Encycl in Neuro Psy

Encyclopedia of Clinical Neuropsychology
Jeffrey S. Kreutzer
John DeLuca
Bruce Caplan
Editors
Encyclopedia of
Clinical Neuropsychology
With 199 Figures and 139 Tables
Editors
Jeffrey S. Kreutzer, PhD, ABPP, FACRM Bruce Caplan, PhD, ABPP
Rosa Schwarz Cifu Professor of Independent Practice
Physical Medicine and Rehabilitation, and Professor of 564 M.O.B. East, 100 E. Lancaster Ave.
Neurosurgery, and Psychiatry Virginia Commonwealth Wynnewood, PA 19096
University Medical Center USA
Department of Physical Medicine and Rehabilitation brcaplan@aol.com
VCU
P.O. Box 980542
Richmond, Virginia 23298-0542
USA
jskreutz@vcu.edu
John DeLuca, PhD, ABPP

Vice President of Research
Kessler Foundation Research Center
1199 Pleasant Valley Way
West Orange, NJ 07052
USA
and
Professor of Physical Medicine and Rehabilitation, and
Neurology and Neuroscience University of Medicine and
Dentistry of New Jersey New Jersey Medical School
jdeluca@kesslerfoundation.org
ISBN 978-0-387-79947-6 e-ISBN 978-0-387-79948-3

Print and electronic bundle ISBN 978-0-387-79949-0
DOI 10.1007/978-0-387-79948-3
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We dedicate the Encyclopedia of Clinical Neuropsychology to our teachers and mentors, the people who taught,
supported, and inspired us to choose and follow careers in the field of clinical neuropsychology.
David Michael Scott, in graduate school, first helped me appreciate the importance of learning about the brain and
nervous system. Alexander Manning taught me about the brain and standardized neuropsychological assessment.
Donald Kausch taught me how to administer and interpret the Halstead Reitan and tests designed by Arthur Benton.
My internship supervisors, Muriel Lezak, Larry Binder, Diane Howieson, Richard Erickson, Orin Bolstad, David Shaw,
and Julian Taplin taught me so much about neuropsychology, how to work with families, and inspired me on to a
career in the field. Jeffrey T. Barth, Ronald Ruff, and Harvey Levin, colleagues I worked with on the Traumatic Coma
Data Bank project, helped me learn neuropsychological research methods, brain injury, and how to be patient and
tenacious. Mitchell Rosenthal, Paul Wehman, and Henry Stonnington taught me about rehabilitation, teamwork,
hope, and how to be practical.
JSK
As an undergraduate, Martin Hahn lit the fire within me regarding an interest in science, which launched my pursuit for
advanced education in brain-behavior relations. Dick Burright taught me about critical thinking in science, through a lot
of hard work. Peter Donovick guided me through graduate school, even when the path ahead seemed unclear, and was
the primary reason I discovered my ultimate career path in human neuropsychology. Keith Cicerone rounded out my
skills and provided me with the finishing touches in my education and training and helped me carve out my particular
niche in neuropsychology, which included both research and clinical activities. Joel DeLisa provided me with the fertile
environment I needed to launch my career in clinical neuropsychology, particularly by supporting a research environ-
ment based on my own interests, approach, and skills, allowing me to pursue a career first dreamed as an undergradu-
ate. Lastly and perhaps most importantly, I dedicate this work to all of my post-doctoral and pre-doctoral trainees, too
numerous to list, who have challenged me professionally and personally, and by far have had the most influence on the
success in my career. I hope that I have had but a fraction of an influence on theirs.
JDL
To: Marcel Kinsbourne, who gets the credit (and blame) for awakening my interest in neuroscience in general and
neuropsychology in particular and exposing me to world-class intellects; Leonard Diller, from whom I learned
the joy of immersion in and struggle to master both the historical and contemporary neuropsychology and
rehabilitation literature; Charles Gibson, who gave me (in retrospect, perhaps unwisely) an inordinate amount of
professional freedom in my first real job; Mitchell Rosenthal, who embodied the lesson I learned from my father,
Jerome Caplan, (Be kind, because everyone you meet is fighting a hard battle) and encouraged me to do the same; and
listed last, but most important, my multifaceted partner, Judy Shechter, my intellectual boomerang colleague and
constant source of entertainment.
BC
Acknowledgement
The conceptualization, compilation, and production of the Encyclopedia of Clinical Neuropsychology spanned more
than four years. We set out to develop a uniquely comprehensive, authoritative, indispensable reference work, and we
are hopeful that our goal has been achieved. We owe an immeasurable debt to the many people who supported us
through the course of the project. Foremost, we are grateful to our families for their enthusiastic support, encourage-
ment, and patience. We are indebted to our cadre of esteemed Associate Editors for helping to develop their sections,
recruit contributors, and ensure the presence of consistently high quality entries. We express our appreciation to the
brilliant group of authors whose efforts form the core of our project. We are immensely indebted to the superb Springer
major reference works team including Janice Stern, Anil Chandy, Lydia Mueller, and Oona Schmid who taught us,
encouraged us, kept us organized and on track, and helped us every step of the way. We are also grateful to our students,
patients, and their families from whom we learned much about facing challenges and the value of being practical.
Jeffrey S. Kreutzer
John DeLuca
Bruce Caplan
Preface
It is doubtful that there is a more rapidly evolving psychological specialty than clinical neuropsychology. Every day,
clinicians are challenged to help patients with a widening variety of cognition-compromising disorders including
traumatic brain injury, vascular conditions, brain tumors, developmental disabilities, psychiatric disturbances, and
neurodegenerative disorders. Some practitioners serve pediatric populations, others treat the elderly, and many serve
general adult populations. Some patients have progressive disorders, while others can achieve substantial improvement
over time. Assessment is typically the starting point, with clinicians addressing a myriad of referral questions, which may
relate to the patients ability to work, return to school, manage personal affairs, drive, live independently, or be
considered eligible for disability benefits. Increasingly, clinicians are involved in civil and forensic proceedings,
contributing to decisions about responsibility, competence, and entitlement to damages for injury.
In fulfilling its clinical mandates, clinical neuropsychology relies strongly on its research base. As a hybrid of
cognitive psychology, neuroscience and clinical psychology, clinical neuropsychology investigations are at the forefront
of translational research in brain-behavior relations. The future of both clinical practice and research lies with our
trainees at all levels undergraduate, doctoral and post-doctoral. Easily accessible and frequently updated knowledge
in clinical neuropsychology provides the foundation for the education and training of our future clinical neuropsychol-
ogists. A fundamental aim of this work has been to provide such a resource and, with the online version, to permit
revision and expansion as the field evolves.
Most neuropsychological reference books focus primarily on assessment, diagnosis, functional neuroanatomy, and
descriptions of various disease entities and their higher cortical consequences. To date, none has been encyclopedic in
format. We see it as a mark of the maturity of the field that such a multi-volume publication is now warranted.
Clinicians, patients, family members, researchers and students all recognize that evaluation and diagnosis is only a
starting point for the treatment and restoration process. Few would be satisfied with an end-product consisting only of a
diagnosis and/or description of the patients cognitive topography. During the past decade, treatment services have
proliferated, and neuropsychologists have been in the forefront of these developments because of their special training
and experience. Neuropsychological clinicians now provide a variety of services in addition to assessment including
psychological counseling, neurobehavioral management, cognitive rehabilitation, family intervention, and vocational
rehabilitation in hospitals and community-based settings. In view of this expanded scope of contemporary practice, we
envisioned an encyclopedia containing information pertinent to these activities.
This encyclopedia will serve as a unified, comprehensive reference for professionals involved in the diagnosis,
evaluation, and rehabilitation of children and adults with neuropsychological disorders. It will also provide students and
scientists with the breadth of knowledge needed to build a scientific basis for interventions and treatment for patients.
We hope Encyclopedia of Clinical Neuropsychology is the first place readers turn for factual, relevant, and comprehen-
sive information to aid in delivering the highest quality services.
September 2010
Jeffrey S. Kreutzer
John DeLuca
Bruce Caplan
Editors
Jeffrey S. Kreutzer, PhD, ABPP, FACRM

Rosa Schwarz Cifu Professor of
Physical Medicine and Rehabilitation, and Professor of
Neurosurgery, and Psychiatry Virginia Commonwealth
University Medical Center
Department of Physical Medicine and Rehabilitation
VCU
P.O. Box 980542
Richmond, Virginia 23298-0542
USA
jskreutz@vcu.edu
John DeLuca, PhD, ABPP

Vice President of Research
USA
and
Professor of Physical Medicine and Rehabilitation,
and Neurology and Neuroscience
University of Medicine and Dentistry of New Jersey
New Jersey Medical School
jdeluca@kesslerfoundation.org
Bruce Caplan, PhD, ABPP

Independent Practice
564 M.O.B. East, 100 E. Lancaster Ave.
Wynnewood, PA 19096
USA
brcaplan@aol.com
Associate Editors
Cristy Akins Ronald A. Cohen

Mercy Family Center Department of Psychiatry and Human Behavior
110 Vetrans Memorial Blvd The Miriam Hospital
Metarie, LA 70005 Brown University
USA 164 Summit Ave
cristy.akins@gmail.com Providence, RI 2906
USA
Carol L. Armstrong RCohen@lifespan.org
The Childrens Hospital of Philadelphia
Neuro-Oncology/Neuropsychology
3535 Market Street, Ste. 1409-1410 John C. Courtney
Philadelphia, Pennsylvania Department of Psychology
USA Childrens Hospital of New Orleans
armstrongc@email.chop.edu 200 Henry Clay Avenue
New Orleans, LA 70118
Shane S. Bush USA
Long Island Neuropsychology, P.C. drjohncc@gmail.com
290 Hawkins Avenue, Suite B
Lake Ronkonkoma, NY 11779
Rik Carl DAmato
USA
University of Macau
drbush@gmail.com
Santa Clara Valley Medical Center
Faculty of Social Sciences and Humanities
Tamara Bushnik
229 Tai Fung Building
Rusk Institute for Rehabilitation Medicine
Taipa, Macau SAR
NYU Langone Medical Center
China
400 East 34th Street, RR115A
rdamato@umac.mo
New York, NY 10016
USA
Tamara.Bushnik@nyumc.org Roberta DePompei
University of Akron
Gordon Chelune Department of Speech Language, Pathology and
Center of Alzheimers Care, Imaging and Research Audiology
University of Utah Akron, OH 44325-3001
650 Komas Dr., Ste 106A USA
Salt Lake City, UT 84108 rdepom1@uakron.edu
USA
gordon.chelune@hsc.utah.edu
Janet E. Farmer
Nancy D. Chiaravalloti University of Missouri-Columbia
Department of Physical Medicine and Rehabilitation Thompson Center for Autism and Neurodevelopmental
UMDNJ-New Jersey Medical School Disorders
1199 Pleasant Valley Way 300 Portland Street, Suite 110
West Orange, NJ 7052 Columbia, MO 65211
USA USA
nchiaravalloti@kesslerfoundation.org farmerje@health.missouri.edu
xiv Associate Editors
Robert G. Frank James F. Malec

College of Public Health Rehabilitation Hospital of Indiana
Kent State University 4141 Shore Drive
P. O. Box 5190 Indianapolis, IN 46254
Kent, OH 44242-0001 USA
USA jim.malec@rhin.com
rgfrank@kent.edu
Paul Malloy
Michael Franzen
The Warren Alpert Medical School of Brown University
Allegheny Neuropsychiatric Institute
Butler Hospital
Allegheny General Hospital
345 Blackstone Blvd.
4 Allegheny Center
Providence, RI 2906
Pittsburgh, PA 15212
USA
USA
PMalloy@Butler.org
mfranzen@wpahs.org
Robert L. Heilbronner John E. Mendoza

Chicago Neuropsychology Group SE LA Veterans Healthcare System
333 N. Michigan Avenue, #1801 Department of Psychiatry and Neurology
Chicago, IL 60601 Tulane University Medical Center
USA 3928 S. Inwood Ave.
rheilbronn@aol.com New Orleans, LA 70131
r-heilbronner@northwestern.edu USA
John.Mendoza2@va.gov
Susan K. Johnson
Department of Psychology
University of North Carolina At Charlotte Randall E. Merchant
9201 University City Blvd. Virginia Commonwealth University Medical Center
Charlotte, NC 28223-0001 Box 980709 MCV Station
USA Richmond, VA 23298-0709
skjohnso@uncc.edu USA
rmerchan@vcu.edu
Douglas I. Katz
Boston University School of Medicine
Sarah A. Raskin
Braintree Rehabilitation Hospital
Department of Psychology and Neuroscience Program
250 Pond Street
Trinity College
Braintree, MA 2184
Hartford, CT 6106
USA
USA
dkatz@bu.edu
Sarah.Raskin@trincoll.edu
Stephanie A. Kolakowsky-Hayner
Director, Rehabilitation Research Stephanie Reid-Arndt
Santa Clara Valley Medical Center School of Health Professions - Health Psychology
Rehabilitation Research Center Ellis Fischel Cancer Center
751 South Bascom Ave. University of Missouri-Columbia
San Jose, CA 95128 Columbia, MO 65211
USA USA
Stephanie.Hayner@hhs.sccgov.org reidarndts@health.missouri.edu
Associate Editors xv
Elliot J. Roth Lyn Turkstra

Feinberg School of Medicine University of Wisconsin, Madison
Physical Medicine and Rehabilitation 7225 Medical Sciences Center
Northwestern University 1300 University Avenue
345 E. Superior Madison, WI 53706-1532
Chicago, IL 60611 USA
USA lsturkstra@wisc.edu
ejr@northwestern.edu
eroth@ric.org Nathan D. Zasler
Concussion Care Centre of Virginia, Ltd.
Bruce Rybarczyk 3721 Westerre Parkway, Suite B
Department of Psychology Richmond, VA 23233
Virginia Commonwealth University USA
Box 842018 nzasler@cccv-ltd.com
Richmond, VA 23284-2018
USA
bdrybarczyk@vcu.edu
Anthony Y. Stringer
Department of Rehabilitation Medicine
Emory University
1441 Clifton Road NE
Atlanta, GA 30322
USA
Anthony.Stringer@emoryhealthcare.org
List of Contributors
GALYA ABDRAKHMANOVA BRITTANY J. ALLEN
Department of Pharmacology Department of Health Psychology, DC 116.88
Virginia Commonwealth University University of Missouri, Columbia
1112 E. Clay Street, P.O. Box 980524 One Hospital Drive
Richmond, VA 23298-0565 Columbia, MO 65212
USA USA
gabdrakhmano@vcu.edu allenbj@health.missouri.edu
THOMAS M. ACHENBACH
JASON VAN ALLEN
University of Vermont
Clinical Child Psychology Graduate Program
2 Colchester Ave.
University of Kansas
Burlington, VT 05405-0134
1000 Sunnyside Ave
USA
Lawrence, KS 66045
thomas.achenbach@uvm.edu
USA
jvanallen@ku.edu
RUSSELL ADAMS
Department of Psychiatry and Behavioral Science
University of Oklahoma Health Sciences Center KARIN ALTERESCU
P.O. Box 26901 Neuropsycholgy Program
Oklahoma City, OK 73190 Queens College and The Graduate Center of the City
USA University of New York
russell-adams@ouhsc.edu Flushing, NY 11367
USA
karin.alterescu@yahoo.com
CRISTY AKINS
Mercy Family Center
110 Vetrans Memorial Blvd AKSHAY AMARANENI
Metarie, LA 70005 Department of Rehabilitation Medicine
USA Emory University
cristy.akins@gmail.com Atlanta, GA 30322
USA
akshay982@gmail.com
AMY ALDERSON
Emory University/Rehabilitation Medicine
1441 Clifton Road
MELISSA AMICK
Atlanta, GA 30322
Department of Psychiatry and Human Behavior
USA
Brown University
amyalderson@gmail.com
Providence, RI 02912
USA
DANIEL N. ALLEN and
Department of Psychology Department of Medical Rehabilitation
University of Nevada Las Vegas Memorial Hospital of Rhode Island
Box 455030; 4505 Maryl and Parkway 111 Brewster Street
Las Vegas, NV 89154-5030 Pawtucket, RI 02860
USA USA
daniel.allen@unlv.edu Melissa_Amick@brown.edu
xviii List of Contributors
HEATHER ANDERSON AMY J. ARMSTRONG

Department of Neurology Department of Rehabilitation Counseling
University of Kansas School of Medicine Virginia Commonwealth University
3599 Rainbow Blvd., MS 2012 P.O. Box 980330
Kansas City, KS 66160 Richmond, VA 23298
USA USA
handerson3@kumc.edu ajarmstr@vcu.edu
GLENN S. ASHKANAZI
STEVEN W. ANDERSON Department of Clinical and Health Psychology
University of Iowa Hospitals and Clinics University of Florida-College of Public Health and
0080-C RCP, 200 Hawkins Drive Health Professions
Iowa City, Iowa 52242 P.O. Box 100165
USA Gainesville, FL 32610-0165
steven-anderson@uiowa.edu USA
gashkana@phhp.ufl.edu
KEVIN M. ANTSHEL
STEPHANIE ASSURAS
Department of Psychiatry and Behavioral Sciences
Neuropsychology Program
Upstate Medical University
Queens College and The Graduate Center of the City
750 East Adams Street
University of New York
Syracuse, NY 13210
Flushing, NY 11367
USA
USA
and
stephassuras@hotmail.com
State University of New York - Upstate Medical
University
1752 Greenspoint Court Syracuse
JANE AUSTIN
Mount Pleasant, SC 29466
USA
William Paterson University
antshelk@upstate.edu
300 Pompton Road
Wayne, NJ 7470
USA
JENNIFER ANN NISKALA APPS austinj@wpunj.edu
Department of Psychiatry & Behavioral Medicine
Childrens Hospital of Wisconsin/Medical College of
Wisconsin BRADLEY AXELROD
9000 W Wisconsin Ave Ste B510 John D. Dingell VA Medical Center
Milwaukee, WI 53226 Psychology Section
USA 4646 John R Street
JApps@chw.org Detroit, MI 48201
USA
Bradley.Axelrod@va.gov
CAROL L. ARMSTRONG
The Childrens Hospital of Philadelphia GLEN P. AYLWARD
Neuro-Oncology/Neuropsychology SIU School of Medicine-Pediatrics
3535 Market Street, Ste. 1409-1410 P.O. Box 19658
Philadelphia, PA 19104 Springfield, IL 62794-9658
USA USA
armstrongc@email.chop.edu gaylward@siumed.edu
List of Contributors xix
SAMANTHA BACKHAUS ERIKA M. BARON

Neuropsychology Rusk Institute of Rehabilitative Medicine Psychology
Rehabilitation Hospital of Indiana Service Pediatrics
4141 Shore Dr. New York University Langone Medical Center
Indianapolis, IN 46254 550 First Avenue
USA New York, NY 10016
samantha.backhaus@rhin.com USA
Erika.Baron@nyumc.org
SANDRA BANKS
Department of Psychiatry
Allegheny General Hospital WILLIAM B. BARR
Four Allegheny Center New York University School of Medicine
Pittsburgh, PA 15212-5234 Medicical Center, Comprehensive Epilepsy Center
USA 403 East 34th Street, EPC - 4th Floor
sbanks@wpahs.org New York, NY 10016
USA
JAMES H. BANOS william.barr@med.nyu.edu
University of Alabama at Birmingham
RUSSELL M. BAUER
619 19th Street South; SRC 530
Department of Clinical and Health Psychology
Birmingham, AL 35249-7330
University of Florida
USA
P.O. Box 100165 Health Science Center
banos@uab.edu
Gainesville, FL 32610-0165
USA
RUSSELL BARKLEY
rbauer@hp.ufl.edu
State University of New York - Upstate Medical
University
1752 Greenspoint Ct.
JESSICA BEAN
Mt. Pleasant, SC 29466
USA
University of Connecticut
DrBarkley@russellbarkley.org
406 Babbidge Road, Unit 1020
Storrs, CT 6269
MARK S. BARON
USA
Neurology
jessica.bean@huskymail.uconn.edu
Virginia Commonwealth University
Southeast/Richmond Veterans Affairs Parkinsons
Disease Research, Education and Clinical Center PELAGIE M. BEESON
(PADRECC) Department of Speech, Language, & Hearing Sciences
Box 980599 The University of Arizona
Richmond, VA Tucson, Arizona 85721-0071
USA USA
mbaron@mcvh-vcu.edu pelagie@u.arizona.edu
IDA SUE BARON

Director of Neuropsychology JAY BEHEL
Inova Fairfax Hospital for Children Department of Behavioral Sciences
Falls Church, VA Rush University Medical Center
10116 Weatherwood Ct. 1653 W. Congress Parkway
Potomac, MD 20854 Chicago, IL 60612
USA USA
ida@isbaron.com jay_behel@rush.edu
xx List of Contributors
STACY BELKONEN JOHN BIGBEE

Department of Rehab Medicine Anatomy and Neurobiology
Mount Sinai School of Medicine Virginia Commonwealth University
5 East 98th Street Box 980709
New York, NY 10029 Richmond, VA 23284
USA USA
Stacy.Belkonen@mountsinai.org jbigbee@vcu.edu
BRIAN D. BELL ERIN D. BIGLER

Department of Neurology Department of Psychology
University of Wisconsin Brigham Young University
600 Highland Ave. 1001 SWKT, P.O. Box 25543
Madison, WI 53792 Provo, UT 84602-5543
USA USA
bell@neurology.wisc.edu erin_bigler@byu.edu
ANDREW BELL NATALIE C. BLEVINS

Department of Anatomy and Neurobiology Department of Psychiatry
Virginia Commonwealth University Adult Psychiatry Clinic and Study Center
1101 East Marshall Street Indiana Universtiy Hospital
Richmond, VA 23298-0709 550 N. University Blvd. Ste 3124
USA Indianapolis, IN 46202
lloydabell4@gmail.com USA
ncblevin@iupui.edu
H. ALLISON BENDER
Neuropsychology
MICHELLE L. BLOCK
Queens College CUNY
Anatomy and Neurobiology
65-30 Kissena Blvd
Flushing, NY 11367
Box 980709
USA
Richmond, VA 23284
and
USA
New York University Langone Medical Center
MBlock@vcu.edu
403 East 34th Street
New York, NY 10016
USA DOUG BODIN
heidibender@aol.com Department of Pediatrics
Nationwide Childrens Hospital and The Ohio State
University
DANIEL B. BERCH
700 Childrens Drive
Child Development and Behavior Branch
Columbus, OH 43205
National Institute of Child Health and Human
USA
Development, NIH
doug.bodin@nationwidechildrens.org
6100 Executive Blvd., Room 4B05
Bethesda, MD 20892-7510
USA ANGELA M. BODLING
and Center for Health Care Quality
Curry School of Education University of MissouriColumbia
University of Virginia One Hospital Drive
Charlottesville, VA 229044260 Columbia, MO 65212
USA USA
dberch@virginia.edu bodlinga@health.missouri.edu
List of Contributors xxi
ROBERT BOLAND ISABELLE BOURDEAU

Department of Psychiatry and Human Behavior Research Centre
The Warren Alpert Medical School of Brown University CHUM, Hotel-Dieu
Butler Hospital 3850, rue Saint-Urbain
Blackstone Blvd. Montreal, QC H2W 1T7
Providence, RI 2906 Canada
USA isabelle.bourdeau@umontreal.ca
robert_boland_1@brown.edu
ALYSSA BRAATEN
JOHN G. BORKOWSKI 1441 Clifton Road, Room 210
Department of Psychology Atlanta, GA 30322
University of Notre Dame USA
118 Haggar Hall alyssabraaten@hotmail.com
Notre Dame, IN 46556
USA LISA A. BRENNER
psych@nd.edu VISN 19 MIRECC
1055 Clermont Street
Denver, CO 80220
USA
JOAN C. BOROD
lisa.brenner@va.gov
ANDREW BRODBELT
Consultant Neurosurgeon
6530 Kissena Blvd.
The Walton Centre for Neurology and Neurosurgery
Flushing, NY 11367
Lower Lane
USA
Liverpool L9 7LJ
and
UK
Mount Sinai School of Medicine
abrodbelt@doctors.org.uk
One Gustave L. Levy Place
New York, NY 10029-6574
JOHN BROWN
USA
Medical College of Georgia
joanborod@optonline.net
1120 15th Street
Augusta, GA 30912
USA
BETH BOROSH johnhbrown@mac.com
Cognitive/Behavioral Neurology Center
Northwestern Feinberg School of Medicine MARGARET BROWN
675 N. Street Clair, Galter 20-100 Mount Sinai School of Medicine
Chicago, IL 60611 272 West 107th Street, Apt. 7A
b-borosh@northwestern.edu USA
margaretbrown@gmail.com
DAWN E. BOUMAN SARAH S. CHRISTMAN BUCKINGHAM

Medical Psychology and Neuropsychology Department of Communication Sciences and Disorders
Drake Center The University of Oklahoma Health Sciences Center
151 W. Galbraith Road 825 NE 14th Street, P.O. Box 26901
Cincinnati, OH 45216-1096 Oklahoma City, OK 73126-0901
USA USA
Dawn.Bouman@healthall.com Sarah-Buckingham@ouhsc.edu
xxii List of Contributors
HUGH W. BUCKINGHAM MERYL A. BUTTERS

Sciences & Disorders and Interdepartmental Program in University of Pittsburgh
Linguistics School of Medicine, WPIC
Louisiana State University 3811 OHara Street
136B Coates Hall Pittsburgh, PA 15213
Baton Rouge, LA 70803-2606 USA
USA ButtersMA@upmc.edu
hbuck@lsu.edu
JEFFREY M. BURNS DEBORAH A. CAHN-WEINER

Department of Neurology UCSF Epilepsy Center
University of Kansas School of Medicine University of California
3901 Rainbow Boulevard 400 Parnassus Avenue
Kansas City, KS 66160 San Francisco, CA 94143-0138
USA USA
jburns2@kumc.edu Deborah.Cahn-Weiner@ucsf.edu
THOMAS G. BURNS
CHARLES D. CALLAHAN
Neuropsychology
Memorial Medical Center
Childrens Healthcare of Atlanta
701 N. 1st Street
1001 Johnson Ferry Road NE
Springfield, IL 62781
Atlanta, GA 30342
USA
USA
Callahan.Chuck@mhsil.com
thomas.burns@choa.org
SHANE S. BUSH
BRUCE CAPLAN
Long Island Neuropsychology, P.C
290 Hawkins Avenue, Suite B
564 M.O.B. East
Lake Ronkonkoma, NY 11779
100 E. Lancaster Ave.
USA
Wynnewood, PA 19096
drbush@gmail.com
USA
brcaplan@aol.com
TAMARA BUSHNIK
Rusk Institute for Rehabilitation Medicine
NYU Langone Medical Center NOELLE E. CARLOZZI
400 East 34th Street, RR115A Outcomes & Assessment Research Laboratory
New York, NY 10016 Kessler Foundation Research Center
USA 1199 Pleasant Valley Way
Tamara.Bushnik@nyumc.org West Orange, NJ 7052
USA
ncarlozzi@kesslerfoundation.org
MELISSA BUTTARO
Brown University, The Miriam Hospital
164 Summit Ave HELEN M. CARMINE
Providence, RI 2906 ReMed
USA Paoli, PA
MButtaro@lifespan.org USA
List of Contributors xxiii
DOMINIC A. CARONE COLBY CHLEBOWSKI

University Hospital Neuropsychology Assessment Department of Psychology
Program University of Connecticut
SUNY Upstate Medical University 406 Babbidge Road, Unit 1020
750 East Adams Street Storrs, CT 6269
Syracuse, NY 13210 USA
USA colby.chlebowski@uconn.edu
caroned@upstate.edu
WOON CHOW
Anatomy & Neurobiology
JENNIFER CASS Virginia Commonwealth University
Department of Pediatrics Box 980709
Nationwide Childrens Hospital and The Ohio State Richmond, VA
University USA
700 Childrens Drive wchow@vcu.edu
Columbus, OH 43205
USA
jennifer.cass@nationwidechildrens.org SHAWN E. CHRIST
University of Missouri
25 McAlester Hall
Columbia, MO 65211-2500
AMIRAM CATZ
USA
DEPARTMENT OF SPINAL
christse@missouri.edu
LOEWENSTEIN REHABILITATION HOSPITAL
278 ACHVZA STREET
RAANANA 43100
SEVERN B. CHURN
ISRAEL
Neurology
AND
TEL-AVIV UNIVERSITY
Box 980599, MCV Station
TEL-AVIV
ISRAEL
USA
amcatz@post.tau.ac.il
schurn@vcu.edu
JESSICA CHAIKEN ANGELA HEIN CICCIA

Media and Public Education Manager Case Western Reserve University
National Rehabilitation Information Center (NARIC) Department of Communication Sciences
8201 Corporate Drieve, Suite 600 11206 Euclid Avenue Room 410
Landover, MD 20785 Cleveland, OH 44106-7154
USA USA
jchaiken@heitechservices.com amh11@case.edu
URAINA CLARK
SANDY SUT IENG CHEANG The Warren Alpert Medical School of Brown University
University of Macau The Miriam Hospital
Department of Psychology Neuropsychology, The CORO Center, 3rd Floor
Av. Padre Tomas Pereira 1 Hoppin Street, Suite 317
Taipa, Macau SAR Providence, RI 2903
China USA
sandycheang@ymail.com UClark@lifespan.org
xxiv List of Contributors
MARY CLARK ADAM CONLEY

University of Missouri Virginia Commonwealth University Medical Center
300 Portland Street, Suite 110 Richmond, VA 23284
Columbia, MO 65211 USA
USA AConley@mcvh-vcu.edu
clarkmj@health.missouri.edu
W. CARL COOLEY
ELAINE CLARK
Medical Director
Department of Educational Psychology
Center for Medical Home Improvement
University of Utah
Crotched Mountain Foundation and Rehabilitation
1705 Campus Center Drive, #327
Center
Salt Lake City, UT 84112-9255
1 Verney Drive
USA
Concord, NH 3047
Elaine.Clark@ed.utah.edu
USA
carl.cooley@crotchedmountain.org
RONALD A. COHEN
The Miriam Hospital PATRICK COPPENS
Brown University SUNY Plattsburgh
164 Summit Ave Communication Disorders and Sciences
Providence, RI 2906 101 Broad Street
USA Plattsburgh, NY 12901
RCohen@lifespan.org USA
patrick.coppens@plattsburgh.edu
MORRIS J. COHEN
Neurology, Pediatrics & Psychiatry STEPHEN CORREIA
Director, Pediatric Neuropsychology, Medical College of Neuropsychology
Georgia Butler Hospital
and Veterans Affairs Medical Center
BT-2601 Childrens Medical Center Warren Alpert Medical School of Brown University
1446 Harper Street 345 Blackstone Blvd.
Augusta, Georgia 30912 Providence, RI 2906
USA USA
mcohen@mail.mcg.edu scorreia@butler.org
RAY COLELLO
JOYCE A. CORSICA
Department of Behavioral Sciences
Rush University Medical Center
Box 980709
1653 W. Congress Parkway
Richmond, VA
Chicago, IL 60612
USA
USA
rcolello@vcu.edu
Joyce_A_Corsica@rsh.net
GRACE COMBS
Applied Psychology and Counselor Education H. BRANCH COSLETT
Department of Psychology, FSL Department of Neurology
University of Northern Colorado University of Pennsylvania, HUP
McKee 248, Box 131 3400 Spruce Street
Greeley, CO 80631 Philadelphia, PA 19104
USA USA
graciecombs@gmail.com hbc@mail.med.upenn.edu
List of Contributors xxv
JOHN C. COURTNEY ANTHONY CUVO

Department of Psychology Center for Autism Spectrum Disorders
Childrens Hospital of New Orleans Southern Illinois University, Mail Code 6607
200 Henry Clay Avenue Carbondale, LL 62901
New Orleans, LA 70118 USA
USA acuvo@siu.edu
drjohncc@gmail.com
RIK CARL DAMATO

DAVID R. COX University of Macau
Neuropsychology & Rehabilitation Consultants, PC Santa Clara Valley Medical Center
600 Market Street Suite 301 Faculty of Social Sciences and Humanities
Chapel Hill, NC 27516 229 Tai Fung Building
USA Taipa, Macau SAR
drcox@iag.net China
rdamato@umac.mo
LAURA CRAMER-BERNESS
KRISTEN DAMS-OCONNOR
Department of psychology
300 Pompton Road
5 East 98th Street Rm B-14
Wayne, NJ 7470
New York, NY 10029-6574
USA
USA
bernessl@wpunj.edu
kristen.dams-oconnor@mountsinai.org
JUDY CREIGHTON
ANDREW S. DAVIS
Department of Educational Psychology
Ball State University
Teachers College Room 524
Flushing, NY
Muncie, IN 47306
USA
USA
judybarry01@gmail.com
davis@bsu.edu
JACQUELINE L. CUNNINGHAM SCOTT L. DECKER

The Childrens Hospital of Philadelphia Counseling and Psychological Services
Department of Psychology, CSH 021 Georgia State University
34th Street and Civic Center Blvd. P.O. Box 3980
Philadelphia, PA 19104-4399 Atlanta, GA 30302-3980
USA USA
cunningham@email.chop.edu cpssld@langate.gsu.edu
SEAN CUNNINGHAM NICK A. DEFILIPPIS

Department of Educational Psychology Georgia School of Professional Psychology
University of Utah Argosy University
1705 Campus Center Drive, #327 980 Hammond Drive NE Bldg. 2, Suite 100
Salt Lake City, UT 84112-9255 Atlanta, GA 30328
USA USA
sean.cunningham@utah.edu ndefilippis@argosy.edu
xxvi List of Contributors
KATHLEEN DEIDRICK BRUCE J. DIAMOND

Department of Health Psychology Department of Psychology
Thompson Center for Autism and Neurodevelopmental William Paterson University
Disorders 300 Pompton Road
University of Missouri-Columbia Wayne, NJ 07470
300 Portland Street, Suite 110 USA
Columbia, MO 65202 DiamondB@wpunj.edu
USA
deidrickk@health.missouri.edu
AIMEE DIETZ
Communication Sciences and Disorders
DEAN C. DELIS University of Cincinnati Hastings and Williams French
University of California Building
San Diego School of Medicine, San Diego Veterans 3202 Eden Avenue (Mail Location 0379)
Affairs Healthcare System Cincinnati, OH 45267-0379
SDVAMC, 3350 La Jolla Village Drive USA
La Jolla, CA 92161 dietzae@ucmail.uc.edu
USA
ddelis@ucsd.edu
MARCEL DIJKERS
JOHN DELUCA
One Gustave Levy Place, Box 1240
Neuropsychology and Neuroscience Laboratory
New York, NY 10029-6574
USA
Marcel.Dijkers@mountsinai.org
USA
jdeluca@kesslerfoundation.org CARL B. DODRILL
Department of Neurology
University of Washington School of Medicine
GEORGE J. DEMAKIS
4488 West Mercer Way
Seattle, WA 98040
University of North Carolina Charlotte
USA
9201 University City Blvd
carl@dodrill.net
Charlotte, NC 28223
USA
Gdemakis@uncc.edu PETER DODZIK
Clinical Psychology & Behavioral Sciences
THESLEE JOY DEPIERO American School of Professional Psychology-
Boston University School of Medicine Schaumburg
Braintree Rehabilitation Hospital Argosy University
250 Pond Street Schaumburg Campus
Boston, MA 2184 999 Plaza Drive, Suite 800
USA Schaumburg, IL 60173
tjdepiero@aol.com USA
pdodzik@edmc.edu
ROBERTA DEPOMPEI
University of Akron JACOBUS DONDERS
Department of Speech Language, Pathology and Mary Free Bed Rehabilitation Hospital
Audiology 235 Wealthy SE
Akron, OH 44325-3001 Grand Rapids, MI 49503-5299
USA USA
rdepom1@uakron.edu jacobus.donders@maryfreebed.com
List of Contributors xxvii
KERRY DONNELLY JEFF DUPREE

VA WNY Healthcare System Anatomy & Neurobiology
University of Buffalo (SUNY) Virginia Commonwealth University
Behavioral Health Careline (116B) Box 980709
3495 Bailey Avenue Richmond, VA
Buffalo, NY 14215 USA
USA jldupree@vcu.edu
kerry.donnelly@va.gov
MOIRA C. DUX
LAUREN R. DOWELL
Rosalind Franklin School of Medicine
Laboratory for Neurocognitive and Imaging Research
University of Maryland Medical Center/Baltimore VA
Kennedy Krieger Institute
226 S. Ann Street
1750 E. Broadway, 3rd Floor
Baltimore, MD 21231
Baltimore, MD 21205
USA
USA
moira.dux@students.rosalindfranklin.edu
dowell@kennedykrieger.org
LINDSEY DUCA NATASHA K. EADDY

Spinal Cord Injury Clinic Neurorehabilitation Specialists
VA Palo Alto Health Care System Baylor College of Medicine
3801 Miranda Ave. (128) Brain Injury and Stroke Program Fellow
Palo Alto, CA 94304 Houston, TX
USA USA
duca@Stanford.edu nkeaddy@aol.com
ALEKSEY DUMER
Queens College and The Graduate Center of the City ANGELA EASTVOLD
University of New York Department of Psychology
NSB A340 University of Utah
6530 Kissena Blvd. Salt Lake City, UT 84112-0251
Flushing, NY 11367 USA
USA angela.eastvold@psych.utah.edu
a.dumer@gmail.com
DAWN M. EHDE
MARY DUNKLE
National Organization for Rare Disorders (NORD)
University of Washington
55 Kenosia Avenue, P.O. Box 1968
Seattle, WA 98195
Danbury, CT 06813-1968
USA
USA
ehde@u.washington.edu
mdunkle@rarediseases.org
KARI DUNNING ERIN E. EMERY

Department of Rehabilitation Sciences Department of Behavioral Sciences
University of Cincinnati Rush University Medical Center
P.O. Box 670394 1653 W. Congress Parkway
Cincinnati, OH 45267-0394 Chicago, IL 60612
USA USA
DUNNINKK@ucmail.uc.edu Erin_Emery@rush.edu
xxviii List of Contributors
ALLISON S. EVANS AMANDA FAULHABER

Department of Pediatrics/Deptartment of Psychiatry William Paterson University
and Human Behavior Department of Psychology, Program in Clinical &
Memorial Hospital of RI Counseling Psychology
Neurodevelopmental Center 300 Pompton Road
555 Prospect Street Wayne, NJ 07470
Pawtucket, RI 2860 USA
USA Psychgrad@wpunj.edu
Allison_Schettini@brown.edu
DEBORAH A. FEIN
DANIEL ERIK EVERHART
406 Babbidge Raod, Unit 1020
Storrs, CT 06269-1020
Eastern Carolina University
USA
Rawl Bldg, East 5th Street
deborah.fein@uconn.edu
Greenville, NC 27858
USA
everhartd@ecu.edu
LEILANI FELICIANO
University of Colorado at Colorado Springs
NATHAN EWIGMAN Colorado Springs, CO
Department of Clinical and Health Psychology USA
University of Florida lfelicia@uccs.edu
Gainesville, FL 32611
USA
newigman@gmail.com WARREN L. FELTON
Neurology
Virginia Commonwealth University Medical Center
NATHALIE DE FABRIQUE Box 980599
Cook County Department of Corrections Richmond, VA
750 N. Dearborn Street, #1504 USA
Chicago, IL 60610 wfeltoniii@mcvh-vcu.edu
USA
ndefabrique@aol.com
ERIC M. FINE
University of California, San Diego
School of Medicine
JOSEPH E. FAIR
San Diego Veterans Affairs Healthcare System
Brigham Young University
1616 9th Ave. Apt. #23
2062 Dakota Ave
La Jolla, CA 92101
Provo, UT 84606
USA
USA
fine.eric@gmail.com
jfairmail@gmail.com
JESSICA FISH
JAELYN R. FARRIS Medical Research Council Cognition and Brain Sciences
Department of Psychology Unit
University of Notre Dame 15 Chaucer Road
Notre Dame, IN 46556 Cambridge, CB2 7EF
USA UK
jfarris@nd.edu jessica.fish@mrc-cbu.cam.ac.uk
List of Contributors xxix
JULIE TESTA FLAADA Winthrop University Hospital

2431 Wilshire Lane NE State University of New York, Stony Brook School of
Rochester, MN 55906 Medicine
USA Mineola, NY
julietestaflaada@gmail.com USA
nancy.foldi@qc.cuny.edu
JENNIFER FLEMING HELENE FORGET

School of Health and Rehabilitation Sciences Universite du Quebec en Outaouais
The University of Queensland Departement de psychoeducation et de psychologie
St Lucia, Brisbane, Queensland 4072 Gatineau, QC
Australia Canada
j.fleming@uq.edu.au helene.forget@uqo.ca
BONNY J. FORREST
FAYE VAN DER FLUIT San Diego Center for Children
University of Wisconsin-Milwaukee 311 4th Avenue Suite 609
Department of Psychology, Gerland Hall San Diego, CA 92111
P.O. Box 413 USA
Milwaukee, WI 53201-0413 bforrest@centerforchildren.org
USA
vanderf2@uwm.edu MICHAEL A. FOX
JAMES R. FLYNN Box 980709
Department of Politics Richmond, VA
The University of Otago USA
P.O. Box 56 mafox@vcu.edu
Dunedin
New Zealand LISA M. FOX
jim.flynn@stonebow.otago.ac.nz Rusk Institute of Rehabilitative Medicine
NYU Langone Medical Center, Psychology Department
400 E. 34th Street
KRISTIN JOAN FLYNN PETERS New York, NY 10016
Department of Health Psychology USA
University of Missouri Health Care, School of Health lisa.fox@nyumc.org
Professions
One Hospital Dr., DC 116.88 LAURA L. FRAKEY
Columbia, MO 65212 Memorial Hospital of Rhode Island and Alpert Medical
USA School of Brown University
flynnpetersk@health.missouri.edu Pawtucket, RI
USA
lfrakey@gmail.com
NANCY S. FOLDI
Psychology Program ROBERT G. FRANK
Queens College and The Graduate Center of the City College of Public Health
University of New York Kent State University
65-30 Kissena Blvd P.O. Box 5190
Flushing, NY 11367 Kent, OH 44242-0001
USA USA
and rgfrank@kent.edu
xxx List of Contributors
MICHAEL FRANZEN PAMELA G. GARN-NUNN

Allegheny Neuropsychiatric Institute Professor of Speech-Language Pathology
Allegheny General Hospital University of Akron
4 Allegheny Center Room 181, Polsky Building, 225 South Main Street
Pittsburgh, PA 15212 Akron, OH 44325-3001
USA USA
mfranzen@wpahs.org garnnun@uakron.edu
KELLI WILLIAMS GARY

SARAH FREEMAN
PM&R Neuropsychology and Rehab Psychology
San Jose Unified School District
Services
210 Tyler Ave.
San Jose, CA 95117
VCU Health Systems/MCV Hospitals and Physicians
USA
1200 E. Broad Street, Room 3-102, Box 980542
sarahfreeman08@gmail.com
Richmond, VA 23298
USA
williamsjonk@vcu.edu
KATHLEEN L. FUCHS
University of Virginia Health System BRANDON E. GAVETT
P.O. Box 800394 Department of Neurology
Charlottesville, VA 22908-0394 Boston University School of Medicine
USA Boston, MA 02118-2526
klf2n@virginia.edu USA
begavett@bu.edu
TERISA GABRIELSON HELEN M. GENOVA

Department of Educational Psychology Neuropsychology and Neuroscience Laboratory
University of Utah Kessler Foundation Research Center
1705 Campus Center Drive, #327 300 Executive Drive, Suite 010
Salt Lake City, UT 84112-9255 West Orange, NJ 7052
USA USA
Terisa.P.Gabrielsen@utah.edu hgenova@kmrrec.org
GLEN GETZ
SHERRI GALLAGHER
Flagstaff Unified School District
2910 N. Prescott Road
Four Allegheny Center
Flagstaff, AZ 86001
Pittsburgh, PA 15212
USA
USA
sherrigallagher@hotmail.com
ggetz@wpahs.org
FRANK J. GALLO GERARD A. GIOIA

University of Wisconsin-Milwaukee George Washington University School of Medicine
Department of Psychology Childrens National Medical Center
P.O. Box 413 14801 Physicians Lane, Suite 173
Milwaukee, WI Rockville, MD 20850
USA USA
fjgallo@uwm.edu ggioia@cnmc.org
List of Contributors xxxi
ELIZABETH LOUISE GLISKY BRAM GOLDSTEIN

Department of Psychology Hoag Hospital Cancer Center
University of Arizona, Department of Gynecologic Oncology
1503 East University Blvd/ P.O. Box 210068 351 Hospital Road, Ste. 507
Tucson, AZ 85721 Newport Beach, CA 92663
USA USA
glisky@u.arizona.edu Bram@gynoncology.com
ASSAWIN GONGVATANA
EMILIE GODWIN
Neuropsychology
Brown University
1223 East Marshall Street
The Miriam Hospital, Coro Bldg. 3-West
One Hoppin Street
USA
eegodwin@vcu.edu
USA
assawin@mac.com
GARY GOLDBERG
Virginia Commonwealth University School of Medicine/ DANIEL GOOD
Medical College of Virginia Brigham Young University
Richmond, VA 395 North 100 East
USA Provo, UT 84062
gary.goldberg.md@gmail.com USA
dag1978@hotmail.com
MYRON GOLDBERG ROBERT M. GORDON

Department of Rehabilitation Medicine Rusk Institute of Rehabilitation Medicine
University of Washington Medical Center New York University Langone Medical Center
1959 NE Pacific Street, Box 356490 400 East 34th Street, Room 507A-RR
Seattle, WA 98195-6450 New York, NY 10016
USA USA
goldbm@u.washington.edu Robert.Gordon@nyumc.org
KIMBERLY A. GORGENS
DIANE CORDRY GOLDEN
Graduate School of Professional Psychology
Association of Assistive Technology Act Programs
University of Denver, MSC 4104
P.O. Box 32
2450 South Vine Street, MSC 4101
Delmar, NY 12054
Denver, CO 80208
USA
USA
dianegolden@sbcglobal.net
kgorgens@du.edu
CHARLES J. GOLDEN JANET GRACE

Center for Psychological Studies Medical Rehabilitation
Nova Southeastern University Memorial Hospital of RI
3301 College Avenue 111 Brewster Street
Fort Lauderdale, FL 33314 Pawtucket, RI 2860
USA USA
goldench@nova.edu Janet_Grace@mhri.org
xxxii List of Contributors
MARTIN R. GRAF AUDREY H. GUTHERIE

Department of Neurosurgery Rehabilitation Research & Development Center of
Virginia Commonwealth University Medical Center Excellence Atlanta Veterans Administration Medical
P.O. Box 980631 Center
Richmond, VA 29298-0631 1670 Clairmont Road
USA Decatur, GA 30033
mgraf@vcu.edu USA
ahgutherie@yahoo.com
LORI GRAFTON KARL HABERLANDT

Carolinas Rehabilitation Department of Psychology
Carolinas HealthCare System Trinity College
Charlotte, NC 28232-2861 300 Summit Street
USA Hartford, CT 6119
Lori.Grafton@carolinashealthcare.org USA
karl.haberlandt@trincoll.edu
MICHAEL R. GREHER
MARTIN HAHN
National Jewish Health and University of Colorado
Department of Biology
Denver School of Medicine
Denver, CO
Wayne, NJ 7470
USA
USA
drgreher@comcast.net
HahnM@wpunj.edu
KATHRINE HAK
MAUREEN GRISSOM
Applied Psychology and Counselor Education
University of Missouri, Department of Health
University of Northern Colorado
Psychology MU Thompson Center for Autism and
McKee 248, Box 131
Neurodevelopmental Disorders
Greeley, CO 80631
300 Portland Street Suite 110
USA
Columbia, MO 65211
Kathrine.Hak@unco.edu
USA
grissommo@health.missouri.edu
MARLA J. HAMBERGER
New York Presbyterian
ELIZABETH STANNARD GROMISCH Columbia Comprehensive Epilepsy Center
Trinity College The Neurological Institute
1005 Smith Ridge Road Columbia University
Hartford, CT 6840 710 West 168 Street, 7th floor
elizabeth.gromisch@trincoll.edu USA
mh61@columbia.edu
WILLIAM GUIDO FLORA HAMMOND

Anatomy & Neurobiology Brain Injury Program Director/Research Director
Virginia Commonwealth University Medical Center Carolinas Rehabilitation
Box 980709 1100 Blythe Blvd
Richmond, VA Charlotte, NC 28203
USA USA
wguido@vcu.edu Flora.Hammond@carolinashealthcare.org
List of Contributors xxxiii
BENJAMIN M. HAMPSTEAD KENNETH M. HEILMAN

Emory University/Rehabilitation Medicine, Atlanta Department of Neurology
VAMC RR&D CoE University of Florida College of Medicine
1441 Clifton Road Suite 150 The Malcom Randall Veterans Affairs Hospital
Atlanta, GA 30322 Box 100236
USA Gainesville, FL 32610
bhampst@emory.edu USA
heilman@neurology.ufl.edu
JANNA L. HARRIS
Hoglund Brain Imaging Center NATHAN HENNINGER
University of Kansas Medical Center Department of Pediatrics
3901 Rainbow Blvd. Mail Stop 1052 Nationwide Childrens Hospital
Kansas City, KS 66160 College of Medicine, Ohio State University
USA 700 Childrens Drive
jharris2@kumc.edu Columbus, OH 43205
USA
Nathan.Henninger@nationwidechildrens.org
ERIC S. HART
University of Missouri Center for Health Care Quality
MARY HIBBARD
Clinical Support and Education Building
Rusk Institute of Rehabilitation Medicine
Columbia, MO 65212
New York, NY 10016
USA
USA
harte@health.missouri.edu
mary.hibbard@mssm.edu
TRISHA HAY
YVONNE HINDES
Hoglund Brain Imaging Center
Division of Applied Psychology
University of Kansas Medical Center
Faculty of Education, University of Calgary
3901 Rainbow Blvd
2500 University Drive N.W
Kansas City, KS 66160
Calgary, AB T2N 1N4
USA
Canada
thay@kumc.edu
ylhindes@ucalgary.ca
AMY HEFFELFINGER MERRILL HISCOCK

Associate Professor of Neurology Department of Psychology
Medical College of Wisconsin University of Houston
9200 W. Wisconsin Ave Houston, TX 77204-5022
Milwaukee, WI 53226 USA
USA mhiscock@uh.edu
AHeffelfinger@mcw.edu
ELISE K. HODGES
ROBERT L. HEILBRONNER Department of Psychiatry
Chicago Neuropsychology Group University of Michigan Health System
333 N. Michigan Avenue, #1801 Neuropsychology Division
Chicago, IL 60601 2101 Commonwealth, Suite C
USA Ann Arbor, MI 48105
rheilbronn@aol.com USA
r-heilbronner@northwestern.edu ekhodges@med.umich.edu
xxxiv List of Contributors
ANNA DEPOLD HOHLER BRADLEY J. HUFFORD

Boston University Medical Center Neuropsychology
720 Harrison Avenue, Suite 707 Rehabilitation Hospital of Indiana
Boston, MA 2118 4141 Shore Drive
USA Indianapolis, IN 46254
Anna.Hohler@bmc.org USA
bradley.hufford@rhin.com
TRACEY HOLLINGSWORTH JOEL W. HUGHES

Nationwide Childrens Hospital Department of Psychology
Developmental Assessment Program Kent State University
187 W. Schrock Road 228 Kent Hall
Columbus, OH 43081 Kent, OH 44242-0001
USA USA
tracey.hollingsworth@nationwidechildrens.org jhughes1@kent.edu
DAVID HULAC
KARIN F. HOTH
Division of Counseling and Psychology in Education
National Jewish Medical and Research Center
University of South Dakota
National Jewish Health
414 E. Clark Street
Denver, CO
Vermillion, SD 57069
USA
USA
psysocmed@njc.org
David.Hulac@usd.edu
EDWARD E. HUNTER
MARIANNE HRABOK
Department of Psychiatry and Behavioral Sciences
University of Victoria
3901 Rainbow Boulevard
P.O. Box 3050, STN CSC
Victoria, BC V8W 3P5
USA
Canada
ehunter@kumc.edu
mhrabok@uvic.ca
SCOTT J. HUNTER
LEESA V. HUANG Department of Psychiatry & Behavioral Neuroscience
Department of Psychology-0234 University of Chicago
California State University 5841 S Maryland Ave., MC 3077
400 West First Street Chicago, IL 60637
Chico, CA 95928-9924 USA
USA shunter@yoda.bsd.uchicago.edu
leesahuang@yahoo.com chgohunt@mac.com
KAREN HUX
DAWN H. HUBER Special Education and Communication Disorders
Pediatric Neuropsychological Services, LLC University of Nebraska Lincoln
1829 S. Kentwood, Suite 108 318N Barkley Memorial Center
Springfield, MO 65804 Lincoln, NE 68583-0738
USA USA
pnsllc@att.net khux1@unl.edu
List of Contributors xxxv
SUMMER IBARRA MATTHEW JACOBS

Rehabilitation Hospital of Indiana Deparment of Psychology
4141 Shore Drive Pennsylvannia State University
Indianapolis, IN 46254 111 Moore Building
USA University Park, PA 16802
summer.ibarra@rhin.com USA
mbj5033@psu.edu
FARZIN IRANI
Psychiatry LISA A. JACOBSON
University of Pennsylvania Department of Neuropsychology
3400 Spruce street, 10 Gates Kennedy Krieger Institute
Philadelphia, PA 19104 Johns Hopkins University School of Medicine
USA 1750 East Fairmount Ave.
firani@upenn.edu Baltimore, MD 21231
USA
jacobson@kennedykrieger.org
CINDY B. IVANHOE
Neurorehabilitation Specialists
KELLY M. JANKE
Baylor College of Medicine
University of Wisconsin-Milwaukee
The Institute for Rehabilitation and Research
1333 Moursund Avenue, D110
P.O. Box 413
Houston, TX 77030
Milwaukee, WI 53201-0413
USA
USA
cbivanhoe@att.net
kmz@uwm.edu
GRANT L. IVERSON
NICHOLAS JASINSKI
Division of Neuropsychology
University of British Columbia
Henry Ford Health System
British Columbia Mental Health & Addictions
1 Ford Place
2255 Wesbrook Mall
Detroit, MI 48202
Vancouver, BC V6T 2A1
USA
Canada
NJasins1@HFHS.ORG
giverson@interchange.ubc.ca
BETH A. JERSKEY
COLLEEN E. JACKSON Department of Psychiatry and Human Behavior
Department of Psychology Alpert Medical School of Brown University
University of Connecticut Butler Hospital
406 Babbidge Road, Unit 1020 Blackstone Blvd.
Storrs, CT 6269 Providence, RI 2906
USA USA
colleen.jackson@uconn.edu Beth_Jerskey@brown.edu
KIMBERLE M. JACOBS CHASMAN JESSE

Department of Anatomy and Neurobiology Department of Psychology
Virginia Commonwealth University University of Connecticut
Box 980709 406 Babbidge Road, Unit 1020
Richmond, VA 23298-0709 Storrs, CT 6269
USA USA
kmjacobs@vcu.edu jesse.chasman@uconn.edu
xxxvi List of Contributors
AMITABH JHA KRISTIN L. JOHNSON

TBIMS National Data and Statistical Center Applied Psychology and Counselor Education
Craig Hospital University of Northern Colorado
3425 South Clarkson Street McKee 248, Box 131
Englewood, CO 80113 Greeley, CO 80631
USA USA
ajha@craighospital.org kristinljohnson@hotmail.com
ERIN JOYCE
MI-YEOUNG JO Pacific Graduate School of PsychologyStanford Doctor
Private Practice of Psychology Consortium
15353 Valerio Street Spinal Cord Injury Clinic
Van Nuys, CA 91406 VA Palo Alto Health Care System
USA 3801 Miranda Ave. (128)
myjo_9@yahoo.com Palo Alto, CA 94304
USA
EEJPsyD@Stanford.edu
SUSAN K. JOHNSON
Department of Psychology AARON N. JUNI
University of North Carolina at Charlotte Neuropsychology and Rehabilitation Psychology
9201 University City Blvd. Department of Physical Medicine & Rehabilitation
Charlotte, NC 28223-0001 The Johns Hopkins School of Medicine
USA 600 North Wolfe Street/Phipps 174
skjohnso@uncc.edu Baltimore, MD 21287
USA
ajuni1@jhmi.edu
JULENE K. JOHNSON
UCSF Epilepsy Center STEPHEN M. KANNE
University of California Thompson Center for Autism and Neurodevelopmental
400 Parnassus Avenue Disorders
San Francisco, CA 94143-0138 University of Missouri
USA 300 Portland, Suite 110
jjohnson@memory.ucsf.edu Columbia, MO 65211
USA
kannest@missouri.edu
JUDY A. JOHNSON
Pasadena Independent School District RICHARD F. KAPLAN
29731 Sullivan Oaks Drive Department of Psychiatry (MC-2103)
Pasadena, TX 77386 UConn Health Center
USA 263 Farmington Ave
jjohnson00708831@comcast.net Farmington, CT 06030-2103
USA
kaplan@psychiatry.uchc.edu
NANCY JOHNSON
Cognitive/Behavioral Neurology Center PAUL E. KAPLAN
Northwestern Feinburg School of Medicine Capitol Clinical Neuroscience
675 N. Street Clair, Galter 20-100 104 Summer Shade Court
Chicago, IL 60611 Folsom, CA 95630-1565
USA USA
johnson-n@northwestern.edu paulek_2000@yahoo.com
List of Contributors xxxvii
EDITH KAPLAN SALLY L. KEMP

Department of Psychology University of Missouri
Suffolk University 1328 Secluded Woods Drive
26 Laconia Street, P.O. Box 476 Columbia, MO 56020
Boston, MA 02420-0005 USA
USA DocSallyKemp@gmail.com
ekaplan@bu.edu
KIMBERLY A. KERNS
NARINDER KAPUR Department of Psychology
Neuropsychology Department University of Victoria
Addenbrookes Hospital Victoria, BC V8W 3P5
R3 Neurosciences, Box 83 Canada
Cambridge, CB2 0QQ kkerns@uvic.ca
UK
narinder.kapur@addenbrookes.nhs.uk
FARY KHAN
Department of Medicine
STELLA KARANTZOULIS University of Melbourne and the Royal Melbourne
Neuropsychology Program Hospital
NYU Langone Medical Center Bldg 21, Royal Park Campus
City University Parkville, VA, VIC 3152
New York, NY Australia
USA Fary.Khan@mh.org.au
skarantz@gmail.com
SO HYUN KIM
DOUGLAS I. KATZ University of Michigan Autism and Communication
Boston University School of Medicine Disorders Center (UMACC)
Braintree Rehabilitation Hospital 2236 East Hall
250 Pond Street Ann Arbor, MI 48109-0406
Boston, MA 2184 USA
USA sohkim@umich.edu
dkatz@bu.edu
TRICIA Z. KING
MICHAEL KAUFMAN Georgia State University
Department of Neurology Department of Psychology
Carolinas Medical Center 140 Decatur Street, Suite 1151
1010 Edgehill Road North Atlanta, GA 30303
Charlotte, NC 28207-1885 USA
USA tzking@gsu.edu
Michael.Kaufman@carolinashealthcare.org
JENNIFER SUE KLEINER

JACOB KEAN Department of Psychology
Department of Physical Medicine and Rehabilitation University of Arkansas for Medical Sciences
Indiana University School of Medicine Blandford Physician Center
200 S. Jordan Avenue Suite 410, 4301 West Markham Street, #568
Indianapolis, IN 47405 Little Rock, AR 72205
USA USA
jakean@indiana.edu jskleiner@uams.edu
xxxviii List of Contributors
BONITA P. KLEIN-TASMAN KATE KRIVAL

Department of Psychology Speech Pathology, School of Health Sciences
University of Wisconsin-Milwaukee Kent State University
2441 E. Hartford Ave. A111 Music and Speech Bldg
Milwaukee, WI 53211 Kent, OH 44242
USA USA
bklein@uwm.edu ckrival@kent.edu
STEPHANIE A. KOLAKOWSKY-HAYNER LAUREN B. KRUPP

Director, Rehabilitation Research Department of Neuropsychology Research
Santa Clara Valley Medical Center Stony Brook University
Rehabilitation Research Center SUNY Stony Brook
751 South Bascom Ave. Stony Brook, NY 11794
San Jose, CA 95128 USA
USA lkrupp@notes.cc.sunysb.edu
Stephanie.Hayner@hhs.sccgov.org
BRAD KUROWSKI
ELIZABETH KOZORA
Cincinnati Childrens Hospital Medical Center
Department of Medicine
University of Pittsburgh
National Jewish Medical, and Research Center
Cincinnati, OH
National Jewish Health
USA
1400 Jackson Street
kurkowskiba@upmc.edu
Denver, CO 80208
USA
KozoraE@NJC.ORG
MATTHEW M. KURTZ
Wesleyan University
JOEL H. KRAMER
Judd Hall 314
UCSF Memory and Aging Center
Middletown, CT 6459
UCSF Med Ctr, 0984-8AC
USA
350 Parnassus Ave, Suite 706
mkurtz@wesleyan.edu
San Francisco, CA 94143
USA
jkramer@memory.ucsf.edu
MONICA KURYLO
MATTHEW KRAYBILL University of Kansas Medical Center
Department of Psychology 3901 Rainbow Blvd
University of Utah Kansas City, KS 66160
Salt Lake City, UT 84112-0251 USA
USA mkurylo@kumc.edu
mkraybill@gmail.com
CHRISTINA KWASNICA
DENISE KRCH Barrow Neurological Institute
Kessler Foundation Research Center 222 W Thomas Road Ste 212
West Orange, NJ Phoenix, AZ 85013
USA USA
dkrch@kesslerfoundation.org Christina.Kwasnica@CHW.EDU
List of Contributors xxxix
DAVID LACHAR GUDRUN LANGE

University of Texas Houston Health Science Center Department of Radiology
1300 Moursund University of Medicine & Denistry of New Jersey
Houston, TX 77030 Pain and Fatigue Study Center, UMDNJ-New Jersey
USA Medical School
david.lachar@uth.tmc.edu 30 Bergen Street, ADMC 1618
Newark, NJ 07103
SUSAN LADLEY-OBRIEN USA
University of Colorado Health Sciences Center langegu@umdnj.edu
Department of Physical Medicine an
Denver Health Medical Center KAREN G. LANGER
777 Bannock Street #0113 Rusk Institute of Rehabilitation Medicine
Denver, CO 80204 NYU Langone Medical Center
USA Department of Psychology
Susan.Ladley-OBrien@dhha.org 400 E. 34th Street, RR-515
Flushing, NY 10016
GINETTE LAFLECHE USA
Memory Disorders Research Center Karen.Langer@nyumc.org
VA Boston Healthcare System and Boston University
School of Medicine
MICHAEL J. LARSON
150 S. Huntington Ave. (151A)
Boston, MA 2130
3032 E. 1530 S.
USA
Provo, UT 84660
lafleche@bu.edu
USA
michael_larson@byu.edu
AUDREY LAFRENAYE
Department of Anatomy and Neurobiology
JENNIFER C. GIDLEY LARSON
Box 980709
University of Utah
USA
USA
forrestad@vcu.edu
jen.larson@utah.edu
SARAH K. LAGEMAN
Division of Neuropsychology and Behavioral Health THOMAS M. LAUDATE
Department of Rehabilitation Medicine Boston University
Emory University Brigham and Womens Hospital
1441 Clifton Road NE 648 Beacon Street, 2nd Floor
Atlanta, GA 30322 Boston, MA 02215-2013
USA USA
sarah.lageman@emoryhealthcare.org tlaudate@yahoo.com
RAEL T. LANGE RONALD M. LAZAR

British Columbia Mental Health and Addiction Services Cerebrovascular Division/Department of Neurology
University of British Columbia Neurological Institute of New York
PHSA Research and Networks Columbia University Medical Center
Suite 201, 601 West Broadway 710 West 168th Street
Vancouver, BC V5Z 4C2 New York, NY 10032
Canada USA
RLange@bcmhs.bc.ca ral22@columbia.edu
xl List of Contributors
VICTORIA M. LEAVITT GEORGE LEICHNETZ

Kessler Foundation Research Center Virginia Commonwealth University
1468 Midland Ave., apt 1B Richmond, VA
West Orange, NJ 10708 USA
USA gleichne@vcu.edu
vleavitt@kesslerfoundation.org
HOYLE LEIGH
SOPHIE LEBRECHT
Brown University
University of California, San Francisco
Visual Neuroscience Laboratory
155 N. Fresno Street
Waterman Street
Fresno, CA 93701
USA
USA
Hoyle.leigh@ucsf.edu
Sophie_Lebrecht@brown.edu
SING LEE JEANNIE LENGENFELDER

Department of Psychiatry Kessler Foundation Research Center
The Chinese University of Hong Kong West Orange, NJ 07052
7A, Block E, Staff Quarters, Prince of Wales Hospital USA
Shatin, HKSAR, PRC jlengenfelder@kesslerfoundation.org
China
singlee@cuhk.edu.hk
MARCUS PONCE DE LEON

ANDREA M. LEE Chief, Neurology Service
University of Manitoba William Beaumont Army Medical Center
1702-72 Donald Street 5005 N. Piedras Street
Winnipeg, MB R3C 1L7 El Paso, Texas 79920-5001
Canada USA
andrea.meredith@gmail.com marcusponce@yahoo.com
KANGMIN D. LEE
TERRY LEVITT
Department of Neurosurgery
1324 College Drive
Box 980631
Saskatoon, Saskatchewan S7N 0W5
Richmond, VA
Canada
USA
tlevitt@sasktel.net
klee2@mcvh-vcu.edu
STACIE A. LEFFARD ALLEN N. LEWIS

Rehabilitation Psychology and Neuropsychology Department of Rehabilitation Counseling
Physical Medicine & Rehabilitation, University of School of Allied Health Professions
Michigan Virginia Commonwealth University
325 E. Eisenhower Parkway P.O. Box 980330
Ann Arbor, MI 48108 Richmond, VA 23298
USA USA
staciele@med.umich.edu anlewis@vcu.edu
List of Contributors xli
PAMELA H. LEWIS CHRIS LOFTIS

Department of Rehabilitation Counseling National Council for Community Behavioral Healthcare
School of Allied Health Professions, Virginia STG International
Commonwealth University 1527 N. Van Dorn Street
980330 Alexandria, VA 22304
Richmond, VA 23298-0330 USA
USA Chris.Loftis@gmail.com
lewisph@vcu.edu
KENNETH J. LOGAN
Department of Communication Sciences & Disorders
DAVID J. LIBON
P.O. Box 117420, 343 Dauer Hall
Drexel University, College of Medicine
Gainesville, FL 32611-7420
New College Building, Mail Stop 423,
USA
245 North 15th Street
klogan@ufl.edu
Philadelphia, PA 19102
USA
dlibon@Drexelmed.edu CATRINA C. LOOTENS
Department of Pediatrics
University of Kansas Medical Center, MS 4004, G005
DEBBIE LICHESKY Miller
American Academy of Pediatrics 3901 Rainbow Blvd.
Elk Grane Village, IL Kansas City, KS 66160-7330
USA USA
clootens@kumc.edu
MARY BETH LINDSAY EDUARDO LOPEZ

Department of Educational Psychology Associate Medical Director/Clinical Services Center for
University of Utah Head Injuries
1705 Campus Center Drive, #327 JFK Johnson Rehabilitation Institute
Salt Lake City, UT 84112-9255 65 James Street
USA Edison, NJ 8818
marybeth.pummel@utah.edu USA
elopag61@aol.com
CASSIE LINDSTROM
CATHERINE LORD
Dept of Psychology
Autism and Communication Disorders Center (UMACC)
UNC-Charlotte
University of Michigan
9201 University City Blvd
300 North Ingalls, 10th Floor
Charlotte, NC 28223
Ann Arbor, MI 48109-0406
USA
USA
cmlinds1@uncc.edu
celord@umich.edu
DONAEC LOCKE JANIS LORMAN

Psychiatry and Psychology The University of Akron
Mayo Clinic School of SpeechLanguage Pathology and Audiology
13400 East Shea Blvd Room 181, Polsky Building, 225 South Main Street
Scottsdale, AZ 85259 Akron, OH 44325-3001
USA USA
locke.dona@mayo.edu JLO101@aol.com
xlii List of Contributors
N. G. LOUISA and
Department of Rehabilitation Medicine Johns Hopkins University School of Medicine
Royal Melbourne Hospital Baltimore, MD 21205
Parkville, Victoria USA
Australia mahone@kennedykrieger.org
Louisa.Ng@mh.org.au
BRI MAKOFSKE
STEPHEN D. LUKE Applied Psychology and Counselor Education
National Dissemination Center for Children with University of Northern Colorado
Disabilities (NICHCY) McKee 248, Box 131
Washington, DC Greeley, CO 80631
USA USA
sluke@aed.org vonf5072@blue.unco.edu
KRISTINE LUNDGREN JAMES F. MALEC

Department of Communication Sciences and Disorders Rehabilitation Hospital of Indiana
University of North Carolina at Greensboro 4141 Shore Drive
323 Ferguson Building P.O. Box 26170 Indianapolis, IN 46254
Greensboro, NC 27402 USA
USA jim.malec@rhin.com
k_lundgr@uncg.edu
AMIT MALHOTRA
JON G. LYON
Kaiser Permanente Medical Center
6344 Hillsandwood Road
280 West MacArthur Boulevard
Mazomanie, WI 53560
Oakland, CA 94611-5693
USA
USA
LyonBlanc@aol.com
amit.x.malhotra@kp.org
DONALD E. LYTLE
Department of Psychology PAUL MALLOY
California State University The Warren Alpert Medical School of Brown University
400 West First Street Butler Hospital
Chico, CA 95928-0234 345 Blackstone Blvd.
USA Providence, RI 2906
DLytle@csuchico.edu USA
PMalloy@Butler.org
ANNA MACKAY-BRANDT
Department of Psychiatry and Human Behavior WILLIAM VICTOR MALOY
Brown University Medical School The Virginia Institute of Pastoral Care
78 Dana Street 2000 Bremo Road, Suite 105
Providence, RI 2906 Richmond VA 23226
USA USA
anna.mackay@gmail.com wvm.vipcare@verizon.net
E. MARK MAHONE CARLYE G. MANNA

Department of Neuropsychology Neuropsychology Program
Kennedy Krieger Institute New York State Psychiatric Institute
1750 E. Fairmount Avenue New York, NY
Baltimore, MD 21231 USA
USA carlyegriggs@hotmail.com
List of Contributors xliii
ASHLEY DE MARCHENA JEANNE W. MCALLISTER

Department of Psychology Center for Medical Home Improvement
University of Connecticut Crotched Mountain
406 Babbidge Road 18 Low Avenue
Storrs, CT 06269-1020 Concord, NH 3301
USA USA
ashley.de_marchena@uconn.edu Jeanne.W.McAllister@Hitchcock.ORG
BERNICE A. MARCOPULOS
Department of Psychiatry and Neurobehavioral DAVID MCCABE
Sciences Queens College and The Graduate Center of the City
University of Virginia, Director, Neuropsychology Lab University of New York
Western State Hospital Department of Psychology
Box 2500 65-30 Kissena Blvd.
Charlottesville, VA 24402-2500 Flushing, NY 11367
USA USA
Bernice.Marcopulos@wsh.dmhmrsas.virginia.gov davidlmc@gmail.com
CHRISTINA R. MARMAROU
Neurosurgery REBECCA MCCARTNEY
Virginia Commonwealth University Emory University/Rehabilitation Medicine
Box 980631 1441 Clifton Road NE
Richmond, VA Atlanta, GA 30322
USA USA
crmarmar@vcu.edu beckygsu@aol.com
GUIDO MASCIALINO
Department of Rehab Medicine DALENE MCCLOSKEY
Mount Sinai School of Medicine Centennial Board of Cooperative Educational Services
5 East 98th Street 16473 Longs Peak Road
New York, NY 10029 Greeley, CO 80631
USA USA
Guido.Mascialino@mountsinai.org dalenemc@what-wire.com
MICAH O. MAZUREK
Thompson Center for Autism and Neurodevelopmental ERICA MCCONNELL
Disorders University of Northern Colorado
University of Missouri 2250 Ironton Street
300 Portland, Suite 110 Greeley, CO 80010
Columbia, MO 65211 USA
USA erica.mcconnell@hotmail.com
mazurekm@missouri.edu
MICHELE M. M. MAZZOCCO MICHAEL A. MCCREA

Johns Hopkins University School of Medicine Executive Director
Kennedy Krieger Institute Neuroscience Center
707 North Broadway 721 American Avenue, Suite 501
Baltimore, MD 21211 Waukesha, WI 53188
USA USA
mazzocco@jhu.edu michael.mccrea@phci.org
xliv List of Contributors
JACINTA MCELLIGOTT LEMMIETTA MCNEILLY

National Rehabilitation Hospital Chief Staff Officer
Rochestown Avenue Speech-Language Pathology, American Speech-
Dun Laoghaire, CO Dublin Language-Hearing Association
Ireland 2200 Research Boulevard,
mcelligottj@gmail.com Rockville, MD 20850-3289
USA
lmcneilly@asha.org
MELISSA J. MCGINN
RORY MCQUISTON
Virginia Commonwealth University School of Medicine
Box 980709
Richmond, VA
Box 980709
USA
Richmond, VA
mjmcginn@vcu.edu
USA
amcquiston@vcu.edu
DAVID E. MCINTOSH
Ball State University LINDA MCWHORTER
Department of Special Education, Teachers College Department of Psychology
Room 722 University of North Carolina at Charlotte
Muncie, IN 47306 9201 University City Blvd
USA North Carolina
demcintosh@bsu.edu Charlotte, NC 28223
USA
lmcwhor1@uncc.edu
MIECHELLE MCKELVEY
Department of Communication Disorders MARY-ELLEN MEADOWS
COE B141, University of Nebraska Kearney Division of Cognitive and Behavioral Neurology
Kearney, NE 68849 Brigham and Womens Hospital
USA 221 Longwood Ave
mckelveyml@unk.edu Boston, MA 2115
USA
mmeadows@partners.org
NICOLE C. R. MCLAUGHLIN
Butler Hospital
MICHAEL S. MEGA
Alpert Medical School of Brown University
Cognitive Assessment Clinic
345 Blackstone Blvd
Providence Brain Institute, Providence Health System
9427 SW Barnes Road, Suite 595
USA
Portland, OR 97225
nmclaughlin@butler.org
USA
michael.mega@providence.org
BRIAN T. MCMAHON
Department of Rehabilitation Counseling STEPHEN S. MEHARG
Virginia Commonwealth University Center for Memory and Learning
P.O. Box 980330 945 11th Ave Suite A
Richmond, VA 23298 Longview, WA 98632
USA USA
bmcbull@vcu.edu smeharg@cfmal.com
List of Contributors xlv
JOHN E. MENDOZA JOHN E. MEYERS

SE LA Veterans Healthcare System Private Practice
Department of Psychiatry and Neurology Neuropsychology
Tulane University Medical Center Schofield Barracks, Concussion Clinic
3928 S. Inwood Ave. 94-553 Alapoai Street # 162
New Orleans, LA 70131 Mililani, HI 96789
USA USA
John.Mendoza2@va.gov jmeyersneuro@yahoo.com
MARK MENNEMEIER DAVID MICHALEC

Neurobiology and Developmental Sciences Division of Psychology
University of Arkansas for Medical Sciences Ohio State University
4301 W Markham Slot 826 Nationwide Childrens Hospital
Little Rock, AR 72205-7199 Developmental Assessment Program
USA 187 W. Schrock Road
msmennemeier@uams.edu Columbus, OH 43081
USA
RANDALL E. MERCHANT david.michalec@nationwidechildrens.org
Box 980709 MCV Station ERIC N. MILLER
Richmond, VA 23298-0709 UCLA Psychology Clinic
USA 2191 Franz Hall
rmerchan@vcu.edu Los Angeles, CA 90095
USA
BRAD MERKER emiller@ucla.edu
Henry Ford Health Systems
1 Ford Place, 1E ETHAN MOITRA
Detroit MI 48202 Drexel University
BMERKER1@HFHS.ORG 509 Windwood Place
Morgantown, WV 26505
GARY B. MESIBOV USA
University of North Carolina at Chapel Hill em742@drexel.edu
CB 7180, 310 Medical School Wing E
Chapel Hill, NC 27599-7180 DORIS S. MOK
gary_mesibov@unc.edu Faculty of Social Sciences and Humanities
University of Macau
TIMOTHY VAN METER Av. Padre Tomas Pereira
Virginia Commonwealth University Taipa, Macau SAR
Richmond, VA China
USA DMok@umac.mo
tevanmet@vcu.edu
ANNA BACON MOORE
LINDA MEYER Department of Rehabilitation Medicine, Division
Communication Services of Neuropsychology
Woodrow Wilson Rehabilitation Center Emory University School of Medicine
P.O. Box 1500 1441 Clifton Road Suite 150
Fishersville, VA 22939-1500 Atlanta, GA 30322
USA USA
L.A.Meyer@wwrc.virginia.gov abmoore@emory.edu
xlvi List of Contributors
AMY C. MOORS LUBA NAKHUTINA

Villanova University New York University Langone Medical Center
Department of Psychology Queens College and The Graduate Center of
800 Lancaster Ave The City University of New York, Room NSB-318
Villanova, PA 19085 65-30 Kissena Blvd
USA Flushing, NY 11367
amy.moors@villanova.edu USA
luba_ny@hotmail.com
LISA MORAN
Department of Psychology AARON P. NELSON
Nationwide Childrens Hospital Division of Cogntive and Behavioral Neurology
700 Childrens Drive Brigham and Womens Hospital
Columbus, OH 43205 Bosten University
USA 221 Longwood Ave
moran.170@osu.edu Boston, MA 2115
USA
anelson@partners.org
JOSEPH E. MOSLEY
Department of psychology
William Paterson University CHRISTINA NESSLER
300 Pompton Road Aphasia/Apraxia Research Program
Wayne, NJ 7470 VA Salt Lake City Healthcare System
USA 500 Foothill Drive, 151-A
mosleyj@optonline.net Salt Lake City, UT 84148
USA
Christina.Nessler@va.gov
MARGARET MOULT
Olin Neuropsychiatry Research Center
ADRIAN NESTOR
Institute of Living
Department of Cognitive and Linguistic Sciences
400 Washington Street
Brown University
Hartford, CT 6106
P.O. 1978
USA
Providence RI 02906
mmoult@harthosp.org
USA
Adrian_Nestor@brown.edu
MARY PAT MURPHY
MSN, CRRN
PAUL NEWMAN
Paoli, PA
Department of Medical Psychology and
USA
Neuropsychology
Drake Center
SUZANNE MUSIL 151 West Galbraith Road
Rush University Medical Center Cincinnati, OH 45216-1096
Chicago, IL USA
USA Paul.Newman@healthall.com
s-musil@northwestern.edu
Suzanne_Musil@Rush.Edu CHRISTINE MAGUTH NEZU
SYLVIE NAAR-KING Drexel UniversityHahnemann Campus
UHC 6d5, 4201 St. Antoine Mail Stop 515, 245 N 15th Street
Detroit, MI 48201 Philadelphia, PA 19102-1192
USA USA
snaarkin@med.wayne.edu christine.nezu@drexel.edu
List of Contributors xlvii
JANET P. NIEMEIER JONATHAN A. OLER

Department of Neuropsychology and Rehabilitation Department of Psychiatry
Psychology University of Wisconsin,
Virginia Commonwealth University, School of Medicine 6001 Research Park Blvd
P.O. Box 980661 Madison, WI 53719
Richmond, VA 23298 USA
USA oler@wisc.edu
jniemeier@mcvh-vcu.edu
KATHLEEN OTOOLE
C. MICHAEL NINA Childrens Healthcare of Atlanta
Department of Psychology Atlanta, GA
William Paterson University USA
300 Pompton Road kathleen.otoole@choa.org
Wayne, NJ 7470
USA
ROHAN PALMER
ninac@wpunj.edu
Institute for Behavioral Genetics
University of Colorado at Boulder
VIRGINIA A. NORRIS
447 UCB
Spinal Cord Injury Clinic
Boulder, CO 80309-0447
VA Palo Alto Health Care System
USA
3801 Miranda Ave. (128)
rohan.palmer@colorado.edu
Palo Alto CA 94304
USA
CHRISTINA A. PALMESE
VANPsyD@Stanford.edu
Beth Israel Medical Center
OLGA NOSKIN
10 Union Square East, Suite 5D
New York, NY 10003
The Neurological Institute of New York
USA
Columbia University
CPalmese@chpnet.org
College of Physicians and Surgeons
710 W 168th Street, NI-6
New York, NY 11032 JUHI PANDEY
onoskin@gmail.com University of Connecticut
THOMAS A. NOVACK Storrs, CT 6269
Department of Psychiatry and Behavioral Neurobiology USA
University of Alabama at Birmingham and
619 19th Street S The Childrens Hospital of Philadelphia
Birmingham, AL 35249-7330 Philadelphia, PA
USA USA
novack@uab.edu pandeyj@email.chop.edu
THOMAS OAKLAND BO CARLOS PANG

Department of Educational Psychology Department of Economics
College of Education Faculty of Social Sciences and Humanities
University of Florida University of Macau
1410 Norman Hall Av. Padre Tomas Pereira
Gainesville, FL Taipa, Macau SAR
USA China
oakland@coe.ufl.edu carlos198769@gmail.com
xlviii List of Contributors
KATHRYN V. PAPP AMY PETERMAN

Department of Psychology Department of Psychology
The University of Connecticut University of North Carolina at Charlotte
406 Babbidge Road, Unit 1020 9201 University City Blvd
Storrs, CT 6269 Charlotte, NC 28223
USA USA
katepapp@gmail.com Ahpeterm@uncc.edu
JO ANN PETRIE
RICK PARENTE
Provo, UT
Towson University
USA
Towson, MD
joann_petrie@cortex.byu.edu
USA
FParente@towson.edu
LEADELLE PHELPS
University at Buffalo, State University of New York
MATTHEW R. PARRY 427 Baldy Hall
Virginia Commonwealth University Buffalo, NY 14260
Richmond, VA USA
USA phelps@buffalo.edu
parrymr@gmail.com
KRISTIN D. PHILLIPS
JANET PATTERSON Medical College of Wisconsin-Milwaukee
Department of Communicartive Sciences and Disorders Department of Neurology, Division of
California State University Neuropsychology
East Bay 9200 W. Wisconsin ave
25800 Carlos Bee Blvd. Milwaukee, WI 53226
Hayward, CA 94542 USA
USA kphillips@mcw.edu
janet.patterson@csueastbay.edu
LINDA L. PHILLIPS
SHELLEY PELLETIER
Board Certified in School Psychology
Box 980709
Shoreline Pediatric Neuropsychology Services, LLC
Richmond, VA
954 Middlesex Turnpike, A2
USA
Old Saybrook, CT 6475
llphilli@hsc.vcu.edu
USA
shelley.pelletier@us.army.mil
WADE PICKREN
Ryerson University
KENNETH PERRINE Department of Psychology, American Psychological
Northeast Regional Epilepsy Group Association
104-20 Queens Blvd., Apt. 10C 350 Victoria Street
Hackensack, NJ 11375 Toronto, ON ON M5B 2K3
USA Canada
krp2003@med.cornell.edu wpickren@psych.ryerson.ca
List of Contributors xlix
ERIC E. PIERSON VICTOR R. PREEDY

Educational Psychology Nutritional Sciences Division
Ball State University Kings College London
2000 W. University Ave. 150 Stamford Street
Muncie, IN 47306 London, SE1 9NH
USA UK
eepierson@bsu.edu victor.preedy@kcl.ac.uk
IRENE PIRYATINSKY ANDREW PRESTON

Butler Hospital and Alpert Medical School of Department of Pediatrics
Brown University Neurodevelopmental Center/ Memorial Hospital of
345 Blackstone Blvd Rhode Island and Warren Alpert Medical School of
Providence, RI 2906 Brown University
USA 555 Prospect Street
Irene_Piryatinsky@brown.edu Pawtucket, RI 2860
USA
Andrew_Preston@brown.edu
KENNETH PODELL
Division of Neuropsychology
Henry Ford Health Systems MICHELLE ANN PROSJE
1 Ford Place, Ste. 1 E University of Florida
Detroit, MI 48202-3450 2036 NW 36th Street
USA Gainesville, FL 32605
kpodell1@hfhs.org USA
michelle@prosje.com
DONNA POLELLE
Department of Commication Sciences and Disorders ADELE S. RAADE
Saint Xavier University Adjunct Assistant Professor
3700 W 103rd Street Boston University Department of Speech
Chicago, IL 60655 Language, & Hearing Sciences
USA 635 Commonwealth Avenue
Polelle@sxu.edu Boston, MA 2215
USA
araade@comcast.net
MATTHEW R. POWELL
Clinical Neuropsychologist
Behavioral Medicine Center VANESSA L. RAMOS
Waukesha Memorial Hospital, Neuroscience Center Department of Psychology
721 American Avenue, Suite 501 Nationwide Childrens Hospital
Waukesha, WI 53188 700 Childrens Drive
USA Columbus, OH 43205
matthew.powell@phci.org USA
Vanessa.ramos@nationwidechildrens.org
TIFFANY L. POWELL
Department of Neurosurgery KATE D. RANDALL
Virginia Commonwealth University Psychology
Box 980631 Univesity of Victoria
Richmond, VA Victoria, BC
USA Canada
tpowell@mcvh-vcu.edu krandall@uvic.ca
l List of Contributors
STEVEN Z. RAPCSAK SHERYL REMINGER

Neurology Service (1-27) Psychology Department
Neurology Section, Southern Arizona VA Health Care University of Illinois at Springfield
System, Department of Neurology, University of Springfield, IL 62703
Arizona USA
3601 S 6th Ave sremi2@uis.edu
Tucson, AZ 85723
USA
szr@email.arizona.edu
KATHRYN K. REVA
SARAH A. RASKIN 51 W 69th Street Apt 4D
Department of Psychology and Neuroscience Program New York, NY 10023
Trinity College USA
Hartford, CT 6106 kathryn.reva@gmail.com
USA
Sarah.Raskin@trincoll.edu
JOSE A. REY
JOSEPH F. RATH College of Pharmacy
Rusk Institute of Rehabilitation Medicine Nova Southeastern University
NYU Langone Medical Center, Department of 3200 South University Dr.
Psychology Ft. Lauderdale, FL 33328
400 East 34th Street USA
New York, NY 10016 joserey@nova.edu
USA
Joseph.Rath@nyumc.org
CECIL R. REYNOLDS
HOLLY RAU Texas A&M Universuty
Department of Psychology 704 Harrington Tower
University of Utah College Station, TX 77843-4225
USA crrh@earthlink.net
holly.rau@psych.utah.edu
ANASTASIA RAYMER JILL B. RICH

Professor of Early Childhood, Speech Pathology and Department of Psychology
Special Education York University
Old Dominion University 4700 Keele Street
110 Child Study Center Toronto, ON M3J 1P3
Norfolk, VA 23529-0136 Canada
USA jbr@yorku.ca
sraymer@odu.edu
CHRISTINE REID ROBERT RIDER

Department of Rehabilitation Counseling Drexel University
Virginia Commonwealth University Department of Psychology
P.O. Box 980330 PSA Building, 3141 Chestnut Street
Richmond, VA 23298 Philadelphia, PA 19104
USA USA
creid@vcu.edu rrider@mail.med.upenn.edu
List of Contributors li
GIULIA RIGHI CAROLE ROTH

Brown University Otolaryngology Clinic, Speech Division
Visual Neuroscience Laboratory Naval Medical Center
Waterman Street 34520 Bob Wilson Drive
Providence, RI 02903 San Diego, CA 92134-2200
USA USA
Giulia_Righi@brown.edu carole.roth@med.navy.mil
DIANA L. ROBINS ELLIOT J. ROTH

Department of Psychology Feinberg School of Medicine
Georgia State University Physical Medicine and Rehabilitation
Department of Psychology Northwestern University
P.O. Box 5010 345 E. Superior
Atlanta, GA 30302-5010 Chicago, IL 60611
USA USA
drobins@gsu.edu ejr@northwestern.edu
eroth@ric.org
DANIEL E. ROHE
Mayo Clinic LINDA ROWLEY
200 First Street Southwest Waisman Center Family Village
Rochester, MN 55905 University of Madison
USA 1500 Highland Avenue
rohe.daniel@mayo.edu Madison, WI 53705-2280
USA
rowley@waisman.wisc.edu
MARYELLEN ROMERO
Assistant Professor of Psychiatry
Department of Psychiatry and Neurology DONALD ROYALL
Tulane University Health Sciences Center The University of Texas Health Center at San Antonio
1440 Canal Street, TB-53 7703 Floyd Curl Dr, Mail Code 7792
New Orleans, LA 70112 San Antonio, TX 78229-3900
USA USA
mmcclai@tulane.edu royall@uthscsa.edu
KATHERINE A. ROOF SHAHAL ROZENBLATT

Department of Psychology Advanced Psychological Assessment
University of North Carolina at Charlotte 50 Karl Avenue, Suite 104
9201 University City Blvd P. C. Smithtown, NY 11787
Charlotte, NC 28223 USA
USA neuro@advancedpsy.com
karoof@uncc.edu
ALEXANDRA RUDD-BARNARD
JON ROSE Rusk Institute of Rehabilitative Medicine Psychology
Spinal Cord Injury Clinic New York University Langone Medical Center
Veterans Affairs Palo Alto Healthcare System Service Psych InPat
3801 Miranda Ave. (128) 550 First Avenue
Palo Alto, CA 94304 New York, NY 10016
USA USA
Jonathon.Rose@VA.Gov Alexandra.Rudd@nyumc.org
lii List of Contributors
RONALD RUFF CATHY RYDELL

San Francisco Clinical Neurosciences & University of American Academy of Neurology
California San Francisco 1080 Montreal Avenue
San Francisco Clinical Neurosci Saint Paul, MN 55116
909 Hyde Street, #620 USA
San Francisco, CA 94109 dhoneyman@aan.com
USA
ronruff@mindspring.com
BONNIE C. SACHS
Department of Psychology & Psychiatry
JESSICA SOMERVILLE RUFFOLO Mayo Clinic College of Medicine
Neuropsychology Clinic 4500 San Pablo Road
The Miriam Hospital Jacksonville, FL 32224
The Coro Center, Suite 317 USA
Providence, RI 2903 Sachs.Bonnie@mayo.edu
USA
jruffolo@lifespan.org
AMANDA L. SACKS
Department of Rehab Medicine
BETH RUSH Mount Sinai Medical Center
Psychiatry and Psychology 5 East 98th Street
Mayo Clinic New York, NY 10029
Davis 4-N, 4500 San Pablo Road USA
Jacksonville, FL 32224 amanda.sacks@mountsinai.org
USA
rush.beth@mayo.edu
DONALD H. SAKLOFSKE
Division of Applied Psychology
MICHELE RUSIN Faculty of Education, University of Calgary
Emory University/Rehabilitation Medicine 2500 University Drive NW
1776 Briarcliff Road NE Calgary, AB T2N 1N4
Atlanta, GA 30306 Canada
USA don.saklofske@ucalgary.ca
mrusin@bellsouth.net
STEPHEN P. SALLOWAY
JULIA RUTENBERG Butler Hospital
Emory University/Rehabilitation Medicine Alpert Medical School of Brown University
Atlanta VAMC RR&D CoE 345 Blackstone Blvd
Atlanta, GA Providence, RI 2906
USA USA
jrutenbe@wellesley.edu Stephen_Salloway@brown.edu
BRUCE RYBARCZYK JEFFREY SAMUELS

Department of Psychology North Broward Medical Center
Virginia Commonwealth University Inpatient Rehabilitation Unit
Box 842018 1 West Sample Road
Richmond, VA 23284-2018 Deerfield Beach, FL 33064
USA USA
bdrybarczyk@vcu.edu hpocmps@gate.net
List of Contributors liii
MARK A. SANDBERG AARON SCHRADER

Independent Practice Applied Psychology and Counselor Education
Community Re-entry Program University of Northern Colorado
St. Charles Hospital McKee 248, Box 131
50 Karl Ave., Suite 104 Greeley, CO 80631
Smithtown, NY 11787 USA
USA aschrader@inbox.com
maspsy@verizon.net
JILLIAN SCHUH
MARLA SANZONE
Independent Practice, Loyola College of Maryland
104-A Annapolis Street
Annapolis, MD 21401
Storrs, CT 6269
USA
USA
docmerri@yahoo.com
jillian.schuh@gmail.com
LYNN A. SCHAEFER
Department of Physical Medicine and Rehabilitation CHRISTIAN SCHUTTE
Nassau University Medical Center John D. Dingell VA Medical Center
2201 Hempstead Turnpike Psychology Section (11MHPS)
East Meadow, NY 11554 4646 John R
USA Detroit, MI 48201-1916
lschaefe@numc.edu USA
Christian.Schutte@va.gov
GERTINA J. VAN SCHALKWYK

Department of Psychology KERRI SCORPIO
Faculty of Social Sciences & Humanities (FSH), Neuropsychology Program
University of Macau Queens College and The Graduate Center of the
Av. Padre Tomas Pereira City University of New York
Taipa, Macau SAR 6530 Kissena Blvd.
China Flushing, NY 11367
gjvs@umac.mo USA
kscorpio100@qc.cuny.edu
PHILIP SCHATZ
Saint Josephs University
DANIEL L. SEGAL
Post Hall #222
University of Colorado at Colorado Springs
1420 Austin Bluffs Parkway
USA
Colorado Springs, CO 80933
pschatz@sju.edu
USA
dsegal@uccs.edu
MIKE R. SCHOENBERG
Associate Professor
Department of Psychiatry and Behavioral Sciences, ROBIN SEKERAK
University of South Florida College of Medicine Waikato District Health Board
3515 E. Fletcher Ave PB 3200
Tampa, FL 33613 Hamilton 2100
USA New Zealand
mschoenb@health.usf.edu sekerakr@gmail.com
liv List of Contributors
SVETLANA SEROVA VICTORIA SHEA

Neuropsychology Postdoctoral Fellow Division TEACCH
Department of Rehabilitation Medicine, Mount Sinai Carolina Institute on Developmental Disabilities
School of Medicine University of North Carolina at Chapel Hill
One Gustave L. Levy Place, Box 1240 Chapel Hill, NC
New York, NY 10029 USA
USA victoria.shea@mindspring.com
Svetlana.serova@mountsinai.org
JUDITH A. SHECHTER
LAURA SHANK 100 East Lancaster Avenue
Rehabilitation Psychology and Neuropsychology Suite 564 East
Physical Medicine & Rehabilitation Wynnewood, PA 19096
University of Michigan USA
325 E. Eisenhower Parkway jshech564@aol.com
Ann Arbor, MI 48108
USA
laurasha@med.umich.edu TAMARA GOLDMAN SHER
Institute of Psychology
Illinois Institute of Technology
3105 S. Dearborn St.
CASEY R. SHANNON
Chicago, IL 60616
USA
Greeley, CO
sher@iit.edu
USA
laurasha@med.umich.edu
ELISABETH M. S. SHERMAN
Alberta Childrens Hospital
ANUJ SHARMA
University of Calgary
Calgary, AB
Richmond, VA
Canada
USA
Elisabeth.Sherman@calgaryhealthregion.ca
sharmaa@vcu.edu
CHERYL L. SHIGAKI
SALLY E. SHAYWITZ Department of Health Psychology
Department of Pediatrics University of Missouri
Yale University School of Medicine One Hospital Drive, DC046.46
P.O. Box 208064 Columbia, MO 65212
New Haven, CT 6520 USA
USA shigakic@health.missouri.edu
sally.shaywitz@yale.edu
GERALD SHOWALTER
BENNETT A. SHAYWITZ Department of Psychiatry and Neurobehavioral
Yale University School of Medicine Sciences
P.O. Box 208064 University of Virginia School of Medicine
New Haven, CT 6520 Charlottesville, VA 22908-0203
USA USA
bennett.shaywitz@yale.edu Gerald.Showalter@wwrc.virginia.gov
List of Contributors lv
SEEMA SHROFF MARIAN L. SMITH

Anatomy & Neurobiology Via Christi Hospital Pittsburg Mt.
Virginia Commonwealth University Carmel
Box 980709 Via Christi Behavioral Health
Richmond, VA Crossroads Counseling Center
USA 200 E. Centennial Avenue, suite 13
shroffiegirl@gmail.com Pittsburg, KS 66762
USA
Marian_Smith@via-christi.org
DAVID H. KEUNG SHUM
Griffith University
School of Psychology, Mt Gravatt Campus Griffith
JILL SNYDER
University
Nathan
Brisbane, Queensland 4111
McKee 248, Box 131
Australia
Greeley, CO 80631
d.shum@griffith.edu.au
USA
jillcsnyder@gmail.com
LINDA SHUSTER
West Virginia University
P.O. Box 6122 MCKAY MOORE SOHLBERG
Morgantown, WV 26506 Communication Disorders and Sciences
USA University of Oregon
lshuster@wvu.edu 5284 University of Oregon
Eugene, OR 97403
USA
SUE ANN SISTO mckay@uoregon.edu
School of Health Technology and Management
Stony Brook University
1500 Stony Brook Road
Stony Brook, NY 11794-6018 SARA S. SPARROW
USA 94, Linsley Lake Road
sue.sisto@stonybrook.edu North Branford, CT 6171
USA
and
Yale University Child Study Center
BETH SLOMINE
230 South Frontage Road
707 North Broadway
New Haven, CT 06471
Baltimore, MD 21205
USA
USA
sara.sparrow@yale.edu
slomine@kennedykrieger.org
AUDREY SMERBECK FERRINNE SPECTOR

School and Educational Psychology Psychology
University at Buffalo McMaster University
The State University of New York 1280 Main Street West
Buffalo, NY 14260-1000 Hamilton, ON L8S4K1
USA Canada
audrey.smerbeck@gmail.com spectof@mcmaster.ca
lvi List of Contributors
APRIL SPIVACK ANTHONY Y. STRINGER

Department of Psychology Department of Rehabilitation Medicine
University of North Carolina - Charlotte Emory University
9201 University City Blvd 1441 Clifton Road NE
Charlotte, NC 28223 Atlanta, GA 30322
USA USA
amurdoch@uncc.edu Anthony.Stringer@emoryhealthcare.org
BETH SPRINGATE RENEE STUCKY

Department of Psychology Health Psychology
University of Connecticut PM&R Rusk Rehab Center
406 Babbidge Road, Unit 1020 Columbia, MO 65211
Storrs, CT 6269 USA
USA StuckyR@health.missouri.edu
beth.springate@uconn.edu
LAUREN STUTTS
Department of Clinical and Health Psychology
SUSAN STEFFANI
CCC-SLP
Gainesville, FL 32611
California State University, Chico, Department of
USA
Communication Sciences and Disorders
lstutts@phhp.ufl.edu
400 West 1st Street
Chico, CA 95929-330
USA
YANA SUCHY
ssteffani@csuchico.edu
University of Utah
380 S. 1530 E., Rm. 502
TARYN M. STEJSKAL
USA
yana.suchy@psych.utah.edu
Virginia, VA
USA
thinktaryn@gmail.com JAMES F. SUMOWSKI
Neuropsychology and Neuroscience
Kessler Medical Rehabilitation Research and Education
WILLIAM STIERS Center
Johns Hopkins University School of Medicine Kessler Foundation Research Center
5601 Loch Raven Boulevard, Suite 406 1199 Pleasant Valley Way
Baltimore, MD 21239 West Orange, NJ 7052
USA USA
wstiers1@jhmi.edu jsumowski@kesslerfoundation.org
ESTHER STRAUSS DONG SUN

Department of Psychology Department of Neurosurgery
University of Victoria Virginia Commonwealth University Medical Center
P.O. Box 3050 P.O. Box 980631 MCV Campus
Victoria, BC V8W 3P5 Richmond, VA 23298
Canada USA
estrauss@uvic.ca dsun@vcu.edu
List of Contributors lvii
ZOE SWAINE RICHARD TEMPLE

Department of Clinical and Health Psychology Clinical Operations
University of Florida CORE Health Care
Gainesville, FL 32611 400 US Hwy 290 West, Bldg B Ste. 205
USA Dripping Springs, TX 78620
zoe@phhp.ufl.edu USA
rtemple@corehealth.com
JOAN SWEARER
Department of Neurology CLAIRE THOMAS-DUCKWITZ
University of Massachusetts Medical School University of Northern Colorado
55 Lake Avenue North 1040 Blue Spruce Drive
Worcester, MA 01655 Greeley, CO 80538
USA USA
swearerj@ummhc.org clairethomasduckwitz@gmail.com
LAWRENCE H. SWEET
JENNIFER TINKER
Brown University, Butler Hospital
Drexel University
345 Blackstone Blvd.
3315 Market Street, 14-308
Providence, RI 2906
USA
USA
sweet@brown.edu
jrt38@drexel.edu
RUSSELL H. SWERDLOW
MICHELLE M. TIPTON-BURTON
University of Kansas School of Medicine
Physical Medicine and Rehabilitation
Landon Center on Aging, MS 2012
3901 Rainbow Blvd
751 South Bascom Avenue
San Jose, CA 95128
USA
USA
rswerdlow@kumc.edu
michelle.tipton-burton@hhs.sccgov.org
MICHAEL J. TARR
Department of Cognitive and Linguistic Sciences and JEFFREY B. TITUS
Brain Science Program Pediatric Neuropsychologist
Brown University Washington University School of Medicine
Waterman Street St. Louis Childrens Hospital
Providence, RI 2903 One Childrens Place, 3S-32
USA St. Louis, MO 63110
Michael_Tarr@Brown.EDU USA
jbt0776@bjc.org
ELLA B. TEAGUE
Neuropsychology program TERI A. TODD
Queens College and The Graduate Center Department of Kinesiology
The City University of New York California State University, Chico
65-30 Kissena Blvd 400 West 1st Street
Flushing, NY 11367 Chico, CA 95929-330
USA USA
ellabjarta@gmail.com tatodd@csuchico.edu
lviii List of Contributors
ALEXANDER I. TROSTER LYN TURKSTRA

Department of Neurology (CB 7025) University of Wisconsin-Madison
University of North Carolina School Medicine 7225 Medical Sciences Center
3114 Bioinformatics Building 1300 University Avenue
Chapel Hill, NC 27599-7025 Madison, WI 53706-1532
USA USA
TrosterA@neurology.unc.edu lsturkstra@wisc.edu
NAM TRAN
Neurosurgery GARY TYE
Virginia Commonwealth University Medical Center Neurosurgery
Box 980631 Virginia Commonwealth University
Richmond, VA Box 980631
USA Richmond, VA
namdtran1@gmail.com USA
gtye@mcvh-vcu.edu
KATHERINE TREIBER
Utah State University
KATHERINE TYSON
Logan, UT 84322
USA
and
University of Massachusetts Medical School
Storrs, CT 6269
Worcester, MA
USA
USA
katherine.tyson@uconn.edu
katietreiber@yahoo.com
ANGELA K. TROYER
JAMIE VANNICE
Division of Psychology
Baycrest Centre for Geriatric Care
3560 Bathurst Street
McKee 248, Box 131
Toronto, ON M6A 2E1
Greeley, CO 80631
Canada
USA
atroyer@baycrest.org
vannice215@gmail.com
THEODORE TSAOUSIDES
Brain Injury Research TODD VAN WIEREN
Mount Sinai School of Medicine Disability Support Services
5 East 98th Street, Room B-15 Indiana University of Pennsylvania
New york, NY 10029 Indiana, PA
USA USA
theodore.tsaousides@mountsinai.org toddvw@iup.edu
JOANN T. TSCHANZ
Utah State University REBECCA VAURIO
Center for Epidemiologic Studies Kennedy Krieger Institute
4450 Old Main Hill 707 North Broadway
Logan, UT 84322-4440 Baltimore, MD 21205
USA USA
joann.tschanz@usu.edu vaurio@kennedykrieger.org
List of Contributors lix
JENNIFER VENEGAS FRED R. VOLKMAR

Department of Educational Psychology Yale University
University of Utah 230 South Frontage Road
1705 Campus Center Drive, #327 New Haven, CT 06520-7900
USA fred.volkmar@yale.edu
Jennifer.venegas@utah.edu
SCOTT VOTA
MIEKE VERFAELLIE Neurology
Memory Disorders Research Center 151A Virginia Commonwealth University
VA Boston Healthcare System and Bosten University Box 980599
School of Medicine Richmond, VA
150 South Huntington Ave USA
Boston, MA 2130 svota@mcvh-vcu.edu
USA
verf@bu.edu
GEORGE C. WAGNER
JEAN VETTEL Rutgers University
Brown University 152 Freylinghuysen Road
Campus Box 1978 Piscataway
Providence, RI 2912 New Brunswick, NJ 8854
USA USA
Jean_Vettel@brown.edu gcwagner@rci.rutgers.edu
CHAD D. VICKERY CHRISTOPHER WAGNER

Neuropsychology Department Department of Rehabilitation Counseling
Methodist Rehabilitation Center Virginia Commonwealth University
1350 E. Woodrow Wilson P.O. Box 980330
Jackson, MS 39216 Richmond, VA 23298
USA USA
chadvickery@hotmail.com chriscwagner@gmail.com
MICHAEL R. VILLANUEVA NATALIE WAHMHOFF

Department of Psychology Department of Educational Psychology
University of North Carolina-Charlotte University of Utah
9201 University City Blvd 1705 Campus Center Drive, #327
Charlotte, NC 28223 Salt Lake City, UT 84112-9255
USA USA
MRVILLAN@uncc.edu Natalie.wahmhoff@hsc.utah.edu
MARTIN A. VOLKER JULIE L. WAMBAUGH

School and Educational Psychology Veterans Affairs Salt Lake City Healthcare System and
University at Buffalo University of Utah
The State University of New York 151 A 500 Foothill Blvd.
Buffalo, NY 14260-1000 Salt Lake City, UT 84148
USA USA
mvolker@buffalo.edu julie.wambaugh@health.utah.edu
lx List of Contributors
SETH WARSCHAUSKY JOHN D. WESTBROOK

Department of Physical Medicine and Rehab National Center for the Dissemination of Disability
University of Michigan Research (NCDDR)
325 East Eisenhower SEDL
Ann Arbor, MI 48108 4700 Mueller Blvd.
USA Austin, TX 78723
sethaw@umich.edu USA
john.westbrook@sedl.org
ADAM B. WARSHOWSKY
Clinical Neuropsychologist, Dual/SCI Unit MICHAEL WESTERVELD
Mount Sinai Medical Center, Shepherd Center Medical Psychology Associates
2020 Peachtree Road Florida Hospital
Atlanta, GA 30309 5165 Adanson Street, Suite 200
USA Orlando, FL 32804
Adam_Warshowsky@Shepherd.org USA
westerm@msn.com
AMANDA WAXMAN
Neuropsychology Program HOLLY JAMES WESTERVELT
Queens College of City University of New York Clinical Neuropsychologist
564 Amsterdam Avenue Apt. 3C Neuropsychology Program
New York, NY 10024 Rhode Island Hospital
USA Alpert Medical School of Brown University
awaxman55@hotmail.com 593 Eddy Street, POB 430
Providence, RI 2903
NADIA WEBB USA
Department of Psychology HWestervelt@lifespan.org
Childrens Hospital of New Orleans
200 Henry Clay Avenue MARNIE J. WESTON
New Orleans, LA 70118 Center for Health Care Quality
USA University of Missouri-Columbia
nwebb@chnola.org One Hospital Drive
Columbia, MO 65212
CHRISTINE J. WEBER-MIHAILA USA
Neuropsychologist westonmk@health.missouri.edu
Northeast Regional Epilepsy Group
104 East 40th Street, Suite 607 KRISTINE B. WHIGHAM
New York, NY 10016 Licensed Psychologist
USA Department of Neuropsychology
christymihaila@yahoo.com Childrens Healthcare of Atlanta
cweber@epilepsygroup.com 1001 Johnson Ferry Road, NE
Atlanta, GA 30342
STEPHEN T. WEGENER USA
Division of Rehabilitation Psychology and kristine.whigham@choa.org
Neuropsychology
Department of Physical Medicine and Rehabilitation GALE G. WHITENECK
The Johns Hopkins School of Medicine Craig Hospital
600 North Wolfe Street, Phipps 174 3425 S. Clarkson Street
Baltimore, MD 21287 Englewood, CO 80113
USA USA
swegener@jhmi.edu gale@craighospital.org
List of Contributors lxi
JOHN WHYTE and

Department of Rehabilitation Medicine University of North Colorado
Thomas Jefferson University Greeley, CO
Moss Rehabilitation Research Institute USA
Albert Einstein Healthcare Network dwitsken518@yahoo.com
60 E. Township Line Road
Elkins Park PA 19027 ERICKA WODKA
USA Center for Autism and Related Disorders
jwhyte@einstein.edu Kennedy Krieger Institute
3901 Greenspring Avenue
ROBERT G. WILL Baltimore, MD 21211
University of Edinburgh USA
Edinburgh wodka@kennedykrieger.org
UK
r.g.will@ed.ac.uk THOMAS R. WODUSHEK
Center for Neurorehabilitation Services, PC
GAVIN WILLIAMS 1045 Robertson Street
Senior Physiotherapist Fort Collins, CO 80524-3926
Epworth Rehabilitation Centre USA
Epworth Hospital twodushek@brainrecov.com
29 Erin Street
Richmond JENNIFER WOEHR
Melbourne, Vic 3121 Department of Neurology
Australia Mount Sinai School of Medicine
gavin.williams@epworth.org.au One Gustave L. Levy Place, Box 1139
New York, NY 10029
BRENDA WILSON USA
Department of Communication Disorders and Sciences jennifer.woehr@mssm.edu
Eastern Illinois University
600 Lincoln Ave EDISON WONG
Charleston, IL 61920-3099 Center for Pain and Medical Rehab
USA 33 Electric Avenue, Suite B03
bmwilson@eiu.edu Fitchburg MA 01420
USA
JILL WINEGARDNER cyberdoc@massmed.org
Northern California Programs
Learning Services MICHAEL S. WORDEN
10855 DeBruin Way Department of Neuroscience
Gilroy, CA 95020 Brown University
USA 185 Meeting Street Box G-LN
and Providence, RI 2912
Princess of Wales Hospital USA
Ely, Cambridgeshire Michael_Worden@brown.edu
UK
jwinegardner@sbcglobal.net JERRY WRIGHT
Rehabilitation Research Center
DEBORAH WITSKEN Santa Clara Valley Medical Center
University of Minnesota Medical School 751 S. Bascom Avenue
2020 Garfield Ave, Apt. 7 San Jose, CA 95128
Minneapolis, MN 55405 USA
USA jerry.wright@hhs.sccgov.org
lxii List of Contributors
FAN WU OSBORN H. ZACHARY

Department of Psychology Behavioural Health Service Line
Faculty of Social Sciences and Humanities Harry S. Truman Memorial Veterans Hospital
University of Macau Columbia, MO 65201
Av. Padre Tomas Pereira USA
Taipa, Macau SAR Zachary.Osborn@va.gov
China
vivienwood1987@hotmail.com
CHRISTINA ZAFIRIS
GLENN WYLIE Applied Psychology and Counselor Education
Neuropsychology and Neuroscience Laboratory University of Northern Colorado
Kessler Medical Rehabilitation Research and Education McKee 248, Box 131
Center Greeley, CO 80631
Kessler Foundation USA
1199 Pleasant Valley Way cmzafiris@hotmail.com
USA
gwylie@kmrrec.org
ROSS ZAFONTE
Spaulding rehabilitation Hospital
KEITH O. YEATES
Harvard Medical School
125 Nashua Street
Nationwide Childrens Hospital
Boston, MA 2114
700 Childrens Drive
USA
Columbus, OH 43205
RZAFONTE@PARTNERS.ORG
USA
keith.yeates@nationwidechildrens.org
NATHAN D. ZASLER
ANGELA YI
Concussion Care Centre of Virginia, Ltd.
3721 Westerre Parkway, Suite B
Richmond, Virginia 23233
5 East 98th Street
USA
New York, NY 10029
nzasler@cccv-ltd.com
USA
angela.yi@mountsinai.org
BRIAN YOCHIM ISLAM ZAYDAN

Department of Psychology Neurology
University of Colorado at Colorado Springs Virginia Commonwealth University
1420 Austin Bluffs Parkway Box 980599
Colorado Springs, CO 80933 Richmond, VA
USA USA
byochim@uccs.edu izaydan@mcvh-vcu.edu
MICHELE L. ZACCARIO
Rusk Institute FADEL ZEIDAN
New York University Langone Medical Center Department of Psychology
Pace University UNC Charlotte
339 East 28th Street 9201 University City Blvd
New York, NY 10016 Charlotte, NC 28223
USA USA
michele.zaccario@nyumc.org fzeidan@uncc.edu
List of Contributors lxiii
DENNIS J. ZGALJARDIC MIRIAM ZICHLIN

Department of Neuropsychology Aging and Dementia Research Center
Transitional Learning Center at Galveston NYU School of Medicine
1528, Postoffice Street 550 First Ave. MHL 310
Galveston, TX 77550 New York, NY 10016
USA USA
dzgaljardic@tlc-galveston.org mlzichlin@gmail.com
ZHENG ZHOU MOLLY E. ZIMMERMAN

Department of Psychology Albert Einstein College of Medicine
St. Johns University 1165 Morris Park Ave Rousso Bldg Rm 310
Queens, NY 11439 Bronx, NY 10461
USA USA
ZHOUZ@stjohns.edu mzimmerm@aecom.yu.edu
A
2 2 Table 7-Item BBS-3P

Contingency Table Berg Balance Scale
2 & 7 Test 15 Item Test

Rey 15 Item Test
Ruff 2&7 Selective Attention Test
504 Plan
3MS
M. J. H OLCOMB 1, DAVID E. M ACINTOSH 2
Modified Mini-Mental State Examination 1
Muncie, IN, USA
2
Muncie, IN, USA
5-HTP
L-Tryptophan Definition
A 504 Plan refers to Section 504 of the Rehabilitation Act of

1973 (Public Law 93-112) and the Americans with Dis-
5-Hydroxytryptophan abilities Act of 1990 (Public Law 101-336), which makes it
illegal to exclude anyone from a federally funded program or
L-Tryptophan activity based on a disability. Section 504, a federal civil
rights law, specifically prohibits discrimination against indi-
viduals with disabilities, within any school system or other
recipient of federal financial assistance. The definition of
recipient is a broad one, as it can include not only schools
6MWD but also states (including their Departments of Education)
or counties, agencies, institutions, or other organizations
Six-Minute Walk Test
that benefit from Federal funds, directly or indirectly.
Current Knowledge
6MWT
A 504 plan documents accommodations for qualified stu-
Six-Minute Walk Test dents which will allow them to have opportunities similar
Jeffrey S. Kreutzer, John DeLuca, Bruce Caplan (eds.), Encyclopedia of Clinical Neuropsychology, DOI 10.1007/978-0-387-79948-3,
# Springer Science+Business Media LLC 2011
2 A AACN Practice Guidelines
to those of their peers. An Individualized Education Plan Historical Background

(IEP) is not a 504 plan because IEPs only cover an inclu-
sive list of students with disabilities. A 504 plan covers a The American Board of Clinical Neuropsychology
far wider range of conditions, including both those that (ABCN) is a specialty board within the American
actually limit one or more major life activities (the crite- Board of Professional Psychology (ABPP). For those
rion for disability under IDEA) and those that do not limit seeking board certification in clinical neuropsychology,
a major life activity but are perceived as limiting by the ABCN is the board responsible for overseeing the exami-
recipient of funding. Thus, individuals who are not eligi- nation process. The American Academy of Clinical
ble for special education services under IDEA may none- Neuropsychology (AACN) is the organization for those
theless be eligible for accommodations under Section 504. awarded board certification by the ABCN. In 2007,
While both laws require provision of a free appropriate AACN produced the first set of practice guidelines,
public education, a comprehensive evaluation is not re- which were intended to . . .facilitate the continued sys-
quired to obtain services under the provisions of Section tematic growth of the profession of clinical neuropsychol-
504. While IDEA provides for comprehensive evaluation ogy, and to help assure a high level of professional
at the expense of the school district, this is not the case for practice.
services requested under Section 504.
In sum, the purpose of 504 legislation is to level the
playing field for those who dont require the significant
level of accommodation and/or assistance needed by Current Knowledge
those who meet criteria for an IEP under IDEA. Examples
of conditions that may qualify for 504 services include Given the recent growth of clinical neuropsychology,
asthma, diabetes, eating disorders, ADHD, depression, coupled with the American Psychological Associations
and conduct disorder. focus on Evidence-Based Practice, the AACN established
(AACN, 2007) guidelines for the practice of neuropsy-
chological assessment and consultation. The guidelines
Cross References are intended to provide standards for competence and
professional conduct within the practice of neuropsy-
Accommodations chology by describing the most desirable and highest
Americans with Disabilities Act (1990) level of professional conduct for clinical neuropsychol-
IDEA ogists providing clinical neuropsychology services. It is
Rehabilitation Act of 1973 important to note that the guidelines are fully compati-
ble with the current APA (2002) Ethical Principles of
Psychologists and Code of Conduct (EPPCC) as well as
the Criteria for Practice Guideline Development and
References and Readings Evaluation (2002) and Determination and Documenta-
tion of the Need for Practice Guidelines (2005). The
Smith, T. E. C., & Patton, J. R. (1998). Section 504 and the public schools.
Austin: TXL Pro-Ed.
AACN practice guidelines include recommendations
for the practice of clinical neuropsychology and they
are not to be regarded as mandatory standards. The
guidelines detail consideration of ethical and clinical
issues as well as specific methods and procedures for
AACN Practice Guidelines the practice of neuropsychology.
There are several major areas of emphasis in the
R OBERT L. H EILBRONNER guidelines. They include: (1) Definitions; (2) purpose and
Chicago Neuropsychology Group scope; (3) education and training; (4) work settings;
Chicago, IL, USA (5) ethical and clinical issues (e.g., informed consent,
patient issues in third party assessments, test security;
underserved populations/cultural issues; and (6) methods
Synonyms and procedures (e.g., review of records, measurement
procedures, test administration and scoring, and
Practice development; Practice guidelines interpretation).
AAMD Adaptive Behavior Scales A 3
References and Readings 2nd edition (ABS-RC: 2) and the Adaptive Behavior
A
Scales-School, 2nd edition (ABS-S: 2). Current versions
American Psychological Association. (2002). Criteria for practice guide- are a comprehensive compilation of the past versions.
line development and evaluation. American Psychologist, 57, These assessments seek to develop an estimate of adaptive
10481051.
behaviors in two scales defined with personal indepen-
American Psychological Association. (2002) Ethical principles of psy-
chologists and code of conduct. American Psychologist, 57,
dence and maladaptive behaviors in individuals with in-
10601073. tellectual disabilities. Items are rated with a yes/no
American Psychological Association. (2005). Determination and docu- response, on a 03 scale, or by frequency. Historically,
mentation of the need for practice guidelines. American Psychologist, the ABS-RC: 2 was used in institutions, but it is now
60, 976978.
also used in community settings, whereas the ABS-S:
Committee on Ethical Guidelines for Forensic Psychologists. (1991).
Specialty guidelines for forensic psychologists. Law and Human
2 was designed for use in school settings.
Behavior, 15, 655665. For both the ABS-RC: 2 and the ABS-S: 2, the
The AACN practice guidelines can be found on the AACNs Web site assessment can be administered by either of two
(www.theaacn.org) and are also published in the AACNs journal: approaches. In one method, the assessment is completed
The Clinical Neuropsychologist, 21, 209231.
by a professional or paraprofessional trained to use the
scales. In the second method, the assessment is adminis-
tered by someone familiar with the individual being
evaluated. Interpretation of results must be completed
AAMD ABS: 2 by an individual with formal training in psychometrics
and these scales.
AAMD Adaptive Behavior Scales The ABS-S: 2 enables an appraisal of an individuals
ability to cope with challenges they encounter in their
school, and aids in the diagnosis of intellectual disabilities
at ages 321. There are nine subscales in the first part of
the assessment, measuring personal independence and
AAMD Adaptive Behavior Scales responsibility of daily living: independent functioning,
physical development, economic activity, language devel-
C RISTA A. H OPP 1, I DA S UE B ARON 2
1 opment, numbers and time, prevocational/vocational ac-
Inova Fairfax Hospital for Children
2 tivity, self-direction, responsibility, and socialization. The
Inova Fairfax Hospital for Children
second part of the assessment, which addresses behavioral
Falls Church, VA, USA
domains, consists of seven subscales: social behavior, con-
formity, trustworthiness, stereotyped and hyperactive
behavior, self-abusive behavior, social engagement,
Synonyms and disturbing interpersonal behavior.
The ABS-S: 2 was normed on 2,074 students with
AAMD ABS: 2; AAMR ABS-RC: 2; AAMR ABS-S: 2
intellectual disabilities and 1,254 of their peers without
intellectual disabilities. Administration takes place in an
interview format with either a parent or teacher and may
Description vary from 20 min to 2 h, dependent on the rater. Scoring
is completed by hand. Raw scores are converted into
The American Association for Mental Deficiency Adap- percentiles, standard scores, and age equivalents for each
tive Behavior Scales (AAMD ABS) is a revised edition subdomain. Five factors can be derived: Personal self-
(1993) of the original assessments that were published in sufficiency, community self-sufficiency, personal social
1969. The American Association for Mental Retardation responsibility, social adjustment, and personal adjust-
(AAMR) (formerly known as the American Association ment. Percentiles, factor standard scores, and age equiva-
for Mental Deficiency) has changed its name to American lents are then reported based on factor scores.
Association on Intellectual and Developmental Disabilities The ABS-RC: 2 is also useful for the assessment of
(AAIDD). Therefore, intellectual disabilities have replaced personal development and social behavior in individuals
mental retardation as the terminology of choice. The with intellectual disabilities, but it has been developed for
behavior scales have been published in two versions, the individuals aged 1879. Like the ABS-S: 2, the assessment
Adaptive Behavior Scales-Residential and Community, has two parts, but there are more subscales in each part.
4 A AAMD Adaptive Behavior Scales
The first part has ten subscales: independent functioning, adaptive behavior as measured in Part II was not related
physical development, economic activity, language develop- to the Vineland Adaptive Behavior Scale and Adaptive
ment, numbers and time, domestic activity, prevocational/ Behavior Inventory (ABI), other measures of maladaptive
vocational activity, self-direction, responsibility, and sociali- behaviors.
zation. The second part contains eight subscales: social
behavior, conformity, trustworthiness, stereotyped and hy-
peractive behavior, sexual behavior, self-abusive behavior,
Clinical Uses
social engagement, and disturbing interpersonal behavior.
The ABS-RC: 2 was normed on a sample of 4,000 adults with
The ABS: 2 assesses the status of individuals with intellec-
intellectual disabilities, and administration times vary be-
tual disability, emotional maladjustment, autism, or de-
tween 15 and 40 min, depending on the informants knowl-
velopmental disability. It enables a professional to assess
edge of the individual being assessed. Raw scores are
strengths and weaknesses of an individual in adaptive
recorded and then converted to standard scores and percen-
areas, document progress, and assess the effectiveness of
tiles. The subscales yield the same five-factor scales as the
intervention/school programs. The manual cautions that
ABS-S: 2.
the examiner should interview a significant informant or
the instrument should be administered by that significant
informant. If an informant is unable to provide needed
Historical Background
information, then another informant needs to be inter-
viewed. Whereas the ABS is a standard assessment used in
The AAMD first published the ABS in 1969 in response to
determining adaptive and maladaptive behavior, its psy-
the definition of mental retardation that was enlarged in
chometric properties are limited, especially compared to
1959 to include adaptive behavior. The ABS-S: 2, first
other measures such as the Vineland Adaptive Behavior
published in 1969 by Nihira, Foster, Shellhaas, and
Scales.
Leland, was revised and standardized in 1974 by Lambert,
Whereas a strength of the ABS-S: 2 is that it was
Windmiller, and Cole and again in 1981 by Lambert and
normed on students with and without intellectual disabil-
Windmiller. The second and current edition was pub-
ities, the ABS-RC: 2s standard scores and percentile ranks
lished in 1993. The ABS-RC:2 were also first published
were not compared to individuals without intellectual
in 1969 by Nihira, Foster, Shellhaas, and Leland. It was
disabilities. Therefore, this assessment may not meet the
revised in 1974, and again in 1993. The goals of the
criteria to make a diagnosis of mental retardation accord-
revisions have been to improve the reliability of the inter-
ing to the AAMR requirements.
viewer in differentiating between individuals with intel-
lectual disabilities who are institutionalized and those
living in the community. Previously, these individuals
had been classified at different adaptive behavior levels
Cross References
according to the AAIDD.
Vineland Adaptive Behavior Scales
Psychometric Data
References and Readings
The authors of the ABS-S: 2 report three types of reli-
ability: internal consistency, stability, and interscorer. Aiken, L. (1996). Assessment of intellectual functioning. Switzerland:
Internal consistency is reported to range from 0.79 to Burkhauser.
Bracken, B., & Nagle, R. (2007). Psychoeducational assessment of preschool
0.98, while measures of stability range from 0.82 to 0.97.
children. New York: Routledge.
For Part I, interscorer reliability ranges from 0.95 to 0.98 Hogg, J., & Langa, A. (2005). Assessing Adults with Intellectual Disabil-
whereas it is 0.96 to 0.99 for Part II. Authors report ities. Malden, MA: Blackwell.
criterion validity in Part 1 moderately correlated with Lyman, W. (2008). Test review In N. Lambert, K. Nihira, & H. Lel (1993).
the ABS and the Vineland Adaptive Behavior Scales, AAMR Adaptive behavior scales: school. Assessment for Affective
Intervention, 33, 5557.
although Part II was not significantly related to either
Reynolds, C., & Fletcher-Janzen, E. (2007). Encyclopedia of special educa-
(Lyman, 2007). tion, a reference for the education of children, adolescents, and adults
The ABS-RC: 2 reports an internal consistency rang- with disabilities and other exceptional individuals (3rd ed., Vol. 1).
ing from 0.81 to 0.97. Concerning discriminant validity, Hoboken, NJ: Wiley.
Abbreviated Injury Scale A 5
AAMR ABS-RC: 2 Abbreviated Injury Scale A
AAMD Adaptive Behavior Scales E DISON WONG

Center for Pain & Medical Rehab
Fitchburg, MA, USA
AAMR ABS-S: 2 Synonyms
AAMD Adaptive Behavior Scales Organ injury scale
Definition
ABAS The Abbreviated Injury Scale (AIS) is an anatomical scor-

ing system first introduced in 1969. It has been revised
Adaptive Behavior Assessment System Second Edition and updated against survival data so that it now provides
a reasonably accurate way of ranking the severity of injury.
Injuries are ranked on a scale of 16, with 1 being
minor, 5 severe, and 6 an unsurvivable injury (Table 1).
This represents the threat to life associated with an
Abasia injury and is not meant to represent a comprehensive
measure of severity. The AIS is not a linear scale, in that
D OUGLAS I. K ATZ the difference between AIS1 and AIS2 is not the same as
Braintree Rehabiltation Hospital that between AIS4 and AIS5. Organ Injury Scales of the
Braintree, MA, USA American Association for the Surgery of Trauma are
Boston University School of Medicine mapped to the AIS score for calculation of the Injury
Boston, MA, USA Severity Score.
Definition
Current Knowledge
This refers to an inability to walk. Abasia may be caused
by a variety of conditions including weakness, spasticity, The latest incarnation of the AIS score is the 2005
cerebellar incoordination, and movement disorders of revision. AIS is monitored by a scaling committee of
various types. the Association for the Advancement of Automotive
Cross References
Abbreviated Injury Scale. Table 1 AIS scores and their
Ataxia definition of injury severity
Spastic Gait AIS Score Injury
1 Minor
2 Moderate
3 Serious
ABAS-II 4 Severe
5 Critical
Adaptive Behavior Assessment System Second
6 Unsurvivable
Edition
6 A Ability Focused
Medicine and has been adopted by the American Associ- ablation is too destructive to neighboring tissues. Even
ation for the Surgery of Trauma since its publication in with sophisticated neurosurgical techniques, ablation of
the Journal of Trauma in 1985. any type in the nervous system may still produce unwanted
motor, sensory, or cognitive-behavioral impairments.
References and Readings Cross References

Copes, W. S., Sacco, W. J., Champion, H. R., & Bain, L. W. (1989).
Commissurotomy
Progress in characterizing anatomic injury. Proceedings of the 33rd
Annual Meeting of the Association for the Advancement of
Craniotomy
Automotive Medicine, pp. 205218. Gamma Knife
Greenspan, L., McClellan, B. A., & Greig, H. (1985). Abbreviated injury Hemispherectomy
scale and injury severity score: A scoring chart. The Journal of Lobectomy
Trauma, 25, 6064.
Lobotomy
Moore, E. E., Shackford, S. R., Pachter, H. L., McAninch, J. W.
Browner, B. D., Champion, H. R., et al. (1989). Organ injury scaling:
Pallidotomy
Spleen, liver, and kidney. The Journal of Trauma, 29, 16646. Prefrontal Lobotomy
Yentis, S. M., Hirsch, N. P., & Smith, G. B. (2004). Anaesthesia and Radiosurgery
intensive care A-Z. New York: Butterworth & Heinemann. Temporal Lobectomy

Ability Focused Krayenbuhl, H., Wyss, O. A., & Yasargil, M. G. (1961). Bilateral thala-
motomy and pallidotomy as treatment for bilateral parkinsonism.
Flexible Battery Journal of Neurosurgery, 18, 429444.
Lord, S. M., & Bogduk, N. (2002). Radiofrequency procedures in chronic
pain. Best Practice & Research. Clinical Anaesthesiology, 16, 597617.
Lunsford, L. D., Flickinger, J. C., & Steiner, L. (1988). The gamma knife.
JAMA, 259, 2544.
Ablation Shah, R. V., Ericksen, J. J., & Lacerte, M. (2003). Interventions in
chronic pain management. 2. New frontiers: Invasive nonsurgical
E DISON WONG interventions. Archives Physical Medicine and Rehabilitation, 84,
Center for Pain and Medical Rehab S3944.
Fitchburg, MA, USA
Synonyms
Abnormal Brain Growth
Resection
Microcephaly
Definition
Ablation is the removal or destruction of an anatomical Abnormal Walking

structure by means of surgery, disease, or other physical or
energetic process. Ablation is employed as a treatment of Gait Disorders
various medical conditions and includes recent advances in
technology. Surgical ablation of neuronal pathways to the
globus pallidus or thalamus has been used historically to
treat parkinsonism. Interventional pain experts use radio-
frequency ablation of nerves in the spine to treat chronic Aboulia
back pain. Gamma radiation or gamma knife surgery is
used to excise brain tumors when traditional surgical Abulia
Absence Epilepsy A 7
an underestimation. It has been suggested that JAE may

ABS A
be as common as juvenile myoclonic epilepsy (JME),
though this has not been well-established. CAE is typically
Agitated Behavior Scale considered to be more common in females.
CAE is associated with a strong family history of
seizures. There is strong concordance among identical
twins, and multiple genes likely account for transmission.
Absence Epilepsy Siblings of patients with CAE have about a 10% chance of
having seizures, and about one-third of patients with CAE
J EFFREY B. T ITUS 1,2 , R EBECCA K ANIVE 1 have a family member with epilepsy. Nevertheless, the
M ICHAEL M ORRISSEY 1 causal influences of CAE are believed to be multifactorial,
1
St. Louis Childrens Hospital depending on both genetic and nongenetic factors. Causal
St. Louis, MO, USA factors in JAE have not been well-studied but may be
2
Washington University School of Medicine similar to what is found in CAE.
St. Louis, MO, USA
Natural History, Prognostic Factors,

Synonyms Outcomes
Petit mal epilepsy; Psychomotor seizures; Pyknoleptic Typical age of onset in CAE is between 3 and 8 years, but
petit mal (childhood absence epilepsy) rare cases of onset prior to 3 years of age have been
reported. Onset of JAE is considered to be between
10 and 17 years. Because onset of CAE has been reported
Definition in cases as old as 10 or 11 years, there is clear overlap
between CAE and JAE. EEG and clinical findings are often
Absence epilepsy is a form of idiopathic generalized useful in differentiating CAE from JAE in older children
epilepsy that is characterized by seizures that involve and younger adolescents. It is unusual for a child to
sudden arrest in activity, awareness, and responsiveness, exhibit features of CAE after the age of 11 years.
and may include some mild motor features. Typical Outcomes in CAE and JAE are generally favorable.
absence seizures usually last less than 10 s and end as Most patients with CAE experience remission of seizures
abruptly as they start. Patients have no recollection of by mid-adolescence, with only a small proportion experi-
the event and often return immediately to their previous encing absence seizures into adulthood. About 40% of
activity with little or no post-ictal alterations in function- patients with CAE also exhibit generalized tonicclonic
ing. Generalized spike-and-wave discharges on EEG are seizures. They often emerge around the time of puberty,
required for the diagnosis and are strongly correlated with are relatively easy to control, and more commonly persist
the clinical events. into adulthood than absence seizures. Tonicclonic seizures
Absence Epilepsy. Table 1 Clinical features of CAE and JAE

Categorization
CAE JAE
Childhood absence epilepsy (CAE). Incidence 28% (of children Unknown
Juvenile absence epilepsy (JAE). with epilepsy)
Age of onset 38 years 1017 years
Seizure frequency Multiple per day One or fewer
Epidemiology per day
Response to Good Good
Incidence reports of absence epilepsy range from 49 to 98
treatment
per 100,000. Among children with epilepsy, 28% have
Seizure freedom Expected Less common
been estimated to have CAE. The incidence of JAE has not
been well-studied. Estimates suggest that JAE accounts for Treatment Through Often through
up to 20% of absence epilepsy cases; however, this may be duration mid-adolescence adulthood
8 A Absence Epilepsy
are more common in JAE and occur in about 8090% of overall intelligence at least one standard deviation below
cases. Some patients with JAE also exhibit myoclonic the mean. Similar rates were found for VIQ and PIQ.
seizures, but they are typically mild and infrequent. While Their spoken language quotient (SLQ), as measured by
most patients with CAE become seizure-free in adoles- various versions of the Test of Language Development,
cence, seizure outcome in JAE is not well known. was average, but it was also lower than controls. A high
CAE is considered to be a benign childhood epilepsy percentage of children with CAE performed at least one
because of relatively good seizure control and functional standard deviation below the mean on language measures.
outcomes. Seizure control is less common in JAE, but In addition to finding a higher rate of cognitive
functional outcomes may be similar. Further research is limitations, Caplan et al. (2008) confirmed that children
needed to examine this. Tonicclonic seizures are believed with CAE also experience emotional and behavioral
to be a marker for poorer seizure outcome in both CAE comorbidities. Among the 69 children with CAE in their
and JAE. Functional outcomes in CAE are thought to be sample, 30% had a diagnosis of attention-deficit/hyperac-
most heavily influenced by psychosocial factors, such tivity disorder (ADHD), with 52% of those children diag-
as family adjustment, support systems, educational atti- nosed as ADHD-inattentive type. Moreover, about 29% of
tudes, and stigma toward the condition. Cognitive and/or their samples were diagnosed with a form of internalizing
behavioral side effects from antiepileptic drug (AED) psychopathology. Among those children, 75% were diag-
therapy may also limit outcomes. nosed with anxiety, 20% with depression, and 5% with
both anxiety and depression. After controlling for IQ and
demographic variables, children with CAE were found to
Neuropsychology and Psychology of have significantly higher ratings on scales of the Child
Absence Epilepsy Behavior Checklist (CBCL) that assess attention pro-
blems, somatic problems, social problems, withdrawal,
Cognitive functioning in CAE is traditionally considered and thought problems. The authors discovered that
benign, because children typically present with normal children with lower intelligence had greater social
intelligence and exhibit no significant impairments in problems, and females in the CAE sample were almost
functional outcomes. However, more recent research has six times more likely to be diagnosed with an anxiety
found evidence that patients with CAE are prone to disorder. In addition, children with CAE were more likely
having cognitive deficits and psychosocial problems, and to be diagnosed with ADHD or anxiety if they had more
they are more likely to receive special education services frequent seizures or a longer duration of illness.
and display low academic achievement. While patients
with poor seizure control exhibit the greatest difficulties,
cognitive and behavioral problems are also experienced by Evaluation
patients with good seizure control. Unfortunately, limited
information is known about cognitive and psychological Children and adolescents with CAE and JAE typically
functioning in JAE. present with no focal neurological abnormalities on
Patients with CAE do not have a characteristic examination. The presence of absence seizures is a defin-
cognitive profile. Cognitive difficulties have been reported ing feature of absence epilepsy, and hyperventilation or
in multiple domains, including attention, memory, and light stimulation can be highly effective at eliciting an
visual-spatial processing. A recent study by Caplan et al. event. In CAE, absence seizures occur multiple times per
(2008) revealed the presence of subtle cognitive impair- day, but, in JAE, they are more rare and may only occur
ments in children with CAE. When compared with con- once per day.
trols, they found that children with CAE (ages 6.711.2 Absence seizures can be either typical or atypical,
years) had significantly lower intelligence, as measured by and discrimination between the two types is usually
the Wechsler Intelligence Scale for Children Revised/Third done off of EEG findings. While typical absence seizures
Edition. While, as a group, children with CAE performed are characterized by clearly delineated episodes of activity
in the average range, they were below the performance of a arrest and impaired consciousness for less than 10 s,
control group. Similar differences were noted on verbal atypical absence seizures are associated with less abrupt
and visual intellectual tasks. The difference in perfor- onset and termination, and they may more commonly
mance IQ (PIQ) was less robust, but still significant, involve various semiological phenomena. Atypical
between children with CAE and controls. Among their absence seizures often last for more than 10 s and cannot
sample of 69 children with CAE, 27% demonstrated be elicited by hyperventilation or light stimulation. Tonic
Absence Seizure A 9
seizures are also frequently present in children with Ethosuximide has also been recommended and may be
A
atypical absence seizures. more appropriate for younger patients. In rare cases of
Typical absence seizures can be subdivided into simple more difficulty in controlling seizures, polytherapy may
and complex. Simple typical absence seizures constitute be needed. In patients with CAE, a seizure-free period of
about 90% of cases and may involve only minor motor 2 years is often recommended prior to discontinuation of
mannerisms (e.g., mild eyelid fluttering). Patients with therapy; however, this should be determined on a case-by-
complex typical absence seizures display more involve- case basis. Patients with JAE will require longer treatment
ment of motor features, such as automatisms or decreased and may continue on AEDs indefinitely. In adolescent
or increased muscle tone. Loss of consciousness may also patients, it is important to educate about the increased
be longer. risk of seizures with poor medication compliance, alcohol
Complex partial seizures can often mimic absence sei- consumption, or sleep deprivation.
zures, particularly when their expression is limited. Typical
absence seizures can be distinguished from complex partial
seizures because they are briefer, more frequent, and have no Cross References
post-ictal impairment. EEG characteristics and the presence
of various seizure types often distinguish atypical absence Petit Mal Seizure
seizures from complex partial epilepsy. Juvenile Myoclonic Epilepsy (JME)
When considering the presence of absence seizures, it
is important to consider whether the episodes can be
accounted for by variations in attention. This is especially
important when considering the high rate of attention
Aicardi, J. (1998). Diseases of the nervous system in childhood. London:
problems in children with epilepsy. Attempting to Mac Keith.
determine the degree of responsiveness during the epi- Berkovic, S. F., & Benbadis, S. (2001). Childhood and juvenile absence
sodes often helps with making the differential diagnosis; epilepsy. In E. Wyllie (Ed.), The treatment of epilepsy: Principles and
however, this can be difficult to determine when episodes practice (3rd ed. pp. 485490). Philadelphia, PA: Lippincott Williams
& Wilkins.
are very brief. Moreover, it is not uncommon for patients
Caplan, R., Siddarth, P., Stahl, L., Lanphier, E., Vona, P., Gurbani, S.,
to have both absence seizures and attention problems. Koh, S., Sankar, R., & Shields, W. D. (2008). Childhood absence
Therefore, a childs ability to respond during an episode epilepsy: Behavioral, cognitive, and linguistic comorbidities.
cannot be used to rule-out the presence of absence seizures. Epilepsia, 49(11), 18381846.
Sometimes a neuropsychological assessment can be helpful
in differentiating between absence seizures and episodes of
inattention. If the examiner has experience with absence
seizures, the neuropsychological assessment can provide Absence Seizure
multiple hours of one-on-one observation and interaction
that might provide opportunities to observe the episodes K ENNETH P ERRINE
and attempt to elicit responses. This can also be helpful if Northeast Regional Epilepsy Group
mental fatigue tends to elicit more events. Hackensack, NJ, USA
On EEG, absence seizures are characterized by parox- Weill-Cornell College of Medicine
ysmal bursts of high amplitude 34 Hz spike and slow New York, NY, USA
waves that are superimposed on a normal background.
The bursts vary in length (310 s), and the clinical absence
is time-locked to the burst period. This activity (clinical Synonyms
and electrographic) can be provoked during a routine
EEG recording using the hyperventilation activation Petit mal seizure; Psychomotor seizures
procedure.
Definition
Treatment
An absence (usually pronounced with a French accent as
Response to AED therapy in CAE and JAE is good, and ab-SAWNS) seizure is a type of generalized seizure
valproic acid is often considered the drug of first choice. caused by a large burst of electrical discharges that
10 A Abstract Reasoning
begins in broad, bilateral brain regions simultaneously (as

opposed to a partial seizure). During an absence seizure, Abstract Reasoning
the patient will lose interaction with the environment,
stare blankly (zone out), and perhaps blink the eyes. DAVID H ULAC
There is no true loss of consciousness or motor functions. University of South Dakota
The seizure is typically short in duration (only several Vermillion, SD, USA
seconds), and patients often resume their ongoing activity
without realizing even that they had a seizure (but will be
amnestic for anything occurring during the episode). Synonyms
There are no postictal problems after the end of the
seizure. Although no first aid is required, the patient Logical reasoning
should be protected from doing anything dangerous dur-
ing the episode (e.g., cooking, crossing the street) but the
episodes are often so brief that intervention is difficult. Definition
The neuropsychological construct of abstract reasoning

Current Knowledge refers to an individuals ability to recognize patterns and
relationships of theoretical or intangible ideas. Abstract
The cause of absence seizures is unknown. Patients with
reasoning is contrary to concrete reasoning whereby an
absence seizures typically have no positive neuroimaging
individual recognizes patterns in information obtained
findings, but usually have bursts of 3-per-s bilaterally
through the immediate senses. When thinking abstractly,
synchronous spike/wave epileptiform activity on a routine
an individual must analyze and synthesize information
EEG (even when not having a seizure). Absence seizures
without the aid of empirical information. Frequently,
can be differentiated clinically from complex partial sei-
abstract reasoning requires an individual to apply con-
zures, in which there is a similar disruption of conscious-
crete information to other scenarios that may not directly
ness and zoning out, by the duration of the episode.
relate to that persons experience.
Absence seizures last only a few seconds, while complex
Abstract reasoning is most closely related to rational
partial seizures usually last 11.5 min. Absence seizures
thought as opposed to empirical thought. While using
typically begin in childhood, respond well to medication,
deductive reasoning, a purely rational thinker does not
and often remit spontaneously by adulthood. Common
look to determine the accuracy of a premise, but seeks
medications for absence seizures include divalproex/
only to understand the relationship between the premises.
valproate sodium (Depakote), ethosuximide (Zarontin),
An example of deductive reasoning, which requires
and lamotrigine (Lamictal). Although the frequency of
abstract reasoning, may go like this:
absence seizures can approach dozens per day, only mild
(at worst) neuropsychological deficits are typically shown 1. Premise 1: Egypt is located in South America.
if the absence episodes occur without other seizure types. 2. Premise 2: The Sphinx lies in Egypt.
They do not have a dramatic impact on academic perfor- 3. Conclusion: The Sphinx is located in South America.
mance. However, absence seizures may occur with other
Empirically and concretely, it is obvious that Egypt is
seizure types in serious disorders such as Lennox-Gastaut
not in South America, but in Africa. To complete the
syndrome, in which case there is considerable cognitive
syllogism, however, the thinker must ignore the concrete
dysfunction and a worse prognosis.
distortion, and instead focus on the two premises and
understand if the conclusion logically flows.
Cross References Common measures of abstract reasoning include the
Similarities, Picture Concepts, and Matrix Reasoning
Epilepsy subtests of the Wechsler scales. During a mental status
exam, abstract reasoning is measured by asking a subject
to describe the meanings of proverbs or to describe word
similarities.
Abstract reasoning, most commonly understood as
Engel, J., & Pedley, T. A. (Eds.). (2008). Epilepsy: A comprehensive textbook
(2nd ed.). New York: Lippincott Williams & Wilkins. being a function of the left hemisphere of the brain, is
www.epilepsyfoundation.org a precursor for using and understanding language and
Academic Ability A 11
mathematics. Individuals who struggle with abstract Cross References A

reasoning benefit when an instructor uses examples to
make the concept more concrete. Frequently, children Action-Intentional Disorders
with learning disabilities have difficulty with these Adynamia
abstract subjects, but achieve greater success in courses Avolition
with more concrete subject matters such as social studies
and science.
Berrios, G. E., & Grli, M. (1995). Abulia and impulsiveness revisited:
References and Readings A conceptual history. Acta Psychiatrica Scandinavica, 92(3),
161167.
Caplan, L. R., Schmahmann, J. D., Kase, C. S., Feldmann, E., Baquis, G.,
Goldstein, G. (2004). Abstract reasoning and problem solving in adults.
Greenberg, J. P., et al. (1990). Caudate infarcts. Archives of neurology,
In M. Hersen (Ed.), Comprehensive handbook of psychological
47(2), 133143.
assessment, Vol. 1: Intellectual and neuropsychological assessment
Drubach, D. A., Zeilig, G., Perez, J., Peralta, L., & Makley, M. (1995).
(pp. 293308). Hoboken, NJ: Wiley.
Treatment of abulia with carbidopa/levadopa. Journal of Neurologic
Rehabilitation, 9, 151155.
Egnelborghs, S., Marien, M. A., Pickut, B. A., Verstraeten, M. A., &
De Deyn, P. P. (2000). Loss of psychic self-activation after parame-
dian bithalamic infarction. Stroke, 31, 17621765.
Forstl, H., & Sahakian, B. A. (1991). A psychiatric presentation of abulia:
Abulia Three cases of frontal lobe ischaemia and atrophy. Journal of the
Royal Society of Medicine, 84, 8991.
I RENE P IRYATINSKY Kumral, E., Evyapan, D., & Balkir, K. (1999). Acute caudate vascular
lesions. Stroke, 30, 100108.
Butler Hospital and Alpert Medical School of Brown
Laplande, D. N. A., Sauron, B., de Billy, A., & Dubois, B. (1992). Lesions
University of the basal ganglia due to disulfiram neurotoxicity. Journal of
Providence, RI, USA Neurology, Neurosurgery & Psychiatry, 55, 925929.
Litvan, I., Paulsen, J. S., Mega, M. S., & Cummings, J. L. (1998). Neuro-
psychiatric assessment of patients with hyperkinetic and hypokinetic
movement disorders. Archives of Neurology, 55, 13131319.
Synonyms Powell, J. H., Al-Adawi, S., Morgan, J., & Greenwood, R. J. (1996).
Motivation deficits after brain injury: Effects of bromocriptine in
Aboulia; Apathy; Athymia; Loss of psychic self-activation; 11 patients. Journal of Neurology, Neurosurgery & Psychiatry, 60,
Psychic akinesia 416421.
Definition Abusive Head Trauma

Abulia refers to a lack of will, drive, or initiative. The word Shaken Baby Syndrome (SBS)
is derived from the Greek abla, meaning non-will.
It should be distinguished from an inability to actually
perform the activity due to cognitive or physical disability.
Abulia is manifested by the lack of motivation, spontane-
ity, and initiation. Some research indicates that abulia ACA
occurs because of malfunction of the brains dopamine-
dependent circuitry, especially bilateral lesions in the Anterior Cerebral Artery
medial frontal lobes, basal ganglia, and their connections.
The following criteria have been suggested for the diag-
nosis of abulia: (1) decreased spontaneity in activity and
speech; (2) prolonged latency in responding to queries, Academic Ability
directions, and other stimuli; and (3) reduced ability to
persist with a task. Academic Competency
12 A Academic Competency
Ma, L., Phelps, E., Lerner, J. V., & Lerner, R. M. (2009). Academic
Academic Competency competence for adolescents who bully and who are bullied. The
Journal of Early Adolescence, 29(6), 862897.
Shapiro, E. S. (2008). From research to practice: promoting academic
T ODD VAN W IEREN
competence for underserved students. School Psychology Review,
Indiana University of Pennsylvania 37(1), 4651.
Indiana, PA, USA
Synonyms Academic Performance

Academic ability; Academic performance; Educational Academic Competency
productivity
Definition Academic Skills

The multidimensional characteristics of a learner C HRISTINA Z AFIRIS
including skills, attitudes, and behaviors that factor University of Northern Colorado
into their academic success. These characteristics can be Greeley, CO, USA
separated and considered in one of two primary domains:
academic skills or academic enablers (DiPerna & Elliot,
2000; Elliot & DiPerna, 2002). Academic skills are both Definition
the basic and complex skills (e.g., reading, writing, calcu-
lating, and critical thinking) needed to access and interact Academic skills refer to a students ability to perform age-
with content-specific knowledge. Academic enablers, appropriate school activities related to writing, reading,
however, are the attitudes and behaviors (e.g., interper- and mathematical problem-solving. Additionally, academ-
sonal skills, motivation, study skills, and engagement) ic skills refer to the information learned which is relevant
that a learner needs in order to take advantage of to school success. Having solid academic skills improves
education. academic progress throughout ones school experience.
Many of the academic skills a child learns are acquired
in the school setting. However, pre-academic skills may
Cross References be obtained in the childs environment prior to the start
of formal schooling. This may be achieved by exposure
Academic Skills to mathematics (such as adding and subtracting objects
Learning at home), coloring, and reading with and to the child.

Edl, H. M., Jones, M. H., & Estell, D. B. (2008). Ethnicity and english Academic Competency
proficiency: Teacher perceptions of academic and interpersonal
Educational Testing
competence in European American and Latino students. School
Psychology Review, 37(1), 3845.
Learning
Elliot, S. N., & DiPerna, J. C. (2002). Assessing the academic competence Reading
of college students: Validation of a self-report measure of skills and
enablers. Journal of Postsecondary Education and Disability, 15(2),
87100.
DiPerna, J. C., & Elliot, S. N. (2000). The academic competence evaluation
scales (ACES college). San Antonio, TX: The Psychological
Association. Burchinal, M. R., Peisner-Feinberg, E., Pianta, R., & Howes, C. (2002).
Hutto, L. (2009). Measuring academic competence in college students: a Development of academic skills from preschool through second
review of research and instruments. Saarbrucken Germany: VDM grade: Family and classroom predictors of developmental
Verlag. trajectories. Journal of School Psychology, 40(5), 415436.
Acalculia A 13
Christian, K., Morrison, F. J., & Bryant, F. B. (1998). Predicting kinder- Alexic acalculia is the inability to read number and
garten academic skills: Interactions among child care, maternal A
correlations with the inability to read text. People with
education, and family literacy environments. Early Childhood
Research Quarterly, 13(3), 501521.
this type of acalculia may focus only on beginning digits
Shapiro, E. S. (2004). Academic skills problems: Direct assessment and (538 is read as 53). For those with alexic acalculia, mental
intervention (3rd ed.). New York: Guilford Press. calculation abilities exceed written calculation abilities
(Ardila & Rosselli, 2002).
Agraphic acalculia is the inability to write numbers.
Like aphasic acalculia, agraphic acalculia correlates with
Acalculia Brocas and Wernickes aphasia. In Brocas aphasia, acal-
culia deficits manifest as omissions, substitutions, and
N ATALIE WAHMHOFF, E LAINE C LARK order reversal. In Wernickes aphasia, difficulties are espe-
University of Utah cially evident when required to write quantities when they
Salt Lake City, UT, USA are orally dictated. Those with Wernickes aphasia also
tend to make paralexias and paragraphias (Ardila & Ros-
selli, 2002; Growth-Marnat, 2000).
Synonyms Frontal acalculia deficits occur in conjunction with
attention difficulties, perseveration, and impairment of
Acquired dyscalculia; Dyscalculia; Mathematics disability more complex math concepts (Dehaene, Cohen, & Chan-
geux, 1998). Difficulties are most apparent with multistep
operations, algorithms, and when planning is required.
Definition While complex concepts are difficult for patients with
frontal acalculia, more basic math concepts are usually
Acalculia, most simply, is the inability to perform mathe-
maintained (Ardila & Rosselli, 2002).
matical tasks. These difficulties can stem from other def-
Spatial acalculia impacts written mathematical tasks
icits or can exist independently. Acalculia deficits can be
more than mental math tasks. A difficulty with writing
global or selective and manifest in a wide variety of num-
numbers is quite apparent in these cases and manifest in
ber processing and calculation abilities.
several ways. Writing on only one side of the page, inability
to write numbers in a straight line, and general disorganiza-
Categorization tion are some of the deficits that impact math performance
(Basso, Burgio, & Caporali, 2000). Patients with spatial
Generally, authors have agreed on two major distinctions: acalculia often forget where to place remainders and car-
primary and secondary acalculia (Growth-Marnat, 2000). ried numbers, despite understanding the basic division
Primary acalculia occurs when mathematical deficits are and multiplication functions. Math procedure signs are
fundamental and are present independently of other defi- often undetected or switched (add instead of subtract).
cits. Deficits in primary acalculia include poor estimation,
number comparison abilities, and difficulty understanding
procedural rules and numerical signs. In primary acalculia, Epidemiology
these deficits will exist regardless of whether tasks are pre-
sented in an oral or written format (Adila & Rosselli, 2002). Acalculia can result from stroke, tumors, and trauma. It is
The secondary acalculias are due to primary deficits in also seen in patients with degenerative dementia (Ardila &
other areas. Aphasic acalculia occurs in patients with Wer- Rosselli, 2002).
nickes and Brocas aphasia. Patients with Brocas aphasia
have problems when translating word representations of
numbers (three hundred and forty-five) to their numeral Prognostic Factors and Outcomes
form (345). They may also read numbers with morpho-
logical errors (15 is read as 50) (Ardila & Rosselli, 2002; There is noted variability in prognosis for acalculia, ranging
Basso, Burgio, & Caporali, 2000). When the secondary from no recovery to full recovery. For primary acalculia,
acalculia stems from Wernickes aphasia, deficits are more improvement is limited. In the case of secondary acalculias,
severe. Reading and writing of numbers often have semantic recovery from the primary deficit, such as aphasia, alexia,
errors, and poor verbal memory often impacts the calcula- and agraphia, occur, the corresponding acalculia deficits
tion abilities of these patients (Grafman & Rickart, 2000). tend to improve as well.
14 A ACC
Neuropsychology and Psychology assessment. This will provide explicit areas to target dur-
of Acalculia ing rehabilitation (Grafman & Rickart, 2000). Long-term
rehabilitation programs should begin simply and progres-
Primary acalculia is associated with left posterior parietal sively work toward more complex tasks. With secondary
lesions. More specifically, damage to the left angular acalculia, focusing rehabilitation on the primary deficit
and supramarginal gyri occurs with primary acalculia may significantly improve the secondary acalculia deficits
(Grafman & Rickart, 2000). It is suggested that there are (Ardila & Rosselli, 2002).
separate neuropathways for rote number knowledge and
semantic number knowledge.
Neuroimaging techniques reveal that several brain Cross References
areas are active when performing calculations and also
that the pattern differs according to what type of calcula- Agraphia
tion is done (Dehaene, Cohen, & Changeux, 1998). This Alexia
occurs to the many abilities that calculation often Aphasia
requires, including verbal, spatial, executive functioning, Gerstmanns Syndrome
and memory. The areas most associated with calculation Spatial Dyscalculia
are the upper cortical surface and anterior aspect of the
left middle frontal gyrus, the bilateral supramarginal and
angular gyrus, the left dorsolateral prefrontal and premo- References and Readings
tor cortices, Brocas area, inferior parietal and left parietal
cortex, and the inferior occipitotempral regions (Ardila & Ardila, A., & Rosselli, M. (2002). Acalculia and dyscalculia. Neuropsychol-
Rosselli, 2002). ogy Review, 12, 179231.
It is important to keep in mind that damage to the Ardila, A., Matute, E., & Inozemtseva, O. (2003). Progressive agraphia,
right hemisphere and the frontal lobes also impact the acalculia, and anomia: a single-case report. Applied Neuropsychology,
10, 205214.
occurrence of acalculia, especially when it is a secondary
Basso, A., Burgio, F., & Caporali, A. (2000). Acalculia, aphasia, and spatial
acalculia. disorders in left and right brain-damaged patient. Cortex, 36,
265280.
Dehaene, S., Cohen, L., & Changeux, J. P. (1998). Neuronal network
Evaluation models of acalculia and prefrontal deficits. In R. W. Parks, D. S.
Levine, & D. L. Long (Eds.), Fundamentals of neural network model-
ing: neuropsychology and cognitive neuroscience (pp. 233255).
The arithmetic section of the Wide Range Achievement Cambridge, MA, USA: MIT.
Test (WRAT) has often been used to test operational skills. Grafman, J., & Rickart, T. (2000). Acalculia. In M. J. Farah & T. E.,
The Key Math, which is designed for children and adoles- Fienberg (Eds.), Patient based approaches to cognitive neurosciences:
cents, tests more targeted and specific abilities that are issues in clinical and cognitive neuropsychology. Cambridge,
Massachusetts: MIT.
suggested for an acalculia assessment (Grafman & Rickart,
Growth-Marnat, G. (Ed.). (2000). Neuropsychological assessment in clini-
2000). Many authors have suggested experimental bat- cal practice. New York: Wiley.
teries that target specific functions and include error Scruggs, T. E. & Mastropieri, M. A. (2000). Acalculia. In Encyclopedia of
analysis. These batteries often assess skills in the following special education (2nd ed., Vol. 1, p. 27). New York: Wiley.
areas: number recognition, number writing, number
transcoding, quantification, magnitude estimation, basic
arithmetic operations, calculation fact verification, multi-
column calculations, magnitude comparison, fractions,
algebra, and numeric knowledge. When possible, these
ACC
skills should be assessed in both written and oral form
Anterior Cingulate Cortex
(Ardila & Rosselli, 2002; Grafman & Rickart, 2000).
Treatment
Accelerated Hypertension
Some authors have suggested beginning rehabilitation
with an error analysis if it was not completed during the Hypertensive Encephalopathy
Accessory Cuneate Nucleus A 15
more likely to demonstrate a diffuse, rather than focal,

Acceleration Injury A
profile of cognitive impairment when cognitive im-
pairment is present. The lateralization of cognitive im-
B ETH R USH pairment that is typically observed in focal brain injury
Mayo Clinic is relatively uncommon following acceleration injury.
Jacksonville, FL, USA A diffuse profile of cognitive impairment in acceleration
injury is due to the disruption of white matter tracts that
are responsible for efficiency and coordination of com-
Synonyms munication between functional brain injuries. As such, a
patient with acceleration injury may demonstrate cogni-
Accelerationdeceleration injury tive slowing, executive dysfunction, and problems with
simple and complex attention as a consequence of his/her
Definition brain injury.
Traumatic injury to the brain resulting from high-speed

acceleration of the brain within the skull cavity in the Cross References
direction of inertial force.
Biomechanics of Injury
Deceleration Injury
Current Knowledge Diffuse Axonal Injury
During acceleration injury, movement of the head is un-

restricted. One of the most common scenarios resulting in
acceleration injury is a high-speed motor vehicle accident.
Primary brain injury results from brain tissue and brain
Bayly, P. V., Cohen, T. S., Leister, E. P., Ajo, D., Leuthardt, E. C., Genin,
structures compressing against one another in the force
G. M. (2005). Acceleration-induced deformation of the human
of inertia. This may result in bruising, hemorrhage, and brain. Journal of Neurotrauma, 22(8), 845856.
shearing of the underlying tensile strength of white matter Sabet, A. A., Christoforou, E., Zatlin, B., Genin, G. M., & Bayly, P. V.
connections deep within the brain. Secondary injury may (2008). Deformation of the human brain induced by mild angular
occur hours or even days after the inciting traumatic head acceleration. Journal of Biomechanics, 41(2), 307315.
event. Secondary effects of injury can include decreased

cerebral blood flow, edema, hemorrhage, increased intra-
cranial pressure, and biochemical changes that may cause
excitotoxicity and more extensive damage to the surround- Accelerationdeceleration Injury
ing brain structures and their associated connections.
Theoretical models of linear acceleration injury now Acceleration Injury
address the heterogeneity of effects that can result from Deceleration Injury
such biomechanical injuries. Although diffuse brain dam-
age may result from this type of injury, a key factor that
predicts the extent of damage following acceleration inju-
ry is the area of initial impact. Given that the structure
and projection pathways of the brain have varying densi- Accessory Cuneate Nucleus
ties and tensile strengths within different regions of the
brain, the point of impact is most likely the key in deter- J OHN E. M ENDOZA
mining the extent of damage that takes place and the Tulane University Medical Center
likelihood and course of recovery that is possible follow- New Orleans, LA, USA
ing injury.
Patients sustaining acceleration injury may experience
headache, photophobia, phonophobia, nausea, and dizzi- Synonyms
ness immediately following injury onset. On neuropsycho-
logical evaluation, patients with acceleration injuries are Lateral cuneate nucleus
16 A Accident Claims
Definition Definition
Nucleus in the dorsolateral portion of the medulla In order to provide students with disabilities the free,
that receives sensory information likely from touch, pres- appropriate public education mandated by IDEA 2004
sure, and stretch receptors in the upper extremities. It and Section 504 of the Rehabilitation Act of 1973, changes
gives rise to the cuneocerebellar tract which enters the typically must be made to a childs educational curric-
cerebellum via the inferior cerebellar peduncle. The acces- ulum or environment. These accommodations include
sory cuneate nucleus is thought to be the equivalent of the changes in the method of presentation of material,
dorsal nucleus of Clarke in the lumbar, thoracic, and classroom seating location, availability of an interpreter
lower cervical cord which is the source of the dorsal for those with hearing impairment, response format,
spinocerebellar tract. These nuclei and tracts provide un- testing time allowed, setting, or other reasonable steps
conscious (as opposed to conscious) sensory feedback that do not significantly alter the content of educational
to the cerebellum in its regulation of individual muscles. material or the validity of tests. To be eligible to receive
Lesions of this nucleus might be expected to produce accommodations, students must be identified as having
cerebellar type symptoms of the ipsilateral upper extrem- a disability consistent with the guidelines presented in
ity (i.e., ataxia/incoordination of movement), but it is IDEA 2004 or Section 504 of the Rehabilitation Act of
relatively small and isolated lesions are likely to be 1973.
extremely rare. Accommodations may also be required in the work-
place under the Americans with Disabilities Act. These
could include installation of a ramp to permit wheelchair
access, flexible working hours, or provision of TTY
machines.
Accident Claims
Personal Injury Cross References
504 Plan, Americans with Disabilities Act
Accident Neurosis References and Readings

Compensation Neurosis
Education, 34 C.F.R. }104.
Individuals with Disabilities Education Improvement Act of 2004, 20 U.S.
C. } 1400 et seq.
Rehabilitation Act, 29 U.S.C. } 794.
Accommodations
J ACOB T. LUTZ 1, DAVID E. M C I NTOSH 2
1
Bell State University
Accumbens Nucleus
Muncie, IN, USA
2 Nucleus Accumbens
Bell State University
Muncie, IN, USA
Synonyms Acetylaspartic Acid

Reasonable accommodations N-Acetyl Aspartate
Acetylcholine A 17
important role in the contraction of skeletal muscles.

Acetylcholine A
Studies also suggest a role in cortical arousal, REM sleep,
and cognitive functions such as attention, learning, and
J OA NN T. T SCHANZ 1, K ATHERINE T REIBER 2 memory. Its presence in cardiac and smooth muscles,
1
Utah State University organs, and salivary, tear, and sweat glands affect auto-
Logan, UT, USA nomic functions (Feldman et al., 1997).
2
Worcester, MA, USA
Current Knowledge
Definition
Applications
Acetylcholine has been identified as a neurotransmitter
substance since the mid-1920s. It is the neurotransmitter Dysfunction in the cholinergic system has been impli-
substance present at the neuromuscular junction and also cated in a number of clinical conditions including Alzhei-
innervates structures of the parasympathetic and sympa- mers disease (AD), diffuse Lewy body dementia (Londos,
thetic nervous systems (Feldman, Meyer, & Quenzer, 1997; Brun, Gustafson, & Passant, 2003), Huntingtons disease,
Iversen, Iversen, Bloom, & Roth, 2009). In the brain, and myasthenia gravis (Iversen et al., 2009). Recent work
cholinergic neurons have a wide distribution. Projections also suggests a reduction in cholinergic activity in Parkin-
emanate from the basal forebrain in the medial septal sons disease that may appear relatively early in the course
nucleus and terminate in the hippocampus and limbic of the condition (Shimada et al., 2009). Acetylchoinester-
cortex. Among other areas receiving cholinergic input are ase inhibitors are used in the palliative treatment of AD
the neocortex, olfactory bulbs, amygdala, neostriatum and myasthenia gravis. Cholinergic or anticholinergic
(caudate nucleus and putamen), the hypothalamus, and compounds are also used as a muscle relaxant for surgery,
various regions in the brain stem (Feldman et al., 1997). treatment of parkinsonism, glaucoma, urinary retention,
Acetylcholine is synthesized from the precursors Acetyl and in nonclinical applications such as insecticides in
CoA and choline in a chemical reaction involving the cata- agriculture and neurotoxins (and their antidotes) in war-
lytic enzyme, choline acetyltransferase (ChAT). The pres- fare (Feldman et al., 1997; Iversen et al., 2009). Much
ence of this enzyme has been used as a marker to locate research is being conducted to develop agents with greater
cholinergic neurons. Acetylcholine degradation (the prima- receptor subtype specificity to better address clinical
ry mode of removal from synapses) is accomplished by the conditions.
activity of a group of enzymes known as cholinesterases.
Acetylcholinesterase is the primary enzyme that breaks
down acetylcholine in the synapse. Thus, to enhance cho- Cross References
linergic function, a number of substances have been devel-
oped that inhibit the activity of this enzyme (Iversen Alzheimers Disease
et al., 2009). Anticholinesterase Inhibitors
Based on differences in the agonists that stimulate Cholinesterase Inhibitors
cholinergic receptors, two receptor subtypes have been
identified, nicotinic and muscarinic. Nicotinic receptors
are stimulated by nicotine, are excitatory, and show a References and Readings
rapid response to stimulation. Muscarinic receptors are
stimulated by muscarine, have either excitatory or inhibi- Feldman, R. S., Meyer, J. S., & Quenzer, L. F. (1997). Acetylcholine. In
tory effects, and show a slower response to stimulation. Principles of neuropsychoparhmacology (pp. 246249). Sunderland,
Further subtypes exist within the nicotinic and muscarin- MA: Sinauer Associates.
ic classes (Feldman et al., 1997; Iversen et al., 2009). Iversen, L. L., Iversen, S. D., Bloom, F. E., & Roth, R. H. (2009). Acetyl-
Acetylcholine is involved in a number of behavioral choline. In Introduction to neuropsychopharmacology (pp. 128149).
New York: Oxford University Press.
processes. As a neurotransmitter substance at the neuro- Londos, E., Brun, A., Gustafson, L., & Passant, U. (2003). Lewy body
muscular junction, it acts on motor neurons of the spinal dementia. Clinical challenges in diagnosis and management. In
cord and cranial motor nerve nuclei, playing an K. Iqbal & B. Winblad (Eds.), Alzheimers disease and related
18 A Acetylcholinergic System
disorders: Research advances (pp. 133142). Bucharest, Romania: (Bartels & Zeki, 2000), patients lose the ability to perceive
Ana Asian International Academy of Aging.
color, and therefore experience the world as varying
Shimada, H., Hirano, S., Shinotoh, H., Aotsuka, A., Sato, K., Tanaka, N.,
et al. (2009). Mapping of brain acetylcholinesterase alterations in
shades of gray. This disorder is termed cerebral achroma-
Lewy body disease by PET. Neurology, 73, 273278. topsia. The loss of color vision in these patients cannot be
explained by the photoreceptors typically damaged or
absent in patients with other types of color blindness.
Acetylcholinergic System
Categorization
Cholinergic System
Cerebral achromatopsia results from bilateral damage to
the V4/V4a region of the color center. If patients experi-
ence complete ablation of V4, they lose color vision in
Acetylcholinesterase Inhibitors their entire visual field. However, if patients experience
unilateral damage to V4, hemi-achromatopsia ensues,
Anticholinesterase Inhibitors where patients only lose color vision in the contralateral
Cholinesterase Inhibitors half of their visual field. In less extreme cases, known as
dyschromatopsia, patients lose the ability to perceive se-
lective colors and/or color constancy. These neuropsycho-
logical disorders, which are the result of damage to the
ACHE Inhibitors cerebral cortex, should not be confused with congenital
achromatopsia, which occurs as a malfunction of the cone
Anticholinesterase Inhibitors photoreceptors.
Epidemiology
AchEIs
Cerebral achromatopsia arises following brain damage to
Anticholinesterase Inhibitors V4/V4a located in the ventral medial region of the occipi-
Cholinesterase Inhibitors tal lobe, typically caused by a tumor, a hemorrhage, or
some sort of brain trauma. Due to the low incidence rate
of cerebral achromatopsia, it is difficult to provide a
reliable estimate of its prevalence. However, it seems safe
Achromatopsia to say that it is extremely rare. A review of the documen-
ted cases showed that of the 27 cases reported, 3 patients
S OPHIE L EBRECHT, M ICHAEL J. TARR recovered, 3 partially recovered, and 21 showed no recov-
Brown University ery (Bartels & Zeki, 2000).
Providence, RI, USA

Synonyms Outcomes
Acquired achromatopsial; Color agnosia; Color blindness; The first cases of cerebral achromatopsia were reported
Cortical color blindness by Verrey (1888). In response to these patients, Verrey
introduced the concept of a color center in the brain.
Continued research confirmed the existence of a cortical
Short Description or Definition region devoted to color processing. Almost a century later,
Meadows demonstrated a correlation between the cor-
Following damage to the ventral medial region of the tical regions sensitive to color, and the damaged cortical
occipital lobe, known as the color center of the brain regions in achromatopsic patients (Meadows, 1974).
Acoustic Aphasia A 19
Neuropsychology and Psychology of occur for up to a year. With regard to the treatment and
A
Achromatopsia diagnosis of cerebral achromatopsia, experimenters re-
port that some patients are not conscious of the absence
The region of damage in the visual field of achromotopsic of color vision. This phenomenon has been explained
patients, V4/V4a, is organized retinotopically; therefore, by the ablation of a color module leaving patients with-
damage to a particular region of V4 results in a loss of out even the concept of color post-lesion. This symp-
color vision at the corresponding location in the visual tom of achromatopsia should be noted when addressing
field. For example, if damage to V4 occurs in the left patients, because pushing a patient to describe a condi-
hemisphere, the patient will lose color vision in the right tion they are not aware of could be distressing for the
half of their visual field. Because V4 is located in the patient.
vicinity of the fusiform gyrus and the lingual gyrus,
known to process faces (Kanwisher et al., 1997), the co-
morbity between achromatopsia and prospoagnosia is
extremely high (Bouvier & Engel, 2006). In addition,
Cross References
patients with achromatopsia also have a higher incidence
Scotoma
of spatial and shape deficits. It has been noted that
patients with complete achromatopsia cannot even imag-
ine color, which means they cannot dream in color or use
color during mental imagery. This absence of color vision References and Readings
often leaves patients with no appetite for foods, which
appear gray, and no desire for intimacy, as flesh appears Bartels, A., & Zeki, S. (2000). The architecture of the color centre in the
gray. An insightful case study of a color-blind painter human visual brain: New results and a review. The European Journal
describes these experiences in detail (Sacks, 1995). of Neuroscience, 12(1), 172193.
Bouvier, S. E., & Engel, S. A. (2006). Behavioral deficits and cortical
damage loci in cerebral achromatopsia. Cerebral Cortex (New York,
N.Y.: 1991), 16(2), 183191.
Evaluation Kanwisher, N., McDermott, J., & Chun, M. M. (1997). The fusiform
face area: A module in human extrastriate cortex specialized
Cerebral achromatopsia can be diagnosed using a range of for face perception. Journal of Neuroscience, 17(11), 43024311.
color vision tests. The simplest test is an explicit color- Meadows, J. C. (1974). Disturbed perception of colors associated with
localized cerebral lesions. Brain: A Journal of Neurology, 97(4),
naming task that requires patients to name the color of 615632.
individual flash cards. The most common test for color Sacks, O. W. (1995). An anthropologist on mars: Seven paradoxical tales.
blindness is the Ishihara plates test. These plates contain New York: Vintage Books.
isoluminant colored dots of varying sizes that together Verrey, D. (1888). Hemiachromatopsie Droite Absolue. Conversation
create the perception of a number embedded in noise. Partielle De La Perception Lumineuse Et Des Formes. Ancien Kyste
Hemorrhagique De La Partie Inferieure Du Lobe Occipital Gauche.
In order to perceive the number, patients must be able to Archives dophtalmologie, 8, 289300.
distinguish between the different colored dots. Another Werner, J. S., & Chalupa, L. M. (2004). The visual neurosciences.
widely-used test is the Farnsworth-Maunsell 100 Hue test, Cambridge, MA: MIT Press.
in which patients are required to order colored caps based
on gradual shifts in hue from light to dark. Patients with
color blindness are unable to perform this task. Rarely, a
diagnosis is made using a Nagel Anomaloscope. This
apparatus is typically used to determine whether a patient ACoA
is a monochromat or a diachromat; however, some
experimenters/practitioners use it in the study of cerebral Anterior Communicating Artery
achromatopsia.
Treatment
Acoustic Aphasia
There is a period of spontaneous recovery for neurovisual
lesions, which typically lasts 3 months post-lesion, but can Pure Word Deafness
20 A Acoustic Neuroma
Acoustic Neuroma
E THAN M OITRA
Drexel University
Morgantown, WV, USA
Synonyms
Neurolemmoma; Vestibular schwannoma
Definition
A benign tumor of the Schwann cells occurring near the

cerebellopontine angle of the brain stem. Typically, it
arises from the vestibulocochlear or eighth cranial nerve,
which connects the brain to the inner ear. It is commonly
associated with neurofibromatosis type 2 and often occurs
bilaterally. Tumor growth is usually slow and may result in Acoustic Neuroma. Figure 2 Courtesy Carol
some hearing loss or deafness, tinnitus, vertigo, and Armstrong. Childrens Hospital of Philadelphia and
vestibular dysfunction. Most acoustic neuromas are diag- the University of Pennsylvania Medical School,
nosed in patients between the ages 30 and 60. Etiology is Department of Neurology
unknown. Treatment options include radiosurgery and
microsurgical removal.
Cross References
Radiosurgery
Radiotherapy
Jrgensen, B. G., & Pedersen, C. B. (1994). Acoustic neuroma. Follow-up

of 78 patients. Clinical Otolaryngology, 19, 478484.
Acquired Achromatopsial
Achromatopsia
Acoustic Neuroma. Figure 1 Courtesy Carol Armstrong. Acquired Dyscalculia

Childrens Hospital of Philadelphia and the University of
Pennsylvania Medical School, Department of Neurology Acalculia
Acquired Immunodeficiency Syndrome (AIDS) A 21
pandemic has killed approximately 25 million people

Acquired Epileptic Aphasia A
worldwide. UNAIDS, a joint program of the United
Nations and the World Health Organization, estimates
LandauKleffner Syndrome that globally, in 2007, 33.2 million people lived with
HIV, 2.5 million became newly infected, and 2.1 million
died from AIDS. In North America alone, 1.3 million
lived with HIV, 46,000 became newly infected, and
21,000 died from AIDS; and approximately, 500,000
Acquired Immunodeficiency have already died from AIDS.
Syndrome (AIDS)
C. M ICHAEL N INA Categorization
Wayne, NJ, USA Differentiation between a diagnosis of HIV or AIDS
depends on CD4+ T cell count and presence of opportu-
nistic infections.
Short Description or Definition
Acquired immunodeficiency syndrome or AIDS is a dis- Etiology/Epidemiology

ease caused by infection with the human immuno-
deficiency virus or HIV. HIV is a viral pathogen that In 1981, the US Centers for Disease Control and Preven-
attacks CD4+ T cells (thymus originating lymphocyte tion (CDC) began receiving reports about unusual cases
cells with cluster determinant 4 + surface receptor sites) of Pneumocystis carinii pneumonia (PCP) and Kaposis
of the human bodys immune system. These CD4+ T cells sarcoma in young gay men and PCP in injection drug
(also called T4 or T helper cells) play a central signaling users. These diseases were not typically seen in individuals
role in the human immune response. In addition, HIV with healthy immune systems. In early 1982, similar dis-
also causes damage to the central nervous system. The ease patterns were seen in blood transfusion recipients,
exact cause of this damage is unclear at this time, but it is hemophiliacs, and heterosexual partners of those already
believed to be caused either by the Trojan horse model infected. In late 1982, the CDC officially named this
or neuroinflammation model. In the Trojan horse model, disease pattern as acquired immune deficiency syndrome
immune system cells known as macrophages conceal and or AIDS. In 1984, a previously unknown human retrovi-
convey HIV into the brain, where they can disrupt rus was discovered in the blood of individuals with AIDS
supportive brain cells such as astrocytes and microglia. by teams in the US and France. In 1986, the retrovirus was
In the neuroinflammation model, the bodys over stimu- named as HIV.
lated immune system causes an increased production of Retroviruses have an RNA (ribonucleic acid) genome,
CD14+ CD16+ monocytes which flood the brain, causing and use an enzyme called reverse transcriptase to convert
inflammation and damage to brain cells and structures. their RNA into DNA (deoxyribonucleic acid), in order to
AIDS is the name given to the end stage of HIV
infection when the bodys ability to fight off microorgan-
isms is compromised, resulting in debilitating or fatal Acquired Immunodeficiency Syndrome (AIDS). Table 1
diseases, which are known as opportunistic infections. Differentiation between human immunodeficiency virus
An individual with HIV infection receives a formal diag- (HIV) infection and acquired immunodeficiency syndrome
nosis of AIDS when the individual has at least one oppor- (AIDS) in individuals infected with HIV
tunistic infection or when the individuals CD4+ T cell Symptom Diagnosis
count is below 200 per mm3 of blood (normal count is
CD4+ T cell count of 200 or higher per HIV infection
typically 5001,500 per mm3).
mm3/blood
In the absence of anti-HIV or antiretroviral drug ther-
CD4+ T cell count below 200 per AIDS
apy, progression to AIDS can take an average of 812 years
mm3/blood
for adults and adolescents, and 3 years from birth in
prenatally infected children. A quarter of a century after Presence of one or more opportunistic AIDS
infection
the first deaths from AIDS were identified, the AIDS
22 A Acquired Immunodeficiency Syndrome (AIDS)
replicate, which is done in the nucleus of infected cells. 3. Transfusion of infected blood or other bodily incor-
HIV is a member of the lentivirus group of retroviruses poration of infected blood
which also includes simian immunodeficiency virus. Len- 4. A fetus or infant exposed to HIV before or during
tiviruses typically have longer incubation periods and birth or through breast feeding
greater genetic complexity than other retroviruses.
The natural progression of HIV infection can be divided
In 1985, a second strain of the virus was discovered,
into three stages: primary infection, clinical latency, and
which was designated as HIV-2. The original strain of the
symptomatic disease stage. The symptomatic disease
virus was designated as HIV-1. HIV-1 is much more
stage is further divided into early and late stages, with
common throughout the world, while HIV-2 is more
AIDS being equated with the late-symptomatic disease
common in certain parts of Africa alone. Also, HIV-2
stage. After a person is initially infected with HIV, a
appears to be milder than HIV-1, with a slower progres-
primary or acute infection stage commences, in which
sion to AIDS. Since its establishment in humans, HIV-1
HIV replicates up to ten billion copies of itself daily;
has undergone mutation of its genome and there are now
high levels of HIV in the blood or viraemia is evident.
three groups of HIV-1.
Approximately, 24 weeks after exposure, nearly 70% of
How HIV is transmitted tends to vary worldwide
those newly infected will experience an acute illness,
depending upon the geographic region. In the United
which has symptoms similar to influenza or mononucle-
States, approximately 45% of current cases of HIV infec-
osis, including fever, fatigue, muscle weakness, headache,
tion were obtained through malemale sexual contact
ocular pain, sensitivity to light, sore throat, diarrhea, and
(men who have sex with men or MSM), 22% were
lymphadenopathy. This illness is due to the temporary
through injecting drug users (IDU), and 5% were through
reduction of CD4+ T cells; it lasts for approximately
individuals who were both MSM and IDU. Approximate-
2 weeks and then resolves spontaneously. It is during
ly, 27% of cases were through malefemale sexual contact.
this stage that the individual typically first begins to
Transmission rates have been changing though, with new
produce antibodies to HIV, which is designated as
cases of infection in older white MSM decreasing. Trans-
seroconversion.
mission rates have been increasing in AfricanAmerican
Serological testing of blood can reliably detect HIV
and Latino MSM and younger white MSM due to
antibodies 26 months after seroconversion. Testing typi-
increases in high-risk sexual practices; approximately,
cally begins with an enzyme-linked immunosorbent assay
50% of new cases are in AfricanAmerican MSM. Rates
(ELISA) or test that looks for antibodies to HIV. A second
of transmission are also increasing in women, primarily
positive ELISA is needed in order to confirm the result.
due to heterosexual contact with MSM and IDU. In
This would then be followed by the Western Blot Proce-
Africa, transmission is primarily due to malefemale sex-
dure to confirm the presence of at least two specific HIV
ual contact. In Eastern Europe, transmission is primarily
antigen groups. A diagnosis of HIV infection is given after
in IDU or malefemale sexual contact. In Southeast
a positive Western Blot test follows two positive ELISA
Asia, transmission is primarily through contact with
tests. If HIV is confirmed, additional tests for plasma viral
commercial sex workers.
RNA (viral load) and CD4+ T cell counts are then typi-
cally completed, in order to assess the state of the immune
system and disease prognosis. Higher viral load counts
Natural History, Prognostic Factors, are typically related to faster disease progression. Lower
Outcomes CD4+ T cell counts are typically related to greater clinical
vulnerabilities.
HIV is not transmitted through casual contact, such as
After the acute illness disappears, the individual enters
touching. It can be transmitted when the bodily fluids of
the clinical latency stage in which symptoms are typically
infected individuals primarily blood, semen, vaginal
absent, other than possibly chronic lymphadenopathy.
fluid, or breast milk comes into contact with the blood-
This stage lasts an average of 10 years. During the clinical
stream or mucosal tissues of uninfected individuals.
latency stage, HIV continues to replicate and attack
Transmission can occur through:
CD4+ T cells, which in turn continues to counter attack.
1. Unprotected sexual contact (anal, vaginal, or oral) As the immune system becomes more compromised,
with an individual infected with HIV individuals eventually enter the early symptomatic disease
2. Sharing needles or syringes with HIV-infected stage, when a variety of symptoms begin to manifest,
individuals including lymphadenopathy, lack of energy, diarrhea,
Acquired Immunodeficiency Syndrome (AIDS) A 23
unintentional weight loss, chronic low-grade fever and Acquired Immunodeficiency Syndrome (AIDS). Table 2 HIV
A
sweats, frequent rashes or fungal infections, headaches, dementia symptoms
or short-term memory loss.
Behavioral difficulties
Finally, individuals enter the late stage of the symp-
Depression
tomatic disease stage or AIDS when the person has at least
Apathy, anhedonia, social withdrawal
one opportunistic infection or when the individuals
CD4+ T cell count is below 200 per mm3 of blood. The Personality changes, including spontaneous sudden and
most common opportunistic infections are PCP, Kaposis strong emotions
sarcoma, HIV wasting syndrome, and HIVencephalopathy Cognitive difficulties
(also known as dementia due to HIV disease or AIDS Confusion
dementia complex). Short-term memory lapses
Loss of concentration
Psychological and Neuropsychological Motor difficulties
Correlates of HIV Infection Lack of muscular coordination
Tremors
As HIV infection progresses, various psychological and Muscle weakness
neuropsychological complications involving both the cen- Loss of balance
tral as well as peripheral nervous systems can become
evident. During primary infection, reports of headaches
and aseptic meningitis are common. During the clinical
latency stage, an acute inflammatory demyelinating neu-
syndrome is characterized by behavioral, cognitive, and
ropathy (similar to Guillain-Barre syndrome; character-
motor declines and difficulties (Table 2). Initial symptoms
ized by progressive muscle weakness) can occasionally
typically manifest as cognitive difficulties (loss of concen-
develop. During the early symptomatic disease stage, pe-
tration and mild deficits in memory) with motor and
ripheral neuropathy is common. This is characterized by
behavioral difficulties frequently occurring. (This early
spontaneous pain (dysesthesia), pain due to light touches
stage is often labeled as HIV-associated minor cognitive
or changes in temperature (hyperesthesia), and weakness
motor disorder.) Later symptoms include partial paraly-
and wasting in arms/legs (distal atrophy).
sis, incontinence, and severe cognitive impairment. Death
It is during the late symptomatic disease stage or AIDS
usually occurs within 16 months after onset of severe
that most major neuropsychological complications devel-
symptoms. Individuals who are coinfected with hepatitis
op, and can include:
C or were IDU, typically display worse symptoms faster.
1. HIV encephalopathy (HIV dementia) As HIV-infected individuals live longer, it is estimated
2. Opportunistic infections that 5075% of all patients with AIDS will evidence
(a) Viral (Cytomegalovirus; Herpes Simplex I and II; some form of HIV dementia.
Herpes Zoster; JC virus, a polyomavirus or While HIV can be present in any part of the brain,
papovavirus which causes PML [progressive HIV is particularly common in the basal ganglia and
multifocal leukoencephalopathy]) central white matter (and to a lesser extent in neocortical
(b) Fungal/Protozoan (Toxoplasmosis, Cryptococcus, gray matter, the brainstem, and the cerebellum) in indi-
Candida, Mycobacterium) viduals not receiving antiretroviral therapy or highly
3. Lymphomas active antiretroviral therapy (HAART) (see below). In
(a) Primary central nervous system lymphomas individuals on HAART, there is evidence of greater
(b) Systemic (metastatic) lymphomas. (The most inflammation in the hippocampus and surrounding en-
common systemic lymphomas are: Hodgkins; torhinal and temporal cortex.
immunoblastic; Burkitts; and non-Hodgkins,
which is particularly prevalent.)
HIV encephalopathy is the term used to describe the Treatment
pathological features of encephalitis of the brain due to
HIV, while HIV dementia (also known as AIDS dementia While there is no cure or vaccine for HIV or AIDS at
complex) is used to describe the clinical syndrome. This this time, there are currently four different classes of
24 A Acquisition of Knowledge
antiretroviral drugs that interfere with the ability of HIV to UNAIDS. (2007). UNAIDS Annual Report 2007: Knowing your epidemic.
Retrieved June 15, 2008 from http://data.unaids.org/pub/Report/
replicate: reverse transcriptase inhibitors (nucleoside and
2008/jc1535_annual_report07_en.pdf
non-nucleoside types); protease inhibitors; entry/fusion Weeks, B. S., & Alcamo, I. E. (2006). AIDS: The biological basis (4th ed.).
inhibitors; and integrase inhibitors. In 1987, the US Food Sudbury, MA: Jones and Bartlett Publishers.
and Drug Administration (FDA) approved Azidothymi-
dine (AZT, also known as Zidovudine), the first nucleo-
side-reverse transcriptase inhibitor (NRTIs). Saquinavir,
the first protease inhibitor was approved in 1995.
Nevirapine, the first non-nucleoside-reverse transcrip- Acquisition of Knowledge
tase inhibitor was approved in 1996. Enfuvirtide, the
first fusion inhibitor was approved in 2003. Maraviroc, Learning
the first entry inhibitor, and Reltegravir, the first inte-
grase inhibitor, were approved in 2007.
In 1996, combination drug therapy or HAART
began. Three or more drugs are used in combination in
order to counter the development of drug resistance by Action Tremor
HIV. Strict adherence to medication intake schedules is
required. Not only is this schedule difficult to follow A NNA D E P OLD H OHLER 1, M ARCUS P ONCE DE LEON2
1
for many individuals, HAART often produces unpleasant Boston University Medical Center
and toxic side effects, including stomach problems and Boston, MA, USA
2
lipodystrophy. If followed correctly, HAART typically and William Beaumont Army Medical Center
drastically reduces viral load, often to undetectable levels El Paso, TX, USA
in the blood, which allows the immune system to re-
bound. Antiretroviral drug therapy and treatments for
opportunistic infections have greatly increased life expec- Synonyms
tancy of those with HIV infection, but due to the presence
of HIV in cells that remain out of reach of antiretroviral Intention Tremors
drugs, eradication of HIV from the human body is unat-
tainable at this time.
Definition
Action tremor is a rhythmic, oscillatory, and involuntary

Cross References
movement of the limb that is seen with movement of an
extremity. It may be seen in isolation with a cerebellar
Dementia
lesion or associated with other tremor types such as the
Encephalitis
postural tremor of essential tremor or the rest tremor of
Meningitis
Parkinsons disease.

Bartlett, J., & Finkbeiner, A. (2006). The guide to living with HIV infection, Essential Tremor
developed at the John Hopkins AIDS clinic (6th ed.). Baltimore: Johns
Parkinsons Disease
Hopkins University Press.
Portegies, P., & Berger, J. (Eds.). (2007). HIV/AIDS and the nervous
system: Handbook of clinical neurology. Amsterdam: Elsevier.
Pratt, R. (2003). HIV & AIDS: A foundation for nursing and healthcare
practice. London: Arnold Publishers.
Sande, M., & Volberding, P. (Eds.). (1999). The medical management of
AIDS (6th ed.). Philadelphia: Saunders. Fahn, S., & Jankovic, J. (Eds.). (2007). Tremors: Diagnosis and treatment.
Stine, G. (2005). AIDS update 2005. San Francisco: Pearson/Benjamin In Movement disorders (pp. 451479). Philadelphia: Churchill
Cummings. Livingstone Elsevier.
Action-Intentional Disorders A 25
or a series of movements that are needed to complete a

Action-Intentional Disorders A
task. The inability to stop a movement or an action pro-
gram when it is no longer required is called motor persev-
K ENNETH M. H EILMAN eration and the inability to withhold a response to a
The Malcom Randall Veterans Affairs Hospital sensory stimulus is called defective response inhibition.
Randall Veterans Affairs Medical Center These motor intentional disorders are parallel to
Gainesville, FL, USA disorders of sensory attention, akinesia being akin
to unawareness, impersistence being the motor parallel
of decreased vigilance, motor perseveration being parallel
Synonyms to failures of extinction or habituation, and defective
response inhibition being similar to distractibility. There
Abulia; Akinesis; Hypokinesis; Motor impersistence are also cognitive defects that mirror four types of inten-
(These terms are not fully synonymous with action- tional motor disorders mention above, but these will not
intentional disorders, but comprise important elements be discussed here.
of the syndrome and are often used when describing In the next section, we briefly describe each of these
specific these elements.) intentional disorders, including subtypes of each category
and in the final section we briefly discuss the possible
pathophysiology.
Definition
In the absence of weakness, patients can have a disability Clinical Manifestations

with initiating (akinesia, hypokinesia, abulia) or sustain-
ing actions (impersistence), inhibiting irrelevant actions Akinesia
(defective response inhibition), and stopping an action
when the task has been completed (motor perseveration). An organism might fail to initiate a movement for many
reasons, but comprehension, attentional, perceptual, sen-
sory, and motor disorders that lead to a failure of move-
Current Concepts ment initiation should not be termed akinesia. In contrast
to these disorders, akinesia is caused by a failure of the
The motor system allows humans to interact with their systems that are responsible for activating the motor
environment and alter themselves as well as others. The system.
human corticospinal motor system together with the There are three methods by which akinesia can be
motor units and muscles can mediate an almost infinite distinguished from extreme weakness. Certain forms of
number of movements and thus the human motor system akinesia are present under certain sets of circumstances
needs to be guided by at least two major types of pro- and absent in others. Thus, using the behavioral method,
grams: praxic and intentional. The praxic programs pro- if it can be demonstrated that a patient makes movements
vide the corticospinal system with the knowledge of how in one set of circumstances (e.g., a motionless left hand is
to make skilled movements (spatial and temporal aspects brought over to the right side of the body and the patient
of movements) and the intentional programs provide the is able to now move this hand) and not in the other, this
corticospinal system with information about when to failure to move is related to an akinesia. If the akinesia is
move. In this section, we will discuss disorders of the not limited to a set of circumstances then the clinician
intentional, or when, systems. When interacting with may have to depend on brain imaging, or physiological
environmental stimuli or the self, there are four when techniques such as magnetic stimulation of the motor
questions that must be addressed: these are (1) when to cortex to demonstrate that the brain lesion did not in-
move, (2) when to persist at a movement or movements, volve the motor system and thus the failure to move is not
(3) when to end a movement or a series of movements, caused by weakness.
and (4) when not to move. The inability to initiate a There are at least three subtypes of akinesia: (1) Body
movement in the absence of a corticospinal or motor part: Akinesia may involve the eyes, the neck and head, a
unit injury is called akinesia. Some patients are able to limb, or the total body; (2) Action space: Akinesia of the
move after a delay and we call this hypokinesia. Motor limbs, eyes, or head may depend on where in space the
impersistence is when a patient cannot sustain a movement body part is moved or in what direction it is moved.
26 A Action-Intentional Disorders
The former is called spatial akinesia (e.g., a hand that does with various body parts including the limbs, eyes, neck,
not move in left hemispace, but does move in right body- eyelids (e.g., keep your eyes closed for until I tell you to
centered hemispace) and the latter is called directional open them), jaw, and tongue. Patients can even demon-
akinesia (e.g., a horizontal gaze palsy where patients can- strate impersistence in activities such as walking. Like
not move their eyes to the left); (3) Stimulusresponse akinesia, it may also be directional (e.g., inability to main-
conditions: Some patients, such as those with Parkinsons tain leftward gaze) or hemispatial (inability to maintain
disease, are impaired in spontaneously initiating a move- dorsiflexion of the wrist in left space with the left arm, but
ment, but in response to a stimulus often have no trouble able to do so in right space).
initiating a movement. We call this endogenously evoked
akinesia (endo-evoked). Patients who fail to move to an
imperative stimulus but will move spontaneously we call
Defective Response Inhibition
exogenously evoked akinesia. A patient may have both exo-
evoked and endo-evoked akinesia, which we term mixed
Not all stimuli require a response and sometimes a re-
or global akinesia.
sponse might interfere with goal-oriented behavior. De-
fective response inhibition is defined as responding when
no response of that body part is required. It can be seen in
Hypokinesia a variety of body parts and might also be directional and
perhaps hemispatial.
A milder defect in the intentional motor (when) sys- There are several forms of defective response inhibi-
tems might not induce a total inability to initiate a re- tion. One means of testing for this disorder is to use the
sponse (i.e., akinesia), but rather these patients crossed response task. A blindfolded patient is instructed to
intentional deficit might be manifested by a delay in raise the hand opposite to that touched. Patients with
initiating a response. We call this delay hypokinesia. The defective response inhibition will often raise the touched
hypokinesias may also be subtyped into body part (e.g., hand first. This type of defective response inhibition may
limb or eyes) and action space (e.g., directional and be termed motor (limb or eye directional) response disinhi-
hemispatial). bition. These can be either contralesional or bilateral. The
eye directional defective response inhibition has also been
called a visual grasp. There are some patients, however,
Motor Extinction who have a perceptual disorder and when stimulated on
one side (e.g., left hand) feel that they were stimulated
Patients with sensory extinction are able to detect single on the other (e.g., right hand). This phenomenon is called
stimuli on either side of their body, but when presented allesthesia and it should not be confused with defective
with two stimuli one on each side of their body they crossed response inhibition.
remain unaware of contralesional stimuli. Motor extinc- Patients with defective response inhibition may also
tion is a form of akinesia or hypokinesia where a patient fail on the types of gono-go tasks described by Luria. For
who is without sensory extinction is asked to respond by example, the patient may be instructed to put up two
moving the hand (or hands) that was (were) touched. The fingers when the examiner puts up one finger and to put
examiner then delivers stimuli to the right, left, and both up no fingers if the examiner puts up two fingers. If the
hands and patients with motor extinction are aware that patient mimics the examiner such that when the examiner
both hands have been touched, but either fail to lift the puts up one finger, the patient puts up one finger and
contralesional hand to simultaneous stimuli or lift it after when the examiner puts up two fingers, the patient puts
a delay. up two fingers, the patient has echopraxia.
Motor Impersistence Motor Perseveration
The inability to sustain a motor act or a series of motor acts When a patient incorrectly repeats a prior response
that are required to complete a goal is called motor imper- or when a patient continues to perform the same act
sistence. Like akinesia, impersistence can be associated when the goal of the act has been completed, it is called
Activa A 27
motor perseveration. In one type of motor perseveration, deficits, injuries, or diseases that injure the basal ganglia,
A
when the task requirements have changed the patient is the substantia nigra (e.g., Parkinsons disease), portions of
unable to switch to a different motor program and incor- the thalamus, as well as the white matter connections can
rectly repeats the movements. Luria (1965) calls this iner- also induce intentional deficits.
tia of program action and Sandson and Albert (1987) call
this recurrent perseveration. In the second type, the patient
continues to perform movements even though the task is Future Directions
completed. Luria (1965) called this efferent perseveration;
however, Sandson and Albert (1987) call this continuous Disorders of intention have received considerably less
perseveration. neuroscientific study than have disorders of sensory selec-
tive attention. There is a need for additional experimental
and clinical neuropsychological studies of these disorders.
Furthermore, assessment batteries are needed that will
Pathophysiology of Intentional facilitate the assessment of the subtypes of motor inten-
Disorders tion disturbances and which may provide additional
quantitative data for experimental analysis and norma-
Intentional motor disorders are often associated with bilat- tive comparison between patient groups and health
eral hemispheric lesions, but when these disorders are individuals.
caused by a unilateral hemispheric lesion they are more
commonly associated with right than left-hemisphere
lesions. The intentional disorders that have been reported Cross References
to be induced by primarily right-hemisphere lesions in-
clude akinesia (e.g., left-sided limbs, leftward arm move- Attention
ments, and even left horizontal gaze), hypokinesia (slowed Directional Hypokinesis
reaction times), motor impersistence of the left-sided Impersistence
limbs, left-sided gaze), and motor (continuous) persevera- Neglect Syndrome
tion. Many of the intentional defects associated with right-
hemisphere dysfunction, however, are not just limited to
the left limbs. For example, patients with a right-hemisphere
lesion are more often abulic, have slowed reaction times of References and Readings
their right hand, and have motor impersistence of eye
closure. These clinical studies suggest that the right hemi- Heilman, K. M., Valenstein, E, Rothi, L. J. G., & Watson, R. T. (2004).
Intentional motor disorders and apraxia. In W. G. Bradley,
sphere may be dominant for intentional control of the
R. B. Daroff, G. M. Fenichel, & J. Jankovic (Eds.), Neurology
motor systems. Studies with normal subjects provide in clinical practice: Principles of diagnosis and management.
further evidence for right-hemisphere intentional domi- (pp. 117130). Phila Penn: Butterworth Heineman.
nance. The anatomic and physiological basis for this domi- Heilman, K. M., Watson, R. T., & Valenstein, E. (2003). Neglect and
nance is not entirely understood. related disorders. In K. M. Heilman, & E. Valenstein (Eds.), Clinical
neuropsychology, (4th ed., pp. 296346). New York: Oxford Univer-
Studies of patients with focal lesions and studies of
sity Press.
monkeys suggest that the frontal lobes may play a critical Heilman, K. M. (2004). Intentional neglect. Frontiers in Bioscience, 9,
role in mediating intentional activity. The most important 694705.
areas of the frontal lobes appear to be the medial and Luria, A. R. (1965). Two kinds of motor perseveration in massive injury
lateral frontal lobes. The frontal cortex has strong projec- to the frontal lobes. Brain, 88, 110.
Sandson, J., & Albert, M. L. (1987). Varieties of perseveration. Neuropsy-
tions to the striatum. The lateral portion of the frontal
chologia, 22, 715732.
lobe projects to the caudate. The premotor cortex projects
to the putamen and the cingulate gyrus projects to the
ventral striatum. The striatum projects to the pars reticu-
laris of the substantia nigra and the globus pallidus. The
globus pallidus projects to specific thalamic nuclei and Activa
these thalamic nuclei project back to the frontal cortex.
Just as injury of the frontal lobes can induce intentional Deep Brain Stimulator (Parkinsons)
28 A Active Limb Activation
Active Limb Activation Active Memory

S ARAH A. R ASKIN Short-Term Memory
Trinity College
Hartford, CT, USA
Activities of Daily Living (ADL)

Synonyms
A NGELA K. T ROYER
Limb activation Baycrest Centre for Geriatric Care
Toronto, Ontario, Canada
Definition
Active limb activation is a rehabilitation technique for
Synonyms
individuals with unilateral neglect. In a series of studies,
Adaptive functions; Functional abilities
Robertson and North (1992, 1993, 1994) and others
(Mattingly, Robertson, & Driver, 1998) have demon-
strated that moving the upper or lower extremity on the
Definition
affected side can reduce neglect symptoms. The effect is
seen only with active movement, as opposed to passive
Activities of daily living (ADLs) are self-care activities that
movement, and only when the limb is moved in the
are important for health maintenance and independent
effected hemispace. However, the limb need not be
living. ADLs comprise a broad spectrum of activities,
observed visually. It should be noted that the effect has
traditionally classified as basic and instrumental ADLs
not been demonstrated universally (e.g., Brown, Walker,
(BADLs and IADLs, respectively). BADLs, also called
Gray, & Findlay, 1999).
physical or self-maintenance ADLs, are life-sustaining
self-care activities such as feeding, grooming, bathing,
dressing, toileting, and ambulation. IADLs are more
Cross References
complex activities that are necessary for independent
living, such as using the telephone, preparing meals,
Attention Training
shopping, managing finances, taking medications,
Behavioral Inattention Test
arranging appointments, and driving. These activities
Cognitive Rehabilitation
are important for participating in ones usual work, social,
Neglect Syndrome
or leisure roles.

Brown, V., Walker, R., Gray, C., & Findlay, J. (1999). Limb activation and
the rehabilitation of unilateral neglect: Evidence of task-specific The evolution of the concept of ADLs is reflected in the
effects. Neurocase, 5, 129142. development of instruments to measure these abilities
Mattingly, J., Robertson, I., & Driver, J. (1998). Modulation of covert (McDowell & Newell, 1996). Measures of BADLs were
visual attention by hand movement: Evidence from parietal extinc-
first developed in the 1940s and 1950s, primarily out of
tion after right hemisphere damage. Neurocase, 4, 245253.
Robertson, I., & North, N. (1992). Spatio-motor cueing in unilateral left
the needs to assess fitness for military duty in World
neglect: The role of hemispace, hand and motor activation. Neurop- War II and to determine the required levels of care for
sychologia, 30, 553563. institutionalized older adults and those with chronic ill-
Robertson, I., & North, N. (1993). Active and passive activation of left nesses. These early measures include the PULSES profile,
limbs: Influence on visual and sensory neglect. Neuropsychologia, 31,
the Barthel Index, and the Katz Index of ADL, among
293300.
Roberson, I., & North, N. (1994). One hand is better than two: Motor
others. Later, in the 1960s and 1970s, there was increased
extinction of left hand advantage in unilateral neglect. Neuropsycho- interest in caring for older and disabled individuals in the
logia, 32, 111. community, and this spawned the need for tools to
Activities of Daily Living (ADL) A 29
measure IADLs that are important for independent living. include the Direct Assessment of Functional Status, the
A
Some of the first of these measures were Lawton and Independent Living Scales, the Structured Assessment of
Brodys IADL Scale and the Disability Interview Schedule. Independent Living Skills, the Medication Management
Abilities Assessment, and many others.
The use of questionnaires administered either on paper
Current Knowledge or by interview allows the sampling of a large number of
behaviors in a short period of time. Self-report question-
ADLs are of interest across various health disciplines. Cur- naires may be appropriate for use with cognitively-normal
rent knowledge in this area is based on research conducted or mildly impaired populations. In the evaluation of
by psychologists, occupational therapists, nurses, psychia- dementia and other cognitive disorders, however, self-
trists, neurologists, and social workers, among others. reported abilities may be difficult to interpret because
of disease-related decreases in self-awareness. The use of
informant-based questionnaires avoids this limitation,
Relevance to Neuropsychology although informants can also be biased in their reports
and may not always be available. Nevertheless, this is one
For the neuropsychologist, an understanding of the of the most common methods for measuring IADLs, and
patients level of independence in ADLs, and in particular a large number of informant-based questionnaires exist,
IADLs, is of interest for several reasons. The diagnosis of such as the Lawton-Brody IADL Scale, the Bristol ADL
a number of cognitive and mental disorders requires an Scale, and the ADL questionnaire.
appraisal of the patients functional ability (American The choice of which particular method of assessment
Psychiatric Association, 2000). For example, impairment to be used will depend, in addition to practical considera-
in adaptive or functional ability is a diagnostic criterion for tions such as time, on the purpose of the assessment.
mental retardation and for schizophrenia. Impaired daily Real-word observations and performance-based measures
functioning is also required for the diagnosis of dementia provide information about what the person is capable
and is one of the defining differences between dementia (in of doing. Questionnaires, on the other hand, measure
which IADLs are impaired) and mild cognitive impairment what the individual is actually doing in his or her day-
(in which IADLs are intact or minimally affected). to-day life.
Increasingly, the evaluation of daily functioning is also
used to identify appropriate treatments for cognitive and
mental disorders. In particular, an important part of Future Directions
determining the effectiveness of behavioral or pharmaco-
logical interventions is measuring the impact of the inter- Although there are a large number of relevant instruments
vention on the patients daily functional ability, in that have been developed to assess ADLs, they vary in terms
addition to cognitive or affective outcomes. of how well their psychometric properties have been
characterized. Systematic literature reviews (e.g., Moore,
Palmer, Patterson, & Jeste, 2007; Sikkes, de Lange-de
Assessment of ADLs Klerk, Pijnenburg, Scheltens, & Uitdehaag, 2009) indicate
that, for many of these measures, there is a need for better
Assessment of ADLs can be accomplished in a number of theoretical justification of the content of the instrument,
ways. Real-world observation of the patient in his or her additional information about test validity and reliability,
own home provides relevant, objective information about indication of what constitutes a meaningful change
daily function. However, this method is obviously time over time, information about the relation between test
and labor intensive, and there are practical limits to the performance and actual real-world functioning, and the
number of behaviors that can be observed within a given development of comprehensive normative data.
time period. An alternative is the use of performance-based
measures, which require the patient to complete function-
al tasks such as preparing a meal, using the telephone, or Cross References
making personal financial transactions that are pre-
sented in a standardized way in the laboratory or clinic. Adaptive Behavior
A number of such instruments have been developed to Basic Activities of Daily Living (B-ADL)
measure single or multiple functional domains. Tests Functional Status
30 A Activities of Daily Living Questionnaire
Instrumental Activities of Daily Living (I-ADL) self-care activities; household care; employment and
Lawton-Brody iADL Scale recreation; shopping and money; travel; and communica-
tion. The informant rates the subjects competence in each
area according to a set of four descriptions of different
competence levels; scores range from 0 to 3 where higher
References and Readings scores indicate greater impairment. A fifth response
option, dont know/has never done is also available, and
American Psychiatric Association. (2000). Diagnostic and statistical
if this option is selected, the item is excluded from scoring.
manual of mental disorders (4th ed., text revision). Washington, DC:
Author. Scores from individual items are summed (with adjustment
Law, M., Baum, C., & Dunn, W. (Eds.). (2001). Measuring occupational for any items marked dont know/has never done) to form
performance: Supporting best practice in occupational therapy. subscale scores and then transformed to a percentage
Thorofare, NJ: Slack. impairment total score. Scores of 033% are classified as
Lawton, M. P., & Brody, E. M. (1969). Assessment of older people: Self-
no/mild impairment, those of 3466% as moderate
maintaining and instrumental activities of daily living. Gerontologist,
9, 179186. impairment, and those of 67100% as severe impairment.
McDowell, I., & Newell, C. (1996). Measuring health: A guide to rating
scales and questionnaires (2nd ed.). New York: Oxford.
Moore, D. J., Palmer, B. W., Patterson, T. L., & Jeste, D. V. (2007). A Historical Background
review of performance-based measures of functional living skills.
Journal of Psychiatric Research, 41, 97118.
Sikkes, S. A. M., de Lange-de Klerk, E. S. M., Pijnenburg, Y. A. L., The first reported use of the ADLQ was in a longitudinal
Scheltens, P., & Uitdehaag, B. M. J. (2009). A systematic review of study looking at cognitive test performance and daily
Instrumental Activities of Daily Living scales in dementia: room for functioning in patients with Alzheimers disease
improvement. Journal of Neurology, Neurosurgery, and Psychiatry, 80, (Locascio, Growdon, & Corkin, 1995). However, the
712.
development and psychometric properties of the measure
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A compendium of
neuropsychological tests (3rd ed.). New York: Oxford. were first reported in Johnson, Barion, Rademaker,
Rehkemper, and Weintraub (2004). Since then, a Chinese
version has been developed and evaluated (ADLQ-CV;
Chu & Chung, 2008), and it has been used in several
studies involving people with non-Alzheimers dementia.
Activities of Daily Living
Questionnaire Psychometric Data
J ESSICA F ISH
Johnson et al. (2004) collected ADLQ data from the
Medical Research Council Cognition & Brain
primary caregivers of 140 people with dementia of various
Sciences Unit
types (Alzheimers disease, vascular/mixed, and fronto-
Cambridge, UK
temporal/primary progressive aphasia). The scale was
completed twice, with a 1 year interval between comple-
tions. Evidence of convergent validity was in the form of
Synonyms
correlations with global severity ratings (clinical dementia
rating r = 0.5 and 0.55 for first/second ratings, respec-
ADLQ
tively; MMSE r = 0.42 and 0.38 for first and second
ratings, respectively). Further evidence of its validity came
from the finding that scores declined significantly over the
Description year-long interval between testings, as would be expected
in people with degenerative conditions. A subgroup of
The activities of daily living questionnaire (ADLQ) was 28 participants took part in a testretest reliability study,
developed to measure the functional abilities of people with a 28 week interval between testings (mean 25.6
with dementia. It is an informant-rated questionnaire and days, SD 12.2). Correlations between first and second
should be completed by the patients primary caregiver. It ratings for the six subscales were high, between 0.86 and
consists of 28 items covering both basic and instrumental 0.92, with the exception of the employment subscale,
activities of daily living, organized into six subscales: which correlated at 0.65. Kappa scores for 25% of scale
Activity Restrictions, Limitations A 31
items were 0.420.60 (classified as moderate), for 54%

Activity Restrictions, Limitations A
of scale items were 0.610.80 (classified as good), and
for 21% of scale items 0.811.0 (classified as very good).
The validity of the ADLQ was investigated via correlations B RIAN YOCHIM
between 29 participants scores on the ADLQ and the University of Colorado at Colorado Springs
record of independent living (RIL), another ADL mea- Colorado Springs, CO, USA
sure. In line with Johnson et al.s predictions, there were
significant correlations between the ADLQ and the activ-
ities and communication subscales of the RIL, but not Definition
the behavior subscale of the RIL.
Chu and Chung (2008) conducted a study examining This idea refers to restrictions prescribed by clinicians
the psychometric properties of a Chinese translation of who treat patients with recent strokes, head injuries, or
the ADLQ (ADLQ-CV), with 125 caregivers of people other neurological conditions, after a neurological event
with moderate Alzheimers disease. The ADLQ-CV was has left the patient with deficits in important areas of
shown to have good internal consistency (a = 0.81), functioning. Patients are often restricted from driving,
testretest reliability at a 2-week interval (intra-class cooking, managing finances, or completing other instru-
correlation (ICC) 0.998), and inter-rater reliability mental activities of daily living after a neurological event.
(ICC 0.997, for primary and secondary caregiver The activities of focus must be tailored to the patient and
ratings). Correlations with the disability assessment for can range from restrictions in playing professional sports
dementia were strong (r = 0.92), suggesting that it is a to restrictions in managing small amounts of cash.
valid measure. A factor analysis also confirmed that the Current Knowledge
ADLQ-CV has a six-factor structure, following the six
proposed subscales. Rehabilitation professionals encounter patients whose
injuries have left them with deficits both in physical and
cognitive realms. Strokes and traumatic brain injuries can
Clinical Uses cause physical impairments in walking, swallowing, use of
an arm and/or leg, communication, and other important
The ADLQ may be used to assist in the diagnosis
skills. Injuries can also lead to cognitive deficits in memory,
of dementia, in decision making regarding necessary
executive functioning, social functioning, language,
intervention and/or assistance, and in monitoring change
visuospatial skills, attention, and/or processing speed.
over time or in response to treatment.
These basic deficits in turn lead to impaired functioning
in everyday life. Rehabilitation professionals must assess
Cross References patients abilities to complete these daily activities and
often must place restrictions on what activities patients
Alzheimers Disease Cooperative Study ADL Scale can continue to complete. If patients are deemed to be
Bristol Activities of Daily Living Scale unable to drive, for example, clinicians must follow
Disability Assessment for Dementia appropriate legal and ethical channels to protect the
Lawton-Brody ADL Scale patient and public.
These limitations in activities can lead to difficulties in
adjustment for the patient, which can sometimes result in
References and Readings depressed mood and other affective symptoms. This
notion is related to the Activity Restriction Model of
Chu, T. K. C., & Chung, J. C. C. (2008). Psychometric evaluation of the
Depressed Affect (Williamson & Shaffer, 2000), which
Chinese version of the activities of daily living questionnaire has been studied as one etiology of depressive symptoms
(ADLQ-CV). International Psychogeriatrics, 20, 12511261. among older adults.
Johnson, N., Barion, A., Rademaker, A., Rehkemper, G., & Weintraub, S.
(2004). The activities of daily living questionnaire: A validation
study in patients with dementia. Alzheimers Disease and Associated Cross References
Disorders, 18, 223230.
Locascio, J. J., Growdon, J. H., & Corkin, S. (1995). Cognitive test
performance in detecting, staging, and tracking Alzheimers disease. Instrumental Activities of Daily Living (IADLs)
Archives of Neurology, 52(11), 10871099. Recommendation
32 A Activity Therapy
References and Readings require voluntariness and instead the actus reus is viewed
in light of the severity of the offense.
Greenwood, R. J., Barnes, M. P., McMillan, T. M., & Ward, C. D. (Eds.).
(2003). Handbook of neurological rehabilitation (2nd ed.). New York:
Psychology Press.
Mills, V. M., Cassidy, J. W., & Katz, D. I. (Eds.). (1997). Neurologic Cross References
rehabilitation: A guide to diagnosis, prognosis, and treatment planning.
Malden, MA: Blackwell Science. Insanity
Williamson, G. M. & Shaffer, D. R. (2000). The activity restriction model
Insanity Defense
of depressed affect: Antecedents and consequences of restricted normal
activities. In G. M. Williamson, D. R. Shaffer, & P. A. Parmelee (Eds.), Mens Rea
Physical illness and depression in older adults: A handbook of theory,
research, and practice. New York: Kluwer Academic/Plenum
Publishers.
Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C. (1997). Psycho-
logical evaluations for the courts: A handbook for mental health profes-
Activity Therapy sionals and lawyers. New York: Guilford.
Recreational Therapy
Acute Brain Failure

Actus Reus Delirium
M OIRA C. D UX
Baltimore, MD, USA
Acute Brain Syndrome
Definition Metabolic Encephalopathy
Actus reus is Latin for guilty act. Under most circum-

stances, a crime consists of at least two factors. The first
factor is the physical conduct or act associated with the
crime, which is known as the actus reus. In order for an Acute Cerebrovascular Attack
individual to be convicted of a crime, it must be demon-
strated beyond a reasonable doubt, that the defendant Stroke
committed the physical act of the crime, or the actus
reus. However, it must concurrently be established that
the defendant also possessed mens reas, which translates
to guilty mind referring to the mental element of
the crime. Thus, a conviction necessitates, beyond reason-
Acute Confusional State
able doubt, establishment of an illegal act coupled
Delirium
with a particular mental state (e.g., intent, knowledge,
Metabolic Encephalopathy
recklessness, or negligence). Description of the actus
reus is typically classified into one of three categories:
commissions, omissions, and/or commonwealth. Com-
mission refers to an affirmative act; omission refers to a
failure to act; and commonwealth refers to a state of Acute Coronary Syndrome
affairs, or circumstances. Commissions and omissions
necessitate causation; commonwealth does not always Myocardial Infarction
Acute Lymphoblastic Leukemia A 33
Current Knowledge A
Acute Encephalopathy
Symptoms
Delirium
Toxic-Metabolic Encephalopathy ALL is characterized by the rapid proliferation of imma-
ture blood cells (lymphoblasts), which crowd out mature,
functional cells. It is associated with the enlargement of
lymphoid tissue in areas including the lymph nodes,
spleen, bone marrow, and lungs, and with increased lym-
Acute Febrile Polyneuritis phocytic cells circulating in blood and in various tissues
and organs. Persons afflicted will experience weakness and
GuillainBarre Syndrome
fatigue, anemia, unexplained fever and infections, weight
loss, or loss of appetite.
Acute Infective Polyneuritis Pathophysiology

GuillainBarre Syndrome Cancer, including ALL, is caused by damage to DNA.
Treatment
Acute Inflammatory
Demyelinating The earlier the ALL is detected, the more effective is its
treatment. The goal is to induce a lasting remission,
Polyradiculoneuropathy (AIDP) considered to be a prevalence of less than 5% of
lymphoblasts in bone marrow. Advances made in the
GuillainBarre Syndrome
ability to match the genetic properties of the blast cells
to treatment options, in association with the availability
of new drugs and improvements made in bone marrow
and stem cell transplantation, have changed the prog-
Acute Lymphoblastic Leukemia nosis for ALL from a zero to a 75% survival rate over
the past 40 years.
J ACQUELINE L. C UNNINGHAM Most (if not all) patients with a childhood history of
The Childrens Hospital of Philadelphia ALL have brain atrophy. Whereas atrophy is associated
Philadelphia, PA, USA with treatment-effects of cranial irradiation therapy
and intrathecal chemotherapy (usually methotrexate), it
can also occur as a result of the condition, itself, rather
Synonyms than as an outcome of treatment, as it appears to cause
atrophy of the brain, which is not specific to certain brain
ALL tissues (Lucy Rorke, MD, personal communication).
Nonetheless, the strongest detrimental impacts on cog-
nition are attributable to treatment-effects and their
Definition damaging influence on the biological substrates of core
neurocognitive abilities, including executive functions
Acute lymphoblastic leukemia (ALL) is a form of cancer and information processing. Such impacts disrupt the
of the white blood cells (leukocytes). ALL is the most secondary abilities, i.e., those that are acquired and
common type of childhood leukemia, and is distingui- knowledge-based. The main approaches to alleviating
shed from chronic lymphoblastic leukemia (CLL) and neurocognitive effects of treatment include cognitive
acute myeloid (or myelogenous) leukemia, which are remediation, pharmacology, and ecological alterations
more prevalent in adults. in the classroom.
34 A Acute Myelogenous Leukemia
Cross References out mature, functional cells. In AML, the cell type is
granuloid, whose cancerous change disrupts its normal
Acute Myelogenous Leukemia ability to form red cells, some types of white cells, and
Leukemia platelets. Resulting symptoms are anemia, easy bruising
Neoplasms and bleeding, and disruption to the bodys ability to
resist infection. Impaired cognition and fatigue are
also strongly associated with AML. Whereas impairments
in these areas have been attributed to effects of chemo-
References and Readings therapy, recent research by Meyers, Albitar, and Estey
(2005) has identified differing cytokine levels present
Butler, R. W., & Mulhern, R. K. (2005). Neurocognitive interventions
for children and adolescents surviving cancer. Journal of Pediatric
prior to chemotherapy as also contributing to these
Psychology, 30, 6578. symptoms.
Crosley, C. J., Rorke, L. B., Evans, A., & Nigro, M. (1978). Central nervous
system lesions in childhood leukemia. Neurology, 28, 678685.
Prassopoulos, P., Carouras, D., Golfinopoulos, S., Evlogias, N.,
Theodoropoulos, V., & Panagiotou, J. (1996). Quantitative assess- Pathophysiology
ment of cerebral atrophy during and after treatment in children
with acute lymphoblastic leukemia. Investigational Radiology, 12,
749754.
The malignant cell in AML is the myeloblast, a mutated
Pui, Ching-Hon (2003). Treatment of acute leukemias: New directions for and immature cell in the granulocytic series, which under-
clinical research. New York: Humana Press. goes combinations with other mutations, to produce a
leukemic clone of cells. Because the process contributes to
much diversity and heterogeneity in cell differentiation, the
diagnosis of AML can be challenging. It remains important,
however, since the chromosomal structure of the leukemic
Acute Myelogenous Leukemia cells is the diseases most critical prognostic factor.
J ACQUELINE L. C UNNINGHAM
Philadelphia, PA, USA Treatment
Treatment in AML consists primarily of chemotherapy,

Synonyms with the goal of achieving remission. Without postre-
mission (consolidation) therapy, almost all patients
Acute myeloid leukemia; AML eventually relapse. Neurocognitive and neuropsychiatric
symptoms are highly prevalent in patients with cancer
and cause significant impairments in their ability to
Definition function. Whereas such impairments are known to be
associated with aggressive cancer treatment, they are
Acute myelogenous leukemia (AML) is a form of cancer additionally attributed to biologic mechanisms underly-
of the white blood cells (leukocytes). It is a relatively ing the cancer itself. Recent research (Meyers et al.,
rare cancer that occurs more commonly in adults than 2005) on AML has made linkages between cytokine-
in children, with more men affected than women. The immunologic activation and factors including cognitive
median age at diagnosis is 63 years. functioning, significant fatigue, and quality of life in AML
patients studied prior to the initiation of treatment.
Current Knowledge
Cross References
Symptoms
Acute Lymphoblastic Leukemia
Acute forms of leukemia are characterized by the rapid Leukemia
proliferation of immature blood cells which rapidly crowd Neoplasms
Acute Respiratory Distress Syndrome A 35
References and Readings A

Acute Respiratory Distress
Meyers, C. A., Albitar, M., & Estey, E. (2005). Cognitive im- Syndrome
pairment, fatigue, and cytokine levels in patients with acute mye-
logenous leukemia or myelodysplastic syndrome. Cancer, 104,
D ONA EC LOCKE
788793.
Pui, C.-H. (2003). Treatment of acute leukemias: New directions for clinical Mayo Clinic
research. New York: Humana Press. Scottsdale, AZ, USA
Synonyms
Acute Myeloid Leukemia Adult respiratory distress syndrome; Respiratory distress
syndrome
Acute Myelogenous Leukemia
Definition
Acute respiratory distress syndrome (ARDS) is the pres-

Acute Radiation Somnolence ence of pulmonary edema in the absence of volume over-
load or depressed left ventricular function, and is
J ACQUELINE L. C UNNINGHAM characterized by the development of sudden breathless-
The Childrens Hospital of Philadelphia ness within hours to days of an inciting event. ARDS is
Philadelphia, PA, USA not a specific disease; instead, it is a type of severe, acute
lung dysfunction that is associated with a variety of dis-
eases and trauma.
Definition
Acute radiation somnolence is a relatively transient and
benign effect of cranial irradiation. It is manifested as In the past, ARDS signified adult respiratory distress
sleepiness occurring during irradiation used to treat brain syndrome to separate this from infant respiratory distress
tumors. It occurs in both children and adults and usually syndrome seen in premature infants. However, this type of
affects daily functioning during the course of treatment. pulmonary edema can also occur in children, so ARDS has
Although it is self-limiting, and resolves with medication gradually evolved to mean acute rather than adult.
and with the termination of irradiation, symptoms can be
upsetting to patients. Nursing intervention which focuses
on preparation through counseling and education serves to Current Knowledge
alleviate distress. Acute radiation somnolence is usually
treated with steroids. ARDS typically develops within 1248 h after the inciting
event, although, in rare instances, it may take up to a few
days. Persons developing ARDS are critically ill, often
with multi-system organ failure. It is a life-threatening
Cross References condition; therefore, hospitalization is required for
prompt management.
Radiation Oncology ARDS is associated with severe and diffuse injury to the
Radiotherapy alveolar-capillary membrane (the air sacs and small blood
vessels) of the lungs. Fluid accumulates in some alveoli of
the lungs, while some other alveoli collapse. This alveolar
References and Readings damage impedes the exchange of oxygen and carbon diox-
ide, which leads to a reduced concentration of oxygen in
Brady, L. W., Heilmann, H. P., Molls, M., & Schlegel, W. (2006). New the blood. Low levels of oxygen in the blood cause damage
techniques in radiation oncology. New York: Springer. to other vital organs of the body such as the kidneys.
36 A Acute Respiratory Distress Syndrome
The 1994 AmericanEuropean Consensus Committee are the most common. This risk is independent of the
defines ARDS as the acute onset of bilateral infiltrates on risk from concurrent aspiration.
chest radiography, a partial pressure of arterial oxygen
Medical Treatment for ARDS:
(PaO2) to fraction of inspired oxygen (FIO2) ratio of less
than 200 mmHg and a pulmonary artery occlusion pres- People with ARDS require hospitalization and treat-
sure of less than 18, or the absence of clinical evidence of ment in an intensive care unit.
left arterial hypertension. There is no specific treatment for ARDS, but rather,
The mortality rate is approximately 3040%. Death treatment is primarily supportive using a mechanical
usually results from multi-system organ failure rather respirator and supplemental oxygen.
than lung failure alone. Diuretics can be given to eliminate fluid from the
Causes: A number of clinical conditions are associated lungs. However, fluids are often given via IV to pro-
with the development of ARDS. vide nutrition and prevent dehydration, but fluids
must be carefully monitored to avoid fluid accumula-
Sepsis and the systemic inflammatory response syn-
tion in the lungs.
drome (SIRS) are the most common conditions asso-
Antibiotic therapy may be administered to treat infec-
ciated with the development of ARDS.
tion, which is often the underlying cause of ARDS.
Severe traumatic injury (especially multiple fractures),
Corticosteroids may sometimes be given late in the
severe head injury, and pulmonary contusion are
process of ARDS or if the patient is in shock. If the
strongly associated with the development of ARDS. In
patient is in shock, drugs to counteract low blood
traumatic injury, factures of the long bones can cause
pressure caused by shock may be administered.
ARDS through fat embolism. In severe brain injury,
If the patient is experiencing anxiety, this can be
ARDS is thought to develop owing to a sudden dis-
treated with anti-anxiety medications.
charge of the sympathetic nervous system, which then
leads to acute pulmonary hypertension and injury to Respiratory therapists may see these patients to provide
the pulmonary capillary bed. In pulmonary contusions, inhaled drugs to decrease inflammation and provide re-
ARDS develops through direct trauma to the lung. spiratory comfort.
Multiple blood transfusions are an independent risk Because of the acute and medically serious nature of
factor for ARDS. The risk is independent of the reason ARDS, it would be unlikely for neuropsychological exam
for the transfusion or the coexistence of trauma. to be requested when a person is acutely ill with ARDS.
The incidence of ARDS increases with the number of Mortality with ARDS is 3040% and the person would
units of blood transfused. If the patient has pre-exist- typically be treated in an Intensive Care Unit. If the person
ing abnormal liver functioning or a coagulation ab- survives, outpatient neuropsychological evaluation could
normality, the risk is further increased. be requested and results may show memory deficits related
Near drowning can be another cause of ARDS. Devel- to the hypoxia as well as neuropsychological deficits
opment of ARDS is slightly more common with salt- related to the underlying medical cause for ARDS (e.g.,
water than with fresh-water. Aspiration leads to an severe TBI, near drowning, sepsis, medication overdose).
osmotic gradient that favors movement of water into
airspaces of the lung. Aspiration may be visible with
chest radiography, although the chest radiograph may Cross References
be normal early in the course of the disease.
Smoke inhalation is another possible cause of ARDS. Anoxia
Smoke inhalation causes lung tissue damage from direct Hypoxia
heat, toxic chemicals, and particulate matter carried
into the lung. Patients with smoke inhalation initially
may be asymptomatic, but patients with airway burns,
exposure to toxic fumes, or exposure to carbon monox- References and Readings
ide should be monitored closely for the development of
Bernard, G. R., Artigas, A., Brigham, K. L., Charlet, J., Falke, K., Hudson, L,
ARDS, even if the symptoms are initially absent.
Lamy M., Legall, J. R., Morris, A., & Spragg, R. (1994). Report of the
Overdoses of narcotics, tricyclic antidepressants, and American-European consensus conference on ARDS: Definitions,
other sedatives have been associated with the develop- mechanisms, relevant outcomes and clinical trial coordination. In-
ment of ARDS. Overdoses of tricyclic antidepressants tensive Care Medicine, 20, 225232.
Adaptive Behavior Assessment System Second Edition A 37
to be a measure of adaptive behavior consistent with

ADA A
current definitions (e.g., those promulgated by the
American Psychiatric Associations (2000) Diagnostic
Americans with Disabilities Act of 1990 and Statistical Manual of Mental Disorders and the
American Association on Intellectual and Developmental
Disabilities (AAIDD, 1992) models of adaptive behavior)
that underscored the importance of ten skill areas:
Adaptation communication, community use, functional academics,
health and safety, home or school living, leisure, self-
Tachyphylaxis care, self-direction, social, and work skills. The ABAS
norm groups were large and included persons 5
through 89. The ABAS was revised shortly after its
publication in response to two issues: a need for the
downward extension of the ABAS for younger children
Adaptive Behavior Assessment and a change in the concept of adaptive behavior embod-
System Second Edition ied in AAIDDs 2002 definition, one that emphasized the
importance of three domains (e.g., conceptual, social, and
T HOMAS OAKLAND practical).
University of Florida The ABAS-II is the only scale of adaptive behavior
Gainesville, FL, USA consistent with models of adaptive behavior advocated
by the AAIDDs 1992 and 2002 definitions and the
American Psychiatric Associations (2000) Diagnostic
Synonyms and Statistical Manual of Mental Disorders. Scaled scores
for 11 adaptive skill areas are provided (Table 1). Ten skill
ABAS; ABAS-II area scores combine to produce standard scores in their
respective domains: conceptual (communication, func-
tional academics, and self-direction), social (social skills
Description and leisure), and practical (self-care, home or school
living, community use, health and safety, and work for
The Adaptive Behavior Assessment System Second Edi- adults); motor skills are assessed for young children. A
tion (ABAS-II; Harrison & Oakland, 2003) provides an General Adaptive Composite Score is derived from the
assessment of adaptive behavior and skills for persons skill scores.
from birth through age 89. Five forms are available:
parent/primary caregiver form (for ages 05), teacher/
day-care provider form (for ages 25), parent form (for Item Data
ages 521), teacher form (for ages 521), and an adult
form (for ages 1689). Its standardization sample is large All items are scored on a four-point scale: 0 (cannot
(>4,000) and representative of US data from 1999 to 2000 perform the behavior), 1 (can perform the behavior
with respect to gender, race/ethnicity, and parental edu- yet does not), 2 (performs the behavior sometimes),
cation, and it is proportional to individuals with dis- and 4 (performs the behavior most or all of the time).
abilities. Forms are available in French-Canadian and This feature is consistent with the World Health Organi-
Spanish. The scales have been adapted for use in Sweden zations International Classification of Functioning
and Taiwan, with plans for extensions to the Czech (Mpofu & Oakland, 2010) effort to distinguish activities
Republic, Denmark, Germany, Romania, and Spain. and performance.
Respondents may indicate that they guessed. Data
from subtests with more than three guesses should not
Historic Background be used. The ABAS-IIs scoring and reporting system
informs clinicians of interventions likely to promote the
The ABAS (Harrison & Oakland, 2000) preceded the development of selected behaviors associated with critical
development of the ABAS-II. The ABAS was developed items.
38 A Adaptive Behavior Assessment System Second Edition
Adaptive Behavior Assessment System Second Edition. Table 1 Adaptive skills and three adaptive domains
Adaptive skills
Communication Speech, language, and listening skills needed for communication with other people, including vocabulary,
responding to questions, and conversation skills
Community use Skills needed for functioning in the community, including use of community resources, shopping skills,
and getting around in the community
Functional Basic reading, writing, mathematics, and other academic skills needed for daily, independent functioning,
academics including telling time, measurement, as well as writing notes and letters
Home living Skills needed for basic care of a home or living setting, including cleaning, straightening, property
maintenance and repairs, as well as food preparation and performing chores
Health and safety Skills needed for protection of health and to respond to illness and injury, including following safety rules,
using medicines, and showing caution
Leisure Skills needed for engaging in and planning leisure and recreational activities, including playing with
others, engaging in recreation at home, and following rules in games
Self-care Skills needed for personal care including eating, dressing, bathing, toileting, grooming, and hygiene
Self-direction Skills needed for independence, responsibility, and self-control, including starting and completing tasks,
keeping a schedule, following time limits, following directions, and making choices
Social Skills needed to interact socially and get along with other people, including having friends, showing and
recognizing emotions, assisting others, and using manners
Work Skills needed for successful functioning and holding a part-time or full-time job in a work setting, including
completing work tasks, working with supervisors, and following a work schedule
Motor skillsa Basic fine and gross motor skills needed for locomotion, manipulation of the environment, and the
development of more complex activities such as sports, including sitting, pulling up to a standing position,
walking, fine motor control, and kicking
Three domains and associated skill areas
Conceptual Includes communication, functional academics, self-direction, and health and safety skills
Practical Includes social skills and leisure skills
Social Includes self-care, home/school living, community use, health and safety, and work skills
a
Although fine and gross motor development is not included as one of the ten skills identified by the American Association on Intellectual and
Developmental Disabilities, it is included in some scales of adaptive behavior.
Psychometric Data between teachers, day-care providers, and parents)

range from the 0.60s to the 0.80s for the skill areas and
Scaled scores generally range from 40 to 120. Consistent are in the 0.90s for the General Adaptive Composite. Its
with all measures of adaptive behavior, the ABAS-II is construct validity is strong as displayed through factor
more sensitive to the assessment of adaptive behavior analyses (Harrison & Oakland, 2003; Wei, Oakland, &
and skills at the lower than the higher ranges. Cut scores Algina, 2008). Its concurrent validity with the Vineland
are not provided by disability category; instead, reliance is Adaptive Behavior Scales Classroom Editions Adap-
placed on diagnostic standards established by state and tive Behavior Composite is high, r = 0.82 (Harrison &
national authorities. Oakland, 2003). See reviews by Burns (2005), Meikamp
The ABAS-II demonstrates suitable psychometric and Suppa (2005), and Rust and Wallace (2004) for addi-
qualities. Internal consistency is high, with reliability tional details.
coefficients of 0.850.99 for the General Adaptive
Composite, three adaptive behavior domains, and
skill areas. Testretest reliability coefficients are in Clinical Uses
the 0.80s and 0.90s for the General Adaptive Com-
posite, three domains, and skill areas (Harrison & Measures of adaptive behavior have been most important
Oakland, 2003). Inter-rater reliability coefficients (e.g., in assessment of persons with mental retardation (now
Addiction A 39
referred to as intellectual disabilities by AAIDD). The of support (10th ed.). Washington, DC: American Association on
Mental Retardation. A
ABAS-II is useful in this diagnosis as well as in interven-
American Psychiatric Association. (2000). Diagnostic and statistical man-
tion planning and monitoring for this and other ual of mental disorders (4th ed., text revision). Washington, DC:
disorders. American Association on Mental Retardation.
The ABAS-II also may assist in promoting an under- Burns, M. K. (2005). Review of the adaptive behavior assessment system
standing of the impact on a persons daily life activities of second edition. In R. Spies & B. Plake (Eds.), The sixteenth mental
measurements yearbook. Lincoln, NE: Buros Institute of Mental
other disorders (e.g., those often diagnosed first during
Measurements.
infancy or early childhood include autism, disorders of Ditterline, J., Banner, D., Oakland, T., & Becton, D. (2008). Adaptive
attention, communication, conduct, elimination, feeding behavior profiles of students with disabilities. Journal of Applied
and eating, learning, motor skills, and pervasive develop- School Psychology, 24, 191208.
mental disorders; Harman, Smith-Bonahue, & Oakland, Harman, J., Smith-Bonahue, T., & Oakland, T. (2009). Assessment of
adaptive behavior development in young children. In E. Mpofu &
2009; Oakland & Harrison, 2008). The ABAS-II is
T. Oakland (Eds.). Rehabilitation and Health Assessment: Applying
useful with children and adolescents who display disor- ICF Guidelines. New York: Springer.
ders including attention deficit/hyperactivity, acquired Harrison, P. & Oakland, T. (2000). Adaptive behavior assessment system.
brain injury, auditory or visual impairment, autism, San Antonio, TX: Harcourt Assessment.
developmental delays, emotional/behavioral disorders, Harrison, P. & Oakland, T. (2003). Adaptive behavior assessment system
second edition. San Antonio, TX: Harcourt Assessment.
learning disabilities, and physical impairments (Ditter-
Meikamp, J., & Suppa, C. H. (2005). Review of the adaptive behavior
line, Banner, Oakland, & Becton 2008; Harrison & assessment system second edition. In R. Spies & B. Plake (Eds.),
Oakland, 2003; Oakland & Harrison, 2008). The sixteenth mental measurements yearbook. Lincoln, NE: Buros
Adults diagnosed with such disorders as anxiety, acute Institute of Mental Measurements.
stress or adjustment disorder, bipolar disorder, depres- Mpofu, E. & Oakland, T. (2010). Assessment in rehabilitation and health.
Upper Saddle River, NJ: Merrill.
sion, mood disorders, psychosis, Parkinsons, postpartum
Oakland, T. & Harrison, P. (2008). Adaptive behavior assessment system-II:
depression, substance abuse, schizophrenia, and sleep Behavior assessment system-II: Clinical use and interpretation.
disturbance may display impairments in their functional New York: Elsevier
daily living skills. Older adults diagnosed with Alzhei- Olley, J. G., & Cox, A. (2008). Assessment of adaptive behavior in adult
mers type dementia and other cognitive and neuropsy- forensic cases: The use of the ABAS-II. In T. Oakland, & P. Harrison,
(Eds.), Adaptive behavior assessment system-II: Clinical use and inter-
chological disorders with late-life onset often display
pretation. Boston: Elsevier
impairments in their functional daily living skills. Al- Rust, J. O. & Wallace, M. A. (2004). Test review: Adaptive behavior
though data from the ABAS-II may not be crucial in the assessment system second edition. Journal of Psychoeducational
diagnosis of some of these disorders, ABAS-II data will Assessment, 22, 367373.
promote an understanding of their impact on daily living Wei, Y., Oakland, T., & Algina, J. (2008). Multigroup confirmatory factor
analysis for the parent form, ages 521, of the adaptive behavior
skills. The ABAS-II is used in the assessment of mental
assessment system-II. American Journal on Mental Retardation. 113,
retardation among death row inmates in light of the 2002 178186.
US Supreme Court Atkins decision (Olley & Cox, 2008).
Adaptive Functions
Cross References
Activities of Daily Living (ADL)
Activities of Daily Living
Activity Restrictions and Limitations
Adaptive Behavior ADD
Intellectual Disabilities
Attention Deficit, Hyperactivity Disorder
Minimal Brain Dysfunction
References
American Association on Intellectual and Developmental Disabilities.

(1992). Definitions, classifications, and systems of supports (9th ed.).
Washington, DC: American Association on Mental Retardation.
Addiction
American Association on Intellectual and Developmental Disabilities.
(2002). Mental retardation: Definition, classification, and systems Substance Abuse Disorders
40 A Adelaide Activities Index
Adelaide Activities Index ADHD, Combined

Frenchay Activity Index Attention Deficit, Hyperactivity Disorder
Adenoma
ADHD, Predominantly
E THAN M OITRA Hyperactive-impulsive Type
Drexel University
Morgantown, WV, USA Attention Deficit, Hyperactivity Disorder
Definition
A benign tumor of glandular origin. There are three types ADHD, Predominantly Inattentive
of adenomas: tubular (most common; tube-like struc- Type
ture), villous (least common; most likely to become can-
cerous; ruffled structure), and tubulovillous (blend of Attention Deficit, Hyperactivity Disorder
tubular and villous structures). Adenomas do not metas- Minimal Brain Dysfunction
tasize, though they can develop into malignancies known
as adenocarcinomas. The tumor may occur throughout
the endocrine system, including the pituitary gland.
Pituitary adenomas occur at a much higher incidence ADI-R
in adults than in children. Because their invasiveness is
local, they are almost always benign and can be difficult to Autism Diagnostic Interview, Revised
detect. There is the secreting and the nonsecreting type.
Clinical symptoms come from the endocrine dysfunction
or from mass effect, and include headaches, hypopituita-
rism, and visual loss (caused by compression in the optic
ADLQ
chiasm). Treatment of pituitary adenomas includes cor-
Activities of Daily Living Questionnaire
rection of electrolyte dysfunction, replacement of pitui-
tary hormones, surgical resection, and radiotherapy.
Cross References Admissibility

Pituitary Adenoma M OIRA C. D UX
Baltimore, MD, USA
Mazzaferri, E. L., & Saaman, N. A. (Eds.) (1993). Endocrine tumors. Definition

Boston: Blackwell Scientific Publications.
Admissibility of evidence refers to any testimonial, docu-
mentary material, or other form of tangible evidence that
can be considered by the trier of fact, most typically
ADHD a judge or a jury, in the context of a judicial or
administrative proceeding. In order for evidence to be
Attention Deficit, Hyperactivity Disorder admissible, it must be relevant, non-prejudicial, and
Minimal Brain Dysfunction possess some indicia of reliability. For example, if
Adoption Studies A 41
evidence consists of a witness testimonial, it must be Greiffenstein, M. F. (2009). Basics of forensic neuropsychology. In
J. Morgan, & J. Ricker (Eds.). Textbook of clinical neuropsychology. A
established that the witness is credible and that he/she
New York: Taylor & Francis.
has knowledge of that which he/she is declaring. For Jenkins v. United States, 307 F. 2d 637 (1962).
neuropsychologists, a central issue is the admissibility Kaufmann, P. M. (2008). Admissibility of neuropsychological evidence in
of ones data and opinions. Rules 401, 402, and criminal cases: Competency, insanity, culpability, and mitigation.
702705 from Article VII of the Federal Rules of Evi- In R. Denney, & J. Sullivan (Eds.). Clinical neuropsychology in the
criminal forensic setting. New York: Guilford.
dence (FRE) relate to Opinions & Expert Testimony.
Perhaps of most relevance to psychologists is rule
FRE 702 which states, If scientific, technical, or other
specialized knowledge will assist the trier of fact to
understand the evidence or to determine a fact in Admissibility of Psychological
issue, a witness qualified as an expert by knowledge, Evidence
skill, experience, training or education, may testify
thereto in the form of an opinion or otherwise. In Jenkins v. U.S. (1962)
other words, the expert should possess some form of
knowledge that a typical judge or juror would not be
expected to know or understand. Rule 703 states, The
facts or data in the particular case upon which an Admissibility of Psychological/
expert bases an opinion or inference may be those
perceived by or made known to the expert at or before Neuropsychological Evidence
the hearing. If of a type reasonably relied upon by
experts in the particular field in forming opinions or Baxter v. Temple (2005)
inferences upon the subject, the facts or data need not
be admissible in evidence in order for the opinion or
the inference to be admitted. Facts or data that are
otherwise inadmissible shall not be disclosed to the Adoption Studies
jury by the proponent of the opinion or inference
unless the court determines that their probative value R OHAN PALMER 1, M ARTIN H AHN 2
1
in assisting the jury to evaluate the experts opinion University of Colorado
substantially outweighs their prejudicial effect. Boulder, CO, USA
2
Several important cases have addressed the admissi- William Paterson University
bility of scientific testimony. In the case of Frye v. United Wayne, NJ, USA
States (1923), the Frye standard was established which
stated that: only scientific methods and concepts with
general acceptance within a particular field are admissi- Definition
ble. In the more recent case of Daubert v. Merrell Dow
(1993), it was determined that scientific testimony has to Adoption studies typically compare pairs of persons, e.g.,
abide by two criteria, the testimony must be: (a) scientifi- adopted child and adoptive mother or adopted child and
cally valid and (b) relevant to the case at hand. biological mother to assess genetic and environmental
influences on behavior.
Cross References Current Knowledge

Daubert v. Merrell Dow Pharmaceuticals (1993)
Design
Familial resemblance of behaviors is due to genetic and/or

References and Readings common familial environmental influences. Adoption
studies provide a direct test of the role of both factors.
A complete list of the Federal Rules of Evidence is available at: http:// This is possible by drawing comparisons between families
judiciary.house.gov/media/pdfs/printers/108th/evid2004.pdf. that share genetic and environmental influences and
42 A ADOS
families that share only genetic or environmental factors. References and Readings
Adoption creates two types of families. The genetic
family consists of pairs of genetically related individuals Bricker, J. B., Stallings, M. C., Corley, R. P., Wadsworth, S. J., Bryan, A.,
who do not share a common family environment (e.g., Timberlake, D. S., et al. (2006). Genetic and environmental
influences on age at sexual initiation in the Colorado adoption
biological parent and adopted-away child). The similar-
project. Behavior Genetics, 36, 820832.
ity between these pairs of relatives provides a direct Petrill, S. A., Plomin, R., DeFries, J. C., & Hewitt, J. K. (2003). Nature,
estimate of genetic effects on behaviors. The second nurture, and the transition to early adolescence. Oxford: Oxford
type family is the environmental family, which is University Press.
made up of pairs of individuals who are not genetically Plomin, R., Fulker, D. W., Corley, R., & DeFries, J. C. (1997). Nature,
nurture, and cognitive development from 1 to 16 years: A parent-
related but who share a common family environment (e.
offspring adoption study. Psychological Science, 8, 442447.
g., adoptive parent and adopted child). The similarity Young, S. E., Rhee, S. H., Stallings, M. C., Corley, R. P., & Hewitt, J. K.
between pairs of relatives from an environmental (2006). Genetic and environmental vulnerabilities underlying
family indicates the presence of environmental influ- adolescent substance use and problem use: General or specific?
ences on behavior. Adoption studies utilize either Behavior Genetics, 36, 603615.
parentoffspring pairs or sibling pairs. Because data
on biological parents and siblings of adoptees are
sometimes rare, comparison between genetic-plus-
environmental families (i.e., intact families) and adoptive
ADOS
families also provides evidence of genetic and environ-
Autism Diagnostic Observation Schedule
mental influences.
Relevance to Neuropsychology Adrenal Hormones

The Colorado Adoption Project has been collecting Minimal Brain Dysfunction
longitudinal data on biological and adoptive parents and
their biological or adopted children for over 30 years
(Petrill, Plomin, DeFries, & Hewitt, 2003). In one set of
analyses from that project reported by Plomin, Fulker, Adrenaline
Corley, and DeFries (1997), parentoffspring correlations
were calculated for children aged 316 years. The results Epinephrine
of the analyses show increasing correlations across those
ages between biological parents and their adopted-away
children on such special cognitive abilities as verbal skills
and perceptual speed. Correlations between adoptive Adrenergic Agonists
parents and adopted children remained about zero across
those ages. The authors interpret the results to indicate Catecholamines
that heritability increases for those special cognitive
abilities with age and that the role of shared environment
is low or nonexistent.
Today, adoption study data are used to assess the
Adrenocorticotropic Hormone
genetic and environmental influence on a variety of
DAVID J. L IBON
clinical outcomes that include drug addiction (Young,
Rhee, Stallings, Corley, & Hewitt, 2006) and age of sexual
Philadelphia, PA, USA
initiation (Bricker et al., 2006), to name a few.
Definition
Cross References
Adrenocorticotropic hormone (ACTH) is produced by
Twin Studies the anterior pituitary gland and is a component of the
Advanced Progressive Matrices A 43
hypothalamic-pituitary-adrenal axis. The release of ACTH Description A

is associated with the biological response to stress. The
production of ACTH from the pituitary gland stimulates First developed in the 1940s as an additional form of the
the adrenal glands to produce cortisol. The ACTH stimu- Ravens progressive matrices, the advanced progressive
lation test is a common procedure used to assess the matrices (APM) were developed to test intellectual
integrity of the adrenal glands. This test is used to identify efficiency in people with greater than average intellectual
a number of medical conditions including adrenal insuffi- ability, and to differentiate clearly between people of
ciency, Addisons disease, and related medical conditions superior ability. A nonverbal test of inductive reasoning,
(Melmed & Kleinberg, 2008). the APM contains 48 items, presented as one set of
12 (Set I), and another of 36 (Set II). As in the standard
version of the test (SPM), items are presented in black ink
on a white background, and become increasingly difficult
Cross References
as progress is made through each set. Although it is an
untimed task, some clinicians administer the APM under
Hypothalamus
time constraints. Set II can be used without a time limit to
assess the examinees total reasoning capacity. In this case,
the examinee would first be shown the problems of Set I as
References and Readings examples to explain the principles of the test, and would
then be given approximately 1 h to complete the task.
Melmed, S., & Kleinberg, D. (2008). Anterior pituitary. In H. M. Alternately, Set I can be given as a short practice test
Kronenberg, S. Melmed, K. S. Polonsky, & P. R. Larsen (Eds.), followed by Set II as a speed test. In this case, 40 min is
Williams textbook of endocrinology (11th edn.). Philadelphia, PA:
the time limit most commonly given for Set II.
Saunders Elsevier.
Adult Respiratory Distress The APM was designed in the 1940s to assess nonverbal
Syndrome abstract conceptualization skills of individuals for whom
the standard version was too easy; that is, those achiev-
Acute Respiratory Distress Syndrome ing a raw score of 50 or above on the SPM. For children
over 10 years of age with high intellectual functioning,
the APM may be the appropriate version to ensure an
adequate ceiling (Mills, Ablard, & Brody, 1993). For
additional information about the historical background
Advanced MS of the original test, please refer to the entry for Ravens
Progressive Matrices.
Secondary-Progressive Multiple Sclerosis
Psychometric Data
Advanced Progressive Matrices Norms for adolescents (ages 1216.5) and adults (1868+;
Sets I and II) for untimed (ages 1270+) and timed (ages
V ICTORIA M. L EAVITT 1728) versions are provided for North America (Raven,
Kessler Foundation Research Center Raven Court, 1998).The reliability of the test is considered
West Orange, NJ, USA good, with high internal consistency of APM Set II, and
split-half reliability coefficients varying between 0.83 and
0.87 (Strauss, Sherman, & Spreen, 2006). Set I, as it has
Synonyms only 12 items, yields lower figures. Reliability of the
original 48-item version was found to be high for adults
APM and children aged 11.5 years+ (>0.80); for younger
44 A Advocacy
children, it was only reasonably reliable (0.76). Overall, Definition

Set II scores increased by three points on retest (Raven
et al., 1998). The process of supporting or acting on behalf of a cause;
facilitating equal community access and participation of
individuals or groups that have typically been socially
Clinical Uses
and/or economically marginalized. There are several
types of advocacy to include:
The SPM and CPM have been found to be sensitive to a
Systems Advocacy: the process in which any system
variety of neurological and neuropsychiatric conditions
(public, private, community based) is made more respon-
( Ravens Progressive Matrices). The APM, designed for
sive to the needs of the individual served by the system.
use with higher functioning individuals, may be more
This process may include increasing awareness of services
appropriately employed for assessing an individuals
and resources available within a community; identifying
capacity for decision-making or strategic planning at
unmet needs of individuals; identifying existing barriers
the management level in the workplace or in a higher
that impede access to community services and resources;
education setting.
developing strategies to eliminate legislative, regulatory,
social and economic barriers that may impede access to
Cross References ones community supports and resources.
Individual Advocacy: the process of increasing
Colored Progressive Matrices awareness of unmet needs and procuring rights or benefits
Ravens Progressive Matrices on behalf of another individual or group of individuals.
Standard Progressive Matrices Self-Advocacy: the process of empowering an individual
to rely upon him or herself to make his/her own choices
and decisions in order to direct the course of his/her life.
The People First movement of the 1970s was a progenitor of
self-advocacy as a civil rights movement. The independent
Mills, C. J., Ablard, K. E., & Brody, L. E. (1993). The Ravens progressive
matrices: Its usefulness for identifying gifted/talented students.
living movement also fostered self-advocacy and provided
Roeper Review, 15, 183186. a foundation for self-advocacy activism.
Raven, J. C. (1965, 1994). Advanced progressive matrices sets I and II.
Oxford: Oxford Psychologists Press.
Raven, J., Raven, J. C., & Court, J. H. (1996). Progressive matrices:
A perceptual test of intelligence. Individual form. Oxford: Oxford Cross References
Psychologists Press. (Original work published 1938)
Raven, J., Raven, J. C., & Court, J. H. (1998). Raven manual: Section 4.
Americans with Disabilities Act
Advanced progressive matrices. Oxford: Oxford Psychologists Press
Ltd. Independent Living
Raven, J., Raven, J. C., & Court, J. H. (2003). Manual for Ravens progres-
sive matrices and vocabulary scales. Section 1: General overview.
San Antonio, TX: Harcourt Assessment.
Strauss, E., Sherman, E. M. S., Spreen, O. (Eds.). (2006). A compendium of References and Readings
neuropsychological tests (3rd ed.). NY: Oxford University Press.
Dell Orto, A. E., & Marinelli, R. P. (Eds.) (1995). Encyclopedia of disability
and rehabilitation. New York: MacMillian Publishing.
Test, D., Fowler, C. H., Wood, W. M., Brewer, D. M., & Eddy, S. (2005).
Advocacy Conceptual framework of self-advocacy for students with disabilities.
Remedial and Special Education, 26, 4354.
Wehmeyer, M. L. (2004). Self-determination and the empowerment of
A MY J. A RMSTRONG people with disabilities. American Rehabilitation, 28, 2229.
Richmond, VA, USA
Synonyms Advocate
Advocate; Support Advocacy
Affective Disorder A 45
Definition A
Adynamia
Affect is the display and experiencing of emotion. It
I RENE S HULOVA -P IRYATINSKY includes positive dimensions such as joy, interest, and
Butler Hospital contentment, as well as negative dimensions of emotion
Providence, RI, USA such as disgust, fear, and anger. Affect is a very rapid
response to internal (e.g., thoughts, memory) or external
stimuli (e.g., other people). It is different from mood,
Synonyms in that it is more momentary and observable by
others, whereas mood is longer-lasting and constitutes a
Asthenia symptom that patients may report (e.g., depression).
Affect can be observed from facial expression, gestures,
Definition posture, and speech (e.g., word choice, tone, rate).
Adynamia refers to a general weakness and lack of energy

evident through lack of verbal or overt behavior due to Cross References
a disease or neurological conditions. It can manifest as
lethargy, loss of strength, weakness in extremities, and Affective Disorder
difficulty initiating activities or completing tasks. Adyna- Emotions
mia can be observed after trauma to the frontal lobes, Mood Disorder
multiple sclerosis, and other conditions. In language, ver-
bal adynamia (lack of spontaneity of speech) is seen with
lesions of the medial frontal lobes and refers to difficulty
in initiation and maintenance of language output.
Batson, C. D., Shaw, L. L., & Oleson, K. C. (1992). Differentiating affect,
Cross References mood and emotion: Toward functionally-based conceptual distinctions.
Emotion. Newbury Park, CA: Sage.
Blechman, E. A. (1990). Moods, affect, and emotions. Hillsdale, NJ:
Abulia Lawrence Erlbaum Associates.
Apathy Ekman, P. (1993). An argument for basic emotion. Cognition and
Transcortical Motor Aphasia Emotion, 6, 169200.
Berrios, G. E. (2008). Classic text no. 76: Asthenia by A. Dechambre Affect Display
(1865). History of Psychiatry, 19(4), 490501.
Caplan, D. (1987). Neurolinguistics and linguistic aphasiology: An Affect
introduction. New York: Cambridge University Press.
Affect Affective Disorder

J OEL W. H UGHES J OEL W. H UGHES
Kent State University Kent State University
Kent, OH, USA Kent, OH, USA
Synonyms Synonyms
Affect display Emotional disorder; Mood disorder

46 A Affective Disorder
Short Description or Definition Bipolar disorder is diagnosed when there is a

manic mood disturbance characterized by markedly
Affective disorder is a mental disorder predominantly expansive, elevated, or irritable mood, lasting at least
characterized by altered mood that results in a significant 1 week. The mood disturbance must be accompanied by
impairment in social, occupational, or other important additional symptoms such as grandiosity, excessive risky
area of functioning. Affective disorders include depressive behavior such as sexual behavior or irresponsible spend-
disorders such as major depressive disorder, minor de- ing, and decreased need for sleep. A mixed episode
pressive disorder, and dysthymia, as well as manic disor- denotes mood disturbances that are characterized by
ders such as bipolar disorder and cyclothymic disorder. both manic and depressive symptoms. A hypomanic
Affective disorders may be primary or caused by medical episode is a less-pronounced elevation of mood that
conditions or substances. would not qualify as a true manic episode. Bipolar dis-
orders follow a course in which periods of elevated
mood alternate with periods of depression, and are
Categorization categorized according to the nature of these episodes.
For example, Bipolar I involves alternating manic and
Mania and depression seem to anchor the ends of an depressive episodes; in Bipolar II, there are alternating
emotional and behavioral continuum, an observation hypomanic and depressive episodes; cyclothymic disor-
that dates from ancient times. In Hippocrates humoral der involves alternating hypomanic and depressive epi-
theory, mania resulted from an excess of yellow bile, and sodes that do not meet full criteria for major depression.
depression to an excess of black bile. In the early twentieth
century, German psychiatrist Emil Kraepelin described
affective disorders as belonging to a manicdepressive Epidemiology
form of psychosis, which he differentiated from dementia
praecox. The term manic depression was replaced by Affective disorders are very common. At any one time,
more contemporary language, including major depressive approximately 10% of the adult population, or nearly
disorder and bipolar disorder in the twentieth century, 20 million Americans, have a depressive illness. Rates of
and, for example, major depressive disorder was first depression are even higher in patients with comorbid medi-
incorporated into the third edition of the Diagnostic cal conditions, and, for example, about 30% of patients with
and Statistical Manual (DSM-III). cardiac disease have clinically significant depression. Bipolar
Depressive disorders include major depressive disor- disorder is much less common than unipolar depression,
der and dysthymic disorder. Diagnosis of major depres- occurring in between 2% and 4% of the population (includ-
sive disorder is made on the basis of symptoms, as there is ing Bipolar I, Bipolar II, and cyclothymic disorder). While
no physiological test that reliably diagnoses depression. depression is twice as common among women as men,
Major depressive disorder requires at least 2 weeks of de- bipolar is equally common in men and women.
pressed mood and/or loss of interest in usually pleasurable
activities (anhedonia). In addition, at least four of the fol-
lowing seven symptoms must also be present; significant Natural History, Prognostic Factors, and
weight gain or loss or appetite changes, sleep disturbance Outcomes
(e.g., early morning awakening with difficulty returning to
sleep), observable disturbances in psychomotor speed Affective disorders often start in adolescence. For exam-
(increased or diminished), loss of energy or excessive ple, the onset of Bipolar disorder is typically 1524 years
fatigue, feelings of low self-worth or inappropriate guilt, of age. However, the most likely ages for a first major
cognitive changes such as the subjective experience of diffi- depressive episode are 3040 years of age. Depressive
culty concentrating, and thinking about or planning suicide. disorders often remit spontaneously, but recurrence is
Dysthymia is similar to major depressive disorder, common, and about 15% of individuals experiencing an
although the depression must be chronic (i.e., two or initial major depressive episode will develop chronic re-
more years of depressed mood), and during the first current depression. The bipolar disorders are highly heri-
2 years of the dysthymia, there must not have been an table, and research continues to determine genetic risk
episode of major depression or a period of longer than markers for bipolar disorder. Brain imaging studies also
2 months with no symptoms. suggest that a broad risk for unstable moods may underlie
Affective Spectrum Disorders A 47
bipolar disorder, but more research is warranted. The have exaggerated responses to negative feedback, includ-
A
causes of depression are not fully understood, but appear ing rumination. Neuropsychological evaluations in de-
to involve the interaction of genetic and environmental pression and bipolar disorder are used frequently in
factors such as stress and disruptions in interpersonal research, as tests with broad clinical utility in the context
relationships. Thus, in addition to female gender, risk of assessing or treating affective disorders have not been
factors for depression include severe life stress such as widely disseminated.
traumatic events and loss of significant relationships. De-
pression is associated with shorter life expectancy from
suicide and other causes of death. For example, depres- Treatment
sion increases risk of cardiac disease, as well as risk of
mortality among individuals with cardiac disease. Depression is often treated with medication and/or psy-
chotherapy. A large number of medications are available
to treat depression, including selective serotonin reuptake
Neuropsychology and Psychology of inhibitors, which typically have relatively milder side
Affective Disorder effects and lower risks than older drugs such as mono-
amine oxidase inhibitors. Treatment of bipolar disorders
Depression is common in neurological conditions such as requires pharmacotherapy. In contrast to major depres-
stroke and traumatic brain injury (Robinson, 2006; sive disorder, bipolar cannot be successfully treated by
Rosenthal, Christensen, & Ross, 1998). Even without an psychotherapy alone.
obvious neurologic insult, individuals with alterations in
executive control, memory, and emotion regulation are at
increased risk for depression. Furthermore, individuals Cross References
with depression often show neuropsychological deficits
in the absence of neurological conditions. The neuropsy- Depressive Disorder
chological deficits specified in the diagnostic criteria for
depression include difficulty concentrating and making
decisions. Thus, depressed patients often exhibit deficits
in executive control, memory, and processing speed. For References and Readings
bipolar disorder, distractibility is typically present, as well
Allen, L. B., McHugh, R. K., & Barlow, D. H. (2008). Emotional disorders:
as impaired decision making reflected in the criterion
A unified protocol. In D. H. Barlow (Ed.), Clinical handbook of
relating to distractibility of excessive involvement in psychological disorders: A step-by-step treatment manual (4th ed.)
activities that present significant risk of negative conse- (pp. 216249). New York: Guilford Press.
quences. Current neuropsychological theories of depres- American Psychiatric Association (2000). Diagnostic and statistical man-
sion emphasize the frontal lobes and basal ganglia, ual of mental disorders (4th ed.). Text Revision. Washington, DC:
American Psychiatric Association.
including abnormalities in neural circuitry involving the
Chamberlain, S. R., & Sahakain, B. J. (2006). The neuropsychology of
prefrontal cortex, mesiotemporal cortex, striatum, amyg- mood disorders. Current Psychiatry Reports, 8, 458463.
dala, and thalamus (Chamberlain & Sahakain, 2006). Clark, L., Chamberlain, S. R., & Sahakian, B. J. (2009). Neurocognitive
These areas may also be implicated in bipolar disorder, mechanisms in depression: Implications for treatment. Annual
as they appear to underlie mood symptoms and treatment Review of Neuroscience, 32, 5774.
Robinson, R. (2006). The neuropsychiatry of stroke (2nd ed.). New York:
effects.
Cambridge University Press.
Rosenthal, M., Christensen, B., & Ross, T. (1998). Depression following
traumatic brain injury. Archives of Physical Medicine and
Evaluation
Assessment of affective disorders focuses on self-report

instruments and clinical interviews. Neuropsychological
testing may reveal deficits in executive function, attention Affective Spectrum Disorders
psychomotor slowing, and biases in the processing of
emotional stimuli. Specifically, depressed individuals Unexplained Illness
48 A Afferent
Cross References
Afferent
Lemniscal System
J OHN B IGBEE
Richmond, VA, USA References and Readings
Luria, A. L. (1976). The working brain: An introduction to neuropsychology.

Synonyms New York: Perseus Books Group.
Sensory
Age Decrements
Definition S ANDRA B ANKS
Afferent is an anatomical term that indicates functional Pittsburgh, PA, USA
directionality. In nervous tissue, afferent is often used
synonymously with sensory information when it refers
to nerves carrying impulses from peripheral receptors Synonyms
toward the central nervous system. Afferent can also be
used in general to refer to any connection coming into a Age-associated cognitive decline
structure within the nervous system. The opposite direc-
tion of conduction is efferent.
Definition
The concept of age decrements in neuropsychology refers

to a decline in cognitive performance due to normal aging
Afferent Paresis rather than due to an extraneous or internal event that is
known to negatively affect cognitive performance, such as
M ARYELLEN R OMERO a traumatic brain injury, stroke, psychiatric symptoms,
Tulane University Health Sciences Center and extensive drug use history.
New Orleans, LA, USA
Current Knowledge
Definition Variability in the performance of aging individuals adds
complexity to the determination of specific age decre-
A deficit in the ability to perform voluntary movements ments on neuropsychological tests. It is generally thought
due to loss of kinesthetic feedback. The primary and that individuals are more likely to retain crystallized
secondary motor cortices have extensive inputs from the knowledge (e.g., that which is practiced, overlearned,
somatosensory areas in the parietal lobes. Following and skill-based) than fluid knowledge (e.g., problem-
lesions to this latter area, particularly the post-central solving). As there are factors that heighten the risk for age
gyrus or to the lemniscal system which provides proprio- decrements, protective factors may counteract the risk.
ceptive information to it, motor difficulties may be ob- For instance, higher levels of education and positive
served either in the limbs or in speech production. health status may slow down the rate of cognitive decline
Although the muscles involved in such activities are not that would otherwise occur with increasing age.
weak per se, the loss of sensory information results in a One concept that illustrates age decrements is Age-
disruption of motor control and an imprecise excitation Associated Memory Impairment (AAMI), which pertains
of muscle groups required to execute specific, voluntary to age-related decline in performance specifically in terms
fine-motor responses. of memory.
Ageusia A 49
Cross References Current Knowledge A

Cognitive Reserve Agenesis can result from various etiologies, including
Memory Impairment genetic predisposition, chromosomal abnormalities, or
intrauterine trauma, such as infection. When present,
this condition is commonly associated with other neuro-
anatomical anomalies, metabolic disturbances, and/or
References and Readings neurobehavioral deficits. The latter might include mental
retardation, seizures, motor deficits, and psychiatric
Lezak, M. D. (2004). Neuropsychological assessment (4th Ed.). New York: disturbances. However, some patients may be relatively
Oxford University Press. asymptomatic, the callosal defect being discovered only
serendipitously late in life. The latter is more likely to
occur when the agenesis is not accompanied by other
neurological or metabolic defects. Whereas disconnec-
tion syndromes are routinely present following surgical
Age Equivalent commissurotomy for intractable epilepsy, they are gener-
ally not present with agenesis.
Mental Age
Age-associated Cognitive Decline Aicardi, J., Chevrie, J.-J., & Baraton, J. (1987). Agenesis of the corpus
callosum. In P. J. Vinken, G. W. Bruyn, & H. L. Klawans (Eds.),
Handbook of clinical neurology (Vol.50, pp. 149173). New York:
Age Decrements Elsevier.
Mild Cognitive Impairment Marszal, E., Jamroz, E., Pilch, J., Kluczewska, E., Jablecka, H., &
Krawczyk, R. (2000). Agenesis of the corpus callosum: Clin-
ical description and etiology. Journal of Child Neurology, 15,
401405.
Zaidel, E., & Iacoboni, M. (2003). The parallel brain: The cogni-
tive neuroscience of the corpus callosum. Cambridge, MA: MIT
Age-Associated Memory Press.
Impairment (AAMI)
Benign Senescent Forgetfulness
Ageusia
M ARYELLEN R OMERO
Agenesis of Corpus Callosum Tulane University Health Sciences Center
J OHN E. M ENDOZA
Tulane University Medical Center
New Orleans, LA, USA Definition
Ageusia is the loss of the sense of taste. The disorder

Definition should be distinguished from a disruption in the ability
to perceive flavor, which requires a combination of olfac-
A developmental defect in which either all or part of the tory, gustatory, and somatosensory functions. Frequently,
corpus callosum fails to develop. complaints of ageusia are often explained by olfactory
50 A Aggravating Factors
dysfunction rather than a disruption in taste perception,

per se. The majority of taste receptors (buds) are located Aggravating Factors
on the tongue and this information is carried by the
VIIth (anterior two thirds) and IXth (posterior third) R OBERT L. H EILBRONNER
cranial nerves, with other taste receptors (cranial nerve Chicago Neuropsychology Group
X) located in other regions of the mouth and throat. Chicago, IL, USA
These taste fibers enter the solitary nucleus (rostral por-
tion) in the upper medulla and from there second-order
neurons travel to the ventral posterior medial nuclei of the Definition
thalamus. Thalamic projections carrying this gustatory
information then project to the post-central gyrus in Refers to any relevant circumstances in correspondence
the region of the parietal operculum and to the underly- with the evidence presented during the trial that, from the
ing insular cortex where the sensation of taste is likely perspective of the jurors, makes the harshest penalty ap-
experienced. propriate. By contrast, mitigating factors refer to evidence
Lesions of the VIIth nerve can result in loss of taste regarding the defendants character or circumstances
in the ipsilateral anterior two thirds of the tongue related to the crime that would provide foundation for a
which is more readily assessable to clinical testing juror to vote for a lesser sentence.
than lesions of the IXth or Xth nerves. However, total
loss of taste (ageusia) is seldom seen as a result of
structural lesions because of the multiple and bilateral
pathways involved. Ageusia (or hypogeusia) is more
In 1972, the U.S. Supreme Court considered the death
likely to result from more systemic problems such
penalty to be a cruel and an unusual punishment because
as treatments for cancer (radiation, chemotherapy),
the manner in which capital sentences were decided in
certain types of influenza, diabetes, or certain med-
Georgia was capricious (Furman v. Georgia, 1972). This
ications. Taste acuity (hypogeusia) can decline with
decision discontinued death penalty litigation in the USA
age and may contribute to the anorexia and weight
at that time because none of the states had a system that
loss often seen in elderly persons. The prognosis in
was substantially different. In 1976 (Gregg v. Georgia), the
acquired ageusia is often correlated directly with the
Court accepted as constitutional Georgias rewrite of their
expected course of the illness or injury causing the
statute which included a capital sentencing process that
dysfunction.
required presentation before a judge or jury of aggravating
and mitigating factors. It required at least one or ten
specified aggravating circumstances to be established be-
Cross References yond reasonable doubt to impose the death penalty.
Some examples include: whether the crime (murder) was
Taste particularly cruel and atrocious, if more than one victim
was murdered, whether the murder occurred during the
commission of a felony, etc.
References and Readings Current Knowledge

Cerf-Ducastel, Van de Moortele, P.-F., MacLeod, P. Le Bihan, D., & Laws regarding how aggravating or mitigating factors
Faurion, A. (2001). Interaction of gustatory and lingual somatosen- should be weighed by jurors vary based on state laws.
sory perceptions at the cortical level in the human: A functional
magnetic resonance imaging study. Chemical Senses, May 1, 26(4),
Neuropsychological assessments in death penalty cases
371383. typically focus on mitigating factors, such as neuropsy-
Doty, R. L., & Kimmelman, C. P. (1992). Lesser20R.P. Smell and taste and chological or neurobehavioral impairments, as there is an
their disorders. In A. K. Asbury, G. M. McKhann, & W. I. McDonald increased body of evidence demonstrating a preponder-
(Eds.), Diseases of the nervous system (2nd ed., pp. 390403). ance of neurocognitive deficits in violent criminals. Neu-
Philadelphia, PA: W.B. Saunders.
Wilson-Pauwek, L., Akesson, E., & Stewart, P. (1988). Cranial
ropsychological assessment with respect to aggravating
nerves: Anatomy and clinical comments. Philadelphia, PA: B.C. factors is less common and typically addresses increased
Decker. risk of future dangerousness.
Agitated Behavior Scale A 51
Cross References 2935 moderate agitation, and 3556 severe agitation.

A
Subscale scores can also be calculated for disinhibition,
Mitigating Factors aggression, and lability although it appears that ABS pri-
marily measures a single construct (Bogner et al., 2000),
so that the total score may be most appropriate when
References and Readings interpreting test results.
Denney, R. L. (2005). Criminal responsibility and other criminal forensic

issues. In G. Larrabee (Ed.), Forensic neuropsychology: A scientific
approach. New York: Oxford University Press. Current Knowledge
Furman v. Georgia, 408 U.S. 238 (1972).
Gregg v. Georgia, 49 L.Ed.2d. 859 (1976). The ABS is often used to perform serial assessments to
track changes in agitation that occur as a natural part of the
logical evaluations for the courts: A Handbook for mental health
professionals and lawyers. (3rd ed.). New York: Guilford Press. recovery process and as a result of treatment. Although
designed with traumatic brain injury in mind, the ABS has
also been used to assess agitation in other populations,
such as patients with progressive dementia (Corrigan,
Agitated Behavior Scale Bogner, and Tabloski, 1996; Tabloski, McKinnon-Howe,
and Remington, 1995). No differences have been found
DANIEL N. A LLEN between males and females with brain injury on the total
University of Nevada score or the subscale scores (Kadyan et al., 2004). Internal
Las Vegas, Nevada, USA consistency estimates range from 0.74 to 0.92 (Bogner
et al., 1999; Corrigan, 1989), with interrater reliability of
0.92 for the total score, and with comparable reliabilities
Synonyms of 0.90, 0.91, and 0.73 for the disinhibition, aggression,
and lability scores, respectively. Subscale to total score
ABS correlations range from 0.43 to 0.55. The construct
validity of the ABS has been supported by factor-analytic
studies that demonstrated the presence of three factors
Description representing disinhibition, aggression, and lability
(Corrigan and Bogner, 1994). ABS scores account for a
The agitated behavior scale (ABS) was designed to eval- substantial portion of the variance (from 36% to 62%) in
uate agitation and other problematic behaviors that independent observations of agitation (Corrigan, 1989)
commonly occur during the acute recovery phase follow- and are able to predict changes in cognition (Corrigan
ing traumatic brain injury (Corrigan, 1989). The ABS is and Mysiw, 1988), which provides additional support for
composed of 14 items that represent a number of com- its validity. Thus, there is evidence that the ABS is a highly
monly occurring problematic behaviors such as short practical measure with sound psychometric properties
attention span, impulsivity, uncooperativeness, violence, that allow for serial assessment of agitation in populations
and angry outbursts. Information that assists in complet- with brain injury.
ing the ABS, including descriptions of the behaviors and
ratings for each item, as well as examples, is available with
the author (Corrigan). Each item is rated on a 14-point Cross References
scale based on intensity of the behavior or frequency of its
occurrence. Additionally, when assigning ratings, the de- Post-traumatic Confusional State
gree to which the behavior interferes with functional Traumatic Brain Injury
behavior is also considered. If the behavior is absent a
rating of 1 is assigned. When the behavior is present a
rating of 2 or greater is assigned, with a rating of 4
indicating that the behavior is present to an extreme
degree. A total score is derived by summing across all 14
Bogner, J. A., Corrigan, J. D., Bode, R. K., & Heinemann, A. W. (2000).
items (range 1456) with scores less than 22 in the Rating scale analysis of the Agitated Behavior Scale. Journal of Head
normal range, scores of 2228 indicating mild agitation, Trauma Rehabilitation, 15, 656659.
52 A Agitation
Bogner, J. A., Corrigan, J. D., Stange, M., & Rabold, D. (1999). Reliability Current Knowledge
of the Agitated Behavior Scale. Journal of Head Trauma Rehabilitation,
14, 9196.
Corrigan, J. D. (1989). Development of a scale for assessment of agitation
There was no consensus on the definition of agitation
following traumatic brain injury. Journal of Clinical and Experimental within the greater health-care profession for many years.
Neuropsychology, 11, 261277. Clinicians in neuro-rehabilitation were using the term in
Corrigan, J. D. & Bogner J. A. (1994). Factor structure of the Agitated the early 1980s to describe a pattern of behavior observed
Behavior Scale. Journal of Clinical and Experimental Neuropsychology,
during recovery from traumatic brain injury. The devel-
16, 386392.
Corrigan, J. D. & Mysiw, W. J. (1988). Agitation following traumatic
opment of the Agitated Behavior Scale by Corrigan and
head injury: equivocal evidence for a discrete stage of cognitive associates in the late 1980s to measure this brain-injury-
recovery. Archives of Physical Medicine and Rehabiltation, 69, related behavior led to a more refined definition of the
487492. term. The term is not limited to just traumatic brain
Kadyan, V., Mysiw, W. J., Bogner, J. A., Corrigan, J. D., Fugate, L. P., &
injury as agitation can manifest in any setting in which
Clinchot, D. M. (2004). Gender differences in agitation after
traumatic brain injury. American Journal of Physical Medicine &
an individual experiences delirium and impaired cogni-
Rehabilitation, 83, 747752. tion (e.g., dementia).
The importance of the concept of agitation and its
measurement was vital to the establishment of the now
accepted viewpoint that recovery from agitation is pre-
ceded by improvement in cognition. Or conversely, inter-
Agitation ventions that decrease arousal and/or cognition can lead
to a worsening of agitation.
PAUL D. N EWMAN
Drake Center
Cincinnati, OH, USA Cross References
Agitated Behavior Scale
Synonyms Behavior Management
Deescalation
Posttraumatic agitation Dementia
Frustration Tolerance
Post-traumatic Confusional State
Definition Traumatic Brain Injury
Agitation is an excess of one or more behaviors that occur

during the course of delirium when cognition is impaired. References and Readings
The behaviors most often in excess during agitation in-
clude aggression, akathisia, disinhibition, and/or emo- Corrigan, J. D. (1989). Development of a scale for assessment of agitation
tional lability. Specific examples of agitated behavior following traumatic brain injury. Journal of Clinical and Experimen-
tal Neuropsychology, 69, 261277.
may include pacing, hand wringing, pulling at tubes or
Sandel, M. E., & Bysiw, W. J. (1996). The agitated brain injured patient.
restraints, inappropriate verbalizations, excessive crying Part 1: Definitions, differential diagnosis, and assessment. Archives of
or laughter, etc. Physical Medicine and Rehabilitation, 77, 617623.
Agitation is often conceptualized to result from an Smith, M., Gardner, L. A., Hall, G. R., & Buckwalter, K. C. (2004).
inability to cope with overstimulation. Stimulation may History, development, and future of the progressively lowered stress
threshold: A conceptual model for dementia care. Journal of the
be internal (e.g., pain or hallucinations) or external (e.g.,
American Geriatric Society, 52, 17551760.
noise, light, or conversation). Ones ability to cope
with stimulation may be viewed as a threshold.
Adverse changes to the brains typical functioning have
the potential to lower this threshold. Thus, individuals
with traumatic brain injury or dementia may become Agnogenic Medial Arteriopathy
agitated at lower levels of stimulation than noninjured
individuals. Cadasil
Agrammatic Speech A 53
Cross References A
Agnosia
Apperceptive Visual Agnosia
A NASTASIA R AYMER Associative Visual Agnosia
Old Dominion University Auditory Agnosia
Norfolk, VA, USA Pure Word Deafness
Tactile Agnosia
Visual Object Agnosia
Definition
Agnosia is a failure to recognize a sensory stimulus that is

not attributable to dysfunction of peripheral sensory References and Readings
mechanisms or to other cognitive impairments associated
with brain damage (Bauer & Demery, 2003). Agnosia is Bauer, R. M., & Demery, J. A. (2003). Agnosia. In K. M. Heilman & E.
often described as a percept that is stripped of its mean- Valenstein (Eds.), Clinical neuropsychology (4th ed., pp. 236295).
ing. The individual can respond to the presence of the New York: Oxford University Press.
Farah, M. J. (1990). Visual agnosia. Cambridge, MA: MIT Press.
stimulus, but has difficulty processing the perceptual
Feinberg, T. E., Rothi, L. J. G., & Heilman, K. M. (1986). Multimodal
information in sufficient detail to make sense of and agnosia after unilateral left hemisphere lesion. Neurology, 36,
meaningfully recognize it. The stimulus can be recognized 864867.
through other sensory modalities. Riddoch, M. J., & Humphreys, G. W. (2001). Object recognition.
In B. Rapp (Ed.), The handbook of cognitive neuropsychology
(pp. 4574). Philadelphia, PA: Psychology Press.
Current Knowledge
Agnosia can occur in any perceptual modality, though it is

most commonly reported to affect the visual modality
(Farah, 1990). Multi-modality forms of agnosia also
Agonist
have been described (Feinberg, Rothi, and Heilman,
Receptor Spectrum
1986). Lesions associated with agnosia will vary across
sensory modalities, usually affecting bilateral post-
Rolandic cortical sensory regions or disconnecting
incoming pathways from one hemisphere to the other
(Bauer & Demery, 2003).
Different forms of agnosia have been described that Agonist Spectrum
depend upon how much incoming information can be
processed. Some forms (e.g., apperceptive agnosia) are Receptor Spectrum
associated with disruption at early stages of perceptual
processing. The person cannot copy or match an incom-
ing percept to a like stimulus and may make perceptual
confusions, yet can conjure up some perceptual informa-
tion from memory (e.g., visual imagery tasks) or answer Agrammatic Aphasia
questions about perceptual attributes of a stimulus. In
other forms of agnosia (e.g., associative agnosia), the Agrammatism
person can copy or match percepts, but is not able to
conjure up information about perceptual characteristics
of a stimulus from memory and also has difficulty
appreciating the meaningfulness of a percept, its category,
context, associated objects and actions. In either case, Agrammatic Speech
accurate processing through that perceptual modality is
disrupted. Telegraphic Speech
54 A Agrammatism
Some authors have argued that agrammatism reflects an

Agrammatism underlying impairment in language representation and/or
processing (Grodzinsky 1986, 1990, 1995; Zurif, Swinney,
LYN T URKSTRA 1, C YNTHIA K. T HOMPSON 2 Prather, Solomon, & Bushell, 1993), while others contend
1
University of Wisconsin-Madison that they represent the speakers strategic adaptation to an
Madison, WI, USA underlying language processing impairment that is not
2
Northwestern University specific to grammar (Kolk & Heeschen, 1990; also see dis-
Evanston, IL, USA cussion in Beeke, Wilkinson & Maxim, 2007). Consistent
with the processing deficit view, individuals with agram-
matic aphasia show problems computing syntactic struc-
Synonyms tures in real time (Dickey, Choy, & Thompson, 2007;
Swinney, Prather, & Love, 2000; but see Blumstein et al.,
Agrammatic aphasia 1998) and also may have deficits that impact both pro-
duction and comprehension, although not always the
Definition same structures (Dickey, Milman, & Thompson, 2008).
Also, the structures that typically are impaired in agram-
Agrammatism refers to language production that is matic aphasia are similar across many languages. In sup-
lacking in grammatical structures. The basic signs of port of the adaptation view, there is evidence that
agrammatism are short phrase length, simplified syntax, the grammatical structures used by individuals with
errors and omissions of main verbs, and omission or agrammatic aphasia vary as a function of the task. For
substitution of grammatical morphemes such as plural example, individuals with agrammatic aphasia may pro-
markers or functors (Saffran, Berndt, & Schwartz, 1989). duce more complex sentences on standardized language
There may also be errors in tense, number, and gender, tests, in which grammatical completeness is the focus,
and difficulty in producing sentences with movement than in conversational interactions, in which the message
of grammatical elements, such as passive sentences, and interaction are the focus and the communication
Wh- questions, and complex sentences (Benedet, Chris- partners are co-constructing a dialog (Beeke, Maxim, &
tiansen, & Goodglass, 1998; Caplan & Hanna, 1998; Wilkinson, 2008).
Goodglass, 1997; Faroqi-Shah & Thompson, 2004). Spo- There is evidence of treatment efficacy for interven-
ken and written production typically shows similar error tions aimed improvement of underlying representation/
patterns. Typically, individuals with agrammatic aphasia processing impairments and deficits in adaptation. Verb
also show impaired comprehension of grammatical struc- as Core (Loverso, Prescott, & Selinger, 1986), Mapping
tures, particularly noncanonical semantically reversible Therapy (Schwartz, Saffran, Fink, & Myers, 1994), and
sentences (e.g., the boy was kicked by the horse; Treatment of Underlying Forms (TUF; Thompson,
Berndt, Mitchum, & Haendiges, 1996; Caramazza & Shapiro, Kiran, & Sobecks, 2003; Thompson, 2008)
Zurif, 1976). focus treatment on verbs and verb argument structure,
training patients to map form to meaning in both simple
Historical Background and complex sentences. Notably, TUF results in strong
generalization from complex to simple structures by
Historically, agrammatism was thought of as a syndrome controlling the lexical and syntactic variables of sentences
typically associated with nonfluent aphasia (Goodglass, trained (see Thompson & Shapiro, 2007, for review).
1997). More recent studies (e.g., Dick et al., 2001) have Various approaches to treatment of grammatical mor-
shown that features of agrammatism are present in the phology, such as deficits in verb tense and agreement,
production of many individuals with various forms of also have been shown to be efficacious (Faroqi-Shah,
aphasia, as well as in normal speakers under stressful 2008; Friedmann, Wenkert-Olenik, & Gil, 2000; Mitchum
conditions, and agrammatism is not attributable to any & Berndt, 1994; Weinrich, Boser, & McCall, 1999).
single site of lesion.
Current Knowledge Cross References
The underlying mechanisms of agrammatism have been Aphasia

debated in the literature over the past several decades. Grammar
Agraphia A 55
Nonfluent Aphasia Loverso, F. L., Prescott, T. E., & Selinger, M. (1986). Cuing verbs:
A treatment strategy for aphasic adults. Journal of Rehabilitation A
Paragrammatism
Research, 25, 4760.
Syntax Mitchum, C., & Berndt, R. (1994). Verb retrieval and sentence construc-
Telegraphic Speech tion: Effects of targeted intervention. In M. J. Riddoch & G. Hum-
phreys (Eds.), Cognitive neuropsychology and cognitive rehabilitation.
Hove, Sussex: Erlbaum.
Saffran, E. M., Berndt, R. S., & Schwartz, M. F. (1989). The quantitative
References and Readings analysis of agrammatic production: Procedure and data. Brain and
Language, 37(3), 440479.
Beeke, S., Maxim, J., & Wilkinson, R. (2008). Rethinking agrammatism: Schwartz, M. F., Saffran, E. M., Fink, R. B., & Myers, J. L. (1994). Mapping
Factors affecting the form of language elicited via clinical test pro- therapy: A treatment programme for agrammatism. Aphasiology, 8,
cedures. Clinical Linguistics and Phonetics, 22(45), 317323. 1954.
Beeke, S., Wilkinson, R., & Maxim, J. (2007). Individual variation in Swinney, D., Prather, P., & Love, T. (2000). The time course of lexical
agrammatism: A single case study of the influence of interaction. access and the role of context: Converging evidence from normal and
International Journal of Language and Communication Disorders, aphasic processing. In Y. Grodzinsky, L. P. Shapiro, & D. Swinney
42(6), 629647. (Eds.), Language and the brain: Representation and processing. New
Benedet, M. J., Christiansen, J. A., & Goodglass, H. (1998). A cross- York: Academic Press.
linguistic study of grammatical morphology in Spanish- and Thompson, C. K., & Shapiro, L. P. (2007). Complexity in treatment
English-speaking agrammatic patients. Cortex, 34(3), 309336. of syntactic deficits. American Journal of Speech and Language
Berndt, R. S., Mitchum, C. C., & Haendiges, A. N. (1996). Comprehen- Pathology, 16, 3042.
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Cognition, 58(3), 289308. of syntactic complexity in treatment of sentence deficits in agram-
Blumstein, S. E., Byma, G., Kurowski, K., Hourihan, J., Brown, T., & matic aphasia: The complexity account of treatment efficacy
Hutchinson, A. (1998). On-line processing of filler-gap construction (CATE). Journal of Speech, Language and Hearing Research, 42,
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Caplan, D., & Hanna, J. E. (1998). Sentence production by aphasic Weinrich, M., Boser, K. I., & McCall, D. (1999). Representation of
patients in a constrained task. Brain and Language, 63(2), 184218. linguistic rules in the brain: Evidence from training an aphasic
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1
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Synonyms
Kolk, H. H. J., & Heeschen C. (1990). Adaptation symptoms and im-
pairment symptoms in Brocas aphasia. Aphasiology, 4, 221231. Written language disorders
56 A Agraphia
Short Description or Definition Epidemiology
Agraphia is the term applied to acquired disorders of Agraphia is commonly observed following damage to the
spelling or writing caused by neurological damage in language-dominant left hemisphere. Although it is most
individuals with normal premorbid literacy skills. There frequently caused by stroke, agraphia can follow any kind
are several different agraphia profiles that variously result of focal damage to the brain regions critical for
from impairments of spelling knowledge, sound-to-letter implementing the various cognitive operations necessary
correspondences, letter-shape information, or motor for normal spelling and writing. Agraphia is also observed
control for handwriting. Although agraphia can occur in individuals with neurodegenerative disorders, including
in relative isolation, it often co-occurs with acquired those with primary progressive aphasia/semantic dementia
impairments of reading (alexia) and spoken language or Alzheimers disease. The specific agraphia profile reflects
(aphasia). the region of cortical damage or atrophy.
Categorization
Several distinct forms of acquired agraphia occur that
Outcomes
reflect specific combinations of impaired and preserved
The prognosis for recovery from agraphia depends on the
spelling and writing abilities following damage to certain
etiology of the lesion and the extent of the underlying
brain regions. Spelling difficulties can result from damage
brain damage. Agraphia following stroke or traumatic
to central linguistic processes supported by the language-
brain injury tends to show some spontaneous recovery
dominant hemisphere in a manner analogous to acquired
in the first months after brain damage occurs, but residual
impairments of reading ( alexia). Agraphia can also
impairments often persist. Additional improvements may
result from disruption of peripheral processing compo-
be achieved with behavioral treatment directed toward
nents that guide the selection and production of appro-
strengthening the weakened cognitive processes that sup-
priate letter shapes.
port spelling or motor control for writing. In individuals
Common central agraphia syndromes
with neurodegenerative disorders, progressive worsening
Phonological agraphia refers to an impaired ability to of the spelling impairment is observed along with the
manipulate the sound system of the language gradual deterioration of other language and cognitive
(phonology) which manifests as a disproportionate functions.
difficulty with the spelling of nonwords (e.g., flig,
merber) compared with real words.
Deep agraphia is characterized by a marked im- Neuropsychology and Psychology
pairment of spelling ability for nonwords, as seen in of Agraphia
phonological agraphia, but with the additional hall-
mark feature of semantic errors (e.g., car for vehicle). Written words are typically produced in response to
Surface agraphia (also called lexical agraphia) is activation of a concept in the semantic system. The
characterized by relatively preserved ability to spell motivation to write a word may be driven by the desire
nonwords and regularly spelled words in the face of to convey a message, or in response to an auditory stimu-
marked impairment of spelling words with irregular lus, as in the context of writing a word to dictation. As
soundletter correspondences, such as choir. depicted in the cognitive model of single-word processing
in Fig. 1, the word meaning (semantics) and the
Common peripheral agraphia syndromes
phonological word form (phonology) both provide access
Allographic agraphia is an impairment of written to spelling knowledge (orthography). In literate adults,
spelling due to errors in letter selection. the spellings of familiar words are easily recalled as whole
Apraxic agraphia is an impairment of the selection words from ones spelling vocabulary (i.e., orthographic
and implementation of graphic motor programs lexicon). In contrast to this lexical approach, spellings can
necessary to move the hand to form letter shapes. be assembled on the basis of the knowledge of sound-to-
Micrographia is the production of abnormally small letter correspondences using a sublexical processing
letters due to defective control of the force, speed, and strategy as depicted in Fig. 1. A sublexical approach is
amplitude of handwriting movements. often employed when one is unsure about the spelling of a
Agraphia A 57
Semantics A
Phonology Orthography
Lexical
Words Words
Spoken word Written word
Sublexical
Auditory Visual
Phonemes Letters
analysis analysis
Motor speech Graphic motor

programs programs
Speech Writing
Agraphia. Figure 1 A cognitive model indicating the component processes involved in spelling and writing
word, or when required to spell an unfamiliar word or a to damage to the sublexical route, while the better
nonword, such as glope. Spelling via soundletter corre- preserved real-word spelling by these patients reflects the
spondences is likely to yield correct responses for regularly residual functional capacity of the lexical and semantic
spelled words, such as drive, but over-reliance on the routes. There is evidence to suggest that phonological
sublexical route will result in phonologically plausible agraphia reflects a central impairment of phonological
errors for irregularly spelled words, such as kwire for processing ability that is also apparent on reading tasks;
choir. Thus, according to a dual-route model as depicted however, the spelling impairment is typically of greater
in Fig. 1, only the lexical route can deliver correct spellings severity due to the fact that spelling is a harder task than
for irregularly spelled words. The final stages of writing reading (Rapcsak et al., 2009). Although spelling accuracy
require translation of abstract spelling knowledge into for words (both regular and irregular) is better preserved
letter shapes and selection and implementation of the than spelling of nonwords, performance is often degraded
graphic motor programs for the appropriate handwriting to some extent relative to premorbid performance. Due to
movements. The various agraphia syndromes reflect the reliance on lexical processing with limited sublexical
specific impairments to these component processes input, real word spelling is typically influenced by lexical-
necessary for spelling and writing. semantic variables such as word frequency (high > low),
imageability (concrete > abstract), and grammatical class
(nouns > verbs > functors). Deep agraphia includes all of
Phonological/Deep Agraphia the characteristic features of phonological agraphia, but it
is distinguished from the latter by the production of
Phonological agraphia is characterized by difficulty in semantic errors (e.g., husband written as wife). In essence,
the generation of spellings on the basis of sound-to-letter deep agraphia can be considered a more severe form of
correspondences. This problem is particularly evident phonological agraphia.
during clinical evaluation when an individual is asked to Like phonological/deep alexia, phonological/deep
generate plausible spellings for nonwords. The dispropor- agraphia is typically encountered in patients with aphasia
tionate difficulty in spelling nonwords compared to syndromes characterized by phonological impairment in-
familiar words gives rise to an exaggerated lexicality effect cluding Brocas, conduction, and Wernickes aphasia. In
(Henry, Beeson, Stark, & Rapcsak, 2007; Rapcsak et al., such cases, there is damage to a network of perisylvian
2009). According to a dual-route model (Fig. 1), poor cortical regions involved in speech production/perception
nonword spelling in phonological agraphia is attributable and phonological processing including Brocas area,
58 A Agraphia
precentral gyrus, insula, Wernickes area, and supramar- representations as observed in individuals with semantic
ginal gyrus (Fig. 2). The contribution of these regions to dementia (Graham, Patterson, & Hodges, 2000). The
phonological processing skills is evident from lesion stud- reduction in the ability to process lexical-semantic
ies, but also in functional imaging studies of healthy information in such individuals results in overreliance
individuals when they perform a variety of written and on sublexical spelling procedures and regularization
spoken language tasks requiring phonological processing errors. As expected, it is not uncommon to observe
(Jobard et al., 2003; Vigneau et al., 2006; Rapcsak et al., co-occurance of surface alexia and agraphia in individuals
2009). In individuals with deep agraphia, the left hemi- with semantic dementia (Graham et al., 2000).
sphere damage tends to be more extensive than that Surface agraphia, like surface alexia, is typically
associated with phonological agraphia, and it has been associated with extrasylvian brain pathology (Fig. 2).
hypothesized that the right hemisphere may be responsi- Focal lesions that give rise to surface agraphia have been
ble for the characteristic deep agraphia profile (Rapcsak, documented in the left inferior occipito-temporal cortex
Beeson, & Rubens, 1991). (Rapcsak & Beeson, 2004). This region includes a portion
of the fusiform gyrus known as the visual word form area
that has been shown to be engaged in healthy adults
Surface Agraphia during reading (Cohen et al., 2002) and spelling tasks
(Beeson et al., 2003) and may represent the neural sub-
Surface agraphia is characterized by difficulty in spelling strate of the orthographic lexicon. Surface agraphia has
irregular words, which contain atypical sound-to-letter cor- also been described following focal damage to posterior
respondences. Regular words are spelled with significantly middle/inferior temporal gyrus and angular gyrus (Rapc-
better accuracy, thus yielding a regularity effect. Nonword sak & Beeson, 2002) and in patients with left anterior
spelling is relatively preserved. In a manner analogous to temporal lobe atrophy (Graham et al., 2000). In these
surface alexia, a dual-route theory attributes surface cases, the spelling deficit may reflect damage to a
agraphia to dysfunction of the lexical spelling route distributed extrasylvian cortical network involved in se-
(Fig. 1). Specifically, it has been suggested that the spelling mantic processing (Fig. 2).
disorder results from damage to the orthographic lexicon
(Rapcsak & Beeson, 2004). The loss of word-specific
orthographic knowledge prompts reliance on a sublexical Allographic Agraphia
phonemegrapheme conversion strategy that produces
phonologically plausible regularization errors on irregular Allographic agraphia refers to a disturbance of the ability
words, a finding that is most pronounced on low to activate or select appropriate letter shapes for the
frequency items (e.g., yot for yacht). Surface agraphia abstract orthographic representations generated by
may also result from damage to central semantic central spelling routes. This impairment of handwriting
Graphomotor control
Phonology
Semantics
Orthography
Agraphia. Figure 2 Cortical regions involved in spelling and writing

Agraphia A 59
is characterized by letter selection errors that often Evaluation A

include the substitution of physically similar letter forms
(e.g., b for h). The allographic difficulty may be specific to Evaluation of individuals with acquired agraphia is
letter case (upper vs. lower) or style (print vs. cursive). structured so that the status of all the relevant component
When allographic agraphia occurs in isolation, oral processes involved in spelling and writing are examined.
spelling is preserved, as well as the ability to correctly Controlled word lists for such assessment can be found in
arrange component letters that make up a word (i.e., the literature (e.g., Beeson & Henry, 2008) or in commer-
anagram spelling) and typing. Allographic agraphia is cially available test batteries (e.g., Kay, Lesser, & Coltheart,
often associated with damage to left temporo-parieto- 1992). A comprehensive battery should include regularly
occipital regions. and irregularly spelled words as well as nonwords. The
evaluation should allow the clinician to identify the na-
ture of the functional impairment and to locate the level
Apraxic Agraphia
of breakdown with reference to a cognitive model of
normal spelling. It is equally important to document
Apraxic agraphia is characterized by poor letter forma-
relatively spared abilities and the use of compensatory
tion in handwriting that is not attributable to allographic
strategies by the patient, as this information is helpful in
disorder or sensorimotor, cerebellar, or basal ganglia
planning treatment.
dysfunction. The difficulty arises at the level of motor
programming for the skilled movements of the hand so
that the spatiotemporal aspects of writing are disturbed.
Individual letters are often difficult to recognize, and Treatment
may simply appear to be meaningless scrawls. Lesions
associated with apraxic agraphia have been noted in the Several behavioral treatment approaches have shown
hemisphere contralateral to the dominant hand. Thus, in positive outcomes in the rehabilitation of agraphia (for a
right-handed individuals, the damage typically involves recent review see Beeson & Henry, 2008). In general,
the left superior parietal lobe in the region of the treatment is directed toward strengthening impaired
intraparietal sulcus, the dorsolateral premotor cortex processes and training the use of compensatory strategies
just anterior to primary motor cortex for the hand, or necessary to bypass the functional deficit. Because written
the supplementary motor area (Fig. 2). spelling tasks inherently involve reading, behavioral treat-
ments for spelling can also serve to strengthen reading.
However, given that spelling is often significantly more
Nonapraxic Disorders of Motor Execution
impaired than reading, it is not uncommon to address
spelling at a lexical level while treating reading at the text
In addition to apraxic agraphia, there are several
level (Beeson & Rapcsak, 2006).
additional disorders of motor execution that affect the
ability to form legible letter shapes. These writing
difficulties include disturbances of the regulation of
movement force, speech, and amplitude. Micrographia Cross References
(the production of small letters with reduced legibility)
is a common example that is associated with the basal Alexia
ganglia pathology in Parkinson disease. Cerebellar pathol- Aphasia
ogy can also result in poor handwriting due to irregular Phonological/Deep Alexia
and disjointed hand movements. Handwriting difficulty Pure Alexia
is also associated with damage to primary sensorimotor Surface Alexia
cortex and/or associated corticospinal tracts that cause
hemiparesis of the dominant hand. When the hemiparesis
is marked, individuals typically shift to writing with the
nondominant hand. Improvement in graphomotor
control of the nondominant hand is apparent with
Beeson, P. M., & Henry, M. L. (2008). Comprehension and production of
practice and often provides a fully functional substitute; written language. In. R. Chapey (Ed.), Language intervention strate-
however, the automaticity of motor movements is rarely gies in adult aphasia (5th ed., pp. 654688). Baltimore, MD: Wolters
comparable to the premorbidly dominant hand. Kluwer/Lippincott, Williams & Wilkins.
60 A Ahylognosia
Beeson, P. M., & Rapcsak, S. Z. (2002). Clinical diagnosis and treatment (weight), or resistance to pressure, with difficulties in
of spelling disorders. In A. E. Hillis (Ed.), Handbook on adult lan-
perceiving size or shape is referred to as amorphogno-
guage disorders: Integrating cognitive neuropsychology, neurology, and
rehabilitation (pp. 101120). Philadelphia: Psychology Press.
sia. While perhaps seeming a bit artificial, according to
Beeson, P. M., & Rapcsak, S. Z. (2006). Treatment of alexia and agraphia. Bauer and Demery (2003), the distinction between ahy-
In J. H. Noseworthy (Ed.), Neurological Therapeutics: Principles and lognosia and amorphognosia apparently traces back to
Practice (2nd ed., pp. 30453060). London: Martin Dunitz. 1935 when a French neurologist, Delay, divided astereog-
Beeson, P. M., Rapcsak, S. Z., Plante, E., Chargualaf, J., Chung, A.,
nosis into two subtypes of deficits: amorphognosia, which
Johnson, S. C., et al. (2003). The neural substrates of writing: A
functional magnetic resonance imaging study. Aphasiology, 17,
was defined as a difficulty in recognizing the size or shape
647665. of an object by touch, and ahylognosia, which was de-
Cohen, L., Lehericy, S., Chochon, F., Lemer, C., Rivaud, S., & Dehaene, S. scribed as a failure to differentiate the molecular quali-
(2002). Language-specific tuning of visual cortex? Functional ties of an object, such as its density, weight, thermal
properties of the Visual Word Form Area. Brain, 125, 10541069.
conductivity, or roughness. Delay also defined a third
Graham, N. L., Patterson, K., & Hodges, J. R. (2000). The impact of
semantic memory impairment on spelling: evidence from semantic
type of astereognosis, tactile asymboly, which was char-
dementia. Neuropsychologia, 38, 143163. acterized as the inability to identify an object by touch
Henry, M. L. Beeson, P. M., Stark, A. J., & Rapcsak, S. Z. (2007). The role in the absence of amorphognosia and ahylognosia. These
of left perisylvian cortical regions in spelling. Brain and Language, same distinctions were followed by Critchley (1969)
100, 4452.
and continue to be used by more recent authors (Bauer
Jobard, G., Crivello, F., & Tzourio-Mazoyer, N. (2003). Evaluation of the
dual route theory of reading: A metaanalysis of 35 neuroimaging
& Demery, 2003). Hecaen and Albert (1978) in their
studies. NeuroImage, 20, 693712. book, Human Neuropsychology, attempted to explain
Kay, J., Lesser, R., & Coltheart, M. (1992). Psycholinguistic assessments these distinctions by suggesting that ahylognosia was
of language processing in Aphasia (PALPA). East Sussex, England: the loss of the capacity to differentiate structural
Lawrence Erlbaum Associates.
components of objects, resulted from impairment of
Rapcsak, S. Z., & Beeson, P. M. (2000). Agraphia. In L. J. G. Rothi, B.
Crosson, & S. Nadeau (Eds.), Aphasia and language: Theory and
intensity analyzers. By contrast, amorphognosia, was
practice (pp. 184220). New York: Guilford. thought to reflect the loss of the capacity to differentiate
Rapcsak, S. Z., & Beeson, P. M. (2004). The role of left posterior inferior forms, resulted from impairment of the analyzers of ex-
temporal cortex in spelling. Neurology, 62, 22212229. tent. Because determining any of these qualities requires
Rapcsak, S. Z., Beeson, P. M., Henry, M. L., Leyden, A., Kim, E. S.,
discriminatory judgments, in the absence of more ele-
Rising, K., et al. (2009). Phonological dyslexia and dysgraphia:
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mentary tactual defects, such disturbances suggest pathol-
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right hemisphere. Brain and Language, 41, 510530. lobe.
Tainturier, M.-J., & Rapp, B. (2001). The spelling process. In B. Rapp
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30, 14141432. Amorphognosis
Astereognosis
Tactile Agnosia
Ahylognosia
J OHN E. M ENDOZA References and Readings
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E. Valenstein (Eds.), Clinical Neuropsychology, (4th ed., pp.
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Critchley, M. (1969). The parietal lobes. New York: Hafner Publishing Co.
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siologie, Topographie. Paris: Masson.
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properties of an object such as its texture, density Disorders of somesthesis and somatognosis). New York: Wiley.
Akelaitis, Andrew John Edward (A.J.) (19041955) A 61
Akathisia Akelaitis, Andrew John Edward A

(A.J.) (19041955)
A NNA D E P OLD H OHLER 1, M ARCUS P ONCE DE LEON2
1
Boston University Medical Center M ICHAEL J. L ARSON , J OSEPH E. FAIR
Boston, MA, USA Brigham Young University
2
William Beaumont Army Medical Center Provo, UT, USA
El Paso, TX, USA
Major Appointments
Synonyms
Dr. A.J. Akelaitis began his career as an assistant pro-
Restlessness fessor in the Department of Medicine, Division of
Psychiatry, at the University of Rochester School of
Medicine and Dentistry. At the same time, he also held
appointments at the clinics of the Strong Memorial
Definition and Rochester Municipal Hospitals in Rochester, New
York. He left these appointments to serve in the Navy
Akathisia is a syndrome characterized by unpleasant
during World War II. Following his service in the war,
sensations of inner restlessness that manifests itself with
Dr. Akelaitis worked as an Assistant Professor of Neu-
an inability to sit still or remain motionless.
rology at the New York Medical College and Assistant
Professor of Clinical Medicine in Neurology at Cor-
nell University Medical College. He also served as the
attending neuropsychiatrist at Mount Vernon (New
Current Knowledge
York) Hospital and on the staff of the Bellevue Hospi-
tal and the New York Hospital.
It is most often seen as a side effect of medications, mainly
neuroleptic antipsychotics. Patients may have difficulty
describing their symptoms, leading to a misdiagnosis of
Major Honors and Awards
anxiety and worsening of the condition upon treatment
with neuroleptic antipsychotic agents. Several medica-
Dr. Akelaitis was a Fellow of the American Psychiatric
tions have been used to treat the condition, including
Association. He was specialty certified by the Ameri-
benztropine and beta-blocking agents. Withdrawal of the
can Board of Psychiatry and Neurology and held
offending agent is often most effective. It may be seen with
membership appointments in the American Medical
Parkinsons disease.
Association, the New York State Medical Society, the
New York Society for Clinical Psychiatry, and the New
York Neurological Society.
Cross References
Parkinsons Disease
Landmark Clinical, Scientific, and
Tardive Dyskinesia
Professional Contributions
Dr. A.J. Akelaitis is best known for his observations of
patients who underwent sectioning of the corpus cal-
References and Readings losum (i.e., split-brain patients). Beginning in the
late 1930s, the neurosurgeon Dr. William P. van
Kumar, A., & Calne, D. (2004). Approach to the patient with a movement
Wagenen pioneered surgical sectioning of the corpus
disorder and overview of movement disorders. In R. L. Watts, & callosum for the treatment of intractable epilepsy
W. C. Koller (Eds.), Movement disorders (2nd ed., p. 9). New York: (Mathews, Linskey, & Binder, 2008). Dr. Akelaitis
McGraw-Hill. worked closely with Dr. van Wagenen and performed
62 A Akelaitis, Andrew John Edward (A.J.) (19041955)
pre and postoperative tests of cognitive and neurolog- Despite his contributions as one of the first indivi-
ical functioning on many of these individuals. Accord- duals to study neurological functioning following
ing to Akelaitis reports, patients who underwent callosotomy, Akelaitis has been criticized for employ-
callosotomy surgery largely did not show lasting ing insensitive or inadequate testing procedures.
changes in cognitive, intellectual, or motor function- However, reviews of his cases have confirmed that
ing, although their seizure activity was consistently his patients did exhibit what are now considered
alleviated. For nearly two decades, Akelaitis reports typical symptoms, although his explanations for
of largely normal functioning after callosotomy per- these manifestations, while consistent with much
petuated the generally accepted belief that sectioning of the research of the time, were often inadequate
the corpus callosum did not impact cognitive or (Sauerwein & Lassonde, 1996). In the 1950s and
motor functioning in humans. 1960s, researchers including Roger Sperry, Michael
Despite his reports of few neurological changes fol- Gazzaniga, Norman Geschwind, Edith Kaplan, and
lowing callosotomy, Akelaitis noted periodic cases Joseph Bogen began to publish articles involving cal-
with hemiplegia and praxic disturbances. He was losotomies in animals and humans, which contra-
slow, however, to include the sectioning of the corpus dicted many of Akelaitis findings. This sparked
callosum in his explanations for these changes; rather, renewed interest in the function of the corpus callo-
he attributed the symptoms to unintended operative sum and eventually earned Sperry the Nobel Prize
damage to adjacent cortical areas. In some cases, post- in 1981.
operative symptoms were seen as exacerbations of Through the course of his short career, Dr. Akelaitis
precallosotomy characteristics or were attributed to made significant contributions toward research on the
preexisting and/or postoperative psychological or be- corpus callosum and advanced the treatment of
havioral factors. Further, many of the symptoms ob- intractable epilepsy. He also published articles regard-
served by Akelaitis were transient and consequently ing the psychiatric aspects of myxedema (severe hypo-
not considered to be conclusively linked with callosal thyroidism), hereditary and vascular cerebral atrophy,
sectioning (Sauerwein & Lassonde, 1996). lead encephalopathy, acute demyelinating processes
Several factors most likely influenced Akelaitis reports (multiple sclerosis), and Picks disease.
of minimal neurological changes following callosotomy
surgery. First, the majority of patients Akelaitis observed
did not have complete callosotomies, nor were neuro-
Short Biography
surgical procedures well standardized at the time. Of the
28 patients he studied, only one third were reported to
Andrew John (A.J.) Akelaitis was born in Baltimore,
have undergone complete callosal sectioning, with the
Maryland, on July 11, 1904. He studied medicine
remainder nearly complete or partial sectioning
at Johns Hopkins University and received his M.D. in
(Bogen, 1995). The patients with only partially sec-
1929. In the early 1930s, he practiced clinical neurology
tioned callosal fibers undoubtedly continued to have
in Rochester, New York. He subsequently became an As-
interhemispheric transmission, thereby contributing
sistant Professor of Medicine at the University of
to Akelaitis findings of generally intact functioning.
Rochester School of Medicine and Dentistry. Dr. Akelaitis
Next, emerging research at the time reported no cogni-
joined the Navy during World War II where he served
tive changes following sectioning of the corpus callo-
with distinction at the rank of Commander. He married
sum. For example, Walter Dandy stated in 1936 that
the former Victoria Chesno. The couple had one son,
when the corpus callosum is split longitudinally. . . no
Andrew, and a daughter, Lillian. Akelaitis died at the
symptoms follow its division. This simple experiment at
New York Hospital on November 24, 1955 at the young
once disposes of the extravagant claims to the functions
age of 51.
of the corpus callosum (see Zaidel, Iacoboni, Zaidel, &
Bogen, 2003). Finally, Akelaitis lacked the technolo-
gies, such as the tachistoscope used by his successors,
to present stimuli to one visual field. Such technology Cross References
would possibly have given him insight into the spe-
cialization of the two hemispheres and interhemi- Corpus Callosum
spheric transfer of information via the corpus Epilepsy
callosum (Mathews, Linskey, & Binder, 2008). Split Brain
Akinetic Mutism A 63
References and Readings Definition A

Akelaitis, A. J. (1941). Psychobiological studies following section of the Akinesis is an absence or paucity of movement, resulting
corpus callosum: A preliminary report. American Journal of Psychia- from an abnormal motor control. It is a problem that may
try, 97, 11471157.
occur in Parkinsons disease when patients develop freez-
Akelaitis, A. J. (1941). Studies on the corpus callosum. II. The higher
visual functions in each homonymous field following complete
ing or inability to initiate movement. It may also occur as
section of the corpus callosum. Archives of Neurology and Psychiatry, a result of a paralyzed muscle, such as with an anesthetic
45, 788796. nerve block.
Akelaitis, A. J., Risteen, W. A., Herren, R. Y., & Van Wagenen, W. P.
(1942). Studies on the corpus callosum. III. A contribution to the
study of dyspraxia and apraxia following partial and complete sec- Cross References
tion of the corpus callosum. Archives of Neurology and Psychiatry,
47, 9711008. Action-Intentional Disorders
Akelaitis, A. J. (1944). Studies on the corpus callosum. IV. Diagonistic
Akinetic Mutism
dyspraxia in epileptics following partial and complete section of the
corpus callosum. American Journal of Psychiatry, 101, 594599.
Bradykinesia
Akelaitis, A. J. (1944). Study on gnosis, praxis, and language following Parkinsons Disease
section of corpus callosum and anterior commisure. Journal of
Neurosurgery, 1, 94102.
Bogen, J. (1995). Some historical aspects of callosotomy for epilepsy.
In A. G. Reeves & D. W. Roberts (Eds.), Epilepsy and the corpus
callosum 2 (pp. 107121). New York: Plenum Press.
Akinetic
Gazzaniga, M. S. (1995). Principles of human brain organization derived
from split brain studies. Neuron, 14, 217228. Akinesis
Gazzaniga, M. S. (2005). Forty-five years of split-brain research and still
going strong. Nature Reviews: Neuroscience, 6, 653659.
Mathews, S., Linskey, M., & Binder, D. (2008). William P. van Wagenen
and the first corpus callosotomies for epilepsy. Journal of Neurosur- Akinetic Mutism
gery, 108, 608613.
Sauerwein, H. C., & Lassonde, M. (1996). Akelaitis investigations of the
M ICHAEL S. M EGA
first split-brain patients. In C. Code, C.-W. Wallesh, Y. Joanette, &
A. R. Lecours (Eds.), Classic cases in neuropsychology (pp. 305317). Brain Institute Providence Health System
Hove, East Sussex: Psychology Press. Portland, OR, USA
Zaidel, E., Iacoboni, M., Zaidel, D., & Bogen, J. (2003). The callosal
syndromes. In K. M. Heilman & E. Valenstein (Eds.), Clinical neu-
ropsychology (pp. 347403). New York: Oxford University Press. Synonyms
A spectrum of motivational impairment has abulia at one
Akinesia end and akinetic mutism at the other. Coma vigil is not
akinetic mutism; it arises when a comatose patient regains
Akinesis the sleep-wake cycle, eyes open during the day and closed
during sleep at night, usually after 2 weeks of a brain
lesion that produces irreversible coma. Coma vigil is also
referred to as a persistent vegatative state. When brain
Akinesis lesions disconnect all descending motor output but pre-
serve conscious awareness the patient is said to be locked
D OUGLAS I. K ATZ in. In akinetic mutism, patients still respond to their
Braintree Rehabilitation Hospital internal and external environment and thus are not in
Braintree, MA, USA coma, and they are not locked in since they can accom-
Boston University School of Medicine plish motor output, given sufficient motivation.
Boston, MA, USA

Synonyms
The fully formed akinetic mute state usually results from
Akinesia; Akinetic bilateral anterior cingulate lesions (Fig. 1). Patients are
64 A Akinetic Mutism
Akinetic Mutism. Figure 1 Arrows show the left greater than right anterior cingulate lesions due to bilateral anterior cerebral
artery (ACA) ischemic stroke. Bilateral ACA lesions usually result in death due to loss of all limbic motivational input to prefrontal
cortex
profoundly apathetic, incontinent, and akinetic. They do area, and the oculomotor circuit, originating in the fron-
not initiate eating or drinking and if speech occurs, it is tal eye fields, are dedicated to motor function. The dorso-
restricted to terse responses. They seem awake, visually lateral prefrontal, lateral orbitofrontal, and anterior
tracking objects, but displaying no emotions even dur- cingulate circuits support executive cognitive functions,
ing painful circumstances, they remain indifferent. The personality, and motivation, respectively (Mega &
akinetic mute state also results from bilateral subcortical Cummings, 1994). Each of the five circuits has the same
paramedian diencephalic and midbrain lesions possibly member structures: the frontal lobe, striatum, globus
affecting the ascending reticular core, medial forebrain pallidus, substantia nigra, and thalamus. There is a
bundles, and isolated bilateral globus pallidus lesions. progressive spatial compaction of the circuits as they
travel through the basal ganglia. A lesion anywhere
along the path of a circuit will produce the same clinical
Categorization result but only in the globus pallidus interna are all the
frontal-subcortical circuits in such a compact spatial
When anterior cingulate lesions are bilateral, limbic, cogni- volume that a relatively small lesion can have profound
tive, and motor activation is disrupted producing profound effects.
akinetic mutism. Loss of ascending input from the reticular
core, due to bilateral lesions of the medial forebrain bundle,
may also produce akinetic mutism. Rarely are complete Epidemiology
bilateral lesions seen in humans, more frequently partial
circuit disruption results in a graded loss in motivation Akinetic mutism is exceedingly rare when permanent,
depending upon which circuit is damaged. since a bilateral lesion is necessary and usually results in
Five frontal-subcortical circuits have been named death. Unilateral anterior cerebral artery (ACA) strokes
according to their function or cortical site of origin: the are the usual cause of transient akinetic mutism, but ACA
motor circuit, originating in the supplementary motor strokes only make up 1% of all cerebral vascular lesions.
Akinetic Mutism A 65
Natural History, Prognostic Factors, skeletomotor effector region. When these two motor
A
and Outcomes regions are spared, motor activity will be normal but the
patient will demonstrate profound indifference, docility,
The natural history of akinetic mutism, when it arises and the loss of motivation to engage in a task. They can be
from a unilateral lesion, is usually a 2-week period of led by the examiner to engage in a task but will fail to self-
gradual improvement from the fully formed syndrome generate sustained directed attention. They lack cognitive
to near-complete recovery presumably enabled by contra- motivation.
lateral limbic activation gaining access to deafferented The role of the anterior cingulate as a cognitive effec-
networks. The outcome from bilateral lesions is usually tor is appreciated within the realm of language. Language,
death, given no ability for cross-hemispheric motivation. a cognitive function, is distinguished from the motor
Thus, prognosis will rely upon neuroimaging document- function of speech. Transcortical motor aphasia
ing the extent of the lesion. (TCMA) is the usual result of left anterior medial or
anterior dorsolateral prefrontal lesions. The classic syn-
drome of TCMA is initial mutism that resolves in days to
Neuropsychology and Psychology weeks, yielding a syndrome featuring delayed initiation of
brief utterances without impaired articulation, excellent
Extracingulate connections support a segregation of the repetition, inappropriate word selection, agrammatism,
cingulate into functional subregions (for a complete dis- and poor comprehension of complex syntax. Activation
cussion of these circuits, Cingulate Gyrus). Paralleling of dorsolateral prefrontal cortices enabling language and
the general distinction between posterior granular sensory speech arises from two sources: the anterior cingulate and
cortices and anterior agranular executive cortices, the the supplementary motor area (with the cingulate skele-
anterior cingulate can be considered an executive region tomotor region). When the executive prefrontal cortex
for affective motivation and cognition, while the posterior (areas 9, 10, and 46) is disrupted, cognitive language
cingulate, with its prominent granular layer IV receiving deficits are prominent (TCMA, type I); when motor
sensory input, is engaged in visuospatial and memory neurons in area 4, devoted to the speech apparatus, are
processing. The interconnections between the anterior disconnected from their activation, speech hesitancy
and posterior cingulate allow for regulatory control by and impoverished output ensues (TCMA, type II).
the anterior executive effector regions over posterior sen- These two functional realms are separable and can be
sory processing and reciprocal modulation of that regu- disconnected anywhere along two pathways. Direct dam-
latory input by the posterior cingulate. age to the supplementary motor area or its outflow to the
Three anterior effector regions include a visceral effec- motor cortex traveling in the anterior superior paraven-
tor region inferior to the genu of the corpus callosum tricular white matter will produce TCMA type II. Direct
encompassing area 25, the anterior subcallosal portions damage to the anterior cingulate, its outflow to areas 9,
of 24ab, and 32; a cognitive effector region that includes 10, and 46, or to the caudate via the subcallosal
most of the supracallosal area 24, and areas 24a0 b0 and fasciculus, just inferior to the frontal horn of the lateral
320 ; and a skeletomotor effector region within the depths of ventricle will disrupt frontal-subcortical circuits
the cingulate sulcus, that includes areas 24c0 /23c on the involved in motivation and executive cognitive function.
ventral bank, with 24c0 g and 6c on the dorsal bank. These The initial muteness has been described by a patient
three cingulate effector regions integrate ascending input after recovery from an anterior cingulate/supplementary
concerning the internal milieu of the organism with motor infarction as a loss of the will to reply to her
visceral motor systems, cognitive-attentional networks, examiners, because she had nothing to say, her mind
and skeletomotor centers to produce the affective motiva- was empty, and nothing mattered (Damasio & Van
tion necessary for the organisms engagement in the Hoesen, 1983).
environment. The loss of will to initiate a motor function results
Circumscribed lesions in humans are rarely confined from supplementary motor or cingulate skeletomotor
to one region of the cingulate. With an anterior lesion, the region damage, while poor initiation of a cognitive pro-
cognitive, skeletomotor, and visceral effector regions are cess results from lesions in supracallosal cingulate areas.
often affected. Bilateral lesions result in an akinetic mute Loss of emotional vigilance ranging from flattened affect
state. The loss of spontaneous motor activity results when to neglect can be produced by surgery in this region.
the lesion involves the supplementary motor area and the Anterior cingulate lesions in monkeys difficult subjects
66 A Akinetic Mutism
in which to evaluate subtle behavioral changes produce (FDG-PET) in frontal cortex has also resulted from
either no observable change or result in a transient pallidal lesions (Laplane, Levasseur, Pillon, Dubois,
stupor with ensuing lethargy, tameness, disturbed intra- Baulac, Mazoyer, et al., 1989) disconnecting their cortical
species social behavior, and decreased pain sensitivity targets. Yet, when pallidal lesions result from carbon
(Pribram & Fulton, 1954). Removal of the anterior cingu- monoxide poisoning, microscopic cortical lesions may
late (areas 24 and 32) in humans (cingulectomy) has been contribute to the functional imaging abnormalities.
employed as a treatment for epilepsy, psychiatric, and Ventral extension of a pallidal lesion appears to discon-
pain disorders. nect the anterior cingulate circuit, in nonhuman primates
The cingulum bundle has also been the site of surgical and humans (Mega & Cohenour, 1997), from limbic
lesions (cingulumotomy when only the bundle is trans- drive. Bilateral paramedian or anterior thalamic lesions
ected, or cingulotomy when cingulate cortex is also (Nagaratnam, Nagaratnam, Ng, & Diu, 2004), caudate
removed) to treat psychiatric and pain disorders. The cin- (Grunsfeld & Login, 2006), or putamen (Ure, Faccio,
gulum contains the efferents and afferents of the cingulate Videla, Caccuri, Giudice, Ollari, et al., 1998) lesions will
to the hippocampus, basal forebrain, amygdala, and all also disrupt the anterior cingulate frontal-subcortical
cortical areas, as well as fibers of passage between hippo- circuit.
campus and prefrontal cortex, and from the median raphe
to the dorsal hippocampus. Surgical ablation of the anterior
portion (sparing fibers relevant to memory function) is
most successful when treating aggression, extreme anxiety,
Evaluation
obsessivecompulsive behaviors, and severe pain. Psychotic
Evaluation of the patient suspected of suffering from
symptoms show only a temporary response. The only pro-
akinetic mutism is to first rule out other causes of possible
spective long-term follow-up of patients undergoing supra-
unresponsiveness. Documenting the response to first ver-
callosal anterior cingulotomy for the treatment of medically
bal stimuli, and then sensory stimuli, will provide evi-
refractory obsessivecompulsive disorder revealed a clear
dence for or against coma. Patients in coma will not
response in 28% and a partial response in 17% (Baer,
respond to internal (e.g., hunger) or external (e.g., pain)
Rauch, Ballantine, Martuza, Cosgrove, Cassem, et al.,
stimuli. All patients who survive the myriad of insults
1995). Including the subcallosal anterior cingulate/medial
producing coma will regain the sleep-wake cycle and will
orbital cortex may provide the best result in treating the
eventually open their eyes spontaneously. They are then
refractory obsessivecompulsive patient (Hay, Sachdev,
described as being in a persistent vegetative state. The
Cumming, Smith, Lee, Kitchener, et al., 1993) due to the
locked-in patient will blink to command and can be
elimination of the visceromotor aspects of the disorder.
taught to use blinking as a form of communication. The
Postsurgical personality changes are subtle after the acute
patient with akinetic mutism will respond to stimuli but
attentional disorder resolves. Although formal cognitive
will not initiate an unprovoked response. When any pa-
testing is unaltered, affect is flattened. Motivation for
tient with limited response is encountered, a brain imag-
previous enjoyments, such as reading, hobbies, and even
ing study is required in their evaluation.
spectator sports, is lost (Tow & Whitty, 1953); subtle
changes that reflect the loss of higher cognitive motivation.
The three anterior cingulate regions, by virtue of the
distinct functional systems they coordinate, are the con- Treatment
duits through which limbic motivation can activate feel-
ing, thought, and movement partial lesions produce Time is the best treatment for unilateral lesions producing
partial aspects of the akinetic mute state depending akinetic mutism since after the acute phase of the lesion
upon their location. (46 weeks) the patients usually recover limbic activation
Subcortical lesions can also produce the fully formed from unaffected regions. When subcortical lesions destroy
syndrome. Carbon monoxide poisoning with resultant ascending dopaminergic fibers in the medial forebrain
apathy and placidity was described in a patient with a bundle, patients may respond to dopaminergic
ventral pallidal lesion who also had hypoperfusion on agonist (Psarros, Zouros, & Coimbra, 2003), or paradoxi-
single photon emission computed tomography (SPECT) cally antagonists of the D2 receptor (Brefel-Courbon
predominately in the cingulate bilaterally (Mori, Yama- et al., 2007) and GABA activation (Spiegel, Casella,
shita, Takauchi, & Kondo, 1996). Hypometabolism on Callender, & Dhadwal, 2008), perhaps due to blocking
18
F-fluorodeoxyglucose positron emission tomography feedback-loop inhibition.
Alcohol Abuse A 67
Cross References A
Alcohol Abuse
Abulia
Amotivation N ATE E WIGMAN
Apathy University of Florida
Cingulate Gyrus Gainesville, FL, USA
References and Readings Synonyms
Baer, L., Rauch, S. L., Ballantine, H. T., Martuza, R., Cosgrove, R., Alcoholism; Binge drinking; Excessive alcohol use
Cassem, E., et al. (1995). Cingulotomy for intractable obsessive-
compulsive disorder: prospective long-term follow-up of 18
patients. Archives of General Psychiatry, 52, 384392.
Brefel-Courbon, C., Payoux, P., Ory, F., Sommet, A., Slaoui, T., Raboyeau, Short Description or Definition
G., et al. (2007). Clinical and imaging evidence of zolpidem effect in
hypoxic encephalopathy. Annals of Neurology, 62(1), 102105. Alcohol abuse refers to a maladaptive pattern of alcohol
Damasio, A. R., & Van Hoesen, G. W. (1983). Focal lesions of the limbic
[use] leading to clinically significant impairment or
frontal lobe. In K. M. Heilman & P. Satz (Eds.), Neuropsychology of
human emotion (pp. 85110). New York: Guilford. distress. The DSM-IV Criteria for alcohol abuse are
Grunsfeld, A. A., & Login, I. S. (2006). Abulia following penetrating brain
injury during endoscopic sinus surgery with disruption of the ante-
rior cingulate circuit: case report. BMC Neurology, 6, 4.
Hay, P., Sachdev, P., Cumming, S., Smith, J. S., Lee, T., Kitchener, P., et al.
DSM-IV-TR Criteria for Alcohol Abuse
(1993). Treatment of obsessive-compulsive disorder by psychosur-
gery. Acta Psychiatrica Scandinavica, 87, 197207. 1. A maladaptive pattern of alcohol abuse leading to
Laplane, D., Levasseur, M., Pillon, B., Dubois, B., Baulac, M., Mazoyer, B., clinically significant impairment or distress, as mani-
et al. (1989). Obsessive-compulsive and other behavioural changes fested by one or more of the following, occurring
with bilateral basal ganglia lesions. Brain: A Journal of Neurology,
within a 12-month period:
112, 699725.
Mega, M. S., & Cohenour, R. C. (1997). Akinetic mutism: a disconnection Recurrent alcohol use resulting in failure to fulfill
of frontal-subcortical circuits. Neurology, Neuropsychology, and Be-
major role obligations at work, school, or home
havioral Neurology, 10, 254259.
Mega, M. S., & Cummings, J. L. (1994). Frontal subcortical circuits and (e.g., repeated absences or poor work perfor-
neuropsychiatric disorders. Journal of Neuropsychiatry and Clinical mance related to substance use; substance-related
Neurosciences, 6, 358370. absences, suspensions, or expulsions from school;
Mori, E., Yamashita, H., Takauchi, S., & Kondo, K. (1996). Isolated or neglect of children or household).
athymhormia following hypoxic bilateral pallidal lesions. Behavioral
Recurrent alcohol use in situations in which it is
Neurology, 9, 1723.
Nagaratnam, N., Nagaratnam, K., Ng, K., & Diu, P. (2004). Akinetic physically hazardous (e.g., driving an automobile
mutism following stroke. Journal of Clinical Neuroscience: Official or operating a machine).
Journal of the Neurosurgical Society of Australasia, 11(1), 2530. Recurrent alcohol-related legal problems (e.g.,
Pribram, K. H., & Fulton, J. F. (1954). An experimental critique of the arrests for alcohol-related disorderly conduct).
effects of anterior cingulate ablations in monkey. Brain: A Journal of
Continued alcohol use despite persistent or recur-
Neurology, 77, 3444.
Psarros, T., Zouros, A., & Coimbra, C. (2003). Bromocriptine-responsive rent social or interpersonal problems caused or
akinetic mutism following endoscopy for ventricular neurocysticer- exacerbated by the effects of the alcohol (e.g.,
cosis. Case report and review of the literature. Journal of Neurosur- arguments with spouse about consequences of
gery, 99(2), 397401. intoxication or physical fights).
Spiegel, D. R., Casella, D. P., Callender, D. M., & Dhadwal, N. (2008).
Treatment of akinetic mutism with intramuscular olanzapine: a case 2. These symptoms must never have met the criteria for
series. Journal of Neuropsychiatry and Clinical Neurosciences, 20(1), alcohol dependence.
9395.
Tow, P. M., & Whitty, C. W. M. (1953). Personality changes after opera- Although alcohol abuse is diagnosed primarily by ob-
tions of the cingulate gyrus in man. Journal of Neurology, Neurosur- served or reported impairment and distress related to
gery, and Psychiatry, 16, 186193.
alcohol use, the Dietary Guidelines for Americans recom-
Ure, J., Faccio, E., Videla, H., Caccuri, R., Giudice, F., Ollari, J., et al.
(1998). Akinetic mutism: a report of three cases. Acta Neurologica mends no more than one drink per day for women and
Scandinavica, 98(6), 439444. two drinks per day for men (USDA, 2005).
68 A Alcohol Abuse
Categorization (Hawkins, Catalano, & Miller, 1992). Another risk factor

appears to be comorbid mental disorders. Epidemiologi-
In the DSM-IV-TR, alcohol abuse is differentiated from cal data suggest that 37% of people who have an alcohol
alcohol dependence in that the former consists of drink- disorder also have another mental disorder (Regier et al.,
ing that impairs functioning without withdrawal symp- 1990), emphasizing the importance of mental and behav-
toms and is thus diagnosed only when dependence is ior health screening. In terms of prognostic factors,
not present (Hasin, Van Rossem, McCloud, & Endicott, Vaillant (1995) suggests that those who achieve long-
1997). An alcohol abuser may continue to drink despite term sobriety usually [are characterized by] (1) a less
awareness of the potential negative physical, social, and harmful, substitute dependency; (2) new relationships;
legal consequences. (3) sources of inspiration and hope; and (4) experiencing
negative consequences of drinking.
In Vaillant (1995) delinquent youth cohort, by age 70,
Epidemiology 54% had already died, 32% were abstinent, 12% were still
abusing alcohol, and 1% were controlled drinkers (i.e.,
Alcohol abuse is associated with diseases of the liver,
drinking but not abusing).
hypertension, neurological damage, and cardiac diseases
such as heart failure. In 2000, alcohol abuse was responsi-
ble for 85,000 deaths in the U.S. National data suggest that
Neuropsychology and Psychology
the prevalence of DSM-IV-TR alcohol abuse (not includ-
of Alcohol Abuse
ing alcohol dependence) was 4.65% in 20012002. At that
time, alcohol abuse was more common among men,
In a review of the literature of neuropsychological deficits
younger respondents, and Whites. From 19911992 to
in chronic alcohol abusers, Chelune and Parker (1981)
20012002, the prevalence of alcohol abuse increased,
found patterns of neurological damage such as cerebral
especially among young African American and Hispanics
atrophy, ventricular enlargement, and decreased cerebral
and in both men and women (Grant et al., 2004). It
blood flow. Approximately 10% of chronic alcohol
appears that alcohol abuse is generally more severe with
abusers have neurocognitive deficits commensurate with
earlier onset in age of alcohol use (Grant, Stinson, &
diagnoses of alcohol-related amnesia or dementia. A large
Harford, 2001). Results from a national survey suggest
portion of those without diagnosable neurocognitive
that close to one fifth of adolescents and adults engaged in
deficits still evince disturbed neuropsychological perfor-
binge drinking one or more times within the last 30 days
mance (Rourke & Grant, 2009). Alcoholics generally
(US DHHS, 2002).
function in the average to above average range on IQ
tests with consistently lower performance IQ (PIQ) scores
Natural History, Prognostic Factors, relative to verbal IQ (VIQ). Their PIQ scores are similar to
Outcomes those of persons with brain damage, whereas VIQ scores
are comparable with those of normal controls (Chelune &
In The Natural History of Alcoholism Revisited, George Parker, 1981; Rourke & Grant, 2009). However, this dis-
Vaillant (1995) described alcohol dependence as a condi- crepancy is not diagnostic of alcoholism. Within the
tion of gradual onset over 515 years of continuous alco- Wechsler subtests, Block Design appears to be the most
hol abuse. He found that the average age of onset was frequently impaired relative to normal controls in all
29 years among a cohort of delinquent youth and 41 studies reviewed. Block Design impairment has been
among a higher educated group. In the cohorts that cited as an effective discriminator between alcoholics
Vaillant (1995) studied, the prevalence of alcoholism and non-alcoholics. Object Assembly and Digit Symbol
increased until age 40 and then declined at a rate of were also impaired relative to normal controls in more
23% per year thereafter. than 3/4 of the studies. Other tests that have revealed
Potential risk factors for alcohol abuse in adolescence impairment in alcoholics include the Category Test,
and early adulthood include being in areas of high Wisconsin Card Sorting Test, Ravens Progressive,
availability and accessibility, sensation seeking and low ShipleyHartford Abstract Age, and other tests of abstract
harm-avoidance in youth, family history of alcohol thinking. Alcoholics also generally perform poorly on Part
abuse, liberal family attitude toward alcohol use, lack B of the Trail Making Test relative to matched control
of family closeness, and early behavioral problems groups (Chelune & Parker, 1981).
Alcohol Abuse A 69
Overall, the most consistently impaired neuro- Have you ever felt Guilty about drinking?

A
psychological domains include verbal and nonverbal Have you ever felt you needed a drink first thing in the
learning and perceptual-motor skills. More broadly, most morning (Eye-opener) to steady your nerves or to get
reviews conclude that abstraction-executive abilities are rid of a hangover?
impaired among alcohol abusers (Rourke & Grant, 2009).
Other brief assessments for alcohol abuse include the
Despite the consistency of these neuropsychological find-
POSIT and CRAFFT for adolescents (Knight, Sherritt,
ings, many of the samples from these studies are recently
Harris, Gates, & Chang, 2003), the Michigan Alcoholism
detoxified adults. Grant and Adams (2009) point out that
Screen Test (MAST) for adults (Magruder-Habib, Stevens,
neuropsychological recovery typically occurs following
& Alling, 1993), and the AUDIT-C for both adults and
the first year and perhaps more of detoxification.
adolescents (Bush et al., 1998). According to Fiellin, Reid,
Although the exact mechanisms of these neuropsy-
and OConnor (2000), the CAGE and the AUDIT are
chological deficits are not known, some of the major
the superior screening instruments in primary care set-
hypotheses attempting to explain these deficits have
tings compared with other alcohol abuse screeners
been (Chelune & Parker, 1981):
and other clinical methods. The CAGE is superior at
1. Chronic alcohol abuse results in premature aging of detecting diagnosable abuse and dependence and the
the brain. AUDIT is superior at detecting at risk and harmful drink-
2. Chronic alcohol abuse leads to global generalized CNS ing (Fiellin et al., 2000).
dysfunction.
3. Chronic alcohol abuse differentially disrupts the right
hemisphere of the brain.
4. Chronic alcohol abuse exerts its detrimental effect on Treatment
the anterior-basal regions of the brain.
5. Chronic alcohol abuse produces a generalized CNS Treatment ranges from support groups to rehabilitation
impairment that is particularly disruptive of the centers. Treatments of alcohol abuse appear to be largely
fronto-parietal association areas of the brain. psychosocial. In a systematic review, brief psychosocial
interventions among primary care patients were found
More recent neural hypotheses of the mechanisms of to be effective at reducing alcohol consumption (Kaner
neuropsychological deficits include reduced regional et al., 2007). Although well-known support groups such
blood flow to the frontal lobes, reduction in metabolites as Alcoholic Anonymous (AA) have been helpful to many
(e.g., NAA) that indicate lack of neuronal integrity, fron- people and likely constitute the most accessible form of
tal-striatal and cerebellar dysfunction manifesting as loss treatment, evidence has not supported AAs effectiveness
of dendritic arbor (Rourke & Grant, 2009). Grant and at reducing alcohol problems (Ferri, Amato, & Davoli,
Adams (2009) note that molecular mechanisms of the 2006). Medical treatments of alcohol abuse focus on
influence of chronic alcohol abuse on neuropsychological reducing craving. Naltrexone (Chick et al., 2000) and
functioning are largely unknown. Acomprosate (Garbutt, West, Carey, Lohr, & Crews,
1999) have been found to be effective at reducing craving.
Evaluation However, most medications are aimed at dependence, not
abuse symptoms.
A common screening tool for alcohol abuse is the CAGE
questionnaire (Ewing, 1984; see An even briefer CAGE
Questionnaire, Table B).The CAGE is highly effective
Cross References
at identifying problem drinkers among adults (Bernadt,
1982). Two yes responses on the CAGE indicate that the
Alcohol Brain Syndrome
respondent should be investigated further. The question-
Alcohol Dependence
naire asks the following questions:
Blood Alcohol Level
Have you ever felt you needed to Cut down on your Fetal Alcohol Syndrome
drinking? Michigan Alcoholism Screen Test
Have people Annoyed you by criticizing your Substance Abuse
drinking? Wernicke-Korsakoff s Syndrome
70 A Alcohol Addiction
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Chelune, G. J., & Parker, J. B. (1981). Neuropsychological deficits asso-
United States Department of Agriculture and United States Department
ciated with chronic alcohol abuse. Clinical Psychology Review, 1,
of Health and Human Services (USDA). (2005). Dietary guidelines for
181195.
Americans: Chap. 9 Alcoholic beverages (pp. 4346). Washington,
Chick, J., Anton, R., Checinski, K., Croop, R., Drummond, D. C.,
DC: US Government Printing Office.
Farmer, R. et al. (2000). A multicentre, randomized, double-blind,
Vaillant, G. E. (1995). The natural history of alcoholism revisited.
placebo-controlled trial of naltrexone in the treatment of alcohol
Cambridge, MA: Harvard University Press.
dependence or abuse. Alcohol, 35, 587593.
Ewing, J. A. (1984). Detecting alcoholism: The CAGE questionnaire.
JAMA, 252, 19051907.
Ferri, M. M. F., Amato L., & Davoli M. (2006). Alcoholics anonymous
and other 12-step programmes for alcohol dependence. Cochrane
Database of Systematic Reviews, Issue 3, Art. No.: CD005032. doi:
Alcohol Addiction
10.1002/14651858.CD005032.pub2
Fiellin, D. A., Reid, M. C., & OConnor, P. G. (2000). Screening for Alcoholism
alcohol problems in primary care: A systematic review. Archives of
Internal Medicine, 160(13), 19771989.
Garbutt, J. C., West, S. L., Carey, T. S., Lohr, K. N., & Crews, F. T. (1999).
Pharmacological treatment of alcohol dependence: A review of the
evidence. JAMA, 281, 13181325. Alcohol Amnesic Disorder
Grant, B. F., Dawson, D. A., Stinson, F. S., Chou, S. P., Dufour, M. C., &
Pickering, R. P. (2004). The 12-month prevalence and trends in DSM-IV Korsakoff s Syndrome
alcohol abuse and dependence: United States, 19911992 and 20012002.
Drug and Alcohol Dependence, 74, 223234.
Grant, I., Adams K. M. (Eds.) (2009). Neuropsychological assessment
of neuropsychiatric disorders (3rd ed., pp. 127158.). New York:
Oxford University Press.
Grant, B. F., Stinson, F. S., & Harford, T. C. (2001). Age at onset of alcohol
Alcohol Dependence
use and DSM-IV alcohol abuse and dependence: A 12-year follow-
up. Journal of Substance Abuse, 13, 493504. G LENN S. A SHKANAZI
Hasin, D. S., Van Rossem, R., McCloud, S., & Endicott, J. (1997). Alcohol University of Florida-College of Public Health and Health
dependence and abuse diagnoses: Validity in a community sample Professions
of heavy drinkers. Alcoholism, Clinical and Experimental Research, Gainesville, FL, USA
21, 213219.
Hawkins, J. D., Catalano, R. F., & Miller, J. Y. (1992). Risk and protective
factors for alcohol and other drug problems in adolescence and early
adulthood: Implications for substance abuse prevention. Psychologi- Synonyms
cal Bulletin, 112, 64105.
Knight, J. R., Sherritt, L., Harris, S. K., Gates, E. C., & Chang, G. (2003). Alcoholism
Validity of brief alcohol screening tests among adolescents: A com-
parison of the AUDIT, POSIT, CAGE, and CRAFFT. Alcoholism,
Clinical and Experimental Research, 27, 6773.
Magruder-Habib, K., Stevens, H. A., & Alling, W. C. (1993). Relative Definition
performance of the MAST, VAST, and CAGE versus DSM-III-R
criteria for alcohol dependence. Journal of Clinical Epidemiology, As described in DSM-IV, alcohol dependence is a set of
46, 435441.
symptoms encompassing dysfunction in cognitive, behav-
Regier, D. A., Farmer, M. E., Rae, D. S., Locke, B. Z., Keith, S. J.,
Judd, L. L., et al. (1990). Comorbidity of mental disorders with
ioral, and physiological domains caused by continued
alcohol and other drug abuse. Results from the epidemiologic catch- alcohol use. A pattern of repeated alcohol ingestion exists,
ment area (ECA) study. JAMA, 264, 25112518. resulting in increasing amounts consumed in order to
Rourke, S. B., & Grant, I. (2009). The neurobehavioral correlates of obtain the desired effect (i.e., tolerance) and characteristic
alcoholism. In I. Grant & K. M. Adams (Eds.), Neuropsychological
symptoms if use is suddenly suspended (i.e., withdrawal).
assessment of neuropsychiatric and neuromedical disorders (3rd ed.,
pp. 398454). New York: Oxford University Press.
There is a perceived loss of control over drinking, exhibited
U.S. Department of Health and Human Services. Substance Abuse and by repeated failed attempts to decrease or quit drinking.
Mental Health Services Administration(US DHHS). (2002). Results Individuals may spend increasing amounts of time
Alcoholic Brain Syndrome A 71
in drinking-related behaviors without being able to stop, alcohol, resulting in significant impairment on normal
A
despite being aware that drinking is causing, or exacerbat- brain functioning (APA Dictionary of Psychology, 2007).
ing, psychological or medical problems. Cognitive conse-
quences can include memory loss, difficulty performing
familiar tasks, poor or impaired judgment, and problems Categorization
with language.
As mentioned in the definition, alcoholic brain syndrome
encompasses several syndromes.
Cross References
1. Alcohol withdrawal delirium: A reversible condition
Alcohol Abuse that develops after cessation of chronic, extreme
Alcohol Dementia alcohol intake. Symptoms include disturbed con-
Alcoholic Brain Syndrome sciousness (e.g., disruption in attention/concentration),
Substance Abuse disruption in memory, orientation, and language be-
Substance Abuse Disorders yond what would be expected from typical alcohol
WernickeKorsakoff Syndrome withdrawal.
2. Alcohol-induced persisting dementia: A chronic condi-
tion that includes multiple cognitive deficits as
References and Readings a result of prolonged alcohol abuse. Cognitive areas
generally impaired include memory, speech, motor/
American Psychiatric Association (1994). Diagnostic and statistical man- sensory functions and executive functions. Global
ual of mental disorders (4th ed.). Washington, DC: American Psychi- impairment in intellectual functioning evolves grad-
atric Association.
ually over time.
3. Alcohol-induced persisting amnestic disorder: A persis-
tent disturbance in memory functioning caused by
chronic alcohol abuse. Memory impairment is severe
Alcoholic Amnestic Disorder enough to cause significant disturbance in occupa-
tional or social functioning.
Wernicke-Korsakoff Syndrome 4. Wernickes encephalopathy (WE): A syndrome resulting
from chronic alcoholism leading to nutritional defi-
ciency (i.e., Vitamin B1 [Thiamine] and characterized
by acute confusion, ataxia, sluggish pupillary reflexes,
Alcoholic Brain Syndrome and nystagmus and memory deficits). The syndrome
can result in coma or death. Lesions are centered in the
G LENN S. A SHKANAZI midbrain, cerebellum, and diencephalon.
University of Florida-College of Public Health 5. Korsakoff s syndrome: This condition often follows
and Health Professions episodes of WE. Thiamine deficiency, as a result of
Gainesville, FL, USA chronic, severe alcohol abuse, leads to a dense antero-
grade and retrograde amnesia. Patients with Korsak-
off s syndrome can store information for only a few
Synonyms seconds before they forget it. The resulting amnesia is
thought to be due to damage in the mammillary bod-
Alcoholic dementia; Alcoholic hallucinosis; Delirium ies, anterior or dorsomedial nuclei (or both) of the
tremens; Korsakoff s syndrome; WernickeKorsakoff thalamus.
syndrome
Another common feature is confabulation, in which
the patient recounts detailed and convincing memories
for events that have never happened.
6. Alcohol-induced psychotic disorder: A condition involv-
Alcoholic brain syndrome is a collection of several syn- ing the presence of delusions and/or hallucinations
dromes associated with the acute or chronic use of due to the physiological effects of alcohol.
72 A Alcoholic Brain Syndrome
Epidemiology Loss of some cognitive functions including memory

in Korsakoff s syndrome may be permanent. Once the
Up to 2 million alcoholics have developed permanent and patient has developed Korsakoff s, the treatment strategies
debilitating conditions that require lifetime custodial care. are not clear. However, it is important for patients to
A number of factors influence how and to what extent remain abstinent from alcohol. Depending on the degree
alcohol affects the brain. These include the age at which the of memory and executive function impairment, and avail-
person started drinking, duration of drinking, amount of ability of family support, patients with Korsakoff s may
alcohol consumed, drinking style/pattern, patients age, require long-term custodial care.
education, genetic background, family history of alcohol-
ism, neuropsychiatric risk factors (e.g., prenatal alcohol
exposure), and general health status. Studies comparing Neuropsychology and Psychology of
men and womens sensitivity to alcohol-induced brain Alcoholic Brain Syndrome
damage have not been conclusive.
Poor nutrition has been a major contributor to the The classic symptom in Korsakoff s syndrome is the in-
development of alcohol-induced brain damage. Up to ability to form new memories (i.e., anterograde amnesia).
80% of alcoholics have a deficiency in thiamine (i.e., However, patients also demonstrate significant deficits in
Vitamin B1). This vitamin is an essential nutrient re- their ability to recall incidents or events from their own
quired by all tissues including the brain. Some of these past as well (i.e., episodic memory). Memory for facts,
people will progress to WE. Approximately 8090% of concepts, and language (i.e., semantic memory) is vari-
alcoholics with Wernickes develop Korsakoff s psychosis, able while perceptual-motor memory is thought to be
which is more prevalent in men aged 4565. Women preserved.
who develop this condition tend to do so at a younger The inability to recall previously learned information
age (i.e., 3555). (i.e., retrograde amnesia) can often extend back 2030
years in a persons life with Korsakoff s patients. General-
ly, a temporal gradient exists such that memories from the
Natural History, Prognostic Factors, more distant past are recalled better than the more recent
and Outcomes ones. The basis of this extensive retrograde amnesia is still
a matter of great controversy.
WE is a medical emergency and requires immediate treat- These patients are typically younger than most
ment, as it can lead to death in approximately 20% of patients presenting to dementia services and because
untreated cases. Symptoms can develop within hours and they often present as initially confused, with concomitant
can be easily missed as many mimic intoxication. If treat- frontal lobe pathology, they are more likely to demon-
ment is given in time, usually through the administration strate aggressive, agitated behaviors and anxiety. Those
of thiamine, progression of symptoms can be slowed or with irreversible brain damage are unlikely to be able to
stopped. Ocular abnormalities usually recover within a live alone but also typically lack available social services.
few days to a few weeks, but ataxia takes 12 months These patients often have a difficult time maintaining
longer to resolve. The acute confusion/delirium usually social and familial relationships and live isolated lives.
improves within 12 days after the treatment but may
take 13 months to completely clear.
If treatment is not provided, then irreversible brain Evaluation
damage, or even death, is possible. Of those who survive,
approximately 85% develop Korsakoff s syndrome. How- For patients who meet the DSM-IV criteria for WE or
ever, not every person who develops Korsakoff s syn- Korsakoff s syndrome, neuropsychological assessment is
drome has a previous episode of Wernickes. Some will useful for documenting functions that are impaired, the
develop Korsakoff s gradually with either no known his- severity of impairment, and the prognostic factors
tory or brief episodes of Wernickes. Some patients are involved in determining the patients ability to manage
initially comatose or semiconscious and only when the daily life either independently or with assistance. Howev-
acute disorder has resolved is the underlying Korsakoff s er, it is preferable for the neuropsychological assessment
syndrome manifest. These patients are still susceptible to to occur when the patient has been abstinent from alcohol
developing Wernickes, especially if drinking were to for a long enough period of time to insure that the acute
continue. symptoms of alcohol withdrawal have subsided.
Alcoholism A 73
Treatment A
Alcoholic Dementia
The primary treatment option for patients experiencing
alcoholic brain syndrome is to stop drinking and remain Alcoholic Brain Syndrome
abstinent. Without additional alcohol exposure, the re-
covery from the delirium caused by alcohol is usually
good. This is obviously the first treatment to be utilized.
As mentioned above, thiamine deficiency is an important Alcoholic Hallucinosis
contributor to alcohol-related brain damage; therefore,
Vitamin B1 supplementation is necessary. Initially, the Alcoholic Brain Syndrome
vitamins can be given intravenously or intramuscularly
followed by oral administration. WE responds well to
high-dose vitamins, and such treatment can prevent the
occurrence of severe, chronic Korsakoffs syndrome. Sec- Alcoholic Polyneuropathy
ondarily, nutritional counseling to promote a vitamin-rich
and balanced diet is also part of this initial treatment pro- Korsakoff s Syndrome
tocol, especially for longer-term recovery and prevention.
Cross References
Alcoholic Psychosis
Alcoholism
Amnesia Korsakoff s Syndrome
Anterograde Amnesia
Dementia
Encephalopathy
Episodic Memory Alcoholism
Korsakoff s Syndrome
Organic Brain Syndrome G LENN S. A SHKANAZI
Retrograde Amnesia University of Florida-College of Public Health and Health
Semantic Memory Professions
Substance Abuse Gainesville, FL, USA
References and Readings Synonyms

Kopelman, M., Thomson, A., Guerrini, I., & Marshall, E. (2009). The Alcohol abuse; Alcohol addiction; Alcohol dependence;
Korsakoff Syndrome: Clinical aspects, psychology and treatment.
Problem drinking; Substance abuse
Alcohol & Alcoholism, 44(2), 148154.
Martin, P., Singleton, C., & Hiller-Sturmhofel, S. (2003). The role of
thiamine deficiency in alcoholic brain disease. Alcohol Research &
Health, 27(2), 134142. Definition
Oscar-Berman, M., & Marinkovic, K. (2003). Alcoholism and the brain:
An overview. Alcohol Research & Health, 27(2), 125133. The term alcoholism has a variety of definitions. For
Parsons, O. (1996). Alcohol abuse and alcoholism. In R. Adams,
some, it is a disease that makes a person dependent on
O. Parsons, J. Culbertson, & S. Nixon (Eds.), Neuropsychology for
clinical practice: Etiology, assessment, and treatment of common neu-
alcohol, causes an obsession with alcohol and inability to
rological disorders. Washington, DC: American Psychological control how much they drink even though their drinking
Association. causes serious problems in their relationships, health,
Rourke, S., & Grant, I. (2009). The neurobehavioral correlates of alco- work, and finances. Others do not define it as a disease
holism. In I. Grant & K. M. Adams (Eds.), Neuropsychological assess-
per se but rather a condition, behavioral in nature,
ment of neuropsychiatric and neuromedical disorders (3rd ed.). New
York, NY: Oxford University Press.
which results in continued consumption of alcohol de-
White, A. (2003). What happened? Alcohol, memory blackouts, and the spite health problems and negative social consequences.
brain. Alcohol Research & Health, 27(2), 186196. For some, the definition must include the concepts of
74 A Alcoholism
addiction and physiological withdrawal mechanisms, reported being current drinkers of alcohol (approximately
while for others, these are consequences of drinking. 109 million). That number drops to 44% when the age is
It is common for laypeople to equate any kind of 18 or older. Approximately 20% of persons aged 12 or older
excessive drinking with alcoholism. Those in the mental participated in binge drinking at least once in 30 days prior
health fields see that disorders related to alcohol use lie to the 2001 survey. Heavy drinking was reported by 5.7%
along a continuum of severity that may include physical of the 12 or older population (12.9 million). The highest
dependency/withdrawal (i.e., alcohol dependence) or may prevalence for both binge and heavy drinking was for those
involve impaired drinking habits that lead to health or in the 1825 age groups with the peak rate occurring at age
social problems/consequences but without dependency/ 21. Studies have found those who begin drinking at an
withdrawal (i.e., alcohol abuse). According to the APA earlier age are at higher risk to develop dependency. Those
Dictionary of Psychology, alcoholism is the popular term Americans who wait till age 21 are 4 times less likely to
for alcohol dependence. become dependent than those who begin drinking before
the age of 15 (i.e., 40% who start before age 15 develop
dependency on alcohol at some point in their lives). The
risk for developing dependency declines with age, as the
prevalence rate for alcoholism in those persons greater than
The term alcoholism was first used in 1849 by a physi-
65 years old is 3%.
cian, Magus Haas, to describe the systematic adverse
There are other nonage risk factors as well. Those with
effects of alcohol overconsumption. In the USA, it became
lower education and lower socioeconomic status are also
a popular term in the 1930s as a result of the growth of
at higher risk. There are also gender differences as men are
Alcoholics Anonymous (AA). Previously, society viewed
at minimum 2.5 times more likely to be defined as alco-
those who drank to excess as immoral, weak of character,
holic as women; however, the proportion of female alco-
and irresponsible. Societys response was punishment and
holics is increasing. White, non-Hispanic, individuals
removal of overconsumers from sober society to protect
are more likely to develop alcoholism than African-
the community. With the rise of AA, and their publication
Americans. The risk for Hispanics is generally the same
(i.e., the Big Book), the view of alcoholism changed
as Whites.
from character flaw to medical disease. AA viewed alco-
Alcoholism is estimated to be the third leading cause
holism as a physical allergy to alcohol accompanied by
of preventable death in the USA (after smoking and obe-
an obsession with drinking. This organization began to
sity). In the USA, 85,000 deaths are attributable to alcohol
dispel the previously held beliefs that alcoholics were
each year at a cost of $185 billion. The NIAAA estimates
unemployable, destitute, and isolated individuals by
that intoxication is present in 3060% of homicides, 22%
demonstrating that some highly respected people who
of suicides, 3350% of automobile accidents, 67% of
had been alcohol dependent had eventually overcome
drownings, and 7080% of fire-related deaths. More
their disorder and went on to lead productive lives.
than 50% of American adults have a close family member
who has or has had alcoholism. Approximately one in four
Epidemiology children younger than 18 in the USA is exposed to alcohol
abuse or alcohol dependence in their family.
The epidemiology of alcoholism can be confusing and Internationally, the World Health Organization esti-
contradictory, depending on the definition being utilized mates that there are 140 million people worldwide that are
and the measurement tool. The generally accepted overall alcohol dependent and they account for 3.5% of the total
rate of occurrence of alcoholism in the USA is 10%. The cases of disease worldwide, which is a higher rate than
U.S. National Longitudinal Alcohol Epidemiologic Study tobacco or illicit drugs.
concluded that alcoholism is prevalent in 20% of adult
hospital inpatients and in 17% of community-based
primary care practices. A 1985 U.S. National Hospital Current Knowledge
Survey found that 528,000 patients were discharged from
hospitals with a primary diagnosis of substance abuse, and Causes
for 81% (428,000), alcohol was the abused substance.
According to a 2001 survey conducted by the National There is no identifiable single cause of alcoholism. Scien-
Institute on Alcohol Abuse and Alcoholism (NIAAA) in tists believe that a myriad of factors play a role in the
the USA, approximately 48% of adults (aged 12 or older) development of alcoholism.
Alcoholism A 75
1. Genetics: Previous twin and adoption studies have more likely to be alcohol dependent. It is not an adequate
A
demonstrated that genes play an important role in measure by itself but can alert a health-care provider to
the development of alcoholism. Researchers found probe further. Another weakness is that it tends to be less
that identical twins (i.e., identical genes) have a higher reliable with populations with lower alcoholism rates
concordance rate for drinking behavior than fraternal (e.g., elderly) and does not identify hazardous drinking.
twins. Other studies have cast some doubt on these
2. Alcohol Use Disorders Identification Test (AUDIT):
twin studies by suggesting the environment of identi-
The AUDIT can detect both hazardous drinking
cal twins is more alike than fraternal twins, thus sug-
and alcohol abuse. It does not need to be administered
gesting a weakening of the argument in favor of genes.
face to face like the CAGE. It was developed by the
In the adoption studies, researchers found that World Health Organization and yields scores for
whether reared by biologic or adoptive parents, the sons consumption, dependency, and alcohol-related
of males with alcohol problems are 4 times more likely problems.
to have alcohol problems than sons of persons who are 3. Alcohol Dependence Data Questionnaire: More sensi-
not. In either case, epidemiologic studies indicate that tive than the CAGE and can distinguish abuse versus
alcoholism tends to run in families. Alcoholics are 6 times dependence.
more likely than nonalcoholics to have blood relatives
who are alcohol dependent. In summary, a persons
genetic makeup can predispose them to alcoholism Diagnosis
or not.
2. Peer influence: Social networks that include heavy Health-care providers most often use the Diagnostic Sta-
drinkers and alcohol abusers increase an individuals tistical Manual of the Mental Disorders, Fourth Edition,
risk for alcoholism. Text Revision (DSM-IV-TR) criterion for alcohol depen-
3. Cultural influence: Cultures that include well-estab- dence. The diagnosis requires three of the following
lished taboos against drunkenness and rules regarding criteria:
drinking have lower alcoholism rates than those who 1. Maladaptive pattern of the use leading to impairment/
do not. distress as manifested by three or more of the below
4. Psychiatric conditions: Certain psychiatric diagnoses occurring in the same 12-month period.
increase the risk of alcoholism. These include Tolerance
ADHD, panic disorder, schizophrenia, and antisocial Withdrawal
personality disorder. Drink more frequently or in larger amounts than
intended
Persistent desire to drink or unsuccessful efforts to
Screening cut down or control use
Great deal of time spent in acquiring/using alcohol
There are a variety of measures for alcoholism including or recovering from its effects
the following: Important social, occupational, or recreational
activities given up or reduced because of alcohol
1. CAGE: The CAGE is named for the four questions Drinking continues despite knowledge of persis-
asked of a patient before any questions regarding tent or recurrent physiological, or psychological
quantities drank are asked. problems caused or exacerbated by drinking
a Have you ever felt the need to Cut down on your
drinking?
b Have people Annoyed you by criticizing your
Treatment
drinking?
c Have you ever felt Guilty about drinking?
There are several well-accepted avenues of treatment.
d Have you ever felt you needed a drink in the morn-
ing to steady your nerves or get rid of a hangover? 1. Psychosocial: Studies have shown that simple, brief
(Eye-opener) interventions can be effective in those not severely
The CAGE has been extensively validated. Those who alcohol dependent. One of those getting an extensive
answer YES to two or more questions are 7 times trial has been Motivation Interviewing based on
76 A Alcoholism
Prochaskas Five Stages of Change Model. A summary afford a private hospital or private psychiatrist could
of the treatment approach is as follows: only find help in state hospitals, jails, or churches.
Precontemplation Patient expresses no interest or AA was the first self-directed approach toward treat-
need for change. The health-care professionals ment. The AA treatment model includes self-help
options are limited. They can point to discrepan- groups, utilizing psychological principles organized
cies between the patients goals and behavior and in small local community groups. The 12 steps of
recommend 2 weeks of abstinence. AA encourage confrontation of denial, admission of
Contemplation Patient expresses ambivalence or powerlessness over alcohol, and strives for people
skepticism about change. The provider should to atone for harm caused by their behavior while
work to influence them in direction of change, drinking. It encourages its members to live ethically
provide information about the dangers of alcohol with a reliance on a higher power. It is this sense
abuse, and recommend an abstinence trial. of AA as a religion that has led to nonreligious self-
Preparation Patient accepts need for change and help groups including rational recovery, LifeRing,
makes plans to accomplish changed drinking goal. and SOS.
Action Patient recognizes problem in drinking
behavior and takes observable steps to decrease
alcohol use. Professional reinforces decision for
change and may introduce self-help groups and/
Future Directions
or medications.
The following are areas needing continued study:
Maintenance Patient and professional work
together to maintain change and prevent relapse. 1. Genetic research current and future studies are look-
ing at individuals with a family history of alcoholism
to pinpoint the location of genes that influence vul-
2. Medications: The most common medications in the nerability to alcoholism. This line of study will assist
treatment of alcoholism are: in the early identification of individuals at risk and of
Disulfiram (Antabuse) Prevents the elimination new, gene-based treatment approaches.
of acetaldehyde, which is a by-product of alcohol 2. Treatment approaches The NIAAA has been funding
metabolism. Results in unpleasant side effects in a study called Project MATCH whose goal is to
persons still drinking including nausea, dizziness, identify variables important in predicting outcome
headache, flushing, vomiting, heart palpitations, based on patient characteristics and treatment design.
and sudden drop in blood pressure. Disulfiram 3. Medications Naltrexone was the first drug approved
needs to be taken daily to be effective. However, by the FDA in 45 years to help alcoholics stay sober
in at least one large clinical trial it did not increase following detoxification. More research is needed.
abstinence.
Naltrexone (ReVia) May work by blocking the
positive effects felt from drinking by blocking opi- Cross References
ate receptors in the brain thereby decreasing crav-
ing for alcohol. Clinical studies have found a Alcoholic Brain Syndrome
modest decrease in relapse (1220%). This drug Fetal Alcohol Syndrome
has an unknown cause of action. Korsakoff s Syndrome
Acamprosate (Campral) Used to maintain Michigan Alcoholism Screening Test
abstinence once alcoholics have stopped drinking. Motivational Interviewing
Thought to work by stabilizing the chemical Substance Abuse Disorders
balance in the brain. In clinical trials, the one Twin Studies
year abstinence rates have been 18% and 12% at WernickeKorsakoff s Syndrome
two years.

3. Self-help groups: Perhaps the best-known organization
involving alcoholism is AA. Until the mid-1930s in the National Institute on Alcohol Abuse and Alcoholism. Etiology and natural
USA, alcohol-dependent persons who could not history of alcoholism. URL Accessed on June 1, 2009 (http://pubs.
Alexia A 77
niaaa.nih.gov/publications/social/module2etiology&naturalhistory/
module2.html). Alexia A
National Institute on Alcohol Abuse and Alcoholism. Helping patients
who drink too much: A clinicians guide. URL Accessed on June 1,
S TEVEN Z. R APCSAK , P ELAGIE M. B EESON
2009 (http://www.niaaa.nih.gov/Publications/EducationTraining-
Materials/guide.htm). The University of Arizona
Schuckit, M. (2000). Drug and alcohol abuse: A clinical guide to Tucson, AZ, USA
diagnosis and treatment. New York, NY: Kluwer Academic/Plenum
Publishers.
U.S. Department of Health and Human Services and SAMHSAs National
Clearinghouse for Alcohol and Drug Information. Accessed URL
on June 1, 2009 (http://ncadistore.samhsa.gov/catalog/facts.aspx?
topic=3). The term alexia is applied to acquired disorders of reading
produced by neurological injury in individuals with
normal premorbid literacy skills. Clinically, patients with
alexia have difficulty in recognizing, pronouncing, or
comprehending written words. Although alexia can
occur in relative isolation, it is more frequently encoun-
Alertness tered in the context of spoken language dysfunction or
aphasia. Most individuals with alexia have concommitant
C HRIS L OFTIS spelling impairment or agraphia, suggesting that reading
STG International and spelling rely on shared cognitive representations
Alexandria, VA, USA and neural substrates. Acquired alexia needs to be
distinguished from developmental dyslexia reflecting a
failure to attain normal reading skills.
Synonyms
Awareness; Consciousness; Watchfulness

Categorization
Alexia is not a single clinical entity. Instead, there are

Definition several distinct forms of alexia characterized by specific
combinations of impaired and preserved reading abilities
A state of being mentally perceptive and responsive to and associated with unique lesion profiles. The three most
external stimuli. A readiness to respond that can be commonly encountered alexia syndromes include pure
detected by Electroencephalography (EEG). Alertness is alexia/letter-by-letter reading, phonological/deep alexia,
susceptible to fatigue; maintaining a constant level of and surface alexia. In order to understand the neuropsy-
alertness is difficult, particularly for monotonous tasks chological mechanisms underlying different subtypes of
demanding continuous attention. Stimulants such as alexia, it is important to briefly review the cognitive
nicotine, caffeine, and amphetamines can temporally processes involved in normal reading.
boost alertness. Diminished alertness is often associated Reading is a complex cognitive skill that requires rapid
with the physiological response of yawning, which may visual discrimination of letters and words, as well as the
boost the alertness of the brain. Impaired alertness is a ability to link information about visual word forms
common symptom of a number of conditions, including (orthography) with knowledge about word sounds
narcolepsy, attention deficit disorder, traumatic brain (phonology) and word meanings (semantics). According
injury, chronic fatigue syndrome, depression, Addisons to an influential dual-route model of reading (Coltheart,
disease, and sleep deprivation. Rastle, Perry, Langdon, & Ziegler, 2001), perceptual
processing of written words begins with visual feature
analysis and letter shape detection (Fig. 1). Following
the letter identification stage, the model postulates two
Cross References distinct procedures or processing routes for deriving
phonology from print. The lexical route requires the
Alertness activation of memory representations of written word
Electroencephalography forms stored in the orthographic lexicon, followed by
78 A Alexia
Semantics
Phonology Orthography
Lexical
Words Words
Spoken word Written word
Sublexical
Auditory Visual
Phonemes Letters
analysis analysis
Motor speech Graphic motor

programs programs
Speech Writing
Alexia. Figure 1 A cognitive model indicating the component processes involved in reading
the retrieval of the corresponding spoken word forms written word comprehension. However, whether semantic
from the phonological lexicon. The lexical route is mediation is also normally required for accurate oral
normally used to read familiar words and can support reading of familiar words is a topic of controversy
the processing of both regular words that have predictable (Coltheart et al., 2001; Plaut, McClelland, Seidenberg, &
spellingsound relationships (e.g., spring) and irregular Patterson, 1996; Woollams, Lambon Ralph, Plaut, &
words that contain atypical lettersound or grapheme Patterson, 2007). In summary, skilled reading depends
phoneme mappings (e.g., choir). By contrast, the sublex- on interactions between visual/orthographic processing,
ical route operates on units smaller than the whole word phonology, and semantics. Damage to these functional
and is thought to rely on the serial conversion of individ- domains or the disruption of the transfer of information
ual graphemes to the corresponding phonemes. The between the cognitive/brain systems that support these
sublexical route is essential for accurate reading of unfa- operations results in alexia.
miliar words or nonwords (e.g., nace) because these novel
items, by definition, do not have preexisting representa-
tions in the orthographic or phonological lexicon. The Epidemiology
sublexical route can also be used to generate plausible
pronunciations for regular words that strictly obey Alexia is commonly observed in right-handed individuals
spellingsound conversion rules. However, processing following damage to the language-dominant left hemi-
irregular words by the sublexical procedure results in sphere. Although it is most frequently caused by stroke,
regularization errors (e.g., have read to rhyme with alexia can follow any kind of focal injury (e.g., trauma,
save). Thus, according to dual-route theory, only the tumor) to the brain regions critical for implementing the
lexical reading route can deliver a correct response to various cognitive operations necessary for normal
irregular words. Note that the model depicted in Fig. 1 reading. Alexia is also often seen in the setting of neuro-
also includes an indirect route from orthography to pho- degenerative disorders, especially in patients with primary
nology via the semantic system. The activation of word progressive aphasia/semantic dementia or Alzheimers
meanings by this semantic reading route is critical for disease. In general, the specific alexia profile is determined
Alexia A 79
not so much by the etiology of the brain damage than by orthographic word forms and result in an abnormal
A
the location of the responsible lesions. word length effect in oral reading.
Pure alexia/letter-by-letter reading is most commonly
seen following left inferior occipito-temporal damage
caused by posterior cerebral artery strokes. It has been
Outcomes
proposed that the critical lesions degrade or disrupt visual
input to the visual word-form area (VWFA) or directly
The prognosis for recovery from alexia depends both on
damage the VWFA itself (Cohen et al., 2003; Epelbaum
the etiology of the lesion and the extent of the underlying
et al., 2008). The VWFA is consistently activated in func-
brain damage. Alexia following stroke tends to show some
tional imaging studies of reading in normal individuals
spontaneous recovery over time, but patients with exten-
and has been localized to the mid-lateral portions of the
sive brain damage may never regain useful reading func-
left fusiform gyrus (BA37) (Cohen et al., 2002; Jobard,
tion and typically stop reading for pleasure. In individuals
Crivello, & Tzourio-Mazoyer, 2003) (Fig. 2). The VWFA
with neurodegenerative disorders, progressive worsening
receives converging input from bilateral posterior occipi-
of the reading impairment is observed along with the
tal areas (BA17,18/19) involved in visual feature analysis
gradual deterioration of other language and cognitive
and letter shape detection and it integrates this informa-
functions.
tion into larger perceptual units corresponding to whole
words (Fig. 2). Activation of the VWFA is sensitive to the
Neuropsychology and Psychology of orthographic familiarity of the letter string, consistent
Alexia with the notion that this cortical region may constitute
the neural substrate of the orthographic lexicon. The
Pure Alexia/Letter-By-Letter Reading orthographic codes computed by the VWFA are subse-
quently transmitted to cortical systems involved in the
In pure alexia, the rapid visual identification of familiar phonological and semantic components of reading
words that characterizes normal skilled reading is dis- (Fig. 3). Importantly, it has been shown that spelling
rupted. Reading is slow and laborious, often relying on a familiar words also activates the VWFA (Beeson et al.,
serial letter-naming strategy known as letter-by-letter 2003). These observations confirm the central role for the
reading. Typically, there is a monotonic increase in VWFA in orthographic processing and support the view
reading latencies as a function of the number of letters that the same orthographic lexical representations medi-
in the word, giving rise to an abnormal word length effect ate reading and spelling. Consistent with this hypothesis,
that is considered the hallmark feature of the syndrome. patients with damage to the VWFA are likely to show
Varying degrees of letter identification difficulty are pres- evidence of reading and spelling impairment attributable
ent and visual reading errors are common (e.g., chain to the loss of word-specific orthographic representations
charm). Collectively, these behavioral observations sug- (Rapcsak & Beeson, 2004).
gest that visual processing impairment plays a critical role
in the pathogenesis of pure alexia (Behrmann, Plaut, &
Nelson, 1998). Although the reading disorder may be Phonological/Deep Alexia
unaccompanied by significant aphasia or agraphia, many
patients with pure alexia demonstrate concommitant Phonological alexia is characterized by a disproportionate
anomia and spelling impairment (Rapcsak & Beeson, difficulty in processing nonwords compared with familiar
2004). Furthermore, patients often perform poorly on words, giving rise to an exaggerated lexicality effect in
nonreading tasks that require fine-grained visual discrim- reading (Crisp & Lambon Ralph, 2006; Patterson &
ination, suggesting that the reading impairment is part of Lambon Ralph, 1999; Rapcsak et al., 2009). Attempts to
a more general visual processing deficit (Behrmann et al., read nonwords often result in real word responses known
1998). Within the framework of the cognitive model as lexicalization errors (e.g., nace name). Although
depicted in Fig. 1, pure alexia is attributable to dysfunc- in phonological alexia reading of familiar words
tion at the visual feature analysis and/or letter identifica- (both regular and irregular) is relatively preserved,
tion stages of reading, or it may be produced by damage to performance is typically influenced by lexical-semantic
the orthographic lexicon. Damage to any of these visual variables including word frequency (high>low), image-
processing components would be expected to interfere ability (concrete>abstract), and grammatical class
with the rapid perceptual identification of familiar (nouns>verbs > functors). Deep alexia includes all the
80 A Alexia
Alexia. Figure 2 Location of the visual word form area (VWFA) (indicated by green circle) as determined by functional
neuroimaging studies of reading. This region receives input from bilateral posterior occipital visual areas (shown in purple).
Arrow indicates callosal transfer of information initially processed by right visual cortex
Phonology
Visual analysis
Semantics
Orthography
Alexia. Figure 3 Cortical regions involved in reading

Alexia A 81
characteristic features of phonological alexia, but it insula, superior temporal gyrus/Wernickes area (BA22),
A
is distinguished from the latter by the production of and supramarginal gyrus (BA40) (Rapcsak et al., 2009).
prominent semantic reading errors (e.g., boy son) Consistent with the phonological deficit hypothesis, there
(Coltheart, Patterson, & Marshall, 1980). Although pho- is an excellent neuroanatomical correspondence between
nological and deep alexia were originally considered sepa- the location of the lesions that produce phonological
rate entities, there is now much evidence to suggest that alexia and the location of the perisylvian cortical areas
the difference between these syndromes is quantitative that show activation in normal individuals during a
rather than qualitative. Thus, phonological and deep alex- variety of written and spoken language tasks requiring
ia are more appropriately considered as points along a phonological processing (Jobard et al., 2003; Rapcsak
continuum, with the latter representing a more severe et al., 2009; Vigneau et al., 2006). As predicted by the
version of the former (Crisp & Lambon Ralph, 2006; continuum model, there is considerable overlap between
Rapcsak et al., 2009). the perisylvian lesion profiles of patients with phono-
Phonological alexia is typically encountered in logical and deep alexia, although the damage in deep
patients with aphasia syndromes characterized by phono- alexia tends to be more extensive. In fact, the massive
logical impairment (i.e., Brocas, conduction, Wernickes). destruction of left-hemisphere language areas in deep
Furthermore, it has been shown that most patients with alexia has lead to the hypothesis that reading perfor-
phonological alexia demonstrate prominent deficits and mance in these patients may be mediated by the intact
increased lexicality effects in spoken language tasks that right hemisphere (Coltheart et al., 1980).
require the manipulation and maintenance of sublexical
phonological information (e.g., repetition, rhyme judg-
ments, phoneme segmentation and blending), and also Surface Alexia
that such non-orthographic measures of phonological
ability correlate with and are predictive of reading perfor- In surface alexia the main difficulty involves reading
mance (Crisp & Lambon Ralph, 2006; Rapcsak et al., irregular words, especially when these items are of low
2009). These observations suggest that the written and frequency. Regular words of comparable frequency are
spoken language impairments in phonological alexia have processed more efficiently, and the discrepancy in perfor-
a common origin and are merely different manifestations mance between words with predictable versus atypical
of a central or modality-independent phonological deficit spellingsound relationships is reflected by an increased
(Crisp & Lambon Ralph, 2006; Patterson & Lambon regularity effect in reading. Nonword reading is typically
Ralph, 1999; Rapcsak et al., 2009). Consistent with this preserved. According to dual-route theory, surface alexia
view, the reading disorder in phonological alexia is usually is attributable to dysfunction of the lexical reading route
accompanied by a qualitatively similar spelling im- (Fig. 1). Specifically, it has been suggested that the reading
pairment (phonological agraphia) (Rapcsak et al., 2009). disorder in some cases may result from damage to the
According to dual-route models (Fig. 1), poor nonword orthographic lexicon (Coltheart et al., 2001; Patterson,
reading in phonological alexia is attributable to damage to Marshall, & Coltheart, 1985). Due to the loss of word-
the sublexical route, while the relatively preserved real specific orthographic knowledge, patients with this type
word reading performance of these patients reflects the of deficit will be forced to rely on a sublexical grapheme
residual functional capacity of the lexical and semantic phoneme conversion strategy that produces phonologi-
routes. The general phonological impairment observed in cally plausible regularization errors on irregular words.
the vast majority of patients suggests that the most com- Low-frequency irregular words are especially vulnerable
mon site of damage may be at the level of the phoneme because the activation of representations in the ortho-
units (with additional damage to the phonological lexicon graphic lexicon is normally modulated by word frequency
in more severe cases), as these phonological processing and the relative refractoriness of low-frequency items may
components are shared between written and spoken be further exaggerated by the brain damage. Consistent
language tasks. with the notion that reading and spelling rely on shared
Phonological alexia is most often associated with orthographic representations, patients with surface alexia
damage to a network of perisylvian cortical regions following damage to the orthographic lexicon show
involved in speech production/perception and phonolog- similar difficulty in spelling irregular words (surface
ical processing in general. Components of this distributed agraphia) (Patterson et al., 1985; Rapcsak & Beeson,
phonological system include posterior-inferior frontal 2004). Alternatively, surface alexia may result from dam-
gyrus/Brocas area (BA44/45), precentral gyrus (BA4/6), age to central semantic representations (Woollams et al.,
82 A Alexia
2007). Specifically, it has been proposed that accurate oral may reflect damage to the orthographic lexicon resulting
reading of low-frequency irregular words normally in the loss of word-specific orthographic knowledge. By
requires additional support from the semantic reading contrast, in patients with anterior temporal lobe lesions,
route and cannot be mediated efficiently by pathways and possibly also in patients with posterior temporo-
that rely on direct transcoding between orthographic parietal damage, surface alexia may be attributable to
and phonological representations (Plaut et al., 1996). the degradation of central semantic representations. The
With the degradation of semantic knowledge, the relative latter hypothesis is supported by functional imaging stud-
inadequacy of non-semantic reading routes is revealed ies of semantic processing in normal individuals that have
and manifests itself as surface alexia. Consistent with the shown activation of a large-scale left-hemisphere extra-
semantic deficit hypothesis, many patients with surface sylvian cortical network that included both anterior tem-
alexia perform poorly on verbal and nonverbal cognitive poral lobe and posterior temporo-parietal sites (Vigneau
tasks requiring semantic processing (e.g., picture naming, et al., 2006; Binder, Desai, Graves, & Conant, 2009)
verbal fluency, spoken word and picture comprehension). (Fig. 3).
Furthermore, the severity of the semantic impairment on
these nonreading tasks has been shown to correlate with
reading accuracy for low-frequency irregular words Evaluation
(Woollams et al., 2007). The proposed central semantic
deficit may also explain the frequent co-occurrence of In evaluating patients with alexia it is important to assess
surface alexia and surface agraphia (Graham, Patterson, the status of all the relevant component processes
& Hodges, 2000). involved in reading (Fig. 1). A comprehensive battery
In contrast to the strong association between perisyl- should include tests of letter and word recognition, as
vian damage and phonological alexia, surface alexia is well as measures of oral reading and reading comprehen-
typically encountered in the setting of extrasylvian brain sion. The evaluation should allow the clinician to identify
pathology. Although uncommon in patients with stroke, the nature of the functional impairment and to locate the
surface alexia has been described in individuals with left level of breakdown with reference to a cognitive model of
temporo-parietal lesions centered on posterior middle/ normal reading. It is equally important to document
inferior temporal gyrus and angular gyrus (BA20/21,37/ relatively spared reading abilities and the use of compen-
39), and also following inferior occipito-temporal lesions satory strategies by the patient, as this information may be
that involved the VWFA (Rapcsak & Beeson, 2004; Vanier helpful in planning treatment. The assessment of alexia is
& Caplan, 1985). As expected, patients with surface alexia best accomplished by the use of commercially available
following VWFA damage also showed evidence of visual reading batteries (e.g., Kay, Lesser, & Coltheart, 1992).
processing impairment and features of pure alexia/letter-
by-letter reading (Rapcsak & Beeson, 2004). A particularly
dramatic and pure form of surface alexia is consistently Treatment
observed in patients with semantic dementia (SD) (Wool-
lams et al., 2007). SD is a subtype of primary progressive A variety of behavioral treatment approaches have shown
aphasia/frontotemporal dementia in which the neurode- positive outcomes in the rehabilitation of alexia. In gen-
generative process has a predilection for left anterior and eral, treatment is directed toward strengthening the im-
inferolateral temporal cortex, including the temporal paired reading procedure/route or it encourages the use of
pole, middle/inferior temporal gyri, and anterior fusiform compensatory strategies to bypass the functional deficit
gyrus (BA38,20/21) (Galton et al., 2001; Mummery et al., (for a review, see Beeson & Rapcsak, 2006).
2000). Surface alexia has also been described in patients
with Alzheimers disease (Patterson, Graham, & Hodges,
1994) and is likely to reflect the frequent involvement of Cross References
left temporo-parietal cortex by the disease process. Al-
though distributed over a large anatomical area, the dis- Agraphia
parate extrasylvian lesion sites in surface alexia seem to Aphasia
have in common the potential for disrupting either lexical Dyslexia
orthographic or semantic processing. Specifically, in Phonological/Deep Agraphia
patients with VWFA involvement the reading disorder Surface Agraphia
Alexithymia A 83
References and Readings Plaut, D. C., McClelland, J. L., Seidenberg, M. S., & Patterson, K. (1996).
A
Understanding normal and impaired word reading: Computational
principles in quasi-regular domains. Psychological Review, 103,
Beeson, P. M., & Rapcsak, S. Z. (2006). Treatment of alexia and
56115.
agraphia. In J. H. Noseworthy (Ed.), Neurological therapeutics: Prin-
Rapcsak, S. Z., & Beeson, P. M. (2004). The role of left posterior inferior
ciples and practice (2nd ed., pp. 30453060), London: Martin Dunitz.
temporal cortex in spelling. Neurology, 62, 22212229.
Beeson, P. M., Rapcsak, S. Z., Plante, E., Chargualaf, J., Chung, A.,
Rapcsak, S. Z., Beeson, P. M., Henry, M. L., Leyden, A., Kim, E. S., Rising,
Johnson, S. C., et al. (2003). The neural substrates of writing: A
K., et al. (2009). Phonological dyslexia and dysgraphia: Cognitive
functional magnetic resonance imaging study. Aphasiology, 17,
mechanisms and neural substrates. Cortex, 45(5), 575591.
647665.
Vanier, M., & Caplan, D. (1985). CT correlates of surface dyslexia. In
Behrmann, M., Plaut, D. C., & Nelson, J. (1998). A literature review and
K. E. Patterson, J. C. Marshall, & M. Coltheart (Eds.), Surface
new data supporting an interactive account of letter-by-letter
dyslexia: Neuropsychological and cognitive studies of phonological
reading. Cognitive Neuropsychology, 15, 751.
reading (pp. 511525). London: Lawrence Erlbaum.
Binder, J. R., Desai, R. H., Graves, W. W., & Conant, L. L. (2009). Where is
Vigneau, M., Beaucousin, V., Herve, P. Y., Duffau, H., Crivello, F.,
the semantic system? A critical review and meta-analysis of 120
Houde, O., et al. (2006). Meta-analyzing left hemisphere language
functional neuroimaging studies. Cerebral Cortex, 19, 27672796.
areas: Phonology, semantics, and sentence processing. NeuroImage,
Cohen, L., Lehericy, S., Chochon, F., Lemer, C., Rivaud, S., & Dehaene, S.
30, 14141432.
(2002). Language-specific tuning of visual cortex? Functional prop-
Woollams, A., Lambon Ralph, M. A., Plaut, D. C., & Patterson, K. (2007).
erties of the visual word form area. Brain, 125, 10541069.
SD-squared: On the association between semantic dementia and
Cohen, L., Martinaud, O., Lemer, C., Lehericy, S., Samson, Y., Obadia,
surface dyslexia. Psychological Review, 114, 316339.
M., et al. (2003). Visual word recognition in the left and right
hemispheres: Anatomical and functional correlates of peripheral
alexias. Cerebral Cortex, 13, 13131333.
Coltheart, M., Patterson, K., & Marshall, J. C. (1980). Deep dyslexia.
London: Routledge & Kegan Paul.
Coltheart, M., Rastle, K., Perry, C., Langdon, R., & Ziegler, J. (2001).
Alexia Without Agraphia
DRC: A dual route cascaded model of visual word recognition and
reading aloud. Psychological Review, 108, 204256. Alexia
Crisp, J., & Lambon Ralph, M. A. (2006). Unlocking the nature of the
phonological-deep dyslexia continuum: The keys to reading aloud
are in phonology ad semantics. Journal of Cognitive Neuroscience, 18,
348362.
Epelbaum, S., Pinel, P., Gaillard, R., Delmaire, C., Perrin, M., Dupont, S., Alexithymia
et al. (2008). Pure alexia as a disconnection syndrome: New diffusion
imaging evidence for an old concept. Cortex, 44, 962974.
Galton, C. J., Patterson, K., Graham, K., Lambon Ralph, M. A., Williams,
J OEL W. H UGHES
G., Antoun, N., et al. (2001). Differing patterns of temporal atrophy Kent State University
in Alzheimers disease and semantic dementia. Neurology, 57, Kent, OH, USA
216225.
Graham, N. L., Patterson, K., & Hodges, J. R. (2000). The impact of
semantic memory impairment on spelling: Evidence from semantic
dementia. Neuropsychologia, 38, 143163.
Definition
Jobard, G., Crivello, F., & Tzourio-Mazoyer, N. (2003). Evaluation of the
dual route theory of reading: A metaanalysis of 35 neuroimaging A deficit in apprehending, experiencing, and describing
studies. NeuroImage, 20, 693712. emotions, including difficulty in perceiving and under-
Kay, J., Lesser, R., & Coltheart, M. (1992). Psycholinguistic assessments of
standing the feelings of others. In particular, difficulty in
language processing in aphasia (PALPA). East Sussex, England: Lawr-
ence Erlbaum Associates.
distinguishing between emotions and bodily sensations
Mummery, C. J., Patterson, K., Price, C. J., Ashburner, J., Frackowiak, that indicate emotional arousal.
R. S. J., & Hodges, J. R. (2000). A voxel-based morphometry study of
semantic dementia: Relationship between temporal lobe atrophy and
semantic memory. Annals of Neurology, 47, 3645.
Patterson, K., Graham, N., & Hodges, J. R. (1994). Reading in dementia Current Knowledge
of the Alzheimer type: A preserved ability? Neuropsychology, 8,
835407.
The term alexithymia was coined by the late psychiatrist
Patterson, K., & Lambon Ralph, M. A. (1999). Selective disorders of
reading? Current Opinion in Neurobiology, 9, 235239.
Peter Sifneos to describe patients who could not find the
Patterson, K. E., Marshall, J. C., & Coltheart, M. (1985). Surface dyslexia: appropriate words to describe their emotional states.
Neuropsychological and cognitive studies of phonological reading. Literally meaning without words for emotions in
London: Lawrence Erlbaum. Sifneos native Greek, Alexithymia is a trait that overlaps
84 A Alice in Wonderland Syndrome
with a number of medical and psychiatric disorders. Short Description or Definition

Alexithymia is associated with somatic complaints such
as headaches, lower back pain, irritable bowel syndrome, Alien hand syndrome (AHS) is a relatively rare manifes-
and fibromyalgia. It is also associated with psychiatric tation of damage to specific brain regions involved in
conditions such as anorexia nervosa, autism spectrum voluntary movement. The core observation is the patient
disorders including Aspergers, major depressive disorder, report that one of his/her hands is displaying purposeful,
panic disorder, posttraumatic stress disorder, and coordinated, and goal-directed behavior over which the
substance abuse. patient feels he/she has no voluntary control. The patient
fails to recognize the action of one of his hands as his own.
The hand, effectively, appears to manifest a will of its
own. This unique involuntary movement disorder is
Cross References characterized by coordinated, well-organized, and clearly
goal-directed limb movements that would otherwise be
Emotional Intelligence indistinguishable from normal voluntary movement. This
definition excludes disordered, non-purposeful, and dys-
kinetic movements associated with other involuntary
movement disorders such as chorea, athetosis, hemibal-
References and Readings lism, and myoclonus.
The alien hand can be engaged in performing a
Sifneos, Peter E. Alexithymia: Past and present. The American Journal of specific goal-directed task or the purposeful use of an
Psychiatry, 153, 137142.
external object. Distinguishing this condition from aso-
Taylor, Graeme J; Bagby, R. Michael and Parker, James DA (1997).
Disorders of Affect Regulation: Alexithymia in Medical and matognosia, there is typically normal awareness and rec-
Psychiatric Illness. Cambridge: Cambridge University Press. ISBN ognition of the limb reported by the patient. However, the
052145610X. patient perceives a lack of self-agency (I am not doing
Taylor GJ, & Taylor HS (1997). Alexithymia. In M. McCallum & that. . .) with regard to the observed behavior of the limb,
W.E. Piper (Eds.) Psychological mindedness: A contemporary
but displays intact ownership (. . .even though I know
understanding. Munich: Lawrence Erlbaum Associates.
this is my hand).
Categorization
Alice in Wonderland Syndrome Three variants of AHS have been described, each with
unique behavioral manifestations and neuroanatomical
Metamorphopsia correlations. These variants include the frontal, callosal,
and posterior forms.
Frontal Form
Alien Hand Syndrome Neuroanatomy

The most common variant is the frontal form. It is
G ARY G OLDBERG , M ATTHEW E. G OODWIN associated with damage to the medial surface of the
Virginia Commonwealth University School of Medicine/ cerebral hemisphere in the frontal region. This variant
Medical College of Virginia has been described in cerebral infarction in the territory
Richmond, VA, USA of the anterior cerebral artery, with tumors involving the
medial surface of the cerebral hemisphere, and in other
conditions affecting the function of the medial frontal
Synonyms lobe region. When the region of injury extends posteriorly
to involve the medial aspect of the prefrontal gyrus
Anarchic hand; Callosal apraxia; Diagnostic dyspraxia; associated with the primary motor cortex (PMC), the
Dr. Strangelove syndrome; Intermanual conflict; Mag- patient may present with crural hemiparesis, with greater
netic apraxia; Wayward hand weakness in the leg as compared to the arm. This
Alien Hand Syndrome A 85
presentation corresponds to the topographical organiza- nondominant hand, they may experience difficulty with
A
tion of the PMC with control of lower limb movement the initiation of spontaneous speech while being able to
located more medially than the areas that control the follow verbal commands and repeat phrases without dif-
upper limb. The frontal variant is seen with involvement ficulty. These findings are consistent with a transcortical
of the medial aspect of the premotor cortex anterior to motor aphasia that affects spontaneous verbalization and
PMC including the supplementary motor area (SMA) and production of propositional language more than repeti-
anterior cingulate cortex (ACC). In functional activation tion and responsive language. Alternatively, this could be
studies, the medial frontal cortex has also been found to understood as an inability to initiate spontaneous verbal
activate spontaneously with complex purposeful move- output. The patient may thus be viewed as partially mute
ments and with internal imaging of voluntary movement, due to the relative akinesia seen with medial frontal cortex
suggesting that it may serve as a higher level system that injury.
modulates the activation of PMC in accordance
with volitional aspects of the performance. The readiness
potential that precedes an overt voluntary movement Callosal Form
by over 1,000 ms arises through activation of the ante-
romedial frontal cortex, suggesting that excitation of this Neuroanatomy
region precedes the appearance of the overt movement and The callosal variant is seen with an isolated lesion of the
activation of the PMC. Activation of the ACC is involved corpus callosum. The voluntary motor systems of the two
in intentional suppression of prepotent responses as tested hemispheres are isolated from each other due to lost
with the Stroop test. These areas may serve as a higher- interhemispheric communication. This variant has been
level system modulating the activation of PMC in described most frequently as a transient condition follow-
accordance with the volitional aspects of the performance. ing callosotomy. It may also be seen following infarction
or tumors selectively involving this structure.
Clinical Presentation
Behaviors seen frequently with the frontal variant in- Clinical Presentation
clude involuntary, visually driven reaching and grasping In the callosal variant of AHS, the appearance of
onto objects, an inability to voluntarily release these intermanual conflict or self-oppositional behaviors
objects, and utilization behavior in which the presence is the predominant feature. Grasping behaviors and exter-
of a frequently encountered object such as a comb or a nally driven reaching movements seen in the frontal vari-
toothbrush elicits behavior in which the object may be ant are notably less prominent. When there is a major
put to use independent of the social context. A grasp disconnection between the two hemispheres resulting
reflex to tactile stimulation is often present in the affect- from callosal injury, the language-linked dominant hemi-
ed hand. The patient may wake themselves up from sleep sphere agent that maintains its primary control over the
by grasping and pulling their own body parts. Patients contralateral dominant limb effectively loses its direct and
may show a prepotent tendency to be drawn toward linked control over the separate agent based in the
external objects. They also may demonstrate alien-asso- nondominant hemisphere (and, thus, the nondominant
ciated sexual self-stimulation or involuntary fondling of limb), which had been previously responsive and obedi-
anothers body, a great source of public embarrassment ent to the dominant agent. The possibility of purposeful
(Ong Hai and Odderson, 2000). Interestingly, while the action in the nondominant limb occurring outside of
patient clearly manifests purposeful involuntary coordi- the realm of influence of the dominant agent thus can
nated behaviors in the affected limb, when they attempt to occur. In the callosal variant, the problematic alien hand is
willfully move the limb, this is effortful and difficult. consistently the nondominant hand, while the dominant
Voluntary movement in the affected limb is often hypo- hand is the identified good controlled hand. The patient
kinetic and hypometric with greater activation of the axial may express frustration and bewilderment at the
and proximal limb muscles compared to the distal mus- conflicting and disruptive behavior of the alien hand
cles controlling the wrist and fingers, even though these whose motivations remain inaccessible to consciousness.
muscles are readily activated in the alien movements. There may be an attentional component that modulates
Generally, these alien behaviors appear in the hand con- the appearance of these episodes of self-oppositional
tralateral to the damaged hemisphere regardless of hemi- behavior since intermanual conflict is observed more
spheric dominance. When the dominant hemisphere is frequently when the patient is fatigued, stressed, or is
damaged, in addition to alien hand behavior in the engaged in effortful multitasking activity. Occasionally,
86 A Alien Hand Syndrome
rather than acting in a contradictory manner, the two from objects approaching the hand in distinct contrast to
hands are observed to be engaged in two different and the reaching and grasping behaviors that are seen in the
entirely unrelated activities as if being guided by frontal variant. The alien hand may assume a characteris-
completely separate and independent intentions. tic posture of fully extended digits with the palmar surface
In a dramatic example of this behavior, one patient retreating from environmental objects, an observation
was observed to initiate smoking a cigarette by pulling the that has been labeled an instinctive avoidance reaction
cigarette out of the package and placing it in her mouth by Denny-Brown and has also been referred to as the
with the controlled dominant hand followed by the alien parietal hand. At times, grasping behaviors can also be
nondominant hand, rather than beginning to light the observed with the posterior variant.
cigarette, suddenly reaching up, pulling it out of the her Alien hand behavior has also been reported in associ-
mouth, and throwing it across the room. Astonished, the ation with subcortical thalamic infarction. In addition to
patient reasoned that perhaps the alien hand was not in having been observed in the context of stroke, tumors and
favor of her smoking! surgical sectioning of the corpus callosum, alien hand
The callosal and frontal variants are often seen in behavior has been described in association with a number
combination with a corresponding overlap of observed of progressive neurodegenerative disorders including cor-
behaviors. For example, following cerebral infarction in ticobasal degeneration, multiple sclerosis, spongiform
the territory of the anterior cerebral artery, there may be encephalopathy, and Alzheimers disease. When AHS
ischemic injury to both the medial frontal lobe and the appears with these progressive encephalopathies, it is
corpus callosum. In this circumstance, there may be both usually accompanied by various forms of motor apraxia,
visually directed reaching and grasping alien behaviors along with multiple additional cognitive disturbances
in the limb contralateral to the area of injury as well as characteristic of the particular condition.
episodes of intermanual conflict. However, a clear differ-
entiation between apparent intermanual conflict due to
attempts to restrain alien behaviors associated with the Epidemiology
frontal variant (e.g., as in the case of self-grasping
described below), and true intermanual conflict, in While there are no epidemiologic studies of the occur-
which the two hands are directed toward independently rence of AHS variants in association with acquired brain
contradictory purposes, may be difficult to differentiate. damage, it can be assumed that this is a relatively rare but
striking manifestation of neurologic pathology.
Posterior or Sensory Form

Pathophysiology and Prognosis
Neuroanatomy
The third identified variant of AHS is the posterior or Adapting the concept developed by Derek Denny-Brown
sensory form, which appears most often with a parietal regarding positive and negative cortical tropisms based in
or parieto-occipital focus of circumscribed damage. As in the parietal lobe and frontal lobes (Denny-Brown, 1956,
the frontal variant, the alien behavior appears in the hand 1966), respectively, a heuristic model has been proposed.
contralateral to the damaged hemisphere. In this model, there are two separable but interactive
components of an intrahemispheric premotor intentional
Clinical Presentation system that modulate the output of the PMC of the
In the patient with the posterior variant, the movement of hemisphere and its direct influence over the spinal
the affected alien limb is typically less organized and often motor nuclei innervating the muscles of the contralateral
has an ataxic instability particularly with visually guided distal upper limb (Goldberg and Bloom, 1990).
reaching. The limb also may show proprioceptive sen- The first component is a posterolateral premotor
sory impairment with hypesthesia, so that kinesthetic system (PLPS) based in the posterior parietal region that
impairment limits the monitoring of limb position. Visu- is involved in generating movements of the contralateral
al field deficits as well as hemi-inattention may be seen on arm and hand that are directed toward external objects
the same side as the alien hand. In this variant, the limb and are responsive to externally sensed contingencies. The
may be observed to lift up off of support surfaces invol- second component is an anteromedial premotor system
untarily and levitate in the air seemingly to avoid con- (AMPS) based in the medial frontal region that is
tact with support surfaces. It may also be seen to withdraw involved in generating movements in the contralateral
upper limb that are directed by an internal action plan commissures linking the two cerebral hemispheres at the
A
and driven by an anticipatory model of future contingen- subcortical level. Thus, conscious human agency can be
cies. It presumably is also involved in activating with- thought of as emerging through the linked and coordinated
drawal movements that pull the limb back and away action of at least four major premotor systems, two in each
from external stimuli. It also functions to withhold action hemisphere. The overall general configuration of this heu-
directly responsive to surrounding objects through inhibi- ristic model is shown in Fig. 1.
tory influence over the PLPS. These two systems are pro- It is proposed that AHS, in its different variants de-
posed to be in a metastable balance through mutually scribed above, appears due to damage either to the corpus
inhibitory influence. Together, these two hemispheric callosum in the callosal variant (Fig. 2), the AMPS of
agency systems form an integrated intrahemispheric agency either hemisphere in the frontal variant (Figs. 3 and 4),
system. Furthermore, each intrahemispheric agency system or to the PLPS of either hemisphere in the posterior
has the capability of acting autonomously in its control over variant (Figs. 5 and 6).
the contralateral limb, although overall unitary control by a The common factor in these anomalous conditions is
conscious agent is maintained through interhemispheric the relative sparing of the PMC region controlling the
communication between these systems via the corpus contralesional alien hand, while the premotor regions
callosum at the cortical level and other interhemispheric involved in the intentional selection of action and the
Alien Hand Syndrome. Figure 1. Heuristic model for understanding alien hand syndrome (AHS).
Abbreviations: RH, Right Hemisphere; LH, Left Hemisphere; CC, Corpus Callosum; PMC, Primary Motor Cortex; AMPS,
Anteromedial Premotor System; PLPS, Posterolateral Premotor System.
This view is shown looking down from above the vertex with the face located at the top of the drawing and the back of the
head noted at the bottom of the drawing, the left side to the left and the right side to the right of the diagram. The open
bidirectional arrow between the AMPS and the PLPS indicates an interaction characterized by mutually interactive inhibition
creating a complementary metastable control of the contralateral hand. Solid arrows indicate facilitatory connections or
connections that maintain synchrony and coherence between the connected structures. Output from PMC is directed primarily
to the contralateral limb with some less potent ipsilateral projections illustrated by a dotted line. See text for further detail.
Note that the left hemisphere is stippled in the diagram designating this as the dominant hemisphere for most individuals in
correspondence with a dominant right hand
Alien Hand Syndrome. Figure 2. The callosal variant of AHS. Theoretical explanatory model for the alien behaviors observed in
callosal damage. In this instance, there are findings consistent with callosal apraxia in addition to intermanual conflict associated
with the complete separation of the two intrahemispheric premotor intentional control systems. The limbs appear to be
operated by two relatively autonomous control systems. The intentional premotor system in the dominant hemisphere is linked
to the language system while that of the nondominant hemisphere is separated from it. The dominant hand is understood as
connected to self while the nondominant hand is not. The alien hand in this variant is the nondominant hand. This is indicated by
the stippled overlay on the left nondominant hand
inhibition of automatic behaviors in response to external conscious voluntary control. The patient may become
factors are impaired. fearful that they will be held accountable for consequences
A recent fMRI study of cortical activation patterns of an action of the alien hand over which they do not feel
associated with alien and non-alien movement has control. The patient may display auto-criticism com-
demonstrated that alien movement is in fact characterized plaining that the alien hand is not doing what it has been
by isolated activation of PMC without concomitant acti- told to do and is therefore characterized as disobedient,
vation of intrahemispheric premotor regions, while vol- wayward, or evil. They may even physically strike the
untary behavior includes the activation of PMC in concert alien hand with the controlled hand as a punishment
with activation of intrahemispheric premotor regions intended to discourage its wayward behavior, or constrain
(Assal, Schwartz, & Vuilleumier, 2007). the movement of the alien hand by grasping tightly onto it
with the controlled hand (self-grasping). They may
verbally address and instruct the hand as if it were an
Neuropsychology and Psychology unruly child acting autonomously and in need of correc-
of AHS tion. Conversely, they may respond to these contrary
actions with amusement.
The presence of AHS can cause the patient significant Given the predicament created, the patient may devel-
psychological distress as the hand seems to possess the op depersonalization and dissociate themselves from the
capability for acting autonomously, independent of their unintended actions of the hand. They often choose to
Alien Hand Syndrome. Figure 3. The nondominant frontal Alien Hand Syndrome. Figure 5. The nondominant posterior
variant of AHS. Theoretical explanatory model for the alien variant of AHS. Theoretical explanatory model for the alien
behaviors observed in the frontal variant associated with behaviors observed in the posterior variant associated with
damage to the AMPS of the nondominant hemisphere. In this damage to the PLPS of the nondominant hemisphere. In this
case, the contralesional nondominant hand develops alien case, the contralesional nondominant hand develops alien
hand findings due to the release by disinhibition of the hand findings due to the release by disinhibition of behaviors
reaching and grasping behaviors driven from the dominant driven from the nondominant AMPS
PLPS
Alien Hand Syndrome. Figure 4. The dominant frontal

variant of AHS. Theoretical explanatory model for the alien
behaviors observed in the frontal variant associated with
damage to the AMPS of the dominant hemisphere. In this Alien Hand Syndrome. Figure 6. The dominant posterior
case, the contralesional dominant hand develops alien hand variant of AHS. Theoretical explanatory model for the alien
findings due to the release by disinhibition of the reaching behaviors observed in the posterior variant associated with
and grasping behaviors driven from the dominant PLPS. In damage to the PLPS of the dominant hemisphere. In this case,
addition, spontaneous expressive language initiation is the contralesional dominant hand develops alien hand
impaired due to the role of the AMPS of the dominant findings due to the release by disinhibition of behaviors
hemisphere in the initiation of verbal output driven from the dominant AMPS
identify an external alien source for the voluntary con- evaluated for evidence of a grasp reflex with both tactile and
trol of the hand, or assign a distinct personality to the visual stimulation. The ability to release objects that have
hand as a way of seeking a satisfactory narrative to explain been grasped should also be assessed. Evaluation for callosal
this perplexing situation. apraxia and impairment of interhemispheric transfer of
From a psychological perspective, it is helpful to information should be included. When the posterior vari-
counsel the patient regarding the organic basis of their ant of AHS is suspected, a visual field assessment and
problem and provide assurance that there is a rational somatosensory examination of the affected limb should be
explanation for their concerns and that there is evidence completed as well as assessment for hemi-inattention. Evi-
that these problems can be treated and may gradually dence of a tendency to withdraw the limb from tactile and
improve over time. visual stimulation should also be elicited and noted.
In AHS, different regions of the brain are able to
command purposeful limb movements, without generat-
ing the conscious feeling of self-control over these move- Treatment
ments. There is thus a dissociation between the actual
execution of the physical movements of the limb and the There is no definitive specific treatment for AHS but a
process that produces an internal sense of voluntary con- number of different rehabilitative approaches have been
trol over the movements. This latter process, impaired in described. Furthermore, in the presence of unilateral
AHS, normally produces the conscious sensation that damage within a single cerebral hemisphere, there is
movement is being internally initiated and produced by often a gradual reduction in the frequency of alien beha-
an active self. Presumably, this process differentiates viors observed over time and a gradual restoration of
between re-afference (i.e., the return of kinesthetic sen- voluntary control over the affected hand. This suggests
sation from the self-generated active limb movement) that neuroplasticity in the bihemispheric and subcortical
and ex-afference (i.e., kinesthetic sensation generated brain systems involved in voluntary movement produc-
from an externally produced passive limb movement). tion can serve to reestablish functional connection be-
It may do this by giving rise to a parallel output signal tween the executive production process and the internal
from motor regions, a so-called efference copy. The self-generation and volitional registration process. Exactly
efference copy is then translated into a corollary dis- how this may occur is not well understood but could
charge, which conveys the expected re-afferent sensory involve a reorganization within residual elements of the
response from the commanded movement. The corollary intrahemispheric premotor systems both at the cortical
discharge can then be used in somatosensory cortex to and subcortical levels. In addition, some degree of ex-
distinguish re-afference from ex-afference and thus differ- panded participation of the intact ipsilateral hemisphere
entiate a self-produced active movement from a move- may be involved in the recovery process by extending
ment resulting from external forces. AHS may thus ipsilateral motor projections.
involve impaired production and transmission of either Different strategies can be used to reduce the interfer-
an efference copy or a corollary discharge signal. ence of the alien hand behavior in the ongoing coherent
controlled actions being performed by the patient. In the
frontal variant, an object such as a cane can be placed in
Evaluation the grip of the alien hand so that it does not reach out to
grasp onto other objects, thus impeding the patients
Evaluation of the patient with AHS involves careful forward progress during walking. In another approach,
observation of limb movement in various naturalistic voluntary control of the limb is developed by training the
contexts, along with reports from the patient regarding patient to perform a specific task with the alien limb, such
their sense of control over these movements. The relative as moving the alien hand to contact a specific object or a
dependence of movement on external context should be highly salient environmental target. Through training to
evaluated through assessment for utilization behaviors enhance volitional control, the patient can effectively
elicited by the presentation of external objects commonly override the alien behavior when it occurs. Recognizing
encountered in daily activities. A phenomenologic ap- that alien behaviors in the frontal variant are often sus-
proach to assessing and documenting the motor behavior tained by tactile input, another approach involves simul-
and linking it to introspective report from the patient is taneously muffling the actions of the alien hand and
essential. Not only should the verbal reports of the patient limiting sensory feedback by placing it in a restrictive
be noted, but also the associated affect. The limb should be cloak such as a specialized soft foam hand orthosis or,
Allele A 91
alternatively, an everyday oven mitt. Of course, this

ALL A
then limits the degree to which the hand can engage in
functional goals. It may also be possible to develop im-
proved participation of ipsilateral hemispheric premotor Acute Lymphoblastic Leukemia
mechanisms by engaging the patient in coordinated bi-
manual activities that necessitate cooperative coordina-
tion mechanisms within residual intact components of
the motor control system in both hemispheres.
Allele
Cross References J OHN D E LUCA
Anterior Cingulate West Orange, NJ, USA
Apraxia
Corpus Callosum
Environmental Dependency Definition
Movement Disorder
Utilization Behavior Allele is an alternate form of a gene, which is the basic unit
of inheritance. A gene is located at a particular site on the
chromosome, and can have several alleles for that locus.
For example, A, B, and O are different alleles for the ABO
blood-type marker locus of a gene. Alleles greatly influ-
ence the expression of physical and behavioral phenotypes
Assal, F., Schwartz, S., & Vuilleumier, P. (2007). Moving with or without
will: Functional neural correlates of alien hand syndrome. Annals of
or traits such as eye color. For instance, the apolipopro-
Neurology, 62, 301306. tein E (APoE) gene is a well-known risk factor for devel-
Biran, I., & Chatterjee, A. (2004). Alien hand syndrome. Archives of oping Alzheimers disease. The APoE gene has three
Neurology, 61, 292294. common alleles: epsilon 2, epsilon 3, and epsilon 4.
Denny-Brown, D. (1956). Positive and negative aspects of cerebral corti-
There is some evidence that carriers of the APoE epsilon 4
cal functions. North Carolina Medical Journal, 17, 295303.
Denny-Brown, D. (1966). The cerebral control of movement. Liverpool:
allele are at a greater risk for the development of
Liverpool University Press. Alzheimers disease. In contrast, the APoE epsilon 3 allele
Frith, C. D., Blakemore, S.-J., & Wolpert, D. M. (2000). Abnormalities in has been suggested as a protective factor in the develop-
the awareness and control of action. Philosophical Transactions of the ment of Alzheimers disease (Plomin, Defries, Craig, &
Royal Society of London, 355, 17711788.
McGuffin, 2003).
Giovanetti, T., Buxbaum, L. J., Biran, I., & Chatterjee, A. (2005). Reduced
endogenous control in alien hand syndrome: Evidence from natu-
ralistic action. Neuropsychologia, 43, 7588.
Goldberg, G., & Bloom, K. K. (1990). The alien hand sign. Localization,
lateralization, and recovery. American Journal of Physical Medicine Cross References
and Rehabilitation, 69, 228238.
Goldberg, G. (1992). Premotor systems, attention to action and beha- Alzheimers Disease
vioural choice. In J. Kien, C. McCrohan, & W. Winlow (Eds.), Apolipoprotein E (ApoE)
Neurobiology of motor programme selection. New approaches to
Chromosome
mechanisms of behavioural choice (pp. 225249). Oxford: Pergamon.
Ong Hai, B. G., & Odderson, I. R. (2000). Involuntary masturbation as a Deoxyribonucleic Acid (DNA)
manifestation of stroke-related alien hand syndrome. Archives of Gene
Physical Medicine and Rehabilitation, 79, 395398. Phenotype
Pack, B. C., Stewart, K. J., Diamond, P. T., & Gate, S. D. (2002). Posterior-
variant alien hand syndrome: Clinical features and response to
rehabilitation. Disability and Rehabilitation, 24, 817818.
Scepkowski, L. A., & Cronin-Golomb, A. (2003). The alien hand: Cases,
categorizations, and anatomical correlates. Behavioral and Cognitive
Neuroscience Reviews, 2, 261277.
Sumner, P., & Husain, M. (2008). At the edge of consciousness: Auto- Plomin, R., Defries, J. C., Craig, W., & McGuffin, P. (2003). Behavioral
matic motor activation and voluntary control. Neuroscientist, 14, genetics in the postgenomic era. Washington, DC: American Psycho-
474486. logical Association.
92 A Allesthesia
Current Knowledge
Allesthesia
Allokinesia is often associated with neglect syndromes,
J OHN E. M ENDOZA usually involving damage to the right hemisphere. It is
Tulane University Medical Center the motor counterpart of alloesthesia. Typically, a patient
New Orleans, LA, USA moves the right limb in response to a request to move
the left limb or moves towards the right, away from the
neglected side, when asked to move toward the neglected
Definition side. In animal models, the phenomena has been
associated with frontal, arcuate gyrus lesions (Heilman,
Misperception of the location of a stimulus. Although it Valenstein, Day, & Watson, 1995) and disconnections of
can occur in other modalities, it is most commonly frontal and posterior parietal cortices (Burcham, Corwin,
elicited by tactile stimulation and is often seen in the Stoll, & Reep, 1997).
presence of other symptoms of unilateral asomatog-
nosia. If a tactual stimulus is applied to the side of
the body contralateral to a hemispheric lesion, the alles-
thetic patient may perceive the nature of the stimulus Cross References
correctly but identify it as being applied to the compara-
ble area on the opposite (unaffected) side of the body. Allesthesia
In some instances the stimulus may be perceived as being Neglect Syndrome
on the same side of the body to which it was applied,
but displaced significantly from the point of the actual
stimulation (usually toward the midline). When present, References and Readings
this phenomenon likely results from post-rolandic
(parietal) lesions of the right rather than the left hemi- Burcham, K. J., Corwin, J. V., Stoll, M. L., & Reep, R. L. (1997).
sphere. More rarely it has been associated with brainstem Disconnection of medial agranular and posterior parietal cortex
lesions. produces multimodal neglect in rats. Behavioural Brain Research,
86(1), 4147.
Heilman, K. M., Valenstein, E., Day, A., & Watson, R. (1995). Frontal lobe
neglect in monkeys. Neurology, 45(6), 12051210.
Cross References
Asomatognosia
Alpha Rhythm
C INDY B. I VANHOE , N ATASHA K. E ADDY
Baylor College of Medicine
Allokinesia Houston, TX, USA
D OUGLAS I. K ATZ
Boston University School of Medicine Synonyms
Boston, MA, USA
Alpha waves; Bergers waves
Definition
Definition
This phenomenon refers to a motor response in
the wrong limb, contralateral to the requested side, Electromagnetic oscillations in the frequency range of
sometimes opposite to the direction requested. 812 Hz arising from synchronous and coherent electrical
Alprazolam A 93
activity of the thalamic pacemaker cells in the human

Alprazolam A
brain. Also called Bergers wave.
J OHN C. C OURTNEY
Current Knowledge New Orleans, LA, USA
Alpha waves are believed to arise from the white matter

of the occipital lobes. They increase during periods of Generic Name
relaxation with eyes closed. Alpha waves are thought
to represent activity in the visual cortex and are asso- Alprazolam
ciated with feelings of calmness and relaxation. Alpha
waves increase when eyes are closed and during medita-
tion and are associated with creativity and mental Brand Name
coordination.
Xanax, Xanax XR
References and Readings Class
Bragatti, J. A., De Moura Cordova, N., Rossato, R., & Bianchin, M. M. Benzodiazepine
(2007). Alpha coma and locked-in syndrome. Journal of Clinical
Neurophysiology, 24(3), 308.
Min, B. K., Busch, N. A., Debener, S., Kranczioch, C., Hansimayr, S., Proposed Mechanism(s) of Action
Engel, A. K., et al. (2007). The best of both worlds: Phase reset
of human EEG alpha activity and additive power contribute to
ERP generation. International Journal of Psychophysiology, 65(1), Binds to benzodiazepine receptors at the GABA-A ligand-
5868. gated channel, thus allowing for neuronal hyperpolariza-
tion. Benzodiazepines enhance the inhibitory action of
GABA via boosted chloride conductance.
Alpha Waves Indication

Generalized Anxiety and Panic Disorders
Alpha Rhythm
Off Label Use
Other anxiety disorders, irritable bowel syndrome, in-

Alphabetic Principle somnia, adjunctive treatment in mania and psychosis,
premenstrual dysphoric disorder.
Phonics
Side Effects
Serious
Alpha-Synuclein Inclusions
Respiratory depression, hepatic dysfunction (rare), renal
Lewy Bodies dysfunction and blood dyscrasias, grand mal seizures
94 A ALS
Common
Altered Testing Procedures
Sedation, fatigue, depression, dizziness, memory pro-
blems, disinhibition, confusion, ataxia, slurred speech Modified Testing

Alternate Forms
Physicians Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson
PDR. Polymorphism
Stahl, S. M. (2007). Essential psychopharmacology: The prescribers guide
(2nd ed.). New York, NY: Cambridge University Press.
Additional Information Alternate Test Forms
Drug Interaction Effects: http://www.drugs.com/drug_interactions.html

K YLE E. F ERGUSON 1, G RANT L. I VERSON 2
1
Drug Molecule Images: http://www.worldofmolecules.com/drugs/ University of British Columbia
Free Drug Online and PDA Software: www.epocrates.com Vancouver, BC, Canada
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs. 2
University of British Columbia & British Columbia
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList Mental Health & Addiction Services
Pill Identification: http://www.drugs.com/pill_identification.html
Vancouver, BC, Canada
Synonyms
ALS
Equivalent forms; Parallel forms
Anterolateral System
Definition
ALSFRS Alternate test forms are designed to avoid or reduce
content- or item-specific practice effects that are associated
Amyotrophic Lateral Sclerosis Functional Rating Scale with repeated administrations of the same neuropsycho-
logical test(s) (Benedict & Zgaljardic, 1998). Examination
of the manuals for many intellectual and neuropsycholog-
ical tests illustrate that practice effects are common,
ALSFRS-R especially over brief retest intervals (e.g., days or weeks).
Regarding test construction, alternate test forms should
Amyotrophic Lateral Sclerosis Functional Rating Scale include the same number of items, and the items should
be of equivalent difficulty. Moreover, the test instructions,
time limits, examples, and format should be identical to
the original instrument developed during standardiza-
Alterations tion, to reduce measurement error (Jackson, 2009). Of
course, measurement error can never be eliminated. For
Polymorphism example, content-sampling error and time-sampling error
inherent in all testretest paradigms are always
concerns in developing alternate test forms (Strauss,
Sherman, & Spreen, 2006). Additionally, alternate test
Altered forms cannot control other factors such as positive
carry-over effect (i.e., developing better test-taking stra-
Transgenic tegies), familiarity with the testing context (i.e., novelty
Alternate Test Forms A 95
effects), performance anxiety, and regression to the mean, provide alternate test forms. With the above caveats in
A
among others (Benedict & Zgaljardic, 1998; Busch, mind, alternate test forms can be useful in serial
Chelune, & Suchy, 2006; Salinsky, Storzbach, Dodrill, & neuropsychological evaluations.
Binder, 2001). This might, to some extent, explain why
some studies show that alternate test forms reduce or
eliminate practice effects, whereas other studies do not. Cross References
Item Response Theory

Current Knowledge Reliable Change Index
Test Construction
Alternate test forms are developed by administering an Test Reliability and Validity
equivalent test comprising items of similar difficulty
to the same group of examinees or normative sample,
shortly before or after being administered the original References and Readings
test form. Scores from the two forms are then correlated
(This is called alternate form reliability, or equivalent or Benedict, R. H., & Zgaljardic, D. J. (1998). Practice effects during repeated
parallel form reliability), which yields a reliability coeffi- administrations of memory tests with and without alternate
forms. Journal of Clinical and Experimental Neuropsychology, 20(3),
cient otherwise known as the coefficient of equivalence.
339352.
If the original and alternate test forms are truly equivalent, Benedict, R. H. B. (2001). Brief visuospatial memory test - revised. Odessa,
then there would be (theoretically) a one-to-one corre- FL: Psychological Assessment Resources.
spondence between the two sets of scores (Petersen, 2008). Brandt, J., & Benedict, R. H. B. (2001). Hopkins verbal learning
Moreover, their means and variances would also be very test-revised. Odessa, FL: Psychological Assessment Resources.
Busch, R. M., Chelune, G. J., & Suchy, Y. (2006). Using norms in neuro-
similar. Therefore, the coefficient of equivalence should be
psychological assessment. In D. K. Attix & K. A. Welsh-Bohmer
high (i.e., >0.80; Sattler, 2001). Of course, though they (Eds.), Geriatric neuropsychology: Assessment and intervention
appear similar, the two forms are often not of equivalent (pp. 133157). New York: Guilford.
difficulty, or otherwise parallel. Thus, in the absence Dorans, N. J., & Holland, P. W. (2000). Population invariance and
of employing special empirical procedures like test equitability of tests: Basic theory and the linear case. Journal of
Educational Measurement, 37, 281306.
equating, which fine-tune the test construction process
Jackson, S. L. (2009). Research methods and statistics: A critical thinking
(Petersen, 2008, p. 99), the two forms cannot be used approach (3rd ed.). Belmont, CA: Wadsworth Cengage Learning.
interchangeably. Kolen, M. J., & Brennan, R. L. (2004). Test equating, scaling, and linking:
Test equating refers to a class of statistical concepts Methods and practices (2nd ed.). New York: Springer.
and procedures that adjust for differences in difficulty Ormea, D., Reeb, M. J., & Riouxc, P. (2001). Premorbid IQ estimates from
a multiple aptitude test battery: Regression vs. equating. Archives of
level on alternate test forms (Please note that these
Clinical Neuropsychology, 16, 679688.
procedures adjust for differences in test difficulty, not Petersen, N. S. (2008). A discussion of population invariance of equating.
differences in content (see Kolen & Brennan, 2004)), so Applied Psychological Measurement, 32, 98101.
that the forms can be used interchangeably (see Kolen & Petersen, N. S., Kolen, M. J., & Hoover, H. D. (1989). Scaling, norming,
Brennan, 2004, pp. 23, for a discussion of this procedure; and equating. In R. L. Linn (Ed.), Educational measurement (3rd ed.,
pp. 221262). New York: Macmillan.
White & Stern, 2003). Test equating establishes, empiri-
Salinsky, M. C., Storzbach, D., Dodrill, C. B., & Binder, L. M. (2001).
cally, a relationship between raw scores on two test forms Test-retest bias, reliability, and regression equations for neuropsy-
that can then be used to express the scores on one form in chological measures repeated over a 1216-week period. Journal of
terms of the scores on the other form (Petersen, Kolen, & the International Neuropsychological Society, 7(5), 597605.
Hoover, 1989, p. 242; see also Dorans & Holland, 2000; Sattler, J. M. (2001). Assessment of children: Cognitive applications
(4th ed.). San Diego: Jerome M. Sattler.
Petersen, 2008). Common types of test equating are Item
Stern, R. A., & White, T. (2003). Neuropsychological assessment battery.
Response Theory (IRT), linear, and equipercentile Lutz, FL: Psychological Assessment Resources.
(Ormea, Reeb, & Riouxc, 2001). Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A compendium of
The Neuropsychological Assessment Battery (Stern & neuropsychological tests: Administration, norms, and commentary
White, 2003), Hopkins Verbal Learning Test-Revised (3rd ed.). New York: Oxford University Press.
White, T., & Stern, R. A. (2003). Neuropsychological assessment battery:
(Brandt & Benedict, 2001), Brief Visuospatial Memory
Psychometric and technical manual. Lutz, FL: Psychological
Test-Revised (Benedict, 2001), and Wide Range Achieve- Assessment Resources.
ment Test-Fourth Edition (Wilkinson & Robertson, 2006) Wilkinson, G. S., & Robertson, G. J. (2006). Wide range achievement test
are several examples of tests (or test batteries) that (4th ed.). Lutz, FL: Psychological Assessment Resources.
96 A Alzheimer, Alois (18641915)
Short Biography
Alzheimer, Alois (18641915)
In the German municipality Marktbreit, Alois Alzheimer
K ATHERINE S. M C C LELLAN 1, A NNA B ACON M OORE 2 was born on June 14, 1864 to Eduard and Theresia
1
Atlanta Veterans Affairs Medical Center Alzheimer. Eduard, a Royal Notary, provided his family
Decatur, GA, USA with a comfortable upbringing. Although Alois had only
2
Emory University School of Medicine an older brother when he was born, six more siblings
Atlanta, GA, USA followed him. Alois spent the first four years of his
education at Catholic school in Marktbreit, until his
family left the area to find a new home with superior
Major Appointments educational opportunities for the children. The familys
chosen residence was in Aschaffenburg, and in 1874, Alois
Intern Mental Asylum at Frankfurt am Main, 1888 moved there in order to study at the Royal Humanistic
1895 Gymnasium. Alois completed his high-school degree in
Senior Physician Mental Asylum at Frankfurt am 1883 with excellent grades. He then decided to study
Main, 18951903 medicine because of his aptitude and fondness for the
Researcher Royal Psychiatric Clinic and District natural sciences, as well as a sense of duty to mankind.
Mental Asylum, Munich, 19031912 He enrolled at the Royal Friedrich Wilhelm Univer-
Assistant Professor Ludwig-Maximilian University, sity in Berlin for the 18831884 winter semester. In his
Munich, 19041912 psychiatry lecture there, he learned of John Conollys
Chief Physician Royal Psychiatric Clinic and District nonrestraint principle. Also called open treatment, the
Mental Asylum, Munich, 19061909 nonrestraint principle proposed the novel view that the
Professor of Psychiatry Psychiatry Clinic of Silesian mentally ill should be treated with a minimal amount of
Friedrich-Wilhelm University, Breslau, 19121915 physical constraint. Although Berlin was the medical
capital of Germany, Alois disliked Berlin and its
distance from his family. Therefore, he was transferred
Major Honors and Awards to the University of Wurzburg (Lower Franconia,
Germany), where his older brother was studying. As an
Extraordinary Professor, Ludwig-Maximilian Univer- aside, due to the influence of his older brother, Alois
sity (1909) joined and later held several officer positions in the
Geheimer Ministerialrat (Cabinet Councillor) (1915) Franconian Corps. His histology professor, Alfred von
Kolliker, gave him his first experience with microscopes
and staining techniques, which lead to his passion for
Landmark Clinical, Scientific, and forensic psychiatry. In the fall of the following year,
Professional Contributions Alois left to spend his winter semester at the Eberhard
Karls University of Tubingen. He returned in 1887 to the
Alois Alzheimer was both an excellent clinician and a Wurzburg Anatomical Institutes department of micros-
notable researcher. He is best remembered for being copy to write his doctoral thesis, On the Earwax
the first to definitively describe the symptoms and Glands. The intricate figures he presented in the
cerebral lesions of the disease now known as Alzhei- paper, as in all his papers, were proof of how scrupu-
mers Disease. Nonetheless, his contributions to sci- lously he conducted his research and clinical work. With
ence and medicine did not begin, nor do they end, the completion of his thesis, Alois Alzheimer received
there. He was one of the leaders of the movement to his doctor of medicine degree. He passed the state med-
implement the nonrestraint principle (explained ical examination and was awarded a license to practice
more fully below) in asylums. His neurohistological medicine in 1888.
work advanced the idea that psychiatric diseases were Shortly thereafter, he became a personal physician to a
biological in origin. And, through his roles as both mentally ill woman and traveled with her for five months.
doctor and scientist, he contributed to our under- Emil Sioli, the director of the Municipal Asylum for the
standing of a variety of conditions such as cerebral Insane and Epileptic in Frankfurt am Main had advertized
atherosclerosis, alcoholism, and general paresis. for an intern, specifically hoping for a competent doctor
Alzheimer, Alois (18641915) A 97
who was also adept with a microscope. Upon his return, reputations of all its doctors. But above all, in 1901,
A
the 24-year old Dr. Alzheimer was hired immediately. Alzheimer met the patient who would immortalize his
Dr. Franz Nissl also was hired as senior physician for the name: Auguste D. Auguste had been admitted to the
asylum. Nissl not only became one of Alzheimers closest asylum because of delusional and excessively forgetful
friends, but also taught him a powerful staining technique behavior. Although at admission she was disoriented,
for highlighting neuronal cell bodies (the Nissl stain), that anxious, and suspicious, over time she became unruly
helped Alzheimer achieve success in his histological stud- and disruptive. Alzheimer was particularly intrigued by
ies. Siolis main goal for the asylum was to fully employ her case for the duration of her stay in the hospital.
the nonrestraint principle. Alzheimer was particularly Alzheimers second child, Hans, was born in 1896,
skilled at gaining the trust of patients through conversa- and his third, Maria, was born in 1900. However, the
tion, and he often documented these conversations. lavish lifestyle he had lived with Cecilie ended when she
The dialogues often were central to diagnosing a patient, died in February 1901. Alzheimers sister, Elisabeth, took
and even more so to research. His talent in clinical inter- over his household. Though she was strict, she became an
viewing was such that clinicians who later read his notes integral part of the family. Without Cecilie, Alzheimer no
had sufficient information to evaluate his opinions and to longer had a reason to stay in Frankfurt. After his appli-
make their own diagnoses. Alzheimer drew on his micros- cation to be director of a regional asylum was rejected,
copy and forensic psychiatry training, to do histological he joined Nissl in Heidelberg in 1903 and went to work
investigations into the physical origins of psychiatric for Emil Kraepelin. The group he joined there was an
disorder. In Frankfurt, his topics of study included epi- international team of researchers. Later that same year,
lepsy, senile dementia, criminal minds, and a variety of Kraepelin was named director of the Royal Psychiatric
psychoses. He established himself as a well-rounded Clinic and the District Mental Asylum in Munich.
physician by publishing papers on a wide variety of topics. Alzheimer followed him, but was not paid in Munich
Aside from his duties as a physician and researcher, he also due to the lack of a position for him, and also his
appeared as an expert before courts and presented at desire to manage his own time. Despite his absence
many scientific meetings. While at Frankfurt, Alzheimer from Frankfurt, Alzheimer still received updates on
became an expert on general paresis, which later became Auguste D.
the subject of his postdoctoral thesis. By this point, Alzheimers thesis on general paresis
In Algeria, a personal physician who had been was finished, but because he moved twice in such a
traveling with a man suffering from general paresis sent short time, he had not yet turned it in. Alzheimer submit-
a telegram to Alzheimer in 1892 to request that he treat ted his postdoctoral thesis to the Ludwig-Maximilian
the worsening patient. Alzheimer obliged and went to University in Munich with the hopes of gaining associate
North Africa. He intended to bring the patient back to professorship. In it, he published not only his clinical
his hospital in Germany, but the patient died before dialogues, but also his postmortem histological findings.
reaching Germany, leaving his wife, Cecilie, a widow. With this paper, he asserted that histological exam-
Alzheimer and Cecilie became close friends, and eventu- inations could definitively show the presence of general
ally the widow asked him to marry her. They were married paresis. Until then, few doctors suspected that syphilis was
in April 1894 in the registry office of Frankfurt. Because a cause of general paresis, but shortly thereafter the link
Cecilie was Jewish, she had to convert to Catholicism between the two was found. His work was surpassed by
before the two could be married by the church in Febru- the discovery of a way to diagnose syphilis, without
ary 1895. On March 10, 1895, their first child, Gertrud, resorting to autopsies. In August 1904, he joined the
was born, and Dr. Nissl was chosen to be her godfather. universitys medical faculty.
But Nissl soon moved to work with Emil Kraepelin in Because of his experience at remodeling the Frankfurt
Heidelberg. Nissls departure created room for Alzheimer clinic, Alzheimer was fundamental in finishing the plans
to be promoted to senior physician within Siolis asylum. for the new Munich clinic. He furnished his anatomic
Also that year, to lessen the overcrowding of the main laboratory with the best equipment and the brightest
hospital, a new branch asylum opened. With this addi- students many of whom went on to make great con-
tion, Sioli and Alzheimer furthered their goal of fully tributions to science, including Ugo Cerletti electrical
implementing the nonrestraint principle by instituting shocks to generate convulsions, Hans Gerhard Creutzfeldt
duration baths rather than isolation. The asylum became and Alfons Jakob Creutzfeldt-Jakob disease, Frederic
known as a revolutionary clinic, and it elevated the Lewy Lewy bodies, and others. Alzheimer was made
98 A Alzheimer, Alois (18641915)
chief physician in 1906, a paid position, but also one that Though he returned to work, his health had not im-
took away much of his time in the laboratory. proved. This did not impede his ability to make signifi-
Two topics that consumed Alzheimer in Munich were cant contributions to science: in 1913 he found the
psychiatric symptoms resulting from pathological anato- syphilis pathogen in the central nervous system of a
my and classification of mental illnesses by etiology. The patient with general paresis.
latter faced much opposition from the scientific commu- After a long illness, Alois Alzheimer died on December
nity. Yet, the most opposition he ever faced was his pre- 19, 1915 from a heart condition and kidney failure.
sentation of the Auguste D. case. Auguste D. had always Though no one immediately took over his pursuit of an
fascinated Alzheimer. He had paid special attention to her, understanding of Alzheimers disease, people recom-
taking copious notes about their conversations. When he menced research on Alzheimers disease cases in the
moved away, he still received updates about her condition, 1950s. Studies of the disease began in earnest after Martin
which worsened progressively until her death. When Roths assertion in the 1960s that Alzheimers disease was
Auguste D. died in 1906, her files, brain, and spinal cord the most common cause of senile dementia. In the 1970s,
were sent to Munich. Alzheimer, along with his student Robert Katzman further propelled the surge of interest
Gaetano Perusini, immediately began examining the case. in Alzheimers disease by stating that it was one of the
In Tubingen, Alzheimer presented her case in a lecture most widespread diseases. Since then, the amount of re-
entitled On a Peculiar Severe Disease Process of the search on Alzheimers disease has increased exponentially,
Cerebral Cortex, in which he described the lesions (now resulting in multiple foundations and centers devoted
known to be neurofibullary tangles) that he believed solely to the disease that Alois Alzheimers colleagues con-
caused Augustes symptoms. Based on records from the sidered trivial.
time, his peers did not bother to ask questions, nor were
there any comments about the lecture in the minutes. He
later published the entire lecture, but still it received little Cross References
attention. He then tasked Perusini to find more patients,
similar to Auguste D. in the clinic. Perusini found four Alzheimers Dementia
cases and published an article entitled On Clinically and Alzheimers Disease
Histologically Peculiar Mental Illnesses in Advanced Age. Paresis
Another student of Alzheimers, Francesco Bonfiglio
found another case of presenile dementia, and also
published on the disease. Spurred by Bonfiglios paper, References and Readings
Kraepelin included a section on Alzheimers Disease, in
the 1910 edition of his text book Clinical Psychiatry. This Engstrom, E. (2007). Researching dementia in imperial Germany: Alois
Alzheimer and the economies of psychiatric practice. Culture, Medi-
publication is acknowledged as the origin of the term.
cine, and Psychiatry, 31, 405413.
Alzheimer himself never referred to it as Alzheimers Graeber, M., Kosel, S., Egensperger, R., Banati, R., Muller, U., Bise, K.,
Disease, though he had later publications on the disease. et al. (1997). Rediscovery of the case described by Alois Alzheimer in
Alzheimer decided to resign his post as chief physician in 1911: Historical and molecular genetic analysis. Neurogenetics,
order to devote more time to research, specifically 1, 73, 80.
Lage, J. (2006). 100 years of Alzheimers disease (19062006). Journal of
traveling to study epilepsy. Although he was no longer
Alzheimers Disease, 9, 1526.
employed by Kraepelin, Alzheimer undertook the respon- Maurer, K., & Maurer, U. (1998). Alzheimer: The life of a physician and the
sibilities of coeditor of Kraepelins Journal of Complete career of a disease. New York: Columbia University Press.
Neurology and Psychiatry. Morris, R., & Salmon, D. (2007). The centennial of Alzheimers disease
Recognition for Alzheimer and the disease carrying and the publication of Uber eine eigenartige Erkankung der
Hirnrinde by Alois Alzheimer. Cortex, 43, 821825.
his name began to spread. In 1912, the Silesian Friedrich-
Small, D., & Cappai, R. (2006). Alois Alzheimer and Alzheimers
Wilhelm University in Breslau asked him to join their disease: A centennial perspective. Journal of Neurochemistry, 99,
faculty as a full professor of psychiatry. During the move 708710.
to Breslau, Alzheimer fell ill, but nevertheless assumed his Snyder, P., & Pearn, A. (2007). Historical note on Darwins consideration
duties with vivacity. His patients and coworkers, includ- of early-onset dementia in older persons, thirty-six years
before Alzheimers initial case report. Alzheimers and Dementia,
ing Georg Stertz, Ottfried Forster, and Ludwig Mann,
3, 137142.
took notice of his kind, yet authoritative presence. In Zilka, N., & Novak, M. (2006). The tangled story of Alois Alzheimer.
1913, his health forced him to visit a private clinic. Bratisl Lek Listy, 107, 343345.
Alzheimers Dementia A 99
AD has also been classified according to the clinical

Alzheimers Dementia A
presentation of symptoms. Its most common presenta-
tion involves early and significant memory impairment.
J OA NN T. T SCHANZ , A ARON A NDERSEN Variants to this presentation have been reported in the
Utah State University literature, and they include a visual (posterior) form
Logan, UT, USA with significant impairment in higher-level processing of
visual stimuli, an aphasic form with significant language
involvement, and a frontal form with prominent im-
Synonyms pairment of executive functions. At autopsy, these var-
iants usually exhibit AD neuropathology in brain regions
Alzheimers disease; Early-onset Alzheimers disease; typically involved in the specific neuropsychological
Familial Alzheimers disease; Senile dementia of the domain (Grabowski & Damasio, 2004).
Alzheimers type
Epidemiology
Prevalence and Incidence. AD is the most common cause of
One of the leading causes of dementia in late-life, dementia in late-life, accounting for 5070% of all cases
Alzheimers disease (AD), is a progressive neurodegenera- (Malaspina Corcoran, Schobel, & Hamilton, 2008).
tive disorder characterized by a gradual onset and pro- Current estimates suggest that 4.5 million individuals
gressive course, affecting memory and other cognitive suffer from AD in the US, and projections based on
domains. For a diagnosis, the cognitive impairments population trends suggest an increase to 13.2 million by
of AD must not occur exclusively in the context of a 2050 (U.S. Department of Health and Human Services,
delirium, and must be of sufficient severity to cause 2006). The overall prevalence of AD is about 56% in
impairment in social or occupational functioning. Diag- individuals aged 65 years or older in North America, and
noses of AD (Possible or Probable AD) are based on the doubles approximately every 5 years after the age of 60.
history and presentation of clinical symptoms, evidence Estimates suggest a prevalence of 1% at age 60, 16%
of cognitive impairment, and the exclusion of other between ages 80 to 85, and 26 to 45% for those above
causes of dementia such as stroke, metabolic disorders, age 85. Incidence rates also exhibit an age-related increase.
or other conditions that may account for the cognitive Studies report differing patterns of AD prevalence and
impairment. A diagnosis of Definite AD is based upon incidence at the upper end of the lifespan, with some
postmortem neuropathological analysis and is made reporting a plateau at very old ages (age 90 or 100;
when there are sufficient numbers of senile plaques and Mendez & Cummings, 2003).
neurofibrillary tangles in specific brain regions. Risk Factors. Increasing age is among the strongest
risk factor for AD. Other risk factors include the 4 allele
of the Apolipoprotein E (APOE) gene, positive family
Categorization history (also in sporadic AD), low education (possibly
due to less neural reserve), female gender (even after
AD may be categorized according to age of onset, accounting for differential survival), and history of head
family history, or presenting clinical features. Age cate- trauma and vascular factors such as high cholesterol and
gories distinguish between senile and pre-senile onset high blood pressure. Some risk factors occurring earlier in
(onset before age 65). Classifications based on family the lifespan affect AD risk. Studies suggest that high blood
history (familial AD vs. sporadic AD) distinguish AD pressure or high serum cholesterol in midlife increases the
forms that show high heritability. Familial AD is rare, risk of AD later in life. Although inconsistent, some stud-
generally of pre-senile onset, and has been associated ies report that treatment with antihypertensive medica-
with mutations in the APP gene on chromosome 21, tions or cholesterol lowing agents reduces the risk for AD
Presenilin 1 gene on chromosome 14, and Presenilin (Soininen, Kivipelto, Laakso, & Hiltunen, 2003). Recent
2 gene on chromosome 1 (Hardy, 2003). Its transmission studies have also examined the role of insulin resistance
resembles an autosomal dominant pattern (Morris & and diabetes in AD risk. Among potential protective
Nagy, 2004). factors, data from epidemiological studies suggest a lower
100 A Alzheimers Dementia
risk of AD among women receiving hormone replacement symptom onset range from 2 to 20 years. The mean
therapy. However, a large randomized clinical trial of survival has been reported as approximately 10 years,
estrogen and estrogen + progesterone in elderly women but some studies have reported considerably shorter du-
suggested an increase in all-cause dementia in those re- ration of 3 years. More rapid rate of disease progression
ceiving the combination hormone treatment. Thus, hor- has been associated with early, prominent language im-
mone therapy is not recommended for cognitive health pairment, frontal features, and extrapyramidal signs
(Malaspina et al., 2008). Other factors under active inves- (Mendez & Cummings, 2003).
tigation are diet, nutrients and nutrient supplements such
as antioxidant vitamins, omega 3 fatty acid, medications
such as non-steroidal anti-inflammatory agents, and life- Neuropsychology and Psychology
style practices such as physical activity and cognitive and of Alzheimers Dementia
social engagement.
Neuropsychological Deficits
Natural History, Prognostic Factors, The neuropsychology of AD follows the clinical progres-
Outcomes sion. In early stages, memory is almost always involved,
with specific deficits in learning new information. Remote
The clinical course of AD is usually one of a gradual onset memory such as memory for autobiographical or other
of symptoms with progressive decline. Many scientists knowledge-based systems (semantic memory) is relatively
believe the disease process starts in the brain decades unaffected. In early stages, standardized testing with
before overt symptoms emerge. A preclinical phase, char- word lists may reveal relative preservation of immediate
acterized primarily by episodic memory deficits, heralds or working memory, but impairment in delayed recall.
the onset of symptoms. This stage, also referred to as There is usually some benefit from cuing or recognition
mild cognitive impairment (MCI), lasts approximately procedures. With progression, cuing is no longer helpful,
13 years. Progression to dementia is characterized by and remote recall is affected. Implicit memory may be
increasing severity of cognitive impairment with severe relatively spared as patients show evidence of learning
memory deficits, visuospatial impairment, and other per- on priming and procedural motor tasks. Orientation to
ceptual disturbances. Language impairment begins with time and place is also affected in AD (Knopman & Selnes,
mild naming difficulties and circumlocutory speech, but 2003).
progresses to include comprehension deficits. Apraxia Language impairments progress from mild anomia
(difficulty performing learned motor tasks in the absence and word finding difficulties in early stages, to include
of impairment in primary motor or sensory functions) impairment in comprehension and writing. Errors in
and impaired executive functions and computational speech (paraphasias) become more common, and word
ability are also apparent. Behavioral changes are common substitutions become progressively less related to the tar-
with indifference, irritability, and sadness, progressing to get words. Repetition of speech may be relatively unaffect-
delusions and, in some individuals, more severe psychiat- ed until late in the disease course (Knopman & Selnes,
ric disturbances such as hallucinations and agitation. In 2003; Mendez & Cummings, 2003). Tests of verbal fluency
end stages, there is severe deterioration of all cognitive and confrontation naming are especially sensitive to early
functions, speech is generally unintelligible, and motor changes in language. Visuospatial disturbances may be
rigidity and urinary and fecal incontinence are present. subtle or nonexistent in the earliest stages of AD. In
Death may occur as the result of other causes such as moderate and severe stages, impairment may be evident
pneumonia or infections (Mendez & Cummings, 2003). on figure copying tasks or judgment of line orientation
On postmortem exam, the brain is characterized by (Knopman & Selnes, 2003). Figure 3 displays characteris-
generalized atrophy and sulcal and ventricular enlarge- tic examples of visuoconstructional impairment in four
ment. Figure 1a displays gross atrophy of an AD brain representative patients with AD.
compared with a brain from a cognitively normal elderly Impaired abstract reasoning, sustained attention,
individual. Figure 2 displays a coronal section of an AD planning, judgment, and problem solving may characterize
brain at the level of the hippocampus. impairment in executive functions. Deficits in executive
The duration of the entire disease course from MCI functions may be demonstrated on tests of verbal fluency,
to death is highly variable. Survival estimates from trailmaking, and set shifting. Tests such as the Rey Complex
Alzheimers Dementia. Figure 1 (a) and (b) display the brains from a cognitively normal elderly individual and an individual who
suffered from advanced AD, respectively. Note the severe atrophy apparent in the AD brain (Photo courtesy of Christine Hulette,
M.D., Bryan Alzheimer Disease Research Center, Duke University. Reproduced with permission from Elsevier Limited)
figure and clock drawing may also elicit impairment in apraxia may involve pantomiming the execution of a
executive functions with poor planning and execution of task. Anosognosia or an unawareness of disability is quite
the tasks. Deficits in working memory may be evident on common (Knopman & Selnes, 2003). Standardized assess-
tasks requiring mental manipulation or divided attention ment approaches are few. Some approaches rely on clini-
(Knopman & Selnes, 2003). cal observation, noting a discrepancy between self-report
Other neurocognitive aspects of AD include apraxia and of cognitive impairment and test performance, or a
anosognosia. In mild AD, deficits in praxis are not common discrepancy between caregiver and patient report of
but emerge later in the disease course. Assessment of impairment.
Alzheimers Dementia. Figure 2 Display of the atrophy in AD in this coronal section including the hippocampi. Note the dilated
lateral ventricles and loss of inferior temporal mass (Photo courtesy of Steven S. Chin, M.D., Ph.D., University of Utah Health
Sciences Center)
Alzheimers Dementia. Figure 3 Display of the visuoconstructional impairments in the drawings of four individuals with
Possible or Probable AD. The stimulus is the left-most figure
Behavioral Symptoms Assessment of behavioral symptoms is particularly im-

portant in an AD evaluation as their presence may suggest
Behavioral changes are extremely common in AD, with other causes of dementia.
nearly all individuals exhibiting at least one symptom at
some point over the disease course. Among the most
common of these changes is apathy, characterized by a Evaluation
lack of interest and indifference. Anxiety, irritability, and
depression are also common, as are delusions. Some A through clinical work-up is important for diagnosing
patients may exhibit hallucinations, and particularly AD or determining the etiology of dementia. Critical
challenging for caregivers and family are disruptive beha- elements of an evaluation include a detailed clinical
viors such as agitation and aggression. The course of history and mental status and physical exams. Due to
behavioral symptoms is variable, with severe episodes inaccurate reporting by patients, interview with a reliable
alternating with milder ones, raising questions about informant is necessary. Laboratory, neuroimaging, and
environmental triggers. Noting the co-occurrence of one neuropsychological testing are important to exclude
or more behavioral disturbances, some scientists believe other causes of dementia. Laboratory testing may include
these symptoms are better conceptualized as behavioral a blood count, routine chemistries, thyroid function,
syndromes, with implications for underlying brain pathol- and B12 levels. Neuroimaging with MRI or CT may reveal
ogy. Several questionnaires are available for assessing generalized cerebral atrophy with associated sulcal widen-
behavioral symptoms, ranging from a single symptom ing and ventricular enlargement. In early stages of the
questionnaire to larger inventories of multiple symptoms. disorder, the brain may appear normal on MRI/CT. PET
ICMRGIc (normalized to Pons)

0.0 0.5 1.0 1.5 2.0
0.0 1.0 2.0 3.0 4.0 5.0

Z-score
Alzheimers Dementia. Figure. 4. Seventy-four year old control subject with normal cognition. The top row shows normal brain
metabolic activity and the bottom row shows very few regions of hypometabolism. The areas of significant hypometabolism
indicated in the medial views are due to this individual having enlarged lateral ventricles relative to normative subjects.
Figures 46 These images are processed FDG-PET images obtained from elderly subjects. The images have been processed using
Neurostat sterotactic surface projections to illustrate the changes of the brain in Alzheimers disease. Subject scans are shown in
two rows in each figure, depicting projections onto six surfaces: R-lateral, L-lateral, R-medial, L-medial, Superior and Inferior. The
top row in each figure displays regional glucose metabolism with cooler colors (purple, blue) reflecting areas of
hypometabolism. The bottom row in each figure displays relative glucose metabolism for each participant as compared with a
normative sample of 27 cognitively normal elderly individuals. In this bottom series, the images display the statistical
significance, expressed as Z-scores, of the hypometabolism when compared to those of the normative sample. The brighter
colors (red, white) represent areas of significant hypometabolism and the cooler colors of blues and purples represent relatively
normal brain metabolism (All photographs courtesy of Norman L. Foster, M.D. and Angela Y. Wang, Ph.D., Center for Alzheimers
Care, Imaging and Research, University of Utah)
Alzheimers Dementia. Figure. 5. Sixty year old subject clinically diagnosed with MCI. The top row shows symmetric decreases
in metabolic activity in both hemispheres of the brain. Abnormalities are primarily in the parietal lobe (shown in the R-lateral and
L-lateral views) and the posterior cingulate cortex (shown in the R-medial and L-medial views), as seen in the green regions. The
bottom row confirms that these regions (green, yellow and red areas) are indeed significantly (Z-scores 2.5) hypometabolic.
This pattern is a distinguishing feature of AD seen in FDG-PET studies (All photographs courtesy of Norman L. Foster, M.D. and
Angela Y. Wang, Ph.D., Center for Alzheimers Care, Imaging and Research, University of Utah)
Alzheimers Dementia. Figure. 6. Seventy-two year old subject clinically diagnosed with AD. This subject shows an even greater
and more widely distributed decrease in glucose metabolism. Parietal and temporal lobes and posterior cingulate cortex (green
and blue region in the top row) are affected. The statistically significant changes in metabolic pattern (red and white regions in
the lower row) are much greater than the MCI case (All photographs courtesy of Norman L. Foster, M.D. and Angela Y. Wang, Ph.
D., Center for Alzheimers Care, Imaging and Research, University of Utah)
imaging is a more sensitive technique for detecting vomiting (Orgogozo, 2003). Memantine, an NMDA glu-
changes in brain function in early stages. Reduced glucose tamate receptor blocker, has been approved for use in
metabolism, usually in the temporoparietal and posteri- moderate and severe AD. This drug is believed to
or cingulate regions, is a consistent pattern in early AD. be effective by reducing neuronal excitotoxicity. Other
Figures 4 through 6 display the pattern of glucose hypo- treatments include the use of psychotropic medications
metabolism in MCI and AD compared with a cognitively (such as antidepressant and antipsychotic medications) to
normal elderly individual. Neuropsychological testing is address the behavioral or neuropsychiatric symptoms.
important to establish the degree of cognitive impairment Cognitive rehabilitation may be attempted early in the
and to identify patterns that may be suggestive of specific disease course while patients are still able to participate.
dementing illnesses. Additional tests such as sampling Psychoeducation, behavioral techniques, music therapy,
cerebrospinal fluid for tau and amyloid-B42 assays may and caregiver support and interventions are also impor-
be helpful as supplemental procedures in complex cases tant elements of clinical care.
(Mendez & Cummings, 2003).
Cross References
Treatment
Alois Alzheimer
Treatment for AD is palliative, with medications and thera- Aricept (Donepezil)
pies providing symptom management. Medications most Cholinesterase Inhibitors
commonly used are cholinesterase inhibitors that func- Dementia
tionally address the cholinergic deficit of AD by blocking Neurofibrillary Tangles
the activity of the acetylcholine degrading enzyme, acetyl- Senile Dementia
cholinesterase. These medications are modestly effective, Senile Plaques
and patients and families may observe an improvement in
some cognitive and behavioral symptoms. However, the
medications do not modify the trajectory of disease pro- References and Readings
gression. In general, cholinesterase inhibitors are well-
tolerated. The use of the first FDA-approved drug of this Grabowski, T. J., & Damasio, A. R. (2004). Definition, clinical features
and neuroanatomical basis of dementia. In M. M. Esiri, V. M.-Y.
class, tacrine, however, is rarely administered now because
Lee, & J. Q. Trojanowski (Eds.), The neuropathology of dementia
of risk of liver toxicity. Other medications include donepe- (2nd ed., pp. 133). Cambridge, UK: Cambridge University Press.
zil, rivastigmine, and galantamine. Side effects include Hardy, J. (2003). The genetics of Alzheimers disease. In K. Iqbal &
gastrointestinal symptoms such as diarrhea, nausea, and B. Winblad (Eds.), Alzheimers disease and related disorders: research
Alzheimers Disease A 105
advances (pp. 151153). Bucharest, Romania: Ana Asian Interna- progressive paranoia, delusional thinking, disorientation,
tional Academy of Aging. A
and poor memory. She was institutionalized for the last
Knopman, D., & Selnes, O. (2003). Neuropsychology of dementia.
In K. M. Heilman & E. Valensteins (Eds.), Clinical neuropsychology
3 years of her life. Upon her death, Alzheimer analyzed her
(4th ed., pp. 574616). New York: Oxford University Press. brain using a silver stain, and described both extracellular
Malaspina, D., Corcoran, C., Schobel, S., & Hamilton, S. P. (2008). and intracellular protein accumulations. The extracellular
Epidemiological and genetic aspects of neuropsychiatric disorders. protein accumulations were termed plaques and the
In S. C. Yudofsky & R. E. Hales (Eds.), Neuropsychiatry and beha-
intraneuronal protein accumulations were called tangles.
vioral neurosciences (5th ed., pp. 301362). Washington, DC:
American Psychiatric Association Press.
Alzheimer presented the results of this autopsy in 1906.
Mendez, M. F., & Cummings, J. L. (2003). Dementia a clinical approach Several other similar cases of relatively presenile (i.e.,
(3rd ed.). Philadelphia: Butterworth. arbitrarily defined as an onset prior to age 5565) clinical
Morris, J. H., & Nagy, Z. (2004). Alzheimers disease. In M. M. Esiri, dementia associated with plaques and tangles were noted
V. M.-Y. Lee, & J. Q. Trojanowski (Eds.), The neuropathology of
by Alzheimer and others over the next 4 years. In 1910,
dementia (2nd ed., pp. 161206). Cambridge, UK: Cambridge Uni-
versity Press.
Alzheimers departmental chair, Emil Kraepelin, pub-
Orgogozo, J.-M. (2003). Treatment of Alzheimers disease with cholines- lished a textbook covering the fields of neurology and
terase inhibitors. An update on currently used drugs. In K. Iqbal & psychiatry, and referred to patients with presenile demen-
B. Winblad (Eds.), Alzheimers disease and related disorders: tia, plaques, and tangles as having Alzheimers disease.
Research advances (pp. 663675). Bucharest, Romania: Ana Asian
Concurrently, other investigators, such as Oscar
International Academy of Aging.
Soininen, H., Kivipelto, M., Laakso, M., & Hiltunen, M. (2003). Genetics,
Fischer, also reported plaque presence in elderly demented
molecular epidemiology and cardiovascular risk factors of individuals. These individuals were older than those
Alzheimers disease. In K. Iqbal & B. Winblad (Eds.), Alzheimers with presenile dementia (i.e., generally older than age
disease and related disorders: Research advances (pp. 5362). 5565). As the commonality of progressive dementia in
Bucharest, Romania: Ana Asian International Academy of Aging.
the elderly was well recognized, the presence of plaques
U.S. Department of Health and Human Services. (2006). Journey
to discovery. 20052006 Progress report on Alzheimers disease.
in elderly demented individuals was felt to represent a
Washington, DC: U.S. Department of Health and Human Services. normal phenomenon. Such individuals were not diag-
nosed with Alzheimers disease. Instead, cognitive decline
in elderly adults was attributed to normal aging or other
poorly described conditions, such as hardening of the
Alzheimers Disease arteries. As a result, Alzheimers disease remained rela-
tively uncommon for a number of subsequent decades.
RUSSELL H. S WERDLOW, H EATHER A NDERSON In the 1960s, investigators began comparing elderly
J EFFREY M. B URNS demented subjects to those diagnosed with presenile
University of Kansas School of Medicine Alzheimers disease. Notable similarities were observed
Kansas City, KS, USA regarding the clinical course (chronic and progressive),
the clinical features (cognitive decline that featured evo-
lution of an amnestic state, followed by behavioral
Definition changes), and histopathology (plaques and tangles). By
the 1970s, the number of demented elderly was growing
A neurodegenerative disease of the brain characterized fast as demographic shifts in the aging population com-
clinically by insidious, chronic, and progressive cogni- bined with increased recognition of the syndrome. At this
tive decline, and histologically by cerebral accumula- point, the original definition of Alzheimers disease (as
tions of the proteins beta amyloid (plaques) and tau described by Alzheimer and named by Kraepelin) was
(tangles). expanded to account for all dementing individuals with
plaques and tangles, although some separation of these
groups was envisioned. Those meeting the original cri-
Historical Background teria of plaque and tangle dementia in presenile adults
were designated as having dementia of the Alzheimer
In 1902, a woman called Auguste D. came under the care type (DAT), while the previously unconsidered elderly
of Dr. Alois Alzheimer, then at the University of Frank- cases were designated as having senile dementia of the
furt. The patient manifested changes in behavior and Alzheimer type (SDAT). With increasing recognition of
cognition. Her clinical course was characterized by the problem, Alzheimers disease very quickly became
106 A Alzheimers Disease
incredibly common, as well as a Western civilization 40 and 42 amino acid-long variants of Ab predominate in
health priority. plaques, and are often designated Ab40 and Ab42. Ab42
In the USA, the 1980s saw the establishment of feder- seems to be particularly important to the formation of the
ally funded Alzheimers disease research centers, which amyloid plaques of Alzheimers disease, probably because
began to systematically study the clinical course of this this version of the protein is quite insoluble. When Ab
progressive dementia, mostly in the common SDAT form. accumulations begin to form in brain, they are not asso-
Academic research began to unravel the chemical make- ciated with disrupted cell elements and are called diffuse
up of plaques and tangles. Investigations into patterns and plaques. Another type of more evolved plaque can also be
causes of neurodegeneration were performed. This ad- found in Alzheimers disease patients, in which Ab
vancing knowledge enhanced the ability of clinicians to becomes condensed at the center of the plaque, and the
diagnose Alzheimers disease at increasingly subtle stages, vicinity of the plaque is associated with disrupted cell
as well as the ability to pharmacologically intervene to elements such as degenerating axons and dendrites. As
achieve partial, temporary symptomatic benefit in at least axons and dendrites are collectively called neurites, this
some individuals. type of plaque is called a neuritic plaque.
The tangles of Alzheimers disease are found primarily
in neurons. Under the microscope tangles have a fibrous
Current Knowledge quality to them, and hence tangles in Alzheimers disease
are referred to as neurofibrillary tangles. Neurofibrillary
Scientific Perspective tangles consist of a protein called tau. Normally, tau is
found in association with microtubules, which act as a
The plaques seen in persons with Alzheimers disease skeleton, or cytoskeleton supporting the cellular struc-
contain several aggregated proteins. The major constitu- ture. The function of tau appears to be the stabilization of
ent is a protein called amyloid beta (Ab). Beta is a these microtubules. Like many proteins, after its produc-
chemical term that specifies a certain pattern of protein tion tau is modified by the addition and subtraction of
folding. Amyloid is a general term that refers to proteins phosphate groups on certain amino acids, especially ser-
that give a particular appearance when exposed to a ine and threonine. During embryonic development, tau is
particular type of stain, Congo red. The beta amyloid, or heavily phosphorylated, but during youth and early adult-
Ab, found in the brains of Alzheimers disease patients hood this heavily phosphorylated pattern is rare if at all
derives from a particular protein called the amyloid pre- seen. In Alzheimers disease, though, tau again takes on
cursor protein (APP). a heavily phosphorylated pattern, which is felt to reflect
In the human brain, the APP is 695 amino acids long. an abnormal physiologic event and is referred to as
It is a transmembrane protein. One end (the carboxy end) tau hyperphosphorylation. Hyperphosphorylated tau
is found inside neurons, in the cytoplasm. The other end molecules begin to pair off, a process called dimeriza-
(the amino end) extends outside the cell. In between the tion. Hyperphosphorylated tau dimers, also called
cytoplasmic and extracellular portions is a stretch that paired helical filaments, are quite insoluble and begin
runs through the membrane. The normal function of to aggregate with each other. This aggregation, typically
APP is not well known. APP is digested by different visible extending from cell bodies into axons, comprises
enzymes, which cut the protein at different points. An the neurofibrillary tangle.
enzyme complex called the beta secretase (BACE) cuts As impressive as this advancing understanding of
APP in its extracellular portion. An enzyme or group of plaque and tangle composition is, recognizing what con-
enzymes referred to as the alpha secretase cuts APP in its stitutes these aggregations does not address why they
intramembrane segment. The gamma secretase cuts APP form. In this regard, genetic studies of DAT subjects who
twice, both times in its intramembrane segment. Both of inherit the disorder in an autosomal dominant fashion
the gamma secretase cuts occur closer to the carboxy end have had a large impact. Several hundred such families
of the APP than the alpha secretase cut. have been documented. In these families the disease
Different cutting combinations generate various APP affects about 50% of each generation, with typical onset
by-products. Cutting of an APP by beta and gamma occurring in the 3rd, 4th, 5th, or 6th decades. A small
secretases generates a 3843 amino acid stretch, and this number of these families have demonstrable mutations in
stretch tends to assume a beta folding conformation and the gene that encodes the APP. This gene is located on
has the features of an amyloid protein (i.e., birefringence chromosome 21, the same chromosome that is present in
under the microscope when stained with Congo red). The excess in Downs syndrome. Downs syndrome patients
invariably accumulate Ab plaques in their 5th decade. with no other systemic or brain diseases that could
A
A somewhat larger number of these families have muta- account for the progressive cognitive decline. A diagnosis
tions in the gene that encodes a protein called presenilin 1. of definite Alzheimers disease can only be diagnosed at
This gene is found in chromosome 14. Presenilin 1 pro- autopsy by the presence of plaques and tangles (although
tein constitutes part of the gamma secretase complex. in some schemas tangles are not requisite) in an individ-
A smaller number of families have mutation of a related ual with a clinical history suggestive of dementia. The
gene on chromosome 1, which encodes a related protein, presence of plaques and tangles in typical brain regions
presenilin 2. Presenilin 2 can also participate in formation (mesial temporal, parietal, and inferior frontal structures)
of the gamma secretase. Mutations in the genes that is quite common in elderly persons with the clinical
encode APP, presenilin 1, and presenilin 2 all enhance syndrome of Alzheimers disease. As a result of the high
the production of Ab42. This has lent support to the prevalence of Alzheimers disease with advancing age (at
amyloid cascade hypothesis, which posits as Ab42 is least one commonly quoted study estimates approximate-
generated it begins to interfere with neuronal function, ly half of those over the age of 85 have it), the specificity of
kill neurons, and generate the other histologic features the clinical diagnosis is high. Recognition of how com-
seen in Alzheimers disease. While the logic underlying mon Alzheimers disease is in later life has also served to
this hypothesis is obvious, it is important to keep in mind enhance clinician awareness, thus improving sensitivity of
it assumes the very small subset of early-onset, autosomal the diagnosis. In the hands of an experienced physician,
dominant Alzheimers disease (which accounts for far less clinical diagnostic accuracy is excellent.
than 1% of those affected) have a similar if not identical Criteria originally designed to facilitate identification
etiology to the common sporadic, late-onset cases that of subjects for clinical trials have helped to standardize
constitute the vast majority. In those subjects, what initi- clinical diagnostic approaches. These criteria, such as
ates Ab42 production remains an open area of debate. those proposed by the National Institute of Neurologic,
Conceivably, population diversity in genes that contribute Communicative Disorders, and Stroke (NINCDS) and
to APP production or processing could cause Ab42 to the Alzheimers Disease and Related Disorders Associa-
appear. Environmental factors could lead to Ab42 formation (ADRDA) in the 1980s emphasize the importance of
tion. Also, a variety of age-related factors promote Ab42 establishing that a progressive dementia exists in a patient.
formation. Two basic approaches are commonly used toward this
Other factors are recognized to play a role in Alzheimers end. One is to demonstrate a pattern of cognitive domain
disease, and where these factors fit into or what they tell us strengths and weaknesses that reliably suggest decline
about the etiologic hierarchy of the disease is unclear. One from a previous level of cognitive function has emerged.
factor relates to the APOE gene on chromosome 19. The For example, defective memory retention in the presence
APOE gene shows population variability due to the pres- of another defective cognitive domain (language, execu-
ence of two polymorphic positions. The common APOE tive function, visuospatial function, and praxis) in an
variants are the e2, e3, and e4 forms. The APOE e4 form elderly patient with cognitive complaints and an other-
is over represented in those with Alzheimers disease, wise unremarkable physical exam is strongly suggestive of
where it seems to move up the age of presentation in Alzheimers disease. The other approach focuses more on
those destined to develop the disorder. Mitochondrial defining the degree and nature of emerging declines in
function is also altered in Alzheimers disease, and these daily living activities. This latter technique focuses exten-
alterations are not limited to the brain. sively on collateral history obtained from family members
or friends of the patient.
The diagnosis is made primarily through clinical im-
Diagnostic Perspective pression, although that impression is influenced by a
small set of recommended laboratory and imaging tests.
Dementia is defined as cognitive decline that has ad- These tests are serologic (vitamin B12 level, thyroid func-
vanced to that point it interferes with activities of daily tion tests, electrolytes with renal and hepatic indices, and
living. While dementia has many different etiologies, a blood cell count) and structural (brain imaging by either
Alzheimers disease is the most common cause of demen- computed tomography or magnetic resonance imaging)
tia, accounting for 5060% of dementia verified by neu- in nature. As currently used, they mostly serve to rule out
ropathological examination of the brain at autopsy. The the presence of concomitant pathologies that can interfere
clinical diagnosis (i.e., diagnosis in life) of Alzheimers with cognition. Although this has contributed to the view
disease is made in patients who have progressive dementia that the Alzheimers disease diagnosis is one of exclusion,
it should be noted that certain patterns of cognitive de- of action in Alzheimers disease has been questioned. In
cline elicited by clinical history or demonstrable by neu- any case, cohorts of patients with moderate or severe
ropsychological testing are so typical of Alzheimers Alzheimers disease, when randomized to memantine,
disease they can be used to support a diagnosis of inclu- perform better on measures of cognitive and functional
sion. It is important to note, though, that at the time of performance than do concurrent placebo treatment
this writing PET and APOE genotyping are not commonly groups. In severe Alzheimers disease, the magnitude of
used in the diagnosis of Alzheimers disease and cannot by observed benefit is similar to that obtained with donepe-
themselves establish a diagnosis of Alzheimers disease. zil. Memantine and donepezil have been studied in com-
bination with each other. Subjects with mini-mental state
exam scores of 514, who were already on donepezil, did
Treatment Perspective better as a group when memantine was added to their
treatment regimen than when placebo was added. De-
Although Alzheimers disease is currently neither revers- monstrable benefits in mild Alzheimers disease are lack-
ible nor curable, it is possible to treat its symptoms. The ing and thus the role of memantine in the mild stages of
first approved treatment for Alzheimers disease was tac- Alzheimers disease is not clear.
rine, a cholinesterase inhibitor. This drug increased levels A single study concluded high-dose vitamin E (2000 iu
of brain acetylcholine by antagonizing its synaptic degra- each day) might slightly slow decline in Alzheimers
dation. Increasing brain cholinergic tone was identified as disease patients. More recent general evidence, though,
a pharmacologic target because Alzheimers disease suggests taking more than 400 iu of vitamin E on a daily
patients show a profound loss of acetylcholine due to basis increases overall mortality. The marginality of any
degeneration of cholinergic neurons in the basal fore- vitamin E benefit, in conjunction with safety concerns, has
brain. Safer cholinesterase inhibitors (donepezil, rivastig- reduced enthusiasm for the use of vitamin E in Alzheimers
mine, and galantamine) have since superseded tacrine. In disease. Although a variety of other prescription medica-
addition to inhibiting acetylcholinesterase, rivastigmine tions (estrogens, statins), nonprescription medications
also inhibits buytrylcholinesterases that also hydrolyze (nonsteroidal anti-inflammatories), and nutraceuticals
acetylcholine, and galantamine is an allosteric modulator (gingko biloba) have been considered for the treatment
of acetylcholine nicotinic receptors. Each agent shows a of Alzheimers disease, published data to date on all other
similar overall degree of efficacy, although the individual treatment options has been at worst negative and at best
with Alzheimers disease may respond to or tolerate one insufficient to earn regulatory approval.
drug better than the other. Treatment cohorts followed for Other drug categories are commonly used to treat
12 weeks to 3 years indicate that as a group, those started targeted symptoms associated with Alzheimers disease.
on cholinesterase inhibitors tend to perform and appear For instance, antipsychotic medications are often used to
slightly improved compared to their immediate pretreat- treat agitated behavior. Some studies do show efficacy
ment baseline. This improvement appears detectable for in this regard, although other studies have argued the
612 months. By 12 months, though, treatment groups limited behavioral benefits antipsychotics may confer is
return to their pretreatment performance as ascertained canceled out by increased morbidity.
by cognitive testing, clinical impression, and caregiver
impression. Beyond 12 months, patients continuously
decline below their pretreatment baseline, although for Future Directions
at least the next several years patients appear to perform
better on cognitive testing than would otherwise be Scientific Perspective
expected. The clinical meaningfulness of this sustained
benefit has fueled considerable debate. Benefits have In the short term, considerable effort will be directed at
been observed on measures of cognitive ability, functional additional studies of Ab dynamics and homeostasis. Re-
ability, behavior, and caregiver stress. search will focus on the toxicities of different degrees of
At the time of this writing, memantine is the only Ab aggregation (especially oligomers, defined as short,
non-cholinesterase inhibitor specifically approved for soluble polymers of amyloid), cellular mechanisms of
the treatment of Alzheimers disease. Under in vitro con- Ab disposal, and tissue-level mechanisms of Ab disposal.
ditions, memantine blocks a cation channel associated Research over the longer term will need to address the
with the NMDA type of glutamate-activated ionotropic fact that the predominant etiologic hypothesis, the amy-
receptors. Whether or not this is its primary mechanism loid cascade hypothesis, cannot yet explain why Ab
homeostasis changes in most of those affected or how Ab amyloid plaques and neurofibrillary tangles can be admi-
A
might give rise to other aspects of Alzheimers disease nistered intravenously, and the degree of brain ligand
pathology. It is possible the amyloid cascade hypothesis retention measured using PET. This approach can provide
will prove valid in those with early onset, autosomal an estimate of an individual patients plaque burden.
dominant Alzheimers disease caused by mutations of Development of techniques such as this will increasingly
the genes encoding APP, presenilin 1, and presenilin 2 pro- render the diagnosis of Alzheimers disease one of inclu-
teins, but not the late-onset cases (the vast majority). sion. Even so, this technology may, like others, turn out to
Disproving the amyloid cascade hypothesis in the serve best as an adjunct to the clinical diagnosis as op-
late-onset cases will likely require two events. First, interposed to the principal determinant of the diagnosis.
ventions that attempt to treat Alzheimers disease by The reason for this is that a substantial percentage of
targeting Ab will need to show absent or limited efficacy. nondemented individuals have relatively high plaque bur-
Second, other hypotheses better able to explain the overall dens. The significance of increased plaque burden in non-
Alzheimers clinical and pathological big picture will need demented individuals will need to be determined with
to demonstrate viability and durability. prospective long-term studies.
Diagnostic Perspective Treatment Perspective
Because it will likely prove easier in the future to prevent None of the treatments approved for use in Alzheimers
neurodegeneration rather than reverse it, the ability to disease are approved for use in MCI, although available
render an early, accurate diagnosis is crucial. Also, the data argue cholinesterase inhibition (at least with done-
ability to treat the disease (either symptomatically or pezil) may provide a marginal benefit. Such a benefit
disease modifying) increases the importance of early di- would not be surprising, especially if MCI represents
agnosis. A confluence of neuropsychologic/clinical longi- very early Alzheimers disease in most people.
tudinal studies performed in conjunction with careful Over a decade of experience with symptomatic treat-
histopathologic correlation has already allowed a syn- ment has made it abundantly clear that disease-modifying
drome called mild cognitive impairment (MCI) to be de- treatments are required. Most current approaches toward
fined. MCI is known to represent a precursor of the disease modification are targeted to Ab homeostasis. In-
Alzheimer syndrome in the majority of those diagnosed hibition of its production (gamma secretase inhibitors
with it, and in more than half the MCI syndrome simply and modifiers), its targeted removal (active and passive
represents early Alzheimers disease. There is an emerging immunization approaches), prevention of its aggregation,
consensus that the line between normal age related cog- and enhancement of enzymatic degradation are all under
nitive decline and clinically excessive cognitive decline, at active pursuit. To date, a phase II Ab vaccination trial
least on an etiologic level, is a blurry one. Accordingly, by (AN1792) was halted when several of the subjects devel-
the time MCI is diagnosable in many individuals, substan- oped encephalitis. Other data obtained through this trial
tial irreversible brain change has occurred. Techniques and suggest the approach was successful in reducing cerebral
technologies for pushing the limits of the diagnosis to amyloid plaques. However, the most extensive published
stages that precede MCI are therefore needed. clinical data from AN1792 indicate that one year after
Most development toward this end focuses on the vaccination, the rate of cognitive decline was similar to
study of potential biomarkers. Biomarkers can be enti- (unchanged from or only very slightly reduced from) the
ties detectable in extractable tissues, such as blood or rate of decline shown by the placebo group of that trial.
cerebrospinal fluid (CSF). For example, CSF tau levels A phase III trial of tramiprosate, which retards Ab aggre-
increase in Alzheimers disease, while CSF Ab levels de- gation, was negative. A phase III trial of a gamma secretase
cline. When used in conjunction with fluorodeoxyglucose modifying agent (R-flurbiprofen) is underway. Phase III
PET, which shows the brains ability to consume glucose, trials of agents intended to humorally remove Ab are
investigators have been able to develop algorithms that scheduled.
predict future cognitive decline in elderly adults with If attacking Ab fails to meaningfully benefit Alzhei-
MCI, and even in individuals before they manifest cogni- mers disease patients, the validity of the amyloid cascade
tive complaints. hypothesis in late-onset, sporadic Alzheimers disease will
Biomarkers can also be demonstrated in vivo. For be called into question. If this happens, new models for
instance, ligands that bind amyloid plaques or both drug design will be needed. Currently, mice expressing a
mutant APP transgene, sometimes in conjunction with Khachaturian, Z. S. (1985). Diagnosis of Alzheimers disease. Archives of
Neurology, 42, 10971106.
other mutant human transgenes, serve as the gold
Klunk, W. E., Engler, H., Nordberg, A., Wang, Y., Blomqvist, G.,
standard for preclinical testing of potential Alzheimers Holt, D. P., et al. (2004). Imaging brain amyloid in Alzheimers
disease treatments. disease with Pittsburgh Compound-B. Annals of Neurology, 55,
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Mayeux, R., Saunders, A. M., Shea, S., Mirra, S., Evans, D., Roses, A. D.,
et al. (1998). Utility of the apolipoprotein E genotype in the diagno-
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Alzheimers Disease Cooperative Study ADL Scale A 111
Data for further details). The entire instrument takes

Alzheimers Disease Cooperative A
1530 min to administer.
Study ADL Scale
J ESSICA F ISH
Medical Research Council Cognition &
The ADCS is a United States-based initiative that aims to
Brain Sciences Unit
conduct research informing the prevention and treatment
Cambridge, UK
of AD, as well as developing measures for use in people
with AD, particularly in clinical trials. The ADCS-ADL
was the first ADL scale to be developed for use specifically
Synonyms in clinical trials with people with AD across the range of
severity. The 23 items in the standard version were
Alzheimers disease co-operative study ADL scale for mild
selected from a pool of 45 items based upon a stringent
cognitive impairment (ADCS-ADL-MCI); Alzheimers
set of psychometric criteria (see Section Psychometric
disease co-operative study ADL scale for severe im-
Data). Using the same criteria, Galasko et al. (2005)
pairment (ADCS-ADL-sev).
developed a version of the ADCS-ADL for more severely
impaired participants, which is known as the
ADCS-ADL-sev, and a version for people with MCI
Description has also been developed (ADCS-MCI-ADL, Perneczky
et al., 2006). The ADCS-ADL has been used in a variety
The ADCS-ADL assesses the competence of patients with
of clinical trials.
Alzheimers Disease (AD) in basic and instrumental
activities of daily living (ADLs). It can be completed by
a caregiver in questionnaire format, or administered by Psychometric Data
a clinician/researcher as a structured interview with a
caregiver. All responses should relate to the 4 weeks Galasko et al. (1997) selected the items for the
prior to the time of rating. The six basic ADL items each ADCS-ADL from a pool of 45 items thought to be
take an ADL (e.g., eating) and provide descriptions of relevant to the target population on the basis of existing
level of competence, with the rater selecting the most scales and clinical experience. To determine which ADLs
appropriate option (e.g., ate without physical help and were most suitable for inclusion, the 45-item version was
used a knife; used a fork or spoon but not a knife; administered at baseline, 6 months and 12 months later to
used fingers to eat; was usually fed by someone else). 64 elderly controls and 242 people with AD, stratified by
The 16 instrumental ADL items follow the format MMSE score at baseline assessment. Half of participants
In the past 4 weeks, did s/he use the telephone, with the were additionally assessed at 1 and 2 months post-
response options of yes/no/dont know. If the response is baseline. An item was included in the final measure if it
yes, a rating is then made regarding his/her competence fit the criteria that it: was performed either premorbidly
according to a set of descriptions tailored to that activity or at baseline by >90% of participants (showing it was
(e.g., for the telephone item, whether the person looked applicable to the target group), had a kappa agreement
up phone numbers and made calls, made calls only to statistic at 12 months of >0.4 (indicating good
well-known numbers without referring to a directory, test-retest reliability), had a significant correlation
made calls only to well-known numbers using a telephone with MMSE score (indicating appropriate scaling and
directory, answered the phone but did not make calls, validity), and showed decline over 12 months in at least
or only spoke when put on the line). Adapted versions 20% of participants (indicating validity and sensitivity
of the scale suitable for people with MCI (ADCS- to change).
MCI-ADL) and moderate-severe AD (ADCS-ADL-sev) Galasko et al. (2005) used the same criteria in
have also been developed. Scores on the 24-item the development of the ADCS-ADL-sev, based on
ADCS-ADL range from 0 to 78, those on the 18-item longitudinal data of 145 patients with Mini-Mental
ADCS-MCI-ADL range from 0 to 57, and on the State Examination (MMSE) scores between 0 and 15.
19-item ADCS-ADL-sev from 0 to 54, where higher scores Galasko et al. reported good test-retest reliability (base-
reflect greater competence (see section Psychometric line-1 month r = 0.94, baseline-2 months r = 0.89,
112 A Alzheimers Disease Co-operative Study ADL Scale for Mild Cognitive Impairment (ADCS-ADL-MCI)
month1month2 r = 0.94), and there was evidence of Galasko, D., Schmitt, F., Thomas, R., Jin, S., Bennett, D., & Ferris, S.
(2005). Detailed assessment of activities of daily living in moderate
convergent validity based upon the strong correlation
to severe Alzheimers disease. Journal of the International Neuropsy-
between ADCS-ADL-sev and other global impairment chological Society, 11, 446453.
measures (ADCS-ADL-sev MMSE r = 0.64; ADCS- Perneczky, R., Pohl, C., Sorg, C., Hartmann, J., Komossa, K.,
ADL-sev Severe Impairment Battery r = 0.71). The Alexopoulos, P., et al. (2006). Complex activities of daily living
mean score on first test was 25.4 (SD 12.7, maximum in mild cognitive impairment: Conceptual and diagnostic issues.
Age and Ageing, 35, 240245.
obtainable 54), with a mean decline of 5.6 points
(SD 7.5) over 6 months and 10.3 points (SD 10.3) over
12 months.
Perneczky et al. (2006) have found that the ADCS-
MCI-ADL scale can discriminate people with MCI from
control participants (a cut-off score of 52 gives sensitivity
Alzheimers Disease Co-operative
of 0.89 and specificity of 0.97). Study ADL Scale for Mild
Cognitive Impairment (ADCS-
ADL-MCI)
Clinical Uses
Alzheimers Disease Cooperative Study ADL Scale
The ADCS-ADL and its variants are the only ADL scales
designed with AD specifically in mind, and can provide a
fairly detailed assessment of competence in a variety of
ADLs. Galasko et al. (2005) state that the measure takes
too long to administer for it to be widely adopted in Alzheimers Disease Co-operative
clinical practice, but it would be useful in intervention
studies, and the ADL-sev in particular where the severity
Study ADL Scale for Severe
of the disorder may render measures such as the MMSE Impairment (ADCS-ADL-sev)
unsuitable due to floor effects. The careful selection of
items for the ADCS-ADL suggests that they are eminently Alzheimers Disease Cooperative Study ADL Scale
suitable for use in clinical trials. Perneczky et al. (2006)
found that even patients with a diagnosis of Mild
Cognitive Impairment exhibit deficits in instrumental
ADLs on the ADCS-ADL-MCI, and that scores can
successfully discriminate patients with MCI from healthy Amantadine
controls; as such, results from this scale may be useful in
forming an MCI diagnosis. Symmetril (Amantadine)
Cross References
Ambidexterity
Bristol Activities of Daily Living Scale
Disability Assessment for Dementia J OHN E. M ENDOZA
LawtonBrody iADL Scale Tulane University Medical Center
The Activities of Daily Living Questionnaire New Orleans, LA, USA
References and Readings Definition

Galasko, D., Bennett, D., Sano, M., Ernesto, C., Thomas, R.,
Ambidexterity is the tendency for one to be more or less
Grundman, M., et al. (1997). An inventory to assess activities of
daily living for clinical trials in Alzheimers disease. The Alzheimers equally proficient in carrying out complex or skilled
disease Cooperative Study. Alzheimers Disease and Associated motor tasks with either the right or the left hand.
Disorders, 11(S2), S33S39. While complete ambidexterity is relatively rare, mixed
American Academy of Clinical Neuropsychology (AACN) A 113
proficiencies or preferences are not uncommon, with men Pujol, J., Deus, J., Losilla, J. M., & Capdevila, A. (1999). Cerebral laterali-
zation of language in normal left-handed people studied by func- A
more frequently demonstrating such mixed preferences
tional MRI. Neurology, 52, 10381043.
than women. Tan (1988) found that approximately 66% Tan, U. (1988). The distribution of hand preference in normal men and
of the population was noted to express a strong right-hand- women. International Journal of Neuroscience, 41, 3555.
ed preference, while a little more than 3% were predomi-
nately left handed. The remaining 30% evidenced mixed
hand preferences. As noted elsewhere in this volume, hand-
edness is a common, but not the only measure of what is Ambiguous Personality
referred to as cerebral dominance. Another of the more Assessment
frequent indices of dominance is language, which is typically
organized primarily in the left hemisphere. While in the Projective Technique
majority of non-brain-injured individuals, the control
of both complex motor skills and language functions rest
within the left hemisphere, this may not always be the case,
particularly for those who are either left handed or ambi- American Academy of Clinical
dextrous. It has been shown that while right hemisphere Neuropsychology (AACN)
dominance for language is quite rare in right-handers, it
could approach 30% in strong left-handers. Individuals R EBECCA M C C ARTNEY
who are ambidextrous or whose parents are left handed Emory University/Rehabilitation Medicine
tend to fall somewhere in between these two groups with Atlanta, GA, USA
regard to the hemispheric localization of language. Further-
more, the localization of language may not be an all-or-none
phenomena. While one hemisphere may be more predomi- Membership
nant, language functions may be mediated to some extent by
both hemispheres. Individuals with mixed or anomalous American Academy of Clinical Neuropsychology
dominance, including those who were ambidextrous, tend (AACN) is an organization for psychologists who have
to have a greater incidence of at least some degree of bilateral achieved board certification in the specialty of Clinical
representation of language. In the event of unilateral strokes, Neuropsychology, under the American Board of Clinical
such individuals may evidence less severe residual aphasic Neuropsychology (ABCN). Membership in the Academy
deficits when compared to patients with strongly lateralized consists of three classes: Active, Senior, and Affiliate. Active
language when that hemisphere is affected. members are elected from among psychologists who have
been certified in clinical neuropsychology by the ABCN in
affiliation with the American Board of Professional Psy-
chology (ABPP). Senior members are elected from among
Cross References Active members who have been Academy members, for a
period of no less than the five preceding years, are age 65 or
Anomalous Dominance older or disabled, and are fully retired from the active
Dominance (Cerebral) practice of clinical neuropsychology. They continue to be
listed in the membership directory of the academy, and
they continue to receive any newsletters distributed to
Academy members. Senior members have no financial
obligations to the Academy and are allowed to continue
to subscribe to any journal available through the Academy.
Benson, D. F., & Geschwind, N. (1985). Aphasia and related disorders:
A clinical approach. In M. Mesulam (Ed.), Principles of behavioral At the time of this publication, there were 367 active senior
neurology (pp. 193238). Philadelphia: F.A. Davis Co. members in the United States and 20 members in Canada.
Knecht, S., Drager, B., Deppe, M., Bode, L., Lohmann, H., Floel, A., et al. Affiliate members are elected from among all others who are
(2000). Handedness and hemispheric language dominance in intellectually interested in the purposes of the Academy and
healthy humans. Brain, 123, 25122518.
wish to participate in its non-voting activities. All members
Pieniadz, J. M., Naeser, M. A., Koff, E., & Levine, H. L. (1983). CT scan
hemispheric asymmetry measurements in stroke cases with global are provided with a subscription to The Clinical Neuropsy-
aphasia: Atypical asymmetries associated with improved recovery. chologist, access to the AACN Clinical Discussion Email
Cortex, 19, 371391. List, and discounted fees to meetings and workshops.
114 A American Academy of Neurology (AAN)
Presidents of the Academy include Byron P. Rourke, Cross References

(19951996), Wilfred van Gorp (19962002), Catherine A.
Mateer (20022004), Robert L. Mapou (20042006), American Board of Clinical Neuropsychology (ABCN)
Jerry J. Sweet (20062008). International Neuropsychological Society
National Academy of Neuropsychology
Major Areas or Mission Statement

AACNs stated mission is to maintain the standards
of Clinical Neuropsychology through support of the Boake, C. (2008). Clinical neuropsychology. Professional Psychology:
Research and Practice, 39(2), 234239.
board certification process of ABCN. The Academy holds
Boake, C., & Bieliauskas, L. A. (2007). Development of clinical neuropsy-
the following objectives: (1) Support for the principles, chology as a psychological specialty: A timeline of major events.
policies, and practices that seek the attainment of the best The ABPP Specialist, 26, 4243.
in clinical neuropsychological patient care. (2) The pursuit Yeates, K. O., & Bieliauskas, L. A. (2004). The American Board of Clinical
of excellence in psychological education, especially as it Neuropsychology and American Academy of Clinical Neuropsy-
chology: Milestones past and present. The Clinical Neuropsychologist,
concerns the clinical neuropsychological sciences. (3) The
18, 489493.
pursuit of high standards in the practice of clinical neuro-
psychology and support of the credentialing activities of
the ABCN. (4) Support for the quest of scientific knowl-
edge by support for research in neuropsychology and
related fields. (5) The communication of scientific and
American Academy of Neurology
scholarly information through continuing education (AAN)
(CE), scientific meetings, and publications. (6) Provision
for communication with other groups and representation C ATHERINE M. RYDELL
for clinical neuropsychological opinion to best achieve and American Academy of Neurology
preserve the purposes of the Academy. Saint Paul, MN, USA
Landmark Contributions Address (and URL)

AACN was founded in 1996. The first appointed president American Academy of Neurology
was Byron Rouke, Ph.D. and the first elected president was 1080 Montreal Avenue
Wilfred Van Gorp, Ph.D. AACN cosponsored the Houston Saint Paul, Minnesota 55116
Conference on Specialty Education and Training in Clinical www.aan.com
Neuropsychology in 1997. This conference was a national (800) 879-1960 (US)
consensus conference of neuropsychological organizations (651) 695-2717 (international)
held with the purpose of establishing training guidelines for (651) 361-4800 (fax)
clinical neuropsychology. The Houston Conference guide-
lines have since become the model for most programs
offering formal training in clinical neuropsychology. Membership
AACN held its first annual conference in 2003. During
that same year, The Clinical Neuropsychologist became The American Academy of Neurology (AAN), established in
AACNs official journal. In 2007, AACN began on-line 1948, is an international professional association of more
Continuing Education (CE) programs. than 21,000 neurologists and neuroscience professionals
dedicated to providing the best possible care for patients
with neurological disorders. The AAN is strongly committed
Major Activities to its mission of ensuring the maintenance of the principles
and standards set forth in the AAN mission statement.
AACN hosts one conference each year. This conference Approximately 22,000 members reside in the USA and
is open to both members and nonmembers. The 4,000 are international members. Membership includes
official journal published by AACN is The Clinical clinicians, academicians, researchers, business adminis-
Neuropsychologist. trators, residents, fellows, and medical students.
American Academy of Neurology (AAN) A 115
Major Areas or Mission Statement Major Activities A

The vision of the AAN is to be indispensable to its Physician Education and Lifelong Learning
members. The mission of the AAN is to promote the
highest-quality neurologic care and enhance member ca- The AANs Annual Meeting is one of the largest
reer satisfaction. To accomplish these purposes, the AAN gatherings of neurology professionals in the world. Held
has established the following organizations to support its each spring, the event attracts nearly 13,000 clinicians,
membership: academicians, researchers, exhibitors, and media repre-
sentatives to share the latest in neurology science and
The American Academy of Neurology Foundation
education. The AAN also offers members three-day re-
(AAN Foundation), established in 1993, raises funds
gional conferences in the fall of each year, and occasional
to support clinical research in neurologic disorders.
workshops. Education activities and programs are
AAN Enterprises, Inc. (AEI), a for-profit subsidiary of
structured to support the ongoing development of neu-
the AAN, was formed in 1999 by the AAN to develop
rology professionals from medical students to
new sources of revenue to pay for state-of-the-art
accomplished clinicians and scientists.
products and services for its membership.
The American Academy of Neurology Professional
Association (AANPA) was established in 2007 Science and Research
and includes all AAN members. The AANPA created
a political action committee, BrainPAC, to repre- The Annual Meeting is a leading forum for sharing the
sent the interests of USA neurologists in latest developments in science and research, as is the
Washington, DC. weekly peer-reviewed journal Neurology. AAN scientific
awards, presented at the Annual Meeting, honor out-
standing achievements in neurology, from aspiring
Landmark Contributions medical students to veteran researchers. Through the
AAN foundation, the AAN provides support to young
The AAN was founded in 1948 by A. B. Baker, MD, chair researchers through more than a dozen clinical research
of the neurology department of the University of Minne- training fellowships, enabling them to pursue research
sota, in response to the difficulties of one of his residents, initiatives and helping them to secure academic appoint-
Joseph Resch, in finding a society that he could join to ments and future fundings.
continue his education and network with fellow neurolo-
gists. Baker was aided by Adolph L. Sahs, MD, of the
Clinical Practice
University of Iowa; Francis M. Forster, of Jefferson Medi-
cal Hospital in Philadelphia; and Russell DeJong, MD, of
The AAN develops clinical practice guidelines to assist
the University of Michigan. Baker served as the first
its members in clinical decision making related to the
Academy president, and Forster and Sahs later had
prevention, diagnosis, treatment, and prognosis of neuro-
terms as president. DeJong was the founding editor-in-
logic disorders. Each guideline makes specific practice
chief of the journal Neurology, which began publication
recommendations based upon a rigorous and compre-
in 1951.
hensive evaluation of all available scientific data. The
The AAN had 52 founding members. The establish-
AAN also develops position statements on a variety of
ment of the Academy, coupled with the increased need for
ethical issues to help guide neurologists and others in
neurologists due to World War II, helped elevate the status
decision making. Members also rely on the AAN for the
of neurology as a practice distinct from psychiatry. In
latest information on coding, reimbursement, quality
1947, there were between 300 and 325 physicians in the
initiatives, patient safety, and practice management issues.
USA who designated themselves as primary neurologists,
and there were 32 residency positions available nation-
wide. By 1970, there were 2,727 primary neurologists and Advocacy
some 700 residents in training. By the end of 2007, there
were more than 16,000 neurologists in the USA. Current- To help foster changes in health care that will benefit
ly, nearly 2,200 residents have memberships with the patients and enhance the practice of neurology, the AAN
AAN. presents advocacy training opportunities for members
116 A American Academy of Pediatrics
through the Donald M. Palatucci Advocacy Leadership many other countries. Members include pediatricians,
Forum, and the Kenneth M. Viste, Jr., MD, Neurology pediatric medical subspecialists, and pediatric surgical
Public Policy Fellowship. Members also participate in the specialists. More than 34,000 members are board-certified
annual Neurology on the Hill visits to the USA Capitol in and called Fellows of the American Academy of Pediatrics
Washington, DC. The AANPAs BrainPAC political action (FAAP).
committee also is instrumental in representing neurol-
ogys interests on the federal level and supporting federal
legislators who support the profession and patients with
neurologic disorders.
The AAP is committed to the attainment of optimal

Publishing physical, mental, and social health and well-being for all
infants, children, adolescents, and young adults.
AAN Enterprises, Inc., has four highly successful publica-
tions published by Lippincott Williams and Wilkins. The
weekly journal Neurology is the most widely read peer- Landmark Contributions
reviewed neurology journal in North America. Neurology
Today, published biweekly, leads all other neurology The AAP was founded in June 1930 by 35 pediatricians
tabloids in readership. Neurology Now, a bimonthly who met in Detroit in response to the need for an inde-
patient-oriented magazine available in AAN member pendent pediatric forum to address childrens needs.
offices, currently has about 256,000 subscribers. Continu- When the AAP was established, the idea that children
um: Lifelong Learning in Neurology, the AANs bimonth- have special developmental and health needs was a new
ly continuing education monograph, is recognized by the one. Preventive health practices now associated with child
American Board of Psychiatry and Neurology as a key tool care such as immunizations and regular health exams
for maintenance of certification. AEI also publishes the were only just beginning to change the custom of treating
monthly member magazine AANnews, which focuses on children as miniature adults.
AAN activities, events, and services; a book series for
patient and their families on treating and living with neuro-
logic disorders; and textbooks geared toward professionals. Major Activities
Cross References One of the AAPs major activities is to further the profes-
sional education of its members. Continuing education
Neuropsychiatry courses, annual scientific meetings, seminars, publica-
tions and statements from committees, councils, and sec-
tions form the basis of a continuing postgraduate
educational program.
More than 30 committees develop many of the AAPs
Visit the AAN online at www.aan.com.
positions and programs. Committees have interests as
varied as injury and poison prevention, disabled children,
sports medicine, nutrition, and child health financing.
American Academy of Pediatrics The AAP currently has six councils and 48 sections
consisting of more than 41,500 members with interest in
D EBBIE L INCHESKY specialized areas of pediatrics. This includes a section for
American Academy of Pediatrics resident physicians with more than 9,000 members. Sec-
Elk Grove Village, IL, USA tions and councils present educational programs for both
their members and the general membership of the AAP in
order to highlight current research and practical knowl-
Membership edge in their respective subspecialties.
The AAP publishes Pediatrics, its monthly scientific
The American Academy of Pediatrics (AAP) has approxi- journal; Pediatrics in Review, its continuing education
mately 60,000 members in the USA, Canada, Mexico, and journal; and its membership news magazine, AAP News.
American Board of Clinical Neuropsychology (ABCN) A 117
It also publishes manuals on such topics as infectious and oral examination. Because the diploma is based on
A
diseases and school health. In its public education efforts, peer review of clinical competency, the majority of ABCN
the AAP produces patient education brochures and a diplomates are active clinicians. However, many also en-
series of child care books written by AAP members. gage in clinical and basic science research, teaching, and a
The AAP executes original research in social, economic, wide range of other professional activities.
and behavioral areas and promotes funding of research. It The ABCN Board of Directors consists of 15 members
maintains a Washington, DC office to ensure that childrens elected by diplomates in good standing. The term of
health needs are taken into consideration as legislation and office is 5 years. Officers of the Board (President, Vice
public policy are developed. The AAPs state advocacy staff President, Secretary, Treasurer) are elected by the Board
provides assistance to chapters, promoting issues such as from among active elected directors. Elected Board mem-
child safety legislation and Medicaid policies that increase bers may serve no more than two consecutive terms.
access to care for low-income children. In addition to elected Board members, there is an exami-
nation chairperson, selected by the Board for a term of
5 years.
American Board of Clinical

Neuropsychology (ABCN) Major Areas or Mission Statement
According to the ABCN bylaws, the organization exists to

M ICHAEL W ESTERVELD 1, K EITH O. Y EATES 2
1 develop and maintain procedures to examine the qualifi-
Florida Hospital
cations of candidates for board certification in Clinical
Orlando, FL, USA
2 Neuropsychology, to conduct the examinations and
Nationwide Childrens Hospital
award certificates to qualified candidates, to maintain a
Columbus, OH, USA
registry of certificate holders, and to serve the public
welfare by identifying practitioners who have obtained
advanced education and training in clinical neuropsy-
Address (and URL)
chology and demonstrated the ability to apply such skills
in a competent manner.
The American Board of Clinical Neuropsychology
(ABCN) is an organization that awards board certification
to practicing clinical neuropsychologists. It is a member
of the American Board of Professional Psychology
Landmark Contributions
(ABPP). Information about ABCN can be obtained from
ABCN was incorporated in 1981. After the findings of the
the ABCN web site (www.theabcn.org) and also at the
joint Division 40-INS task force on Education, Accredita-
ABPP web site (www.abpp.org).
tion, and Credentialing in 1981 (published in 19845 and
Mail correspondence for ABCN can be directed to:
republished in the first issue of The Clinical Neuropsychol-
Department of Psychiatry (F6248, MCHC-6) ogist in 19877) established requisite education and train-
University of Michigan Health System ing experiences, the need for a means of identifying well-
1500 East Medical Center Drive, SPC 5295 trained and competent practitioners was recognized.
Ann Arbor, MI 48109-5295 A planning group (Linas Bieliauskas, Louis Costa, Edith
Kaplan, Muriel Lezak, Charles Matthews, Steven Mattis,
Manfred Meier, and Paul Satz) incorporated ABCN
Membership in Minneapolis in 1981. The organization was formed
with the intention of affiliating with the ABPP, a unifying
As of May, 2010 ABCN had awarded 748 diplomas. governing body for independently incorporated specialty
Diplomates from throughout the USA, District of examining boards akin to the ABMS for medical
Columbia, and Canada are represented among the ranks specialties. After the first examinations were completed
of ABCN. Awarding of the ABCN diplomate is based in 1983, ABCN formally affiliated with ABPP (also in
primarily on clinical knowledge and skill, as demon- 1983) and the first ABPPABCN diplomas were awarded
strated throughout the examination process which in 1984. The first President of ABCN was Manfred Meier,
includes a written examination, practice sample review, who served from 1983 until 1991.
118 A American Board of Clinical Neuropsychology (ABCN)
ABCN was initially established as an organization boards and recognition of special competencies of existing
solely charged with awarding diplomas to applicants board members. As a result, the Pediatric Special Interest
successfully demonstrating competency through the group was formed, and held the first meeting in 2009
examination process. In 1988, it became a membership during the AACN Conference.
organization and began charging dues so that resources Table 1 presents a timeline summary of major land-
for further development of the organization could be marks for ABCN.
built. This included creation and maintenance of a written
examination in consultation with Professional Examina-
tion Services (PES). After years of development and pilot Major Activities
testing to assure validity and reliability of the written
examination, in 1993, ABCN began to require that new ABCNs primary activities are developing, maintaining,
candidates pass the written examination prior to submit- and conducting the examination. The examination pro-
ting practice samples. The written examination is regular- cess consists of four distinct steps. First, the education and
ly reviewed for content updates to remove outdated items training experiences of the applicant are reviewed, initially
and assure that advances in clinical practice and knowl- at the ABPP central office, where the application is exam-
edge in the field are reflected in the examination. ined for graduate training, internship, and licensure sta-
The American Academy of Clinical Neuropsychology tus. Applications are then forwarded to ABCN for review
(AACN), an organization originally comprised of ABCN of advanced specialty training. Any practicing clinical
diplomates, was formed in 1996. ABPP had received legal neuropsychologist with a doctoral-level degree who pos-
advice that there was potential for conflict of interest in sesses a valid license to practice psychology is eligible to
the roles of credentialing bodies that also engaged in
advocacy. As a result, the academy was formed to fulfill
the advocacy and professional development role. AACN
has grown significantly and now includes an affiliate American Board of Clinical Neuropsychology (ABCN).
member category for neuropsychologists who have not Table 1 Timeline for major ABCN milestones
yet received their ABCN diploma, and for affiliated pro- 1981 ABCN incorporated in Minnesota
fessionals who are not neuropsychologists. Although
1983 First set of examinations completed
ABPP has recently received a different legal opinion that
1983 Formal affiliation between ABCN and ABPP
allowed member boards to once again merge with their
established
academies, ABCN and AACN have grown and function
1984 First ABCN/ABPP diplomates awarded
well in their complementary roles and at this time have no
plans to merge. 1988 ABCN bylaws revised to create membership
In 1997, a landmark conference regarding education organization
and training for clinical neuropsychologists was held in 1989 ABCN designated Specialty Council in Clinical
Houston (the Houston Conference on Specialty Educa- Neuropsychology by ABPP
tion and Training in Clinical Neuorpsychology). Attend- 1993 Written examination formally instituted
ing the conference were representatives from each of the 2002 AACN establishes mentoring program to promote
professional neuropsychology organizations, and the pro- board certification through ABCN
ceedings were published in 1998. In 2002, the ABCN 2002 ABCN votes to adopt Houston Conference guidelines
Board of Directors voted to adopt the Houston Confer- for eligibility for board certification, beginning in 2005
ence training guidelines as requisite training to be eligible 2002 Written examination updated to reflect Houston
for the ABCN diplomate. Candidates who received their Conference guidelines
degrees after January 1, 2005 are expected to have had 2004 500th ABCN diploma awarded
training and experience consistent with the guidelines laid 2004 BRAIN Website and Listserv group formed
out in the Houston Conference proceedings. 2005 Houston Conference education and training
In 2007, ABCN began to consider subspecialization requirements implemented
within the field, and address examination and recog- 2007 Committee to study subspecialization formed
nition of special competencies, such as pediatric neuro-
2009 700th diploma awarded
psychology. At that time, ABPP did not have a model for
2009 Pediatric Neuropsychology special interest group
subspecialization, and worked with ABCN to develop a
formed
framework to address issues such as overlap with other
American Board of Clinical Neuropsychology (ABCN) A 119
apply. Beginning in 2005, applicants for the ABCN presented with a brief description of a case, and is asked
A
diploma are expected to complete training consistent to inquire about background history, test data, and related
with the Houston Conference on Specialty Education medical information to arrive at a clinical diagnosis and
and Training in Clinical Neuropsychology. This includes conclusion. Along the way, the candidate may be asked
coursework in the areas outlined in the Houston Confer- about their rationale for test selection, their differential
ence, and completion of a formal 2-year postdoctoral diagnostic considerations, and how test results may
residency program in Clinical Neuropsychology. Howev- support or otherwise aid in diagnosis and treatment
er, recognizing that the field has evolved, applications planning. The professional and ethical portion of the
from candidates who obtained their graduate training examination is an opportunity for the candidate to dem-
prior to implementation of the Houston Conference stan- onstrate knowledge of important ethical considerations in
dards are evaluated according to the standards in place at the practice of neuropsychology, as well as discuss impor-
the time their degree was granted, provided they can tant issues for the field.
demonstrate that the pertinent requirements were met A comprehensive overview of the examination process
during their training (see www.theabcn.org for detailed was published in 2008 (Armstrong, et al., 2008).
requirement listings). Candidates who are respecializing Currently, ABCN conducts written examinations at
in neuropsychology, or who recently completed respecia- four major conferences each year:
lization programs, are expected to have education and
International Neuropsychology Society (INS North
training experiences consistent with the requirements in
American Meeting)
place at the time of their respecialization, not the date of
American Academy of Clinical Neuropsychology (AACN)
their original degree.
American Psychological Association (APA)
Once an applicants credentials have been reviewed
National Academy of Neuropsychology (NAN)
and accepted, the next step in the examination process is
a written examination. The written examination consists Oral examinations are conducted twice annually in
of 100 multiple-choice questions that cover a range of Chicago, Illinois, hosted by Rush University Medical Cen-
topics in neuropsychology. It is intended to evaluate the ter. One examination is conducted each autumn (usually
candidates breadth of knowledge and to assure that they late October, or early November) and the other in the
have the foundational knowledge necessary for competent spring (usually early May).
practice in clinical neuropsychology. It is administered The AACN holds an annual conference for continuing
at major conferences, including the AACN conference, education, professional development, and furthering the
National Academy of Neuropsychology (NAN) annual growth of the profession through advocacy. The meeting
meeting, International Neuropsychology Society (INS) is held annually in June.
North American Meeting, and the American Psychologi-
cal Association (APA) meeting. It was developed and is
maintained in association with PES.
Once a candidate has passed the written examination, Cross References
the next step is submission of a practice sample consisting
of two typical cases in the candidates practice. The prac- American Academy of Clinical Neuropsychology
tice samples are reviewed by at least three independent, (AACN)
board certified neuropsychologists. American Board of Professional Psychology (ABPP)
Following acceptance of the practice sample, the can- American Psychological Association (APA)
didate is invited to sit for the oral examination that con- International Neuropsychology Association (INS)
sists of three parts practice sample, fact-finding, and Meier, Manfred John (19292006)
ethics/professional development. The practice sample sec- National Academy of Neuropsychology (NAN)
tion of the orals provides the candidate an opportunity to
discuss their practice as applied to the specific cases they
submitted. The cases also serve as a starting point leading
to more in-depth discussion of differential diagnosis, and
general information about the nature of the disorder in
Armstrong, K., Beebe, D. W., Hilsabeck, R. C., & Kirkwood, M. W.
the case and related conditions. The fact-finding section (2008). Board certification in clinical neuropsychology: A guide to
of the oral examination is an opportunity for the candi- becoming ABPP/ABCN certified without sacrificing your sanity.
date to demonstrate clinical skills. The candidate is Oxford Press.
120 A American Board of Pediatric Neuropsychology
Bieliauskas, L. A., & Matthews, C. G. (1987). American Board of Clinical training in pediatric neuropsychology (from graduate
Neuropsychology: Policies and procedures. The Clinical Neuropsy-
school to continuing education), written examination, a
chologist, 1, 2128.
Bieliauskas, L. A., & Matthews, C. G. (1990). American Board of Clinical
practice sample submission, and an oral examination. The
Neuropsychology Update, 1990. The Clinical Neuropsychologist, 4, ABPdN does not have a grand fathering policy, and
337343. thus, all existing board members were required to com-
Bieliauskas, L. A., & Matthews, C. G. (1997). The American Board of plete all new phases of the examination process to ensure
Clinical Neuropsychology, 1996 update: Facts, data, and information
equality of standards among boarded members.
for potential candidates. The Clinical Neuropsychologist, 11, 222225.
Hannay, H. J., Bieliauskas, L., Crosson, B. A., Hammeke, T. A., Hamsher,
As of early 2010, 111 neuropsychologists have submit-
K. deS., & Koffler, S. (Eds.). (1998). Proceedings of the Houston ted applications to ABPdN and 75 members have passed
Conference on specialty education and training in clinical neuorp- the ABPdN examination process. At present, there are
sychology. Archives of Clinical Neuropsychology, 13, 157250. 57 active and five emeritus members of the board from
Ivnik, R. J., Haaland, K. Y., & Bieliauskas, L. A. (2000). American Board of
21 states, Canada, and Puerto Rico.
Clinical Neuropsychology special presentation. The Clinical Neurop-
sychologist, 14, 261268.
Report of the Division 40/INS Joint Task Force on Education, Accredita-
tion, and Credentialing (1984). Division 40 Newsletter, Vol. 2, no. 2,
pp. 38.
Reports of the ins - division 40 task force on education, accreditation, and Board certification in pediatric neuropsychology serves to
credentialing (1987). The Clinical Neuropsychologist, 1(1), 2934. assist consumers by offering supportive evidence of the
Yeates, K. O., & Bieliauskas, L. A. (2004). The American Board of
competence of the pediatric neuropsychologists. The
Clinical Neuropsychology and American Academy of Clinical
Neuropsychology: Milestones past and present. The Clinical Neurop-
ABPdN is the only board certification organization with
sychologist, 18, 489493. the sole purpose of examining and certifying competence
in pediatric neuropsychology.
American Board of Pediatric
Members of ABPdN practice in a variety of settings includ-
Neuropsychology ing universities, teaching hospitals, general hospitals, hos-
pital trauma centers, private practices, rehabilitation
P ETER D ODZIK facilities, stroke centers, memory disorder centers, group
American School of Professional Psychology-Schaumburg practices, and child development centers. Current members
Schaumburg, IL, USA hold academic affiliations at over 40 colleges and universi-
ties. Several members have developed tests commonly used
in the practice of pediatric and general neuropsychology.
Membership Member accomplishments include past president of APA
Division 40, current and past presidents of four State Psy-
The American Board of Pediatric Neuropsychology chology Boards, past president of National Academy of
(ABPdN) was developed in 1996 by a coalition of clinical Neuropsychology, past and present editor of Archives of
practitioners, representing institutions hiring pediatric Clinical Neuropsychology, past editor of Journal of School
neuropsychologists. The original group conceived the Psychology, and the owner/moderator of PEDS-NPSY, a
board to advance their belief that a unique interplay pediatric list-serve with over 1,600 members.
exists between neurodevelopmental issues and neuropsy-
chological assessment that requires special sets of exper-
tise not readily assessed by the then existing boarding Major Activities
entities. Following discussion with colleagues who were
members of medical practice and psychology boards, The ABPdN is the board-certifying arm of the American
the coalition elected to establish an independent certi- Academy of Pediatric Neuropsychology (AAPN), which is
fying authority. The examination process evolved into devoted to training and promotion of the field of pediat-
a comprehensive and multilevel process that includes a ric neuropsychology. The AAPN, in affiliation with the
written application including clinical case vignettes used American College of Professional Neuropsychology, holds
to determine decision-making strategies of the applicant, an annual conference each spring with topics related to
scope of practice and a thorough assessment of organized the field of pediatric neuropsychology.
American Board of Pediatric Neuropsychology A 121
The primary activity of ABPdN is conducting the 2. Continuing education

A
board certification process. Board examination through a) Verification of CEUs in pediatric neuropsychology
the ABPdN involves several stages. The format of the for the past 3 years
ABPdNs examination processes has been constant since 3. Clinical work
the examinations held in 2004, but the procedures con- a) Clinical appointment verification contact
tinue to be reviewed and amended. The purpose of the information
ABPdN examination process is to ensure that the exam- b) Breakdown of clinical practice by age, disorders,
inee has demonstrated competency to practice pediatric and ethnic background
neuropsychology. The specific stages are discussed below c) Completion of clinical vignettes
and more detail can be obtained from the ABPdN web site 4. Educational appointment (if applicable)
(Beljan, Bos, Courtney, & Dodzik, 2006). The overall pass a) Academic institution verification contact
rate for each stage of the examination process is between information
73% and 81%.
The application is first reviewed by the Examination
Chair for completion and accuracy of documents and
licensure status. The application is then reviewed by a
Credential Review panel of three reviewers. A passing score by two of the
three reviewers is required to move to the next stage of the
Minimum training and education standards include com- examination. Each reviewer evaluates the application for
pletion of a doctoral degree from a regionally accredited consistent and thorough training in pediatric neuropsy-
program in applied psychology that was, at the time the chology at multiple levels of training.
degree was granted, accredited by the APA, CPA, or was
listed in the publication Doctoral Psychology Programs
Meeting Designation Criteria (ASPPB National Register Practice Sample
designation committee, 2008). Membership in the
National Register of Health Service Providers in Psychol- The purpose of the practice sample is to determine the
ogy, the Canadian Register of Health Service Providers, or applicants clinical knowledge. While the written exami-
those holding the Certificate of Professional Qualification nation was designed to assess content-specific knowledge
qualify as meeting the doctoral requirements for member- with regard to pediatric neuropsychology, the practice
ship. Licensure or certification at the independent practice sample allows the board to evaluate the day-to-day skills
level as a psychologist in the state, province, or territory in of the applicant. To that end, the sample should reflect a
which the psychologist actively practices is also required. typical patient seen in the applicants clinical practice.
The applicant must be practicing as a pediatric neurop- Practice samples may include assessment or intervention
sychologist and must have completed an Association of techniques. After an application is reviewed and the can-
Psychology Postdoctoral and Internship Center (APPIC) didate is determined to be board-eligible, they will then be
or APA accredited internship that included a documented invited to provide a practice sample that reflects their
rotation or concentration in neuropsychology, and 2 years typical work in pediatric neuropsychology. Prior to taking
of postdoctoral supervised experience in neuropsycholo- the objective and oral examination, the candidate must
gy, at least 50% of that being pediatric-oriented. In addi- prepare and tender a written sample of an original pedi-
tion, each applicant reviewed by the Board must provide atric neuropsychological examination performed solely by
the following: the candidate. Appropriate samples may also include case
analysis/interventions and supervision sessions.
1. Education
a) Undergraduate degree transcript
b) Graduate degree transcript Written Examination
c) Internship verification contact information
d) Postdoctoral residency verification contact The third step is the written exam, a 100 question, multiple-
information choice instrument designed and constructed by other pedi-
e) Postdoctoral fellowship verification contact infor- atric neuropsychologists whose purpose is to assess the
mation (if applicable) candidates breadth of knowledge in pediatric neuropsy-
f) Detailed description of training in pediatric neu- chology. The questions were first assessed for face validity,
ropsychology (narrative) clustered for content area, rank-ordered, deleted or refined,
122 A American Board of Pediatric Neuropsychology
reanalyzed, debated, approved, and then compiled into a ability to articulate the major findings and their rationale.
larger item pool for random selection by domain each year. Candidates discuss their rationale in such areas as:
A passing score of 70% is required. Each exam includes the
(1) Test selection (if applicable): psychometric proper-
following basic core areas:
ties, test validity/reliability, limitations for use, and
Psychometrics exclusion of all competing diagnoses.
Pediatric Neurosciences (2) Test interpretation (if applicable): alternate interpre-
Psychological and Neurological Development tations of findings, conflict resolution within the
Neuropsychological and Neurological Diagnostics data, discussion of strengths and weaknesses, and
Ethics and Legal Issues environmental and cultural factors.
Research Design Review for Clinical Application (3) Diagnostic conclusions: alternate diagnosis, ultimate
Intervention Techniques understanding of neuropathology, prognosis, pro-
Consultation and Supervisory Practices gression, lateralizing/localizing effects, pathognomic
signs, causality, environmental conditions, and
effects on neural development.
Oral Examination
(4) Recommendations and treatment planning: best
practices for treatment, availability, prognosis, fund-
This part of the examination process is comprised of a
ing, delivery options, cost/benefit analysis, iatrogenic
review of the candidates practice sample, the nature and
outcomes, parental compliance/agreement, and ethi-
application of neuropsychological knowledge to their cur-
cal issues.
rent practice, appreciation for ethical issues and obligations,
(5) Consultation and supervision (if applicable): best
and a review of the candidates views and philosophy on
practices for communication of data, delivery
pediatric neuropsychology. The oral examination also
options, supervisee needs/relationships, and rap-
includes a mock case review, in which the candidate is
port/therapeutic relationship.
given information about a fictional case, and they develop
and articulate their working hypothesis. The oral examina- This process is intended to be collegial and the examiners
tion is intended to be a collegial opportunity for the endeavor to be sensitive to the different and yet equally
reviewers to validate the candidates ability to think on viable approaches within pediatric neuropsychology. The
their feet and discern their preparation and readiness for purpose is to ascertain the Candidates logic and thought
board certification. processes and to allow them to demonstrate these skills.
The first portion of the oral examination permits the During the ethics segment, there is discussion of one or
examination team to consider the scope of the candidates two standardized vignettes, and the candidate is expected to
body of training and how they practice pediatric neuro- present relevant comments on the ethical dilemmas,
psychology (e.g., acute care, rehabilitation, outpatient, thoughtfully weighing them in the light of the APA ethics
assessment, and/or treatment) so that the fact-finding principles, professional practice standards, and relevant
and practice sample review can be conducted in the most statutes.
relevant fashion. This section is broken into two parts:
Part I: The examinee will explain their background.
Cross References
The examinee will provide a history of their educational
and professional background. Special consideration American Psychological Association (APA), Division 40
should be given to their pediatric neuropsychological National Academy of Neuropsychology (NAN)
training and background.
The examinee will explain their current role as a
pediatric neuropsychologist and the issues their typi- References and Readings
cal clientele present.
ASPPB National Register designation committee (2008). Retrieved
Part II: The examinee will demonstrate pertinent knowl- October 1, 2009 from http://www.nationalregister.org/designate_
edge of practical pediatric neuropsychology. stsearch.html
Beljan, P., Bos, J., Courtney, J., & Dodzik, P. (2006). Preparation guide for
The next segment of the oral examination allows the
examination and certification by the American Board of Pediatric
candidate to present the material in their practice sample Neuropsychology. Retrieved from http://abpdn.org/docs/study-
and to provide an overview of the history, evaluation pro- guide.pdf
cess, and outcome of the case. The examiners evaluate their For additional information please see the web site at www.abpdn.org.
American Board of Professional Psychology (ABPP) A 123
their specialties. Examples of these might include clinical

American Board of Professional A
and cognitive-behavioral, clinical neuropsychology and
Psychology (ABPP) rehabilitation, or counseling and group.
For a licensed psychologist to be board eligible,
C HRISTINE M AGUTH N EZU each of the 13 boards require that he or she meets both
Drexel University Hahnemann Campus generic and specialty eligibility criteria concerning
Philadelphia, PA, USA education, professional training, and licensure in the
jurisdiction where professional services are provided.
Once an individuals credentials are reviewed and
Membership approved, the individual seeking board certification
moves to the next phase of their candidacy process. In
The American Board of Professional Psychology (ABPP) clinical neuropsychology and forensic specialties, this
has 3,074 currently active board-certified specialists in necessitates passing a written examination. In all other
membership. As a national-in-scope credentialing organi- specialties, the candidates are not required to take a
zation in professional psychology, its membership is written exam, and may move directly to the final phases
comprised doctoral-level psychologists who provide pro- in the process. For all specialties, this includes first sub-
fessional services and consultation and are licensed to mitting a professional practice sample. After the practice
practice psychology in the jurisdiction in which they sample is approved, the oral examination (final phase) is
practice. Completion of a doctoral degree, completion of typically scheduled. Specialty boards may also provide a
a qualified internship, relevant postdoctoral experience, senior option regarding practice samples submitted by
and relevant jurisdictional licensure as a psychologist are candidates with at least 15 years of experience post licen-
the minimum prerequisites for approval to take an ABPP sure who may submit samples of their professional work
board certification exam. such as publications, treatment manuals, program man-
uals, or a comprehensive summary of their professional
practice, to satisfy the requirements of a professional
Major Areas or Mission Statement practice sample.
With regard to both practice samples and oral exams,
The American Board of Professional Psychology (ABPP) the candidates competency is assessed across various
is a national-in-scope credentialing organization that domains. These competency domains may be functional
has been awarding board certification in professional in nature, and include the day-to-day activities of specialty
psychology specialties for over 60 years (Bent, Packard & practice, such as assessment, intervention, and/or consul-
Goldberg, 1999; Finch, Simon & Nezu, 2006; Packard tation that are informed by a scientific literature base.
& Reyes, 2003). ABPP describes the value of its credential They also include foundational competencies, such as
as one that provides peer and public recognition of ethics, individual and cultural diversity, and interper-
demonstrated competence in an approved specialty sonal competence, which cut across all of a specialists
area in professional psychology (American Board of other activities. The competency model upon which
Professional Psychology, 2008). Moreover, ABPP ABPP board certification is based, draws from several
board certification is increasingly associated with important sources such as the APA-sponsored Compe-
greater opportunities for career growth, including em- tencies Conference in 2002 and resulting Task Force on
ployment opportunities, practice mobility between jur- Assessment of Competence in Professional Psychology
isdictions, and financial compensation (American Board (Kaslow et al., 2007), and a review of competency assess-
of Professional Psychology; Sweet, Nelson & Moberg, ment models developed both within (e.g., Assessment
2006). of Competence Workgroup from Competencies Confer-
ABPP is currently a unique and unitary umbrella ence Roberts, Borden, Christiansen, & Lopez, 2005;
organization with multiple specialty boards that Leigh et al, 2007) and outside (e.g., American Council
include cognitive-behavioral, clinical, clinical child and for Graduate Medical Education and American Board
adolescent, clinical health, clinical neuropsychology, of Medical Specialties, 2000) of the profession of
counseling, couples and family, forensic, group, school, psychology.
rehabilitation, organizational, business, and consulting, There is a strong consensus among many professional
and psychoanalysis. Many professional psychologists psychologists that the American Board of Professional
seek dual certifications that reflect the full scope of Psychology represents a high degree of integrity regarding
124 A American Board of Professional Psychology (ABPP)
specialty board certification and serves as a gold standard For interested applicants, it contains application instruc-
for demonstration of specialty competency in professional tions as well as other helpful information. The organiza-
psychology. tion will publish its first book, Becoming Board Certified by
the American Board of Professional Psychology (ABPP) in
2009.
The origins of ABPP can be traced back to its establish-

ment in 1947 as the American Board of Professional
Cross References
Examiners in Psychology (Bent et al., 1999). The intention
American Academy of Clinical Neuropsychology
of the original board was to ensure that individuals were
(AACN)
qualified to perform the professional service activities
American Board of Clinical Neuropsychology (ABCN)
associated with clinical and counseling psychology.
American Board of Rehabilitation Psychology (ABRP)
However, as professional psychology expanded its scope
and depth, the organization changed its name to the
American Board of Professional Psychology to reflect the
expansion of specialization activities that were emerging References and Readings
for professional psychologists. As a result, the number
of its affiliated specialty boards and associated academies American Council for Graduate Medical Education and American Board
has grown from 3 to 13, reflecting this professional of Medical Specialties (2000). Toolbox of assessment methods.
expansion and the breadth of specialties that have Chicago, IL: American Council for Graduate Medical Education
and American Board of Medical Specialties.
emerged over that past 5 decades (Finch et al., 2006;
American Board of Professional Psychology (2008). Retrieved June 25,
Packard & Reyes, 2003). 2008, from http://www.abpp.org
Bent, R. J., Packard, R. E., & Goldberg, R. W. (1999). The American board
of professional psychology. Professional Psychology: Research and
Major Activities Practice, 30, 6573.
Datillio, F. M. (2002). Board certification in psychology: Is it
really necessary? Professional Psychology: Research and Practice, 33,
Each of the psychology specialty boards under the ABPP 5457.
umbrella has an elected trustee who participates as a Finch, A. J., Simon, N. P., & Nezu, C. M. (2006). The future of clinical
member of the ABPP Board of Trustees as the overall psychology: Board certification. Clinical Psychology: Science and
governance group of the ABPP. Each specialty board Practice, 13, 254257.
Kaslow, N. J., Rubin, N. J., Bebeau, M. J., Leigh, I. W., Lichtenberg, J. W.,
assumes the responsibility for developing and carrying
Nelson, P. D., Portnoy, S. M., & Smith, I. L. (2007). Guiding princi-
out the ABPP specialty examinations. The ABPP central ples and recommendations for the assessment of competence. Pro-
office, under the management of a full-time Executive fessional Psychology: Research and Practice, 38, 441451.
Officer, executes important day-to-day functions for all Leigh, I. W., Smith, I. L., Bebeau, M. J., Lichtenberg, J. W., Nelson, P. D.,
of the 13 specialty boards. These include generic candida- Portnoy, S., Rubin, N. J., & Kaslow, N. J. (2007). Competency
assessment models. Professional Psychology: Research & Practice, 38,
cy verification of applicants, budget maintenance and
463473.
accounting responsibilities, record keeping, development Nezu, C. M., Finch, A. J., & Simon, N. P. (Eds.) (2009, in press), Becoming
and maintenance of an ABPP Directory, development and board certified by the American board of professional psychology
editing responsibility for the ABPP website, monitoring (ABPP). New York: Oxford University Press.
the organization relative to ethical/legal issues, planning Packard, T., & Reyes, C. J. (2003). Specialty certification in professional
psychology. In M. J. Prinstein & M. D. Patterson (Eds.), The portable
of conference and governance activities, and general ad-
mentor: Expert guide to a successful career in psychology (pp. 191
ministrative support. The primary publication of the or- 208). New York: Plenum.
ganization, The Specialist, is published twice annually and Roberts, M. C., Borden, K. A., Christiansen, M. D., & Lopez, S. J. (2005).
available to all members in both electronic and printed Fostering a culture shift: Assessment of competence in the education
format. The organization website (www.ABPP.org) and careers of professional psychologists. Professional Psychology:
Research and Practice, 36, 355361.
contains important information regarding the mission,
Sweet, J. J., Nelson, N. W., & Moberg, P. J. (2006). The TCN/AACN
governance, and organizational documents. For the 2005 Salary Survey: Professional practices, beliefs, and incomes
public, the website contains listings of board-certified of U.S. Neurophysiologists. The Clinical Neuropsychologist, 20,
specialists across specialties and practice jurisdictions. 325364.
American Board of Professional Neuropsychology (ABN) A 125
the diplomate process to maintain membership. At this

American Board of Professional A
time, an oral examination and essay examination were
Neuropsychology (ABN) added to the case study reviews, and all previous members
were allowed the opportunity to undergo the expanded
J OHN E. M EYERS examination process. Those who successfully completed
Private Practice, Neuropsychology the process, including the new oral examination, were
Mililani, Hawaii, USA given full diplomate status in ABN.
After 1991, those who did not successfully complete
the additional oral examination were no longer listed
Membership as diplomates through ABN. The oral examination in-
cluded three 1 h sessions dealing with ethics, the work
The American Board of Professional Neuropsychology sample, and general knowledge. ABN no longer required
(ABN) comprises 350 (as of 2010) neuropsychologists letters of competency from supervisors but instead
who have doctoral degrees, and they are licensed as psy- required letters of recommendation from other
chologists and have completed the ABN diplomate exam- neuropsychologists.
ination process. In 2004, the diplomate evaluation process was again
ABN was established in 1982 by a group of clinical reevaluated and work began on substituting a multiple-
neuropsychologists, all of whom were diplomates of the choice general knowledge examination for the oral exam-
American Board of Professional Psychology (ABPP), to ination on the same subject. This process took several
provide peer regulation of the practice of professional years to complete, and as of January 1, 2009, all applicants
neuropsychology. The process of obtaining the ABN dip- were required to complete the multiple-choice written
lomate is a dynamic one which has changed over the years examination; the essay examination was dropped in
and is expected to evolve as the field of neuropsychology favor of the multiple-choice exam. In 2008, the original
evolves. Initially, in addition to obtaining a doctoral acronym for ABN was changed from ABPN to ABN to
degree, licensure as a psychologist, and completing a avoid confusion with the American Board of Psychiatry
number of years of postdoctoral experience in neuropsy- and Neurology.
chology, early applicants were required to show evidence The current examination procedure includes:
of specialized training in neuropsychology and to provide
1. Review of credentials and letters of recommendation
supervisory evaluations of their competency in profes-
2. A 100-question multiple-choice examination
sional neuropsychology.
3. A case study-work samples review
Between 1982 and 1985, following a review of creden-
4. A 1-h ethics oral examination and
tials and supervisory evaluations, work samples were re-
5. A 1-h work style oral examination
quired. These were graded by multiple examiners on a
pass/fail basis. Individuals who passed this final step were The multiple-choice written examination covers areas of
awarded a diplomate. Individuals who did not pass eval- general knowledge based on the recommended guidelines
uation were allowed to apply for a Certificate in Profes- of the Houston Conference. The ethics examination
sional Neuropsychology, indicating that they had some addresses ethical situations and current ethical dilemmas,
training in neuropsychology but not sufficient to be and the work style examination covers clinical vignettes
awarded diplomate status. This was initially intended as and clinical decision-making.
an interim credential as part of the process of obtaining
a diplomate. After 1985, this process was abandoned as
increasing numbers of neuropsychology training pro- Major Areas or Mission Statement
grams became available.
In February of 1989, the ABN was reorganized and the ABN recognizes and encourages the pursuit of excellence
bylaws were modified. An annual dues structure was in the practice of clinical neuropsychology. ABNs prima-
instituted and ABN became a membership organization ry objective is the establishment of professional standards
whose only credential is a diplomate. This newly estab- of expertise for the practice of clinical neuropsychology.
lished organization mandated continuing education for Through its credentialing and examination processes and
active membership. It was required that all those who had its continuing education requirement, the ABN offers to
a Certificate in Professional Neuropsychology complete the medical community, the public, and to individuals
126 A American Board of Rehabilitation Psychology
who have a need for applied neuropsychological services, locations throughout the country. A workshop on the
a process whereby competent professional neuropsychol- ABN examination process is held at least once a year.
ogists can be identified. Individual candidate mentoring is offered throughout
To achieve the standards set forth by the ABN for the year.
competent professional practice of neuropsychology, the
following outcome objectives have been developed:
Validate the skills of clinical practitioners
Identify competent practitioners http://www.neuropsychologyboard.org/
Provide public information about professional Bennett, T. L., Horton, A. M., Jr. & Elliott, R. W. (1999). American Board
of Professional Neuropsychology (ABPN). Bulletin of the National
neuropsychology
Academy of Neuropsychology, 14, 79.
Document the maintenance of competence of profes- Elliott, R. W., & Horton, A. M., Jr. (1994). Philosophy of the American
sional neuropsychology practitioners with continuing Board of Professional Neuropsychology. Bulletin of the National
education requirements Academy of Neuropsychology, 11, 1415.
Provide individuals, organizations, and agencies who Elliott, R. W., & Horton, A. M., Jr. (1995). History and current status of
the American Board of Professional Neuropsychology. The Indepen-
use neuropsychology services with a referral directory
dent Practitioner, 15, 175177.
of ABN diplomates Goldstein, G. (2001). Board certification in clinical neuropsychology:
Some history, facts and opinions. Journal of Forensic Neuropsychol-
Recognition by ABN signifies to the public and to other
ogy, 2, 5765.
health professionals a high level of competency in applied Horton, A. M. Jr., Crown, B. M., & Reynolds, C. R. (2001). American
neuropsychology. The ABN does not ascribe to any spe- Board of Professional Neuropsychology: An Update-2001. Journal of
cific theoretical framework. While recognizing the impor- Forensic Neuropsychology, 2, 6778.
tance and contribution of a graduate education in
neuropsychology and subsequent specialty training, the
ABN believes that the critical element in the practice of
professional neuropsychology is the application of that American Board of Rehabilitation
training to client issues and needs. Psychology
DANIEL E. R OHE
Landmark Contributions Mayo Clinic
Rochester, Minnesota
Applied Neuropsychology, a peer reviewed edited
journal, is the official journal of the ABN.
Membership
Major Activities The American Board of Rehabilitation Psychology

(ABRP) is one of 13-member boards of the American
ABN holds annual board of directors meetings in the Board of Professional Psychology (ABPP). The ABRP
spring and at the National Academy of Neuropsychology consists of 135 (as of 2010) doctoral-level psychologists
(NAN) conference. Associated with ABN is the American who are primarily engaged in provision of clinical services
College of Professional Neuropsychology (ACPN) whose to individuals and their families affected by a wide range
purpose is to provide continuing education programs in of disabilities and chronic health conditions including
neuropsychology. brain injury, spinal cord injury, amputations, chronic
The ACPN is approved by the American Psychological pain, multiple sclerosis, cancer, and sensory impairment
Association to provide continuing education programs. such as blindness and deafness. In addition to clinical
Every year, ACPN offers continuing education at an an- services, the majority of the members also engage in
nual conference and at general membership meetings held research, teaching, and administration of rehabilitation
in conjunction with other neuropsychological or psycho- programs. Rehabilitation psychologists are also involved
logical organizations. Twice a year, the board of directors in interdisciplinary teamwork with other medical and
and committee chairs meet to organize ABNs profession- rehabilitation providers. Rehabilitation psychologists
al activities. ABN candidate examinations and examiner who are boarded in the specialty reside in 30 states
training workshops are held a minimum of twice a year at and Canada.
American Board of Rehabilitation Psychology A 127
Major Areas or Mission Statement 19942000), Bernard Brucker (vice-president), Mitchell

A
Rosenthal (secretary), Daniel Rohe (treasurer). The mem-
The mission of the ABRP is to protect the public and bers at large were: Bruce Caplan, David Cox, Harry Parker,
enhance the quality of health care by certifying rehabilita- Anthony Ricci, James Whelan, and Mary Willmuth. Sub-
tion psychologists who demonstrate the knowledge, skills, sequent board presidents have been Mitchell Rosenthal
and attitudes essential to maximize quality of life for (20002004), Bernard Brucker (20042008), and Daniel
individuals with disabilities and chronic illness. The vi- Rohe (current president).
sion of the ABRP is that all psychologists practicing in The second major contribution is the crafting of an
rehabilitation will be boarded in the specialty. Psycholo- organization that reflected the values of the professionals
gists who obtain the diplomate in rehabilitation psychol- who created it. The ABRP devised an innovative exami-
ogy must meet the generic requirements for specialty nation process that is user-friendly, collegial, competency-
certification by the ABPP that include a doctoral degree based, and affirming of the candidate. The ABRP was the
in psychology from an accredited degree program and first board to devise a proactive mentoring program that
licensure as a psychologist for independent practice in has a credentialed colleague personally guide the appli-
the USA or Canada. The ABRP-specific eligibility require- cant through each step of the process.
ments include: completion of a recognized internship The third major contribution is cosponsorship of
program and 2 years of supervised practice in rehabilita- the annual Rehabilitation Psychology meeting with
tion psychology. In addition, the candidate must have the Division of Rehabilitation Psychology that began
completed at least 3 years of experience in rehabilitation in 1999. The annual meeting has become an institutio-
psychology. Given the diverse training experiences of nalized opportunity for leaders in the field to meet,
rehabilitation psychologists, the credential review present research, and promote the specialty to new
includes significant reliance on the ratings of supervisors students.
(two required) and the endorsement of colleagues and
peers (two required). The candidate then submits a two-
part practice sample (typically two case reports) that is
evaluated by three ABRP examiners. Finally, the candidate
Major Activities
completes an oral examination on: two clinical vignettes,
The major activity of ABRP is cosponsorship of the
their practice sample, and an ethics examination. The
Annual Conference of Rehabilitation Psychology with
entire examination process is designed to ensure that
Division 22 of the American Psychological Association.
each candidate demonstrates the foundational and the
This conference occurs the last weekend of February
functional competencies required of the diplomate in re-
and provides the opportunity to earn continuing educa-
habilitation psychology. The foundational competencies
tion credits. The conference provides ABRP sponsored
fall in four domains: interpersonal interactions, individual
educational sessions that explain the process of attain-
and cultural diversity, ethical and legal foundations, and
ing the diplomate in rehabilitation psychology to inter-
professional identification. The functional competencies
ested candidates. The conference features nationally
encompass science base and application, assessment, in-
recognized leaders in the field of rehabilitation psy-
tervention, consultation, and consumer protection.
chology. The ABRP board works in tandem with the
American Academy of Rehabilitation Psychology
(AARP). The AARP is a separate organization with over-
Landmark Contributions lapping board membership with the ABRP board. The
AARP contributes the operational support required for
The primary contribution of ABRP is providing the op-
organizing the Annual Conference of Rehabilitation
portunity for psychologists who are dedicated to the
Psychology.
health and welfare of individuals with disabilities and
chronic illness to be certified as rehabilitation psycholo-
gists. The ABRP began as a Credentials Committee
within the Division of Rehabilitation Psychology in 1993. Cross References
This committee met throughout 1993 and 1994 and
incorporated as the American Board of Rehabilitation American Board of Professional Psychology (ABPP)
Psychology in 1995. On December 4, 1994 they established American Psychological Association (APA), Division 22
bylaws and elected officers: Richard Cox (president, Rehabilitation Psychology
128 A American College of Professional Neuropsychology (ACPN)
References and Readings Landmark Contributions
Frank, R., Rosenthal, M., & Caplan, B. (Eds.). (2009). Handbook of In addition to the continuing education benefit, ACPN
rehabilitation psychology (2nd ed.). Washington, DC: American Psy- also has an official quarterly journal, Applied Neuropsy-
chological Association.
chology, which is dedicated to the presentation of
Nezu, C., Finch, A., Jr., & Simon, N. (Eds.). (2009). Becoming
board certified by the American board of professional psychology.
practitioner-based scholarly research.
New York, NY: Oxford University Press, Inc. Diplomates of the ABN who are in good standing are
automatically Fellows of ACPN and may use the acronym
FACPN on their signature line. Members of other neuro-
psychological organizations may also join the ACPN as
Affiliate members and receive a subscription to Applied
American College of Professional Neuropsychology, and participate in ACPN continuing
Neuropsychology (ACPN) education programs.
J OHN E. M EYERS Major Activities

Private Practice, Neuropsychology
Mililani, Hawaii, USA ACPN is accredited by the American Psychological
Association to sponsor continuing education for psychol-
ogists. ACPN has two general meetings a year. One
Address (and URL) meeting, National Academy of Neuropsychology (NAN)
annual conference, a continuing education breakfast, is
The American College Of Professional Neuropsychology typically held at the fall. The second yearly meeting is a
(ACPN) multiday conference, usually held in the spring. This is a
c/o Michael Raymond, Ph.D., ABN much larger conference with multiple speakers, presenta-
Executive Director for ABN tions, and a poster session highlighting recent clinically
John Heinz Institute of Rehabilitation Medicine, relevant studies and papers.
Neuropsychology Services
150 Mundy Street
Wilkes-Barre. PA 18702
Cross References
Tel.: (570)826-3771
American Board of Professional Neuropsychology
http://www.neuropsychologyboard.org/
(ABN)
Membership
American Congress of
The American College of Professional Neuropsychology
Rehabilitation Medicine
(ACPN) is a membership organization formed on
September 1, 1995 that is composed of 350 (2009) Neu-
M ARCEL P. J. M. D IJKERS
ropsychologists who have doctoral degrees, are licensed
as psychologists, and have completed the Diplomate
New York, NY, USA
examination process.
Membership
Membership is about 800, consisting of clinicians and
The academic arm of the American Board of Professional nonclinicians with an interest in medical rehabilitation
Neuropsychology (ABN) is the ACPN. The mission of the research, and training in medicine, psychology, occupa-
ACPN is to promote and provide the highest levels of tional and physical therapy, nursing, speech and language
services related to professional neuropsychology, for the pathology, political science, etc. Medical rehabilitation
benefit of the public and the profession. concerns restoration of function for individuals who as a
American Congress of Rehabilitation Medicine A 129
result of stroke, traumatic brain injury, spinal cord injury, 2008). Reflecting the ongoing differentiation between
A
amputation, and other disorders have impairments and radiologists and what (much later) would be called
activity limitations that are primarily physical in nature, physiatrists, the name was changed to American Congress
but often also include cognitive and behavioral deficits; it of Physical Therapy in 1925. To emphasize its link to
is to be distinguished from psychiatric rehabilitation, medicine rather than allied health, the organization
addictions rehabilitation, etc., although there is overlap renamed itself American Congress of Physical Medicine
in methods and sometimes clientele. Members share an in 1944.
interest in rehabilitation research, and the translation of While World War I had given rise to the development of
research-based knowledge into formats that are of use to rehabilitation, the involvement of physicians had been
medical rehabilitation clinicians. About 70 members are limited rehabilitation was centered on the vocational
located outside the USA, especially in Canada. rehabilitation of discharged servicemen. During and after
World War II, however, a number of physicians became
specialists in rehabilitation and started to apply methods
Mission Statement they had used with servicemen to the treatment of civilians
with amputations, spinal cord injury, stroke, and develop-
The mission of the American Congress of Rehabilitation mental disabilities such as cerebral palsy. To avoid the
Medicine is to enhance the lives of persons living with creation of a separate organization involving physicians
disabilities through a multidisciplinary approach to reha- with very similar interests and therapeutic regimens, a
bilitation, and to promote rehabilitation research and its shotgun marriage between physiatrists and rehabilita-
application in clinical practice (About ACRM, 2008). tion physicians was acknowledged in 1952 with expansion
The American Congress of Rehabilitation Medicine of the name of the organization to American Congress of
serves people with disabling conditions by promoting Physical Medicine and Rehabilitation (Zeiter, 1954).
rehabilitation research and facilitating information dis- In the 1960s, the Congress opened its membership to
semination and the transfer of technology. We value re- nonphysician rehabilitation professionals, first only those
habilitation research that promotes health, independence, holding a doctoral degree (1965), then also to nurses and
productivity, and quality of life for people with disabling therapists with an (earned) masters degree (Anonymous,
conditions. We are committed to research that is relevant 1998). To acknowledge the diminishing emphasis on
to consumers, educates providers to deliver best practices, physical medicine, the Congress changed its name again,
and supports advocacy efforts that ensure adequate public to American Congress of Rehabilitation Medicine, in
funding for our research endeavors (About ACRM, 1966. ACRM accepted rehabilitation professionals with a
2008). bachelors degree as members starting in 1986. The first
To develop and implement our vision, ACRM will nonphysician to become president of the organization
seek the involvement of rehabilitation professionals, in- took office in 1977; neuropsychologists who have served
cluding clinicians, senior level service managers, admin- as president include Leonard Diller, Mitchell Rosenthal,
istrators, educators, and researchers. We will call upon the and Wayne Gordon.
leaders in rehabilitation to identify current best practices In recent years, ACRM has redefined itself as an orga-
and best providers at all levels of care. We will disseminate nization focusing on rehabilitation science, with strong
this information to the field at our regional and national interest in both generating knowledge through research
meetings, through directed position papers, and in our and knowledge translation to bring research results to the
journal, Archives of Physical Medicine and Rehabilitation clinic in a format that practitioners can use (Hart, 1997;
(About ACRM, 2008). Heinemann, 2006; Wilkerson, 2004). It now is primarily
a group of creators, transmitters, and consumers of
research-based rehabilitation knowledge, both those
Landmark Contributions with clinical training (physicians, occupational and phys-
ical therapists, psychologists, etc.) and those without
The American Congress of Rehabilitation Medicine was (engineers, political scientists, etc.), bound by the convic-
established in 1923 as the American College of Radiology tion that collaboration of disciplines is the best way to
and Physiotherapy, a professional organization of physi- solve the problems inherent in disablement and the reha-
cians who had a clinical interest in diagnostic and thera- bilitation of persons with impairment, activity limita-
peutic radiology, as well as the therapeutic application of tions, and participation restrictions. The insignia of the
electricity and other physical therapies (About ACRM, organization still reflects ACRMs roots in physical
130 A American Congress of Rehabilitation Medicine
medicine, including the traditional symbols for the four grant programs supported by the National Institute on
elements: water, earth, fire, and air. Disability and Rehabilitation Research since 1987). There
also is considerable overlap between the membership of
the BI-ISIG and Divisions 22 (Rehabilitation Psychology)
and 40 (Clinical Neuropsychology) of the American Psy-
Major Activities
chological Association. The BI-ISIG publishes a newslet-
ter, Moving Ahead. Intense collaboration in research and
ACRM communicates with its members through its
clinical care occurs among the BI-ISIG members, who
scientific journal (the Archives of Physical Medicine and
have their own task forces and come together in an addi-
Rehabilitation APM&R), a newsletter (Rehabilitation
tional annual meeting.
Outlook) and weekly E-news, an electronic digest of
APM&R began in 1920 as the Journal of Radiology, the
time-sensitive news. An annual scientific meeting of 34
private property of a Dr. Albert A. Tyler (Cole, 1999). The
days, often held jointly with other scientific and profes-
journal changed its name to the Archives of Physical Ther-
sional organizations, brings together members and non-
apy, X-ray, Radium, in 1926; in 1930, Dr. Tyler gave the
members to discuss research findings, research methods,
journal to ACRM (then still named the American Con-
and issues relevant to the funding, implementation, and
gress of Physical Therapy) as a debt-free, unencumbered
dissemination of rehabilitation research.
gift. The later changes in the name of the journal parallel
A number of standing committees offer members an
the changes in the name of its owner. It became the
opportunity to work on issues of special interest. Current
Archives of Physical Therapy in 1938, the Archives of
committees include the International Committee (focus-
Physical Medicine in 1945; in 1953, the journal became
ing on the communications between US and foreign re-
the Archives of Physical Medicine and Rehabilitation, the
habilitation research specialists), the Clinical Practice
name it still has (Nelson, 1969). However, the content has
Committee (dealing with issues of evidence-based prac-
shifted gradually from emphasis on physical medicine,
tice and related matters), and the Involving Consumers in
with a fairly low research basis, to an accent on rehabilita-
Rehabilitation Research Committee. The Early Career
tion as carried out by all disciplines that play a role in
Committee aims to assist individuals new to rehabilita-
medical rehabilitation. It now is almost exclusively a re-
tion research in mastering the scientific, administrative,
search journal, with non-US contributions constituting
and personal aspects of a career in rehabilitation research.
over half the contents (Dijkers, 2009).
Over the years, a number of interdisciplinary special
The journal probably gives the best indication of the
interest groups (ISIGs) have existed under the aegis of
role of neuropsychology in rehabilitation settings, and of
ACRM; current groups include ISIGs focused on spinal
neuropsychologists in ACRM. The first paper with neu-
cord injury, stroke, the measurement of participation, and
ropsycholog* in its title or abstract was published in 1975.
traumatic brain injury.
Almost 200 have been published since, but they did not
The Brain Injury ISIG (BI-ISIG) grew out of the
become an annual presence until 1984. The number now
ACRM Head Injury Task Force, first called together in
averages ten a year. In scanning the contributions of
1979. The BI-ISIG, which attracts large numbers of psy-
neuropsychologists to APM&R, a number of characteristics
chologists and especially neuropsychologists, has played a
of neuropsychology in rehabilitation stand out:
crucial role in the development of services for individuals
with traumatic brain injury (TBI) in the United States. A Many of these papers are coauthored with representa-
definition of mild TBI often used in the literature emerged tives of other disciplines, especially physicians.
from the work of this group (American-Congress-of- Several straddle neuropsychology and rehabilitation
Rehabilitation-Medicine.-Head-Injury-Interdisciplinary- psychology, reflecting the fact that in many rehabilita-
Special-Interest-Group, 1993). The Journal of Head Trau- tion programs psychologists need to wear multiple
ma Rehabilitation (JHTR) was founded by a physician hats.
(Sheldon Berrol) and a psychologist (Mitchell Rosenthal) The focus, especially in recent years, is as much on
who were active in the BI-ISIG, as well as involved with treatment as on diagnosis, with cognitive rehabilita-
the fledgling National Head Trauma Foundation, now the tion for TBI and other diagnostic groups most
Brain Injury Association of America. There is significant prominent.
overlap between the BI-ISIG membership and both the A great variety of diagnostic groups have been studied,
Editorial Board of JHTR and the leadership of the TBI including those with peripheral vascular disease
Model Systems of Care (demonstration and research amputations, post-polio fatigue, multiple sclerosis,
American Psychological Association (APA) A 131
sickle-cell disease, progressive supranuclear palsy, Wilkerson, D. L. (2004). Individual, science, and society: ACRMs mis-
sion and the body politic. Archives of Physical Medicine and Rehabil- A
myotonic muscular dystrophy, and spinal cord injury.
itation, 85(4), 527530.
However, over the years and especially recently, stroke Zeiter, W. J. (1954). The history of the American Congress of Physical
and TBI have been the etiologies of disability that Medicine and Rehabilitation. Archives of Physical Medicine and
rehabilitation neuropsychologists have most often Rehabilitation, 35(11), 683688.
been concerned with.
While the American Congress of Rehabilitation Med-
icine is not an organization of psychologists, let alone
neuropsychologists, it is safe to say that it has played
American National Adult Reading
a key role in the development of neuropsychology for Test (ANART)
medical rehabilitation patients in the United States. In
the foreseeable future, it probably will continue to be the Weschlers Adult Reading test
forum in which these specialists, especially those who are
interested in research, interact with nurses, speech/lan-
guage pathologists, neuroscientists, and other specialties
that contribute to rehabilitation.
American Psychological
Association (APA)
WADE P ICKREN
References and Readings Ryerson University
Toronto, ON, Canada
About ACRM. (2008). Retrieved August 25, 2008, from http://www.acrm.
org/about/index.cfm
American-Congress-of-Rehabilitation-Medicine.-Head-Injury-Interdisci-
plinary-Special-Interest-Group. (1993). Definition of mild trau- Address and URL
matic brain injury. Journal of Head Trauma Rehabilitation, 8(3),
8687. 750 First Street NE, Washington, DC 20002-4242 (www.
Anonymous. (1998). Development of the American Congress of Rehabil- apa.org)
itation Medicine into a multidisciplinary professional society: Final
report of the Professional Development Committee, 19691972.
Archives of Physical Medicine and Rehabilitation, 79(12 Suppl. 2),
412. Membership
Cole, T. M. (1999). ACRM presidential address. In the clothing of chal-
lenge. American Congress of Rehabilitation Medicine. Archives of 150,000 as of 2010
Physical Medicine and Rehabilitation, 80(2), 127129.
Dijkers, M. P. (2009). International Collaboration and Communication
in Rehabilitation Research. Archives of Physical Medicine and
Rehabilitation, 90(5), 711716.
Hart, K. A. (1997). Rehabilitation research: The new focus of the Ameri-
can Congress of Rehabilitation Medicine. Archives of Physical Medi- The mission of the APA is to advance the creation, com-
cine and Rehabilitation, 78(12), 12871289. munication, and application of psychological knowledge
Heinemann, A. W. (2006). ACRMs evolving mission: Opportunities to to benefit society and improve peoples lives.
promote rehabilitation research. Archives of Physical Medicine and
Rehabilitation, 87(2), 157159.
Kottke, F. J., & Knapp, M. E. (1988). The development of physiatry before
1950. Archives of Physical Medicine and Rehabilitation, 69 Spec No,
414.
Krusen, F. H. (1969). Historical development in physical medicine and
rehabilitation during the last forty years. Walter J. Zeiter Lecture. The American Psychological Association (APA) was
Archives of Physical Medicine and Rehabilitation, 50(1), 15. founded in 1892 by a small group of men interested in
Nelson, P. A. (1969). History of the Archives A journal of ideas and what was called the new psychology. Its founding at this
ideals. Archives of Physical Medicine and Rehabilitation, 50(7),
particular time can best be understood as part of the large
367405.
Rusk, H. A. (1969). The growth and development of rehabilitation
number of changes occurring in the USA at that time.
medicine. Archives of Physical Medicine and Rehabilitation, 50(8), The emergence of a number of what are now standard
463466. academic disciplines, psychology, economics, political
132 A American Psychological Association (APA)
science, biochemistry, physiology, in the last 2 decades association that was much more broadly based than
of the nineteenth century was part of a reorganization of before the War and that was organized around an increas-
American knowledge production, reflecting a division of ingly diffuse conceptualization of psychology. Now, the
intellectual labor similar to the division of manufactory associations scope included professional practice and
labor. Like its fellow disciplines, the new psychology grew the promotion of human welfare, as well as the practice
and prospered as it responded to the needs of American of the science of psychology. This flexibility in scope has
society. remained to the present time, as new challenges and
Within the modern university system that emerged demands have arisen.
after the U.S. Civil War, the new disciplines quickly Psychology boomed after the end of World War II,
developed advanced degrees that provided credentials, with the greatest increase in membership coming between
which served to validate the disciplines members as 1945 and 1970. This was due to intense interest in the
experts in their special field. This occurred in parallel field, especially in the domains of clinical and applied
with the progressive movement in politics, which called psychology, among returning serviceman, many of
for a more efficient, less corrupt, social order. The whom saw the great need for better psychological services
synergism of these two developments, specialized exper- firsthand during the war. Institutional or structural fac-
tise and rationalized government, helped create the de- tors that facilitated this growth included the GI Bill, the
mand for trained personnel to fill the new professional new Veterans Administration Clinical Psychology training
niches created by the demands for a more efficient program, and the creation of the National Institute of
society. Psychology was one of the most successful of Mental Health. For the first time, psychology was a field,
the new disciplines to make itself useful for the social both science and practice, that was richly funded for
management of an increasingly complex and diversified training and research. This was, as one scholar termed it,
society. The Golden Age of Psychology. The rapid and incredible
In July 1892, G. Stanley Hall (18441924) met with a growth in APAs membership reflected this trends, as
small group of men to discuss the possibility of organizing membership grew 630% from 1945 to 1970, from 4,183
a psychological association. Although the details of the members (1945) to 30,839 (1970). By comparison, from
meeting are not known, the group elected 31 individuals, 1970 to 2000, APA membership grew to 88,500, with
including themselves, to membership, with Hall as the another 70,500 affiliates.
first President. The first meeting of the new American Part of what facilitated this growth was the new divi-
Psychological Association (APA) was held in December sional structure of the APA that grew out of the reorgani-
1892 at the University of Pennsylvania. The basic gover- zation plan during World War II. Now, members could
nance of the APA at this time was consisted of a small join a special interest group within APA and find other
council with an executive committee. This plan remained like-minded members. Of course, this also facilitated the
in effect until the reorganization of APA during World fractionation of psychology and pushed the field away
War II. from any sense of unity that it may have held prior to
Membership growth of the APA was modest over the the war. Nineteen divisions were approved in 1944, with
first 50 years of its existence. From 31 members in 1892, the two most numerous being clinical and personnel (now
there were 125 members in 1899, 308 in 1916, 530 in 1930, counseling). This reflected the sectional structure of the
and 664 in 1940. In 1926, a new class of nonvoting American Association of Applied Psychology (AAAP, f.
membership was formed, associate, and most of the 1937), which had emerged in 1937 as the chief rival to the
growth occurred in that class after 1926, so that there APA and had been the chief reason for the reorganization.
were 2,079 associate members in 1940. Many of these Because the Psychometric Society (Division 4) decided
associates were individuals doing practical or applied not to join and after Division 11, Abnormal Psychology
work in psychology and who also belonged to one of the and Psychotherapy, merged with Division 12, Clinical
applied associations that emerged in this time. Realizing Psychology, the number of active divisions was reduced
that the growth of applied psychology represented to 17. Growth in the number of divisions was slow until
a potential threat to its preeminence, the leaders of APA the 1960s, only three more were added, in part because
sought to reorganize the association during World War II. many of the older members, then in leadership positions,
Under this reorganization plan, the APA merged with were quite resistant to increasing the number of divisions.
other psychological organizations and created divisions The growth in the number of divisions since the 1960s has
to represent special fields of interest. There were initially been consistent, with 54 divisions now part of the APA
17 divisions (19 were proposed). The result was an structure. Many of the newer divisions reflect the growth
American Psychological Association (APA) A 133
of particular practice areas, for example, Division 50, the mid- to late 1980s, as tensions between those who
A
Addictions. However, there has also been growth in spe- wanted APA to remain a primarily scientific organization
cial interest areas that belie any simple science/practice and those who sought a greater emphasis by the associa-
dichotomy, for example, Society for the Psychology of tion on professional practice rose to a boil. A proposed
Women, Society for the History of Psychology, Interna- reorganization plan was defeated by a vote of the mem-
tional Psychology, Media Psychology, or the Study of Men bership and almost immediately a large group of dissident
and Masculinity. psychological scientists, including former APA Presidents,
left the APA to form what is now the Association for
Psychological Science (APS). Still, after a period of strug-
Major Activities gle, both organizations are strong, stable representatives
of psychology, with many psychologists belonging to both
The effect on APA governance of the divisional structure associations.
and the growth of state and provincial psychological One result of the split that led to the formation of
organizations has been marked. As mentioned, prior to APS is that professional interests have grown stronger
World War II, APAs governance structure was a small within APA. As the number of psychologists devoted to
council with an executive committee. After the reorga- professional practice grew and gained greater influence
nization and the end of the war, the Council of Repre- in the APA governance structure, a new unit was estab-
sentatives has grown in number to accommodate lished in the APA Central Office. The Office of Profes-
representation from each division and from state and sional Practice was created in the mid-1980s with a
provincial psychological associations, thus making gover- mandate to focus on applied practice activities, especial-
nance somewhat unwieldy. Various plans have been tried ly the promotion of health-care practice. To finance the
over the years to ensure a voice for each of the areas and expansion of activities, a special assessment was levied
interests groups in psychology on the council and it on psychologists licensed for health-care practice. With
remains a dynamic situation. One result of the growth this money, the office was able to engage in consultation,
of professional psychology, especially clinical and technical assistance, and legal and legislative assistance
counseling psychology, on governance has been the infor professionals. The office also began to work closely
crease in the representation of professional interests, for with state associations to enhance practice issues and
example, licensing, specializations, etc., in the delibera- support efforts relevant to legislation in state legislatures.
tions of the council. At times, this has led to tension Within a few years, the range of activities led to the need
between the representatives of psychological science and to create the Practice Directorate within APA. Since that
those whose main commitment is to advancing time, the Practice Directorate has played the important
professional practice. In historical retrospect, it seems roles of handling all practice-related programs and has
clear that this tension was inherent in the reorganization been responsible for the coordination of practice efforts
of APA, as the association reflected developments in the in legal and legislative arenas. The special assessment and
field. the Practice Directorate represented a special moment
As a membership organization, APA has often been in APAs history in that they enhanced the power of
perceived as inadequately representing one or more clinical and professional practice both within and
its constituencies. It has been the case, more often than without APA.
not, that the resulting tension was resolved and the un- Even so, APA has maintained a commitment to the
happy parties remained within the association. However, promotion of psychological science. It publishes more
there have also been more serious disagreements that have than 40 peer-reviewed scientific journals. Internally, in
resulted in new organizations being formed. In the late the APA Central Office, this is represented by the Science
1950s, a group of experimental psychologists grew Directorate. Since the late 1980s, the Central Office has
unhappy with what they perceived as APAs drift from been reorganized to better represent the diverse constitu-
scientific psychology. By the end of 1959, this group encies of the membership. Beginning with the formation
formed the Psychonomic Society in order, they asserted, of the Practice Directorate in the late 1980s, other Direc-
to foster psychology as a science without a need to attend torates were formed in the hope that the interests of all the
to professional issues. The Psychonomic Society remains a membership would be better represented. As of 2009,
very viable and valuable organization of scientists to the there were the Practice, Education, Science, and Public
present moment; many of its members remained APA Interest Directorates. From a historical perspective, it is
members, as well. A more serious division occurred in too soon to determine whether this approach represents
134 A American Psychological Association (APA), Division 22
an advance for the association or a further balkanization Major Areas or Mission Statement
of the field.
APA remains the worlds largest membership organi- The Division of Rehabilitation Psychology works to unite
zation of psychologists. It has a fascinating past, marked psychologists and others interested in the prevention and
by growth, conflict, and increasing diversification. rehabilitation of disability and chronic illness. Rehabilita-
tion Psychology Practice is a specialty within the domain
of professional healthcare psychology, which applies psy-
Cross References chological knowledge and skills on behalf of individuals
with disabilities and chronic health conditions in order to
Advocacy; Entries 7786 (excluding 84); Entries maximize their health and welfare, independence and
376, 377 choice, functional abilities, and role participation. Such
American Psychological Association Division 22 disabilities include spinal cord injury, brain injury,
American Psychological Association Division 40 stroke, amputations, burns, work-related injuries, multi-
ple traumatic injuries, chronic pain, cancer, heart disease,
multiple sclerosis, neuromuscular disorders, AIDS, devel-
opmental disorders, psychiatric impairment, substance
References and Readings abuse, impairments in sensory functioning, and other
physical, mental and/or emotional impairments. The
Dewsbury, D. A. (1997). On the evolution of divisions. American Psychol- broad field of Rehabilitation Psychology also includes
ogist, 52, 733741.
rehabilitation program development and administration,
Evans, R. B., Sexton, V. S., & Cadwallader, T. C. (Eds.). (1992).
The American Psychological Association: A historical perspective.
research, teaching, public education and development of
Washington, DC: American Psychological Association. policies for injury prevention and health promotion, and
Fernberger, S. W. (1932). The American Psychological Association: advocacy for persons with disabilities and chronic health
A historical summary, 18921930. Psychological Bulletin, 29, 189. conditions.
Guthrie, R. V. (1998). Even the rat was white: A historical view of psychol-
ogy. Boston: Allyn and Bacon.
Pickren, W. E., & Schneider, S. F. (Eds.). (2005). Psychology and the
National Institute of Mental Health: A historical analysis of science, Landmark Contributions
practice, and policy. Washington, DC: APA Books.
1. Rehabilitation psychologists have worked in medical
settings as part of teams of healthcare professionals for
more than half a century, long before psychologists
were regularly involved in other healthcare settings.
American Psychological 2. Division 22 was established in 1958, one of the earlier
Association (APA), Division 22 divisions in APA.
3. Division 22 members conducted the initial research
W ILLIAM S TIERS on individual, interpersonal, and social changes
Johns Hopkins University School of Medicine related to changes in appearance and physical capacity,
Baltimore, MD, USA as well as the social psychology of stereotyping and
prejudice faced by persons with disability.
4. Division 22 members were among the pioneers help-
Membership ing psychology understand the world of work, how the
same can be affected by impairment and disability,
The American Psychological Association (APA) Division and issues about vocational rehabilitation.
22 Rehabilitation Psychology is composed of over 1,111 5. Rehabilitation psychologists have developed the
(2009) psychologists who provide clinical services (91%), principles of cognitive rehabilitation, and have served
teach (65%), conduct research (41%), manage rehabilita- as leaders in the federal model systems programs
tion programs (37%), and perform other activities too. for traumatic brain injury, spinal cord injury, and
They work in hospitals and clinics (40%), in university, burns.
college, medical school (27%), and other settings, and are 6. Board Certification in Rehabilitation Psychology was
also in independent practice (28%). established in 1997.
American Psychological Association (APA), Division 40 A 135
Major Activities the years from its initial one representative to the current
A
allotment of four seats. This trend coincides with Division
The journal Rehabilitation Psychology is published 40s increasing influence within APA and increasing recog-
quarterly by the APA. nition of neuropsychology as a clinical specialty.
Division 22, in conjunction with the American Board Eligibility for membership is based on the criteria re-
of Rehabilitation Psychology, holds an annual conference quired for Associate, Member, or Fellow status in the APA.
in the spring. Additional requirements include demonstrated interest
in the field of neuropsychology and its scientific develop-
ment, public dissemination, and/or clinical applications.
All members of the division have rights and privileges to
Cross References hold office and serve on division committees, vote in
regular elections, attend various meetings of the division,
American Psychological Association (APA) and receive publications of the division. Information for
Rehabilitation Psychology joining Division 40 can be obtained on the divisions web-
site at http://www.div40.org/membership.html.
APA statistics indicate that the majority of Division
40 members are women (55%). Ethnic minority members
References and Readings constitute 8% of the membership, consistent with larger
APA trends. Approximately, 80% of the division member-
American Psychological Association. (2008). A closer look at Division 22: ships have Ph.D. in clinical psychology or a related field.
A growing field meets the challenges of war. Monitor on Psychology,
Nearly half (42%) of the members work in independent
38(8), 5455.
Frank, R., Rosenthal, M., & Caplan, B. (Eds.). (2009). Handbook of settings. Most other members work in medical schools,
rehabilitation psychology (2nd ed.). Washington, DC: American Psy- hospitals, and university settings. Many combine their
chological Association. work in institutional and private-practice settings. Mem-
Larson, P., & Sachs, P. (2000). A history of Division 22. In D. A. Dewsbury bership surveys have indicated that psychologists in Divi-
(Ed.), Unification through division: Histories of the divisions of the
sion 40 spend a substantially larger amount of time
American Psychological Association (Vol. 5, pp. 3358). Washington,
DC: American Psychological Association. (>40%) in assessment activities than other APA members
(<15%). Approximately, one third of the members are
actively involved in research activities. Approximately,
40% are involved in clinical training.
American Psychological
Association (APA), Division 40 Major Areas or Mission Statement
W ILLIAM B. B ARR Division 40 was formed in 1980 with the mission of
New York University School of Medicine enhancing the understanding of brain-behavior relation-
New York, USA ships and the application of such knowledge to human
problems. Activities of the division encompass the areas
of science (e.g., presentations at the annual meeting of
Membership APA, awards for outstanding scientific contributions),
practice (e.g., Current Procedural Terminology CPT
The Division of Clinical Neuropsychology (Division 40) is billing codes, educational brochures for patients), edu-
one of 56 specialty divisions recognized by the American cation and training (e.g., neuropsychology graduate
Psychological Association (APA). Since its inception, it has student organization), and specialty public interest
become one of APAs largest and most active divisions. In its groups (e.g., women, minorities, geriatrics, rural, etc.).
nearly 30 years, membership has grown from 433 psychol- The division upholds APA bylaws and enacted its own
ogists to its current numbership of 5,315, which currently divisional bylaws in 1980, which were subsequently re-
makes it the second largest of all APA divisions behind only vised to their current form in 1997. Over the years, Divi-
the Independent Practice Division (Division 42). The division 40 has provided published guidelines on many aspects
sions representation to the APA council has grown over of neuropsychological practice and training while also
136 A American Psychological Association (APA), Division 40
fostering continued development of the science of neuro- Dr. Harold Goodglass with Dr. Gerald Goldstein serving
psychology through activity of its committees. The divi- as both the Secretary and Treasurer. The presidents of the
sion advances scientific knowledge in the field of division include many of the most prominent names in the
neuropsychology through its support of publication and field of neuropsychology (Table 1).
presentation of scientific papers at professional confer- One of the divisions earliest activities included work-
ences, including the APAs annual convention. ing with the INS Task Force on Education, Accreditation,
and Credentialing (TFEAC) in establishing guidelines for
doctoral, internship, and postdoctoral training in clinical
Landmark Contributions neuropsychology. Recommendations provided by that
group, calling for a combination of training experiences
Psychologists interested in the developing field of neuro- in psychology and the neurosciences, continues as the
psychology began participating on a regular basis at APA fields dominant model of training. The INS task force
meetings during the 1960s. The origins of Division 40 can was eventually discontinued as it became increasingly
be traced back to the development of the International evident that professional issues were becoming the domain
Neuropsychological Society (INS), which is known as the of Division 40. A listing of publications of other profes-
field of neuropsychologys first formal organization. Infor- sional guidelines and statements developed by Division
mal meetings of psychologists interested in neuropsycho- 40 committees and task forces are provided in Table 2.
logical issues were held at the annual APA meeting dating The purpose of these guidelines was to facilitate an adher-
back to 1965. The INS was formally organized in 1967 as ence to standards for professionals in the field of clinical
an outgrowth of these meetings with the goal of serving as neuropsychology with the ultimate goal of ensuring the
a scientific and educational organization. The need for quality of services provided to consumers.
formal representation in APA became increasingly appar- During the 1990s, a task force from Division 40 led
ent as professional issues regarding practice, education, by Manfred Meier successfully submitted a petition for
and training in neuropsychology began to emerge. Leaders clinical neuropsychology to become the first psycholog-
in the field, including Arthur Benton, Louis Costa and ical specialty recognized by the APAs Commission on
Manfred Meier, saw the need for the development of an Recognition of Specialties and Proficiencies in Profes-
organization to promote the growing specialty of clinical sional Psychology (CRSPP). Recognition of clinical
neuropsychology that was independent of INS and APAs neuropsychology as a specialty became official in 1997.
Division of Clinical Psychology (Division 12). The appli- This was followed by a set of activities, working in
cation to establish a Division of Clinical Neuropsychology conjunction with the National Academy of Neuropsy-
was submitted to APA and approved by its Council of chology (NAN), American Board of Clinical Neuro-
Representatives in September 1979. The formation of psychology (ABCN), American Academy of Clinical
Division 40 was made effective in January 1980, consistent Neuropsychology (AACN), and the Association of
with APA procedures. The divisions first President was Postdoctoral Programs in Clinical Neuropsychology
American Psychological Association (APA), Division 40. Table 1 Presidents of division 40 (clinical neuropsychology)
1980s 1990s 2000s

19791980 Harold Goodglass 19891990 Charles G. Matthews 19992000 Gordon J. Chelune
19801981 Harold Goodglass 19901991 Raymond S. Dean 20002001 Jason Brandt
19811982 Louis Costa 19911992 Steven Mattis 20012002 Allan F. Mirsky
19821983 Nelson M. Butters 19921993 Oscar Parsons 20022003 Antonio Puente
19831984 Thomas J. Boll 19931994 Robert K. Heaton 20032004 Kathleen J. Haaland
19841985 Lawrence C. Hartledge 19941995 Carl Dodrill 20042005 Robert J. Ivnik
19851986 Manfred J. Meier 19951996 Kenneth M. Adams 20052006 Russell M. Bauer
19861987 Edith F. Kaplan 19961997 Eileen B. Fennell 20062007 Keith O. Yeates
19871988 Byron P. Rourke 19971998 Linas A. Bieliauskas 20072008 Thomas A. Hammeke
19881989 Gerald Goldstein 19981999 Cecil R. Reynolds 20082009 Glenn E. Smith
American Psychological Association (APA), Division 40 A 137
American Psychological Association (APA), Division 40. The division has four standing committees including
A
Table 2 Published guidelines from division 40 committees Membership, Fellowship, Elections, and Program Com-
and task forces mittees and four continuing committees consisting of the
Science Advisory, Education Advisory, Practice Advisory,
Year Activity
and Public Interest Advisory Committees. Special Com-
1987 Guidelines for Doctoral Training Programs in Clinical mittees, including Task Force Committees, can also be
Neuropsychology established by vote of the Executive Committee, when the
1987 Task Force Report on Computer-Assisted need arises. The Committee on APA Relations and the
Neuropsychological Evaluation Publications and Communications Committee are exam-
1988 Guidelines of Continuing Education in Clinical ples of these. The President, in consultation with the EC,
Neuropsychology appoints chairs of all divisional committees and task forces.
1989 Definition of a Clinical Neuropsychologist Summaries of divisional activities, minutes of executive
1989 Guidelines Regarding the Use of Nondoctoral committee meetings, and committee reports are published
Personnel in Clinical Neuropsychological Assessment biannually in Newsletter 40, the official division newsletter.
1991 Recommendations for Education and Training of Continued commitments to training have been demon-
Nondoctoral Personnel in Clinical Neuropsychology strated by the formation of the Division 40 Association for
1991 Guidelines for Computer-Assisted Neuropsychology Students in Training (ANST) and the
Neuropsychological Rehabilitation and Cognitive establishment of an Early Career Psychologists committee.
Remediation Committees and mentoring programs have been estab-
lished for women entering the field and for ethnic minority
members. Brochures describing an introduction to clinical
(APPCN) in developing an integrated model for spe- neuropsychology are available through the divisions Public
cialty training in clinical neuropsychology. Representa- Interest Advisory Committee (PIAC). The Practice Adviso-
tives from these organizations and various training ry Committee (PAC) provides monitoring of legislative
programs across the USA met in 1997 for what was activities and both local and national activities affecting
termed The Houston Conference on Specialty Training the practice of clinical neuropsychology. This committee is
in Clinical Neuropsychology. The conference led to the also responsible for interactions with government agencies
development and publication of a document describing such as the Centers for Medicare and Medicaid Services
an integrated model of education and training. Interac- (CMS). The PAC worked with other organization in estab-
tions between Division 40 and these other groups con- lishing a new set of CPT testing codes aimed at optimizing
tinue through an organization called the Clinical reimbursement for neuropsychological services. These
Neuropsychology Synarchy (CNS). codes were officially implemented in 2006.
The division has maintained its goal of integrating
science and practice. The Science Advisory Committee
Major Activities (SAC) continues in its role of producing scientific pro-
grams for the APAs annual convention. Studies on neu-
Officers of Division 40 include President, President-Elect, rologic syndromes, assessment, and developmental issues
Past President, Secretary, and Treasurer. These positions are among the topics most commonly presented in the
are elected by the general membership with the term of Division 40 program at the annual APA meeting. The SAC
President lasting 1-year and the roles of Secretary and also provides a number of awards for students and early
Treasurer lasting 3-years. The officers serve on an Execu- career psychologists establishing careers in neuropsycho-
tive Committee (EC) joined by various Division Commit- logical research. More recent SAC activities include inte-
tee Chairs, Divisional Representatives to APA Council, gration of neuropsychologys scientific activities with APA
and three Members-at-Large. Meetings of the EC are and government agencies such as the National Institutes
held twice yearly, with one of the meetings held at the of Health (NIH).
North American meeting of the INS in mid-winter and Division 40 does not publish or provide an official
the other coinciding with the APA convention in the journal. However, over the years, the division has main-
summer. Presidents of the division preside at meetings tained a close relationship with The Clinical Neuropsychol-
and serve as the Chairperson of the EC. Terms of office ogist (TCN), a journal focusing on clinical issues relevant
begin and end at the completion of the annual business to neuropsychologists. The journal has published a num-
meeting held during the summer. ber of statements and guidelines prepared by Division 40
138 A American Speech-Language-Hearing Association (ASHA)
task forces relevant to the practice of neuropsychology for 140,000 members and affiliates who are speech-language
and abstracts from Division 40s scientific program at pathologists, audiologists, and speech, language, and
APA. In 1989, TCN also began to publish regular listings hearing scientists in the USA and at the international level.
of training programs in neuropsychology. In 2006,
a user-interactive revision of the list was developed by
the Education Advisory Committee (EAC) and trans-
ferred to the Division 40 web site. The listing currently
Vision: Making effective communication a human right,
includes 31 doctoral training programs, 42 internships,
accessible, and achievable for all.
and 78 sites offering postdoctoral residencies for specialty
training in clinical neuropsychology. The web site also
includes descriptions of other divisional activities and Mission
links to the divisions archival material.
Empowering and supporting speech-language patholo-
gists, audiologists, and speech, language, and hearing
Cross References scientists by:
American Academy of Clinical Neuropsychology (AACN) Advocating on behalf of persons with communication
American Psychological Association (APA) and related disorders
International Neuropsychological Society Advancing communication science
National Academy of Neuropsychology Promoting effective human communication
References and Readings Landmark Contributions
Adams, K. M., & Rourke, B. P. (Eds.) (1992). The TCN guide to professional ASHA has had several names during its 83-year history.
practice in clinical neuropsychology. Berwyn, PA: Swets & Zeitlinger. The first was the American Academy of Speech Correction
Costa, L. (1998). Professionalization in neuropsychology: The early years. (1925). The current name, The American Speech-Language-
Hearing Association (ASHA), was adopted in 1978. ASHA
Meier, M. J. (1992). Modern clinical neuropsychology in historical per-
spective. American Psychologist, 47, 550558.
is the nations leading professional, credentialing, and
Meier, M. J. (2002). In search of knowledge and competence. In scientific organization for speech-language pathologists,
A. Y. Stringer, E. L. Cooley, & A-L. Christensen (Eds.), Pathways to audiologists, and speech/language/hearing scientists.
prominence in neuropsychology: Reflections of twentieth century ASHA has been the guardian of these professions for
pioneers. New York: Psychology Press.
over 75 years, initiating the development of national
Puente, A. E., & Marcotte, A. C. (2000). A history of Division 40 (clinical
neuropsychology). In D. A. Dewsbury (Ed.), Unification through
standards for each discipline and certifying professionals
division: Histories of the divisions of the American Psychological for 55 years.
Association, Volume V. Washington, DC: American Psychological ASHA began in 1925 at an informal meeting of the
Association Press. National Association of Teachers of Speech (NATS) in
Iowa City, IA, an organization of people working in the
areas of rhetoric, debate, and theater. Robert W. West was
the first president of the association from 1925 to 1928.
American Speech-Language- Its members were becoming increasingly interested in
Hearing Association (ASHA) speech correction and wanted to establish an organization
to promote scientific, organized work in the field of
L EMMIETTA M C N EILLY speech correction. Accordingly, in December of that
American Speech-Language-Hearing Association year, the American Academy of Speech Correction
Rockville, MD, USA ASHAs original predecessor was born.
ASHA has grown exponentially since its inception
from 25 members in 1925 to 140,000 in 2010. ASHA
Membership opened its first national office on January 1, 1958 in
Washington, DC. The association subsequently moved
The American Speech-Language-Hearing Association is four times, most recently settling in its current location
the professional, scientific, and credentialing association in Rockville, MD in 2008. ASHAs new national office is
American Speech-Language-Hearing Association Functional Assessment of Communication Skills for Adults A 139
a LEED certified green building the first nonprofit behaviors at the level of disability, based on direct obser-
A
companys building of that distinction in Maryland. vations by speech-language pathologists or significant
others who are familiar with the clients typical commu-
nication performance across the following domains:
Major Activities Social Communication; Communication of Basic Needs;
Reading, Writing, and Number Concepts; and Daily
Publications: The ASHA Leader; American Journal of Planning. Within each domain, specific functional beha-
Audiology; American Journal of Speech-Language viors are rated on a 7-point scale of independence, rang-
Pathology; Journal of Speech, Language, and Hearing ing from does the activity fully independently, through
Research; Language, Speech, and Hearing Services in five levels of does with varying degrees of assistance to
Schools; and Perspectives. does not perform the activity. For example, Social
Conferences: Annual convention and three niche confer- Communication concerns the ability to use names of
ences: Healthcare, Schools, and State Policy Workshop familiar people, exchange information on the telephone,
as well as several web events annually. answer yes/no question and follow directions, under-
stand facial expressions and tone of voice, comprehend
References and Readings nonliteral meaning, and understand TV and radio pro-
grams. Communication of Basic Needs assesses ability to
Interdisciplinary approaches to Brain Damage written by the joint com-
recognize familiar faces and voices, express feelings and
mittee http://www.asha.org/docs/html/PS199000093.html make known needs and wants, and respond in an emer-
Selected practice documents related to Adult Neurogenics are featured gency. Reading, Writing, and Number Concepts examine
in ASHAs Online Practice Policy documents. http://www.asha.org/ the ability to understand simple signs, use reference
academic/curriculum/slp-aneuro/deskref
materials, understand printed material and follow writ-
Structure and Function of an Interdisciplinary Team for Persons with
Acquired Brain Injury http://www.asha.org/docs/html/GL2007
ten directions, complete forms, write messages, and
00288.html make money transactions. Finally, Daily Planning eval-
Memory Assessment on an Interdisciplinary Rehabilitation Team: A uates the ability to tell time, sequence numbers for using
Theoretically Based Framework. http://ajslp.asha.org/cgi/content/full/ a telephone, maintain a schedule of appointments and
16/4/316?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=
use a calendar, and read a map. Each domain is rated
&fulltext=memory+assessment&searchid=1&FIRSTINDEX=0
&sortspec=relevance&resourcetype=HWCIT
globally on the basis of a Scale of Qualitative Dimensions
(i.e., adequacy, appropriateness, promptness, and com-
munication sharing). The measure yields domain and
dimension mean scores, overall scores, and profiles of
American Speech-Language- both Communication Independence and Qualitative
Dimensions.
Hearing Association Functional The ASHA-FACS includes:
Assessment of Communication
A 117-page manual
Skills for Adults A CD version to allow automatic tabulation of the
measures for recording incremental client assessments
C AROLE R OTH in MS Excel used in PC or Apple/Macintosh
Naval Medical Center A paper-and-pencil version with score summary and
San Diego, CA, USA profile forms that purchasers can copy
A rating key on a 5 x 7 card
An electronic index of ICD-9-CM codes
Synonyms
ASHA-FACS Historical Background
ASHA-FACS evolved from the wave of healthcare ac-

Description countability and the widespread need for an effective
instrument to measure the functional communication of
The ASHA-FACS was designed as a quick and easily adults who have speech, language, or cognitive impair-
administered measure of functional communication ments for purposes of justifying payment, defining service
140 A American Speech-Language-Hearing Association Functional Assessment of Communication Skills for Adults
eligibility, and judging the value of care. Developed in independence scores had high interrater agreement
1995 by ASHA, it reflects the collaborative effort of (mean correlation = 0.95) as did overall scores (mean
more than 70 individuals, both ASHA members and correlation = 0.90). Intrarater reliability for communica-
related professionals. The first version of the measure, tion independence mean scores by assessment domain
the ASHA Functional Communication Measures (Frattali, ranged from 0.95 to 0.99 and intrarater reliability of
C.M.1998), was developed for use with both children and overall communication independence scores was 0.99.
adults. The FCMs consisted of 12 rating scales, each Intrarater reliability of qualitative dimension mean scores
representing a separate communication process and ranged from 0.94 to 0.99 and 0.99 for the overall qualita-
rated on an 8-point scale of independence. Development tive dimension scores.
of the FCMs was funded by the National Institute on The ASHA-FACS was moderately correlated with
Child Health and Human Development, National Insti- other measures of language and cognitive function as
tutes of Health. The FCMs were determined to be unsuit- demonstrated by external criterion measures used with
able for use with children, and as a result of other subjects with aphasia and cognitive-communication
limitations, a second group of experts specifically in impairments from traumatic brain injury. A significant
adult communication disorders edited the FCMs, pro- correlation of 0.76 (a = 0.05 level) was obtained be-
posed a multidimensional scoring system, and renamed tween Western Aphasia Battery (WAB) (Kertesz, 1982),
the instrument. Aphasia Quotients (AQs), and ASHA-FACS overall
Further revisions in 1992 included a reconceptualiza- scores. Statistically significant correlations were obtained
tion of the framework to measure at the level of disability, between ASHA-FACS domain scores and WAB subtest
consistent with the World Health Organizations Interna- scores, with the exception of correlations between WAB
tional Classification Scheme, resulting in the final title, fluency scores and reading and writing domain scores
the ASHA Functional Assessment of Communication from the ASHA-FACS. Correlations between the ASHA-
Skills for Adults (ASHA-FACS). The design of the FACS domain score and overall score and each of the
ASHA-FACS was based on a definition of functional Functional Independence Measure (FIM) scales (FIM
communication formulated in 1990 by an ASHA advisory 4.0; SUNY at Buffalo Research Foundation, 1993) were
group: the ability to receive or to convey a message, statistically significant (ranging from 0.42 to 0.82), with
regardless of the mode, to communicate effectively and the exception of the social interaction scale of the FIM.
independently in natural environments (cited in Frattali, External validation data for the subjects with cognitive-
C.M.1995). communication impairments ranged from 0.76 to 0.85
between the Scales of Cognitive Ability for Traumatic
Brain Injury (SCATBI) (Adamovich & Henderson,
Psychometric Data 1992) severity scores and the ASHA-FACS scores, and a
0.84 correlation between the ASHA-FACS overall scores
The usability, sensitivity, reliability, and validity of the with the SCATBI severity scores. These correlations were
ASHA-FACS were demonstrated through two separate all statistically significant at the a = 0.05 level. Statisti-
pilot tests and one field test. The first version was piloted cally significant correlations were found between ASHA-
in 1993 to determine the measures usability, resulting FACS domain and overall scores with the Rancho Los
in the development of a 7-point observational rating Amigos Levels of Cognitive Functioning (Hagen,
scale. A second pilot test confirmed the usability of the Malkmus, & Durham, 1979) (correlations ranged from
revised version, and acceptable levels of reliability and 0.64 to 0.83) and FIM scores (correlations ranged from
validity were found. A more sensitive scoring system for 0.50 to 0.80). Nonsignificant correlations were obtained
capturing qualitative information about the nature of a from SCATBI subtest scores and ASHA-FACS domain
clients functional communication led to the addition of scores obtained from the mild to moderately impaired
a second scoring feature, the 5-point Scale of Qualitative TBI group.
Dimensions. High internal consistency and social validity were
To establish interrater reliability, the ASHA-FACS reported. Internal consistency indicated that most item
was completed independently for 51 subjects by two scores covered the full 7-point rating scale, showed high
examiners within a 48-h period. Interrater reliability inter-item correlations between items within assessment
correlations on the seven assessment domain scores domains, were internally consistent with respect to as-
ranged from 0.72 to 0.92. Overall communication sessment domain, and that all items were measuring the
American Speech-Language-Hearing Association Functional Assessment of Communication Skills for Adults A 141
same underlying construct. The data indicated that all References and Readings A
domain scores correlated with overall ASHA-FACS
scores. Evaluation of social validity was accomplished Adamovich, B., & Henderson, J. (1992). Scales of cognitive ability for
by correlating overall ASHA-FACS scores with measures traumatic brain injury. Chicago: Riverside.
Davidson, B., & Worrall, L. (2002). The assessment of activity limitation
scored by family members or friends of subjects. These
in functional communication: Challenges and choices. In A. E. Hillis
measures included the Communicative Effectiveness (Ed.), The handbook of adult language disorders: Integrating cognitive
Index (CETI; Lomas et al., 1989) and a Rating of Overall neuropsychology, neurology, and rehabilitation (pp. 1934). New
Communication Effectiveness, a single overall index of each York: Psychology Press.
subjects communication effectiveness rated on a scale from Davidson, B., Worrall, L., & Hickson, L. (2003). Identifying the commu-
nication activities of older people with aphasia: Evidence from
1 (lowest) to 7 (highest). These data indicated high positive
naturalistic observation. Aphasiology, 17(3), 243264.
correlations between ASHA-FACS overall scores and Rat- Donovan, N. J., Rosenbek, J. C., Ketterson, T. U., & Velozo, C. A.
ings of Overall Communication Effectiveness by clinicians (2006). Adding meaning to measurement: Initial Rasch analysis of
(i.e., r = 0.81). ASHA-FACS overall scores did not correlate the ASHA FACS Social Communication Subtest. Aphasiology,
well with family members or friends Ratings of Overall 20(24), 362373.
Frattali, C. M. (Ed.) (1998). Measuring modality-specific behaviors,
Communication Effectiveness or CETI scores. CETI ratings
functional abilities, and quality of life. In Measuring outcomes in
were consistently higher than those measured using the speech-language pathology. (P. 203). New York: Thieme.
ASHA-FACS. Frattali, C. M., Thompson, C. K., Holland, A. L., Wohl, C. B., & Ferketic,
M. M. (1995). The American Speech-Language-Hearing Association
Functional Assessment of Communication Skills for Adults (ASHA
FACS). Rockville, MD: ASHA.
Clinical Uses Frattali, C. M., Thompson, C. M., Holland, A. L., Wohl, C. B., & Ferketic,
M. M. (1995). The FACS of life ASHA FACSa functional outcome
ASHA-FACS was designed for clinicians to rate functional measure for adults. ASHA, 37(4), 4046.
communication behaviors of adults with speech, lan- Hagen, C., Malkmus, D., & Durham, P. (1979). Levels of
guage, and cognitive-communication disorders resulting cognitive functioning. In Rehabilitation of the head-injured adult:
Comprehensive physical management (Appendix C., pp. 8789).
from left hemisphere stroke and from traumatic brain
Downey, CA: Professional Staff Association of Rancho Los Amigos
injury. Hospital.
In a review of the evidence leading to recommended Kagan, A., Simmons-Mackie, N., Rowland, A., Huijbregts, M., Shumway,
best practices for assessment of individuals with cogni- E., McEwen, S., Threats, T., & Sharp, S. (2008). Counting what
tive-communication disorders after TBI, the ASHA-FACS counts: A framework for capturing real-life outcomes of aphasia
intervention. Aphasiology, 22(3), 258280.
was one of a few standardized, norm-referenced tests that
Kertesz, A. (1982). Western Aphasia Battery. New York: Grune & Stratton.
met most established criteria for validity and reliability Lomas, J., Pickard, L., Bester, S., Elbard, H., Finlayson, A., & Zoghaib, C.
for use with this clinical population (Turkstra, Coelho, & (1989). The Communicative Effectiveness Index: Development
Ylvisaker, 2005). It was one of only four of the 31 tests and psychometric evaluation of a functional communication
reviewed that evaluated performance outside clinical set- measure for adults. Journal of Speech and Hearing Disorders, 54,
113124.
tings. It was unique in that it was based on research about
Ross, K. B., & Wertz, R. T. (2002). Relationships between language-based
daily communication needs in the target population and disability and quality of life in chronically aphasic adults. Aphasiol-
incorporated consumer feedback about ecological validity ogy, 16(8), 791800.
into the design. The research is rich in the many clinical State University of New York at Buffalo Research Foundation.
benefits of the ASHA-FACS. For example, this instrument (1993). Guide for use of the Uniform Data Set for Medical
Rehabilitation: Functional independence measure. Buffalo, NY:
has been used to measure communication disability rela-
Author.
tive to quality of life in chronically aphasic adults (Ross & Turkstra, L. S., Coelho, C., & Ylvisaker, M. (2005). The use of standar-
Wertz, 2002; Davidson, Worrall, & Hickson, 2003), to dized tests for individuals with cognitive-communication disorders.
evaluate the effectiveness of functionally based communi- Seminars in Speech and Language, 26(4), 215222.
cation therapy (Worrall & Yiu, 2000), and to evaluate real- Worrall, L., & Yiu, E. (2000). Effectiveness of functional communication
therapy by volunteers for people with aphasia following stroke.
life outcomes of aphasia interventions (Kagan et al.,
Aphasiology, 14(9), 911924.
2008). Using Rasch analysis of the ASHA-FACS Social Worrall, L., McCooey, R., Davidson, B., Larkins, B., & Hickson, L. (2002).
Communication Subtest (SCS), Donovan, Rosenbek, The validity of functional assessments of communication and the
Ketterson, & Velozo (2006) demonstrated that caregivers activity/participation components of the ICIDH-2: Do they reflect
were reliable respondents who could use the SCS to rate what really happens in real-life? Journal of Communication Disorders,
35(2), 107137.
therapy progress and functional outcomes.
142 A Americans with Disabilities Act of 1990
perform an essential function of the job, (c) reasonable

Americans with Disabilities Act of accommodations, and (d) threats to others. The
1990 reasonable accommodations are typically broken
down by short-term accommodations as well as long-
R OBERT L. H EILBRONNER term accommodations.
Chicago Neuropsychology Group
Chicago, IL, USA
Historical Background Americans with Disabilities Act of 1990, 42 U.S.C. 1210112213 et seq.
Bell, C. (1997). The Americans with disabilities act, mental disability and
The Americans with Disabilities Act (ADA) was signed by work. In R. Bonnie, & J. Monahan (Eds.), Mental disorder, mental
disability and the law. Chicago: University of Chicago Press.
President George Bush in 1990 and went into effect in
Foote, W. M. (2003). Forensic evaluation in Americans with disabilities
1992. It is regarded by many as the most sweeping civil act cases. In A. Goldstein (Ed.), Handbook of psychology (Vol. 11).
rights legislation since the Civil Rights Act of 1964, with Forensic psychology. New Jersey: Wiley.
its intent to assist people with disabilities to obtain jobs Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C. (1997).
and achieve the goal of full functioning in the workplace. Psychological evaluations for the courts: A handbook for mental health
professionals and lawyers. New York: Guilford.
The ADA contains provisions that outlaw discrimination
More detailed information regarding the Americans with Disabilities Act
against people with disabilities (including those with of 1990 can be found at www.ada.gov
learning disabilities and mental disorders) in hiring,
training, compensation, and benefits (Bell, 1997) and
mandates that employers provide reasonable accommo-
dations for disabled workers who could qualify for jobs if
such assistance is provided. It also protects individuals Amitriptyline
against retaliation for filing charges or otherwise being
involved in an Equal Employment Opportunity Commis- J OHN C. C OURTNEY
sion (EEOC)-related action. The act requires that people Childrens Hospital of New Orleans
with disabilities be treated like nondisabled persons, un- New Orleans, LA, USA
less it is determined that a certain individuals disability
produces significant hindrances to ones involvement in a
particular endeavor. It was established due to Congresss Generic Name
recognition of a large number of Americans with one or
more disabilities and the discrimination experienced by Amitriptyline
such individuals with respect to employment and access
to services.
Brand Name
Elavil
Current Knowledge
The ADA includes several sections that cover different

types of activities, most notably, employment (Title I), Class
public services (Title II), public accommodations and
services operated by private entities (Title III), access to Tricyclic Antidepressant
telecommunications (Title IV), and miscellaneous pro-
visions (Title V). Psychologists often conduct evalua-
tions of disabled individuals to determine reasonable Proposed Mechanism(s) of Action
accommodations in accordance with the ADA. The
most common referral involves Title 1, employment Increases available norepinephrine and serotonin, blocks
issues. The ADA requires that an evaluator assesses serotonin reuptake and may desensitize both serotonins
four distinct areas: (a) disability, (b) qualifications to 1A and beta adrenergic receptors.
Amnestic Disorder A 143
Indication A
Amnesia
Depression
G INETTE L AFLECHE
Memory Disorders Research Center, Boston University
School of Medicine and VA Boston Healthcare System
Off Label Use Boston, MA, USA
Neuropathic pain, fibromyalgia, headache, and insomnia

Definition
Amnesia refers to the loss of ability to recall facts, events,

Side Effects
or concepts encountered prior to the onset of illness
(retrograde amnesia) or to the loss of ability to form
Serious
new memories (anterograde amnesia), or both. Although
anterograde and retrograde amnesia can occur in isola-
Paralytic ileus, hyperthermia, lowered seizure threshold,
tion, they most often appear together following a single
sudden death, cardiac arrhythmias, tachycardia, QTc pro-
cause. That cause is most frequently a neurologic insult or
longation, hepatic failure, mania, potential for activation
illness, but can also be psychogenic. In most cases, the
of suicidal ideation
memory loss is permanent, but it can be temporary, as for
example, in transient global amnesia.
Common
Blurred vision, constipation, urinary retention, increased Cross References

appetite, dry mouth, diarrhea, heartburn, weight gain,
fatigue, weakness, dizziness, anxiety, sexual dysfunction, Anterograde Amnesia
sweating, rash, and itching Memory Impairment
Retrograde Amnesia
Transient Global Amnesia
PDR.
(2nd ed.). New York, NY: Cambridge University Press. Baddeley, A. D., Kopelman, M. D., & Wilson, A. W. (2002). The handbook
of memory disorders. Chichester, UK: Wiley.
Additional Information
Drug Molecule Images: http://www.worldofmolecules.com/drugs/ Amnestic Disorder
Free Drug Online and PDA Software: www.epocrates.com
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs. B ETH S PRINGATE
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList
Storrs, CT, USA
AML Synonyms
Acute Myelogenous Leukemia Global amnesia

144 A Amnestic Disorder
Short Description or Definition Natural History, Prognostic Factors,

and Outcomes
Amnestic disorders are defined by a global loss in explicit
memory that is persistent and stable. The hallmark fea- The amnestic disorder is exemplified by the case study of
ture of this disorder is extreme anterograde amnesia H.M. H.M. had intractable epilepsy that was treated with
(impairment in the ability to form new explicit mem- a radical, experimental surgery in which his medial tem-
ories) in the absence of any other extensive cognitive poral lobes were removed bilaterally. His resection includ-
losses. Individuals with amnestic disorders may display ed the hippocampal formation and adjacent structures
an impairment in memory which is not lasting (e.g., including most of the amygdala and parahippocampal
transient global amnesia), progressive (e.g., Alzheimers gyrus, including the entorhinal cortex. Following surgery,
disease), or occurs in combination with declines in other H.M. developed severe anterograde amnesia which mani-
cognitive domains. fested as deficient episodic and semantic memory. In ad-
dition, he developed partial retrograde amnesia for events
within 19 months before his surgery. However, earlier
Categorization memories were unaffected, and his working memory and
procedural memory (skill learning) also remained intact
Amnestic disorders can result from a variety of causes, (Corkin, 2002; Scoville & Milner, 1957).
including hypoxic/anoxic events, infections (e.g., herpes Course: Onset is often acute due to the nature of the
simplex encephalitis), and lesions such as those that pathological processes that cause amnestic disorders (e.g.,
occur following stroke or surgical ablation, and are asso- cerebrovascular events, anoxic/hypoxic events, surgical ab-
ciated with damage to several brain regions. Two subtypes lation, and infections such as herpes encephalitis). As
of amnestic disorders have received the most attention: amnestic disorders are caused by the destruction of brain
bitemporal amnesia and diencephalic amnesia (e.g., structures, deficits are persisting and stable without expec-
Korsakoff s syndrome and patients with discrete thalamic tation of improvement or further decline barring any addi-
or mammillary body lesions). A third subtype, basal tional injury.
forebrain amnesia, is viewed as clinically distinctive and General neuropsychological profile: Patients exhibit
has been studied to a lesser degree (Bauer, Grande, and deficits in explicit memory marked by significant antero-
Valenstein, 2003). grade amnesia. They may also exhibit retrograde amnesia
(disruption in the ability to recall previously learned
information), although this is typically less severe and
Epidemiology exhibits a temporal gradient with older memories less
likely to be disturbed. Attention, working memory, pro-
Amnestic disorders can be observed in several classes cedural memory, implicit learning, and general cognition
of patients including following viral infections (e.g., remain largely intact.
herpes encephalitis), anoxic/hypoxic events (e.g., after Amnestic disorders resulting from bitemporal or dien-
heart attack or near-drowning), Korsakoff s syndrome, cephalic insults are the most frequently studied and similar
bilateral temporal lobectomies, and cerebrovascular in their neuropsychological profiles. Although early studies
events. However, global amnestic syndromes themselves suggested that individuals with bitemporal amnesias have a
are relatively rare. For example, herpes simplex encepha- more rapid forgetting rate, McKee and Squire (1992) found
litis carries a 70% mortality rate without treatment. The equivalent forgetting curves for pictures when severity of
cognitive impairments in survivors are ranging, and in amnesia was controlled. Both subtypes of amnesia display
one study of long-term survivors 19 of 22 participants a degree of retrograde amnesia (Kopelman, Stanhope, &
experienced some form of memory impairment although Kingsley, 1999). Bauer, Grande, and Valenstein (2003)
only five subjects had memory difficulties that were argue that despite these similarities, some deficits are
categorized as severe (Utley et al., 1997). In a review of unique to patients with diencephalic amnestic disorders;
studies of cerebral anoxia, Caine and Watson (2000) con- although some studies suggest patients with Korsakoff s
clude that while 54% of case studies describe memory syndrome display a unique deficit in memory for tempo-
impairments, only 19% report memory deficits in ral order (e.g., Squire, 1982; Kopelman et al., 1999), others
isolation. fail to support this finding (Downes et al., 2002).
Amnestic Disorder A 145
Basal forebrain amnesia typically results from vascu- famous individuals. The aspects of memory that remain
A
lar lesions or aneurysm surgery in the region of the intact in classic amnestic disorder patients (such as se-
anterior communicating artery. After basal forebrain mantic memory and motor skill learning) should also be
damage, patients may demonstrate extensive anterograde assessed.
amnesia (Bottger et al., 1998; Tidswell et al., 1995). The main differential diagnoses to consider include
Confabulation is common and may relate to the extent delirium and dementia. Delirium is defined by a distur-
of orbitofrontal involvement (Hashimoto, Tanaka, & bance in attention and consciousness, both of which are
Nakano, 2000), but it often subsides following the acute intact in amnestic disorders. Although dementias present
phase while the amnestic state remains. There is evidence similarly to amnestic disorders in that patients often pres-
that patients with basal forebrain amnesia benefit from ent with memory impairments, cognitive decline (rather
the presentation of cues to enhance recall (Osimani et al., than stability) occurs and impairments in other cognitive
2006). domains such as language or executive functions are
present.
Evaluation
Treatment
As amnestic disorders are defined by deficits in new
learning, memory is the cognitive domain that should Treatment of amnestic disorders is nonspecific and
be emphasized within a neuropsychological evaluation focused primarily on management of symptoms. Cogni-
that also includes assessment of other areas of cognitive tive rehabilitation and memory training programs, which
function such as orientation, attention, language, execu- emphasize the teaching of mnemonic strategies or the
tive functions, visuospatial skills, and psychological func- use of external memory aids such as note-taking or
tioning. Patients fitting the classic amnestic disorder audiotaping in order to enhance patients functioning in
profile will exhibit deficits in memory with generally daily life, have been used to improve memory in indivi-
intact cognition within other domains. duals with dementia and other disorders. Theoretically,
It is important to establish the specific nature of these programs would be useful for individuals with
patients memory impairments. Immediate memory amnestic disorders. However, without the ability for
span (typically assessed through tests such as Digit and patients to consciously recall they have learned these
Spatial Span from the Wechsler Memory Scales) should strategies and remember to implement them, these pro-
be within the normal range. Anterograde learning may grams are likely of little value for patients with amnestic
be assessed with measures such as list learning, story disorders.
learning, or figure memory. While patients will be able The use of pharmacologic agents to treat amnestic
to retain items and repeat them back as long as they disorders is not well studied, and large randomized con-
can keep them in memory, learning curves are typically trolled trials are lacking. In an open-label pilot study,
flat, and an intervening distractor task will cause items Benke et al. (2005) administered donepezil, a cholinester-
to be lost completely. The use of cues or yes/no recogni- ase inhibitor, to patients with a chronic amnestic syn-
tion format, which typically facilitates memory in drome from a ruptured and repaired aneurysm of the
most individuals, will not aid recall in these patients. anterior communicating artery, anterior cerebral, or
Explicit anterograde learning will be equally impaired pericallosal artery. Some measures of performance on a
regardless of the type of memory test (free recall, cued list-learning task improved significantly during the
recall, and recognition), stimulus material (e.g., words, 12-week medication administration period, suggesting
pictures, and sounds), and sensory modality through future double-blinded controlled studies would be useful
which information is acquired (e.g., visual, auditory, to more thoroughly examine the potential utility of
and somatosensory). cholinergic medications.
In addition, retrograde amnesia and memory for re- In addition, due to their memory impairment, patients
mote events can be examined in a qualitative manner are likely to experience impairments in their social and
by inquiring about autobiographical events as well as vocational activities and may also require supervised
memories that one can assume to be present in most living situations and a guardian for legal and medical
people from a given society such as pictures of concerns.
146 A Amnestic Syndromes
Cross References
Amnestic Syndromes
Amnesia
Amnestic Syndrome G INETTE L AFLECHE , M IEKE V ERFAELLIE
Dissociative Amnesia VA Boston Healthcare System and Boston University
Korsakoff s Syndrome School of Medicine
Temporal Lobectomy Boston, MA, USA

The amnesic syndromes are a collection of neurological
Bauer, R. M., Grande, L., & Valenstein, E. (2003). Amnesic disorders. In disorders characterized by a dense global amnesia that
K. M. Heilman, & E. Valenstein (Eds.), Clinical neuropsychology (pp. includes both anterograde and retrograde components
495573). New York: Oxford University Press.
( Anterograde Amnesia and Retrograde Amnesia).
Benke, T., Koylu, B., Delazer, M., Trinka, E., & Kemmler, G., (2005).
Cholinergic treatment of amnesia following basal forebrain lesion
due to aneurysm rupture an open-label pilot study. European
Journal of Neurology, 12, 791796.
Categorization
Bottger, S., Prosiegel, M., Steiger, H., & Yassouridis, A. (1998). Neurobe-
havioral disturbances, rehabilitation outcome, and lesion site in The amnesic syndromes can be classified according to
patients after rupture and repair of anterior communicating artery cause or site of damage. Etiologically, they are caused by
aneurysm. Journal of Neurology, Neurosurgery, and Psychiatry, 65,
cerebrovascular disease, herpes simplex encephalitis,
93102.
Caine, D., & Watson, J. D. G. (2000). Neuropsychological and neuropath-
WernickeKorsakoff syndrome, anoxia, anterior commu-
ological sequelae of cerebral anoxia: a critical review. Journal of the nicating artery aneurysm (ACoA), and tumors. Neuro-
International Neuropsychological Society, 6, 8699. pathologically, amnesia can arise from damage to the
Corkin, S. (2002). Whats new with the amnesic patient H.M.? Nature medial temporal lobes, the midline diencephalic nuclei,
Reviews: Neuroscience, 3, 153160.
the basal forebrain, or from disruption of some of their
Downes, J. J., Mayes, A. R., MacDonald, C., & Hunkin, N. M.
(2002). Temporal order memory in patients with Korsakoff s
interconnections such as the fornix. Most amnesic syn-
syndrome and medial temporal amnesia. Neuropsychologia, 40, dromes are chronic, and are due to structural damage to
853861. critical brain structures, but amnesia can also be transient,
Hashimoto, R., Tanaka, Y., & Nakano, I. (2000). Amnesic confabulatory due to functional disruption of these brain structures (see
syndrome after focal basal forebrain damage. Neurology, 54,
Transient Global Amnesia).
978980.
Kopelman, M. D., Stanhope, N., & Kingsley, D. (1999). Retrograde
amnesia in patients with diencephalic, temporal lobe or frontal
lesions. Neuropsychologia, 37, 939958.
Neuropsychology of the Amnesic
McKee, R. D., & Squire, L. R. (1992). Both hippocampal and diencephalic Syndromes
amnesia result in normal forgetting for complex visual material.
Journal of Clinical and Experimental Neuropsychology, 14, 103. Herpes Simplex Encephalitis (HSE)
Osimani, A., Vakil, E., Blinder, G., Sobel, R., & Abarbanel, J. M. (2006).
Basal forebrain amnesia: a case study. Cognitive and Behavioral
HSE is a viral infection of the brain that begins as a flu-
Scoville, W. B., & Milner, B. (1957). Loss of recent memory after bilateral like illness with headaches and fever, followed by lethargy,
hippocampal lesions. Journal of Neurology, Neurosurgery, and Psychi- confusion, and disorientation. If left untreated, amnesia,
atry, 20, 1121. agnosia, and aphasia can develop. Patients who do not
Squire, L. R. (1982). Comparisons between forms of amnesia: some undergo a complete recovery can suffer a broad range of
deficits are unique to Korsakoff s syndrome. Journal of Experimental
cognitive deficits that persist, but some are left with only
Psychology: Learning, Memory, and Cogntion, 8, 560571.
Tidswell, P., Dias, P. S., Sagar, H. J., Mayes, A. R., & Battersby, R. D. E. an isolated amnesic syndrome. Their Presentation is sim-
(1995). Cognitive outcome after aneurysm rupture: relationship to ilar to that of HM who became unable to form new
aneurysm site and perioperative complications. Neurology, 45, memories after undergoing a neurosurgical operation in
875882. which a large portion of the medical temporal region of
Utley, T. F. M., Ogden, J. A., Gibb, A., McGrath, N., & Anderson, N. E.
his brain was removed bilaterally.
(1997). The long-term neuropsychological outcome of herpes sim-
plex encephalitis in a series of unselected survivors. Neuropsychiatry, Neuropathologically, the virus preferentially infects
Neuropsychology, and Behavioral Neurology, 10, 180189. limbic regions in the temporal lobe including the
Amnestic Syndromes A 147
hippocampus and adjacent entorhinal, perirhinal and functioning are particularly common (Lim et al., 2004).
A
parahippocampal cortices, as well as the amygdala and In a minority of patients, anoxic injury leads to isolated
polar limbic cortices. Damage often extends to the lateral amnesia.
aspect of the temporal lobe, damaging the anterolateral Relatively selective developmental amnesia has been
aspect, the inferior aspect, or both. Anterior extension of documented in children and adolescents who experienced
damage into ventromedial areas such as the insular cortex an anoxic event shortly after birth. Gadian et al. (2000)
and the basal forebrain has also been documented. The reported on five cases, all of whom had selective bilateral
severity of memory impairment following HSE shows hippocampal atrophy. Neuropsychological results revealed
substantial variation that is directly proportional to the that all of the children performed poorly on tasks of epi-
extent of medial temporal lobe damage (Stefanacci, Buf- sodic memory, but attention, reasoning abilities, and vi-
falo, Schmolck, & Squire, 2000). Lesions are often asym- suospatial skills were intact. Strikingly, these children were
metrical, and this will define the clinical presentation. If able to acquire a considerable amount of new semantic
damage to the left temporal region is greater, verbal knowledge, as indicated by the fact that they were success-
memory problems dominate, whereas if right temporal fully able to attend mainstream schools. The relative pres-
damage is greater, nonverbal aspects of memory are pre- ervation of semantic learning in these children has been
dominantly impaired, such as memory for faces and ascribed to the integrity of subhippocampal cortical areas,
designs. Patients whose lesions extend into lateral tempo- including entorhinal and perirhinal cortices.
ral regions may also suffer from a severe retrograde am-
nesia that is thought to be due to damage to convergence
WernickeKorsakoff Syndrome
zones in anterior temporal areas. Damage primarily to
right anterior temporal regions is more likely to result in a
WernickeKorsakoff Syndrome.
loss of personal episodic memories (OConnor, Butters,
Miliotis, Eslinger, & Cermak, 1992), and that to the left
temporal cortex is associated with loss of semantic knowl- Cerebrovascular Accidents
edge (DeRenzi, Liotti, & Nichelli, 1987). Cases with un-
usual category-specific semantic impairments have also Bilateral posterior cerebral artery (PCA) infarction is a
been described, such as differential loss of knowledge of well-recognized cause of amnesia. Because the left and
concrete versus abstract concepts or animate versus inan- right PCA arise from the bifurcation of a common source,
imate concepts. strokes that occur upstream from the bifurcation can affect
the medial temporal lobes bilaterally, causing a dense
global amnesia. Neuroanatomical studies of patients with
Anoxia PCA infarction have revealed that lesions in the posterior
parahippocampus or the collateral isthmus (a pathway
Anoxic brain injury can result from any of a number of connecting the posterior parahippocampus to association
diverse etiologies including cardiac arrest, respiratory dis- cortex) are critical for the memory impairment (Von
tress, carbon monoxide poisoning, or drug overdose. Cramon, Hebel, & Schuri, 1988). When damage extends
These clinical conditions all diminish or cut off the supply posteriorly to include occipitotemporal cortices, deficits
of oxygen to the brain, either through reduced blood flow beyond amnesia are often seen.
or reduced blood oxygen saturation. The physiological Early in their clinical course, patients with PCA in-
consequences of such anoxic events are complex. Brain farction exhibit a global confusion that eventually resolves
areas particularly vulnerable to anoxic injury include the into an isolated amnestic syndrome or may be associated
hippocampus, basal ganglia, and watershed areas of the with additional neuropsychological deficits, such as visual
cerebral cortex. The clinical manifestations of anoxia are field defects, alexia, color agnosia, or anomia. The mem-
highly variable, but memory impairment is a common ory disturbance is characterized by a classic profile of
manifestation. A review of 58 studies of cerebral anoxia consolidation deficits in the context of normal working
showed that while damage to hippocampal structures was memory and normal intelligence. There may or may not
common, damage restricted to the hippocampus was seen be associated retrograde amnesia. Memory problems have
in only 18% of patients (Caine & Watson, 2000). Accord- also been described with unilateral, usually left, PCA
ingly, in a majority of patients, memory impairment infarction. In such cases, the memory impairment can
occurs in the context of generalized cognitive impairment. be transient or permanent, and is typically limited to
Significant changes in executive abilities and motor verbal material. Memory deficits in patients with right
148 A Amnestic Syndromes
PCA have been less well studied, but such examination is tests, particularly following a delay. This reflects a disrup-
complicated by the perceptual problems that frequently tion of strategic retrieval processes that allow access to
accompany right PCA infarction. information stored in memory. Deficient strategic mem-
Thalamic strokes can also lead to significant memory ory processes also contribute to poor encoding, and the
loss. Because the relevant thalamic centers are small and use of organizational strategies at encoding can enhance
adjacent to one another, it is difficult to establish associa- patients performance. A failure to adequately monitor
tions between site of damage and clinical deficits. A recent the outcome of memory search can also occur, and this
review (Van der Werf et al., 2000) suggests that damage to manifests as a tendency toward high level of false alarms
the mammillo-thalamic tract (MTT) invariably causes in recognition tests. In extreme cases, this can lead to
anterograde amnesia, and that no amnesia occurs in the impairment in recognition memory that exceeds that
absence of damage to the MTT. Medial dorsal lesions seen in recall. Other features linked to frontal dysfunction
cause a memory disturbance that is mild in comparison include impaired source memory and temporal tagging.
to the severe amnesia that arises when the lesion extends
to the MTT. Patients with thalamic amnesia exhibit exec-
utive dysfunction, increased sensitivity to interference, Evaluation
and variability in the persistence and extent of retrograde
amnesia. Although a primary focus of the assessment in amnesia is
on memory function, it is important to assess other cog-
nitive domains as well, including general intelligence,
ACoA Aneurysm attention, executive functions, language, semantic knowl-
edge, and visuospatial skills. Such a comprehensive ap-
Rupture of ACoA can result in a memory disorder that proach is required to distinguish whether a patient
ranges from mild to severe. The ACoA provides blood presents with a pure amnesic syndrome or with memory
supply to the basal forebrain, the anterior cingulate, the impairment in the context of more pervasive cognitive
anterior hypothalamus, the anterior columns of the for- difficulty. New learning abilities should be assessed by
nix, the anterior commissure, and the genu of the corpus measures of free recall, cued recall, and recognition, and
callosum. The pathological consequences of a ruptured should examine both immediate and delayed retention.
aneurysm may be a result of infarction directly, or sec- Information derived from specific aspects of perfor-
ondary to subarachnoid hemorrhage, vasospasm, and mance, such as the shape of the learning curve, compari-
hematoma formation. Because of the various neuropath- son of recall and recognition performance, and effects of
ological consequences, the clinical profiles associated with delay, all provide important pointers to the nature of the
ACoA aneurysm are more variable than those seen with memory breakdown (e.g. inefficiencies in encoding, re-
diencephalic or medial temporal lobe injuries, and the trieval, or consolidation) and may inform remediation.
impairments are often more global in nature (DeLuca & A variety of standardized tests are available to assess
Diamond, 1995). memory function, and the reader is referred to Lezak,
The acute phase of recovery following rupture and Howieson, & Loring, 2004, for specific examples. The
repair of ACoA aneurysm is characterized by a severe most commonly used standardized memory test is the
confusional state and a marked attentional disorder. As Wechsler Memory Scale-III or IV, which consists of a
the confusion resolves, memory problems become more series of subtests that probe various aspects of verbal
apparent. These can vary from mild impairments to se- and nonverbal memory in different formats. Assessment
vere amnesia. A temporally graded retrograde amnesia is of remote memory should cover knowledge of public
also frequently present. Other symptoms, including exec- events and people, personal facts, and autobiographical
utive dysfunction, confabulation, and poor insight, are events. Such assessment can be challenging, because there
likely to be part of the resulting clinical syndrome if the are few standardized measures available, and corrobora-
lesion extends to the medial frontal lobes. The clinical tion from a caregiver may be needed to establish the
outcome of patients with more extensive lesions is typi- accuracy of reported personal memories. With respect to
cally worse than that of patients with lesions limited to the general fund of knowledge, areas of assessment include
basal forebrain. knowledge of famous names and faces, public news
The amnesia associated with ACoA aneurysm has a events, and new vocabulary that has recently entered the
marked frontal dysexecutive component. Performance on language. Several structured interviews have been devel-
recognition tests is often better preserved than on recall oped to examine recollection of personal events and facts.
Amnestic Syndromes A 149
Treatment impaired forms of memory through the use of internal

A
strategies. The choice of strategy will be dependent on
There is no pharmacological or cognitive treatment that the nature of the memory process that appears defective.
can restore memory in amnesia. However, cognitive reha- Examples of such techniques include enhanced organi-
bilitation approaches have been developed that aim at zation of the to-be-learned information through chunk-
fostering routines and habits that will increase indepen- ing or categorizing, and elaboration of the material,
dence, productivity, and quality of life. The choice of whether through verbal associations or the creation of
rehabilitation approach should be informed by both cog- visual images. Such strategies fall under the category of
nitive and psychosocial/emotional factors. Cognitive fac- internal memory aids.
tors include premorbid skills and abilities and current There are no specific methods of treatment available
neuropsychological functioning. A clear delineation of to restore memories from the past. Information and pic-
impaired and preserved aspects of memory is critical to tures of emotionally neutral facts about ones life can be
guide rehabilitation efforts, as is identification of other reintroduced and incorporated in the selected treatment
areas of cognitive impairment that might hamper thera- approach. However, emotionally laden facts, such as the
peutic efforts. Of the psychosocial/emotional factors, in- death of a family member, can trigger repeated emotional
sight and motivation are perhaps the two most influential responses that can interfere with adjustment and are best
predictors of rehabilitation success. Patients need to have avoided in the early stage of treatment. By nature,
some awareness of their deficits and have some degree of relearned personal experiences about ones life will be
internal drive to understand the value of, and engage in, recalled without the emotional texture of the original
the rehabilitation process. event; however, they can play an important role in helping
Several treatment approaches take advantage of pre- patients fill in the narrative of their own life.
served nondeclarative memory abilities to teach patients
new information or skills. One approach that capitalizes
on preserved implicit perceptual memory is the vanishing Cross References
cues technique. Patients are guided to provide the correct
information in response to perceptual cues, through the Anterograde Amnesia
use of implicit memory. Once successful, cues are gradu- Retrograde Amnesia
ally reduced, eventually leading to the spontaneous gener- Transient Global Amnesia
ation of the to-be-learned information. This technique has
proven successful for learning new vocabulary and con-
cepts. Important caveats, however, are that such learning is References and Readings
a slow and laborious process, and the information learned
Baddeley, A. D., Kopelman, M. D., & Wilson, A. W. (2002). The handbook
is typically inflexible and only accessible in the exact form
of memory disorders. Chichester, UK: Wiley.
it was learned. An important consideration in the use of Caine, D., & Watson, J. D. G. (2000). Neurospsychological and neuro-
implicit memory techniques is the avoidance of errors, as pathological sequelae of cerebral anoxia: A critical review. Journal of
patients have no recollection of their mistakes and conse- the International Neuropsychological Society, 6, 8699.
quently, errors, just like correct responses, can be primed. DeLuca, J., & Diamond, B. J. (1995). Aneurysm of the anterior commu-
nicating artery: A review of neuroanatomical and neuropsychologi-
Other methods capitalize on preserved procedural
cal sequelae. Journal of Clinical and Experimental Neuropsychology,
learning and use repetition to teach skills and habits that 17, 100121.
support activities of daily living. Examples of external DeRenzi, E., Liotti, M., & Nichelli, P. (1987). Semantic amnesia with
compensatory aids that rely on procedural memory are preservation of autobiographical memory: A case report. Cortex, 23,
the use of notebooks, diaries, and alarm clocks. Electronic 578597.
Gadian, D. G., Aiardi J., Watkins, K. E., Porter, D. A., Mishkin, M., &
devices such as computers, smartphones, and paging sys-
Vargha-Khadem, F. (2000). Developmental amnesia associated with
tems have great flexibility as compensatory aids, but train- early hypoxic-ischaemic injury. Brain, 123, 499507.
ing in the use of such technology requires very lengthy Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuropsychologi-
practice sessions, and transfer of learning outside the cal assessment. New York: Oxford University Press.
training sessions can be difficult. It is therefore most ap- OConnor, M. G., Butters, N., Miliotis, P., Eslinger, P., & Cermak, L. S.
(1992). The dissociation of anterograde and retrograde amnesia in a
propriate for individuals who have premorbid experience
patient with herpes simplex encephalitis. Journal of Clinical and
with such devices and are highly motivated to use them. Experimental Neuropsychology, 14, 159178.
For individuals with milder memory impairments, it Stefanacci, L., Buffalo, E. A., Schmolck, H., & Squire, L. R. (2000).
may also be possible to directly focus on enhancing Profound amnesia after damage to the medial temporal lobe: A
150 A Amnion Rupture
neuroanatomical and neuropsychological profile of patient E. P. The

Journal of Neuroscience, 20, 70247036. Amorphosynthesis
Van der Werf, Y. D., Witter, M. P., Uylings, H. B., & Jolles, J. (2000).
Neuropsychology of infarctions in the thalamus: A review. Neurop-
Hemiinattention
sychologia, 38, 613627.
Von Cramon, D., Hebel, N., & Schuri, U. (1988). Verbal memory and Neglect
learning in unilateral posterior cerebral infarction, Brain, 111, Neglect Syndrome
10611077. Visual Neglect
Amnion Rupture
Amotivational
Anencephaly
Apathy
Amorphognosis
J OHN E. M ENDOZA Amoxapine
New Orleans, LA, USA J OHN C. C OURTNEY
Definition
Amorphognosis is that aspect of tactile agnosia which Generic Name
refers specifically to deficits in the ability to appreciate
(identify) the external form of an object such as its shape, Amoxapine
size, or other contour features by tactual manipulation
alone. In the absence of more elementary somatosensory
disturbances resulting from either peripheral nerve or the
dorsal column system, such deficits suggest lesions in the Brand Name
contralateral postcentral gyrus of the parietal lobe or in its
adjacent association cortices. Ascendin
Cross References
Class
Ahylognosia
Astereognosis Tetracyclic antidepressant
Tactile Agnosia
References and Readings Proposed Mechanism(s) of Action

Bauer, R. M., & Demery, J. A. (2003). Agnosia. In K. Heilman & E. Amoxapine inhibits reuptake of norepinephrine and nor-
Valenstein (Eds.), Clinical neuropsychology (4th ed., pp. 236295).
adrenaline. It is also known to antagonize Serotonin 2A
Hecaen, H., & Albert, M. L. (1978). Chapter 6. Disorders of somesthesis receptors, thus increasing presynaptic release of amines.
and somatognosis. In Human neuropsychology. New York: Wiley. Mild Dopamine 2 blockade.
Amphetamine A 151
Indication A
Amphetamine
Reactive depressive disorder, psychotic depression, and
depression accompanied by anxiety or agitation. J OA NN T. T SCHANZ 1, K ATHERINE T REIBER 1,2
1
Logan, UT, USA
2
Off Label Use Worcester, MA, USA
Depressive phase of a bipolar disorder, anxiety, insomnia,

neuropathic pain, and treatment resistant depression. Synonyms
D-Amphetamine; Dextroamphetamine; Dexedrine

Side Effects
Definition
Serious
Amphetamine refers to a group of synthetic chemicals with
Paralytic ileus, hyperthermia, lowered seizure threshold, psychoactive stimulant effects. There are two forms, dex-
sudden death, cardiac arrhythmias, tachycardia, QTc pro- tro-amphetamine (D-amphetamine) and levo-amphet-
longation, hepatic failure, intraocular pressure, mania, amine (L-amphetamine), of which D-amphetamine is the
and potential for activation of suicidal ideation. more biologically active. Chemical modifications to the
basic structure have produced derivatives with even more
potent psychoactive properties. For example, addition of
a second methyl group to the chemical structure creates
Common methamphetamine, a highly addictive drug. Modification
of the benzene ring of the amphetamine structure creates
Blurred vision, constipation, urinary retention, increased methylenedioxy-methamphetamine (MDMA) or Ecstasy,
appetite, dry mouth, diarrhea, heartburn, weight gain, another drug with high addiction and abuse potential
fatigue, weakness, dizziness, anxiety, sexual dysfunction, (Iversen, Iversen, Bloom, & Roth, 2009).
sweating, rash, and itching. Can cause extrapyramidal The behavioral effects of amphetamine include
symptoms such as akathisia and potentially tardive increased alertness, confidence, and euphoria. The drug
dyskinesia. also reduces fatigue and enhances performance on cogni-
tive tasks, possibly by increasing attention and working
memory. However, cognitive enhancement is not a uni-
versal effect. Reportedly, working memory is enhanced
only among those with poor ability and may be detrimen-
tal to those with high ability (Iversen et al., 2009).
PDR. In animals, there is a dose-dependent effect of increasing
Stahl, S. M. (2007). Essential psychopharmacology: The prescribers guide activity such as locomotion and at higher doses, stereo-
(2nd ed.). New York, NY: Cambridge University Press. typed motor behaviors. The reinforcing properties of
amphetamine have been demonstrated in operant condi-
tioning studies. The drug also increases systolic and dia-
stolic blood pressure, respiration, and heart rate, among its
Additional Information other autonomic nervous system effects (Feldman, Meyer,
& Quenzer, 1997). Amphetamine or its derivatives have
Drug Interaction Effects: http://www.drugs.com/drug_interactions.html been used for clinical purposes (see History). However, its
Drug Molecule Images: http://www.worldofmolecules.com/drugs/
clinical use has been limited due to its abuse potential and
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.com: dangerous autonomic effects (Iversen et al., 2009).
8080/cgi bin/ddiD4?ver=4&task=getDrugList The biological mechanism underlying the psychoac-
Pill Identification: http://www.drugs.com/pill_identification.html tive effects of amphetamine is believed to occur by
152 A AMPS
enhancing the release and blocking the reuptake of the occur in amphetamine psychosis vs. schizophrenia;
monoamine neurotransmitters dopamine, norepineph- Iversen et al., 2009). As reported above, other negative
rine, and serotonin (Feldman et al., 1997; Iversen et al., effects of chronic amphetamine abuse include neurotoxic
2009). At high doses, the drug also inhibits the metabo- damage to neurotransmitter systems. Impairments in atten-
lism of catecholamines by the enzyme monoamine oxi- tion and memory have also been reported which may persist
dase. Chronic use of amphetamine has been associated even after a period of prolonged abstinence (Gouzoulis-
with damage to selective dopamine and serotonin Mayfrank & Daumann, 2009; Iversen et al., 2009).
neurons and receptors (Feldman et al., 1997; Gouzoulis-
Mayfrank & Daumann, 2009). Methamphetamine is also
a potent neurotoxin, although its toxic effects predomi- Future Directions
nantly involve the serotonergic system (Feldman et al.,
1997; Gouzoulis-Mayfrank & Daumann, 2009). The rein- Research into the psychoactive and behavioral effects of
forcing properties of amphetamine are hypothesized to amphetamine has helped advance knowledge of the psy-
reflect increased dopamine neurotransmission in the sub- chological role of several monoamine neurotransmitters
cortical structure, the nucleus accumbens. and their relevance to clinical conditions such as addic-
tion and schizophrenia and the neurochemistry underly-
ing some cognitive processes such as attention and
Historical Background and Clinical working memory. Future research will undoubtedly uti-
Relevance lize advances in technology to elucidate the neural struc-
tures and pathways associated with reward circuits
First introduced and marketed as a nasal or bronchial involved in addictions, examine the neuroplasticity of
decongestant in the 1930s, amphetamine was sought for the nervous system after chronic abuse, and clarify the
its psychoactive effects and as an appetite suppressant. It moderating role of genetics in the behavioral response to
was used in the military to enhance attention and coun- amphetamine and other compounds (Iversen et al., 2009).
teract the effects of sleep deprivation (Iversen et al., 2009;
Meyer & Quenzer, 2005). Amphetamine and its deriva-
tives have also been used for the treatment of narcolepsy, Cross References
attentional problems, and as a stimulant in the general
population (Meyer & Quenzer, 2005). D-Amphetamine
Over time, the addictive properties of amphetamine Dopamine
were realized, particularly of its potent derivatives. The
acute effects of amphetamine-based drugs are enhanced
by use of a rapid route of administration such as intrave-
nous injection. Following a short-term rush however, a
Feldman, R. S., Meyer, J. S., & Quenzer, L. F. (1997). Stimulants: Am-
period of restless agitation, depression, irritability, and
phetamine and cocaine. In Principles of neuropsychopharmacology
other negative symptoms ensues. Repeated, continuous (pp. 549568). Sunderland, MA: Sinauer Associates.
administrations are followed by a let down, with a pro- Gouzoulis-Mayfrank, E., & Daumann, J. (2009). Neurotoxicity of drugs
longed period of sleep. This alternating cycle, when re- of abuse-the case of methylenedioxyamphetamines (MDMA,
peated, results in a substantial physical toll on the body. ecstasy), and amphetamines. Dialogues in clinical Neuroscience, 11,
305317.
As with other drugs of abuse, dependence and tolerance
Iversen, L. L., Iversen, S. D., Bloom, F. E., & Roth, R. H. (2009). Psychos-
can develop with chronic use, leading to the administra- timulants. In Introduction to neuropsychopharmacology (pp. 447
tion of increasing doses to achieve the desired effects. 472). New York: Oxford University Press.
With sustained chronic use, negative effects may emerge. Meyer, J. S., & Quenzer, L. F. (2005). Psychomotor stimulants: Cocaine
These include repetitive, stereotyped behaviors as well as and the amphetamines. In Psychopharmacology: Drugs, the brain and
behavior (pp. 292300). Sunderland, MA: Sinauer Associates.
a psychotic syndrome consisting of hallucinations and
paranoid delusions. This syndrome, known as amphet-
amine psychosis is notably similar to the symptoms of
paranoid schizophrenia and has provided some support
for the dopamine hypothesis of schizophrenia. However, AMPS
qualitative differences between the two conditions also
exist (e.g., greater tendency for visual hallucinations to Assessment of Motor Process Skills
Amygdala A 153
Historical Background A
Amusia
The amygdala was originally described by Burdach in the
J OHN E. M ENDOZA late nineteenth century as an almond-shaped structure
Tulane University Medical Center situated deep in the anterior temporal lobe of the central
New Orleans, LA, USA nervous system. The amygdala was subsequently shown to
be important for the appropriate processing of emotional
information in nonhuman primates by Kluver and Bucy
Current Knowledge in the 1930s. This permitted McLean to include the amyg-
dala in the group of brain structures that make up the
Music involves both complex qualities such as familiar limbic system thought to be involved in processing
melodies, rhythm, or tempo, and more elementary of emotional information. Since then progress has
aspects such as discrimination of timbre, pitch, or continued toward understanding the role that the amyg-
tone. While lesions of the temporal lobes are fairly dala plays in processing and encoding emotional informa-
consistently implicated, the hemispheric localization of tion in the mammalian central nervous system.
lesions responsible for specific deficits has been more
controversial. Music, like language, is composed of indi-
vidual, temporally sequenced stimuli (musical notes, Current Knowledge
melodies, tunes), each capable of being analyzed with
regard to particular features such as pitch and timbre, The amygdala is an almond-shaped structure located in
functions that would appear to be more in keeping with the medial temporal lobe of mammals. However, the first
the suspected operations of the left hemisphere. By con- description of this almond-shaped structure only referred
trast, melodies may also be perceived as a gestalt, which to a portion of the amygdala called the basal nucleus.
is more characteristic of right hemisphere functions. Currently, the amygdala is described as a collection of
There is evidence that well-trained musicians come to different subnuclei or subareas, one of which is the basal
rely more heavily on the left hemisphere for processing nucleus. The nuclei have been grouped together based on
certain aspects of music when compared with non-musi- their phylogenetic similarities or similarities in their neu-
cians. However, the right hemisphere evidences superi- ronal elements. Older phylogenetic nuclei include the
ority for both the perception and expression of music in olfactory areas (i.e., cortical nucleus and nucleus of the
studies of non-musicians. Thus, the strategies by which olfactory tract) and the central and medial nuclei. More
various musical elements are approached, as well as the recent phylogenetic structures include areas similar to the
leading hemisphere in appreciating those elements, are neocortex such as the lateral, basal, and accessory basal
most likely determined in part by ones prior musical nuclei, which are collectively referred to as the basolateral
experience or training. In summary, while both the right region or complex. Based on similarities in their neuronal
and left hemispheres are apparently involved in the components, various nuclei of the amygdala have been
expression and perception or appreciation of music, the defined as neocortical-like nuclei (such as the basolateral
specific contributions of each are still somewhat of a complex) that consist of glutamatergic pyramidal-like neu-
mystery. rons or striatal-like nuclei (such as the central and medial
nuclei) that consist of GABAergic medium spiny neurons.
In humans, the amygdala is located under the uncus
of the limbic lobe at the anterior end of the hippocampus.
Amygdala It also merges with the periamygdaloid cortex and abuts
the putamen and tail of caudate nucleus. As a whole, the
R ORY M C Q UISTON amygdala receives diverse inputs from throughout the
Virginia Commonwealth University central nervous system. The basolateral complex receives
Richmond, VA, USA inputs encoding somatosensory, visual, auditory, gustato-
ry, olfactory, and visceral information from the dorsal
thalamus, prefrontal cortex, cingulate, parahippocampal
Synonyms gyrus, insular cortex, and sensory associational areas.
The central and medial nuclei receive inputs from olfac-
Amygdaloid body; Amygdaloid nucleus tory centers, hypothalamus (ventromedial and lateral),
154 A Amygdala
dorsomedial and medial nuclei of the thalamus, and vis- amygdala innervate the lateral nuclei. The lateral nuclei
ceral inputs from the parabrachial nuclei, solitary nucleus are the most dorsally located within the amygdala, medial
and periaqueductal gray of the brainstem. Outputs from to the piriform cortex, and underneath the striatum. The
the amygdala are equally diverse. They leave via two lateral nuclei receive associational inputs encoding a sin-
predominant pathways. The central nucleus contributes gle sensation (somatosensory, visual, auditory, gustatory,
to the stria terminalis where its efferents make connec- olfactory, or visceral). This is the first stage where sensory
tions with the hypothalamus (preoptic nuclei, ventrome- input is assigned emotional value and also where some
dial nucleus, anterior nucleus, and lateral hypothalamic emotional memories may be stored (however, the amyg-
areas), nucleus accumbens, septal nuclei, and rostral por- dala as a site for storing emotional memories remains a
tions of the caudate and putamen. However, the primary contentious issue). Although the lateral nuclei projects to
output of the amygdala is the ventral amygdalofugal multiple areas within and outside the amygdala, a major
pathway. Through this pathway, the basolateral complex output is the basal nuclei (located ventral to the lateral
sends inputs to the hypothalamus, septal nuclei, sustantia nuclei) where the initial sensory processing of the lateral
innominata, prefrontal, cingulate, insular, and inferior nuclei is integrated with inputs from highly processed
temporal cortices. Through the same pathway, the central areas including polymodal sensory areas and areas
nucleus projects diffusely in the brainstem innervating the involved in memory formation like the hippocampus.
dorsal vagus, raphe, locus coeruleus, parabrachial nuclei, The lateral and basal nuclei project medially to the central
and the periaqueductal gray. It is the interplay between the nucleus either directly or indirectly through intercalated
diverse afferents projecting to the amygdala, processing cells (intercalated cells separate the basolateral complex
within the amygdala, and the effect of the amygdala on its from the central and medial nuclei). The central nuclei
targets that contribute to the emotional assessment of send much of the processed emotional content from the
incoming sensory information and coordinated behavior- amygdala to the rest of the brain. Thus, the central nucle-
al responses. us is seen as the output region of the amygdala. The central
Most of what is known about human amygdala nucleus produces emotional responses through its effects
function comes from studies of patients with damage to on its various targets throughout the central nervous sys-
the amygdala. However, most damage in humans is not tem. For example, the central nucleus produces arousal
restricted to the amygdala alone and patients with damage through its innervation of modulatory systems in the
to larger areas of the medial temporal lobe have more brain stem that release norepinephrine, dopamine, seroto-
profound deficits. Nonetheless, patients with temporal nin, and acetylcholine. Its input to the periaqueductal gray
lobe damage including the amygdala display a number produces freezing, startle, analgesia, and cardiovascular
of emotional and inappropriate behavioral deficits. changes associated with fear. It also innervates the parabra-
These include impaired fear responses, hypersexuality, chial nucleus where it affects pain processing. Its inputs to
hyperorality, and hyperattention. These behaviors were the dorsal motor vagal nucleus controls parasympathetic
originally described by Kluver and Bucy in nonhuman nervous system function and it also affects vagal nerve
primates. function through its projection to the solitary nucleus.
Much of what is known about functional circuitry Finally, the central nuclei projects to the hypothalamus
within the amygdala and how it relates to encoding of where it controls the release of hormones and activates
emotion has been gleaned from studies in rodents. The the sympathetic nervous system.
amygdala can be divided into many subareas based on In summary, the amygdala is a complex group of
functional circuitry. Lateral to the amygdala is the piri- nuclei that receive diverse inputs from various regions of
form cortex, which encodes olfactory information. Olfac- the central nervous system to assess emotional value.
tory information from the piriform cortex, and other Similarly, after extensive processing, its outputs innervate
olfactory structures, projects to the most ventral and a diverse group of regions in the central nervous system to
lateral portion of the amygdala, the cortical nuclei. The exert its effect. The result is that the amygdala is involved
cortical nuclei in turn project medially to the ventrally in encoding fear, reward, aggression, sexual, maternal, and
located medial nuclei, which is a major output for olfac- ingestive behaviors. This results in effects on cognition,
tory information from the amygdala. However, less is attention, perception, and memory formation. Therefore,
known about the ventrally located olfactory associated it is not surprising that amygdala dysfunction has been
amygdala nuclei compared to the more dorsal multisen- associated with anxiety disorders such as posttraumatic
sory nuclei. The more dorsal nuclei receive information stress disorder, phobias and panic attacks, depression, and
from all sensory modalities. The major inputs to the schizophrenia.
Amyloid Plaques A 155
Future Directions A
Amygdaloid Nucleus
Most of what is known about emotional information
processing performed by the amygdala has been gleaned Amygdala
from studies of fear conditioning. However, the amygdala
also likely plays a role in the encoding of positive emo-
tions associated with rewarding stimuli. Currently, efforts Amyloid Plaques
are being made toward understanding the different types
of emotional values encoded in the amygdala. Also, it J OA NN T. T SCHANZ
remains somewhat contentious whether emotional mem- Utah State University
ory is actually stored by the amygdala. It is of great Logan, UT, USA
interest to determine where emotional memories are
stored in the amygdala (possibly the lateral nuclei) and
precisely what types of memories are being stored by the Synonyms
amygdala, that is, whether these memories are of con-
scious declarative forms or more procedural reflexive Diffuse plaques; Neuritic plaques; Senile plaques
forms. Understanding how the amygdala contributes to
the formation of different forms of emotional memory
will likely provide insights for the treatment of several
Definition
psychiatric illnesses such as posttraumatic stress disorder,
Amyloid plaques refer to an aggregation of beta amyloid
phobias, anxiety, and depression.
protein found in the extracellular space between neurons in
the brain. Amyloid plaques may be of diffuse, pre-amyloid
type, or neuritic, mature senile type. The latter is recog-
Cross References
nized as one of the neuropathological hallmarks of Alzhei-
mers disease (AD). Mature amyloid plaques are spherical
Efferent
in shape and consist of a central beta-amyloid core, fibril-
Insular Lobe
lary outward extensions, and surrounding dystrophic
Limbic System
neurites (elements of degenerating neurons). Unlike the
Locus Ceruleus
mature and senile plaques, diffuse plaques have an amor-
Midbrain Raphe
phous, irregular shape, and lack the surrounding neurites.
Neocortex
Striatum
Temporal Lobes Current Knowledge
It is unknown if the diffuse plaques later form into senile

References and Readings plaques. Both plaque types contain the amyloid b protein
(Ab), a portion of a larger neuronal transmembrane pro-
Ledoux, J. (2007). The amygdala. Current Biology, 17, 868874. tein of unknown function. Other differences between
Ledoux, J. E. (2000). Emotion circuits in the brain. Annual Review of senile and diffuse plaques include their regional distribu-
Neuroscience, 23, 155184.
tion in the brain. Diffuse plaques are common in the basal
Phelps, E. A., & Ledoux, J. E. (2005). Contributions of the amygdala to
emotion processing: from animal models to human behavior. Neu-
ganglia structures of the caudate nucleus and putamen as
ron, 48, 175187. well as the cerebellum, where neuritic plaques are rare. In
Sah, P., Faber, E. S., Lopez De Armentia, M., & Power, J. (2003). The AD, neuritic plaques are more commonly found in the
Amygdaloid complex: anatomy and physiology. Physiological neocortex (Morris & Nagy, 2004).
Reviews, 83, 803834.
Morris, J. H., & Nagy, Z. (2004). Alzheimers disease. In M. M. Esiri,

Amygdaloid Body V. M.-Y. Lee, & J. Q. Trojanowski (Eds.), The neuropathology of
dementia (2nd ed., pp. 161206). Cambridge, UK: Cambridge Uni-
Amygdala versity Press.
156 A Amyotrophic Lateral Sclerosis
motor neurons (or both), showing features of bulbar palsy

Amyotrophic Lateral Sclerosis (facial weakness, limited palatal movement and lingual
atrophy, weakness, and fasciculation) and/or pseudobul-
A LEXANDER I. T ROSTER bar palsy (emotional lability, dysarthria, and brisk jaw
University of North Carolina School of Medicine jerk). Persons with cervical onset can also show upper
Chapel Hill, NC, USA and or lower motor neuron involvement and have upper
limb signs. Such signs may include proximal weakness
(shoulder abduction as required in toothbrushing or
Synonyms combing) or distal weakness (carrying out pincer grip
movements). Lumbar onset patients have involvement of
Lou Gehrigs disease lower motor neurons and proximal weakness (e.g., diffi-
culty in climbing stairs) or foot drop (resulting in
Short Description or Definition tripping).
The most widely accepted clinical diagnostic criteria
The features of amyotrophic lateral sclerosis (ALS) were (the El Escorial criteria) define definite ALS by the pres-
first described by Charcot in the nineteenth century. ALS ence of both upper and lower motor neuron signs in three
is a progressive, fatal neurodegenerative disease affecting regions, probable ALS by signs in two regions, possible
upper and lower motor neurons, although increasingly ALS by signs in one region, and suspected ALS by only
ALS is recognized as a multisystem disorder whose mani- lower or upper motor neuron signs in one or more
festations may also include cognitive and behavioral regions. The suspected ALS category may be the most
changes. Most patients present with motor neuron symp- controversial, and some consider the presence of only
toms at disease onset, and as the disease progresses, upper motor neuron signs to represent primary lateral
persons with ALS demonstrate impairments in speech, sclerosis, while the presence of only lower motor neuron
swallowing, breathing, and use of upper and lower signs represents spinal muscular atrophy.
limbs, with eventual paralysis. The cognitive changes, Also controversial is the notion that FTD and ALS are
the prevalence of which is not well studied but estimates part of the same spectrum of disorders. This idea is
range from about 20 to 50%, most often involve executive supported by observations that persons with ALS may
dysfunction. Deficits in visuospatial, language, and mem- develop FTD and persons with FTD or primary progres-
ory functions are more inconsistently observed. When sive aphasia (PPA) may develop ALS as well as by patho-
dementia is seen, it resembles a frontotemporal lobar logic (ubiquitin-positive, tau-negative, and synuclein-
degeneration or frontotemporal dementia characterized negative neuronal inclusions in some forms of ALS and
by personality change, irritability, diminution of insight, FTD) and genetic findings. Nonetheless, some propose a
poverty of planning, abstraction and initiation, and categorization of ALS dependent upon the presence or
obsessiveness. absence of cognitive and behavioral features, namely ALS,
ALS with cognitive impairment, ALS with behavioral im-
pairment, and ALS with FTD. This categorization appar-
Categorization ently fails to consider that about 25% of patients may have
both cognitive and behavioral abnormalities.
Categorizations can be based on genetics, neurological
levels inferred from symptoms, and diagnostic probability.
At least eight familial variants of ALS (ALS 18) have been Epidemiology
identified, though the vast number of cases (about 90%) is
sporadic. Of these eight, six forms are inherited The incidence of ALS is about 1.52.5 per 100,000 per
in autosomal dominant manner, and two in autosomal year and a prevalence of about 6 per 100,000. Prevalence
recessive manner. and incidence of cognitive impairment is not well studied,
Three neurological levels are most often identified in but it has been estimated that cognitive impairment
the expression of ALS symptoms: bulbar, cervical, and occurs in 2050% of patients. Although one study in a
lumbar. A fourth (thoracic) level is rarely encountered specialty clinic indicated a prevalence of FTD features in
clinically. Persons with bulbar onset demonstrate pro- about 40% of patients with ALS, this might represent an
blems with speech (dysarthria) and/or swallowing (dys- overestimate, given sampling bias, and the figure may be
phagia), and may have disease that affects lower or upper as low as 5%.
Amyotrophic Lateral Sclerosis A 157
Natural History, Prognostic Factors, toward echolalia, stereotypy of expression, and persevera-
A
Outcomes tion in ALS.
When deficits in memory are observed in ALS,
Incidence of ALS peaks in the 60s and drops rapidly they are more likely to be evident on immediate than
thereafter. A broad estimate of mortality is that 50% of delayed recall tasks. Some take this to implicate poorer
patients do not survive beyond 3 years from symptom executive control over encoding processes, whereas others
onset, but that some may survive 10 years or more. Three might invoke slowed information processing as an expla-
epidemiologic studies provide fairly consistent survival nation. The finding that patients can benefit dispropor-
data using time of diagnosis as the reference point tionately from the provision of recognition cues relative
(though diagnostic confirmation may lag onset by 1318 to free recall formats suggests that retrieval deficits might
months): 78% at 1 year, 56% at 2 years, and 32% at also be implicated, or that shallow levels of encoding are
4 years. Several factors are associated with poorer prog- sufficient to support recognition but not recall.
nosis: low-forced vital capacity, bulbar onset (often less Concerning behavioral changes, rating scales have
tolerant of forced ventilation), older age at onset, and revealed that as many as two thirds of persons with ALS
shorter interval between first symptom and presentation. show one or more of irritability, disinhibition, inflexibili-
Patients attending tertiary and specialized ALS clinics ty, restlessness, and apathy. Apathy and questionable or
tend to show longer survival and treatment with riluzole, poor social judgment are more likely to be observed in
on average, extends life by 3 months. Longer survival is patients with bulbar onset ALS. Surprisingly, although
seen in persons with only upper or lower motor neuron reactive depressive reactions may occur after diagnosis,
disease, though as noted, it is controversial whether var- major depression is quite rare among ALS patients (about
iants such as primary lateral sclerosis are ALS. 10%). Symptoms of depression are common, occurring in
about half of patients. Persons with ALS may in particular
experience hopelessness and end-of-life concerns. Patho-
Neuropsychology and Psychology logical laughing or crying, as seen in pseudobulbar syn-
of Amyotrophic Lateral Sclerosis dromes, should not be confused with depression.
Most common among cognitive declines in ALS is execu-

tive dysfunction. Card sorting tasks demanding of concep- Evaluation
tualization and cognitive flexibility are less sensitive to
executive deficits in ALS than are verbal fluency tasks Although consensus guidelines for assessment of cogni-
demanding initiation and deployment of efficient word tion in ALS are expected in the future; currently only older
retrieval strategies. Retrieval of verbs, putatively more de- suggestions are available. Experimental modifications of
pendent upon frontal lobe integrity than upon phonemic tests to eliminate timing and minimize motor require-
or semantic fluency tasks (requiring word retrieval by ments, while facilitating patient performance, have
initial sound or membership in semantic categories, re- unknown sensitivity. Persons with hypophonic speech
spectively) may be the most susceptible to ALS. Verbal might be provided an amplifier. Computers as augmenta-
fluency decrements are observed even if one controls for tive communication devices, while not practical in tradi-
motor and speech impairments. Another task sensitive to tional neuropsychological assessment, can be helpful in
deficits in ALS, and particularly to pseudobulbar ALS, are interviewing the patient. Yesno or forced-choice recog-
Tower tasks that place a premium on spatial working nition paradigms might allow patients to demonstrate
memory and planning. Similarly, another test of working knowledge of memoranda.
memory (digit span backward, requiring examinees to Verbal fluency tests are likely to be helpful in determin-
repeat increasingly long series of digits in reverse order of ing which patients might require fuller evaluations because
presentation) has also been shown to be sensitive to ALS. traditional screening instruments, such as the Mini Mental
Language (unlike motor speech) is less likely dis- State Exam, are not sensitive to cognitive impairment in
rupted by ALS, although language task impairments are ALS. In addition to measures of executive function, naming,
observed in patients with ALS and dementia. Despite and memory, it is important to include in assessments self-
performing well on nonverbal semantic knowledge and or informant rating scales capturing behavioral changes
grammar tasks, patients with ALS and dementia perform such as apathy, irritability, depression, disinhibition, etc.
poorly on verbal tasks, making semantic paraphasic errors Such measures are helpful in identifying those persons
on naming tests. Some studies have observed tendencies with behavioral changes or the behavioral variant of FTD.
158 A Amyotrophic Lateral Sclerosis Functional Rating Scale
Treatment amyotrophic lateral sclerosis. Alzheimer Disease and Associated

Disorders, 21, S31S38.
Brownlee, A., & Palovcak, M. (2007). The role of augmentative commu-
There are no curative treatments for ALS. The only drug nication devices in the medical management of ALS. Neurorehabil-
approved for ALS is riluzole, a glutamate release inhibitor itation, 22, 445450.
that shows moderate benefit and extends life on an aver- Lewis, M., & Rushanan, S. (2007). The role of physical therapy and
age of 3 months. Palliative care (symptomatic control and occupational therapy in the treatment of amyotrophic lateral sclero-
sis. Neurorehabilitation, 22, 451461.
quality of life optimization in the absence of a cure) is
Logroscino, G., Traynor, B. J., Hardiman, O., Chio, A., Couratier, P.,
recommended from the outset, and numerous ameliora- Mitchell, J. D., et al. (2008). Descriptive epidemiology of amyo-
tive therapies, often multidisciplinary, are available. trophic lateral sclerosis: New evidence and unsolved issues. Journal
Cramps and spasticity can be treated with a variety of of Neurology, Neurosurgery and Psychiatry, 79, 611.
medications including, for example, carbamazepine, qui- Lomen-Hoerth, C. (2008). Amyotrophic lateral sclerosis: From bench to
bedside. Seminars in Neurology, 28, 205211.
nine, baclofen, and tizanidine. Drooling can be treated
McCluskey, L. (2007). Palliative rehabilitation and amyotrophic lateral
with anticholinergics such as scopolamine, although sclerosis: A perfect match. Neurorehabilitation, 22, 407408.
there is a risk of confusion and memory problems in Mitchell, J. D., & Borasio, G. D. (2007). Amyotrophic lateral sclerosis.
older patients, and amitriptyline, which may also alleviate Lancet, 369, 20312041.
depression and pathological laughing and crying, may be Mitsumoto, H., & Rabkin, J. G. (2007). Palliative care for patients with
amyotrophic lateral sclerosis: Prepare for the worst and hope for
preferable. Speech therapy is helpful both for swallowing
the best. Journal of the American Medical Association, 298, 207216.
problems and dysarthria, although ultimately, severe Phukan, J., Pender, N. P., & Hardiman, O. (2007). Cognitive impairment
swallowing problems necessitate change in diet and chok- in amyotrophic lateral sclerosis. Lancet Neurology, 6, 9941003.
ing may necessitate percutaneous endoscopic gastrostomy Radunovic, A., Mitsumoto, H., & Leigh, P. N. (2007). Clinical care of
(PEG) placement. When communication becomes too patients with amyotrophic lateral sclerosis. Lancet Neurology, 6,
913925.
difficult due to speech problems or difficulty breathing,
Strong, M. J., Grace, G. M., Orange, J. B., & Leeper, H. A. (1996).
computers can be used to facilitate communication, Cognition, language, and speech in amyotrophic lateral sclerosis: A
in some cases even when paralysis is present. Because review. Journal of Clinical and Experimental Neuropsychology, 18,
breathing difficulty and shortness of breath can be dis- 291303.
tressing to the patient, a benzodiazepine or morphine use
is recommended. Respiratory insufficiency can be alle-
viated with noninvasive ventilation and later invasive
ventilation. Mood disturbances and family bereavement Amyotrophic Lateral Sclerosis
issues can be dealt with by counseling and social work Functional Rating Scale
intervention. Physical and occupational therapy may also
be helpful to facilitate mobility and, perhaps to lesser M ICHELLE M ARIE T IPTON -B URTON
extent, strength and range of motion. Santa Clara Valley Medical Center
San Jose, CA, USA
Cross References
Synonyms
Assistive Technology
Cortical Motor Pathways ALSFRS; ALSFRS-R
Frontal Lobes
Frontal Temporal Dementia
Frontotemporal Lobar Degeneration Description
Speech
The Amyotrophic Lateral Sclerosis Functional Rating
Scale is a validated instrument designed to assess the
References and Readings functional status and the disease progression in patients
with amyotrophic lateral sclerosis (ALS). It is a tool that
Averill, A. J., Kasarskis, E. J., & Segerstrom, S. C. (2007). Psychological
can be used to monitor functional change in a patient
health in patients with amyotrophic lateral sclerosis. Amyotrophic
Lateral Sclerosis, 8, 243254.
over time. The ALSFRS is a 10-item functional inventory
Boeve, B. F. (2007). Links between frontotemporal lobar degeneration, which was devised for use in therapeutic trials in ALS.
corticobasal degeneration, progressive supranuclear palsy, and Each item is rated on a 04 scale, (with 0 being severely
Analysis of Variance A 159
impaired and 4 being normal) by the patient and/or hospital length of stay and survival time in ALS patients
A
caregiver, yielding a maximum score of 40 points. The treated with tracheostomy-intermittent positive-pressure
ALSFRS assesses the patients levels of self-sufficiency in ventilation. Through observation and interview the eva-
areas of self-feeding, grooming, ambulation and commu- luator assesses the following measures: speech, salivation,
nication, and swallowing. swallowing, handwriting, cutting food/handling utensils,
turning in bed and adjusting bed clothes, walking,
climbing stairs, and breathing.
The ALSFRS was developed because then current used Cross References
clinimetric scales being utilized at the time were contami-
nated with impairment measurements did not measure Amyotrophic Lateral Sclerosis
the broad range of disabilities that result from ALS, and
did not lend themselves to sub-score analysis that was
based entirely on disability components (Feinstein, 1987;
Louwerse et al., 1990; Streiner & Norman, 1989).
ALS CNTF Treatment Study (ACTS) Phase 111 Study Group. (1996).
The ALSFRS is a validated rating instrument for mon- The Amyotrophic Lateral Sclerosis Functional Rating Scale. Assess-
itoring the progression of disability in patients with ALS. ment of activities of daily living in patients with Amyotrophic
One weakness of the ALSFRS, as it was originally Lateral Sclerosis. Archives of Neurology, 53, 141147.
designed, was that it granted disproportionate weighting Cedarbaum, J. M., & Stambler, N. (1997). Performance of the
Amyotrophic Lateral Sclerosis Functional Rating Scale (ALSFRS)
to limb and bulbar, as compared to respiratory dysfunc-
in multicenter clinical trials. Journal of the Neurological Sciences,
tion. The ALS Functional Rating Scale Revised version 152(Suppl 1), S1S9.
that is also validated incorporates additional assessments Herndon, R. M. (2006). Handbook of neurologic rating scales (p. 96).
of dyspnea, orthopnea, and the need for ventilator New York: Demos Medical Publishing.
support. The Revised ALSFRS (ALSFRS-R) retains the Lo Coco, D., Marchese, S., La Bella, V., Piccoli, T., & Lo Coco, A. (2007).
The amyotrophic lateral sclerosis functional rating scale predicts
properties of the original scale and shows strong internal
survival time in amyotrophic lateral sclerosis patients on invasive
consistency and construct validity. mechanical ventilation. Chest, 132(1), 6469.
Psychometric Data
Analysis of Covariance
The ALSFRS was developed as an internally consistent,
reliable, and valid measure of disability in ALS patients ANCOVA/MANCOVA
as part of the Amyotrophic Lateral Sclerosis Ciliary Neu-
rotrophic Factor (ALS CNTF) Treatment Study (ACTS
Phase 111 Study Group, 1996). The ability of the ALSFRS
to be responsive to change in the clinical status of ALS Analysis of Variance
patients was evaluated cross-sectionally and prospectively
over time in phase 1 and phase 2 studies of CNTF in ALS. M ICHAEL D. F RANZEN
The ALSFRS has been validated both cross-sectionally Allegheny General Hospital
and longitudinally against muscle strength, the Schwab and Pittsburgh, PA, USA
England ADL rating scale, the Clinical Global Impression
of Change (CGIC) scale, and independent assessments of
patients functional status (Cedarbaum & Stambler, 1997). Synonyms
ANOVA
Clinical Uses
The ALSFRS is a straightforward instrument that can be Definition

utilized across disciplines to assess the functional status of
an individual diagnosed with ALS. The tool has also been Analysis of variance (ANOVA) is a method of examining
utilized to evaluate the disease progression, predict and evaluating possible statistical relations among
160 A ANAM
variables. ANOVA involves a general model of indepen- Definition

dent and dependent variables as well as a mathematical
model of calculating statistical relations among the vari- Anarthria is speechlessness due to a severe loss of neuro-
ables. The independent variables are categorical in nature muscular control over the speech musculature (Duffy,
and the dependent variables are continuous in nature. 2005). The term typically refers to the most severe form
Although ANOVA is frequently used to evaluate potential of dysarthria. Language and cognition of the anarthric
causality in an experiment, a significant finding in an patient may be intact but their disordered neuromuscular
ANOVA does not automatically indicate a casual relation. system prevents speech. Anarthric patients have an intact
The determination of causality requires experimental ma- drive or motivation to speak but are unable. Writing
nipulation of the independent variables with subsequent remains intact (Marcie & Hecaen, 1979). A lesion in the
changes in the dependent variables. A finding of statistical outflow pathway from Brocas area leads to anarthria
significance in ANOVA indicates the likelihood of a sys- (Caplan & Chertkow, 1989, p. 295).
tematic relation between variables.
Cross References Cross References
Analysis of Covariance (ANCOVA) Dysarthria

Multivariate Analysis of Variance
References and Readings References and Readings

Caplan, D., & Chertkow, H. (1989). In D. P. Kuehn, M. L. Lemme, & J. M.
Iverson, G. R., & Norpoth, H. (1987). Analysis of variance. Newbury Park,
Baumgartner (Eds.), Neural bases of speech, hearing, and language.
CA: Sage Publications.
Chapter 10 Neurolinguistics (pp. 292302). Boston: College-Hill,
Watson, P. (2009). Review of analysis of variance and covariance: How to
Little, Brown.
choose and construct models for the life sciences. Psychological
Duffy, J. R. (2005). Motor speech disorders: Substrates, differential diagno-
Medicine, 39, 695696.
sis, and management. St. Louis, MO: Elsevier Mosby.
Marcie, P., & Hecaen, H. (1979). Agraphia: writing disorders associated
with unilateral cortical lesions. In K. M. Heilman & E. Valenstein
(Eds.), Clinical Neuropsychology (Chapter 4, p. 96). Oxford: Oxford
ANAM University Press.
Automated Neuropsychological Assessment Metrics
ANCOVA/MANCOVA
Anarchic Hand
M ICHAEL F RANZEN
Alien Hand Syndrome Allegheny Neuropsychiatric Institute
Pittsburgh, PA, USA
Anarthria
Synonyms
C AROLE R OTH
Naval Medical Center Analysis of covariance
San Diego, CA, USA
Definition
Synonyms
ANCOVA or analysis of covariance is a variant of the
Speechlessness ANOVA model in which the statistical effect of a
Anencephaly A 161
nuisance variable is removed mathematically from the Watson, P. (2009). Review of Analysis of variance and covariance: How to
choose and construct models for the life sciences. Psychological A
analysis in order to clarify the relations between the
Medicine, 39, 695696.
independent and the dependent variables. The optimal Wildt, A. R. & Ahtola, O. T. (1978). Analysis of covariance. Beverly Hills:
situation would be if the independent variable levels or Sage.
groups were not related to the nuisance variable. Howev-
er, if the nuisance variable is related to the dependent
variable and if the nuisance variable is systematically
represented among the independent variables, ANCOVA
may be used to partial out the statistical effect of the Anencephaly
nuisance variable or covariate. This is not a substitute for
removing the effect through experimental design. For E RIN D. B IGLER , J O A NN P ETRIE
example, level of education may be statistically related Brigham Young University
to performance on a memory test. If two groups of Provo, Utah, USA
depressed and nondepressed individuals differ systemati-
cally on the basis of their level of education, any
difference found with regard to performance on a Synonyms
memory test might be due to the different level of
education. By employing ANCOVA and using education Amnion rupture; Congenital defects; Exencephaly; Lack
level as the covariate, the researcher may have a of neural tube closure; MRI; Neural tube defects
clearer understanding of the relation between the
presence of depression and performance on the memory
test. Short Description or Definition
Although there are different mathematical methods
for conducting an ANCOVA including the use of multi- Using an in front of an anatomical descriptor signifies
ple regression (which see), ANCOVA under the general absence. Cephalic is Greek for head with encephalon
linear model provides a useful conceptualization of the specifically referring to the brain. Therefore, the term
underlying idea. We can think of calculating the regres- anencephaly is used to denote a congenital defect in the
sion between the covariate and the dependent variable development of the head, including the meninges, the
and then residualizing the influence of the covariate. cranium, and the scalp and, in particular, abnormal
Then an ANOVA can be conducted on the residual brain growth, with an almost completely diminished
values. In order to use ANCOVA, the data must satisfy prosencephalon (telencephalon diencephalon) or fore-
a few basic assumptions. There must be a linear relation brain and only rudimentary development of the brain
between the covariate and the dependent variable. The stem.
slope of the regression for each group or level of the
independent variable must be the same. The error term
should be normally distributed with a mean of zero. The
covariate should not be affected by the independent Categorization
variable.
Anencephaly results from the failure of closure of the
headend of the neural tube in early fetal development
(first 34 weeks) with subsequent neural tube defects
Cross References (NTD) including lack of formation of the brain, skull
and scalp. Loss of the forebrain includes loss of the two
Analysis of Variance (ANOVA)
cerebral hemispheres, the connecting corpus callosum,
neocortex, thalamus, hypothalamus and other structures
of the limbic system the amygdala, hippocampus, cau-
References and Readings date nucleus, ventricles, etc., and all of their connections
(Kolb & Whishaw, 2008). These structures comprise the
Belin, T. R., & Normand, S.-L. T. (2009). The role of
majority of human brain tissue and are required for
ANCOVA in analyzing experimental data. Psychiatric Annals, 39, almost all sensation perception and basic physiological
753759. functions including body temperature control, eating,
162 A Anencephaly
sleeping, and motor function, and cognition, language, Natural History, Prognostic Factors,
memory, emotion, thought processing, inhibition, deci- and Outcomes
sion making, and/or reasoning.
With the major portion of an infants brain being
undeveloped, particularly the cerebrum, and coupled
with the brain often being exposed in utero, the anence-
Epidemiology
phalic infant is frequently stillborn. An infant born alive
with anencephaly is, as a rule, blind, deaf, unconscious,
Anencephaly results from NTD (Cohen, 2002; Detrait
and may only reflexively respond. With only a basic brain
et al., 2005; Dias & Partington, 2004; Mitchell, 2005)
stem and a nonfunctioning cerebrum, prognosis is poor;
with approximately 1 in 1,000 births born with NTD;
anencephalic infants will never gain consciousness and
these may be associated with genetics, nutrition, environ-
will only have minimal reflex actions such as breathing.
ment, or a combination of all three. There is a known
There may be intermittent sound or touch responses;
higher prevalence of females born with anencephaly NTD
however, no further progress can be expected (see
as compared to males (James, 1980). Over the past 3
National Institute of Neurological Disorders and
decades, worldwide research has found an association
Stroke, 2010).
between prenatal folic acid deficits leading to folate defi-
ciencies (National Institutes of Health: Office of Dietary
Supplements, 2009) and NTD (see also Calvo & Biglieri, Neuropsychology and Psychology
2008; Kondo, Kamihira, & Ozawa, 2009; Wolff, Witkop, of Anencephaly
Miller, & Syed, 2009). While all the causes of open NTD
are not known, research indicates that daily consumption There is essentially no assessment that neuropsychological
of 4 mg/day of folic acid by women before and during testing can offer given the absence of cortical development
pregnancy brings about a 70% reduction in NTD (Centers in the anencephalic infant who does survive. Such chil-
for Disease Control and Prevention, 1991, 2008; Cornel & dren have reflexive function only (i.e., breathing and
Erickson, 1997; McLone, 2003; MRC Vitamin Study some responses to sound or touch can manifest) and
Research Group, 1991). will rarely survive longer than a few hours or days.
a b c
Anencephaly. Figure 1 Magnetic resonance imaging (MRI) findings of the head and neck 8 h after birth. (a) Sagittal
T1-weighted, (b) sagittal T2-weighted, and (c) coronal T1-weighted images show cranial schisis. The normal skin stops at the skull
base and encircles abnormally developed cerebral structures, the so-called area cerebrovasculosa (white arrows). Along the
border of the skull defect the skin seems to be in continuity with the superficial layer of the area cerebrovasculosa, probably the
pia mater (curved white arrow). The posterior fossa is funnel-shaped. A rudimentary brain stem (curved black arrows) and
primordium of cerebellum (small black arrows) are present. The cervical spine is normal (From Calzolari et al., 2004, With
permission)
Anencephaly A 163
Neuropsychologists should have an empathetic awareness Calzolari, F., Gambi, B., Garani, G., & Tamisari, L. (2004). Anencephaly:
MRI findings and pathogenetic theories. Pediatric Radiology, A
of this condition; they may be asked to consult with
34, 10121016.
parents and families about the nature of the infants Centers for Disease Control and Prevention (1991). Use of folic acid
deficits and the poor prognosis (Ashwal, 2005). for prevention of spina bifida and other neural tube defects
19831991. MMWR Morbidity and Mortality Weekly Report, 40,
513516.
Evaluation Centers for Disease Control and Prevention (2008). Prevalence of neural
tube defects and folic acid knowledge and consumption puerto
Although the pathogenesis of anencephaly is still not fully rico, 19962006. MMWR Morbidity and Mortality Weekly Report,
57, 1013.
understood, several studies suggest that exencephaly or the
Cohen, M. M., Jr. (2002). Malformations of the craniofacial region:
lack of skull growth or separation following NTD allows Evolutionary, embryonic, genetic, and clinical perspectives. American
the cerebral tissue to be exposed in utero causing damage Journal of Medical Genetics, 115, 245268.
from the amniotic fluid (Calzolari, Gambi, Garani, & Cook, R. J., Erdman, J. N., Hevia, M., & Dickens, B. M. (2008). Prenatal
Tamisari, 2004). As can be seen in Fig. 1, even though management of anencephaly. International Journal of Gynecology &
Obstetrics, 102, 304308.
there are other anomalies of physical development
Cornel, M. C., & Erickson, J. D. (1997). Comparison of national policies
associated with the presence of anencephaly, the most on periconceptional use of folic acid to prevent spina bifida and
dramatic is a failure of brain development. anencephaly (SBA). Teratology, 55, 134137.
Detrait, E. R., George, T. M., Etchevers, H. C., et al. (2005).
Human neural tube defects: Developmental biology, epidemiology,
Treatment and genetics. Neurotoxicology and Teratology, 27, 515524.
Dias, M. S., & Partington, M. (2004). Embryology of myelomeningocele
Ultimately, mortality rate is 100% with anencephaly. and anencephaly. Neurosurgical Focus, 16, E1.
Some anencephalic children do survive from hours to James, W. H. (1980). The sex ratios of anencephalics born to anencephalic-
days but rarely longer and in a persistent vegetative state prone women. Developmental Medicine and Child Neurology,
22, 618622.
(Payne & Taylor, 1997); thus, treatment is purely support-
Kolb, B., & Whishaw, I. Q. (2008). Fundamentals of human neuropsychol-
ive. The presence of a surviving infant with anencephaly ogy. New York: Worth Publishers.
raises numerous ethical questions about care, treatment, Kondo, A., Kamihira, O., & Ozawa, H. (2009). Neural tube defects:
and maintenance (Batavia, 2002; Cook, Erdman, Hevia, & Prevalence, etiology and prevention. International Journal of Urology,
Dickens, 2008; Obeidi, Russell, Higgins, & ODonoghue, 16, 4957.
McLone, D. G. (2003). The etiology of neural tube defects: The role of
2010), including the importance of continued research
folic acid. Childs Nervous System, 19, 537539.
for better ways to prevent and treat neurological birth Mitchell, L. E. (2005). Epidemiology of neural tube defects. American
defects. Journal of Medical Genetics. Part C. Seminars in Medical Genetics,
135C, 8894.
MRC Vitamin Study Research Group (1991). Prevention of neural tube
Cross References defects: Results of the medical research council vitamin study.
Lancet, 338, 131137.
Ethics in the Practice of Neuropsychology National Institute of Neurological Disorders and Stroke. (2010, January
14, 2010). NINDS anencephaly information page. National Insti-
Forebrain
tutes of Health: Reducing the burden of neurological disease Re-
National Institute of Neurological Disorders and Stroke trieved March 16, 2010, from http://www.ninds.nih.gov/disorders/
National Institutes of Health (NIH) anencephaly/anencephaly.htm
National Institutes of Health: Office of Dietary Supplements. (2009, 4/15/
2009). Dietary supplement fact sheet: Folate. Dietary Supplement
References and Readings Fact sheets Retrieved March 16, 2010, from http://dietary-
supplements.info.nih.gov/factsheets/folate.asp
Ashwal, S. (2005). Recovery of consciousness and life expectancy of Obeidi, N., Russell, N., Higgins, J. R., & ODonoghue, K. (2010). The
children in a vegetative state. Neuropsychological Rehabilitation, natural history of anencephaly. Prenatal Diagnosis. doi:10.1002/
15, 190197. pd.2490.
Batavia, A. I. (2002). Disability versus futility in rationing health Payne, S. K., & Taylor, R. M. (1997). The persistent vegetative state and
care services: Defining medical futility based on permanent anencephaly: Problematic paradigms for discussing futility and
unconsciousness pvs, coma, and anencephaly. Behavioral Sciences rationing. Seminars in Neurology, 17, 257263.
& The Law, 20, 219233. Wolff, T., Witkop, C. T., Miller, T., & Syed, S. B. (2009). Folic acid
Calvo, E. B., & Biglieri, A. (2008). [impact of folic acid fortification on supplementation for the prevention of neural tube defects: An
womens nutritional status and on the prevalence of neural tube update of the evidence for the U.S. Preventive services task force.
defects]. Archives of Argentina Pediatrics, 106, 492498. Annals of Internal Medicine, 150, 632639.
164 A Aneurysm
consciousness is a presenting feature in about 20% of

Aneurysm cases. Commonly observed systemic complications and
sequelae are vasospasms, rebleeding, hydrocephalus, her-
B RUCE J. D IAMOND niation, seizures, cardiodysrhythmias, and respiratory de-
William Paterson University pression (Bonner & Bonner, 1991).
Wayne, NJ, USA
Neuropsychological and Medical

Synonyms Outcomes
Blood-filled dilatation Symptoms and signs can include retinal hemorrhage,
papilledema, and meningeal signs with seizure activity
commonly observed. Focal signs are prominent within
Short Description or Definition the first 24 h (e.g., parenchymal dissection, hyperfusion
distal to the aneurysm site, cerebral edema). Vasospasm
An aneurysm is an abnormal blood-filled dilatation of a may be the cause of focal signs within the 4872 h window.
blood vessel that can occur in vascular innervated areas Cognitive, psychiatric, and behavioral impairments fol-
(Websters New Explorer Medical Dictionary, 2006). lowing aneurysm rupture will depend on the site and
Aneurysms generally develop due to trauma, infections, extent of damage, secondary sequelae, complications,
congenital defects, or degenerative diseases (Parkin & and pre-morbid health (see Table 1).
Leng, 1993).
Assessment and Treatment

Categorization
The Hunt-Hess grading scale is used for prognosis and for
timing of surgical interventions. Diagnostic evaluations
Intracranial aneurysms are commonly classified as saccu-
commonly include CT scans, angiography, and MR angi-
lar, mycotic, traumatic, arteriosclerotic, dissecting, or
ography. Surgical treatment consists of clipping and
neoplasmic. Giant aneurysms greater than 2.5 cm in
endovascular embolization of the aneurysm, and pharma-
diameter are believed to be congenital anomalies and
cologic interventions may include calcium channel block-
mostly are located on the anterior and middle cerebral,
ers (e.g., nimodipine) in order to reduce the severity of
and carotid and basilar arteries (Ropper, Brown, Adams,
vasospasm (Bonner & Bonner, 1991).
& Victor, 2005).
Epidemiological Factors
Aneurysm. Table 1 Symptoms that may be associated with
Ruptured aneurysms, specifically the saccular type, are the ruptured and unruptured cerebral aneurysms (From Bonner &
most common cause of subarachnoid hemorrhage (SAH) Bonner, 1991)
after 20 years of age. This type of aneurysm accounts for
Ruptured
about 80% of nontraumatic aneurysms. aneurysms Unruptured aneurysms
Parenchymal Headache, nuchal rigidity
dissection
Natural History, Prognostic Factors, and Hyperfusion Neurologic deficit
Outcomes
Cerebral edema Drowsiness, confusion, focal
neurologic deficit
Unruptured aneurysms may be symptomatic and mani-
Cognitive Decerebrate rigidity/vegetative
fested as cranial nerve palsies. Ruptured cerebral aneur-
impairments disturbance possible
ysms can be associated with states of consciousness
Disturbances in Deep coma
ranging from lethargy to coma. Outcome depends on
personality
location and severity of bleeding. A sudden loss of
Angelman Syndrome A 165
Cross References Categorization A

Anterior Cerebral Artery Deletion or mutation of genetic material on chromosome
Anterior Communicating Artery 15q1113 can result in one of two distinct neurodevelop-
Herniation Syndromes mental disorders, depending upon whether the genetic
Hydrocephalus material is from the maternal or paternal chromosome.
This parent of origin effect is known as imprinting.
Note that the 15q1113 region is differently imprinted
References and Readings in maternal and paternal chromosomes, and both
imprintings are needed for normal development. If a
Bonner, J. S., & Bonner, J. J. (1991). The little black book of neurology: A maternal deletion occurs, the result is Angelman syn-
manual for neurologic house officers (2nd ed.). St Louis, MO: Mosby- drome; but if paternal, then the result is PraderWilli
Year Book.
syndrome. Therefore, Angelman and PraderWilli have
Parkin, A., & Leng, R. C. (1993). Neuropsychology of the amnestic syn-
drome. Hove, UK: Lawrence Erlbaum.
been termed sister syndromes or sister disorders.
Ropper, A. H., Brown, R. H., Adams, R. D., & Victor, M. (2005). Adams & There are four main classes of Angelman syndrome,
Victors principles of neurology. New York: McGraw-Hill. based upon four primary genetic mechanisms by which it
Websters new explorer medical dictionary (new ed.). (2006). Springfield, occurs (Clayton-Smith & Laan, 2003). Each of these clas-
MA: Merriam-Webster.
ses involves expression of the maternal chromosome
region 15q1113, which includes the UBE3A gene. In
the general population, UBE3A is expressed only from
the maternal chromosome in particular regions of the
Aneurysmal Subarachnoid brain, and the UBE3A gene on the paternal chromosome
Hemorrhage is inactive. In Angelman syndrome, as a result of the
deletion, only about 10% of UBE3A is expressed
Subarachnoid Hemorrhage (Williams, 2005).
Epidemiology
Exact prevalence rates of Angelman syndrome are
Angelman Syndrome unknown but have been estimated between 1/10,000 and
1/40,000 (Clayton-Smith & Laan, 2003). See Table 1 for
K RISTIN D. P HILLIPS 1, B ONITA P. K LEIN -TASMAN 2
1 estimates by subtype.
Medical College of Wisconsin
Milwaukee, WI, USA
2
University of Wisconsin-Milwaukee Natural History, Prognostic Factors,
Milwaukee, WI, USA and Outcomes
Angelman syndrome was first described by Dr. Harry

Short Description or Definition Angelman in 1965. He observed several pediatric patients
whom he referred to as puppet children, in light of their
Angelman syndrome is a neurodevelopmental disorder happy expressions and jerky movements. This term was
caused by one of several genetic mechanisms involving later abandoned, and the disorder came to be known as
maternal chromosome 15, specifically the region 15q11 Angelman syndrome. Diagnostic clinical criteria were
13. Characteristic physical features include a large chin, developed by Williams and colleagues in 1995 and revised
deep-set eyes, a wide mouth, and microcephaly. Addition- in 2006 (Williams et al., 2006).
ally, seizure disorder, ataxia, hypotonia, developmental The prenatal and perinatal history of children with
delays, and a lack of expressive language are commonly Angelman syndrome is typically unremarkable, and de-
observed. Behaviorally, individuals with Angelman velopmental delays first become evident around 612
syndrome are known for a happy temperament, frequent months of age (Cassidy et al., 2000). In addition to mi-
laughter, inattention/hyperactivity, and stereotyped crocephaly, a flat occiput (microbrachycephaly) is com-
behaviors (Clayton-Smith & Laan, 2003). monly observed. Puberty typically occurs on time. There
166 A Angelman Syndrome
Angelman Syndrome. Table 1
Genetic
mechanism Incidence Definition
De novo 70% Deletion on maternal
deletion chromosome region 15q1113
Uniparental 23% Both copies of chromosome 15
disomy are inherited from the father,
rather than one from each parent
Imprinting 25% Genes become inactivated as a
defect result of a disruption in genes
controlling the imprinting
process itself, or the imprinting
center
UBE3A 1015%
mutation
Unknown 1015%
(Cassidy, Dykens, & Williams, 2000; Clayton-Smith & Laan, 2003;
Williams, 2005)
is generally no evidence of reduced lifespan, although the

severity of associated medical conditions (e.g., seizures) Angelman Syndrome. Figure 1
certainly impacts health and the overall quality of life.
Additionally, the longstanding motor difficulties in this
population often translate into mobility issues later in life
(Clayton-Smith & Laan, 2003).
Although epilepsy is common in Angelman syn-
drome, it is not universal, with estimates of about 80%
in this population (Clayton-Smith & Laan, 2003).
A variety of seizure types has been reported, including
atypical absence, myoclonic, atonic, and tonicclonic.
Seizures usually appear in early childhood, with some
indication of improvement during late childhood/adoles-
cence, although the majority of adults continue to have
seizures. EEGs are typically abnormal, and characteristic
EEG patterns have been described.
Variability is evident in the phenotypic expression of
Angelman syndrome depending upon the specific genetic
mechanism by which it occurs. Those with Angelman
syndrome due to a de novo deletion appear most severely
affected, including more severe medical and physical pro-
blems, as well as greater motor and language deficits (e.g.,
Clayton-Smith & Laan, 2003; Levitas, Dykens, Finucane, &
Kates, 2007). In contrast, those with uniparental disomy
have less-severe ataxia and seizures, better nonverbal
communication skills, and fewer dysmorphic facial fea-
tures. Individuals with Angelman syndrome due to an
imprinting center defect also appear to have milder clini-
cal presentations. Those with UBE3A mutations have
been found to have the more-severe medical and physical
problems seen in individuals with de novo deletions, but Angelman Syndrome. Figure 2
Angelman Syndrome A 167
fewer difficulties with motor and language skills than typically employed to identify genetic deletions, whereas
A
these individuals (Clayton-Smith & Laan, 2003). DNA-methylation testing can be used to detect uniparental
disomy or imprinting defects.
Neuropsychology and Psychology of
Angelman Syndrome
Treatment
Neuroanatomical findings have demonstrated anomalous
There is no cure for Angelman syndrome itself. Given
Sylvian fissures in individuals with Angelman syndrome
the high incidence of seizure disorder, management and
(Leonard et al., 1993), in addition to marked cerebellar
follow-up by a neurologist is usually necessary. Anticon-
atrophy (Jay, Becker, Chan, & Perry, 1991). Cognitive
vulsant medications have been utilized to manage sei-
functioning typically falls in the severe-to-profound
zures. Clonazepam, valproic acid, and phenobarbital
range of intellectual disability (Peters, Goddard-Finegold,
appear to be most effective in addressing seizures in
Beaudet, Madduri, Turcich, & Bacino, 2004). Similarly,
Angelman syndrome. Sleep difficulties have successfully
adaptive functioning is delayed, with a relative strength
been addressed through behavioral and pharmacological
in socialization and a relative weakness in motor skills
intervention.
(Peters et al., 2004). A primary feature of Angelman
Involvement in interventions such as occupational,
syndrome is limited expressive language, typically ranging
physical, and speech/language therapy is typically recom-
from no language to very few single words. There are
mended to address language and motor deficits. In addition
relative strengths in nonverbal communication and recep-
to speech/language therapy, alternative communication
tive language. Marked deficits occur in fine motor skills.
methods typically need to be explored. Special education
A happy temperament has been reported among
programming is also indicated in light of cognitive deficits.
individuals with Angelman syndrome, characterized by
Very few behavioral intervention studies have been con-
frequent smiling and laughter, which persists across the
ducted for individuals with Angelman syndrome. Behavior-
lifespan and is most evident in social interactions (e.g.,
al training has been used to increase communication and
Clayton-Smith, 2001; Clayton-Smith & Laan, 2003).
daily living skills.
Parents have rated their children with Angelman syn-
drome lower on irritability and lethargy, in comparison
to individuals with other developmental disabilities Cross References
(Summers & Feldman, 1999). A variety of behavioral
difficulties have been reported, the most common includ- Ataxia
ing inattention and hyperactivity (Clarke & Marston, Developmental Delay
2000; Summers, Allison, Lynch, & Sandler, 1995). Epilepsy
However, there is some indication that these behavioral Intellectual Disabilities
difficulties improve with age (Clayton-Smith, 2001). Microcephaly
Stereotyped behaviors, such as hand flapping, have been PraderWilli Syndrome
observed. In addition, individuals with Angelman syn- Seizure
drome often have an attraction to water and shiny objects. Syndrome
These latter findings have led to the conclusion that the
incidence of autism spectrum disorders is high in this
population; however, this may be overdiagnosed References and Readings
in Angelman syndrome given the severe-to-profound
intellectual disability. Sleep problems are common, in- Angelman Syndrome Foundation, Inc. (2009). Retrieved November 6,
cluding issues like falling asleep, staying asleep, and 2008, from http://www.angelman.org/
being easily roused from sleep. Feeding problems have Cassidy, S. B., Dykens, E., & Williams, C. A. (2000). Prader-Willi and
Angelman syndromes: Sister imprinted disorders. American Journal
also been reported.
of Medical Genetics, 97, 136146.
Clarke, D. J., & Marston, G. (2000). Problem behaviors associated with
15q- Angelman syndrome. American Journal on Mental Retardation,
Evaluation
105, 2531.
Clayton-Smith, J. (2001). Angelman syndrome: Evolution of the pheno-
Angelman syndrome is confirmed through genetic test- type in adolescents and adults. Developmental Medicine and Child
ing. Fluorescence in-situ hybridization (FISH) testing is Neurology, 43, 467480.
168 A Angiitis
Clayton-Smith, J., & Laan, L. (2003). Angelman syndrome: A review of the Definition
clinical and genetic aspects. Journal of Medical Genetics, 40, 8795.
Jay, V., Becker, L. E., Chan, F. W., & Perry, T. L. Sr. (1991). Puppet-like
syndrome of Angelman: a pathologic and neurochemical study.
Angiography refers to a set of procedures designed to
Neurology, 41, 416422. image the arterial circulation. As such, cerebral angio-
Leonard, C. M., Williams, C. A., Nicholls, R. D., Agee, O. F., Voeller, K. K., graphy refers specifically to the imaging of the cerebral
Honeyman, J. C., et al. (1993). Angelman and Prader-Willi arterial tree.
syndrome: A magnetic resonance imaging study of differences in
cerebral structure. American Journal of Medical Genetics, 46, 2633.
Levitas, A., Dykens, E., Finucane, B., & Kates, W. (2007). Behavioral
phenotype of genetic disorders. In R. Fletcher, E. Loschen, Current Knowledge
C. Stavrakaki, & M. First (Eds.), Diagnostic manual intellectual
disability: A textbook of diagnoses of mental disorders in persons with Historical background: Angiography was initially intro-
intellectual disability. Kingston, NY: NADD Press.
duced into medical practice in the late 1940s. Traditional
Peters, S. U., Goddard-Finegold, J., Beaudet, A. L., Madduri, N.,
Turcich, M., & Bacino, C. A. (2004). Cognitive and adaptive beha-
catheter angiography involves introduction of a catheter
vior profiles of children with Angelman syndrome. American Journal through a large peripheral artery (typically the femoral
of Medical Genetics, 128, 110113. artery), threading it to its desired location, and injection
Summers, J. A., Allison, D. B., Lynch, P. S., & Sandler, L. (1995). of radio-opaque contrast medium while obtaining radio-
Behaviour problems in Angelman syndrome. Journal of Intellectual
graphic images. The introduction of computerized tomo-
Disability Research, 39, 97106.
Summers, J. A., & Feldman, M. A. (1999). Distinctive pattern of
graphic angiography (CT angiography) in the 1970s
behavioral functioning in Angelman syndrome. American Journal allowed the administration of contrast material intrave-
on Mental Retardation, 104, 376384. nously rather than intra-arterially, since the reconstructed
Williams, C. A. (2005). Neurological aspects of the Angelman syndrome. tissue slices allow visualization of the contrast in the
Brain & Development, 27, 8894.
arteries or organs of interest. Magnetic resonance (MR)
Williams, C. A., Beaudet, A. L., Clayton-Smith, J., Knoll, J. H.,
Kyllerman, M., Laan, L. A., et al. (2006). Angelman syndrome
angiography was added to the diagnostic armamentarium
2005: Updated consensus for diagnostic criteria. American Journal in the early 1990s. MR digital subtraction angiography
of Medical Genetics, 140, 413418. can visualize the arterial circulation via detection of
moving water molecules in blood, without the attendant
risks of toxicity from the contrast medium or radiation
exposure (Fig. 1). It has the additional advantage of
Angiitis revealing abnormalities in the vessel wall, not merely
luminal filling defects. However, contrast agents designed
Vasculitis for visibility in MR scanning, and administered intrave-
nously, can further enhance visualization.
Psychometric data: The sensitivity, specificity, and pos-
itive predictive value of the various forms of angiography
Angio are dependent on the disorder under study and its preva-
lence in the sample being investigated. Overall, however,
Carotid Angiography less invasive forms of angiography have increasingly
supplanted the catheter-based methods, because of compa-
rable accuracy. In one recent porcine model, for example,
estimated degree of arterial narrowing did not differ
Angiography, Cerebral significantly between catheter and digital subtraction
imaging methods, and the correlation between methods
J OHN W HYTE was highly significant.
Moss Rehabilitation Research Institute Clinical uses: Angiography can be performed to
Albert Einstein Healthcare Network visualize occult vascular pathology such as unruptured
Elkins Park, PA, USA aneurisms, arteriovenous malformations, or the abnor-
mal vascular supply of tumors. It can also be performed
to localize the source of clinically significant bleeding, as
Synonyms in the case of ruptured aneurisms, or to locate the sites of
narrowing or occlusion by atherosclerotic plaque, throm-
(Cerebral) arteriography bus, arterial dissection, or external compression.
Angioma, Cavernous Angioma A 169
Angioma, Cavernous Angioma A
J ENNIFER T INKER
Drexel University
Synonyms
Cavernous hemangioma; Cavernoma; Cerebral cavernous

malformation (CCM); Cavernous venous malformation
Definition
Cavernous angiomas are benign vascular malformations

found within the CNS. They are typically found supra-
tentorially (approximately 80%), predominantly in the
frontal and temporal lobes. Infratentorially, cavernous
Angiography, Cerebral. Figure 1 Figure CA1 shows a large angiomas are most commonly found in the pons and
arteriovenous malformation in the left frontal lobe as revealed cerebellar hemispheres (Sage & Blumbergs, 2001). Origi-
by an unenhanced MR angiogram nally thought to be relatively rare and most commonly
detected during autopsy, the advent of MRI has led to an
increased detection, with incidence rates now estimated
Cross References between 0.02% and 0.8% of the general population.
The size of the well-circumscribed, mulberry-like mass
Computed Tomography can range from less than 1 cm to greater than 4 cm.
Digital Subtraction Angiography Prevalence rates are relatively equivalent among men
Magnetic Resonance Imaging and women. While it can remain asymptomatic lifelong,
symptomatic presentation is most commonly seen in
References and Readings the third and fourth decades of life. However, newly
symptomatic cases have been well-reported throughout
Anzalone, N., Scotti, R., & Iadanza, A. (2006). MR angiography of the
the life span. Clinical manifestations, when present, vary
carotid arteries and intracranial circulation: Advantage of a high
relaxivity contrast agent. Neuroradiology, 48(Suppl. 1), 917.
significantly and generally correlate to location of the
Bracard, S., Anxionnat, R., & Picard, L. (2006). Current diagnostic lesion. Most commonly reported symptoms include
modalities for intracranial aneurysms. Neuroimaging Clinics of headache (665%), seizure (2352%), focal neurological
North America, 16(3), 397411. deficit (2045%), and intracranial hemorrhage (1325%)
Paciaroni, M., Caso, V., & Agnelli, G. (2005). Magnetic resonance imag-
(Conway & Rigamonti, 2006). Despite the regional affini-
ing, magnetic resonance and catheter angiography for diagnosis of
cervical artery dissection. Frontiers of Neurology and Neuroscience,
ty for frontal and temporal regions, no studies have spe-
20, 102118. cifically examined for selective neuropsychological
Rhee, T. K., Park, J. K., Cashen, T. A., Shin, W., Schirf, B. E., Gehl, J. A. deficits. Treatment can include observation, surgical re-
et al. (2006). Comparison of intraarterial MR angiography at 3.0 T section, or stereotactic radiosurgery.
with x-ray digital subtraction angiography for detection of renal
artery stenosis in swine. Journal of Vascular and Interventional
Radiology, 17(7), 11311137. References and Readings
Conway, J. E., & Rigamonti, D. (2006). Cavernous malformations: A

review and current controversies. Neurosurgery Quarterly, 16(1),
1523.
Angioma Sage, M. R., & Blumbergs, P. C. (2001). Cavernous haemangiomas
(angiomas) of the brain. Pathological-Radiological Correlation, 45,
Hemangioma 247256.
170 A Angioplasty
complications are rare, but they include allergy, bleeding,

Angioplasty clotting, stroke, kidney failure, and reblockage of the newly
opened artery. After the procedure, patients usually remain
E LLIOT J. R OTH on bedrest for a short time and are instructed to use anti-
Northwestern University platelet medications. It is estimated that more than one
Chicago, IL, USA million people with heart disease undergo angioplasty
every year in the USA.
Synonyms
Coronary angioplasty; Percutaneous transluminal coro- Cross References

nary angioplasty (PTCA)
Angiography
Atherosclerosis
Cerebrovascular Disease
Definition Coronary Disease
Myocardial Infarction
Angioplasty is a minimally invasive clinical procedure to Peripheral Vascular Disease
dilate blood vessels narrowed or blocked by atherosclerosis. Stent
Current Knowledge References and Readings

Angioplasty is most commonly performed on the coronary American College of Cardiology, American Heart Association, Society
arteries that supply blood to the heart muscle, but it is also for Cardiovascular Angiography and Interventions: ACC/AHA/
performed on carotid arteries, peripheral blood vessels in SCAI 2005 Guideline Update for Percutaneous Coronary Interven-
the limbs, and elsewhere. Angioplasty may be used to treat tion: A Report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines (ACC/
coronary artery disease, which often presents with persis-
AHA/SCAI Writing Committee to Update the 2001 Guidelines for
tent angina (chest pain) or a myocardial infarction (heart Percutaneous Coronary Intervention) (2006). Circulation, 113,
attack), as well as cerebrovascular disease causing stroke or e166e286.
transient ischemic attacks, renal artery stenosis causing
kidney dysfunction, and peripheral artery disease, usually
in the blood vessel of the leg.
In this procedure, a small incision is made over the skin
of a peripheral artery (usually the femoral artery in the Angular Acceleration
thigh), and the artery is punctured to gain access into
the blood vessel. A thin catheter is then inserted into the Rotational Acceleration
blood vessel, and both blood vessels and catheter are visua-
lized by radiographic fluoroscopy. The catheter is then
pushed further into the vessel (guided by fluoroscopic
images). When the tip of the catheter reaches the target
blood vessel, a previously folded balloon at the end of the Angular Gyrus Syndrome
catheter is inflated to flatten the plaque in the vessel wall,
thereby reducing the blockage and expanding the diameter Gerstmanns Syndrome
of the artery. Usually, a stent, a metal mesh tube of small
diameter that was also at the end of the catheter, is then
placed inside the vessel and expanded by manipulating the
catheter tip. The result is a dilated artery and improved
blood flow through the vessel. Anhedonia
This procedure is done to prevent the vessel from be-
coming blocked again. It is a relatively safe procedure, and Apathy
Anomia A 171
Cross References A
Anomalous Dominance
Dominance (Cerebral)
J OHN E. M ENDOZA
New Orleans, LA, USA References and Readings
Geschwind, N., & Galaburda, A. M. (1987). Cerebral lateralization:

Synonyms Biological mechanisms, associations, and pathology. Cambridge, MA:
MIT Press.
Mixed dominance Geschwind, N., & Galaburda, A. (1985). Cerebral lateralization. Archives
of Neurology, 42, 428459; 521552; 634654.
Herron, J. (Ed) (1980). Neuropsychology of left-handedness. New York:
Academic.
Definition
Anomalous dominance describes any pattern of cerebral

organization of function in which the left hemisphere is
not primarily responsible for initiating propositional
speech and processing written or spoken language. Anomia
A NASTASIA R AYMER
Current Knowledge Old Dominion University
Norfolk, VA, USA
Since the left hemisphere primacy for language is typical
of most right-handers (who represent the vast majority of
the population), it is considered to be the dominant Synonyms
pattern of brain organization. Hence, any pattern that
differs from this is considered to be anomalous. Most Naming impairments; Word finding difficulties
deviations occur in left-handers, approximately 30% of
whom exhibit some form of anomalous dominance for
language where these functions are organized either pri- Definition
marily in the right hemisphere (reversed dominance) or
are more bilaterally represented. Although anomalous Anomia generally refers to instances of word finding
dominance can occur in right-handers, this is rare and, difficulty that occur during the course of conversational
when present, is often a consequence of some early devel- discourse. It is often documented clinically in confrontation
opmental defect or brain trauma. Other associations that picture naming tasks.
have been reported to be related to anomalous patterns
of hemispheric organization of language are female gen-
der, mixed hand preference (ambidexterity), and family Current Knowledge
history of sinistrality. In these situations, there is an
increased tendency for language functions to be organized Anomia can occur in healthy individuals who occasionally
in both hemispheres. Support for this hypothesis comes in experience difficulty in thinking of an intended word
part from radiographic studies which show a tendency for during conversation, also known as the tip-of-the-tongue
males when compared with females to have greater ana- state (Biedermann, Ruh, Nickels, & Coltheart, 2008). It is
tomical asymmetry in the region of the frontal operculum a frequent occurrence in individuals with left hemisphere
(Brocas area) and in the temporal operculum (planum brain damage and aphasia (Raymer, 2005). Typically
temporale), both key language areas. This apparent ten- associated with difficulties for nouns, anomia also can
dency for greater bilateral representation of language has affect the ability to retrieve other classes of words, such
been suggested as a possible explanation for (1) the earlier as verbs and adjectives. Word finding requires several
development (on average) of language in females than in steps, including semantic processes in which the speaker
males, and (2) the superior recovery of language functions has an idea or meaning to convey and phonological
following strokes seen in some left-handers. processes in which the speaker selects an appropriate
172 A Anomic Aphasia
word to express that meaning (Raymer & Rothi, 2008). Raymer, A. M., & Rothi, L. J. G. (2008). Cognitive neuropsychological
approaches to assessment and treatment: Impairments of lexical
These different steps in word finding engage different
comprehension and production. In R. Chapey (Ed.), Language in-
parts of the brain distributed throughout the left cere- tervention strategies in adult aphasia (5th ed., pp. 607631).
bral hemisphere. Therefore, when brain damage occurs, Baltimore: Lippincott, Williams & Wilkins.
anomia will accompany different types of aphasia, and
different types of anomic errors can arise. It is important
to note that anomia and anomic aphasia are not synony-
mous. Anomia is the primary symptom of anomic aphasia
Anomic Aphasia
and also can be observed in virtually all other forms of
A NASTASIA R AYMER
aphasia (e.g., Brocas aphasia, Wernickes aphasia), both as
Old Dominion University
initial and residual signs when other signs and symptoms
Norfolk, VA, USA
of aphasia have resolved.
When anomia occurs, a number of errors can be seen
(Goodglass, Kaplan, & Barresi, 2001). At times, the
moment of anomia leads to complete inability to retrieve
Definition
a word. Other times, an inappropriate word is retrieved,
Anomic aphasia is the language impairment that involves
also known as a paraphasia. Sometimes, the error word
only word finding difficulties or pure anomia in contrast
is somehow related to the intended word in meaning
to other forms of aphasia (Goodglass et al., 2001). Other
(semantic paraphasia, e.g., saying dog for cat) or sound
language modalities typically are intact, including auditory
characteristics (phonologic paraphasia, e.g., saying
comprehension of language, repetition of words and
crat for cat). Sometimes, the moment of word finding
sentences, and spontaneous generation of sentences.
difficulty is filled with a description of the intended word
or circumlocution (e.g., That thing that meows and has
whiskers. I cant think of the name.). In severe forms of Current Knowledge
anomia, neologisms may occur in which the uttered word
may not be recognizable at all (e.g., saying bilan for cat). Anomic aphasia is a form of language disorder associated
with acquired brain damage typically affecting the left
cerebral hemisphere (Raymer, 2005). Anomic aphasia
Cross References can be manifest as a difficulty in retrieving specific
intended words, often nouns, but sometimes verbs,
Circumlocution during the course of sentence generation. The grammati-
Confrontation Naming cal characteristics of the sentence remain intact. The
Paraphasia moments of word retrieval difficulty lead to long pauses,
Phonemic Paraphasia insertion of filler words, or selection of wrong words
Semantic Paraphasia (paraphasias) during conversation or other word retrieval
Word Finding activities, most commonly in tasks requiring individuals
to name pictures. Also common in anomic aphasia is
circumlocution, in which the speaker cannot think of
References and Readings the intended word and instead describes or provides
associated information about the word.
Biedermann, B., Ruh, N., Nickels, L., & Coltheart, M. (2008). Information When anomic aphasia occurs as a result of an acute
retrieval in tip of the tongue states: New data and methodological neurologic event (e.g., stroke), it can be accompanied by
advances. Journal of Psycholinguistic Research, 37, 171198.
pure alexia and difficulties with color identification
Goodglass, H., Kaplan, E., & Barresi, B. (2001). The assessment of aphasia
and related disorders (3rd ed.). Philadelphia: Lippincott, Williams, &
(Goodglass et al., 2001). Acutely, anomic aphasia has
Wilkins. been described following left temporal/occipital lesions
Goodglass, H., & Wingfield, A. (Eds.) (1997). Anomia: Neuroanatomical (e.g., area 37) and left thalamic lesions (Raymer, Moberg,
and cognitive correlates. San Diego: Academic Press. Crosson, Nadeau, & Rothi, 1997; Raymer, Foundas et al.,
Laine, M., & Martin, N. (2006). Anomia: Theoretical and clinical aspects.
1997). Anomic aphasia also can be seen chronically as
New York: Psychology Press.
Raymer, A. M. (2005). Naming and word retrieval problems. In
individuals recover from other forms of aphasia. In that
L.L. LaPointe (Ed.), Aphasia and related neurogenic language case, the accompanying symptoms and neural correlates
disorders (3rd ed., pp. 7286). New York: Thieme. of anomic aphasia vary.
Anosmia A 173
Cross References ability to perceive odors. Hyposmia is a more precise term

A
to describe decreased ability to perceive smells, whereas
Anomia hyperosmia is the increased ability to perceive odors.
Circumlocution Dysosmia (a.k.a. parosmia) refers to distortions in the
Confrontation Naming sense of smell, including cacosmia (distortion of a smell
Paraphasia as particularly unpleasant) and phantosmia (an olfactory
Phonemic Paraphasia hallucination, or the sensation of a smell in the absence
Semantic Paraphasia of a stimulus).
Word Finding
Epidemiology
Olfactory dysfunction is present in at least 1% of indivi-
Goodglass, H., Kaplan, E., & Barresi, B. (2001). The assessment of duals under the age of 65, with some estimates suggesting
aphasia and related disorders (3rd ed.). Philadelphia: Lippincott, total anosmia in as much as 5% of the population. Rates
Williams, & Wilkins. of impairment increase dramatically with age, with
Goodglass, H. & Wingfield, A. (Eds.) (1997). Anomia: Neuroanatomical
approximately 25% of older adults showing deficits in
and cognitive correlates. San Diego: Academic Press.
Laine, M. & Martin, N. (2006). Anomia: Theoretical and clinical aspects. olfaction (Murphy et al., 2002). In patients presenting to
New York: Psychology Press. chemosensory clinics, olfactory deficits are reported to be
Raymer, A. M. (2005). Naming and word retrieval problems. In related to disability and quality of life, though most
L. L. LaPointe (Ed.), Aphasia and related neurogenic language individuals with olfactory deficits are unaware of them.
disorders (3rd ed., pp. 7286). New York: Thieme.
It is well established that throughout the lifespan, women
Raymer, A. M., Foundas, A., Maher, L., Greenwald, M., Morris, M.,
Rothi, L. J. G. et al. (1997). Cognitive neuropsychological analysis show more acute olfactory abilities than men.
and neuroanatomic correlates in a case of acute anomia. Brain and
Language, 58, 137156.
Raymer, A. M., Moberg, P., Crosson, B., Nadeau, S., & Rothi, L. J. G. Causes
(1997). Lexical-semantic deficits in two patients with dominant
thalamic infarction. Neuropsychologia, 35, 211219.
The causes of olfactory impairments are typically
categorized as: (1) conductive/transport impairments,
(2) sensory/sensorineural deficits, or (3) central olfactory
neural impairment, though these categories are not
Anosmia mutually exclusive. The understanding of the potential
causes of olfactory deficits will be enhanced by a brief
H OLLY J AMES W ESTERVELT, N ICOLE C. R. M C L AUGHLIN review of the olfactory system, though it is noted that the
Alpert Medical School of Brown University olfactory pathways within the central nervous system
Providence, RI, USA (CNS) are not entirely agreed upon.
Synonyms Anatomy of the Olfactory System
Anosphrasia The sensation of smell is the brains perception of odor in

response to odorants activating olfactory receptors. Odors
enter the nose, where they come in contact with the
Short Description or Definition olfactory epithelium, made up of olfactory receptors.
Olfactory receptor cells (first order neurons) send signals
Anosmia is defined as a lack of the sense of smell or an along the olfactory nerve (first cranial nerve) to the mitral
inability to detect odors of any kind. In the strictest sense, cells of the olfactory bulb, where olfactory axons synapse
anosmia refers to a total lack of olfactory ability, though with second-order neurons in the olfactory bulb. Each
the term is often used more loosely to refer also to partial olfactory receptor type sends a signal to a particular
or diminished sense of smell. There are multiple additional region of the olfactory bulb. Mitral cell axons project
terms describing olfactory abilities. Normosmia is the intact through the olfactory tract and lateral olfactory stria to
174 A Anosmia
the primary olfactory cortex, which is primarily made up Anosmia. Table 1 Sampling of disorders associated with
of the piriform cortex. Other structures receiving direct olfactory deficits
input include the anterior olfactory nucleus, olfactory
Alcoholism/Korsakoffs
tubercle, amygdala, and rostral entorhinal cortex
syndrome Multiple sclerosis
(Gotfried & Zald, 2005). Projections from these primary
areas extend to secondary olfactory regions in the hippo- Alzheimers disease Multiple system atrophy
campus, hypothalamus, thalamus, amygdala, and agranular Amyotrophic lateral Parkinson dementia complex
insula, enabling encoding of odors into memory as well sclerosis of Guam
as emotional processing of specific odors (Gotfried & Corticobasal degeneration Parkinsons disease
Zald, 2005). There are also projections to the orbitofrontal Dementia with Lewy Progressive supranuclear
cortex (OFC), and it is believed that the OFC mediates bodies palsy
conscious perception of odors; lesions to this area often Diabetes mellitus REM sleep behavior disorder
lead to impaired olfactory abilities (Gotfried & Zald, Downs syndrome Restless leg syndrome
2005). In addition to the activation of the first cranial Frontotemporal dementia Schizophrenia
nerve, certain smells may also activate the trigeminal
Head injury Sjogrens syndrome
nerve (CNV), which mediates sensations associated with
certain odorants, including burning, cooling, irritation, Human immunodeficiency Syphilis
virus
or tickling sensations. Activation of the trigeminal nerve
may allow the detection of some odors, even in the Huntingtons disease Temporal lobe epilepsy
presence of primary olfactory impairments. Cranial Mild cognitive impairment Vascular dementia
nerve zero (nervus terminalis) may also play some role
in olfaction, though its function is poorly understood
in humans. loss. Given the vast number of disorders that have
shown olfactory deficits, theories have been postulated
Conductive/Transport Impairment that olfactory impairment may be a nonspecific marker
Olfactory impairment within this category arises from of CNS dysfunction. This is likely not the case, given
obstruction of nasal passages. Typical causes of obstruc- that the degree of deficit can differ widely among
tion include nasal inflammation, such as from allergies or disorders, there exists significant range of deficits
upper respiratory infection (URI), or other structural among patients within disorders, and the deficits can
interference, such as nasal polyps. URI is the most be unrelated to disease stage or magnitude of disease
common cause of smell loss, and is often transient. symptoms in some diseases but not others. Rather, it is
Permanent smell loss due to URI can occur, presumably probable that the presence and degree of olfactory
reflecting direct insult to the neuroepithelium, and involvement is related to the relative degree of structural
becomes more likely in older age. or biochemical damage to the specific regions of the
brain involved in olfactory transduction.
Sensorineural/Central Olfactory Neural
Impairment Neurodegenerative Diseases
Olfactory deficits within these categories arise from Interest in olfaction in neurodegenerative disorders began
damage to the neuroepithelium and/or impairment or most intensely in the 1980s, with a focus on Alzheimers
impingement of central olfactory structures from CNS disease (AD) and Parkinsons disease (PD). It was initially
disease. There are numerous congenital, endocrine, thought that these two disorders, which were often
neurological/neurodegenerative, nutritional/metabolic, thought of as the prototypical examples of cortical and
and psychiatric disorders that have been shown to be subcortical diseases, would share an early and notable
associated with olfactory deficits (for a review of these deficit. Olfactory deficits were then identified in a variety
causes, see Murphy, Doty, & Duncan, 2003). In addition, of neurodegenerative disorders, making olfactory loss a
injury, medications (for review see Doty & Bromley, nonspecific finding, though the degree of impairment
2004), environmental toxins (for review see Upadhyay & may be useful in distinguishing some disorders.
Holbrook, 2004), structural lesions, and medical/surgical The cause of olfactory deficits in neurodegenerative
interventions (for review see Murphy et al., 2003) can diseases is unknown (for a review of potential causes, see
affect neural functioning. The Table 1 provides a small Smutzer, Doty, Arnold, & Trojanowski, 2003). The deficits
sampling of disorders that can be associated with olfactory may be due at least in part to neurotransmitter system
Anosmia A 175
alterations, especially dopamine and acetylcholine. disease progression. Although group studies have shown
A
Damage to central processing areas is also a likely expla- consistent deficits in odor identification, it should be
nation, particularly involvement of the olfactory bulb and noted that the presence of deficits is not a universal
tracts, as relevant neuropathologic changes (e.g., neurofi- finding among patients with AD, making odor identifica-
brillary tangles, amyloid plaques, dystrophic neurites, tion tests imperfect screening instruments for the disorder.
Lewy bodies, and disproportionate neuronal loss) are Odor identification has also been studied recently in
often seen in these areas. Other relevant central proces- patients with mild cognitive impairment (MCI) and
sing areas (e.g., entorhinal cortex), however, also show cognitively intact older adults with and without genetic
neuropathologic changes, as may peripheral structures risk for future cognitive decline. Several longitudinal
(e.g., olfactory epithelium). studies have demonstrated that odor identification has a
strong relationship with memory performance, even in
Parkinsons Disease Olfactory impairment is a promi- healthy older adults performing within normal limits on
nent, common, and early feature of Parkinsons disease cognitive measures (Devanand et al., 2000; Wilson et al.,
(PD; see Doty, 2003a, b, for a review). The deficits tend to 2007). These studies also show that odor identification is a
be bilateral, and are more common than some of the unique and significant predictor of future cognitive
hallmark symptoms of PD, such as tremor. Olfactory decline above and beyond baseline memory performance,
deficits may be present before the motor symptoms as well as a good predictor of conversion to dementia in
become evident, and are apparent with both threshold patients with MCI. In cross-sectional studies of MCI
and identification tasks. The size of the effect is astoun- subtypes, patients with both amnestic and non-amnestic
ding (ranging from 1.17 to 12.15 in a meta-analysis; subtypes perform modestly worse than healthy older
Mesholam, Moberg, Mahr, & Doty, 1998), though the adults but better than patients with dementia (Devanand
majority of patients are not completely anosmic. Deficits et al., in press; Westervelt, Bruce, Coon, & Tremont,
do not appear to correlate with the extent of cognitive or 2008). In using olfactory performance to distinguish
motor involvement, do not respond to treatment, and do MCI subtypes, results are mixed, though when significant
not appear to be progressive over time. differences have been found between subtypes, the
magnitude of the difference is of questionable clinical
Other Parkinsonian Spectrum Disorders Other Parkinso- significance. Together, these studies suggest that when a
nian disorders, such as corticobasal degeneration (CBD), notable olfactory deficit is observed in patients with MCI,
multiple system atrophy, and progressive supranuclear there is substantial risk of future decline. However, odor
palsy, are also associated with olfactory deficits, though identification measures may not be particularly clinically
the impairments tend to be more mild than is seen in useful in early detection or early differential diagnosis for
PD (Doty, 2003a, b). These findings suggest that olfactory the modal patient.
functioning may be useful in distinguishing PD from
other parkinsonian disorders, though a more recent Dementia with Lewy Bodies Olfaction in dementia with
study of olfaction in CBD raises some question of Lewy bodies (DLB) was first described in a study that
potentially more notable deficit in this disorder than crudely measured anosmia with a brief detection task
was previously described (Pardini, Huey, Cavanagh, & (McShane et al., 2001). Forty percent of patients with
Grafman, 2009). DLB were found to be anosmic, in contrast with 16%
of patients with AD, and 6% of the healthy controls.
Alzheimers Disease and Mild Cognitive The presence of smell loss was not found to be associated
Impairment There has been fairly good consistency in with concurrent AD and DLB pathology on autopsy.
the literature for most of the studies examining olfaction Subsequent studies confirmed anosmia to be more
in Alzheimers disease (AD; see Doty, 2003a, b, for a common in DLB than in AD, with anosmia present in
review). The size of the effect is extremely large, ranging 5665% of patients with DLB (and some degree of smell
from 0.98 to 8.55 in a meta-analysis (Mesholam et al., loss in nearly 90%), but in only 1123% of AD patients
1998), though, as in PD, patients are typically not (Olichney et al., 2005; Westervelt, Stern, & Tremont,
completely anosmic. Odor identification deficits are al- 2003). Assessment of anosmia has been shown to improve
ways found; odor detection deficits are more inconsis- the sensitivity of diagnostic criteria for DLB, with mini-
tently demonstrated and may be a later symptom. The mal loss of specificity (Olichney et al., 2005). Combined,
odor identification deficit does not seem to be primarily these few studies raise the possibility that olfactory
due to a general cognitive deficit and deficits worsen with measures may be useful in distinguishing AD from DLB.
176 A Anosmia
Other Dementias Olfactory deficits have also been occurrence of any event associated with the deficit (e.g.,
described in other dementias, including recent, consistent head injury, illness). Fluctuations in symptoms may be
findings of smell deficits in frontotemporal dementia that most suggestive of obstructive causes, but need to be
are generally of the magnitude of deficits seen in AD distinguished from paroxysmal events. Medical history
(Luzzi et al., 2007; McLaughlin & Westervelt, 2008; should be carefully assessed, as multiple medical condi-
Pardini et al., 2009), and, in vascular dementia to a similar tions and medications may be associated with olfactory
or lesser extent to that seen in AD (Gray, Staples, Murren, alterations. Referral for an ENT evaluation may be war-
Dhariwal, & Bentham, 2001; Knupfer & Spiegel, 1986). ranted. Olfactory hallucinations, in particular, require
careful work-up as they may be indicative of seizure or
Head Injury tumor, and are less likely of primary psychiatric origin.
Olfactory loss is fairly common following head injury (for
review, see Costanza, DiNardo, & Reiter, 2003), with the
Classes of Assessment
incidence of anosmia ranging from approximately 5 to 60%.
These latter estimates represent the incidence among
There are three classes of olfactory assessment methods:
patients with severe head injury, though total anosmia
psychophysical, electrophysiological, and psychophysio-
can occur even after very mild injury. Partial or unilateral
logical, with psychophysical assessment being the most
loss may be less likely to be detected than total anosmia.
common and most clinically relevant.
Deficits may be caused by a variety of mechanisms, includ-
ing sinus/nasal injury, shearing of the olfactory nerve, or Psychophysiological
contusion/hemorrhage in central processing regions. In Psychophysiological assessment of olfactory abilities relies
regard to shear injuries, the axons of the olfactory receptor on the measurement of changes in the autonomic nervous
cells are particularly susceptible to injury as they pass system after presentation of an odorous stimuli, through
through the body ridges of the cribiform plate. Coup and such methods as heart rate and blood pressure. These
contra-coup forces are likely to result in anosmia, with methods are rarely used.
occipital blows most frequently causing smell loss.
Electrophysiological
Schizophrenia Electrophysiological assessments examine electrical
Olfactory deficits have been well-studied in schizophrenia activity generated in response to an odorant and are
(for review, see Doty, 2003a, b). Deficits have been shown primarily research tools. Electro-olfactograms (EOG)
to be of lesser magnitude than typically seen in AD and use electrodes placed on the human olfactory epithelium
PD, progress with disease duration, and are most asso- to directly assess olfactory abilities. Olfactory event-
ciated with negative symptoms of the disease. In patients related potentials (ERP) are recorded from the scalp
showing olfactory deficits, the impairments appear early surface, measuring electroencephalographic activity after
in the disease, perhaps in prodromal stages. There does presentation of brief, precisely defined odorous stimuli.
not appear to be any notable relationship with antipsy- For example, chemosensory ERPs can be obtained after
chotic medication use or cigarette smoking. Odor identi- stimulation of olfactory nerve (olfactory ERPs) or the
fication deficits correlate most strongly with measures of trigeminal nerve (somatosensory ERPs). Absence of
executive functioning in this population, rather than olfactory ERPs in presence of somatosensory ERPs
those of medial temporal lobe functioning. All aspects of suggests olfactory deficits. These measures are sensitive
olfaction appear to be impaired (i.e., identification, to age and gender effects. Chemosensory evoked poten-
threshold, discrimination, and memory). tials are unable to discern where the impairment is within
the olfactory pathway, but are considered among the only
objective ways of establishing smell loss.
Evaluation
Psychophysical
Clinical History Psychophysical methods are the most commonly used
assessment practices in both clinical and research settings.
Obtaining a detailed clinical history is critical in assessing In these techniques, stimuli are presented, and the patient or
olfactory deficits. Symptoms should be clearly defined, participant reports their perception (detection, discri-
and the clinician should attempt to determine the extent mination, identification); this category can be further
and duration of the perceived loss, as well as the sub-divided into threshold and suprathreshold tasks.
Anosmia A 177
Threshold Testing Odor Memory Test Odor memory test involve having the
A
Threshold testing is used to determine at what concen- individual smell an odor (or group of odors), and after a
tration a patient or participant can accurately detect the specified period of time, recognize the odor from a set of
presence of an odor. Two methods have been developed to distracters. Often, novel, non-descript odors are utilized
determine this threshold: the method of limits procedure to minimize the ability to label, and interference tasks are
and the single staircase procedure. In the method of limits introduced during delays to minimize rehearsal of the
procedure, a low concentration of a specific odor is odor labels/qualifiers.
presented, and the concentration is increased until it can
be detected. In the single staircase procedure, the concen-
tration is increased following trials in which the partici- Other Olfactory Assessment Tools
pant cannot detect the odor, and decreased following
correct detection. There are commercially available smell The Sniff Magnitude Test
threshold tests, for example, using felt-tipped pens and The sniff magnitude test is a recently developed clinical
squeeze bottles. Olfactometers can be used to present measure of olfaction based on the reflex-like reduction in
precise amounts of odorants through constant airflow. sniffing that occurs in response to detection of odors
However, many of these techniques can be cumbersome (especially unpleasant odors), but does not occur when
for clinical use. sniffing non-odorized air (Frank, Dulay, & Gestland,
2003). This response is observed in people with normal
Suprathreshold Tasks sense of smell, but is absent in those with anosmia. The
Suprathreshold tasks include rating scales/magnitude task involves having the patient sniff a canister that
estimation scales, odor identification tasks, and odor releases either a blank or an odor, while wearing a nasal
memory/recognition tasks. When using rating scales, the cannula connected to a device to measure the negative
participant rates the amount of the attribute perceived pressure created by the sniff. The test is quick to administer
(e.g., pleasantness); these may include category scales (about 5 min) and has minimal, if any, reliance on
(which category describes sensation) and line scales cognition, linguistic ability, and familiarity of odors.
(placement of mark on line with descriptors). When
using a magnitude estimation scales, a participant will Neuroimaging
assign a number to stimuli in relation to relative intensity. Imaging, particularly MRI, is clearly important for
identification of structural lesions that may be impinging
Odor Identification Tasks Odor identification tasks also on the olfactory system, or in assisting in diagnosis of
suprathreshold tasks, require participants to identify other neurologic disorders that may account for smell
odors, often by presenting scratch-and-sniff items, loss. CT is frequently used in identifying sinonasal disease.
tinctures in jars, or odorant-soaked tampons. These tasks MRI can also be useful in evaluating changes in olfactory
almost invariably include multiple choice options, as odor bulb volume due to viral, traumatic, or idiopathic olfac-
identification is otherwise extremely challenging even for tory dysfunction, with good relationship demonstrated
individuals with intact olfactory abilities. These tasks are between objective olfactometry (with chemosensory
easy to administer and the most frequent type of task used evoked potentials) and bulb volume. Functional scans,
in clinical settings, but can be somewhat costly depending in particular fMRI and PET, are also often used as research
on the task. The most widely used odor identification task tools in studying the functional organization of olfaction.
is the University of Pennsylvania Smell Identification These studies have shown involvement in the amygdala,
Task (UPSIT), which consists 40 micro-encapsulated piriform cortex, OFC, insula, anterior cingulate,
odorants presented in a 4-option, multiple choice format. thalamus, caudate, subiculum, upper pons, and cerebellar
Other, briefer measures include 12-item versions vermis, with different activation patterns depending on
(e.g., Cross-Cultural Smell Identification Test/Brief Smell the nature of the task (e.g., sniffing, smelling single odors,
Identification Test (BSIT), the BSIT-A designed especially discrimination, identification, etc.).
for AD, the BSIT-B designed especially for PD) and a
3-item screen (Pocket Smell Test). The UPSIT and BSIT
both have associated norms. Sniffin Sticks includes both a Treatment
threshold task and an odor identification task, and is
extensively normed in European samples (Hummell, Treatment is most promising in patients with smell loss
Kobal, Gudziol, & Mackay-Sim, 2007). associated with conduction problems. For example,
178 A Anosmia
antibiotic treatment, steroids, and allergy management Doty, R. L. (Ed.). (2003b). Handbook of olfaction and gustation (2nd ed.).
New York: Marcel Dekker.
may be helpful in reducing deficits associated with
Doty, R. L., & Bromley, S. M. (2004). Effects of drugs on olfaction and
inflammatory disease. Surgical removal of other obstruc- taste. Otolaryngologic Clinics of North America, 37, 12291254.
tions, such as nasal polyps, can also be effective in Frank, R. A., Dulay, M. F., & Gestland, R. C. (2003). Assessment of
restoring olfactory ability. In contrast, treatment of the Sniff Magnitude Test as a clinical test of olfactory function.
sensorineural/central neural problems is often less Physiology & Behavior, 78, 195204.
Gotfried, J. A., & Zald, D. H. (2005). On the scent of human olfactory
effective. Exceptions may include resection of tumors
orbitofrontal cortex: Meta-analysis and comparison to non-human
impinging on the olfactory system and, in some cases, primates. Brain Research Brain Research Review, 50, 287304.
resection of epileptogenic foci associated with olfactory Gray, A. J., Staples, V., Murren, K., Dhariwal, A., & Bentham, P. (2001).
seizures. Iatrogenic effects of medications are typically Olfactory identification is impaired in clinic-based patients
reversible with discontinuation of the medication and with vascular dementia and senile dementia of the Alzheimer type.
International Journal of Geriatric Psychiatry, 16, 513517.
eventual improvement in smell is expected after cessation
Hummell, T., Kobal, G., Gudziol, H., & Mackay-Sim, A. (2007).
of smoking. Recent work also suggests that olfactory Normative data for the sniffinsticks including tests of odor
training may improve olfaction in some patients identification, odor discrimination, and olfactory thresholds: an
(Hummel et al., 2009). Zinc or vitamin therapies are at upgrade based on a group of more than 3000 subjects. European
times prescribed to treat olfactory loss, but there is little Archives of Otorhinolaryngology, 264, 237243.
Hummel, T., Rissom, K., Reden, J., Hahner, A., Weidenbecher, M., &
evidence of benefit in the absence of associated defici-
Huttenbrink, K. B. (2009). Effects of olfactory training in patients
encies. Typically, the more severe and long-standing the with olfactory loss. Laryngoscope, 119, 496499.
smell loss, the less likely recovery is in sensorineural/ Knupfer, L., & Spiegel, R. (1986). Differences in olfactory test
central neural disorders. Especially for individuals performance between normal aged, Alzheimer and vascular type
who do not respond to treatment, education about the dementia individuals. International Journal of Geriatric Psychiatry,
1, 314.
safety implications of smell loss is important, given
Luzzi, S., Snowden, J. S., Neary, D., Coccia, M., Provinciali, L., & Lambon
concerns of the patients failure to detect hazardous Ralph, M. A. (2007). Distinct patterns of olfactory impairment in
odors (e.g., smoke) or spoiled food. Nutritional status Alzheimers disease, semantic dementia, frontotemporal dementia,
may also be compromised in patients with olfactory and corticobasal degeneration. Neuropsychologia, 45, 18231831.
deficits, and use of flavor enhancements in foods can be McLaughlin, N., & Westervelt, H. J. (2008). Odor identification deficits in
frontotemporal dementia: A preliminary study. Archives of Clinical
helpful in improving food intake (Schiffman, 2000).
Neuropsychology, 23, 119123.
McShane, R. H., Nagy, Z., Esiri, M. M., King, E., Joachim, C., Sullivan, N.,
et al. (2001). Anosmia in dementia is associated with Lewy
Cross References bodies rather than Alzheimers pathology. Journal of Neurology,
Neurosurgery, and Psychiatry, 70, 739743.
Mesholam, R. I., Moberg, P. H., Mahr, R. N., & Doty, R. L. (1998).
Cranial Nerves
Olfaction in neurodegenerative disease. A meta-analysis of olfactory
Olfaction functioning in Alzheimers and Parkinsons diseases. Archives of
Olfactory Bulb Neurology, 55, 8490.
Olfactory Tract Murphy, C., Doty, R. L., & Duncan, H. J. (2003). Clinical disorders of
olfaction. In R. L. Doty (Ed.), Handbook of olfaction and gustation
(2nd ed.). New York: Marcel Dekker.
Murphy, C., Schubert, C. R., Cruickshanks, K. J., Klein, B. E., Klein, R., &
References and Readings Nondahl, D. M. (2002). Prevalence of olfactory impairment in
older adults. Journal of the American Medical Association, 288,
Costanza, R. M., DiNardo, L. J., & Reiter, E. R. (2003). Head injury and 23072312.
olfaction. In R. L. Doty (Ed.), Handbook of olfaction and gustation Olichney, J. M., Murphy, C., Hofstetter, C. R., Foster, K., Hansen, L. A.,
(2nd ed.). New York: Marcel Dekker. Thal, L. J., et al. (2005). Anosmia is very common in the Lewy body
Devanand, D. P., Michaels-Marston, K. S., Liu, X., Pelton, G. H., variant of Alzheimers disease. Journal of Neurology, Neurosurgery,
Padilla, M., Marder, K., et al. (2000). Olfactory deficits in patients and Psychiatry, 76, 13421347.
with mild cognitive impairment predict Alzheimers disease at Pardini, M., Huey, E. D., Cavanagh, A. L., & Grafman, J. (2009). Olfactory
follow-up. American Journal of Psychiatry, 157, 13441405. function in corticobasal syndrome and frontotemporal dementia.
Devanand, D. P., Tabert, M. H., Cuasay, K., Manly, J. J., Schupf, N., Archives of Neurology, 66, 9296.
Brickman, A. M., et al. (in press). Olfactory identification deficits Schiffman, S. S. (2000). Intensification of sensory properties of food for
and MCI in a multi-ethnic elderly community sample. Neurobiology the elderly. Journal of Nutrition, 130, 92759305.
of Aging. Smutzer, G. S., Doty, R. L., Arnold, S. E., & Trojanowski, J. Q. (2003).
Doty, R. L. (2003a). Odor perception in neurodegenerative diseases. In Olfactory system neuropathology in Alzheimers disease Parkinsons
R. L. Doty (Ed.), Handbook of olfaction and gustation (2nd ed.). disease, and schizophrenia. In R. L. Doty (Ed.), Handbook of
New York: Marcel Dekker. olfaction and gustation (2nd ed.). New York: Marcel Dekker.
Anosognosia A 179
Upadhyay, U. D., & Holbrook, E. H. (2004). Olfactory loss as a result of day to the next. The more common hypotheses are that
toxic exposure. Otolaryngologic Clinics of North America, 37, A
the anosodiaphoria likely reflects the same type of neglect
11851207.
Westervelt, H. J., Bruce, J. M., Coon, W. G., & Tremont, G. (2008). Odor
or inattention that results in the original anosognosia,
identification in mild cognitive impairment subtypes. Journal of only less severe, is a result of a general emotional flatten-
Clinical and Experimental Neuropsychology, 30, 151156. ing or indifference that can follow right hemispheric
Westervelt, H. J., Stern, R. A., & Tremont, G. (2003). Odor identification lesions, or a combination of the two. (Heilman, Blonder,
deficits in diffuse Lewy body disease. Cognitive and Behavioral
Bowers, & Valenstein, 2003).
Wilson, R. S., Schneider, J. A., Arnold, S. E., Tang, Y., Boyle, P. A., &
Bennett, D. A. (2007). Olfactory identification and incidence of mild
cognitive impairment in older age. Archives of General Psychiatry, Cross References
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Anosognosia
Denial (of Illness)
Anosodiaphoria
J OHN E. M ENDOZA
Tulane University Medical Center Adair, J. C., Schwartz, R. L., & Barrett, A. M. (2003). Anosognosia. In
K. Heilman & E. Valenstein (Eds.), Clinical neuropsychology (4th ed.,
Critchley, M. (1969). The parietal lobes. New York: Hafner.
Heilman, K. M., Blonder, L. X., Bowers, D., & Valenstein, E. (2003).
Definition Emotional disorders associated with neurological diseases. In K. M.
Heilman & E. Valenstein (Eds.), Clinical neuropsychology (4th ed.,
Anosodiaphoria is defined as the failure to fully appreciate
Prigatano, G. P., & Schacter, D. L. (Eds.), (1991). Awareness of deficit after
the significance of a neurological deficit as a result of a brain injury. New York: Oxford.
brain lesion.
Current Knowledge Anosognosia

Following certain injuries to the brain, most commonly
K ENNETH M. H EILMAN
strokes in the right hemisphere, a patient may fail to
University of Florida College of Medicine and the Malcom
recognize (deny) the resulting neurological deficit(s),
Randall Veterans Affairs Medical Center
such as paralysis. This latter condition is known as ano-
Gainesville, FL, USA
sognosia. With time, patients typically show increased
awareness of the deficit. For example, if asked, they
might acknowledge that a stroke has occurred and that
Synonyms
their ability to use their arm or leg has been affected.
However, the patient might fail to fully appreciate the
Self-awareness
extent or functional implications of the deficit, attribute
it to another more benign factor (such as being right-
handed), or otherwise appear relatively unconcerned Definition
about it. This latter condition has been termed anosodia-
phoria (Adair, Schwartz, & Barrett, 2003; Critchley, 1969). Anosognosia is a disorder characterized by denial of ill-
Thus, while acknowledging that his arm and/or leg are/is ness or lack of awareness of disability.
weak, a patient may talk about his plans to return to
work in the near future, although that may be totally
unrealistic, given the severity of his condition and the Historical Background
nature of his work. There does not appear to be any
clear consensus as to the etiology of this condition, the In the clinic, it is very common to see patients who suffer
level of denial of which might be seen to vary from one with a neurological disease, such as stroke, but who
180 A Anosognosia
appear to deny illness or be unaware of their disabilities. body (hemiparesis). Many of these patients will be un-
Seneca, the Stoic philosopher noted this about 2,000 aware of their weakness and when asked about the pres-
years ago, but the first modern description of a patient ence of weakness, they will deny this disability. Several,
with unawareness-denial was by von Monakow (1885). not mutually exclusive, mechanisms have been used to
Although there were other investigators who wrote about explain this phenomenon.
this striking disorder, it was Babinski (1914), who coined Psychological denial. Weinstein and Kahn (1955) who
the term anosognosia. This word comes from three roots: brought modern attention to this syndrome, posited
a = without, noso = disease, gnosis = knowledge. In that for many people having a stroke with weakness was
addition to describing patients who were unaware of a psychologically traumatic event, and the means by
their illness or disability, Babinski described other patients which some people deal with this trauma is to use
who appeared to be aware but remained unconcerned. He psychological denial. To test this hypothesis, Weinstein
called this disorder, anosodiaphoria. and Kahn studied patients who had anosognosia and
There are many forms of anosognosia and these found that even before their stroke these patients
forms are related to the nature of a patients disability. frequently used this denial defense mechanism.
When Babinski first used this term, the patients he Some investigators have noted that anosognosia for
described denied or were unaware of their hemiparesis. hemiplegia is more often associated with a left than right
Anton (1898) described patients who were unable to see hemiparesis. The psychological denial theory of anosog-
because they had destroyed their primary visual cortex, nosia cannot explain this asymmetry. Many patients with
but were unaware or denied their blindness. Patients left hemisphere injury, however, are aphasic and have
with Korsakoff s amnesic disorder are unaware of their problems with both the comprehension of questions
memory loss and aphasic patients such as those with (What is wrong with you? Are you weak?) as well as
Wernickes aphasia appear to be unaware of their jargon speakinganswering questions. Thus, Weinstein and
speech. Kahn thought what appeared to be a hemispheric asym-
metry was induced by a sampling bias.
Using selective hemispheric anesthesia (the Wada
Current Knowledge study) and questioning the patient after they recover
from anesthesia revealed that unawareness of the hemi-
Although of great academic interest, the presence of ano- plegia (anosognosia) was more common with the right
sognosia or anosodiaphoria has important medical impli- than left hemisphere anesthesia (Gilmore et al., 1992).
cations. For example, there are now treatments for stroke After the selective hemispheric anesthesia has worn off
that must be given within hours of the onset of symptoms. there is no aphasia or a need for psychological denial. The
The patients who are unaware of their disabilities or rightleft hemisphere asymmetries found were within
undervalue their importance might not seek immediate subjects, and thus premorbid personality can also not
medial attention. In addition, people who have disabilities account for this asymmetry. Although this study suggests
but are not aware of these disabilities might inadvertently that denial cannot entirely explain anosognosia for hemi-
injure themselves and/or others. Rehabilitation works plegia, denial might be used by many people to help deal
best, when patients are strongly motivated to get well. with diseases and disabilities.
When a person is either unconcerned or unaware of Failure of feedback. To know something is impaired, a
their disabilities, they are not motivated and unmotivated person requires feedback. Many investigators have sug-
patients are less likely to benefit from these treatments. gested that it is a failure of feedback, induced by either
They might even refuse to undergo rehabilitation and sensory loss (e.g., proprioception and hemianopia) or
they might not take their medications that can reduce inattention neglect, spatial or personal, that accounts for
their disability or possibly prevent further possible anosognosia of hemiplegia. That inattention neglect is
brain damage. more commonly associated with right hemisphere injury
might also account for the asymmetries of anosognosia.
Studies from our laboratory have revealed when
Possible Mechanisms of Anosognosia for undergoing selective right hemisphere anesthesia, during
Hemiplegia the time these patients demonstrate shoulder weakness
their shoulder proprioception is intact. To learn if this
Patients with hemispheric strokes often develop an inabil- disorder could be related to neglect, spatial or personal,
ity to use the arm-hand on the contralesional side of their we brought their hemiplegic left forelimb over to the right
Anosognosia A 181
side of their body and to their right visual field. To make Phantom movements. Limb amputation is often associated
A
certain subjects see their hand, we wrote a number on with a perception that the limb is still present and this
their hand and subjects were able to read these numbers. perception is thought to be related to the continued
Despite these strategies many, but not all, patients still presence of a brain representation of that missing phan-
denied weakness of that hand. Thus, a failure of feedback tom limb. When patients with a hemiparesis are asked to
can only explain anosognosia in some patients. In support move a limb, many often perceive that the paretic limb is
of this postulate, several investigators have reported dis- moving, and this phantom movement in combination
sociations between the presence of spatial neglect and with impaired feedback might account for anosognosia.
anosognosia. During selective hemispheric anesthesia (Wada test), we
Asomatognosia hypothesis. While patients with personal had blindfolded subjects with left hemiplegia attempt to
neglect might be unaware of the parts of their body, raise their paretic left arm and we then asked them to raise
patients with asomatognosia do not feel or claim that their right (non-paretic) arm to the same level as they
certain body parts belong to them. It has been posited perceived left arm. Some of the patients we tested did raise
that asomatognosia is caused by the alteration of the their right arm, suggesting that they had phantom move-
brains representation of the body, a body schema. Like ments, but we found no significant relationship between
spatial and personal neglect, asomatognosia is more com- phantom movements and anosognosia.
monly associated with right than left hemisphere lesions. Intentional motor disorder. Patients with right hemisphere
If patients with right hemisphere injury do not believe lesions often demonstrate contralesional limb akinesia
their left arm-hand belongs to them, they will not recog- also called motor neglect. Many of these patients do not
nize their own weakness. During right hemispheric anes- attempt to spontaneously move their akinetic arm and
thesia, the patients with left hemiplegia were shown their while less common some do not even attempt to move
left hand or someone elses left hand in a restricted view this arm to command. Limb akinesia can occur both with
box that projected to their right visual field. The patients and without a hemiplegia. Patients with limb akinesia
were asked if the hand they were viewing was their own or might not discover that they are weak because they do
another persons hand. We found that there were some not attempt to move this left arm. If they do not attempt
patients who had anosognosia who also had asomatogno- to move this arm, they will not experience a dissociation
sia, but only a small proportion. Thus, asomatognosia can between their expectations and performance, and it is this
also not fully account for this disorder. dissociation that alerts people that there is a problem.
Disconnection hypothesis. When a patient with a complete Providing external motivation such as suggestions or
callosal disconnection receives a stimulus to the left visual commands might entice patients to attempt a movement
field or on the left side of the body and is asked to tell the and with these commands some patients do discover their
examiner the nature of the stimulus, the left language weakness. Electromyographic studies have also provided
speech hemisphere often confabulates a response. evidence in support of this akinesia hypothesis.
Geschwind (1965) noted that large right hemisphere Summary. Based on the above discussion it appears that
lesions can both injure the right hemispheres cortex and several mechanisms might contribute to the presence of
intrahemispheric networks, as well as induce a interhemi- anosognosia for hemiplegia.
spheric disconnection. Thus, when asked about weakness,
the left hemisphere which is disconnected from the right
will confabulate a response I am not weak. The obser- Possible Mechanisms of Anosognosia for
vation mentioned above, where during the right hemi- Amnesia and Cortical Blindness
sphere anesthesia the patients left hand is brought over to
the right visual field and thus has access to the left lan- Damage to three interconnected brain networks can pro-
guagespeech dominant hemisphere, also tests this dis- duce amnesia, an impairment in the episodic memory
connection hypothesis. As mentioned, in few patients system: (1) the medial temporal lobe Papez circuit
when their arm could be visualized in the right visual (e.g., hippocampus, entorhinal and perirhinal cortex, for-
field left hemisphere, they did recognize their weakness. nix, the mammillary bodies, the mammillothalamic tract,
In these cases, we cannot be sure if their anosognosia was the anterior thalamus, and the retrosplenial cortex);
induced by a failure in feedback or a disconnection. Fu- (2) the dorsomedial thalamus; and (3) the basal forebrain
ture research will have to learn if these mechanisms can be (medial septal nucleus and the diagonal band of Broca),
dissociated. However, as mentioned above this procedure which provide acetylcholine to the hippocampus. Amne-
only helps a small minority of patients. sic patients with medial temporal lesions are often aware
182 A Anosognosia
of their disability and patients with damage to the basal suggesting that their unawareness might have been related
forebrain and to the medial thalamus are often unaware of to not being able to closely attend to their output. These
their memory deficit. aphasic patients might have focused their attention on
The reason for this dichotomy is not fully known, but what they were attempting to say rather than how they
the dorsomedial thalamic nucleus is heavily connected said it.
with the frontal lobes and damage to this dorsomedial
nucleus induces frontal dysfunction. Damage to the basal
forebrain is also often associated with frontal dysfunction.
Frontal lobe dysfunction is often associated with impaired
Future Directions
recall but not recognition, suggesting that the problem is
Anosognosia, the failure to recognize a disease or a dis-
not with the consolidation of memories, but rather re-
ability, might delay treatment, interfere with rehabilita-
trieval. The patients with amnesia from a thalamic or
tion, and put people in danger. Patients might be
basal forebrain injury, more often confabulate memories
anosognosic for a variety of neurological disorders such
than do those with medial temporal lobe damage. Since
as weakness, sensory loss, personal and spatial neglect,
these patients retrieve memories and have no means of
memory loss, and aphasia. There appears to be a variety
testing these memories veracity, they might be unaware
of mechanism that might account for anosognosia includ-
that their recall is incorrect and therefore they might be
ing psychological denial, impaired and false feedback,
unaware of their memory disorder.
alterations of the body schema, failures to test systems,
Blindness. Patients with Antons syndrome have blindness
and to initiate behaviors. Future research is needed. In
from damage to their primary visual cortex, usually from
addition to continuing to define and test possible
stroke. These patients often deny their blindness, confab-
mechanisms, effective treatments for these disorders are
ulate responses, and are unaware they are blind, anosog-
needed.
nosic. The reason why these patients are not aware of their
blindness is not known. We examined a patient with
Antons syndrome who had intact visual imagery. Perhaps
since these patients have intact visual imagery and cannot Cross References
receive visual input, this imagery is mistaken for online
input. Attention
Awareness
Consciousness
Possible Mechanisms for Unawareness Impaired Self-Awareness
of Aphasia
Patients with Wernickes aphasia speak in jargon, cannot

comprehend, name, or repeat. Many are not aware that References and Readings
they are aphasic and that they are speaking in jargon. For
example, we saw a patient, who when speaking jargon, Anton, G. (1898). Blindheit nach beiderseitiger Gehirnerkrankung mit
Verlust der Orienterung in Raume. Mitt. Ver. Arzte Steirmark, 33,
became angry when he was not understood. It has been
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posited that Wernickes aphasia is induced by injury to the Babinski, J. (1914). Contribution a letude des troubles mentaux dans
phonological lexicon a store of learned word sounds. To lhemiplegie organique cerebrale (anosognosie). Revue Neurologique,
be aware that an error has been made, a person needs to 27, 845847.
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the gap between theory and practice. New York: Psychology Press.
Since patients with Wernickes aphasia have destroyed
Geschwind, N. (1965). Disconnexion syndromes in animals and man.
their representations of word sounds when they speak Brain, 88, 237294, 585644.
jargon, they have no representations with which to com- Gilmore, R. L., Heilman, K. M., Schmidt, R. P., Fennell, E. M., &
pare their speech and are thus unaware of their errors. Quisling, R. (1992). Anosognosia during Wada testing. Neurology,
We have also reported patients who appear to have an 42, 925927.
Prigatano, G. P., & Schacter, D. L. (1991). Awareness of deficit after brain
intact input lexicon (e.g., can understand speech) but who
injury: Clinical and theoretical issues. New York: Oxford University
make phonological errors and are not aware that they Press.
made these errors. If these patients speech is recorded von Monakow, C. (1885). Experimentelle und pathologisch-anatomische
and played back to them, they do detect their errors, Untersuchungen uber die Beziehungen der sogenannten Sehphare zu
Anoxia A 183
den infrakorticalen Opticuscentren und zum N. opticus. Archiv fur The CA1 cells of the hippocampus contain high
Psychiatrie und Nervenkrankheiten, 16, 151199. A
concentrations of glutamate and they are particularly
Weinstein, E. A., & Kahn, R. L. (1955). Denial of illness: Symbolic and
physiological aspects. Springfield, IL: Charles C. Thomas.
vulnerable to subnormal oxygenation levels. Therefore,
it appears that the action of glutamate on these cells is
the putative mechanism mediating cell death in this
region of the hippocampus and helps explain many
of the signs and symptoms associated with anoxia
Anosphrasia (Bonner & Bonner, 1991).
Anosmia
Signs and Symptoms
Anoxia often results in impairments in memory,

ANOVA executive, and motor function. This is likely due to the
fact that anoxia is associated with damage to limbic and
Analysis of Variance subcortical regions, in addition to the frontal lobes and
the cerebellum (Golden, Zillmer, & Spiers, 1992).
Neuropsychological and Psychological

Anoxia Outcomes
B RUCE J. D IAMOND Anoxia can result in impairments in anterograde
William Paterson University memory (which in its most severe form may manifest as
Wayne, NJ, USA an amnestic disorder). Presenting symptoms may also
include impairments in awareness and affect as well as
confabulatory behavior. Anoxia associated with cardiac
Synonyms arrest may include amnesia, in addition to bibrachial
paresis, cortical blindness, and visual agnosia. Carbon
Oxygen deficiency; Severe hypoxia monoxide poisoning may be associated with affective
disturbances as well as cortical and anoxia induced
dysfunction (Aminoff, Simon, & Greenberg, 2005).
Definition
Anoxia refers to a hypoxia (i.e., deficiency in the Cross References
oxygenation of the arterial blood) of sufficient severity
to result in permanent neurologic damage (Websters New Carbon Monoxide Poisoning
Explorer Medical Dictionary, 2006). The brain has little to Glutamate
no reserve of oxygen or glucose, consequently an anoxic Hippocampus
episode of 46 min can result in neuronal cell death or
necrosis because of impairment in cellular metabolism. In
contrast to anoxia, hypoxia refers to a reduction in References and Readings
oxygenation, rather than a complete loss of oxygenation
(Zillmer & Spiers, 2001). Aminoff, M. J., Simon, R. P., & Greenberg, D. A. (2005). Clinical
neurology. New York: McGraw-Hill.
Bonner, J. S., & Bonner, J. J. (1991). The little black book of neurology:
A manual for neurologic house officers. (2nd ed.). St Louis: Mosby-
Etiology Year Book.
Golden, C. J., Zillmer, E. A., & Spiers, M. V. (1992). Neuropsychological
Anoxia can result from a number of conditions includ- assessment and intervention. Springfield, IL: Charles C.Thomas.
Websters new explorer medical dictionary (New Edition). (2006).
ing cardiac arrest, carbon monoxide poisoning, stroke, Springfield, MA: Merriam-Webster.
brain injury, and complications due to anesthesia. It is Zillmer, E. A., & Spiers, M. V. (2001). Principles of neuropsychology.
thought that cells exposed to anoxia release glutamate. Belmont, CA: Wadsworth/Thomson Learning.
184 A Anoxic Encepathopathy
Categories
Anoxic Encepathopathy
The ACA can be divided into five segments A1A5,
Anoxia although it should be noted that some of the literature is
describing the A1 segment when referring to the ACA
(Sawada & Kazui, 1995).
Antagonist Medical, Neuropsychological, and

Psychological Symptoms
Receptor Spectrum
Infarctions in the territory of this artery are associated
with a variety of clinical signs and symptoms involving
gait, limb sensation, abulia, lack of spontaneous activity,
urinary incontinence, frontal and memory impairments,
Anterior Aphasia in addition to emotional dysregulation (apathy)
(Brust, 1995).
Brocas Aphasia
Cross References
Anterior Communicating Artery

Anterior Cerebral Artery
B RUCE J. D IAMOND
William Paterson University Brust, J. C. M. (1995). Agitation and delirium. In J. Bogousslavsky, &
Wayne, NJ, USA L. Caplan (Eds.), Stroke syndromes (pp. 134139). Cambridge: Cam-
bridge University Press.
Ropper, A. H., Brown, R. H., Adams, R. D., & Victor, M. (2005). Adams &
Victors principles of neurology. New York: McGraw-Hill.
Synonyms Sawada, T., & Kazui, S. (1995). Anterior cerebral artery. In J. Bogousslavsky,
& L. Caplan (Eds.), Stroke syndromes (pp. 235246). Cambridge:
ACA; Cerebral artery Cambridge University Press.
Definition Anterior Cingulate Cortex

The anterior cerebral artery (ACA) arises as the medial R ONALD A. C OHEN , A NNA M AC K AY-B RANDT
branch of the bifurcation of the internal carotid artery Brown University
(ICA) (Sawada & Kazui, 1995) and supplies the anterior Providence, RI, USA
three-quarters of the medial surface of the frontal and
parietal lobes, the anterior 80% of the corpus callosum,
the frontal basal cerebral cortex, the anterior diencepha- Synonyms
lon, and deep structures. Innervated areas also include the
medial-orbital surface of the frontal lobe, frontal pole, ACC
and a small strip of the lateral surface of the cerebral
hemisphere along the superior border (Ropper, Brown,
Adams, & Victor, 2005). The largest branch (Heubners Structure
artery) supplies the head of the caudate, the anterior
globus pallidus, and the anterior limb of the internal The anterior cingulate cortex (ACC) is a mesocortical
capsule. paralimbic area located anterior to the corpus callosum
Anterior Cingulate Cortex A 185
and posterior to the prefrontal cortex. The ACC was once severe depression and schizophrenia. While frontal lobot-
A
viewed as a single limbic structure, forming an important omy resulted in a reduction in agitation and other severe
part of the Papez circuit, though in reality analysis of its psychiatric symptoms, surgical removal of the frontal lobe
cytoarchitecture indicates that it consists of regions with caused severe cognitive dysfunction. Given that the orbital
different cell types. Its cell characteristics are agranular, frontal region was considered to be particularly important
and therefore are distinct from the cortex. for the control of impulses and emotional regulation,
The ACC encompasses several Broadmann areas, subsequent psychosurgical approaches typically restricted
including areas 24, 25, 32, and 33. The ACC wraps around ablation to these areas, often through leukotomy.
the corpus callosum, having the appearance of a collar Unfortunately, patients undergoing this procedure often
or belt. In fact, the term cingulum means belt in Latin. exhibited marked personality change, with flattening of
A large volume of the ventral ACC consists of Area 24, affect, apathy, and other undesirable effects. A third gen-
which merges with the posterior cingulate cortex eration of psychosurgical procedures ensued with efforts
(Area 23) along the posterior half of the corpus callosum. to target brain areas more selectively. The ACC was a
The division between the ACC and posterior cingulate is point of focus because of its association with both limbic
undifferentiated to a large extent, though these areas can areas as well as the frontal cortex. Beginning in the late
be separated based on the cortical layer IV in the posterior 1950s, cingulotomy was developed as an alternative to
cingulate. Anterior to Area 24 is the subgenual cortex frontal ablation. Early studies suggested that it had few
(Area 25), which may be considered to be distinct from adverse cognitive effects, and that it seemed helpful
other ACC areas. Anterior to this region is the dorsal for certain patients, particularly those with intractable
ACC, including areas 32 and 33. The midanterior section obsessivecompulsive symptoms, chronic pain, and
of the ACC is often termed midcingulate (mACC), while opiate dependence. There was also some evidence that it
the more posterior section is termed perigenual cingulate was helpful for patients with severe chronic depression,
(pACC). These areas have distinct cell characteristics, and though the basis for these effects may relate to reductions
there is strong evidence of functional differences across in emotional tension, obsessive thought processes, and
subareas of the ACC. other depression-associated problems.
Primary afferent input to the ACC is received via Literature on the psychosurgical effects of cingulotomy
axons from the midline and intralaminar thalamic nuclei, provided compelling evidence that the ACC plays a role
with the anterior nucleus receiving input from mamillary in human emotional experience and regulation. Further-
neurons, which in turn has projections from the subicu- more, there is also evidence that the ACC influences
lum. The ACC is associated with a large white-matter autonomic nervous system response, including heart
bundle, the cingulum, through which signals are trans- rate, blood pressure, and galvanic skin response, with
mitted to other limbic areas. As a paralimbic area, the these responses showing alterations in the rate of habitua-
ACC is a transition area between subcortical and limbic tion following cingulotomy (Cohen et al., 1995). Yet, most
structures, such as the amygdala and cortical areas, most early studies of the effects of cingulotomy suggested that
notably in the frontal lobes. The posterior ACC has heavy the ACC had little impact on intellectual ability or most
input from the amygdala, whereas the mid-ACC receives neuropsychological functions. Postsurgery patients tended
greater input from parietal areas. Connections between not to experience significant memory, language, or visual
the ACC and the mesial, ventral, and orbital frontal areas change. Subsequent controlled studies indicated that while
appear to be particularly important for emotional and these functions are largely spared following cingulotomy,
behavioral regulation. there are alterations in some attention-related functions,
most notably attentional focus, intention, and response
selection and control (Cohen et al., 2001). These changes
Function correspond with reductions in emotional tension and
distress, and also a tendency for reduced self-initiation
Current knowledge regarding the functions of the ACC of behavior (Cohen et al., 2001).
has its origins in the psychosurgical efforts of the mid- Recent experimental evidence suggests a functional
twentieth century. At that time, the role of the frontal dissociation between the posterior and middle ACC. The
lobes in emotion and behavioral control were recognized, mid-ACC plays a role in response selection and control,
and frontal lobotomy was experimented with as a means including intention and planning to act or to engage
of treating a variety of psychiatric conditions, including in cognitive operations. It has also been implicated in
186 A Anterior Cingulate System
processing new motor programs, working memory, and implicated in substance abuse, including opiate addiction
mismatch detection. In contrast, the posterior ACC and nicotine dependence. Citalopram binds to the sero-
appears to play a more direct role in emotional proces- tonin transporter at very high levels in the posterior ACC,
sing, though these areas are likely highly interconnected, which may account for the effects of this type of drug on
enabling the integration of emotional and attentional reducing mood, anxiety, and pain symptoms. There is
processes (Bush, Luu, & Posner, 2000). also evidence that functional response of the ACC varies
Interest in the functional significance of ACC as a function of risk-reward dynamics, appetitive state,
increased dramatically with the advent of functional neu- and motivation. Neuroimaging studies have begun to
roimaging methods. Activation of the ACC is evident point to its role in a variety of behavior problems, such
across a wide range of tasks. In fact, it is among the as obesity and inactivity.
most responsive areas of the brain on fMRI. This probably
reflects the fact that it plays an increased role when tasks
require motivation and drive to complete and where there Cross References
is demand for attentional effort and focus.
The ACC plays a significant role in response to the Apathy
conflict during cognitive tasks associated with decision Executive Function
making and the need to resolve competing or discrepant Intention
information (Botvinick et al., 1999). Some cognitive neu- Psychosurgery
roscientists argue that conflict monitoring is the primary
function of the ACC, though it seems likely that this
capacity is closely associated with the broader functions References and Readings
of regulation of drive, emotion, attention, and response
intention; and selection, initiation, and persistence Ballentine, H. T. Jr., Levey, B. A., Dagi, T. F., & Diriunas, I. B. (1977).
relative to situational demands. Neurosurgical treatment in psychiatry, pain, and epilepsy. In W. H.
Sweet, S. Obrador, & J. G. Martin-Rodriques (Eds.), Cingulotomy
for psychiatric illness: Report of 13 years experience (pp. 333353).
Illness Baltimore, MD: University Park Press.
Bush, G., Luu, P., & Posner, M. I. (2000). Cognitive and emotional
influences in anterior cingulate cortex. Trends in Cognitive Sciences,
Focal brain diseases affecting only the ACC are rare. 4(6), 215222.
However, the ACC is vulnerable to the effects of tumor, Botvinick, M., Nystrom, L. E., Fissell, K., Carter, C. S., & Cohen, J. D.
stroke, and other neurological conditions involving ante- (1999). Conflict monitoring versus selection-for-action in anterior
rior cortical infarction or mass action. Unilateral ablation cingulate cortex. Nature, 402(6758), 179181.
Cohen, R. A., Kaplan, R. F., Meadows, M. E., & Wilkinson, H. (1994).
of the ACC in laboratory studies of primates, and also
Habituation and sensitization of the orienting response
secondary to stroke, has been shown to produce hemi- following bilateral anterior cingulotomy. Neuropsychologia, 32(5),
neglect syndrome, providing further evidence that the 609617.
ACC plays an important role in attention. There is evi- Cohen, R. A., Kaplan, R. F., Zuffante, P., Moser, D. J., Jenkins, M. A.,
dence of ACC dysfunction secondary to atrophy asso- Salloway, S., et al. (1999). Alteration of intention and self-initiated
action associated with bilateral anterior cingulotomy. Journal of
ciated with neurodegenerative conditions, such as
Neuropsychiatry and Clinical Neurosciences, 11(4), 444453.
Alzheimers disease, which may contribute to symptoms Cohen, R. A., Paul, R., Zawacki, T. M., Moser, D. J., Sweet, L., &
of apathy and behavioral inertia in certain patients. How- Wilkinson, H. (2001). Emotional and personality changes following
ever, these changes are usually part of a much more global cingulotomy. Emotion, 1(1), 3850.
pattern of brain abnormality. Devinsky, O., Morrell, M. J., & Vogt, B. A. (1995). Contributions of
anterior cingulate cortex to behaviour. Brain, 118(Pt. 1), 279306.
The ACC plays a more obvious role in psychiatric
illness and also the range of normal behavior. Activation
of the ACC occurs in association with increased levels of
distress and emotional tension and anxiety. It also tends
to be associated with obsessive rumination and preoccu- Anterior Cingulate System
pation with internal states and signals, such as pain and
impulses to seek reward. Accordingly, the ACC has been Mesial Frontal System
Anterior Communicating Artery A 187
Anterior Commissure Anterior Communicating Artery A
J OHN E. M ENDOZA B RUCE J. D IAMOND

Tulane University Medical Center William Paterson University
New Orleans, LA, USA Wayne, NJ, USA
Synonyms Synonyms
Interhemispheric commissure Communicating artery; ACoA
Description
Definition
The anterior communicating artery (ACoA) intercon-
A relatively small commissure in the basal forebrain lying nects the two anterior cerebral arteries just rostral to the
above the optic chiasm and anterior to the main columns optic chiasm and resides at the anterior portion of the
of the fornix that connects homologous areas of the mid- Circle of Willis.
dle and inferior temporal gyri, including parts of the Ruptured ACoA aneurysms may impact a variety
olfactory cortices (Fig. 1). of neurologic, neuropsychological, and psychological
functions. This may, in part, be due to the fact that
the perforating branches of the ACoA supply the anteri-
or hypothalamus, mesial anterior commissure, lamina
termininalis, and areas implicated in executive function,
memory, and affect (e.g., fornix and basal forebrain, septal
nuclei, nucleus accumbens, diagonal band, and the medial
Acq Tm substantia innominata) (DeLuca & Diamond, 1995;
Sawada & Kazui, 1995). The profound memory disorders
that may be associated with ACoA aneurysm rupture do
not appear to directly involve neuroanatomic areas tradi-
tionally implicated in amnesia, which makes the ACoA
artery of both clinical and theoretical interest.
Etiology
ACoA aneurysms may develop as a result of trauma,
infections, degenerative diseases, or a congenital defect
(Parkin & Leng, 1993). Aneurysms often become symp-
tomatic as a result of subarachnoid hemorrhage (SAH)
following rupture (Riina, Lemole, & Spetzler, 2002). SAH
has an overall incidence of 10 to 16 per 100,000 and is a
major cause of mortality and morbidity (Clinchot,
Kaplan, Murray, & Pease, 1994).
Mechanisms
Ruptured ACoA aneurysms alter the hemodynamic circu-

Anterior Commissure. Figure 1 lation of the anterior portion of the Circle of Willis, often
188 A Anterior Communicating Artery
resulting in cerebral infarction and impairments in cogni- differences most notable on tests of executive and memo-
tion, personality, and functional activities (DeLuca & ry function. Relationships between recovery of executive
Diamond, 1995; McCormick, 1984). Damage to the function and temporal gradients in retrograde amnesia
basal forebrain region may help account for many of the have been reported, with improvements in executive func-
cognitive impairments that are observed in ACoA aneu- tion accompanied by parallel improvements in the severi-
rysm due to the fact that the basal forebrain region con- ty of retrograde amnesia. Improvement in the recall of
tains cholinergic neurons that project to the hippocampus complex visual-spatial information and an enhanced abil-
and amygdala, via the medial forebrain bundle to the ity to benefit from an executive learning strategy have also
entire cerebral cortex. Damage to this area would, there- been reported with little improvement on traditional
fore, particularly interfere with cholinergic activation of measures of memory or executive function (Diamond,
structures and circuits implicated in memory within the DeLuca, & Kelley, 1997a). Recovery from neuropsycho-
medial temporal lobe (Schnider & Landis, 1995). More- logical disturbances is generally poorer in patients with
over, vascular compromise of the perforating branches of ventral frontal lesion compared to those with basal fore-
the ACoA are believed to impact functional areas (e.g., brain and striate lesions.
executive function, memory, and affect) that are inner- Surgical outcome and prognosis following aneurysms
vated by these vascular branches. There is general agree- depend on multiple factors (e.g., initial clinical status,
ment in the literature suggesting that personality changes localization of aneurysm, age, and the morphological
following ACoA aneurysm are a result of frontal lobe characteristics of the aneurysm). Comparisons of clipping
dysfunction, particularly in the medio-basal zones along versus endovascular embolization procedures have shown
the distribution of the anterior cerebral artery. The sub- that, in a number of studies, clipped patients have more
callosal perforating artery has, in fact, been implicated in severe cognitive impairments than embolization patients
and may mediate personality changes and memory and that 33% of clipped patients had impairments in
impairments. memory and executive functioning (Chan, Ho, & Poon,
2002).
Generally, the severity of cognitive impairment has
Epidemiological Factors predictive value for functional status particularly with
respect to levels of required supervision at discharge
Rupture of cerebral aneurysms strikes at a mean age of
(Saciri & Kos, 2002).
50 years and accounts for 510% of all strokes (Dombovy,
Some work suggests that recovery of executive func-
Drew-Cates, & Serdans, 1998), and approximately
tion and not short- and long-term memory may, in fact,
8595% of all aneurysms develop at the anterior portion
be the best predictor of the ability to return to work
of the cerebral arterial supply, primarily at the Circle of
(DeLuca & Diamond, 1995).
Willis (Adams & Biller, 1992; Ropper, Brown, Adams, &
Victor, 2005). The ACoA is one of the most common sites
of cerebral aneurysm and is the most frequent site of
Neuropsychological and Psychological
cerebral infarct following aneurysm rupture (DeLuca &
Diamond, 1995; McCormick, 1984). About 3040% of
Outcomes
cerebral aneurysms affect the ACoA artery, and 90% of
Neuropsychological
cases are asymptomatic (Beeckmans, Vancoillie, & Michiels,
1998; Manconi, Paolino, Casetta, & Granieri, 2001) with
It is generally concluded that verbal intellectual skills,
various reports suggesting that the incidence of rupture is
language functions, visuo-spatial skills, and attention/
highest between 40 and 70 years of age (McCormick,
concentration are within normal limits or only mildly
1984; Sethi, Moore, Dervin, Clifton, & MacSweeney,
impaired, although complex concentration appears to be
2000) and that rupture occurs more frequently in females
reduced. An increased sensitivity to interference may be a
(i.e., 60% of cases) (Adams & Biller, 1992).
defining feature among ACoA amnesics and between
ACoA amnesics and diencephalic-mesial and temporal
Natural History, Prognostic Factors, and amnesics. More severe impairments are seen in delayed
Outcomes versus immediate memory and in executive function
(DeLuca & Diamond, 1995). Impairments in spatio-
With respect to impairment and chronicity, acute ACoA temporal discrimination appear similar to other popula-
patients are more impaired than chronic ones with tions with frontal lobe dysfunction (Schacter, 1987).
Anterior Communicating Artery A 189
Implicit memory involving data- and concept-driven re- statements or actions that involve distortions that are
A
trieval processes and behavioral and physiological indices unintentional (Moscovitch & Melo, 1997) with two dis-
(Diamond, Mayes, & Meudell, 1996) appears to be rela- tinct types of confabulation generally recognized in the
tively intact, although the evidence is sparse. Procedural literature, spontaneous and provoked (Kopelman, 1987).
memory on serial reaction time and mirror-reading tasks The key difference between provoked and spontaneous
also appears to be preserved. confabulation is that in spontaneous confabulation the
Spatial working memory in ACoA patients has been confabulation guides actions. Recovery from confabula-
reported to be impaired, and the impairment profile is tion appears to parallel improvement in temporal context
similar to patients with temporal lobe excisions. ACoA confusion, and recovery can occur in the absence of sig-
patients have displayed impairments in semantic memo- nificant improvement on traditional tests of memory and
ry, and difficulties to both the acquisition and recall of executive function.
verbal information showing little initial learning, a passive With respect to psychosocial outcomes, a significant
learning style, a flat learning slope, and impaired recogni- percentage of SAH survivors are left with cognitive,
tion discrimination, in addition to emitting a high num- emotional, and behavioral changes that can profoundly
ber of intrusions and false positives (Diamond, DeLuca, & impact their daily lives. Compared with controls,
Kelley, 1997b). ACoAs have shown impairments in infor- SAH patients display an increased incidence of mood
mation processing and autobiographical memory (espe- disturbance, cognitive impairment, and lower levels of
cially for events associated with context). ACoA amnesics independence, and participation on measures that reflect
(i.e., with putative basal forebrain damage) have exhibited social functioning. Levels of productive employment
impairments in delay eyeblink classical conditioning are generally reduced and many patients show clinically
(Myers et al., 2001), event-related potentials (ERPs), and significant posttraumatic stress symptomatology (see
in prospective remembering. Table 1 for a list of neuropsychological and psychological
impairments).
Psychological
Assessment and Treatment
ACoAs have displayed increased risk-taking on tasks in
which choices were associated with different magnitudes Given the wide range of impairments associated with
of reward and punishment. Confabulation is observed in ACoA aneurysm, it may be advisable for clinicians to
a subset of ACoA aneurysm patients and is manifested by use assessments that focus on those impairments that
Anterior Communicating Artery. Table 1 Neuropsychological and psychological impairments associated with ACoA aneurysm
Awareness, self-monitoring, and personality Memory Cognitive/executive/mood

Disorders of awareness: Semantic Memory Attention
Confabulation Prospective Memory Cognitive Estimation
Anosognosia Visuo-Spatial Decision-making
Executive dysfunction Working Memory Dual Task Performance
Intrusions Recall/Recognition Learning
Proactive Interference
Mood
Delay eyeblink conditioning
Motor/sensory Language Autonomic and event-related potentials (ERP)
Paraparesis syndrome Dichotic listening Electrocardiogram (ECG)
Visuomotor skill learning Phonemic fluency Delayed ERP (P300): Auditory
Alien hand syndrome Verbal fluency Delayed ERP (P300): Visual
Visual-sensory function (unruptured aneurysms) Prolonged QTc intervals
190 A Anterior Communicating Artery
are most salient and have the greatest impact on activities Cross References
of daily living (ADLs). Impairments in memory, executive
function, and attention/concentration as well as mood Activities of Daily Living (ADLs)
figure prominently following ACoA aneurysm rupture Amnesia
and should be part of routine assessment. For example, Aneurysm
assessments should examine set-shifting (e.g., Wisconsin Anterior Cerebral Artery
Card Sort Test (WCST) and Trails B), verbal and visual Confabulation
fluency (e.g., CFT/FAS and Design Fluency Test), verbal Executive Functioning
recall and recognition (e.g., California Verbal Learning Rey Complex Figure Test
Test (CVLT)), visual recall (e.g., ReyOsterreith Complex
Figure Test (ROCFT)), sustained attention (e.g., Cancel-
lation Test), information processing speed (e.g., n-back References and Readings
tasks), and impaired abstraction (e.g., Cognitive Estima-
tion Test (CET)). Adams, H. P., & Biller, J. (1992). Hemorrhagic intracranial vascular
In some cases, modification of existing assessment disease. In A. B. Baker & R. J. Joynt (Eds.), Clinical neurology
tools can be an effective way to enhance the assessment (vol. 2). Philadelphia: J. B. Lippincott.
process. For example, the ReyOsterrieth Organizational Beeckmans, K., Vancoillie, P., & Michiels, K. (1998). Neuropsychological
deficits in patients with an anterior communicating artery syn-
and Extended Memory (ROEM) test, which is a modifi-
drome: A multiple case study. Acta Neurologica Belgica, 98(3),
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mechanisms underlying the nature of the impaired mem- Chan, A., Ho, S., & Poon, W. S. (2002). Neuropsychological sequelae of
ory in ACoA amnesics by using measures of recall and patients treated with microsurgical clipping or endovascular embo-
recognition (e.g., subunit recognition, spatial arrange- lization for anterior communicating artery aneurysm. European
ment, and whole figure recognition). Moreover, encoding
Clinchot, D. M., Kaplan, P., Murray, D. M., & Pease, W. S. (1994).
and recall were improved by using an executive organiza- Cerebral aneurysms and arteriovenous malformations: Implications
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of 40% of the patients (Dombovy, Drew-Cates, & Serdans,
anterior communicating artery aneurysm and multiple sclerosis
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tioning (Ravnik et al., 2006). 35(7), 10171034.
Anterograde Amnesia A 191
Myers, C. E., DeLuca, J., Schultheis, M. T., Schnirman, G. M., Ermita, age 27, HM underwent bilateral resection of the medial
B. R., Diamond, B. J., Warren, S. G., & Gluck, M. (2001). Impaired A
temporal lobes for alleviation of refractory seizures, which
delay eyeblink classical conditioning in individuals with anterograde
amnesia resulting from anterior communicating artery aneurysm.
had become progressively more severe following a head
Behavioral Neuroscience, 115(3), 560570. injury he had suffered at age 9. The resection was success-
Parkin, A., & Leng R. C. (1993). Neuropsychology of the amnestic syn- ful in reducing his seizures but, unexpectedly, following
drome: Hove, U.K.: Lawrence Erlbaum. the treatment he was unable to remember his normal
Prignatano, G., & DeLuca, J. (1999). Methodological issues in research on
daily activities. For example, he could not recall eating
neuropsychological and intellectual assessment. In P. C. Kendall,
J. Butcher, & G. Holmbeck (Eds.), Handbook of research methods in
his meal within minutes of having finished it, and he
clinical psychology (pp. 241250). New York: Wiley. could not remember having had a conversation minutes
Ravnik, J., Starovasnik, B., Sesok, S., Pirtosek3, Z., Svigelj, V., Bunc, G., after it ended. He was unable to remember his regular
et al. (2006). Long-term cognitive deficits in patients with good caregivers, even though he could converse and interact
outcomes after aneurysmal subarachnoid hemorrhage from anterior
normally with them when they were present. These find-
communicating artery. Croat Medical Journal, 47, 253263.
Riina, H. A., Lemole, G. M., Jr., & Spetzler, R. F. (2002). Anterior
ings established that intact medial temporal lobes are
communicating artery aneurysms. Neurosurgery, 51(4), 993996. critical for normal memory function. HMs medial tem-
Ropper, A. H., Brown, R. H., Adams, R. D., & Victor, M. (2005). Adams & poral lobe resection had left him with a dense anterograde
Victors principles of neurology. New York: McGraw-Hill. amnesia, despite his having intact intelligence, attention,
Saciri, B. M., & Kos, N. (2002). Aneurysmal subarachnoid haemorrhage:
language function, and social skills. With respect to his
Outcomes of early rehabilitation after surgical repair of ruptured
intracranial aneurysms. Journal of Neurology Neurosurgery and Psy-
memory for the events that preceded his surgery, it was
chiatry, 72(3), 334337. initially thought that his retrograde amnesia ( Retro-
Sawada, T., & Kazui, S. (1995). Anterior cerebral artery. In J. Bogousslavsky grade Amnesia) was limited to approximately 2 years
& L. Caplan (Eds.), Stroke Syndromes (pp. 235246). Cambridge: prior to the operation, but more recent findings indicate
that he had a more extensive retrograde amnesia that
Schnider, A., & Landis, T. (1995). Memory loss. In J. Bogousslavsky &
L. Caplan (Eds.), Stroke syndromes (pp. 145150). Cambridge, MA:
extended to 11 years before the surgery. Subsequent neu-
Cambridge University Press. ropsychological studies of HM and other amnesic indivi-
Schacter, D. L. (1987). Implicit memory: History and current status. duals have further informed our current understanding of
Journal of Experimental Psychology: Learning, Memory and Cognition, both impaired and preserved memory function in amnesia
13, 501518.
(Corkin, 1984).
Sethi, H., Moore, A., Dervin, J., Clifton, A., & MacSweeney, J. E. (2000).
Hydrocephalus: Comparison of clipping and embolization in aneu-
rysm treatment. Journal of Neurosurgery. 92(6), 991994.
Neuropsychology of Anterograde
Amnesia
Anterograde Amnesia Patients suffering from anterograde amnesia have great

difficulty in bringing to mind information to which they
G INETTE L AFLECHE , M IEKE V ERFAELLIE were exposed following the onset of their illness. These
VA Boston Healthcare System and Boston University patients have preserved immediate memory, in that they
School of Medicine can hold in mind a current topic of conversation and can
Boston, MA, USA repeat a string of digits with no delay, but, following any
distraction or delay, memory for the information is lost.
Episodic memory or memory for personal events is se-
Short Description or Definition verely impaired and, as a result, patients no longer form a
record of their lives. The nature of this loss is global, in
Anterograde amnesia is an inability to recall or recognize that it includes both verbal and nonverbal information in
events, facts, or concepts to which one was exposed all sensory modalities. It encompasses both personally
following the onset of illness. experienced events (episodic memory) and impersonal
facts or concepts (semantic memory). Together these
two forms of memory comprise declarative (or explicit)
Brief Historical Background memory, and are what the plain term memory refers to
in common usage. An important insight to arise from the
Current scientific understanding of anterograde amnesia study of patients with anterograde amnesia is that not all
began largely with the study of patient HM. In 1953, at forms of long-term memory are impaired. Forms of
192 A Anterograde Amnesia
memory that do not require deliberate reference to a prior contribute to explicit memory; the first is recollection,
experience, often referred to as nondeclarative (or implic- the intentional, effortful process by which aspects of a past
it) memory, remain intact. episode are recovered. The second is familiarity, a sub-
Failure of declarative memory in amnesia can arise jective feeling that arises when information is processed
from a number of different etiologies. These include an- fluently and comes to mind easily. Whereas performance
oxia, herpes simplex encephalitis (HSE), anterior commu- on recall tasks depends on the ability to recollect contex-
nicating artery aneurysm (ACoA), WernickeKorsakoff tually appropriate information, performance on recogni-
syndrome (WKS), and stroke. The amnesia is a direct tion tasks can be supported by either recollection or
consequence of damage to the medial temporal lobes familiarity. Thus, the pattern of performance of patients
(i.e., HSE; anoxia), the midline diencephalon (i.e., WKS; with limited hippocampal lesions is thought to reflect
stroke), basal forebrain structures (i.e., ACoA), or some of impaired recollection, but preserved familiarity. Such a
the fiber tracts that link these regions. These amnesias pattern is consistent with findings from neuroimaging
are usually permanent. In contrast, in transient global am- and neurophysiological studies that suggest that the hip-
nesia (TGA) there is temporary dysfunction of memory- pocampus proper is critical for recollection, whereas
related brain structures including the hippocampal for- familiarity is supported by the perirhinal cortex. If the
mation and thalamus. Episodes of TGA typically last no damage is more extensive and extends beyond the hippo-
more than 24 h, after which the patients new-learning campus to include other medial temporal lobe structures
returns to normal, but a permanent amnesic gap remains such as the perirhinal cortex, then both recollection and
for the period of the attack ( Transient Global Amnesia). familiarity are affected, leading to striking impairments
The ability to remember newly encountered infor- on tests of recognition as well as recall.
mation depends on a number of stages, including the The degree of impairment in new semantic learning is
processing and representation of immediate experience also a function of the extent of the medial temporal lobe
(encoding), the transfer of that encoded information to lesion. Patients with injury limited to the hippocampus
long-term storage (consolidation), and its re-manifes- are able to acquire some new facts and concepts post-
tation in consciousness upon deliberate recall (retrieval) morbidly, although inefficiently, but patients with more
at a later time. Disruption of any one of these stages extensive medial lobe damage show minimal ability to do
could lead to anterograde amnesia. In patients with so (Verfaellie, 2000).
medial temporal or diencephalic lesions, encoding and In patients who suffered anoxia or a rupture of an
retrieval are thought to be relatively intact. Such aneurysm of the anterior communicating artery, frontal
patients perform normally on intelligence tests, and lobe impairments may be superimposed on the core amne-
on short-term memory tests, suggesting adequate sia ( Amnestic Syndromes). In such cases the antero-
encoding (Baddeley, 1995). Furthermore, impaired re- grade amnesia will be exacerbated by additional
trieval is unlikely to be the cause of their failed explicit impairments in encoding and retrieval. Executive functions
memory, because memories from many years ago can still such as planning, organizing, monitoring, and control of
be retrieved. Therefore, it is assumed that their impair- attention, all depend on the integrity of the frontal lobes.
ments reflect deficient consolidation. The medial tempo- Executive impairments will interfere with the ability to
ral lobes, through interactions with neocortical regions, mentally manipulate and organize information during de-
are thought to be critical for consolidation. They bind liberate encoding, and will also disrupt initiation and eval-
together into a coherent representation the different uation of memory search during effortful retrieval. The
aspects of an event that are neocortically represented latter can lead to unusually high levels of intrusions in
(Eichenbaum, 2006). recall, or false alarms in recognition, a phenomenon
Generally, the size of the causative brain lesion is known as enhanced susceptibility to false memory.
directly proportional to the density of the amnesia, but Despite such pervasive impairments in declarative
the specific location of the lesion will also impact on the memory, patients with anterograde amnesia show intact
nature of the memory impairment. For example, if the performance in a variety of forms of nondeclarative mem-
damage is limited to the hippocampal formation, perfor- ory. These include procedural learning (the acquisition of
mance on recall tasks is impaired, but performance on new skills or habits), eyeblink conditioning (learning to
recognition tasks can remain intact (Mayes, Holdstock, blink the eyes in response to a tone because of the repeat-
Isaac, Hunkin & Roberts, 2002). To account for these ed association of the tone with an air puff to the eye), and
findings, it has been suggested that two distinct processes repetition priming (improved accuracy or speed of
Anterograde Amnesia A 193
performance for stimuli to which an individual was re- and the choice among them should be informed by cog-
A
cently exposed) (Verfaellie & Keane, 2002). These forms of nitive factors such as premorbid abilities and skills as well
nondeclarative memory depend on neural circuits in the as post-morbid neuropsychological strengths and weak-
basal ganglia, cerebellum, or neocortex that remain spared nesses, including the severity of amnesia. Contributing
in amnesia (Squire, 1994). non-cognitive factors include premorbid lifestyle and
habits, and educational background. Contributing emo-
tional factors include insight and motivation, which are
Evaluation essential for any treatment choice, because the absence of
either will undermine rehabilitation efforts.
Anterograde amnesia refers to a severe and permanent Remediation of patients with severe amnesia relies
inability to learn new information in the presence of largely on those aspects of memory that are preserved,
otherwise normal intelligence, attention span, perception, such as procedural learning and priming. Techniques
reasoning, and language ability. The evaluation of antero- that capitalize on procedural learning use repetition to
grade amnesia must therefore, as a first step, include a drill skills and habits, ranging from essential activities
comprehensive neuropsychological work-up to determine of daily living to simple assembly tasks and cognitive
whether other areas of cognitive functioning are intact skills. Such skill learning is frequently involved when
and, if not, whether any deficits found contribute to the teaching a patient to use an external memory aid, such as
memory disorder. With regard to assessment of memory a memory notebook, calendar, diary, appointment book,
functioning itself, there are a variety of standardized tests or written reminders. The memory notebook is a preferred
available, and Lezak, Howieson, and Loring (2004) pro- compensatory instrument for amnesics because it is
vide a comprehensive review of the most commonly used divided into sections that are personally tailored to a
ones. Assessing performance on recall and recognition patients life (i.e., daily tasks, future plans, notes section,
tests is an essential component of the evaluation, because and so on). More sophisticated technology, in the form
their comparison can reveal the nature of the memory of computerized paging systems, electronic assistants,
processes that are affected. Both verbal and nonverbal alarms, and timers, is most useful for individuals who
memory should be examined, and memory should be had some proficiency in the use of such devices premor-
tested both shortly after learning and following a longer bidly. Learning to use such devices de novo may pose high
delay, to assess the rate of forgetting. Other factors of demands on working memory or episodic memory, which
diagnostic importance are a patients sensitivity to inter- is problematic for memory disordered patients. In such
ference and his or her ability to use organizational strate- instances, it is important to break the task down into
gies at encoding and retrieval. While a comprehensive small steps that can be practiced independently. Once
assessment of anterograde memory typically includes a the steps become automatized, they can then be gradually
variety of different tests, each developed for a specific integrated.
purpose, the use of a single standardized memory battery Other methods rely on preserved priming abilities
that evaluates all major aspects of new learning can (Verfaellie, 2000). One technique is the vanishing cues
provide a good overview of memory functioning. The technique, which has been used to teach amnesics
Wechsler Memory Scale-III (Wechsler, 1997) is probably computer-related vocabulary, business-related terms,
the most widely-used instrument for this purpose. In and novel concepts, through gradual reduction of cues
addition to indices of Immediate Memory and General that elicit correct answers. Another technique is errorless
(Delayed) Memory, it provides an index of Working learning. Error elimination requires explicit recollection
Memory, and, in patients with anterograde amnesia, a of the learning episode, and thus densely amnesic patients
split on the order of 20 points is to be expected between have great difficulty eliminating errors. Their perfor-
Working Memory and Immediate/General Memory. mance relies primarily on implicit memory, which typi-
cally leads to production of the strongest response. If that
response is incorrect, the error is likely to be further
Treatment strengthened across subsequent learning trials, thus inter-
fering with learning the correct response.
Rehabilitation interventions in amnesia aim at increasing For patients with milder memory impairments,
day-to-day functional adaptation and independence. strategies aimed at strengthening the impaired form of
A wide array of intervention techniques is available, memory are more appropriate. Such patients may
194 A Anterolateral System
benefit from rehearsal and relearning of the material.

Spaced repetitions, across different time intervals and Anterolateral System
different spatial locations, are especially beneficial as
they enhance the likelihood that information will be J OHN E. M ENDOZA
richly encoded, thus enhancing the chances that a free- Tulane University Medical Center
standing memory will be integrated with preexisting New Orleans, LA, USA
memories. For patients whose memory impairment
reflects impairment in effortful encoding and retrieval,
techniques that promote enhanced organization (e.g., Synonyms
chunking, thematic organization) and elaboration (e.g.,
verbal mnemonics, visual imagery) at the time of ALS; Spinothalamic tract
learning may be useful. In a sense, elaboration provides
the learner with alternative retrieval routes that may
enhance recall. Definition
One of two ascending pathways in the spinal cord that

carry conscious sensory information from the upper and
Cross References lower extremities, trunk, and posterior portion of the
head to the brain (the other being the lemniscal system).
Amnesia
Retrograde Amnesia
Current Knowledge
Of the two ascending somatosensory pathways (the

References and Readings other being the posterior columns or lemniscal system)
the anterolateral system (ALS) is the more primitive
Baddeley, A. D. (1995). The psychology of memory. In A. D. Baddeley, and polysynaptic and is primarily responsible for the
B. A. Wilson, & F. N. Watts (Eds.), Handbook of memory disorders
sensations of pain, temperature, and crude (less well
(pp. 325). New York: John Wiley & Sons.
Corkin, S. (1984). Lasting consequences of bilateral medial temporal
defined) or simple touch. Input into the ALS is derived
lobectomy: Clinical course and experimental findings in H. M. from both specialized cutaneous receptors and free
Seminars in Neurology, 4, 249259. nerve endings in the skin. These sensory impulses then
Eichenbaum, H. (2006). Memory binding in hippocampal travel centrally (toward the cord) in the peripheral
relational networks. In H. D. Zimmer, A. Mecklinger, & U. Linder-
nerves. Just outside the cord, the peripheral nerves
berger (Eds.), Handbook of binding and memory: Perspectives from
cognitive neuroscience (pp. 2551). New York: Oxford University
bifurcate into the dorsal and ventral nerve roots. The
Press. dorsal roots, which carry sensory information, then
Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuropsychologi- synapse in the gray matter of the cord (dorsal horns)
cal assessment (4th ed.). New York: Oxford University Press. on the same side in which they enter. Secondary fibers
Mayes, A. R., Holdstock, J. S., Isaac, C. L., Hunkin, N. M., & Roberts, N.
then cross the midline of the cord in the ventral white
(2002). Relative sparing of item recognition memory in a patient
with adult-onset damage limited to the hippocampus. Hippocampus,
commissure and ascend in the ventrallateral portion of
12, 325340. the spinal cord as the ventral and lateral spinothalamic
Squire, L. S. (1994). Declarative and nondeclarative memory: Multiple tracts. While these two tracts were once described as
brain systems supporting learning and memory. In D. L. Schacter, & carrying different and distinct types of sensory infor-
E. Tulving (Eds.), Memory systems 1994 (pp. 203232). Cambridge,
mation, the current thinking is that they have extensive
MA: MIT Press.
Verfaellie, M. (2000). Semantic learning in amnesia. In L. S. Cermak
functional overlap and hence should be considered as a
(Ed.), Handbook of neuropsychology (2nd ed., pp. 335354). single anterolateral system. These second-order fibers of
Amsterdam: Elsevier Science. the ALS ascend in the ventral lateral portion of the cord
Verfaellie, M., & Keane, M. M. (2002). Impaired and preserved memory and then in the lateral and later in the dorsolateral
processes in amnesia. In L. R. Squire, & D. L. Schacter (Eds.),
portions of the brainstem. These ascending pathways
Neuropsychology of memory (3rd ed., pp. 3546). New York: Guilford
Press.
continue to ventral posterior lateral nucleus of the thal-
Wechsler, D. (1997). WMS-III manual. New York: Psychological amus. From the thalamus, third-order neurons project
Corporation. to the somatosensory cortices in the parietal lobes of the
Anticholinergic A 195
brain. Because the nerve fibers making up the ALS cross Anticholinergic. Table 1 Anticholinergic medications
A
the midline within a few vertebral segments of where clinically used for the antimuscarinic effects
they enter the cord, lesions affecting the ALS will result
Medications for Oxybutynin (Ditropan),
in contralateral deficits. neurogenic bladder tolterodine (Detrol), trospium
including urge (Sanctura), solifenacin
incontinence, for (Vesicare), darifenacin
Cross References overactive bladder (Enablex)
Anticholinergic Benztropine (Cogentin),
Medial Lemniscus (Posterior Columns)
antiparkinsons medication trihexyphenidyl (Artane)
Antivertigo medication Meclizine (Antivert),
scopolamine (Transderm
References and Readings Scop)
Gastrointestinal Diphenoxylate/atropine
Mendoza, J. E., & Foundas, A. L. (2008). The somatosensory systems. In
antispasmodics (Lomotil), belladonna
J. E. Mendoza & A. L. Foundas (Eds.), Clinical neuroanatomy A
neurobehavioral approach (pp. 2347). New York: Springer.
medications (Donnatal)
Medications for Tiotropium (Spiriva),
bronchospasm ipratropium (Atrovent)
Anti-Anxiety Drugs
Anticholinergic. Table 2 Anticholinergic medications not
Anxiolytics primarily targeting the cholinergic receptors
Sedating Diphenhydramine (Benadryl),
antihistamines hydroxyzine (Vistaril), cyproheptadine
Anti-Anxiety Medications (Periactin)
Tricyclic Amoxaprine (Asendin), amytriptyline
Anxiolytics antidepressants (Elavil), desipramine (Norpramin),
imipramine (Tofranil), nortriptyline
(Pamelor)
Certain Clozapine (Clozeril), olanzapine
Anticholinergic antipsychotics (Zyprexia), risperidone (Risperdal)
Muscle relaxants Dantrolene (Dantrium), cyclobenzaprine
M ARY PAT M URPHY
(Flexeril)
MSN, CRRN
Paoli, PA, USA
blockers. The receptor subtypes affect the brain, salivary
glands, smooth muscle, and ciliary muscles of the eye.
Synonyms Categories of medications are clinically used for the
antimuscarinic effects and include medications for uri-
Anticholinergic medications
nary spasmodics and overactive bladder, anticholinergic
antiparkinsons agents, antivertigo medications, gastro-
Definition intestinal antispasmodics, mydriatic medications, and
medications for bronchospasm. Another group of med-
Anticholinergic agents alter the balance of neurotransmitters ications not primarily targeting the cholinergic receptors
in the central and peripheral nervous system inhibiting include sedating antihistamines, tricyclic antidepressants,
parasympathetic nerve impulses. Specifically, the agents muscle relaxants, some antipsychotics, antiarrythmics,
diminish acetylcholine and allow for the increase of and antiemetics. Neuropsychologists should be aware
dopamine. Anticholinergic medications are divided into of the medications their patients are taking and the
three categories based on their specific receptor targets in potential impact on neuropsychological test results. It
the nervous system and in other sites in the body: is necessary to differentiate between medication side-
antimuscarinic, ganglionic blockers, and neuromuscular effects and true consequences or neurologic disorder.
196 A Anticholinergic Medications
Current Knowledge clinical severity of delirium symptoms in older medical inpatients.

Archives of Internal Medicine, 161(8), 10991105.
Lieberman, J. A. (2004). Managing anticholinergic side effects. Journal of
Anticholinergic medications are used in treating a variety Clinical Psychiatry, 6(Suppl. 2), 2023.
of medical conditions. Anticholinergic drugs are used in
treating a variety of conditions including Parkinsons dis-
ease and other Parkinsonian-like disorders; gastrointestinal Anticholinergic Medications
disorders such as diverticulitis; respiratory disorders such
as asthma; and genitourinary disorders such as prostatitis. Anticholinergic
Side Effects
Anticholinesterase Inhibitors
Anticholinergic side effects can be caused by a wide range
of medications. Anticholinergic medications have periph- J OA NN T. T SCHANZ 1, K ATHERINE T REIBER 1,2
1
eral and central side effects including dry mouth, blurred Utah State University
vision, urinary retention or difficulty initiating voiding, Logan, UT, USA
2
constipation or bowel obstruction, decreased sweating, University of Massachusetts Medical School
increased heart rate, ataxia, increased body temperature, Worcester, MA, USA
agitation, confusion, delirium, memory impairment,
decreased attention, dizziness, and drowsiness.
Certain populations are at greater risk for adverse events Synonyms
related to anticholinergic medications. They include older
adults who already experience a decrease in acetylcholine Acetylcholinesterase inhibitors; ACHE inhibitors; AchEIs;
production; men with benign prostatic hypertrophy, Cholinesterase inhibitors
patients with glaucoma, and individuals with dementia
who are already taking cholinesterase inhibitors.
The elderly and patients with brain injury are often Definition
prescribed medications with anticholinergic properties to
address medical issues for bladder management, increased Anticholinesterase inhibitors are a class of substances that
muscle tone, and behavior (atypical antipsychotics). affect the cholinergic neurotransmitter system and are
There may be a cumulative effect of taking multiple often used for clinical purposes in the treatment of mem-
medications which act on the cholinergic system. ory disorders such as Alzheimers disease (AD). Nonclini-
Anticholinergic side effects in older adults include an cal uses include agricultural applications such as pesticides
increase in delirium, diminished ADLs, and decrease in and military applications such as the development of neu-
cognition (Fick et al., 2003; Han et al., 2001). rotoxins. Acetylcholine is normally released by the presyn-
patic neuron and activates receptors on the postsynaptic
cell. Acetylcholinesterase is the primary enzyme that breaks
Cross References down acetylcholine in the synaptic cleft. Cholinesterase
inhibitors block the activity of this enzyme, allowing the
Acetylcholine neurotransmitter substance to remain in the synaptic cleft
Dopamine longer to stimulate postsynaptic receptors.
Neurotransmitters
Current Knowledge
Clinical Indications
Fick, D. M., Cooper, J. W., Wade, W. E., Waller, J. L., Maclean, J. R., &
Beers, M. H. (2003). Updating the Beers criteria for potentially Cholinesterase inhibitors are often used in the treatment
inappropriate medication use in older adults: results of a US con-
of memory and other cognitive disorders. In AD, degener-
sensus panel of experts. Archives of Internal Medicine, 163(22),
27162724.
ation of brain cholinergic neurons has been associated
Han, L., McCusker, J., Cole, M., Abrahamowicz, M., Primeau, F., & Elie, with progressive cognitive deterioration. Because cholines-
M. (2001). Use of medications with anticholinergic effect predicts terase inhibitors do not reverse or stop the progressive
Anticoagulation A 197
degeneration of cholinergic neurons, their effectiveness is

Anticoagulation A
greatest early in the course of the disease, while existing
neurons are able to continue to produce and release ace-
tylcholine (Orgogozo, 2003). Other compounds such as E LLIOT J. R OTH
memantine (which acts on the glutamatergic system) have Northwestern University
been approved for use in moderate to severe dementia. Chicago, IL, USA
Formulation and Side Effects Synonyms

Several cholinesterase inhibitors are available, such as Antithrombotic therapy
donepezil, galantamine, and rivastigmine. The primary
mode of intake is oral, although a cutaneous route through
a dermal patch has been developed. Common side effects
Definition
of cholinesterase inhibitors include nausea, vomiting, di-
arrhea, and anorexia. Less common are insomnia and
Anticoagulation refers to the prevention of blood from
cardiovascular symptoms such as bradycardia. Drug toler-
clotting.
ability may be enhanced by varying dosing and titration
rates to achieve therapeutic levels (Orgogozo, 2003).
Current Knowledge
Other Applications
An anticoagulant is a chemical that prevents coagulation.
In addition to its distribution in the brain, acetylcholine is The body contains a number of naturally occurring phys-
also present at the neuromuscular junction and plays an iological anticoagulants, but other anticoagulants are used
important role in the bodys motor functions. Cholines- as pharmacological agents to prevent and treat thrombotic
terase inhibitors developed for agricultural or military disorders such as coronary artery disease causing ischemic
applications may affect the motor system by causing an heart disease, cerebrovascular disease causing stroke, pe-
accumulation of acetylcholine at the neuromuscular junc- ripheral arterial disease causing limb ischemia, and venous
tion leading to excessive excitation of muscles and a thromboembolic disease.
cessation of muscle contraction (due to overexcitation). Commonly used anticoagulation medications in-
Autonomic functions may also be affected due to cholin- clude warfarin (Coumadin), heparin, and low molecu-
ergic innervation of cardiac and smooth muscles. Thus, lar weight heparin compounds such as enoxaparin
cholinesterase inhibitors are potent neurotoxins that are (Lovenox), tinzaparin (Innohep), and dalteparin
used as insecticides or in warfare (Iversen, Iversen, Bloom, (Fragmin).
& Roth, 2009). New anticoagulants are under development. Dosages
of these medications can be adjusted using blood tests
that measure the levels of certain clotting functions,
Cross References which can be used to monitor the effectiveness of the
medication regimen. Optimum ranges for the results of
Acetylcholine these tests are available for specific conditions and clini-
Alzheimers Disease cal situations.
Predictably, adverse effects of these medications are
References and Readings largely hemorrhagic in nature. Prolonged bleeding from
simple superficial lacerations, internal hemorrhage into
Iversen, L. L., Iversen, S. D., Bloom, F. E., & Roth, R. H. (2009). Acetyl- gastrointestinal system, brain, or muscles in the pelvis or
choline. Introduction to neuropsychopharmacology (pp. 128149). leg occurs with greater frequency, depending on the level
New York: Oxford University Press. of anticoagulation. Rarely, a paradoxical thrombotic
Orgogozo, J.-M. (2003). Treatment of Alzheimers disease with disorder might occur as a result of using one of these
cholinesterase inhibitors. An update on currently used drugs. In
medications. On balance, the benefits of using certain
K. Iqbal, & B. Winblad (Eds.), Alzheimers disease and related
disorders: Research advances (pp. 663675). Bucharest: Ana Asian anticoagulants in selected situations outweigh the risks
International Academy of Aging. of the medications, but primarily in controlled
198 A Anticonvulsants
circumstances when clinical and laboratory monitoring is monotherapy is the goal for the treatment of epilepsy,
feasible and when the patient does not have risk of falls, choosing medications targeting seizure control with
injuries, or other contraindications. fewest side effects. Monotherapy also makes it easier to
monitor side effects. Usually, if one drug fails, another
medication is trialed. If the initial AED fails, the physician
Cross References typically will wean this medication and try another first-
line drug. If monotherapy fails, polytherapy may be tried.
Atherosclerosis The physician will maximize the first-line dose and then
Central Venous Thrombosis add a second-line medication. General monitoring for
Cerebral Embolism AEDs includes the frequency and severity of seizures,
Heparin adverse events and side effects, and monitoring of plasma.
Thrombosis The chart below identifies FDA indications for commonly
Venous Thrombosis used AEDs.
Warfarin
Mechanism of Action for AEDs

Phenytoin, carbamazepine, lamotrigine, gabapentin,
Dentali, F., Douketis, J. D., Gianni, M., Lim, W., Crowther, M. A. (2007) topiramate, and valproate block sodium channel and
Meta-analysis: Anticoagulant prophylaxis to prevent symptomatic impede generation of high-frequency action potentials.
venous thromboembolism in hospitalized medical patients. Annals Some of the drugs may also reduce high-threshold calci-
of Internal Medicine, 146, 278288.
Hirsh, J., Guyatt, G., Albers, G. W., Harrington, R., Schunemann, H. J.
um currents, resulting in a decrease in excitatory trans-
(2008). Executive summary: antithromotic and thrombolytic thera- mitter release. In therapeutic ranges, barbiturates and
py, 8th Edition: American College of Chest Physicians evidence- diazepam derivatives enhance GABA responses. Topira-
based clinical practice guidelines. Chest, 133, 71S105S. mate may enhance GABAergic inhibition. Gabapetin may
promote nonsynaptic GABA release. Phenobarbital is a
long-acting barbiturate with sedative, hypnotic, and
anticonvulsant properties. It acts on the GABA receptors,
increasing synaptic inhibition. This has the effect of
Anticonvulsants
M ARY PAT M URPHY Anticonvulsants. Table 1 Commonly used AED
MSN, CRRN
Partial seizures Tonicclonic Absence
Paoli, PA, USA
First-line drugs Carbamazepine Valproate Ethosuximide
Phenytoin Phenytoin Valproate
Synonyms Valproate Carbamazepine
Topiramate Topiramate
Antiepileptic drugs (AED) Second-line
drugs
(alternative
therapy)
Definition Primidone Lamotrigine
Gabapentin Gabapentin
A group of medications used in the management of Phenobarbital Primidone Clonazepam
epilepsy. Primidone Phenobarbital Primidone
Valproate Topiramate
Felbamate Felbamate
Current Knowledge (use when other (use when other
alternative alternative
The selection of an AED depends on the type of seizure, medications medications
have failed) have failed)
age of patient, and gender. According to the literature,
Anticonvulsants A 199
elevating the seizure threshold and reducing the spread of hypontension, bradycardia, dysrhythmias, and cardiac
A
seizure activity in the brain. Phenobarbital may also in- changes, as well as venous irritation and
hibit calcium channels. thrombophlebitis.
Other adverse events/side effects include gingival
hyperplasia, hirstism, rash, hepatitis, megaloblastic
First-Line Medications anemia, thrombocytopenia, StevensJohnson syndrome,
systemic lupus Erythematosus, and folic acid deficiency.
Valproate (Depakote)
Drug interactions
Indication Drug interactions are many and include (but are not
Labeled indications include control of epilepsy (seizures limited to) chloramphenicol, dexamethasone, doxycycline,
disorders). As an AED, it can be used as monotherapy and furosemide, haloperidol, meperidine, methadone, oral
adjunctive treatment of tonicclonic, partial complex contraceptives, theophylline, and warfarin. Non-AEDs
seizures, and simple and complex absence seizures. It that effect phenytoin levels include alcohol, antacids, folic
can be used as an adjunctive treatment in patients who acid, rifampin, tube feedings, alcohol, cimetidine,
have multiple types of seizures. fluoxetine, imipramine, INH, omeprazole, propoxyphene,
sulfonamides, and trazadone.
Contraindications
The medication should be prescribed cautiously for Carbamazepine (Tegretol)
individuals with liver disease and urea cycle disorders
and for pregnant women. Indication
Carbamazepine is indicated as a first-line drug for use as
Adverse events/side effects an anticonvulsant for partial seizures, generalized tonic
Weight gain, thrombocytopenia, and elevated liver clonic, and mixed seizures, but not absence seizures. It is
enzymes may be dose related. When initially starting generally nonsedating within therapeutic range. It is also
the medication, patients may complain of nausea and indicated in the treatment of trigeminal neuralgia.
diarrhea. Hyperammonemia has been reported and may
be present despite normal liver function testing. In the Adverse events/side effects
elderly, there is a possible increase in somnolence. Adverse events associated with carbamazepine include
aplastic anemia and agranulocytosis. Pretreatment hema-
Drug interactions tology testing should be completed to obtain a baseline.
Medications that may increase valproate levels include The patient should be monitored and treatment should be
felbamate, rifampin, and chlorpromazine; medications that discontinued with hematology changes. StevensJohnson
valproate may affect include carbamazepine, amitriptyline, syndrome (an exfoliating dermatitis) has been reported.
nortriptyline, clonazepam, ethosuximide, lamotrigine, Carbamazepine has mild anticholinergic properties, so
phenobarbital, phenytoin, tolbutamide, and lorazepam. patients with intraocular eye pressure should be moni-
tored. Carbamazepine should not be used in pregnant
Phenytoin (Dilantin) women. Patients should be cautioned against drinking
alcohol.
Indication In the beginning of treatment, patients report side
Phenytoin is the oldest and one of the most effective effects including dizziness, drowsiness, nausea, and
medications in the treatment of a wide range of seizure vomiting.
types. The labeled use is for tonicclonic and partial
complex seizures. It is often used as a first-line drug Medications that affect carbamazepine plasma
choice for monotherapy. The usual dose is 300 to 400 levels
mg/day. An extended-release capsule allows for onetime a Drugs that increase plasma levels include cimetidine,
day dosing. The therapeutic range is 1020. danazol, macrolides, erythromycin, troleandomycin,
fluoxitine, nefazoned, loratadine, terfenadine, INH,
Adverse events/side effects propoxyphene, verapamil, grapedfruit juice, protease
Phenytoin can be administered intravenously. As a result, inhibitors, and valproate. Medications that decrease
specific adverse events/side effects can include carbamazepine plasma levels include cisplatin, felbamate,
200 A Anticonvulsants
rifampin, phenobarbital, phenytoin, primidone, meth- Lamotrigine (Lamictal)

suximide, and theophylline.
Lamotrigine is effective as monotherapy for individuals
with partial complex seizures; it is also considered
Topamax (Topiramate) effective as an adjunctive therapy for partial complex
seizures and generalized tonicclonic seizures. It is
Topiramate is considered effective as a monotherapy for thought to inhibit voltage-sensitive sodium channel
individuals with partial complex or generalized tonic mechanisms. It is well tolerated and does not seem to
clonic seizures. It is also effective as an adjunctive treatment have cognitive altering side effects. A therapeutic plasma
for partial complex and generalized tonicclonic seizures. concentration has not been established for lamotrigine.
Adverse events/side effects Side effects/adverse events

Metabolic acidosis is an adverse event associated Include rash, fatigue, dizziness, diplopia, and ataxia.
with topiramate. Conditions that predispose individuals Angioedema, nystagmus, and hematuria also may occur.
include renal disease, severe respiratory disorders, status
epilepticus, and diarrhea. Measurement of baseline and Drug interactions
periodic sodium bicarbonate is recommended. Other side Medications that decrease lamotrigines effectiveness
effects/adverse events include kidney stones, paresthesia include carbamazepine, valproate, phenobarbital, primi-
of the extremities, acute myopia and glaucoma, decreased done, and acetaminophen.
sweating and hyperthermia, cognitive-related dysfunc- Febamate (Felbatol) has been approved for adjunc-
tion, psychiatric/behavioral disturbances, and somno- tive therapy or monotherapy for individuals with partial
lence or fatigue. complex or tonicclonic seizures. This medication is
recommended when other therapies have been tried and
Drug interactions have failed.
Concomitant administration of topiramate and valproate
has been associated with hyperammonia. Topiramate con- Adverse events/side effects
centrations affect phenytoin and valproate. Topiramate This medication potentially causes aplastic anemia or
concentrations are affected by phenytoin, carbamazepine, hepatotoxicity and should be used with extreme care by
valproate, and lamotrigine. a knowledgeable physician when other therapies have
Ethosuximide (Zarontin) has been approved for been tried. Other side effects/adverse events include
absence (petit mal) seizures. Adverse events/side effects anorexia, vomiting, and insomnia.
include blood dyscrasias; decreased cognition including
drowsiness, dizziness, irritability, hyperactivity, and Drug interactions
fatigue; and ataxia. There have been reports of increased Felbatol affects phenytoin, valproate, and carbamazepine
tonicclonic seizures. concentrations.
Second-Line Medications
Barbiturates (Second Line)
Gabapentin (Neurontin)
Phenobarbital
Gabapentin is effective as an adjunctive therapy in the treat-
ment of partial seizures with and without generalization.
Indication
Labeled indications include control of epilepsy (seizures
disorders) and as a sedative/hypnotic medication for
Adverse events/side effects short-term treatment of insomnia. As an AED, it can be
Include dizziness, ataxia, weight gain, gi upset, somno-
used as monotherapy in the treatment of generalized
lence, and other symptoms of CNS depression.
(tonicclonic), simple, or partial complex seizures; for
myoclonic epilepsy; and for neonatal and febrile seizures
Drug interactions in children. It has also been prescribed for eclamptic
Antacids decrease their bioavailability. seizures during pregnancy.
Antidepressants A 201
Contraindications tachycardia, chest pain, headache, constipation, nausea,

A
The medication should be prescribed cautiously for and ataxia.
individuals with liver disease, CHF, and hypovolemic Medications include the following:
shock and for pregnant women. The medication does Clonazepam (Klonopin) is effective as an adjunctive
cause both physical and psychological drug dependence; medication for individuals with absence, tonicclonic, and
for this reason, it is not a first-line medication of choice myoclonic seizures. Diazepam (Valium) and Lorazepam
for individuals with drug dependence. If prescribed for (Ativan) can be used to treat status epilepticus.
sleep, it should not be used longer than 2 weeks and
prescribed for the elderly because of its long half-life.
Patients should avoid alcohol and other CNS depressants Cross References
while taking phenobarbital. Other contraindications in-
clude preexisting CNS depression, severe uncontrolled Epilepsy
pain (may mask symptoms) porphyria, and severe GABA
respiratory disease with obstruction or dyspnea. Abrupt Seizure
discontinuation may cause seizures.

Adverse events/side effects
Adverse affects include sedation, ataxia, cognitive
Lanctot, K., Herrmann, N., Mazzotta, P., Khan, L., & Ingber, N. (2004).
impairment, may cause a paradoxical effect including GABAergic function in Alzheimers disease: Evidence for
hyperactivity and problems with sleep, megablastic dysfunction and potential as a therapeutic target for the treatment
anemia (responds to folic acid) and rash, exfoliative of behavioural and psychological symptoms of Dementia. Canadian
dermatitis and Stevens-Johnson Syndrome. Journal of Psychiatry, 49(7), 439453.
MacQueen, G., & Young, T. (2003). Cognitive effects of atypical
antipsychotics: focus on bipolar spectrum disorders. Bipolar
Non-AEDs affected by phenobarbital Disorders, 5, 5361.
Phenobarbital may interfere with the effectiveness of acet- Yasseen, B., Colantonio, A., & Ratcliff, G. (2008). Prescription medication
aminophen and increase liver damage. The effectiveness of use in persons many years following traumatic brain injury. Brain
beta-blockers except Atenolol, Levobunolol, Metiprano- Injury, 22(10), 752757.
lol, and Nadolol, oral contraceptives, chloramphenicol,
chlorpromazine, cimetidine, corticosteroids, cyclospor-
ine, desipramine, doxycycline, folic acid, griseofulvin,
haloperidol, meperidine, methadone, nortriptyline, quin- Antidepressant Responsive
idine, theophylline, and warfarin may be compromised
when taking phenobarbital.
Disorders
Unexplained Illness
Non-AEDs affecting phenobarbital levels
Chloramphenicol, propoxyphene, and quinine may in-
crease phenobarbital levels. Chlorpromazine, folic acid,
and prochlorperazine may decrease phenobarbital levels.
There may be increased toxicity with benzodiazapines, Antidepressants
CNS depressants, and methylphenidate.
Primidone (Mysoline) is related in structure to barbi- J OA NN T. T SCHANZ 1, K ATHERINE T REIBER 1,2
1
turates. It is used in the management of tonicclonic, partial Utah State University
complex, and focal seizures. The adverse events/side affects Logan, UT, USA
2
and drug interactions are similar to phenobarbital. University of Massachusetts Medical School
Worcester, MA, USA
Benzodiazepines
Definition
This class of medication is not typically used as first-line
medications. As a class, they can produce CNS depression Antidepressants are a class of medications that are
and behavioral changes. Other adverse reactions include used primarily in the treatment of clinically severe
202 A Antidepressants
mood or anxiety disorders. The majority of effective orthostatic hypotension, and weight gain. A concern with
antidepressants currently in use enhance neurotrans- this medication is the narrow therapeutic index, which
mission of serotonin and/or norepinephrine. General- raises the risk of death with overdose. SSRIs do not carry
ly, this is achieved by blocking the reuptake of the the same health concerns as MAOIs or TCAs. Common
neurotransmitter substance(s), inhibiting the enzymes side effects of SSRIs include nausea and sexual dysfunc-
responsible for its metabolism, or directly stimulating tion. A topic of much controversy is a possible increase in
the postsynaptic receptors (Iversen, Iversen, Bloom, & risk of suicidal ideation and behavior (see Current Knowl-
Roth, 2009). Several antidepressants are also used in edge). Side effects reported with mixed SSRINRIs (e.g.,
treating generalized anxiety disorder, panic disorder, and velaxafine), include headache, dry mouth, sedation, hyper-
obsessivecompulsive disorder (Bourin & Lambert, tension, and constipation (Iversen et al., 2009).
2002). Other conditions for which antidepressants have
demonstrated efficacy include eating disorders (Powers &
Bruty, 2009), neuropathic pain (OConnor & Dworkin, Current Knowledge
2009), stress incontinence, nocturnal eneuresis, ejaculatory
disorders (Michel, Ruhe, de Groot, Castro, & Oelke, 2006), Approximately 6070% of persons treated with antide-
migraine headaches, fibromyalgia (Stone, Viera, & Parman, pressants show a positive response. The lack of response in
2003), attention-deficit/hyperactivity disorder (Chung, 3040% of depressed individuals (at least to SSRIs) may
Suzuki, & McGough, 2002), smoking, insomnia, and pos- be due in part to the effects of genes. Variations in the
sibly pathological gambling (Grant & Grosz, 2004). serotonin transporter gene (often referred to as
There are several classes of antidepressant medica- 5-HTTLPR) modify the response of depressed persons
tions. Tricyclic antidepressants (TCAs) block the reuptake to SSRIs. Compared to those with a long (L) allele of
of monoaminergic neurotransmitters and monoamine this gene, persons with a short allele exhibit poorer
oxidase inhibitors (MAOIs) inhibit their metabolism. response to SSRI treatment. Variations in 5-HTTLPR
Other compounds are more selective in blocking the may also influence the experience of side effects
reuptake of specific neurotransmitters (selective serotonin (Horstmann & Binder, 2009).
reuptake inhibitors or SSRIs and noradrenergic reuptake The response rate to placebo in clinical trials of
inhibitors or NRIs). Compounds with dual serotonergic antidepressants is relatively high, ranging from 30 to
and noradrenergic actions have also been developed 50%. The placebo response is greater among individuals
(Iversen et al., 2009). with mild depressive symptoms, and recent meta-analyses
Regardless of the type of antidepressant, the com- of clinical trials of second-generation antidepressants
pounds are similar in their effectiveness and the time indicate significant treatment effects only among those
course of their effects. The lag between the initiation of with severe symptoms (Fournier et al., 2010; Kirsch
antidepressant treatment and the alleviation of symptoms et al., 2008).
generally takes 26 weeks for the maximal response. The Significant concerns of an increased risk of suicidal
delay in treatment response suggests that the therapeutic ideation and behavior (suicidality) have arisen over
effects may result from downstream events that reflect the use of new-generation antidepressants. The US Food
the brains adaptation to treatment (Iversen et al., 2009). and Drug Administration (FDA) has released several
Alternative treatments with a shorter treatment lag are advisories that antidepressant use may increase the risk
under active investigation (see Future Directions). of suicidality among children, adolescents, and young
Antidepressant medications differ in their profile of adults (http://www.fda.gov/NewsEvents/Newsroom/Press
side effects. First-generation MAOIs, which inhibit the Announcements/2007/ucm108905.htm). A meta-analysis
activity of both MAO-A and MAO-B, were known for of clinical trial data with SSRIs has confirmed a moderate
potentially serious side effects if patients also consumed increase in risk of suicidality among pediatric patients
foods containing tyramine (fermented products such as (Hammad, Laughren, & Racoosin, 2006). These observa-
wine or cheese). Potential effects included headache, tions are in contrast to epidemiological data that indicate
hypertension, cerebral hemorrhage, and death. Newer- reduced rates of completed suicides. Some have hypothes
generation MAOIs that act more selectively on MAO-A ized that the higher risk of suicidality with antidepressant
do not require the dietary restriction from tyramine- treatment likely occurs in a subset of high-risk patients
containing foods. Common side effects associated with with agitated major depression or unrecognized bipolar
TCAs include dry mouth, urinary retention, sedation, disorder (Rihmer & Akiskal, 2006).
Antihistamines A 203
Future Directions Horstmann, S., & Binder, E. B. (2009). Pharmacogenomics of antidepres-

A
sant drugs. Pharmacology and Therapeutics, 124, 5773.
Iversen, L. L., Iversen, S. D., Bloom, F. E., & Roth, R. H. (2009). Anti-
More research is needed to examine the safety of antide- depressants and Anxiolytics. Introduction to Neuropsychopharmacol-
pressant treatment in pediatric and young adult popula- ogy (pp. 306335). New York: Oxford University Press.
tions. Thorough characterization of patients may help Kirsch, I., Deacon, B. J., Huedo-Medina, T. B., Scoboria, A., Moore, T. J.,
clarify whether certain subgroups are more vulnerable to Johnson, B. T. (2008). Initial severity and antidepressant benefits:
A meta-analysis of data submitted to the food and Drug
develop suicidal behaviors while receiving antidepres-
Administration. PlOS Medicine, 5, e45.
sants. Additionally, antidepressants are not effective for Michel, M. C., Ruhe, H. G., de Groot, A. A., Castro, R., & Oelke, M.
3040% of depressed patients. Current work is exploring (2006). Tolerability of amine uptake inhibitors in urologic diseases.
alternative treatments, for example, testing antagonists of Current Drug Safety, 1, 7385.
NMDA glutamate receptors for an antidepressant effect. OConnor, A. B., & Dworkin, R. H. (2009). Treatment of neuropathic
pain: An overview of recent guidelines. American Journal of
This approach stems from observations in animal models
Medicine, 122(Suppl. 10), S2232.
that exposure to an inescapable stressor (shock) produces Powers, P. S., & Bruty, H. (2009). Pharmacotherapy for eating disorders
learned helplessness and also disrupts long-term potenti- and obesity. Child Adolescent Psychiatric Clinics of North America, 18,
ation in the hippocampus, an NMDA-dependent process. 175187.
It is hypothesized that NMDA receptors may also play a Rihmer, Z., & Akiskal, H. (2006). Do antidepressants t(h)reat(en)
depressives? Toward a clinical judicious formulation of the antide-
role in the development of learned helplessness, and simi-
pressant-suicidality FDA advisory in light of declining national
lar to the effects of antidepressants, antagonism of these suicide statistics from many countries. Journal of Affective Disorders,
receptors may block its development. Initial clinical stud- 94, 313.
ies with ketamine, an NMDA antagonist, show a signifi- Skolnick, P., Popik, P., & Trullas, R. (2009). Glutamate-based antidepres-
cant antidepressant effect within 2 h. In addition to a sants: 20 years on. Trends in Pharmacological Sciences, 30, 563569.
Stone, K. J., Viera, A. J., & Parman, C. L. (2003). Off-label applications for
more rapid treatment effect, it is hoped that glutamate-
SSRIs. American Family Physician, 68, 498504.
based therapies will alleviate depressive symptoms among
those unresponsive to current treatments (Skolnick,
Popik, & Trullas, 2009).
Antiepileptic Drugs (AED)

Cross References Anticonvulsants
Depression
Selective Serotonin Reuptake Inhibitors (SSRIs)
Serotonin Antihistamines
S TEPHANIE A. KOLAKOWSKY-H AYNER
Santa Clara Valley Medical Center,
References and Readings Rehabilitation Research Center
San Jose, CA, USA
Bourin, M., & Lambert, O. (2002). Pharmacotherapy of anxious disorders.
Human Psychopharmacology: Clinical Experimental, 17, 383400.
Chung, B., Suzuki, A. R., & McGough, J. J. (2002). New drugs for
treatment of attention-deficit/hyperactivity disorder. Expert Opinion Synonyms
Emerging Drugs, 7, 269276.
FDA Press Release. Extracted from http://www.fda.gov/NewsEvents/ Histamine antagonist; Inverse histamine agonists
Newsroom/PressAnnouncements/2007/ucm108905.htm on 1/21/2010
Fournier, J. C., DeRubeis, R. J., Hollon, S. D., Dimidjian, S., Amsterdam,
J. D., Shelton, R. C., et al. (2010). Antidepressant drug effects and
depression severity: A patient-level meta-analysis. JAMA, 303, 4753. Definition
Grant, J. E., & Grosz, R. (2004). Pharmacotherapy outcome in older
pathological gamblers: A preliminary investigation. Journal of Antihistamines are commonly used to treat allergies; H1
Geriatric Psychiatry and Neurology, 17, 912.
Hammad, T. A., Laughren, T., & Racoosin, J. (2006). Suicidality in
receptor inverse agonists typically reduce swelling and
pediatric patients treated with antidepressant drugs. Archives of vasodilation within the nasal area. H1 receptor antagonists
General Psychiatry, 63, 332339. include cetirizine, diphenhydramine also known as
204 A Antihypertensives
benadryl, desloratadine, doxylamine, ebastine, fexofena-

dine, loratadine, pheniramine, and promethazine. H2 in- Antihypertensives
verse agonists reduce gastric acid and are used to treat
ulcers and reflux. H2 receptor antagonists include cimeti- M ARY PAT M URPHY
dine, famotidine, lafutidine, nizatidine, ranitidine, and MSN, CRRN
roxatidine. H3 and H4 receptor antagonists are experi- Paoli, PA, USA
mental in nature and are being investigated for their
cognitive enhancing and immunomodulation abilities.
Additionally, antihistamines may be used to treat off- Definition
label issues such as motion sickness, anxiety, and
insomnia. Antihypertensives are pharmacologic agents used to lower
Neuropsychologists must be aware of the potential blood pressure to normal levels or near normal levels. The
effects of antihistamines on the physical, emotional, and initiation and intensity of drug treatment depends on blood
cognitive functioning of their patients. Side effects of pressure level, the individuals risk factors (smoking,
antihistamine use may include dry nose and mouth, dyslipidemia, diabetes mellitus, older than 60, male, post-
drowsiness, dizziness, headache, upset stomach, loss of menopausal women, and family history of cardiovascular
appetite, irritability, motor slowness, diminished proces- disease for women under 65 and men under 55 years of age),
sing speed, and impaired visual skills. Antihistamine and target organ damage (e.g., stroke or TIA, ne-
effects are exacerbated by the use of alcohol and other phropathy, peripheral artery disease, retinopathy)
substances, which in turn will be of further detriment to or cardiovascular disease. Cardiovascular risks decrease
neuropsychological testing. when the blood pressure is below 139/89. Typical agents
for treating hypertension include diuretics, beta-blockers,
ACE (angiotensin converting enzyme) inhibitors, calcium
Cross References channel blockers, peripheral alpha selective blockers, cen-
tral alpha2 agonists, direct vasodilators, and adrenergic
Pharmacodynamics antagonists.
Pharmacokinetics
Psychopharmacology
Current Knowledge
Hypertension is a risk factor for stroke, myocardial infarc-
tion, renal failure, congestive heart failure, progressive
Hindmarch, I., & Shamsi, Z. (1999). Antihistamines: Models to assess
sedative properties, assessment of sedation, safety and other side-
atherosclerosis, and dementia. Treatment reduces the
effects. Clinical & Experimental Allergy, 29, 133142. risks of heart disease as well as cardiovascular morbidity.
Parsons, M., & Ganellin, C. (2006). Histamine and its receptors. British For Stage I hypertension, the blood pressure ranges from
Journal of Pharmacology, 147, S127S135. 140/90 to 159/99; Stage II and Stage III blood pressure, the
Theunissen, E., Vermeeren, A., van Oers, A., van Maris, I., & Ramaekers, J.
systolic number is greater than 160 and diastolic is greater
(2004). A dose-ranging study of the effects of mequitazine on actual
driving, memory and psychomotor performance as compared to
than 100.
dexchlorpheniramine, cetirizine and placebo. Clinical & Experimen- Monotherapy is preferred initially. The first line of
tal Allergy, 34(2), 250258. treatment is beta-blockers and diuretics for uncomplicated
van Ruitenbeek, P., Vermeeren, A., Smulders, F., Sambeth, A., & Riedel, W. hypertension individuals who do not have preexisting
(2009). Histamine H1 receptor blockade predominantly impairs
coronary disease, diabetes, or proteinuria. In patients
sensory processes in human sensorimotor performance. British
Journal of Pharmacology, 157(1), 7685.
with diabetes mellitus, renal disease or CHF, ACE
Vuurman, E., Rikken, G., Muntjewerff, N., de Halleux, F., & Ramaekers, J. inhibitors and angiotensin receptor antagonists are the
(2004). Effects of desloratadine, diphenhydramine, and placebo on appropriate initial therapy. Typically, the patient is started
driving performance and psychomotor performance measurements. on a low dose of long-acting, once daily drug, and the
European Journal of Clinical Pharmacology, 60(5), 307313.
dose is titrated until the blood pressure is lowered. If
Zlomuzica, A., Ruocco, L., Sadile, A., Huston, J., & Dere, E. (2009).
Histamine H1 receptor knockout mice exhibit impaired spatial mem-
blood pressure is not controlled with the dose of a
ory in the eight-arm radial maze. British Journal of Pharmacology, 157 single drug, a second agent from a different class is
(1), 8691. recommended. Combination therapy provides more
Antihypertensives A 205
rapid control of hypertension and is recommended for Beta-blockers should not be discontinued abruptly but
A
patients with stages II and III hypertension. Triple-drug should be tapered over 14 days to prevent withdrawal
therapy may be required if the blood pressure control is which includes unstable angina, myocardial infarction,
not achieved. Some patients have resistant hypertension. and death.
A fourth line of medications may be required.
ACE Inhibitors
This class of antihypertensives inhibits ACE which
Classes of Antihypertensives converts angiotensin I to II a potent vasoconstrictor.
This is a first-line therapy for patients with diabetes and
Diuretics proteinuria. Mediations include Lotensin, Capoten,
Diuretics decrease blood pressure by causing diuresis, Vasotec, Monopril, Zestril, Univasc, Accupril, Altace, and
which results in decreased blood volume, cardiac output, Mavik.
and stroke volume. They fall into three categories: Side effects include cough, hypotension, hyperkalemia,
thiazides, loop diuretics, and potassium-sparing diuretics. rash, loss of taste, leukopenia, and neutropenia. They are
Thiazides onset of action occurs within 23 h. Their half- contraindicated in pregnancy and for patients with
life is 812 h allowing for once daily dosing. Trade names bilateral real artery stenosis.
include Hygroton, Hydrodiuril, Lozol, and Zaroxolyn.
Loop diuretics act in the loop of Henle in the kidney Calcium Channel Blockers
and are less effective in the long term. Their duration is Calcium channel blockers relax the cardiac and smooth
6 h. These agents are indicated with CHF or nephrotic muscle by blocking calcium channels that allow calcium
syndrome. Bumex, Edecrin, Lasix, and Demadex are trade into the cells. The result is vasodilation. They also
names. decrease the heart rate and slow cardiac conduction.
Potassium-sparing agents cause minimal diuresis Medications include Calan, Cardizem, Norvasc, Plendil,
and are relatively ineffective in lowering the blood pres- Procardia Cardene, Sular, and DynaCirc.
sure. The medications correct thiazide-induced potassium
and magnesium losses. Medication trade names include Side Effects
Midamor, Aldactone, and Dyrenium. Side effects include GI upset, edema, and hypotension.
Rare side effects include bradycardia, CHF, and AV
Adverse Events block. Other adverse effects include dizziness, headache,
Most complications occur related to dose and duration of shortness of breath, gingival hyperplasia, and edema.
use. Hypokalemia is a side effect, but can be managed
with potassium chloride or use of potassium-sparing Contraindications
agents. Calcium channel blockers should not be prescribed for
Acute gouty arthritis, muscle cramps, development of individuals with second- and third-degree heart block or
diabetes, nocturia or incontinence, and sun sensitivity left ventricular dysfunction.
have been noted as clinical side effects.
Other Classes of Antihypertensives
Beta-Blocking Agents Peripheral alpha1- receptors (Cardura, Minipress, and
Beta1-receptors are located in the heart and kidneys and Hytrin), central alpha2 (Clonidine, Aldomet, Tenex,
regulate heart rate and cardiac contractility. Beta2- and Wytension), direct vasodilators (Apresoline and
receptors regulate bronchodilation and vasodilation. Loniten), and adrenergic antagonists (Serpasil, Ismelin
Beta-blockers decrease blood pressure by blocking the and Hylorel) are the remaining categories of antihyper-
beta-receptors. Some beta-blockers are cardioselective tensives. They are mainly used as second- and third-line
that is, they do not block the beta2-receptors, therefore medications.
do not cause bronchoconstriction. These medications
include Lopressor, Kerlone, Tenormin, Sectral and Zebeta,
Corgard, Inderal, and Cartrol. Cross References
Side Effects Psychopharmacology
The most common side effects of beta-blockers are Stroke
fatigue, dizziness, bronchospasm, nausea, and vomiting. Transient Ischemic Attack (TIA)
206 A Antiplatelet Therapy
References and Readings attack and stroke in certain situations, for primary and
secondary prevention. This favorable effect is based on
August, P. (2003). Initial treatment of hypertension. New England Journal the ability of these agents to inhibit the chemicals that
of Medicine, 348, 610617. cause platelets to clump together initiating blood clot
Cranwell-Bruce, L. (2008). Antihypertensives. MEDSURG Nursing, 17(5),
formation.
337341.
Ernst, M., & Moser M. (2009). Use of diuretics in patients with
Aspirin is the prototypical antiplatelet agent. Other
hypertension. New England Journal of Medicine, 361, 21532164. currently available antiplatelet agents include ticlopidine
Houston, M. C., Pulliam Meador, B., & Moore Schipani, L. (2000). (Ticlid), clopidogrel (Plavix), and dipyridamole
Handbook of antihypertensive therapy (10th ed.). Philadelphia: (Persantine).
Hanley & Belfus.
Staessen, J., & Birkenhager, W. (2005). Evidence that new antihypertensives
are superior to older drugs. Lancet, 366(9489), 869871. Cross References
Atherosclerosis
Antiplatelet Therapy Cerebrovascular Disease
Coronary Disease
E LLIOT J. R OTH Ischemic Stroke
Northwestern University Myocardial Infarction
Chicago, IL, USA Peripheral Vascular Disease
Stent
Thrombosis
Definition
Antiplatelet therapy uses specific pharmacological agents
(antiplatelet agents) to inhibit the ability of platelets to
Tran, H., & Anand, S. S. (2004). Oral antiplatelet therapy in cerebrovas-
clump together to form blood clots, or thromboses, pri- cular disease, coronary artery disease, and peripheral arterial disease.
marily in arteries. It is commonly used in people with JAMA, 292, 18671874.
atherosclerosis (narrowing of the arteries).
Current Knowledge Antipsychotic

Platelets are naturally occurring cells (actually, portions of Neuroleptics
cells) that circulate in the blood. They clump, or aggregate,
under certain conditions to initiate the formation of blood
clots. These platelet clumps are then further bound togeth-
er by the protein, fibrin. Together, the fibrin and the platelet
Antipsychotic Medications
clump comprise the thrombus or blood clot. Thrombi are
Antipsychotics
useful in that they stop bleeding in normal circumstances.
When there is a break in an artery, allowing blood to leave
the vessel, platelets become activated by attaching to the
wall of the blood vessel at the site of the bleeding, and by Antipsychotics
attracting fibrin and other coagulation factors to the area to
stop the bleeding. However, if the blood clot forms inside H ELEN M. C ARMINE
the artery, it can block the flow of blood to the tissue that ReMed
is supplied by the artery, which can result in tissue dam- Paoli, PA, USA
age. A clot forming in the coronary artery causes ischemic
heart disease (which may present as angina or myocardial
infarction), and when the blood clot forms in the carotid Synonyms
or cerebral arteries, it may cause a stroke.
Many studies have demonstrated the effectiveness of Antipsychotic medications; Atypicals (antipsychotics);
aspirin and other antiplatelet agents in preventing heart Conventional antipsychotics; High-potency/low-potency
Antipsychotics A 207
groups of antipsychotics; Neuroleptics; Standard the serotonin, dopamine, and GABA neurotransmitter
A
antipsychotics systems. This multiple pathway approach may help with
the individualization and selection of the best agent based
on the individuals response.
Definition
Agents used for the treatment of psychotic disorders, Current Knowledge

severe mental illnesses, and mood/behavior disorders
not responsive to other medication/behavioral interven- Standard antipsychotics have been used since the 1950s
tions. Broader application/often off-label use of these for their sedating effects on individuals with psychosis/
medications to address thought/behavior disorders in psychotic symptoms. As phenothiazines were known to
various populations including adults with dementia, produce these effects as postoperative sedation agents, the
traumatic brain injury, developmental disorders with sedating effect led to the development of additional
behavioral symptoms unresponsive to other treatments, standard antipsychotic agents produced and utilized
and individuals with depression who are not responsive through the 1980s, including, but not limited to agents
to antidepressant therapy alone. Specifically in TBI such as Thorazine, Mellaril, Stelazine, Prolixin, Navane,
populations, according to B.C. McDonald et al. (2002), and Trilafon. These standard antipsychotic agents were
individuals with TBI whose cognition and behaviors are divided into high- and low-potency groups based on their
disorganized, and agitated, there may be a role for neuro- profiles indicating desirable/undesirable effects including
leptics agents. Another study by Ahmed and Fuiji (1998) sedation, anticholinergic/parasympathetic side effects
identified that individuals who have a brain injury including urinary and bowel retention, dry mouth and
experience a two- to fivefold greater risk of developing cardiovascular effects, and extrapyramidal symptoms as
psychosis than the general population, and may require a result of their dopamine blockade, their effects on
treatment with atypical antipsychotics to help restore sympathetic blockade/alpha adrenergic blockade leading
behavioral and cognitive stability. to hypotension and dizzinesss and the effects of
neurotramsission leading to involuntary movements
(tardive dyskinesias) and extrapyramidal symptoms.
Historical Background Other adverse effects noted with typical antipsychotics
include lowering seizure threshold, thermal dysregulation,
Antipsychotic medications according to Preston, hormonal dysregulation including hyperprolactinemia,
Neal, and Talaga (2006) have truly revolutionized the and a fatal but rare side effect known as neuroleptic
treatment of psychotic disorders. Conventional/Typical malignant syndrome characterized by fever, rigidity, and
Antipsychotics act primarily through blockade of confusion. Obviously, all medication agents require close
dopamine D2 receptors. Chlorpromazine(Thorazine)/a monitoring and may also require other agents to address
phenothiazine was first used in 1952 as a postoperative undesired effects, or lowering of the antipsychotic agent
agent, but quickly became a standard treatment for seda- or change in administration time to minimize untoward
tion and reducing psychotic symptoms of psychiatric effects.
patients, and soon many other phenothiazines were Newer atypical or novel agents with Clozaril
developed (Preston, Neal, and Talaga, 2006). The role of (Clozapine) as the first agent in this category have
dopamine 2 postsynaptic receptor blockade led to the been noted to be effective in significantly reducing the
development of future dopamine blockers that are chem- symptoms of psychosis, particularly when other agents
ically targeted to reduce and selectively block/weakly are unsuccessful by targeting specific dopamine
block dopamine to minimize side effects. Since that receptors, or block/ inhibit reuptake of serotonin. The
time, off-label use of these agents has benefited other most significant difference is in the reduction of the
populations. These agents were called neuroleptics negative symptoms and the lower risk of developing
because as a result of their dopamine blockade, they also tardive dyskinesias. However, Clozaril effects on the bone
lead to other neurological side effects/undesired effects. marrow may lead to a severe blood disorder/agranulocy-
The newer antipsychotics, known as atypicals, are tosis. Clozaril requires adherence to an FDA protocol for
strong serotonin blockers (5-HT2A and 5-HT2C) and Complete Blood Count/ANC monitoring based on
produce varying degrees of dopamine blockade, weakly threshold values. Newer atypical agents were developed
blocking D2 receptors and D1 receptors and also act on to improve the reduction of negative symptoms, improve
208 A Antithrombotic Therapy
cognition, decrease risk of tardive dyskinesias, and other Savitz, J., van der Merwe, L., Stein, D., Solms, M., & Ramesar, R. (2008).
Neuropsychological task performance in bipolar spectrum illness:
neurological changes resulting from these agents.
genetics, alcohol abuse, medication and childhood trauma. Bipolar
Newer atypical/novel antipsychotic agents have in- Disorders, 10(4), 479494.
cluded Risperidone, Zyprexa, Seroquel, Geodon, Abilify, Voruganti, L., & Awad, A. (2004). Neuroleptic dysphoria: Towards a new
and, most recently, Saphris. However, with these newer synthesis neuroleptic dysphoria. Psychopharmacology, 171(2),
atypical antipsychotics, other concerning side effects 121132.
Wozniak, J., Block, E., White, T., Jensen, J., & Schulz, S. (2008). Clinical
have been exposed including metabolic changes leading
and neurocognitive course in early-onset psychosis: a longitudinal
to alterations in carbohydrate and lipid metabolism, pos- study of adolescents with schizophrenia-spectrum disorders. Early
sible diabetes, and excessive weight gain. All of these Intervention in Psychiatry, 2(3), 169177.
newer agents require routine monitoring of weight,
blood sugar, and lipid profile studies to control the
potential adverse effects while achieving improvement in
both positive/negative symptoms of psychosis. Treatment
duration with these agents is individually maximized Antithrombotic Therapy
based on response to reduction in positive symptoms of
chronic thought disorders/psychosis. Shorter treatment Anticoagulation
durations may be possible in acute onset of delirium,
acute psychoses, or brief reactive psychosis.
Future Directions Anxiety

The use of the newer atypical agents has been shown to J OEL W. H UGHES
produce a reduction in hostility and aggression in Kent State University
schizophrenic patients, elderly patients with dementia, Kent, OH, USA
and empirically with individuals experiencing aggression
and agitation in TBI. The next generation of agents will be
directed at further reducing overall side effects while Synonyms
maximizing treatment response and symptom reduction
while returning to optimal daily functioning and Fear
cognitive, mood, and behavioral stability.
Definition
Cross References
Anxiety is an unpleasant state characterized by affective,
Neuroleptics cognitive, and physiological elements such as fear, worry,
Psychopharmacology apprehension, and tension.
Psychotic Disorder Anxiety is similar to the emotion of fear, although the
function of chronic anxiety is often to avoid or mask true
fear through mechanisms of anxiety such as worry and
References and Readings anticipation of negative future outcomes. The physiologi-
cal manifestations of anxiety include increased blood
Ahmed, I. I., & Fuiji, D. (1998). Posttraumatic Psychosis. Seminars in
pressure, increased breathing rate (often shallow),
Clinical Neuropsychology, 3(1), 2333.
McDonald, B. C., Flashman, L. A., & Saykin, A. J. (2002). Executive increased heart rate, other cardiac symptoms (e.g., pain,
dysfunction following traumatic brain injury: neural substrates and skipped beats), gastrointestinal distress including nau-
treatment strategies. NeuroRehabilitation, 17(4), 333344. sea, stomach aches, increased motility of the gut, and
Meredith, C., Jaffe, C., Ang-Lee, K., & Saxon, A. (2005). Implications of diarrhea, generalized bodily distress such as fatigue and
chronic methamphetamine use: A literature review. Harvard Review
pain. Cognitively, anxiety is frequently characterized by an
of Psychiatry, 13(3), 141154.
Preston, J., ONeal, J. H., & Talaga, M. C. (2006). Child and adolescent overestimation of the probability of a negative future
clinical psychopharmacology made simple. Oakland, CA, US: New outcome and an exaggeration of the consequences of the
Harbinger Publications. negative outcome. For example, an anxious person may
Anxiolytics A 209
believe that it is likely that they will fail a test with habituation. Exposure can be in vivo or imaginal, and
A
catastrophic consequences. therapy frequently uses cognitive techniques to modify
Anxiety often occurs in response to external stressors. anxiety-generating cognitions. Anxiolytic medication is
It can be a normal reaction to stress, in which case anxiety also often prescribed.
can help coping behavior by focusing attention, mobiliz-
ing energy, and increasing goal-directed behavior.
However, anxiety can also be a reaction to internal (phys- Cross References
iological) cues or a generalized and pervasive mood with-
out identifiable precipitants. When anxiety is an excessive Anxiolytics
reaction, or present in the absence of any true challenges Beck Anxiety Inventory
or dangers, it is considered pathological. Individuals with
pathological levels of anxiety are typically high in trait
anxiety, which is a stable and enduring tendency to re- References and Readings
spond with anxiety to a wide variety of situations. Indi-
viduals high in trait anxiety are often also high in Allen, L. B., McHugh, R. K., & Barlow, D. H. (2008). Emotional disorders:
neuroticism. A unified protocol. In D. H. Barlow (Ed.), Clinical handbook of
psychological disorders: A step-by-step treatment manual (4th ed.,
pp. 216249). New York, NY: Guilford Press.
American Psychiatric Association (2000). Diagnostic and statistical
Historical Background manual of mental disorders (4th ed.), Text Revision. Washington,
DC: American Psychiatric Association.
Anxiety is basic to human experience and has been docu-
mented and treated since the beginning of recorded his-
tory. The relation between anxiety and health complaints
has been recognized since the seventeenth century, although Anxiolytics
psychiatric nosology did not become well developed
until the last century. A number of anxiety disorders S TEPHANIE A. KOLAKOWSKY-H AYNER
have been delineated in contemporary psychiatric writ- Santa Clara Valley Medical Center,
ings and are described in the most recent edition of the Rehabilitation Research Center
Diagnostic and Statistical Manual of Mental Disorders San Jose, CA, USA
published by the American Psychiatric Association.
Synonyms
Current Knowledge
Anti-anxiety drugs; Anti-anxiety medications
Although anxiety can be learned, it is thought to have a
biological basis in the amygdala and hippocampus. When
individuals are exposed to potentially dangerous or harm- Definition
ful stimuli, brain imaging often shows increased activity
in the amygdala accompanied by participant reports of Anxiolytics are prescription drugs used to reduce the
increased anxiety. Excessive anxiety can also compromise severity and extent of symptoms due to anxiety-related
performance on neuropsychological tests, especially by disorders. Often known as benzodiazepines, these drugs
interfering with attention and cognitive efficiency. are used to treat generalized anxiety disorder, panic attacks,
When suspected, the level of anxiety should be phobias, and other ongoing issues of excessive fear and
assessed. Anxiety is often measured using the Beck Anxi- dread. Medical illness often associated with high levels of
ety Inventory or Hamilton Anxiety Scale. They do not anxiety also includes brain injury, heart disease, and COPD.
diagnose anxiety disorders, but give a dimensional mea- There are six approved anxiolytics in the USA today includ-
sure of anxiety. ing the popular Diazepam (Valium), Lorazepam (Ativan),
Effective treatment of anxiety almost always involves and Alprazolam (Xanax). Anxiolytics are designed to im-
exposure to the feared stimulus. Treatments are based pact neurotransmitters in the amygdala by increasing
on the principles of classical conditioning, and the goal gamma-aminobutyric acid (GABA), an inhibitory neuro-
is to extinguish the fear response through exposure and transmitter that diminishes the fear response.
210 A Apallesthesia
Neuropsychologists must be aware of the potential

effects of anxiolytics on the physical, emotional, and Apallic Syndrome
cognitive functioning of their patients. Anxiolytics are
highly addictive and are often abused when used as a Persistent Vegetative State
recreational drug. Patients may also become dependant
on their medication if on increased doses for long
periods of time. Side effects of anxiolytics may include
excessive drowsiness to the point of sedation; suicidal
thoughts; unexplained excitement, rage, anger, or hos-
Apathy
tility; confusion and cognitive slowing; balance and
L AURA L. F RAKEY
dizziness issues; diminished motor and visual skills;
Memorial Hospital of Rhode Island and Alpert Medical
and breathing issues. Negative side effects may impact
School of Brown University
neuropsychological testing and treatment and these
Pawtucket, RI, USA
effects should be considered in treatment planning and
recommendations.
Synonyms
Cross References
Abulia; Amotivational; Anhedonia; Negative symptom
Benzodiazepines
Diazepam
GABA Short Description or Definition
Psychopharmacology
In the vernacular, the word apathy generally refers to
indifference or a lack of feeling or concern. In clinical
References and Readings settings, apathy is often conceptualized as a lack of
drive or motivation, a lack of responsiveness (behavioral
Cosci, F., Schruers, K., Faravelli, C., & Griez, E. (2004). The influence of or emotional) to stimuli, or a lack of initiation, or a
alcohol oral intake on the effects of 35% CO2 challenge: A study in reduction in self-generated, purposeful behavior.
healthy volunteers. Acta Neuropsychiatrica, 16(2), 107109.
Deacon, R., Bannerman, D., & Rawlins, J. (2002). Anxiolytic effects of
cytotoxic hippocampal lesions in rats. Behavioral Neuroscience, 116
(3), 494497. Epidemiology
Karl, T., Duffy, L., Scimone, A., Harvey, R., & Schofield, P. (2007). Altered
motor activity, exploration and anxiety in heterozygous neuregulin 1 Apathy has been described in a variety of psychiatric,
mutant mice: Implications for understanding schizophrenia. Genes,
neurological, and medical conditions, including depres-
Brain & Behavior, 6(7), 677687.
Lanctot, K., Herrmann, N., Mazzotta, P., Khan, L., & Ingber, N. (2004).
sion, schizophrenia, Alzheimers disease, frontotemporal
GABAergic function in Alzheimers disease: Evidence for dysfunc- dementia, mild cognitive impairment (MCI), Parkinsons
tion and potential as a therapeutic target for the treatment of disease, progressive supranuclear palsy, Huntingtons dis-
behavioural and psychological symptoms of dementia. Canadian ease, cortical basal degeneration, dementia with Lewy
Journal of Psychiatry, 49(7), 439453.
bodies, stroke, vascular dementia, cerebral autosomal
McHugh, S., Deacon, R., Rawlins, J., & Bannerman, D. (2004). Amygdala
and ventral hippocampus contribute differentially to mechanisms of
dominant arteriopathy with subcortical infarcts and
fear and anxiety. Behavioral Neuroscience, 118(1), 6378. leukoencephalopathy (CADASIL), traumatic brain injury
Treit, D., & Menard, J. (1997). Dissociations among the anxiolytic (TBI), anoxic encephalopathy, WernickeKorsakoff syn-
effects of septal, hippocampal, and amygdaloid lesions. Behavioral drome, hydrocephalus, human immunodeficiency virus
Neuroscience, 111(3), 653658.
(HIV), multiple sclerosis, apathetic hyperthyroidism,
chronic fatigue syndrome, vitamin B12 deficiency, Lyme
disease, and drug intoxication and withdrawal.
Following an extensive review of the literature, van
Apallesthesia Reekum et al. (2005) summarized the prevalence rates of
apathy in many of the above-named conditions derived
Pallanesthesia from studies that employed a variety of assessment
Apathy A 211
measures (see below). Combining data from multiple it does appear as a nonspecific symptom for several other
A
studies, these authors report point prevalence rates of disorders. The merits of including apathy as a stand-alone
60.3% in Alzheimers disease, 46.7% in TBI, 60.3% in disorder in the upcoming DSM-V revision are currently
persons with focal frontal lesions, 33.8% in vascular de- being debated.
mentia, 34.7% poststroke, 22.2% in dementia with Lewy Prognostically, there is evidence to suggest that apathy
bodies, 29.8% in HIV, 20.5% in multiple sclerosis, and may be associated with more severe impairment and
53.3% in patients with major depression. Studies examin- negative outcomes. For example, a longitudinal study
ing apathy in other neurological conditions have found examining apathy in persons with Alzheimers disease
prevalence rates of 41% in CADASIL (Reyes et al., 2009), found that apathy at the baseline was associated with
90% in frontotemporal dementia, 91% in progressive faster cognitive and functional decline at follow-up
supranuclear palsy, 59% in Huntingtons disease, and (Starkstein et al., 2006) There is also some evidence that
33% in Parkinsons disease (Levy et al., 1998). Apathy is apathy may precede the development of Alzheimers dis-
also one of the most commonly observed neuropsychia- ease. One longitudinal study of patients with MCI found
tric symptoms in MCI (Apostolova and Cummings, that those patients who converted to Alzheimers disease
2008). had higher rates of apathetic symptomatology (91.7%)
While the above-described findings related to clinic- than those patients who did not convert (26.9%) (Robert
based samples, apathy has also been reported in a et al., 2006). Apathy has also been found to be significant-
community-based sample of older adults with prevalence ly associated with lower cognitive functioning and more
rates of 1.4% in cognitively normal elderly, 3.1% in mild severe motor symptoms in persons with Parkinsons dis-
cognitive syndrome, and 17.3% in dementia (Onyike ease (Pedersen et al., 2009). Apathetic symptomatology
et al., 2007). Apathy also appears to be quite common in has also been found to be negatively associated with
nursing home settings, with one study reporting a preva- functional improvement in rehabilitation settings after
lence rate of 84.1% (Wood et al., 2000). Apathy may also strokes (Hama et al., 2007) and increased risk for mortal-
appear as an adverse effect of some prescription drugs, ity in nursing home residents with dementia (van Dijk
including selective serotonin reuptake inhibitors (SSRIs) et al., 1994).
(Hoehn-Saric et al., 1990). Studies have also found that apathy is associated with
decreased performance of activities of daily living (ADLs)
in persons with stroke (Mayo et al., 2009; Starkstein et al.,
Natural History, Prognostic Factors, 1993), vascular dementia (Zawacki et al., 2002), fronto-
Outcomes temporal dementia (Kipps et al., 2009), dementia with
Lewy bodies (Ricci et al., 2009), and major depression
The word apathy comes from the Greek word apatheia, (Steffens et al., 1999). Alzheimers disease patients with
meaning, an absence of feeling. The Stoic philosophers apathy are more likely to be impaired on basic activities of
used this term to connote the total freedom from emo- daily living (dressing, bathing, toileting, transferring,
tions and passions which were thought to compromise walking, and eating) than nonapathetic Alzheimers dis-
rationality and the desired state of mental tranquility. ease patients, even when matched on degree of cognitive
However, over the centuries, the term apathy came to impairment (Albert et al., 1996; Stout et al., 2003). In
refer to a lack of reactivity and became viewed as patho- addition, apathy has been found to account for 27% of
logical rather than desirable. the variance in instrumental activities of daily living
While apathy can be observed as a symptom asso- scores (medication management, shopping, finances) in
ciated with a variety of psychiatric, neurological, and patients with Alzheimers disease (Boyle et al., 2003).
medical conditions, some authors have argued that apa- Finally, apathy does not only impact the patient. Due
thy, in some circumstances, may represent a neuropsy- to impairments in motivation, individuals with apathy
chiatric syndrome as well. Marin (1991) defined an apathy can require more support and management, which can,
syndrome as a loss of motivation which could not be in turn, result in increased caregiver burden and stress.
attributed to emotional distress, intellectual impairment, The caregivers of patients with Alzheimers disease-related
or a diminished level of consciousness. In contrast, apa- apathy have been shown to report significantly elevated
thy, as a symptom, was defined as a loss of motivation due levels of distress and perceived burden compared to those
to a disturbance of intellect, emotion, or level of con- who are caring for less apathetic patients with a similar
sciousness (Marin, 1991). Apathy is not considered an level of cognitive impairment (Kaufer et al., 1998). Care-
independent syndrome in the current DSM-IV, though giver distress secondary to neuropsychiatric symptoms,
212 A Apathy
including apathy, has been implicated in the eventual mood states, dysphoric versus emotionally indifferent, is
institutionalization of many patients with Alzheimers the most useful characteristic in making a differential
disease (Scott et al., 1997; Steele et al., 1990). diagnosis between apathy and depression. Apathy can be
thought of as a syndrome of primary motivational loss
and diminished emotional reactivity, while depression
reflects a syndrome of mood disturbance.
The mechanisms of apathy are not fully understood,
of Apathy
though most theories suggest it involves disruption of the
frontal-subcortical neural circuit. This circuit begins with
In clinical practice and research, apathy is often mistaken
the anterior cingulate cortex, and continues to the ventral
for depression, though it is a distinct syndrome that can
striatum, the globus pallidus, and the thalamus, before
be distinguished from depression (Levy et al., 1998;
looping back to the anterior cingulate cortex. It has been
Marin, 1991; Starkstein et al., 2001). The syndromes of
hypothesized that neuropathological changes and altera-
depression and apathy share some symptoms (Table 1)
tions in regional chemistry, especially acetylcholine, do-
and may co-occur in that same individual, making diag-
pamine, and serotonin, in this circuit, are responsible for
nosis a challenging exercise. (Damsio and Van Hosen,
the clinical manifestation of apathy (David et al., 2008;
1983). For example, an apathetic demented patient who
Franceschi et al., 2005; Landes et al., 2001; Mega &
presents with fatigue, sleep disturbance, poor appetite and
Cummings, 1994). Apathy with impaired motivation
weight loss, poor concentration, and anhedonia, may be
and indifference has most strongly been associated with
diagnosed with a major depressive disorder even in the
damage to anterior cingulate cortex (ACC) (Damsio &
absence of dysphoria (Ishii et al., 2009). A number of
Van Hosen, 1983). In the most extreme cases, damage to
studies have found apathy to be correlated with high
the ACC results in akinetic mutism, and a complete loss of
scores on various depression measures (Rabkin et al.,
initiation and motivation. Single photon emission com-
2000; Ready et al., 2003; Starkstein et al., 2006). However,
puted tomography (SPECT) studies of patients with
this correlation may be due to the fact that many clinical
Alzheimers disease found that apathy was strongly and
measures of depression include questions assessing the
inversely correlated with right anterior cingulate activity
symptoms of both apathy and depression, which may
(Benoit et al., 1999) or with a bilateral reduction in
lead to misdiagnosis.
cingulate activity (Migneco et al., 2001).
Apathy may be distinguished from depression by the
Frontal regions have also been implicated in the man-
absence of dysphoric mood symptoms such as sadness,
ifestation of apathy. Neuroimaging studies have found
guilt, hopelessness, and helplessness. The difference in
apathy in AD patients to be correlated with hypoperfu-
sion in frontotemporal regions (Benoit et al., 1999; Craig
et al., 1996). In one study, apathetic stroke patients
Apathy. Table 1 Symptoms of apathy and depression
showed reduced regional cerebral blood flow in the right
Symptoms of Overlapping Symptoms of dorsolateral prefrontal cortex and the left frontotemporal
apathy symptoms depression regions (Okada et al., 1997). Subcortical regions may also
Loss of motivation Lack of interest in Dysphoria
be implicated in the presence of apathy. In one study,
and initiation events or activities apathy was seen in 80 stroke patients with lesions to
posterior limb of the internal capsule (Starkstein et al.,
Lack of persistence Lack of energy Hopelessness
1993). Apathy has also been observed with lesions to the
Diminished Psychomotor slowing Guilt
right hemisphere subcortical structures following TBI
emotional
reactivity
(Finset & Andersson, 2000).
Evidence from neuropsychological studies suggests
Reduced social Fatigue Pessimism
that apathy may be associated with cognitive impairment,
engagement
in particular, executive dysfunction. Apathetic patients
Poor insight Suicidal
with Alzheimers disease have been shown to have greater
ideation
executive functioning deficits, abilities thought to be
Loss of
mediated by the frontal lobes, than depressed patients
appetite
with Alzheimers disease (Kuzis et al., 1999). Another
Sleep
study found that apathetic patients with Alzheimers dis-
problems
ease showed significantly greater deficits on measures of
Apathy A 213
executive functioning, but performed similarly on other disinhibition, and executive dysfunction. This allows for
A
neuropsychological measures not dependent on executive an estimation of the extent to which current problem
function (McPherson et al., 2002). Apathy has also been behaviors represent a change from premorbid function-
associated with executive dysfunction in other clinical ing. T-scores greater than 65 are clinically significant. The
populations, including TBI (Andersson & Bergedalen, FrSBe has been shown to be reliable, valid, and sensitive to
2002), Parkinsons disease (Starkstein et al., 1992), pro- behavior change due to frontal lobe damage (Grace et al.,
gressive supranuclear palsy (Litvan et al., 1998), and HIV 1999), Alzheimers disease (Stout et al., 2003), TBI (Lane-
(Castellon et al., 2000). Brown & Tate, 2009), and a variety of other neurological
conditions.
The NPI is a structured interview conducted with
Evaluation an informant designed to assess for the presence of 12
neuropsychiatric symptoms, including apathy (Cum-
Formal assessment measures for apathy focus on those mings, 1997). A positive response to a screening question
symptoms of apathy that are distinct from depression. indicates the presence of the symptom and leads to fur-
The most commonly employed assessment instruments ther questions about the behavior and eventual ratings of
for apathy in clinical and research settings include the the symptom severity (mild, moderate, or severe) and the
Apathy Evaluation Scale (AES), the Neuropsychiatric amount of caregiver distress it causes. The Neuropsychia-
Inventory (NPI), and the Frontal Systems Behavior tric Inventory Questionnaire (NPI-Q) (Kaufer et al.,
Scale (FrSBe). Less commonly used but validated 2000) is a self-administered questionnaire completed by
measures include the Dementia Apathy Interview and a caregiver or informant that assesses for the presence of
Rating, the Lille Apathy Rating Scale, the Apathy Inven- the same 12 symptoms and asks for ratings of severity and
tory, the Behavior Rating Scale for Dementia, and the caregiver distress using the same rating scale as the NPI
Scale for the Assessment of Negative Symptoms in Alz- interview. Importantly, both of these versions of the NPI
heimers disease. Of note, while several of these measures include separate questions for depression and apathy. The
include self-report versions, these may fail to identify NPI asks caregivers to consider whether the behavior has
apathy in patients with reduced insight, and, therefore, been present for the past month. The NPI has been shown
informant measures may be more helpful in assessing for to have good reliability and validity; however, unlike the
apathy. other measures discussed, there is no recommended cut-
The AES comes in a clinician-administered version, off score for clinical significance. Of note, while the AES
an informant version, and a self-report version, all of and FrSBe provide more nuanced assessments of apathy,
which have been shown to have satisfactory reliability the NPI is the most widely reported measure of apathy
(Marin et al., 1991). The clinician-administered version reported in the literature. This is likely due to the fact that
(AES-C) of this measure is a semi-structured interview the NPI assesses for a wide array of neuropsychiatric
which includes 18 items and is focused on behavior that symptomatology, and is often used in intervention studies
has been present during the past month. Each item falls for a variety of conditions of which apathy may be one
into one of four categories (cognitive, behavior, emotion- symptom, but not a cardinal feature of a disorder.
al, or other) and is rated on a 4-point Likert scale, with
higher scores representing a greater degree of apathy.
A recent study examined the AES-C and found it to be Treatment
valid and reliable for identifying and quantifying apathy,
and found that using a cut-off score of 40.5 resulted in Nonpharmacologic interventions for apathy tend to focus
good sensitivity and moderate specificity (Clarke et al., on introducing new sources of interest and stimulation.
2007a; Clarke et al., 2007b). Pet therapy, art therapy, and physical therapies may be
The FrSBe (Grace & Malloy, 2001) was specifically useful in decreasing apathy, though the efficacies of these
designed to assess for behavioral changes associated with interventions have not been examined in a systematic
frontal lobe dysfunction and comes in a self-report and fashion with apathetic patients. Increasing opportunities
informant version. This questionnaire consists of 46 items for socialization and encouraging participation in social
and asks the respondent to rate the patients behavior on activities may also be helpful. Patients should be encour-
each item using a five-point Likert scale. Respondents are aged to be as functionally autonomous as possible. Senso-
asked to rate the patients behavior both before and after ry deficits and pain should be managed so that these do
the onset of illness or injury. Subscales assess apathy, not interfere with activities. Implementing exercise
214 A Apathy
programs and scheduled activities may also be beneficial commonly used to treat attention deficit/hyperactivity
in enhancing initiation and motivation. While there have disorder (AD/HD) and narcolepsy. These medications
been few studies on behavioral interventions specifically have also been used to treat apathy in Alzheimers disease,
for apathy, there is some evidence that behavioral therapy normal pressure hydrocephalus, Parkinsons disease,
may be helpful in reducing apathetic symptomatology. cerebrovascular accidents, and depression (Chatterjee &
One randomized controlled study comparing reminis- Fahn, 2002; Jansen et al., 2001; Keenan et al., 2005; Padala
cence therapy (a treatment modality designed to facili- et al., 2007b; Spiegel et al., 2009). However, most of
tate recall of experiences from the past to promote the evidence for the efficacy of these medications on
intrapersonal and interpersonal functioning) to a time apathy comes from case reports or case series. These
and attention control group (one-on-one time with an medications can also have negative side effects, including
activity therapist) found that apathy was reduced for both insomnia, loss of appetite, anxiety, and higher blood
groups of patients with dementia (Politis et al., 2004). pressure, which may deter their use with vulnerable popu-
Another study showed that individualized functional lations (Ishii et al., 2009). Other stimulating medications
and occupational training reduced apathy in patients such as modafinil (Padala et al., 2007a) and selegiline
with mild to moderate-stage dementia (Lam et al., (Newburn & Newburn, 2005) have been reported to
2010). Behavioral activation therapy (BA) is an interven- reduce apathy in case studies, however, further study is
tion which focuses on alleviating depression by increasing needed.
the individuals exposure to rewarding and reinforcing Reductions in apathy with the use of dopaminergic
stimuli by increasing activation and decreasing avoidance agents such as bromocriptine (Powell et al., 1996) and
behaviors (Dimidjian & Davis, 2009). This behavioral amantadine (Swanberg, 2007; van Reekum et al., 1995)
approach includes goal setting, activity scheduling, prob- have been reported in a few case studies, but no rando-
lem solving, and self-monitoring, to get patients to mized clinical trials have been conducted to date.
become more active and, thus, increase exposure to re- Apathetic-type symptoms and behavior may be seen in
ward, and positive reinforcement to combat depressive schizophrenic patients with negative symptoms. Atypical
symptomatology. It has been shown to be comparable antipsychotic medications such as risperidone, olanza-
to cognitive behavior therapy and pharmacotherapy pine, and clozapine have been shown to be helpful in
(paroxetine) in reducing depressive symptomatology in reducing negative symptoms in schizophrenia (van
placebo-controlled studies (Dimidjian et al., 2006; Reekum et al., 2005). However, none of the studies to
Sturmey, 2009). While this intervention has not been date has specifically examined apathy, and these medica-
examined in the treatment of apathy, its focus on tions can be associated with serious negative side effects
increased activity and exposure to pleasant, rewarding such as tardive dyskinesia, akathisia, extra pyramidal
experiences would appear to be particularly well-suited symptoms, and orthostatic hypotension.
to address the lack of interest, motivation, and anhedonia As previously noted, apathy is the most common
that characterize apathy. Future research may show this to neuropsychiatric symptom associated with Alzheimers
be a promising intervention for both depression and disease, and modest improvements in apathy have
apathy. been seen in patients with Alzheimers disease who are
Psychoeducation for families and caregivers can also treated with acetylcholinesterase inhibitor medications
be beneficial. Oftentimes, apathy is mischaracterized as a (Cummings, 2000; Mega et al., 1999). Currently, there
willful behavior (e.g., stubbornness or laziness) by care- are three acetylcholine inhibitor medications approved
givers who do not recognize that these behaviors are for use in the United States: donepezil, galantamine, and
related to neurological, psychiatric, and medical comor- rivastigmine. A recent meta-analysis identified 14 rando-
bidities. Educating families on the underlying causes for a mized, placebo-controlled trials of monotherapy with
patients low initiation and motivation may help lessen these medications in patients with Alzheimers disease
perceived caregiver burden and stress. that reported a behavioral outcome (Rodda et al., 2009).
Currently, there is no FDA-approved pharmacological Of these, only four were specifically designed to assess
intervention for apathy, however, many different medi- behavioral outcomes, and the rest used behavioral out-
cations, including acetylcholinesterase inhibitors, psy- comes as secondary measures. Overall, three of the 14
chostimulants, dopaminergic drugs, and atypical studies reviewed reported a statistically significant im-
antipsychotics, have been used off-label to treat apa- provement in the overall score on the Neuropsychiatric
thetic symptomatology. Methylphenidate and dextroam- Inventory, and only one found a significant reduction in
phetamine are psychostimulant medications that are apathy, specifically (Gauthier et al., 2002).
Apathy A 215
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Aphasia A 217
Steffens, D. C., Hays, J. C., & Krishnan, K. R. (1999). Disability in of behavioral symptoms such as impairment in auditory
geriatric depression. American Journal of Geriatric Psychiatry, 7(1), A
comprehension, reading comprehension, naming,
3440.
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(2003). Frontal behavioral syndromes and functional status in prob- writing, and presence of paraphasic (substitution) sound
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Categorization
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ciated Disorders, 21(2), 164166.
van Dijk, P. T., Dippel, D. W., & Habbema, J. D. (1994). A behavioral Many systems have been proposed to classify aphasia
rating scale as a predictor for survival of demented nursing types (Kertesz, 1979). Each system represents a theoretical
home patients. Archives of Gerontology and Geriatrics, 18(2), perspective of aphasia and identifies aphasia types accord-
101113.
ing to the constellation of behavioral characteristics.
van Reekum, R., Bayley, M., Garner, S., Burke, I. M., Fawcett, S., Hart, A.,
et al. (1995). N of 1 study: Amantadine for the amotivational
Classification systems can be dichotomous (e.g., fluent
syndrome in a patient with traumatic brain injury. Brain Injury, vs. nonfluent or comprehension deficit vs. production
9(1), 4953. deficit), anatomically and behaviorally based (e.g., Boston
van Reekum, R., Stuss, D. T., & Ostrander, L. (2005). Apathy: Why care? classification system of aphasia types, such as Brocas
Journal of Neuropsychiatry and Clinical Neurosciences, 17(1), 719.
aphasia), behaviorally based (e.g., Schuells system of
Wood, S., Cummings, J. L., Hsu, M. A., Barclay, T., Wheatley, M. V.,
Yarema, K. T., et al. (2000). The use of the neuropsychiatric invento-
multimodality, unidimensional impairment, such as
ry in nursing home residents. Characterization and measurement. aphasia with visual involvement), based on severity (e.g.,
American Journal of Geriatric Psychiatry, 8(1), 7583. mild, moderate, or severe), or follow a processing model
Zawacki, T. M., Grace, J., Paul, R., Moser, D. J., Ott, B. R., Gordon, N., (e.g., cognitive neuropsychological model of naming; Kay,
et al. (2002). Behavioral problems as predictors of functional abil-
Lesser, & Coltheart, 1996). Classification systems are use-
ities of vascular dementia patients. Journal of Neuropsychiatry and
Clinical Neurosciences, 14(3), 296302.
ful for a general understanding of an individuals
communication ability; however, controversy exists
regarding their clinical utility. Some individuals with
aphasia show symptoms that match more than one type
of aphasia and others show symptoms that do not fit into
Aphasia any of the classification categories. Studies examining
classification report 3570% success in classifying
J ANET PATTERSON participants as one aphasia type. Table 1 shows three
East Bay classification systems, with general characteristics of
Hayward, CA, USA each aphasia type.
Epidemiology
Aphasia resulting from stroke occurs in approximately
Aphasia is an acquired communication disorder caused
80,000 people each year, affecting about 30% of indivi-
by brain damage, characterized by impairments of
duals who have a first-ever ischemic or hemorrhagic
language modalities; speaking, listening, reading and
stroke. Approximately, one million people in the United
writing; it is not the result of a sensory or motor deficit,
States are living with aphasia following stroke. Aphasia
a general intellectual deficit, confusion or a psychiatric
resulting from traumatic brain injury and other causes is
disorder (Hallowell & Chapey, 2008, p. 3). Aphasia is
difficult to estimate.
typically acquired suddenly as a result of a stroke and can
also appear following traumatic brain injury or other
neurological events such as tumor or disease. When Natural History, Prognostic Factors,
aphasia develops slowly over time and is the only Outcomes
behavioral symptom present, the diagnosis is typically
primary progressive aphasia (PPA). Aphasia is often Reports of language disorder following brain injury have
classified according to the appearance of a constellation existed for hundreds of years, initially primarily as case
218 A Aphasia
Aphasia. Table 1 Three examples of aphasia classification systems showing aphasia types and general characteristics
of each type
Dichotomous classification
Type Characteristics
Nonfluent aphasia Limited speech output
Effortful speech output
Content words retained; function words omitted
May or may not have articulation difficulties
Melodic contour altered
Fluent aphasia Approximates normal rate and sentence length
Content words omitted in severe fluent aphasia
Circumlocution present in mild fluent aphasia
Melodic contour preserved
Anatomical and behavioral classification
Brocas aphasia Nonfluent aphasia; expressive aphasia
Effortful output
Reduced phrase length and syntactic complexity; content words
usually preserved
Auditory comprehension may or may not be impaired
Impairments in reading, writing, naming, and repetition
Right hemiplegia often present
Wernickes aphasia Fluent aphasia; receptive aphasia
Auditory comprehension usually impaired
Impairments of reading, writing, naming, and repetition
Paraphasic errors
Melodic contour retained
Conduction aphasia Fluent aphasia
Auditory comprehension preserved
Impairment in repetition
Naming may be impaired
Error recognition typically preserved
Global aphasia Nonfluent aphasia
Impairments in auditory comprehension, reading writing, naming, and repetition
Limited functional communication often preserved
Anomic aphasia Fluent aphasia
Auditory and reading comprehension and repetition preserved
Word retrieval deficit
Transcortical motor aphasia Nonfluent aphasia
Auditory comprehension and naming may be impaired
Repetition preserved
Paraphasic errors and perseveration present
Aphasia A 219
Aphasia. Table 1 (Continued)

A
Transcortical sensory aphasia Fluent aphasia
Auditory comprehension impaired
Paraphasic errors
Repetition preserved
Naming may be impaired
Behavioral classification
Simple aphasia Mild impairment
Multimodality impairment (comprehension of spoken language; speech;
reading; writing)
No specific perceptual, sensorimotor, or dysarthric components
Aphasia with visual involvement Mild aphasia
Central impairment of visual modality
Aphasia with persisting dysfluency Mild aphasia
Verbal dysfluency
Aphasia with scattered findings Moderate aphasia
Impairments in one or more modalities
Functional communication preserved
Aphasia with sensorimotor involvement Severe aphasia
Impaired output
Aphasia with intermittent auditory Severe aphasia
imperception Impaired auditory comprehension
Irreversible Aphasia syndrome Severe aphasia
Impairments in all modalities (comprehension of spoken language;
speech; reading; writing)
reports. Paul Broca and Carl Wernicke in the late 1800s do not systematically influence prognosis (Pedersen,
presented clinical data relating behavioral and anatomical Jorgensen, Nakayama, Raaschou, & Olsen, 2004).
information, localizing language ability to the left hemi- Aphasia recovery occurs most rapidly immediately
sphere, and ultimately having their names adopted to following the brain injury, as the brain begins to heal
identify anatomical areas in the brain related to patterns itself. Studies have shown that recovery also continues
of language behavior. Current studies of persons with for years post stroke and treatment (Moss & Nicholas,
aphasia use neuroimaging techniques to further elucidate 2006). Outcome measures documenting change are
the behavioral and anatomical relationship. impairment-based (e.g., change in naming ability) or
Aphasia in the first few months after a stroke is the activity/participation-based (e.g., increased participation
acute stage and is often characterized by spontaneous in social activities), following the World Health Organiza-
recovery of language and communication deficits. In the tions International Classification of Functioning, Disabil-
chronic stage, an individual learns to live with aphasia and ity and Health (ICF; WHO, 2001). Some persons with
return to life activities. Prognosis for recovery is variable aphasia recover to near normal premorbid language and
and dependent upon both internal patient factors (e.g., communication performance while others remain severe-
severity of aphasia, type and extent of lesion, or concomi- ly aphasic. Almost every person has the potential for some
tant medical problems) and external factors (e.g., family level of functional communication, from being an inde-
support or communication interaction opportunities). pendent communicator in a variety of communication
Personal variables such as age, education, and gender interactions to being dependent upon an alternative or
220 A Aphasia
augmentative communication system or a conversational breadth and depth of an individuals support and
partner. communication networks (e.g., Blackstone & Berg,
2003). Several scales have been developed to screen for
depression. Some have a linguistic bias or rely on caregiver
Neuropsychology and Psychology report while others have been adapted to be aphasia
of Aphasia friendly and not depend exclusively on complex written
sentences. Three examples of instruments to examine
Cognitive neuropsychology has brought to aphasia depression are the Stroke Aphasia Depression Question-
evaluation and treatment a set of models of human naire (SADQ) (Lincoln, Sutcliffe, & Unsworth, 2000), the
cognitive mechanisms and processes thought to underlie Aphasia Depression Questionnaire (Benaim, Cailly,
language performance. An individuals performance on Perennou, & Pelissier, 2004) and the Visual Analog
several linguistic tasks is examined for patterns of Mood Scale (Stern, Arruda, Hooper Wolfner & Morey,
impaired and spared cognitive processes to infer the 1997). The SADQ while designed for persons with aphasia
cognitive architecture that underlies the performance. has a linguistic bias and is intended to rely on caregiver
For example, in a model of lexical processing, the linguistic report. The ADQ is a nine item tool used to assess post-
tasks might be lexical recognition (word/nonword stroke depression in persons who are hospitalized after
identification), auditory comprehension (pointing to a a stroke. The VAMS is an example of a non-linguistic
named word), and naming a picture (confrontation mood scale used for self-report of depressive symptoms.
naming). An individual who scores high on auditory
comprehension and reading words tasks but low on
confrontation naming may be inferred to show a deficit Evaluation
in phonological output lexicon but have an intact
semantic system and ability to use phonic skills to read Approaches to evaluation of aphasia vary with the
a word. That is, the individual may have intact semantic conceptualization of aphasia.
knowledge and be aware of the phonological form of a Some approaches take an impairment-based
word and be able to read it, but lack the phonological approach, viewing aphasia as a disorder of selected
skills to generate the verbal label. The performance abilities while others, such as the Life Participation
pattern serves to direct treatment to the impaired process- Approach to Aphasia (Chapey et al., 2008) take an activi-
es, using the spared processes as strengths. Cognitive ty/participation approach, viewing aphasia as a disrup-
neuropsychological models of language processing tion to communication and placing the person with
frequently used in aphasia assessment and treatment, aphasia and his or her family at the center of clinical
however, are not without criticism as being descriptive and decision-making activities. (Schuell, Jenkins & Jimenez-
not prescriptive, and requiring time-consuming assessment. Pabon, 1964) proposed a Stimulation-Facilitation model
In contrast to the deficit-specific models of cognitive based on auditory comprehension stimuli that are indi-
neuropsychology, the psychology of aphasia in assessment vidually adapted to persons with aphasia. Chapey et al.
and treatment recognizes the importance of an support a Cognitive Stimulation model, which views
individuals psychosocial state, quality of life, functional communication as a problem-solving and decision-
communication abilities, and communication network. making task. Following the World Health Organization
Tanner (2003) proposed an eclectic approach to examine ICF (2001), models of assessment and treatment typically
the psychology of aphasia from three perspectives: incorporate information at levels of impairment and ac-
effects of brain injury, psychological defenses and coping tivity/participation. Group treatment has gained popular-
styles, and responses to loss. This view speaks to the ity in recent years, recognizing the value of social
importance of an individuals premorbid personal connectedness (Avent, 1977; Kearns & Elman, 2008).
characteristics, their ability to adjust to change, and Lubinski (2008) discussed an environmental model, sug-
their external support network as they and their family gesting that clinicians consider physical and social envir-
learn to live with aphasia. Several models and tools exist onments of a person with aphasia to enhance treatment
to guide assessment and treatment in these areas. For effects. Finally, psychosocial models of intervention focus
example, quality-of-life scales ask questions about topics on integrating an individual into a communicating society
such as family support and general outlook on life (e.g., and promoting their participation in personally relevant
Communication-Related Quality of Life Scale; Cruice activities (Simmons-Mackie, 2008). Regardless of the ap-
et al., 2003). Social network diagrams illustrate the proach, in order to understand the linguistic and
Aphasia A 221
communicative abilities and needs of an individual, it is characterized by spontaneous recovery of language and
A
important to conduct an evaluation within a culturally communication deficits, while in the chronic stage of
sensitive framework. aphasia an individual learns to live with aphasia and
Three types of aphasia tests are commonly used to return to life activities. There are many well-validated,
assess language and communication abilities in persons effective techniques for aphasia rehabilitation, particular-
who have aphasia: screening tests (short assessments that ly for chronic aphasia. These range from general stimula-
may be administered at bedside), comprehensive aphasia tion approaches to treatments aimed at specific signs of
tests (batteries containing several subtests such as naming, aphasia, and are chosen according to the patients
reading, and writing), and tests of specific linguistic or individual needs, goals, aphasia characteristics, and
communicative function (e.g., syntactic function or etiology. For aphasia due to acute-onset causes (e.g.,
naming) (Patterson, 2008). In addition, assessment of vascular etiologies or trauma), therapy has been demon-
aphasia and its impact on a persons life includes testing strated to be effective both early after onset as well in the
cognitive abilities (e.g., memory), testing executive chronic stage. For aphasia due to progressive etiologies,
functioning (e.g., divided attention), observing a person therapy has been shown to be effective in maintaining
in activities of daily communication, and interviewing the functional communication and maximizing quality of
person with aphasia and family members about the communication life to the extent possible given the med-
impact of aphasia on life participation and functional ical diagnosis.
communication. Pharmacological intervention for aphasia may be
In aphasia assessment it is as important to determine undertaken for direct treatment of the language deficit
the presence or absence of aphasia, and presence of or administered to address a concomitant disorder, such
concomitant disorders, as well as to classify aphasia type as depression. Although research in this area is encouraging,
or describing aphasia symptoms. Examples of disorders to date no pharmacologic treatment has emerged
that may accompany aphasia but that are not aphasia are as consistently improving linguistic function without
apraxia of speech, dysarthria, dementia, memory im- adverse side effects (Greener, Enderby, & Whurr, 2001;
pairment, or psychiatric problems. These concomitant Murray & Clark, 2006; Troisi et al., 2002).
disorders will affect treatment planning and task selection. Treatment for aphasia historically focused primarily
Medical conditions, such as diabetes, cardiovascular dison restitution of function using impairment-based
ease, and any medications the patient takes may affect treatment techniques, with treatment targets such as
performance and should also be noted in the assessment word or sentence production, or writing. Examples of
report. these treatment techniques are Melodic Intonation
The goals of evaluation will vary depending upon Therapy, a semantic or phonologic cueing hierarchy,
factors such as severity of aphasia, age, and time post- and confrontation naming. More recently, treatment
onset. For example, an individual with mild aphasia who goals have expanded to include activity/participation
anticipates returning to work should have an assessment based treatments such as functional communication
that includes detailed information on linguistic proces- and group therapy. Examples of activity/participation
sing and a job task analysis to determine the linguistic treatment methods are book groups for persons with
requirements of the position. This information may be aphasia (with the linguistic level of the book modified
used to determine the individuals ability to return to a to be aphasia friendly), reciprocal scaffolding (e.g.,
job, to identify communication requirements of the job, Avent, Patterson, Lu, & Small, 2009), and supported
and to guide employment-related treatment. In contrast, conversation (e.g., Kagan, Black, Duchan, Simmons-
evaluation for an individual with severe aphasia and Mackie, & Square, 2001).
concomitant severe apraxia of speech may require an The four principles of evidence-based practice,
evaluation focused on functional communication current best practices, clinical expertise, client/patient
strategies to use with familiar communication partners values, and context of treatment, guide treatment
within a contained environment. planning. Clinical practice research and clinical trials
support the efficacy and effectiveness of aphasia therapy.
Systematic reviews, such as the one for constraint-induced
Treatment language therapy (Cherney, Patterson, Raymer, Frymark, &
Schooling, 2008), and meta-analyses (e.g., Robey, 1998)
The acute stage of aphasia is the first few months after a report the evidence from group studies and single-subject
stroke as the brain recovers from injury, and is often research studies for a specific treatment or aphasia
222 A Aphasia
therapy in general. Cherney and Robey (2008) and the References and Readings
Academy of Neurological Communication Disorders
and Sciences (ANCDS, 2008) present analyses of Academy of Neurological Communication Disorders and Sciences.
treatment effect sizes of aphasia treatment for specific (2008). Practice guidelines of the ANCDS: Evidence based practice
guidelines for the management of communication disorders in
treatment areas such as syntax and language
neurologically impaired individuals. http://www.ancds.org/index.
comprehension. php?option=com_content&view=article&id=9&Itemid=9. Accessed
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Cross References New York: Elsevier.
Avent, J., Patterson, J., Lu, A., & Small, K. (2009). Reciprocal scaffolding
Agnosia treatment: A person with aphasia as clinical teacher. Aphasiology,
Agrammatism 23, 110119.
Benaim, C., Cailly, B., Perennou, D., & Pellissier, J. (2004). Validation of
Agraphia
the Aphasic Depression Rating Scale. Stroke, 35, 16921969.
American Speech-Language-Hearing Association (ASHA) Blackstone, S., & Hunt Berg, S. (2003). Social networks: A communication
Anarthria inventory for individuals with complex communication needs and their
Anomic Aphasia communication partners. Monterey, CA: Augmentative Communica-
Aphasia Tests tion Inc.
Chapey, R., Duchan, J. F., Elman, R. J., Garcia, L. J., Kagan, A., Lyon, J.,
Apraxia of Speech
et al. (2008). Life participation approach to aphasia: A statement of
Augmentative or Alternative Communication (AAC) values for the future. In R. Chapey (Ed.), Language intervention
Boston Diagnostic Aphasia Examination strategies in aphasia and related neurogenic communication disorders
Boston Naming Test (5th ed., pp. 279289). Philadelphia: Wolters Kluwer.
Brocas Aphasia Cherney, L. R., Patterson, J. P., Raymer, S. M., Frymark, T., &
Schooling, T. (2008). Evidence-based systematic review: Effects of
Carl, Wernicke
intensity of treatment and constraint-induced language therapy
Conduction Aphasia for individuals with stroke-induced aphasia. Journal of Speech-
Crossed Aphasia Language-Hearing Research, 51, 12821299.
Cue Cherney, L. R., & Robey, R. R. (2008). Aphasia treatment: recovery,
Dysarthria prognosis and clinical effectiveness. In R. Chapey (Ed.),
Language intervention strategies in aphasia and related neurogenic
Dysgraphia
communication disorders (5th ed., pp. 186202). Philadelphia:
Edith Kaplan Wolters Kluwer.
Evidence-Based Practice Cruice, M., Worral, L., Hickson, L., & Murison, R. (2003). Finding focus
Fluent Aphasia for quality of life with aphasia: Social and emotional health, and
Global Aphasia psychological well-being. Aphasiology, 17, 333353.
Davis, G. A. (2006). Aphasiology: Disorders and clinical practice.
Harold Goodglass
Englewood Cliffs, NJ: Prentice Hall.
Melodic Intonation Therapy Greener, J., Enderby, P., & Whurr, R. (2001). Pharmacological treatment for
Multilingual Aphasia Examination aphasia following stroke. Cochrane Database of Systematic Reviews.
Neurosensory Center Comprehensive Examination Issue 4. Art. No.: CD000424. doi: 10.1002/14651858.CD000424.
for Aphasia Hallowell, B., & Chapey, R. (2008). Introduction to language intervention
strategies in aphasia. In R. Chapey (Ed.), Language intervention
Paragrammatism
strategies in aphasia and related neurogenic communication disorders
Paraphasia (5th ed., pp. 319). Philadelphia: Wolters Kluwer.
Paul Broca Kagan, A., Black, S. E., Duchan, J. F., Simmons-Mackie, N., & Square, P.
Pragmatic Communication (2001). Training volunteers as conversational partners using
Progressive Aphasia Supported Conversation for Adults with aphasia (SCA):
A controlled trial. Journal of Speech-Language-Hearing Research,
Semantic Paraphasia
44, 624638.
SpeechLanguage Therapy Kay, J., Lesser, R., & Coltheart, M. (1996). Psycholinguistic assessments
Subcortical Aphasia of language processing in aphasia (PALPA): An introduction.
Telegraphic Speech Aphasiology, 10, 159215.
Transcortical Motor Aphasia Kearns, K., & Elman, R. (2008). Group therapy for aphasia: Theoretical
and practical considerations. In R. Chapey (Ed.), Language interven-
Transcortical Sensory Aphasia
tion strategies in aphasia and related neurogenic communication
Wernickes Aphasia disorders (5th ed., pp. 376398). Philadelphia: Wolters Kluwer.
Wernicke-Lichtheim Model of Aphasia Kertesz, A. (1979). Aphasia and associated disorders: Taxonomy localization
Western Aphasia Battery and recovery. New York: Grune & Stratton.
Aphasia Diagnostic Profiles A 223
Lincoln, N. B., Sutcliffe, L. M., & Unsworth, G. (2000). Validation of

the Stroke Aphasic Depression Questionnaire (SADQ) for use Aphasia Diagnostic Profiles A
with patients in hospital. Clinical Neuropsychological Assessment, 1,
8896.
J ANET PATTERSON
Lubinski, R. (2008). Environmental approach to adult aphasia. In
R. Chapey (Ed.), Language intervention strategies in aphasia and California State University
related neurogenic communication disorders (5th ed., pp. 319349). East Bay, Hayward, CA, USA
Philadelphia: Wolters Kluwer.
Moss, A., & Nicholas, M. (2006). Language rehabilitation in chronic
aphasia and time postonset: A review of single-subject data. Stroke, Description
37, 30433051.
Murray, L. L., & Clark, H. M. (2006). Neurogenic disorders of language:
Theory driven clinical practice (Chap. 10). Clifton Park, NY:
The Aphasia Diagnostic Profiles (ADP; Helm-Estabrooks,
Thompson Delmar Learning. 1992) is an impairment-based measure (World Health
Patterson, J. P. (2008). Assessment of language disorders in adults. In Organization, 2001) designed to assess language and
R. Chapey (Ed.), Language intervention strategies in aphasia and communication skills in persons with aphasia, primarily
related neurogenic communication disorders (pp. 64160). Baltimore:
following stroke. The ADP consists of nine subtests, each
Wolters Kluwer.
Pedersen, P. M., Jorgensen, H. S., Nakayama, H., Raaschou, H. O., &
of which yields a standard score and percentiles. The
Olsen, T. S. (2004). Aphasia in acute stroke: Incidence, determinants, subtests assess speech, language, and communication in
and recovery. Annals of Neurology, 38, 659666. all modalities (verbal and written) and the test emphasizes
Robey, R. R. (1998). A meta-analysis of outcomes in the treatment conversational interaction; verbal instructions to the
of aphasia. Journal of Speech-Language-Hearing Research, 41,
patient are written in an informal style in the manner of
172187.
Schuell, H., Jenkins, J., & Jimenez-Pabon, E. (1964). Aphasia in adults.
conversation (e.g. Well now, thats out of the way, Im
New York: Harper medical Division. going to turn on the tape recorder).
Simmons-Mackie, N. (2008). Social approaches to aphasia intervention. Responses are typically scored on a five-point scale:
In R. Chapey (Ed.), Language intervention strategies in aphasia and immediately correct; mostly correct; some correct; fully
related neurogenic communication disorders (5th ed., pp. 290318).
incorrect; no response. Scores from the subtests are com-
Philadelphia: Wolters Kluwer.
Stern, R. A., Arruda, J. E., Hooper, C. R., Wolfner, G. D., & Morey, C. E.
bined to produce five profiles describing the level of
(1997). Visual analog mood scales to measure internal mood state in impairment of aphasia. The profiles are the Aphasia Classi-
neurologically impaired patients: Description and initial validity fication Profile, the Aphasia Severity Profile, the Alternative
evidence. Aphasiology, 11, 5971. Communication Profile, the Error Profiles, and the
Tanner, D. C. (2003). Eclectic perspectives on the psychology of aphasia.
Behavioral Profile. Other scores of interest are the ADP
Journal of Allied Health, 32, 256260.
Troisi, E., Paolucci, E., Silvestrini, M., Matteis, M., Vernieri, F.,
Phrase length (average length of longest three phrases);
Grasso, M. G., et al. (2002). Prognostic factors in stroke rehabilita- Correct Information Units (new pieces of information),
tion: The possible role of pharmacological treatment. Acta and Index of Wordiness (Correct Information Units
Neurologica Scandinavica, 105, 100106. relative to total number of words). Table 1 shows the
World Health Organization. (2001). International Classification of
titles and a brief description of the nine subtests and five
Functioning, Disability and Health. Geneva: Author. http://www.
who.int/classifications/icfbrowser/. Accessed 30 March, 2010.
profiles.
The ADP is used to classify an individuals aphasia type
as nonfluent, borderline fluent, or fluent. Using the lexical
retrieval score, ADP phrase length, auditory comprehension
score, and repetition score, the ADP further classifies the
aphasia type as global, mixed nonfluent, Brocas, transcor-
Aphasia Assessment tical motor, Wernickes, transcortical sensory, conduction,
or anomic aphasia, following the conventions of the Boston
Aphasia Tests aphasia classification system.
The ADP was created in part to address the need for a
comprehensive aphasia battery that could be adminis-
tered in a relatively brief time (4050 min) in a medical
setting. The manual is clearly written with explicit
Aphasia Diagnosis administration and scoring instructions. The record
form is easy to use and facilitates the completion of the
Aphasia Tests profile scores.
224 A Aphasia Diagnostic Profiles
Aphasia Diagnostic Profiles. Table 1 Aphasia diagnostic profiles: Nine subtests and five profiles
ADP Subtests
Subtest Description
Personal information Verbal response to questions
Writing Complete Patient Information Sheet
Reading Read items on Patient Information Sheet
Fluency Produce connected speech in three contexts
Naming Name familiar pictured items
Auditory language comprehension Answer questions word, sentence, and story levels
Repetition Repeat words and phrases
Elicited gestures Pretend to complete action
Singing Sing 3 familiar songs
ADP Profiles
Profile Description
Aphasia Classification Profile Identifies aphasia type (based on the Boston
classification system)
Aphasia Severity Profile Indicates specific strengths and weaknesses
Alternative Communication Profile Identifies patients strongest response modalities
and guides therapy
Error Profiles Identify the communicative value of a patients
responses
Behavioral Profile Indexes the patients overall emotional state during
testing
Historical Background Clinical Uses
The ADP was first published in 1992 and since then has Three characteristics make the ADP a valuable clinical
been frequently used in clinical and research activities. assessment tool: the theoretical foundation and close re-
Numerous studies of aphasia treatment use the ADP as a lationship to the Boston aphasia classification system, the
measure of behavior change following intervention. structure of the test and clarity of the administration
manual, and the amount of administration and scoring
time required. It is also notable that both verbal and
Psychometric Data nonverbal modalities of communication are included in
the assessment. One limitation of the ADP is that it does
The ADP manual reported that it was standardized on 290 not examine any linguistic, psycholinguistic, or neuropsy-
adults with neurological impairments (222 potentially chological behavior in detail; additional tests in specific
aphasic adults) and 40 nonaphasic adults. The median areas would be required to obtain in-depth information as
age of these individuals was 70 years. The manual further part of an extensive diagnostic evaluation.
reported reliability coefficients (inter-item consistency)
for subtest raw scores that ranged from 0.73 (Behavioral
Score) to 0.96 (Repetition), with most of the coefficients Cross References
in the 0.90s. Testretest coefficients ranged from 0.64
(Elicited Gestures) to 0.91 (Information Units). The ADP Anomia
has a strong theoretical and psychometric foundation Anomic Aphasia
but has not been subjected to additional psychometric Aphasia
evaluation. Aphasia Tests
Aphasia Tests A 225
Boston Diagnostic Aphasia Examination communicative function (Patterson, 2008). In addition,

A
Brocas Aphasia assessment of aphasia and its impact on a persons life
Carl, Wernicke includes testing cognitive abilities and related disorders
Conduction Aphasia (e.g., memory), testing executive functioning (e.g., atten-
Edith Kaplan tion and planning), observing a person in activities of
Global Aphasia daily communication (e.g., social functional communica-
Harold Goodglass tion or work-related communication), interviewing the
Repetition person with aphasia and family members, and determin-
Speech/Communication Disabilities ing an individuals candidacy for use of alternative and
Speech-Language Therapy augmentative communicative systems (e.g., an alphabet
Transcortical Motor Aphasia board to spell words, drawing, or a commercially available
Transcortical Sensory Aphasia device).
Wernickes Aphasia
Aphasia has been assessed more or less systematically for
Helm-Estabrooks, N. (1992). Aphasia diagnostic profiles. Austin, TX: Pro many years. Clinical observation was the earliest method
Ed Inc.
of assessment, and the first standardized test was
World Health Organization. (2001). International classification of func-
tioning, disability and health. http://www.who.int/classifications/ published in 1926 by Henry Head. In the ensuing years,
icfbrowser/ several comprehensive aphasia tests and specific linguistic
tests appeared. Each comprehensive test is based upon a
theoretical model of aphasia, and although the tests
contain common subtests (e.g., sentence repetition), the
Aphasia Evaluation test results and aphasia diagnoses vary. For example, the
Minnesota Test for Differential Diagnosis of Aphasia
Aphasia Tests (Schuell, 1965) assesses language performance across
several modalities and rests upon Schuells theory of
aphasia as a unitary reduction in language across
Aphasia Tests modalities with or without accompanying perceptual or
motor deficits. In contrast, the Boston Diagnostic Aphasia
J ANET PATTERSON Examination (Goodglass, Kaplan, & Baressi, 2001) relates
California State University speech and language behavioral deficits to neurological
Hayward, CA, USA lesions. With yet a different perspective, Luria (1966)
proposed a comprehensive examination for aphasia
through nonstandardized observation of language perfor-
Synonyms mance in several modalities, but without specific subtests.
In recent years, several tests have emerged to assess
Aphasia assessment; Aphasia diagnosis; Aphasia evaluation specific language or communication functions in PWA.
For example, the ASHA-FACS (Frattali et al., 1995)
assesses functional communication skills such as partici-
Description pating in conversation, while the Reading Comprehension
Battery for Aphasia (LaPointe & Horner, 1998) evaluates
Tests of aphasia are used to diagnose the type and reading performance in several contexts, such as single
severity of aphasia and related disorders and to plan words and paragraphs.
intervention for the speech, language, and communica-
tion deficits demonstrated by persons who have aphasia
following brain injury (PWA). Three types of aphasia tests Psychometric Data
are commonly used to assess language and communica-
tion abilities in PWA: screening tests, comprehensive The availability of psychometric data for aphasia tests
aphasia tests, and tests of specific linguistic or ranges from prolific and well documented for some tests
226 A Aphasia Tests
to minimal or nonexistent for others, and the data Examination (Benton, Hamsher, Rey, & Sivan, 1994), and
appear in scholarly journals as well as in the test manuals. the Neurosensory Center Comprehensive Examination for
Spreen and Risser (2003) and Strauss, Sherman, and Aphasia (Spreen & Benton, 1977).
Spreen (2006) provide overviews of psychometric data
for many general aphasia tests and supplemental language
tests. Few studies, and none recently, compared psycho- Tests of Specific Linguistic or
metric data across tests. In evaluating a general or supple- Communication Function
mental test for aphasia, several factors should be
considered, including size and definition of the standar- Tests of specific functions provide detailed information
dization sample; reports of item, concurrent and predic- about a persons abilities in one area of linguistic
tive validity; test-retest, interrater and intrarater or communication ability and are particularly useful
reliability; report of raw score means, standard deviations, for persons who have severe or minimal aphasia and for
and ranges; information about test development, examiner whom comprehensive aphasia batteries would understate
qualifications, administration instructions, scoring, and communication strengths and weaknesses. Three
interpretation; and normative data. examples are the Revised Token Test (McNeil & Prescott,
Although it is difficult to judge which of the many 1978) for auditory comprehension, the Boston Naming
aphasia tests best meets all the factors mentioned above, Test (Goodglass, Kaplan & Weintraub, 2001) for
there are four tests that are frequently used in clinical oral naming, and the Psycholinguistic Assessments of
settings and have the most psychometric data published Language Processing in Aphasia (Kay, Lesser, & Coltheart,
about them: Boston Diagnostic Aphasia Examination, 1992).
Boston Naming Test, Token Test (and Revised Token Test),
and Western Aphasia Battery.
Tests of Cognitive-Communication Abilities
and Related Functions
Clinical Uses
Tests of cognitive-communicative abilities related to
Screening Tests for Aphasia language functions have been included as part of com-
prehensive aphasia batteries (e.g., the Ravens Progres-
Screening tests for aphasia are brief and may be adminis- sive Matrices [Raven, Raven, & Court, 1995] as part of the
tered at bedside. Their purpose is to rapidly determine Cortical Quotient in the WAB) or administered indepen-
the presence of aphasia or the need for further assessment. dently (e.g., Wechsler Memory Scale; Wechsler, 2009).
A screening test may be independent (e.g., Quick Assess-
ment for Aphasia; Tanner & Culbertson, 1999) or a short-
ened form of a comprehensive aphasia battery, such as the Tests of Functional Communication
Western Aphasia Battery (WAB; Kertesz, 2006).
Functional communication abilities in PWA are assessed
through observation or the use of specific tests. Func-
Comprehensive Aphasia Batteries tional communication includes verbal and nonverbal
methods of conveying information in activities of daily
A comprehensive aphasia battery is based on a theoretical living, such as reading signs, greeting individuals and
model of aphasia and contains several subtests. For participating in conversation. Functional communica-
example, the Boston Diagnostic Aphasia Examination tion assessed through observation can be contextually
(Goodglass et al., 2001) has 34 subtests and the perfor- bound, such as assessing conversation with familiar or
mance pattern is used to classify an individual with an unfamiliar partners. Tests of functional communication
aphasia type (e.g., Brocas aphasia). Although some are intended to simulate activities of daily living but
subtests of comprehensive aphasia batteries may appear typically are acontextual. Two examples of tests of
similar, the data obtained from each of the subtests and functional communication are the Communicative
the resulting aphasia diagnosis will vary according to the Activities of Daily Living 2 (Holland, A. L., Frattali, C.
theoretical model of aphasia which underlies the test. M. & Fromm, D. 1999) and the Assessment of Language-
Other comprehensive aphasia batteries are the Western Related Functional Activities (Baines, Heeringa, & Martin,
Aphaisa Battery (Kertesz, 2006), the Multilingual Aphasia 1999).
Aphonia A 227
Cross References Spreen, O., & Risser, A. H. (2003). Assessment of aphasia. Oxford: Oxford
A
University Press.
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A compendium
Activities of Daily Living of neuropsychological tests: Administration, norms and commentary
Aphasia (3rd ed.). Oxford: Oxford University Press.
Augmentative or Alternative Communication Wechsler, D. M. (2009) Wechsler Memory Scale - 4th Edition. San Antonio
Boston Diagnostic Aphasia Examination TX: Psychological Corporation.
Boston Naming Test
Luria, Alexander Romanivich (19021977)
Multilingual Aphasia Examination
Neurosensory Center Comprehensive Examination
for Aphasia Aphonia
Wechsler Memory Scales
Western Aphasia Battery LYN T URKSTRA
University of Wisconsin-Madison
Madison, WI, USA
Baines, K. A., Martin, K. W., & Heeringa, H. M. (1999). ALFA: Assessment Synonyms
of Language Related Functional Acclivities. Austin TX: Pro-Ed.
Benton, A. L., Hamsher, K. deS., Rey, G. J., & Sivan, A. B. (1994). Mutism
Multilingual Aphasia Examination (MAE-3). Lutz FL: Psychological
Assessment Resources Inc (PAR).
Davis, G. A. (2007). Aphasiology: Disorders and clinical practice (2nd ed.).
Boston: Pearson Allyn & Bacon.
Frattali, C. M., Thompson, C. K., Holland, A. L., Wohl, C. B., &
Definition
Ferketic, M. M. (1995). The American Speech-Language-Hearing As-
sociation Functional Assessment of Communication Skills in Adults. Mutism is the complete absence of voice, i.e., adduction
Rockville, MD: The American Speech-Language-Hearing Association. and vibration of the vocal folds is insufficient for vocal
Goodglass, H., Kaplan, E., & Weintraub, S. (2001). Boston Naming Test
production. Aphonia may be associated with vocal fold
(2nd ed.). Austin TX: ProEd.
Goodglass, H., Kaplan, E., & Baressi, B. (2001). Boston Diagnostic Aphasia
paralysis; trauma; severe cases of inflammation, edema,
Examination (3rd ed.). San Antonio, TX: Psychological Corporation. or scarring of the vocal folds; benign or malignant
Head, H. (1926). Aphasia and kindred disorders of speech. New York: diseases of the vocal folds that interfere with vocal
MacMillan. fold closure; neurologically based movement disorders
Holland, A. L., Frattali, C. M., & Fromm, D. (1999). Communicative
(e.g., spasmodic dysphonia); overuse of the voice; or
Activities of Daily Living - 2nd Edition. San Antonion: Psychological
Corporation.
somatoform disorders (e.g., in forms of elective mut-
Kay, J., Lesser, R., & Coltheart, M. (1992) Psycholinguistic Assessment of ism). Aphonia may be intermittent or episodic. For
Language Processes in Aphasia. London: Taylor & Francis Group. example, individuals with spasmodic dysphonia may
Kertesz, A. (2006). Western Aphasia Battery. New York: Grune & Stratton. have periodic, abnormal abduction or adduction of
LaPointe, L. L., & Horner, J. (1998). Reading Comprehension Battery for
the vocal folds that may be perceived as voice breaks.
Aphasia (RCBA2). San Antonio TX: Pearson.
Luria, A. R. (1966). Higher cortical functions in man. New York:
Individuals who stutter also may have periodic voice
Basic Books. breaks, in this case associated with tight adduction of
McNeil, M. R., & Prescott, T. E. (1978). Revised Token Test. Austin, the vocal folds.
TX: Pro-Ed. When voice loss is incomplete, or when vocal quality
Patterson, J. P. (2008). Assessment of language disorders in adults.
is affected without complete loss of voice (e.g., if the voice
In R. Chapey (Ed). Language intervention strategies in aphasia and
related neurogenic communication disorders (5th ed., pp. 64160).
is hoarse), it is referred to as dysphonia. Aphonia and
Baltimore: Wolters Kluwer. dysphonia refer specifically to abnormal sound output
Raven, J., Court, & Raven, J. C. (1995). Ravens Progressive Matrices. from the phonatory sound source (i.e., the larynx), and
San Antonio: The Psychological Corporation. should be distinguished from anarthria or dysarthria,
Schuell, H. (1965). Minnesota Test for Differential Diagnosis of Aphasia.
which are disorders of articulation, i.e., related to the
Minneapolis: University of Minnesota Press.
Spreen, O., & Benton, A. L. (1977). Neurosensory Center Comprehensive
movements of the tongue, lips, jaw, and soft palate.
Examination for Aphasia. Victoria BC: University of Victoria Accordingly, dysphonia or aphonia can occur indepen-
Neuropsychology Laboratory. dently from anarthria or dysarthria.
228 A APM
Cross References been implicated in atherosclerosis and AD, and impaired

cognitive functioning. More specifically, ApoE-4 has been
Dysphonia shown to be a major risk factor for development of AD
and has been associated with subtle neuropsychological
deficits in preclinical AD. Brain changes associated with
References and Readings ApoE-4 in AD include: increased counts of amyloid pla-
ques and neurofibrillary tangles; smaller medial temporal
Merati, A., & Bielamowicz, S. (Eds.). (2007). Textbook of voice disorders. lobe structures; reduced glucose metabolism; and deple-
San Diego: Plural Publishing. tion of cholinergic markers in the hippocampus, frontal,
Stemple, J. C., Glaze, L. E., & Klaben, B. G. (2000). Clinical voice pathology,
and temporal cortices. ApoE-4 has also been associated
theory & management (3rd ed.). Thompson Learning (now Florence,
KY: Cengage Learning).
with adverse recovery after traumatic brain injury (TBI).
Person with TBI with the ApoE-4 allele are ten times more
likely to develop AD than those without the ApoE-4 allele.
In multiple sclerosis, ApoE-4 has been found to be asso-
ciated with rapid disease progression and increased cog-
APM nitive impairment, although the findings for cognitive
impairment have been inconsistent.
Advanced Progressive Matrices
Cross References
Alzheimers Disease
APOE
Apolipoprotein E References and Readings
Plomin, R., Defries, J. C., Craig, I. W., & McGuffin, P. (2003). Behavioral
genetics in the postgenomic era. Washington DC: American Psycho-
Apolipoprotein E logical Association.
J OHN D E LUCA
West Orange, NJ, USA Apoptosis
K ATHLEEN L. F UCHS
Definition University of Virginia Health System
Charlottesville, VA, USA
Apolipoprotein E (ApoE) is a polymorphic plasma glyco-
protein that transports cholesterol and other lipids, and
has been shown to be involved in the growth and repair of Synonyms
neurons. There is also some evidence to suggest that ApoE
is involved in lipid redistribution after demyelination. The Programmed cell death
ApoE protein is mapped to chromosome 19 and is poly-
morphic with three major isoforms, each of which trans-
lates into three alleles of the gene: ApoE-2, ApoE-3, and Definition
ApoE-4. ApoE-2 is associated with the genetic disorder
type III hyperlipoproteinemia. There is also some evi- Apoptosis is both a normal developmental process to
dence that this allele may serve as a protective role in the rid the body of overproduced cells as well as a sign of
development of Alzheimers disease (AD). ApoE-3 is pathology in mature neural systems. Apoptosis involves
found in approximately 64% of the population, and is activation of caspases proteins that cleave other pro-
considered as the neutral ApoE genotype. ApoE-4 has teins in order to inactivate or modulate them to trigger
Apperceptive Visual Agnosia A 229
pro-death molecular pathways. The resulting cellular Locked-in Syndrome

A
debris is then removed by microglia in the central nervous Minimally Conscious State
system. Abnormal protein cleavage and cell death has Minimally Responsive State
been implicated in neurodegenerative disorders such as
Alzheimers disease as well as autoimmune disorders such
as multiple sclerosis. References and Readings
(May 26, 1994). Medical Aspects of the Persistent Vegetative StateFirst

Cross References of Two Parts. NEJM, 330, 14991508.
Multi-society Task Force on PVS. Medical Aspects of the Persistent
Vegetative State-Second of Two Parts. NEJM, 330,15721579.
Alzheimers Disease
Multiple Sclerosis
References and Readings Apperceptive Visual Agnosia

Hengartner, M. O. (2000). The biochemistry of apoptosis. Nature, J OHN E. M ENDOZA
407, 770776. Tulane University Medical Center
Yuan, J., & Yankner, B. A. (2000). Apoptosis in the nervous system. New Orleans, LA, USA
Nature, 407, 802809.
Definition
Appalic Syndrome Inability or marked difficulty in visually identifying an
object or picture of an object as a result of impaired
D ONA E C L OCKE
perceptual abilities. In apperceptive agnosia, in addition
Mayo Clinic
to problems in the visual identification of an object,
Scottsdale, AZ, USA
patients show impairment in reproducing (e.g., by draw-
ing) the object or image and even matching the item to a
similar one within a visual array. This contrasts with
Synonyms
associative visual agnosia in which identification may
also be impaired but the patient can usually render a
Persistent vegetative state
reasonable representation (e.g., a drawing or graphomo-
tor copy) of the object that cannot be visually identified
Definition and can visually match it to a sample. Apperceptive visual
agnosia likely results from a defect in the secondary asso-
Appalic syndrome is an older term that has been replaced ciation areas of the visual cortex and is usually found in
by persistent vegetative state. The vegetative state is a patients who complain of general loss or reduction in
clinical condition of complete unawareness of the self and visual acuity.
the environment, accompanied by sleepwake cycles with
either complete or partial preservation of hypothalamic
and brain-stem autonomic functions. A thorough clinical Cross References
evaluation may be required to distinguish between persis-
tent vegetative state and other conditions, including Associative Visual Agnosia
coma, brain death, and locked-in syndrome.

Cross References
Bauer, R. M., & Demery, J. A. (2003). Agnosia. In K. Heilman &
Brain Death E. Valenstein (Eds.), Clinical neuropsychology (4th ed., pp.
Coma 236295). New York: Oxford University Press.
230 A Applied Behavior Analysis
DeRenzi, E., & Spinnler, H. (1966). Visual recognition in patients with Rationale or Underlying Theory
unilateral cerebral disease. Journal of Nervous and Mental Disease,
142, 513525.
DeRenzi, E., Scotti, G., & Spinnler, H. (1969). Perceptual and associative
From a behavioral systems perspective, behavioral devel-
disorders of visual recognition. Relationship to the side of the opment is a function of the reciprocal interaction of a
cerebral lesion. Neurology, 19, 634642. persons: (a) genetic-constitutional makeup, (b) history of
interactions, (c) current physiological conditions, (d) cur-
rent environmental conditions, and (e) behavioral dy-
namics or behavior change over time (Novak & Pelaez,
Applied Behavior Analysis 2004). Treatment providers should consider all these fac-
tors when developing behavioral programs for individuals
A NTHONY C UVO
with neuropsychological disorders. A major conceptual
Southern Illinois University
focus of ABA is to understand, explain, and control the
Carbondale, IL, USA
operant behavior of humans in their environment.
The most basic form of operant conditioning is the
probabilistic strengthening of a response by its reinforcing
Definition consequences and the weakening of a response by its
punishing consequences. For example, access to extra
Applied behavior analysis (ABA) is the science in which
computer time might reinforce the timely completion of
tactics derived from the principles of behavior are applied
academic work by students with attention deficit disorder,
to improve socially significant behavior and experimenta-
and loss of free play might punish their noncompliance.
tion is used to identify the variables responsible for the
In addition to control of behavior by its consequences,
improvement in behavior (Cooper, Heron, & Heward,
behavior can be evoked by stimuli that precede it. For
2007, p. 690).
example, a written or pictorial prompt might evoke a
medication taking response by a person with acquired
Historical Background head injury. The beneficial treatment effects and avoid-
ance of adverse effects by not taking the medication might
The most notable figure in ABA is B. F. Skinner whose increase the probability that the person will take it.
book, The Behavior of Organisms (1938), described his The probability that a response actually will occur at a
animal research on operant conditioning. Skinner given time can be influenced by contextual variables. For
explained how behavior operates on the environment example, severe symptoms of allergies on a particular day
and is a function of its environmental consequences. might increase the aversiveness of otherwise tolerable
Subsequently, Skinner explained the application of behav- academic task demands on a student with attention deficit
ioral principles and processes discovered in the animal disorder and increase the probability that the student will
laboratory to a utopian society (1948), human behavior engage in task escape behavior that day.
(1953), verbal behavior (1957), teaching (1968), and During the past decade, there has been a growing body
other issues related to ABA. of research on relational responding and relational frame
Research on the application of basic behavioral prin- theory (e.g., Hayes, Barnes-Holmes, & Roche, 2001;
ciples and processes to important societal concerns began Sidman, 1994) that has provided the conceptualization
to emerge in the middle of the twentieth century. The and supporting empirical data to account for a broader
Journal of Applied Behavior Analysis, the flagship journal range of phenomena relevant to ABA. For example, the
of the discipline, began publication in 1968 as an outlet theory explains how individuals who experience painful
for the emerging ABA research. In the initial issue of that medical procedures can develop a wide range of fears to
journal, the defining characteristics of ABA were identi- various persons, settings, and objects (Friman, 2007).
fied as being applied, behavioral, analytical, technological,
conceptually systematic, effective, and capable of produc-
ing generalizable outcomes (Baer, Wolf, & Risley, 1968). Goals and Objectives
Since then, ABA research has found a welcome home in
numerous professional journals in various disciplines. ABA treatment goals, regardless of neuropsychological
The Association for Behavior Analysis-International was population, can be broadly classified as efforts to promote
established in 1974 and is ABAs principal professional the acquisition, maintenance, fluency (i.e., rate), and
organization. generalization of adaptive behavior, as well as the
Applied Behavior Analysis A 231
reduction of challenging behavior. An individuals treat- people in their environment (e.g., staff, parents). Treat-
A
ment goals and objectives should be determined by an ment participants have been of diverse ages, diagnoses,
analysis of the persons behavioral excesses and deficits and severity of disability. Intervention has occurred in
based on their expectations in the environmental context both laboratory and natural settings for numerous adap-
(i.e., goals should be socially valid). tive and challenging behaviors to meet goals and objec-
The social validity of treatment goals can be deter- tives, such as those previously stated. The largest body of
mined more formally either by social comparison or sub- research and application can be found for persons with
jective evaluation techniques (Kazdin, 1977). The former developmental disabilities, especially intellectual disabili-
relies on considering an individuals behavior with respect ty, and more recently autism spectrum disorders. For
to that of an appropriate comparison group. For example, approximately 50 years, research and application for indi-
the classroom out-of-seat behavior of a child with hyper- viduals with intellectual disability has occurred across the
activity could be compared with that of his classmates lifespan, severity of the disability, behavioral topogra-
who serve as the social validation criterion. Does the phies, and in institutional and community settings. ABA
childs out-of-seat behavior fall unacceptably outside the research and applications to autism have been more lim-
range of his or her peers? Subjective evaluation relies on ited, but noteworthy, with children being the most fre-
the opinion of key persons in the environment as a social quent recipient of treatment. There is a much smaller, but
validation criterion. For example, the teacher might rate nevertheless important, body of ABA treatment demon-
the childs out-of-seat behavior daily with respect to its strations for individuals with other neuropsychological
acceptability. Is the childs out-of-seat behavior unaccept- disorders, including acquired head injury, Alzheimers
able in the opinion of the teacher? Treatment participants disease, attention deficit/hyperactivity disorder, cerebral
also could assist in setting their own goals as part of a self- palsy, dementia, epilepsy, learning disabilities, schizophre-
management program. nia, and Tourettes syndrome. ABA based treatments have
The specific behavioral topographies that are the goals much to offer these under-studied populations, their
of change might differ across individuals (e.g., by popula- families, and the staff who serve them. The breadth of
tion, type and severity of disability, setting). Treatment applicability of ABA-based treatments across clinical and
goals also can have commonality across different clinical nonclinical populations can be attributed to the generality
populations (e.g., rate of performing academic behavior by of the underlying principles and processes of the science
children with attention deficit/hyperactivity disorder and of behavior.
cerebral palsy; reduction of physically aggressive behavior
by individuals with acquired head injury and encephalitis).
Thus, practitioners should focus on understanding the Treatment Procedures
personcontext relationship when formulating treatment
goals, and not solely on a persons diagnosis. As previously stated, ABA is the science of behavior and
Individuals with various neuropsychological disorders not a treatment per se. Treatments typically include a
have had treatment goals related to specific target beha- number of components that are applications of the sci-
viors, such as: (a) acquired brain injury (aggression, vo- ence of behavior; however, claims about the efficacy of
cational behavior); (b) attention deficit/hyperactivity individual components cannot be made independently of
disorder (off-task, academic behavior); (c) autism (com- the whole treatment package. A common component of
munication, social skills); (d) cerebral palsy (conversa- ABA treatment packages is differential reinforcement (i.e.,
tion, walking); (e) dementia, including Alzheimers reinforcing the desired response and withholding rein-
disease (incontinence, wandering); (f) encephalitis (sexu- forcement or using a behavior reduction tactic for unde-
al and violent behavior); (g) epilepsy (diet compliance, sired responses). For example, the pathological tongue
seizure awareness); and (h) Tourettes syndrome (vocal thrust during mealtime of a 10-year old boy with mental
and motor tics). retardation and spastic cerebral palsy was treated by pre-
senting food when his tongue was in and pushing the
tongue back into his mouth with a spoon when he thrust
Treatment Participants out his tongue and expelled food (Thompson, Iwata, &
Poynter, 1979). Amount of attention was differentially
ABA has had wide application of its treatment procedures provided to control breath-holding for a 7-year old girl
to various clinical and nonclinical populations, including with mental retardation and Cornelia-de-Lange syn-
those with neuropsychological disorders, as well as key drome (Kern, Mauk, Marder, & Mace, 1995) and the
bizarre vocalizations of an adult with schizophrenia involves performing a functional behavioral assessment
(Wilder, Masuda, OConner, & Baham, 2001). Noncon- to form a hypothesis regarding the cause of challenging
tingent attention (i.e., increasing attention overall with- behavior. For example, treatment for a persons self-inju-
out respect to a specific target behavior) has been used rious behavior should be developed based on an under-
effectively for reducing disruptive vocalizations by elderly standing of why that persons problem behavior occurs in
dementia patients (Buchanan & Fisher, 2002); noncontin- a given context. The specific self-injurious behavior might
gent escape (i.e., allowing escape from an activity regard- be reinforced by receiving social attention or tangible
less of behavior) has been used for treating aggression items from others, escape or avoidance from aversive
during bathroom routines for the same population stimuli (e.g., task demands, irritation from eczema), au-
(Baker, Hanley, & Mathews, 2006). tomatic reinforcement (e.g., sensory self-stimulation), or
To increase the likelihood that response consequences a combination of these consequences. Functional behav-
serve a reinforcing function, stimulus preference assess- ioral assessment procedures include various descriptive,
ments are formally conducted. For example, the relative indirect (e.g., interview, rating scales), and experimental
preference of 33 food items was assessed to help a 15-year methods. Treatment procedures are then derived from the
old girl with uncontrolled epilepsy maintain compliance hypothesized function of the problem behavior indicated
to a ketogenic diet (Amari, Grace, & Fisher, 1995). Highly by the functional behavioral assessment. For example, the
preferred foods were used to reinforce compliance to the inappropriate sexual behavior of a 9-year old boy with
diet. Allowing individuals to make choices among activ- acquired brain injury was determined to be reinforced by
ities to be performed is another tactic to promote desired social attention (Fyffe, Kahng, Fittro, & Russell, 2004).
behavior (e.g., on-task by individuals with traumatic Treatment derived from that hypothesis consisted of func-
brain injury) and reduce challenging behavior. tional communication training and withholding attention
Several behavioral components are important when for the inappropriate behavior.
teaching new behavior. Often, shaping by successive An example of a comprehensive treatment package with
approximations is required to teach behavior. For exam- multiple components is a study that evaluated the efficacy
ple, a 5-year old child with mental retardation and spina of training children with autism to pass the state mandated
bifida was taught the use of crutches by breaking the task vision screening when they started school (Simer & Cuvo,
down into a 10-step sequence (Horner, 1971). Prompts or 2009). The package included components to teach the
cues usually are required to evoke an unlearned response. visual discriminations required (i.e., preference assess-
Examples include physical prompts (e.g., physically guid- ment, choice making, match-to-sample discrimination
ing a child to use crutches), modeling (e.g., video demon- discrete trial training, transfer of stimulus control, differ-
strating a typically developing child undergoing a medical ential reinforcement), and additional components to re-
exam), visual prompts (e.g., picture or written memory duce escape/avoidance behavior (i.e., desensitization,
aides for adults with Alzheimers disease or acquired brain extinction, reinforcement of alternative behavior).
injury), and verbal instructions (i.e., telling people what Behavioral principles and processes can explain the
to do). ABA research has also demonstrated procedures to behavior of social units at all levels (e.g., individual, fami-
transfer control of responding from the prompt to natural ly, staff, organizations), and ABA interventions can be
cues (e.g., from the memory aide that prompts going to applied to each of these social levels. Treatment programs
the next activity to the time on the clock). are individualized with respect to frequency and duration,
Environmental arrangements are also helpful in with a general goal to assist the social unit achieve as
controlling behavior. A visual cloth barrier on an unsafe much independence as feasible. The distinguishing fea-
restricted area reduced entry to that area by dementia ture of ABA treatments is that they are based on an
patients who wandered (Feliciano, Vore, LeBlanc, & analysis of the function of behavior in its environmental
Baker, 2004). Furniture was rearranged to be more con- context, derived from the science of behavior (i.e., pri-
ducive to conversation, and mealtime routines were rear- marily operant conditioning), and assessed for efficacy at
ranged to improve behavior in dementia patients (Melin the level of individuals and not groups as a whole.
& Gotestam, 1981). Classroom environmental arrange-
ments of various types are standard practice to control
the behavior of children with autism. Efficacy Information
There is a considerable literature base on ABA
approaches to reduce the challenging behavior of persons The efficacy of ABA derived treatments most typically has
with neuropsychological disorders. Best practice today been established by small n single subject experimental
Applied Behavior Analysis A 233
designs that control for threats to internal validity. Exter- client, preferably to supplement objective observation by
A
nal validity is established by multiple systematic replica- others.
tions that expand the generality of the findings. The body Behavior should be analyzed at its most microscopic
of ABA treatment efficacy research has increased signifi- level (e.g., trial or session data for an individual) initially
cantly over the decades since the 1960s. There are sub- before aggregating across more macroscopic levels (e.g.,
stantial treatment efficacy and effectiveness data for basic trial blocks, days, persons). Most often, data are plotted in
behavioral processes and their application to persons with a figure (e.g., line graph) and analyzed visually. For re-
neuropsychological disorders. Thousands of studies have search purposes, data are typically collected in the context
demonstrated the efficacy of interventions that teach or of the requirements of a single subject experimental de-
strengthen behavior. Efficacy has been demonstrated for sign. For routine clinical practice, it is advisable to have at
procedures that involve basic reinforcement processes, least baseline and treatment data.
token reinforcement, self-management, shaping, chain- Since ABA-based treatment programs should address
ing, prompting, transfer of stimulus control, and other socially valid goals for an individual, outcome measure-
behavioral processes and techniques. Likewise, numerous ment largely relies on a consideration of whether treat-
studies have provided evidence for the efficacy of behavior ment effects have attained those goals. Most often, that
reduction procedures based on processes such as extinc- determination can be made by visual inspection of the
tion, punishment, response cost, timeout, and differential data. Behavior analysts are interested in clinically mean-
reinforcement of various types. During the past 25 years, ingful (i.e., visually obvious on a figure) results and not
the efficacy of deriving treatment hypotheses for challeng- less impressive improvement, even if it is unlikely to have
ing behavior from a functional behavioral assessment occurred by chance.
has been clearly demonstrated by a large number of The social or clinical significance of outcomes can be
systematic replications. measured more formally either by social comparison or
Although there is a substantial body of ABA efficacy subjective evaluation techniques (Kazdin, 1977) as previ-
research that demonstrates the generality of behavioral ously described. For example, does the out-of-seat behav-
principles and processes across target behaviors, popu- ior of a child with hyperactivity after treatment compare
lations, and settings, the amount of efficacy research favorably to that of his classmates who serve as the social
differs across specific populations with neuropsycholog- comparison criterion? Does the teacher who serves as the
ical disorders. An ABA approach to intervention has subjective evaluation criterion rate the childs out-of-seat
been best practice for decades for individuals with in- behavior as acceptable after treatment?
tellectual disability, especially for those with more se- Since the goal of ABA research and treatment is to
vere disability. Since the 1960s beginning with Lovaas produce socially significant outcomes for individuals and
seminal work, efficacy of an ABA approach to treat not for samples from a population, the role of statistical
young children with autism has been demonstrated analysis as a decision making tool is rather limited. De-
and earned support by the US Surgeon General (1999) scriptive statistics are sometimes used to supplement vi-
and others. A recent meta-analysis of behavioral treat- sual analysis and social validation. Descriptive statistics
ments for attention-deficit/hyperactivity disorder sup- can serve as an aide by summarizing certain key charac-
ported the efficacy of ABA for that population (Fabiano teristics of the data set (e.g., measures of central tendency,
et al., 2009). variability, trend, effect size). When inferential statistics
are used, they are employed to make inferences from a
sample of an individuals behavior (i.e., data collected) to
Outcome Measurement the universe of that individuals behavior, and not to
population parameters.
The primary method of measuring treatment outcomes in Another outcome evaluative criterion is theoretical
ABA is direct and systematic observation of the objective- significance. Are treatment outcomes consistent with the
ly defined behavioral topography of interest (e.g., its fre- behavioral conceptualizations that underlie treatment se-
quency, duration, intensity). That measurement could be lection for the target behaviors? For example, is behavior
either continuous (i.e., each event) or sampled from the reduction treated by extinction (i.e., withdrawing rein-
individuals universe of behavior (e.g., by interval or time forcement from a previously reinforced response) consis-
sampling recording). Observers should be reliability tent with what we know about extinction as a basic
trained and observe and record independently of each behavioral process? Because of the idiographic nature of
other. Some ABA programs include self-observation by a ABA treatment, standardized instruments based on
normative data for measuring treatment outcome are References and Readings
generally eschewed in favor of individualized measure-
ment as previously described. Nevertheless, individualized Amari, A., Grace, N. C., & Fisher, W. W. (1995). Achieving and main-
rating scales, logs, and standardized tests are sometimes taining compliance with the ketogenic diet. Journal of Applied Be-
havior Analysis, 28, 341342.
used as secondary measures.
Baer, D. M., Wolf, M. M., & Risley, T. R. (1968). Some current dimensions
of applied behavior analysis. Journal of Applied Behavior Analysis,
1, 9197.
Qualifications of Treatment Providers Baker, J. C., Hanley, G. P., & Mathews, M. R. (2006). Staff-administered
functional analysis and treatment of aggression by elder with de-
mentia. Journal of Applied Behavior Analysis, 39, 469474.
The principal credential for applied behavior analysts is Buchanan, J. A., & Fisher, J. E. (2002). Functional assessment and non-
national certification that is administered by The Behav- contingent reinforcement in the treatment of disruptive vocalization
ior Analyst Certification Board, a nonprofit corporation. in elderly dementia patients. Journal of Applied Behavior Analysis, 35,
There are two levels of professional certification. The 99103.
Cooper, J. O., Heron, T. E., & Heward, W. L. (2007). Applied behavior
Board Certified Behavior Analyst (BCBA): (a) holds a
analysis (2nd ed.). Upper Saddle River, NJ: Pearson.
masters or doctoral degree, (b) has had the required Fabiano, G. A., Pelham, W. E. Jr., Coles, E. K., Gnagy, E. M., Chronis-
number of coursework hours in certain core content Tuscano, A., & OConnor, B. (2009). A meta-analysis of behavioral
areas of behavior analysis (i.e., ethics, behavioral princi- treatments for attention-deficit/hyperactivity disorder. Clinical Psy-
ples, behavioral assessment and selecting interventions, chology Review, 29, 129140.
Feliciano, L., Vore, J., LeBlanc, L. A., & Baker, J. C. (2004). Decreasing
experimental evaluation, behavioral measurement, and
entry into a restricted area using a visual barrier. Journal of Applied
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passed a written test. The Board Certified Assistant In P. Sturmey (Ed.), Functional analysis in clinical treatment
Behavior Analyst (BCABA) holds a Baccalaureate degree, (pp. 335355). Burlington, MA: Elsevier.
Fyffe, C. E., Kahng, S. W., Fittro, E., & Russell, D. (2004). Functional
has passed a written test, and has had similar coursework
analysis and treatment of inappropriate sexual behavior. Journal of
and supervised clinical experience as the BCBA but to Applied Behavior Analysis, 37, 401404.
a lesser degree. BCBAs and BCABAs can hold their Hayes, S. C., Barnes-Holmes, D., & Roche, B. (2001). Relational frame
required academic degrees in any discipline as long as theory. New York: Plenum.
they meet the other requirements. Psychologists can Horner, R. D. (1971). Establishing use of crutches by a mentally
retarded spina bifida child. Journal of Applied Behavior Analysis, 4,
be certified in Behavioral Psychology, with a concentra-
183189.
tion in ABA by the American Board of Behavioral Kazdin, A. E. (1977). Assessing the clinical or applied importance of
Psychology, an affiliate of the American Board of Profes- behavior change through social validation. Behavior Modification,
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Stimulus Generalization Century-Crofts.
Apraxia A 235
Thompson, G. A. Jr., Iwata, B. A., & Poynter, H. (1979). Operant control deficits or weakness, discoordination, movement disor-
of pathological tongue thrust in spastic cerebral palsy. Journal of A
ders, and sensory loss.
Applied Behavior Analysis, 12, 325333.
U. S. Department of Health and Human Services. (1999). Mental health:
Assessment: Assessment for apraxia involves asking a
A report of the surgeon general. Rockville, MD: Department of Health patient to carry out pantomimes of movements (e.g.,
and Human Services, Substance Abuse and Mental Health Services show me how you would salute . . . brush your teeth
Administration, Center for Mental Health Services, National Insti- with a toothbrush. . . blow out a candle). If the response
tute of Mental Health.
in not correct, the examiner may evaluate the patients
Wilder, D. A., Masuda, A., OConnor, C., & Baham, M. (2001). Brief
functional analysis and treatment of bizarre vocalizations in adult
response to imitation of the movement or ability to
with schizophrenia. Journal of Applied Behavior Analysis, 34, 6568. produce the movement using actual objects or tools.
The patient may also be tested for recognition of skilled
movements produced by the examiner.
Classification of Apraxia: Apraxias may be differentiated
Applied Behavioral Analysis by the body elements involved in the impaired movement,
using the terms limb apraxia, oral or buccofacial apraxia,
Behavior Modification trunk or axial apraxia. These disorders have different
neuroanatomical underpinnings and may occur separate-
ly in different individuals. For instance, patients with oral
apraxia may demonstrate normal function on tests of
Apprehension Span limb praxis.
Apraxia has been subclassifed into ideational apraxia,
Span of Apprehension ideomotor apraxia, and limb-kinetic apraxia (Liepmann,
1900). Ideational apraxia is a loss of the conception of a
gesture or skilled movement. In this form, the patient
does not seem to know what to do, and the motor activity
Apraxia is not facilitated by the use of actual objects. Ideomotor
apraxia affects the implementation of the movement,
D OUGLAS I. K ATZ producing spatial and timing errors. The patient seems
Boston University School of Medicine to know what to do but cannot carry the movement out
Braintree, MA, USA properly. Limb-kinetic apraxia is the inability to make
finely graded, precise limb movements. It has been
difficult to separate this form of apraxia from motor
Definition dysfunction related to elemental motor disturbance, and
it remains controversial that this is actually an apraxic
The inability to correctly carry out a learned, skilled disorder of learned skilled movement.
motor act despite the preserved capability of the Neuropathological localization: Apraxias are almost al-
sensorimotor system to produce the intended movement. ways associated with lesions in the dominant hemisphere.
The left parietal lobe is most often implicated in limb
apraxia in right-handers. Portions of the frontal lobes,
Current Knowledge including the supplementary motor area, have been
implicated in some forms of apraxia. Lesions in and
Apraxia is thought to involve a loss of representations or around Brocas area are most often implicated in cases
the inability to adequately access representations of of oral apraxia. Lesions affecting transmission of informa-
learned movements and motor skills in the damaged tion between the cerebral hemispheres, including lesions
brain. This may lead to a loss of recall of the concept or of the corpus callosum, may lead to apraxia of just the left
configuration of the movement, or the inability to limbs because of disconnection of movement engrams in
transform or implement the representational knowledge the left hemisphere from motor control areas in the right
of the movement into a well-coordinated, properly con- hemisphere (callosal apraxia).
figured, and sequenced gesture. The diagnosis of apraxia Other disorders: A number of disorders have labels that
requires the exclusion of cognitive and sensorimotor include the term apraxia but have no relationship with
impairments that may affect the ability to carry out the apraxia according to the usual definition. These include:
motor skill, such as arousal, attention, intention, language Dressing apraxia difficulty orienting clothes to the body,
236 A Apraxia of Speech
often associated with left neglect, and usually occurring (e.g., aphemia, phonemic disintegration, cortical dysar-
with superior parietal right hemisphere lesions; construc- thria, dyspraxia of speech). Currently, there are no
tional apraxia difficulty drawing or copying pictures or acceptable synonyms in use. The descriptor, stroke in-
designs; gait apraxia difficulty initiating or maintaining duced (SI), has occasionally been used to specify AOS
a normal gait pattern as can be seen in normal pressure resulting from stroke (e.g., SI-AOS).
hydrocephalus; apraxia of gaze difficulty directing eye
movements as seen in Balints syndrome. Apraxia of speech
is a disorder that affects the sequencing of sounds in Short Description or Definition
words and syllables. It can be developmental or acquired
and people with this disorder have difficulty coordinating AOS is a neurologic, motoric disorder of speech produc-
articulatory motor activities necessary for speech. It is tion that is characterized by slowed rate of speech, diffi-
controversial whether this represents an apraxia consis- culties in sound production, and disrupted prosody. AOS
tent with the definitions described above, or a subtype is not a disorder of language, although it rarely occurs
of language or elemental motor disorders affecting without aphasia. Consequently, there is no impairment of
articulatory sequencing. comprehension or production of language in pure AOS.
Cross References Categorization

Balints Syndrome AOS is not divided into categories. Childhood Apraxia of
Brocas Aphasia Speech (CAS) is a related disorder, but not a category of
Frontal Lobes AOS.
Movement Disorders
Supplementary Motor Area
Epidemiology
References and Readings Duffy (2005) reported that AOS was the primary com-
munication disorder in 7.6% of 6,101 cases of neurologic
De Renzi, E. (1990). Apraxia. In F. Boller & J. Grafman (Eds.), Handbook
motor speech disorders. As a secondary diagnosis (e.g.,
of neuropsychology (Vol. 2, pp. 245263). New York: Elsevier.
Heilman, K. M. (1997). Disorders of skilled movements: limb apraxia.
accompanying aphasia), AOS can be expected to occur
In T. E. Feinberg & M. J. Farah (Eds.), Behavioral neurology and more frequently.
neuropsychology (pp. 227235). New York: McGraw Hill.
Liepmann, H. (1900). Das Krankheitsbild der Apraxie (motorische
Asymbolie) auf Grund eines Falles von einseitiger Apraxie.
Monatschrift Psychiatrie und Neurologic, 8, 1544,
Rothi, L. J. G., & Heilman, K. M. (1997). Apraxia: The neuropsychology of
Outcomes
action. East Sussex: Psychology Press.
The establishment of AOS as a distinct clinical entity is
typically credited to Dr. Fredrick Darley, who in the late
1960s stimulated much of the early discussion and re-
Apraxia of Speech search concerning the nature and characteristics of this
disorder. Since that time, the definition and descriptors of
J ULIE L. WAMBAUGH AOS have continued to evolve, with continuing research
Veterans Affairs Salt Lake City Healthcare System efforts being likely to result in further refinement of our
and University of Utah knowledge concerning this disorder.
Salt Lake City, UT, USA The most frequent cause of AOS is cerebral vascular
accident involving the language-dominant hemisphere.
Other causes of focal brain damage (e.g., penetrating
Synonyms head injury, neoplasm resection) may also result in
AOS. Areas of injury that have been most often asso-
Historically, acquired apraxia of speech (AOS) has been ciated with AOS include the regions in the premotor
known under a variety of terminological designations cortex (notably, the left posterior, inferior frontal
Apraxia of Speech A 237
gyrus), parietal lobe, and insula (see Wambaugh and Unlike the dysarthrias, AOS is not associated with problems
A
Shuster, 2008 for a review). with muscle tone, weakness, reflexes, or sensory processing.
Little objective evidence exists concerning the natural
course of AOS, including the factors affecting prognosis.
Duffy (2005) indicates that mutism associated with AOS Evaluation
rarely lasts beyond 2 weeks unless other speech, language,
or cognitive deficits are also present. Diagnosis of AOS requires that the primary symptoms of
Treatment can be expected to result in the improvement reduced rate of speech, distorted sound production, and
in symptoms of AOS, even when AOS is chronic. Treatment disrupted prosody be present. Behaviors such as difficul-
guidelines for AOS have been developed, which provide ties with speech initiation or articulatory groping (see
effectiveness ratings for different types of treatment based above) may also be observed, but should not be used
on the existing published evidence (see below; Wambaugh, alone for purposes of differential diagnosis (Wambaugh
Duffy, McNeil, Robin, and Rogers, 2006a, 2006b). et al., 2006a). Screening for AOS typically involves eli-
citing a variety of speech samples and determining the
presence or absence of AOS symptoms. For example,
Neuropsychology and Psychology Duffy (2005) provides a tool that may be used to evaluate
of AOS speech production across tasks such as sound, monosyllabic
word, multisyllabic word, and sentence repetition; repeated
AOS is a neurogenic, motoric speech disorder that is word productions; alternate and sequential motion rates,
characterized by reduced rate of speech, disrupted pro- reading aloud; and connected speech production. The
duction of speech sounds, and disordered prosody. These Apraxia Battery for Adults second edition (Dabul, 2000)
symptoms may be accompanied by behaviors such as also provides tasks that may be used for examining speech
articulatory groping (silent and/or audible), speech initi- production in adults with suspected AOS. However, the
ation difficulties, increasing number of sound errors with criteria for diagnosis of AOS provided by this test will not
increasing word length or phonetic complexity, awareness differentiate AOS from phonemic paraphasia.
of speech errors, and motoric perseverations. Its severity
ranges from a total inability to speak to negligible speech
disruptions (McNeil, Robin, and Schmidt, 2009; Wam- Treatment
baugh et al., 2006a).
AOS is thought to be caused by difficulties in the Behavioral treatment has been demonstrated to have
process of converting correctly selected and ordered positive outcomes for persons with AOS. An AOS prac-
sounds into previously learned movement information tice guidelines report revealed four general approaches to
necessary for the implementation of intended speech AOS treatment: (1) articulatory-kinematic treatments
movements. That is, it is assumed that sounds are cor- (techniques focused on improving articulation of
rectly selected and sequenced at a linguistic level of pro- sounds), (2) rate/rhythm control treatments (therapies
cessing. However, there is difficulty in accessing stored involving manipulating rate of speech production or
movement plans/programs needed to articulate those imposing an external rhythm on speech), (3) alterna-
chosen sounds. These difficulties cause disruptions in tive/augmentative communication approaches (therapies
the selection, positioning, and movement timing of the involving training the use of methods/devices for supple-
articulators (e.g., tongue, lips, etc.). Consequently, sound menting or replacing speech), and (4) intersystemic fa-
productions may be inaccurate, transitions between cilitation/reorganization treatments (therapies utilizing a
sounds may be disrupted, and prosody may be abnormal. relatively intact system/modality such as singing or ges-
Sound durations as well as the intervals between sounds, turing to facilitate speech production) (Wambaugh et al.,
syllables, and words tend to be prolonged. Sound produc- 2006b). On the basis of objective evaluation of the existing
tion errors are relatively consistent in location and invari- evidence, the AOS guideline developers determined that
able in type across repeated productions (McNeil, Robin, articulatory-kinematic approaches were probably
and Schmidt, 2009). effective rate/rhythm control approaches and intersyste-
AOS typically occurs with aphasia and rarely occurs mic approaches were possibly effective; and AAC
without it. The symptoms of AOS, however, are not approaches had insufficient support to warrant a rating.
attributable to disruptions in language. AOS may also There are currently no published reports of restorative
occur with another motor speech disorder, dysarthria. neurological treatments applied specifically to AOS
238 A Apraxic Agraphia
(e.g., neuropharmaceutical treatment, electrical cortical speech used in addition to words to convey specific mean-
stimulation, transcranial magnetic stimulation), but ing and emotional information (Leon & Rodriguez, 2008;
such reports are likely to be available in the future. Wymer, Lindman, & Booksh, 2002). Aprosodia is tradi-
tionally characterized as linguistic or affective (Wymer
Cross References et al., 2002). Linguistic prosody aids meaning, e.g., convict
vs. convict or the dog and the cat in the cage are mine vs. the
Aphasia dog, and the cat in the cage, are mine allow unambiguous
Dysarthria discrimination of the semantic target. Affective prosody
Phonemic Paraphasia conveys attitude, e.g., incredulity, sadness, or anger, e.g.,
depending on the prosodic intonation, oh, yeah, Im just
great may be a sincere expression of a good feeling, or an
References and Readings equally sincere communication that the speaker is angry
or frustrated. Linguistic aprosodia is associated with both
Dabul, B. (2000). Apraxia battery for adults (2nd ed.). Austin, TX: Pro-ed.
Duffy, J. R. (2005). Motor speech disorders: Substrates, differential
left and right hemisphere lesions; affective aprosodia is
diagnosis, and management (2nd ed.). St. Louis, MO: Elsevier Mosby. more consistently associated with lesions of the right hemi-
McNeil, M. (2002). Apraxia of speech: From concept to clinic. Seminars sphere (Baum & Pell, 1999; Pell, 2006; Ross & Monnot,
in Speech and Language, 23(4), 221222. 2008). Additionally, the basal ganglia appear to play a key
McNeil, M. R., Robin, D. A., & Schmidt, R. A. (2009). Apraxia of speech:
role in processing and further distributing the meaning
Definition and differential diagnosis. In M. R. McNeil (Ed.), Clinical
management of sensorimotor speech disorders (2nd ed., pp. 249268).
associated with the prosodic characteristics (Cancelliere &
New York: Thieme. Kertesz, 1990; Pell & Leonard, 2003).
Wambaugh, J. L., & Shuster, L. I. (2008). The nature and management of Clinically, aprosodia is most often considered in terms
neuromotor speech disorders accompanying aphasia. In R. Chapey of whether receptive, expressive, or both aspects of pro-
(Ed.), Language intervention strategies in aphasia and related neuro-
sodic ability are diminished in an individual. However,
genic communication disorders (5th ed., pp. 10091042).
Philadelphia, PA: Lippincott Williams & Wilkins.
Ross and various colleagues have proposed a categoriza-
Wambaugh, J. L., Duffy, J. R., McNeil, M. R., Robin, D. A., & Rogers, M. tion system for the aprosodias, which is similar to that
(2006a). Treatment guidelines for acquired apraxia of speech: A used to categorize aphasia types. The system is based on a
synthesis and evaluation of the evidence. Journal of Medical Speech combination of deficit profile and site-of-lesion informa-
Language Pathology, 14(2), xvxxxiii.
tion: motor (in the area of the frontal operculum), sensory
Wambaugh, J. L., Duffy, J. R., McNeil, M. R., Robin, D. A., & Rogers, M.
(2006b). Treatment guidelines for acquired apraxia of speech: Treat-
(posterior temporal operculum), conduction (arcuate fas-
ment descriptions and recommendations. Journal of Medical Speech ciculus), transcortical (anterior or posterior watershed),
Language Pathology, 14(2), xxxvixvii. or global deficits (Ross, 1981, 2000; Ross & Monnot,
2008). For example, an individual with motor aprosodia
might not express affective or emotional prosody when
speaking; one with sensory aprosodia might not recognize
Apraxic Agraphia the affective meaning of prosodic signals in anothers
speech. These nondominant hemisphere anatomic corre-
Agraphia lates of prododic deficits do have modest empirical support
(see Ross & Monnot, 2008 for a summary of related inves-
tigations). Ross motor aprosodia should not be confused
with prosodic production impairments that arise from def-
Aprosodia icits in speech production due to dysarthria (Duffy, 2005).
Assessment of aprosodia is generally accomplished
K ATE K RIVAL through careful observation; however, the Florida Affect
Kent State University Battery (Bowers, Blonder, & Heilman, 1998) and the
Kent, OH, USA Aprosodia Battery (Ross, Thompson, & Yenkosky, 1997)
may be useful additions to standard testing regimes. Man-
agement of aprosodic impairments has received little at-
Definition tention in the literature; however, emerging evidence
suggests that behavioral therapies may have some effect
Aprosodia is a deficit in comprehending or expressing (Bornhofen & MacDonald, 2008; Leon et al., 2005; Rosen-
prosody, i.e., variations in pitch, loudness, or rhythm of bek et al., 2004). Future work that will focus on the design
Arachnoid Cyst A 239
and implementation of treatment for both expressive and Ross, E. D., & Monnot, M. (2008). Neurology of affective prosody and its
functionalanatomic organization in right hemisphere. Brain and A
receptive aprosodia is anticipated.
Language, 104(1), 5174.
Ross, E. D., Thompson, R. D., & Yenkosky, J. P. (1997). Lateralization of
affective prosody in brain and the callosal integration of hemispheric
Cross References language functions. Brain and Language, 56, 2754.
Wymer, J. H., Lindman, L. S., & Booksh, R. L. (2002). A neuropsycholog-
ical perspective of aprosody: Features, function, assessment and
Apraxia of Speech
treatment. Applied Neuropsychology, 9(1), 3747.
Dysarthria
Prosody

Arachnoid Cyst
Baum, S. R., & Pell, M. D. (1999). The neural bases of prosody:
Insights from lesion studies and neuroimaging. Aphasiology, 13,
B ARBARA S PACCA 1, A NDREW B RODBELT 2
1
581608. Childrens Hospital Anna Meyer
Bornhofen, C., & McDonald, S. (2008). Comparing strategies for treating Florence, Italy
emotion perception deficits in traumatic brain injury. Journal of 2
The Walton Centre for Neurology and Neurosurgery
Head Trauma Rehabilitation, 23(2), 103115.
Lower lane, Liverpool, UK
Boutsen, F. R., & Christman, S. S. (2002). Prosody in apraxia of speech.
Seminars in Speech and Language, 23, 245255.
Bowers, D., Blonder, L., & Heilman, K. M. (1998). The Florida
affect battery. Gainesville, FL: University of Florida Brain Institute. Synonyms
Cancelliere, A. E. B., & Kertesz, A. (1990). Lesion localization in acquired
deficits of emotional expression and comprehension. Brain and
Temporal lobe agenesis
Cognition, 13(2), 133147.
Duffy, J. R. (2005). Motor speech disorders: Substrates, differential diagno-
sis, and management. St. Louis, MO: Mosby.
Emmorey, K. D. (1987). The neurological substrates for prosodic aspects
of speech. Brain and Language, 30, 305320. Short Description or Definition
Karow, C. M., & Connors, E. C. (2003). Affective communication in
normal and brain-damaged adults: An overview. Seminars in Speech
and Language, 24(2), 6991.
Arachnoid cysts are benign intracranial space occupying
Leon, S. A., & Rodriguez, A. D. (2008). Aprosodia and its treatment. lesions. An arachnoid membrane surrounds a collection
Perspectives on Neurophysiology and Neurogenic Speech and Language of clear fluid, identical to cerebrospinal fluid (CSF).
Disorders, 18, 6672. Arachnoid cysts present due to mass effect, sudden hem-
Leon, S. A., Rosenbek, J. C., Crucian, G. P., Heiber, B., Holiway, B.,
orrhage, or incidentally.
Rodriguez, A. D., et al. (2005). Active treatments for aprosodia
secondary to right hemisphere stroke. Journal of Rehabilitation Re-
search and Development, 42(1), 93102.
Monrad-Krohn, G. H. (1948). Dysprosdy or altered melody of language.
Brain, 70, 405415.
Categorization
Pell, M. D. (2006). Cerebral mechanisms for understanding emotional
prosody in speech. Brain and Language, 96(2), 221.
Pell, M. D., & Leonard, C. L. (2003). Processing emotional tone from Arachnoid cysts are classified according to their location
speech in Parkinsons disease: a role for the basal ganglia. Cognitive, as intracranial or spinal. Intracranial arachnoid cysts can
Affective, & Behavioral Neuroscience, 3(4), 275288. be further subclassified (Table 1). Middle fossa cysts
Rosenbek, J. C., Crucian, G. P., Leon, S. A., Hieber, B., Rodriguez, A. D.,
(MFAC) can also be classified according to their size and
Holiway, B., et al. (2004). Novel treatments for expressive aprosodia:
A phase I investigation of cognitive linguistic and imitative inter-
distortion of surrounding structures based on Galassi
ventions. Journal of the International Neuropsychological Society: classification (Galassi et al., 1982). Type I cysts are small,
JINS, 10(5), 786793. biconvex, and have no mass effect (Fig. 1a); type II cysts
Ross, E. D. (1981). The aprosodias: Functional-anatomical organization have a rectangular shape and involve proximal and inter-
of the affective components of language in the right hemisphere.
mediate segments of the Sylvian fissure (Fig. 1b); type III
Archives of Neurology, 38, 561569.
Ross, E. D. (2000). Affective prosody and the aprosodias. In M. M.
cysts entirely involve the Sylvian fissure and can produce
Mesulam (Ed.), Principles of behavioral and cognitive neurology. midline shift (Fig. 1c). Arachnoid cysts may also be classi-
New York: Oxford University Press. fied as primary congenital or acquired (Di Rocco, 1990;
240 A Arachnoid Cyst
Arachnoid Cyst. Table 1 Frequency and distribution of intracranial arachnoid cysts (Rengachary, Watanabe, & Brackett, 1978)
Position Incidence (%) Position Incidence (%)

Supratentorial 76.8 Infratentorial 23.2
Middle cranial fossa 38.6 CerebelloPontine Angle 15.7
Sellar, intrasellar, suprasellar 13.3 Vermal 6.3
Convexity 11.5 Clival 1.2
Interemispheric fissure 8.3
Quadrigeminal plate 5.1
Arachnoid Cyst. Figure 1 Classification of middle fossa arachnoid cysts. (a) bilateral type I middle fossa arachnoid cyst
demonstrating small size, biconvex appearance, and absence of mass effect; (b) type II middle fossa arachnoid cysts are
rectangular; (c) type III middle fossa arachnoid cyst are large and often have significant mass effect
Oberbauer, 1999). Midline posterior fossa arachnoid cysts structural anomalies such as agenesis of the corpus callo-
must not be confused with the DandyWalker complex. sum (occurring in 68% of patients), and a post fossa
The DandyWalker complex describes hypoplasia or agen- arachnoid cyst- like structure that is not a true arachnoid
esis of the cerebellar vermis, associated hydrocephalus, cyst (Wilkinson & Winston, 2008).
Epidemiology Originally thought to be due to congenital hypoplasia

A
of the brain (e.g. temporal lobe agenesis), this concept
Arachnoid cysts are estimated to account for 1% of all has been questioned, as postoperative imaging confirms
nontraumatic intracranial lesions and are incidentally that the brain expands after cyst decompression (Fig. 2).
found in 1 per 1,000 autopsies (Boop & Teo, 2000; Di Most arachnoid cysts are now considered to be the result
Rocco, 1990; Oberbauer, 1999; Wilkinson & Winston, of a defect in early fetal development. Between the 6th and
2008). They present in the first 2 decades of life, with a the 8th week of gestation, the meninx primitiva differ-
mean age at diagnosis of 6 years. There is a male predom- entiates into the pia and arachnoid mater. Congenital
inance (23:1). Arachnoid cysts are mainly localized to duplication or splitting of the arachnoid layer at this
one side, but case reports of bilateral cysts have been time is thought to lead to formation of primary congenital
described (Ziaka, Kouyalis, Boviatsis, & Sakas, 2008). arachnoid cysts (Bright, 1831; Gosalakkal, 2002; Miyajima
Familial presentations occur (glutaric aciduria type I) et al., 2000; Rengachary & Watanabe, 1981; Schachenmayr
(Jamjoom, Okamoto, Jamjoom, al-Hajery, & Abu- & Friede, 1978, 1979) (Fig. 3).
Melha, 1995). Imaging and endoscopic evidence exists demonstrat-
ing that at least in some arachnoid cysts, enlargement is
due to a unidirectional valve type mechanism (Gosalakkal,
Etiology/Pathology 2002; Miyajima et al., 2000; Santamarta, Aguas, & Ferrer,
1995; Schroeder & Gaab, 1997 ). A secretory mechanism
Microscopic examination demonstrates splitting of the from the cyst wall has been suggested, although others
arachnoid membrane at the margin of the cyst, a thick have disputed this because of a lack of microscopic
layer of collagen, hyperplastic arachnoid cells, and numer- evidence of secretion including pineocytosis (Go, Houth-
ous blood vessels in the cyst wall, and an absence of off, Blaauw, Havinga, & Hartsuiker, 1984; Gosalakkal,
traversing trabeculae although fine blood vessels may be 2002; Schachenmayr & Friede, 1979). Water movement
present (Miyajima et al., 2000; Rengachary & Watanabe, along an osmotic pressure gradient due to repeated small
1981). Arachnoid cysts can communicate or be separate intracystal hemorrhage has also been suggested (Di Rocco,
from the subarachnoid space (SAS), but appear to contain 1990). Arachnoid cysts can also be acquired following
fluid similar in composition to CSF (Miyajima et al.; hemorrhage, head injury, or surgery (Kutlay, Colak,
Rengachary & Watanabe; Yildiz et al., 2005). Demircan, & Akin, 1998).
Arachnoid Cyst. Figure 2 Middle fossa arachnoid cyst both before (a) and after (b) surgery. Note the significant brain
re-expansion, an observation used to refute the suggestion of a congenital hypoplastic origin
Arachnoid Cyst. Figure 3 Foetal magnetic resonance image Arachnoid Cyst. Figure 4 Quadrigeminal Plate arachnoid cyst
demonstrating an interemispheric arachnoid cyst

Outcomes, Symptoms, and Signs
The natural history of arachnoid cysts is unpredictable.

Cysts can grow in size, remain stable, rarely reduce, or
disappear completely. Spontaneous hemorrhage or hem-
orrhage occurring after minor head injury have been de-
scribed. In patients with middle fossa arachnoid cysts, the
annual risk of symptomatic hemorrhage is less than 0.1%
(Parsch, Krauss, Hofmann, Meixenberger, & Roosen,
1997). Hemorrhage can be asymptomatic, or, at worst,
present as a life-threatening acute subdural hematoma.
Subdural hygromas can also develop due to rupture of
the cyst wall. Symptomatic patients may complain of Arachnoid Cyst. Figure 5 Intraoperative photograph
symptoms related to raised ICP or specific to the cyst demonstrating microsurgical fenestration of an arachnoid cyst
location. Described symptoms and signs include irritabili-
ty, lethargy, headache, nausea, vomiting, diplopia, papille-
dema, cranial nerve dysfunction, and in infants, also been described (Boop & Teo, 2000; Di Rocco, 1990;
macrocrania, a tense fontanelle, displayed sutures, failure Oberbauer, 1999; Wilkinson & Winston, 2008).
to thrive, or to reach developmental milestones. Patients with sellar and suprasellar cysts typically pres-
In MFAC, bone deformities are common with large ent with endocrine dysfunction, manifesting as failure to
cysts and usually consist of macrocrania, temporal bone thrive or precocious puberty. Optic pathway compression
thinning, and bossing. Less commonly, downward displace- can result in loss of visual fields or acuity, while hypotha-
ment of the temporal floor and upward and forward dis- lamic pressure can produce eating and behavioral disor-
placement of the lesser wing of the sphenoid may lead to ders. Thinning and displacement of the floor of the sella
proptosis, and in extreme cases visual loss, facial numbness, turcica and an empty sella can be observed with intrasellar
and ocular palsies. Long tract compression can lead to cysts. Rarely, Suprasellar Cysts compressing the third ven-
sensory and motor limb signs. Seizures are common, occur- tricle present with bobble-head doll syndrome, whose
ring in up to 40% of patients. Developmental delays, behav- pathogenesis is unknown, consisting in involuntary
ioral disorders, memory, and attention dysfunction have movement of the head forward and backward at a rate
Arachnoid Cyst. Figure 6 Appearance before (a) and during (b) endoscopic fenestration of a middle fossa arachnoid cyst
of 23 times/s (Hagebeuk, Kloet, Grotenhuis, & Peeters, suggesting that arachnoid cysts may suppress cognitive
2005). Cerebral convexity cysts often present with cranial and cortical function (Baroey Raeder, Helland, Hugdahl,
deformity and asymmetry alone. Quadrigeminal Plate & Wester, 2005; Wester & Hugdahl, 2003). However,
Cysts (Fig. 4) can present with obstructive hydrocephalus larger series do not support significant clinical improve-
or upward gaze palsies. Spinal arachnoid cysts usually ment after surgery in patients with severe developmental
present with myelopathy or nerve root compression (Di and behavior problems (Arai et al.; Levy, Wang, Aryan,
Rocco, 1990). Yoo, & Meltzer, 2003). In patients with developmental
delay, behavioral disorders, and an arachnoid cyst, or in
very young patients with large cysts, preoperative neu-
Neuropsychology and Psychology of ropsycological testing, EEG, and/or SPECT may have a
Arachnoid Cysts role in supporting surgical intervention (Wilkinson &
Winston).
Large arachnoid cysts may present with failure to reach
developmental milestones and psychomotor delay. Cases
of dementia in adults have been reported (Harsh, Evaluation
Edwards, & Wilson, 1986). Cerebellar signs may be mis-
diagnosed as motor delay. MFAC and convexity cysts can Diagnosis and follow-up are based on clinical evaluation
be associated with cognitive problems, developmental and imaging. Arachnoid cysts appear as cavities filled with
delay, behavioral disorders, and memory and attention fluid with the same characteristics as CSF, surrounded
deficits in up to 7.8% of patients (Arai, Sato, Wachi, by a thin wall that is not calcified and does not enhance
Okuda, & Takeda, 1996). Symptoms can be potentiated after contrast. Magnetic resonance imaging (MRI) is the
with antiepileptic drugs and sedatives. The relationship diagnostic tool of choice because of image resolution for the
between arachnoid cysts and developmental and behav- cyst and surrounding anatomy (Wilkinson & Winston,
ior problems is poorly understood. Functional magnetic 2008).
resonance imaging demonstrates no alterations in Blood
Oxygen Level Dependant responses (BOLD) yet Single
Photon Emission Computed Tomography (SPECT) Treatment
images can demonstrate reduced cerebral blood flow
and glucose metabolism even in the contralateral hemi- Indications
sphere (Wilkinson & Winston, 2008). Pre- and postop- Arachnoid cysts causing a focal neurological deficit, raised
erative cognitive testing, in small series, demonstrate ICP, or enlarging should be treated. The management of
improved performance in specific tasks after treatment, asymptomatic patients or patients with functional
symptoms, such as seizures and developmental delay, is Gosalakkal, J. A. (2002). Intracranial arachnoid cysts in children: A
review of pathogenesis, clinical features, and management. Pediatric
controversial. Asymptomatic cysts without mass effect
Neurology, 26(2), 9398.
may have a lower risk of bleeding if treated (Wilkinson Hagebeuk, E. E., Kloet, A., Grotenhuis, J. A., & Peeters, E. A. (2005).
& Winston, 2008; Parsch et al., 1997). Seizure control may Bobble-head doll syndrome successfully treated with an endoscopic
be improved, but a causal link is not always apparent. ventriculocystocisternostomy. Case report and review of the
Currently, treatment in patients with severe developmental literature. Journal of Neurosurgery, 103(3 Suppl), 253259.
Harsh, G. R., Edwards, M. S. B., & Wilson, C. B. (1986). Intracranial
delay does not appear to confer a significant functional
arachnoyd cysts in children. Journal of Neurosurgery, 64, 835842.
improvement (Arai et al., 1996; Levy et al., 2003). Jamjoom, Z. A., Okamoto, E., Jamjoom, A. H., al-Hajery, O., &
Abu-Melha, A. (1995). Bilateral arachnoid cysts in the Sylvian region
Surgical Options in female siblings with glutaric aciduria type I. Journal of Neurosur-
Three surgical options exist. These include shunt inser- gery, 82, 10781081.
Karabatsou, K., Hayhurst, C., Buxton, N., OBrien, D. F., & Mallucci, C. L.
tion, open exploration, or endoscopic fenestration (Lena
(2007). Endoscopic management of arachnoid cysts: An advancing
et al., 1996, Kaufman & Park, 2000). Commonly, a cysto- technique. Journal of Neurosurgery, 106(6 Suppl Pediatrics),
peritoneal shunt is placed, although revision rates due to 455462.
infection or system failure remain at 2040% at 8 years Kaufman, B. A., & Park, T. S. (2000). Treatment of arachnoid cysts. In
(Arai et al., 1996; Oberbauer et al., 1992). Cyst fenestra- D. G. McLane (Ed.), Pediatric neurosurgery Philadelphia, PA: WB
Saunders.
tion consists of opening a window in both the superficial
Kutlay, M., Colak, A., Demircan, N., & Akin, O. N. (1998). Iatrogenic
and deep walls of the cyst to allow communication be- arachnoid cyst with distinct clinical picture as a result of bone defect
tween the cyst and the subarachnoid space (Figs. 5 and 6). in the floor of the middle cranial fossa: Case report. Neurosurgery,
Both microsurgical and endoscopic approaches demon- 43(5), 12151218.
strate improvement in up to 90% of patients (Karabatsou Lena, G., Erdincler, P., Van Calenberg, F., Genitori, L., & Choux, M.
(1996). Arachnoid cysts of the middle cranial fossa in children. A
et al., 2007; Levy et al., 2003; Spacca et al., 2009). Endo-
review of 75 cases, 47 of which have been operated in a comparative
scopic fenestration is less invasive, and series suggest study between membranectomy with opening of cisterns and
reduced morbidity (Karabatsou et al., 2003; Spacca cystoperitoneal shunt. Neurochirurgie, 42(1), 2934.
et al., 2009). Treatment of an associated subdural hemor- Levy, M. L., Wang, M., Aryan, H. E., Yoo, K., & Meltzer, H. (2003).
rhage or hygroma may lead to resolution of the arachnoid Microsurgical keyhole approach for middle fossa arachnoid cyst
fenestration. Neurosurgery, 53(5), 11381145.
cyst (Parsch et al., 1997).
Miyajima, M., Arai, H., Okuda, O., Hishii, M., Nakanishi, H., & Sato, K.
(2000). Possible origin of suprasellar arachnoid cysts: Neuroimaging
and neurosurgical observations in nine cases. Journal of Neurosurgery,
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Oberbauer, R. W. Haasa, J., & Pucher, R. (1992). Arachnoid cysts in
treated with cystoperitoneal shunting. Neurosurgery, 39(6), 11081113.
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Neurology, 64, 160162. (1997). Arachnoid cysts associated with subdural hematomas and
Boop, F. A., & Teo, C. (2000). Congenital intracranial cysts. In D. G. hygromas: Analysis of 16 cases, long-term follow-up and review of
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Bright, R. (1831). Reports of medical cases selected with a view of illustrat- intracranial arachnoid cysts. Surgical Neurology, 9, 139144.
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Di Rocco, C (1990). Arachnoid cysts. In Youmans: Neurological arachnoid cysts: Endoscopic and cine-mode MRI evidence of a
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Arcuate Fasciculus A 245
Schroeder, H. W., & Gaab, M. R. (1997). Endoscopic observation of a slit- long been used in labor, construction, and securities regu-
valve mechanism in a suprasellar prepontine arachnoid cyst: Case A
lation, but is gaining popularity in other disputes.
report. Neurosurgery, 40(1), 198200.
Spacca, B., Kandasamy, J., Mallucci, C. L., & Genitori, L. (2009). Endoscopic
treatment of middle fossa arachnoid cysts: a series of forty patients
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patients with intracranial arachnoid cysts. Journal of Neurology, 250, Mediation
3641.
Wilkinson, C. C., & Winston, K. R. (2008). Congenital arachnoid cysts
and the Dandy-Walker complex. In A. L. Albright, I. F. Pollack, &
P. D. Adelson (Eds.), Principles and practice of pediatric neurosurgery References and Readings
(pp. 162186). New York: Thieme.
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et al. (2005). Evaluation of communication between intracranial
arachnoid cysts and cisterns with phase-contrast cine MR imaging.
AJNR American Journal of Neuroradiology, 26(1), 145151.
Ziaka, D. S., Kouyalis, A. T., Boviatsis, E. J., & Sakas, D. E. (2008).
Asymptomatic massive subdural hematoma in a patient with bitem- Arcuate Fasciculus
poral agenesis and bilateral temporal arachnoid cysts. The Southern
Medical Journal, 101(3), 324326.
M ARTIN R. G RAF
Richmond, VA, USA
Arachnoid Mater
Meninges Definition
The arcuate fasciculus is a large bundle of nerve fibers that

curves around the lateral sulcus to connect Brocas area in
Arbitration the frontal cortex to Wernickes area located in the poste-
rior portion of the temporal lobe. This white matter
R OBERT L. H EILBRONNER pathway is essential for language processing in which the
Chicago Neuropsychology Group arcuate fasciculus connects the region associated with
Chicago, IL, USA the ability to produce spoken language, Brocas area, to
that of the ability to process spoken words that are heard
which is associated with Wernickes area. This language
Definition loop is located in the left hemisphere in approximately
90% of the population. Lesions disrupting the arcuate
Arbitration is an alternative means of settling a dispute by fasciculus result in conduction aphasia, which is charac-
impartial person(s) without proceeding to a court trial. It is terized by paraphasic errors in which incorrect words or
sometimes preferred as a means of settling a matter in order sounds are substituted and word repetition is impaired,
to avoid the expense, delay, and acrimony of litigation. although these individuals generally show reasonably nor-
There is no discovery and there are simplified rules of mal speech and comprehension.
evidence in arbitration. The arbitrator(s) are selected di-
rectly by the parties or are chosen in accordance with the
terms of the contract in which the parties have agreed to use Cross References
a court-ordered arbitrator(s) or an arbitrator(s) from the
American Arbitration Association. If there is no contract, Superior Longitudinal Fasciculus
usually each party chooses an arbitrator and the two arbi-
trators select a third to comprise the panel. When parties
submit to arbitration, they agree to be bound by and References and Readings
comply with the arbitrators decision. The arbitrators de-
cision is given after an informal proceeding where each LaPointe, L. L. (2005). Aphasia and related neurogenic language disorders.
party presents evidence and witnesses. Arbitration has New York: Thieme.
246 A Arcuate Fibers
Off Label Use

Arcuate Fibers
Other psychotic disorders, acute mania, bipolar mainte-
Associational Fibers nance, bipolar depression, behavioral disturbances asso-
ciated with dementias, behavioral disturbances in children
and adolescents, and impulse control disorders.
Aricept
Side Effects
Donepezil
Serious
Neuroleptic malignant syndrome, seizures.

Aripirozole
J OHN C. C OURTNEY 1, C RISTY A KINS 2
1
Common
2 Insomnia, dizziness, activation, akathisia, nausea, and
Mercy Family Center
vomiting.
Metarie, LA, USA
Generic Name References and Readings
Aripirozole Physicians Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson
PDR.
Brand Name
Abilify Additional Information

Class Free Drug Online and PDA Software: www.epocrates.com
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.com:
Atypical Neuroleptic 8080/cgi bin/ddiD4?ver=4&task=getDrugList
Proposed Mechanism(s) of Action

Partial agonism at dopamine 2 receptors. Also inhibits
5HT2a receptors, thus increasing presynaptic release of
Arithmetic Reasoning
related catecholamines.
Z HENG Z HOU
St. Johns University
Queens, NY, USA
Indication
Schizophrenia, Bipolar (mixed/manic), Adjunctive by for Synonyms
Major Depressive Disorder, Autistic irritability in children
and teens. Numerical reasoning; Quantitative reasoning
Arousal A 247
Definition Zhou, Z. (in press). Mathematical reasoning. In J. S. Kreutzer, J. Deluca, &

A
B. Caplan (Eds.), Encyclopedia of clinical neuropsychology. New York:
Springer.
Mathematical reasoning is the mathematical methodology
of axiomatic reasoning, logical deduction, and formal
inference.
Current Knowledge Arousal

R ONALD A. C OHEN
Research in evolutionary genetics and neuroscience
Brown University
suggests important neurological differences between
Providence, RI, USA
mathematical capacities that are evolutionary primitive
(e.g., counting) and those (e.g., arithmetic) that are more
culturally taught (Geary, 1995). Empirical data demon-
strate that mathematical reasoning and language are
Synonyms
functionally and neuroanatomically independent,
Cortical activation; Cortical arousal; Delirium; Wakefulness
suggesting (a) there is a common and domain-general
syntactic mechanism that underpins both language and
mathematics, but that mathematical expressions can gain
direct access to this system without translation into a Definition
language format, and (b) autonomous, domain-specific
syntactic mechanisms exist for language and mathematics The psychological and physiological state of wakefulness,
(Varley, Klessinger, & Romanowski, Siegal, 2005). Studies excitement, and/or activation enables readiness for action,
on sex differences provide evidence that math reasoning increased sexual desire, and readiness. From a neuropsy-
develops from a set of biologically based cognitive chological perspective, arousal refers to the tonic state of
capacities that males and females share (Spelke, 2005). cortical activity elicited by subcortical reticular formation
Male infants show no advantage in the processing of that results in increased wakefulness, alertness, muscle tone,
objects, space, or number. Highly selected male and autonomic response (e.g., heart rate and respiration).
and female students show equal abilities to learn mathe-
matics. However, other studies found male advantage in
arithmetical reasoning mediated by male advantages in Historical Background
both computational fluency and spatial cognition.
The concept of arousal played a key role in many of the
earliest psychological theories. Physiologists of the nine-
Cross References teenth century, such as Brucke, focus on the basis of
bioenergetics as they attempted to understand the basis
Abstract Reasoning of cell function. This influenced Freud who posited that
Academic Competency bioenergetics were the driving forces underlying psycho-
Academic Skills logical experience and behavior and accounted for his
Problem Solving construct of Id. William James proposed that emotional
experience involved the labeling of arousal and behavioral
response associated with affective stimuli. Classical con-
References and Readings ditioning theory was also routed in Pavlovs observations
of autonomic and behavioral unconditioned response
Geary, D. C. (1995). Reflections on evolution and culture in childrens
to stimuli, such as foods that have appetitive value
cognition: Implications for mathematical development and (i.e., unconditioned stimuli). His concept of the orienting
instruction. American Psychologist, 50(1), 2437. response was one of the first constructs that directly
Spelke, E. (2005). Sex differences in intrinsic aptitude for mathematics linked arousal and learning to an attentional response.
and science? American Psychologist, 60(9), 950958.
Subsequently, the arousal became a key construct in the
Varley, R. A., Klessinger, N. J. C., Romanowski, C. A. J., & Siegal, M.
(2005). Agrammatic but numerate. Proceedings of the
development of the field of psychophysiology in its efforts
National Academy of Science of the United States of America, 102, to characterize the relationship between psychological
35193524. experience and physiological response. The
248 A Arousal
demonstration by Moruzzi and Magoun (1949) shows perform cognitive challenges that are stressful or that
that the brain-stem reticular formation plays a key role require rapid response for adequate performance tend to
in generating brain activation as evident by electroen- result in increased fast wave EEG activity as well as
cephalography. This spurred subsequent neurophysiolog- autonomic nervous system responses such as increased
ical inquiry into the factors underlying arousal and their heart rate and respiration, metabolic activity, and a diver-
mediation of higher order cognitive functions. Early sion of blood from the gastrointestinal system to skeletal
efforts to understand the actions of neurotransmitters in muscle. These responses are associated with a readiness to
the brain were closely linked to the concept of arousal, respond, a key element of attention, the specific nature
based on the effects of norepinephrine on the sympathetic of this attention response depends on whether the task
nervous system response and wakefulness. Pribram and demands involve passive vigilance or more effortful
McGuinness (1975) posited dissociations between arousal, directed attention.
activation, and effort in the control of attention, an There is now strong evidence that multiple neural
important theoretical neuropsychological work that tied systems are involved in the maintenance, control, and
these processes to underlying brain mechanisms. Heilman allocation of arousal throughout the cortex. At least four
and Valensteins (1979) attention-arousal hypothesis neurotransmitter systems (acetylcholine, norepinephrine,
proposed that the arousal associated with reticular dopamine, and serotonin) mediate the energetic state of
activation interacted with a number of distinct cortical the brain, though a variety of peptides influence the
and subcortical systems involved in the control of neural response across specific brain systems. While hier-
attention, and that unilateral brain lesions across these archically the arousal originates in the brainstem, the
brain systems occur in patients with hemineglect nuclei of the hypothalamus play a critical role in the
syndrome. specificity of arousal relative to specific appetitive beha-
viors. For example, while damage to the reticular system
of the brain stem often results in coma, hypothalamic
Current Knowledge nuclei such as the suprachiasmatic nucleus exert control
over wakefulness, by maintaining circadian rhythm.
The concept of arousal has evolved substantially from its Furthermore, the arousal associated with drives such
original conception. Some neuroscientists argue that the as eating and sexual response are directly governed
concept has outlived its usefulness because the term by hypothalamic functions, with higher level limbic
arousal is used to refer to a broad range of different (e.g., amygdala) and cortical control.
behavioral and physiological phenomena with very The most obvious clinical manifestations of disor-
different underlying mechanisms. This has led to over- dered arousal occur in conjunction with delirium. How-
generalization of the construct. Yet, arousal continues to ever, factors that influence the level of arousal have direct
have an important role in neuropsychological theories. effects on performance, as described at the turn of the last
There is compelling evidence that brain stem and subcor- century in the YerkesDodson law. There are data from a
tical activity influences cortical activity and also auto- wide range of cognitive, behavioral, and neuropsycholo-
nomic response. At a behavioral and phenomenological gical studies demonstrating supporting the principle that
level, arousal provides a construct that links the more task performance varies as a function of arousal, with
primitive bioenergetic responses of the brain with higher optimal performance occurring at some intermediate level.
cortical functions. This is most obvious when considering Pathological states that cause lethargy usually reduce
levels of consciousness that can range from deep sleep attentional performance. Similarly, drugs, anxiety, or other
or coma to normal wakefulness to states of extreme factors that lead to excessive arousal also have detrimental
excitement, hyperactivity, or agitation. Altered arousal is consequences on performance. Disturbances of arousal are
a key feature of delirium that can occur due to transient commonly associated with both intoxication as well as
disruptions in brain function due to metabolic or drug withdrawal from drugs like alcohol and barbiturates,
influences. electrolyte imbalances, trauma to brain from closed
Stimulation of the sympathetic nervous system and an head injury, and various neurological disorders including
increase in the secretion of epinephrine and norepineph- encephalitis, tumors, advanced Alzheimers disease, and
rine increase the brain activity on EEG, along with stroke. Conditions that affect the brain stem, hypothalamus,
behavioral response toward greater wakefulness, where thalamus, limbic areas (e.g., amygdala), and frontal and
drugs like barbiturates and alcohol have the opposite temporal lobes are most likely to alter arousal, and there-
effect. The task that requires intense focused attention to by affect attention too.
Arteriovenous Malformation (AVM) A 249
From a neuropsychological perspective, arousal is an References and Reading A

important factor influencing the intensity of attentional
focus and also the ability of people to sustain attention. Cohen, R. A. (1993). Neuropsychology of attention. New York: Plenum
Kahneman (1973) proposed that arousal is a governing Publishing.
Heilman, K. M., & Valenstein, E. (1979). Mechanisms underlying
factor underlying attentional capacity. Cohens (1993)
hemispatial neglect. Annals of Neurology, 5(2), 166170.
four-factor attention framework and other neuro- Kahneman, D. (1973). Attention and effort. Englewood Cliffs, NJ:
psychological theories of attention posit that capacity Prentice-Hall.
limitations associated with the overall level of behavioral Moruzzi, G., & Magoun, H. W. (1949). Brain stem reticular formation
and physiological arousal constrain attention by influen- and activation of the EEG. Electroencephalography and Clinical
Neurophysiology, 1(4), 455473.
cing the intensity of focus that is possible, which in turn
Pribram, K., McGuinness, D. (1975). Arousal, activation, and effort in the
affects other aspects of attention, most notably sustained control of attention. Psychological Review, 82(2), 116149.
performance.
Future Directions Arteriography, Cerebral

Arousal appears to be a necessary and durable construct Angiography, Cerebral
within neuropsychology. Yet, some of the concerns
of neuroscientists regarding the overuse and overgenerali-
zation of the term have merit. As knowledge increases
regarding the functional neuroanatomy of specific Arteriosclerotic Vascular Disease
white-matter pathways projecting from subcortical to
cortical regions, there will be a need for further refine-
or ASVD
ment of the arousal construct. Efforts to more clearly
Atherosclerosis
demonstrate the linkage between behavioral and physio-
logical arousal in the clinical context are needed, given
that they are not always coupled. The example of de-
creased frontal lobe activation associated with hyperactiv-
ity and impulsivity in attention deficit disorder illustrates Arteriovenous Malformation
this fact. At this point in time, arousal is typically not (AVM)
directly assessed as part of neuropsychological evalua-
tions, except through behavioral observation. However, B RUCE J. D IAMOND, J OSEPH E. M OSLEY
with advances in the functional neuroimaging, it is possi- William Paterson University
ble to demonstrate both activation as well as deactivation Wayne, NJ, USA
of particular brain regions, and to observe how these
responses change in association with not only momentary
task demands but also tonic state of arousal. Accordingly, Synonyms
in the future physiological measurement of arousal and
activation across brain systems, it is likely to be a Brain arteriovenous malformation; Cerebral malforma-
more common element of standard neuropsychological tion; Vascular malformation
assessment.
Cross References Arteriovenous malformation (AVMs) are irregular, anom-

alous, abnormal, or faulty formations or structures con-
Attention necting the arteries and veins (Websters New Explorer
Consciousness Medical Dictionary, 2006). AVMs have been associated
Orienting Response with aneurysms in 1050% of patient groups, depending
Reticular Activating System on the type of angiographic techniques employed
YerkesDodson Law (Al-Shahi & Warlow, 2001).
250 A Arteriovenous Malformation (AVM)
Arteriovenous Malformation (AVM). Figure 1
Etiology to grow, regress, and regenerate following obliteration

by surgery or radiosurgery (Moftakhar, Hauptman,
AVMs arise about 3 weeks after conception at the time Malkasian, & Martin, 2009). Currently, it is thought
when blood vessels are dividing into veins and arteries that the altered expression of more than 900 genes is
(Stein & Wolpertson, 1980). Recent studies have sug- involved in the pathogenesis of AVMs (Moftakhar et al.,
gested that AVMs are dynamic and have the ability 2009).
Arteriovenous Malformation (AVM) A 251
Epidemiology Assessment and Treatment A

AVMs are the most common type of clinically significant The AVM is often recognized clinically between the ages of
vascular malformation, occurring exclusively within 10 and 30, presenting as a seizure disorder, an intracere-
the brain or involving extension of vessels from the bral hemorrhage, a subarachnoid hemorrhage, a nonspe-
subarachnoid space into brain parenchyma (Frosch, cific or migraine headache, and less frequently as pulsatile
Anthony, & De Girolami, 2005). AVM sizes may vary tinnitus (Al-Shahi & Warlow, 2001; Frosch et al., 2005;
from a few millimeters to several centimeters (Warlow, et al., 2005; Warlow, 2001).
2001), with males being affected twice as frequently as The most commonly affected site is the middle cere-
females. bral artery, particularly its posterior branches, but AVMs
may occur anywhere along the midbrain, cerebellum, or
spinal cord (Frosch et al., 2005). Because the presence of
Mechanisms an AVM exposes patients to the risk of permanent neuro-
logical deficits or death, surgical intervention is usually
Cognitive improvements have been attributed to im- necessary (Zhao et al., 2005). The preferred treatment
proved cerebral blood flow and reduction of hypoperfu- method is generally surgical excision (Ropper, Brown,
sion (Lantz & Meyers, 2008). Surgery may result in severe Adams, & Victor, 2005; Zhao et al., 2005). However,
neuropsychological complications for some patients, in- advances in interventional neuroradiology and stereotac-
cluding executive dysfunction and aphasia (Lantz & tic radiosurgery (SRS) have allowed for the development
Meyers, 2008; Zhao et al., 2005). of alternatives to traditional microsurgery, such as gamma
knife SRS and proton beam radiosurgery (Ropper et al.,
2005; Zhao et al., 2005). In addition, the treatment of
Neuropsychological and Psychological giant cerebral AVMs (>6 cm in diameter) may require
Outcomes endovascular embolization as an adjunct to surgical inter-
vention (Zhao et al., 2005).
The actual occurrence of cognitive deficits in AVM is
difficult to determine (Lantz & Meyers, 2008) because
much of the data have been pooled from patients with Cross References
ruptured and unruptured AVMs. Patients with AVM may
exhibit below normal performance on tests of intelligence, Anterior Communicating Artery
attention, and memory (Lantz & Meyers, 2008). Some Gamma Knife
research has demonstrated postsurgical improvement in Intracarotid Sodium Amytal Test
patients neuropsychological functioning, including better Radiosurgery, Stereotactic Radiation Therapy
performance on tasks requiring executive function (Lantz Shunts
& Meyers, 2008). Wada Test
Recently, researchers have demonstrated brain reorga-
nization of language function in patients with AVM by
using selective Wada testing (intracarotid amobarbital References and Readings
sodium and xylocaine procedure), magnetic resonance
imaging, and functional magnetic resonance imaging Al-Shahi, R., & Warlow, C. (2001). A systematic review of the frequency
(Lantz & Meyers, 2008). Other research has demonstrated and prognosis of arteriovenous malformations of the brain in adults.
structural reorganization involving the motor cortex Brain, 124, 19001926.
Aminoff, M. J., Greenberg, D. A. & Simon, R. P. (2005). Clinical neurology.
(Lantz & Meyers, 2008). Patients with AVM are more
New York: McGraw-Hill.
likely to report developmental learning disorders than Frosch, M. P., Anthony, D. C., & De Girolami, U. (2005). The central
patients with tumors or aneurysms, with AVM patients nervous system. In V. Kumar, A. K. Abbas, & N. Fausto (Eds.),
reporting four times the rate of learning disability com- Pathologic basis of disease (pp. 13471420). Philadelphia: Elsevier.
pared to the normal population (Lantz & Meyers, 2008; Lantz, E. R., & Meyers, P. M. (2008). Neuropsychological effects of brain
arteriovenous malformations. Neuropsychology Review, 18, 167177.
Lazar et al., 1999). This finding may suggest that disorders
Lazar, R. M., Connaire, K., Marshall, R. S., Pile-Spellman, J.,
of learning and intellectual function may serve as a Hacein-Bey, L., Solomon, R. A., et al. (1999). Developmental deficits
marker for early cerebral dysfunction in patients with in adult patients with arteriovenous malformations. Archives of
AVMs (Lazar et al., 1999). Neurology, 56, 103106.
252 A Arteriovenous Malformations
Moftakhar, P., Hauptman, J. S., Malkasian, D., & Martin, N. A. (2009). Cross References
Cerebral arteriovenous malformations. Part 1: cellular and molecu-
lar biology. Neurosurgical Focus, 26(5), 115.
Ropper, A. H., Brown, R. H., Adams, R. D., & Victor, M. (2005). Adams &
Apraxia of Speech
Victors principles of neurology. New York: McGraw-Hill. Articulation Disorder
Stein, B. M., & Wolpertson, S. M. (1980). Arteriovenous malformations Ataxia
of the brain. I: Current concepts and treatments. Archives of Neurol- Dysarthria
ogy, 37, 6975.
Dystonia
Warlow, C. (2001). Stroke, transient ischemic attacks, and intracranial
venous thrombosis. In M. Donaghy (Ed.), Brains diseases of the
Phoneme
nervous system (pp. 775896). New York: Oxford University Press. Phonics
Websters new explorer medical dictionary (New Ed.). (2006). Springfield, Speech-Language Pathology
MA: Merriam-Webster.
Zhao, J., Wang, S., Li, J., Qi, W., Sui, D., & Zhao, Y. (2005). Clinical
characteristics and surgical results of patients with cerebral arterio-
venous malformations. Surgical Neurology, 63, 156161. References and Reading
Hulit, L. M., & Howard, M. R. (2005). Born to talk: an introduction to
speech and language development (4th ed.). Boston: Pearson A & B.
Plante, E., & Beeson, P. M. (2008). Communication and communication
Arteriovenous Malformations disorders: a clinical introduction (3rd ed.). Boston: Pearson A&B.
Vascular Malformations
Articulation Disorders
Arteritis PAMELA G. G ARN -N UNN
University of Akron
Vasculitis Akron, OH, USA

Articulation
An articulation disorder is a failure to acquire a
J ANET PATTERSON speech sound or sounds of a particular language by the
California State University East Bay expected normative age due to some type of motoric
Hayward, CA, USA problem. Speech sound errors in articulation disorders
include
Substitutions: replacing a standard speech sound with
Definition a different standard speech sound e.g., Wabbit for rabbit,
thpoon for spoon, or bery for very.
Articulation is (1) the juncture between bones or carti- Omission: omission of a standard speech sound e.g.,
lages in the skeleton of a vertebrate; (2) the movement ba for bat, gin for green. (Widespread omissions often
pattern and relationship of oral structures such as the indicate a phonological disorder, however.)
tongue and lips, to produce the sounds of speech. Articu- Distortions: replacement of a standard speech sound
lation develops gradually and consistently across children by a nonstandard sound e.g., s in soup sounds slushy.
of all cultures, and the earliest sounds made by infants are Additions: addition of a sound or syllable e.g., cart for
undifferentiated. As a child matures and motor control car or chiminey for chimney. Additions are the least com-
becomes increasingly well-coordinated, the childs speech monly occurring type of articulation error.
becomes intelligible within the linguistic community. While some of these sound changes are common for
Articulation is evaluated through tests of single sounds toddlers and early preschoolers, children should master
and words, and in contexts such as oral reading and con- the speech sounds of English by the age of 8.
versation. Articulation disorders can disrupt speech intelli- NOTE: However, individuals whose sound substitutions
gibility temporarily or for extended periods of time. or omissions reflect a dialectic variation or acquisition of
Articulation Disorders A 253
English as a second language are not considered to have an Articulation Disorders. Table 1
A
articulation disorder.
By age 3: p m h w b (emerging between ages 1 and 3)
By age k g d t f y (girls only) (emerging between ages
Categorization 3 : 2 and 3 )
By age 4: y (boys)
An articulation disorder is a type of speech sound disor- By age 5: s-blends (emerging between ages 3 and 5)
der. It is associated with a motoric inability to produce a By age v
speech sound or sounds (rather than a failure to acquire 5 :
the speech sound rules of a particular language) by the By age 6: sh ch j (girls)
expected normative age. ( Phonological Disorder.) Ar-
By age 7: sh ch j (boys) th (as in that)
ticulation and phonological disorders can co-occur.
By age 8: r s ng l z th (as in thumb) zh (as in measure)
Epidemiology motor skills and perceptual development but also the

sound make-up and length of a word. Nevertheless, re-
Incidence figures are available for speech sound disorders, search indicates that the following sounds should be mas-
of which articulation disorders are one type. Figures cited tered by the ages indicated:
for preschoolers are 89% with approximately 5% still
demonstrating a speech sound disorder by first grade. Inci- Vowels: should all be acquired by age 3 with the
dence of speech sound disorders in children is higher than exception of the er sound in words like bird and
in adults. Some children will outgrow their errors, while hammer.
others will require treatment from a speech-language Consonants: these represent ages of mastery; prior to
pathologist to develop understandable speech (see these ages, correct production will vary
Evaluation). For children who do not meet these milestones, test-
During the process of speech development, articula- ing and possible treatment by a certified speech-language
tion disorders occur more often in children with pathologist is required. A person who continues to exhibit
Genetic syndromes such as Down syndrome or other articulation errors past age 8 should also be evaluated
syndromes associated with cognitive delays unless their sound usage is characteristic of a dialect or
Childhood apraxia of speech first language.
Neurological disorders such as cerebral palsy
Orofacial anomalies such as cleft palate Neuropsychology and Psychology of
Myofunctional disorders (sometimes referred to as Disorder
tongue thrust disorders)
In some cases, no definitive etiological factor will be In some cases, an articulation disorder may be associated
found. with damage to the central or peripheral nervous system.
For school-aged children, articulation disorders can Specific neurological correlates usually are not found except
be a continuation of an earlier phonological or articula- in cases of dysarthria or apraxia. When misunderstood,
tion problem or the result of some type of neurological some children may react by refusing to speak or withdraw-
injury. Similarly, in adults, a speech sound disorder can ing from others. Children who are unable to communicate
consist of residual errors of an earlier disorder or a new due to an articulation disorder can become frustrated and
disorder due to a variety of neurological causes. Dysar- act out because they cannot make basic needs and wants
thria and apraxia for further information on these adult known. The childs family can also become frustrated at
causes of speech sound disorders. their inability to communicate with their child. However,
this type of behavior is much more likely to occur in
conjunction with phonological disorders rather than artic-
Natural History, Prognostic Factors, ulation disorders. For adults with speech sound disorders
Outcomes due to apraxia or dysarthria, the effect on communication
will depend on the number of sounds affected, the degree of
A childs acquisition of the speech sounds is a gradual speech understandability, and the patients reaction to the
process. Correct articulation can depend not only on communication problem.
254 A AS
Evaluation
ASEBA
Evaluation of articulation disorders is designed to
determine: Child Behavior Checklist
1. Existence of a problem
2. Nature of the problem (sounds in error, patterns
intelligibility)
3. Possible etiology(ies) of the problem, e.g., structural
ASHA-FACS
problem or neurological disorder
American Speech-Language-Hearing Association Func-
4. Probable course of treatment
tional Assessment of Communication Skills for Adults
5. Prognosis
To meet these goals, the following components should be
included in an evaluation for speech sound disorders:
1. Case history
2. Hearing screening
Ashworth Spasticity Scale (and
3. Oral mechanism evaluation Modified Version)
4. Phonemic sound-by-position tests
5. Language testing K ARI D UNNING
6. Other tests as appropriate University of Cincinnati
Cincinnati, OH, USA
Treatment
Synonyms
For patients with simple articulation disorders, a tradi-
tional, phonetic approach can be successful. Phonolog- AS; MAS
ical Disorders and Articulation Disorders for more
information on treatment.
Description
Cross References The Ashworth Scale (AS) and Modified Ashworth Scale
(MAS) measure spasticity. During the administration of
Apraxia
both AS (Ashworth, 1964) and MAS (Bohannon & Smith,
Articulation Disorder
1987), the examiner passively moves the joint being tested
Dysarthria
and rates the perceived level of resistance in the muscle
Phonological Disorder
groups opposing the movement. Both scales are single-
Phonology
item measures ranging from 0 to 4, where 0 indicates no
increase in muscle tone and 4 indicates that the affected
References and Readings part is rigid in flexion or extension. The AS is considered
an ordinal scale, whereas the MAS is considered a nominal
American Speech-Language-Hearing Association. (2007). Speech sound scale due to ambiguity created by the addition of the 1
disorders: Articulation and phonological disorders, from www.asha. grade between 1 and 2 (Pandyan, Johnson, Price, Curless,
org/public/speech/disorders/SpeechSoundDisorders. Barnes, & Rodgers, 1999).
American Speech-Language-Hearing Association. (2008). Incidence and
prevalence of communication disorders and hearing loss in children
(2008 Ed.), from www.asha.org/members/research/reports/children.
The AS was first described by Ashworth in 1964 (Ashworth,

AS 1964) and was subsequently modified with the addition
of a 1 grade by Bohannon in 1987 with the intent to
Ashworth Spasticity Scale (and Modified Version) increase sensitivity (Bohannon & Smith, 1987). However,
ASIA Impairment Scale A 255
this addition may have decreased the reliability of the References and Readings A
MAS for heavier limbs (see below) (Ansari, Naghdi, Arab,
& Jalaie, 2008; Pandyan et al., 1999; Platz, Eickhof, Ansari, N. N., Naghdi, S., Arab, T. K., & Jalaie, S. (2008). The interrater
Nuyens, & Vuadens, 2005). and intrarater reliability of the Modified Ashworth Scale in the
assessment of muscle spasticity: Limb and muscle group effect.
NeuroRehabilitation, 23(3), 231237.
Psychometric Data Ashworth, B. (1964). Preliminary trial of carisoprodol in multiple sclero-
sis. Practitioner, 192, 540542.
Bohannon, R. W., & Smith, M. B. (1987). Interrater reliability of a
Inter- and intra-rater reliability of the AS and MAS show
modified Ashworth scale of muscle spasticity. Physical Therapy,
wide variation (Pandyan et al., 1999; Platz et al., 2005), 67(2), 206207.
which cannot be attributed to any one factor (Platz et al., Fleuren, J. F., Voerman, G. E., Erren-Wolters, C. V., et al. (2009). Stop
2005), although some evidence suggests that the inter- using the Ashworth Scale for the assessment of spasticity. Journal of
rater reliability of the MAS is lower for heavier limbs Neurology, Neurosurgery, and Psychiatry, 81(2), 4652.
Lance, J. W. (1980). Symposium synopsis. In R. G. Feldman, R. R. Young,
(Ansari et al., 2008; Pandyan et al., 1999; Platz et al.,
& W. P. Koella (Eds.), Spasticity: Disordered motor control (pp.
2005). Both scales have demonstrated responsiveness to 485494). Chicago, IL: Year Book Medical Publishers.
treatment (Platz et al., 2005). Pandyan, A. D., Gregoric, M., Barnes, M. P., et al. (2005). Spasticity:
Spasticity is characterized by an involuntary muscle Clinical perceptions, neurological realities and meaningful measure-
activity (Pandyan et al., 2005) and has been traditionally ment. Disability and Rehabilitation, 27(12), 26.
Pandyan, A., Johnson, G., Price, C., Curless, R., Barnes, M., & Rodgers, H.
defined as a velocity-dependent increase in muscle tone
(1999). A review of the properties and limitations of the Ashworth
due to a hyperactive stretch reflex (Lance, 1980). The and modified Ashworth Scales as measures of spasticity. Clinical
construct validity of the AS and MAS as spasticity assess- Rehabilitation, 13(5), 373383.
ments is inadequate because they do not address velocity Platz, T., Eickhof, C., Nuyens, G., & Vuadens, P. (2005). Clinical scales for
dependence. Rather, these scales measure passive resis- the assessment of spasticity, associated phenomena, and function:
A systematic review of the literature. Disability and Rehabilitation,
tance to movement (hypertonia), which is influenced by
27(12), 718.
spasticity but also altered by biomechanical factors unre-
lated to involuntary muscle activation (Fleuren, Voerman,
& Erren-Wolters, 2009; Pandyan et al., 1999; Platz et al.,
2005). Thus, AS and MAS scores are only moderately ASIA (American Spinal Injury
associated with reflexes (Platz et al., 2005) and electro-
myographic assessments (Fleuren et al., 2009; Pandyan Association) Exam
et al., 1999; Platz et al., 2005) and more strongly asso-
ciated with objective measures of resistance (Fleuren et al., ASIA Impairment Scale
2009; Pandyan et al., 1999; Platz et al., 2005).
Clinical Uses ASIA Impairment Scale

Despite the fact that the AS and MAS are actually only A MITABH J HA
valid assessments of hypertonia (Fleuren et al., 2009; Craig Hospital
Pandyan et al., 1999; Platz et al., 2005), these scales are Englewood, CO, USA
the most commonly used clinical tools to assess spasticity
(Pandyan et al., 1999; Platz et al., 2005). Both scales have
been used to describe treatment response for persons with Synonyms
a wide range of upper motor neuron disorders, including
traumatic brain injury, stroke, multiple sclerosis, cerebral ASIA (American Spinal Injury Association) exam; Frankel
palsy, and spinal cord injury (Platz et al., 2005). scale; International standards for the neurological
classification of spinal cord injury
Cross References Description

Severe Brain Injury The International Standards for Neurological Classification
Spinal Cord Injury of SCI (ISNCSCI) is a widely accepted and readily
256 A ASIA Impairment Scale
administered guide to document neurological function addition, the ASIA Impairment Scale (AIS) grade classi-
after spinal cord injury (SCI) and is intended to be a fication, an indicator of injury completeness similar to
standard for measuring neurological outcomes in both the Frankel scale, is assigned based on this information.
clinical and research settings. Briefly, these standards AIS A denotes a complete injury with no sensory or
utilize a two-step process consisting of a specific neuromotor function below the level of injury. Incomplete
logical examination followed by a classification proce- injuries are graded as AIS B if there is sensory but no
dure based on the results of the exam. The systematic motor function below the injury level, AIS C if there is
neurological examination assesses sensory and motor some motor sparing, AIS D for substantial motor
function of each spinal segmental level. Sensation of sparing, and AIS E for normal neurological examination
light touch and pinprick (PP) stimuli is scored as 0 for (Fig. 1).
absent, 1 for impaired, and 2 for normal. Motor func-
tion is scored on a scale of 0 for total paralysis to 5 for
normal strength. All 28 dermatomes are tested bilaterally Historical Background
for sensory function, and ten key muscles are tested
bilaterally for motor function, yielding sensory/light ISNCSCI has been used extensively in clinical practice
touch (LT) and sensory/pinprick (PP) summed scores and research since 1982. The standards and
ranging from 0 to 112 and motor summed scores rang- accompanying reference manual have undergone se-
ing from 0 to 100. The neurological level is assigned as quential revisions, most recently in 2000 and 2003,
the lowest level with normal neurological function. In respectively.
Patient Name_ ___________________________________
Examiner Name _________________________________ Date/Timeof Exam ___________________
STANDARD NEUROLOGICAL CLASSIFICATION

OF SPINAL CORD INJURY
(scoring on reverse side)
(distal phalanx of middle finger)

(little finger)
Comments:
REV 03/06
ASIA Impairment Scale. Figure 1 International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI)
Asomatognosia A 257
Psychometric Data A
Asomatognosia
Published studies have found total motor score ICCs from
0.98 to 0.99 for intra-rater reliability and 0.97 for inter- J OHN E. M ENDOZA
rater reliability. Total sensory scores intra-rater reliability Tulane University Medical Center
has ranged from 0.76 to 0.98, and 0.88 to 0.96 for inter- New Orleans, LA, USA
rater. One study reported agreement on individual
muscles with Kappas ranging from 0.3 to 0.89 for each
myotome, 0.02 to 0.83 for dermatome assessment Synonyms
using pinprick, and 0.17 to 1 when assessed using light
touch. Disturbance of body schema
Clinical Uses Definition

The exam is used to document sensory and motor func- Disturbance in the normal awareness of ones own
tion after SCI. It has been used to diagnose SCI, as an body, typically characterized by one or more of the
outcome measure in studies to treat spinal cord patholo- following symptoms: (1) a tendency to ignore or ne-
gy, as well as a tool to predict outcomes such as indepen- glect one side of the body, (2) a failure to recognize or
dence with activities of daily living, employment, life difficulty in identifying a specific part of the body
satisfaction, and life expectancy. (usually a limb or part of a limb), (3) difficulty in
differentiating the right from the left side of the body,
or (4) recognizing an impairment in a part of the body
(anosognosia).
Cross References
Sensorimotor Assessment
Spinal Cord Injury
Current Knowledge
Asomatognosia most commonly results from acute or

References and Reading subacute brain lesions and may affect one or both sides
of the body. Unilateral neglect generally involves an entire
American Spinal Injury Association. (2002). International standards for
side of the body, more commonly the left. This might be
neurological classification of spinal cord injury (Revised 2002). reflected in a failure to shave the affected side of the face,
Chicago: American Spinal Injury Association. putting a glove only on one hand, or reduced use of the
American Spinal Injury Association. (2003). Reference manual for the involved limb for certain activities, even though it is
international standards for neurological classification of spinal
physically capable of doing so. If a limb is paralyzed, the
cord injury (Revised 2003). Chicago: American Spinal Injury
Association. patient may either deny or minimize the impairment
Furlan, J. C., Fehlings, M. G., Tator, C. H., & Davis, A. M. (2008). Motor (anosognosia), or may even deny ownership of the affected
and sensory assessment of patients in clinical trials for limb. If the affected side or a part of the body is stimu-
pharmacological therapy of acute spinal cord injury: Psychometric lated, the individual may report that the homologous area
properties of the ASIA standards. Journal of Neurotrauma, 25(11),
on the intact side was touched (allesthesia). Patients may
12731301.
Kirshblum, S. C., Memmo, P., Kim, N., Campagnolo D., & Millis, S.
also have difficulty localizing or identifying parts of their
(2002). Comparison of the revised 2000 American spinal injury own body (autotopagnosia). This is most commonly
association classification standards with the 1996 guidelines. expressed as difficulty naming or identifying individual
American Journal of Physical Medicine & Rehabilitation, 81(7), fingers (especially the three middle digits) either of their
502505.
own hands or those of others (finger agnosia). This deficit
Mulcahey, M. J., Gaughan, J., Betz, R. R., & Johansen, K. J. (2007). The
international standards for neurological classification of spinal cord
is usually expressed bilaterally. Rightleft disorientation is
injury: Reliability of data when applied to children and youths. generally also considered a form of asomatognosia. Here,
Spinal Cord, 45(6), 452459. the individual has difficulty reliably identifying the right
258 A Asperger Syndrome
and left sides of his or her own body or those of the

examiner. Aspergers Disorder
Although asomatognosia strictly refers to impaired
awareness or attention to parts of ones own body, S TEPHEN M. K ANNE , M ICAH O. M AZUREK
personal neglect often extends into extrapersonal space. Thompson Center for Autism and Neurodevelopmental
Thus, a patient may fail to attend to visual or auditory Disorders
stimuli on the affected side, despite intact visual fields Columbia, MO, USA
or the fact that auditory stimuli enter both ears.
This can be very disconcerting for family members if
they are not made aware of these phenomena, Synonyms
perhaps believing the patient is purposely ignoring their
presence. Asperger syndrome
Unilateral neglect or anosognosia type disorders are
most commonly found, following acute lesions (such as
strokes) of the right hemisphere. Although improvement Short Description or Definition
is typically seen over time, subtle degrees of deficit may
persist indefinitely. By contrast, those deficits that present Aspergers disorder is a neurodevelopmental disorder that
bilaterally (such as finger agnosia and rightleft disorien- is associated with impairment in social relatedness and
tation) are usually the result of posterior left-hemispheric repetitive or restricted behaviors and interests. Social dif-
lesions. ficulties that are characteristic of Aspergers disorder in-
clude nonverbal aspects of social interaction (e.g., eye
contact, gestures, and facial expressions) as well as social
Cross References and emotional reciprocity (e.g., sharing interests, taking
turns, demonstrating empathy). Behaviorally, individuals
Allesthesia with Aspergers often exhibit intense and narrow circum-
Anosognosia scribed interests, insistence on sameness or routine, and
Autotopagnosia behavioral rigidity (American Psychiatric Association,
Finger Agnosia 1994). While overall level of intellectual functioning
RightLeft Disorientation (i.e., IQ) is not impaired in individuals with Aspergers
disorder, their cognition is often compromised in other
areas such as executive functioning (see Neuropsychology
and Psychology of Aspergers Disorder below).
Hecaen, H., & Albert, M. L. (1978). Human neuropsychology (pp. 303 Categorization
330). New York: Wiley.
Heilman, K. M., Watson, R. T., & Valenstein, E. (2003). Neglect and Aspergers disorder is currently classified in the DSM-IV
related disorders. In K. Heilman & E. Valenstein (Eds.), Clinical
as one of five separate pervasive developmental disorders
neuropsychology (pp. 296346). New York: Oxford University Press.
Kortte, K. B., & Wegener, S. T. (2004). Denial of illness in medical (which also include autistic disorder, Retts disorder,
rehabilitation populations: Theory, research and definitions. Reha- childhood disintegrative disorder, and pervasive develop-
bilitation Psychology, 49, 187199. mental disorder NOS). Aspergers disorder is a fairly
Prigatano, G. P., & Schacter, D. L. (1991). Awareness of deficit after brain recent addition to the DSM, first appearing only in
injury: Clinical and theoretical issues. New York: Oxford University
the latest version, the DSM-IV (1994). According to the
Press.
DSM-IV, to meet criteria for Aspergers disorder, an
individual must demonstrate impairment in social
interaction (exhibiting at least two out of four possible
symptoms) and restricted and repetitive patterns of beha-
viors or interests (exhibiting at least one out of four
Asperger Syndrome possible symptoms). In addition, an individual must not
have a history of developmental delays in language,
Aspergers Disorder cognition, or adaptive functioning. Of note, the criteria
Aspergers Disorder A 259
for Aspergers disorder are identical to those for autistic a result, Wing (1981) published an influential paper
A
disorder (i.e., autism) in the areas of social impairment reintroducing Aspergers original ideas and arguing for
and restricted and repetitive behavior. However, autistic broadening the definition of autism to include Aspergers
disorder requires an additional criterion of impairment in disorder on the autism continuum. Eventually, a separate
communication (i.e., delays in language development, diagnosis of Aspergers disorder was added to the fourth
impairment in conversation, stereotyped language, or edition of the DSM (1994). Since that time, debate has
lack of pretend play). Additionally, there is not a require- continued as to whether or not Aspergers disorder should
ment in the criteria for autistic disorder that cognitive, remain a separate diagnosis from autism. The prevailing
language, and adaptive development fall within the current view is that Aspergers disorder and autism are
normal range in childhood (as is the case in Aspergers not distinctly different, and that Aspergers disorder
disorder) (American Psychiatric Association, 1994). may simply represent the milder end of the autism
spectrum. As a result, Aspergers disorder is often used
synonymously with the term high-functioning autism
Epidemiology (which typically refers to individuals meeting criteria for
Autistic Disorder whose IQ levels are above 70).
Prevalence estimates have varied widely from 0.3/1,000 With regard to developmental course, Aspergers
to 6/1,000 (see Mattila et al., 2007 for review). Based on a disorder is generally diagnosed much later than autistic
review of the literature, Fombonne (2003, 2005) esti- disorder, with an average age of diagnosis being 11 years
mated the prevalence rate for Aspergers disorder to be (possibly due to the lack of early developmental delays).
approximately 2/10,000. Such wide variations in prevalence It follows a continuous course throughout the lifespan,
rates are likely due to differences in diagnostic procedures although for some individuals symptoms remit as a result
and operational definitions used in each study. In fact, of early intervention (see Frith, 2004 for review). Research
recent rates from the same study varied from 1.6/1,000 into prognostic factors and outcome in Aspergers
to 2.9/1,000 depending on the specific criteria used for disorder is sparse, particularly since it has only been
diagnosis (Mattila et al., 2007). In terms of sex differences, recognized as an official diagnosis for little over a decade;
males are overrepresented in Aspergers disorders, with however, IQ and language ability have been found to be
an estimated sex ratio of 4:1 (see Schopler, Mesibov, & strong predictors of outcomes in autism spectrum
Kunce, 1998 for review). disorders in general.
Natural History, Prognostic Neuropsychology and Psychology

Factors, Outcomes of Aspergers Disorder
Aspergers disorder takes its name from the Austrian By definition, social interactions are impaired in Asper-
physician, Hans Asperger, whose 1944 paper on autistic gers disorder. However, the underlying processes by
psychopathy described a group of children who showed which social interactions are disrupted have been the
deficits in social behaviors, insistence on sameness, a lack source of recent attention. First, there is clear evidence
of nonverbal communication, repetitive movements, and that individuals with Aspergers disorder have impair-
average intelligence. Asperger (in 1944) and Leo Kanner ments in their ability to understand complex emotions
(in 1943), although unaware of one anothers work, were and a resulting inability to recognize and empathize with
the first to describe this cluster of symptoms. While Leo others feelings. Individuals with Aspergers disorder
Kanners seminal work describing autistic behaviors was (as well as autistic disorder), also have impairments
the subject of much discussion and resulted in the even- in what is known as theory of mind. As such, they
tual inclusion of autism in the DSM (in 1980), Aspergers have difficulty automatically attributing mental states to
paper did not receive wide attention after publication and others. Although there are no formal criteria concerning
was not translated into English until 1991 (see Frith, communication skills for Aspergers disorder, clinical and
1991). After the appearance of autism in the DSM-III, it research accounts highlight the presence of social
became apparent that there was a group of individuals communication difficulties. Specifically, difficulties with
who did not meet the criteria for the narrowly defined pragmatic language and difficulties with turn-taking in
definition of infantile autism, but who demonstrated conversation are common (see Klin, Volkmar, & Sparrow,
deficits in social interaction and repetitive behaviors. As 2000 for review).
260 A Aspergers Disorder
Aspergers Disorder. Table 1 DSM-IV criteria for Aspergers disorder
Social impairment (2 or more) Restricted and repetitive behavior (1 or more) Lack of delays in
1. Impaired nonverbal behavior 1. Abnormal and intense preoccupation with Language
stereotyped or restricted interest
2. Impaired peer relationships 2. Inflexible and nonfunctional routines or rituals Cognitive development
3. Lack of seeking to share enjoyment, 3. Stereotyped and repetitive motor mannerisms Self-help skills
interests, or achievements
4. Lack of social or emotional reciprocity 4. Preoccupation with parts of objects Adaptive behavior
(other than social)
Curiosity about the
environment
Source: From Diagnostic and Statistical Manual of Mental Disorders, fourth edition, by American Psychiatric Association, 1994, Washington, DC
Aspergers disorder is also associated with cognitive great deal of overlap among these conditions, empirical
features that affect functioning outside the social findings have been equivocal. Some studies have found
domain. Studies have shown that individuals with visual-spatial impairments (with strengths in Verbal IQ)
Aspergers disorder have very uneven cognitive profiles. in Aspergers disorder, while others have not demonstrated
One explanation for this common finding is that these this pattern (see Klin et al., 2000). Further work with more
individuals have weak central coherence. That is, they stringent diagnostic criteria is needed in this area.
are more likely to process information as discrete units
rather than processing them as a unified whole. There is
some evidence that bottom-up processing occurs without Coexisting Conditions
accompanying top-down control. As a result, high levels
of details are perceived, while global information may be In addition to the core symptoms, Aspergers disorder
missed (see Frith, 2004). Studies have also shown may also be accompanied by co-occurring disorders.
consistent deficits in overall executive function among Studies have shown that a large percentage of children
individuals with Aspergers disorder (as is also the case with Aspergers disorder also exhibit problems with atten-
in autistic disorder). Specifically, poor performance has tion and impulse control (similar to those found in
been shown on both the Wisconsin Card Sorting Test and ADHD). However, the DSM-IV prevents an additional
the Tower of Hanoi. Particular deficits have been noted in diagnosis of ADHD when there is an existing pervasive
the ability to shift response set and in overall planning. developmental disorder diagnosis. In adolescence and
Consistent with this, individuals with Aspergers disorder adulthood, case studies indicate relatively high rates of
are often described as having difficulty adjusting to depression, anxiety, and bipolar disorder among indivi-
changes in routine or task demands, and as having a duals with Aspergers disorder (see Ghaziuddin, 2002 for
strong need for sameness (see Klin et al., 2000). review). Recent evidence has also demonstrated that indi-
Some studies, including Wings (1981) original de- viduals with Asperger disorder have significant adaptive
scription, have found significantly higher verbal IQ scores impairments as well (see Saulnier & Kim, 2007).
than performance IQ scores among individuals with
Aspergers disorder (the reverse of which is typically
found in autistic disorder). Motor clumsiness has also Evaluation
been observed among children with Aspergers disorder
since Hans Aspergers original paper, although it has Diagnostic assessment of Aspergers disorder is best con-
never been a part of the formal diagnostic criteria ducted using multiple methods and observers. Due to the
(see Frith, 1991). As a result, researchers have been complexity of the disorder, and its effects on broad areas
interested in potential similarities between Aspergers dis- of functioning, interdisciplinary assessment is recom-
order and nonverbal learning disorders (NVLD) or right mended. First, because Aspergers is a neurodevelopmen-
hemispheric dysfunction. These profiles are marked by tal disorder, parent report of early history and
relative strengths at rote verbal skills, with deficits in social development, as well as structured observations of current
understanding and motor coordination. While there is a behavior, are essential. Currently, the two gold-standard
Aspergers Disorder A 261
tools for diagnosis of autism spectrum disorders are based on the region, they may range from specialized
A
the Autism Diagnostic Interview Revised (ADI-R) and schools designed to serve students with Aspergers
the Autism Directed Observation Schedule (ADOS). disorder to modifications within general education class-
These are the most widely studied measures in the field, rooms. Some students may get benefit and support
and reliability and validity have been well established. The from paraprofessional aides in the classroom, while others
ADI-R is a comprehensive interview that assesses past and may require only slight academic modifications. Most
current functioning in the areas of communication, social students with Aspergers disorder benefit greatly from
interaction, and restricted or repetitive behavior. The communication interventions aimed at improving prag-
Autism Directed Observation Schedule (ADOS) is anoth- matic and social skills (see Klin et al., 2000; Mesibov et al.,
er diagnostic tool that allows for clinic-based observations 2001 for review).
across various structured activity- and conversation- Family support, parent training, and instruction on
based interactions. Despite their advantages, however, behavior management strategies can also be helpful when
neither tool was designed to measure Aspergers disorder disruptive behaviors accompany the clinical picture. For
specifically, or to differentiate between Aspergers disorder adolescents and adults, there are emerging data showing
and other PDDs. A number of other scales have been that both individual and group-based cognitive behavioral
developed to assess Aspergers disorder, but systematic therapy are promising in the treatment of co-occurring
research is lacking as of yet (see Matson & Boisjoli, 2008; symptoms of depression and anxiety. Individual work
Mesibov, Shea, & Adams, 2001 for review). with counsellors or mental health professionals could
In addition to assessing the core symptoms of Asper- also focus on social and communication skills training as
gers disorder, assessment should focus on cognitive, well as bolstering adaptive functioning. In addition, med-
adaptive, and communication skills. General measures of ications may be prescribed to treat associated symptoms
intelligence, such as the Wechsler Scales and the Stanford (particularly inattention, depression, and anxiety).
Binet Intelligence Scales are useful in assessing overall
functioning as well as particular strengths and weaknesses.
Additionally, it is helpful to include measures of visual- Cross References
spatial and visual-motor processing, particularly since
these areas are typically weaker in Aspergers disorder. Autistic Disorder
Given common deficits in executive function and atten- Nonverbal Learning Disabilities
tion, neuropsychological assessment of these functions is Pervasive Developmental Disorder NOS
recommended. Measures of social communication and
pragmatic language, and adaptive skills, also add informa-
tion to the clinical picture and help inform intervention References and Readings
recommendations (see Klin et al., 2000 for review).
manual of mental disorders (4th ed.). Washington, DC: American
Treatment Psychiatric Publishing, Inc.
Fombonne, E. (2005). The changing epidemiology of autism. Journal of
Applied Research in Intellectual Disabilities, 18, 281294.
There is, as of yet, no available treatment that provides a
Fombonne, E., & Tidmarsh, L. (2003). Epidemiologic data on Asperger
cure for the core impairments of Aspergers disorder. disorder. Child and Adolescent Psychiatric Clinics of North America,
However, there are a number of interventions that target 12, 1521.
specific symptoms. In addressing social deficits in Frith, U. (Ed.). (1991). Autism and Asperger syndrome. Cambridge: Cam-
Aspergers disorder, there have been several promising bridge University Press.
Frith, U. (2004). Emanuel Miller lecture: Confusions and controversies
studies of social competence interventions among children
about Asperger syndrome. Journal of Child Psychology and
and adolescents with Aspergers disorder and autism. Such Psychiatry, 45, 672686.
interventions can be delivered in educational or outpatient Ghaziuddin, M. (2002). Asperger syndrome: Associated psychiatric and
clinic-based settings, and typically include cognitive and medical conditions. Focus on Autism and Other Developmental
behavioral components (including direct instruction, Disabilities, 17, 138144.
Klin, A., Volkmar, F. R., & Sparrow, S. (Eds.). (2000). Asperger syndrome.
modelling skills, and skills practice) (see Klin et al., 2000).
New York, NY: The Guilford Press.
Educationally, students with Aspergers disorder often Matson, J. L., & Boisjoli, J. A. (2008). Strategies for assessing Aspergers
benefit from modifications and supports provided syndrome: A critical review of data based methods. Research in
through special education. Although services vary widely Autism Spectrum Disorders, 2, 237248.
262 A Assessment of Consent
Mattila, M., Kielinen, M., Jussila, K., Linna, S., Bloigu, R., Ebeling, H., responsibilities, interpersonal relationships, community
et al. (2007). An epidemiological and diagnostic study of Asperger
life, education, employment, and recreation (classified as
syndrome according to four sets of diagnostic criteria. Journal of the
American Academy of Child & Adolescent Psychiatry, 46, 636646.
social roles). The long form includes 31 subsections, es-
McLaughlin-Cheng, E. (1998). Asperger syndrome and autism: A sentially covering the listed domains with a greater degree
literature review and meta-analysis. Focus on Autism and Other of specificity. Each item is rated on a 4-point level of
Developmental Disabilities, 13, 234245. accomplishment scale (with an additional option to
Mesibov, G. B., Shea, V., & Adams, L. W. (2001). Understanding Asperger
state not applicable), a 5-point level of satisfaction
syndrome and high-functioning autism. New York, NY: Kluwer
Academic/Plenum Publishers.
scale, as well as a rating regarding the type and level of
Saulnier, C. A., & Klin, A. (2007). Brief report: Social and communication assistance required (i.e., no assistance, assistive device,
abilities and disabilities in higher functioning individuals with adaptation, human assistance). A score for each item is
autism and Asperger syndrome. Journal of Autism and Developmental obtained with reference to a scoring template included in
Disorders, 37(4), 788793.
the manual, grading according to the level of difficulty and
Schopler, E., Mesibov, G. B., & Kunce, L. J. (Eds.). (1998). Asperger
syndrome or high-functioning autism? New York, NY: Plenum Press.
level of assistance. Item scores range from 0 (not accom-
Wing, L. (1981). Aspergers syndrome: A clinical account. Psychological plished) to 9 (performed with no difficulty and no assis-
Medicine, 11, 115130. tance), with mid-scale examples being 3 (performed with
difficulty and human assistance), and 6 (performed with
difficulty and technical aid or adaptation). Scores can then
be weighted by the number of applicable activities to
Assessment of Consent obtain domain-level scores, or a simple formula can be
used to obtain an overall score.
Informed Consent
Assessment of Life Habits (LIFE-H) Noreau, Fougeyrollas, and Tremblay (2005) stated that the
LIFE-H was developed to assess social participation in
J ESSICA F ISH people with disabilities, regardless of the nature of those
Medical Research Council Cognition & disabilities, and based upon the Disability Creation Process
Brain Sciences Unit model, which views handicap as the situational result of
Cambridge, UK the interaction of two causal dimensions: the characteristics
of the individual and those of the environment. Version
2.0 of the scale was developed following a content validity
Synonyms study that involved 12 experts in rehabilitation medicine
evaluating the scale (in terms of clarity and pertinence of
The abbreviation LIFE-H is consistent, but version num- content, classifications used in the measurement scales,
bers are often appended (e.g., LIFE-H 1.0, 2.0, 3.0, 3.1) etc.); modifications included reversing the scoring of the
accomplishment section such that higher scores reflected
the competence in the activity. Version 3.0 incorporated a
Description greater number of items within particular domains and
added additional filter questions to some sections (e.g., if
The Assessment of Life Habits (LIFE-H) is a self-report you are not currently employed, skip to section x). Version
measure of social participation of people with disabilities. 3.1 is a short form based upon version 3.0.
The original version of the scale consisted of 298 items;
later versions have reduced the number of items to 240
(version 3.0). Various short forms are also available (5577 Psychometric Data
items), with the most recent being the 77-item version 3.1.
The long form is said to take between 20 and 120 min to Fougeyrollas et al. (1998) reported that the LIFE-H v1.0
complete, and the short form, 2060 min. In the short demonstrated acceptable internal consistency in adults
form (version 3.1), items are organized into 12 categories: and children (Intra-class Correlation (ICCs) > 0.5 for
nutrition, fitness, personal care, communication, housing, each life habit), and good testretest reliability in children
mobility (classified as activities of regular living) and and adults with spinal cord injury (ICC children r = 0.73,
Assessment of Motor Process Skills A 263
and adults r = 0.74). Inter-rater reliability was examined and disabilities: Conceptual approach and assessment of handicap.
International Journal of Rehabilitation Research, 21(2), 127141. A
in a group of 20 stroke patients (Beaulieu et al., 1996;
Noreau, L., Desrosiers, J., Robichaud, L., Fougeyrollas, P., Rochette, A., &
Cited in Noreau et al., 2002), with ICCs for 6/12 accom- Viscogliosi, C. (March 18, 2004). Measuring social participation:
plishment ratings of life habits above 0.6, and 10/12 Reliability of the LIFE-H in older adults with disabilities. Disability &
satisfaction ratings for life habits above 0.6. Similar Rehabilitation, 26(6), 346352.
findings have been reported for inter-rater reliability of Noreau, L., Fougeyrollas, P., & Tremblay, J. (2005). The measure of life
habits (LIFE-H) users manual. RIPPH. http://www.ripph.qc.ca/?
LIFE-H scores for people with physical disabilities, with
rub2=4&rub=15&lang=en. Accessed 23 Apr 2010.
ICCs of r > 0.75 for 7/10 categories, and r = 0.89 for the Noreau, L., Fougeyrollas, P., & Vincent, C. (2002). The LIFE-H: Assess-
whole scale (Noreau et al., 2004). ment of the quality of social participation. Technology and Disability,
Several studies have examined the predictive validity of 14(3), 113118.
the LIFE-H. Desrosiers et al. (2003) presented evidence of Rochette, A., Desrosiers, J., & Noreau, L. (2001). Association between
personal and environmental factors and the occurrence of handicap
the convergent validity of the LIFE-H in the form of high
situations following a stroke. Disability & Rehabilitation, 23(13),
correlations with the Functional Autonomy Measurement 559569.
System (SMAF), and moderate correlations with the Func-
tional Independence Measure (FIM). Further, LIFE-H
scores were lower in stroke patients than neurologically
healthy controls. A comprehensive review of the psycho-
metric properties of the LIFE-H is available online (http://
Assessment of Motor Process
www.medicine.mcgill.ca/Strokengine-assess/module_lifeh_ Skills
indepth-en.html#section3).
K ELLI W ILLIAMS G ARY
Clinical Uses Richmond, VA, USA
The LIFE-H is available in Dutch, English, and French

versions. Adapted forms suitable for use with children Synonyms
aged 04 and 513 are available (for which a proxy re-
spondent is required). The LIFE-H has been used to AMPS
evaluate social participation in many patient groups, in-
cluding children with cerebral palsy, adults with Spinal
Cord Injury, Traumatic Brain Injury, and stroke. Description
The Assessment of Motor Process Skills (AMPS) is a stan-

Cross References dardized observational assessment widely used by occupa-
tional therapists to measure the quality of performance in
Functional Autonomy Measurement System activities of daily living (ADL) of persons across the age
Functional Independence Measure spectrum beginning at 3 years. Specifically, the AMPS tests
functions that relate to purposeful, goal-oriented daily life
tasks that a person wants, needs, and is expected to perform;
References and Readings it does not evaluate neuromuscular, biomechanical, cogni-
tive, and psychosocial impairments (Fisher, 2006). The
More information is available on http://www.medicine.mcgill.ca/ current version of the assessment contains 83 calibrated
Strokengine-assess/module_lifeh_indepth-en.html#section3. Accessed ADL tasks that permit evaluation of 36 skills (16 motor,
12 May 2009.
20 process); AMPS-trained raters must observe two or
Desrosiers, J., Rochette, A., Noreau, L., Bravo, G., Hebert, R., & Boutin, C.
(Sept.Oct. 2003). Comparison of two functional independence more specific tasks in 1020 min increments.
scales with a participation measure in post-stroke rehabilitation. A multi-perspective approach is used to rate each task by
Archives of Gerontology and Geriatrics, 37(2), 157172. observing various motor and process skills in terms of
Desrosiers, J., Noreau, L., Rochette, A., Bravo, G., & Boutin, C. (2002). physical effort, efficiency, safety, and independence. The 16
Predictors of handicap situations following post-stroke rehabilita-
tion. Disability & Rehabilitation, 24(15), 774785.
motor skills reflect the ability to use body positions, obtain
Fougeyrollas, P., Noreau, L., Bergeron, H., Cloutier, R., Dion, S. A., & and hold objects, move self and objects, and sustain perfor-
St-Michel, G. (1998). Social consequences of long term impairments mance during ADL task performance. The 20 process skills
264 A Assisted Living
pertain to sustaining performance, applying knowledge, tasks to the clients daily life needs. Therefore, the environ-
temporal organization, organizing space and objects, and ment should be naturalistic and approximate the conditions
adapting performance. Scores are based on observation of in which the client can comfortably perform tasks. Settings
the client from certified raters. Motor and process skills are for AMPS observation can vary based on the space available
rated simultaneously utilizing a 4-point ordinal criterion and can include fully equipped clinic kitchens, laundry
referenced rating scale with the highest score denoting com- rooms, outdoor, and the clients own room in the hospital
petent performance, followed by questionable, inefficient, or nursing home.
and markedly inefficient performance. AMPS computer The primary advantage of the AMPS is that it can be
scoring software converts ordinal raw scores of easy skill used with persons of virtually any age, diagnosis, or disabil-
items for persons of low ability and hard skill items for ity. However, the scope and breadth of evidence for AMPS
persons of high ability along a single common equal-interval use is limited in psychiatric, neurologic, and pediatric set-
linear scale (Fisher, 1994). tings. Geriatric settings have offered the most research evi-
dence for those with cognitive impairments and dementias,
followed by a sizable proportion of research for people with
Historical Background learning disabilities (Hitch, 2007).
The genesis of the AMPS is found in the psychiatric assess- Cross References
ment of clients with schizophrenia and depression in Hali-
fax, Canada (Fisher & Bernspang, 2007). In 1994, the basic Activities of Daily Living
idea was further developed and a specific tool was stan- Instrumental Activities of Daily Living
dardized by Anne G. Fisher, ScD, OTR and colleagues from Occupational Therapy
the Division of Occupational Therapy, Umea University in
Umea, Sweden. Currently, the AMPS is used in at least 20 References and Readings
countries. In 2006, the most recent version (sixth version)
was published to increase applicability across populations, Fisher, A. G. (1994). Development of a functional assessment that adjusts
diagnoses, disabilities, cultural background, nationality, ability measures for task simplicity and rater leniency. In M. Wilson
and age groups by adding additional tasks (Fisher, 2006). (Ed.), Objective measurement: Theory into practice (Vol 2, pp. 145
175). Norwood, NJ: Ablex.
Fisher, A. G. (2006). Assessment of motor and process skills. Vol. 1: Devel-
opment, standardization, and administration manual (6th ed.). Fort
Psychometric Data Collins, CO: Three Star.
Fisher, A. G., & Bernspang, B. (2007). Response to: A critique of the
The AMPS has robust psychometric properties. Interrater Assessment of Motor and Process Skills (AMPS) in mental health
and intrarater reliability are high with 95% of calibrator practice. Mental Health Occupational Therapy, 12, 1011. (Available
from http://www.ampsintl.com/documents/MHOT%20March%
raters demonstrating goodness-of-fit to the many-faceted
202007.pdf)
Rasch model. Testretest reliability is high on a diagnosti- Hitch, D. (2007). A reply from Danielle Hitch to the Fisher and Bern-
cally heterogeneous sample of older adults with r = 0.90 to spang response to: A critique of the Assessment of Motor and
0.91 for AMPS process scale and motor scale, respectively Process Skills (AMPS) in mental health practice. Mental Health
(Fisher, 2006). Studies have found good validity of the Occupational Therapy, 12, 14. (Available from http://www.ampsintl.
com/documents/MHOT%20March%202007.pdf)
AMPS when applied to groups of different racial, ethnic,
and cultural backgrounds, across gender, and with multi-
ple diagnoses.
Assisted Living
Clinical Uses J AY B EHEL
Rush University Medical Center
Fisher (2006) states: the AMPS provides occupational Chicago, IL, USA
therapy practitioners with a powerful and sensitive tool
that can assist with planning effective ADL interventions
and documenting change. Because of the AMPS unique Synonyms
and innovative design, occupational performance is
evaluated based on the familiarity and relevance of the Domiciliary care; Residential care
Assistive Technology A 265
Definition A
Assistive Technology
Assisted living is a care arrangement that provides
supervision and assistance to individuals who are unable D IANE C ORDRY G OLDEN
to live independently but do not require the level of care Association of Assistive Technology Act Programs
provided in conventional nursing homes. Delmar, NY, USA
Current Knowledge Definition
Assisted living arrangements may take place in structured Assistive technology (AT) is a term used to refer to both
assisted living facilities, small group homes, or an indivi- AT devices and AT services. A formal, legal definition
duals own home or the home of a family member. These of AT devices and services was first published in the
arrangements have as their goal the preservation of a Technology-Related Assistance for Individuals with Dis-
degree of autonomy and privacy at home or in a home- abilities Act of 1988 as follows:
like setting. When sited in ones home, assistance may be " assistive technology device means any item, piece of
provided by a combination of paid caregivers, family equipment, or product system, whether acquired com-
members, and other paid or unpaid assistants to help mercially, modified, or customized, that is used to in-
with housekeeping, laundry, cooking, and transpor- crease, maintain, or improve functional capabilities of
tation. Assistance provided may include supervision for individuals with disabilities
safety, medication management, meal preparation, and
accompaniment and assistance during community-based " assistive technology service means any service that direct-
activities. Assisted living facilities may also offer social ly assists an individual with a disability in the selection,
activities and specialized services for individuals with acquisition, or use of an assistive technology device
cognitive impairment. Basic Activities of Daily Living AT devices include a vast array of items such as wheel-
(BADL) such as hands-on bathing, dressing, and feeding chairs, eyeglasses, hearing aids, Braille printers, electronic
are usually not considered as a part of an assisted living note-takers and organizers, augmentative communica-
arrangement as the consistent need for such basic care is tion systems, text-to-speech software, speech synthesizers,
often seen as an indication that nursing home or a home- adaptive keyboards, alternative pointing devices, voice
based parallel thereof is the more appropriate level of care. recognition software, aids for daily living, etc. AT services
Assisted living typically is not covered by private include evaluation/assessment services, selecting, fitting,
insurance or Medicare, and access to such care may be customizing, and repairing devices, delivering training
limited by an individuals finances. Moreover, there is a and technical assistance supports, and coordinating fund-
considerable variability in how care facilities, clinicians, ing and other necessary interventions to support device
and professional literature define and discuss assisted acquisition and use.
living. Consequently, the appropriate role of assisted liv- The definition of AT devices and services has remained
ing in the continuum of care remains unclear, and refine- unchanged through numerous reauthorizations of the
ment and redefinition of this role likely will be ongoing Assistive Technology Act and has been adopted in other
for some time. statutes, such as the Individuals with Disabilities Education
Act. The same definition has also been used in promulgat-
ing federal rules, such as the Electronic and Information
Cross References Technology Accessibility Standards developed pursuant to
Section 508 of the Rehabilitation Act (http://www.access-
Life Care Planning board.gov/sec508/standards.htm).

Stone, R. I., & Reinhard, S. C. (2007). The place of assisted living in long-
term care and related service systems. Gerontologist, 47(Spec. No. 3), A precise history of AT is difficult to depict because of the
2332. diversity of devices and services included in the definition
266 A Assistive Technology
of AT. The history of hearing aids can be traced back to Goals and Objectives
Alexander Graham Bells pioneering work on develop-
ment of the telephone. Modern wheelchairs are patterned AT goals and objectives begin with a primary focus on
after the first folding, tubular steel wheelchair developed ameliorating and/or compensating for a specific function-
in the 1930s; while the first dedicated wheelchair (called al deficit. For example, electronic organizers can be used
an invalids chair) is thought to have been invented to address memory or information processing problems;
4 centuries ago for Phillip II of Spain. Some devices text-to-speech software can be used to address reading
were developed as AT and evolved into mainstream tech- deficits; augmentative communication systems can be
nology. For example, in 1948 the National Bureau of used to address communication limitations, etc. In most
Standards developed specifications for a low-cost reliable cases, secondary goals are also targeted for outcomes
talking-book machine for the blind that became the including increasing academic success, fostering gainful
tape recorder. Conversely, some items developed as main- employment, supporting independent community living,
stream technology became AT such as voice recognition decreasing inappropriate behaviors, etc. With expanding
software originally developed for dictation that is used by legal mandates for integration of individuals with
individuals with motor disabilities who are unable to use a disabilities into all societal settings (Individuals with
keyboard for computer access. Disabilities Education Act, Section 504 of the Rehabilita-
In recent years, technology use has become more tion Act, and the Americans with Disabilities Act), AT
commonplace for everyone. Similarly, AT use is now goals and objectives continue to expand into new
more frequent across the disability spectrum, addressing outcome areas.
deficits in hearing, vision, motor, social, organizational,
cognitive, speech, language, information processing, etc.
Especially critical today is the use of information technol- Treatment Participants
ogy (IT), including telecommunications. IT use is now
critical to success in education, employment, independent AT is an appropriate intervention option to consider
living, and community integration and AT is the interface when functional limitations are encountered. Candidacy
that makes IT accessible (http://www.albritton.us/AThis- for AT is not limited by age, disability diagnosis, or
tory.html). severity/combination of deficits. There are no prerequi-
sites for AT consideration and AT should not be relegated
to a last resort intervention after all other interventions
have been tried and abandoned.
Rationale or Underlying Theory AT can address a variety of human functions and is
frequently grouped into areas such as vision, hearing,
Today, AT intervention is rooted in the disability rights communication, daily living, computer access, learning/
movement and self-determination efforts of individuals cognition, environmental adaptations, mobility/seating/
with disabilities and their advocates. These initiatives positioning, vehicle modifications, and recreation/leisure.
helped to delineate the difference between the medical/ For almost all functional limitations, there is a range of AT
rehabilitation and independent living models of interven- intervention that can be considered as a treatment option
tion for individuals with disabilities. The medical model (Cook & Hussey, 2001).
identifies a physical or mental impairment or lack of
certain skills and treatment is delivered to remediate the
deficit(s). With the medical model the locus of the Treatment Procedures
problem lies with the individual and the goal is to fix
the individual in some way through professional Consideration for AT begins with assessment by a quali-
treatment. Under the independent living model the prob- fied team of individuals who are knowledgeable about the
lem is defined as a lack of supports and accommodations, individual, their strengths and limitations and the range
inaccessibility, and/or autonomy the problem lies with of potential AT options available to address the indivi-
the environment or the interaction with the environment, duals functional needs. Best practice includes conducting
rather than within the person. In this model, AT plays a structured device trials with various AT devices in the
major role in addressing/ameliorating interaction environment(s) in which the individual will be using the
difficulties, typically without overtly attempting to fix technology (e.g., home, school, work, community, etc.).
the disability itself (DeJong, 1979; Pelka, 1997). This allows for comparative analysis of different device
Assistive Technology A 267
features and functions to determine which best addresses and Do we understand the commitment? (DeRuyter,
A
the individuals needs. 1995; Trachtmann, 1994). In these articles, the authors
Once AT has been acquired for an individual, training postulated that stakeholders and AT providers must be
and support must be provided for the user, their family, prepared to show how their devices/services make a dif-
and other critical individuals such as teachers, therapists, ference in the lives of individuals who receive an AT
etc. More complex AT (computer-based software applica- intervention.
tions, assistive listening systems, augmentative communi- Today, outcome measurement is occurring in all AT
cation devices, etc.) frequently requires significant service areas (medicine, education, employment/voca-
investment of time and resources in initial programming, tional rehabilitation, and independent living) through a
fitting, and set-up, in addition to training on device use variety of interdisciplinary activities. Some are driven by
(Galvin & Scherer, 1996). policy needs, in particular, accountability for public dol-
lars spent on AT (e.g., Medicare, Medicaid, special educa-
tion, vocational rehabilitation, etc.) and justification for
Efficacy Information
private insurance expenditures on AT. Others are driven
by an overarching goal of quality service delivery and
Efficacy research on AT includes basic documentation of
continuous program improvement.
changes in functional skill areas (those the AT is intended
The most direct outcome measure for AT intervention
to address) and potential secondary improvements in
is demonstration of functional skills, independence, well-
academic, social, behavioral, and other areas. Much of
being, and quality of life. Administration of standardized
this efficacy is self-evident and is reported by the AT
assessments in the aided condition (using AT) can be
users themselves (Scherer, 1993).
useful in measuring outcomes in discreet skill areas (e.g.,
No discussion of AT efficacy would be complete with-
auditory discrimination, memory, expressive communi-
out addressing the issues of device abandonment and
cation, etc.). In addition, some global assessment of AT
cost/benefit. For many types of AT, consumer discontinu-
outcomes can be helpful such as the Psychosocial Impact
ing use of the device after acquisition has been a historic
of Assistive Devices Scales (PIADS) (Jutai & Day, 2002),
problem (Wessels, Dijcks, Soede, Gelderblom, & De
the Quebec User Evaluation of Satisfaction with Assistive
Witte, 2003). Factors shown to mitigate abandonment
Technology (QUEST) (Demers, Weiss-Lambrou, & Ska,
include active consumer and family involvement in the
1996), and similar instruments. A number of online
selection and implementation of AT and the relative ad-
resources are also available with extensive data on AT
vantage of AT within the array of intervention options
outcome tools and research such as the Adaptive Technol-
available (Alper & Raharinirina, 2006; Riemer-Reiss &
ogy Resource Center (http://atrc.utoronto.ca/index.php?
Wacker, 2000).
option=com_content&task=view&id=175&Itemid=69),
As technology continues to improve, the problem of
the Assistive Technology Outcomes Measurement System
device abandonment steadily abates. Today the greater chal-
(ATOMS) Project (www.uwm.edu/CHS/atoms), the Con-
lenge is in justifying the cost/benefit of AT to secure funding
sortium for Assistive Technology Outcomes Research
from private insurance, local, state, federal, and other fund-
(www.atoutcomes.org), and the Quality Indicators for
ing sources. Some types of AT, such as durable medical
Assistive Technology Services (www.qiat.org).
equipment, have a longer history of cost/benefit data in-
cluding prevention of secondary disabilities making funding
more readily available. Other types of AT, such as electronic
Qualifications of Treatment Providers
organizers used to remediate/compensate for cognitive lim-
itations, are relatively new with little cost/benefit data
AT intervention can be provided by an extensive list of
making funding difficult to secure (Gillette & DePompei,
professionals, usually specialists in the type of the AT
2004; Hart, Buchhofer, & Vaccaro, 2004).
provided. For example, hearing aids are typically provided
by audiologists or hearing instrument dispensers, eye-
Outcome Measurement glasses by optometrists and ophthalmologists, etc. How-
ever, as the AT becomes less prescriptive in nature, the
The field of AT outcomes is quite young with most pub- range of providers expands. Electronic note-takers and
lished work emerging in the 1990s. Two of the first organizers can be provided by a whole host of providers,
focused articles on evaluating AT outcomes posed the special educators, rehabilitation counselors, behavior
questions Are we ready to answer the tough questions? therapists, occupational therapists, AT practitioners, etc.
268 A Association Areas
The Rehabilitation Engineering and Assistive Technology

Association of North America (RESNA) administers a cer- Association Areas
tification program for Assistive Technology Professionals
(ATPs) with associated standards of practice (http://www. M ARYELLEN R OMERO
resna.org/assets/240_standardsofpracticefinal1.pdf). Tulane University Health Sciences Center
Cross References Synonyms
Americans with Disabilities Act of 1990 Association cortex

Augmentative and Alternative Communication
Independent Living Centers
Definition
Individuals with Disabilities Education Act
Section 504 of the Rehabilitation Act of 1973
It is recognized that the brain is neither holistic nor rigidly
localized with respect to cognitive functions. However,
higher-order cognitive capabilities depend on specialized
regions within the brain that process, link or integrate
References and Readings elementary or new, as well as stored information into
increasingly complex wholes. Such regions are termed
Alper, S., & Raharinirina, S. (2006). Assistive technology for individuals
with disabilities: A review and synthesis of literature. Journal of
association areas and are thought to be the neuroanatomi-
Special Education Technology, 21(2), 4764. cal substrate for such higher functions as memory, emotion,
Cook, A., & Hussey, S. (2001). Assistive technologies: Principles and prac- perception, language, spatial and problem-solving skills, as
tice (2nd ed.). California: Mosby Year-Book, Inc. well as the planning and execution of behavioral responses.
DeJong, G. (1979). Independent living: From social movement to analytic
Three major association areas are recognized:
paradigm. Archives of Physical Medicine and Rehabilitation, 60,
435446. (1) Frontal association cortices, as the name implies, are
Demers, L., Weiss-Lambrou, R., & Ska, B. (1996). Development of the
located in the more anterior aspects of the frontal
Quebec user evaluation of satisfaction with assistive technology
(QUEST). Assistive Technology, 8, 313.
lobes and include dorsolateral, orbitofrontal, and pre-
DeRuyter, F. (1995). Evaluating outcomes in assistive technology: Do we motor areas. While various feedback loops are likely
understand the commitment? Assistive Technology, 7(1), 316. involved including those from the posterior and lim-
Galvin, J. C., & Scherer, M. J. (1996). Evaluating, selecting and using bic association areas, conceptually, the initial decisions
appropriate assistive technology. Gaithersburg, MD: Aspen Publish-
and planning regarding executive or motor responses
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Gillette, Y., & DePompei, R. (2004). The potential of electronic organizers
to a given situation are generally thought to flow from
as a tool in the cognitive rehabilitation of young people. NeuroReh- the prefrontal (most anterior) cortices to the premo-
abilitation, 19(3), 233243. tor cortex that organizes, coordinates, and sequences
Hart, T., Buchhofer, R., & Vaccaro, M. (2004). Portable electronic devices the actions essential to the successful completion of
as memory and organizational aids after traumatic brain injury:
the response. From there, commands are believed to
A consumer survey study. Journal of Head Trauma Rehabilitation,
19(5), 351365.
be forwarded to the primary motor area (precentral
Jutai, J., & Day, H. (2002). Psychosocial impact of assistive devices scale gyrus) that then actually executes the motor response.
(PIADS). Technology and Disability, 14(3), 107111. The orbitofrontal cortex is shared with limbic associa-
Pelka, F. (1997). ABC-CLIO companion to the disability rights move- tion cortex (see below) that underscores the impor-
ment. Santa Barbara, CA: ABC-CLIO, Inc.
tance of the integration of emotion, memory, and
Riemer-Reiss, M. L., & Wacker, R. R. (2000). Factors associated with
assistive technology discontinuance among individuals with disabil-
behavior. Lesions to prefrontal association cortices
ities. Journal of Rehabilitation, 66(3), 4450. often affect self-monitoring, planning, and executive
Scherer, M. J. (1993). Living in the state of stuck: How technology impacts functions, including behavioral inhibition.
the lives of people with disabilities. Cambridge, MA: Brookline Books. (2) The limbic association cortex includes ventromedial
Trachtmann, L. (1994). Outcome measures: Are we ready to answer the
frontal lobe, medial parietal lobe, temporal pole, and
tough questions? Assistive Technology, 6, 9192.
Wessels, R., Dijcks, B., Soede, M., Gelderblom, G. J., & De Witte, L.
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Association for Postdoctoral Programs in Clinical Neuropsychology (APPCN) A 269
association areas is received and projected to other

Association Cortex A
areas of the cortex, including the prefrontal cortex
discussed above, again permitting the integration of
emotions, cognition and perceptions, and memory. Association Areas
Dysfunction is often expressed as emotional/behav- Homotypic Cortex
ioral dysregulation and memory impairment.
(3) The locations of the parieto-temporal-occipital associ-
ation cortices are described by their names and are Association for Postdoctoral
typically divided into secondary and tertiary areas.
The former are unimodal in nature (respond more or
Programs in Clinical
less exclusively to a single sensory modality) and lie Neuropsychology (APPCN)
adjacent to their respective primary cortical sensory
projection areas. They are thought to be responsible J ACOBUS D ONDERS
for further integrating and processing sensory input Mary Free Bed Rehabilitation Hospital
into potentially meaningful percepts. Hence, lesions of Grand Rapids, MI, USA
these secondary association areas will commonly result
in modality-specific perceptual disturbances or agno-
sias. By contrast, the tertiary or heteromodal association Address (and URL)
areas receive input from all sensory modalities. Because
of this and their central location, they are sometimes APPCN
referred to as the PTO (parietal-temporal-occipital) P.O. Box 69037, Pleasant Ridge, MI 48069
cortex. Because of their crossed or multimodal inputs, www.appcn.org
these latter areas, which are very highly developed in
man, are thought to represent the foundations for Membership
higher-order conceptual and intellectual abilities, in-
cluding abstraction, language, and visual-spatial and The Association of Postdoctoral Programs in Clinical
mathematical problem solving, any or all of which can Neuropsychology (APPCN) is an organization of approx-
be adversely affected by lesions to these areas. imately 50 member programs that offer comprehensive,
integrated postdoctoral residencies.
Cross References
Association Pathways
The mission of APPCN is to foster the provision of ad-
Heteromodal Cortex
vanced specialty education and training to promote the
Secondary Cortex
competencies that are necessary for practice in the specialty
Unimodal Cortex
of clinical neuropsychology (Boake, Yeates, & Donders,
2002).
Kupermann, I. (1991). Localization of higher cognitive and affective
functions: The Association cortices. In E. R. Kandel, J. H. Schwartz, Formally incorporated in 1992, APPCN contributed to the
& T. M. Jessel (Eds.), Principles of neural science (3rd ed., pp. 823
Houston Conference, which established that completion
838). East Norwalk, CT: Appleton & Lange.
Mendoza, J. E., & Foundas, A. F. (2008). Clinical neuroanatomy: a behav-
of two years of formal postdoctoral residency training is a
ioral approach. New York: Springer. uniform requirement for entry into the professional prac-
Mesulam, M.-M. (2000). Principles of behavioral and cognitive neurology. tice of clinical neuropsychology (Hannay, Bieliauskas,
New York: Oxford University Press. Crosson, Hammeke, Hamsher, & Koffler, 1998). In more
Pandya, D. N., & Seltzer, B. (1982). Association areas of the cerebral
recent years, APPCN has been a key representative to inter-
cortex. Trends in Neurosciences, 5, 385390.
Pandya, D. N., & Yeterian, E. H. (2003). Cerebral cortex: architecture and
organizational groups like the Clinical Neuropsychology
connections. In Encyclopedia of the neurological sciences (pp. 594 Synarchy, and the Inter-Organizational Summit on Educa-
604). USA: Elsevier Science. tion and Training.
270 A Association for Postdoctoral Programs in Clinical Neuropsychology (APPCN)
Major Activities APPCN has also strived to make the process of

education and evaluation as part of postdoctoral residen-
APPCN is not an accrediting organization, a role which is cy training in clinical neuropsychology more standar-
left to the Commission on Accreditation of the American dized. For this purpose, a 50-item written examination
Psychological Association (APA). However, a growing has been developed by APPCN to be used with residents
number of the APPCN members are currently accredited who are near completion of their first postdoctoral train-
by APA as a postdoctoral specialty program in clinical ing year, to evaluate their knowledge of major content
neuropsychology. Details about individual APPCN mem- areas like functional neuroanatomy, adult and pediatric
ber programs, including focus on adult v. pediatric neu- syndromes, psychometrics, etc. This exam is not intended
ropsychology, accreditation status, primary diagnostic to give residents a grade; rather, it is to be used as an
groups served, and other characteristics, are available on educational tool, to identify relative strengths and weak-
the APPCN website. nesses in the residents working knowledge base, so that
The major standards for program membership in the relative lacunae can be addressed during the sub-
APPCN include the following: (1) the duration of training sequent training year. During that second year, APPCN
is for a minimum of 2 years, or for an equivalent time member programs also have the opportunity to start
on no less than a half-time basis, at a fixed site with preparing residents for board certification, by means of
regular, on-site supervision; (2) the program includes an ethics vignettes and mock oral fact finding case materi-
organized and integrated combination of at least 50% als that are very similar in format and level of difficulty to
clinical service, at least 10% didactic/educational activ- those used by ABPPCN.
ities, and at least 10% research or other scholarly activ- Finally, the most recent initiative of APPCN has
ities; and (3) the program director is board-certified in involved advocacy with the United States Department
Clinical Neuropsychology through the American Board of Veterans Affairs for the development of more postdoc-
of Professional Psychology (ABBPCN). One of the major toral training programs in clinical neuropsychology,
accomplishments of APPCN is the development and im- primarily because of the high number of traumatic brain
plementation, in collaboration with National Matching injuries among US service personnel involved in the
Services, of a computerized system for matching of appli- combat in Iraq. When more than a dozen of these training
cants for postdoctoral residency training in clinical neu- programs became available in the Fall of 2007, APPCN
ropsychology to programs that offer such training. This contacted the programs, provided mentoring as needed,
electronic system, instituted in 2001, is the most fair to and waived their first-time participation fee in the
applicants, and the most efficient for programs, with all electronic match. APPCN has also continued to offer assis-
APPCN programs that have open positions in any given tance to new programs as they seek specialty accreditation
year taking part in this electronic match. Postdoctoral through the APA. APPCN will continue to embrace addi-
programs that are not members of APPCN are also tional organized and integrated postdoctoral training pro-
allowed to participate as long as they meet APPCN stan- grams in clinical neuropsychology.
dards #1 and #2 above, and if they agree to respect all
other conditions of the match, including prohibition of
pre-emptive offers, and adherence to the binding nature Cross References
of the match outcomes. Further details are available at
http://www.natmatch.com/appcnmat/. American Board of Clinical Neuropsychology (ABCN)
APPCN is dedicated to education of aspiring neurop American Board of Professional Psychology (ABPP)
sychologists about what it takes to become a competitive American Psychological Association (APA)
candidate for postdoctoral residency training. For this
purpose, several educational seminars are offered on
a regular basis, some in collaboration with other organi- References and Readings
zations, such as Division 40 ( Clinical Neuropsycholo-
gy) of the APA and the Association of Neuropsychology Boake, C., Yeates, K. O., & Donders, J. (2002). Association of Postdoctoral
Students in Training (ANST). Over the past several years, Programs in Clinical Neuropsychology: update and new directions.
APPCN program directors have also consistently provided
Hannay, H. J., Bieliauskas, L., Crosson, B. A., Hammeke, T. A., Hamsher,
a special topic presentation about postdoctoral residency K., & Koffler, S. P. (1998). The Houston Conference on specialty
training at the annual meeting of the National Academy of education and training in clinical neuropsychology. Archives of
Neuropsychology (NAN). Clinical Neuropsychology, 13, 157250.
Associative Aphasia A 271
Cross References A
Commissures, Cerebral
J OHN E. M ENDOZA Projection Pathways
Definition Associational Fibers

M ELISSA J. M C G INN
Fiber pathways that lie within the cerebrum that connect
one part of the cerebral cortex with another within the
Richmond, VA, USA
same hemisphere. Association pathways are thus con-
trasted with commissures that generally interconnect ho-
mologous areas of the two halves of the brain, and
projection pathways that are fiber tracts interconnecting
Synonyms
cortical and subcortical structures. They may be very long
Arcuate fibers
(typically termed fasciculi) or very short. The latter may
consist of U-shaped fibers connecting one gyrus with an
adjacent one or horizontal connections within a gyrus
itself (e.g., bands of Baillarger). These various pathways
Definition
allow different areas of the brain to communicate with
Associational fibers are white matter fibers that connect
one another. Some of the major association pathways are
various cortical regions within the same cerebral hemi-
shown in Fig. 1.
sphere. Being the most prevalent type of neuronal tracts
found in the cortex, associational fibers permit bidirec-
tional communication between different cortical areas,
allowing the cortex to function as a coordinated whole.
Associational fibers arise from cortical layer II/III pyrami-
dal neurons and can be classified as either short associ-
ational fibers, which connect adjacent gyri within the
same lobe, or long associational fibers, interconnecting
more distant regions located in different lobes. The major
long associational fibers tracts in the brain include the
superior longitudinal fasciculus, arcuate fasciculus, unci-
nate fasciculus, and cingulum.
Cross References
Arcuate Fasciculus
Cerebral Cortex
Cingulum
U
Superior Longitudinal Fasciculus
U
SLF White Matter
AF arcuate fasciculus
IOF inf. occiptofrontal fasc. AF
SLF sup. longitudinal fasc. IOF
UF
U U-fibers
UF uncinate fasciculus
Associative Aphasia
Association Pathways. Figure 1 Conduction Aphasia
272 A Associative Memory
perceptual problem) from an inability to recognize familiar

Associative Memory faces (generally considered an associative problem). Thus,
in the latter instance, while the patient might be able to
Paired-Associate Learning match the face or picture of a familiar person to one within
an array of pictures, he would not be able to identify the
face or the picture as that of his wife, his daughter, or other
Associative Visual Agnosia famous person with whom he might be familiar.
While the specific lesions causing specific associative
J OHN E. M ENDOZA visual agnosias are not well defined, they are generally
Tulane University Medical Center thought to represent a disconnection type syndrome in-
New Orleans, LA, USA volving the temporal, occipital, and/or parietal regions of
the left hemisphere with some disruption of fiber path-
ways or connections between the unimodal (visual) and
Definition heteromodal cortices.
Regardless of modality, an associative agnosia implies that

Cross References
although perception is intact, the particular stimulus has
no meaning (associative value) to the individual. The
Alexia
stimulus can neither be named nor linked to other personal
Apperceptive Visual Agnosia
or sensory experiences. Hence, associative visual agnosia
Color Agnosia
refers to the inability to identify or categorize a visually
Color Anomia
presented stimulus despite adequate visual perception.
Disconnection Syndrome
Heteromodal Cortex
Prosopagnosia
Current Knowledge Unimodal Cortex
Individuals with this disorder should be able to match the
visual stimulus to a sample and copy or draw what is seen, References and Readings
thus distinguishing associative from apperceptive visual
Bauer, R. M., & Demery, J. A. (2003). Agnosia. In K. Heilman &
agnosia. In the latter condition, visual object recognition
E. Valenstein (Eds.), Clinical neuropsychology, (4th ed., pp. 236
is also impaired, but primarily as a result of a disturbance 295). New York: Oxford University Press.
of perception. In addition to having difficulty naming DeRenzi, E., & Spinnler, H. (1966). Visual recognition in patients with
visually presented objects, a patient suffering from associa- unilateral cerebral disease. Journal of Nervous and Mental Disease,
tive visual agnosia would likely be unable to describe their 142, 513525.
DeRenzi, E., Scotti, G., & Spinnler, H. (1969). Perceptual and associative
use or purpose, or indicate to which category of objects
disorders of visual recognition. Relationship to the side of the cere-
they may belong. However, in pure visual associative agno- bral lesion. Neurology, 19, 634642.
sia, identification should be possible if the patient were
allowed to hold the object(s) (tactile recognition).
An associative visual agnosia may differentially affect
recognition of objects, words, colors, or faces. In visual Astasia-Abasia
agnosia for words (also known as pure alexia or pure word
blindness), visual word recognition is impaired. But the D OUGLAS I. K ATZ
individual may be able to read if allowed to trace the Braintree Rehabilitation Hospital
letters with a finger, thus permitting tactile or kinesthetic Braintree, MA, USA
recognition of individual letters. In associative color Boston University School of Medicine
agnosia, the individual may be able to match colors, but Boston, MA, USA
neither name them nor identify objects with which they
might be associated (such as cherries or apples for the color
red). Facial agnosia (prosopagnosia) is a bit complex in that Synonyms
one may differentiate the inability to make discriminations
among unfamiliar faces (thought to be more of a Blocqs disease
Astereognosis A 273
Definition also called morphognosia, reflect impairments in recog-

A
nizing the physical features of the object (e.g., weight or
An inability to stand and walk in a normal and coordinated texture). Secondary recognition deficits reflect a specific
manner. Astasia means inability to maintain standing and impairment in object recognition with spared primary
abasia refers to impaired coordination of gait. The term is recognition (for review see De Renzi, 1982).
usually applied to unusual, often bizarre patterns of gait
and stance that appear to have no neuropathophysiologic
basis. Conversion disorder is frequently the underlying
cause. Patients may sway in a staggering, unstable manner, Epidemiology
often catching themselves before falling. This syndrome is
also referred to as Blocqs disease. Astereognosis can be common after stroke with one re-
port indicating that up to 90% of patients demonstrate
astereognosis (Connell, Lincoln, & Radford, 2008).
Cross References Damage to the cortical regions important for haptic
input integration can cause astereognosis. This disorder,
Abasia therefore, is common and can occur in the
Gait Disorders presence of many neurological disorders including
Psychogenic Disorder brain (e.g., Knecht, Kunesch, & Schnitzler, 1996), or
spinal cord tumors (Lesoin, Rousseaux, Martin, Petit, &
Jomin, 1986), and traumatic brain injury (Hom & Reitan,
1982).
Morris, J.G., Mark de Moore, G., Herberstein, M. (2006). Psychogenic
Gait: An example of Deceptive Signaling. In: C.R. Cloninger, &
M. Hallett (Eds.), Psychogenic movement disorders: neurology and
neuropsychiatry. Philadelphia: Lippincott Williams & Wilkins. Natural History, Prognostic Factors,
Okun, M.S., & Koehler, P.J. (2007). Paul Blocq and (psychogenic) astasia Outcomes
abasia. Movement Disorder, 22, 13731378.
Connell et al. (2008) followed 58 stroke survivors over a
period of 6 months (baseline, 2, 4, and 6 months) and at
each time period participants completed the Nottingham
Astereognosis Sensory Assessment (see below). Stereognosis significantly
improved during the observation period, with the greatest
M ELISSA A MICK changes occurring within the first 4 months (baseline rela-
VA Boston Healthcare System tive to 4-month performance). Regression analyses indi-
Boston, MA, USA cated that stroke severity and motor performance of the
upper limb were predictive of the presence of impaired
stereognosis at the baseline assessment.
Synonyms
Object agnosia; Tactile agnosia

of Astereognosis
Astereognosis can occur after injury to either the left or
Astereognosis is defined as the inability to identify objects right hemisphere. A specialized role for the right hemi-
through touch without visual input. sphere in stereognosis has been proposed, however this
finding has not been consistently observed (for review see
Zaidel, 1998 and De Renzi, 1982). Initially astereognosis
Categorization was thought to be due to damage to the primary
somatosensory cortex; however, posterior parietal lesions
Astereognosis has been subdivided into primary and sec- have also been associated with this impairment (Knecht
ondary recognition deficits. Primary recognition deficits, et al., 1996).
274 A Asthenia
Evaluation Cross References
Astereognosis is often examined with non-standardized Ahylognosia

methods. In the typical neurological examination, aster- Amorphognosis
eognosis is assessed by asking the patient to identify an Parietal Lobe
object through touch without visual input. Common Somatosensory Cortex
objects used for identification can include coins, keys, Stereognosis
paper clips, or screws. For patients with hemiparesis, the Tactile Agnosia
examiner may manipulate the patients hand to assist in Tactile Form Recognition
object identification. Standardized assessments of aster- Tactual Performance Test
eognosis do exist. The Tactile Form Recognition Test from
the HalsteadReitan Neuropsychological Test Battery
(Reitan & Wolfson, 1993) requires participants to manip-
ulate a flat plastic shape with one hand obscured from References and Readings
vision, while the other hand points to the same shape
mounted on a board with three other potential distrac- Benton, A. L. (1969). Stereognosis test; Manual of instructions. Neuropsy-
tors. In the Benton Stereognosis Test (Benton, 1969), chology Laboratory, Department of Psychology, University of
Victoria.
10 cards with fine grain, sandpaper figures pasted on top
De Renzi, E. (1982). Disorders of space exploration and cognition.
are felt by the participant out of view. The participant has New York: Wiley.
30 s to explore the card and 45 s to respond. Responses are Connell, L. A., Lincoln, N. B., & Radford, K. A. (2008). Somatosensory
made by pointing to the corresponding line drawing impairment after stroke: Frequency of different deficits and their
mounted in full view of the respondent. The Nottingham recovery. Clinical Rehabilitation, 22, 758767.
Gaubert, C. S., & Mockett, S. P. (2000). Inter-rater reliability of the
Sensory Assessment includes an assessment of astereog-
Nottingham method of stereognosis assessment. Clinical Rehabilita-
nosis (Gaubert & Mockett, 2000). In this task the partici- tion 14(2), 153159.
pant is blindfolded and asked to name the object placed in Hom, J., & Reitan, R. M. (1982). Effect of lateralized cerebral damage
their hand. Presentation of the objects is time limited. upon contralateral and ipsilateral sensorimotor performances. Jour-
Objects to be identified include coins, comb, sponge, nal of Clinical Neuropsychology 4(3), 249268.
Knecht, S., Kunesch, E., & Schnitzler, A. (1996). Parallel and
pencil, scissors, a cup, and a glass. Responses are scored
serial processing of haptic information in man: Effects of parietal
on a scale of 0-2 depending upon the quality of the verbal lesions on sensorimotor hand function. Neuropsychologia, 34,
response. 669687.
Lesoin, F., Rousseaux, M., Martin, H. J., Petit, H., & Jomin, M. J. (1986).
Astereognosis and amyotrophy of the hand with neurinoma of the
second cervical nerve root. Neurology, 233, 5758.
Treatment Lincoln, N. B., Crow, J. L., Jackson, J. M., Waters, G. R., Adams, S. A., &
Hodgson, P. (1991). The unreliability of sensory assessment. Clinical
Astereognosis has been observed to spontaneously im- Rehabilitation, 5, 273282.
prove over time (Connell et al., 2008). One study has Reitan, R. M., & Wolfson, D. (1993). The Hasltead-Reitan neuropsycho-
found that stereognosis improves following systematic logical test battery: Theory and clinical interpretation. Tucson, AZ:
Neuropsychology Press.
hand retraining in stroke survivors who were at least
Yekutiel, M., & Guttman, E. J. (1993). A controlled trial of the
2 years post stroke. Yekutiel & Guttman (1993) had 25 retraining of the sensory function of the hand in stroke
participants receive three, 45-min hand-retraining ses- patients. Journal of Neurology, Neurosurgery, and Psychiatry, 56,
sions weekly for a period of 6 weeks. The therapy was 241244.
customized for each participant but everyone received Zaidel, E. (1998). Stereognosis in the chronic split brain: Hemispheric
differences, ipsilateral control and sensory integration across the
education to improve insight about their impairment
midline. Neuropsychologia, 36, 10331047.
and exercises were intended to be appropriately challeng-
ing, designed to promote self-efficacy, used vision and the
less affected hand to aid sensory function, and provided
frequent breaks and novel stimuli. Unlike the control
group, the patient group showed a statistically significant
improvement on the stereognosis assessment. These find- Asthenia
ings suggest that functional gains through therapy can
occur in the years following stroke. Adynamia
Asymmetry A 275
Astrocytoma Asymmetry A
R OBERT R IDER M ARYELLEN R OMERO

Drexel University Tulane University Health Sciences Center
Philadelphia, PA, USA New Orleans, LA, USA
Definition Synonyms
Astrocytomas are the most frequently diagnosed tumors, Hemispheric specialization

are usually slow-growing, and may develop a cystic com-
ponent. Arising in astrocytic cells anywhere throughout Definition
the central nervous system, they may occur in any age
group, but are most frequently diagnosed in middle-aged Asymmetry is the discordance between the right and left
males. The highest incidence of brain stem astrocytomas sides of the brain in respect to structure and/or function.
is found in children. Grading systems focus on the degree
of resemblance to normal astrocytes, with higher grades Current Knowledge
associated with more rapid growth and greater likelihood
of metastasis. Three common types of astrocytomas are: Although not initially linked to brain asymmetry, the first
low-grade astrocytomas, which are often benign and tend behavioral asymmetry that was likely noted was the superi-
to occur in the cerebellum (especially in children) but ority of motor skills exhibited by one hand, most common-
may also occur in the cerebrum in adults; anaplastic ly the right, over the other. The next real breakthrough with
astrocytomas, which are malignant; glioblastoma multi- regard to asymmetry is generally thought to have occurred
forme, which are thought to arise from astrocytomas and in the nineteenth century with the discovery that acquired
are the most malignant. The specific symptoms associated language deficits (aphasia) were typically associated with
with astrocytomas depend on the region of the CNS that lesions of the left hemisphere. Since then, other asymme-
is affected. tries, both functional and structural, have been identified
with regard to the two cerebral hemispheres.
Cross References Structural Asymmetries

Fibrillary Astrocytoma
Structural asymmetries of the brain were first noted around
Oligoastrocytoma
the beginning of the twentieth century, but it was not until
Pilocytic Astrocytoma
the late 1960s that these were first strongly correlated with
Xanthroastrocytoma
functional differences between the hemispheres. In a study
of 100 postmortem brains, Geschwind and Levitsky (1968)
noticed that the planum temporale, located in the tempo-
References and Readings ral operculum, was larger in 65% of the brains studied as
compared with only 11% in which the right was larger.
Louis, D., Ohgaki, H., Cavenee, W., & Wiestler, O. (2007). WHO classifi- They concluded that this difference was likely related to
cation of tumours of the central nervous system (4th ed.). World the left hemispheres association with the production of
Health Organization. language in most individuals. Subsequent studies have
demonstrated that this asymmetry can be shown to pres-
ent even prior to birth, reinforcing the genetic predispo-
sition to left-hemispheric dominance for language.
Since the advent of more sophisticated imaging tech-
Astrocytosis niques that allow for large-scale in vivo studies of the
brain, other structural differences have been documented.
Gliosis The inferior frontal gyrus in the left hemisphere,
276 A Asymmetry
corresponding to Brocas area, has been shown to be more ability to use numbers is thought to be a function nor-
highly developed on the left side for most individuals. The mally carried out by the left hemisphere, the disturbance
gyri and sulci associated with the motor strip (Brod- of which following a lesion to the left hemisphere may be
manns area 4) are more prominent in the left hemisphere defined as acalculia (dyscalculia). However, most complex
of right-handers. Fairly consistent differences in the later- arithmetical operations also have a spatial component.
al fissure have been found, with the posterior ascending For example, precise alignment of rows and columns of
ramus of this sulcus making a more abrupt upward turn numbers is critical in mathematical operations, whether
in the right hemisphere as compared with the left. This completed mentally or on paper. These spatial relations
would suggest likely differences in the distribution of the can be disturbed following right-hemispheric lesions,
supramarginal and angular gyri in the inferior parietal resulting in what has been termed spatial dyscalculia.
lobules of the two hemispheres. Even on a more micro- It is known that the hemisphere contralateral to the
level, differences in the size and organization of individual hand being used to carry out some motor tasks is imme-
cells or cell columns have been identified in the two diately responsible for the execution of these movements.
hemispheres. However, the motor programs or engrams for overlearned
It is reasonable to speculate that some structural dif- motor skills are believed to reside in the left hemisphere,
ferences likely relate to functional differences between the certainly for the vast majority of right-handers, as well as
two hemispheres, particularly behaviors such as language many left-handers. Thus, any lesion that either directly
and handedness. However, functional asymmetries have interferes with those engrams or the ability of that infor-
either been demonstrated or are suspected well beyond mation to reach the premotor cortex of either hemisphere
those which can currently be explained by structural dif- can result in an impaired performance, especially if the
ferences. The following represent a sampling of some of individual is asked to demonstrate the action in the ab-
the functional differences that have been observed. sence of the actual object. This latter condition is referred
to as an ideomotor apraxia.
Perceptual abilities appear to be differentially
Functional Asymmetries distributed between the two hemispheres. It has already
been noted that the left hemisphere is normally the lead-
It has been well established that language expression ing hemisphere in interpreting verbal (semantic) infor-
and comprehension are normally mediated primarily, mation, while the right appears to be better adapted to
if not exclusively, by the left hemisphere, even among processing certain types of emotional cues. It seems that
left-handers. However, the right hemisphere has also the right hemisphere is also the more proficient in proces-
been shown to play an important role in communication. sing many types of visual-spatial or visual-gestalt infor-
Verbal communication is not just about using words in mation. Thus, the right hemisphere has been found to be
sentences or paragraphs; emotional tone or nuances of the generally superior in carrying out certain constructional
speaker often convey important meaning. In some com- tasks, making judgments regarding the orientation of
munications, such as those with a sarcastic intent, the real lines in space, in making discriminations regarding unfa-
message is carried by the tone rather than by the words, miliar faces, and in recognizing familiar tunes or environ-
which, if interpreted literally, might actually convey a very mental sounds. On the other hand, the left hemisphere
different message. The ability to use as well as interpret appears to be the leading hemisphere when it comes to
these emotional components of speech, known as proso- perception of certain aspects of ones own body. Problems
dy, is primarily mediated by the right hemisphere; damage of rightleft orientation and difficulty recognizing indi-
to this side of the brain may produce various forms of vidual fingers of ones hands (finger agnosia) are typically
aprosodia. With regard to using or interpreting the lan- associated with lesions of the left inferior parietal lobule.
guage of others, the right hemisphere is also believed to Functional MRI studies have demonstrated consistent
play an important role in identifying the central theme or activation of right hemisphere structures during tests of
point of the discourse of others and being able to stay on vigilance and directed attention. However, divided atten-
point when speaking or writing. It appears to be impor- tion tasks have been shown to selectively activate left
tant in appreciating verbal (as well as nonverbal) humor prefrontal cortex. PET imaging studies have demon-
and in detecting meaning from the differential inflections strated increased blood flow in the right prefrontal and
given to individual words in speech. superior parietal cortex during tasks requiring sustained
In addition to words, numbers also have their own attention, regardless of the type of stimulus (verbal, visu-
symbolic meaning. Hence, as might be expected, the al, etc.) or where it is introduced (left vs. right).
Ataxia A 277
Differences between the two hemispheres have also Davidson, R. J., & Hugdahl, K. (Eds.). (1996). Brain asymmetry. Cam-
bridge, MA: Bradford Books. A
been demonstrated in learning and memory tasks and
Gazzaniga, M. S. (2000). The new cognitive neurosciences. Boston: MIT
other cognitive domains. Of the two, the left hemisphere Press.
has been more strongly associated with learning verbal Gazzaniga, M. S., Ivry, R. B., & Mangun, G. R. (2002). Cognitive neuro-
information. While many studies have shown that the science: The biology of the mind. New York: W.W. Norton &
right hemisphere is perhaps better at learning certain Company.
Geschwind, N., & Levitsky, W. (1968). Left-right asymmetry in temporal
nonverbal or visual-spatial type information, the
speech region. Science, 161, 186187.
findings are generally less robust compared to the left Good, C. D., Johnsrude, I., Ashburner, J., Henson, R. N. A., Friston, K. J.,
hemisphere and verbal memory. One frequent explana- & Frackowiak, R. S. J. (2001). Cerebral asymmetry and the effects of
tion for this is that when faced with any memory task, sex and handedness on brain structure: A voxel-based morphometric
humans have a natural tendency to try to verbally encode analysis of 465 normal adult human brains. Neuroimage, 14,
685700.
the stimulus, thus bringing the left hemisphere into play.
Kinsbourne, M. (Ed.). (1978). Asymmetrical function of the brain. New
It has also been suggested that the two hemispheres York: Cambridge University Press.
play different roles in attention. The much more frequent Mendoza, J. E., & Foundas, A. L. (2008). Clinical neuroanatomy:
association of disorders such as unilateral neglect and A neurobehavioral approach. New York: Springer.
anosognosia with right hemispheric lesions have led to Ross, E. (2000). Affective prosody and the aprosodias. In M. Mesulam
(Ed.), Principles of behavioral and cognitive neurology. New York:
the hypothesis that while, as might be expected, the left
hemisphere attends to the right side of space (both per- Walsh, K. (1994). Neuropsychology: A clinical approach. New York:
sonal and extrapersonal), the right hemisphere focuses on Churchill Livingstone.
both right and left space.
Finally, the association of the right hemisphere and
emotional expression would appear to go beyond the Ataxia
affective intonations of speech as described above. It is
commonly observed, both by health-care professionals as A NNA D E P OLD H OHLER 1, M ARCUS P ONCE DE LEON2
well as the spouses and other family members of persons 1
Boston University Medical Center
with brain injury that individuals with right hemisphere Boston, MA, USA
lesions often behave differently than those with left-sided 2
William Beaumont Army Medical Center
lesions. While the latter seem to remain emotionally at- El Paso, TX, USA
tached, even if that emotion is often one of anger, frustra-
tion, or sadness, right hemispherically damaged patients
are more likely to be described as apathetic, indifferent, Synonyms
emotionally flat, both in terms of their verbal and facial
expressions and their interpersonal relationships. Clumsiness
Cross References Definition
Anosognosia Ataxia describes a lack of coordination while performing

Directed Attention voluntary movements. It is associated with damage to the
Dominance, Cerebral cerebellum or its afferent or efferent pathways. It may
Ideomotor Apraxia appear as clumsiness, inaccuracy, or instability. It
Language may affect any part of the body. When ataxia affects the
Unilateral Neglect arms and hands, it may cause tremor due to overcorrection
Wada Test of inaccurate movements. It may produce dysmetria or an
inability to gauge distance correctly. It may cause past-
pointing when an attempted reach overshoots the target.
References and Readings It may also cause dysdiadochokinesia or poor perfor-
mance of regular, repeated movements. Cerebellar injury
Corballis, P. M. (2003). Visuospatial processing and the right-hemisphere
interpreter. Brain and Cognition, 53, 171176.
may contribute to nystagmus, hyper and hypometric
Davidson, R. J. (1992). Emotion and affective style: Hemispheric sub- saccades, scanning speech, titubation, and difficulties
strates. Psychological Science, 3, 3943. with gait and balance.
278 A Atheromatous Plaque
Current Knowledge Neuropsychology
There are a number of different types of damage to the Cerebellar syndromes may be associated with cognitive
cerebellum. These range from fixed damage (e.g., stroke, slowing.
trauma, hypoxic injury) to chemical and metabolic, and Evaluation includes a detailed neurological examina-
degenerative. Cerebellar injury related to vitamin tion, magnetic resonance imaging, and laboratory inves-
deficiency (e.g., E, B12, and thiamine) may be reversible tigation for reversible or genetic causes.
and should be identified and treated. Metabolic diseases Treatment depends on the underlying insult.
such as Hartnups, Refsums, and the mitochondrial dis-
orders are less treatable. A deficiency of Coenzyme Q10
Cross References
has been described in patients with cerebellar ataxia, usu-
ally with childhood onset and often associated with sei-
Cerebellum
zures. The symptoms may respond to Coenzyme Q10
Dysdiadochokinesia
treatment. There are a number of hereditary cerebellar
ataxias. Most of the autosomal recessive and autosomal
dominant ataxias have no treatments. An exception is References and Readings
vitamin E deficiency, which is an autosomal recessive
disorder. It is due to a mutation in the gene coding for Gilman, S. (2004). Clinical features and treatment of cerebellar disorders.
the alpha tocopherol transfer protein located on the long In R. L. Watts & W. C. Koller (Eds.), Movement disorders (2nd ed.,
pp. 723736). New York: McGraw-Hill.
arm of chromosome 8. It is characterized by childhood
onset of ataxia, dysarthria, areflexia, proprioceptive defi-
cits, extensor plantar responses, and skeletal deformities.
The episodic ataxias, which are inherited in an Atheromatous Plaque
autosomal dominant fashion, may also have some
symptomatic treatment regimens. Episodic Ataxia Type 1 Atherosclerosis
is related to a chromosome 12 mutation in the potassi-
um channel gene. Clinically, the disease manifests with
episodes of ataxia lasting seconds to minutes. Patients
may also suffer from myokymia during and between
Atherosclerosis
attacks of ataxia. The ataxia may be induced by startle or
E LLIOT J. R OTH
exercise. Episodic Ataxia Type 2 is related to a defect
Northwestern University
located on chromosome 19. It is due to a mutation in a
Chicago, IL, USA
voltage-dependent calcium channel. Clinically, patients
present with nystagmus. Attacks last minutes to hours
and may be induced by a change in posture. Patients
may also complain of vertigo. As the disease progresses,
Synonyms
ataxia becomes permanent.
Arteriosclerotic vascular disease or ASVD; Atheromatous
plaque; Hardening of the arteries
Epidemiology
Definition
Ataxia is a common sign associated with inherited,
acquired, toxic, and traumatic events. Atherosclerosis is the progressive pathological process of
buildup of plaque inside the blood vessels, resulting in
blockage of blood flow through the vessels.
Natural History
The genetic syndromes that are associated with ataxia Current Knowledge
tend to be progressive. Individuals with static insults
such as strokes or trauma may show improvement in The plaque that causes atherosclerosis is comprised of
function over time. fatty substances, cholesterol, cells, calcium, and fibrin, a
Atkins v. Virginia A 279
stringy material found normally in the blood to help clot References and Readings A
the blood. The plaque formation process stimulates the
cells of the artery wall to produce substances that then Stary, H. C., Chandler, A. B., Dinsmore, R. E., Fuster, V., Glagov, S., Insull,
accumulate in the vessel wall. Fat builds up within W., et al. (1995). A definition of advanced types of atherosclerotic
lesions and a histological classification of atherosclerosis: A report
these cells and around them, and they form connective
from the Committee on Vascular Lesions of the Council on Arterio-
tissue and calcium. The artery wall thickens, the arterys sclerosis, American Heart Association. Circulation, 92, 13551374.
diameter is reduced, and blood flow and oxygen delivery
are decreased. Plaques can rupture or crack open, causing
the sudden formation of a blood clot (thrombosis).
Atherosclerosis can cause angina or myocardial infarction Atherosclerotic Dementia
if it blocks the blood flow in the coronary arteries that
supply the heart muscle, stroke if it blocks the carotid Vascular Dementia
arteries that supply the brain, kidney disease if it blocks
the renal arteries or gangrene possibly leading to amputa-
tion if it blocks the peripheral arteries that supply the
limbs. Atherosclerotic Heart Disease
Atherosclerosis may be asymptomatic for many years.
Risk factors for this disease have been well studied. It is Coronary Disease
thought that atherosclerosis is caused by a response to
damage to the endothelium from high cholesterol, high
blood pressure, and cigarette smoking. A person who has
all three of these risk factors is eight times more likely to Atherothrombotic Brain
develop atherosclerosis than is a person who has none. Infarction
Physical inactivity, diabetes, and obesity are also risk
factors for atherosclerosis. Heredity, advancing age, and Ischemic Stroke
racial background are less-significant risk factors.
Treatment options include lifestyle changes, use of
lipid-lowering and other drugs, angioplasty, and various
surgical procedures, depending on the location of the
plaque. Many lifestyle changes that prevent disease Athymia
progression also prevent the onset of the disease; these
include a low-fat, low-cholesterol diet, weight loss, exer- Abulia
cise, blood pressure control, diabetes management, and
smoking cessation.
Atkins v. Virginia
Cross References
R OBERT L. H EILBRONNER
Angioplasty Chicago Neuropsychology Group
Anticoagulation Chicago, IL, USA
Antiplatelet Therapy
Atherosclerosis
Cerebrovascular Disease Synonyms
Cholesterol
Coronary Disease Mental retardation defense
Ischemic Stroke
Peripheral Vascular Disease Historical Background
Stent
Thrombolysis Daryl Atkins and William Jones abducted Eric Nesbitt
Thrombosis from a convenience store and after finding only $60 in
280 A Atomoxetine
his wallet, Atkins and Jones used Nesbitts vehicle to drive were tainted. Thus, Atkins was set to be executed on
to an ATM and forced him to withdraw $200. Thereafter, 2 December 2005. However, the decision was recently
Atkins and Jones drove Nesbitt to an isolated location reversed again by the Virginia Supreme Court, as a result
where he was shot eight times and subsequently died. of state procedural grounds.
Atkins and Jones were quickly tracked down by police
and in custody, it was determined that Jones story claim-
ing that Atkins pulled the trigger was more coherent than Current Knowledge
Atkins story implicating Jones as the shooter. Thus,
Atkins was charged and convicted of abduction, armed Forensic psychological and neuropsychological assess-
robbery, and capital murder. This took place despite the ments of mentally retarded individuals being considered
results of an IQ test completed by a clinical psychologist, for the death penalty are highly important. Specifically,
in which Atkins score of 59 placed him in the mildly the U.S. Supreme Court did not specify the degree of
mentally retarded range. Nonetheless, he was sentenced mental retardation required to circumvent the death
to death. penalty and instead left such determinations up to the
The Supreme Court of Virginia was in agreement with discretion of the states. It is important to note that
the judgment of the trial court and the appeal was taken to sub-average intelligence alone does not warrant a label
the U.S. Supreme Court. In July of 2002, the U.S. Supreme of mental retardation. Impairments in adaptive function-
Court reversed the judgment of the trial court and the ing and evidence of mental retardation prior to the age of
Supreme Court of Virginia and referred the case back to 18 years are needed for a diagnostic determination of
the sentencing court to render a sentence other than the mental retardation.
death penalty. The U.S. Supreme Court ruled that
the punishment was excessive and thus prohibited by
the eighth Amendment as cruel and unusual if it is not Cross References
graduated and proportioned to the offense. An excessive
judgment is judged by current societal standards. Thus, Intellectual Disabilities
societys standards of decency, albeit subject to change, Intelligence
must prove that they are influenced by objective factors
to the maximum possible extent. Furthermore, it was
ruled that mental retardation does not preclude a persons References and Readings
capability to discriminate right from wrong, though
mental retardation does lead to a diminished capacities Atkins v. Virginia, 153 L. Ed 2d 335 (2002).
to process and comprehend information, reduces com- Cunnningham, M. D., & Goldstein, A. M. (2003). Sentencing determina-
tions in death penalty cases. In A. Goldstein (Ed.). Forensic psychology
munication abilities, and decreases ones ability to learn
(Vol 11). Handbook of psychology. New Jersey: Wiley.
from mistakes and experiences, reason logically, inhibit Denney R. L. (2005). Criminal responsibility and other criminal forensic
impulses, and understand the emotions and behaviors of issues. In G. Larrabee (Ed.). Forensic neuropsychology: a scientific
others. The U.S. Supreme Court concluded that mentally approach. New York: Oxford University Press.
retarded individuals are not exempt from criminal Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C. (2007). Psycho-
logical evaluations for the courts: A handbook for mental health
sanctions, though a decrease in personal culpability is
professionals and lawyers (3rd ed.). New York: Guilford Press.
warranted. Thus, due to the conclusions that the purposes
of retribution and deterrence are not accomplished in the
execution of mentally retarded individuals, coupled with
the increased risk that the death penalty will be imposed Atomoxetine
erroneously; the U.S. Supreme Court ruled that the eighth
Amendment precludes execution of mentally retarded J OHN C. C OURTNEY
persons. Childrens Hospital of New Orleans
Despite the courts ruling, in July of 2005 a Virginia New Orleans, LA, USA
jury determined that Atkins was intelligent enough to be
executed due to the fact that another IQ score had been
recorded at above 70. Moreover, the prosecution claimed Generic Name
that his poor performance in school was related to use of
alcohol and drugs and that earlier assessments of his IQ Atomoxetine
Atrophy A 281
Brand Name Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.com:

A
8080/cgi bin/ddiD4?ver=4&task=getDrugList
Strattera
Class
Norepinephrine reuptake inhibitor Atrophy

Proposed Mechanism(s) of Action J OA NN T. T SCHANZ
Inhibits the presynaptic reuptake of norepinephrine and Logan, UT, USA
theoretically increases dopamine in the prefrontal cortex
via the same mechanism.
Synonyms
Indication Degenerative; Wasting
Attention Deficit Hyperactivity Disorder.

Definition
Off Label Use
Atrophy refers to loss of cells of any tissue. In the
Treatment resistant depression and anxiety. brain, atrophy refers to a loss of neurons that may be
generalized (e.g., diffuse atrophy) or focal, reflecting
Side Effects
Serious
Increased cardiac rate, potential hypertension, orthostatic

hypotension, rare liver damage, potential for induction of
mania, and suicidal ideation.
Common
Sedation in children, decreased appetite, dry mouth, con-

stipation, nausea, vomiting, dysmenorrhea, erectile dys-
function, and impaired libido.

PDR.
Atrophy. Figure 1 Display of diffuse atrophy of the cerebral
hemispheres. Note the shrunken gyri and prominent, widened
Drug Molecule Images: http://www.worldofmolecules.com/drugs/ sulci (Photo courtesy of Steven S. Chin, M.D., Ph.D., University
Free Drug Online and PDA Software: www.epocrates.com of Utah Health Sciences Center)
282 A Attendant Care
circumscribed regional cell loss. With atrophy, there adequate training of an attendant, and financial issues
is also a corresponding loss of neural connections including paying a competitive wage to personal
(synapses). Features of atrophy include sulcal widening, attendants. Funding sources of attendant care may include
shrunken gyri, and enlarged ventricles. Focal atrophy may private resources such as: Health Insurance; Auto Insur-
occur as a result of trauma or cerebrovascular lesions, for ance; and Workers Compensation; or public resources
example. Generalized atrophy may occur with neurode- such as: Medicaid; Department of Vocational Rehabili-
generative conditions such as Alzheimers disease. Atro- tation; Department of Veterans Affairs; Crime Victims
phy may be viewed on gross inspection of the brain Compensation and/or other State-funded programs.
postmortem or antemortem with structural imaging tech-
niques such as MRI or CT scan. Figure 1 displays diffuse
brain atrophy of the cerebral hemispheres viewed from Cross References
the top.
Assisted Living
Attendant Care References and Readings

A MY J. A RMSTRONG Rodriguez-Banister, K. (2006). The Personal Care Attendant Guide:
Virginia Commonwealth University The Art of Finding, Keeping, or Being One. New York: Demos Medical
Publishing.
Richmond, VA, USA
Definition
Attention
Attendant care involves the provision of services to assist
individuals with mental and/or physical disabilities in the R ONALD A. C OHEN
performance and/or conduct of activities of daily living in Brown University
order to maximize community inclusion and indepen- Providence, RI, USA
dent living. The intent of attendant care is to promote
independence, participation, and quality of life of the
individual while also preventing medical problems. Typi- Synonyms
cally, the individual receiving attendant services is unable
to perform such tasks independently, or may perform them Concentration; Focus; Vigilance
with great difficulty. Attendant services include, but are not
limited to activities such as: bathing, dressing, feeding,
toileting, transferring, mobility, cooking, cleaning, Definition
laundering, cognitive assistance and monitoring. Services
may also relate to sustaining health such as dispensing Cognitive processes that enable the selection of, focus on,
medications etc. and sustained processing of information. The object of
Attendant care may be provided by a family member attention can either be environmental stimuli actively
such as a spouse, partner, sibling or parent, or by a hired being processed by sensory systems, or associative infor-
employee. Typically, attendant care is provided by persons mation and response alternatives generated by ongoing
who have been trained to provide the service/s within the cognitive activity.
home and/or community. The independent living model
of attendant care contends that individuals with disabil-
ities should be empowered, to the highest degree possible, Historical Background
to recruit, screen and hire, train and terminate their
respective personal attendants, thereby ensuring Attention is subjectively self-evident to all people, and
self-determination and choice. Additional considerations terms that referred to attention-type experiences have
related to the provision of attendant care include where been described by philosophers through the ages. The
and how to locate and access quality service providers, concept of attention is strongly linked in the philosophy
Attention A 283
to the nature of consciousness, self-awareness, and most cognitive science. In particular, the application of infor-
A
theories of the mind. Accordingly, attention has been mation processing models and signal detection methods
the subject of psychological inquiry from the beginning of to the study of communication led to a resurgence of
this scientific discipline. The writings of William James research interest in attention. This is not surprising con-
captured this fact, as evident from this well-known ex- sidering the fact that signal detection and selection, the
cerpt from his Principles of Psychology (1898). basic elements of almost all theories of selective attention,
are also central to information and communication theo-
" Everyone knows what attention is. It is the taking posses-
ry. This approach emphasized the probabilistic nature of
sion by the mind, in clear and vivid form, of one out of what
information detection and selectivity, a conceptual depar-
seem several simultaneously possible objects or trains of
ture from earlier psychophysical methods used to study
thought. Focalization, concentration, of consciousness are
perception. The application of information processing
of its essence. It implies withdrawal from some things in
approaches to the study of attention was a logical step, as
order to deal effectively with others
one of the primary problems for any communication or
While written over 100 years ago, this description very information processing system is reducing the total
succinctly captures essential aspects of the phenomena of amount of incoming signal to manageable levels to enable
attention, and remains apropos even today. The under- subsequent processing of this information.
standing of cognitive, behavioral, and neuropsychological Broadbent (1958) proposed the first formal model of
bases, influences, and effects of attention have dramatically selective attention based on the information processing
evolved since the time of William James. Yet, the under- theory. He maintained that attention occurs because there
lying subjective and behavioral experiences characterized is an information bottleneck as the large quantity of
by James and the other psychologists of his time remain environmental information that is available during paral-
largely consistent with current phenomenology of atten- lel processing is subject to channel capacity limitations
tion. Different types of attention were described, such later in the stream of processing due to serial processing
as directed, divided, focused, sustained, selective, and constraints. Broadbent posited that the primary require-
volitional attention, many of which continue to be used ment for attention to occur was a filtering process (as
to describe the varieties of attentional experience. The shown in Fig. 1) that occurred soon after sensory registra-
primary limitation of these early efforts was the lack of tion and served to separate relevant from irrelevant signals
experimentation that would have enabled operationaliz- in order to enable meaningful information to be available
ing of these constructs and understanding of the processes for subsequent serial processing through limited capacity
underlying them. information channels. This model presumed a somewhat
Following the initial efforts of early psychologists to passive system by which this filtering occurred, with se-
study attention from perspectives of structuralism and lection driven by the salience of the stimuli themselves.
functionalism, a rather long period ensued dominated by However, the nature of this filtering process was not fully
behaviorism during which cognitive processes, like atten- operationalized in this initial model. In the years that
tion, were largely viewed as outside of the realm of empiri- followed, a number of variations on this model of atten-
cal psychological inquiry. Attention was considered to be a tion were proposed by other investigators working in the
construct that could be explained by more basic behavioral newly emerging field of cognitive psychology.
principles, such as discrimination learning, cue domi- Most notably, Treisman proposed an attenuation theo-
nance, anticipation, and expectation. Classical condition- ry of attention, which was similar to Broadbents model in
ing theory provided an essential framework for behavioral which he postulated a single process that occurred early in
analysis of attention, as the orienting response to novel the information processing stream, soon after sensory reg-
stimuli, and its subsequent habituation, provided the istration (Treisman & Gelade, 1980). According to attenua-
behavioral and neural building blocks for simple forms tion theory, selective attention requires distinguishing
of attention, in the absence of long-term memory forma- between messages on the basis of their physical character-
tion (i.e., conditioning). The concepts of motivation and istics, such as location, intensity, and pitch, as well as
drive which played a major role in neobehaviorism, also content. In this model of attention, stimuli naturally differ
helped to bridge attention theory and learning principles. in their threshold for activating awareness of a stimulus,
Information theory (Shannon & Weaver, 1949), which and the process of attention effectively decreases (i.e.,
evolved out of technological advances in radio communi- attenuates) the strength (e.g., loudness) of irrelevant sti-
cation and also radar detection during World War II, was a muli. This attenuation process was considered to occur in
major impetus for the subsequent re-emergence of conjunction with a feature integration process that enabled
284 A Attention
Sensory
Messages Filter Detector To memory
store
Attended
message
Attention. Figure 1 Model depicting filtering process as proposed by Broadbent (1958)
perceptual experience. This line of research was noteworthy linkages between arousal, activation, and effort in the
for the use of dichotic listening paradigms in which atten- control of attention (Pribram & McGuinness, 1979).
tion is divided between the two ears, and information must A large body of cognitive studies of attention followed
be selected from one of the two channels of input. this pioneering work. Several of these are particularly
The bottleneck models proposed by Broadbent and important in a historical context. Posner (1979) made
Treisman proposed that selection occurs at a very early an important distinction between overt and covert shifts
stage of processing soon after sensory registration, thereby of attention that occur in the context of visual selective
linking attention squarely with sensory selection. Essen- attention. Overt attention is characterized by the act of
tially, selective attention filters inhibits focus on informa- intentionally directing attention (i.e., looking) toward a
tion occurring in the unattended ear in dichotic listening stimulus, whereas covert attention occurs without intention
experiments before semantic analysis and other cognitive when focus is drawn to a particular stimulus or location,
processes have time to occur. Other investigators (e.g., typically as a result of cues or other types of information of
Deutch and Deutch (1963) argued that attention is strong- which the person may have little conscious awareness. Pos-
ly influenced by the response demands of a situation and ner also refined the use of chronometric methods
that it likely occurred at a later stage of processing, and that to demonstrate the costs associated with these attention
in reality both ears analyze incoming information seman- shifts. His research also made a distinction between two
tically, though response demands creates a bias toward primary processes, selection and focus, that were necessary
one ear over the other. This led to heated debates in the to account attentions intensity and spatial distribution.
1960s and 1970s over the location of the bottleneck. While Shiffrin and Schneider (1979) conducted seminal stud-
considerable experimental evidence indicated that early ies that distinguished automatic from controlled attention.
sensory selection occurs prior to a point in time when They varied the number of targets to be detected and the
semantic information has been processed, there is also consistency of target location based on either fixed or
other paradigms that demonstrate that in most situations variable memory demands. By creating greater variability
selection is greatly influenced by semantics and the rein task characteristics, subjects could not rely on memory
sponse requirements that exist. to facilitate performance, which slowed their response
Subsequent researchers took this a step further by time. Under these conditions, automaticity was no longer
demonstrating that capacity limitations constrain atten- feasible. Besides demonstrating the distinction between
tion and the intensity of attentional focus that is possible automatic and controlled attention, these findings also
at any given point in time. Kahenmans (1983) capacity illustrated the relationship between attention and memory,
theory of attention proposed that peoples capacity for and set the stage for a long line of research examining
attentional focus is not static, but instead varies as a working memory in relationship to attention.
function of factors such as the reward characteristics of
the task, arousal level, and other biological determinants.
This theory of attention was extremely important in that Neuropsychological Models and
it brought to the forefront the fact that attention should Frameworks
not be conceptualized in purely mechanical terms as was
the case in early attention models based solely on infor- Over the past 2 decades, research efforts have been direct-
mation processing theory. Rather attention needed to be ed at organizing these varieties of attention into coherent
viewed in the context of the biological factors that drive it. frameworks. Furthermore, researchers have proposed
This helped to catalyze an emphasis on the study of neuropsychological models of attention that seek to char-
focused attention, a shift that coincided with information acterize the functional neuroanatomic systems involved
coming from psychophysiological studies that showed in attention, the processes for which these systems are
Attention A 285
responsible, and also how these functional brain areas efficient use of available attention capacity and the inten-
A
interact. The models described below are not meant to sity of focus. Similarly, some tasks that are weighted more
be an exhaustive review of the literature in this regard, but demand for sensory selective attention, while others place
rather highlights some of the key elements of current greater demand on response intention and selection. In
theoretical frameworks and the extent to which there is other words, while these four components need to be
consistency across models. accounted for in explaining attention across all situations,
Alan Mirsky provided one of the first neuropsycho- particular tasks may require minimal demands for sus-
logical frameworks to account for what he described tained attention, but intense demands on capacity and
as the elements of attention. This framework pro- focus. Validation efforts directed at this framework have
posed five elements of attention: (1) selection, (2) focus, shown the principal factors to be highly reliable, internally
(3) execute, (4) switch, and (5) sustain. This theoretical consistent, and valid with respect to their weighting relative
framework was derived from factor analyses of neuropsy- to specific brain disorders and conditions. For example,
chological test results obtained from a large sample from patients with attention-deficit disorder have greatest im-
his clinical practice. pairment on tasks requiring sustained attention, whereas
Cohen (1993) proposed a similar component process patients with diminished speed of processing have greatest
framework of attention that hypothesized four primary problems on tasks requiring capacity and focus. It is note-
components of attention (Fig. 2): (1) sensory selective worthy that the analyses conducted by both Mirsky and
attention; (2) response intention, selection, and control; Cohen yielded very similar factor structures and validity
(3) capacity-focus; and (4) sustained attention. A primary data, providing strong evidence that four to five primary
goal of Cohens model was to include components reflect- components processes exist that account for most varieties
ing similar levels of analysis. The components of this frame- of attention. These attentional component processes are
work were also derived from factor analysis of clinical described in greater detail below.
neuropsychological data with efforts made to retain only
the minimum number of factors necessary to account for
maximum variance in the data, with an effort to make Selective Attention
conservative interpretation of the component processes
associated with each factor. Each component was hypothe- A fundamental aspect of all attentional processes is that it is
sized to be a function of other more basic subcomponent selective. Attention enables the selective deployment of
processes. This model posits that these four components of cognitive resources for the processing of information from
attention are not completely orthogonal or functionally either the external environment or internal cognitive pro-
independent, but instead rather share common component cesses or associative representations. Attention also requires
subprocesses, processes depending on the task at hand. a shift from less salient information. Processes that enable
A simplified version of the model is shown. or facilitate the selection of salient information for further
In everyday situations, attention depends on the inter- cognitive processing are collectively referred to as selective
action of all four of these component processes. However, attention (Treisman, 1969; Triesman & Geffen, 1967).
for some tasks, the primary demand may be for sustained Individuals are constantly flooded with an infinite num-
attention or vigilance, whereas for another task it may be ber of signals from both outside and within. By reducing
Attention. Figure 2 Simplified neuropsychological model of the components of attention

286 A Attention
the amount of information that will receive additional switching. Not only do these processes account for the
processing, attention constrains incoming information control of simple motor responses, they also provide the
to the individuals available capacity at a given point in foundation for more complex cognitive processes, such as
time, thereby keeping the level of information to be pro- planning, problem solving, and decision making, as well as
cessed at a manageable level. While selective attention is conceptual processes such as categorization, organization,
necessary and beneficial for cognitive function, there and abstraction. Executive control is strongly dependent on
are costs associated with selectively attending. By attend- the actions of prefrontal-subcortical systems. Executive
ing to a particular stimulus, the likelihood of detecting control is dependent on the ability of the system to act
other potentially relevant stimuli or choosing an alterna- with intention, to initiate responding, to inhibit responding
tive response strategy is reduced. Optimal selective atten- based on new information, and to efficiently shift from one
tion depends on the system being flexible and adaptive, response alternative to another in accordance with chang-
with the capacity to select and focus on certain stimuli, ing environmental demands.
but then to shift to other stimuli or cognitive processing
when task conditions change. Selective attention thereby
serves as a gating mechanism for the flow of information Focused Attention and Capacity Limitations
processing and the control of behavior.
Attention is also characterized by having intensity and by
the extent to which it is allocated in either a focal or
Response Selection and Control diffuse manner. The intensity of attentional focus is a
function of both situational and task demands and organ-
Attention has traditionally been viewed as a process closely ismic factors, such as motivation and drive. Focused at-
related to perceptual processing. It prepares the individual tention is constrained by capacity limitations (Kahneman,
for sensory intake, perceptual analysis, and integration with 1973) that limit the intensity of focus that is possible on a
other cognitive processes. Yet, there are many situations in moment-by-moment basis. Attentional capacity is influ-
which attention is not directed at incoming sensory infor- enced by both structural and energetic factors (Cohen,
mation, but rather selection response alternatives, and the 1993). Energetic capacity limitations tend to be state
control of responding once a selection has been made. Even dependent and reflect the changing energetic conditions
when a task primarily requires selective attention, there of the brain, including motivation, and the incentives to
are usually coexisting response demands. While sensory attend that are present in the situation. Structural factors
selection may be automatically elicited by the occurrence tend to be more stable and dependent on each persons
of salient external stimuli, more often than not the act intrinsic information processing capacity. Factors that in-
of attending is linked to a planned, goal-directed course of fluence structural capacity include the processing speed
action. In this regard, attention and responding are directed capacity that is a function of the integrity of neural trans-
to obtain information that will optimize behavior. mission, memory encoding, storage and retrieval limita-
The processes associated with response selection and tions, and temporalspatial processing dynamics that vary
control range from simple behavioral orienting, such as across people. Given these factors that limit attentional
turning ones head in response to a sound source to more capacity, focused attention varies relative to the cognitive
complex cognitive processes involving intention, planning, demands and type of information to be processed, and
and decision making. Response selection and control form situational incentive. Focused attention can occur relative
the basis for what humans typically experience as volitional to either sensory selective attention, or intention and
action. Before responding, individuals generate a large response selection, and in fact often involves the coordi-
number of response alternatives. These response alterna- nation of sensory and response selection. Such coordina-
tives are evaluated prior to making an actual motor re- tion is quite effortful (Pribram & McGuinness, 1975).
sponse, leading to response bias, that is, the probability of Arousal and activation vary as a function of the existing
selecting specific responses. demands for focused attention, with greater activation
The attentional processes involved in response selec- occurring when there is more utilization of available
tion and control are related to a broader class of cognitive capacity because of the need to focus.
processes, commonly referred to as executive functions
(Fuster, 1989; Luria, 1966). Several processes associated Automatic Versus Controlled Attention
with response generation underlie executive control: in- An important distinction exists between automatic and con-
tention, selection, initiation, inhibition, facilitation, and trolled attentional processing (Schneider & Shiffrin, 1977;
Attention A 287
Hasher & Zacks, 1979). Automaticity occurs most com- brightest students would encounter tremendous dif-
A
monly in the context of sensory selective attention, par- ficulties sustaining their focus for a lecture that lasted
ticularly for tasks requiring simple detection of a target 12 consecutive hours.
from a set of stimuli, and also on tests of attention span. Vigilance refers to sustained attention directed toward
With automaticity, there is usually relatively little demand specific targets, in which a state of readiness is required to
placed on attentional capacity, and often attention can detect and respond to stimuli occurring at variable and often
occur without much awareness or subjective effort (e.g., infrequent intervals (e.g., Colquhoun & Baddeley, 1967;
attending to other cars while driving on an empty high- Corcoran et al., 1977). Detecting rare targets with lengthy
way). Automaticity can be interfered with increase in size intervals between responses can be difficult. This type of
and complexity of the environment to be attended to. sustained attention is quite common in everyday life. For
Spatial selective attention is particularly well suited for example, a watchman may spend the entire night attend-
automatic attentional processing since visual information ing to the possibility of an intruder without this event ever
typically occurs in parallel with a vast array of information occurring. Attention to low-frequency events has different
reaching the brain almost instantaneously. Automaticity processing requirements than responding to high-
is more difficult to achieve for tasks that require sequen- frequency events and, for many people, is more difficult.
tial cognitive operations, though some degree of automa- Vigilance and sustained attention are under the influence
ticity may be attainable through practice. Controlled of sustained motivational level, boredom, and fatigue,
attention is typically required for tasks in which there which are sensitive to the dynamics of temporal tasks.
are working memory demands, or other requirement of
other cognitive processes, such as memory encoding and
retrieval, rapid processing speed, or executive control. The Current Clinical and Experimental
demand for focused intensity varies as a function of require- Evidence
ments for controlled attention that exist for a particular
task. Generally, response intention, selection, and control Neuropsychological Studies
are not very amenable to automatic attentional processing,
as behavioral responding typically requires complex motor Twenty years ago the clinical and experimental neuropsy-
sequencing with executive control demands. However, the chological literature on impairments of attention associated
fact people are able to perform certain tasks such as typing with neurological and psychiatric disorders affecting the
or playing a musical instrument with considerable automa- brain was quite limited. Much of the neuropsychological
ticity illustrates that automaticity is attainable for well- focus on attention was on the assessment of attention span
learned motor programs. in the context of psychometric analysis of performance on
tests such as digit span. This probably reflected the fact that
adequate attention was once viewed more as a necessary
Sustained Attention condition for other cognitive functions to occur optimally,
but not particularly important in its own right in consid-
Attention varies as a function of the temporal dynamics of erations of brainbehavior relationships. This attitude has
the task to be performed and the situation, and all humans changed dramatically, and attention is now widely regarded
experience some degree of performance variability, par- as a critical cognitive process that reflects not only the
ticularly when long periods of sustained performance interface between both the external environment and inter-
are required. Sustained attention refers to processes that nal cognitive functions, but also moment-by-moment in-
enable the maintenance of performance over time. Com- formation processing. A literature review conducted about
pared to other cognitive processes, such as language and 2 decades ago revealed less than 500 studies focused on the
visual perception, attention is inherently variable by ne- neuropsychology of attention. Recent literature reviews
cessity, as it must be responsive to changing stimulus suggest that this number is now over 40, 000. This increase
conditions, task demands, and motivational and energetic in interest in attention reflects the fact that: (1) attention
states. Problems with sustained attention commonly occur disturbances are one of the most common by-products
on tasks requiring attentional persistence for long dura- of brain, (2) attention is closely tied to the human experi-
tions when there are high levels of demand for effortful ences of consciousness, awareness, and cognitive control,
processing. All people have limits in their capacity for (3) major advances have occurred in the methodology for
sustained attention. Sitting in a 1-hour lecture is not a studying and assessing attention, and (4) for a number of
problem for most bright college students, but even the reasons, there has been an increased societal interest in
288 A Attention
attention disturbances, perhaps in part because of the in- Alzheimers and Neurodegenerative Dementias
tense information processing demands and pace of life that Attention disturbance is usually not described as a prima-
people now experience. ry feature of Alzheimers disease (AD) and histori-
Impairments of attention may be either specific or cally tended to be viewed as one cognitive function that
nonspecific. Specific impairments occur when only aspect was largely spared. This conclusion is misleading. While
of attention is affected. Often this occurs when impaired patients with early-stage AD typically do not show overt
attention is directly associated with a particular type of symptoms of severe inattention, they frequently have
cognitive operation, such as spatial processing. These marked difficulty with focused attention and executive
impairments are often associated with focal brain distur- control, particularly when tasks required controlled atten-
bances affecting specific cortical or subcortical systems tional processing. This reflects a distinction between per-
necessary for the cognitive operation. Nonspecific distur- formance on tests of simple and complex attention, as
bances of attention are much more common, often occur- conclusions about spared attention in AD have often been
ring due to disorders that affect arousal, motivation, or based on the observation of preserved attention span on
other factors that reduce attentional capacity, and as a tests such as digit span. Patients with early AD are often
result of more diffused nonlocalized brain disorders. Both usually alert, energetic, and able to maintain their general
types of attentional disturbance provide insights into the focus on the assessment process. Yet, most will have con-
cognitive processes of attention and the brain mechan- siderable difficulty on tasks requiring focused and divided
isms that underlie these processes. Though localized attention, suppression of interference (e.g., Stroop), in-
lesions provide the best vehicle for analysis of the role of formation processing speed and efficiency (e.g., Symbol
specific brain structures in attentional control, nonspecific Coding), and working memory. As the disease progresses,
attentional impairments illustrate the influence of meta- performance becomes impaired on most tasks requiring
bolic and neurotransmitter abnormalities on information effortful attentional processing. Pervasive disturbance
processing rate, arousal, and other energetic and structural eventually develops affecting all aspects of attention,
factors that may affect attentional capacity and focus. including self-awareness.
Attentional capacity is a direct function of level of con-
sciousness, making this an essential part of the clinical
assessment of attention. Levels of consciousness range
Multiple Sclerosis
Multiple sclerosis (MS), one of the most common neu-
from normal states of alertness and awareness to coma.
rologic in young adults, often affects learning, memory,
A brief summary of the attentional disturbances asso-
and executive control. Given the fact that the disease
ciated with several common neurological and psychiatric
affects the myelin of the white matter, deficits in these
conditions is provided below. For more detailed consider-
areas are often strongly associated with attentional
ation see Cohen (1993).
impairments and slowed inefficient information
processing. Attentional capacity is typically reduced
Stroke and Neglect Syndrome
with performance decrements usually evident under
Unilateral stroke affecting the nondominant cortex often
conditions of increased informational load. Fatigue is
causes hemi-neglect syndrome, perhaps the most well
the most common of all symptoms in MS and is asso-
known and dramatic form of attention disturbance. The
ciated not only with motor effort but also with attend-
defining feature of neglect syndrome is the failure to attend
ing to and performing cognitive tasks. Patients with MS
to, respond to, or be aware of stimuli on one side of space.
experience difficulty maintaining consistent effort on
Many variants of neglect syndrome may be observed clini-
tasks.
cally. Most patients with neglect exhibit impairments of
sensory selective attention, although some may have pri-
mary problems with hemi-spatial response selection and HIV
control. Experimental investigations have confirmed the Similar to MS, HIV-infected patients who have not
role of attention in hemi-neglect syndrome. Manipulation developed severe AIDS dementia typically show primary
of attentional parameters demonstrates that symptoms of impairments in the areas of psychomotor and informa-
hemi-neglect change as attentional demands are modified tion processing speed, focused and sustained attention,
(Kaplan et al., 1989). Regardless of which attentional pro- and executive functioning. This reflects the fact that when
cess is most affected, all patients with neglect syndrome not adequately treated, HIV tended to initially have great-
have a fundamental disorder involving the spatial distri- est effects on subcortical systems, including the basal
bution and allocation of attention. ganglia.
Attention A 289
Closed Head Injury irrelevant stimuli and thoughts has long been considered to
A
The most common effects of closed head trauma are diffuse be a major element of the disorder, which has been linked to
axonal damage due to shearing forces and frontal lobe dis- the dopamine system. Schizophrenics often encounter dif-
turbances. Consequently, attention and executive dysfunc- ficulties on tests of sensory selective attention because of
tion are among the most common associated cognitive their susceptibility to distraction. Slowed reaction time and
problems. Persistent distractibility, poor concentration, apa- processing speed also contribute to problems with atten-
thy, and fatigability are prominent sequelae. Deficits of arous- tional capacity, and both focused and sustained attention
al and poor performance on measures of selective, focused, (Nuechterlein, 1977).
divided and sustained attention, processing speed, and exec-
utive functioning tend to occur, which may contribute to Attention-Deficit Disorder (ADD)
associated learning and memory retrieval problems as well. A developmental disorder of attention, ADD is the most
widely recognized of all attention disturbance. Problems
Epilepsy with sustained attention and distractibility are key features
Transient changes in the level and quality of conscious- of the disorder, along with hyperactivity among a subset
ness, common in seizure disorder, typically cause marked of children. While there is general agreement regarding
alterations in attention around the time of the seizure. the existence of ADD, there continues to be considerable
During the time between seizures, patients with epilepsy debate about its manifestations and pathophysiology, par-
may have greater problems than healthy individuals ticularly in light of the fact that ADD tends to occur along
on tests of focused and divided attention. These deficits with other comorbid conditions.
appear to be related in part to slowed speed of processing
and its effects on attentional capacity. Pharmacological
effects associated with anticonvulsant therapy likely con- Primate Studies
tribute in part to these attentional effects.
Understanding of the neural substrates of attention was
greatly enhanced by the use of neurophysiological meth-
Metabolic Disturbances ods in primates. The value of these studies is that they
Factors that affect the metabolic function often cause provided directed recording of electrical activity from
delirium, or more subtle alterations in attention and brain areas implicated in attention both by past clinical
arousal. Accordingly, metabolic disturbance is one of the studies of patients with neurological disorders and also
most common reasons for transient alterations in atten- ablation studies involving laboratory animals. In the
tion among people without other neurological or psychi- 1970s, Robert Wurtz, Michael Goldberg and their collea-
atric illness. Metabolic disturbances that affect the brain gues (1982) began electrophysiological studies from the
can be the result of a wide variety of factors, including brain of monkeys trained on specific attention para-
drug effects and systemic illnesses, such as liver and kid- digms. The earliest of these studies showed that the
ney disease, and diabetes. superior colliculus exhibits increased firing rates during
visual attention, providing the first direct evidence of the
Psychiatric Disorders involvement of a neural area in this process. Subsequent-
Difficulties with focused and sustained attention are ex- ly, a large number of studies were conducted that showed
tremely common among patients with psychiatric disor- the contribution of other brain regions, particularly in
ders, including affective disorders (major depression and posterior visual areas to specific aspects of visual selec-
bipolar disturbance) and schizophrenia. Severe anxiety tive attention. This work both confirmed the role of areas
states can also interfere with attention. A strong relationship like the inferior parietal cortex that had been suspected
exists between expenditure of effort and performance on of being involved in visual selective attention based on
tests of attention and other demanding cognitive functions studies of hemi-neglect syndrome. Over time, there has
for patients with major affective disorders. Impairments been increasing emphasis on the role of frontal brain
tend to be somewhat proportional to severity of depression, systems in relationship to these posterior brain areas.
with performance improving when the depression resolves. There is now a large body of research on this topic,
Diminished attentional capacity is particularly evident on supporting to general conclusions about selective atten-
tasks that require psychomotor speed, attentional focus, tion: (1) Visual selective attention is controlled by mul-
and effortful demands for mental control. Abnormal atten- tiple interacting brain areas that comprise a functional
tion is also a central feature of schizophrenia, as filtering of system. (2) Selective attention involves not only
290 A Attention
posterior visual brain areas, but also frontalstriatal sys- and attention usually must be assessed within the context
tems that provide executive response control. Active of performance on tasks that load on one or more these
investigation continues using primate models with par- other domains. Attentional performance is often assessed
ticular emphasis on source analysis of how particular as derived measure obtained by comparing performance
types of neurons are tuned to optimize attention to across tasks that control for key attentional parameters
particular types of signals. This research has been instru- (e.g., targetdistractor ratio). Absolute performance often
mental in characterizing the functional brain systems provides less informative measures of performance incon-
governing attention in humans. sistencies in the assessment of attention. For example,
how performance varies as a function of time, spatial
characteristics, or memory load provides more informa-
Functional Neuroimaging tion about attentional dynamics than simply considering
total errors on a visual detection task. Since attention
Attention was one of the first cognitive functions to be is not the by-product of a unitary process, or a single
demonstrated through the use of functional imaging meth- sensory modality, it cannot be adequately assessed on the
ods, such as functional MRI and PET. The fact that atten- basis of findings from one specific test. For example,
tional parameters can be easily manipulated in the context conclusions based on digit span performance are mis-
of the scanner and that attention reflects the moment-by- guided. Attentional assessment requires a multifactorial
moment information processing of the brain makes it very approach. The specific attention measures used in an
conducive to study through functional brain imaging. evaluation depends on the overall level of functioning of
These efforts have largely confirmed the involvement of the particular patient. For patients with global cognitive
inferior parietal and frontal brain systems in attention, dysfunction, it may be difficult to use certain tasks that
with studies showing the relative contribution of specific require overly complex responses. For patients with rela-
areas in selective, focused, and sustained attention. This is tively high overall cognitive abilities, tasks should be cho-
a rapidly growing area of neuropsychological inquiry. To sen that require multiple component processes. If the
date, results of functional neuroimaging experiments have patient is able to perform well on these tasks, then severe
largely supported evidence from earlier cognitive, neuro- attention disturbance involving specific attentional com-
psychological, psychophysiological, and primate studies ponent processes can be ruled out. The Stroop and Trail-
with respect to the neural substrates of attention. Making tests are examples of tasks that require multiple
attentional processes. If impairments are found on such
tasks, then more extensive testing of specific component
Clinical Assessment Considerations processes can be conducted. When possible, efforts should
be made to use tasks that incorporate signal detection
Although an essential cognitive process, attention is more methods, even when not evaluating sensory selective
difficult to directly observe or measure than other cogni- attention per se. This methodology provides the best
tive functions like language, visual perception, or memory. means of accurately summarizing performance relative
Attention fluctuates in accordance with changes in task to all types of possible errors, and easily integrates with
demands and the processing capacity of the patient over response time measures.
time. Unlike other cognitive functions, performance may Attentional parameters that should be considered.
be quite different across different points in time, and it is A thorough assessment of attention should be based on
this variability that in fact defines attention. Attention is analysis of data from a comprehensive battery of atten-
often situation specific. This accounts for why some chil- tional tests that sample underlying component processes
dren with ADD perform well in a controlled laboratory (Cohen, 1993). Accordingly, tasks should be used that are
setting, despite reports of gross problems with inattention differentially sensitive to the following attentional para-
in school or the home. meters: (1) spatial characteristics, (2) temporal dynamics,
Unlike most other cognitive processes, attention pri- (3) memory demands, (4) processing speed requirements,
marily serves a facilitative function. Attention enhances (5) perceptual complexity, (6) demands for response
or inhibits perception, memory, motor output, and exec- sequencing and control, (7) cognitive complexity of the
utive functions, including problem solving. Yet, attention task, (8) effort required to complete task, and (9) task
is always measured as a function of performance on tasks salience, relevance, and reward value.
that also loads on one or more of these other cognitive While multifactor neuropsychological assessment
domains. Therefore, pure tests of attention do not exist, provides the best means of evaluating attentional
Attention A 291
impairments, a comprehensive attentional evaluation Colquhoun, W. P., & Baddeley, A. D. (1967). Influence of signal proba-
bility during pretraining on vigilance decrement. Journal of Experi- A
may not be feasible in everyday clinical practice, because
mental Psychology, 73, 153155.
of time constraints, the patients overall severity of cogni- Desimone, R., & Gross, C. G. (1979). Visual areas in the temporal cortex
tive impairment, or the fact that other cognitive functions of the macaque. Brain Research, 178, 363380.
must be assessed in greater detail because of the referral Deutsch, J. A., & Deutsch, D. (1963) Attention: Some theoretical con-
questions. Consequently, clinicians should be aware of the siderations. Psychological Review, 70, 8090.
Fuster, J. M. (l989). The prefrontal cortex: Anatomy, physiology, and neu-
information that can be obtained from different levels of
ropsychology of the frontal lobe. New York: Raven.
attentional assessment. A few primary tests of attention Goldberg, M. E., & Bushnell, M. D. (l981). Behavioral enhancement of
should be included in all neuropsychological evaluations. visual response in monkey cerebral cortex. II. Modulation in frontal
The continuous performance test (CPT) paradigm pro- eye fields specifically related to saccades. Journal of Neurophysiology,
vides an excellent measure for assessing sustained atten- 46, 783787.
Hasher, L., & Zacks, R. T. (1979). Automatic and effortful processes in
tion and other related indices. Tests of focused and
memory. Journal of Experimental Psychology: General, 108, 356388.
selective attention are also now widely available. Several Heilman, K. M., Watson, R. T., & Valenstein, E. (l993). Neglect and
attention batteries have also been developed that may related disorders. In K. M. Heilman & E. Valenstein (Eds.), Clinical
facilitate the comprehensive assessment of the elements neuropsychology (3rd ed., pp. 279336). New York: Oxford Universi-
of attention. ty Press.
Heilman, K. M., Bowers, D., Coslett, H. B., & Watson, R. T. (l983).
Directional hypokinesia in neglect. Neurology, 2(33), 104.
Heilman, K. M., Watson, R. T., Valenstein, E., & Goldberg, M. E. (1988).
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Kahneman, D. (1973). Attention and effort. Englewood Cliffs, NJ:
the ability of neuropsychologists in the future to assess
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moment-by-moment variations in attention associated Kahneman, D., & Treisman, A. (1984). Changing views of attention and
with task performance. There continues to be the need automaticity. In R. Parasuraman & D. R. Davies (Eds.), Varieties of
to attentional batteries that are theoretically coherent and attention. New York: Academic.
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Psychological Review, 84, 166.
Cohen, R. A. (1993) Neuropsychology of Attention. New York: Plenum. Shannon, C. E., & Weaver, W. (1949). The mathematical theory of com-
Cohen, R. A., Meadows, M. E., Kaplan, R. F., & Wilkinson, H. (1994) munication. Urbana, Illinois: The University of Illinois Press.
Habituation and sensitization of the OR following bilateral cingulate Treisman, A., & Gelade, G. (1980). A feature-integration theory of atten-
damage. Neuropsychologia, 32(5), 609617. tion. Cognitive Psychology, 12, 97136.
292 A Attention Deficit Disorder
Verfaellie, M., Bowers, D., & Heilman, K. M. (1988). Attentional factors accounting for roughly half of the ADHD cases. ADHD-
in the occurrence of stimulus-response compatibility effects.
H/I is far less common, is most often observed in pre-
Neuropsychologia, 26, 435444.
Watson, R. T., Heilman, K. M., Cauthen, J. C., & King, F. A. (1973).
school and early elementary school aged children, and is
Neglect after cingulotomy. Neurology, 23, 10031007. probably just the earlier developmental stage to the C-
Wurtz, R. H., Goldberg, M. E., Robinson, D. L. (1982). Brain mechanisms type in many instances. In general, hyperactive-impulsive
of visual attention. Scientific American, 246(6), 124135. symptoms decline more steeply as children age (although
feelings of restlessness may persist), but inattentive symp-
toms remain relatively constant.
Children with ADHD-H/I and ADHD-C are at higher
Attention Deficit Disorder risk for conduct problems. Youth with ADHD-I are at
higher risk for learning disorders, anxiety and possibly
Attention Deficit, Hyperactivity Disorder depression. While some argue that ADHD-I is a distinct
disorder from ADHD-C and ADHD-HI, others have not
found consistent differences between the subtypes on
neuropsychological or laboratory measures. Though diag-
nosed as a categorical disorder, ADHD may actually rep-
Attention Deficit, Hyperactivity resent an extreme end along a normal continuum for
Disorder the traits of attention, inhibition and the regulation of
motor activity.
K EVIN M. A NTSHEL , R USSELL B ARKLEY
State University of New York - Upstate Medical University
NY, Mount Pleasant, SC, USA Epidemiology
The population prevalence of ADHD is estimated to be

Synonyms 39% of school-age children and 45% of adults. ADHD
is more prevalent in males and those with chronic health
ADD; ADHD; ADHD, combined; ADHD, predominantly problems, family dysfunction, low socioeconomic status,
hyperactive-impulsive type; ADHD, predominantly presence of a developmental impairment, or urban living.
inattentive type; Attention deficit disorder; Hyperkinetic ADHD is a worldwide disorder found in most countries
disorder with rates similar to if not higher than those found in
North America. Differences across ethnic groups within
the North America are sometimes found but seem to be
Short Description or Definition more a function of social class than ethnicity.
Attention deficit/hyperactivity disorder (ADHD) is char-

acterized by developmentally inappropriate degrees of
Outcomes
inattention, impulsiveness, and/or hyperactivity that
most often arise in early to middle childhood, result in
The syndrome of attention difficulties, impulsive behav-
functional impairment across multiple domains of daily
ior and overactivity has been known since the late 1700s
life activities, and remain relatively persistent over time.
and certainly since the early 1900s. Numerous attempts
have been made at definition and nomenclature, including
Strauss syndrome, minimal brain dysfunction or damage,
Categorization hyperkinetic child syndrome (or hyperkinesis), and atten-
tion deficit disorder with and without hyperactivity.
DSM-IV-TR defines three ADHD subtypes: Predomi- ADHD can exist without other psychiatric disorders
nantly Inattentive type (ADHD-I), Predominantly Hyper- in 2530% of ADHD cases (MTA Collaborative Group,
active/Impulsive type (ADHD-H/I) and Combined type 1999) but is more often associated with co-morbidity.
(ADHD-C). ADHD-C is the most prevalent subtype in Oppositional defiant disorder (4565%) is the most com-
clinically-referred samples yet the true population preva- mon psychiatric co-morbidity in ADHD. As many as half
lence of ADHD-C and ADHD-I is likely comparable, each of these oppositional children will progress to early onset
Attention Deficit, Hyperactivity Disorder A 293
conduct disorder such as lying, stealing, fighting and household and maintaining health are also consistently
A
otherwise violating the rights of others. Major depressive reported in adults with ADHD. For example, employer
disorder (2030%) and anxiety disorders (1030%) are ratings are lower for adults with ADHD and adults with
also relatively common co-morbid conditions in pediatric ADHD have more part-time employment and change
ADHD. jobs more often.
Longitudinal research following children with ADHD There are some data to suggest that ADHD is more
into adulthood suggests that 5086% of children with functionally impairing than most other outpatient psychi-
ADHD continue to show impairing symptoms as they atric disorders in these domains. While the relationship
age. The fact that some children do not continue to have between ADHD symptoms and impairment in children
an ADHD diagnosis may be due in part to the finding that with ADHD is modest (r = 0.3), these relationships may
ADHD symptoms decline as a function of age in typically be more robust in adults (r = 0.7).
developing populations. However, it may also simply reflect
that DSM symptoms and symptom thresholds may be
developmentally inappropriate and too restrictive, respec- Neuropsychology and Psychology of
tively, to be applied to outside of childhood. For example, ADHD
DSM-IV inattentive symptoms are more common in ado-
lescents than DSM-IV hyperactive/impulsive symptoms. A meta-analysis suggested that children with ADHD have
While this may infer that inattention persists at higher levels an IQ about nine points lower than typically developing
than hyperactivity/impulsivity, it may also simply reflect peers. Similar data have been reported in adults with
the developmental insensitivity of the DSM-IV symptoms. ADHD. Lower performance on the WAIS-III Arithmetic
Genetics also appear to be a large factor in those who and Digit Symbol may account for a substantial portion of
continue to demonstrate clinically significant ADHD the IQ differences noted between adults with ADHD and
post-childhood versus those whose symptoms are in re- community controls.
mission. For example, prevalence rates of ADHD among Controlled processing deficits are commonly observed
the relatives of children with persistent ADHD are signifi- in pediatric ADHD. Children with ADHD perform less well
cantly higher than rates in relatives of children with re- on laboratory tasks that assess vigilance, motoric inhibition,
mitted ADHD. In addition, a history of major depressive organization, planning, complex problem solving, and ver-
disorder before age 13 is a predictor of the syndromic bal learning and memory. Adults with ADHD are impaired
persistence of ADHD into adolescence as is having a on these same cognitive domains.
below average IQ. Both children and adults with ADHD perform less well
By definition, individuals with ADHD need to be on tasks that require vigilance, or the ability to sustain
functionally impaired in two or more domains of major attention. There is also some evidence that rare target
life activities. In children, academic, social and family paradigms (few targets, many non-targets) such as the
functioning domains are the most frequently impaired Gordon Diagnostic System appear to be more difficult
(MTA Collaborative Group, 1999). Educational impair- for adults with ADHD than those paradigms with higher
ments including academic underachievement and learning signal probabilities.
disabilities are well documented in the pediatric ADHD Response inhibition has been hypothesized to play a
literature. central role in pediatric ADHD. Continuous performance
In adolescents and young adults, academic impair- test (CPT) commission errors are a common laboratory
ments continue to persist; young adults with ADHD com- measure of this construct. Unlike attention deficits (which
pleted fewer years of education, with nearly 1/4 failing to seem to emerge more reliably in rare target CPTs), re-
complete high school. Others have similarly reported that sponse inhibition deficits emerge more reliably in higher
relatively few young adults with ADHD attempt college signal probabilities such as the Conners CPT. Several
(20%) and even fewer graduate (5%) from college. Com- studies have reported that adults with ADHD make
pared to children with ADHD who are followed into more errors of commission on high signal CPTs relative
adulthood, clinically diagnosed adults with ADHD appear to both clinical and community control participants.
to have higher intellectual levels, have graduated from high Executive functioning deficits are present in both pediat-
school and have at least attempted college. ric and adult ADHD. Thus, it is surprising that performance
In addition to educational impairments, impairments on one of the most well established tests of executive func-
in domains such as occupational, dating/marital relations, tioning, the Wisconsin Card Sorting Test is not impaired in
financial management, driving, child-rearing, managing a adults with ADHD. Multiple studies have failed to report a
294 A Attention Deficit, Hyperactivity Disorder
significant difference between adults with ADHD and com- which normative data are available. These include broad
munity controls on WCST categories completed and num- band questionnaires, such as the Behavioral Assessment
ber of errors, both perseverative and non-perseverative. System for Children 2nd edition or Child Behavior Che-
Verbal fluency is impaired in adult ADHD. The most cklist for screening the major dimensions of childhood
widely used verbal fluency task in adult ADHD popula- psychopathology (e.g. anxiety, depression, attention,
tions has been the Controlled Oral Word Association Test. hyperactivity, aggression, etc.). Narrow band question-
Multiple studies have reported significant differences be- naires specifically evaluate the symptoms of ADHD as set
tween community controls and adults with ADHD. forth in DSM-IV. Rating scales can reliably, validly and
Given the importance of attention and working mem- efficiently measure DSM-IV-based ADHD symptoms.
ory to memory encoding and storage, it is not surprising Some examples of instruments demonstrating appropriate
that adults with ADHD have been demonstrated to have psychometric properties with a strong normative base
memory deficits. They also appear to have more difficulty include the ADHD Rating Scale IVand the Conners Rating
managing auditory/verbal information relative to visual Scales 3rd edition.
information. Although differences emerge between adults A number of specific tests have been devised to provide
with ADHD and community controls on the WAIS-III objective measures of a subjects vigilance and impulse
Digit Span, the effect size of the differences are much control, such as the Gordon Diagnostic System, Conners
larger on the California Verbal Learning Test. For exam- Continuous Performance Test or the Test of Variables of
ple, adults with ADHD perform less well on overall rates Attention, among others. Research suggests, that these tests
of learning, recall, recognition and semantic clustering. are not especially accurate at classifying children as ADHD;
The weaker performance on the semantic clustering index while the presence of abnormal scores on such tests indi-
may indicate failure to adopt a strategy. cates the presence of a disorder in as many as 90% of
children who perform poorly, such scores cannot indicate
the specific disorder present. Moreover, the ecological va-
Evaluation lidity of these tests is low thus precluding the ability to
predict from the test scores how the child will function in
The American Academy of Child and Adolescent Psychia- more natural settings, such as home and school. These tests
try (Pliszka, 2007) has established guidelines for the are therefore not recommended for routine diagnostic eva-
assessment and treatment of ADHD. No neurological, luations of children with ADHD, although they may be
genetic, neuropsychological or behavioral tests have used in clinics specializing in ADHD as part of research or
sufficient positive and negative predictive power to accu- drug trials. More useful information is likely to be obtained
rately classify ADHD cases with sufficient success to recom- from the parent and teacher rating scales discussed above.
mend them for clinical diagnosis. Clinical diagnosis is based
largely on careful history taking, use of structured interviews
containing DSM-IV criteria for ADHD and related disor- Treatment
ders, and the expert knowledge of the clinician in the differ-
ential diagnosis among childhood mental disorders. Treatment for ADHD in children typically involves three
Paramount in the evaluative process is the time to listen to components: parent and child education and support,
parental concerns, probe for details concerning nature, classroom accommodations, and medication. Substantial
onset, and course, elaborate the specific impairments result- evidence exists to show that training parents in child
ing from these concerns, and place them in the larger behavior management skills can be of significant benefit
framework of the clinical taxonomy of mental disorders. in the reduction of parentchild conflict and improvement
The clinical interview is then supplemented with the use of in child success within the home (MTA Collaborative
parent and teacher behavior rating scales to assess develop- Group, 1999). The school setting frequently requires ad-
mental deviance of symptoms, screening of intelligence and justment to meet the special needs of the child with
academic achievement skills by standardized testing, brief ADHD. School interventions often include alterations to
observation of the child during unstructured and structured the curriculum and work load to better mesh with the
activities, contact with school personnel concerning class- limited attention, persistence, and disorganization of the
room functioning and compilation of prior school and child with ADHD; increases in sources of positive rein-
mental health records available on the child. forcement for work productivity; occasional use of imme-
Other sources of information essential for the diagnos- diate and systematic negative consequences for disruptive
tic process are behavioral rating scales or checklists on or inappropriate behavior; implementation of a daily
Attention Deficit, Hyperactivity Disorder A 295
school behavior report card (the ratings on which are What constitutes the psychosocial component, however,
A
linked to a home token economy). appears to be somewhat different in adult ADHD relative
The mainstay of treatment for many children with to pediatric ADHD. For example, neither cognitive behav-
ADHD is medication, frequently psychostimulants. Three ioral therapy (CBT) nor cognitive therapy has much re-
classes of medication appear to be useful for management of search support in pediatric ADHD. Nonetheless, there are
ADHD, these being: psychostimulants (methylphenidate, some data to suggest that CBT may be more efficacious in
amphetamines), noradrenergic reuptake inhibitors (ato- adults with ADHD. For example, in the adult ADHD
moxetine), and antihypertensive medications (clonidine, literature, there is some evidence that CBT is efficacious
guanfacine). for reducing functional impairments in adults concur-
Stimulant medications, especially extended release rently treated with stimulants.
formulations, are a front-line management strategy in
pediatric ADHD; approximately 70% of children with
ADHD will show an efficacious response to stimulant
Cross References
medications such as Methylphenidate or mixed-salt amphe-
tamines. The side effects of stimulants are fairly benign,
Americans with Disabilities Act
short-lived, dose related, and often managed through dose
Attention; Attention/Executive Functions
or timing adjustments, or by switching to a different deliv-
Atomoxetine; Behavior Assessment System for
ery system or stimulant.
Children (BASC)
Atomoxetine is a nonstimulant approved for man-
Cognitive Behavioral Therapy
agement of ADHD. Atomoxetine is an exclusive norad-
Conners 3rd edition
renergic reuptake inhibitor and is the first drug indicated
Continuous Performance tests
for ADHD that is not a Schedule II controlled substance
D-amphetamine
with low potential for abuse, making it more convenient
Executive Functioning
than the stimulants for sampling, prescribing, and titrat-
Individuals with Disabilities Education Act
ing. Clonidine and guanfacine are alpha2-noradrenergic
Learning Disability
agonists that have some effectiveness for the manage-
Metacognition
ment of hyperactive-impulsive ADHD symptomatology.
Methylphenidate
They are also considered off-label for treatment of
Section 504 of the Rehabilitation Act of 1973
ADHD as they have not as yet been specifically
Stimulants
approved by the FDA for treatment of ADHD. An extend-
Working Memory
ed release form of guanfacine received FDA approval
in 2009.
In adults, stimulant medications are effective in ap-
proximately 70% of individuals with ADHD. Atomoxe- References and Readings
tine may be particularly effective for adults with ADHD
and co-morbid depression or for those with a co-morbid Barkley, R. A. (2006). Attention deficit hyperactivity disorder:
substance use disorder. A handbook for diagnosis and treatment (3rd ed.). New York:
Guilford Press.
Managing psychiatric co-morbidity is a significant
Barkley, R. A., & Murphy, K. R. (2006). Attention deficit hyperactivity
component of pediatric ADHD. The same dictum appears disorder: A clinical workbook (3rd ed.). New York: Guilford.
central to managing ADHD in adults. While uncompli- MTA Collaborative Group. (1999). A 14-month randomized clinical
cated ADHD exists in about 25% of the adults with trial of treatment strategies for attention-deficit/hyperactivity
ADHD, most adults with ADHD have significant psychi- disorder. The MTA Cooperative Group. Multimodal treatment
study of children with ADHD. Archives of General Psychiatry, 56
atric co-morbidity that requires clinical attention and
(12), 10731086.
management. One aspect in which the psychiatric co- Nigg, J. (2006). What causes ADHD: Understanding what goes wrong and
morbidity is evident in treatment strategies is phar- why. New York: Guilford.
macotherapy. Although the evidence for the efficacy of The ADHD Report, a bimonthly newsletter for clinicians edited by
polypharmacy is limited at this time, multiple researchers Dr Barkley with contributions from leading clinicians and research-
ers. Guilford Publications, New York.
have asserted that polypharmacy may be more likely in
Pliszka, S. (2007). Practice parameter for the assessment and treatment of
adult ADHD than pediatric ADHD. children and adolescents with attention-deficit/hyperactivity disor-
Similar to pediatric ADHD, a psychosocial treatment der. Journal of the American Academy of Child and Adolescent Psychi-
component is typically recommended in adult ADHD. atry, 46(7), 894921.
296 A Attention Network Test (ANT)
is printed (e.g., red ink) when the word itself spells out a
Attention Network Test (ANT) different color (e.g., BLUE). Brain areas implicated in the
executive attention system include frontal midline regions
M ICHAEL S. WORDEN such as the anterior cingulate cortex and the lateral
Brown University prefrontal cortex. The neurotransmitter dopamine is
Providence, RI, USA important in the functioning of this network.
The Attention Network Task (ANT) was developed by
Jin Fan, Michael Posner, and colleagues at the Sackler
Attention is often subdivided by researchers into a Institute for Developmental Psychobiology. Using subtrac-
number of separate systems. Although there is certainly tive methodology, the ANT is designed to assess each of
some interaction between them, these systems play differ- these three attentional networks using a single reaction-
ent roles in terms of their effect on information processing time paradigm. The fundamental task of the participant is
and the control of behavior. Further, there is evidence that simple. On each trial, the participant looks at a small
different attentional systems are associated with different, fixation cross in the center of a computer screen and a
largely nonoverlapping brain regions and rely to a large small arrow, called the target, is briefly displayed either
extent on different neurotransmitter systems. One such above or below the fixation. The participant is required to
framework advanced by Michael Posner and colleagues respond by pressing one of two buttons as quickly and
defines three separate attention systems or networks: accurately as possible indicating whether the arrow is
alerting, orienting, and executive control. pointing to the left or right. On some presentations, the
The alerting system is responsible for helping the target is preceded by a briefly presented cue stimulus while
organism reach and maintain an alert state. This state, on other trials it is presented with no advanced warning.
which is separate from arousal, is characterized by a These cues are either predictive or non-predictive. Orient-
readiness to perceive and process incoming stimuli. The ing cues are presented either above or below the central
alerting system has been associated with superior fixation and indicate the location at which the upcoming
parietal, right frontal, and thalamic brain regions and arrow will be shown. Non-orienting cues are presented
the norepinephrine neurotransmitter system. either at the center of the screen or else both above and
The orienting system is responsible for selecting and below fixation simultaneously. Both types of cues indicate
giving preference to specific sensory information, often in that the target is about to appear but only orienting cues
terms of spatial location. Attentional orienting in space provide information regarding the location of the
may be done overtly by, for example, moving the head or impending target. Finally, in some cases, the target
covertly, that is, without moving the eyes or head. For arrow is flanked on either side by other stimuli. These
example, a football player might look down the field with flanking stimuli may be arrows pointing in the same
his eyes while attending covertly to the location and move- direction as the target (called congruent trials) or they
ments of other players in his peripheral vision. Attended may be arrows pointing in the opposite direction as the
items are generally processed faster and more accurately target (called incongruent trials).
than nonattended items. Brain areas that have been linked The efficiency of the three attention networks may be
to the orienting system include areas of the parietal cortex assessed independently for each participant by use of the
and the frontal eye fields, and the cholinergic neurotrans- subtractive method. Both reaction time and accuracy may
mitter system appears to play an important role. be examined. To assess the alerting network, scores from
The executive attention system is involved in monitor- trials in which no cue was presented are compared to
ing ones performance in the context of current task scores from trials in which there was a cue presented.
demands and providing control signals that help other The difference in mean reaction times between these two
systems adapt to changing contexts and conflicting trial types constitutes an efficiency score for the alerting
information. Executive attention is especially important network and is indicative of the extent to which the
for detecting and responding to situations in which there alerting network was able to use the information provided
is stimulusresponse conflict. Such conflict arises when by the cue to improve behavioral performance. In a
two or more stimuli or two or more aspects of the same similar manner, an efficiency score for the orienting
stimulus are associated with different behavioral network may be derived by subtracting mean scores
responses. A common example is the Stroop task in from trials with orienting cues from the scores for trials
which subjects are presented with printed words and with non-orienting cues. Both of these trial types include
they must name the color of the ink in which the word a cue so there should be no difference in terms of a
Attention Training A 297
contribution from the alerting network. The difference in Fan, J., McCandliss, B. D., Fossella, J., Flombaum, J. I., & Posner, M. I.
(2005). The activation of attentional networks. Neuroimage, 26(2), A
scores measures the degree to which the orienting system
471479.
could take advantage of the predictive cues to orient to a http://www.sacklerinstitute.org/users/jin.fan/
specific spatial location. In the case of the non-orienting Posner, M. I., & Rothbart, M. K. (2007). Research on attention networks
cues, the participant could not predict whether the target as a model for the integration of psychological science. Annual
would appear above or below the fixation point and Review of Psychology, 58, 123.
therefore could not improve performance by orienting
to one or the other spatial location. An efficiency score
is derived for the executive attention system by comparing
scores on trials with congruent flankers to trials with Attention Process Training
incongruent flankers. Subjects will tend to be slower and
less accurate for incongruent trials than for congruent Attention Training
trials, and the size of these differences indicates the extent
to which the individual is able to suppress conflicting
response tendencies.
A number of intriguing findings have come from Attention Span
studies that have utilized the ANT. Supporting the notion
that the three attention networks assessed by the ANT Span of Apprehension
constitute independent systems, a large-scale study of
over 200 individuals found that there was very little cor-
relation in efficiency scores among the three networks. In
other words, the particular score of an individual on any
Attention Training
one of the three attention networks does not tend to
predict that individuals scores on the other two networks.
M C K AY M OORE S OHLBERG
A high efficiency score for the alerting network, for exam-
University of Oregon
ple, does not suggest what ones scores are likely to be for
Eugene, OR, USA
either the orienting or executive attention networks.
Using electroencephalographic (EEG) recordings from
the surface of the scalp, it was found that each of these
Synonyms
three attention systems is associated with distinct patterns
of neural oscillations. A number of variations on the
Attention process training, direct attention training,
original ANT have been developed to address specific
process training
questions and for the study of special populations. For
example, child-friendly versions of the ANT that use
cartoon pictures of fish instead of arrows have been used
Definition
to study the development of attention systems.
Attentional deficits are a hallmark of many psychiatric
Attention training is based on the premise that attentional
and neurological disorders. The ANT has been used to
abilities can be improved by activating particular aspects
assess the relative impact of many disorders on the differ-
of attention through a stimulus drill approach. The
ent attention systems and to help distinguish between or
repeated stimulation of attentional systems via graded
establish subtypes of particular disorders. Among others,
attention exercises is hypothesized to facilitate changes
variations on the ANT have proven useful in the study
in attentional functioning. Most attention training
of attention deficit hyperactivity disorder, Alzheimers
programs assume that aspects of cognition can be isolated
disease, autism, borderline personality disorder, traumatic
and discretely targeted with training exercises.
brain injury, substance abuse, and schizophrenia.
Fan, J., McCandliss, B. D., Sommer, T., Raz, A., & Posner, M. I. (2002).
The aspects of attention that are trained vary widely
Testing the efficiency and independence of attentional networks. among interventions and frequently depend upon a
Journal of Cognitive Neuroscience, 14(3), 340347. theoretical model of attention. Attention models,
298 A Attentional Response Bias
regardless of their operational framework, appear to in- Cicerone, K. D., Dahlberg, C., Kamar, K., Langenbahn, D. M., Malec, J. F.,
Bergquist, T. F. et al. (2000). Evidence-based cognitive rehabilitation:
clude functions related to sustaining attention over time
Recommendations for clinical practice. Archives of Physical Medicine
(vigilance), capacity for information, shifting attention, & Rehabilitation, 81, 316321.
speed of processing, and screening out distractions. Some Galbiati, S., Recla, M., & Pastore, V. (2009). Attention remediation
attention efficacy studies evaluate attention interventions following traumatic brain injury in childhood and adolescence.
that focus on particular attention components such as Neuropsychology, 23(1), 4049.
Park, N. W., & Ingles, J. L. (2001). Effectiveness of attention rehabilitation
reaction time and sustained attention for visual informa-
after acquired brain injury: A meta-analysis. Neuropsychology, 15,
tion (e.g., Ponsford and Kinsella, 1988). Other efficacy 199210.
studies use attention training programs that include Park, N. W., Proulx, G., & Towers, W. M. (1999). Evaluation of the
hierarchical tasks to address a continuum of attention attention process training programme. Neuropsychological Rehabili-
components from basic sustained attention to more com- tation, 9, 135154.
Sohlberg, M. M., Avery, J., Kennedy, M., Ylvisaker, M., Coelho, C.,
plex mental control (e.g., Park, Proulx, & Towers, 1999;
Turkstra, L., & Yorkston, K. (2003). Practice guidelines for direct
Sohlberg, McLaughlin, Pavese, & Heidrich, 2001). attention training. Journal of Medical Speech Language Pathology,
Evidence supports the effectiveness of attention train- 11(3), xixxxxix.
ing beyond the effects of nonspecific cognitive stimulation Sohlberg, M. M., McLaughlin, K. A., Pavese, A., Heidrich, A., &
for patients with traumatic brain injury or stroke during Posner, M. (2001). Evaluation of attention process training and
brain injury education in persons with acquired brain injury. Journal
the postacute phase of recovery and rehabilitation (Butler,
of Clinical and Experimental Neuropsychology, 22, 656676.
2008; Cicerone et al., 2000). Evidence-based practice
guidelines for attention training were generated from
examination of the intervention research literature
(Sohlberg et al., 2003). Analysis of nine Class I and Class
II studies suggested that certain aspects of attention train- Attentional Response Bias
ing are helpful in improving attention performance in
some adults with traumatic brain injury. Treatment R ONALD A. C OHEN
parameters found to influence positive outcomes includ- Brown University
ed high frequency of attention training, combining Providence, RI, USA
attention training with metacognitive training (e.g, self
monitoring and strategy training), and individualizing
training to match the clients attention profile. The effects Definition
of attention training may be relatively small or task-
specific, and the research encourages clinicians to actively Attentional response bias refers to the tendency to re-
facilitate and monitor the impact of attention training on spond to the targets of attention on a particular task or
functional, everyday activities. in a given context. This tendency is often operationalized
using signal detection theory based on possible error types
that can occur; that is, either misses (errors of omission)
Cross References or false positive (errors of commission). The proportion
of these types of errors can be expressed as an index
Attention corrected relative to the total number of errors of all
Attention/Executive Functions types made (b: beta). A person who makes a much larger
Neuropsychological Rehabilitation number of errors of commission than errors of omission
Plasticity (misses) is exhibiting a response bias toward responding
Process Training by indicating they detected the target even when it was not
presented, which in many cases reflects excessive impul-
sivity or inhibitory control problems. Conversely, a ten-
dency to miss targets, but to rarely make false positive
References and Readings efforts, suggests that the patient may be trying hard to
never make an error, which in turn results in not respond-
Butler, R. W., Copeland, D. R., Fairclough, D. L., Mulhern, R. K.,
ing when they should. This is often observed in patients
Katz, E. R., Kazak, A. E. et al. (2008). A multicenter, randomized
clinical trial of a cognitive remediation program for childhood
who lack motivation, are depressed, or who experience
survivors of a pediatric malignancy. Journal of Consulting and problems because of slowed processing speed. In healthy
Clinical Psychology, 76(3), 367378. individuals, response bias can be influenced by
Atypical Teratoid/Rhabdoid Tumor (AT/RT) A 299
instructional set, reward, or other factors that shift the References and Readings A
likelihood of responding or not responding.
Larrabee, G. (2005). Forensic neuropsychology: A scientific approach.
Stern, B. H., & Brown, J. (2007). Litigating brain injuries. New York:
Cross References Thomson Reuters.
Continuous Performance Test

Signal Detection Theory
Atypical Antipsychotic
Attention-Deficit/Hyperactivity Neuroleptics
Disorder (ADHD)
Atypical Autism
Pervasive Developmental Disorder NOS
Attorney
M OIRA D UX
Rosalind Franklin School of Medicine
Baltimore, MD, USA Atypical Teratoid/Rhabdoid
Tumor (AT/RT)
Definition J ENNIFER T INKER
Drexel University
An attorney is defined as one who is legally appointed on Philadelphia, PA, USA
anothers behalf. An attorney-at-law is an individual who
has achieved the necessary educational requirements
(J.D.) and is licensed to practice law by the highest court Definition
of a state or some other form of jurisdiction. In civil cases
(e.g., personal injury, medical malpractice), there are Atypical Teratoid/Rhabdoid Tumor (AT/RT) is a rare,
plaintiff and defense attorneys. The plaintiff attorney highly malignant tumor of early childhood, most com-
represents the injured party (e.g., plaintiff) in an action monly diagnosed in infants who are less than 2 years. First
against the party they allege to be responsible for the described by Rorke and colleagues in 1987 (Lefkowitz,
damages; the defense attorney represents the defendant Rorke, & Packer, 1987), the AT/RT received its designation
(e.g., insurance company, hospital, and doctor). In crimi- because of its complex histological components. Progno-
nal matters, there are prosecution and defense attorneys. sis is extremely poor with a median survival of 611
The prosecuting attorney represents the party (e.g., Fed- months. Over half of AT/RTs identified are located within
eral, State, or local government) who has accused and the posterior fossa (brainstem, cerebellum, and pre-
wants to convict the offender of some type of criminal dominantly the cerebello-pontine angle) (Rorke, Packer,
action (e.g., murder, assault). The defense attorney repre- & Biegel, 1996). Clinical presentation varies largely by
sents the party (e.g., defendant) who has been accused of tumor location and size. Infants, in particular, may present
committing the crime. with nonspecific symptoms, including lethargy and
failure to thrive. Older children (>3 years of age) may
demonstrate more specific problems, including head tilt,
Cross References cranial nerve palsy, headache, and hemiplegia (Rorke &
Biegel, 2000). Often histologically confused with PNET/
Litigation medulloblastoma.
300 A Atypicals (antipsychotics)
Cross References condition, appreciation of certain aspects of musical

sounds might also be compromised (amusia). For this
Medulloblastoma syndrome to be diagnosed, other higher order deficits
Primitive Neuroectodermal Tumor that might more readily explain the deficit (such as aphasic
disorder) should be ruled out. In auditory-verbal agnosia
there is impairment of ones ability to process, interpret, or
References and Readings comprehend speech sounds or spoken language. Patients
may report that it is like hearing someone speaking in a
Lefkowitz, I. B., Rorke, L. B., & Packer, R. J. (1987). Atypical teratoid foreign language. Reading, writing, and speaking are in-
tumor of infancy: definition of an entity. Annals of Neurology, 22, tact, although speaking may be slightly problematic due to
5665.
the distortions in auditory feedback heard as speech is
Rorke, L. B., & Biegel, J. A. (2000). Atypical teratoid/rhabdoid tumour. In
P. Kleihues & W. K. Cavenee (Eds.), World health organization
attempted. In auditory-verbal agnosia (pure word deaf-
classification of tumours. Pathology & genetics. tumours of the nervous ness), the ability to match nonspeech or environmental
system (pp. 145148). Lyons, France: IARC Press. sounds (e.g., a barking dog, the ringing of a bell, or a train
Rorke, L. B., Packer, R. J., & Biegel, J. A. (1996). Central nervous system whistle) to corresponding pictures may remain intact.
atypical teratoid/rhabdoid tumors of infancy and childhood: defini-
Conversely, one may have difficulties identifying or match-
tion of an entity. Journal of Neurosurgery, 85, 5665.
ing nonspeech sounds, while retaining the ability to pro-
cess and interpret spoken language. Some degree of
impairment in ones ability to recognize musical sounds
Atypicals (antipsychotics) is commonly, but not invariably, present in these disorders.
Select patients may have difficulty recognizing familiar
Antipsychotics tunes or melodies, while retaining their ability to produce
them spontaneously. Others may be impaired at matching
tones, rhythms, or timbre, for example, identifying the
sound of a particular musical instrument.
Auditory Agnosia Auditory agnosia is thought to result from either (1)
unilateral or bilateral lesions of the unimodal (secondary)
J OHN E. M ENDOZA
auditory association cortex in the middle portions of the
superior temporal gyrus and/or (2) a disconnection syn-
drome involving the primary auditory cortex (Heschls
gyrus) of one hemisphere and the subcortical projections
from the opposite hemisphere to the unimodal auditory
Synonyms association cortex on that same side. Such lesions would
allow elementary sounds to be heard (as one or both of
Auditory-sound agnosia; Auditory-verbal agnosia; Pure
Heschls gyri are intact), but would produce impaired
word deafness
higher level processing due to damage or inaccessibility to
the unimodal cortex. With critically placed bilateral lesions
Definition of the superior temporal gyri, an agnosia for all types of
complex auditory input may be present. Auditory-verbal
Rare condition in which sounds, although heard, are not agnosia is more likely to result from left-sided lesions as
properly interpreted and thus have little or no meaning described above, while auditory agnosia for nonspeech
for the patient. sounds is more likely to be associated with right hemi-
spheric lesions. Agnosia for musical sounds may also be
differentially affected, but in an even less consistent manner.
Current Knowledge
When present, auditory agnosia, is usually primarily lim- Cross References

ited to impaired recognition of either language sounds or
nonlanguage (environmental) sounds. The former is Agnosia
known as auditory-verbal agnosia or pure word deafness. Amusia
No commonly used term is applied to the latter. In either Disconnection Syndromes
Auditory Discrimination A 301
References and Readings Heschls gyrus. The primary auditory cortex receives direct
A
input from the medial geniculate nuclei of the thalamus,
Bauer, R. M., & Demery, J. A. (2003). Agnosia. In K. Heilman & E. which it is thought to process auditory input at a very basic
Valenstein (Eds.), Clinical neuropsychology (4th ed., pp. 236295). level with little, if any, distinction between the right and left
hemispheres. The secondary auditory cortex (primarily
Brodmanns area 22) surrounds the primary cortex and,
for the most part, is located in the lateral portion of the
superior temporal gyrus. The posterior portion of this
Auditory and Visual Evoked secondary cortex in the left hemisphere constitutes
Potentials Wernickes area. These secondary cortices are thought to
be responsible for the further refinement of auditory
Event-Related Paradigms input, organizing it into meaningful or potentially mean-
ingful percepts. Lesions of Wernickes area (left hemi-
sphere) are associated with severe comprehension and
other language-related deficits, whereas comparable
Auditory Brainstem Response lesions in the right hemisphere may be associated with
difficulty recognizing or interpreting nonlanguage
Audiometry sounds. Such lesions in the right hemisphere might help
account for the inability of some patients to comprehend
Brainstem Auditory Evoked Responses or interpret the emotional tones or inflections in spoken
language, which may convey more meaning than the
actual words themselves (i.e., receptive aprosodia).
Auditory Brainstem Responses

Cross References
(ABR)
Aprosodia
Brainstem Auditory Evoked Responses Auditory Agnosia
Homotypic Cortex
Idiotypic Cortex
Auditory Cortex
J OHN E. M ENDOZA Auditory Discrimination
New Orleans, LA, USA B ETH K UCZYNSKI 1, S TEPHANIE A. KOLAKOWSKY-H AYNER 2
1
University of California
Davis, CA, USA
2
Definition Santa Clara Valley Medical Center,
That portion of the cerebral cortex devoted exclusively to San Jose, CA, USA
the processing of input from the medial geniculate nuclei
(auditory information).
Synonyms
Current Knowledge Auditory processing
Located in the superior portion of the temporal lobe of

each hemisphere, the auditory cortex consists of both Definition
primary (idiotypic) and secondary (unimodal homotypic)
cortices. The former is located in the temporal operculum Auditory discrimination is the ability to recognize differ-
(Brodmanns area 41 and part of 42) and is referred to as ences in phonemes (the smallest unit of sound in a
302 A Auditory Evoked Response (AER)
language), including the ability to identify words and Current Knowledge

sounds that are similar and those that are different. Audi-
tory discrimination tests are performed to measure a per- From the Outer Ear to the Cochlear Nuclei
sons phonological awareness, such as the ability to focus
on and manipulate phonemes within spoken words. Im- Sound is transmitted through the air as longitudinal
paired auditory discrimination should be addressed early waves, enters the outer ear, and vibrates the tympanic
in child development as it is pertinent to learning and membrane. The three ossicles (malleus, incus, and stapes)
development. amplify and transmit these vibrations to the oval window,
producing waves in the scala vestibuli, a fluid-filled
compartment within the coil-shaped cochlea of the
Cross References inner ear. These fluid waves distort the stiff basilar mem-
brane. Residing on the membrane, hair cells within the
Language organ of Corti transduce the minute movements of
Phonological Disorders the membrane into the graded release of glutamate onto
Phonology the peripheral processes of bipolar afferent fibers, whose
cell bodies are located in the spiral ganglion. The central
processes exit the base of the cochlea, form the auditory
References and Readings trunk of the vestibulocochlear nerve (eighth cranial nerve,
CN VIII), and project ipsilaterally to the ventral and
Gordon-Brannan, M. E., & Weiss, C. E. (2008). Clinical management of dorsal cochlear nuclei in the brainstem.
articulatory and phonologic disorders (3rd ed.). Philadelphia, PA:
Lippincott Williams & Wilkins.
Moller, A. R. (2000). Hearing: Its physiology and pathophysiology. San
Diego, CA: Academic Press. From the Cochlear Nuclei to the Superior
Warren, R. M. (1999). Auditory perception: A new synthesis (2nd ed.).
Olivary Nuclei
New York: Cambridge University Press.
Warren, R. M. (2008). Auditory perception: An analysis and synthesis
(3rd ed.). New York: Cambridge University Press. Fibers from the dorsal cochlear nucleus decussate to the
contralateral inferior colliculus via the lateral lemniscus.
Fibers from the ventral cochlear nuclei project ipsilater-
ally to the superior olivary nucleus and also decussate
via the trapezoid body to the contralateral superior
Auditory Evoked Response (AER) olivary nucleus. This circuit provides temporal and in-
tensity differences in the horizontal plane between right
Brainstem Auditory Evoked Responses and left ear to aid in sound source localization. Because
of the bilateral nature of these afferent projections,
central lesions rarely result in total unilateral hearing
loss.
Auditory Pathway
From the Superior Olivary Nuclei to the
WOON C HOW Medial Geniculate Nuclei
Richmond, VA, USA Afferent fibers from the superior olivary nuclei merge
with other audition-associated ascending fibers and proj-
ect via the lateral lemniscus to the inferior colliculus. The
Definition inferior colliculus receives bilateral inputs from almost all
audition-related nuclei and acts as a nearly obligatory
The auditory neural pathway in the central nervous relay in the ascending auditory pathway. It is here that
system transmits and processes sound signals from the horizontally oriented and vertically oriented sound source
ear to the cortex. The configuration of the pathway is localization data is fully and finally integrated. Ascending
multisynaptic and bilaterally projecting. fibers from the inferior colliculus project ipsilaterally to
Auditory Processing A 303
the last subcortical relay station, the medial geniculate

Auditory Perceptual Disorder A
nucleus.
Located in the posteroinferior portion of the (APD)
thalamus, the medial geniculate nucleus is a relay between
the inferior colliculus in the brainstem and the auditory Central Auditory Processing Disorder
cortex. The medial geniculate nucleus plays a role in
directing and maintaining attention.
From the Medial Geniculate Nuclei to Auditory Processing

Heschls Gyri
S COTT L. D ECKER , J ESSICA A. C ARBONI
Outputs from the medial geniculate nucleus project via Georgia State University
the internal capsule to the ipsilateral primary auditory Atlanta, GA, USA
cortex located in the posterior portion of the superior
temporal gyrus of Heschl. At the cortical level, detected
sound is finally perceived. Bilateral lesions of the auditory Definition
cortex remove the conscious perception of sounds, but
because of extensive subcortical processing, an individual Auditory processing is a term used to describe the process
may still react reflexively to a sound without actually in which sound waves are transduced into neurological
hearing it. impulses and decoded by the primary auditory cortex
in the temporal lobe of the brain. Further processing
involves general sound detection and language sounds.
Object vibration causes molecules of air surrounding
Tonotopic Mapping it to condense and pull apart, producing waves that travel
away from the object. Receptor cells within our ears will
One idea of note is tonotopy, which is the spatial arrange- be stimulated if the vibration ranges between approxi-
ment of where particular frequencies of sound are relayed mately 30 and 20,000 times per second (Carlson, 2007).
and processed within the auditory system. In the cochlea, These waves will then be perceived as sound.
high frequency sounds are detected by hair cells at the There are three dimensions of sound: pitch, loudness,
base and low frequency sounds at the apex. This tonotopic and timbre. The pitch of an auditory stimulus is deter-
organization is preserved systematically all the way up to mined by the frequency of vibration or cycle per second
the primary auditory cortex, where higher frequency (Hertz). Intensity of sound is a function of loudness,
sounds are mapped to a more medial location on the whereas vigorous vibrations of an object produce more
superior temporal gyrus whereas lower frequency sounds intense sound waves thus producing louder sounds. In-
are mapped to a more anterolateral location. formation regarding the nature of sound is produced
through timbre.
Our ears are able to detect stimuli, determine the
Cross References spatial location of those stimuli, and recognize the
identity of such stimuli.
Auditory Cortex
Auditory System
Cochlea Cross References
Cochlear Nuclei (Dorsal and Ventral)
Heschls Gyrus Auditory Discrimination
Inferior Colliculi Auditory Pathway
Internal Capsule
Lateral Lemniscus
Medial Geniculate Nuclei References and Readings
Trapezoid Body
Vestibulocochlear Nerve Carlson, N. R. (2007). Physiology of behavior (8th ed.). Boston: Pearson.
304 A Auditory Processing Disorder (APD)
equalization of pressure on either side of the tympanic

Auditory Processing Disorder membrane. The semicircular canals, the vestibule, and the
(APD) cochlea comprise the inner ear. The first two constitute
the end organs for the vestibular system, whereas the
Central Auditory Processing Disorder cochlea and organ of Corti contained within it represent
the origin of the nerve impulses that eventually are trans-
lated into sounds.
The second set of structures in the auditory system is
the brainstem nuclei associated with hearing. The dorsal
Auditory Sensory Memory and ventral cochlear nuclei located in the region of the
pontinemedullary junction represent the origin of the
Echoic Memory second-order auditory fibers. Next in line are the superior
olivary nuclei, which lie in the pons and are the first
nuclear group to receive auditory input from both ears.
The next and final major nucleus concerned with hearing
in the brain stem is the inferior colliculus, a paired struc-
Auditory Spatial Processing ture in the dorsal portion of the midbrain.
The brain itself might be considered the third portion
Spatial Processing of the auditory system. The two most critical structures
here are the medial geniculates of the thalamus, and
Heschls gyri (Brodmanns area 41) which lie in the tem-
poral operculum (within the lateral fissure) of each hemi-
sphere. It is this last structure, in conjunction with its
Auditory System adjacent secondary auditory cortices, which is responsible
for processing the auditory input into meaningful
M ARYELLEN R OMERO information.
Tulane University Health Sciences Center Finally, there are the major pathways that interconnect
New Orleans, LA, USA these various structures. The auditory portion of the
vestibulo-cochlear nerve (CN VIII) is the first-order neu-
ronal pathway in the auditory system. It has its origins in
Structure the organ of Corti and terminates in the dorsal and
ventral cochlear nuclei. The acoustic stria (dorsal, ventral,
The structure and function of the human auditory system and intermediate) form the second-order neurons of the
was first postulated by the physicist George Ohm more auditory system. What is important to note is that while
than 100 years ago. Dr. Ohm theorized that the auditory most fibers cross the midline, some remain ipsilateral,
systems main function was to translate complex sound thus at a very early stage there is bilateral input from
material into highly specialized vibratory signals that each ear. The trapezoid body of the pons represents one
could then be processed in the brain and recoded as such major crossing of these auditory fibers (primarily
recognizable entities. At a very basic level, the auditory those from the ventral acoustic stria). Most of these
system might be considered as being composed of three second-order fibers synapse in the superior olivary nuclei,
primary structures and their interconnections. The first of although some proceed directly to the inferior colliculi.
these is the ear, which itself is typically divided into three The lateral lemniscus, again consisting of both crossed and
components. The outer or external ear is that which is uncrossed fibers, interconnects the superior olivary nuclei
visible, the pinna and the auditory meatus or ear canal with the inferior colliculi. From there, the brachium of the
which terminates at the tympanic membrane or ear drum. inferior colliculi carries auditory signals to the medial
Next is the middle ear which primarily consists of a linked geniculates which, in turn, project ipsilaterally to the
series of three small bones, the malleus, incus, and stapes, primary auditory cortices. It should be noted that, due
which act together as a system of levers. The former is to the arrangement of the auditory pathways, by the time
attached to the tympanic membrane and the latter to the these signals reach the cortex they are derived from both
oval window of the inner ear. The middle ear is connected ears, with approximately 60% coming from the contralat-
to the oral cavity by the eustachian tube which allows for eral ear and 40% from the ipsilateral one.
Auditory System A 305
Function normally implies damage no higher than the cochlear

A
nuclei. Pure word deafness (intact hearing with the inabil-
Joseph Fourier, a French mathematician, identified the ity to understand spoken language without other major
physical and mathematical properties of sound waves aphasic deficits) can result from a relatively rare occur-
and described the transformation of such stimuli into rence of damage to Heschls gyrus on the left and a
frequency, amplitude, and phase, which govern discrete dissociation of input to the secondary association areas
elements of sound such as loudness and pitch. In its raw, from the non-dominant hemisphere. Damage at interme-
unprocessed state, sound exists in the form of vibration diate levels may result in poor localization of sounds.
that results in alterations in the pressure of the air in the Aside from ponto-medullary strokes, unilateral (or bilat-
immediate environment. These alterations in pressure eral) hearing loss is most commonly the result of damage
take the form of waves that have a specific frequency or to the middle or inner ear or the nerves that emanate from
combination of frequencies as well as intensity. The fre- the latter. Any of many causes could be the problem, from
quency of the sound wave, as measured by hertz (Hz) is prolonged exposure to loud noises, trauma, infections,
the major determinant of the pitch of the resulting sound, medications, and, of course, simply aging. While formal
experienced by the listener as high or low. The amplitude assessments of hearing loss are best left to audiologists, a
of the wave, or its height, is the major determinant of the gross assessment of hearing acuity is important to better
loudness of the resulting sound, measured in decibels (dB). understand why a particular patient may be having diffi-
The human ear is capable of capturing sound over a con- culty either on examination of mental status or coping at
siderable frequency range, approximately 2020,000 Hz. home or on the job. Given a hearing loss, neurologists will
The transduction of sound waves into the perception often try to differentiate its particular nature. Two types of
of sound is complex. Vibrations entering the external peripheral hearing loss (i.e., not due to a lesion of the
auditory meatus strike the tympanic membrane, causing brain stem or above) are typically identified, conductive
it to vibrate. This vibration is transferred directly to the and sensorineural. The former, which is generally more
ossicles; first the malleus, which is attached to the tympanic amenable to treatment, is a result of a problem with the
membrane, followed by the incus and then the stapes external or middle ear, while the latter implies damage to
which sets the oval window of the inner ear in motion. the inner ear. These can often be distinguished by a couple
The vibration is then picked up by the fluids (perilymph of procedures using a tuning fork (preferably 512 Hz). In
and endolymph) of the cochlea, first setting the perilymph the first, the ability of the patient to hear the vibration is
of the scala vestibuli and then the endolymph of the organ tested by comparing air to bone conduction (Rinne test).
of Corti and basilar membrane upon which its rests, and Here the base of the vibrating tuning fork is applied to the
finally the perilymph of the scala tympani from where it is mastoid process just behind the ear. When the sound is
dissipated via the round window of the inner ear. In the said to have dissipated, the ends of the fork are immedi-
course of this activity, the basilar membrane is differen- ately moved near the auditory canal (air conduction). If
tially affected depending on the frequency of the waves the problem is in the middle ear, the sound will not be
causing the hair cells along its length to be stimulated, heard. Conversely, if the sound is heard better via air than
initiating patterns of nerve impulses that correspond to bone conduction, a sensorineural (inner ear) deficit is
the particular pitch. This very discrete information is suspected. It should be noted that for normals, air con-
picked up by the auditory nerve (CN VIII) in the form duction will be superior to bone conduction, but one
of bioelectrical nerve impulses, which then are propagated should be looking for relative differences in acuity, not
through the various pathways described above until absolute auditory thresholds as the latter will likely low-
eventually reaching the cerebral cortex where they are ered in the affected ear. A second procedure is to press the
eventually interpreted as speech or other sounds. base of the tuning fork on the middle of the forehead.
If there is a sensorineural loss, the sound will be localized
to the unaffected ear, while it will be localized (sound
Illness louder) in the affected ear in a conductive hearing loss.
This latter procedure is referred to as the Weber test.
Damage to any part of the auditory system, from cerumen Another common problem associated with hearing is
(wax) in the auditory canal to bilateral cortical lesions tinnitus, a buzzing, ringing, or other repetitive noxious
(exceedingly rare) can result in hearing deficits. Because sound in one or both ears. It can be relatively brief or
of the multiple crossings and ipsilateral connections with- chronic. If the latter, it can be very disturbing to the
in the system, hearing loss which is confined to one ear patient. The causes can be multiple, including certain
306 A Auditory Verbal Learning
drugs (e.g., aspirin), aftereffects of exposure to loud and/or recognize them at a later time. These tasks assess
noises, infections, or occasionally may represent the initial acquisition and retrieval components of memory, includ-
symptoms of a more serious condition such as a brain- ing encoding, learning characteristics, storage, consolida-
stem tumor. Unfortunately, treatment options for this tion over short- or long-time intervals, and subsequent
condition are quite limited. Having background noise, access to the information either by free retrieval or recog-
such as music, is often helpful. nition. The nature of the test composition, the instruc-
tions to the individual, and the scoring dictate what
conclusions are drawn from the task.
Cross References Auditory verbal learning tasks (AVLTs) are used in
both clinical and research settings, and are a hallmark of
Aphonia memory assessment. Recent versions of these tests include
Auditory Cortex the California Verbal Learning Test-II (CVLT-II; Delis,
Auditory Pathway Kaplan, Kramer, & Ober, 2000), Hopkins Verbal Learning
Cochlea Test-R (HVLT-R; Brandt & Benedict, 2001), World Health
Pure Word Deafness Organization/UCLA Auditory Verbal Learning Test
Tinnitus (WHO/UCLA AVLT; Maj et al., 1993), Rey Auditory
Weber Test Verbal Learning Test (RAVLT; Schmidt, 1996),
Neuropsychological Assessment Battery (NAB; Stern &
White, 2003), and List Learning in the Center to Establish
References and Readings Registry for Alzheimers Disease (CERAD; Morris et al.,
1989; Welsh, Butters, Hughes, Mohs, & Heyman, 1991).
Bradley, W. G., Daroff, R. B., Fenichel, G. M., & Jankovic, J. (2004). Other commonly used list-learning tasks (e.g., ADAS-
Neurology in clinical practice: Principles of diagnosis and management COG; Rosen, Mohs, & Davis, 1984), like the Free and
Fourth Edition. Philadelphia, PA: Butterworth-Heineman.
Cued Selective Reminder Task (FCSRT; Buschke, Sli-
Wilson-Pauwek, L., Akesson, E. J., Stewart, P. A., & Spacey, S. D. (2002).
Cranial nerves in health and disease. Hamilton, ONT: B.C. Decker,
winski, Kuslansky, Katz, Verghese, & Lipton, 2006; Gro-
Inc. ber, Merling, Heimlich, & Lipton, 1997), are not solely
auditory, adding visual words or picture presentations of
items.
List-learning tasks share many design features. The
Auditory Verbal Learning number of words in the to-be-learned list (e.g., 1216
items) has been designed to exceed the typical vigilance
J UDY C REIGHTON 1, H. A LLISON B ENDER 2 span of seven items and to stress learning demands. The
S TEPHANIE A SSURAS 1, J ENNIFER WOEHR 3 learning phase is the presentation of the list across several
J OAN C. B OROD 1,3 , N ANCY S. F OLDI 1,4 trials. Following each trial, the examinee is asked to recall
1
Queens College and The Graduate Center of the as many items as possible. Once the learning is complete,
City University of New York a short time interval elapses, usually including interfer-
Flushing, NY, USA ence tasks designed to prevent rehearsal of the list items.
2
New York University Langone Medical Center The examinee is then asked to recall items from the list,
New York, NY, USA constituting a short term recall. After another longer
3
Mount Sinai School of Medicine interval, again containing some distraction, a recall is
New York, NY, USA requested. These short- and long-term retrieval assess-
4
State University of New York, Stony Brook ments capture the examinees ability to store, consolidate,
School of Medicine and maintain information, as well as to retrieve it on
Mineola, NY, USA command. Tests can include a subsequent multiple- or
forced-choice task to facilitate access, capturing the items
that were encoded but could not be accessed on free
Description retrieval.
Despite commonalities, instruments vary in content
An auditory verbal learning task typically requires indivi- and administration. List construction on some tests (e.g.,
duals to hear a list of items, learn those items, and recall CVLT-II, HVLT-R, WHO/UCLA AVLT, and
Auditory Verbal Learning A 307
NAB) incorporates semantic categories, whereas others Historical Background A

do not (e.g., RAVLT, CERAD, and ADAS-COG).
Examinees are not initially informed of these categories Word lists have been used to assess learning and memory
in order to determine whether they can exploit semantic for over a century. Ebbinghaus (1885) was early to observe
information to their advantage and to facilitate their and describe the serial position phenomenon. Eduoard
ability to organize, encode, and learn more items. To Claparede (Boake, 2000) assessed learning and memory in
ensure and document that any particular item is fully his work on child pedagogy in 1916 using a 15-item word
encoded with semantic knowledge, the FCSRT adopts an list, which was adapted by Andre Rey to develop the
alternate use of semantic organization by cueing exami- RAVLT in 1941. The RAVLT, first published in France,
nees with the semantic category while the word is being has been adapted since its development and modified
learned and by prompting the category immediately af- for use in multiple languages. In 1996, the RAVLT
terward. Another variation among tests is the use of manual (Schmidt, 1996) was published, providing stan-
interference lists. For instance, after the initial learning dard instructions on administration, scoring, and
phase of the target lists in the CVLT-II and NAB, an interpretation. The original CVLT, published in 1987
alternate list is administered, designed to share some but (Delis, Kramer, Kaplan, & Ober, 1987), incorporated
not all of the semantic categories of the target list. This semantic categories, scorings of learning characteristics,
helps to address susceptibility to interference and source use of semantic strategy, and contrast measures of learned
learning. Other tests (e.g., HVLT-R and FCSRT) do and retrieved items. The CVLT-II revision (Delis et al.,
not have prescribed interference tasks, although other 2000), published in 2000, adopted new norms.
word-list or naming tasks should not be used during the The CVLTChildrens Version (Delis, Kramer, Kaplan, &
delay. Delayed recall is commonly tested after a 2030- Ober, 1994) is appropriate for children in the age group
min interval. There are various methods to assess the of 516 years. The HVLT (Brandt, 1991) was introduced
recognition memory of the target list. Examinees can with six alternate forms designed for longitudinal, repeat-
identify target-list words among a list of distracters ed testing, and the revised version (Brandt & Benedict,
(CVLT-II, HVLT-R, and NAB) or identify targets in 2001) incorporated delayed recall and recognition trials.
forced- (CVLT-II) or multiple-choice (FCSRT) recogni- The newest list-learning task from the NAB (Stern &
tion trials. While most tasks use recognition after short- White, 2003) has been normed on individuals up to 97
(NAB) or long-term (CVLT-II and HVLT-R) free recall, years of age. The WHO/UCLA AVLT was designed by the
one test (ADAS-COG) relies exclusively on the immediate WHO in 1993 to better evaluate examinees worldwide
recognition to assess learning. (Maj et al., 1993). When designing this instrument,
AVLTs reveal significant information about learning the authors were careful to select words that were familiar
and memory processes. The multiple trial exposure gen- across multiple cultures. Similar to the CVLT-II, the
erates an individuals learning curve, indicating whether words comprising the WHO/UCLA AVLT can be classi-
information learned on an earlier trial is maintained and fied into categories. However, the categories of the
appended with new information. Learning characteristics, WHO/UCLA AVLT are universally familiar (i.e., body
particularly serial position effects (i.e., primacy and re- parts, animals, tools, household objects, and transporta-
cency effects), provide insight about how learning occurs. tion vehicles). Of note, the WHO/UCLA AVLT is a
For instance, the dual storage model (Raaijmakers & component of the Neuropsychological Screening Battery
Shiffrin, 1981) suggests that items from primacy and for Hispanics (Ponton et al., 1996).
middle regions of the lists are thought to reflect long-
term storage, whereas recent items remain in immediate
working memory. The position of an item in the list, Psychometric Data
known as the distinctiveness feature, can also aid in later
recall, with the distinct first or last items having prefer- Normative data for AVLTs span an age range of 797 years.
ence. Susceptibility to proactive and/or retroactive inter- Groups used in normative data include healthy adults,
ference of the interference list or shared semantic men, women, and Hispanic individuals. Stratified norms
categories of target items are analyzed. Long-term reten- according to age, sex, ethnicity, educational level, and
tion of verbal information can be parsed into storage and region of the country (e.g., Northeast) are also available.
retrieval components via examination of free-recall versus Many tests (e.g., CVLT-II and CERAD) have been
recognition scores. normed for European, Asian, and Southeast Asian groups.
308 A Auditory Verbal Learning
Direct translation of word lists into other languages verbal learning, providing detailed information about an
should be avoided, as words may have been selected to individuals capacity to acquire, consolidate, store, and
accommodate word frequency within a language or ap- retrieve information, thus revealing significant aspects of
propriateness within a culture. Some AVLTs are targeted the learning and retrieval processes. Learning character-
for certain populations using shorter versions and more istics, particularly primary and recency serial position
age-appropriate word lists (e.g., CVLT-C). Shorter effects (Foldi, Brickman, Schaefer, & Knutelska, 2003),
forms have also been adopted for more impaired indivi- are highly informative in differentiating clinical popula-
duals (e.g., CVLT-II, Short Form; Delis et al., 2000). tions and provide insight about how learning is occurring.
Verbal learning tests are used to evaluate memory A detailed step-by-step exploration of each individuals
performance over time. Testretest reliability using the learning process enables the clinician or researcher to
same version of the test has been evaluated for 1-month identify specific areas of vulnerability and can guide
as well as 1-year intervals. Many tests have adopted alter- intervention strategies.
nate or multiple forms. Whereas alternate versions can Auditory verbal learning tasks have been instrumental
reduce practice effects, there is evidence that these effects in assessing change in memory over time. The auditory
are not completely eliminated (Houx et al., 2002) due to verbal learning paradigm has been very sensitive in
procedural learning. Therefore, examiners must be very discriminating between healthy and memory-impaired
cognizant of practice effects. Even after 2 years, healthy groups. A vast literature demonstrates the sensitivity of
older adults showed practice effects on the CVLT-II (Blasi, these tests to the detection of prodromal Alzheimers
Zehnder, Berres, Taylor, Spiegel, & Monsch, 2009). disease.
Construct validity of adult and child versions of the
CVLT in assessing learning and memory has been exam-
ined in several studies. Attention span, learning efficiency, Cross References
delayed recall, and inaccurate recall represent one example
of a four-factor model that was identified by a factor California Verbal Learning Test-II
analysis in a sample of children with traumatic brain California Verbal Learning Test-II, Childrens Version
injury (Mottram & Donders, 2005). Variability across Consortium to Establish a Registry for Alzheimers
studies may be a result of methodological differences, Disease (CERAD)
demographic differences, severity of patient population, Hopkins Verbal Learning Test Revised
and/or time elapsed between disease onset and assessment. Memory
In terms of inter-test relationships, tests are not Neuropsychological Assessment Battery
interchangeable, as word lists and administrations vary Rey Auditory Verbal Learning Test
significantly. However, the RAVLT correlates moderately
with the CVLT-II. The CVLT-II is now incorporated into
the Wechsler Memory Scale IV as a valid component of References and Readings
the memory indices. The HVLT-R also shows a high
correlation with the CVLT-II, although it may be more Blasi, S., Zehnder, A. E., Berres, M., Taylor, K. I., Spiegel, R., &
appropriate for greater disease severity. Monsch, A. U. (2009). Norms for change in episodic memory as a
prerequisite for the diagnosis of mild cognitive impairment (MCI).
Boake, C. (2000). Edouard Claparede and the Auditory Verbal Learning
Clinical Uses Test. Journal of Clinical and Experimental Neuropsychology, 22,
286292.
Verbal learning tests are ubiquitous in assessments of Brandt, J. (1991). The Hopkins Verbal Learning Test: Development of a
new memory test with six equivalent forms. The Clinical Neuropsy-
memory-impaired populations. Amnesic disorders, de-
chologist, 5, 125142.
generative dementias (including Alzheimers, Parkinsons, Brandt, J., & Benedict, R. (2001). Hopkins Verbal Learning Test-Revised.
and Huntingtons disease), temporal lobe epilepsy, Lutz, FL: Psychological Assessment Resources.
traumatic brain injury, depression, and focal stroke are Buschke, H., Sliwinski, M. J., Kuslansky, G., Katz, M., Verghese, J., &
diseases that have not only benefited from these tests, but Lipton, R. B. (2006). Retention weighted recall improves dis-
crimination of Alzheimers disease. Journal of the International
also have promoted refinements and further development
Neuropsychological Society, 12, 436440.
to extend our knowledge of the neuropsychological Delis, D. C., Kaplan, E., Kramer, J. H., & Ober, B. A. (2000). California
underpinnings of memory function. These instruments Verbal Learning Test II (2nd ed.). San Antonio, TX: The Psycho-
evaluate both quantitative and procedural aspects of logical Corporation.
Augmentative and Alternative Communication (AAC) A 309
Delis, D. C., Kramer, J., Kaplan, E., & Ober, B. A. (1994). California Verbal
Learning Test Childrens Version. San Antonio, TX: Pearson. Augmentative and Alternative A
Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (1987). California
Verbal Learning Test: Adult Version. New York: The Psychological Communication (AAC)
Corporation.
Ebbinghaus, H. (1885). Memory: A contribution to experimental psychology D IANE C ORDRY G OLDEN
(H. A. Ruger & C. E. Bussenenues, Trans., 1913). New York: Teachers Association of Assistive Technology Act Programs
College, Columbia University.
Delmar, NY, USA
Foldi, N. S., Brickman, A. M., Schaefer, L. A., & Knutelska, M. E. (2003).
Distinct serial position profiles and neuropsychological measures
differentiate late life depression from normal aging and Alzheimers
disease. Psychiatry Research, 120, 7184. Definition
Grober, E., Merling, A., Heimlich, T., & Lipton, R. B. (1997). Free and
cued selective reminding and selective reminding in the elderly.
Augmentative and alternative communication (AAC) is a
Journal of Clinical and Experimental Neuropsychology, 19, 643654.
Houx, P. J., Shepherd, J., Blauw, G. J., Murphy, M. B., Ford, I., Bollen, E. L., set of procedures and processes by which an individuals
et al. (2002). Testing cognitive function in elderly populations: communication skills can be maximized for functional and
The PROSPER study. Journal of Neurology, Neurosurgery, and effective communication. AAC approaches supplement or
Psychiatry, 73, 385389. replace natural speech with aided options that incorporate
Maj, M., DElia, L., Satz, P., Janssen, R., Zaudig, M., Uchiyama, C., et al.
the use of some type of device ranging from simple picture
(1993). Evaluation of two new neuropsychological tests designed to
minimize cultural bias in the assessment of HIV-1 seropositive per- communication systems to complex speech generating
sons: AWHO study. Archives of Clinical Neuropsychology, 8, 123135. devices and/or unaided options that involve only the indi-
Morris, J. C., Heyman, A., Mohs, R. C., Hughes, J. P., van Belle, G., viduals body, such as sign language. AAC may be used to
Fillenbaum, G., et al. (1989). The Consortium to Establish a Registry augment understanding as well as written or oral expres-
for Alzheimers Disease (CERAD). Part I. Clinical and neuropsycho-
sion. A multimodal approach that includes both devices
logical assessment of Alzheimers disease. Neurology, 39, 11591165.
Mottram, L., & Donders, J. (2005). Construct validity of the California and unaided strategies may be most effective in meeting
Verbal Learning Test-Childrens Version (CVLT-C) after pediatric the individuals communication needs.
traumatic brain injury. Psychological Assessment, 17, 212217.
Ponton, M. O., Satz, P., Herrera, L., Ortiz, F., Urrutia, C. P., Young, R.,
et al. (1996). Normative data stratified by age and education for the Historical Background
Neuropsychological Screening Battery for Hispanics (NeSBHIS):
Initial report. Journal of the International Neuropsychological Society,
2, 96104. Prior to about 1970, AAC was not a widely accepted
Raaijmakers, J. G. W., & Shiffrin, R. M. (1981). Search of associative intervention technique and could even be described as
memory. Psychological Review, 88, 93134. contraindicated in the professional literature. At that
Rosen, W. G., Mohs, R. C., & Davis, K. L. (1984). A new rating scale for time, it was thought that the act of vocal production was
Alzheimers disease. American Journal of Psychiatry, 141, 13561364.
Schmidt, M. (1996). Rey Auditory Verbal Learning Test: A handbook. Los
a critical building block of human language development.
Angeles: Western Psychological Services. As a result, interventionists believed that providing an
Stern, R. A., & White, T. (2003). Neuropsychological Assessment Battery. alternative to speech production would deter speech
Lutz, FL: Psychologial Assessment Resources. (and thus language) development because the child
Welsh, K., Butters, N., Hughes, J., Mohs, R., & Heyman, A. (1991). would choose to use the easier alternative mechanism
Detection of abnormal memory decline in mild cases of Alzheimers
disease using CERAD neuropsychological measures. Archives of
(Bates, 1976; Fourcin, 1975).
Neurology, 48, 278281. In the late 1960s and in the 1970s, research evidence
indicated speech was actually a secondary component to
language function and that robust receptive and expres-
sive language could be developed without vocal produc-
Auditory-Sound Agnosia tion. In many cases, the use of alternatives to speech
production was found to actually support (and in no
Auditory Agnosia way deter) vocal production (Schlosser & Wendt, 2008;
Silverman, 1980; Zangari, Lloyd, & Vicker, 1994). In 1980,
the American Speech-Language-Hearing Association
(ASHA) established an Ad Hoc Committee on Commu-
Auditory-Verbal Agnosia nication Processes and Nonspeaking Persons that devel-
oped a position statement outlining the concept of AAC
Auditory Agnosia as a set of intervention techniques using a variety of
310 A Augmentative and Alternative Communication (AAC)
symbol sets and communication interaction behaviors. systems have been developed to meet this need with some
This became the framework for the field of AAC today. specifically focused on individuals with neuropsychological
At about the same time, new computer technologies disabilities such as autism (Glennen & DeCoste, 1997).
were exploding onto the scene creating previously un- While the core goal of AAC is to provide effective com-
imaginable opportunities for AAC device development. munication, related objectives can include decreasing
The Trace Research and Development Center, part of the problem behaviors and increasing successful education,
College of Engineering at the University of Wisconsin- employment, and community living outcomes.
Madison, was formed in 1971 to address the communica-
tion needs of people with severe disabilities who were
nonspeaking. The Center was an early leader and inno-
Treatment Participants
vator in the augmentative communication field and pio-
Early in the history of AAC, two misconceptions thrived
neered development of electronic communication aids in
regarding candidacy for AAC that a set of prerequisite skills
the 1970s and 1980s that became prototypes for the
(usually cognitive and motor) was required before AAC
speech generating devices (SGDs) of today (Vanderheiden,
could be considered and AAC should only be implemented
1978; Vanderheiden & Grilley, 1976).
after all traditional forms of speech therapy had failed. Both
have been proven unsubstantiated as many successful AAC
users have severe motor and/or cognitive impairments, and
Rationale or Underlying Theory
research has shown no justification for waiting to implement
AAC as it can support speech development (Shane & Bashir,
Today the widespread acceptance of AAC is a valid inter-
1980). As a result, candidacy for AAC is not limited by
vention option to develop viable means of effective com-
age, disability diagnosis or prerequisite cognitive or motor
munication for any individual with limited natural
skills. Individuals who can benefit from AAC may be of all
speech, as well as to enhance comprehension for those
ages, including infants and toddlers with disabilities, and
who are not hearing impaired, but who have difficulty
may have diagnoses including apraxia, dysarthria, apha-
understanding spoken language. In 1992, the National
sia, autism, ALS, cerebral palsy, multiple sclerosis, Parkin-
Joint Committee for the Communication needs of Per-
sons, mental retardation, etc.
sons with Severe Disabilities issued a Communication Bill
of Rights that unequivocally states, All persons, regard-
less of the extent or severity of their disabilities, have a Treatment Procedures
basic right to affect, through communication, the condi-
tions of their own existence. A set of 12 specific rights are The challenges for those providing intervention are main-
described in the Bill of Rights including, the right to have taining current knowledge of the vast array of available
access at all times to any needed augmentative and alter- AAC device options, appropriately matching the skill sets
native communication devices and other assistive devices of individuals with disabilities to available AAC systems,
and to have those devices in good working order. securing funding to acquire the system, improving com-
munication opportunities and environments, and
providing supports sufficient to ensure effective use of
Goals and Objectives the system.
Consideration for aided AAC intervention begins with
Most of the early history of AAC focused on individuals with assessment by a qualified team of individuals who are
neuromotor impairments that limited oral-motor skills knowledgeable about the individual and his other
such as cerebral palsy and amyotrophic lateral sclerosis. strengths and limitations especially in the areas of speech,
However, with the passage of landmark legislation such as language, and motor skills. One or more team members
the Education of Handicapped Childrens Act (P.L. 94142), should be knowledgeable about the range of potential
Section 504 of the Rehabilitation Act, and later the AAC alternatives available and those that are viable
Americans with Disabilities Act, individuals with all types options to meet the individuals communication needs.
of disabilities have become more integrated into education, Appropriate practice in assessment includes conducting
employment, community living, and society in general. This structured device trials with various AAC devices in the
change created a widespread need for individuals with environment(s) in which the individual will be using
all types of disabilities to have an effective, functional com- the technology (e.g., home, school, community, etc.).
munication system. More complex and efficient AAC This allows for comparative analysis of different device
Augmentative and Alternative Communication (AAC) A 311
features and functions to determine which best address Any number of standardized communication measures
A
the individuals functional communication needs. can be used to document communication efficacy using
The result of an AAC assessment is identification of the AAC system. In addition, the Adaptive Technology
the system features appropriate for an individual includ- Resource Center had identified a variety of outcome
ing specification of device input features (selection tech- measurement tools that focus on the functional efficiency
niques), message characteristics, and output features. and functional gains achieved through the use of assistive
Once an appropriate AAC system has been acquired, technologies including AAC, see http://atrc.utoronto.ca/
training and support for the user, their family, and others index.php?option = com_content&task = view&id =
(e.g., teachers, therapists, etc.) must be implemented. 178&Itemid = 69.
More complex AAC systems frequently require initial
programming and device setup as part of user support
services. Short and long-term communication goals
should be developed using the AAC system and therapy Qualifications of Treatment Providers
services implemented to support goal achievement
(Beukleman, Garrett, & Yorkston, 2007; Beukelman & AAC intervention is typically provided by speech-
Mirenda, 2005; www.aac-rerc.com). language pathologists (SLPs) who are licensed by states
as health care providers, educated at the graduate level
in the study of human communication, its develop-
Efficacy Information ment and its disorders. Medicare requires an SLP who
provides AAC assessments or treatment to hold the
Efficacy research on AAC ranges from observation of Certificate of Clinical Competence (CCC) in speech-
changes in functional communication skills to potential language pathology from the American Speech-
secondary improvements in academic, social, behavioral, Language-Hearing Association. In addition to SLPs,
and other areas. For individuals with limited or no some other types of professional providers may be
functional communication, an AAC system that delivers members of the intervention team providing AAC
basic communication ability can be deemed effective by services, especially in the educational environment, e.
self-verification of communication occurring (Fried- g., special educators, occupational therapists, assistive
Oken & Bersani, 2000). Beyond this basic gauge of AAC technology practioners, etc. (ASHA, 2002; ASHA, 2004;
efficacy, research has been done on a variety of specific ASHA, 2005).
outcomes such as decreasing problem behaviors through
the use of AAC (Vaughn & Horner, 1995), enhancing the
rate of AAC communication, (Venkatagiri, 1993), and
even nuances such as speech synthesizer intelligibility Cross References
(Mirenda & Beukelman, 1990) all in an effort to support
AAC efficacy. Articulation
Seminal work on AAC efficacy done by Ralf Schlosser Articulation Disorder
(2003) addressed a wide range of AAC efficacy issues Assistive Technology
including the role of AAC in facilitating or hindering Speech
natural speech development, literacy development in Speech/Communication Disabilities
AAC users, and the effects of speech output (use of speech Speech-Language Pathology
generating devices). In 2001, Medicare began coverage of Speech-Language Therapy
speech generating devices (SGDs) based on acceptance of Speech Sound Disorders
AAC efficacy research. Since then, a number of private
insurance carriers have followed suit and now cover
SGDs as do most state Medicaid programs.
American Speech-Language-Hearing Association. (1981). Position state-
Outcome Measurement ment on non-speech communication. ASHA, 23, 577581.
American Speech-Language-Hearing Association. (2002). Augmentative
The most direct outcome measure for AAC intervention is and alternative communication: Knowledge and skills for service delivery
demonstration of effective and efficient communication. [Knowledge and Skills]. Retrieved from www.asha.org/policy
312 A Aura
American Speech-Language-Hearing Association. (2004). Roles and

responsibilities of speech-language pathologists with respect to Aura
augmentative and alternative communication: Technical report
[Technical Report]. Retrieved from www.asha.org/policy
K ENNETH P ERRINE
American Speech-Language-Hearing Association. (2005). Roles and
responsibilities of speech-language pathologists with respect to augmen- Northeast Regional Epilepsy Group
tative and alternative communication: Position statement [Position Hackensack, NJ, USA
Statement]. Retrieved from www.asha.org/policy Weill-Cornell College of Medicine
Bates, E. (1976). Language and context: The acquisition of pragmatics. New New York, NY, USA
York: Academic Press.
Beukleman, D., Garrett, K., & Yorkston, K. (2007). Augmentative and
alternative communication strategies for adults with acute or
chronic medical conditions. Baltimore: Paul H. Brookes Publishing Definition
Company.
Beukelman, D., & Mirenda, P. (2005). Augmentative and alternative An aura is a paroxysmal episode that occurs before several
communication: Management of severe communication disorders in
types of neurologic events. It is a type of warning heralding
children and adults (3rd ed.). Baltimore: Paul H. Brookes Publishing
Company. the onset of the ictal event such as a migraine or an epilep-
Fourcin, A. J. (1975). Language development in the absence of expressive tic seizure. Auras usually last longer in migraines (up to
speech. In E. H. Lenneberg & E. Lenneberg (Eds.), Foundations of minutes) than in seizures (typically several seconds).
language development (Vol. II). New York: Academic Press. Episodes longer in duration or more remote from the
Fried-Oken, M., & Bersani, H. (2000). Speaking up and spelling it out:
ictus in both migraine and seizures are called prodromes.
Personal essays on augmentative and alternative communication. Bal-
timore: Paul H. Brookes Publishing Company. In both disorders, auras can represent any disruption of
Glennen, S. L., & DeCoste, D. C. (1997). Handbook of augmentative neurologic function, the specific phenomena of which
and alternative communication. San Diego: Singular Publishing arise from the localization of their onset in the brain.
Group.
Mirenda, P., & Beukelman, D. (1990). A comparison of intelligibility
among the natural speech and seven speech synthesizers with listen-
ers from three age groups. Augmentative and Alternative Current Knowledge
Communication, 6, 6168.
National Joint Committee for the Communication Needs of Persons with
Auras can consist of disruptions or activations of primary
Severe Disabilities. (1992). Guidelines for meeting the communi-
cation needs of persons with severe disabilities. ASHA, 34(Suppl. 7),
sensory modalities (touch, hearing, smell, taste, vision),
18. Retrieved from www.asha.org/policy or www.asha.org/njc including paresthesias (somatosensory hallucinations that
Schlosser, R. W. (2003). The efficacy of augmentative and alternative feel like tingling or pins and needles) or numbness,
communication: Toward evidence-based practice. San Diego: unformed (noises, distortions) or formed (voices, songs,
Academic Press.
commercial jingles) auditory hallucinations or transient
Schlosser, R. W., & Wendt, O. (2008). Effects of augmentative and
alternative communication intervention on speech production in
deafness, and olfactory or gustatory hallucinations
children with autism: A systematic review. American Journal of (usually noxious, such as burned rubber). Visual halluci-
Speech-Language Pathology, 17, 212230. nations are especially common in migraine, and can in-
Shane, H., & Bashir, A. S. (1980). Election criteria for the adoption of an clude loss of vision such as blind spots or hemianopsia
augmentative communication system: Preliminary considerations.
(loss of vision on one side), positive phenomena such as
Journal of Speech and Hearing Disorders, 45, 408414.
Silverman, F. (1980). Communication for the speechless. Englewood Cliffs,
scintillating scotoma (flickering spots of light that may
NJ: Prentice-Hall. begin centrally and extend to arcs of flickering white or
Vanderheiden, G. C. (1978). Non-vocal communication resource book. colored lights), or zig-zag or other geometric lines or
Baltimore: University Park Press. patterns. Formed visual hallucinations can occur (especially
Vanderheiden, G. C., & Grilley, K. (1976). Non-vocal communication
in epilepsy), which are usually described as animals or
techniques and aids for the severely physically handicapped. Austin,
TX: Pro-Ed.
cartoon characters. Visual distortions can also occur, such
Vaughn, B., & Horner, R. (1995). Effects of concrete versus verbal choice as macropsia/micropsia (seeing objects larger/smaller) and
systems on problem behavior. Augmentative and Alternative telescopia/micropsia (seeing objects farther away/closer). In
Communication, 11, 8992. epilepsy, more complex somatosensory auras can occur,
Venkatagiri, H. S. (1993). Efficiency of lexical prediction as a communi-
such as a rising epigastric sensation (feeling the stomach
cation acceleration technique. Augmentative and Alternative
Communication, 9, 161167.
rising up to the mouth) or ineffable feelings that the
Zangari, C., Lloyd, L. L., & Vicker, B. (1994). Augmentative and alterna- patient cannot elucidate. Complex experiential psychic
tive communication: A historic perspective. Augmentative and Alter- auras can also occur (especially in epilepsy), such as
native Communication, 10, 2759. deja vu, out-of-body experiences, depersonalization,
Autism Diagnostic Interview, Revised A 313
derealization, bizarre perceptual phenomena, etc. Psy- Description A

chological symptoms such as anxiety, panic, and fear
are also common. In migraines, auras are thought to The current edition of the Autism Diagnostic Interview-
be caused by the vascular phenomena causing the head- Revised (ADI-R; Rutter, Le Couteur, & Lord, 2003) is a
ache. Of note, migraine auras can occur without any standardized, semistructured, and investigator-based
subsequent headache. In epilepsy, auras are actually sim- interview for parents or caregivers of individuals with
ple partial seizures produced by epileptiform electrical autism. It provides a diagnostic algorithm for the ICD-10
discharges that affect one brain region alone; they do definition of autism (World Health Organization [WHO],
not disrupt consciousness, and can be recalled by the 1992) and DSM-IV (American Psychiatric Association
patient after the ictus. [APA], 1993). The interview is appropriate for the diag-
nostic assessment of any person within the age range
extending from early childhood to adult life, provided
Cross References that they have a non-verbal mental age above 2 years.
The ADI-R includes 93 items in three domains of func-
Epilepsy tioning language/communication, reciprocal social
Partial Seizures interactions, and restricted, repetitive, and stereotyped
behaviors and interests, as well as other aspects of beha-
References and Readings viors. Up to 42 of the interview items are systematically
combined to produce a formal, diagnostic algorithm for
Allan Ropper, A. H., & Samuels, M. (2009). Adams and Victors principles
autism as specified by the authors, or a general diagnosis
of neurology (9th ed.). New York: McGraw-Hill. of autism spectrum disorders (ASD) as used in several
Engel, J., & Pedley, T. A. (Eds.). (2008). Epilepsy: A comprehensive textbook collaborative studies (Risi et al., 2006). All items in the
(2nd ed.). New York: Lippincott Williams & Wilkins. ADI-R are coded in terms of whether the behavior is
www.epilepsyfoundation.org
currently occurring, and whether it ever occurred,
or occurred during a specifically defined period in pre-
school years. The diagnostic algorithm is based on the
ever/most abnormal codes in preschool years, but cur-
Authoritative Reference rent scores can be used to facilitate a clinical diagnosis.
Most of the ADI-R pertains to behaviors that are rare
Learned Treatise in individuals who do not have ASD and/or who do not
have profound intellectual disabilities. Thus, numerical
estimates of the typical scores of general population
have not been obtained. Researchers have used scores in
Autism the domains or overall as estimates of severity of autistic
symptoms. However, the validity of this approach has
Autistic Disorders
not been directly tested. Scores have been published for
many research populations but not yet systematically
dimensionalized.
Autism Diagnostic Interview,

Revised Historical Background
S O H YUN K IM , C ATHERINE L ORD The WPS Edition of the ADI-R (2003) is a modified
University of Michigan Autism version of the 1994 version (Lord, Rutter, & Le Couteur,
and Communication Disorders Center (UMACC) 1994), which was based on the original Autism Diagnostic
Ann Arbor, MI, USA Interview (ADI; Le Couteur et al., 1989). The 1994 version
was somewhat shorter than the original in order to make
the interview more appropriate for clinical, as well as
Synonyms research, usage. The diagnostic algorithm developed for
the 1994 version remains unaltered (apart from minor
ADI-R changes in age cutoff).
314 A Autism Diagnostic Interview, Revised
Psychometric Data associated with ASD, but requires approximately two

hours to administer and substantial practice to do so
Psychometric properties for the original ADI were reliably.
provided for a carefully selected, blindly interviewed and The Diagnostic Algorithms are sets of rules that allow
coded, sample of 16 autistic and 16 mentally handicapped classification of patterns of behavior according to whether
children and adults covering a range of IQs and chrono- or not they meet the current DSM-IV or ICD-10 diagnos-
logical ages. Inter-rater reliability was assessed for a sam- tic criteria of autism and nonautistic ASD. One caveat for
ple of ten children with autism and ten without, with clinical users is that they should be aware that diagnostic
multirater kappas ranging from 0.55 to 0.94 for each algorithm result and a true clinical diagnosis are not the
item and intraclass correlations above 0.94 for all subdo- same. Clinical diagnosis is based on multiple sources of
main and domain scores. The majority of individual items information, including direct observation. Thus, even
showed good discriminative validity showing diagnostic though the ADI-R provides broader contexts including
differences across autistic and mentally handicapped the information about history or functioning of a child
groups (Le Courteur et al., 1989). than observations, ADI-R alone cannot be used to make a
Psychometric properties for the current ADI-R were complete standard diagnosis.
provided for a carefully selected, blindly interviewed and Current Behavior Algorithms can be used to assess the
coded, sample of 25 autistic and 25 mentally handicapped participants current behavior. This can be used in clinical
children ranged in chronological age from 36 to 59 settings to assess changes brought about by intervention
months, with mental ages ranging from 21 to 74 months. or changes reflecting increasing developmental maturity
Inter-rater reliability was assessed, with multirater kappas or changing life circumstances.
ranging from 0.63 to 0.89 for each item and intraclass The ADI-R should only be used by appropriately
correlations above 0.92 for all subdomain and domain experienced clinicians. Interviewers must be familiar
scores. Following the initial standardization study of the with the concepts of ASD and relevant behaviors. Training
ADI-R, a further study was undertaken of a separate workshops and videotapes are available to help clinicians
sample of 53 children with autism and 41 nonautistic understand the scoring and administration of the ADI-R.
children with mental handicap or language impairments
(Lord et al., 1993). Inter-rater reliability was as high as the
initial study, with multirater kappas ranging from 0.62 to Cross References
0.96 for individual items. Test-retest reliability was very
high, with all coefficients being in the 0.930.97 range. Autism Diagnostic Observation Schedule
Majority of individual items showed good discriminative Autistic Disorder
validity showing diagnostic differences across autistic and Childhood Autism Rating Scales
mentally handicapped groups (see Lord et al., 1994). The Modified Checklist for Autism in Toddlers (M-CHAT)
algorithm cutoffs were determined by identifying the also CHAT
point within each area that yielded the best combination
of sensitivity and specificity both exceeding 0.90.
American Psychiatric Association. (1993). Options book for DSM-IV.

Clinical Uses Washington, DC: Author.
DiLavore, P., Lord, C., & Rutter, M. (1995). The pre-linguistic autism
The ADI-R offers a profile of a child in different areas diagnostic observation schedule (PL-ADOS). Journal of Autism and
including language/communication, reciprocal social Developmental Disorders, 25, 355379.
Le Couteur, A., Rutter, M., Lord, C., Rios, P., Robertson, S.,
interactions, and restricted, repetitive, and stereotyped
Holdgrafer, M., et al. (1989). Autism diagnostic interview: A
behaviors and interests based on the parents detailed semistructured interview for parents and caregivers of autistic persons.
descriptions of the history and behaviors of the child. It Journal of Autism and Developmental Disorders, 19, 363387.
can provide a comprehensive description of a child both Lord, C., Rutter, M., & Le Couteur, A. (1994). Autism diagnostic
currently and in earlier ages, but must be used in interview-revised: A revised version of a diagnostic interview for
caregivers of individuals with possible pervasive developmental
conjunction with observations and/or direct testing in
disorders. Journal of Autism and Developmental Disorders, 24(5),
making a diagnosis of ASD. The ADI-R can provide a 659685.
useful structure to obtain history and understand a Risi, S., Lord, C., Gotham, K., Corsello, C., Chrysler, C., Szatmari, P., et al.
parents perspective on their childrens symptoms (2006). Combining information from multiple sources in the
Autism Diagnostic Observation Schedule A 315
diagnosis of autism spectrum disorders. Journal of the American order to make judgments about social and communicative
Academy of Child and Adolescent Psychiatry, 45, 10941103. A
abilities as independent as possible from the effects of
Rutter, M., Le Couteur, A., & Lord, C. (2003). Autism diagnostic
interview-revised. Los Angeles: Western Psychological Services.
absolute level of language delay. Each module has its own
World Health Organization. (1992). The ICD-IO classification of mental protocol, which contains a schedule of activities designed
and behavioral disorders: Clinical descriptions and diagnostic guide- for use with children or adults at particular developmental
lines. Geneva: Author. and language levels. Recently, the Toddler Module of the
ADOS was developed for use in children between 12 and 30
months of age in addition to the original four modules
(Lord, Luyster, Gotham, & Guthrie, in press).
Module 1 is intended for children who do not use
Autism Diagnostic Observation spontaneous phrase speech consistently. It consists of 10
Schedule activities with 29 accompanying ratings. Module 2 is
intended for children with some flexible phrase speech
S O H YUN K IM , C ATHERINE L ORD who are not verbally fluent. It consists of 14 activities with
University of Michigan Autism and Communication 28 accompanying ratings. Module 3 provides 13 activities
Disorders Center (UMACC) and 28 ratings. It is intended for verbally fluent children
Ann Arbor, MI, USA for whom playing with toys is age-appropriate. The oper-
ational definition of verbal fluency is the spontaneous,
flexible use of sentences with multiple clauses that de-
Synonyms scribe logical connections within a sentence. It requires
the ability to talk about objects or events not immediately
ADOS present. Module 4 contains the socioemotional questions,
along with interview items about daily living and addi-
tional tasks. It is intended for verbally fluent adults and
Description for adolescents who are not interested in playing with toys
such as action figures (usually over 1216 years). This
The Autism Diagnostic Observation Schedule (ADOS; module consists of 1015 activities with 31 accompanying
Lord, Rutter, DiLavore, & Risi, 2001) is a semistructured, ratings. The difference between Modules 3 and 4 lies
standardized assessment of communication, social interac- primarily in whether information about social communi-
tion, and play or imaginative use of materials for individuals cation is acquired during play or through a conversational
who have been referred because of possible autism spectrum interview. It is important to note that adolescents or
disorders (ASD). As part of the schedule, planned social adults may feel uncomfortable when presented with the
occasions, referred to as presses (Lord, Rutter, Goode, & toys for young children that are available in modules 1
Heemsbergen, 1989) are created in which a range of social and 2; suggestions for modifying the earlier modules to be
initiations and responses is likely to appear. In the same appropriate for older children or adults who are less
way, communication opportunities are designed to elicit verbal are available from the authors. In addition to the
a range of interchanges. Play situations are included four modules, the Toddler Module is intended for chil-
to allow observation of a range of imaginative activities dren between 12 and 30 months of age who should have a
and social role-play. A variety of structured activities nonverbal age equivalent of at least 12 months and be
and materials, and less structured interactions, provide walking independently. It consists of 11 activities with 41
standard contexts within the ADOS in which the social, accompanying ratings (Lord et al., in press).
communicative, and other behaviors relevant to the The ADOS provides the diagnostic algorithms that are
understanding of ASD are observed. sets of rules that allow classification of autism or ASD.
The ADOS consists of four modules. Each module is Separate diagnostic algorithms for each module can be
appropriate for children and adults at different develop- generated using subsets of items in each module. Items
mental and language levels, ranging from no expressive or and the thresholds for the classification of autism and of
receptive use of words, to fluent, complex language in an ASD in the algorithms differ for each module. However,
adult. Only one module, lasting about 30 minutes, is admi- the general principles and procedures for computation are
nistered to any individual at a given point of time. In the the same across modules and similar to the DSM-IV
ADOS, the examiner uses the module that best matches the (American Psychiatric Association, 1993) and ICD-10
expressive language skills of the individual child or adult in (World Health Organization, 1992). The algorithms for
316 A Autism Diagnostic Observation Schedule
Module 1, 2, and 3 were recently revised from the previ- there was a need to extend the age and verbal limits of the
ous algorithms (Gotham, Risi, Pickles, & Lord, 2007). ADOS to be appropriate for younger and nonverbal chil-
Reflecting recent research, the revised algorithms now dren. The PL-ADOS was then created based on the grow-
consist of two new domains, Social Affect and Restricted, ing interest in using the instruments in clinical settings,
Repetitive Behaviors, combined to one score to which which addressed the concerns of parents and fit the abil-
thresholds are applied, resulting in generally improved ities of children functioning at infant and toddler levels.
predictive validity compared to the previous algorithms. As a result, it included more flexible, briefer activities and
The module 1 consists of no words and some words greater use of play materials for nonverbal young children
algorithms by language level. The module 2 includes that served as a downward extension for the ADOS, rather
Younger than 5 and Greater or Equal to 5 algorithms than a replacement. The PL-ADOS was effective in dis-
by chronological age. Module 3 includes a single algo- criminating 25-year-old-children with autism from chil-
rithm. All items appearing on the new algorithms con- dren with non-autism spectrum developmental delays
tribute to a single score with two classification thresholds, (DiLavore et al., 1995). However, it tended to be under-
one for autism and another for ASD. There are the inclusive for children with autism who had some expres-
Toddler Module algorithms for children between 12 and sive language. Thus, a tool was required to address the
30 months, who do not have phrase speech; once children needs of children who fell between the PL-ADOS and
have developed phrase speech, they should be adminis- ADOS in language skills. Furthermore, the ADOS con-
tered module 2. Since differential diagnosis can be chal- sisted primarily of activities intended for school-age chil-
lenging especially in toddlers, the toddler module dren. Additional or alternative tasks were needed for
algorithms generate range of concern (little-or-no con- adolescents and adults. The current edition of the ADOS
cern; mild-to-moderate concern; moderate-to-severe was designed in response to these factors. The current
concern) rather than strict classifications. ADOS differs from the preceding instruments in a way
Most of the ADOS pertains to behaviors that are rare that it is aimed at providing standard contexts for the
in individuals who do not have ASD and/or who do not observation of behavior for a broader developmental and
have profound intellectual disabilities. Thus, numerical age range of individuals suspected of having autism. Thus,
estimates of the typical scores of general population the current ADOS includes additional items developed for
have not been obtained. Scores from module 1 to 3 have verbally fluent, high-functioning adolescents and adults
now been calibrated for children with ASD to yield a as well as younger and nonverbal children.
standard severity score based on a large sample (see However, even though this updated version of the
below; Gotham, Pickles, & Lord, in press). ADOS did indeed extend the usefulness of the original
ADOS below a language level of 3 years, research has indi-
cated that it remained of limited value for children with
Historical Background nonverbal mental age below 16 months. Thus, a standar-
dized diagnostic measure applicable for infant and young
In its present form, the current WPS Edition of the ADOS toddlers was also needed for early identification (Gotham
(Lord et al., 2001) is a combination of two similar diag- et al., 2007). The recent development of the Toddler Mod-
nostic instruments: the 1989 version of the ADOS (Lord ule of the ADOS reflects this need for the measure to be
et al., 1989) and the Pre-Linguistic ADOS (PL-ADOS; applicable to very young children from 12 to 30 months.
DiLavore, Lord, and Rutter, 1995). The ADOS was first The original algorithms included two domains, social
introduced in the 1980s as a method of standardizing interaction and communication. Recently, Gotham et al.
direct observations of social behavior, communication, (2007) revised algorithms for module 1, 2, and 3, and
and play in children suspected of having autism. It was the existing social and communication domains were
intended to be administered to children between the ages merged, and the domain of Restricted Repetitive Beha-
of 5 and 12, who had expressive language skills at least at viors (RRB) was newly included. The revised algorithms
the 3-year-old level. It was proposed as a complementary resulted in increased specificity and sensitivity proving
instrument to the Autism Diagnostic Interview (ADI; Le increased diagnostic validity compared to the previous
Couteur et al., 1989), an investigator-based parent or algorithms. Furthermore, even though the inclusion of
caregiver interview that yielded a description of history, the RRB domain did not improve predictive value of the
as well as current functioning, in areas of development ADOS in differentiating individuals with autism from
related to autism. Because children under age five consti- those with pervasive developmental disorder not
tute the bulk of referrals for a first diagnosis of autism, otherwise specified (PDD-NOS; also referred as ASD), it
Autism Diagnostic Observation Schedule A 317
aided in distinguishing PDD-NOS from non-spectrum Psychometric properties for the Toddler Module were
A
cases. provided for a sample of 182 different participants. The
sensitivity of each algorithm ranged from 83% to 91%
and specificity from 86% to 94%. Inter-rater item and
Psychometric Data domain reliability was greater than .71, and inter-rater
algorithm reliability ranged from .60 to .90. Intraclass
Psychometric properties for the original ADOS were correlations ranged from .74 to .99 for all algorithm
provided for a carefully selected, blindly interviewed and domains and total scores (Lord et al., in press).
coded, sample of 223 children and adults with autistic
disorder (autism), pervasive developmental disorder
not otherwise specified (PDD-NOS) or non-spectrum Clinical Uses
(NS) diagnoses. Inter-rater reliability was assessed, with
mean multirater kappas of all items for each module rang- Use of the ADOS is related to the examiners clinical skills
ing from .65 to .78 and intraclass correlations above .82 for and experience with the instrument. Examiners need to be
all subdomain and domain scores. Test-retest reliability sufficiently familiar with the ratings and the activities so
varied by subdomain ranging from .59 to .82. In the origi- that they can focus their attention on observation of the
nal sample, the ADOS algorithms generally achieved 94% individual being assessed, rather than on administration
correct classification. The exceptions were the ASD versus of tasks. The examiner should have sufficient practice in
non-spectrum (NS) module 2 specificity of 87% and observation of ASD symptoms and scoring of the ADOS
module 3 sensitivity of 90%, and the PDD-NOS versus items, as well as in administering the activities. Examiners
NS Module 2 specificity of 88% and sensitivity of 89% are encouraged to attend workshops, use videotapes, or
and module 3 sensitivity of 80% (Lord et al., 2001). work with colleagues to obtain inter-rater reliability be-
Psychometric properties for the newly revised algo- fore administering the ADOS for clinical or research pur-
rithms were provided for a sample of 1,139 different poses (Lord et al., 2001). Examiners should note that the
participants. The revised algorithms resulted in increased Toddler Module and module 1 are always administered
specificity in classifying non-autism ASD in lower func- with parents or caregivers in the room, which provides an
tioning populations, evidenced by the 1231% increase in opportunity to show a parent, examples of behaviors that
specificity for children without any words (depending on define ASD, and get information from a parent about the
nonverbal mental age) and the modest gain in specificity validity of the childs behaviors during the testing session.
for older children who have not progressed beyond phrase Because the ADOS consists of codings made from a single
speech. During module 1, no words improved in each observation, it does not include information about histo-
diagnostic comparison (e.g., from the sensitivity of 19% ry or functioning in other contexts. This means that the
to 50% for children with nonverbal mental age of 15); ADOS alone cannot be used to make a complete standard
the specificity of both module 2 groups improved for diagnosis, but used in conjunction with other testing.
non-autism ASD versus NS (e.g., from 77% to 83% Lord and her colleagues suggested several strategies
for children greater or equal to 5). For autism versus that clinicians or researchers may take to measure how
non-spectrum and for ASD versus NS, the new and old behaviors of individual may have changed over time by
algorithms performed approximately equally well in using the ADOS item and domain scores (Lord et al.,
terms of sensitivity. For non-autism ASD versus non- 2000). If an individual has been administered the same
spectrum, sensitivity of the new algorithm was somewhat module more than once, raw scores on individual items
lower in module 1, no words (as was necessary to raise and on algorithm domains can be compared. If an indi-
specificity; e.g., 100% in old algorithm versus 97% in new vidual has changed modules, raw scores on items that
algorithm for children under nonverbal mental age under remain constant across modules (about two thirds of
15), but it showed improvement from the old algorithm each contiguous module) can be compared, yet compari-
in the higher-functioning modules 1 (AUT versus NS; son of raw domain scores is not meaningful. However, the
from 88% to 97%) and module 2 (ASD versus NS; from ADOS calibrated scores recently developed by Gotham
76% to 84%) cells. Inter-rater reliability on the ADOS was et al. (in press) can be used in this case to compare
monitored through joint administration and scoring by assessments across modules and time. The calibrated
two different examiners for at least 1 in 10 cases and, in scores have more uniform distributions across age- and
some cases, through scoring of videotapes. Agreement language-groups compared to raw totals, which make it
remained at greater than 85% (Gotham et al., 2007). possible to compare childrens scores longitudinally across
318 A Autism Spectrum Disorder
distinct algorithms. Thus, calibrated scores can be useful DiLavore, P., Lord, C., & Rutter, M. (1995). Pre-linguistic autism diag-
nostic observation schedule (PL-ADOS). Journal of Austism and
in clinical settings to test treatment responsiveness and
Developmental Disorders, 25, 355379.
other clinical outcomes in individuals with ASD. Gotham, K., Pickles, A., & Lord, C. (in press). Standardizing ADOS
In addition, it was suggested that more detailed scores for a measure of severity in autism spectrum disorders.
coding of communication samples or particular behaviors Journal of Autism and Developmental Disorders.
(e.g., pragmatics, sentence structure, gestures) may also be Gotham, K., Risi, S., Pickles, A., & Lord, C. (2007). The autism diagnostic
observation schedule: Revised algorithms for improved
carried out from videotapes of the ADOS. Other observa-
diagnostic validity. Journal of Autism and Developmental Disorders,
tional coding schemes that address specific aspects of 37, 613627.
behavior in more detail may also be applied using the Le Couteur, A., Rutter, M., Lord, C., Rios, P., Robertson, S.,
ADOS as a way of obtaining a discrete sample of behavior Holdgrafer, M., et al. (1989). Autism diagnostic interview: A
in standard contexts. Often, clinicians carrying out diag- semistructured interview for parents and caregivers of autistic per-
sons. Journal of Autism and Developmental Disorders, 19, 363387.
nostic assessments may wish to make programming
Lord, C. E., Luyster, R., Gotham, K., & Guthrie, W. J. (in press). Autism
suggestions for parents/caregivers, therapists, or teachers. diagnostic observation schedule toddler module. Los Angeles, CA:
Many of the activities and codes of the earlier modules Western Psychological Services.
have fairly straightforward implications both for how to Lord, C., Risi, S., Lambrecht, L., Cook, E. H., Leventhal, B. L., DiLavore,
teach an individual child and for the content of appropri- P., et al. (2000). The autism diagnostic observation schedulegeneric:
A standard measure of social and communication deficits associated
ate goals. For example, module 1 provides opportunities
with the spectrum of autism. Journal of Autism and Developmental
for children to make requests in a number of circum- Disorders, 30(3), 205223.
stances, including requests for action (i.e., the examiner Lord, C., Rutter, M., DiLavore, P. C., & Risi, S. (2001). Autism diagnostic
to blow a balloon), requests for food, requests to continue observation schedule. Los Angeles, CA: Western Psychological
a social game, and requests for an object or activation of Services.
Lord, C., Rutter, M., Goode, S., & Heemsbergen, J. (1989). Autism
that object (i.e., operating a bubble gun). Noting how
diagnostic observation schedule: A standardized observation of
children make requests and in what circumstances they communicative and social behavior. Journal of Autism and Develop-
are most easily able to communicate their interest or mental Disorders, 19(2), 185212.
needs, allows the clinician to create goals to teach new Lord, C., Rutter, M., & Le Couteur, A. L. (1994). Autism diagnostic
request behaviors and to help the children generalize interview-revised: A revised version of a diagnostic interview for
caregivers of individuals with possible pervasive developmental dis-
existing behaviors across contexts. Generating program-
orders. Journal of Autism and Developmental Disorders, 24(5),
ming goals from modules 3 and 4 may be somewhat more 659685.
complex, because fewer codes describe specific behaviors World Health Organization. (1992). The ICD-IO classification of mental
that may be usefully taught in a direct fashion. Realizing and behavioral disorders: Clinical descriptions and diagnostic
the degree to which adults with autism have limited guidelines. Geneva, Switzerland: Author.
insight into the nature of social relationships, or having
the opportunity to observe adolescents describing the
emotions of the main characters in a story, can be helpful
in representing the strengths they may have and
difficulties they experience in social interaction. Autism Spectrum Disorder
Pervasive Developmental Disorder NOS
Cross References
Autism Diagnostic Interview-Revised (ADI-R)
Autistic Disorder Autistic Disorder
Childhood Autism Rating Scales
Modified Checklist for Autism in Toddlers (M-CHAT) F RED R. VOLKMAR
also CHAT Yale University
New Haven, CT, USA

Synonyms
American Psychiatric Association. (1993). Options book for DSM-IV.
Washington, DC: Author. Childhood autism; Infantile autism; Kanners syndrome
Autistic Disorder A 319
Short Description/Definition Rates of autistic disorder are typically three to four

A
times higher in boys than in girls. The nature of this
Autistic disorder is a neurodevelopmental condition char- gender difference remains unclear, but speculation has
acterized by marked problems in social interaction, com- centered on lower thresholds for expression of the con-
munication/play, and a set of unusual behaviors related to dition in boys. An early impression of increased rates in
difficulties in tolerating change in the environment. The better educated families appears to have been due to
condition is of early onset. In most cases, it appears to be referral bias and has not been supported by later work.
congenital, but perhaps in 20% of cases, a period of
normal development is observed. The condition always
appears before 3 years of age.
Outcomes
Categorization
Issues of diagnosis can be complex in infants as not all
Autism was first described by Leo Kanner in 1943 (Kanner, required features may be exhibited until around age 3
1943). Early controversy centered around the idea that (Lord & Venter, 1992). After that time, diagnostic agree-
autism might be a form of schizophrenia, but several lines ment increases substantially. By school age, autistic chil-
of evidence suggest this is not the case. Changes in dren become more sociable and may make significant
approaches to the definition of autism have occurred academic gains although behavioral difficulties are prom-
over time. Currently, both the American Psychiatric inent. During adolescence, some children make
Association (DSM-IV-TR) (World Health Organization, substantial gains and others lose skills. There is increased
2000) and International (ICD-10) (World Health Organi- risk for development of epilepsy throughout the develop-
zation, 1994) categorization systems define autistic disor- mental period, with peak frequencies of new onset of
der in essentially the same way. Autistic disorder is one or epilepsy in early childhood and adolescence (Volkmar &
a group of conditions referred to as the pervasive devel- Nelson, 1990).
opmental disorders (PDD). Other conditions in that class The first studies of long-term outcome in children
include Aspegers disorder (in which marked social defi- with autism were relatively pessimistic with only 23%
cits are observed but some aspects of language are rela- of cases being able to achieve adult independence and self-
tively preserved); Retts disorder (a condition largely sufficiency. Several factors appear to significantly improve
confined to girls and characterized by marked deteriora- prognosis: cases are now detected at early ages (when
tion in motor, cognitive, and communicative skills); child- intervention may be more effective (National Research
hood disintegrative disorder (a rare condition where at Council, 2001), and in many countries, educational ser-
least 2 years of normal development precedes the emer- vices are now mandated). It appears that at least 20% or
gence of an autistic like illness); and PDD-NOS (not more of children with autism are capable of self-sufficiency
otherwise specified) a term reserved for cases exhibiting in adulthood with at least another 1520% able to be
some features of autism but not the full syndrome. largely independent (Howlin, 2005). Major predictors of
long-term outcome include nonverbal cognitive ability
and the capacity to use language to communicate only
Epidemiology around age 5. Adaptive abilities (the ability to cope with
real world situations) are also important particularly as
A number of epidemiological studies have been undertaken
the person becomes older.
around the world. Their interpretation is complicated by
methodological differences including case finding and defi-
nitions used. The earliest studies reported rates on the
order of 1 in 2,000 children, but more recent work suggests Neuropsychology and Psychology
that a figure of 1 in 8001,000 children is probably more of Autistic Disorder
accurate; the broader PDD spectrum is much more ambig-
uously defined and probably affects as many as 1 in 150 The first attempts to develop psychological models of
children (Fombonne, 2005). Much debate has centered on autism centered around the notion that experiential fac-
whether autism is increasing in frequency, but this issue tors might be involved. As evidence of brain involvement
remains unclear despite better methods of case detection accumulated, theories shifted to focus on neurocognitvie
and greater public awareness (Fombonne, 2005). and brain-based mechanisms.
320 A Autistic Disorder
Several neurocognitive models/theories have been

proposed. One approach posits difficulties in executive
functioning skills; this model would account for some of
the problems with shifting set and perseveration typical of
individuals with autism (Ozonoff et al., 2005). However,
deficits in these areas are not specific to autism and are
not strongly related to the extent of social vulnerability.
Another approach has focused on difficulties in what is
termed Central Coherence or the capacity to integrate
information into coherent or meaningful wholes (Happe,
2005). This model centers on problems resulting from
difficulties in selective attention and appreciation of social
meaning. Another approach posits difficulties in under-
standing and empathizing with others (Baron-Cohen,
1989). This Theory of Mind hypothesis has been very
Autistic Disorder. Figure 1 Visual focus of an autistic man
productive for research. It presumes that difficulties
and a normal comparison subject showing a film clip of a
arise as a result of an inability to understanding feelings,
conversation. Typically developing person (top line) goes back
intention, and social meaning. Weaknesses of this
and forth between the eyes in viewing a social scene, a high
approach include the fact that more able individuals
functioning person with autism goes back and forth between
with autism can solve usual theory of mind type pro-
the mouths of the speakers. Reprinted with permission from
blems; a second problem arises because many of the first
Klin, Jones, Schultz, Volkmar, and Cohen (2002)
features of autism appear before usual theory of mind
skills are established in typically developing infants. A
amount of social-affective information (Klin, Jones
relatively newer approach, Enactive Mind, has attempted
et al., 2002).
a synthesis of insights from studies of social cognitive
Beginning with the first twin studies of autism in the
information processing in autism with normal develop-
late 1970s a considerable body of work has strongly impli-
mental perspectives (Klin, Jones et al., 2003) (Fig. 1).
cated genetic factors in the pathogenesis of autism. There
A focus on specific brain mechanisms was suggested
are significantly increased rates of autism in identical
by high rates of epilepsy and various neurological signs
twins and a higher risk in siblings both of autism and a
and symptoms (e.g., persistence of primitive reflexes,
range of other developmental problems. It appears that
delayed development of hand dominance, etc.). A range
multiple genes are involved and several candidate genes
of abnormalities has been found in post-mortem studies.
are now being studied (Rutter, 2005).
Lesion studies, e.g., of the amygdala or hippocampus,
have produced some behaviors in monkeys similar to
some of those seen in autism (Bachevalier, 1996). Other Evaluation
studies have focused on abnormalities in the cerebellum
and overall brain size which appears to be increased in Evaluation of the child with autism typically involves
autism (Courchesne et al., 2004). the efforts of members of several different disciplines
Other approaches have focused on specific neuropsy- psychology, speech-language pathology, medicine, occu-
chological processes. For example, Scultz and colleagues pational and physical therapy, and special education.
(Schultz et al., 2000) used fMRI techniques to demon- Goals for evaluation include clarification of the diagnosis
strate that more cognitively able individuals with and establishment of patterns of strengths/weakness that
autism process faces differently than typical controls; have implications for programming. Medical evaluations
essentially they fail to activate the fusiform face area. are indicated to look for conditions like Fragile X syn-
This observation is of interest given a large body of drome and seizures sometimes associated with autism
experimental work on differences in face processing in (Volkmar et al., 1999).
autism. Another work, e.g., using eye tracking technol-
ogy, has revealed marked differences in scanning of the Treatment
environment during social situations with more able
individuals with autism tending to focus on the lower Over the past decade a considerable body of work on
half of the face or objects, thus losing a considerable intervention has become available. In its influential 2001
Autobiographical Memory A 321
review a panel from the US National Research Council Kanner, L. (1943). Autistic disturbances of affective contact. Nervous
Child, 2, 217250. A
systematically evaluated ten treatment programs for youn-
Klin, A., Jones, W., Schultz, R., Volkmar, R., & Cohen, D. (2002). Visual
ger children with autism. Although differing in some fixation patterns during viewing of naturalistic social situations as
respects these programs shared many similarities including predictors of social competence in individuals with autism. Archives
intensive individualized programs and structured teach- of General Psychiatry, 59(9), 809816.
ing. Many, although not all, of these programs make ex- Klin, A., Jones, W., Schultz, R., & Volkmar, F. (2003). The enactive mind,
or from actions to cognition: Lessons from autism. Philosophical
tensive use of applied behavior analytic principles to teach
Transactions of the Royal Society of London, Series B: Biological
basic skills which can then be expanded. Increasing social Sciences, 358(1430), 345360.
and communication abilities are important goals. Psycho- Klin, A., Jones, W., Schultz, R., Volkmar, F., & Cohen, D. (2002). Defining
therapy is not a mainstay of treatment but is sometimes and quantifying the social phenotype in autism. American Journal of
used in older and more able individuals but is to be Psychiatry, 159, 895908.
Lord, C., & Venter, A. (1992). Outcome and follow-up studies of high-
problem-focused in nature.
functioning autistic individuals. In E. Schopler & G. B. Mesibov
Drug treatments can be helpful relative to certain symp- (Eds.), High-functioning individuals with autism current issues in
toms (e.g., agitation, stereotyped mannerisms) but do not autism (Vol. xviii, pp. 187199; 316). Plenum: NY.
address the core social deficit (Scahill & Martin, 2005). National Research Council. (2001). Educating young children with autism.
Washington, DC: National Academy Press.
Ozonoff, S., South, M., & Provencal, S. (2005). Executive functions.
Cross References In F. R. Volkmar, A. Klin, R. Paul, & D. J. Cohen (Eds.), Handbook
of autism and pervasive developmental disorders (3rd edn,
Adaptive Behavior pp. 60627). New York: Wiley.
Rutter, M. (2005). Genetic influences and autism. In F. R. Volkmar,
ADI
A. Klin, R. Paul, & D. J. Cohen (Eds.), Handbook of autism and
ADOS pervasive developmental disorders (Vol. 1, pp. 425452). Hoboken,
Applied Behavior Analysis NJ: Wiley.
Asperger Disorder Scahill, L., & Martin, A. (2005). Psychopharmacology. In F. R. Volkmar,
Behavior Modification A. Klin, R. Paul, & D. J. Cohen (Eds.), Handbook of autism and
pervasive developmental disorders (Vol. 2, pp. 11021122). Hoboken,
Epilepsy
NJ: Wiley.
Executive Functioning Schultz, R. T., Gauthier, I., Klin, A., Fulbright, R. K., Anderson, A. W.,
Intellectual Disability Volkmar, F. (2000). Abnormal ventral temporal cortical activity
TEACCH during face discrimination among individuals with autism and
Vineland II Asperger syndrome. Archives of General Psychiatry, 57(4), 331340.
Volkmar, F., Cook, E. Jr., Pomeroy, J., Realmuto, G., Tanguay, P. (1999).
Summary of the practice parameters for the assessment and treat-
References and Readings ment of children, adolescents, and adults with autism and other
pervasive developmental disorders. Journal of the American Academy
American Psychiatric Association. (2000). Diagnostic and statistical man- of Child and Adolescent Psychiatry, 38(12), 16111616.
ual (4th ed., Text Rev.). Washington, DC: APA Press. Volkmar, F. R., & Nelson, D. S. (1990). Seizure disorders in autism.
Bachevalier, J. (1996). Brief report: Medial temporal lobe and autism: Journal of the American Academy of Child and Adolescent Psychiatry,
A putative animal model in primates. Journal of Autism and 29(1), 127129.
Developmental Disorders, 26(2), 217220. World Health Organization. (1994). Diagnostic criteria for research.
Baron-Cohen, S. (1989). The theory of mind hypothesis of autism: Geneva: World Health Organization.
A reply to Boucher [comment]. The British Journal of Disorders of
Communication, 24(2), 199200.
Courchesne, E., Redcay, E., Kennedy, D. P. (2004). The autistic brain: Birth
through adulthood. Current Opinion in Neurology, 17(4), 489496.
Fombonne, E. (2005). Epidemiological studies of pervasive develop- Autobiographical Memory
mental disorders. In F. R. Volkmar, A. Klin, R. Paul, & D. J. Cohen
(Eds.), Handbook of autism and pervasive developmental disorders
K ATHERINE T YSON
(Vol. 1, pp. 4269). Hoboken, NJ: Wiley.
Happe, F. (2005). The weak central coherence account of autism. In University of Connecticut
F. R. Volkmar, A. Klin, R. Paul, & D. J. Cohen (Eds.), Handbook of Storrs, CT, USA
autism and pervasive developmental disorders (Vol. 1, pp. 640649).
Hoboken, NJ: Wiley.
Howlin, P. (2005). Outcomes in autism spectrum disorders. In
F. R. Volkmar, A. Klin, R. Paul, & D. J. Cohen (Eds.), Handbook of
Synonyms
autism and pervasive developmental disorders (Vol. 2, pp. 201222).
Hoboken, NJ: Wiley. Memory; Personal memory; Recollective memory
322 A Autobiographical Memory
Definition problems as they examine lessons from past events and

think about how future events and behavior might turn
Autobiographical memory (AM) is the memory of events out.
or information involving the self. Researchers generally As a cultural mechanism, in particular, AM helps not
conceptualize AM as episodic, as opposed to semantic. only to shape the individual self, but also to provide the
AMs are temporally defined (e.g., by the date of the individual with a sense of identity in relation to a wider
remembered event) and involve a sense of recollection or community (Bluck, 2003). In EuroAmerican societies,
reliving of the original event (Greenberg & Rubin, 2003). AM appears to emerge around three-and-a-half years of
age, as adults begin to share memories with their children.
Some cultural differences have emerged in the nature of
Historical Background AM. Asian societies, for example, may report fewer AMs
and have fewer and later memories from earlier childhood
Levin, Benton, and Grossman (1982) are sometimes cred- compared to EuroAmericans. Whereas collective identity
ited with originating the term AM. However, AM research may be the focus in these societies, Americans tend to
dates back to Francis Galtons 1879 study of his own recall focus on creating a unique identity; AM is essential to this
of events in his personal past. Galton sampled his own development of a self.
episodic memories by finding associations between words In its role of aiding self-development, AM may also
and events from his past and dating those events. In 1974, drive positive perceptions of self and emotion regula-
Crovitz and Schiffman modified Galtons technique to tion. Research by Wilson and Ross (Bluck, 2003) has
create what became a widely used method for studying shown that remembering positive events often brings
AM (see Rubin, 1999). Their revised technique involved about a positive mood. Furthermore, the third person,
asking participants to think of memories associated with observers perspective from which people often remember
words presented to them. In 1983, Nigro and Neisser negative life events gives them distance from those events,
pioneered studies examining the effect of point of view which may also promote well-being. Sharing of AMs with
on AM in their studies of field memories (viewed from the others may aid emotion regulation.
same viewpoint as originally experienced) and observer As a facilitator of social interaction AM helps people
memories (viewed from an observers perspective). to reflect on and share recollections of the past with one
They found that older memories were more often viewed another. Fivush et al. (Bluck, 2003) have suggested that in
from the observer point of view than recent memories motherchild relationships, sharing of AMs may help
(see Rubin, 1999). Current research has spanned a variety children to learn how to deal with and express emotions,
of areas, including examining AMs functional mechan- particularly negative ones.
isms, studying psychopathologys potential effects on AM, In its directive function, AM guides current behavior
and investigating AMs neuropsychological underpin- and functioning. Both everyday and traumatic memories
nings through imaging studies. guide peoples present decisions and actions.
Current Knowledge Methods in AM Research
Phenomenology Several methods have been developed for studying AM.

Given its complexity and the lack of consensus about
Much of the recent research on AM has concentrated on how AM works, no single method has emerged as a
AMs function. Pillemer (1992) posited that AM has gold standard; rather, these methods are often used in
three basic functions: self-related, communicative (so- combination.
cial), and directive (planning for present and future Open-ended methods include the word-cue method,
events) (Bluck, 2003). In serving the self, AM helps people similar to Galtons original method. Participants are
to develop a sense of coherence and continuity in defining presented with cue words or other stimuli and asked to
who they are through memories. In its communicative think of memories. Typically, after the cued portion of
role, AM provides the content of conversations and facil- such a study, the researcher will ask the participants to
itates building intimacy in social relationships. Sharing of date the memories. This method has tended to provide
AMs can also inform and teach others about the sharers consistent results, lending support to expected findings:
world. As a directive tool, AM can help people solve childhood amnesia of early life memories, retention of the
Autobiographical Memory A 323
memories of the most recent two decades, and for people with her mother on Tuesdays, as opposed to remembering
A
over age 40, an increase in memories about adolescence a specific one of those Tuesday lunches.
and early adulthood (Wenzel & Rubin, 2005). This cueing Research also indicates that trauma and non-trauma
method is most commonly applied using the Autobio- memories differ substantially in clinical, but not in healthy
graphical Memory Test, first described in 1986 by populations (Dalgleish & Brewin, 2007). While involun-
Williams and Broadbent (Wenzel & Rubin, 2005). A second tary memory may be enhanced in some clinical popula-
open-ended method involves simply asking a participant tions, voluntary memory is often fragmented, incomplete,
about his or her life. A more structured approach, the and disorganized, particularly in people with a trauma
involuntary-memory-diary method, asks participants to history. PET and fMRI studies have suggested that the
keep a diary record of involuntary AMs as they occur. retrieval of trauma memories in PTSD patients is char-
Some other methods for delving into AM are more acterized by increased activity of limbic and paralimbic
closed-ended. The Autobiographical Memory Interview, areas, including the amygdala. Additionally, researchers
developed by Kopelman, Wilson, and Baddeley, was have found deactivation of the medial prefrontal areas
designed to be used with neuropsychological patients and Brocas area and decreased hippocampal activity in
(Wenzel & Rubin, 2003). The interview asks for specific PTSD patients when they processed emotional, rather
kinds of memories from specific time periods. The partic- than neutral material.
ipant is not provided a choice as to the types of memories In looking at depressed individuals, studies have
he or she will share. In the diary recall method, partici- suggested that cues reflecting personal characteristics
pants record events and subsequently receive a memory are more likely to promote a shift to processing of infor-
test for these events. Unlike the other methods, the diary mation within the long-term view of the self, increasing
recall method can provide some measure of the accuracy the likelihood that self-related semantic information will
of memories. A final method, the questionnaire method, be provided in response to cues on the Autobiographical
asks participants to report on a series of properties Memory Test. In a different, but related line of research,
of AMs; this method is often used in conjunction euthymic individuals with a history of depression and
with other approaches. Recently, Sutin and Robins patients with a borderline personality disorder retrieved
(2007) have developed The Memory Experiences Question- less specific AMs in response to cue words that matched
naire, a measure designed to assess a comprehensive range highly endorsed attitudes or schema. This finding suggests
of dimensions of AM. that an impaired retrieval of specific memories may be the
In developing methods to study such a multifaceted result of certain cues activating generic, higher-order
phenomenon as AM, researchers focus on several variables mental representations in people with both psychopathol-
of interest. These variables include: whether the memory is ogy histories and present diagnoses (Dalgleish & Brewin,
general or specific, latency to retrieve a memory, number of 2007; Hermans et al., 2006). Generally dysfunctional atti-
omissions (i.e., when a person does not present a specific tudes, whether in an individual exhibiting psychopathol-
personal memory for certain stimuli presented), age of mem- ogy or in a healthy individual, could play a part in an
ories, and affective tone. Studies have shown that the last of individuals inability to retrieve specific memories.
these variables, affective tone, can potentially differentiate
AMs of people with psychopathology from AMs of people
without psychopathology (Dalgleish & Brewin, 2007). Neuropsychology
Although researchers have studied the neuropsychology

AM and Psychopathology of AM specifically, knowledge about the neuropsychology
of memory in general is much more substantial. By look-
In studying the relationship between psychopathology ing at the broad memory literature, researchers have been
and AM, researchers have found that certain aspects of able to make some claims about the neuropsychology of
AM in clinical populations do differ from those of healthy AM and to suggest areas for future study.
populations. Evidence suggests that AM in patients with AM appears to be distributed throughout the brain.
suicidal ideation, current or past depression, and trauma Retrieval of personally experienced events has been linked
history may be overgeneral compared to the specific to medial temporal lobe, visual cortex, posterior parietal
memories that healthy individuals recall (Hermans, midline, and prefrontal cortex activity (Daselaar et al.,
Raes, Philippot, & Kremers, 2006). For example, a de- 2008; Greenberg & Rubin, 2003). AMs emotional and
pressed patient might report a memory of going to lunch sensory components may involve still other brain areas.
324 A Autoimmune Disorders
Daselaar et al. (2008) have worked to map the time looking at schema activation and overgeneral AMs may
course of AM, including emotional and reliving aspects of be important to understanding why clinical populations
AM. Through functional magnetic resonance imaging remember AMs differently from nonclinical populations.
(fMRI), Daselaar et al. examined both initial accessing of Taking a closer look at the neuropsychology of AM
memories and subsequent elaboration of the memories. will be necessary as we find better ways to define AM
As a person first began to recall a personal memory, behaviorally. Correlating behavioral changes with the
hippocampal, retrosplenial, and medial and right prefron- brain changes we can see through imaging will be
tal cortex activation occurred (Daselaar et al., 2008). As a significant area for future study so that we develop a
participants rated memories, brain areas associated with clearer idea of what structures make up the AM circuitry
emotion and sensory function were activated, including the in the brain.
amygdala and hippocampus for initial emotion ratings,
and visual cortex and ventromedial and inferior prefrontal
cortex for reliving ratings. This line of research underlines Cross References
AMs dynamic involvement of multiple brain areas.
The visual, auditory, and olfactory systems all appear Declarative Memory
to be potential parts of the broad AM system. Research Episodic Memory
has demonstrated that visual imagery is central to AM, False Memory
especially when considering long-term visual memories Forgetting
(Greenberg & Rubin, 2003). The medial-temporal lobes Memory Impairment
and the frontal lobes have been implicated in case study Remote Memory
research examining visual imagerys role in AM. Auditory Working Memory
imagery may also be involved in AM, but so far studies
have not shown autobiographical amnesias to be related
specifically to damage of the auditory cortices. As with References and Readings
visual imagery, further research may provide more
information on this aspect of AM. Bluck, S. (Ed.). (2003). Autobiographical memory: Exploring its
functions in everyday life [Special issue]. Memory, 11.
In addition to its sensory dimensions, AM also seems
Dalgleish, T., & Brewin, C. R. (Eds.). (2007). Autobiographical memory
to be closely related to language. However, with only one and emotional disorder [Special issue]. Memory, 15(3).
exception, semantic dementia, AM impairment does not Daselaar, S. M., Rice, H. J., Greenberg, D. L., Cabeza, R., LaBar, K. S., &
seem to be related to language-related neuropsychological Rubin, D. C. (2008). The spatiotemporal dynamics of autobio-
impairments (Greenberg & Rubin, 2003). In semantic graphical memory: Neural correlates of recall, emotional intensity,
and reliving. Cerebral Cortex, 18, 217229.
dementia, patients display better recall for recent
Greenberg, D. L., & Rubin, D. C. (2003). The neuropsychology of
memories than for older ones. A patient with semantic autobiographical memory [Special issue]. Cortex, 39, 687728.
dementia experiences loss of AM, as well as a loss of the Hermans, D., Raes, F., Philippot, P., & Kremers, I. (Eds.). (2006).
ability to maintain semantic memories in storage. Autobiographical memory specificity and psychopathology. New York:
Psychology Press.
Levin, H. S., Benton, A. L., & Grossman, R. G. (1982). Neurobehavioral
consequences of closed head injury. New York: Oxford University
Future Directions Press.
Rubin, D. C. (Ed.). (1999). Remembering our past: Studies in autobio-
Future research on AM should concentrate on defining graphical memory. New York: Cambridge University Press.
and specifying AM both behaviorally and through Sutin, A. R., & Robins, R. W. (2007). Phenomenology of autobiographical
memories: The memory experiences questionnaire. Memory, 15(4),
neuropsychological techniques, including functional and
390411.
structural imaging. Continuing to consider and revise a Wenzel, A., & Rubin, D. C. (Eds.). (2005). Cognitive methods and their
conceptual model of AM, such as Pillemers, is important application to clinical research. Washington, DC: American Psycho-
to providing researchers a better, more definite way to logical Association.
conceptualize AM. Looking at AM cross-culturally may
help to determine whether this type of memory plays
distinct roles in different cultures and societies. Individual
differences in AM are also an important area for Autoimmune Disorders
study, given researchers focus on AM as important to
the formation of self. In research on psychopathology, Myasthenia Gravis
Automated Neuropsychological Assessment Metrics A 325
ANAM tests in order to assess more specific areas of

Autoimmune Thyroiditis A
functioning (Vincent et al., 2008). The most recent ver-
sion of ANAM uses a Windows platform and can be found
Hypothyroidism at the Center for the Study of Human Operator Perfor-
mance at the University of Oklahoma (Jones, Loe, Krach,
Rager, & Jones, 2008).
Administration time can range from a few minutes for
Automated Interpretation a single subtest to 90 minutes for the entire battery (U.S.
Army Medical Department, 2009). Scoring for the ANAM
Test Interpretations: Computer Based is computer generated. Scores for ANAM subtests can be
calculated in a variety of ways, including the percentage of
correct responses (accuracy score), mean response time
for accurate responses (MS), and the ratio of accuracy and
Automated Neuropsychological speed or number of correct responses per minute
(throughput score) (Jones et al., 2008).
Assessment Metrics
S UMMER I BARRA Historical Background
Rehabilitation Hospital of Indiana
Indianapolis, IN, USA The ANAM was originally developed by the US Depart-
ment of Defense as a means of monitoring changes in
human performance when encountering environmental
Synonyms challenges, but has now become a common assessment
instrument for use in several clinical populations (Kane,
ANAM Roebuck-Spencer, Short, Kabat, & Wilken, 2007) and
research applications (Vincent et al., 2008). The current
ANAM is the result of 30 years of research and is directly
Definition linked to older standardized test batteries, including the
Unified Tri-Service Cognitive Performance Assessment
The Automated Neuropsychological Assessment Metrics Battery (Reeves et al., 2007).
(ANAM) is a computer-based battery of tests designed to
measure an individuals neurocognitive skills including
areas such as sustained attention, processing speed, work- Current Knowledge
ing memory, and visuospatial ability. It consists of 31 test
modules as well as forms for recording demographic Various combinations of ANAM subtests have been
information (see Fig. 1; Center for the Study of Human employed to investigate neurocognitive changes and im-
Operator Performance; Reeves, Winter, Bleiberg, & Kane, pairment in medical and neurological conditions includ-
2007). The entire battery of tests can be administered or ing acquired brain injury, multiple sclerosis, Parkinsons
the administrator can elect to customize a subset of the disease, systemic lupus erythematosus (Kane et al., 2007),
ANAM executive module Participant information Sleepiness scale Mood scale

2-Choice reaction time Code substitution Logical reasoning Matching grids
Matching to sample Mathematical processing Memory search Running memory CPT
Simple reaction time Tapping Procedural reaction time Spatial processing
Manikin Switching Tower puzzle Standard CPT
Pursuit tracking Stroop test Spatial processing delayed Grammatical reasoning
Complex reaction time 4-Choice reaction time Relative judgment Symbolic reaction time
Digit reaction time Visual vigilance Unstable tracking Dual task
Automated Neuropsychological Assessment Metrics. Figure 1

326 A Automated Neuropsychological Assessment Metrics
migraine headache (Roebuck-Spencer, Sun, Cernich, for accurate responses (MS), and the ratio of accuracy and
Farmer, & Bleiberg, 2007) and Alzheimers dementia speed or number of correct responses per minute
(Levinson, Reeves, Watson, & Harrison, 2005). Currently, (throughput score) (Jones et al., 2008).
in an effort to better identify the occurrence of traumatic
brain injury (TBI), the ANAM is also being used by the
US military to establish a baseline of neurocognitive Psychometrics
functioning prior to deployment for all Service members
(U.S. Army Medical Department, 2009). The subtests of the ANAM were selected from previously
Data from over nine studies suggest that varying established assessment instruments (e.g., Walter Reed Per-
combinations of ANAM subtest batteries are sensitive formance Assessment Battery, the Air Force Criterion
and specific in detecting neurocognitive change among Task Set, Navy Performance Evaluation Tests for Environ-
individuals with neurological disorders (Kane et al., mental Research) with research supporting their respec-
2007). Common uses include screening and triage, moni- tive sensitivity, reliability, and validity (Reeves et al.,
toring of disease progression, and detection of treatment 2007). As researchers have attempted to gather psycho-
and medication effects (Kane et al., 2007). metric data for the current ANAM, many have included
Other uses of the ANAM include evaluation of cogni- only subsets of the subtests in their studies rather than the
tive functioning in determining fitness for duty, neuro- entire ANAM battery.
toxicology, human factors engineering, and various fields Various combinations of ANAM subtests have been
of medicine such as aerospace, undersea, military opera- shown to be both sensitive and specific in detecting cog-
tions, and sports (Reeves et al., 2007). nitive changes in a number of neurological conditions
(Kane et al., 2007).
Through the process of multiple baseline administra-
Advantages tions, testretest reliabilities across several ANAM subtest
throughput scores ranged from 0.50 to 0.91 with 9 of the
The ANAM has been noted as an ideal instrument for 10 estimates <0.77(Short, Ivins, & Kane, manuscript in
assessing change in neurocognition (Roebuck-Spencer preparation).
et al., 2007). Through randomization of stimuli, practice Construct validity has been established between sev-
effects are minimized across numerous testing sessions eral of the commonly used ANAM subtests (e.g., Math,
(Roebuck-Spencer et al., 2007). Further, subtle changes Running Memory, Code Substitution Delayed Memory,
in response time can be more precisely detected as and Logical Reasoning) and more traditional measure of
compared to manual calculation of response time neurocognitive function such as Trail Making Test A&B,
(Roebuck-Spencer et al., 2007). Other advantages include Animal Naming, Controlled Oral Word Association Test,
time efficiency and cost-effectiveness, both of which are and the Digits Backward and Digit Symbol subtests of the
helpful when attempting to triage large numbers of WAIS-III (Short, Cernich, Wilken, & Kane, 2007).
patients (Kane et al., 2007).
Limitations Future Directions
Research findings indicate that varying combinations of The use of the ANAM in various fields of medicine and
the ANAM batteries are not as thorough as more extensive science continues to develop as evidenced by recent stud-
neurocognitive assessments. ies attempting to validate specified subsets of the ANAM
battery. Examples include validation of the ANAM-sports
medicine battery (ASMB) designed for surveillance and
Administration management of sports related concussions (Cernich,
Reeves, Sun, & Bleiberg, 2007), use of ANAM tests to
Administration time can range from a few minutes for a assess the effects of extreme environmental stressors
single subtest to 90 minutes for the entire battery (U.S. such as high altitude, toxins, and radiation exposure
Army Medical Department, 2009). Scoring for the ANAM (Lowe et al., 2007), and assessment of medication efficacy
is computer generated. Scores for ANAM subtests can be and potential medication side effects, specifically for
calculated in a variety of ways, including the percentage of CNS-active drugs (Wilken, Sullivan, Lewandowski, &
correct responses (accuracy score), mean response time Kane, 2007).
Automatic Language A 327
Cross References assessment metrics (ANAM): Issues and challenges. Archives of Clin-
A
ical Neuropsychology, 22, S79S87.
Short, P., Cernich, A., Wilken, J. A., & Kane, R. L. (2007). Initial construct
Cognitive Functioning validation of frequently employed ANAM measures through struc-
Concussion tural equation modeling. Archives of Clinical Neuropsychology, 22S,
Mild Brain Injury S63S77.
Traumatic Brain Injury Short, P., Ivins, B. J., & Kane, R. L. (manuscript in preparation). Reliabil-
ity characteristics of select Automated Neuropsychological Assess-
ment Metrics (ANAM) measures.
U.S. Army Medical Department (2009). Automated Neuropsychological
References and Readings Assessment Metrics (ANAM). www.medicine.army.mil/prr/anam.
html. Retrieved on 10 March 2009.
Vincent, A. S., Bleiberg, J., Yan, S., Ivins, B., Reeves, D. L., Schwab, K.,
Jones, W. P., Loe, S. A., Krach, K., Rager, R. Y., & Jones, H. M. (2008). et al. (2008). Reference data from the automated neuropsychological
Automated neuropsychological assessment metrics (ANAM) and assessment metrics for use in traumatic brain injury in an active duty
Woodcock-Johnson III tests of cognitive ability: A concurrent valid- military sample. Military Medicine, 173, 836849.
ity study. The Clinical Neuropsychologist, 22, 305320. Wilken, J. A., Sullivan, C. L., Lewandowski, A., & Kane, R. L. (2007). The
Kane, R. L., Roebuck-Spencer, T., Short, P., Kabat, M., & Wilken, J. use of ANAM to assess the side-effect profiles and efficacy of medi-
(2007). Identifying and monitoring cognitive deficits in clinical cation. Archives of Clinical Neuropsychology, 22S, S127S133.
populations using Automated Neuropsychological Assessment
Metrics (ANAM) tests. Archives of Clinical Neuropsychology, 22S,
S115S126.
Reeves, D. L., Winter, K. P., Bleiberg, J., & Kane, R. L. (2007). ANAM
genogram: Historical perspectives, description, and current endea- Automatic Behavior
vours. Archives of Clinical Neuropsychology, 22S, S15S37.
Roebuck-Spencer, T., Sun, W., Cernich, A. N., Farmer, K., & Bleiberg, J. Automatism
(2007). Assessing change with the automated neuropsychological
Stimulus-Bound Behavior
assessment metrics (ANAM): Issues and challenges. Archives of Clin-
ical Neuropsychology, 22, S79S87.
References ANAM Automatic Language

R OBERTA D E P OMPEI
Center for the Study of Human Operator Performance. (nd). ANAM tests
and associated modules. http://c-shop.ou.edu/anam42.htm. Re- The University of Akron
trieved on 10 March 2009. Akron, OH, USA
Cernich, A., Reeves, D., Sun, W., & Bleiberg, J. (2007). Automated
neuropsychological assessment metrics sports medicine battery.
Archives of Clinical Neuropsychology, 22S, S101S114.
Jones, W. P., Loe, S. A., Krach, K., Rager, R. Y., & Jones, H. M. (2008).
Synonyms
Automated neuropsychological assessment metrics (ANAM) and
Woodcock-Johnson III tests of cognitive ability: A concurrent valid- Nonpropositional language
ity study. The Clinical Neuropsychologist, 22, 305320.
Kane, R. L., Roebuck-Spencer, T., Short, P., Kabat, M., & Wilken, J.
(2007). Identifying and monitoring cognitive deficits in clinical
populations using automated neuropsychological assessment
Definition
metrics (ANAM) tests. Archives of Clinical Neuropsychology, 22S,
S115S126. Automatic language is the use of nonpropositional language
Levinson, D., Reeves, D., Watson, J., & Harrison, M. (2005). Automated forms. Even if the patient is unable to converse at all, he
neuropsychological assessment metrics (ANAM) measures of cogni- or she may produce automatic responses. These responses
tive effects of Alzheimers disease. Archives of Clinical Neuropsychol-
may be: (a) automized sequences: counting, reciting the
ogy, 20, 403408.
Lowe, M., Harris, W., Kane, R. L., Banderet, L., Levinson, D., & Reeves, D. alphabet, saying the days of the week; (b) memorized
(2007). Neuropsychological assessment in extreme environments. sequences: prayers pledge of allegiance; (c) recurrent social
Archives of Clinical Neuropsychology, 22S, S89S99. speech: Have a nice day, How are you?; (d) emotional
Reeves, D. L., Winter, K. P., Bleiberg, J., & Kane, R. L. (2007). ANAM speech: cursing or a typically stated sentence when emotion-
genogram: Historical perspectives, description, and current endea-
ally upset. It is important to note that these types of
vours. Archives of Clinical Neuropsychology, 22S, S15S37.
Roebuck-Spencer, T., Sun, W., Cernich, A. N., Farmer, K., & Bleiberg, J. responses are not clearly thought out and are not under
(2007). Assessing change with the automated neuropsychological the cognitive control of the patient. These responses do not
328 A Automaticity
represent propositional language skill and should not be instead name the color of the stimulus. Reaction time
considered as a conscious attempt to participate in conver- tends to be slower when the color word and the color of
sational situations. Automatic language can be found in the stimulus are incongruent when compared to the time
severe aphasias and in many dementias. It may also occur to name the color of a series of Xs or a noncolor word.
in mental health problems such as schizophrenia.
Cross References
Cross References
Controlled Attention
Stereotypy Orienting Response
Reading Fluency
Stroop Effect
Alajouanine, T. (1956). Verbal realization in aphasia. Brain, 79, 128.

Blanken, G., & Marini, V. (1997). Where do lexical speech automatisms
come from? Journal of Neurolinguistics, 10(1), 1931.
Chapey, R. (Ed.). (2001). Language intervention strategies in aphasia and MacLeod, C. M. (1992). The Stroop task: The gold standard of atten-
related neurogenic communication disorders (4th ed.). Philadelphia: tional measures. Journal of Experimental Psychology: General, 121,
Lippincott, Williams & Wilkins. 1214.
Stroop, J. R. (1935). Studies of interference in serial verbal reactions.
Journal of Experimental Psychology, 18, 643662.
Automaticity
Automatism
A NNA M AC K AY-B RANDT
Brown University Medical School D OUGLAS I. K ATZ
Providence, RI, USA Boston University School of Medicine
Boston, MA, USA
Definition
Synonyms
A mental operation that proceeds without voluntary
control and without requiring capacity or processing Automatic behavior
resources.
Definition
Current Knowledge
This is a complex movement that occurs without
Automatic processes are usually found in the context of conscious awareness or purposeful intent.
stimulus information that is well integrated into the indi-
viduals memory through either a classical conditioning,
an overlearned behavior (e.g., reading), or an evolution- Current Knowledge
arily adaptive response (e.g., orienting response). The
Stroop effect (Stroop, 1935; MacLeod, 1992) is a good Automatisms may occur in the setting of complex-partial
example of the influence of automaticity on behavior. seizures. Typical simple movements include lip smacking,
Reading becomes automatic at a level of proficiency chewing, or finger rubbing. More complex automatisms
acquired by most school-aged children, such that it is include walking, running, undressing, and speaking. Emo-
out of an individuals control not read a presented word. tional expressions, such as laughing or crying, may also
This involuntary response is captured in the interference occur as automatisms. Automatisms may occur during
it produces when one attempts to ignore a color word and seizures or as post-ictal phenomena. Speech automatisms
Autonomic Nervous System A 329
tend to lateralize to the left hemisphere but lateralization is Definition A

not predictable for other automatisms (Rasonyi, Fogarasi,
Kelemen, Janszky, & Halasz, 2006). Responsiveness is usu- The autonomic nervous system is a complex and vital
ally lost when automatisms occur during seizures. Rarely, system that helps to maintain homeostasis and adaptation
patients may have preserved responsiveness in the pres- throughout the human body. It is composed of both
ence of seizure-induced automatisms, and only with sei- central and peripheral components that provide thermo-
zures that arise from right hemisphere foci (Ebner, regulation, arterial blood pressure adaptation, as well as
Dinner, Noachtar, & Luders, 1995). alterations in regional blood flow in response to metabolic
In addition to epileptic seizures, automatisms may also demands, micturition, gastrointestinal motility, and sex-
be observed in other situations including intoxication, ual function.
sleep walking, hypoglycemia, and psychological disorders,
such as dissociative fugue states. Forensic assessments
aimed at determining culpability often center around the
Current Knowledge
differential diagnosis of automatisms (Fenwick, 1990).
Central Component
Cross References The central components of the autonomic nervous system

are located within the cerebral cortex, thalamus, hypo-
Complex Partial Seizures thalamus, hippocampus, and cerebellum. These compo-
nents are integrally connected via a network of ascending
and descending pathways see Fig. 1. This provides a high
Ebner, A., Dinner, D. S., Noachtar, S., & Luders, H. (1995). Automatisms
Insular cortex
with preserved responsiveness: A lateralizing sign in psychomotor
seizures. Neurology, 45(1), 6164.
Fenwick, P. (1990). Automatism, medicine and the law. Psychological
Medicine. Monograph Supplement, 17, 127. Paraventricular
Rasonyi, G., Fogarasi, A., Kelemen, A., Janszky, J., & Halasz, P. (2006). nucleus
Lateralizing value of postictal automatisms in temporal lobe
epilepsy. Epilepsy Research, 70(23), 239243. Central nucleus
of the amygdala
Lateral hypothalamic area
Autonomic Dysregulation Periaqueductal

gray matter
Hemodynamic Response
Parabrachial
region
Autonomic Nervous System
S COTT VOTA Nucleus of the
Virginia Commonwealth University tractus solitarius
Richmond, VA, USA
Nucleus ambiguus
Ventrolateral
Synonyms medulla
Internal regulation system; Involuntary nervous system; Autonomic Nervous System. Figure 1 Central components
Visceral nervous system of the autonomic nervous system
330 A Autonomic Nervous System
level of control over autonomic function. These intercon- gland (producing lacrimation) and the cerebral and cra-
nections ultimately descend to specific cells within the nial blood vessels (eliciting vasodilatation). Axons also
brainstem and spinal cord. The thoracolumbar outflow travel to the submandibular ganglion, providing secreto-
consists of fibers that arise in the intermediolateral cell motor and vasodilator inputs to the corresponding sali-
column of the thoracic and first two lumbar segments of vary glands. The inferior salivatory nucleus sends axons
the spinal cord. This is the origin of the sympathetic via the glossopharyngeal nerve to ultimately synapse on
division of the autonomic nervous system. The cranial the otic ganglion, stimulating parotid gland secretion.
outflow, arising from cranial nerve nuclei III, VII, IX, and Most preganglionic parasympathetic output from the
X, and the sacral outflow, arising from cell bodies in the brainstem is mediated by the vagus nerve, which receives
intermediate cell column of sacral segments 2 through 4, input from the dorsal motor nucleus of the vagus and the
form the parasympathetic division of the autonomic lateral portion of the nucleus ambiguus. The vagus nerve
nervous system. innervates the heart, respiratory tract, and the entire
gastrointestinal tract with the exception of the descending
colon and rectum.
Peripheral Component The sacral preganglionic output arises from neurons
of the sacral preganglionic nucleus located in the lateral
The peripheral part of the autonomic nervous system is gray matter of the sacral spinal cord. These axons travel to
then composed of sympathetic and parasympathetic the pelvic splanchnic nerves, which join the inferior hy-
pathways. These pathways arise from two distinct ana- pogastric plexus to innervate the descending colon, blad-
tomic portions of the brainstem and spinal cord. The der, and sexual organs. These outputs elicit contraction of
parasympathetic fibers arise from the craniosacral por- the bladder detrusor muscle and circular smooth muscle
tion, and the sympathetic fibers arise from the thoraco- of the rectum as well as regulating vasodilatation of the
lumbar region. Although anatomically separated, the two cavernous tissue of the penis required for erection.
parts are complementary in maintaining a balance in
the activities of many visceral structures and organs. The Sympathetic Nervous System
preganglionic neurons for both the parasympathetic and The sympathetic preganglionic neurons are primarily lo-
sympathetic divisions release acetylcholine, but the differ- cated in the intermediolateral nucleus in the thoracic and
ence lies in the postganglionic neurotransmitter release. upper lumbar regions of the spinal cord. The pregangli-
The parasympathetic postganglionic fibers release norepi- onic sympathetic axons exit through the ventral roots and
nephrine and epinephrine and thus are referred to as pass on to the corresponding spinal nerve to reach the
cholinergic. The sympathetic postganglionic fibers release paravertebral sympathetic chain. The majority of the pre-
norepinephrine and epinephrine and thus are classified as synaptic fibers branch and run rostrally or caudally along
adrenergic. The terminals of sympathetic fibers on sweat the sympathetic chain and synapse on the paravertebral
glands, however, do not follow this pattern and are cho- ganglia. The remaining fibers pass through the paraver-
linergic (see Figs. 2 and 3). tebral chain without synapsing. These form the splanch-
nic nerves which innervate prevertebral ganglia.
Parasympathetic Nervous System The paravertebral sympathetic ganglia are primarily a
Parasympathetic outputs arise from the preganglionic relay station for preganglionic inputs. They innervate
neurons located in the nuclei of the brainstem and sacral all tissues and organs except those in the abdomen, pelvis,
spinal cord. Preganglionic parasympathetic axons travel a and perineum. For example the superior cervical ganglion
long distance before eventually reaching their target gang- sends postganglionic axons to innervate the eye, facial
lia, which are typically close to, or within the target end sweat glands, salivary glands, pineal, thyroid, and para-
organ. thyroid glands. These outputs elicit pupil dilatation, con-
The cranial preganglionic parasympathetic nuclei traction of the Muller muscle of the eyelid, facial sweating,
(Edinger Westphal Nuclei) projects through the oculomo- and vasoconstriction in facial and cerebral circulation.
tor nerve. These preganglionic axons synapse on neurons The stellate ganglion, which receives preganglionic input
of the ciliary ganglion. The neurons innervate the iris and from the mid thoracic segment, sends postganglionic
ciliary muscles, eliciting pupillary constriction and ac- axons to innervate blood vessels and sweat glands in
commodation of the lens. The superior salivatory nucleus the upper limbs and trunk. These outputs produce either
located in the pons projects via the facial nerve to the vasoconstriction or vasodilatation in the skin and muscle,
sphenopalatine ganglion. This innervates the lacrimal sweating, or piloerection. Outputs from the stellate
Autonomic Nervous System A 331
Ciliary ganglion
A
Ciliary muscle
Sphenopalatine CN III
ganglion
Lacrimal gland
Submandibular CN VII
ganglion
Salivary glands
Parotid gland
CN IX
Otic ganglion
1
2
Larynx and trachea (CN X) 3
Lungs Vagus 4
Heart 5
6
Gastrointestinal tract 7
8
Abdominal organs
9
10
11
12
Large intestine 1
2
3
S24
Kidney
Bladder
Sex organs
Autonomic Nervous System. Figure 2 Parasympathetic Nervous System
ganglion also elicit cardiac acceleration and bronchodila- vasoconstriction, smooth muscle relaxation of the bladder
tion. The lumbar paravertebral ganglia subsequently and rectum, constriction of the internal sphincter of the
innervate the blood vessels and sweat glands in the lower bladder and rectum, and ejaculation.
limb.
The prevertebral ganglia are located anterior to the
abdominal aorta. Preganglionic input from the lower Diagnosing Autonomic Dysfunction
thoracic segments is carried by the splanchnic nerves to
the celiac and superior mesenteric ganglia and provides Medical History
postganglionic fibers to the celiac plexus that innervates As the autonomic nervous system innervates all organ
all abdominal viscera, with the exception of the descend- systems, a detailed medical history and physical examina-
ing colon. These outputs produce vasoconstriction and tion is paramount. This will help develop a proper differ-
inhibition of the gastrointestinal tract motility. Pregangli- ential diagnosis and laboratory evaluation. The goals of
onic axons from the lumbar spinal segments travel via the clinical evaluation are to identify the presence, loca-
the lumbar splanchnic nerves to synapse in the inferior tion, and time course of autonomic dysfunction. This will
mesenteric ganglion. These axons innervate the descend- help to determine which part(s) of the autonomic ner-
ing colon, rectum, bladder, and sexual organs eliciting vous system may be involved: sympathetic noradrenergic,
332 A Autonomic Nervous System
Ciliary muscle
Lacrimal gland
Salivary glands C1
Larynx and 1
T1
trachea 2
3
Lungs 4
5
Celiac
ganglion 6
Heart
7
Stomach 8
Small intestine 9
10
Adrenal medulla 11
12
1
Superior mesenteric 2
ganglion 3
Large intestine
L1
Kidney
Bladder
Inferior
Sex organs mesenteric
ganglion
Autonomic Nervous System. Figure 3 Sympathetic Nervous system
sympathetic cholinergic, parasympathetic cholinergic, making note of acrocyanosis, pallor, mottling, diaphore-
or adrenomedullary. Specific questions should be asked sis, alopecia, or erythema should be performed. An
to determine if the patient may have symptoms of ortho- eye exam can also be valuable. Attention should be given
static hypotension, anhydrosis, weight change, constipa- to pupillary shape, size, and the response to light and
tion, sexual dysfunction, sialorrhea, or urinary retention. accommodation.
Questions related to aggravating and relieving factors
need to be considered. Examples include: relationship to Diagnostic Testing
meals; environmental temperature; and diurnal variation. A workup to uncover an etiology for autonomic dys-
A complete listing of all prescribed medications, as well as function should begin with routine serologic testing.
over the counter herbal and dietary supplements need to This includes serum electrolytes, glucose, hepatic function
be reviewed. tests, protein electropheresis, and a complete blood count.
Further serologic testing may include cortisol levels, para-
Examination neoplastic autoantibodies, and plasma catecholamines.
An exam should start with a general overview of the An EKG and echocardiogram should also be performed.
patient making note of facial expression, posture, and A variety of more specialized tests, both invasive and
height. Vital signs should be checked in the supine, seated, noninvasive, may also need to be considered. These in-
and standing positions. A thorough skin examination clude, but are not limited to the following: deep breathing
Autotopagnosia A 333
and valsalva ratio, isometric handgrip and cold pressor

Autoreceptor A
tests, thermoregulatory sweat and skin sympathetic tests,
quantitative sudomotor axon reflex testing, power spec-
tral analysis of heart rate variability, tilt table testing, and B ETH K UCZYNSKI 1, S TEPHANIE A. KOLAKOWSKY-H AYNER 2
1
neuroimaging such as PET scanning. University of California
Davis, CA, USA
2
Treatment Rehabilitation Research Center
Both nonpharmacologic and pharmacologic treatments San Jose, CA, USA
are available to treat patients with autonomic dysfunc-
tion. For certain disorders, surgical intervention may be
needed. The goal is to ameliorate all symptoms while
Synonyms
avoiding side effects.
Heteroreceptor; Receptor
Nonpharmacologic measurements start with patient
education. Symptoms such as rising slowly from a seated
position, or modifying sodium intake may be enough in Definition
some autonomic disorders to provide patients with a
symptom free life. An autoreceptor is a receptor located on the neuron (term-
Pharmacotherapy may include medications to in- inals, soma, and/or dendrites), and the function is to bind a
crease central blood volume, such fludrocortisones, specific ligand (such as neurotransmitters or hormones) re-
vasopressin analogues, acetylcholinesterase inhibition, or leased by that same neuron. The autorecptor is mainly used as
caffeine. a feedback mechanism to monitor neurotransmitter synthesis
and/or release. Dopaminergic neurons can have autorecep-
tors that regulate the release of dopamine. Autoreceptor
regulation is very effective in modulating neurotransmission
Cross References and is of interest for pharmacological intervention.
Anticholinergic
Arousal
Cross References
Cerebellum
Hormones
Cholinergic System
Neurotransmitters
Hippocampus
Hypothalamus
Thalamus
Carey, R., DePalma, G., Damianopoulos, E., Muller, C., & Huston, J.
(2004). The 5-HT1A receptor and behavioral stimulation in the rat:
References and Readings Effects of 8-OHDPAT on spontaneous and cocaine-induced behav-
ior. Psychopharmacology, 177(1/2), 4654.
Meltzer, H. (1980). Relevance of dopamine autoreceptors for psychiatry:
Benarroch, E. E., Westmoreland, B. F., Daube, J. R., Reagan, T. J., & Preclinical and clinical studies. Schizophrenia Bulletin, 6(3), 456475.
Sandok, B. A. (1999). Medical neurosciences: An approach to
anatomy, pathology, and physiology by systems and levels (4th ed.).
Philadelphia: Lippincott Williams and Wilkins.
Bradley, W. G., Daroff, R. B., Fenichel, G., & Jankovic, J. (2004). Neuro-
Autotopagnosia
logy in clinical practice (4th ed.). Boston: Butterworth-Heinemann.
Gilman, S., Newman, S. W., Manter, J. T., & Gatz, A. J. (2003). Manter J OHN E. M ENDOZA
and Gatzs essentials of clinical neuroanatomy and neurophysiology Tulane University Medical Center
(10th ed.). Philadelphia: F.A. Davis Company.
Netter, F. H. (1991). Nervous system, Part 1: Anatomy and physiology
(Vol. 1) (Ciba collection of medical illustrations). Summit, NJ:
Ciba-Geigy Corporation.
Ropper, A. H., & Brown, R. H. (2005). Adams and Victors principles of
Definition
neurology (8th ed.). New York: McGraw-Hill.
Rowland, L. P. (2005). Merritts neurology (11th ed.). Philadelphia: Disturbance of body schema involving the loss of ability to
Lippincott Williams and Wilkins. localize, recognize, or identify the specific parts of ones body.
334 A AVMs
Current Knowledge Definition
While some reported cases exhibit impaired knowledge of Avolition is a severe problem with initiation, volitional, or
most body parts, autotopagnosia is most frequently man- willed action, and production of goal-directed behavior. It
ifested as difficulty in identifying or naming specific fingers may reflect a general lack of motivation and drive.
(finger agnosia), especially the three middle fingers. The Avolition is commonly seen as one of the negative
problem extends to identifying comparable body parts on symptoms in patients with schizophrenia, and is also
the examiner or graphic representations of body parts. The common in frontal lobe disorders affecting medial frontal
deficit usually involves both sides of the body, thus distin- systems.
guishing it from unilateral neglect. While not typically
classified as such, right-left disorientation likely reflects
another form or subtype of autotopagnosia. In this condi- Cross References
tion, patients are unable to reliably identify the right and left
sides of their bodies or those of others. Both finger agnosia Abulia
and right-left disorientation are frequently present at the Apathy
same time, particularly following lesions of the left angular Cingulate Gyrus
gyrus and may be a part of what has been defined as Gerst-
manns syndrome. The latter would also include deficits in
writing (agraphia) and arithmetical operations (acalculia).
Cross References
Foussias, G., & Remington, G. (2008). Negative symptoms in schizophre-
nia: Avolition and Occams Razor. Schizophrenia Bulletin Advance
Finger Agnosia Access 10.10.1093/schbul/sbn094.
Gerstmanns Syndrome Liddle, P. F. (1994). Volition and schizophrenia. In A. S. David &
Right-Left Disorientation J. C. Cutting (Eds.), The neuropsychology of schizophrenia
(pp. 3948). Hillside, UK: Lawrence Erlbaum.
Rummel, C., Kissling, W., & Leucht, S. (2005). Antidepressants as add-on
References and Readings treatment to antipsychotics for people with schizophrenia and pro-
nounced negative symptoms: A systematic review of randomized
Benton, A. L., & Sivan, A. B. (1993). Disturbances of the body schema. In trials. Schizophrenia Research, 80, 8597.
K. M. Heilman & E. Valenstein (Eds.), Clinical neuropsychology
(pp. 123140). New York: Oxford University Press.
Denberg, N. L., & Tranel, D. (2003). Acalculia and disturbances of the
body schema. In K. M. Heilman & E. Valenstein (Eds.), Clinical
neuropsychology (pp. 161184). New York: Oxford University Press.
Avonex
AVMs Beta-Interferons
Vascular Malformations
Avolition Awareness
I RENE P IRYATINSKY, PAUL M ALLOY Alertness
Butler Hospital and Alpert Medical School of Brown Consciousness
University
Providence, RI, USA
Synonyms Awareness of Illness

Apathy Insight, Effects on Rehabilitation
Axon Sheath A 335
Dolan, 2002). Core skills for social awareness include

Awareness, Social Awareness A
perspective taking and the ability to read the emotions
of others using nonverbal cues. Deficits in social aware-
T ERISA G ABRIELSEN , E LAINE C LARK ness are often found among individuals with various
University of Utah developmental disorders, including autism and nonverbal
Salt Lake City, UT, USA learning disabilities. Social awareness skills are key
components in social learning and social skill interven-
tions (e.g., Bellini, 2006).
Synonyms
Social cognition; Theory of mind References and Readings
Beland, K. (2007). Boosting social and emotional competence.

Definition Educational Leadership, 64(7), 6871.
Bellini, S. (2006). Building social relationships. Shawnee Mission, KS:
Social awareness is defined as the ability to recognize Autism Asperger Publishing Co.
another persons thoughts and feelings, predict and Kolb, B., & Whishaw, I. Q. (2003). Fundamentals of human neuropsy-
understand anothers behaviors based on the perception chology (5th ed.) New York: Worth.
Markova, G., & Legerstee, M. (2006). Contingency, imitation, and affect
of anothers mental state, and empathize with others.
sharing: Foundations of infants social awareness. Developmental
Psychology, 42(1), 132141.
Sperry, R. W., Zaidel, E., & Zaidel, D. (1979). Self recognition and social
Current Knowledge awareness in the deconnected minor hemisphere. Neuropsychologia,
17, 153166.
Social awareness is required for people to live successfully Winston, J. S., Strange, B. A., ODoherty, J., & Dolan, R. J. (2002).
in complex social groups and requires the ability to Automatic and intentional brain responses during evaluation of
perceive and process subtle social signals (e.g., recognition trustworthiness of faces. Nature Neuroscience, 5, 277283.
and interpretation of facial expression and vocal tone).
Areas of the brain that are thought to be involved in social
awareness include: right temporal lobe (facial recognition
and expression), superior temporal sulcus (biological
motion), and orbitofrontal and prefrontal cortex, Axon Sheath
amygdala, and possibly insular cortex (social cognition)
(Kolb & Whishaw, 2003; Winston, Strange, ODoherty, & Myelin
B
they do after suffering neurological or psychiatric
Babcock, Harriet (18071952) disorders. Babcock believed that mental disorders do
not affect tests of prior knowledge acquisition (e.g.,
A NTHONY Y. S TRINGER vocabulary). She further identified a number of tests
Medicine Emory University that she thought were sensitive to mental disorders,
Atlanta, GA, USA including tests familiar to contemporary neuropsy-
chologists (e.g., reverse digit span and various
reasoning tasks). Babcock quantified mental efficiency
Major Appointments by contrasting performance on these two kinds of
tests, a forerunner of the holddont hold test com-
Manhattan State Hospital, New York, 19231925 parison ( HoldDont Hold Tests).
New York University, New York, 19311952 Babcocks contemporary influence is also evident in her
story memory format. In this format, a story is initially
Major Honors and Awards presented and recall is tested. The story is presented a
second time followed by 10 min of interpolated activity
Babcock was elected to the New York Academy of and a final recall test. This format has been adopted
Science and was a Diplomate of the American Board in some contemporary memory batteries and has the
of Examiners in Professional Psychology. advantage of allowing the neuropsychologist to test
both immediate and delayed recall, as well as learning
with repetition. Although the original Babcock Story is
Landmark Clinical, Scientific, and rarely used today, some current memory batteries incor-
Professional Contributions porate its format ( Wechsler Memory Scale). In this
and other respects, Babcocks work continues to influ-
In the 1930s, Babcock began a longitudinal study of ence clinical and scientific neuropsychology.
syphilitic patients, a project that was less notable for
its outcomes (many of which were not subsequently
replicated) than for its methodology. Classic neurologi- Short Biography
cal studies from the time of Paul Broca and Karl Wer-
nicke were centered around clinical case observation. In Little has been written concerning Babcocks personal life.
a departure from this classic tradition, Babcock adopted She was born in 1877 in Westerly, Rhode Island. She
the methods of scientific psychology to study the cog- began her career late in life, earning her doctoral degree in
nitive effects of neurological disease. Her research meth- her 50s. Prior to this, she lived a traditional life as a home-
ods were well-characterized and repeatable, she utilized maker. She initially gained experience working in psychiat-
standardized psychometric measures, and she ric facilities, but after earning her doctorate, she spent the
incorporated normal control comparison groups in her balance of her career on the faculty at New York University.
research. Anticipating later batteries of neuropsycholog- Despite her late beginning, Babcocks work was an impor-
ical tests, Babcock attempted to quantify deficits in tant forerunner to the emergence of neuropsychology as a
discrete mental abilities and used an efficiency index scientific field. Babcock died on December 12, 1952.
to summarize the overall functioning of her patients.
Babcock based her efficiency index on the idea that Cross References
intellectual function varies over time. More specifical-
ly, people may exhibit a higher level of intellectual HoldDont Hold Tests
function while healthy and in the prime of life, than Intelligence
338 B Babinksi Reflex
Intelligence Quotient infants exhibit an extensor response from birth, which

Wechsler Memory Scale converts to a flexor response during ages 1218 months
given normal development; developmental delay may
result in a persistent positive response. Indifferent
References and Readings responses may be found in normal individuals but may
also indicate the presence of a lower motor neuron or
Hartman, D. E. (1991). Reply to reitan: Unexamined premises and the other peripheral nervous system injury that interferes
evolution of clinical neuropsychology. Archives of Clinical Neuropsy- with the expression of a flexor response.
chology, 6, 147165.
Stringer, A. Y., & Cooley, E. L. (2002). Neuropsychology: A twentieth-
century science. In A. Y. Stringer, E. L. Cooley, & A.-L. Christensen
(Eds.), Pathways to prominence in neuropsychology: Reflections Cross References
of twentieth century pioneers (pp. 326). New York: Psychology Press.
Developmental Delay
Multiple Sclerosis
Spinal Cord Injury
Stroke
Babinksi Reflex Traumatic Brain Injury
E DISON WONG
Center for Pain & Medical Rehab References and Readings
Fitchburg, MA, USA
Babinski, J. (1896). Sur le reflexe cutane plantaire dans certaines
affections organiques du systeme nerveux central. Comptes rendus
Synonyms des seances de la Societe de biologie et de ses filiales, 48, 207208.
Campbell, W. W. (2005). DeJongs the neurological examination (pp. 324,
331, 339). Philadelphia: Lippincott, Williams & Wilkins.
Long tract sign; Plantar reflex; Upper motor neuron sign Getz, C. (1985). Introduction to the motor systems. In E. R. Kandel &
J. H. Schwartz (Ed.), Principles of neural science (pp. 429442).
New York: Elsevier.
Definition Landau, W. M., & Clare, M. H. (1959). The plantar reflex in man, with
special reference to some conditions where the extensor response is
unexpectedly absent. Brain, 82, 321335.
The Babinksi reflex or sign is elicited by making contact
along the lateral side of the plantar foot with a blunt
implement and not causing pain, discomfort or injury
to the skin; the implement is run from the heel along a
curve to the metatarsal pads. There are three responses
possible:
Background Information
Extensor (positive or pathological): hallux (great toe) History (Medical, Social, Psychological)
extension and the other toes abduct
Flexor (negative or normal): all toes flex and the
foot everts
Indifferent: no response
Backward Digit Task
Current Knowledge Digit Span
A positive response signifies pathology in the upper

motor neuron pathways, either in the spinal cord and/or
brain, such as in multiple sclerosis, stroke, traumatic brain
injury, or spinal cord injury. It may be the sole sign of Backward Masking
upper motor neuron damage and is the most popular
reflex that checks these pathways for the lower limbs. All Temporal Inhibition
Balance Disorders B 339
Epidemiology
BADS
Aging may also affect balance. Approximately 40% of B
Behavioral Assessment of the Dysexecutive Syndrome people older than age 65 suffer falls each year. Vertigo is
the most common form of dizziness.
BAER Natural History

Brainstem Auditory Evoked Responses Balance disorders associated with neurodegenerative
diseases tend to be progressive.
BAI Neuropsychology and Psychology

of Balance
Beck Anxiety Inventory
Neurodegenerative disorders associated with balance that
affect the cortex can also be associated with cognitive
difficulties.
Balance Disorders
A NNA D E P OLD H OHLER 1, M ARCUS P ONCE DE LEON2 Evaluation
1
Boston, MA, USA The history and physical examination often lead to a diag-
2
William Beaumont Army Medical Center nosis. At times, laboratory tests and imaging are obtained for
El Paso, TX, USA confirmation or to rule out harmful diagnoses. If a reversible
cause is found and treated, significant recovery may occur.
However, if the balance problem is due to a permanent
Definition or progressive neurological deficit, the patient may need
training to manage their gait and balance difficulties.
Normal balance requires the integration of three sensory
systems: visual, vestibular (found in the inner ear), and
somatosensory (sensations from the skin, muscles, tendons, Treatment
and joints) in addition to muscle strength. When these
systems are impaired, individuals may experience episodes Physical therapy and vestibular rehabilitation may be
of spinning, light-headedness, trouble focusing their eyes, useful in appropriate cases. They may improve current
and/or poor balance or falls. functioning and potentially decrease the potential for
progression of deficits and complications from falls.
Categorization
Cross References
Balance may be affected by disturbances of strength in
the trunk or legs, sensation deficits, or difficulties with Ataxia
coordination. Multiple systems may be affected. A Parkinsons Disease
detailed history and neurological examination may help
detect the affected area. Balance may be impaired after a
focal event such as a stroke or may develop during the References and Readings
course of a neurodegenerative disease such as Parkinsons
disease. Medications and infections of the brain or inner Ackley, S., Newell Decker, T., & Limb, C. J. (2007). An essential guide to
ear may also contribute to balance difficulties. hearing and balance disorders. Psychology Press.
340 B Balint, R. (Rezso (Rudolf) Balint) (18741929)
metabolism and the treatment of diabetes. He is most

Balint, R. (Rezso (Rudolf) Balint) well-known in his home country of Hungary for the
(18741929) treatment of gastric ulcer with the use of alkali.
Rezso Balint died of thyroid cancer in 1929 at the
A LYSSA B RAATEN age of 56.
Atlanta, GA, USA
Cross References
Major Appointments Neglect

Optic Ataxia
University of Budapest, Budapest, Hungary, 1910
1929
Hecaen, H., & Ajuriaguerra, J. (1954). Balint Syndrome (psychic paralysis

Major Honors and Awards of visual fixation) and its minor forms. Brain, 77, 373400.
Husain, M., & Stein, J. (1988). Reszo Balint and his most celebrated case.
Balints work was honored by the later naming of his Archives of Neurology, 45, 8993.
triple-syndrome complex as Balints Syndrome by Rezso Balint (physician). From Wikipedia: http://en.wikipedia.org/wiki/
Hecaen and Ajuriaguerra (Hecaen & Ajuriaguerra, rezs. Retrieved January 7, 2009.
1954).
Landmark Clinical, Scientific, and Balints Syndrome

U RAINA C LARK
Hungarian physician Rezso Balints first writings, The Warren Alpert Medical School of Brown University,
published while he was still a medical student, were The Miriam Hospital, Neuropsychology
case studies examining muscular atrophy in hemiple- Providence, RI, USA
gia. He went on to study tabes dorsalis and the treat-
ment of epilepsy. In 1907, Dr. Balint recorded his
observations of a patient who suffered from a unique Short Description or Definition
constellation of neurologic symptoms including fixa-
tion of gaze, neglect of objects in his periphery, and Balints syndrome was first described by Rezso Balint
misreaching for target objects. The patient was noted in 1909. It consists of three visuospatial abnormalities:
to first experience these symptoms following damage simultanagnosia, optic ataxia, and ocular motor apraxia.
to the posterior parietal lobes. This triple-syndrome The syndrome typically occurs in the absence of visual
complex was later named Balints Syndrome. field deficits. Individuals with Balints syndrome experi-
ence significant perceptual limitations. Patients with this
syndrome cannot perceive more than one object at a
Short Biography time. They experience great impairments in their ability
to explore visual space: they have difficulty navigating
Rezso Balint was born in 1874 to a German-Jewish family through their environment, they get lost easily, and they
in Budapest, Hungary. He attended the University of experience difficulty reaching for or grasping items in need.
Budapest, where he received his degree in medicine in Balints syndrome is usually associated with large bilat-
1897. Balint was a student of Friedrich von Koranyi. He eral lesions in the dorsal occipitoparietal region, and is
was employed as a Lecturer at the University of Budapest consequently rare. The most common causes of Balints
in 1910 and was promoted to Professor of Internal Medi- syndrome include ischemia (particularly watershed infarc-
cine in 1917. tions) and degenerative disorders (e.g., Alzheimers disease,
At the onset of World War I, Dr. Balint turned his posterior cortical atrophy). Balints syndrome can also re-
research focus from neurology to tuberculosis and sult from trauma, tumors, leukoencephalopathies, and
Balints Syndrome B 341
prion disorders. In individuals with HIV-AIDS, Balints Evaluation

syndrome can develop secondary to HIV encephalitis or
progressive multifocal leukoencephalopathy. Transient Before a diagnosis of Balints syndrome can be made, B
symptoms of Balints syndrome have been reported in more general cognitive dysfunction (e.g., hemineglect,
association with migraine onset. visual impairments) should be ruled out. It is important
that the patients visual fields be assessed fully as some
types of visual field abnormalities (e.g., extensive periph-
Natural History, Prognostic Factors, eral scotomata) can result in symptoms that are very
Outcomes similar to Balints syndrome.
A typical method of assessing for simultanagnosia
The prognosis for patients with Balints syndrome varies includes asking the patient to examine and describe the
depending on the etiology of the syndrome. Patients with events depicted in a complex visual image (e.g., the Cookie
posterior cortical atrophy usually experience a declining Theft Picture from the Boston Diagnostic Aphasia Exami-
course, while some patients with acute infarction may nation). In such a task, it is helpful if key elements of the
demonstrate improved functioning with time. image are presented in all four quadrants of the picture in
order to assess visual attention more fully across the quad-
rants. Individuals with hemineglect may describe items on
Neuropsychology and Psychology one side of the picture only. Patients with Balints syn-
of Balints Syndrome drome often are able to identify discrete items in the
picture; however, they are frequently unable to integrate
As noted above, individuals with Balints syndrome the various elements of the picture into a coherent story.
display three classic symptoms, including simultanagnosia, Patients will show impairments on visual search and count-
optic ataxia, and ocular motor apraxia. Simultanagnosia ing tasks. Letter identification and reading abilities may
is generally considered to be a disruption in spatial atten- also be assessed for functional purposes.
tion, which is associated with an inability to direct ones In assessing for optic ataxia, one may place several items
attention to more than one or a few objects at a time. It is at different locations on a table and ask the patient to touch
not uncommon for patients with this syndrome to ignore or grasp each of the items. It is important to assess whether
or neglect all other objects once one object in the visual the patient is able to grasp items within both hemifields
field has been fixated upon. Although patients can per- with each hand independently. Patients with unilateral
ceive and name individual objects regardless of the lesions typically demonstrate greater impairment when
objects location within the visual field, they exhibit an reaching for items located in the hemispace that is contra-
inability to perceive and interpret the gestalt of the scene. lateral to the lesion, using the contralateral hand. Indivi-
The second symptom associated with Balints syndrome duals with Balints syndrome are impaired when reaching
is optic ataxia, which is defined as a deficit in reaching for visual targets in all locations within the visual field;
under visual guidance despite normal limb strength and however, some patients with Balints syndrome may dem-
position sense. As a result of this symptom, patients demonstrate reaching difficulties in which one arm is more
onstrate an inability to manually respond to visual stimuli affected than the other. Patients with this syndrome are
and they often make location errors when pointing to or noted to be clumsy when grasping items and they may
grasping for visual targets. Some of the impairments noted often mislocate objects in space when reaching for or point-
on tests of reaching abilities include: increased action ing to items. In contrast, reaching to somatosensory targets
latency, poor control of hand trajectory, increased varia- such as parts of the patients own body (e.g., knee, shoulder)
bility at the end of the reach, tendency to reach to one side, on command is frequently intact; however, patients with
and dissociations of distance and direction control. The significant parietal spatial representation abnormalities may
third symptom of Balints syndrome includes ocular aprax- demonstrate impairments in both reaching for objects as
ia, which is manifested by an inability to voluntarily shift well as reaching to somatosensory targets.
gaze toward a new visual target. The ability to make a In assessing for ocular motor apraxia, the patients
saccade on command is significantly impaired and is next ability to make saccadic eye movements to targets on
to impossible for patients with Balints syndrome, whereas command can be compared to their ability to make
the ability to make reflexive saccades (e.g., those made to reflexive saccades to targets that appear suddenly in
suddenly appearing visual objects or sudden noises) and their field of vision. The former can be tested by asking
random spontaneous saccades remains intact. the patient to saccade between the clinicians left and right
342 B Barbiturates
index fingers, spaced far apart and held at various loca- one of the most common inhibitory neurotransmitter
tions across the patients visual field. The latter can be systems in the brain. Their behavioral effects include
tested in response to a person passing by or to a loud relaxation, drowsiness, and feelings of euphoria. However,
unexpected noise occurring in the periphery. their widespread effects also result in the depression of
reflexes and cardiovascular and respiratory functions,
particularly at higher doses (Feldman et al., 1997).
Treatment
The psychoactive effects of barbiturates increase
their risk for drug dependence and abuse. Symptoms of
Relatively little is known about treatment of patients with
tolerance and withdrawal develop with chronic use; how-
Balints syndrome. Rehabilitation often utilizes a func-
ever, greater tolerance develops to the psychoactive effects,
tional approach in which the patients strengths are used
but less so to the respiratory depressant effects of
to offset impairments. There is some evidence to suggest
barbiturates, resulting in an increased risk of a toxic
that cognitive and perceptual rehabilitation approaches
overdose (Feldman et al., 1997). Cross tolerance with
using verbal cues and organizational search strategies
other substances may also occur. For example, alcohol
can improve visual function and reaching abilities
use may also increase tolerance to barbiturates, further
(Perez, Tunkel, Lachmann, & Nagler, 1996).
increasing the risk of a toxic overdose.
Cross References
Current Knowledge
Hemiinattention
The use of barbiturates has declined significantly with the
Simultanagnosia
development of other anxiolytic and anticonvulsant
Visual Field Deficit
medications. Benzodiazepines, which are also anxiolytic
compounds that interact with the GABAA receptor
References and Readings (although a different site than barbiturates), have a larger
therapeutic window than barbiturates and have replaced
Perez, F. M., Tunkel, R. S., Lachmann, E. A., & Nagler, W. (1996). Balints their use as a safer alternative for the treatment of anxiety.
syndrome arising from bilateral posterior cortical atrophy or infarc-
tion: Rehabilitation strategies and their limitation. Disability and
Rehabilitation, 18, 300304. Cross References
Benzodiazepines
Gamma-Aminobutyric Acid (GABA)
Barbiturates
J OANN T. T SCHANZ 1, K ATHERINE T REIBER 1,2 References and Readings
1
Feldman, R. S., Meyer, J. S., & Quenzer, L. F. (1997). Sedative-hypnotic
Logan, UT, USA
2 and anxiolytic drugs. In Principles of neuropsychoparhmacology
University of Massachusetts Medical School (pp. 673729). Sunderland, MA: Sinauer.
Worcester, MA, USA
Definition Barefoot v. Estelle (1983)

Barbiturates belong to a class of medications known as R OBERT L. H EILBRONNER
sedative-hypnotics. Initially, they were prescribed for their Chicago Neuropsychology Group
anxiolytic and relaxing properties. Later, they were also Chicago, IL, USA
used as anticonvulsants, and shorter-acting forms were
developed for use as anesthetics in surgery (Feldman,
Meyer, & Quenzer, 1997). Synonyms
Barbiturates affect a subtype of the receptors of the
neurotransmitter, gamma-aminobutyric acid (GABA), Prediction of future dangerousness
Barona Index B 343
Historical Background Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C. (1997).
Psychological evaluations for the courts: A handbook for mental health
professionals and lawyers. New York: Guilford.
Thomas A. Barefoot burned down a bar and shot and Monahan, J. (1992). Mental disorder and violent behavior: Perceptions B
killed a police officer who was investigating the arson. and evidence. American Psychologist, 47, 511521.
Barefoot was convicted by the jury of capital murder of Monahan, J., & Steadman, H. J. (1994). Toward a rejuvenation of risk
a police officer. During the death penalty phase of the assessment research. In J. Monahan, & H. J. Steadman (Eds.),
Violence and mental disorder: Developments in risk assessment.
case, the state used psychiatric testimony to demonstrate
Chicago: University of Chicago Press.
that Barefoot posed a threat to society in the future. Mossman, D. (1994). Assessing predictors of violence: Being accurate
Specifically, the state had Drs. John Holbrook and James about accuracy. Journal of Consulting and Clinical Psychology,
Grigson review a hypothetical fact situation based on 62, 783792.
evidence from the case and asked each of the doctors if
the convicted individual would commit violent acts in the
future or would pose a threat to society. Both doctors
testified that the criminal would be a continued threat
to society. In fact, Dr. Grigson concluded that there was
Barona Index
a one hundred percent and absolute probability
G LEN E. G ETZ
that Barefoot would commit violent acts in the future
and thus pose a continued threat to society. The judge
Pittsburgh, PA, USA
sentenced Thomas A. Barefoot to death. Barefoot
appealed the decision and in the Court of Criminal
Appeals raised several concerns about the way his trial
was handled, most notably with respect to the probability
Synonyms
that he would commit future violent acts. Barefoot argued
Premorbid intelligence regression model
that the psychiatrists testifying against him had not even
examined him and were making determinations based on
a hypothetical fact-based situation. Moreover, Barefoot
called into question the ability of psychiatrists to predict Definition
future dangerousness. The Court of Criminal Appeals
rejected all of Barefoots arguments and the U.S. Supreme Barona Index is a demographically based regression
Court rejected Barefoots suggestion that psychiatrists method to estimate premorbid intelligence in terms of
are not competent to make determinations regarding index scores on the Wechsler Adult Intelligence Scale-
dangerousness in future. The U.S. Supreme Court Revised (WAIS-R).
ruled that psychiatrists are no less reliable than laypersons
and that laypersons testimony of future dangerousness is
indeed permissible. The Court upheld that the use of Historical Background
hypothetical questions to establish future dangerousness
is just because such testimony is supported by the Federal Attempts have long been made to estimate premorbid
Rules of Evidence (FRE) that death penalty cases do not intellectual functioning. A frequent method in clinical
present special evidentiary problems. Furthermore, there practice is to estimate the level of premorbid cognitive
is evidence (e.g., Monahan, 1992; Monohan & Steadman, skill by subjectively considering aspects of the individuals
1994; Mossman, 1994) to suggest that mental health history such as education and occupation. Another com-
professionals do indeed predict violence significantly mon approach to estimate premorbid IQ is to use tests of
better than chance when relevant factors are included present ability, which are thought to be relatively resistant
in the determination. to change even during the phases of a psychiatric disorder
or those following a neurologically based disorder. A
variant is the best performance method in which the
References and Readings highest score obtained by an individual is assumed to be
the most likely premorbid level ( Best Performance
Method). Research has been inconsistent as to the
issues. In G. Larrabee (Ed.), Forensic neuropsychology: A scientific effectiveness of this approach. In an attempt to reduce
approach. New York: Oxford University Press. the error in estimating intelligence based on current
344 B Barona Index
functioning and eliminate the subjectivity inherent in these equations resulted in less IQ variance and larger
clinical judgment, demographically based regression standard errors of estimate, cross validation studies were
equations were created to statistically predict intelligence successful.
test scores. A later method of combining demographic
information and current performance on IQ has also been
Current Knowledge
found to be relatively effective.
It is well established that demographic variables, such
Currently, premorbid estimation of IQ functioning
as education, social class and education, are correlated
includes the WAIS-III (Wechsler, 1997). Algorithms
with measured IQ. Wilson et al. (1978) created a regres-
derived from the WAIS-III with demographic variables
sion equation to predict WAIS IQ from demographic
have been developed by the Oklahoma Premorbid Intelli-
variables. They used regression modeling with WAIS Full
gence Estimate (OPIE-3). Four sets of algorithms using
Scale IQ, Verbal IQ, and Performance IQ as criteria and
between one and four WAIS-III subtests have been devised.
age, education, sex, race, and occupation as predictors.
Research consistently suggests that OPIE-3 methods are
With the development of the WAIS-Revised (WAIS-R),
reasonably effective in estimating premorbid intelligence.
further models were needed to estimate premorbid intel-
ligence. Baron, Reynolds, and Chastain (1984) generated
demographic equations for the estimation of premorbid Future Directions
WAIS-R IQ. Subsequently, research demonstrated suc-
cessful discrimination of neurologically based patients As we are on the brink of the release and utilization of
from non-neurologically based patients utilizing the the Wechsler Adult Intelligence Scale-IV, it is quite likely
WAIS-R. As demonstrated in Fig. 1, the predictor vari- that future regression models to estimate premorbid func-
ables incorporated into the model included those origi- tioning as indexed by scores on this test will be developed.
nally utilized by Wilson et al. (1978) as well as urban/rural It is necessary to continue to improve our methods of
residency, geographic location, and handedness. Although estimating premorbid abilities. Future models will most
Barona Index. Figure 1 Barona et al. (1984) regression formulas for pre-morbid IQ
Barthel Index B 345
likely consider other variables and/or include more spe- grooming, dressing, bowel and bladder continence, toilet-
cific criteria for the existing models. For example, the ing, transfers, mobility, and stair use. Items are weighted
expansion of technology along with fewer labor-based and scored according to their perceived importance. B
jobs will very likely influence the occupations used for Higher scores indicate better performance. In the most
the equation. As age expectancy increases, the role of age commonly used version, the maximum score of 100 indi-
on premorbid functioning will quite likely become a more cates full independence. Several versions of the Barthel
important variable as well. Index and their associated scoring methods exist. (Shah
et al. 1989) expanded the scoring categories to improve
the scale discriminability. Others have simplified the scor-
ing system, while incorporating additional categories,
Cross References
to sum to a maximum of 20 points.
Best Performance Method
Intelligence
Premorbid Estimate
Premorbid Functioning
The BI evolved over a 10-year period from the mid-1950s
until its publication in 1964. It was developed to per-
References and Readings mit nursing staff to assess the ability of patients with
neuro-muscular and musculoskeletal disorders to care
Barona, A., & Chastin, R. L. (1986). An improved estimate of premorbid for themselves. It was one of the first measures of activities
IQ for black and whites on the WAIS-R. International Journal of
of daily living (ADL) to be developed. Since its initial
Barona, A., Reynolds, C. R., & Chastain, R. (1984). A demographically
publication, it has been modified to both expand and
based index of premorbid intelligence for the WAIS-R. Journal of restrict the item scoring. The BI is widely used in rehabili-
Consulting and Clinical Psychology, 52, 885887. tation centers, despite subsequent investigations identify-
Schoenberg, M. R., Scott, J. G., Duff, K., & Adams, R. L. (2002). Estima- ing problems with the scaling and sum-scoring system.
tion of WAIS-III intelligence from combined performance and de-
The BI remains popular as it includes the key physical and
mographic variables: Development of the OPIE-3. The Clinical
Neuropsychologist, 16, 426438.
self-care items important for discharge planning and is
Wilson, R. S., Rosenbuam, G., Broan, G., Rourke, D., Whitman, D., & simple to use.
Grisell, J. (1978). An index of premorbid intelligence. Journal of Following the appearance of the BI, many other
Consulting and Clinical Psychology, 46, 15541555. indices of function have been developed, underlining the
importance of this type of tool in rehabilitation practice.
The BI and the Functional Independence Measure (FIM)
are the two most widely used measures of ADL in stroke
research. The BI tends to be used more frequently in
Barthel Index Europe while the FIM is more likely to be used in North
America.
G AVIN W ILLIAMS
Epworth Hospital
Melbourne, Victoria, Australia
Psychometric Data
Synonyms The original version of the BI was developed without the
investigation of content validity for item inclusion or
BI
validity of the scoring system. Many authors have ques-
tioned and subsequently suggested modifications to the
scoring system. Most recently, de Morton et al. (2008)
Description used Rasch analysis to investigate the validity of item
score summation for the BIs original and modified ver-
The Barthel Index (BI) measures ten functions that are sions. They found that score summation was not valid and
important for independent living feeding, bathing, although rescoring may improve the validity of the data
346 B Basal Forebrain
collected at discharge, methods for rescoring outcome

measures are not commonly used in rehabilitation. Basal Forebrain
Many studies have found the BI to have high inter-
rater and retest reliability. The low number of scoring R ANDALL E. M ERCHANT
categories for some individual items means that the BI Virginia Commonwealth University Medical Center
is less likely to be as discriminative or responsive to Richmond, VA, USA
change as scales such as the Functional Independence
Measure (FIM), which has seven scoring categories for
each item. Definition
Despite problems with some psychometric properties
of the BI, it has good clinical utility in that it requires little The basal forebrain is a collection of nuclei and tracts
staff training, is quick and easy to administer, and costs that lie near the bottom and front of the brain. It
nothing. includes the nucleus basalis, diagonal band of Broca,
and medial septal nuclei. This areas neurons are
major producers of acetylcholine which is then
distributed throughout the brain and most important-
Clinical Uses ly to the cerebral cortex and amygdala. The basal
forebrain is most commonly damaged by an aneurysm
The BI is widely used in inpatient rehabilitation settings. It of the anterior communicating artery. When this
encompasses most of the important physical aspects of occurs, there is a reduction in the amount of acetyl-
daily function, but does not directly address impairment choline in the brain, leading to impaired learning,
to communication, cognition, or hearing and vision. The amnesia, and confabulation. A decrease in cholinergic
BI is simple and easy to use with well-defined categories; output by neurons of the basal forebrain is also known
so minimal training or familiarization is required. to occur in cases of Alzheimers disease and senile
dementia.
Cross References
Cross References
Functional Independence Measure (FIM)
Rivermead Mobility Index Anterior Communicating Artery

Basal Ganglia
de Morton, N., Keating, J., & Davidson, M. (2008). Rasch analysis of the
Barthel index in the assessment of hospitalized older patients after
C HRISTINA M ARMAROU, M ATTHEW R. PARRY
admission for an acute medical condition. Archives of Physical Medi-
cine and Rehabilitation, 89(4), 641647.
Mahoney, F., & Barthel, D. (1965). Functional evaluation: The Barthel Richmond, VA, USA
Index. Maryland State Medical Journal, 14, 6165.
McDowell, I., & Newell, C. (1996). Measuring health a guide to rating
scales and questionnaires (2nd ed., pp. 5663). New York: Oxford
Synonyms
University Press.
Sangha, H., Lipson, D., Foley, N., Salter, K., Bhogal, S., Pohani, G., &
Teasell, R. W. (2005). A comparison of the Barthel Index and Basal nuclei
the Functional Independence Measure as outcome measures in
stroke rehabilitation: patterns of disability scale usage in clini-
cal trials. International Journal of Rehabilitation Research, 28(2),
135139.
Definition
Shah, S., Vanclay, F., & Cooper, B. (1989). Improving the sensitivity of the
Barthel Index for stroke rehabilitation. Journal of Clinical Epidemi- The basal ganglia refer specifically to a group of sub-
ology, 42(8), 703709. cortical structures considered as extrapyramidal motor
Basal Ganglia B 347
Cortex Studies in Parkinsons disease (PD) patients uncover the

importance of the basal ganglia in attention the behavior
of target-focusing in the presence of distractors (Brown, B
Soliveri, & Jahanshahi, 1998). Levodopa therapy among
Putamen PD patients improves motor behavior and attentional set-
Indirect shifting; the absence of striatal dopamine has been shown
Thalamus to impair dual-task performance and self-monitoring
VL / VA / CM (Brown & Marsden, 1991; Brown, Soliveri, & Jahanshahi,
Direct
1998; Taylor, Saint-Cyr, & Lang, 1986). For example, PD
patients demonstrate significant impairment in Petrides
self-ordered pointing task (Petrides & Milner, 1982; West,
Ergis, Winocur, & Saint-Cyr, 1998).
The basal ganglia have been shown to regulate tempo-
ral coupling and ordering of both motor and nonmotor
Globus pallidus
sequences (Malapani et al., 1998; Kotz, Schwartze, &
Schmidt-Kassow, 2009). Interestingly, a role in auditory
Int Ext
rhythm detection and generation has been supported
(Grahn & Brett, 2007, 2008); this is analogous to the
well-established role of the basal ganglia in motor timing
Subthalamic nucleus and pattern generation, making the circuitry a rhythm-
pattern generator both in executive (motor) and percep-
tual (cognitive) realms. The implications of this and sim-
ilar work for the perceptual and executive aspects of
Dopaminergic, excitatory language are well-demonstrated (Kotz, Schwartze, &
Glutamatergic, excitatory Schmidt-Kassow, 2009). For example, Smits-Bandstra
GABAergic, inhibitory et al. have described the basal ganglia in the setting of
Basal Ganglia. Figure 1 Basal ganglia circuitry. Diagram persons who stutter (Smits-Bandstra & De Nil, 2007).
illustrates only major direct and indirect circuits. Significant The basal ganglia are involved in a number of other
cortical input is active at every level (not shown) higher-order cognitive functions. For instance, problem-
solving tasks that activate the prefrontal cortex also acti-
vate the basal ganglia. Recent research has shown that
the basal ganglia are significantly involved in learning,
components. These components include caudate and
including motor skill learning, sequence learning, habit
putamen, substantia nigra, subthalamic nucleus, and glo-
learning, and category learning. In addition, the basal
bus pallidus (GP). Figure 1 depicts major circuitry within
ganglia are involved in a number of other cognitive
the basal ganglia.
functions including working memory, attentional sys-
tems, and executive decision making and control. In
addition, the basal ganglia are important for performing
Current Knowledge tasks automatically. While many of the behaviors
engaged in seem simple and are taken for granted, these
Role in behavior and cognition. Rosvold demonstrated a daily behaviors are really patterns of highly organized
topographical coupling between the prefrontal cortex and behaviors with very specific goals and purposes. As tasks
caudate nucleus (Rosvold, 1972; Johnson, Rosvold, & are learned and practiced, they become automated, and
Mishkin, 1968). Considering the major outflow of the require little to no conscious control. The basal ganglia
basal ganglia to the thalamus, it is not surprising that play a critical role in the smooth and efficient operation
a substantial amount of research strongly supports the of such highly automated behavior, and as such are part
role of the basal ganglia in higher-order behavioral and of the complex executive system of the brain. Thus, the
cognitive tasks. Much of this research relies on striatal basal ganglia play a critical in performing everyday prac-
dopaminergic deficit and cortical lesion models in both tical tasks in an effortless and efficient manner (Koziol &
human patients and animal models. Budding, 2009).
348 B Basal Ganglia
Organization. The striatal complex is composed of the GP (Haines, 2004). Three major fiber tracts are associated
neostriatum (caudate and putamen) and ventral striatum with the STN: the subthalamic fasciculus (STF), the ansa
(nucleus accumbens and olfactory tubercle) (Haines, lenticularis (AL), and the lenticular fasciculus (LF). The
2004). Embryologically the same, the caudate and puta- STF connects the STN and GP, crossing the internal cap-
men are separated by the internal capsule. Striosomes and sule; the AL connects the GPi and the thalamus and differs
matrix constitute a chemical and functional separation of from the STF in that it does not directly cross the internal
the striatal complex: striosomes are areas of low acetyl- capsule. Lastly, the LF crosses the internal capsule and
cholinesterase and high neuropeptide content, whereas ultimately joins the AL to form the thalamic fasciculus
matrix regions are rich in acetylcholinesterase (Bernacer, (or the H1 Field of Forel).
Prensa, & Gimenez-Amaya, 2007). This difference in Subthalamic function. The STN is thought to modu-
acetylcholinesterase content provides a convenient histo- late the entire circuitry of the basal ganglia (Hamani,
chemical differentiation between neostriatal regions Saint-Cyr, Fraser, Kaplitt, & Lozano, 2004).
(DiFiglia, Pasik, & Pasik, 1976). The GP consists of two segments: internal (medial,
Striatal function. The GABAergic cells of the striatum GPi) and external (lateral, GPe). The nucleus is bounded
project to the internal segment of GP and substantia nigra medially by the internal capsule, and laterally by
(striosomes project mainly to pars compacta; matrix pro- the putamen (Haines, 2004). Frequently, the term lenti-
jects mainly to pars reticulata). These nuclei also receive form nucleus is used to refer to the GP and putamen
substance-P and enkephalinergic input from the striatum together.
(Menguala, de las Herasb, Erroa, Lanciegoa, & Gimenez- Pallidal function. The internal segment tonically inhi-
Amaya, 1999). The striatum tonically inhibits its pallidal bits the ventroanterior and ventrolateral nuclei of the
and nigral targets. thalamus. The external segment tonically inhibits the
The striatum itself receives inhibitory GABAergic pro- STN and provides transient inhibition to the internal
jections from substantia nigra pars reticulata (Boyes & segment (DeLong & Wichmann, 2007). It is convenient
Bolam, 2007). Major excitatory input is found in gluta- to consider the GP as the gateway between the basal
matergic projections from thalamus (centromedian and ganglia and the thalamus. The thalamus, in turn, relays to
parafascicular nuclei) and cortex (several motor areas), as the motor areas of the cortex.
well as dopaminergic input from substantia nigra pars The basal ganglia have been described in terms of
compacta (Kubota et al., 1987). The latter dopaminergic functionally opposing direct and indirect pathways.
input terminates in both D1 and D2 dopamine receptor Broadly, the direct pathway promotes VA/VL thalamic
subtypes, an important determinant in excitation or inhi- relay to cortex, while the indirect pathway inhibits such
bition of striatal neurons (Surmeier, Ding, Day, Wang, & traffic. The following description of direct and indirect
Shen, 2007). pathways is a summary and integration of previous
The substantia nigra (SN) generally refers to two nu- sources.
clei, pars compacta and pars reticulata (SNpc, SNpr, Direct pathway. The VA/VL thalamic complex is under
respectively). The SN lies within the midbrain, caudal to tonic inhibition from both GPi and SNpr; transient inhi-
the crus cerebri and rostral to the red nucleus (Haines, bition of these nuclei is provided by the striatum. In this
2002). The SNpc contains dopaminergic neurons, while way, excitation of the striatum inhibits GPi output to the
the SNpr contains mostly GABAergic neurons. Intra- thalamus, and the net effect is disinhibition of the VA/VL
nigral connections serve as modulatory loops: GABAergic thalamic complex. The activation of striatal GABAergic
input to SNpc decreases dopaminergic activity within the projections to SNpr and GPi has two sources: cortical
pars compacta; dopaminergic input to SNpr decreases glutamatergic stimulation and nigral dopaminergic stim-
GABAergic activity (Boyes & Bolam, 2007; DeLong & ulation acting upon D1 striatal receptors. In this way, the
Wichmann, 2007). direct pathway is a case of thalamic disinhibition by
Nigral function. The pars reticulata provides tonic suppression of GPi activity.
inhibition of the thalamus, while the major function of Indirect pathway. If the direct pathway is considered as
the pars compacta is dopaminergic input to the striatum a suppression of GPi activity leading to disinhibition of
(Haines, 2002). the thalamus, the indirect pathway is described as sup-
The subthalamic nucleus (STN) is inferior to the thal- pression of the GPe leading to disinhibition of STN. Tonic
amus and medial to the GP; a biconvex-shaped structure, inhibition of STN comes from GPe (whereas tonic inhibi-
the STN is surrounded by dense bundles of myelinated tion of thalamus comes from GPi). The striatum serves to
fibers. The internal capsule separates the STN from the transiently inhibit GPe (as well as inhibit GPi as
Basal Ganglia B 349
previously described). The striatum contains both D1 and Corticostriatal: glutamatergic, from primary-, pre-,
D2 dopamine receptors. While the direct pathway uses D1 supplementary-, and cingulate-motor areas
receptors, the D2 subtype is the main striatal receptor of Nigrostriatal: dopaminergic from pars compacta; B
the indirect pathway. SNpc inhibits striatal output to GPe fibers terminate on two separate dopamine receptor
through these D2 receptors. types; also GABAergic from pars reticulata
In general terms, activity through the direct pathway
promotes thalamocortical activity by disinhibition of the
thalamus; the indirect pathway suppresses thalamocor- Efferent
tical activity. This opposing circuitry is thought to mod- Striatopallidal: GABAergic and substance-P projections to
ulate the net effect of the basal ganglia on thalamic internal segment; GABAergic and enkephalin projections
output. to external segment of globus pallidus
Striatonigral: striosomal GABAergic projections to
pars compacta; matrix GABAergic and enkephalinergic
Illness projections to pars reticulata
Huntington disease, hyperkinetic, choreiform disease, auto-

somal dominant inheritance, pathological CAG trinucleo- Globus Pallidus: Internal, External Segments
tide repeats (Shao & Diamond, 2007). Mechanism of
disease may include enhanced corticostriate activity and Afferent
enhanced thalamic disinhibition (Centonze, Bernardi, & Striatopallidal (see above)
Koch, 2007). The Unified Huntingtons Disease Rating Subthalamopallidal: glutamatergic mainly to internal
Scale is widely accepted to represent an array of disease segment
signs and symptoms (Huntington Study Group, 1996). Nigropallidal: dopaminergic to external segment
Dopamine and glutamate antagonists, as well as GABAer-
gic therapy have been described (Bonelli, Wenning, &
Efferent
Kapfhammer, 2004). Speech and gait therapy are often
Pallidothalamic: GABAergic from internal segment main-
employed. Depression is common among Huntingtons
ly to ventral anterior nucleus of thalamus
disease patients, and antidepressant treatment has been
Pallidonigral: GABAergic from external segment to
described (Korenyi & Whittier, 1967).
pars reticulata
PD, late idiopathic onset, early onset, signs include
Pallidosubthalamic: GABAergic from external seg-
resting tremor, oculomotor disturbance, loss of postural
ment to subthalamic nucleus
reflexes, among other dyskinesias. Pathology includes loss
of nigral dopaminergic neurons, although the cause is
multivariable (Nagatsu & Sawada, 2007; Bergman et al., Substantia Nigra: Pars Compacta, Pars Reticulata
1998). Treatment can involve levodopa therapy and de-
carboxylase antagonists, among a variety of other phar- Afferent
macological agents (Pahwa, 2006). Surgical intervention is Striatonigral and pallidonigral (see above)
a relatively recent development, often targeting STN and Subthalamonigral: glutamatergic to pars reticulata
GPi (Kern & Kumar, 2007).
Other basal ganglia disorders: Wilson disease, Syden-
ham chorea, and ballismus Efferent
Nigrostriatal and nigropallidal (see above)
Nigrosubthalamic: dopaminergic from pars compacta
Summary of Major Components and to subthalamus
Circuitry (See Fig. 1) Nigrothalamic: GABAergic to ventromedian and ven-
trolateral nuclei of thalamus
Striatum: Caudate, Putamen
Afferent Subthalamic Nucleus

Thalamostriatal: glutamatergic, mainly from caudal intra-
laminar nuclei (centromedian and parafascicular nuclei); Afferent
glutamatergic Pallidosubthalamic and nigrosubthalamic (see above)
350 B Basal Ganglia
Efferent Thalamus
Subthalamopallidal and subthalamonigral (see Tremor
above)
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Neostriatal cholinergic neurons receive direct synaptic inputs from
Nucleus Basalis of Meynert B
dopaminergic axons. Brain Research, 413, 179184.
Malapani, C., Rakitin, B., Levy, R., Meck, W., Deweer, B., Dubois, B., et al.
(1998). Coupled temporal memories in Parkinsons disease: A
dopamine-related dysfunction. Journal of Cognitive Neuroscience,
10, 316331.
Menguala, E., de las Herasb, S., Erroa, E., Lanciegoa, J. L., & Gimenez-
Amaya, J. M. (1999). Thalamic interaction between the input and Base Rate (Population)
the output systems of the basal ganglia. Journal of Chemical Neuro-
anatomy, 16(3), 185197. M OLLY E. Z IMMERMAN
Nagatsu, T., & Sawada, M. (2007). Biochemistry of postmortem brains in
Albert Einstein College of Medicine
Parkinsons disease: Historical overview and future prospects. Jour-
nal of Neural Transmission Supplement, 72, 113120. Bronx, NY, USA
Pahwa, R. (2006). Understanding Parkinsons disease: An update on
current diagnostic and treatment strategies. Journal of the American
Medical Directors Association, 7(7 Suppl. 2), 410. Definition
Petrides, M., & Milner, B. (1982). Deficits on subject-ordered tasks after
frontal and temporal lobe lesions in man. Neuropsychologia, 20,
601604. The population prevalence of a variable of interest is
Rosvold, H. (1972). The frontal lobe system: Cortical-subcortical inter- known as the base rate.
relationships. Acta Neurobiologica Experimentalis (Warsaw), 32,
439460.
Shao, J., & Diamond, M. I. (2007). Polyglutamine diseases: Emerging
concepts in pathogenesis and therapy. Human Molecular Genetics, 15
Current Knowledge
(16) Spec No. 2, R115R123.
Smits-Bandstra, S., & De Nil, L. (2007). Sequence skill learning in persons
who stutter: Implications for cortico- striato-thalamo-cortical dys- Base rates can be calculated using the following formula
function. Journal of Fluency Disorders, 32(4), 251278. (Gouvier, 1999):
Surmeier, D. J., Ding, J., Day, M., Wang, Z., & Shen, W. (2007). D1 and
D2 dopamine-receptor modulation of striatal glutamatergic signal- #cases with condition of interest
Base Rate
ing in striatal medium spiny neurons. Trends in Neurosciences, 30(5), #cases in a population
228235.
Taylor, A., Saint-Cyr, J., & Lang, A. (1986). Frontal lobe dysfunction in
Parkinsons disease: The cortical focus of neostriatal outflow. Brain, In neuropsychological settings, base rates are often
109, 845883. used to characterize diagnostic accuracy and interpret
West, R., Ergis, A., Winocur, G., & Saint-Cyr, J. (1998). The contribution the sensitivity and specificity of a clinical assessment.
of impaired working memory monitoring to performance of the
The sensitivity of a test is the probability of correctly
self-ordered pointing task in normal aging and Parkinsons disease.
Neuropsychology, 12, 546554. identifying an individual with impaired functioning as
actually being impaired, while the specificity of a test
is the probability of correctly identifying an individual
with normal functioning as actually being normal
(Lezak, Howieson & Loring, 2004). When the base rates
of a condition are low, the sensitivity of a test may
Basal Ganglia-Thalamocortical be misleading. When the base rates of a condition are
Circuit high, the specificity of a test may be misleading (Podell,
DeFina, Barrett, McCullen & Goldberg, 2003). The neu-
CorticalSubcortical Loop ropsychologist should consider base rates of a disorder
when selecting tests for use in a specific population.
Knowledge of base rates may also indicate that im-
pairment cutoff scores should be adjusted to interpret
diagnostic accuracy. Assessments of malingering or sub-
Basal Nuclei optimal effort should also be conducted with consider-
ation of base rates for a particular condition of interest
Basal Ganglia (Gouvier, 1999).
352 B BASI
Cross References Forms
Sensitivity There are two forms: a comprehensive form and a survey

form. The comprehensive form comprises six timed
subtests: vocabulary, spelling, language mechanics,
reading comprehension, math computation, and math
References and Readings application. The survey form is a screening tool compris-
ing two subtests: verbal skills and math skills. The subtests
Gouvier, W. D. (1999). Base rates and clinical decision making in neuro- can be administered independently to measure specific
psychology. In J. J. Sweet (Ed.), Forensic neuropsychology (pp. 2738).
skills or in any combination. There are four grade levels
Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuropsychologi-
(IIV), 3rd to 4th grade, 5th to 6th grade, 7th to 8th, and
cal assessment. Oxford: Oxford University Press. 9th to 12th. Student progress can be assessed through
Podell, K., Defina, P. A., Barrett, P., McCullen, A., & Goldberg, E. (2003). Form A with Fall norms (August to December) and
Assessment of neuropsychological functioning. In I. B. Weiner, Form B with Spring norms (January to July). A growth
D. K. Freedheim, J. A. Schinka, & W. F. Velicer (Eds.), Handbook of
scale value (GSV) is also made available to measure the
psychology (pp. 443466). New York: Wiley.
progress of students.
Administration
BASI
The tests can be administered individually or in groups,
Basic Achievement Skills Inventory timed or untimed; the comprehensive form takes about
2 h and the survey form takes about 50 min to complete.
Scoring and Report

Basic Achievement Skills
Scoring for the comprehensive form is available through
Inventory Q local software, mail-in scoring, or hand-scoring. There
are two reports (student summary report with parent
D ORIS S. M OK
summary report, and adult summary report). The student
University of Macau
summary report includes standard scores, percentile
Taipa, Macau SAR, China
scores, age equivalents, and grade equivalents as well as
classification (low average, average to above average) by
learning objective. The adult summary report includes
Synonyms
percent correct, grade equivalent, and classification by
learning objective.
BASI
Scoring for the survey form can be obtained through
Q local software and hand-scoring but not mail-in
scoring. In addition to the summary report, an employ-
Description ment report is available for the survey form, providing
standard scores compared to those of adults with different
The Basic Achievement Skills Inventory (BASI) is a education levels.
commercially published, norm-referenced achievement
test that assesses math, reading, and language skills
for children and adults. Information on the test is easily Historical Background
accessible through the publishers webpage (http://www.
pearsonassessments.com/basi.aspx), which includes rele- Achilles N. Bardos, PhD, is the author of the test.
vant excerpts from the manual, a flash demo, sample (http://www.unco.edu/cebs/SchoolPsych/faculty/BASI/
reports and others. index.html)
Basic Achievement Skills Inventory B 353
The BASI is a newly developed test published in 2004. It students; (4) make placement decisions for ESL, GED, and
was developed with the assistance of teachers who wrote the program placement; (5) track academic progress, etc.
test items, which were then reviewed by curriculum experts. Specific applications in four settings are proposed in the B
Content was based on curriculum standards from The BASI Flash Demo (http://www.pearsonassessments.
Model Curriculum and Assessment Database (MCAD), a com/basidemo/basi.swf): (1) K-12 school/educational
database used by educators to align with district, state, and setting, (2) corrections setting for intake and evaluation of
national curriculum requirements and standards. offenders for placement in programs, (3) public safety for
employment screening, and (4) adult and child clinical
setting. Since BASI is a relatively new test, there are limited
research data to support its use across the wide variety of
Psychometric Data proposed settings. Literature search using PSYCINFO and
ERIC databases identifies one study (Griffith, 2006) using
Standardization is reportedly based on stratified random
the BASI with military students.
sampling to match closely with the US Census 2000.
Rhoades (2007) and Trevisan (2007) cautioned against
For the comprehensive form, a grade-appropriate sample
individual administration of the BASI due to the lack of
was stratified according to gender, race, parental educa-
standardization procedures. In adult and child clinical set-
tion, and region. Standardization of Form A was based on
tings, the BASI Comprehensive Form is recommended to
2,439 students tested during Fall 2002 and standardiza-
be used as a time- and cost-effective screening, providing an
tion of Form B was based on 2,130 students tested in
overview of achievement or alternative for individually
Spring 2003. The survey form included a school-age stan-
administered achievement test when detailed information
dardization sample of 2,518 students (aged 818) tested in
is not needed. The test is not recommended for diagnostic
school settings and an adult sample of 2,452 adults (aged
purposes but serves only as a screener to assist in the
1980) recruited in a variety of settings.
diagnostic process. There is no current support of its use
The test has good reliability. Buros Institute test
in neuropsychological testing. BASI appears best for cost-
reviewers (Rhoades, 2007; Trevisan, 2007) reported the
effective, group-based assessment and has been selected to
testretest stability, internal consistency, and alternate-
be used in educational and forensic settings such as pre- and
forms reliability to be fairly strong, with estimates ranging
posttesting under the Florida Juvenile Justice Common
from 0.54 to 0.96 for individual subtest scores and
Assessment Program. When more research data are avail-
0.670.98 for composite scores.
able, the potential use of the BASI can be reexamined.
Test validity is established through the Iowa Tests of
Basic Skills (ITBS), the Iowa Tests of Education Develop-
ment (ITED), the Tests of Adult Basic Education (TABE),
the Wechsler Individual Achievement Test Second Cross References
Edition (WIAT-II) and the Woodcock Johnson Psycho-
educational Battery III (WJ-III). A review of the data Academic Skills
(http://www.pearsonassessments.com/basi-correlation.
htm) indicates that intercorrelations between subtests are
supported; correlation coefficients range from low to References and Readings
high. Rhoades (2007) noted that correlations between
subtests with similar constructs are not particularly Griffith, R. (2006). An examination of factors influencing differences in
academic performance among active duty military students and
strong. Since some of the correlation studies were based
naval reserve officer training corps scholarship students in a univer-
on small sample size of students (around 40), unstable sity setting. Dissertation Abstracts International Section A, 67, 2071.
correlations are not unusual (Trevison, 2007). Retrieved from PsycINFO database.
Rhoades, E. K. (2007). Test review of the basic achievement skills inven-
tory. In K. F. Geisinger, R. A. Spies, J. F. Carlson, & B. S. Plake (Eds.),
The seventeenth mental measurements yearbook [Electronic Version].
Clinical Uses Retrieved February 17, 2009, from the Buros Institutes Test Reviews
Online website: http://unl.edu/buros
Trevisan, M. S. (2007). Test review of the basic achievement skills inven-
The author proposes that the comprehensive form provides
tory. In K. F. Geisinger, R. A. Spies, J. F. Carlson, & B. S. Plake (Eds.),
a complete evaluation of academic skills to (1) determine The seventeenth mental measurements yearbook [Electronic Version].
academic strengths and weaknesses; (2) screen for and assist Retrieved February 17, 2009, from the Buros Institutes Test Reviews
in diagnosing learning disabilities; (3) place for college Online website: http://unl.edu/buros
354 B Basilar Artery
Basilar Artery Battery Approach

E LLIOT J. R OTH M OLLY E. Z IMMERMAN
Northwestern University Albert Einstein College of Medicine
Chicago, IL, USA Bronx, NY, USA
The basilar artery provides blood to the brain. This artery A battery approach to neuropsychological assessment is
and the two vertebral arteries comprise the vertebrobasilar the administration of multiple measures that cover a wide
system, which supplies blood to the posterior part of circle range of cognitive abilities to fully characterize an indivi-
of Willis and connects (anastomoses) with blood sup- duals neuropsychological strengths and weaknesses.
plied to the anterior part of the circle of Willis from the
carotid arteries. It arises from the confluence of the two
vertebral arteries, next to the lower brain stem, ascends Current Knowledge
parallel to the brain stem, and gives rise to the anterior
inferior cerebellar artery, which supplies part of the cere- The battery approach is predicated on the existence of a
bellum, some smaller branches that supply the brain stem, variety of instruments that have been empirically devel-
and the superior cerebellar artery. It finally divides into oped to measure myriad aspects of neuropsychological
the two posterior cerebral arteries (PCA). These supply function. Neuropsychological batteries generally contain
the upper brain stem, the occipital lobe, and the posterior a measure of general intellectual functioning or premor-
portion of the temporal lobes. bid functioning as well as assessments of basic neuropsy-
chological functions that may include attention, executive
Current Knowledge function, language, memory, visuospatial perception and
construction, and psychomotor function. Performance on
The clinical manifestations of basilar artery occlusion a test of general intellectual function serves as a context in
depend on the location of the occlusion, the extent of which performance across neuropsychological domains
thrombus, and the collateral flow. Normally, the blood can be considered. Selection of individual tests that com-
flows in an anterograde fashion from the vertebral arteries prise a neuropsychological battery is very likely to depend
to the basilar artery up to its terminal branches. This on the assessment setting, nature of the presenting prob-
pattern of flow may vary. If the proximal segment of the lem and differential diagnosis, and the theoretical orien-
basilar artery is occluded and the occlusion resulted from a tation of the clinician.
slowly progressive stenosis, collateralization occurs within One of the first battery approaches was what is com-
the cerebellum into the circumferential branches of the monly referred to today as the fixed battery. In the fixed
basilar artery. In addition, flow can be reversed from the battery approach, test selection is predetermined irrespec-
PCAs into the distal basilar artery. Thrombosis of the tive of the patients presenting problem. A comprehensive
basilar artery causes various clinical syndromes that result battery of tests is administered to all patients in the same
from brainstem ischemia, including cranial nerve dysfunc- standardized manner. Collection of collateral medical and
tion, difficulty in swallowing and breathing, and at its most social history is obtained following administration and
severe, locked-in syndrome. Basilar artery thrombosis is the scoring of the neuropsychological data to avoid response
most common cause of locked-in syndrome. Mortality rate bias on the part of the test administrator. Examples of this
of basilar artery occlusion is 70%, but this can be reduced psychometrically oriented, data-driven approach include
substantially through the use of antithrombotic agents. the LuriaNebraska Battery and the HalsteadReitan Bat-
tery. An advantage of the fixed battery approach is that it
Cross References facilitates comparison of test scores across patient groups
and assessment settings. Another advantage of the battery
Circle of Willis approach, when using standardized tests, is that this
Posterior Cerebral Artery approach facilitates the use of technicians in the adminis-
Vertebrobasilar System tration of the tests. This approach can also facilitate the
Battle Sign B 355
development of data banks for research purposes. A dis- flexible battery approach increased from 54% in 1989 to
advantage, however, is that it is often time-consuming, 70% in 1999. These data reflect the relative popularity of
cost-prohibitive, and may produce excessive testing ses- this approach, and suggest that it is likely to remain in B
sions that are poorly tolerated by patients (Mitrushina, favor in the coming years.
Boone, Razani, & DElia, 2005).
An alternative neuropsychological assessment method
is the flexible battery approach. In this hypothesis-driven Cross References
approach, initial test selection is guided by the patient
referral question, presenting problem, and the clinical Boston Process Approach
interview. A modest range of measures that survey a broad Fixed Battery
range of cognitive functions is specifically chosen to probe Flexible Battery
and characterize the patients presumed strengths and
weaknesses. Following this initial assessment, which is
sometimes referred to as a core or screening battery, References and Readings
the clinician will then select additional tests based on the
patients performance on the core battery and reported Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuropsychologi-
cognitive concerns (Strauss, Sherman, & Spreen, 2006). cal assessment. Oxford: Oxford University Press.
Mitrushina, M., Boone, K. B., Razani, J., & DElia, L. F. (2005). Handbook
The flexible battery approach is more focused on each
of normative data for neuropsychological assessment. Oxford: Oxford
individual patients presenting problem and differential University Press.
diagnosis than the fixed battery approach. As a result, the Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A compendium of
total assessment period is restricted and may be more neuropsychological tests: Administration, norms, and commentary.
cost-effective. However, inherent in the flexible battery Oxford: Oxford University Press.
Sweet, J. J., Moberg, P. J., & Sucy, Y. (2000). Ten-year follow-up survey of
approach is the inconsistent administration of tests across
clinical neuropsychologists: Part 1. Practices and beliefs. The Clinical
patient groups. That is, not all of a neuropsychologists Neuropsychologist, 14, 1837.
patients will receive the same tests, thereby limiting com-
parisons of findings across patient groups or settings
(Mitrushina et al., 2005).
A variant of the flexible battery approach is the pro-
cess approach, also known as the Boston process approach Battle Fatigue
(Lezak, Howieson, & Loring, 2004). This method entails
emphasis on the more qualitative aspects of neuropsycho- Posttraumatic Stress Disorder
logical performance. When completing a task, patients are
closely observed for strategy formation and execution.
Atypical performances will be further probed by the clini-
cian with direct questioning or modified re-administra- Battle Sign
tion of the task to more fully examine the nature of
the behavioral dysfunction. This approach affords a B ETH R USH
more in-depth characterization of the patients neuropsy- Mayo Clinic
chological abilities. However, it has been criticized for its Jacksonville, FL, USA
lack of normative data and standards for the reliability
and validity of its methods (Strauss et al., 2006).
Synonyms
Future Directions Periauricular or mastoid ecchymosis
Although all battery approaches to neuropsychological

assessment have advantages and disadvantages, results Definition
from a recent survey from Sweet, Moberg and Sucy
(2000) suggest that the flexible battery approach is the Crescent-shaped bruise wrapping behind the base of the
method that is most preferred by clinicians. According to ear lobe and extending posteriorly towards the point of
this report, the percentage of clinicians who endorsed the the neck where the base of the skull meets the neck. This
356 B Baxter v. Temple (2005)
clinical symptom indicates the presence of a skull fracture. opinion that neuropsychologists were not competent to
A patient with this symptom may present with bloody offer expert testimony on brain malfunctions from motor
discharge of the ear. The bruise results from the force of vehicle accidents. The appellate court held that to exclude
impact, which forces the flow of blood out of the vascular such testimony on physical matters by psychologists
endothelium of a vessel into adjacent skin tissue. The would be to ignore present medical and psychological
battle sign may occur a few days following the onset of practice. Most states allow neuropsychological testimony
the skull fracture. about brain damage (Richardson & Adams, 1992) while
there is a greater diversity of opinion as to testimony
about causation.
Cross References
Current Knowledge
Depressed Skull Fracture
In Baxter v. Temple (2005), defense filed a motion in
limine to exclude the testimony of a neuropsychologist
References and Readings in a case of lead exposure as insufficiently unreliable
because opinions were based on results from a flexible
Victor, M., & Ropper, A. H. (2001). Principles of neurology (7th ed., neuropsychological test battery. The defense argued suc-
pp. 925953). New York: McGraw-Hill. cessfully that the neuropsychologists testimony should be
excluded because the Boston Approach had not been
subject to peer review and publication, has no known or
potential error rate, and is not generally accepted in the
Baxter v. Temple (2005) appropriate scientific literature. In other words, Daubert
factors were used by the trial judge to exclude expert
R OBERT L. H EILBRONNER neuropsychological evidence. Furthermore, the court
Chicago Neuropsychology Group made an important distinction between the roles of a
Chicago, IL, USA clinical provider and forensic examiner, emphasizing
that neuropsychologists in forensic practice must employ
objective methods that allow them to be unbiased truth
Synonyms seekers. The defendant motion in limine was granted.
Some (Reed, 1996) have argued that Daubert challenges
Admissibility of psychological/neuropsychological evidence of idiosyncratic (flexible) test combinations will eliminate
the use of flexible neuropsychological batteries in forensic
consulting. However, recent surveys of neuropsycholo-
gists show that the majority of neuropsychologist practi-
Historical Background tioners use a carefully constructed battery approach
specifically tailored to the patient/examinees specific
One of the first decisions to address the admissibility of
issues. In 2008, the New Hampshire Supreme Court
expert testimony by a psychologist or neuropsychologist
reviewed the neuropsychological literature, practices of
as to the existence of a brain injury or mental defect was
neuropsychologists, considered relevant Daubert stan-
Jenkins v. United States (1962). This was a criminal trial in
dards and various amicus briefs, and concluded that the
which the jury was instructed to disregard the testimony
exclusion of the neuropsychological testimony in Baxter v.
of the psychologists on the grounds that they could not
Temple (2005) was in error.
give a medical opinion as to mental disease or defect
because they did not have medical training. The appellate
court reversed the decision holding that the expert did not Cross References
need to be a medical practitioner. A later opinion, in
United States v. Riggleman (1969) supported the position Admissibility
that psychologists were not excluded from testifying Daubert v. Merrell Dow
about criminal sanity solely because they lacked medical Expert v. Treater Role
training. Simmons v. Mullins (1975) was an early appellate Federal Rules of Evidence
court decision that essentially reversed a trial court Kumho Tire v. Carmichael
Bayley Scales of Infant and Toddler Development B 357
References and Readings five domains: Cognitive (91 items), Language (49 recep-
tive and 48 expressive), Motor (66 fine motor and 72 gross
Chapple v. Ganger, 851 F. Suppl. 1481 (E. D. Wash, 1994). motor), Social-Emotional, and Adaptive. Like its prede- B
Greiffenstein, M. F. (2009). Basics of forensic neuropsychology. In cessors, the BSID-III is a modified power test. Assessment
J. Morgan & J. Ricker (Eds.), Textbook of clinical neuropsychology.
of the first three domains is accomplished by item admin-
Greiffenstein, M. F., & Cohen, L. (2005). Neuropsychology and the law:
istration, while the latter two are completed using care-
Principles of productive attorneyneuropsychologists relations. giver response to a questionnaire. A Behavior Observation
In G. Larrabee (Ed.), Forensic neuropsychology: A scientific approach. Inventory is completed by both the examiner and the care-
New York: Oxford University Press. giver, and allows assessment of the childs behavior during
Jenkins v. United States (1962). 307 F. 2d 637.
testing and at home. The Language scale includes Receptive
Kaufmann, P. M. (2008). Admissibility of neuropsychological evidence in
criminal cases: Competency, insanity, culpability, and mitigation.
Communication and Expressive Communication subtests;
In R. Denney & J. Sullivan (Eds.), Clinical neuropsychology in the the Motor scale includes a Fine Motor and a Gross Motor
criminal forensic setting. New York: Guilford Press. subtest. The BSID-III Social-Emotional scale is an adapta-
Richardson, R. E. L., & Adams, R. L. (1992). Neuropsychologists as expert tion of the Greenspan Social-Emotional Growth Chart: A
witnesses: Issues of admissibility. The Clinical Neuropsychologist, 6,
Screening Questionnaire for Infants and Young Children
295308.
Simmons v. Mullins (Pa. Super Ct. 1975). 331 A2D 892, 897.
(Greenspan, 2004). The Adaptive Behavior scale is com-
United States v. Riggleman (4th Cir. 1969). 411 F.2d 1190. posed of items from the Parent/Primary Caregiver Form
of the Adaptive Behavior Assessment System-Second Edi-
tion (Harrison & Oakland, 2003). This scale measures
areas such as communication, community use, health
and safety, leisure, self-care, self-direction, functional
Bayley pre-academics, home living, social and motor, and yields
a General Adaptive Composite (GAC). Discrepancies
Bayley Scales of Infant and Toddler Development
between scaled scores can be reviewed to determine
whether the differences between subtests are statistically
significant.
Bayley Scales of Infant and

Toddler Development Historical Background
G LEN P. AYLWARD The original BSID (Bayley, 1969) evolved from versions of
SIU School of Medicine-Pediatrics developmental tests that were administered to infants
Springfield, IL, USA enrolled in the landmark National Collaborative Perinatal
Project. It was considered the reference standard for the
assessment of infant development and administered to
Synonyms infants over the first 2 years. The BSID was theoretically
eclectic and borrowed from different research and test
Bayley; BSID-III instruments. The test contained three components: the
Mental Developmental Index (MDI), the Psychomotor
Developmental Index (PDI) (M = 100, SD = 16) and the
Description Infant Behavior Record, and was applicable from 2 to
30 months.
The Bayley Scales of Infant and Toddler Development- The BSID subsequently was revised into the BSID-II
Third Edition (BSID-III; 2006) is often considered to be (Bayley, 1993), this due in part to the upward drift
the reference standard for developmental assessment. It is of approximately 11 points on the MDI and 10 points
an individually administered test, applicable from 1 to on the PDI, reflecting the Flynn effect. Although the
42 months of age. The stated primary purpose of the mean remained the same, the SD was now 15. When
BSID-III is to identify children with developmental delay compared to the original BSID, the BSID-II scores
and to provide information for interventions. were 12 points lower on the MDI and 10 points lower
The BSID-III was normed on 1,700 children (divided on the PDI. The Behavior Rating Scale was devel-
into 17 age groups) and development was assessed across oped to enable the assessment of state, reactions to
358 B BBA
the environment, motivation, and interaction with peo- levels of development. Repeated administration can docu-
ple. The age range of the BSID-II was expanded to span ment the effects of an intervention program. However,
142 months. The instrument contained 22 item sets changes in test content and alteration of scales in conjunc-
and basal and ceiling rules that differed from the origi- tion with the Flynn effect and the more recent increase in
nal BSID. These rules were controversial because if mean scores (in comparison to the previous version) make
correction for prematurity was used to determine the longitudinal comparisons of scores difficult in individual
item set to begin administration, or if an earlier item children or cohorts. Extracting language items from the
set was employed because of developmental problems, cognitive scale also affects comparability with the MDI
scores tended to be somewhat lower, because the child found in previous versions. Conversely, the five domains
was not automatically given credit for passing the lower now allow the BSID-III to be more compatible with early
item set. The BSID-II was also criticized because it intervention requirements (IDEA; PL 108446, Part C). A
did not provide area scores compatible with IDEA criticism of the test is that it can take an exceptionally long
requirements for cognitive, motor, communication, so- time to administer and this can be very problematic when
cial, and adaptive function. testing young children. The BSID-III can be used in mul-
tidisciplinary clinics, NICU follow-up programs, or as a
follow-up evaluation after a child has been identified by
Psychometric Data the use of a screening test.
On the BSID-III, norm-referenced scaled scores (M = 10,

SD = 3), composite scores (M = 100, SD = 15), percentile References and Readings
ranks, and growth scores are provided in addition to
confidence intervals for the scales and developmental Bayley, N. (1969). The Bayley scales of infant development. San Antonio,
age equivalents. Composite scores range from 55 to 155, TX: The Psychological Corporation.
Bayley, N. (1993). The Bayley scales of infant development (2nd ed.). San
depending on the scale. Internal consistency of the subt-
Antonio, TX: The Psychological Corporation.
ests range from .86 to .93; intercorrelations between Cog- Bayley, N. (2006). Bayley scales of infant and toddler development
nitive and Language composites was .52, for Cognitive (3rd ed.). San Antonio, TX: The Psychological Corporation.
and Motor composites, .50, and the intercorrelation be- Greenspan, S. I. (2004). Greenspan social-emotional growth chart. A
tween Language and Motor composites was .49. Growth screening questionnaire for infants and young children. San Antonio,
TX: Harcourt Assessment, Inc.
scores are new and are used to longitudinally plot the
Harrison, P. L., & Oakland, T. (2003). Adaptive behavior assessment system
childs growth over time for each subscale. This metric is (2nd ed.). San Antonio, TX: The Psychological Corporation.
calculated based on the subtest total raw score and ranges Newborg, J. (2005). The battelle developmental inventory (2nd ed.). Itasca,
from 200 to 800 (M = 500, SD = 100). Similar to the IL: Riverside Publishing.
original BSID, there are basal rules (passing the first three
items at the appropriate age start-point) and ceiling or
discontinue rules (a score of 0 for five consecutive items).
The correlation between the BSID-III Language Com- BBA
posite and the previous BSID-II MDI is .71, the Motor
Composite and the BSID-II PDI = .60, and the Cognitive Brunel Balance Assessment
Composite and the BSID-II MDI = .60. However, in con-
trast to the expected Flynn effect, the Bayley-III Mental
and Motor composite scores are approximately 7 points
higher than the corresponding BSID-II MDI and PDI.
This phenomenon has also been reported with other BBS
developmental tests such as the Battelle Developmental
Inventory-Second Edition (Newborg, 2005). Berg Balance Scale
Clinical Uses
BCRS
Administration of the BSID-III provides quantitative and
qualitative data that give insight into the childs current Brief Cognitive Rating Scale
Beck Anxiety Inventory B 359
Beck Anxiety Inventory. Table 1 Anxiety Level by Score

BCT (Beck & Steer, 1993)
Category Test Anxiety Level Minimal Mild Moderate Severe B

Score 07 815 1625 2663
asked to rate each item on a 4-point scale ranging from

BDAE 0 (not at all) to 3 (severely, can barely stand it). Ratings are
for the past week. Items are summed to obtain total scores
Boston Diagnostic Aphasia Examination
ranging from 0 to 63 (Beck & Steer, 1993).
Time to complete the measure is 10 min. An additional
5 min is required for scoring. Although the age range
stated in the manual is between 17 and 80, studies have
BDI been conducted with younger populations (Osman,
Hoffman, Barrios, Kopper, Breitenstein, & Hahn, 2002),
Beck Depression Inventory providing support for its use among adolescents. The
Inventory can be administered and scored by hand.
Administration via interview or computer is possible,
and computerized scoring is available.
BDI-II
Beck Depression Inventory
The measure was developed to assess cognitive and psy-
chological symptoms of anxiety, with the goal of reliably
discriminating between anxiety- and depression-related
Bearing symptoms. An initial item pool (86 items) was compiled
from three existing scales (the Anxiety Checklist [Beck,
Orientation Steer, & Brown, 1985], Physicians Desk Reference Check-
list [Beck, 1978], and Situational Anxiety Checklist [Beck,
1982]). These measures contained items regarding the
wide range of symptoms reported by those with anxiety
disorders (Beck et al., 1988). A series of analyses were
Beck Anxiety Inventory conducted to reduce the item pool to 21 (Beck et al.,
1988). Initially, redundant items were eliminated. Succes-
L ISA A. B RENNER sive iterated principal factor analyses were used to achieve
VISN 19 MIRECC further item reduction (Beck et al., 1988). Remaining
Denver, CO, USA items were evaluated (validity and reliability analyses)
and results yielded a 21-item scale (Beck et al., 1988).
Synonyms
Psychometric Data
BAI
Work by Beck et al. (1988) suggests high internal consis-
tency (0.92) and test-retest reliability over 1 week, r(81) =
Description 0.75. The Inventory was shown to discriminate between
those with and without anxiety-related disorders. The BAI
The Beck Anxiety Inventory (BAI) (Beck, Epstein, Brown, & was also moderately correlated with the revised Hamilton
Steer, 1988; Beck & Steer, 1993) is a 21-item scale developed Anxiety Rating Scale, r(150) = 0.51. In addition, the
to assess the severity of anxiety symptoms. Respondents are validity of the BAI has been supported by findings
360 B Beck Anxiety Inventory
which suggest that the BAI and the Beck Depression note that scores should be interpreted based on normative
Inventory (BDI) (Beck, Rush, Shaw, & Emery, 1979) mea- data taking into account gender, age, and living situation.
sure different symptoms (Hewitt & Norton, 1993). In addition to its use with general clinical populations,
A number of factor-analytic studies have been the BAI has demonstrated utility in neuropsychological
conducted regarding the BAI and results have provided populations. The BAI has been used in clinical trials of
two- (cognitive and somatic components) (Hewitt and psychotropic interventions for depression following trau-
Norton, 1993), four- (subjective, neurophysiological, matic brain injury (TBI) (Ashman et al., 2009), and as a
autonomic, and panic) (Beck and Steer, 1991), five- (sub- measure of anxiety following TBI (Cantor et al., 2005).
jective fear, somatic nervousness, neurophysiological, Trahan, Ross, and Trahan (2001) used the BAI to study
muscular/motoric, and respiration) (Borden, Peterson, the relationship between self-reported post-concussive
& Jackson, 1991), six- (somatic distress, fear, autonomic and psychiatric symptoms in neurologically normal
hyperactivity, panic, nervousness, and motor tension) young adults and those recovering from mild TBI. They
(Morin, Landreville, Colecchi, McDonald, Stone, & found correlations between a composite of measure of
Ling, 1999) factor solutions. Hewitt and Norton (1993) post-concussive symptoms and the BAI. The BAI has
suggest that this range in number of identified factors also been used to measure anxiety following stroke
may, in part, be related to the inconsistency of specific (Moon, Kim, Kim, Won, & Kim 2004), though some
items composing the factors (somatic and cognitive) and research suggests that caution is warranted in its use
differences in factor-analytic approaches used. In psychi- with this population due to the potential overlap between
atric patients, Hewitt and Norton (1993) provided evi- somatosensory anxiety symptoms and neurological con-
dence to support that their two-factor structure was sequences of stroke (Schramke, Stowe, Ratcliff, Goldstein,
similar for men and women, despite the fact that & Condray, 1998).
women seemed to report more anxiety than men. Explor-
ing the psychometric properties of the BAI with older
adults, Morin et al.s six-factor solution included multi- Cross References
ple subjective, motoric, and physiological dimensions of
anxiety. A trend for older subjects to obtain slightly Anxiety
higher scores was also noted. Given the lack of consensus Beck Depression Inventory
regarding underlying factors for the BAI, use of the total
score, as recommended in its initial development (Beck &
Steer, 1993), remains the predominant approach for mea- References and Readings
suring anxiety with this instrument.
Ashman, T. A., Cantor, J. B., Gordon, W. A., Spielman, L., Flanagan, S.,
Ginsberg, A., et al. (2009). A randomized controlled trial of sertra-
line for the treatment of depression in persons with traumatic brain
Clinical Uses injury. Archives of Physical Medicine & Rehabilitation, 90(5),
733740.
The BAI appears to adequately measure anxiety-related Beck, A. T. (1978). PDR checklist. Philadelphia: University of Pennsylva-
symptoms, but may be more sensitive to physiological nia, Center for Cognitive Therapy.
Beck, A. T. (1982). Situational anxiety checklist (SAC). Philadelphia:
aspects of anxiety disorders (Ferguson, 2000). This is likely
University of Pennsylvania, Center for Cognitive Therapy.
in part related to the fact that items were selected to Beck, A. T., Epstein, N., Brown, G., & Steer, R. A. (1988). An inventory for
adequately discriminate between those with anxiety ver- measuring clinical anxiety: Psychometric properties. Journal of Con-
sus depression. As such, Ferguson (2000) notes that the sulting and Clinical Psychology, 56, 893897.
BAI may not be sensitive to detecting anxiety disorders Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive therapy
of depression: A treatment manual. New York: Guilford Press.
where psychophysiological arousal was not a prominent
Beck, A. T., & Steer, R. A. (1991). Relationship between the Beck Anxiety
feature, (p. 520). He also notes that the instrument has a Inventory and the Hamilton Anxiety Rating Scale with anxious
high level of face validity and, as such, respondent moti- outpatients. Journal of Anxiety Disorders, 5, 213223.
vation may impact reporting. In general clinical settings, Beck, A. T., & Steer, R. A. (1993). Beck Anxiety Inventory manual. San
the Inventory may be best used in conjunction with addi- Antonio, TX: Psychological Corporation.
Beck, A. T., Steer, R. A., & Brown, G. (1985). Beck anxiety checklist.
tional findings to diagnose anxiety-related disorders and
Unpublished manuscript, University of Pennsylvania.
assess treatment needs and responses. Borden, J. W., Peterson, D. R., & Jackson, E. A. (1991). The Beck Anxiety
Although it has been suggested the BAI is a valuable Inventory in nonclinical samples: Initial psychometric properties.
screen tool for older adults, Morin and colleagues (1999) Journal of Psychopathology and Behavioral Assessment, 13, 345356.
Beck Depression Inventory B 361
Cantor, J. B., Ashman, T. A., Schwartz, M. E., Gordon, W. A., Hibbard, Steer, 1987). A more substantial revision led to the devel-
M. R., Brown, M., et al. (2005). The role of self-discrepancy theory in
opment of the Beck Depression Inventory-II in 1996
understanding post-traumatic brain injury affective disorders: A
pilot study. Journal of Head Trauma Rehabilitation, 20(6), 527543.
(BDI-II; Beck, Steer, & Brown, 1996). B
Ferguson, R. (2000). Using the Beck Anxiety Inventory in primary care. The BDI-II is comprised of 21 individual items reflecting
In M. E. Maruish (Ed.), Handbook of psychological assessment in specific cognitive, affective, and physical symptoms of de-
primary care settings (pp. 509536). Mahwah, NJ: Lawrence Erlbaum pression. Each item includes four statements that vary in the
Associates, Inc.
description of symptom severity. Scores range from 0 to 3,
Hewitt, P. L., & Norton, G. R. (1993). The Beck Anxiety Inventory:
A psychometric analysis. Psychological Assessment, 5, 408412.
with a score of 3 indicating severe symptoms and a score of
Morin, C. M., Landreville, P., Colecchi, C., McDonald, K., Stone, J., & 0 indicating an absence of concern with that particular
Ling, W. (1999). The Beck Anxiety Inventory: Psychometric proper- aspect of depressive symptomatology (Lezak, Howieson,
ties with older adults. Journal of Clinical Geropsychology, 5, 1929. Loring, Hannay, & Fischer, 2004). The total score is the
Moon, Y. S., Kim, S. J., Kim, H. C., Won, M. H., & Kim, D. H. (2004).
sum of all endorsed statements. If more than one statement
Correlates of quality of life after stroke. Journal of the Neurological
Sciences, 224(12), 3741.
from a given item is chosen by the patient, only the statement
Osman, A., Hoffman, J., Barrios, F. X., Kopper, B. A., Breitenstein, J. L., & of greatest severity is scored. The maximum total score is 63.
Hahn, S. K. (2002). Factor structure, reliability, and validity of the As per the BDI-II Manual, the instrument requires
Beck Anxiety Inventory in adolescent psychiatric inpatients. Journal approximately 510 min to complete. This, of course,
of Clinical Psychology, 58(4), 443456.
may vary depending on the patient. The BDI-II is typically
Schramke, C. J., Stowe, R. M., Ratcliff, G., Goldstein, G., & Condray R.
(1998). Poststroke depression and anxiety: Different assessment
self-administered, but the examiner may read the items
methods result in variations in incidence and severity estimates. aloud to the patient if difficulties with reading or vision
Journal of Clinical & Experimental Neuropsychology, 20(5), 723737. are evident. The administration instructions differ
Trahan, D. E., Ross, C. E., & Trahan, S. L. (2001). Relationship among depending on the mode of administration (self or exam-
postconcussional-type symptoms, depression, and anxiety in neuro-
iner). The BDI-II instructs individuals to respond to the
logically normal young adults and victims of mild brain injury.
Archives of Clinical Neuropsychology, 16, 435445.
items based on how they felt during the past 2 weeks,
including today. The time frame was increased from 1
week in the original instrument to 2 weeks in the BDI-II
to remain consistent with the American Psychiatric Asso-
ciations Diagnostic and Statistical Manual on Mental
Beck Depression Inventory Disorders-Fourth Edition (American Psychiatric Associa-
tion, 1994) diagnostic criteria for clinical depression. The
D ENNIS J. Z GALJARDIC BDI-II is applicable to patients aged 1380 years.
Transitional Learning Center at Galveston
Galveston, TX, USA
Synonyms The original BDI was developed with the use of descriptors
provided by psychiatric patients (predominantly with de-
BDI; BDI-II pression). These descriptors were then consolidated and
adopted into 21 items, several of which differ from those
in the BDI-II. In an attempt to remove alternative wordings
and double negatives from the original BDI instrument,
Description Beck and colleagues (1979) developed the BDI-IA. Fifteen
of the 21 original items were modified. Moran and Lam-
The Beck Depression Inventory (BDI; Beck, Ward, Men- bert (1983) discovered that the BDI met only six of the
delson, Mock, & Erbaugh, 1961) is one of the most widely nine criteria for depression listed in the American Psychi-
used self-report inventories to assess depressive symptom atric Associations Diagnostic and Statistical Manual on
severity in adolescent and adult populations. It has been Mental Disorders-Third Edition (American Psychiatric
employed as a screening instrument in over 2,000 studies Association, 1980). Further, they reported that the BDI
(Richter, Werner, Heerlein, Kraus, & Sauer, 1998). An lacked items addressing psychomotor activity and agita-
amended version of the original 1961 instrument (BDI- tion and permitted only the endorsement of decreases
IA; Beck, Rush, Shaw, & Emery, 1979) was developed in (not increases) in appetite and sleep (which was inconsis-
1979, with publication of its manual in 1987 (Beck & tent with DSM-III criteria for clinical depression).
362 B Beck Depression Inventory
Further changes to the diagnostic criteria for clinical replicated Beck and colleagues (1996) two-factor solution
depression following the publications of the DSM-III-R in a sample of 414 undergraduates. However, in their
(1987) and-DSM-IV (1994) led to further revision of the model, the Pessimism and Loss of Interest in Sex
instrument. Changes implemented for what became the items significantly loaded onto the Cognitive-Affective
BDI-II included rewording of select statements, as well as factor. The internal consistency for both cognitive and
(1) introduction of the items of Agitation, Worthless- somatic factors were reported to be good (a = 0.87 and
ness, Concentration Difficulty, and Loss of Energy; (2) 0.74, respectively).
modifications to the Insomnia and Loss of Appetite
items to reflect both increases and decreases in sleep and
appetite; and (3) the removal of the Body Image Change, Clinical Uses
Work Difficulty, Weight Loss, and Somatic Preoccupa-
tion items. The BDI-II Manual designates the following raw score
classifications of depression severity: 13 = minimal;
1419 = mild; 2028 = moderate; 29 = severe. The
Psychometric Data instruments developers suggested that different cut-off
scores may be required depending on the characteristics
Standardization data for the BDI-II was obtained from 500 of the sample and the purpose for using the instrument.
psychiatric outpatients and 120 undergraduates. Internal Hence, on an individual basis, clinical judgment must be
consistency was high for each sample (a = 0.92 and 0.93, used, as the cut-off score ranges should be viewed as
respectively). These coefficient alphas are consistent with guidelines (Lezak et al., 2004). As per the BDI-II Manual,
those reported in independent study samples including: clinicians may give particular consideration to items
140 psychiatric outpatients (mean age = 37.6 years) 2 (Pessimism) and 9 (Suicidal Thoughts or Wishes) to
(a = 0.91; Beck, Steer, Ball, & Ranieri, 1996), 408 psychi- gauge suicide risk in a given psychiatric patient.
atric adolescents (age range = 1317 years) (a = 0.93; Given the burgeoning ethnic and cultural diversity of
Osman, Kopper, Barrios, Gutierrez, & Bagge, 2004), 414 psychiatric and neurological patient populations, there is an
nonclinical undergraduates (age range = 1739 years) ever-increasing need for linguistically and culturally sensi-
(a = 0.90; Storch, Roberti, & Roth, 2004), 414 nonclinical tive psychiatric inventories. Wiebe and Penley (2005) re-
high-school-aged students (age range = 1418 years) port on the psychometric properties of a Spanish
(a = 0.92; Osman, Barrios, Gutierrez, Williams, & Bailey, translation of the BDI-II using a sample of 895 undergrad-
2008), and 147 nonclinical community-dwelling older uates. They administered the English and/or Spanish ver-
adults (age range = 5990 years) (a = 0.86; Segal, Cool- sion of the BDI-II twice to each participant, with a 1-week
idge, Cahill, & ORiley, 2008). Test-retest reliability of the interval between administrations. The two versions of the
BDI-II was assessed in a sample of 26 psychiatric out- instrument were administered to English-only speaking or
patients (Beck et al., 1996), yielding a statistically signifi- bilingual participants. In their design, the monolingual
cant correlation coefficient (r = 0.93). participants (n = 539) received the English version of the
Beck et al. (1996) demonstrated the convergent and BDI-II at each time-point. One subset of the bilingual
discriminant validity of the BDI-II in 87 psychiatric out- participants (n = 355) were administered the Spanish ver-
patients by correlating BDI-II scores with scores from the sion of the BDI-II at each time-point, whereas the remain-
Hamilton Psychiatric Rating Scale for Depression (Hamil- ing bilingual subset (n = 254) were randomized in the
ton, 1960) and the Hamilton Rating Scale for Anxiety administration of the Spanish and English versions of the
(Hamilton, 1959). Here, the BDI-II was more positively BDI-II at each time-point. Internal consistencies for the
correlated with the Hamilton depression scale (r = 0.71) English only and Spanish only administration were good
than the Hamilton anxiety scale (r = 0.47). While asses- (a = 0.89 and 0.91, respectively). Test-retest reliabilities
sing the factor validity of the BDI-II, Beck and colleagues were statistically significant for each version across condi-
(1996) reported a two-factor solution using their outpa- tion (English only [r = 0.73], Spanish only [r = 0.86], and
tient standardization sample that yielded a Somatic- randomized administration [r = 0.76]). Confirmatory
Affective factor (12 items) and a Cognitive-Affective factor analyses revealed that their data from both English
factor (9 items). Items that did not significantly load onto and Spanish versions of the BDI-II demonstrated good
either factor included Pessimism and Loss of Interest fit with the factor solution reported in the BDI-II Manual.
in Sex. Similar findings were replicated using their stan- Cognitive complexity of a given instrument of depres-
dardization sample of undergraduates. Storch et al. (2004) sive symptom severity is important to consider, as such
Beck Depression Inventory B 363
measures may be administered to patient populations with (2009) stressed that, while the BDI-II can provide adequate
known cognitive impairment (e.g., Parkinsons disease means in assessing the severity of depression in patients
[Zgaljardic, Borod, Foldi, & Mattis, 2003] and Traumatic with TBI, the separate dimensions of depression need to B
Brain Injury [Draper & Ponsford, 2008]). Shumway, Sen- be addressed by considering all three score subtypes in
tell, Unick, and Bamberg (2004) demonstrated that three this patient population in order to avoid misattributing
versions of the BDI including the original instrument, the somatic symptoms of TBI to symptoms of depression.
BDI-II, and the BDI-Primary Care (BDI-PC; Beck, Guth, The BDI-II was developed to correspond with depres-
Steer, & Ball, 1997) had high overall complexity based on sive disorder criteria set forth by the DSM-IV. The reli-
the characteristics of (1) number of instructions, ques- ability and validity of the instrument have been
tions, and response options; (2) item length; (3) readabili- established across several studies including psychiatric
ty (grade level); and (4) linguistic problems (likely to result and neurological patients as well as nonclinical commu-
in memory overload). Nevertheless, good reliability and nity-dwelling individuals. This appears to extend to eth-
validity of the BDI-II have been demonstrated in patients nic and culturally diverse populations as well. The BDI-II
with significant cognitive impairment (Powell, 2003). is not intended to be used for the sole purpose of speci-
There has been concern that the somatic complaint fying a clinical diagnosis, but rather as an indicator of the
items included in the BDI-II may be confounded in select existence and severity of depressive symptoms (Beck et al.,
patients, such as the elderly or those with movement 1996). Further, that depression may occur concurrently
disorders (e.g., Parkinsons disease [PD]) (Lezak et al., with other psychiatric diagnoses (e.g., apathy) across pa-
2004). In these patient populations, physical sequelae tient populations also mandates caution when interpreting
might mimic somatic symptoms of depression, leading findings from the BDI-II.
to greater endorsement of somatic items on the BDI-II
and resulting in false classifications of depressive symp-
tomatology. Using the original BDI instrument, Levin,
Llabre, and Weiner (1988) reported that among patients
Cross References
with PD, somatic complaints were associated with the
Center for Epidemiologic Studies-Depression
depression and not the PD symptomatology (e.g., brady-
Geriatric Depression Scale
kinesia), suggesting that the BDI is a valid measure of
Hamilton Rating Scale for Depression
depression in this particular patient population. Internal
Self-Report Measures
consistency for the total score of the BDI was acceptable
Zung Self-Rating Depression Scale
(a = 0.88). When the scores for the somatic items were
removed from the total score, the internal consistency
remained relatively unchanged (a = 0.89). Green, Fel-
mingham, Baguley, Slewa-Youan, and Simpson (2001) References and Readings
administered the BDI to 117 patients with Traumatic
Brain Injury (TBI) 2 years after discharge from a residen- American Psychiatric Association (1980). Diagnostic and statistical man-
tial brain injury rehabilitation program. Internal consis- ual of mental disorders. Washington, DC: American Psychiatric
tency was high (a = 0.92). A principal component factor Association.
American Psychiatric Association (1987). Diagnostic and statistical man-
analysis using the BDI total score yielded a three-factor
ual of mental disorders (3rd ed., Rev.). Washington, DC: American
solution. The affective factor accounted for the largest Psychiatric Association.
percentage of variability, followed by negative attitudes American Psychiatric Association (1994). Diagnostic and statistical man-
toward the self and somatic disturbance factors. Their ual of mental disorders (4th ed.). Washington, DC: American Psychi-
findings were relatively consistent with the findings from atric Association.
Beck, A. T., Guth, D., Steer, R. A., & Ball, R. (1997). Screening for major
studies using non-TBI samples and suggest that BDI
depression disorders in medical inpatients with the Beck Depression
scores, at least for moderate levels of depression, did not Inventory for primary care. Behavior Research and Therapy, 35,
appear to be influenced by high incidences of somatic 785791.
complaints. Siegert, Walkey, and Turner-Stokes (2009) Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive therapy
reported on the existence of three-factor solution, yielding of depression. New York: Guilford Press.
Beck, A. T., & Steer, R. A. (1987). Manual for the Beck Depression
a depression factor (all 21 BDI-II items) as well as a
Inventory. San Antonio, TX: The Psychological Corporation.
somatic (11 items) and a cognitive/affective (8 items) Beck, A. T., Steer, R. A., Ball, R., & Ranieri, W. (1996). Comparison of
factor in a sample of patients with TBI. Internal consistency Beck Depression Inventories -IA and -II in psychiatric outpatients.
for item scores from each factor was strong. Siegert et al. Journal of Personality Assessment, 67(3), 588597.
364 B Beery Developmental Test of Visual-Motor Integration (VMI)
Beck, A. T., Steer, R. A., & Brown, G. K. (1996). Beck Depression Inventory
Manual (2nd ed.). San Antonio, TX: The Psychological Corporation. Beery Developmental Test of
Beck, A., Ward, C. H., Mendelson, l., Mock, J., & Erbaugh, J. (1961). An
inventory for measuring depression. Archives of General Psychiatry, Visual-Motor Integration (VMI)
4, 561571.
Draper, K., & Ponsford, J. (2008). Cognitive functioning ten years follow- K ELLY C ROTTY, I DA S UE B ARON
ing traumatic brain injury and rehabilitation. Neuropsychology, 22 Inova Fairfax Hospital for Children
(5), 618625.
Falls Church, VA, USA
Green, A., Felmingham, K., Baguley, I. J., Slewa-Younan, S., & Simpson, S.
(2001). The clinical utility of the Beck Depression Inventory after
traumatic brain injury. Brain Injury, 15(12), 10211028.
Hamilton, M. (1959). The assessment of anxiety states by rating. British Synonyms
Journal of Medical Psychology, 32, 5055.
Hamilton, M. (1960). A rating scale for depression. Journal of Neurology
Beery VMI; Developmental test of visual motor
and Neurosurgical Psychiatry, 23, 5662.
Levin, B. E., Llabre, M. M., & Weiner, W. J. (1988). Parkinsons disease integration
and depression: Psychometric properties of the Beck Depression
Inventory. Journal of Neurology, Neurosurgery & Psychiatry, 51(11),
14011404.
Lezak, M. D., Howieson, D. B., Loring, D. W., with Hannay, H. J., & Description
Fischer, J. S. (2004). Neuropsychological assessment (4th ed.).
New York: Oxford University Press. The BeeryBuktenica Developmental Test of Visual-
Moran, P. W., & Lambert, M. J. (1983). A review of current assessment
Motor Integration (VMI; Beery, Buktenica, & Beery,
tools for monitoring changes in depression. In J. S. Lambert, E. R.
Christensen, & S. DeJulio (Eds.), The assessment of psychotherapy
2004) is designed to identify deficits in visual-motor inte-
outcome (pp. 263303). New York: Wiley. gration, visual perception, and motor coordination. This
Osman, A., Barrios, F. X., Gutierrez, P. M., Williams, J. E., & Bailey, J. brief paper and pencil test requires the examinee to copy
(2008). Psychometric properties of the Beck Depression Inventory-II geometric designs of increasing complexity arranged in
in nonclinical adolescent samples. Journal of Clinical Psychology, 64
a developmental sequence. The 5th edition (2004) pro-
(1), 83102.
Osman, A., Kopper, B. A., Barrios, F., Gutierrez, P. M., & Bagge, C. L.
vides standardized normative data for individuals aged
(2004). Reliability and validity of the Beck Depression Inventory-II 218 years, and more recent norms have been established
with adolescent psychiatric inpatients. Psychological Assessment, 16 using 1,021 adults aged 19100 years. The VMI has a
(2), 120132. Full Form and a Short Form, both of which can be
Powell, R. (2003). Psychometric properties of the Beck Depression Inven-
administered to a group or individuals in approximately
tory and the Zung Self Rating Depression Scale in adults with mental
retardation. Mental Retardation, 41(2), 8895.
1015 min. The Short Form, for children aged 27 years,
Richter, P., Werner, J., Heerlein, A., Kraus, A., & Sauer, H. (1998). On the has 21 items and the Full Form extends to 30 items. Each
validity of the Beck Depression Inventory. A review. Psychopathology, reproduction of a geometric form is scored as 1 point if
31(3), 160168. correct and 0 if incorrect, with a discontinuation rule of
Segal, D. L., Coolidge, F. L., Cahill, B. S., & ORiley, A. A. (2008). Psycho-
three consecutive failures. Raw scores are converted to age-
metric properties of the Beck Depression Inventory II (BDI-II) among
community-dwelling older adults. Behavior Modification, 32(1), 320.
based standard scores, percentiles, and scales scores. Two
Shumway, M., Sentell, T., Unick, G., & Bamberg, W. (2004). Cognitive optional subtests use the same stimulus forms as the VMI,
complexity of self-administered depression measures. Journal of the visual perception test and the motor coordination test.
Affective Disorders, 83, 191198. These subtests are useful to compare visual-motor integra-
Siegert, R. J., Walkey, F. H., & Turner-Stokes, L. (2009). An examination
tion efficiency to pure visual or pure motor performance.
of the factor structure of the Beck Depression Inventory-II in a
neurorehabilitation inpatient sample. Journal of the International
Neuropsychological Society, 15(1), 142147.
Storch, E. A., Roberti, J. W., & Roth, D. A. (2004). Factor structure,
concurrent validity, and internal consistency of the Beck Depression
Inventory-Second Edition in a sample of college students. Depression
& Anxiety, 19(3), 187189. The Beery VMI, originally known as the Developmental
Wiebe, J. S., & Penley, J. A. (2005). A psychometric comparison of the Form Sequence, began to be developed in 1961. While
Beck Depression Inventory-II in English and Spanish. Psychological
other design-copying measures were available, they did
Assessment, 17(4), 481485.
Zgaljardic, D. J., Borod, J. C., Foldi, N. S., & Mattis, P. (2003). A review of
not comprise a sequence of designs that increased in
the cognitive and behavioral sequelae of Parkinsons disease: Rela- complexity or that reflected normal development. Keith
tionship to frontostriatal circuitry. Cognitive & Behavioral Neurology, Beery believed that visual-motor integration correlated
16(4), 193210. with academic achievement and wanted to construct a
Behavior B 365
measure of such skill development. He began with 72 and clinical interpretation. Even children who perform well
designs administered to 600 children in Illinois. Thirty on the visual-motor integration portion may have deficits
designs were selected and administered to another 600 in the subareas of visual perception and motor coordina- B
children, leading to the selection of the final 24 forms tion (Kulp & Sortor, 2003). In fact, visual perception spe-
administered today. cifically has been associated with math and reading ability
Beery VMI was published in 1967 by Keith Beery, (Sortor & Kulp, 2003). Research has also found a signifi-
Norman Buktenica, and Natasha Beery, with normative cant relation between visual-motor integration and aca-
data obtained in 1964 on 1,030 children. The Beery VMI demic achievement (Sortor & Kulp, 2003); however, these
has since been re-normed on more than 10,000 children. two areas are not exclusively correlated. Beery VMI is more
Updated editions of the Beery VMI were published in strongly correlated with chronological age than academic
1982 (2nd Edition), 1989 (3rd Edition), 1997 (4th Edi- achievement. Poor performance on the Beery VMI may or
tion), and 2004 (5th Edition). Each edition offered may not indicate academic achievement impairments.
updated norms. The most recent 5th Edition includes
standardized norms for children of 2 years of age and
provides visual-motor teaching methods from birth
Cross References
through early elementary school.
Beery Developmental Test of Visual-Motor Integration
(VMI)
Psychometric Data Bender-Gestalt, Second Edition
Rey-Osterrieth Complex Figure Test (ROCF)
The manual reports overall average reliabilities at .92 for
visual-motor integration, .91 for visual perception, and .90
for motor coordination. Beery VMI correlates .52 with the References and Readings
Wide Range Assessment of Visual Motor Abilities
(WRAVMA) drawing subtest and .75 with the Develop- Beery, K. E., Buktenica, N. A., & Beery, N. A. (2004). The Beery-Buktenica
mental Test of Visual Perception (DTVP-2) copying subtest. developmental test of visual-motor integration: Administration, scoring
Strong correlations between the Beery VMI and other visual and teaching manual. Minneapolis, MN: NCS Pearson.
motor assessments highlight the tests validity. Normative Kulp, M. T., & Sortor, J. M. (2003). Clinical value of the Beery visual-
motor integration supplemental test of visual perception and motor
scores are valid for both individual and group administra-
coordination. Optometry and Vision Science, 80(4), 312315.
tion, but it is recommended that those who perform below Malloy, P., Belanger, H., Hall, S., Aloia, M., & Salloway, S. (2003). Asses-
average be individually tested. It is also suggested that sing visuocontructional performance in AD, MCI and normal elder-
preschoolers be screened individually to maintain validity. ly using Beery visual-motor integration test. The Clinical
Neuropsychologist, 17(4), 544550.
Sortor, J. M., & Kulp, M. T. (2003). Are the results of the Beery-Buktenica
developmental test of visual motor integration and its subtests
Clinical Uses related to achievement test scores? Optometry and Vision Science,
80(11), 758763.
The Beery VMI is designed to be an early screening tool to

identify children with visual-motor deficits that may lead
to learning, neuropsychological, and behavioral pro-
blems. Beery VMI is primarily used for children because Beery VMI
of its ability to assess age appropriate development. Beery
VMI is also beginning to be used as an early screening tool Beery Developmental Test of Visual-Motor Integration
for dementia in adults. Research has found that visuocon- (VMI)
structional deficits may be an early indicator of dementia
(Malloy, Belanger, Hall, Aloia, & Salloway, 2003). Other
uses of the Beery VMI are to test the effectiveness of
educational and early intervention programs.
While the manual states that the visual perception and Behavior
motor coordination subtests are optional, research has
shown that all areas should be assessed for optimal results Behavior Assessment System for Children (BASC)
366 B Behavior Assessment System for Children (BASC)
dimensions. The BASC-2 is a revision of the BASC

Behavior Assessment System (Reynolds & Kamphaus, 1994). Users of the original
for Children (BASC) BASC can shift easily to using the BASC-2. The BASC-
2 retains all of the key features of the BASC and makes
C ECIL R. R EYNOLDS 1, R ANDY W. K AMPHAUS 2, numerous improvements such as: improved reliabilities
K IMBERLY J. VANNEST 1 and additional scales (functional communication, TRS
1 and PRS; activities of daily living, PRS; adaptability,
Texas A&M University
College Station, TX, USA TRSA and PRSA; and attention problems and hyperac-
2 tivity on SRP) without lengthening the forms; a standar-
Georgia State University
Atlanta, GA, USA dization sample matched to recent US population figures
(Current Population Survey, 2001); greater similarity of
item content across levels and between the TRS and PRS; a
Synonyms reduction in the length of the TRS; newly devised content
scales that can be used as an aid in interpreting the
Behavior; Behavioral assessment; Diagnosis; primary scales and to broaden the coverage of the behav-
Psychopathology ior areas assessed by BASC-2; a mixed item-response for-
mat on the SRP, which improves both scale reliability and
the ability to measure at the extremes of the score ranges;
Description expanded age range for assessing students through age 21
years who are still attending secondary school, and, on the
The Behavior Assessment System for Children, Second SRP, students aged 18 through 25 attending postsecond-
Edition (BASC-2; Reynolds & Kamphaus, 2004) is a mul- ary institutions; and more detailed clinical norms.
timethod, multidimensional system of related instru- Scoring and interpretive software programs are avail-
ments used to evaluate the behavior and self-perceptions able for the BASC-2 that make actuarial as well as
of children, adolescents, and young adults aged 2 through content matches to the educational classification of emo-
25 years. The BASC-2 is multimethod in that it has the tional disturbance, and also to various DSM-IV-TR clin-
following components, which may be used individually or ical diagnoses. The most popular and useful of the
in any combination: programs is the BASC-2 Plus program, which also scores
and interprets the Content Scales, which other programs
1. Two rating scales, one for teachers (Teacher Rating
do not.
Scales, or TRS) and one for parents (Parent Rating
The BASC-2 was designed to facilitate the differential
Scales, or PRS), which gather descriptions of the
diagnosis and educational classification of a variety of
childs observable behavior, each divided into age-
emotional and behavioral disorders of children and to aid
appropriate forms
in the design of treatment plans. When used individually,
2. A self-report scale (Self-Report of Personality, or
the BASC-2 components are reliable and psychometrically
SRP), on which the child or young adult can describe
sophisticated instruments that provide an array of benefi-
his or her emotions and self-perceptions
cial data. When used as a total system, the BASC-2 pro-
3. A Structured Developmental History (SDH) form
vides information about a child from a variety of sources,
4. A form for recording and classifying directly observed
providing the clinician with a coordinated set of tools for
classroom behavior (Student Observation System, or
evaluation, diagnosis, and treatment planning.
SOS), which is also available for PDA applications as
As a system, the BASC-2 components afford a trian-
an electronic version known as the BASC-2 POP or
gulated view of the childs behavioral problems by
Portable Observation Program
(1) examining behavior in multiple settings (at home
5. A self-report for parents of children ages 218 years,
and school); (2) evaluating the childs emotions, person-
designed to capture a parents perspective on the
ality, and perceptions of self; (3) providing important
parentchild relationship in such domains as commu-
background information, useful when making education-
nication, disciplinary styles, attachment, involvement,
al classifications or clinical diagnoses, an area commonly
and others.
shortchanged in educational settings; and (4) a software
The BASC-2 is multidimensional in that it measures nu- that provides a sophisticated means for evaluating change
merous aspects of behavior and personality, including or progress of individuals over time in response to
positive (adaptive) as well as negative (clinical) interventions.
Behavior Assessment System for Children (BASC) B 367
Key Features of the BASC-2 available and updated information on these versions
can be obtained by contacting Pearson Assessments
The BASC-2 has numerous features that make it a sophis- (www.pearsonassessments.com). Estimates from sales fig- B
ticated and reliable system of behavior assessment. The ures indicate the BASC-2 is one of the frequently, if not
BASC-2 assesses a wide range of distinctive dimensions. the most, administered individual psychological tests in
In addition to evaluating personality and behavioral pro- the public schools of the United States.
blems and emotional disturbance, the BASC-2 identifies
positive attributes that can be capitalized on in the treat-
ment process, attributes that are valuable but too often
ignored in clinical assessment.
The range of dimensions assessed helps in making
The original BASC (Reynolds & Kamphaus, 1994) was
differential diagnosis of specific categories of disorder,
published by American Guidance Service following
such as those denoted in the Diagnostic and Statistical
7 years of development work. The original BASC was
Manual of Mental Disorders (DSM-IV-TR; American
standardized for use with ages 2.5 through 18 years,
Psychiatric Association, 2000), as well as general cate-
and was rapidly adopted as the most frequently adminis-
gories of problems, such as those addressed by The Indi-
tered behavior scales in the schools in the United States.
viduals with Disabilities Education Act. The BASC-2 is
Versions were subsequently developed for international
highly relevant to federal regulations concerning the diag-
applications by TEA Ediciones in Spain. Clinical settings
nosis of severe emotional disturbance among children in
also began to adopt and use the BASC throughout North
the schools and also is sensitive enough to detect even
America as research demonstrated strong sensitivity and
mild behavior problems among children in other disability
specificity in diagnostic applications. The original BASC
categories, including learning disabilities and mental
has been used in more than 125 such research studies,
retardation.
many of which were large-scale, longitudinal analyses of
The BASC-2 allows information from multiple
both developmental psychopathology and treatment effi-
sources to be compared using instruments with overlap-
cacy. Once the BASC-2 was released in 2004, use grew
ping norms to help achieve reliable and accurate diag-
geometrically in all areas of practice.
noses. The software programs available for the BASC-2 will
also compare data from each of the BASC-2 components
and assess them for similarities and differences statistically
and graphically. Psychometric Data
Each BASC-2 component is designed for a specific
setting or type of respondent because some constructs The BASC-2 scales were designed to be highly interpret-
or behaviors are more important or measurable in some able and are built around clearly specified constructs with
settings than in others. This also gives clinicians a clear matching item content, developed through a balance of
view of the generalizability of the individuals behavior as theory and empirical data. Experienced clinicians wrote
well as the setting-specific nature of any behavior pro- the initial items and they were assigned initially to scales
blems that occur principally in one type of surrounding. using expert methods but refined iteratively using an
The BASC-2, PRS, SRP, and SDH are available in empirical approach based on the responses of nearly
Spanish as well as English and are also available on 50,000 individuals. Scales are consistent not only across
audio for nonreaders. The BASC-2 can be either hand sex and age levels but also between the teacher and parent
scored or computer scored (manual or scannable item forms. This provides a basis for consistent interpretation
entry). The BASC-2 Spanish version sold in the United of scales and for meaningful across-source and across-
States was developed simultaneously with the English time score comparisons. BASC-2 norms are based on
version and thus is far more than a translation, being a large, US Census Bureau representative samples and are
fully developed scale with yoked items (see Reynolds & differentiated according to the age, sex, and clinical status
Kamphaus, 2004, for a more detailed explanation). of the child. Clinicians have a choice of sex-based norms
The BASC-2 has been widely used and is available or combined-sex norms when deriving standard scores for
throughout the English-speaking world from Pearson the various subscales and composites. The BASC-2 covers
Assessments of Bloomington, MN and throughout the full age range, 2 through 21 years, of students in
the Spanish-speaking world from TEA Ediciones in preschool through high school settings, while maintaining
Madrid. Versions in several other languages are also developmental sensitivity and continuity of constructs.
The BASC-2 also offers a version of the SRP for ages 18 Academic difficulties are frequently linked to behavior
through 25 for use in technical schools, colleges, and problems. Syndromes such as attention-deficit hyperactivity
universities. disorder (ADHD) and depression have known academic
The BASC-2 scales and composites have high inter- consequences; learning disabilities and mental retardation
nal consistency and testretest reliability. Most alpha are often associated with adjustment problems such as low
coefficients for the BASC-2 subscales and composites self-concept or anxiety. It is strongly suggested that every
exceed 0.80 and are sufficiently reliable for application child experiencing academic difficulties receive a behavioral
to diagnostic and treatment issues. Additionally, the assessment. Additionally, research demonstrates that good
BASC-2 offers various types of validity checks to help behavioral assessment of constructs such as attitude to
the clinician detect careless or untruthful responding, school, attitude to teachers, study skills, attention problems,
misunderstanding, or other threats to validity. The and adaptability, in tandem with cognitive assessment,
BASC-2 Manual demonstrates validity evidence for the improves the prediction of both school performance and
proposed applications of the BASC-2 scales that is exten- response to intervention.
sive and covers both theoretical and actuarial bases. The BASC-2 is also useful for assessing severe emo-
Correlations with numerous other rating scales and tional disturbance. The rating scales can help distinguish
self-reports are given as well as studies of a large number between children with conduct disorders or social malad-
of clinical groups. justment on the one hand and those with severe emotional
disturbance on the other, as called for by Federal laws.
With its various components, the BASC-2 can help assess
Clinical Uses all aspects of the federal definition of severe emotional
disturbance.
Clinical Diagnosis The BASC-2 may be particularly useful in designing
individual educational plans (IEPs) for emotionally dis-
The BASC-2 aids in the clinical diagnosis of disorders that turbed children. It allows the selection of target behaviors
are usually first apparent in childhood or adolescence. as well as clusters of behaviors to delineate syndromes that
It assesses a variety of symptoms that are noted in the are an important focus of the IEP.
DSM-IV-TR. The BASC-2 rating scales and the SOS were also
Because the components of the BASC-2 can be used designed for use at the preschool level to help develop
separately or in combination, the BASC-2 may be used family service plans (FSPs) for 4- and 5-year-olds with
easily in residential settings, in clinics, or by private prac- disabilities. The SDH is well suited to identifying the
titioners. The PRS and SDH can be completed by a parent service needs of families.
while the child is being evaluated by the practitioner, thus The BASC-2 is also useful in manifestation
reducing the practitioners time in the data collection determination.
process. The rating scales, the SRP, and the SOS can be Manifestation determination refers to a process
repeated on a regular basis to monitor a childs progress for determining the origin of behavior. The procedure is
and response to treatment. commonly encountered in special education and in 504
It is highly desirable that diagnosis be linked clearly to proceedings related to disciplinary actions or conduct
intervention. In this respect, treatment planning can also problems. Prior to the application of any adverse action
be facilitated by the BASC-2. Problem behaviors can be against a student with a disability, a multidisciplinary
delineated and targeted in a program leading to their team must determine that the behavior in question was
reduction. A similar strategy can be used with deficits in not a direct result of the students disability. The method
adaptive skills. is based on the premise that students with a disability
Differential diagnosis is becoming an increasingly im- should not be punished for behavior that is considered to
portant issue in school settings. This is partly because the be a manifestation of the disability. For example, suppose
complexity of many childrens problems requires an array a child with schizophrenia is experiencing auditory
of interventions that must be tailored to the individual hallucinations at school and tells a teacher that another
childs needs. Consequently, the BASC-2 is designed to be child is threatening to commit a violent act. Because these
sensitive to numerous presenting problems in the class- auditory experiences were a manifestation of the childs
room, including deficiencies in social skills, study skills, or disability, he or she should not be punished for reporting
other adaptive skills. them as actual threats.
Behavior Assessment System for Children (BASC) B 369
In most cases, the BASC-2 will prove helpful in the the admissibility of expert testimony based on test results.
manifestation determination process. The BASC has a Reynolds and Kamphaus (2002) provides examples of
long history of effectiveness in differentiating social mal- uses of the original BASC in forensic situations such as B
adjustment and conduct disorder from behavior asso- child custody evaluations, personal injury litigation, and
ciated with an emotional disturbance (Reynolds & juvenile certification. This manual contains considerable
Kamphaus, 2002). The BASC-2 content scales such as information on the reliability of BASC-2 scores and asso-
anger control, bullying, and executive functioning en- ciated standard errors of measurement, on the normative
hance its utility for such purposes. samples, and on validation studies, all of which are consid-
ered by judges in determining admissibility of testimony
based partially or wholly on test data. Also presented
Assessment of Individuals with Limitations here are additional crucial data on the ability of the
of Vision and Hearing BASC to measure child and adolescent psychopatholo-
gy and to discriminate among various diagnostic
The BASC-2 scales can be used to evaluate the behavioral groups, capabilities that also are included in the con-
and emotional status of children and adolescents with sideration of admissible evidence. The BASC is well
sensory impairments. The interpretation of BASC-2 test established in clinical environments such as schools,
scores for these individuals requires specialized training, child guidance centers, university clinics, and private
expertise, and supervised experience in working with practice settings in the United States and abroad. The
groups with sensory impairment. use of tests in a wide variety of settings is important in
establishing credibility and admissibility in various legal
proceedings.
When choosing instruments for forensic evaluations,
Program Evaluation it is also important for clinicians to evaluate the instru-
ments ability to detect dissimulation (Reynolds & Kam-
Repeated use of the BASC-2 TRS, PRS, SRP, and SOS can phaus, 2002). In court proceedings, individuals may have
aid in identifying a childs progress in specific programs. much to gain by appearing to have more or fewer pro-
Improvement in designated areas of behavior and in affec- blems than actually exist. Because nearly any behavioral or
tive states may be noted, and the strengths and weaknesses emotional problem or disorder can be minimized or exag-
of programs thus identified. The original BASC was shown gerated, objective methods are needed to determine
in a number of evaluation studies to be sensitive to the whether dissimulation has occurred. The BASC-2 has
effects of various intervention programs for young chil- scales designed and tested for the detection of dissimula-
dren (including the evaluation component of Head Starts tion in responding by parents, teachers, and children.
Project Mastery) and adolescents (e.g., the evaluation by In particular, the BASC-2 validity scales can identify exag-
the Civilian Health and Medical Program of the Uniformed gerated responding, minimization of problem reporting,
Services, or CHAMPUS, of the effectiveness of residential inconsistencies, random answering patterns, and other
treatment for adolescents). These and other applications of response methods that lead to inaccurate depictions of
the BASC in program evaluation are reviewed in Reynolds the childs or adolescents behavior. Because of the strength
and Kamphaus (2002). With the improved score reliabil- of its validity scales, its documented psychometric proper-
ities and broadened content coverage in both clinical and ties, and the validity of its application in behavior evalua-
adaptive domains, the BASC-2 is expected to surpass the tion and differential diagnosis, the BASC-2 provides
BASC in the evaluation of programs and of interventions support to educate professionals or those challenged in
at both the individual and program levels. legal proceedings regarding their diagnostic or placement
decisions.
Forensic Evaluation
The Behavioral and Emotional Screening
The BASC-2 is appropriate for use in legal or forensic System (BESS)
settings. According to several US Supreme Court rulings
of the 1990s, evidence of the psychometric properties of The BESS (Kamphaus & Reynolds, 2007, a member of
tests used in a forensic setting is crucial for determining the BASC-2 system or family of assessment devices), is a
variant of the BASC-2 designed to identify risk for behav- and social skills. Each of these areas is assessed in detail
ioral or emotional problems and predict mental health (along with numerous others) on the assessment compo-
and educational outcomes. The BESS includes two parent nents of the BASC-2.
rating forms for ages 3 through 5 and 6 through 18, two Each chapter provides a theoretical framework,
teacher rating forms for the same age groups, and one annotated bibliography citing selections of the research
self-report form for ages 8 through 18. Each form of the literature, and the essential elements of each interven-
BESS is brief and, therefore, practical at less than 30 items tion followed by procedural steps and considerations
each and taking about 510 min of informant time and no for application. The BASC-2 Intervention Guide is a
prior training and coaching of the informant. comprehensive source book (472 pp.) of interventions.
Using the same item response formats as the BASC-2, The essential elements and the procedural steps are
each BESS form produces a single score indicating nor- designed for use by psychologists, counselors, or other
mal (T = 2060), elevated (6170), or extremely school professionals with mental health training (unlike
elevated risk (T = 71 or higher). Validity indexes are the assessment components of the BASC-2 which re-
provided for each form, and Spanish adaptations and quire more extensive training and supervised experience
translations for parent and teacher forms. Test scoring in clinical assessment and are considered to be Level C
software is designed for large-scale screening of entire products).
classes, grade levels, or school systems by incorporating Corresponding Classroom guides include evidence
scanned data entry of forms and sophisticated individual based interventions appropriate for classroom settings
and group reporting options, and a tracking report option organized by both externalizing and internalizing groups
for community monitoring of behavioral and emotional of behaviors and contain some sample lesson plans and
adjustment status. forms for common interventions and procedures. Parent
The BESS manual includes a detailed discussion of Tip Sheets present information about each type of prob-
development procedures and a separate chapter devoted lem for communication with parents or caregivers on how
to validity and reliability evidence collected to date. to help at home.
Articles by DiStefano and Kamphaus (2007) and Kam-
phaus et al. (2007) provide additional validity evidence
associated with pilot studies of the BESS. Virtually all reli-
ability coefficients exceed 0.90 and predictive validity stud- References and Readings
ies of behavioral, emotional, and educational outcomes
from 2 to 4 years in length are reported, as well as correla- American Psychiatric Association. (2000). Diagnostic and statistical man-
tions with numerous behavior rating scale measures of ual of mental disorders (4th ed., text revision). Washington, DC:
Author.
adjustment.
Current Population Survey (2001). United Stated Bureau of the Census,
The BESS manual also provides a detailed discussion Current Population Survey, Washington, DC: US Bureau of the
of promising screening practices, including the use of Census.
multiple gates and informants, desired age or grade DiStefano, C., & Kamphaus, R. W. (2007). Development and validation
groups for screening, and linking screening to early inter- of a behavioral screener for preschool-age children. Journal of Emo-
tional and Behavioral Disorders, 15, 93102.
vention aimed at preventing the onset of mental health
Kamphaus, R. W., & Reynolds, C. R. (2007). Behavior assessment system
disorders or unsuccessful educational outcomes. for children second edition (BASC-2): Behavioral and emotional
screening system (BESS). Bloomington, MN: Pearson.
Kamphaus, R. W., Thorpe, J. S., Winsor, A. P., Kroncke, A. P., Dowdy,
BASC-2 Intervention Guide for Emotional E. T., & VanDeventer, M. (2007). Development and predictive va-
lidity of a teacher screener for child behavioral and emotional
and Behavioral Problems
problems at school. Educational and Psychological Measurement, 6,
115.
The BASC-2 Intervention Guide, another component of Ramsay, M., Reynolds, C. R., & Kamphaus, R. W. (2002). Essentials of
the BASC-2, (Vannest, Reynolds, & Kamphaus, 2008) behavioral assessment. New York: Wiley.
provides an articulation of evidence-based practices for Reynolds, C. R., & Kamphaus, R. W. (1994). Behavior assessment system
for children. Bloomington, MN: Pearson Assessments.
each of 11 common types of emotional and behavioral
Reynolds, C. R., & Kamphaus, R. W. (2002). The clinicians guide to the
problems: aggression, conduct problems, hyperactivity, at- behavior assessment system for children. New York: Guilford.
tention problems, academic problems, anxiety, depression, Reynolds, C. R., & Kamphaus, R. W. (2004). Behavior assessment system
somatization, functional communication, adaptability, for children (2nd ed.). Bloomington, MN: Pearson Assessments.
Behavior Modification B 371
Vannest, K. J., Reynolds, C. R., & Kamphaus, R. W. (2008). Behavior

assessment system for children second edition (BASC-2) intervention Behavior Modification
guide for emotional and behavioral problems. Bloomington, MN:
Pearson.
S TEPHANIE A. KOLAKOWSKY-H AYNER B
San Jose, CA, USA
Behavior Management
G LENN S. A SHKANAZI
Synonyms
University of Florida-College of Public Health and
Health Professions
Applied behavioral analysis; Behavior therapy; Cognitive-
Gainesville, FL, USA
behavioral modification
Techniques used to control or modify an action or perfor- Behavior modification is the use of basic learning techni-
mance of a subject. This is a less-intensive version of behav- ques, such as conditioning, biofeedback, assertiveness
ior modification in which the goal is to develop, strengthen, training, positive or negative reinforcement, hypnosis, or
maintain, decrease, or eliminate behaviors in a planned or aversion therapy, to change unwanted individual or group
systematic way. Behavior management skills are particularly behavior. A technique, typically based on functional
important to enhance the probability that individuals, or assessment, used to reinforce adaptive behaviors while
groups, choose behaviors that are pro-social. Prosocial diminishing or extinguishing maladaptive behaviors.
behaviors are typically seen as personally fulfilling, produc- Seven characteristics of behavior modification, identified
tive, and socially acceptable. Persons surviving a traumatic by Martin and Pear (2007), include:
brain injury (TBI) often have behavioral disturbances such A strong emphasis on defining problems in terms of
as disinhibition and/or agitation. Due to learning impair- measurable behavior
ments as a result of their TBI, the traditional behavior Making environmental adjustments to improve
management approaches, which are based on learning the- functioning
ory principles, are modified. For example, behavior man- Precise methods and rationales
agement approaches with TBI survivors may focus more on Dynamic real-life application of techniques
stimulus control (e.g., controlling environmental cues) than Techniques grounded in learning and behavior theory
operant conditioning (e.g., recalling the contingency be- Scientific demonstration linking the imposed tech-
tween behaviors and the resulting consequences). nique with behavior change
Strong emphasis on accountability
Cross References
Cross References
Behavior Analysis
Behavior Modification Applied Behavior Analysis
Behavior Therapy Behavior Management
Behavioral Therapy Behavioral Analysis
Behavioral Assessment
Behavioral Therapy
Jacobs, H. E. (1993). Behavior analysis guidelines and brain injury rehabil- References and Readings
itation: People, principles and programs. Gaithersburg, MD: Aspen.
Karol, R. L. (2003). Neuropsychological intervention: The practical treat- Crum, C. (2004). Using a cognitive-behavioral modification strategy to
ment of severe behavioural dyscontrol after acquired brain injury. Boca increase on-task behavior of a student with a behavior disorder.
Raton, FL: CRC Press. Intervention in School & Clinic, 39(5), 305.
372 B Behavior Rating Inventory for Executive Functions
Hicinbothem, J., Gonsalves, S., & Lester, D. (2006). Body modification The BRIEF-P measures the behavioral manifestations of
and suicidal behavior. Death Studies, 30(4), 351.
executive function in preschool children aged 25. The
Lindsey, N., Reif, J., Bachand, A., & Seys, S. (2005). Behavior modifica-
tion following a diagnosis of hepatitis C infection. American Journal
BRIEF-P consists of a single form completed by parents
of Health Behavior, 29(6), 512519. and/or teachers/caregivers to rate the childs executive func-
Martin, G. L., & Pear, J. (2007). Behavior modification: What it is and how tions within the home and preschool settings. The question-
to do it (8th ed.). Upper Saddle River: Pearson Prentice Hall. naire consists of 63 items comprising five theoretically and
Ntinas, K. (2007). Behavior modification and the principle of normaliza-
empirically derived clinical scales measuring: Inhibit, Shift,
tion: clash or synthesis? Behavioral Interventions, 22(2), 165177.
Emotional Control, Working Memory, and Plan/Organize.
These scales form three factor-derived indexes: Inhibitory
Self-Control, Flexibility, and Emergent Metacognition and
one composite score the GEC. The BRIEF-P also includes
Behavior Rating Inventory for two validity scales Inconsistency and Negativity.
Executive Functions The BRIEF-SR is an 80-item adolescent self-report
behavior rating scale designed for older children and
G ERARD A. G IOIA 1, P ETER K. I SQUITH 2 adolescents, ages 1118 years with a fifth-grade or higher
1
Childrens National Medical Center reading ability, to complement the BRIEF Parent and
Rockville, MD, USA Teacher Forms. The 80 items yield information for eight
2
Dartmouth Medical School non-overlapping clinical scales measuring: Inhibit, Shift,
Lebanon, NH, USA Emotional Control, Monitor, Working Memory, Plan/
Organize, Organization of Materials, and Task Comple-
tion. The clinical scales form two broader indexes the
Synonyms Behavioral Regulation Index (BRI) and the Metacognition
Index (MI) and yield an overall summary score, the
BRIEF; BRIEF-A; BRIEF-P; BRIEF-SR GEC. The BRIEF-SR also includes the Negativity and
Inconsistency validity indexes.
The BRIEF-A measures the adults executive functions
Description in his or her everyday home and work environments. Two
formats are used a self-report and an informant report.
The Behavior Rating Inventory of Executive Function The Self-Report Form is designed to be completed by
(BRIEF) family of measures are rating scales completed adults 1890 years of age while the Informant Report
by parents and teachers of school children aged 518 years Form is administered to an adult who is familiar with
(BRIEF), by parents and caregivers of preschool children the rated individuals everyday functioning. The latter
aged 25 years (BRIEF-Preschool Version; BRIEF-P), by form can be used alone when the rated individual is
adolescents aged 1118 years (BRIEF-Self-Report Version; unable to complete the Self-Report Form or has limited
BRIEF-SR), or by adults aged 1890 years and their awareness of his or her own difficulties, or with the Self-
informants (BRIEF-Adult Version; BRIEF-A). Each Report Form to gain multiple perspectives on the indivi-
version facilitates assessment of the everyday behavioral duals functioning. The BRIEF-A is composed of 75 items
manifestations of executive dysfunction in the home, within nine nonoverlapping clinical scales measuring:
school, and/or work environments. Inhibit, Self-Monitor, Plan/Organize, Shift, Initiate, Task
The BRIEF consists of two forms, a parent question- Monitor, Emotional Control, Working Memory,
naire and a teacher questionnaire, designed to assess exec- Organization of Materials. The clinical scales form two
utive function behaviors of children and adolescents aged broader factor-based indexes: BRI and MI, and these
518 years in the home and school environments. It indexes form the overall summary score, the GEC. The
includes 86 items within eight non-overlapping clinical BRIEF-A also includes three validity scales Negativity,
scales measuring Inhibit, Shift, Emotional Control, Inconsistency, and Infrequency.
Initiate, Working Memory, Plan/Organize, Organization
of Materials, and Monitor. The BRIEF also includes two Historical Background
validity scales Inconsistency and Negativity. The eight
scales form two broader indexes based on the factor struc- Executive functions have been historically evaluated using
ture, Behavioral Regulation and Metacognition, as well as laboratory-based performance tests. While these types of
an overall score, the Global Executive Composite (GEC). measures offer the advantages of control over extraneous
Behavior Rating Inventory for Executive Functions B 373
variables and potential to fractionate and examine com- as well as the cerebellum. Furthermore, studies of indivi-
ponents of executive function separately such as planning duals with acquired focal lesions in non-frontal brain
versus working memory, they are limited in ecological regions such as the basal ganglia have provided further B
validity, or the ability to predict functioning in the support for a distributed circuitry model of executive
everyday environment. Fundamentally, executive func- functions. Damage to any given component of this
tions are necessary for organization of goal-directed be- circuitry may result in executive dysfunction.
havior in the everyday, real world, environment. Thus, The BRIEF was originally developed beginning in
in addition to assessing these functions with clinical 1994 by the authors following a commonly accepted
performance measures, it is important to also capture developmental model of executive function. The impetus
behavioral manifestations of executive function or dys- arose from frequent observations in clinical practice that
function. The BRIEF was developed to measure executive parent and teacher reports of a childs functioning in the
function through the assessment of individuals behavior everyday environment did not always, or even often, fit
in their everyday environments. Given the challenges of with the same childs test performance on putative
executive function assessment in the laboratory and executive function performance tests. Although originally
inherent limitations to applicability in the everyday intended for the authors own clinical and research use,
environment and to treatment, attention has increasingly the measure found acceptance initially in the pediatric
turned to alternative methods of evaluation that offer neuropsychology domain, and was published first in
enhanced ecological validity. Assessment methods that 2000, with subsequent versions published in the ensuing
reliably tap the individuals everyday executive problem- years. Since then, the several versions of the BRIEF have
solving in natural settings offer a complementary become widely used across the age spectrum and across
approach to clinical performance-based assessment. clinical, school, and research settings. Since publication, a
Executive function is generally viewed as a broad substantial body of literature has developed examining
umbrella term that encompasses a set of interrelated BRIEF profiles with a wide range of clinical groups
subdomains. Although authors vary in which functions (Strauss, Sherman, & Spreen, 2006).
are viewed as executive function domains, they typically
include: initiation of goal-directed behavior, inhibition of
competing actions or stimuli, planning and selection of Psychometric Data
relevant task goals, organization of behavior to solve
complex problems, flexible shifting of problem-solving BRIEF (Age 518 Years; Parent,
strategies when necessary, and monitoring and evaluation Teacher Forms)
of problem-solving behavior. In support of these
behaviors, working memory capacity plays a fundamental Standardization: Normative data are based on 1,419
role in holding information actively on-line in the parents and 720 teachers from rural, suburban, and urban
service of problem-solving, including planning and areas, reflecting 1999 US Census estimates for distributions
organization. Importantly, the executive functions are of SES, ethnicity, and gender. Separate normative tables,
not exclusive to cognition; emotional control is also including T scores, percentiles, and confidence intervals,
relevant to effective problem-solving activity and should are provided for four age groups for boys and girls sepa-
be considered in any definition. Historically, executive rately, with norms for both the parent and teacher forms.
functions have been closely associated with the integrity Clinical data are based on 212 parents and 120 teachers
of the frontal lobes of the brain. Much of the evidence rating children with developmental disorders or acquired
supporting a role for the frontal lobes in executive neurological disorders (e.g., learning disabilities, attention-
functions has come from studies of individuals with deficit/hyperactivity disorder (ADHD), traumatic brain
acquired focal damage to this region. More recently, injury (TBI), Tourettes syndrome, mental retardation,
studies using advanced brain imaging techniques such as epilepsy, and language disorders).
positron emission tomography (PET) and functional Reliability: High internal consistency (Cronbachs
magnetic resonance imaging (fMRI) have shown that alpha = 0.800.98 for both parent and teacher forms).
the frontal lobes play an essential role in executive func- Test retest reliability (Mean r = 0.82 for normative sample
tions. However, these same studies have also clearly shown parent ratings, Mean r = 0.88 for clinical sample teacher
that executive functions are not subserved by the frontal ratings). Inter-Observer (teacherparent) reliability
lobes alone, but rather by distributed neural circuitry that reflected in moderate correlations (Mean r = 0.32 for
includes other cortical regions and subcortical structures normative samples, Mean r = 0.34 for clinical samples).
374 B Behavior Rating Inventory for Executive Functions
Validity: Evidence of validity is demonstrated by 1118 years. The normative sample includes 1,118 parti-
several lines of evidence including high inter-rater cipants from a wide range of racial/ethnic backgrounds,
agreement for item-scale assignments by expert panel, educational backgrounds, as well as geographic regions
factor analytic studies, and structural equation modeling. that are matched to US Census data.
Convergent and divergent validity evidence is demon- Reliability: The BRIEF-SR scales demonstrate appro-
strated by convergence with scales of inattention and priate reliability. Internal consistency is high for the GEC
impulsivity and divergence of behavioral/emotional func- (a = 0.96) and moderate to high for the clinical scales
tioning from executive functioning using the ADHD-IV, (a = 0.720.96). Temporal stability is strong (r = 0.89 for
Behavior Assessment System for Children (BASC), CBCL, the GEC over a period of approximately 5 weeks), and
and CRS. Principal factor analysis of the BRIEF Parent there is strong inter-rater agreement for the GEC with
and Teacher Forms yielded a consistent 2-factor solution parent ratings on the BRIEF (r = 0.56). Teacher ratings on
(i.e., Behavioral Regulation, Metacognition) for norma- the BRIEF correlated less strongly with adolescent ratings
tive and clinical samples. Two of the Scales, Working on the BRIEF-SR (GEC r = 0.25) but were well within
Memory and Inhibit, are clinically useful in detecting expectations.
and predicting the diagnosis of ADHD. Validity: Principal factor analysis of the BRIEF-SR
yielded a 2-factor solution (i.e., Behavioral Regulation,
Metacognition) for normative and clinical samples. Corre-
BRIEF-Preschool (BRIEF-P; Age 25 Years; lational analyses with other self-report behavior rating
Parent, Caretaker Forms): scales (i.e., Child Behavior Checklist/Youth Self-Report
(CBSL/YSR), Behavior Assessment System for Children
Standardization: Normative data based on child ratings Self-Report of Personality (BASC-SRP), Child Health
from 460 parents and 302 teachers from urban, suburban, Questionnaire (CHQ), Profile of Mood States-Short Form
and rural areas, reflecting 1999 US Census estimates for (POMS-SF)) provide evidence of convergent and divergent
race/ethnicity, gender, socioeconomic status, and age. validity for the BRIEF-SR. Examination of BRIEF-SR pro-
Clinical samples included children in the following files in a variety of clinical groups provides further evidence
diagnostic/clinical groups: ADHD, low birth weight/ of validity based on clinical utility. BRIEF-SR ratings for
prematurity, language disorders, autism spectrum groups of adolescents with ADHD-I, ADHD-C, Insulin-
disorders, and a mixed clinical group. Dependent Diabetes Mellitus, Autism Spectrum Disorders,
Reliability: High internal consistency (a = 0.800.95 and Anxiety and Depressive Disorders showed different
for parent sample and a = 0.900.97 for teacher sample); patterns of scale elevations for each group compared to
testretest reliability (r = 0.780.90 for parents and matched control groups. Correlations between adolescent
0.640.94 for teachers); and modest correlations between and parent ratings for the clinical groups were strong,
parent and teacher ratings (r = 0.140.28). suggesting good agreement much of the time.
Validity: Convergent and discriminant validity
evidence established with other measures of inattention,
hyperactivity-impulsivity, depression, atypicality, anxiety, BRIEF-Adult (BRIEF-A; Self-Report, Informant
and somatic complaints (ADHD-IV-P, CBCL/15, Report)
BASCPRS). Factor analytic studies provide support for
a three-factor model of executive functioning embodied Standardization: The BRIEF-A was standardized and
by the three indexes in the parent and teacher normative validated for use with men and women from ages 18 to
groups, respectively. The Working Memory and the 90 years. The normative sample includes adults from a
Plan/Organize scales define the first component; the wide range of racial/ethnic backgrounds, educational
Shift and Emotional Control scales comprise the second backgrounds, as well as geographic regions that are
component; and the Inhibit and Emotional Control scales matched to US Census data.
define the third component. Reliability: The BRIEF-A has demonstrated multiple
lines of evidence for reliability. Internal consistency was
moderate to high for the Self-Report normative sample
BRIEF-Self-Report (BRIEF-SR): (a = 0.730.90 for clinical scales; 0.930.96 for indexes
and GEC) and high for the Informant Report normative
Standardization: The BRIEF-SR was standardized and sample (a = 0.800.93 for clinical scales; 0.950.98 for
validated for use with children and adolescents aged indexes and GEC). Using a mixed sample of clinical or
Behavior Rating Inventory for Executive Functions B 375
healthy adults who were seen for clinical evaluation or such as ADHD, TBI, lesions of the frontal lobes, Type 1
research study participation, internal consistency was Diabetes Mellitus, autism spectrum disorders, learning
high for the Self-Report Form (a = 0.800.94 for clinical disabilities, myelomeningocele and hydrocephalus, B
scales; 0.960.98 for indexes and GEC) and the Informant Tourettes syndrome, phenylketonuria, bipolar disorder,
Report Form (a = 0.850.95 for clinical scales; 0.960.98 obstructive sleep apnea, 22q11 deletion syndrome, galac-
for indexes and GEC). Test-retest correlations over a tosemia, sickle cell disease, and early focal frontal lesions.
4-week period across the clinical scales ranged from The BRIEF-Adult Version has been examined in indivi-
r = 0.820.93 for the Self-Report Form (n =0.50) and duals with Mild Cognitive Impairment, ADHD, Multiple
from r = 0.91 to 0.94 for the Informant Report Form Sclerosis, Alzheimers disease, epilepsy, and TBI. The
(n = 0.44). Correlations between Self-Report ratings and measures also show promise for veridicality, i.e., predict-
Informant Report ratings were moderate, ranging from ing behavior in the natural environment. The measures
r = 0.44 to 0.68 for the clinical scales and from 0.61 to 0.63 are increasingly being examined in relationship to other
for the indexes and the GEC. indications of everyday functioning. Correlational
Validity: The BRIEF-A exhibits multiple lines of analyses suggest strong, logical relationships between
validity evidence as an ecologically sensitive measure executive function and everyday behaviors such as impul-
of executive functioning in individuals with a range of sivity with aggression and working memory with atten-
conditions across a wide age range. In terms of convergent tion problems. Correlations with other real-world
validity evidence, the Self- and Informant Report Form of functioning such as adaptive functioning are reported in
the BRIEF-A scales, indexes, and GEC demonstrated individuals with developmental disabilities and scholastic
significant correlations in the expected direction with achievement. Teacher ratings of executive function on the
self- and informant reports on the Frontal Systems BRIEF predict student performance on high-stakes
Behavior Scale, Dysexecutive Questionnaire, and testing. While there are modest correlations between the
Cognitive Failures Questionnaire. Validity was further BRIEF and performance tests that tap aspects of executive
demonstrated via concurrent profiles of BRIEF-A scores functions, there are more intriguing relationships between
in clinical populations such as ADHD, multiple sclerosis, the BRIEF and biological markers such as genetic
epilepsy, mild cognitive impairment, and TBI. Validity conditions (e.g., 22q11 deletion syndrome), brain injuries
studies also are reported in the Professional Manual (e.g., frontal lobe lesions), metabolic conditions (e.g.,
comparing the BRIEF-A with the Clinical Assessment of phenylketonuria), and structural and functional imaging
Depression, the Geriatric Depression Scale, the Beck (e.g., frontal volume and activation). Finally, certain
Depression Inventory-II, and the State Trait Anxiety profiles of executive function in the everyday environ-
Inventory. Factor analysis of Self-Report Form data ment predict diagnosis of ADHD.
yielded a 2-factor solution (i.e., Behavioral Regulation, An understanding of the individuals profile of execu-
Metacognition) for normative and mixed clinical/healthy tive function strengths and weaknesses can lead to targeted
adult samples, accounting for 73 and 76% of the variance, pharmacological, behavioral, cognitive, or other therapeu-
respectively. Factor analysis of Informant Report Form tic interventions. Such strategies may be specifically tar-
data also yielded a similar 2-factor solution for the geted toward one area of executive functions such as
normative and mixed clinical/healthy adult samples, antecedent management for children with inhibitory con-
accounting for 81 and 78% of the variance, respectively. trol deficits, or may be more programmatic, such as the
comprehensive cognitive rehabilitation programs. The
BRIEF has potential uses for clinical treatment design,
Clinical Uses monitoring, and outcome measurement. Data from the
BRIEF can help the clinician focus on potentially problem-
Given the central importance of the executive functions to atic areas requiring further assessment. The same data may
the direction and control of dynamic real world behav- inform decisions about targets for treatment and types of
ior, the BRIEF was designed for a broad range of indivi- interventions based on the potential for ameliorating real-
duals with developmental, neurological, psychiatric, and world problems. Given that the BRIEF captures the patients
medical conditions. Deficits in various subdomains of the everyday functioning, the scales can suggest specific pro-
executive functions are central characteristics of many blems for which treatment goals and strategies can be
developmental and acquired neurological disorders across targeted. For example, an individual who is described as
the lifespan. Executive function deficits measured via the disinhibited in the everyday world might have treatments
BRIEF have been demonstrated in a variety of populations and supports targeted specifically toward boosting
376 B Behavior Therapy
inhibitory control or limiting opportunity for impulsive Gioia, G. A., Isquith, P. K., & Kenealy, L. (2008). Assessment of behavioral
aspects of executive function. In V. Anderson, R. Jacobs, & P. Anderson,
behavior. A child with difficulties shifting set might benefit
(Eds.), Executive functions and the frontal lobes: A life span approach.
from teaching and intervention strategies that incorporate Sussex, England: Psychology Press.
use of routines and schedules to reduce agitation and anxi- Gioia, G. A., Isquith, P. K., Kenworthy, L., & Barton, R. M. (2002). Profiles
ety when change is needed. of everyday executive function in acquired and developmental
Finally, behavioral assessment of executive function disorders. Child Neuropsychology, 8, 121137.
Isquith, P. K., Crawford, J. S., Espy, K. A., & Gioia, G. A. (2005). Assess-
can also contribute to treatment monitoring and eventual
ment of executive function in preschool children. Mental Retardation
outcome evaluation. Given the inherent difficulty in and Developmental Disability Research Review, 11, 209215.
administering performance measures of executive Malloy, P., & Grace, J. (2005). A review of rating scales for measuring
function in a repeated fashion, behaviorally anchored behavior change due to frontal systems damage. Cognitive and
measures may be more suited to such within-subjects Behavioral Neurology, 18, 1827.
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). Behavior rating
methods. For example, a patient concerned about
inventory of executive function (BRIEF). A compendium of
attentional difficulties might reveal problems with inhibi- neuropsychological tests, administration, norms, and commentary
tory control and working memory on the BRIEF. After (3rd ed., pp. 10901099). New York: Oxford University Press.
appropriate interview and clinical diagnosis, treatment
methods might include medication and cognitive-behavior
therapy. To evaluate effectiveness of treatment, the measure
may be administered again after starting medication, and Behavior Therapy
again after a longer period to determine whether the effects
of treatment are maintained. Ratings can be provided by Behavior Modification
the individual themselves or an informant in their environ-
ment who has the opportunity to regularly observe their
behavior (e.g., parent, teacher, spouse). More frequent
monitoring might also be appropriate in some cases, such
Behavior/Behavioral Analysis
as for individuals who sustain a mild TBI, where full
neuropsychological evaluation may not be feasible or
appropriate at the time, but rapid, timely assessment of
functioning is important for determining when the
individual may return to normal activities. Behavior/Behavioral Observation
Cross References
Attention Deficit/Hyperactivity Disorder

Attention/Executive Functions Behavioral Assessment
Concussion
Frontal Systems Behavior Scale (FrSBe) DAWN E. B OUMAN
Traumatic Brain Injury Drake Center
Cincinnati, OH, USA

Synonyms
Baron, I. S. (2000). Behavior rating inventory of executive function
[Test Review]. Child Neuropsychology, 6, 235238.
Gioia, G. A., & Isquith, P. K. (2004). Ecological assessment of executive
Behavior/behavioral analysis; Behavior/behavioral
function in traumatic brain injury. Developmental Neuropsychology, observation
25, 135158.
Gioia, G. A., Isquith, P. K., & Guy, S. C. (2001). Assessment of executive
functions in children with neurologic impairment. In R. J. Simeonsson
Definition
& S. Rosenthal (Eds.), Psychological and developmental assessment:
Children with disabilities and chronic conditions. New York: Guilford Behavioral assessment is a systematic collection of data,
Press. obtained through direct observation, often in natural
Behavioral Assessment of the Dysexecutive Syndrome B 377
settings, rather than sole administration of standardized Description

tests. Behavior assessment can be informal or formal and
standardized. Based on learning theory, behavioral assess- The BADS (Wilson, Alderman, Burgess, Emslie, & Evans, B
ment considers the context of a persons actions, includ- 1996) is a test battery designed to predict everyday dif-
ing antecedents that precede and might trigger the action, ficulties that arise as a result of Dysexecutive Syn-
as well as consequences that follow the behavior which drome (DES). It consists of six subtests and a 20-item
might reinforce the behavior. Behavior assessment can be questionnaire that assesses executive functioning in an
used to describe a persons functioning (i.e., arousal, ecologically valid way. The subtests are the Rule Shift
initiation, or agitation) and evaluate effectiveness of ther- Cards Test, Action Program Test, Key Search Test, Tempo-
apy interventions or medications. In persons who have ral Judgment Test, Zoo Map Test, and Modified Six Ele-
behavioral disorders due to neurological causes, behavior ments Test.
assessment is the first step for evaluating the situation so The Rule Shift Cards Test is a measure of cognitive
that remediation recommendations can be made. Patients flexibility that consists of 21 spiral-bound cards that are
are often directly observed in physical or occupational used to assess the ability to respond correctly to a rule and
therapy sessions and in the home or classroom. to shift from one rule to another. It is scored based on how
long it takes to complete the task and number of errors. In
the first part, examinees are asked to respond Yes to a
Cross References red card and No to a black card. This component
establishes a pattern of behavior that is designed to in-
Behavior Assessment System for Children (BASC) crease the probability of perseverative errors in the second
Behavior Management part, when the rules are changed. In the second part,
Behavior Modification examinees are asked to respond Yes if the card just
Behavior Rating Inventory for Executive Functions turned over is of the same color as a previously turned
Behavioral Analysis card and No if it is different.
Behavioral Assessment of the Dysexecutive Syndrome The Action Program Test involves five steps that re-
Behavioral Therapy quire simple skills that are typically part of most peo-
Conners Comprehensive Behavior Rating Scale ples repertoires. It requires examinees to determine what
Functional Assessment needs to be done prior to concentrating on how that
Functional Assessment Measure end is to be achieved. The test consists of a rectangular
stand with a thin transparent tube with a removable lid
and a cork on the bottom, while at the other end, there is a
beaker that is two thirds full of water. An L-shaped rod
that is not long enough to reach the cork is to the left
of the stand. Examinees are asked to get the cork out of
Jacobs, H. E. (1993). Behavior analysis guidelines and brain injury rehabil-
itation. Gaithersburg, MD: Aspen. the tube by using any of the available objects without
lifting the stand, the tube, or the beaker, and without tou-
ching the lid with their fingers.
In the Key Search Test, examinees are presented with
an A4-sized piece of paper with a 100 mm square in the
Behavioral Assessment of the middle and a small black dot 50 mm below it. Examinees
Dysexecutive Syndrome are told to pretend that the square is a field in which they
lost their keys and are asked to draw a line, starting at the
S HAHAL R OZENBLATT black dot, demonstrating how they would go about
Advanced Psychological Assessment, P.C. searching the field. The test is scored based on the effi-
Smithtown, NY, USA ciency of the search process.
The Temporal Judgment Test comprises four questions
concerning everyday events, which range from requiring a
Synonyms few seconds to several years. Examinees are asked to make
a sensible guess as to how long an event will take (e.g., How
BADS long do most dogs live?).
378 B Behavioral Assessment of the Dysexecutive Syndrome
In the Zoo Map Test, examinees are asked to show Shallice and Burgess (1991) developed the Six Elements
how they would visit a series of designated locations on a Test, which required examinees to carry out six tasks
map of a zoo, while following certain rules. In the high in a limited time frame without violating certain rules.
demand component, examinees incur a high number of It was tailored to a difficulty level that was consistent
errors by simply visiting the locations in the order given in with the high level of functioning of Shallices and
the instructions. In the low demand component, exam- Burgesss patients. Wilson et al. (1996) modified the Six
inees are simply required to follow the instructions to Elements Test, simplifying it for the more severely im-
produce an error-free performance. The goal of the test paired and less intellectually able patients who are often
is to assess spontaneous planning abilities. seen by neuropsychologists. These modifications evolved
The Modified Six Elements Test requires the completion into the BADS.
of three tasks (i.e., dictation, arithmetic, and picture nam-
ing), each of which is divided into parts A and B. Examinees
are required to attempt at least a part from each of the six Psychometric Data
subtests within a 10-min period and are instructed not to
complete both parts of the same task consecutively. The Multiple studies established the psychometric properties
goal of this component is to determine the examinees of the BADS. Wilson et al. (1996) found that inter-rater
ability to plan, organize, and monitor behavior. reliability was high, ranging from 0.88 to 1.00. Testretest
The Dysexecutive Questionnaire (DEQ) consists of reliability was also examined, with examinees generally
21 items that sample the range of problems commonly performing slightly, but not significantly, higher after the
associated with the Dysexecutive Syndrome. Four broad second administration. Correlations between the first
areas are sampled: emotional or personality changes, mo- and second test administrations were moderate, with the
tivational changes, behavioral changes, and cognitive exception of the Zoo Map Test, where virtually no corre-
changes. Items are scored on a 5-point (04) Likert lation was found. This lack of correlation was attributed
scale, ranging from Never to Very Often. Two versions to the presence of outliers and small sample size (n = 25).
are available, one completed by the examinee and another The testretest reliability of the BADS was similar in
by an informant. pattern to other tests of frontal lobe functioning admi-
nistered at the same time (e.g., Modified Card Sorting
Test; Nelson, 1976).
Historical Background The validity of the BADS was assessed across varied
populations. Bennett, Ong, and Ponsford (2005) investi-
The BADS is designed to evaluate patterns of deficits that gated the sensitivity of the BADS to executive dysfunc-
are typically subsumed under the functions of the frontal tion in a sample of 64 Australian patients who were
lobes. Rylander (1939) enumerated the deficits as involv- involved in motor vehicle or workplace accidents. All
ing disturbances in attention, increased distractibility, the patients experienced a loss of consciousness and
impaired ability to learn new tasks, and deficits contend- varying degrees of post-traumatic amnesia (PTA). The
ing with complex information. Shallice (1982) described authors concluded that scores derived from the BADS
this pattern of deficits as comprising impairment in atten- and other measures used in their study were only mod-
tional control, which he termed the supervisory system. erately useful in assessing executive dysfunction. In con-
Baddeley (1986) analogized the supervisory system to the trast, several studies found the BADS to discriminate
central executive component of working memory and between patients and control subjects. Krabbendam, de
suggested the term Dysexecutive Syndrome as a way of Vugt, Derix, and Jolles (1999) were able to discriminate
characterizing patients with this pattern of impairment. between schizophrenic patients and controls. Additional-
Such patients are most likely to present as impulsive, ly, Katz, Tadmor, Felzen, and Hartman-Maeir (2007) were
distractible, unable-to-use feedback to modify responses, able to discriminate between acute and chronic schizo-
and to behave inappropriately in social situations. phrenics, with the latter evidencing greater executive
The BADS was developed because patients who dysfunction. Verdejo-Garcia and Perez-Garcia (2007)
exhibited obvious impairments with executive function- examined the usefulness of the BADS in determining
ing in their day-to-day functioning often performed executive dysfunction in a Spanish sample of substance-
adequately on traditional tests of executive function- dependent examinees (SDI). They concluded that the
ing such as the Wisconsin Card Sorting Test or the BADS yielded greater effect sizes for differences between
Stroop Color Word Test. To address this discrepancy, SDI and controls than did traditional measures of
Behavioral Regulation B 379
executive function. SDI performance on the BADS was

also useful as a predictor of problems in daily activities. Behavioral Control
Additionally, deficits in BADS scores persisted following B
protracted abstinence, even when other neuropsychologi- Self-Regulation
cal indices showed recovery.
Clinical Uses Behavioral Inattention Test

Wilson et al. (1996) developed the BADS to aid those Rivermead Behavioral Inattention Test
involved in the assessment of examinees with brain injury
to determine the extent of executive dysfunction and the
likelihood that the dysfunction interferes with everyday
life. The BADS can also be used to determine the presence Behavioral Marital Therapy
of executive dysfunction in other patient groups, such as
persons with schizophrenia and problems with substance Cognitive Behavioral Couples Therapy
abuse. The BADS can be a useful part of the rehabilitation
process as a tool that can detect subtle difficulties with
planning and organization, which then become targets of
intervention.
Behavioral Memory Aids
Cognitive Correctors
Cross References
Frontal Lobe
Behavioral Prothestics
References and Readings Cognitive Correctors
Baddeley, A. D. (1986). Working memory. Oxford: Clarendon Press.

Bennett, P. C., Ong, B., & Ponsford, J. (2005). Assessment of executive
dysfunction following traumatic brain injury: Comparison of the
BADS with other clinical neuropsychological measures. Journal of Behavioral Psychology
the International Neuropsychological Society, 11, 606613.
Katz, N., Tadmor, I., Felzen, B., & Hartman-Maeir, A. (2007). The
Behaviorism
Behavioural Assessment of the Dysexecutive Syndrome (BADS) in
schizophrenia and its relation to functional outcomes. Neuropsycho-
logical Rehabilitation, 17, 192205.
Krabbendam, L., de Vugt, M. E., Derix, M. M. A., & Jolles, J. (1999). The
Behavioural Assessment of the Dysexecutive Syndrome as a tool to
assess executive functions in schizophrenia. The Clinical Neuropsy- Behavioral Redirection, Cognitive
chologist, 13, 370375.
Nelson, H. E. (1976). A modified card sorting test sensitive to frontal lobe
Shifting, Cognitive Redirection,
defects. Cortex, 12, 313324. Refocusing
Rylander, G. (1939). Personality changes after operations on the frontal
lobes. Acta Psychiatrica et Neurologica, Suppl. 20, 581.
Redirection
Shallice, T., & Burgess, P. (1991). Deficits in strategy application following
frontal lobe damage in man. Brain, 114, 727741.
Verdejo-Garcia, A., & Perez-Garcia, M. (2007). Ecological assessment of
executive functions in substance dependent examinees. Drug and
Alcohol Dependence, 90, 4855.
Wilson, B. A., Alderman, N., Burgess, P. W., Emslie, H., & Evans, J. J.
Behavioral Regulation
(1996). Behavioural assessment of the dysexecutive syndrome. Bury St
Edmunds, UK: Harcourt Assessment. Self-Regulation
380 B Behavioral Therapy
learning experiments, later to be termed classical condi-

Behavioral Therapy tioning. In classical conditioning, also called respondent
conditioning, Pavlov found that dogs would naturally
salivate (unconditioned response) when presented
G LENN S. A SHKANAZI with food (unconditioned stimulus). If he paired the
University of Florida-College of Public Health and presentation of the unconditioned stimulus with a previ-
Health Professions ously neutral stimulus, like a bell (conditioned stimu-
Gainesville, FL, USA lus), the previously neutral stimulus produced the same
unconditioned response as the unconditioned stimulus,
even if the unconditioned stimulus was absent. The un-
Synonyms conditioned response thus became the conditioned re-
sponse to the newly acquired conditioned stimulus. In
Behavior management; Behavior modification other words, Pavlov found that if he rang a bell before
feeding the dogs (who naturally salivated when the food
was presented), eventually the bell ringing alone would
Definition make the dogs salivate whether or not the food appeared.
An important behavioral therapy principle derived from
Behavioral therapy is a type of psychotherapy that focus- this work is that if the conditioned stimulus (bell) is
es on changing and gaining control over unwanted beha- repeatedly presented without the unconditioned stimulus
viors based upon the principles of classical and operant (food), the conditioned response (salivation) decreases
conditioning. It is useful in the treatment of depres- in intensity. This process is termed extinction and can
sion, anxiety disorders, phobias, smoking cessation, be found in human behavioral therapy in the treat-
weight loss, stuttering, enuresis, tics, and other medical ment of phobias. For example, Wolpe treated phobic
conditions. patients with a technique he named systematic desensi-
tization, which involves gradually exposing a patient to
an anxiety-provoking stimulus until the anxiety reaction
is extinguished.
Historical Background Burrhus Frederick Skinner (19041990) expanded on
the work of Pavlov with his concept of operant condi-
Attempts to help people solve behavioral problems tioning, which postulates that behavior can be affected
through attempts that closely mirror todays behavioral by rewards and punishments. In a famous operant condi-
therapy has a very long history. Nineteenth-century Brit- tioning experiment, a rat is in a box equipped with an
ish penal colonies used token economies to reinforce automatic food dispenser. When the rat hears the dispens-
inmates for obeying prison rules. The early Romans used er release food pellets, it moves to the food tray and eats.
aversive conditioning (e.g., placement of putrid spi- Next, a lever is placed in the box that dispenses a few
ders in the glasses of alcohol abusers) in order to decrease pellets of food when pressed. When the rat touches the
problem drinking. Seventeenth-century French physicians lever, food is dispensed. Soon the rat is pressing the lever
were using thought stopping to treat cases of obses- repeatedly to obtain the food. Through operant condi-
sional thinking. tioning, the rats behavior of pressing the lever is rein-
Behavioral therapys philosophical roots are from the forced as the rat learns to pair the pressing of the lever
School of Behaviorism, which posits that psychological with the reward. In terms of behavioral therapy, human
matters can be studied scientifically by observing behavior can be affected by reinforcement in that desired
overt behaviors and without reference to internal mental behaviors can be rewarded (reinforced) and thereby in-
states. Some of the early behavior therapists included crease in frequency while undesired behaviors can be cut
Joseph Wolpe (South Africa) and Hans Eysenck (United off from their reinforcement and extinguished. Skinner
Kingdom). Perhaps the most well-known contributors to found that the frequency and timing of the rewards given
the early development of behavioral therapy are Ivan also affected how fast the new behaviors were acquired
Pavlov and B.F. Skinner. and how hard it was to extinguish them. These became
Ivan Pavlov (18491936) was a Russian physician known as schedules of reinforcement. The work of
and physiologist who published extensively in the early Skinner also led to what is called shaping, in which the
part of the twentieth century on his conditioned desired behavior (e.g., training a chicken to peck a piano)
Behavioral Therapy B 381
could be gradually acquired by rewarding approximations fear of heights, etc.). The phobic behavior can be defined
to the behavior. as avoidance of, or escape from, the phobic stimulus (e.g.,
escaping/running away from a spider or avoiding sit- B
uations involving public speaking). By escaping from
Current Knowledge the phobic stimulus patients can reduce their anxiety.
The behavior of escape/avoidance is reinforced since the
Behavioral therapy has been successfully used for a variety reduction of the anxiety is reinforcing for the individual
of problem behaviors including, but not limited to, chronic (negative reinforcement is a concept derived from operant
pain, substance abuse, depression, phobias, autism, obesity, conditioning). In SD, patients are gradually exposed to
managing stress, smoking cessation, anorexia, obsessive the phobic stimuli, allowing them to acclimate themselves
compulsive disorder, and attention-deficit/hyperactivity to it, until they are able to tolerate it. Patients create a
disorder. It has been extensively used in patients with hierarchy of fear steps that they must overcome to reach
developmental disabilities, severely disturbed psychotic the last step, the phobic stimulus. These hierarchies can be
patients, survivors of brain injury, and others where in- imaginable, pictures or actual exposure. Patients deal with
sight-oriented or cognitive therapies may not be effective. each successive step until the hierarchy is completed.
There are a myriad of methods involved including: Typically, patients are taught relaxation skills to control
fear responses during exposure to the hierarchy.
Systematic desensitization (SD)
Behavioral therapy treatment tends to be of shorter
Exposure and response prevention
duration than more traditional modes of psychotherapy
Contingency management
(e.g., psychodynamic). Initial sessions are dedicated to
Flooding
the explanation of the basic tenets of behavioral change
Modeling
(e.g., reinforcement, extinction, punishment, etc.). Once
Applied behavior analysis
established, a variety of techniques may be utilized
Operant conditioning
including:
Respondent conditioning
Role-playing therapist models desired behaviors or
Some of these techniques are used in everyday life. For
reactions.
example, parents and teachers place stars on a refrigerator
Skills training patient is taught new desired beha-
chart or bulletin board to reward desirable behavior by
viors to replace undesired ones for parenting, social
children. Some techniques involve accumulating points
situations, public speaking, etc.
for performing a desired behavior, points that can later be
Flooding form of systematic desensitization where
exchanged for some desirable reinforcer. These token
the patient is exposed directly to the feared stimulus
economies are a variation of operant conditioning and
to extinguish the fear response.
are used in a variety of settings. In addition, extinction of
Homework patients are to try out new behaviors
undesired behavior has penetrated the mainstream as seen
learned in therapy in real-life situations.
by the use of time out, a technique involving the re-
Conditioning application of reinforcement to in-
moval of a child from reinforcement, seen by the child as
crease a desired behavior or the removal of reinforce-
somewhat aversive, or punishing, with the hope of de-
ment to decrease an unwanted behavior (e.g., token
creasing the unwanted behavior.
economies).
Behavioral therapy is based on the concepts that (1)
Relaxation training used to help patients relieve
targeted behaviors can be modified by a variety of behav-
anxiety/tension. An important component of system-
ioral techniques and (2) that the newly acquired behaviors
atic desensitization.
will be more adaptive than the undesired ones. These
techniques tend to be empirical (data-driven) and observ- The use of behavioral therapy in the treatment of sur-
able. They do not rely for their effectiveness on any mental vivors of severe traumatic brain injury (TBI) can be
(cognitive) constructs like unconscious motivations. They problematic. Those who demonstrate severe behavioral
simply identify a behavior to change and change it rather dyscontrol as a result of their TBI also likely possess
than trying to understand why the individual was cognitive sequelae that hinder the successful therapeutic
performing that behavior. An example of one of these use of these techniques. Persons with severe memory
techniques is the use of SD. deficits may not be able to recall the behavior they
This technique is often used with people who have a performed to earn a reinforcer in a contingency manage-
specific phobia (e.g., fear of snakes, fear of closed spaces, ment system. Memory problems may also interfere
382 B Behavioral Variant Frontotemporal Dementia
with a survivors ability to recall that a particular behavior Kazdin, A., & Hersen, M. (1980). The current status of behavior therapy.
Behavior Modification, 4(3), 283302.
led to a particular consequence. Without this ability
Masters, J., Burish, T., Holton, S., & Rimm, D. (1987). Behavior therapy:
to recall contingencies, survivors are likely to not be able Techniques and empirical findings. San Diego: Harcourt Press
to make different choices (i.e., make behavior changes) Jovanovich.
for which behavior they exhibit in given situations. There- Wilson, K. (1997). Science and treatment development: Lessons from the
fore, behavior management strategies place special em- history of behavior therapy. Behavior Therapy, 28, 547558.
phasis on controlling environmental stimuli in order
to reduce problem behaviors (e.g., disinhibition and
agitation).
The goal of behavior therapy with moderate or mild Behavioral Variant
TBI survivors is to provide the patient with a behavioral
repertoire that they can use to solve daily life problems
Frontotemporal Dementia
as a result of cognitive deficits (i.e., compensatory ap-
proaches). Critical behavioral therapy techniques utilized
Picks Disease
include self-monitoring, scheduling of activities, role-
playing, modeling, and contingency contracting.
Future Directions Behaviorism

Chronic diseases have replaced acute illness as the leading A NTHONY Y. S TRINGER
cause of premature death. These chronic conditions often Medicine Emory University
have unhealthy behaviors at their root cause. Examples Atlanta, GA, USA
include cigarette smoking, obesity, and lack of exercise,
poor nutritional habits, substance abuse, and medical
noncompliance. For this reason, behavioral therapy has Synonyms
demonstrated great clinical value in the treatment and
prevention of chronic health problems. An example of Behavioral psychology; Cognitive behaviorism
behavioral therapys potential can be seen in the work of
Carl Simonton in the treatment of cancer patients. His
results confirm that patients who have received behavioral Definition
treatment plus conventional oncology treatment live
twice as long as patients who had received conventional Behaviorism is a psychological theory (and branch of
cancer treatment alone. psychology), focusing on observable behavior rather
than mental phenomena, that attempts to explain behav-
ior by learning principles such as classical and operant
Cross References
conditioning. In classical conditioning, an unconditioned
stimulus already eliciting a response is paired with a
Behavioral Analysis
neutral stimulus. With repeated pairing, the neutral
(conditioned) stimulus begins to elicit the same response
Behaviorism
as the unconditioned stimulus. Operant conditioning
focuses on environmental consequences that increase
Homework
(positive reinforcement) or decrease (negative reinforce-
Psychotherapy
ment) the frequency of behavior. Early behaviorists fo-
Relaxation Training
cused exclusively on observable behavior while more
Social Skills Training
recent cognitive behaviorists have applied learning prin-
ciples to patterns of thought. As behaviorism historically
References and Readings attempted to account for behavior solely in terms of
environmental factors, neuropsychology has had limited
Gelder, M. (1997). The future of behavior therapy. Journal of Psychother- impact on the development of this approach to psychol-
apy Practice, 6(4), 285293. ogy. In contrast, neuropsychologists have attempted to
Bells Palsy B 383
understand the neural mechanisms of learning, a notable occurring around the mean and increasingly fewer obser-
example being Donald Hebbs seminal postulate that vations/scores occurring farther (above/below) from the
concordant firing in synaptically coupled neurons mean (68.26% of observations/scores fall within one B
increases the strength of the connection between the standard deviation of the mean; 95.44% fall within two
two neurons. This early postulate proved highly influen- standard deviations of the mean). A normal distribution
tial in subsequent research on the neural mechanisms of of observations is typical in large samples acting additively
learning. and independently, and is assumed in parametric statists
(e.g., t-tests, ANOVA). Standardized scores derived from
neuropsychological measures are based upon (assume)
Cross References normal distribution of the standardization sample, and
provide for direct comparison of performance between
Behavior Modification
different measures.
Cognitive Behavior Therapy
Learning
Cross References
Base Rate (Population)
Beggs, J. M., Brown, T. Y., Byrne, J. H., Crow, T., LeDoux, J. E., LeBar, K. Cut Off Scores, Cutting Scores
(1999). Learning and memory: Basic mechanisms. In M. J. Zigmond, Intelligence Quotient
F. E. Bloom, S. C. Landis, J. L. Roberts, & L. R. Squire (Eds.), Funda-
Mental Age
mental neuroscience (pp. 14111454). San Diego, CA: Academic Press.
Mills, J. A. (1998). Control: A history of behavioural psychology. New York: Percentiles
New York University Press. Standard Scores
ODonohue, W. T. (2001). The psychology of B.F. Skinner. Thousand Oaks,
CA: Sage.
Staddon, J. E. R. (2000). The new behaviorism: Mind, mechanism, and
society. Philadelphia, PA: Psychology Press. References and Readings
Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuropsychological

assessment (pp. 154156). New York: Oxford University Press.
Sattler, J. M. (2001). Assessment of children: Cognitive applications
Behavioral Inattention Test (pp. 9192). La Mesa, CA: Jerome M. Sattler.
Rivermead Behavioral Inattention Test
Bells Palsy
Bell Curve
T HESLEE J OY D E P IERO
E RICKA WODKA Boston University School of Medicine
Kennedy Krieger Institute Boston, MA, USA
Baltimore, MD, USA
Synonyms
Synonyms
Idiopathic facial paralysis
Gaussian distribution; Normal curve; Normal
distribution
Definition
Definition
Bells palsy is the acute onset of paralysis of the muscles
A normal distribution of observations/scores is shaped innervated by the facial nerve, not due to obvious causes
like a bell, with the majority of observations/scores such as trauma, stroke, or local infection.
384 B Belle Indifference
Current Knowledge Lyme disease can also cause Bells palsy. In endemic
areas, Lyme disease antibody tests should be done.
Anatomy Ramsay-Hunt syndrome refers to Bells palsy caused
by Varicella-Zoster (the virus that causes chicken-
The facial nerve innervates the muscles that control pox and shingles). The distinguishing characteristic of
the forehead and eyebrow, close the eyelids, and move Ramsay-Hunt is the presence of vesicles (small fluid filled
the cheeks and lips. It also supplies taste to the anterior blisters) in the eternal auditory canal or on the eternal ear.
two thirds of the tongue, and innervates the stapedius
muscle (a small muscle in the middle ear, connecting the
tympanic membrane to the stapes, that dampens excessive
vibration in the tympanic membrane due to loud noises). Treatment
Antiviral agents are not effective in idiopathic cases.

Clinical Presentation
Steroids (prednisone is most common) decrease the prob-
ability of permanent paralysis, or aberrant re-innervation.
The onset of paralysis may be preceded by pain behind the
Because of the paralysis of the muscles that close the eye,
ear for 1 or 2 days. The paralysis is complete in 2 days in
the cornea must be protected, especially at night. Artificial
half the patients, and by 5 days in almost all the patients. If
tears, liquid or ointment, and taping the eye shut are
the stapedius muscle is involved, there may be sensitivity
common treatments.
to noise. Taste is impaired in almost all patients. Clinical-
Antiviral treatment is indicated in Ramsay-Hunt, as is
ly, the forehead is unfurrowed, the eye cannot close fully,
antimicrobial treatment in Lyme positive patients.
the lower eyelid droops, and tears may run down the
cheek. Due to weakness of the oral muscles, saliva may
drip from the corner of the mouth on the effected side.
This is distinguished from a central facial palsy Prognosis
(e.g., due to stroke), by forehead weakness and weakness
of eye closure. In a central facial weakness, there is little or Eighty percent recover within a few weeks to 2 months.
no forehead involvement. In the Bells palsy, the forehead Recovery of some motor function in the first week is a
is unfurrowed, the eyebrow is lower than on the unin- good prognostic sign.
volved side, and cannot be voluntarily raised. In a central
facial weakness, the eyelid closes fully, though closure may
be weaker than on the uninvolved side. In Bells palsy,
eye closure is incomplete, and the lower sclera and Cross References
cornea may be reddened due to exposure to air without
lubrication from tears. Lyme Disease
Epidemiology
Incidence: 23/100,000 annually.
Cases in women and men are equal. Gilden, D. (2004). Clinical practice. Bells palsy. New England Journal of
Season: no seasonal preference. Medicine, 351, 13231331.
Age: occurs equally in all age groups. Hazin, R., Azizzadeh, B., & Bhatti, M. (2009). Medical and surgical
management of facial nerve palsy. Current Opinion in Opthalmology,
20(6), 440450.
Etiology
The etiology of Bells palsy is thought to be viral. The

genome of herpes simplex virus type 1 has been identified
in the fluid surrounding the facial nerve in several cases, Belle Indifference
but there is no convincing evidence that this is the case in
the majority of cases. La Belle Indifference
Bender VisualMotor Gestalt Test II B 385
programming controlling seems to be the largest

Bender VisualMotor Gestalt source of variance on test performance (Decker, Allen, &
Test II Choca, 2006). B
S COTT L. D ECKER , J ESSICA A. C ARBONI
Georgia State University Historical Background
Atlanta, GA, USA
The BenderGestalt has historically been one of the most
used measures in psychology. The BenderGestalt
Synonyms originated from Lauretta Benders research in perception
and psychopathology. She adapted designs used by
BenderGestalt, second edition; BG-II Wertheimer (1923) to be used as a measure of develop-
ment and psychopathology. Initially, performance was
qualitatively interpreted but a need for standardized
scoring systems emerged. Numerous scoring systems
Description have been developed, with the most notable being the
Pascal and Suttell (1951) method, the Koppitz (1963)
As with any measure, research identifies various measure- developmental scoring system, and Lacks (1999) scoring
ment, scoring, and standardization issues. Recent research system for screening for brain dysfunction. The various
culminated in the revision of the test, the BenderGestalt scoring systems and the multifaceted use of the
second edition, which was revised by Brannigan and BenderGestalt test, whether used as a warm-up prior
Decker in 2003. The BenderGestalt second edition main- to more intellectually challenging tasks or to screen for
tains many of the historical properties of the test that brain injury, have contributed to the long-standing and
appealed to clinicians while improving the psychometric continued use of the measure.
adequacy of the test. Similar to its predecessor, the
BenderGestalt second edition requires the copying of
various geometric line drawing images on a blank piece
of paper. The drawing productions are rated on a 5-point Clinical Uses
scale (Global Scoring System) based on the similarity
with the original line drawings, which are shown on The BenderGestalt was initially utilized by Lauretta
individual cards and displayed in a sequential order. Bender as a measure of perception and psychopathology.
Additionally, a memory recall period ensues after the The BenderGestalt, second edition has been used
copy period. extensively for educational, medical, and other purposes.
Like the original, the BenderGestalt second edition In particular, it has been utilized in education as a
has high reliability and validity and discriminates perfor- determinant of fine motor or visualspatial difficulties.
mance in individuals with a variety of learning and
psychological problems. It is this latter finding that
individuals from a wide variety of clinical conditions References and Readings
show poor performance on line copy tasks that contri-
butes to the tests clinical utility. Unfortunately, theoreti- Bender, L. (1938). A visual motor Gestalt test and its clinical use. New York:
cal explanations for poor performance as well as American Orthopsychiatric Association.
Decker, S. L., Allen, R., & Choca, J. P. (2006). Construct validity of the
explanations for qualitative errors, such as figure rotations
Bender-Gestalt II: Comparison with Wechsler intelligence scale for
and perseverations, are still lacking. Although previous children III. Perceptual and Motor Skills, 102, 113141.
research incorporated the use of psychodynamic and per- Koppitz, E. M. (1963). The Bender Gestalt test for young children.
sonality paradigms, the most evidence-based supported New York: Grune and Stratton.
inference of performance on the BenderGestalt second Lacks, P. (1999). Bender Gestalt screening for brain dysfunction (2nd ed.).
New York: Wiley.
edition is as a measure of visual/perceptualmotor
Pascal, G. R., & Suttell, B. J. (1951). The Bender Gestalt test. New York:
integration. Although many subcomponents are required Grune & Stratton.
in performance such as visual acuity and graphomotor Wertheimer, M. (1923). Studies in the theory of Gestalt psychology.
skills, the integration of a visual percept with a motor Psychologische Forschung, 4, 301350.
386 B BenderGestalt, Second Edition
midtemporal or lower rolandic region. Clinical seizures

BenderGestalt, Second Edition are consistent with simple partial seizures, with behavioral
semiology suggestive of onset in the lower portions of the
Bender VisualMotor Gestalt Test II pre- and postcentral gyri.
Epidemiology
Benign Epilepsy of Childhood
It is estimated that 1525% of school-aged children with
with Centrotemporal Spikes epilepsy meet diagnostic criteria for BRE. Males are be-
(BECTS) lieved to be more affected (3:2). Perinatal complications,
head trauma, central nervous system infections, or other
Benign Rolandic Epilepsy minor neurological insults have been associated with
about 10% of cases.
BRE is presumed to be genetically determined, with a
family history of seizures documented in 2132% of cases.
The electrographic abnormality seen in BRE is believed to
Benign Rolandic Epilepsy be the inherited trait and follows a transmission method of
autosomal dominance. The gene associated with the elec-
J EFFREY B. T ITUS 1,2 , R EBECCA K ANIVE 1, trographic trait is located on chromosome 15q14, though
M ICHAEL M ORRISSEY 1 the expression of the gene appears to be complex and likely
1
St. Louis Childrens Hospital affected by a multitude of genetic, environmental, and
St. Louis, MO, USA pathological factors. As such, only about 10% of children
2
Washington University School of Medicine with the electrographic trait exhibit clinical seizures.
St. Louis, MO, USA
Synonyms Natural History, Prognostic Factors,

Outcomes
Benign epilepsy of childhood with centrotemporal spikes
(BECTS); Rolandic epilepsy; Sylvian seizures Typical age of seizure onset in BRE is between the ages of
2 and 13 years, but seizures have been known to begin as
early as 1 year of age and as late as 15 years. About 75% of
cases experience seizure onset between the ages of 7 and
Definition 10 years.
Children with BRE typically have an excellent out-
Benign rolandic epilepsy (BRE) is one of the most common come. The majority of patients will experience fewer
epilepsy syndromes and belongs to a class of epilepsy syn- than ten seizures, and it is not uncommon for a patient
dromes called idiopathic partial epilepsies of childhood. to have only one seizure. Most patients experience seizure
These syndromes are characterized by seizure onset between remission within 1 or 2 years of onset. Even in cases that
the ages of 18 months and 13 years and seizure remittance involve difficult to control seizures, full recovery is
during childhood or adolescence. Exclusionary criteria for expected and seizures beyond the age of 16 years are
these syndromes include the following: absence of brain rare. Only about 2% of patients with BRE will experience
damage as evidenced on clinical examination or imaging additional seizures as an adult.
techniques; absence of generalized tonicclonic seizures; BRE is associated with good neurocognitive and social
and absence of long-term neuropsychological impairment. outcomes. While transient neurodevelopmental concerns
A family history of idiopathic epilepsy is typical, but it is not have been elucidated in more recent research, it is typically
required for diagnosis. believed that there is no long-term impact of BRE on adult
BRE is the most common idiopathic partial epilepsy functioning. There also appears to be no relation between
in childhood and is distinguished by focal epileptiform seizure frequency and the duration of BRE on functional
discharges that are typically localized over the outcome.
Benign Rolandic Epilepsy B 387
Neuropsychology and Psychology of BRE While neurodevelopmental problems have been veri-
fied in the active phase of BRE, it is not yet clear whether
BRE has been traditionally thought to be a benign syn- these problems remit after resolution of the EEG abnorm- B
drome, resulting in few if any neurodevelopmental pro- alities. The evidence thus far would suggest no long-term
blems. However, more recent research has suggested that impairment, but this needs to be verified through longi-
BRE can be associated with some neurocognitive problems, tudinal studies.
particularly during the active phase of the syndrome.
Among the available research, children with BRE, as a
group, have been consistently demonstrated to have av- Evaluation
erage intelligence. Nevertheless, more extensive neuro-
psychological assessment has revealed evidence of at least The diagnosis of BRE can only be made when charac-
mild neurocognitive difficulties in up to 78% of children teristic electrographic abnormalities and seizures are
with BRE. Almost 56% are estimated to have neurocog- present concurrently. Individual seizures are brief (up to
nitive difficulties in more than one area. The types of 12 min), simple partial seizures that are typically senso-
reported difficulties experienced by this population are rimotor in expression. Oropharyngolaryngeal symptoms
varied, including problems with motor coordination, are common and are associated with unilateral numbness
visualmotor integration, spatial processing, language and motor features that result in gurgling and grunting
processing, memory, attention, and executive function- noises. Hemifacial motor movements often occur and
ing. However, absence of control groups, questionable consist of sudden clonic contractions of the lower lip.
quality of some cognitive measures, and variability in Ipsilateral tonic deviation of the mouth is also a common
the definition of a deficit in cognitive functioning among accompanying feature. Ictal speech arrest can occur in
the available studies has made it difficult to make gen- about 40% of cases, regardless of the side of seizure
eralizations about the presence of neurocognitive pro- focus. The neurological examination is typically normal.
blems in BRE. Eighty percent of children with BRE experience sei-
A 2005 study out of Australia identified the presence of zures during sleep or the waking period. About 75% of
cognitive deficits in a relatively large sample of children seizures occur in non-REM sleep, shortly after initiating
with BRE. These included problems with verbal memory sleep or shortly before waking. Secondary generalizing
and visual memory, with about 10% of children falling seizures occur in about 20% of cases and typically occur
below two standard deviations on the verbal memory later in the sleep cycle. Partial seizures have a tendency to
index of the wide range assessment of memory and occur at the beginning or end of the sleep cycle.
learning (WRAML). In contrast, only 5% were below two The characteristic EEG pattern of BRE involves frequent
standard deviations on the visual memory index. However, to occasional unilateral or bilateral centrotemporal (rolan-
33% were below two standard deviations on the Rey Figure dic) sharp and slow waves that are superimposed on a
Delay. Deficits in phonological processing were also noted normal EEG background. Interictal activity can be present
and were believed to correspond with reading and spelling while the patient is awake and is markedly activated during
problems in the sample (Northcutt et al., 2005). NREM sleep. The rolandic sharp and slow waves have a
A more recent study in 2008 also confirmed the pres- voltage dipole that is negative in the rolandic and sylvian
ence of academic problems in children with BRE. Specifi- fissures and positive in the frontal head regions.
cally, children with BRE were found to have normal
intelligence levels but higher rates of reading, writing, and
mathematics disorders than children in a control group. Treatment
Attention problems were not identified. Of note, the study
reported that children with BRE who had a younger age of BRE is associated with spontaneous remission of seizures,
seizure onset were more likely to have a learning disability, regardless of whether the patient is treated with an anti-
and children with BRE who had prolonged interictal EEG epileptic medication. The decision to treat a child with
abnormalities in sleep were significantly more likely to have BRE is often based upon the impact of the seizures on
a learning disability. It was concluded that children with quality of life. Because the seizures typically occur infre-
BRE who have seizure onset prior to 8 years of age and have quently and most commonly during sleep, many clini-
EEG abnormalities that persist for more than 1 year are at cians chose not to initiate treatment. If the events are
greater risk for developing learning disabilities (Piccinelli frequent and potentially frightening to the child or par-
et al., 2008). ent, treatment with an antiepileptic medication may be
388 B Benign Senescent Forgetfulness
considered. However, there is currently no formal consen- Definition

sus on the best treatment for BRE. Carbamazepine is likely
the medication most commonly used, particularly due to The term benign senescent forgetting was coined by
the side effects associated with phenobarbital and phenyt- V.A. Kral (see Kral, 1962) to describe an age-related
oin. Valproic acid or gabapentin may also be helpful. In memory decline that is distinct from memory im-
most cases, polytherapy should be avoided. There is cur- pairment due to known neurological damage or disease.
rently no information about whether treatment with an
antiepileptic medication can help avoid or minimize the
neurocognitive difficulties associated with BRE.
Current Knowledge
Cross References Changes in cognitive functioning are prevalent in aging
populations. It has become clear that there is most
Carbamazepine likely a continuum between normal and abnormal men-
Gabapentin tal function in those individuals who will ultimately
Partial Seizure (Simple) develop dementia. Recent studies focusing on the char-
Valproate acterization of the earliest stages of cognitive im-
pairment have identified an intermediate period
between the cognitive changes of normal aging and
dementia (see Petersen, Stevens, Ganguli, Tangalos,
Cummings, & DeKosky, 2001). This transitional zone
has been described using a variety of terms, including
Aicardi, J. (1998). Diseases of the nervous system in childhood. London:
Mac Keith. benign senescent forgetfulness (BSF), age-associated
Ferrie, C. D., Nordli, D. R., & Panayiotopoulos, C. P. (2008). Benign focal memory impairment (AAMI), age-associated cognitive
epilepsies of childhood. In J. M. Pellock, B. F. D. Bourgeois, & decline (ACCD), cognitive impairment-no dementia
W. E. Dodson (Eds.), Pediatric epilepsy: Diagnosis and therapy (CIND), and, most recently, mild cognitive impairment
(3rd ed., pp. 335350). New York: Demos.
(MCI). AAMI differs from BSF in that it includes specific
Loiseau, P. (2001). Idiopathic and benign partial epilepsies. In E. Wyllie
(Ed.), The treatment of epilepsy: Principles and practice (3rd ed., memory test performance criteria of 1 SD below young-
pp. 475484). Philadelphia: Lippincott Williams & Wilkins. adult levels (see Larrabee & Crook, 1994). AACD expands
Northcutt, E., Connolly, A. M., Berroya, A., Sabaz, M., McIntyre, J., the definition to decrements in performance in other
Christie, J., et al. (2005). The neuropsychological and language cognitive domains. MCI further refined the definition to
profile of children with benign rolandic epilepsy. Epilepsia, 46,
include the presence of memory complaints, normal activ-
924930.
Piccinelli, P., Borgatti, R., Aldini, A., Bindelli, D., Ferri, M., Perna, S., et al. ities of daily living, normal global cognitive functioning,
(2008). Academic performance in children with rolandic epilepsy. but abnormal memory performance compared to age- and
Developmental Medicine and Child Neurology, 50, 353356. education-matched controls (see Smith & Rush, 2006).
The clinical concept of MCI is important because it is a
significant risk factor for dementia. While conversion
rates vary widely, most researchers estimate that indivi-
duals with MCI develop dementia at a rate of 1015% per
Benign Senescent Forgetfulness year, in contrast to the rate of 12% per year for age-
matched controls.
R ICHARD F. K APLAN
UConn Health Center
Farmington, CT, USA
Cross References
Synonyms
Age Decrements
Age-associated memory impairment (AAMI); Late-life Mild Cognitive Impairment
forgetfulness Normal Aging
Benton, Arthur (19092006) B 389
References and Readings Education and Training
Kral, V. A. (1962). Senescent forgetfulness: Benign and malignant. Journal He received his B.A. and M.A. degrees from Oberlin B
of the Canadian Medical Association, 86, 257260. College, and completed his Ph.D. at Columbia University
Larrabee G. J., & Crook, T. H. (1994). Estimated prevalence of age-
in 1935 under the mentorship of Carney Landis, followed
associated memory impairment derived from standardized tests of
memory function. International Psychgeriatrics, 6, 95104.
by clinical training at the Payne Whitney Psychiatric
Petersen, R. C., Stevens, J. C., Ganguli, M., Tangalos, E. G., Cummings, Clinic of New York Hospital.
J. L., & DeKosky, S. T. (2001). Practice parameter: Early detection of
dementia: Mild cognitive impairment (an evidence-based review).
Report of the Quality Standards Subcommittee of the American
Academy of Neurology. Neurology, 56, 11331142. Major Appointments
Smith, G., & Rush, B. K. (2006). Normal aging and mild cognitive
impairment. In D. K. Attix & K. A. Welch-Bohmer (Eds.), Geriatric Dr. Benton volunteered for military service in the US
neuropsychology assessment and intervention (pp. 2756). New York:
Guilford.
Navy in 1941, and was commissioned as a lieutenant
in the medical department. His active duty ended in
1945, but he continued to serve in the US Navy Re-
serve for many years, eventually retiring at the rank of
captain. In 1946, he accepted a position in the Psy-
chology Department at the University of Louisville. In
1948, he became a professor at the University of Iowa,
Benton, Arthur (19092006) where he would remain for over 50 years. He initially
was appointed Professor and Director of Graduate
S TEVEN W. A NDERSON
Training in Clinical Psychology, and then accepted a
University of Iowa Hospitals and Clinics
joint appointment in the departments of Psychology
Iowa City, Iowa, USA
and Neurology in 1958. He officially retired in 1978,
but remained active in research, teaching, and other
professional activities for another 20 years.
Landmark Clinical, Scientific, and
Arthur Benton was one of the pioneering figures in Major Honors and Awards
clinical neuropsychology. Beginning in the 1940s, he
introduced and applied novel and objective assess- President, American Orthopsychiatric Association,
ment techniques that provided a basis for fundamen- 1965
tal brain-behavior studies in aphasia, visuospatial President, International Neuropsychological Society,
abilities, hemispheric specialization, and other 1970
cognitive processes. Through the development of Secretary-General, Research Group on Aphasia of the
standardized tasks that stressed specific abilities, to- World Federation of Neurology, 19711978
gether with collection of data from neurological Distinguished Professional Contribution Award,
patients and normal comparison subjects, he was American Psychological Association, 1978
able to bring increased reliability and sensitivity to Outstanding Scientific Contribution Award, Interna-
the mental status exam, helping to establish neuro- tional Neuropsychological Society, 1981
psychology as a valuable clinical entity. He devel- Samuel Torrey Orton Award, Orton Dyslexia Society,
oped a number of neuropsychological tests that have 1982
been in wide use in clinical and research settings Distinguished Service and Outstanding Contribution
worldwide for several decades, including the Visual Award, American Board of Professional Psychology,
Retention Test, Judgment of Line Orientation, 1985
Three-Dimensional Block Construction, and Facial Distinguished Clinical Neuropsychologist Award, Na-
Recognition. He advocated a flexible approach to tional Academy of Neuropsychology, 1989
clinical assessment, with the content and scope of Gold Medal Award for Life Achievement in the Appli-
testing determined by the referral question, context, cation of Psychology, American Psychological Foun-
and patient abilities. dation, 1992
390 B Benton, Arthur (19092006)
Biography Maurice Van Allen (Iowa City VA Hospital). From its

inception, his neuropsychology program was dedicated
Arthur Benton was born in New York City on October 16, to the tripartite goals of scientific investigation, patient
1909. Educated at Oberlin and Columbia, he was a great care, and student training, united by a focus on develop-
historian who could trace his academic lineage to the ing objective psychological measures for the impairments
earliest psychologists. During his military assignment to resulting from brain dysfunction. The beginnings of the
the San Diego Naval Hospital prior to beginning his program were quite humble, with the original neuropsy-
academic career, he worked with neurologist Morris chology unit being housed in a windowless 50 60 room
Bender and examined servicemen with traumatic brain shared with the Department of Urology, which utilized it
injury. This experience helped convince him of the value for special purposes.
of standardized clinical tests, and led to the development The laboratory rapidly expanded, and with access to
of the Benton Visual Retention Test. the high volume of neurological patients at the University
During his first academic appointment at the Univer- Hospitals and other nearby institutions, Benton and his
sity of Louisville, Benton cowrote with Spafford Ackerly students systematically approached each of the primary
the seminal paper on childhood-onset damage to prefron- domains of cognition, devising and validating tests of
tal cortex. This detailed neuropsychological and neuroan- language, memory, attention, visual perception, visuomo-
atomical study of a single patient dispelled the notion that tor abilities, auditory recognition, tactile perception, body
early damage to the brain was always followed by good schema, and more. The enduring value of their empirical
recovery, and presaged later work illuminating the pre- approach is reflected in the fact that several of these tests
frontal cortex as a critical region underlying social and remain in the batteries of most neuropsychologists today.
emotional behavior. Benton advocated a hypothesis-testing approach to
In 1948, Benton began his long career at the Universi- neuropsychological evaluation. According to this flexible
ty of Iowa when he took the position of Professor and approach, hypotheses regarding the patients condition
Director of Graduate Training in Clinical Psychology. Two would arise from behavioral observations, the patients
years later, A. L. Sahs, Chairman of the Department of history, and performances on an initial brief battery of
Neurology at the University of Iowa Hospitals and Clinics tests. These hypotheses would then be tested with
invited him to set up a laboratory in the hospital for the subsequent targeted behavioral tests. I think that we
purpose of studying behavioral impairments related to should regard neuropsychological assessment in the
brain disease, a move strongly supported by Drs. Russell same way as we view the physical or neurological exami-
Meyers (Chairman of the Division of Neurosurgery) and nation, i.e., as a logical, sequential decision-making pro-
cess rather than as simply the administration of a fixed
battery of tests (Benton, 1985). He was a strict empiricist
and did not hesitate to challenge popular beliefs if his data
indicated otherwise. Perhaps best known was his charac-
terization of the Gerstmann syndrome as . . . a fiction; it
is simply an artifact of defective and biased observations
(1961), based on his systematic observation that the com-
ponents of the Gerstmann syndrome did not co-occur
with one another any more than with deficits not consid-
ered part of the syndrome.
Benton was instrumental in bringing together the
international neuropsychological community. He used
his knowledge of French, German, and Italian to translate
and bring to attention reports of neurological syndromes
that had been largely overlooked because they were pub-
lished in languages other than English. He was a visiting
scholar at the University of Milan (1964), the Neurosur-
gical Clinic, Hospital Sainte-Anne, Paris (1968), the
Hebrew University Medical School, Jerusalem (1969),
Benton, Arthur (19092006). Figure 1 the Free University of Amsterdam (1971), the University
Benton, Arthur (19092006) B 391
of Helsinki (1974), the Tokyo Metropolitan Institute of Clinical Neuropsychology

Gerontology (1974), the University of Melbourne (1977), Facial Recognition Test
LEcole des Hautes Etudes, Paris (1979), the University of Flexible Battery B
Victoria, British Columbia (1980), the University of Min- Frontal Lobes
nesota Medical School (1980), and the University of Gerstmanns Syndrome
Michigan (1986). Hemispheric Specialization
In the context of all of his professional accomplish- Hypothesis Testing Approach (to Evaluation)
ments, Dr. Bentons dedication to education in neuropsy- Judgment of Line Orientation
chology was perhaps his greatest contribution. During Mental Status Examination
neuropsychologys formative years, he was instrumental Multilingual Aphasia Examination
in developing training standards for the field. At the first National Academy of Neuropsychology (NAN)
scientific session of the INS, held in Washington D.C. in Standardized Tests
1967, he moderated an afternoon symposium on the de-
velopment of a comprehensive training program in neu-
ropsychology, and he remained active in refining these References and Readings
standards over the years. At the University of Iowa, he
Ackerly, S. S., & Benton, A. L. (1948). Report of a case of bilateral frontal
supervised 46 doctoral dissertations and 24 masters the-
lobe defect. The Frontal Lobes; Proceedings of the Association for
ses, and he provided consultation to leading neuropsy- Research in Nervous and Mental Disease 1947, 27 (pp. 479504).
chology centers around the world. He was known for Baltimore: Williams and Wilkins.
supervision characterized by frankly honest feedback, Benton, A. L. (1945). A visual retention test for clinical use. Archives of
often bruising to the students ego, but always accompa- Neurology and Psychiatry, 54, 212216.
Benton, A. L. (1955). Right-left discrimination and finger-localization
nied by sage guidance for improving the situation.
in defective children. Archives of Neurology and Psychiatry, 74,
Dr. Benton officially retired in 1978, at which time the 383389.
Benton Laboratory of Neuropsychology in the Depart- Benton, A. L. (1956). The concept of pseudofeeblemindedness. Archives
ment of Neurology was dedicated. His retirement was of Neurology and Psychiatry, 75, 379388.
incomplete, however, as he continued to provide guidance Benton, A. L. (1960). Motivational influences on performances in brain-
damaged patients. American Journal of Orthopsychiatry, 30, 313321.
for the neuropsychologists at Iowa and elsewhere and
Benton, A. L. (1961). The fiction of the Gerstmann Syndrome. Journal
continued writing for more than another 2 decades. of Neurology, Neurosurgery, and Psychiatry, 24, 176181.
Today, the Benton Neuropsychology Laboratory at the Benton, A. L. (1962). Behavioral indices of brain injury in school chil-
University of Iowa Department of Neurology remains a dren. Child Development, 33, 199208.
vital program for research, training, and patient care, in Benton, A. L. (1964). Contributions to aphasia before Broca. Cortex, 1,
314327.
the tradition established by Dr. Benton more than a half
Benton, A. L. (1964). Developmental aphasia and brain damage. Cortex,
century ago. 1, 4052.
Bentons wife, Rita, was a professor of musicology at Benton, A. L. (1967). Problems of test construction in the field of aphasia.
the University of Iowa, where she was the first head of the Cortex, 3, 3258.
Music Library in 1957. Arthur and Rita met in 1939 while Benton, A. L. (1969). Development of a multilingual aphasia battery:
Progress and problems. Journal of Neurological Sciences, 9, 3948.
they both were vacationing in Paris, and they married
Benton, A. L. (1977). Interactive effects of age and brain disease on
later that year. Upon Rita Bentons death in 1980, the reaction time. Archives of Neurology, 34, 369370.
Music Library was named in her honor. They had three Benton, A. L. (1985). Some problems associated with neuropsychological
children: Raymond, Abigail, and Daniel. Arthur Benton assessment. Bulletin of Clinical Neurosciences, 50, 1115.
died in Glenview, Illinois on December 27, 2006 from Benton, A. L., & Fogel, M. L. (1962). Three-dimensional constructional
praxis. Archives of Neurology, 7, 347354.
complications of emphysema, at the age of 97.
Benton, A. L., Hamsher, K. deS., Varney, N. R., & Spreen, O. (1983).
Contributions to neuropsychological assessment. New York: Oxford
University Press.
Cross References Benton, A. L., & Howell, I. L. (1941). The use of psychological tests in the
evaluation of intellectual function following head injury. Psychoso-
matic Medicine, 3, 138151.
ABPP
Benton, A. L., & Van Allen, M. W. (1968). Impairment in facial recogni-
APA tion in patients with unilateral cerebral disease. Cortex, 4, 344358.
Aphasia Levin, H. S., & Benton, A. L. (1975). Temporal orientation in patients
Benton Visual Retention Test with brain disease. Applied Neurophysiology, 38, 5660.
392 B Benton Face Recognition Test
construction. Now in its fifth edition (Sivan, 1992),

Benton Face Recognition Test the test consists of three equivalent forms (Forms C, D,
and E), each composed of 10 items of visual stimuli. Most
Facial Recognition Test items include three geometric forms presented along a
horizontal plane, making the test particularly sensitive to
visual neglect (Sivan, 1992).
The following description of the BVRT was adapted
Benton Faces from Strauss, Sherman, and Spreen (2006). The test
includes four alternative methods of administration
Facial Recognition Test
(A, B, C, and D) that assess different aspects of func-
tioning. The most common administration (A) assesses
immediate recall of a visual display. After presenting a
stimulus card for 10 s, the card is removed, and the
Benton Test examinee is asked to draw the design from memory.
Administration B follows the same procedure as A, but
Benton Visual Retention Test with a 5-s exposure interval. Administration C allows
the examiner to dissociate memory functioning from
perceptual and motor aspects of the task by asking the
examinee to reproduce the designs while each item is in
Benton Visual Form plain view. There is no time limit, but individuals who
Discrimination Test work very slowly should be encouraged to increase their
speed. In Administration D, a 15-s interval is inserted
Visual Form Discrimination between the 10-s encoding phase and the figure repro-
duction, allowing the examiner to assess short-term
retention of visual information. Scoring consists of
both the number of correct designs and the number
Benton Visual Retention Test of six different types of errors: omissions, distortions,
perseverations, rotations, misplacements, and size
C ARLYE G. M ANNA 1,2 , K ARIN A LTERESCU 2, errors. Administration time for each form is approxi-
J OAN C. B OROD 2,3 , H. A LLISON B ENDER 4 mately 5 min. Several sets of norms are available and
1
New York State Psychiatric Institute reflect different demographic characteristics, including
New York, NY, USA age ranges and education levels (Mitrushina, Boone,
2
Queens College and The Graduate Center of the City Razani, & DElia, 2005; Strauss et al., 2006). A multi-
University of New York ple-choice recognition administration (Administration
Flushing, NY, USA M, with alternate forms F and G) is also sometimes
3
Mount Sinai School of Medicine used, particularly with patients who have visuoconstruc-
New York, NY, USA tional and motor coordination deficits (Amieva, Gaestel,
4
New York University Langone Medical Center & Dartigues, 2006). For Administration M, the examinee
New York, NY, USA views a target stimulus for 10 s and, after it has been
removed, is required to identify it from among four
choices. Although not part of the English-language ver-
Synonyms sion, materials for this special administration are available
in the German (Sivan & Spreen, 1996) and French
Benton Test; BVRT (Benton, 1965) editions.
Description Historical Background

The Benton Visual Retention Test (BVRT) is a widely used Dr. Arthur L. Benton developed the Visual Retention Test as
test of visual memory, visual perception, and/or visual a brief measure of immediate nonverbal memory to
Benton Visual Retention Test B 393
supplement the popular auditory digit span test in neuro- brain disease for the adult norms, and 236 children, aged
psychological evaluations (Benton, 1945). It was first pub- 613 years, enrolled in public schools in Iowa and
lished in 1946. Memory-for-designs tasks had appeared Wisconsin, for the child and adolescent norms. B
earlier in the century as part of larger intelligence tests,
but included only a few designs and did not have separate
normative data. As an addition to the digit span test, the Clinical Uses
BVRT was intended to provide a broader assessment of
short-term memory, and its format was selected for its As it recruits a number of different cognitive functions, the
resistance to emotional influence, employment of differ- BVRT is sensitive to many forms of brain damage
ent sensorimotor components (graphomotor versus audi- and disease; however, its ability to discriminate among
tory-vocal), and minimal examiner-subject interaction diagnoses is low (for a review, see Mitrushina et al.,
(freedom from interpersonal demands). The initial ver- 2005). An individuals global performance, quantified as
sion included seven cards and two parallel forms. A 1955 either the number correct score or error score, provides the
revision increased the number of designs and alternate best indicator of impairment. According to the manual,
forms, and added norms for children aged 816 years. measures of specific error types, such as omissions, perse-
Later editions included a design copy administration verations, and distortions, are not by themselves diagnos-
and updated norms. The most recent revision was tic, but may raise hypotheses for further testing. For
authored by Abigail Benton Sivan in 1992 and is avail- example, a high number of perseverative errors suggests
able from its publisher, Pearson Assessments (http:// possible frontal lobe damage, particularly if supported by
pearsonassess.com). other test and behavioral data. Omission of peripheral
figures may raise suspicion of brain damage and is most
frequently associated with left hemispatial neglect as a
Psychometric Data result of damage to right parietal lobe regions. In contrast,
global performance has not been found to consistently
Information on reliability and validity may be found in distinguish between patients with unilateral right and left
the manual. Test-retest reliability is 0.85. Alternate form brain damage. Though the BVRT is sensitive to the visuo-
reliability ranges from 0.79 to 0.84. There is evidence that spatial disturbance that is often observed in patients with
Form C is slightly less difficult than Forms D and E under right hemisphere damage, studies have shown that indivi-
Administration A. Correlations between immediate (Ad- duals with unilateral left hemisphere damage can exhibit
ministration A) and delayed (Administration D) recall are similarly poor results on Administration A (Vakil, Blach-
positive and range from 0.40 to 0.83, depending on the stein, Sheleff, & Grossman, 1989), as well as on copy and
combination of forms used. Construct validity has been multiple-choice administrations (Arena & Gainotti,
demonstrated through moderate correlations (0.460.62) 1978). This indicates that memory for the BVRT designs,
of the BVRT with nonverbal subtests from the Wechsler many of which can be verbalized, is mediated by both
Adult Intelligence Scales, including Block Design, Digit hemispheres. However, the presence of a delay interval
Symbol, and Object Assembly. may differentially affect verbally and visually encoded
Child and adolescent normative data are included for material and therefore help to discriminate between left-
Administrations A and C. The normative data for each and right-sided brain damage. Participants with right
method of administration are based on different standar- hemisphere damage achieved a lower total correct score
dization samples, and sample characteristics are provided on Administration D than on Administration A, whereas
for Administrations A, B, and C. (Normative data for individuals with left hemisphere damage had the opposite
Administration D are not included in the manual.) The pattern of performance, benefitting from the delay. In
standardization sample for Administration A is based on a contrast, scores from healthy participants did not differ
compilation of three separate studies totaling over 1,300 between the two administrations (Vakil et al., 1989).
participants, ranging in age from 869 years. (See manual Both copy and memory administrations are highly
for discussion of participant inclusion criteria for each of sensitive to early dementia, and may also help to identify
these studies.) The standardization sample for Adminis- individuals who are at risk for developing dementia in the
tration B is based on 103 medical inpatients and out- future. In one such study, participants with six or more
patients, aged 1660 years, with no evidence or history errors on Administration A were nearly twice as likely to
of brain disease. The standardization samples for Admin- develop Alzheimers Disease 1015 years later, when com-
istration C are 200 medical patients with no history of pared to participants who had fewer errors (Kawas et al.,
394 B Benton Visual Retention Test
2003). The BVRT also aids in identifying children with a Visuoperceptual

learning disability and discriminating among types of Wechsler Memory Scale
learning disabilities, with reading deficits associated with
the lowest levels of performance (Snow, 1998). Children
with Attention-Deficit/Hyperactivity Disorder receiving
stimulant medication have also been shown to perform References and Readings
more poorly on the BVRT than healthy participants (Ris-
Amieva, H., Gaestel, Y., & Dartigues, J. (2006). The multiple-choice
ser & Bowers, 1993). Poorer performance is evident in a
formats (Forms F and G) of the Benton Visual Retention Test as a
subset of patients with schizophrenia and may result, at tool to detect age-related memory changes in population-based
least in part, from abnormal patterns of visual scanning studies and clinical settings. Nature Protocols, 1, 19361938.
and fixation related to deficient attention (Obayashi, Mat- Arena, R., & Gainotti, G. (1978). Constructional apraxia and visuoper-
sushima, Ando, Ando, & Kojima, 2003). The BVRT may ceptive disabilities in relation to laterality of lesions. Cortex, 14,
463473.
also be useful in detecting malingering, which has been
Benton, A. L. (1945). A visual retention test for clinical use. Archives of
characterized by a greater number of errors, particularly Neurology and Psychiatry, 54, 212216.
distortion ones, than seen in neuropsychologically im- Benton, A. L. (1965). Manuel pour lapplication du Test Retention Visuelle.
paired patients (Benton & Spreen, 1961; Suhr, Tranel, Paris, France: Les Editions du Centre de Psychologie Appliquee.
Wefel, & Barrash, 1997). Benton, A. L. (1974). Revised Visual Retention Test: Clinical and
experimental applications (4th ed.). New York: Psychological
In evaluating results, it is important to consider that
Corporation.
the BVRT may be sensitive to individual differences that Benton, A. L., & Spreen, O. (1961). Visual Memory Test: The simulation
do not necessarily reflect neuropathology. Stratified nor- of mental incompetence. Archives of General Psychiatry, 4, 7983.
mative data confirm that age is negatively correlated and Kawas, C. H., Corrada, M. M., Brookmeyer, R., Morrison, A.,
that baseline intellectual functioning is positively corre- Resnick, S. M., Zonderman, A. B., et al. (2003). Visual memory
predicts Alzheimers disease more than a decade before diagnosis.
lated with the BVRT number correct score. The associa-
Neurology, 60, 10891093.
tion with baseline intellect is strongest in the lower than Mitrushina, M. N., Boone, K. B., Razani, J., & DElia, L. F. (2005).
average IQ ranges. Education-stratified norms are also Handbook of normative data for neuropsychological assessment
available, and indicate a positive relationship between (2nd ed.). New York: Oxford University Press.
years of education and the number correct score (Strauss Obayashi, S., Matsushima, E., Ando, H., Ando, K., & Kojima, T. (2003).
Exploratory eye movements during the Benton Visual Retention
et al., 2006). The BVRT is used worldwide, and norma-
Test: Characteristics of visual behavior in schizophrenia. Psychiatry
tive data have been published from more than a dozen and Clinical Neurosciences, 57, 409415.
countries (Mitrushina et al., 2005). While relatively Risser, M. G., & Bowers, T. G. (1993). Cognitive and neuropsychological
few in number, studies involving direct cross-cultural characteristics of attention deficit hyperactivity disorder children
comparisons demonstrate generally good consistency; receiving stimulant medications. Perceptual and Motor Skills, 77,
10231031.
however, caution is recommended when testing indivi-
Rosselli, M., Ardila, A., Bateman, J. R., & Guzman, M. (2001). Neuropsy-
duals with very low levels of education (Mitrushina et al., chological test scores, academic performance, and developmental
2005). Comparisons of elderly people living in the US and disorders in Spanish-speaking children. Developmental Neuropsy-
Canada suggest similar levels of performance when edu- chology, 20, 355373.
cation and/or reading ability are controlled. Results from Sivan, A. B. (1992). Benton Visual Retention Test (5th ed.). San Antonio,
TX: Psychological Corporation.
a large Columbian sample of school-aged children did not
Sivan, A. B., & Spreen, O. (1996). Der Benton-Test (7th ed.). Bern,
differ from North American norms (Rosselli, Ardila, Bate- Switzerland: Verlag Hans Huber.
man, & Guzman, 2001), suggesting that when educational Snow, J. H. (1998). Clinical use of the Benton Visual Retention Test for
quality is similar, as is increasingly more common in children and adolescents with learning disabilities. Archives of
developed countries, cross-cultural differences, if present, Clinical Neuropsychology, 13, 629636.
are relatively small. Most studies have shown no gender
neuropsychological tests: Administration, norms, and commentary
differences. (2nd ed.). New York: Oxford University Press.
Suhr, J., Tranel, D., Wefel, J., & Barrash, J. (1997). Memory performance
after head injury: Contributions of malingering, litigation status,
psychological factors, and medication use. Journal of Clinical and
Experimental Neuropsychology, 19, 500514.
Cross References Vakil, E., Blachstein, H., Sheleff, P., & Grossman, S. (1989). BVRT-scoring
system and time delay in the differentiation of lateralized hemi-
Short Term Memory spheric damage. International Journal of Clinical Neuropsychology, 11,
Visual-Motor Function 125128.
Ben-Yishay, Yehuda (1933 ) B 395
individuals with brain injuries combined contributions

Ben-Yishay, Yehuda (1933 ) from neuropsychology, behavioral psychology, cogni-
tive-behavioral psychotherapy, special education, social B
A MY A LDERSON psychology, and psychodrama. He adapted these mod-
Emory University alities to the needs and capabilities of his patients, sys-
Atlanta, GA, USA tematically applying them in therapeutic community
settings to reach maximal effectiveness. Through his
holistic approach to the treatment of brain injury, a
Major Appointments foundation for cognitive and neuropsychological reha-
bilitation was established.
1967-present New York University Medical Center, The holistic rehabilitation approach developed by
Rusk Institute of Rehabilitation Medicine Dr. Ben-Yishay includes a number of components
19741976 Clinical Director of Israel Head Trauma in addition to traditional cognitive retraining, including:
Project, New York University Medical Center, Rusk development of a therapeutic milieu or community,
Institute, and Israel Ministry of Defense Joint Re- psychotherapy, regular involvement of family and
search Project, Afeka, Israel. caregivers, psychoeducation, and transitional work
19761983 Visiting Clinical Director, New York Uni- opportunities. Within the therapeutic milieu or com-
versity Medical Center, Rusk Institute, and Israel Min- munity, persons with brain-injury not only participate
istry of Defense Joint Research Project, Afeka, Israel. in activities aimed at adaptation to and compensation
19951997 Clinical Director, Kurt Goldstein Institute for their deficits but also meet regularly with staff mem-
for Holistic Neuropsychological Rehabilitation bers to monitor their progress. Interaction with other
Stravbing, Germany individuals with brain injury is also an important part of
the therapeutic milieu. During individual and group
psychotherapy, persons with brain injury address the
many adjustment issues associated with their deficits.
Major Honors and Awards In addition, the involvement of family and caregivers in
the rehabilitation process not only provides additional
1976 Howard A. Rusk Award for Outstanding Accom- support for the person with a brain injury as they com-
plishments in Rehabilitation plete therapies but also assists with the transition back to
1982 William F. Caveness Award for Distinguished the community by providing realistic education and
Contributions in the field of Head Injury, National information regarding the persons progress and injury.
Head Injury Foundation. Finally, transitional work opportunities provide impor-
1988 Thomas J. Dean Award of Excellence in Head tant information regarding individuals abilities outside
Injury Rehabilitation, Dallas, Rehabilitation of structured settings and help to provide additional
Foundation. functional goals for rehabilitation therapies.
1991 Distinguished Career Achievement Award, The work of Dr. Ben-Yishay has been researched and
American Board of Medical Psychotherapists. applied both within the United States and abroad, and
2006 Outstanding Life-Time Scientific Contributions premiere rehabilitation institutes around the world
to Rehabilitation Psychology. American Psychological utilize his model of cognitive rehabilitation as the
Association, Division 22. foundation for their own brain injury programs. His
teaching methods are studied by students and profes-
sionals from all over the world, and he is internation-
ally known as a clinician, teacher, researcher, and
Landmark Clinical, Scientific, and expert in the field of holistic rehabilitation.
Dr. Ben-Yishay is the father of holistic brain injury Short Biography
rehabilitation. Initially developed in Israel for war veter-
ans with head injuries and later transitioned to the New Yehuda Bin-Yishay was born February 11, 1933 in Cluj,
York University School of Medicine at the Rusk Institute, Romania. He grew up in Israel and served in the Israeli
Dr. Ben-Yishays treatment interventions with army. In 1957, he received a B.A. degree in Sociology and
396 B Benzodiazepines
Special Education from Hebrew University in Jerusalem, Cross References

Israel. Then, in 1958, he came to the United States on a
scholarship from the New School University in New York Cognitive Rehabilitation
City. There, he studied under Kurt Goldstein. He com- Goldstein, Kurt (18781965)
pleted an internship in Clinical Psychology in 1960 at
Trenton State Hospital in Trenton, NJ. His Masters degree
in Personality Psychology was completed in 1961. References and Readings
After completing his Masters degree, Dr. Ben-Yishay
served as the psychologist for an experimental program in Ben-Yishay, Y., & Diller, L. A primer holistic neuropsychological rehabilita-
the Department of Rehabilitation at the Albert Einstein tion. New York, NY: Oxford University Press, In Press.
College of Medicine in New York. The study tested the Prigatano, G., & Ben-Yishay, Y. (1999). Psychotherapy and psychothera-
effectiveness of a therapeutic community model of peutic intervention. In M. Rosenthal (Ed.), Rehabilitation of the
adult and child with traumatic brain injury (3rd Ed.). Philadelphia:
rehabilitation.
F.A. Davis.
In 1964, Dr. Ben-Yishay joined the faculty at New York
University. He obtained his Ph.D. from New York University,
following the completion of studies investigating the effects
of normobaric oxygen on stroke patients performances on
neurologic, sensory-motor, and cognitive measures. While at Benzodiazepines
New York University, Dr. Ben-Yishays research over the next
several years focused on three key areas: 1) rehabilitation J OANN T. T SCHANZ 1, K ATHERINE T REIBER 1,2
1
outcome prediction studies; 2) comparisons between normal Utah State University
controls and brain injured individuals across a variety of Logan, UT, USA
2
measures; and 3) development and efficacy studies of cogni- University of Massachusetts Medical School
tive rehabilitation modules. Worcester, MA, USA
From 19741977 Dr. Ben-Yishay conducted a pilot
study in Israel to investigate the effects of holistic brain
injury rehabilitation on Israeli war veterans. The results Definition
were impressive, and the study was followed in September
of 1978 by the New York University-Rusk Head Trauma Benzodiazepines belong to a class of medications
Program, a fully funded five-year research grant-based known as sedative-hypnotics. They bind to the sub-
program. type A of the common inhibitory neurotransmitter
Throughout his career, Dr. Ben-Yishay trained substance, gamma-aminobutyric acid (GABA). They
numerous rehabilitation neuropsychologists, who have have wide ranging effects. Their popular use is
gone on to institute his model of cognitive rehabilitation. reflected in their anxiolytic, muscle relaxant, sedative,
Individuals such as Anne-Lise Christensen, Ph.D. and anesthetic, and anticonvulsant properties. Due to their
George Prigatano, Ph.D. have been greatly influenced by safety profile, benzodiazepines became very popular in
the work of Dr. Ben-Yishay and established programs the 1970s, replacing older drugs such as barbiturates
built upon principles learned under his tutelage. and meprobamate for the treatment of anxiety symp-
Dr. Ben-Yishays work in the area of holistic brain toms, insomnia and other sleep disorders (Iversen,
injury rehabilitation has continued to the present day, Iversen, Bloom & Roth, 2009), and alcohol withdrawal
and he has been recognized extensively for his work syndrome (Ntais, Pakos, Kyzas, & Ioannidis, 2005). How-
worldwide. He has receiving numerous awards and hon- ever, negative effects of benzodiazepine use have also been
ors, including the 2006 Lifetime Scientific Contributions reported. Although these side effects vary depending
to Rehabilitation Psychology Award from Division 22 of upon the original indication for benzodiazepine use, some
the American Psychological Association. of the unwanted effects include drowsiness, decreased con-
In addition to the numerous international committee centration, memory impairment, psychomotor slowing
and consultant positions that he has held, Dr. Ben-Yishay (Buffett-Jerrott & Stewart, 2002), and postural instability
has also served on a number of important editorial (with increased risk of falls) among the elderly (Allain,
boards, including: Archives of Physical Medicine and Re- Bentue-Ferrer, Polard, Akwa, & Patat, 2005). Chronic use
habilitation, Journal of Head Trauma Rehabilitation, Brain also carries the risk of substance dependence and abuse,
Injury, and Neuropsychological Rehabilitation. and cognitive impairment with prolonged use at high
Berg Balance Scale B 397
doses (Stewart, 2005; Barker, Greenwood, Jackson, & Montplaisir, J., Hawa, R., Moller, H., Morin, C., Fortin, M., Matte, J.,
Reinish, L., & Shapiro, C. M. (2003). Zopiclone and zaleplon vs
Crowe, 2004). For these and other reasons, medications
benzodiazepiones in the treatment of insomnia: Canadian consensus
in this class are now more commonly used on a short- statement. Human Psychopharmacology: Clinical and Experimental, B
term rather than a long-term basis (Iversen et al., 2009). 18, 2938.
Ntais, C., Pakos, E., Kyzas, P., & Ioannidis, J. P. (2005). Benzodiazepines
for alcohol withdrawal. Cochrane Database of Systematic Reviews,
Current Knowledge 20, CD005063.
As reported above, chronic use of benzodiazepines

has declined, particularly for the treatment of anxiety
disorders and insomnia. Tricyclic antidepressants Berg Balance Scale
(TCAs) and selective serotonergic agents are increasingly
being prescribed over benzodiazepines for the treatment K ARI D UNNING
of anxiety disorders. For example, selective TCAs are University of Cincinnati
reportedly as effective as benzodiazepines in the treatment Cincinnati, OH, USA
of generalized anxiety disorder and certain selective
serotonin reuptake inhibitors, and TCAs are effective in
the treatment of panic and obsessivecompulsive disor- Synonyms
ders (Bourin & Lambert, 2002).
With respect to insomnia, benzodiazepines were the BBS; 7-item BBS-3P
treatment of choice over barbiturates. However, negative
effects such as the development of tolerance, residual day-
time sleepiness, aggravation of respiratory conditions, and Description
reduced duration of slow-wave (restorative) and REM
sleep were also reported. Newer, nonbenzodiazepine hyp- The Berg Balance Scale (BBS) is a 14-item performance
notic compounds such as zopiclone and zaleplon are also observation measure that assesses balance on a scale from
effective in treating insomnia, yet have fewer side effects 0 to 4 for each item, yielding a total score range of 056,
than those of benzodiazepines (Montplaisir et al., 2003). where higher scores indicate better balance. The BBS tests
both static and dynamic balance with items meant to
mimic balance challenges encountered in daily life.
Cross References
Barbiturates
GABA Historical Background
In 1989, Berg developed the BBS to fill the need for a

References and Readings quantitative balance assessment tool to screen older adults
for fall risk. The BBS has subsequently become the best
Allain, H., Bentue-Ferrer, D., Polard, E., Akwa, Y., & Patat, A. (2005). known clinical balance instrument. Shorter versions of
Postural instability and consequent falls and hip fractures associated the BBS, such as the seven-item BBS-3P (which also has
with use of hynotics in the elderly. A comparative review. Drugs in
a condensed rating scale) have also been developed and
Aging, 22, 749765.
Barker, M. J., Greenwood, K. M., Jackson, M., & Crowe, S. F. (2004).
validated.
Cognitive effects of long-term benzodiazepine use. A meta-analysis.
CNS Drugs, 18, 3748.
Bourin, M., & Lambert, O. (2002). Pharmacotherapy of anxious disor-
ders. Human Psychopharmacology: Clinical and Experimental,
Psychometric Data
17, 383400.
Buffett-Jerrott, S. E., & Stewart, S. H. (2002). Cognitive and sedative The high reliability, validity, and sensitivity of the BBS,
effects of benzodiazepine use. Current Pharmaceutical Design, including predictive validity for fall risk, are well docu-
8, 4558.
mented in the literature. Some authors initially dichoto-
Iversen, L. L., Iversen, S. D., Bloom, F. E., & Roth, R. H. (2009). Anti-
depressants and anxiolytics. Introduction to neuropsychopharmacology
mized the scale, using the threshold value <45 points as
(pp. 306335). New York: Oxford University Press. an indication of fall risk. However, more rigorous study
398 B Bergers Waves
has determined that a gradient of fall risk exists over the Blum, L., & Korner-Bitensky, N. (2008). Usefulness of the berg balance
scale in stroke rehabilitation: A systematic review. Physical Therapy,
entire scale. A retrospective study of community-dwelling
88(5), 559566.
persons with stroke demonstrated that changing from 3 to Chou, C. Y., Chien, C. W., Hsueh, I. P., Sheu, C. F., Wang, C. H., & Hsieh,
4 for the standing on one leg item had a sensitivity of C. L. (2006). Developing a short form of the berg balance scale for
0.90 and a specificity of 0.50 for predicting the history of people with stroke. Physical Therapy, 86(2), 195204.
multiple falls. Internet Stroke Center (2007). Berg balance scale. http://www.strokecen-
ter.org/Trials/scales/berg.html. Accessed May 19, 2010.
Mao, H., Hsueh, I., Tang, P., Sheu, C., & Hsieh, C. (2002). Analysis and
comparison of the psychometric properties of three balance mea-
Clinical Uses sures for stroke patients. Stroke, 33(4), 10221027.
Muir, S. W., Berg, K., Chesworth, B., & Speechley, M. (2008). Use of the
The BBS is available online (Internet Stroke Center, 2007). berg balance scale for predicting multiple falls in community-dwelling
Administration requires 1020 min, a chair, a step, a elderly people: A prospective study. Physical Therapy, 88(4), 449459.
ruler, and a stopwatch. Balance ability is sometimes Stevenson, T. J. (2001). Detecting change in patients with stroke using the
berg balance scale. Australian Journal of Physiotherapy, 47, 2938.
grossly categorized as good, fair, or poor for score ranges Tyson, S. F., & Connell, L. A. (2009). How to measure balance in clinical
from 56 to 41, 4021 and 200, respectively. As stated practice. A systematic review of the psychometrics and clinical utility
above, a gradient of fall risk exists over the entire scale. of measures of balance activity for neurological conditions. Clinical
BBS scores are used when prescribing mobility aids and Rehabilitation, 23(9), 824840.
treatment interventions, identifying safe and unsafe activ-
ities, and to measure treatment effect. When assessing the
treatment effect for individual patients with stroke, a
score change of 6 points has been shown to represent Bergers Waves
real change, beyond measurement error, with 90%
confidence. Alpha Rhythm
Although originally designed to screen older adults for
fall risk, the BBS has subsequently been validated for
persons with stroke, multiple sclerosis, and Parkinsons
Disease. Best Performance Method
G LEN E. G ETZ
Cross References Allegheny General Hospital
Pittsburgh, PA, USA
Balance Disorders
Multiple Sclerosis
Parkinsons Disease Synonyms
Reliability
Sensitivity Cognitive potential
Specificity
Stroke
Definition
Neuropsychologists typically do not have an opportunity

References and Readings to evaluate patients before the onset of neurological illness
or injury. Judgments about impairment are often made by
Alzayer, L., Beninato, M., & Portney, L. G. (2009). The accuracy of
comparing obtained test scores with estimates of premor-
individual berg balance scale items compared with the total berg
score for classifying people with chronic stroke according to fall bid ability. There are several approaches to estimating
history. Journal of Neurologic Physical Therapy: JNPT, 33(3), 136143. premorbid level of ability. One such approach is the Best
Berg, K., Wood-Dauphinee, S., & Williams, J. I. (1995). The balance scale: Performance Method. Using this method, data are collect-
Reliability assessment with elderly residents and patients with an ed from multiple sources, including, but not limited to,
acute stroke. Scandinavian Journal of Rehabilitation Medicine, 27(1),
test scores, observations, interviews, reports from family,
2736.
Berg, K., Wood-Dauphinee, S., Williams, J. I., & Gayton, D. (1989). and historical data. After the data are collected, the
Measuring balance in the elderly: Preliminary development of an data source that yields the highest level of functioning is
instrument. Physiotherapy Canada, 41, 304311. the set standard to which all other aspects of functioning are
Beyond a Reasonable Doubt B 399
compared. The Best Performance Method assumes that one and Rebif (INF-b1a). These medications are adminis-
performance level exists for each persons cognitive abilities. tered via injection, and each has been shown to reduce the
A notable discrepancy between a patients best and other frequency of MS relapses, reduce MRI evidence of brain B
performances is indicative of neuropsychological impair- lesions, and possibly reduce disability progression.
ment. The Best Performance Method also assumes that
performance should be consistent across all areas of func- Cross References
tioning. For example, very superior intellectual and other
abilities would be expected from a patient who has earned a Multiple Sclerosis
doctoral degree in engineering. The method has been criti-
cized by some who believe that there is a high likelihood of
overestimating premorbid ability.
National Clinical Advisory Board of the National Multiple Sclerosis
Cross References Society. (2007). Disease management consensus statement. Retrieved
February 15, 2010, from http://www.nationalmssociety.org/down-
load.aspx?id=8
Deficit Measurement Noseworthy, J., Miller, D., & Compston, A. (2006). Disease-modifying
Premorbid Estimate treatments in multiple sclerosis. In A. Compston, C. Confavreux,
Premorbid Functioning H. Lassman, I. McDonald, D. Miller, J. Noseworthy, et al. (Eds.),
Premorbid Intelligence McAlpines multiple sclerosis (4th ed., pp. 729802). Philadelphia:
Elsevier.
Zhang, J., Hutton, G., & Zang, Y. (2002). A comparison of the mechan-
References and Readings isms of action of interferon beta and glatiramer acetate in the
treatment of multiple sclerosis. Clinical Therapeutics, 24, 19982021.
Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). The rationale
of deficit measurement. In Neuropsychological Assessment (4th ed.,
Mortensen, E. L., Gade, A., & Reinisch, J. M. (1991). Best Performance Betaseron
Method in clinical neuropsychology. Journal of Clinical and
Experimental Neuropsychology, 13, 361371. Beta-Interferons
Beta-Interferons Between-session Assignments

K ATHLEEN L. F UCHS Homework
University of Virginia Health System
Charlottesville, VA, USA
Beyond a Reasonable Doubt
Synonyms R OBERT L. H EILBRONNER
Avonex ; Betaseron ; Rebif
Chicago, IL, USA
Definition
Definition
Interferon b is a disease-modifying drug currently indi-
cated for treatment of relapsing forms of multiple sclero- Beyond a reasonable doubt is the standard of proof
sis. Its mechanism of action is complex and is presumed required in most criminal cases within an adversarial
to inhibit immune system T-cell activation and migration system. Generally, the prosecution bears the burden of
into the central nervous system as well as modulate the proof and is required to prove their version of events to
action of some pro-inflammatory proteins (cytokines). this standard. This means that the proposition being
There are three FDA approved beta interferons available presented by the prosecution must be proven to the
in the US Avonex (INF-b1a), Betaseron (INF-b1b), extent that there is no reasonable doubt in the mind
400 B BG-II
of a reasonable person that the defendant is guilty. References and Readings

There can still be a doubt, but only to the extent that it
would not affect a reasonable persons belief regarding Denney, R. L. (2005). Criminal forensic neuropsychology and assessment
whether or not the defendant is guilty. The shadow of of competency. In G. Larrabee (Ed.), Forensic neuropsychology:
A scientific approach. New York: Oxford University Press.
a doubt is sometimes used interchangeably with rea-
Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C. (2007).
sonable doubt, but this extends beyond the latter to the Psychological evaluations for the courts: A handbook for mental health
extent many believe is an impossible standard. Reason- professionals and lawyers (3rd ed.). New York: Guilford.
able doubt is therefore used. If doubt affects a rea-
sonable persons belief that the defendant is guilty, the
jury is not satisfied beyond a reasonable doubt. The
precise meaning of words such as reasonable and BG-II
doubt is usually defined within jurisprudence of the
applicable country. Bender VisualMotor Gestalt Test II
The standard that must be met by the prosecutions
evidence in a criminal prosecution is that no other logical
explanation can be derived from the facts except that the
defendant committed the crime, thereby overcoming the
presumption that a person is innocent until proven guilty.
BHS
If the jurors or judge have no doubt as to the defendants
Personality Inventory for Children
guilt, or if their only doubts are unreasonable doubts, then
the prosecutor has proven the defendants guilt beyond
a reasonable doubt and the defendant should be
pronounced guilty. The term reasonable doubt con-
notes that evidence establishes a particular point to a
BI
moral certainty and that it is beyond dispute that any
Barthel Index
reasonable alternative is possible. It does not mean that
no doubt exists as to the accuseds guilt, but only that no
reasonable doubt is possible from the evidence presented.
Beyond a reasonable doubt is the highest standard
of proof that must be met in any trial. In civil litigation, BIAA
the standard of proof is either proof by a preponder-
ance of the evidence or proof by clear and convincing Brain Injury Association of America
evidence. These are lower burdens of proof. A prepon-
derance of the evidence simply means that one side
has more evidence in its favor than the other, even by
the smallest degree. Clear and convincing proof is evi- Bias
dence that establishes a high probability that the fact
sought to be proven is true. The main reason that the R OBERT L. H EILBRONNER
high-proof standard of reasonable doubt is used in Chicago Neuropsychology Group
criminal trials is that such proceedings can result in Chicago, IL, USA
the deprivation of a defendants liberty or even in his
or her death. These outcomes are far more severe than
in civil trials, in which money damages are the common Synonyms
remedy.
Partiality; Prejudice
Cross References
Definition
Burden of Proof
Clear and Convincing Evidence Faust, Ziskin, and Hiers (1991) and Wedding and Faust
Preponderance of the Evidence (1989) explain chief forms of bias related to clinical
Bicycle Drawing Test B 401
judgment and decision making in neuropsychology. First, References and Readings

hindsight bias is the tendency to believe, after the outcome
of an incident is determined, that the outcome could have Faust, D., Ziskin, J., & Hiers, J. B., Jr. (1991). Brain damage claims: Coping
B
been more reliably predicted than is actually true. This with neuropsychological evidence. Marina del Rey, CA: Law &
Psychology Press.
form of bias suggests that being aware of an event via a
Larrabee, G. J. (2000). Forensic neuropsychological assessment. In R. D.
clients clinical history may lead the clinician to conclude Vanderploeg (Ed.), Clinicians guide to neuropsychological assessment
that they can determine the outcome of the event and (2nd ed., pp. 301335). Mahwah, NJ: Lawrence Erlbaum.
make diagnostic determinations. Confirmation bias refers Sweet, J. J., & Moulthrop, M. A. (1999). Self-examination questions as a
to the tendency to seek confirming evidence while failing means of identifying bias in adversarial assessments. Journal of
Forensic Neuropsychology, 1, 7388.
to consider disconfirming evidence when generating di-
Van Gorp, W., & McMullen, W. (1997). Potential sources of bias in
agnostic impressions. Thus, a clinician seeks to confirm forensic neuropsychological evaluations. The Clinical Neuropsychol-
initial hypotheses, while failing to gather information ogist, 11, 180187.
related to alternative hypotheses. Moreover, it has been Wedding, D., & Faust, D. (1989). Clinical judgment and decision-making
demonstrated that clinicians tend to stop hypothesis eval- in neuropsychology. Archives of Clinical Neuropsychology, 4, 233265.
uation once information in support of an initial hypothe-
sis has been gathered, thus potentially terminating the
evaluation prior to adequate consideration of competing
hypotheses.
To combat against bias in neuropsychological assess- Bicycle Drawing Test
ment and testimony, Wedding and Faust (1989) and
Sweet and Moulthrop (1999) provided a number of stra- R ONALD A. C OHEN
tegies for clinicians to consider when testifying and pre- Brown University
paring reports. First and foremost, they recommended Providence, RI, USA
that clinicians be familiar with the scientific literature
regarding human judgment and decision making. More-
over, they recommend that clinicians begin with consid- Definition
eration of the most valid information, generating
alternative diagnostic hypotheses, and then gathering As the name suggests, the Bicycle Drawing Test requires
and considering evidence for each and providing an outpatients to draw a picture of a bicycle in freehand using a
line of disconfirmatory information. Thus, in the context pencil. It can be a useful measure of visualspatial and
of a neuropsychological evaluation, it is recommended visualmotor impairments, and also has been used in the
that clinicians generate a list of test findings that support assessment of hemi-neglect syndromes. Typically, the
specific hypotheses, but also list data that disputes such patient is asked to draw a copy of a simple line drawn
hypotheses. Larrabee (2000) suggests a four-component picture of a bicycle. Many clinicians first ask the patient
consistency analysis for neuropsychological decision to draw a bicycle in freehand from their own memory, to
making, including asking the following four questions: assess their constructional ability in the absence of a model.
(a) Are the data consistent within and between neuropsy-
chological domains? (b) Is the neuropsychological pro-
file consistent with the suspected etiologic condition? History and Clinical Evidence
(c) Are the neuropsychological data consistent with the
documented severity of injury? and (d) Are the neuro- The Bicycle Drawing Test is widely associated with Piagets
psychological data consistent with the subjects behav- (Piaget, 1955) investigations of cognitive development,
ioral presentation? Several pieces of data must be though similar tests seem to have been employed earlier
analyzed in order to address the aforementioned ques- (Poppelreuter, 1990; Veiders, 1934). Neuropsychological
tions: comprehensive interview, meticulous record review, investigations of focal unilateral lesions (Hecaen & Assal,
and comprehensive and redundant neuropsychological 1970) have demonstrated differences in performance be-
tests within each domain (language, perception, sensori- tween patients with left- and right-sided posterior brain
motor functioning, attention/information processing, lesions. Such comparisons have also suggested qualitative
psychomotor speed, verbal and visual learning and differences in the types of errors made among patients
memory, intelligence, problem solving, motivation, and with left- and right-sided lesions (Angenent, 1971). Such
personality). findings led to the inclusion of this test as a measure of
402 B Bilateral Acoustic Neurofibromatosis
constructional ability. One study compared the Bicycle References and Readings
Drawing test to the BenderGestalt test (Greenberg,
Rodriguez & Sesta, 1994), and found bicycle drawing to Angenent, H. L. (1971). The development of thought structure among
be more sensitive to brain dysfunction in children with normal and mentally retarded children. Nederlands Tijdschrift voor
de Psychologie en haar Grensgebieden, 26(4), 215232.
visualspatial problems than the BenderGestalt test.
Greenberg, G. D., Rodriguez, N. M., & Sesta, J. J. (1994). Revised scoring,
Interestingly, improvements in bicycle drawing perfor- reliability, and validity investigations of Piagets Bicycle Drawing
mance have been described in studies of patients with Test. Assessment, 1(1), 89101.
Parkinsons disease, multiple sclerosis, and Tourettes syn- Hecaen, H., & Assal, G. (1970). A comparison of constructive deficits
drome (Sandyk, 1994; Sandyk, 1997a, 1997b), with rever- following right and left hemispheric lesions. Neuropsychologia, 8(3),
289303.
sal of spatial orientation in Parkinsons patients when they
Piaget, J. (1955). Perceptual and cognitive (or operational) structures in
received electromagnetic pulses to their brain (Sandyk, the development of the concept of space in the child. Acta Psycholo-
1998). The quality and complexity of the drawing pro- gica, 11, 4146.
duced by children and adults has also been linked to their Poppelreuter, W. (1990). Disturbances of lower and higher visual capacities
intellectual ability (Sharma, 1972). caused by occipital damage: with special reference to the psychopatho-
logical, pedagogical, industrial, and social implications. Oxford/
New York: Clarendon Press/Oxford University Press.
Sandyk, R. (1994). Reversal of a visuoconstructional deficit in
Parkinsons disease by application of external magnetic fields: A
Current Clinical Use report of five cases. International Journal of Neuroscience, 75(34),
213228.
Formal scoring systems exist for the Bicycle Drawing test Sandyk, R. (1997a). Progressive cognitive improvement in multiple scle-
(Greenberg et al., 1994) providing a means for deriving rosis from treatment with electromagnetic fields. International Jour-
quantitative results when using this test. Studies compar- nal of Neuroscience, 89(12), 3951.
Sandyk, R. (1997b). Reversal of a visuoconstructional disorder by weak
ing the drawings of amateurs with artists have also shown
electromagnetic fields in a child with Tourettes syndrome. Interna-
that observational, experimental, and neuropsychological tional Journal of Neuroscience, 90(34), 159167.
methods for scoring drawings can provide systemic differ- Sandyk, R. (1998). Reversal of the bicycle drawing direction in Parkin-
ences in cognitive skills among individuals (van Sommers, sons disease by AC pulsed electromagnetic fields. International Jour-
Lange-Kuttner & Thomas, 1995). Yet, most clinicians nal of Neuroscience, 95(34), 255269.
Sharma, T. R. (1972). Measuring intelligence through bicycle drawings.
currently use the Bicycle Drawing test in conjunction with
Indian Educational Review, 7(1), 130.
other constructional tests, including coping or freehand van Sommers, P. (1995). Observational, experimental and neu-
drawing tasks (e.g., cube, house), and examine results ropsychological studies of drawing. In C. Lange-Kuttner, &
qualitatively for gross spatial distortion, or omissions. G. V. Thomas (Eds.) Drawing and looking: Theoretical approaches
Other tests, such as copying of the Rey Complex Figure to pictorial representation in children (pp. 4461). Hertfordshire:
Harvester Wheatsheaf.
are now more widely used for visualmotor assessment.
Veiders, E. (1934). Analyse der Fahigkeit zum raumlichen Denken. Anal-
Yet, the bicycle drawing test is an easy-to-administer task ysis of the ability for spatial thinking. Psychotechnisches Zeitschrift,
that can yield valuable information about the visual- 9, 5260.
spatial and constructional abilities of patients. It can also
detect hemi-neglect syndrome, as some patients may omit
one side of the bicycle. IT can yield information about
additional information on intellectual development when
used in the assessment of children. Generally, it should Bilateral Acoustic
not be used as a stand-alone test, but should rather be Neurofibromatosis
used in conjunction with other tests of visual construc-
tional functioning. Neurofibromatosis Type 2
Cross References
BenderGestalt Bilateral Simultaneous

Block Design Stimulation
Clock Drawing
Rey Complex Figure Test Double Simultaneous Stimulation
Bilingual Aphasia B 403
linguistic processing and neuroanatomical correlates of

Bilingual Aphasia language for bilinguals and monolinguals, language func-
tion of a bilingual speaker is not equivalent to that of a B
H ENRIKE K. B LUMENFELD 1, M ARGARITA K AUSHANSKAYA 2 monolingual speaker. With two language systems instead
1
San Diego State University of one, bilinguals have been shown to activate their two
San Diego, CA, USA languages in parallel and experience interaction and in-
2
University of Wisconsin-Madison terference between them. In addition, bilinguals frequent-
Madison, WI, USA ly switch and translate between languages.
There is still considerable debate regarding the func-
tional localization of language in bilinguals. The evidence
Definition to date indicates that the extent of overlap in representa-
tion of languages depends on the speakers language profi-
Bilingual aphasia is a term referring to aphasia in an ciency and the age at which the second language was
individual who is bilingual or multilingual. The degree acquired. Recent imaging research suggests that different
and nature of impairment vary widely, and depend on the languages are most likely to share the same brain regions
interplay among a number of factors, including site and when the second language is acquired earlier (Paradis, 2000;
size of the lesion, the individuals premorbid language Wartenburger et al., 2003), and when both languages are
learning and experience history, and proficiency and im- highly proficient (e.g., Chee et al., 1999; Golestani, Alario,
mersion in each language. Current evidence suggests that Meriaux, Le Bihan, Dehaene, & Pallier, 2006; Klein,
the same classification/diagnosis of aphasia (e.g., fluent, Milner, Zatorre, Zhao, & Nikelski, 1999; Perani et al.,
nonfluent) tends to hold across both languages, with 2003). Even in languages that are structurally different
varying degrees of impairment and recovery trajectories from each other, at least partially shared representations
(Paradis, 1998). In the USA, 45,000 new cases of bilingual have been identified (e.g., English/Chinese; English/ASL,
aphasia are expected each year (Paradis, 2001). Chee et al., 1999; Emmorey, Mehta, & Grabowski , 2007).
Additional brain areas have also been identified dur-
Historical Background ing bilingual language processing. Bilinguals may engage
the prefrontal cortex to a larger extent when they process a
Knowledge of bilingual aphasia is primarily based on a less proficient language than when they process a more
history of case studies (for reviews, see Pearce, 2005; proficient language (e.g., Golestani et al., 2006; Indefrey,
Lorenzen & Murray, 2008), including documented cases 2006; Marian et al., 2007; Perani et al., 2003; Sakai, Miura,
as early and varied as a patient who could read Latin but Narafu, & Muraishi, 2004). Increased activation in dorso-
not German (Gesner, 1770); a patient in Southern France lateral prefrontal cortex, anterior cingulate gyrus, and
who, after brain damage, showed a selective deficit in supramarginal gyrus has been observed during language
French but not Occitan (Lordat, 1843); and a trilingual switching (Hernandez, Martinez, & Kohnert, 2000; Price,
patient who recovered French and Spanish, but lost the Green, & von Studnitz, 1999; Wang, Xue, Chen, Xue, &
ability to even understand Italian (Pitres, 1895). Based on Donga, 2007), while increased activation in anterior
early case studies, a number of predictions have been cingulate gyrus and basal ganglia has been noted
made about patterns of impairment and recovery in during translation (Price et al., 1999). Finally, bilinguals
bilingual individuals with aphasia, including better recov- show activation of the left caudate nucleus and anterior
ery of the mother tongue (Ribots Law, 1882), the most cingulate gyrus for naming tasks in a bilingual context
familiar language (Pitres Rule, 1895), the language dom- (Abutalebi et al., 2007). Abutalebi and Green (2007) pro-
inant in the environment (Bychowsky, 1919), and the posed that the neural network that supports language
language closest to our heart (Minkowski, 1927). control in bilinguals likely includes anterior cingulate
cortex, prefrontal cortex, caudate nucleus, and left inferi-
or parietal lobule.
Current Knowledge Bilingual individuals with aphasia typically go
through a variety of changes in their language abilities,
A systematic and theoretical understanding of bilingual where their languages are available to different degrees
aphasia relies on an understanding of the bilingual lan- during the acute phase of recovery (up to 4 weeks post
guage system and its neural correlates. While more simi- onset). During this phase, availability of representations
larities than differences have been observed with regard to may vary because of diaschisis. As impairment patterns
404 B Bilingual Aphasia
stabilize during the post-acute phase (up to 5 months around. Translation without comprehension is a preserved
post-onset), language impairment becomes more directly ability to translate without an ability to comprehend the
related to site of lesion and damage to specific language meaning of either translation. Finally, spontaneous trans-
representations. lation is the involuntarily production of translations that
cannot be inhibited.
The heterogeneity of the bilingual population makes it
Clinical Variants and Recovery Patterns difficult to link language profiles and lesion site/size with
specific impairment and recovery patterns in individuals
Bilingual individuals with aphasia show great variability in with bilingual aphasia. However, a number of linguistic
impairment and recovery patterns. Paradis (2001), in factors in impairment and recovery patterns have been
a review of 132 cases of bilingual aphasia, found that identified. Naming and translation of cognate words
61% showed parallel recovery of their two languages, (that share sound and meaning in the two languages,
18% showed differential recovery of their two languages, e.g., lamp-lampara) is typically less impaired in bilingual
7% showed blended recovery, and 5% showed selective individuals with aphasia than naming and translation of
recovery (for similar distributions on a sample of 20 noncognate words (key llave, Goral, Levy, & Obler, 2006;
ItalianFriulian patients, see Fabbro, 2001). Reports of Kohnert, 2004; Roberts & Deslauriers, 1999). In general,
atypical and pragmatically inappropriate language swit- aspects of bilinguals languages that are more shared
ching behaviors in bilingual individuals with aphasia have are also more resistant to impairment (e.g., Kiran &
also appeared (Munoz, Marquardt, & Copeland, 1999). Tuctenhagen, 2005). Linguistic features that differ be-
Parallel impairment refers to aphasia of the same type tween languages (e.g., different grammatical systems)
and severity in both languages. The two languages are may result in differences in how symptoms of aphasia
impaired and recover simultaneously (relative to premor- are expressed even if the same underlying deficit exists.
bid language proficiency). Differential impairment refers For example, a morphologically rich language can theo-
to aphasia of the same type in both languages (e.g., fluent retically undergo greater morphological breakdown, and
vs. nonfluent) with crosslinguistic differences in severity morphological deficits may look more severe. Therefore,
levels. In contrast, differential aphasia refers to different cross-linguistic differences in the symptoms and recovery
aphasia symptoms in each language. Differential recovery patterns of bilingual aphasia frequently occur at points
refers to one language recovering better than the other where the two linguistic systems diverge.
(relative to premorbid levels). Blended impairment Another explanation for divergent recovery patterns
refers to the inappropriate combination of two or more in bilingual aphasia is the Cue Strength hypothesis (e.g.,
languages (e.g., the patient may lose the ability to discrim- Wulfeck, Bates, & Capasso, 1991). According to this hy-
inate between languages). Pathological mixing, character- pothesis, the linguistic importance of a grammatical
ized by inadvertent and uncontrolled language switches, is structure or the contribution it makes to the linguistic
typically associated with blended impairment. In contrast, message may account for crosslinguistic differences in
pathological fixation is an inability to switch languages. syntactic deficits, with more important cues being more
Antagonistic recovery refers to a pattern where one lan- likely to be preserved. For example, English-speaking
guage recovers first, and starts regressing when the other individuals with aphasia have been found to be more
language starts to recover. Alternating antagonism refers to sensitive to word-order errors during grammaticality
repetition of the antagonistic pattern, with the two lan- judgments while Italian-speaking individuals with apha-
guages alternating in availability (cycles may range from sia were more sensitive to morphological errors. Similarly,
hours to months). Selective impairment refers to aphasia differences in reading impairments have been found
in only one language, while the other language remains across languages with different orthographies. Readers
intact (relative to premorbid language proficiency). In are referred to a detailed review of current knowledge
addition, a variety of deficits have been identified in about bilingual aphasia by Lorenzen and Murray (2008).
bilingual aphasics ability to translate from one of their
languages to the other. An inability to translate is reflected
in bilinguals inability to translate either forward (from Assessment
their native language to their second language) or back-
ward (from their second language to their native lan- An important part of assessment in bilingual aphasia
guage). Paradoxical translation is an ability to translate consists of establishing premorbid proficiency levels as
from one language to the other, but not the other way accurately as possible and determining the nature and
Bilingual Aphasia B 405
extent of impairment in each language relative to these than the ability to retrieve known information. A clinician
premorbid proficiency levels. Self-reports, questionnaires may explain a new grammatical rule and test the clients
about the history of language use (e.g., code-switching), ability to generalize it. If the client generalizes the rule B
reports from family members or friends, and written or easily, then weak linguistic performance is likely due to
recorded samples of patients language abilities are typi- the influence of the non-target language or low profi-
cally used to establish premorbid proficiency levels. Once ciency in the target language, rather than aphasia.
premorbid proficiency levels have been established, it is
important to assess both of the patients languages in
Treatment
order to gauge their full linguistic capacity and impair-
ments across languages.
Assessment of both languages, together with the social
There are currently no assessment measures for bilin-
communication needs of the client, will inform choice
gual aphasia that meet all standards for measurement
of therapy language and specific therapy goals. A primary
validity. The bilingual aphasia test (BAT, Paradis, 1987)
goal in the treatment of bilingual individuals with aphasia
is the most comprehensive tool available and provides
is to maximally benefit both languages even if treatment
systematic ways to assess aphasia in many languages.
occurs in only one language.
Tasks on the BAT are equivalent in linguistic complexity
Treatment may be conducted to target both languages
across languages, and cover assessment of linguistic levels
directly. During bilingual treatment, language-switching
(phonological, lexical-semantic, morphological, syntac-
may be encouraged as a compensatory strategy to allow
tic), linguistic skills (comprehension, formulation, repeti-
the client to use his/her full linguistic capacity. Translation
tion, judgment, lexical access), and linguistic units (words,
may be used in a similar manner to aid lexical access. For
sentences, paragraphs). The BAT assumes that the test-
example, switch-back through translation (SBT) treat-
taker has pre-morbid proficiency in each language that is
ment (Ansaldo & Marcotte, 2007) is a procedure where
equivalent to at least 400 language-learning hours. The test
the client is cued to translate the word back into the other
is administered in each language on different days. Where
language whenever an inadvertent switch occurs.
it is not feasible to obtain all language versions of the BAT,
If resources are only available to treat in English, the
its principles may be followed during assessment.
speechlanguage pathologist may work to identify outside
Additional tasks that may be useful in examining
resources in helping to rehabilitate the clients other
bilingual individuals language impairments include the
languages. Such linguistic resources may include
type-token ratio in each language based on comparable
language-specific community groups, or guidance of fam-
language samples, number of verbs and grammatical
ily members. Crosslinguistic generalization is most likely
clauses per utterance, semantic acceptability, confabulation,
to occur when shared representations are targeted for
and total number of words or utterances within a set time
treatment, crosslinguistic associative links are used, or
window (fluency measures). Preservation of links between
similar cognitive processes are a focus of intervention
languages may be assessed by testing participants transla-
(e.g., reading in alphabetic languages). Current evidence
tion abilities from the native language to the second
suggests that treatment in the persons weaker language
language and vice versa. As part of cognitive assessment,
may generalize to his/her stronger language, especially
language switching behaviors may be examined. Patho-
when treatment targets are similar across languages
logical mixing can be distinguished from nonpathological
(Edmonds & Kiran, 2004). However, generalization from
mixing: For example, in nonpathological mixing, subject
the stronger to the weaker language is less likely. General-
and verb should be in the same language, and switches
ization across languages has been shown when cognate
should not occur on prepositions.
words are used in treatment (Kohnert, 2004), semantic
If, due to limitations in resources, assessment and
features are treated (Edmonds & Kiran, 2004, 2006), and
treatment are done only in English, the clinician may
general cognitive function is treated (Kohnert, 2004).
obtain information on the structure of the clients other
However, cross-linguistic generalization does not always
language in order to identify crosslinguistic influences in
occur (e.g., Galvez & Hinckley, 2003).
the clients English output. This may allow the clinician to
distinguish low premorbid proficiency in English from a
disorder. The dynamic assessment approach provides an Future Directions
alternative method for examining deficits in situations of
low premorbid language proficiency. Dynamic assessment In 2000, 18% of the population older than 5 years of age
focuses on the ability to learn new information, rather (47 million people) spoke a language other than English
406 B Bilingual Aphasia
at home, up from 14% in 1990 and 11% in 1980 (U.S. Abutalebi, J., & Green, D. (2007). Bilingual language production: The
neurocognition of language representation and control. Journal of
Census, 2000). As the bilingual population grows, with
Neurolinguistics, 20, 242275.
special growth in older adults, the need for accommoda- Ansaldo, A. I., & Marcotte, K. (2007). Language switching and mixing in
tion of bilingual individuals with aphasia will increase. the context of bilingual aphasia. In J. G. Centeno, L. K. Obler, & R. T.
Among Mexican Americans, stroke incidence is slightly Anderson (Eds.), Studying communication disorders in Spanish speak-
higher (1.63%) than in non-Latino white peers (1.36%), ers: Theoretical, research, and clinical aspects. Clevedon, UK: Multi-
lingual Matters.
and transient ischemic attacks are more frequent at youn-
Bialystok, E., Craik, F. I. M., Klein, R., & Viswanathan, M. (2004). Bilin-
ger ages (Lorenzen & Murray, 2008). The US Department gualism, aging, and cognitive control: Evidence from the Simon task.
of Health and Human Services found that Latino indivi- Psychology and Aging, 19, 290303.
duals were 33% less likely to receive necessary health- Bychowsky, Z. (1919). Concerning the restitution of language loss
care services, compared to non-Latino white peers subsequent to a cranial gunshot wound in a polyglot aphasic. In
M. Paradis (Ed.), Readings on aphasia in bilinguals and polyglots
(Lorenzen & Murray, 2008). With these changes in popu-
(pp. 130144). Montreal, QC: Didier.
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the efficacy of various treatment approaches for bilingual (1999). Processing of visually presented sentences in Mandarin and
aphasia has become increasingly necessary. English studied with fMRI. Neuron, 23, 127137.
One particularly promising avenue of research in Edmonds, L., & Kiran, S. (2004). Confrontation naming and semantic
relatedness judgments in Spanish/English bilinguals. Aphasiology, 18,
bilingual aphasia is in the area of cognitive control. Lan-
567579.
guage production requires cognitive control skills. These Edmonds, L., & Kiran, S. (2006). Effect of semantic naming treatment on
skills may be honed with bilingual experience, as bilin- crosslinguistic generalization in bilingual aphasia. Journal of Speech,
guals must suppress one language in favor of another Language, and Hearing Research, 49(4), 729748.
language every time they speak. Balanced bilinguals have Emmorey, K., Mehta, S., & Grabowski, T. (2007). The neural correlates of
sign versus word production. Neuroimage, 36, 202208.
been shown to have cognitive advantages over monolin-
Fabbro, F. (2001). The bilingual brain: Bilingual aphasia. Brain and
guals on nonlinguistic executive function tasks, especially Language, 79, 201210.
as they age (Bialystok, Craik, Klein, & Viswanathan, 2004; Galvez, A., & Hinckley, J. J. (2003). Transfer patterns of naming
Kave, Eyal, Shorek, & Cohen-Mansfield, 2008; Zied et al., treatment in a case of bilingual aphasia. Brain and Language, 87,
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Gesner, J. A. P. (1770). Sammlung von Beobachtungen aus der
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Arzneygelehrtheit und Naturkunde (pp. 17691776). Nordlingen:
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integrity of the cognitive control system in bilingual indi- Golestani, N., Alario, F. X., Meriaux, S., Le Bihan, D., Dehaene, S., &
viduals with aphasia. It is also possible that cognitive- Pallier, C. (2006). Syntax production in bilinguals. Neuropsycholo-
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Goral, M., Levy, E. S., & Obler, L. K. (2006). Neurolinguistic aspects of
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Ribots laws. European Neurology, 54, 2731. Binswangers disease (BD) is a type of subcortical vascular
Perani, D., Abutalebi, J., Paulesu, E., Brambati, S., Scifo, P., Cappa, S. F., dementia caused by widespread, microscopic damage
et al. (2003). The role of age of acquisition and language usage in
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early, high-proficient bilinguals: A fMRI study during verbal fluency.
Human Brain Mapping, 19, 170182. of atherosclerosis (i.e., narrowing of arterial blood
Pitres, A. (1895). Etude sur laphasie chez les polyglottes. Revue de vessels) that reduces the supply of blood to subcortical
Medicine, 15, 873899. areas of the brain, causing tissue to die. The characteristic
Price, C. J., Green, D. W., & von Studnitz, R. (1999). A functional imaging pattern of BD-damaged brain tissue can be seen using
study of translation and language switching. Brain, 122, 22212235.
brain imaging techniques such as computed tomography
Roberts, P. M., & Deslauriers, L. (1999). Picture naming of cognate and
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Sakai, K. L., Miura, K., Narafu, N., & Muraishi, Y. (2004). Correlated sities also called leukoaraiosis, and more sensitive MRI
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sequences.
U.S. Census Bureau: Language Use. (2000). Retrieved November 20,
2009, from http://www.census.gov/population/www/socdemo/ There is some controversy in the literature about
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Wang, Y., Xue, G., Chen, C., Xue, F., & Donga, Q. (2007). Neural bases describes the result of different neuropathologies that
of asymmetric language switching in second-language learners: An affect subcortical white matter (Caplan, 1995; Hachinski
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et al., 2006; Olsen and Clasen, 1998; Pantoni and Garcia,
Wartenburger, I, Heekeren, H. R., Abutalebi, J., Cappa, S. F.,
Villringer, A., & Perani, D. (2003). Early setting of grammatical 1995). Although the precise cause of BD is unclear, it is
processing in the bilingual brain. Neuron, 37, 159170. frequently associated with diabetes, cardiovascular dis-
Wulfeck, B., Bates, E., & Capasso, R. (1991). A cross-linguistic study of ease, previous cerebrovascular accident, malnutrition
grammaticality judgments in Brocas aphasia. Brain and Language, and, most notably, hypertension. The age of onset for
41, 311336.
BD is typically between ages 60 and 79 years, with
Zied, K. M., Phillipe, A., Karine, P., Valerie, H. T., Ghislaine, A.,
Arnaud, R., et al. (2004). Bilingualism and adult differences in men and women equally affected. Estimates about the
inhibitory mechanisms: Evidence from a bilingual stroop task. incidence of BD range from 312% (Babikian and
Brain and Cognition, 54, 254256. Ropper, 1987).
408 B Biological Cycles
Current Knowledge healthy diet, exercising, and not smoking or drinking too
much alcohol. Controlling vascular risk factors can help
Neuropathology improve cognition and may even help prevent the devel-
opment of dementia (Roman, 2005).
Gross pathology of brain tissue affected by BD is charac-
terized by gyral atrophy and widening of the sulci result-
ing from the loss of cerebral white matter. Lateral Prognosis
ventricles are also typically enlarged. Lacunar infarctions
can be found in the white matter, pons, and basal ganglia BD is a progressive disease and there is currently no cure.
as well as occasionally in the cerebellum. Microscopic The course of BD can be variable and deterioration can
pathology of BD is marked by diffuse and patchy white occur suddenly or gradually and then progress in a step-
matter demyelination with areas of reactive gliosis and wise manner (Santamaria Ortiz and Knight, 1994).
decreased nerve fibers. The small arteries of the white
matter also show fibrous thickening, which is associated
with hypertension and cardiovascular disease. BD is be- Cross References
lieved to result from ischemic injury of frontal lobe white
matter and is distinct from the lacunar state of small vessel Leukoaraiosis
disease that also causes dementia but results from infarc-
tions in the basal ganglia and internal capsule.
Clinical Symptoms Babikian, V., & Ropper, A. H. (1987). Binswangers disease: a review.
Stroke, 18(1), 212.
BD typically has a slow, insidious onset that eventually Caplan, L. R. (1995). Binswangers disease revisited. Neurology, 45(4),
626633.
manifests in cognitive and motor dysfunctions related
Hachinski, V., Iadecola, C., Petersen, R. C., Breteler M. M., Nyenhuis,
to the disruption of subcortical neural circuits. Specifical- D. L., Black S. E. et al. (2006). National Institute of Neurological
ly, patients exhibit executive dysfunction (e.g., impaired Disorders and Stroke-Canadian Stroke Network vascular cognitive
initiation, inhibition, monitoring of goal-directed behav- impairment harmonization standards. Stroke, 37(9), 22202241.
ior, and verbal fluency), psychomotor slowing, inatten- Lezak, M. D., Howieson, D. B., & Loring, D. (2004). Neuropsychological
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tion, and short-term memory loss with poor retrieval
Olsen, C. G., & Clasen, M. E. (1998). Senile dementia of the Binswangers
but intact recognition (Roman, 2003). Other symptoms type. American Family Physician, 58(9), 20682074.
include changes in speech, an unsteady gait, postural Pantoni, L., & Garcia, J. H. (1995). The significance of cerebral white
instability, changes in personality or mood (including matter abnormalities 100 years after Binswangers report. A review.
apathy, irritability, and depression), as well as urinary Stroke, 26(7), 12931301.
Roman, G. C. (2003). Neurological aspects of vascular dementia:
incontinence (Babikian and Ropper, 1987; Caplan, 1995;
Basic concepts, diagnosis, and management, In P. A. Lichtenberg,
Lezak, Howieson, & Loring, 2004; Roman, 2003). D. L. Murman, & A. M. Mellow (Eds.), Handbook of dementia -
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sis. Cerebrovascular Diseases, 20(Suppl. 2), 91100.
Santamaria Ortiz, J., & Knight, P. V. (1994). Review: Binswangers disease,
Treatment of BD is often targeted at specific symptoms. leukoaraiosis and dementia. Age Ageing, 23(1), 7581.
For example, medications such as donepezil and meman- Sink, K. M., Holden, K. F., & Yaffe, K. (2005). Pharmacological treatment
tine may be used to treat the cognitive symptoms asso- of neuropsychiatric symptoms of dementia: a review of the evidence.
ciated with BD. Individuals with depression may be Jama, 293(5), 596608.
treated with antidepressant medications (e.g., serotonin-
specific reuptake inhibitors (SSRIs) such as sertraline or
citalopram) and individuals with agitation or disruptive
behavior can be treated with atypical antipsychotic med-
ications such as risperidone or olanzapine (Sink, Holden, Biological Cycles
& Yaffe, 2005). Other treatment interventions are often
focused on reducing cardiovascular risk factors by eating a Circadian Rhythms
Biopsy B 409
understanding of the biomechanics underlying brain injury

Biomechanics of Injury has led to the development of protective headgear in high-
speed or direct-impact sports such as biking, motor racing, B
B ETH R USH football, and hockey.
Mayo Clinic
Jacksonville, FL, USA
Cross References
Definition
Acceleration Injury
An inclusive term to explore and describe the mechan- Deceleration Injury
ical and physical factors that result in traumatic brain Diffuse Axonal Injury
injury. Rotational Acceleration
Traumatic Brain Injury
Current Knowledge
Biomechanical injuries typically occur without the direct
impact of an outside object on the skull or brain, but Bayly, P. V., Cohen, T. S., Leister, E. P., Ajo, D., Leuthardt, E. C., Genin,
rather in the context of accelerationdeceleration injuries. G. M. (2005). Acceleration-induced deformation of the human
brain. Journal of Neurotrauma, 22, 845856.
High-speed situations such as motor vehicle accidents
Ommaya, A. K., Goldsmith, W., & Thibault, L. (2002). Biomechanics and
and sports provide mediums for these inertia-based inju- neuropathology of adult and pediatric head injury. British Journal of
ries. The structure of the skull includes sinuses and bony Neurosurgery, 16, 220242.
protective regions. Underlying brain tissue is held in sus-
pension underneath the skull not only by the meninges,
but also by a cushion of cerebral spinal fluid. Different
inertial forces such as linear acceleration, rotation of the
head, or massive vibration or air pressure changes in Biopsy
the environment can result in a wide range of potential
damage to these underlying substances. These disruptions B RAM G OLDSTEIN
may include skull fracture, linear acceleration injury, Hoag Hospital Cancer Center
rotational injury, and the effects of vibration of the skull Newport Beach, CA, USA
and brain against one another.
Superficial or deep lesions may result in parenchy-
mal injury depending on the type of mechanical force Definition
that occurred at the time of head trauma. Linear accel-
eration injuries are most often associated with superfi- A biopsy is a medical examination entailing the removal
cial brain injuries such as cerebral contusions, while of cellular tissue via a needle or surgical resection.
rotational injuries are most often associated with dis- In particular, an incisional or core biopsy involves a
ruptions to deep white matter tracts and projections, select sample of tissue, whereas an excisional biopsy
and centrally located brain structures and neural net- necessitates a larger specimen. The biopsy results are
works. Consequently, rotational injuries may be more typically evaluated microscopically by a pathologist, who
severe with regard to effects on cognition, motor skills, determines if a lesions pathology is benign or malignant.
and functional status. Concussion with or without loss Although histological confirmation of tumor diagnosis
of consciousness is also a consequence of biomechanical can be achieved, a biopsy sampling error can result if
forces and the subsequent effects on underlying brain the specific tissue section does not contain the most
tissue. representative cellular features. When the biopsy is
The biomechanics of injury differentially affect initial abnormal, the cell structure may be unusual and
and long-term recovery from acquired brain injury. Under- indicative of malignancy. However, further pathological
standing these different mechanical forces may help one to examination is often required to make a definitive
improve understanding of injury severity. Increased diagnosis.
410 B Biorhythms
Cross References Historical Background
Psychopathology Blast injuries can occur in any setting, civilian or military.

Radiosurgery However, exposure to the effects of explosive forces is
much more associated with military populations, and
has been since the advent of modern warfare. Awareness
of the effect of blast injuries began to emerge in earnest
References and Readings with the phenomenon of shell shock during the First
World War. That war exposed staggering number of sol-
Yu, X., Liu, Z., Tian, Z., Li, S., Huang, H., Xiu, B., et al. (2006). Stereo- diers to explosive injuries, far more than had previous
tactic biopsy for intracranial space-occupying lesions: clinical analy- conflicts. As a result, an ever-increasing number of mili-
sis of 550 cases. Stereotactic and Functional Neurosurgery, 75,
tary personnel presented with vague but incapacitating
103108.
complaints that prevented them from returning to active
(particularly frontline) duty. Initially, these symptoms
were considered secondary to organic central nervous sys-
tem injury. Over time however, others favored a more
psychological or even intentional (i.e., malingering) expla-
Biorhythms nation, citing the fact that many shell-shocked servicemen
did not appear to have been as close to the explosion as
Circadian Rhythms would seem necessary to truly be negatively affected. The
nature of the shell-shock symptoms was further obscured
by the lack of diagnostic methods, absence of a clear defini-
tion of the syndrome, and even political factors (e.g., super-
iors being able to justify returning much-needed soldiers to
BIT frontline duty if their complaints reflected psychological or
constitutional weaknesses rather than neurological/organic
Rivermead Behavioral Inattention Test injuries). This debate of psychological versus neurologi-
cal causes has continued throughout subsequent wars and
is a particular focus of the present conflicts in the Middle
East, given the high incidence of explosives utilized by
terrorists and non-Coalition combatants.
BJLOT
Judgment of Line Orientation Current Knowledge
With improvements in medical care of trauma and the

development of more effective defensive equipment (i.e.,
body and vehicle armor), a greater number of servicemen
Blast Injury and women injured in combat are surviving than ever
before: The mortality rate for wounded personnel has
B RADLEY J. H UFFORD declined from approximately 30% during the Second
Rehabilitation Hospital of Indiana World War to approximately 10% today. As a result, a
Indianapolis, IN, USA greater number of the wounded are surviving with trau-
matic brain injury than in the past from under 20%
during the Vietnam conflict to perhaps near 50% in the
Definition current wars in Afghanistan and Iraq. Overall, it has been
estimated that possibly as many as 22% of all combat
A trauma sustained as a result of exposure to an explosion troops in Operations Iraqi Freedom and Enduring Free-
or its effects. Technically, blast injury can affect any physi- dom may have incurred an acquired brain injury of some
cal system/function; its neurological effects are high- degree. The majority of these combat-related brain inju-
lighted here. ries are sustained as a result of exposure to an explosion.
Blast Injury B 411
Explosions may cause injury through four Typically, an individual is exposed to more than one
mechanisms: mechanism, making the contributions of one particular
mechanism difficult to separate from others. B
1. Primary Blast Injury
Approximately 60% of explosion-related injuries in
A primary injury is one sustained from exposure to combat lead to an acquired brain injury. As is the case
the shock/pressure waves initiated by the explosion. with other etiologies, the majority of traumatic brain
When explosive munitions are detonated, a shockwave injuries resulting from explosions are classified as mild
approaching a speed of 8000 meters/second is generated. in nature. Similar to civilian settings, mild traumatic
The waves generated from a blast can cause life-threaten- brain injury (mTBI) has not been consistently defined in
ing injuries when they strike an individual directly, or if the literature, which is a substantial limitation in making
they reflect off nearby surfaces and then come into con- meaningful comparisons between studies. Despite this,
tact with the person. The force generated is of such a definitions such as that proposed by the American Con-
magnitude that it often results in an instant fatality or in gress of Rehabilitation Medicine are coming into wider
trauma to multiple body systems. Body organs that are acceptance, and have largely been adopted by the military.
relatively solid or fluid-filled tend to sustain a lesser The ACRM definition of mTBI includes at least one
degree of injury than those that are gas-filled or have a symptom such as less than half an hour of loss of con-
gas-fluid interface, such as the tympanic membrane, sciousness, less than 24 hours of post-traumatic amnesia,
lung, and colon. Although not fully understood, research any retrograde or anterograde amnesia, mental status
suggests that the explosion may injure the central ner- changes immediately after injury, and transient/perma-
vous system directly, as in a concussion, but may also nent neurological impairments. The literature cautions
indirectly affect the brain. The latter case may occur when that a mild TBI from an explosion may not be equivalent
peripheral somatic areas are impacted by the blast, to mild TBI from other etiologies (e.g., motor vehicle
setting in motion events that ultimately impact the cen- accidents, sports injuries), as the former may affect the
tral nervous system (CNS), such as chemical/metabolic brain more diffusely and tend to involve trauma to other
cascades, physical sequelae (i.e., cerebral infarction organ systems, thereby complicating the patients clinical
caused by an air embolism), and/or kinetic events (e.g., presentation and recovery. However, studies have indi-
transfer of shock/pressure wave energy from the body, up cated that factors such as loss of consciousness and cog-
the vasculature into brain tissue). It has been postulated nitive deficits do not appear to significantly differ between
that the severity and number of the patients physical blast victims and those injured by other means, tentatively
wounds from primary blasts often overshadow symp- suggesting that knowledge gleaned from studying these
toms of traumatic brain injury, delaying diagnosis and other etiologies has at least some applicability to blast
treatment for these injuries. injury survivors.
Cognitive (e.g., memory, attention), somatic (e.g.,
2. Secondary Blast Injury
dizziness, headache, sleep initiation/maintenance difficul-
Secondary injuries occur when shrapnel, debris, or other ties), and emotional (e.g., irritability, nervousness) symp-
objects are caught up by the blast and propelled against/ toms are commonly seen initially. In civilian samples,
into an individual. Many of these injuries are therefore mild TBI symptoms appear to resolve quickly, with most
penetrating in nature. individuals showing rapid recovery within the first week.
However, over one third may continue to experience
3. Tertiary Blast Injury
significant post-concussion symptoms, and as many as
This type of injury is sustained when the person is caught 15% may continue to experience persistent symptoms
up and propelled by the blast wind that follows the initial after 12 months (Persistent Post-Concussion Syn-
shock wave, and is thrown against objects, structures, the drome). Unfortunately, post-concussion symptoms
ground, other individuals, etc., often resulting in blunt have not been consistently defined, and many point out
force wounds. that the constellation of symptoms present are vague and
lack the specificity needed to identify them as constituting
4. Quaternary Blast Injury
a true syndrome.
Quaternary blast injuries are those that arise from the This debate over whether the more chronic symptom
aftereffects of an explosion. Examples include being ex- constellation after mild TBI reflects a true neurological
posed to radiation, fire, chemicals, dust, or toxic sub- syndrome has particular relevance in blast injury, as the
stances that were precipitated by the explosive event. brief history of shell shock above illustrates. Those
412 B Blast Injury
favoring a neurological position cite animal models in helpful in identifying post-concussive symptoms and clar-
which direct and indirect exposure to primary blasts ifying the diagnostic picture, enabling education and
causes structural, chemical, and electrophysiological treatment efforts to proceed more quickly.
changes in the brain. Those weighing psychological fac- The profile of cognitive weaknesses resulting from
tors more heavily in terms of causation point to the mTBI blast injuries is quite variable. Slowed attention and in-
literature that indicates non-neurological factors, such as formation processing speed, motor slowness, and execu-
premorbid psychological coping resources and external tive and memory difficulties are common. As such,
stressors, appear to influence the development of concus- neuropsychological assessment should ideally be broad-
sion symptoms in some individuals. The fact that mTBI based, with all major cognitive domains sampled. As is the
symptoms overlap considerably with anxiety disorders case in sports concussions, the symptom picture for many
such as post-traumatic stress disorder is particularly note- individuals may evolve relatively rapidly, arguing for use
worthy, given the high incidence of PTSD in military of tests that have alternate forms (e.g., California Verbal
personnel who have experienced combat: Gaylord, Coo- Learning Test 2nd Edition, Hopkins Verbal Learning
per, Mercade, Kennedy, Yoder, and Holcomb (2008) Test-Revised). Tracking somatic symptoms (e.g., Post-
found that nearly 20% of military persons who incurred Concussion Scale-Revised) over time may also have utili-
blast and burn injuries were appropriate for both mild ty. Because of the high degree of PTSD and other affective
brain injury and PTSD diagnoses. Hoge, McGurk, Thom- disorders, a thorough psychological evaluation should
as, Cox, Engel, and Castro (2008) reported that approxi- always be performed (e.g., MMPI-2, PAI) and observation
mately 15% of soldiers surveyed after being returned for these symptoms should be an ongoing effort, not
home might meet criteria for both an mTBI and PTSD; simply one restricted to an initial evaluation. Given the
these servicemen and women were more likely to have high degree of lowered effort present in civilian mTBI
been exposed to a blast injury. In addition, their survey cases, effort testing (e.g., Test of Memory Malingering) is
indicated that the presence of affective distress might be often advocated, with the caveat that poor performances
the major factor in maintaining chronic health difficul- on these tests should not automatically be interpreted as
ties, including mTBI symptomatology. A compromise signs of intentional feigning of symptoms, but as a sign
position of sorts posits mTBI symptoms are likely neuro- that further investigation is warranted as to the cause of
logical in origin but are subsequently maintained by emo- the lowered effort.
tional/psychological factors, and that the presence of After a thorough diagnostic assessment has been per-
PTSD and similar affective disturbances can complicate formed, treatments generally have proceeded along the
healing from and coping with mTBI and vice versa. The lines advocated for mild brain injuries attributed to
fact that PTSD symptoms can arise long after the actual non-blast causes. Specifically, reassurance and education
trauma indicates that these emotional disturbances may regarding the nature and general recovery of cognitive and
influence a person at virtually any point in his or her brain other symptoms is delivered, and problematic symptoms
injury recovery. are treated with medication (e.g., analgesics for pain,
Treatment approaches of blast injuries have paralleled soporific medication for insomnia, antidepressants for
treatment efforts in mild TBI. Treatment begins with a affective symptoms) and other strategies (e.g., relaxation
thorough diagnostic assessment. The Armed Services have strategies for anxiety symptoms, psychotherapy for PTSD
made significant improvements in their endeavors to symptoms). Aggressive, evidence-based cognitive rehabil-
standardize comprehensive screening and interviewing itation efforts have been advocated and research programs
methods to identify service personnel who may have in this area have been proposed.
experienced an acquired brain injury, beginning on the
battlefield and continuing throughout the militarys med-
ical system. Efforts have also been made to carefully screen
the wounded for other symptoms (e.g., tinnitus) that Future Directions
place them at higher risk for having sustained a TBI in a
blast. Any assessment should include a thorough medical The research literature in blast injury is still in an early
evaluation and comprehensive interview that elicits his- stage of development. The following is a partial list of
torical information about past psychological treatment/ necessary future research efforts: clarifying definitions of
coping, substance use, and combat exposure. Neuropsy- mTBI and post-concussive symptom constellations; sepa-
chological evaluation as early as possible would also be ration of the effect of different blast mechanisms (e.g.,
Blessed Dementia Scale B 413
primary, secondary) on the brain; standardization of re-

search methodology with respect to inducing blast inju- Blessed Dementia Rating Scale
ries in animal subjects; comparison of mTBI symptoms, (BDRS) B
course and recovery between blast injury survivors and
those who have injuries from sports or other sources; Blessed Dementia Scale
investigation of the effect of multiple blast exposures;
investigation of how PTSD/affective distress differs from
and interacts with mTBI. More prospective research is
clearly needed. Within neuropsychology, development of
alternate forms for many tests is encouraged. Blessed Dementia Scale
AVRIL J. K ELLER 1, E LISABETH M. S. S HERMAN 1,
E STHER S TRAUSS 2
1
Cross References Alberta Childrens Hospital, University of Calgary
Calgary, AB, Canada
Concussion 2
Mild Brain Injury Victoria, BC, Canada
Post-Concussion Disorder (Syndrome)
Post-Traumatic Stress Disorder
Traumatic Brain Injury Synonyms
Blessed dementia rating scale (BDRS); Blessedroth DS;

Dementia scale (DS); Modified blessed dementia scale
References and Readings (DS); Newcastle DS; Revised dementia scale (RDS)
Batten, S., Beal, S., Bleiberg, J., et al. (2009). Defense Centers of Excellence
for Psychological Health and Traumatic Brain Injury and Defense
and Veterans Brain Injury Center consensus conference on cognitive Description
rehabilitation for mild traumatic brain injury. Washington, D.C.
Cernak, I., Wang, Z., Jiang, J., Bian, X., & Savic, J. (2001). Ultrastructural The Blessed Dementia Scale (DS) was developed in 1968
and functional characteristics of blast injury-induced neurotrauma.
by Blessed and colleagues in an attempt to quantify the
The Journal of Trauma, Injury, Infection, and Critical Care, 50,
695706.
degree of intellectual and personality deterioration
Gaylord, K., Cooper, D., Mercade J., Kennedy, J., Yoder, L., & Holcomb, J. (p. 799) in the elderly.
(2008). Incidence of posttraumatic stress disorder and mild trau- This rating scale consists of 22 items that reflect (1)
matic brain injury in burned service members: Preliminary report. changes in performance of everyday activities (8 items;
The Journal of Trauma, Injury, Infection, and Critical Care, 64,
e.g., using money and finding ones way), (2) changes in
S200S206.
Hoge, C., McGurk, D., Thomas, J., Cox, A., Engel, C., & Castro, C. (2008).
habits including self-care (3 items; i.e., eating, dressing
Mild traumatic brain injury in U.S. soldiers returning from Iraq. The and continence), and (3) changes in personality, interests,
New England Journal of Medicine, 358(5), 453463. and drives (11 items; e.g., evaluation of rigidity and
Jackson, G., Hamilton, N., & Tupler, L. (2008). Detecting traumatic brain affect). A close friend or relative is asked to provide
injury among veterans of operations enduring and Iraqi freedom.
these behavior ratings of the examinee over the past six
North Carolina Medical Journal, 69(1), 4347.
Jones, E., Fear, N., & Wessely, S. (2007). Shell shock and mild traumatic
months; when unavailable, medical records can be used.
brain injury: A historical review. American Journal of Psychiatry, 164, The DS is scored on a 028 point scale, where higher
16411645. numbers indicate a larger decrement in functional capac-
ity. On everyday activity items, a score of 1 is given for
total inability to perform a task, a score of is given for
partial, variable, or intermittent inability to perform
an activity, and a score of 0 is given if the patient is able
Bleeding to perform the task. The changes in habits section is
scored on a 4-point scale (i.e., 03), resulting in a stronger
Hemorrhage contribution to the total score. Personality changes
414 B Blessed Dementia Scale
are scored 1 if present or 0 if absent (Blessed, Tomlinson, Heyman, 1988). Additional analysis of the scale has indi-
& Roth, 1968; Blessed, Tomlinson, & Roth, 1988). A total cated that the items can be subdivided into four groups,
cut-off score of 4 out of 28 is typically used to differentiate each with its own score (Cognitive, items 17, score range
patients with dementia versus those without. Scores of 07; Personality Change, items 1217, score range 06;
49 indicate mild impairment, whereas scores of 10 or Apathy/Withdrawal, 18, 20, and 21, score range 03;
higher suggest moderate to severe impairment (Eastwood, Basic Self-Care, 911, score range 03), in order to aid
Lautenschlaegar, & Corbin, 1983). Stern, Mayeux, Sano, in interpretation (Stern, Hesdorffer, Sano, & Mayeux,
Hauser, and Bush (1987) have suggested 15 as the thresh- 1990).
old for moderate impairment.
The original DS also included a second section com-
prised of a brief battery of simple cognitive tasks, called Psychometric Data
the Information-Memory-Concentration Test (IMCT;
Blessed et al., 1968; Blessed et al., 1988). Similar to other In community-dwelling individuals, testretest reliabil-
brief mental status instruments, the IMCT incorporates ity after 4 weeks was r = 0.79; the first 11 items show
12 items of information/orientation, 11 items of long- marginal reliability (r = 0.68; Erkinjuntti et al., 1988).
term memory, a brief test for the 5-min recall of a persons Cole (1990) found an interrater reliability of r = 0.59
name and address, and three sequencing tasks requiring when comparing DS ratings by two independent raters
concentration (Blessed et al., 1968; Blessed et al., 1988). who each interviewed the caretakers of 47 dementia
This sub-component is typically no longer included in patients.
the DS. The initial study employing the DS showed that scores
increased as the presence of senile plaques increased
(r = 0.77; Blessed et al., 1968). Also, the DS showed
Historical Background discriminative validity in identifying senile dementia
patients compared with depressed, paraphrenia, delirious,
The original Dementia Scale (DS) evaluated informant- and physically ill patients (Blessed et al., 1968). Others
reported changes in behavior and daily functioning and have also noted that the DS is able to discriminate
also included cognitive tasks given to the patient. It was between dementia patients and community residents
developed by Blessed, Tomlinson, and Roth in 1968 in (Erkinjuntti et al., 1988; Lam et al., 1997). When a cut-
an attempt to compare the deterioration of intellect off of 4/28 was used, the DS was shown to have a sensitiv-
and personality with underlying brain neuropathology ity of 90% and a specificity of 84% (Erkinjuntti et al.,
(Blessed et al., 1968; Blessed et al., 1988). The Revised 1988). Moderate to high correlations have been reported
Dementia Scale (RDS) was introduced in 1988 and in- with other measures such as the CERAD Total score
cluded only items reflecting informant-rated changes (r = 0.40; Chandler et al., 2005), the Mini-Mental Status
in everyday activities and habits (items 1 through 11; Exam (r = 0.80; Hendrie et al., 1988), and the CAMDEX
Erkinjuntti, Hokkanen, Sulkava, & Palos, 1988). The sen- (r = 0.77; Hendrie et al., 1988). Additionally, Stern et al.
sitivity and specificity of the revised scale was higher than (1987) reported that disease progression can be moni-
that of the original DS, possibly due to lower dementia- tored using the DS; cognitive deficiencies affecting
specificity of the excluded items (i.e., changes in person- instrumental activities of daily living (e.g., handling
ality, interests, and drive; Lawson, Rodenburg, & Dykes, money, remembering short lists) were evident early
1977). However, the 4-week testretest reliability for the and worsened throughout the disease course, whereas
revised scale was lower (r = 0.68) than the original changes in basic self-care did not occur until 45 years
(r = 0.79), potentially due to the inclusion of fewer into the illness (Stern et al., 1990).
items (Erkinjuntti, et al., 1988). A cut-off of 1.5 on the RDS yields a sensitivity of
Items from the DS have been included in the standar- 93% and a specificity of 97% in discriminating between
dized interview with relatives that is part of the Cam- demented and non-demented subjects, regardless of
bridge Mental Disorders of the Elderly Examination level of dementia (Erkinjuntti et al., 1988). The RDS
(CAMDEX; Roth et al., 1986). Elements of this scale is also highly correlated with the Activities of Daily
have also been incorporated in the standardized battery Living Scale, the Instrumental Activities of Daily Living
of the Consortium to Establish a Registry for Alzheimers Scale, and the Functional Activities Questionnaire (Juva
Disease (CERAD; Morris, Mohs, Rogers, Fillenbaum, & et al., 1997).
Blessed Dementia Scale B 415
The DS appears minimally affected by demographic Chandler, M. J., Lacritz, L. H., Hynan, L. S., Barnard, H. D. Allen, G.,
Deschner, M., et al. (2005). A total score for the CERAD neuropsy-
factors. Age correlates moderately with DS scores
chological battery. Neurology, 65(1), 102106.
(r = 0.31), but when degree of dementia is taken into Cole, M. G. (1990). Interrater reliability of the Blessed Dementia Scale. B
account, age does not have a significant effect (Erkinjuniti Canadian Journal of Psychiatry, 35(4), 328330.
et al., 1988). Education appears unrelated to DS scores Eastwood, M. R., Lautenschlaegar, E., & Corbin, S. (1983). A comparison
(Erkinjuniti et al., 1988). AfricanAmerican patients score of clinical methods for assessing dementia. Journal of the American
Geriatrics Society, 31(6), 342347.
higher on the DS than white patients (Hargrove, Stoeklin,
Erkinjuntti, T., Hokkanen, L., Sulkava, R., & Palos, J. (1988). The Blessed
Haan, & Reed, 1998). The DS has been translated Dementia Scale as a screening test for dementia. International Jour-
and validated in Chinese, Korean, and Czech (Lam et al., nal of Geriatric Psychiatry, 3, 267273.
1997; Lee et al., 1999; Vajdickova, Kolibas, Heretik, & Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975). Mini Mental State:
Kosc, 1995). A practical method for grading the cognitive state of patients for the
clinician. Journal of Psychiatric Research, 12(3), 189198.
Hargrove, R., Stoeklin, M., Haan, M., & Reed, B. (1998). Clinical aspects
of Alzheimers disease in Black and White patients. Journal of the
Clinical Uses National Medical Association, 90, 7884.
Hendrie, H. C., Hall, K. S., Brittain, H. M., Austrom, M. G., Farlow, M.,
Parker, J., et al. (1988). The CAMDEX: A standardized instrument for
The DS offers a blend of items commonly found on the diagnosis of mental disorder in the elderly: A replication with a U.S.
mental status exams, activities of daily living scales, and Sample. Journal of the American Geriatric Society, 36(5), 402408.
instrumental activities of daily living scales. It is quick and Juva, K., Maela, M., Erkinjuntti, T., Sulkava, R., Yukoski, R., Valvanne, J.,
easy to administer, and additionally provides a quantifi- et al. (1997). Functional assessment scales in detecting dementia. Age
and ageing, 26(5), 393400.
cation of the degree of dementia severity. As such, it is
Lam, L. C. W., Chiu, H. F. K., Li, S. W., Chan, W. F., Chan, C. K. Y,
ideal for use by general practitioners and specialized Wong, M., et al. (1997). Screening for dementia: A preliminary study
medical and mental health care professionals to gauge on the validity of the Chinese version of the Blessed-Roth Dementia
initial status, as well as to track disease progression. Scale. International Psychogeriatrics, 9(1), 3946.
The DS may also provide more useful information in Lawson, J. S., Rodenburg, M., & Dykes, J. A. (1977). A dementia rating
scale for use with psychogeriatric patients. Journal of Gerontology, 32,
a clinical setting than the MMSE and other cognitive
153159.
assessment scales (Mant, Eyland, Pond, Saunders, & Lee, D. Y., Yoon, J. C., Lee, K. U., Jhoo, J. H., Kim, K. W., Lee, J. H., et al.
Chancellor, 1988) because it measures functional aspects (1999). Reliability and validity of the Korean version of Short Blessed
of dementia. Test (SBT-K) as a dementia screening instrument. Journal of the
Korean Neuropsychiatric Association, 38, 13651375.
Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuropsychologi-
cal assessment (4th ed.). New York: Oxford.
Cross References Mant, A., Eyland, E. A. Pond, D. C., Saunders, N. A., & Chancellor, A. H. B.
(1988). Recognition of dementia in general practice: Comparison of
general practicioners opinion with assessments using the Mini-
Activities of Daily Living Scale
Mental State Examination and the Blessed Dementia Scale. Family
Alzheimers Disease Practice, 5(3), 184188.
CERAD Morris, J. C., Mohs, R. C., Rogers, H., Fillenbaum, G., & Heyman, A.
Clinical Dementia Rating (1988). Consortium to establish a registry for Alzheimers disease
Dementia (CERAD) clinical and neuropsychological assessment of Alzheimers
disease. Psychopharmacology Bulletin, 24(4), 641651.
Dementia Rating Scale
Roth, M., Tym, E., Mountjoy, C. Q., Huppert, F. A., Hendrie, H.,
Lawton-Brody Instrumental Activities of Daily Living Verma, S., et al. (1986). CAMDEX: A standardized instrument for
Scale the diagnosis of mental disorders in the elderly with special reference
to early detection of dementia. British Journal of Psychiatry, 149,
698709.
Stern, Y., Hesdorffer, D., Sano, M., & Mayeux, R. (1990). Measurement
References and Readings and prediction of functional capacity in Alzheimers disease.
Neurology, 40(1), 814.
Blessed, G., Tomlinson, B. E., & Roth, M. (1968). The association between Stern, Y., Mayeux, R., Sano, M., Hauser, W. A., & Bush, T. (1987).
quantitative measures of dementia and of senile changes in the Predictors of disease course in patients with probable Alzheimers
cerebral gray matter of elderly subjects. British Journal of Psychiatry, disease. Neurology, 37(10), 16491653.
114(512), 797811. Vajdickova, K., Kolibas, E., Heretik, A., & Kosc, M. (1995). Application of
Blessed, G., Tomlinson, B. E., & Roth, M. (1988). Blessed-Roth Dementia behavioural scale in the diagnosis of dementia of advanced age.
Scale (DS). Psychopharmacology Bulletin, 24(4), 705708. Ceska a Slovenska Psychiatrie, 91(1), 714.
416 B BlessedRoth DS

BlessedRoth DS Outcomes
Blessed Dementia Scale The first cases of blindsight were observed in war veterans
with damage to their occipital lobe (Poppel et al., 1973).
These veterans had no conscious perception of stimuli in
the damaged portion of their visual field, yet were able to
track a moving light presented there. The most extensive
Blindsight experimental work in this area was completed with pa-
tient DB, who was diagnosed in the 1970s. DBs case is
S OPHIE 1, L EBRECHT 1, M ICHAEL J. TARR 2 extensively reviewed in the seminal book on blindsight
1
Brown University (Weiskrantz, 1986) is written.
Providence, RI, USA
2
Carnegie Mellon University
Pittsburgh, PA, USA
Neuropsychology and Psychology of. . ..
(syndrome/illness)
The area of impaired vision in the visual field of a blind-
Blindsight is a neuropsychological disorder that results sight patient is referred to as a scotoma defined as an
from damage to the primary visual cortex (V1). Such island of visual loss surrounded by an area of normal
localized cortical damage produces localized visual im- visual acuity (Fig. 1). It is important to note that the
pairment in the patients visual field contralateral to the visual impairment manifests in the region of the visual
site of the damage. Critically, despite the nominal loss of
vision, patients with blindsight preserve the ability to
detect and discriminate visual stimuli presented in the
impaired region of their visual field. Lawerence
Weiskrantzs (1986) observation of this ability to see
stimuli in a blind visual field led him to refer to this
disorder as blindsight.
Categorization
There are two types of blindsight, termed Type I and Type II.
Patients with Type I blindsight report no conscious aware-
ness of stimuli presented in the damaged region of their
visual field, yet preserve the ability to detect stimuli pre-
sented there. Patients with Type II blindsight, report a faint
conscious perception of stimuli in the damaged region of
their visual field, yet preserve the ability to detect stimuli
with higher precision than their conscious perception.
Epidemiology
Blindsight results from brain damage to the primary

visual cortex (V1) located in the posterior region of the
occipital cortex, typically caused by a tumor, a hemor-
rhage, or some sort of brain trauma. Blindsight. Figure 1 The visual perception of a scotoma
Blindsight B 417
field contralateral to the hemisphere where the brain motion, and recent evidence suggests some patients
injury has occurred. For example, damage to the left can even differentiate between different wavelengths of
hemisphere of V1 results in impairment to the right color and form presented simultaneously in their scotoma B
visual field. Typically, because early visual brain areas (Trevethan, Sahraie & Weiskrantz, 2007). Primate studies
are retinotopically mapped, the extent of the damage support the claim that this unconscious perception is
to occipital lobe corresponds to the extent of the not subserved by islands of undamaged tissue. When
impairment in the visual field. For example, if an the striate cortex of primates is cortically ablated, like
entire hemispheres occipital lobe is ablated then the humans, they have no conscious perception of stimuli
entire contralateral visual field is damaged a condi- presented in their scotoma, but do retain unconscious
tion is termed hemianopia. Likewise, if a quarter of perception. The strongest neural evidence supporting
V1 is damaged (i.e., one half of one hemispheres the existence of blindsight comes from the identifica-
occipital lobe), a quarter of the contralateral visual tion subcortical connections from the Lateral Genicu-
field is damaged a condition is termed quadranopia. late Nucleus (LGN) directly to the extrastriate cortex.
Figure 2 illustrates the pattern of visual impairment and These pathways, unaffected by V1 damage, are potential
the corresponding scotoma that arises when only a small mediators for the unconscious visual perception ob-
region of occipital lobe is damaged. Although a patient served in blindsight. The identification of this pathway
with such a pattern of sparing and loss might experience has prompted a fascinating debate regarding the role
blindsight in such a restricted scotoma, the most interest- of V1 in the neural representation of consciousness.
ing cases of blindsight have been where patients have Scientists have posited that if there is perception, but
lost all conscious visual experience, that is, there is not conscious perception, without V1, then V1 must
injury covering early visual brain areas across both play a critical role as a neural correlate of conscious-
hemispheres. ness; this remains an active area of research (for review
Note that not all patients with scotomas experience see Tong, 2003).
blindsight. The functional definition is that despite an
absence of conscious perception, patients with blindsight
retain the ability to detect and discriminate stimuli pre- Evaluation
sented in their scotoma. For example, patients can localize
moving and stationary stimuli using saccades or pointing. Because blindsight patients experience no conscious
They can also discriminate line orientations, detect awareness of stimuli presented in their scotoma,
Right optic tract
Right LGN
Optic radiation
Scotoma
Area of damage
Primary visual cortex
Blindsight. Figure 2 The relationship between a region of damage in visual cortex (V1) and the corresponding impairment in the
visual field (Adapted from Bear, Connors, & Paradiso, 2006)
418 B Blitz-Nick-Salaam Krampfe
experimenters rely on a two-alternative forced-choice explanation cannot account for now-present circular
(2AFC) procedure to diagnose and evaluate the symp- form discrimination (Trevethan et al., 2007). One possi-
toms of the disorder. The 2AFC procedure, typically bility is that DBs improvement in form perception is the
used to assess behavioral performance in nonspeaking result of the large number of hours DB spent completing
primates, presents patients with a target stimulus, a experimental testing.
probe stimulus (matched to target), and a distractor One point to consider when diagnosing or treat-
stimulus (non-matched to target); the target can be pre- ing patients with blindsight is that Type I patients have
sented either prior to or simultaneously with the paired no conscious access to the stimuli presented in the sco-
probe and distractor. The patient must select either the toma. Consequently, experimenters should be cautious
probe or the distractor as matching the target. The patient in asking for specific answers when running a 2AFC task
is not allowed to respond, I dont know, so in this way in that this task may be distressing to a patient who
the task is a forced-choice. In a variant of this procedure experiences no conscious visual perception. That is,
used to assess blindsight, experimenters present an image they may find such a task irrelevant to their personal
both to the scotoma and the hemisphere of normal visual experience.
acuity then ask subjects to report whether the two stimuli
are the same or different (Weiskrantz, 1986). Given that
chance performance in these procedures is 50%, it is Cross References
interesting to note that patients estimate their success
rate on these tasks to be roughly 50%, but in reality Cortical Blindness
their success rate is closer to 90%, illustrating the discon- Hemianopia
nect between conscious and unconscious vision in blind- Scotoma
sight. Similar results have been observed using a Visual Field Deficit
somewhat different procedure designed to measure the
unconscious perception of visual motion in blindsight
patients: saccades tracking or pointing in which a moving
object is presented within the visual field of the scotoma
Bear, M. A., Connors, B. W., & Paradiso, M. A. (2006). Neuro-
and the patient is asked to track the object with their eyes
science exploring the brain. Baltimore, MD: Lippincott Williams &
or with their finger. Wilkins.
Dineen, J., & Keating, E. G. (1981). The primate visual system after
bilateral removal of striate cortex. Survival of complex pattern
Treatment vision. Experimental Brain Research. Experimentelle Hirnforschung.
Experimentation Cerebrale, 41(34), 338345.
Poppel, E., Held, R., & Frost, D. (1973). Residual visual function after
There is a period of spontaneous recovery for neurovi- brain wounds involving the central visual pathways in man. Letters to
sual lesions, typically up to 3 months post lesion, but has Nature, 243, 295296.
been reported to extend to up to a year. Following this Sahraie, A., Trevethan, C. T., MacLeod, M. J., Murray, A. D., Olson, J. A.,
period, active discrimination of stimuli presented in the & Weiskrantz, L. (2006). Increased sensitivity after repeated stimu-
lation of residual spatial channels in blindsight. Proceedings of the
scotoma seems to be the best strategy for improvement
National Academy of Sciences of the United States of America, 103(40),
in humans (Sahraie, Trevethan, MacLeod, Murray, 1497114976.
Olson, & Weiskrantz, 2006), and nonhuman primates Tong, F. (2003). Primary visual cortex and visual awareness. Nature
(Dineen & Keating, 1981). As such, blindsight patients Reviews. Neuroscience, 4(3), 219229.
that participate as experimental subjects sometimes show Trevethan, C. T., Sahraie, A., & Weiskrantz, L. (2007). Can blindsight be
superior to sighted-sight?. Cognition, 103(3), 491501.
large improvements in their visual discrimination abil-
Weiskrantz, L. (1986). Blindsight: A case study and its implications. Net
ities. For example patient DB, the first blindsight patient Library, USA: Oxford University Press.
studied extensively (Weiskrantz, 1986), was recently Werner, J. S., & Chalupa, L. M. (2004). The visual neurosciences.
retested, 30 years after his right striate cortex was surgi- Cambridge, MA: MIT Press.
cally removed during treatment of a nonmalignant ve-
nous tumor. Patient DB can now discriminate complex
circular forms presented in his scotoma, for example, he
can discriminate a circle from an oval. Previously the Blitz-Nick-Salaam Krampfe
ability to distinguish form was accounted for by DBs
ability to distinguish line orientations; however, this West Syndrome
Block Design B 419
differed from Maxfield and Town in that he asked children

Block Design to use blocks to copy two-dimensional designs printed on
stimulus cards rather than from models constructed by B
B RIANNE M AGOUIRK B ETTCHER 1, DAVID J. L IBON 2 the examiner using identical blocks, a method adopted by
E DITH K APLAN 3, R OD S WENSON 4, DANA L. P ENNEY 5 Wechsler. Kohs (1920, 1923) specifically used block con-
1
Temple University struction as a means to assess intelligence. Consistent with
Philadelphia, PA, USA the prevailing views of the day, Kohs viewed intelligence
2
Drexel University College of Medicine as a unitary or global construct. The Kohs BD test con-
Philadelphia, PA, USA sisted of a series of 17 designs (culled from a corpus of 35
3
Suffolk University original designs). Kohs (1920, 1923) clearly viewed his test
Boston, MA, USA as equal to the existing Binet scales in measuring general
4
University of North Dakota Medical School intellectual ability. He also viewed the performance
Fargo, ND, USA (Kohs, 1920) or nonverbal nature of his test as a means
5
The Lahey Clinic to assess intelligence in children where it was either not
Burlington, MA, USA possible or problematic to use language or language
related tests. As adopted by Wechsler later, Kohs awarded
bonus points for speed. Interestingly, a separate scoring
Synonyms system was also derived to measure moves or each
separate and distinct change in the position of the
Kohs blocks block (Kohs, 1920). All these early researchers readily
acknowledged the multidimensional aspect of their
block construction procedures and commented on the
Description qualitative features of childrens block construction
strategies.
The Block Design (BD) test is a subtest from the Wechsler
corpus of intelligence tests that requires the examinee to
use three-dimensional blocks to construct a model from a Psychometric Data
two-dimensional stimulus card. Blocks consist of sides
that are all white, all red, or diagonally half red and Successful completion of the BD test requires a host
white. Performance is timed. Although bonus points are of cognitive abilities (Kramer, Kaplan, Blusewicz, & Pre-
awarded for speed, the score is either all or none, that is, a ston, 1991) including specific analytic and synthetic
score is awarded only if the model is correctly produced problem-solving strategies (Schorr, Bower, & Kiernan, 1982).
within the prescribed time limit. Analytic strategies refer to mental segmentation of the
stimulus design into individual blocks. Upon mentally di-
viding the blocks into segments the blocks are subsequently
Historical Background arranged to match each unit. This strategy might capital-
ize on the presence of perceptual edge cues and implicit
Hutt (1925) notes that the first documented use of block grid information when constructing the design (Kaplan,
construction as a psychological test was by Francis N. 1988; Kaplan et al., 1991). Synthetic strategies emphasize
Maxfield, working at the University of Pennsylvania Psy- the design as a whole, and may not rely on segmentation
chology Laboratory and Clinic, who devised a color for test completion. Examinees who utilize this strategy
cube test to study imageability in children. The proce- focus primarily on the gestalt or overall form of the
dures devised by Maxfield were also used by Clara Town design. Specific BD test items tend to pull for one
(1921, cited in Hutt, 1925). Both of these researchers were strategy versus the other. However, over reliance on either
interested in studying analytic problem-solving strategies problem-solving approach will ultimately lower an exam-
in children. However, it was Samuel Calmin Kohs (1916 inees test score and could be highly suggestive of either
1960) who derived the Block Design (BD) test that was focal or lateralized neurological insult.
ultimately adapted by David Wechsler. It appears that The BD test is often viewed as a measure of so-called
Maxfield, Town, and Kohs used the same commercially constructional apraxia (Kleist, 1923, cited in Benton &
available blocks, that is, all blocks were constructed with Tranel, 1993) and has been naively associated with right
four colors red, white, blue, and yellow. Kohs procedure parietal brain damage (Kaplan, 1988). Clear evidence
420 B Block Design
of the multidimensional cognitive skills necessary for test performance. These are listed below and are part of
optimal performance on the BD test comes from two the WAIS-R-NI corpus (Kaplan et al., 1991).
sources: patients with cerebral disconnection (Geschwind,
1. Providing Additional Blocks Rather than constraining
1979; Kaplan, 1988); and patients with focal brain lesions.
the examinees performance by providing only 4 or 9
For example, patients who have undergone a commissur-
blocks as prescribed by the Wechsler test manual,
otomy (Geschwind, 1979; Kaplan, 1988) provided a
Kaplan et al. (1991) suggests presenting the patient
unique opportunity to study BD problem-solving strate-
with 9 blocks on all 4-block test items and 12 blocks
gies because these patients serve as their own controls.
on all 9-block test items. Attempting to construct
Since these patients have undergone resection of the corpus
designs with too few or too many blocks conveys
callosum and the anterior commissure, sensory informa-
additional information about possible spatial as well
tion cannot be transferred between the hemispheres. Illus-
as executive impairment.
trations provided by Geschwind (1979) and Kaplan
2. Flow Charting Documenting the patients perfor-
(1988) show that when commissurotomized patients use
mance with a flow chart is mandatory to the cogent
their right hand, that is, when BD constructions are guid-
analysis of BD test performance. Examples of the rich
ed by the left hemisphere with no input from the right
data which can be obtained with a flow chart are
hemisphere, the inherent 2 2 or 3 3 matrix is violated
illustrated by Kaplan et al. (1991, Figure 6). As de-
and there is a tendency for blocks to pile up on the right
scribed above, focal right-hemisphere lesioned
side of the design reflecting an inattention of left hemi-
patients tend to break the 2 2 or 3 3 grid config-
space suggestive right hemisphere dysfunction (Kaplan,
uration of the stimulus matrix and often produce
1988, Figures 12). Very different errors occur with com-
distorted responses. Kaplan et al. (1991) provides
missurotomized patients attempting BD using their
examples of BD constructions produced by right-an-
left hand, that is, when constructions are guided by the
terior and right-posterior lesioned patients in Figures
right hemisphere with no input from the left hemi-
6c and 6d, respectively (see p. 90). The 3 3 grid
sphere. Now, the 2 2 or 3 3 grid matrix is rarely
configuration is broken by both patients. However, the
violated. However, blocks tend to be rotated so that the
construction of a patient with a right-posterior lesion
internal details of individual blocks do not match
is measurably more distorted than the construction
the model. Thus, Geschwind (1979) and Kaplan (1988)
produced by a right-anterior lesioned patient suggest-
show that regardless of which hand is used commissur-
ing greater perceptual-spatial impairment. Thus, as
otomized patients produce zero point responses, but the
suggested many years ago by Kohs (1920, 1923) an
underlying brain-behavior relationships responsible for
analysis of BD moves provides important
these response strategies are very different. Kaplan,
information.
Palmer, Weinstein and Baker (1981) noted that similar
3. Errors Subtypes The WAIS-R-NI (Kaplan et al., 1991)
behavior occurs in patients with focal right and left hemi-
suggests a variety of error scores that supplement
sphere lesions. Patients with right-sided lesions often
the traditional total Wechsler scale score. The scoring
break the 2 2 or 3 3 matrix inherent in the stimulus
techniques described below are designed to supplement
resulting in highly distorted responses, blocks continue to
standardized scoring procedures and help in iden-
collect on the right side of hemi-space, and constructions
tifying underlying brain pathology.
are often initiated on the right-side with patients working
(a) Rotational errors scored when a blocks surface
from right to left. Patients with left-sided lesions respect
coloring is incorrect. This type of internal detail
the inherent grid configuration of the BD stimuli. These
error could be associated with a left hemisphere
patients often make single-block, rotational errors or mis-
lesion.
align internal details (Kaplan et al., 1991) with responses
(b) Broken configuration scored when the 2 2 or
initiated on the left side of hemi-space.
3 3 grid matrix of the design is violated. As
noted above, such errors are often seen in
patients with right hemisphere lesions.
Clinical Uses While rotational and broken configuration errors often
occur in patients with circumscribed stroke, patients
Kaplan and colleagues (Kaplan, 1988; Kaplan et al., 1991) with epilepsy (Zipf-Williams, 2000) or brain injury
have suggested a number of additional testing and scoring (Wilde et al., 2000) lateralized to one side of the brain
procedures to extract detailed information from the BD may also make these errors.
Block Design B 421
(c) Orientation errors scored when a block(s) is incor- have been debated. Joy et al. (2001) provided a compre-
rectly oriented, that is, when the final product or hensive evaluation of the reported age-related decline in
elements of the final product are shifted or misor- BD test performance and offered normative data for the B
iented about 30 degrees in relation to the model. clinical interpretation of BD in healthy older adults.
Spatial, perceptual, or executive problems might un- In addition to standard passfail scoring, these researchers
derlie this difficulty. also utilized proportional scoring methods as well as
(d) Perseverations scored when incorrect block pla- the supplemental measures detailed in the WAIS-R-NI.
cements persist either within or between successive Results confirmed a moderate negative correlation be-
BD trials. Gross perseverative behavior is often tween standard BD score and age (r = 0.455); however,
seen in patients with frontal lobe or frontal sys- the use of proportion scores, elimination of time con-
tems lesions. Less severe perseverative behavior straints, and termination of time-bonuses significantly
might occur in conjunction with rotational and reduced the documented age differences. These authors
broken configuration errors and may suggest dys- interpreted this finding as evidence for less severe age-
executive behavior associated with a specific brain related impairment in visuospatial and constructional
region. abilities in healthy older adults than traditional scoring
(e) Stimulus bound examples include instances when techniques suggest. In general, it is important to carefully
the examinee is drawn to build their construction consider the role of psychomotor slowing and error types
either right next to or under the stimulus booklet or when administering the standard block design test to
even pile blocks on top of the stimulus booklet. healthy older adults in order to avoid differently penaliz-
Less egregious, but no less important stimulus ing individuals based on age. Older adults diagnosed with
bound errors occur when patients are aware of but a neurodegenerative disorder exhibit different patterns of
unable to self-correct errors. errors depending upon their neuropsychological profile
(f) Response latency patients with bradyphrenia may and diagnosis. Stimulus bound errors, broken configura-
ultimately produce a correct construction and might tions, and psychornotor slowing are all more prevalent in
be able to self-correct errors but may complete a individuals diagnosed with a dementia relative healthy
correct design only after the time limit as prescribed older adult controls.
in the test manual has passed. Such behavior might be
associated with subcortical syndromes. However,
slow time to completion often occurs in patients
with alcohol abuse, brain injury, multiple sclerosis, Cross References
or epilepsy.
(g) Start position using a flow chart, documenting the Constructional Apraxia
start position of the first block also allows for exami- Visuoconstruction
nation of a preferred side, and can be indicative of
lateralized brain dysfunction (Akshoomoff-Haist
et al., 1989).
Akshoomoff-Haist, N. A., Delis, D. C., & Kiefner, M. G. (1989).

Block Design Use with Additional Block constructions of chronic alcoholic and unilateral brain-
Populations: damaged patients: A test of the right hemisphere vulnerability
hypothesis of alcoholism. Archives of Clinical Neuropsychology, 4,
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Visuoconstructional Disorders. In K. M. Heilman & E. Valenstein
An observed pattern of developmental cognitive change (Eds.) Clinical Neuropsychology (3rd ed.). New York: Oxford
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abilities coupled with a significant diminution in visuo-
ment of a test of visuospatial analysis. Neuropsychology, 6, 385394.
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that the BD test differentiates between younger and American, 241, 180199.
older adults (Kaufman, 1990; Troyer et al., 1994), but Hutt, R. B. W. (1925). Standardization of a color cube test. The Psycho-
the specific cognitive functions that underlie this behavior logical Clinic, 16, 7797.
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tative features of block design performance among healthy older Blood Alcohol Level
adults. Archives of Clinical Neuropsychology, 16, 157170.
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A brainbehavior based analysis. Paper presented at the annual Cincinnati, OH, USA
European meeting of the International Neuropsychological Society,
Bergen, Norway.
Kaplan, E., Fein, D., Morris, R., & Delis, D. (1991). The WAIS-R as a
neuropsychological instrument. San Antonio, TX: The Psychological Synonyms
Corporation.
Kaufman, A. S. (1990). Assessing adolescent and adult intelligence. Boston: Blood alcohol concentration; Blood alcohol content
Allyn & Bacon.
Kohs, S. C. (1920). The block design tests. Journal of Experimental
Psychology, 3, 357376.
Kohs, S. C. (1923). Intelligence measurement. New York: Macmillan. Definition
Kramer, J. H., Kaplan, E., Blusewicz, M. J., & Preston, K. A. (1991). Visual
hierarchical analysis of block design configural errors. Journal of Measure of alcohol in the blood.
Clinical and Experimental Neuropsychology, 13, 455465.
Lezak, M., Howison, D. B., & Loring, D. W. (2004). Neuropsychological
assessment (4th ed.). New York: Oxford University Press. Current Knowledge
Schorr, D., Bower, G. H., & Kiernan, R. (1982). Stimulus variables in the
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50, 479487.
Blood alcohol levels are typically expressed as milligrams
Troyer, A. K., Cullum, C. M., Smernoff, E. N., & Kozora, E. (1994). Age or grams of ethanol per deciliter (e.g., 100 mg/dL or 0.10
effects on block design: Qualitative performance features and g/dL). A level of 2030 mg/dL typically results from the
extended-time effects. Neuropsychology, 8, 9599. ingestion of one to two drinks. One drink corresponds to
Wilde, M. C., Boake, C., & Sherer, M. (2000). Wechsler Adult Intelligence
340 mL (12 oz.) of beer, 115 mL (4oz) of wine, and 43 mL
Scale-Revised Block Design broker configuration errors in
non-penetrating traumatic brain injury. Applied Neuropsychology,
(1.5 oz) of a shot. Blood alcohol levels as low as 2080 mg/
7, 208214. dL can lead to decreased inhibitions and decreased cogni-
Zip-Williams, E. M., Shear, P. K., Strongin, D., et al., (2000). Qualitative tive and motor performance, while levels of 300400 mg/
Block Design performance in epilepsy patients. Archives of Clinical dL can lead coma or death. Blood alcohol levels typically
correlate inversely with cognitive and motor performance
(i.e., as blood alcohol levels increase, cognitive and motor
performance decrease). Specifically, increased blood alco-
hol levels correlate with slower reaction time and inversely
correlate with frontal executive function. Additionally,
Blocqs Disease speed of cognitive performance recovers as alcohol levels
return to drug-free levels; however, accuracy may contin-
Astasia-Abasia
ue to remain impaired.
Cross References
Blood Alcohol Concentration Coma
Executive Function
Blood Alcohol Level Frontal Lobe
Domingues, S. C., Mendonca, J. B., Laranjeira, R., Nakamura-Palacios,

Blood Alcohol Content E. M. (2009). Drinking and driving: A decrease in executive frontal
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Blood Oxygen Level-Dependent B 423
Schweizer, T. A., & Vogel-Sprott, M. (2008). Alcohol-impaired speed and There are four different types of Doppler US studies
accuracy of cognitive functions: A review of acute tolerance and
currently being utilized by physicians. Continuous wave
recover of cognitive performance. Experimental and Clinical Psycho-
pharmacology, 16(3), 340350.
Doppler is typically used at the bedside and only produces B
Harrisons Online Harrisons principles of internal medicine, 16th edn. sound from the transducer which the practitioner uses
Chapter 372: Alcohol and Alcoholism. to listen for blockage or stenosis of the vessel. Duplex
Doppler produces both a picture of the blood vessel and
a graph representing the speed and direction of blood flow
(hence the name duplex). Color Doppler uses a com-
puter to convert the Doppler sounds into colors and
Blood Clot
overlay those colors on an image of the blood vessel.
Power Doppler is more sensitive than color Doppler in
Hematoma
detecting blood flow. It combines the results given by
color Doppler with duplex Doppler. It is commonly
used to evaluate the flow of blood through vessels within
solid organs.
Blood Flow Studies Transcranial Doppler (TCD) is used to measure
the blood flow through the brains blood vessels. It is
C INDY B. I VANHOE , N ATASHA K. E ADDY becoming more widely used to evaluate for embolus,
Neurorehabilitation Specialists stenosis, vasospasm, and the risk of stroke.
Houston, TX, USA
Cross References
Synonyms Doppler Ultrasound
Regional Cerebral Blood Flow
Duplex/Doppler ultrasound (US); Vascular ultrasound Transcranial Doppler

Definition
Blaivas, M. (2007). Ultrasound in the detection of venous thromboem-
A blood flow study is a noninvasive imaging technique bolism. Critical Care Medicine, 35(Suppl. 5), S224234.
which is used to measure blood flow and pressure through Hamper, U. M., DeJong, M. R., & Scoutt, L. M. (2007). Ultrasound
arteries, veins, or chambers and valves of the heart. evaluation of the lower extremity veins. Radiologic Clinics of North
Doppler US may be used to diagnose vascular conditions America, 45(3), 525547.
Rubens, D. J., Bhatt, S., Nedelka, S., & Cullinan, J. (2006). Doppler
such as thrombosis, vascular stenosis, valvular heart
artifacts and pitfalls. Radiologic Clinics of North America, 44(6),
disease, peripheral vascular and aneurysmal disease. It 805835.
may also be used to evaluate the condition of bypass grafts Weber, T. M., Lockhart, M. E., & Robbin, M. L. (2007). Upper extremity
and blood flow to transplanted organs. venous Doppler ultrasound. Radiologic Clinics of North America, 45,
513524.
Current Knowledge
Blood Oxygen Level-Dependent
Blood flow studies such as Doppler US uses a transducer
that sends high-frequency sound waves which bounce off J OHN W HYTE
of solid objects including red blood cells. The sound waves Moss Rehabilitation Research Institute
are reflected back to the transducer. Moving objects, Albert Einstein Healthcare Network
such as the red blood cells, cause a change in pitch of Elkins Park, PA, USA
the sound waves (also known as the Doppler effect).
These reflected waves are sent to and processed by a
computer which translates the waves into pictures or Synonyms
graphs. The images are representative of the flow of
blood through the vessel. BOLD
424 B Blood Oxygen Level-Dependent
Definition with a neural event) to allow the BOLD signal to be

related to specific behavioral and cognitive events that
BOLD imaging is a version of magnetic resonance are assumed to require neural processing. The hemody-
imaging that depends on the different magnetic proper- namic response function can be modeled in a normative
ties of oxygenated versus deoxygenated hemoglobin and sense (i.e., the shape of the blood flow response in a
thus, indirectly, on variations in local tissue perfusion. typical organism) or in the individual subject.
The utility of BOLD imaging for functional magnetic Although the BOLD signal is not a direct measure of
resonance imaging (fMRI) also depends on the physiolog- neural activity, a number of studies that have simulta-
ical phenomenon by which metabolically active cerebral neously recorded direct measures of cerebral blood flow
tissue demands more perfusion than less-active tissue. or actual neuronal firing rates have suggested that, in
Thus, populations of neurons that are particularly active most circumstances at least, there is a reasonably tight
during a cognitive or motor task actually elicit a relative coupling of neural activity and the BOLD signal. Less
surplus of perfusion which, in turn, results in an increase research, however, has been conducted on animals or
in the ratio of oxygenated to deoxygenated hemoglobin, humans with known abnormalities of cardiovascular
detectable as a change in the BOLD signal. function, so that the possibility remains that the coupling
assumptions underlying the use of this method are vio-
lated in certain research contexts.
Historical Background The BOLD signal provides relative information about
changes in flow, rather than an absolute measure of
As early as 1890, Roy and Sherrington noted that regional
perfusion in cc/gm/min as can be obtained from PET,
cerebral blood flow increased in areas of neural activity.
or perfusion MRI. However, when contrasted to or sub-
This increase in perfusion became detectable in vivo with
tracted from some control condition, the change in the
the advent of positron emission tomography (PET), in
BOLD signal can help to localize the brain areas that are
which radioactive tracers are injected and their emitted
specifically active in the condition of interest when com-
radiation detected. It was not until the discovery of BOLD
pared to the control condition.
contrast by Ogawa and colleagues at Bell Laboratories,
BOLD imaging studies in human neuroscience most
however, that it was possible to measure these neurally
often make use of one of the two common experimental
mediated changes in flow without radiation exposure
designs: blocked or event-related (Fig. 1). In the blocked
using MRI and, hence, to allow a broader range of studies
design, the subject is asked to perform a particular cogni-
with normal control subjects and with repeated studies of
tive or motor task in blocks that alternate with other
the same individuals.
blocks of a contrasting task or rest. The BOLD signal is
then statistically averaged across the two types of blocks,
Current Knowledge and a measure of the difference between them is mapped
onto each voxel in the MR image, thus showing those
Because of its dependence on the state of oxygenation of areas of the brain that had the largest change in BOLD
the blood, the BOLD signal is several steps removed from signal between the two conditions. A contrasting rest
the typical phenomenon of interest: changes in neural block is typically used when one is interested in the
activity. All measures of cerebral blood flow are indirect, brain areas involved in all aspects of the task, although
in the sense that they can be influenced by cardiovascular this method has been criticized because there is no stan-
factors (e.g., changes in cardiac output, vascular resis- dardization of the subjects mental activity during rest.
tance) as well as changes in metabolic demand by neural Alternatively, if one is interested in the brain areas
(as well as nonneural tissue, e.g., glia) tissue. But BOLD involved with a specific task process, one might alternate
has the additional limitation that it represents the rela- the experimental task with a control task that shares most
tionship between oxygen delivery and oxygen extraction, but not all of the features of the experimental task. For
rather than oxygen consumption itself a more direct example, if a research subject performs alternating blocks
measure of tissue metabolic activity. In addition, there is a of finger tapping in response to a visual signal versus
delay of several seconds between the changes in neural viewing the visual signal without tapping, areas involved
activity and the changes in associated blood flow. Thus, in the perception of the visual signal will tend to be
BOLD imaging typically involves mathematical modeling canceled out across conditions whereas neural networks
of the hemodynamic response function (the increase specifically involved in the tapping response will be
and subsequent return to baseline of flow associated highlighted. In this way, a wide range of cognitive and
Blood Oxygen Level-Dependent B 425
the performance of specific mental activities. By assessing

how strongly changes in the BOLD signal in different
regions are correlated over time, one can derive a measure B
of functional connectivity, assessed either at rest or dur-
ing the performance of specific tasks. Measures of func-
tional connectivity do not specify the actual anatomical
connections between regions, but merely demonstrate the
degree to which their activity levels are linked over time.
With any of these experimental designs, the BOLD
signal must also be mapped to an anatomical model of the
brain. This is done by modeling the signal separately in each
voxel of the MRI image and then contrasting the signal in
each voxel between the experimental conditions of interest.
This may require additional manipulations, such as warping
each subjects image to a standard template, smoothing
the signal so that the activity in collections of voxels rather
than individual voxels is highlighted, and deriving statis-
tical maps that code the reliability of the change of interest
across brain regions and individual subjects. Several forms
of computer software are available for processing raw
fMRI data into analyzable maps and statistical results.
Although BOLD and other functional MRI techniques
are extremely powerful research tools, they incorporate a
Blood Oxygen Level-Dependent. Figure 1 This axial slice of large number of data transformations and assumptions
the brain shows the areas of most significant BOLD activation between the raw signal acquisition and interpretations at
across 18 control subjects, obtained while they attended to the level of brain activity and behavior. As noted above,
three randomly moving visual stimuli. Higher visual areas in conclusions reached by these techniques can be under-
the occipital cortices (motion areas V5/MT+) and superior mined by alterations in the coupling between neural
colliculi show the greatest activation activity and blood flow, by failure to accurately under-
stand the cognitive and motor processes required by the
motor tasks have been studied in normal subjects as a task, and by invalid application of the many analytical
way of localizing the neural networks involved in their and statistical methods that transform the measured
performance; and in patient subjects, as a way of BOLD signal into statistical maps of brain activity. Thus,
exploring how that localization may have been altered investigators seeking to use these methods typically need
by pathology or recovery. extensive training in their application.
In event-related BOLD designs, experimental trials of
different types can be delivered in a random sequence and
averaged in a time-locked fashion. The timing between Cross References
trials is sometimes jittered (i.e., randomly varied) so
that, even though the hemodynamic responses from indi- Functional Imaging
vidual trials overlap, their individual effects can be sepa- Magnetic Resonance Imaging
rately modeled (deconvolved), by incorporating the
known temporal spacing between them.
More recently, the BOLD signal has been used to References and Readings
understand how activities in different parts of the
brain are interrelated. Modern neuroscience posits the Buxton, R. B., Uluda, K., Dubowitz, D. J., & Liu, T. T. (2004). Modeling
presence of distributed neural networks, rather than the hemodynamic response to brain activation. Neuroimage,
23(Suppl. 1), S220233.
focal regions, supporting specific cognitive and motor
Jamie Shorey, History of functional MRI. Retrieved October 15, 2007
processes. Since components of these neural networks from http://www.ee.duke.edu/jshorey/MRIHomepage/fmri.html
may be separated by considerable distances, it is of interest Huettel, S. A., Song, A. W., & McCarthy, G. (2004). Functional magnetic
to understand how they communicate with each other in resonance imaging. Suderland, MA: Sinauer Associates.
426 B Blood Thinner
Kida, I., & Hyder, F. (2006). Physiology of functional magnetic resonance resistance, and lack of pinocytic vesicles, provide limited
imaging: Energetics and function. Methods in Molecular Medicine,
and selective access to this highly specialized organ. Only
124, 175195.
Logothetis, N., & Pfeuffer, J. (2004). On the nature of the BOLD
lipophilic molecules less than 600 Da can passively diffuse
fMRI contrast mechanism. Magnetic Resonance Imaging, 22(10), through the BBB. This protects the brain from toxins,
15171531. microorganisms (i.e., bacteria) and peripheral neuro-
Nair, D. G. (2005). About being BOLD. Research Brain Research transmitters. This selective barrier can potentially limit
Reviews, 50(2), 229243.
entry of large substances required for normal brain func-
Stephan, K. E., Harrison, L. M., Penny, W. D., & Friston, K. J. (2004).
Biophysical models of fMRI responses. Current Opinion in Neuro-
tion, including insulin, amino acids, and glucose. In order
biology, 14(5), 629635. to circumvent this problem, the BBB has developed highly
Steward, C. A., Marsden, C. A., Prior, M. J., Morris, P. G., & Shah, Y. B. specialized transport mechanisms on both the luminal
(2005). Methodological considerations in rat brain BOLD contrast and albuminal membrane surfaces, such as Na-K-Cl
pharmacological MRI. Psychopharmacology, 180(4), 687704.
cotransporter, g-glutamyl transpeptidase (GGTP), and
the GLUT-1 glucose transporter. The protective BBB can
be at a disadvantage in that it prevents the entry of
pharmacologic agents that are often hydrophilic.
Blood Thinner Also unique to brain microvascular endothelium is
their intimate association with astrocytes, forming the
Warfarin (Coumadin)
glia limitans. Astrocytes are thought to participate in
the induction and maintenance of the endothelial BBB
phenotype. In vitro studies have shown that astrocytes
cocultured with endothelial cells can induce BBB pheno-
Blood-Brain Barrier typic features, including tight junctions and increased
electrical resistance. Astrocytic membranes and superna-
N AM T RAN
tant from astrocytic cultures share similar inductive
properties. The mechanisms of this induction and the
Richmond, VA, USA
inductive factor(s) have yet to be fully elucidated.
In addition to its regulatory role, studies of the BBB
are beginning to emerge to demonstrate its function in
Synonyms
establishing a unique brain milieu. In vitro BBB models
have shown decreased tissue plasminogen activator and
Cerebral microvasculature
then anticoagulant protein thrombomodulin expression
and increased plasminogen activator inhibitor-1 expres-
Definition sion by brain endothelium compared with endothelium
from the periphery. These findings suggest a procoagulant
The blood-brain barrier (BBB) maintains brain homeo- environment in the brain that may predispose the brain
stasis by regulating the movement of compounds across to strokes.
the endothelium of cerebral capillaries.
Cross References
Current Knowledge
Neuroglia
BBB serves to maintain brain homeostasis by regulating
the influx and efflux of compounds to and from the brain.
The presence of a barrier was first documented by Paul Blood-Filled Dilatation
Ehrlich in the late nineteenth century. However, it was not
until the advent of the electron microscope that the Aneurysm
makeup of the BBB was begun to be understood. The
brain microvascular endothelium comprises the BBB. In
contrast to endothelium from other vascular beds, the Blue Spot
morphologic features unique to the brain microvascular
endothelium, such as tight junctions, increased electrical Locus Ceruleus
Body Schema B 427
difficulties in identifying body parts and/or appreciating

BNT their relative relations to one another. Care should be
taken to differentiate asomatognosia from unilateral ne- B
Boston Naming Test glect or anomia. In the former, the deficit is restricted to
one side of the body; in the latter, difficulties with naming
extend beyond just parts of the body. More commonly,
Body Schema autotopagnosia is restricted to difficulty identifying indi-
vidual fingers, especially the middle three. The deficit
J OHN E. M ENDOZA is usually bilateral and will frequently involve not only
Tulane University Medical Center difficulties with regard to the patients own fingers,
New Orleans, LA, USA but also those of the examiner or pictorial representations
of a hand. Deficits are often found whether tested visually
or tactually and whether verbal or nonverbal (e.g., match-
Synonyms ing to a model) responses are required. Unilaterally
expressed deficits in finger recognition using only tactile
Somatognosis stimulation likely reflect a more basic somatosensory
disturbance.
Right-left disorientation, the inability to reliably distin-
Definition guish the right from the left sides of ones body in the
absence of a more generalized aphasic disorder, is another
General term for the personal awareness of ones body, commonly cited example of a disturbance of body sche-
including the location and orientation of its various parts ma. As with finger agnosia, difficulties extend beyond the
and their relative motion in space and time, as well as its patients themselves to include problems with extraperso-
functional integrity. nal right-left discriminations. Anosognosia and anosodia-
phoria (a milder form of anosognosia), along with
unilateral neglect or hemi-inattention are sometimes
Current Knowledge viewed as specialized forms of a body schema disorder.
One major difference is that these latter syndromes are
Although usually taken for granted, to effectively carry generally limited to one side of the body, whereas auto-
out normal motor activities one needs to appreciate both topagnosia, the more restricted finger agnosia, and right-
the static and kinetic state of the body as a whole as well as left disorientation affect both sides of the body. The one
its individual parts. This information is derived from a notable exception to this rule is Antons syndrome, a form
number of sensory feedback loops, including signals from of anosognosia in which the patient denies blindness
receptors in the muscles, tendons, ligaments and the skin where both right and left visual fields are involved.
(proprioceptive, kinesthetic, and tactile information), the While there is some potential variability with regard to
inner ear or vestibular sense (orientation, direction, and localizations of lesions, asomatognosia, when bilaterally
speed of movement of the head), and vision. Perhaps as a expressed, is most commonly associated with lesions of
result of collective experiences with such discrete sensory the left parietal region, typically involving the inferior
input, it has been suggested that individuals eventually parietal lobule. Unilateral neglect or hemi-inattention
develop what might be considered a superordinate sense syndromes may occur following anterior or posterior
of ones own body, independent of its movement in space lesions of either hemisphere, although they are most
or time. This knowledge, at least to some extent, trans- common following right posterior lesions. Antons syn-
cends ones own body and allows insights into bodies in drome is typically associated with bilateral lesions involv-
general. Because awareness of body schema is such a fun- ing the posterior cerebral arteries.
damental operation of the central nervous system, it al-
most functions at a subliminal level. One is normally only
aware of its operation when it becomes dysfunctional. Cross References
Disorders of body schema, known as asomatognosias,
can take on various guises. Although relatively rare, auto- Allesthesia
topagnosia represents what might be considered the quin- Anosodiaphoria
tessential body schema disturbance. This deficit involves Anosognosia
428 B BOLD
Autotopagnosia
Cortical Blindness Boston Diagnostic Aphasia
Finger Agnosia Examination
Hemiinattention
Right-Left Disorientation C AROLE R OTH
Naval Medical Center
San Diego, CA, USA
Adair, J. C., Schwartz, R. L., & Barrett, A. (2003). Anosognosia. In K. M.

Heilman & E. Valenstein (Eds.), Clinical neuropsychology (4th ed.,
Synonyms
Denburg, N. L., & Tranel, D. (2003). Acalculia and disturbances of BDAE
body schema. In K. M. Heilman & E. Valenstein (Eds.), Clinical
neuropsychology (4th ed., pp. 161184). New York: Oxford
University Press. Description
Goldenberg, G. (2003). Disorders of body perception and representation.
In T. E. Feinberg & M. J. Farah (Eds.), Behavioral neurology
and neuropsychology (2nd ed., pp. 285294). New York, NY: Boston Diagnostic Aphasia Examination (3rd ed.)
McGraw-Hill. (BDAE-3) Authors: Harold Goodglass, Edith Kaplan,
Prigatano, G. P., & Schacter, D. L. (Eds.). (1991). Awareness of deficit after Barbara Barresi, 2001, Publisher: Pro-Ed, 8700 Shoal
brain injury: Clinical and theoretical issues. New York: Oxford Creek Blvd, Austin, TX 78757-6897, http://www.proe-
University Press.
dinc.com (also available through Psychological Assess-
ment Resources (http://www.parinc.com)).
The BDAE-3 test kit includes test manual, stimulus
cards, and test booklets for Standard and Short forms, and
BOLD the 60-item Boston Naming Test with record booklets.
The manual is provided within the test kit.
Blood Oxygene Level-Dependent The Boston Diagnostic Aphasia Examination (BDAE)
is a comprehensive, multiple subtests instrument for
investigating a broad range of language impairments
that are common consequences of brain damage. It is
Bonnet Syndrome designed as a comprehensive measure of aphasia. The
examination provides materials and procedures to evalu-
Charles Bonnet Syndrome ate five language-related sections and an additional sec-
tion on praxis. The five language domains include
conversational and expository speech, auditory compre-
hension, oral expression, reading, and writing. In addi-
BonnevieUllrich Syndrome tion to individual subtest scores, the test yields three
broader measures: the Severity Rating Scale (a rating of
Turner Syndrome the severity of observed language/speech disturbance), the
Rating Scale Profile of Speech Characteristics (a rating of
observed speech characteristics and of scores in two main
language domains), and the Language Competency Index
Borderline Schizophrenia (a composite score of language performance on BDAE-3
subtests). The extended version includes a sixth section,
Schizotypal Personality Disorder Praxis, which examines natural and conventional ges-
tures, use of pretend objects, and bucco-facial and
respiratory movements. Suggestions for administering,
scoring, and interpreting performance on subtests in the
Borreliosis BDAE are given in the test manual, as well as directions
for plotting and interpreting patient profiles. Percentiles
Lyme Disease or standard scores can be derived for each subtest.
Boston Diagnostic Aphasia Examination B 429
Administration Italian, Dutch, Hindi, Finnish, Mandarin Chinese, Japa-

nese, and Portuguese.
The 44-page test booklet provides instructions for test B
administration. This booklet is available at the back of
Psychometric Data
the hardbound text by Goodglass, Kaplan, and Barresi
(2001a) published by Lippincott Williams & Wilkins,
Norms
which is included in the complete test package. The
Short Form and Extended Form items are specified in
Standardization of the BDAE-3 is based on an aphasic
the test booklet and are also presented in different type-
population referred concurrently by field examiners
face; the Short Form items are presented in bold typeface,
working in inpatient, outpatient, and private practice
and the Extended Form items appear in italics. The
settings. Means and standard deviations for the BDAE-3
Standard administration includes all of the bold Short
subtests for aphasic subjects are provided in the test
Form items in addition to regular typeface items.
manual. The number of subjects varies from a maximum
of 85 to a low of 31, depending on the subtest. Means are
also provided for 15 normal subjects who, on average,
Historical Background failed less than one item per subtest.
The BDAE is designed to meet three goals: to enable
diagnosis of aphasia syndromes, to measure the breadth Reliability
and severity of aphasic disturbance, and to provide a
comprehensive assessment of language to guide therapy. KuderRichardson reliability coefficients for subtests re-
Initially published by Goodglass and Kaplan in 1972, it was flect variability, ranging between <0.65 and < 0.95 with
revised in 1983 and again in 2001. Changes from the about two thirds of the coefficients reported in the man-
previous edition include the addition of abbreviated and ual (Goodglass et al., 2001a), ranging from 0.90 upwards.
expanded testing formats, incorporation of the Boston Since testretest reliability is difficult if not impossible to
Naming Test, addition of a Language Competence Index attain with patients with aphasia, the current reliability
and clarification of scoring procedures and definitions. coefficients demonstrate very good internal consistency in
The revision also was designed to integrate recent advances terms of what the items within the subtests are measuring
in neurolinguistics research, including methods to assess (Goodglass et al., 2001a). For most subtests, correlations
narrative and discourse complexity, category-specific dis- are very high between the Short and Standard Forms
sociations in lexical production/comprehension, syntax (>0.90; Goodglass et al., 2001a).
comprehension, and analysis of grapheme-phoneme con- Validity: A correlation matrix was obtained for all
version during reading. The ultimate goal for the authors the scores in the battery and the correlation coefficients
in developing the test was clinical utility. 0.60 or greater are displayed in the manual (Goodglass
The BDAE-3 consists of more than 50 subtests that et al., 2001a), with severity partialled out, showing inter-
can be administered in three different formats: Standard, correlations between BDAE-3 subtests for the standardiza-
Short, and Extended. The Standard format most closely tion sample. Based on these, a number of sharply defined
resembles earlier versions of the BDAE. The new Short clusters are indicated by the authors (p. 16). Although no
Form of the test provides a brief assessment. The extended current studies have examined the factor structure of the
version offers a comprehensive neurolinguistic profile BDAE-3, based on data for earlier versions of the BDAE,
that includes evaluation of spontaneous narrative, proces- Goodglass and Kaplan (1972) found a strong general
sing of word categories, syntax comprehension, and language factor, and factors covering spatial-quantitative-
reading/writing. The BDAE-3 allows both a quantitative somatagnostic, articulation-grammatical fluency, auditory
and a qualitative evaluation of language. The examination comprehension, and paraphasia domains. Goodglass and
is based on an assumption that the nature of the aphasic Kaplan (1983) described a second factor analysis using a
deficit is determined by (1) organization of language in sample of 242 aphasic patients, concluding that auditory
the brain, (2) the location of the lesion causing the comprehension, repetition-recitation, reading, and writing
aphasia, and (3) interactions among parts of the language were factors of equal importance. Similar findings in
system. normal individuals were reported by Pineda et al. (2000).
The BDAE has been adapted and translated for use in Correlations between earlier versions of the BDAE and
many languages including Spanish, French, German, other measures have been described. For example, the
430 B Boston Naming Test
BDAE oral apraxia task has been correlated with other Brocas Aphasia
articulation tasks (Sussman et al., 1986); correlations for Conduction Aphasia
the auditory comprehension measure on the BDAE and Praxis
the Token Test and with respective measures of the Porch Wernickes Aphasia
Index of Communicative Ability (PICA) have been
reported (Divenyl & Robinson, 1989). Brookshire and References and Readings
Nichols (1984) found the BDAE auditory comprehension
subtest did not predict auditory paragraph comprehen- Brookshire, R. H., & Nicholas, L. E. (1984). Comprehension of directly
sion of independent standardized material. and indirectly stated main ideas and details in discourse by brain-
Goodglass and Kaplan designed the BDAE to assess damaged and non-brain-damaged listeners. Brain and Language, 21,
various components of language function for the purpose 2136.
Crary, M. A., Wertz, R. T., & Deal, J. L. (1992). Classifying aphasias:
of discriminating among different patterns of CNS lesions
Cluster analysis of Western Aphasia Battery and Boston Diagnostic
indicative of types of aphasia. Studies to date have not Aphasia Examination. Aphasiology, 6, 2936.
determined decision rules for the diagnosis of individual Davidoff, M., & Katz, R. (1985). Automated telephone therapy for im-
subtypes of aphasia (Crary et al., 1992; Reinvang & proving comprehension in aphasic adults. Cognitive Rehabilitation,
Graves, 1975). 3, 2628.
Divenyl, P. L., & Robinson, A. J. (1989). Nonlinguistic auditory capabil-
Ecological validity of the BDAE for predicting prog-
ities in aphasia. Brain and Language, 37, 290326.
ress in speech therapy has been described by various Goodglass, H., & Kaplan, E. (1972). Boston Diagnostic Aphasia Examina-
authors (Davidoff & Katz, 1985; Helm-Estbrooks & tion (BDAE). Philadelphia: Lea & Febiger.
Ramsberger, 1986; Marshall & Neuberger, 1994). Goodglass, H., & Kaplan, E. (1983). The assessment of aphasia and related
disorders (2nd ed.). Philadelphia: Liea & Febiger.
Goodglass, H., Kaplan, E., & Barresi, B. (2001a). The assessment of aphasia
Clinical Uses and related disorders (3rd ed.). Philadelphia: Lippincott Williams &
Wilkins.
Goodglass, H., Kaplan, E., & Barresi, B. (2001b). Boston diagnostic aphasia
The BDAE is derived from samples of adult patients
examination (3rd ed.). Philadelphia: Lippincott Williams & Wilkins.
with stroke and therefore is most useful when assessing Helm-Estabrooks, N., & Ramsberger, G. (1986). Aphasia treatment de-
inpatient or outpatient adult populations with language livered by telephone. Archives of Physical Medicine and Rehabilita-
impairments resulting from strokes, but it can be used tion, 67, 5153.
effectively with persons who have sustained traumatic Marshall, R. C., & Neuburger, S. I. (1994). Verbal self-correction and
improvement in treated aphasia clients. Aphasiology, 8, 535547.
brain injury. The BDAE offers a comprehensive look at
Pineda, D. A., Rosselli, M., Ardila, A., Mejia, S. E., Romero, M. G., &
language function from a neuropsychological perspective. Perez, C. (2000). The Boston Diagnostic Aphasia Examination-
Complete administration of this battery requires approx- Spanish Version: The influence of demographic variables. Journal
imately 90 min. The Short Form requires approximately of the International Neuropsychological Society, 6, 802814.
4060 min. The BDAE is one of the most popular Reinvang, I., & Graves, R. (1975). A basic aphasia examination: Descrip-
tion with discussion of first results. Scandinavian Journal of Rehabil-
batteries for use by speechlanguage pathologists for eval-
itation Medicine, 7, 129135.
uation of aphasia and other neurologic language impair- Spreen, O., & Risser, A. H. (Eds.). (2003). Assessment of aphasia.
ments. In addition to its strength as a comprehensive New York: Oxford University Press.
assessment of language, the BDAE provides useful Sussman, H., Marquardt, T., Hutchinson, J., & MacNeilage, P. (1986).
instructions for observing and recording specific types of Compensatory articulation in Brocas aphasia. Brain and Language,
27, 5674.
error responses (e.g., paraphasia) found in individuals
with aphasia, reflecting what has been termed the Boston
school approach to aphasia classification. The detailed
examination of conversational and expository speech is an
Boston Naming Test
important and unique aspect of the BDAE and is well
C AROLE R OTH
described in the manual (Goodglass et al, 2001a).
San Diego, CA, USA
Cross References
Anomic Aphasia Synonyms
Aphasia
Boston Naming Test BNT
Boston Naming Test B 431
Description Correct responses following a phonemic cue are not in-

cluded in the total correct score.
Boston Naming Test-2 (BNT-2) B
Authors: Kaplan, Edith, Goodglass, Harold, Weintraub,
Sandra
Second edition 2001
The test was originally published by Kaplan and collea-
Publisher: Pro-Ed, 8700 Shoal Creek Blvd, Austin, TX
gues in 1978 as an experimental version with 85 items. It
787576897
was revised to a 60-item test in 1983. The current version
http://www.proedinc.com
(BNT-2) retains the same 60 items and includes a short
Also available as part of the revised BDAE-2 (Goodglass
15-item version as well as a multiple-choice version.
et al., 2000) from Pro-Ed.
Short-forms of the BNT have been developed to reduce
The Boston Naming Test (BNT), consisting of 60
test time. These include: Fastenau et al. (1998), Graves
black and white line drawings of objects, is a measure of
et al. (2004), Lansing et al. (1999), Mack et al. (1992),
confrontation naming that takes into account the finding
Saxton et al. (2000), Teng et al. (1989), and Williams et al.
that patients with dysnomia often have greater difficulties
(1989). The 15-item short-form 4 (Mack SF4) developed
with the naming of low frequency objects. Thus, instead
by Mack et al. (1992) was adopted by the authors of the
of a simple category of anomia, naming difficulties may
BNT-2 and can be found at the beginning of the stimulus
be rank ordered along a continuum. Items on the BNT
booklet and answer sheet. The new BNT-2 also includes
are ordered according to their ability to be named, which
a multiple-choice version that can be administered fol-
is thought to be correlated with their frequency. This
lowing the standard presentation, specifically to further
type of picture-naming vocabulary test is useful in the
assess the subjects recognition of the lexicon for items
examination of children with learning disabilities and the
previously missed. The BNT-2 is available separately and
evaluation of adults with brain injury or dysfunction.
as part of the revised BDAE-2.The BNT has been adapted
When used in conjunction with the Boston Diagnostic
and translated for use in at least a dozen languages includ-
Aphasia Examination, inferences can be drawn regarding
ing a 30-item adaptation for Spanish-speaking people in
language facility and possible localization of cerebral
the United States.
damage.
Psychometric Data
Administration
Reliability, Validity, and Norms:
The Boston Naming Test assesses naming abilities of
children, aphasic adults, and normal adults. The drawings
Reliability
are shown to the examinee one at a time, and the exam-
inee is asked to name each of them. Familiarity decreases
Internal consistency for the 60-item form has been
as the test progresses. Following presentation of each
reported to range between 0.78 and 0.96. Reliability coef-
picture stimulus, two types of cues may be presented
ficients have been lower for the abbreviated versions; for
when there is an error response: a stimulus cue (de-
example, the Mack SF4 version ranges between 0.49 and
scriptive) and a phonemic cue. A stimulus cue is pre-
0.84. Testretest reliability is high over short intervals. For
sented when the subject clearly misperceives the picture or
longer time intervals, such as 1112 months, testretest
indicates a lack of recognition of the picture. A phonemic
reliability was marginal to high; for example, in a healthy,
cue is presented after each error response, including fol-
elderly Caucasian adult population, testretest reliability
lowing a stimulus cue. The subject is given up to 20 s to
ranged between 0.62 and 0.89 (Mitrushina & Satz, 1995);
respond following each stimulus presentation, including
and high retest reliability (0.92) in a normal or neurolog-
the cues. All responses are recorded as a correct re-
ically stable adult population (Dikmen et al., 1999).
sponse or as an error with the actual error response
recorded for later coding by type. Types of cues presented
are recorded as stimulus cue or phonemic cue; re- Validity
sponse latencies in seconds are also recorded. The total
correct score is the sum of the accurate responses pre- The BNT has been shown to correlate highly with other
sented spontaneously and following a stimulus cue. language-related measures; including the Visual Naming
432 B Boston Naming Test
Test of the Multilingual Aphasia Examination (Axelrod for 663 primarily Caucasian individuals older than 55
et al., 1994; Schefft et al., 2003); as well as with measures years of age, derived from the Mayo Older Americans
of intelligence; including the Verbal Comprehension Fac- Normative Studies (the MOANS projects). Raw scores
tor of the WAIS-R and the Standard Raven Progressive are converted to age-corrected scaled scores having a
Matrices in children aged 612 years (Storms et al., 2004). mean of 10 and a standard deviation (SD) of 3 (Strauss
Poor performance on the BNT has been described in et al., 2006). Additional studies have expanded the utility
subjects with neurologic disease; including: left- of the MOANS project by providing age- and IQ-adjusted
hemisphere and brainstem strokes, anoxia, multiple percentile equivalents of MOANS Age-adjusted BNT
sclerosis, Parkinsons disease, Alzheimers disease, and scores, for individuals over 55 years (Steinberg et al.,
closed head injuries. 2005); age- and education-adjusted normative data
based on African Americans from the Mayo Older African
American Normative studies (MOAANS) project (Lucas
Norms et al., 2005) (Strauss et al., 2006).
Data on BNT norms for children is limited. The test
The norms available in the test booklet are limited authors provide norms for ages 5 years 0 months (50)
to small groups of adults ranging in age between 18 and through 125, based on small groups of participants. The
79 (N = 178) and of children ranging in age between data were collected in 1987 and the normative data are
50 years and 125 years (N = 356). Information about believed to be largely from Caucasian boys and girls who
geographical region, ethnicity, or time reference for this were attending public and private schools and living with
normative data is not provided. middle class families in suburban or urban areas of
Cross-sectional studies suggest that age (Heaton et al., the northeastern United States. There is a gap in the
2004; Ivnik et al., 1996; MacKay et al., 2005; Mitrushina BNT norms for adolescents between the ages of 14 and
et al., 2005) and verbal intelligence affect the BNT scores 17 years.
(Killgore & Adams, 1999; Steinberg et al., 2005;
Tombaugh & Hubley, 1997). Gender has been reported
to be unrelated to BNT performance (Henderson et al.,
1998; Ivnik et al., 1996; Lucas et al. 2005; Riva et al., 2000). Clinical Uses
Other studies suggest men outperform women in older
samples, possibly because of male-biased items The BNT, a visual confrontation naming test, is recom-
(Randolph et al., 1999). Reading vocabulary is strongly mended as a supplement to the Boston Diagnostic Apha-
correlated with BNT performance (Graves & Carswell, sia Examination. It can be used to assess naming abilities
2003; Senior et al., 2001). Geographic region and ethnicity of children, aphasic adults, and typical adults, although
have been shown to affect performance (Heaton et al., there is limited and poorly described normative data, and
2004; Lucas et al., 2005). Linguistic background also no testretest reliability for children.
affects test scores according to Roberts et al. (2002).
In the literature can be found a number of normative
reports for adult English speakers (see pp. 905907,
Strauss, Sherman, & Spreen, 2006). For example, Heaton Cross References
et al. (2004) reviewed studies over a 25-year period and
presented age, gender, and educational norms for two Anomia
ethnicity groups: Caucasians and African Americans. Boston Diagnostic Aphasia Examination
Mitrushina et al. (2005) compiled data from 14 studies,
comprising a total of 1,684 educated participants with
above-average intelligence who were administered the
60-item version. Their data was presented in 5-year incre-
ments, ranging from ages 25 to 84 years. The data is
Axelrod, B. N., Ricker, J. H., & Cherry, S. A. (1994). Concurrent validity
considered to be similar to those provided by Kaplan
of the MAE visual naming test. Archives of Clinical Neuropsychology,
et al. (2001) and may overestimate expected performance 9, 317321.
for individuals with lower educational and intellectual Dikmen, S. S., Heaton, R. K., Grant, I., & Temkin, N. R. (1999). Test
levels. Ivnik et al. (1996) provided age-corrected norms retest reliability and practice effects of expanded HalsteadReitan
Boston Process Approach B 433
neuropsychological test battery. Journal of the International Neuro- Roberts, P. M., Garcia, L. J., Desrochers, A., & Hernandez, D. (2002).
psychological Society, 5, 346356. English performance of Proficient bilingual adults on the Boston
Fastenau, P. S., Denburg, N. L., & Mauer, B. A. (1998). Parallel short Naming Test. Aphasiology, 16, 635645.
forms for the Boston Naming Test: Psychometric properties and Saxton, J., Ratcliff, G., Munro, C. A., Coffery, C. E., Becker, J. E., Fried, L., B
norms for older adults. Journal of Clinical and Experimental Neuro- & Kuller, L. (2000). Normative data on the Boston Naming Test and
psychology, 20, 828834. two equivalent 30-item short-forms. The Clinical Neuropsychologist,
Goodglass, H., Kaplan, E., & Barresi, B. (2000). The assessment of aphasia 14, 526534.
and related disorders (3rd ed.). Philadelphia: Lea & Febiger. Schefft, B. K., Testa, S. M., Dualy, M. F., Privitera, M. D., & Yeh, H. S.
Graves, R. E., Bezeau, S. C., Fogarty, J., & Blair, R. (2004). Boston Naming (2003). Preoperative assessment of confrontation naming ability and
Test Short Forms: A comparison of previous forms with new item intrictal paraphasia production in unilateral temporal lobe epilepsy.
response theory based forms. Journal of Clinical and Experimental Epilepsy and Behavior, 4, 161168.
Neuropsychology, 26, 891902. Steinberg, B. A., Beiliauskas, L. A., Smith, G. E., Langellotti, C., & Ivnik,
Heaton, R. K., Miller, S. W., Taylor, M. J., & Grant, I. (2004). Revised R. J. (2005). MAYOs Older Americans Normative Studies: Age- and
comprehensive norms for an expanded Halstead Reitan Battery: De- IQ-adjusted norms for the Boston Naming Test, the MAE Token
mographically adjusted neuropsychological norms for African Ameri- Test, and the Judgment of Line Orientation Test. The Clinical Neu-
can and Caucasian adults, Lutz, FL: PAR. ropsychologist, 19, 280328.
Henderson, L. W., Frank, E. W., Pigatt, T., Abramson, R. K., & Houston, Storms, G., Saerens, J., & De Deyn, P. P. (2004). Normative data for the
M. (1998). Race, gender and educational level effects on Boston Boston Naming Test in native Dutch-speaking Belgian children and
Naming Test scores. Aphasiology, 12, 901911. the relation with intelligence. Brain and Language, 91, 274281.
Ivnik, R. J., Malec, J. F., Smith, G. E., Tangalos, E. G., & Peterson, R. C. Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A compendium of
(1996). Neuropsychological test norms above age 55: COWAT, BNT, neuropsyschological tests: Administration, norms, and commentary
MAE Token, WRAT-R Reading, AMNART, Stroop, TMT, and JLO. (3rd ed. pp. 901915). New York: Oxford University Press.
The Clinical neuropsychologist, 10, 262278. Teng, E. L., Wimer, C., Roberts, E., Damasio, A. R., Eslinger, P. J.,
Kaplan, E., Goodglass, H., & Weintrab, S. (1983). The Boston naming Folstein, M. F., Tune, L. E., Whitehouse, P. J., Bardolph, E. L.,
test. Philadelphia: Lea & Febiger. Hui, H. C., & Henderson, V. W. (1989). Alzheimers dementia:
Killgore, W. D. S., & Adams, R. L. (1999). Prediction of Boston Naming Performance on parallel forms of the Dementia Assessment Battery.
Test performance form vocabulary scores: Preliminary guidelines for Journal of Clinical and Experimental Neuropsychology, 11, 899912.
interpretation. Perceptual and Motor Skills, 89, 327337. Tombaugh, T. N., & Hubley, A. (1997). The 60-item Boston Naming Test:
Lansing, A. E., Ivnik, R. J., Cullum, C. M., & Randolph, C. (1999). An Norms for cognitively intact adults aged 25 to 88 years. Journal of
empirically derived short form of the Boston Naming Test. Archives Clinical and Experimental Neuropsychology, 19, 922932.
of Clinical Neuropsychology, 14, 481487. Van Gorp, W., Satz, P., Kiersch, M., & Henry, R. (1986). Normative data
Lucas, J. A., Ivnik, R. J., Smith, G. E., Ferman, T. J., Willis, F. B., Petersen, on the Boston naming test for a group of normal older adults.
R. C., 7 Graff-Radford, N. R. (2005). Mayos Older African Amer- Journal of Clinical and Experimental Neuropsychology, 8, 702705.
icans Normative Studies: Norms for Boston Naming Test, Controlled Welch, L. W., Doineau, D., Johnson, S., & King, D. (2002). Educational
Oral Word Association, Category Fluency, Animal naming, Token and gender normative data for the Boston naming test in a group of
Test, WRAT-3 Reading, Trail Making Test, Stroop Test, and Judgment older adults. Brain and Language, 53(2), 260266.
of line Orientation. The Clinical Neuropsychologist, 19, 243269. Williams, B. W., Mack, W., & Henderson, V. W. (1989). Boston naming
Mack, W. J., Freed, D. M., Williams, B. W., & Henderson, V. W. (1992). test in Alzheimers disease. Neuropsychologiea, 27, 10731079.
Boston Naming Test: Shortened version for use in Alzheimers dis-
ease. Journal of Gerontology, 47, 164168.
MacKay, A., Connor, L. T., & Henderson, V. W. (2005). Dementia does
not explain correlation between age and scores on Boston Naming
Test. Archives of Clinical Neuropsychology, 20, 129133.
Boston Process Approach
Mitrushina, M., & Satz, P. (1995). Repeated testing of normal elderly with
the Boston Naming Test. Aging Clinical and Experimental Research, S HAHAL R OZENBLATT
7, 123127. Advanced Psychological Assessment, P.C.
Mitrushina, M. M., Boone, K. B., Razani, J., & DElia, L. F. (2005).
Smithtown, NY, USA
Handbook of normative data for neuropsychological assessment
(2nd ed.). New York: Oxford University Press.
Neils, J., Baris, J. M., Carter, C., Dellaira, A. L., Nordloh, S. H., & Weiler, E.
(1995). Effects of age, education, and living environment on Boston Synonyms
naming test performance. Journal of Speech and Hearing Research,
38, 11431149.
BPA
Nicholas, L. E., Brookshire, R. H., MacLennan, D. L., Schumacher, J. G.,
& Porrazzo, S. A. (1988). The Boston naming test: Revised adminis-
tration and scoring procedures and normative information for non-
brain-damaged adults. Clinical Aphasiology, 18, 103115.
Description
Randolph, C., Lansing, A., Ivnick, R. J., Cullum, C. M., & Hermann, B. P.
(1999). Determinants of confrontation naming performance. Born out of the work of A. R. Luria (e.g., Higher Cortical
Archives of Clinical Neuropsychology, 14, 489496. Function in Man, 1966), the Boston Process Approach
434 B BPA
(BPA) to neuropsychological assessment is a method of provides a number of standard scores, enabling compar-
exploring the patients approach to a task and the process isons with a normative sample. In addition, they provide
involved in attaining a specific test score (Loring, 1999). the clinician with a way of understanding the patients
Its aim is to provide a more accurate characterization of approach to the task. For example, on the CVLT-II, wheth-
neuropsychological function and dysfunction and the er the examinee makes use of semantic categories (e.g.,
nervous system components involved than is achieved types of animals) to aid in recall of the word list is consid-
with a purely psychometric approach (Kaplan, 1988; ered and quantified.
Strauss, Sherman, & Spreen, 2006). Despite the growing popularity of the BPA, there
have been criticisms. As outlined by Strauss et al. (2006),
criticisms of the approach include insufficient norms, lim-
Current Knowledge ited information about reliability and validity, and pro-
blems with readministration due to nonstandard initial
According to Edith Kaplan (1988, 1990), the achieve- administration.
ment oriented approach to assessment is flawed, in that
it assumes that the scores obtained are reflective of an
underlying unitary mechanism. As an example, two indi-
viduals could arrive at a similar score via distinctly differ- Cross References
ent processes that are dependent on distinctly different
neural structures and/or pathways. The inherent loss of Hypothesis Testing Approach
data that occurs by focusing on composite or total scores
resulted in the development of an approach that focused
on how a specific result was obtained. This avenue of
investigation led to the Boston Process Approach (BPA). References and Readings
In addition to careful observation of the strategies used
during the completion of a task, the BPA emphasizes the Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (2000). California
importance of demographic variables (e.g., age, gender, verbal learning test. Adult version manual (2nd ed.). San Antonio,
socioeconomic status, education, and occupational TX: The Psychological Corporation.
status), medical history, and mental health history, be- Kaplan, E. (1988). A process approach to neuropsychological assessment.
In T. Boll, & B. K. Bryant (Eds.), Clinical neuropsychology and brain
cause each of these variables can influence a patients
function: Research, measurement, and practice. Washington, DC:
performance. American Psychological Association.
The BPA differs from the fixed and flexible battery Kaplan, E. (1990). The process approach to neuropsychological assess-
approaches to testing in that the final score is deempha- ment of psychiatric patients. Journal of Neuropsychiatry, 2, 7287.
sized; that is, whether a response is right or wrong is less Loring, D. W. (1999). INS dictionary of neuropsychology. New York:
important than how it was attained (Kaplan, 1990). In
Luria, A. R. (1966). Higher cortical function in man. New York: Basic
addition, the test may be administered differently from the Books.
standardized approach, and additional measures may be Milberg, W. P., Hebben, N., & Kaplan, E. (1986). The Boston process
introduced to better understand the component processes approach. In I. Grant, & K. M. Adams (Eds.), Neuropsychological
that influence or are involved in the performance of a assessment of neuropsychiatric disorders. New York: Oxford
University Press.
particular task. Modified materials may also be used to
gain a better understanding of the errors or unusual neuropsychological tests: Administration, norms, and commentary
approaches that were noted on a task (Milberg, Hebben, (3rd ed.). New York: Oxford University Press.
Kaplan, 1986). Wechsler, D., Kaplan, E., Fein, D., Kramer, J., Morris, R., et al. (2004).
Although right or wrong answers are deemphasized in Wechsler intelligence scale for children integrated (4th ed.). San Antonio,
TX: Harcourt Assessment.
the BPA, it is essential for the qualitative observations to
be quantifiable and subjected to statistical analyses
(Kaplan, 1990). This approach contributed to the devel-
opment of a wide variety of measures including the
Wechsler Intelligence Scale for Children, 4th Edition
Integrated (Wechsler, Kaplan, Kramer, Morris, 2004) BPA
and California Verbal Learning Test, 2nd Edition (Delis,
Kramer, Kaplan, & Ober, 2000). Each of these measures Boston Process Approach
Brain Abscesses B 435
BPRS Bradykinesia
Brief Psychiatric Rating Scale A NNA D E P OLD H OHLER 1, M ARCUS P ONCE DE LEON2 B
1
Boston, MA, USA
2
Brachytherapy El Paso, TX, USA
B RAM G OLDSTEIN
Hoag Hospital Cancer Center Definition
Newport Beach, CA, USA
Bradykinesia is a slowness of movement. It is often seen
in parkinsonian individuals and is a cardinal feature of
Synonyms Parkinsons disease. It can be seen in movements of small
muscles when an individual is asked to rapidly open and
Internal radiation therapy close a hand, tap a finger, or move an arm back and forth
to grab an object. It can involve any limb in isolation, such
as decreased arm swing during gait evaluation, or the
Definition entire body at once, evident in the abnormal stillness of
a patient with Parkinsons disease. It may fluctuate during
Brachytherapy is a form of radiation therapy, and the day depending on fatigue and medication levels in the
often indicated for the treatment of specific, recurrent case of Parkinsons disease.
brain tumors and head or neck cancers. The procedure
involves the placement of radioactive (e.g., iridium-192,
palladium-103, or iodine-125) seeds inside or adjacent to
Cross References
a targeted lesion. The primary advantage of brachythera-
py is that the treatment allows for a higher radioactive
Parkinsons Disease
dose to be delivered to the tumor bed without damaging
the surrounding, healthy brain tissue (Sneed, Prados,
Phillips, Weaver, & Wara, 1992). In particular, High
Dose Rate brachytherapy utilizes catheters to mitigate References and Readings
exposure and accelerate the treatment time. Intracavitary
brachytherapy is another subtype that involves the use of Fahn, S., & Jankovic, J. (Eds.). (2007). Parkinsonism: Clinical features and
a balloon catheter which delivers localized radiation diagnosis. In Movement disorders (pp. 79100). Philadelphia:
Churchill Livingstone Elsevier.
therapy to the affected area. Following the completion of
radiotherapy, the radiation source and balloon catheter
are then removed. Brachytherapy is a safe procedure,
although reported side effects include infection, seizures,
and headaches. Brain Abscesses
M ICHAEL R. V ILLANUEVA , S USAN K. J OHNSON
Cross References University of North Carolina-Charlotte
Charlotte, NC, USA
Radiation Therapy

Brain abscesses are an intracranial mass of immune cells,
Sneed, P. K., Gutin, P. H., Prados, M. D., Phillips, T. L., Weaver, K. A.,
Wara, W. M., et al. (1992). Brachytherapy of brain tumors. Stereo- pus (i.e., collection of dead neutrophils), and other mate-
tactic and Functional Neurosurgery, 59, 157165. rials stemming from a bacterial or fungal infection.
436 B Brain Arteriovenous Malformation
Current Knowledge Treatment
Etiology Brain abscesses are treated as medical emergencies and

may require hospitalization. If the infectious agent is
Brain abscesses may arise by direct infection of organisms, bacterial in nature, antibiotics are usually the treatment
local extension from adjacent focal areas, or distribution of choice. However, if the infection is determined to be
by way of the bloodstream. Moreover, they form as an of fungal origin, then antifungal medications may be
inflammatory response to bacteria or fungal infections prescribed. Surgery is usually indicated if intracranial
within the brain. This inflammatory response leads to a pressure continues to increase, medications fail to reduce
localization of infected brain cells, immune cells, and the size of the abscesses, or the abscesses are at risk
microorganisms within an area of the brain (Kumar, of rupture (www.nlm.nih.gov/medlineplus/ency/article/
Abbas, & Fausto, 2004). This area becomes encapsulated 000783.htm).
by an abscess wall, which is formed by adjacent cells to
prevent further infection of neighboring structures. This
results in the formation of an encapsulated, purulent
(pus-filled) mass within the brain. While this inflamma- Cross References
tory response can serve to protect the brain from further
injury, it can also have significant negative consequences. Brain Swelling
If the abscess ruptures, it can lead to inflammation of Cyst
the ventricles (i.e., fluid-filled cavities containing cerebral Inflammation
spinal fluid) within the brain in addition to inflammation
of the meninges (i.e., membranes that surround the brain
and spinal cord). If the brain begins to swell, the mass References and Readings
may raise intracranial pressure and promote progressive
herniation within the brain, which can be fatal (Kumar Kumar, V., Abbas, A., & Fausto, N. (2004). Robbins and Cotran patha-
et al., 2004). logic basis of disease (7th ed.). Philadelphia, PA: W.B. Saunders
Company.
See also http://www.nlm.nih.gov/medlineplus/ency/article/000783.htm.
Symptoms
Clinically, cerebral abscesses can be devastating and often

lead to an increase in intracranial pressure and localized
deficits (Kumar et al., 2004). Additionally, symptoms
Brain Arteriovenous
associated with brain abscesses can develop slowly (i.e., Malformation
within a 2-week period) or suddenly. A nonexhaustive list
of symptoms may include the following: headaches, gait Arteriovenous Malformation (AVM)
disturbances, disequilibrium, changes in mental status,
vomiting, and stiffness/aching of the neck, shoulders, or
back.
Brain Attack
Prognosis
Stroke
If brain abscesses are left untreated, death is the most
likely outcome. On the other hand, treatment can signifi-
cantly reduce the mortality rate to about 10 percent.
Earlier treatment predicts a better outcome, although
long-term neurological deficits may persist despite all Brain Commissures
intervention approaches (Kumar et al., 2004 and http://
www.nlm.nih.gov/medlineplus/ency/article/000783.htm). Commissures, Cerebral
Brain Death B 437
make the diagnosis; however, in some states, a specialist in

Brain Death the field of neuroscience is required to make the assess-
ment. Certain criteria should be met before a diagnosis of B
T IFFANY L. P OWELL brain death is considered in order to determine the pres-
Virginia Commonwealth University ence of unequivocal neurologic devastation. These in-
Richmond, VA, USA clude interpreting relevant imaging studies and
excluding the presence of conscious altering drugs.
(Table 1, Wijdicks, 2000).
Synonyms When the assessment for neurologic devastation is
complete, a focused and methodical clinical examination
Death should follow with emphasis on the documentation of
coma, absence of brainstem reflexes, and demonstration
of apnea following maximal stimulation of respiratory
Definition centers (Table 2).
In some instances, the clinical determination of brain
Brain death is the irreversible loss of all brain function. death is not possible because of a patients extreme hemo-
Including the lack of capacity for consciousness and dynamic or respiratory instability. In these cases, certain
respirations (Presidents Commission for the Study of confirmatory testing can be completed to make the
Ethical Problems in Medicine, 1981). Brain death is diagnosis. These often include cerebral angiography,
equivalent to traditional circulatory death, which is de- transcranial doppler, electroencephalography (EEG), or
fined by cessation of tissue perfusion and the absence of
pulses. However, with brain death the heart will continue
to beat and spinal cord reflexes may persist for a short Brain Death. Table 1 Assessment of Neurologic Devastation
time (Canadian Neurocritical Care Group, 1999).
Clinical or radiographic evidence of catastrophic and
irreversible brain injury
Exclusion of drug intoxication, sedatives, or paralytic
Current Knowledge agents
Correction of severe electrolyte, acid-base, or endocrine
History of the Definition of Brain Death disturbances
Core body temperature >32 C
In 1959, Mollaret and Goulon first introduced the term
coma depasse (beyond coma) to describe irreversible brain
damage (Mollaret & Goulon, 1959). The modern scie-
ntific concept of brain death is largely based on this
original description of 23 comatose patients who exhib- Brain Death. Table 2 Clinical criteria for brain death
ited loss of brainstem reflexes, respirations, and flat ele-
1. Coma, profound state of unconsciousness
ctroencephalograms (EEG). Several years later, the
Harvard ad hoc committee formalized the definition of 2. Pupils fixed at midposition and dilated
brain death using neurological criteria and published 3. Absence of papillary response to light
their landmark article in 1968. These publications helped 4. Absence of pupil movement with head manipulation or
to define current practice guidelines, now widely accepted injection of cold water into the EAC (external auditory
by clinicians, involved in the diagnosis of brain death. canal)
5. Absence of motor response
6. Absence of corneal and gag reflexes
Criteria for the Diagnosis of Brain Death 7. Absence of coughing in response to tracheal suctioning
in Adults 8. Absence of respiratory drive at Paco2 60mmHg or
20mmHg above patients baselinea
The determination of brain death is largely a clinical a
Paco2 is the partial pressure of arterial carbon dioxide
diagnosis. Any experienced physician should be able to Reprinted from Wijdicks (2001) with permission
438 B Brain Disease
nuclear imaging. These tests are not required for the

standard diagnosis of adult brain death. Brain Injury Association of
America
T HOMAS R. WODUSHEK 1, M ICHAEL R. G REHER 2
References and Readings 1
Center for Neurorehabilitation Services, PC
Fort Collins, CO, USA
Ad Hoc Committee of the Harvard Medical School. (1968). A definition 2
National Jewish Health & University of Colorado
of irreversible coma. Report of the Ad Hoc Committee of the Denver School of Medicine
Harvard medical school to examine the definition of brain death.
Journal of the American Medical Association, 205, 337340.
Denver, CO, USA
Canadian Neurocritical Care Group. (1999). Guidelines for the diagnosis
of death. Canadian Journal of Neurological Sciences, 26, 6466.
Mollaret, P., Goulon, M. (1959). Le coma depasse. Revue Neurologique, Synonyms
101, 315.
Presidents Commission for the Study of Ethical Problems in Medicine.
(1981). Guidelines for the determination of death. Journal of the
BIAA
American Medical Association, 246, 21842186.
Wijdicks, E. F. (2000). Brain death. Philadelphia: Lippincott Williams &
Wilkins.
Wijdicks, E. F. (2001). The Diagnosis of Brain Death. New England
Membership
Journal of Medicine, 344, 12151221.
The Brain Injury Association of America (BIAA) consists
of more than 40 state affiliates as well as hundreds of local
chapters and support groups. A portion of the individuals
involved at these various levels subscribe to the national
mailing list which includes the names of approximately
Brain Disease 19,000 individuals. Approximately two-thirds of the list
are traumatic brain injury (TBI) survivors and their fam-
Encephalopathy
ily members while the remaining represent a wide variety
of professional providers and researchers (G. Ayotte, per-
sonal communication, November, 2008).
Brain Hemorrhage Major Areas or Mission Statement

Hemorrhagic Stroke
BIAA Mission Statement: Creating a better future
through brain injury prevention, research, education,
and advocacy.
Brain Imaging Landmark Contributions

Neuroimaging The BIAA, formerly the National Head Injury Founda-
tion, was founded in 1980 by Marilyn and Marty Spivack
and other family members of brain injury survivors.
Among BIAAs landmark contributions was its success in
securing Congressional approval of the 1996 Traumatic
Brain Injury Brain Injury Act (PL 104166), later re-authorized as Title
XIII of the Childrens Health Act of 2000 (PL 106310),
Head Injury and most recently as the S. 793 TBI Act of 2008. The
Penetrating TBI original bill created the Federal TBI program to address
Traumatic Brain Injury (TBI) the struggles of many persons with TBI in gaining access
Brain Injury Association of America B 439
to appropriate community-based care. It is the only states to plan reforms in treatment, transportation,
Federal law that addresses the millions of Americans housing, education, and social support, in order to inte-
who suffer permanent disability as a result of traumatic grate brain injury survivors (among others) into the least B
brain injury. The law allowed the Health Resources and restrictive setting possible. To aid state agencies working
Services Administration (HRSA) to develop a grant toward compliance, the BIAA partnered with Indepen-
program for states to aid in the treatment of persons dent Living Research Utilization to provide regional train-
with TBI. The bill authorized appropriations to the Na- ing workshops regarding the content of the Olmstead
tional Institutes of Health (NIH) for TBI research and to decision, its intended effect, and potential strategies to
the Centers for Disease Control and Prevention (CDC) meet the community needs of individuals with cognitive
for a public information campaign regarding the conse- disabilities who might otherwise be wrongly placed in
quences and prevention of brain injury. The ability to institutional settings.
achieve successive appropriation bills has been due in The BIAA in coordination with the Brain Trauma
part to the work of the BIAA and others to persuade Foundation, the American Association of Neurological
approximately 100 members of Congress to join the Surgeons, and other professional contributors, developed
Congressional Brain Injury Task Force. The task force was and published Guidelines for the Management of Severe
established in 2001 to provide guidance to Congress and Brain Injury (2000). The BIAA was also involved in
other federal agencies regarding policies relevant to the care authoring Management and Prognosis of Penetrating
and treatment of those with traumatic brain injury. Brain Injury (Aarabi et al. 2001). These publications
In 1992, the BIAA was integral in shaping the Defense were created to provide up-to-date, evidence-based
and Veterans Head Injury Program, later renamed the guidelines and protocols to improve the outcome of TBI
Defense and Veterans Brain Injury Center (DVBIC). patients.
This organizations mission is to develop and provide As part of its ongoing legislation efforts to increase
advanced TBI evaluation and treatment for veterans as private insurance, Medicare, and TriCare coverage for
well as active duty military personnel and their depen- cognitive rehabilitation, the BIAA published Cognitive
dents. The program has lead to the development of six Rehabilitation: The Evidence, Funding, and Case for
additional Department of Defense and Veterans Affairs Advocacy of Brain Injury (Katz, Ashley, OShanick, and
treatment sites that offer specialized care for military Connors, 2006), which included ten recommendations to
survivors of brain injury. The DVBIC includes a number increase access and delivery of cognitive rehabilitation
of collaborating partners to provide medical care, clinical services across the nation.
research, and brain-injury education. It was named the In 1996, the BIAA founded the American Academy for
TBI operational component of the recently established the Certification of Brain Injury Specialists (AACBIS)
Defense Centers of Excellence for Psychological Health which to date has certified 2,800 members. The mission
and Traumatic Brain Injury. of AACBIS is to improve the care provided to individuals
In 1999, the US Supreme Court decided the case of with brain injury through enhanced education and train-
L.C. & E.W. vs. Olmstead. Justice Ruth Bader Ginsburg ing of their health care providers. Training is provided by
delivered the opinion of the Court, holding that under volunteers and based primarily upon The Essential Brain
Title II of the Americans with Disabilities Act states are Injury Guide (American Academy for the Certification of
required to place persons with mental disabilities in Brain Injury Specialists, 2007), which was also published
community settings rather than in institutions when the by the BIAA. Certification is granted to those with appro-
States treatment professionals have determined that com- priate work experience who have successfully completed
munity placement is appropriate, the transfer from the training and written examination.
institutional care to a less restrictive setting is not opposed
by the affected individual, and the placement can be
reasonably accommodated, taking into account the Major Activities
resources available to the State and the needs of others
with mental disabilities. Although the case was not spe- The BIAA has demonstrated a long-term commitment to
cific to brain-injury survivors, the ruling allowed the shaping public policy and partnering with governmental
BIAA and others to advocate for these individuals, many agencies. It has repeatedly worked to preserve and expand
of whom had been inappropriately placed in psychiatric rehabilitation options for persons with brain injury,
hospitals or other institutional settings that were not particularly Medicare and Medicaid beneficiaries. It has
designed for their unique needs. The ruling tasked the worked to secure federal funding for research and public
440 B Brain Plasticity
education. The BIAA remains active in disability advocacy Defense and Veterans Brain Injury Center. (n.d.). Defense and veterans
brain injury center: Home of defense and veterans head injury
and has provided consultation and assistance in develop-
program. Retrieved December 20, 2008, from http://www.dvbic.org
ing numerous legislative proposals that benefit those who Katz, D. I., Ashley, M. J., OShanick, G. J., & Connors, S. H. (2006).
have sustained brain injury. Encouraging private/public Cognitive rehabilitation: The evidence, funding, and case for advocacy
partnerships, particularly in the care of military service- of brain injury. McLean, VA: Brain Injury Association of America.
related brain injury, has been a crucial area of interven-
tion. Public policy initiatives that enhanced trauma care,
child abuse prevention, transportation safety, education,
and respite care were among the associations 2007 Brain Plasticity
accomplishments (G. Ayotte, personal communication,
November, 2008) J ENNIFER S UE K LEINER
The BIAA views brain injury prevention and aware- University of Arkansas for Medical Sciences
ness as a primary component of its mission. The associa- Little Rock, AR, USA
tion has distributed information kits, produced public
service announcements, and provided access to subject
matter experts for a number of media outlets. The BIAA Definition
also publishes TBI Challenge!, a quarterly newsletter with
a distribution that includes 25,000 households. The BIAA Plasticity refers to the brains ability to change its struc-
hosts/co-hosts a number of educational meetings and ture in response to development, the environment, or
conferences, maintains a comprehensive website, and injury.
publishes the National Directory of Brain Injury Rehabil-
itation Services to provide survivors and/or family mem- Current Knowledge
bers with helpful information about services in their
community. On an annual basis the BIAA responds to Brain plasticity, or neuroplasticity, refers to the brains
over 100,000 requests for assistance through either its ability to change in response to development, to the
national information call center or its website. Each environment (including learning), and in response to
March the BIAA circulates 10,000 information kits to injury or aging. While it was once conceptualized that
mark Brain Injury Awareness Month. once the brain ceases development, that it would then be
resistant to change, or in effect be static. Research over the
last several decades has demonstrated that the brain con-
Cross References tinues to be capable of change, or restructuring, through-
out the life span. While much research with respect to
Traumatic Brain Injury brain plasticity focuses on outcomes following injury,
brain plasticity also refers to developmental changes that
occur in the brain throughout the life span, including
References and Readings synaptic changes that occur in response to the acquisition
of new learning and memories. As such, plasticity is seen
Aarabi, B., Alden, T. D., Chestnut, R. M., Downs J. H., Ecklund, J. M.,
as an intrinsic property of the central nervous system in
Eisenberg, H. M., et al. (2001). Management and prognosis of
penetrating brain injury. Journal of Trauma, Injury, Infection and
that the brain is constantly restructuring and reorganizing
Critical Care, 51, S1S86. in response to new learning. Specifically, studies of
American Academy for the Certification of Brain Injury Specialists learning new behaviors, such as learning Braille, result in
(2007). The essential brain injury guide (4th ed.). McLean, VA: the rapid, but transient onset of cortical enlargement that
Brain Injury Association of America.
gives way to a more stable but less dramatic cortical
Brain Injury Association of America. (n.d.). Brain injury association USA
home page. Retrieved December 20, 2008, from http://www.biausa.
enlargement associated with plasticity.
org Research has demonstrated that a variety of factors
Brain Injury Association of America (2005). Academy of certified brain affect plasticity of neural reorganization and proliferation.
injury specialists (ACBIS). Retrieved December 20, 2008, from http:// One such environment includes the richness of the envi-
www.aacbis.net/index.html
ronment in which an organism is grown. Specifically,
Brain Trauma Foundation, American Association of Neurological
Surgeons, Joint Section on Neurotrauma and Critical Care (2000).
organisms that grow in a richly stimulating environment
Guidelines for the management of severe traumatic brain injury. in which a variety of experiences are encountered have
Journal of Neurotrauma, 17, 451627. greater plasticity than individuals who are reared in less-
Brain Reserve B 441
stimulating environments. Empirical experimentation in loss of a large area of the brain. The learning of alternative
humans and animals alike have demonstrated that the communication techniques, such as Braille, requires the
dendrite length as well as the density of synapses in adaptation of new behavior; research has demonstrated B
organisms with enriched motor and sensory environ- that individuals who have learned Braille have larger
ments surpass those raised in less-stimulating environ- sensory maps related to the finger pad used in reading
ments. However, these differences appear only to exist as compared to the contralateral equivalent or as com-
with early learning environments, as adolescents and pared to individuals who do not read Braille. Further-
adults show no such sensitivity to environmental factors. more, not only do blind individuals develop enlarged
Both gender and hormone differences also appear to play corresponding sensory maps, it has also been demon-
a role in neural plasticity, with specific respect to cortical strated that the occipital, or visual, cortex is subsequently
areas; for example, while males are more sensitive to recruited for tactile information processing, as well as
experience related to the visual cortex, females are more auditory information processing.
sensitive to development in the hippocampal area. The advancement of technology has furthered our
However, the concept of brain plasticity may be best understanding of the existence of, and mechanisms be-
understood by examining the processes by which the hind, neuroplasticity. The ability to specify and character-
brain changes in response to injury. Responses to injury ize brain function via visualization of glucose and oxygen
may result in the loss of a previously held behavior, release metabolism has allowed for exploration of mechanisms of
of a previously suppressed behavior, the assumption of a plasticity. Processes of functional neuroimaging, includ-
function by a neighboring neuronal network, or the de- ing positron emission tomography as well as functional
velopment of new behaviors (which may be adaptive or magnetic resonance imaging allows for indirect visualiza-
maladaptive). Physiologically, reorganization can occur tion of synaptic activity; experimentation involving tasks
by changing the balance between excitatory and inhibito- being performed while the brain is being imaged allows
ry synaptic and membrane responses as well as by for examination of synaptic changes. Magnetic resonance
strengthening or weakening synaptic connections. Brain spectroscopy is thought to be a promising technique that
plasticity can also involve the growth of new dendrites and allows for analysis of the connection between neurochem-
axons to form new synaptic connections. Research sug- ical changes and behaviors. Electroencephalography and
gests that the age of onset of the injury is critical in the magnetoencephalography allows to direct measurement
development of new connections, as long connections are of neuronal activity; however, it lacks structural specifici-
more difficult to form in the mature brain, whereas the ty. Transcranial magnetic stimulation also allows for di-
young brain may be more capable of forming long con- rect analysis of neural activity by temporarily suppressing
nections due to the existence of excess connectivity. brain regions, allowing for direct assessment of brain-
Changes in connectivity can occur through the strength- behavior relationships in conjunction with functional
ening or weakening of synaptic density or the rearrange- neuroimaging techniques.
ment of synaptic connections. While the concept of
neuroplasticity does at times result in recovery of adaptive References and Readings
behavioral changes, plasticity may also lead to unmasking
of previous suppressed and maladaptive behaviors as well Galaburda, A., & Pascual-Leone, A. (2003). Mechanisms of plasticity and
as the development of dysfunctional behaviors. behavior. In T. E. Feinberg & M. J. Farah (Eds.), Behavioral neurology
Brain plasticity may occur via multiple difference & neuropsychology (2nd ed., pp. 5770). New York, NY: McGraw-
Hill.
mechanisms. Perhaps the most common, and best under-
Kolb, B. (1995). Brain plasticity and behavior. Mahwah, NJ: Erlbaum.
stood, mechanism includes the expansion of a specified Kolb, B., Gibb, R., & Robinson, T. E. (2003). Brain plasticity and behavior.
area of circuitry or the recruitment of either a local or Current Directions in Psychological Science, 12(1), 15.
distal area of circuitry. Such reorganization of function is Kolb, B., & Whishaw, I. Q. (1998). Brain plasticity and behavior. Annual
a common post-injury response and occurs shortly fol- Review of Psychiatry, 49, 4364.
Nelson, C. A., & Luciana, M. (2001). Handbook of developmental cognitive
lowing the injury and continues to develop years follow-
neuroscience. Boston, MA: Massachusetts Institute of Technology.
ing the injury as the organism adapts. Remodeling or
reorganization occurs both at the cortical and subcortical
level, and can occur both within and between functional
modalities. For example, much literature exists examining Brain Reserve
the reorganization of neuronal circuitry in response to
blindness. Early onset blindness results in the functional Cognitive Reserve
442 B Brain Reserve Capacity
Current Knowledge
Brain Reserve Capacity
Research consistently demonstrates that the underlying
G LEN E. G ETZ neuropathology is not consistent with behavioral distur-
Allegheny General Hospital bance caused by dementia. Brain reserve capacity partially
Pittsburgh, PA, USA explains this phenomenon. It appears that symptomatic
behaviors are less likely to be prevalent in individuals
with greater brain reserve capacity. Research has also
Synonyms consistently found that cognitive reserve capacity, that is
the lifestyle approaches that encourage cognitive activity,
Global reserve; Reserve plays an important role in functional ability despite neu-
ropathological changes. It appears plausible that brain
reserve capacity, such as increased amount of neurons
Definition and neuronal connections, is at least in part due to beha-
viors that encourage cognitive reserve capacity, such as
Brain reserve capacity is the brains resilience to patho- education and occupation. The interplay of cognitive
logical damage or changes. The greater the brain reserve activity and brain reserve capacity is being carefully
capacity, the less likely an individual will demonstrate studied in an attempt to understand the relationship.
behavioral disturbance associated with a disease.
Future Directions
Historical Background Identifying factors that increase the likelihood of brain
reserve capacity has the possibility of being an invaluable
Research has attempted to understand the role of various tool toward improving the quality of elderly peoples
factors involved in cognitive decline. Frequent central lives and potentially reducing the risk of developing
nervous system disorders occur in the elderly, which Alzheimers disease. The National Institute of Aging and
increase the likelihood of cognitive decline. Age, in itself, other federally funded programs have invested millions of
is a factor known to alter cognitive functioning. Brain dollars to better understand the factors in improving
reserve capacity is the brains ability to effectively manage brain reserve capacity. Studies will continue to better
the increasing changes in normal aging and to cope understand factors that increase brain cells, synaptic
with pathological damage. connections, and other neurophysiological markers.
Post-mortem examination of elderly individuals The implementation and advancement of technology
provides evidence that that there is a discrepancy between will assist in providing a clearer understanding of these
the clinical manifestation of Alzheimers disease and the factors as well.
neuropathology of the disorder (Katzman et al., 1998).
Specifically, this early study found that a subset of
individuals whose brains were found to have a high
degree of pathology associated with Alzheimers disease
Cross References
did demonstrate minimal clinical symptoms associated
Alzheimers Disease
with the disease. Interestingly, the results from this study
Cognitive Reserve
suggested that the weight of the brains in this subset of
patients was higher. These patients were also found to
have more neurons. It was subsequently concluded that
perhaps these patients larger brains and their possession References and Readings
of more neurons were protective against dementia symp-
toms. While subsequent studies have been inconclusive, Katzman, R., Terry, R., DeTeresa, R., Brown, T., Davies, P., Fuld, P., et al.
many studies have suggested that head circumference, (1988). Clinical, pathological and neurochemical changes in demen-
tia: a subgroup with preserved mental status and numerous neocor-
brain volume, intracranial volume, and genetic influ-
tical plaques. Annals of Neurology, 23, 138144.
ences also play an important role in brain reserve Stern, Y. (2006). Cognitive Reserve, Theory and Application. Series Editor
capacity. L. Bieliauskas. New York, NY: Psychology Press.
Brain Tumor B 443
hypothermia, and using an electronic intracranial pressure

Brain Storming monitor with a valve to adjust pressure over time.
Hemodynamic Response B
Cross References
Edema
Intracranial Pressure
Brain Swelling
B ETH R USH
Mayo Clinic Marmarou, A. (2007). A review of progress in understanding the
Jacksonville, FL, USA pathophysiology and treatment of brain edema. Neurosurgery
Focus, 22, E1.
Definition
Brain Tumor
Expansion of the size of the brain that occurs following
head trauma and brain injury. E THAN M OITRA
Drexel University
Current Knowledge
Together with brain edema, brain swelling can elevate Definition

intracranial pressure. Once intracranial pressure is elevat-
ed, oxygen, glucose, and blood have difficulty reaching all An abnormal mass of tissue in which some cells (glial or
portions of the brain. Blood vessels are no longer efficient non-glial) grow and multiply uncontrollably. A tumor can
in carrying blood, oxygen, and nutrients throughout the be benign or malignant. It is associated with damage or
brain. As a consequence, increased intracranial pressure mutation to the TP53 gene on human chromosome 17.
complicates the degree of brain injury and also the brains P53 regulates the cell cycle and functions in tumor sup-
natural response to trauma. pression. A tumor can cause damage by increasing pres-
Brain swelling can occur in 1520% of severe brain sure in the brain, by shifting the brain or pushing against
injuries. The exact mechanism that leads to brain swelling the skull, and by invading and damaging nerves and
is poorly understood, but once trauma is sustained, the healthy brain tissue. Some tumors may be truly indolent
brain tissue swells to compress harder and harder against in their growth, growing so slowly that they are present for
the rigid skull. Brain swelling must be managed emergently an unknown length of time because symptoms are less
following brain injury because patients experiencing brain gross and disruptive. Those that are actively growing may
swelling are at a higher risk of death. The brain may swell to be more likely to present with the following symptoms,
a point in which portions of the brain herniate through depending on tumor locus: headaches; nausea or vomit-
openings in the skull. Brain swelling may compress the ing; seizures or convulsions; difficulty in thinking,
brainstem, the area of the brain that maintains conscious- speaking, or finding words; personality changes; weakness
ness, and critical life functions, such as cardiac function or paralysis in one part or one side of the body; loss of
and respiration. Methods of managing brain swelling balance; vision changes; confusion and disorientation;
involve administering medications to constrict blood and memory loss (Levin, Leibel, & Gutin, 2001; Price,
vessels, drilling a burr hole or conducting decompressive Goetz, & Lovell, 2007).
craniotomy to relieve pressure, temporarily removing a
portion of the skull in a decompressive craniectomy to Cross References
relieve pressure (and replacing the skull fragment once
pressure is normalized), placing an external drain to relieve Astrocytoma
pressure and excess fluid from the surface of the brain, Glioma
placing the patient on artificial respirator so that carbon Neuroblastoma
dioxide does not accumulate in the brain, inducing Neurocytoma
444 B Brain with Excessive Weight
References and Readings of electrical waves generated from different anatomical

parts of the brain-ear system are plotted as summarized
Levin, V. A., Leibel, S. A., & Gutin, P. H. (2001). Neoplasms of the central below (Lew, Lee, Pan, & Chiang, 2007):
nervous system. In V. T. DeVita, S. Hellman, & S. A. Rosenberg
(Eds.), Cancer: principles and practice of oncology (pp. 21002160). Wave I: Cochlear nerve (CN VIII)
Philadelphia, PA: Lippincott, Williams, & Wilkins. Wave II: Cochlear nucleus (CN VIII)
Price, T. R. P., Goetz, K. L., & Lovell, M. R. (2007). Neuropsychiatric Wave III: Superior olivary complex
aspects of brain tumors. In S. C. Yudofsky & R. E. Hales (Eds.), The
Wave IV: Lateral lemniscus
American psychiatric publishing textbook of neuropsychiatry and be-
havioral neurosciences (5th ed., pp. 735764). Washington, DC:
Wave V: Inferior colliculus
Waveform delays may indicate an abnormality in
function along the auditory pathway. Unilateral delays
suggest a lesion to cranial nerve VIII along its pathway
or in the brainstem. BAER may be abnormal in acoustic
Brain with Excessive Weight neuroma, demyelinating disease, migraine headaches,
multiple sclerosis, brainstem tumor, brainstem stroke, or
Megalencephaly brain injury of various etiologies. Common uses of BAER
include acoustic neuroma detection, multiple sclerosis
diagnosis, and intraoperative monitoring during cere-
bellopontine angle tumor resection. Magnetic resonance
Brainstem Auditory Evoked imaging (MRI) may provide greater anatomic detail and
would be preferable for detecting a small lesion. However,
Potentials (BAEP) BAER may be particularly useful in an individual who
cannot undergo MRI.
Brainstem Auditory Evoked Responses
Current Knowledge
Brainstem Auditory Evoked BAER results are generally not affected by the effect of
Responses anesthesia and medications, or peripheral vestibular
pathology. BAER is sometimes used for prognostic
F LORA H AMMOND 1, LORI G RAFTON 2 purposes after brain injury, but its use is limited for this
1
Indiana University purpose. Complete absence of responses is considered an
Indianapolis, IN, USA ominous sign (Lew et al., 2007), and abnormal BAER may
2
Carolinas Rehabilitation confirm suspicion of brainstem injury, while normal
Charlotte, NC, USA BAER simply indicates preservation of the auditory
pathways through the brain. BAER does not reveal
information about damage that may have occurred
Synonyms elsewhere in the brain, and thus, normal BAER does not
necessarily predict good outcome (Lew et al., 2007;
Auditory brainstem responses (ABR); Auditory brainstem Zafonte, Hammond, & Peterson, 1996).
response audiometry; Auditory evoked response (AER);
Brainstem auditory evoked potentials (BAEP); BAER; Cross References
Brainstem response (BSR)
Evoked Potentials
Definition
Brainstem auditory evoked responses (BAER) test the
function of the auditory nerve and auditory pathways of Huszar, L. (2006). Clinical utility of evoked potentials. eMedicine.
the brain by measuring the electrophysiologic responses Retrieved July 9, 2007 from http://www.emedicine.com/neuro/
to repeated clicks presented to each ear. The response time topic69.htm
Brainstem Strokes B 445
Lew, H. L., Lee, E. H., Pan, S. S. L., & Chiang, J. Y. P. (2007). Electrophys- one of three anatomical locations within the brain stem.
iologic assessment techniques: evoked potentials and electroen-
Pontine brainstem gliomas are associated with the poorest
cephalography. In N. D. Zasler, D. I. Katz, R. D. Zafonte (Eds.),
Brain Injury Medicine (p. 158). New York: Demos.
prognosis for survival, while tectal and cervicomedullary B
Zafonte, R. D., Hammond, F. M., & Peterson, J. (1996). Predicting gliomas are associated with longer survival. Tectal brain-
outcome in the slow to respond traumatically brain-injured patient: stem gliomas are often associated with hydrocephalus as a
Acute and subacute parameters. NeuroRehabilitation, 6, 1932. result of compression of the fourth ventricle. Typical
manifestations of cervicomedullary tumors include dys-
phagia, unsteadiness, nasal speech, and sensory loss in the
face. Pontine brainstem gliomas are associated with cra-
nial nerve or long tract symptoms, including problems
Brainstem Glioma with the control of facial muscles, ocular movements, and
swallowing. Diffuse brainstem gliomas, once thought to
R OBERT R IDER be a single entity, are now thought to comprise a group of
Drexel University tumors with varying courses and outcomes. Brainstem
Philadelphia, PA, USA gliomas can also occur in the cervicomedullary junction,
pons, midbrain, and tectum; prognosis is worse and very
grim for diffuse brainstem gliomas. Diffuse brainstem
Synonyms gliomas do not typically enhance on MRI. They are not
responsive to radiotherapy, and treatment is usually lim-
Midbrain glioma; Pontine glioma ited to chemotherapy.

Definition
Albright, L., Pollack, I., Adelson, P., Humphreys, R., George, T., Painter, M.,
Brainstem gliomas are highly aggressive tumors of the et al. (2007). Principles and practice of pediatric neurosurgery
central nervous system occurring more frequently in (2nd ed.). New York: Thieme.
children than in adults (Fig. 1). These type of tumors Donaldson, S., Laningham, F., & Fisher, P. (2006). Advances toward an
often originate from the left side and typically involve understanding of brainstem gliomas. Journal of Clinical Oncology,
24(8), 12661272.
Brainstem Response (BSR)

Brainstem Auditory Evoked Responses
Brainstem Strokes
E LLIOT J. R OTH
Chicago, IL, USA
Definition
A stroke that is caused by ischemia or hemorrhage in the
Brainstem Glioma. Figure 1 Picture credit: Michael Phillips midbrain, pons, or medulla is called a brainstem stroke.
and Peter C. Fisher There are many brainstem stroke clinical syndromes, the
446 B Breathing Tube
presentation of each depending on the specific location in Thalamic Hemorrhage

the brain stem that is involved. Most brainstem stroke Vertebrobasilar System
syndromes result from ischemia due to partial blockage or
complete occlusion of arteries in the vertebrobasilar sys- References and Readings
tem located at the posterior region of the brain.
Chua, K., & Kong, K. (1996). Functional outcome in brain stem stroke
patients after rehabilitation. Archives of Physical Medicine and Reha-
bilitation, 77, 194197.
Current Knowledge Dauby, J-D. (1996). The diving bell and the butterfly: A memoir of life in
death. New York: Vintage.
Localization of the brainstem lesion can usually be made Nelles G., et al. (1998). Recovery following lateral medullary infarction.
by recognizing the specific pattern of clinical deficits and Neurology, 50, 14181422.
understanding the anatomical basis for these clinical
manifestations. Many of these strokes cause dysfunction
of one or more of the many cranial nerves that originate
from the brain stem. The specific clinical dysfunction, Breathing Tube
typically involving head and neck functions, localizes the
tissue injury to the side that is ipsilateral to the clinical Endotracheal Tube
deficit. Some also involve motor or sensory deficits of the
body, which localize the injury to the side that is contra-
lateral to the clinical deficit. When cerebellar signs such as BRI
ataxia and discoordination are present in association with
other brainstem findings, this localizes the lesion to the Sick Building Syndrome
ipsilateral side, and usually to the pons. When unilateral
facial and contralateral body sensory deficits exist, this
also localizes the lesion to the brain stem. Other symp-
toms, such as vertigo, double vision, nausea, and selected
BRIEF
tremors, are also reflective of dysfunction of certain spe-
Behavior Rating Inventory for Executive Functions
cific brainstem structures. Because the brain stem also
contains the life support centers that control respiration,
blood pressure, and heart rate, a brainstem stroke has the
potential to be fatal. Brief Cognitive Rating Scale
In its most severe form, an infarction of the ventral
pons can interrupt the function of all motor pathways, DANIEL N. A LLEN
causing locked-in syndrome, in which the patient can University of Nevada Las Vegas
receive and understand sensory stimuli, but has no Las Vegas, NV, USA
motor control, resulting in complete total body paralysis
and inability to speak, while maintaining awareness and
sensation. Synonyms
MRI scanning usually facilitates the diagnosis of
brainstem stroke. BCRS
Cross References Description
Basilar Artery The Brief Cognitive Rating Scale (BCRS; Reisberg & Ferris,
Cerebrovascular Disease 1988) is used to assess functional and cognitive abilities in
Lacunar Infarction both normal aging and progressive dementia. The BCRS
Locked-In Syndrome is part of the Global Deterioration Scale Staging System
Posterior Cerebral Artery (GDS; Reisberg, Ferris, de Leon, Crook, 1993) which is
Posterior Communicating Artery composed of three separate rating scales that include the
Pure Motor Stroke GDS, the Functional Assessment Staging (FAST; Reisberg,
Brief Psychiatric Rating Scale B 447
1988), and the BCRS. The BCRS provides objective rat- Mini-Mental State Examination
ings of a number of domains that include various cogni- Multi-Infarct Dementia
tive functions as well as functional abilities, mood, and B
behavior, and is made up of two parts. Part I includes
ratings for Concentration, Recent Memory, Remote
Memory, Orientation, and Functioning and Self Care,
Foster, J. R., Sclan, S., Welkowitz, J., Boksay, I., & Seeland, I. (1988).
while Part II allows for ratings of Speech and Language Psychiatric assessment in medical long-term care facilities: Reliabili-
Abilities, Motoric Capacities, Mood and Behavior, Praxis ty of commonly used rating scales. International Journal of Geriatric
Ability, Calculation Ability, and Feeding Capacity. Psychiatry, 3, 229233.
Each of the domains is rated on a 17 point scale that Ihl, R., Frolich, L., Dierks, T., Martin, E., & Maurer, K. (1992). Differential
validity of psychometric tests in dementia of the Alzheimer type.
ranges from normal (rating of 1) to profound im-
Psychiatry Research, 44, 93106.
pairment (rating of 7). For each domain, a behavioral Reisberg, B. (1988). Functional assessment staging (FAST). Psychophar-
anchor is provided for each point on the rating scale. The macology Bulletin, 24, 653659.
authors provided examples of questions that might be Reisberg, B., & Ferris, S. H. (1988). Brief cognitive rating scale (BCRS).
used to elicit information needed to complete the BCRS Psychopharmacology Bulletin, 24, 629636.
Reisberg, B., Ferris, S. H., de Leon, M. J., & Crook, T. (1988). Global
as well as guidelines for scoring each domain. Ratings are
deterioration scale (GDS). Psychopharmacology Bulletin, 24,
completed based on interviews with the patient and an 661663.
informant who is knowledgeable regarding the patients Reisberg, B., Ferris, S. H., Steinberg, G., Shulman, E., de Leon, M. J., &
day-to-day activities and functioning. Interviews may Sinaiko, E. (1989). Longitudinal study of dementia patients and aged
be conducted in person or over the telephone. The controls. In M. P. Lawton, & A. R. Herzog (Eds.), Special research
methods for gerontology (pp. 195231). Amityville, NY: Baywood.
BCRS has been translated into a number of languages
Reisberg, B., Sclan, S. G., de Leon, M. J., Kluger, A., Torossian, C., Shulman,
including Chinese, French, Polish, Spanish and Swedish, E., Steinberg, G., Monteiro, I., McRas, T., Mackell, J., & Ferris, S. H.
among others. (2007). The GDS staging system. In A. J. Rush (Ed.), Handbook of
psychiatric measures (pp. 431435). Washington, DC: American Psy-
chiatric Publishers.
Current Knowledge
From a psychometric standpoint, the BCRS has excellent

interrater reliability when completed by trained clinicians, Brief Evaluation
and test-retest reliability is also high (Foster et al., 1988;
Reisberg et al., 1989). Validity studies indicate the BCRS Neuropsychological Screening Examination
has strong correlations with the GDS, the Mini-Mental
State Examination, some neuropsychological measures of
memory abilities, as well as measures of activities of daily
living and quality of life. Relationships have also been
Brief Psychiatric Rating Scale
demonstrated between BCRS scores and neuropathology
E DWARD E. H UNTER 1, M EGHAN M URPHY 2
measured using a variety of techniques (EEG, PET, SPECT, 1
neurological examination). BCRS scores are sensitive to
Kansas City, KS, USA
the progression of Alzheimers disease, with significant 2
University of Missouri-Kansas City
declines in scores as the disease progresses (Ihl, Frolich,
Kansas City, MO, USA
Dierks, Martin, Maurer, 1992). Thus, the BCRS is useful in
both research and clinical settings where it can provide
valuable information regarding progression of cognitive
decline, as well as the impact that such decline has on
Synonyms
behavior and function.
BPRS
Cross References Definition

Alzheimers Dementia The Brief Psychiatric Rating Scale (BPRS) (Overall &
Alzheimers Disease Gorham, 1962, 1988) consists of a series of 18 items
448 B Brief Psychiatric Rating Scale
assessing the following psychiatric symptoms: somatic con- (1988). Versions are also widely available online, includ-
cern, anxiety, emotional withdrawal, conceptual disorgani- ing at: http://www.public-health.uiowa.edu/icmha/out-
zation, guilt feelings, tension, mannerisms and posturing, reach/documents/BPRS_expanded.PDF.
grandiosity, depressive mood, hostility, suspiciousness, hal-
lucinatory behavior, motor retardation, uncooperativeness,
unusual thought content, blunted affect, excitement, and
Cross References
disorientation. The instrument takes approximately 510
min to complete, following an interview with the patient.
Affective Disorder
The clinician rates each item on a scale ranging from 1 (not
Alzheimers Dementia
present) to 7 (extremely severe). The inventory is geared
Alzheimers Disease
toward serious psychopathology. While the ratings on
Anxiety
individual items are meaningful, the BPRS can yield an
Clinical Interview
overall score, and sets of items can be grouped into
Dementia with Lewy Bodies
categories.
Parkinsons Dementia
Parkinsons Disease
Psychosis
Current Knowledge
Psychotic Disorder
Structured Clinical Interview for DSM-IV (SCID)
The BPRS has acceptable psychometric properties and
enjoys widespread clinical use. Several authors have devel-
oped versions of the BPRS with behavioral anchors to
improve reliability, or training methods to accomplish the
same (Ventura, Green, Shaner, & Liberman, 1993). Using a References and Readings
behaviorally anchored approach and no specific interview
format or rater training, Lachar et al. (2001) obtained Cummings, K. R., Raman, R., & Thai, L. (2007). Quetiapine for agitation
weighted kappa agreement between psychiatrists on the or psychosis in patients with dementia and parkinsonism. Neurology,
68, 13561363.
majority of items at above 0.75. Scores on the BPRS are
Devanand, D. P. (1998). A randomized, placebo-controlled dose-
highly correlated with those of other similar instruments comparision of a trial of haloperidol for psychosis and disruptive
although, as with all such clinician-rated scales, relation- behaviours in Alzheimers disease. American Journal of Psychiatry,
ships with external criteria are modest (Mortimer, 2007). 155, 15121520.
Initially developed for use with psychiatric populations, Dunayevich, E., Sethuraman, G., Enerson, M., Taylor, C. C., & Lin, D.
(2006). Characteristics of two alternative schizophrenia remission
the BPRS is one of the most common scales used to track
definitions: Relationship to clinical and quality of life outcomes.
outcomes in schizophrenia research (Dunayevich, Sethura- Schizophrenia Bulletin, 86, 300308.
man, Enerson, Taylor, & Lin, 2006). It has been used Lachar, D., Bailley, S. E., Rhoades, H. M., Espandas, A., Aponte, M.,
effectively with individuals having other psychiatric dis- Cowan, K. A., et al. (2001). New subscales for an anchored version
orders (e.g., bipolar disorder; Picardi et al., 2008), as well of the Brief Psychiatric Rating Scale: Construction, reliability and
validity in acute psychiatric admissions. Psychological Assessment, 13,
as those with neurological conditions having psychotic or
384395.
other psychiatric symptoms, including Alzheimers dis- Levin, H. S., High, W. M., Goethe, K. E., Sisson, R. A., Overall, J. E.,
ease, dementia with Lewy bodies, and Parkinsons disease Rhoades, H. M., Eisenberg, H. M., Kalisky, Z., & Gary, H. E. (1987).
(Cummings, Raman, & Thai, 2007; Devanand, 1998; Tar- The neurobehavioural rating scale: Assessment of the behavioural
iot, Profenno, & Ismail, 2004). It has also been used in a sequelae of head injury by the clinician. Journal of Neurology, Neuro-
surgery and Psychiatry, 50, 183193.
modified form with persons with traumatic brain injury
Mortimer, A. M. (2007). Symptom rating scales and outcome in schizo-
(Levin et al., 1987). In neuropsychological practice, the phrenia. British Journal of Psychiatry Supplement, 50, s7s14.
BPRS can enable the clinician to organize and quantify Overall, J. E., & Gorham, D. R. (1962). The brief psychiatric rating scale.
observations of psychotic symptoms or other seriously Psychological Reports, 10, 790812.
disordered behavior, both as part of an evaluation and Overall, J. E., & Gorham, D. R. (1988). The Brief Psychiatric Rating Scale
(BPRS): Recent developments in ascertainment and scaling. Psycho-
in tracking the course of the clinical condition over time.
pharmacology Bulletin, 24, 9799.
The BPRS is in the public domain, and may be found Picardi, A., Battisti, F., de Girolamo, G., Morosini, P., Norcio, B., Bracco,
in Overall & Gorham (1988). A behaviorally anchored R., et al. (2008). Symptom structure of acute mania: A factor study of
format may be found in Woemer, Mannuzza, and Kane the 24-item Brief Psychiatric Rating Scale in a national sample of
Brief Symptom Inventory B 449
patients hospitalized for a manic episode. Journal of Affective Dis- be hand- or computer-administered to individuals ages 13
orders, 108, 183189.
and older (BSI) or 18 and older (BSI-18). Respondents
Tariot, P. N., Profenno, L. A., & Ismail, M. S. (2004). Efficacy of atypical
antipsychotics in elderly patients with dementia. Journal of Clinical
rate the extent to which a specific problem has distressed B
Psychiatry, 65(Suppl. 11), 1115. them in the past 7 days (although evaluations over other
Ventura, J., Green, M. F., Shaner, A., & Liberman, R. P. (1993). time intervals may be specified), using a 5-point scale
Training and quality assurance on the Brief Psychiatric Rating (0 = not at all to 4 = extremely). Administration is
Scale. International Journal of Methods in Psychiatric Research, 3,
straightforward, taking 4 (BSI-18) to 810 min (BSI) to
221244.
Woerner, M. G., Mannuzza, S., & Kane, J. M. (1988). Anchoring the
complete.
BPRS. Psychopharmacology Bulletin, 24, 112117. Scores are determined by summing values for each
symptom dimension and then dividing by number of
items endorsed in the respective dimension. A GSI can
be calculated for either measure by adding the scores for
all subscales, as well as the additional items (in the BSI),
Brief Symptom Inventory and then dividing by number of responses. For the BSI
only, the PST is determined by counting the number of
J OSEPH F. R ATH , L ISA M. F OX items endorsed with a positive (nonzero) response, and
NYU Langone Medical Center the PSDI is derived by dividing the sum of the item
New York, NY, USA values by the PST. Raw scores can be converted to
standardized T scores, generating a profile that graphi-
cally illustrates a respondents current psychological
Synonyms symptom presentation. Interpretation of the BSI can
be done at three levels: global scores, primary symptom
BSI; BSI-18 dimensions, and discrete symptoms (Derogatis &
Melisaratos, 1983). Computer administration, scoring,
and interpretation programs are available for both
Description instruments.
Advantages of the BSI and the BSI-18 are that they can
The BSI (Derogatis & Melisaratos, 1983) is a shortened, be completed quickly and used for repeated assessments.
53-item version of the Symptom Checklist-90 (SCL-90; Also, both measures are reported to be sensitive to mild-
Derogatis, Lipman, & Covi, 1973) that measures to-severe psychological distress, making them useful with
emotional-behavioral functioning in nine dimensions: many populations. Limitations include typical concerns
somatization, obsessivecompulsive, interpersonal sensi- associated with self-report measures, such as possible
tivity, depression, anxiety, hostility, phobic anxiety, para- patient response bias and over or underreporting, as well
noid ideation, and psychoticism. Four additional items as limited utility with some medical populations (e.g.,
not specific to any one domain load on several different neurologic), given the paucity of acceptable norms and
dimensions. In addition, three global indices Global concerns that certain items on the BSI may be closely
Severity Index (GSI), Positive Symptom Total (PST), related to physical and cognitive symptoms (Slaughter,
and Positive Symptom Distress Index (PSDI), provide Johnstone, Petroski, & Flax, 1999).
more general assessment of psychological well-being.
The BSI-18 (Derogatis, 2000), an 18-item shortform of
the BSI intended as a screen for psychiatric disorders and
psychological distress, consists of three six-item subscales: Historical Background
somatization, depression, and anxiety. A GSI also can be
calculated. In response to the need for briefer evaluation tools rele-
Not intended for use as diagnostic tools, both instru- vant in a variety of assessment settings, including medical
ments are designed to identify psychological symptoms and industrial research studies, the BSI and BSI-18 were
in medical populations, psychiatric patients, and commu- derived from the SCL-90, a 90-item checklist that includes
nity non-patients, with separate norms for males and the same nine symptom dimensions and three global
females. Written at a sixth grade reading level and avail- indices as the BSI. The SCL-90, itself, was developed in
able in over 24 languages, these self-report measures can 1973 (Derogatis et al., 1973) and was derived from the
450 B Brief Symptom Inventory
Hopkins Symptom Checklist (Derogatis, Lipman, Rickels, Lindner, 1988) found the BSI to be a strong and reliable
Uhlenhuth, & Covi, 1974). The BSI was published in 1983 predictor of psychological distress; whereas, the BSI-18
(Derogatis & Melisaratos, 1983), and the BSI-18 followed has been demonstrated to predict levels of distress in
in 2000 (Derogatis, 2000). cancer patients (e.g., Recklitis, Parsons, Shih, Mertens, &
Robison, 2006).
Some concern has been raised about the factor struc-
Psychometric Data ture and discriminant validity of the BSI and BSI-18.
For example, Boulet and Boss (1991) found that BSI
The most recent BSI manual (Derogatis, 1993) provides subscales correlated with nonanalogous scales on the
normative data from four samples: (1) 1,002 heteroge- MMPI, suggesting poor discriminant validity. In terms of
neous psychiatric outpatients; (2) 914 adult non-patients; factor structure, moderate to high intercorrelations were
(3) 423 psychiatric inpatients; and (4) 2,408 adolescent found among BSI subscales, with one factor explaining
non-patients. The BSI-18 was normed on two samples: over 70% of the variance in a principal-components anal-
(1) 1,134 community adults and (2) 1,543 adult cancer ysis (Boulet & Boss, 1991). Several cross-cultural studies
patients. Additional norms have been developed for such of the BSI-18 (e.g., Asner-Self, Schreiber, & Marotta,
diverse samples as older adults (Hale, Cochran, & Hedge- 2006) found only the GSI (versus the three subscales) to
path, 1984), college students (Cochran & Hale, 1985), be a valid indicator of psychological distress. These
individuals with spinal cord injury (Heinrich, Tate, & researchers suggested that the BSI and BSI-18 assess the
Buckelew, 1994), British psychiatric outpatients (Ryan, degree, but not the exact nature of psychopathology,
2007) and community-dwelling adults (Francis, Rajan, & and therefore GSI scores should be considered the most
Turner, 1990), Israeli adolescents (Canetti, Shalev, & De- useful indicator of psychological distress derived from the
Nour, 1994), and others (see Derogatis, 1993). Internal measures.
consistency coefficients are strong for both the BSI (0.71
0.83) and BSI-18 (0.740.89). Testretest reliability also is
good, ranging from 0.68 to 0.91 (BSI) and 0.68 to 0.84 Clinical Uses
(BSI-18).
BSI and BSI-18 manuals cite a variety of studies sup- The BSI and BSI-18 are widely used measures of psycholog-
porting validity in a range of settings and populations, ical distress employed with a variety of populations includ-
including psychoneuroimmunology, psychopathology, ing inpatient and outpatient medical and psychiatric
pain assessment and management, HIV research, student patients, individuals receiving treatment for substance
mental health, and general clinical studies. For example, abuse, and college students. Individuals who are of extreme-
in symptomatic adults, convergent validity between the ly low intelligence, delirious, psychotic, or have motivation
BSI and the Minnesota Multiphasic Personality Inventory to distort their responses are not good candidates for either
(MMPI) was shown to be 0.300.72 (Derogatis & Meli- measure. Given factor-structure concerns noted above (e.g.,
saratos, 1983) for the Wiggins content scales (i.e., 13 scales Boulet & Boss, 1991), the instruments may be used most
tapping content areas such as social maladjustment and appropriately as screening tools to alert clinicians to ele-
authority conflict) and Tryon cluster scales (i.e., seven scales vated levels of psychological distress, rather than as diag-
assessing conceptual clusters such as social introversion and nostic indicators. According to the BSI manual
bodily symptoms). Convergent validity also has been (Derogatis, 1993), the measures are most useful in clini-
demonstrated between the BSI and several other scales in cal and research settings where time is a major limiting
predicting affective status among chronic pain patients variable.
(Kremer, Atkinson, & Ignelzi, 1982). High correlations Both measures can be used as onetime assessments or
were also found between the SCL-90 and the BSI (0.92 administered repeatedly to evaluate treatment efficacy or
0.96; Derogatis, 1993) and BSI-18 (0.910.96; Derogatis, trends over time. Both are reported to have been used
2000). In terms of predictive validity, the BSI has been successfully in primary care settings to assess significant
shown to be a good predictor of psychopathology in changes in psychological distress and symptoms in
several populations, including a community unipolar de- patients with medical problems. The measures can be
pression cohort (Amenson & Lewinsohn, 1981), drug- used in nonclinical populations (e.g., to assess caregiver
using adults (Buckner & Mandell, 1990), and the elderly distress) as well.
(Hale et al., 1984). Screening studies completed with Both the BSI and BSI-18 may be useful tools for
medical cohorts (e.g., Kuhn, Bell, Seligson, Laufer, & inclusion in neuropsychological assessments, given their
BRIEF-P B 451
brevity and utility for repeated administrations. The BSI- Cochran, C. D., & Hale, W. D. (1985). College student norms on the Brief
Symptom Inventory. Journal of Clinical Psychology, 41, 777779.
18 was reported to be a valid screening measure for the
Derogatis, L. R. (1993). Brief Symptom Inventory (BSI): Administration,
overall level of psychological distress in both inpatients scoring, and procedures manual (3rd ed.). Minneapolis, MN: National B
and outpatients with traumatic brain injury (Meachen, Computer Systems.
Hanks, Millis, & Rappaport, 2008). However, the obser- Derogatis, L. R. (2000). Brief Symptom Inventory-18 (BSI-18): Adminis-
vation that most items in the BSI obsessivecompulsive tration, scoring, and procedures manual. Minneapolis, MN: National
Computer Systems.
scale are more reflective of cognitive complaints (e.g.,
Derogatis, L. R., Lipman, R. S., & Covi, L. (1973). SCL-90: An outpatient
concentration and memory problems) than classic obses- psychiatric rating scale: Preliminary report. Psychopharmacology
sivecompulsive disorder traits (Slaughter et al., 1999) Bulletin, 9, 1328.
highlights an issue of particular concern to neuropsychol- Derogatis, L. R., Lipman, R. S., Rickels, K., Uhlenhuth, E. H., & Covi, L.
ogists. Given the overlap between many items and cogni- (1974). The Hopkins Symptom Checklist (HSCL): A self-report
inventory. Behavioral Science, 19, 115.
tive and physical symptoms, clinicians are urged to
Derogatis, L. R., & Melisaratos, N. (1983). The Brief Symptom Inventory:
interpret elevations cautiously and remain vigilant against An introductory report. Psychological Medicine, 13, 595605.
misusing scale names for diagnostic purposes. It is crucial Francis, V. M., Rajan, P., & Turner, N. (1990). British community norms
not to rely on psychiatric interpretations of elevated scales for the Brief Symptom Inventory. British Journal of Clinical Psychol-
in neurological patients who have no history of emotional ogy, 29, 115116.
Hale, W. D., Cochran, C. D., & Hedgepath, B. E. (1984). Norms for the
difficulties; instead, BSI and BSI-18 item responses
elderly on the Brief Symptom Inventory. Journal of Clinical and
might best be examined individually and used to guide Consulting Psychology, 52, 321322.
treatment. Heinrich, R. K., Tate, D. G., & Bucklew, S. P. (1994). Brief Symptom
Inventory norms for spinal cord injury. Rehabilitation Psychology, 39,
4956.
Kremer, E. F., Atkinson, J. H., & Ignelzi, R. J. (1982). Pain measurement:
Cross References The affective dimensional measure of the McGill Pain Questionnaire
with a cancer pain population. Pain, 12, 153163.
Beck Anxiety Inventory Kuhn, W. F., Bell, R. A., Seligson, D., Laufer, S. T., & Lindner, J. E. (1988).
Beck Depression Inventory The tip of the iceberg: Psychiatric consultations on an orthopaedic
Brief Psychiatric Rating Scale service. International Journal of Psychiatry in Medicine, 18,
375382.
Center for Epidemiologic Studies-Depression
Meachen, S. J., Hanks, R. A., Millis, S. R., & Rapport, L. J. (2008). The
Geriatric Depression Scale reliability and validity of the Brief Symptom Inventory-18 in persons
Hamilton Rating Scale of Depression with traumatic brain injury. Archives of Physical Medicine and Reha-
Millon Clinical Multiaxial Inventory bilitation, 89, 958965.
Minnesota Multiphasic Personality Inventory Recklitis, C. J., Parsons, S. K., Shih, M., Mertens, A., & Robison, L. L.
(2006). Factor structure of the Brief Symptom Inventory-18 in adult
Personality Assessment Inventory
survivors of childhood cancer: Results from the childhood cancer
Self-Report Measures survivor study. Psychological Assessment, 18, 2232.
Symptom Checklist-90-Revised Ryan, C. (2007). British outpatient norms for the Brief Symptom Inven-
Zung Self-Rating Depression Scale tory. Psychology and Psychotherapy: Theory, Research, and Practice,
80, 183191.
Slaughter, J., Johnstone, G., Petroski, G., & Flax, J. (1999). The usefulness
of the Brief Symptom Inventory in the neuropsychological evalua-
References and Readings tion of traumatic brain injury. Brain Injury, 13, 125130.
Amenson, C. S., & Lewinsohn, P. M. (1981). An investigation into the

observed sex difference in prevalence of unipolar depression. Journal
of Abnormal Psychology, 90, 113.
Asner-Self, K. K., Schreiber, J., & Marotta, S. A. (2006). A cross-cultural BRIEF-A
analysis of the Brief Symptom Inventory-18. Cultural Diversity and
Ethnic Minority Psychology, 12, 367375.
Behavior Rating Inventory for Executive Functions
Boulet, J., & Boss, M. W. (1991). Reliability and validity of the brief
symptom inventory. Psychological Assessment, 3, 433437.
Buckner, C. J., & Mandell, W. (1990). Risk factors for depressive symp-
tomatology in a drug-using population. American Journal of Public
Health, 80, 580585.
Canetti, L., Shalev, A. Y., & De-Nour, A. K. (1994). Israeli adolescents
BRIEF-P
norms of the Brief Symptom Inventory (BSI). Israel Journal of
Psychiatry and Related Sciences, 31, 1318. Behavior Rating Inventory for Executive Functions
452 B BRIEF-SR
impairment and to reflect changes in understanding of

BRIEF-SR disability (particularly in light of the 2001 WHO frame-
work) since the scale was developed. Bucks and Haworth
Behavior Rating Inventory for Executive Functions (2002) also stated that studies evaluating a revised BADLS
are underway, but no papers reporting these studies have
been published to date (information correct as of
02.06.09).
Bristol Activities of Daily
Living Scale Psychometric Data
J ESSICA F ISH
The 22-item preliminary version of the BADLS had good
Medical Research Council Cognition &
testretest reliability (r = 0.95, for kappa scores for
Brain Sciences Unit
individual items see Bucks et al., 1996), and evidence of
Cambridge, UK
its validity was found through correlations between the
BADLS and MMSE scores (r = 0.55), and between BADLS
and observed performance ratings (r = 65). The final
Synonyms 20-item version of the BADLS, completed by 50 caregivers
of people with dementia (mixed diagnoses), found
Bristol ADL scale (BADLS); Revised bristol activities of
estimates of reliability and validity consistent with the
daily living scale (BADLS-R)
previous version, with BADLSMMSE scores correlating
at 0.67. Principal components analysis identified a four-
factor structure consisting of instrumental ADLs (7 items
Description explaining 40.3% of variance), self care (6 items explain-
ing 10.3% of variance), orientation (5 items explaining
The Bristol ADL scale is an informant-rated measure that 7.5% of variance), and mobility (2 items explaining 7%
covers 20 ADLs, both basic and instrumental. Items are of variance). Byrne et al. (2000) found that the BADLS
rated on a four-point scale (from totally dependent to was a good measure of change in ADL proficiency over
totally independent, with an additional not applicable time in people with Alzheimers disease (AD) receiving
option). anticholinesterase inhibitors, as judged by its correlations
with MMSE and ADAS-Cog scores, and sensitivity of 74%
and specificity of 65% in detecting improvement/stability
Historical Background versus decline, in comparison with clinician-rated
judgments.
The BADLS was developed specifically for use in people A recent systematic review of 12 instrumental ADL
with dementia, as existing scales were felt to be insensitive scales for persons with dementia (Sikkes, de Lange-de
to change in this group, having been designed for healthy Klerk, Pijnenburg, Scheltens and Uitdehaag, 2009) con-
older adults or people with physical disabilities. Initially, cluded that the BADLS was of moderate quality, the
22 items were included based on the rationale that they highest rating awarded in the review, which was given to
appeared in at least two existing ADL measures. only two measures, BADLS and the Disability Assessment
Caregivers of people with dementia completed the for Dementia.
questionnaire by mail, including feedback on the rele-
vance and importance of the items and response options.
Some modifications were made to the scale, with the next Clinical Uses
version incorporating different response options. Two
items on which participants scored at floor and ceiling Wicklund et al. (2007) noted that the Bristol ADL scale is
respectively were removed, leading to the final 20-item heavily weighted towards basic ADLs rather than instru-
version. Bucks and Haworth (2002) stated that the mental ADLs, so this should be borne in mind when
measure is regularly used in 58% of memory clinics considering using it. Nonetheless, the BADLS has been
in the United Kingdom, but that a revision was needed used as a primary or secondary outcome measure in a
in order to increase sensitivity to mild cognitive number of clinical trials, including those of
Broca, Pierre Paul (18241880) B 453
pharmaceutical and psychosocial interventions in people Woods, R. T., Bruce, E., Edwards, R. T., Hounsome, B., Keady, J.,
Moniz-Cook, E. D., et al. (2009). Reminiscence groups for people
with dementia. Recent examples include open-label and
with dementia and their family carers: Pragmatic eight-centre
controlled trials on the safety of aspirin (AD2000 Collab- randomised trial of joint reminiscence and maintenance versus B
orative Group, 2008) and neuroleptic treatments (Ballard usual treatment: A protocol. Trials, 10, 64.
et al., 2008) in people with AD, a comparison of cholines-
terase inhibitor and glutamate agonist treatment in mod-
erate-severe AD (Jones et al., 2009), and RCTs of
reminiscence therapy (Woods et al., 2009) and interper-
Bristol ADL Scale (BADLS)
sonal psychotherapy (Burns et al., 2005) for people with
Bristol Activities of Daily Living Scale
Azheimers disease and other dementias. Bucks and
Haworth (2002) have noted that completing the question-
naire may be in itself helpful for caregivers, as it can help
them to understand the effects of dementia in real-life Broadmann Area 17
terms.
Cuneus
Cross References
Alzheimers Disease Cooperative Study ADL Scale Broadmann Areas 18, 19

Disability Assessment for Dementia
LawtonBrody IADL Scale Extrastriate
The Activities of Daily Living Questionnaire
References and Readings Broca, Pierre Paul (18241880)

AD2000 Collaborative Group. (2008). Aspirin in Alzheimers disease M ICHAEL J. L ARSON
(AD2000): A randomised open-label trial. Lancet Neurology, 7, 4149. Brigham Young University
Ballard, C., Lana, M. M., Theodoulou, M., Douglas, S., McShane, R., Provo, UT, USA
Jacoby, R., et al. (2008). A randomised, blinded, placebo-controlled
trial in dementia patients continuing or stopping neuroleptics
(the DART-AD trial). PLoS Medicine, 5, 587599.
Bucks, R. S., Ashworth, D. L., Wilcock, G. K., & Siegfried, K. (1996). Name and Degrees
Assessment of activities of daily living: Development of the Bristol
Activities of Daily Living Scale. Age and Ageing, 25, 113120. Pierre Paul Broca received a bachelors degree of letters (a
Bucks, R. S., & Haworth, J. (2002). Bristol Activities of Daily Living Scale:
A critical evaluation. Expert Reviews in Neurotherapeutics, 2, 669676.
subject that includes history and literature) in 1840 from
Burns, A., Guthrie, E., Marino-Francis, F., Busby, C., Morris, J., his hometown Sainte-Foy-la-Grande College, and subse-
Russell, E., et al. (2005). Brief psychotherapy in Alzheimers disease. quently received a Bachelor of Science degree in mathe-
British Journal of Psychiatry, 187, 143147. matics. He began his study of medicine in 1841 at the age
Byrne, L. M. T., Wilson, P. M. A., Bucks, R. S., Hughes, A. O., & of 17 at the Faculty of Medicine at the University of Paris.
Wilcock, G. K. (2000). The sensitivity to change over time of the
Bristol Activities of Daily Living Scale in Alzheimers Disease.
He completed his formal medical training there in 1848.
International Journal of Geriatric Psychiatry, 15, 656661. Broca was studious and progressed rapidly during his
Jones, R., Sheehan, B., Phillips, P., Juszczak, E., Adams, J., Baldwin, A., medical studies. He was named externe of the Faculty of
et al. (2009). DOMINO-AD protocol: Donepezil and memantine in Medicine hospitals following a competitive application in
moderate to severe Alzheimers disease a multicentre RCT. Trials, 1843, interne in 1844, and interne laureate, with a 1-year
10, 57.
Sikkes, S. A. M., de Lange-de Klerk, E. S. M., Pijnenburg, Y. A. L.,
extension in 1847. He competed successfully to receive the
Scheltens, P., & Uitdehaag, B. M. J. (2009). A systematic review of positions of Anatomy Assistant of the Faculty of Medicine
Instrumental Activities of Daily Living scales in dementia: room for in 1846 and Prosector of Anatomy to the Faculty in 1848.
improvement. Journal of Neurology Neurosurgery and Psychiatry, 80, His mentors included such renowned individuals as
712. Francois Leuret at the Bicetre, Philippe Ricord at the
Wicklund, A. H., Johnson, N., Rademaker, A., Weitner, B. B., &
Weintraub, S. (2007). Profiles of decline in activities of daily living
Hopital du Midi, Langier at the Hopital Beaujon, Pierre
in non-Alzheimers dementia. Alzheimers Disease and Associated Nicolas Gerdy at the Faculty of Medicine (Paris), and
Disorders, 21, 813. Philippe-Frederic Blandin at the Hotel-Dieu.
454 B Broca, Pierre Paul (18241880)
Major Appointments cancer cells can penetrate the venous and lymphatic
systems as they metastasize. In the early 1850s, he
Following the completion of his medical studies, performed the first experiment in Europe using hyp-
Broca served as a lecturer at the Faculty of Medicine notism as surgical anesthesia.
in Paris. He lectured on topics in anatomy and surgery Broca was a prolific writer. He wrote several medical
until a formal competition for a professorship at the classics early in his career, including an extensive
Faculty of Medicine opened in 1853. That year, at the treatise on brain aneurysms, Des aneurysms et de leur
age of 29, Broca successfully competed to achieve the traitment, published in 1856 and a memoir on cancer,
distinction of Professor Agrege and Chirurgien du Memoir sur lanatomie pathologique du cancer, pub-
Bureau Central (also known as Chirurgien des Hopi- lished in 1853.
taux or Surgeon of the Hospitals) at the Faculty of
Medicine. In 1867, he was selected to chair the patho-
logie externe. Broca received the distinction of a pro- Speech and Localization of Function
fessor of clinical surgery in 1868. That same year, he
was elected a member of the Academie de Medicine, Brocas most well-known observations were made in
and resigned his chair of the pathologie externe in 1861 and the several years that followed. During that
order to accept the chair of Clinical Surgery. He held time, there was considerable fervor regarding the
this position until his death. During his tenure as the plausibility of cortical localization of functions, as
chair of Clinical Surgery, Broca worked in several Franz Joseph Galls early nineteenth-century phrenol-
Parisian hospitals, including the Hopital St. Antoine, ogy had fallen out of favor. Gall, based on his observa-
the Pitie, the Hotel des Cliniques, and the Hopital tions of skull shape, placed the ability to speak and
Necker. recall words in the inferior aspect of the frontal lobes.
Jean Baptiste Bouillaud followed Galls localizationist
views and hypothesized that the anterior lobes of the
Major Honors and Awards brain contained a center for speech production.
Bouillaud even offered a prize to the first individual
Broca became widely recognized throughout France
who reported a case with loss of speech without lesion
for his work. In 1865, he was elected president of the
to the frontal lobes.
Paris Societe de Chirurgie. In 1868, he was appointed
In February 1861 at a meeting of the Societe dAnthro-
to the Academie de Medicine and named a member of
pologie de Paris, a heated debate ensued when Pierre
the French Legion of Honor. He was elected to a
Gratiolet, another well-respected scientist of the time,
permanent seat in the French Senate in 1880, just
proposed total brain volume as a meaningful correlate
before his death. Broca also received many posthu-
of intelligence, and indicated that the functions of all
mous honors, including the eponymous naming of
parts of the brain were essentially identical. These
Brocas area, Brocas aphasia, and the diagonal band of
views were vehemently opposed by Bouillaud and his
Broca.
student and son-in-law Simon Alexandre Ernest
Aubertin. Broca was present during these debates as
Landmark Clinical, Scientific, the secretary of the Societe dAnthropologie. As he
and Professional Contributions considered the views presented, Broca eventually
sided with Bouillaud and Aubertin and became less
Early Career willing to accept the idea that all parts of the cerebral
hemispheres function in the same way (Finger, 2000).
Although Broca is best known for his work on speech On April 12, 1861, a Monsieur Leborgne was admitted
and the localization of brain functions, he first estab- to Brocas surgical service at the Bicetre for cellulitis
lished his reputation as a physician and scientist using and gangrene of the right leg. Affected by epilepsy since
the microscope to study diseases (Finger, 2004). He childhood, Leborgne developed considerable limita-
described in detail the histology of articular cartilage tions in his ability to speak along with right hemipar-
(the type of cartilage that covers the end of bones), the esis at age 30. He could comprehend speech and
histology of Rickets, and demonstrated that muscular communicate using pantomime, but his speech output
dystrophy is primarily a disease of the muscles. Broca was limited to the monosyllabic phrase tan, which
was among the first to use a microscope to show that became his nickname.
Broca, Pierre Paul (18241880) B 455
Leborgne died due to complications from the cellulitis for reporting on the localization of language functions,
and gangrene on April 17, 1861. Broca quickly com- although there were others who may have preceded
pleted an autopsy and presented his preliminary find- him. In 1836, Marc Dax presented a work indicating B
ings at the meeting of the Societe dAnthropologie de that disturbances in language production were due to
Paris the following day. He reported atrophy of both lesions of the left hemisphere. Daxs work remained
hemispheres of Leborgnes brain, with extensive soft- largely unknown until his son Gustave Dax presented
ening of left-frontal areas originating from the third and published his deceased fathers work in the years
left-frontal convolution. He further examined after 1863 (see Buckingham, 2006 and Finger, 2000).
Leborgnes brain specimen and presented his in-
depth findings at the Societe in August 1861. His
Surgery
presentation included a description of Leborgnes ep-
ilepsy and physical difficulties, including right-sided
Broca focused heavily on the relation between the skull
paralysis and loss of speech, along with a description
and the brain. In June 1871, he treated a 38-year-old
of the growth of a lesion from the third left-frontal
laborer who was kicked in the left-frontal region of the
convolution to other areas of the brain. Over time, the
skull by a horse. There was no fracture; nevertheless, the
area of the third left-frontal convolution became
patient showed difficulties with speech production after
known as Brocas area as a result of this case.
approximately 1 month. He eventually lost his full ability
Later in 1861, Brocas surgical service was referred a
to express himself through speech and lapsed into a coma.
Monsieur Lelong who had fractured his left femur
Broca suspected an abscess in the area of the third frontal
after a fall. Lelong was an 84-year-old man who had
convolution and performed a craniotomy at this approxi-
been admitted to the Bicetre 8 years previously for
mate location based on his hypothesis. He successfully
senility. In the spring of 1860, Lelong had suddenly
drained the abscess, but the patient slipped back into
collapsed and fallen unconscious. Upon recovery, he
coma after approximately 11 h and died. Autopsy revealed
was able to produce only four French words: oui,
a left-sided, predominantly frontal, meningoencephalitis
non, toujours, and trios, though his pantomimes
(Jay, 2002). This surgery based on Brocas findings regard-
were nearly always correct (Lee, 1981). Lelong lived
ing the localization of speech functions is likely the first
for only 12 days after he was referred to Brocas ser-
practical application of the theory of cortical localization
vice. Following Lelongs death, Broca performed an
(Finger, 2004; Stone, 1991).
autopsy and found lesions in the second and third
frontal convolutions. Presenting the findings from the
case of Lelong to the Societe dAnthropologie de Paris Anthropology
in November 1861, Broca indicated that the findings
confirmed those from his study of Leborgne, and From approximately 1866 until his death, Broca focused
hypothesized Lelongs left-frontal lesion was due to the majority of his efforts on the advancement of anthro-
an old hemorrhage that had occurred at the time pology. Indeed, due to his interest in anthropology and
Lelong lost his speech in 1860 (Lee, 1981). the remains of early humans, he did not write any papers
Broca called the inability to produce language in the at all on speech and the brain after 1877 (Finger, 2000).
context of intact comprehension, as seen in the cases Brocas initial interest in anthropology was piqued after
of Leborgne and Lelong, aphemie (Armand Trous- serving on a commission examining excavations in the
seau subsequently renamed such disturbances apha- cemetery of the Celestins in 1847. The discovery of Nean-
sia in 1864). Broca published several additional cases derthal Man in 1856, the publishing of Charles Darwins
of aphemie with lesions to the left hemisphere. For controversial ideas in On the Origin of Species in 1859,
example, in 1863, he published a series of eight cases and the subsequent controversy on the origins of man
showing primarily left-frontal lesions with language furthered Brocas desire to study anthropology.
production deficits. In an 1865 manuscript, Broca Much of Brocas anthropological research focused on
firmly asserted that the left hemisphere is the domi- the comparative study of skulls and the cranium circum-
nant seat for language production. ference across ethnic groups. He devised various instru-
Brocas declaration that the left hemisphere is predom- ments, standardized techniques and methods to examine
inantly responsible for language is among the clearest the structure and topography of the brain based on mea-
and most dramatic examples of localization of neural surements from prehistoric craniums. He invented at least
functions. Broca continues to receive the primary credit 27 instruments to determine the relation between the
456 B Broca, Pierre Paul (18241880)
brain and skull, including a goniometer (instrument to several societies, schools, and laboratories. In 1848, he
measure angles), craniograph (instrument used to depict established a society of free-thinking individuals, many
the outline of the skull), and several stereographic instru- of whom were sympathetic to Charles Darwins contro-
ments (Cowie, 2000). versial theories. He started the anthropology laboratory at
In 1869, Broca published the first description of the the Ecole des Hautes Etudes in Paris in 1858, the Societe
Gibraltar skull. Discovered in 1848, the Gibraltar skull was dAnthropologie de Paris, the first-known anthropologi-
among the earliest skeletal remains identified as belonging cal Societe in the world, in 1859, the Revue dAnthropo-
to the early species of Homo sapiens neanderthlensis. Broca logie in 1872, and the Ecole dAnthropologie in Paris in
was also fascinated with the topic of neolithic trephina- 1876. Broca held leadership positions in many of these
tion, the process, whereby a hole is scraped or drilled into societies, including secretary of the Societe Anatomique,
the skull. His interest in trephination began in 1867 after general secretary of the Societe dAnthropologie de Paris,
he examined an Incan skull with cross-hatched cuts. He president of the Societe de Chirurgie, and director of the
hypothesized that the operations were performed to treat Ecole dAnthropologie.
internal maladies in children (Finger, 2004), and was Broca married Lugol Augustine, the daughter of
among the first to speculate that trephination was a ther- Dr. Jean Guillaume Auguste Lugol, who propagated the
apeutic practice that was survived postoperatively based use of iodine in the treatment of disease, on July 6, 1857.
on the signs of inflammation at the wound margins The couple had three children, one daughter and two
(Cowie, 2000). sons. Just as Broca followed in his fathers footsteps by
Broca was very active in the study of anthropology becoming a physician, his two sons succeeded him as well-
during the final years of his life. Indeed, he was known to respected medical scientists.
spend many hours per day in the Ecole dAnthropologie he Pierre Paul Broca died on July 9, 1880 in Paris at the
founded. During the last 2 decades of his life, Broca pub- age of 56. Autopsy showed that all organs were apparently
lished over 240 papers and monographs on anthropologi- sound, although some have speculated his cause of death
cal topics (Schiller, 1992), including a five-volume work to be heart disease (Finger, 2000, 2004). Following his
entitled, Memoires dAnthropologie, published in 1871. autopsy one of his students remarked, We shall probably
not be far from the truth in attributing the catastrophe to
cerebral exhaustion, arising from too protracted a course
Short Biography of severe intellectual exertion (Memoir of Paul Broca,
1881). He was buried at the Montparnasse Cemetery in
Pierre Paul Broca was born on June 28, 1824, in Sainte- Paris. In his life, Broca published over 500 books and
Foy-la-Grande, a small town near Bordeaux, France. He articles. His influence on ideas regarding cortical localiza-
was raised under the Calvinist Protestant tradition. His tion, speech, and anthropology endures today. Indeed,
maternal grandfather, in addition to serving as mayor of many scientists would agree that the foundations of mod-
Bordeaux during the French revolution, was a pastor. His ern neuropsychology and cognitive neuroscience were
mother, Annette Thomas, was the sister of a Protestant laid by Pierre Paul Broca (Dronkers et al., 2007).
minister. His father, Jean Pierre (known as Benjamin)
Broca, was a physician who served for several years as a Cross References
surgeon in the French Army and was present at the Battle
of Waterloo (Finger, 2000). Aphasia
Following his undergraduate education, Broca sought Brocas Aphasia
to study engineering at the Ecole Polytechnique in Paris Localization
(Schiller, 1992). The death of his only sibling, a sister Speech
named Leontine, in 1840, along with pressure from his Tan
parents to remain closer to home and follow his fathers Wernickes Aphasia
career path, led to his decision to change his course of
study to medicine in 1841.
Broca showed considerable interest in the scientific
societies that prevailed in Paris both during his study of
Buckingham, H. W. (2006). The Marc Dax (17701837)/Paul Broca
medicine and throughout his career. He joined the Societe (18241880) controversy over priority in science: Left hemisphere
Anatomique (Anatomical Society) in 1847 and the Societe specificity for seat of articulate language and for lesions that cause
de Chirurgie (Surgical Society) in 1849. He also founded aphemia. Clinical Linguistics & Phonetics, 20, 613619.
Brocas Aphasia B 457
Clower, W. T., & Finger, S. (2001). Discovering trepanation: The con- words and lacks functors, bound morphemes, and other
tributions of Paul Broca. Neurosurgery, 49, 14171425.
grammatical elements. Paraphasic errors are also present.
Cowie, S. E. (2000). A place in history: Paul Broca and cerebral localiza-
tion. Journal of Investigative Surgery, 13, 297298.
Reading and writing performance generally mirrors that B
Dronkers, N. F., Plaisant, O., Iba-Zizen, M. T., & Cabanis, E. A. (2007). of auditory comprehension and oral expression. Some
Paul Brocas historic cases: High resolution MR imaging of the brains individuals with Brocas aphasia have agrammatism, a
of Leborgne and Lelong. Brain, 130, 14321441. lack of grammatical structure in their extemporaneous
Finger, S. (1994). Origins of neuroscience. New York City: Oxford
or repeated output that is often associated with impaired
University Press.
Finger, S. (2000). Minds behind the brain. New York City: Oxford
comprehension of grammatical structures. Personality
University Press. and intelligence are typically intact, and, in general, non-
Finger, S. (2004). Paul Broca (18241880). Journal of Neurology, 251, linguistic cognitive functions are relatively preserved, but
769770. this is difficult to test the given role of language in cogni-
Greenblatt, S. H. (1970). Hughlings Jacksons first encounter with the
tive functions.
work of Paul Broca: The physiological and philosophical back-
ground. Bulletin of the History of Medicine, 44, 555570.
Grodzinsky, Y., & Amunts, K. (Eds.). (2006). Brocas region. New York
City: Oxford University Press. Categorization
Hothersall, D. (2004). History of psychology (4th ed.). New York City:
McGraw-Hill.
Brocas Aphasia is a type of aphasia that is characterized
Jay, V. (2002). Pierre Paul Broca. Archives of Pathology and Laboratory
Medicine, 126, 250251.
by speech that is effortful, sparse, and halting, with
Lee, D. A. (1981). Paul Broca and the history of aphasia: Roland P. impaired repetition and relatively intact language
Mackay Award Essay, 1980. Neurology, 31, 600602. comprehension.
Memoir of Paul Broca (1881). The Journal of the Anthropological Institute
of Great Britain and Ireland, 10, 242261.
Schiller, F. (1983). Paul Broca and the history of aphasia. Neurology,
33, 667.
Schiller, F. (1992). Paul Broca: Founder of French anthropology, explorer of and Outcomes
the brain. New York: Oxford University Press.
Schreider, E. (1966). Brain weight correlations calculated from original The prognosis for recovery of functional communication
results of Paul Broca. American Journal of Physical Anthropology, 25,
in individuals with Brocas aphasia depends on the under-
153158.
Stone, J. L. (1991). Paul Broca and the first craniotomy based on cerebral
lying cause of the aphasia as well as factors such as the size
localization. Journal of Neurosurgery, 75, 154159. of the lesion and the patients age, premorbid language
skills, and comorbid health conditions. Individuals who
initially present with Brocas aphasia often evolve to a
clinical profile of anomic aphasia, with relatively good
Brocas Aphasia auditory and reading comprehension, and deficits pri-
marily in word-finding and the comprehension and pro-
LYN T URKSTRA duction of complex syntax.
Madison, WI, USA
of Brocas Aphasia
Synonyms
Brocas aphasia has been traditionally associated with
Anterior aphasia; Expressive aphasia; Motor aphasia lesions to Brodmanns areas 44 and 45 in the frontal
lobe of the dominant (typically left) hemisphere. Autopsy
data and neuroimaging studies, however, have shown
Short Description or Definition both the absence of Brocas aphasia in individuals with
lesions in this region and also the reverse (Yang, Zhao,
It is a type of aphasia that is characterized by speech that is Wang, Chen, & Zhang, 2008). The debate about the local-
effortful, sparse, and halting, and impaired repetition, ization of Brocas aphasia is part of a larger theoretical
with relatively intact language comprehension. The spo- discussion of the modularity of language and other cog-
ken output of individuals with Brocas aphasia often is nitive functions (for the treatment implications of this
described as telegraphic, as it contains primarily content debate, see discussion in Basso & Marangolo, 2000).
458 B Brocas Aphasia
Depression is a common psychological consequence Treatment

of aphasia, and is significantly more common after ante-
rior left-hemisphere lesions (including those associated There is a wide variety of validated treatment techniques
with nonfluent aphasia) than lesions in other areas for nonfluent aphasia, particularly for Brocas aphasia.
(Carson et al., 2000). The most commonly used tools These range from traditional stimulation-type therapies,
for evaluation of depression rely heavily on language which have been the staple of aphasia therapy since the
processes and thus have limited utility for individuals second world war, to current treatments such as conver-
with aphasia (Turner-Stokes & Hassan, 2002). Scales sational script training (Manheim, Halper, & Cherney,
designed to limit verbal demands, such as the Cornell 2009), constraint-induced aphasia therapy (Cherney,
Depression Scale (Alexopoulos, Abrams, Young, & Patterson, Raymer, Frymark, & Schooling, 2008), training
Shamoian, 1988), have been used in studies of aphasia of communication partners (Kagan, Black, Duchan,
but have not been validated for this population Mackie, & Square, 2001), and direct training of underly-
(Townend, Brady, & McLaughlan, 2007). A systematic ing grammatical structures (Thompson & Shapiro, 2005).
review of measures of depression in aphasia (Townend Most of the treatment literature has focused on indivi-
et al., 2007) indicated that adaptation of existing scales duals with vascular disorders, primarily stroke. For these
and use of other informants were common approaches to patients, speechlanguage therapy interventions have
the diagnosis of depression in individuals with aphasia, been found to be effective in improving both impairments
and recommended collaboration between mental health and functional communication ability even several years
and language experts in the diagnostic process. after the stroke.
Cross References
Evaluation
Aphasia
Aphasia is typically evaluated using a combination of Nonfluent Aphasia
standardized language tests and careful observation of Paraphasia
extemporaneous communication. Assessment of cogni- SpeechLanguage Therapy
tive functions such as attention, memory, and executive
functions is challenging in this group, given both the
verbal demands inherent in the structure of most neuro-
psychological tests and the complex interplay of language References and Readings
and other cognitive functions. Cognitive tests considered
Academic of Neurologic Coaammunication Disorders and Sciences.
to have relatively low language demands (e.g., the Cogni-
Evidence-based practice guidelines (Association). Retrieved October
tive Linguistic Quick Test, Helm-Estabrooks, 2001; or 1, 2008, from www.ancds.org
Ravens Standard Progressive Matrices, Raven 1938, in- Alexopoulos, G. S., Abrams, R. C., Young, R. C., & Shamoian, C. A.
cluded in the Western Aphasia Battery) are sometimes (1988). Cornell scale for depression in dementia. Biological Psychia-
used to test cognitive abilities other than language, with try, 23(3), 271284.
Basso, A., & Marangolo, P. (2000). Cognitive neuropsychological rehabili-
the caveat that language impairments are likely to influ-
tation: The emperors new clothes? Special issue: Cognitive neuropsy-
ence performance on these tests as well (Beeson, Bayles, chology and language rehabilitation. Neuropsychological Rehabilitation,
Rubens, & Kaszniak, 1993). 10(3), 219229.
The specific tests and measures used depend on the Beeson, P. B., Bayles, K. A., Rubens, A. B., & Kaszniak, A. W. (1993).
goals of the assessment (e.g., diagnosis vs. prediction of Memory impairment and executive control in individuals with
stroke-induced Aphasia. Brain and Language, 45, 253275.
functional performance vs. treatment planning), the time
Carson, A. J., MacHale, S., Allen, K., Lawrie, S. M., Dennis, M., House, A.,
post-onset (e.g., comprehensive test batteries are not et al. (2000). Depression after stroke and lesion location: A system-
appropriate in the context of acute stroke), and the atic review. Lancet, 356(9224), 122126.
patients clinical presentation. As lesions typically asso- Cherney, L. R., Patterson, J. P., Raymer, A., Frymark, T., & Schooling, T.
ciated with Brocas aphasia affect motor structures in the (2008). Evidence-based systematic review: Effects of intensity of
treatment and constraint-induced language therapy for individuals
frontal lobe, many patients with Brocas aphasia also have
with stroke-induced Aphasia. Journal of Speech, Language, and
apraxia of speech and hemiplegia or hemiparesis, which Hearing Research, 51(5), 12821299.
poses a particular challenge in assessment of language and Goodglass, H. (1993). Understanding aphasia. San Diego, CA: Academic
other cognitive functions. Press.
Bromocriptine B 459
Helm-Estabrooks, N. (2001). Cognitive linguistic quick test (1st ed.). San Current Knowledge
Antonio, TX: Psychological Corporation.
Kagan, A., Black, S., Duchan, J., Mackie, N., & Square, P. (2001). Training
volunteers as conversation partners using supported conversation
In some cases, the boundary identified by Brodmann is B
for adults with Aphasia (SCA): A controlled trial. Journal of Speech, also a functional boundary. For instance, primary visual
Language, and Hearing Research, 44, 624638. cortex is contained in Brodmanns area 17. Brodmanns
Manheim, L. M., Halper, A. S., & Cherney, L. (2009). Patient-reported area 18 is considered to be higher-order visual cortex.
changes in communication after computer-based script training for
Somatosensory functions are associated with Brodmanns
aphasia. Archives of Physical Medicine and Rehabilitation, 90(4),
623627.
areas 3, 1, and 2, with part of area 3 being recognized
Raven, J. C. (1938). Progressive matrices: A perceptual test of intelligence. as primary somatosensory cortex. Brodmanns areas 41
London: H.K. Lewis. and 42 are associated with audition (hearing). Primary
Thompson, C. K., & Shapiro, L. P. (2005). Treating agrammatic aphasia motor cortex (the output for motor commands) is asso-
within a linguistic framework: Treatment of underlying forms.
ciated with Brodmanns area 4, while premotor cortex
Aphasiology, 19(10/11), 10211036.
Townend, E., Brady, M., & McLaughlan, K. (2007). A systematic evalua-
(where the decision to move likely arises) is found in
tion of the adaptation of depression diagnostic methods for stroke Brodmanns area 6.
survivors who have aphasia. Stroke, 38(11), 30763083. A different interpretation of cytoarchitechtonic regions
Turner-Stokes, L., & Hassan, N. (2002). Depression after stroke: A review (107 areas) was published by Constantin von Economo and
of the evidence base to inform the development of an integrated care
Georg N. Koskinas in 1925.
pathway. Part 1: Diagnosis, frequency and impact. Clinical Rehabili-
tation, 16(3), 231247.
Yang, Z. H., Zhao, X. Q., Wang, C. X., Chen, H. Y., Zhang, Y. M. (2008).
Neuroanatomic correlation of the post-stroke aphasias studied with Cross References
imaging. Neurological Research, 30(4), 356360.
Auditory Cortex
Cerebral Cortex
Neocortex
Somatosensory Cortex
Brodmanns Area 17 Visual Cortex
Visual Cortex
Brodmann, K. (2005). Brodmanns: Localisation in the cerebral cortex.
(L. J. Carey Trans.). Berlin: Springer.
Brodmanns Areas of the Cortex Falk, D., & Gibson, K. R. (Eds.). (2008). Evolutionary anatomy of the
primate cerebral cortex. Cambridge: Cambridge University Press.
K IMBERLE M. J ACOBS
Richmond, VA, USA
Bromocriptine
Definition DAVID J. L IBON
Brodmanns areas of the cortex refer to 52 regions of the Philadelphia, PA, USA
cerebral cortex that were identified in 1909 by German
Neurologist, Korbinian Brodmann, based on cytoarchi-
tectonic (cell size, spacing or packing density, and lami- Definition
nation) differences. Brodmanns areas are typically shown
on a map of the brain surface, but each region is conti- Bromocriptine is one of the group of medicines classified
nued through the depth of cerebral cortex. These regions as ergot alkaloids. Bromocriptine acts to block the release
were originally identified based on Nissl-stained sections of prolactin which is produced by the pituitary gland.
of human brain; however, Brodmann believed that they Bromocriptine is used to treat a variety of medical con-
applied to all mammals. ditions including problems with menstruation, infertility,
460 B BrownSequard Syndrome
Parkinsons disease, neuroleptic malignant syndrome, horn of the cord on the same side in which they entered.
and pituitary adenomas. When used in conjunction From there, their second-order neurons cross the midline
with diet, bromocriptine can also be used to treat type of the cord in the ventral while commissure and
2 diabetes. then ascend contralaterally as the ventral and lateral
spinothalamic tracts (anterolateral system).
Thus, a lesion that transects one-half of the spinal
References and Readings cord will cause motor symptoms on the same side of the
body as a result of severing the lateral corticospinal tract
Ropper, A. H., & Samuels, M. A. (2009). Adams and Victor principles of on that side. This will result in residual upper motor
neurology (9th ed.). New York: McGraw Hill. neuron type deficits below the level of the lesion (e.g.,
spastic paralysis, hyperreflexia, clonus, loss of superficial
reflexes, and a positive Babinski). As the lesion also affects
the ventral horns, lower motor neuron signs (flaccid pa-
ralysis, severe atrophy, hyporeflexia, and fasciculations)
BrownSequard Syndrome are potentially discernable at the level of the lesion.
Because the posterior columns are affected, the individual
J OHN E. M ENDOZA will also demonstrate a loss of proprioception, fine tactual
Tulane University Medical Center discrimination, and vibratory sense below the level of the
New Orleans, LA, USA lesion on that same side. Finally, as a result of a disruption
of the ascending spinothalamic tracts, there will be a loss
of pain and temperature. However, because these latter
Synonyms tracts represent sensory information that has crossed over
from the opposite side of the cord, the loss of pain and
Hemisection of spinal cord temperature will be contralateral to the lesion (and one of
the sides opposite to the motor and posterior column
symptoms). Because the fibers carrying signals for pain
Definition and temperature ascend and descend a couple of spinal
segments before decussating, the level of loss of pain and
BrownSequard syndrome is a neurological condition in temperature will be slightly below that of proprioception
which, as a result of a lesion affecting one half of the spinal and stereognosis.
cord, there is paralysis and loss of proprioception, vibra- A BrownSequard syndrome usually results from a
tion, and fine tactile discrimination on one side of the penetrating injury as might be found in a knife or bullet
body and loss of pain and temperature on the other. wound. Because such wounds lack anatomical precision,
exactly one half of the cord is rarely severed, but the term
is applied if the clinical picture generally matches that
Current Knowledge which was described above.
To fully appreciate this syndrome, it is helpful to under-

stand some basic anatomy of the spinal cord. Recall that Cross References
the lateral corticospinal tract, which carries voluntary
motor impulses originating in the cortex, descends in Anterolateral System
the lateral portion of the cord after having crossed the Lateral Corticospinal Tracts
midline (decussated) in the medulla. On the sensory side, Posterior Columns
fibers that mediate position sense (proprioception), fine
tactual discrimination (stereognosis), and vibration enter
the cord through the dorsal nerve roots and, without
synapsing, travel up the same side of the cord from
which they enter (via the posterior columns or lemniscal Bruise
system) until they synapse in the medulla. By contrast,
those dorsal root (sensory) fibers that carry information Cortical Contusion
regarding pain and temperature synapse in the dorsal Hematoma
BSID-III B 461
by comparing BBA scores during in-hospital admission

Brunel Balance Assessment within 24 weeks after stroke to scores on the Barthel Index
and Rivermead Mobility Index at 3 months post-stroke in B
TAMARA B USHNIK 102 individuals (Tyson, Hanley, Chillala, Selley, & Tallis,
Rusk Institute for Rehabilitation Medicine - NYU 2007). Individuals who had limited sitting balance during
Langone Medical Center hospitalization showed little recovery of functional mobility
New York, NY, USA independence. Individuals who were able to walk (with or
without assistive equipment) during hospitalization were
mostly independent at 3 months post-stroke in transfers,
Synonyms walking, and stairs. For those individuals with limited stand-
ing balance during hospitalization, the majority regained the
BBA ability to walk, conduct transfers, and navigate stairs, al-
though more of these individuals required assistance.
Definition
Cross References
The Brunel Balance Assessment (BBA) clinical assessment
tool is designed as an outcome measure to assess balance Barthel Index
before and after stroke physiotherapy interventions. Berg Balance Scale
It consists of 12 items that progress from easy to difficult Motor Assessment Scale
in a hierarchical manner to form an ordinal scale. The Rivermead Mobility Index
easiest item is static sitting balance with upper limb
support; a mid-range item is dynamic standing balance; References and Readings
the hardest item is advanced change of the base of support.
Each item is assessed by evaluating performance on a specif- Tyson, S. F., & Connell, L. A. (2009). How to measure balance in clinical
ic task with task-specific criteria for succeeding; for example, practice. A systematic review of the psychometrics and clinical utility
dynamic standing balance is assessed by evaluating the of measures of balance activity for neurological conditions. Clinical
distance that the individual can reach beyond arms length. Rehabilitation, 23, 824840.
Tyson, S. F., & DeSouza, L. H. (2004). Development of the Brunel Balance
Success at this task is set at a minimum reach of 7 cm. The
Assessment: A new measure of balance disability post stroke. Clinical
BBA items are arranged into three subscales which can be Rehabilitation, 18, 801810.
used individually: sitting; standing; and stepping balance. Tyson, S. F., Hanley, M., Chillala, J., Selley, A. B., & Tallis, R. C. (2007).
The relationship between balance, disability, and recovery after
stroke: Predictive validity of the Brunel Balance Assessment.
Current Knowledge Neurorehabilitation and Neural Repair, 21, 341346.
Homogeneity of the scale: All items have item-total correla-

tions of more than 0.20. Cronbachs alpha, a measure of
internal consistency, was 0.93 (Tyson & DeSouza, 2004). BSI
Therefore, the scale was deemed homogeneous and
internally consistent. Brief Symptom Inventory
Reliability: Test-retest reliability was assessed using
observations on consecutive days, while inter-rater reliabil-
ity was assessed using two independent raters. There was
100% agreement for both forms of reliability (Tyson & BSI-18
DeSouza, 2004).
Validity: Criterion validity was assessed by comparison Brief Symptom Inventory
with the sitting section of the Motor Assessment
Scale (sitting balance), the Berg Balance Test (standing bal-
ance), and the Rivermead Mobility Index (stepping balance/
functional mobility). The correlation coefficients were 0.83 BSID-III
(Motor Assessment Scale), 0.97 (Berg Balance Test), and 0.95
(Rivermead Mobility Index). Predictive validity was assessed Bayley Scales of Infant and Toddler Development
462 B Bucco-facial Apraxia
Side Effects
Bucco-facial Apraxia
Serious
Apraxia
Seizures, hypomania, induction of mania, and activation
of suicidal ideation (controversial)
Building-related Illness
Common
Sick Building Syndrome
Dry mouth, constipation, nausea, weight loss, insomnia,
dizziness, headache, agitation, tremor, abdominal pain,
tinnitus, and sweating
Bupropion
J OHN C. C OURTNEY 1, C RISTY A KINS 2 References and Readings
1
New Orleans, LA, USA Physicians Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson
2
Mercy Family Center PDR.
Metarie, LA, USA Stahl, S. M. (2007). Essential psychopharmacology: the prescribers guide
Generic Name
Bupropion
Brand Name Free Drug Online and PDA Software: www.epocrates.com
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.
Wellbutrin, Wellbutrin SR, Wellbutrin XL, Zyban Pill Identification: http://www.drugs.com/pill_identification.html
Class
Antidepressant Burden of Proof

M OIRA C. D UX
Proposed Mechanism(s) of Action University of Maryland Medical Center/Baltimore VA
Baltimore, MD, USA
Increases norepinephrine/noradrenaline and dopamine,
blocks norepinephrine reuptake pump, may increase do-
pamine neurotransmission in the frontal cortex, blocks Synonyms
dopamine reuptake pump.
Standards of proof
Indication
Major depressive disorder, nicotine addiction

Definition
This refers to the duty to provide evidence for allegations

Off Label Use raised in the context of legal action. The Standard of Proof
is the degree of proof needed in a legal action to persuade
Bipolar-disorder, ADHD the court (e.g., judge or jury) that a given allegation is
Buspirone B 463
indeed founded or true. There are three main types of Brand Name
standards of proof: beyond a reasonable doubt, clear and
convincing evidence, and a preponderance of the evi- Buspar B
dence. Artificial percentages have been associated with
each of these standards of proof with beyond reasonable
doubt coinciding with 9095% certainty, clear and Class
convincing evidence 75%, and a preponderance of the
evidence associated with just over 50%. Each of these Anxiolytic
standards is used during different inquiries in criminal
procedure (e.g., insanity defense, competency to stand
trial, and competency to be executed) and there are Proposed Mechanism(s) of Action
other standards used by appellate courts when reviewing
trial court records. Under the current Mental Penal Code Serotonin 1A partial agonist, thus diminishing the overall
Standard for Insanity, The defendant has the burden of serotonergic activity at those receptor sites
providing the defense of insanity by clear and convincing
evidence.
Indication
Cross References Anxiety disorders
Beyond a Reasonable Doubt

Clear and Convincing Evidence
Off Label Use
Preponderance of the Evidence
Mixed anxiety and depression, treatment resistant
References and Readings depression
Denney, R. L. (2005). Criminal forensic neuropsychology and assessment

of competency. In G. Larrabee (Ed.), Forensic neuropsychology: A Side Effects
scientific approach. New York: Oxford University Press.
logical evaluations for the courts: A handbook for mental health profes-
Serious
sionals and lawyers (3rd ed.). New York: Guilford Press.
Very rare cardiac symptoms
Buschke Selective Reminding Test Common
Selective Reminding Test Dizziness, sedation, nervousness, and nausea

Buspirone
PDR.
J OHN C. C OURTNEY
Stahl, S. M. (2007). Essential psychopharmacology: the prescribers guide
Childrens Hospital of New Orleans (2nd ed.). New York, NY: Cambridge University Press.
New Orleans, LS, USA
Generic Name
Buspirone Drug Molecule Images: http://www.worldofmolecules.com/drugs/
464 B Butters, Nelson (19371995)
Free Drug Online and PDA Software: www.epocrates.com International Neuropsychological Society (Secretary-
Treasurer 19741977; Board of Governors 19781981;
Treasurer 19801983; President, 19841985)
National Academy of Neuropsychology (Fellow;
President 19921993)
American Psychological Society (Fellow, 1988)
Butters, Nelson (19371995) American Board of Clinical Neuropsychology
(Founding Fellow, Vice-President 19911993)
M ERYL A. B UTTERS , J AMES T. B ECKER Distinguished Clinical Neuropsychologist Award from
University of Pittsburgh School of Medicine the National Academy of Neuropsychology (1991)
Pittsburgh, PA, USA Meritorious Service Award from the Department of
Veteran Affairs (1993)
Distinguished Service Award from the American
Major Appointments Board of Professional Psychology (1993)
NIMH Postdoctoral Research Fellow at the Neuropsy-

chology Section of NIMH, Bethesda, MD (19641966) Landmark Clinical, Scientific, and
Instructor, College of General Studies, George Professional Contributions
Washington University (19651966)
Assistant Professor, Ohio State University (19661967) Nelson Butters authored or coauthored over 200 peer-
Lecturer in Psychology, Antioch College (19661967) reviewed scientific articles, 60 invited monographs
Lecturer in Psychology, Wellesley College (19671968) and book chapters and reams of abstracts. He coedited
Lecturer in Psychology, University of Massachusetts or coauthored six books and delivered a multitude of
(Boston) (19671983) invited lectures and presentations. Butters expended
Research Career Scientist, Boston Veterans Adminis- much professional energy demonstrating the existence
tration Medical center (19671983) of distinct dissociations among cognitive functions,
Professor of Neurology (Neuropsychology), Boston especially memory, within and between patients with
University School of Medicine (19671983) various forms of cerebral dysfunction. He was unusu-
Senior Lecturer, Northeastern University, University ally successful (perhaps uniquely so) at integrating
College (19671983) neuroanatomy and cognitive theory with applied neu-
Affiliate Professor of Psychology, Clark University ropsychology. As a result, one of the most distinguish-
(19731983) ing features of his career was that his work was very
Chief, Psychology Service, San Diego Department of highly regarded by cognitive and clinical researchers as
Veteran Affairs Medical Center (19831995) well as practicing clinicians. He was especially proud of
Professor of Psychiatry, University of California this cross-professional appeal.
School of Medicine (San Diego) (19831995) Butters earliest work was conducted in primates. Two
tests in particular could reveal memory loss in
monkeys the delayed response (DR) and delayed
Major Honors and Awards alternation (DA) tasks. For both DR and DA, the
animals had to hold information in memory for a
Phi Beta Kappa, Summa Cum Laude, A.B. with Honors short time before making a response to obtain a
NIH Predoctoral Research Fellowship (19611964) reward. Lesions in the prefrontal cortex, in particular
NIMH Postdoctoral Research Fellowship (19641966) along the sulcus principalis, severely disrupted the
Member of the Collegium of the Distinguished monkeys ability to either perform or learn the tasks.
Alumni of the College of Liberal Arts of Boston In 1969, Butters, in collaboration with Deepak Pandya,
University (elected 1974) demonstrated that the middle third of the sulcus prin-
Fellow, American Association for the Advancement cipalis was the critical region associated with impair-
of Science ments of DR and DA. In 1971, they described functional
American Psychological Association (Fellow Divisions differentiation along the axis of the sulcus principalis;
3, 6, 40; President of Division 40 19821983; the middle third differed from the anterior and posteri-
Representative to APA Council 19901992) or portions with regard to their efferent (outgoing)
Butters, Nelson (19371995) B 465
projections of the prefrontal cortex. In 1972, with their and extent of changes in cognition across patients
student Gary Van Hoesen, they reported on the afferent with different forms of brain damage, we advance
(incoming) projections to the entorhinal cortex around our understanding of the neuroanatomical basis of B
the hippocampus another brain region critical for the cognitive process in question, the organization of
memory functions. the process itself, and how these affect the individual
At the same time, Butters was working closely with patient. This concept became a theme sometimes
Donald Stein and Jeffrey Rosen on recovery of func- explicit, sometimes implicit that was woven into the
tion following frontal lobe lesions in nonhuman pri- fabric of Butters research career.
mates. They showed that if one removed sections of An early series of studies in the 1970s with Ina Samuels
the frontal lobes in monkeys in serial fashion, that is, exemplified this approach. Together they systematically
over a series of operations, the resulting deficit was examined visual and auditory short-term memory in
less than that exhibited by monkeys who experienced individuals with a variety of lesions. In the early 1970s
the same lesion, in one step. They concluded that cognitive psychologists were debating the relative mer-
these results demonstrated at least partial recovery of its of serial versus parallel processing in normal human
function. This finding in adult monkeys was impor- memory. Butters work with Laird Cermak on patients
tant because at the time, it was believed that if a brain with amnesic disorders was among the first to examine
lesion occurred after 12 months of age (in the monkey), this and other central topics of cognitive psychological
recovery was not possible. Patricia Goldman was research. The Butters and Cermak collaboration was
showing that infant macaques with brain lesions particularly fruitful because it directly influenced the
could fully recover some functions, but not others development of models of normal human memory
the data from the Rosen, Stein, and Butters series shed particularly the notion that memory is neither a serial
light on the question of whether, and by how much, nor parallel process, but rather that the type or intensity
older animals (and by extension, humans) could re- of the processing was what was critical (i.e., levels of
cover function after a brain lesion. processing argument espoused by Fergus Craik).
One of his earliest human studies (published with While in Boston, Butters and his colleagues made
Melvin Barton in 1970) on the role of the frontal and great strides in elucidating the neuropsychological
parietal lobes in concrete operations, shaped much of effects of alcoholism. The papers that emanated
Butters philosophy of neuropsychology and laid the from studies of chronic, non-amnestic alcoholics (in
groundwork for his career examining the brain struc- collaboration with Christopher Ryan, James Becker,
tures that mediate abnormal cognition. They took Kathleen Montgomery, and Barbara Jones) had a last-
concepts and methods that were popular in human ing influence on the way that the neuropsychology of
cognition at that time and used them to examine the alcoholism was viewed and studied. Butters work also
role of various brain structures in these cognitive pro- focused on the amnesic syndrome associated with
cesses. For example, humans with damage to the pari- chronic, severe alcoholism. With Laird Cermak, his
etal lobes have difficulty reversing or changing their systematic series of studies focused on the role of
behavior. That is, once taught a rule, they have difficul- interference and encoding in the short-term memory
ty deviating from that rule. What was unclear at the defects of patients with alcoholic Korsakoff s syn-
time was whether this deficit was a fundamental deficit drome. It is noteworthy that Butters developed
in reversal or a consequence of a deficit in retention personal relationships with many of these patients,
the ability to remember the old rule or learn the new venturing out to their homes (sometimes state hospi-
one. The results of these experiments not only in- tals or nursing homes) and repeatedly reevaluating
formed investigators on the nature of the behavioral them for different projects. This work was important
and cognitive changes that follow focal brain damage, not only because of what it revealed about both nor-
but lent insight into the cognitive processes themselves. mal and pathological memory, but also because it
Butters made exemplary use of what Hans-Lukas clearly demonstrated that a long-term consequence
Teuber referred to as the natural fracture lines of of alcoholism can be an amnestic disorder (a matter
behavior. That is, when a patient suffers a brain that was hotly debated at the time). Perhaps the most
injury, behavior and cognition fail neither completely enduring legacy of Butters and Cermaks work from
nor in a random manner. Rather, the breakdown this period was the 1980 publication of Alcoholic Kor-
occurs at points where different cognitive processes sakoff s Syndrome: An Information Processing Approach
intersect. By comparing and contrasting the nature to Amnesia. The title was not an accident they
466 B Butters, Nelson (19371995)
wanted to emphasize the role of neuropsychology in included Alzheimers disease, which he considered
analyzing information processing, and how this re- the prototypical cortical dementia. In San Diego
search informed our models of normal memory and his work with David Salmon, William Heindel, Wil-
memory systems. The publication of this text marked liam Beatty, Munro Cullum, Eric Granholm, Alexan-
the beginning of the modern era of cognitive der Troster, Agnes Chan, Andreas Monsch, and a host
neuroscience. of other students and colleagues focused on three
Another trend in Butters research during the middle- main areas, yielding a significant scientific contribu-
to-late 1970s was prompted by his desire to better tion in each.
understand retrograde amnesia, which had not yet Butters work with David Salmon and their colleagues
been studied in any systematic way, due in part, to demonstrated that the memory disorders of cortical
the lack of suitable test instruments. He collaborated and subcortical dementias are dissociable, with Alz-
with Marilyn Albert, who took on the task of develop- heimers disease characterized by poor consolidation
ing the Boston Retrograde Amnesia Battery, which and rapid forgetting due to limbic damage and Hun-
became the first carefully validated and well-normed tingtons disease by poor retrieval associated with
retrograde memory battery applicable to individuals fronto-striatal dysfunction. Butters work with trainee
of various ages. This productive collaboration, which Mark Bondi and others in his research group was
later included Jason Brandt and Donald Stuss, firmly among the first to show that the neuropsychological
established that the retrograde memory impairment characteristics of very early Alzheimers disease dif-
exhibited by Korsakoff s patients had a clear temporal fered from the benign cognitive changes of normal
gradient, suggesting that the neural substrates of aging and could therefore be used for the early and
memory change with the passage of time. That is, even pre-clinical detection of the disease, presaging
over time, episodic memories mediated by similar findings in HD. Finally, researchers were be-
the hippocampal circuitry are actively recalled, there- ginning to investigate the phenomenon of implicit
by losing their spatial and temporal markers, becom- memory, and Butters work with William Heindel,
ing part of semantic memory, stored elsewhere (likely David Salmon, Jane Paulsen, and others showed that
the temporalparietal association cortices). various forms of implicit memory could be dissociated
During his last years in Boston, Butters devoted in Alzheimers disease, Huntingtons disease, and Par-
considerable time to studying the cognitive effects of kinsons disease. These studies were the first to dis-
Huntingtons disease (HD), demonstrating a func- sociate priming and procedural learning in the brain,
tional dissociation between the locus of the lesions showing that procedural learning deficits were asso-
in HD (the basal ganglia) and those found in Korsak- ciated with basal ganglia dysfunction while priming
off s syndrome (the limbic system). This research deficits were linked with neocortical damage that
predated the identification of the HD gene and devel- occurs in Alzheimers disease. Any one of these con-
opment of a test to determine whether the offspring of tributions would have been impressive; together they
HD patients were destined to develop the disease. As represent a truly remarkable accomplishment.
part of the Center Without Walls, Butters worked In 1986 the American Psychological Association
with people at risk for HD (i.e., who had a parent (APA) acquired the journal Neuropsychology and But-
with the disease) to determine whether measures of ters was appointed Editor. APA tradition allows new
cognition administered earlier in life could predict editors to choose the colors of the journals binding
those who would ultimately develop the disease. and Butters chose a white background with (Boston)
In 1983 Butters accepted an offer to join the Depart- Celtic green for the text (he was a lifelong fan of his
ment of Psychiatry at the University of California- hometown basketball team). Butters goal for the
San Diego (UCSD), where he relished the opportunity journal was that it should become one of the journals
to develop a clinical service with neuropsychologists of record for basic, applied, and clinical research in
who conducted research as well as provided clinical neuropsychology. This will be another of his lasting
care. In addition to developing a first-rate psychology legacies.
service, Butters maintained his prolific research pub- Most important to Butters were his students his
lication rate. Soon after arriving in San Diego, UCSD academic children (and in some cases grandchildren)
was designated an Alzheimers Disease Research Cen- were almost as important to him as his biologic chil-
ter, which provided Butters with the opportunity to dren, Meryl, Paul, and Lisa. His attraction was inter-
expand his research on memory. His studies now national (e.g., John Hodges, Narinder Kapur, Matti
Butters, Nelson (19371995) B 467
Laine), and his mentees continue to lead the field (e. and scholar. A concussion sustained playing football left
g., Kathie Welsh-Bohmer, Terry Jernigan). him with lifelong anosmia, an irony not lost on him when
A narrative of Butters contributions to neuropsychol- he later published articles on the importance of assessing B
ogy would be woefully incomplete without a personal olfaction in brain-damaged patients. In addition to his
description. He possessed tremendous internal drive, obvious academic talent, he took great pride in his care-
and held both his students and colleagues to the high fully crafted image as a motor scooter-riding bad boy,
standards he applied to himself. Every Butters student emulating James Dean and Marlon Brando. Later in life,
carries distinct memories of the red ink and blunt he took great pleasure in recounting tales of his friendship
reviews accompanying their manuscript drafts. His with his classmate, the late social and political activist
academic rigor notwithstanding, Butters was univer- Abbie Hoffman. Butters particularly enjoyed retelling
sally known as an involved, supportive mentor and stories of drag racing against Hoffman from Worcester
colleague. His role extended to that of job-broker and to Boston, MA, and attending wild parties at Hoffmans
he devoted an inordinate amount of time and energy home. Somehow surviving high school, he went on to
to assisting and advising a vast array of students and attend the University of Chicago and Boston University.
colleagues about both professional and personal Butters was at first unsure of his professional goals.
matters. He was described as being biologically inca- His parents had pushed for him to become a physician or
pable of tolerating an unhappy student (a term that lawyer, but neither profession held much appeal. Public
he applied quite broadly); he had to help make things speaking came rather easily to him, and he was excited by
right (even if the student did not immediately appre- the idea of being a positive influence in the lives of college
ciate his wisdom). In his later years he took tremen- students. Therefore, during the second or third year of
dous pleasure in referring to himself as the college he decided to become a psychology teacher.
Godfather of Neuropsychology. Butters entered the doctoral program in psychology at
Butters was blunt, brash, and famously irreverent. Clark University in the fall of 1960. At the time Clark had
While his lifestyle was decidedly mainstream, he one of the leading psychology programs in the world. He
reveled in characterizing himself as something of a was awarded a Woodrow Wilson Fellowship for his first
rebel. He was unendingly curious about those who year of graduate school because of his commitment to
walked to the beat of a different drummer. His per- college teaching. During his second or third year in grad-
sonal role models included Marlon Brando, Lenny uate school, he ran across a research article by Mortimer
Bruce, and Woody Allen. He had a keen sense for Mishkin and H. Enger Rosvold about delayed alternation,
and appreciation of the absurd and ironic and found reversal learning, and the frontal lobes in monkeys.
humor in the darker side of life, though he never took Butters became fascinated with the concept that one could
himself too seriously. On more than one occasion he examine the neurological structures that underlie cognitive
was heard saying: If I hadnt become a neuropsychol- and psychological processes. At the time he was particularly
ogist, I wouldve been a comedian. At every APA and interested in what went on in the brain and what brain
INS meeting social hour, Butters could be found, structures played a part in the development of concrete or
beer in hand, listening to and recounting hilarious formal operations in the thinking processes of children.
stories about friends, colleagues, and family. Most of At the end of his third year of graduate school, Butters
the time, he played a leading role in these comedic wrote to Hal Rosvold, a researcher at the National Insti-
tales. In sum, Butters rare combination of intellectual tutes of Health (NIH), asking whether he would consider
creativity, drive, irreverence, and appreciation of taking him as a postdoctoral fellow. A visit to Rosvolds
satire allowed him to make his mark both in the lab led to a postdoctoral fellowship with Rosvold and
field of neuropsychology and in the hearts of his Mishkin from 1964 to 1966. His work at the NIH focused
contemporaries. on the roles of the septal nuclei, basal forebrain, and
caudate nucleus in reversal learning and delayed alterna-
tion performance. Butters was fulfilling his plan to spend
Short Biography a couple of years studying physiological psychology
and perhaps do a few studies on the neurological
Nelson Butters was born on May 7, 1937, in Boston, MA. bases of cognition before resuming the path toward his
He initially attended public school in Brookline, MA, and teaching career.
then Worcester Academy, a private boarding school, grad- Butters resumed his teaching path in 1966 by taking
uating first in his class. He was an accomplished athlete teaching positions at Wright State University and Antioch
468 B BVRT
College in Ohio. However, the few studies he had Cross References

conducted while at NIH caught the attention of Harold
Goodglass and Norman Geschwind of the Boston Veter- Alzheimers Disease
ans Administration Hospital and Department of Neurol- Amnesia
ogy of the Boston University School of Medicine. Amnestic Disorder
Moreover, Butters and Goodglass had become acquainted Amnestic Syndrome
during the formers years at Clark. The personal relation- Anterograde Amnesia
ship, combined with Butters cutting-edge animal work, Dementia
led to an invitation from Geschwind and Goodglass to Episodic Memory
join their burgeoning Aphasia Research Center. Butters Goodglass, Harold (19202002)
eagerly accepted the opportunity to join this exciting Implicit Memory
group and to return home to Boston. While he initially Kaplan, Edith
studied nonhuman primates, he took the opportunity to Korsakoff s Syndrome
learn about human neuropsychology from the early pio- Mammillary Bodies
neers, many of whom resided in Boston. In addition to Medial Temporal Lobe
Geschwind and Goodglass, he reveled in learning from Memory
and exchanging ideas with the likes of Edith Kaplan, Memory Impairment
Marlene Oscar Berman, Howard Gardner, Edgar Zurif, Mishkin, Mortimer (1926 )
and many others. The unparalleled atmosphere at the Parkinsons Dementia
Boston VA Hospital led to Butters first studies in Parkinsons Disease
human neuropsychology. During 19671970 he con- Procedural Memory
ducted both animal and human research and after 1970 Retrograde Amnesia
his work focused exclusively on human cognition. Semantic Memory
In 1983 Butters moved to San Diego, CA, to join the Subcortical Dementia
Department of Psychiatry at UCSD, where he continued Temporal Lobes
to flourish. Continuing his research program, Butters also Thalamus
built a psychology service with a particular emphasis on
training. He surrounded himself with superb colleagues
including, among others, Robert Heaton and Dean Delis. References and Readings
In early 1993 Butters developed oral motor weakness
and by March 1993 it was clear that he had amyotrophic Butters, N. (1996). Memoirs, in Nelson Butters remembered. APA
lateral sclerosis. He was 55 years old and at the height of Division 40 Newsletter, 14(3), 1, 37.
Butters, M., Becker, J. T., & Brandt, J. (1996). A legend in his own time:
his career. He handled his nearly 3-year battle with ALS in
tribute to Nelson Butters, in Nelson Butters remembered. APA
typical Butters fashion, continuing to work and socialize Division 40 Newsletter, 14(3), 2, 78.
until the week before his death. He took the opportunity Butters, M. A., & Butters, N. M. (2002). Nelson M. Butters: One step
to tell his students, colleagues, and family how grateful he ahead. In A. Y. Stringer, E. L. Cooley, & A. L. Christensen (Eds.),
was to have had them in his life. When he lost the ability Pathways to prominence: Reflections of 20th century neuropsycho-
logists. New York: Psychology Press.
to speak, he used adaptive computer equipment to com-
Cermak, L. S. (Ed.). (1994). Neuropsychological explorations of memory
municate. The week before he died, he was still telling off- and cognition: Essays in Honor of Nelson Butters. New York:
color and self-deprecating jokes by laboriously typing Plenum.
with his big toe, irreverent and irrepressible until the end.
Acknowledgment
We would like to thank Christopher Ryan and David BVRT
Salmon for very helpful comments on an earlier draft of
this chapter. Benton Visual Retention Test
C
progresses to transient ischemic attacks (TIA), and recur-
C/NC rent strokes. The migraine attacks are often reported to be
particularly long lasting or severe and may even include
Coma/Near Coma Scale symptoms of hemiplegia. The strokes are typically lacu-
nar, occurring in subcortical white matter or basal ganglia
and, in some cases, occur in the brain stem and spinal
cord. Recurrent subcortical infarcts lead to cognitive de-
CABG cline, pseudobulbar palsy, motor impairment, psychiatric
symptoms (most commonly depression), and ultimately
Coronary Artery Bypass Graft total motor impairment and subcortical vascular demen-
tia. Cognitive decline is most prominently seen as execu-
tive dysfunction, slowed processing speed, and reduced
attentional abilities. As the disease progresses, memory
Cadasil and other areas of cognitive functioning begin to decline.
The total amount of white matter involvement associated
A NGELA E ASTVOLD, YANA S UCHY
with the lacunar lesions and the degree of atrophy predict
University of Utah
severity of cognitive and motor impairment.
Salt Lake, UT, USA
Cause: CADASIL is caused by mutations or deletions in
the Notch3 gene on chromosome 19, which plays an
important role in cell differentiation during development.
Synonyms
While the pathogenetic mechanism has yet to be deter-
mined, the resulting pathophysiology includes thickening
Agnogenic medial arteriopathy; Chronic familial vascular
of arterial walls, accumulation of granular osmiophilic
encephalopathy; Familial Binswangers disease; Familial
material (GOM) in arterial walls (this distinguishes it
disorder with subcortical ischemic strokes, dementia, and
from arterial hypertension), gradual destruction of vascu-
leukoencephalopathy; Hereditary multi-infarct dementia
lar smooth muscle cells leading to fibrosis, progressive
thickening of arterial walls, and narrowing of the lumen
Short Description or Definition of cerebral arteries. This eventually causes thrombosis,
reduced blood flow, destruction of small- and medium-
Cerebral autosomal dominant arteriopathy with subcor- sized arteries, and consequently focal infarcts. MRI typi-
tical infarcts and leukoencephalopathy (CADASIL) is a cally reveals characteristic periventricular or white matter
rare autosomal dominant, adult-onset inherited cerebral hyperintensities, as well as infarcts in the basal ganglia and
vascular disease, characterized by migraines, recurrent brain stem. The cerebral cortex remains relatively intact.
transient ischemic attacks, and strokes leading to cogni- Diagnosis: Identification of a Notch3 mutation provides
tive decline and dementia. the most certain diagnosis, in addition to the presence of
GOM in arterial walls, which can be detected with a skin
biopsy. Positive MRI findings are often detected in even
Current Knowledge asymptomatic individuals. History of particularly severe
migraines may be the earliest indication.
Clinical Manifestation: The typical age of onset is Treatment and prognosis: Currently, there is no cure or
30500 years of age. The initial clinical manifestation disease-modifying therapy for CADASIL, and only symp-
often begins with migraines with aura, and slowly tom management and supportive care are available for
470 C CAGE Questionnaire
affected individuals. Death typically occurs 1020 years to steady your nerves or to get rid of a hangover (eye-
after the onset of symptoms. Angiography and anticoagu- opener)? Individual item responses are scored in a binary
lants should be avoided as they may provoke cerebrovascu- fashion (0 = no and 1 = yes). The total score can
lar accidents. range from 0 to 4. A score of 2 or greater is typically
considered a positive finding, that is, an indication of
alcohol misuse.
Cross References
Binswangers Disease Historical Background

Lacunar Stroke
Small Vessel Ischemic Disease The CAGE was developed by Ewing and Rouse (1968)
for detection of alcoholism and was first introduced
as a formal screening instrument 2 years later (Ewing &
References and Readings Rouse, 1970). Final item selection for the CAGE was
based on examination of 130 randomly selected, general
Kalaria, R. N., Viitanen, M., Kalimo, H., Dichgans, M., & Tabira T. hospital patients; items selected were those that resulted
(2004). The pathogenesis of CADASIL: An update. Journal of Neu- in a minimal set of items that usefully divided
rological Sciences, 226, 3539.
responders into two groups, patients with alcoholism
Kalimo, H., Ruchoux, M. M., Viitanen, M., & Kalaria, R. N. (2002).
CADASIL: A common form of hereditary arteriopathy causing
(confirmed by physician impressions and chart
brain infarcts and dementia. Brain Pathology, 12(3), 371384. study) and patients without indication of alcoholism
Kalimo, H., Viitanen, M., Amberia, K., Juvonen, V., Marttila, R, (Ewing, 1984).
Poyhonen, M., et al. (1999). CADASIL: Hereditary disease of arteries Over the years, several modifications to the original
causing brain infarcts and dementia. Neuropathology and Applied
instrument have been recommended, including placing a
Neurobiology, 25, 257265.
time frame reference on the four questions (e.g., in the last
year), as well as adding questions regarding frequency of
use, tolerance, and perceived history of drinking problems
(Bradley, Kiviahan, Bush, McDonell, & Fihn, 2001;
National Institute on Alcohol Abuse and Alcoholism,
CAGE Questionnaire 1995; McQuade et al., 2000).
M YRON G OLDBERG
University of Washington Medical Center
Seattle, WA, USA Psychometric Data
Testretest reliability of the CAGE over a 7-day period was

Definition 0.80 in a psychiatric sample and 0.95 in a nonclinical
sample (Teitelbaum & Carey, 2000); mean CAGE score
The CAGE is one of a number of brief screening changes for each group across this same time period
instruments designed to help in the detection of alcohol were nonsignificant. Convergent validity has been reason-
misuse. The instruments name is an acronym for ably good, though somewhat variable, with reported
questions about Cutting down on drinking, Annoyance correlations ranging from 0.48 to 0.70 with other
at others concern about drinking, feeling Guilty about alcohol-screening instruments (see Dhalla & Kopec,
drinking, and using alcohol as an Eye-opener in the 2007 for review).
morning. The CAGE can be rapidly administered in an A number of studies have examined the validity of
interview format or written format and consists of the CAGE in detecting alcohol misuse. Aertgeerts, Buntinx,
following four items: (1) Have you ever felt that you and Kester (2004) performed a meta-analysis of 10 studies
should cut down on your drinking?; (2) Have people of the utility of the CAGE in detecting alcohol abuse or
annoyed you by criticizing your drinking?; (3) Have alcohol dependency in general clinical populations using
you ever felt bad or guilty about your drinking?; and criteria from the Diagnostic and Statistical Manual for
(4) Have you ever had a drink first thing in the morning Mental Disorders (DSM-III-R APA, 1987). With a cutoff
CAGE Questionnaire C 471
score at 2, pooled sensitivities across studies were 0.87 in Cross References
hospital inpatients, 0.71 in primary care patients, and 0.60
in ambulatory medical patients; specificities were 0.77, Alcohol Abuse
0.91, and 0.92, and positive predictive validities were Alcohol Dependence
0.57, 0.74, and 0.82, respectively. Aertgeerts et al. (2004) Alcoholic Brain Syndrome C
concluded that the CAGE is only of limited value as a Alcoholism
screening instrument using a cutoff score of 2 and Blood Alcohol Level
recommended that additional information about alcohol Fetal Alcohol Syndrome
use patterns be obtained from any patient who gives one Korsakoff s Syndrome
positive answer on the instrument. Michigan Alcoholism Screen Test
Dhalla and Kopec (2007) provided a more recent Substance Abuse
review of the CAGE validity literature, considering, in Substance Abuse Disorders
part, the sensitivity, specificity, and positive predictive WernickeKorsakoff s Syndrome
value associated with different cutoff scores. The authors
concluded that the CAGE has adequate validity in
screening medical and surgical inpatients, psychiatric
inpatients, and ambulatory medical patients for alcohol
Aertgeerts, B., Buntinx, F., & Kester, A. (2004). The value of the CAGE in
misuse and that use of a cutoff score of 2 affords the screening for alcohol abuse and alcohol dependence in general
best combination of sensitivity, specificity, and positive clinical populations: A diagnostic meta-analysis. Journal of Clinical
predictive value. At the same time, they cautioned that the Epidemiology, 57, 3039.
CAGE has not performed well with Caucasian women, American Psychiatric Association (1987). Diagnostic and statistical man-
ual of mental disorders (3rd rev. ed.). Washington, D.C.: American
prenatal women, and college students.
Psychiatric Press.
Fiellin, Carrington, and OConner (2000) also provide Bradley, K., Kiviahan, D., Bush, K., McDonell, M., & Fihn, S. (2001).
a noteworthy review of validity studies, concluding that in Variations on the CAGE alcohol screening questionnaire: Strengths
primary care settings, the CAGE questionnaire was more and limitations in VA general medical patients. Alcoholism: Clinical
effective in identifying patients with alcohol abuse or and Experimental Research, 25, 14721478.
Cherpitel, C. J. (2000). A brief screening instrument for problem drinking
dependency than in detecting patients with at risk,
in the emergency room: The RAPS4. Journal of Studies on Alcoholism,
hazardous, or harmful drinking. 61, 447449.
Dhalla, S., & Kopec, J. (2007). The CAGE questionnaire of alcohol
misuse: A review of reliability and validity studies. Clinical & Inves-
Clinical Uses tigative Medicine, 30, 3341.
Ewing, J. A. (1984). Detecting alcoholism: The CAGE questionnaire.
Journal of the American Medical Association, 252, 19051907.
The CAGE has enjoyed wide popularity in primary care Ewing, J. A., & Rouse, B. A. (1970). Identifying the hidden alcoholic.
settings as an alcohol-screening instrument for a number Presented at the 29th international congress on alcohol and drug
of reasons, as it is brief, easy to administer, and can be dependence, Sydney, Australia, February 3, 1970.
incorporated into more extensive interviews or question- Fiellin, D., Carrington, R., & OConner, P. (2000). Screening for alcohol
problems in primary care: A systematic review. Archives of Internal
naires (Bradley et al., 2001). However, support for its
Medicine, 160, 19771989.
validity across different populations has been mixed. It National Institute on Alcohol Abuse and Alcoholism (1995). The physicians
appears to perform best when used to screen for alcohol guide to helping patients with alcohol problems (NIH publication
abuse or dependence in clinical populations and less 95-3769). Bethesda: U.S. Department of Health and Human
well in detecting current hazardous drinking. Caution Services, Public Health Service, National Institutes of Health.
Pokorny, A., Miller, B., & Kaplan, H. (1972). The brief MAST: A short-
should be used especially when interpreting results for
ened version of the Michigan Alcoholism Screening Test. American
nonclinical respondents (i.e., general population) as well Journal of Psychiatry, 129, 342.
as for women and college students, as the CAGE has been Saunders, J. B., Aasland, O. G., Babor, T. F., De La Fuente, J. R., & Grant,
noted to under-perform in these populations. In addition, M. (1993). Development of the Alcohol Use Disorders Identification
as several authors have recommended, a positive finding Test (AUDIT): WHO collaborative project on early detection of
persons with harmful alcohol consumption-II. Addiction, 88,
on the CAGE, regardless of cutoff score level (i.e., 1
791804.
or 2), should be followed up by further examination Teitelbaum, L., & Carey, K. (2000). Temporal stability of alcohol
of alcohol consumption patterns, using established stan- screening measures in a psychiatric setting. Psychology of Addictive
dard criteria. Behaviors, 14, 401404.
472 C CalCAP
(what) streams to the parieto-occipital association

CalCAP cortex and occipitotemporal association cortices,
respectively.
California Computerized Assessment Package
Illness
Calcarine Cortex The calcarine cortex is perfused by the calcarine artery,

which is a limb off the posterior cerebral artery. Our
M ARY-E LLEN M EADOWS visual system has evolved such that damage to one eye
Brigham and Womens Hospital does not result in blindness in one visual field. Damage
Boston, MA, USA to either the right or left calcarine cortex results in a
contralateral field cut, a hemianopia. Macular sparing
usually occurs because of collateral blood supply from
Synonyms branches of the middle cerebral artery. Isolated lesions
of the primary visual cortex results in discrete blind
Primary visual cortex; Striate cortex spots (scotomas) in the corresponding area of the
visual field.
Structure
Cross References
This is the term for the primary visual cortex, V1, or
Calcarine Fissure
Brodmanns area 17. The area encompasses the medial
Calcarine Sulcus
surface and a small lateral surface of the occipital lobe,
Occipital Lobe
and is within the calcarine sulcus. It is located at the most
Scotoma
posterior portion of the cerebral hemisphere. The optic
Unimodal Cortex
radiations terminate in layer IV of the calcarine cortex.
Visual Cortex
Layer IV is rather thick and is subdivided into sublaminae.
The calcarine cortex is also sometimes referred to as
the striate cortex because of a strip of myelin (Stria of
Gennari) that can be visualized. The area is organized in References and Readings
a retinotopic fashion; that is, there is point-to-point
representation from the retina to the cortex. For instance, Netter, F. (1991). The CIBA collection of medical illustrations: Volume I
fibers in the right half of each retina (perceives information nervous system, part I: anatomy and physiology. West Caldwell, NJ:
in the left visual field) project to the right calcarine cortex, CIBA-Geigy.
and fibers in the left half of each retina (perceives informa-
tion in the right visual field) project to the left calcarine
cortex.
Calcarine Fissure
Function J OHN E. M ENDOZA
From a functional perspective, the calcarine cortex is im- New Orleans, LA, USA
portant in determining orientation, spatial-frequencies,
and color properties of the visual stimulus. The infor-
mation is then projected to other areas in the occip- Synonyms
ital lobe for further visual analysis. This occurs via
transmission to the dorsal (where) and the ventral Calcarine sulcus
California Computerized Assessment Package C 473
California Computerized
Assessment Package
E RIC N. M ILLER C
UCLA Psychology Clinic
Los Angeles, CA, USA
Synonyms
CalCAP
Description
Calcarine Fissure. Figure 1 Mid-sagittal view of the brain
(MRI) showing calcarine fissure separating the cuneus and the The California Computerized Assessment Package (Cal-
lingual gyrus of the occipital lobe CAP; 1999) presents a series of brief reaction time tasks
designed to assess speeded information processing and
psychomotor functioning. The Standard CalCAP consists
Definition of 4 Simple and 6 GoNo Go reaction time subtests that
require 2025 min to complete. The individual reaction
The calcarine fissure is a deep sulcus located on the medial time measures were designed to assess a number of cog-
surface of the occipital lobe (see Fig. 1). The superior nitive domains, including speed of processing (reaction
(cuneus) and inferior (lingual gyrus) banks of this sulcus time), lexical discrimination (real word vs. nonsense
represent the primary cortical projection area for vision. word), rapid visual scanning, form discrimination and
Visual information that is first received in the upper matching, working memory (1-back and 2-back tasks),
portions of the retina is represented along the upper and sustained and divided attention. Each task includes a
banks of the fissure (cuneus), while that derived from practice session that must be completed with 100% accu-
the lower retina projects to its lower bank. Thus, lesions racy to proceed to the main 2-min procedure, a method
confined to the upper bank (cuneus) will result in con- that ensures that subjects understand the task instructions
tralateral inferior visual field defects, while damage to and that minimizes practice effects in longitudinal study
the lower bank (lingual gyrus) will produce upper field designs. Subjects are asked to focus on a display field and
deficits. Lesions destroying tissue along both the upper respond only to specific types of visual stimuli. For exam-
and lower banks may result in a contralateral homony- ple, in the form discrimination task, they are asked to
mous hemianopia. press a key only when two out of three non-nameable
figures are identical.
The core measures of reaction time, hits and false-
positives, and signal detection parameters allow investiga-
Cross References tors to measure accuracy and general speed of processing,
as well as relative differences among conceptually distinct
Cuneus decision tasks. Four iterations of a Simple reaction time
Lingual Gyrus routine at various points in the test allow direct measure-
Visual System ment of the subjects ability to maintain focus throughout
the 20-min testing procedure. The computer scores each
task using age- and education-specific norms derived from
641 men ranging from 21 to 58 years of age, with a mean
education of 16 years. Final scores are available immediate-
Calcarine Sulcus ly in tabular and graphical formats. Additional norms have
been derived for elementary school children (3rd, 5th, and
Calcarine Fissure 6th grades), women, and older individuals. The CalCAP
474 C California Computerized Assessment Package
also includes a 4-subtest language-independent abbreviated GoNo Go paradigms, the simple reaction time measures
battery weighted toward measures of speeded processing have relatively low testretest reliability (0.200.29), sug-
and working memory. These test batteries are well suited gesting that the psychomotor skills measured by the sim-
for collecting reliable information on psychomotor func- ple reaction time tasks vary considerably depending on
tioning in a brief period of time, and can be used effectively state variables such as mood, attention, fatigue, and time
for assessing changes over time. Stimulus materials are of day (Miller, 2008).
available in English, Spanish, French, Norwegian, Danish, CalCAP reaction time correlates most highly with age,
and Flemish. and, to a lesser extent, with years of education. Two
studies of gender effects on CalCAP reaction time have
shown no differences between men and women on any of
Historical Background the CalCAP indices (Berg, 1994). The psychometric prop-
erties of the CalCAP are unstable for 3rd graders, but
The CalCAP was originally developed by Dr. Eric Miller essentially the same as found in adults by the 5th grade
in the late 1980s as an automated substitute for (Budzinski, 1994).
traditional neuropsychological testing. The Standard
battery, developed in consultation with Dr. Paul Satz
and Dr. Ola Selnes, was designed to measure aspects of Clinical Uses
language and visuoperceptual skills, working memory,
speeded information processing, attention, learning and The CalCAP has been widely used in cross-sectional and
memory, visual scanning, and reaction time. While the longitudinal studies of HIV/AIDS (Miller et al., 1991;
reaction time tasks that comprise the Standard CalCAP Gonzalez et al., 2003), drug abuse (Chang et al., 2002;
battery do assess many of these areas of cognitive func- Volkow et al., 2001), depression (Stordal et al., 2004),
tioning, studies have shown that the tasks correlate only epilepsy (Hessen, Lossius, M. I., Reinvang, I., & Gjerstad,
modestly (0.20.4) with traditional neuropsychological 2008), traumatic brain injury (Waterloo, Ingebrigtsen, &
measures (Miller, Satz, & Visscher, 1991). Factor analyses Romner, 1997), and hyperbaric oxygen treatments
using the CalCAP and other neuropsychological test (Hjalmarsen, Waterloo, Dahl, Jorde, & Viitanen, 1999;
batteries show that the reaction time indices form two Van Hoof, Coomans, De Becker, De Meirleir, & Cluydts,
primary factors best characterized as simple reaction 2002). It is particularly sensitive to the psychomotor
time and decision speed. These factors are distinct changes seen in these disorders and, unlike most psycho-
from traditional neuropsychological measures and motor tasks, has minimal practice effects, making it par-
most researchers and clinicians now use the CalCAP ticularly appropriate for research paradigms such as
and other reaction time measures primarily as indices clinical trials and epidemiologic studies that require re-
of these types of speeded information processing and peated testing.
attention. The abbreviated version of the CalCAP specif- The cognitive functions assessed by the CalCAP pro-
ically excludes measures designed to look at visuoper- gram are best described as timed psychomotor skills re-
ceptual and language skills and focuses primarily on quiring focused or sustained attention. Impaired reaction
these core indices of reaction time, working memory, time across multiple measures is usually indicative of
and attention. generalized motor slowing or slowed information pro-
cessing. Impaired reaction time on specific measures,
particularly when coupled with scores outside of normal
Psychometric Data bounds on true-positive responding, is suggestive of a
more specific functional deficit, such as language skills
All the subtests in the CalCAP have high internal consis- (lexical discrimination task), visuoperceptual deficits
tency reliability (0.770.96). Six-month testretest reli- (form discrimination), or working memory (1-back and
ability for the GoNo Go paradigms is comparable with 2-back tasks).
levels seen for conventional neuropsychological proce- The standard CalCAP program classifies subjects as
dures (0.430.68), but there is less evidence of the practice outliers if they perform two standard deviations or
effects commonly seen with psychomotor measures. The lower on two or more of the tasks. Using these
reduced practice effects may be due to the requirement criteria, approximately 10% of subjects are classified as
that all subjects complete practice trials with 100% outliers. This base rate of 10% includes individuals with
accuracy before proceeding to the actual test. Unlike the premorbid conditions such as prior head injury, learning
California Verbal Learning Test (California Verbal Learning Test-II) C 475
disability, preexisting neurologic conditions, as well as Waterloo, K., Ingebrigtsen, T., & Romner, B. (1997). Neuropsychological
function in patients with increased serum levels of protein S-100
individuals who are simply on the low end of normal
after minor head injury. Acta Neurochirurgica, 139, 2632.
functioning.
Cross References
C
California Verbal Learning Test
Attention/Executive Functions (California Verbal Learning
Continuous Performance Tests
Information Processing Speed Test-II)
Speed of Information Processing
VisualMotor Function A NGELA Y I
Mount Sinai Medical Center
New York, NY, USA
Berg, D. (1994). Adults reaction time as affected by age and education level.
Synonyms
B.A. Honours Thesis supervised by Dr. Frank Spellacy, University of
Victoria. CVLT
Budzinski, L. M. (1994). An exploration of simple and choice reaction times
in children. B.A. Honours Thesis supervised by Dr. Frank Spellacy,
Victoria, B.C., University of Victoria.
Chang, L., Ernst, T., Speck, O., Petal, H., DeSilva, M., Leonido-Yee, M., Description
et al. (2002). Perfusion MRI and computerized cognitive tests
abnormalities in abstinent methamphetamine users. Psychiatry Re-
search, 114, 6579.
The California Verbal Learning Test-II (CVLT-II) is the
Gonzalez, R., Heaton, R. K., Moore, D. J., Letendre, S., Ellis, R. J., latest (2000) version of a widely used verbal learning and
Wolfson, T., et al. (2003). HIV Neurobehavioral Research Center memory test. The current version contains recalling
Group. Computerized reaction time battery versus a traditional and recognition of two lists of words over immediate
neuropsychological battery: detecting HIV-related impairments. and delayed trials. List A includes 16 words and requires
Journal of International Neuropsychological Society, 9, 6471.
Hessen, E., Lossius, M. I., Reinvang, I., & Gjerstad, L. (2008). Improve-
the examinee to recall the list over five trials. List B
ment in speeded cognitive processing after anti-epileptic drug with- (interference), which is also 16 words, is administered
drawal a controlled study in mono-therapy patients. Progress in after List A for one trial. Short-delay free recall and
Neurotherapeutics and Neuropsychopharmacology, 3, 199209. cued recall are administered after List B. A 20-min delay
Hjalmarsen, A., Waterloo, K., Dahl, A., Jorde, R., & Viitanen, M. (1999). follows the short-delay recalls, followed by nonverbal
Effect of long-term oxygen therapy on cognitive and neurological
dysfunction in chronic obstructive pulmonary disease. European
testing. Long-delay recall, long-delay-cued recall, and yes/
Neurology, 42, 2735. no-recognition trials of List A follow the 20-min delay.
Miller, E. N. (1999). CalCAP California Computerized Assessment Package A revision of the CVLT-II is the addition of a forced choice
Manual (2nd ed.). Los Angeles: Norland Software. recognition after a 10-min delay following the yes/no trial.
Miller, E. N. (2008). CalCAP California Computerized Assessment Pack- Another revision of the CVLT-II is the inclusion of a
age. Retrieved October 16, 2008 from http://www.calcaprt.com
Miller, E. N., Satz, P., & Visscher, B. (1991). Computerized and conven-
short form (nine words) and an alternate form. The short
tional neuropsychological assessment of HIV-1 infected homosexual form was created for the purpose of screening or for
men. Neurology, 41, 16081616. patients who may have more severe brain damage and
Stordal, K. I., Lundervold, A. J., Egeland, J., Mykletun, A., Asbjornsen, A., may feel overwhelmed by the long form. This short form
Landro, N. I., et al. (2004). Impairment across executive functions takes 15 min to administer and also has a 15-min delay.
in recurrent major depression. Nordic Journal of Psychiatry, 58,
4147.
The alternate form has been statistically equated with the
Van Hoof, E., Coomans, D., De Becker, O., De Meirleir, K., & Cluydts, R. standard form.
(2002). Hyperbaric oxygen therapy for chronic systemic infections in The CVLT-II was normed from a national standardi-
chronic fatigue syndrome. International Journal of Psychophysiology, zation sample of 1,087 of ages 1689, which was demo-
45, 8283. graphically matched to the US population. It takes 30 min
Volkow, N. D., Chang, L., Wang, G. J., Fowler, J. S., Leonido-Yee, M.,
Francesci, D., et al. (2001). Association of dopamine transporter
to administer and includes 30 min of delay. The test is
reduction with psychomotor impairment in methamphetamine administered with paper and pencil format, with the
abusers. American Journal of Psychiatry, 158, 377382. examiner recording the responses. The responses are
476 C California Verbal Learning Test Childrens Version
scored using the Comprehensive Scoring System, which of the literature of clinical populations from 1987 to
computes raw scores and standardized scores for over 1999, summarizing the key findings of CVLT perfor-
50 learning and memory variables. The raw scores can mance across various clinical populations, which include
be scored manually, although there are limits to how anterior temporal lobectomy, Korsakoff s syndrome,
much information can be derived. Alzheimers disease, Huntingtons disease, Parkinsons
The CVLT-childrens (CVLT-C) version can be adminis- disease, head injury, schizophrenia, depression and
tered to children aged 516 and can assist professionals in other affective disorders, chronic alcohol and drug
diagnosing memory impairment secondary to learning dis- abuse, posttraumatic stress disorder, systemic medical
abilities, attention-deficit disorder, mental retardation, and disease (HIV, chronic fatigue syndrome, Lyme disease,
other neurological disorders and psychiatric problems. The eosinophilia myaligia syndrome, cardiac transplant can-
administration is similar to the format of the CVLT-II, didates), insufficient effort, and predictor for everyday
although forced choice recognition is not included. functioning.
Historical Background Cross References
The first edition of the CVLT was originally published in Buschke Selective Reminding Test
1987 from the work of Delis, Kramer, Kaplan, and Ober Childrens Memory Scale
(1987). They created one of the first tests to incorporate Hopkins Verbal Learning Test
principles from cognitive science to measure learning and Rey Auditory Verbal Learning Test
memory. This test provided a measurement of not only Rivermead Behavioral Memory Test
what an individual remembers, but how they remember Selective Reminding Test
and what errors are made. This refuted previous beliefs Wechsler Abbreviated Scale of Intelligence
that memory dysfunction was limited to recall and Wechsler Memory Scale All Versions
recognition.

Psychometric Data
Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (1987). The California
verbal learning test: Research edition, adult version. San Antonio, TX:
CVLT-II: Split-half reliability coefficients based on split-
The Psychological Corporation.
ting immediate-recall trials ranged from 0.89 to 0.94. Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (1993). The California
Coefficient alphas based on word category scores across verbal learning test for children. San Antonio, TX: The Psychological
immediate-recall trials ranged from 0.71 to 0.82. The split- Corporation.
half reliability based on the number of times each word was Elwood, R. W. (1995). The California verbal learning test: Psychometric
characteristics and clinical application. Neuropsychology Review, 5(3).
correctly recalled across immediate-recall trials ranged
from 0.68 to 0.79. The CVLT-II is correlated with the
Wechsler Abbreviated Scale of Intelligence (WASI).
CVLT-C: The internal consistency reliability across
five trials ranged from 0.84 to 0.91. Reliability coefficients California Verbal Learning Test
for across-semantic category consistency ranged from Childrens Version
0.64 to 0.80.
E RIC M. F INE , D EAN C. D ELIS
University of California, San Diego, School of Medicine
Clinical Uses San Diego Veterans Affairs Healthcare System
La Jolla, CA, USA
The CVLT-II manual states that the test measures multi-
ple aspects of how verbal memory occurs or fails to
occur, therefore providing a comprehensive assessment Synonyms
of each patients profile of verbal learning and memory
strengths and weaknesses. The manual reports a review CVLT-C
California Verbal Learning Test Childrens Version C 477
Description false-positive errors in recognition memory (Table 1 for

CVLT-C variable definitions).
Overview of Test Procedures
The California Verbal Learning Test Childrens Version Standardization Sample C

(CVLT-C) is a relatively brief, individually administered
measure designed to assess the strategies and processes The CVLT-C was normed on a sample of 920 children
involved in learning and remembering verbal materials from 12 age groups ranging from 5 through 16 years of
(Delis, Kramer, Kaplan, & Ober, 1994). Like the adult age. The sample was stratified based on data from the
versions of this measure (CVLT; Delis, Kramer, Kaplan, 1988 U.S. Census (for additional information regarding
& Ober, 1987; CVLT-II; Delis, Kramer, Kaplan, & Ober, the sample characteristics, see the test manual; Delis et al.,
2000; California Verbal Learning Test (California Verbal 1994). In addition, normative data for 4-year-olds was
Learning Test-II), the CVLT-C adopts a process-oriented provided by a study by Goodman, Delis, and Mattson
approach for parsing a variety of learning and memory (1999).
components, which facilitates the identification of dis-
tinct memory profiles associated with clinical disorders.
The CVLT-C uses words presented as part of two Score Conversions and Contrast Scores
shopping lists (i.e., a Monday list and a Tuesday
list) and measures both recall and recognition of the Raw scores for the various CVLT-C indices are converted
words over a number of trials. The use of a shopping- into an age-based T or z scores (see test manual for
list format makes the procedure more relevant for a description of procedures used to derive these standar-
child and provides information regarding how the child dized scores; Delis et al., 1994). Although the test manual
approaches an everyday memory task. Specifically, in the includes tables for converting the numerous raw scores to
first five trials, the child is asked to recall words from the standardized scores, these scores are computed automati-
Monday list (List A), which consists of 15 words, with cally using the CVLT-C computer scoring software. The
five words from each of three semantic categories (i.e., standard score for List A trials 15 total is presented in a
fruits, clothing, and toys). An interference Tuesday list T-score metric, with a mean of 50 and a standard devia-
(List B) of 15 words is then presented on one trial. Words tion of 10. The remaining standardized scores are pre-
from the Tuesday list are divided equally across three sented in a z-score metric, with a mean of 0 and a
semantic categories (i.e., fruits, furniture, and desert). standard deviation of 1.
The Tuesday trial is followed by short-delay free- and Examination of contrast scores (i.e., z-score differ-
cued-recall trials of the first (Monday) list. For cued- ences between two variables) allows for the assessment of
recall trials, the examinee is asked to recall words from particular learning and memory processes. For example,
the three semantic categories contained in List A. A comparing List B (Tuesday list) recall with List A (Monday
20 min delay occurs next, during which nonverbal mea- list) Trial 1 recall provides a measure of a childs suscep-
sures should be administered. After the delay interval, tibility to proactive interference. As another example, con-
long-delay free-recall, long-delay cued-recall, and yes/no trasting List A long-delay free recall with List A short-delay
recognition memory trials of the Monday list (List A) are free recall can be used to identify rapid forgetting across
administered. delays (Delis et al., 1994; Delis et al., 2000; Donders &
With these procedures, the CVLT-C evaluates not only Minnema, 2004).
the level of a childs memory performance, but also the
learning strategies used and types of errors made (Delis
et al., 1994). Numerous learning and memory variables Historical Background
are quantified on the CVLT-C, including level of total
recall and recognition on all trials, type of learning strate- In the past, the clinical neuropsychological assessment of
gy employed (e.g., semantic clustering and serial cluster- memory relied on tests designed primarily to assess the
ing), serial position effects, degree of vulnerability to presence or absence of memory dysfunction per se. This
proactive and retroactive interference, retention of infor- goal was accomplished by scoring memory tests only in
mation over short and longer delays, enhancement of terms of the level of correct recall or recognition. Howev-
recall performance by category cuing and recognition er, over the past 25 years or so, numerous studies from
testing, perseveration and intrusion errors in recall, and cognitive neuropsychology have documented qualitatively
478 C California Verbal Learning Test Childrens Version
California Verbal Learning Test Childrens Version. Table 1 CVLT-C variable definitions
Variable
List A total Total number of words recalled across the five learning trials
List A1 Number of words recalled from the first trial
List A5 Number of words recalled from the fifth trial
List B Number of words recalled from the interference list (List B)
List A short-delay free Number of words recalled from List A immediately after the presentation of the interference list
recall (List B)
List A short-delay cued Number of words recalled from List A with semantic cueing
recall
List A long-delay free Number of words recalled from List A after a 20 min delay
recall
List A long-delay cued Number of words recalled from List A with semantic cueing after a 20 min delay
recall
Semantic clustering Number of consecutively recalled words from the same semantic category (i.e., consecutive words
from the same semantic category), which reflects the extent to which the subject has actively
imposed a semantic organization on the list of words
Serial clustering Number of consecutively recalled words in the same order as they were presented (i.e., a serial
cluster)
Primacy % Percentage of words correctly recalled from the beginning of List A (first four words)
Middle % Percentage of words correctly recalled from the middle of List A (middle seven words)
Recency % Percentage of words correctly recalled from the end of List A (last four words)
Learning slope Average number of new words acquired across the five List A immediate-recall trials (e.g., a score of 1
means that the examinee learned approximately one new word per trial)
Consistency % Percentage of target words recalled once on each of the four learning trials that were also recalled on
the very next trial; reflects ability to maintain a consistent learning strategy
Perseverations Total number of target words repeated within a trial (called repetitions on the CVLT-II; Delis et al.,
2000)
Free-recall intrusions Total number of extra-list intrusions on all the free-recall trials
Cued intrusions Total number of extra-list intrusions on all the cued-recall trials
Total intrusions Total number of extra-list intrusions made on free- and cued-recall trials
Recognition hits Total number of target words correctly identified on recognition testing as belonging to List A
(yes/no format)
Recognition Accuracy of distinguishing target from distracter words on recognition testing; calculated using
discriminability signal detection methods
False positives Total number of distractor words incorrectly identified as belonging to List A during recognition
testing
Response bias Tendency to favor yes or no responses on recognition testing (positive scores reflect a yes bias)
distinct patterns of memory dysfunction associated with neuroscience, and modeled in part after the Rey Auditory
various neurological and psychiatric populations. These Verbal Learning Test (Rey AVLT; Rey, 1964), the CVLT-C,
findings emphasize the multicomponential nature of like its adult counterpart ( California Verbal Learning
learning and memory, and, as such, the importance of Test (California Verbal Learning Test-II)), was developed
developing clinical memory tests that allow for the to facilitate the quantification of multiple learning and
evaluation of both qualitative and quantitative features memory parameters (Delis et al., 1987; Delis, Freeland,
of memory performance. Informed by principles of Kramer, & Kaplan, 1988; Delis et al., 1994; Delis et al.,
learning/memory from cognitive science and cognitive 2000).
California Verbal Learning Test Childrens Version C 479
Psychometric Data Because the reliability characteristics of the primary

CVLT-C performance indices (e.g., the total words
Reliability and Validity recalled during the learning trials) are stronger than for
the process or strategy-use variables (e.g., semantic
The reliability of the CVLT-C was assessed using measures clustering), it has been recommended that clinicians C
of internal consistency and testretest reliability (Delis place greater emphasis on the main performance variables
et al., 1994). The internal consistency coefficient for the and interpret process-variables cautiously (Strauss et al.,
five trials of the Monday list ranged from .84 to .91 (with a 2006). In order to evaluate learning and memory in other
mean of .88) and the across-semantic-category consisten- formats (e.g., story memory) or modalities (visual), the
cy coefficient ranged from .64 to .80 (with a mean of .72). CVLT-C can be complemented with measures from other
Testretest stability (median retest interval of 28 days) standardized childrens memory assessment batteries
ranged from .90 to .17, with higher testretest correlations (e.g., Childrens Memory Scale and Wide Range Assess-
typically occurring for measures of overall level of perfor- ment of Memory-Second Edition).
mance (e.g., total words recalled during the five learning
trials and long-delay free recall). Practice effects were
fairly large for certain conditions. For example, trials Cross References
15 total recall improved by an average of five words for
8-year-olds, by six words for 12-year-olds, and by nine California Verbal Learning Test (California Verbal
words for 16-year-olds. The average improvement on List B, Learning Test-II)
the short-delay, and long-delay trials ranged from one to Childrens Memory Scale
two words across all the groups. Rey Auditory Verbal Learning Test
Evidence supporting the validity of CVLT-C comes
from factor analyses of the original standardization
sample and studies of CVLT-C performance in various References and Readings
neurological and neurodevelopmental populations. As
described in the test manual, exploratory principal com- Delis, D. C., Freeland, J., Kramer, J. H., & Kaplan, E. (1988). Integrating
ponents analysis of the primary CVLT-C performance clinical assessment with cognitive neuroscience: Construct valida-
tion of the California Verbal Learning Test. Journal of Consulting and
indices produced a six-factor solution that closely paral-
Clinical Psychology, 53(1), 123130.
leled the adult version (CVLT; Delis et al., 1987). In Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (1987). The
addition, Donders (1999) employed confirmatory factor California verbal learning test - Adult version. San Antonio, TX:
analysis to reanalyze the CVLT-C standardization sample, The Psychological Corporation.
and found a five-factor solution that included attention Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (1994). The
California verbal learning test-Childrens version. San Antonio, TX:
span (List A, Trial 1; List B; middle region recall), learning
The Psychological Corporation.
efficiency (List A, Trial 5; semantic clustering; recall Delis, D. C., Kramer, J., Kaplan, E., & Ober, B. A. (2000). California verbal
consistency), free delayed recall (ahort-delay free recall, learning test - Second Edition. San Antonio, TX: The Psychological
long-delay free recall), cued-delay recall (short-delay cued Corporation.
recall, long-delay cued recall), and inaccurate recall (total Donders, J. (1999). Structural equation analysis of the California verbal
learning test - Childrens version in the standardization sample.
intrusions, recognition false positives).
Developmental Neuropsychology, 15, 395406.
Donders, J., & Minnema, M. (2004). Performance discrepancies on the
California verbal learning test - Childrens version (CVLT-C) in
Clinical Uses children with traumatic brain injury. Journal of the International
Neuropsychological Society, 10, 482488.
Goodman, A. M., Delis, D. C., & Mattson, S. N. (1999). Normative data
The CVLT-C was designed to assess subtle to severe verbal
for 4-year-old children on the California verbal learning test -
learning and memory deficits in child clinical populations. Childrens version. The Clinical Neuropsychologist, 13(3), 274282.
The extant literature indicates that the CVLT-C has utility Miller, L. J., & Donders, J. (2003). Prediction of educational outcome
for characterizing the learning and memory deficits asso- after pediatric traumatic brain injury. Rehabilitation Psychology, 48,
ciated with a wide-range of clinical disorders (for review, see 237241.
Rey, A. (1964). Lexamen clinique en psychologie. Paris: Presses Universi-
Strauss, Sherman, & Spreen, 2006). In addition, CVLT-C
taires de France.
performance has been shown to be predictive of long- Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A compendium
term educational outcomes in children who have suffered of neuropsychological tests (3rd ed.). New York: Oxford University
a traumatic brain injury (Miller & Donders, 2003). Press.
480 C Callosal Apraxia
Current Knowledge
Callosal Apraxia
The CANTAB includes two products: CANTABeclipse
Alien Hand Syndrome and CANTABelect. The CANTABeclipse is composed
Apraxia of 22 tests grouped in specific functional dimensions
measuring executive functioning, visual memory, atten-
tion, semantic/verbal memory, and decision making/
response control. A sixth functional category labeled in-
Callosal Disconnection Syndrome duction is comprised of two very short tests whose pur-
pose is to familiarize examinees with the general idea of
Split-Brain responding by touching the screen and to identify those
examinees who cannot reliably participate in the exami-
nation. Details of each subtest are described in Table 1.
The CANTAB offers users flexibility by providing subtests
that can be selected for administration based upon the
Cambridge Neuropsychological specific clinical question. All subtest stimuli are delivered
Testing Automated Battery nonverbally, although adequate receptive language func-
tions are necessary to understand task demands. The
M ARK A. S ANDBERG publisher regards the majority of CANTAB tests to be
Independent Practice independent of language and culture.
Smithtown, NY, USA CANTABelect is described as a bespoke service
geared toward conducting pharmaceutical clinical trials.
In this case, CCL configures a battery to meet the specific
Synonyms research needs and requirements of the investigator.
Research supporting the use of the CANTAB in the
CANTAB evaluation of brainbehavior relations is reasonably ex-
tensive, with many peer reviewed articles available for
review on the companys website www.cantab.com. Stud-
ies are available supporting the validity and utility of
Description the CANTAB in measuring the impact of pharmaco-
therapy on neuropsychological performance, and in the
The Cambridge Neuropsychological Testing Automated assessment of Attention Deficit Hyperactivity Disorder,
Battery (CANTAB) is a neuropsychological measure de- affective disorders, schizophrenia, senile dementia of the
veloped at the University of Cambridge and currently Alzheimers type and Parkinsons disease. Although consid-
marketed by Cambridge Cognition Limited (CCL). The erable research is available attesting to the usefulness of the
CANTAB is a theoretically derived instrument, predomi- CANTAB with adult populations, it has not been studied to
nantly measuring non-language functions. The current the same extent in the assessment of brain-behavior rela-
version is a Windows-based program operating on a PC tions and their developmental evolution among children.
platform utilizing interactive touch screen technology. More recent is the investigation of the CANTAB as
CANTAB tests are described as having sufficient sensitiv- a tool to assess the neuropsychological functioning of
ity to discern changes in cognitive functioning brought children. Luciana (2003) noted that because the format
about by CNS disorders and medications. and test items can be used in the assessment of all age
groups, the test allows for complex cognitive functions to
be measured from the time they developmentally emerge
Historical Background to the point where they begin to diminish. DeLuca and
colleagues (2003) studied the development of executive
Originally created in the late 1980s to diagnose dementia capacities during childhood and beyond. Using a sample
in elderly individuals (Fray et al., 1996), the CANTAB is of participants ranging in age from 8 to 64 years, they
used, and has been studied, across age groups and with found functional gains in the efficiency of working mem-
patients presenting with both psychiatric and neurologi- ory capacity, planning, and problem solving abilities be-
cal conditions. tween ages 15 and 19 and again from ages 2029 years. In
Cambridge Neuropsychological Testing Automated Battery C 481
Cambridge Neuropsychological Testing Automated Battery. Table 1 CANTAB tests
Subtest Functional category Skill measured

Motor screening Induction Capacity to undergo CANTAB assessment
Big little circle Induction Rule following C
Delayed matching to sample Visual memory Forced choice recognition
Paired associates learning Visual memory Episodic memory
Pattern recognition memory Visual memory Recognition memory for patterns
Spatial recognition memory Visual memory Recognition memory for spatial locations
Intra-extra dimensional set shift Executive function Attentional set shifting
One touch stockings of Cambridge Executive function Planning and working memory
Stockings of Cambridge Executive function Planning and motor control (Tower of London task)
Spatial span Executive function Working memory capacity
Spatial working memory Executive function working memory/strategic thinking
Choice reaction time Attention Alertness and motor speed
Reaction time Attention Simple reaction time
Match to sample visual search Attention Visual search and discrimination
Rapid visual information processing Attention Continuous performance task
Simple reaction time Attention Alertness and motor speed
Graded naming test Semantic/verbal memory Lexical access/naming
Verbal recognition memory Semantic/verbal memory Immediate and delayed verbal memory
Affective go/no-go Decision making/response control Information processing
Cambridge gambling task Decision making Decision making and risk taking
Response control
Information sampling task Decision making Pre-decisional contemplation
Response control
Stop signal task Decision making Inhibition of prepotent responses
Response control
contrast, the developmental vulnerability of executive cost will also be prohibitive to many private practitioners
skills was suggested by a decline in CANTAB performance and organizations.
among subjects in the 5064 year old sample (Luciana & Software requirements described by the publisher
Nelson, 2002). include Microsoft Windows 2000 or Windows XP
Reliability studies have been completed internally by operating systems, with minimal hardware requirements
Cambridge Cognition which described test-retest reli- being a PC with 800 MHz Pentium III processor, 256 MB
ability coefficients ranging from 0.40.87. Those findings of RAM, 100 MB free disk space, sound card and speakers,
are consistent with stability coefficients reported by CD-ROM drive, serial port and USB port. A touch screen is
Lowe and Rabbitt (1998). Luciana (2003) reported con- also required, which Cambridge Cognition offers to supply.
sistency coefficients ranging from .73 for a measure of
reaction time latency to .95 for performance on the self-
ordered search task. Future Directions
Limitations of CANTAB include its exclusion of
language based measures, thus leaving the examiner to Pharmaceutical companies have been using CANTAB
supplement the battery with additional tests to assess internationally in multi-site clinical trials for more than
relevant brain-behavior issues such as those involving 20 years. The company is in the process of developing a
laterality (e.g., auditory-verbal memory). CANTABs version of CANTAB for the health care market.
482 C Cancellation Tests
References and Readings individuals make few, if any, errors (Weintraub, 2000).
Standardized versions of cancellation tests, such as the
Elliott, R., McKenna, P. J., Robbins, T. W., & Sahakian, B. J. (1995). Ruff 2 & 7, show good testretest reliability. In addition,
Neuropsychological evidence for frontostriatal dysfunction in on the Ruff 2 & 7 younger adults performed better than
schizophrenia. Psychological Medicine, 25, 619630.
older adults and performances improved with higher
Luciana, M. (2003). Practitioner review: Computerized assessment of
neuropsychological function in children: Clinical and research appli-
levels of education. There were no gender effects
cations of the Cambridge Neuropsychological Testing Automated (Mitrushina, Boone, Razani, & DElia, 2005).
Battery (CANTAB). Journal of Child Psychology and Psychiatry,
44(5), 649663.
Luciana, M., & Nelson, C. A. (2002). Assessment of neuropsychological Clinical Uses
function through use of the Cambridge Neuropsychological Testing
Automated Battery: Performance in 4- to 12-year-old children. Cancellation tests have been shown to be sensitive in
Developmental Neuropsychology, 22(3), 595624.
detecting deficits in attention related to right hemisphere
Prouteau, A., Verdoux, H., Briand, C., Lesage, A., Lalonde, P., Nicole, L.,
Reinharz, D., & Stip, E. (2004). The crucial role of sustained
lesions, traumatic brain injuries, schizophrenia, and
attention in community functioning in outpatients with schizo- AIDS-related cognitive impairment. Cancellation tests
phrenia. Psychiatry Research, 129, 171177. are particularly useful in assessing visuospatial neglect.
Sweeney, J. A., Kmiec, J. A., & Kupfer, D. J. (2000). Neuropsychologic Unlike normal individuals who begin searching for target
impairments in bipolar and unipolar mood disorders on the
stimuli on the left side of the page and systematically
CANTAB neurocognitive battery. Biological Psychiatry, 48, 674685.
move rightward, neglect patients begin on the right
using a disorganized search pattern omitting many targets
on the left side of the page (Weintraub, 2000). By decreas-
Cancellation Tests ing the attentional demands of a letter cancellation test by
reducing the number of nontarget stimuli, right hemi-
R ICHARD F. K APLAN sphere damaged patients showed decreased left-sided ne-
UConn Health Center glect, suggesting that the neglect syndrome is the result of
Farmington, CT, USA an attentional bias (Kaplan et al., 1991).
Synonyms Cross References
Vigilance tests Attention

Neglect and Hemi-inattention
Neglect Syndrome
Description Vigilance
Cancellation tests are designed to measure sustained and

selective attention. References and Readings
Kaplan, R. F., Verfaellie, M., Meadows, M. E., Caplan, L. R., Pessin, M. S., &
Historical Background DeWitt, L. D. (1991). Changing attentional demands in left hemi-
spatial neglect. Archives of Neurology, 48, 12631266.
Mitrushina, M., Boone, K. B., Razani, J., & DElia, L. F. (2005). Handbook
Numerous variations of cancellation tests have been
of normative data for neuropsychological assessment (2nd ed.,
developed to assess sustained, selective attention, and pp. 160170). New York: Oxford.
spatial inattention following hemispheric lesions. The Weintraub, S. (2000). Neuropsychological assessment of mental state. In
patient is typically required to scan through an array M. Mesulam (Ed.), Principles of behavioral neurology (2nd ed.,
of stimuli and find (cancel) specific target stimuli (e.g., pp. 121173). New York: Oxford.
bells).
Psychometric Data CANTAB

There is relatively little normative data for cancellation Cambridge Neuropsychological Testing Automated
tests, and most comparative studies show that normal Battery
Capacity Limitations C 483
Capacity Capacity Limitations

R OBERT L. H EILBRONNER A NNA M AC K AY-B RANDT
Chicago Neuropsychology Group Brown University Medical School
Chicago, IL, USA Providence, RI, USA
C
Synonyms Definition
Competency The constraints on processing of internal and external

stimuli dependent upon the structure of, and the processes
related to, the cognitive system.
Definition
In the most basic sense, capacity refers to the ability to

make decision(s) with regard to oneself. Specifically, this
refers to ones ability to understand and appreciate the
Fundamental research in attention emerged in the
consequences of ones actions. Legal capacity remains
1950s with information processing theories. D.E. Broad-
in effect until death, unless a court rules that one is inca-
bent published an influential book in 1958, Perception
pacitated. If a person is ruled by a court of law to be legally
and Communication, which was in turn influenced by
incapacitated, this can remove all or part of a persons right
the contemporary work of communication theorists in
to make decisions. Specifically, one can be deemed incapa-
engineering. Broadbent used the communication sys-
ble of managing financial affairs, but ruled capable of
tem as a metaphor for relationships within the human
making medical decisions, for example. If a person is
brain. Each brain system (i.e., sensory, memory, re-
ruled to lack full legal capacity, then they are prohibited
sponse generation) was conceptualized in terms of a
from entering into a contract, giving a power of attorney,
communication system, with an information source, a
creating a will, or consenting to medical treatment. A ruling
transmission channel(s), and a receiver. The channel by
of legal incapacity typically results in the appointment of a
which a message is transmitted has a capacity, which
guardian or conservator to make decisions for the person.
limits the rate by which information can be transmitted.
There are several types of capacity that are relevant to
A property of communication systems is that the
forensic neuropsychology including: capacity to consent
transmission of information within a system can never
to treatment, to manage financial affairs, and others.
exceed the capacity of the channel divided by the
information source output. This theoretical conceptu-
alization sets the stage for future research, describing the
Cross References limits in sensory and cognitive systems and mechanisms
to deal with the processing of information in these
Testamentary Capacity
systems.

Marson, D. C., & Hebert, K. (2005). Assessing civil competencies in older
In response to the observation that one is not able to
adults with dementia: Consent capacity, financial capacity, and
testamentary capacity. In G. Larrabee (Ed.), Forensic neuropsychology:
attend to all stimuli in the environment at the same
A scientific approach. New York: Oxford University Press. time, hypotheses have developed to explain the limita-
Marson, D. C., Sawrie, S., Snyder, S., McInturff, B., Stalvery, T., tions on the capacity for cognitive processing, particularly
Boothe, A., et al. (2000). Assessing financial capacity in patients in the areas of attention and memory (Broadbent, 1971;
with Alzheimers disease: A conceptual model and prototype
Miller, 1956; Shiffrin & Schnieder, 1977; Kahneman,
instrument. Archives of Neurology, 57, 877884.
Willis, S. (1996). Everyday cognitive competence in elderly persons:
1973). Cohen (1993) organized attentional capacity in
Conceptual issues and empirical findings. The Gerontologist, 36, terms of structural and energetic limitations. Structural
595601. capacity limitations can be thought of in terms of
484 C CAPD
optimal processing characteristic of the system such as References and Readings

channel capacity, working-memory capacity, processing
speed, and temporalspatial characteristics of the sys- Broadbent, D. E. (1958). Perception and communication. London:
tem. These structural elements are influenced by vari- Pergamon.
Broadbent, D. E. (1971). Decision and stress. London: Academic Press.
ables such as performance required on more than one
Cohen, R. (1993). The neuropsychology of attention. New York: Plenum.
task (e.g., dual task): task complexity, memory de- Duncan, J., & Humphreys, G. W. (1989). Visual search and stimulus
mand, high or low rate of target event occurrence, similarity. Psychological Review, 96, 433458.
and task duration. Energetic capacity limitations are Jacoby, L. L. (1991). A process dissociation framework: Separating auto-
considered to be natural or imposed variations within matic from intentional uses of memory. Journal of Memory and
Language, 30, 513541.
an individual that includes arousal, motivation, and
Kahneman, D. (1973). Attention and effort. Englewood Cliffs, NJ: Pren-
generated effort. A clear indicator of the influence of tice-Hall.
energetic factors on performance is performance varia- Miller, G. A. (1956). The magical number seven, plus or minus two: Some
bility over time. limits on our capacity for processing information. Psychological
Researchers of cognition have used the debate over Review, 63, 8197.
Shiffrin, R. M., & Schnieder, W. (1977). Controlled and automatic
whether particular processes are limited or unlimited in
human information processing: 2. Perceptual learning, automatic
capacity as a fruitful ground for study. For example, attending and a general theory. Psychological Review, 84, 127190.
theories of serial and parallel processing have emerged Treisman, A., & Gelade, G. (1980). A feature integration theory of
in both the attention and memory literature in support attention. Cognitive Psychology, 12, 97136.
and rejection of capacity limited processes. Although not Wolfe, J. M. (1994). Guided search 2.0: A revised model of visual search.
Psychonomic Bulletin & Review, 1, 202238.
strictly coupled, serial processing is often considered in
the context of limited capacity, whereas paral-
lel processing is thought to be unlimited in capacity.
This coupling bears out in visual search studies that
have found preattentive processes that are thought
CAPD
to be parallel and unlimited in capacity, versus focal
Central Auditory Processing Disorder
attentive processes that are serial and limited in capacity
(Duncan & Humphreys, 1989; Treisman & Gelade, 1980;
Wolfe, 1994). Similarly, in memory research, Jacoby
(1991) distinguished automatic from controlled proces- Capgras Syndrome
sing, with similar parallel and unlimited capacity (auto-
matic) versus serial and limited capacity (controlled) PAUL M ALLOY
distinctions. Alpert Medical School of Brown University
Providence, RI, USA
Future Directions
Synonyms
A relatively recent emphasis has been placed on the inter-
action of neural and cognitive limitations with factors Reduplication delusion; Reduplicative paramnesia
such as arousal, motivation, and effort.
Cross References Delusions are defined as false beliefs based on incorrect

inference about external reality, and firmly sustained in
Attention spite of the opinions of others or contrary evidence
Attention/Executive Function (American Psychiatric Association, 1987).
Parallel Processing Capgras syndrome (Capgras & Reboul-Lachaux, 1923)
Serial/Sequential Processing is a type of reduplication delusion involving the belief that
Short-Term Memory persons well-known to the patient, such as family
Span Test members, have identical doubles or are imposters. The
Working Memory double or imposter is sometimes perceived as differing
Capgras Syndrome C 485
slightly in some physical characteristic from the found that the delusion actually had a 15% incidence in
genuine person, but the patient may have difficulty their sample of adult inpatients previously diagnosed as
verbalizing the precise nature of this difference. having schizophrenia. Several researchers have found
that about 25% of Alzheimer patients display delusions
involving misidentification of people (e.g., Mendez, C
Categorization Martin, Smyth, & Whitehouse, 1992). Large-scale
epidemiological studies are lacking to date.
Several variations of Capgras syndrome have been identi-
fied. Doppleganger or subjective doubles is the belief that
the patient himself has a double or impersonator
(Christodoulou, 1978). Fregoli syndrome is the belief that
a person is capable of taking on the appearance of others,
Outcomes
while retaining his/her own psychological identity (Courbon
About 58% of Capgras patients who receive adequate
& Fail, 1927). Intermetamorphosis is the belief that people
neurodiagnostic workups are found to display primary
are changing in both physical and psychological identity
psychiatric disorder, uncomplicated by demonstrable
to become another person (Courbon & Tusques, 1932).
neurologic disease (Dohn & Crews, 1986). Although
Capgras syndrome must be distinguished from purely
psychological factors can be important in the production
perceptual or hallucinatory disturbances, and from
of delusions, a critical review of the literature by Malloy
generalized disturbance of cognition. That is, in order to
and Richardson (1994) demonstrated that delusions can
be properly and convincingly diagnosed as a delusion, the
also result from identifiable neurologic disease, from
disturbance must involve a mistaken belief (not merely a
generalized disturbances to focal lesions.
misperception) and must be persistent (not a transitory
They found that Capgras and its variants have been
effect of confusion). For example, in autoscopy, the patient
reported in association with a variety of systemic diseases
experiences a second self, as in the subjective doubles
and diffuse neurologic disorders. Systemic etiologies have
variant of Capgras. However, the phenomena differ in
included: Metabolic disturbances such as myxedema,
that the double is actually seen in autoscopy, rather than
pseudohypoparathyroidism, anemia, hepatic dysfunction,
believed to be active elsewhere, as in subjective doubles. The
B12 deficiency; intoxication and reactions to drugs inclu-
prosopagnosic person may fail to recognize his wife, where-
ding cocaine, chloroquine, disulfiram, digoxin, and
as the Capgras patient will insist that the present person is
lithium; cerebral infections such as encephalitis and
an imposter and that the real wife is somewhere else.
AIDS; subarachnoid hemorrhage; migraine; post-ECT
Patients in confusional states or dementia may express
confusion; minor head trauma; and degenerative dementia.
strange beliefs, but the beliefs typically change from hour
In terms of focal lesions such as tumors and stroke,
to hour and do not persist once the confusion resolves. Thus
that review demonstrated that the right hemisphere or
this problem should not be termed delusional.
bilateral lesions were invariably found on neuroimaging,
Patients with Capgras syndrome are usually described
with no exclusively left-hemisphere lesions. EEG and neu-
as forthcoming and cooperative. Although they insist that
rologic exam findings also implicated right-hemisphere
their delusional beliefs are true, they often admit to puzzle-
pathology. In terms of specific localization, 72% of cases
ment or bemusement regarding aspects of the delusion.
with CT or MRI scans had right frontal, temporal, or
Rather than escalate their defenses by becoming hostile,
frontotemporal involvement. Neuropsychological testing
they are more likely to confabulate an explanation. For
documented spatial, executive, and nonverbal memory
example, a patient with a delusion of duplication (Malloy,
problems, consistent with the right frontotemporal
1991) was asked how she could have two sets of children
localization on neuroimaging studies.
with identical names. She appeared momentarily puzzled
and then stated, My husband was in the Navy, and we
moved around a lot; it was hard to keep that straight.
Capgras Syndrome
Epidemiology
Capgras and its variants represent either underidentifica-
Dohn and Crews (1986) observed that Capgras syndrome tion or overidentification of the object of the delusion
was frequently overlooked in psychiatric patients and (Vie, 1930). Thus, in Capgras syndrome, the patient
486 C Capgras Syndrome
mistakenly perceives the person as unfamiliar due to Treatment

underidentification. In Fregoli syndrome, on the other
hand, the patient misperceives diverse persons as the In degenerative dementia, duplication delusions are usually
same person due to overidentification. transitory phenomena, occurring in the early-to-middle
Feinberg and Shapiro (1989) emphasized the stages and disappearing when cognitive deficits become
importance of the right temporal lobe in producing severe. In other etiologies such as cerebrovascular disease,
misidentification delusions. They reviewed the evidence they often occur acutely and persist for many months or
from stimulation and seizure studies indicating that the years. Prognosis appears to vary with the type of delusion
right temporal lobe plays an important role in producing and the underlying etiology.
the experience of familiarity. Cutting (1991) has put forth Many underlying systemic causes (e.g., infections,
a similar argument regarding the role of the right toxic reactions, metabolic disturbances) of duplication
hemisphere in identification. delusions are readily treated, resulting in elimination of
Crucial factors in the persistence of delusions may be the delusion. For example, Santiago, Stoker, Beigel, Yost,
the length of time the perceptual distortion continues, and Spencer (1987) reported resolution of Capgras
and the ability of the patient to correct the misperception following treatment of underlying thyroid disease.
on the basis of new information. Frontal lesions may Spontaneous resolution of Capgras delusions has also
impact on the latter self-corrective function, making it been reported (Ruff & Volpe, 1981).
impossible to resolve conflicting information, resulting On the other hand, Joseph (1987) described a patient
in unconcern and confabulation when the conflicts are whose chronic psychosis and intermittent psychotic mis-
confronted (Joseph, 1986). Alexander, Stuss, and Benson identification of the Capgras and intermetamorphosis
(1979) were the first to report a Capgras delusion clearly types were refractory to neuroleptic treatment. Upon
related to a specific neurologic structural lesion, involving administration of a trial of clorazepate, complete
the right hemisphere with predominantly frontal and remission of psychotic symptoms was achieved for the
temporal lobe damage. They noted the importance of first time in 19 years, but these recurred when the patient
frontal damage in Capgras, both in terms of the inability discontinued her clorazepate.
to resolve conflicts, and confabulation of a second The effectiveness of psychological interventions may
persona. vary with the type of delusion, and the degree to which
Psychodynamic or functional interpretations for the neurologic factors are involved. Unfortunately, there has
development of delusions are not incompatible with this been no systematic treatment follow-up research, and
neuropsychological explanation. data are limited to uncontrolled case studies.
Evaluation Cross References
Careful clinical interview with both patient and family Reduplicative Paramnesia
members will help to elicit evidence of Capgras delusions.
In the course of family disputes and initial evaluations,
patients may learn to minimize or deny their delusions. References and Readings
Demented patients may forget instances of misidentifica-
tion. Hence, family informants may be extremely helpful. Alexander, M., Stuss, D. T., & Benson, D. F. (1979). Capgras syndrome:
The literature is replete with case reports positing a A reduplicative phenomenon. Neurology, 29, 334339.
psychodynamic explanation for Capgras, but with no
manual of mental disorders-third edition-revised (DSM-III-R).
workup to rule out neurologic etiology. Since Capgras is Washington, DC: American Psychiatric Press.
commonly associated with neurologic illness; full workup Capgras, J., & Reboul-Lachaux, J. (1923). Lillusion des sosies dans
including neuroimaging and neuropsychological testing is un delire systematise. Bulletin de Societe Clinical Medicine Mentale,
essential. Neuropsychological testing often reveals deficits 11, 616.
Christodoulou, G. N. (1978). Syndrome of subjective doubles. The
in frontal/executive and visuospatial functions (Malloy &
American Journal of Psychiatry, 135, 249251.
Richardson, 1994). Facial recognition and memory Courbon, P., & Fail, G. (1927). Syndrome dillusion de Fregoli et
should be tested to rule out alternative explanations for schizophrenie. Bulletin de Societe Clinical Medicine Mentale, 88,
the patients problems, such as prosopagnosia. 214237.
Carbamazepine C 487
Courbon, P., & Tusques, J. (1932). Lillusion de intermetamorphose et de Brand Name

charme. Annales Medico-Psychologiques, 90, 401406.
Cutting, J. (1991). Delusional misidentification and the role of the right
hemisphere in the appreciation of identity. The British Journal of
Tegretol, Carbatrol
Psychiatry, 159(Suppl. 14), 7075.
Dohn, H. H., & Crews, E. L. (1986). Capgras syndrome: A literature review
C
and case series. The Hillside Journal of Clinical Psychiatry, 8, 5674. Class
Feinberg, T. E., & Shapiro, R. M. (1989). Misidentification-reduplication
and the right hemisphere. Neuropsychiatry, Neuropsychology, and
Behavioral Neurology, 2, 3948.
Anticonvulsant
Foerstl, H. (1990). Capgras delusion: An example of coalescent psycho-
dynamic and organic factors. Comprehensive Psychiatry, 31, 447449.
Joseph, A. B. (1987). Delusional misidentification of the Capgras and Proposed Mechanism(s) of Action
intermetamorphosis types responding to clorazepate. A case report.
Acta Psychiatrica Scandinavica, 75, 330332.
Carbamazepine is a use-dependent blocker of voltage-
Joseph, R. (1986). Confabulation and delusional denial: Frontal lobe and
lateralized influences. Journal of Clinical Psychology, 42, 507520.
sensitive sodium channels, it interacts with the open chan-
Malloy, P. (1991). Differential diagnosis of primary and secondary nel conformation of voltage-sensitive sodium channels, it
Capgras delusions. Neuropsychiatry, Neuropsychology, and Behavioral interacts at alpha pore-forming subunit of voltage-sensitive
Neurology, 4, 90108. sodium channels, and inhibits release of glutamate.
Mendez, M. F., Martin, R. J., Smyth, K. A., & Whitehouse, P. J. (1992).
Disturbances of person identification in Alzheimers disease. A retro-
spective study. The Journal of Nervous and Mental Disease, 180, 9496.
Ruff, R. L., & Volpe, B. T. (1981). Environmental reduplication associated Indication
with right frontal and parietal lobe injury. Journal of Neurology,
Neurosurgery, and Psychiatry, 44, 382386. Complex partial seizures, generalized tonicclonic seizures,
Santiago, J. M., Stoker, D. L., Beigel, A., Yost, D., & Spencer, P. (1987).
mixed seizure patterns, and trigeminal neuralgia pain.
Capgras syndrome in a myxedema patient. Hospital & Community
Vie, J. (1930). Un trouble de lidentification des personnes: Lillusion des
sosies. Annales Medico-Psychologiques, 88, 214237. Off Label Use
Glossopharyngeal neuralgia, bipolar disorder, psychosis,

schizophrenia, and personality disorders.
Capital Punishment
Death Penalty Side Effects
Serious
CARB Aplastic anemia, agranulocytosis, Stevens Johnson Syn-

drome, cardiac problems, induction of psychosis or
Computerized Assessment of Response Bias mania, and increased frequency of seizures.
Common
Carbamazepine
Sedation, dizziness, confusion, headache, nausea, and
J OHN C. C OURTNEY vomiting.

Generic Name PDR.
Carbamazepine Second edition. New York, NY: Cambridge University Press.
488 C Carbon Monoxide Poisoning
Additional Information Exposure to carbon monoxide is the most common

form of poisoning worldwide. With increased awareness
Drug Interaction Effects: http://www.drugs.com/drug_interactions.html of its potential dangers, the majority of these exposures
Drug Molecule Images: http://www.worldofmolecules.com/drugs/ can be prevented.
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList Natural History, Prognostic Factors,
Pill Identification: http://www.drugs.com/pill_identification.html Outcomes
Compared to normal oxyhemoglobin (i.e., when oxygen

binds to hemoglobin), carboxyhemoglobin is bright red;
thus, an early sign of carbon monoxide poisoning is a
Carbon Monoxide Poisoning cherry-red skin color.
Acute exposure to lower concentrations of carbon
G EORGE C. WAGNER monoxide will result in a slowly developing hypoxia that
Rutgers University triggers peripheral vasodilation. Paradoxically, when there
New Brunswick, NJ, USA is a slow increase in carboxyhemoglobin saturation, com-
pensatory changes in respiratory rate may lag. Thus, the
symptoms of dizziness, weakness, headache, and nausea
Synonyms will precede fainting. Once unconscious, increased respi-
ration and tachycardia will be followed by convulsions
Carboxyhemoglobinemia and coma, and death will ensue as the carboxyhemoglobin
climbs and remains above 50% saturation.
Chronic exposure to low concentrations of carbon
Short Description monoxide can occur in heavy smokers as well as in indi-
viduals whose occupations involve protracted exposure to
Carbon monoxide (CO) is a colorless, odorless gas gen- exhaust fumes. The binding of carbon monoxide to he-
erated during the combustion of carbon-containing fuels. moglobin is fully dissociable though these individuals
When inhaled into the lungs, it readily competes with may manifest carboxyhemoglobin saturation at 10%,
oxygen for binding sites on hemoglobin. The affinity of which is 20-fold higher than normal. Symptoms asso-
carbon monoxide binding to hemoglobin is more than ciated with chronic exposure include headache, fatigue,
200-fold greater than that of oxygen. Thus, at atmospheric nausea, difficulty in concentrating, and impaired memory
concentrations as low as 0.1%, carbon monoxide will (Kao & Nanagas, 2005).
achieve a 50% saturation of the hemoglobin, resulting in
carboxyhemoglobinemia and a significant reduction in Neuropsychological Assessment
the blood oxygen levels.
Acute carbon monoxide poisoning, for example, fol- The Carbon Monoxide Neuropsychological Screening
lowing exposure to automobile exhaust (which generates Battery (CONSB) has been developed to screen for cogni-
about 5% to 7% carbon monoxide) will rapidly saturate tive impairment following acute carbon monoxide poi-
the hemoglobin and cause death within minutes with soning (Messier & Myers, 1991). The CONSB battery
virtually no prior symptoms. begins with an assessment of general orientation of the
patient, and this is followed by the Digit Span, Trail
Making, Digit Symbol, Aphasia Screening, and Block De-
Epidemiology sign tests. Use of this battery in an emergency room
setting allows for the early detection of cerebral im-
Exposure to low concentrations of carbon monoxide con- pairment in the exposed individuals.
sequent to the operation of faulty furnaces or gas-powered
engines is the leading cause of accidental poisoning in the Evaluation
United States. Exposure to high concentrations of carbon
monoxide is the most common form of intentional poi- The long-term consequences of acute carbon monoxide
soning in the United States. poisoning may, in part, be consequent to the damage to
Carotid Angiography C 489
the bloodbrain barrier during the period of hypoxic Messier, L. D., & Myers, R. A. M. (1991). A neuropsychological screening
battery for emergency assessment of carbon-monoxide-poisoned
coma. Following apparent recovery from the acute expo-
patients. Journal of Clinical Psychology, 47(5), 675684.
sure, a delayed toxicity with abrupt onset may appear Prockop, L. D., & Chichkova, R. I. (2007). Carbon monoxide intoxica-
with symptoms of confusion together with motoric tion: an updated review. Journal of the Neurological Sciences, 262,
symptoms resembling Parkinsons disease (incoordina- 122130.
C
tion, muscular weakness, and muscular rigidity). These
neurological signs reflect extensive damage to the basal
ganglia and white matter of the brain with a demyelin-
ation that spares the neuronal axons. Neuroimaging Carboxyhemoglobinemia
scans will most likely appear normal 24 h after exposure;
lesions may begin to appear 2 weeks later. Functional Carbon Monoxide Poisoning
changes associated with these later-appearing lesions are
variable but attempts have been made to relate these to
the severity of the initial exposure. Acute exposure result-
ing in carboxyhemoglobin saturation of 25% or more will
result in later onset cognitive impairments in as many as Cardiac Ultrasound
50% of the patients. The cognitive deficits include agno-
sia, aphasia, and apraxia as well as impaired memory, Echocardiogram
impaired executive function, and a general decrease
in intellect. In addition, visuomotor performance dete-
rioriates. Finally, late-appearing changes in affect are
frequently reported as are obsessivecompulsive tenden- Career Counseling for Individuals
cies and anxiety (Hopkins & Woon, 2006). with Disabilities
Vocational Counseling
Treatment
Effective treatment entails removal from the source of the

carbon monoxide and providing oxygen; when breathing
Career Maintenance
air, the half-life of carboxyhemoglobin is about 5 h and
this time can be reduced to 1.5 h with oxygen supplemen-
Job Retention
tation. Indeed, supplementation with oxygen immediately
after exposure remains as the most effective strategy for
reducing the severity of the later-appearing neural and
functional consequences following carbon monoxide poi-
soning (Prockop & Chichkova, 2007). Carotid Angiography
PAUL E. K APLAN
Capitol Clinical Neuroscience
Cross References Folsom, CA, USA
Neurotoxins
Synonyms
References and Readings Angio
Hopkins, R. O., & Woon, F. L. M. (2006). Neuroimaging, cognitive

and neurobehavioral outcomes following carbon monoxide Definition
poisoning. Behavioral and Cognitive Neuroscience Reviews, 5(3),
141155.
Kao, L. W., & Nanagas, K. A. (2005). Carbon monoxide poisoning. Angiography is the evaluation of the blood vessels
Medical Clinics of North America, 89, 11611194. of the central nervous system and associated
490 C Carotid Artery
cervicocerebral vasculature applying radiography to the

simultaneous injection of intravascular contrast media. Carotid Artery
Femoral or axillary nonselective approaches can be
used to catheterize the aortic arch or selective means Internal Carotid Artery
employed to catheterize the carotid artery. Contrast
media is then injected through the catheter and X-
rays taken. Digital subtraction, computed tomography
(CT) scanning, and MRI techniques too can be applied Carotid Endarterectomy
at this point. Obstructions, stenosis, aneurysms, and
A-V malformations can all be identified. Finer and A NUJ S HARMA
more selective views are realized by using microcath- Virginia Commonwealth University
eters. Some of the disease entities studied include is- School of Medicine
chemic cerebrovascular disease, aneurysms, vascular Richmond, VA, USA
malformations, neoplasms, and brain injuries. Two
special carotid lesions could be evaluated with carotid
angiography. Arterial dissections develop when blood Synonyms
is extravasated within the arterial wall itself narrowing
the arterial lumen. The carotid artery between C2 and CEA
the base of the skull is frequently a target for the
formation of a pseudoaneurysm. Pain, bruits, with
cranial nerve palsies will be present. Angiography will Definition
be useful. Another condition where carotid angiogra-
phy is useful is the carotid-cavernous fistula a high CEA is an elective surgical procedure that removes plaque
pressure, high-flow connection between the carotid from the lumen of the carotid artery. After anesthesia, the
artery and the cavernous sinus veins. Patients will surgeon clamps the carotid artery proximal and distal to
present with visual loss, a bruit, proptosis. the stenosis temporarily. The surgeon may place a shunt
proximal to the clamp to reroute blood to the brain. Next,
an incision is made over the area of blockage. The plaque
is scraped out and separated from the inner lining of the
Current Knowledge
artery. After it is removed, the artery is sutured together,
the clamps are removed, and any bleeding is stopped.
Can be part of the evaluation process of patients with
Finally, the skin incision is closed.
cerebrovascular disease.
Current Knowledge
Cross References
The arch of the aorta gives off three branches: the
Angioma innominate, the left common carotid, and the left sub-
Glioma clavian. The innominate artery, also known as the bra-
Hemangioma chiocephalic artery, gives rise to the right subclavian
Hemiplegia artery and the right common carotid artery. The com-
mon carotid arteries bilaterally split into internal and
external carotid arteries. The right and left internal ca-
References and Readings rotid arteries, along with the vertebral arteries, branches
of the subclavian artery, are the major blood vessels
Dumolin, C. L., & Hart, H. R. (1986). Magnetic resonance angiography. supplying the brain.
Radiology, 161, 717. As plaque builds in the carotid artery, atherosclerosis,
Faro, S. H., Haselgrove, J. C., Wang, Z., et al. (1993). Carotid MR or hardening of arteries, develops. Carotid stenosis, or
angiography. Radiology, 189, 243.
narrowing of the carotid artery, may also develop and is
Love, B. B., & Biller, J. (2003). Neurovascular System. In C. G. Goetz (Ed.),
Textbook of clinical neurology (2nd ed.) (pp. 395424). Philadelphia: most common at the origin of the internal carotid artery
Saunders. or less commonly, at the distal common carotid artery.
Case Coordination C 491
If the stenosis is severe, it may result in decreased is inserted through the groin and is guided until it
perfusion of brain tissue, and consequently ischemia. reached the site of stenosis. After the location of the
Another mechanism by which ischemia can develop is catheter is confirmed, a balloon inflates and attaches a
by the development of a thrombus over the plaque. metal-mesh stent into the artery. The balloon is then
When this occurs, an embolus may break off and may deflated and the catheter is gently removed. However, C
result in the occlusion of a vessel distally. long-term studies have not proven this method to be
A stroke may develop if the brain is deprived of its superior to a CEA.
blood supply, resulting in a sudden loss of neurologic
function. However, transient ischemic attacks (TIA)
may be the diagnosis if symptoms, such as loss of sensory
or motor function in the extremities, inability to com- Cross References
prehend or initiate speech, or loss of vision in one
eye described a shade coming down over one eye (amau- Ischemia
rosis fugax), last for a few minutes to hours and Magnetic Resonance Angiography
resolve completely in twenty-four hours. Patients with Stroke
a history of stroke or TIA are at increased risk of a
subsequent stroke and should be further evaluated with
imaging studies. According to the North American
Symptomatic Carotid Endarterectomy Trial (NASCET),
patients with symptomatic carotid artery stenosis of
Chaturvedi, S., Bruno, A., Feasby, T., Holloway, R., Benavente, O.,
greater than 70% have a 26% risk of recurrent stroke Cohen, S. N. et al. (2005). Carotid endarterectomy an evidence-
over two years. based review: Report of the Therapeutics and Technology Assess-
The diagnosis of a TIA is made by carotid duplex ment Subcommittee of the American Academy of Neurology.
ultrasound. This type of imaging bounces high-frequency Neurology, 65, 794801.
Roffi, M., & Luscher, T. F. (2008). Management of carotid artery stenosis.
sound waves off blood vessels and the blood within the
Herz, 33, 490497.
lumen to determine blood flow and any abnormalities Rothwell, P. M., Eliasziw, M., Gutnikov, S. A., Fox, A. J., Taylor, D. W.,
within the vessels themselves. Other modalities useful in Mayberg, M. R. et al. (2003). Analysis of pooled data from the
the diagnosis of a TIA include computed tomography randomised controlled trials of endarterectomy for symptomatic
angiography (CTA), magnetic resonance angiography carotid stenosis. Lancet, 361, 107116.
(MRA), and angiography. In each of these, a contrast
dye, or gadolidium in the case of MRA, is injected into
the arteries. This helps identify any areas of poor blood
flow and determine the degree of stenosis.
If there is greater than 70% blockage of the carotid CARS
artery, a CEA is recommended if the patient is symptomatic
with a history of TIA or nondisabling stroke, or even if Childhood Autism Rating Scales
the patient is asymptomatic. However, a CEA should not
be performed during a stroke or TIA or if the patient
experiences a stroke that leaves him severely disabled.
If there is less than a 70% blockage and the patient
is asymptomatic, a CEA is not recommended. In this
case, the patient should be treated medically with a baby
CAS
aspirin daily. In addition, other risk factors that may cause
Cognitive Assessment System
further damage to the vessels, such as smoking, diabetes,
hypertension, and hypercholesterolemia, should be treated
medically. A CEA is only recommended for 5069% steno-
sis if the patient has had recurrent TIAs unresponsive to
medical management.
For patients that are high risk for the CEA, other Case Coordination
surgical interventions, such as angioplasty and stenting,
can be considered. During this procedure, a catheter Case Management
492 C Case Management
patients or cases. People with disabilities often find the

Case Management term, case manager, to be pejorative as in, I am not a
case and I will not be managed. Case managers do not
B RIAN T. M C M AHON manage patients, but instead, they manage the rehabilita-
Virginia Commonwealth University tion process. Indeed, the planning, organizing, directing,
Richmond, VA, USA and controlling of the rehabilitation process from the
initial point of contact to the realization of outcomes is
the ultimate mission of the case manager. For example,
Synonyms life-care planning ( Life Care Planning) is often depicted
as the ultimate case management plan because of its
Case coordination; Case planning inherently comprehensive nature. It is hard to conceive
of a successful life-care planner who is not a professional
case manager.
Definition Another appropriate way to understand case manage-
ment is to review the core body of knowledge for CCMs.
Case management is a widely used (and often misused) These include: case management concepts, principles, and
term that has become commonplace in health care and strategies; psychosocial and support systems; health-care
human services. In its most professional use, case manage- management and service delivery; health-care reimburse-
ment is a collaborative process that assesses, plans, implement; and vocational concepts and interventions. Case
ments, coordinates, monitors, and evaluates the options management requires one to go well beyond the direct
and services required to meet the patients health and/or patient services of ones core profession and intervene
human service needs. It is characterized by advocacy, com- in the systems, services, and supports available in the
munication, and resource management and promotes community to achieve intended outcomes. For example,
quality and cost-effective interventions and outcomes. it is not unusual for a case manager to work with multi-
ple stakeholders in a single case including payers,
service providers, family members, attorneys, employers,
Current Knowledge advocacy organizations, and, of course, the patient. The
case manager sees all of these parties as important and
In recent years, case management has become a freestand- is keenly aware that any single individual in this
ing profession, but it is actually an overlay upon ones core system has the wherewithal to completely sabotage a
profession. The certified case manager (CCM) must first well-conceived plan if neglected or marginalized. In
hold a professional license or certification in a recognized essence, the case manager is not only the primary architect
health care or human service profession before he or she of the rehabilitation plan, but must also sell that plan to all
is eligible for case management certification. The core of the key stakeholders in order to maximize the plans
profession must involve a postsecondary degree in a field implementation and outcomes.
that promotes the psychological, medical, or vocational Case management is among the most misused
well-being of the person being served. The license or terms in health care. Because it is unprotected by most
certification that follows the degree in ones core profession state departments of professional regulation, the term is
must be one that is required by law for independent often used in reference to discharge planners, utilization
practice without the supervision of another licensed reviewers, claims adjusters, and a host of paraprofes-
professional. Most CCMs are graduate-trained in rehabili- sionals. However, CCMs are professionally prepared and
tation counseling, rehabilitation or occupational health evaluated along the lines described above. They are also
nursing, or clinical social work. held to strict scope-of-practice guidelines, ethics, and
The essential functions of a case manager include continuing education requirements.
assessment and coordination; development, monitoring,
implementation and evaluation of the rehabilitation plan;
and achievement of outcomes. It is worth noting that case
managers are managers in a very real sense. Generally Cross References
speaking, management theory states that the primary
functions of a manger are to plan, organize, direct, and Life Care Planning
control. This is precisely what case managers do but not to Recommendation
Catatonic Behavior C 493
References and Readings that has become too difficult or is perceived as being too
difficult. Typically, persons experiencing catastrophic
Case Management Society of America (2002). CMSA standards of reactions are not fully aware of their increasing lability
practice. Little Rock, AR: Case Management Society of America. and cannot respond to logic and reason, but they
Chan, F., & Leahy, M. (2005). Health care and disability case management,
benefit from decreased demands and calm reassurance. C
(2nd ed.). Lake Zurich, IL: Vocational Consultants Press.
Huber, D. (2005). Disease management: A guide for case managers.
Catastrophic reactions were initially thought to be
St. Louis: Elsevier Saunders. associated only with dominant hemisphere damage and
Mullahy, C. (2004). The case managers handbook (3rd ed.). Sudbury, MA: accompanying language impairment, but they can follow
Jones and Bartlett. any neurological problem that interferes with adaptive
coping and executive functioning.
Case Planning Cross References
Case Management Agitation

De-Escalation
Frustration Tolerance
CAT Scan
Computed Tomography
Callahan, C. D. (2009). The assessment and rehabilitation of executive
function disorders. In B. Johnstone & H. H. Stonnington (Eds.),
Rehabilitation of neuropsychological disorders (2nd edn., pp. 75106).
Philadelphia, PA: Psychology Press.
Catastrophic Condition Goldstein, K. (1948). Language and language disturbances: Aphasic
symptom complexes and their significance for medicine and theory of
Catastrophic Reaction language. New York: Grune and Stratton.
Holland, D., & Larimore, C. (2009). The assessment and rehabilitation of
language disorders. In B. Johnstone & H. H. Stonnington (Eds.),
Rehabilitation of Neuropsychological Disorders (2nd edn., pp. 137166).
Philadelphia, PA: Psychology Press.
Catastrophic Reaction Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuropsychological
Assessment (3rd edn., p. 62). New York: Oxford University Press.
DAWN E. B OUMAN
Drake Center
Cincinnati, OH, USA
Catatonia
Synonyms Catatonic Behavior
Catastrophic condition
Catatonic Behavior
Definition
S OLOMON K ALKSTEIN , FARZIN I RANI
This term coined by Goldstein (1948) describes acute University of Pennsylvania
distress, agitation, and disorganized behavior occurring Philadelphia, PA, USA
when overwhelmed by a situation with which the person
cannot cope, typically following brain injury or other
neurological impairment. Rapid and extreme anxiety, Synonyms
depression, and frustration can result when a person
becomes over-stimulated or overwhelmed with a task Catatonia
494 C Catatonic Behavior
Short Description Diagnostically, since catatonic behavior has numerous

disease causes (Gelenberg, 1976), care must be taken to
Catatonic behavior is characterized by marked distur- distinguish the above-listed conditions from other syn-
bances in psychomotor movements that occur within dromes, which may present with similar features. Specifi-
the context of a psychiatric or medical condition. Accord- cally, DSM-IV TR notes that a separate diagnosis is not
ing to the Diagnostic and Statistical Manual of the Mental given if the catatonia occurs exclusively during the course
DisordersFourth edition (DSM-IV TR) catatonic fea- of a delirium. Additionally, catatonic-like symptoms may
tures are identified, or the catatonic subtype is recognized, occur in the context of one of the medication-induced
when there are at least two of the following: movement disorders, such as neuroleptic-induced parkin-
sonism or neuroleptic malignant syndrome, or as a fea-
Motoric immobility as shown during catalepsy (in-
ture of akinetic parkinsonism, malignant hyperthermia,
cluding waxy flexibility) or stupor
locked-in syndrome, stiff-person syndrome or elective
Excessive motor activity (apparently purposeless and
mutism (Taylor & Fink, 2003).
independent of external stimuli)
Extreme negativism (motiveless resistance to instruc-
tions, maintenance of rigid postures against attempts
to be moved) or mutism
Epidemiology
Peculiarities of voluntary movement as shown during
Catatonia is currently rare in North America and Europe;
posturing (voluntary assumption of inappropriate or
however, reports of its prevalence vary widely among
bizarre postures)
studies. Bleulers initial estimates of catatonic
Stereotyped movements, prominent mannerisms, or
symptomatology among schizophrenia patients were sig-
prominent grimacing
nificantly higher than those that are found today. Numer-
Echolalia (repetition of a word or phrase just spoken
ous surveys of catatonia among psychiatric patients using
by another) or echopraxia (repetitive imitation of
duration criteria of several to 24 h have yielded prevalence
movements of others).
rates ranging from 7.6% to 38% (Taylor & Fink, 2003).
When including studies in which systematic rules of ex-
amination are used and catatonia rating scales are applied
Categorization this range narrows from 7% to 15% (Fink & Taylor, 2006).
Although numerous reports of catatonia among children
The DSM-IV TR lists three conditions during which cata-
and adolescents have been documented, particularly in
tonic features may be observed:
autistic and pervasive developmental disorders popula-
1. Schizophrenia Catatonic Subtype (295.20) tion, the syndrome appears to be more common in adults
2. Mood Disorder Catatonic Features Specifier with prevalence rates for children and adolescents ranging
3. Catatonia due to a General Medical Condition from approximately 117% (Weder, Muralee, Penland, &
(293.89) Tampi, 2008).
Catatonic subtype of schizophrenia: This is a subtype of
schizophrenia characterized by marked psychomotor
disturbance that involves at least two of the six symp- Natural History, Prognostic Factors,
toms identified above. Outcomes
Mood disorder Catatonic features specifier: The speci-
fier With Catatonic Features can be applied to the Catatonia was first formally described in the late nine-
current (or most recent) episode in major depressive teenth century by the German physician, Dr. Karl Lud-
disorder and bipolar I or II disorder when at least two wig Kahlbaum, as a disorder characterized by mood
of the six symptoms listed above are present. symptoms, stupor, confusion, and eventually, dementia.
Catatonia due to a general medical condition: When Additionally, he noted unusual motor symptoms and
evidence is present that catatonic behavior, presenting carefully documented the character and course of the
as at least two of the six symptoms listed above, is illness. Subsequently, Kraepelin classified patients who
the direct physiological consequence of a general med- exhibited symptoms of catatonia within his dementia
ical condition, the syndrome is specified as Catatonic praecox disorder and Bleuler, adopting this formulation,
Disorder Due to. . . and the medical condition is interpreted catatonic symptoms as features of his newly
listed. named schizophrenia. This model of catatonia as a
Catatonic Behavior C 495
subtype within schizophrenia persisted through early psychopharmacological studies. Neuroimaging studies have
and recent versions of the DSM. Only with the publica- not been conclusive and have revealed various cortical and
tion of DSM-IV was consideration given to catatonia subcortical brain regions to be associated with the illness, a
occurring within the context of other psychiatric and finding that may explain observed clinical differences
medical conditions. This was due to important articles in symptom presentation (Weder et al., 2008). Neuropsy- C
published in the 1970s, which established co-occurrence chological evaluation of catatonic psychiatric inpatients
of catatonia and mood disorders (Abrams & Taylor, as compared with a psychiatric control group revealed
1976) and emphasized the association between catatonia relatively poorer performance on measures of working
and neurological or general medical conditions (Gelen- memory and those visualspatial abilities related to right
berg, 1976). Several reports have also suggested the pres- parietal functioning. Additionally, significant differences
ence of a genetic form of catatonia not captured by between catatonic patients and healthy controls were
DSM-IV TR criteria (Taylor & Fink, 2003). Thus, the observed on attentional and executive tests associated with
conceptualization and classification of catatonia con- frontal functioning. These results suggest attentional-motor
tinues to evolve. and frontoparietal dysfunction in catatonia (Northoff,
An additional area of controversy involves categoriza- Nagel, Danos, Leschinger, Lerche, & Bogerts, 1999).
tion. Advocates have argued for DSM reclassification of
catatonia into a syndrome rather than a subtype of schizo-
phrenia. They claim that the current model fails to ade- Evaluation
quately recognize catatonia in other psychiatric illnesses
and limits treatment of catatonic behavior to protocols Although DSM-IV requires two of the six symptoms of
focusing on antipsychotic drugs. Fink and Taylor (2003, catatonic behavior listed previously in order to establish
2006) have therefore proposed a change in nomenclature, presence of catatonia, definitions of catatonia, as well as
suggesting that catatonia be reclassified separately from its basic signs and symptoms, are still the subject of
other syndromes, akin to delirium or dementia, with three debate and no authoritative set of criteria has been uni-
syndrome subtypes (nonmalignant, delirious, and malig- versally accepted (Caroff & Ungvari, 2007). Several rating
nant) and four specifiers (secondary to: mood disorders, scales have been developed to assess for the presence of
general medical conditions or toxic states, neurological dis- catatonia; however, the number of signs and symptoms
orders, or psychotic disorders). However, this reclassifica- that are included range from 10 to 40 for almost all
tion system remains controversial. instruments (Taylor & Fink, 2003). Several reviews have
Numerous risk factors for catatonia have been listed the most commonly listed signs and symptoms of
reported including history of perinatal infections, epilep- the syndrome as mutism, posturing, negativism, staring,
sy, medication effects, and frontal or basal ganglia dis- rigidity, echophenomena, stereotypes, grimacing, and
eases (Weder et al., 2008). Additionally, various aspects of perseveration (Weder et al., 2008). In terms of the num-
comorbid psychiatric conditions including age of onset ber of symptoms required to justify a diagnosis, mini-
and severity of symptoms are considered risk factors and mum thresholds vary among scales. While some scales
contribute significantly to prognosis. Although highly resemble the DSM-IV TR in requiring the presence of
variable, overall prognosis appears to be relatively better 2 or 3 symptoms out of a list of 11 or 12 (Lohr &
for recurrent catatonia and mood disorders with cat- Wisniewski, 1987; Rosebush, Hildebrand, Furlong, &
atonia as compared with catatonic schizophrenia. One Mazurek, 1990), other instruments assign greater weight
review study indicated that while acute treatment prog- to certain cardinal symptoms over other secondary symp-
nosis is excellent, long-term prognosis depends on the toms (Bush, Fink, Petrides, Dowling, & Francis, 1996).
underlying condition that elicited catatonia (Taylor & Other scales group symptoms by category (i.e., motor,
Fink, 2003). affective, and behavioral) and require a symptom from
each category in order to establish a diagnosis (Northoff
et al., 1999). Most authors accept a range from several
Neuropsychology and Psychology to 24-hours duration as being necessary in order to defin-
of Catatonic Behavior itively establish the presence of catatonia (Weder et al.,
2008). Attempts have been made to identify individual
Although the pathophysiology of catatonia remains poorly clusters within the catatonia syndrome based on dis-
understood, both the GABA and dopaminergic neurotrans- crete symptom-groups and duration of illness (acute/
mitter systems have been implicated in numerous chronic); however, further research in this area is
496 C Catecholamines
necessary before the existence of subtypes can be estab- Bush, G., Fink, M., Petrides, G., Dowling, F., & Francis, A. (1996).
Catatonia. I. Rating scale and standardized examination. Acta Psy-
lished (Weder et al., 2008).
chiatrica Scandanavica, 93, 129136.
Caroff, S. N., & Ungvari, G. S. (2007). Expanding horizons in catatonia
research. Psychiatric Annals, 37(1), 79.
Treatment Fink, M., & Taylor, M. A. (2003). Catatonia: A clinicians guide to diagnosis
and treatment. Cambridge: Cambridge University Press.
Fink, M., & Taylor, M. A. (2006). Catatonia: Subtype or syndrome in
Treatment for catatonic symptoms differs depending on DSM? American Journal of Psychiatry, 163, 18751876.
the underlying cause. Catatonia is currently viewed by Gelenberg, A. J. (1976). The catatonic syndrome. Lancet, 1(7973),
most clinicians from a predominantly biological frame- 13391341.
work (Penland, Weder, & Tampi, 2006). Generally, benzo- Lohr, J., & Wisniewski, A. A. (1987). Catatonia. In J. Lohr & A. A.
Wisniewski (Eds.), Movement disorders: A neuropsychiatric approach.
diazepines such as lorazepam are considered to be the first
New York: Guilford Press.
treatment of choice. If patients fail their initial trial, the Northoff, G., Nagel, D., Danos, P., Leschinger, A., Lerche, J., & Bogerts, B.
use of bilateral electroconvulsive therapy is usually con- (1999). Impairment in visual-spatial function in catatonia:
sidered. Although these are the best-studied treatments A neuropsychological investigation. Schizophrenia Research, 37,
of the syndrome, the efficacy of other approaches, such 133147.
Penland, H. R., Weder, N., & Tampi, R. R. (2006). The catatonic dilemma
as transcranial magnetic stimulation, continues to be
expanded. Annals of General Psychiatry, 5(14), 19.
explored. Catatonic schizophrenia may be treated by a Rosebush, P. I., Hildebrand, A. M., Furlong, B. G., & Mazurek, M. F.
variety of pharmacotherapeutic and psychotherapeutic (1990). Catatonic syndrome in a general psychiatric inpatient popu-
methods. Hospitalization may be necessary to protect lation: Frequency, clinical presentation, and response to lorazepam.
the patients safety and supportive psychotherapy and Journal of Clinical Psychiatry, 51, 357362.
Taylor, M. A., & Fink, M. (2003). Catatonia in psychiatric classification:
family education may help patients and their families
A home of its own. American Journal of Psychiatry, 160, 12331241.
adjust to problems created by the illness. Other support- Weder, N. D., Muralee, S., Penland, H., & Tampi, R. R. (2008). Catatonia:
ive services as sheltered workshops and special education A review. Annals of Clinical Psychiatry, 20(2), 97107.
may also be helpful. When catatonic symptoms are due to
a mood disorder, episodes may be treated with mood
stabilizers or antidepressant medications. Catatonic
symptoms caused by a medical disorder require correct Catecholamines
diagnosis of the underlying medical condition, followed
by appropriate treatment. For example, levodopa and M ARLA S ANZONE
amantadine (symmetrel) have shown some effectiveness Independent Practice
in reducing catatonic symptoms due to postencephalitic Annapolis, MD, USA
Parkinsons disease. Hospitalization and careful supervi-
sion of persons with catatonic symptoms may be neces-
sary to ensure that they do not harm themselves or others Synonyms
and to prevent malnutrition, exhaustion, or fever.
Adrenergic agonists; Direct- and indirect-acting adrenergic
receptor agonists; Dopamine agonists; Dopaminergic
Cross References agonists; Sympathomimetic amines/drugs/agents/
compounds
Delusion
Mood Disorder
Schizophrenia Definition
Catecholamines are a class of biologically active water

soluble hormones comprising catechol and amine
References and Readings compounds. They are derivatives of the amino acid
tyrosine. Tyrosine is converted from phenylalanine as a
Abrams, R., & Taylor, M. A. (1976). Catatonia: A prospective clinical
function of the hydroxylation by the enzyme phenylala-
study. Archives of General Psychiatry, 33(5), 579581.
American Psychiatric Association. (2000). Diagnostic and statistical man-
nine hydroxylase, and can also be directly ingested from
ual of mental disorders (4th edn., text revised). Washington, DC: dietary proteins (Catecholamines, 2002; Catecholamines,
American Psychiatric Association. 2008; Catecholamines, 2009a, b).
Catecholamines C 497
Catecholamines are sympathomimetic amines, a group involuntary movement disorder and tends to develop
of compounds including dopamine, epinephrine, and during middle adulthood. Anxiety can precipitate and
norepinephrine whose molecular structure is similar to exacerbate the amplitude of the tremor. It is generally
that of a larger class of neurotransmitters, the monoa- treated with beta blockers such low doses of propranolol
mines. The specific molecular structure of catecholamines and with lesser efficacy with Atenolol and anxiolytics C
is a benzene ring with two hydroxyl groups, an intermedi- such as alprazolam (Kaufman, 2007).
ate ethylamine to the side and an amine terminal group. Chemodectoma (nonchromaffin paraganglioma)
The chromaffin cells in the adrenal medulla and sympa- Benign chemoreceptor system tumors. The most common
thetic nervous system postganglionic fibers are the primary types are glomus jugulare tumor and carotid body tumor.
site of catecholamine production (Hoffman, 2004). Dopamine-b-hydroxalase Deficiency Severe orthostatic
During times of physiological and/or psychological hypotension of a congenital nature caused by the inability
stress neurons in the central and peripheral sympathetic to generate the enzyme, dopamine-b-hydroxalase.
nervous systems secrete catecholamines via hypothalamic Familial Paraganglioma Syndrome Genetic slow-
and adrenomedullary activation. Catecholamine toxicity, growing chromosomal (11q23) benign tumors primarily
also referred to as catecholamine dump or storm can of the head and neck. These unusual conditions are inher-
occur from trauma, causing over-stimulation, excessive ited from the father. Disfiguring facial swelling, hearing
production and circulation of catecholamines in the loss, tinnitus, pain, persistent cough, or other head/neck
central nervous system, and/or lesions of nuclei affecting anomalies as a function of cranial nerve damage from
the sympathetic nervous system in the brainstem. the tumor.
Catecholamines affect metabolic rate, temperature Neuroblastoma, produces catecholamines, and follow-
regulation, smooth muscle functions, cardiovascular and ing brain tumors is the second most common solid tumor
nervous systems. Epinephrine and norepinephrine auto- in childhood. Testing for the catecholamine metabolites,
nomically prepare the body for crisis such as cold, fatigue, vanillylmandelic acid and homovanillic acid, are
danger, and shock. Dopamine is produced as an interme- identified in the urine.
diate process in the synthesis of epinephrine and is critical Pheochromocytoma is a benign tumor that secretes
to the regulation of many neurological processes, includ- norepinephrine and epinephrine. It originates in
ing smooth fine and gross motor movements, energy sympathetic paraganglia or adrenal medulla.
regulation, motivation, executive functioning and formal Tetrahydrobiopterin deficiency is a genetic condition
thought regulation. Sympathomimetic drugs used to treat that results in the inability to manufacture the enzymes
conditions associated with these biological functions required to synthesize catecholamines. This leads to a defi-
mimic the actions of epinephrine, norepinephrine or do- ciency of the neurotransmitters, norepinephrine, epineph-
pamine (Sympathomimetic drug, 2008; Venes, Thomas, rine, and dopamine (Catecholamines, 2002; Myers, 2006).
Egan, Houska, 2001). Such drugs include those used to
treat a variety of abnormalities associated with central and
sympathetic nervous system processes (e.g., blood pressure, Mechanisms of Action
cardiac anomalies, premature labor, glaucoma, bronchitis,
asthma, emphysema, blood glucose metabolism, movement The adrenergic or sympathomimetic drugs act at
disturbances and psychosis). In addition, numerous disor- sympathetic postganglionic terminal by activating the
ders involve catecholamine disturbances of congenital, ge- catecholaminergic hormones, epinephrine (adrenaline),
netic, or familial origin such as dopamine-b-hydroxalase norepinephrine (noradrenaline), and/or dopamine in
deficiency, paraganglioma syndrome, and tetrahydrobiop- various ways. Some compounds have cross-reactivity
terin deficiency, but also those with unknown precipitating such that they act on catecholamines by more than one
mechanisms, including chemodectina, neuroblastoma, and mechanism of action (Sympathomimetic drug, 2008).
pheochromocytoma (Catecholamines, 2002). Directly activating adrenergic postsynaptic receptors
(Direct-Acting Adrenergic Agonists) include a-adrenergic
agonists and b-adrenergic agonists. There are five types:
Catecholamine-Related Conditions a1, a2, b1, b2, and b3. Adrenergic agonists stimulate one or
more of these receptor types. Adrenergic antagonists
Benign Familial Tremor/Essential Tremor is an inherited inhibit one or more of the actions of these receptors.
autosomal dominant condition suggestive of excessive Some agents have stimulating and blocking actions on
systemic adrenergic activity. It is the most common different receptors simultaneously. Receptor selectivity
Catecholamines. Table 1 Sympathomimetic Action & Function
Primary
neurotransmitter
actions Mechanism of action Examples of compounds Clinical uses
Alpha (a) Direct-acting alpha- Alpha (a1, a2) adrenergic Used to treat glaucoma by decreasing the
adrenergic adrenergic agonists agonists production of aqueous fluid; as vasopressors, nasal
agonists Promote decongestants and to dilate the pupil for eye
vasoconstriction, exams
mydriasis, body
tissue-building,
inhibition
of endogenous
testosterone release
a1 Agonists a1 Agonists Oxymetazoline, Used to treat anemias caused by deficient
stimulate phenylephrine production of red blood cells, aplastic anemia,
phospholipase C hypotension, shock, paroxysmal supraventricular
activity tachcardia
a2 Agonists a2 Agonists inhibit Clonidine (a2 and a2 Agonists reduce sympathetic nervous system
adenylyl cyclase imidazoline-I1 agonist) activation. They are used to treat opiate and
activity Guanfacine (affinity for alcohol withdrawal symptoms, as
preference for a2a antihypertensives, gestational hypertension, to
adrenoceptor) decrease peripheral resistance and as sedatives.
More recently they are being used to treat
Methyldopa is
neuropathic pain, sleep hyperhidrosis, and off-
approximately 50%
label, to counter the side effects of stimulant
absorbed from the gut,
medications
metabolized in the
intestines and liver and
alpha-methylnorepineprine,
its metabolite, stimulates
central a2- receptors
Mixed a, b1, Undetermined or Epinephrine, amidephrine, Mixed alpha- beta- agonists such as epinephrine
b2 agonists mixed alpha- beta- ergotamine, are used to treat anaphylaxis, acute asthmatic
stimulation norepinephrine, synephrine reactions, cardiac arrest, open-angle glaucoma
and nasal congestion. It stimulates alpha, beta1
and beta2 adrenergic receptors, increasing cardiac
output, dilating bronchials, skeletal muscle
vasulature, and pupils dilation due to constriction
of dilatory muscles
b Antagonists Direct-acting beta- Cardiac stimulants Beta blockers are used to treat heart block,
(beta blockers) adrenergic agonists ventricular tachcardia, cardiac arrest, asthma,
block the action of stimulate adenylyl chronic bronchitis, emphysema, hypovolemic and
epinephrine and cyclase activity and septic shock, low cardiac output or hypoperfusion,
norepinephrine open calcium congestive heart failure
channels
b1 Agonists Direct-acting b1- Albuterol, dobutamine Asthma, Chronic Obstructive Pulmonary Disease
adrenergic agonists (COPD), sinus congestion
Catecholamines. Table 1 (Continued)
Primary
neurotransmitter
b2 Agonists Direct-acting b2- Metaproterenal, formoterol, A moderately selective b2 agonist. It acts on C
adrenergic agonists salmeterol, terbutaline smooth muscle in the lungs, uterus, and skeletal
stimulate muscle vasculature. Used to treat asthma, COPD,
postsynaptic premature labor
b2 receptors of the The enzyme intracellular adenyl cyclase catalyzes
intracellular enzyme, the conversion of ATP to cAMP. Elevated cAMP
adenylyl cyclase. levels are associated with bronchial
Closes calcium smooth muscle relaxation and regulation of mast
channels, relaxing cells activation
smooth muscle
Mixed b Isoproterenol (b1 and Cardiogenic shock, bradyarrhythmias, heart block,
antagonists b2 agonist) cardiac arrest, brochospasm associated with
anesthesia, asthma, chronic
bronchitis, emphysema, hypovolemic and
septicemic shock
COMT-inhibitors Indirectly inhibiting Entacapone, tolcapone Adjunctive Parkinsons treatment
epinephrine and
norepinephrine
metabolism
Dopamine Stimulate production Bromocriptine, Hypertensive crisis through vasodilation in
agonists and release at D1 apomorphine, fenoldopam coronary, renal, mesenteric and peripheral arteries
receptors Pramipexole (pre- and Pramipexole used to treat idiopathic parkinsonism
postsynaptic D2 and 3 signs. It stimulates caudate neurons
receptor agonism) by D3 agonism
Prolongs Levodopa (I-Dopa) Parkinsonianism Levodopas efficacy is as a
dopaminergic activity prodrug. It is a precursor of catecholamines
when combined with
COMT-inhibitors
and dopa
decarboxylase
inhibitors
(e.g., benserazide
or carbidopa)
Dopamine Increase Cocaine, Methylphenidate Cocaine used recreationally and highly subject to
Reuptake norepinephrine Amphetamines abuse. Ophthalmically used as local anesthetic.
Inhibitors (DRIs) release at central Amphetamines and methylphenidate are used
noradrenergic primarily to treat ADHD, narcolepsy, occasionally
neurons. Release of in geriatric depression, post-stroke and cancer
dopamine at to increase alertness and counteract
mesolimic areas in chemotherapy lethargy. All DRIs and stimulant-
high doses. acting drugs elevate mood, increase focusing
ability and physical energy in most, increase
respiration and heart rate, blood pressure and
decrease appetite. They can cause euphoria,
rebound depression and anxiety particularly
if over-used or used inappropriately to treat
depressive disorders
Primary
neurotransmitter
Dopamine Blockade of Antipsychotic agents Schizophrenia, Bipolar I, mania
antagonists dopamine (more D2
than D1 receptor
affinity).
Moderate a
adrenergic and
histaminic
antagonism.
Monoamine Stimulate production Phenelzine (Nardil) Treatment resistant depression, atypical
Oxidase Inhibitors and release of depression, panic disorder
(MAOIs) catecholamines in
CNS
Chronic use Tranylcypromine (Parnate)
downregulates a2 or
b adrenergic and
serotonin receptors
Norepinephrine Prevent re-uptake of Most non-SSRI Atypical depression, dysthymia, anxiety, ADD, post
reuptake norepinephrine at antidepressants: Tricyclic traumatic stress disorder
inhibitors postsynaptic antidepressants (TCAs
receptors mixed catecholamine
stimulation and inhibition)
Atomoxetine (Strattera)
serotonin and
norepinephrine reuptake
inhibition Duloxetine
(Cymbalta) Venlafaxine
(Effexor) selective
norepinephrine reuptake
inhibition
Norepinephrine- Increase availability of Bupropion, pyrovalerone, ADHD, depression, chronic fatigue, obesity
dopamine monoamines, mazindol (also classified as a
reuptake inhibitor dopamine and TCA), phenethylamines
norepinephrine, due
to inhibiting re-
uptake, causing a
stimulating effect
Norepinephrine Stimulate production Mirtazapine (classified as a Depression, mixed anxiety-depression with sleep
releasers and release of tetracyclic and a disruption
catecholamines noradrenergic specific
serotonergic antidepressant
NaSSA)
Mianserin is a tetracyclic
antidepressant
Primary
neurotransmitter
Stimulants Stimulate direct Amphetamine salts, ADD/ADHD increases alertness, concentration, C
production and methylphenidate, focus, attention, executive functions, endurance
release of dexamphetamine, mentally and physically. Diminishes verbal and
catecholamines, dextroamphetamine, physical impulsivity
particularly phentermine Narcolepsy to help maintain alertness
norepinephrine and
Major depressive disorder occasionally used to
dopamine from
augment antidepressant treatment
storage vesicles
Weight management phentermine is used to
suppress appetite
Also increase Schedule IV controlled substances in the US
norepinephrine and
dopamine levels via
reuptake inhibition
and binding to the
MAO protein
transporter
Stimulate production Modafinil, adrafinil Narcolepsy to maintain alertness, and counteract
and release of abnormal states that diminish alertness
catecholamines Night shift work to counteract fatigue
Over-the-counter Synthetic and plant- Ephedrine, To suppress appetite, increase alertness, enhance
stimulants based herbal pseudoephedrine, MDMA, athletic performance
preparations with cocaine, ephedra, Ma huang, Cocaine, a tropane derivative, is made from South
significant abuse guarana American coca bush leaves. It is occasionally used
potential thought to legally as an ophthalmic local anesthetic, but no
stimulate release of longer prescribed for its stimulant properties
catecholamines
Aminoff (2004); Hoffman (2004); Kaufman (2007); Katzung (2004); Psychoactive drug (2009); Stimulant (2009); Sympathomimetic drug (2008);
Williams and Turner (2008).
addresses strength of affinity toward a particular receptor norepinephrine. If the enzyme is inhibited, it prevents the
rather than absolute specific selectivity of one receptor only. removal of epinephrine and norepinephrine from the sys-
Direct-acting dopamine agonists are used to treat tem which induces sympathomimetic effects. Similarly,
hypertensive crisis and parkinsonian signs and symptoms. with COMT-Inhibitors, the enzyme catechol-O-methyl
Indirect-acting, norepinephrine transporter antagonists transferase (COMT) is an intracellular enzyme in the
such as ephedra, cocaine, and amphetamines. They block postsynaptic neuron that degrades epinephrine and nor-
and reverse the activity of the norepinephrine transporter epinephrine. This enzyme effectively deactivates them by
proteins. These proteins functionally terminate the effects of inducing S-adenosyl methionine (SAM) to add a methyl
norepinephrine and to a lesser degree, dopamine, by remov- group to the catecholamines. The COMT-Inhibitors
ing these neurotransmitters from the synapse and repacka- prevent this deactivation by blocking the breakdown/
ging them in their vesicles for later use (Katzung, 2004). reuptake process, and enabling the utility of the catecho-
Indirectly inhibiting epinephrine and norepinephrine lamines (Catechol-O-methyl transferase, 2009).
metabolism such as COMT-Inhibitors (e.g., entacapone Stimulating production and release of catecholamines as
and tolcapone) and MAOIs such as Parnate and Nardil do MAOIs and amphetamines. These agents are known to
(Aminoff, 2004) that raise the level of all the catecholamines increase cardiac output and blood pressure as a function of
in the blood. Monoamine oxidase (MAO) is the enzyme constricting peripheral blood vessels which increases the
primarily responsible for metabolism of epinephrine and force and rate of cardiac muscle contractions. They can
502 C Categorical Data
also lead to elevations in blood lipid levels due to fat Catecholamines. (2009b). In Merriam-Webster online dictionary.
Retrieved January 13, 2009, from http://www.merriam-webster.
catabolism and blood glucose levels due to glycogenolysis
com/dictionary/catecholamines
of skeletal and hepatic muscle (Sympathomimetic drug, Hoffman, B. B. (2004). Adrenoceptor-activating & other sympathomi-
2008). As discussed above, monoamine oxidase (MAO) is metic drugs. In B. Katzung (Ed.), Basic and clinical pharmacology
the enzyme primarily responsible for degrading catechola- (9th ed., pp. 122141). New York: Lange Medical Books/McGraw-
mines. It has a half-life of several minutes. MAOIs and Hill.
Katzung, B. G. (2004). Introduction to autonomic pharmacology.
psychoactive stimulants bind to the enzyme, inhibiting
In B. Katzung (Ed.), Basic and clinical pharmacology (9th ed.,
the break down of the catecholamines, and largely for this pp. 7593). New York: Lange Medical Books/McGraw-Hill.
reason the effects of amphetamines last longer than those of Kaufman, D. M. (2007). Clinical neurology for psychiatrists (6th ed.,
cocaine or crack. Amphetamines are among the adrenergic pp. 97, 190, 193, 430431). Philadelphia: Saunders Elsevier.
agents with dual mechanisms of action or cross-reactivity. Myers, T. (2006). Catecholamine (definition). In Myers, T. (Ed.),
Mosbys dictionary of medicine, nursing & health professions
The production of all the catecholamines, dopamine, epi-
(7th ed., pp. 323). Missouri: Mosby Elsevier.
nephrine, and norepinephrine is stimulated and the reup- Psychoactive drug. (2009). In Wikipedia. Retrieved January 16, 2009, from
take, particularly of norepinephrine, is inhibited. http://en.wikipedia.org/wiki/Psychoactive_drug
Stimulant. (2009). In Wikipedia. Retrieved January 15, 2009, from http://
en.wikipedia.org/wiki/Stimulant
Specific Compounds and Properties Sympathomimetic drug. (2008). In Wikipedia. Retrieved January 13,
2009, from http://en.wikipedia.org/wiki/Sympathomimetic
Venes, D., Thomas, C., Egan, E., & Houska, A. (2001). Catecholamine
All sympathomimetic amines can be conceptualized to be (definition), In D. Venes, et al. (Eds.), Tabers medical dictionary
part of a broad group of stimulant drugs due to their (19th ed., pp. 357). Philadelphia: FA Davis Company.
sympathetic nervous system and/or central nervous Williams, F. M., & Turner, T. J. (2008). Adrenergic pharmacology:
system activating properties. However, due to multiple Biochemistry & physiology of adrenergic function. In D. E. Golan,
A. H. Tashjian, E. J. Armstrong, & A. W. Armstrong (Eds.), Principles
mechanisms of action sympathomimetics are classified
of pharmacology: The pathophysiologic basis of drug therapy
accordingly and as a function of their use in the treatment (pp. 129139). Philadelphia: Lippincott Williams & Wilkins.
of specific conditions (Table 1).
Cross References Categorical Data

Adrenergic Agonists Qualitative Data
Dopamine
Epinephrine
Monoamine Oxidase
Norepinephrine Category Fluency
Sympathomimetic Amines
Controlled Oral Word Association Test
Verbal Fluency
Aminoff, M. J. (2004). Pharmacologic management of parkinsonism &

other movement disorders. In B. Katzung (Ed.), Basic and clinical
pharmacology, (9th ed., pp. 447461). New York: Lange Medical Category Test
Books/McGraw-Hill.
Catechol-O-methyl transferase. (2009). In Wikipedia. Retrieved January
15, 2009, from http://www.answers.com/topic/catechol-o-methyl-
N ICK A. D E F ILIPPIS
transferase Argosy University
Catecholamines. (2002). In MedicineNet. Retrieved January 15, 2009, Atlanta, GA
from http://www.medterms.com
Catecholamines. (2008). In Wikipedia. Retrieved January 13, 2009, from
http://en.wikipedia.org/wiki/Catecholamines
Catecholamines. (2009a). In The free dictionary by Farlex, Retrieved
Synonyms
January 13, 2009, from http://medical-dictionary.thefreedictionary.
com/Catecholamines BCT; CT; HCT
Category Test C 503
Description which to base approaches to new and unfamiliar stimuli.

Although Halstead found his test to discriminate frontal
The Category Test (CT) was first published by Ward lobe-damaged patients from others, this finding was never
Halstead (Halstead & Settlage, 1943). Over the years, validated by other researchers. Various researchers have,
there have been several versions of the test, all retaining however, identified the CT as one of the most sensitive C
the essential format of the original and the goal of mea- measures of brain injury in the Halstead Reitan Battery
suring concept formation ability. All versions involve the (Choca, Laastch, Wetzel, & Agresti, 1993).
presentation of visual images of different shapes to the The existence of various versions of the CT has raised
examinee. The examinee is to determine which underly- the issue of comparability of these newer forms with the
ing concept is presented by the image and choose a num- original CT. To date, there has been no research indicating
ber from 1 to 4 to identify the concept. For example, the effects of CT test apparatus on the performance of exam-
examinee may choose the number corresponding to inees. Numerous studies demonstrated comparable
the number of items in the image, the proportion of the results, regardless of the test format. Kupke (1983) point-
image that is drawn continuously, etc. The examinee is ed out that the modification of a test apparatus in a purely
given feedback after each choice to indicate if he or she cognitive task, such as that presented by the CT, should
was correct in their decision. By a process of utilizing this have little effect on performance. However, this analysis
feedback to monitor performance, the examinee then would only pertain to versions that retain the original
learns the concepts. The number of errors is used to test stimuli and administration instructions. A self-
determine the overall performance. administered version of the test that drastically changed
The original version of the test was administered by instructions and allowed the examinee to view earlier
way of a drum with images on it and a slit for examinees responses does not meet this requirement. Also, various
to view them. Feedback was given with a bell (correct) or short forms of the CT have not been studied sufficiently to
buzzer (incorrect). Sometime during the 1940s or 1950s determine their comparability to the original length test.
(the exact date being unclear), the test was reduced from A number of investigators have attempted to determine
its original 360 items and 9 subtests to 208 items and if the CT can generate more scores than just the number of
7 subtests. The final subtest asks the examinee to recall errors. Factor analytic studies have indicated that there
previously presented concepts in order to respond cor- may be different abilities tapped by the test, prompting
rectly, constituting a memory component to the test. research into the possibility of developing scores for differ-
More recent versions have included a projection of images ent abilities. Scales for spatial positional reasoning, propor-
using slides, a card format, a self-administered version, tional reasoning, perseveration, loss of set, and memory,
a booklet version, and various computer versions. The have all been proposed, along with a measure of effort.
various versions are available from different publishers: Recent research has found concurrent validity for a num-
Slide projector version (Reitan Labs), Booklet version ber of these measures, and efforts to standardize them for
(Psychological Assessment Resources), and Computer ver- clinical use continue (Minassian et al., 2003).
sions (Psychological Assessment Resources and Mental
Health Systems). Feedback has varied by version and
includes the original bell or buzzer, computer approxima- Psychometric Data
tions of the bell or buzzer, or examiner feedback of correct
and incorrect. Test administration time is 3045 min. Demonstrated testretest validity of the CT ranges from
0.60 in normal populations to 0.96 for brain-damaged
participants. A problem in identifying retest stability for
Historical Background the CT has to do with the substantial learning aspect of
the test. Although there has been no adequate analysis of
Halstead (1940) reported the preliminary findings of expected gain on re-administration of the test, reliability
studies dating back to the 1920s using concept formation data suggest an improvement of about 15 points for
tests in which brain-damaged participants grouped normal individuals and 25 points for brain-damaged
objects into categories. It was clear from subjective ana- individuals, with a retest interval of 23 months. Internal
lyses that brain damage affected this ability. Halstead consistency, perhaps a better marker of reliability for this
hypothesized that his test measured abstraction and the test, has been shown to be very high at 0.97, as is split half
process of developing sets or frames of reference on reliability at 0.98.
504 C Caudate Nucleus
Numerous studies have demonstrated the CTs ability related to perseveration, attention, and possibly other
to discriminate brain damaged from normal examinees, aspects of their performance on the CT.
with analyses indicating statistically significant discrimi-
nation at the 0.05 to 0.001 levels. However, utilizing only
the suggested cut-off score of 50 errors to separate groups
Cross References
has resulted in a false positive rate of as high as 18%. The
need to correct for age and education has been firmly
COWA
established, as these variables account for a significant
Ruff Figural Fluency
variance of CT error scores. Including these corrections
Tower of London
significantly reduces classification errors (Heaton, Grant,
Trail Making Test
& Matthews, 1991).
Wisconsin Card Sorting Test
The original intent of Halstead to utilize the CT as a
measure of frontal lobe functioning has not been vali-
dated by researchers. Also, the CT has been found to be
relatively ineffective in lateralizing damage to the brain. References and Readings
The test, as is the case with many neuropsychological
instruments, is significantly impacted by severe psychiat- Choca, J. P., Laastch, L., Wetzel, L., & Agresti, A. (1993). The
ric disturbance and inadequate effort. Halstead Category Test: A fifty year perspective. Paper presented at
the annual meeting of the American Psychological Association,
Toronto, Canada.
Halstead, W. C. (1940). Preliminary analysis of grouping behavior in
Clinical Uses patients with cerebral injury by the method of equivalent and non-
equivalent stimuli. American Journal of Psychiatry, 96, 12631294.
The category test is generally grouped in most textbooks Halstead, W. C., & Settlage, P. H. (1943). Grouping behavior of normal
persons and of persons with lesions of the brain. Archives of Neurol-
in the field with other measures of executive function-
ogy and Psychiatry, 49, 489503.
ing. This concept can be loosely defined as the ability to Heaton, R. K., Grant, I., & Matthews, C. G. (1991). Comprehensive norms
utilize feedback to organize and plan ones approach to for an expanded Halstead-Reitan Battery: Demographic corrections,
deal with a novel problem-solving task. Taking this defi- research findings, and clinical applications. Odessa, FL: Psychological
nition, the CT seems to qualify as a measure of this Assessment Resources.
Kupke, T. (1983). Effects of subject sex, examiner sex, and test apparatus
ability. In fact, clinicians who use the test typically in-
on Halstead Category and Tactual Performance Tests. Journal of
clude it in their battery of tests as an executive function- Consulting and Clinical Psychology, 51, 624626.
ing measure. This approach is supported by the test Minassian, A., Perry, W., Carlson, M., Pelham, M., & DeFilippis, N.
format and some research, but should not involve reli- (2003). The Category Test Perseveration, Loss of Set, and Memory
ance on the CT as the sole measure of executive func- scales: Three new scales and their relationship to executive function-
ing measures. Assessment, 10, 213221.
tioning. As previously discussed, the test does not
identify only frontal lobe dysfunction, but is sensitive
to any type of brain injury.
Unfortunately, the only validated and normed score
for the CT is the total error score. The original cut-off of
50 errors should not be used without also looking at age Caudate Nucleus
and education adjusted scores. The sex of the examinee
does not appear to have a significant effect on test per- S EEMA S HROFF
formance, and although norms are frequently broken Virginia Commonwealth University
down by sex, this demographic variable can largely be Richmond, VA, USA
ignored. The clinician can view CT performance as in-
dicative of the overall cortical integrity of his or her
patient. There is also some evidence that the test assesses Definition
fluidity of thinking and may be related to rehabilitation
outcome. The caudate nucleus is an arcuate mass deep into the
Ongoing research will hopefully provide the clinician cortical hemispheres forming a part of the basal ganglia.
more information concerning his or her patients abilities Apart from being involved in the smooth orchestration of
Caudate Nucleus C 505
motor actions, it has been recently implicated in other the direct pathway that increases motor activity. An
functions like learning, memory, emotion, and language. indirect pathway, involving the subthalamic nucleus,
decreases motor activity. The activity of these pathways
is further modulated by dopamine from the nigrostrial
Nomenclature tract and ACh from the interneurons. C
Striatum/Neostriatum = Caudate Nucleus (nucleus
caudatus) + Putamen Physiology and Pathophysiology
Corpus striatum (Dorsal division) = Caudate Nucleus +
Putamen + Globus Pallidus The caudate nucleus is mainly involved in motor planning
and execution of smooth movement. Degeneration of the
caudate is associated with dyskinesias and involuntary
Current Knowledge movements. Caudate pathology manifests in choreiform
movements (brisk, jerky, and purposeless), as seen in
Anatomy Sydenhams chorea (minute caudate hemorrhages and
capillary emboli post streptococcal infection in children)
The caudate nucleus has a globular head, tapering body, or Huntingtons disease (an adult onset degenerative he-
and down curving tail. The head lies in the floor and reditary disorder). Athetosis (slow, sinuous, and aimless
lateral wall of the anterior horn of the lateral ventricle, movements involving distal musculature) is also seen in
whereas the body runs in the floor. Medially, the caudate striatal pathology. Loss of nigrostriatal input in Parkin-
nucleus abuts the thalamus; in the floor of the ventricle, sons disease leads to akinesia and rigidity characteristic of
this junction forms a groove known as the sulcus the disease.
terminalis that lodges the stria terminalis of the choroids Recently, the caudate nucleus has been implicated in
plexus. The corpus callosum runs above the head and functions other than motor planning. Using functional
body. The caudate nucleus is separated from the lenti- imaging, Crinion et al. (2006), have shown activation of
form nucleus by the anterior limb of the internal capsule. the caudate nucleus during language processing in bilin-
gual persons. Initial degeneration in the caudate is
thought to be responsible for the dysphoria in early Hun-
Histology tingtons disease (Paradiso et al., 2008). The caudate nu-
cleus has also been theorized to envision positive
The caudate nucleus and putamen show similar histology. emotional events in the near future (DArgembeau et al.,
Small and large neurons (in a 20:1 ratio) with spherical or 2007) and provide complimentary information of the
ovoid dendritic fields populate the neostriatum making outcomes of actions (Lau & Glimcher, 2007).
connections within the nucleus or with the globus palli-
dus. Most small neurons contain GABA and either
enkephalin or substance P. Enkephalinergic neurons ex- Cross References
press D2 dopamine receptors whereas those with sub-
stance P have D1 receptors. Large neurons with spiny Globus Pallidus
dendrites contain acetylcholine esterase (AChE) and cho- Putamen
line acetyltransferase (CAT). Thalamus
Circuitry
Corticostriate, thalamostriate, and nigrostriate fibers
form the major input to the striatum. Cortical areas Crinion, J., Turner, R., Grogan, A., Hanakawa, T., Noppeney, U.,
Devlin, J. T., et al. (2006). Language control in the bilingual brain.
involved in motor planning and execution project to the
Science, 312(5779), 15371540.
caudate and putamen. Striatal neurons relay to the globus D Argembeau, A., Xue, G., Lu, ZL., Van der Linden, M., & Bechara, A.
pallidus that sends information to the thalamus (VA/VL), (2007). Neuroimage [Epub ahead of print].
which in turn feeds back to cortical motor areas forming Grays Anatomy (1995). (38th ed.). Pearson Professional Limited.
506 C Causal Modeling
Lau, B., & Glimcher, B. W. (2007). Action and outcome encoding in

the primate caudate nucleus. Journal of Neuroscience, 27(52), CDR
1450214514.
Murray, B., & John, K. (1983). The human nervous system An anatomical
Clinical Dementia Rating
viewpoint (4th ed.). Philadelphia: Harper and Row, Publishers, Inc.
Paradiso, S., Turner, B. M., Paulsen, J. S., Jorge, R., Ponto, L. L., &
Robinson, R. G. (2008). Neural bases of dysphoria in early Hunting-
tons disease. Psychiatry Research, 162(1), 7387.
CEA
Carotid Endarterectomy
Causal Modeling
Path Analysis
Ceiling Effect
S ANDRA B ANKS
Cavernoma Allegheny General Hospital
Pittsburgh, PA, USA
Angioma, Cavernous Angioma
Synonyms
Cavernous Hemangioma Ceiling level
Angioma, Cavernous Angioma

Definition
A ceiling effect is observed when an examinee obtains very

Cavernous Venous Malformation high or maximum scores on a particular test. This may
lead to an underestimation of the examinees true ability
Angioma, Cavernous Angioma level because the test does not allow for higher levels of
performance to be assessed.
CBCL Current Knowledge
Child Behavior Checklist A ceiling effect in a large number of participants in a

normative sample may prevent the examiners ability to
gauge a particular individuals personal ceiling, or highest
level of performance, when compared with others in the
standardization sample because the maximum level of
CBCT performance within the sample cannot be assessed.
For example, on a list-learning memory test that con-
Cognitive Behavioral Couples Therapy tains only four words, the majority of examinees will most
likely recall most or all of the words. Four bits of
information (in this case, words in a list) place very little
demand on the average persons memory ability. To say
CCT that any particular examinee who learns all four words is
demonstrating intact memory abilities may underesti-
Childrens Category Test mate that examinees actual memory span. Adding at
Center for Epidemiological StudiesDepression C 507
least five more words would allow for an investigation of cut-off scores may be more appropriate with medical
that individuals upper limit of learning or memory populations.
capacity.
Historical Background C
Cross References
In 1971, the National Institute of Mental Health (NIMH)
Floor Effect began development of the CES-D to measure depressive
Testing the Limits symptoms in epidemiological research (Brantley,
Mehan, & Thomas, 2000). Selection of original compo-
nents of depressive symptomatolgy (e.g., depressed
mood, worthlessness) was based on factor analytic stud-
Ceiling Level ies and clinical literature (Radloff, 1977); specific items
were chosen from established measures. Following
Ceiling Effect minor revisions, items were added to the NIMH
structured interview and used in a large-scale study
(Brantley et al., 2000).
Follow-up studies support use of the CES-D with
diverse populations, including those with neurological
Center for Epidemiological compromise. Recent efforts have also focused on creating
StudiesDepression shorter versions of this measure (e.g., Iowa, Boston) to
facilitate use and decrease participant burden. Kohout
L ISA A. B RENNER and colleagues (1993) found that when assessing older
VISN 19 MIRECC adults (65 and older) shorter versions adequately evalu-
Denver, CO, USA ated the same symptom dimensions as the original mea-
sure. Findings from Carpenter et al. (1998), who pooled
data from 832 women (6 population), support use of the
Synonyms Iowa form over the Boston.
CES-D
Psychometric Data
Description Psychometric properties of the CES-D were initially
established with members of the general population
The Center for Epidemiological Studies Depression (household interview survey) and those receiving ser-
Scale (CES-D; Radloff, 1977) is a 20-item self-report vices in a psychiatric setting (Radloff, 1977). Validity
measure that assesses the presence and severity of depres- (content, construct, and criterion) was confirmed via
sive symptoms over the previous week. The CES-D has item choice and patterns of correlations with clinical
been used with adult and adolescents. Individuals com- ratings and alternate self-report measures. CES-D scores
pleting the Scale rate each item on a four-point Likert differentiated between psychiatric inpatients and mem-
scale ranging from 0 (rarely or none of the time) to 3 (most bers of the general population (Radloff, 1977): 70% of
or all of the time). Four items require reverse scoring. the patients versus 21% of the general population scored
Administration time is approximately 5 min. Responses above 16. Internal consistency, based on coefficient
are summed to obtain a total score of 060, with higher alpha and Spearman-Brown split-halves method, is gen-
scores indicating a greater frequency of symptoms. Scores erally high approximately 0.85 in the general population
of 16 or higher were suggested to identify subjects with and approximately 0.90 in the patient sample. Consistent
depressive illness (Radloff, 1977). Work by Pandya, Metz, with the expectation that shorter test-retest intervals
and Patten (2005) supports the use of this cut-off in those would produce higher correlations, test-retest reliabilities
with multiple sclerosis (MS). Earlier work by Zich, ranged from 0.32 (12 months) to 0.67 (4 weeks). Follow-
Attkisson, and Greenfield (1990) suggest that alternate up studies appear to support Radloff s (1977) original
508 C Center for Epidemiological StudiesDepression
reliability and validity statistics (Brantley et al., 2000). A Cross References

four factor structure (depressed affect, positive affect,
somatic and retarded activity, and interpersonal) was Beck Depression Inventory
initially reported (Radloff, 1977), and has been supported Geriatric Depression Scale
by subsequent confirmatory analyses. However, findings Hamilton Rating Scale of Depression
suggest that among minority populations alternate mod- Structured Clinical Interview for DSM-IV (SCID)
els may provide a better fit (Brantley et al., 2000). Zung Self-Rating Depression Scale
Clinical Uses References and Readings
Bay, E., Hagerty, B. M., & Williams, R. A. (2007). Depressive symptom-

The CES-D is a widely accepted measure of depressive
atology after mild-to-moderate traumatic brain injury: A compari-
symptoms that has been used with a range of popula- son of three measures. Archives of Psychiatric Nursing, 21(1), 211.
tions, including those with a history of neuropsycholog- Brantley, P. J., Mehan, J., & Thomas, J. L. (2000). The beck depression
ical impairments secondary to disease (e.g., MS), inventory (BDI) and the center for epidemiological studies depres-
acquired insult (e.g., stroke), or injury (e.g., traumatic sion scale (CES-D). In M. E. Maruish (Ed.), Handbook of psychologi-
cal assessment in primary care settings (pp. 391422). Mahwah, NJ:
brain injury, TBI). The CES-D has been relied on to
Lawrence Erlbaum Associates, Inc.
document the incidence and severity of depression in Bush, B. A., Novack, T. A., Schneider, J. J., & Madan, A. (2004). Depres-
individuals with MS, including those who received dis- sion following traumatic brain injury: The validity of the CES-D as a
ease-modifying treatments (Patten, Fridhandler, Beck, & brief screening device. Journal of Clinical Psychology in Medical
Metz, 2003; Chwastiak et al., 2002), and to assess for Settings, 11, 195201.
Carpenter, J. S., Andrykowski, M. A., Wilson, J., Hall, L. A., Rayens, M. K.,
potential adverse psychiatric side effects of Interferon
Sachs, B., et al. (1998). Psychometrics for two short forms of the
treatment (Patten & Metz, 2001). It has also been used center for epidemiologic studies-depression scale. Issues in Mental
to explore the relationship between depression and cogni- Health Nursing, 19, 481494.
tive complaints in individuals with MS (Maor, Olmer, & Chwastiak, L., Ehde, D. M., Gibbons, L. E., Sullivan, M., Bowen, J. D., &
Mozes, 2001), and study whether depression may be a Kraft, G. H. (2002). Depressive symptoms and severity of illness in
multiple sclerosis: Epidemiologic study of a large community sam-
risk factor for increased mortality after stroke (Gump
ple. The American Journal of Psychiatry, 159(11), 18621868.
et al., 2005). Dikmen, S. S., Bombardier, C. H., Machamer, J. E., Fann, J. R., & Temkin,
Confirmatory factor analysis supports the use of N. R. (2004). Natural history of depression in traumatic brain injury.
this measure for those with mild to moderate TBI Archives of Physical Medicine & Rehabilitation, 85(9), 14571464.
(McCauley et al., 2006); acceptable reliability of the Gump, B. B., Matthews, K. A., Eberly, L. E., Chang, Y. F., & MRFIT
Research Group. (2005). Depressive symptoms and mortality in
CES-D with individuals with TBI has also been docu-
men: Results from the multiple risk factor intervention trial. Stroke,
mented (Bush, Novack, Schneider, & Madan, 2004). 36(1), 98102.
Moreover, Bay, Hagerty, and Williams (2007) argue that Kohout, F. J., Berkman, L. F., Evans, D. A., & Cornoni-Huntley, J. (1993).
the CES-Ds psychometric properties and ease of use Two shorter forms of the CES-D depression symptoms index. Jour-
render it an appropriate measure for depression screening nal of Aging and Health, 5, 179193.
Maor, Y., Olmer, L., & Mozes, B. (2001). The relation between objective
in persons with TBI. The CES-D has also been used in
and subjective impairment in cognitive function among multiple
longitudinal research on the incidence of depression sclerosis patientsthe role of depression. Multiple Sclerosis, 7(2),
following TBI (Dikmen et al., 2004) and in studies of 131135.
depression in caregivers of individuals with TBI (Rivera McCauley, S. R., Pedroza, C., Brown, S. A., Boake, C., Levin, H. S.,
et al., 2007). Goodman, H. S., et al. (2006). Confirmatory factor structure of the
center for epidemiologic studies-depression scale (CES-D) in mild-
Of note, although findings from the CES-D may be
to-moderate traumatic brain injury. Brain Injury, 20, 519527.
useful in identifying certain symptoms of depression, the Pandya, R., Metz, L., & Patten, S. B. (2005). Predictive value of the CES-D
measure only addresses mood during the week prior to in detecting depression among candidates for disease-modifying
administration and, therefore, does not permit the clini- multiple sclerosis treatment. Psychosomatics, 46, 131134.
cian to assign a formal diagnosis of a mood disorder. As Patten, S. B., Fridhandler, S., Beck, C. A., & Metz, L. M. (2003). Depres-
sive symptoms in a treated multiple sclerosis cohort. Multiple Scle-
such, in a clinical setting it may be best used in conjunc-
rosis, 9, 616620.
tion with additional findings (e.g., structured clinical in- Patten, S. B., & Metz, L. M. (2001). Interferon beta-1 a and depression in
terview, additional measures) to diagnose depressive relapsing-remitting multiple sclerosis: An analysis of depression data
disorders and assess treatment needs. from the PRISMS clinical trial. Multiple Sclerosis, 7(4), 243248.
Center for Medical Home Improvement C 509
Radloff, L. S. (1977). The CES-D Scale: A self-report depression scale for adults, and their families may require more than the
research in the general population. Applied Psychological Measure-
usual well child and/or adult, preventive care, and acute
ment, 1, 385401.
Rivera, P., Elliott, T. R., Berry, J. W., Grant, J. S., & Oswald, K. (2007).
illness interventions. It involves explicit changes in the
Predictors of caregiver depression among community-residing families roles of providers and office staff aimed at improving).
living with traumatic brain injury. Neurorehabilitation, 22(1), 38.
Zich, J. M., Attkisson, C. C., & Greenfield, T. K. (1990). Screening for
1. Access to needed services C
depression in primary care clinics: The CES-D and the BDI. Interna- 2. Communication with specialists, schools, and other
tional Journal of Psychiatry in Medicine, 20, 259277. resources
3. Outcomes for children and families
Center for Medical Home
Improvement The story of the medical home extends from the 1935
Social Security Legislation Act that called for Maternal
W. C ARL C OOLEY, J EANNE W. M C A LLISTER and Child Health (MCH) Title V Programs to locate,
Crotched Mountain diagnose, and treat crippled children to todays emphasis
Concord, NH, USA on providing planned primary health care in the context
of the families and communities in which patients live.
Community-based care in a medical home is increasingly
Membership accepted as one of the means of achieving optimal out-
comes for children, youth, adults, and their families. The
The Center for Medical Home Improvement (CMHI) is a term medical home was coined in 1967 by the Council
nonprofit organization affiliated with Crotched Mountain. on Pediatric Practice, a subgroup of the American Acade-
(Crotched Mountain is a charitable organization employing my of Pediatrics, and has been described with a variety of
more than 900 people, whose mission is to serve individuals applications and definitions since then. The CMHI began
with disabilities and their families, embracing personal its efforts in 1993 with a capacity building endeavor for
choice and development, and building communities of pediatric practices serving children with special healthcare
mutual support. It provides specialized education, rehabili- needs. In 1997, the CMHI developed and implemented an
tation, community and residential support services for improvement model with multiple New Hampshire, Ver-
more than 2,000 individuals living in New England and mont, and Maine healthcare teams. These teams (physi-
New York.) It is founded in 1993 by Dr. Carl W. Cooley, cian leader and practice-based care coordinator)
Medical Director and Ms. Jeanne W. McAllister, R.N., M.S., partnered with patients and families to redesign primary
M.H.A., Director. Along with the founders, Dr. Cooley and care services. In 2003, the CMHI published the Medical
Ms. McAllister, the CMHI is staffed by Lora Council, M.D. Home Index (MHI) as a validated measurement to assess
(Quality Consultant), Lori Keehl-Markowitz, R.N., B.S.N. quality and monitor improvements in a primary care
(Program Manager), Leah Reed (Program Coordinator), practice (this tool is now available for adult care). Practice
and Kathleen Sherrieb, R.N., M.S., M.P.H. (Data Manage- improvement activities in multiple states have consistent-
ment Consultant). ly demonstrated sustained increases of greater than 30%
in MHI scores overall. A companion Medical Home Fam-
ily Index and Survey used by these practices has shown
Major Areas or Mission Statement significant improvement in clinical, functional, satisfac-
tion, and cost outcomes and an increase in the use of
The mission of the CMHI is to promote high-quality written and portable care plans. During 20012004, the
primary care in the medical home and secure health CMHI spread its model to ten additional practices in
policy changes critical to the future of primary care. The Vermont and New Hampshire and partnered with the
CMHI defines the medical home as a community-based National Initiative for Childrens Healthcare Quality
primary care setting which provides and coordinates high (NICHQ) in two national medical home learning collabora-
quality, planned, family-centered health promotion, acute tives. These efforts spread the CMHIs model to 20 state
illness care and chronic condition management (chronic Title V Programs, 40 primary care practices, and multiple
condition management acknowledges that children, family advocacy organizations. The CMHI and NICHQ
510 C Center for Medical Home Improvement
adapted the widely recognized Chronic Care Model as 2. Develop supports for primary care practices to im-
the Care Model for Child Health in a Medical Home. prove their medical homeness
A health resources and services administration 3. Align statewide efforts toward an investment in the
(HRSA) systems grant was awarded to the CMHI in future of primary care
2004 and a contract for a medical home outcomes re-
Following initial Council meetings, the New Hampshire
search study. Early findings from this research show that
Endowment for Health funded the CMHI to convene and
enhanced chronic condition management and care coor-
lead the New Hampshire Primary Care Task Force. This
dination, as outlined in the MHI, are associated with
group will issue consensus statements crafted to further
reductions in emergency room use, hospitalizations, and
detail the resources and supports necessary to develop and
visits to specialists. Starting in 2007, the CMHI Medical
provide relationship-centered primary care. The Task
Director, Dr. Carl Cooley began convening and chairing a
Force will comment on what they would like a future
Medical Home Work Group to design and develop a pilot
medical home pilot effort to look like in New Hampshire.
program to test a new process of primary care medical
The CMHI plans to develop and provide technical assis-
home-based, longitudinal care of children with genetic
tance to help primary care practices pass the National
conditions identified through newborn screening includ-
Committee for Quality Assurance (www.ncqa.org) medi-
ing the potential use of registries, planned care methods,
cal home recognition measure, a requirement to enter a
decision support mechanisms, comanagement with spe-
medical home pilot demonstration and receive enhanced
cialists, and application of family-and-patient-centered
payment. The CMHI is working with the New Hampshire
practices. This project is called the New England Genetics
Citizens Health Initiative and a public private multi-
Collaborative (NEGC) and is funding through the Uni-
payer and stakeholders group to craft New Hampshires
versity of New Hampshires Office of Sponsored Research.
pilot to stimulate a transformative process in primary care
A similar medical home project entitled Leadership Edu-
for the twenty-first century. In conclusion, the CMHI
cation in Autism Spectrum Disorders (LEASD) will begin
provides content expertise, education, and consultation
in the fall of 2008. The CMHI will work in partnership with
focused on medical home development to a variety of states,
Dartmouth Medical School (DMS) and the University of
centers, and initiatives including the American Academy of
New Hampshire Leadership in Education in Neurodeve-
Pediatrics, the commonwealth fund, various HRSA gran-
lopmental and Related Disabilities (LEND) program to
tees, and numerous state and regional programs.
assure that all children in New Hampshire are screened
for autism and spectrum disorders at 18 and 24 months to
assure early diagnosis and access to early intervention and
Major Activities
family-centered care for optimal development outcomes.
The providence for the medical home model has gained
2001: Medical Home Index (MHI), pediatric version, a
substantial momentum that in 2007, the American Acade-
validated measurement to assess quality and monitor
my of Pediatrics, American Academy of Family Physicians,
improvements in a primary care practice (available at
and the American College of Physicians as well as Family
www.medicalhomeimprovement.org). 2001: Developed
Voices and the National Association of Pediatric Nurse
a companion Medical Home Family Index and Survey
Practitioners endorsed the medical home as the model
(available at www.medicalhomeimprovement.org). 2001:
for twenty-first-century primary care (www.pcpcc.org).
Medical Home Improvement Tool Kit (available at www.
States are looking for better ways to effectively support
medicalhomeimprovement.org). 2003: Parent Partners
the healthcare needs of its citizens and the organizational
Creative Forces on Medical Home Improvement Teams
and operational needs of those providing health care.
(available at www.medicalhomeimprovement.org).
However, there is a looming crisis in primary care that
2006current: New Hampshire Council on the Future of
raises concerns about current and future capacity, recruit-
Primary Care Medical Home. 2007current: New Hamp-
ment, and reimbursement. In response to the current
shire Primary Care Task Force 2007: Medical Home Prac-
struggle inherent to primary care, the CMHI, in partner-
tice-Based Care Coordination, Workbook (available at
ship with New Hampshire Special Medical Services regu-
www.medicalhomeimprovement.org). 20072008: New
larly convenes the New Hampshire Council on the Future
England Genetics Collaborative (NEGC), Regional Genet-
of the Primary Care Medical Home with explicit goals to:
ics and Newborn Screening Collaborative. 2008: Leader-
1. Build and spread awareness of the medical home ship Education in Autism Spectrum Disorders (LEASD).
model of primary care 2008: Extra-Ordinary Care: Improving Your Medical
Center for Outcome Measurement in Brain Injury (COMBI) C 511
Home, Guide and Workbook (available at www.medical- measures for persons with brain injury. The measures
homeimprovement.org). included in the COMBI are commonly used in the field
2008: Medical Home Index (MHI), Adult version of brain injury rehabilitation and assessment. The
(available at www.medicalhomeimprovement.org). COMBI is a collaborative project of 16 brain injury
facilities or centers, with each center contributing infor- C
mation on one or more measures. For most supported
measures, there are syllabus and training information,
rating forms, background information on validity and
Cooley, W. C., McAllister, J. W., Sherrieb, K., & Clark, R. (2003).
The medical home index: Development and validation of a new
reliability, a reference list of published studies, and test-
practice-level measure of implementation of the medical home ing materials. A Frequently Asked Question (FAQ) sec-
model. Ambulatory Pediatrics, 3, 173180. tion is also included, compiled from past training
Cooley, W. C., & McAllister, J. W. (2004). Building medical homes:
Improvement strategies in primary care for children with special
health care needs. Pediatrics, 113, 14991506.
Dillon, A., & McAllister, J. W. (2006). Do you have a medical home? EP Center for Outcome Measurement in Brain Injury (COMBI).
Magazine (www.eparent.com), August, 2228.
Table 1 COMBI-featured scales/measures
Joint Principles of the Patient-Centered Medical Home (2007). http://
www.aafp.org/online/etc/medialib/aafp_org/documents/policy/fed/ Agitated Behavior Scale (ABS)
jointprinciplespcmh0207.Par.0001.File.dat/022107medicalhome.pdf
Apathy Evaluation Scale (AES)
McAllister, J. W., Pressler, E., & Cooley, W. C. (2007). Practice-based care
coordination: A medical home essential. Pediatrics, 120, e723e733. Awareness Questionnaire (AQ)
doi: 10.1542/peds.2006-1684. Cognitive Log (Cog-Log)
Takachand, M., Kaye, N., & Beesla, R. (2008). Strategies states can use to
Coma/Near Coma Scale (CNC)
support the infrastructure of medical homes. State Health Policy
Briefing. www.nashp.org/Files/shpbriefing_pcmhsupport.pdf. Coma Recovery Scale-Revised(CRS-R)
Confusion Assessment Protocol (CAP)
Community Integration Questionnaire (CIQ)
The Craig Handicap Assessment and Reporting Technique
Center for Outcome Measurement (CHART)
The Craig Handicap Assessment and Reporting Technique
in Brain Injury (COMBI) Short Form (CHART SF)
The Craig Hospital Inventory of Environmental Factors
J ERRY W RIGHT
(CHIEF)
Disability Rating Scale (DRS)
San Jose, CA, USA
The Family Needs Questionnaire (FNQ)
Functional Assessment Measure (FAM)
Membership Functional Independence Measure (FIM)(TM)
Glasgow Outcome Scale (GOS)
The Center for Outcome Measurement in Brain Injury Extended Glasgow Outcome Scale (GOS-E)
(COMBI) is a collaborative project of 16 brain injury High Level Mobility Assessment Tool (HiMAT)
facilities or centers, most of them Traumatic Brain
Level of Cognitive Functioning Scale (LCFS)
Injury Model Systems (funded by the National Institute
Mayo Portland Adaptability Inventory (MPAI)
on Disability and Rehabilitation Research). The product is
an informational web site that is oriented primarily to- Mississippi Aphasia Screening Test (MAST)
wards clinicians and researchers, but is also freely avail- Neurobehavioral Functioning Inventory (NFI)
able to the general public. The Orientation Log (O-Log)
The Patient Competency Rating Scale (PCRS)
Participation Objective, Participation Subjective
Major Areas Satisfaction With Life Scale (SWLS)
Service Obstacle Scale (SOS)
The COMBI is an online resource for those needing
Supervision Rating Scale (SRS)
detailed information and support in regards to outcome
512 C Centers for Medicare and Medicaid Service
information and submitted questions. The COMBI was

designed to provide accessible and consistent informa- Centers for Medicare and
tion regarding brain injury outcome measures to clini- Medicaid Service
cians and researchers.
R OBERT G. F RANK
Kent State University
Landmark Contributions Kent, OH, USA
The COMBI is coordinated by Santa Clara Valley Medical

Center and is supported by funds from the National Membership
Institute on Disability and Rehabilitation Research
(NIDRR). It has been a collaborative project of the The Centers for Medicare and Medicaid (CMS) served
NIDRR-funded Traumatic Brain Injury Model Systems 102 million Americans enrolled in Medicare, Medicaid,
since 1998. and the Childrens Health Insurance Program (CHIP)
in FY 11.
Major Activities
Major Areas
Currently, the COMBI has 28 featured scales, with 25
scales available for immediate download. Table 1 shows CMS is part of the Department of Health and Human
the COMBI-featured scales as of August 2008. Additional Services. The primary offices are not located in Washing-
information is available about measuring employment ton D.C. but in Baltimore. With a budget of approximate-
and substance abuse after brain injury. The COMBI web ly $650 billion, serving almost 90 million beneficiaries,
site also conducts testing and certification for the Disabil- CMS has a dominant role in American health care. The
ity Rating Scale (DRS). The COMBI web site (www.tbims. top position in CMS, the Administrator, is nominated by
org/combi) receives over 1,200 visitors per day, with well the President of the USA but must be confirmed by the
over one million visits in total. Senate. Most administrators have come to CMS from
academia or have been industry lobbyists. The position
of Administrator is complex and demanding. Nancy-Ann
DePearle, who served as Administrator at the end of the
Cross References Clinton administration, during one of the few periods in
which federal spending for CMS declined, noted that
Agitated Behavior Scale (ABS) the Administrator has . . .many bosses, including 535
Coma/Near Coma Scale (CNS) members of Congress, the White House, the Inspector
Coma Recovery Scale (CRS) General, the US Government Accountability Office
National Institute on Disability and Rehabilitation (GAO) (Health Affairs: W-5337).
Research (NIDRR) The Department of Health and Human Services,
Neurobehavioral Functioning Inventory (NFI) through CMS, issues regulations and policy clarifications
Orientation Log guiding the provision of services for Medicare benefici-
Rancho Los Amigos Scale aries. All psychologists who provide health-care services
Traumatic Brain Injury to Medicare recipients, particularly neuropsychologists,
Traumatic Brain Injury Model System interact with CMS. Each psychologist who provides ser-
vices to Medicare beneficiaries must obtain National Pro-
vider Identification (NPI) from CMS. Medicare fiscal
intermediaries oversee payment for Medicare services
References and Readings including the electronic fund transfer. Each state has a
fiscal intermediary overseeing Medicare Part A (inpatient
http://www.tbims.org/combi
services) and Part B (professional services). CMS regula-
Wright, J. M., Bushnik, T., & OHare, P. (2000). The center for outcome
measurement in brain injury (COMBI): An internet resource you
tions now guide the care of all Medicare beneficiaries. In
should know about. Journal of Head Trauma Rehabilitation, 15(8), addition, the size and impact of Medicare have made the
734738. agency a predictor of many coverage choices by private
Centigray C 513
insurers. When CMS issues proposed rules in the Federal Medicare program (health insurance for people aged 65
Register (the federal governments daily journal), all and over, younger people receiving social security disabil-
providers have the opportunity to comment. Final rules ity benefits, and persons with end-stage kidney disease)
that guide reimbursement by CMSs fiscal intermediaries as well as the Medicaid program (providing medical
are then issued. assistance from state and federal governments for eligible C
low-income persons). Although the federal government
regulates Medicaid, state governments actually operate
Landmark Contributions the program). HCFA also provided federal oversight for
quality control initiatives.
In July 1965, at the home of President Harry Truman, Between 1989 and 2000, the number of Medicare
President Lyndon B. Johnson signed the Social Security claims rose from 70% to more than 800 million claims.
Act of 1965. Titles XVIII and XIX of the Act fostered a new Despite this staggering volume, Medicares administrative
view of health care in the USA, responding to more than costs were only 2%. HCFA was viewed as having a bias
20 years of legislative initiatives aimed at creating an toward providers. In 2001, the Bush administration,
insurance program to cover hospitalization, health ser- believing that HCFA was perceived as bureaucratic, unre-
vices, and skilled nursing care for the elderly as well as sponsive, and biased toward physicians and hospitals,
coverage for low-income children. When implemented in sought a new image for the agency. In an effort to improve
1966, Medicare (created by Title XVIII) provided cover- the agencys image, the Bush administration changed the
age for more than 19 million elderly Americans. Medicaid name to the Centers for Medicare and Medicaid CMS
(created in Title XIX), covered almost 15 million people (Scully, 2005), heralding an effort to streamline the many
and was administered by the Social Rehabilitation administrative processes overseen by CMS. Despite the
Administration, an agency managing poverty and welfare new name, CMS continued the responsibilities of HCFA:
programs. Medicare, end-stage renal disease, quality, and coordina-
The inclusion of Medicare and Medicaid within the tion of Medicaid with the states.
Social Security Act reflected political compromises need-
ed for the passage of both programs. Wage and price
controls imposed during World War II prompted many
employers to offer health-care coverage. This de facto
DePearle, N. A. (2005). What does it take to run Medicare and Medicaid?
wage increase determined that health insurance became a Health Affairs, W-5337338.
common employer benefit, but one that excluded the Derzon, R. A. (2005). The Genesis fo HCFA. Health Affairs, W5326.
elderly and unemployed. By 1960, the inadequacy of Scully, T. A. (2005). Policy high oints: Medicare and medicaid in the New
health services for older Americans had become a political Millennium. Health Affairs, W5339.
issue. In order to secure enough votes to pass Medicare,
President Johnson created the concept of the medically
indigent thereby linking welfare to health care for the
elderly. Centigray
Medicare and Medicaid were administered separately
during the Johnson and Nixon administrations. Joseph B RAM G OLDSTEIN
Califano, Secretary of Health Education and Welfare Hoag Hospital Cancer Center
(HEW) under Jimmy Carter, believed that ineffective Newport Beach, CA, USA
oversight of health programs permitted spiraling health
costs and health-care spending inflation (Derzon, 2005).
Califano knew the separate administration of Medicare Synonyms
and Medicaid reflected the political compromises needed
to create coverage for the elderly and the poor through cGY
linking coverage for the elderly to welfare. The split ad-
ministration of Medicare and Medicaid, however, made Definition
the two mammoth programs less manageable. Califano
moved quickly, in secret and combined Medicare and Centigray (cGY) is the preferred measurement of
Medicaid, forming the Health Care Financing Admin- absorbed radiation and is equivalent to one-hundredth
istration (HCFA). HCFA provided oversight to the (10-2) of a gray, or 1 rad. The gray measures the deposited
514 C Central Auditory Processing Disorder
energy of radiation. The daily dose of radiation is also symptoms diagnosed by audiologists and/or speech and
referred to as a fraction, since each dose is a percentage of language specialists using the audiology code of ICD-9
the cumulative prescribed dose. The dose is given in code 388.4 (Abnormal Auditory Processes).
sublethal fractions, which protracts the dose to facilitate The American Speech-Language Hearing Association
the occurrence of repair kinetics. Hence, radiation oncol- (ASHA, 2005) defines CAPD as difficulties in the per-
ogists use fractions to take advantage of the differential ceptual processing of auditory information in the central
recovery rates for normal and neoplastic tissue, thereby nervous system (CNS). It presents in the form of poor
permitting repopulation of normal cells and inducing performance in one or more of the following abilities
radiosensitivity via increased oxygen to the remaining or skills: sound localization and lateralization, auditory
tumor cells. Fractionated dose radiotherapy enhances discrimination, auditory pattern recognition, temporal
the treatment efficacy by targeting the cancer cells aspects of audition (including temporal integration,
while mitigating the damage to healthy tissue. This is temporal discrimination/gap detection, temporal order-
determined using a therapeutic ratio, which compares ing, and temporal masking), auditory performance in
the damage to both cancerous and healthy cells (Potters, competing acoustic signals (including dichotic listen-
Timmerman, & Larson, 2005). Moreover, the biological ing), and auditory performance with degraded acoustic
effects on the relevant tissue vary according to the signals.
radiation type and intensity.
Categorization
Cross References
Neither CAPD nor SI is listed in the DSM-IVor DSM-IV-TR
Radiation Therapy manuals which provide diagnostic codes for psychologists,
psychiatrists, and speech and language specialists. When
References and Readings individuals from these fields assess problems that are
language based, they use language tests and assign diag-
Potters, L., Timmerman, R., & Larson, D. (2005). Stereotactic body
nostic codes associated with specific language disorders
radiation therapy. Journal of the American College of Radiology, 2, (e.g., ICD-9: 315.3, Developmental Speech or Language
676680. Disorder; ICD-9: 389.9, Unspecified Hearing Loss).
While the diagnosis of CAPD has a 50-year history,
there is much controversy about its legitimacy (Carneol,
2008). In part, this stems from its extensive comorbidity
Central Auditory Processing with a variety of impairments in attention/concentration,
Disorder language, memory, IQ, academic achievement, and other
behavioral/emotional disorders. Children with the CAPD
J UDITH A. S HECHTER 1, S ARAH J. L EINEN 2 diagnosis typically demonstrate poor listening skills,
1
Wynnewood, PA, USA difficulty filtering linguistic information from back-
2
Widener University ground noise, problems following oral instructions, poor
Chester, PA, USA auditory discrimination skills, distractibility/inattentive-
ness, and often need additional time to complete tasks
(Bloom & Hynd, 2008). In addition, there is no compel-
Synonyms ling research that reliably provides specific neurobiologi-
cal bases for CAPD when compared to findings that
Auditory perceptual disorder (APD); Auditory processing link specific brain regions with language-based learning
disorder (APD); CAPD; Sensory integration-C/APD disabilities and Attention Deficit Hyperactivity Disorder
(SI-C/APD) (Bloom & Hynd, 2008). Together, these factors have
called into question the validity of CAPD as a distinct
diagnosis.
Short Description or Definition It is important to understand the complicated neuro-
physiological constructs of hearing to better understand
Central Auditory Processing Disorder (CAPD) is not a the etiological basis of CAPD. That is, one must know
neuropsychological diagnosis. It refers to an amalgam of how sound travels from the outer ear through the middle
Central Auditory Processing Disorder C 515
and inner ear structures through the eighth auditory contribute to outcome trajectories (e.g., comorbid
nerve to Heschls gyrus in the left temporal lobe of the ADHD, LD) (Bloom & Hynd, 2008).
brain. At that point, the brain begins to recognize nerve
impulses as sound and then initiates interpretation of
these impulses as either speech or nonverbal auditory C
stimuli. These stimuli are then analyzed bilaterally by Neuropsychology and Psychology
auditory stimulus networks distributed within the brain of CAPD
(Carneol, 2008).
Some researchers have proposed CAPD subgroups The immense overlap of CAPD symptoms with other de-
such as Auditory Decoding Deficit (primary left auditory velopmental disorders such as ADHD continues to fuel
cortex dysfunction), Prosodic Deficit (nonprimary right debate among psychologists, neuropsychologists, audiolo-
auditory cortex and associated areas dysfunction), and gists, and speech-language pathologists over the existence of
Integration Deficit (corpus callosum dysfunction) (Bellis, this diagnosis. While a definition of CAPD as a unimodal
2003; Bellis & Ferre, 1999; Katz, 1992). These subtypes disorder is a useful tool in the conceptualization of the
may help clinicians design intervention strategies specific symptoms associated with it, the notion of CAPD as sepa-
to an individuals presenting problems However, these rate and distinct from language-based LD and ADHD has
models are theoretical in nature and not universally not been well documented in the literature.
agreed upon (ASHA, 2005; Jutras et al., 2007). In a sample of 30 913-year-olds, approximately 50%
of children diagnosed with CAPD also met diagnostic
criteria for ADHD (Riccio, Hynd, Cohen, Hall, & Molt,
1994). Based on ratings from audiologists and pediatri-
Epidemiology
cians, Chermak, Tucker, and Seikel (2002) identified
exclusive behavior sets characterizing CAPD and ADHD.
No truly authoritative population or prevalence studies
CAPD was not characterized by hyperactivity and
regarding CAPD are available (Castrogiovanni, 2008).
difficulties with impulse control.
Chermak and Musiek (1997) estimate a prevalence rate
Some individuals with CAPD may have difficulties
of 23% in children, with the disorder occurring twice as
with speech and language. Varying combinations of audi-
frequently in males than females. Cooper and Gates
tory processing deficits may be associated with different
(1991) estimate that the prevalence in older adults is
functional deficits in speech and language. Differential
1020%.
diagnosis between CAPD and language disorders can be
quite challenging due to shared symptomatology. For
example, a core deficit in phonological processing under-
Natural History, Prognostic Factors, lies dyslexia. Similarly, children with CAPD may have
and Outcomes difficulty discriminating and manipulating the phonetic
aspects of auditory input. It has been suggested that
The etiology of CAPD is unknown. CAPD may present as auditory processing problems in developmental dyslexia
a developmental or acquired disorder. The maturation of are specific to the encoding of speech, whereas CAPD is
the central auditory pathway may be delayed (Bamiou, characterized by a general dysfunction encoding all
Musiek, & Luxon, 2001). Prenatal or perinatal factors auditory stimuli.
(e.g., hyperbilirubenemia, anoxia or hypoxia, ototoxic Academic difficulties are often a characteristic of
drugs, Rh incompatibility, prematurity/low birth weight, children who carry a CAPD diagnosis (ASHA, 2005).
birth complications, maternal diabetes, or infections), ear They may have a difficult time encoding/learning spoken
infections, heavy metal exposure, cerebrovascular disor- information or information presented with background
ders, epilepsy, Lyme disease, and traumatic brain injury noise. They are more likely to have behavioral, emotional,
may be risk factors for the constellation of symptoms that and social difficulties secondary to poor communica-
characterize the CAPD diagnosis (Bamiou, Musiek, & tion skills (ASHA, 2005). The preceding, combined
Luxon, 2001; Musiek & Chermak, 2009; Riccio & with associated learning difficulties, can compromise
Hynd, 1996). self-esteem and contribute to emotional withdrawal, so-
It is not clear if problems in auditory processing matization, conduct disorders, depression, anxiety, and
resolve with age, if children are able to compensate for interpersonal problems (Riccio, Cohen, Garrison, &
auditory processing deficits, and what factors may Smith, 2005).
516 C Central Auditory Processing Disorder
Evaluation educational programming. These would be written in the

form of an Individual Education Program (Individuals
Since CAPD is an auditory deficit, an audiologist is the with Disabilities Education Improvement Act of 2004,
professional best-qualified to diagnose CAPD (ASHA, 20 U.S.C. 1400; Public Law 108446) that would provide
2005). Although psychologists and speech-language such accommodations under the category of Other
pathologists (SLPs) may screen for auditory processing Health Impaired.
difficulties, speech-language and psychological measures
should not be used to diagnose CAPD (ASHA, 2005).
Screening processes involve systematically observing lis- Cross References
tening behavior and assessing performance on tests of
auditory function (ASHA, 2005). Multidisciplinary as- ADD
sessment including other professionals such as psycholo- ADHD
gists and SLPs should be conducted to help delineate American Speech-Language-Hearing Association (ASHA)
cognitive communication and language-related factors Americans with Disabilities Act
associated with CAPD, determine the functional impact Auditory System
of CAPD, and guide treatment (ASHA, 2005). Cognitive Communication Disorder
The audiologists central auditory diagnostic test D-amphetamine
battery, which aims to examine the integrity of the central Dyslexia
auditory nervous system (ASHA, 2005) may include au- Executive Functioning
ditory discrimination tests, auditory temporal processing Learning Disability
and patterning tests, dichotic speech tests, monaural Section 504 of the Rehabilitation Act of 1973
low-redundancy speech tests, binaural interaction tests, Stimulants
electroacoustic measures, and electrophysiologic mea-
sures (ASHA, 2005). Auditory processing tests include
elements of attention and memory, but also appear to References and Readings
assess processes not tapped by measures of these con-
structs (Riccio et al., 2005). A diagnosis of CAPD typically American Speech-Language-Hearing Association. (2005). (Central)
auditory processing disorders [Technical Report]. Available from
requires performance, two standard deviations below the
www.asha.org/policy.
mean on two or more auditory processing tests. The Bamiou, D., Musiek, F., & Luxon, L. (2001). Aetiology and clinical
audiologist must also consider the confounding effects presentations of auditory processing disorders A review. Archives
of fatigue, poor attention, memory, and motivation on of Disease in Childhood, 85, 361365.
test performance. Bellis, T. J. (2003). Assessment and management of central auditory proces-
sing disorders in the educational setting: From science to practice
(2nd ed.). Clifton Park, NY: Delmar Learning.
Bellis, T. J., & Ferre, J. M. (1999). Multidimensional approach to the
differential diagnosis of auditory processing disorders in children.
Treatment Journal of the American Academy of Audiology, 10, 319328.
Bloom, J. S., & Hynd, G. (2008). Dysfunctions of attention, learning, and
central auditory processing: Whats the difference? In K. McBurnett &
Collaboration among educators, school psychologists,
L. Pfiffner (Eds.), ADHD, concepts, controversies, new directions.
speech-language pathologists, audiologists, neuropsy- (pp. 6370). New York: Informa Health Clinic USA Inc.
chologists, and physicians may be necessary to identify Carneol, S. O. (2008). Elusive, inclusive, or conclusive? (central)
and implement interventions aimed at ameliorating auditory processing disorder. In J. Apps, R. F. Newby, &
symptoms that resemble those associated with the L. W. Roberts (Eds.), Pediatric neuropsychology case studies: From
the exceptional to the commonplace. (pp. 307323). New York, NY:
CAPD diagnosis.
Springer Business & LLC.
While there is some evidence that methylphenidate Castragiovanni, A. (2008). Incidence and prevalence of hearing loss and
may ameliorate symptoms in children with the diagnosis hearing aid used in the United States 2008 Edition. Available from
of CAPD, research is inconclusive. More typical interven- www.asha.org/research/reports/hearing.
tions for CAPD symptoms include perceptual training, Chermak, G., & Musiek, F. (1997). Central auditory processing disorders:
New perspectives. San Diego: Singular Publishing Group.
instruction in linguistic and cognitive compensatory stra-
Chermak, G., Tucker, E., & Seikel, J. (2009). Behavioral considerations of
tegies, environmental modifications (e.g., preferential auditory processing disorder and attention-deficit hyperactivity dis-
seating, use of a stereo system in the classroom, use of order: Predominantly inattentive type. Journal of American Academy
area rugs), assistive technology alternatives, and specific of Audiology, 13, 332338.
Central Executive C 517
Cooper, J., & Gates, G. (1991). Hearing in the elderly the Framingham several types of memory in the intact human mind.
cohort, 19831985: Part II. Prevalence of central auditory processing
Although philosophers have long been theorizing about
disorders. Ear and Hearing, 12, 304311.
Jutras, B., Loubert, M., Dupuis, J., Marcoux, C., Dumont, V., & Baril, M.
distinctions within memory, there has been experimental
(2007). Applicability of central auditory processing disorder models. evidence supporting the divisions of memory for only the
American Journal of Audiology, 16, 100106. past 3040 years (Baddeley, 1999). C
Katz, J. (1992). Classification of auditory processing disorders. In J. Katz,
N. Stecker, & D. Henderson (Eds.), Central auditory processing:
A transdisciplinary view (pp. 8191). Baltimore: Mosby-Yearbook.
Musiek, F., & Chermak, G. (2009). Diagnosis of (central) auditory
processing disorder in traumatic brain injury: Psychophysical
and electrophysiological approaches. Washington, DC: The ASHA
Leader. Retrieved from http://www.asha.org/publications/leader/ Baddeley and Hitch (1974) developed a theory of a WM
2009/091124/CAPD.htm. system that has become the dominant theory in cognitive
Riccio, C., Cohen, M., Garrison, T., & Smith, B. (2005). Auditory pro- psychology for the organization of WM (Fig. 1). Baddeleys
cessing measures: correlation with neuropsychological measures of
model addressed weaknesses of previous short-term
attention, memory, and behavior. Child Neuropsychology, 11,
363372.
memory (STM) models, including the failure to address
Riccio, C., & Hynd, G. (1996). Relationship between ADHD and central nonverbal processing. Baddeleys model, which has
auditory processing disorder: A review of the literature. School undergone changes throughout the years, is a theoretical
Psychology International, 17, 235252. concept and was not originally developed to directly cor-
Riccio, C., Hynd, G., Cohen, M., Hall, J., & Molt, L. (1994). Comorbidity
respond with specific neuroanatomical regions, though
of central auditory processing disorder and attention-deficit hyper-
activity disorder. Journal of the American Academy of Child and
research that attempts to do so has been completed. The
Adolescent Psychiatry, 33, 849847. original theory proposed the existence of three compo-
nents (Fig. 1). Baddeley envisioned this system as consist-
ing of a central executive, which is a limited capacity
subsection that controls certain subsystems. The central
executive controls slave systems, which are mainly used
Central Executive for the temporary storage of information. Information
that is not needed right now, but will soon be needed,
N ICOLE C. R. M C L AUGHLIN can be stored within these slave systems to free up the
Butler Hospital, central executive for other tasks. One of the slave systems
Alpert Medical School of Brown University is the articulatory or phonological loop, which is a verbal
Providence, RI, USA store. Subvocalization of verbal material creates a record
in a phonological buffer. The central executive then reads
the phonological buffer, and the cycle begins again. For
Definition most of this cycle, the central executive is not needed.
Another slave system is the visuospatial sketchpad, which
Working memory (WM) has been defined as the is used to rehearse visual or spatial materials. Manipulation
blackboard of the mind and the mental sketchpad of information within either the phonological loop or vi-
(Baddeley, 1986). It enables the online holding and mental suospatial sketchpad does not affect information being
manipulation of information. Human beings use WM retained in the other system; they have been shown to be
processes all the time. For example, WM is used to distinct systems in regard to interference effects (Brooks,
perform rapid mathematical functions in our heads and 1968). Another component, the episodic buffer
to understand the inherent meaning in speech and (described in detail below), was added in 2000 to address
writing. WM is also important for reasoning and problem some of the perceived weaknesses of the earlier model.
solving (Baddeley, 1999). Psychologists have posited The current multicomponent model describes fluid
Visuospatial Central executive Phonological

sketchpad loop
Central Executive. Figure 1 Initial three-component model of working memory (WM) (Baddeley & Hitch, 1974)
518 C Central Executive
Central executive
Phonological Loop Episodic buffer Visuospatial sketchpad
Visual Episodic Language

semantic long-term memory
Central Executive. Figure 2 Multicomponent model of working memory (WM) (Baddeley, 2000)
capabilities (such as temporary storage) and crystallized are prevented from rehearsing items by being required to
abilities that are involved in long-term knowledge (Fig. 2). state an irrelevant word (such as the. . .the. . .the), perfor-
Phonological Loop. The phonological loop is most mance declines. There also appears to be a word-length
similar to the earlier concept of STM (Baddeley, 1992) effect such that longer words are more difficult to remem-
and is the most studied component within this theory. ber, potentially because participants are subvocalizing
There are two components within the phonological loop: words, and thus, there is more time for information to
a phonological store and an articulatory rehearsal system. deteriorate (Baddeley, 2000).
The phonological store can temporarily hold acoustic People frequently use the phonological store in every-
material for 12 s and is involved in speech perception. day life, subvocalizing when counting and when reading.
The articulatory rehearsal system can maintain material Adult fluent readers use this component less than poor
by subvocal repetition and can take visually presented readers, or individuals learning to read, but show diffi-
material and register this material by subvocalization. culties picking up errors in written text when their sub-
There are several pieces of evidence that have supported vocalization capabilities are disrupted (Baddeley, 1999).
the presence of the phonological loop. The simplest piece The phonological store may also be important for new
of evidence is that it appears clear that our verbal store language acquisition as well as native language acquisition
holds only a limited amount of information. The phono- (Baddeley, 1999); some researchers have indicated that the
logical similarity effect indicates that sequences of items phonological loops primary purpose is for language
with similar phonological sounds are more difficult to acquisition (Baddeley, Gathercole, & Papagno, 1998).
remember than those with disparate sounds (e.g., mad A deficit in phonological STM appears to stem from a
can cap man is more difficult than pen day cow bar rig) defective phonological store. Articulatory rehearsal appears
(Baddeley, 1966b). In addition, it demonstrates the ten- to be defective in aphasic patients with dyspraxia, as they
dency for participant errors to be phonologically similar are unable to carry out the speech motor codes needed for
to the correct item (i.e., F for S and B for G). Similarity of articulation (Waters, Rochon, & Caplan, 1992). Dysarthric
meaning does not seem to be important for the phono- patients do not appear to have a deficit in articulatory
logical store (Baddeley, 1966b), whereas long-term stor- rehearsal, likely because their deficits are peripheral, not
age is affected by similarity of meaning, but not sound central (Baddeley & Wilson, 1985). Neuroanatomically,
(Baddeley, 1966a). The irrelevant speech effect shows that based upon lesion studies, the inferior parietal cortex
exposure to irrelevant speech either at the same time or appears to be related to the temporary phonological store,
directly after stimuli material can disrupt immediate re- whereas the articulatory rehearsal system uses brain areas
call of the stimulus; meaningless noise does not disrupt necessary for speech production, such as Brocas area and/
stimuli material. This effect is the same for phonologically or the supplementary motor area (Muller & Knight, 2006).
similar or dissimilar items (Salame & Baddeley, 1987). Visuospatial Sketchpad. Similar to the function of the
Preventing rehearsal (articulatory suppression) further phonological loop for verbal material, the visuospatial
decreases performance (Baddeley, 1999); when participants sketchpad allows for the maintenance of temporary
Central Executive C 519
representations of visuospatial information. The visuo- override the CS when the CS fails or no known schema
spatial sketchpad is involved in such tasks as visual imag- exists (Shallice, 1982).
ery and mental rotation. Evidence for this system comes Additional attentional processes that have been ascribed
from the finding that visuospatial immediate memory can to the central executive include focusing, dividing, and
be disrupted by visual tracking, but not by verbal coding switching attention, as well as serving as the interface be- C
(Baddeley, 1999). There seems to be separate subsystems tween the subsystems described above and long-term mem-
involved in the maintenance of visual information (shape, ory (Baddeley, 2001). With regard to focusing attention,
color) and spatial information, independent of the central participants in a chess game were impaired by interference
executive (Klauer & Zhao, 2004). In addition, there also from a random digit generation task; this was thought to
appears to be a dissociation of this system into two com- place a heavy load on the central executive (Robbins et al.,
ponents, a passive store that maintains information, and 1996). With regard to dividing attention, participants
a more active device that manipulates it (Bruyer & with Alzheimers disease who have long-term memory and
Scailquin, 1998). attentional deficits are impaired on dual-task paradigms,
The visuospatial sketchpad appears to be principally yet are able to do the same tasks individually (MacPherson
represented within the right hemisphere (Baddeley, 2000). et al., 2007). There is a question as to whether switching is
Within this component, as noted above, past research has primarily an executive process, though there also appears
indicated that there is a neuroanatomical differentiation to be a strong relationship between the phonological loop
between object and spatial information. Using evidence and switching.
from the parietal and temporal visual streams, it is likely Research has indicated that the prefrontal cortex,
that the parietal lobe (dorsal stream) processes spatial especially the dorsolateral prefrontal region, is critical
information (i.e., where the relation of objects across for executive functioning (Collette et al., 1999; DEsposito
coordinates) while the temporal lobe (ventral stream) et al., 1995; Owen, Evans, & Petrides, 1996; Salmon et al.,
processes nonspatial (i.e., what as in a visual image or 1996). However, more recent studies have indicated that,
object information); this subdivision also possibly although the PFC appears essential for executive function-
extends into dorsal and ventral regions of the prefrontal ing, other brain regions may also be important for these
cortex, and these regions are most relevant for short-term, functions (Baddeley & Wilson, 1988; Baker et al., 1996;
or working memory processes (Goldman-Rakic & Leung, Berman et al., 1995; Nagahama et al., 1996).
2002). Episodic Buffer. As mentioned above, the episodic buff-
Central Executive. The central executive has been er was developed in response to a need for a component to
described as a homunculus, or little man who makes relate between working and long-term memory (Baddeley,
decisions as to how the slave systems should be used. It is a 2000). The episodic buffer is envisioned as a temporary
limited capacity attentional system that is in charge of the storage system controlled by the central executive, as well
phonological loop and visuospatial sketchpad (Baddeley, as an interface between multiple systems. The central
1999). Although the central executive may be considered executive can retrieve information from the store, and
the most important component of this model, given the potentially manipulate or modify it. There were multiple
apparent complexity of this system, it is difficult to investi- weaknesses to the initial three-component theory that this
gate. Baddeley (1986) coined the term dysexecutive syn- multicomponent model has attempted to address. For
drome (DES) to describe dysfunctions of the central example, with articulatory suppression (interference of
executive. encoding of numbers) of the phonological loop, short-
Baddeley has compared the central executive to Norman term span becomes shorter, but does not completely dis-
and Shallices ideas of the supervisory attentional system appear (Baddeley, 1984). In addition, participants can
(SAS; Shallice, 1982), which is used in planning, decision- remember more in sentences or in paragraphs than
making, novel situations, and difficult situations. Cont- would be anticipated solely based upon the phonological
ention scheduling (CS) is a process that chooses one store. There appears to be a distinction between immedi-
response and inhibits another, in a crude and fast way. ate recall and delayed prose recall, with disparate subsys-
CS modulates the selection of an action schema when it is tems implicated in each (Wilson & Baddeley, 1988). The
routine, or unconscious, selecting the schema with the episodic buffer appears to be preserved in patients with
strongest triggers. The SAS is a higher level system that impaired LTM (Baddeley, 2000), and plays an important
is slow and flexible. It is utilized when a selection is role in sending information to and retrieving information
more complex, and adjusts the activation level of the from LTM. Although there is minimal research specifically
action schemas. Therefore, the SAS can actually examining the neuroanatomical basis of this component,
520 C Central Executive
it appears likely that the frontal lobes are involved in Berman, K. F., Ostrem, J. L., Randolph, C., Gold, J., Goldberg, T. E.,
Coppola, R., et al. (1995). Physiological activation of a cortical
these processes. Specifically, there appears to be greater
network during performance of the Wisconsin card sorting test: A
right frontal activation for integration of information positron emission tomography study. Neuropsychologia, 33(8),
(Prabhakaran, Narayanan, Zhao, & Gabrieli, 2000). 10271046.
Baddeleys theory provided a framework for the Brooks, L. R. (1968). Spatial and verbal components of the act of recall.
initial study of working memory processes, addressing Canadian Journal of Psychology, 22, 349368.
Bruyer, R., & Scailquin, J. C. (1998). The visuospatial sketchpad for
weaknesses of earlier models of STM that did not suffi-
mental images: Testing the multicomponent model of working
ciently account for many important pieces of information. memory. Acta Psychologica (Amsterdam), 98(1), 1736.
Although there have been additions to the model since its Collette, F., Salmon, E., Van der Linden, M., Chicherio, C., Belleville, S.,
initial conception, Baddeleys ideas continue to be relevant Degueldre, C., et al. (1999). Regional brain activity during tasks
today, and this work has informed, and continues to in- devoted to the central executive of working memory. Cognitive
Brain Research, 7(3), 411417.
form, multiple avenues of research within the field.
DEsposito, M., Detre, J. A., Alsop, D. C., Shin, R. K., Atlas, S., &
Grossman, M. (1995). The neural basis of the central executive
system of working memory. Nature, 378(6554), 279281.
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Cerebellar Cognitive Affective Syndrome C 521
pressure results from the thrombosis, then surgical

Central Neurocytoma placement of a ventriculoperitoneal shunt is considered.
Survival rate exceeds 90%, full recovery occurs in 88% of
Neurocytoma the survivors, and recurrence rate is about 2%.
C
Cross References
Central Venous Thrombosis
Anticoagulation
E LLIOT J. R OTH Antiplatelet Therapy
Northwestern University Cerebrovascular Disease
Chicago, IL, USA Heparin
Ischemic Stroke
Thrombolysis
Synonyms Thrombosis
Venous Thrombosis
Cerebral thrombophlebitis; Cerebral venous thrombosis; Warfarin
Dural sinus thrombosis; Intracranial venous thrombosis;
Sagittal sinus thrombosis; Sinus thrombosis
Ferro, J. M., Canhao, P., Bousser, M. G., Stam, J., & Barinagarrementeria,
Definition F. (2005). Cerebral vein and dural sinus thrombosis in elderly
patients. Stroke, 36, 19271932.
Central venous thrombosis is a rare form of stroke Stam, J. (2005). Thrombosis of the cerebral veins and sinuses.
that results from thrombosis (blood clot) of the veins in New England Journal of Medicine, 352(17), 17911798.
the dura mater that surround and drain blood from
the brain.
Current Knowledge Cephalalgia

Headache
Symptoms may include headache, abnormal vision,
Post-traumatic Headache
seizures, and any of the symptoms of stroke such as
weakness of the face and limbs on one side of the body.
Diagnosis is usually made by computed tomography
(CT/CAT) or magnetic resonance imaging (MRI) scan-
ning, using radiocontrast to demonstrate obstruction of
the venous sinuses by thrombus. In about 80% of patients CERAD
with this condition, it occurs in the setting of a preexisting
underlying clotting disorder such as Protein C deficiency, Consortium to Establish a Registry on Alzheimers
Protein S deficiency, hyperhomocysteinemia, nephrotic Disease
syndrome, antiphospholipid antibody syndrome, preg-
nancy, oral contraceptive use, systemic lupus erythemato-
sus, Wegeners granulomatosis, and sarcoidosis, and
infections such as otitis, mastoiditis, and meningitis. For
this reason, a search for these conditions should be Cerebellar Cognitive Affective
undertaken. Syndrome
Treatment relies on the administration of anticoagu-
lants, or rarely, thrombolytic agents. If raised intracranial Cognitive Affective Syndrome
522 C Cerebellar Hemorrhage
Salvati, M., Cervoni, L., Raco, A., & Delfini, R. (2001). Spontaneous
Cerebellar Hemorrhage cerebellar hemorrhage: Clinical remarks on 50 cases. Surgical
E LLIOT J. R OTH
Chicago, IL, USA
Cerebellar Mutism
Synonyms J ACQUELINE L. C UNNINGHAM
Posterior fossa hemorrhage Philadelphia, PA, USA
Definition
Definition
A cerebellar hemorrhage is a bleeding into the cerebellum,
A transient speech disorder typically associated with re-
the portion of the brain located posteriorly, that controls
section of cerebellar tumors, particularly medullo-
balance, coordination, and related functions.
blastomas involving the cerebellar vermis. Cerebellar
mutism can also result from stroke in the cerebrovascular
Current Knowledge distribution, affecting the cerebellar peduncles and brain-
stem. Cerebellar mutism forms part of a syndrome of
It is estimated that 10% of all intracerebral hemorrhages, or deficits, known as the posterior fossa syndrome (PFS).
about 12% of all strokes, are cerebellar hemorrhages. It
can be caused by high blood pressure, heavy alcohol con-
sumption, cocaine use, anticoagulant use, clotting disor- Current Knowledge
ders, cerebral vascular abnormalities such as arteriovenous
malformations and aneurysms, and cerebral amyloid Symptoms
angiopathy. Approximately two-thirds are thought to result
from hypertension. Symptoms of the hemorrhage include As part of PFS, cerebellar mutism is associated with de-
headaches, especially at the posterior and inferior area of creased or absent speech, irritability, hypotonia, ataxia,
the skull, nausea and emesis, stiff neck, dizziness and verti- and the inability to coordinate voluntary movements,
go, blurred or double vision, balance and coordination including the volitional motor aspects of speech. Mutism
deficits, speech difficulty, and altered consciousness. The occurs within the first week of surgery (or cerebrovascular
onset of symptoms is generally abrupt and dramatic. This event) and its duration may be a matter of days or weeks.
is a medical emergency, requiring immediate neurosurgical It is expected to resolve within 4 months. However, even
attention. It is diagnosed using CTor MRI scanning. Treat- with the return of functional speech, the quality of voca-
ment relies on reducing intracranial pressure and surgically lizations may lack normalcy in being hypernasal, mono-
removing the hemorrhage as quickly as possible. tone, high pitched, slowed, and/or sparse.
Cross References
Pathophysiology
Hemorrhagic Stroke
Intracerebral Hemorrhage Information obtained from single photon emission
Intracranial Hemorrhage computerized tomography (SPECT) studies have sup-
ported the theory that cerebellar mutism results from
the effects of decreased cerebral and cerebellar blood
flow upon cell functioning in particular brain pathways.
These cause disruption in the cerebellar modulation
Kirollos, R. W., Tyagi, A. K., Ross, S. A., van Hille, P. T., &
Marks, P. V. (2001). Management of spontaneous cerebellar hema-
of neural circuits that link prefrontal, posterior parietal,
tomas: A prospective treatment protocol. Neurosurgery, 49, superior temporal, and limbic cortices with the
13781386. cerebellum.
Cerebellum C 523
Treatment voluntary movements as well as the control of

equilibrium.
The treatment of cerebellar mutism resides in speech
language therapy, with early goals of therapy including
the teaching of nonverbal communication as a compen- Current Knowledge C
satory strategy as well as the direct strengthening of oral-
motor functioning through the systematic practicing Embryology
of tongue and lip movements. Moreover, since cerebellar
mutism occurs within a context of broad cognitive The cerebellum originates from the metenencephalic
and affective change, a comprehensive assessment of division of the rhombencephalon, sharing the same
speech and language skills is important to identify embryologic origin with the pons.
and treat language deficits more broadly. Problems in
higher-level cognitivelinguistic functioning can include
difficulty in areas like planning and initiating communi- Anatomy
cation, verbal fluency, abstract reasoning, and working
memory. The cerebellum consists of three main lobes: anterior
(paleocerebellum or spinocerebellum), posterior (neocer-
ebellum or cerebrocerebellum), and flocculonodular
Cross References (archicerebellum or vestibulocerebellum). These lobes
are further divided to ten small lobules: lingula, folium,
Brain Tumor central lobule, tuber, culmen, pyramid, declive, uvulae,
Cerebellum and tonsils.
Cognitive Affective Syndrome
Medulloblastoma Cerebellar Peduncles
Posterior Fossa The cerebellar peduncles are bundles of nerve fibers,
Posterior Fossa Syndrome connecting the cerebellum with the brain stem. There
are three bundles: inferior, middle, and superior cerebellar
peduncles.
The inferior cerebellar peduncle (ICP) contains the
References and Readings dorsal spinocerebellar tract (DSCT), cuneocerebellar tract
(CCT), olivocerebellar tract (OCT), and vestibulocerebel-
Keating, R. F., Goodrich, J. T., & Packer, R. J. (2001). Tumors of the
lar tract (VCT). DSCT fibers arise from cells in the ipsi-
pediatric central nervous system. New York: Thieme.
Schmahmann, J. D., & Caplan, D. (2006). Cognition, emotion and the lateral Clarkes column in the spinal cord (C8-L3). CCT
cerebellum. Brain, 129, 290292. fibers arise from the ipsilateral accessory cuneate nucleus.
Schweizer, T. A., Levine, B., Rewilak, D., et al. (2008). Rehabilitation of The largest component of the OCT fibers arises from the
executive functioning after focal damage to the cerebellum. Neuror- contralateral inferior olive. VCT fibers arise from cells in
ehabilitation and Neural Repair, 22, 7277.
both the vestibular ganglion and the vestibular nuclei, and
pass in the inferior cerebellar peduncle to reach the
cerebellum.
The middle cerebellar peduncle (MCP) contains the
Cerebellum pontocerebellar tract (PCT). These fibers arise from the
contralateral pontine gray matter.
I SLAM Z AYDAN The superior cerebellar peduncle (SCP) is the prima-
Virginia Commonwealth University ry efferent peduncle of the cerebellum. It contains fibers
Richmond, VA, USA that arise from several deep cerebellar nuclei. These
fibers pass ipsilaterally and then cross at the level of the
inferior colliculus to form the decussation of the SCP.
Definition From the SCP, these fibers will then continue rostrally
to terminate in the red nucleus and the motor nuclei of
The cerebellum, one of the three major portions of the ventral anterior (VA) and ventral lateral (VL)
the brain, is involved with the coordination of thalamus.
524 C Cerebellum
To thalamus and red nucleus cells. Golgi cells are intermediary cells located in the
Corticopontine granular layer. They receive stimulatory input (GABA)
fibers Superior cerebellar from the granular layer to inhibit granule cells.
peduncle
Cerebellum
Nuclei
Pons Purkinje cells can transmit inhibitory signals to the deep
To vestib. nuclei of the cerebellum. The most lateral nucleus,
nuclei
Pontine dentate, receives its input from the OCT and PCT and
Dentate
mossy fibers Interposed
carries planning information from the posterior parietal
Fastigial area. The interpositus nucleus (globose and emboliform)
Middle receives its Purkinje cell input from the OCT and PCT
cerebellar fibers carrying information from primary motor cortex
peduncle (area 4), DSCT, and CCT. Medially located fastigial
Inferior cerebellar nucleus receives input from the DSCT and CCT. Vestibu-
peducncle lar nuclei receive proprioceptive input from the spinal
Climbing fibers Proprioceptive cord and medullary olive.
from inferior olive information from
spinocerebellar tract
(mossy fibers) Fibers
Climbing fibers go to all parts of the cerebellum. They are
Cerebellum. Figure 1
not restricted to a particular zone. A climbing fiber sends
a collateral synapse to the deep cerebellar nuclei, which is
excitatory. The climbing fiber then climbs up, synapsing
Histology on the dendrites of the Purkinje cell. Each Purkinje cell
receives input from only one climbing fiber axon, but
Cortex each climbing fiber axon can split to innervate several
The cerebellar cortex consists of three layers from outer- Purkinje cells. The climbing fiber-Purkinje cell synapses
most to innermost: molecular, Purkinje (pyriform), and are excitatory. The OCT terminates directly on Purkinje
granular layers. The molecular layer consists mainly of cells, by-passes granule cells, and causes complex spikes in
neuropil and is the site of synapses. The majority of cells Purkinje cells.
in this layer are stellate and basket cells in addition to a Mossy fibers are the axons of DSCT, CCT, vestibulo-
few neurons. Purkinje cell layer consists of a single layer of cerebellar (VCT) and PCT carrying input to the cerebellar
large (25 micrometer) pear-shaped neurons. It is consid- cortex. They terminate and excite granule cells. Each
ered the largest cells in the nervous system. The granular mossy fiber branches profusely in the white matter. Each
layer is dense with 37 million neurons per cubic mm, Purkinje cell receives input from approximately >20,000
consisting of small cells with a granular cytoplasm. mossy fibers and only one climbing fiber.
Beneath the cortex lies white matter that forms the core Parallel fibers are the long axons of granule cells that
of the foliae. pass dorsally through the granule and Purkinje cell layers
to reach the molecular layer of the cerebellar cortex,
Cells where they bifurcate and run parallel to the long axis of
The cerebellum is formed of several complex cells. Stellate the folium. Parallel fibers excite a row of Purkinje cells
cells project local inhibitory output (taurine). Basket cells and in addition to a few basket cells that in turn will
also project local inhibitory output (GABA). They feed inhibit distant Purkinje cells outside the field of
forward inhibition on Purkinje cells. Purkinje cells are excitation.
stimulatory, transmitting impulses from the cerebellar The aminergic fibers originate in the Raphe nuclei and
cortex via efferent pathways. They project inhibitory out possess serotonergic input, modulating the granule and
(GABA). Granule cells have axons that run parallel to the molecular layers. This category of fibers also includes
longitudinal axis of the lobes. Granule cell excite by way of those originating from the locus ceruleus possessing
glutamate. Granule cells are only excitatory in the cere- noradrenergic input and terminating in all three cortical
bellar cortex, terminating on Golgi, basket, and Purkinje layers.
Cerebral Amyloid Angiopathy C 525
Function References and Readings
The cerebellum receives input from all areas of the Albus, J. S. (1971). A theory of cerebellar function. Mathematical
central and peripheral nervous systems. Continuous Biosciences, 10, 2561.
Miller, N., & Newman, N. (2005). Walsh and Hoyts clinical neuro-
flow of information from the spinal centers and cortical C
ophthalmology (6th ed.). Philadelphia, Pennsylvania: Lippincott
areas are integrated in the cerebellar cortex. The cere- Williams and Wilkins.
bellar output then guides the precision of different cere- Ramnani, N. (2006). The primate cortico-cerebellar system: anatomy and
bral functions namely equilibrium, planned voluntary function Nature Reviews Neuroscience, 7, 511522.
movements, and muscle tone. The cerebellar modula- Ropper, A., & Brown, R. (2005). Adams and Victors principles of
neurology (11th ed.). USA: McGraw-Hill Inc.
tion of motor control is executed through its inhibitory
Strick, P. L., Dum, R. P., & Fiez, J. A. (2009). Cerebellum and nonmotor
output to the motor cortex and the descending motor function. Annual Review Neuroscience, 32, 413434.
tracts. Guided by visual, proprioceptive, and vestibular
spinal input, the cerebellum compares the intended
force needed to execute a planned voluntary movement
with the appropriate muscle power needed to execute it. Cerebral Amyloid Angiopathy
It then modulates the tone of the agonist and antagonist
muscles through inhibitory input to the motor cortex, E LLIOT J. R OTH
the pyramidal and extrapyramidal tracts, aiming at the Northwestern University
execution in a precise manner. While this voluntary Chicago, IL, USA
movement is executed, maintenance of equilibrium re-
gardless of movement or body position is achieved
through the cerebellar output to the antigravity muscles Definition
and the vestibular centers. Eye movements are also
maintained during body movement via extensive con- Cerebral amyloid angiopathy is a syndrome characterized
nections with the occulomotor nuclei in the brain stem. by recurrent spontaneous lobar cerebral hemorrhages of
More recent data has shown that the cerebellum is various sizes and in various locations. Each hemorrhage
involved in cognitive, behavioral, and emotional proces- may be asymptomatic or may cause all of the symptoms
sing, including executive control, attention, working of lobar hemorrhages resulting from increased intracranial
memory, learning, language, pain, and emotion (Strick pressure, including severe headache, seizure, stiff neck, and
et al., 2009). vomiting; altered consciousness; paralysis or weakness and
sensory loss; cognitive and language dysfunction, often
Lesions leading to dementia after multiple episodes.
Damage to the cerebellar center or to either its inflow
or outflow tracts leads to loss of cerebellar fine tuning
Current Knowledge
modulation on different cerebral functions. Vestibulocer-
ebellar lesions can result in disequilibrium, nystagmus,
The pathological process that causes this disease is the depo-
abnormal gait, and recurrent falls. Truncal ataxia and
sition of a protein, beta-amyloid, in the walls of the arteries of
scanning speech are seen with spinocerebellar lesions.
the brain. Interestingly, this protein is identical to the one
Patients with corticocerebellar lesions can display signs
found in high quantities in the brains of patients with Alz-
of dysmetria, asynergia (decomposition of the voluntary
heimers disease. The incidence of cerebral amyloid angio-
movement), hypotonia, dysdiadochokinesia, and inten-
pathy is difficult to estimate, but is known to increase with
tion tremors.
advancing age. It is thought to account for 15% of all intra-
cerebral hemorrhages in patients over 60 years and up to
Cross References one-half of lobar intracerebral hemorrhages in patients older
than 70, totaling about 20 per 100,000 per year in that group.
Ataxia Diagnosis is usually made based on the clinical presentation
Dysdiadochokinesia and imaging of recurrent spontaneous lobar hemorrhages,
Glutamate with no other predisposing problems, usually associated with
Nystagmus progressive decline in function, and most often associated
Proprioception with dementia. The recurrences can occur simultaneously,
526 C Cerebral Angiitis
clustered in time, or separated by years. The definitive normal, but magnetic resonance imaging of the brain is
diagnosis, based on pathological findings, is most typically abnormal in more than 90% of patients. However, the
made postmortem. Treatment is usually supportive, consist- pattern of abnormal findings is not specific. Cerebrospi-
ing of observation, symptom relief, and rehabilitation. nal fluid analysis usually reveals elevations in total protein
level or white blood cell count. Angiography has a low
sensitivity and low specificity. Treatment usually includes
Cross References cyclophosphamide and prednisone.
Hemorrhagic Stroke
Lobar Hemorrhage
Cross References
References and Readings Lupus Cerebritis

Moyamoya Disease
Kinnecom, C., Lev, M. H., Wendell, L., et al. (2007). Course of cerebral Vasculitis
amyloid angiopathy-related inflammation. Neurology, 68, 14111416. Vasospasm

Cerebral Angiitis
Birnbaum, J., & Hellmann, D. B. (2009). Primary angiitis of the central
nervous system. Archives of Neurology, 66, 704709.
E LLIOT J. R OTH Calabrese, L. H., Duna, G. F., & Lie, J. T. (1997). Vasculitis in the central
Northwestern University nervous system. Arthritis & Rheumatism, 40, 11891201.
Chicago, IL, USA Younger, D. S. (2004). Vasculitis of the nervous system. Current Opinion
in Neurology, 17, 317336.
Synonyms
Cerebral vasculitis Cerebral Artery

Anterior Cerebral Artery
Definition Internal Carotid Artery
Middle Cerebral Artery
Cerebral angiitis or cerebral vasculitis is a relatively rare Posterior Cerebral Artery
disease, characterized by inflammation of the blood ves-
sels inside and leading to the brain. It may be caused
either by a primary disease of the blood vessel walls
producing inflammation or as a secondary phenomenon Cerebral Autoregulation
resulting from a systemic inflammatory disease such as
systemic lupus erythematosus or certain infections. Cerebral Blood Flow
Current Knowledge
Cerebral Blood Flow
Angiitis that is confined to the brain is relatively uncom-
mon, and is called primary angiitis of the central nervous E LLIOT J. R OTH
system (PACNS), isolated CNS vasculitis, primary CNS Northwestern University
vasculitis, or granulomatous angiitis of the nervous sys- Chicago, IL, USA
tem. It usually affects small- and medium-sized cerebral
blood vessels, but does not involve blood vessels outside
of the CNS. Headache and encephalopathy are the most Synonyms
frequent symptoms. Stroke occurs in about 20% of
patients. Blood tests reflecting inflammation are usually Cerebral autoregulation; Cerebral perfusion pressure
Cerebral Cortex C 527
Definition
Cerebral Cortex
Cerebral blood flow is the amount of blood that goes
through the arterial tree in the brain in a given amount K IMBERLE M. J ACOBS
of time. Virginia Commonwealth University
Richmond, VA, USA
C
Current Knowledge Synonyms

In adults, cerebral blood flow is typically 750 ml per Cerebrum surface; Cortex
minute, or about 50 ml per 100 grams of brain tissue
per minute. This amount is equivalent to about 15% of
the total cardiac output. Cerebral blood flow is highly
Definition
regulated, through autoregulation, in order to meet
the metabolic demands of the functioning brain. If it is
The cerebral cortex is a structure lying on the outer
too high, it can cause elevated intracranial pressure, which
surface of the vertebrate cerebrum that is responsible for
will compress and damage brain tissue. If it is too low, it
consciousness and higher brain functions.
will fail to meet the demands of the brain, resulting
in cerebral ischemia if blood flow is less than 20 ml per
100 grams of brain tissue per minute and in cerebral
infarction if blood flow is less than 10 ml per 100 grams
of brain tissue per minute. Cerebral blood flow is affected
The cerebral cortex is a structure lying on the outer
by blood viscosity, blood vessel size, intracranial pressure
surface of the vertebrate cerebrum that is responsible for
level, and systemic blood pressure.
consciousness and higher brain functions, including sen-
sory perception, voluntary movement, language,
reasoning, memory, and planning. Cerebral comes from
Cross References the Latin word cerebrum, meaning brain. Cortex comes
from the Latin word for bark, which is typically an outer
Atherosclerosis layer or covering. In large mammals, this structure is
Diffusion-Weighted Imaging folded forming ridges known as gyri and grooves known
Ischemic Penumbra as sulci. Gyri and sulci normally form in the same relative
Ischemic Stroke locations from one individual to another. This folding
Perfusion-Weighted Imaging increases the cortical surface area while allowing for con-
Transcranial Doppler Ultrasonography straints on skull circumference. Abnormal folding of the
Vasospasm cortex is associated with neurological deficits. Absent or
reduced folding in humans is known as lissencephaly
(smooth brain) and is associated with mental retardation
References and Readings and epilepsy (Leventer, Mills, & Dobyns, 2000). The ab-
normality of small regions of increased folding is known
Aaslid, R., Lindegaard, K. F., Sorteberg, W., & Nornes, H. (1989). Cerebral as polymicrogyria (many small ridges), and can also be
autoregulation dynamics in humans. Stroke, 20, 4552.
associated with developmental delay and epilepsy (Piao
Kandel, E. R., Schwartz, J. H., & Jessell, T. M. (2000). Principles of neural
science (4th ed., p. 1305). New York: McGraw-Hill.
et al., 2005).
Current Knowledge
Cerebral Cavernous Malformation Structurally, the cerebral cortex can be divided into four
(CCM) lobes named after the overlying cranial bones: frontal,
parietal, temporal, and occipital. Prominent sulci define
Angioma, Cavernous Angioma the borders of these lobes. Primary functions of the lobes
528 C Cerebral Cortex
can be ascribed as follows: occipital: vision; parietal: sense

of touch (somatosensation) and body position; frontal:
planning of action and control of movement; and tempo-
ral: hearing, visual identification, and memory. These
lobes are present in each of the two hemispheres (left
and right).
The cerebral cortex can also be divided on the basis of
phylogeny into archicortex, paleocortex, and neocortex
(oldest to newest). Archicortex consists of the hippocam-
pus, which is associated with the acquisition of memories.
Paleocortex is primarily associated with the function of
olfaction. Only mammals have neocortex. In humans, the
majority of the cerebral cortex is made up of neocortex. In
addition, as a percentage of total brain tissue, humans have
more neocortex than other species (see for example,
human relative to rat, Swanson, 1995). This is unique to
the neocortex, since evolution has not increased the size of
other brain structures, such as the cerebellum (Clark,
Mitra, & Wang, 2001). This increase in proportion is due
to increased surface area, and not to a change in the thick-
ness of the cortex, which is from 13 mm thick in all species. Cerebral Cortex. Figure 1 Cortical Lamination. Cresyl Violet
Cortex is made up of gray matter, where cell bodies stained coronal section from rat, showing neocortex above
predominate, and white matter that consists primarily of hippocampus (archicortex). Neocortical layers are indicated by
myelinated axons. All cortex is laminated, but the gray Roman numerals. Layer V is commonly divided into subparts
matter of neocortex has six layers (Fig. 1), while that of with layer Va containing callosal projection neurons, and Vb
the older archi-and paleocortices has three layers. Cortical containing the largest pyramidal neurons that project to
layers are differentiated based on their cellular compo- spinal cord and other subcortical locations. Within this section
nents. The basic components and lamination of cortex are of neocortex, slight differences in cytoarchitectonics can be
consistent across phylogeny. Within neocortex, the layers seen between the somatosensory cortex (Brodmanns area 3)
are given names that represent the predominant neuronal to the right and motor cortex (Brodmanns area 4) to the left.
cell type. The outermost layer (identified by Roman nu- Most obvious is the lack of a clear layer IV within motor cortex.
meral I), contains mainly dendrites and axons and is WM neocortical white matter; s.o. stratum oriens; s.p. stratum
called the molecular layer. Layer II is called the external pyramidale; s.r. stratum radiatum, all of the CA1 region of the
granule layer and consists of small, spherical cells. Layer hippocampus
III primarily contains small to medium pyramidal neu-
rons and is called the external pyramidal layer. Layer IV instance sending the result of motor cortical processing to
contains spiny stellate neurons and is called the internal the motor neurons of the spinal cord. Layer VI provides a
granule cell layer. Layer V contains large pyramidal neu- return feedback to the thalamus.
rons and is called the internal pyramidal layer. Layer VI Different functional regions of cortex are considered
has a variety of morphological cell types and is therefore to have primary, secondary, and association components.
called the polymorphic cell layer. These layers have differ- In sensory cortex, the primary cortical area is the region
ential functions that are consistent across different neo- that first receives information about that sense from the
cortical areas (Fig. 2). Layer I is a modulatory region and periphery (traveling by way of the thalamus). The second-
receives input from higher order cortical regions. Layers II ary cortical area is considered higher order because the
and III perform intracortical processing, receiving input input it receives is the result of cortical processing from
from the deeper layer IV, as well as from adjacent layers II the primary cortical area. Association cortex receives
and III and from the homologous cortical region in the input from several different cortical regions.
opposite hemisphere. Layer IV is the major input layer The general function of the layers is maintained across
and receives specific thalamocortical afferents in sensory cortical regions; however, there are slight changes in cell
areas of cortex. Layer V is the major cortical output, for size and packing density (cytoarchitecture) from one
Cerebral Cortex C 529
cortical area to another. These cytoarchitectonic differ-

ences were used by Korbinian Brodmann in 1909 to draw
I boundaries presumed to identify functionally different
cortical areas.
Perpendicular to the plane of the cortical layers are C
II
functional modules called cortical columns. The idea that a
column of cortex represents a fundamental processing unit
Callosal was brought to light by Vernon Mountcastle of Johns
Hopkins University (Mountcastle, 1957). Within a column,
III neurons tend to have similar response properties. For
instance, within somatosensory cortex, the neurons within
a column have similar receptive fields (area of the receptive
surface that causes the neuron to fire action potentials).
IV Neurons of different columns have nonoverlapping recep-
tive fields. The result of evolution then has been to add
cortical columns or additional processing units.
Head trauma, stroke, and tumor may all result in
Callosal lesions of the cerebral cortex. The function lost will be
V dependent on the location of the lesion. For example,
lesion of Brodmanns area 17 will result in loss of vision,
while lesion of Brodmanns area 3 will result in some loss
of somatosensation including touch and pain discrimina-
tion. Damage to Brodmanns area 4 will result in loss of
VI motor function. Lesions of the frontal cortex can cause
severe personality changes. Memory loss is typically asso-
Modulatory ciated with cortical lesions. The inability to speak occurs
Specific Nonspecific
DA
Thalamic
after destruction of Brocas area in the ventral portion of
NE To Thalamic
Afferents the frontal lobe, typically in the left hemisphere
5-HT Spinal Cord Afferents
Superior Colliculus (Brodmanns areas 44 and 45). Incoherent speech or
ACh
word salad results from the destruction of Wernickes
Cerebral Cortex. Figure 2 Diagram of typical excitatory area in the upper portion of the temporal lobe (part of
neuronal cell types and connections of neocortex. Layer I, the Brodmanns area 22).
modulatory cell layer, contains the tufts of deeper lying
pyramidal neurons, nonspecific thalamic afferents, and input
from brainstem modulatory transmitter systems. Layer II Cross References
contains primarily small granule cells. Layer III has small
pyramidal neurons that perform intracortical processing, Association Cortex
sending their axons horizontally within layer III. Layer IV Auditory Cortex
contains spiny stellate neurons that send their output to layer Brodmanns Areas of the Cortex
III. Specific thalamic afferents make excitatory synapses within Heteromodal Cortex
layer IV on the spiny stellate cells as well as on the apical Homotypic Cortex
dendrites of deeper lying pyramidal neurons. These specific Neocortex
thalamic afferents have a smaller projection to layer VI, near Prefrontal Cortex
the border with layer V. Layer V is the major output layer for Primary Cortex
the cortex, and contains medium and large pyramidal Secondary Cortex
neurons. Layer VI contains neurons with a variety of shapes. Somatosensory Cortex
Note that inhibitory cells that make up 20% of the neurons Striate Cortex
in the neocortex are not shown here. Modulatory: Modulatory Tertiary Cortex
neurotransmitters; DA: Dopamine; NE: Norepinephrine; 5-HT: Unimodal Cortex
Serotonin; and ACh: Acetylcholine Visual Cortex
530 C Cerebral Dominance
References and Readings Vasogenic edema involves a disruption in the blood

brain barrier with leakage of fluid from the intravascular
Clark, D. A., Mitra, P. P., & Wang, S. S. (2001). Scalable architecture in space.
mammalian brains. Nature, 411, 189193. In cytotoxic edema, the bloodbrain barrier is
Jones, E. G., & Peters, A. (Eds.). (1990). Cerebral cortex: Volume 8A:
intact, and there is an increase in the intracellular fluid
Comparative structure and evolution of the cerebral cortex, part I.
New York: Springer.
compartment.
Jones, E. G., & Peters, A. (Eds.). (1990). Cerebral cortex: Volume 8B:
Comparative structure and evolution of the cerebral cortex, part II.
New York: Springer. Cross References
Leventer, R. J., Mills, P. L., & Dobyns, W. B. (2000). X-linked malforma-
tions of cortical development. American Journal of Medical Genetics, Cerebral Perfusion Pressure
97, 213220.
Mountcastle, V. B. (1957). Modality and topographic properties of single
neurons in cats somatic sensory cortex. Journal of Neurophysiology,
20, 408434.
Piao, X., Chang, B. S., Bodell, A., Woods, K., Benzeev, B., Topcu, M., et al. References and Readings
(2005). Genotype-Phenotype analysis of human frontoparietal poly-
microgyria syndromes. Annals of Neurology, 58(5), 680687. Beaumont, A., Marmarou, A., & Ward, J. D. (2001). Intracranial Hyper-
Rasmussen, W., & Penfield, T. (1957). The cerebral cortex of man: A tension Mechanisms and Management. In D. G. McClone (Ed.),
clinical study of localization of function. New York: Macmillan Pediatric Neurosurgery (pp. 619633). Philadelphia: W. B. Saunders.
Company. Greenberg, M. S. (1997). Handbook of Neurosurgery. Lakeland, FL:
Swanson, L. W. (1995). Mapping the human brain: Past, present, and Greenberg Graphics.
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and contribution to brain swelling. J Neuropathol Exp Neurol, 66(9),
771778.
Cerebral Dominance
Cerebral Embolism
Hemispheric Specialization
E LLIOT J. R OTH
Chicago, IL, USA
Cerebral Edema
Synonyms
G ARY T YE 1, J OHN B ROWN 2
1
Virginia Commonwealth University Embolic stroke
Richmond, VA, USA
2
Augusta, GA, USA Definition
A cerebral embolism is a blood clot (thrombus) that starts
Synonyms from the heart or blood vessel where the clot originates
and stops in an artery that leads to or rests within the
Cytotoxic edema; Vasogenic edema brain. The result is occlusion of the vessel and obstruction
of the flow of oxygen and blood to the brain tissue
supplied by that artery.
Definition
Current Knowledge
Cerebral edema is an increase in the water content of the
brain that leads to brain swelling. It may be divided into Cerebral embolisms cause about 1520% of all strokes and
two broad categories: vasogenic and cytotoxic. about one-quarter of all ischemic strokes. It occurs most
Cerebral Palsy C 531
frequently in patients who have known heart disease, in-

cluding atrial fibrillation and other arrhythmias, valve dis- Cerebral Hemisphere
ease, mural thrombus (a blood clot sitting in the left
ventricle of the heart), or other conditions. It causes symp- Frontal Lobe
toms similar to those of thrombotic strokes, but the pre- Occipital Lobe
Parietal Lobe
C
sentations of embolic strokes tend to be more abrupt and
dramatic. These can include sudden onset of hemiplegia, Temporal Lobe
sensory loss, facial weakness, cognitive deficits, or speech
disturbance. Seizures or headaches are relatively common in
embolic strokes, and both of these symptoms are relatively
rare in ischemic strokes. In addition, there may be multiple Cerebral Hemorrhage
diffuse simultaneous neurological findings, which may re-
sult from multiple simultaneous emboli, known as showers Hemorrhagic Stroke
of emboli. Usually, management requires addressing the
cardiac condition and preventing subsequent emboli by
using anticoagulants, in addition to the treatment of the
cerebral infarction and its neurological consequences. Cerebral Infarction
Ischemic Stroke
Cross References
Anticoagulation
Echocardiogram Cerebral Leukencephalopathy
Infarction
Ischemic Stroke Periventricular Leukomalacia
Thrombosis
Warfarin
Cerebral Malformation
References and Readings Arteriovenous Malformation (AVM)
DiTullio, M. R., & Homma, S. (2002). Mechanisms of cardioembolic

stroke. Current Cardiology Reports, 4, 141148.
Fuster, V., Ryden, L. E., Cannom, D. S., Crijns, H. J., Curtis, A. B., &
Ellenbogen, K. A. (2006). ACC/AHA/ESC 2006 Guidelines for the Cerebral Microvasculature
Management of Patients with Atrial Fibrillation: A report of the
American College of Cardiology/American Heart Association Task
Force on Practice Guidelines and the European Society of Cardiolo- Blood-Brain Barrier
gy Committee for Practice Guidelines (Writing Committee to Revise
the 2001 Guidelines for the Management of Patients With Atrial
Fibrillation): Developed in collaboration with the European Heart
Rhythm Association and the Heart Rhythm Society. Circulation,
114, e257e354. Cerebral Palsy
Hart, R. G., Pearce, L. A., & Aguilar, M. I. (2007). Meta-analysis:
antithrombotic therapy to prevent stroke in patients who have non- K ATHLEEN K EELY M C C ANN D EIDRICK
valvular atrial fibrillation. Annals of Internal Medicine, 146, 857867. University of Missouri-Columbia
Columbia, MO, USA
Cerebral Evoked Potentials Synonyms

Event-Related Potentials Static encephalopathy
532 C Cerebral Palsy
Short Description or Definition birth raises the risk of CP, with a recent study reporting a
diagnosis of cerebral palsy among 20% of children born at
As defined by the International Workshop on the Definition or before 27 weeks of gestation versus diagnosis of 56%
and Classification of Cerebral Palsy, Cerebral Palsy (CP) is: of children born between 28 and 31 weeks (Ancel et al.,
2006). Reviewers note that overall rates of CP are climb-
" a group of permanent disorders of the development of
ing, while rates of CP among full-term infants have
movement and posture, causing activity limitation, that
remained stable (1.1/1,000). This suggests that increases
are attributed to non-progressive disturbances that oc-
are largely due to greater survival of preterm infants
curred in the developing fetal or infant brain. The motor
(Mukherjee & Gaebler-Spira, 2007).
disorders of cerebral palsy are often accompanied by
disturbances of sensation, perception, cognition, commu-
nication, and behavior, by epilepsy, and by secondary Natural History, Prognostic Factors,
musculoskeletal problems (Rosenbaum et al., 2007). and Outcomes
Etiology varies by birth status (preterm or full-term) and

Categorization type of CP (Menkes & Sarnat, 2000). For preterm infants,
the most common causes of CP are intraventricular hemor-
Classification schemes are critical to providers attempt-
rhage and/or periventricular leukomalacia. Risk factors for
ing to describe the disorder, measure change in func-
CP in full term infants include prenatal infections, anoxic or
tion, and provide prognostic information (Rosenbaum
ischemic injuries, genetic syndromes, brain malformations,
et al., 2007). Historically, classification has focused on two
or stroke. Atypical CP with athetoid movements is typically
features: (a) tone and (b) body part involvement (Menkes
caused by basal ganglia damage secondary to hyperbiliru-
& Sarnat, 2000). Table 1 for a summary.
binema (Mukherjee & Gaebler-Spira, 2007). A variety of
Spastic forms of CP are more common, with spastic
symptoms are associated with CP, which vary by severity
diplegia being the most common (Menkes & Sarnat, 2000).
and type of CP (Menkes & Sarnat, 2000; Mukherjee &
However, there is disagreement regarding classification
Gaebler-Spira, 2007). See Table 2 for a summary.
schemes, largely due to poor reliability (Accardo & Hoon,
2008). Recent attempts to improve classification schemes
include: (a) development of standardized examination pro- Neuropsychology and Psychology
cedures and diagnostic algorithms and (b) use of the Gross of Cerebral Palsy
Motor Functional Classification System (GMFCS), which
focuses on functional mobility without identifying abnor- As many as 3050% of children with CP may have a
malities of tone or affected limbs (Rosenbaum et al., 2007). diagnosis of mental retardation, with increased incidence
for children with quadriplegia, more severe motor deficits,
Epidemiology full-term birth, and/or a coexisting seizure disorder
(Menkes & Sarnat, 2000; Mukherjee & Gaebler-Spira,
Prevalence rates vary from 1.3 to 3/1,000 and are stable 2007). Estimates of intellectual functioning can be diffi-
across country of origin (Clark & Hankins, 2003). Preterm cult to obtain, as apraxic speech, visual difficulties, and
Cerebral Palsy. Table 1 Traditional categorization of cerebral palsy
Type Description
Spastic cerebral palsy Increased muscle tone with movement
Spastic quadriplegia Spasticity of upper and lower limbs
Spastic diplegia Greater involvement of the legs than the arms
Spastic hemiparesis Greater involvement of one side of the body (more often the right); greater impairment
of the arm than the leg
Extrapyramidal cerebral palsy Involuntary and abnormal muscle movements: dystonia (fluctuating tone and abnormal
body postures) and/or athetoid movements (writhing movements in the extremities)
Hypotonic cerebral palsy Persistent, low muscle tone
Mixed and atypical cerebral palsy Mixture of spasticity and extrapyramidal symptoms
Cerebral Palsy C 533
Cerebral Palsy. Table 2 Symptoms associated with CP
Domain Symptoms
Secondary muscular and Delayed development of adaptive motor skills
orthopedic symptoms Gait abnormalities C
Oral-motor difficulties and problems with speaking and drooling
Contracture (shortening of the muscle)
Bone deformities (e.g., hip subluxation/dislocation)
Scoliosis
Osteoporosis
Reduced limb growth
Neurologic symptoms Seizure disorder
Sensory Visual problems
Homonomous hemianopsia (in spastic hemiplegia)
Strabismus
Nystagmus
Visual sequela related to prematurity
Tactile/perceptual deficits
Stereognosis
Poor two-point discrimination (in spastic hemiplegia)
Neglect of affected side of the body (in spastic hemiplegia)
Hearing loss
Feeding/gastrointestinal Dysphagia and aspiration
Malnutrition requiring gastrostomy
Gastroesophageal reflux
Constipation
Incontinence or difficulty voiding
Dental Malocclusion
Poor tooth enamel
Pain and fatigue Pain associated with primary (e.g., spasticity and contractures) and secondary
(e.g., constipation) disease processes
Pain related to medical procedures
Fatigue secondary to poor mobility
fine motor deficits can limit participation in traditional disability (e.g., attractiveness, social interaction, athletics,
tests (Fennell & Dikel, 2001). Little is known about cog- academics) (Miyahara & Cratty, 2004). Adolescent girls
nitive functioning among children with CP who do not may be at particularly increased risk for low self-concept
have a diagnosis of mental retardation, reports of deficits (Shields, Murdoch, Loy, Dodd, & Taylor, 2006). Studies of
in learning (specifically arithmetic), visual-perceptual Quality of Life (QOL) suggest lower QOL for children
processing (particularly in spastic diplegia), working with CP, particularly in areas associated with CP and its
memory, and executive functioning are emerging (Blon- sequella (e.g., academics, social interaction) and most
dis, 2004; Jenks et al., 2007). notably for children with quadriplegia/more severe CP
The empirical literature regarding mental health in (Livingston, Rosenbaum, Russell, & Palisano, 2007).
children with CP is sparse. Overall, studies of children Transition to adulthood is understudied, but issues re-
with physical disabilities suggest that difficulties with garding reduced involvement in age-appropriate social
adjustment are atypical, with the exception of poor self- activities and roles, employment, and leisure activities
concept in areas directly impacted by the physical are of concern (Liptak, 2008).
534 C Cerebral Palsy
Evaluation Jongerius, & Rotteveel, 2007). Pain can be life-limiting

and may be underrecognized due to communication def-
Given the broad variability in etiology and the sparse icits and atypical pain responses in children with CP
knowledge base regarding neuropsychological function- (Houlihan, ODonnell, Conaway, & Stevenson, 2004).
ing in CP, evaluations should be tailored to the child and Adaptation of common self-report pain assessment scales
situation. Prior to the evaluation, medical evaluations and/or use of measures that have been developed for
clarifying the childs vision and hearing will be critical. children who have communication problems may help
Assessment measures should be chosen carefully to avoid the team to adequately evaluate and treat pain (Hadden
underestimates of function due to motor or verbal output & von Baeyer, 2005). Fatigue due to increased energy
problems (e.g., use of nonverbal tests of intelligence that expenditure during daily tasks can also impact function
minimize requirements for motor output) (Fennell & and should be addressed (Berrin et al., 2007).
Dikel, 2001). In children with marked communication
deficits, parents and educators may be interested in possi-
ble methods for alternative communication (e.g., picture Cross References
exchange systems, complex computerized devices), a
question which can be addressed through a multi-disci- Assistive Technology
plinary evaluation including a psychologist, speechlan- Augmentative and Alternative Communication
guage pathologist, and occupational therapist. For Constraint Induced Therapy
children who are less impaired, evaluations should in- Encephalopathy
clude a broad overview of neuropsychological functions Hemiparesis
with attention to executive functioning, visual-perceptual Hemiplegia
processing, and academics. Assessments should include Interdisciplinary Team Rehabilitation
formal or informal evaluation of pain, fatigue, and psy- Periventricular Leukomalacia
chological and behavioral functioning. Prematurity and Low Birthweight
Treatment References and Readings

Accardo, P. J., & Hoon, A. H., Jr. (2008). The challenge of cerebral
Multidisciplinary treatment is considered the standard of palsy classification: The ELGAN study. Journal of Pediatrics, 153,
care for children with CP (Braddom, 2007). Children are 451452.
involved in medical and therapeutic treatments designed Ancel, P.-Y., Livinec, F., Larroque, B., Marret, S., Arnaud, C., Pierrat, V.,
to decrease spasticity and increase function (e.g., botox et al. (2006). Cerebral palsy among very preterm children in relation
to gestational age and neonatal ultrasound abnormalities: The
injections, baclofen pump, surgical interventions, splinting
EPIPAGE cohort study. Pediatrics, 117, 828835.
and casting, physical and occupational therapies, early inter- Berrin, S. J., Malcarne, V. L., Varni, J. W., Burwinkle, T. M., Sherman,
vention services). Although promising, treatment efficacy is S. A., Artavia, K., et al. (2007). Pain, fatigue, and school functioning
unknown for many of these interventions (Tupper, 2007). in children with cerebral palsy: A path-analytic model. Journal of
Interventions developed from a rehabilitation psy- Pediatric Psychology, 32(3), 330337.
Blondis, T. A. (2004). Neurodevelopmental motor disorders: Cerebral
chology perspective are integral to the treatment
palsy and neuromuscular diseases. In D. Dewey & D. E. Tupper
plan, including behaviorally-based treatments to increase (Eds.), Developmental motor disorders: A neuropsychological approach
function and assessment and intervention of pain and (pp. 113136). New York: Guilford Press.
fatigue. Constraint-induced movement therapy (CIMT) Braddom, R. L. (Ed.). (2007). Physical medicine and rehabilitation (3rd
is a promising approach that attempts to overcome ed.). Philadelphia: Elsevier, Inc.
Clark, S. L., & Hankins, G. D. V. (2003). Temporal and demographic
learned non-use of the affected limb and to promote use
trends in cerebral palsy fact and fiction. American Journal of
of the affected limb through brain re-organization Obstetrics and Gynecology, 188, 628633.
(Hoare, Wasiak, Imms, & Carey, 2007). Patients are re- Fennell, E. B., & Dikel, T. N. (2001). Cognitive and neuropsychological
strained from using the unaffected limb through a sling or functioning in children with cerebral palsy. Journal of Child Neurol-
glove for 23 weeks and behavioral techniques (e.g., shap- ogy, 16, 5863.
Hadden, K. L., & von Baeyer, C. L. (2005). Global and specific behavioral
ing, massed practice, scaffolding, and positive reinforce-
measures of pain in children With Cerebral Palsy. Clinical Journal of
ment) are used to encourage use of the affected limb. Pain, 21(2), 140146.
Also promising are behavioral treatments that address Hoare, B. J., Wasiak, J., Imms, C., & Carey, L. (2007). Constraint-induced
problems with drooling (Van der Burg, Didden, movement therapy in the treatment of the upper limb in children
Cerebral Ventricles C 535
with hemiplegic cerebral palsy. Cochrane Database of Systematic the mean arterial pressure (MAP) and the intracranial
Reviews (2), CD004149.
pressure (ICP).
Houlihan, C. M., ODonnell, M., Conaway, M., & Stevenson, R. D.
(2004). Bodily pain and health-related quality of life in children
with cerebral palsy. Developmental Medicine and Child Neurology,
46(5), 305310.
Jenks, K. M., de Moor, J., van Lieshout, E. C. D. M., Maathuis, K. G. B.,
Cross References C
Keus, I., & Gorter, J. W. (2007). The effect of cerebral palsy on
arithmetic accuracy is mediated by working memory, intelligence, Cerebral Blood Flow
early numeracy, and instruction time. Developmental Neuropsycholo- Intracranial Pressure
gy, 32, 861879.
Liptak, G. S. (2008). Health and well being of adults with cerebral palsy.
Current Opinion in Neurology, 21, 136142.
Livingston, M. H., Rosenbaum, P. L., Russell, D. J., & Palisano, R. J. References and Readings
(2007). Quality of life among adolescents with cerebral palsy: What
does the literature tell us? Developmental Medicine and Child Neu-
Diringer, M. N., & Axelrod, Y. (2007). Hemodynamic manipulation
rology, 49(3), 225231.
in the neuro-intensive care unit: cerebral perfusion pressure therapy
Menkes, J. H., & Sarnat, H. B. (2000). Perinatal asphyxia and trauma.
in head injury and hemodynamic augmentation for cerebral vaso-
In J. H. Menkes & H. B. Sarnat (Eds.), Child neurology (6th ed.,
spasm. Current Opinion in Critical Care, 13(2), 156162.
pp. 401466). Philadelphia: Lippincott Williams & Wilkins.
Wright, W. L. (2007). Multimodal monitoring in the ICU: when could
Miyahara, M., & Cratty, B. J. (2004). Psychosocial functions of children
it be useful? Journal of the Neurological Sciences, 261(12), 1015.
and adolescents with movement disorders. In D. Dewey & D. E.
Tupper (Eds.), Developmental motor disorders: A neuropsychological
perspective (pp. 427442). New York: Guilford.
Mukherjee, S., & Gaebler-Spira, D. J. (2007). Cerebral palsy. In R. L.
Braddom (Ed.), Physical medicine and rehabilitation (3rd ed.,
pp. 12431267). Philadelphia: Elsevier. Cerebral Seizures
Rosenbaum, P., Paneth, N., Leviton, A., Goldstein, M., Bax, M., Damiano,
D., et al. (2007). A report: The definition and classification
Epilepsy
of cerebral palsy April 2006. Developmental Medicine and Child
Neurology Supplementum, 109, 814.
Shields, N., Murdoch, A., Loy, Y., Dodd, K. J., & Taylor, N. F. (2006).
A systematic review of the self-concept of children with cerebral
palsy compared with children without disability. Developmental
Medicine and Child Neurology, 48, 151157. Cerebral Thrombophlebitis
Tupper, D. E. (2007). Management of children with disorders of motor
control. In S. J. Hunter & J. Donders (Eds.), Pediatric neuropsycho- Central Venous Thrombosis
logical intervention: A critical review of science and practice
(pp. 338365). Cambridge, UK: Cambridge University Press.
Van der Burg, J. J. W., Didden, R., Jongerius, P. H., & Rotteveel, J. J.
(2007). Behavioral treatment of drooling: A methodological critique
of the literature with clinical guidelines and suggestions for future
research. Behavior Modification, 31, 573594. Cerebral Vasculitis
Cerebral Angiitis
Cerebral Perfusion Pressure
G ARY T YE 1, J OHN B ROWN 2
1
Cerebral Venous Thrombosis
Richmond, VA, USA
2
Central Venous Thrombosis
Augusta, GA, USA
Definition
Cerebral Ventricles
Cerebral perfusion pressure (CPP) is the net pressure of
flow of blood to the brain, which is the difference between Ventricles
536 C Cerebrovascular Accident (CVA)
injury is irreversible, this causes a completed stroke,

Cerebrovascular Accident (CVA) which is defined as the neurological manifestations of
disease of blood vessels of the brain. Other forms of
Stroke cerebrovascular disease also can occur. Inflammation
of blood vessel walls (vasculitis), bleeding into the
cerebral vessel walls (dissection), and hemorrhage, or
extravasation of blood outside of the vessels themselves
and into the brain tissue, also can cause brain damage.
Cerebrovascular Dementia These can give rise to strokes.
Multi-infarct Dementia
Cross References
Atherosclerosis
Cerebral Angiitis
Cerebrovascular Disease Cerebral Embolism
Dissection
E LLIOT J. R OTH Hemorrhagic Stroke
Northwestern University Infarction
Chicago, IL, USA Intracerebral Hemorrhage
Ischemic Stroke
Stroke
Definition Subarachnoid Hemorrhage
Thrombosis
Cerebrovascular disease refers to the group of conditions Transcranial Doppler Ultrasonography
characterized by disease of the blood vessels that supply Vascular Dementia
blood to the brain. It can occur in the blood vessels that Vascular Malformation
lead to the brain or in the blood vessels inside the brain. Vasculitis
While it usually presents with symptoms of a stroke (the
group of clinical manifestations of cerebrovascular disease),
it can be asymptomatic, in which case it is usually detected
either by physical examination or selected imaging References and Readings
techniques.
The term cerebrovascular accident (or CVA) is Wolf, P. A., & Grotta, J. C. (2000). Cerebrovascular disease. Circulation.
incorrect and should be avoided, as there is nothing 102, IV-75.
accidental about a stroke. The term cerebrovascular
disease is a more general term than is stroke, because
cerebrovascular disease includes asymptomatic or sub-
clinical disease, in addition to the clinically manifest
strokes.
Most cerebrovascular disease is obstructive in nature,
Cerebrum Surface
caused by atherosclerotic plaques that line the blood
Cerebral Cortex
vessel walls and block the blood flow. If the blockage is
only partial, and is not severe enough to impair brain
function, then the disease remains asymptomatic. How-
ever, if the obstruction is severe enough to reduce blood
supply to the extent that brain injury occurs, then symp-
toms suggesting a stroke ensue. If these symptoms are CES-D
temporary and completely reversed, the phenomenon is
known as a transient ischemic attack. If the brain Center for Epidemiological StudiesDepression
Chapple v. Ganger C 537
involved, especially neuropsychologists. These types of

CFL Test challenges question the scientific basis of one or more
of the experts methods, measures, or conclusions. Chal-
Controlled Oral Word Association Test lenges to specific methods are brought under Frye v.
F-A-S Test United States (1923) and Daubert v. Merrell Dow (1993)
Verbal Fluency
C
rulings.
Cross References
CGY
Daubert v. Merrell Dow
Centigray
Chandler Exterminators v. Morris Chandler Exterminators Inc. v. Morris, 200 Ga. App. 816 (1992).
Schudel v. General Electric, 120 F. 3d 991 (1995).
(1992)
Chicago, IL, USA Chapple v. Ganger
Definition Chicago Neuropsychology Group
Chicago, IL, USA
The testimony of neuropsychologists is commonly
challenged by defense attorneys in cases relating to infer-
ences of subtle brain changes associated with neurotoxic Historical Background
brain injury. In the case of Schudel v. General Electric
(1995), plaintiffs accepted neuropsychological evidence In the cause of Daubert v. Merrell Dow (1993), it was ruled
for brain damage caused by organic solvents and poly- that for scientific testimony to be admissible, it has to be:
chlorinated biphenyls (PCBs). However, the federal (a) scientifically valid, and (b) relevant to the case at
appeals court from the Ninth Circuit ruled that neuro- hand. The court provided a list of guidelines intended
psychological testimony is limited only to damages and to aid in the determination of scientific validity (e.g.,
cannot determine physical causation. The court opined peer reviewed, fasifiability, acceptable error rate, etc.).
that determination of causation is relegated to medical The Daubert ruling along with subsequent related rulings
doctors (MDs) or left to the discretion of the jury to (e.g., General Electric v. Joiner, 1997, Kumho Tire v.
make connections between neurocognitive deficits pre- Carmichael, 1999), generated significant debate among
sented and exposure to toxins. In the case of Chandler psychologists and neuropsychologists, and many other
Exterminators v. Morris (1992), the Georgia Supreme disciplines. Specifically, Reed (1996) viewed the Daubert
Court ruled in favor of the trial courts decision to ruling to necessitate the utilization of commercially avail-
prohibit neuropsychological testimony that proposed a able fixed batteries only, such as the HalsteidReitan Bat-
link between neurotoxicants and impaired neuropsycho- tery. However, most neuropsychologists employ a flexible
logical test scores. In response to this case, Georgia legis- battery approach; thus, contradicting Reeds assertions
lature wrote a new law permitting neuropsychologists to implying that most neuropsychologists would not be suit-
provide testimony related to causation of brain injuries ed for involvement in forensic work. In support of his
in Georgia. Challenges to specific neuropsychological conclusion, Reed referenced the case of Chapple v. Ganger
tests and test batteries occur with some degree of fre- (1998), a brain injury claim. Review of the judges written
quency, and they should be taken seriously by all parties decision in Chapple v. Ganger outlined that all
538 C Charles Bonnet Syndrome
neuropsychological testimony (even partial HRB proto- Categorization

cols from two other neuropsychologists) was admitted
into evidence and the fact that the judge had placed The images associated with CBS are often rich in detail,
more emphasis on testimony from a fixed battery advo- and their clarity frequently contrasts sharply with suf-
cate was completely unrelated to the determination of the ferers blurred perception of real objects (Menon, Rah-
test battery. Indeed, there was no Daubert challenge to a man, Menon, & Dutton, 2003). They are sometimes
flexible test battery approach. In this particular case, only referred to as pseudo-hallucinations to indicate that
the testimony of a vocational specialist who conducted no the person experiencing them is aware that the images
testing and provided no evidence in the form of a peer- are not real. Hallucinations may vary greatly in terms of
reviewed study to support his claims, was subject to a color, clarity, movement, and bizarreness (Plummer, Klei-
Daubert hearing from the defense. nitz, Vroomen, & Watts, 2007). Nevertheless, common
themes and figures have been described, including
humans and animals, extended landscapes, and ornate
References and Readings structures (Plummer et al., 2007). Ffytche and Howard
(1999) classified their patients hallucinations into eight
Chapple v. Ganger, 851 F. Supp. 1481, E.D. of Washington (1994). categories (Table 1).
Daubert v. Merrell Dow Pharmaceuticals, 509 U.S. 579 (1993). While the clinical validity of this classification system
General Electric co. v. Joiner, 522 U.S. 136 (1997).
has not yet been established, it does share some simila-
Principles of productive attorney-neuropsychologists relations. In
rities with known functional and anatomical networks
G. Larrabee (Ed.), Forensic neuropsychology: A scientific approach. within the visual association cortex (Plummer et al.,
New York: Oxford University Press. 2007).
Kumho Tire Co. v. Carmichael, 526 U.S. 137 (1999).
Reed, J. E. (1996). Fixed versus flexible neuropsychological test batteries
under the Daubert standard for the admissibility of scientific
Epidemiology
evidence. Behavioral Sciences and the Law, 14, 315322.
1. Prevalence: Once considered rare, CBS is becoming

increasingly more common (Rovner, 2006). The larger
number of reported CBS cases may be related to the
Charles Bonnet Syndrome growing population of older adults and the more
common occurrence of visual disorders such as age-
M ELISSA B UTTARO related macular degeneration, glaucoma, and cataracts
Brown University (Rovner, 2006). It has also been argued that past prev-
Providence, RI, USA alence estimates of CBS were spuriously low due to a
Synonyms/Associated Terms Charles Bonnet Syndrome. Table 1
Bonnet syndrome Hallucination Category Description

Tessellopsia Regular, overlapping patterns
Short Description or Definition Hyperchromatopsia Hyperintense, vivid, brilliant

colors
Charles Bonnet syndrome (CBS) is characterized by the Prosopometamorphopsia Facial distortions
following features (Eperjesi & Akbarali, 2004): Dendropsia Branching forms
Perseveration True percept that persists after
1. The presence of well-formed, complex, repetitive or the individual looks away
persistent visual hallucinations
Illusory visual spread Spread of a non-hallucinated
2. Full or partial retention of insight into the unreal
pattern
nature of the hallucinations
Polyopia Multiple copies of a percept
3. Absence of hallucinations in other sensory modalities
(e.g., auditory, olfactory) Micropsia/macropsia Miniaturized/larger than life
images
4. Absence of delusions
Charles Bonnet Syndrome C 539
general lack of awareness of the syndrome in the medi- Charles Bonnet Syndrome. Table 2
cal community, as well as patients reluctance to dis-
Factors Favoring the Recurrence of Hallucinations
close their hallucinatory symptoms for fear of being
labeled psychotic or demented (Plummer et al., 2007). Dimly lit conditions
One estimate suggests that the prevalence of complex States of drowsiness C
visual hallucinations in patients with visual impairment Physical and social isolation
is between 11% and 15% (Menon et al., 2003).
2. Age of onset: CBS may occur at any age, but it is more
common in the elderly. Average age of onset tends to be
in the 70s and 80s (Plummer et al., 2007). The
increased prevalence of CBS in older adults is likely Charles Bonnet Syndrome. Table 3
related to the greater incidence of sudden visual loss
Factors that May Help Relieve Hallucinations
and/or isolation in this age group (Menon et al., 2003).
Rapid blinking
Sustained eye closure
Natural History, Prognostic Factors, Diversionary activities
Outcomes Limiting exposure to dim lighting
Walking away
Historical background: Charles Bonnet syndrome is
Looking at or approaching images
named after the eminent Swiss philosopher and naturalist
who first described this phenomenon in 1760 (Hedges,
2007). In a book entitled Essai Analytique sur les Faculties
de LAme [Analytical Essays Concerning the Faculties of
the Mind], Charles Bonnet described how his cognitively It has been argued that CBS is more commonly asso-
intact, 89-year-old grandfather with failing eyesight began ciated with higher degrees of visual impairment, and with
to experience well-formed visual hallucinations, which he bilateral as opposed to unilateral ocular pathology
was aware were not actually physically present. Interest- (Menon et al., 2003). It has also been suggested that it is
ingly, Charles Bonnet began to have similar experiences not the specific lesion site or the severity of impairment,
later in his own life. At the age of 22, he began to experi- but rather the rate of development of the visual im-
ence severe eye pain and progressively worsening loss of pairment that best predicts CBS (Plummer et al., 2007).
vision that made it difficult for him to use a microscope, That is, hallucinations may be more common in the
and he ultimately turned to more abstract philosophical context of sudden or unexpected decrease in visual func-
pursuits and theoretical questions in biology. In his re- tion (Menon et al., 2003).
tirement, he experienced formed visual hallucinations Outcomes: The course of CBS can be unpredictable.
associated with many of the common attributes of the While the onset is generally sudden, it may also be gradual
syndrome that shares his name, including blindness, in- (Menon et al., 2003). Hallucinations can last from seconds
tact cognition, and occurrence in quiet and reflective to hours, or even days. Clustering of episodes across days
settings. Another native of Geneva, George de Morsier, or weeks is not unusual. Three patterns of the syndrome
proposed in 1967 that visual hallucinations in older men have been described (Menon et al., 2003). The episodic
without mental deficiency be designated the syndrome of pattern, characterized by hallucinations that happen over
Charles Bonnet. a period of days to months and then permanently cease, is
Current thinking/prognostic factors: The question of reportedly the least common. In the periodic pattern,
whether visual impairment is necessary for the develop- phases of hallucinatory activity alternate with phases of
ment of CBS has been the matter of debate. Some argue remission. The continuous pattern, as its name suggests, is
that CBS is almost invariably associated with impaired characterized by unremitting hallucinations (i.e., no hal-
vision, and it may occur whenever sensory input to the lucination-free intervals) (Menon et al., 2003). Overall,
brain is decreased sufficiently to allow release phenomena. the duration of CBS can extend from days to years, and
Other researchers report that visual dysfunction, though spontaneous recurrence after a symptom-free interval is
common, is not mandatory for diagnosis, and note that possible. Interestingly, some sufferers have reported per-
CBS has been found in individuals with intact vision manent remissions of CBS in conjunction with ongoing
(Terao & Collinson, 2000). visual decline (Plummer et al., 2007).
540 C Charles Bonnet Syndrome
Neuropsychology and Psychology of Treatment

Charles Bonnet Syndrome
Treatment for CBS may not always be necessary, since
The exact pathophysiology of CBS is unclear. Although visual hallucinations often resolve spontaneously, either
Charles Bonnet suggested that the primary pathology in response to improvement or further deterioration of
was restricted to the eye, subsequent research has suggest- visual function (Menon et al., 2003). In addition, many
ed that complex hallucinations can occur in the context of patients are not distressed by their hallucinations and may
visual impairment secondary to pathology anywhere along even enjoy them. However, if hallucinations are frequent
the central visual pathway, from the orbit to the occipital or distressing, the following treatment options are
cortex (Menon et al., 2003). A leading hypothesis is that available:
complex visual hallucinations result from deafferentation
1. Optimizing visual acuity: Patients should initially
of the visual association cortex following lesions among
be referred to a low-vision specialist, who may be
the central visual pathway. Age-related macular degenera-
able to reduce or alleviate hallucinations by optimiz-
tion is a commonly cited cause of CBS, but other ocular
ing visual function (e.g., via prescription eyeglasses or
pathologies include glaucoma, central retinal artery oc-
visual aids). If appropriate, the patient might be con-
clusion, and optic neuritis (Plummer et al., 2007). Extrao-
sidered for surgery (e.g., cataract surgery or neurosur-
cular and central visual axis pathologies associated with
gical procedures). Several reports indicate that
CBS include lesions of the pituitary and optic chiasm,
improvement of visual function, either spontaneously
meningioma, and occipital stroke.
or by intervention, can effectively decrease or even
eliminate hallucinations (Menon et al., 2003).
Evaluation 2. Supportive treatment: A key component in the man-
agement of CBS is supportive. Patients may derive
The evaluation of CBS should begin with a clinical comfort from sympathetic explanations that their hal-
interview, which should be approached carefully in lucinations are not uncommon, are not necessarily a
light of sufferers frequent reluctance to disclose hallu- marker of psychiatric disease, and may represent a
cinatory experiences. The clinician should assess the release phenomenon in the context of visual im-
nature of the hallucinations, the modalities in which pairment. Using the analogy of phantom visions,
they occur, the presence of delusions, and the patients similar to a phantom limb syndrome, may be helpful
insight. It is important to note that insight into the (Rovner, 2006).
illusory nature of the hallucinations may not occur 3. Psychotherapeutic strategies: Psychotherapeutic techni-
immediately; in fact, there may be a period of initial ques used for phantom limb pain, including distrac-
deception, especially if the perceived images are not tion, hypnosis, relaxation training, and cognitive
uncommon and fit realistically into the patients sur- restructuring can help reduce the unpleasant effects
roundings (Menon et al., 2003). Referrals to an ophthal- of intrusive and upsetting visual hallucinations
mologist, low-vision specialist, and neuropsychiatrist may (Menon et al., 2003). Support or psychoeducational
be helpful. groups are useful settings in which sufferers can meet,
A key issue for clinical neuropsychologists is the differ- obtain reassurance, and be given advice about specific
ential diagnosis of CBS from other causes of visual hallu- techniques for reducing hallucinations (Eperjesi &
cinations. Conditions belonging in the differential include Akbarali, 2004).
migraine, occipital seizures, peduncular hallucinosis (usu- 4. Behavioral/environmental modifications: Approaches
ally from rostral brainstem infarct), drug-induced states, such as rapid eye blinking, sustained eye closure,
psychiatric disease, delirium, and dementia. In particular, minimizing fatigue and stress, and engaging in dis-
CBS may occur in the early stages of dementia with Lewy tracting activities (e.g., listening to the radio and
bodies (DLB), and as cognitive function declines, insight attending to household chores) may help reduce hal-
about the unreal nature of the hallucinations vanishes lucinations. Limiting exposure to dim lighting (e.g.,
(Terao & Collinson, 2000). Some have suggested the by increasing lighting in the home in the evening) and
term Charles Bonnet Plus or CBS plus to describe visual taking steps to reduce glare may also be helpful. Look-
hallucinations that occur in the presence of a neuropsy- ing directly at the images, attempting to approach
chiatric disorder (Eperjesi & Akbarali, 2004; Menon et al., them, and conversing with them have also been
2003). reported to stop hallucinations (Menon et al., 2003).
CHART Short Form C 541
Since solitude and loneliness, particularly during the

evening hours, tend to heighten hallucinations, CHART
strengthening social networks and increasing the
amount of time spent interacting with others may be Craig Handicap Assessment and Reporting Technique
useful (Plummer et al., 2007). C
5. Pharmacological interventions: Referral to a specialist
for pharmacological therapy may be helpful. A few
case studies have reported efficacy of pharmacological
agents in alleviating symptoms, such as sodium
CHART Short Form
valproate, olanzapine, and carbamazepine (Plummer
G ALE G. W HITENECK
et al., 2007). Use of other medications (e.g., risperi-
Craig Hospital
done, gabapentin, and diazepam) has also been
Englewood, CO, USA
described (Eperjesi & Akbarali, 2004).
6. Follow-up: Since some cases of CBS do go on to devel-
op dementia, it is recommended that clinicians follow
patients with complex visual hallucinations carefully
Synonyms
over time (Menon et al., 2003). Though most patients
CHART-SF; Craig handicap assessment and reporting
experience no practical problems associated with CBS,
technique (CHART) short form
continuous visual hallucinations can interfere with
navigation and driving, and patients ability to per-
form daily activities safely should be monitored over
time (Menon et al., 2003).
Definition
The Craig Handicap Assessment and Reporting

Technique Short Form (CHART-SF) is a 19-item measure
Cross References of handicap or level of societal participation. Released in
1998, the CHART-SF is the short version of the 32-item
Dementia with Lewy Bodies CHART instrument designed to provide a simple,
Macropsia objective measure of the degree to which impairments
Micropsia and disabilities result in handicaps (societal participation
Visual Hallucinations limitations) for adolescents and adults (15 years and
older) in the years after initial rehabilitation. Like its
precursor, the CHART-SF includes six subscales (physical
independence, cognitive independence, mobility, occupa-
References and Readings tion, social integration, and economic independence),
which closely reflect the disablement model developed
Eperjesi, F., & Akbarali, N. (2004). Rehabilitation in Charles Bonnet by the World Health Organization, published in 1980
syndrome: A review of treatment options. Clinical and Experimental
and revised in 2001. Each subscale contains from 2 to 5
Optometry, 87(3), 149152.
Ffytche, D. H., & Howard, R. J. (1999). The perceptual consequences of
questions, which together quantify the extent to which
visual loss: Positive pathologies of vision. Brain, 122(Pt 7), individuals fulfill various social roles. CHART-SF focuses
12471260. on objective, observable criteria that are easily quantifi-
Hedges, T. R. (2007). Charles Bonnet, his life, and his syndrome. Survey of able and unlikely to be open to subjective interpretation.
Ophthalmology, 52(1), 111114.
Each of the domains or subscales of the instrument have a
Menon, G. J., Rahman, I., Menon, S. J., & Dutton, G. N. (2003). Complex
visual hallucinations in the visually impaired: The Charles Bonnet
maximum score of 100 points, which is considered the
Syndrome. Survey of Ophthalmology, 48(1), 5872. level of performance typical of the average non-disabled
Plummer, C., Kleinitz, A., Vroomen, P., & Watts, R. (2007). Of Roman person. High subscale scores indicate less handicap, or
chariots and goats in overcoats: The syndrome of Charles Bonnet. higher social and community participation.
Journal of Clinical Neuroscience, 14(8), 709714.
Although originally developed for use with persons
Rovner, B. W. (2006). The Charles Bonnet syndrome: A review of recent
research. Current Opinion in Ophthalmology, 17(3), 275277.
with spinal cord injury, the CHART and the CHART-SF
Terao, T., & Collinson, S. (2000). Charles Bonnet syndrome and demen- have proven to be appropriate measures of societal
tia. Lancet, 355(9221), 2168. participation that can be used with individuals having a
542 C CHART-SF
range of physical or cognitive impairments. The CHART-

SF was designed to be administered by interview, either in CHEIs
person or by telephone and takes approximately 57 min
to administer. There is no set time period for administering Cholinesterase Inhibitors
the CHART-SF; however, it is recommended that multiple
measurements be taken over the course of a persons
lifetime to assess the changes with adaptation to the
disability and to gain insight into changes in participation, Chelation
which may occur over time.
The 19-item CHART-SF with subscales closely B RUCE J. D IAMOND, A MANDA FAULHABER
approximating the subscale scores for the CHART long William Paterson University
form is recommended for those populations for whom Wayne, NJ, USA
time is at a minimum.
Synonyms
Current Knowledge EDTA therapy
In an effort to reduce the number of items in the original

CHART, a short form was developed. A multidimension- Short Description or Definition
al analysis was performed which showed that fewer vari-
ables were needed to obtain CHART scores. Regression Chelation therapy has been used in allopathic and in
analyses were performed on each subscale with the complementary and alternative (CAM) forms of medi-
dependent measure being the scale score and the variables cine. Claims that chelation therapy with ethylene diamine
contributing to the subscale acting as the predictor variables. tetraacetic acid (EDTA) is an effective technique for
All CHART subscale scores could be reduced by fewer controlling and treating cardiovascular disease are not
questions to reach 90% explained variance except Economic supported by systematic reviews of the literature (Ernst,
Self-Sufficiency, which using the main variables could Pittler, Stevinson, White & Eisenber, 2001; Seely, Wu &
only explain 45%. Mills, 2005). However, Chelation therapy does appear to
be highly effective and is the treatment of choice in treat-
ing heavy metal poisoning (Ernst et al., 2001). Recent
research also suggests that Chelation therapy may have
Cross References applications in the treatment of malaria (Mabeza, Love-
vsky, Gordeuk & Weiss, 1999). The therapy involves the
Craig Handicap Assessment and Reporting Technique
intravenous administration of EDTA, which binds ions in
the blood, and is often used in combination with vita-
mins, trace elements, and iron supplements.
Whiteneck, G., Brooks, C. A., Charlifue, S., Gerhart, K. A., Mellick, D.,
Categorization
Overholser, D., et al. (1998). Guide for use of the CHART: Craig
handicap assessment and reporting technique. www.craighospital. While Chelation therapy has been used for treating lead
org/Research/CHART December 28, 2009. poisoning and vascular occlusive disease, oral chelation ther-
apy with the a-ketohydroxypyridine chelator 1,2-dimethyl-
3-hydroxypyrid-4-one (L1, INN/BAN: deferiprone) has
also been used in iron- and aluminum-overloaded patients.
A number of iron(III) chelators have also shown antimalar-
CHART-SF ial activity in vitro with the proposed mechanism of activ-
ity involving the withholding of iron from metabolic
CHART Short Form pathways of the intra-erythrocytic parasite and the forma-
Craig Handicap Assessment and Reporting Technique tion of toxic complexes with iron.
Chemical AIDS C 543
History levels (Kontoghiorghes, 1995). Toxic side effects include

six cases of reversible agranulocytosis, 030% incidence of
Chelation therapy began in the early 1950s and was pri- transient musculoskeletal and joint pains, 06% of gastric
marily used to treat metal poisoning of the blood. How- intolerance, and 02% zinc deficiency. In the treatment of
ever, both allopathic and CAM practitioners have claimed malaria, iron chelation therapy with desferrioxamine, C
that the technique can be used to reverse the arterioscle- which is the only compound of this nature that is available
rotic disease process (e.g., peripheral arterial occlusive for use in humans, has shown clinical activity in both
disease (PAOD)). uncomplicated and severe malaria in humans (Mabeza
et al., 1999).
Evaluation
Adverse Side Effects
Studies examining the efficacy of Chelation therapy have
shown mixed results. In one authoritative systematic re-
In one systematic review, adverse effects were character-
view, it was stated that proponents of chelation therapy
ized as rare but cases of hypocalcemia and a single case of
adhere to pathophysiological models of arteriosclerosis,
increased creatinine was noted in a patient on the EDTA
which are inconsistent with current knowledge and prac-
intervention (Seely, Wu & Mills, 2005). Moreover, it was
tice (Ernst et al., 2001). In a systematic review of chelation
emphasized that if the treatment is used in lieu of proven
therapy in the treatment of malaria, it was concluded that
therapies, indirect harm to the patient could result. In
when used via oral administration, its efficacy and low
another systematic review, it was reported that EDTA
cost make it more accessible than desferrioxamine for the
treatment may be associated with life-threatening adverse
majority of patients needing iron chelation (Mabeza et al.,
effects, such as hypocalcemia and severe kidney damage,
1999).
in addition to prolonged bleeding and respiratory distress
(Ernst et al., 2001).
Treatment and Mechanisms
Typically, Chelation therapy is administered in multiple Cross References

sessions with each treatment lasting for over an hour. The
putative mechanism underlying chelation therapy is the Lead Exposure
binding of ions in the blood by EDTA. The therapy is,
generally, considered to be effective in heavy metal poi-
soning. In CAM applications, it has been used as an References and Readings
alternative to bypass surgery, based on the idea that che-
lation therapy removes harmful plaque build-up in the Ernst, E., Pittler, M. H., Stevinson, C., White, A., & Eisenber, D.
arteries (unblocking arteriosclerotic arteries) and helps (Eds.) (2001). The desktop guide to complementary and alternative
medicine: An evidence based approach. Amsterdam: Elsevier Health
prevent strokes. The mechanism is believed to involve
Sciences.
the extraction of calcium out of arteriosclerotic plaques Kontoghiorghes, G. J. (1995). New concepts of iron and aluminum
via the chelating mechanism. In a systematic review of chelation therapy with oral L1 (deferiprone) and other chelators:
randomized, placebo-controlled, double-blind trials, it A review. Analyst, 120, 845851.
was concluded that Chelation therapy for PAOD is not Mabeza, G. F., Loyevsky, M., Gordeuk, V. R., Weiss, G. (1999). Iron
chelation therapy for Malaria: A review. Pharmacology & Therapeu-
superior to placebo, that it is associated with considerable
tics, 81, 5375.
risks and costs, and that it should now be considered Seely, D. M., Wu, P., & Mills, E. J. (2005). EDTA Chelation therapy for
obsolete (Ernst et al., 2001). However, it should also be cardiovascular disease: A systematic review. BMC Cardiovascular
noted that using oral chelation therapy, in doses ranging Disorders, 5, 3238.
from 55 to 100 mg kg1 of L1 (a-ketohydroxypyridine
chelator 1,2-dimethyl-3-hydroxypyrid-4-one (L1, INN/
BAN: deferiprone)), a majority of iron-loaded patients
showed urinary iron excretion levels greater than those Chemical AIDS
accumulating from transfusions (1535 mg d1) and also
reductions in serum ferritin and liver iron to near normal Multiple Chemical Sensitivity
544 C Chemical Hypersensitivity Syndrome
-thalidomide. The specific manner in which chemothera-

Chemical Hypersensitivity py achieves the intended effect is contingent upon the
Syndrome particular drug(s) employed. However, cytotoxicity
usually occurs when the cell attempts to divide and before
Multiple Chemical Sensitivity the repair occurs (Chabner & Longo, 2004). The proba-
bility of the intended effect on the targeted molecules
reflects the appropriate concentration of drugs, amount
or dose and timing of drug administration. Drug absorp-
tion, distribution, and penetration are also significant
Chemotherapy factors inherent in the efficacy of chemotherapy. The
precise drug dosage can be complicated because if
B RAM G OLDSTEIN the amount is too low, it may be ineffective against the
Hoag Hospital Cancer Center tumor. Conversely, if the dosage is too high, patients may
Newport Beach, CA, USA suffer from excessive toxicity. Since chemotherapy
damages healthy cells during the therapeutic process, the
treatment is associated with several harmful side effects,
Synonyms such as myelosuppression. For example, bone marrow,
which produces white blood cells, red blood cells, and
Systemic therapy blood platelets, can be damaged during chemotherapy
treatment. In particular, white blood cells and platelets
frequently drop transiently after chemotherapy, so that
Definition patients are at increased risk for infection and bleeding
during and post chemotherapy. Many chemotherapy
Chemotherapy is a systemic treatment for cancer, com- patients also suffer from nausea and vomiting because
prising cytoxic agents that target cancer cells. Normally, the drugs irritate the stomach lining and bowel. Certain
cells develop and die in an orderly and determined chemotherapy drugs also cause alopecia, or hair loss. This
fashion. However, when cancer manifests itself, the cells condition results from the chemotherapy agent adversely
intractably divide and proliferate. Chemotherapy drugs affecting the growth of hair cells, causing them to become
target these cancer cells by destroying them before they brittle and eventually break. Several chemotherapies also
continually multiply and divide. In particular, chemo- result in anorexia, severe loss of appetite, and significant
therapy interferes with or impairs the targeted molecules weight loss. Fatigue, diarrhea, and constipation are also
(e.g., DNA, proteins) during designated cellular stages, very common side effects from cancer and chemotherapy.
such as synthesis or mitosis. The majority of chemothera- Additionally, specific chemotherapy agents can cause
py drugs damage or interfere with the replication of DNA stomatitis, a condition that results in sores manifesting
and/or RNA, and are used to treat several malignancies, inside the mouth or throat. Chemotherapy is most often
particularly brain tumors, lymphomas, and leukemias. given intravenously, whereby a thin needle is inserted
Some of the chemotherapies include: alkylating agents into a patients vein on the hand or lower arm. Intrave-
(such as cisplatin, carboplatin, cyclophosphamide, and nous chemotherapy can also be delivered through cathe-
temozolomide) to treat brain tumors, lymphomas, and ters, ports, and pumps. The treatment is frequently given
leukemias; nitrosoureas (e.g., carmustine and lomustine) in cycles (i.e., specified treatment periods) that reflect
are indicated for the treatment of brain tumors and alternating rest periods. This is necessary because
lymphomas; antimetabolites (such as methotrexate) to patients require substantial relief to permit the body to
treat leukemias; anthracycline and related drugs recuperate, build healthy new cells, and restore strength.
(e.g., doxorubicin), which have toxic effects on the Treatment regimens may be given daily, weekly, or
heart; topoisomerase inhibitors (such as topotecan, monthly and are based upon a drugs efficacy or toxicity.
irinotecan, and etoposide); mitotic inhibitors (e.g., vin- Chemotherapy is usually administered before (neo-ad-
blastine and vincristine), which can cause peripheral juvant) surgery or post (adjuvant) surgery. Neoadjuvant
nerve damage; and corticosteroid hormones, which can chemotherapy is intended to decrease the primary
be used to kill or slow the growth of cancer cells. There tumors size. This potentially mitigates the harmful
are other chemotherapies that are excluded from these effects of surgery or radiotherapy and enhances the effi-
categories, namely L-asparaginase, -hydroxyurea, and cacy of chemotherapy.
Chemotherapy C 545
Adjuvant chemotherapy may also reduce the proba- the cell attempts to divide and before repair occurs
bility of tumor resistance to drug therapy in the event of (Chabner & Longo, 2004).
disease recurrence (Chabner & Longo, 2004). Further- The probability of the intended effect on the targeted
more, adjuvant chemotherapy is effective at destroying molecules reflects the appropriate concentration of drugs,
residual cancer cells that have spread to distal parts of amount or dose and timing of drug administration. Drug C
the body (i.e., metastasis), particularly because rapidly absorption, distribution, and penetration are also signifi-
proliferating lesions are very amenable to treatment. cant factors inherent in the efficacy of chemotherapy.
Palliative chemotherapy is indicated when the curative The precise drug dosage can be complicated because if
potential is very low and the primary goals are to decrease the amount is too low, it may be ineffective against the
the patients tumor burden and prolong life expectancy. tumor. Conversely, if the dosage is too high, patients may
suffer from excessive toxicity.
Since chemotherapy damages healthy cells during the
Current Knowledge therapeutic process, the treatment is associated with
several harmful side effects, such as myelosuppression.
Recent neuropsychological research has indicated that For example, bone marrow, which produces white blood
chemotherapy can also adversely impact cognitive cells, red blood cells, and blood platelets, can be damaged
functioning, both short-term and delayed. In particular, during chemotherapy treatment. In particular, white
neuropsychological research studies have provided blood cells and platelets frequently drop transiently after
evidence discussing the impact of chemotherapy on atten- chemotherapy, so that patients are at increased risk for
tion, memory, and concentration (Armstrong, Gyato, infection and bleeding during and after chemotherapy.
Awadalla, Lustig, & Tochner, 2004). Consequently, many Many chemotherapy patients also suffer from nausea
of these chemotherapy-induced cognitive impairments and vomiting because the drugs irritate the stomach lining
can significantly impair patients daily activities, such as and bowel. Certain chemotherapy drugs also cause alope-
working, being involved in a committed relationship, and cia or hair loss. This condition results from the chemo-
attending to personal responsibilities. Research has therapy agent adversely affecting the growth of hair cells,
suggested that many of these impairments are temporary causing them to become brittle and eventually break.
but some may be more long-term, or even permanent. Several chemotherapies also result in anorexia, severe
The cognitive effects are not uniform, and the severity loss of appetite, and significant weight loss. Fatigue, diar-
appears to reflect a higher concentration and/or larger rhea, and constipation are also very common side effects
dose of chemotherapy. from cancer and chemotherapy. Additionally, specific
Most of the different types of chemotherapy drugs chemotherapy agents can cause stomatitis, a condition
damage or interfere with the replication of DNA and/or that results in sores manifesting inside the mouth or throat.
RNA, and are used to treat several malignancies, particu- Chemotherapy is most often given intravenously,
larly brain tumors, lymphomas, and leukemias. Some of involving a thin needle, which is inserted into a patients
the chemotherapies include: alkylating agents (such as vein on the hand or lower arm. Intravenous chemotherapy
cisplatin, carboplatin, cyclophosphamide, and temozolo- can also be delivered through catheters, ports, and pumps.
mide) to treat brain tumors, lymphomas, and leukemias; The treatment is frequently given in cycles that reflect
nitrosoureas (e.g., carmustine and lomustine) to treat brain specified treatment periods which are alternated with
tumors and lymphomas; antimetabolites to treat leukemias rest periods. This is necessary because patients require
(such as methotrexate); anthracycline and related drugs substantial relief to permit the body to recuperate, build
(e.g., doxorubicin), which have toxic effects on the heart; healthy new cells, and restore strength.
topoisomerase inhibitors (such as topotecan, irinotecan, Treatment regimens may be given daily, weekly,
and etoposide); mitotic inhibitors (e.g., vinblastine and or monthly and are based upon a drugs efficacy or
vincristine), which can cause peripheral nerve damage; toxicity. Chemotherapy is usually administered before
and corticosteroid hormones, which can be used to kill or (neo-adjuvant) surgery or post (adjuvant) surgery.
slow the growth of cancer cells. There are other che- Neo-adjuvant chemotherapy is intended to decrease the
motherapies that are excluded from these categories, such primary tumors size. This potentially mitigates the harm-
as L-asparaginase, -hydroxyurea, and -thalidomide. The ful effects of surgery or radiotherapy and enhances the
specific manner in which chemotherapy achieves the efficacy of chemotherapy.
intended effect is contingent upon the particular drug(s) Adjuvant chemotherapy is employed when there is
employed. However, cytotoxicity usually occurs when scant evidence of residual disease, but there is an increased
546 C Chief Sensory Nucleus of V
risk of cancer recurrence. Adjuvant chemotherapy may cuneatus and gracilis in the medulla, which mediate simi-
also reduce the probability of tumor resistance to drug lar input from the trunk and extremities. It gives rise to
therapy in the event of disease recurrence (Chabner & trigeminothalamic fibers, which terminate in the ventral
Longo, 2004). Furthermore, adjuvant chemotherapy is posterior medial nucleus of the thalamus.
effective at destroying residual cancer cells that have
spread to distal parts of the body (i.e., metastasis), partic-
ularly since rapidly proliferating lesions are very amenable Current Knowledge
to treatment. Palliative chemotherapy is indicated when
the curative potential is very low and the primary goals Because of its size and density, it is rare for brainstem
are to decrease the patients tumor burden and prolong lesions to be isolated to a single nucleus or pathway.
life expectancy. Theoretically, lesions which involve this nucleus might
most readily be distinguished on a routine neurological
exam by changes (asymmetries) in two-point discrimina-
Cross References tion on the ipsilateral face. In practice, however, such
lesions are likely to involve other brainstem nuclei and
Systemic Therapy pathways, including the adjacent motor nucleus of V,
spinal trigeminal tract and/or nucleus, spinal thalamic
tracts, lateral portions of the medial lemniscus, and mid-
dle cerebellar peduncles resulting in ipsilateral muscle
References and Readings weakness of the jaw muscles, ipsilateral changes in pain
and temperature in the face and diminished or abolished
Armstrong, C. L., Gyato, K., Awadalla, A. W., Lustig, R., & Tochner, Z. A. corneal reflex, contralateral loss of pain and temperature
(2004). A critical review of the clinical effects of therapeutic irradia-
in the extremities, diminished or loss of proprioception,
tion damage to the brain: the roots of controversy. Neuropsychology
Review, 14, 6586. stereognosis, and vibration in the contralateral extremities
Chabner, B. A., & Longo, D. L. (2004). Cancer chemotherapy and biother- (leg > arm), and ipsilateral cerebellar signs.
apy: Principles and practice. Hagerstown, MD: Lippincott, Williams &
Wilkins.
Gilman, S., & Newman, S. W. (2003). Manter and Gatzs essentials of

clinical neuroanatomy and neurophysiology. Philadelphia: F.A. Davis.
Chief Sensory Nucleus of V Wilson-Pauwek, L., Akesson, E. J., Stewart, P. A., & Spacey, S. D. (2002).
Cranial nerves in health and disease. Hamilton, ON: B.C. Decker.
J OHN E. M ENDOZA
Child Behavior Checklist
Synonyms T HOMAS M. A CHENBACH
University of Vermont
Principal sensory nucleus of the trigeminal nerve; Princi- Burlington, VT, USA
pal sensory nucleus of V
Synonyms
Definition
ASEBA; CBCL
Nucleus responsible for proprioceptive feedback from the
muscles of facial expression, stereognosis or fine tactual
discrimination, and vibratory sensations from the face. Description
Located in the dorsolateral pons just medial to the middle
cerebellar peduncle and inferior to the superior cerebellar The Achenbach System of Empirically Based Assessment
peduncle, it is the functional equivalent of the nuclei (ASEBA) comprises a family of forms for rating
Child Behavior Checklist C 547
behavioral/emotional problems and adaptive characteris- interviewer who administers the SCICA to 6- to 18-year-
tics. For ages 1 to 90 years, developmentally appropri- olds and the Test Observation Form (TOF), which test
ate forms are designed to be completed by collaterals who examiners use to rate the behavior observed during the
know the person who is being assessed. These forms administration of individual ability and achievement tests
include versions of the Child Behavior Checklist to 2- to 18-year-olds. Table 1 summarizes the ASEBA C
(CBCL), completed by parent figures for 1- to 5-year- forms, ages covered, who completes the forms, and refer-
olds and for 6- to 18-year-olds; the Caregiver-Teacher Re- ences to manuals for each form.
port Form (C-TRF) for ages 15, completed by daycare
providers and preschool teachers; the Teachers Report
Form (TRF) for ages 618, completed by teachers and Normed Profiles
other school personnel; the Adult Behavior Checklist
(ABCL) for ages 1859, completed by spouses, partners, Scores obtained from all ASEBA forms are displayed on
family members, friends, therapists, and other collaterals; profiles in relation to norms that are based on distribu-
and the Older Adult Behavior Checklist (OABCL) for ages tions of scale scores obtained by large samples of peers.
60 and older, completed by caregivers as well as by For the collateral and self-report forms for ages 1 to
collaterals. 90 years, norms are based on a US national probability
The ASEBA also includes parallel forms completed by sample of people who had not received mental health or
the people being assessed, including the Youth Self-Report substance abuse services in the preceding 12 months. For
(YSR) for ages 1118, the Adult Self-Report (ASR) for the CBCL/618, TRF, and YSR, norms are provided for
ages 1859, and the Older Adult Self-Report (OASR) for many cultures in addition to the USA, as detailed later
ages 60 and older. The collateral and self-report forms (Achenbach & Rescorla, 2007a, b). Multicultural norms
assess functioning in everyday contexts over periods of for the CBCL/15 and C-TRF were released in 2010. For
26 months. the DOF, SCICA, and TOF, norms are based on ratings of
In addition to the collateral and self-report forms, children observed in the contexts for which these instru-
other ASEBA forms are designed for rating behavior ob- ments are designed.
served in specific situations. These forms include the Each profile displays an individuals scale scores in
Direct Observation Form (DOF), which is completed by terms of standard scores (T scores) and percentiles based
observers who rate two or more 10-min samples of chil- on the normative sample of that individuals peers, as
drens behavior observed in classrooms and other group rated by a particular type of informant (e.g., parent,
settings; the Semistructured Clinical Interview for Chil- teacher, self). The profiles also display demarcations be-
dren and Adolescents (SCICA), which provides an inter- tween the normal range, borderline clinical range, and
view protocol and a rating form completed by the clinical range on each scale. Figure 1 illustrates a profile
Child Behavior Checklist. Table 1 ASEBA assessment instruments
Instrument Ages Completed by Reference

CBCL/15 15 Parent figures Achenbach and Rescorla (2000)
C-TRF 15 Daycare providers, preschool teachers Achenbach and Rescorla (2000)
CBCL/618 618 Parent figures Achenbach and Rescorla (2001, 2007a)
TRF 618 Teachers Achenbach and Rescorla (2001, 2007a)
YSR 1118 Youths Achenbach and Rescorla (2001, 2007a)
TOF 218 Psychological examiner McConaughy and Achenbach (2004)
DOF 611 Observer McConaughy and Achenbach (2009)
SCICA 618 Interviewer McConaughy and Achenbach (2001)
ASR 1859 Adults Achenbach and Rescorla (2003)
ABCL 1859 Collaterals Achenbach and Rescorla (2003)
OASR 60 Older adults Achenbach, Newhouse, and Rescorla (2004)
OABCL 60 Collaterals Achenbach, Newhouse, and Rescorla (2004)
548
YSR/1118 - Syndrome scale scores for Boys (2001 version)
C
ID: 2301251405003 Date filled: 01/08/2001 Informant: Self
Gender: Male
Name: Wayne webster Birth date: 03/03/1986 Relationship: Self
Age: 15
Clinician: Dr. Barrett Agency: CMHC
Internalizing Verified: Scanned Externalizing
100
C
95
L
90 I
T 85 N
I
S 80
C
C 75 A
O
70 L
R
E 65
N
60 O
55 R
M
50
Anxious/ Withdrawn/ Somatic Social Thought Attention Rule-breaking Aggressive A
L
depressed depressed complaints problems problems problems behavior behavior
Total score 12 12 6 14 14 9 5 14
T score 70-C 83-C 64 80-C 77-C 63 56 67-B
Percentile >97 >97 92 >97 >97 90 73 96
1 14.Cries 2 5.EnjoysLittle 2 47.Nightm ares 2 11.Dependent 2 9.MindOff 0 1.ActsYoung 1 2.Alcohol 2 3.Argues
0 29.Fears 2 42.PreferAlone 1 51.Dizzy 2 12.Lonely 0 18.HarmSelf 0 4.FailsToFinish 0 26.NoGuilt 1 16.Mean
0 30.FearSchool 2 65.WontTalk 1 54.Tired 1 25.NotGetAlong 1 40.HearsThings 2 8.Concentrate 0 28.BreaksRules 0 19.DemAtten
0 31.FearDoBad 2 69.Secretive 0 56a.Aches 0 27.Jealous 2 46.Twitch 0 10.SitStill 0 39.BadFriends 1 20.DestroyOwn
0 32.Perfect 0 75.Shy 1 56b.Headaches 2 34.OutToGet 0 58.PicksSkin 2 13.Confused 0 43.LieCheat 0 21.DestroyOther
2 33.Unloved 0 102.LacksEnergy 0 56c.Nausea 2 36.GetsHurt 2 66.RepeatsActs 1 17.Daydream 0 63.PreferOlder 1 22.DisobeyHome
2 35.Worthless 2 103.Sad 0 56d.EyeProb 1 38.Teased 0 70.SeesThings 1 41.Impulsive 0 67.RunAway 1 23.DisobeySchl
2 45.Nervous 2 111.Withdrawn 1 56e.SkinProb 2 48.NotLiked 2 76.SleepsLess 1 61.PoorSchool 1 72.SetsFires 1 37.Fights
0 50.Fearful 0 56f.Stomach 1 62.Clumsy 0 83.StoresUp 2 78.Inattentive 0 81.StealsHome 0 57.Attacks
0 52.Guilty 0 56g.Vomit 1 64.PreferYoung 1 84.StrangeBehav 0 82.StealsOther 0 68.Screams
1 71.SelfConsc 0 79.SpeechProb 2 85.StrangeIdeas 1 90.Swears 1 86.Stubborn
2 91.ThinkSuic 2 100.SleepProb 1 96.ThinksSex 2 87.MoodChang
2 112.Worries 0 99.Tobacco 2 89.Suspicious
0 101.Truant 0 94.Teases
1 105.UsesDrugs 2 95.Temper
0 97.Threaten
0 104.Loud
Copyright 2001 T.M. Achenbach B = Borderline clinical range; C = Clinical range Broken lines = Borderline clinical range
Child Behavior Checklist. Figure 1 Syndrome profile scored from the Youth Self-Report completed by 15-year-old Wayne Webster (From Achenbach & Rescorla, 2001, p. 33)
of syndrome scales scored from the YSR completed by McConaughy, & Howell, 1987). Consequently, profes-
15-year-old Wayne Webster (not his real name). sionals who work with children recognize the need to
obtain reports from multiple informants. Meta-analyses
of correlations between collateral and self-reports of
Scales on Which ASEBA Instruments adult psychopathology have also revealed only modest C
Are Scored correlations that argue for using multi-informant data to
assess adults (Achenbach, Krukowski, Dumenci, &
ASEBA problem items are scored on scales for syn- Ivanova, 2005).
dromes derived empirically via exploratory factor ana- Because each informant may provide valid and useful
lyses (EFAs) and confirmatory factor analyses (CFAs). information that differs from what other informants
These empirically derived syndromes reflect patterns of provide, data from multiple informants should be com-
problems found to co-occur in ratings by each kind of pared. Software for scoring ASEBA forms facilitates cross-
informant. informant comparisons by printing scores obtained from
In addition to the syndrome scales, each form is parallel forms on parallel profiles. In addition, it prints
scored on DSM-oriented scales constructed by having side-by-side comparisons of ratings by up to eight infor-
experts from many cultures select ASEBA problem items mants on all problem items that have counterparts on
that are very consistent with particular diagnostic cate- forms completed by different informants. It also prints Q
gories of the American Psychiatric Associations (1994) correlations that measure the degree of agreement be-
Diagnostic and Statistical Manual-Fourth Edition (DSM- tween each pair of informants and compares them with
IV). Like the syndrome scales, the DSM-oriented scales Q correlations between pairs of informants in large refer-
are displayed on profiles in terms of T scores, percentiles, ence samples.
and normal, borderline clinical, and clinical ranges. Most An especially useful kind of comparison between
forms are also scored on scales comprising critical items informants reports is illustrated in Fig. 2. This is a com-
that are of particular concern to clinicians. parison between syndromes scored from the YSR com-
The collateral and self-report forms are additionally pleted by Wayne Webster, CBCLs completed by Waynes
scored on scales for favorable characteristics, such parents, and TRFs completed by three of Waynes tea-
as competence, adaptive functioning, and personal chers. For each syndrome, such as the Anxious/Depressed
strengths. The particular items and scales are geared to syndrome shown in the upper left-hand corner, the bars
the developmental level of people being assessed and to reflect the magnitude of standard scores (T scores)
the informants knowledge of people being assessed. For obtained from ratings by each kind of informant. Because
example, parents of 6- to 18-year-olds provide data re- the T scores are based on ratings by each kind of infor-
garding their childrens involvement in sports, nonsports mant for a normative sample of children, the height of the
activities, organizations, jobs and chores, friendships, and bar indicates the level of the problems reported by a
relationships with parents, siblings, and peers. Teachers particular kind of informant compared to problems
provide data on childrens academic performance and reported by that kind of informant for a normative sam-
adaptive characteristics at school. For adults, data are ple of children. For example, the leftmost bars indicate
requested regarding friendships, relations with spouse or that the Anxious/Depressed syndrome scores obtained
partner, children, job, and enrolment in educational pro- from CBCL ratings by Waynes parents are above the top
grams. Only the items relevant to the adult being assessed broken line compared to parents CBCL ratings of a
are scored. For example, adults who lack a spouse or normative sample of adolescent boys. As scores above
partner, children, job, or enrolment in educational pro- the top broken line are in the clinical range, the CBCL
grams are not scored on those items. Adult forms also bars indicate that Waynes parents reported more pro-
have normed scales for substance use. blems of this syndrome than were reported by parents of
97% of boys in the normative sample.
Cross-Informant Comparisons
Multicultural Norms
Meta-analyses have revealed that correlations between
parent, teacher, and self-reports of childrens problems Norms obtained in one society may not be generalizable
are typically only low to moderate (Achenbach, to other societies. To determine the degree of
550
Cross-informant comparison - CBCL/TRF/YSR Syndrome scale T Scores (2001 version)
C
ID: 2301251405 Name: Wayne webster Gender: Male Birth date: 03/03/1986 Comparison date: 04/13/2001
Form Eval ID Age Informant name Relationship Date Form Eval ID Age Informant name Relationship Date
CBC1 001 15 Alice N. Webster Biological mother 04/04/2001 TRF5 005 15 Carmen Hernandez Classroom teacher {F} 04/11/2001
CBC2 002 15 Ralph F. Webster Biological father 04/05/2001 TRF6 006 15 Charles Dwyer Classroom teacher {M} 04/12/2001
YSR3 003 15 Self Self 04/08/2001
TRF4 004 15 George jackson Classroom teacher {M} 04/10/2001
Anxious/depressed Withdrawn/depressed Somatic complaints

100
90
80
70
60
50
72C 72C 70C 68B 61 63 82C 70C 83C 79B 74C 74C 58 61 64 50 58 62
CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6
Social problems Thought problems Attention problems

100
90
80
70
60
50
69B 69B 80C 70C 65B 69B 69B 66B 77C 70C 60 66B 71C 76C 63 68B 65B 64
CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6
Rule-breaking behavior Aggressive behavior

100
B = Borderline clinical range; C = Clinical range
90 Broken lines = Borderline clinical range
80 {F} = Female {M} = Male
70
60
50
57 62 56 63 53 53 73C 73C 67B 82C 65B 67B
CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6
Child Behavior Checklist. Figure 2 Cross-informant comparisons of syndrome scores for Wayne Webster (From Achenbach & Rescorla, 2001, p. 39)
generalizability across societies, the same assessment instruments, theory, and applications, as well as directions
instruments must be administered to large representative in which the ASEBA is now moving. Translations are
samples of people in different societies. This has been available in 85 languages. Over 6,500 publications by
done with ASEBA instruments in many societies. CFAs some 9,000 authors report use of the ASEBA in 80 cultural
of CBCL, TRF, and YSR data from many societies support groups and societies (Berube & Achenbach, 2010). ASEBA C
the generalizability of syndromes that were initially instruments are available in paper and Internet-based
derived from US samples. Comparisons of scale scores electronic versions in many countries around the world
show that the distributions of CBCL, TRF, and YSR scores for practical assessment in clinical, educational, forensic,
in many societies approximate those obtained in the USA. and other services, as well as for research on countless
However, some societies have substantially lower or topics, such as genetics, medical conditions, outcome
higher mean scores. To take account of societal differences evaluations, epidemiology, development, diagnosis, and
in scale scores, separate sets of norms have been con- multicultural comparisons. Because the ASEBAs concep-
structed for the societies obtaining relatively low scores, tual framework is open ended and generative, it continues
societies obtaining intermediate scores, and societies to advance in multiple directions (Achenbach, 2009).
obtaining relatively high scores. Because parent, teacher,
and self-ratings often yield different scores, the multicul-
tural CBCL, TRF, and YSR norms were constructed sepa- Psychometric Data
rately. For some societies, problem scores obtained from
one kind of informant are relatively low, while scores Table 2 summarizes psychometric data for all ASEBA
obtained from another kind of informant are intermedi- instruments in terms of mean alphas, test-retest reliability,
ate or high. For example, CBCL and TRF problem scores and the percentage of variance in ASEBA scale scores
obtained from Japanese parents and teachers are in the accounted for by clinical referral status, after partialing
low range, whereas YSR scores obtained from self-ratings out demographic effects. Many additional psychometric
by Japanese youths are in the intermediate range. findings including goodness of fit obtained from CFAs
To enable practitioners and researchers to compare in diverse samples are reported in ASEBA manuals and
CBCL, TRF, and YSR scores with culturally appropriate in refereed publications listed by Berube and Achenbach
norms, the scoring software provides options for displaying (2010).
problem scale scores in relation to norms for low-scoring,
intermediate-scoring, and high-scoring societies. For ex-
ample, CBCL and TRF scores for a Japanese youth would Clinical Uses
typically be displayed in relation to norms for low-scoring
societies. However, the youths YSR scores would be dis- ASEBA instruments have numerous clinical uses. Berube
played in relation to norms for intermediate-scoring socie- and Achenbach (2010) list publications reporting use of
ties. If the Japanese youth lived in the USA and attended an the ASEBA in relation to over 150 medical conditions.
American school, the TRF scores would be displayed in Some 600 publications report use of the ASEBA for eval-
relation to US norms for teachers ratings. If the youths uating treatments and outcomes for many kinds of psy-
parents were well acculturated to the USA, the CBCL scores chopathology and other problems.
could be displayed in relation to US norms and also in ASEBA instruments can be used at many stages of
relation to Japanese norms to see whether the scores were clinical processes, including screening to identify needs
clinically deviant according to either set of norms. for help, documentation of problems and adaptive func-
tioning for use in clinical referrals, and intake assessment
on which to base treatment decisions. During the course
Historical Background of treatment, ASEBA instruments are useful for determin-
ing whether goals are being met. Following the treatment,
The ASEBA stems from Achenbachs (1966) factor- ASEBA instruments can be readministered to evaluate
analytic derivation of syndromes of child and adolescent outcomes and subsequent functioning. At any point,
psychopathology. Since then, over 4 decades of research ASEBA instruments can be used to assess behavioral/
and practical experience have produced ASEBA instru- emotional concomitants of neuropsychological and med-
ments for ages 1 to 90 years. Achenbach (2009) docu- ical disorders. The availability of similar ASEBA instru-
ments the historical development of ASEBA research, ments for children and adults facilitates family
552 C Child Behavior Checklist
Child Behavior Checklist. Table 2 Summary of ASEBA psychometric data
Alphaa Reliabilityb Validityc

Instrument Narrow Broad Narrow Broad Narrow Broad
CBCL/15 0.76 0.92 0.82 0.89 11 17
C-TRF 0.80 0.94 0.78 0.85 13 20
CBCL/618 0.83 0.94 0.88 0.92 24 32
TRF 0.86 0.94 0.84 0.90 15 20
YSR 0.78 0.92 0.78 0.85 10 14
TOF 0.82 0.90 0.76 0.84 9 14
DOF 0.68 0.79 0.51 0.72 7 20
SCICA 0.70 0.84 0.75 0.80 9 16
ASR 0.78 0.93 0.84 0.91 10 14
ABCL 0.80 0.94 0.84 0.88 6 8
OASR 0.80 0.96 0.86 0.95 13 20
OABCL 0.83 0.97 0.94 0.95 19 29
Narrow, mean for syndrome and DSM-oriented scales; broad, mean for internalizing, externalizing, and total problems. Data are from manuals
listed in the Further Reading.
a
Cronbachs coefficient alpha for the internal consistency of scales.
b
Pearson rs for test-retest reliability over 8- to 16-day intervals. SCICA rs are between ratings by different interviewers who interviewed children
over intervals averaging 12 days.
c
Percentage of variance accounted for by clinical referral status (referred vs. nonreferred) in multiple regressions of referral status on ASEBA scale
scores with demographic variables partialed out.
assessment, as well as close coordination between inter- Achenbach, T. M., & Rescorla, L. A. (2003). Manual for the ASEBA adult
forms & profiles. Burlington, VT: University of Vermont, Research
ventions for parents and their children.
Center for Children, Youth, and Families.
Achenbach, T. M., & Rescorla, L. A. (2007a). Multicultural supplement to
the manual for the ASEBA school-age forms & profiles. Burlington,
References and Readings VT: University of Vermont Research Center for Children, Youth, and
Families.
Achenbach, T. M. (1966). The classification of childrens psychiatric symp- Achenbach, T. M., & Rescorla, L. A. (2007b). Multicultural understanding
toms: A factor-analytic study. Psychological Monographs, 80, (No. 615). of child and adolescent psychopathology: Implications for mental health
Achenbach, T. M. (2009). The Achenbach system of empirically based assessment. New York: Guilford Press.
assessment (ASEBA): Development, findings, theory, and applications. Achenbach, T. M., & Reescorla, L. A. (2010). Multicultural guide to the
Burlington, VT: University of Vermont, Research Center for manual for the ASEBA preschool forms & profilies. Burlington, Ver-
Children, Youth, and Families. mont, University of Vermont Research Center for Children, Youth,
Achenbach, T. M., Krukowski, R. A., Dumenci, L., & Ivanova, M. Y. and Families.
(2005). Assessment of adult psychopathology: Meta-analyses and American Psychiatric Association (1994). Diagnostic and statistical man-
implications of cross-informant correlations. Psychological Bulletin, ual of mental disorders (4th ed.). Washington, DC: Author.
131, 361382. Berube, R. L., & Achenbach, T. M. (2010). Bibliography of published
Achenbach, T. M., McConaughy, S. H., & Howell, C. T. (1987). Child/ studies using the Achenbach system of empirically based assessment
adolescent behavioral and emotional problems: Implications of (ASEBA). Burlington, VT: University of Vermont, Research Center
cross-informant correlations for situational specificity. Psychological for Children, Youth, and Families.
Bulletin, 101, 213232. McConaughy, S. H., & Achenbach, T. M. (2001). Manual for the semi-
Achenbach, T. M., Newhouse, P. A., & Rescorla, L. A. (2004). Manual for structured clinical interview for children and adolescents (2nd ed.).
the ASEBA older adult forms & profiles. Burlington, VT: University of Burlington, VT: University of Vermont, Research Center for Chil-
Vermont, Research Center for Children, Youth, and Families. dren, Youth, and Families.
Achenbach, T. M., & Rescorla, L. A. (2000). Manual for the ASEBA McConaughy, S. H., & Achenbach, T. M. (2004). Manual for the test
preschool forms & profiles. Burlington, VT: University of Vermont, observation form for ages 218. Burlington, VT: University of
Research Center for Children, Youth, and Families. Vermont, Research Center for Children, Youth, and Families.
Achenbach, T. M., & Rescorla, L. A. (2001). Manual for the ASEBA school- McConaughy, S. H., & Achenbach, T. M. (2009). Manual for the ASEBA
age forms & profiles. Burlington, VT: University of Vermont, direct observation form for ages 611. Burlington, VT: University of
Research Center for Children, Youth, and Families. Vermont, Research Center for Children, Youth, and Families.
Childhood Autism Rating Scales C 553
and the CARS was published as an appendix to the 1980

Childhood Autism article by Schopler, Reichler, DeVellis, and Daly. It was
originally intended for use by trained diagnosticians
Autistic Disorder making ratings based on observation; however, the mea-
sure has been expanded for use by others (e.g., physicians, C
speechlanguage pathologists, special educators, and
audiologists) as well as to include information from
Childhood Autism Rating Scales other sources such as parent report and classroom obser-
vations. It is important to note that the CARS was devel-
M AUREEN G RISSOM
oped prior to the DSM-IV concept of Autism as a
University of Missouri
spectrum of disorders (Magyar & Pandolfi, 2008).
Columbia, MO, USA
Synonyms Psychometric Data
The CARS Manual (1988) describes high internal consis-

CARS
tency reliability (alpha = 0.94) and an average interrater
reliability of 0.71 for two independent raters across 280
Description cases. Testretest reliability for 91 cases rated 1 year apart
by two separate raters was 0.88. The sensitivity of the
The childhood autism rating scale (CARS) is a 15 item CARS was 100% for a sample of 54 children with autistic
measure intended to assist in distinguishing children with disorder in a study by Rellini et al. (2003). However, there
autism spectrum disorder (ASD) from children with other is concern that the CARS may overdiagnose children with
types of delays. It is an observational scale in which each cognitive impairments as having autism with lower IQ
item is rated from 1 (within normal limits) to 4 (severely scores correlating with higher CARS scores (Perry, Con-
abnormal) and ratings include consideration of peculiarity, dillac, Freeman, Dunn-Geier, & Belair, 2005). In addition,
frequency, and duration of the behavior rated (Schopler, sensitivity in the Rellini et al. study was not as great for
Reichler, & Renner, 1988). It yields a total score ranging distinguishing children with Aspergers disorder and per-
from 15 to 60. Scores of 3036.5 suggest mild to moderate vasive developmental disorder-not otherwise specified
Autism and 3760 suggest severe Autism. However, when (PDD-NOS) from children with attention-deficit/hyper-
used with adolescents and adults, the cut-off has been activity disorder (ADHD) and language delay. Despite the
decreased to 28 (Schopler et al., 1988). fact that the CARS was initially published during the time
The CARS was initially developed using a sample of of the DSM-III, the CARS has shown good agreement
1,606 children, approximately three quarters of whom were with clinical diagnosis with the DSM-IV/ICD-10 criteria
male. Sixty seven percent of the sample was white, 30% (Perry, Condillac, Freeman, Dunn-Geier, & Belair, 2005).
African American, and 3% was of other racial descent. Several studies have looked at the relations between
Within the male and female samples, the age distribution the CARS and other measures intended to assist in the
was similar with 56% age 5 years or younger, 32% between diagnostic process. In one study, the CARS and the Au-
ages 6 and 10 years, and 11% age over 10 years. Seventy one tism Diagnostic Interview-Revised (ADI-R) were found
percent of the sample had an IQ (as determined by one of to correlate 91.8% for cases in which a child received a
various measures) below 70, 17% with an IQ between 70 and diagnosis of Autism and 44.4% for those in which an
84, and 13% with an IQ above 84 (Schopler et al., 1988). Autism diagnosis was not given (Pilowsky, Yirmiya, Shul-
man, & Dover, 1998). More recently, Saemundsen, Mag-
nusson, Smari, and Sigurdardottir (2003) found a
Historical Background correlation of 0.81 between the CARS (having a total
score greater than 30) and the ADI-R (meeting cut-offs
The CARS was developed at the University of North in all three domains) in a study that included 54 children.
Carolina at Chapel Hill and was used to evaluate children Several factor analyses of the 15 items comprising the
referred to the TEACCH program. The CARS has been in CARS have been conducted. Magyar and Pandolfi
use since 1971 (Reichler & Schopler, 1971) at which point (2007) found that four components: (1) a social com-
it was called the childhood psychosis rating scale (CPRS) ponent, (2) a negative emotionality construct, (3) a
554 C Childhood Epileptic Encephalopathy with Diffuse Slow Spike-and-waves
sensory and stereotypy construct, and (4) an activity Rating Scale (CARS). Journal of Autism and Developmental Disorders,
10, 91103.
level and consistency of intellectual response compo-
Schopler, E., Reichler, R. J., & Renner B. (1988). The Childhood Autism
nent, accounted for 57% of the variance in ratings. Rating Scale (CARS). Los Angeles, CA: Western Psychological
Services.
Clinical Uses
The CARS can be used as part of multimodal approach to

the diagnosis of ASD that includes observation of the Childhood Epileptic
child, caregiver interview, assessment of developmental
levels, detailed developmental history, and screening
Encephalopathy with Diffuse
for associated disorders such as Fragile X (Magyar & Slow Spike-and-waves
Pandolfi, 2007, p. 1787).
LennoxGastaut Syndrome
Cross References
Autism Diagnostic Interview-Revised

Aspergers Disorder Childhood or Adolescent Brain
Attention-Deficit/Hyperactivity Disorder Injury
Autism Diagnostic Observation Schedule
Autistic Disorder Pediatric Traumatic Brain Injury
Pervasive Developmental Disorder Not Otherwise
Specified
TEACCH
Childrens Category Test

VANESSA L. R AMOS , K EITH O. Y EATES
Magyar, C. I., & Pandolfi, V. (2007). Factor structure evaluation of the Nationwide Childrens Hospital
Childhood Autism Rating Scale. Journal of Autism and Developmen-
tal Disorders, 37, 17871794.
Columbus, OH, USA
Perry, A., Condillac, R. A., Freeman, N. L., Dunn-Geier, J., & Belair, J.
(2005). Multi-site Study of the Childhood Autism Rating Scale
(CARS) in Five Clinical Groups of Young Children. Journal of Autism Synonyms
and Developmental Disorders, 35, 625634.
Pilowsky, T., Yirmiya, N., Shulman, C., & Dover, R. (1998). The Autism
Diagnostic Interview-Revised and the Childhood Autism Rating
CCT
Scale: Differences between diagnostic systems and comparison be-
tween genders. Journal of Autism and Development Disorders, 28,
143151.
Reichler, R. J. & Schopler, E. (1971). Observations on the nature of Description
human relatedness. Journal of Autism and Childhood Schizophrenia,
1, 283296. The Childrens Category Test (CCT) is an abbreviated
Rellini, E., Tortolani, D., Trillo, S., Carbone, S., & Montecchi, F. (2004). version of the original Halstead Category Test (HCT;
Childhood Autism Rating Scale (CARS) and Autism Behavior
Checklist (ABC) Correspondence and Conflicts with DSM-IV
Reitan & Wolfson, 1992). The CCT is an individually
Criteria in Diagnosis of Autism. Journal of Autism and Developmen- administered instrument designed to measure nonverbal
tal Disorders, 34, 703708. learning and memory, concept formation, and problem-
Saemundsen, E., Magnusson, P., Smari, J., & Sigurdardottir, S. (2003). solving abilities. The CCT consists of two levels. Level 1 is
Autism Diagnostic Interview-Revised and the Childhood Autism given to children aged 58 and consists of five subtests
Rating Scale: Convergence and discrepancy in diagnosing Autism.
Journal of Autism and Developmental Disorders, 33, 319328.
and 80 items. Level 2 is given to children aged 916 and
Schopler, E., Reichler, R. J., DeVellis, R. F., & Daly, K. (1980). Toward consists of six subtests and 83 items. The childs task is to
objective classification of childhood autism: Childhood Autism identify the single conceptual rule underlying the items in
Childrens Category Test C 555
each subtest. The last subtest on both levels requires the deficits or speech/language difficulties (Boll, 1993). The
child to remember and reapply the conceptual rules from CCT can provide insights regarding a childs cognitive
previous subtests. abilities and learning strategies in terms of difficulties in
The CCT was normed on a stratified representative memory or shifting between conceptual ideas (MacNeil
sample of 920 children in 12 age groups ranging from Horton, 1996). However, a poor score on the CCT does C
5 years to 16 years, 11 months. Administration requires not necessarily indicate a neurologically based disorder;
approximately 1520 min. The raw score is the total rather it indicates a disruption in mental processing
number of errors (CCT Total), which is converted into (Boll, 1993).
an age-normed T-score (M = 50, SD = 10). The CCT is Studies of the CCTs sensitivity to brain dysfunction
easy to administer and score. indicate that the measure is not consistently sensitive to
structural brain damage or neurodevelopment disorders
in children (Bello, Allen, & Mayfield, 2008; Donders,
Historical Background 1996). Results from studies examining the sensitivity of
the CCT to various forms of brain dysfunction suggest
The CCT was developed in an effort to provide an efficient that the CCT assesses multiple dimensions of problem
and well-normed childrens version of the HCT, which is solving, rather than a general construct of abstraction
well documented to be sensitive to cerebral impairment (Nesbit-Greene & Donders, 2002), which has led some
(Reiten & Wolfson, 1992), and the previous childrens to caution against relying on the total error score as the
versions of the Category Test (Reiten & Wolfson, 1993). sole index of brain dysfunction (Allen, Knatz, & Mayfield,
Concerns about lengthy administration times and expen- 2006; Bello et al., 2008). The use of the CCT with brain-
sive, bulky equipment led to the development of various injured children may be hampered by the fact that the
short forms of these tests (e.g., Short Category Test Book- overall T-score is based on six different subtests that differ
let Format), with the most comprehensive of these efforts in their sensitivity to the severity of the injury (Nesbit-
resulting in the CCT (Boll, 1993). The CCT and California Greene & Donders, 2002). Another problem with using the
Verbal Learning Test-Childrens Version (CVLT-C) were CCT with brain-injured children is that it is untimed and
standardized and normed on the same population. children are provided with corrective feedback throughout
the test administration, and these features may compensate
for any deficits in processing speed or executive function
Psychometric Data that the child may be experiencing (Donders & Nesbit-
Greene, 2004). Overall, studies investigating the use of the
Median internal consistency reliability for the CCT Total CCT with brain-injured children suggest that caution is
score is 0.88 for Level 1 and 0.86 for Level 2, with average needed in interpreting the results, and that it should be
standard errors of measurement of 3.46 and 3.74, respec- supplemented with psychometric data from additional
tively (Boll, 1993). The separate age-level values and neuropsychological tests (Donders & Nesbit-Greene,
averaged coefficients indicate that the CCT possesses a 2004; Moore, Donders, & Thompson, 2004).
high degree of internal consistency across ages. The
manual reports a variety of studies demonstrating that
the CCT consistently and significantly correlates with Cross References
other measures of achievement or cognitive ability, such
as the WISC-R and CVLT-C. Concept Learning
Delis-Kaplan Executive Function System
Halstead-Reitan Neuropsychological Test Battery
Clinical Uses Memory (Including Memory Impairment)
Nonverbal Learning Disabilities
The CCT is a widely used test of the ability to solve Problem Solving
problems by developing and modifying strategies of
responding to various visual designs and patterns References and Readings
(Nesbit-Greene & Donders, 2002). The CCT does not
require demonstration of acquired skills, ability, or Allen, D. N., Knatz, D. T., & Mayfield, J. (2006). Validity of the childrens
knowledge, and eliminates potential confounding vari- category test-level 1 in a clinical sample of heterogeneous forms of
ables because it can be used with children with motor brain dysfunction. Archives of Clinical Neuropsychology, 21, 711720.
556 C Childrens Memory Scale
Bello, D. T., Allen, D. A., & Mayfield, J. (2008). Sensitivity of the childrens of both immediate and delayed (30 min) recall. Each
category test level 2 to brain dysfunction. Archives of Clinical
Auditory/Verbal subtest also provides a measure of recogni-
Boll, T. (1993). Childrens category test. San Antonio, TX: Psychological
tion recall.
Corporation. After administration of the core subtests (Table 1), the
Donders, J. (1996). Validity of short forms of the intermediate Halstead examiner can derive eight index scores: Attention/Con-
category test in children with traumatic brain injury. Archives of centration, Verbal Immediate, Verbal Delayed, Delayed
Recognition, Visual Immediate, Visual Delayed, Learning,
Donders, J., & Nesbit-Greene, K. (2004). Predictors of neuropsychologi-
cal test performance after pediatric traumatic brain injury.
and General Memory (Fig. 1). The learning Index is
Assessment, 11(4), 275284. derived using subtest scores from the Auditory/Verbal
MacNeil Horton, A. (1996). Book and test reviews. Archives of Clinical (Word Pairs) and the Visual/Nonverbal (Dot Locations)
Neuropsychology, 11, 171173. domains. The General Memory Index is a measure of
Moore, B. A., Donders, J., & Thompson, E. H. (2004). Validity of the
global memory functioning and is generated using both
childrens category test-level 1 after pediatric traumatic brain injury.
Archives of Neuropsychology, 19, 19.
the immediate and delayed memory indexes from the
Nesbit-Greene, K., & Donders, J. (2002). Latent structure of the childrens Auditory/Verbal and Visual/Nonverbal domains.
category test after pediatric traumatic head injury. Journal of Clinical The immediate portion of the core battery takes
and Experimental Neuropsychology, 24(2), 194199. approximately 3040 min to administer, with an additional
Reiten, R. M., & Wolfson, D. (1992). Neuropsychological evaluation of
1020 min required for administration of the delayed
older children. South Tucson, AZ: Neuropsychology Press.
Reiten, R. M., & Wolfson, D. (1993). The Halstead-Reitan neuropsycho-
recognition sections. Two record forms are provided for
logical test battery: Theory and clinical interpretation (2nd ed.). South students of 58 and 916 years. Scoring tables in the
Tucson, AZ: Neuropsychology Press. manual or computer software allow for conversion of raw
scores to scaled scores (mean = 10; SD = 3) at the individ-
ual subtest level and standard scores (mean = 100; SD = 15)
at the index level. Table 1 provides a brief description of
the core subtests.
Childrens Memory Scale
M ORRIS J. C OHEN
Medical College of Georgia Historical Background
Augusta, Georgia, USA
Development of the CMS began in 1985 to provide clin-
icians with a comprehensive, well-standardized, individu-
Synonyms ally administered instrument that would assess the
important processes involved in learning and memory
CMS within the pediatric population. Prior to this, traditional
psychological evaluation of children with neurological and
neurodevelopmental disorders included tests of intelli-
gence, achievement, and behavior/emotional functioning
Description with little if any attention paid to the childs ability to learn
and remember new information. This was the case despite
The Childrens Memory Scale (CMS), published in 1997,
the fact that most referrals were in some way related to the
provides a comprehensive assessment of learning and mem-
students inability to learn and remember school-related
ory in children and adolescents of ages 5 through 16 years.
content. As a result, the CMS was developed with five goals
The CMS is individually administered and designed to be
in mind:
used as part of a standard psychological or neuropsycho-
logical evaluation. It assesses declarative learning and mem- 1. The development of an instrument that was consistent
ory functions across three domains: Auditory/Verbal, with current theoretical models of learning and memory.
Visual/Nonverbal, and Attention/Concentration (working 2. The development of an instrument that was sensitive
memory). Each domain contains two core subtests and to developmental changes over time.
one supplemental subtest. The subtests comprising the 3. To evaluate the relationship between memory and
Attention/Concentration domain provide measures of at- intelligence and provide the clinician with a mecha-
tention and working memory. Each subtest in the Auditory/ nism to meaningfully evaluate discrepancies between
Verbal and Visual/Nonverbal domains provide measures IQ and learning/memory performance.
Childrens Memory Scale C 557
Childrens Memory Scale. Table 1 Description of CMS core index and subtest components
Core
Core Index Subtest Subtest Description
Verbal Memory Indexes Stories Two stories (age-dependent 58-, 912-, and 1316-year olds) are read.
(Immediate, Delayed, and Immediately after presentation of each story, the child is asked to repeat as
C
Recognition) much of the story as can be remembered. In the delayed portion, the child
retells the stories and then answers questions about the stories (recognition
recall).
Word Pairs A list of 10 or 14 (age-dependent 58-year olds; 916-year olds) related and
unrelated word pairs are read; thereafter the stem is read and the child recalls the
associate. Three learning trials are administered followed by a free recall. In the
delayed portion, the child is asked to recall the word pairs spontaneously
followed by a recognition section.
Visual/Non-Verbal Memory Dot The child is shown an array of dots (blue) located within a rectangle in a stimulus
Indexes (Immediate and Locations book. This page is removed and the client is asked to replicate the spatial location
Delayed) of the dots by placing chips on a 3 4 or 4 4 rectangular grid (depending on
age 6 dots for 58-year olds; 8 for dots 916-year olds). Three learning trials are
administered followed by presentation of a distractor array (red dots) after which
an immediate recall trial is presented. In the delayed portion, the child is asked to
reproduce the original blue dot array.
Faces The child is presented with a series of 12 (58-year olds) or 16 (916-year olds)
pictured human faces one at a time. In the immediate and delayed recall sections,
the child is asked to identify the stimulus faces from a different set of foils (36 or
48 colored photos).
Attention/Concentration Numbers A digit span forwards and backwards task (similar to the WISC-III subtest).
Index Sequences The client is asked to mentally sequence or manipulate information as quickly as
possible. The 12 items include such tasks as reciting numbers, days of the week
and months in forward and reverse order, and counting by 2s, 4s, and 6s. Scoring
is based upon accuracy and speed.
4. The inclusion of a diversified selection of clinically and Psychometric Data

educationally relevant tasks that would allow clini-
cians to indentify and characterize learning and mem- The CMS was standardized on a representative US sample
ory disorders in children and help them to design of 1,000 children. The sample was stratified according to age
remedial and compensatory programs based upon (10 age groups ranging in age from 5 to 16 years; 100 per age
the childs performance. group), sex (equal number of males and females in each age
5. The development of an instrument that could be suc- group), race/ethnicity (White, African American, Hispanic,
cessfully administered within a standardized testing and other), geographic region (northeast, north central,
situation and also be child friendly. south, west), and parent education level (five categories
ranging from <8th grade to university degree). Further,
As such, the CMS focused upon the assessment of de-
the CMS is the only memory assessment instrument to
clarative memory with no attempt made to formally
provide a linking sample co-normed with an individually
evaluate procedural memory, which involves skill
administered intelligence scale (WISC-III and WPPSI-R).
learning and classical conditioning. Further, the CMS
This sample was comprised of 300 children (ages 516; 50%
was unable to provide measures of long-term memory
male 50% female) and provided the examiner with an
beyond 30 min due to the time restriction of a traditional
empirically grounded basis for predicting the level of mem-
assessment and the logistical problems inherent in the
ory performance from IQ and determining when a childs
reevaluation of the standardization sample over a longer
memory performance deviated significantly from IQ
time interval.
558 C Childrens Memory Scale
Domain Subtests Indexes

Stories* Verbal
Word pairs* Immediate
Word lists**
Auditory/verbal
Stories 2* Verbal
Word pairs 2* Delayed
Word lists 2**
Delayed
Recognition
Learning
Dot locations* Visual

Faces* Immediate
Family pictures**
Visual/nonverbal
Dot locations 2* Visual

Faces 2* Delayed
Family pictures 2**
Numbers* Attention/
Attention/concentration Sequences* Concentration
Picture locations**
Note: *Core subtest; **Supplemental subtest
Childrens Memory Scale. Figure 1 Structure of the childrens memory scale
expectancy. With the release of the WISC-IV in 2004, a With respect to validity, the results of confirmatory
smaller correlation study was conducted involving 126 chil- factor analysis yielded a three-factor solution consisting of
dren of ages 616 years (Drozdick, Holdnack, Rolfhus, & Auditory/Verbal memory, Visual/Nonverbal memory,
Weiss, 2005). The authors provide tables which allow for and Attention/Concentration. The manual also provides
ability-memory discrepancy analysis using the predicted concurrent validity studies with different measures of
actual or simple difference methods and base rates. intelligence and achievement, which consistently show a
The CMS manual provides both split-half and test- moderate positive correlation. The CMS correlations with
retest reliability coefficients for the index scores and subt- measures of executive functioning and language were low
ests. For the indexes, average split-half reliability estimates to moderate. Finally, with respect to other measures of
ranged from .76 to .91. Average split-half reliability esti- memory, moderate to high correlation were obtained
mates for the subtests ranged from .71 to .91. Test-retest across the indexes of the CMS and Wechsler Memory
reliability (mean re-test interval 59.6 days) was assessed ScaleIII, and low to moderate correlations were obtained
across three age bands using a sample of 125 students. across the indexes of the CMS and the Wide Range As-
Reliability estimates ranged from .29 to .89 for the indexes. sessment of Learning and Memory. More recently, perfor-
Due to the nature of memory assessment and psychometric mance on both the CMS and WRAML-2 was reported as
considerations (restriction of range), decision consistency low to moderate in the latter tests Examiners Manual
test-retest coefficients were also calculated. These ranged (Sheslow & Adams, 2003).
from .61 to .93 for the indexes and from .71 to .93 for the
core subtests. Results indicated a general practice effect of
up to one standard deviation, similar to what was obtained Clinical Uses
on the WISC-III. Inter-rater reliability was also assessed on
subtests requiring subjective scoring (e.g., stories) and was As previously stated, the CMS was designed to be used as
found to be high. part of a standard psychological or neuropsychological
Chlordiazepoxide C 559
evaluation in order to provide a comprehensive assess-

ment of learning and memory in children and adolescents Chi-square
of ages 516 years. The clinical sensitivity and usefulness of
the CMS was demonstrated by the inclusion of case studies M ICHAEL D. F RANZEN
and clinical validity studies in the test manual. These in- Allegheny General Hospital
Pittsburgh, PA, USA
C
cluded individual studies comparing the performance of
children with temporal lobe epilepsy, traumatic brain inju-
ry, brain tumors, learning disabilities, ADHD, and specific
language impairment to that of normal controls. Additional Definition
studies have been published examining learning and mem-
ory performance in children with dyslexia and/or ADHD Chi-square is a nonparametric statistic that evaluates the
(Kibby & Cohen, 2008), and specific language impairment likelihood that two observed distributions are different.
(Riccio, Cash, & Cohen, 2007). The relationship between The first step to calculating a chi-square is to construct a
continuous performance testing and performance on the contingency table in which observations are plotted
CMS has been investigated in a clinic sample (Riccio, on the basis of the values of the relevant variables. For
Garland, & Cohen, 2007). Studies have also been reported example, a contingency table might be constructed
on learning and memory performance of children with where one axis is gender and the other axis is diagnosis.
complex partial epilepsy of temporal origin, using an The chi-square would describe whether female and male
experimental version of the CMS (Cohen, 1992; Cohen, patients have approximately the same distribution of
Holmes, Campbell, Smith, & Flanigan, 1990). diagnoses.
Cross References
Cross References
Memory
Wechsler Memory Scale Correlation Coefficients
Wide Range Assessment of Memory and Learning
Cohen, M. J. (1992). Auditory/verbal and visual/spatial memory in chil- Castellan, N. J. Jr. (1965). On the partitioning of contingency tables.
dren with complex partial epilepsy of temporal lobe origin. Brain Psychological Bulletin, 64, 330338.
and Cognition, 20, 315326.
Cohen, M. J. (1997). Childrens memory scale. Administration manual.
San Antonio, Texas: The Psychological Corporation.
Cohen, M. J., Holmes, G. L., Campbell, R., Smith, J. R., & Flanigan, H. F.
(1990). Memory performance following unilateral electrical stimu-
lation of the hippocampus in a child with right temporal lobe
Chlordiazepoxide
epilepsy. Journal of Epilepsy, 3, 115122.
Drozdick, L. W., Holdnack, J., Rolfus, E., & Weiss, L. (2005). Technical J OHN C. C OURTNEY
report #5 WISC-IV and childrens memory scale. San Antonio, Texas: Childrens Hospital of New Orleans
Harcourt Assessment. New Orleans, LA, USA
Kibby, M. Y., & Cohen, M. J. (2008). Memory functioning in children
with reading disorders and/or attention-deficit/hyperactivity disor-
der: A clinical investigation of their working memory and long-term
memory functioning. Child Neuropsychology, 14, 525546. Generic Name
Riccio, C. A., Cash, D. L., & Cohen, M. J. (2007). Learning and memory
performance of children with specific language impairment (SLI). Chlordiazepoxide
Applied Neuropsychology, 14, 255261.
Riccio, C. A., Garland, B. H., & Cohen, M. J. (2007). Relations between
the test of variables of attention (TOVA) and the childrens memory
scale (CMS). Journal of Attention Disorders, 11, 167171.
Sheslow, D., & Adams, W. (2003). Wide range assessment of memory
Brand Name
and learning -2. Administration manual. Wilmington, DE: Jastak
Associates. Librium, Librax
560 C Chlorpromazine
Class
Chlorpromazine
Anxiolytic
J OHN C. C OURTNEY 1, C RISTY A KINS 2
1
Proposed Mechanism(s) of Action 2
Mercy Family Center
Metarie, LA, USA
Chlordiazepoxide binds to the GABA-A ligand-gated
chloride channel complex and, thereby, enhances the in-
hibitory effects of GABA. Generic Name
Chlorpromazine
Indication
Anxiety disorders, symptoms of anxiety, preoperative ap- Brand Name

prehension and anxiety, and withdrawal from acute
alcoholism. Thorazine
Side Effects Class
Serious Conventional antipsychotic
Respiratory depression, kidney dysfunction, and liver

disorders (rare).
Blocks dopamine 2 receptors; dopamine D2, histamine

Common H1, and cholinergic M1 blockade in the vomiting center
(area postrema)
Sedation, dizziness, depression, forgetfulness, confusion,
and hyperexcitability.
Indication
References and Readings Schizophrenia, nausea, vomiting, restlessness before sur-

gery, manic episodes of bipolar disorder, tetanus
PDR.
(2nd ed.). New York, NY: Cambridge University Press. Off Label Use
Bipolar disorder
Side Effects
Serious
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList Neuroleptic malignant syndrome, jaundice, agranulocy-
Pill Identification: http://www.drugs.com/pill_identification.html tosis, seizures
Cholesterol C 561
Common cholesterol. In the presence of high circulating concentra-

tions, LDL-cholesterol gradually builds up in and on the
Neuroleptic-induced deficit syndrome, akathisia, extrapy- walls of the coronary, cerebrovascular, or peripheral
ramidal symptoms, priapism, amenorrhea arteries. Together with coagulation factors and platelets,
cholesterol deposits on the vessel walls can form thick C
hard plaques which, over time, can occlude the blood
References and Readings vessels in a process called atherosclerosis. Therefore,
a high level of LDL-cholesterol (usually greater than
Physicians Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson 160 mg/dL) indicates an increased risk of heart disease
PDR. and, to a lesser extent, stroke. For this reason, LDL-choles-
terol is often called bad cholesterol. About one-third of
the circulating cholesterol is transported by high-density
lipoprotein (HDL), which more commonly carries the cho-
lesterol away from the arteries, and toward the liver where
it is metabolized and eliminated. It has been suggested
that HDL removes excess cholesterol from plaques, and
consequently HDL-cholesterol is known as good choles-
Free Drug Online and PDA Software: www.epocrates.com terol because a high HDL-cholesterol level seems to
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs. protect against coronary heart disease. Typically, the
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList liver meets all of the bodys requirements for cholesterol
by manufacturing it, which means that dietary cholesterol
is not needed for nutritional purposes. In foods, saturated
fatty acids, and to a lesser extent, trans fats, are the main
sources of elevated blood cholesterol levels. Measures to
Cholesterol reduce elevated cholesterol levels include reductions in
dietary cholesterol intake, cholesterol-lowering medica-
E LLIOT J. R OTH tions, increases in physical activity levels (which increase
Northwestern University HDL-cholesterol), and cessation of smoking.
Chicago, IL, USA
Cross References
Synonyms
Atherosclerosis
Fats; Lipids Cerebrovascular Disease
Coronary Disease
Ischemic Stroke
Definition Myocardial Infarction
Peripheral Vascular Disease
Cholesterol is a naturally occurring lipid found in the Stent
bloodstream and in cells throughout the body. It is an Thrombosis
important component of cell membranes and some hor-
mones. However, hypercholesterolemia, or high blood References and Readings
concentrations of cholesterol, is a major risk factor for
heart disease and stroke. Fletcher, B., Berra, K., Ades, P., Braun, L. T., Burke, L. E., Durstine, J. L.
et al. (2002). Managing abnormal blood lipids: A collaborative
approach. Circulation, 112, 31843209.
Current Knowledge National Cholesterol Education Program Expert Panel on Detection,
Evaluation, and Treatment of High Blood Cholesterol in Adults
(Adult Treatment Panel III): Third Report of the National Choles-
Cholesterol does not typically exist on its own in the blood; terol Education Program (NCEP) Expert Panel on Detection, Evalu-
it is transported to and from cells by lipoprotein molecules. ation, and Treatment of High Blood Cholesterol in Adults (Adult
Low-density lipoprotein (LDL) is the major carrier of Treatment Panel III). (2002). Circulation, 106, 31433421.
562 C Cholinergic System
When acetylcholine binds to the nicotinic receptor, it

Cholinergic System generates the opening of the ion pore, causing a rapid
influx of cations. There are four nicotinic receptor
C OLLEEN E. J ACKSON subtypes (N1, N2, N3, and N4), as well as a, b, d, and g
University of Connecticut subunits for each subtype.
Storrs, CT, USA Muscarinic: The muscarinic acetylcholine receptor
type forms G protein-coupled channels in the membranes
of neurons receptive to acetylcholine. When acetylcholine
Synonyms binds to one of these metabotropic channels, it generates a
cascade of information transduction within the cell via
Acetylcholinergic system intracellular proteins. There are five muscarinic receptor
subtypes (M1, M2, M3, M4, and M5). All five receptor
subtypes are present in the central nervous system;
Definition however, M1, M2, and M4, are more predominant.
The cholinergic system is composed of organized nerve

cells that use the neurotransmitter acetylcholine in
the transduction of action potentials. These nerve cells Cholinergic Projections
are activated by or contain and release acetylcholine dur-
ing the propagation of a nerve impulse. The cholinergic The cholinergic system is formed by a broadly projecting
system has been associated with a number of cognitive circuitry, as well as local circuitry. Long-projection cho-
functions, including memory, selective attention, and linergic neurons originating in the nuclei of the basal
emotional processing. forebrain project widely throughout the brain. For exam-
ple, the nucleus basalis of Meynert and the diagonal band
of Broca, both structures within the basal forebrain, trans-
Current Knowledge mit acetylcholine to the cerebral cortex. In addition, cho-
linergic projections exist between the septal nucleus and
Acetylcholine Synthesis and Metabolism the hippocampus. Local cholinergic circuitry within the
striatum has important interactions with nigrostriatal
The synthesis of acetylcholine, the neurotransmitter used dopamine neurons and striatal GABAergic neurons
by nerve cells in the cholinergic system, requires choline, a involved in extrapyramidal movement.
natural amine found in the lipid bilayer of the cell mem-
brane, and acetyl coenzyme A (acetyl-CoA), a thioester
used in metabolic reactions and an acceptor and donor of Cognitive Role of the Cholinergic System
acetyl groups. These molecules are catalyzed by choline
acetyltransferase, an enzyme found only in acetylcholiner- The cholinergic system has been implicated in a number
gic cells, in order to produce acetylcholine. of cognitive abilities, including attention, memory, and
In the metabolism of acetylcholine, acetylcholinester- emotional processing. Both human and animal studies
ase degrades the molecule to produce choline and acetic indicate that cholinergic input originating in the basal
acid. The choline molecules generated through this reac- forebrain mediates sustained attentional performance
tion are transported, via a high-affinity choline uptake (see Sarter, Givens, & Bruno, 2001 for review). In addi-
protein, back to the nerve terminal. They are then used to tion, the cholinergic system also acts as a modulator of
synthesize new acetylcholine molecules. level of processing (e.g., primitive responses such as
reflexes vs. limbic system responses vs. evaluative and
discriminative executive functioning processes). Broadly,
Cholinergic Receptor Types and Subtypes activation of the cholinergic system supports attentional
processing of threat-related stimuli (Berntston, Sarter, &
Nicotinic: The nicotinic acetylcholine receptor type forms Cacioppo, 1998), while specific projections to the medial
ligand-gated ion channels in the membranes of neurons prefrontal cortex influence anxious responses to contex-
receptive to acetylcholine. As an ionotropic receptor, the tual stimuli (Hart, Sarter, & Bernston, 1999). By influen-
nicotinic receptor is directly linked to an ion channel. cing arousal and attention, acetylcholine also impacts
Cholinergic System C 563
working memory and the attentional processes required agent is currently being assessed as a treatment for schizo-
for error detection (see Sarter, Gehring, & Kozak, 2006 for phrenia (Lameh et al., 2007).
review). Emotional processing is also intricately related to
the cholinergic system; additionally, cholinergic inputs
to the frontoparietal cortex may influence how attention Future Directions C
is directed toward emotional information (Bentley, Vuilleu-
mier, Thiel, Driver, & Dolan, 2003). As would be expected Future research focused on the interaction between the
from a system influencing such a variety of cognitive cholinergic system and other neurotransmitters (e.g., nor-
functions, decreased cholinergic tone, associated with epinephrine, dopamine, and serotonin), and neuromodu-
Alzheimers disease, results in impaired cognitive perfor- lators (e.g., substance P) will be important in
mance broadly extending to memory, attention, and understanding the complexities that exist within the
executive functioning (Terry & Buccafusco, 2003). brain and body regarding the communication of chemical
signals. Further development of biomarkers (e.g., behav-
ioral, electrophysiological, and neuroimaging) associated
Pharmacological Agents Acting on the with cholinergic decline will allow for improved identifi-
Cholinergic System cation of disorders associated with the cholinergic system.
A continued focus on the role of the cholinergic system in
Pharmacological agents impact the cholinergic system in Alzheimers disease, as well as the development of phar-
a number of different ways. At the receptor level, nicotinic maceutical interventions targeting the cholinergic system
acetylcholine agonists stimulate cholinergic activity large- in the treatment of this disease (e.g., alpha-7 subunit
ly in peripheral acetylcholine neurons. However, nicotine, nicotinic agonists), remains critical, particularly with the
a nicotinic acetylcholine agonist acts at nicotinic receptors continued rise in the elderly population. Finally, research
in the central nervous system. Nicotinic acetylcholine on the role of the cholinergic system in a number of
antagonists acting on cells in the central nervous system psychological disorders, including stress, affective and
are rarely used in clinical practice. panic disorders, and schizophrenia, will continue to high-
Pilocarpine is an example of a muscarinic acetylcho- light the broad implications on mental health that this
line agonist that acts on the parasympathetic nervous system has.
system. While pilocarpine is not used clinically to treat
central nervous system disorders, it has a range of side
effects, including excessive sweating and salivation, which Cross References
are related to its action on muscarinic receptors in the
parasympathetic nervous system. Muscarinic acetylcho- Alzheimers Disease
line antagonists, such as scopolamine and atropine, block Cholinesterase Inhibitors
muscarinic receptors. Their anticholinergic effects on the Memory
parasympathetic nervous system result in side effects such Memory Impairment
as dry mouth, constipation, and tachycardia. Mild Cognitive Impairment
Acetylcholinesterase inhibitors, such as tacrine and
donepezil, block the breakdown of acetylcholine in the
synaptic cleft. The result is sustained levels of acetylcho- References and Readings
line in the synapse that are capable of transmitting
chemical information to other cells. Acetylcholinester- Bentley, P., Vuilleumier, P., Thiel, C., Driver, J., & Dolan, R. (2003).
ase inhibitors are commonly used in the treatment of Cholinergic enhancement modulates neural correlates of selective
attention and emotional processing. Neuroimage, 20, 5870.
Alzheimers disease, as well as Lewy Body dementia.
Bodick, N. C., Offen, W. W., Levey, A. I., Cutler, N. R., Gauthier, S. G.,
Presently, there is a developing focus on the choliner- Satlin, A., et al. (1997). Effects of xanomeline, a selective muscarinic
gic system in the treatment of schizophrenia. Xanomeline, receptor agonist, on cognitive function and behavioral symptoms in
an M1/M4 muscarinic acetylcholine agonist that was Alzheimer disease. Archives of Neurology, 54, 465473.
initially assessed as a possible treatment for Alzheimers Lameh, J., Burstein, E. S., Taylor, E., Weiner, D. M., Vanover, K. E., &
Bonhaus, D. W. (2007). Pharmacology of N-desmethylclozapine.
disease, has shown efficacy in treating psychotic
Pharmacology & Therapeutics, 115, 223231.
symptoms (Bodick et al., 1997). In addition, N-des- Sarter, M., Givens, B., & Bruno, J. P. (2001). The cognitive neuroscience of
methylclozapine (norclozapine, NDMC), a metabolite of sustained attention: Where top-down meets bottom-up. Brain Re-
the antipsychotic clozapine, is a partial M1 agonist. This search Reviews, 35, 146160.
564 C Cholinesterase Inhibitors
Sarter, M., Gehring, W. J., & Kozak, R. (2006). More attention must be
paid: the neurobiology of attentional effort. Brain Research Reviews, Chorea
51, 145160.
Terry, A., & Buccafusco, J. (2003). The cholinergic hypothesis of age
A NNA D E P OLD H OHLER 1, M ARCUS P ONCE DE LEON2
and Alzheimers disease-related cognitive deficits: recent challenges 1
and their implications for novel drug development. Journal of Phar- Boston University Medical Center
macology and Experimental Therapeutics, 306, 821827. Boston, MA, USA
2
El Paso, TX, USA
Cholinesterase Inhibitors
Synonyms
J OA NN T. T SCHANZ
Utah State University Dance-like
Logan, UT, USA
Synonyms Definition
Acetylcholinesterase inhibitors; AchEIs; Anticholinester-
Chorea is characterized by brief, irregular muscle
ase inhibitors; CHEIs
contractions that are not repetitive or rhythmic,
but appear to flow from one muscle to the next.
Definition They may appear as dance-like movements of the
limbs, trunk, or head. Typical movements include facial
Cholinesterase inhibitors are a class of medications used in grimacing, shoulder adduction, and finger extension
the treatment of Alzheimers disease (AD) that targets the and contractions. They can be associated with snakelike
cholinergic neurotransmitter system. The treatment is writhing movements of the hands or feet known as
based on the observation of a cholinergic deficiency in athetosis.
AD. Cholinesterase inhibitors block the activity of acetyl-
cholinesterase, the primary enzyme that breaks down ace-
tylcholine, and allows the neurotransmitter substance to
remain in the synaptic cleft longer in order to stimulate Current Knowledge
postsynaptic receptors. These drugs do not prevent the
further degeneration of cholinergic neurons. They are mod- Chorea is a feature of Huntingtons disease, and may be
estly effective in the short-term improvement of attention, present with rheumatic fever. It can be seen as a side effect
concentration, memory, and some behavioural symptoms, of the medication levodopa or the dopamine agonists and
but are not thought to alter the progression of the disease. may result from metabolic disorders, endocrine disorders,
and vascular incidents.
Cross References
Alzheimers Dementia Cross References

Alzheimers Disease
Anticholinesterase Inhibitors Huntingtons Disease
Orgogozo, J.-M. (2003). Treatment of Alzheimers disease with cholines-

terase inhibitors. An update on currently used drugs. In K. Iqbal &
B. Winblad (Eds.), Alzheimers disease and related disorders: Research Marshall, F. J. (2004). Clinical features and treatment of Huntingtons
advances (pp. 663675). Bucharest, Romania: Ana Asian Interna- disease. In R. L. Watts, & W. C. Koller (Eds.), Movement disorders
tional Academy of Aging. (2nd ed., pp. 589603). New York: McGraw-Hill.
Christensen, Anne-Lise (1926 ) C 565
qualitatively oriented LNI continues to be used in Eur-

Christensen, Anne-Lise (1926 ) ope, and somewhat less frequently in the USA
A NTHONY Y. S TRINGER
Emory University Education and Training C
Atlanta, GA, USA
19541955 Visiting research fellow at Radcliffe
University
Landmark Clinical, Scientific, and 1956 Master of Arts in Psychology, University of
Professional Contributions Copenhagen, Denmark
1957 Doctor of Philosophy, University of Copenha-
In 1966, Anne-Lise Christensen reviewed a newly gen, Denmark
published English translation of Aleksandr Lurias
Christensen began attending the University of Copenha-
(1966) Higher Cortical Functions in Man and instantly
gen in 1945, shortly after the liberation of Denmark from
realized its value in the clinical bedside examination of
the Nazi occupation. She writes about the overwhelming
cognitive function in neurological patients. Luria
experience of freedom and peace . . . [when] the borders
provided a comprehensive theory of the brain organi-
were opened, and we were full of hope and expectations
zation, from which cognitive tasks could be developed
for the future (Christensen, 2002, p. 119). Her studies
to measure various cortical functions. However, Lur-
were interrupted for 6 years by marriage and mother-
ias scholarly presentation required some adaptation
hood, but she returned to the university in 1952, dividing
before it could be practically applied by clinicians.
her time between literature and psychology. Christensen
Christensen began to translate Lurias methods into
was accepted at Radcliffe University in 1954, where she was
her native Danish as well as adapt them for use in the
exposed to the work of Talcott Parsons, Gordon Allport,
clinic. Responding to Lurias invitation, Christensen
Gardner Lindzey, and George Mandler. She cites, Jerome S.
visited him in Moscow and presented her Danish
Bruner, however, as her greatest influence. In his work,
translation. Luria labeled it a vulgarization of his
Christensen was exposed to New Look Psychology
method, but added he had always wanted someone
which took the methods of the psychophysics laboratory
to do this. He encouraged Christensen to do an En-
and applied them to everyday perceptual experience.
glish translation. Five years later, Christensen pre-
Christensen returned to Denmark in 1955 and
sented the first English draft to Luria on her second
completed her doctoral studies at the University of
visit to Moscow. Luria made edits and provided a
Copenhagen in 1957. Bruner continued to influence
paper for Christensen to translate and include in the
Christensens career for more than a decade later when
final draft. Christensen published Lurias Neuropsy-
he insisted she introduced herself to Luria at a 1969
chological Investigation (LNI) in 1975, including a
conference in London. Impressed with her attempts at
textbook, manual, and stimulus cards.
using his method in Denmark, Luria invited Christensen
The LNI introduced a qualitative approach to neuro-
to visit him in Moscow, but a sudden heart attack pre-
psychological examination, which contrasted with the
vented his participation in the conference. Nonetheless,
predominant quantitative batteries used in the USA.
an official invitation arrived in Denmark, and Christensen
The LNI is one of the few theory-based assessment
made her visit to the Bourdenko Neurosurgical University
approaches in neuropsychology and has been lauded
Institute to work with Luria in September 1970 (Chris-
for its flexible administration, brevity, and qualitative
tensen, 2002). This began the collaboration between
focus (Kolb & Wishaw, 1990). It has also been criti-
the two, which resulted in the introduction of the LNI
cized for its lack of norms and insensitivity to mild
to the West.
impairment (Lezak, 1983). Though Christensen de-
clined to collaborate, Charles Golden and colleagues
(Golden, Purisch, & Hammeke, 1979) in the USA Major Appointments
attempted to standardize the administration of the
LNI and establish a normative base for interpretation. University Hospital of Aarhus (Psychiatry and Neuro-
This unfortunately violated the original qualitative surgery Departments), Jutland, Denmark, 19591968
focus of the LNI and generated considerable contro- University Hospital of Aarhus (Head of Clinical Psy-
versy and criticism. Nonetheless, Christensens original chological Department), Jutland, Denmark, 19691981
566 C Chromosome
University of Copenhagen (Research Neuropsycholo- Luria, Alexander Romanovich (19021977)

gist), Denmark, 19811985 Luria Nebraska Neuropsychological Battery
Center for Rehabilitation of Brain Injury (Founder Qualitative Neuropsychological Assessment
and Director), University of Copenhagen, Denmark,
19851998
University of Copenhagen (Professor of Neuropsy-
chological Rehabilitation), Denmark, 19851998
Christensen, A.-L. (1975). Lurias neuropsychological investigation. Manual
and test materials. New York: Spectrum Publications.
Major Honors and Awards Christensen, A.-L. (2002). Lifelines. In A. Y. Stringer, E. L. Cooley, & A.-L.
Christensen (Eds.), Pathways to prominence in neuropsychology:
1987 Lady of the Dannebrog Order (bestowed by the Reflections of twentieth-century pioneers (pp. 119137). New York:
Psychology Press.
Queen of Denmark) Golden, C. J., Purisch, A. D., & Hammeke, T. A. (1979). The Luria-
1994 Philosophia Doctor Honoris Causa, University Nebraska neuropsychological battery. Lincoln: University of Nebraska
of Lund, Sweden Press.
Kolb, B., & Wishaw, I. Q. (1990). Fundamentals of human neuropsychology
(3rd ed.). New York: Freeman.
Lezak, M. (1983). Neuropsychological assessment (2nd ed.). New York:
Short Biography Oxford University Press.
Luria, A. R. (1966). High cortical functions in man (2nd ed.). New York:
A deep and lasting penchant for collaboration is evident Basic Books.
both in Anne-Lise Christensens personal and professional
lives. At 19, she married Niels Egmont Christensen, a
former classmate. Their careers progressed in tandem.
While Anne-Lise was at Radcliffe, Niels was at Harvard.
They were at the University of Aarhus together beginning Chromosome
in 1959, and Niels became the Chair of the Philosophy
Department just a year before Anne-Lise became the M ARTIN H AHN 1, R OHAN PALMER 2
1
Chair of Clinical Psychology. Over the course of her William Paterson University
career, Christensen has had many distinguished collabora- Wayne, NJ, USA
2
tors, colleagues, and mentors. Besides Bruner and Luria, University of Colorado at Boulder
she cites the noted neuropsychologists Elkhonon Gold- Boulder, CO, USA
berg (whom she met in Moscow while training with
Luria), Edith Kaplan, and Muriel Lezak, and neuroscien-
tists Donald Stein and Stanley Finger (Christensen, 2002). Definition
Her collaborations have always been international
in scope, stretching across Europe and the Americas. Chromosomes are threadlike structures made of proteins
Her collaboration with her husband Niels came to a sad and nucleic acids. They are found in the nucleus of
ending with his suicide in 1980 after battling bipolar eukaryotic cells and carry genetic information along
disorder. Yet, even after retiring, her international colla- their length in the form of genes. In the early 1900s, Walter
borations continued, with Christensen recently serving Sutton and Theodor Boveri argued that the understanding
on the Board of Consultants for the SARAH Network of chromosomes was consistent with Mendelian genetics,
Hospitals in Brazil, a complex of facilities, she believes and the result of their thinking is called the chromosome
bridge the chasm between humanistic and empirical theory of heredity. A part of that theory is that Mendelian
scientific approaches to rehabilitation (Christensen, genes have specific locations (or loci) on chromosomes a
2002, p. 134). topic under heavy research since that time.
Chromosomes differ in overall length and the length
of their parts, and they have distinctive banding patterns
Cross References that allow them to be recognized. Humans have 23 pairs
or 46 chromosomes. Of those 23 pairs, one pair is called
Kaplan, Edith (19242009) the sex chromosomes, and the remaining 22 pairs are
Lezak, Muriel called autosomes.
Chronic Fatigue Syndrome C 567
Cross References defined by the Centers for Disease Control (CDC) study
group (Holmes et al., 1988); they named the condition
Deoxyribonucleic Acid (DNA) Chronic Fatigue Syndrome (CFS). In subsequent years,
Gene case definitions for CFS were created in Australia, Great
Britain (Sharpe et al., 1991; Wessely, 1995), and Canada C
(Carruthers et al., 2003), and a pediatric case definition
for ME/CFS was published in 2006 (Jason et al., 2006).
Chronic Bronchitis Currently, the most common case definition used in the
United States for the clinical diagnosis of CFS is a version
Chronic Obstructive Pulmonary Disease of the original 1988 CDC case definition revised in 1994
by an International CFS Study Group (Fukuda, Straus,
Hickie, Sharpe, Dobbins, & Komaroff, 1994).
The diagnosis of CFS cannot be made if the following
are present and could account for the presence of persis-
Chronic Familial Vascular tent fatigue: (1) permanent medical exclusions include
Encephalopathy organ failure, chronic infections, rheumatic and chronic
inflammatory diseases, major neurologic diseases requir-
Cadasil ing systemic treatment, major endocrine diseases, and
primary sleep disorders; (2) temporary medical exclu-
sions include treatable conditions that require evaluation
over time to determine the extent to which they contrib-
Chronic Fatigue Immune ute to the fatiguing illness such as conditions discovered
at onset or initial evaluation (e.g., effects of medications,
Deficiency Syndrome (CFIDS) sleep deprivation, untreated hypothyroidism, untreated
or unstable diabetes mellitus, active infection), conditions
Chronic Fatigue Syndrome that resolve (e.g., pregnancy), cardiac conditions, and
morbid obesity specified as BMI > 45; 3) permanent
psychiatric exclusions include lifetime diagnoses of bipo-
lar affective disorders, schizophrenia of any subtype, de-
Chronic Fatigue Syndrome lusional disorders of any subtype, dementias of any
subtype, organic brain disorders, and alcohol or substance
G UDRUN L ANGE abuse within 2 years before onset of the fatiguing illness,
UMDNJ-New Jersey Medical School any past or current diagnosis of major depressive disorder
Newark, NJ with psychotic or melancholic features, anorexia nervosa,
or bulimia.
If none of the exclusions apply, using the 1994 case
Synonyms definition, CFS is diagnosed based on the following cri-
teria: (1) fatigue is of new or definite onset, not due to
Chronic Fatigue Immune Deficiency Syndrome (CFIDS); exertion, not relieved by rest, and must result in substan-
Medically unexplained symptoms (MUS); Myalgic ential reductions in previous levels of educational, occupa-
cephalitis (ME); Post-infectious fatigue syndrome tional, social, or personal activities, (2) fatigue is of at least
(PFIS). Nomenclature used by patients or healthcare pro- 6 months duration, and (3) concurrent with at least four
viders is generally based on their etiologic perspective of the following eight symptoms that could not have
predated the onset of fatigue: impairment in short-term
memory or concentration severe enough to result in
Short Description or Definition substantial reductions in previous levels of educational,
occupational, social, or personal activities, painful lymph
Chronic fatigue syndrome is a complex illness defined by nodes in front or back of the neck or under the arms, sore
unexplained disabling fatigue and a combination of non- throat, muscle pain, pain in more than one joint without
specific accompanying symptoms that can have sudden or accompanying redness or swelling, headaches of a new
gradual onset. The diagnosis of the condition was initially type, unrefreshing sleep, postexertional malaise lasting
568 C Chronic Fatigue Syndrome
more than 24 h. These symptoms are nonspecific and dysfunction, cortisol dysregulation, small white matter
variable in both nature and severity over time. They lesions in the frontal regions of the brain, orthostatic
were selected on the basis of consensus clinical opinion and cognitive dysfunction. Most abnormalities are found
and were not identified empirically. in CFS patients who do not suffer from comorbid psychi-
atric disorder, most commonly depression. Treatments,
especially cognitive behavioral and graded exercise treat-
Categorization ments, enhance the prognosis for improvement. If un-
treated, complete recovery from CFS is rare.
Only a small percentage of patients complaining of fatigue
will be categorized as having CFS. Most patients either have
prolonged fatigue, defined as self-reported, persistent fa- Neuropsychology and Psychology of
tigue of 1 month or longer, or chronic fatigue defined as Chronic Fatigue Syndrome
self-reported persistent or relapsing fatigue of 6 or more
consecutive months (Fukuda et al., 1994). Other conditions CFS patients typically complain of difficulties with concen-
of unexplained etiology with similar symptom profiles tration, memory, and thinking, yet neuropsychological
are often comorbid with CFS and can include Fibromyalgia testing does not generally confirm the reported cognitive
Syndrome (FMS), Temporo-Mandibular Syndrome dysfunction. Available data suggest that the main cognitive
(TMS), Irritable Bowel Syndrome (IBS), Multiple Chemi- deficit in individuals with CFS is slowed information pro-
cal Sensitivity (MCS), Gulf War Syndrome (GWS), Major cessing, which can affect memory as well as executive
Depressive Disorder (MDD), and anxiety disorders. function. Depression is a very common comorbid condi-
tion (Tiersky, Johnson, Lange, Natelson, & DeLuca, 1997).
Epidemiology Neuroimaging data increasingly provide evidence for de-
creased cerebral blood flow and functional activation of
In the United States, CFS occurs in up to about 0.5% of brain areas suggesting increased cognitive effort (Lange,
the general population. It is most commonly found in Wang, Deluca, & Natelson, 1998; Lange et al., 2005).
middle-aged women and is most common in Latinos,
followed by African Americans, and Whites. The illness
affects women (predominantly between the ages of 40 Evaluation
and 59) more often than men (Reyes et al., 2003). In
general, the expression of the syndrome is not gender- A neuropsychological testing battery for individuals with
specific (Buchwald, Pearlman, Kith, & Schmaling, 1994). CFS should include measures of overall current and pre-
Chronic Fatigue Syndrome can also occur in children and morbid cognitive function (i.e., Wechsler Test of Adult
adolescents. While gender distribution is similar to that of Reading, Wechsler Adult Intelligence Scale III/IV), simple
adults, prevalence rates are significantly lower. and complex attention as well as information processing
and working memory (i.e., Continuous Performance
Test, Gordon, Trails, Paced Auditory Serial Addition
Natural History, Prognostic Factors, Test), executive function (i.e., subtests of DelisKaplan
Outcomes Executive Function System including verbal fluency,
towers test; Wisconsin Card Sort Test), memory
Disorders with similar symptom profiles have been des- (i.e., Wechsler Memory Scale III/IV, California Verbal
cribed for at least two centuries and have been known Learning Test II, Rey Osterrieth Complex Figure Test),
under a variety of names including neurasthenia, language function (i.e., Boston Naming Test), visual
Akureyri disease, Epstein Barr Syndrome, and chronic perceptual function (i.e., Judgment of Line Orientation,
mononucleosis. Although many hypotheses exist about Hooper), and motor function (i.e., grip strength, finger
the causes for CFS, the etiology of the condition is still tapping, pegboard). It is also recommended to test the
unclear. Some believe that CFS is a latent form of depres- level of motivation and effort expanded during neuropsy-
sion and anxiety disorder, while others view the syndrome chological testing as well as emotional functioning to
as a sleep disorder, attribute it to endocrine dysfunction improve interpretability of test results.
or abnormalities within the central nervous system When an individual is diagnosed with CFS, it may be
(CNS). Abnormalities identified in individuals with desirable to evaluate the intensity and severity of symp-
CFS include HypothalamicPituitaryAdrenal Axis toms associated with CFS using self-report
Chronic Fatigue Syndrome C 569
questionnaires. To assess fatigue intensity, several mea- Dietrich, & Oxman, 2000). Medication management
sures have been used including the Chalder Fatigue Scale of fatigue is in its infancy; presently, there is no FDA
and the Krupp Fatigue Scale; both have acceptable psy- approved drug for fatigue. Over the counter medications
chometric properties. The Chalder Fatigue Scale is a 14- offer a first line of therapeutic possibilities. Stronger med-
item instrument with a 4-choice format and separates ications, including stimulants and antidepressants, re- C
mental and physical fatigue (Chalder et al., 1993). The quire a physicians prescription. In general, medications
Krupp Fatigue Severity Scale includes nine items rated on used to treat depression, anxiety, and pain are very often
7-point scales and is sensitive to different aspects and used for the pharmacologic treatment of CFS. It is impor-
gradations of fatigue severity. Most items in the Krupp tant to recognize that fatigue is not solely due to disease
scale are related to behavioral consequences of fatigue processes, but can occur as an indirect consequence of
(Krupp, LaRocca, Muir-Nash, & Steinberg, 1989). The decreased physical activity and conditioning. Graded aer-
Checklist Individual Strength (CIS) is a 20-item inventory obic exercise training is a safe and effective treatment for
with four subscales commonly used to measure fatigue CFS and has been shown to improve quality of life. The
severity, concentration, reduced motivation, and physical primary goal of exercise is to avoid the spiral of decon-
activity. The CIS focuses on fatigue over the preceding ditioning that is common in most fatiguing diseases.
2 weeks (Vercoulen, Swanink, Fennis, Galama, Van der
Meer, & Bleijenberg, 1994). Another commonly used in-
strument to measure fatigue severity is the Multidimen- Cross References
sional Fatigue Inventory, also a 20-item questionnaire
providing scores for severity of general fatigue, physical Epstein Barr Syndrome
fatigue, mental fatigue, as well as reduced motivation and Gulf War Syndrome
activity (Smets, Garssen, Bonke, & De Haes, 1995). Neurasthenia
Another symptom that might warrant additional in- Unexplained Illness
vestigation is pain. Five of the eight CFS-defining symp-
toms reflect pain (headaches of a new type, pattern, or
severity, muscle pain, and multi-joint pain without
swelling or redness, sore throat, tender cervical/axillary
lymph nodes). In many cases, pain may be the primary
Buchwald, D., Pearlman, T., Kith, P., & Schmaling, K. (1994). Gender
determinant of disability for some individuals with CFS. differences in patients with chronic fatigue syndrome. Journal of
The McGill Pain Questionnaire (MPQ) is a well-validated General International Medicine, 9, 397401.
questionnaire that can be used to further characterize Chalder, T., Berelowitz, G., Pawlikowska, T., Watts, L., Wessely, S., Wright,
pain or follow the course of pain in CFS (Melzack, 1975). D., et al. (1993). Development of a fatigue scale. Journal of Psychoso-
matic Research, 37, 147153.
The MPQ includes four components: (1) a human figure
Carruthers, B. M., Jain, A. K., De Meirleir, K. L., Peterson, D. L., Klimas,
drawing on which patients are asked to mark the location N. G., Lerner, A. M. et al. (2003). Myalgic Encephalomyelitis/
of their pain; (2) a series of adjectives divided into groups Chronic Fatigue Syndrome: clinical Working Case Definition,
from which patients identify their experience by circling Deagnostic and Treatment Protocols. Journal of Chronic Fatigue
word descriptors; (3) questions about prior pain experi- Syndrome, 11, 7115.
DeLuca, J. (2008). Fatigue as a window to the brain. London, UK: MIT
ence, pain location, and information on the use of pain
Press.
medication; and (4) a present pain intensity index. Fukuda, K., Straus, S. E., Hickie, I., Sharpe, M. C., Dobbins, J. G., &
Komaroff, A. (1994). The chronic fatigue syndrome: a comprehensive
approach to its definition and study. International Chronic Fatigue
Treatment Syndrome Study Group. Annals of Internal Medicine, 121, 953959.
Holmes, G. P., Kaplan, J. E., Gantz, N. M., Komaroff, A. L., Schonberger,
L. B., Straus, S. E., et al. (1988). Chronic fatigue syndrome: a working
Effective treatment needs to be tailored to each individual case definition. Annals of Internal Medicine, 108, 387389.
diagnosed with CFS and often consists of a combination Jason, L. A., Bell, D. S., Rowe, M. D., van Hoof, E. L. S. J. K., Lapp, C.,
of behavioral, pharmacological, and physical interven- et al. (2006). A pediatric case definition for myalgic encephalomyeli-
tions. Behavior modification or cognitive restructuring tis and chronic fatigue syndrome. Journal of Chronic Fatigue Syn-
drome, 13, 144.
are two cognitive behavioral therapy (CBT) approaches
Kroenke, K., Taylor-Vaisey, A., Dietrich, A. J., & Oxman, T. E. (2000).
used to treat CFS. Using this modality, reductions in Interventions to improve provider diagnosis and treatment of men-
the effect of fatigue on functional ability and quality of tal disorders in primary care. A critical review of the literature.
life have been shown in CFS (Kroenke, Taylor-Vaisey, Psychosomatics, 41, 3952.
570 C Chronic Multisymptom Illnesses
Krupp, L. B., LaRocca, N. G., Muir-Nash, J., & Steinberg, A. D. (1989). Short Description or Definition
The fatigue severity scale. Application to patients with multiple
sclerosis and systemic lupus erythematosus. Archives of Neurology,
46, 11211123.
The Global Initiative for Chronic Obstructive Lung Disease
Lange, G., Steffener, J., Cook, D. B., Bly, B. M., Christodoulou, C., Liu, (GOLD) Workshop defines COPD as a disease state char-
W. C., et al. (2005). Objective evidence of cognitive complaints in acterized by airflow limitation that is not fully reversible.
Chronic Fatigue Syndrome: a BOLD fMRI study of verbal working The airflow limitation is usually both progressive and asso-
memory. Neuroimage, 26, 513524.
ciated with an abnormal inflammatory response of the
Lange, G., Wang, S., Deluca, J., & Natelson, B. H. (1998). Neuroimaging
in chronic fatigue syndrome. American Journal of Medicine, 105,
lungs to noxious particles or gases. The GOLD committee
50S53S. was organized by the World Health Organization (WHO)
Melzack, R. (1975). The McGill pain questionnaire: major properties and and the US National Heart Lung and Blood Institute
scoring methods. Pain, 1, 277299. (NHLBI). Additional information about definitions, diag-
Reyes, M., Nisenbaum, R., Hoaglin, D. C., Unger, E. R., Emmons, C.,
nosis, treatment, and research can be found at www.gold
Randall, B., et al. (2003). Prevalence and incidence of chronic fatigue
syndrome in Wichita, Kansas. Archives of Internal Medicine, 163,
copd.com.
15301536.
Sharpe, M. C., Archard, L. C., Banatvala, J. E., Borysiewicz, L. K., Clare,
A. W., David, A., et al. (1991). A reportchronic fatigue syndrome:
guidelines for research. Journal of the Royal Society of Medicine, 84,
Categorization
118121.
Smets, E. M., Garssen, B., Bonke, B., & De Haes, J. C. (1995). The
Multidimensional Fatigue Inventory (MFI) psychometric qualities COPD has traditionally been defined by severity of airflow
of an instrument to assess fatigue. Journal of Psychosomatic Research, limitation. Indeed, the GOLD COPD classification system
39, 315325. relies on measures of airflow limitation to stratify COPD
Tiersky, L. A., Johnson, S. K., Lange, G., Natelson, B. H., & DeLuca, J.
severity (i.e., Forced Expiratory Volume in 1 Second (FEV1)
(1997). Neuropsychology of chronic fatigue syndrome: a critical
review. Journal of Clinical and Experimental Neuropsychology, 19,
and Forced Expiratory Volume in 1 Second/Forced Vital
560586. Capacity(FEV1/FVC ratio)). This staging system is cur-
Vercoulen, J. H., Swanink, C. M., Fennis, J. F., Galama, J. M., Van der rently the primary determinant of treatment guidelines.
Meer, J. W., & Bleijenberg, G. (1994). Dimensional assessment of Heterogenity in the pathophysiology underlying COPD
chronic fatigue syndrome. Journal of Psychosomatic Research, 38,
has been increasingly recognized over the past decade
383392.
Wessely, S. (1995). The epidemiology of chronic fatigue syndrome.
including chronic bronchitis, peripheral airways disease,
Epidemiological Review, 17, 139151. and emphysema (Friedlander, Lynch, Dyar, & Bowler,
2007). At times, asthma has also been included in group-
ing of patients with COPD.
Chronic Multisymptom Illnesses

Epidemiology
Unexplained Illness
COPD is the fourth leading cause of death in United
States. Worldwide mortality from COPD is predicted to
increase owing to the increased tobacco consumption in
third world countries, and COPD mortality among
Chronic Obstructive Pulmonary women is increasing faster than mortality among men
Disease (Anthonisen & Manfred, 2004). The third National
Health and Nutrition Examination Survey, conducted
E LIZABETH KOZORA , K ARIN F. H OTH between 1988 and 1994, demonstrated that between 5%
National Jewish Health and 8% of the US population had COPD as defined by
Denver, CO, USA physiological parameters (NHANES III). The worldwide
prevalence of COPD in 1990 was estimated by the WHO/
World Global Burden of Disease Study to be 9.34 per
Synonyms 1,000 in men and 7.33 per 1,000 in women. In the US,
COPD death rates are low among people under the age of
Chronic bronchitis; COPD; Emphysema 45, but increase with age.
Chronic Obstructive Pulmonary Disease C 571
Natural History, Prognostic Factors, in daily activity, increased disease severity, and impaired
Outcomes health status (Hopkins & Bigler, 2001; McSweeny &
Labuhn, 1996).
Risk factors for COPD include both environmental and
host-related variables. Cigarette smoke has been identified C
as the most important external risk factor, followed by pipe
Evaluation
and cigar smoke, occupational dusts and chemicals, history
of severe childhood respiratory infections, HIV infection,
Neuropsychological evaluation for cognitive problems
outdoor pollution, and IV drug use. Host-related factors
associated with COPD typically involves measurement of
include airways hyper-responsiveness, genetic factors, se-
attention, learning and memory, reasoning and executive
vere hereditary alpha1-antitrypsin deficiency, low birth
functioning skills, visuomotor speed, and visuoperceptual
weight, and maternal cigarette smoking during gestation
function. Psychological evaluation typically involves mea-
(Anthonisen & Manfred, 2004).
sures of depression, anxiety, and health-related quality
of life.
COPD
Treatment
Empirical studies have documented neuropsychological
(i.e., cognitive) deficits in patients with chronic airway Research to date suggests that a variety of therapeuticap-
obstruction and COPD. Two of the largest studies proaches utilized in COPD patients (including oxygen
conducted in the 1980s were the Nocturnal Oxygen therapy, comprehensive rehabilitation programs, and
Therapy Trial (NOTT) and the Intermittent Positive surgical techniques) improve psychological and cognitive
Pressure Breathing Trial (Prigatano & Levin, 1988). The functioning. Long-term (greater than 6 months) use of
pattern and extent of cognitive dysfunction reported oxygen therapy improves cognitive performance in
in COPD vary across patients and appear to be associated COPD, probably due to direct effects of improved oxygen
with disease severity. In COPD patients with moderate delivery to the central nervous system (Prigatano & Levin,
to severe hypoxemia, deficits have been identified in sim- 1988). Early studies reported improvement in visual
ple motor movement and overall strength, perceptual- memory, verbal memory, and motor speed among the
motor integration, abstract reasoning, attention to COPD subjects following 6 months of continuous oxygen
auditory stimuli, learning and memory, and language therapy. Large multisite studies have also demonstrated
skills. In patients with mild hypoxemia, impairments in benefits of oxygen for cognitive function in COPD.
higher cerebral functioning include abstract reasoning, For example, in the Nocturnal Oxygen Therapy Trial,
auditory and visual attention, verbal and nonverbal COPD patients receiving continuous oxygen therapy for
learning and recall, and reasoning and motor skills 12 months experienced greater improvements in cognitive
(Kozora et al., 2008). There is some evidence that cogni- performance than did patients receiving only nocturnal
tive impairment has an independent impact on patients oxygen therapy.
daily functioning, medical regimen adherence, and quali- There is also evidence suggesting that comprehensive
ty of life, although results have been mixed (McSweeny & multidisciplinary rehabilitation programs can improve
Labuhn, 1996). cognitive functioning and psychological status in emphy-
Psychological changes and emotional distress have also sema patients. Comprehensive rehabilitation programs
been noted in COPD patients. To date, depression and for treatment of COPD are well established and typically
anxiety are the most commonly observed psychological include assessment, education, instruction on respiration,
problems in COPD (Hynninen, Breitve, Wiborg, Pallesen, & psychosocial support, and exercise training with the
Nordhus, 2005) with estimates of the prevalence of dep- goal of restoring patients to the highest level of indepen-
ression ranging from approximately 25% to 50%. Some of dent function (Make, 2004). As noted in a recent review
the discrepancies in prevalence estimates across studies article (Kozora et al., 2008), Emery and colleagues first
may be related to differences in the method used to assess reported in 1991 improved complex attention in COPD
depression. In addition to emotional distress, multiple patients following a 30-day exercise rehabilitation pro-
studies have demonstrated poor quality of life in patients gram that included instructional/educational compo-
with COPD, which has been associated with restrictions nents, psychosocial counseling, and stress reduction. In a
572 C Chronic Organic Brain Syndrome
subsequent study published in 1998, they reported im- J. B. Karlinsky, & T. E. King (Eds.), Baums textbook of pulmonary
diseases (7th ed.). Philadelphia: Lippincott, Williams & Wilkins.
provement in verbal fluency and reduction in symptoms
Friedlander, A. L., Lynch, D., Dyar, L. A., & Bowler, R. P. (2007). Pheno-
of anxiety and depression in a group participating in types of chronic obstructive pulmonary disease. COPD: Journal of
exercise, stress reduction, and education programs when Chronic Obstructive Pulmonary Disease, 4(4), 355384.
compared to a control group participating in stress reduc- Hopkins, R. O., & Bigler, E. D. (2001). Pulmonary disorders. In R. E.
tion and education treatment only. This finding high- Tarter, M. Butters, & S. R. Beers (Eds.), Medical neuropsychology
(2nd ed., pp. 247266). New York: Kluwer/Plenum.
lighted the utility of the exercise component toward
Hynninen, K. M., Breitve, M. H., Wiborg, A. B., Pallesen, S., & Nordhus,
improved cognitive and psychological functions. In I. H. (2005). Psychological characteristics of patients with chronic
2002, Kozora and colleagues also reported improvement obstructive pulmonary disease: A review. Journal of Psychosomatic
in visual attention and semantic fluency, among COPD Research, 59(6), 429443.
patients following a 3-week comprehensive rehabilitation Kozora, E., Emery, C., Kaplan, R. M., Wamboldt, F. S., Zhang, L., & Make,
B. J. (2008). Cognitive and psychological issues in emphysema.
program when compared to untreated COPD and
Proceedings of the ATS, 5(4), 556560.
healthy control subjects similar in age, education, and Make, B. (2004). Pulmonary rehabilitation. In J. D. Crapo, J. Glassroth,
gender. This program included exercise, educational, in- J. B. Karlinsky, & T. E. King (Eds.), Baums textbook of pulmonary
structional, and psychosocial components. In addition to diseases (7th ed., pp. 289307). Philadelphia: Lippincott Williams
cognitive changes, significant improvement in depressive and Wilkins.
McSweeny, A. J., & Labuhn, K. T. (1996). The relationship of neuropsy-
symptoms was reported. Together, these studies indicate
chological functioning to health-related quality of life in systemic
improved cognitive performance and psychological medical disease: The example of chronic obstructive pulmonary
status following comprehensive rehabilitation with an disease. In I. Grant & K. M. Adams (Eds.), Neuropsychological assess-
exercise component. Many studies have also reported ment of neuropsychiatric disorders (pp. 577602). New York: Oxford
increased quality of life following comprehensive reha- University Press.
Prigatano, G. P., & Levin, D. C. (1988). Pulmonary system. In R. E. Tarter,
bilitation (Make, 2004).
D. H. Van Theiel, & K. L. Edwards (Eds.), Medical neuropsychology
Finally, studies have suggested some improvement in (pp. 1126). New York: Plenum.
cognition for moderate to severe COPD patients follow-
ing lung volume reduction surgery (LVRS). In an ancillary
study of the National Emphysema Treatment Trial
(NETT), Kozora and colleagues (Kozora et al., 2008)
examined neuropsychological and psychological func-
Chronic Organic Brain Syndrome
tioning of patients receiving LVRS when compared to
Organic Brain Syndrome
patients receiving only medical therapy (MT). The LVRS
group showed significant improvement compared to the
MT group at 6 months on a measure of psychomotor
speed, delayed recall for verbal information, and trends
toward improved sequential thinking, and psychomotor Chronic Progressive Multiple
speed and naming to confrontation. LVRS patients Sclerosis
also experienced significant reduction in depression at
6 months, as reflected in total Beck Depression Inventory Primary Progressive Multiple Sclerosis
score. There was no direct evidence that improved cogni-
tion in LVRS was related to improved physical capacity
(workload and 6 min walk) or pulmonary function.
Chronic Widespread Pain
Cross References Disorder
Fibromyalgia
Anoxia

Cingulate Cortex
Anthonisen, N. R., & Manfred, J. (2004). Epidemiology of chronic
obstructive pulmonary disease. In J. D. Crapo, J. Glassroth, Cingulate Gyrus
Cingulate Gyrus C 573
the more rostral olfactory piriform paleocortex unites the

Cingulate Gyrus orbitofrontal, insular, and temporopolar regions, while
the more caudal archicortex of the hippocampus provides
M ICHAEL M EGA the nidus for developmental spread through parahippo-
Providence Brain Institute campal and entorhinal regions into the posterior cingu-
Portland, OR, USA
C
late. Both paralimbic belts reflect a different emphasis
within the cingulate (Fig. 1). The orbitofrontal-centered
belt processes the internal affective state of the organism.
Synonyms The more recent hippocampal-centered belt is the exter-
nally directed evaluative arm of the limbic system.
Cingulate cortex; Subcallosal; Subgenual Both work in concert, enabling the selection of envi-
ronmental stimuli based on the internal relevance those
stimuli have for the organism. Although both areas 24 and
Structure 32 are part of the hippocampal belt, the more rostral
connections of area 24 contrast with the more caudal
The cingulate gyrus, first named by Burdach in 1822, was sensory connections of area 23, distinguishing the anteri-
combined with the anterior olfactory region and hippo- or executive from the posterior evaluative cingulate.
campus by Broca to form the ring of olfactory processing Appreciating that the major reciprocal connections
he termed the grand lobe limbique. Anatomic studies between the orbitofrontal trends are with the anterior
revealed extensive connections between the anterior cingulate, while the hippocampal trends are with the
thalamus, known to be associated with the hippocampus posterior cingulate, will assist the understanding of cin-
and hypothalamus, and the cingulate. In 1937, Papez gulate function.
combined these anatomic results with the clinical reports Three anterior effector regions and a posterior proces-
of emotional disturbances following lesions to the cingu- sing region also emerge through a review of the efferent
late and other limbic structures to propose a mechanism and afferent connections of the cingulate. The three ante-
of emotion based on a limbic circuit. For Papez, the rior regions include a visceral effector region inferior to the
integration of internal feelings and emotional responsive- genu of the corpus callosum encompassing area 25, the
ness with the functions of the lateral cerebral cortex oc- anterior subcallosal portions of 24ab, and 32; a cognitive
curred in the cingulate. The limbic circuit of Papez effector region, which includes most of the supra-callosal
however did not find anatomical evidence to support area 24, and areas 24ab and 32; and a skeletomotor
the closing connection of the cingulate to the hippocam- effector region within the depths of the cingulate sulcus
pus until 1975, when Shipley and Srensen documented that includes areas 24c/23c on the ventral bank, with
that the presubiculum, which receives a dense cingulate 24cg and 6c on the dorsal bank. These three cingulate
outflow, projects heavily to layer III of the entorhinal effector regions integrate ascending input concerning the
cortex the origin of the perforant pathway into hippo- internal milieu of the organism with visceral motor sys-
campal pyramidal cells. tems, cognitive-attentional networks, and skeletomotor
Understanding the function of the cingulate in the
integration of internal feelings and emotional responsive-
ness with movement and thought begins with an apprecia-
tion of its cytoarchitecture. Brodmanns original
cytoarchitectonic separation of anterior and posterior
cingulate cortex into areas 24 and 23 based upon the
presence of agranular cortex in area 24 contrasted with
the granular cortex of area 23 has been refined by more
accurate studies of the progressive cytoarchitectonic elabo-
ration in the ventral to dorsal direction. Two main centers
of isocortical development can be traced phylogenetically
and through cytoarchitectonic progression. These two
developmental trends, termed paralimbic belts, are transi-
tional cortical zones from less-differentiated allocortex to Cingulate Gyrus. Figure 1 The Orbiotfrontal (red) and
more-differentiated isocortex with two functional centers: hippocampal (blue) paralimbic trends
574 C Cingulate Gyrus
centers to produce the affective motivation necessary for nucleus of the vagus, and the nucleus accumbens/olfacto-
the organisms engagement in the environment. The pos- ry tubercle of the ventral striatum.
terior sensory processing region (areas 23ab and 29/30) Brain areas that have reciprocal connections with the
assists in the memory and processing of environmental visceral effector region, except the claustrum that supplies
stimuli targeted as relevant to the organism based on their auditory input, also influence visceral function when sti-
motivational valence. The following sections will explore mulated. This results from their amygdalar connections
the connections of these four cingulate regions (Figs. 2 that convey the visceral state of the organism to paralimbic
and 3) and their function as observed from electrical areas. The orbitofrontal cortex mediates empathic, civil,
stimulation, imaging, and clinical data. and socially appropriate behavior. Rostral auditory associ-
ation cortex in the superior temporal area also provides
auditory information to the visceral effector region. No
Function visual information has direct access to the subcallosal area.
The dorsolateral prefrontal lobe, functioning as an
Visceral effector region. Major reciprocal connections with executive processor, provides nonreciprocal input
the visceral effector region are with the basal and accesso- from areas 9 and 46 to the subcallosal anterior cingulate
ry basal amygdala, medial orbitofrontal cortex areas 11, region. Executive functions permit an organized behav-
12, and 13, anterior superior temporal pole area 38, and ioral response to solve a complex problem. This includes
the anterior ventral claustrum. Major nonreciprocal pro- the activation of remote memories, self-direction, and
jections from the visceral effector region target the para- independence from environmental contingencies, shifting
sympathetic nucleus of the solitary tract, the sympathetic and maintaining behavioral sets appropriately, generating
thoracic intermediolateral column, the dorsal motor motor programs, and using verbal skills to guide behavior.
Dorsolateral prefrontal efferents into the subcallosal cin-
gulate provide feedback inhibition on the basic drives of
hunger, aggression, and reproductive urges. Table 1 for a
summary of these anatomic connections.
Subcallosal cingulate processing modulates visceral
output from brain-stem sympathetic and parasympathetic
centers. Access to the basal ganglia, via the ventral striatum,
allows processing of the internal milieu of the organism to
influence the skeletal motor system as well. This visceral
motor network encompasses the bulk of the orbitofrontal-
centered paralimbic belt dedicated to assessing the emo-
Cingulate Gyrus. Figure 2 Cytoarchitectonic divisions of the tional valence of objects based upon internal motivating
cingulate and adjacent areas drives. Patients with lesions in this area are often
Cingulate Gyrus. Table 1 Major reciprocal connections and

nonreciprocal targets for the visceral effector region of the
cingulate cortex
Reciprocal connections
Basal and accessory basal amygdala
Medial orbitofrontal areas 11, 12, and 13
Superior temporal pole area 38
Anterior ventral claustrum
Nonreciprocal targets
Parasympathetic nucleus of solitary tract
Cingulate Gyrus. Figure 3 The four functional divisions of the Sympathetic intermediolateral column
cingulate. The visceral effector region (1), the cognitive
Dorsal motor nucleus of the vagus
effector region (2), the skeletomotor effector region (3), and
Nucleus accumbens and olfactory tubercle
the posterior cingulate (4)
disinhibited with irritability, lability, tactlessness, and fatu- reticular activating system and its control over arousal.
ous euphoria. Patients act upon visceral drives without Table 2 for a summary of these anatomic connections.
regard to social decorum. Skeletomotor effector region. Major reciprocal connections
Cognitive effector region. Major reciprocal connections with the skeletomotor effector region are with the primary
with the cognitive effector region are with the basal amyg- and supplementary/premotor motor cortex areas 4 and 6, C
dala, prefrontal areas 8, 9, 10, and 46, caudal orbitofrontal prefrontal areas 8, 9, and 46, parietal areas 1, 2, 3a, 5, and
area 12, inferior temporal pole area 38, rostral insula, 7b, and caudal insula. Major nonreciprocal projections
anterior parahippocampal areas 35 and 36, and the ante- from the skeletomotor area target the lateral putamen,
rior medial claustrum. Areas reciprocally connected to the spinal cord, ventromedial parvocellular division of the red
cognitive effector region share a general similarity with nucleus, and the ventrolateral pontine gray matter.
the subcallosal anterior region underscoring their com- Primary motor cortex has very limited input. The me-
mon membership in the orbitofrontal paralimbic belt. dial supplementary, lateral premotor, and cingulate skeletal
The cognitive effector region is more developed in its motor regions are the only forebrain inputs to the primary
cytoarchitecture, than the subcallosal cingulate, and thus motor cortex. The skeletomotor region in the banks of the
has stronger connections with more phylogenetically re- cingulate sulcus conveys limbic influence to the medial
cent neocortex of dorsolateral prefrontal areas 8, 9, 10, supplementary, lateral premotor, and primary motor cor-
and 46 devoted to executive function. The amygdala pro- tex. Frontal eye fields in area 8 also share reciprocal connec-
vides internal affective input to the supracallosal anterior tions with the skeletal motor effector region. Areas 9 and 46
cingulate. The distribution of amygdala efferents deline- of the dorsolateral prefrontal cortex contribute executive
ates the dorsal boundary of the cingulate as a functional input to the limbic motor system. Thus, executive and
system. Auditory input arises from the anterior medial limbic systems gain access to primary motor area 4 indi-
claustrum as well as a minor link with the auditory asso- rectly. The cingulate skeletal motor region receives the
ciation area of the superior temporal gyrus. The rostral greatest outflow from executive prefrontal cortex than
insula and anterior parahippocampal areas provide addi- all other motor cortices underscoring its influence over
tional reciprocal connections with the cognitive effector goal-directed behavior. Sensory-motor parietal areas 1, 2,
region not associated with the subcallosal region. Rostral 3a, and 5 also have reciprocal connections with the skeletal
insular cortex is a transitional paralimbic region that motor center within the banks of the cingulate sulcus. The
integrates visceral alimentary input with olfactory and rostral parietal area 7b has a strong relationship with the
gustatory afferents. Connections with the anterior para- premotor cortex, while the granular cortex of the caudal
hippocampal areas 35 and 36 allow the supracallosal cin-
gulate to influence multimodal sensory afferents entering
the hippocampus. Cingulate Gyrus. Table 2 Major reciprocal connections and
Major nonreciprocal projections of the supracallosal nonreciprocal targets for the cognitive effector region of the
anterior cingulate include the auditory association cortex cingulate cortex
of anterior superior temporal area 22, allowing the cognitive
effector region to influence language and the access of Reciprocal connections
semantic stores. The posterior parietal area 7a and the Basal amygdale
dorsomedial head of the caudate are also targets. Parietal Prefrontal areas 8, 9, 10, and 46
area 7a is the sensory component in the extrapersonal Caudal orbitofrontal cortex area 12
attentional network linked with the dorsolateral prefrontal Inferior temporal pole area 38
executive system. The head of the caudate is also a target Rostral insula
of this executive prefrontal cortex. Cingulate input to the
Anterior parahippocampal areas 35 and 36
caudate assists in the initiation of vocalization behavior as
Anterior medial claustrum
well as executive function. Emotional vocalizations occur-
ring during stimulation in monkeys requires intact cingu- Nonreciprocal targets
late efferents to the periaqueductal gray that produce Anterior superior temporal area 22
similar behaviors when stimulated. The most caudal amyg- Parietal area 7a
dalar projections to 24c, extending into anterior 24c, inner- Dorsomedial head and body of caudate
vate a face representation region that may have direct
Periaqueductal gray
connections with the facial nucleus in the pons. Efferents
Dorsomedial pontine gray matter
to the dorsomedial pons provide cingulate influence on the
insula is a somatosensory limbic region. More corticospinal The posterior granular sensory cortices are distin-
neurons are found in the cingulate than are found in the guished from the anterior agranular executive cortices.
supplementary motor cortex, and the cingulate has about The posterior cingulate, with its prominent granular
40% of the amount found in primary motor cortex. Table 3 layer IV, is dedicated to visuospatial and memory proces-
for a summary of these anatomic connections. sing. Major reciprocal connections are with the dorsal
Sensory processing region. Major reciprocal connections visual system of the inferior parietal lobe dedicated to
with the sensory processing region are with caudal parie- spatial processing and with the frontal eye fields in area
tal area 7a, frontal eye fields area 8, posterior perirhinal 8. Reciprocal connections with lateral prefrontal area 46
area 35, presubiculum, posterior parahippocampal area allow an interaction between executive and sensory/mne-
36, prefrontal area 46, and the ventral caudal claustrum. monic processing, which may mediate perceptual work-
Major nonreciprocal projections from the sensory proces- ing memory tasks. Posterior parahippocampal and
sing region target the dorsal caudate, posterior superior perirhinal areas 36 and 35, as well as the presubiculum,
temporal gyrus area 22, and orbitofrontal area 11. These are reciprocally connected to the sensory processing re-
regions are shown in Table 4. gion of the posterior cingulate. These connections modu-
late the multimodal efferents entering the entorhinal layer
III cells that form the perforant pathway into the hippo-
Cingulate Gyrus. Table 3 Major reciprocal connections and campus. Feedback from these areas to the cingulate pro-
nonreciprocal targets for the skeletomotor effector region of vides highly processed sensory information, and the
the cingulate cortex ventral visual system involved in feature analysis can
Reciprocal connections influence the posterior cingulate through these connec-
Primary motor area 4 tions. Although in cats dorsal caudal claustrum is related
Supplementary motor area 6 to visual processing, while the ventral caudal claustrum
receives auditory input, it is possible that in primates
Prefrontal areas 8, 9, and 46
visual information may reach the posterior cingulate via
Parietal areas 1, 2, 3a, 5, and 7b
the ventral caudal claustrum.
Caudal insula The nonreciprocal targets of the posterior sensory
Nonreciprocal targets processing region include the dorsal caudate which also
Lateral putamen receives input from area 7a of the caudal inferior parietal
Spinal cord lobe. This shared connection between the dorsal head of
the caudate and the dorsal visual system of area 7a sup-
Red nucleus
ports the role of the posterior cingulate in visual atten-
Ventrolateral pontine gray matter
tion. Output to posterior superior temporal area 22 will
influence auditory association cortex. Limited efferents to
the rostral portion of area 11 provide the only overlap
with the orbitofrontal-centered belt.
Cingulate Gyrus. Table 4 Major reciprocal connections and Electrical stimulation of the cingulate. Electrical stimula-
nonreciprocal targets for the sensory processing region of the tion studies of the cingulate in humans and animals are
cingulate cortex difficult to interpret because differing techniques have
Reciprocal connections been used in these investigations. With varying intensity,
Caudal parietal area 7 time course, and location of stimulation, it is not
surprising that a spectrum of results is noted. Despite
Frontal eye fields area 8
technical variations, stimulation of the anterior cingulate
Prefrontal area 46
in humans regularly produces visceral motor and affective
Posterior parahippocampal areas 35 and 36 changes, speech alterations, and automatic motor beha-
Presubiculum viors (Meyer, McElhaney, Martin, & McGraw, 1973). In
Ventral caudal claustrum contrast to inhibitory responses elicited by the stimula-
Nonreciprocal targets tion of primary motor cortex, which cannot be controlled,
Dorsal caudate
respiratory arrest from cingulate stimulation can be over-
come volitionally (Penfield & Jasper, 1954). Automatic
Posterior superior temporal area 22
behaviors noted include unilateral and bilateral move-
Orbitofrontal area 11
ments and repetitive tic like movements of the hands,
lips, or tongue. These movements can also be consciously cingulate skeletomotor region is also activated (Grafton,
suppressed; implicating the cingulate as an unconscious Woods, & Tyszka, 1994).
effector supports its role in the pathophysiology of
obsessivecompulsive disorder (behaviors that respond
well to cingulotomy). Fear, pleasure, agitation, euphoria, Illness C
and a sense of well being affective phenomena also
common after limbic stimulation have been reported Structural and functional abnormalities. Seizures originat-
(Meyer, McElhaney, Martin, & McGraw, 1973). Involun- ing in the anterior cingulate can alter visceral activity,
tary vocalizations and speech arrests are less common in produce involuntary skeletomotor output, result in dis-
humans than in animals with stimulation of areas 32, 24, turbed attention, and cause interictal behavior abnormal-
and the rostral part of 25 (Vogt & Barbas, 1988). ities. The severity and specific abnormality will depend
Functional activation of the cingulate. In functional activa- upon the location of the seizure focus and ensuing dam-
tion studies, the cognitive effector region of the anterior age that affects interictal brain function. A diverse assort-
cingulate is activated when sustained attention to novel ment of atonic, absence, speech arrest, autonomic, and
tasks is required. Tasks spanning motor, language, mem- complex partial seizures with secondary generalization
ory, and visuospatial paradigms all produce supracallosal have been described. Inaccessibility of the medial hemi-
anterior cingulate activation. When memory encoding is sphere to surface electrode recording is the greatest obsta-
combined with a motor task demanding sustained cle to the elucidation of cingulate seizures.
divided attention (Fletcher et al., 1995), only the anterior In a study involving 36 cases (Mazars, 1970), depth
cingulate is activated due to the sustained vigilance electrodes revealed near-instantaneous bilateral spread to
demanded by dividing effort between the two tasks. the frontal poles when the focus was in the anterior
When motivation to master a task is no longer required, cingulate; posterior foci spread to the contralateral cingu-
and accurate performance of a task becomes routine, the late within seconds, followed by involvement of the con-
anterior cingulate returns to a baseline activity level vexities with generalized tonicclonic seizures. Emotional
(Raichle et al., 1994). The acquisition of novel cognitive stress often precipitated the seizures. Psychoses and
strategies requires the dynamic vigilance of the supra- episodic rage were common interictal behavioral abnorm-
callosal cingulate, but with practice the motivation realities that responded to the removal of the anterior cin-
quired to entrain new cognitive networks to a novel task gulate and occasionally the frontal pole as well.
is no longer necessary. A distinction between motivation Consciousness may be altered and automatisms can be
and attention is important. A task is still attended to and voluntarily inhibited or integrated with ongoing move-
completed correctly after the motivating influence of the ments (Geier et al., 1977).
supracallosal cingulate has initiated the acquisition of an An 11-year-old girl who initially had atonic seizures at
efficient cognitive routine. Through the activation of the age 30 months was reported to develop complex partial
anterior supracallosal cingulate limbic motivation directs seizures with blinking, lip smacking, automatisms, and
the selection of the best cognitive strategy among many humming (Levin & Duchowny, 1991). An obsessive
competing contingencies. Thus, activation studies using compulsive disorder developed over a 5-year period, and
varied tasks consistently activate the cognitive effector by age 8, she became preoccupied with Satan and her
region in normals motivated to succeed in whatever task personal hygiene. Seizure focus, recorded from depth
is given them. The contribution to an extrapersonal at- electrodes, was in the right anterior cingulate. The
tentional network involving direct links between the patients behavioral abnormalities responded well to a
anterior cingulate, dorsolateral executive frontal area, 4-cm ablation of the right anterior cingulate.
and the inferior parietal lobule provided by the cogni- Another case of a right anterior cingulate focus with
tive effector region is the motivation to engage in a cogni- accompanying behavioral abnormalities has been de-
tive challenge. scribed (Devinsky, Morrell, & Vogt, 1995). One year
Functional imaging has also confirmed the role of the after mild head trauma, a 42-year-old male developed,
skeletomotor effector region in the preparation of motor over a 15-year period, sociopathic behavior and complex
output and motor learning. When a motor task is only partial seizures unresponsive to medical treatment. Sei-
imagined, the cingulate cortex inferior and anterior to the zures were usually nocturnal and frequent (1020 per
supplementary motor area (dorsal bank of the cingulate night), with stereotypic motor output: facial contortions,
sulcus) shows significant activation. During the acquisi- tongue thrusting, a strangulated yell, flexion of the neck
tion of procedural learning in a rotory pursuit task, the and trunk, bilateral extremity extension, and thrashing
with preserved consciousness. Occasionally, generali- lesions, possibly affecting the ascending reticular core. Fail-
zation to tonicclonic seizures developed with loss of ure of response inhibition on go-no-go tests is the major
consciousness. neuropsychological deficit in the patient with an anterior
Irritability, disinhibition, and sexual deviancy were medial frontal damage. The loss of spontaneous motor
behavioral complications in a police officer who was dis- activity results when the lesion involves the supplementary
missed from the force because of brutality and the use of motor area and the skeletomotor effector region. When
confiscated drugs. Surface and sphenoidal electroenceph- these two motor regions are spared, motor activity will be
alogram showed rhythmic bifrontal theta. Magnetic reso- normal but the patient will demonstrate profound indif-
nance imaging (MRI) and [18F]-fluorodeoxyglucose ference, docility, and the loss of motivation to engage in a
positron emission tomography (FDG-PET) were essen- task. They can be led by the examiner to engage in a task
tially normal, but depth electrodes revealed a right cingu- but will fail to self-generate sustained directed attention.
late focus which spreads to the ipsilateral orbitofrontal They lack cognitive motivation.
area and contralateral anterior cingulate in 300 ms. Re- The role of the anterior cingulate as a cognitive effec-
section of the right cingulate and anterior corpus callo- tor is appreciated within the realm of language. Language,
sum relieved 90% of the spells with only brief axial flexion a cognitive function, is distinguished from the motor
being the residual seizures. The behavioral abnormalities function of speech. Transcortical motor aphasia
were reported to improve with the patient married and (TCMA) is the usual result of left anterior medial or
employed as a fast-food restaurant manager. anterior dorsolateral prefrontal lesions. The classic syn-
Both stimulation and seizure activity can discharge drome of TCMA is initial mutism that resolves in days to
the functional centers of the cingulate to produce a vis- weeks, yielding a syndrome featuring delayed initiation of
ceral effect, a cognitive or behavioral change, and a speech brief utterances without impaired articulation, excellent
or motor output. Appreciating the functional centers repetition, inappropriate word selection, agrammatism,
within the cingulate assists the interpretation of the and poor comprehension of complex syntax. Activation
signs and symptoms exhibited when it discharges. The of dorsolateral prefrontal cortices enabling language and
interictal behavioral abnormalities of anterior cingulate speech arises from two sources: the anterior cingulate and
epilepsy reflects the dysfunction of limbic networks the supplementary motor area (with the cingulate skele-
which, if affecting infracallosal and orbitofrontal cortex, tomotor effector region). When the executive prefrontal
will result in visceral motor disturbances and disinhibi- cortex (areas 9, 10, and 46) is disrupted, cognitive lan-
tion with socially inappropriate behavior. Obsessive guage deficits are prominent (TCMA, type I); when
compulsive features may occur with dysfunction of the motor neurons in area 4, devoted to the speech apparatus,
cognitive component of the supracallosal cingulate. This are disconnected from their activation, speech hesitancy
abnormal dynamic vigilance exerted by the cognitive and impoverished output ensues (TCMA, type II). These
effector region in obsessivecompulsive disorders can two functional realms are separable and can be discon-
occur from a well-circumscribed seizure focus in this nected anywhere along two pathways. Direct damage to
region (Levin & Duchowny, 1991) and is relieved by the supplementary motor area or its efferent pathway to the
surgical ablation of this region or its outflow (Tow & motor cortex traveling in the anterior superior paraventri-
Whitty, 1953). cular white matter will produce TCMA type II. Direct
Focal lesions and syndromes. Well-circumscribed lesions in damage to the anterior cingulate, its outflow to areas 9,
humans are rarely confined to one region of the cingulate. 10, and 46, or to the caudate via the subcallosal fasciculus,
With an anterior lesion, both the cognitive, skeletomotor just inferior to the frontal horn of the lateral ventricle will
and visceral effector regions are often affected. Bilateral disrupt frontal-subcortical circuits involved in motivation
lesions result in an akinetic mute state ( Akinetic Mut- and executive cognitive functions. The initial muteness has
ism). Patients are profoundly apathetic. Rarely moving, been described by a patient after recovering from an anteri-
and incontinent, they eat and drink only when fed, and if or cingulate/supplementary motor infarction as a loss of the
speech occurs it is limited to monosyllabic responses to will to reply to her examiners, because she had nothing
questioning. Patients appear awake with eyes tracking to say, her mind was empty, and nothing mattered
objects. Displaying no emotions, even when in pain, ( Akinetic Mutism).
patients show complete indifference to their circumstance. The cingulum bundle has also been the site of surgical
Transient akinetic mutism with similar features occurs with lesions (cingulumotomy, or cingulotomy when cingulate
unilateral lesions. The akinetic mute state can also result cortex is also removed) to treat psychiatric and pain dis-
from bilateral paramedian diencephalic and midbrain orders. The cingulum contains the efferents and afferents
of the cingulate to the hippocampus, basal forebrain, and the hippocampus during encoding and may also be
amygdala, and all cortical areas, as well as fibers of passage important in the storage of long-term information.
between hippocampus and prefrontal cortex, and from Synthesizing cytoarchitectonic refinements, nonhu-
the median raphe to the dorsal hippocampus. Surgical man primate tracer studies, clinical-behavioral correla-
ablation of the anterior portion (sparing fibers relevant tion data, and functional neuroimaging results have C
to memory function) is most successful when treating been refined but have not significantly added to the
aggression, extreme anxiety, obsessivecompulsive beha- basic description of cingulate function offered by Papez:
viors, and severe pain. Psychotic symptoms show only a
" It is thus evident that the afferent pathways from the recep-
temporary response. The three anterior cingulate regions,
tor organs split at the thalamic level into three routes, each
by virtue of the distinct functional systems they access, are
conducting a stream of impulses of special importance. One
the conduits through which limbic motivation can acti-
route conducts impulses through the dorsal thalamus and
vate feeling, thought, and movement.
the internal capsule to the corpus striatum. This route
Lesions of the posterior cingulate disrupt memory func-
represents the stream of movement. The second conducts
tion in animals and humans. The closing link in the circuit
impulses from the thalamus through the internal capsule to
of Papez, from the anterior thalamic efferents traveling
the lateral cerebral cortex. This route represents the stream
through the posterior cingulum to areas 32 and 29/30, is
of thought. The third conducts a set of concomitant
the cingulate projection sent to the presubiculum. Anterior
impulses through the ventral thalamus to the hypothala-
cingulotomy will not disrupt this memory circuit but rarely
mus and by way of the mamillary body and the anterior
pathologic lesions will extend into, and beyond, the poste-
thalamic nuclei to the gyrus cinguli, in the medial wall of the
rior cingulate. If the lesion extends inferior to the splenium
cerebral hemisphere. This route represents the stream of
of the corpus callosum, it may also disrupt the fornix, thus
feeling. In this way, the sensory excitations which reach the
disconnecting the efferents from the hippocampus to the
lateral cortex through the internal capsule receive their
diencephalon. If the lesion extends posteriorly, it may dam-
emotional coloring from the concurrent processes of hypo-
age the supracommissural portion of the hippocampus
thalamic origin which irradiate them from the gyrus cinguli.
the gyrus fasciolaris and the fasciola cinerea. A large left-
(Papez, 1937)
sided lesion that extended beyond the posterior cingulate
into the fornix and supracommissural hippocampus after
the surgical repair of an arteriovenous malformation
resulted in a persistent amnesia (Cramon & Schuri, 1992). References and Readings
Disruption of septo-hippocampal pathways in the cingu-
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important components of Papezs circuit had clearly been
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cannot determine if the posterior cingulate cortex, rather vidual subject performance. Human Brain Mapping, 1, 221234.
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stroy neurons but spare fibers of passage can clarify this tactic cingulotomy with results of acute stimulation and serial psy-
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Raichle, M. E., Fiez, J. A., Videen, T. O., MacLeod, A.-M. K., Pardo, J. V., Fellgiebel, A., Muller, M. J., Wille, P., Dellani, P. R., Scheurich, A.,
Fox, P. T., et al. (1994). Practice-related changes in human brain Schmidt, L. G., et al. (2005). Color-coded diffusion-tensor-imaging
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and spatial memory; a microlimnology analysis. In B. A. Vogt & Gholkar, A., et al. (2007). Atrophy is associated with posterior
M. Gabriel (Eds.), Neurobiology of cingulate cortex and limbic thala- cingulate white matter disruption in dementia with Lewy bodies
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gery & Psychiatry, 16, 186193. resonance imaging and neuropsychological performance in amnestic
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Cingulum
CIQ
I RENE P IRYATINSKY
Butler Hospital and Alpert Medical School of Brown Community Integration Questionnaire
University
Providence, RI, USA
Circadian Clock
Definition
Circadian Rhythms
The cingulum is a collection of white matter fibers project-
ing from the cingulate gyrus to the entorhinal cortex in the
brain, allowing for communication between components
of the limbic system. The cingulum connects the medial
temporal lobe with the posterior cingulate gyrus. Diffusion
Circadian Rhythms
tensor imaging studies have reported cingulum bundle
B RUCE J. D IAMOND
disruption in mild cognitive impairment and Alzheimers
disease. In addition, some research indicates that in Alzhei-
Wayne, NJ, USA
mers disease, the posterior cingulate cortex hypofunction
is due to the indirect effect of the degeneration of cingulum
fibers secondary to medial temporal lobe atrophy.
Synonyms
Cross References Biological cycles; Biorhythms; Circadian clock
Cingulate Gyrus
The pervasive characteristics of living organisms are
Catani, M., Howard, R. J., Pajevic, S., & Jones, D. K. (2002). Virtual
rhythmic biological and behavioral changes, which are
in vivo interactive dissection of white matter fasciculi in the human expressed at varying levels of organization ranging from
brain. NeuroImage, 17(1), 7794. basic cellular to the highly complex level. These rhythms
Circadian Rhythms C 581
are generally referred to as circadian rhythms and they Developmental factors may also mediate some of the
organize a variety of behaviors, including sleep, which is variations in circadian rhythms. For example, the aging
characterized by a 90-min Rapid Eye Movement (REM) process is often accompanied by changes in circadian
cycle and the wakefulnesssleep cycle, which is organized rhythms that may affect sleep and place older adults at a
around an approximate 24-h cycle (Carlson, 1999). higher risk for sleep disturbance (Lee-Chiong, 2005). C
Categorization History and Impact

The core body temperature rhythm and the sleepwake Endogenous biological clocks were demonstrated over
cycle are among the most extensively studied of the 200 years ago (Kolb & Wishaw, 2005) and entrainment
human biorhythms (Waterhouse & DeCoursey, 2004b) was identified as the most important property for deter-
with the 24-h circadian rhythms represented most prom- mining the phase relationship of a circadian clock
inently in the research literature. This is because these (Johnson, Elliot & Foster, 2004). Circadian rhythms
rhythms impact daily life (e.g., work, school, medical may confer an adaptive value on an organism, since the
psychological status) and are of relatively brief duration, organism can anticipate environmental changes (Clark,
so they are amenable to study (Clark, 2005). There is also 2005), and physiological functions synchronized with
a developmental progression in how rhythmicity is the time of day are associated with enhanced efficiency
expressed from birth to old age (Waterhouse & DeCour- (Quigg, 2006). Disruption in circadian rhythms can ad-
sey, 2004b). There are a number of biological rhythms versely impact individuals involved in shift and night work,
characterized by different time periods (Table 1). who suffer jet lag or whose schedules are temporally irregu-
lar. The impact is more profound when task demands
involve vigilance and reaction time (Costa, 1999) and are,
Mechanisms therefore, more vulnerable to the effects of fatigue. Atten-
tional regulation over both incoming information and
Circadian rhythms are modulated by both internal clocks outgoing responses may also be vulnerable to time of
(e.g., pacemakers) and external triggers that can entrain day effects. Disturbances in sleepwake cycles and
biorhythms, acting as zeitgebers (e.g., changes in illumi- biological rhythms have been associated with affective
nation). The superchiasmic nucleus (SCN) of the hypo- disorders including depression.
thalamus has been identified as the principal biological
clock (Carlson, 1999) based on lesion studies and day
night changes in activity levels. The mechanisms med- Evaluation
iating communication and synchronization between
neurons appear to be chemical in nature. Both the SCN There are large differences in circadian cycles between
and the pineal gland exert an influence on seasonal younger and older adults. Clinicians should assess the
rhythms with SCN-induced melatonin secretion involved quantitative and qualitative nature of cognitive decline
in synchronizing circadian rhythms (Carlson, 1999). in the elderly with attention to circadian influences
(with the elderly tending to be morning oriented)
(Hasher, Goldstein & May, 2005). In evaluating clients
for possible disruptions in circadian rhythms, clinicians
Circadian Rhythms. Table 1 Biological rhythms
would be well advised to determine if clients engage in
Biological shift work, have experienced jet lag or changes in sched-
rhythms Time period Activity ule, or exhibit fatigue, sleep disorders, excessive daytime
drowsiness, or decrements in job-related performance
Infradian Period of less Eating behaviors
than 24 h
(Costa, 1999).
Circadian Period of about Sleepwake
24 h
Treatment
Ultradian Period of about Human female
28 days menstrual cycle
While the circadian clock of healthy humans is entrained
Circannual Yearly Migratory birds
to a period of about 24 h, the precise timing varies on an
582 C Circle of Friends
intraindividual and interindividual basis. At a certain Quigg, M. (2006). Circadian rhythms: Problems with the body clock.
In N. F. Watson & B. V. Vaughn (Eds.), Clinicians guide to sleep
point, these deviations may be considered clinical abnor-
disorders (pp. 277304). Philadelphia: Taylor & Francis.
malities (i.e., seasonal affective disorder). In fact, seasonal Waterhouse, J. M., & DeCoursey, P. J. (2004a). Human circadian organi-
affective disorder has been treated using phototherapy, zation. In J. C. Dunlap, J. J. Loros, & P. J. DeCoursey (Eds.),
which involves the use of light boxes, whereby a patient Chronobiology: Biological timekeeping (pp. 291323). Sunderland,
is exposed to light each winter morning or evening and MA: Sinauer.
Waterhouse, J. M., & DeCoursey, P. J. (2004b). The relevance of circadian
the circadian rhythm becomes entrained in ways that
rhythms for human welfare. In J. C. Dunlap, J. J. Loros, &
induce circadian phase shifts (Kolb & Wishaw, 2005). P. J. DeCoursey (Eds.), Chronobiology: Biological timekeeping
Individuals who make substantial changes to their sleep (pp. 325356). Sunderland, MA: Sinauer.
wake cycles during night work or after trans-meridian
travel could be helped using a chronobiological treatment.
The treatment would involve exposure to appropriate
circadian synchronizers and basing therapy on phase re-
sponse curves for light and melatonin (Waterhouse & Circle of Friends
DeCoursey, 2004a). By making accommodations in the
timing of work-related activities (Hasher et al., 2005), Circles of Support
performance efficiency can be improved and fatigue
decreased, thus enhancing health and safety (Costa, 1999).
And in treating patients with bipolar disorder, psychoso-
cial therapies should identify areas of vulnerability includ- Circle of Willis
ing unhealthy circadian rhythms (Newman, 2006).
E LLIOT J. R OTH
Cross References
Chicago, IL, USA
Fatigue
Sleep Disturbance
Definition
References and Readings The circle of Willis is the anatomical name given to
the formation of arteries at the base of the brain that
Carlson, N. R. (1999). Foundations of Physiological Psychology (4th edn.).
contribute the overwhelming majority of blood supply
Boston: Allyn & Bacon. to the brain.
Clark, A. V. (Ed.). (2005). Causes, role and influence of mood states.
Hauppauge, NY: Nova Biomedical Books.
Costa, G. (1999). Fatigue and biological rhythms. In D. J. Garland, J. A.
Wise, & D. V. Hopkin (Eds.), Handbook of aviation human factors Current Knowledge
(pp. 235255). Mahwah, NJ: Lawrence Erlbaum.
Hasher, L., Goldstein, D., & May, C. P. (2005). Its about time: Circadian
rhythms, memory, and aging. In C. & Izawa N. Ohta (Eds.), Human The circle of Willis is formed by the connections between
learning and memory: Advances in theory and application: The 4th the predominantly horizontal branches that derive from
Tsukuba international conference on memory (pp. 199217). the middle cerebral arteries anteriorly and from the
Mahwah, NJ: Lawrence Erlbaum. basilar artery posteriorly. The right and left middle cere-
Johnson, C. H., Elliot, J., & Foster, R. (2004). Fundamental properties of
bral arteries each give off an anterior cerebral artery
circadian rhythms. In J. C. Dunlap, J. J. Loros, & P. J. DeCoursey
(Eds.), Chronobiology: Biological timekeeping (pp. 67105). Sunder- (forming the anterolateral borders of the circle of Willis),
land, MA: Sinauer Associates. which goes forward to supply blood to the frontal lobe.
Kolb, B., & Wishaw, I. Q. (2005). An introduction to brain and behavior. These anterior cerebral arteries are connected to each
New York: W. H. Freeman. other by the anterior communicating artery, which
Lee-Chiong, T. L. (2005). Sleep: A comprehensive handbook. Hoboken, NJ:
forms the front of the circle. Posteriorly, the basilar
Wiley.
Newman, C. F. (2006). Bipolar disorder. In F. Andrasik (Ed.), Compre- artery bifurcates into the right and left posterior cerebral
hensive handbook of personality and psychopathology: Vol. 2: Adult arteries, which supply the occipital and posterior tem-
psychopathology (pp. 244261). Hoboken, NJ: Wiley. poral lobes and the cerebellum, forming the posterior
Circles of Support C 583
border of the circle. Each posterior cerebral artery is personal goals. It is one of many tools addressing life
connected to the middle cerebral artery on its planning from a functional or strategic assessment ap-
corresponding side by a posterior communicating artery, proach known as person-centered planning. Person-
forming the posterolateral borders of the circle. There centered planning replaces more traditional assessment
are several clinical implications of the circle pattern approaches associated with the medical model of services. C
of these arteries. Perhaps most importantly, because Circles of support originated in Canada and have experi-
of the interconnectedness of the arteries that result enced widespread use in North America. Circles view
from this circle format, if one of the main arteries is people as individuals and assist them to attain self-
occluded, the distal smaller arteries that it supplies determination focusing upon empowerment and
can potentially receive blood from the other arteries not dependence of the individual. It is capacity oriented
that make up the circle, a phenomenon known as and identifies strengths, preferences, likes, and dislikes of
collateral circulation. This helps to prevent cerebral the individual. The circle will also identify support needs
ischemia and stroke. The circle of Willis also is a in order to achieve a particular goal.
common site for cerebral aneurysms, with the greatest The focus person leads the process and decides who
numbers involving the anterior communicating artery, will participate in the circle and the direction which the
posterior communicating arteries, and middle cerebral planning will take. Typically, a facilitator is selected
arteries. from within the circle to help energize the group. The
first circle is the circle of intimacy and includes
the people most intimate in the focus persons life. The
Cross References second circle, the circle of friendship, includes good
friends and close relatives. The third circle, the circle
Anterior Cerebral Artery of participation includes the people and organizations
Anterior Communicating Artery the focus person is involved with. The fourth circle is the
Basilar Artery circle of exchange and includes those that are paid to
Internal Carotid Artery be in the focus persons life. Members are not paid to be
Middle Cerebral Artery involved in a circle of support, but are involved in the
Posterior Cerebral Artery focus persons life in some capacity. Members use their
Posterior Communicating Artery skills, knowledge, and networks to help the focus person
Vertebrobasilar System accomplish goals. The circle develops and monitors
the plan, making sure that it is current with the wishes
of the focus person. It is as ongoing process that is
dynamic.
Circles of Support
A MY J. A RMSTRONG Cross References
Richmond, VA, USA Inclusion
Medical Model
Synonyms
Circle of friends
Falvey, M. A., Forest, M., Pearpoint, J., & Rosenberg, R. (1994). All my
lifes a circle. Using the tools: Circles, MAPs and PATH. Toronto,
Definition Canada: Inclusion Press.
OBrien, C. L., & OBrien, J. (2000). The origins of person-centered
planning: A community of practice perspective. Retrieved from
A circle of support is a group of people that forms a http://thechp.syr.edu/PCP_History.pdf
community around a specific individual (focus person) OBrien, J., & Lyle OBrien, C., (Eds.). (1998). A little book about person
with significant disabilities to assist him or her to achieve centered planning. Toronto: Inclusion Press.
584 C Circumduction
are often used by persons with aphasia when having

Circumduction difficulty recalling or retrieving a word. In place of the
target word, a description of the word is used. Circumlo-
T HESLEE J OY D E P IERO cutions, or substitutions of object description (e.g., snow/
Boston University School of Medicine soft, white/cold) and instrumental function (e.g., watch/
Braintree, MA, USA knowing the hour) can be observed in aphasic output
(Benson & Ardila, 1996; p. 53). They occur frequently
with a posterior (sensory) aphasia.
Synonyms Circumlocutions can represent a positive symptom
of anomia in which, upon failure to retrieve a word,
Spastic gait the subject talks around the word by defining it, describ-
ing a referent, or even making sound effects. Pointing
Definition to his wrist, a patient might say, I wear it right here,
and I tell time with it; mine goes tick, tick. The use
Circumduction describes the movement of the leg of a of circumlocutions is indicative of intact semantic activa-
person with hemiplegia, hemiparesis or paraplegia, tion and a general capacity to retrieve lexical forms
paraparesis. Lesions of the pyramidal tract cause more (Davis, p. 109).
weakness in the flexors of the leg than the extensors
(hip and knee flexors and ankle dorsiflexors). Because of
this weakness, the foot cannot be raised from the floor, Cross References
and the leg cannot be advanced in a straight line forward,
as it would do normally. The leg moves away from the Anomia
trunk, then it is advanced toward it during walking, in a Aphasia
circular pattern. The medial side of the shoe scrapes the
floor, causing excessive wear in that area.
Cross References
Benson, D. F., & Ardila, A. (1996). Aphasia: A clinical perspective.
Chapter 4, Linguistic analysis of aphasia, 4660. New York: Oxford
Hemiparesis University Press.
Hemiplegia Davis, G. A. (2000). Aphasiology: Disorders and clinical practice. Chap. 1,
Pyramidal Tract Introduction to acquired language disorders, 119 (p. 7); Chap. 5,
Investigating symptoms and syndromes, (92119). Needham Heights,
MA: Allyn & Bacon.
Victor, M., & Ropper, A. H. (2001). Adams and victors principals of
neurology (7th ed.). New York: McGraw-Hill.
Circumstantiality
R OBERT F RANK
Circumlocution Kent State University
Kent, OH, USA
C AROLE R. R OTH
San Diego, CA, USA Definition
Circumstantiality is circuitous thinking and speech that

Definition digresses from the essential point. It differs from tangen-
tiality in which the individual ultimately fails to address
The use of an unnecessarily large number of words the main idea. In circumsatantiality, the main point is
to express an idea. Evasion in speech. Circumlocutions never lost but may be clouded and its appearance
Civil Law C 585
delayed by excess and repeated material. Circumstantial Off Label Use

thinking is a characteristic of thought disorders.
Premenstrual dysphoric disorder, obsessive compulsive
disorder, panic disorder, generalized anxiety disorder,
Cross References posttraumatic stress disorder, and social anxiety disorder. C
Tangentiality
Side Effects
Serious
Seizures, mania, and suicidal ideation (all rare).

Circumventricular Organ
Subfornical Organ
Common
Sexual dysfunction, gastrointestinal upset, insomnia, se-

dation, tremor, headache, dizziness, sweating, bruising
Citalopram and very rare bleeding, rare hyponatremia, and a potential
for SIADH (syndrome of inappropriate antidiuretic hor-
J OHN C. C OURTNEY mone secretion).
Generic Name Physicians Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson
PDR.
Citalopram Stahl, S. M. (2007). Essential psychopharmacology: The prescribers guide
Brand Name
Celexa
Class Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.
Selective Serotonin Reuptake Inhibitor Pill Identification: http://www.drugs.com/pill_identification.html

Civil Action
Citalopram blocks the presynaptic serotonin reuptake
pump and desensitizes serotonin receptors, theoretically
Litigation
increases serotonin neurotransmission, and is a mild
antihistamine.
Indication Civil Law

Depression. Personal Injury
586 C Civil Litigation
Civil Litigation CJD

M OIRA C. D UX Creutzfeldt-Jakob Disease
Baltimore, MD, USA
Definition Classical Model of Aphasia

Civil law is a division of the law that deals primarily with WernickeLichtheim Model of Aphasia
disputes between individuals and/or organizations, in
which some form of compensation may be awarded to
the victim. Typically, civil law involves filing of a lawsuit
by a private party, called the plaintiff. Civil litigation
commonly involves hearing related to disputes regarding Classical Test Theory
torts, contracts, probate of wills, trusts, property, admin-
istrative law, commercial law as well as a plethora of other M ICHAEL D. F RANZEN
matters related to private parties and organizations. Allegheny General Hospital
Civil litigation primarily aims to correct an injustice, Pittsburgh, PA, USA
uphold an agreement, or settle a dispute. If compensation
is awarded to the victim, then the person/organization
responsible for the injustice is responsible for covering the
Definition
compensation. In civil litigation, the burden of proof is
usually placed on the plaintiff, though exceptions do exist.
Classical test theory is the body of concepts and methods
Punishment related to civil litigation is typically limited
that have formed the basis for psychological assessment.
to reimbursement for loses incurred by the plaintiff as a
Classical test theory posits that observed scores are the
result of actions/inactions committed by the defendant.
additive function of true scores and error terms. True
Incarceration is not a punishment rendered via civil liti-
scores are the ideal value of a construct in a particular
gation. Civil litigation and criminal litigation are not
person or situation. The error term is the effect of factors
mutually exclusive entities. For example, an individual
extraneous to the construct of interest. Error terms are
involved in a criminal case may seek compensation in
assumed to be independent of (or uncorrelated with)
civil court. For neuropsychologists, civil litigation typi-
the true scores. Analysis of the reliability of a score can
cally involves determination of causation, damages, and
be accomplished by manipulating factors thought to be
disability in disputes in which neuropsychological func-
influencing the error term. For example, in order to
tioning is of relevance (e.g., personal injury, medical
examine the effect of factors related to time or instance
malpractice).
of measurement, a test might be administered to the same
individuals on two different occasions. The relation
between the two observed scores, determined by calculat-
ing a correlation coefficient or by performing an analysis
of variance, helps to estimate the magnitude of the error
term and the proportion of the observed score that is
Greiffenstein, M. F. (2009). Basics of forensic neuropsychology. In
J. Morgan & J. Ricker (Eds.), Textbook of clinical neuropsychology. likely to be true score.
New York: Psychology Press.
Principles of productive attorney-neuropsychologists relations. Cross References
In G. Larrabee (Ed.), Forensic neuropsychology: A scientific approach.
Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C. (2007). Item Response Theory
Psychological evaluations for the courts (3rd ed.). New York: Guilford Reliability
Press. Sources of Error
Clinical Dementia Rating C 587
Embretson, S. E. (Ed.). (2010). Measuring psychological constructs: Beyond Reasonable Doubt

Advances in model-based approaches. Washington, DC: American Burden of Proof
Psychological Association.
Preponderance of Evidence C
Lord, F. M., & Novick, M. R. (2008). Statistical theories of mental test
scores. New York: Information Age Pub Inc.

Psychological evaluations for the courts: A handbook for mental
Clear and Convincing Evidence health professionals and lawyers (3rd ed.). New York: Guilford
Press.
Chicago, IL, USA
Client Generated Index (CGI)

Definition
Patient Generated Index
The burden of proof is the obligation to shift the as-
sumed conclusion away from an oppositional opinion
to ones own position: it may only be fulfilled by evi-
dence. Under the Latin maxim, necessitas probandi Clinical Dementia Rating
incumbit ei qui agit, the general rule is that the neces-
sity of proof lies with he who complains. The burden of J ING E E TAN 1, E STHER S TRAUSS 1,
proof, therefore, usually lies with the party making the E LISABETH M. S. S HERMAN 2
1
claim. The exception to this rule is when a prima facie University of Victoria
case has been made. He who does not carry the burden Victoria, BC, Canada
2
of proof carries the benefit of assumption, meaning he Alberta Childrens Hospital, University of Calgary
needs no evidence to support his claim. Fulfilling the Calgary, AB, Canada
burden of proof effectively captures the benefit of as-
sumption, passing the burden of proof off to another
party. Clear and convincing evidence is a burden of Synonyms
proof required of a plaintiff for him to win the lawsuit.
This standard is higher than mere preponderance of the CDR
evidence. Proof of fraud, for example, usually requires
clear and convincing evidence. Clear and convincing
evidence is the higher level of burden of persuasion Description
and is most often employed in civil litigation. To
prove something by clear and convincing evidence, The Clinical Dementia Rating (CDR; Hughes, Berg, Dan-
the party with the burden of proof must convince the ziger, Coben, & Martin, 1982) is a semi-structured,
trier of fact that it is substantially more likely than clinician-rated interview widely used to stage the progres-
not that the thing is in fact true. This is a lesser require- sion of dementia using information provided by the pa-
ment than proof beyond a reasonable doubt, which tient and an informant. A global CDR score is generated
requires that the trier of fact be close to certain of the to stage the severity of dementia. It is based on ratings
truth of the matter asserted, but a stricter requirement of the patients functioning in six domains commonly
than proof by preponderance of the evidence, which affected in Alzheimers disease (AD): memory, orienta-
merely requires that the matter asserted seem more tion, judgment and problem solving, community affairs,
likely true than not. home and hobbies, and personal care. The CDR rates only
588 C Clinical Dementia Rating
impairments due to cognitive deficits rather than to phys- that uses a total score generated from the sum of boxes
ical disability. Based solely on clinical information (CDR-SB) has gained popularity to quantify progression
obtained from the patient and informant, and without of AD in longitudinal clinical trials of experimental thera-
reference to psychometric performance, a box score de- pies (e.g., Petersen et al., 2005).
scribing the level of impairment is generated for each
domain. The box score ranges from 0 to 3, representing
none to severe impairment. Using a scoring algo- Psychometric Data
rithm, one of five possible stages is then derived from
the individual box scores as follows: CDR = 0 (no demen- Interrater Reliability
tia); CDR = 0.5 (questionable dementia); CDR = 1 (mild
dementia); CDR = 2 (moderate dementia); CDR = 3 (se- Most of the psychometric studies on the CDR have
vere dementia). Although not part of the original proto- focused on interrater reliability in multicenter clinical
col, CDR = 4 (profound) and CDR = 5 (terminal) can also trials. These studies have concluded that experience
be used to classify the later stages of dementia. An alter- using the CDR increases reliability estimates, although
native method that generates a total score (range 018) adequately trained inexperienced raters may also demon-
from the sum of boxes (CDR-SB) has also been used for strate a high level of agreement (kappa = 0.83 or higher;
quantification purposes in longitudinal studies (e.g., Schafer et al., 2004; Tractenberg, Schafer, & Morris, 2001).
Cortes et al., 2008). The CDR takes about 90 min to The CDR also shows good reliability among raters of
administer. various qualifications. There were no major differences in
The CDR has been used in clinical practice and mul- reliability among physicians, nurses, PhDs, social workers,
ticenter clinical trials, as well as in cross-cultural dementia psychometrists, or research assistant raters (85% for
studies around the world. The CDR protocol is available non-MDs and 82% for MDs; Oremus, Perrault, Demers,
in over 60 languages and dialects, including English, & Wolfson, 2000). Kappas between physician raters range
French, Spanish, Italian, Portuguese, Dutch, Czech, from 0.75 to 0.94 for the six individual domain scores and
Bulgarian, Russian, Tagalog, Afrikaans, Greek, German, CDR-SB score. Kappas between nurses, or between nurses
Hebrew, Indian dialects, Chinese dialects, Japanese, and and physicians, range from 0.66 to 0.77 (Oremus et al.,
Korean. These translations can be downloaded free of cost 2000).
on the CDR Web site (http://alzheimer.wustl.edu/cdr/
default.htm).
An online training video on the use of the CDR is Construct Validity
available free for individual users, and takes about 89 h to
complete. Detailed scoring algorithms, including tie-break Evidence for construct validity of the CDR appears solid.
rules, and an online scoring worksheet are available on the In the original study, the CDR had strong correlations
CDR Web site. with the Blessed Dementia Scale (BDS; r = 0.74) and the
Pfeiffer Short Portable Mental Status Questionnaire
(SPMSQ; r = 0.84) among individuals with CDR ratings
Historical Background between no dementia and very mild dementia (Hughes
et al., 1982). Correlations with various cognitive measures
The CDR was originally developed at the Washington ranged from small to large in community-dwelling sam-
University School of Medicine in 1979 to evaluate the ples (Folsteins Mini-Mental State Examination = 0.33;
progression of AD (Hughes et al., 1982). The original BDS = 0.74; SPMSQ = 0.84). Similar correlations were
protocol has evolved somewhat over the years, with box found with neuropsychological measures such as the
descriptors updated to sharpen the distinction between CERAD Boston Naming Test, list learning, and verbal
severity levels within each domain, and new scoring rules fluency (Oremus et al., 2000).
added to resolve scoring ambiguity (Morris, 1993). Alter- In terms of neuropathology, CDR = 0.5 (a proxy for
native scoring methods have also been suggested to im- mild cognitive impairment; MCI) has been associated
prove scoring accuracy (Gelb & St. Laurent, 1993). An with multiple pathological signs including those related
extension of this scale to include CDR = 4 (profound) and to AD, Lewy body dementia, or vascular dementia, as
CDR = 5 (terminal) to classify the later stages of dementia well as nonspecific pathology (Saito & Murayama,
(Dooneief, Marder, Tang, & Stern, 1996) among nursing 2007). Further, increased microglia activation, an inflam-
home elderly has been proposed. As well, another method matory biomarker of AD, was seen with advancing CDR
Clinical Dementia Rating C 589
stages (Xiang, Haroutunian, Ho, Purohit, & Pasinetti, populations (Lim, Chin, Lam, Lim, & Sahadevan, 2005;
2006). A negative association was also found between the Senanarong, Chen, & Orgogozo, 2006), although empiri-
CDR-SB score and glucose metabolism in the right poste- cal validation of various translations is needed.
rior cingulate gyrus (Perneczky, Hartmann, Grimmer, The CDR presents several advantages over psychomet-
Drzezga, & Kurz, 2007). ric tests. First, it is an assessment option for patients who C
are illiterate and/or have limited English language profi-
ciency. Moreover, it can also be used in the presence of
aphasia, a condition common among patients with
Predictive Validity
dementing disorders. Lastly, the administration of the
CDR does not require a standardized set of instructions,
There is evidence that individuals with higher CDR-SB
but is dependent upon a set of guidelines. As such, the
scores are more likely to develop dementia in the future
CDR is easily adapted for cross-cultural use (e.g., Lim
(Lynch et al., 2006). In addition, CDR scores predict
et al., 2005). A disadvantage of the CDR is that it is
survival in individuals with suspected dementia. Using
somewhat lengthy to administer.
survival as outcome, the median survival was 1 year for
CDR = 5, 2 years for CDR = 4, 2.5 years for CDR = 3,
3 years for CDR = 2, and 3.5 years for CDR = 1 (Dooneief
Cross References
et al., 1996). Use of the CDR as a screening tool for
dementia revealed a sensitivity of 92% and specificity of
Alzheimers Disease
94% for mild dementia in a community sample of adults
CERAD
older than age 75 (Juva et al., 1995).
Dementia
Clinical Uses
The original focus of the CDR was to assess community-
dwelling older adults, since its anchor points probe for Cortes, F., Nourhashemi, F., Guerin, O., Cantet, C., Gillette-Guyonnet, S.,
examples of ones engagement with the home and com- Andrieu, S., et al. (2008). Prognosis of Alzheimers disease today: A
two-year prospective study in 686 patients from the REAL-FR study.
munity. However, it has also been adapted for use in
Alzheimers and Dementia, 4(1), 2229.
chronic long-term care facilities (Marin et al., 2001). Dooneief, G., Marder, K., Tang, M. X., & Stern, Y. (1996). The Clinical
The global CDR is widely used primarily for the staging Dementia Rating scale: community-based validation of profound
of AD. It has also been used to stage other dementing and terminal stages. Neurology, 46, 17461749.
disorders such as Parkinsons disease and frontotemporal Gelb, D. J., & St. Laurent, R. T. (1993). Alternative calculation of the
global clinical dementia rating. Alzheimer Disease & Associated
dementia. In recent years, CDR = 0.5 has been used to
Disorders, 7(4), 20211.
characterize MCI; however, there is evidence that a large Hughes, C. P., Berg, L., Danziger, W. L., Coben, L. A., & Martin, R. L.
proportion (29.7%) of individuals at CDR = 0.5 also meet (1982). A new clinical scale for the staging of dementia. British
ICD-10 criteria for mild dementia (Lynch et al., 2006). Journal of Psychiatry, 140, 566572.
In terms of longitudinal studies of AD progression, Juva, K., Sulkava, R., Erkinjuntti, T., & Ylikoski, R. (1995). Usefulness of
the Clinical Dementia Rating scale in screening for dementia. Inter-
both the global CDR and the CDR-SB appear to be
national Psychogeriatrics, 7(1), 1724.
useful for tracking cognitive changes over a 23 year Lim, W. S., Chin, J. J., Lam, C. K., Lim, P. P. J., & Sahadevan, S. (2005).
period (e.g., Cortes et al., 2008; Meguro et al., 2004). Clinical Dementia Rating: experience of a multi-racial Asian
Of the two scoring methods, the CDR-SB is more population. Alzheimer Disease and Associated Disorders, 19(3),
commonly used in clinical drug trials because it was 135142.
Lynch, C., Walsh, C., Blanco, A., Moran, M., Coen, R., Walsh, J., et al.
found to be sensitive to changes within 12 months follow-
(2006). The clinical dementia rating sum of box score in
ing baseline measurement in donepezil drug trials, where- mild dementia. Dementia and Geriatric Cognitive Disorders, 21(1),
as the global CDR was not (e.g., Petersen et al., 2005). 4043.
There is also evidence that the CDR-SB is more useful Marin, D., Flynn, S., Mare, M., Lantz, M., Hsu, M., Laurans, M., et al.
than the global CDR in distinguishing mild cognitive (2001). Reliability and validity of a chronic care facility adaptation of
the Clinical Dementia Rating scale. International Journal of Geriatric
deficits from dementia (Lynch et al., 2006).
Psychiatry, 16(8), 745750.
In addition to western populations, use of the CDR Meguro, K., Shimada, M., Yamaguchi, S., Sano, I., Inagaki, H.,
has also been accepted as an appropriate comprehensive Matsushita, M., et al. (2004). Neuropsychosocial features of very
measure for studies of dementia patients in Asian mild Alzheimers Disease (CDR 0.5) and progression to dementia
590 C Clinical Depression
in a community: The Tajiri Project. Journal of Geriatric Psychiatry

and Neurology, 17(4), 183189. Clinical Interview
Morris, J. C. (1993). The clinical dementia rating (CDR): Current version
and scoring rules. Neurology, 43(11), 24122414.
K IMBERLY A. G ORGENS
Oremus, M., Perrault, A., Demers, L., & Wolfson, C. (2000). A review of
outcome measurement instruments in Alzheimers disease drug University of Denver
trials: Psychometric properties of global scales. Journal of Geriatric Denver, CO, USA
Psychiatry and Neurology, 13(4), 197205.
Perneczky, R., Hartmann, J., Grimmer, T., Drzezga, A., & Kurz, A. (2007).
Cerebral metabolic correlates of the clinical dementia rating scale in
mild cognitive impairment. Journal Of Geriatric Psychiatry And
Synonyms
Neurology, 20(2), 8488.
Petersen, R. C., Thomas, R. G., Grundman, M., Bennett, D., Doody, R., Diagnostic interview; Intake; Intake interview; Unstruc-
Ferris, S., et al. (2005). Vitamin E and Donepezil for the treatment tured clinical interview
of Mild Cognitive Impairment. New England Journal of Medicine,
352(23), 23792388.
Saito, Y., & Murayama, S. (2007). Neuropathology of mild cognitive
impairment. Neuropathology, 27(6), 578584. Definition
Schafer, K., Tractenberg, R., Sano, M., Mackell, J., Thomas, R., Gamst, A.,
et al. (2004). Reliability of monitoring the clinical dementia rating in A skillfully conducted clinical interview is the cornerstone
multicenter clinical trials. Alzheimer Disease & Associated Disorders,
of psychological assessment. This interaction, typically a
18(4), 219222.
Senanarong, V., Chen, C., & Orgogozo, J. (2006). Third Asia- face-to-face meeting that lasts between 30 min and 2 h,
Pacific Regional Meeting of the International Working Group generates a tremendous amount of data for the clinician via
on Harmonization of Dementia Drug Guidelines: Meeting both observation and direct questioning. Information
Report Summary. Alzheimer Disease & Associated Disorders, 20(4), obtained through observation during the clinical interview
311312.
is considered qualitative or descriptive, and can include
Tractenberg, R., Schafer, K., & Morris, J. (2001). Interobserver disagree-
ments on clinical dementia rating assessment: Interpretation and impressions about cognition, attention, orientation, lan-
implications for training. Alzheimer Disease & Associated Disorders, guage, sensorimotor deficits, affect, insight, attitude toward
15(3), 155161. assessment, acculturation, hygiene, interpersonal relations,
Xiang, Z., Haroutunian, V., Ho, L., Purohit, D., & Pasinetti, G. M. (2006). and coping mechanisms, among other variables. In addi-
Microglia activation in the brain as inflammatory biomarker of
tion, the verbal exchange between patient and clinician
Alzheimers disease neuropathology and clinical dementia. Disease
Markers, 22(12), 95102. yields information about current life circumstances, in-
cluding the reason for referral and history of the presenting
problem, as well as an account of developmental/medical/
family history, educational and occupational achievement,
legal problems, sociocultural/religious considerations, sub-
stance abuse, and other relevant psychiatric issues. Together
Clinical Depression with test data and collateral information, interview materi-
al is an invaluable tool for clinical hypothesis formulation
Major Depression
and testing, as well as treatment planning.
Current Knowledge
Clinical Extender There are three types of clinical interview, reflecting
the degree to which the content and questions are scripted:
Psychometrician structured, semi-structured, and unstructured. A struc-
tured interview (e.g., the Structured Clinical Interview for
DSM-IV-Clinical Version [SCID-I]; First, Gibbon, Spitzer,
& Williams, 2001), like any standardized assessment tool,
gathers specific data that allows clinicians to make com-
Clinical Importance parisons between client and normative group function.
Criticisms of structured clinical interviews include a frus-
Clinical Significance tration with lengthy questionnaires and the missed
Clinical Neuropsychology C 591
opportunity for meaningful dialogue (Maruish, 2008). An Referral Question

unstructured clinical interview, on the other hand, is Self-Report Measures
principally reliant on clinical skill for direction. An opti- Structured Clinical Interview for DSM-IV (SCID-I)
mal unstructured clinical interview involves moving from Structured Interview of Reported Symptoms (SIRS)
broad content areas to more specific ones, from open- C
ended to more directive questions seeking yes/no re-
sponses. While the goals of clinical interviewing remain References and Readings
much the same regardless of format, critics have argued
that bias is more easily introduced into unstructured First, M., Gibbon, M., Spitzer, R. L., & Williams, J. B. W. (2001). Users
clinical interviews than standardized approaches. A hy- guide for the Structured Clinical Interview for DSM-IV Axis I disor-
brid, the semi-structured clinical interview, offers many ders. New York: Biometrics Research.
of the benefits of its structured and unstructured counter- Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuro-
parts, with breadth and depth chief among them. The psychological assessment, (4th ed.). New York, NY: Oxford
University Press.
semi-structured format ensures that all areas of potential Maruish, M. M. (2008). The clinical interview. In R. P. Archer & S. R.
clinical concern are assessed, while affording the clinician Smith (Eds.), Personality assessment. New York: Routledge.
the flexibility to dictate the degree of attention each con- Rogers, R. (2001). Diagnostic and structured interviewing. A handbook for
tent area receives. In addition, the semi-structured clinical psychologists. New York: Guilford Press.
interview can be altered to accommodate disabilities, it Sbordone, R. J. (2000). The assessment interview in clinical neuropsy-
chology. In G. Groth-Marnat (Ed.), Neuropsychological assessment in
can be abbreviated to meet the needs of the client (e.g., clinical practice (pp. 94126). New York: Wiley.
fatigue) or the setting (e.g., bedside assessment), and it Shedler, J. (2002). A new language for psychoanalytic diagnosis. Journal of
can be amended to include additional lines of inquiry. the American Psychoanalytic Association, 50, 429456.
As well as yielding information regarding patient Zimmerman, M. (1994). Interview Guide for Evaluating DSM-IV Psychi-
history and current functioning, a clinical interview offers atric Disorders and the Mental Status Examination. East Greenwich,
RI: Psych Products Press.
opportunities to build rapport and foster a working al- Zimmerman, M., & Mattia, J. I. (1999). Psychiatric diagnosis in clinical
liance. In addition to promoting satisfaction with the practice: Is comorbidity being missed? Comprehensive Psychiatry,
assessment process, the development of rapport may pro- 40(3), 182191.
mote compliance from a reluctant patient and provide a
foundation for follow-up discussions and interventions
that may be indicated. Also, the dialogue during a clinical
interview allows a clinician to provide important patient
education. The initial conversation may explicitly address Clinical Neuropsychology
confidentiality, insurance/fee setting, the nature and pur-
pose of the examination, the intended use of assess- A NTHONY Y. S TRINGER
ment data, and a summary of follow-up plans including Emory University
feedback sessions (Lezak, Howieson, & Lorig, 2004). Atlanta, GA, USA
Despite routine use in clinical practice, there is consid-
erable debate about the reliability of clinical interviews.
Many believe the variability in questioning undermines the Definition
utility of the tool itself. Some research has suggested that
unstructured clinical interviews often fail to detect psychiat- Clinical neuropsychology is a specialty within psychology
ric and comorbid conditions (Zimmerman & Mattia, 1999). that applies the science of brain-behavior relations to the
Other researchers find empirical rigor in skillful clinical assessment, diagnosis, treatment, and rehabilitation of
interviewing (Shedler, 2002, p. 429). This argument not- patients across the life span with neurological, medical,
withstanding, the clinical interview remains a staple as- neurodevelopmental, psychiatric, or other cognitive and
sessment tool, as fallible or effectual as the clinician. learning disorders (Barth et al., 2003). The American
Psychological Association (APA) defines a clinical neu-
ropsychologist as a professional psychologist who applies
Cross References principles of assessment and intervention based upon the
scientific study of human behavior as it relates to normal
Behavioral Assessment and abnormal functioning of the nervous system (APA,
Mental Status Examination 1989, pp. 22).
592 C Clinical Neuropsychology
Clinical neuropsychology is recognized as a specialty intended to measure what he termed biological intelli-
by APA, the American Board of Professional Psychology, gence. The influence of Galtons statistical methods is
and the Canadian Psychological Association. Though seen in Halsteads factor analysis of his test battery. Hal-
there is no agreed upon date for the emergence of the stead proposed a four-factor theory of biological intelli-
field, clinical neuropsychology began to be recognized as a gence in his 1947 book Brain and Intelligence. Halsteads
distinct professional discipline following a 1948 sympo- book was severely criticized by contemporary scholars,
sium at the APA annual meeting appropriately entitled and ultimately had little influence on theories of intelli-
Neuropsychology. In this symposium, Hans-Lukas gence (Hartman, 1991). Halsteads test battery, however,
Teuber described procedures he and Morris Bender devel- did prove highly influential. Ralph Reitan, a student of
oped to study the behavioral effects of penetrating missile Halstead, established a laboratory at the University of
wounds to the brain (Benton, 1987). Indiana Medical Center in 1950. Over the course of sever-
Clinical neuropsychology had many forerunners. In al decades, Reitan expanded upon Halsteads initial bat-
the 1880s, Sir Francis Galton opened a laboratory in tery, adding procedures for detecting aphasia and sensory
London where for a few pennies, people could take tests perceptual impairments and for comparing performances
of visual acuity, reaction time, and various psychophysical of the two sides of the body. Reitan developed adaptations
abilities. A cousin of Charles Darwin, Galtons ideas about of the original adult battery for children and adolescents,
eugenics have made him a historically controversial fig- collected normative data, and used discriminant function
ure. Nonetheless, factor analytic statistical methods grew analysis to validate the ability of the various batteries to
out of his work and became critical for the development discriminate brain damaged from neurologically healthy
and validation of mental ability tests. His work was put to individuals. The HalsteadReitan Neuropsychological
practical use in early twentieth-century France when psy- Test Battery set a standard of excellence for test develop-
chologists Alfred Binet and Theodore Simon developed ment in neuropsychology and for a time was the most
intellectual tests to identify and place children in need of widely used approach in clinical neuropsychological
special education. World War I also stimulated interest in assessment.
his work in the USA, as the military sought tests that Reitans students were also prolific (Reed, 1985). They
could efficiently identify the strengths and weaknesses of include Hallgrim Klve who studied with Reitan in the
large numbers of military recruits. As many as one million 1950s and then established a laboratory at the University
soldiers underwent mental ability testing during World of Wisconsin. Another student, Homer Reed, directed the
War I (Hartman, 1991). Neuropsychology Laboratory at the New England Medical
Just after World War I, the German American psychol- Center in Boston where he concentrated on use of the
ogist Shepherd Ivory Franz (1919) published detailed battery with pediatric patients. Phillip Rennick, who did
descriptions of tests of tactile sensation, motor coordina- fellowship training with Reitan, went on to establish a
tion, praxis, language, attention, memory, visuospatial laboratory at the former (now defunct) Lafayette Clinic
perception, reasoning, and intelligence. By 1924, hand in Detroit, and developed a repeatable neuropsychological
dynamometers, finger tapping keys, motor steadiness battery for situations in which serial testing is needed.
tests, form perception boards, and tests of color vision, Just as World War I provided an impetus for the
vibration sense, attention, and memory were available development of psychological ability tests, World War II
(Hartman, 1991). Though these tests were quickly stimulated the development of neuropsychological assess-
adopted by researchers (see Neuropsychology, Science of), ment and treatment methods because of the large number
clinical application came a few decades later. Franz advo- of veterans who returned having survived penetrating
cated for their clinical use in a series of lectures to the missile wounds to the brain. Reitans early work involved
Government Hospital for the Insane, starting in 1910 the examination of brain-injured World War II veterans.
(Hartman, 1991) and in 1904 was instrumental in estab- This population also provided the impetus for Hans-
lishing a psychological laboratory at Mclean Hospital in Lukas Teubers work in the USA and Aleksandr Romano-
Boston. This was the first such laboratory in a hospital vich Lurias work in Russia.
setting in the USA Teuber immigrated from Germany and served as a
In 1935, the experimental psychologist Ward Halstead noncommissioned naval officer before establishing the
opened a laboratory at the University of Chicago for the Psychophysiological Laboratory with the neurologist
psychological study of neurology and neurosurgery Morris Bender at New York University (Weinstein,
patients. Adopting techniques used to test animals in 1985). Besides being the focal point for numerous seminal
ablation studies, Halstead designed a series of tests studies, Teubers laboratory was the incubator for many
Clinical Neuropsychology C 593
neuropsychologists who went on to make important con- neuropsychology practitioners and researchers. Dr.
tributions including Joseph Altman, Lila Ghent, Rita Kaplan and her associates in Boston developed the pro-
Rudel, Josephine Semmes, and Sidney Weinstein. cess-approach to neuropsychological assessment, recog-
Meanwhile, working with Russian World War II veterans nizing that tests are complex and multifactorial and that
at the Burdenko Neurosurgical Institute in Moscow, Luria patients can take different paths to the same test score. C
developed a richly qualitative approach to neuropsycho- According to this approach, only by systematically analyz-
logical assessment that was in stark contrast to the quan- ing the process(es) by which patients arrive at their
titative and normatively based test batteries that were in responses, often by parsing a test into fine-grained com-
use in the USA Luria also was an exponent of neuropsy- ponents, can a neuropsychologist truly understand what
chological approaches to rehabilitation and to use of aspect of brain functioning is compromised.
pharmacologic agents to enhance recovery of function Activity was not confined to North America. Clinical
(Gualtieri, 1988). neuropsychology got its South American start when C.
Besides having cognitive disorders, many injured Mendilaharsu and S. Acevedo de Mendilaharsu established
World War II veterans were aphasic, sparking neuropsy- the first South American neuropsychological laboratory
chological interest in language and the brain. Kurt in 1958 at the Neurological Institute in Montevideo,
Goldsteins ( Goldstein, Kurt) book Language and Lan- Uruguay (Ardila, 1990). Despite sometimes challenging
guage Disorders, published in 1948, combined his theories economic conditions, South American neuropsycholo-
about abstracting ability with neurologys classic anato- gists conducted investigations of constructional ability,
mico-clinical syndrome approach to aphasia. The num- dementia, and language. The field spread to Mexico,
bers of aphasic veterans available for study along with Peru, Columbia, Chile, Argentina, Brazil, Honduras,
Goldsteins influential book attracted experimental neu- Nicaragua, and elsewhere.
ropsychologists and psycholinguists to the study of lan- Clinical neuropsychology as a profession has be-
guage disorders (Goodglass, 1985). Aphasia research come increasingly organized since its inception. The
centers began to appear in the USA, among them being International Neuropsychological Society (INS), the
a laboratory established by Arthur Benton. National Academy of Neuropsychology (NAN), and
In 1948, the year of Teubers seminal APA presenta- the APA Division of Clinical Neuropsychology (Divi-
tion, Arthur Benton accepted an appointment as Profes- sion 40) are the most well-known professional neuro-
sor of Psychology at the University of Iowa, and by 1950 psychological organizations within the USA. Founded
established a neuropsychological testing unit at the Uni- in 1967, INS has a membership that exceeds 3,500.
versity of Iowa Hospitals (Hamsher, 1985). There, Benton NAN, formed in 1974, includes more than 3,000 mem-
and his students and colleagues conducted normative bers. Division 40 of the American Psychological Associ-
studies, examining the effects of age, gender, and educa- ation, incorporated in 1980, is the most recent of these
tion. They also developed a variety of tests for use in professional organizations, with a membership of over
studying what had previously been vaguely defined clini- 4,000 neuropsychologists. Although smaller in member-
cal disorders such as the Gerstmann syndrome ship, neuropsychologists have formed similar profes-
( Gerstmann Syndrome). Over the next 2 decades, Ben- sional organizations throughout Europe, Asia, South
tons laboratory was home to numerous neuropsychology America, Australia, and Africa (see, for example, Jodzio,
pioneers including Max Fogel, Donald Shankweiler, Kerry 1998; Nihashi, 1998; Preilowski, 1997).
deS. Hamsher, Nils Varney, Scott Lindgren, Otfried Formal courses and organized programs of instruc-
Spreen, and Harvey Levin (Hamsher, 1985). Bentons tion in clinical neuropsychology began to appear in the
laboratory conducted important studies of aphasia using 1960s, with one of the first offered in the Biological
control group designs, psychological test construction Psychology Doctoral Program at the University of
methods, statistical analysis, and psycholinguistic theory. Oklahoma Health Sciences Center (Parsons, 1991). Qual-
The behavioral neurologist Norman Geschwind, along ity and content of instruction varied from program to
with his colleagues Davis Howes and Harold Goodglass, program as they multiplied in the 1970s. In 1979,
established an aphasiology center at the Boston Veterans Dr. Manfred Meier initiated an effort to establish stan-
Administration Hospital, continuing the more rigorous dards of training and competence for neuropsychologists
neuropsychological approach to language disorders. The in the USA. This effort culminated first in the establish-
Boston VA became a major center for neuropsychological ment of the American Board of Clinical Neuropsychology
training and research with Dr. Edith Kaplan famously (ABCN) in 1981. A year later, the American Board of
serving there as mother to a generation of Professional Neuropsychology (ABN) was established
594 C Clinical Neuropsychology
with a similar goal of establishing standards of profes- International Neuropsychological Society

sional expertise in neuropsychology. These two certifica- Luria, Alexander Romanovich (19021977)
tion bodies continue to function autonomously, though National Academy of Neuropsychology
ABCN affiliated with the American Board of Professional Neuropsychiatry
Psychology (ABPP) in 1984, joining other boards that Neuropsychology, Science of
conduct peer review of the credentials, knowledge, and Reitan, Ralph (1922 )
practice of clinical psychologists seeking subspecialty cer- Teuber, Hans-Lukas (19161977)
tification in the USA.
In 1987, APA Division 40 published guidelines for
doctoral, internship, and postdoctoral training in neuro- References and Readings
psychology and a year later formally adopted the defini-
tion of a clinical neuropsychologist quoted above. American Psychological Association Division 40 (1989). Definition of a
clinical neuropsychologist. The Clinical Neuropsychologist, 3, 22.
Included in this definition (but not quoted) were explicit
Ardila, A. (1990). Neuropsychology in Latin America. The Clinical Neu-
training, supervision, licensing, and peer review require- ropsychologist, 4, 121132.
ments that must be met by neuropsychologists. APA also Barth, J. T., Pliskin, N., Axelrod, B., Faust, D., Fisher, J., Harley, J. P., et al.
recognized attainment of the ABCN/ABPP diploma as (2003). Introduction to the NAN 2001 definition of a clinical neu-
the clearest evidence of competence as a Clinical Neu- ropsychologist. Archives of Clinical Neuropsychology, 18, 551555.
Benton, A. (1987). Evolution of a clinical specialty. In K. M. Adams, &
ropsychologist (APA Division 40, 1989). As of 2010, over
B. P. Rourke (Eds.), The TCN guide to professional practice in clinical
500 practicing clinicians have attained ABPP/ABCN dip- neuropsychology (pp. 14). Amsterdam: Swets & Zeitlinger.
lomate status in neuropsychology and over 350 neurop- Goldstein, K. (1948). Language and language disorders. Orlando, FL:
sychologists had attained ABN certification. Grune & Stratton.
Though ABCN and ABN initially differed in their Goodglass, H. (1985). Aphasiology in the United States. International
Journal of Neuroscience, 25, 307311.
examination procedures, currently both boards require a
Groth-Marnat, G. (2000). Introduction to neuropsychological assessment.
peer review of credentials, a multiple-choice written In G. Groth-Marnat (Ed.), Neuropsychological assessment in clinical
exam, and a 1 h ethics oral exam. The two boards differ, practice: A guide to test interpretation and integration (pp. 325).
however, in other aspects of their oral examination. In New York, NY: Wiley.
particular, ABCN, but not ABN, conducts an oral fact- Gualtieri, C. T. (1988). Pharmacotherapy and the neurobehavioural se-
quelae of traumatic brain injury. Brain Injury, 2, 101129.
finding examination in which candidates solicit informa-
Hamsher, K. D. (1985). The Iowa Group. International Journal of Neuro-
tion about a neuropsychological patient in order to arrive science, 25, 295305.
at a diagnostic formulation and clinical recommenda- Hartman, D. E. (1991). Reply to Reitan: Unexamined premises and the
tions. Nonetheless, the two boards have grown more evolution of clinical neuropsychology. Archives of Clinical Neuropsy-
similar since their inception, and have discussed merger, chology, 6, 147165.
Jodzio, K. (1998, Spring). Neuropsychology in Poland: Past and present.
but these efforts have been unsuccessful. One milestone
International Neuropsychological Society Liaison Committee Newslet-
likely to occur in the USA in the twenty-first century is the ter, 5, 13.
achievement of widespread ABCN or ABN diplomacy Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). The practice of
among those identifying neuropsychology as their prima- neuropsychological assessment. In Neuropsychological assessment
ry area of specialization. This milestone would signal (4th ed., pp. 314). New York, NY: Oxford University Press.
Nihashi, N. (1998, Spring). Neuropsychology in Japan. International
the professional and organizational maturity of clinical
Neuropsychological Society Liaison Committee Newsletter, 5, 13.
neuropsychology. Parsons, O. A. (1991). Clinical neuropsychology 19701990: A personal
view. Archives of Clinical Neuropsychology, 6, 105111.
Preilowski, B. (1997). Establishing clinical neuropsychology in Germany:
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Reed, J. (1985). The contributions of Ward Halstead, Ralph Reitan and
American Board of Clinical Neuropsychology (ABCN) their associates. International Journal of Neuroscience, 25, 289291.
American Board of Professional Neuropsychology Stringer, A. Y., & Cooley, E. L. (2002). Neuropsychology: A twentieth-
American Psychological Association (APA), Division 40 century science. In A. Y. Stringer, E. L. Cooley, & A.-L. Christensen
Benton, Arthur (19092006) (Eds.), Pathways to prominence in neuropsychology: Reflections of twen-
tieth century pioneers (pp. 326). New York, NY: Psychology Press.
Forensic Neuropsychologist
Weinstein, S. (1985). The influence of Hans-Lukas Teuber and the
Forensic Neuropsychology psychophysiological laboratory on the establishment and develop-
Geschwind, Norman (19261984) ment of neuropsychology. International Journal of Neuroscience, 25,
Halstead, Ward (19081968) 277288.
Clinical Practice Guidelines C 595
guide the allocation of health care resources, and

Clinical Practice Guidelines (5) reduce the risk of liability for negligent care
(IOM, 1992).
A NDREA M. L EE In addition to patients and their families, health care
University of Manitoba providers, and health care institutions, others such as
Winnipeg, Manitoba, Canada
C
payers, health care benefit providers, and public policy
makers have a stake in clinical practice guidelines. Legis-
lators, regulators, and health care purchasers take an
Synonyms interest in studying them to assist them in making deci-
sions that control health care costs. It is assumed that if
Practice guidelines the most appropriate care is administered, better health
outcomes will be achieved and health care costs will be
lowered. Although some guidelines could likely achieve
such hopes for decreased health care costs, other guide-
Definition lines may not.
The Agency for Healthcare Research and Quality
According to the Institute of Medicines 1990 report, (AHRQ), formerly known as the AHCPR, created a
Clinical Practice Guidelines: Directions for a New Program, central public resource for evidenced-based clinical prac-
clinical practice guidelines are systematically developed tice guidelines called the National Guideline Clearing-
statements to assist practitioner and patient decisions house (NGC) that can be accessed at http://www.
about appropriate health care for specific clinical guideline.gov/
circumstances. For a clinical practice guideline to be included on the
NGC, the following criteria must be met: (1) The guide-
line must contain systematically developed recommenda-
tions, strategies, or information that assist in the decision
Historical Background making of appropriate health care in specific clinical
situations by healthcare providers and patients; (2) the
Recommendations for appropriate care have been found guideline must be produced by a medical specialty associ-
in ancient writings (IOM, 1992). Modern guidelines have ation, professional societies, public or private organiza-
been developed by professional organizations for over tions, government agencies, or health care organizations
50 years. It was only in the 1990s, however, that the or plans; (3) a documentation should be produced that
systematic, evidence-based guidelines began to appear verifies that a systematic literature search and review of
with any regularity. In November 1989, the Agency for scientific literature was performed during the guideline
Health Care Policy and Research (AHCPR) was created development; (4) the guidelines should have been
with, among other responsibilities, a mandate to devel- reviewed or produced within 5 years and should be avail-
op, disseminate, and evaluate clinical practice guidelines. able in print or electronic format in the English language
The AHCPR then enlisted the Institute of Medicine (National Guideline Clearinghouse, 2009). These criteria
(IOM) for advice. The result was the 1990 report gener- ensure minimum quality of guidelines submitted to
ated by the IOM, called Clinical Practice Guidelines: the NGC.
Directions for a New Program, that aimed to encourage
standardization and consistency in the development of
guidelines.
Future Directions
An ongoing challenge is the implementation of clinical
Current Knowledge practice guidelines and ensuring their application by
health care providers. Factors such as information over-
The five major purposes of clinical practice guidelines load, habitual practice patterns, fears of malpractice, and a
are to: (1) aid in clinical decision-making by patients lack of economic incentives create barriers to guideline
and health care providers, (2) educate individuals application and each must be addressed on an individual
or groups, (3) assess and ensure quality of care, (4) and systemic level.
596 C Clinical Relevance
Cross References Clinical significance also refers to a static condition of

import for example, a functionally relevant discrepancy
AACN Practice Guidelines between cognitive abilities in different domains (e.g., lan-
guage vs. visual-perceptual abilities). The term can also
refer to the level of distress or impairment related to
References and Readings psychological symptoms as criteria for a DSM-IV TR
disorder diagnosis.
IOM. (1990). In M. J. Field & K. N. Lohr (Eds.), Clinical Practice guide- While clinical significance may be supported by sta-
lines: Directions for a new program. Washington, DC: National tistically significant differences on quantitative measures
Academy Press. of functioning, statistical significance cannot be equated
IOM. (1992). In M. J. Field & K. N. Lohr (Eds.), Guidelines for clinical
with clinical significance.
practice: From development to use. Washington, DC: National
Academy Press.
National Guideline Clearinghouse. (2009). Inclusion criteria. Retrieved
October 13, 2009, from the National Guideline Clearinghouse Web
site: http://www.guideline.gov/submit/inclusion.aspx Cross References
Functional Assessment
Premorbid Functioning
Clinical Relevance Quality of Life
Reliable Change Index
Clinical Significance Response to Intervention
Statistical Significance
Clinical Significance References and Readings

M ONICA K URYLO 1, J ASON VAN A LLEN 2 American Psychiatric Association. (2000). Diagnostic and statistical man-
1
The University of Kansas Medical Center ual of mental disorders (Rev. 4th ed.). Washington, DC: American
Kansas, KS, USA Psychiatric Association.
2 Jacobson, N. S., Roberts, L. J., Berns, S. B., & McGlinchey, J. B. (1999).
University of Kansas
Methods for defining and determining the clinical significance of
Lawrence, KS, USA treatment effects: Description, application, and alternatives. Journal
of Consulting and Clinical Psychology, 67, 300307.
Jacobson, N. S., & Truax, P. (1991). Clinical significance: A statistical
Synonyms approach to defining meaningful change in psychotherapy research.
Journal of Consulting and Clinical Psychology, 59, 1219.
Kazdin, A. E. (1999). The meanings and measurement of clinical
Clinical importance; Clinical relevance significance. Journal of Consulting and Clinical Psychology, 67,
332339.
Kazdin, A. E. (2003). Clinical significance: Measuring whether interven-
Definition tions make a difference. In A. E. Kazdin (Ed.), Methodological issues
and strategies in clinical research (3rd ed., pp. 691710). Washington,
DC: American Psychological Association.
Clinical significance is a perceived, valued, and function- Spitzer, R. L., & Wakefield, J. C. (1999). DSM-IV diagnostic criterion for
ally relevant discrepancy in symptoms/abilities that clinical significance: Does it help solve the false positives problem?
reflects an important change in functioning. This can American Journal of Psychiatry, 156, 18561864.
involve either an improvement (usually as a result of
treatment or intervention) or a decline (typically due
progression of illness or disorder) as measured by symp-
toms or impairment level. The relevance and value of
this to difference may be determined by the client, mental Clinical Target Volume
health professional, and/or the clients significant
other(s). Involved Field Radiotherapy
Clock Drawing C 597
Disorders of Speech (1926), assessed aphasic patients using

Clock Drawing a wide number of drawing tests including the clock test
(p. 214) to assess deficits in understanding and executing
DAVID J. L IBON 1, E DITH K APLAN 2, R OD S WENSON 3, complex propositional speech and deficits associated with
DANA L. P ENNEY 4 symbol formation. In describing propositional speech and
1
Drexel University College of Medicine
C
symbolic formation deficits associated with aphasia, Head
Philadelphia, PA, USA (1926) wrote any act of mental expression, which
2
Suffolk University demands symbolic formulation, tends to be defective
Boston, MA, USA and the higher its propositional value the greater the
3
North Dakota School of Medicine difficulty it will present (p. 212). Head (1926) provided
Fargo, ND, USA many examples of aphasic patients who demonstrated
4
The Lahey Clinic striking impairment in executing the propositional com-
Burlington, MA, USA mand to set the clock hands for a specified time. For
example, Head described an aphasic patient who was
able to set clock hands correctly at 3:40, but not when
Description he was told to place the hands at 20 minutes to 4. For
this latter test condition (20 minutes to 4), Head com-
Clock Drawing Test (CDT) is a widely used and popular mented that his patient appeared doubtful of the mean-
neuropsychological test. Rubin, Barr, and Burton (2005) ing of the words 20 minutes to. Other researchers have
reported that the CDT appears in the top 40 tests most used the CDT to assess deficits in symbolic formation in
commonly used by neuropsychologists. The CDT is often neurologic patients (Mayer-Gross, 1935; McFie & Zangwill,
considered to be a visuoconstructional test. Modern ver- 1960; Van Horst, 1934).
sions of the CDT usually contain at least two parts clock Classically trained neurologists often associate the
drawing to command and clock drawing to copy. In the CDT as a means to assess constructional apraxia. Kleist
command condition, patients are presented with a blank (1912, cited in Benton & Tranel, 1993) described con-
sheet of paper and are asked to draw the face of a clock structional apraxia as deficits in formative activities nec-
showing the numbers and the two hands set for ten after essary to assemble parts into a meaningful whole. For
eleven. In the copy condition, a pre-drawn model of a Kleist, the essential defect in constructional apraxia was
clock with numbers and hands set for 10 after 11 is the ineffective translation of visuoperceptual information
presented, and the patient is asked to copy the model. into an effective motor act. In this sense, the concepts of
Clock drawing with hands set for ten after eleven is Kleist are consistent with the constructs Head (1926) used
an innovation introduced by Edith Kaplan (Kaplan, to understand impaired clock drawings produced by
1988, 1990). aphasic patients. Interestingly, Kleist tended to associate
As described below, other versions of the CDT ask the constructional apraxia with lesions in the left posterior
patient to set the hands for other times. Also, some ver- cortex. This is in stark contrast to the anecdotal point of
sions of the CDT include a clock subtest in which patients view that tends to automatically associate defective clock
are presented with pre-drawn clock faces with and withdrawing (or any other impaired figure copying test for
out numbers and/or hands and are asked to either draw that matter) with a right parietal lesion. While it is cer-
clock hands to designate specific times or read the speci- tainly true that patients with right parietal lesions often
fied time (Borod, Goodglass, & Kaplan, 1980; Leach, produce very spatially impaired clock drawings, it is naive
Kaplan, Reweilak, Richards, & Proulx, 2000; Tuokko, to automatically associate impaired clock drawing with
Hadjustavropoulos, Miller, & Beattie, 1992). either a lesion in any single brain region, or as a measure
of any single cognitive operation. As described below,
defective clock drawings to command and copy can be
Historical Background associated with a wide array of neurologic lesions and
underlying cognitive disorders.
Since the late 1980s, a profusion of research using the Many time settings have been used in the CDT. Kaplan
CDT as an assessment tool for dementia has emerged. (1988, 1990) recommends using ten after eleven. First,
However, some of the more interesting historical roots clock setting for ten after eleven requires the patient to
of the CDT came from research with aphasic patients. disambiguate a complex propositional command. Sec-
Henry Head, in his magnum opus Aphasia and Kindred ond, since the numbers 10 and 11 are on the clock,
598 C Clock Drawing
patients need to resist the temptation to be pulled to the patients are presented with a blank page and asked to
numbers 10 and 11. Thus, clock setting to ten after draw a clock with numbers and set the hands for ten
eleven tends to elicit a variety of stimulus-bound errors. after eleven, (3) a pre-drawn clock face where patients
In a survey of neuropsychologists and neurologists are asked to put in all the numbers and set the hands for
described by Freedman, Leach, Kaplan, Shulman, and 20 after 8, (4) a clock reading test with hands, but without
Delis (1994), other commonly used clock settings include numbers where patients are asked to identify a specified
20 after 8 and 3 oclock. time, and (5) a clock reading test with numbers and hands
where patients are, again, asked for the specified time. For
clock drawing to command and copy, behavior related to
Psychometric Data the drawing of the clock face, the numbers, and hands,
and the representation of the clock hands originating
Some scoring guidelines for the CDT can be found as part from the center of the clock are each scored using a
of the Boston Diagnostic Aphasia Examination supple- 13-point scoring system. The pre-drawn clock face condi-
mentary language tests (BDAE; Goodglass & Kaplan, tion is scored using an 11-point scoring system. Thus, for
1972, 1983; Goodglass, Kaplan, & Baresi, 2001). In this portion of the test scores have a 037 point range.
the original BDAE (with the rakishly purple cover [see Each clock reading subtest contains six test stimuli. Per-
Hollands forward to the third edition of the BDAE, formance on the three clock drawing test conditions are
2001]), the CDT test was one of several tests believed to combined with a score measuring the copy of a complex
be sensitive to parietal lobe injury. As described in the figure for a combined age-corrected scale score. The two
BDAE corpus, clock drawing is one of six figures where clock reading subtests are scored separately (range 06).
patients are asked to draw to command and copy (i.e., a For these two tests, age-related percentile cut scores are
clock with hands set for 10 after 11, a daisy, an elephant, provided.
a red cross, a three-dimensional cube, and a house). For Freedman, Leach, Kaplan, Shulman, and Delis (1994)
the clock drawing portion of the test, a three-point described a very comprehensive clock scoring system
scoring system was described awarding a point for an using a variety of clock drawing conditions and clock
approximately circular clock face, symmetry of number settings. Normative data was collected and grouped by
placement, and correctness of numbers. No scoring for decade from age 20 to 80. Separate scales were devel-
the representation of the clock hands was suggested. oped to assess the drawing of the clock face, the drawing
Normative data for the entire figure drawing test of the numbers, the presence and drawing of the clock
(range 013 for the separate command and copy test hands, and the degree to which the clock hands emanated
conditions) is provided. Separate normative data for from the center of the clock face. Base rates for a wide
the CDT is not included. Additional normative informa- range of clock drawing behavior are provided. These data
tion is provided by Borod, Goodglass, and Kaplan show that certain errors occur more frequently with age.
(1980). In this report, norms are also provided for two For example, for clock setting using ten after eleven, the
additional clock assessment procedures clock setting representation of the clock hands tends to be differentially
with numbers and clock setting without numbers. In affected by age.
both tests, the patient is presented with pre-drawn clock As noted above, a wide number of clock drawing
faces with and without numbers and are asked to draw the procedures have been reported (Lezak, Howison, & Lor-
hands to read 1:00, 3:00, 9:15, and 7:30. Performance is ing, 2004); however, most researchers follow Kaplans
assessed using a 12-point scoring system. Borod and col- (1988, 1990) suggestion and ask patients to set the
leagues (1980) described both age and educational effects hands for ten after eleven (Freedman et al., 1994). It is
for this clock assessment procedure. Other researchers important to understand that many CDT scoring proce-
have commented on the effects of education on clock dures are essentially atheoretical, that is, the administra-
drawing test performance (Marcopulos, McLean, & tion and scoring procedures were devised with an
Giuliano, 1997). eye toward sensitivity to brain damage or neurological
The Kaplan-Baycrest Neuropsychological Survey insult rather than to assess for deficits involving specific
(KBNS; Leach et al., 2000) contains a comprehensive cognitive constructs. Recent research, particularly in
clock test consisting of five parts: (1) clock drawing to using the CDT as part of a dementia evaluation, suggests
command where patients are asked to draw the face that the command and copy conditions are related to
of clock put in all the numbers and set the hands for different underlying cognitive mechanisms (Cosentino,
10 after 11, (2) a clock drawing to copy condition where Jefferson, Chute, Kaplan, & Libon, 2004; Libon, Swenson,
Clock Drawing C 599
Barnoski, & Sands, 1993; Libon, Malamut, Swenson, & in the command condition may be due to a deficit in
Cloud, 1996; Rouleau, Salmon, Butters, Kennedy, & visuospatial memory. Tranel, Rudrauf, Vianna, and
McGuire, 1992). Equally important, different results are Damasio (2008) administered the CDT to a large group
obtained depending on test instruction (see Cosentino of focal lesioned patients. Imaging studies found errors on
et al., 2004 for a review). These considerations are criti- the CDT were associated with right parietal (supramargi- C
cally important when the task at hand is to differentiate nal gyrus) and left inferior frontal-parietal opercular
between say, dementia subtypes. brain damage. These researchers also noted that visuospa-
tial errors were predominant in patients with right hemi-
sphere damage, whereas time-setting errors were
Clinical Uses predominant in patients with left hemisphere lesions.
Dementia As noted above, since the late 1980s, there
Focal lesions Clock drawing has not been extensively has been a plethora of research demonstrating the value
studied in non-dementia, focal lesioned patients. None- of the clock drawing test as both a screening test for
theless, specific patterns of deficits can be associated with dementia as well as a means of investigating cognitive
specific neurologic lesions. Freedman et al. (1994) and constructs that may differentiate between dementia sub-
Kaplan (1988, 1990) provide some instructive exemplars. types (see Cosentino et al., 2004 for a review). Rouleau
For example, patients with left posterior brain lesion et al. (1992, 1996) examined patients with Alzheimers
resulting in a Wernickes aphasia often present with lan- disease (VaD) and Huntingtons disease (HD) adminis-
guage comprehension deficits. While these patients may tering a clock drawing test to command and copy with
demonstrate general understanding of the clock drawing hands set for ten after eleven. An analysis of errors proved
instructions, numbers may be omitted entirely with hatch effective in differentiating between dementia subtypes.
marks used as substitutes (Freedman et al., 1994). Patients AD patients made more conceptual errors while HD
with a left anterior lesion presenting with a Brocas apha- patients produced more graphomotor errors. These
sia often have difficulty in understanding functor words authors speculated that semantic knowledge deficits
such as to and after. These patients, therefore, may be might underlie the deficits produced on the CDT by AD
apt to draw the clock hands pointing to the numbers 10 patients whereas executive dysfunction might underlie the
and 11. Further assessment is required to see if this kind errors produced by HD patients. When the command and
of error is caused by a language-related deficit or repre- copy conditions were compared, AD, but not HD patients
sents an executive deficit. Patients with left hemisphere improved from the command to copy test conditions.
lesions might initiate their drawing on the left side of the Rouleaus research was the impetus for a series of studies
clock, that is, on the side contralateral to their intact right conducted by Libon and colleagues (Cosentino et al., 2004;
hemisphere. Thus, numbers may be written correctly but Libon et al., 1993, 1996) that examined differences on
in a counterclockwise direction (Freedman et al., 1994). the CDT between patients with AD and vascular dementia
Interesting dissociations can be found in clock draw- (VaD). In their original study, Libon et al. (1993) found
ings to command versus copy in focal lesion patients. no difference in errors between AD and VaD patients in
Kaplan (1990) provides several instructive examples. An the command condition. However, similar to Rouleau,
analysis of clock drawings produced by a patient with a AD patients improved, that is, made fewer errors than
right parietal lesion demonstrates differential impairment VaD patients in the copy condition. These findings
in the copy versus the command test conditions. In the were replicated in a second study (Libon et al., 1996),
copy test condition, many numbers were omitted on the that is, AD patients generally improved from the com-
left side of the drawing. The clock drawing to command mand to copy test conditions compared to VaD patients.
did not demonstrate this behavior and was generally Cosentino et al. (2004) grouped dementia patients diag-
intact compared to the copy test condition. Kaplan nosed clinically with either AD or VaD on the basis of
(1988) demonstrated the opposite profile in a patient MRI white matter alterations (MRI-WMA). These groups
with a right temporal lesion. Here, there was differential were compared to dementia patients with Parkinsons
impairment in the command condition. For this patient, disease (PD). Patients presenting with minimal to mild
the clock drawing to copy was generally intact. For the MRI-WMA continued to improve from the command to
right parietal lesioned patient, the differential impairment copy test conditions, that is, produce fewer errors in the
in the copy condition likely reflected a deficit involving copy versus the condition test conditions, compared to
visually mediated neglect of left hemi-space. For the left patients with moderate to severe MRI-WMA and PD
temporal lobe patient, the visuospatial impairment seen patients. Errors produced the copy condition were
600 C C-Log
correlated with poor performance on executive tests. Libon, D. J., Malamut, B. L., Swenson, R., & Cloud, B. S. (1996). Further
analyses of clock drawings among demented and non-demented
Errors produced in the command condition were corre-
subjects. Archives of Clinical Neuropsychology, 11, 193211.
lated with overall dementia severity and tests related to Libon, D. J., Swenson, R., Barnoski, E., & Sands, L. P. (1993). Clock
semantic knowledge. Cahn-Weiner (2003) correlated CDT drawing as an assessment tool for dementia. Archives of Clinical
performance with MRI measures of atrophy and found Neuropsychology, 8, 405416.
that impaired CDT performance was attributable to im- Marcopulos, B. A., McLean, A., & Giuliano, A. J. (1997). Cognitive
impairment or inadequate norms: A study of healthy, rural, older adults
pairment in multiple cognitive domains but was primarily
with limited education. The Clinical Neuropsychologist, 11, 111131.
related to volume loss involving the right temporal cortex. Mayer-Gross, W. (1935). Some observations on apraxia. Proceeding of the
Taken as a whole, this research suggests that different Royal Society of Medicine, 28, 12031212.
cognitive constructs underlie impaired clock drawing in McFie, J., & Zangwill, O. L., (1960). Visuo-constructive disabilities asso-
patient with cortical versus subcortical dementia. ciated with lesions of the left cerebral hemisphere. Brain, 83,
243260.
Rouleau, I., Salmon, D. P., & Butters, N. (1996). Longitudinal analysis of
Cross References clock drawing in Alzheimers disease patients. Brain and Cognition,
31, 1734.
Rouleau, I., Salmon, D. P., Butters, N., Kennedy, C., & McGuire, K.
Constructional Apraxia (1992). Quantitative and qualitative analyses of clock drawings in
Alzheimers and Huntingtons disease. Brain and Cognition, 18, 7087.
Rubin, L. A., Barr, W. B., & Burton, L. A. (2005). Assessment practices of
References and Readings clinical neuropsychologists in the United States and Canada: A
survey of INS, NAN, and APA Division 40 members. Archives of
Benton, A., & Tranel, D. (1993). Visuoperceptual, visuospatial, and Clinical Neuropsychology, 20, 3365.
visuoconstructional disorders. In K. M. Heilman & E. Valenstien, Tranel, D., Rudrauf, D., Vianna, E. P. M., & Damasio, H. (2008). Does the
(Eds.), Clinical neuropsychology (3rd ed.). New York: Oxford clock drawing test have focal Neuroanatomical correlates? Neuropsy-
University Press. chology, 22, 553562.
Borod, J. C., Goodglass, H., & Kaplan, E. (1980). Normative data on the Tuokko, H., Hadjustavropoulos, T., Miller, J. A., & Beattie, B. L. (1992).
Boston diagnostic aphasia examination, parietal lobe battery, and the The clock test: A sensitive measure to differentiate normal elderly
Boston Naming Test. Journal of Clinical Neuropsychology, 2, 209216. from those with Alzheimer disease. Journal of the American Geriatrics
Cahn-Weiner, D. A., Williams, K., Grace, J., Tremont, G., Westervelt, H., Society, 40, 579584.
& Stern, R. A. (2003). Discrimination of dementia with lewy bodies Van der Horst, L. (1934). Constructional apraxia: Osychological views on
from Alzheimer disease and Parkinson disease using the clock draw- the conception of space. Journal of Nervous and Mental Disease, 80,
ing test. Cognitive and Behavioral Neurology, 16, 8592. 645650.
Cosentino, S., Jefferson, A. J., Chute, D. L., Kaplan, E., & Libon, D. L.
(2004). Clock drawing errors in dementia: Neuropsychological and
Neuroanatomic considerations. Cognitive and Behavioral Neurology,
17, 7483. C-Log
Freedman, M., Leach, L., Kaplan, E., Shulman, K. I., & Delis, D. C. (1994).
Clock drawing: A neuropsychological analysis. New York: Oxford
University Press.
Cognitive-Log
Goodglass, H., & Kaplan, E. (1972). Assessment of aphasia and related
disorders (1st ed.). Philadelphia, PA: Lea and Febiger.
Goodglass, H., & Kaplan, E. (1983). Assessment of aphasia and related
disorders (2nd ed.). Philadelphia, PA: Lea and Febiger. Clomipramine
Goodglass, H., Kaplan, E., & Baresi, B. (2001). Assessment of aphasia and
related disorders (3rd ed.). Philadelphia, PA: Lippincott, Williams. J OHN C. C OURTNEY
Head, H. (1926). Aphasia and kindred disorders of speech. New York:
Macmillan.
Kaplan, E. (1988). A process approach to neuropsychological assessment. New Orleans, LA, USA
In T. Boll & B. K. Bryant (Eds.), Clinical neuropsychology and brain
function: Research, measurement, and practice. Washington, DC:
American Psychological Association. Generic Name
Kaplan, E. (1990). The process approach to neuropsychological assess-
ment of psychiatric patients. Journal of Neuropsychiatry and the
Clinical Neurosciences, 2, 7287. Clomipramine
Leach, L., Kaplan, E., Rewilak, D., Richards, B., & Proulx, G.-B. (2000).
The kaplan baycrest neurocognitive assessment. San Antonio, TX: The
Psychological Corp.
Brand Name
Lezak, M., Howison, D. B., & Loring, D. W. (2004). Neuropsychological
assessment (4th ed.). New York: Oxford University Press. Anafranil
Clonazepam C 601
Class Additional Information
Tricyclic antidepressant Drug Interaction Effects: http://www.drugs.com/drug_interactions.html

Gene-Based Estimate of Drug interactions: http://mhc.daytondcs. C
Proposed Mechanism(s) of Action com:8080/cgi bin/ddiD4?ver=4&task=getDrugList
Boosts neurotransmitters serotonin and norepinephrine/
noradrelaline; blocks serotonin transporter; apparently
desensitizes both serotonin 1A receptors and beta adren-
ergic receptors Clonazepam
J OHN C. C OURTNEY
Indication Childrens Hospital of New Orleans
Obsessive-compulsive disorder, depression, cataplexy
syndrome
Generic Name
Off Label Use Clonazepam
Anxiety, insomnia, chronic pain

Brand Name
Side Effects Klonopin
Serious
Class
Paralytic ileus, hyperthermia, lowered seizure threshold
Anxiolytic
and rare seizures, orthostatic hypotension, sudden death,
arrhythmias, tachycardia, QTc prolongation, increased
intraocular pressure, hepatic failure, extrapyramidal
symptoms, mania, and suicidal ideation
Binds to benzodiazepine receptors at the GABA-A ligand-
gated channel, thus allowing for neuronal hyperpolariza-
Common tion. Benzodiazepines enhance the inhibitory action of
GABA via boosted chloride conductance.
Blurred vision, constipation, increased appetite, urinary
retention, dry mouth, nausea, diarrhea, heartburn,
strange taste in mouth, weight gain, fatigue, weakness, Indication
dizziness, headache, anxiety, nervousness, restlessness, se-
dation, sexual dysfunction, sweating Panic disorders (with or without agoraphobia), Lennox
Gastaut syndrome, akinetic seizures, myoclonic seizure,
absence seizures
Off Label Use
PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The prescribers guide Atonic seizures and other anxiety disorders, acute psycho-
(2nd ed.). New York, NY: Cambridge University Press. sis, insomnia
602 C Clonidine
Side Effects Proposed Mechanism(s) of Action
Serious Centrally acting alpha 2 agonist

dysfunction and blood dyscrasias, Grand mal seizures Indication
Hypertension
Common
Sedation, fatigue, depression, dizziness, memory pro- Off Label Use

blems, dysinhibition, confusion, ataxia, slurred speech
Attention deficit hyperactivity disorder, Tourettes syn-
drome, anxiety disorders including PTSD and social anx-
References and Readings iety disorder, substance withdrawal including opiates and
alcohol, menopausal flushing, clonadine-induced hyper-
Physicians Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson salavation, severe pain in cancer patients
PDR.
(2nd ed.). New York, NY: Cambridge University Press. Side Effects
Serious
Sinus bradycardia, atrioventricular block during with-
drawal, hypertensive, encephalopathy, cerebrovascular
accidents, and death
Pill Identification: http://www.drugs.com/pill_identification.html Common
Dry mouth, dizziness, constipation, sedation, major de-

pression, weakness, fatigue, impotence, loss of libido,
Clonidine insomnia, headache, dermatologic reactions, hypoten-
sion, occasional syncope, nervousness, agitation, tachy-
J OHN C. C OURTNEY cardia, nausea, vomiting
Generic Name Physicians Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson
PDR.
Clonidine
Brand Name
Duraclon, Catapres, Catapres-TTS, Clorpres
Drug Inter action Effects: http://www.drugs.com/drug_interactions.html
Class Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.
Antihypertensive Pill Identification: http://www.drugs.com/pill_identification.html
Closure C 603
Common
Clorazepate
Sedation, fatigue, depression, dizziness, memory pro-
J OHN C. C OURTNEY blems, dysinhibition, confusion, ataxia, and slurred
Childrens Hospital of New Orleans speech.
C

Generic Name
Clorazepate PDR.
Brand Name
Azene, Tranxene Additional Information

Class Free Drug Online and PDA Software: www.epocrates.com
Gene-Based Estimate of Drug interactions: http://mhc.daytondcs.com:
Anxiolytic 8080/cgi bin/ddiD4?ver=4&task=getDrugList

Binds to benzodiazepine receptors at the GABA-A ligand- Closure
gated channel, thus allowing for neuronal hyperpolariza-
tion. Benzodiazepines enhance the inhibitory action of R ONALD A. C OHEN
GABA via boosted chloride conductance. Clorazepate is Brown University
also hypothesized to inhibit neuronal activity in amgy- Providence, RI, USA
dala-centered fear circuits.
Synonyms
Indication
Visual integration; Visual synthesis
Anxiety Disorder, symptoms of anxiety, and acute alcohol
withdrawal.
Definition
Off Label Use Visual closure refers to the ability to perceive and recog-
nize objects, shapers, features, or symbols from incom-
Partial seizures (as an adjunct). plete or degraded visual stimuli. It reflects the capacity of
humans to fill in missing information from incomplete
sensory input to achieve a meaningful percept.
Side Effects
Serious Historical Perspective

Respiratory depression, hepatic dysfunction (rare), renal The principle of visual closure had its roots in Gestalt
dysfunction and blood dyscrasias, and Grand mal psychology (Ellis, 1938; Harlow, 1938; Kohler, 1929).
seizures. Gestalt psychology theorized that operationally brain
604 C Clot Buster
functions (i.e., perception and cognition) are holistic impairments on tests such as the Gollin Figures and
consisting of analog processes that occur in a parallel Mooney Closure tests. This may reflect the fact that impair-
manner and are self-organizing. This led to the well- ments on this type of task tend to be embedded in other
known conclusion regarding perception, and cognition visual perception deficits that are more striking. However,
more generally, that the whole is greater than the sum it is also clear that closure paradigms have not been system-
of its parts. Based on this framework, all perceptual atically implemented into standard neuropsychological
processes act to achieve optimal organization and recon- batteries using modern computerized methods, so that
ciliation with the objects that are being perceived. A definitive conclusions regarding impairments of closure
critical principle driving Gestalt perception is pragnanz secondary to localized and global brain disorders cannot
(law of conciseness), which maintains that people orga- be reached at this point.
nize their experience in an orderly, symmetric, and simple
manner when possible. Visual closure was one of the
five laws of pragnanz, with others including the laws Cross References
of similarity, proximity, symmetry continuity, and com-
mon fate. Gollin Figures
While each of these laws has potential value in ac- Hooper Visual Organization Test
counting for elements of visual integration, the law of Simultanagnosia
visual closure seems to have had the most direct impact,
particularly with respect to clinical neuropsychology.
Early clinical studies of the effects of posterior cortical
lesions on visual perception indicated that certain patients
had difficulty in simultaneously processing all the ele-
Ellis, W. D. (1938). A source book of Gestalt psychology. New York:
ments of their visual sensorium to achieve a unified
Harcourt, Brace & World.
percept, a syndrome that was labeled simultagnosia Foreman, N. (1991). Correlates of performance on the Gollin and
(Poppelreuter, 1990). Mooney tests of visual closure. Journal of General Psychology, 118
(1), 1320.
Harlow, R. F. (1938). Philosophys contribution to Gestalt psychology.
Journal of Psychology: Interdisciplinary and Applied, 5, 185200.
Current Knowledge Holmes, D. S. (1968). Search for closure in a visually perceived pattern.
Psychological Bulletin, 70(5), 296312.
The idea that visual perception occurs as a function by- Jones, E. C., & Dennis, M. E. (1972). Perceptual closure as a function of
product of active self-organizing processes is now widely gap size. Perceptual and Motor Skills, 35(1), 126.
accepted by most visual scientists, though many would Kohler, W. (1929). Gestalt psychology. New York: H. Liveright.
Mooney, C. M., & Ferguson, G. A. (1951). A new closure test. Canadian
reject a pure holistic view. Instead, visual perception and
Journal of Psychology/Revue Canadienne de Psychologie, 5(3),
higher-order visual processes tend to be conceptualized as 129133.
the by-product of computational processes carried out by Poppelreuter, W. (1990). Disturbances of lower and higher visual capacities
modular neural networks responsible for specific opera- caused by occipital damage: with special reference to the psychopatho-
tions. Visual closure is thought to result from such pro- logical, pedagogical, industrial, and social implications. Oxford/New
York: Clarendon Press/Oxford University Press.
cesses occurring in extra-striatal systems found primarily
in the parietal cortex. Psychometric studies of closure
have tended to employ tests such as the Gollin Figures
and Mooney test (Foreman, 1991; Holmes, 1968; Jones &
Dennis, 1972; Mooney & Ferguson, 1951). In healthy Clot Buster
adults, the ability to recognize line drawings that have
been degraded has been shown to be a function of the Recombinant Tissue Plasminogen Activator
size of gaps in the drawing (Jones & Dennis, 1972), which
in turn reflects the amount of missing information. Per-
formance on closure tests has been shown to not be
strongly associated with visual search performance, sug-
gesting that these are distinct visual processes (Foreman, Clot Busting
1991). While tests of closure have existed for over 40 years,
there are relatively few studies demonstrating consistent Thrombolysis
Clustering C 605
Side Effects
Clotting
Serious
Thrombosis
Agranulocytosis, neuroleptic malignant syndrome, sei- C
zures, pulmonary embolism, myocarditis, hyperglycemia.
Clozapine Common
J OHN C. C OURTNEY 1, C RISTY A KINS 2 Increased risk for diabetes, sweating, and increased
1 salivation.
2
Mercy Family Center References and Readings
Metarie, LA, USA
PDR.
Generic Name Stahl, S. M. (2007). Essential psychopharmacology: The prescribers guide
Clozapine
Brand Name Drug interaction effects: http://www.drugs.com/drug_interactions.html

Drug molecule images: http://www.worldofmolecules.com/drugs/
Free drug online and PDA software: www.epocrates.com
Clozaril, Leponex Gene-based estimate of drug interactions: http://mhc.daytondcs.
Pill identification: http://www.drugs.com/pill_identification.html
Class
Atypical Neuroleptic Clumsiness

Ataxia
Blocks dopamine 2 receptors, inhibits serotonin 2A recep- Cluster Analysis

tors, thus increasing presynaptic release of related
catecholamines Clustering
Indication
Clustering
Schizophrenia (treatment-resistant), reduction of suicidal
M ICHAEL D. F RANZEN
behavior.
Pittsburgh, PA, USA
Off Label Use

Synonyms
Bipolar disorder (treatment-resistant), violence, and ag-
gression associated with psychosis or brain dysfunction. Cluster analysis
606 C Cmax
Definition elimination. The maximum concentration of a drug in

blood plasma represents a drugs peak effect. Cmax is one
Clustering can be thought of as the obverse of factoring. In of the primary pharmacokinetic measures for evaluating
factor analysis, observations are correlated with each other how the body acts upon a drug.
and the correlation matrix is examined to see which items The same dose of a drug may result on different
covary among themselves. In cluster analysis, the correla- plasma levels because the body is not a passive recipient.
tion matrix is examined to see which individuals or obser- Plasma levels of a drug can be altered by the route of
vations covary among themselves. Once the groups of administration, the ease of absorption, the distribution of
individuals are composed, they are compared to each the drug with the body, the bioavailability or accessible
other in order to see if some external correlate exists. concentration of the drug, and the efficiency with which a
For example, a large group of patients might be drug is metabolized or eliminated.
administered a series of cognitive measures. The scores Common factors that affect plasma levels of a drug
on those measures are examined to see which individuals could include the size of the molecule and its fat solubility;
seem to be most similar to each other. Once the groups the patients gastric pH, physical health or age, and
are empirically formed, their characteristics are examined the presence of other medications or foods that may expe-
to see if age or diagnosis or injury severity discriminates dite or slow absorption from the gastrointestinal tract into
among the groups. general circulation or alter the drugs metabolism and
excretion. These factors may require changes in dosing in
order to achieve therapeutic levels of a drug or alterations
Cross References in diet, such as to take a drug with or without food. It may
also include recommendations to avoid particular foods
Correlation Coefficients
that are known to induce or inhibit the specific enzyme
Factor Analysis
pathways that metabolize the drug (e.g., grapefruit juice).
Drugdrug interactions can alter the plasma levels of a
References and Readings drug, including its peak effect.
There are also mediations that inhibit metabolism with-
Corter, J. (1996). Tree models of similarity and association. Thousand in a particular liver-mediated enzyme system, thus altering
Oaks, CA: Sage. the availability of other agents of that drug itself. This can
Kaufman, L., & Rousseeuw, P. (2005). Finding groups in data: An
alter the availability of a drug, including its Cmax. Fluox-
introduction to cluster analysis. Hoboken, NJ: Wiley.
McIntyre, R. M., & Blashfield, R. K. (1980). A nearest-centroid technique
etines impact on codeine is a good example. Codeine is
for evaluating the minimum-variance clustering procedure. ultimately synthesized into morphine and via a transforma-
Multivariate Behavioral Research 15, 22252238. tion that requires an enzyme that makes this change possi-
ble. Fluoxetine appears to inhibit this process, thus
dramatically reducing the pain control intended via the
administration of codeine.
Cmax For some drugs, there is no clear relationship be-
tween the concentration of a drug in blood plasma and
N ADIA W EBB its pharmacological effect. For other drugs, the concen-
Childrens Hospital of New Orleans tration must be tightly monitored, typically through
New Orleans, LA, USA regular plasma assessments of drug levels (assays). As a
rule of thumb, adverse drug reactions and side effects
become more likely as the dose of a drug increases.
Synonyms Consequently, adverse drug effects are more likely at
the time of Cmax.
Maximum concentration; Peak concentration
Cross References
Definition
p450 Cytochrome System
Plasma concentrations reflect a time curve from the ad- Pharmacokinetics
ministration of a drug through its peak effect and eventual Side Effects
Cochlear Nuclei (Dorsal and Ventral) C 607
References and Readings waves in the cochlea are transduced into bioelectrical
nerve impulses. The acoustic division of the eighth cranial
Brunton, L. B., Lazo, J. S., & Parker, K. L. (Eds.). (2005). Goodman & nerve has its cell bodies in the spiral ganglion of the
Gilmans the pharmacological basis of therapeutics (11th ed.). cochlea.
New York: McGraw Hill.
Stahl, S. M. (2008). Stahls essential psychopharmacology: Neuroscientific C
basis and practical applications. New York: Cambridge University
Press.
Cross References
Auditory System
CMS
Childrens Memory Scale
Ropper, A. H., & Brown, R. J. (2005). Deafness, dizziness, and disorders
of equilibrium. In Adams and Victors principles of neurology.
CNC
Coma/Near Coma Scale
Cochlear Nerve
Vestibulocochlear Nerve
CNS Lupus
Lupus Cerebritis
Cochlear Nuclei (Dorsal
and Ventral)
J OHN E. M ENDOZA
Cochlea Tulane University Medical Center
K ERRY D ONNELLY
University at Buffalo/SUNY
Buffalo, NY, USA
Definition
Cochlear nuclei is the nuclei that receive first-order
Definition auditory input from the organ of Corti in the cochlea of
the inner ear.
The cochlea, a small conical structure, is the part of the
inner ear that converts mechanical energy (vibrations)
into nerve impulses sent to the brain. It is also known as
the organ of hearing. The word cochlea is a Latin word Current Knowledge
derived from the Greek kokhlos, which refers to the land
snail. A coiled tube, the cochlea winds around a central The cochlear nuclei are divided into a dorsal and a
axis, forming the anterior part of the labyrinth. It contains ventral group. The dorsal cochlear nuclei give rise to
the organ of Corti, which includes the hair cells that the dorsal acoustic stria, which immediately cross the
constitute the primary mechanisms by which pressure midline and contribute fibers that ascend contralaterally
608 C Coding
in the lateral lemniscus. The ventral cochlear nuclei are

the source of two other auditory pathways, the interme- Cogniform Disorder
diate and the ventral acoustic stria. The former also
crosses the midline and, like the dorsal acoustic stria, D EAN C. D ELIS
ascends in the contralateral lateral lemniscus. Fibers San Diego School of Medicine
making up the ventral acoustic stria, the largest of these San Diego Veterans Affairs Healthcare System
three pathways, take three different paths after leaving La Jolla, CA, USA
the nucleus. They (1) synapse in both the ipsilateral or
contralateral superior olivary nuclei, which in turn send
tertiary fibers to the inferior colliculi via the ipsilateral Synonyms
and contralateral lateral lemniscus, and (2) send fibers
directly to the contralateral inferior colliculi, bypassing Conversion disorder; Malingering; Somatoform disorders
the superior olivary nuclei.
The crossing fibers of the ventral acoustic stria make
up what is known as the trapezoid body of the pontine Definition
tegmentum. The dorsal and ventral cochlear nuclei them-
selves are located laterally in the rostral medulla at the In neuropsychology, the assessment of test-taking effort
pontinemedullary junction near the vestibulocochlear has captured the focus of considerable research and de-
nerve. bate. In the past 20 years, over 500 studies have been
Since the first-order neurons from the auditory nerve published in peer-reviewed neuropsychological journals
terminate in the cochlear nuclei and the decussations that address the breadth and scope of this problem (see
within the auditory system only begin with the second- reviews by Hom & Denny, 2002; Iverson & Binder, 2000;
order neurons originating in the cochlear nuclei, these Larrabee, 2005; Sweet, 1999). Considerable advances have
nuclei receive input only from one ear. Hence, unilateral been made in the development of empirically based meth-
pontine lesions affecting the dorsal and ventral cochlear ods for identifying individuals who are simulating cogni-
nuclei would be expected to result in ipsilateral hearing tive problems, including the use of instruments designed
deficits (loss). specifically to assess cognitive validity (Binder, 1993;
Frederick, 1997; Green et al., 1999; Tombaugh, 1996),
analysis of atypical performances on standard ability
tests (Larrabee, 2003; Millis et al., 1995), and analysis of
Cross References
testretest profile inconsistencies (Hom & Denny, 2002;
Iverson & Binder, 2000). In addition, specific guidelines
Auditory System
and criteria have been developed for diagnosing subopti-
mal effort and malingering on neuropsychological tests
(e.g., Slick et al., 1999). Using these methods and guide-
lines, neuropsychologists have found that the frequency of
individuals exhibiting excessive or exaggerated cognitive
Wilson-Pauwek, L., Akesson, E. J., Stewart, P. A., & Spacey, S. D. (2002).
Cranial nerves in health and disease. Hamilton, ONT: B.C. Decker. symptoms in medicolegal evaluations often ranges from
20% to 40% (Miller, 2001; Millis et al., 1995; Mittenberg
et al., 2002). In light of the pervasiveness of this problem,
it is now generally accepted that cognitive validity testing
Coding is an important part of the neuropsychological assessment
process, particularly for evaluations that occur in the
Digit Symbol Substitution Test context of medicolegal or disability-application settings
(Bush et al., 2005).
While considerable advances have been made in the
methods used to detect individuals who are exhibiting
inadequate effort and symptom exaggeration on cognitive
Cog-Log testing, neuropsychologists often find themselves in a quan-
dary in terms of the diagnostic labels to ascribe to these
Cognitive-Log individuals once they have been identified. The DSM-IV
Cogniform Disorder C 609
offers several possible categories for diagnosing individuals (b) Undifferentiated Somatoform Disorder requires
with excessive cognitive symptoms (e.g., Malingering and one or more physical complaints, with no reference
Conversion Disorder); however, shortcomings of these con- made to cognitive difficulties.
ditions have been noted in the literature. In particular, (c) Conversion Disorder requires one or more symp-
Malingering has been the subject of considerable debate toms or deficits affecting voluntary motor or sensory C
and criticism, especially with regards to the objectivity with function [emphasis added], without mention of
which clinicians can assess if feigned symptoms were inten- cognitive or memory difficulties among the specific
tionally or unintentionally produced. Improvements have criteria.
been made in establishing criteria for this condition (e.g., (d) Pain Disorder requires only excessive pain
Slick et al., 1999), but clinicians nevertheless often remain symptoms.
reluctant to use any diagnosis that requires them to make (e) Somatoform Disorder NOS could conceivably in-
judgments about intentionality of symptom exaggeration. clude individuals with predominantly excessive cog-
Clinicians often face three general problems in trying nitive symptoms; however, soma denotes physical
to use existing DSM-IV categories to classify individuals rather than cognitive problems, and the list of exam-
with excessive cognitive symptoms. These problems in- ple cases provided in the DSM-IV for this catchall
clude (a) lack of a diagnostic category that adequately category makes no reference to excessive cognitive
targets the specific features of this relatively common symptoms.
condition, (b) the use of criteria that require the clinician (f) Dissociative Amnesia requires one specific type of
to make judgments about internal states that are exceed- cognitive problem, namely, an inability to recall
ingly difficult to evaluate in an objective manner (e.g., important personal information, usually of a trau-
intentional versus unintentional production of excessive matic or stressful nature [emphasis added]. Howev-
symptoms), and (c) difficulties in determining the relative er, individuals presenting with excessive cognitive
role that external incentive and sick-role factors may play symptoms do so in a myriad of ways (Bush et al.,
in the symptom production. 2005; Delis & Jacobson, 2000; Larrabee, 2003). Some
Symptom Specificity. The existing DSM-IV cate- people endorse problems in all cognitive domains
gories addressing excessive symptomatology can be queried, including attention, language, math, visual-
divided into two general types: symptom-specific versus spatial functions, higher-level executive functions,
symptom-nonspecific conditions. Symptom-specific con- new learning and memory, and remote recall of im-
ditions are those that require amplification of only certain portant personal information. In contrast, other
types of symptoms. The DSM-IV offers a relatively small individuals endorse difficulties in only one or a few
number of symptom-specific categories, which fall only specific cognitive skills (e.g., short-term memory and
among the somatoform disorders (e.g., Somatization Dis- concentration), while denying problems in other cog-
order and Conversion Disorder) and dissociative disor- nitive domains, including recall of important person-
ders (e.g., Dissociative Amnesia and Dissociative Fugue). al information. In fact, cases of isolated difficulty in
In addition, the DSM-IV offers two symptom-nonspecific remembering important autobiographical informa-
conditions, Malingering and Factitious Disorder, which tion are relatively rare, illustrating the limited utility
are discussed in the next section. of this diagnostic category for the vast majority of
A major problem in trying to subsume individuals cases with excessive cognitive symptoms.
with excessive cognitive complaints or invalid test perfor- (g) Dissociative Fugue not only requires one specific
mances into one of the symptom-specific diagnoses is that cognitive difficulty (inability to recall some or all
the cognitive symptoms of many of these cases simply fail of ones past), but carries the added stipulation that
to fit adequately in these categories. Following are expla- this difficulty must surface in the context of a sud-
nations of this problem for each of the symptom-specific den, unexpected, travel away from home or ones
categories provided in the DSM-IV: customary place of daily activities [emphasis
added]. These cases are extremely rare among indi-
(a) Somatization Disorder requires at least four pain
viduals presenting with excessive cognitive symp-
symptoms, two gastrointestinal symptoms, one sex-
toms, thereby precluding the use of this category
ual symptom, and one pseudoneurological symp-
for almost all cases.
tom. However, many individuals who present with
(h) Dissociative Identity Disorder is thought to occur
primarily excessive cognitive symptoms have few if
in individuals with multiple personalities in which
any physical complaints (Larrabee, 2005).
they exhibit an inability to recall important
610 C Cogniform Disorder
information about one or more personality states goal-directed motivation. An individual may be both
when they are in a different personality state. How- conscious of producing feigned behavior (e.g., is capable
ever, cases of multiple personalities are relatively of admitting to self and others that he or she is simulating
rare, particularly in clinicalneuropsychological symptoms) and motivated to do so for some type of
practice, and thus this diagnosis is seldom applicable personal gain; these features would meet criteria for a
to individuals with excessive cognitive symptoms. DSM-IV diagnosis of Malingering. However, someone
(i) Dissociative Disorder NOS is another catchall cate- may be largely unconscious of the feigned behavior (e.g.,
gory that, conceivably, could encompass individuals has convinced himself or herself that the excessive symp-
with excessive cognitive complaints. However, the toms are real), yet the feigned behavior may still arise due
tenor of this category is for individuals who exhibit to a specific, goal-directed purpose. For example, it was
an inability to recall personal information that was of noted during World War II that some soldiers, when faced
a traumatic or stressful nature, thereby greatly limit- with the prospect of entering the frontlines of battle,
ing the utility of this category for most cases of would develop psychogenic paralysis (what would now
excessive cognitive symptoms. be diagnosed as Conversion Disorder given that the symp-
tom amplification occurred primarily in the motor do-
Taken together, the aforementioned nine symptom-spe-
main). These individuals often appeared to truly believe
cific categories either fail to include cognitive complaints,
they were paralyzed, thereby suggesting an unconscious
target only highly specific, relatively rare types of cogni-
(conversion) process. However, their exaggerated behav-
tive problems, or require that other, qualitatively different
ior (paralysis) was clearly goal-directed, because it was
symptoms or conditions also be present (e.g., extensive
manifested in the context of an external incentive (avoid-
physical symptoms for Somatization Disorder). For these
ance of danger). In these cases, the conscious component of
reasons, these diagnoses generally fail to capture the vast
intentionality may have been absent, but the goal-directed
majority of individuals presenting with excessive cogni-
motivational component for producing the symptom was
tive symptoms.
likely present.
Intentionality. Another difficulty in using existing
In neuropsychological practice, the same type of disso-
DSM-IV categories has to do with required criteria related
ciation may occur in which individuals may produce exces-
to intentional/unintentional or voluntary/involuntary
sive cognitive symptoms in reaction to an external incentive
control over the production of the excessive complaints
(e.g., litigation), thereby suggesting goal-directed motiva-
or symptoms. For example, a key required criterion for
tion for the symptom production. However, these indivi-
the two symptom-nonspecific categories Malingering
duals may have nevertheless convinced themselves that their
and Factitious Disorder is that the clinician must deter-
symptoms are real, thereby suggesting a lack of a conscious
mine if the excessive symptoms were generated in an
component to the symptom production. Thus, for these
intentional or volitional manner. The problem here is
individuals, only certain components of intentionality may
that this criterion reflects a causative internal state that,
be present, with the lack of conscious awareness calling
for the majority of cases, is difficult if not impossible to assess
into question whether they would adequately meet the
in an objective manner. That is, the degree to which a person
required criteria for a diagnosis of Malingering. Another
may be exhibiting excessive symptoms or behaviors in an
complicating factor in the assessment of intentionality is
intentional, voluntary, or conscious manner versus an un-
that conscious awareness likely exists on a continuum, with
intentional, involuntary, or unconscious manner represents
individuals varying from being fully conscious, to semicon-
an untestable diagnostic hypothesis for many cases (see also
scious, to largely unconscious of the production of the
Slick et al., 1999). A clinician may have a hunch about
feigned behavior. Although an operational definition of
whether an individuals excessive complaints or symp-
intentionality is beyond the scope of this chapter, the im-
toms were under the voluntary or involuntary control of
portant point here is that intentionality of symptom pro-
the person, but usually these impressions are not substan-
duction not only refers to an elusive internal state, but
tiated by objective data, such as a disclosure or confession
it likely has component features that exist on a continuum
made by the individual to a clinician or other uninvolved,
(e.g., levels of conscious awareness), thereby making this
reliable third party.
construct exceedingly difficult for clinicians to assess in an
Another difficulty in this area of diagnosis is that
objective manner. Consequently, many clinicians are reluc-
intentionality is likely multifactorial in nature. For exam-
tant to use diagnoses such as Malingering, Factitious Disor-
ple, there may be at least two key components of inten-
der, and Conversion Disorder at least in part because of
tionality that can be dissociated: conscious awareness and
difficulty in objectively assessing the presence or absence
of intentionality in the generation of the excessive As another example, some individuals may begin to
symptom. feign symptoms intentionally and consciously in reaction
External Incentive. A third difficulty in using existing to an external incentive (e.g., a lawsuit). However,
DSM-IV categories to diagnose individuals with excessive these individuals may gradually, and perhaps uncon-
cognitive symptoms is related to another required criteri- sciously, assume a progressively worsening sick role due C
on for the two symptom-nonspecific categories Malin- to (a) a prolongation in obtaining the external incentive
gering and Factitious Disorder regarding the presence or (e.g., caused by delays in the lawsuit); and (b) increased
absence of external incentive in the production of the skepticism and questioning on the part of family mem-
symptoms. Specifically, external incentive is a required bers, coworkers, or health providers about the authentici-
inclusionary criterion for Malingering and required exclu- ty of the individuals complaints. This prolonged scrutiny
sionary criterion for Factitious Disorder. (If there is an may be overwhelming to these individuals, compelling
absence of external incentive, then the clinician must them to adopt the sick role and exhibit illness behavior
make a further determination of whether or not an indi- in widespread areas of their lives, to the point where they
vidual has adopted the sick role in order to diagnose may even convince themselves of the authenticity of their
Factitious Disorders). However, the criterion of external symptoms. In other words, while the DSM-IV treats
incentive carries its own inherent difficulties for clinicians external incentive and sick role as mutually exclusive diag-
to identify when considering these diagnoses. First, for nostic criteria for differentiating Malingering and Facti-
many cases, practitioners may not have access to sufficient tious Disorder, in reality, as is the case for most psychiatric
background information about a persons life to be able to conditions, they may co-occur in varying degrees (Slick
assess if external incentives are operative in the case. That et al., 1999).
is, a practitioner may be unaware that a patient has or is Given these limitations in the DSM-IV, the following
planning to apply for disability or to initiate a civil lawsuit two diagnostic categories were proposed by Delis and
in the future, or has committed a crime and fears that he Wetter (2007) to encompass cases of excessive cognitive
or she may soon be apprehended. This lack of knowledge complaints or poor (invalid) test performances in the
about possible covert sources of external incentives makes absence of sufficient evidence of intentionality of symp-
it difficult to utilize the diagnoses of Malingering or tom production to warrant a diagnosis of Malingering.
Factitious Disorder for a number of cases, especially
given that such information is a required criterion rather
than an optional one for these categories. Neuropsychology of Cogniform Disorder
Second, as currently written, the DSM-IV criteria do
not allow for the possibility that a comorbidity may occur The essential feature of Cogniform Disorder is a pattern of
between the adoption of the sick role and the presence cognitive complaints or low scores on psychometric cog-
of external incentives (see also Slick et al., 1999). nitive tests that are considered to be excessive because they
For example, some individuals may gradually develop cannot be fully explained by a neurological disorder, by
into a progressively worsening sick role without the pres- another mental disorder that is associated with CNS dys-
ence of external incentives. However, after a period of function (e.g., schizophrenia), by a general medical con-
time, these individuals may present as so disabled that dition known to affect CNS function (e.g., renal disease),
they begin to receive disability payments, without neces- by the direct effects of a substance (e.g., opioid medica-
sarily having actively sought out such compensation. The tions), or by other factors known to affect cognitive func-
financial gain, however, likely buttresses and propagates tioning (e.g., developmental learning disorder, insomnia,
the continuation of the sick role. According to the and normal aging process). If the cognitive complaints or
DSM-IV, these individuals would have started out as poor test performances occur in the presence of a known
having Factitious Disorder, but as soon as the external neurological or mental disorder or any other factor
incentive was initiated and became a reinforcing factor, known to affect CNS function (e.g., medication), the
the diagnosis of Factitious Disorder would be called into cognitive symptoms are in excess of what would be
question (again, because external incentive is a required expected from the history, physical examination, labora-
exclusionary criterion for this condition). However, for tory tests, or psychometric validity testing. Findings from
these cases, the predominant causative factor for the ex- the clinical interview or psychometric testing of cognitive
cessive symptomatology may still be the adoption of the functions do not substantiate the degree of cognitive
sick role, with the external incentive playing a secondary complaints or symptoms because of the presence of at
or supportive role in the continuation of the symptoms. least two of the following features:
612 C Cogniform Disorder
(a) Cognitive complaints or poor test performances that reporting significant cognitive complaints and dysfunction
are rare for patients with documented mild to mod- in their daily lives.
erate generalized brain damage (e.g., loss of remote The primary distinguishing feature between Cogniform
autobiographical memories and inability to perform Disorder and Cogniform Condition (see below) concerns
overlearned verbal skills like reading, spelling, or the degree to which the individual presents as cognitively
simple math) impaired in widespread areas of his or her life. Specifically, a
(b) Inconsistencies between the individuals excessive diagnosis of Cogniform Disorder should be made if there is
cognitive complaints or poor test performances and reasonable evidence that the individual exhibits excessive
the relatively mild nature of the injury or illness as cognitive symptoms in most if not all areas of his or her life
documented in the medical records and seemingly at all times, thereby suggesting a conversion-
(c) Inconsistencies between the individuals excessive like adoption of the sick role manifested primarily as cogni-
cognitive complaints or poor test performances and tive dysfunction. In addition, in Cogniform Disorder, the
observed behavior degree of claimed disability in performing activities of daily
(d) Delayed onset of excessive cognitive complaints or living will often parallel the individuals complaints of cog-
symptoms after an injury and/or significant worsen- nitive dysfunction and poor (invalid) cognitive test perfor-
ing of symptoms over time without an adequate mance. For example, the individual not only obtains
explanation for the decline in functioning (e.g., severely deficient (and likely invalid) scores on tests of
subsequent neurological complications) visual-motor and visual-spatial functioning, but he or she
(e) Significant inconsistencies in cognitive test scores or also ceases to drive a vehicle because of the perceived cogni-
profiles across repeat evaluations tive problems. In many ways, Cogniform Disorder is analo-
(f) Patterns of cognitive test scores within an examina- gous to the somatoform condition of Conversion Disorder,
tion that are rare for brain-damaged patients but with the excessive symptoms manifested primarily in
(g) Significant inconsistencies in cognitive complaints or terms of cognitive dysfunction rather than deficits affecting
symptoms over time primarily motor or sensory functions (e.g., nonepileptic
(h) Evidence of insufficient test-taking effort or exagger- seizures). For this reason, Cogniform Disorder should be
ation on tests designed specifically to assess validity considered as a new subtype of the somatoform disorders.
of cognitive performance
(j) Evidence of insufficient test-taking effort or exagger-
ation on specific measures obtained from standard
Neuropsychology of Cogniform
ability tests that have been empirically found to assess
Condition
validity of cognitive performance
The essential features of Cogniform Condition are the
Considerable individual differences are found in the per- same as those of Cogniform Disorder in every respect,
formances of people with this condition on psychometric with the exception of the degree to which the individual
tests of cognitive skills (Larrabee, 2003; Slick et al., 1999). exhibits cognitive dysfunction in widespread areas of his
Some individuals obtain markedly low scores on most or her everyday life. That is, in Cogniform Condition,
cognitive tests administered; these individuals are often there is (a) a lack of reasonable evidence that the individ-
less sophisticated about medical and psychological condi- ual presents as cognitively dysfunctional in many areas of
tions and more blatant in their symptom amplification. his or her life, and (b) evidence of significant inconsis-
Other people may obtain low and invalid scores on only a tencies between the individuals excessive cognitive com-
few tests administered (e.g., memory tasks); these indivi- plaints or poor test performances in an evaluation and his
duals may be more subtle in their symptom exaggeration or her higher level of everyday functioning. For example,
and, as a result, more difficult to identify. Occasionally, an an individual may obtain severely deficient (and likely
individual may perform within expected ranges on most invalid) scores on tests of visual-motor and visual-spatial
cognitive tests administered, including cognitive validity functioning and yet continues to drive a vehicle without
tests, and yet continue to complain of extensive cognitive apparent difficulty. In other words, in Cogniform Condi-
problems and dysfunction in their daily lives. These indivi- tion, the individual is not given a diagnosis of disorder,
duals may have learned from other sources (e.g., Internet; because there is a lack of reasonable evidence that the
attorney coaching) that neuropsychological tests are capa- individual is acting out the sick role of being cognitively
ble of detecting poor test-taking effort, and consequently dysfunctional in widespread areas of his or her life despite
exert adequate effort on psychometric tests despite presenting to the clinician in a manner that suggests that
he or she should be markedly impaired in everyday As proposed here, a diagnosis of Cogniform Disorder or
functioning. Cogniform Condition does not exclude the possibility of
intentional production of the excessive symptoms; rather,
these categories imply only that there is insufficient evidence
Cogniform Disorder and Condition Versus at the time of the assessment to formulate a diagnosis of C
Malingering: Similarities and Differences intentionality and therefore Malingering. Indeed, an ad-
vantage of having diagnostic categories such as Cogni-
Cogniform Disorder, Cogniform Condition, and Malin- form Disorder and Cogniform Condition is that they
gering (when manifested in the form of cognitive dysfunc- allow the clinician to label the cognitive symptoms as
tion) are similar in that the individual may present with excessive using more neutral terms that avoid the accusa-
excessive cognitive complaints or exhibit evidence of tory implications of Malingering when there is a lack of
inadequate effort and exaggeration on formal neuropsy- clear evidence to make that diagnosis. In addition, as
chological testing. However, a diagnosis of Cogniform discussed above, intentionality is likely multifactorial in
Disorder or Cogniform Condition should not be made if nature and is comprised of at least two key components:
there is reasonable evidence that the excessive cognitive conscious awareness and goal-directed motivation. The
symptoms are produced in an intentional or volitional individual who has convinced himself or herself that the
manner, in which case a diagnosis of Malingering may be feigned behavior is real may not be fully or even partially
warranted. As noted above, however, this determination conscious of his or her symptom amplification, but this
can be difficult to make for many cases due to inherent person may nevertheless have developed the symptoms in
problems in objectively assessing the internal state of the reaction to the presence of external or interpersonal
intentionality of simulated behavior. For this reason, it is incentives for personal gain. The categories Cogniform
likely that many cases of excessive cognitive symptoms Disorder and Cogniform Condition allow the clinician
would receive the more neutral diagnosis of Cogniform to acknowledge the presence of incentives that may
Condition, and possibly a diagnosis of Cogniform Disor- have played a significant role in the goal-directed motiva-
der if the individual exhibits cognitively dysfunctional tion for the excessive symptomatology without having to
behavior in widespread areas of his or her life. However, make the difficult determination of whether the individu-
when evidence emerges that implicates at least a conscious al is conscious or unconscious of these dynamics.
component in the production of the excessive cognitive
symptoms, then a diagnosis of Malingering (or Malin-
gered Neuropsychological Dysfunction; Slick et al., 1999)
may be warranted. Following are different examples of
Binder, L. M. (1993). Assessment of malingering after mild head trauma
evidence that can be supportive of a diagnosis of with the Portland Digit Recognition Test. Journal of Clinical and
Malingering: Experimental Neuropsychology, 15, 170182.
Binder, L. M., Storzbach, D., Anger, W. K., Campbell, K. A., & Rohlman,
(a) On psychometric testing, an individual obtains an D. S. (1999). Subjective cognitive complaints, affective distress, and
accuracy score on a forced-choice recognition memory objective cognitive performance in Persian Gulf War Veterans.
test that falls significantly below a chance level. Such a Archives of Clinical Neuropsychology, 14, 531536.
score provides empirical evidence that the individual Bush, S. S., Ruff, R. M., Troster, A. I., Barth, J. T., Koffler, S. P., & Pliskin,
N. H. (2005). Symptom validity assessment: Practice issues and
correctly remembered the right answers above a
medical necessity. Archives of Clinical Neuropsychology, 20, 419426.
chance level and used this knowledge to frequently Delis, D. C., & Jacobson, M. (2000). Neuropsychological testing. Encyclo-
select the wrong answer (Larrabee, 2003; Millis, 1992). pedia of Psychology. New York: American Psychological Association/
(b) A person who is involved in two separate personal- Oxford University Press.
injury lawsuits for different accidents complains of Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (2000). The
California verbal learning test (2nd ed.). San Antonio: The Psycho-
one set of symptoms and injuries to doctors asso-
logical Corporation.
ciated with one lawsuit and different symptoms and Delis, D. C., & Wetter, S. R. (2007). Cogniform disorder and cogniform
injuries to other doctors associated with the second condition: Proposed diagnoses for excessive cognitive symptoms.
lawsuit. Such selective reporting of symptoms that Archives of Clinical Neuropsychology, 22, 589604.
correspond to the different lawsuits suggests a con- Frederick, R. I. (1997). Validity indicator profile. Minnetonka: NCS
Assessments.
scious component to the symptom amplification.
Gervais, R. O., Russell, A. S., Green, P., Allen, L. M., Ferrari, R., & Pieschl,
(c) An individual confesses to intentionally per- S. D. (2001). Effort testing in patients with fibromyalgia and disabil-
forming poorly when taking cognitive tests. ity incentives. Journal of Rheumatology, 28, 18921899.
614 C Cognistat
Green, P., Rohling, M. L., Lees-Haley, P. R., & Allen, L. M. (2001). Effort for Level of Consciousness is also provided. The various
has a greater effect on test scores than severe brain injury in com-
subscales are modeled after more extensive and well-vali-
pensation claimants. Brain Injury, 15, 10451060.
Hom, J., & Denney, R. L. (2002). Detection of response bias in forensic
dated neuropsychological tests but in an abbreviated from.
neuropsychology. Journal of Forensic Neuropsychology, 2, 1166. For example, Attention is assessed using digit repetition
Iverson, G. L., & Binder, L. M. (2000). Detecting exaggeration and similar to that used on the Wechsler scales. Unlike other
malingering in neuropsychological assessment. The Journal of Head screening procedures that yield a single summary score,
Trauma Rehabilitation, 15, 829858.
Cognistat is designed to yield a score for each domain and
Iverson, G. L., & Franzen, M. D. (1996). Using multiple objective memory
procedures to detect stimulated malingering. Journal of Clinical and
thus produce a differentiated profile of cognitive abilities.
Experimental Neuropsychology, 18, 3851. Cognistat also employs an adaptive testing approach (re-
Larrabee, G. J. (2003). Detection of malingering using atypical perfor- ferred to as a screen and metric approach) to decrease the
mance patterns on standard neuropsychological tests. The Clinical time spent in administration. In this approach, an item that
is of average difficulty is first administered for each subtest.
Larrabee, G. J. (2005). Assessment of malingering. In G. L. Larrabee (Ed.),
Forensic Neuropsychology. New York: Oxford University Press.
If that item is passed, no other items are administered from
Millis, S. R. (1992). The recognition memory test in the detection of that subtest, but if it is failed, additional easier items are
malingered and exaggerated memory deficits. The Clinical Neurop- administered. The raw scores for each subscale are then
sychologist, 6, 406414. plotted on a standard profile form, and performance is
Millis, S. R., Putnam, S. H., Adams, K. M., & Ricker, J. H. (1995). The
classified as being in the average range or as indicative of
California verbal learning test in the detection of incomplete effort.
Psychological Assessment, 7, 463471.
mild, moderate, or severe impairment.
Mittenberg, W., Patton, C., Canyock, E. M., & Condit, D. C. (2002). Base
rates of malingering and symptom exaggeration. Journal of Clinical
and Experimental Neuropsychology, 24, 10941102.
Slick, D. J., Sherman, E. M. S., & Iverson, G. L. (1999). Diagnostic criteria
Current Knowledge
for malingered neurocognitive dysfunction: Proposed standards for
clinical practice and research. The Clinical Neuropsychologist, 13, Because extensive validity and normative information
545561. were not available when Cognistat was originally pub-
Sweet, J. J. (1999). Malingering: Differential diagnosis. In J. J. Sweet (Ed.),
lished, a number of studies have subsequently examined
Forensic Neuropsychology. Lisse: Swets and Zeitlinger.
Tombaugh, T. N. (1996). Test of memory malingering. New York: Multi
its sensitivity to brain damage as well as the influence
Health Systems. of demographic variables on test performance. Research
revealed that the Cognistat may be more sensitive to brain
damage than the Mini Mental State Exam, Cognitive Ca-
pacity Screening Examination, and Mattis Dementia Rating
Cognistat Scale (e.g., Drane et al., 2003). Cognistat has also been
found to be sensitive to a variety of neurological and
DANIEL N. A LLEN
psychiatric disorders, and to age-related changes
University of Nevada Las Vegas
in cognitive abilities (for brief review see Doninger,
Las Vegas, NV, USA
Ehde, Bode, Knight, Bombardier, & Heinemann, 2006).
Correlations between its various subtests and neuropsycho-
logical measures of similar abilities provide evidence for its
Synonyms construct validity (Nabors, Millis, & Rosenthal, 1997).
The Cognistat battery also has limitations. For exam-
Neurobehavioral cognitive status examination (NCSE)
ple, performance is influenced by demographic variables,
including age and education. Although the original valida-
Description tion study of the Cognistat demonstrated no differences in
performance between age groups (Kiernan, Mueller,
The Cognistat test battery (Kiernan, Mueller, & Langston, Langston, & Van Dyke, 1987), subsequent investigations
1995), formerly called the Neurobehavioral Cognitive found that increased age is associated with poorer perfor-
Status Examination, is a screening tool designed to as- mance on the Construction, Memory, Similarities, Atten-
sess a number of different cognitive domains including tion, and Calculation domains, with Construction and
Orientation, Attention, Language Abilities (Comprehen- Memory appearing to be the most consistently impacted
sion, Repetition, Naming), Construction, Memory, Calcu- by age (Drane & Osato, 1997). Additionally, years of
lations, and Reasoning (Similarities, Judgment). A rating education and low levels of educational attainment are
Cognitive Affective Syndrome C 615
associated with diminished performance (Macauly et al.,

2003; Ruchinskas et al., 2001). With only limited norma- Cognition
tive data available to correct for these influences (Drane
et al., 2003), interpretation of performance in the elderly Cognitive Functioning
and those with limited education must be tentative. C
Finally, a recent study of community dwelling and hospi-
talized individuals with traumatic brain injury suggests Cognitive Affective Syndrome
that the Cognistat should not be used to profile neuro-
cognitive strengths and weaknesses because measurement R OBERT R IDER
error accounted for the majority of variance in subtest Drexel University
scores (Doninger et al., 2006). Thus, the Cognistat pro- Philadelphia, PA, USA
vides a useful method to screen patients with a variety of
neurological and psychiatric disorders for neurocognitive
impairment, although additional research appears war- Synonyms
ranted before that it can be used to make inferences
regarding impairment of discrete cognitive abilities, and Cerebellar cognitive affective syndrome
more extensive normative data is needed.
Definition
Cross References
First described by Schmahmann and Sherman (1997),
Mattis Dementia Rating Scale (DRS)
cerebellar cognitive affective syndrome (CAS) refers to
Mini Mental State Exam (MMSE)
a cluster of impairments involving higher-order cognitive
processes and affective functioning. Symptoms tend to
References and Readings cluster in executive dysfunction, including problems
with planning, set shifting, verbal fluency, abstract
Doninger, N. A., Ehde, D. M., Bode, R. K., Knight, K., Bombardier, C. H., & reasoning, perseveration, attentional dysregulation, hy-
Heinemann, A. W. (2006). Measurement properties of the neurobe- peractivity, impulsivity and disinhibition, and deficits in
havioral cognitive status examination (Cognistat) in traumatic brain working memory. However, symptoms may also include
injury rehabilitation. Rehabilitation Psychology, 51(4), 281288.
Drane, D. L., & Osato, S. S. (1997). Using the neurobehavioral cognitive
visuospatial disorders, expressive language disorders,
status examination as a screening measure for older adults. Archive of affective abnormalities, difficulties with visuospatial orga-
Clinical Neuropsychology, 12(2), 139143. nization, visual memory, logical sequencing, and blunted
Drane, D. L., Yuspeh, R. L., Huthwaite, J. S., Klingler, L. K., Foster, L. M., or inappropriate affect (Schmahmann & Sherman, 1997).
Mrazik, M., & Axelrod, B. N. (2003). Healthy older adult perfor-
mance on modified version of the Cognistat (NCSE): Demographic
issues and preliminary normative data. Journal of Clinical and Current Knowledge
Experimental Neuropsychology, 25(1), 133144.
Kiernan, R. J., Mueller, J., & Langston, J. W. (1995). Cognistat (Neurobe- Causes and Correlates of CAS
havioral Cognitive Status Examination). Lutz, FL: Psychological
Assessment Resources.
Kiernan, R. J., Mueller, J., Langston, J. W., & Van Dyke, C. (1987). The The co-occurrence of these cognitive and affective symp-
Neurobehavioral Cognitive Status Examination: A brief but quanti- toms arises from the disruption of neuroanatomical cir-
tative approach to cognitive assessment. Annals of Internal Medicine, cuits connecting the cerebellum with frontal, parietal,
107(4), 481485. temporal, and limbic cortices. Damage to these connec-
Macaulay, C., Battista, M., Lebby, P. C., & Mueller, J. (2003). Geriatric
performance on the Neurobehavioral Cognitive Status Examination
tions can occur in association with cerebellar infarct
(Cognistat) what is normal? Archives of Clinical Neuropsychology, 18, (Schmahmann and Sherman, 1997), cerebellar atrophy
463471. associated with severe alcoholism (Fitzpatrick, et al.,
Nabors, N. A., Millis, S. R., & Rosenthal, M. (1997). Use of the Neuro- 2008), cerebellar tumor or tumor resection (Levihson,
behavioral Cognitive Status Examination (Cognistat) in traumatic
et al., 2000; Konczak, 2005), trauma, neurodegenerative
brain injury. Journal of Head Trauma Rehabilitation, 12(3), 7984.
Schrimsher, G. W., Parker, J. D., & Burke, R. S. (2007). Relation between
disorders, or cerebellitis. Affective symptoms have been
cognitive testing performance and pattern of substance use in males associated with damage to the cerebellar vermis (Levihson,
at treatment entry. Clinical Neuropsychologist, 21(3), 498510. et al., 1997). Lesions of the anterior lobe of the cerebellum
616 C Cognitive Archives
tend to produce only minor changes in executive and The Planning scale consists of: matching numbers,
visualspatial functions. Children with a cognitive affective planned codes, and planned connections.
syndrome can also have autistic characteristics, and diag-
1. Matching numbers The individual is asked to
nosis of autism can be confounded by cerebellar lesions.
locate and underline a pair of matching numbers.
The task begins with 1 digit and progressively moves
References and Readings into 7 digit numbers.
2. Planned codes A client is requested to complete a
Schmahmann, J., & Sherman, J. (1998). The cerebellar cognitive affective series of boxes according to a corresponding code
syndrome. Brain, 121, 561579. provided at the beginning of each item.
Schmahmann, J., Weilburg, J. D., Sherman, J. B., & Janet, C. (2007). The
3. Planned connections This subtest is similar to
neuropsychiatry of the cerebellum - insights from the clinic. Cere-
bellum, 6(3), 254267.
the original trail making task. In this subtest, both
numerical and alphabetical sequences are employed.
The Attention scale encompasses: number detection,
expressive attention, and receptive attention.
Cognitive Archives 1. Number detection This subtest consists of rows of
numbers with both target and distracter stimuli.
At the top of each item page, a key is printed with
the target numbers. Children are instructed to under-
line only the target specified.
Cognitive Assessment System 2. Expressive attention Children aged 57 are to
identify the size of an assortment of animals, in spite
L EESA V. H UANG of the size depicted on the page. For children aged
California State University 817, this subtest is similar to the Stroop Test.
Chico, CA, USA Color words are presented in a different colors of ink
(e.g., the word red might be in blue ink) and the
children are requested to name the color of the ink.
Synonyms 3. Receptive attention First, a series of pictures or words
are presented in which the client must identify and
CAS underline identical stimuli. Second, children are
requested to recognize and identify two items that
Description share a common characteristic. This subtest is omitted
for the Basic Battery.
The DasNaglieri Cognitive Assessment System (CAS;
The Simultaneous Processing scale includes: nonverbal
Naglieri & Das, 1997a, 1997b) is a cognitive assessment
matrices, verbalspatial relations, and figure memory.
to assess children aged 5 years, 0 months to 17 years,
11 months. Individual administration time is approximate- 1. Nonverbal matrices A variety of pictures with
ly 1 h. The CAS is arranged in three separate, yet interrelat- geometrical shapes or patterns are shown to the
ed levels of scores: individual subtests, PASS (Planning, student. The student needs to select one option that is
Attention, Simultaneous, and Successive) composite scales, consistent with the presented relationship or pattern.
and a Full Scale quotient. Twelve subtests comprise the CAS 2. Verbal spatial relations The individual receives
and each subtest generates a scaled score (M = 10; SD = 3). auditory information and determines which picture
The Standard Battery utilizes 12 subtests with three subt- best represents the verbal description given. Presented
ests per PASS process, while the Basic Battery includes in a multiple-choice format, the series of pictures
eight subtests, two subtests for each PASS process. Each of allows the student to demonstrate understanding of
the four PASS composite scores (M = 100; SD = 15) is a logical, grammatical, and spatial information.
combination of the subtests included in each respective 3. Figure memory A client is required to trace geometric
process. Finally, the Full Scale Score (M = 100; SD = 15) is design previously observed, which is embedded within
the aggregate total of the four PASS cognitive processes a larger and more intricate geometrical design. This is
scales, which are equally weighed. omitted from the Basic Battery.
Cognitive Assessment System C 617
The Successive Processing scale consists of: word series, position to a collective whole (Naglieri, 2005). Successive
sentence repetition, sentence questions, and speech rate. Processing is described as the unidirectional, consecutive
organization of stimuli (Naglieri & Das, 2005).
1. Word series Individuals are instructed to repeat a
series of commonly used words in the same consecutive
order given. The difficulty level increases as the word C
list starts with two words and ends with nine words.
Psychometric Data
2. Sentence repetition This subtest demands that
The standardization sample of 2,200 children is represen-
individuals repeat sentences that gradually become
tative of the US population on nine criteria (Naglieri &
longer. The sentences in this subtest utilized color
Das, 1997b). The internal consistency of the CAS subtests
words to reduce the contextual meaning and possible
range from 0.75 to 0.89, with a median reliability of 0.82.
interference with simultaneous processing. The score
The Standard Battery had average reliabilities of 0.88
is based on the total number of correctly repeated
(Planning), 0.88 (Attention), 0.93 (Simultaneous), and
items.
0.93 (Successive). The reliability coefficient range for the
3. Speech rate This subtest is administered only to
Full Scale score was 0.950.97.
children aged 57. Children are verbally presented
The theoretical premise of the CAS was constructed
with a series of three word combinations and are
on a four-factor model; however, factor analyses
requested to repeat each combination as quickly and
generated empirical support for both three- and four-
as many times as possible within 30 s.
factor models depending upon the age category. Further
4. Sentence questions Administered to children aged 817
research has provided support for the CAS as a measure of
instead of speech rate. In an extension of the sentence
g. Weak correlations were found between the CAS
repetition task, this subtest requires that children re-
Standard Battery Full Scale and PASS scales (ranging
spond to a question about a nonsensical sentence.
from 0.37 to 0.67) with the Wechsler Intelligence Scale
for Children-third edition (WISC-III; Wechsler, 1991).
Historical Background Predictive validity was moderately established with cluster
and subtest scores from the WoodcockJohnson Psycho-
The CAS is one of few cognitive processing instruments Educational Battery-Revised Tests of Achievement
which incorporate a neuropsychological foundation. The (Woodcock & Johnson, 1989).
theoretical basis of the CAS is an extension of Alexander S.
Lurias work relating to the brains three functional units
Clinical Uses
(Naglieri, 1999, 2005). It was modified and refined by Das,
Naglieri, and Kirby into four processing components:
The purpose of the CAS is to provide an analysis of an
Planning, Attention, Simultaneous, and Successive Pro-
individuals cognitive abilities through the measurement
cessing, otherwise known as PASS, to explain differences
of the PASS processes (Naglieri, 2005). The authors
in cognitive processing of children (Das & Naglieri, 2001).
suggested that the CAS is a valuable alternative tool
The Planning subtests require individuals to engage in
to the traditional Wechsler or StanfordBinet scales,
a problem-solving sequence to complete novel tasks
when assessing individuals who may have attention-
(Naglieri, 1999). The development, selection, application,
deficit/hyperactivity disorders (ADHD), LD, mental
and evaluation of strategies are crucial to the success of
retardation, traumatic brain injury, serious emotional
performance (Naglieri & Das, 1997b). Subtests in the
disturbance, giftedness, and planning problems (Naglieri
Attention scale require a combination of three com-
& Das, 1997b). Furthermore, possessing an under-
ponents: focused, selective, and sustained attention
standing of an individuals PASS profile will provide
(Naglieri, 2005). Focused attention involves the act of
essential information for the selection and evaluation of
attending to presented stimuli in the environment.
instructional recommendations (Das & Naglieri, 2001;
Selective attention is the concentration of attention to
Naglieri & Das, 1997b).
chosen stimuli while disregarding nonessential or com-
peting stimuli. Sustained attention is the differential
effort (over time, especially) an individual applies to- References and Readings
ward task completion. Simultaneous Processing subtests
require the ability of an individual to incorporate and Das, J. P., & Naglieri, J. A. (2001). The Das-Naglieri cognitive assessment
comprehend unconnected entities and its relation/ system in theory and practice. In J. J. W. Andrews, D. H. Saklofske, &
618 C Cognitive Assessors
H. L. Janzen (Eds.), Handbook of psychoeducational assessment: Definition

Ability, achievement, and behavior in children (pp. 3363).
San Diego, CA: Academic Press.
Naglieri, J. A. (1999). Essentials of CAS assessment. New York: Wiley.
Cognitive Behavioral Couples Therapy (CBCT) has
Naglieri, J. A. (2005). The cognitive assessment system. In D. P. Flanagan become one of the most well researched approaches for
& P. L. Harrison (Eds.), Contemporary intellectual assessment: the treatment of marital and couple distress, with growing
Theories, tests, and issues (2nd ed., pp. 441460). New York: The empirical support for it effectiveness. Theoretically
Guilford Press.
grounded in both social learning and social exchange
Naglieri, J. A., & Das, J. P. (1997a). Cognitive assessment system:
Administration and scoring manual. Itasca, IL: Riverside Publishing.
theories, the premise of CBCT is that an individuals
Naglieri, J. A., & Das, J. P. (1997b). Cognitive assessment system: behavior both influences and is influenced by his/her
Interpretive handbook. Itasca, IL: Riverside Publishing. environment. When applied to a marriage or other long-
Naglieri, J. A., & Das, J. P. (2005). Planning, attention, simultaneous, and term relationship, this premise suggests that one partners
successive (PASS) theory: A revision of the concept of intelligence.
behavior influences and is influenced by the actions of the
In D. P. Flanagan & P. L. Harrison (Eds.), Contemporary intellectual
assessment: Theories, tests, and issues (2nd ed., pp. 120135).
other. CBCT typically focuses on two aspects of this
New York: The Guilford Press. process: (a) exchanges of positive and negative behaviors;
Wechsler, D. (1991). Wechsler intelligence scale for children-third edition. (b) communication skills that influence the interaction
San Antonio, TX: Psychological Corporation. process (Epstein, Baucom, & Daiuto, 1997).
Woodcock, R. W., & Johnson, M. B. (1989). WoodcockJohnson psycho-
educational battery-revised, tests of achievement. Itasca, IL: Riverside.
Current Knowledge
Couples and Health
Cognitive Assessors
A patients ongoing, long-term relationship can influence
Cognitive Correctors a range of psychosocial variables related to health
behaviors. The health-enhancing properties of intimate
and long-term relationships have been repeatedly
documented (Kiecolt-Glaser & Newton, 2001; Wilson,
Cognitive Assistive Technology 2001). Various mechanisms of action for this relationship
have been proposed, including selection and protection
Prosthetic Memory Aids (Kiecolt-Glaser & Newton, 2001). That is, healthier people
are more likely to be in and stay in intimate relationships,
and they tend to have more resources and take care of
themselves better than their counterparts without such
Cognitive Awareness relationships. Additional research has investigated other
mechanisms for the protective benefits of long-term
Metacognition relationships, including partner attitudes or behaviors, and
caretaking (Keefe et al., 1996; Wilson, 2001).
Treatment Procedures
Cognitive Behavioral Couples
Therapy A CBCT approach to treatment with both relationship
distressed and health impaired couples focuses on three
TAMARA G OLDMAN S HER factors: behavioral factors, affective/emotional factors,
Illinois Institute of Technology and cognitive factors. The behavioral component
Chicago, IL, USA includes increasing positive behaviors such as spending
more time together and decreasing negative behaviors
such as criticizing or nagging. In addition, because com-
Synonyms munication problems are the most commonly reported
presenting complaint of distressed couples, the behavior-
Behavioral marital therapy; CBCT; Cognitive behavioral al aspects of the treatment also typically involve a skills-
marital therapy; Couples therapy; Marital therapy oriented approach to communication change where the
Cognitive Behavioral Therapy C 619
value and skills of working together to solve a problem References and Readings
are the foci.
Affect is a focus of therapy insomuch as it is an Baucom, D. H., Shoham, V., Mueser, K. T., Daiuto, A. D., & Stickle, T.
indicator of significant relationship distress and for its (1998). Empirically supported couple and family interventions
for marital distress and adult mental health problems. Journal of
ability to direct the therapist in exploring links between C
Consulting and Clinical Psychology, 66, 5388.
the emotions of the partners and their behaviors. Affect Epstein, N. B., & Baucom, D. H. (2002). Enhanced cognitive-behavioral
can be approached with a skills approach in helping therapy for couples. Washington, DC: American Psychological
partners learn to express their own and listen to the Association.
other persons emotions and by linking specific emotions Epstein, N. H., Baucom, D. H., & Daiuto, A. (1997). Cognitive-behavioral
couples therapy. In W. K. Halford, & H. J. Markman (Eds.), Clinical
to specific relationship issues.
handbook of marriage and couples intervention (pp. 415449). West
The third factor in CBCT is cognition. As Epstein et al. Sussex, England: Wiley.
(1997) note, the importance of cognitive factors in Halford, W. K., & Markman, H. J. (Eds.). (1997). Clinical handbook of
relationship functioning lies in the fact that objectively marriage and couples intervention. New York: Wiley.
observable behavioral events are often subjectively experi- Keefe, F. J., Caldwell, D. S., Baucom, D. H., Salley, A., Robinson, E.,
Timmons, K., et al. (1996). Spouse-assisted coping skills training
enced quite differently by the partners. The therapist
in the management of osteoarthritic knee pain. Arthritis Care and
works to uncover underling cognitive factors shaping the Research, 9(4), 279291.
behavior and affect of the partners in order to increase Kiecolt-Glaser, J. K., & Newton, T. L. (2001). Marriage and health: His
understanding and promote behavioral change. and hers. Psychological Bulletin, 127(4), 472503.
Schmaling, K., & Sher, T. G. (2000). The psychology of couples and illness:
Theory, research, and practice. Washington, D.C.: American Psycho-
logical Association.
Efficacy Information Shadish, W. R., & Baldwin, S. A. (2003). Meta-analysis of MFT inter-
ventions. Journal of marital and family therapy, 29, 547570.
CBCT, and its predecessor, Behavioral Marital Therapy Shadish, W. R., & Baldwin, S. A. (2005). Effects of Behavioral Marital
(BMT) have been one of the most researched forms of Therapy: A Meta-analysis of randomized controlled trials. Journal of
couples therapy (Shadish & Baldwin, 2003, 2005). Results Consulting and Clinical Psychology, 73(1), 614.
Wilson, S. E. (2001). Socioeconomic status and the prevalence of health
of efficacy trials repeatedly demonstrate that those who
problems among married couples in later midlife. American Journal
receive either CBCT or BMT report less distress than those of Public Health, 91(1), 131135.
who receive no treatment and that this finding remains
not only for couples presenting with general marital
distress, but also for depression, agoraphobia, and alcohol
abuse (Baucom, Shoham, Mueser, Daiuto, & Stickle,
1998). Based upon recent meta-analyses of studies using Cognitive Behavioral Marital
CBCT, Shadish and Baldwin (2003, 2005) reported an Therapy
overall mean effect size ranging from 0.59 to 0.84 for
couples therapy generally, with no differential effective- Cognitive Behavioral Couples Therapy
ness across theoretical orientation found.
Qualifications of Providers
CBCT can be conducted by a variety of treatment
providers, specifically trained in its use with various TARYN M. S TEJSKAL
populations. This includes neuropsychologists, clinical Virginia Commonwealth University Medical Center
psychologists, marriage and family therapists, counselors, Richmond, VA, USA
social workers, and clergy.
Definition
Cross References
Cognitive behavioral therapy (CBT) is a theoretical
Behaviorism framework based on the premise that a persons
Cognitive Behavior Therapy cognitions influence their emotions and behavior. CBT
620 C Cognitive Behavioral Therapy
provides considerable utility in addressing a variety of alleviation. To reduce the emotional experience of frustra-
common emotional consequences of neurological disor- tion, a neuropsychologist working with a brain-injured
ders including anxiety and depression, as well as behavior patient would encourage the patient to appreciate the
modification for brain injury survivors. gains made since the injury. In order to avoid unrealistic
expectations for post injury functioning that could create
frustration; the patient would be cautioned against com-
Historical Background paring present capabilities to preinjury functioning.
CBT grew out of Albert Elliss (Ellis, 1975) work on

Rational Emotive Behavioral Therapy (REBT) and Treatment Participants
examination of irrational beliefs in the 1950s. Ellis
concluded that irrational beliefs (e.g., I am powerless to CBT is broadly applicable to a variety of clinical neuro-
solve my problems; I am unlovable) were associated with logical diagnoses including anxiety, depression, obsessive
the development of mood disorders. Beck, Rush, Shaw, compulsive disorder (OCD), and posttraumatic stress
and Emery (1979) developed Cognitive Therapy on the disorder (PTSD). CBT can be used with individuals,
premise that cognitive errors (e.g., over-generalizing, couples, and families. Further, CBT can be used with
magnification, personalization) were associated with the patients at developmental levels from young children to
development of depression and anxiety. Further, they older adults. CBT therapists act more as coaches colla-
viewed depression as accompanied by of a triad of borating with patients alter processes of thinking, feeling,
negative cognitions consisting of a negative view of self, and action as opposed to an analyst making expert
the world, and the future. interpretations.
Arnold Lazarus (1971) was the first to introduce the
term behavior therapy into the professional literature.
Further expanding the lens of CBT, Lazarus and Folkman Treatment Procedures
(1984) developed the stress, appraisal, and coping
model (1984) that acknowledges the importance of how CBT encompasses a variety of clinical interventions for
an individual views the environment (primary appraisal) individuals with a neurological disorder as well as couples
and their available coping resources (secondary apprais- and families in which a member has a neurological
al). Finally, attribution theory, proposed by Fritz Heider diagnosis or injury. Within all CBT interventions,
(1958) posits that people can interpret events as caused by behaviors, cognitions, and emotions are integrally related;
internal (i.e., factors within the person such as a persons though interventions may focus on behavior or cognition,
own intelligence and behavior) or external factors (i.e., these distinctions are often made for heuristic purposes
factors external to the person such as the weather or luck). (Epstein & Baucom, 2002). Further, CBT posits that
When internal attributions are made, people are said to change in one domain will produce changes in others
have an internal locus of control, or hold cognitions that domains. In the past, behavior-oriented therapies have
support their sense of efficacy in affecting what happens been ripe with skills training in areas such as problem-
to them. When external attributions are paramount, peo- solving, communication, and relaxation with the idea
ple are said to have an external locus of control, that being that maladaptive patterns arise around areas of
is, they believe that they exert less control over their skill deficits. Though CBT therapists also deliver a
environment. judicious amount of skills-based training, therapy moves
beyond behavior modification to the meaning and inter-
pretations made as a result of interactions and experience.
Goals and Objectives
Neuropsychologists using CBT as a conceptual framework Behavior-Focused Interventions

work toward modifying maladaptive cognitions such as
negative attributions, unattainable expectations and Patients with neurological diagnoses have a host of behav-
standards, and faulty belief systems. Through the modifi- ior patterns amenable to CBT intervention. One such
cation of these problematic (i.e., schemas), CBT seeks to pattern, negative reciprocity, is the idea that negative
alter peoples emotional and behavioral responses in behavior increases the propensity that a person will
service of symptom management, reduction, and respond to expressed negative behavior with more
Cognitive Behavioral Therapy C 621
negative behavior (Epstein & Baucom, 2002). For exam- encouraging healthy compartmentalization of emotion
ple, family members may respond angrily toward a pa- (Epstein & Baucom, 2002). In cases of neurological diag-
tient who acts aggressively after a brain injury. Over time nosis or injury, emotions may either be exacerbated or
negative reciprocity pervades relationships, invading minimized. To enhance the expression of emotions, thera-
cognitions and emotions such that family members pists may ask probing questions to bring awareness to C
make global negative attributions about another persons emotional experience such as: What happens to you
intentions and behavior (Epstein & Baucom, 2002). when. . .What is it like for you when. . .How do you feel
An important aspect of CBT is skills-based training; as you listen to your son expressing his experience. . .
meant to enhance positive behavior and decrease negative (Epstein & Baucom, 2002). In this way, individuals and
behavior. In an instance where a person receives a diagnosis family members can be encouraged to share their emo-
of schizophrenia, a CBT clinician may intervene with a tional experience in the context of a safer therapeutic
family to teach communication skills. Empirical literature environment.
has discussed the detrimental impact of expressed emotion
(EE) in families with a schizophrenic family member.
Further, the family members may be overwhelmed and Efficacy Information
have many questions, concerns, and emotions they need
to express surrounding the diagnosis. Communication CBT has been empirically validated for the treatment of
skills training teaches families how to communicate more many disorders including anxiety (Barlow, OBrien, &
productively with one another about complex issues and Last, 1984), sexual dysfunction (Baucom, Shoham,
reduce detrimental patterns of interaction such as EE. Mueser, Daiuto, & Stickle, 1998), depression (Beach,
Sadeen, & OLeary, 1990), bipolar disorder, schizophre-
nia, and bulimia nervosa (Baucom et al., 1998). CBT is
Cognition-Focused Interventions often used in conjunction with medication for a variety of
mental health concerns. In addition, CBT effectively
The manner in which a person cognitively ascribes mean- enhances coping skills for adults with chronic illness
ing to behavior is an important factor in CBT. Therapy (Rybarczyk, DeMarco, DeLaCruz, Lapidos, & Fortner,
often focuses on reassessing and amending these 2001) and caregivers (Gallagher-Thompson, Lovett,
cognitions. Areas of inquiry often include attributions, Rose, McKibbin, Coon, et al., 2000).
expectancies, assumptions, standards, and beliefs. In Recently, advances in computer software have given
order to evaluate and modify existing cognitions, clinicians rise to computerized versions of CBT. Though computer-
intervene using guided discovery during which clients are ized cognitive behavioral therapy (CCBT) is not meant t o
asked to identify and evaluate their cognitions (Epstein & replace face-to-face therapy, it does provide an additional
Baucom, 2002). When a patient is depressed about a treatment option. CCBT allows clients to participate in
neurological diagnosis or injury, clinicians may intervene therapy when there is a paucity of available therapists,
at the cognitive level challenging catastrophic thinking the associated costs are prohibitive, or the prospect of
(e.g., I will never get better). A therapist may focus speaking to someone face-to-face seems off-putting. In
decreasing negative self talk (e.g., I am worthless the way 2006, the United Kingdoms National Institute of Health
I am now) by encouraging the patient to keep a journal of and Clinical Excellence (NICE) provided guidelines
thoughts occurred and the impact of the thoughts on the recommending CCBT as a result of randomized
patients mood (Epstein & Baucom, 2002). controlled trials for mild to moderate depression and
anxiety (NICE, 2006).
Emotion-Focused Interventions
Outcome Measurement
Interventions within the realm of emotions may range
from expanding minimized emotional experience to con- Many clinicians used standardized instruments to assess
taining heightened emotional experience. Clinicians may the presence and severity of a variety of neuropsychologi-
draw on a variety of strategies to access, heighten, or limit cal diagnoses. With regard to depression, clinicians may
emotional experience including normalizing emotional use self-report inventories such as the Beck Depression
responses, metaphor, acceptance of emotional expression, Inventory (BDI II; Beck, Steer, & Brown, 1996) Finally, the
enhancing tolerance for distressing emotions, and Beck Anxiety Inventory (BAI: Kabacoff, Segal, Hersen, &
622 C Cognitive Behaviorism
Van Hasselt, 1997) has shown considerable utility in Inventory and the State-Trait Anxiety Inventory with older adult
psychiatric outpatients. Journal of Anxiety Disorders, 11(1), 3347.
diagnosing anxiety and identifying the severity of the
Lazarus, A. A. (1971). Behavior therapy and beyond. New York: McGraw-
anxiety symptoms. Hill.
Lazarus R. S., & Folkman, S. (1984). Stress, appraisal and coping.
New York: Springer.
Qualifications of Treatment Providers Leahy, R. L. (Ed.) (1997). Practicing cognitive therapy: A guide to inter-
ventions. Northvale, NJ: Jason Aronson.
National Institute of Health and Clinical Intervention (NICE). (2006).
CBT can be used by a variety of treatment providers such Depression and anxiety computerized cognitive behavioral therapy
as neuropsychologists, clinical psychologists, marriage (CCBT). Retrieved on July 17, 2007 at http://guidance.nice.org.uk/
and family therapists (MFTs), counselors, and social TA97
workers. Treatment providers using CBT should have OFarrell, T. J., Choquette, K. A., Cutter, H. S. G., Brown, E. D., &
appropriate clinical training in the model. Further, McCourt, W. F. (1993). Behavioral marital therapy with and without
additional couples relapse prevention sessions for alcoholics and
clinical providers learning to use CBTas a conceptual frame- their wives. Journal of Studies on Alcohol, 54, 652666.
work to guide therapy should seek supervision from an Rybarczyk, B., DeMarco, G., DeLaCruz, M., Lapidos, S., & Fortner, B.
experienced individual trained in the model of CBT. (2001). A classroom mind-body wellness intervention for older
adults with chronic illness: Comparing immediate and one year
benefits. Behavioral Medicine, 27, 1527.
Cross References
Behaviorism
Behavior Modification Cognitive Behaviorism
Psychotherapy
Behaviorism
Barlow, D. H., OBrien, G. T., & Last, C. G. (1984). Couples treatment of Cognitive Control
agoraphobia. Behavior Therapy, 15, 4158.
Baucom, D. H., Shoham, V., Mueser, K. T., Daiuto, A. D., & Stickle, T. R.
(1998). Empirically supported couples and family therapies for
adult problems. Journal of Consulting and Clinical Psychology, 66,
5388.
Beach, S. R. H., Sadeen, E. E., & OLeary, K. D. (1990). Depression in
marriage: A model for etiology and treatment. New York: Guilford
Press.
Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive therapy
of depression. New York: Guilford. R ICK PARENTE
Beck, A. T., Steer, R. A., & Brown, G. K. (1996). Manual for the Beck Towson University
Depression Inventory-II. San Antonio, TX: Psychological
Towson, MD, USA
Corporation.
Beck, J. S. (1995). Cognitive therapy: Basics and beyond. New York:
Guilford.
Dattilio, F. M., & Freeman, A. (Eds.). (2003). Cognitive-behavioral strate- Synonyms
gies in crisis intervention (3rd ed.). New York: Guilford.
Ellis, A. (1975). A new guide to rational living. Englewood Cliffs: Prentice
Behavioral memory aids; Behavioral prothestics; Cogni-
Hall.
Epstein, N. B., & Baucom, D. H. (2002). Enhanced cognitive-behavioral
tive archives; Cognitive assessors; Cognitive monitors;
therapy for couples. Washington: American Psychological Association. Cognitive orthotics; Cognitive robots; Cognitive trainers;
Gallagher-Thompson, D., Lovett, S., Rose, J., McKibbin, C., Coon, D., External aids; Prosthetic devices
Futterman, A., & Thompson, L.W. (2000). Impact of psycho-
educational interventions on distressed family caregivers. Journal of
Clinical Geropsychology, 6, 91110.
Definition
Heider, F. (1958). The psychology of interpersonal relations. New York:
Wiley.
Kabacoff, R. I., Segal, D. L., Hersen, M., & Van Hasselt, V. B. (1997). A device, external to the mind, that enhances or replaces
Psychometric properties and diagnostic utility of the Beck Anxiety a memory or cognitive function.
Cognitive Functioning C 623
Current Knowledge Cognitive trainers and archives teach a skill and/or

store large searchable databases. For example: academic
Parente and Herrmann (2010) defined several different remediation software teaches basic academic skills; cogni-
external aids that take over a deficient cognitive or memory tive remediation software provides drill and practice exer-
function. Table 1 surveys the various types of cognitive cises that improve cognitive skills; skills training software C
correction devices. teaches skills like typing or the use of specific software
Cognitive prosthetics refer to a general class of devices packages (e.g., Microsoft Office). Cognitive archives (e.g.,
that take over some memory process. Examples of partic- electronic encyclopedias) store large amounts of informa-
ularly useful prosthetics include: color coding, which cre- tion and provide a search engine for finding specific topics.
ates simplistic visual organization; checklists, which
improve consistency and sequential ordering; medication
organizers, which organize medications and remind a References and Readings
person which ones to take on each day; notepads and post-
it notes, which are useful for quickly writing a message or Parente, R., & Herrmann, D. (2010). Retraining cognition: Techniques and
for placing a written message somewhere where it will be applications. Austin, TX: ProEd Publishers.
seen later; appointment calendars and diaries, which
remind the person of important appointments and pro-
vide a record of daily activities.
Cognitive robots carry out a repetitive task for an
individual. For example: calculators perform the same Cognitive Exercises
mathematical operations; cycling timers turn appliances
on and off at preset times; telememo wrist watches remind Homework
the person of appointments at the same time every day,
week, month, or year; motion-sensitive detectors automat-
ically turn lights on and off when motion or the lack
thereof is sensed; smart irons turn themselves off after a Cognitive Flexibility
short period of disuse.
Cognitive Orthotic Devices replace some cognitive Mental Flexibility
function. For example: spelling machines find the correct Stroop Effect
spelling by keying in a close match; internet search engines
search the internet using key words and Boolean logic;
grammar checkers check a document for accuracy of
grammar.
Cognitive Functioning
C HRISTINA A. PALMESE
Beth Israel Medical Center
Cognitive Correctors. Table 1 Kinds of cognitive correctors
New York, NY, USA
Behavioral Changes in behavior that are specifically
prosthetics designed to remind a person to do
something Synonyms
Cognitive Carries out the same task consistently and
robot correctly Cognition; Mentation; Thinking
Cognitive Performs a thinking task
orthotic
Cognitive Help the person to learn new skills and to Definition
trainers practice them
Cognitive Maintain knowledge and records of past Cognitive functioning is a general term used to describe
archives experience so that a person does not have the different ways that people think. It refers to faculties
to store and retain this information
such as attention, mental processing speed, executive
internally in his or her memory
functions, language, visual spatial skills, memory, and
624 C Cognitive Functioning
fine motor dexterity. Different cognitive functions are sup- radio or television nearby. Divided attention allows us to
ported by distinct cortical and subcortical brain regions. pay attention to two or more tasks simultaneously. At the
Disruption of neural processes in these brain regions can top of the hierarchy is alternating attention, which is the
result in a range of cognitive deficits and syndromes. most complex form of attention that involves shifting of
attention from one task to another.
Many neuropsychological measures have been
Historical Background designed to evaluate attention. One such measure is the
digit span test. This task assesses basic attention capacity
In the 1600s, Descartes, a philosopher, was one of the first through repetition of series of numbers of increasing
scholars to establish the idea that the brain controls be- length (e.g., 1-2-3-etc). Continuous performance tests
havior. In the late 1700s, Franz Gall, a forefather of phre- are computerized assessment tools that evaluate attention
nology (the study of behavior based on the size and shape capacity over an extended time period of 1015 min.
of the skull) helped identify that different parts of the Higher level attention skills can be examined using tests
brain regulate distinct aspects of thought, personality, and involving mental arithmetic, more complex mental arith-
behavior. Later on in the 1800s and 1900s,Wilder Penfield, metic, connecting numbers and letters in alternating
Hughlings Jackson, Paul Broca, and Carl Wernicke, to sequence (e.g., 1-A-2-B-3-etc), and resequencing of
name only a few researchers who contributed significantly numbers and letters in numeric and alphabetic order
to the field of neuropsychology, used epilepsy and lesion (e.g., transform 8-K-2 to 2-8-K).
models to delineate distinct neuroanatomical correlates of Attention problems can be seen across the lifespan.
cognitive and motor functions. More recently, functional In children, poor concentration, distractibility, and trou-
(e.g., fMRI, PET) and structural (e.g., MRI, CT) neuro- ble regulating behavior can be related to an Attention
imaging techniques have provided an even more well Deficit Disorder, a diagnosis that is made when pervasive
defined understanding of brain-behavior relationships. attention difficulties are demonstrated prior to age seven
years and are observable in at least two different environ-
ments. However, attention difficulties in children also
Current Knowledge may develop secondary to anxiety, language disorders,
or neurological disorders such as epilepsy. In adults, at-
Attention tention deficits may manifest secondary to a variety of
neurological and medical conditions, including sub-
Attention refers to the ability to concentrate on informa- arachnoid hemorrhage, epilepsy, dementia, head injury,
tion that is heard and seen in the environment in both diabetes, and hypothyroidism. Stress, depression, and med-
the presence and absence of distractions. It also allows ication side effects often contribute to attention problems
us to concentrate on two things at once, such as balancing in adults, as well.
a checkbook while talking on the phone. It is regulated
by the frontal lobes, although pathways involving the
pons, parietal lobe, and thalamus are involved in the Mental Processing Speed
mediation of attention, as well. Dysfunction along these
pathways can contribute to various types of attention Mental processing speed, a term used synonymously with
problems. reaction time, refers to the speed at which an individual
Attention is hierarchically organized, and disruption thinks and completes activities. It is largely regulated by
of the most basic attention skills leads to disruption of the frontal lobes and subcortical regions, and it has global
more complex attention abilities. Focused attention is the effects on cognition. That is, if mental processing speed is
most rudimentary level of attention that permits us to poor slowness also is observed in areas of attention, lan-
concentrate or be vigilant to something in the environ- guage, and spatial processing abilities. This mental slow-
ment for a very brief time period. Sustained attention ing is referred to as bradyphrenia.
refers to maintenance of concentration for minutes or Reaction time can be evaluated in several ways. Mea-
hours. Selective attention requires even greater attention sures requiring manual transcription of numbers and
capacity that allows us to attend to a particular task while shapes are very sensitive to bradyphrenia. Other tasks
filtering out irrelevant, background information. For ex- may involve rapid reading of color names and naming
ample, this form of attention is used when we read the of colors, timed symbol search, and rapid generation of
newspaper and are not distracted by noises such as the words.
Cognitive Functioning C 625
Bradyphrenia is commonly observed in medical and Cognitive Correctors. Table 1

neurological conditions across the lifespan, including de-
Aphasia
mentia, brain injury, and Parkinsons disease.
syndrome Neuroanatomy Symptom(s)
Brocas Posterior, Poor articulation,
(expressive) lateral frontal telegraphic, non-fluent,
C
Executive Functions
aphasia lobe limited speech, intact
comprehension
Executive functioning refers to some of the most highly
complex aspects of thinking. It includes skills such as Wernickes Anterior, lateral Poor comprehension,
(receptive) temporal lobe fluent speech, nonsensical
problem solving ability, task execution and efficiency,
aphasia speech content
self-monitoring, strategizing, mental flexibility, planning,
Anomic Temporal- Poor naming, intact
and conceptualization. Executive functions are largely
aphasia parietal border comprehension, intact
mediated by the frontal lobes, and they are highly sensitive
fluency
to cerebral dysfunction.
Deficits in executive functioning can occur secondary
to neurodevelopmental immaturity, such as seen in atten-
tion deficit disorder. For the most part, however, execu- commonly observed language problems in adults is a
tive dysfunction is either acquired through brain injury naming deficit (which is synonymous with word finding
(e.g., stroke, head injury) or associated with neurodegen- difficulty, dysnomia, and tip of the tongue experiences),
erative diseases, such as Alzheimers disease, multiple auditory naming tests have proven to be useful for identi-
sclerosis, and Huntingtons disease. fication of anomia, as well. Similar measures are used
during evaluation of pediatric populations. In addition,
examination of children also should include assessment of
Language phonics, grammar, syntax, language formulation, and
language organization skills.
At the most fundamental level, language can be broken
down into two categories: receptive and expressive lan-
guage. Receptive language refers to the ability to under- Visual Spatial Processing
stand language; it is mediated by the posterior region
of the superior temporal gyrus, which is known as Cognitive abilities such as basic spatial perception, visual
Wernickes area. Expressive language, on the other hand, construction, and nonverbal problem solving ability are
pertains to oral and written expression and it is regulated characterized as spatial processing skills. These faculties
by the posterior frontal/anterior temporal lobe. This re- involve identifying what and where items are in space.
gion commonly is referred to as Brocas area. The what, or ventral, pathway is mediated by the right
Deficits in receptive and expressive language can be (nondominant) temporal lobe. Disruption of this pathway
idiopathic (i.e., of unknown origin) or acquired. If lan- by acquired brain injury can result in agnosia, which is a
guage problems are idiopathic, they typically are identi- loss of awareness and inability to recognize entities in the
fied during a childs development and are referred to as a environment. Agnosias can be domain specific, affecting
developmental language delay. As some children mature, auditory, visual, or somatosensory functioning. Prosopag-
their language difficulties might resolve; however, other nosia is a unique agnosia in which there is an inability to
children experience residual language deficits throughout recognize faces.
adulthood. On the other hand, acquired language deficits The where or dorsal pathway is regulated by the
such as those resultant from stroke, head injury, and parietal lobe. Dysfunction in the parietal lobe can contrib-
tumor are characterized as aphasia. Depending on the ute to spatial neglect in which a portion of space is
location of brain injury, different aphasia syndromes can neglected or ignored. Neglect can be detected during
be observed. Listed below are three of the most commonly visual field screening and on line bisection and drawing
referenced syndromes. tasks. An individual with spatial neglect will not respond
Traditionally, language skills in adults are assessed to information presented in part or all of the visual field.
with an aphasia battery (e.g., Boston Diagnostic Aphasia Left hemispatial neglect, in which the entire left side of
Examination (BDAE)), letter and category fluency, and space is ignored, is the most commonly observed form of
visual confrontation naming tasks. As one of the most neglect that results from damage to the right parietal lobe.
626 C Cognitive Functioning in the Elderly
Memory Cross References
Memory involves learning, retrieval, retention, and recog- Agnosia

nition of information. Memory functions are lateralized, Agraphia
with verbal memory regulated by left (dominant) tempo- Alexia
ral regions and visual-spatial memory regulated by the Amnesia
right temporal lobe. In order for new learning to occur, we Anomia
must be able to attend to the material and store it tempo- Aphasia
rarily in our short-term memory. Consolidation of this Attention
information into long-term memory stores occurs within Learning
the CA1-CA3 regions of the hippocampus, a subcortical Memory
brain region rich in acetylcholine. Once learned, informa- Processing Speed
tion is then stored in various neural networks throughout Syndrome
the brain. Verbal Fluency
Learning deficits can be attributed to depletion of Visuoperceptual
acetylcholine or loss of brain cell within the hippocam-
pus. This type of memory problem typically is associated
with cortical dementia, such as Alzheimers disease. References and Readings
Cholinesterase inhibitors, which are medications that
promote cholinergic availability, are common treatment Hamberger, M. J., Goodman, R. R., Perrine, K., & Tamny, T. (2001).
options to delay or slow the progression of a learning Anatomic dissociation of auditory and visual naming in the lateral
temporal cortex. Neurology, 56(1), 5661.
deficit. Retrieval deficits, on the other hand, are charac-
Heilman, K. M., & Valenstein, E. (2003). Clinical neuropsychology
terized by poor spontaneous recall, yet adequate recog- (4th ed.). New York, NY: Oxford University Press.
nition of newly learned material. They are associated Kolb, B., & Wishaw, I. (2008). Fundamentals of human neuropsychology
with cell loss and neurochemical depletion of dopamine (6th ed.). New York, NY: Worth Publishers, Inc.
and glutamate in the basal ganglia and other subcortical Lezak, M., Howieson, D. B., & Loring, D. W. (2004). Neuropsy-
chological assessment (4th ed.). New York, NY: Oxford University
regions. Retrieval deficits are observed in subcortical
Press.
dementias, including Parkinsons disease and Hunting- Squire, L. R., & Schacter, D. L. (2002). Neuropsychology of memory
tons disease. Although cholinesterase inhibitors can be (3rd ed.). New York, NY: The Guilford Press.
used to treat subcortical memory dysfunction, their effi-
cacy is relatively weaker in subcortical versus cortical
dementia populations.
Cognitive Functioning in the

Elderly
Motor
Normal Aging
Motor abilities refer to skills such as hand-eye coordina-
tion, manual dexterity, and visual-motor integration.
These skills all have contralateral representation within
the parietal lobes. That is, right sided motor functions Cognitive Impairment No
are regulated by left parietal lobe regions, and vice versa.
Motor dysfunction can be observed in children with de-
Dementia (CIND)
velopmental delay, as well as in adults and children with
Mild Cognitive Impairment
medical conditions including cerebral palsy, spasticity,
and dementia. It often manifests as clumsiness, poor
handwriting, or trouble tying shoe laces and buttoning
shirts. Motor abilities can be evaluated using tasks requir-
ing rapid placement of pegs into a pegboard, drawing, Cognitive Log
imitation of hand movements, finger tapping, and grip
strength. Cognitive-Log
Cognitive Processing Speed C 627
psychology approach to better understanding cognitive

Cognitive Monitors processing has been through the development of computa-
tional models, such as artificial intelligence.
Cognitive Correctors In cognitive neuroscience research, cognitive proces-
sing concepts are used to explore the relation between C
brain and behavior, as exemplified by George Millers
research (1956) on the capacity of short-term memory
to hold seven plus or minus two items and Baddeleys
Cognitive Orthotics theory (1974) of a central executive, phonological loop,
and visuospatial sketchpad.
Prosthetic Memory Aids
Current Knowledge
The cognitive processing model is currently used in

Cognitive Potential the assessment and treatment of learning disabilities,
alcohol and drug addictions, and trauma and abuse.
Best Performance Method This model emphasizes how new information is pro-
cessed, internalized, and retrieved in the context of a
persons existing mental representations of information,
and of his/her beliefs, desires, knowledge, preferences,
and intentions.
Cognitive Processing
D ENISE K RCH
Kessler Foundation Research Center Cross References
West Orange, NJ, USA
Attention
Definition Learning
Memory
Cognitive processing is a general term to describe a Metacognition
series of cognitive operations carried out in the creation Perception
and manipulation of mental representations of informa- Reasoning
tion. Cognitive processes may include attention, per- Retrieval, Retrieval Techniques
ception, reasoning, emoting, learning, synthesizing, Short Term Memory
rearrangement and manipulation of stored information,
memory storage, retrieval, and metacognition. These
functions can be conscious (e.g., learning a concept) or References and Readings
unconscious (e.g., learning a skill) and can be internally
generated (e.g., recalling a memory) or initiated by a Coren, S., Ward, L., & Enns, J. (2004). Sensation and perception. New York:
novel sensory input from the environment (e.g., solving Harcourt Brace.
Groome, D., Brace, N., Edgar, H., Esgate, A., Pike, G., Stafford, T., et al.
a problem).
(2006). An introduction to cognitive psychology: Processes and disor-
From a cognitive psychology perspective, cognitive ders (2nd ed.). London: Routledge.
processing is approached as a sequence of ordered stages
wherein sensory input is transformed, reduced, elaborated,
stored, recovered, and utilized. Early views of cognitive
processing emphasized linear temporal processing, whereas
contemporary models assume a less linear, more complex Cognitive Processing Speed
flow of dynamics, including bottom-up (sensory-driven)
and top-down (concept-driven) processes. One cognitive Information Processing Speed
628 C Cognitive Rehabilitation
Rationale or Underlying Theory

CR is multidisciplinary and draws from a range of fields,
M ARIANNE H RABOK , K IMBERLY A. K ERNS including neuropsychology, learning theory, cognitive
University of Victoria behavioral therapy and psychotherapy, among many
Victoria, BC, Canada others. One main category of theories underlying CR is
that specific to the cognitive or behavioral domain of CR
focus. For example, attention rehabilitation programs are
Synonyms based on theoretical models of attention, memory reha-
bilitation programs on theoretical models of memory, and
Cognitive Remediation so on. A theory-driven approach provides a rational and
empirical basis for intervention, and guidance on the
structure and delivery of CR (Levine & Downey-Lamb,
Definition 2002; Sohlberg & Mateer, 2001).
Another major theory underlying many forms of CR
Cognitive rehabilitation (CR) can be defined as efforts is neuroplasticity (Kolb & Cioe, 2004), the concept that
to promote maximal adaptive cognitive functioning in the brain is amenable to change in structure and func-
people with neurologically induced cognitive deficits tion. These changes occur at multiple levels, and are
(Barrett & Gonzalez-Rothi, 2002). manifest in various ways, including changes at the syn-
apse, changes in neurotransmitter systems, and changes
in neural networks (Barrett & Gonzalez-Rothi, 2002;
Historical Background Sohlberg & Mateer, 2001). Neuroplasticity has many
implications to CR, including the type and timing of
The field of CR has grown rapidly over the last few CR, and the effect of environmental factors on recovery
decades, but historically can be traced to the 1800s of cognitive function following brain injury (Barrett &
(Ponsford, 2004; Sohlberg & Mateer, 2001). For example, Gonzalez-Rothi, 2002).
Broca administered language rehabilitation in the 1800s
and until the 1980s most rehabilitation programs focused
on remediation of language deficits (as reviewed by Goals and Objectives
Ponsford, 2004). Many further developments in CR were
a result of the confluence of societal influences and CR aims to foster natural recovery, decrease the develop-
scientific and technological advances. During WWI, ment of maladaptive patterns, and increase functional
Goldstein established CR programs for brain-injured recovery (Sohlberg & Mateer, 2001). The primary goal
soldiers. During WWII, Luria advanced the field of CR of CR is to help people achieve an optimal level of func-
through his theoretical model of brain functioning, tioning in the context of impairments. CR emphasizes
recovery, and rehabilitation (Ponsford, 2004). improving function in everyday contexts, rather than on
Advances in medical practice and an increase in the specific cognitive tasks per se.
number of survivors of traumatic brain injury (TBI) led
to a greater awareness of the needs of people who sus-
tained TBI, and an expansion of the number and focus of Treatment Participants
CR programs (the era of proliferation; Coelho, 1997, as
cited by Sohlberg & Mateer, 2001). However, current CR has been used with a variety of populations, including
trends in service delivery have resulted in an era of but not limited to: TBI, stroke, acquired brain injury
consolidation, a term describing the significant down- (ABI) of varying etiology, developmental disorders,
sizing of CR programs. It has been suggested that the Alzheimers dementia, and schizophrenia. CR has been
reduced length of inpatient stays, outpatient health most commonly used among people who have sustained
coverage, and more limited support for CR programs TBI and stroke. Research on CR aimed at neurocognitive
have made evidence and theory-based CR practices deficits associated with schizophrenia has been growing
increasingly relevant to contemporary practice (Cicerone over the last 10 years (Kurtz & Nichols, 2007).
et al., 2005; Levine & Downey-Lamb, 2002; Sohlberg & Variables contributing to the pattern and degree
Mateer, 2001). of recovery following brain injury include: demographic
Cognitive Rehabilitation C 629
(e.g., age, education, gender, culture), injury-related (e.g., rapid recovery than diffuse injury (Sohlberg & Mateer,
time since injury, extent, and severity of injury), and 2001).
psychological characteristics (e.g., therapeutic alliance,
comorbid psychological disorders, awareness).
Psychological Factors C
Demographic Variables Therapeutic Alliance: CR should be an interactive partner-
ship between the client, their significant others, and the
Age : Younger adults show better levels of recovery therapist. Cultivating a relationship characterized by
than older adults (Teuber, 1975 as cited by Sohlberg & attentiveness, respect, trust, commitment, and rapport is
Mateer, 2001). ABI in older adults may be complicated a critical component of CR. Open communication and
by a number of factors, including the superimposition involvement of the client and family in goal setting can
of effects of ABI on declining cognitive abilities (Richards, also enhance engagement in rehabilitation (Sohlberg &
2000 as cited by Sohlberg & Mateer, 2001), and psycho- Mateer, 2001).
social difficulties more prevalent in the population, Comorbid Psychological Disorders: Depression and
including reduced levels of social support and financial anxiety are frequently associated with brain injury (e.g.,
resources (Goleburn & Golden, 2001). However, it Anson & Ponsford, 2006). These can impede CR and
has also been suggested that older adults often have a adjustment following injury due to their propensity
greater degree of stability, coping skills, fewer life to decrease motivation and contribute to a feeling of
demands, and effective compensatory techniques, which hopelessness (Sohlberg & Mateer, 2001).
may be helpful to promoting recovery (Sohlberg & Awareness: Lack of awareness can occur following
Mateer, 2001). brain injury, and has been associated with poor self-
Education and Intelligence: Premorbid intelligence and regulation, disengagement in CR programs (Allen &
education are significantly related to recovery and adjust- Ruff, 1990), and poorer outcome.
ment (Anson & Ponsford, 2006). Although these factors provide important informa-
Gender: Some research suggests that women have tion related to the pattern and degree of recovery follow-
better recovery following left hemisphere lesions than ing brain injury, it should also be noted that much more
men (Kimura, 1983), and circulating sex hormones have research is needed to better identify therapy factors and
also been shown to have neuroprotective effects (e.g., client characteristics that optimize clinical outcomes of
Roof, Duvdevani, & Stein, 1993). CR (Cicerone et al., 2005).
Culture: Culture influences beliefs regarding the
nature and cause of loss, service utilization, degree of
personal responsibility for health, role of family, and Treatment Procedures
many other facets of psychological and behavioral
functioning relevant to recovery and participation in CR Examples of domains that have been a focus of CR
(Sohlberg & Mateer, 2001). include: attention, memory, language, visuoperceptual
difficulties, executive functions, and socioemotional
and behavioral disturbances. CR encompasses a range
Injury Related Variables of interventions. These can be broadly divided into
two types of techniques. The first are those that aim to
Time since Injury: Spontaneous recovery typically occurs restore or enhance function, by targeting the underlying
at a faster rate immediately following brain injury, partic- impairment (Glisky & Glisky, 2002; Sohlberg & Mateer,
ularly within the first 6 months, with significant recovery 2001). For example, Attention Process Training (APT) is a
also occurring up to 2 years following injury (Sohlberg & theoretically-driven program that contends that attention
Mateer, 2001). However, it is important to note that can be improved through repeated activation of atten-
compensatory techniques can be implemented and tional systems (Sohlberg & Mateer, 1987, 2001). APT
underlying motor and cognitive skills improved years consists of a group of hierarchically organized tasks
after injury (e.g., Shaw et al., 2005). that exercise different components of attention (e.g.,
Extent and Severity of Injury: Relatively mild injuries sustained, selective, alternating, divided attention). In
are associated with faster recovery rate and better CR of memory deficits, restorative/generalized memory
outcomes. Focal injuries are often associated with more approaches aim to improve specific memory systems
630 C Cognitive Rehabilitation
across tasks and contexts (e.g., prospective memory train- compared to a number of alternate treatment conditions,
ing, Raskin & Sohlberg, 1996 as cited by Sohlberg & with no comparison demonstrating a benefit for an
Mateer, 2001). Various approaches to executive function alternate treatment condition.
rehabilitation provide practice in executive skills (e.g., Although implementation of CR programs results in
planning) and guiding behavior through self-talk positive change, a number of methodological problems
(e.g., self instructional training, Cicerone & Giacino, 1992). have been identified in the CR literature, including but
The second category of CR interventions is compen- not limited to:
satory techniques, which aim to compensate for, or bypass
1. Variability in client characteristics and treatment
deficits (Sohlberg & Mateer, 2001; Wilson & Zangwill,
settings
2003). These include environmental supports (e.g.,
2. Insufficient description of samples
organization of physical space, manipulation of physio-
3. Small sample sizes
logical factors such as sleep, nutrition etc.) and external aids
4. Inadequate description of interventions
(e.g., calendars, pagers, checklists, etc.; Manly, Ward, &
5. A lack of standardized treatment protocols and
Robertson, 2002; Wilson & Zangwill, 2003). Compen-
treatment approaches (including type of intervention,
satory techniques can be helpful in managing diverse
length, and intensity)
types of cognitive difficulties (Sohlberg & Mateer, 2001).
6. Lack of appropriate control conditions (e.g., no
A third approach involves the use of specialized
treatment or alternate treatment)
approaches to teaching and stabilizing new behaviors
7. Lack of uniform outcome measures
and knowledge in people with memory difficulties.
These include instructional techniques such as errorless Evidence-based standards of CR are frequently
learning, in which mistakes are minimized (Wilson, identified as important in advancing the field of CR, both
Baddeley, Evans, & Shiel, 1994), the method of vanishing in terms of quality of treatment and for fiscal support at
cues (Glisky & Glisky, 2002) and traditional behavioral an organizational level (e.g., Sohlberg & Mateer, 2001).
shaping and training techniques. Cicerone et al. (2005) reviewed evidence for CR inter-
Psychosocial support or psychotherapy (e.g., sup- ventions used with TBI and stroke populations. A number
ported listening, brain injury education, relaxation training) of interventions with strong empirical support were
can also be an integral part of a rehabilitation program, identified. Strategy training (e.g., APT or Time Pressure
depending on the needs of the client (Sohlberg & Mateer, Management) was effective during postacute rehabilita-
2001). Computer programs can be used as an adjunct tion for TBI. A number of visuospatial rehabilitation
to CR, but should not be the sole form of CR (Cicerone techniques were empirically supported for improving ne-
et al., 2005). It has been recommended that computer glect following right hemisphere stroke (e.g., visuospatial
CR programs be focused, structured, monitored, and rehabilitation, scanning training). Specific gestural or
ecologically valid. A successful rehabilitation program strategy training was found to be effective in the treatment
typically involves a combination of interventions, speci- of apraxia following left hemisphere stroke. A number of
fically tailored to the individuals level of disability language interventions were shown to have empirical
and personal goals (Manly et al., 2002; Solhberg & support, including cognitive linguistic therapies,
Mateer, 2001). pragmatic conversational skills, interventions for specific
The duration and frequency of CR varies widely (e.g., language impairments (e.g., reading comprehension), and
Geusgens, Winken, van Heugten, Jolles, & van den adjunctive computer-based interventions. Strong empiri-
Heuvel, 2007; Kurtz & Nichols, 2007). CR has been cal support was shown for memory strategy training (e.g.,
delivered both on an individual and on a group basis. visual imagery and external aids, such as memory
Significant others (e.g., family) are viewed as an integral notebooks). Some empirical support was found for self-
part of treatment (Sohlberg & Mateer, 2001). instruction and self-monitoring interventions for
executive functions. Empirical support was found for
comprehensive-holistic CR programs, which address
Efficacy Information multiple aspects of impairment.
Interventions that meet criteria for inclusion as an
Cicerone et al. (2005) examined differential treatment empirically supported treatment do not represent an
effects of CR compared to alternate treatment conditions exhaustive list of CR interventions that may be effective,
in 46 class I studies with TBI and stroke populations. but reflect the empirical status of the field of CR research
Their review suggested a clear differential benefit of CR and practice. A successful rehabilitation program typically
Cognitive Rehabilitation C 631
involves a combination of interventions, specifically standardized observations of simulated performance of

tailored to the individuals level of disability and personal daily tasks in a laboratory environment, and standardized
goals (Manly et al., 2002; Solhberg & Mateer, 2001). and nonstandardized reports of transfer to daily function-
Therefore, clinical considerations may demand CR inter- ing (Geusgens et al., 2007). There is a need for further
ventions with strong empirical support, as well as those development of standardized measure of transfer with C
that have less empirical support but may be beneficial to good psychometric properties (Geusgens et al., 2007). It
the client. A discussion of limitations and strengths of has been recommended that generalization should not be
empirically supported and empirically validated inter- expected, but should be programed throughout the
ventions can be found elsewhere (e.g., Chambless & CR program (Sohlberg & Mateer, 2001).
Ollendick, 2001).
There is less empirical study of CR with populations
beside TBI and stroke. A review of CR with children who Qualifications of Treatment Providers
have sustained ABI concluded that there is a sufficient
amount of evidence to recommend attention remedia- CR is typically provided by registered psychologists, and
tion, involvement of family members in the treatment occupational therapists. Speech and language therapists
plan, and provision of psychoeducation to guardians typically provide rehabilitation for language and
(Laatsch et al., 2007). A review of studies of CR with communication deficits.
people with early stage Alzheimers disease suggested CR
could be beneficial, particularly when flexible to the needs
of clients, of sufficient duration, and involving caregivers Cross References
(Clare, 2003). A review of studies of CR with people
with schizophrenia has suggested improvements on Assistive Technology
memory and executive functions, although it should be Attention Training
noted that this is an emerging field so is based on a Behavioral Memory Aids
small number of studies (Kurtz & Nichols, 2007). Brain Plasticity
A review of CR for people with multiple sclerosis sug- Compensatory Strategies
gested empirically based support for verbal learning and Environmental Modifications
memory intervention, and suggested additional research Errorless Learning
support is needed (OBrien, Chiaravalloti, Govereover, & Head Injury
DeLuca, 2008). Insight, Effects on Rehabilitation
Interdisciplinary Team Rehabilitation
Memory
Outcome Measurement Neglect and Heminattention
Neuropsychological Rehabilitation
Levine and Downey-Lamb (2002) recommend inclusion Prosthetic Memory Aids
of both specific outcome measures that relate closely to Rehabilitation Psychology
the construct addressed by the intervention, and well as Traumatic Brain Injury
general measures of functional outcomes, such as return
to work/school, interpersonal relationships, and leisure
activities. When possible, measures should have known References and Readings
psychometric properties, and be completed by both the
client and significant others. Allen, C. C., & Ruff, R. M. (1990). Self-rating vs. neuropsychological
performance of moderate vs. severe head-injured patients. Brain
Neuropsychological assessment can be a valuable tool
Injury, 4, 717.
at various points to: predict outcome, guide appropriate Anson, K., & Ponsford, J. (2006). Coping and emotional adjustment
rehabilitation strategies, guide vocational and educational following traumatic brain injury. The Journal of Head Trauma
planning, explain behavior, and help evaluate the extent Rehabilitation, 21, 248259.
of injury in conjunction with other information Barrett, A. M., & Gonzalez-Rothi, L. J. (2002). Theoretical bases
for neuropsychological interventions. In P. J. Eslinger (Ed.),
(Bergquist & Malec, 2002).
Neuropsychological interventions: Clinical research and practice
Measurement of transfer of training to everyday life (pp. 1637). London: The Guilford Press.
has been measured through assessment of performance Bergquist, T. F., & Malec, J. F. (2002). Neuropsychological assessment
on tasks similar to tasks used during training, for treatment planning and research. In P. J. Eslinger (Ed.),
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Neuropsychological interventions: Clinical research and practice (pp. Sohlberg, M. M., & Mateer, C. A. (1987). Effectiveness of an attention
3858). London: The Guilford Press. training program. Journal of Clinical and Experimental Neuropsy-
Chambless, D. L., & Ollendick, T. H. (2001). Empirically supported chology, 19, 117130.
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Cicerone, K. D., Dahlberg, C., Malec, J. F., Langenbahn, D. M., Wilson, B. A., Baddeley, A. D., Evans, J. J., & Shiel, A. (1994). Errorless
Felicetti, T., Kneipp, S., et al. (2005). Evidence-based cognitive learning in the rehabilitation of memory impaired people.
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Cicerone, K. D., & Giacino, J. T. (1992). Remediation of executive tation: Theory and practice. Exton, PA: Psychology Press.
function deficits after traumatic brain injury. Neurorehabilitation,
2, 7383.
Clare, L. (2003). Cognitive training and cognitive rehabilitation for
people with early-stage dementia. Reviews in Clinical Gerontology,
13, 7583. Cognitive Remediation
Geusgens, C. A. V., Winken, S. I., van Heugten, C. M., Jolles, J., & van den
Heuvel, W. J. A. (2007). Occurrence and measurement of transfer in
cognitive rehabilitation: A critical review. Journal of Rehabilitation
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In P. J. Eslinger (Ed.), Neuropsychological interventions: Clinical
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Goleburn, C. R., & Golden, C. J. (2001). Traumatic brain injury outcome
in older adults: A critical review of the literature. Journal of Clinical Cognitive Reserve
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Kimura, D. (1983). Sex differences in cerebral organization for
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J ESSE C HASMAN
1935. Brown University
Kolb, B., & Cioe, J. (2004). Neuronal organization and change after Providence, RI, USA
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bilitation: From neurobiology to clinical practice (pp. 729). London:
The Guilford Press.
Kurtz, M. M., & Nichols, M. C. (2007). Cognitive rehabilitation for
Synonyms
schizophrenia: A review of recent advances. Current Psychiatry
Reviews, 3, 213221. Brain reserve; Neural compensation; Neural reserve
Laatsch, L., Harrington, D., Hotz, G., Marcantuoro, J., Mozzoni, M. P., &
Walsh, V., et al. (2007). An evidence-based review of cognitive and
behavioral rehabilitation treatment studies in children with ac-
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Levine, B., & Downey-Lamb, M. M. (2002). Design and evaluation of
Cognitive reserve is a concept often used to describe how
rehabilitation experiments. In P. J. Eslinger (Ed.), Neuropsychological
interventions: Clinical research and practice (pp. 80104). London:
individual differences mediate the clinical expression of
The Guilford Press. brain damage. In this context, some individuals may cope
Manly, T., Ward, S., & Robertson, I. (2002). The rehabilitation of atten- better than others and function within relatively normal
tion. In P. J. Eslinger (Ed.), Neuropsychological interventions: Clinical limits, despite the presence of neuropathology.
research and practice (pp. 105136). London: The Guilford Press.
OBrien, A., Chiaravalloti, N. D., Govereover, Y., & DeLuca, J. (2008).
Evidenced based cognitive rehabilitation for persons with multiple
sclerosis: A review of the literature. Archives of Physical Medicine and Historical Background
Ponsford, J. (2004). Introduction. In J. Ponsford (Ed.), Cognitive and
behavioral rehabilitation: From neurobiology to clinical practice
Historically, one of the earliest observations of cognitive
(pp. 16). London: The Guilford Press. reserve was described in a study that found characteristic
Roof, R. L., Duvdevani, R., & Stein, D. G. (1993). Gender influences senile plaques and neurofibrillary tangles commonly asso-
outcome of brain injury: Progesterone plays a protective role. Brain ciated with Alzheimers pathology present in healthy, cog-
Research, 607, 333336.
nitively unimpaired elderly (Blessed, Tomlinson, & Roth,
Shaw, S. E., Morris, D. M., Uswatte, G., McKay, S., Meythaler, J. M., &
Taub, E. (2005). Constraint-induced movement therapy for recovery
1968). Similar observations between brain pathology and
of upper-limb function following traumatic brain injury. Journal of performance variability frequently have been described in
Rehabilitation Research and Development, 42, 769778. the extant literature.
Cognitive Stimulation C 633
Current Knowledge activities, such as education, occupation, exercise, or so-

cial involvement, may provide buffers within neural net-
While the underlying mechanisms that support cognitive works to help delay the behavioral symptoms associated
reserve remain unclear, current theories focus on how the with brain pathology.
brain may develop alternative or more efficient networks C
to compensate for pathology. One theory proposed by
Satz (1993) holds that brain mass and neuronal count Future Directions
or brain reserve capacity (BRC) may raise or lower the
brains threshold to withstand a lesion or degenerative An important implication of this concept may be the
process. In this model, lower BRC would make an indi- development of interventions that aim enhances cognitive
vidual more vulnerable to neurological insult and increase reserve. In aging research, for instance, growing interest
test sensitivity in detecting impairment. Similarly, greater has revolved around the effectiveness of brain training
BRC would provide a higher threshold before the effects games, exercise, or lifestyle modifications that may
of neuropathology are observed. For instance, one study strengthen and/or expand neural networks, and improve
(Katzman et al., 1988) compared a high-functioning cognitive functioning.
group of nursing home residents with Alzheimers pathol-
ogy with a group of healthy nursing home controls. When
compared across several cognitive domains, the Alzhei- Cross References
mers group performed at or above the levels of healthy
controls. In this study, the observed cognitive deficits were Brain Plasticity
much lower than predicted, given the level of brain pa- Brain Reserve Capacity
thology in these individuals. This was explained, in part,
by the finding that those in Alzheimers group had larger
brains with more neurons than the control group, which
may have helped those individuals compensate for their
Blessed, G., Tomlinson, B. E., & Roth, M. (1968). The association between
neuropathology. Genetics may play a primary role in
quantitative measures of dementia and of senile change in the
building greater BRC by increasing overall brain mass, cerebral grey matter of elderly subjects. The British Journal of Psychi-
synaptic density, or neurogenesis, all of which could pro- atry, 114(512), 797811.
vide greater resiliency against lesions or a degenerative Katzman, R., Terry, R., DeTeresa, R., Brown, T., Davies, P., Fuld, P., et al.
process. (1988). Clinical, pathological, and neurochemical changes in de-
mentia: A subgroup with preserved mental status and numerous
By contrast, the concept of cognitive reserve suggests
neocortical plaques. Annals of Neurology, 23(2), 138144.
that individual differences in genetics or life experiences Satz, P. (1993). Brain reserve capacity on symptom onset after brain
provide a buffer to the effects of brain disease, including injury: A formulation and review of evidence for threshold theory.
dementia. Neural reserve or neural compensation models Neuropsychology, 7(3), 273295.
(Stern, 2002) are proposed as potentially active processes Stern, Y. (2003). The concept of cognitive reserve: A catalyst for research.
Journal of Clinical and Experimental Neuropsychology, 25(5),
that facilitate the brains attempts to adapt to disease
589593.
pathology. Various lines of animal studies have supported Stern, Y. (2006). Cognitive reserve: Theory and application (studies on
this model noting the benefits of enriched environments neuropsychology, neurology, and cognition). New York: Psychology
on neurogenesis and plasticity in the brain. In humans, Press.
years of education and occupational attainment are asso-
ciated with the preservation of cognitive functions. For
instance, individuals with lower education often demon-
strate clinical manifestations of dementia earlier in the Cognitive Robots
disease process compared to those with higher education
(Stern, 2003). Cognitive Correctors
One of the important implications of the cognitive
reserve construct is that lifetime experiences can influence
individuals level of functioning. It is important to high-
light that current research does not suggest that cognitive Cognitive Stimulation
reserve prevents neuropathology from developing. Rather,
it is believed that a lifetime spent engaging in stimulating Reality Orientation
634 C Cognitive Trainers
nondegenerative and degenerative neurologic diseases (in-

Cognitive Trainers cluding the dementias) (ASHA, 2005).
CCDs were recognized in the early 1980s as research
Cognitive Correctors mounted, illustrating the interdependency of cognition
and language, particularly with regard to the roles of
attention and memory in language processing and with
regard to the pervasive impact that cognitive impairments
Cognitive-Behavioral have on functional communication abilities (Bayles &
Modification Tomoeda, 2007; Myers & Blake, 2008; Ylvisaker, Szekeres,
& Feeney, 2008). Speech-language pathologists (SLPs)
Behavior Modification now routinely assess and treat those aspects of cognition
that either support, or are influenced by, speech, lan-
guage, and communication; other clinicians such as
neuropsychologists, rehabilitation psychologists, and
cognitive remediation specialists may do so as well.
Cognitive-Communication
Disorder
Categorization
S ARAH S. C HRISTMAN B UCKINGHAM
The University of Oklahoma Health Sciences Center CCDs are differentiated from linguistic impairments
Oklahoma, OK, USA (aphasias) and from motor speech disorders (dysarthrias
and apraxia of speech) by the use of overly concrete,
poorly organized, and socially insensitive communication
Synonyms despite preserved speech and language skills. CCDs may
be caused and/or complicated by impairments of atten-
Cognitive-communication impairment; Language of con- tion, memory, executive functions, and pragmatics.
fusion; Language of generalized intellectual impairment; Symptoms will vary by etiology, patterns of brain damage,
Right hemisphere impairment/disorder and individual differences in the neural organization of
cognitive functions.
Short Description or Definition Epidemiology

The American Speech-Language-Hearing Association Approximately 1.4 million individuals will suffer stroke-
(ASHA) has defined cognitive-communication disorders related CCDs each year (CDC, 2007; Tomkins, 1995).
(CCDs) as those that, . . .encompass difficulty with any One to two million children will acquire post-traumatic
aspect of communication that is affected by disruption of CCDs annually (Blosser & DePompei, 2003; CDC, 2001;
cognition. Communication may be verbal or nonverbal and Ylvisaker et al., 2008), whereas adult and elderly indivi-
includes listening, speaking, gesturing, reading, and writing duals will sustain head injuries at rates approximating
in all domains of language (phonologic, morphologic, syn- 100200 per 100,000, respectively (Bruns & Hauser,
tactic, semantic, and pragmatic). Cognition includes cogni- 2003). The number of individuals expected to be living
tive processes and systems (e.g., attention, perception, with dementia of the Alzheimers type (DAT), and thus
memory, organization, executive function). Areas of func- living with CCDs, is expected to increase from 4 million
tion affected by cognitive impairments include behavioral (in the year 2000) to 31.2 million people by the year 2050.
self-regulation, social interaction, activities of daily living,
learning and academic performance, and vocational perfor-
mance. Cognitive-communication disorders may be con- Natural History, Prognostic Factors,
genital or acquired. Congenital etiologies include but are and Outcomes
not limited to genetic disorders and pre, peri, and postnatal
neurologic injuries and diseases. Acquired etiologies in- The natural history and prognosis for improvement of
clude but are not limited to stroke, brain tumor, traumatic cognitive-communication dysfunction are tied to many
brain injury, anoxic or toxic encephalopathy, and factors, including etiology, initial severity of disorder,
Cognitive-Communication Disorder C 635
the presence or absence of comorbid illnesses, and of the cerebrum may cause difficulty with pragmatics,
the nature of specific individual variables such as age, context-sensitive semantics, and expressive affective pros-
gender, and psychological state. In the absence of con- ody, obscuring indications of mood and compromising
founding circumstances, improvement of CCD is antici- the ability to communicate successfully in social situa-
pated when caused by stroke, excisable tumor, remitting tions. Egocentrism may impair recognition of these pro- C
disease, or traumatic brain injury. When caused by problems and reduce insight into the communication needs
gressive debilitating conditions such as non-excisable of others. Deficits in vigilance, sustained and selective
tumors or dementing diseases, CCD will worsen over attention, and/or in attention switching can cause salient
time. CCD of greater initial severity has a poorer prog- information to be missed, and reduce the sequential
nosis than CCD of mild or moderate initial severity, or simultaneous processing of information from multiple
although in the case of recovery from TBI, the degree sources. Difficulties drawing inferences, extracting themes
of functionality at hospital discharge may be more pre- and topics in discourse, interpreting nonliteral language,
dictive than the initial severity of injury (Testa, Malec, and/or reading affective and prosodic cues for mean-
Moessner, & Brown, 2005). The presence of co-occurring ing during conversational exchanges may be present
illnesses may compromise the speed and extent of recov- (Ylvisaker et al., 2008). A tangential communication
ery from CCD at any severity level; CCDs arising from style often emerges, where excessive, vaguely relevant
traumatic injuries causing diffuse brain damage, for ex- details are inserted inappropriately into narratives and
ample, are likely to be accompanied by paralysis, motor discourse (Myers & Blake, 2008).
speech disorders, and injuries to vital organs. Damage to the right parietal association cortex and to
Recovery from CCD differs by etiology. Re- the right parietal-temporal-occipital (PTO) cortex can
covery after stroke is usually most rapid in the first lead to contralateral inattention, impeding reading,
3 months post onset. Recovery from thrombo-embolic writing, and listening for stimuli in left hemispace.
stroke may continue after 6 months post onset, where- Lesions in PTO cortex can also cause visual-spatial per-
as recovery from hemorrhagic stroke may plateau at the ception and recognition deficits (including topographical
6-month point. Functional improvement in cognitive- and geographical agnosias), which can impair navigation
communication abilities after severe traumatic brain in- in familiar environments if verbal mediation strategies are
jury is generally slower at the outset when compared not used to compensate. Damage to secondary (superior
with stroke and typically proceeds in a stairstep fashion temporal) association cortex may reduce the efficiency of
over months or years. Recovery from mild stroke or auditory language processing if stimuli are complex or if
brain injury often seems rapid in comparison. Many they must be processed quickly. Damage may also impair
individuals with mild brain injuries appear to recover the interpretation of affective prosody when produced by
quickly (Ylvisaker et al., 2008), but as many as 1520% others. Lesions to prefrontal, parietal, and temporal cor-
suffer from persistent fatigue and reduced information tex have been associated with anosognosia, the failure to
processing speed for years after injury. Frequently unrec- recognize the existence or presence of illness and a prob-
ognized and untreated, these deficits cause lifelong cogni- lem that can reduce compliance with treatment activities
tive challenges that threaten social adjustment and (Myers, 2001; Myers & Blake, 2008; Tomkins, 1995).
successful community reentry. In contrast to stroke and When damage to the cerebral cortex is bilateral, def-
TBI, recovery from dementing illness is not expected. Early icits across multiple systems may interact to impair com-
stages of cognitive decline in DAT are accompanied by munication to different degrees. Bilateral cortical
forgetfulness, word-finding difficulties, and changes in so- damage, for example, can cause impairments in the self-
cial pragmatics; mid stages are characterized by increased regulation of communicative behaviors that range from
memory loss, anomia, and social withdrawal; and late failure to organize discourse efficiently to failure to in-
stages are associated with loss of most useable cognitive hibit inappropriate utterances and actions. It can also
and physical functions (Bayles & Tomoeda, 2007). diminish the ability to focus attention and memory so
as to make them useful during conversational exchanges
(Ylvisaker et al., 2008). However, if bilateral damage
Neuropsychology and Psychology of involves subcortical hippocampal structures, then funda-
Cognitive-Communication Disorder mental disruptions of declarative (semantic, episodic, and
lexical) and explicit memory may occur. Hippocampal
Damage to the prefrontal and frontal association regions damage/deterioration is common with brain injury/
of the right (or nonlanguage-dominant) hemisphere dementing disease, and it can lead to a host of
636 C Cognitive-Communication Disorder
impairments ranging from difficulty learning new infor- 5. The ability to discriminate relevant from irrelevant
mation to the presence of a severe, unremitting amnesia. detail and integrate disparate parts into a coherent
Bilateral damage to lower brain stem reticular activat- whole can be evaluated with scene description tasks.
ing circuits can severely compromise arousal, alertness, 6. Cognitive flexibility and functional problem-solving
and awareness. This can lead to brief losses of conscious- abilities can be assessed with tasks that require the
ness or to intractable coma. When caused by dementing generation of multiple strategies for achieving a goal
disease, coma is most likely followed by death. However, and that require repairs of failed communicative inter-
recovery from traumatic coma frequently leads to return changes with others (Myers, 1999).
of function through increasing levels of responsivity,
Standardized tests used to assess cognitive-communication
communication, orientation, self-regulation, and cogni-
functions subsequent to right hemisphere impairment in-
tive integration. A common sequela of traumatic brain
clude the Mini-Inventory of Right Brain Injury (Pimental &
injury is a period of post-traumatic amnesia (PTA), that
Kingsbury, 1989), The Rehabilitation Institute of Chicago
is, inability to form new memories of events happening
Clinical Management of Right Hemisphere Dysfunction
after brain injury with disorientation to time, place, or
(Halper, Cherney, & Burns, 1996), and The Burns Brief
person. In individuals who are verbal, confabulation may
Inventory of Communication and Cognition (Burns, 1997).
be present until disorientation and confusion diminish.
While these instruments will elicit symptoms of CCD
As cognitive functioning improves, individuals with brain
associated with right hemisphere damage, findings must
injuries will benefit from environmental structure and
be interpreted with a view toward evaluating impair-
external direction to support increasingly purposive, flex-
ments of underlying neuropsychological processes, for it
ible, and goal-oriented behavior.
is here that treatment will be most profitably directed
(Myers, 1999).
Standardized tests used to assess CCD after TBI in-
Evaluation
clude the American Speech-Language-Hearing Association
Functional Assessment of Communication Skills in Adults
Evaluation of a suspected CCD requires examination of
(Frattali, Thompson, Holland, Wohl, & Ferketic, 1995),
cognition as it affects and interacts with skills of speech
the Behavioral Rating Inventory of Executive Function
planning and execution, language comprehension and
(Roth, Isquith, & Gioia, 2005), the Brief Test of Head
production, and pragmatic/discourse aspects of commu-
Injury (Helm-Estabrooks & Hotz, 1991), the Ross Infor-
nication in everyday social contexts (Turkstra, Cohelo, &
mation Processing Assessment-2 (Ross-Swain, 1996), and
Ylvisaker, 2005).
the Scales of Cognitive Ability for Traumatic Brain Injury
Tests of cognitive-communication skills are used to
(Adamonovich & Henderson, 1992). The Glasgow Coma
evaluate the effects that deficits in attention, orientation,
Scale (Jennett & Teasdale, 1981) and the Rancho Los
perception, memory, organization, and executive func-
Amigos Levels of Cognitive Function Scale (Hagen,
tions can have on communication. Examples of tasks
Malkmus, Durham, & Bowman, 1979) or its revisions,
frequently included in formal and informal assessments
including a version adapted for children under 14 years of
are provided for illustration:
age (Blosser & DePompei, 2003), are frequently used to
1. Attention to left hemispace is frequently tested with assess consciousness and track recovery of cognitive func-
line-bisection, cancellation, and drawing tasks as well tions after coma.
as with more complex reading, writing, and listening Informal situational assessments of cognition and
tasks that require individuals to process communica- communication may yield valuable information that can-
tion stimuli from both right and left sides of body not be obtained from formal standardized tests (Blosser &
midline. DePompei, 2003; Turkstra et al., 2005). This naturalistic
2. Inferencing abilities are tested by asking patients to approach to assessment has been termed, functional,
interpret humor, to recognize indirect requests for collaborative, context-sensitive, hypothesis-testing assess-
actions, and to follow the themes of conversations. ment, and it should be conducted with the purpose of
3. Orientation is assessed by asking patients to respond identifying situational variables that can be manipulated
to questions about time, place, and person. to improve the successful participation of injured indivi-
4. Memory for facts, events, and procedures is evaluated duals as they operate within their everyday environments
with yes/no questions, narratives, and performance of (Ylvisaker et al., 2008). Best-practice assessment proce-
familiar routines. dures for individuals who have suffered brain injuries
Cognitive-Communication Disorder C 637
should, therefore, include (1) completion of formal test- functional merits (p. 209), improving fundamental cog-
ing in specific skill domains and (2) completion of obser- nitive processes will have the greatest automatic generali-
vational checklists (or quality of life inventories) where zation to the many untrained tasks where those processes
children (or adults) may be evaluated in natural environ- are needed.
ments (Blosser & DePompei, 2003; Turkstra et al., 2005). Generalization may be more difficult to achieve when C
This type of assessment might include administration of CCD is associated with diffuse brain injury versus focal
the Functional Assessment of Verbal Reasoning and Execu- stroke. Rehabilitation approaches that are more contextu-
tive Strategies test (MacDonald, 2005), a tool that was alized (implemented in natural settings) and more func-
developed for evaluation of cognitive-communication tion oriented (designed to support activities of daily
skills specifically related to reading, writing, and living) than traditional methods are ideal for promoting
reasoning (Turkstra et al., 2005), and the Quality of Com- rapid skill mastery and transfer. Ylvisaker et al. (2008)
munication Life Scale (Paul et al., 2005). suggest that treatment strategies designed to compensate
Assessment of CCD in dementia employs standar- for impaired executive functions and self-regulation abil-
dized screening tests, severity staging instruments, and ities will most often lead to successful rehabilitation after
comprehensive assessment batteries (Hopper & Bayles, brain injury. They advocate practicing essential cognitive-
2008). Screening tests include the Story Retelling Subtest communication tasks (such as conversing with family
of the Arizona Battery for Communication Disorders members or taking notes during lectures) within support-
of Dementia (Bayles & Tomoeda, 1993) and the FAS ive real-world environments, where stimuli likely to trig-
Verbal Fluency Test (Borkowski, Benton, & Spreen, ger errors have been removed and where the use of
1967). Tests for estimating the severity of cognitive de- external aids is encouraged.
cline include the Mini-Mental State Examination Intervention for CCD in DAT emphasizes manage-
(Folstein, Folstein, & McHugh (1975)) and the Global ment rather than rehabilitation. Goals are designed
Deterioration Scale (Reisberg, Ferris, deLeon, & to help individuals maintain functional competence for
Crook (1982)). Comprehensive assessment batteries as long as possible. Decontextualized errorless learning
include the Arizona Battery for Communication Disorders activities that drill attention and memory can bolster the
of Dementia (Bayles & Tomoeda, 1993) and the Function- encoding and retrieval of factual information in early
al Linguistic Communication Inventory (Bayles & stages of dementia. Intervention tasks that employ exter-
Tomoeda, 1994), the latter being most useful for indivi- nal memory aids that recruit long-term (remote) mem-
duals with severe dementia (Hopper & Bayles, 2008). ory (such as reminiscing about past events) and that
Assessment findings can help families work with SLPs to draw on procedural memory for familiar routines
understand and compensate for the symptoms of cogni- (such as describing how to get home) can help promote
tive decline. social communication and safety while capitalizing
on those aspects of cognition that are available in mid-
stage dementia. Tangible sensory stimuli (including dolls
and stuffed animals) can help support communication
Treatment and reduce agitation as dementia advances (Bourgeois,
1990, 1991, 1992; Hoerster, Hickey, & Bourgeois, 2001;
Treatment for CCD has traditionally been decontextua-
Hopper & Bayles, 2008).
lized (implemented in rehabilitation settings or at
bedside) and deficit oriented (designed to improve/
support impaired cognitive-communication processes).
Conventional pencil/paper or computer tasks are used to Cross References
stimulate underlying cognitive processes (e.g., attention,
memory) with the expectation that as they improve, so Attention
will the related functional skills (e.g., readiness to listen to Brain Injury
speakers taking turns, remembering a set of instructions Cognitive Functioning
given by ones boss). Myers (1999) advocates the use Cognitive Processing
of decontextualized treatments to facilitate cognitive- Cognitive Rehabilitation
communication skills in individuals who have acquired Dementia
CCD from right hemisphere stroke. She argues that al- Executive Functioning
though the value of any treatment approach rests on its Functional Neuroanatomy
638 C Cognitive-Communication Impairment
Memory Impairment Hoerster, L., Hickey, E. M., & Bourgeois, M. S. (2001). Effects of memory
aids on conversations between nursing home residents with demen-
Mild Brain Injury
tia and nursing assistants. Neuropsychological Rehabilitation, 11(3/4),
Mild Cognitive Impairment 399427.
Moderate Brain Injury Hopper, T., & Bayles, K. A. (2008). Management of neurogenic commu-
Pragmatic Communication nication disorders associated with dementia. In R. Chapey (Ed.),
Severe Brain Injury Language intervention strategies in aphasia and related neurogenic
communication disorders (5th ed., pp. 9881008). Philadelphia:
Lippincott Williams & Wilkins.
Jennett, B., & Teasdale, G. (1981). Management of severe head injuries.
Philadelphia: F. A. Davis.
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executive strategies. Guelph, Ontario: CCD Publishing.
Adamonovich, B., & Henderson, J. (1992). Scales of cognitive ability for Myers, P. S. (1999). Right hemisphere damage: Disorders of communication
traumatic brain injury. Chicago, IL: Riverside. and cognition. San Diego: Singular Publishing Group.
American Speech-Language-Hearing Association. (2005). Roles of speech- Myers, P. S. (2001). Toward a definition of RHD syndrome. Aphasiology,
language pathologists in the identification, diagnosis, and treatment of 15, 913918.
individuals with cognitive-communication disorders: Position state- Myers, P. S., & Blake, M. L. (2008). Communication disorders
ment [Position Statement]. www.asha.org/policy. associated with right-hemisphere damage. In R. Chapey (Ed.), Lan-
Bayles, K. A., & Tomoeda, C. (1993). The arizona battery for communica- guage intervention strategies in aphasia and related neurogenic com-
tion disorders of dementia. Austin, TX: Pro-Ed. munication disorders (5th ed., pp. 963987). Philadelphia: Lippincott
Bayles, K. A., & Tomoeda, C. (1994). The functional linguistic communi- Williams & Wilkins.
cation inventory. Austin, TX: Pro-Ed. Paul, D., Frattali, C. M., Holland, A. L., Thompson, C. K., Caperton, C. J.,
Bayles, K. A., & Tomoeda, C. (2007). Cognitive-communication disorders & Slater, S. (2005). Quality of communication life scale. Rockville,
of dementia. San Diego, CA: Plural Publishing. MD: American Speech-Language-Hearing Association.
Blosser, J. L., & DePompei, R. (2003). Pediatric traumatic brain injury: Pimental, P. A., & Kingsbury, N. A. (1989). Mini inventory of right brain
Proactive intervention (2nd ed.). Clifton Park, NY: Delmar Learning. injury. Austin, TX: Pro-Ed.
Borkowski, J. G., Benton, A. L., & Spreen, O. (1967). Word fluency and Reisberg, B., Ferris, S. H., deLeon, M. J., & Crook, T. (1982). The global
brain damage. Neuropsychologia, 5, 135140. deterioration scale (GDS): An instrument for the assessment of
Bourgeois, M. S. (1990). Enhancing conversation skills in patients primary degenerative dementia (PDD). American Journal of Psychi-
with Alzheimers disease using a prosthetic memory aid. Journal of atry, 139(1), 136139.
Applied Behavior Analysis, 23(1), 2942. Ross-Swain, D. (1996). Ross information processing assessment (RIPA-2).
Bourgeois, M. S. (1991). Communication treatment for adults with Austin, TX: Pro-Ed.
dementia. Journal of Speech and Hearing Research, 34(4), 831844. Roth, R. M., Isquith, P. K., & Gioia, G. A. (2005). Behavior rating
Bourgeois, M. S. (1992). Evaluating memory wallets in conversations inventory of executive function- Adult Version. Lutz, FL: Psychological
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Chicago, IL: Riverside. Cognitive-Communication Disorder
Cognitive-Log C 639
Reliable serial assessment is crucial to document the

Cognitive-Log rapid changes in behavior and cognition during recovery
from acquired brain disorders. Therefore, there is a need
T HOMAS A. N OVACK for a brief, bedside evaluation instrument to assess other
University of Alabama at Birmingham areas of cognition that are frequently affected by acquired
Birmingham, AL, USA
C
brain injuries. Existing scales are typically too lengthy or
involved to present as part of morning rounds. Other
scales fail to adequately capture the primary limitations
Synonyms resulting from acquired brain injury. The brief scales that
have been created for serial administration in an inpatient
C-Log; Cog-Log; Cognitive Log setting have been presented without adequate psychomet-
ric properties or scaling. The Cog-Log was created to serve
as a brief bedside measure to chart neurocognitive recov-
Description ery and assist in planning rehabilitation interventions with
a wide variety of patients.
The Cog-Log is a ten-item scale designed for serial bed-
side measurement of cognitive functions in individuals
completing inpatient rehabilitation. The scale includes Psychometric Data
items assessing orientation, immediate and delayed verbal
recall, concentration, executive function, response inhibi- The reliability and validity of the Cog-Log have been
tion, and praxis. All responses are scored according to the assessed in several ways. A sample of 150 individuals with
following criteria: 3 points = spontaneously correct re- acquired brain injury was examined with the Cog-Log.
sponse, no errors; 2 points = correct on logical cueing Most of the sample (80%) had sustained moderate to severe
(e.g., That was yesterday, so today is?) or in the presence TBI, with the remainder including patients with CVA and
of 1 error; 1 point = correct on multiple-choice cueing or anoxia. Internal consistency analysis (Cronbachs alpha) was
in the presence of 2 errors; 0 points = incorrect despite conducted for the total Cog-Log score. Inter-rater reliability
cueing, more than 2 errors, unable to complete. Points for estimates (Spearmans rho) were calculated using a subset of
time estimation are calculated as follows: 3 points = 19 patients (75 total observations). High internal consisten-
correct within 5 s; 2 points = correct within 10 s; cy (Cronbachs alpha = 0.778) was demonstrated with a
1 point = correct within 15 s. Incorrect/absent standard error of measurement of 0.53. Inter-rater reliabili-
responses are followed by cueing at the next level for the ty coefficients for each of the ten Cog-Log items ranged
orientation and delayed memory items. Multiple-choice from 0.749 (Go/No-go task) to 1.0 (Time Estimation).
cueing, used only with the orientation items, involves Standard errors of measurement were no more than 0.10
provision of three choices, varying the location of the for single item scores, which range from 0 to 3.
correct response. Item scores are summed to provide a Factor analysis of the Cog-Log using principal com-
total score ranging from 0 to 30. Daily scores can be ponents extraction (N = 150) revealed a unitary factor
plotted to permit quick visual analysis of recovery trends. (Eigenvalue = 3.48), with all items loading on that factor.
The following specific items are included in the Cog- The highest loadings were for delayed recall of verbal
Log: three items assessing the orientation to the date, time, information and recitation of months backwards, suggest-
and hospital name; two items assessing immediate and ing a stronger contribution of complex working memory
delayed recall for a short address; counting backwards and verbal recall to this unitary factor.
from 20; reciting the months in reverse order; and estimat- The Cog-Log exhibited a significant correlation with
ing when 30 s has passed. Two motor tasks involving hand neuropsychological assessment completed on the same day,
gestures a movement sequence (fist-edge-palm) and a including tests such as immediate and delayed recall of the
response inhibition task (go/no-go) are also included. Wechsler Memory Scale-III Logical Memory subtest, Rey
Auditory Verbal Learning Test, Digit Span subtest of the
Wechsler Adult Intelligence Test-III, and the Trail Making
Historical Background Test. The lowest Cog-Log score obtained during acute
rehabilitation also significantly predicted 1-year outcome
Measurement of orientation and higher neurocognitive pro- in three of six neuropsychological domains (attention,
cesses are important aspects of early neurorehabilitation. executive functioning, and visuospatial abilities) after
640 C Collaborative Care
controlling for demographics and injury severity. The Cog- Lee, D., LoGalbo, A. P., Banos, J. H., & Novack, T. A. (2004). Prediction of
cognitive abilities one year following TBI based on cognitive screen-
Log was also significantly correlated with the results of the
ing during rehabilitation. Rehabilitation Psychology, 49, 167171.
Mini Mental State Examination, a well-known cognitive Penna, S., & Novack, T. (2007). Further validation of the orientation and
screening test (r = 0.75, P < 0.001). Cognitive Log relative to the mini mental status exam. Archives of
Physical Medicine and Rehabilitation, 88, 13601361.
Clinical Uses
Individuals without known neurological insult received Collaborative Care
average total Cog-Log scores of 28 ( 2), and mean
individual item scores were greater than or equal to Family-Centered Care
2.4. Age, education, and gender did not predict total or
individual item scores (p > 0.05). Stepwise discriminant
analyses on a sample of 82 persons with brain injury and
82 normal controls matched for age, education, and gen-
der revealed that a cut-off score of 25 correctly classified Collagen Vascular Disease
88.4% of individuals in their respective groups.
The Cog-Log is a companion instrument to the Ori- E LLIOT J. R OTH
entation Log (O-Log). Generally, the Cog-Log is not Northwestern University
administered until a score of at least 15 is achieved on Chicago, IL, USA
the O-Log, indicating that the person is responding and
able to respond correctly to some orientation questions.
Administering the Cog-Log prior to this point has not Synonyms
proven fruitful. The Cog-Log can be administered every
day, but typically three times a week is sufficient to moni- Connective tissue disease
tor progress or detect deterioration.
Efficiency and ease of assessment were considered
when choosing items; tasks requiring additional stimuli Definition
(e.g., block construction) or extended administration
times were not included. The Cog-Log was designed for Collagen vascular diseases are a group of conditions that are
flexible administration to patients with severe cognitive characterized by malfunction of the tendons, bones, and
and behavioral disturbances. Administration time ranges connective tissue, that are supported by collagen. Their
from 7 to 10 min for confused patients, but can be as short pathogenesis is autoimmune in nature.
as 5 min for those who perform well.
Current Knowledge
Cross References The most common collagen vascular disorders include
rheumatoid arthritis, systemic lupus erythematosus,
scleroderma, and dermatomyositis. Others include poly-
Galveston Orientation and Amnesia Test
myositis, polyarteritis nodosa, ankylosing spondylitis, and
Mini Mental State Examination
a number of vasculopathies. These diseases are frequently
associated with diffuse inflammatory changes, abnormal
immunity. Vascular abnormalities that result from these
conditions serve as frequent causes of various types of
References and Readings vasculitis. Common features include arthritis, skin
changes, eye changes, pericarditis, pleuritis, myocarditis,
Alderson, A. L., & Novack, T. A. (2003). Reliable serial measurement of nephritis, and vasculitis of the brain, peripheral nerves, or
cognitive processes in rehabilitation: The Cognitive-Log. Archives of
extremities. They also may have a variety of hematological
Physical Medicine and Rehabilitation, 84, 668672.
Center on Outcome Measurement in Brain Injury (COMBI). www.tbims. changes causing clotting or bleeding, and a number of
org/combi. Accessed May 26, 2009. abnormal circulating blood proteins.
Color Agnosia C 641
The cause of most of these diseases is unknown. color perception (i.e., retaining the ability to match
Hereditary factors and deficiencies, autoimmunity, envi- colors or to identify the numbers on the Ishihara plates).
ronmental antigens, infections, allergies, and antigen- They also have difficulty matching colors, either verbally
antibody complexes in various combinations are probably or visually, to familiar colored objects (e.g., identifying
involved. the color normally associated with cherries, lettuce, C
or bananas).
Relatively rare, pure color agnosia must be distin-
Cross References guished from other disturbances of color perception
and color naming (color anomia). In color blindness,
Cerebral Angiitis the individual is unable to perceive or distinguish either
Lupus Cerebritis certain colors or possibly all color. In the latter case,
Vasculitis the world is seen in shades of black and white. While
color blindness is usually congenital, it can also be ac-
quired, a condition known as central achromatopsia.
References and Readings The latter is a perceptual deficit thought to result
from lesions in the visual cortices (e.g., lingual gyrus
Klippel, J. H., Stone, J. H., Crofford, L. J., & White, P. H. (Eds.). (2008).
and the occipitotemporal (fusiform) gyrus). In this dis-
Primer on the rheumatic diseases (13th ed.). New York: Springer. order, the patient may have difficulty verbally naming a
visually presented color, pointing to a color named by
the examiner, or simply matching or sorting colored
objects to others of a similar hue, yet still be able
to indicate (name) the colors normally associated with
Collapsed Lung common objects (e.g., the colors of the outside, inside,
and seeds of a watermelon). In a milder form of this
Pneumothorax condition (dyschromatopsia), colors are described as
dull, washed out, or faded. In color anomia, the
problem is not one of perceptions, but of language.
The patient can perceive and match colors, but has diffi-
Colliculi culty naming specific colors or pointing to colors named
by the examiner.
Inferior Colliculi In the few published cases, lesions associated with
color agnosia tend to occur in the left or bilateral occipi-
totemporal area.
Color Agnosia
J OHN E. M ENDOZA Cross References
New Orleans, LA, USA Achromatopsia
Color Anomia
Definition
Literally, a loss of previous color knowledge. References and Readings
Bauer, R. M., & Demery, J. A. (2003). Agnosia. In K. Heilman & E.
Current Knowledge Valenstein (Eds.), Clinical neuropsychology (4th ed., pp. 236295).
Tranel, D. (2003). Disorders of color processing. In T. E. Feinberg & M. J.
In pure color agnosia, patients have difficulty naming Farah (Eds.), Behavioral neurology and neuropsychology (pp. 243
or pointing to named colors, despite relatively preserved 256). New York: McGraw-Hill.
642 C Color Anomia

Color Anomia
Bauer, R. M., & Demery, J. A. (2003). Agnosia. In K. Heilman, &
J OHN E. M ENDOZA E. Valenstein (Eds.), Clinical neuropsychology (4th ed.) (pp. 236
Tulane University Medical Center 295). New York: Oxford University Press.
New Orleans, LA, USA Tranel, D. (2003). Disorders of color processing. In T. E. Feinberg, & M. J.
Farah (Eds.), Behavioral neurology & neuropsychology (pp. 243256).
Definition
Anomia is the inability to name colors in the absence

of a more global anomia associated with an aphasic Color Blindness
disorder.
Achromatopsia
Current Knowledge
To be classified as a color anomia, the disorder should

Color Imagery
occur in the absence of problems with color perception
J OHN E. M ENDOZA
or recognition (i.e., the patient should be able to match
or sort colors). Two subtypes of the disorder have been
identified. In one, the problem is limited to an inability
to name colors that are visually presented or to point to
colors named by the examiner. This type of color
anomia is usually associated with the syndrome of alex-
Definition
ia without agraphia and results from lesions involving
The ability to visualize a color in its absence. When
the primary visual cortex of the dominant hemisphere
asked, most individuals would be able to identify
(resulting in a right homonymous hemianopsia) and
the outer color of a watermelon as well as that of the
the splenium of the corpus callosum. Visual informa-
inside of the rind, the fleshy part of the melon, and its
tion is thus restricted to the left visual field (right
seeds. Color imagery is more than an ability to simply
hemisphere) and the color information cannot cross
recall a particular visual image; it also involves the
the involved splenium of the corpus callosum to reach
capacity to mentally conjure up and manipulate colors
the left (verbal) hemisphere. In the second subtype,
at will. For example, one may imagine a blue horse or a
specific color anomia, the patient has difficulty with purely
person wearing an article of clothing of a specific color,
verbal color naming tasks, in addition to difficulty in
never having seen either before. While disturbances of
naming visually presented colors. Thus, there would be a
color perception and color imagery are frequently
naming deficiency if the patient were asked to name the
linked, in some cases the two can be distinguished clini-
colors associated with the inside and outside of a water-
cally. Thus, while a given patient may be able to name
melon. As in the first case, color matching or sorting
or match colors presented visually, that same patient
should be intact. In specific color anomia, other aphasic
may not be able to name the color of an apple in its
(naming) deficits may be present, but color names are
absence. Similarly, while accurately identifying the color
most affected.
red from an array, the patient may not be able to match
it to a black-and-white picture of the fruit, although
the latter may be identified by its shape. While the
Cross References exact anatomical site responsible for disturbances of
color imagery has not been firmly established, the left
Alexia Without Agraphia temporal-occipital cortex is believed to be involved in
Color Agnosia most cases.
Colored Progressive Matrices C 643
Cross References D, and E of the standard progressive matrices (SPM) so

that intellectual capacity can be more accurately
Apperceptive Visual Agnosia assessed (the score for set Ab would be omitted to
Associative Visual Agnosia determine a percentile based on SPM scoring).
Color Agnosia C
Color Anomia
For information about the historical background of the

References and Readings original test, please refer to Raven Progressive Matrices.
Farah, M. J. (2003). Disorders of visual-spatial perception and cognition.

In K. M. Heilman & E. Valenstein (Eds.), Clinical neuropsychology Psychometric Data
(4th ed., pp. 146160). New York: Oxford University Press.
Tranel, D. (2003). Disorders of color processing. In T. E. Feinberg & M. J. Norms for ages 5.511.5 for North America are presented
Farah (Eds.), Behavioral neurology and neuropsychology (2nd ed.,
by Raven, Raven and Court (1998, 2000). By age 9 years, a
pp. 243256). New York: McGraw-Hill.
nearly perfect score is obtained (35/36) by the upper 5%
of the sample. Education corrected norms are available
for an abbreviated version (sets A and B, excluding Ab
which is correlated >0.90 with the sum of A and B) for
ages 5585. In children, split-half reliability has been
Colored Progressive Matrices shown to be high (>0.80) (Raven et al. 1998), as is
test-retest reliability following days or weeks (>0.80).
V ICTORIA M. L EAVITT Over longer intervals (6 months to 1 year) these values
Kessler Foundation Research Center decline (0.590.79).
West Orange, NJ, USA
Clinical Uses
Description
The CPM was designed for use with children, older
The colored progressive matrices (CPM) are an alter- people, for anthropological studies, and for clinical
nate form of the Ravens progressive matrices (RPM) work. Its format makes it valuable for individuals who
that was published in the 1940s. Shorter and simpler cannot understand English; people with physical disabil-
than the original, this version was designed for younger ities, aphasias, cerebral palsy, or deafness; and people with
children (ages 511 years), the elderly (over 65 years), below normal intelligence. The colored backgrounds were
and people with moderate or severe learning difficul- introduced to attract the patients attention; the test
ties. As such, it also tends to be used more frequently in can be administered in the form of illustrations in a
research protocols, although it is important to note booklet or as boards with moveable pieces. Patients with
that the CPM and the RPM are not interchangeable, left hemisphere damage perform better on the colored
nor may derived scores from the two tests be inter- matrices than on the standard form (as described in
preted the same. CPM contains 36 items, grouped into Lezak, Howieson, & Loring, 2004). This is likely attribut-
three sets (A, Ab, B) of 12 items each: A and B from the able to the fact that while only one-fifth of RPM items test
original version, with the addition of set Ab. Most visuospatial skills almost exclusively, fully one-third of
items are presented on a colored background to make items on the CPM are predominantly visuospatial, with
the test visually stimulating for participants; the bright other items involving more problem-solving. Also likely
background does not seem to detract from the clarity due to the visuospatial task demands, individuals with
of the stimuli. As the last few items in set B are exactly Lewy body dementia tend to have more difficulty on the
the same as they appear in the standard version, an CPM than Alzheimers patients with similar levels of
examinee who succeeds on these may go on to Sets C, dementia.
644 C Coma
Cross References rating, and include the Glasgow Coma Scale (Teasdale &
Jennett, 1976) and the FOUR Score (Wijdicks, Bamlet,
Advanced Progressive Matrices Maramattom, Manno, & McClelland, 2005).
Ravens Progressive Matrices
Standard Progressive Matrices
Prognosis
References and Readings Mortality rates for patients in coma vary with etiology,
but commonly reach or exceed 50%. Early prognostic
Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuropsycho- variables of poorer outcome include lower Glasgow
logical assessment (4th ed.). New York: Oxford University Press. Coma Scale scores (Teasdale & Jennett, 1976), increased
Raven, J. C. (1938, 1996). Progressive Matrices: A perceptual test of
intelligence. Oxford: Oxford Psychologists Press Ltd.
age, absent pupillary responses, systolic blood pres-
Raven, J., Raven, J. C., & Court, J. H. (1998). Raven manual: Section 2. sure <90 mm Hg, and computed tomography abnormal-
Colored progressive matrices. Oxford: Oxford Psychologists Press Ltd. ities, including compression, effacement, or blood within
Raven, J., Raven, J. C., & Court, J. H. (2000). Raven manual research the basal cisterns, or extensive traumatic subarachnoid
supplement 3: American norms, neuropsychological applications. hemorrhage (Posner et al., 2007).
Oxford: Oxford Psychologists Press Ltd.
Raven, J., Raven, J. C., & Court, J. H. (2003). Manual for Ravens
progressive matrices and vocabulary scales. Section 1: General
overview. San Antonio, TX: Harcourt Assessment. Cross References
Strauss, E., Sherman, E. M. S., & Spreen, O. (Eds.). (2006). A compendium
of neuropsychological tests (3rd ed.). New York: Oxford University Decerebrate Posturing
Press.
Decorticate Posturing
Glasgow Coma Scale
Loss of Consciousness
Minimally Conscious State
Coma Stupor
Vegetative State
J ACOB K EAN
Indiana University School of Medicine
Indianapolis, Indiana, USA References and Readings
Posner, J. B., Saper, C. B., Schiff, N. D., & Plum, F. (2007). Plum and
Definition Posners diagnosis of stupor and coma. New York: Oxford University
Press.
Coma is a state of unconsciousness in which the patient is Teasdale, G., & Jennett, B. (1976). Assessment and prognosis of coma
incapable of being awake, and is unarousable, even with after head injury. Acta Neurochirurgica, 34, 4555.
Wijdicks, E. F. M., Bamlet, W. R., Maramattom, B. V., Manno, E. M., &
vigorous stimulation. Coma is usually the result of dis- McClelland, R. L. (2005). Validation of a new coma scale: The FOUR
ease or injury, and rarely lasts for more than 4 weeks. score. Annals of Neurology, 58, 585593.
While comatose, a patient may respond to painful stimuli
but lack the ability to demonstrate localized response or
defensive movements (Posner, Saper, Schiff, & Plum,
2007).
Coma Recovery Scale
Current Knowledge M ARK A. S ANDBERG
Diagnosis Smithtown, NY, USA
The diagnosis of patients in coma necessarily involves

examination of physiological functions, including arous- Synonyms
al, pupillary responses, respiration, motor function, and
reflexes. Several diagnostic scales are available for severity CRS; CRS-R; JFK coma recovery scale
Coma/Near Coma Scale C 645
Definition Kalmar, K., & Giacino, J. (2005). The JFK coma recovery scale-revised.
Neuropsychological Rehabilitation, 15(34), 454460.
The CRS-R, including administration and scoring information and rating
The Coma Recovery Scale (CRS-R) is a 23-item instru- forms, is available as a PDF file at www.tbims.org/combi/crs/index.
ment used to assist with differential diagnosis, prognostic html.
assessment, and treatment planning with patients having C
disorders of consciousness.
Current Knowledge
Coma Vigile
The Coma Recovery Scale was initially developed by
Vegetative State (Persistent)
Giacino and colleagues in 1991 and thereafter was revised
in 2004 as the JFK Coma Recovery Scale-Revised (Giacino,
Kalmar, & Whyte, 2004). The scale was developed with the
goal of helping to identify the neurobehavioral character-
istics of persons diagnosed with disorders of conscious- Coma/Near Coma Scale
ness, thus allowing for increased prognostic clarity and
refinement of treatment methods. In its revised form, M ARK A. S ANDBERG
the CRS-R is composed of 23 items, which coalesce into Independent Practice
six subscales addressing auditory, visual, motor, oromo- Smithtown, NY, USA
tor, communication, and arousal functions. Each subscale
is composed of hierarchically arranged items associated
with the brain stem, subcortical, and cortical processes. Synonyms
Items receiving higher scores are more likely to reflect
cognitively mediated activity. The test syllabus offers be- C/NC; CNC
havioral criteria, which provide the user with operationa-
lized characteristics used to determine whether a specific
response to sensory stimuli has been demonstrated by the
Description
patient. A rating form is included as part of the syllabus,
which allows the user to perform serial assessments.
The Coma/Near Coma (CNC) Scale was designed to
Based on the 2004 study by Giacino, Kalmar and Whyte,
measure small changes in neurobehavioral status among
interrater and testretest reliability were described as high
patients who have sustained severe brain injuries and
for CRS-R total scores, although some systematic scoring
whose clinical functioning is consistent with vegetative
differences between raters were found on the visual and
or near-vegetative states. The CNC Scale is useful when
oromotor/verbal subscales. The CRS-R has been translated
reliable, valid, and economical assessment of patients func-
into Spanish, Italian, German, French, Dutch, and Norwe-
tioning is required so as to substantiate clinical change or
gian. The CRS-R offers a reliable method for measuring the
lack thereof in patients whose functioning is at markedly
trajectory of consciousness following severe brain injury,
low levels. The CNC Scale expands the levels of the
and in assisting in the differential diagnosis of patients in a
Disability Rating Scale (DRS). It has five levels and is
minimally conscious state from those in a vegetative state.
composed of 11 items. The items assess dysfunction in
the sensory and perceptual dimensions and describe the
severity of primitive response deficits.
Cross References
Coma/Near Coma Scale

Recognizing a need for rehabilitation professionals to

systematically identify and chart changes in functioning
in patients whose clinical status is best characterized as
Giacino, J. T., Kalmar, K., & Whyte, J. (2004). The JFK coma recovery
scale- revised: measurement characteristics and diagnostic utility. approximately vegetative, the CNC Scale was developed
Archives of Physical Medicine and Rehabilitation, 85(12), 20202029. as a supplement to the Dementia Rating Scale (DRS). Use
646 C Coma/Near Coma Scale
Coma/Near Coma Scale. Table 1 Coma/near coma scale overview
Item # Dimension assessed Stimulus used Response elicited

1 Auditory Ringing bell Eye opening/orientation
2 Command Responsivity Verbal request Response to command
3 Visual Flashing light Fixation or avoidance
4 Visual Say Look at me Fixation & Tracking
5 Threat Quick movement of hand to eyes Eye blinking
6 Olfactory Ammonia capsule Withdrawal or grimacing
7 Tactile Shoulder tap Head/eye orientation or shoulder movement
8 Tactile Swab to each nostril Withdrawal/eye blink or mouth twitch
9 Pain Firm pinch to finger tip Withdrawal or agitation
10 Pain Firm ear pinch Withdrawal or agitation
11 Vocalization None; listen for any verbalization Words or sounds
of the CNC Scale is recommended whenever the DRS accuracy. Following this training, it is noted that while
score is greater than 21 (Extremely Severe Disability). single ratings can be used, a minimum of two indepen-
The scoring form also notes that in cases in which DRS dent ratings per patient is encouraged for purposes of
scores are < 21, CRC Scale ratings should be conducted promoting reliability (Rappaport, 2000). It is also recom-
monthly in conjunction with the DRS. mended that rating be taken at approximately the same
time each day whenever possible.
The CNC Scale includes 11 items representing 8 res-
Current Knowledge ponse dimensions (see Table 1). Each item includes
3 score options (0, 2, 4); 4 referring to no responsivity
As described by Rappaport, Dougherty, and Kelting (1992) to sensory stimulation. The CNC Total Score is com-
and as detailed by the Center for Outcome Measurement puted by adding the ratings (0, 2, 4) from each of the
in Traumatic Brain Injury (COMBI; www.tbims.org/ 11 items and dividing that score by the number of items
combi/cnc/index.html), interrater reliability calculated at rated. Categorical descriptions are offered to coincide
three time periods was 0.97. The lowest interrater inter- with the Total Score attained (i.e., No Coma through
correlation of 0.86 was found to exist on item 8 (nasal Extreme Coma).
swab). The internal consistency as determined using
alpha coefficients were 0.43, 0.65, and 0.65 for CNC Scale
scores taken at 1, 8, and 16 weeks post injury, respectively Cross References
(Rappaport, Dougherty, & Kelting, 1992).
A rank order correlation between CNC Scale and DRS Coma Recovery Scale
scores was 0.69 (p < 0.02). The correlation between CNC Dementia Rating Scale
Scale ratings and the prominence of sensory (auditory,
visual, and somatosensory) abnormality as determined
through evoked potential studies was 0.52 (p < 0.05) References and Readings
(Rappaport, Dougherty, & Kelting, 1992).
Discussion regarding training in the use of the CNC Rappaport, M. (2000). The coma/near coma scale. The center for outcome
Scale is offered by COMBI (www.tbims.org/combi/cnc/ measurement in brain injury. Accessed 1/6/08 from www.tbims.org/
cnctat.html). It is recommended that proper use of combi/cnc.
the instrument follows a period during which evaluations Rappaport, M. (2005). The disability rating scale and coma/near coma
scales in evaluating severe head injury. Neuropsychological Rehabili-
are performed simultaneously with several raters indepen-
tation, 15(3/4), 442453.
dently offering judgments for each item. Interrater com- Rappaport, M., Dougherty, A., & Kelting, D. L. (1992). Evaluation of
parisons and discussion concerning the reasons for making coma and vegetative states. Archives of Physical Medicine and Reha-
specific judgments are encouraged to refine observational bilitation, 73, 628634.
Commission on Accreditation of Rehabilitation Facilities (CARF) C 647
CARF is governed by its President/CEO and a

Commission on Accreditation 12-member Board of Directors. The Board of Directors
of Rehabilitation Facilities consists of individuals with expertise, experience, and per-
spective on CARF-related issues. Current CARF leadership
(CARF) includes individuals with a diverse range of expertise, in- C
cluding individuals with psychology, physical therapy, and
S ARAH K. L AGEMAN
speech-language pathology expertise, social work back-
Emory University
grounds, as well as past surveyors and individuals with
Atlanta, GA, USA
business and legal training. Other perspectives on issues
CARF International offices
related to CARF-accreditation and other matters are gained
Tucson, AZ
through individuals and organizations that are members of
CARF Canada
CARFs International Advisory Council (IAC).
Edmonton, AB, Canada
The International Advisory Council (IAC) creates a
CARFCCAC
partnership for CARF and IAC members to promote
Washington, DC
quality in human services and enhance the lives of per-
sons served. It also provides a forum for guidance and
input into standards development and the accreditation
Membership
process and insight on issues affecting the fields in which
CARF provides accreditation services. IAC members
Commission on Accreditation of Rehabilitation Facilities
support CARFs mission, purposes, values, and vision.
(CARF) is an independent, nonprofit organization that is
The IAC is composed of organizational and individual
an accreditor of human service providers. It was formed
members who represent a broad spectrum of stake-
in 1966 when the Association of Rehabilitation Centers
holders, including persons served, providers, profes-
(ARC) and the National Association of Sheltered Work-
sionals in the field, and purchasers. Current members
shops and Homebound Programs (NASWHP) joined
of the IAC include American Academy of Neurology,
forces to further develop their interests in setting stan-
American Academy of Orthopedic Surgeons, American
dards. Since its inception, CARF has grown significantly
Academy of Pain Medicine, American Academy of Phys-
in size and informally adopted CARF International as its
ical Medicine and Rehabilitation, American Occupa-
registered name after accrediting programs in Canada,
tional Therapy Association, Inc., American Physical
Europe, and South America.
Therapy Association, American Psychological Associa-
CARF International currently provides accreditation
tion, American Speech-Language-Hearing Association,
services in the following areas, called customer service
American Therapeutic Recreation Association, and the
units: aging services; child and youth services; behavioral
U.S. Psychiatric Rehabilitation Association, in addition
health; durable medical equipment, prosthetics, ortho-
to many other established agencies and associations
tics, and supplies (DMEPOS); employment and com-
documented on the CARF web site, http://www.carf.
munity services; medical rehabilitation; and opioid
org/About/IAC/.
treatment programs. The CARF family of organizations
currently accredits more than 6,000 providers at more
than 20,000 locations on five continents. More than Major Areas or Mission Statement
8.3 million persons of all ages are served annually by
CARF-accredited providers. In 2002, CARF Canada was The mission of CARF is to promote the quality, value,
developed as a private, nonprofit organization serving and optimal outcomes of services through a consultative
Canadian providers. CARF acquired the Continuing accreditation process that centers on enhancing the lives of
Care Accreditation Commission (CCAC) in 2003. The the persons served (retrieved June 29, 2010, from http://
CCAC provides accreditation of continuing care retire- www.carf.org/About/Mission/). CARF has identified three
ment communities and aging services networks. Finan- core values as central to its mission, and these values are
cial support for CARF includes fees from accreditation prioritized in all CARF accreditation, research, and edu-
surveys, sales of publications, grants from public and cational activities. The following are the three CARF core
private entities, fees from seminars and conferences, values: (1) all people have the right to be treated with
and contributions from International Advisory Council dignity and respect, (2) all people should have access
(IAC) members. to needed services that achieve optimum outcomes, and
648 C Commission on Accreditation of Rehabilitation Facilities (CARF)
(3) all people should be empowered to exercise informed accreditation for rehabilitation organizations providing
choice. services to workers with occupational disabilities.
In support of its mission, CARF has identified numer- CARF has also expanded the types of services for
ous purposes that are the focus of the agency, including which it provides accreditation. In September 1997,
the following (retrieved June 29, 2010, from http://www. CARF was awarded a contract by the Department of
carf.org/About/Mission/). Health and Human Services, Substance Abuse and Mental
Health Services Administration for the development and
To develop and maintain current, field-driven stan-
implementation of opioid treatment program accredi-
dards that improve the value and responsiveness of
tation. After successful development of the program
the programs and services delivered to people in need
accreditation, CARF was recognized in November 2001
of rehabilitation and other life enhancement services.
by the Substance Abuse and Mental Health Services
To recognize organizations that achieve accreditation
Administration (SAMHSA)/Center for Substance Abuse
through a consultative peer-review process and dem-
Treatment (CSAT) as an approved accrediting organiza-
onstrate their commitment to the continuous improve-
tion for opioid treatment programs. As noted previously,
ment of their programs and services with a focus on the
CARF acquired the Continuing Care Accreditation
needs and outcomes of the persons served.
Commission (CCAC) in 2003. Acquisition of the CCAC
To conduct accreditation research emphasizing out-
promoted CARFs vision of being an independent re-
comes measurement and management, and to provide
source that identifies high-quality care providers for indi-
information on common program strengths as well as
viduals of all ages, including children and older adults.
areas needing improvement.
More recently, in February 2007, CARF began accrediting
To provide consultation, education, training, and
suppliers of certain durable medical equipment, prosthet-
publications that support organizations in achieving
ics, orthotics, and supplies (DMEPOS) after the Centers
and maintaining accreditation of their programs and
for Medicare & Medicaid Services (CMS) approved CARF
services.
as a national authority for DMEPOS suppliers.
To provide information and education to persons
Over the decades, CARF has steadily grown and
served and other stakeholders on the value of
expanded its accreditation services to serve individuals in
accreditation.
other countries. In 1969, CARF accredited its first program
To seek input and to be responsive to persons served
in Canada and the first program in Europe was accredited
and other stakeholders.
in August 1996. CARF Canada was incorporated in Sep-
CARF also collaborates with partners who share CARF tember 2002 in Edmonton, Alberta. Further expansion of
vision and goals, while remaining politically neutral. CARF services included accreditation of the first program in
partners include professional associations, advocacy groups, South America in December 2005. The value of CARF
governmental agencies, or individuals who are committed accreditation is extensive and includes benefits such as
to enhancing the lives of persons who receive services. business improvement, risk management, funding access,
positive visibility, accountability, peer network, in addi-
tion to other benefits detailed on the CARF web site.
One of the key developments in the history of CARF was Major Activities
the passing of a resolution by the Council of State Admin-
istrators of Vocational Rehabilitation in April 1970, which CARF accreditation outcomes for CARF and CARF
urged state agencies to support a CARF accreditation Canada consist of a three-year accreditation, a one-year
requirement for all organizations providing rehabilitation accreditation, provisional accreditation, nonaccreditation,
services. As CARFs services became increasingly recog- and preliminary accreditation. CARF-CCAC accreditation
nized by organizations and agencies, additional support of outcomes include a five-year accreditation and nonaccre-
CARF accreditation services has occurred. In November ditation. CARF currently has close to 1,500 surveyors
1974, Goodwill Industries of America recognized CARF throughout the North and South America and Europe.
as the accrediting organization for all Goodwill organiza- The steps to accreditation involve a year or more of
tions. Another resolution, adopted in November 1980 by preparation prior to the site survey and ongoing quality
the Association of Trial Lawyers of America, urged state improvement following the survey. CARF designates a
workers compensation agencies to require CARF CARF Resource Specialist to organizations seeking
Commission on Accreditation of Rehabilitation Facilities (CARF) C 649
accreditation to provide guidance and technical assistance its accreditation areas (Behavioral Health, Employment
regarding the accreditation process. Other resources are and Community Support, and Medical Rehabilitation).
also available to facilitate the preparation process, includ- Then in 1996, CARF published the first edition of the
ing standards manuals for the various programs and Accreditation Sourcebook. A significant contribution to
services an organization can seek accreditation for and accreditation services occurred in 1998, when CARF C
the CARF Accreditation Sourcebook, which explains the rewrote its standards to be unidimensional as part of its
accreditation process. CARF accreditation requires that an commitment to implementing the Standards Confor-
organization must implement and use the standards in its mance Rating System. Additional standards were pub-
programs for at least 6 months prior to the survey. During lished in 1999, including standard manuals for Adult
this time, an organization conducts a self-study and eval- Day Services Programs and the Veterans Health Adminis-
uation of conformance to the standards using the stan- tration Comprehensive Blind Rehabilitation Services.
dards manual in conjunction with the survey preparation Moreover, that same year, CARF extended its practice of
questions. Then the organization submits the Intent to disclosing information to the public regarding an organi-
Survey, which includes detailed information about lead- zations survey report from just the Medical Rehabilitation
ership, programs, and services that the organization is Standards Manual to also include the Behavioral Health
seeking to accredit and the service delivery location(s). Standards Manual and the Adult Day Services Standards
CARF selects a survey team by matching program or Manual. CARFs public information policy was extended
administrative expertise and relevant field experience to include all areas later in 2003. Standards manuals for
with the organizations unique requirements. During the assisted living programs were published in 2000, followed
survey, the survey team determines the organizations by the Child and Youth Services Standards Manual in 2005,
conformance to all applicable standards on site through the Aging Services Standards Manual in 2006, and Stan-
the observation of services, interviews with persons served dards for Dementia Care in 2006. In addition to these
and other stakeholders, and review of documentation. publications, CARF has continued to implement new
The survey team shares findings related to the standards standards in many of its areas of accreditation.
with the organization at an exit conference before the CARF has implemented new electronic programs
team leaves the site and this information is also submitted designed to support and further develop its mission. In
to CARF. CARF then renders the accreditation decision 2007, CARF released the uSPEQ (pronounced you speak;
and a written survey report approximately 68 weeks after http://www.uspeq.org/) Consumer Experience Survey, fol-
the survey. Organizations have 90 days after notification lowed by the uSPEQ Employee Climate Survey. Both survey
of an accreditation award to fulfill an accreditation condi- tools are designed to assist organizations with their well-
tion by submitting to CARF a Quality Improvement Plan being and performance improvement. CARF launched its
(QIP) outlining actions that have been or will be imple- extranet Customer Connect (http://customerconnect.carf.
mented in response to the recommendations made in the org) for accredited organizations and those seeking accred-
survey report. CARF maintains communication with itation to manage their individual contact information,
organizations throughout the tenure of accreditation. view up-to-date information about their organizations
CARF has published numerous standard manuals surveys, and access information about the accreditation
which have identified program evaluation standards, result- process. Most recently in 2008, CARFs ASPIRE to Excel-
ing in improved services and programs provided to clients lence quality framework has been implemented in all
receiving rehabilitation services. The first publication of a standards manuals. This framework provides a logical,
new section of standards manuals for Rehabilitation Facil- action-oriented approach to ensure that organizational
ities in November 1973 became a springboard for future purpose, planning, and activity result in desired outcomes.
CARF contributions to program evaluation. In January Each year, CARF sponsors numerous in-person and
1986, standards for two new program areas (Respite Pro- web-based seminars to help providers maintain confor-
grams and Alcoholism and Drug Abuse Treatment Pro- mance to the CARF standards. The in-person seminars are
grams) were published in the 1986 Standards Manual for held in cities across the United States, Canada, and Europe.
Organizations Serving People with Disabilities. The 1988
Standards Manual for Organizations Serving People with
Disabilities included new standards in areas of Post-Acute Cross References
Brain Injury Programs and Community Mental Health
Programs. CARF published a separate volume of its 1995 Americans with Disabilities Act of 1990
Standards Manual and Interpretive Guidelines for each of Individuals with Disabilities Education Act
650 C Commissural Fibers
National Center for the Dissemination of Disability Definition

Research
National Dissemination Center for Children with The right and left cerebral hemispheres are connected
Disabilities by three tracts of nerve fibers or axons, which are collec-
National Institute on Disability and Rehabilitation tively referred to as commissures, cerebral. These trans-
Research verse, nerve fiber bundles connect to the homologous
National Institute of Neurological Disorders and Stroke regions of each hemisphere and are known as the corpus
National Rehabilitation Information Center callosum, the anterior commissure and the posterior
No Child Left Behind Act of 2001 commissure. The corpus callosum, also referred to as
Rehabilitation Counseling the great cerebral commissure, is the largest, and it
Rehabilitation Psychology interconnects the greatest portion of the cerebral hemi-
Section 504 of the Rehabilitation Act of 1973 spheres, permitting the cerebral cortex to operate as a
whole. The corpus callosum is often the site for commis-
surotomy, surgical bisection, to treat certain psychiatric
References and Readings disorders and epilepsy. The anterior commissure is a
smaller bundle of nerve fibers that interconnect parts
CARF accreditation (http://www.carf.org/Accreditation/Accreditation
of the temporal lobes. The posterior commissure is an-
Process/StepstoAccreditation/). other fiber bundle that crosses beneath the pineal gland
CARF IAC (http://www.carf.org/About/IAC/). to connect the midbrain regions of the cerebral
CARF mission (http://www.carf.org/About/Mission/). hemispheres.
CARF overview (http://www.carf.org/About/).
CARF partners (http://www.carf.org/Resources/IACResources/).
CARF structure (http://www.carf.org/About/WhoWeAre/).
Value of CARF Accreditation (http://www.carf.org/Accreditation/Valueof
Accreditation/).
Cross References
Commissurotomy
Corpus Callosum
Commissural Fibers
Commissurotomy
C HRISTINA K WASNICA
Barrow Neurological Institute
Commissural Magna Phoenix, AZ, USA
Corpus Callosum
Synonyms
Split-brain
M ARTIN R. G RAF Definition
Richmond, VA, USA The term referring to the medical procedure in which
interconnecting fibers between the cerebral hemispheres
are lesioned. The anatomic location includes either
Synonyms or both anterior and posterior fibers. When posterior
fibers are resected, connections to the hippocampus may
Brain commissures; Commissural fibers also be affected.
Community Integration Questionnaire C 651
Current Knowledge key social and interpersonal bonds (staying close and
connected with individuals who matter most in daily
The neurosurgical technique is based on the premise life). Thus, effective communication depends as much
that when stimuli enters the brain it is rapidly communi- on nonverbal behaviors such as facial expression, touch,
cated via the corpus callosum to the other hemisphere. In and vocal intonation as on the exchange of words. C
refractory epilepsy, severing the corpus callosum Acquired deficits to communication ability can occur in
may prevent the spread of electrical activity between hemi- the absence of a notable loss in intelligence or nonlinguistic
spheres and generalization of the seizure activity. This cognitive functions, as in aphasia, dysarthria, dysphonia/
procedure prevents the communication of the two hemi- aphonia, and apraxia of speech.
spheres thus resulting in a clinical scenario of a split
brain. Clinical disconnection syndromes in these patients
have been studied across a large number of neurocognitive
Cross References
tasks. These surgical lesions have allowed for the study of
Language
sensory perceptual processes and lateralization. Deficits
Speech
have been seen in the area of perception, attention, memo-
ry, language, and reasoning. In studies of these patients, it
has become clear that the left hemisphere has limitations in
perceptual functions while the right hemisphere has more Communication Disorders
striking limitations in cognitive functions. The split brain
studies have also led to theories of consciousness and a Speech/Communication Disabilities
neurocognitive framework for the human experience.
References and Readings Community Adjustment

Community Re-entry
Bogen, J. E., Fisher, E. D., & Vogel, P. J. (1965). Cerebral commissurot-
omy: A second case report. JAMA, 194, 13281329.
Gazzaniga, M. S. (2000). Cerebral specialization and interhemispheric
communication: Does the corpus callosum enable the human con-
dition? Brain, 123, 12931313.
Community Integration
Community Re-entry
Communicating Artery
Community Integration
Anterior Communicating Artery
Questionnaire
M ARCEL D IJKERS
Communication Ability Mount Sinai School of Medicine
New York, NY, USA
J ON G. LYON
Mazomanie, WI, USA
Synonyms
Definition CIQ
Commonly refers to the ease, efficiency, and accuracy of

the exchange of information or content between parties Description
regardless of form, i.e., spoken, written, gestured, drawn,
or using augmentative and assistive devices (communi- The Community Integration Questionnaire (CIQ) mea-
cation boards or computers). Human communication sures what the International Classification of Disability,
relies primarily on the preservation and maintenance of Functioning and Health (ICF) currently designates as
652 C Community Integration Questionnaire
Participation. The CIQ consists of 15 items relevant to resulting instrument, sometimes designated the CIQ-R,
home integration (H) (living), social integration (S) dropped one item and reassigned two to different sub-
(loving), and productive activities (P) (working). It is scales (Sander et al., 1999). The CIQ-R has been used
scored to provide subtotals for each of these domains, as infrequently. In 2002, The TBIMS dropped the CIQ, and
well as a total community integration score. The basis for replaced it (in 2007) with the Participation Assessment
scoring is primarily frequency of performing activities or with Recombined Tools (PART).
roles, with secondary weight given to whether or not
activities are done jointly with others and the nature
of these other persons (for example, with/without dis- Psychometric Data
ability). The CIQ can be completed by either the index
person or a proxy in 1015 min. The optimal method Psychometric information for the CIQ is spread out over
of data collection is an in-person interview, but a number of sources. In addition to the three papers by
telephone interviewing is quite common, and the Trau- Willer et al. (Willer, Linn, et al., 1994; Willer, Ottenbacher,
matic Brain Injury Model Systems (TBIMS) have also et al., 1994; Willer, Rosenthal, et al., 1993) key texts
utilized self-administered CIQs. No formal training are those by Corrigan and Deming (1995), Sander et al.
and credentialing process for the administration of the (1999); Sander et al. (1997) and Tepper, Beatty and
CIQ exists. DeJong (1996). Dijkers critically summarized psychomet-
ric information available through 1997 (Dijkers, 1997),
and some later sources are given in Reistetter and Abreus
Historical Background 2005 article (Reistetter and Abreu, 2005).
Reliability. Results of reliability studies have been
The CIQ was developed in the early 1990s by Barry Willer, mixed. Based on the (Pearson) correlations reported in
Ph.D. and a group of professionals and consumers to the earliest study, the interrater reliability of the CIQ
provide a measure of community integration after trau- appears to be in the acceptable range. However, the
matic brain injury (TBI) that could be used in the TBIMS intraclass correlation coefficient (ICC), a more appropri-
research program (Willer, Linn, & Allen, 1994; Willer, ate measure, resulted in much lower numbers, according
Ottenbacher, & Coad, 1994; Willer, Rosenthal, Kreutzer, to a later investigation, especially for the Home (H)
Gordon, & Rempel, 1993). They used the following design dimension. More recent research also suggests that in
criteria: brevity; suitable for use in in-person or telephone home integration there is the greatest discrepancy
interviews with the person with TBI or a proxy; focus on between reports by subjects with TBI and those by their
behaviors rather than feeling states; no biases resulting proxies. In the latter study, the person with TBI tended
from age, gender, or socioeconomic status; sensitive to a to report higher values than the proxy for all three
wide variety of living situations; and value neutral. The components. Subscale ICCs ranged from 0.43 (H) to
instrument has been translated (not always using formal 0.81 (P) fairly low values.
backtranslation methods) into French, Spanish, Japanese, For the CIQ total score, three out of four studies have
Korean, Dutch, Swedish, and Norwegian, among others. reported internal consistency levels that exceed the
It is the most extensively used measure of community criterion of a coefficient alpha above 0.80. However, the
integration/ participation in research on TBI, but has corresponding values for the S and P dimensions
also been applied in investigations of other types of are much lower, especially for the latter quite likely
brain injury (including stroke and brain tumors), spinal due to the fact that alpha is based on only two variables,
cord injury, burns, trauma in general, mobility disabil- which are very dissimilar from one another: work/study/
ities, and post-polio syndrome. The most common appli- volunteering, and travel.
cations are in program evaluation and the study of the Distribution issues. Corrigan and Deming noted
natural history of TBI and other impairments, but the negatively skewed distributions for the premorbid data
CIQ has also been used in clinical trials of interventions to for CIQ total, positive skews for H for all four samples,
improve post-injury functioning, and in construct valida- negative skews for all samples for the S dimension, and
tion studies of newly proposed participation measures. negative skew for P for the TBI-premorbid sample, but
Because the assignment of items to subscales by Willer positive skew for the three others. Various kurtosis pro-
et al. was based on a correlation matrix calculated for a blems were also noted. They recommended that the P
small sample, Sander et al. performed a factor analysis subscale not be used independently from its contribution
involving all CIQ items for a much larger sample. The to the CIQ total score. Distribution problems were also
Community Integration Questionnaire C 653
noted by Willer et al. and Sander et al., among others. use of the CIQ is freely given but should be requested, by
Unless these can be resolved through transformations, contacting him at the Center for Research on Community
nonparametric statistics need to be used in order to deal Integration at the Ontario Brain Injury Association,
with the nonnormal distributions. 3550 Schmon Parkway, Thorold, Ont L2V 4Y6, Canada,
Validity. No formal content or face validity studies of email: willer@vaxxine.com C
the CIQ have been done, but it was developed utilizing
a panel consisting of both consumers and professionals
with expertise in TBI outcome studies. Cross References
CIQ subscales and total score have been found to
correlate with subscales and total score on CHART CHART Short Form
(another measure of community integration), impairment Community Re-entry
and disability, time since injury, CIM (a measure of subjec- Craig Handicap Assessment and Report Technique
tive community integration), and subjective quality of life, Frenchay Activity Index
according to multiple reports. Most researchers find Glasgow Outcome Scale
negative correlations between CIQ and its subtotals (except Glasgow Outcome Scale Extended
sometimes H) and age. Females tend to have higher CIQ Impact on Participation and Autonomy Questionnaire
scores for total, H and S than males, but lower P scores. Instrumental Activities of Daily Living (I-ADL)
Sensitivity. The available research shows that the CIQ LawtonBrody IADL scale
can validly distinguish between persons with TBI and LIFE-H
nondisabled people. Persons with TBI are less integrated Outcome, Outcome Measurement
along all dimensions than nondisabled comparison Participation Measure for Post Acute Care (PM-PAC)
groups in most research. In one study, CIQ scores distin- Participation Objective Participation Subjective
guished between three groups of persons with TBI living Reintegration to Normal Living Index
in settings differentiated by supervision/support level: Social and Occupational Functioning Scales (SOFAS)
independent in the community, in the community with Traumatic Brain Injury Model System
some (natural) support, and in an institution such as a
nursing home, rehabilitation facility, etc. Willer et al.
reported gain in CIQ (sub)scores for people with TBI References and Readings
receiving residential rehabilitation services between the
second and third anniversary of injury, while a control Corrigan, J. D., & Deming, R. (1995). Psychometric characteristics of the
group who received no or minimal home-based services community integration questionnaire: Replication and extension.
did not show a gain. Corrigan et al. found trends toward Journal of Head Trauma Rehabilitation, 10, 4153.
Dijkers, M. (1997). Measuring the long-term outcomes of traumatic
improvement in all three subscales and total score in a
brain injury: A review of the community integration questionnaire.
cross-sectional study covering injury anniversaries one Journal of Head Trauma Rehabilitation, 12, 7491.
through four. However, in another investigation, a very Reistetter, T. A., & Abreu, B. C. (2005). Appraising evidence on
small increase from the first to the second anniversary of community integration following brain injury: A systematic review.
injury was reported for a group that in large majority did Occupational Therapy International, 12, 196217.
Sander, A. M., Seel, R. T., Kreutzer, J. S., Hall, K. M., High, W. M., Jr., &
not receive rehabilitation services any longer.
Rosenthal, M. (1997). Agreement between persons with traumatic
brain injury and their relatives regarding psychosocial outcome
using the community integration questionnaire. American Journal
Clinical Uses of Physical Medicine and Rehabilitation, 78, 353357.
Sander, A. M., Fuchs, K. L., High, W. M., Jr., Hall, K. M., Kreutzer, J. S., &
In several TBI community integration programs, the CIQ Rosenthal, M. (1999). The community integration questionnaire
revisited: An assessment of factor structure and validity.
is used to monitor patients progress. However, due to the
American Journal of Physical Medicine and Rehabilitation, 80,
lack of norms and the dependence of community 13031308.
functioning on the environment, the clinical applicability Tepper, S., Beatty, P., & DeJong, G. (1996). Outcomes in traumatic brain
of the CIQ is very much limited. injury: Self-report versus report of significant others. Brain Injury,
10, 575581.
Willer, B., Linn, R., & Allen, K. (1994). Community integration
Note and barriers to integration for individuals with brain injury. In
Barry Willer Ph.D., who was the principal investigator in M. A. J. Finlayson & S. H. Garner (Eds.). Brain injury rehabilitation:
developing the CIQ, holds the copyright. Permission for clinical considerations. Baltimore: Williams and Wilkins.
654 C Community Re-entry
Willer, B., Ottenbacher, K. J., & Coad, M. L. (1994). The community Cross References
integration questionnaire. A comparative examination. American
Journal of Physical Medicine and Rehabilitation, 73, 103111.
Willer, B., Rosenthal, M., Kreutzer, J. S., Gordon, W. A., & Rempel, R.
Quality of Life
(1993). Assessment of community integration following rehabili-
tation for traumatic brain injury. Journal of Head Trauma
Rehabilitation, 8, 7587. References and Readings
Americans with Disabilities Amendments Act of 2008, Pub. L. No. 110

325, 122 Stat. 3553 (2008).
Huey, K. (1980). Patient re-entry into the community. Hospital and
Community Re-entry Community Psychiatry, 31, 5156.
Liberman, R. P., & Silbert, K. (2005). Community re-entry: Develop-
ment of life skills. Psychiatry: Interpersonal and Biological Processes,
A LLEN N. L EWIS J R ., PAMELA H. L EWIS 68(3), 220229.
Virginia Commonwealth University McColl, M. A., Carlson, P., Johnston, J., Minnes, P., Shue, K., Davies, D.,
Richmond, VA, USA et al. (1998). The definition of community integration: Perspectives
of people with brain injuries. Brain Injury, 12(1), 1530.
National Institute on Disability and Rehabilitation Research. (2006).
Long-range plan for fiscal years 2005 through 2009.
Synonyms Presidents New Freedom Commission Report on Mental Health (2003).
Achieving the promise: Transforming mental health care in America.
Community adjustment; Community integration Substance abuse and mental health services administration of the
U.S. Department of Health and Human Services.
Definition
Community re-entry is the extent that an individual who

is initially unable to fully function in the community due Community-Based Rehabilitation
to disability is eventually returned to the community to
work and live independently, using natural supports and A LLEN N. L EWIS J R ., PAMELA H. L EWIS
exercising full access, choice, autonomy, and striving for Virginia Commonwealth University
actualization. Actualization is the degree to which there is Richmond, Virginia
the achievement of a respectable quality of life.
The Americans with Disabilities Act (ADA) of 1990
attempted to legislate community integration by remov- Synonyms
ing physical barriers related to access and making it illegal
to discriminate on the basis of disability. However, In vivo services; Milieu-based services; Outpatient
30 years since the ADAs passage and after the recent rehabilitation
passage of the ADA Restoration Act in late 2008, there is
still significant concern that United States society does
not fully possess nor embrace the attitudes and values Definition
commensurate with full inclusion and community
integration for individuals with disabilities. The provision of restorative or rehabilitative services
Community re-entry programs teach skills necessary targeted toward the amelioration of a disability (disability:
along a continuum of services that afford persons the any illness, condition, or impairment [congenital or
opportunity to learn behaviors needed to live full lives acquired] that interferes with functioning in a major life
with a disability. Such programs provide services and domain) and/or the mitigation of functional limitations
supports to enable the successful transition of an individ- resultant from a disability to the maximum extent possible
ual with a disability from facility-based services to a viable in a non-acute care, non-facility-based service setting.
community placement. Community-based rehabilitation services attempt to
maximize the individuals ability to function in vivo
Note within major life pursuits such as independent daily living
The authors are not related by blood or marriage. and work.
Compartmentalization C 655
Community-based rehabilitation attempts to en- into well-perfused organs. Muscle, fat, and bone are
hance the quality of life for individuals with disabilities saturated last. These tissues can serve as storage depots
and their families. This includes meeting basic needs, for substances, contributing to the half-life of a drug and
but also going beyond to promote inclusion and partici- potentially to interaction effects days or weeks after a drug
pation. Community-based rehabilitation typically has been discontinued. C
involves several domains of functioning such as health, The body may be inappropriately be treated as a single
education, work, socialization, and ones sense of entity or compartment. In a single-compartment model,
empowerment. Reaching a point of social acceptance in drugs are theoretically presumed to diffuse through tis-
the 1970s and 1980s, the original mission of community- sues and the differences in absorption and retention of a
based rehabilitation was to offer individuals with dis- drug are not treated as significant. This single-compart-
abilities access to programming and supports in their ment model is sufficient in many situations, but is less
own home communities using local resources. Further, useful when drugs may be preferentially retained in one
community-based rehabilitation ostensibly attempts to type of tissue. Dosage predictions fail if they do not
optimize the provision of rehabilitative services, equal- account for the gradual ambient leaching of the drug
ize opportunity, reduce poverty, and promote full social from fat or bone into general circulation.
inclusion. The instances in which a multi-compartment model
is most relevant are for individuals who are medically ill,
have unusually high or low body fat, are pregnant, have
an abnormality in pH or illnesses which impact the liver
References and Readings or kidneys (and thus profoundly alter the pharmacoki-
netics of drug metabolism). Differences in the propor-
Church, J., Saunders, D., Wanke, M., & Pong, R. (1995). Organizational
models in community based health care: A review of the literature.
tion of fatty tissue can influence dosing decisions since
Health Promotion and Programs Branch,Ottawa: Health Canada. mg/kg may be less appropriate for drugs that are less fat-
World Health Organization, (2004). CBR: A strategy for rehabilitation, soluble. One common example of this reduced alcohol
equalization of opportunities, poverty reduction and social inclu- tolerance in women since fatty tissues do not readily
sion of people with disabilities: Joint position paper/International
absorb alcohol.
Labour Organization, United Nations Educational, Scientific and
Cultural Organization and the World Health Organization.
Another form of compartmentalization is ion
trapping, in which the pH alters the ease with which a
drug is transferred into or out of a particular tissue. For
example, neonatal blood is typically more acidic than
adult blood, making it more difficult for slightly alkaline
drugs to diffuse back into maternal circulation. Similarly,
Comorbid the GI tract is more acidic than blood plasma. Weakly
acidic drugs diffuse more readily to blood than weakly
Dual Diagnosis alkaline drugs.
Cross References
pH
Compartmentalization Pharmacokinetics
N ADIA W EBB
New Orleans, LA, USA References and Readings
Brunton, L. B., Lazo, J. S., & Parker, K. L. (Eds.). (2005). Goodman &
Definition Gilmans the pharmacological basis of therapeutics (11th ed.).
Stahl, S. M. (2008). Stahls essential psychopharmacology: Neuroscientific
Drugs do not saturate tissues within the body at the same basis and practical applications. New York: Cambridge University
rate. They are quickly absorbed into blood plasma and Press.
656 C Compensation Neurosis
Compensation Neurosis Compensatory Education

Approach
B ETH K UCZYNSKI 1, S TEPHANIE A. KOLAKOWSKY-H AYNER 2
1
University of California J ILL S NYDER
Davis, CA, USA University of Northern Colorado
2
Santa Clara Valley Medical Center, Greeley, CO, USA
San Jose, CA, USA
Definition
Synonyms Compensatory educational approaches require teachers
to present material in a different format, providing
Accident neurosis students an alternative way to master a particular concept
and demonstrate knowledge.
Definition
Current Knowledge
Compensation neurosis is a condition in which
symptoms are associated with a real or presumed dis- The goal of education is to help students acquire skills and
ability (possibly exaggerated) that may bring financial master concepts that will be useful in daily living.
compensation. This type of neurosis is believed to be Generally, two approaches are used when instruction
motivated by the desire for, and hope of, monetary or fails to help students learn. These include compensatory
interpersonal gain. Many factors are involved in com- education approaches and/or remedial education
pensation neurosis, such as the psychological factors approaches ( Remedial Education Approach). Compen-
before and after the presumed injury, the additional satory educational approaches require teachers to present
effects on the quality of life, and the possible influences material in a different format, providing students an
of legal or insurance processes. The term is often used alternative way to master a particular concept and dem-
in litigation and seems to be quite controversial in onstrate knowledge. They are used when students lack the
psychiatry. ability to acquire a certain skill or concept. For example, a
deaf student who is unable to speak may be taught sign
language as an alternate form of communication; or, a
student with a math calculation disability may be taught
Cross References to use a calculator. When students fail to make progress in
a certain skill area, evidence-based strategies and methods
Fake Bad Scale must be employed to help the student attain expected
Malingering learning outcomes. In these cases, education must be
adjusted by offering different activities that facilitate the
same results. This approach in isolation does not repre-
sent best practice, and in keeping with the educational
and neuro-developmental literature, practitioners should
References and Readings offer both remedial and compensatory approaches,
depending on students specific academic needs. Educa-
Brown, J. T. (October 1996). Compensation neurosis rides again: tors must be careful to distinguish between the education-
A practitioners guide to defending PTSD claims
al content in which a student struggles (e.g., reading or
(post traumatic stress disorder). Defense Counsel Journal, 63(4),
467482.
math), and the method in which a particular concept may
Rogers, R. (2008). Clinical assessment of malingering and deception (3rd be successfully integrated. Offering a compensatory ap-
Ed.). New York: Guilford Press. proach should be a last resort on the educational
Compensatory Strategies C 657
continuum, and should be supported by a comprehensive Examples of behavioral strategies would include repeating
neuro-psychological evaluation. phrases during social interactions to ensure accurate pro-
cessing of conversation, or associating words with images
to enhance recall.
Cross References C
Academic Competency
Current Knowledge
Academic Skills
Compensatory Education Approach
Compensatory strategies have shown efficacy in rando-
Remedial Education Approach
mized, controlled studies for improving the ability to
Strength-Based Education Approach
remember to complete activities in the future (prospective
memory) in neurologically impaired people with cogni-
tive difficulties. For example, Wilson, Emslie, Quirk, and
References and Readings Evans (2001) used an external pager in 143 people be-
tween 8 and 83 with a range of neurological illnesses or
DAmato, R. C., & Rothlisberg, B. A. (1996). How education should trauma. Results revealed that more than 80% of clients
respond to students with traumatic brain injury. Journal of Learning
improved in carrying out self-care activities and meeting
Disabilities, 29(6), 670683.
DAmato, R. C., Rothlisberg, B. A., & Work, P. L. H. (1999). Neuropsy-
appointments, as well as other life skills, relative to the
chological assessment for intervention. In C. R. Reynolds, & T. B. baseline period, and effects were maintained seven weeks
Gutkin (Eds.), The handbook of school psychology (pp. 452475). after return of the pager. Environmental modifications,
New York: Wiley. including use of signs, removal of distracting environ-
Gaddes, W. H., & Edgell, D. (1994). Learning disabilities and brain
mental stimuli, and checklists have been used effectively
function: A neuropsychological approach (3rd ed.). New York:
Springer.
in randomized, controlled trials to enhance adaptive func-
tioning and quality of life in people with severe psychiatric
illnesses as well (Velligan, Prihoda, Ritch, Maples, Bow-
Thomas, & Dassori, 2002).
Compensatory Strategies
M ATTHEW M. K URTZ Cross References
Wesleyan University
Middletown, CT, USA Cognitive Rehabilitation
Environmental Modifications
Mnemonic Techniques
Definition Neuropsychological Rehabilitation
Prosthetic Memory Aids
Compensatory strategies are environmental modifica-
tions or behavioral strategies designed to bypass persistent
impairment in attention, memory, executive-function,
and/or other cognitive skills as a means to achieve desired
rehabilitation goals. Environmental modifications could
Velligan, D. I., Prihoda, T. J., Ritch, J. L., Maples, N., Bow-Thomas, C., &
include the use of external aids or modifying the setting in Dassori, A. (2002). A randomized, single-blind pilot study of com-
which activities take place. The use of an alphanumeric pensatory strategies in schizophrenia outpatients. Schizophrenia Bul-
pager and a checklist for a person with memory and letin, 28, 283292.
executive-function deficits to ensure completion of daily Wilson, B. A. (2008). Neuropsychological rehabilitation. Annual Review
of Clinical Psychology, 4, 141162.
tasks at specific times would be an example of external
Wilson, B. A., Emslie, H. C., Quirk, K., & Evans, J. J. (2001). Reducing
aids. Working in a distraction-free room to enhance con- everyday memory and planning problems by means of a paging
centration skills in a person with symptoms of disinhibi- system: a randomised control crossover study. Journal of Neurology,
tion would be an example of modifying an environment. Neurosurgery and Psychiatry, 70, 477482.
658 C Competence to Testify
financial affairs, execute a will, drive, manage medica-

Competence to Testify tions, live independently, and handle even the most
basic activities of daily life (ADLs).
Jenkins v. U.S. (1962) In the criminal realm, competency relates to a defen-
dants current ability to understand and partake in legal
proceedings. The Dusky standard states that: The test
must be whether he (the defendant) has sufficient present
ability to consult with his lawyer with a reasonable degree
Competency of rational understanding and whether he has a rational
as well as factual understanding of the proceedings against
M OIRA C. D UX him. (p. 402). The Dusky standard outlines the minimal
University of Maryland Medical Center/Baltimore VA level of competency necessary in accordance with the U.S.
Baltimore, MD, USA Constitution for all criminal jurisdictions. Grisso (1988)
outlined five areas of analysis suggested for psychologists/
neuropsychologists conducting competency evaluations:
Synonyms (1) functional description of specific abilities, (2) causal
explanations for deficits in competency abilities, (3) in-
Capacity teractive significance of deficits in competency ability,
(4) conclusory opinions about legal competency and
incompetency, and (5) prescriptive remediation for defi-
Definition cits in competency abilities. In an attempt to operationa-
lize the Dusky ruling, the Group for the Advancement of
Competency is a legal determination to be made by a legal Psychiatry (1974) developed a 21-point list of abilities
professional (i.e., judge). It relates to a persons capacity derived from competency assessment instruments avail-
(a clinical status as judged by a health care professional) to able at the time and included items such as: understand
make determinations/decisions or to perform certain current legal situation, understand legal defenses available
functions. In a legal context, competency typically relates in the defendants behalf, tolerate stress at the trial and
to ones understanding of issues related to involvement while awaiting trial, and protect self by using available
in a legal proceeding (Reisner & Slobogin, 1990). Such an legal safeguards. As a result of Wieter v. Settle (1961), the
understanding necessitates some degree of acknowledg- U.S. District Court outlined several minimal ability
ment regarding the nature of the procedure, the risks requirements for criminal competency including (but
involved, success estimates, possible alternative options/ not limited to): mental capacity to appreciate his or her
approaches, and the pros and cons of specific courses of presence in relation to time, place, and thing; apprehends
action. Issues related to competency can be raised at any that there is a judge on the bench; apprehends that there
time during the criminal judicial process. Specific compe- is, or will be, a jury present to pass on evidence adduced as
tencies in the criminal realm include: competence to to his or her guilt or innocence of such charge; he or she
confess (or waive rights at pretrial investigations), com- has memory sufficient to relate those things in his or her
petency to plead guilty, competency to waive right to own personal manner.
counsel, competency to stand trial, competency to be Currently, there are a number of instruments designed
sentenced, competency to waive further appeal (when to assess competency (primarily in the criminal realm),
facing capital punishment), and competency to be exe- which are referred to as competency assessment tools
cuted. Competency evaluations are the most common (CATs). Examples include: the Competency Assessment
referral of mental health professional in criminal foren- Inventory-Revised, the Fitness Interview Test-Revised, the
sics. A defendants competency can be questioned by Georgia Court Competency Test, the Competency Assess-
attorneys and judges. In the civil realm, impairment of ment for Standing Trial for Defendants With Mental
competency, or decision-making capacity, is often a con- Retardation, and the MacArthur Competency Assessment
sequence of various types of dementias and other organic Tool-Criminal Adjudication. It is important to note
brain syndromes. Impairments in memory, judgment, that none of the aforementioned CATs have been vali-
reasoning, and planning can affect a persons capacity dated with brain-injured or neurological populations.
to: make medical decisions, consent to research, manage Marson and colleagues (cf. Marson & Hebert, 2005)
Complex Partial Seizure C 659
have developed instruments to assess consent capacity in Definition

older adults.
Formerly known as psychomotor seizures, complex par-
tial seizures (CPS) are defined by the International League
Cross References Against Epilepsy as focal seizures with impaired con- C
sciousness as the central feature.
Financial Capacity A CPS may begin with a simple partial seizure, also
referred to as an aura. This commonly consists of feelings
References and Readings of emotional, ideational, or sensory changes. Once con-
sciousness becomes impaired, individuals with CPS may
Denney, R. L., (2005). Criminal forensic neuropsychology and assessment experience automatisms, which are often characterized as
of competency. In G. Larrabee (Ed.), Forensic neuropsychology: repetitive, semi-purposeful involuntary movements.
A scientific approach. New York: Oxford University Press. These may be oropharyngeal (e.g., lip smacking), emo-
Dusky v. United States, 362 U.S. 402 (1960).
tional (e.g., fear), gestural (e.g., picking), ambulatory (e.
Grisso, T. (1988). Competency to stand trial evaluations: A manual for
practice. Sarasota, FL: Professional Resource Exchange.
g., walking), or verbal in nature. In some cases, focal CPS
Group for the Advancement of Psychiatry (1974). Misuse of psychiatry in secondarily progresses into a generalized event (i.e.,
the criminal courts: Competency to stand trial. New York: Commit- tonicclonic seizure). The specific paroxysmal behavior
tee on Psychiatry and Law. changes correspond to the seizure focus and the progres-
Marson, D. C., & Hebert, K. (2005). Assessing civil competencies in older
sion represents the spread of epileptiform activity. Indi-
adults with dementia: Consent capacity, financial capacity, and tes-
tamentary capacity. In G. Larrabee (Ed.), Forensic neuropsychology: A
viduals with CPS often experience brief postictal
scientific approach. New York: Oxford University Press. confusion and are usually amnestic for their ictal
Reisner, R., & Slobogin, B. (1990). Law and the mental health system behavior.
(2nd ed.). St. Paul, MN: West.
Wieter v. Settle (1961). 193 F. Supp. 318 (W.D. Mo., 1961).
Current Knowledge
Epidemiologically, CPS comprises an estimated 42% of all

Competency to Proceed partial seizures and 20% of all epilepsies. Approximately
6080% of CPS arise from the temporal lobe, particularly
Legal Competency the neocortex and inferomedial (limbic) structures. While
commonly equated with temporal lobe seizures, it is now
known that forms of CPS can originate from other brain
regions, most notably the frontal lobes. A diagnosis of
Complex Figure Test (CFT) CPS can be identified through a neurological history and
description of the events. However, the electroencephalo-
Rey Complex Figure Test
gram (EEG) remains the gold standard for diagnosis.
Patients with CPS often exhibit abnormal discharges on
interictal recordings and a characteristic pattern of onset
and spread of activity when seizures are recorded. CPS is
Complex Partial Seizure most commonly treated with antiepileptic drugs. Surgical
intervention for intractable CPS has been increasingly
W ILLIAM B. B ARR , H EIDI A. B ENDER pursued in recent years. Successful outcomes are most
NYU Comprehensive Epilepsy Center often achieved following temporal lobectomy or lesion
EPC resection in CPS patients with underlying mesial tempo-
New York, USA ral sclerosis.
Synonyms Cross References

Partial epilepsy; Psychomotor seizures; Temporal lobe Aura
seizure Generalized Tonic-Clonic Seizures
660 C Complex Partial Seizures with Automatisms
Temporal Lobe
Temporal Lobe Epilepsy Computed Tomography
R OBIN S EKERAK
Waikato District Health Board
References and Readings Hamilton, New Zealand
Browne, T. R., & Feldman, R. G. (Eds.). (1983). Epilepsy: Diagnosis and

management (p. 39). Boston, MA: Little, Brown, & Company. Synonyms
Kotagal, P., & Loddenkemper, T. (2005). Focal seizures with impaired
consciousness. In E. Wyllie, A. Gupta, & D. K. Lachwani (Eds.), The
treatment of epilepsy: Principles & practice (4th ed., pp. 441442).
CAT Scan; Computerized axial tomography; CT
Philadelphia, PA. Lippincott Williams & Wilkins.
Lee, G. P., & Clason, C. L. (2008). Classification of seizure disorders
and syndromes, and neuropsychological impairment in adults
with epilepsy. In J. E. Morgan, & J. H. Ricker (Eds.), Textbook of
Definition
clinical neuropsychology (pp. 439440). United Kingdom: Taylor &
Francis. CT is an imaging modality that generates cross-sectional
Oxbury, J. M., & Duchowny, M. (2000). Diagnosis and classification. In images of the body with very good anatomical detail.
J. Oxbury, C. Polkey, & M. Duchowny (Eds.), Intractable focal This is accomplished by an X-ray tube rotating 360
epilepsy (pp. 1516). London: W.B. Saunders.
around the body as it moves through the CT scanner.
During rotation a collimated (focused) X-ray beam is
transmitted through the body which is attenuated by
the tissues. The attenuated X-rays are sensed by an
array of detectors on the opposite side as they leave
Complex Partial Seizures with the body. The signal from the detectors is processed by
a computer to reconstruct a cross-sectional image.
Automatisms Images in axial (dividing the body into superior and
inferior sections), cornal (dividing the body into anteri-
Psychomotor Epilepsy
or and posterior sections), and sagittal (dividing
the body into left and right) planes, as well as 3D,
can be reconstructed the data accquired. Images in the
axial (dividing the body into inferior and superior seg-
ments), sogittal (dividing the body into left and right
Comprehensive Driving segments), and coronal (dividing the body into anterior
Assessment and posterior segments) planes, as well as 3D images,
can be reconstructed from the data accquired. The
Driving Assessment image is stored electronically and displayed on the com-
puter screen. Hard copies of the image can be photo-
graphed onto film. The image is made up of a matrix of
2D cells called pixels, similar to a digital camera. The
pixels are 2D representations of 3D volumes of tissue
called voxels.
Comprehensive System (CS) Different scanning geometries can be obtained includ-
ing helical (or spiral) and multi-slice acquisition. In heli-
Rorschach cal scanning contiguous slices are obtained with
simultaneous continuous X-ray tube rotation and patient
movement. Multiple rings of detectors can be activated by
single rotation of the X-ray tube enabling multiple slices
to be obtained. CT images are produced so that you view
Compulsory Self-Incrimination the films as if looking toward the patients feet with the
patient lying on their back; therefore, the right side of the
Self-Incrimination body is to ones left and vice-versa.
Computer-Aided Assessment C 661
The density of tissues (the attenuation coefficient) is Current Knowledge

expressed in Hounsfield units. All tissues are measured
relative to the density of water which is set at 0. Less dense Advantages of CT
materials, such as air, appear black; more dense materials,
Excellent anatomical detail
such as bone, appear white. Tissue densities in between C
Rapid imaging time
appear as various shades of gray.
Less expensive than MRI
Less movement artifact than MRI
Disadvantages of CT:
CT in Identifying Neurologic Disorders
Relatively high dose of radiation
Bony areas can cause artifact, limiting use in the
Traumatic brain injury: CT is useful in moderate to severe
posterior fossa, spine, bone/parenchyma interface,
acute head trauma. It can accurately diagnose hemor-
and pelvis
rhage, pneumocephalus, foreign bodies, and fractures
Metallic objects also cause artifact if not MRI
(C1-C3 should be included, as upper cervical spine frac-
compatible
ture is associated with 10% of severe head injuries). Sec-
Not good at allowing relative dating and evolution of
ondary effects of trauma such as edema and cerebral
intraparenchymal hemorrhage
herniation are easily detected by CT. MRI may show
subtle vascular dissections, diffuse axonal injuries and
infarctions not initially evident on CT, as well as, evolu-
tion of hemorrhages that allows better dating of injuries
than CT. Cross References
Hemorrhage/stroke: Non-contrast CT is the preferred
investigative modality for presentation of acute stroke, in Angiography, Cerebral
order to rule out a bleed. CT has a higher sensitivity than Magnetic Resonance Imaging
spin-echo MRI for detecting acute hemorrhage. MRI can Neuroimaging
detect site and volume of acute infarct. Some literature
suggests that a T2-weighted MRI has the same sensitivity
for acute hemorrhage as CT. However, rapid imaging,
less motion artifact, availability, cost, and compatibility
Bushberg, J. T., Seibert, J. A., Leidholdt, E. M., Jr., & Boone, J. M. (2001).
with ferromagnetic metals (pacemakers, foreign bodies), The essential physics of medical imaging (2nd ed., pp. 327372).
maintain CT as the primary imaging modality in acute Baltimore, MD: Lippincott Williams & Wilkins.
stroke. Bushong, S. (2004). Radiologic science for technologists (pp. 422457).
Gray/White matter differentiation and subtle lesions: Philadelphia: Elsevier Mosby.
Graham, D., & Cloke, P. (2003). Principles of radiological physics
CT may not be sensitive enough to detect lesions with
(pp. 384385). Edinburg: Churchill Livingstone.
subtle contrast. MRI has better gray/white differentiation Howlett, D., & Ayers, A. (2004). The hands-on guide to imaging
and can detect subtle lesions within white matter. There- (pp. 1213). Oxford: Blackwell Publishing.
fore, it is preferred for subtle lesions such as encephalitis, Novelline, R. (2004). Squires fundamentals of roentgenology (pp. 2934).
hippocampal sclerosis, suspected intracranial tumors, Cambridge: President and Fellows of Harvard College.
Patel, P. (2005). Lecture notes: Radiology (2nd ed., pp. 89). Oxford:
multiple sclerosis, and acute ischemic stroke.
Blackwell Publishing.
Bony Detail: Bony pathology such as a fracture, mas- Slone, R. (2000). CT techniques and protocols. In R. M. Slone, A. J.
toiditis, or sinusitis is better imaged with CT than an Fisher, P. J. Pickhardt, F. R. Gutierrez, & D. M.Balfe (Eds.), Body CT:
MRI. However, since X-ray photons are preferentially A practical approach. New York, NY: McGraw-Hill.
absorbed by bone this can cause streaky bone artifact Wolbarst, A. B. (2000). Physics of radiology (2nd ed., p. 95). Madison, WI:
Medical Physics Publishing.
(called cupping) when trying to view brain tissue at
the skull base. MRI is the preferred modality for brain-
stem lesions as there are fewer bony artifacts.
Hydrocephalus and Cerebral Atrophy: CSF containing
spaces are clearly shown on a CT and thus ventricular/ Computer-Aided Assessment
sulcal size, shape, and proportionality are easily
evaluated. Test Interpretations: Computer Based
662 C Computer-Based Test Interpretation
Computer-Based Test
Interpretation CARB was designed and published by Conder, Allen, and
Cox (1992) to provide a computerized tool for adminis-
Test Interpretations: Computer Based tration of the forced-choice, digit recognition tasks that
were gaining popularity in assessment of effort during
neuropsychological testing. Hiscock and Hiscock (1989)
had described the use of forced-choice methods in detect-
Computerized Assessment of ing malingering, and Binder (1990) had also studied
Response Bias this method of assessing effort. The authors of CARB
elected to name the test with the phrase response bias
DAVID R. C OX (as opposed to malingering or effort) to clarify that the
Chapel Hill, NC, USA test was not diagnosing malingering, but measuring a
bias in the response.
Several versions of CARB have been published and
Synonyms studied. The original version (Conder et al., 1992) utilized
three distinct trials of 37 items each. Each item includes
CARB presentation of a five digit number that is to be remem-
bered followed by a short delay during which the examin-
ee is to count silently backward from 20. The examinee
Description then selects the presented number from two choices the
target and a foil. The groups of trials differ from one
The Computerized Assessment of Response Bias (CARB) another in that the delay between stimulus presentation
is a computer-based tool for evaluating effort. The CARB and forced-choice presentation increases from 3 to 6 and
is one of many measures characterized as symptom valid- 9 s, respectively. Initial studies of this version of CARB
ity tests (SVT), indices of response bias used to assess determined that performance at or below 89% correct
possible malingering, poor effort, or exaggeration of defi- falls more than two standard deviations below the sample
cit. The test is a computerized version of the digit recog- of individuals with documented brain injury (Conder
nition paradigm in a forced choice format, akin to the et al., 1992); performance below 90% was therefore
procedures described by Hiscock and Hiscock (1989) and deemed to be biased.
Binder (1990). Frequently, statistical determination of Subsequent versions of CARB include CARB-97
below chance performance (based on the binomial theo- (Allen, Conder, Green, & Cox, 1997) and another revi-
rem) has been used with tests such as these to identify sion referenced in Green and Iverson (2001). CARB-97
persons showing poor effort. This method requires an added auditory feedback to the original version such that
extremely low score to reach a statistically significant correct responses are followed by a pleasant tone and
level. However, as the CARB is an easy test, it allows the incorrect responses are followed by an unpleasant tone.
clinician to detect inadequate effort using above-chance The third revision shortened the delays between stimulus
cutoff scores (Millis, 2008). The test has been studied with presentation and forced choice presentation to 1.5, 2.5,
a wide variety of populations, including persons with and 3.5 s. Each CARB version has been utilized in pub-
head injury, chronic fatigue syndrome, musculoskeletal lished studies, although the original version may continue
injuries, pain disorders, and psychiatric or emotional dis- to be the most widely used (Larrabee, 2007).
turbances such as depression. Published studies have in-
cluded both adults and children. Administration time can
vary depending on the protocol used; however, it typically Psychometric Data
can be completed in no more than 1015 min. CARB
performance results include percent correct for each As with many, if not most, symptom validity tests the
group of trials as well as the overall percent correct. Also nature of CARB presentation of a relatively easy task
reported are the response latency for each item, average that may be perceived to be much more difficult than it
latency per group of trials, and overall, as well as other, actually is leads to a distribution of scores that is highly
information. An interpretive summary can also be skewed toward the upper end. Individuals who put forth
provided, if desired. effort on the test get all, or nearly all, of the items correct.
Computerized Assessment of Response Bias C 663
This appears to be true regardless of the presence or appropriate in any clinical population. The concept of
absence of brain injury or other cognitive deficits. CARB the binomial theorem and evaluation of performance
was originally validated on a small sample (8) of indivi- against chance levels is a useful and reasonably valid
duals who had documented severe brain injury. That measure. Clearly, however, there is support for the use of
group performed at 98.6% (SD = 3.6) correct (Conder CARB with cutoff scores at above-chance levels in assess- C
et al., 1992). Internal consistency across items is therefore ment of those groups of whom scientific studies have been
also quite high among individuals putting forth adequate published.
effort; biased responding with suboptimal effort is pre-
sumed, by the nature of the construct, to be more variable.
Individuals who perform at a passing level on CARB Cross References
yielded 96.697.6% accuracy across the blocks of trials,
whereas those who performed at a non-passing level Dissimulation
yielded accuracy scores ranging from 62.4 to 74.6% Effort
(Allen et al., 1997; Allen, Richards, Green, Iverson, & Forensic Neuropsychologist
Conder, 1998). An accuracy difference of 10% or more Forensic Neuropsychology
between any two blocks of the test correlates highly Forensic Psychology
with poor (non-passing) scores on CARB (Allen et al., Hiscock Forced-Choice Test
1997). Testretest reliability (1-week interval) is quite Malingering
high (r = 0.97) (de Armas, 1996). Portland Digit Recognition Test
Response Bias
Rey 15-Item Test
Clinical Uses Symptom Validity Assessment
Word Memory Test
Clinically, CARB is used to assess response bias and level
of effort and assist in the detection of symptom exaggera-
tion and/or malingering. Published studies have primarily References and Readings
involved populations of individuals alleging brain injury
Allen, L. M., Conder, R. L., Green, P., & Cox, D. R. (1997). CARB 97
via closed head trauma, although other diagnostic group-
manual for the computerized assessment of response bias. Durham:
ings have also been examined. These include chronic CogniSyst.
fatigue syndrome, fibromyalgia, stroke, chronic pain, Allen, L. M., Iverson, G. L., & Green, P. (2003). Computerized assessment
multiple sclerosis, brain aneurysm, and brain tumor of response bias in forensic neuropsychology. Journal of Forensic
(Allen, Iverson, & Green, 2003). Neuropsychology, 3(2), 205225.
Allen, L. M., Richards, P. M., Green, W. P., Iverson, G. L., & Conder, R. L.
Additional studies have used samples of persons with
(1998). Performance patterns on the computerized assessment
brain injury, alleging brain injury, or with alleging other of response bias in 1752 compensation cases (Abstract). Archives of
disorders that may affect cognition. The variable of seek- Clinical Neuropsychology, 13, 1516.
ing versus not seeking compensation as a result of an Binder, L. M. (1990). Malingering following minor head trauma. The
injury or condition is a significant one in the realm of Clinical Neuropsychologist, 4, 2536.
Conder, R., Allen, L., & Cox, D. (1992). Manual for the computerized
assessing effort. Lending support to the notion that sec-
assessment of response bias. Durham: CogniSyst.
ondary gain can be a major factor in these cases. Gervais, de Armas, A. (1996). Detection of malingering in forensic psychological
Green, Allen, and Iverson (2001) reported that 100% of evaluations. The Forensic Examiner, JulyAugust, 2628.
the individuals with fibromyalgia and rheumatoid arthri- Flaro, L., Green, P., & Allen, L. M., III. (2000). Symptom validity test
tis who were not seeking compensation performed in a results with children: CARB and WMT. Archives of Clinical Neuro-
psychology, 15(8), 840.
fashion that indicated adequate effort. Age does not ap-
Gervais, R., Green, P., Allen, L., & Iverson, G. (2001). Effects of coaching
pear to be a significant factor influencing performance on on symptom validity testing in chronic pain patients presenting for
CARB. Flaro, Green, and Allen (2000) reported on chil- disability assessments. Journal of Forensic Neuropsychology, 2(2),
dren performing at or above normal adult performance 119.
levels on CARB. Allen et al. (2003) summarized a number Green, P., & Iverson, G. L. (2001). Validation of the computerized assess-
ment of response bias in litigating patients with head injuries. The
of studies providing validation for the utility of CARB
Clinical Neuropsychologist, 15, 492497.
with a variety of diagnostic groupings. Hiscock, M., & Hiscock, C. K. (1989). Refining the forced-choice method
CARB appears to be an appropriate measure of effort for the detection of malingering. Journal of Clinical and Experimental
across a very large age range, and would in theory be Neuropsychology, 11, 967974.
664 C Computerized Axial Tomography
Larrabee, G. J. (2007). Assessment of malingered neuropsychological defi- Hypothesis testing is a persons ability to try out several
cits. New York: Oxford University Press.
possible concepts, solutions, or rules in a systematic way
Millis, S. R. (2008). Assessment of incomplete effort and malingering in
the neuropsychological examination. In Morgan, & Ricker (Eds.),
to determine which is the most useful. Cognitive psychol-
Textbook of clinical neuropsychology. New York: Taylor & Francis. ogists define concept learning as the development of
prototypes, schemas, attributions, or exemplars (Lamberts &
Shanks, 1997). Prototypes are learned typical representa-
tions of the concept. For example, a compact car is small,
gets good gas mileage, and is a Toyota. Schemas are scripts
Computerized Axial Tomography that are learnt for behaving or for evaluating behavior.
For example, an introduction usually involves a greeting,
Computed Tomography a smile, and a handshake. Attributions are collections of
behavior adjectives and adverbs that define the notion of a
person, place, or behavior. For example, Republicans are
white, rich, and drive Hummers. Exemplars are collections
Concentration of examples of concepts that are stored in memory. For
example, observing people at the mall defines the concept
Attention of an everyday person. Humans use several different
strategies to form concepts. Conservative focus involves
gradual manipulation of one aspect of a complex concept
at a time until the concept clarifies. Focus gambling tests
several possible hypotheses at the same time instead of
Concept Learning one at a time. Scanning involves forming global hypoth-
eses about a concept, then modifying them in accordance
R ICK PARENTE with rewards and punishments. Trial and error is the
Towson University tendency to just keep trying until something works.
Towson, MD, USA Aspects of the task that improve concept acquisition
include an orderly arrangement of the items that the
person must use to form the concept. A compact display
Synonyms in which all the aspects of the concept are present also
improves acquisition. Sequential problems that present a
Hypotheses; Rules consistent concept also improve concept acquisition. The
saliency, novelty, and complexity of the concept, and
whether feedback is provided affect how quickly a person
Definition learns it (Hunt & Ellis, 2003).
An abstract or general idea that is inferred or derived from

specific instances. References and Readings
Hunt, R. R., & Ellis, H. C. (2003). Fundamentals of cognitive psychology.

Current Knowledge Madison, WI: Brown & Benchmark.
Lamberts, K., & Shanks, D. (Eds.). (1997). Knowledge, concepts, and
A concept is a special combination of ideas that has a categories. Cambridge, MA: MIT Press.
Parente & Herrman (2010). Retraining conceptual skills (chap. 16). In
particular meaning. Rules are concepts that direct
Retraining cognition: Techniques and applications. Austin, TX: Pro-Ed
behavior because there are consequences attached to Publishers.
them. A hypothesis relates two or more concepts with a
prediction (Parente & Herrmann, 2010). Hypothesis test-
ing, rule learning, concept learning, and problem solving
are all interrelated skills. Concept learning is how humans
learn to divide their environment into examples and Conceptual Knowledge
nonexamples of things they understand. Rule learning is
the process of associating concepts with consequences. Semantic Memory
Concussion C 665
post-traumatic anterograde amnesia (PTA), retrograde am-

Concordance nesia, and Glasgow Coma Scale (GCS; Teasdale & Jennett,
1974). Standard neurological examination and imaging
Inter-rater Reliability studies are frequently normal following concussion (i.e.
have limited sensitivity) so should not be relied on to C
diagnose concussion. Among clinical and scientific
experts, a concussion is synonymous with mild traumatic
brain injury (MTBI). Please see MTBI for a more detailed
Concurrent Validity discussion of issues related to diagnosis, management,
recovery, and outcome post concussion.
Test Validity
Current Knowledge
Concussion Epidemiology
M ATTHEW R. P OWELL , M ICHAEL A. M C C REA Current epidemiology statistics likely grossly underesti-
Neuroscience Center mate the true incidence and prevalence of concussion
Waukesha, WI, USA because of imprecise surveillance systems (e.g., many
individuals with concussive injury never seek medical
care and those who do seek care are frequently not hospi-
Synonyms talized), and because current estimates are clouded by
variable research methodologies and inconsistent defini-
Mild traumatic brain injury; Sport-related concussion tions of concussion (McCrea, 2008; National Center for
Injury Prevention and Control, 2003). As discussed in
greater detail under MTBI entry, best estimates would
Definition suggest an incidence of at least 100/100,000 and perhaps
as high as 500/100,0000 population depending on study
A concussion refers to a trauma-induced alteration in methodologies (McCrea, 2008).
neurological function. Giza and Hovda (2001) and
Hovda et al. (1990) discuss the abnormal neurometabolic
processes associated with concussion. Early clinical signs
Recovery and Outcome Post Concussion
of concussion include alteration of mental status or be-
havior, and can be accompanied by other symptoms out-
Concussions fall under the general rubric of MTBI, and are
lined below.
frequently graded by severity (e.g., grade 13 concussion).
More significant concussive injury is associated with great-
er length of altered consciousness, LOC, or amnesia, al-
Diagnosis though concussive injury often occurs without observed
LOC or measurable amnesia. Generally speaking, acute
Diagnosis of concussion is made based on identifying neurologic, behavioral, or cognitive symptoms begin
an event with adequate biomechanical force to cause a acutely and resolve within 710 days, with a small percent-
concussive injury and by examining acute injury severity age of individuals exhibiting symptoms beyond 3 months
indicators. Frequent events associated with a direct trauma (Belanger & Vanderploeg, 2005; Iverson, 2005; McCrea,
or blow to the head to cause concussion include a fall, 2008). Providers should expect a relatively rapid and full
motor vehicle accident, or sports collision. In addition to a recovery for patients following a single concussion. There
direct blow to the head, a concussion can result from rapid is no apparent difference in outcome across the various
acceleration, deceleration, rotational or percussive forces grades of concussion, though there are reports of longer
that affect brain tissue. Injury severity indicators frequent- recovery periods for complicated cases, such as those
ly used to diagnose concussion include alteration of with intracranial abnormalities identified via imaging
consciousness (confusion), loss of consciousness (LOC), (Williams, Levin & Eisenberg, 1990).
666 C Conditioned Stimulus
Evaluation and Management Post References and Readings

Concussion
Belanger, H. G., & Vanderploeg, R. D. (2005). The neuropsychological
Early evaluation of symptoms and neurological status is impact of sports-related concussion: A meta-analysis. Journal of the
International Neuropsychological Society, 11, 345357.
essential following concussion to diagnose severity of injury
Giza, C. C., & Hovda, D. A. (2001). The neurometabolic cascade of
and to rule out complications such as intracranial abnorm- concussion. Journal of Athletic Training, 36, 228235.
alities or other comorbid injuries. Computed tomography Hovda, D. A., Prins, M., Becker, D. P., Lee, S., Bergsneider, M., & Martin,
(CT) imaging of the brain is frequently ordered by medical N. A. (1999). Neurobiology of concussion. In J. E. Bailes, M. R.
specialists because it continues to be the most sensitive Lovell, & J. C. Maroon (Eds.), Sports-related concussion (pp. 1251).
St. Louis, MO: Quality Medical.
procedure for detecting acute intracranial abnormalities
Iverson, G. L. (2005). Outcome from mild traumatic brain injury. Current
post injury. Opinion in Psychiatry, 18, 301317.
While spontaneous improvement over days to weeks Kelly, J. P., & Rosenberg, J. H. (1997). Diagnosis and management of
is the hallmark of recovery following concussion, it is concussion in sports. Neurology, 48(3), 575580.
generally accepted that behavioral management (e.g., ed- McCrea, M. (2008). Mild traumatic brain injury and postconcussion syn-
drome: The new evidence base for diagnosis and treatment. New York:
ucation about MTBI, recovery and outcome; teaching
cognitivebehavioral strategies to manage symptoms) Mittenberg, W., Canyock, E. M., Condit, D., & Patton, C. (2001). Treat-
may minimize the likelihood of a suboptimal outcome ment of Post-concussion syndrome following mild head injury.
and may contribute to improved quality of life for Journal of Clinical & Experimental Neuropsychology, 23(6), 829836.
patients, perhaps because of greater understanding of Mittenberg, W., Tremont, G., Zielinski, R. E., Fichera, S., & Rayls, K.
(1996). Cognitive-behavioral prevention of postconcussion syn-
ones injury and greater appreciation for the expected
drome. Archives of Clinical Neuropsychology, 11(2), 139145.
recovery following injury. Pharmacologic intervention National Center for Injury Prevention and Control. (2003). Report to
for certain symptoms, such as pain, sleep abnormalities, congress on mild traumatic brain injury in the United States: Steps to
or mood disturbance, may also be indicated to help with prevent a serious public health problem. Atlanta, GA: Centers for
early adjustment and quality of life issues following con- Disease Control and Prevention.
Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired
cussion. Post-acute evaluation and monitoring is crucial
consciousness: A practical scale. The Lancet, 2(7872), 8184.
for tracking a persons recovery following injury. This will Williams, D. H., Levin, H. S., & Eisenberg, H. M. (1990). Mild head
help providers determine when it is appropriate for injury classification. Neurosurgery, 27(3), 422428.
patients to resume prior activities, such as collision sports,
academics, or work. Individuals recovering from concus-
sion appear to be more vulnerable for re-injury or cata-
strophic injury. See Kelly and Rosenberg (1997) for an Conditioned Stimulus
excellent discussion of issues involved in management of
sports-related concussion, principles of which can be ap- Stimulus Control
plied to management of concussions resulting from any
mechanism.
Neuropsychological consultation is particularly help-
ful in the evaluation and management of patients follow-
Conduction Aphasia
ing concussion. Neurocognitive testing is sensitive to
LYN T URKSTRA
early, post-acute, and subtle symptoms associated with
concussion, objectively tracks cognitive recovery over
Madison, WI, USA
time, and provides valuable information to inform return
to activity decision-making. Without neuropsychological
data, medical specialists must rely solely on a persons
subjective report about residual neurocognitive symptoms.
Synonyms
Education and cognitive behavioral therapy techniques
Associative aphasia
are important treatment tools frequently employed by
neuropsychologists or other behavioral management
specialists to help prevent or treat persisting postconcussive Short Description
symptoms (Mittenberg, Canyock, Condit, & Patton,
2001; Mittenberg, Tremont, Zielinski, Fichera, & Rayls, Conduction aphasia is a subtype of fluent aphasia that is
1996). characterized by fluent speech and relatively intact
Conduction Aphasia C 667
language comprehension, but significantly impaired rep- utterances (stereotypies). This is consistent with the
etition. Utterance length is normal or increased, and finding that the arcuate fasciculus is spared in many
speech has normal prosody and grammar and is produced patients with conduction aphasia (Quigg et al., 2006).
with normal effort. There is a reduction in content words, By contrast to the localization or modular view of
paraphasic errors are common, and oral reading is Geschwind and others, researchers in connectionist theo- C
impaired. ry have conceptualized language as the product of a
distributed cortical network that can be disrupted in
various ways to produce similar phenotypes. The advent
of functional imaging resurrected the notion of dis-
Categorization connection syndromes and more modular notions of lan-
guage (Catani & Ffytche, 2005), and the current view is
Conduction aphasia is differentiated from other types of somewhere in between a modular and connectionist
fluent aphasia (Wernickes aphasia, transcortical sensory perspective.
aphasia, and anomic aphasia) by the disproportionate
impairment in repetition relative to comprehension and
spontaneous production. It is differentiated from Wer-
nickes aphasia in particular by the patients awareness of Evaluation
his or her paraphasic errors.
The signs and symptoms of conduction aphasia will
be revealed only with testing of auditory and reading
comprehension, spontaneous language (e.g., asking the
Natural History, Prognostic Factors, patient to describe a picture), and repetition, so that
Outcomes the relative performance in these modalities can be
compared.
The prognosis for recovery of functional communication
in individual with conduction aphasia depends on the
underlying cause of the aphasia as well as factors such as
the size of lesion and the patients age, premorbid lan- Treatment
guage skills, and comorbid health conditions. Individuals
who initially present with conduction aphasia often There is no specific treatment for conduction aphasia,
evolve to a clinical profile of anomic aphasia, with rela- beyond therapies that are appropriate for aphasia in gen-
tively good auditory and reading comprehension, and eral ( Aphasia).
deficits primarily in word-finding and the comprehension
and production of complex syntax.
Cross References
Aphasia
Nonfluent Aphasia
Conduction Aphasia
Conduction aphasia historically has been attributed to the
interruption of white matter pathways, notably the arcuate References and Readings
fasciculus (part of the superior longitudinal fasciculus),
that connect posterior and anterior cortical structures Catani, M, & Ffytche D. H. (2005). The rises and falls of disconnection
involved in language comprehension and production. syndromes. Brain, 128(Pt 10), 22242239.
Thus, conduction aphasia historically was referred to as Geschwind, N. (1965). Disconnexion syndromes in animals and man. II.
a disconnection syndrome (Geschwind, 1965). Lesion Brain 88, 585644.
Goodglass, H. (1993). Understanding Aphasia. San Diego, CA: Academic
and imaging studies have revealed, however, that conduc-
Press.
tion aphasia may result from lesions in a variety of loca- Quigg, M., Geldmacher, D. S., & Elias, W. J. (2006). Conduction aphasia
tions, and that arcuate fasciculus lesions are instead as a function of the dominant posterior perisylvian cortex: Report of
implicated in the production of repetitive, stereotypic two cases. Journal of Neurosurgery 104, 845848.
668 C Confabulation
described as brief, partially accurate responses often

Confabulation inaccurately localized in time (Victor & Ropper, 2001).
Fantastic or productive confabulations have been described
FARZIN I RANI 1, DAVID J. L IBON 2 as more elaborate fictitious stories (Berlyne, 1972).
1
University of Pennsylvania Further distinctions have been made between confabula-
Philadelphia, PA, USA tions that are provoked by direct questions, often in the
2
Drexel Medical College context of memory testing, or spontaneous confabulations
Philadelphia, PA, USA occurring without any external trigger (Kopelman, 1987).
The boundaries between provoked/spontaneous and
momentary/fantastic confabulations are often blurred,
Description with many authors mixing these characteristics when
describing the symptoms. Some have argued against
Korsakoff initially described pseudo-reminiscences in such categorizations and instead suggested that confabu-
alcoholic patients with amnesia who made up fictitious lation should be regarded as a continuous variable,
stories about events that did not occur. In their translation ranging from minor distortions to more dramatic
of Kosakoff s original work, Victor and Yakovlev note that fantasies (Metcalf et al., 2007).
Korsakoff first identified patients with a psychic disorder
in conjunction with multiple neuritis who presented
with a derangement of memory and of the association
of ideas along with other symptoms of the now well- Neuropsychology of Confabulation
known Korsakoff syndrome (Korsakoff, 1955). Later, the
term confabulation was introduced and defined as the Studies using neuropsychological test performance to
falsification of memory occurring in clear consciousness examine mechanisms of confabulation have not yielded
in association with an organically derived amnesia consistent results. Observations of perseverative responses
(Berlyne, 1972). It has also been referred to as true in individuals who confabulate have implicated frontal
memories that have been misplaced in both time and executive dysfunction (e.g., Kopelman, Stanhope, &
place (Kopelman, 1987) as well as the spontaneous Kingsley, 1997). Others have argued for more prominence
narrative reports of events that never happened. More of memory impairments rather than executive dys-
recently, confabulation has been defined as statements or function (e.g., Dalla Barba, 1993). A combination of
actions that involve distortions of memories (Metcalf, executive and memory deficits may be involved. Memory
Langdon & Coltheart, 2007). impairment may explain the presence or absence of
Confabulation, as a symptom, has been described in a confabulation, but the severity of confabulation may be
number of disorders including strokes (particularly influenced by the extent of executive dysfunction (Fischer,
anterior communicating artery), traumatic brain injuries, Alexander, DEsposito, & Otto, 1995). Clinical lesion
dementia, metabolic disorders, and psychiatric disorders. studies have implicated the medial prefrontal cortex in
Confabulations are mentioned as a probable symptom in spontaneous confabulations, particularly the orbitofrontal
most of the descriptions of Korsakoff s syndrome despite region (Schnider, 2003). Damage to limbic structures
ambiguous clinical diagnostic guidelines (Borsutzky, involved in memory is also likely to be required for
Fujiwara, Brand, & Markowitsch, 2008). For instance, confabulations to occur (Fischer et al., 1995). The litera-
the ICD-10 mentions confabulations as a probable but ture on anterior communicating artery aneurysms
not obligatory symptom for diagnosing an Alcohol- (ACoA) has implicated frontal structures as a necessary
Induced Amnesic Syndrome while the DSM-IV site of neuropathology in confabulation, although cases of
(American Psychiatric Association, 1994) does not nonamnestic ACoA patients with frontal lesions who do
include confabulations in its guidelines for diagnosing not confabulate have suggested that both frontal lobe and
Alcohol-Induced Amnesic Syndrome. basal forebrain structures may be needed for spontaneous
confabulations (DeLuca & Diamond, 1995).
Four types of cognitive models have been proposed to
account for confabulations:
Categorization
1. Source monitoring theory. This view was initially
There are different descriptions of confabulation used by promoted by Johnson, Hashtroudi, and Lindsay
several authors. Momentary confabulations have been (1993) who argued that individuals who confabulate
Confabulation C 669
are unable to accurately monitor the source of their 4. Three-factor cognitive-neuropsychological theory.
memories which results in errors and confusion. Metcalf et al. (2007) propose a 3-factor combined
According to this view, patients who confabulate can- model that hypothesizes interplay between an execu-
not accurately identify where or when events occur. tive control retrieval deficit, an evaluation deficit, and
They may also be unable to differentiate between a persons individual emotional/motivational biases. C
whether a representation is real or not due to Specifically, according to this view confabulatory
impairments in being able to access qualitative symptoms and content are the result of a failure of
characteristics of the representation such as details executive control that causes an impaired search and
about perceptual, contextual, affective, and semantic selection of appropriate memories from the autobio-
information. Furthermore, secondary evaluation graphical episodic memory store. Confabulators are
deficits may also lead to the over-inclusive acceptance purportedly unable to critically evaluate material from
of memories. their autobiographical or general semantic store and
2. Temporal context theory. Dalla Barba, Mantovan, accept confabulations as real memories. Further,
Cappelletti, and Denes (1998) have suggested that the personal biases may be involved in the preferential
primary impairment in confabulation is a difficulty selection of memories that are emotionally biased.
with temporal consciousness. According to this
view, patients who confabulate are confused about the
temporal order of information retrieved from memory. Evaluation
While knowledge of time is preserved and patients are
aware of a past, present, and future, they are unable to Since Korsakoff s initial description in 1955 of pseudo-
make correct temporal judgments about their mem- reminiscences in alcoholic patients with amnesia who
ories, resulting in sequencing errors. Schnider (2003) made up fictitious stories about events that did not
has also argued that there is confusion between pres- occur, there has been considerable variability in how con-
ently relevant and irrelevant memories, resulting in a fabulation is defined, identified, assessed, and understood.
failure to suppress activated but presently irrelevant For instance, it remains debated whether confabulations
memory traces. Neuroanatomically, Schnider et al. are readily differentiated from delusions. Some have ar-
have linked confabulation with the posterior orbito- gued that confabulations are not different from delusions
frontal cortex and the anterior limbic structures di- since both are held firmly over time. Others have viewed
rectly connected with it. Schnider argues that the confabulations, delusions, hallucinations, and insight as
adaptation of thought and behavior to ongoing reality part of a continuum. Still others have argued that delu-
is mediated by the anterior limbic system which acts sions and confabulations differ since confabulations tend
by suppressing activated memory traces that do not to be associated with partially valid memories that can be
pertain to ongoing reality. In patients who confabu- traced to real events. Further debate ensues about whether
late, this monitoring of ongoing reality in thought confabulations are deliberate attempts to compensate for
goes awry and appears to be related to the brains memory gaps due to embarrassment or whether they
reward system. involve source monitoring, temporal context, or retrieval
3. Retrieval theory. This view has been primarily promoted difficulties that result in an implausible or fictional out-
by Moscovitch and Melo (1997) who argue that put. Confabulation, particularly following ACoA aneur-
deficient strategic retrieval processes and monitoring ysms has also been viewed as representing differences in
deficits influence confabulation. Specifically, confabu- degree and not kind. Other important variables identi-
lation is thought to be the result of a faulty strategic fied in the understanding of confabulation have included
retrieval search and inaccurate ordering and making the distinction between an unaware or
placement of memories in context. According to this aware process, premorbid personality factors, the
view, strategic retrieval is dependent upon executive need for coexistence of amnesia, differentiation from
processes and is self-initiated and goal-directed, while an acute confusional state, disconnection syndrome,
associative retrieval is automatic and independent of and whether indifference/apathy or deceit/lying is
executive processes. Confabulators are thought to involved (DeLuca, 2000). There has been further varia-
show deficiencies in strategic retrieval, influenced by bility in decisions on how to label an individual as a
deficiencies in the neocortical/prefrontal/hippocampal confabulator. Some have used the term based on clinical
network hypothesized to be involved in strategic observations of spontaneous or provoked production of
retrieval. fabricated stories following brain injury. Other researchers
670 C Confabulation
have labeled individuals as confabulators based on the num- Cross References

ber, or quality of intrusions/confabulations produced dur-
ing standardized neuropsychological tests or experimental Capgras Syndrome
tasks. Overall, the concept of confabulation remains elusive Delusion
and its underlying mechanisms remain an area requiring Intrusion Errors
further understanding. Reduplicative Paramnesia
WernickeKorsakoff Syndrome
Treatment
Treatment is determined in part by etiology. Some have References and Readings

proposed that rehabilitation efforts should avoid mem-
American Psychiatric Association: Diagnostic and Statistical Manual of
ory training and repeated questions about orientation.
Mental Disorders, Fourth Edition, Text Revision. Washington, DC,
For instance, according to Schnider (2003) it may be American Psychiatric Association, 2000.
easier for a confabulating patient to accept that her Berlyne, N. (1972). Confabulation. The British Journal of Psychiatry,
baby has already received food than to convince her that 120(554), 3139.
her baby is over 30 years old. Instead, it may be more Borsutzky, S., Fujiwara, E., Brand, M., & Markowitsch, H. J. (2008).
Confabulations in alcoholic Korsakoff patients. Neuropsychologia,
beneficial to promote the engagement of patients in com-
46(13), 31333143.
mon everyday activities and accept their false interpreta- Dalla Barba, G. (1993). Different patterns of confabulation. Cortex, 29(4),
tion of reality until spontaneous confabulations resolve 567581.
(Schnider). Many spontaneous confabulations eventually Dalla Barba, G., Mantovan, M. C., Cappelletti, J. Y., &
resolve. In a study of eight spontaneous confabulators, Denes, G. (1998). Temporal gradient in confabulation. Cortex, 34
(3), 417426.
almost all stopped confabulating 18 months later and
DeLuca, J. (1992). Rehabilitation of confabulation: The issue of unaware-
regained correct orientation in time and place, as well as ness of deficit. NeuroRehabilitation, 2(3), 2330.
the ability to refer thinking and acting to ongoing reality DeLuca, J. (2000). A cognitive neuroscience perspective on confabulation.
(Schnider, Ptak, von Daniken, & Remonda, 2000). Specif- Neuro-Psychoanalysis, 2(2), 119132.
ically, temporal context confusion based on an inability DeLuca, J., & Diamond, B. J. (1995). Aneurysm of the anterior
communicating artery: A review of neuroanatomical and neuropsy-
to suppress intrusions of currently irrelevant memory
chological sequelae. Journal of Clinical and Experimental Neuropsy-
traces into ongoing thinking paralleled the course of chology, 17(1), 100121.
spontaneous confabulations in this study. Patients with DeLuca, J., & Locker, R. (1996). Cognitive rehabilitation following
isolated, less extensive, orbitofrontal lesions stopped con- anterior communicating artery aneurysm bleeding: A case report.
fabulating within a few weeks and had the best neuropsy- Disability and Rehabilitation, 18(5), 265272.
Fischer, R. S., Alexander, M. P., DEsposito, M., & Otto, R. (1995).
chological outcomes. Patients with additional basal
Neuropsychological and neuroanatomical correlates of confabula-
forebrain lesions continued to confabulate for several tion. Journal of Clinical and Experimental Neuropsychology, 17(1),
months and remained amnestic. One patient with exten- 2028.
sive orbitofrontal damage and perirhinal cortex damage Johnson, M. K., Hashtroudi, S., & Lindsay, D. S. (1993). Source moni-
continued to confabulate after more than 3 years. Inter- toring. Psychological Bulletin, 114(1), 328.
Kopelman, M. D. (1987). Two types of confabulation. Journal of Neuro-
disciplinary approaches for the rehabilitation of confabu-
logy, Neurosurgery, and Psychiatry, 50(11), 14821487.
lation in the treatment of patients with ACoA aneurysms Kopelman, M. D., Stanhope, N., & Kingsley, D. (1997). Temporal
have also been suggested, including a three-tiered ap- and spatial context memory in patients with focal frontal,
proach focused on improving (1) intellectual awareness, temporal lobe, and diencephalic lesions. Neuropsychologia, 35(12),
the ability to understand that one has an impairment, (2) 15331545.
Korsakoff, S. S. (1955). Psychic disorder in conjunction with peripheral
emergent awareness, the ability to recognize a problem
neuritis, Neurology, 5, 394406.
when it is occurring, and (3) the ability to anticipate that a Metcalf, K., Langdon, R., & Coltheart, M. (2007). Models of confabula-
problem (confabulation) is going to occur (DeLuca, tion: A critical review and a new framework. Cognitive Neuropsy-
1992). In one case, improvements in executive function- chology, 24(1), 2347.
ing using this rehabilitation approach removed obstacles Moscovitch, M., & Melo, B. (1997). Strategic retrieval and the frontal
lobes: Evidence from confabulation and amnesia. Neuropsychologia,
to vocational activity and social functioning by improving
35(7), 10171034.
the patients awareness of his difficulties and enabling Schnider, A. (2003). Spontaneous confabulation and the adaptation of
utilization of compensatory strategies (DeLuca & Locker, thought to ongoing reality. Nature Reviews. Neuroscience, 4(8),
1996). 662671.
Conflict C 671
Schnider, A., Ptak, R., von Daniken, C., & Remonda, L. (2000). Recovery References and Readings
from spontaneous confabulations parallels recovery of temporal
confusion in memory. Neurology, 55(1), 7483.
American Psychological Association. (2002). Ethical principles of psychol-
Victor, M., & Ropper, A. H. (Eds.). (2001). Principles of neurology
ogists and code of conduct. American Psychologist, 57, 10601073.
(7th ed.). New York: The McGraw-Hill Companies, Inc.
Committee on Ethical Guidelines for Forensic Psychologists (1991).
Specialty guidelines for forensic psychologists. Law and Human C
Behavior, 15, 655665.
Confidentiality Psychological evaluations for the courts (3rd ed.). New York: Guilford.
Chicago, IL, USA
Confirmatory Bias
M OLLY E. Z IMMERMAN
Albert Einstein College of Medicine
Definition
Bronx, NY, USA
Confidentiality has been defined as containing informa-
tion whose unauthorized disclosure could be prejudicial to
the national interest. In psychology, it is one of the most
Definition
important components of the Ethical Principles of Psychol-
Confirmatory bias occurs when a clinician preferentially
ogists and Code of Conduct (2002) and the Specialty
accepts or seeks evidence that confirms an initial hypoth-
Guidelines for Forensic Psychologists (1991). The bound-
esis at the expense of thorough consideration of emerging
aries of confidentiality vary based on the setting, that is,
contradictory evidence (Garb, 2003). For example, a cli-
whether it is in the clinical versus forensic realm and
nician may formulate an initial impression that a client
whether it is in the civil versus criminal realm. In treatment
has dementia based on a referral question. During the
settings, clinicians consider confidentiality of paramount
clinical interview, the clinician may focus on questions
importance and they are reluctant to disclose information
relating to memory and change in activities of daily living
obtained from a client even when there are explicit legal or
while failing to ask questions that specifically pertain
countervailing ethical mandates to do so (such as when a
to differential diagnoses, such as major depressive
patient may harm another). Such a position is unrealistic in
disorder. In neuropsychological settings, this generally
the forensic context because the results of forensic evalua-
unintentional bias may impair judgment, hamper
tions (be it civil or criminal) are routinely disclosed to third
decision-making, produce false reports, and negatively
parties. In both clinical and forensic contexts, psychologists
impact the assessment approach and interpretation of
provide examinees with adequate informed consent
findings. To address this bias, the clinician should system-
prior to engaging in the examination. In the forensic con-
atically review all available data within a hypothesis-
text, it is the duty of forensic psychologists to inform clients
testing framework in an effort to remain as impartial as
of their legal rights regarding the purpose of an evaluation,
possible (Weiner & Greene, 2007).
the anticipated forensic service, the nature of procedures to
be utilized, the limits of confidentiality, who has retained
the examiner for the evaluation, who the report may be References and Readings
directed to, and that anything which is said during the
examination could be included in a report or come up Garb, H. N. (2003). Clinical judgment and mechanical prediction. In
during deposition or trial testimony. Some jurisdictions I. B. Weiner, D. K. Freedheim, M. Gallagher, J. A. Schinka, & R. J.
do not provide for confidentiality of mental health evalua- Nelson (Eds.), Handbook of psychology (pp. 2742). New York: Wiley.
Weiner, I. B., & Green, R. L. (2007). Handbook of personality assessment.
tions. For example, when an evaluation is conducted as a
New York: Wiley.
result of direct court order, confidentiality is not provided.
Cross References Conflict

Privilege Contraindication
672 C Conformal Techniques
Conformal Techniques Confrontation Naming

Involved Field Radiotherapy A NASTASIA R AYMER
Old Dominion University
Norfolk, Virginia, USA
Confound
Confounding Variables Synonyms
Word finding
Confounding Variables
J AMES H. B ANOS
Definition
University of Alabama at Birmingham
Confrontation naming involves the selection of a specific
Birmingham, AL, USA
label corresponding to a viewed stimulus, usually a
picture, of a viewed object or action. Confrontation
naming also refers to a type of task used in assessment
Synonyms
when problems with naming are of concern.
Confound; Extraneous variable; Lurking variable
Current Knowledge
Definition
Confrontation naming tasks often are incorporated as part
A confounding variable is an extraneous variable that
of clinical language testing to detect impairments of word-
obscures the true relation between two other variables or
finding abilities in individuals with various types of neuro-
groups of interest. In experimental research designs, a con-
logic impairments typically affecting the left hemisphere of
founding variable often presents as an unintended
the brain (Spreen & Risser, 2003). Although word finding
or undesirable systematic difference between groups
takes place during the course of sentence generation in
(the independent variable) that is also systematically related
conversational speech, it is most often tested clinically in
to the outcome of interest (dependent variable). It hinders
confrontation naming tasks where the vocabulary tested is
the ability to infer a causal relation between the variables
constrained to known, identified target words. Therefore,
and can lead to misattributing a causal effect to the inde-
word-finding functions are at times referred to as naming
pendent variable (a threat to internal validity). Potential
abilities (e.g., Chialant, Costa, & Caramazza, 2002).
confounding variables are most effectively addressed during
The most common published test of confrontation
study design (e.g., via random assignment, case control
naming is the Boston Naming Test (Kaplan, Goodglass,
matching), but may be addressed to some extent during
& Weintraub, 2001); other published confrontation
statistical analysis (e.g., handled as a covariate).
naming tests also exist for use in children and adults
with word-finding difficulties (An Object and Action
Cross References Naming Battery, Druks, & Masterson, 2000; Test of
Adolescent/Adult Word Finding, German, 1990). Con-
Analysis of Covariance (ANCOVA)
frontation naming tests assess the ability to retrieve
Error, Sources of
different types of words, including pictures of objects to
test noun retrieval, or pictures of actions to test verb
References and Readings retrieval. Although most tests of confrontation naming
test stimuli from a variety of semantic categories, some
Kazdin, A. E. (Ed.). (2003). Methodological issues & strategies in clinical
tests can differentiate pictures according to the semantic
research (3rd ed.). Washington, DC: American Psychological
Association.
category to which they belong, including pictures from a
Pearl, J. (2009). Causality: Models, reasoning, and inference. Cambridge: variety of natural categories such as animals, fruits, and
Cambridge University Press. vegetables, and man-made categories such as furniture,
Congestive Heart Failure C 673
clothing, tools, and transportation (e.g., Goodglass, Definition

Kaplan, & Barresi, 2001).
Congestive heart failure (CHF) or heart failure is a condi-
tion in which the heart muscle is unable to pump suffi-
Cross References
cient blood to adequately supply the bodys organs. C
Anomia
Anomic Aphasia
Current Knowledge
References and Readings Common causes of CHF include coronary artery disease,
myocardial infarction, hypertension, cardiac valve dis-
Chialant, D., Costa, A., & Caramazza, A. (2002). Models of naming. ease, cardiomyopathy (heart muscle disease), congenital
In A. E. Hillis (Ed.), The handbook of adult language disorders heart disease, and endocarditis (heart infection). In CHF,
(pp. 123142). New York: Psychology Press. the heart continues to pump, but exercise and activity
Druks, J., & Masterson, J. (2000). An object and action naming battery.
cause shortness of breath (dyspnea on exertion or
Hove, UK: Psychology Press.
German, D. J. (1990). Test of adolescent/adult word finding. Austin, TX: DOE), fatigue, weakness, light-headedness, or syncope.
Pro-Ed. Because the heart is not pumping the blood completely
Goodglass, H., Kaplan, E., & Barresi, B. (2001). The assessment of aphasia and effectively, the blood backs up into the heart
and related disorders (3rd ed.). Philadelphia, PA: Lippincott, chambers, and ultimately into the venous system. This
Williams & Wilkins.
causes congestion of the tissues, and edema in the legs
Kaplan, E., Goodglass, H., & Weintraub, S. (2001). The Boston naming
test. Philadelphia: Lippincott, Williams & Wilkins. and internal organs, including the lungs (pulmonary
Laine, M., & Martin, N. (2006). Anomia: Theoretical and clinical aspects. edema), often resulting in shortness of breath, especial-
New York: Psychology Press. ly when lying supine (orthopnea). Electrocardiogram
Spreen, O., & Risser, A. H. (2003). Assessment of aphasia. Oxford: Oxford and certain blood tests are usually abnormal, and chest
University Press.
x-ray shows congestion of the lungs. Echocardiography
Tranel, D., Adolphs, R., Damasio, H., & Damasio, A. R. (2001). A neural
basis for the retrieval of words for actions. Cognitive Neuropsychology, is noninvasive and highly revealing, and has the potential
18(7), 655670. to provide a quantitative measure of severity of heart
failure as indicated by the proportion of blood in the left
ventricle that can be pumped out by the muscle (ejec-
tion fraction).
Congenital Defects CHF is a chronic condition with acute exacerbations
during which patients may experience moderate or signif-
Anencephaly icant distress. Chronic congestive heart failure can be
managed using a combination of interventions that help
the patient to compensate for the problems caused by
CHF. Acute pulmonary edema is a medical emergency.
Congenital Hypothryroidism Treatment of acute CHF episodes usually consists of rest,
salt reduction, identification, and removal of the precipi-
Hypothyroidism
tating factor (such as infection, cardiac arrhythmia, or
other cause), and the use of select medications that help
to improve the pumping ability (contractility) of the
Congestive Heart Failure heart muscle and the capacity of the blood vessels to
provide blood supply to other organs. These medications
E LLIOT J. R OTH include angiotensin-converting enzyme inhibitors, beta-
Northwestern University blockers, digoxin, diuretics (water pills), and vasodilators.
Chicago, IL, USA At times, valve disease warrants valve replacement sur-
gery, and extremely severe heart damage may require
cardiac transplantation to prevent death. Usually, mild
Synonyms to moderate congestive heart failure can be treated with
medications, adjustments of exercise and activity levels,
Heart failure and medical supervision.
674 C Conjugate Gaze
Cross References can result, which can then cause diplopia. The mechan-
isms for horizontal eye movements are better understood
Coronary Disease than vertical eye movements. As individuals age, the abil-
Echocardiogram ity to look upward tends to decline. Cerebral structures
control when and where the eyes move, and the brain
stem structures control how they move.
References and Readings The centers for lateral conjugate gaze are in the frontal
and occipital cortices. In the frontal lobe, this area is in the
Jessup, M., Abraham, W. T., Casey, D. E., Feldman, A. M., Francis, G. S., posterior aspect of the frontal lobes, referred to as the
Ganiats, T. G., et al. (2009). Focused update: ACCF/AHA guidelines frontal eye fields. This area is close to the motor strip.
for the diagnosis and management of heart failure in adults: A report The function of the frontal centers is to control voluntary
of the American College of Cardiology Foundation/American Heart
conjugate eye movements to the opposite side. The frontal
Association Task Force on Practice Guidelines, Developed in collab-
oration with the International Society for Heart and Lung Trans-
eye fields (FEF) receive inputs from peristriate, parietal
plantation. Circulation, 119, 19772016. and superior temporal cortex, medial pulvinar, and the
dorsomedial nucleus of the thalamus. Stimulation of FEF
results in contralateral saccades. In strokes that affect this
area, one may see an eye deviation toward the side of the
lesion and away from the paralyzed limb. This usually
Conjugate Gaze occurs only in the acute phase of an infarct. At some
point, the patient may be unable to move the eyes away
M ARY-E LLEN M EADOWS from the lesion on command. However, they may be able
Brigham and Womens Hospital to follow an object to the opposite side if the occipital lobe
Boston, MA, USA center is not damaged. The occipital lobe centers for
lateral conjugate gaze control eye movement when an
individual is following an object to the opposite side.
Synonyms Lesions of the occipital lobe that control lateral conjugate
gaze are less common than lesions of the frontal centers.
Eye movements; Versional movements Conjugate gaze can be disrupted by stroke or trauma,
depending on the location of the damage. For instance, an
intracerebral hemorrhage in the caudate nucleus or puta-
Definition men will cause conjugate deviation of eye movements to the
side of the lesion. Pineal tumors, which can press upon the
Conjugate gaze is the ability of the eyes to work together midbrain, can cause paralysis of upward gaze. Deeper dam-
or in unison. It refers to the motion of both eyes in the age can affect downward saccades. Given the extensive
same direction at the same time. The eyes can look later- anatomy of control of the visual system, damage or dys-
ally (left/right), upward, or downward. Disorders in con- function along any of the nuclei or tracts integral to eye
jugate gaze refer to the inability to look in a certain movements can result in abnormalities. Eye movements
direction with both eyes. utilize the basal ganglia and cerebellum in their planning
and coordination. Patients with basal ganglia disorders may
have involuntary, small, or slow eye movements. Patients
Current Knowledge with parkinsonian symptoms may have a restriction of
upgaze. In patients with progressive supranuclear palsy, a
Conjugate gaze is mediated in the brain stem by the cardinal feature is the restriction of upgaze, and these
medial longitudinal fasciculus, which is a nerve tract patients initially complain of difficulties with reading. The
that connects the abducens, trochlear, and oculomotor flocculus of the cerebellum is important for suppression of
nuclei. These nuclei, in turn, are responsible for the mus- vestibular reflex and for smooth pursuit movements. Parts
cles that control eye movements. The left pontine center of the vermis help to coordinate saccades, and damage can
connects with the right frontal center for conjugate gaze result in dysmetric saccades. Patients with long-standing
to the left, and the right pontine center connects with the frontal lobe lesions cannot inhibit inappropriate saccades
left frontal center for conjugate gaze to the right. If extrao- from a fixation to a peripheral, visually attractive stimulus
cular muscles are not working properly, dysconjugate gaze that appears suddenly. Frontal seizures with a focus in or
Conners 3rd Edition (Conners 3; Conners 2008) C 675
near one eye field may manifest by turning of the eye and from the individual. These are critical for binocular single
head away from the side of the lesion. vision and depth perception.
Evoked eye movements (dolls eye test or oculocepha-
lic reflex) and the caloric response can be used in the
examination of an unresponsive patient. However, if a Cross References C
patient is in a comatose state due to drug intoxication
or hypothermia, these tests may show no response. The Dysconjugate Gaze
assessment is as follows: Lateral Gaze Palsy
Dolls eye test This test can be used in either the Saccadic Eye Movements
comatose or conscious patient. Hold the patients eyes
open and rapidly move/rotate the head to one side and
hold it there. If the brain stem reflexes are intact, the eyes References and Readings
will move conjugately in the direction opposite to the head
rotation. If the injury is in the brain stem, the eyes do not Lavin, P. J. M., & Weissman, B. (2000). Neuro-Opthalmology. In W. G.
Bradley, R. B. Daroff, G. M. Fenichel, & C. D. Marsden (Eds.),
move. If a patient is conscious and can follow commands,
Neurology in clinical practice: Principles of diagnosis and management.
have them fixate on an object. This test should not be used Boston, MA: Butterworth-Heinemann.
in a patient who has possible cervical injuries. Marshall, K. G. (2006). Cranial nerve III, IV and VI: Disorders of conju-
Caloric test This test can be done in the comatose gate Gaze. Patient Care Canada, 17, 5157.
patient. The patients ear canal is irrigated with 20 ml of Ross, R. T. (1999). How to examine the nervous system (3rd ed.). Stamford,
CT: Appleton and Lange.
ice-cold water. The eyes should move toward the ear that
is irrigated. If the patients eyes do not move, the lesion is
in the brain stem. This test should not be used in a patient
who has possible cervical injuries, or who has blood in the
ear canal or a perforated eardrum. Connectionist Model of Aphasia
Conjugate eye movements allow the eyes to get an
image onto the fovea and keep it there. Fast movements WernickeLichtheim Model of Aphasia
or saccades allow images onto the fovea and slower move-
ments keep them there. Smooth pursuit movements com-
pensate for target movement. There are several ocular
motor systems: Connective Tissue Disease
Saccadic system moves the eyes rapidly (up to 800 /s)
in order to fixate on new targets in the visual fields. These Collagen Vascular Disease
can be voluntary or a response to a verbal command.
Reflex saccades can also occur to stimuli that are threat-
ening or to a sound in the periphery.
Pursuit system enables the eyes to track slowly moving
targets (approximately 70 /s) so the image is stable on the Conners 3rd Edition (Conners 3;
fovea. Conners 2008)
Vestibular eye movement subsystem maintains a stable
image on the retina during head movements. The vesti- C. K EITH C ONNERS 1, J ENNI P ITKANEN 2, S ARA R. R ZEPA 2
1
bulo ocular reflex maintains the eyes in the same direction Duke University Medical School
in space during head movements. This is controlled by the Durham, North Carolina, USA
2
semicircular canals, which respond to rotational accelera- Multi-Health Systems Inc.
tion of the head. Toronto, Ontario, Canada
Optokinetic system complements the vestibular eye
movement system. It uses reference points in the environ-
ment to maintain orientation. This system uses fixation Description
and pursuit in humans.
Vergence system enables the eyes to move dysconju- The Conners 3rd Edition (Conners 3; Conners, 2008), the
gately (converge and diverge) in the horizontal axis to latest version of the Conners Rating Scales, is a thorough
maintain fixation on a moving target toward or away assessment of attention deficit/hyperactivity disorder
676 C Conners 3rd Edition (Conners 3; Conners 2008)
(ADHD) and its most commonly associated problems (including all three ADHD subtypes: ADHD predomi-
and disorders in school-aged youth. The Conners 3 is a nantly inattentive type, ADHD predominantly hyperac-
multi-informant assessment with forms for parents, tive-impulsive type, and ADHD combined type),
teachers, and youth. Parent and teacher ratings can be disruptive behavior disorders, learning disorders, anxiety
obtained about youth aged 618 years, and youth aged disorders, major depressive disorder, bipolar disorder, and
818 years can complete the self-report. pervasive developmental disorders.
The assessment features multiple content scales that
assess ADHD-related concerns such as inattention and
hyperactivity as well as related problems in executive func- Historical Background
tioning, learning, aggression, and peer/family relations.
Symptoms of distinct diagnoses can be assessed with scales The first versions of the Conners Parent and Teacher
that link directly to the Diagnostic and Statistical Manual Rating Scales were developed at the Harriet Lane Clinic
of Mental Disorders (DSM-IV-TR; American Psychiatric of the John Hopkins Hospital in the 1960s during
Association, 2000) symptomatic criteria for ADHD, con- Dr. Leon Eisenbergs controlled studies of psychotherapy
duct disorder (CD), and oppositional defiant disorder and medications. The purpose of the original scales was to
(ODD). Anxiety and Depression Screener items are also serve as the basis for a detailed interview about a childs
included in order to provide coverage of two internalizing problems. The first version of the parent scale contained
problems frequently associated with ADHD. The Conners items grouped in terms of problems (e.g., sleep, eating,
3 also provides two index scores: the Conners 3 ADHD temper, friendships, school). The teacher scale included
Index and the Conners 3 Global Index. The assessment items related to functioning within the classroom setting
also includes validity scales (positive impression, negative (e.g., group participation, attitude towards authority).
impression, and inconsistency index), severe conduct crit- The earliest research studies on the scales supported the
ical items, impairment items (home, school, and social research properties of the scales. For example, the very
settings), and open-ended additional questions (addition- first study on the teacher scales (Conners, 1969) demon-
al concerns, strengths). strated adequate test-retest reliability. In addition, good
The Conners 3 offers full-length, short, and index form sensitivity to drug treatment and nondrug therapy effects
options. The full-length forms convey the most detailed were established.
information of all the forms. The short forms are useful The scales were first formally published in 1989 as the
when the administration of the full-length version is not Conners Rating Scales (CRSTM, Conners, 1989, 1990) and
possible or practical (e.g., when multiple administrations offered a standard format with normative data, detailed
over time are required). The index forms are useful in information about the psychometric properties and the
screening and treatment monitoring situations. Adminis- proper use of the scales, and the hand-scorable
tration requires approximately 20 min for the full-length QuikScoreTM form allowing for easy administration
forms, 10 min for the short forms, and approximately 5 and scoring. The CRS was later revised (CRS-R; Conners,
min for the index forms. Raw scores are converted to age- 1997) to offer a self-report component and scales
and gender-based standard scores (including T-scores and linked to the Diagnostic and Statistical Manual of Mental
percentiles). Results from the DSM-IV-TR symptom Disorders Fourth Edition (American Psychiatric Associ-
scales are also reported in terms of symptom counts, ation, 1994) criteria for ADHD. The Conners 3, the latest
that is, whether or not the minimum symptom require- revision of the Conners Rating Scales, incorporates the
ments set by the DSM-IV-TR have been met. The Conners key features of its predecessors with updated normative
3 ADHD Index produces a probability score, which indi- data and psychometric properties, an age range specific
cates whether the youths scores are more like youth with to the assessment of school-aged children, and an
ADHD, or with those from the general population. increased focus on the assessment of ADHD, associated
The Conners 3 normative sample consists of 3,400 features, and the disorders most commonly comorbid
assessments (1,200 parent, 1,200 teacher, and 1,000 with ADHD.
self-report assessments) including 50 boys and 50 girls
from each age (618 years for the parent and teacher
report, 818 years for the self-report). The racial/ethnic Psychometric Data
distribution of this sample closely matches the US
population. Approximately 2,100 clinical cases were also Results of reliability analyses revealed that the Conners 3
collected from youth with following diagnoses: ADHD forms have high levels of internal consistency, with
Conners 3rd Edition (Conners 3; Conners 2008) C 677
Cronbachs alpha ranging from 0.77 to 0.97 (mean Clinical Uses

Cronbacha alpha = 0.90), and excellent temporal stability,
with test-retest correlations ranging from 0.71 to 0.98 The Conners 3 can be used as an assessment tool as well as
(mean r = 0.83, all correlations, p < 0.001). There is also a in planning and monitoring treatment plans. Standar-
great deal of consistency between multiple parent and/or dized scores allow for the objective comparison of an C
teacher ratings of the same youth, with inter-rater reliabil- individual with age- and gender-based expectations.
ity coefficients ranging from 0.52 to 0.94 (mean r = 0.77, Correspondence of items with DSM-IV-TR symptomatic
all correlations, p < 0.001). criteria for ADHD, CD, and ODD in combination with
The Conners 3 Manual reports a variety of studies information about associated features and level of
demonstrating convergent/divergent validity through cor- impairment facilitates differential diagnosis decisions in
relations of Conners 3 scales scores with other related clinical practice. The Conners 3 offers a scoring feature,
measures of childhood psychopathology. Overall, scales which links the assessment results to areas of eligibility
that assess similar constructs tended to be moderately to under the Individuals with Disabilities Improvement Act
strongly intercorrelated, while scales that did not assess of 2004 (IDEA 2004) making the assessment useful for
similar constructs tended to have smaller correlations. identification of appropriate educational classification
Table 1 provides highlights from these analyses. and/or services for students in the public school system.
Results from discriminative validity analyses indicated The Conners 3 can also be used as an assessment tool in
that the Conners 3 scores accurately discriminate between screening and research contexts.
relevant groups. Results from a series of multivariate In addition to being an assessment tool, the Conners
analysis of covariance revealed that, for all scales, the 3 forms can be employed as a tool for planning, monitoring,
means for the target clinical groups were significantly and evaluating treatment plans. Elevated scores from the
higher than the means for the general population Conners 3 suggest areas to target in treatment, with individ-
and other clinical groups (e.g., youth diagnosed with ual item responses can be used to guide decisions about
ADHD, predominantly hyperactive-impulsive type scored specific behaviors requiring intervention. The assessment
significantly higher on the hyperactivity/impulsivity and can also be used in treatment monitoring situations, for
ADHD hyperactive-impulsive scales than did youth example to monitor the effectiveness of an individuals re-
without a clinical diagnoses, as well as youth diagnosed sponse to treatment or to evaluate an intervention program.
with other disorders). The sizes of the group membership The Conners 3, at the time of writing, is too recent to
effects (as determined with partial Z2) were moderate to have generated research literature, but empirical studies
large, on average, accounting for 19.1% of the variance in with earlier versions of the forms have demonstrated
scores. In terms of the classification accuracy of the scores the utility of the assessment in treatment outcome studies,
(as determined by a series of discriminant function epidemiological and etiological studies of ADHD and other
analyses), the mean overall correct classification rate was behavior problems, construct and discriminative validity
75.6% across all forms. studies, correlational studies, and cross-cultural studies.
Conners 3rd Edition (Conners 3; Conners 2008). Table 1 Overview of Correlations between the Conners 3 and Other Measures
Conners 3 scales Other measures r (range)

Inattention, ADHD inattentive BASC-2: Attention problems 0.520.89
ASEBA: Attention problems 0.720.96
Hyperactivity/Impulsivity, ADHD BASC-2: Hyperactivity 0.410.91
hyperactive-impulsive BRIEF: Inhibit 0.760.92
Executive functioning BASC-2: Executive functioning 0.430.68
BRIEF: Plan/Organize 0.700.87
Aggression, conduct disorder, oppositional BASC-2:Aggression 0.590.95
defiant disorder ASEBA: Aggressive behavior 0.580.93
Peer relations ASEBA: Social problems 0.720.84
Note. All rs significant, p <.05. BASC-2 = Behavior Assessment System for Children, Second Edition; ASEBA = Achenbach System of Empirically
Based Assessment; BRIEF = Behavior Rating Inventory of Executive Function.
678 C Conners Comprehensive Behavior Rating Scale
Cross References compulsive behaviors, violence potential, and physical

symptoms. Scales are also included to assess the Diagnostic
Attention Deficit Hyperactivity Disorder and Statistical Manual of Mental Disorders (DSM-IV-TR;
Conners Comprehensive Behavior Rating Scales American Psychiatric Association; APA, 2000) diagnostic
Conners Continuous Performance Test-II criteria for symptoms of generalized anxiety disorder, sep-
Individuals with Disabilities Education Act aration anxiety disorder, social phobia, obsessive compul-
sive disorder, major depressive episode, manic episode
autistic disorder, Aspergers Disorder, attention deficit/hy-
References and Readings peractivity disorder (ADHD), conduct disorder, and oppo-
sitional defiant disorder. Other clinical indicators are also
included for other potential problem areas, including bul-
manual of mental disorders (4th ed., text Rev.). Washington, DC:
American Psychiatric Association. lying, enuresis/encopresis, panic attack, pervasive develop-
American Psychiatric Association. (1994). Diagnostic and statistical mental disorder, pica, post-traumatic stress disorder,
manual of mental disorders (4th ed.). Washington, DC: American specific phobia, substance use, tics, and trichotillomania.
Psychiatric Association. The assessment also includes the Conners Clinical Index
Conners, C. K. (1969). A teacher rating scale for use in drug studies with
(Conners CI), Severe Conduct and Self Harm Critical
children. American Journal of Psychiatry, 126, 884888.
Conners, C. K. (1997). Conners rating scales-revised technical manual. items, Validity scales (Positive Impression, Negative Im-
Toronto, Ontario, Canada: Multi-Health Systems. pression, and Inconsistency Index), Impairment items
Conners, C. K. (1989, 1990). Conners rating scales technical manual. (home, school, and social settings), and open-ended Addi-
Toronto, Ontario, Canada: Multi-Health Systems. tional Questions (additional concerns, strengths).
Conners, C. K. (2008). Conners 3rd edition manual. Toronto, Ontario,
In addition to the Conners CBRS form, the assessment
Canada: Multi-Health Systems.
Individuals with Disabilities Education Improvement Act of 2004 also offers the Conners CI as a standalone form. The Con-
(IDEA), Pub. L. No. 108446, 118 Stat. 2647 (2004). [Amending ners CBRS forms provide a comprehensive view of a youths
20 U.S.C. 1400 et seq.]. behavioral, social, emotional, and academic functioning.
The Conners CI is a brief 24-item index with items from
the Conners CBRS form that best differentiate youth with
a clinical diagnosis from youth in the general population.
Conners Comprehensive Administration requires approximately 25 min for the
Behavior Rating Scale Conners CBRS forms and 10 min for the Conners Clinical
Index form. Raw scores are converted to age- and gender-
C. K EITH C ONNERS 1, J ENNI P ITKANEN 2, S ARA R. R ZEPA 2 based standard scores (including T-scores and percen-
1
Duke University Medical School tiles). Results from the DSM-IV-TR symptom scales are
Durham, NC, USA also reported in terms of symptom counts, that is, whether
2
Multi Health Systems Inc. or not the minimum symptom requirements set by the
Toronto, ON, Canada DSM-IV-TR have been met. The Conners CI produces a
probability score, which indicates whether the youths
scores are more like youth with a clinical diagnosis
Description (disruptive behavior disorder, learning/language disorder,
mood disorder, anxiety disorder, or ADHD) or with those
The Conners Comprehensive Behavior Rating Scales from the general population.
(Conners CBRS; Conners, 2008) is a comprehensive The Conners CBRS normative sample consists of
assessment tool, which can be used to assess a wide range 3,400 assessments (1,200 parent, 1,200 teacher, and
of behavioral, emotional, social, and academic issues in 1,000 self-report assessments) including 50 boys and
school-aged youth. The Conners CBRS is a multi-infor- 50 girls from each age (618 years for the parent and teacher
mant assessment with forms for parents, teachers, and report, 818 years for the self-report). The racial/ethnic
youth. Parent and teacher ratings can be obtained about distribution of this sample closely matches the US
youth aged 618 years, and youth aged 818 years can population. Approximately 2,000 clinical cases were also
complete the self-report. The assessment features multiple collected from youth with following diagnoses: ADHD,
Content scales that assess emotional distress, aggressive disruptive behavior disorders, learning disorders, anxiety
behaviors, academic difficulties, hyperactivity/impulsivity, disorders, major depressive disorder, bipolar disorder, and
social problems, separation fears, perfectionistic and pervasive developmental disorders.
Conners Comprehensive Behavior Rating Scale C 679
Historical Background with test-retest correlations ranging from 0.56 to 0.96

(mean r = 0.81, all correlations, p < 0.001). There is also
The Conners CBRS is a new assessment tool, which is a great deal of consistency between multiple parent and/or
built on the foundation of the Conners Rating Scales. teacher ratings of the same youth, with inter-rater reliabil-
The Conners Rating Scales are a widely used and well ity coefficients ranging from 0.53 to 0.89 (mean r = 0.74, C
validated assessment of ADHD and related issues. When all correlations, p < 0.001).
updating and revising the latest version of the scales The Conners CBRS Manual reports a variety of stud-
(Conners 3rd Edition; Conners, 2008), the need for a ies demonstrating convergent/divergent validity through
comprehensive assessment of behavioral, social, emotional, correlations of Conners CBRS scales scores with other
and academic concerns became evident. The Conners related measures of childhood psychopathology. Overall,
CBRS was therefore developed to provide clinicians with scales that assess similar constructs tended to be moder-
an assessment and treatment planning/monitoring tool, ately to strongly intercorrelated, while scales that did not
which would address a broad range of clinical issues in assess similar constructs tended to have smaller correla-
school-aged youth and which could be linked to diagnos- tions. Table 1 provides highlights from these analyses.
tic and intervention systems such as the DSM-IV-TR Results from discriminative validity analyses indicated
(APA, 2000) and Individuals with Disabilities Education that the Conners CBRS scores accurately discriminate
Improvement Act of 2004. between relevant groups. Results from a series of multi-
variate analysis of covariance revealed that, for all scales,
the means for the target clinical groups were significantly
Psychometric Data higher than the means for the general population and
other clinical groups (e.g., youth diagnosed with a disrup-
Results of reliability analyses revealed that the Conners tive behavior disorder scored significantly higher on the
CBRS assessments have high levels of internal consistency, Aggressive Behavior and Violence Potential scales than
with Cronbachs alpha ranging from 0.69 to 0.97 (mean did youth without a clinical diagnoses, as well as youth
Cronbacha alpha = 0.86), and excellent temporal stability, diagnosed with other disorders). The sizes of the group
Conners Comprehensive Behavior Rating Scale. Table 1 Overview of correlations between the Conners CBRS
and other measures
Conners CBRS Scale Other measures r

Conners CBRS Content Scales Emotional distress BASC-2: Anxiety 0.470.87
ASEBA: Anxious/Depressed 0.530.85
Academic difficulties BASC-2: Learning problems 0.780.93
Aggressive behaviors, violence potential ASEBA: Aggressive behavior 0.600.96
Physical symptoms BASC-2 somatization 0.590.78
DSM-IV-TR Symptom Scales ADHD inattentive ASEBA: Attention problems 0.720.91
ADHD hyperactive-impulsive BRIEF: Inhibit 0.740.89
Major depressive episode BASC-2: Depression 0.380.71
Generalized anxiety disorder BASC-2: Anxiety 0.460.67
Social Phobia MASC: Social anxiety 0.620.68
Separation anxiety disorder MASC: Separation/Panic Scale 0.420.53
Autistic disorder, Aspergers disorder BASC-2: Developmental social disorders 0.430.69
ASEBA: Social problems 0.640.80
Note. All rs significant, p < .05. BASC-2 = Behavior Assessment System for Children, Second Edition; ASEBA = Achenbach System of Empirically
Based Assessment; BRIEF = Behavior Rating Inventory of Executive Function; MASC = Multidimensional Anxiety Scale for Children.
680 C Conners Rating Scales
membership effects (as determined with partial Z2) were Conners, C. K. (2008). Conners 3rd Edition manual. Toronto, Ontario,
Canada: Multi-Health Systems.
moderate to large, on average, accounting for 14.5% of
Individuals with Disabilities Education Improvement Act of 2004
the variance in scores. In terms of the classification (IDEA), Pub. L. No. 108446, 118 Stat. 2647 (2004). [Amending
accuracy of the scores (as determined by a series of 20 U.S.C. 1400 et seq.].
discriminant function analyses), the mean overall correct
classification rate was 78% across all forms.
Conners Rating Scales

Clinical Uses
A LLISON S. E VANS 1, A NDREW P RESTON 2
1
The Conners CBRS can be used as an assessment tool as Pawtucket, RI, USA
2
well as in planning and monitoring treatment plans. Brown University Medical School
Standardized scores allow for the objective comparison Providence, RI, USA
of an individual with age- and gender-based expectations.
Correspondence of items with DSM-IV-TR, symptomatic
criteria for a number of disorders in combination with Synonyms
information about the youths level of impairment, facil-
itates differential diagnosis decisions in clinical practice. CPRS; CRS
The Conners CBRS offers a scoring feature, which links
the assessment results to areas of eligibility under the
Individuals with Disabilities Improvement Act of 2004 Description
(IDEA, 2004), making the assessment useful for identifi-
cation of appropriate educational classification and/or The Conners Rating Scales are used as a general screening
services for students in the public school system. The tool for the detection of problematic behaviors, and At-
Conners CBRS forms can also be used as an assessment tention Deficit Hyperactivity Disorder (ADHD) symp-
tool in screening and research contexts. toms in particular, in children and, more recently, in
In addition to being an assessment tool, the Conners adults.
CBRS can be employed as a tool for planning, monitoring,
and evaluating treatment plans. Elevated scores from the
Conners CBRS suggest areas to target in treatment, with Historical Background
individual item responses can be used to guide decisions
about specific behaviors requiring intervention. The assess- Rating scales and symptom checklists provide an effective,
ment can also be used in treatment monitoring situations, for quick, and standard approach to the measurement of prob-
example to monitor the effectiveness of an individuals re- lematic behaviors observed in children. The Conners rating
sponse to treatment or to evaluate an intervention program. scales were initially developed as comprehensive checklists
of basic presenting problems of children. A re-standardiza-
tion took place in the late 1990s, which was designed to
Cross References provide a stronger empirical base and a more narrowed
focus of common behavioral problems in childhood. The
Conners 3rd Edition revised scales were developed with norms derived from a
Conners Continuous Performance Test large, representative sample of North American children,
Differential Diagnosis using confirmatory factor analyses to develop a definitive
Individuals with Disabilities Education Act factor structure. The revised scales focused on behaviors
directly related to ADHD and its associated behaviors. The
item content was updated to reflect the recent knowledge
References and Readings and developments concerning ADHD. The revised scales
content contained fewer items, yet the authors claimed that
with greater focus on ADHD-related behaviors and concor-
manual of mental disorders (4th ed., Rev. Ed.). Washington, DC:
dance between scale items and current conceptualizations
Conners, C. K. (2008). Conners comprehensive behavior rating scales of ADHD, the CPRS-R provided better discriminatory
manual. Toronto, Ontario, Canada: Multi-Health Systems. power for detecting ADHD children than previous versions.
Conners Continuous Performance Test (CPT) C 681
Psychometric Data References and Readings
The authors report that the psychometric properties of Conners, C. K. (1989). Conners Rating Scale Manual. New York: Multi-
the revised scale are adequate as demonstrated by good Health Systems, Inc.
Conners, C. K., Erhardt, D., & Sparrows, E. (1999). Conners Adult ADHD
internal reliability coefficients, high testretest reliability, C
Rating Scales (CAARS). North Tonawanda, NY: Multi-Health
effective discriminatory power, and predictive and struc- Systems, Inc.
tural validity. Various researchers have suggested three Conners, C., Sitarenois, G., Parker, J. D., & Epstein, J. N. (1998).
main areas for the application of Conners scales: as a The revised Conners Parent Rating Scale (CPRS-R): factor struc-
general screening tool for the detection of problematic ture, reliability, and criterion validity. Journal of Abnormal Child
Psychology, 26, 257268.
behaviors in children, as a complimentary tool for clarify-
Conners, C., Sitarenois, G., Parker, J. D., & Epstein, J. N. (1998). Revision
ing a specific diagnosis, and as a measurement tool for the and restandardization of the Conners Teacher Rating Scale (CTRS-R):
assessment of treatment results. Factor structure, reliability, and criterion validity. Journal of Abnor-
mal Child Psychology, 26, 279291.
Clinical Uses
The Conners scales are designed to assess symptoms as
reported by various informants (e.g., parents, teachers,
self-report for adolescents) using corresponding factor
Conners Continuous
structures. There are also short and long forms that vary Performance Test (CPT)
from approximately 20 to 80 items. The Conners ratings
have also been compared across cultures, including (for C. K EITH C ONNERS 1, G ILL S ITARENIOS 2
1
example) Italian, British, Chinese, Brazilian, and New Duke University Medical School
Zealand cultures and, consequently, translated into a num- Durham, NC, USA
2
ber of different languages, including Sudanese Arabic, Multi Health Systems Inc.
Turkish, and Hindi. Toronto, ON, Canada
The Conners Adult ADHD Rating Scale (CAARS) was
more recently developed to assess ADHD symptomato-
logy in adults. The rating scale was designed to be com- Description
pleted by respondents about themselves or about a
significant other. Factor analyses used to select items and The Conners Continuous Performance Test - 2 (CPT-2;
determine the structure of the CAARS scale were Conners, 2000) is a computer administered test that is
based on data from a derivation sample consisting of designed to assess problems with attention. The Con-
839 normal adults and from a clinical sample consisting ners CPT-2 presents 360 stimuli trials (i.e., individual
of 167 adult. Four major dimensions were reported: three letters) on the screen, with 1, 2, or 4 s between the
corresponded to the core features of ADHD seen in chil- presentation of letters (ISI: Inter-Stimulus Interval).
dren and the fourth, a secondary consequence of ADHD: The 360 trials are divided into 18 blocks of 20 trials
(1) Inattention/Executive Functioning, (2) Hyperactivity/ each. The ISIs are counterbalanced across these blocks.
Restlessness, (3) Impulsivity/Emotional Lability, and (4) Respondents are instructed to press the spacebar or the
Problems with Self-Concept. Internal reliability coefficients appropriate key on the mouse for any letter that
for the CAARS scales for four different age groups (18 years appears, except the letter X. The CPT takes fourteen
plus) were reported to be excellent (coefficient alphas min to administer excluding the recommended practice
ranging from 0.86 to 0.92 for males and females) and test. Over the duration of the test, 324 non-X stimuli
testretest reliability over a month was felt to be strong (i.e., targets) appear, and the letter X (nontarget)
(0.800.91). appears 36 times. One of the primary advantages of
this paradigm is the high proportion of targets that
appear, yielding a larger pool of responses for generat-
Cross References ing the statistical output. Many statistics are computed
including omission errors (i.e., failing to respond to a
Conners 3rd Edition (Conners 3; Conners 2008) target letter), commission errors (i.e., responding to a
Conners Comprehensive Behavior Rating Scales nontarget), hit reaction time (the average speed of
682 C Conners Continuous Performance Test (CPT)
correct presses to target letters), hit reaction time stan- was initially released as a DOS application (Conners
dard error (which assesses the consistency of responses CPT 3.0; Conners, 1994), and later renormed and
to targets), detectability (the ability to discriminate converted into a windows application (Conners, 2000).
between targets and nontargets), response style
(assesses speed vs accuracy response tendencies), per-
severations (reaction times less than 100 ms), hit reac-
tion time by block (change in reaction time as the test Psychometric Data
progresses), standard error by block (change in re-
sponse consistency as the test progresses), reaction Reliability. Split-half reliability results were computed for
time by ISI (change in mean reaction time across the original standardization sample (Conners, 1994,
ISI), and standard error by ISI (change in response 2000). The mean split-half reliability was 0.83 (range
consistency across ISI). These statistics are converted 0.66 to 0.95). Test-retest reliability is reported in Conners
to T-scores and can be interpreted in terms of various (2000) and is based on a small sample (n = 23). Test-retest
aspects of attention including inattention, impulsivity, correlation was high for the confidence index (r = 0.89),
and vigilance. The CPT-2 also provides a confidence and moderate to high for omissions, commissions,
index probability (expressed as a percentage out of 100) Hit Reaction Time, Hit Reaction Time Standard Error,
of the results being from a clinical as opposed to a non- Variability, Detectability, and Response Style (range
clinical case. r = 0.43 to r = 0.84). The Block change and ISI change
T-scores are computed using General Population (not statistics were less consistent across test administrations
pre-identified with a clinical condition) norms (Conners, (r = 0.05 to r = 0.51).
2000) obtained for children and adults aged 6 years and Validity. Validation of the CPT-2 focused on its two
above. The test is based on a total of 1,920 normative primary clinical uses: to help identify clinical problems
cases, out of which 52.8% of the cases were female, 47.0% with attention or potential neurological impairments and
were White, 27.0% Black, and 21.4% of other ethnic to monitor treatment effects. Conners (2000) compares
origin. Demographic information for age is shown in means from the General Population normative data
Table 1. T-scores are computed based on the age and (n = 1483), and ADHD cases (n = 271) in an ANCOVA
gender of the respondent. Data was also collected for controlling for age and gender for 617 year olds.
378 ADHD cases, and 223 neurologically impaired cases Performance of the ADHD group was significantly worse
(e.g., post-concussive, other organic brain syndrome, on the CPT-2 for all of the measures except commissions
dementia). where no significant difference was found. Discriminant
Function Analysis was also used to examine classification
accuracy for the CPT-2. For 617 year olds, sensitivity is
Historical Background reported at 83% and specificity at 82%. Similar analyses
were conducted on the adult samples. In addition to
The acronym CPT was first introduced by Rosvold, General Population data (n = 437), ADHD data
Mirsky, Sarason, Bransome, and Beck (1956) who used a (n = 107), neurologically impaired data was also available
particular version to detect attention lapses in subjects (n = 223). Performance of the ADHD group and
with petit mal epilepsy. In early CPTs such as the one neurologically impaired group was significantly worse
they used, subjects were required to press a key when a than the General Population group for all of the CPT-
target letter (e.g., X) appeared or when the target 2 measures. The neurologically impaired group also
letter appeared preceded by another letter (e.g., AX). scored significantly worse than the ADHD group on
While the CPT was being explored in clinical settings, several measures. They made significantly more omission
Mackworth (1957) initiated basic vigilance studies. errors, had significantly slower reaction times, had more
By changing basic test parameters, different CPT variable reaction times, and their standard error was
paradigms could be constructed. The CPT-2 paradigm affected more by letter presentation speed (ISI).
Conners Continuous Performance Test (CPT). Table 1 Age distribution of CPT-2 Normative Sample
Age 67 89 1011 1213 1415 1617 1834 3554 55+
n 88 283 369 258 261 224 237 146 54
Consciousness C 683
Discriminant Function Analyses comparing ADHD to Cross References

General Population cases yielded 87% specificity
and 88% sensitivity. When comparing neurologically Attention Deficit, Hyperactivity Disorder
impaired cases to General Population cases, specificity Conners 3rd Edition (Conners 3; Conners 2008)
was 92% and sensitivity was 85%. Conners Comprehensive Behavioral Rating Scale C
In terms of treatment sensitivity, Conners, Casat,
Gualtieri, and Weller (1996) examined the efficacy of
bupropion in the treatment of children with ADHD and References and Readings
used the Conners CPT as one of the efficacy assessment
tools. A double-blind procedure was used with 72 ADHD Boonstra, A. M., Kooij, J. J., Oosterlaan, J., Sergeant, J. A., &
children and 32 ADHD control children aged 612. Buitelaar, J. K. (2005). Does methylphenidate improve inhibition
and other cognitive abilities in adults with childhood-onset ADHD?
Subjects were randomized to receive 36 mg/kg of
buproprion per day or placebo twice daily. Significant Conners, C. K. (1994). Conners Continuous Performance Test computer
treatment effects were found. Epstein et al. (2006) exam- program 3.0 Users manual. Toronto, ON: Multi Health Systems Inc.
ined mean differences between 190 children who took a Conners, C. K. (2000). Conners Continuous Performance Test (CPT-2)
stimulant medication on the day of neurological testing computer program for windows, technical guide, and software manual.
Toronto, ON: Multi Health Systems Inc.
and 126 children who took no stimulant medication of
Conners, C. K., Casat, C. D., Gualtieri, C. T., & Weller, E. (1996).
the day of testing. Children who were not on medication Bupropion hydrochloride in attention deficit disorder with hyperac-
made significantly more omission errors and commission tivity. Journal of the American Academy of Child and Adolescent
errors, had significantly slower reaction times, and were Psychiatry, 35, 13141321.
significantly more variable in their response speed. Boon- Conners, C. K., Epstein, J. N., Angold, A., & Klaric, J. (2003). Continuous
Performance Test performance in a normative epidemiological
stra, Kooij, Oosterlaan, Seargeant, and Buitelaar (2005)
sample. Journal of Abnormal Child Psychology, 31, 555.
tested 43 adults with ADHD in a double-blind, cross-over, Epstein, J. N., Conners, C. K., Hervey, A. S., Tonev, S. T., Arnold, L. E.,
and placebo controlled study. The CPT-2 was adminis- Abikoff, H., et al. (2006). Assessing medication effects in the MTA
tered during the third week of titrated treatment with study using neuropsychological outcomes. Journal of Child
methylphenidate and during the third week of treatment Psychology and Psychiatry, 47, 446456.
Epstein, J. N., Erkanli, A., Conners, C. K., Klaric, J., Costello, J. E., &
with placebo. Large medication effects were observed for
Angold, A. (2003). Relations between Continuous Performance
commission errors, standard error of hit reaction time, Test measures and ADHD behaviors. Journal of Abnormal Child
and inattentiveness. A moderate effect was also observed Psychology, 31, 543554.
for hit reaction time. Hervey, A. S., Epstein, J. N., Curry, J. F., Tonev, S., Arnold, L. E.,
Conners, C. K., et al. (2006). Reaction time distribution analysis of
neuropsychological performance in an ADHD sample. Child
Clinical Uses Mackworth, N. H. (1957). Some factors affecting vigilance. Advancements
in Science, 53, 389393.
Although the CPT-2 cannot be used alone to make a Rosvold, H. E., Mirsky, A. F., Sarason, I., Bransome, E. D., Jr., &
diagnosis, it provides performance based information Beck, L. H. (1956). A continuous performance test of brain damage.
Journal of Consulting Psychology, 20, 343350.
that aids in the diagnostic process. The performance
based information from the CPT-2 complement infor-
mant reports commonly obtained from parents, teachers,
or by self-report. Response patterns on the CPT-2 enable
practitioners to better understand the type of deficits that Consciousness
might be present (e.g., Epstein, Erkanli, Conners, Klaric,
Costello, & Angold, 2003; Hervey et al., 2006). For R ONALD A. C OHEN
example, some response patterns might suggest inatten- Brown University
tiveness or impulsivity, while other response patterns may Providence, RI, USA
indicate activation/arousal problems or difficulties main-
taining vigilance. The CPT-2 has also commonly been
used as a way of assessing treatment effectiveness. Careful Synonyms
charting of CPT scores while testing different drug
dosages can often be helpful in determining optimal Alertness; Awareness; Mindfulness; Self-awareness;
dosage levels. Wakefulness
684 C Consciousness
Definition was a primary task for psychology. He postulated that

apperception represented the core activity of the mind
Consciousness comes from the Latin word conscientia and was the interface between internal and external experi-
which means knowledge-within, or knowledge that is ence. Notably, Wundts primary method for exploring these
shared. Today the term is used to describe the experience processes was introspection, which essentially is the process
of self as distinct from the external environment. It is of looking inward or self-reflection. These ideas evolved
characterized by experiences of alertness, self-awareness, into structuralism, the first dominant theoretical school of
and attention of oneself relative to the environment rela- psychology.
tive to the self; i.e., identify, which in turn involves aware- A dramatic shift away from consideration of con-
ness of ones own perceptions, associations, emotional sciousness occurred during much of the twentieth century
experience, and the cognitive interpretation of these as behaviorism became the dominant perspective, as con-
experiences. More narrowly, consciousness is often de- sciousness was viewed as metaphysical and beyond em-
fined level of arousal, wakefulness, alertness, responsive- pirical observation. Even cognitive scientists tended to
ness, and adaptability in contrast to states of coma or steer away from tackling this construct, probably because
sleep. of the difficulties associated with experimentally studying
However, consciousness has defied unitary definition, it. Yet, for clinicians working with the subjective experi-
perhaps because it is intrinsically bound to subjective ences of their neurological and psychiatric patients, con-
experience. sciousness was difficult to avoid. When the neurologist
Babinski (1914) first described patients who were unaware
of their own deficits (i.e., anosognosia) he was essentially
Historical Background addressing the issue of consciousness and self-awareness.
Initially, the problem of consciousness was handled by
The nature of human consciousness has been a primary narrowing the meaning of the term to refer to the state
topic of philosophical inquiry throughout the ages. The of being awake, alert and aware, in contrast to coma,
ancient Greek philosophers contemplated questions re- stupor, or sleep, which in turn led to the idea of level of
garding the relationship between external and objective consciousness, which remains a standard part of mental
reality. For example, Plato recognized that humans can status examinations.
think and speak, and yet not be fully aware of their larger
realm and whether their observations were valid with
respect to external reality. His cave allegory was an effort Current Neuropsychological Knowledge
to describe this problem. For medieval religious philoso-
phers (e.g., Aquinas), it referred to the act of applying Over the past 2 decades there has been a major resurgence of
moral knowledge to ones actions. Descartes extended the interest and research effort directed at the nature of con-
concept of conscientia to include the idea that it sciousness, along with growing recognition that the con-
involves a psychological state of mind, and used separate struct is a necessary one, as consciousness describes an
terms to explain this level of experience from moral important element of human experience, the sense of self.
knowledge, though he did not formally employ the mod- A number of scientific developments set the stage for this
ern concept of consciousness in his dualism of mind shift in zeitgeist. The evolution of the field of cognitive
body interaction. John Locke later wrote I may be held science provided empirical methods for studying covert
morally responsible for the act of which I am conscious of mental processes. Also as cognitive processes such as
having achieved; and my personal identity; my-self goes as attention and memory were better understood, foundations
far as my consciousness extends itself , its first modern were established for studying phenomena like intention and
usage associated with the idea of self and personal self-awareness. Computational neuroscience was also influ-
identity. Interestingly, Locke still linked consciousness ential in this regard. It is quite difficult to operationalize or
to the ideas of morality and responsibility. The nature conceptualize consciousness as a single node in a top-down
of consciousness was a recurrent theme of renaissance modular cognitive framework. This is less of a problem for
philosophers. computational theories that take a bottom-up approach,
The quest to better understand the nature of conscious- such as the parallel distributed processing (PDP) models
ness dominated the new science of psychology at it evolved proposed by Rummelhart and McClelland (1986), as con-
in the late nineteenth century. Wilhelm Wundt believed sciousness can be conceptualized as an emergent byproduct
that identifying the constituents of human consciousness of associative networks acting together with feedback or
Consciousness C 685
feed-forward organization. Another major impetus for con- In contrast to AD, patients with certain other degenera-
sciousness becoming an acceptable topic for scientific in- tive conditions often show general preservation of con-
quiry was advances in the field of neuroscience itself. sciousness despite having marked impairments of other
Functional imaging methods have made it easier to measure functions. For example, patients with severe Parkinsons
brain responses associated with subjective cognitive states, disease typically have major motor symptoms, cognitive C
providing evidence that these states have valid neurobiolog- control problems, including executive and attention dys-
ical underpinnings. Furthermore, growing recognition function. They may also show blunting of emotional re-
of the brains complexity has played an important role. sponse and altered emotional functioning. Yet, they are
There is now general consensus that cognition involves often painfully aware of their deficits, and have greater
interactions among large networks of cortical neurons, preservation of sense of self than the AD patient. Similarly,
which communicate across larger functional systems in an patients with Multiple Sclerosis (MS) sometimes exhibit
integrated manner. This perspective enabled cognitive neu- pseudobulbar affect. They are affectively labile with dramat-
roscientists to shift away from having to view consciousness ic shift in the outward expression of emotion, but yet they
as a unitary process sitting on top of the pyramid of cogni- report not feeling the emotion that corresponds to this
tive functions. expression. Despite these problems with affective and be-
Several lines of research and clinical evidence have had havioral control, patients with MS typically are very aware
particular bearing on current knowledge regarding the of their deficits and may feel locked in because of their
neuropsychology of consciousness. The effect of various symptoms.
types of drugs, most notably hallucinogens, opiates, and Alterations in self-awareness and consciousness also
alcohol on conscious experience provides one of the most occur as a result of damage to specific brain regions. This
clear cut illustrations of the fact that even among healthy fact is significant since it suggests that certain functional
people consciousness is not a static phenomenon. Ones anatomic systems play an important role in the experience
sense of reality, identify and self-awareness can be dra- of consciousness, though probably not as a function of
matically altered by drugs such as LSD, presumably any one of these systems alone. Subcortical lesions affect-
by altering the flow of information processing. Case stud- ing the mid-brain, brain stem and thalamus often cause
ies have consistently shown that disruption of self-aware- dramatic alterations in level of consciousness. The reticu-
ness as a function of damage to specific brain regions. lar system which generates ascending activation to cortical
Furthermore, clinicians working with patients experien- areas plays a well established role in this phenomenon,
cing neurodegenerative dementias have long been aware with damage to this system contributing to problems with
of dramatic impoverishment in the quality of conscious arousal and alertness. Damage to these areas frequently
experience as the disease progresses, corresponding underlies coma, and the electrical activity measured by
with the extent of cortical atrophy. Among patients with EEG is amplified by generators in these systems. Persistent
Alzheimers disease (AD) and other neuronal dementias, a vegetative state is a clinical illustration of this, as these
loss of self is one of the hallmark features of the end- unfortunate patients exhibit impaired higher cortical
stage condition. In fact, it is when AD patients lose their functions, have persevered circadian sleep-wake cycles
ability to respond to people who are familiar and mean- and autonomic function. Compared to healthy people
ingful to them, and when they lose awareness of their own who are awake, patients with this syndrome have im-
identify, their personal memories, and the nature of their paired connectivity between brainstem and thalamic
cognitive problems that families typically experience areas and the cortex. This results in a reduced cortical
greatest despair. In fact, it is often this change, along activation, with generalized slowing consistent with coma.
with an inability for self-care that leads to nursing home These subcortical areas are clearly essential for maintain-
placement rather than the amnestic disturbance per se. ing normal consciousness, since disconnecting them from
The loss of identity in AD patients usually corresponds cortical areas impairs alertness, attention, and other cog-
with personality changes and profound impoverishment nitive functions linked to consciousness. The activation
in abstraction and associative ability. While other cogni- and arousal associated with this functional anatomic sys-
tive functions like language are often also severely tem makes an essential contribution to is a necessary part
impaired at this point, it may be difficult to fully appreci- of the maintaining consciousness, thought this activation
ate these changes, though the quality of emptiness and is not sufficient to account for the full dynamic of con-
loss of self that may ultimately be the characteristic that sciousness (i.e., self-awareness and sense of identity).
best defines severe dementia rather than impairment in a The thalamus appears to play an important role in
particular cognitive domain. consciousness, but as a convergence site of reticular
686 C Consciousness
activation from lower brain systems and because of its There is strong evidence from studies of neglect syn-
role in integrating this activation with cortical input. drome that medial frontal and anterior cingulate cortical
Bilateral ablation of the central medial zone of the intra- areas play a major role in intention (Cohen, 1993). The
laminar nucleus of the thalamus produces coma and intent and plan for action seems to be an important
persistent vegetative states. This thalamic area is affected element of consciousness, as this capacity is linked to
by general anaesthetics and drugs that cause sedation, the experience of drive and spontaneity. An illustration
suggesting that it is necessary for anti-psychotic drugs. of this is seen in patients who undergo cingulotomy, as
This evidence suggests that a functioning thalamus is their primary long-term neurocognitive deficit involves
necessary, but not sufficient, for human consciousness, diminished performance on tests requiring intention, and
though again this area alone is not sufficient to account also reduced spontaneity, initiative, and creative impulse.
for all aspects of consciousness. Cortical and limbic func- It is also noteworthy that syndromes that result in altera-
tions are necessary elements of normal consciousness. tions of consciousness that involve delusions and a frac-
Patients with bilateral occipital damage who exhibit tured sense of reality, such as reduplicative para-amnesia
blind sight are clearly experiencing some alteration in and Capgrass syndrome, tend to occur among patients with
consciousness and self-awareness. Yet, this disturbance frontal lobe damage, often involving the non-dominant
may be relative focal and limited to vision. For these hemisphere. In cases of reduplicative paramnesia, patients
individuals, altered consciousness has not affected all may feel with certainty that while the house in which they
aspects of self-awareness and identity. Damage to other are living looks identical to their real home, that it is in fact a
cortical areas may also produce specific impairments of replica of their home. When queried these patients usually
awareness and self-consciousness. For example, the ne- acknowledge the logical implausibility of their belief, but
glect syndrome commonly associated with right inferior state that they are certain because of some feeling they have,
parietal damage often results in anosognosia and im- suggesting a relationship between emotional response and
paired awareness of what is being neglected. For some of the processing of these frontal systems. Primate studies
these patients, the alteration in awareness and conscious- support the role of the frontal cortex in this regard, and
ness extends beyond the limits of the spatial disturbance led Crick and Koch (1995) to propose that consciousness is
that is observed. Yet, typically patients with these lesions largely dependent on the resonance of thalamo-cortical
do not lose their sense of self completely. They may show systems acting in a recursive manner.
diminished ability for self-reflect, but usually show abil- The role of memory and its underlying functional
ities in this regard as long as not tied to the types of spatial neuroanatomic systems raises a number of interesting
processing that is affected. issues for consciousness. Patients like HM, who have
The frontal cortex seems to have be the cortical area suffered bilateral damage to hippocampal or paralimbic
with greatest influence on consciousness, self-regulation areas, lose their ability to form new episodic memories.
and self-referential processes. The famous case of Phineus Yet, they typically retain retrograde memory for events
Gage, the railroad worker who suffered severe frontal that happened earlier in their life, which enables them to
damage when a spike penetrated his brain provided his- retain some sense of personal identity based on these
torical illustration of this. Following his injury Gage recollections. Yet, they have lost the ability to update
became indifferent to social consequences and showed these memories or to adapt these memories to new cir-
little self-regard for his own behavior (Harlow, 1848). cumstances. Clearly this results in an alteration of con-
While it is impossible to accurately evaluate the nature sciousness, though they may still report knowing who
of change in his subjective sense of consciousness and self- they are or what they think about certain topics.
awareness based on the historical record, it seems clear In addition to the contribution of specific cortical
from clinical descriptions that his self-awareness was dra- and subcortical areas to the experience of consciousness,
matically altered. In modern case study, Eslinger and his there is a rich history of research on brain laterality,
colleagues (1986) have demonstrated impaired empathy specifically the effects of disconnection between the left
associated with frontal lobe disturbance, which affects and right hemisphere of the brain. The corpus callosum
social reasoning, judgment and perspective taking. Inter- provides the white matter linkage between the hemi-
estingly, this disorder of empathy also involves problems spheres. Roger Sperry observed remarkable alterations
with moral reasoning, a notion consistent with early phil- in consciousness and awareness among patients who
osophical ideas regarding consciousness, which as dis- underwent surgical severing of the corpus callosum
cussed earlier conceptualized consciousness as tied to (split brain) for treatment of intractable seizures. When
mans capacity for moral knowledge. the two hemispheres are no longer able to communicate,
Consciousness C 687
each processes and interprets information presented to it likely play a significant role, by linking emotional valence
in different ways. For example, the left hemisphere is to particular associative information. In interaction with
typically more involved in language processing, and cortical areas, these limbic areas enable amplification of
therefore tended to be aware of verbal elements of infor- affective signals, and also their regulation, providing for
mation during tasks compared to the right hemisphere. the intensity and richness of emotional affective experi- C
Because of a lack of integration between the cortical ence. (5) Some type of mechanism that enables temporal
hemispheres, it is possible to dissociate elements of con- binding of associative experiences in an integrated way
sciousness tied to each side of the brain. Yet, following likely occurs that creates the feeling of a unified conscious
this procedure, it was only under experimentally con- experience and sense of single identity, I.
trolled conditions that major dissociations occurred. Some of the distinctions that exist between theories of
Post-surgically, people still experienced a single identity consciousness relate to the emphasis that is placed on
in everyday experience, suggesting that splitting the two particular cognitive functions. Some recent investigators
hemispheres does not completely disrupt the sense of a have emphasized the role of posterior brain systems
unified consciousness. involved in visual processing to a greater extent. A num-
ber of theories emphasize the role of frontal brain systems.
For example, one of the first neuroscientific models of
Neuropsychological Models of consciousness proposed by Shalice (1978) viewed con-
Consciousness sciousness as a byproduct of dominant action systems
that govern the stream of thought processes. As discussed
Consideration of the neuropsychological literature to date previously, many models have focused on frontal systems
has established the foundations for the cognitive neuro- with varying degrees of emphasis on particular processes.
science of consciousness. Over the past 15 years, theoreti- Damasios model of consciousness emphasizes the critical
cal models have been developed to explain how the role of emotional processing systems, as well as the so-
brain creates mind and consciousness. These models matic or visceral activity of the body as a whole.
include contributions from philosophers (Dennett, 1991; Perhaps the greatest distinction between theories of
Churchland, 2005), neuropsychologists/behavioral neu- consciousness stems from the extent to which it is
rologists (Cohen, 1993; Damasio, 1995, 2000) and cogni- viewed as distinct from the physical processes that com-
tive neuroscientists (Shallice, 1978; Eccles, 1994; Crick prise, or essentially indistinguishable from these physical
and Koch, 1995; McClelland et al., 1997; Grossberg, processes, as Dennett argues. Furthermore, some of these
1999). It is beyond the current scope to review each of models take more of a top-down approach, whereas others
their models. However, there are several features common view consciousness from a bottom-up perspective, as an
to each, as well as a few fundamental distinctions between emergent byproduct of all of the more basic associative
these models, as summarized below. processes that underlie cognition. The PDP approach of
Most current models of consciousness take the per- McClelland and Rummelhart (1986, 1997), and other neu-
spective that consciousness is not localized to a single rocomputational theories (e.g., Grossberg, 1999) take a
brain region, but rather is an emergent function of multi- more bottom-up approach and tend to view conscious-
ple systems acting in an integrated fashion. (1) Almost all ness as the sum total of these distributed processes. De-
researchers and theorists agree that lower brain areas (e.g., spite these differences, there seems to be little
reticular system) that energize the brain and lead to alter- disagreement that consciousness is a complex cognitive
ing levels of activation are a necessary requirement for phenomenon that results from the interaction of multiple
consciousness, but not sufficient to explain the phenome- brain systems and processes, which in an integrated co-
non. (2) The thalamus seems to play and essential role, herent manner provides for the sense of self, universally
particularly as a nexus for this activation and for integra- experienced by healthy humans.
tion and gating of cortical information. (3) Frontal
regions appear to play several important roles, including
the generation and sustaining of intention, switching and Future Directions
gating of information, and the enabling of feedback, and
feed-forward mechanisms that enable reprocessing of cer- The cognitive and neurobiological bases of consciousness
tain associative information and feedback control for remain major frontiers in neuropsychology. Clinicians
gating of this information as it flows from posterior evaluating patients following acute brain injury routinely
cortical systems. (4) Limbic areas, such as the amygdala, assess level of impaired consciousness is (i.e., the degree of
688 C Consolidation
coma, stupor or lethargy), though this level of analysis Crick, F., & Koch, C. (1990). A framework for consciousness. Nature
Neuroscience, 6(2), 119126.
does not fully capture the richness of normal conscious
Damasio, A. R. (1995). Consciousness. Knowing how, knowing where.
experience. None the less, clinical research is likely to yield Nature, 375, 106107.
greater precision in the assessment of levels of Damasio, A. R. (2000). The feeling of what happens: Body and emotion in
consciousness. the making of consciousness. New York: Vintage.
Some progress has been made in understanding how Damasio, H., Grabowski, T., Frank, R., et al. (1994). The return of
Phineas Gage: Clues about the brain from the skull of a famous
consciousness arises as a by-product of other cognitive
patient. Science, 264, 11021105.
functions, most notably emotional experience, attention Dennett, D. (1991). Consciousness explained. Boston: Little & Company.
and executive functioning. Computation neuroscience Eccles, J. C. (1994). How the self controls its brain. Berlin: Springer.
has offered a perspective for explaining consciousness as Eslinger, P. J. (1998). Neurological and neuropsychological bases of em-
an emergent property of complex neural systems. Yet, the pathy. European Neurology, 39, 193199.
Grossberg, S. (1999). The link between brain learning, attention, and
measurement of the qualitative experience that comprises
consciousness. Consciousness and Cognition, 8, 144.
consciousness is still far from becoming part of main- Harlow, J. M. (1848). Passage of an iron rod through the head. Boston
stream neuropsychological assessment, or from being Medical and Surgical Journal, 39, 389393.
fully operationalized as a cognitive construct or neuropsy- Harlow, J. M. (1868). Recovery from the passage of an iron bar through
chological domain. Greatest progress has been made with the head. Publications of the Massachusetts Medical Society, 2,
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respect to the study of anosognosia, and recent efforts to
McClelland , J. L., Cohen, J. D., & Schooler, J. W. (1997). The neural basis
better understand the relationship between subjective ex- of consciousness and explicit memory: Reflections on Kihlstrom, Man-
perience of cognitive impairments and also cognitive and dler and Rumelhart. Scientific approaches to consciousness (pp. 499
emotional experience and neuropsychological perfor- 509). Lawrence Erlbaum Associates.
mance. This seems to be a fertile area of continued inves- Rumelhart, D. E., McClelland, J. E., & the PDP Research Group (1986).
Parallel distributed processing: Explorations in the miccrostructure
tigation. Functional imaging approaches have provided
of cognition, Vol. 1: Foundations. Cambridge, MA: Bradford/MIT
considerable insight into the neural bases of conscious- Press.
ness and likely will continue to be on the cutting edge of Shallice, T. (1978). The dominant action system: An information proces-
these efforts, since they provide a means for observing sing approach to consciousness. In K. S. Pope & J. L. Singer (Eds.),
brain response associated with subjective experience. Evi- The stream of consciousness: Scientific investigations into the flow of
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dence of the attentional default network that emerged
Wundt, W. (1902). Outlines of psychology (Trans., 2nd ed.). Oxford.
from functional imaging research illustrates the type of Engelmann:
insight about the neural bases of consciousness that can
be achieved from these approaches.
Cross References
Consolidation
Anosognosia
Attention E LIZABETH S TANNARD G ROMISCH
Capgras Syndrome Trinity College
Minimally Conscious State Hartford, CT, USA
Parallel Distributed Processing
Reduplicative Paramnesia
Reticular Activating System Synonyms
Split-Brain
Memory consolidation
Churchland, P. S. (2002). Self-representation in nervous systems. Science,

Definition
296, 308310.
Churchland, P. S. (2005). A neurophilosophical slant on consciousness Consolidation is the process of converting short-term
research. Progress in Brain Research, 149, 285293. memory to permanent long-term memory through the
Cohen, R. A. (1993). Neuropsychology of attention. New York: Plenum.
formation of new synapses.
Consolidation C 689
Current Knowledge Assessment and Measurement
History Assessment of consolidation is done through testing

short-term memory with material modality tests, then
The first written evidence of consolidation was by Marcus measuring long-term memory after a delay or a distrac- C
Fabius Quintilian, who stated curious fact, of which the tion. The participants will be given a list of words, for
reason is not obvious, that the interval of a single night example, and asked to repeat them back to the examiner.
will greatly increase the strength of the memory and the After a period of time has passed (delay), the participants
power of recollection, which is the most important ele- will be prompted to repeat the words again. The examiner
ment of memory, undergoes a process of ripening and may also measure consolidation by using a distraction to
maturing during the time which intervenes. The term prevent the participants from rehearsing the information.
consolidation was coined by Georg Elias Muller and To effectively measure consolidation, conditions must be
Alfons Pilzecker, whose conducted research between controlled when testing both short-term memory and
1892 and 1900 and found that memory takes time to long-term memory.
consolidirung. Published in their article Experimen-
telle Beitrage zur Lehre vom Gedachtnis, Muller and
Pilzecker found that it takes time to form memories, Neuroimaging
and that these new memories can be disrupted for some
time after formation. Research by Takashima et al. tracked the brains activity
during the process of consolidation. As the brain conso-
Process of Consolidation lidates short-term memories into long-term memories,
the functional magnetic resonance imaging (fMRI)
The process of consolidation occurs in the neocortex of shows an increase in activity in the hippocampus. Once
the brain, with memory information sent from the hip- the brain switches from consolidation to memory retriev-
pocampus. Two specific processes are involved in consoli- al, the hippocampal activity decreases and the ventral
dation based on the period of time needed to create long- medial prefrontal region increases. Sterpenich et al. used
term memories from the short-term memories. Synaptic fMRI to examine consolidation during sleep. The activa-
consolidation occurs the quickest, consolidating mem- tion in the hippocampus decreased over time (3 days
ories within the first few hours of learning. System con- compared to 6 months), indicating that the memories
solidation, on the other hand, takes between weeks to were being stored in the neocortex and no longer depen-
years for hippocampus-dependent memories to become dent on the hippocampus. After 6 months, activity
independent of the hippocampus. Consolidation can increased in the ventral medial prefrontal region.
occur more rapidly if new information is incorporated
with an already existent schema. In addition, the largest
amount of consolidation happens during rapid eye move- Cross References
ment (REM) sleep.
Memory
Long-Term Memory Short-Term Memory
Studies in anterograde amnesia, such as with Patient H.

M., have shown that lesions on the medial temporal lobe References and Readings
prevent long-term memory formation. Long-term mem-
ory is information that has been consolidated and is Dudai, Y. (2004). The neurobiology of consolidations, or, how stable is
permanently stored in the brain. While consolidation is the engram? Annual Review of Psychology, 55, 5186.
initiated in the limbic system, specifically in the hippo- Lechner, H. A., Squire, L. R., & Byrne, J. H. (1999). 100 years of consoli-
dationremembering Muller and Pilzecker. Learning and Memory,
campus, long-term memories are stored throughout the
6, 7787.
cortex. When the memory is retrieved, it can be modified Riberio, S., Goyal, V., Mello, C. V., & Pavlides, C. (1999). Brain gene
with recently acquired memories, thus strengthening the expression during REM sleep depends on prior waking experience.
original memory. Learning and Memory, 6, 500508.
690 C Consortium to Establish a Registry on Alzheimers Disease
Sterpenich, V. et al. (2009). Sleep promotes the neural reorganization of nition (delayed) conditions, and a constructional praxis
remote emotional memory. The Journal of Neuroscience, 29(16),
test that requires examinees to copy four line drawings of
51435152.
Takashima, A., et al. (2005). Declarative memory consolidation in
increasing complexity (Rosen, Mohs, & Davis, 1984).
humans: A prospective functional magnetic resonance imaging Administration time for the battery is 2030 min for
study. Proceedings of the national academy of sciences of the United persons with AD; persons without AD may complete the
States of America, Vol. 103, no. 3, 756761. battery in less time (Morris et al., 1989). As may be
Tronson, N. C., & Taylor, J. R. (2007). Molecular mechanisms of memory
expected given the brevity of the battery and the range
reconsolidation. Nature Reviews Neuroscience, 8, 262275.
Weingartner, H., & Parker, E. S., (Eds.). (1984). Memory consolidation:
of cognitive ability of the target populations, floor and
psychobiology of cognition. Hillsdale, NJ: Lawrence Erlbaum ceiling effects have been noted for individuals with later
Associates. stage AD and for individuals without AD, respectively
(Morris et al., 1989). Normative data are available based
on the CERAD program control sample (Welsh et al.,
1994), as well as from studies of specific demographic
groups (see Clinical Uses).
Consortium to Establish a
Registry on Alzheimers Disease
S USAN VANDERHILL 1, E STHER S TRAUSS 1
E LISABETH M. S. S HERMAN 2
1 The Consortium to Establish a Registry for Alzheimers
Disease (CERAD) was first funded by the National Insti-
Victoria, BC, Canada
2 tute on Aging in 1986 in response to a US Congressional
University of Calgary
mandate to collect epidemiological data concerning the
Calgary, AB, Canada
incidence of AD. A nationwide consortium of 24 univer-
sity medical centers (the CERAD program) developed,
standardized, and evaluated methods for clinical, neuro-
Synonyms psychological, neuropathologic, and neuroimaging
assessments of AD. Data from the study population, in-
CERAD
cluding 1,094 patients with AD and 463 controls evalu-
ated annually between 1987 and 1996, are available on
CD-ROM for research purposes (CERAD, Box 3203,
Description Duke University Medical Center, Durham, NC 27710).
As the bulk of the CERAD data collection took place
The Consortium to Establish a Registry for Alzheimers
before the widespread use of cholinesterase inhibitor
Disease (CERAD) neuropsychological battery was
treatment for AD, these data provide a rich source of
designed to provide an efficient, standardized method to
information as to the natural history of AD. A special
evaluate cognitive functioning in individuals with Alzhei-
issue of Neurology (49, suppl. 3) published in 1997 com-
mers disease (AD). Originally employed in a large-scale
memorated the tenth anniversary of the CERAD program
longitudinal research program, tests were selected to pro-
and reviewed study design, implementation, and key find-
vide coverage of the primary cognitive deficits associated
ings from wide-ranging investigations of AD.
with AD (e.g., memory, language, praxis, and intellectual
status) and to have a range of difficulty appropriate for
use through much of the course of the disease (Morris
et al., 1989). Individual tests within the battery include Psychometric Data
well-known, commonly used measures such as the Mini-
Mental State Exam (MMSE; Folstein, Folstein, & Psychometric data for the CERAD neuropsychological
McHugh, 1975), a 15-item modified Boston Naming battery reported for participants enrolled over the first
Test (Kaplan, Goodglass, & Weintraub, 1978), and an 19 months of the study indicated good interrater reliabil-
Animal Naming verbal fluency test (Isaacs & Kennie, ity across all tests, with intraclass correlation coefficients
1973). Also included are a ten-item word list memory ranging from 0.92 to 1.0 (Morris et al., 1989). One
test, with free recall (immediate and delayed) and recog- month testretest data showed variable reliability
Consortium to Establish a Registry on Alzheimers Disease C 691
(rs from 0.36 to 0.90), with lower correlation coefficients impact test performance. Normative data for patients
for measures whose variance may have been constrained with AD have also been reported, in addition to annual
by ceiling effects (Morris et al., 1989). The efficacy of rates of change on CERAD test scores over a 4-year period
CERAD battery measures (individually and in combina- (Morris et al., 1993).
tion) for detecting AD and for staging dementia severity The CERAD battery has been extensively translated. C
has been evaluated using discriminant function models Normative data for the CERAD are available for a wide
(Welsh, Butters, Hughes, Mohs, & Heyman, 1991; Welsh, range of racial/cultural/demographic groups (Bertolucci
Butters, Hughes, Mohs, & Heyman, 1992). The word list et al., 2001; Fillenbaum, Heyman, Huber, Ganguli, &
delayed recall measure was shown to most effectively Unverzagt, 2001; Fillenbaum et al., 2005; Ganguli et al.,
differentiate those with AD from controls (correctly 1991; Ganguli et al., 1996; Guruje et al., 1995; Whyte et al.,
identifying 94% of controls and 86% of mild AD 2005). Beeri et al. (2006) provide normative data for
patients), although the ability of this measure to distin- individuals over the age of 85.
guish dementia severity groups was limited due to floor Methods for deriving a single summary score for the
effects. For those with impaired scores on delayed recall, CERAD battery (excluding the MMSE) and normative
performance on the naming measure was shown to mod- data for this summary score for unimpaired, mild cogni-
estly increase the discrimination of those with mild from tive impairment (MCI), and AD groups have been pub-
moderate AD (improvement in overall accuracy from lished (Chandler et al., 2005). This total score was
65 to 71%). Verbal Fluency and Constructional Praxis reportedly more consistent at differentiating these three
performances were shown to increase discrimination of groups from one another compared to the MMSE total
those with moderate from severe AD (improvement in score, which showed limited ability to distinguish patients
overall accuracy from 66 to 81%). Within a cognitively with MCI from unimpaired individuals, and the word list
impaired sample, the CERAD battery has also been found delayed recall score, which showed limited ability to dis-
to distinguish those with AD from those with schizophrenia tinguish MCI from AD.
(Davidson et al., 1996). Clinicalpathological correlations Some authors have described an overreliance of the
have shown association between CERAD neuropsycho- CERAD battery on using verbal modalities of testing, at
logical performance and AD pathology on autopsy the expense of other relevant information. To address this
(Hulette et al., 1998). Data from the CERAD program issue, a visual memory measure based on recall of the
have been used to identify predictors of time to institu- Constructional Praxis test items has been proposed. Ad-
tionalization in patients with AD, but information from ministration instructions and psychometric properties of
the CERAD neuropsychological battery (with the excep- a delayed recall and recognition condition of this measure
tion of the MMSE) was not considered in this study have been reported (Spangenberg, Henderson, & Wagner,
(Heyman, Peterson, Fillenbaum, & Pieper, 1997). 1997).
In sum, the brevity of the CERAD neuropsychological
battery, combined with the vast associated research base,
make the CERAD a useful tool for assessment of cognitive
Clinical Uses function in cases of suspected dementia where factors
such as fatigue, motivation, or incapacity prevent a more
The chief objective of the CERAD neuropsychology task extensive neuropsychological examination of cognitive
force was to develop a brief, reliable battery of neuropsy- capacities (Welsh et al., 1994). Assessment in specialized
chological tests that would be widely used by researchers memory clinics, however, would typically employ a more
and clinicians to assess the cognitive status of patients extensive neuropsychological battery.
with AD at entry and during long-term annual follow-
up (Welsh-Bohmer & Mohs, 1997). The CERAD neuro-
psychological battery has been widely used in research Cross References
studies, including those completed at many of the NIH-
sponsored Alzheimers Disease Centers. Normative data Alzheimers Disease
based on 413 CERAD control subjects aged 5089 have Blessed Dementia Screen
been published to facilitate clinical application (Welsh Clinical Dementia Rating Scale (CDR)
et al., 1994). These data are stratified by age, education, Mattis Dementia Rating Scale (DRS)
and gender, as these factors were shown to differentially Mini-Mental State Exam (MMSE)
692 C Constraint Induced Therapy
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Morris, J. C., Heyman, A., Mohs, R. C., Hughes, J. P., van Belle, G.,
et al. (2006). Age, gender, and education norms on the CERAD
Fillenbaum, G., et al. (1989). The Consortium to Establish a Registry
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Rosen, W. G., Mohs, R. C., & Davis, K. L. (1984). A new rating scale for
Neto, J., & Ramos, L. R. (2001). Applicability of the CERAD Neuro-
Alzheimers disease. The American Journal of Psychiatry, 141(11),
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Chandler, M. J., Lacritz, L. H., Hynan, L. S., Barnard, H. D., Allen, G.,
recall and recognition condition to assess visual memory in the
Deschner, M., et al. (2005). A total score for the CERAD Neuropsy-
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Davidson, M., Harvey, P., Welsh, K. A., Powchik, P., Putnam, K. M., &
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Welsh, K. A., Butters, N., Hughes, J., Mohs, R., & Heyman, A. (1991).
a comparison of elderly schizophrenic patients and patients with
Detection of abnormal memory decline in mild cases of Alzheimers
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F. W. (2001). Performance of elderly African American and
(1992). Detection and staging of dementia in Alzheimers disease.
White community residents on the CERAD Neuropsychological
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Constraint Induced Therapy
et al. (1991). Effects of age, gender, and education on cognitive
tests in a rural elderly community sample: Norms from the Mono- M ARIANNE H RABOK , K IMBERLY A. K ERNS
ngahela Valley Independent Elders Survey. Neuroepidemiology, 10(1), University of Victoria
4252. Victoria, BC, Canada
Guruje, O., Unverzargt, F. W., Osuntokun, B. O., Hendrie, H. C.,
Baiyewu, O., Ogunniyi, A., et al. (1995). The CERAD Neuropsycho-
logical Test Battery: Norms from a Yoruba-speaking Nigerian sam-
ple. West African Journal Of Medicine, 14(1), 2933. Definition
Heyman, A., Peterson, B., Fillenbaum, G., & Pieper, C. (1997). Predictors
of time to institutionalization of patients with Alzheimers disease: Constraint induced therapy (CIT) typically refers to a
the CERAD experience, part XVII. Neurology, 48(5), 13041309.
therapeutic intervention involving restraint of a non-
Hulette, C. M., Welsh-Bohmer, K. A., Murray, M. G., Saunders, A. M.,
Mash, D. C., & McIntyre, L. M. (1998). Neuropathological and
affected upper extremity combined with intensive practice
neuropsychological changes in normal aging: Evidence for pre- with the affected upper extremity (e.g., Alberts, Butler, &
clinical Alzheimer disease in cognitively normal individuals. Journal Wolf, 2004; Charles & Gordon, 2005; Taub & Uswatte,
of Neuropathology and Experimental Neurology, 57(12), 11681174. 2005, 2006).
Isaacs, B., & Kennie, A. T. (1973). The Set test as an aid to the detection of
dementia in old people. The British Journal of Psychiatry: The Journal
of Mental Science, 123(575), 467470.
Kaplan, E., Goodglass, H., & Weintraub, S. (1978). The Boston Naming
Test. Boston, MA: Veterans Administration Medical Center.
Morris, J. C., Edland, S., Clark, C., Galasko, D., Koss, E., Mohs, R., et al. CIT has its origins in primate unilateral deafferentation
(1993). The Consortium to Establish a Registry for Alzheimers studies, where it was observed that animals avoided use
Constraint Induced Therapy C 693
of their deafferented limb unless the intact limb was to rehabilitation strategies that focus on developing com-
restrained (e.g., Taub & Uswatte, 2005, 2006). Concepts pensatory techniques, CIT aims to optimize and develop
from CIT were then applied to humans in single case residual functions (Lillie & Mateer, 2006). Although CIT
studies, case series, and small group studies, primarily has been shown to result in significant gains in motor
with people who had sustained hemiplegia following stroke activity, it should not be expected to restore or normalize C
(Taub et al., 1993). The Extremity Constraint Induced movements to pre-injury levels (Taub & Uswatte, 2005).
Treatment (EXCITE) study is a randomized clinical trial
involving over 200 individuals enrolled at 39 months
post-stroke, using uniform CIT methods and measure- Treatment Participants
ment at six testing sites in the USA (Nichols-Larsen,
Clark, Zeringue, Greenspan, & Blanton, 2005; Winstein CIT has been applied in a variety of populations, includ-
et al., 2003; Wolf et al., 2006). ing upper limb hemiparesis following stroke, traumatic
brain injury, and children with hemiplegia (Charles &
Gordon, 2005; Lillie & Mateer, 2006; Shaw et al., 2005).
Rationale or Underlying Theory Research has suggested significant improvement in a
number of populations, including those with chronic
CITreflects the integration of a wide variety of research fields,
TBI (identified as > 1 year post-TBI; Shaw et al., 2005)
including neuroplasticity, motor learning, and behavioral
and both subacute and chronic stroke (identified as <
therapy (Sterr, Szameitat, Shen, & Freivogel, 2006). Two
1 year post-stroke and > 1 year post-stroke, respectively;
mechanisms are typically proposed as the basis for
Page, Levine, & Leonard, 2005).
increased use of affected extremities in CIT: overcoming
Adherence to treatment and level of residual motor
learned nonuse, and induction of use-dependant cortical
function prior to CIT is positively related to treatment
organization (Morris & Taub, 2001).
gains (Shaw et al., 2005; Taub & Uswatte, 2005). Cognitive
Learned nonuse is said to occur following brain injury
impairment is linked to less improvement (Morris et al.,
because unsuccessful motor attempts with the affected
2006). An inherent assumption in CIT is that a residual
extremity leads to punishment (e.g., pain, incoordination,
level of motor function remains in the affected extremity,
failure to meet the goal of the movement). Compensatory
which enables a degree of positive reinforcement for its
behavior also occurs when use of the non-affected extrem-
use (Taub & Uswatte, 2006). A minimal level of residual
ity is positively reinforced.
motor function is often specified as an inclusion criterion
CIT aims to counter-condition learned nonuse. For
in research studies of CIT, as is a lack of general cognitive
example, in animals, the functional limb is restrained and
impairment (e.g., Nichols-Larsen et al., 2005).
the animals complete forced, repetitive movements with
Due to the higher degree of neural plasticity early in
the affected limb. This results in an alteration in the
development, it has been suggested that children may
contingencies of reinforcement, such that compensatory
benefit from CIT to an even greater extent than adults
use of the non-affected limb is no longer reinforced, and
(e.g., Taub & Crago, 1995 as cited by Charles & Gordon,
use of the affected limb is reinforced.
2005). Specific modifications have been made to make
Use-dependant cortical reorganization is a second
CIT more amenable to childhood populations, including
primary mechanism thought to underlie CIT. Neuroim-
conducting CIT in the home environment and practice
aging and transcranial magnetic stimulation studies of the
sessions in the context of play (DeLuca, Echols, Law, &
brain prior to and following CIT have suggested cortical
Ramey, 2005).
reorganization around the infarct site, and recruitment of
a large portion of neurons adjacent to those originally
involved in the control of the limb (Dong, Dobkin, Cen,
Wu, & Winstein, 2006; Morris & Taub, 2001; Park, Butler, Treatment Procedures
Cavalheiro, Alberts, & Wolf, 2004).
CIT is generally administered as a package treatment,
incorporating restraint of the unaffected limb, and
Goals and Objectives structured practice (e.g., shaping and repetitive practice)
with the affected limb. A transfer package involving
A major goal of CIT is to increase the use of the affected limb behavioral techniques used to promote transfer of gains
in real world environments (Sterr et al., 2006). In contrast from the laboratory to daily life is emphasized in CIT
694 C Constraint Induced Therapy
(Taub & Uswatte, 2005). Structured practice with the measured in a laboratory setting, and it is therefore
affected arm involves everyday functional tasks (Alberts recommended that these dimensions be assessed separately
et al., 2004), such as eating lunch, throwing a ball, etc. (Uswatte & Taub, 2005).
(Glover, Mateer, Yoell, & Speed, 2002). The Wolf Motor Function Test is a frequently used
Conventional CIT treatment aims for restraint of the measure of laboratory motor performance (e.g., Uswatte
unaffected limb for 90% of waking hours, and structured & Taub, 2005). Functional outcome is most often studied
practice 68 h per day (Kaplon, Prettyma, Kushi, & through use of Motor Activity Log (MAL), a semistruc-
Winstein, 2007). The treatment period for restraint and tured interview of extremity use in real-life settings (e.g.,
structured practice is 5 days per week, for 23 consecutive Winstein et al., 2003).
weeks with a 1:1 therapistpatient ratio.
The intensive nature of CIT has prompted concerns
regarding its applicability to clinical settings, due to insti-
Qualifications of Treatment Providers
tutional and clinical factors. For example, facilities may
lack the space, therapist time, and associated financial
Physiotherapists most frequently provide services. Occu-
resources to administer CIT (Levine & Page, 2004).
pational therapists have also been identified as providing
Concerns have also been raised regarding attrition rates,
services (e.g., Brogardh, 2006). Specialized training in
compliance, and health care coverage (Levine & Page,
CIT is recommended (DeLuca et al., 2005; Winstein
2004; Page & Levine, 2003).
et al., 2003).
Because these factors can impede service delivery and
the aims of CIT, modifications of treatment protocols
have been introduced. For example, group delivered CIT
(Brogardh, 2006), automatized delivery of CIT with less Cross References
therapist involvement (AutoCITE; Lum, Uswatte, Taub,
Hardin, & Mark, 2006; Taub, Lum, Hardin, Mark, & Brain Plasticity
Uswatte, 2005), and fewer hours of restraint and shorter Cognitive Rehabilitation
practice sessions over longer periods (Levine & Page, Head Injury
2004; Page & Levine, 2003; Page, Sisto, Johnston, & Hemiparesis
Levine, 2002) have all resulted in significant treatment Hemiplegia
gains, often comparable to the gains of conventional Physical Therapy
CIT (e.g., Levine & Page, 2004; Lum et al., 2006). Current Rehabilitation Psychology
research suggests that particularly important features are Traumatic Brain Injury
prolonged rehearsal on specific tasks involving the affect-
ed limb and shaping in effort to improve everyday activity
(Pomeroy & Tallis, 2002). References and Readings
Alberts, J. L., Butler, A. J., & Wolf, S. L. (2004). The effects of constraint-
induced therapy on precision grip: A preliminary study. Neuroreh-
Efficacy Information abilitation and Neural Repair, 18, 250258.
Brogardh, C. (2006). Constraint-induced movement therapy in patients
CIT has been shown to significantly improve performance with stroke: A pilot study on effects of small group training and of
extended mitt use. Clinical Rehabilitation, 20, 218227.
on laboratory tests of motor ability and functional out-
Charles, J., & Gordon, A. M. (2005). A critical review of constraint-
come measures. The effect sizes for functional outcome induced movement therapy and forced use in children with hemiplegia.
measures tend to be very large in magnitude (Taub & Neural Plasticity, 12, 245261.
Uswatte, 2005). Effect sizes on laboratory tests tend to DeLuca, S. C., Echols, K., Law, C. R., & Ramey, S. L. (2005). Intensive
be more variable (as reviewed by Lillie & Mateer, 2006). pediatric constraint-induced therapy for children with cerebral
palsy: Randomized, controlled, crossover trial. Journal of Child
Dong, Y., Dobkin, B. H., Cen, S. Y., Wu, A. D., & Winstein, C. J. (2006).
Motor cortex activation during treatment may predict therapeutic
Outcome Measurement gains in paretic hand function after stroke. Stroke, 37, 15521555.
Glover, J. E., Mateer, C. A., Yoell, C., & Speed, S. (2002). The effectiveness
There can be significant discrepancies between real of constraint induced movement therapy in two young children with
world spontaneous functional use and motor ability as hemiplegia. Pediatric Rehabilitation, 5, 125131.
Constructional Apraxia C 695
Kaplon, R. T., Prettyma, M. G., Kushi, C. L., & Winstein, C. J. (2007). Six constraint-induced movement therapy. Rehabilitation Psychology,
hours in the laboratory: A quantification of practice time during 50, 3442.
constraint-induced therapy (CIT). Clinical Rehabilitation, 21, Winstein, C. J., Miller, J. P., Blanton, S., Taub, E., Uswatte, G., Morris, D.,
950958. et al. (2003). Methods for a multisite randomized trial to investigate
Lillie, R., & Mateer, C. A. (2006). Constraint-based therapies as a pro- the effects of constraint-induced movement therapy in improving
posed model for cognitive rehabilitation. Journal of Head Trauma
upper extremity function among adults recovering from a
cerebrovascular stroke. Neurorehabilitation and Neural Repair, 17,
C
Levine, P., & Page, S. J. (2004). Modified constraint-induced therapy: 137152.
A promising restorative outpatient therapy. Topics in Stroke Rehabil- Wolf, S. L., Winstein, C. J., Miller, J. P., Taub, E., Uswatte, G., Morris, D.,
itation, 11, 110. et al. (2006). Effects of constraint-induced movement therapy on
Lum, P. S., Uswatte, G., Taub, E., Hardin, P., & Mark, V. W. (2006). upper extremity function 3 to 9 months after stroke: The EXCITE
A telerehabilitiation approach to delivery of constraint-induced randomized clinical trial. JAMA, 296, 20952103.
movement therapy. Journal of Rehabilitation Research and Develop-
ment, 43, 391400.
Morris, D. M., Shaw, S. E., Mark, V. W., Uswatte, G., Barman, J., &
Taub, E. (2006). The influence of neuropsychological characteristics
on the use of CI therapy in persons with traumatic brain injury.
Neurorehabilitation, 21, 131137. Constructional Apraxia
Morris, D. M., & Taub, E. (2001). Constraint-induced therapy approach
to restoring function after neurological injury. Topics in Stroke A MY K. B YERLEY, A NDREW S. DAVIS
Rehabilitation, 8, 1630. Ball State University
Nichols-Larsen, D. S., Clark, P. C., Zeringue, A., Greenspan, A., &
Muncie, Indiana, USA
Blanton, S. (2005). Factors influencing stroke survivors quality of
life during subacute recovery. Stroke, 36, 14801484.
Page, S., & Levine, P. (2003). Forced use after TBI: Promoting plasticity
and function through practice. Brain Injury, 17, 675684. Synonyms
Page, S. J., Levine, P., & Leonard, A. C. (2005). Modified constraint-
induced therapy in acute stroke: A randomized controlled pilot
Constructional dyspraxia
study. Neurorehabilitation and Neural Repair, 19, 27.
Page, S. J., Sisto, S., Johnston, M. V., & Levine, P. (2002). Modified
constraint-induced therapy after subacute stroke: A preliminary
study. Neurorehabiliation and Neural Repair, 16, 290295. Short Description or Definition
Park, S. W., Butler, A. J., Cavalheiro, V., Alberts, J. L., & Wolf, S. I. (2004).
Changes in serial optical topography and TMS during task perfor-
mance after constraint-induced movement therapy in stroke: A case
Constructional apraxia is an inability to reproduce pat-
study. American Society of Neurorehabiliation, 18, 95105. terns or join component parts into a whole. This condition
Pomeroy, V., & Tallis, R. (2002). Neurological rehabilitation: A science is assessed through observation of a patient completing
struggling to come of age. Physiotherapy Research International, activities such as drawing, copying, or building three-
7, 7689.
dimensional objects (Lezak, Howieson, & Loring, 2004).
Shaw, S. E., Morris, D. M., Uswatte, G., McKay, S., Meythaler, J. M., &
Taub, E. (2005). Constraint-induced movement therapy for recovery
Impairments in processing spatial forms observed in con-
of upper-limb function following traumatic brain injury. Journal of structional apraxia can occur in the absence of apraxia of
Rehabilitation Research and Development, 42, 769778. singular motor movements (Benton, 1969).
Sterr, A., Szameitat, A., Shen, S., & Freivogel, S. (2006). Application of
CIT concepts in the clinical environment: Hurdles, practicalities, and
clinical benefits. Cognitive Behavioral Neurology, 19, 4853.
Taub, E., Lum, P. S., Hardin, P., Mark, V. W., & Uswatte, G. (2005).
Categorization
AutoCITE: Automated delivery of CIT with reduced effort by
therapists. Stroke, 36, 13011304. Recent studies suggest qualitatively different types of con-
Taub, E., Miller, N. E., Novack, T. A., Cook, E. W. III, Fleming, W. C., structional apraxia determined by the location of brain
Nepomuceno, C. S., et al. (1993). Technique to improve chronic
insult. In general, patients with right hemisphere im-
motor deficit after stroke. Archives of Physical Medicine and Rehabil-
itation, 74, 347354.
pairment make more coordinate type errors (e.g., distance
Taub, E., & Uswatte, G. (2005). Use of CI therapy for improving motor and angular distortions), whereas those with left hemi-
ability after chronic CNS damage: A development prefigured by Paul spheric impairment tend to commit categorical errors
Bach-Y-Rita. Journal of Integrative Neuroscience, 4, 465477. (e.g., position exchanges and pattern reversals) (Laeng,
Taub, E., & Uswatte, G. (2006). Constraint-induced movement therapy:
2006). Patients with right hemispheric impairment gener-
Answers and questions after two decades of research. Neurorehabil-
itation, 21, 9395.
ally experience difficulties with the overall gestalt of the
Uswatte, G., & Taub, E. (2005). Implications of the learned non-use constructional task. Their approach to the task may ap-
formulation for measuring rehabilitation outcomes: Lessons from pear to be more fragmented and disjointed, not coming
696 C Constructional Apraxia
together as a whole. Constructions created by patients treatment, while others may have symptoms spontane-
with right hemisphere impairment may make drawing ously diminish. For other patients, symptoms may be
that are sparse or may be significantly distorted with permanent. Further research for prognostic factors of
regard to perspective or proportion. Some patients with constructional apraxia is warranted.
right hemisphere injury may create overdetailed or repet-
itive drawings, while others may draw elaborate pictures
that are missing important components. Additionally, Neuropsychology and Psychology of
patients with right hemispheric lesions frequently dem- Constructional Apraxia
onstrate left-sided visual inattention and include more
details on construction tasks. Symptoms associated with constructional apraxia fre-
In contrast, those with left hemisphere impairment quently indicate deficits associated with right parietal
may be able to construct the overall concept and propor- dysfunction, or the non-dominant hemisphere and
tions accurately, and their constructions may also be global cognitive processing impairment. However, re-
symmetrical. However, they often tend to generate draw- cent research has shown involvement of both hemi-
ings with fewer details (McFie & Zangwill, 1960). Patients spheres, namely the parietal lobes, in constructional
with left hemisphere impairment may perform construc- apraxia. Furthermore, neuroimaging research has
tion tasks better when given a model rather than working implicated the ventral premotor area, posterior part
on command. They tend to focus on overall shape rather of the inferior temporal sulcus, and occipital cortex
than specific details. Overall, construction deficits tend to in constructional deficits (Makuuchi, Kaminaga, &
be more common when the lesion is located in the poste- Sugishita, 2003; Nielson, Cummings, & Cotman, 1996).
rior portion of the brain rather than the anterior areas. Constructional apraxia should not be conceptualized as a
Furthermore, while patients with cortical lesions make the unitary syndrome caused by discrete lesions (Guerin, Ska,
same types of constructional errors as patients with sub- & Belleville, 1999), but as resulting from impairment in
cortical lesions, those with subcortical impairment appear lateralized perceptual processing of spatial abilities
to have more significant impairment. (Laeng, 2006). Constructional apraxia manifests more
frequently in patients with lesions in the non-dominant
hemisphere (De Renzi, 1997). Consequently, construc-
Epidemiology tional apraxia often co-occurs with deficits in visual-spa-
tial perception (Benton, 1982), although both conditions
A review of literature revealed no known reports of preva- may exist independently. Therefore, the presentation of
lence of constructional apraxia. In fact, constructional constructional apraxia differs among patients; some
apraxia is generally included as a subcategory of apraxia, struggle with copying figures, whereas others demonstrate
which is listed as a rare disease by the office of rare difficulty constructing designs with blocks (Lezak et al.,
diseases (ORD) of the National Institutes of Health 2004).
(NIH). Therefore, apraxia is known to affect less than
200,000 people in the population of the USA. Thus, as a
subcategory of apraxia, constructional apraxia affects even Evaluation
fewer individuals. Common causes of constructional aprax-
ia include dementia (e.g., Alzheimers Disease) and stroke, The utility of constructional apraxia as an estimate of
which are two of the most frequent neurological diseases. global cognitive functioning has a well-established his-
tory in neurology, neuropsychology, and rehabilitative
settings. Tasks commonly utilized to assess construc-
Natural History, Prognostic Factors, and tional apraxia include copying, drawing, or construct-
Outcomes ing simple figures, such as clocks or crosses. These
efficient, brief, and easy-to-administer construction
Constructional apraxia is not in itself a disease but a tasks are attractive to clinicians for use with patients
symptom of another neurological illness. Therefore, prog- with impaired test-taking skills. The tasks used to
nosis of the condition is related to the prognosis of the assess constructional apraxia have proven to be re-
underlying neurological condition. Prognosis for indivi- markably sensitive to global neurological impairment
duals with constructional apraxia varies and has not been because of the involvement of various cognitive pro-
well studied. Some patients may improve via continued cessing domains necessary for completing construction
Content-Referenced Testing C 697
tasks. Construction tasks can require complex cogni- Benton, A. L. (2009). Constructional apraxia: Some unanswered ques-
tions. In A. L. Benton (Ed.), Brain & behavior: Research in clinical
tive processes, including visual-spatial and visuoper-
neuropsychology (pp. 129141). Chicago: Aldine.
ceptual abilities, receptive language skills, numerical De Renzi, E. (1997). Visuospatial and construction disorders. In T. E.
knowledge, graphomotor skills, and intact executive Feinberg, & M. J. Farah (Eds.), Behavioral neurology and neuropsy-
functioning (Freedman et al., 1994; Lezak et al., 2004; chology (pp. 297304). New York: McGraw-Hill.
C
Shulman, 2000). The sensitivity of construction tasks to Fischer, J. S., & Loring, D. W. (2004). Construction. In M. D. Lezak,
D. B. Howieson, & D. W. Loring (Eds.), Neuropsychological assess-
global cognitive impairment renders these tasks advanta-
ment (4th ed., pp. 531568). New York: Oxford University Press.
geous in the assessment of patients with known or Freedman, M., Leach, L., Kaplan, E., Winocur, G., Shulman, K., & Delis,
suspected neurological impairment, including those D. C. (1994). Clock drawing: A neuropsychological analysis. New York:
with Alzheimers Disease, Huntingtons Disease, Parkin- Oxford University Press.
sons Disease, aphasia, seizures, CVAs, and TBIs. As an Guerin, F., Ska, B., & Belleville, S. (1999). Cognitive processing of drawing
abilities. Brain and Cognition, 40:464478.
example, construction tasks have been shown to be useful
Laeng, B. (2006). Constructional apraxia after left or right unilateral
as screening tools and markers for disease progression stroke. Neuropsychologia, 44:15951606.
with Alzheimers patients. Furthermore, the presence of Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). Neuropsychologi-
constructional apraxia early in the course of Alzheimers cal Assessment (4th ed.). New York: Oxford University Press.
Disease has been shown to be a predictor of accelerated Makuuchi, M., Kaminaga, T., & Sugishita, M. (2003). Both parietal lobes
are involved in drawing: A functional MRI study and implications
cognitive decline (Smith, Esiri, Barnetson, King, & Nagy,
for constructional apraxia. Brain Research, 16:338347.
2001). McFie, J., & Zangwill, O. L. (1960). Visual construction disabilities
associated with lesions of the left cerebral hemisphere. Brain,
83:243260.
Treatment Nielson, K., Cummings, B., & Cotman, C. (1996). Constructional apraxia
in Alzheimers disease correlates with neuritic neuropathology in
occipital cortex. Brain Research, 741:284293.
While physical and occupational therapies may modestly Shulman, K. L. (2000). Clock-drawing: Is it the ideal cognitive screening
improve the functioning of an individual with construc- test? International Journal of Geriatric Psychiatry, 15:548561.
tional apraxia, no specific medical treatment has been Smith, M., Esiri, M., Barnetson, L., King, E., & Nagy, Z. (2001). Con-
found to be effective with significantly improving constructional apraxia in Alzheimers disease: Association with occipital
lobe pathology and accelerated cognitive decline. Dementia and
structional deficits. Furthermore, medications that target
Geriatric Cognitive Disorders, 12:281288.
the slowing of dementia do not appear to help with
constructional apraxia. The most beneficial approach for
treatment of individuals with constructional apraxia
involves ensuring their environments are safe. For exam-
ple, it is important to arrange furniture in the home in a
way that the patient can navigate safely. Constructional Dyspraxia
Constructional Apraxia
Cross References
Apraxia
Dementia
Stroke
Visual-Motor Function Content Validity
Test Validity
Benton, A. L. (1969). Constructional apraxia: Some unanswered ques-

tions. In A. L. Benton (Ed.), Contributions to clinical neuropsychology
(pp. 128141). Chicago: Aldine.
Benton, A. L. (1982). Spatial thinking in neurological patients:
Historical aspects. In M. Potegal (Ed.), Spatial abilities: Development
Content-Referenced Testing
and physiological foundations (pp. 253271). New York: Academic
Press. Domain Referenced Test Interpretation
698 C Contextual Memory
Contingency Table. Table 2

Contextual Memory
TBI No TBI
Source Memory Test + 35 15 50
Test 5 45 50
40 60 100
Cond. = Condition
Contingency Table
C HRISTIAN S CHUTTE , B RADLEY A XELROD In this example, hit rate would be calculated by adding
John D. Dingell VA Medical Center the number of true negatives and false negatives and then
Detroit, MI, USA dividing them by the number of total decisions ((TP +
FN)/total decisions). This allows for a relatively simple
way to assess the relationships between categorical
Synonyms variables.
A concrete example would be a group of 100 patients,
2 2 Table 40 of whom have a true diagnosis of traumatic brain injury
(TBI) who are administered a brief test to diagnose the
presence of the disorder. By comparing the obtained scores
to a cutting score, 55 patients are tagged as having the
Definition disorder and 45 patients as not having the disorder. Using
this information, a contingency table to find hit rate can
A contingency table is generally a representation of cate- quickly be defined, sensitivity, and specificity, as well as
gorical data in a tabular format, such as a 2 2 table, positive and negative predictive power.
though the table can have three or more variables. One can then calculate hit rate ((TP + FN)/total
decisions) or (35 + 5)/100 = .4, sensitivity (TP/(TP +
FN)) or 35/(35 + 5) = .875, specificity (TN/(TN + FP))
Current Knowledge or 45/(45 + 15) = .75, positive predictive power (TP/(TP +
FP)) or 35/(35 + 15) = .70, and negative predictive power
There are row variables on the horizontal axis and column (TN/(TN + FN)) or 45/(45 + 5) = .90. In verbal form, hit
variables on the vertical axis. It represents mutually exclu- rate is a proportion of the number of correctly identified
sive variables. Good examples of contingency tables are TBI patients and incorrectly ruled out TBI patients divided
hit rate, sensitivity, and specificity, as well as positive and by the total number of patients (40% in this case) or
negative predictive power. In the case of hit rates to assess sensitivity is computed by the percentage of people who
the number of correct classification decisions that result actually have the disorder who were appropriately detected
from the use of a particular test or measure, one would by the test (87.5% in this case).
enter the number of true positives, true negatives, false More complex contingency tables can be used, such as
positives, and false negatives into a contingency table like 3 2, 3 3, or more, though relationships between
the one below. variables are less clear owing to difficulties with interac-
tion effects. More complex contingency tables are often
analyzed with more complex statistical procedures, such
as log-linear analysis.
Contingency Table. Table 1
Cond. + Cond. Cross References

Test + True + (TP) False + (FP) Total + Decisions
Negative Predictive Power
Test False (FN) True (TN) Total Decisions
Positive Predictive Power
Base Rate Cond. Absent Total of all decisions Sensitivity
Cond. = Condition Specificity
Continuous Performance Tests C 699
more commonly used in standard neuropsychological eva-

Continuous Performance Tests luations. In fact, the CPT was one of the first neuropsycho-
logical paradigms widely adapted for computerized
R ONALD A. C OHEN assessment. Subsequently, impairments on this paradigm
Brown University were demonstrated across various disorders, most notably
Providence, RI, USA
C
schizophrenia (Nuechterlein, 1983) and attention deficit
disorder (Epstein et al., 2003).
Synonyms
Psychometric Data
CPT
In its original form, the CPT provided measures of accu-
racy and response bias over the course of a fixed time
Description period using signal detection methodology. Although the
tests may vary in terms of length and type of stimulus
An attention paradigm that has evolved into a class used, the underlying paradigm is the same across versions
of neuropsychological tests used to assess sustained of the test. Patients are presented with series of letters
attention. There is not a single continuous performance (typically) or other stimuli on a screen, and are told to
test (CPT) test, as a number of commercially available and push a response key only when they see the target
research CPT tasks exist and have been published in the stimulus. They are instructed not to respond when they
neuropsychological literature. The common characteristic see any other stimuli. The letter x has often been used
of all CPT tests is that they involve sequential presentation as the target in CPT paradigms, with the task to respond
of stimuli, usually letters or numbers, over an extended to this letter while ignoring other letters that flash before
period of time. The task demand is to attend and respond them. Several common variations of the standard CPT
to particular target stimuli, while ignoring other stimuli paradigm exist, in particular, a conditional task, in which
that serve as nontarget distractors. the patient must only respond to the target letter when
another stimulus occurs immediately before it (e.g., A-X),
which increases the difficulty of the task.
Historical Background In recent years, a variety of tests based on computer-
ized CPT paradigms have been developed, with varying
Early efforts by psychologists to assess attention in the degree of sensitivity and specificity to clinical disorders of
context of intellectual or other cognitive testing typically attention. At the present time, the most widely used
relied on tests such as digit span, which provided a commercially available CPT tests are versions by Conners,
useful measure of attentional focus and span, but did not Epstein, Angold, and Klaric (2003) and the Test of
address other important elements of attention, such as the Variables of Attention (TOVA), though a variety of others
patients ability to selectively attend to information or to exist, such as VIGIL (1990) and the d2 Test of Attention
sustain attention (Cohen, 1993). Sustained attention was (Brickenkamp, 1992). Typically, a CPT is included as part
particularly difficult to assess using traditional paper-and- of a more comprehensive battery of tests of attention and
pencil tests, as it required the measurement of signal detec- executive functioning.
tion performance over extended periods of time. Psycholo- Given that the CPT paradigm is based on signal detec-
gists typically relied on behavioral observation or analysis of tion theory and method, there are certain indices common
patterns of inconsistency in test performance over time to to all versions of the test; correct responses, errors of
derive evidence of sustained attention problems. The devel- omission (misses), errors of commission (false positives),
opment of the tachistoscope for rapid presentation of visual and response time (RT). Correct responses are based on the
stimuli with controlled timing provided a means of circum- sum of the number of times the patient correctly responds
venting this problem. Mirsky et al. (1956) described the to the target and correctly avoids responding to distractors.
continuous performance paradigm and provided research Omission errors (misses) are errors involving a failure to
data supporting its sensitivity in detecting brain damage. respond to the target, while commission errors (false posi-
The advent and widespread availability of computer tech- tives) are errors involving a response to nontargets. Errors
nology in the decades that followed led to more widespread of commission reflect a failure to inhibit responding. High
experimentation with this paradigm and it eventually being omission rates indicate that either the patient is not
700 C Continuous Performance Tests
focusing adequately on the stimuli or that their processing of consistency across versions of the tests, particularly
speed is slow and they are unable to respond rapidly with respect to basic parameters such as the duration of
enough. CPT tests usually also provide a measure of the interstimulus interval (ISI), the total duration of the
mean response time (RT), which reflects the processing task, and the task demand. For example, a task requiring
speed of the patient during the task. Higher rates of correct detection of a single letter is much easier than a condi-
detections indicate better attention performance. tional paradigm requiring detection of a letter sequence
From these primary measures, signal detection indices (A-X). Furthermore, the duration of a typical CPT test
are usually derived based on a comparison of error types. can range from several minutes to over 20 min. Versions
Based on the total number of errors of commission with a long ISI tend to be relatively easy to perform, but
and omission on the CPT, a discrimination index (d0 ) is are tedious, with behavioral challenge arising from the
calculated which provides a measure of accuracy based on monotony of the task, which over a long test period is
standardized scores (z-scores) from normative samples. A really a test of vigilance. In contrast, versions that have a
measure of response bias (b) is also usually derived based short ISI with conditional task demands or other char-
on the difference in standard scores for each type of error. acteristics that increase difficulty tend to be more sensi-
Response bias indices provide a better way of interpreting tive to sustained attention in the context of greater
tendencies to make one type of error or the other because information processing demand and requirement for
they account for the total number of errors of each type. focused attention. Adaptive-rate continuous perfor-
Receiver operator characteristics (ROC) metrics can also mance methods provide a means of circumventing this
be derived, which provide a way of interpreting the issue. For example, the adaptive-rate continuous perfor-
tendency to make errors of each type as a function of mance test (ARCPT; Cohen, 1993) adjusts its ISI over the
the signal detection parameters of the task, such as course of the test based on accuracy of response to
percentage of targets to nontargets. General equations compensate for the slow speed of processing. The final
for d0 and b are shown below. ISI that is maintained by the end of the test provides a
strong measure of capacity limitations related to proces-
d0 zmisses zfalse positives sing speed deficits. Also the ARCPT provides separate
vigilance decrement and inconsistency indices to enable
b zmisses zfalse positives=z total errors assessment of the temporal dynamics of performance
over 10 blocks of time over the duration of the test.
In the past, many versions of the CPT provided only these The ARCPT measures attentional performance on a
basic indices, which limited their usefulness in rapid and challenging task which is less subject to bore-
characterizing problems with sustained attention. While dom. Therefore, the ARCPT provides enables the assess-
d0 and b provide excellent measures of detection accuracy, ment of sustained attention during a cognitively
response deposition, and overall attention performance, demanding task compared to standard CPT paradigms.
they do not directly provide measures of performance Also, because the ISI adjusts to shorter durations when a
over time. Recent versions of the Conners and other CPT patient is performing well, the test can typically be com-
tests tend to now include a measure of temporal variability pleted in about 10 min. The ARCPT also provides several
in performance. While there are a variety of ways that the metrics that enable assessment of temporal inconsisten-
temporal nature of performance can be determined, two cies in performance.
general types of measures exist: (1) performance decrement Despite the fact that CPT tests vary in a variety of
and (2) performance inconsistency. Performance decre- ways, many of the commonly used measures (e.g., Con-
ment provides a measure of the change in performance ners CPT) report good testretest reliability in healthy
between the beginning and end of the test. In theory, if a adults. CPT performance tends to correlate well with
person is failing to sustain attention, their performance performance on other information processing-based
should worsen the longer they stay on task. However, measures and performance on speeded tests of attention
often this measure is not impaired except when there is a and executive function, such as the Stroop and trail-
severe problem with sustained attention and fatigue after making test. Validation studies conducted with the
several minutes of effort. Performance inconsistency ARCPT indicate strong reliability (r = .95) for accuracy
indices provide an alternative temporal measure based on of performance (d0 ) across samples and strong validity as
variance across time, as opposed to linear decrement. indicated by the sensitivity of CPT indices to measures of
A primary problem in interpreting the meaning and structural and functional brain and systemic physiological
clinical significance of CPT findings stems from the lack disturbances as discussed in greater detail below.
Contraindication C 701
Clinical Uses Sustained Attention

Vigilance
CPT tests should be included in all comprehensive neu-
ropsychological batteries designed to provide a thorough
assessment attention, executive functioning, and proces- C
sing speed. There is a well-established research and clinical
Brickenkamp, R. Z. E. (1992). The d2 test of attention. Seattle, WA:
literature demonstrating that this paradigm is highly Hogrefe & Huber.
sensitive to brain dysfunction. The fact that the CPT yields Cohen, R. A. (1993). Neuropsychology of attention. New York: Plenum.
measures of information processing characteristics based Cohen, R., Lohr, I., Paul, R., & Boland, R. (2001). Impairments of atten-
on a task with controlled timing and consistency of tion and effort among patients with major affective disorders. Journal of
Neuropsychiatry and Clinical Neurosciences, 13(3), 385395.
stimulus presentation makes it a valuable addition to
Conners, C. K., Epstein, J. N., Angold, A., & Klaric, J. (2003). Continuous
standard paper-and-pencil tests of cognitive function. performance test performance in a normative epidemiological
Performance deficits on the CPT are evident in sample. Journal of Abnormal Child Psychology, 31(5), 555562.
patients with various forms of brain dysfunction Epstein, J. N., Erkanli, A., Conners, C. K., Klaric, J., Costello, J. E., &
(Rosvold, Mirsky, Sarason, Bransome, & Beck, 1956). Angold, A. (2003). Relations between continuous performance test
performance measures and ADHD behaviors. Journal of Abnormal
The most obvious use for the CPT is in the assessment
Child Psychology, 31(5), 543554.
of attention deficit disorder (ADD), for which the objec- Gunstad, J., Cohen, R. A., Paul, R. H., & Gordon, E. (2006). Dissociation
tive assessment of sustained attention is central to the of the component processes of attention in healthy adults. Archives of
diagnosis. However, there is now an extensive research Clinical Neuropsychology, 21(7), 645650.
literature demonstrating deficits or outright impairments Jerskey, B., Cohen, R. A., Jefferson, A. L., Hoth, K. F., Haley, A. P.,
Gunstad, J. J., et al. (2009). Sustained attention is associated with left
of CPT performance among patients with a wide range of
ventricular ejection fraction in older adults with heart disease. Journal
neurological and psychiatric conditions. For this reason, of the International Neuropsychological Society, 15(1), 137141.
impaired CPT performance should be considered a highly Leark, R. A., Greenberg, L. K., Kindschi, C. L., Dupuy, T. R., & Hughes,
sensitive measure of functional attention impairment and S. J. (2007). Test of variables of attention: Clinical manual. Los
brain dysfunction, though not necessarily specific to one Alamitos: The TOVA Company.
Nuechterlein, K. H. (1983). Signal detection in vigilance tasks and behav-
type of neurological or psychiatric condition.
ioral attributes among offspring of schizophrenic mothers and among
Impairments of CPT are evident in patients with neu- hyperactive children. Journal of Abnormal Psychology, 92(1), 428.
rodegenerative disorders like Alzheimers disease, as well Rosvold, H. E., Mirsky, A. F., Sarason, I., Bransome, E. D., Jr., & Beck,
as disorders affecting subcortical and white matter brain L. H. (1956). A continuous performance test of brain damage.
systems, such as multiple sclerosis, HIV, and Journal of Consulting Psychiatry, 20, 343350.
VIGIL: A continuous performance test. (1990). New Hampshire:
cerebrovascular disease. In fact, patients with cardiovas-
Forethought.
cular disease show a relationship between cardiac output
and CPT performance (Jerskey et al., 2009). Among
patients with severe affective disorders, CPT performance
is often impaired and associated with problems with Contraindication
effort (Cohen, Lohr, Paul, & Boland, 2001). CPT has
been shown to be sensitive to sustained attention and M ARLA S ANZONE
information processing deficits associated with neurotox- Independent Practice
ic exposure to lead, solvents, drugs, or other substances. Annapolis, MD, USA
An important clinical determination that needs to be
made when examining performance on the CPT is whether
there is evidence of an actual problem with sustained Synonyms
performance, or whether a broader problem with focused
and selective attention exists that occurs regardless of the Conflict; Counterindicant
time spend on task.
Definition
Cross References
A contraindication is a circumstance, condition, symptom,
Attention Deficit Disorder (ADD) or factor that increases the risk associated with a medical
Signal Detection procedure, drug, or treatment. A contraindication refers to
702 C Contrecoup Injury
any intervention considered inappropriate or inadvisable results from accelerationdeceleration events during
based upon unique factors of the situation such as potential which the force impacting the head causes the brain to
harmful interactions between drugs or medical conditions slam into the skull on the opposite side of the blow. Motor
that renders an individual vulnerable if implemented. vehicle accidents, falls, sports injuries, and physical
A contraindication may be absolute or relative. Absolute assaults with blunt objects frequently result in contrecoup
contraindications are those which are inadvisable without injuries. Skull characteristics make the most probable
exception or qualification. They are either permanently sites of injury in the frontal and temporal lobes, as tips
recommended against, or temporarily until the disqualifying of the skull can more easily be forced into the under-
condition is remediated. The use of the atypical antipsychot- lying brain tissue in the frontal and temporal lobes.
ic medication, clozapine carries a risk of agranulocytosis, a Neuropsychological evaluation can help to identify cog-
sever low white blood cell disorder condition. Clozopine nitive impairments arising from both the primary and
would be an absolute contraindication in an individual secondary sites of injury.
with a history of bone marrow suppression
Relative contraindications refer to circumstances in
which procedures or treatments are considered in com- Cross References
parative terms. They are contingent upon a risk/benefit
analysis of the relevant factors. The proportionate value of Acceleration Injury
an intervention is compared with its potential for negative Biomechanics of Injury
consequences. An example of a relative contraindication Cortical Contusion
would be the use of an anti-convulsant/mood stabilizing Traumatic Brain Injury
medication in the ongoing treatment of a pregnant
woman with severe bipolar mania and suicidality, but
whose has been asymptomatic only while on lithium. References and Readings
Cross References Graham, D. I., Saatman, K. E., Marklund, N., Copnte, V., Morales, D.,
Royo, N., & McIntosh, T. K. (2006). The neuropathology of trauma.
In R. W. Evans (Eds.), Neurology and trauma (2nd ed., pp. 4594).
Extrapyramidal Side Effects New York: Oxford University Press.
Iatrogenic
Signs

Mosby. (2006). Contra- (definition). In T. Myers (Ed.), Mosbys dictionary
of medicine, nursing & health professions (7th ed., pp. 453). Missouri:
A NNA M AC K AY-B RANDT
Mosby Elsevier.
Venes, D., Thomas, C., Egan, E., & Houska, A. (2001). Contraindication Brown University Medical School
(definition). In D. Venes, et al. (Eds.), Tabers medical dictionary Providence, RI, USA
(19th ed., pp. 479). Philadelphia: FA Davis Company.
Synonyms
Contrecoup Injury
Central executive; Cognitive control; Supervisory atten-
B ETH R USH tional system
Mayo Clinic
Definition
Definition Higher-order cognitive processes that influence the

regulation of behavioral responses and the selection of
Contrecoup injury is an injury to the brain tissue directly information to be attended to are based on task-related
beneath the skull, opposite to the point of impact. It goals.
Controlled Oral Word Association Test C 703
Current Knowledge Frontal Lobe

Vigilance
Neuroanatomical
From a neuroanatomical perspective, brain networks

C
other than those related to frontal lobe functions can be
Anderson, M. C., & Green, C. (2001). Suppressing unwanted memories
involved in controlled aspects of attention. For example,
by executive control. Nature, 410, 366369.
parietal lobe structures appear to be important for Baddeley, A. D., & Hitch, G. (1974). Working memory. In G. H. Bower
response intention and sensory selective attention. How- (Ed.), The psychology of learning and motivation: advances in research
ever, control behaviors such as response planning, selec- and theory (Vol. 8, pp. 4789.). New York: Academic Press.
tion, and execution are associated with networks of Cohen, R. (1993). The neuropsychology of attention. New York: Plenum.
Miyake, A., Friedman, N. P., Emerson, M. J., Witzki, A. H., Howerton, A.,
cortical and subcortical regions linked to the frontal
& Wager, T. D. (2000). The unity and diversity of executive functions
lobes. It is these functions that are most commonly and their contributions to complex frontal lobe tasks: A latent
refer to when discussing control functions of the brain. variable analysis. Cognitive Psychology, 41, 49100.
Although there is not a clear anatomical mapping, studies Monsell, S., & Driver, J. (2000). Attention and performance XVIII: Control
suggest that different regions of the frontal lobe (and of cognitive processes. Cambridge, MA: MIT Press.
OReilly, R. C., Braver, T. S., & Cohen, J. D. (1999). A biologically-based
associated networks) relate to different aspects of control,
neural network model of working memory. In P. Shah & A. Miyake
such that there is a heterogeneity of functioning that (Eds.), Models of working memory. New York: Cambridge University
would argue against any unitary conceptualization of Press.
attentional control (Cohen, 1993). Shallice, T. (1988). Form neuropsychology to mental structure. Cambridge:
Shallice, T., Stuss, D. T., Picton, T. W., Alexander, M. P., & Gillingham, S.
(2008). Mapping task switching in frontal cortex through neuropsy-
Cognitive chological group studies. Frontiers in Neuroscience, 2(1), 7985.
Similarly, cognitive researchers have made an effort to

move away from a homunculus view of control functions,
pointing out that terms such as central executive (Baddely Controlled Oral Word Association
& Hitch, 1974), supervisory attentional system (Shallice, Test
1988), and executive control (e.g., Anderson & Green,
2001) all take on the role of a poorly defined black box J ANET PATTERSON
and give the impression of a unitary concept. These terms California State University East Bay
may have been useful as placeholders, while cognitive Hayward, CA, USA
researchers worked out the details of other related systems,
such as the slave systems of Baddely and Hitchs (1974)
model of working memory. However, with an emerging Synonyms
focus on attentional control and with new tools for the
direct study of phenomena such as task switching, re- Category fluency; CFL test; COWA; COWAT; F-A-S test;
sponse inhibition, goal formation, and planning in the Letter fluency; Phonemic fluency; Verbal fluency
form of functional neuroimaging (e.g., Shallice, Picton,
Alexander, & Gillingham, 2008), computational modeling
(OReilly, Braver, & Cohen, 1999), and statistical model- Description
ing techniques (Miyake et al., 2000), there is a growing
body of information that specifies the subprocesses The Controlled Oral Word Association Test (COWAT) is a
involved in these selection functions with increasing clar- measure of verbal fluency and is a subtest of the Multilin-
ity (see also Monsell & Driver, 2000 for a review). gual Aphasia Examination (MAE; Benton, Hamsher, &
Sivan, 1994). The COWAT uses the three letter set of C,
F, and L to assess phonemic fluency. Individuals are given
Cross References 1 min to name as many words as possible beginning with
one of the letters. The procedure is then repeated for the
Divided Attention remaining two letters (see Strauss, Sherman, & Spreen,
Focused Attention 2006 and Benton, Hamsher, Rey, & Sivan, 1994 for
704 C Controlled Oral Word Association Test
specific administration instructions). Several tests of pho- more difficult, while results for the F-A-S form appeared
nemic fluency exist, some of which are part of larger test more variable. In addition, COWAT scores have been
batteries (e.g., the MAE or the Neurosensory Center Com- correlated with neuropsychological measures such as
prehensive Examination for Aphasia; Spreen & Benton, reading tests and IQ tests.
1977) and others that can be administered independently
(e.g., the F-A-S Test).
Verbal fluency is a cognitive function that facilitates Clinical Uses
information retrieval from memory. Successful retrieval
requires executive control over cognitive process such as Scoring for the COWAT and other verbal fluency tests is
selective attention, mental set shifting, internal response straightforward. The examiner writes each word as it is
generation, and self-monitoring. Tests of verbal fluency produced by the individual. The transcript is reviewed
evaluate an individuals ability to retrieve specific informa- and inadmissible words (i.e., repetitions, proper names,
tion within restricted search parameters (Lezak, Howieson, or slang) are eliminated. The test score is the total number
Loring, Hannay, & Fischer, 2004). The two most common of different words produced for all three letters (see
parameters are semantic fluency and phonemic fluency. Strauss et al., 2006 and Benton et al., 1994 for specific
administration instructions).
Supplementary scoring measures for the COWAT and
Historical Background other phonemic fluency tests provide additional informa-
tion in clinical diagnosis and treatment. Supplementary
Borkowski, Benton, and Spreen (1967) were early propo-
scorning measures are error analysis, and cluster and
nents of systematically examining word fluency in persons
switching analysis (see Table 1). In error analysis, the
with brain damage. They recognized that so-called word
examiner notes any observable pattern of production of
fluency tasks had been used in neuropsychological inves-
errors that suggests a loosening of executive control over
tigation of patients with brain damage and undertook two
cognitive processes that would result in errors. For exam-
studies of the task. The first established the relations
ple, a pattern of multiple repetitions of previous responses
between word fluency and various English letters; the
suggests perseveration and inefficient self-monitoring.
second examined word fluency data for persons with
Error patterns provide qualitative performance data and
brain damage and control patients. They presented nor-
may appear as common patterns such as repetition of a
mative data for the first study and comparative data for
word, or idiosyncratic patterns. Clustering and switching
the second, clearly supporting their hypotheses of the
analyses evaluate the depth of the searchable knowledge
utility of word fluency assessment.
base (clusters) and the cognitive flexibility within and
Since publication of these data, word fluency tasks,
across categories (switching) (Troyer, Moscovitcvh, &
and the COWAT in particular, have been investigated in
Winocur, 1977). An example of an efficient search strategy
detail. Spreen and Risser (2003) suggest that this assess-
would be identifying a cluster or subcategory within the
ment tool in its various forms has been one of the most
category (e.g., words that begin with cr in the COWAT
frequently and thoroughly investigated neuropsychologi-
task of naming words that begin with C) and producing as
cal assessment measures for unimpaired and neurologi-
many items in that category as possible and then switch-
cally impaired persons. A search of electronic databases
ing clusters (e.g., to words beginning with cl). Clusters
confirms this suggestion.
are scored by counting the number of clusters and calcu-
lating the mean cluster size; switches are scored by count-
Psychometric Data ing the number of transitions between clusters. Rules for
scoring cluster size and number of switches appear in
Psychometric data for the COWAT and other phonemic Troyer et al. (1997) and normative data for healthy adults
fluency tests, as well as other verbal fluency tasks (e.g., appear in Troyer (2000).
semantic fluency) are readily available. Norms have been Scores from the COWAT are useful in evaluation of
published for children and adults of varying ages, levels of persons with neurogenic communication disorders, such
education, ethnic diversity, and geographical diversity as aphasia following stroke, traumatic brain injury, and
(Loonstra, Tarlow, & Sellers, 2001; Strauss et al., 2006). dementia. Studies have included COWAT in the diagnos-
Some differences have been noted between test forms, tic batteries given to several patient populations and also
most notably, between the COWAT and F-A-S Test in treatment studies as measures of behavioral change.
(Barry, Bates, & Labouvie, 2008); the CFL form appeared The utility of the COWAT in identifying the nature
Controlled Oral Word Association Test C 705
Controlled Oral Word Association Test. Table 1 An example of F-A-S Test results and cluster and switch scoring for a person
with aphasia
Responses Clusters and Switches

FAS-Test: F fast, fun, fickle, fuschsia, finger of fate, Clusters = 8 (mean size = 1.1)
four, fifty-four, forty, fornicate fast
C
fun
Words = 9 fickle
fuchsia
finger of fate
four
fifty-four
forty, fornicate
Switches = 7
FAS-Test: A apple, aardvark, alpaca, Clusters = 5 (mean size = 1)
ammonia, arsenic apple
aardvark
Words = 5 alpaca
ammonia
arsenic
Switches = 4
FAS-Test: S substantial, sum, subtraction, Clusters = 5 (mean size = 1.8)
stuck, structure, symbol, sympathy, stroke, sixty substantial, sum, subtraction
stuck, structure
Words = 9 symbol, sympathy
stroke
sixty
Switches = 4
Total Words = 23 Clusters = 18
Mean size = 1.27
Switches = 15
and severity of performance deficits in clinical popula- Boston Diagnostic Aphasia Examination
tions has been supported; however, conflicting findings Circumlocution
have been reported. Typically, the total number of ac- Clustering
ceptable responses is the reported test result; however, Cognitive-Communication Disorder
increasingly cluster and switching scores are reported as Cognitive Functioning
well. The COWAT is valuable in detecting cognitive Cognitive Processing
dysfunction, but it requires further study before defini- Cue
tive conclusions are possible with regard to performance Cued Recall
patterns that can be linked with specific neurogenic Error Recognition and Correction
behavioral deficits. Free Recall
Mayos Older American Normative Studies (MOANS)
National Adult Reading Test
Cross References Phonemic Cue
Semantic Cue
Aphasia Semantic Fluency
Aphasia Tests Verbal Mediation
Benton, Arthur Western Aphasia Battery
706 C Contusion (Cerebral)

Convulsion
Barry, D., Bates, M. E., & Labouvie, E. (2008). FAS and CFL forms of
verbal fluency differ in difficulty: A meta-analytic study. Applied Grand Mal Seizure
Benton, A. L., Hamsher, K., Rey, G. L., & Sivan, A. B. (1994). Multilingual
Aphasia Examination (3rd ed.). Iowa City, IA: AJA Associates.
Borkowski, J. G., Benton, A. L., & Spreen, O. (1967). Word fluency and Convulsive Disorder
brain damage. Neuropsychologia, 5, 135140.
Goodglass, H., Kaplan, E., & Baressi, B. (2001). Boston Diagnostic Aphasia
Examination (3rd ed.). San Antonio TX: Psychological Corporation.
Epilepsy
Kertesz, A. (2006). Western Aphasia Battery. New York: Grune & Stratton.
Lezak, M. D., Howieson, D. B., Loring, D. W., Hannay, H. J., & Fischer,
J. S. (2004). Neuropsychological assessment (4th ed.). New York:
Oxford University Press. COPD
Loonstra, A. S., Tarlow, A. R., & Sellers, A. H. (2001). COWAT metanorms
across age, education and gender. Applied Neuropsychology, 8, Chronic Obstructive Pulmonary Disease
161166.
Spreen, O., & Benton, A. L. (1977). Neurosensory Center Comprehensive
Examination for Aphasia. Victoria BC: University of Victoria Neuro-
psychology Laboratory.
Spreen, O., & Risser, A. H. (2003). Assessment of aphasia. Oxford: Oxford
Coping
University Press.
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). Compendium of J OEL W. H UGHES
neuropsychological tests: Administration, norms, and commentary Kent State University
(3rd ed., p. 502). Oxford: Oxford University Press. Kent, OH, USA
Troyer, A. K. (2000). Normative data for clustering and switching on
verbal fluency tasks. Journal of Clinical and Experimental Neuropsy-
chology, 22, 370378.
Troyer, A. K., Moscovitch, M., & Winocur, G. (1997). Clustering and Synonyms
switching as two components of verbal fluency: Evidence from
younger and healthy adults. Neuropsychology, 11, 138146. Stress management
Definition
Contusion (Cerebral)
Coping is responding to environmental stimuli, events,
Cortical Contusion and circumstances for the purpose of minimizing or
managing stress, solving problems, and modulating phys-
iological and emotional responses. Coping is often paired
with stress (as the latter elicits the former) in what has
Conventional Antipsychotics become the stress and coping literature associated with
Richard Lazarus and Susan Folkman. Stress responses
Antipsychotics typically involve appraising the stimulus or event, which
begins the process of assigning value (e.g., distressing)
and determining responses (e.g., fight, flight, freeze).
Coping is a process that follows stress appraisals, and
Conversation Analysis coping responses seek to manage stress with cognitive,
physiological, and behavioral responses. Various coping
Discourse Assessment strategies have been categorized, such as appraisal-
focused, problem-focused, or emotion-focused coping.
Conversion Disorder Cross References
Cogniform Disorder Self-Regulation

Somatization Stages of Adjustment
Coronary Artery Bypass Graft C 707
Stress Patients undergo general anesthesia and a midline

Stress Management incision (median sternotomy) allows the surgeon to
visualize the heart and vessels. The artery or vein grafts
are then harvested. Frequently used vessels include the
References and Readings internal thoracic arteries, radial arteries, and saphenous C
veins. The heart is then stopped using a special mixture of
Carver, C. S., Scheier, M. F., & Weintraub, J. K. (1989). Assessing coping
chemicals and the patient is placed on cardiopulmonary
strategies: A theoretically based approach. Journal of Personality and bypass where the blood flow returning to the heart is
Social Psychology, 56, 267283. diverted through a heartlung machine that provides ex-
Lazarus, R. S., & Folkman, S. (1984). Stress, appraisal and coping. tracorporeal circulation and oxygenation. The graft is then
New York: Springer.
sewn into place and the heart is restarted. The sternum is
then closed with wires, and the incision is sutured.
Core Battery Current Knowledge

Flexible Battery In the early years of cardiac surgery several investigators
noted transitive postoperative delirium, whereas others
reported immediate postoperative neurological abnormal-
ities, however, no well-conducted or controlled studies were
Coronary Angioplasty available. More recent studies have shown a short-term
neuropsychological decline in the 714 days after CABG,
Angioplasty including deficits in psychomotor speed, attention, verbal
learning, and memory. Studies have reported an 1175%
incidence of postoperative cognitive decline (POCD) after
cardiac surgery. Age is considered to be the strongest pre-
Coronary Artery Bypass Graft dictive factor of postoperative cognitive dysfunction. It is
hypothesized that off-pump surgery causes less cognitive
F LORA H AMMOND 1, LORI G RAFTON 2 decline as it avoids extracorporeal circulation, but studies
1
Indiana University have not shown this to be true. Other potential causes of
Indianapolis, IN, USA neurocognitive decline include intraoperative cerebral oxy-
2
Carolinas Rehabilitation gen desaturation or microemboli.
Charlotte, NC, USA

Synonyms
Eagle, K. A., Guylon, R. A., Davidoff, R., Ewy, G. A., Fonger, J.,
Gardner, T. J., et al. (1999). http://circ.ahajournals.org/cgi/content/
CABG
full/100/13/1464
Jensen, B. ., Rasmussenb, L. S., & Steinbruchel, D. A. (2008). Cognitive
outcomes in elderly high-risk patients 1 year after off-pump versus
Definition on-pump coronary artery bypass grafting. A randomized trial.
European Journal of Cardio-Thoracic Surgery, 34(5), 10161021.
Slater, J. P., Guarino, T., Stack, J., Vinod, K., Bustami, R. T., Brown, J. M.,
Coronary artery bypass surgery (CABG) is a surgical
III, et al. (2009). Cerebral oxygen desaturation predicts cognitive
procedure for coronary artery disease in which arteries decline and longer hospital stay after cardiac surgery. Annals of
or veins from other parts of the body are grafted from the Thoracic Surgery, 87(1), 3644, discussion 4445
aorta to the coronary arteries in order to bypass the Tarter, R. E., Butters, M., Beers, S. R. (2001). Medical neuropsychology
blocked portions. Indications for surgery include disease (2nd ed., pp. 6971). New York: Kluwer Academic.
http://www.nlm.nih.gov/medlineplus/ency/article/002946.htm. Accessed
of the left main coronary artery and/or disease of all three
29 August, 2007.
coronary arteries and abnormal ventricular function. It http://www.sts.org/sections/patientinformation/adultcardiacsurgery/cabg/
may be performed in patients with severe angina which is index.html?CFID=3659926&CFTOKEN=93793791. Accessed 29 Au-
unresponsive to medical management. gust, 2007.
708 C Coronary Artery Disease
cardiac stress tests, and direct visualization on coronary

Coronary Artery Disease angiography or other imaging studies. The treatment
includes the use of beta-blockers, calcium channel blockers,
Coronary Disease angiotensin converting enzyme inhibitors, nitroglycerine,
aspirin, or other medications; antihypertensive and lipid-
lowering agents; diet, exercise, and lifestyle changes; throm-
bolysis; angioplasty with coronary stent placement; and
coronary bypass graft surgery.
Coronary Disease
E LLIOT J. R OTH
Northwestern University Cross References
Chicago, IL, USA
Angioplasty
Anticoagulation
Synonyms Antiplatelet Therapy
Atherosclerosis
Atherosclerotic heart disease; Coronary artery disease; Cholesterol
Coronary heart disease; Ischemic heart disease Congestive Heart Failure
Infarction
Ischemia
Definition Myocardial Infarction
Stent
Coronary disease, or coronary artery disease (CAD), results Thrombosis
from atherosclerosis, or narrowing of the arteries that Tissue Plasminogen Activator
provide blood supply to the heart muscle (myocardium). Vasospasm
Current Knowledge
Atherosclerosis, which is the process by which cholesterol
and fat deposits adhere to the inside walls of blood vessels, Hansson, G. K. (2005). Inflammation, atherosclerosis, and coronary
creates plaques that block the blood supply through blood artery disease. New England Journal of Medicine, 352, 16851695.
Virmani, R., Kolodgie, F. D., Burke, A. P., Farb, A., & Schwartz, S. T.
vessels. When this narrowing or occlusive process blocks the
(2000). Lessons from sudden coronary death: a comprehensive mor-
coronary artery, the accompanying obstruction to blood phological classification scheme for atherosclerotic lesions. Arterio-
flow reduces the supply of oxygen and nutrients to the sclerosis, Thrombosis, and Vascular Biology, 20, 12621275.
heart muscle, creating ischemia that causes chest pain (an-
gina pectoris), or death of the cells of the heart (myocar-
dial infarction). At times, it can cause other problems such
as arrhythmias (abnormal heart rhythm) or congestive heart
failure, in which the heart is unable to pump sufficient blood
to the remainder of the body. CAD is the most common type
Coronary Heart Disease
of heart disease and the leading cause of death in the USA.
Coronary Disease
Risk factors for CAD have been well studied; these include
smoking, diabetes, hypertension, hyperlipidemia, obesity,
sedentary lifestyle, excessive alcohol intake, and family his-
tory. Although chest pain is the most common symptom,
dyspnea, palpitations, diaphoresis, nausea, radiation of the
pain to the neck and left arm, and no symptoms at all, also Corporis Callosi
are possible. The diagnosis relies on electrocardiogram,
blood levels of cardiac enzymes, echocardiography, select Corpus Callosum
Correction Factor C 709
vary widely but are generally reported to range between

Corpus Callosum 0.3 and 0.7% in the general population and as high as 3%
in individuals with development disabilities. Agenesis of
J EFF D UPREE the corpus callosum results in symptoms ranging from
Virginia Commonwealth University asymptomatic with normal intelligence to intellectual
Richmond, VA, USA
C
retardation, seizures, hydrocephalus, and spasticity. In
individuals suffering from severe epilepsy, a surgical pro-
cedure known as corpus callostomy may be performed,
Synonyms which involves the partial or complete transaction of the
corpus callosum. This procedure is only performed in
Commissural magna; Corporis callosi; Interhemispheric patients who are at risk of accidental injury resulting
commissure from severe seizures. The laymans term for this condition
is split brain due to the loss of interhemispheric com-
munication. Much of the original research detailing the
Definition consequence of corpus callostomy was conducted by
Dr. Roger Wolcott Sperry.
Corpus callosum is the largest axonal tract of the adult
brain that provides symmetrical connections between the
two hemispheres. Cross References
Ganglion
Gazzaniga, M. S. (1939 )
Current Knowledge Sperry, Roger Wolcott (19131994)
Split-brain
The corpus callosum is the largest commissure of the
adult brain that provides a bridge for the passing of
information from one cerebral hemisphere to the other References and Readings
by 200300 million myelinated and unmyelinated axons.
The size of the corpus callosum varies greatly but is Barr, M., & Kiernan, J. (1983). The human nervous system An anatomical
generally larger in females than in males. In the human, viewpoint (4th ed.). Philadelphia: Harper and Row.
the corpus callosum begins development around the 11th Gazzaniga, M. S. (2005). Forty-five years of split-brain research and still
going strong. Nature Reviews Neuroscience, 6(8), 653659.
week of gestation and continues through adolescence.
Haines, D. (2006). Fundamental neuroscience for basic and clinical appli-
Initially, the corpus callosum is composed of astrocytic cations (3rd ed.). Philadelphia: Churchill Livingstone Elsevier.
processes, which serve as conduits for growing axons Kandel, E., Schwartz, J. H., & Jessel, T. M. Principles of neural science
extending to the contralateral hemisphere. This inter- (4th ed.). New York: McGraw-Hill.
hemispheric commissure lies beneath the cortex at the Paul, L. K., Brown, W. S., Adolphs, R., Tyszka, J. M., Richards, L. J.,
Mukherjee, P., et al. (2007). Agenesis of the corpus callosum:
bottom of the cerebral longitudinal fissure. It forms
Genetic, developmental and functional aspects of connectivity.
much of the roof of the lateral ventricles and is composed Nature Reviews Neuroscience, 8(4), 287299.
of four parts: the rostrum, the genu, the body (also known
as the trunk), and the splenium. Each portion of the
corpus callosum is responsible for connecting symmetri-
cal regions of the two hemispheres with the rostrum and
genu connecting portions of the prefrontal and premotor Corpus Mamillare
cotices, the body interconnecting the premotor, motor,
supplementary motor, and the posterior parietal cortices, Mammillary Bodies
while the splenium connects portions of the temporal,
occipital, and parietal lobes. Although being the largest
white matter tract of the brain, the corpus callosum is not
essential for life. The complete or partial absence of the Correction Factor
corpus callosum is known as agenesis of the corpus callo-
sum. This condition is rare, and estimates of incidence K Scale
710 C Correlation Coefficients
plot of the data. The values of a correlation can range

Correlation Coefficients between 1 and 1 with these two extremes representing
perfect relationships, which rarely if ever occur in
C HRISTIAN S CHUTTE , B RAD N. A XELROD research, and a correlation coefficient of 0 would
John D. Dingell VA Medical Center represent no relationship, given certain assumptions are
Detroit, MI, USA made. A line can be drawn through data that are related
that generally approximates a regression line, which is
how Galton identified the first regression line in his
Synonyms heritability studies with peas. Correlation is a measure
of the strength of the relationship between two variables.
Pearson r, r, rho Thus, if data in a scatter plot are randomly scattered, such
as in the example below, then there is no relationship, as
no single line adequately represents the data and the
Definition correlation would be roughly 0.
A measure of the strength of the relationship between two

10
variables, x and y.
8
Historical Background 6
y
4
The correlation, or co-relation, coefficient is typically
attributed to Karl Pearson who developed the formalized
2
idea of correlation during the mid- to late 1800s. However,
the beginning of the idea of correlation may have 0
come from Sir Francis Galton, cousin of Charles Darwin.
0 2 4 6 8 10
Galton worked on genetic heritability of sweet peas. x
Through his work on heritability, he developed the
If data are positively related, such that as one variable
beginnings of regression and correlation. Pearson, who
increases in value so does the other, then one would be
worked in Galtons lab and was later his biographer, attrib-
able to draw a line that would approximately represent
uted the development of the regression slope to Galton.
the data. The below example illustrates an ideal relation-
Pearson then generalized Galtons work into the Pearson
ship that rarely occurs in research of a 1 correlation
Product Moment Correlation (PPMC), or moment
such that for every one unit that x goes up, y goes up one
meaning the average of a set of products. The PPMC is
unit.
often identified as r, which Galton originally used to
denote regression and Pearson later used as notation
for correlation. In 1896, Pearson published an article in 30
which he credited Bravais for developing the rudiments of
the correlation formula. In this work published in the 25
Philosophical Transactions of the Royal Society of London,
Pearson showed that the optimum values for the regres- 20
y
sion line and correlation could be derived from the prod-

uct moment or S xy=n, where x and y are deviations from
15
their respective means, usually expressed as standard z
scores and n is the number of pairs.
10
0 5 10 15 20
Current Knowledge x
There may also be negative associations, such that

A correlation, or co-relation, of two variables can be for every unit that x goes up, y goes down, or a 1
visually scanned initially by simply looking at a scatter relationship, such as the below idealized example.
Correlation Coefficients C 711
The correlation coefficient is therefore a measure of the

10 extent to the relation of pairs of observed data points can
be expressed as a linear function. The greater the summed
8
square of differences between the observed data and the
values described by the linear function, the lower the cor- C
6
relation coefficient. The closer the observed data points lie
y
4 to the line of best fit, the higher the correlation coefficient.

There are several forms of correlation that need to
2 be addressed including those for continuous variables,
categorical variables, and correlations that are better
0 descriptions of nonlinear and skewed relationships. The
0 2 4
x
6 8 10 scope of this article is to cover the basic foundations of
correlation coefficients. The use of correlation ranges far
However, typically a scatter plot will not be as obvious and wide and a thorough examination of this subject is
and the data will look more like an ellipse such as in the the subject of chapters and entire texts referenced below.
example below, which still illustrates a strong correlation The object of this entry is to cover foundational
of over .8. issues related to correlation coefficients. There are more
correlation coefficients than those presented below,
though several different forms of correlation and their
properties are considered.
8
It is important to note that correlation, even a strong
correlation, does not infer causation. In other words,
6
simply because two variables are related does not mean
that one causes the other. For example, you need light to
y
read this text. Simply because the light is on while you are
4 reading does not mean that light is causing you to read,
they are certainly related, as there will always be some
light source when you read, but one does not cause the
2 other. A determination of causation requires adequate
0 2 4
x
6 8 10 experimental design.
There are certain important components that underlie
The above examples show linear relationships between
most correlations. Correlations are most meaningful
variables, which is an assumption of most correlation
when certain criteria are met, and different correlation
coefficients. An examination of scatter plots can also
coefficients are affected differently by failure to meet
show nonlinear relationships, which are not well repre-
different assumptions. The Pearson product moment
sented by standard correlation coefficients, such as the
correlation coefficient has the most stringent set of
PPMC, but can be shown with other methods, such as
assumptions. These include:
eta. The below example has a near 0 Pearson r, but the
variables are clearly related nonlinearly. 1. The data are interval: The level of measurement must
at least be interval as opposed to nominal or ordinal,
25 though this can be managed if it is violated.
2. The data must have a linear relationship: Most correla-
20 tions assume that the data are linearly related, as op-
posed to nonlinear. To the degree which the data are
15
better explained by a nonlinear relationship correlation
y
10
coefficients will underestimate the relationship. Prior to
completing a correlation analysis this can be examined
5 by looking at a scatter plot, as discussed above.
3. The variables have similar and normal underlying
0 distributions (more formally in a bivariate correlation,
0 5 10 15 20 such as the Pearson r): To the degree that the
x
712 C Correlation Coefficients
distributions of the different variables differ, the cor- also other methods that are more robust to violations of
relation will attenuate the relationship between them. the above assumptions, such as Spearmans rho or eta in
For example, if correlating a variable that is normally the case of a nonlinear relationship. The correlation
distributed, like height, with one that is highly skewed coefficient is considered a measure of effect size, which is
like ability to walk. This is done when correlating a a measure of how different two distributions are. By
continuous variable with a dichotomous variable or convention a correlation of .1 is small, .3 moderate and
when correlating interval data with ordinal. If this .5 large (Cohen, 1988), at least in the behavioral sciences
assumption is violated to a significant degree then that can expect weaker relationships in general due to
rank order correlation may be used, such as the the complexity of the subject matter. For example, the
Spearmans rho or other nonparametric correlations. correlation between IQ and academic achievement is
4. The data must have homoscedasticity: The error, or approximately .55 (Griffenstein & Baker, 2003), but one
random variance in X and Y, contained in the data, is would expect no effect for a correlation between IQ and
assumed to be equal along the entire distribution. If, height. The correlation coefficient can also be squared to
for example, one portion of the distribution has a give the coefficient of determination, which is the amount
much larger random variance, then the correlation of variance in one variable that is accounted for by
may overrepresent the relationship because it would another. For example, if one had a correlation of .55
underrepresent the amount of variance that is between IQ and academic achievement then the coeffi-
attributable to error. If data are heteroscedastic, then cient of determination (r 2) would be .30, which means
the distribution will not be normal and the correlation that approximately 30% of the variance in academic
may misrepresent the data. achievement is accounted for by IQ.
5. The data has no or limited outliers: Correlation is
1. PPMC or r: The PPMS is an association of two
sensitive to outliers. Some forms of correlation are
continuous variables that shows the degree of linear
more robust to a violation of this assumption than
relationship between them. It can be calculated using
others, but normally correlation is a representation of
raw scores, deviation scores, or by using a covariance
deviations of mean values. Thus, to the degree that the
formula. A common method is to calculate the
mean is affected by outliers then the correlation will be
standard score (or z score) and sum the products of
also. If there are many outliers, or few that are large,
the two variables and divide them by the degrees of
this problem can be managed through use of a
freedom (n 1) or S xy=n S 1.
Spearman rho, which ranks data.
2. Point-biserial or rpb: This is a special case of the PPMC
6. There is limited measurement error present in the
for use when there is a continuous variable, such as
sample: It is assumed that the measurement is relative-
height, and a dichotomous nominal variable, such as
ly free from or has limited error. In other words, if one
gender. The point-biserial correlation is for naturally
has an invalid test that only measures error then
dichotomous variables, such as gender, not artificially
the correlation will be near zero, as the data will be
dichotomized variables, such as taking a naturally
random and show little relationship. It is rare in
continuous distribution, such as intelligence, and
behavioral research to be free from error, but limiting
making it into high and low intelligence.
it is an important aspect of experimental control.
3. Phi: This is a special case of the PPMC for use when
7. The data have adequate variance: In order to
both variables are dichotomous and nominal. Note that
adequately assess relationships among variables there
as with rpb this is for naturally dichotomous variables,
must be variance among the variables. In general, the
such as gender, not artificially dichotomized variables.
more variance the higher the correlation will be.
4. Biserial or rb: This is for use when there is one contin-
To the extent that these criteria are violated, which they uous variable, such as height, and a dichotomized
often are, the correlation coefficient is more or less im- variable, such as high and low intelligence. So, the
pacted depending on the type of correlation. biserial correlation measures the relationship between
There are several different methods calculating basic X and Y as if Y were not artificially dichotomized. This
correlation coefficients depending on the type and char- is similar to the point-biserial, but the formula is
acteristics of the data being analyzed. There are several designed to replace some of the variance that is lost.
different types of correlation that depend on the level of One of the important components listed above is that
measurement (nominal, ordinal, interval, ratio) being the data have adequate variance. However, when a
made. Most are special cases of the Pearson r. There are variable is dichotomized much of the variance is lost.
Cortical Blindness C 713
Thus, the biserial formula replaces some of that Cross References

variance, which always yields a higher correlation
than a point-biserial correlation. Statistical Significance
5. Tetrachoric: This is similar to the phi, except that it is z Score
assumed that there is a continuous distribution C
underlying the dichotomized variables and it thusly
replaces some of that variance, as opposed to phi References and Readings
that assumes that the two variables are naturally
dichotomous, such as gender and employment status. Chen, P., & Popovich, P. (2002). Correlation: Parametric and nonparametric
measures. Thousand Oaks, CA: Sage.
6. Spearmans rho or rs or r: Spearmans rho is a non-
Cohen, J. (1988). Statistical power analysis for the behavioral sciences
parametric statistic. In other words, it makes no (2nd ed.). New Jersey: Erlbaum.
assumptions about the underlying distribution of the
variables. One of the primary components of the
typical PPMC is that there is a normal or bell-shaped
distribution underlying the variable. However, in
many cases, distributions are highly skewed. For
Cortex
example, if one were to look at a distribution of people
Cerebral Cortex
who live into adulthood in the USA, the distribution
would likely be very skewed to the left, meaning that
the vast majority of people live at least until they are of
adult age. Relate that distribution to the number of
people who vote, which would be positively skewed, Cortical Activation
meaning that few people of adult age vote proportion-
ally and a PPMC would not yield an inaccurate repre- Arousal
sentation, as this distribution significantly violates the
assumptions of the PPMC. Thus, one could convert
raw scores into ranks and complete the correlation.
This is more robust to violations of some of the Cortical Arousal
underlying components of correlation.
7. Measures of nonlinear relationships: Eta is a measure Arousal
of association that can be used if the data are nonline-
ar, as in the final scatter plot above. It is a measure of
the strength of the effect and is always positive. Eta is
always higher than jrj and is therefore a biased
estimate of the effect. Cortical Blindness
In practical usage, many of the different correlation coef-
S TEVEN Z. R APCSAK , G. A LEX H ISHAW
ficients are calculated using the same method, such as the
University of Arizona
PPMC and the point-biserial, given the ubiquity of com-
Tucson, Arizona, USA
puter statistical packages. What is important to note with
any correlation being used are the number and degree of
the components that are violated and what impact that
Synonyms
has on the relationship between the variables. For exam-
ple, if one is using a PPMC to assess highly skewed data
Antons syndrome; Blindsight
then the relationship may be very low, where actually, if a
nonparametric method is used, such as the Spearmans
rho, then the relationship may be significant. Conversely,
if a PPMC is used on data that have many large outliers Short Description or Definition
the relationship may look strong and be significant, but in
reality it is the impact of those large outliers that are Cortical blindness refers to severe visual loss produced
falsely raising the strength of the associations. by bilateral damage to the geniculostriate visual
714 C Cortical Blindness
pathways. The underlying pathophysiological mecha- currently unclear whether recovery of visual capacity in
nism involves direct destruction and/or de-afferentation cortical blindness is mediated by spared neural tissue
of primary visual cortex (striate cortex, Brodmann area within primary visual cortex, or whether it reflects the
17, or V1). The term Antons syndrome is applied to strengthening and increasing utilization of alternative
patients with cortical blindness who demonstrate explic- visual pathways to extrastriate cortical regions that bypass
it denial or unawareness (anosognosia) of their visual the damaged geniculostriate system, or both. Anosogno-
impairment. sia for visual loss in patients with Antons syndrome also
tends to diminish over time, often parallel to the resolu-
tion of the visual impairment, but partial defects of aware-
ness are not uncommon. In cases of transient cortical
Categorization
blindness due to RPLS, full recovery of vision can occur
within a few days along with complete resolution of the
Although no universally agreed upon classification system
characteristic neuroradiological abnormalities.
exists, patients with cortical blindness differ in terms of the
severity of the visual loss, the presence/absence of spared
visual abilities (conscious or unconscious), the degree of
awareness of the deficit, and the extent of functional recov-
ery. There are also variations across cases with respect to the
capacity to generate internal visual representations using
Cortical Blindness
mental imagery and the susceptibility to experience abnor-
In severe cases of cortical blindness, all forms of conscious
mal visual sensations/hallucinations. The precise neurobio-
visual perception may be abolished. However, this type
logical mechanisms underlying these individual differences
of total visual loss is relatively uncommon and many
in clinical presentation remain to be determined.
patients retain at least some rudimentary visual awareness
of motion or light. Visual form discrimination is pro-
foundly impaired and objects, faces, or written words can-
Epidemiology not be identified. Visuospatial orientation is also severely
compromised and patients may repeatedly bump into
Cortical blindness is a relatively rare condition, typically objects when attempting to navigate in their environment.
caused by bilateral occipital strokes in the territory of the Although individuals with cortical blindness do not
posterior cerebral arteries. Other less common etiologies have normal conscious awareness of visual events, they
include anoxic brain damage, carbon monoxide poison- can sometimes demonstrate surprising ability to respond
ing, head trauma, and occipital lobe tumors. Transient to stimuli presented within the blind portions of their
cortical blindness can be seen in the context of the revers- visual fields. Specifically, patients may be able to detect,
ible posterior leukoencephalopathy syndrome (RPLS) locate, and discriminate visual stimuli that they claim not
related to hypertensive encephalopathy, the use of chemo- to see. Residual visual capacity within the cortically blind
therapeutic and immunosuppressant drugs, or the injec- field in the absence of conscious awareness has been
tion of radiological contrast agents during cerebral referred to as blindsight (Weiskrantz, 1986; Stoerig &
angiography. Cowey, 1997, 2007; Stoerig, 2006). The fact that blindsight
can be observed in patients with extensive destruction or
de-afferentation of primary visual cortex suggests that the
Natural History, Prognostic Factors, preserved visual abilities of these individuals are mediated
Outcomes by neural pathways from retina to extrastriate visual cor-
tex that bypass the damaged geniculostriate system. There
Although some recovery of visual function is observed in are in fact a number of alternative non-geniculostriate
most cases of cortical blindness, patients with neuroim- pathways capable of transmitting visual information to a
aging evidence of extensive structural damage to occipital variety of temporo-parietal extrastriate cortical areas via
cortex typically do not regain full normal vision. Residual subcortical relay nuclei in the midbrain and diencephalon
visual field defects are common, and cortical blindness (Weiskrantz, 1986; Stoerig & Cowey, 1997, 2007; Stoerig,
may evolve into visual agnosia characterized by a persis- 2006). The specific visual functions retained in blindsight
tent inability to recognize objects, faces, or words despite may depend on which of these multiple parallel visual
the return of more elementary visual functions. It is pathways are available to patients. For instance, the
residual capacity to detect motion and to locate and visual imagery may provide faulty input to an otherwise
manually grasp targets presented in the blind field may intact monitor. The loss of normal visual input following
depend on projections from the retina to the superior damage to primary visual cortex may in fact give rise to
colliculus, with additional connections to the pulvinar frequent release hallucinations in patients with cortical
and to middle temporal (MT/V5) and dorsal parietal blindness due to increased cortical excitability in de-affer- C
cortex (Danckert & Rossetti, 2005). Other alternative ented extrastriate areas. Furthermore, since visual percep-
pathways from retina to ventral extrastriate cortex or tion and imagery are mutually inhibitory under normal
amygdala might be involved in mediating unconscious circumstances, the absence of bottom-up activation by
visual form discrimination (Trevethan, Sahraie, & Wei- geniculostriate afferent signals may be accompanied by a
skrantz, 2007) and implicit recognition of emotional fa- relative enhancement of visual imagery mediated by unop-
cial expressions (Morris, DeGelder, Weiskrantz, & Dolan, posed top-down activation of sensory representations in
2001; Pegna, Khateb, Lazeyras, & Seghier, 2005). Func- extrastriate cortex. Patients may deny blindness because
tional imaging studies in patients with blindsight are con- they continue to experience internally generated visual sen-
sistent with the notion that unconscious processing of sations and may mistake these for veridical perceptions
visual information depends on non-geniculostriate visual resulting from retinal stimulation by external visual events.
pathways. Specifically, these investigations have demon- To understand anosognosia for visual loss, it is useful
strated activation in midbrain/thalamic nuclei, extrastriate to briefly consider what is currently known about
cortical areas, and the amygdala in the absence of concomi- the neural correlates of normal visual awareness. In this
tant activity in the lesioned primary visual cortex during context, it is important to emphasize that conscious
visual stimulation of the blind field (Sahraie, Weiskrantz, awareness of visual events normally entails the capacity
Barbur, Simmons, Williams, & Brammer, 1997; Stoerig, to acknowledge, describe, reflect upon, and make appro-
2006; Morris et al., 2001; Pegna et al., 2005). priate cognitive judgments about ongoing visual ex-
Patients with cortical blindness may demonstrate un- periences (Weiskrantz, 1997; Block, 2005; Dehaene,
awareness of their profound visual impairment. This Changeux, Naccache, Sackur, & Sergent, 2006). Thus,
striking clinical condition is referred to as Antons syn- awareness and the ability to provide introspective report
drome. Anosognosia for visual loss can take several dif- or commentary about the quality, content, and veridi-
ferent forms. In extreme cases, patients emphatically deny cality of visual perceptions are closely related functions.
being blind and produce confabulatory responses when Although localized neural activity in cortical visual areas
questioned about their visual abilities. Other patients (striate and extrastriate cortex) is obviously necessary for
acknowledge a change in their vision but they typically visual information to reach this commentary stage of
offer a variety of excuses to explain the difficulty, attribut- conscious awareness, it is by itself not sufficient (Wei-
ing it to poor lighting conditions or to a problem skrantz, 1997; Rees, Kreiman, & Koch, 2002; Dehaene
with their eyeglasses. A number of theories have been et al., 2006). In particular, evidence from recent neuroim-
advanced to explain anosognosia for blindness (Bisiach aging studies suggests that conscious vision requires the
& Geminiani, 1991; Heilman, 1991; Celesia, Brigell, & additional recruitment of dorsolateral prefrontal and pa-
Vaphiades, 1997; Adair, Schwartz, & Barrett, 2003). For rietal cortical regions implicated in visual attention and
instance, it has been proposed that normal visual aware- working memory (Rees, Kreiman, & Koch, 2002; Dehaene
ness depends on a hypothetical monitor located in extra- et al., 2006). Prefrontal cortex is also involved in mediat-
striate visual association areas that receives afferent input ing strategic cognitive operations necessary for critically
from primary visual cortex (Heilman, 1991). In addition evaluating and interpreting the meaning and signific-
to evaluating activity within the visual areas of the brain, ance of visual experiences in order to determine the
the monitor also sends efferent information to cortical most appropriate behavioral response.
language areas enabling subjects to verbally comment on Activation of frontal and parietal regions by input
their visual experiences. Lesions that disrupt the input from cortical visual areas is also likely to play an essential
and/or output connections of the visual monitor, or pro- role in awareness of abnormal visual function. Specifi-
duce damage to the monitor itself, result in anosognosia cally, damage to primary visual cortex and extrastriate
for visual impairment that may include verbal denial of areas may give rise to visual field defects and/or domain-
the deficit and the production of confabulatory responses specific impairments in processing distinct visual stimu-
by the disconnected language areas. It has also been sug- lus attributes (e.g., form, color, motion). If the same lesions
gested that in cases of cortical blindness, internally gener- also interfere with the bottom-up activation of the fronto-
ated visual experiences in the form of hallucinations or parietal cortical network that normally enables conscious
716 C Cortical Blindness
awareness and introspective report about visual experi- movement, or identity of objects presented in their blind
ences, anosognosia for the visual impairment ensues. De- field using a forced-choice response method (e.g., was it a
fective awareness of visual function may also result from key or a coin?). Better than chance performance on these
direct damage to the putative fronto-parietal network that types of tasks is taken to be indicative of blindsight. Alter-
provides the critical top-down attentional amplification natively, patients can be asked to try to reach for and grasp
required for perceptual information processed within objects in their blind field. Regardless of the testing method
visual cortical modules to enter consciousness, or it may used, it is important to establish after each trial whether
be produced by lesions that disrupt feedforward/feedback the patient had any conscious awareness of the visual
connections between fronto-parietal cortex and visual stimulus. Visual imagery can be tested by asking the sub-
processing areas. In summary, conscious awareness of jects to answer questions about the visual attributes of
both normal and abnormal vision requires dynamic re- familiar objects or animals (e.g., do polar bears have long
ciprocal interactions between cortical visual areas and or short tails?). Patients should be questioned about ab-
specialized regions within frontal and parietal cortex. normal visual perceptions and hallucinations. Unaware-
Lesions that disrupt the spatial distribution, intensity, ness of deficit may be revealed by spontaneous comments
or timing of activation across the different functional or behavior, but patients should also be specifically asked
components of this large-scale neural system may give to describe the quality and content of their visual experi-
rise to a variety of clinical conditions characterized by ences. The severity of anosognosia can be quantified by
unawareness of preserved or impaired visual processing, simple rating scales (Bisiach & Geminiani, 1991; Celesia,
including blindsight, visual neglect, and anosognosia for Brigell, & Vaphiades, 1997).
blindness. Structural neuroimaging (CT/MRI) studies in
patients with cortical blindness due to stroke typically
reveal extensive bilateral infarctions involving primary
Evaluation visual cortex and underlying white matter, often with
evidence of lesion extension into adjacent extrastriate
Neuro-ophthalmological examination in cortical blind- visual association areas (Brodmann areas 18/19, 37)
ness confirms the normal fundoscopic appearance of the (Figure 1). SPECT/PET scans frequently demonstrate
retinas and optic nerves. The pupillary light response is blood flow/metabolic abnormalities that extend beyond
characteristically preserved, as the retinal fibers that me- the boundaries of the lesions seen on CT/MRI, providing
diate this reflex leave the optic tract prior to the origin of evidence that the cortical visual areas that appear spared
the geniculostriate pathways. Reflexive blinking to threat- by structural imaging studies are in fact functionally
ening visual gestures is usually absent, and in the majority compromised. In patients with transient cortical blind-
of cases optokinetic nystagmus cannot be elicited by ness due to RPLS, neuroimaging studies have demon-
moving a striped object in front of the patients eyes. strated reversible bilateral subcortical white matter
The dissociation between preserved pupillary light re- abnormalities in posterior occipito-temporo-parietal
sponse and absent optokinetic nystagmus can have diag- regions attributable to vasogenic edema.
nostic utility in distinguishing patients with cortical
blindness from patients with severe peripheral visual loss
due to bilateral eye or optic nerve pathology in whom
both responses are lost, and also from individuals with Treatment
psychogenic blindness in whom both responses are
retained. A number of behavioral approaches have been tried with
Clinical evaluation of visual function in patients with varying degrees of success to restore visual function in the
cortical blindness should include tests of visual acuity, cortically blind field and/or help patients learn alternative
determination of light and motion perception in different strategies to compensate for their visual impairment
sectors of the visual field, tests of spatial localization, as (Kerkhoff, 2000). Attempts to increase awareness of the
well as assessments of color perception, object and face visual deficit in patients with anosognosia constitute an
recognition, and reading ability. Studying blindsight usu- important component of the treatment program. It has
ally requires the use of specialized testing equipment in an been shown that blindsight performance can be improved
experimental laboratory environment. However, in the by training, and the use of these techniques may aid the
clinical setting blindsight can be tested by requiring recovery of vision in individuals with cortical blindness
patients to guess the presence/absence, location, (Stoerig, 2006; Sahraie et al., 2006).
Cortical Blindness. Figure 1 Diffusion-weighted MRI scan in a patient with cortical blindness following bilateral posterior
cerebral artery strokes. Note massive destruction of primary visual cortex (Brodmann area 17), with lesion extension into ventral
extrastriate visual association areas (Brodmann areas 18,19,37). This individual demonstrated complete denial of blindness
(anosognosia), consistent with Antons syndrome
Cross References Kerkhoff, G. (2000). Neurovisual rehabilitation: Recent developments

and future directions. Journal of Neurology, Neurosurgery, and Psy-
chiatry, 68, 691706.
Anosognosia Morris, J. S., DeGelder, B., Weiskrantz, L., & Dolan, R. J. (2001). Differ-
Visual Hallucinations ential extrageniculostriate and amygdala responses to presentation
of emotional faces in a cortically blind field. Brain, 124, 12411252.
Pegna, A. J., Khateb, A., Lazeyras, F., & Seghier, M. L. (2005). Discrimi-
nating emotional faces without primary visual cortices involves right
References and Readings amygdala. Nature Neuroscience, 8, 2425.
Rees, G., Kreiman, G., & Koch, C. (2002). Neural correlates of conscious-
Adair, J. C., Schwartz, R. L., & Barrett, A. M. (2003). Anosognosia. In ness in humans. Nature Reviews Neuroscience, 3, 261270.
K. M. Heilman & E. Valenstein (Eds.), Clinical neuropsychology Sahraie, A., Weiskrantz, L., Barbur, J. L., Simmons, A., Williams, S. C. R., &
(pp. 193197). New York: Oxford University Press. Brammer, M. J. (1997). Pattern of neural activity associated with
Bisiach, E., & Geminiani, G. (1991). Anosognosia related to hemiplegia conscious and unconscious processing of visual signals. Proceedings
and hemianopia. In G. P. Prigatano & D. L. Schacter (Eds.), of the National Academy of Sciences, 94, 94069411.
Awareness of deficit after brain injury: Clinical and theoretical issues Sahraie, A., Trevethan, C. T., MacLeod, M. J., Murray, A. D., Olson, J. A., &
(pp. 1739). New York: Oxford University Press. Weiskrantz, L. (2006). Increased sensitivity after repeated stimula-
Block, N. (2005). Two neural correlates of consciousness. Trends in tion of residual spatial channels in blindsight. Proceedings of the
Cognitive Sciences, 9, 4652. National Academy of Sciences, 103, 1497114976.
Celesia, G. G., Brigell, M. G., & Vaphiades, M. S. (1997). Hemianopic Stoerig, P. (2006). Blindsight, conscious vision, and the role of primary
anosognosia. Neurology, 49, 8897. visual cortex. Progress in Brain Research, 155, 217234.
Danckert, J., & Rossetti, Y. (2005). Blindsight in action: what can the Stoerig, P., & Cowey, A. (1997). Blindsight in man and monkey. Brain,
different sub-types of blindsight tell us about the control of visually 120, 535559.
guided actions? Neuroscience and Biobehavioral Reviews, 29, 10351046. Stoerig, P., & Cowey, A. (2007). Blindsight. Current Biology, 17,
Dehaene, S., Changeux, J. -P., Naccache, L., Sackur, J., & Sergent, C. R822R824.
(2006). Conscious, preconscious, and subliminal processing: A test- Trevethan, C. T., Sahraie, A., & Weiskrantz, L. (2007). Form discrimina-
able taxonomy. Trends in Cognitive Sciences, 10, 204211. tion in a case of blindsight. Neuropsychologia, 45, 20922103.
Heilman, K. M. (1991). Anosognosia: Possible neuropsychological Weiskrantz, L. (1986). Blindsight: A case study and implications. Oxford:
mechanisms. In G. P. Prigatano & D. L. Schacter (Eds.), Awareness Clarendon Press.
of deficit after brain injury: Clinical and theoretical issues (pp. 5362). Weiskrantz, L. (1997). Consciousness lost and found. Oxford: Oxford
New York: Oxford University Press. University Press.
718 C Cortical Color Blindness
Cross References
Cortical Color Blindness
Contrecoup Injury
Achromatopsia Edema
Focal Lesion, Contusion
Cortical Contusion References and Readings
B ETH R USH Bigler, E. D. (2001). The lesions in traumatic brain injury: Implications
Mayo Clinic for clinical neurophysiology. Archives of Clinical Neuropsychology,
16, 95131.
Graham, D. I., Saatman, K. E., Marklund, N., Conte, V., Morales, D.,
Royo, N., & McIntosh, T. K. (2006). The neuropathology of trauma.
In R. W. Evans (Eds.), Neurology and Trauma (2nd ed., pp. 4594).
Synonyms New York: Oxford University Press.
Bruise; Contusion (cerebral)
Cortical Deafness
Definition
Pure Word Deafness
Cortical contusions are bruises on the brain tissue that
form from the small blood vessel leaks (veins and arteries
covering the parenchymal tissue), or a series of microhe-
morrhages following trauma. Trauma is usually the result
of physical blows to the head such as those sustained in a Cortical Lewy Body Disease
motor vehicle accident, direct blow to the head from (CLBD)
assault, or significant sports-related injuries. Veins and
arteries on the surface of the brain are damaged, which Dementia with Lewy Bodies
results in bleeding and bruising. When the blood vessel is
torn, blood escapes from the vessel at a rate that is faster
than the blood that can be absorbed by the brain. Conse-
quently, cortical contusions commonly result in edema
and increased intracranial pressure.
Cortical Magnification
R ONALD A. C OHEN
Current Knowledge Brown University
Providence, RI, USA
Second to diffuse axonal injury, cortical contusion is the
most common type of intra-axial lesion following brain
trauma. By radiologic definition, a cortical contusion Definition
must involve some portion of the superficial gray matter.
Because gray matter has more vasculature than white Cortical magnification refers to the fact that the number
matter, most cortical contusions are hemorrhagic, where- of neurons in the visual cortex responsible for processing
as diffuse axonal injuries are rarely hemorrhagic. The the visual stimulus of a given size varies as a function of
frontal and temporal lobes are the most common sites the location of the stimulus in the visual field. Stimuli
of cortical contusions. When present, cortical contusions occurring in the center of the visual field that have been
are usually found bilaterally. Compared to diffuse axonal detected in the fovea of retina are processed by a very large
injury lesions, cortical contusions are much less likely to number of neurons in the primary visual cortex of
involve an initial presentation of coma or altered loss of the occipital lobe, though these neurons handle only a
consciousness. very small region of the central visual field. Conversely,
Cortical Mapping C 719
stimuli detected in the peripheral visual field tend to be specific informational characteristics (e.g., shape, color,
processed by a much smaller number of neurons in the texture, position, movement), neurons with greatest sen-
primary visual cortex. sitivity to these dimensions vary as a function of cortical
magnification factors and a tradeoff of size of the recep-
tive field and the number of neurons dedicated to each C
Current Knowledge part of the field.
Cortical magnification reflects an important concept in

the field of cognitive neuroscience; the cortical volume,
and ultimately the number of neurons allocated to a
Cross References
particular function, typically varies as a function of the
Feature Detection
significance of the function. For example, since the
Magnocellular Neurons
sense of touch is particularly important for the hands,
Parvocellular Neurons
there are many more nerve receptors in the finger tips
Spatial Frequencies
than in the trunk of the body. Similarly, the volume of
Spatial Processing
motor cortex dedicated to controlling the hands and
mouth in humans is much greater than the volume
dedicated to large muscle groups with more limited
action. Given the critical role that vision plays in References and Readings
human cognition, tremendous magnification of neu-
rons is dedicated to visual processing, with this magni- Daniel, P. M., & Whitteridge, D. (1961). The representation of the visual
fication occurring at various processing stages along the field on the cerebral cortex in monkeys. Journal of Physiology, 159,
203221.
visual pathways beginning in the retina. The extent of
cortical magnification is often expressed as a ratio of
millimeters of cortical surface per degree of visual
angle. This ratio varies across visual areas. Among
primates, neurons devoted to processing foveal input
from the retina are about 100 times more prevalent Cortical Malformation
than neurons devoted to peripheral stimuli in the pri-
mary visual cortex (Daniel & Whitteridge, 1961). Heterotopia
The principle of cortical magnification indicates an
important relationship between the number of neurons
dedicated to big or small visual angles and the receptive
field of those neurons. When a large number of neurons
are involved in a small visual angle, there is inherently a Cortical Mapping
large processing capacity being assigned to a smaller area
of visual focus. Conversely, a smaller number of neurons M ARLA J. H AMBERGER
handling a visual angle are indicative of a larger receptive Columbia University
field, as each neuron must be sensitive to changes occur- New York, NY, USA
ring across a larger area of space. This creates an inherent
relationship between the spatial frequency of the visual
information being processed and the size of the receptive Synonyms
field that is essential for considering how neurons across
different visual cortical areas are tuned to respond to the Direct stimulation mapping; Electrical stimulation
featural and spatial characteristics of visual input. A mapping (ESM); Functional mapping
consequence of this organization for the primary visual
cortex is that visual acuity and the ability to detect small
features of stimuli are best in the center of the visual field Description
and poorest in the periphery. Yet, broad spatial changes
with movement are easily detected at the periphery. Cortical mapping is an invasive procedure in which
Since visual cortical areas differ in their emphasis on electrical stimulation is applied briefly to the cortical
720 C Cortical Mapping
surface for the purpose of identifying areas critical for is based on negative responses, thorough mapping of
sensory, motor or language function. This procedure is language cortex requires administration of tasks assessing
utilized when brain surgery involves the removal or a range of language functions.
disruption of potentially functional cortical areas. Sites Depending on the location of the area identified and
identified via cortical mapping are typically spared the nature of the response elicited by stimulation, it is
from resection, with the goal of preserving function generally held that removal of a positive sensory, motor,
postoperatively. or language site identified by stimulation will result in
Stimulation is applied using a bipolar stimulator, usu- impaired function postoperatively. Of the few clinical
ally via pairs of adjacent subdural electrodes. The procedure series published, results suggest that postoperative
can be conducted intra-operatively in a conscious patient function is best preserved when the resection margin
before resection of brain tissue, or extra-operatively, if sub- exceeds 1 cm from the functional site. On the other
dural electrodes have been implanted, most commonly in hand, there is some evidence that certain sites identified
pharmacologically resistant epilepsy patients who require by stimulation can be removed without concern of
intracranial EEG monitoring to delineate the region of postoperative decline. These include motor sites identi-
seizure onset (Fig. 1). The identification of sensory and fied in the supplementary motor area, tongue, and lower
motor sites is based on stimulation-evoked positive face areas (due to their bilateral representation), and
responses, such as a subjective sensation (e.g., tingling) possibly, language sites identified in the basal temporal
or an observable movement (e.g., muscle twitch). In con- region, although this is somewhat controversial.
trast, stimulation of language cortex elicits no experiential For motor and sensory mapping, the duration of elec-
or observable response in an inactive patient. Rather, trical stimulation is typically 2 s, whereas language
cortical language mapping relies on negative responses, mapping typically requires 48 s of stimulation, depending
in that the patient must be engaged in a language task on the particular task under assessment. The level of stim-
and stimulation of language cortex will disrupt task ulation administered ranges from 1 mA to a maximum of
performance. Thus, for language mapping, stimulation 17 mA, with motor and sensory cortex typically utilizing
produces a discrete, reversible lesion, theoretically en- <10 mA and language cortex typically requiring >10 mA.
abling the examiner to observe the functional conse- Under normal circumstances, cortical stimulation causes
quences of damage to the site(s) stimulated. Stimulation neither pain nor discomfort. One risk of stimulation, how-
of frontal language cortex typically produces speech ar- ever, is the evocation of a seizure, particularly in patients
rest, whereas stimulation of posterior (temporal/parietal) with epilepsy, due to a likely lower seizure threshold in
language cortex typically elicits comprehension, naming epileptogenic areas. To minimize the probability of a stim-
or reading difficulties. Because cortical language mapping ulation induced seizure, EEG is monitored on an ongoing
Cortical Mapping. Figure 1 Implanted subdural electrode grid used for EEG recording and electrical stimulation mapping
Cortical Motor Pathways C 721
basis, and the stimulation intensity is lowered when location of posterior temporal and parietal language
abnormal discharges are associated with stimulation. Nev- sites appears to vary more among individuals, although
ertheless, benzodiazepines are typically kept close at hand this might merely reflect alterations in the distribution of
for IV administration for instances when a seizure occurs language sites in patients with epileptogenic cortex in the
and fails to resolve rapidly on its own. temporal region. C
Clinical Uses
Alteration of function via cortical stimulation in both
One of the main challenges with brain surgery involving
animals and humans dates back to the mid 1800s. The
cortical regions is to remove a sufficient amount of
procedure came into clinical use in the early twentieth
pathological tissue without removing areas critical for
century in association with surgical resection of epilepto-
function. Cortical mapping is used to identify cortical
genic cortex in patients with pharmacologically refractory
regions critical for function, in order to spare these areas
epilepsy. Initially used to identify sensory and motor
from resection or protect them from damage during
cortex, Wilder Penfield and colleagues pioneered the tech-
surgical procedures. Cortical mapping is typically
nique in the 1950s for use in the identification of language
performed when there is concern that resective brain
cortex. Stimulation-based language mapping was further
surgery (e.g., tumor resection, epilepsy surgery) might
refined by George Ojemann and colleagues who essential-
impinge upon, or possibly overlap with cortical regions
ly established the current clinical standards. In addition to
necessary for function.
its clinical utility, investigators have used the opportunity
provided by clinical stimulation to investigate structure-
function relations. These studies build upon the lesion
model, contributing more precise information regarding Cross References
functional localization due to both the controlled setting,
and the smaller, more discrete lesions induced Epilepsy
temporarily by stimulation than that typically found Functional Imaging
with naturally occurring lesions. Localization
Psychometric Data References and Readings

Cortical mapping procedures remain unstandardized.
Hamberger, M. (2007). Cortical language mapping in epilepsy: A critical
Due to its highly invasive nature, data from cortical review. Neuropsychology Review, 4, 477489.
mapping are based on clinical rather than normal popu- Ojemann, G. A. (1983). Electrical stimulation and the neurobiology of
lations, and therefore, classic psychometric data are language. The Behavioral and Brain Sciences, 2, 221230.
unavailable. It has also been difficult to assess reliability,
as cortical mapping is rarely performed more than once
in the same patient. Nevertheless, patients with indwell-
ing subdural grids who undergo mapping over 2 or more
days, and patients who require a second surgery involv- Cortical Motor Pathways
ing adjacent brain regions provide opportunities for
repeat mapping, although these circumstances are rela- C HRISTINA R. M ARMAROU
tively infrequent. In the absence of published studies Virginia Commonwealth University
addressing this issue, anecdotal reports suggest a reason- Richmond, VA, USA
able level of consistency in the location of simulation-
identified sites within individuals. Across individuals,
consistency is relatively high for the location of motor Synonyms
and sensory cortex. Frontal language cortex is slightly
more variable, with most positive sites clustered in the Corticospinal tract; Pyramidal tract; Voluntary motor
frontal opercular region, anterior to the tongue area. The tract
722 C Cortical Motor Pathways
Definition pyramidal decussation, ultimately terminating in the

ventral horn of the cervical-through-lumbar spinal
The cortical motor pathway consists of four regions of the cord. These cortical motor pathways work in tandem
cerebral cortex (primary motor cortex, posterior parietal with other cortical motor areas of the brain notably
cortex, premotor cortex, and supplementary motor cor- the cerebellum and subcortical motor nuclei (the basal
tex) whose neuronal cell bodies are located in layer V ganglia) to execute planning and control of voluntary
(five) and whose projections are involved with the execu- motor activity. Other projections from layer V of M-I
tion of muscle contraction largely on the contralateral side include the corticostriatal fibers to the striatum (caudate
of the body. and putamen), corticorubral fibers to the red nucleus,
and projections that terminate in the reticular forma-
tions with the medulla and pons of the brain stem. M-I
projections also modulate other motor areas within the
Current Knowledge
cortex and include reciprocal connections with the sup-
plementary motor area, the premotor and posterior
The cortical motor pathway describes a trajectory of fibers
parietal motor areas. These fibers are part of a vast
whose cells of origin are located in layer V of the cerebral
reciprocal network that cross via the corpus callosum
motor cortex. The cerebral motor cortex is a term that
and are referred to as callosal connections. The SMA
describes the four main areas of the cerebral cortex that
contributes to the corticospinal tract and has reciprocal
contribute to the planning, control, and execution of
callosal projections to contralateral areas of the motor
voluntary motor fibers; the primary motor cortex (M1),
cortex. The premotor cortex (PMC) contributes to the
secondary motor cortices, premotor cortex, and the sup-
corticospinal tract and also has extensive reciprocal con-
plementary motor area (SMA).
nections to both SMA and MI.
Cortical Location and Overall Function

Cross References
The primary motor cortex (M1) is located in the frontal
lobe of the brain and the cells of origin, in layer V, are Cerebral Cortex
found within the precentral gyrus. These cells generate Decerebrate Posturing
neural impulses that control the execution of movement Decorticate Posturing
directed to skeletal muscles on the contralateral side of the Hemiplegia
body. Other regions of the cortex that contribute to Homunculus
the cortical motor pathway termed secondary motor Internal Capsule
cortices include the posterior parietal area (PMA), the Periventricular White Matter
premotor cortex (PMC) and the supplementary motor Precentral Gyrus
area (SMA). The posterior parietal cortex is responsible Pyramidal System
for transforming visual information into motor com- Sensorimotor Assessment
mands relayed via the premotor and supplementary Supplementary Motor Area
motor area. The premotor cortex is involved in sensory
guidance of movement and control of proximal and trunk
muscles of the body. The supplementary motor area is
involved in the planning and coordination of complex References and Readings
movements, such as those requiring coordination of
two-handed movement. Berne, R. M., & Levy, M. N. (2000). Principles of physiology. St. Louis,
Multiple pathways arise from the efferent projections MO: Mosby.
of the motor cortices. Neuronal cell bodies located in layer Fix, J. (1995). Neuroanatomy. Baltimore, MD: Williams & Wilkins.
V of the M1, SMA, and premotor cortex send vast projec- Haines, D. E. (2000). Neuroanatomy. Philadelphia, PA: Lippincott
Williams & Wilkins.
tions that collectively give rise to the largest single path-
Haines, D. E. (2004). Neuroanatomy: An atlas of structures, sections, and
way, the pyramidal or corticospinal tract. The tract systems. Philadelphia, PA: Lippincott Williams & Wilkens.
descends through the internal capsule and forms the Kandel, E. R., Schwartz, J. H., & Jessel, T. M. (1991). Principles of
pyramids of the medulla, crossing midline at the neuroscience. Norwalk, CT: Appleton and Lange.
CorticalSubcortical Loop C 723
inhibition related to social context or emotional subject

CorticalSubcortical Loop matter. In this loop, the lateral orbitofrontal cortex
(OFC) projects via the ventromedial caudate nucleus to
J ANNA L. H ARRIS VA and MD thalamic nuclei, which in turn send projec-
University of Kansas Medical Center tions back to lateral OFC.
Kansas, KS, USA
C
Affective-motivational loop. This loop is also called
the Limbic loop. This circuit plays a role in emotional
and motivational behaviors. Widespread areas of limbic
Synonyms cortex including the anterior cingulate gyrus, medial
OFC, and portions of the temporal lobe all send projec-
Basal ganglia-thalamocortical circuit; Cortico-basal tions via the nucleus accumbens to MD thalamus. The
ganglia loop circuit is completed by thalamocortical projections from
MD to the anterior cingulate and medial OFC.
Definition
The corticalsubcortical loop describes a class of distinct,

Clinical Disorders and Treatment
parallel circuits that connect specific regions of cerebral
Approaches
cortex with the basal ganglia and specific thalamic nuclei.
The thalamic nuclei complete the loop by projecting back to
An understanding of the architecture of corticalsubcortical
the same regions of cortex from which the circuits originate.
loops has given rise to a prevailing view of numerous clinical
disorders as essentially circuit disorders, arising from abnor-
Current Knowledge mal neuronal activity at some stage of the finely tuned
circuit. The best-studied examples involve the motor loop,
Several distinct, anatomically segregated corticalsubcor- where disturbances within the circuit can result in either
tical loops may be characterized based on the functional hypokinetic movement disorders (e.g., Parkinsons disease)
role of the cortical regions involved. or hyperkinetic disorders (e.g., chorea, ballismus, and dys-
Motor loop. The motor loop plays a role in the prep- tonia). In addition, abnormal activity within the non-motor
aration and execution of movement. Primary motor cor- loops may be associated with disorders as diverse as obses-
tex and associated premotor areas project via the putamen sivecompulsive disorder, schizophrenia, and Tourette syn-
to the ventral tier nuclei of the thalamus, which then drome. Recently, interventions that surgically remove or
complete the loop with projections back to motor cortex. modify (e.g., with deep brain stimulation) the dysfunctional
Somatotopic organization is maintained through all component of the corticalsubcortical loop have met with
stages of this circuit. considerable success. These promising treatment approaches
Oculomotor loop. The oculomotor loop is involved are the subject of intensive ongoing research.
in the control of eye movements. The frontal eye fields
(FEF) and supplementary eye fields (SEF) project via the
body of the caudate nucleus to the ventral anterior (VA) Cross References
and mediodorsal (MD) thalamic nuclei, which complete
the loop by projecting back to FEF and SEF. Basal Ganglia
Prefrontal associative loops. The prefrontal associa- Deep Brain Stimulator (Parkinsons)
tive loops describe two distinct components, which sub- Parkinsons Disease
serve different aspects of higher cognitive processing.
The dorsolateral prefrontal loop plays a role in cogni-
tive processes including spatial memory and working References and Readings
memory. In this circuit, the dorsolateral prefrontal cor-
tex (PFC) projects via the dorsolateral head of the cau- Alexander, G. E., Crutcher, M. D., & DeLong, M. R. (1990). Basal ganglia-
date to VA and MD thalamic nuclei, which then project thalamocortical circuits: Parallel substrates for motor, oculomotor,
prefrontal and limbic functions. Progress in Brain Research, 85,
back to dorsolateral PFC. The lateral orbitofrontal
119146.
loop plays a role in cognitive processes including the DeLong, M. R., & Wichmann, T. (2007). Circuits and circuit disorders of
ability to select and shift behavioral sets, and response the basal ganglia. Archives of Neurology, 64(1), 2024.
724 C Corticobasal Degeneration
complex of disorders (Kertesz, 2003). Given the clinically

Corticobasal Degeneration heterogeneous presentation of CBD, and the fact that the
core features of CBD can be produced by other condi-
A LEXANDER I. T ROSTER tions, it has been recommended that the term corticobasal
University of North Carolina syndrome (CBS) be applied to the core clinical features of
Chapel Hill, NC, USA CBD regardless of etiology. In contrast, the term cortico-
basal degeneration (CBD) should be reserved for the
distinctive neuropathological condition of CBD, regard-
Synonyms less of its clinical presentation (Lang, 2003).
From a neuropathologic standpoint, CBD, like fron-
Corticobasal syndrome; Corticodentatonigral degenera- totemporal lobar degeneration, has been categorized as a
tion with neuronal achromasia tauopathy. Tau is a microtubule-associated protein that
promotes the polymerization of tubulin and thus, micro-
tubule assembly. The human tau gene, containing 16
Short Description or Definition exons, is located on the long arm of chromosome 17
and encodes for the six isoforms of tau found in the
First described as corticodentatonigral degeneration with central nervous system. The isoforms differ by the pres-
neuronal achromasia by Rebeiz et al. in 1968, corticobasal ence or absence of amino acid inserts encoded by exons 2,
degeneration (CBD) was long thought to be predomi- 3, and 10. Whether the transcript of exon 10 is spliced in
nantly a motor disorder. Indeed, the original description or out of the final tau protein product determines whether
of the disorder emphasized the relative preservation of the isoform has three or four repeated microtubule-bind-
mental faculties. More recently, emphasis has been placed ing domains (three isoforms have three repeats and three
on the neurobehavioral features of CBD, and the over- isoforms have four repeats). The four repeat isoforms of
lapping clinical and neuropathological features of CBD tau (4R tau) promote microtubule assembly at more than
with frontotemporal lobar degenerations continue to gen- twice the rate of the three repeat (3R tau) isoforms.
erate debate about the classification and nosology of the Although the expression of 3R and 4R tau is cell-type
disorder. specific, the 3R tau expression in normal human brain
The motor presentation of CBD most often involves is 11.5-fold higher than the 4R expression level. In
an asymmetric, progressive, akinetic-rigid parkinsonism spontaneous and genetic CBD, 4R tau represents the
of gradual onset that responds minimally if at all to main pathological inclusion. Recent findings that
levodopa and is sometimes accompanied by dystonia or mutations associated with parkinsonism (in LRRK2)
myoclonus. Cortical signs that are common in CBD and frontotemporal lobar degeneration (in progranulin)
include asymmetric apraxia, cortical sensory signs can be seen in some cases presenting with corticobasal
(e.g., astereognosis, graphesthesia), and alien hand sign. syndrome further highlight the heterogeneity of cortico-
The latter may involve a sense of lack of ownership of the basal syndrome (CBS).
limb in the absence of visual cues, involuntary purposeful Autopsy in CBD cases reveals asymmetric frontal and
movements, or frank interference of one limb with the parietal atrophy, depigmentation of the substantia nigra
others execution of purposeful movement. These motor without Lewy bodies, and often the presence of ballooned
and cortical signs are core features of CBD. cells in cortex. Tau-positive astrocytic plaques, oligoden-
droglial coiled bodies, and threadlike lesions are seen in
white and gray matter, especially the superior frontal and
Categorization parietal gyri and the pre- and post-central gyri, and in the
striatum.
The neurobehavioral expression of CBD can be quite
variable, and cases with confirmed CBD neuropathology
have presented with features suggestive of primary pro- Epidemiology
gressive aphasia and frontotemporal dementia. Coupled
with the recognition of CBD as a tauopathy, the occasion- Prevalence and incidence of CBD are unknown, and poor
al neurobehavioral resemblance of CBD to frontotem- diagnostic accuracy no doubt contributes to this. Al-
poral dementia and primary progressive aphasia has lead though the H1/H1 tau haplotype has been identified as
some to argue that CBD is a member of the Pick heightening susceptibility to both CBD and progressive
Corticobasal Degeneration C 725
supranuclear palsy, no clear genetic etiology has been retrieval deficits. Remote memory has been little studied
identified. Dementia and other cognitive and behavioral in CBD, but the pattern of poor recall but intact recogni-
abnormalities were thought to be rare in CBD until the tion on remote memory tasks suggests a retrieval deficit.
last decade, but it is now appreciated that the frequency of Visuospatial impairments have been observed.
neurobehavioral abnormalities observed as a presenting With respect to emotional and neuropsychiatric C
problem or during the course of the condition is quite issues, depression is common in CBD (73% of patients),
high. It might be that the inconsistent incidence and though apathy (40%), irritability (20%), and agitation
prevalence estimates of cognitive impairment in CBD (20%) also occur with frequency.
are a function of whether patients were drawn from
movement disorder, dementia, or psychiatry clinics.
Evaluation
Natural History, Prognostic Factors, The selection of specific neuropsychological tests in CBD,
Outcomes like any other condition, should be guided by the referral
questions and the patients ability to cooperate and meet
Disease onset is usually in the sixth decade of life, and task demands. However, tests of executive function (e.g.,
mean time to death from diagnosis is about 7 years. planning, abstraction, and cognitive flexibility), praxis,
visuospatial functions, attention, learning and memory,
and word retrieval should be employed. Symptom
Neuropsychology and Psychology of inventories relating to apathy, depression, and frontal
Corticobasal Degeneration behavior syndromes, such as the Neuropsychiatric
Inventory, Hamilton depression scale, and Frontal
CBD involves an asymmetric apraxia, most often of the Systems Behavior Scale can be helpful in characterizing
ideomotor type, but ideational and limb kinetic apraxias neuropsychiatric features of CBD.
also occur. Thus, patients most often have difficulty
demonstrating the use of tools. Poor drawing (construc-
tional apraxia) is also commonly seen. Language distur- Treatment
bance occurs early or during progression of the syndrome,
and the aphasia is most often non-fluent (about 56% of Some cases may show transient improvement in parkin-
cases) or anomic (30%). The pattern of performance on sonian features with levodopa treatment; dopamine ago-
language tests in patients with the traditional CBD pre- nists are generally even less helpful than levodopa.
sentation is somewhat inconsistent across studies, but Tremor, if present, may be alleviated by benzodiazepines.
phonological impairments may be an important feature. Antidepressants with anticholinergic profiles are to be
Performance on verbal fluency tests, especially lexical or avoided given possible adverse cognitive side effects, but
phonemic fluency tests, is usually impaired either due to selective serotonin reuptake inhibitors may be helpful in
the executive demands of those tasks or aphasia. Perfor- treating depression. Speech therapy is helpful in treating
mance on semantic memory tasks such as conceptual dysphagia.
matching and visual confrontation naming and expressive
vocabulary is relatively preserved and impaired in a mi-
nority of patients, although some studies have reported Cross References
considerable impairment on semantic tasks early in the
disease. When naming is impaired, disproportionate Basal Ganglia
benefit is derived from cuing suggesting a retrieval rather Corticobasal Degeneration
than semantic memory deficit. Comprehension is typical- Frontal Lobes
ly preserved early, but comprehension of grammatically Frontal Temporal Dementia
complex material declines with disease progression. Frontotemporal Lobar Degeneration
Executive dysfunction, as indicated by poor perfor- Gait Disorders
mance on tasks such as the card sorting tasks and the Movement Disorders
Trailmaking test is common. Episodic memory impair- Parkinson Plus Syndromes
ments in CBD are relatively mild early in the course of the Parkinsons Disease
condition and appear to involve both encoding and Parkinsonian Movement
726 C Cortico-Basal Ganglia Loop
Striatum
Tauopathy Corticoliberin
Corticotropin-Releasing Hormone
Belfor, N., Amici, S., Boxer, A. L., Kramer, J. H., Gorno-Tempini, M. L.,
Rosen, H. J., et al. (2006). Clinical and neuropsychological features
of corticobasal degeneration. Mechanisms of Ageing and Develop-
ment, 127, 203207.
Boeve, B. F. (2007). Parkinson-related dementias. Neurologic Clinics, 25,
Corticospinal Tract
761781.
Geda, Y. E., Boeve, B. F., Negash, S., Graff-Radford, N. R., Knopman, Cortical Motor Pathways
D. S., Parisi, J. E., et al. (2007). Neuropsychiatric features in 36
pathologically confirmed cases of corticobasal degeneration. Journal
of Neuropsychiatry and Clinical Neurosciences, 19, 7780.
Graham, N. L., Bak, T. H., & Hodges, J. R. (2003). Corticobasal degener-
ation as a cognitive disorder. Movement Disorders, 18, 12241232.
Kertesz, A. (2003). Pick complex: An integrative approach to frontotem- Corticotropin-Releasing Factor
poral dementia: Primary progressive aphasia, corticobasal degenera-
tion, and progressive supranuclear palsy. The Neurologist, 9, 311317.
(CRF)
Lang, A. E. (2003). Corticobasal degeneration: Selected developments.
Movement Disorders, 18(Suppl. 6), S5156. Corticotropin-Releasing Hormone
Litvan, I., Cummings, J. L., & Mega, M. (1998). Neuropsychiatric features
of corticobasal degeneration. Journal of Neurology, Neurosurgery, and
Murray, R., Neumann, M., Forman, M. S., Farmer, J., Massimo, L.,
Rice, A., et al. (2007). Cognitive and motor assessment in autopsy-
proven corticobasal degeneration. Neurology, 68, 12741283. Corticotropin-Releasing Hormone
Sha, S., Hou, C., Viskontas, I. V., & Miller, B. L. (2006). Are frontotem-
poral lobar degeneration, progressive supranuclear palsy and corti- B ETH K UCZYNSKI 1, S TEPHANIE A. KOLAKOWSKY-H AYNER 2
cobasal degeneration distinct diseases? Nature Clinical Practice 1
University of California
Davis, CA, USA
Troster, A. I., & Fields, J. A. (2008). Parkinsons disease, progressive 2
supranuclear palsy, corticobasal degeneration, and related disorders Santa Clara Valley Medical Center,
of the frontostriatal system. In J. E. Morgan & J. H. Ricker (Eds.), Rehabilitation Research Center
Textbook of clinical neuropsychology (pp. 536577). New York: Psy- San Jose, CA, USA
chology Press.
Synonyms
Cortico-Basal Ganglia Loop
Corticoliberin; Corticotropin-releasing factor (CRF)
Definition
Corticobasal Syndrome
Corticotropin-releasing hormone (CRH) is a hormone
Corticobasal Degeneration that is primarily produced by the hypothalamus and is
involved in the stress response. It is released from the
paraventricular nucleus of the hypothalamus with the
Corticodentatonigral primary action within the anterior lobe of the pituitary
to initiate the release of adrenocorticotropic hormone
Degeneration with Neuronal (ACTH). CRH (41 amino acids long) is derived from a
Achromasia 191 amino acid preprohormone. Other areas of CRH
synthesis include peripheral tissues, and it is highly
Corticobasal Degeneration expressed in the placenta.
CPT C 727
Cross References
Counterindicant
Hormone
Contraindication
C
Bennett, M. (2008). Stress and anxiety in schizophrenia and depression:

Glucocorticoids, corticotropin-releasing hormone and synapse re- Couples Therapy
gression. Australian & New Zealand Journal of Psychiatry, 42(12),
9951002. Cognitive Behavioral Couples Therapy
Fabricio, A., Tringali, G., Pozzoli, G., & Navarra, P. (2005). Mirtazapine
acutely inhibits basal and K-stimulated release of corticotropin-
releasing hormone from the rat hypothalamus via a non-genomic
mechanism. Psychopharmacology, 178(1), 7882.
Guendelman, S., Lang Kosa, J., Pearl, M., Graham, S., & Kharrazi, M.
(2008). Exploring the relationship of second-trimester corticotropin
releasing hormone, chronic stress and preterm delivery. Journal of COWA
Maternal-Fetal & Neonatal Medicine, 21(11), 788795.
Watts, A., Kelly, A., & Sanchez-Watts, G. (1995). Neuropeptides and Controlled Oral Word Association Test
thirst: The temporal response of corticotropin-releasing hormone F-A-S Test
and neurotensin/neuromedin N gene expression in rat limbic fore-
brain neurons to drinking hypertonic saline. Behavioral Neurosci-
Verbal Fluency
ence, 109(6), 11461157.
Weber, M., & Richardson, R. (2001). Centrally administered
corticotropin-releasing hormone and peripheral injections of strych-
nine hydrochloride potentiate the acoustic startle response in pre-
weanling rats. Behavioral Neuroscience, 115(6), 12731282. COWAT
Controlled Oral Word Association Test
F-A-S Test
Verbal Fluency
Cortisteroids
Steroids
CPM
Coumadin Raven Matrices
Warfarin (Coumadin)
CPRS
Counseling
Conners Rating Scales
Psychotherapy
Counseling Relationship CPT

TherapistPatient Relationship Continuous Performance Tests
728 C Craig Handicap Assessment and Reporting Technique
The CHART was designed to be administered by

Craig Handicap Assessment and interview, either in person or by telephone and takes
Reporting Technique approximately 15 min to administer. Participant-proxy
agreement across disability groups on the CHART has
G ALE G. W HITENECK provided evidence in support of the use of proxy data
Craig Hospital for persons with various types of disabilities (Cusick,
Englewood, CO, USA Brooks, & Whiteneck, 2001). There is no set time period
for administering the CHART; however, it is recom-
mended that multiple measurements be taken over the
Synonyms course of a persons lifetime to assess changes with
adaptation to the disability and to gain insight into
CHART; CHART-SF changes in participation, which may occur over time.
Description Historical Background

The Craig Handicap Assessment and Reporting Technique WHO describes a conceptual model of disablement that
(CHART) is a 32-item instrument designed to provide a includes impairment at the organ level, disability de-
simple, objective measure of the degree to which impair- scribing functional status, and handicap, or more re-
ments and disabilities result in handicaps (societal partici- cently, participation, encompassing the roles one plays
pation limitations) for adolescents and adults (15 years and in the world and society. Despite its importance as a
older) in the years after initial rehabilitation. The CHART rehabilitation goal, handicap (absence of social partici-
includes six subscales (physical independence, cognitive pation) is the least often measured of all rehabilitation
independence, mobility, occupation, social integration, outcomes. A great deal of work has been done in devel-
and economic independence), which closely reflect the oping tools to measure and document impairment and
disablement model developed by the World Health disability; however, limited attempts have focused on the
Organization (WHO, 1980, 2001). Each subscale contains measurement and assessment of long-term participation
37 questions, which together quantify the extent to which limitations (handicap), despite the fact that psychosocial
individuals fulfill various social roles. CHART focuses on adjustment is clearly regarded as the ultimate outcome
objective, observable criteria that are easily quantifiable and of rehabilitation. The CHART was specifically developed
unlikely to be open to subjective interpretation. Each of the to help fill this gap to assess the WHO dimensions of
domains or subscales of the CHART has a maximum score handicap and to provide a simple, objective measure of
of 100 points, which is considered to be the level of perfor- the degree to which impairments and disabilities result
mance typical of the average nondisabled person. High in participation limitations in the years after initial
subscale scores indicate less handicap or higher social and rehabilitation.
community participation. The model of disablement suggested by the WHO
The CHART was developed in 1992 for use with provides useful conceptual distinctions for impairment,
persons with spinal cord injury (SCI) and originally did disability, and handicap (WHO, 1980). In practical terms,
not address the WHO handicap dimension described as impairment occurs at the organ level, representing any loss
orientation (Whiteneck, Charlifue, Gerhart, Overhos- or abnormality of psychological, physiological, or
ler, & Richardson, 1992). The current CHART was revised anatomical structure or function. Disability occurs at the
in 1995 with the addition of a Cognitive Independence person level, demonstrated as any restriction or lack of
subscale (to assess orientation) and has proven to be an ability (resulting from impairment) to perform any
appropriate measure of societal participation that can be activity in the manner or within the range considered
used with individuals having a range of physical or cogni- normal for a human being. Handicap occurs at the societal
tive impairments (Mellick, Walker, Brooks, & Whiteneck, level. It is a disadvantage for a given individual, resulting
1999). A 19-item Short Form with subscales closely from an impairment or a disability that limits or prevents
approximating the subscale scores for the CHART long the fulfillment of a role that is normal (depending on age,
form is recommended for those applications or popula- sex, and social and cultural factors) for that individual.
tions in which time is at a minimum (Whiteneck et al., The initial disablement model, the International Classi-
1998). fication of Impairment, Disability and Health (ICIDH)
Craig Handicap Assessment and Reporting Technique C 729
(WHO, 1980), was later revised as the International factors included in this subscale include household com-
Classification of Functioning, Disability and Health position, romantic involvement; the number of relatives,
(ICF) (WHO, 2001). The domain of handicap was business associates, and friends with whom regular writ-
reconceptualized and changed to participation. The ten or oral contract is maintained, and the frequency of
migration away from the use of handicap toward the initiating conversations with strangers. C
more widespread use of participation is evident in Economic Self-Sufficiency is the individuals ability to
literature published since 2001. According to the WHO, sustain customary socioeconomic activity and indepen-
handicap (participation) describes the total effects and dence. This dimension is defined as the remaining dispos-
interplay of all the consequences of disability: social, able household family income after nonreimbursed
economic, cultural, and environmental. medical expenses have been excluded.
Each CHART dimension of handicap is characterized
by directly observable qualities which lend themselves to
easy quantification. While an infinite number of factors Psychometric Data
might have been included, to keep the instrument to a
practical length the following dimensions have been Initial calibration of the CHART scoring system was based
operationalized based on the WHO definitions. on administration of the instrument to 88 able-bodied
Physical Independence is the individuals ability to individuals and 100 persons with SCI. Once the norms
sustain a customarily effective independent existence. had been established, two studies were conducted to
The major component of this subscale is the number of assess the psychometric properties. CHART showed high
hours per day someone is needed to provide routine or testretest reliability 0.93 for the total score and from
occasional assistance (whether paid or unpaid). Indivi- 0.80 to 0.95 for the subscales. The correlation of subject
duals are viewed as somewhat less handicapped if they proxy scores was 0.83 for the total CHART score. Rasch
take primary responsibility for instructing and directing analysis established that CHART is a well-calibrated linear
people who are providing assistance to them. scale, with a good fit of both items and persons to its data
Cognitive Independence is the individuals ability to (Whiteneck et al., 1992).These studies established the
sustain a customary level of independence without the CHART as a reliable and valid instrument, as well as a
need for supervision. The factors included in this subscale well-calibrated linear scale (Whiteneck et al.; Dijkers,
reflect the amount of hours that a person needs supervi- 1991). A decade later, subsequent testing on a group of
sion both inside and outside the home, as well as the 236 persons with SCI reported similar results testretest
amount of difficulty an individual has in remembering, correlations of 0.87 and subjectproxy correlations of 0.85
communicating, and managing money. were reported (Whiteneck, Brooks, & Mellick, 1997).
Mobility is the individuals ability to move about The Revised CHART which included the Cognitive
effectively in his/her surroundings and is demonstrated Independence subscale was tested on 1,110 persons in
by the hours per day out of bed, days per week out of the six impairment categories SCI, traumatic brain injury,
house, nights per year spent away from home, accessibility stroke, multiple sclerosis, amputation, and burn
of the home, and transportation utilization. (Whiteneck , Brooks et al., 1997). Results indicated that
Occupation is the individuals ability to occupy time in the cognitive subscale of the CHART was reliable and
the manner customary to that persons sex, age, and enhanced the appropriateness of the CHART in assessing
culture. The time spent in various activities is used to handicap among persons having cognitive impairments
measure this dimension. The relative value society places (Mellick et al., 1999). Participant-proxy agreement across
on different activities is used to weight the time in each the six disability groups provided evidence in support of
category. Although there was a potential for subjective the inclusion of proxy data for persons with various types
bias based on value judgments in developing the scale in of disabilities (Cusick et al., 2001)
this dimension, priority has been give to gainful employ- In an effort to reduce the number of items in the
ment, schooling, and active homemaking and mainte- CHART, a short form was developed. A multidimensional
nance, and this prioritization has been supported by analysis was performed which showed that fewer variables
validity and reliability testing. Other elements documen- were needed to obtain CHART scores. Regression analyses
ted include volunteer work, recreational pursuits, and were performed on each subscale with the dependent mea-
self-improvement activities. sure being the scale score and the variables contributing to
Social Integration is the individuals ability to partici- the subscale acting as the predictor variables. All CHART
pate in and maintain customary social relationships. The subscale scores could be reduced by fewer questions to reach
730 C Craig Handicap Assessment and Reporting Technique (CHART) Short Form
90% explained variance except Economic Self-Sufficiency, Mellick, D., Walker, N., Brooks, C. A., & Whiteneck, G. (1999). Incorpor-
ating the cognitive independence domain into CHART. Journal of
which using the main variables could only explain 45%.
Rehabilitation Outcome Measures, 3(3), 1221.
For additional information about the development, Segal, M. E., & Schall, R. R. (1995). Assessing handicap of stroke
testing, and scoring procedures for the CHART and survivors. A validation study of the Craig handicap assessment and
CHART-SF please consult the Guide for use of the reporting technique. American Journal of Physical Medicine &
CHART: Craig Handicap Assessment and Reporting Rehabilitation, 74, 276286.
Walker, N., Mellick, D., Brooks, C. A., Whiteneck, G. G. (2003).
Technique at www.craighospital.org/Research/CHART.
Measuring participation across impairment groups using the Craig
handicap assessment and reporting technique. American Journal of
Physical Medicine and Rehabilitation, 82(12), 936941.
Clinical Uses Whiteneck, G., Brooks, C. A., Charlifue, S., Gerhart, K. A., Mellick, D.,
Overholser, D., et al. (1998). Guide for use of the CHART: Craig
handicap assessment and reporting technique. www.craighospital.
The CHART is a useful tool to measure handicap
org/Research/CHART December 29, 2009.
(participation limitations) in populations with injury or Whiteneck, G. G., Brooks, C. A., & Mellick, D. C. (1997). Handicap
chronic illness with or without rehabilitation interven- assessment Final report. Rehabilitation research and training center
tion. The CHART is designed as an interview tool, on functional assessment and evaluation of rehabilitation outcomes.
which can be administered face-to-face or by telephone. Buffalo, NY: State University of New York.
Whiteneck, G. G., Charlifue, S. W., Gerhart, K. A., Overhosler, J. D., &
Each item on the instrument has been carefully and con-
Richardson, G. N. (1992). Quantifying handicap: A new measure of
cisely worded to minimize ambiguity of interpretation. It long-term rehabilitation outcomes. Archives of Physical Medicine and
is possible to use the instrument as a mailed question- Rehabilitation, 73, 519526.
naire, although some valuable data potentially would be Whiteneck, G. G., Fougeyrolles, P., & Gerhart, K. A. (1997). Elaborating
lost in the absence of interaction with an interviewer the model of disablement. In M. Fuhrer (Ed.), Assessing medical
rehabilitation practices: The promise of outcomes research. Baltimore:
providing consistent prompts. There is no set time period
Paul H. Brooks Publishing Co.
for administering the CHART; however, it is recom- World Health Organization. (1980). International classification of impair-
mended that multiple measurements be taken over the ments, disabilities and handicaps: A manual of classification relating to
course of a persons lifetime to assess changes with adap- the consequences of disease. Geneva: World Health Organization.
tation to the disability and to gain insight into changes in World Health Organization. (2001). International classification of func-
tioning, disability and health. Geneva: World Health Organization.
participation which may occur over time. CHART has
been demonstrated to be a reliable measure of societal
participation limitations in a variety of populations in-
cluding people with physical and/or cognitive functional
limitations.
Craig Handicap Assessment and
Reporting Technique (CHART)
Cross References Short Form
CHART Short Form
CHART Short Form

Cusick, C. P., Brooks, C. A., & Whiteneck, G. G. (2001). The use of
proxies in community integration research. Archives of Physical Cramping
Medicine and Rehabilitation, 82(8), 10181024. Manuscript in
development. Dystonia
Cusick, C. P., Gerhart, K. A., & Mellick, D. C. (2000). Participant-proxy
reliability in traumatic brain injury outcome research. Journal of
Head Trauma Rehabilitation, 15(1), 739749.
Dijkers, M. (1991). Scoring CHART: Survey and sensitivity analysis.
Journal of the American Paraplegia Society, 14, 8586.
Hall, K. M., Dijkers, M., Whiteneck, G., Brooks, C. A., & Krause, J. S.
(1998). The Craig handicap assessment and reporting technique
Cranial Aerocele
(CHART): Metric properties and scoring. Topics in Spinal Cord
Injury Rehabilitation, 4(1), 1630. Pneumocephalus
Cranial Nerves C 731
may be considered mixed nerves, meaning that they

Cranial Nerves carry a combination of motor and sensory fibers (CNs
V, VII, IX, and X). As a general rule, the brainstem nuclei
M ELISSA J. M C G INN associated with sensory cranial nerve fibers are located
Virginia Commonwealth University School of Medicine more laterally in the brainstem, while the motor nuclei
Richmond, VA, USA
C
are positioned more medially. The sulcus limitans is the
landmark that demarcates the boundary between these
efferent (motor) and afferent (sensory) nuclear zones in
Definition the brainstem, which are typically arranged in a longitu-
dinal columnar manner according to functional compo-
Cranial nerves serve as conduits for communication nents (see Functional Components below). Motor
between the brain and the body, providing motor and neurons that comprise these brainstem nuclei send axo-
sensory innervation to structures in the head and neck nal projections, via cranial nerves, to control glandular
as well as the thoracic and abdominal viscera. There are tissue secretions and the contraction of various types of
12 pairs of cranial nerves, each of which is designated by a muscle (skeletal, smooth, and cardiac muscle). Con-
Roman numeral and a name (see Table 1). Roman numer- versely, the sensory cranial nerve fibers typically origi-
als IXII indicate the rostrocaudal order in which cranial nate from sensory neurons located in sensory ganglia
nerves originate from the brain, while the name desig- (collections of neurons residing outside of the brain)
nated to each pair of cranial nerves denotes either its and function to transmit sensation from various types
function or distribution. of sensory receptors (i.e., pain and temperature recep-
tors on the skin) to the brainstem.
Functional Components. In addition to the generalized
Historical Background classification of cranial nerves as sensory, motor, or mixed
nerves, the fibers that comprise each CN can be further
The enumeration of the cranial nerves can be traced back categorized according to the specific nature of the afferent
to second century Greek physicianphilosopher Galen; or efferent information being transmitted and the types
whose initial description included 7 of the 12 currently of structures innervated. These fiber classifications,
accepted pairs. English physician and neuroanatomist which are often referred to as functional components
Thomas Willis reclassification of the cranial nerves in include somatic motor, visceral motor, branchial motor,
the seventeenth century consisted of nine pairs and super- somatic sensory, visceral sensory, and special sensory
seded Galens previous description. German anatomist fibers. A cranial nerve can carry one or several of these
Samuel Thomas von Soemmerring introduced the con- functional components.
temporary classification system, comprising 12 pairs of Motor Cranial Nerves. Three of the six functional
cranial nerves, in the late eighteenth century. classifications of cranial nerve fibers convey motor inner-
vation: somatic motor, branchial motor, and visceral
motor fibers. Somatic motor fibers originate in motor
nuclei located in the medial-most cell column of the
Current Knowledge brainstem and function to transmit motor impulses to
voluntary skeletal muscle (of developmental somatic
Cranial Nerve Nuclei. The majority of cranial nerves myotome origin) in the head and neck. CNs III, IV, and
(CNs) originate from collections of neurons (nuclei) VI carry somatic motor fibers that innervate the extrao-
located within the brainstem (exceptions to this rule cular muscles, CNXI provides somatic motor innervation
are CNs I and II, which are associated with the forebrain to two muscles located within the neck/shoulder region
and diencephalon, respectively). CNs III and IV emerge and CN XII conveys somatic motor information to the
from the midbrain portion of the brainstem, CNs VVIII intrinsic muscles of the tongue.
arise from the pons, and the remaining cranial nerves Branchial motor fibers are similar to somatic motor
(CNs IXXII) originate in the medulla. Taken together, fibers in that they provide motor innervation to voluntary
the cranial nerves convey both motor and sensory inner- striated muscles located within the head and neck region.
vation. However, individual cranial nerves may transmit However, branchial motor fibers and the muscles that
sensory information only (CNs I, II, and VIII), motor they innervate are afforded a separate classification
innervation only (CNs III, IV, VI, XI, and XII), or they based on their embryologic derivation from branchial/
732 C Cranial Nerves
Cranial Nerves. Table 1 List of cranial nerves
Functional Deficits/symptoms
Number Name componenta Function of dysfunction
I Olfactory N. Special sensory Olfaction (smell) Hyposmia and anosmia
II Optic N. Special sensory Vision Anopsia
III Oculomotor N. Somatic motor Extraocular muscles (superior, inferior, and Diplopia and ptosis
medial rectus muscles)
Visceral motor Ciliary and pupillary constrictor muscles Pupil dilation
IV Trochlear N. Somatic motor Extraocular muscle (superior oblique muscle) Diplopia
V Trigeminal N. Somatic sensory Face, mouth/jaw, teeth, sinuses, meninges, Trigeminal neuralgia
oral and nasal mucosa
Branchial motor Muscles of mastication Asymmetric chewing
VI Abducens N. Somatic motor Extraocular muscle (lateral rectus muscle) Diplopia and medial
deviation of eye
VII Facial N. Special sensory Taste (anterior 2/3 of tongue) Loss of taste
Somatic sensory Skin on ear and tympanic membrane
Branchial motor Muscles of facial expression Facial paralysis and Bells
palsy
Visceral motor All salivary glands (excluding the parotid
gland) and lacrimal glands
VIII Vestibulocochlear N. Special sensory Audition and balance Deafness, tinnitus, and
vertigo
IX Glossopharyngeal N. Special sensory Taste (posterior 1/3 of tongue) Loss of taste
Somatic sensory Skin on ear, tympanic membrane, posterior
1/3 of tongue, and tonsillar fossa
Branchial motor Stylopharyngeus muscle
Visceral motor Parotid gland
Visceral sensory Carotid body and carotid sinus Blood pressure
regulation deficits
X Vagus N. Special sensory Taste (epiglottis) Loss of taste
General sensory Skin on external ear
Branchial motor Muscles of the larynx and pharynx Dysphagia and
dysphonia
Visceral motor Glands, smooth and cardiac muscle in the
neck, thorax, and abdomen
Visceral sensory Pharynx, larynx, and thoracic and abdominal
viscera
XI Spinal Accessory N. Somatic motor Trapezius and sternocleidomastoid muscles Shoulder drop and
weakened neck rotation
XII Hypoglossal N. Somatic motor Muscles of the tongue Tongue deviation
a
Alternative names for the functional components include following: General somatic efferent (GSE), somatic motor; general visceral efferent
(GVE), visceral motor; special visceral efferent (SVE), branchial motor; general somatic afferent (GSA), somatic sensory; general visceral afferent
(GVA), visceral sensory; special somatic afferent (SSA) and special visceral afferent (SVA), special sensory.
pharyngeal arches and the fact that branchial motor nu- expression (innervated by CN VII), the pharyngeal and
clei are located in distinct brainstem columns (immedi- laryngeal muscles (innervated by CNs IX, X and the
ately adjacent and lateral to the somatic motor nuclei). cranial portion of CN XI), and the muscles of mastication
Muscles of branchial origin include the muscles of facial (innervated by CN V).
Cranial Nerves C 733
Visceral motor fibers provide autonomic (parasympa- relating to olfaction (CN I), vision (CN II), audition (CN
thetic) innervation to the head, neck, thoracic, and ab- VIII), balance (CN VIII), and taste (CNs VII, IX, and X).
dominal viscera, where they control glandular secretions This special sensory designation is an all-encompassing
and smooth and cardiac muscle contraction. The motor classification in that it does not distinguish between the
neurons that regulate parasympathetic visceral motor somatic senses (vision, audition, and balance) and the C
processes are typically positioned immediately lateral to more visceral sensations (olfaction and taste).
the branchial motor nuclei column in the brainstem. Intracranial Courses. Cranial nerves must traverse
Visceral motor fibers in CN III transmit parasympathetic through foramina (small holes) within the skull in order
innervation to structures in the eye that regulate pupil to navigate the path between the brain and the various
constriction and lens accommodation. CN VII regulates structures to which they provide innervation. Often, cra-
the secretion of tears (via the lacrimal glands) and salivary nial nerves will travel through these foramina together in
gland secretions (along with CN IX). CN X conveys vis- groups as they exit the cranium. For example, CNs IX, X,
ceral motor innervation to glandular tissue, smooth and and XI pass through the jugular foramen on their descent
cardiac muscles of the gastrointestinal, pulmonary, and to structures in the neck, thoracic, and abdominal cav-
cardiovascular systems. CN X has the most extensive ities; while CNs III, IV, and VI all traverse the superior
distribution of the cranial nerves, with its innervation orbital fissure to enter into the orbit to innervate the
spanning structures within the head and neck down to extraocular muscles. Knowledge of the origins of cranial
the thoracic and abdominal regions. nerves (i.e., brain stem nuclei), their intracranial course
Sensory Cranial Nerves. The remaining three func- and the cranial foramina through which they pass is
tional classifications of cranial nerve fibers convey sensory crucial to any neurological exam, as the diagnosis of
information and include somatic sensory, visceral sen- dysfunction of specific nerves can help to pinpoint the
sory, and special sensory fibers. As previously mentioned, site of and provide valuable information about damage or
the brainstem nuclei associated with these sensory fibers injury to the brain. For example, one of the early symp-
are located more laterally in the brainstem relative to toms of a pituitary adenoma is impaired vision, which
motor nuclei and are arranged in longitudinal columns results from the close proximity between the pituitary
according to functional components (from lateral to me- gland and fibers of CN II, which can become compressed
dial: special sensory, somatic sensory, and visceral sensory as a result of the tumor bulk. Similarly, CN VI has a very
nuclei). Somatic sensory fibers carry information from long intracranial course and, due to its emergence near
exteroreceptors and proprioceptors in the skin, muscles, the bottom of the brain and its course through the cav-
tendons, and joints of the head and neck, mediating the ernous sinus, it is often the first cranial nerve to be
perception of pain, temperature, touch, and propriocep- affected in the case of elevated intracranial pressure, com-
tion. CN V is the major somatic sensory nerve of the head, mon symptoms of which include painful eye movement
mediating cutaneous and proprioceptive sensation from and blurred or double vision (diplopia). Unlike the ma-
the skin, muscles, and joints in the face, mouth, and jaw as jority of cranial nerves, which exit from the ventral surface
well as sensory innervation of the teeth, oral and nasal of the brainstem, CN IV exits the midbrain dorsally and
mucosa, sinuses, and meninges. CN IX also transmits wraps around the lateral surface of the brainstem to enter
somatic sensory information from a portion of the oral the orbit. Due to this long peripheral course around
mucosa (the posterior third of the tongue and tonsillar the brainstem, CN IV is particularly susceptible to head
fossa) and, together with CNs VII and X, mediates sensa- trauma, where damage to this nerve is manifested by
tion of the skin on the outer ear. diplopia or blurred vision. Such examples demonstrate
In contrast to somatic sensory fibers, visceral sensory the manner in which cranial nerve dysfunction can pro-
fibers receive sensory input from receptive endings in vide insight into the various pathological situations that
visceral structures, such as walls of blood vessels or of can occur in the brain.
the digestive tract. Congruent with its expansive distribu- Cranial Nerve Dysfunction. Cranial nerve dysfunction
tion, CN X mediates the majority of visceral sensation in is not uncommon and can result from a variety of under-
the pharynx, larynx, thoracic, and abdominal cavities. CN lying pathologies, ranging from brain trauma to various
IX transmits visceral sensory information from the carotid forms of neurological disease. Common cranial nerve
sinus and carotid body, important structures in the regula- dysfunctions/disorders include Trigeminal Neuralgia
tion of blood pressure and respiration. (CN V), Bells Palsy (CN VII), Ramsay Hunt Syndrome
The final category of sensory cranial nerve fibers is the (CN VII), acoustic neuroma (CN VIII), Glossopharyngeal
special sensory fibers, which convey sensory information Neuralgia (CN IX), eye movement-related cranial nerve
734 C Cranial Pneumocyst
palsies (CNs III, IV, and VI), hyposmia/anosmia (CN I),

and various anopsias (CN II), among others. Due to its Cranial Pneumocyst
expansive innervation, CN X damage/dysfunction can re-
sult in a variety of deficits relating to visceral processes in Pneumocephalus
the heart, lungs, and abdomen. Interestingly, CN X nerve
stimulation is an emerging adjunctive treatment for certain
types of intractable epilepsy and refractory (treatment-re- Craniectomy
sistant) depression; however, the manner in which CN X
stimulation exerts its therapeutic effects is yet to be fully J AMES F. M ALEC
established. Mayo Clinic
Indianapolis, IN, USA
Cross References
Synonyms
Acoustic Neuroma
Anosmia Decompressive craniectomy
Auditory Pathway
Auditory System
Autonomic Nervous System Definition
Bells Palsy
Deaf/Hearing Impairment Craniectomy or decompressive craniectomy is a surgical
Diplopia procedure in which a section of the skull is removed
Dysphagia and not immediately replaced (Hutchinson, Timofeev, &
Dysphonia Kirkpatrick, 2007; Aarabi, Hesdorffer, Ahn, Aresco,
Medulla Scalea, & Eisenberg, 2006). This procedure is most fre-
Midbrain quently used when increased intracranial pressure follow-
Neurologic Examination ing traumatic brain injury does not respond to other less
Olfaction aggressive interventions. Following brain trauma, the
Olfactory Bulb brain may expand within the skull. The resulting
Optic Nerve increased intracranial pressure can compromise brain
Optic Neuropathy function, particularly in the brain stem. Compression of
Pons the brain stem can compromise its basic life support
Ptosis functions, that is, cardiac and respiratory regulation, cre-
Pupillary Light Response ating a life-threatening situation. By removing part of the
Taste skull, the swelling brain is provided room to expand,
Tinnitus reducing intracranial pressure and pressure on the brain-
Trochlear Nerve stem. Although the section of the skull that is removed
Vestibulocochlear Nerve in a craniectomy is not immediately replaced, the bone
Visual Field Deficit removed may be stored and replaced at a later date when
Visual System brain swelling is reduced and stable. Artificial materials
Vertigo may also be used to replace the removed skull. In a
craniotomy, a section of the skull is removed and replaced
as part of the initial surgical procedure. Craniotomy is
more frequently performed as part of surgical interven-
References and Readings tion for disorders such as brain tumor or arteriovenous
malformation. However, a craniectomy may be preferred
Kandel, E. R., Schwartz, J. H., & Jessell, T. M. (2000). Principles of neural
in such cases if the condition appears to be associated with
science (4th ed.). New York: McGraw-Hill.
Shaw, J. P. (1992). A history of the enumeration of cranial nerves by brain swelling. Craniectomy may have no advantage over
European and British Anatomists from the time of Galen to 1895, craniotomy in long-term outcome after severe brain
with comments on nomenclature. Clinical Anatomy, 5(6), 466484. injury (Woertgen, Rothoerl, Schebesch, & Albert, 2006).
Cranioplasty C 735
However, standard craniectomy appears to result in better

outcomes than limited craniectomy (Jiang et al., 2005).
Cross References C
Brain Swelling
Craniotomy
Aarabi, B., Hesdorffer, D., Ahn, E., Aresco, C., Scalea, T. M., &
Eisenberg, H. M. (2006). Outcome following decompressive craniect-
omy for malignant swelling due to severe head injury. Journal of
Neurosurgery, 104, 469479.
Hutchinson, P., Timofeev, I., & Kirkpatrick, P. (2007). Surgery for brain
edema. Neurosurgical Focus, 22(5), E14.
Jiang, J. Y., Xu, W., Li, W. P., Xu, W. H., Zhang, J., Bao, Y. H., et al. (2005).
Efficacy of standard trauma craniectomy for refractory intracranial
hypertension with severe traumatic brain injury: A multicenter, Craniopharyngioma. Figure 1 Courtesy Michael Fisher, MD,
prospective, randomized controlled study. Journal of Neurotrauma, Peter C. Phillips, MD. The Childrens Hospital of Philadelphia
22(6), 623628.
Woertgen, C., Rothoerl, R. D., Schebesch, K. M., & Albert, R. (2006).
Comparison of craniotomy and craniectomy in patients with acute References and Readings
subdural haematoma. Journal of Clinical Neuroscience, 13(7),
718721. Fahlbusch, R., Honegger, J., Paulus, W., Huk, W., & Buchfelder, M.
(1999). Surgical treatment of craniopharyngiomas: experience with
168 patients. Journal of Neurosurgery, 90, 237250.
Craniopharyngioma
Cranioplasty
E THAN M OITRA
Drexel University J ACINTA M C E LLIGOTT
Morgantown, WV, USA National Rehabilitation Hospital
Dun Laoghaire Co., Dublin, Ireland
Definition
Definition
Craniopharyngioma is a slow-growing, extra-axial,
epithelial-squamous, calcified cystic tumor. It occupies Cranioplasty or replacement of bone flap or prosthesis is a
the suprasellar/sellar region and shows benign histology surgical procedure usually performed to fill in, or replace
but malignant behavior, as it may invade surrounding a defect in the skull following a craniectomy or removal
areas and recur after the treatment (Fahlbusch, Honegger, of a bone flap (Fig. 1).
Paulus, Huk, & Buchfelder, 1999). Craniopharyngiomas
may develop embryogenetically, arising from remnants
of the craniopharyngeal duct and/or Rathke cleft or meta- Further Reading
plastically because of residual squamous epithelium. The
most common presenting symptoms are endocrine dys- Cranioplasty can be performed using the patients own
function, headache, and visual disturbances. Craniophar- bone flap, which has been frozen or stored in the patients
yngiomas are treated with surgery or surgery followed by abdomen, or multiple materials such as titanium mesh,
radiotherapy. hydoxyapatite, and polymethylmethacrylate can be used
736 C Craniospinal Irradiation
Gardner, W. J. (1945). Closure of defects of the skull with tantalum.

Surgery, Gynecology Obstetrics, 80, 303312.
Long, D. F. (2007). Diagnosis and management of late intracranial com-
plications of TBI. In N. D. Zasler, D. L. Katz, & R. D. Zafonte (Eds.),
Brain injury medicine. Principles and practice. New York: Demos.
Winder, R. J., Cooke, R. S., Gray, J., Fannin, T., & Fegan, T. (1999).
Medical rapid prototyping and 3D CT in the manufacture of custom
made cranial titanium plates. Journal of Medical Engineering and
Technology, 23(1), 2628.
Craniospinal Irradiation
Craniospinal Radiotherapy
Cranioplasty. Figure 1 Source: Winder, Cooke, Gray, Fannin,

and Fegan (1999)
as alternative to create a cranioplasty flap, where necessary
computerized techniques may be used to generate a J ACQUELINE L. C UNNINGHAM
custom made cranioplasty (Long, 2007). Childrens Hospital of Philadelphia
The decision to perform and the timing of the cranio- Philadelphia, PA, USA
plasty to replace the skull defect following craniectomy
can be variable. Originally considered to be largely a
cosmetic rather than a therapeutic procedure, cranio- Synonyms
plasty may be now be performed to prevent late neuro-
logical complications associated and identified with Craniospinal irradiation; CSI
craniectomy including the so called syndrome of
trephined (Dujovny, Agner, & Aviles, 1999; Long,
2007). Characteristics of this syndrome include headache, Definition
dizziness, irritability, epilepsy, discomfort, and psychiatric
symptoms, and in addition, the skin overlying the skull Craniospinal radiotherapy is an irradiation that is
defect may become indented (Dujovny, Aviles, Fernandez, & directed at the whole brain and length of the spinal axis,
Charbel, 1997). The pathophysiology of the the including the meninges, as part of the cancer treatment to
syndrome of the trephined is unknown, however, a control malignant cells. It serves as a radical (curative)
number of factors have been implicated including antineoplastic therapy, as a prophylaxis against a neo-
atmospheric pressure, cerebral blood flow, and cerebro- plasms involvement with the central nervous system, or
spinal fluid changes (Dujovny et al., 1997). Neurological as a palliative recourse when cure is impossible. Craniosp-
and functional improvements have been shown to inal irradiation (CSI) is technically challenging, and is
improve following cranioplasty in this syndrome, for used with computed tomography (CT) simulation and
example, in 1945 Gardner described the improvement in multimodality MRI registration to define a large target
symptoms in some patients following cranioplasty with volume, which spares healthy tissues, and assures exact
tantalum (Dujovny et al., 1997; Gardner, 1945). reproducibility of treatment from day-to-day.
MRI evidence of the craniospinal radiation injury to
the brain has been seen in lHermittes sign (a side effect of
radiotherapy on the spinal cord, experienced as shock
sensations), telangiectasia (dilated capillaries), white mat-
Dujovny, M., Agner, C., & Aviles, A. (1999). Syndrome of the trephined:
Theory and facts. Critical Reviews in Neurosurgery: CR, 9(5), 271278.
ter changes, basal ganglia change, necrosis, and cerebral
Dujovny, M., Aviles, A., Fernandez, P., & Charbel, F. T. (1997). Cranio- atrophy. Although the differential sensitivity of specific
plasty: Cosmetic or therapeutic? Surgical Neurology, 47, 238241. brain regions to radiotherapy has not been determined,
Craniotomy C 737
factors relating to total dose, dose per fraction, and inter- Definition
val between fractions have been identified as important
variables influencing the brains response to radiation. Neurosurgical procedure involving the opening of the
Present research focuses on the development of treatment skull as a means of decreasing intracranial pressure
protocols based on the efficacy in tumor control while and/or for purposes of removal of a mass lesion. C
using the least dose of craniospinal radiotherapy
(1,800 cGy), often in conjunction with chemotherapy, as
the efficacy of CSI dose reduction in ameliorating neuro- Current Knowledge
endocrine and neurocognitive sequelae remains unclear.
Today, in contrast to the much higher doses used in the Craniotomy as a treatment for increased ICP from a mass
past decades, CSI doses of 2,400 and 3,600 cGy (with daily lesion has its foundation early in the history of neurosur-
fractions of 150 or 180 cGy) are standard. Studies contin- gery. Decompressive craniotomy (DC) initially was intro-
ue to evaluate how low a dose will remain effective in a duced to lower the intracranial pressure (ICP) in patients
risk-adapted setting. Controversy also exists on the with inoperable tumors and in managing uncontrolled
expression of radiation effects on specific neurocognitive ICP after traumatic brain injury (Brit & Hamilton,
domains. Attention and memory are known to bear a 1978). In recent years, DC has been recommended as an
vulnerability to neurotoxicity, but issues of individual alternative treatment for space occupying acute hemi-
differences, including premorbid and disease-related risk spheric infarction with or without massive medically
factors, are expected to influence neuropsychological uncontrolled brain edema (Schwab, 1998). During the
outcomes. acute period following cerebral infarction, neurologic
decline is often attributed to surrounding edema. Apart
from relieving the mass effect, restoration of the micro-
Cross References circulation around the infarcted area is the target of DC.
The management of increased intracranial pressure is a
Radiation Injury common clinical scenario in neurosurgery. Strategies for
Radiation Oncology the management of ICP fall into two general categories:
Radiotherapy to reduce the volume of the intracranial compartment
(medical management) and to remove the mechanical
constraints imposed by the cranial vault (surgical).
In patients who sustain a severe non-penetrating
References and Readings head injury, overall 2545% require a craniotomy for
evacuation of a hemorrhagic mass lesion, including epi-
Armstrong, C. L., Gyato, K., Awadalla, A. W., Lustig, R., & Tochner, Z. A.
(2004). A critical review of the clinical effects of therapeutic irradia-
dural, subdural, and intracerebral hematomas (Miller,
tion damage to the brain: The roots of controversy. Neuropsychology 1981). There is little debate in the surgical management
Review, 14, 6586. of a rapidly deteriorating patient with a focal neurological
Brady, L. W., Heilmann, H. P., Molls, M., & Schlegel, W. (2006). New deficit and neuroimaging findings of an expanding intra-
techniques in radiation oncology. New York: Springer.
cranial hematoma associated with significant mass effect
and midline shift. For less obvious situations controversy
remains given the lack of class I and II data to support any
treatment standard. Complete removal of a brain tumor
without inflicting neurological deficits is a desirable end
Craniotomy result in neurosurgical practice. Craniotomy was tailored
to encompass tumor plus adjacent areas presumed to
E DUARDO L OPEZ contain eloquent cortex. Magnetic brain stimulation or
Johnson Rehabilitation Institute intraoperative cortical stimulation can be used to guide
Edison, NJ, USA resection of functional cortex.
DC remains a controversial procedure in spite of a
number of studies published in the literature on its use
Synonyms in the treatment of intracranial hypertension secondary
to malignant cerebral edema, traumatic brain injury,
Craniectomy; Trephination aneurysmal subarachnoid hemorrhage, central venous
738 C Cretinism
thrombosis, encephalitis, intracerebral hematoma, and conditions are characterized pathologically by neuronal
metabolic encephalopathies. It has been shown to be loss, spongiform change, and astrocytic gliosis. Cell loss
effective in reduction of ICP refractory to medical therapy can be seen microscopically as multiple perforations to
but evidence supporting an improvement in clinical out- the brain tissue creating the characteristic sponge-like
come has not been conclusive. appearance. Prion diseases are caused by infectious
agents, which are abnormal self-replicating forms of a
normal brain protein, prion protein.
Cross References
Temporal Lobectomy
Categorization and Epidemiology
CreutzfeldtJakob Disease (CJD) may be sporadic (that is
References and Readings develop spontaneously without apparent cause), familial
(inherited), or acquired (transmitted by infection).
Brit, R., & Hamilton, R., (1978). Large decompressive craniotomy in the
treatment of acute subdural hematoma. Neurosurgery, 2(3), 195200.
CJD occurs worldwide with a mean annual incidence
Bullock, R., Chestnut, R., Ghajar, J., Gordon, D., Hartl, R., Newell, D. W., of approximately 12 cases per million population
et al. (2006). Surgical management of subdural hematoma. (Ladogana et al., 2005). Except for variant and iatrogenic
Neurosurgery, 58(3), S216S224. CJDs, which are in decline, the disease has a relatively
Chen, C., Smith, E., Ogilvy, C., Carter, B. S., (2006). Decompressive
stable incidence with no convincing evidence of geo-
craniectomy: Physiological rationale, clinical indications, and
surgical considerations. 5, 7080.
graphical clustering (although there are regions with an
increased incidence of familial cases). The gender inci-
dence is equal.
Cretinism Natural History, Prognostic Factors,

Hypothyroidism
Outcomes
Sporadic and familial CJDs have been recognized as prion

Creutzfeldt-Jakob Disease diseases for many years, showing wide geographical spread;
however, variant CJD has been confined largely to the
K ARI H AWKINS 1,2 , R. G. W ILL 1, N ARINDER K APUR 2 United Kingdom, with the first cases reported in 1996.
1
University of Edinburgh It is thought that meat products intended for human con-
Edinburgh, UK sumption contained contaminated brain and spinal cord
2
Addenbrookes Hospital from animals affected by the epidemic of a prion disease in
Cambridge, UK cattle (Bovine Spongiform Encephalopathy) in the 1980s
(Hilton, 2006). Initial fears of a catastrophic epidemic
of vCJD among humans have been partially quelled,
Synonyms with a peak in new cases during 2000 reducing steadily
to only one new case in 2007 (http://www.cjd.ed.ac.uk).
CJD; Prion disease; Transmissible spongiform encepha- However, all vCJD cases to date have shared a common
lopathy (TSE) genotype (Methionine/Methionine) raising the possibil-
ity of subsequent peaks, which occur due to lengthened
incubation times among other genotypic groups. In addi-
Short Description or Definition tion, evidence from Kuru, an acquired prion disease aris-
ing from cannibalistic funeral practices among the Fore
CreutzfeldtJakob Disease (CJD) is a rare, fatal neurode- people of Papua New Guinea carried out until 1950s,
generative disease, which is one of the transmissible spon- suggests that incubation times for acquired prion disease
giform encephalopathies or prion diseases. These may stretch to several decades (Collinge et al., 2006). It is
Creutzfeldt-Jakob Disease C 739
also possible for a person-to-person spread to occur, as has Variant CJD presents with a psychiatric syndrome,
been seen in four cases of blood transfusion-associated including depression and anxiety, for about 6 months
vCJD infection (most recent incidence figures are available before there is a progressive neurological and cognitive
from http://www.cjd.ed.ac.uk). decline as in sCJD, although chorea and dystonia occur as
well as myoclonus. The mean survival is 14 months, and C
vCJD affects a younger age group, with the mean age
Natural History and Prognosis being 29 years at death.
Different CJD phenotypes develop and progress at differ-

ent rates, although all subtypes develop profound demen- Neuropsychology and Psychology of
tia and multiple neurological features progressing to loss CreutzfeldtJakob Disease
of awareness and death. A summary of clinical presenting
features is given in Table 1. The Presentation of the CJD Patient
sCJD presents with cumulative multifocal neurological
deficits in association with a rapidly progressive dementia. The differential diagnosis is often the question at refer-
The cardinal clinical signs are dementia and myoclonus, ral, in particular, the distinction between a psychiatric
with a significant proportion of cases exhibiting ataxia or neurological basis for the presenting symptoms or to
and paratonic rigidity of the limbs. The mean survival distinguish CJD from other neurological conditions. A
from onset to death is only 4 months, although patients in thorough history, as always, is essential in establishing
the younger age groups often survive for more than a year. both the profile of the presenting symptoms and the
sCJD affects predominantly the older age groups with the course of the illness, and care should be taken to obtain
mean age being 65 years at death. corroborative reporting from relatives given the diffi-
The clinical presentation in familial CJD is often sim- culties of accurate history taking in individuals with
ilar to sCJD, but the age of onset is about 10 years earlier, cognitive decline. Sporadic CJD can often be distin-
and in some forms, there may be early ataxia and/or slow guished from other disorders by the speed and degree
progression. of cognitive decline, the short duration of illness, and
Iatrogenic CJD may present as in sCJD, but human the associated neurological signs. Some cases of fCJD
pituitary hormone recipients typically develop progressive present very similarly to sCJD; however, in fCJD, there is
ataxia and cognitive impairment develops late, if at all. often a younger age of onset, a longer disease duration,
Creutzfeldt-Jakob Disease. Table 1 Forms, causes, and incidence of CJD
Form Phenotype Cause Incidence

Sporadic Sporadic Unknown. Approximately one case per million
Creutzfeldt population. Accounts for around 85% of CJD
Jakob Disease cases.
(sCJD)
Familial Familial Inheritance of mutation in the PrP gene. Approximately 1015% of CJD cases are
Creutzfeldt familial.
Jakob Disease
(fCJD)
Acquired Iatrogenic Case-to-case transmission via contaminated Less than 1% of CJD cases arise through
neurosurgical instruments, human dura mater acquired infection.
grafts, or exposure to human pituitary
hormones. The variant form of CJD can also be
transmitted via blood transfusion.
Variant CJD Ingestion of contaminated meat products from 166 cases in total in the UK, 23 cases in
(vCJD) cattle infected with Bovine Spongiform France, and a total of 18 cases elsewhere in
Encephalopathy. the world (as of May 2008).
740 C Creutzfeldt-Jakob Disease
Creutzfeldt-Jakob Disease. Table 2 Clinical presentation of CJD
Approximate
duration of Early clinical
Form Age at onset illness features Neuropsychological findings Exceptions
Sporadic 90% of cases 4 months (65% of Neurological signs Areas of early cognitive deficit Rare cases occur
between 50 cases survive <6 including cerebellar vary in this heterogeneous younger than 50.
and 80 years, months from ataxia, cognitive group, but there is often marked Young cases may
mean 65 years symptom onset). impairment (global impairment by the time of a present with some
dementia or referral for testing. Most cases psychiatric
specific deficits in show rapid progression to a symptoms
earlier stages), wide-ranging dementia initially, similar to
followed by including verbal and nonverbal the vCJD
myoclonus, rigidity, memory, executive dysfunction, presentation, and
and rapid and nominal skills. Poor memory may have longer
deterioration to loss and/or attention are often early disease duration.
of speech, features, but there may be 19% sCJD cases
voluntary occasional cases where initial have a disease
movement, and deficits reflect dysphasia or visual duration >12
awareness. disturbance. months
Heidenhain form:
very focal visual
difficulties for
weeks/months
before other
cognitive
symptoms.
Look for: Rapid cognitive decline Brownell
over multiple test sessions. Oppenheimer
Fluctuations in responsiveness form: pure
and distractibility. cerebellar
syndrome for
Intrusion errors.
several weeks or
Verbal and motor perseveration. months before
cognitive decline
Familial Dependent on Dependent on the Dependent on fCJD cases may demonstrate less Some cases can
the specific specific mutation, mutation, may severe/rapid cognitive decline at have an illness
mutation of but on average present in a similar the early stages of a longer duration of years.
the prion 25 years fashion to sCJD or disease course than sCJD or vCJD Fatal Familial
protein gene, with predominant cases. A single case in 2000 Insomnia: early
but most often sleep and showed specific isolated deficits sleep disturbance
between the autonomic in delayed verbal memory and and autonomic
ages of 30 and disturbance or word finding prior to global dysfunction is
50 years. cerebellar ataxia involvement. One study suggests prominent
(see Exceptions, that naming ability may be
Gerstmann
right). Deterioration preserved in some cases in
Straussler
is usually slower comparison to sCJD and vCJD.
syndrome:
than in vCJD or Look for: Family history of CJD or
progressive
sCJD with a longer other (possibly misclassified)
cerebellar ataxia
disease course. neurological disease
Creutzfeldt-Jakob Disease. Table 2 (Continued)
Approximate
duration of Early clinical
Form Age at onset illness features Neuropsychological findings Exceptions
Iatrogenic Dependent on Following dura Human growth Dependent on mode of C
age at mater graft similar hormone infection: transmission; human growth
exposure. to sCJD, With progressive hormone patients present with
Incubation human pituitary cerebellar ataxia with relatively preserved
period hormones 1218 syndrome, delayed cognitive function until later
following months onset of dementia stages, while intracerebral cases
intracerebral Human dura mater present with broad-ranging
exposure is infection: rapidly dementia with rapid
1946 months, progressive deterioration as seen in sCJD.
extending to dementia, similar to Look for: Rapid cognitive decline
many years or sCJD over multiple test sessions for
decades with intracerebral exposure cases.
peripheral History of relevant exposure to
exposure. differentiate from sCJD.
Variant Median age 28 Median 14 Most commonly, Measurable impairments on tests In 15%,
(range 1274) months initial presentation of both verbal and nonverbal neurological
is psychiatric memory, executive function, symptoms
disturbance speed of attention, and nominal precede
including skills have characterized psychiatric.
depression, descriptions of published cases.
agitation, and Language, verbal reasoning, and
behavioral changes, visuoperceptual skills may be less
although in some frequently impaired, although
cases cognitive this may reflect an earlier disease
changes may be stage at the time of testing. One
the first sign of study suggests possible
abnormality. preserved ability in some
A delay of months components of visuoperception
is possible before in comparison to patients
distinct suffering from sCJD or fCJD.
neurological signs, Global involvement follows with
although cognitive rapid disease progression.
changes may be Look for: Fluctuating attention
found earlier in the and effort during testing.
disease course. Cognitive impairment more
Sensory symptoms profound than expected for
such as pain or odd depression or including areas of
sensation in limbs deficit unusual for psychiatric
or face may be disorders.
reported. Ataxia, Significant cognitive decline over
myoclonus, and follow-up assessment sessions.
significant
cognitive
impairment (such
as memory)
develop as the
disease progresses
Sources of information for this table are referenced under References and Readings.
742 C Creutzfeldt-Jakob Disease
Creutzfeldt-Jakob Disease. Table 3 Investigations used in the diagnosis of CJD
Phenotype MRI EEG CSF 1433 Tonsil biopsy Blood test History
Sporadic Important in In 6080% of A positive 14-3-3 Negative At codon 129
(sCJD) excluding other cases, generalized CSF immunoassay of the prion
conditions. High bi- or triphasic is strongly protein gene:
signal on FLAIR or periodic sharp supportive of a 70%
DWI sequences in wave complexes diagnosis of sCJD methionine
the caudate and at 1/s. May not in the appropriate homozygous
putamen in about appear until later clinical context
70% of cases stages of the i.e., rapidly
disease progressive
dementia. Positive
in 90% of cases of
sCJD
Familial Some cases Characteristic Positive less Negative Analysis of Positive family
(fCJD) similar to sCJD periodic pattern is frequently than the prion history of CJD in
less frequently sCJD protein gene about 30% of
seen than in sCJD. for mutations cases
Iatrogenic Similar to sporadic Characteristic Positive in a Negative Mainly Relevant
CJD periodic pattern is proportion of homozygous exposure risk
less frequently cases methionine such as
seen than in sCJD. or valine treatment with
cadaveric
derived human
growth hormone
or human dura
mater graft
Variant Characteristic Normal or Positive in 50% of As vCJD, unlike All tested
(vCJD) high signal in the nonspecifically cases, but does the other CJD cases
posterior thalamic abnormal. not distinguish phenotypes, methionine
region (the Characteristic from sCJD involves the homozygous
pulvinar sign) in periodic pattern lymphoreticular
over 90% of cases in two cases late system, abnormal
on FLAIR or DWI in clinical course. protein may be
sequences. found in the
biopsy of tonsil
tissue in about
90% of cases.
Adapted from The National CreutzfeldtJakob Disease Surveillance Unit website (http://www.cjd.ed.ac.uk/investigations.htm).
and a family history of either CJD or another neurolog- Neuropsychological Testing

ical disorder. In iatrogenic cases, there should be a clear
history of a relevant exposure. The history in vCJD cases Patients with CJD often present at too late a stage for
includes early psychiatric symptoms (including mood, formal testing with a full neuropsychological battery. This
delusion, and agitation) and may also reveal cognitive is reflected in the literature, in which reports focus on
decline in everyday activities, of the type that might small cohorts and case studies. Efforts should be made to
typically be attributed to depression. In some cases, obtain sufficient breadth across cognitive domains when
neuropsychological symptoms may precede psychiatric testing to aid diagnosis and enable repeat testing if appro-
or neurological indicators that develop as the disease priate. Observations of test behavior will also be helpful.
progresses. The early presenting features in all CJD A study is currently underway to establish whether a brief
subtypes are summarized in Table 2. bedside screening test might be sufficient to give an
indication of whether the degree or pattern of impairment professionals in supporting individuals and their families
seen in a patient could indicate CJD. through a period of acceptance, adjustment, loss, and
ultimately grief. Provision might also be made for the
counselling of healthcare staff involved in these distressing
Evaluation cases. C
Neuropsychological testing may occur prior to, in parallel
with, or following medical investigations and may provide
support for a diagnosis of CJD or prompt the clinician to
Cross References
instigate more extensive investigation than would usually
Prion Disease
be undertaken in patients presenting, for example, with
Spongiform Encephalopathy
primarily psychiatric complaints as in vCJD. A number of
further investigations may be used in the diagnosis of CJD
(Table 3).
Treatment Clare, L. (2007). Neuropsychological rehabilitation and people with demen-

tia. Hove, England: Psychology Press.
Collinge, J., Whitfield, J., McKintosh, E., Beck, J., Mead, S., Thomas, D. J.,
CJD is fatal. There is currently no effective treatment for et al. (2006). Kuru in the 21st century an acquired human prion
the disease itself, despite ongoing trials of Quinacrine, disease with very long incubation periods. Lancet, 367(9528),
Pentosan Polysulfate, and Flupirtine (Stewart, Rydzewska, 20682074.
Keogh, & Knight, 2008; see the MRC New Therapies Cordery, R. J., Alner, K., Cipolotti, L., Ron, M., Kennedy, A., Collinge, J.,
et al. (2005). The neuropsychology of variant CJD: a comparative
Scrutiny Group for Prion Disease website for up-to-date
study with inherited and sporadic forms of prion disease. Journal of
information concerning recent treatment studies). Medi- Neurology, Neurosurgery and Psychiatry, 76, 330336.
cal management should focus on alleviating discomfort, Creutzfeldt-Jakob Disease Foundation website. http://www.cjdfoundation.
including the use of medication to manage myoclonic org
jerks or pain and, as the disease progresses, the manage- Gass, C. S., Luis, C. A., Meyers, T. L., & Kuljis, R. O. (2000). Familial
Creutzfeldt-Jakob disease: a neuropsychological case study. Archives
ment of issues such as feeding or continence. Intervention
of Clinical Neuropsychology, 15(2), 165175.
may be needed for the management of mood or psychotic Hilton, D. A. (2006). Pathogenesis and prevalence of variant Creutzfeldt-
symptoms. Since a high level of care will inevitably be- Jakob disease. Journal of Pathology, 208(2), 134141.
come necessary, planning for the provision of this should Kapur, N., Abbott, P., Lowman, A., & Will, R. G. (2003). The neuropsy-
begin early, in consultation with the family. In the case of chological profile associated with variant Creutzfeldt-Jakob disease.
Brain, 126, 26932702.
a diagnosis of familial CJD, the family will face difficult
Ladogana, A., Puopolo, M., Croes, E. A., Budka, H., Jarius, C., Collins, S.,
decisions regarding genetic screening and should be guid- et al. (2005). Mortality from Creutzfeldt-Jakob disease and related
ed through such a process by an appropriately qualified disorders in Europe, Australia, and Canada. Neurology, 64,
professional. 15861591.
It is often the case that the cognitive symptoms of Medical Research Council New Therapies Scrutiny Group for Prion
Disease website http://www.mrc.ac.uk/PolicyGuidance/PolicyDeve-
CJD show extremely rapid deterioration and, in view of
lopment/NewTherapiesScrutinyGroupforPrionDisease.
this, cognitive rehabilitative efforts are unlikely to pro- National Creutzfeldt-Jakob Disease Surveillance Unit (NCJDSU) website.
duce helpful returns. However, in cases with early refer- http://www.cjd.ed.ac.uk
ral or a longer disease course, supportive aids (such as a National Prion Clinic website. http://www.nationalprionclinic.org
calendar for orientation) or environmental adaptations Smith-Bathgate, B. (2005). Creutzfeldt-Jakob disease: diagnosis and
nursing care issues. Nursing Times, 101, 5253.
may produce improvements in activities of daily living,
Snowden, J. S., Mann, D. M. A., & Neary, D. (2002). Distinct neuropsy-
self-efficacy, and mood, at least in the early days, as is the chological characteristics in Creutzfeldt-Jakob disease. Journal of
case in other dementias (Clare, 2007; Smith-Bathgate, Neurology, Neurosurgery and Psychiatry, 73, 686694.
2005). Spencer, M. D., Knight, R. S. G., & Will, R. G. (2002). First hundred cases
While the patients themselves are likely to lose aware- of variant Creutzfeldt-Jakob disease: retrospective case note review
of early psychiatric and neurological features. British Medical Jour-
ness of their predicament as their cognitive ability
nal, 324, 14791482.
declines, their families observe a devastating deterioration Stewart, L. A., Rydzewska, L. H. M., Keogh, G. F., & Knight, R. S. G.
in their loved ones. There is a role for the clinical psychol- (2008). Systematic review of therapeutic interventions in human
ogist, nurse practitioner, or other qualified healthcare prion disease. Neurology, 70, 12721281.
744 C Criminal Forensics
Denney, R. L., & Sullivan, J. P. (2008). Clinical neuropsychology in the

Criminal Forensics criminal forensic setting. New York: Guilford.
Denney, R. L., & Wynkoop, T. F. (2000). Clinical neuropsychology in the
criminal forensic setting. Journal of Head Trauma Rehabilitation, 15,
M OIRA C. D UX
804828.
University of Maryland Medical Center/Baltimore VA Mrad, D. (1996). Criminal responsibility evaluations. Paper presented at
Baltimore, MD, USA issues in forensic assessment symposium. Atlanta, GA: Federal Bu-
reau of Prisons.
Definition
Within the field of forensic psychology, the utilization of Criminal Litigation

clinical neuropsychological expertise for criminal forensic
cases can be considered a subspecialty of the field. Denney M OIRA C. D UX
and Wynkoop (2000) modified Mrads (1996) multiple University of Maryland Medical Center/Baltimore VA
data source model (MDSM) to the practice of criminal Baltimore, MD, USA
forensic neuropsychology. The purpose of the model is to
provide a framework for clinicians to evaluate all relevant
sources of information, most notably information relevant Definition
to the defendants mental state at the time of the offense.
The model covers three time points of analysis: present, In civil litigation, a lawsuit is filed by a private party,
time of offense, and prior history. Moreover, the model seeking damages from another party as a result of some
assesses symptoms/behaviors, explanations, etc. via the type of injury, negligence, or malpractice. In criminal
self-report of the defendant as well as via other sources of litigation, the case is filed by the government against a
data (e.g., neuropsychological tests, mental status exam, defendant whom the government believes has committed
medical/neurological exam, arrest reports, witness state- a crime. Crimes are classified into one of two categories:
ments, physical evidence, hospital/psychiatric records, misdemeanors or felonies. Punishment for misdemeanors
employment records, family/friend reports, etc.). Once involve a maximum possible sentence of less than 1 year of
all of the relevant pieces of information are gathered, incarceration; felonies carry a maximum possible sen-
spanning the three time points, it is the role of the forensic tence of more than 1 year of incarceration. The burden
neuropsychologist to consolidate the information and of proof in criminal litigation is always assumed by the
formulate opinions. Evaluators involved in criminal for- state. Thus, it is the states responsibility to prove that
ensics typically have very different roles compared to gen- the defendant is guilty of having committed a crime.
eral practitioners. Specifically, in forensic evaluations, the However, if a defendant claims insanity (e.g., cannot
client is typically not the person being examined, and the appreciate the wrongfulness of the act nor conform their
ultimate goal is to evaluate the facts, not to maintain an conduct to the requirements of the law), then the burden
alliance with the examinee as is the case in a clinical of proof in proving ones insanity falls on the defendant.
context. Moreover, forensic criminal evaluations typically Under criminal litigation, the state must demonstrate that
involve much more extensive application of corroborative the accused satisfied each element of the statutory
information as well as validated assessments of negative definition of the crime and prove the defendants involve-
response bias, symptom validity, and malingering. ment beyond a reasonable doubt. In the context of
criminal litigation, forensic neuropsychologists often
provide determinations regarding mens rea (e.g., guilty
Cross References
mind) or not guilty by reason of insanity (NGRI),
competent waiver of Miranda rights, and/or competence
Criminal Litigation
to proceed (e.g., stand trial, to be sentenced, etc.).

Cross References
issues. In G. Larrabee (Ed.), Forensic neuropsychology: A scientific Actus Rea
approach. New York: Oxford University Press. Criminal Forensics
Crisis Intervention C 745
Insanity related issue. Nonetheless, neuropsychologists are

Mens Rea increasingly being called upon to determine whether or
not brain pathology may contribute to criminal behavior
(Barr, 2008).
References and Readings C
Denney, R. L., & Sullivan, J. P. (2008). Clinical neuropsychology in the
criminal forensic setting. New York: Guilford. Cross References
Principles of productive attorney-neuropsychologist relations. In Actus Rea
G. Larrabee (Ed.), Forensic neuropsychology: A scientific approach. Diminished Capacity
Diminished Responsibility
Insanity
Intent
Mens Rea
Criminal Responsibility
R OBERT L. H EILBRONNER References and Readings
Chicago, IL, USA Barr, W. B. (2008). Neuropsychological approaches to criminality and
violence. In R. Denney, & J. Sullivan (Eds.), Clinical neuropsychology
in the criminal forensic setting. New York: Guilford.
Definition issues. In G. Larrabee (Ed.), Forensic neuropsychology: A scientific
approach. New York: Oxford University Press.
Criminal responsibility, or the conclusion of guilt for a Heilbronner, R. L., & Waller, D. (2008). Neuropsychological consultation
in the sentencing phase of capital cases. In R. Denney, & J. Sullivan
criminal offense, centers on four elements: (1) The
(Eds.), Clinical neuropsychology in the criminal forensic setting.
defendant must have committed the act (actus reus). New York: Guilford.
(2) The defendants actions must have caused the crime. Shapiro, D. L. (1999). Criminal responsibility evaluations: A manual for
(3) The defendant must have committed the crime with a practice. Sarasota, FL: Professional Resource Press.
guilty state of mind (mens rea). (4) There must be no Wrightsman, L. S., Greene, E., Nietzel, M. T., & Fortune, W. H. (2002).
Psychology and the legal system (5th ed.). Belmont, CA: Wadsworth,
circumstance constituting a legal defense for the charged
Thompson Learning.
crime (e.g., self-defense). In short, there must be the Yates, K. F., & Denney, R. L. (2008). Neuropsychology in the assessment
criminal act and the criminal intent and both must be of mental state at the time of the offense. In R. Denney, & J. Sullivan
proven, beyond a reasonable doubt. Mental health profes- (Eds.), Clinical neuropsychology in the criminal forensic setting.
sionals are typically involved with establishing intent and New York: Guilford.
mens rea, which involves the assessment and professional
opinions related to a defendants sanity and/or dimin-
ished capacity (which includes a decreased level of intent).
Criminal responsibility evaluations are also called san-
ity evaluations or assessment of mental state at the time of Crisis Intervention
the offense evaluations. Determining whether or not a
defendant was sane at the time of the offense is one of E LISE K. H ODGES 1, J EFFREY G. K UENTZEL 2
1
the most controversial questions forensic examiners are University of Michigan Health System
asked to address given that the purpose of the exam is to Ann Arbor, MI, USA
2
identify individuals who should not be held morally Wayne State University
responsible (not guilty by reason of insanity) for their Detroit, MI, USA
acts (Yates & Denney, 2008). An insanity plea is pursued
in about 9 out of 1,000 cases, and it is successful approxi-
mately 25% of the time (Wrightsman, Greene, Nietzel, & Synonyms
Fortune, 2002). It is very rare when a defendant is
acquitted secondary to insanity caused by a brain-injury- Emergency mental health treatment
746 C Criterion Validity
Definition Roberts (2005) developed a seven-stage crisis inter-

vention model:
Crisis intervention techniques target the resolution of an
1. Conduct a biopsychosocial/imminent danger assessment
immediate crisis and restoration of the affected indivi-
2. Establish a collaborative relationship
duals previous level of functioning. Roberts (2005)
3. Identify the major problems and crisis precipitants
defines a crisis as a period of psychological disequilibri-
4. Encourage exploration of feelings
um, experienced as a result of a hazardous event or situa-
5. Generate alternatives and new coping strategies
tion that constitutes a significant problem that cannot be
6. Restore functioning via implementation of an action
remedied by using familiar coping strategies.
plan
7. Plan follow-up and booster sessions
Hospitals, clinics, and schools typically have in place a set
Current Knowledge
of policies and procedures for how staff should intervene
in the crisis situations that are most likely to be encoun-
It is important to stress that most individuals who expe-
tered. Staff trainings on these protocols should be con-
rience a crisis or traumatic event tend to recover on their
ducted routinely to ensure a high level of preparedness.
own accord (i.e., crisis intervention may not be needed).
Cross References
Crisis Intervention Approaches
Stress Management
Critical incident stress management (CISM; Mitchell &
Everly, 1993) is an approach to crisis intervention that has
garnered considerable attention since its initial develop- References and Readings
ment in the 1980s. A key component of CISM is the critical
incident stress debriefing (CISD), a group session held Mitchell, J. T., & Everly, G. S. (1993). Critical incident stress debriefing: An
shortly after an incident. Led by CISM-trained facilitators, operations manual for the prevention of traumatic stress among emer-
gency services and disaster workers. Ellicott City, MD: Chevron.
the CISD session allows participants to share their experi-
National Child Traumatic Stress Network and National Center for PTSD
ences of the incident, and the leaders provide psychoedu- (2006). Psychological first aid: Field operations guide, (2nd ed.). Re-
cation about stress reactions and recommended coping trieved March 5, 2010, from http://www.ncptsd.va.gov/ncmain/
strategies. In the 1990s, a controversy developed surround- ncdocs/manuals/PFA_V2.pdf.
ing CISM, as research evidence mounted that failed to National Institute of Mental Health (2002). Mental health and mass
violence: Evidence-based early psychological intervention for victims/
show its effectiveness. A National Institute of Mental
survivors of mass violence. A workshop to reach consensus on best
Health (NIMH) report (2002) suggested that stand-alone practices. NIH Publication No. 02-5138, Washington, D.C.: U.S.
CISD does not consistently prevent post-traumatic disor- Government Printing Office.
ders, and that some individuals, such as those with high Roberts, A. R. (2005). Crisis intervention handbook: Assessment, treatment,
arousal, may be put at heightened risk for adverse out- and research. (3rd. ed.). New York: Oxford University Press.
comes as a result of CISD-type interventions. Thus, man-
datory participation in group debriefing sessions is
considered very questionable.
An alternative to CISM is psychological first aid
(PFA; National Child Traumatic Stress Network and
Criterion Validity
National Center for PTSD, 2006). PFA is an evidence-
Test Validity
informed, pragmatic approach that targets acute stress reac-
tions and the immediate needs of persons exposed to a
critical incident (NIMH, 2002). The goals of PFA include
enhancement of safety (both objective and subjective), re-
duction of stress-related symptoms, restoration of rest and Criterion-Referenced Testing
sleep, linkage with resources, and facilitation of social
support. Domain Referenced Test Interpretation
Cross-Examination C 747
sinistrality. However, familial sinistrality is absent in the

Critical Periods majority (63%) of reported CA cases (Coppens, Hungerford,
Yamaguchi, & Yamadori, 2002). Further, there does not
Sensitive Periods seem to be any difference in CA symptomatology when
comparing patients with and without familial sinistrality, C
and the presence of familial sinistrality does not increase
the number of anomalous cases, as could be expected if
Crossed Aphasia language laterality were weak (Coppens et al., 2002).
Individuals with CA also often display typical right-
PATRICK C OPPENS
hemisphere symptoms (e.g., left-side neglect, visuospa-
SUNY Plattsburgh
tial/visuoconstruction problems, affective dysprosody,
Plattsburgh, NY, USA
and spatial agraphia) which indicates that those skills
may lateralize independent of language. The aphasic dif-
ficulties may obscure these right-hemisphere signs, but
Definition
these represent a major difference in symptomatology
between CA and LHA.
Crossed aphasia is an acquired language impairment fol-
lowing a lesion in the right hemisphere in a right-handed
individual.
Cross References
Current Knowledge Aphasia
Handedness
The term crossed aphasia (CA) was coined by Byrom
Bramwell (1899) to indicate an aphasia caused by a cere-
bral lesion ipsilateral to the dominant hand regardless of References and Readings
handedness. Currently, CA only refers to right-handed
individuals. The frequency of CA among stroke survivors Alexander, M. P., Fischette, M. R., & Fischer, R. S. (1989). Crossed
is rare (13%). aphasias can be mirror image or anomalous. Brain, 112, 953973.
Although some earlier authors considered CA to Basso, A., Capitani, E., Laiacona, M., & Zanobio, M. E. (1985). Crossed
aphasia: One or more syndromes? Cortex, 21, 2545.
be the consequence of a weaker language lateralization,
Bramwell, B. (1899). On crossed aphasia. Lancet, 14731479.
it appears that individuals with CA have language as Coppens, P., Hungerford, S., Yamaguchi, S., & Yamadori, A. (2002).
strongly lateralized as those with left-hemisphere aphasia Crossed aphasia: An analysis of the symptoms, their frequency, and
(LHA), mainly because both populations show a similar a comparison with left-hemisphere aphasia symptomatology. Brain
prognosis. and Language, 83, 425463.
Fujii, T., Yamadori, A., Fukatsu, R., Ogawa, T., & Suzuki, K. (1997).
CA can be mirror image or anomalous (Alexander,
Crossed mixed transcortical aphasia with hypernomia. European
Fischette, & Fischer, 1989). Mirror-image CA denotes Neurology, 37, 193194.
the expected correspondence between symptomatology
and lesion location within the language-dominant
hemisphere, whereas anomalous CA implies the presence
of unexpected language symptoms given the lesion loca- Cross-Examination
tion (e.g., Wernickes aphasia following a frontal lesion
[Basso, Capitani, Laiacona, & Zanobio, 1985], a mixed M OIRA C. D UX
transcortical aphasia with preserved naming [Fujii, University of Maryland Medical Center/Baltimore VA
Yamadori, Fukatsu, Ogawa, & Suzuki, 1997]). Close to Baltimore, MD, USA
two thirds of CA cases are mirror image. The CA language
symptomatology is virtually indistinguishable from LHA,
and all aphasia types have been reported in CA. Definition
The cause of CA is essentially unknown, but the influ-
ence of left-handedness in the family has long been consid- A deposition or actual trial testimony consists of two
ered an important causal factor, a hypothesis called familial parts: the direct examination and the cross-examination.
748 C CRS
Direct examination precedes the cross-examination and

involves testimony brought forth by the retaining attor- CRS-R
ney. Cross-examination occurs immediately after the
direct examination and is carried out by the opposing Coma Recovery Scale
attorney. The main purpose of cross-examination is to
test the reliability, accuracy and credibility of witnesses
testimony produced during the direct examination.
Questions posed during cross-examination typically fall
into two categories: those intended to expose weaknesses Crystallized Intelligence
or errors in the expert witnesses data acquisition or
interpretations, and those related to expose biases in the Intelligence
testimony. During cross-examination, expert witnesses
are expected to give responsive answers. That is, they
are to provide relevant answers, but the answers need
not be those implicitly desired by the opposing attorney.
The opposing attorney may use several tactics during
cross examination including: challenging credibility,
CSI
establishing doubt, leading questions, feigned ignorance,
the cut-off (e.g., testimony of witness terminated to stop
the witness from providing further information that
could be detrimental to the opposing attorneys position),
intentional ambiguity, implying impropriety, rattling the
witness, and many others.
CS-PFP
Physical Functional Performance
Cross References
Direct Examination
CS-PFP10
Physical Functional Performance
Brodsky, S. L. (2004). Coping with cross-examination and other pathways
to effective testimony. Washington, DC: American Psychological
Association.
(1975). Federal rules of evidence for United States courts and magistrates.
St. Paul, MN: West Publishing.
Greiffenstein, M. F., & Cohen, L. (2005). Neuropsychology and the law: CT
Principles of productive attorney neuropsychologist relations. In
G. Larrabee (Ed.), Forensic neuropsychology: A scientific approach. Category Test
Computed Tomography
CRS
CT Scan
Coma Recovery Scale
Conners Rating Scales Computed Tomography
Cue C 749
may appear spontaneously as a behavior is unfolding

Cue in order to effect immediate change. For example,
when one sees the cue of a deer running into the
J ANET PATTERSON road one veers away to avoid a collision, or when one
California State University is engaged in conversation and hears the cue of his or
Hayward, CA, USA
C
her sentence that does not adequately express the
intended meaning one immediately changes the sen-
tence. Cues may also appear as a learned strategy and
Synonyms be repeated in a consistent format. For example, dri-
vers know that when the yellow traffic light appears
Discriminative stimulus; Prime; Prompt they should slow the car in preparation to stop when
the red traffic light appears, or in a communication
Definition interaction when another individual offers a greeting
one should respond. Some examples of self-generated,
A cue is a verbal or nonverbal instruction to induce internal cues are reminders for future action (e.g.,
behavior change. Cues are self-generated or may come remember to walk the dog), mental sequences used in
from the environment (including an examiner). They the tip-of-the-tongue state (e.g., telling oneself that the
Present Cue # 1 Present Cue # 4

Present a picture and say, Say the name of this, or Say It starts with ___ and say the first sound
Whats this or Tell me the name of this
If correct response
If correct response (a) Say correct or right
(a) Say correct or right (b) Present Cue #3
(b) Ask for five repetitions
(c) Move to next picture item If incorrect response
(a) Present Cue #5
If incorrect response
(a) Present Cue #2
Present Cue # 5
Present Cue # 2 Say The word is ___ and say the name of the item
Say It goes with ____ and give the semantic cue

If correct response
If correct response (a) Say correct or right
(1) Say correct or right (b) Present Cue #4
(2) Present Cue #1
If incorrect response (a) Repeat cue and ask for repetition
(a) Present Cue #3 (b) If unable to repeat item name after three
consecutive presentations of Cue #5
Present Cue # 3 move to next picture item
Say It sounds like ___ and give the rhyme cue
If correct response
(a) Say correct or right
(b) Present Cue #2
(a) Present Cue #4
Cue. Figure 1 An example of a cueing hierarchy for oral naming using semantic and phonological cues
750 C Cue Dominance
name rhymes with sock), or teaching/treatment strate- Definition

gies (e.g., using an association strategy for naming,
such as reciting the alphabet to cue the name). Exam- Cue dominance refers to the tendency to perceive or
ples of external cues are environmental signs (e.g., respond to a particular stimulus or class of stimuli over
walk/do not walk signals), preprogrammed reminders others in the environment. Stimuli may either have in-
(e.g., alarm clock), or teaching/treatment techniques trinsic properties that give them strength or dominance
(e.g., semantic-phonological cueing hierarchy). A cue- based on physical attributes (e.g., loudness, color), or may
ing hierarchy is a set of cues progressing from weak cues acquire dominance (i.e., propensity to elicit a response) as
providing little information about the target response, to a function of associative learning and task demands.
strong cues providing much information (Wambaugh,
Linebaugh, Doyle, Martinez, Kalinyak-Fliszar, & Spencer,
2001) (Fig. 1). Current Knowledge
Cue dominance is an important principle derived from

behavioral studies of animal conditioning and learning the-
Cross References ories. It provides a theoretical foundation for the neurosci-
ence of selective attention, linking basic behavioral and
Cue Dominance
learning processes with higher order information processing.
Cued Recall
In the context of behavioral conditioning, cues refer
Free Recall
to stimuli that have the capacity to elicit an orienting
Phonemic Cue
response, anticipation, subsequent attention, and re-
Recency Effect
sponse intention and preparation. Cues lack the inherent
Semantic Cue
biological salience of unconditioned stimuli, and do not
Semantic Fluency
elicit unconditioned Pavlovian responses, but can become
Verbal Fluency
conditioned stimuli through associative learning. Studies
of discrimination learning conducted in the middle of the
twentieth century established many of the operational
References and Readings characteristics underlying cue dominance. For example,
studies examining intrinsic cue dominance demonstrated
Patterson, J. P., & Hinnach, S. E. (2005). Word familiarity effects during that monkeys have a natural preference for response to
naming and discourse production in aphasia. Presentation to the color over other perceptual dimensions, such as size and
American Speech-Language-Hearing Association Annual Conven- shape (Draper, 1965). Experiments with human infants
tion. San Diego. demonstrated cue dominance for certain shapes over
Wambaugh, J. L., Linebaugh, C. W., Doyle, P. J., Martinez, A. L.,
others based on whether they resembled the shape of a
Kalinyak-Fliszar, M., & Spencer, K. A. (2001). Effects of two cueing
treatments on lexical retrieval in aphasic speakers with different human face (Fantz & Miranda, 1975). While certain stim-
levels of deficit. Aphasiology, 15(10/11), 933950. ulus features have intrinsic cue dominance across many
animal species, the ability to form complex cues based on
the association of simple cues appears greatest among
humans, as is the ability to exhibit reversal learning in
order to shift response from one cue to another (Kendler &
Ward, 1972; Kendler, 1971).
Cue Dominance In neuropsychological studies and assessment meth-
ods, cues are often used to either facilitate attention to
R ONALD A. C OHEN particular spatial locations, semantic information, or re-
Brown University sponse demands. Alternatively, cues are used to create
Providence, RI, USA interference to test the effects of distraction or the redi-
rection of attention away from the primary demands of a
task. This is a fundamental element of the spatial selective
Synonyms attention paradigms that involve cueing to spatial loca-
tions (Posner, Snyder, & Davidson, 1980). Furthermore,
Cue salience; Orienting stimulus; Stimulus strength the tendency of the semantic value associated with a word
Cued Recall C 751
to be dominant over color and to interfere with attention from free recall in that a cue or word is presented that is
to and naming of the actual color that is being presented related to the information being remembered. This aides
underlies the Stroop effect. Researchers and clinicians in the process of memory retrieval. Some examples of
studying or assessing attentional processes need to ac- cued recalls are the names of the categories in which
count for both the inherent and acquired cue dominance words were originally grouped or the presentation of C
of stimuli being used in the context of particular tasks. related words. For instance, in remembering the word
feather, the word bird may be used as a cued recall.
Cross References Current Knowledge

Enhancement
Tests of Cued Recall
Selective Attention
Visual Discrimination
There are many tests of cued recall. One of the most
commonly used tests of cued recall is the California Verbal
Learning Test (CVLT) developed by Delis et al. This se-
References and Readings mantic test, like many other tests of memory, utilizes both
free and cued recall.
Draper, W. A. (1965). Cue dominance in oddity discriminations by
rhesus monkeys. Journal of Comparative and Physiological Psychology,
60(1), 140141. Clinical Uses of Cued Recall Testing
Fantz, R. L., & Miranda, S. B. (1975). Newborn infant attention to form
of contour. Child Development, 46(1), 224228.
Kendler, T. S. (1971). Continuity theory and cue-dominance. In H. H.
In addition to the use of free recall tests, tests of cued
Kendler & J. T. Spence (Eds.), Essays in neobehaviorism: A memorial recall may be used in identifying memory impairments in
volume to Kenneth W. Spence. East Norwalk: Appleton-Century- a wide array of disorders including mild cognitive im-
Crofts. pairment and Alzheimers disease. In some instances, tests
Kendler, H. H., & Ward, J. W. (1972). Reversal learning: The effects of
of cued recall may be more accurate than free recall tests
conceptual and perceptual training in the absence of differential
observing responses. Psychonomic Science, 28(6), 346348.
in detecting cognitive changes. For example, Ivanoiu et al.
Posner, M. I., Snyder, C. R., & Davidson, B. J. (1980). Attention and the (2005) found that a cued recall test is more reliable in
detection of signals. Journal of Experimental Psychology: General, testing memory impairment in Alzheimers disease than
109(2), 160174. free recall testing. While both tests of memory are im-
paired in such individuals, cued recall may be a more
accurate measure of cognitive decline. This is because
deficits other than pure memory deficits, such as impaired
Cue Salience attention or depression, may account for a decreased
performance in free recall. Conversely, cued recall tests
Cue Dominance may be used to more directly measure the encoding and
retrieval that takes place in memory tasks.
Cross References
Cued Recall
California Verbal Learning Test (California Verbal
M ARGARET M OULT Learning Test-II)
Institute of Living Hartford Cue
CT, USA Free Recall

Definition
Carpenter, S. K., Pashler, H., & Vul, E. (2006). What types of learning are
Cued recall is the retrieval of memory with the help of enhanced by a cued recall test? Psychonomic Bulletin & Review, 13,
cues. Such cues are often semantic. Cued recall differs 826830.
752 C Cultural Diversity in Neuropsychology
Ivanoiu, A., Adam, S., Van der Linden, M., Salmon, E., Juillerat, A. C., Recent studies emphasize that the deconstruction of
Mulligan, et al. (2005). Memory evaluation with a new cued recall
race is critical for improved clinical care of ethnically di-
test in patients with mild cognitive impairment and Alzheimers
disease. Journal of Neurology, 252, 4755.
verse populations. The construct has been identified as a
Vogel, A., Morentsen, L., Gade, A., & Waldemar, G. (2007). The category proxy for more meaningful but complex variables such as
cued recall tests in very mild Alzheimers disease: Discriminative acculturation and indicators of quality of education, which
validity and correlation with semantic memory functions. European account for significant proportions of racial and ethnic
Journal of Neurology, 14, 102108.
differences in neuropsychological test scores (Romero
et al., 2009, p. 765). However, increasing emphasis has
been placed on the importance of the clinician knowing
when to apply race- and ethnic-based norms, as their use
can actually reduce detection of neuropsychological im-
Cultural Diversity in pairment. The complexity of this issue was demonstrated
Neuropsychology in one of the Mayos Older African American Normative
Studies (MOAANS) project studies. In this study, adjust-
S ARAH K. L AGEMAN ment of test scores for reading level surprisingly reduced
Emory University detection of cognitive impairment in African Americans.
Atlanta, GA, USA Lucas and colleagues (2005) suggest that their findings
indicate that cohort differences in reading level may be
more reflective of individual differences in cognitive abil-
Definition ity rather than contextual differences such as educational
backgrounds. While race may be a very efficient and
The term cultural diversity generally refers to the differ- parsimonious variable for clinicians to use at times, the
ences in defining cultural features that exist between confounding of causes and effects of these variables pre-
people (or within a given population), such as language, sents a significant challenge. The Diversity Summit parti-
dress, and traditions, as well as more abstract concepts cipants unanimously agreed that guidelines for
involving significant variations in societal organization neuropsychological practice among ethic and racial mino-
and interaction styles between individuals and environ- rities are needed to further improve clinical service for
ments. With respect to neuropsychology, the term ethic and racial minorities.
encompasses the racial and ethnic diversity among neu- In an effort to initiate the development of practical
ropsychologists themselves and the populations they in- guidelines regarding the use of demographic corrections,
teract with, as well as issues related to the influences of clinical criteria have been developed. As detailed in the
race and ethnicity on neuropsychological evaluations and Diversity Summit proceedings, demographic corrections
treatments. are useful to identify and characterize acquired neurocog-
nitive impairments in adults who (1) are natives of the
country of assessment, (2) developed normally, (3) received
Current Knowledge mainstream education, and (4) speak English as their first
language (for the U.S. norms). Demographic corrections
Multicultural competency is a developing area of focus are sometimes useful to identify and characterize acquired
within the field of neuropsychology. As the ethnic and neurocognitive impairments in (1) teenagers or young
racial diversity of the United States increases, so do efforts adults who have not completed their education, (2) adults
to provide neuropsychological services to ethnic minori- who may have had a mild developmental disorder, or (3)
ties. Thus, clinical and research studies have begun to anyone with a linguistic, cultural, or educational back-
examine how cultural variables influence performance ground not well represented in the normative subject
on neuropsychological measures. While the past decade sample. Demographic corrections are not recommended
has witnessed some publications providing test norms for when the clinician is asked (1) to characterize absolute
specific racial and ethnic groups, the use of racial and levels of functioning, (2) to identify or characterize possi-
ethnic norms for neuropsychological measures remains a ble acquired impairment in capital punishment cases or
contentious issue. Readers are encouraged to examine the when determining qualifications for special services,
summary of the 2008 Diversity Summit for additional or (3) in cases of possible acquired impairment in indivi-
details (Romero et al., 2009). Highlights of the summit duals who have developmental disability, (4) to character-
and recent literature are provided below. ize acquired cognitive impairment in individuals who
Cultural Diversity in Neuropsychology C 753
have major background differences from the normative importance of training in cross-cultural neuropsychology
sample, (5) to predict future performance in employment will become increasingly important as the Spanish-
or academic settings, and (6) for employment selection speaking Latino population in the United States grows.
decisions. In addition to these clinical guidelines, empha- In keeping with the demographic changes in the
sis is being increasingly placed on correctly using proba- United States, training programs and national organiza- C
bilistic statistics to predict group membership (i.e., tions are brainstorming ways to promote recruitment and
diagnosis) for individuals. Readers are encouraged to retention of students with diverse racial and ethnic back-
review recent publications regarding likelihood ratios, grounds in the study of neuropsychology. Emphasis has
which express the risk associated with certain test scores been placed on student exposure to neuropsychology
(Smith, Ivnik, & Lucas, 2008). earlier in academic careers, mentoring with minority
While additional study of the deconstruction of race is and nonminority faculty who are sensitive to diversity
needed, development of ethnic group norms itself is a issues and financial support of minority students. The
challenging and complex task. Test publishers are increas- study of cultural diversity itself has gained support and
ingly making efforts to include important background many licensing bureaus require documentation of diver-
variables in normative samples. However, the cost of sity training in graduate school for licensure. Numerous
recruiting and assessing large cohorts is prohibitive for organizations, including the American Psychological
individual centers and researchers and is often even a Association (APA) Division 40, the International Neuro-
challenge for larger test publishing companies. While psychological Society (INS), and the National Academy of
inclusion of demographic variables in research articles is Neuropsychology (NAN), promote awareness of diversity
an important piece to further develop this area, federal issues and foster collaborations among clinicians and
and foundation-funded grants may be necessary to sup- researchers interested in diversity issues. Readers are
port multicenter partnerships, ideally suited to study encouraged to review current guidelines, including the
large, diverse cohorts. APA Ethical Principles (2002) and the APA Multicultural
Despite the development of racially and ethnically Guidelines (2002) for further details.
diverse norms, including the widely used Heaton norms Diversity in neuropsychology has become of increasing
for African American and Caucasian adults, the almost interest and importance; however, measures to improve
endless variety possible with regard to individuals language, diagnostic assessment of ethnic minorities may not fully
culture, and education backgrounds limits the application address the issue of improving clinical care of ethnic mino-
of demographically corrected norms for every possible clin- rities, given limited health care access of non-English-
ical situation (Heaton, Miller, Taylor, & Grant, 2004). Local speaking patients. Access to care and other factors affecting
norms may be helpful for clinicians working with popu- ethnic minority patient outcomes have increasingly been
lation groups with less common background variables; examined in the field of neuropsychology. Readers are
however, integration of test scores with a persons individ- encouraged to review two issues of the Journal of Head
ual context is ultimately critical for formulation of an Trauma Rehabilitation, dedicated to U.S. and international
accurate diagnosis. In clinical practice, other issues re- cultural issues in the rehabilitation of survivors of traumatic
garding assessment of ethnic, linguistic, and cultural head injury (Cultural Issues, 2007 and International
minorities are also present. The use of translated tests, Programs and Perspectives, 2007). Articles in these issues
interpreters, and bilingual psychometrists are all current highlight complex relationships between functional out-
methods for evaluating non-English-speaking patients. comes, disability severity, return to work, and utilization
However, the shear complexity of language fluency is of professional psychological services in ethnic minority
important to consider. Language fluency of an individual groups. The international issue describes models of care
can vary widely with regard to (1) age of acquisition, (2) used in the context of various health care systems as well
proficiency, (3) manner of learning, (4) amount of lan- as international perspectives on research and develop-
guage exposure, (5) predominant mode of bilingual inter- ment in the field of traumatic brain injury rehabilitation.
action, and (6) language structure variables (i.e., alphabetic The study of health disparities among ethnic minority
versus logographic languages and phonemic versus non- populations is a complex, but critical field of research.
phonemic status). Currently, the use of translated tests and Multiple dimensions of disparity exist, including many of
official interpreters or bilingual psychometrists are pre- the variables discussed regarding the deconstruction of
ferred over using family members as interpreters and site race such as ethnicity, education, income, occupation,
translation, which refers to the practice of quickly translat- and geography. Continuous study of these variables is
ing a test with no standardization procedures. The critical to improve clinical care for ethnic minorities.
754 C Cultural Sensitivity
Cross References ethnic minorities: Summit proceedings. The Clinical Neuropsycholo-

gist, 23, 761779.
Smith, G. E., Ivnik, R. J., & Lucas, J. (2008). Assessment techniques:
AACN Practice Guidelines Tests, test batteries, norms, and methodological approaches. In
Clinical Practice Guidelines J. E. Morgan & J. H. Ricker (Eds.), Textbook of clinical neuropsychol-
Cultural Sensitivity ogy (pp. 3857). New York: Taylor & Francis.
Culture Fair Tests Uzzell, B. P., Ponton, M., & Ardila, A. (Eds.). (2007). International
handbook of cross-cultural neuropsychology. Mahwah, NJ: Lawrence
Ethics in the Practice of Neuropsychology
Erlbaum Associates, Inc.

Cultural Sensitivity
American Academy of Clinical Neuropsychology (AACN). Multicultural
references. Retrieved March 16, 2010, from the AACN Web site:
http://www.theaacn.org/position_papers/AACN_multicultural_ref
C HRISTIAN S CHUTTE , B RADLEY A XELROD
erences.pdf John D. Dingell VA Medical Center
American Psychological Associations Ethical Principles of Psychologists Detroit, Michigan, USA
and Code of Conduct with the 2010 Amendments (http://www.apa.
org/ethics/code/index.aspx)
American Psychological Associations Ethnic Minority Affairs Office
(http://www.apa.org/pi/oema/index.aspx)
Synonyms
American Psychological Associations Minority Fellowship Program
(http://www.apa.org/pi/mfp/) Multicultural
American Psychological Associations Division 45, Society for the Psy-
chological Study of Ethnic Minority Issues (http://www.apa.org/
divisions/div45/) Definition
American Psychological Association. (2002). Guidelines on multicultural
education, training, research, practice, and organizational change for Awareness of how a patients background, including eth-
psychologists. Retrieved June 30, 2010, from http://www.apa.org/
nicity and demographic factors, affects treatment, assess-
practice/guidelines/multicultural.pdf
Arango-Lasprilla, J. C., & Niemeier, J. (Eds.). (2007). Cultural issues in
ment, and research.
the rehabilitation of TBI survivors: Recent research and new fron-
tiers. Journal of Head Trauma Rehabilitation, 22(2), 73139.
Ardila, A., Rosselli, M., & Puente, A. (1994). Neuropsychological evalua-
Current Knowledge
tion of the Spanish speaker. New York: Plenum Press.
Board of Directors (2007). American Academy of Clinical Neuropsychol- There are a couple of pertinent definitions, or applications,
ogy (AACN) Practice Guidelines for Neuropsychological Assessment of cultural sensitivity to the field of neuropsychology.
and Consultation. The Clinical Neuropsychologist, 21, 209231. Re-
The position of the American Psychological Associa-
trieved March 16, 2010, from http://www.theaacn.org/position_
papers/AACNPractice_Guidelines.pdf
tion (APA), which is reflected in the 2002 APA ethical
Ferraro, F. R. (Ed.). (2002). Minority and cross-cultural aspects of neuro- principles of psychologists and code of conduct, state
psychological assessment. Lisse, Netherlands: Swets & Zeitlinger. Psychologists are aware of and respect cultural, individ-
Fletcher-Janzen, E., Strickland, T. L., & Reynolds, C. R. (Eds.). (2000). ual, and role differences, including those based on age,
Handbook of cross-cultural neuropsychology. New York: Kluwer
gender, gender identity, race, ethnicity, culture, national
Academic/Plenum Publishers.
Heaton, R. K., Miller, S. W., Taylor, M. J., & Grant, I. (2004). Revised
origin, religion, sexual orientation, disability, language,
comprehensive norms for an expanded Halstead-Reitan battery: demo- and socioeconomic status and consider these factors
graphically adjusted neuropsychological norms for African American and when working with members of such groups. Psycholo-
Caucasian adults. Lutz, FL: Psychological Assessment Resources, Inc. gists try to eliminate the effect on their work of biases
International Programs and Perspectives on Traumatic Brain Injury Re-
based on those factors, and they do not knowingly partic-
habilitation. (2007). Journal of Head Trauma Rehabilitation, 22(4),
209256.
ipate in or condone activities of others based upon such
Lucas, J. A., Ivnik, R., Willis, F., Ferman, T., Smith, G., Parfitt, F., et al. prejudices.
(2005). Mayos Older African American Normative Studies: Norma- Cultural sensitivity is also reflected in the 2002 APA
tive data for commonly used clinical neuropsychological measures. Guidelines on multicultural education, training, research,
practice, and organizational change for psychologists.
Nell, V. (1999). Cross-cultural neuropsychological assessment: Theory and
practice. Mahwah, NJ: Lawrence Erlbaum Associates, Inc.
The APA defines multicultural specifically as referring
Romero, H. R., Lageman, S. K., Kamath, V., Irani, F., Sim, A., Suarez, P., to interactions with individuals from minority ethnic
et al. (2009). Challenges in the neuropsychological assessment of and racial groups in the United States and the dominant
Culture Fair Test C 755
European-American culture. This document states that Heaton, R. K., Miller, S. W., Taylor, M. J., & Grant, I. (2004). Revised
comprehensive norms for an expanded Halstead-Reitan Battery: demo-
all individuals are in a social, political, and economic
graphically adjusted neuropsychological norms for African American and
context. Therefore, it is increasingly important for psy- Caucasian Adults. Lutz, FL: Psychological Assessment Resources Inc.
chologists to be aware of the specific needs of individuals Nagra, A., Skeel, R. L., & Sbrage, T. P. (2007). A pilot investigation on the
based on their ethnic/racial heritage and social group effects of stress on neuropsychological performance in Asian-Indians
C
identity. Guidelines relating to research direct psycho- in the United States. Cultural Diversity & Ethnic Minority Issues, 13,
5463.
logists to recognize the importance of conducting cul-
Smith, G. E., Ivnik, R. J., & Jucan, J. (2008). Assessment techniques:
ture-centered and ethical psychological research among tests, test batteries, norms and methodological approaches. In
persons from ethnic, linguistic, and racial minority J. E. Morgan, & J. H. Ricker (Eds.), Textbook of clinical neuropsycho-
backgrounds. logy (pp. 3857). New York: Taylor & Francis.
A second area of cultural sensitivity that directly
relates to neuropsychology is the impact of culture on
testing and on normative data. It is important that an
individual examinees test performance be related to indi-
viduals of similar backgrounds. For example, the norma- Culturally Reduced Test
tive group of an elderly, well-educated African American
man should closely match his background. Without close Culture Fair Test
matching of cultural, demographic, and educational
background, unacceptable problems with misclassifica-
tion of normal test results as abnormal can result in
misdiagnosis of the patient. There is evidence that exam-
iners belonging to a culture different from that of the
examinee can elicit some anxiety, which may have a dele-
Culture Fair Test
terious effect on test scores on more demanding cognitive
G LEN E. G ETZ
tasks (Nagra, Skeel, & Sbrage, 2007). Additionally, cultural
background, demographics and educational history, can
Pittsburgh, PA, USA
have a sizeable impact on normative data. Smith, Ivnik
and Jucan (2008) discuss the development of norms spe-
cifically for older adults on commonly used neuropsy-
Synonyms
chological tests. They subsequently developed more
specific norms for older African Americans, as it was
Culture free test; Culturally reduced test
found that culture had a significant impact on normative
data. Heaton, Miller, Taylor and Grant (2004) have pub-
lished norms that take into account age, education, and
cultural background. This area of cultural sensitivity plays Definition
an important role in neuropsychology in terms of diag-
nosis and test evaluation. Culture fair test is a test that is equally fair to all cultural
groups. Fairness is related to a lack of bias in the inter-
pretation or use of a test to classify or diagnose. In a
Cross References culture fair test, the validity of the interpretation is
similar across different cultural groups. It is unlikely
Cultural Diversity that any test can entirely eliminate the influence of
Normative Data learning and cultural experience, given that the test con-
tent, language, directions, and validity criteria are cul-
turally bound. However, avoiding culturally loaded
References and Readings items, items that are found to be unfair to certain groups
of people, increases the likelihood of it being a culturally
American Psychological Association. (2002). Ethical principals of psychol-
fair test. Culturally loaded items, such as those that
ogists and code of conduct.
American Psychological Association. (2002). Guidelines on multicultural
utilize pictures or general information that are differen-
education, training, research, practice and organizational change for tially prevalent for certain cultures, decrease the likeli-
psychologists. hood of a culturally fair test.
756 C Culture Free Test
Cross References is part of the occipital lobe, corresponding to Broadmann

area 17. Pyramidal cells in the cuneus (striate cortex)
Cultural Sensitivity project to extrastriate cortices (Broadmann areas 18
Ravens Progressive Matrices and 19). The cuneus consists of both striatal and extra-
striatal visual cortex consisting of five layers. The striatal
areas are largely posterior and are idiotypic homomodal
(Mesulams classification), while the extrastriatal areas
contain heterotypic cell types that respond to more com-
plex visual information. The cuneus receives input from
Jensen, A. R. (1974). How biased are culture-loaded tests? Genetic
Psychology Monographs, 90, 185244.
the contralateral superior retina corresponding to the
Scarr, S. (1994). Culture fair and culture free test. In R. J. Sternberg (Ed.), lower visual field. From the extrastrial areas of cuneus,
Encyclopedia of human intelligence. New York: Macmillan. information is processed through both ventral and dorsal
pathways. The dorsal pathway is particularly important
for higher spatial analysis and visual integration.
Culture Free Test Function
The cuneus plays as essential role in primary visual proces-

Culture Fair Test
sing. The striatal regions that contain primary visual pro-
cessing areas contain neurons with small receptive fields
that are sensitive to very basic visual frequency information
related to position, local orientation, spatial-frequency, and
color (Beason-Held et al., 1998; Jeannerod, 2004; Ulbert,
Cuneate Nucleus Karmos, Heit, & Halgren, 2001; Ungerleider & Pribram,
1977). However, more anterior to the primary visual areas
Nucleus Cuneatus are neurons that respond to more complex information
contained in the visual information processed by the
primary receptors (Ungerleider & Haxby, 1994). Accord-
ingly, the cuneus plays a role in both primary and second-
ary visual processing. Extrastriatal areas of the cuneus are
known to respond to reward, anticipatory, attention, and
Cuneus working memory manipulations, and there is even evi-
dence that posterior striatal areas respond to attentional
R ONALD A. C OHEN
signals, providing evidence that this cortical plays some
Brown University
role in higher cognitive function involving basic visual
Providence, RI, USA
information.
Synonyms
Illness
Broadmann area 17
Damage to the cuneus would typically occur among
patients experiencing focal brain lesions. Most often
such lesions occur secondary to cerebral infarction
Structure (stroke) typically involving the posterior cerebral circula-
tion, though neurosurgery to remove neoplasm may re-
The term cuneus comes from the Latin term for wedge, sult in focal damage to the cuneus as well. Some atypical
which reflects the shape of this occipital brain area. The neurodegenerative diseases are also known to cause tissue
cuneus is a wedge-shaped cortical area located in the loss in this occipital area. The effects of focal damage to
medial occipital gyri, superior to the calcarine fissure the cuneus are known primarily from experimental abla-
and posterior to the parietaloccipital fissure. The cuneus tion in primate studies and to some extent from single-
Cuneus C 757
tral
Cen
us
sulc Paracentr
al
eu
s lobule Su
n p fr
cu ont
ae al g
Pr Cing
ulate yru
s
C
Pa Cingulate gyrus sul
cus
ri
eto
-oc
m
callosu
Cuneus Corpus
cip
.
nix
For
Fi
Fissure
ss
ur
ine
y
Isthmus tor
fac
r
rol
lca
Lingual gyrus Pa ea
Ca
Hippo Uncus a r
camp
al gyr
Fusif us
Infr orm
Inf. T temp. gyrus
emp.
Gyru
s sulcus
Cuneus. Figure 1 Sagital illutration showing the cuneus in the posterior cortex
case studies of stroke. Posterior cuneus lesions tend to What System

disrupt primary visual perception, particularly response Where System
to stimuli occurring in the lower visual fields. Damage to
more anterior areas of the cuneus also affects visual func-
tions (e.g., movement perception), though often for
higher level operations involved in object perception and References and Readings
spatial analysis, including attention (De Weerd, Peralta,
Desimone, & Ungerleider, 1999). Beason-Held, L. L., Purpura, K. P., Krasuski, J. S., Maisog, J. M., Daly,
Interestingly, there is also evidence that cuneus vol- E. M., Mangot, D. J., et al. (1998). Cortical regions involved in visual
texture perception: A fMRI study. Brain Research Cognitive Brain
ume is related to other behavioral processes not obviously
Research, 7(2), 111118.
tied in a direct way to visual processing. For example, one Crockford, D. N., Goodyear, B., Edwards, J., Quickfall, J., & el-Guebaly, N.
recent study found greater cuneus volume to be associated (2005). Cue-induced brain activity in pathological gamblers.
with greater inhibitory control among patients with bipo- Biological Psychiatry, 58(10), 787795.
lar disorder affective disorder (Haldane, Cunningham, De Weerd, P., Peralta, M. R., III, Desimone, R., & Ungerleider, L. G.
(1999). Loss of attentional stimulus selection after extrastriate corti-
Androutsos, & Frangou, 2008). Another study found
cal lesions in macaques. Nature Neuroscience, 2(8), 753758.
that compulsive gamblers had increased activity in dorsal Haldane, M., Cunningham, G., Androutsos, C., & Frangou, S. (2008).
visual processing pathways, including the cuneus when Structural brain correlates of response inhibition in Bipolar Disorder I.
compared with controls (Crockford, Goodyear, Edwards, Journal of Psychopharmacology, 22(2), 138143.
Quickfall, & el-Guebaly, 2005). Whether such findings Jeannerod, M. (2004). Visual and action cues contribute to the self-other
distinction. Nature Neuroscience, 7(5), 422423.
reflect a specific role of the cuneus in these psychiatric
Ulbert, I., Karmos, G., Heit, G., & Halgren, E. (2001). Early discrimina-
disorders versus more incidental findings needs to be tion of coherent versus incoherent motion by multiunit and synaptic
determined in future investigations. activity in human putative MT + . Human Brain Mapping, 13(4),
226238.
Ungerleider, L. G., & Haxby, J. V. (1994). What and where in the
human brain. Current Opinion in Neurobiology, 4(2), 157165.
Cross References
Ungerleider, L. G., & Pribram, K. H. (1977). Inferotemporal versus
combined pulvinar-prestriate lesions in the rhesus monkey: Effects
Feature Detection on color, object and pattern discrimination. Neuropsychologia,
Spatial Frequency Analysis 15(45), 481498.
758 C Cushings Syndrome
peripheral circulation and reaches cells in the cortex of the

Cushings Syndrome adrenal gland where cortisol biosynthesis is initiated. Cor-
tisol itself exerts negative feedback control on ACTH and
I SABELLE B OURDEAU 1, H ELENE F ORGET 2 CRH secretion, maintaining a normal secretion rate in case
1
CHUM-Hotel-Dieu of HPA activation, in stress for example (Fig. 1). ACTH is
Montreal, QC, Canada released physiologically in a series of secretory episodes,
2
Universite du Quebec en Outaouais followed by an equal number of cortisol bursts in plasma.
Gatineau, QC, Canada Thus, plasma cortisol levels are maximum in the early
morning hours around awakening, gradually decline
throughout the morning, and reach nadir values late in
Short Description or Definition the evening. Midnight serum cortisol >200 nmol/L strong-
ly suggests the diagnosis of CS (Stewart, 2008). Variations
Endogenous Cushings syndrome (CS) is a rare disorder of ACTH and cortisol values constitute the normal cir-
occurring in about 0.72.4 per million population per cadian rhythm. CS is caused by pituitary or adrenal
year (Newell-Price, Bertagna, Grossman, & Nieman, abnormalities or may be secondary to ectopic ACTH or
2006). CS includes symptoms and signs resulting from CRH secretion by various nonpituitary tumors, such as
chronic supraphysiological exposure to glucocorticoids lung carcinoma. CS is classified into ACTH-dependent
(GC). The classical clinical features of CS are centripetal and -independent causes which are described in Table 1.
obesity with abnormal fat distribution, mainly affecting Cushings disease refers to CS due to excessive pituitary
the face, neck, trunk, and abdomen, and sparing the ACTH secretion from pituitary tumors.
extremities. Other findings are facial plethora, easy
bruisability, purple abdominal striae, hirsutism, muscle
weakness, hypertension, and glucose intolerance (Stewart, Evaluation or Diagnosis
2008). In addition, mood alterations and psychiatric
diseases mainly depressive and anxiety disorders as The diagnosis of endogenous CS may be challenging and
well as cognitive impairment are highly prevalent in CS require the expertise of an endocrinologist. Authors will
patients (Bourdeau et al., 2005). briefly discuss the evaluation and various tests used to
The principal aim of this chapter is to present diagnose CS. The first step is to confirm CS by biochemi-
psychiatric and cognitive data on adult patients with CS. cal investigation. Then, the cause of the disease should be
The recognition of psychoneurological abnormalities
associated with hypercortisolism is of clinical importance
in the management of patients affected by CS.
Hypothalamus
Etiology
CRH
Exogenous CS refers to iatrogenic CS resulting from chron-
ic GC therapy. GC, which have potent anti-inflammatory Pituitary
and immunologic actions, are widely used for the treat-
ment of various diseases such as inflammatory bowel
disease, asthma, rheumatoid arthritis, and organ transplan- ACTH
tation. Thus, exogenous CS is the most common form of
CS. Endogenous CS may be caused by dysregulation at
Adrenal gland
various levels of the hypothalamicpituitaryadrenal axis
(HPA), resulting in cortisol overproduction. The regulation
of cortisol synthesis and secretion is mediated by the hypo- Cortisol
thalamus, the pituitary, and the adrenal glands. Corticotro-
pin (ACTH) is synthesized and secreted by corticotrophs of Cushings Syndrome. Figure 1 Schematic representation of
the pituitary which are mainly regulated by two hypotha- the hypothalamuspituitary axis. Normally cortisol negatively
lamic hormones, corticotropin-releasing hormone (CRH), regulates corticotropin-releasing hormone (CRH) and ACTH
and arginine-vasopressin. Pituitary ACTH is secreted in the secretion
Cushings Syndrome C 759
Cushings Syndrome. Table 1 Classification of the etiologies and cognition, has increased considerably in the recent
of endogenous Cushings syndrome (CS) years. McEwen, Weiss, and Schwartz (1968) demonstrated
the presence of glucocorticoid receptors (GR) in the rat
ACTH-dependent CS (80% of cases)
brain. Loss of brain volume was documented in patients
Pituitary adenoma (Cushings disease) (80%)
with endogenous and exogenous CS (Bourdeau et al., C
Ectopic ACTH or corticotropin-releasing hormone (CRH)
2002). In addition, cerebral magnetic resonance spectros-
secretion from nonpituitary neoplasms (20%)
copy revealed abnormalities of cerebral metabolism in
ACTH-independent CS (20% of cases) patients with CS (Khiat et al., 1999).
Adrenal adenoma (60%) Psychiatric disturbances occur in patients with both
Adrenal carcinoma (40%) exogenous and endogenous CS. Interestingly, patients
Bilateral ACTH-independent macronodular adrenal with endogenous depression frequently have high corti-
hyperplasia (rare) sol levels, and present HPA axis dysregulation, disclosed
Bilateral micronodular adrenal hyperplasia (primary by abnormal suppression on the dexamethasone test.
pigmented nodular adrenocortical disease and However, diurnal rhythm is usually maintained in de-
nonpigmented adrenal hyperplasia) (rare) pressed patients, and they do not develop physical signs
of CS. CS is also associated with an increased prevalence
of cognitive impairments, particularly of attention,
learning, and memory. Patients with CS represent a
identified. During the investigation, it is important to natural model that illustrates the interactions between
evaluate patients for other illnesses, drugs, alcohol, or hypercortisolism and brain function. The following sec-
depression. All these conditions may lead to misinterpre- tion focuses on the psychiatric and neuropsychological
tation of the endocrine test results. The overnight 1-mg anomalies in CS.
dexamethasone suppression test, a screening tool for the
diagnosis of CS, consists of administering 1 mg of dexa-
methasone at bedtime (23:00 h) with measurement of Psychiatric Disorders Associated with CS
plasma cortisol the following morning (08:0009:00 h).
Normal subjects should suppress plasma cortisol to less Depression is a frequent feature of CS. In fact, several
than 50 nmol/L. Measurement of free cortisol in 24- reports indicate that more than 50% of CS patients pres-
h urine collection is useful to confirm the diagnosis; ent severe depressive symptoms that reach the threshold
values fourfold greater than the upper limit of normal of a major depressive disorder. Haskett (1985) observed a
are highly suggestive of CS. More recently, late-night lifetime history of psychiatric symptoms and signs in
salivary cortisol has proven useful in the diagnosis of CS patients with proven CS. He found that the majority of
(Nieman et al., 2008). Once a diagnosis of CS is con- them experienced psychiatric disturbances that closely
firmed, the next step is to establish the etiology. Plasma resembled typical syndromes, with episodes of major
ACTH will distinguish between ACTH-dependent and - affective disorder (endogenous depression, mania, or
independent CS. ACTH values lower than 1.1 pmol/L hypomania). Moreover, Haskett (1985) noted that there
indicate ACTH-independent CS, and CT imaging of the were no significant differences between pituitary-
adrenal glands should be performed (Newell-Price et al., dependent and -independent forms of CS in the occur-
2006). ACTH values above 3.3 pmol/L suggest ACTH- rence of major depression. His observations were later
dependent CS, and further endocrine investigations confirmed by independent investigations (Kelly, 1996;
should be undertaken, including magnetic resonance im- Sonino, Fava, Belluardo, Girelli, & Boscaro, 1993). Using
aging of the pituitary glands and other tests that are DSM-III criteria (American Psychiatric Association,
beyond the scope of this chapter. 1980), Hudson, Hudson, Griffing, Melby, and Pope
(1987) reported a high lifetime diagnosis of mood
disorders in CS patients, of whom 14% were assessed to
Psychiatric Diseases and have major affective disorder. Loosen, Chambliss, DeBold,
Neuropsychological Disturbances Shelton, and Orth (1992) recognized major depressive
Associated with CS disorder in 68% of adult patients with CS. In addition,
this disorder was frequently associated with anxiety
Understanding the importance and complexity of adrenal disorder (generalized anxiety disorder and/or panic dis-
hormones impacting cerebral function, particularly affect order), indicating a syndrome of anxious depression in
760 C Cushings Syndrome
patients with active CS (Loosen et al., 1992). Focusing on reported generalized impairment of cognitive functions
Cushings disease, Sonino, Fava, Raffi, Boscaro, and Fallo (decreased concentration and memory, perceptual distor-
(1998) found major depression in more than half of their tions). More recently, Starkman, Gebarski, Berent, and
patients studied. Moreover, major depression was signifi- Schteingart (1992) observed moderate-to-severe deficits
cantly correlated with older age, female gender, higher in a wide variety of language and nonverbal subtests
pretreatment urinary cortisol levels, and more severe among more than two-thirds of their CS patients.
clinical conditions. Kelly, Kelly, and Faragher (1996) Difficulties with reasoning ability, comprehension, and
reported that some patients with CS were diagnosed to processing of new information also were found. Deficits
have depression and were more depressed than patients in these areas of cognition were confirmed in a recent
with other pituitary tumors. Concentrating on the controlled study of 19 CS patients (Forget, Lacroix,
question of whether depression in CS more consistently Somma, & Cohen, 2000). In fact, memory was the most
resembles any of the clinical subcategories, Dorn et al. studied function in CS because the emphasis was on the
(1995) established that patients with active endogenous hippocampus which is rich in GR. However, the distribu-
CS exhibited significant psychopathology, expressed pri- tion of GR in many areas of the cerebral cortex suggests
marily by atypical depression. This concept of atypical that extrahippocampic sites could also be the target of
depression refers to the presence of weight gain or cortisol, and generalized impairment of cognitive func-
increased appetite, fatigue, hypersomnia, leaden paralysis, tions after chronic hypercortisolism may be related to this
and longstanding interpersonal rejection sensitivity wide dispersion of GR.
(American Psychiatric Association, 1994).
In summary:
Treatment
1. More than 50% of patients with CS report severe
depressive symptoms
The goal of CS treatment is to correct the hypersecretion
2. There are no significant differences between ACTH-
of adrenal hormones. In most cases, tumor-specific
dependent and -independent forms of CS in the
surgery will be performed. In Cushings disease, pituitary
occurrence of major depression
tumors should be resected, and in adrenal CS adrenalec-
3. Major depressive disorders are commonly associated
tomy performed. In cases of ectopic ACTH secretion
with anxiety disorders
secondary to benign tumors, the latter should be
4. Major depression is significantly correlated with
removed; but in most cases, there are metastatic malig-
older age, female gender, higher pretreatment urinary
nant tumors. If surgery is unsuccessful, drugs that block
cortisol levels, and more severe clinical conditions
steroid synthesis may be administrated to achieve
5. A high prevalence of atypical depression features is
eucortisolism (Biller et al., 2008; Stewart, 2008).
seen in CS
Neuropsychological Disorders Associated Natural History, Prognostic Factors,

with CS Outcomes
Neuropsychological disorders have been detected in about The reversibility of brain volume loss after the correction
two-thirds of patients with CS. The first such investiga- of hypercortisolism in patients affected by CS was previ-
tion evaluated unselected CS patients on the Michigan ously demonstrated (Bourdeau et al., 2002). Similarly,
Neuropsychological Test Battery (Whelan Schteingart, treatment of hypercortisolism is often efficacious in
Starkman, & Smith, 1980). This test battery included decreasing the depressive components of illness. Signifi-
standardized and objective measures with a broad range cant improvement in depressive symptoms was observed
of discrete language, verbal and nonverbal reasoning, when patients with CS were assessed by psychometric
auditory and visual memory, and sensory and motor methods before and after the treatment of their endo-
functions. The study revealed diffuse bilateral cerebral crine condition, (Dorn et al., 1997; Forget, Lacroix, &
dysfunction in CS with impairment in nonverbal, visual Cohen, 2002; Kelly et al., 1996; Starkman, Giordani,
ideational, visual-memory, and spatialconstructional Gebarski, & Schteingart, 2006; Starkman, Schteingart, &
abilities. Starkman, Schteingart, and Schork (1981) Schork, 1986). In a longitudinal study of depressive and
Cushings Syndrome C 761
neuropsychological symptoms in CS, Forget et al. (2002) References and Readings

reported a significant improvement in Beck Depression
Inventory scores 1 year after the correction of hypercorti- van Aken, M. O., Pereira, A. M., Biermasz, N. R., van Thiel, S. W.,
solism. More recently, Starkman et al. (2006) showed Hoftijzer, H. C., Smit, J. W. A., et al. (2005). Quality of life in patients
after long-term biochemical cure of Cushings disease. The Journal of
significant changes in depression and anxiety subscales C
Clinical Endocrinology and Metabolism, 90, 32793286.
on SCL-90-R after the successful treatment of hypercor- American Psychiatric Association. (1980). Diagnostic and statistical
tisolism in CS. However, psychological distress does not manual of mental disorders (3rd ed.). Washington, DC: American
always disappear upon proper treatment. For example, Psychiatric Association.
Dorn et al. (1997) disclosed that the incidence of atypical American Psychiatric Association. (1994). Diagnostic and statistical
manual of mental disorders (4th ed.). Washington, DC: American
depression progressively decreased after the correction of
Psychiatric Association.
hypercortisolism this disorder, however, continued to be Biller, B. M., Grossman, A. B., Stewart, P. M., et al. (2008). Treatment of
the prevailing psychiatric diagnosis after the successful adrenocorticotropin-dependent Cushings syndrome: A consensus
cure of CS. It is likely that the psychopathology symptoms statement. The Journal of Clinical Endocrinology and Metabolism,
still seen after the correction of CS may be related to the as 93, 24542462.
Bourdeau, I., Bard, C., Forget, H., Boulanger, Y., & Cohen, H., Lacroix, A.
yet unexplored interaction between endocrine and
(2005). Cognitive function and cerebral assessment in patients with
psychosocial factors. Indeed, despite the correction of Cushings syndrome. In J. W. Findling & H. Raff (Eds.), Cushings
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(Lindsay, Nansel, Baid, Gumowski, & Nieman, 2006; van Bourdeau, I., Bard, C., Noel, B., Leclerc, I., Cordeau, M. P., Belair, M.,
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in these patients (Heald et al., 2004). 19491954.
Few studies have objectively examined the reversibility Dorn, L. D., Burgess, E. S., Dubbert, B., Simpson, S. E., Friedman, T.,
of cognitive disorders after successful treatment. Mauri Kling, M., et al. (1995). Psychopathology in patients with endoge-
nous Cushings syndrome: Atypical or melancholic features.
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Clinical Endocrinology, 43, 433442.
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tor functions 6 months after surgery. No changes in other Chrousos, G. P. (1997). The longitudinal course of psychopathology
cognitive functions could be detected. On the other hand, in Cushings syndrome after correction of hypercortisolism. The
no differences between Cushings patients and their Journal of Clinical Endocrinology and Metabolism, 82, 912919.
Dorn, L. D., & Cerrone, P. (2000). Cognitive function in patients with
controls were found in cognitive function 12 months
Cushing syndrome. Clinical Nursing Research, 9, 420440.
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(2002) evaluated subjects who presented with CS on a pairment following surgical treatment of Cushings syndrome. Psy-
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Hudson, J. I., Hudson, M. S., Griffing, G. T., Melby, J. C., & Pope, H. G.,
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Kelly, W. F., Kelly, M. J., & Faragher, C. (1996). A prospective study

of psychiatric and psychological aspects of Cushings syndrome. Customized Job Retention
Clinical Endocrinology, 45, 715720.
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in Cushings syndrome as monitored by proton magnetic resonance
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Richmond, VA, USA
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Job retention is the process of facilitating the tenure of an
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McEwen, B. S., Weiss, J. M., & Schwartz, L. S. (1968). Selective retention job retention services begin with the completion of a thor-
of corticosterone by limbic structures in rat brain. Nature, 220, ough assessment to determine the individuals strengths,
911912. interests and preferences, and support needs. The results of
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guideline. The Journal of Clinical Endocrinology and Metabolism, including promoting consumer choice and involvement,
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earned, benefits, inclusion, and opportunities for career
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Clinical correlates of major depression in Cushings disease. Psycho- cant disabilities. Retention services may also include sup-
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Starkman, M. N., Gebarski, S. S., Berent, S., & Schteingart, D. E. (1992).
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756765. expectations and stressors associated with the respective
Starkman, M. N., Giordani, B., Gebarski, S. S., & Schteingart, D. E. position. Retention services must also ensure that the
(2006). Improvement in mood and ideation associated with increase
needs of the employer are understood and met.
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of the standard error, to place an education-altering
TX: Pro-Ed. label on that child. If such standards are not followed,
Wagner, C. C., Armstrong, A. J., Fraser, R. T., Vandergoot, D., & Thomas, then clinicians run the risk of basing a decision on a C
D. F. (2006). Evidence-based employment practices in vocational false-positive (the discovery of a limitation when none
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a limitation when one truly exists).
pay: Inclusive employment for people with disabilities. Baltimore, MD: To consider an example, a cutoff score may be the
Paul H. Brookes. score differentiating between intact performance and im-
pairment on a particular test. To speak in terms of diag-
nosing cognitive impairment, in a normal distribution of
scores, a cutoff score would be any score below 95% which
is obtained by the intact group within a particular stan-
Cut Scores dardization sample.
Clinicians may adjust cutoff scores because of individ-
Cut Off Scores, Cutting Scores ual or cultural variables that render the reliability of a
test nonapplicable to the individual or sample being
assessed. Otherwise, the clinician could run the risk of
pathologizing an individual who does not truly exhibit
the pathology.
Cut Off Scores, Cutting Scores

S ANDRA B ANKS References and Readings
Pittsburgh, PA, USA Nunnally, J. C., & Bernstein, I. H. (1994). Psychometric theory (3rd ed.).
Synonyms
Cut scores
CVA
Definition Stroke
Cutoff scores, also referred to as cutting scores, are scores

that differentiate the levels of performance.
CVLT
Current Knowledge California Verbal Learning Test (California Verbal

Learning Test-II)
The reliability of a measure is an essential factor to con-
sider when using cutoff scores. Nunnally and Bernstein
(1994) suggest that a test must have an internal consis-
tency coefficient of at least 0.90, and ideally above 0.95, to
designate a particular score as a diagnostic cutoff point, CVLT-C
although this might be a high standard. For instance, if a
child is demonstrating a learning disorder, the tests used California Verbal Learning Test Childrens Version
764 C Cyst
major role in drug metabolism and is the cause for some

Cyst adverse drug reactions. Metabolism and clearance of a
drug are presumed to be stable, allowing for basic predic-
E THAN M OITRA tions about a drugs dose, blood levels, and pharmacolog-
Drexel University ical effects. Drugs are typically metabolized by a limited
Philadelphia, PA, USA number of mechanisms, some of these include the P450
enzyme pathways. Drugs, foods, or herbal preparations
that alter the efficiency of those pathways may also alter
Synonyms the plasma concentration of some drugs by inhibiting
or inducing (increasing) the efficiency of a particular
Nodule; Polyp enzymatic pathway. There are drugs/herbs that can simul-
taneously induce and inhibit different isoenzymes
(St. Johns Wort), or simply induce their own metabolism
Definition (carbamazepine).
Although over the counter preparations are less likely
Cyst refers to an abnormal growth of benign cells, typically to be mentioned, some effect P450 enzyme pathways (e.g.,
containing normal cerebrospinal fluid. Central nervous cigarettes or the topical antifungal ketoconazole). Smo-
system cysts may occur as neoplasms or subsequent to kers, for example, may require increased doses of drugs
leptomeningitis, hemorrhage, or surgery. Most patients because cigarette smoking has the ability to induce an
presenting with cyst are asymptomatic, though headache; enzyme that deactivates some medication. As a corollary,
calvarial bulging; intracranial hypertension; craniome- an abrupt cessation of smoking would then increase the
galy; developmental delay; visual loss; precocious puberty; plasma level of these drugs unless and until the dose is
and seizures, with focal neurologic signs can occur. Addi- modified.
tional cognitive consequences may include symptoms of P450 isoenzymes are widely distributed, but often
dementia and inattention. Arachnoid cysts represent the thought of as liver enzymes because the liver metabolizes
most common form of benign cyst and occur in the drugs through oxidation as well as reduction and hydro-
cerebrospinal axis. Size of arachnoid cysts is not directly lysis. The p450 cytochrome system is critical to a number
affected by changes in the ventricular system. of oxidative reactions (the addition of an oxygen molecule
or the removal of hydrogen from a molecule). The P450
Cross References isoenzymes share a heme (iron) cofactor, although they
may use a number of different molecules as a basis for
Neoplasm enzyme reactions. The term cytochrome arose because the
isoenzymes were differentiated by their cellular (cyto)
location and their color (chrome) or wavelength during
spectrophotometric studies. P450 enzymes absorb light at
Cytochrome P450 450 nm. Specific CYP enzyme pathways are noted in
shorthand (e.g., CYP3A4 or CYP 2D6). Typically, authors
N ADIA W EBB include the prefix CYP before a three character alphanu-
Childrens Hospital of New Orleans meric 3A4, but it may be abandoned if the author is
New Orleans, LA, USA writing casually or for an audience familiar with the
terms. The alphanumeric denotes the gene family, sub-
family, and individual gene. The three most common
Synonyms isoenzymes involved in human drug metabolism are
CYP3A4, CYP2D6, and CYP2C9.
P450 isoforms; P450 isoenzymes; P450 system
Definition Cross References
The liver-mediated cytochrome P450 isoenzymes (abbre- Cmax

viated as CYP) constitute an enzyme family that plays a p450 Cytochrome System
Cytotoxic Edema C 765
Pharmacokinetics Stahl, S. M. (2008). Stahls essential psychopharmacology: Neuroscientific

basis and practical applications. New York: Cambridge University
Side Effects
Press.
References and Readings C

Brunton, L. B., Lazo, J. S., & Parker, K. L. (Eds.). (2005). Goodman &
Cytotoxic Edema
Gilmans the pharmacological basis of therapeutics (11th ed.).
New York: McGraw Hill. Cerebral Edema
D
Professor (University of Iowa, Iowa City, IA, 1980
DAD 2005)
President (Academy of Aphasia, 1983)
Disability Assessment for Dementia President (Behavioral Neurology Society, 1985)
Adjunct Professor (The Salk Institute for Biological
Studies, La Jolla, CA, 1989-present)
David Dornsife Professor of Neuroscience (University
DAFS of Southern California, Los Angeles, CA, 2005present)
Director, Brain and Creativity Institute (University of
Direct Assessment of Functional Status
Southern California, Los Angeles, CA, 2006Present)
Selected Honors and Awards

DAI
Sandoz Prize in Neurology (Portuguese Society of
Diffuse Axonal Injury Neurology, 1971, 1973, 1974)
William Beaumont Prize (American Medical Associa-
tion, 1990)
European Academy of Arts and Sciences (Elected 1993)
Damasio, Antonio R. (1944 ) Institute of Medicine of the National Academy of
Sciences (Elected 1994)
J OHN RYAN , T RICIA Z. K ING American Academy of Arts and Sciences (Elected 1997)
Georgia State University Bavarian Academy of Sciences (Elected 2002)
Atlanta, GA, USA Signoret Prize in Cognitive Neuroscience (shared with
Hanna Damasio, 2004)
Prince of Asturias Award for Scientific and Technical
Education and Training Research (2005)
University of Lisbon Medical School, Portugal

(M.D.; 1969) Landmark Clinical, Scientific, and
Aphasia Research Center (Research Fellowship with Nor- Professional Contributions
man Geschwind; 1967)
University of Lisbon, Portugal (Ph.D.; 1974) Antonio Damasio is a prominent neurologist, neuro-
University Hospital, Lisbon, Portugal (Residency in scientist, and author. His research investigating the
Neurology, 19701972) relations between brain damage and functioning has
had a major influence on both Psychology and Philos-
ophy, especially in the domains of emotion and deci-
Major Appointments sion-making. He has made major contributions in the
areas of language, memory, and perception as well. His
Language Research Laboratory (Center de Estudos Somatic Marker Hypothesis posits that emotional
Egas Moniz, Lisbon, Portugal, 19711975) states actually occurring in the body or simulated in
Chief, Division of Behavioral Neurology & Cognitive the brain can influence decision-making.
Neuroscience (Department of Neurology, University As a neuropsychologist, Damasios work has spanned
of Iowa, Iowa City, IA, 19772005) numerous domains. Early in his career, his primary
768 D Damasio, Antonio R. (1944 )
focus was on the relation between the brain and lan- Short Biography
guage, but his interests expanded to include memory,
perception, and autism in the 1980s. By the late 1980s, Antonio Damasio was born in Lisbon, Portugal in 1944.
his research focused on how brain injuries can teach He attended the University of Lisbon Medical School,
about how concepts and categories are stored in the and received his M.D. in 1969 followed by his Ph.D. in
brain. He proposed a neural architecture for learning 1974 from the University of Lisbon. In 1967, he studied
and recall based on convergence/divergence of signals with Norman Geschwind at the Aphasia Research
from critical nodes called convergencedivergence Center (Boston, MA) and later returned to America in
zones. Throughout his career, he has focused primar- 1975 when he became an Assistant Professor at the
ily on the study of how brain damage affects psycho- University of Iowa, earning the distinction of Full
logical functioning, thereby inferring how the healthy Professor in 1980. His association with the Salk Institute
brain operates. began in the 1980s. He remained at the University of
Damasios largest influence has been his theories on Iowa until 2005 when he moved to the University of
emotion and decision-making. Before 1995, the Southern California as the director of the Brain and
study of judgment and decision-making rarely or Creativity Institute, and Professor of Psychology,
tangentially considered how emotion could influ- Neuroscience, and Neurology.
ence behavior. In Descartes Error, Damasio advanced
the hypothesis that not only could emotion aid
reason in decision-making, but reason itself evolved
Cross References
from emotion and the two remain critically
interconnected. Central to Damasios theory is the
Geschwind, Norman (19261984)
Somatic Marker Hypothesis, which proposes that,
when making decisions, options are marked either
negatively or positively, consciously or unconscious-
ly, thus deterring an individual from making a nega- References and Readings
tive choice or, on the contrary, promoting a positive
choice. Damasio, A. R. (1989a). Time-locked multiregional retroactivation:
In the years since this revolutionary idea, numerous A systems level proposal for the neural substrates of recall and
recognition. Cognition, 33, 2562.
studies have lent support to the idea that emotion and Damasio, A. R. (1989b). The brain binds entities and events by multire-
reason are interdependent. These studies have includ- gional activation from convergence zones. Neural Computation, 1,
ed patients with ventromedial prefrontal damage who 123132.
are unable to monitor visceral states and, as a result, Damasio, A. R. (1996). The somatic marker hypothesis and the possible
functions of the prefrontal cortex. Transactions of the Royal Society
make poor decisions. The Somatic Marker Hypothesis,
(London), 351, 14131420.
however, has not been immune to criticism. Recently, Damasio, A. R. (1999, 2000). The feeling of what happens: Body and
these criticisms have focused on the extensive reliance emotion in the making of consciousness. New York: Harcourt.
of the hypothesis on the Iowa Gambling Task and Damasio, A. R. (2003). Looking for Spinoza: Joy, sorrow and the feeling
sometimes-conflicting evidence from other labora- brain. New York: Harcourt.
Damasio, A. R. (2005). Descartes error: 10th anniversary edition, with a
tories regarding the mediational role of the ventrome-
new author preface. New York: Penguin Books.
dial prefrontal cortices. Damasio, A. R., Grabowski, T. J., Bechara, A., Damasio, H., Ponto, L. L.
Since the publication of Descartes Error, Damasio has B., Parvizi, J., et al. (2000). Subcortical and cortical brain activity
extended his work on emotion to include research and during the feeling of self-generated emotions. Nature Neuroscience,
philosophy on the nature of feelings, morality, and 3, 10491056.
Damasio, A. R., & Meyer, K. (2008a). Behind the looking-glass. Nature,
consciousness. He has proposed that, in addition to
454, 167168.
mapping representations of the external world and Damasio, A. R., & Meyer, K. (2008b). Consciousness: An overview of the
internal states, regions such as the posterior cingulate phenomenon and of its possible neural basis. In S. Laureys &
cortex and related cortices (the postero-medial corti- G. Tononi (Eds.), The neurology of consciousness. Oxford: Elsevier.
ces) create a second-order representation which Dunn, B. D., Dalgleish, T., & Lawrence, A. D. (2006). The somatic marker
hypothesis: A critical evaluation. Neuroscience and Biobehavioral
allows an organism to develop a sense of self. These
Reviews, 30, 239271.
studies have begun to form a bridge between neuro- Gluck, A. (2007). Damasios error and descartes truth: An inquiry into
psychology and philosophy, posing testable hypoth- consciousness, metaphysics, and epistemology. Scranton, PA: Universi-
eses regarding metacognition. ty of Scranton Press.
Daubert v. Merrell Dow Pharmaceuticals (1993) D 769
amphetamine abuse include possible neurotoxic damage

D-Amphetamine to the dopamine system with reduced numbers of trans-
porters and receptors. Impairments in attention and mem-
J OANN T. T SCHANZ 1, K ATHERINE T REIBER 1,2 ory have been reported with abuse (Iversen et al., 2009).
1
Logan, UT, USA
2
University of Massachusetts Medical School Cross References
Worcester, MA, USA
D
Amphetamine
Synonyms References and Readings

Dextroamphetamine; Dexedrine Feldman, R. S., Meyer, J. S., & Quenzer, L. F. (1997). Stimulants:
Amphetamine and Cocaine. In Principles of neuropsychoparhmacology
(pp. 549568). Sunderland, MA: Sinauer.
Definition Iversen, L. L., Iversen, S. D., Bloom, F. E., & Roth, R. H. (2009). Psychos-
timulants. In Introduction to neuropsychopharmacology (pp. 447472).
Dextroamphetamine (D-amphetamine) is one of two New York: Oxford University Press.
chemical forms of the synthetic stimulant amphetamine,
and is a potent central nervous system stimulant that
increases the release and blocks the reuptake of the mono-
aminergic neurotransmitters, dopamine, norepinephrine,
Dance-like
and serotonin. Acute administration of the stimulant is
Chorea
associated with increased alertness, confidence, euphoria,
and cognition. In animals, there is a dose-dependent effect
of increasing activity such as locomotion and at higher
doses, stereotyped motor behaviors. D-amphetamines
reinforcing properties and potential for abuse are thought
DAS-II
to reflect increased dopamine neurotransmission in the
Differential Ability Scales (DAS and DAS-II)
nucleus accumbens. The drug also increases both systolic
and diastolic blood pressure and increases respiration and
heart rate, among other autonomic nervous system effects
(Feldman, Meyer, & Quenzer, 1997; Iversen, Iversen, Daubert v. Merrell Dow
Bloom, & Roth, 2009).
Pharmaceuticals (1993)
Current Knowledge R OBERT L. H EILBRONNER
Although historically, D-amphetamine has had clinical Chicago, IL, USA
uses for narcolepsy, as an appetite suppressant, and cog-
nitive enhancer, much has been written of its addictive
properties. As with other drugs of abuse, dependence and Definition
tolerance can develop with chronic use, resulting in the
administration of increasing doses to achieve the desired This case involved two persons, Jason Daubert and Eric
effects. Repetitive, stereotyped behaviors may emerge with Schuller, who had been born with severe birth defects.
sustained use. With chronic abuse, a psychotic syndrome Along with their parents, they sued Merrell Dow Pharma-
resembling the symptoms of paranoid schizophrenia may ceutical Inc., based on the claim that the drug Bendectin
emerge. Although some differences between amphet- had caused their birth defects. Merrell Dow had the case
amine-induced psychosis and schizophrenia have been placed in federal court and moved for summary judgment
identified, this observation has provided some support due to the fact that their expert witness provided
for the dopamine hypothesis of schizophrenia (Iversen documents indicating that no published scientific study
et al., 2009). Other negative effects of chronic existed to provide support for a causal relationship
770 D DCT
between Bendectin and birth defects. By contrast, Daubert Cross References

and Schuller provided their own expert evidence which
indicated that Bendectin could indeed lead to birth defects. Admissibility
This expert testimony was based primarily on in vitro and Chapple v. Ganger
in vivo animal studies, pharmaceutical studies, and a re- Joiner v. General Electric (1997)
analysis of already published studies. However, because Kumho Tire v. Carmichael
such methodologies had not garnered acceptance within
the scientific community, the court awarded summary References and Readings
judgment to Merrell Dow. Daubert and Schuller appealed
the decision to the Ninth Circuit Court. The Court deemed Chapple vs. Ganger, 851 F. Supp. 1481, E.D. of Washington, (1998).
that the district court had correctly granted summary Daubert vs. Merrell Dow, 509, U.S. 579 (1993).
judgment since the plaintiffs evidence was not deemed Frye v. U.S. D.C. Cir., 293 F. 1013 (1923).
as utilizing reliable methodologies as determined by the Greiffenstein, M. F., & Cohen, L. (2005). Neuropsychology and the law:
Principles of productive attorney Neuropsychologist relations.
scientific community. Additionally, it appeared as if the
In G. Larrabee (Ed.), Forensic neuropsychology: A scientific approach.
evidence produced by the plaintiff seemed to be created New York: Oxford University Press.
only for the purpose of litigation. The case was reviewed by Joiner v. General Electric, 522 U.S. 136 (1997).
the U.S. Supreme Court who determined that the Federal Kumho Tire v. Carmichael 526 U.S. 137 (1999).
Rules of Evidence (FRE) govern the admissibility of scien- Reed, J. E. (1996). Fixed versus flexible neuropsychological test batteries
under the Daubert standard for admissibility of scientific evidence.
tific evidence presented in federal court. Moreover, it was
Behavioral Sciences and the Law, 14, 315322.
decided that the judge is to act as the gatekeeper prior to
admitting evidence in order to ensure that the evidence is
scientifically valid and relevant to the particular case. The
court provided certain criteria to make determinations DCT
regarding the scientific validity of information presented.
For example, the guidelines include: falsifiability (has the Dot Counting Test
methodology been tested), peer review (has the methodol-
ogy been subjected to peer-review process), acceptable
error rate, general acceptance of methods or principles, De Renzi, Ennio (1924 )
technical manual/guide for use of instrument, etc.
M ICHELLE P ROSJE
Current Knowledge Gainesville, FL, USA
The decision in the Daubert case has created some

controversy within the field of psychology in general Major Appointments
and forensic neuropsychology more specifically. Most
notably, Reed (1996) viewed the Daubert ruling as Fellowship (School of Medicine, University of Pavia,
implying that only fixed battery, commercially acceptable, 19531956)
neuropsychological batteries may be admissible. Given Faculty (Department of Nervous and Mental Diseases,
that most neuropsychologists employ a flexible battery University of Modena, 19561957)
approach, this created unrest among the neuropsycholog- Faculty (University of Milan, 19581969)
ical community. However, many have challenged Reeds Professor of Neurology (University of Trieste, 1969
interpretation of the Daubert case and subsequent rulings 1971)
(e.g., Chapple v. Ganger) have deemed neuropsycholog- Chair of Nervous and Mental Diseases (School of
ical data based on flexible batteries as admissible. Chal- Medicine, University of Trieste, 19691971)
lenges to scientific information relayed by expert Professor of Neurology (University of Milan, 1971
witnesses are referred to as Daubert or Frye and such 1974)
hearings are held in limine, or away from the jury. Specifi- Professor and Head (Department of Neurology, Uni-
cally, the judge listens to the pros and cons of the scientific versity of Modena, 19742002)
evidence and the attorneys usually argue for or against Honorary Visiting Professor (University of Aberdeen,
admissibility of a specific test or conclusion. 1996)
De Renzi, Ennio (1924 ) D 771
Major Honors and Awards De Renzis initial studies on aphasia were conducted in
collaboration with Luigi A. Vignolo and took Gesch-
President of the European Brain and Behavior Society winds model into consideration. Vignolo had com-
(19731974) pleted a thesis on aphasia and had considerable
Carlo Riquier Award (University of Pavia, 1988) training in language and its disorders. De Renzi and
Honorary Degree in Psychology (University La Vignolo garnered the assistance of a local mime group
Sapienza of Rome, 1993) to study the potential role of nonverbal information in D
Member of the Academia Europea (1994) the aphasics comprehension deficit (De Renzi, 1998).
Honorary Member of the American Neurological The group presented short sketches miming everyday
Association (1995) actions (e.g., hammering a nail). In support of their
Honorary Member of the Academy of Neurology original impairment hypothesis, De Renzi and Vig-
(1995) nolo found that aphasics demonstrated significant
Honorary Member of the British Neuropsychological comprehension deficits. For the Seventh International
Society (1996) Congress of Neurology, they submitted a presentation
Professor Emeritus (University of Modena, 2002) about the aphasics impairment hypothesis including
Member by Election, Academy of Aphasia their recent findings about comprehension dysfunc-
Member of Research Group on Aphasia of the World tion. Arthur L. Benton reviewed their manuscript,
Federation of Neurology providing encouragement and prompting them to
Member of International Neuropsychological Symposia contemplate the behavior of normal subjects. This
first contact with Benton soon evolved into a lifelong
mentorship and friendship for De Renzi. Benton not
Landmark Clinical, Scientific, and only shared knowledge and presented lectures, but
Professional Contributions also pushed De Renzi to develop strong methodologi-
cal discipline during his time in Iowa City as a Fullb-
Ennio De Renzis fame stems from his heartfelt devo- right Professor. Bentons influence became evident
tion to establishing neuropsychology as a scientific during the 1960s and 1970s when De Renzi began to
discipline in Italy. One of the most influential postwar shift his focus from examining small groups of select-
neuropsychologists (Milner, 1997), De Renzi contrib- ed patients to studying unselected clinical cases.
uted greatly to the understanding of a broad range of Vignolo and De Renzi, together with other members of
neurological phenomena, including aphasia, apraxia, an interdisciplinary group which originally included
agnosia, topographical amnesia, and disorders of lan- such well-known scientists as Henry Hecaen, Hans Teu-
guage, spatial cognition, and memory. His seminal ber, and Clemens Faust, met to discuss various neuro-
works in these areas, particularly hemispheric special- logical phenomena, namely aphasia, constructional
ization and neuropsychological deficits in patients apraxia, alexia, cerebral dominance, effects of unilateral
with localized brain lesions, were ahead of his time. versus bilateral lesions, and disorders of time sense and
His insatiable exploration into unchartered neurolog- body schema. In 1962, the efforts of De Renzi, Vignolo,
ical and psychological territories spanned more than Brenda Milner, Klaus Poeck, and Oliver Zangwill
40 years and prompted further neuropsychological renewed the group that formally adopted the name of
research. the International Neuropsychological Symposium
During his early years studying neurology and psychi- (Stringer & Cooley, 2002). Also in 1962, De Renzi
atry, De Renzi worked closely with Professor Gildo and Vignolo collaborated on a paper about the
Gastaldi from the University of Pavia at two psychiat- Token Test, which has been one of De Renzis most
ric and two neurological wards. Gastaldi ultimately influential works.
asked De Renzi to join his group in the Department of During the early 1960s, establishing research proto-
Nervous and Mental Disease at the University of cols was challenging in light of scarce grant funding.
Modena. A few years later when Gastaldi accepted a De Renzi put forth great effort to assemble a group of
new position and moved to Milan to become the colleagues willing to devote countless hours in ex-
Chair of Nervous and Mental Disease, De Renzi fol- change for name recognition on papers. This group
lowed in Gastaldis footsteps, subsequently deciding came to be known as the Milan Group and consisted
to put aside his interest in psychiatry and devote of Vignolo, Pietro Faglioni, Hans Spinnler, and Anna
himself entirely to neurology. Basso. Piero Faglioni, an Italian neurologist with a
772 D De Renzi, Ennio (1924 )
passion and expertise for statistical analysis, played a 1969, De Renzi was called to hold the Chair of Ner-
principal role in influencing De Renzis approach to vous and Mental Diseases by the School of Medicine
experimental design. De Renzis application of clinical at the University of Trieste.
cases and appropriate methodology fostered inferen- Following his tenure in Milan and Gastaldis death in
tial thinking about his patients with unilateral hemi- 1973, De Renzi accepted a position as Chair of Ner-
spheric damage and consequently prompted vous and Mental Diseases in Modena. He acted as
examination of the interplay between specialization/ chief of a department with 70 neurological beds and
asymmetry and anteriorposterior lesion location. 40 psychiatric beds. In 1982, De Renzi published his
In 1964, one year after Henry Hecaen established the influential book Disorders of Space Exploration and
journal Neuropsychologia, De Renzi founded Cortex. Cognition, a book that remains a cornerstone in the
Cortex was created as an international journal devoted field of neuropsychology, with particularly rich insight
not only to the anatomy of the central nervous system, into perceptual and visuomotor disorders. He elo-
but more so to a focus on cognition and the relation quently and perceptively combined pertinent animal
between the central nervous system and mentation. Of research with detailed discussions of human neuropsy-
particular interest was the behavior of patients, includ- chological research in his book.
ing children, with acquired brain lesions versus normal Over the span of his 50-year devotion to neuropsy-
controls. In addition, the journal sought to provide chology, De Renzi has published on a broad range of
insight into the use of functional neuroimaging tech- topics. He distinguished four levels in the processing of
niques to record brain activity. De Renzi noted that the spatial information, including exploration, percep-
only way to subject ones research to a broader audition, memory, and conceptualization. He described
ence and to contribute to the field was to publish in the phenomena of constructional apraxia, hand and
international journals rather than burying (it) in eye forced deviation, and disorders of space percep-
Italian journals (2006). With the birth of this journal, tion. De Renzi and his group examined hemispatial
De Renzi embarked on a challenging mission to ac- neglect and developed a purely acoustic test for audi-
quire not only the English language, but also a specific tory neglect. He also directed attention toward agno-
manner in which to report statistical data. The first sia. Along with Faglioni and Spinnler, De Renzi
editorial board of the journal included numerous devised a strategy to tackle recognition disorders by
prominent intellectual critics of the time, namely, Ar- investigating each hemispheres contribution to visual
thur Benton, George Ettlinger, Norman Geschwind, information processing. As technology advanced, De
Harold Goodglass, and Klaus Poeck. Gastaldi, one of Renzi utilized computed tomography scans to enhance
De Renzis early teachers, was the editor in chief. When his research. From prosopagnosia and Balints syn-
Gastaldi died in 1973, De Renzi assumed the role of drome to memory disorders and frontal signs, De
editor in chief and actively held this position until Renzis extensive research agenda contributed much
2000 when Sergio Della Sala succeeded him. to the field of neuropsychology as it is know today. In
During the 1960s, the European Brain and Behavior fact, he more recently examined the anatomy of dis-
Society was formed, whose aim was to provide an orders in depth perception (Turnbull, Driver, &
opportunity for international scientists to assemble to McCarthy, 2004) and focused on tactile agnosia as
share interests and beliefs about the biological founda- his final area of research.
tions of behavior. De Renzi actively participated in the De Renzi has considered himself primarily as a clinician
preliminary discussions to create the society and was who engages in research and teaching not only for self-
nominated as president for 19711973. In 1969, the edification, but also to shed light on the patients con-
Italian Society of Neurologys invitation to De Renzi ditions and optimal interventions. De Renzi believed
to present about hemispheric dominance represented that the pure essence of neuropsychology dwells in the
a momentous shift in the field. At the meeting, De Renzi interface of the patients treatment, research protocols,
reviewed his findings from the previous 6 years of and teaching. I always felt the opportunity to shift
research on a wide range of neuropsychological topics. from patient examinations to research and teaching,
At this time, neuropsychology seemed to be gaining in far from causing loss of concentration and dissipation
popularity as young students became impressed with of energy, is an asset because it keeps your mind open
neuropsychology, and an increasing number of psycho- and inquisitive on a wide range of practical and theo-
logical and neurophysiological departments were retical aspects of reality and can be immensely gratify-
emerging around the world (De Renzi, 1998). In ing (De Renzi, 1998).
Deaf D 773
Short Biography stage of his life. He commented that he sees his life as
positive and gratifying in that his interest and curiosity
Ennio De Renzi was born in the agricultural hub of about culture have enriched every day on earth, and he
Cremona, Italy on December 18, 1924. The atmosphere has led both the family and career life he has desired (De
in Italy during the first 20 years of his life was filled Renzi, 1998).
with fascist propaganda and devoid of any freedoms or
liberties. As such, De Renzi noted it was repressive, D
untruthful, and boring (De Renzi, 1998). His maternal Cross References
grandfather played a large role during De Renzis early
years, prompting him to devour as many books as Agnosia
possible. As a voracious reader during his school Anomic Aphasia
years, De Renzi learned to read literature in the original Apraxia
languages of French and German. Fortunately, De Arthur L. Benton
Renzis book knowledge flourished at a time when he Balints Syndrome
was required to relocate to 14 different cities during the Hemispatial Neglect
first 17 years of his life due to his fathers military Hemispheric Specialization
career. Unfortunately, he had significant difficulties Prosopagnosia
establishing strong interpersonal relationships with
classmates and teachers.
Interestingly, De Renzi had no interest in the
sciences during secondary school. So, he decided to
De Renzi, E. (1996). Balint-Holmes syndrome. In C. Code (Ed.), Classic
study law at the university. Patriotic propaganda
cases in neuropsychology (pp. 123144). New York, NY: Psychology.
permeated the political climate at that time while De Renzi, E. (1998). Ennio De Renzi. In L. R. Squire (Ed.), The history of
underneath the country was struggling. De Renzi noted neuroscience in autobiography (Vol. 5, pp. 227269). The Society for
that after the Nazi occupation of Italy and his attempt to Neuroscience. http://www.sfn.org/skins/main/pdf/history_of_neur-
locate a niche in the free part of the country, he enlisted oscience/hon_vol_5/c5.pdf. Retrieved 19 June 2009.
De Renzi, E. (1999). Agnosia. In G. Denes & L. Pizzamiglio (Eds.),
as a private and served alongside his father as a colonel
Handbook of clinical and experimental neuropsychology (pp. 371408).
in the Italian army (1998). Even though he had already New York, NY: Psychology.
passed seven law examinations, De Renzi was drawn to De Renzi, E. (2000). Prosopagnosia. In M. J. Farah & T. E. Feinberg
medicine, particularly during wartime turmoil. After (Eds.), Patient-based approaches to cognitive neuroscience (pp. 8595).
reading a book about brain functioning, he became Cambridge, MA: MIT.
De Renzi, E., Cavalleri, F., & Facchini, S. (1996). Imitation and utilization
fascinated with the workings of the mind and decided
behavior. Journal of Neurology, Neurosurgery, and Psychiatry, 61,
to abandon law, take his medical entrance exams, and 396400.
forge ahead into the field of medicine. In 1945, he De Renzi, E., Lucchelli, F., Muggia, S., & Spinnler, H. (1997). Is memory
accepted a position at the Ghislieri College in Pavia, loss without anatomical damage tantamount to a psychogenic deficit?
Italy. This institution was one of the few that offered The case of pure retrograde amnesia. Neuropsychologia, 35(6), 781794.
Milner, A. D. (1997). Ennio De Renzi. In N. Sheehy, A. J. Chapman,
deserving students from less-affluent families the oppor-
& W. Conroy (Eds.), Biographical dictionary of psychology
tunity for a university education free of charge. And (pp. 137138). New York, NY: Routledge.
so began his odyssey into the field of neurology and Stringer, A. Y., & Cooley, E. L. (2002). Neuropsychology: a twentieth-
ultimately neuropsychology. century science. In A. Y. Stringer, E. L. Cooley, & A.-L. Christenson
From his early childhood years, De Renzi sought to (Eds.), Pathways to prominence in neuropsychology: reflections of
twentieth- century pioneers (pp. 326). New York, NY: Psychology.
broaden his cultural horizons. As a youngster, he avidly
Tesak, J., & Code, C. (2008). Milestones in the history of aphasia: Theories
read literature from various countries. During college, and protagonists. New York, NY: Psychology.
he desired to interact with friends from different regions Turnbull, O. H., Driver, J., & McCarthy, R. A. (2004). 2D but not 3D:
of the world. He established the international journal, Pictorial-depth deficits in a case of visual agnosia. Cortex, 40, 723738.
Cortex, to facilitate international communication and
dissemination of knowledge. De Renzi firmly believed
that visiting foreign cities and spending time with collea-
gues around the world were added bonuses to his profes- Deaf
sion. He gleaned intimate knowledge about other places
and expanded his cultural horizons throughout every Deaf/Hearing Impairment
774 D Deaf/Hearing Impairment
intensities (measured by decibels). Audiologists classify

Deaf/Hearing Impairment hearing loss as normal (015 db loss), mild (2540 db
loss), moderate (4155 db loss), moderately severe (5670
D EBORAH W ITSKEN db loss), severe (7190 db), or profound (>90 db). Degree
University of Northern Colorado of hearing loss may also be delineated based on functional
Greeley, CO, USA descriptions of the hearing loss impact (e.g., those
with mild hearing loss may be able to communicate using
the telephone whereas those with a profound hearing loss
Synonyms often cannot understand spoken language via telephone).
Deaf; Hard of hearing; Hearing impaired; Hearing loss

Epidemiology
Short Description or Definition The World Health Organization (2005) estimates indicate
278 million people worldwide have moderate to profound
Medical definitions of deafness refer to impairment in the hearing loss in both ears. Eighty percent of individuals
physical structures necessary for hearing and understand- with hearing loss live in low- and middle-income
ing language. The term deaf refers to a degree of hearing countries. Men are more likely to experience hearing
loss that significantly impacts access to auditory language; loss than women. The majority of individuals experien-
hard of hearing typically refers to hearing loss that still cing hearing loss are over 30 years old. In the United
allows for some access to auditory information. Medical States, although estimates vary, most indicate that one
and functional definitions of deafness do not necessarily to six per 1,000 babies are born with severe to profound
correspond with an individuals cultural identity. The congenital hearing loss (ASHA, 2009).
cultural definition (commonly indicated by the capita- The most common cause of conductive hearing loss is
lized term Deaf ) refers to individuals who reject the chronic otitis media. Causes of sensorineural hearing loss
medical notion that deafness represents impairment per include genetics, premature birth, anoxia, maternal rubella
se and identify with a community of individuals that share during pregnancy, use of ototoxic drugs, infectious dis-
common experiences, a rich cultural heritage, and a eases (e.g., meningitis, measles, mumps), head injury,
shared language sign language (Lane et al., 1996). foreign bodies blocking or damaging the ear canal, and
prolonged exposure to excessive noise.
Categorization
Hearing is commonly defined according to where the Outcomes
problem occurs and the degree of hearing loss. Conduc-
tive hearing impairment refers to problems occurring in The impact of hearing loss varies widely depending on the
the outer or middle ear, which are commonly medically or cause, level, and type of hearing impairment and the age of
surgically treatable (i.e., otitis media). Sensorineural onset. Onset prior to the development of speech and language
hearing impairment typically refers to a failure in the is associated with greater difficulties with language acquisi-
cochleas ability to translate mechanical energy produced tion, academic achievement, and social and occupational
by the middle ear into neural impulses sent to the eigth functioning. Research indicates that early identification of
nerve. Mixed hearing loss refers to simultaneous occur- hearing loss and intervention yields significant benefits on
rence of both difficulties. Conductive and sensorineural language, academics, and social-emotional development
hearing losses are differentiated from various types of (Calderon & Naidu, 2000; Yoshinaga-Itano, Sedey, Coulter,
central hearing loss, often referred to as cortical deafness, & Mehl, 1998). With the adoption of newborn infant
which refers to impairment in the ability to interpret hearing screening procedures, many children are identi-
sounds despite adequate functional mechanisms for fied with hearing loss in the first months of life, compared
hearing (e.g., pure word deafness, auditory agnosia). to an average age of 18 months prior to universal screen-
Degree of hearing loss is typically defined by ones ings (Mertens, Sass-Lehrer, & Scott-Olson, 2000).
ability to perceive sounds of different frequencies Full access to language has a significant impact on
(measured by hertz or cycles per second) and at different predicted outcomes. Research has indicated that reading
Deaf/Hearing Impairment D 775
levels of deaf and hard of hearing high school graduates lobes are activated in individuals using sign language and
have traditionally hovered around the 4th grade level those relying on spoken language. However, in native sign
while deaf undergraduate college students with deaf par- language users, there is additional activation in the right-
ents read on average at 11th grade level (Hauser, 2001; hemisphere superior temporal and inferior parietal
Traxler, 2000). Recognizing the importance of communi- regions (Newman, Bavelier, Corina, Jezzard, & Neville,
cation, many families struggle to determine the most 2002). Other subtle differences in cognitive organization
appropriate method for augmenting hearing and have been found among individuals with hearing loss D
providing access to communication whether in English who prefer to communicate using sign language, including
and/or through a signed language. No single solution has improved peripheral visual attention, mental rotation,
emerged as panacea for all individuals with hearing loss. image generation, and face processing (for review, see Hau-
Regardless of communication modality, positive parent ser, Wills, & Isquith, 2006; Marscharck & Hauser, 2009).
child interaction has been identified as a predictor of the Despite these subtle differences, research has indicated
childs linguistic development (Calderon & Naidu, 2000; that when assessed nonverbally by an evaluator familiar
Pressman, Pipp-Siegel, Yoshinaga-Itano, & Deas, 1999). with their preferred communication mode, individuals
Research indicating that over 90% of children who are who are deaf and hard of hearing perform similarly to
deaf have parents who are hearing highlights the common hearing peers on standardized, nonverbally administered
struggle experienced by many families to find a suitable intelligence tests (Braden, 1994; Maller, 2003).
communication system (Mitchell & Karchmer, 2002). Considerable controversy exists regarding whether
Struggles with literacy secondary to limited access to there exists a psychology of deafness, that is, whether
spoken English often translate into career challenges. Un- there are certain traits that are uniquely associated with
fortunately, compared to hearing peers, unemployment individuals who are deaf or hard of hearing (Paul &
rates are higher for individuals who are deaf and hard of Jackson, 1993). Others suggest that this viewpoint repre-
hearing and large numbers receive Supplemental Security sents a culturally biased perspective (Lane, 1988). Some
Disability Insurance (SSDI) (Danek & Busby, 1999). researchers have suggested that there may be indirect
However, the employment challenges of individuals with developmental consequences of growing up with hearing
hearing loss are not significantly different from other loss in a world that relies heavily on auditory input
individuals with disabilities. For example, there is no (Hauser et al., 2006). Compared to same-age hearing
difference in the probability of employment between peers, individuals who are deaf and hard of hearing may
youth with learning disabilities and those with hearing be more likely to be exposed to risk factors that can
loss (Wagner, Newman, Cameto, Garza, & Levine, 2005). contribute to developmental and behavioral challenges.
Notably, these group means may overshadow the satisfac- These factors may include academic difficulties, low self-
tory quality of life attained by many individuals who are esteem, inconsistent discipline, and sexual/physical abuse
deaf and hard of hearing, many of whom attain successful (Black & Glickman, 2005; Simeonsson, Wax, & White,
careers in areas such as education, psychology, neuropsy- 2001). Although children with hearing loss develop
chology, medicine, and law. Advances in technology and attachments to caregivers similarly to their peers, the
legal precedent established through the Americans with diagnosis of a childs hearing loss may impact parents
Disability Act continue to broaden opportunities avail- attachment to their child and contribute to difficult
able to individuals who are deaf and hard of hearing. parentchild interactions (Meadow-Orlans, 1990).
Children who have not developed adequate language
and communication skills regardless of modality are
Neuropsychology and Psychology more likely to demonstrate difficulties with self-regula-
of Deafness/Hearing Loss tion and social skills (Rhine-Kahlback, 2004). Findings of
greater prevalence of psychopathology among individuals
Neuropsychologists should be cognizant that many causes with hearing loss are controversial and may reflect meth-
of hearing loss, particularly nongenetic causes, are com- odological flaws. Greater rates of psychopathology may
monly associated with other neurological factors that may not be attributable to hearing loss per se, but rather
have a severe impact on functioning. When isolated from may reflect characteristics of dysfunctional families such
comorbid neurological conditions, hearing loss has been as those commonly associated with greater rates of psy-
shown to impact cognitive organization but not intellec- chopathology among individuals who do not have
tual functioning (Braden, 1994). fMRI studies have indi- hearing loss (Powers, Elliott, Patterson, & Shaw, 1995).
cated that similar regions in the left frontal and temporal Limited communication skills in any modality are
776 D Deaf/Hearing Impairment
associated with poor psychosocial functioning and may neuropsychological evaluations with individuals from
significantly limit access to therapeutic intervention (Black this unique population. Neuropsychologists are strongly
& Glickman, 2005). Clinicians who are not skilled in encouraged to consult with and refer to clinicians trained
working with deaf clients may be more likely to provide in deafness.
a narrow range of diagnoses to clients who are deaf and
may over diagnose psychotic disorders. In contrast, when
assessed by deafness mental health specialists, lower rates Treatment
of psychosis and a greater range of less severe psychiatric
problems are reported (Black & Glickman, 2009). Treatment varies depending on the cause and nature of
the hearing loss as well as ones cultural perspective. No
one treatment approach has been demonstrated to be
Evaluation effective for all individuals who are deaf or hard of
hearing. Conductive hearing losses are often treated with
Hearing loss is typically identified through audiological antibiotics or minor surgeries, such as insertion of
assessment which may include behavioral, electroacous- pressure-equalization tubes. Individuals with sensorineu-
tic, and electrophysiological measures. Immittance audio- ral hearing loss may benefit from use of hearing aids or a
metry identifies outer and middle ear function. cochlear implant (CI) (refer to Pisoni et al., 2008 for a
Audiological evaluation also involves obtaining a pure- review of factors impacting outcomes of CI users). Reha-
tone audiogram which depicts an individuals hearing bilitation may include use of an amplification system in
sensitivity at varying frequencies and intensities. New- addition to language stimulation programs, use of assis-
born infant hearing screening procedures, which allow tive devices, auditory training, and speech therapy. Envi-
for early diagnosis of hearing loss, may include otoacous- ronmental accommodations (e.g., preferential seating),
tic emissions screening (OAE) and auditory brain stem use of adaptive technology to improve access (e.g., flash-
response screening (ABR). ing light systems), and communication repair strategy
Numerous factors impact the validity and reliability of training are also essential.
neuropsychological assessment of individuals who are The mental health needs of individuals who are deaf
deaf and hard of hearing. Misdiagnoses of mental retar- and hard of hearing traditionally have been underserved.
dation, learning problems, and psychopathology are com- Referral to a mental health professional trained in deaf-
mon when assessed by individuals not appropriately ness, preferably one with fluency in the clients preferred
trained to form clinical diagnoses based on an under- communication mode, reflects best practice. Indirect
standing of the dynamic interplay between deafness and communication through an interpreter during therapy
its associated causes, language functioning and accessibil- may negatively impact the therapeutic process by inter-
ity, and family dynamics. Factors complicating the assess- fering with the patienttherapist relationship, increasing
ment process include the match between the evaluator the likelihood of miscommunication, and interfering with
and clients preferred communication modality, selection the therapists ability to reliably assess the clients mental
of assessments demonstrated to be valid and reliable with status (Leigh, Corbett, Gutman, & Morere, 1996; Sussman
clients who are deaf, use of interpreters, and interpreta- & Brauer, 1999). When interpreters must be used, it is
tion of test results. Translation into a different communi- preferable to use a consistent, certified interpreter.
cation modality or use of other accommodations may
alter an assessments underlying construct and its psycho-
metric properties, therefore invalidating the results. As an Cross References
example, one of the most commonly used assessments of
intelligence, the Wechsler Intelligence Scale for Children Auditory Cortex
III, has been demonstrated to measure the construct of Auditory System
intelligence among children with hearing loss differently
than same-age hearing peers at the factor and item levels
(Maller & Ferron, 1997). Nonverbal assessment tools References and Readings
which do not rely heavily on verbal content reflect best
practice when assessing individuals with hearing loss American Speech-Language-Hearing Association (2009). The prevalence
(Braden, 1994; Maller, 2003). Specialized training is re- and incidence of hearing loss in children. Retrieved June 11, 2009,
quired to adequately conduct psychological and from http://www.asha.org/public/hearing/disorders/children.htm
DeanWoodcock Neuropsychological Assessment System D 777
Black, P., & Glickman, N. (2005). Language dysfluency in the deaf additional disabilities. Journal of Childhood Communication Disor-
inpatient population. JADARA, 39(1), 303321. ders, 17, 1519.
Black, P., & Glickman, N. (2009). Language and learning challenges in Pressman, L., Pipp-Siegel, S., Yoshinaga-Itano, C., & Deas, A. (1999). The
the deaf psychiatric population. In Cognitive-behavioral therapy relation of sensitivity to child expressive language gain in deaf and
for deaf and hearing persons with language and learning challenges hard-of-hearing children whose caregivers are hearing. Journal of
(pp. 146). New York: Taylor & Francis. Deaf Studies and Deaf Education, 4, 294304.
Braden, J. P. (1994). Deafness, deprivation, and IQ. New York: Plenum. Rhine-Kahlback, S. (2004). The assessment of developmental language
Calderon, R., & Naidu, S. (2000). Further support for the benefits of early differences, executive functioning, and social skills in deaf
identification and intervention for children with hearing loss. The children. Unpublished doctoral dissertation, Gallaudet University, D
Volta Review, 100(5), 5384. Washington, DC.
Danek, M. M., & Busby, H. (1999). Transition planning and programming: Simeonsson, R. J., Wax, T. M., & White, K. (2001). Assessment of children
empowerment through partnership. Washington, DC: Gallaudet who are deaf or hard of hearing. In R. Simeonsson & S. Rosenthal
University Press. (Eds.), Psychological and developmental assessment: Children
Hauser, P. C. (2001). Deaf readers phonological encoding: An electro- with disabilities and chronic conditions (pp. 248266). New York:
myogram study of covert reading behaviour. Dissertation Abstracts Guilford.
International, 62, 4B. (UMI No. AAI3012772). Sussman, A. E., & Brauer, B. A. (1999). On being a psychotherapist with
Hauser, P. C., Wills, K., & Isquith, P. K. (2006). Hard-of-hearing, Deaf clients. In I. W. Leigh (Ed.), Psychotherapy with deaf clients from
deafness, and being Deaf. In J. E. Farmer, J. Donders, & S. A. diverse groups (pp. 322). Washington, DC: Gallaudet University
Warschausky (Eds.), Treating neurodevelopmental disabilities Press.
(pp. 119131). New York: Guilford. Traxler, C. B. (2000). The Stanford achievement test, 9th edition: Nation-
Lane, H. (1988). Is there a psychology of the deaf ? Exceptional Children, al norming and performance standards for deaf and hard of
55, 719. hearing students. Journal of Deaf Studies and Deaf Education, 5(4),
Lane, H., Hoffmeister, R., & Bahan, B. J. (1996). A journey into the deaf- 337348.
world. San Diego, CA: Dawn Sign Press. Wagner, M., Newman, L., Cameto, R., Garza, N., & Levine, P. (2005). After
Leigh, I., Corbett, C. A., Gutman, V., & Morere, D. A. (1996). Providing high school. A first look at the postschool experiences of youth
psychological services to deaf individuals: A response to new percep- with disabilities. A report from the National Longitudinal Transition
tions of diversity. Professional Psychology: Research and Practice, 27, Study 2 (NLTS-2). Menlo Park, CA: SRI International. Retrieved June
364371. 1, 2009, from http://www.nlts2.org/pdfs/afterhighschool_ report.pdf
Maller, S. J. (2003). Intellectual assessment of deaf people: A critical WHO (2005). Deafness and Hearing Impairment. Retrieved 6/11/2009,
review of core concepts and issues. In M. Marshark & P. E. Spencer from http://www.who.int/mediacentre/factsheets/fs300/en/print.
(Eds.), Oxford handbook of deaf studies, language, and education html
(pp. 451463). New York: Oxford University Press. Yoshinaga Itano, C., Sedey, A. L., Coulter, D. K., & Mehl, A. L. (1998). The
Maller, S. J., & Ferron, J. (1997). WISC-III factor invariance across deaf language of early and later identified children with hearing loss,
and standardization samples. Educational and Psychological Mea- Pediatrics, 102, 11611171.
surement, 7, 987994.
Marscharck, M., & Hauser, P. C. (Eds.). (2009). Deaf cognition: Founda-
tions and outcomes. New York: Oxford University Press.
Meadow-Orlans, K. P. (1990). Research on developmental aspects of
deafness. In D. E. Moores & K. P. Meadow-Orlans (Eds.), Education
and developmental aspects of deafness (pp. 283298). Washington,
DeanWoodcock
DC: Gallaudet University Press.
Mertens, D. M., Sass-Lehrer, S., & Scott-Olson, K. (2000). Sensitivity in DeanWoodcock Neuropsychological Assessment System
family professional relationships: Potential experiences of families
with young deaf and hard of hearing children. In P. T. Spencer,
C. J. Erting, & M. Marschark (Eds.), The deaf child in the family at
school (pp. 133150). Mahwah, NJ: Erlbaum.
Mitchell, R. E., & Karchmer, M. A. (2002). Chasing the mythical ten DeanWoodcock
percent: Parental hearing status of deaf and hard of hearing students
in the United States. Sign Language Studies, 4, 138163.
Neuropsychological Assessment
Newman, A. J., Bavelier, D., Corina, D., Jezzard, P., & Neville, H. J. (2002). System
A critical period for right hemisphere recruitment in American Sign
Language processing. Nature Neuroscience, 5, 7680.
Paul, P. V., & Jackson, D. W., (1993). Toward a psychology of deafness.
S COTT L. D ECKER
Needham Heights, MA: Allyn & Bacon. University of South Carolina
Pisoni, D., Conway, C., Kronenberger, W., Horn, D. L., Karpicke, J., & Columbia, SC, USA
Henning, S. C. (2008). Efficacy and effectiveness of cochlear
implants in deaf children. In M. Marscharck & P. C. Hauser (Eds.),
Deaf cognition: foundations and outcomes (pp. 52101). New York:
Synonyms
Powers, A. R., Elliott, R. N., Patterson, D., & Shaw, S. (1995). Family
environment and deaf and hard of hearing students with mild DeanWoodcock; DW; DWNB
778 D DeanWoodcock Neuropsychological Assessment System
Description Each psychiatric symptom is rated on a rating scale of

severity and duration. The last section, Clinical Observa-
The DeanWoodcock Neuropsychological Battery (DWNB) tions and Impressions, provides an assessment of behav-
(Dean & Woodcock, 2003) consists of a Sensory-Motor ior based on clinical judgment.
Battery (SMB), Structured Neuropsychological Interview, The Structured Neuropsychological Interview covers
and Emotional Status Exam. The DWNB contains many all major background elements important for a clinical
components of a traditional neuropsychological assess- evaluation. Information is directly collected from the
ment. The SMB consists of measures traditionally subject or parent and covers biographical information,
found in other neuropsychological batteries such as the referral concerns, medical history, psychiatric history,
HalsteadReitan. Although the DWNB may be used with social history, family history, and development. Informa-
any cognitive measure, it was co-normed with the tion obtained from the Structured Neuropsychological
WoodcockJohnson Third Edition (Woodcock, McGrew, Interview, as well as the Emotional Status Examination,
& Mather, 2001). are useful in helping to provide meaningful interpretation
The SMB includes one measure of laterality, six sen- to the performance measures in either the sensorimotor
sory measures, and seven motor measures. The sensory exam or from tests of cognition or achievement.
tests assess a variety of functions including peripheral
and near point visual acuity, auditory acuity, and a
variety of tactile functions. The motor measures assess Historical Background
gross motor (i.e., Gait and Station and Romberg), visual-
motor construction and coordination, and a variety of Subtests of the DWNB are based on theories of neuro-
other motor functions including finger tapping and grip psychological functioning and examination procedures
strength. Once the test is administered, raw scores are historically used in neurology. Many of the neurological
converted into W-scores. W-scores are Rasch-based exams grew from the historic roots of early clinical
measures with equal-interval properties. Next, the W- observations of brainbehavior correspondence. For
score is subtracted from a Reference W, which represents example, Brocas early observations of the left-inferior
the average W-score for a particular age range. Qualita- frontal lobe involvement in language production are
tive interpretation of impairment based on scores now viewed as a type of aphasia and assessed through
includes the labels within normal limits, mild im- language measures on the DWNB. One primary differ-
pairment, moderate impairment, and severe ence between subtests of the DWNB and the historic
impairment. Since many tests include lateralized indica- counterparts from neurology is the use of psychometric
tors of functioning (right and left), lateralized im- measurement theory. Whereas neurologists may use sim-
pairment may be easier to detect in the summary of ilar procedures, the DWNB provides standardization
scores by marking the impairment label with an L for procedures and normative information. Normative in-
left and an R for right. Standard scores are not formation is useful for developmentally sensitive mea-
provided because of the non-normal distribution of sures where less than perfect performance is normal.
scores for most of the tests. Base rates for frequency of Additionally, base rates of impairment help determine
impairment are provided in the manual. Total composite the likelihood of performance across various clinical
of sensory and motor functioning may be obtained by conditions such as apraxia, agnosia, aphasia, dysarthria,
adding W-scores across tests, although the validity of somesthesia, etc.
such indices is unknown. Spanish administration proce-
dures are identical to English procedures.
The Emotional Status Examination and the Neuro- Psychometric Data
psychological Interview are important components of the
DWNB. The Emotional Status Examination consists of Numerous reliability studies were reported from both
three sections. The first section records relevant demo- the manual and published resources. Reliability esti-
graphic information such as name and age. The second mates for each measure are reported across the develop-
section systematically reviews 50 psychiatric symptoms mental age range and in general are satisfactory for their
sampled from a large variety of psychiatric illnesses. The intended purpose. The normative information is based
purpose is to cover a large number of disorders relatively on a sample of 1,011 subjects from age 4 to 80.
quickly. Endorsement of particular psychiatric signs or The sample was matched to the U.S 2000 census by
symptoms may require additional follow-up or testing. gender and race. Numerous validity studies were also
Death Penalty D 779
reported including content, developmental, and con- Definition

struct validity.
The death penalty, otherwise known as capital
punishment, is one of three possible punishments ren-
Clinical Uses dered for defendants found guilty of murder or other
capital crimes. The death penalty involves execution of
The DWNB provides a fairly comprehensive neuropsy- the defendant. The U.S. Supreme Court has determined D
chological battery that assesses most areas of relevance that the death penalty is not typically a violation of the
in neuropsychology. Additionally, its psychometric Eight Amendments ban on cruel and unusual punish-
properties increase its value in clinical assessment. Clin- ment. Moreover, the Sixth Amendment does not neces-
icians familiar with the components can complete the sitate a jury trial in order to sentence someone to death.
battery in about an hour. Scoring software may be pur- Capital punishment in the USA is a highly controversial
chased separately and reduces the chances of calculation issue as evidenced by the prohibition of capital punish-
errors. ment in certain states. Moreover, various religious
affiliations possess disparate views related to the moral
grounds of the death penalty. There are several issues for
Cross References forensic neuropsychologists to consider related to capital
punishment. First and foremost, it is crucial that prior to
HalsteadReitan Neuropsychological Test Battery accepting a role in a capital case, that the practitioner
Neuropsychology evaluate his/her personal positions on the death penalty
and in accordance with ethical standards. If ones per-
sonal views hold the potential to impede with ones
References and Readings professional role, then they should not assume the role
of a consultant or expert in a capital case. Neuropsychol-
Dean, R. S., & Woodcock, R. W. (2003). Dean-Woodcock neuropsychologi- ogists involved with death penalty cases usually are
cal battery. Itasca, IL: Riverside. involved with determinations of competency to be
Dean, R. S., Woodcock, R. W., Decker, S. L., & Schrank, F. A. (2003).
executed, competency to waive death penalty appeals,
A cognitive neuropsychology assessment model. In F. A. Schrank &
D. Flanagan (Eds.), WJ III clinical use and interpretation: Scientist-
assessment of mental retardation, and other mitigating
practitioner perspective (pp. 345377). SanDiego, CA: Academic. factors (e.g., brain damage, effects of a history of
Woodcock, R. W., McGrew, K. S., & Mather, N. (2001). Woodcock- abuse, etc.)
Johnson III. Itasca, IL: Riverside.
Cross References
Death Aggravating Factors
Atkins v. Virginia
Brain Death Mitigating Factors
Death Penalty References and Readings
Cunningham, M. D., & Goldstein, A. M. (2003). Sentencing determina-

R OBERT L. H EILBRONNER tions in death penalty cases. In A. Goldstein (Ed.), Handbook of
Chicago Neuropsychology Group psychology (Vol. 11). Forensic psychology, New Jersey: Wiley.
Chicago, IL, USA Heilbronner, R. L., & Waller, D. (2008). Neuropsychological consultation
in the sentencing phase of capital cases. In R. Denney, & J. Sullivan
(Eds.), Clinical neuropsychology in the criminal forensic setting. New
York: Guilford.
Synonyms Reynolds, C., Price, J. R., & Niland, J. (2003). Applications of neuropsy-
chology in capital felony (death penalty) defense. Journal of Forensic
Capital punishment Neuropsychology, 3, 89123.
780 D Deceleration Injury
Cross References
Deceleration Injury
Acceleration Injury
B ETH R USH Biomechanics of Injury
Mayo Clinic Diffuse Axonal Injury
Synonyms References and Readings
Accelerationdeceleration injury Barth, J. T., Freeman, J. R., Broshek, D. K., & Varney, R. N. (2001).
Acceleration-deceleration sport-related concussion: The gravity of
it all. Journal of Athletic Training, 36(3), 253256.
Meythaler, J. M., et al. (2001). Archives of Physical Medicine and Rehabili-
Definition tation, 82, 14611471.
Olvey, S. E., et al. (2004). Neurosurgery, 54, 672677.
Deceleration injury is a traumatic injury to the brain,
typically following an acceleration injury to the brain in
a high-speed situation such as a motor vehicle accident or
high-impact sports. Deceleration injuries typically result
in additive damage to an acceleration injury after Decerebrate Posturing
the speed and inertia of momentum is obstructed. In
this situation, the brain that is moving forward in the J ACOB K EAN
direction of inertia falls backward in the opposite direc- Indiana University School of Medicine
tion, which may result in further compression of the Indianapolis, Indiana, USA
underlying brain tissue and white matter connections.
Synonyms
Current Knowledge
Extensor posturing
Similar to acceleration injuries, primary injury in decel-
eration injury results in bruising, hemorrhage, and
shearing of the underlying tensile strength of white mat-
ter connections deep within the brain. Secondary injury Definition
may occur hours or even days after the inciting traumatic
event. Secondary effects of injury can include decreased Decerebrate posturing is a pattern of movement com-
cerebral blood flow, edema, hemorrhage, increased in- monly produced by extensive forebrain lesions including
tracranial pressure, and biochemical changes that may the subcortex. It is characterized by rigidity, extension of
cause excitotoxicity and more extensive damage to the the arms with wrists pronated, extension of the legs,
surrounding brain structures and their associated downward pointing of the toes, and sometimes arching
connections. of the spine. Decerebrate posturing may be partial or
Acceleration and deceleration injuries are not uncom- asymmetric. Decerebrate (or extensor) posturing is
mon in high-impact sports such as football and hockey. distinguished from decorticate (or flexor) posturing by
Neuropsychologists are now often involved in baseline the extension of the arms. Decerebrate posturing is
cognitive screens for professional sports players and in generally the result of massive and bilateral forebrain
subsequent cognitive evaluations following a traumatic lesions or other damage that includes upper brainstem
event in which a concussion or traumatic brain injury and sometimes the rostral pons. Common causes include
is suspected. Professional sports organizations strongly cerebral infarction (stroke), intracranial hemorrhage, pri-
endorse the use of helmets in such sports activities to mary brain tumor, secondary brain tumor, traumatic
reduce the amount of free range of motion in the head head injury, increased intracranial pressure from any
that can potentially cause a more severe acceleration cause, brainstem tumor, and metabolic or hepatic
deceleration injury. encephalopathies.
Declarative Memory D 781
Cross References Declarative (Explicit)

Memory

Episodic Memory Semantic Memory
Posner, J. B., Saper, C. B., Schiff, N. D., & Plum, F. (2007). Plum and - Experiences and events localized in - Not localized in time and space
D
time and space
Posners diagnosis of stupor and coma. New York: Oxford University - Not connected to experience where
- Awareness of the personal acquired
Press. experience
- Factual information
Declarative Memory. Figure 1 Components of declarative

Declarative Memory memory
J ILLIAN S CHUH
University of Connecticut procedures remains largely intact. One famous patient,
Storrs, CT, USA H.M., described by Brenda Milner and William Beecher
Scoville in a classic 1957 paper, underwent surgery to
reduce seizures caused by intractable epilepsy. After the
Synonyms bilateral removal of his hippocampus and medial tempo-
ral lobes, H.M. suffered profound anterograde amnesia.
Explicit memory He was no longer able to store new declarative memories
and had a limited ability to retrieve previously stored
memories (Corkin, 1968; Milner, 1965). However, his
Definition ability to learn new skills (procedural memory) appeared
largely unaffected. For example, in a task of mirror draw-
Declarative memory refers to long-term memory, which ing, H.M.s accuracy improved with each testing session.
stores information that can be consciously discussed or However, H.M. was unable to recognize the details of the
declared. Declarative memory, which is the form of testing environment, and thought each session to be
memory as viewed by most lay people, involves the novel, as though he were encountering the testing materi-
deliberate encoding of information for objects, events, als for the first time (Milner, 1965; Scoville & Milner,
or facts. One of several distinct memory systems (Lezak, 1957). H.M.s case provides an example of anatomic dis-
Howieson, & Loring, 2004), declarative memory is often sociation, in which tasks that differ in their declarative
contrasted with non-declarative or procedural memory, versus procedural memory demands are associated with
which refers to the unconscious encoding of procedures, distinct neuroanatomical structures. This anatomic disso-
routines, or patterned information for learning skills or ciation suggests that declarative and procedural tasks may
processes. Declarative memory is further divided into rely on distinct memory storage and retrieval systems in
episodic, the memory for experiences localized in time the brain.
and space, and semantic, the memory for learned
knowledge that is not time locked to a specific event;
e.g., rote memorization of a historical fact or the letters Current Knowledge
of the alphabet (Fig. 1).
Since the time of H.M., many studies have examined
memory in a variety of neurological presentations. In
Historical Background particular, the consolidation of declarative memory has
been an area of interest and debate. While several memory
The theory of multiple memory systems largely began functions have been identified, there is controversy over
with the distinction between declarative and procedural the stages involved in the formation of declarative mem-
memory. This distinction is observed in patients with ories (Parkin & Rapp, 2001). For example, there is long-
anterograde amnesia, who have an inability to store new standing debate as to whether short term memory is a
declarative memories, while memory for skills or distinct function or one element in the consolidation
782 D Declarative Memory
process (Fuster, 2003; McGeoch, 1932). Many studies The consolidation of long-term memories is thought
suggest that there are three stages that are clinically useful to occur through a process known as long-term poten-
(Loring, 1999): sensory memory, short term/immediate tiation (LTP; Tranel & Damasio, 2002). LTP, lasting
memory, and long term/secondary memory (Fig. 2). anywhere from hours to months, is the simultaneous
In the first stage, lasting several seconds at the most, stimulation of two or more neurons that results in an
information is held in a sensory store, while extraneous increased synaptic strength, improving communication
stimuli in the environment are filtered out (Crowder, between the synapses (Cooke & Bliss, 2006). This stimu-
Surprenant, & Kazdin, 2000). The information either lation of a neural network primes the system for learning.
quickly decays or is further processed as short-term mem- Long-term memory formation occurs when continued stim-
ory if there is rehearsal or additional support for its ulation increases synaptic strength, allowing the learning to
salience. Short-term memory, known as immediate mem- be retained. Memory storage does not occur at particular
ory, serves as a temporary store. Lasting from roughly 30 s sites in the brain, but rather results from the contribution of
to several minutes (Lezak et al., 2004), this storage allows many cortical networks (Markowitsch, Tulving, & Craik,
for the integration of relevant perceptual information. If 2000). Several areas of the brain have been identified as
the memory trace is not processed for long-term consoli- particularly critical in declarative memory consolidation.
dation, the memory quickly dissipates. For example, upon These include the hippocampus, midline diencephalon,
receiving the new phone number of a friend, you may medial temporal lobe, mammillary bodies, thalamus, for-
remember it for the several minutes before dialing. nix, and frontal lobes (Parkin & Rapp, 2001).
However, it may be difficult to recall that number several
hours later. The number is retained while it is relevant,
but after a short period of time this memory dissipates. Future Directions
Memory traces can be retained for up to several hours
through rehearsal (the engagement of repetitive mental While it is clinically useful to organize the process of
processes; Brown, Craik, & Tulving, 2000). If this number declarative memory formation into distinct stages, these
was important to remember, you might repeat it several stages may be functionally interdependent. For example,
times or use a mnemonic device (a word or phrase recent research suggests that short-term memory may
representing the numbers) to enhance your memory. simply be the early part of the consolidation process in
The process of rehearsal increases the chance of that memory formation (Fuster, 2003). Additionally, the dis-
information being retained or encoded in long-term tinction between episodic and semantic memory can also
memory. However, it does not guarantee long term be fuzzy. If you learn that Nouakchott is the capital of
storage, as conscious rehearsal can only be maintained Mauritania, tomorrow you are likely to remember the
temporarily. Rehearsal techniques often imply that long- event of learning it (e.g., reading this article, where you
term memory formation happens through effortful were when reading, what happened before and after, etc.),
attention. However, memories may also form through making it an episodic memory. However, what happens if
incidental learning, which requires little conscious effort. tomorrow, a radio program has a feature on Mauritania?
If you repeatedly hear this fact, the episodic memory will
become a semantic memory. Conversely, if you have the
semantic knowledge that Nouakchott is the capital of
Sensory memory
(milliseconds to several seconds)
Mauritania, and then help your friend with a geography
project on Mauritania, you now have an episodic memory
Repetition
involving a semantic memory. It is likely these compo-
Short term/ Immediate
nents are not separate memory systems, but rather two
Memory
(thirty seconds to several minutes) processes that are closely intertwined (Willingham, 2004).
Even the distinction between declarative and procedural
memory can become blurred. Some researchers speculate
Long term/ Secondary
Memory that there is a developmental progression during learning
(hours to years)
upon which knowledge moves from more implicit
representations to more declarative representations as
Memory decay/
Forgetting the learner matures (Alibali & Koedinger, 2000).
Research continues to address these relationships, and it
Declarative Memory. Figure 2 Stages of declarative memory is likely that a multidisciplinary approach will further the
Decorticate Posturing D 783
knowledge of declarative memory. Brain imaging studies are Fuster, J. M. (2003). Cortex and mind: Unifying cognition. New York:
improving the understanding of the anatomical networks
Lezak, M. D., Howieson, D., & Loring, D. (2004). Neuropsychological
involved in declarative memory processes. Such an under- assessment (4th ed.). New York: Oxford University Press.
standing will guide the examination of declarative memory Loring, D. W. (1999). INS dictionary of neuropsychology. New York:
formation at the cellular level, so that we will not only be able Oxford University Press.
to understand the anatomical areas important for declara- Markowitsch, H. J., Tulving, E., & Craik, F. I. M. (2000). Neuroanatomy
of memory. The Oxford handbook of memory (pp. 465484).
tive memory, but have better insight into the formation of D
declarative memory. Additionally, computational modeling McGeoch, J. A. (1932). Forgetting and the law of disuse. Psychological
can shed insight into how one memory processes may inter- Review, 39(4), 352370.
act with another. Finally, much of the research on declarative Milner, B. (1965). Memory disturbance after bilateral hippocampal
memory in humans has focused on typical adults or patients lesions. In P. Milner & S. Glickman (Eds.), Cognitive processes and
the brain. Princeton: Van Nostrand.
with lesions occurring later in life (as in the cases of studies
Ofen, N., Kao, Y. C., Sokol-Hessner, P., Kim, H., Whitfield-Gabrieli, S., &
of anterograde amnesia). While this has given immense Gabrieli, J. D. (2007). Development of the declarative memory
knowledge of the declarative memory system, relatively little system in the human brain. Nature Neuroscience, 10(9), 11981205.
empirical work has examined the development of this sys- Parkin, A. J., & Rapp, B. (2001). The structure and mechanisms of
tem. One imaging study by Ofen et al. (2007) comparing memory. The handbook of cognitive neuropsychology: What deficits
reveal about the human mind (pp. 399422). New York: Psychology
children to adults found increased activation in the pre-
Press.
frontal cortex with increasing age. Additionally, activation Scoville, W. B., & Milner, B. (1957). Loss of recent memory after bilateral
in the prefrontal cortex correlated with developmental hippocampal lesions. Journal of Neurology, Neurosurgery, and Psychi-
gains in the ability to remember details of an experience. atry, 20(1), 1121.
Further examination of developmental processes will not Tranel, D., & Damasio, A. R. (2002). Neurobiological foundations of
human memory. In A. D. Baddeley, B. A. Wilson, & F. N. Watts
only provide insight on the maturational trajectory of
(Eds.), Handbook of memory disorders. (2nd ed., pp. 2750). Oxford:
declarative memory, but also help further the understand- John Wiley & Sons.
ing of the relationship between those memory systems Willingham, D. T. (2004). Cognition: The thinking animal (2nd ed.).
which appear seemingly distinct. Upper Saddle River, NJ: Pearson/Prentice Hall.
Cross References
Alzheimers Dementia Decompressive Craniectomy

Alzheimers Disease
Anterograde Amnesia Craniectomy
Dementia
Episodic Memory
Procedural Memory
Semantic Memory
J ACOB K EAN
References and Readings Indiana University School of Medicine
Indianapolis, Indiana, USA
Alibali, M. W., & Koedinger, K. R. (2000). The developmental progression
from implicit to explicit knowledge: A computational approach.
Behavioral and Brain Sciences, 22(05), 755756.
Brown, S. C., Craik, F. I. M., & Tulving, E. (2000). Encoding and retrieval Synonyms
of information. The Oxford handbook of memory (pp. 93107).
New York: Oxford University Press. Flexor posturing
Cooke, S. F., & Bliss, T. V. P. (2006). Plasticity in the human central
nervous system. Brain: A Journal of Neurology, 129(7), 16591673.
Corkin, S. (1968). Acquisition of motor skill after bilateral medial Definition
temporal-lobe excision. Neuropsychologia, 6(3), 255265.
Crowder, R. G., Surprenant, A. E. M., & Kazdin, A. E. (2000). Sensory
stores. Encyclopedia of psychology (Vol. 7) (pp. 227229). Decorticate posturing is a pattern of movement produced
Washington, DC: American Psychological Association. by extensive lesions in white matter, internal capsule, or
784 D De-efferented State
thalamus, and characterized by rigidity, flexion of the Definition

arms, fists and fingers, and extension of the legs. Decorti-
cate (or flexor) posturing may be partial or asymmetric, Bilateral implantation of electrode leads into target areas
and is distinguished from decerebrate (or extensor) pos- of the brain to treat movement disorders.
turing by the flexion in the arms, which positions the
hands close to the heart.
Current Knowledge
Cross References
DBS was first performed in 1987 to treat tremor of
Parkinsons disease and essential tremor. The exact
Decerebrate Posturing
mechanism of action for DBS is unknown, though it is
likely related to the inhibition/blockade of excitatory
membrane potentials. In Parkinsons disease, leads are
References and Readings usually implanted in the subthalamic nucleus and inter-
nal part of the globus pallidus (GPi). The procedure is
Posner, J. B., Saper, C. B., Schiff, N. D., & Plum, F. (2007). Plum and performed with stereotactic localization of the selected
Posners diagnosis of stupor and coma. New York: Oxford University nuclei and can be performed in one or two surgeries
Press.
depending on regional preferences and standard of
care. DBS generally allows for reduction in the need for
medications for the symptoms of Parkinsons disease.
Motor fluctuations and tremor are most affected by
DBS. Improvements in tremor, rigidity, and bradykine-
De-efferented State sia are sustained. DBS is considered a reversible
procedure.
Locked-In Syndrome
Cross References
Parkinsons Disease
Deep Brain Stimulation (DBS) Tremor
Deep Brain Stimulator (Parkinsons)

Erola, T., Heikkinen, R. R., Haapaniemi, T., Tuominen, J., Juolasmaa, A.,
& Myllyla, V. (2006). Efficacy of bilateral subthalamic nucleus (STN)
stimulation in Parkinsons disease. Acta Neurochirurgica, 148,
Deep Brain Stimulator 389394.
(Parkinsons) Kleiner-Fisman, G., Fisman, D., Sime, E., Saint-Cyr, J. A., Lozano, A. N.,
& Lang, A. (2003). Long term follow up of bilateral deep brain
stimulation of the subthalamic nucleus in patients with advanced
C INDY B. I VANHOE Parkinson disease. Journal of Neurosurgery, 99, 489495.
Baylor College of Medicine Krause, M., Fogel, W., Mayer, P., Kloss, M., & Tronnier, V. (2004).
Houston, TX, USA Chronic inhibition of the subthalamic nucleus in Parkinsons
disease. Journal of the Neurological Sciences, 219, 119124.
Vesper, J., Chabardes, S., Fraix, V., Sunde, N., & Ostergaard, K. (2002).
Dual Channel deep brain stimulation system (kinetra) for
Synonyms Parkinsons disease and essential tremor: a prospective multicenter
open clinical study. Journal of Neurology, Neurosurgery, and
Activa; Deep brain stimulation (DBS); Kinetra Psychiatry, 73, 275280.
Default Network D 785
Deep Venous Thrombosis Default Network

Venous Thrombosis L AWRENCE H. S WEET
Brown University
Providence, RI, USA
De-escalation D
Synonyms
DAWN E. B OUMAN
Drake Center, Default mode network; Task-negative network
Cincinnati, OH, USA
Definition
Definition
The default network is a system of brain regions that is
De-escalation is the reduction in the intensity of out-of- active when there are no external cognitive demands. The
control, agitated behavior and the prevention of further greatest brain activity is observed in this system during
behavioral crisis. Following a traumatic brain injury or unstructured rest, and the least activity is observed during
other neurological disorder, including stroke or brain tasks that require concerted external focus. The existence
tumor, some people become more easily confused, over- and core location of the default network are widely ac-
whelmed, threatened, fearful, uncertain, impulsive, and cepted; however, its function and subsystems remain
less able to control their behavior, resulting in increasing under investigation. The default network is distributed
levels of verbal and physical aggression. De-escalation bilaterally and is comprised of at least two core midline
techniques including decreasing stimulation, offering regions, the posterior cingulate cortex and medial frontal
calm reassurance, redirecting, and reorienting can gyrus, plus the inferior parietal lobule and areas in the
decrease agitation and lessen the intensity of a behavioral medial and lateral temporal lobe.
outburst.
Cross References Identification of the default network emerged unexpectedly

from functional neuroimaging studies that administered
Agitation paradigms with a variety of active cognitive challenges.
Behavior Management Functional neuroimaging designs frequently sample brain
Catastrophic Reaction activity during resting states in order to provide a baseline
Crisis Intervention to which the task-elicited brain response to active experi-
mental challenges are compared. During the middle of the
1990s, it became apparent that a set of brain regions con-
sistently exhibited greater activity during the resting base-
References and Readings line periods compared to different active experimental
challenges. This surprisingly consistent pattern of resting
Gervasio, A. H., & Matthies, B. K. (1995). Behavioral management of
activity appeared as deactivation when compared to the
agitation in the traumatically brain-injured person. Neurorehabilita-
tion, 5, 309316.
active experimental conditions on maps of significant brain
response. Moreover, this significant deactivation was often
as robust as the expected task-related activation. This dis-
covery motivated discussions about improving experimen-
tal designs to better control baseline assessments and much
Default Mode Network greater attention to deactivation patterns. Although deac-
tivation patterns were often not even reported in early
Default Network studies, within a decade, they became a major focus of
786 D Defective Visual Localization
functional neuroimaging research. An early meta-analysis uncontrolled baseline processing. The research focus very
of visual processing generated the first major interest in quickly transitioned from explaining observed deactivation
deactivation patterns in 1997. Schulman and colleagues patterns, to mapping the default network, and finally to the
found common deactivation patterns across studies that larger implications for cognitive neuroscience and neuro-
administered different visual tasks. These deactivations psychiatry. Although core regions have been well described
corresponded to regions now known as the default net- and empirically supported, the full anatomical extent and
work. In 2001, Raichle and colleagues first labeled this specific functions of this network remain under investiga-
baseline activity a default mode of brain function in a tion. Future work will likely be aimed at narrowing and
series of influential papers that substantially increased re- integrating the broad cognitive functions that have been
search interest in this system. attributed to the default network and its subsystems, for
example, the theory that the default network serves as an
imagery simulator for creative thinking. These and other
cognitive constructs associated with the default network
Current Knowledge
will require reliable and valid operational definitions that
are feasible to use in functional neuroimaging environ-
Investigation of default network activity has revealed con-
ments. Integration of the default network with other
sistent inverse relationships with a wide variety of exter-
brain systems such as the task-positive network and atten-
nally focused tasks that range from visual processing
tional systems is also likely to be a major goal of future
to more complex working memory tasks. Consistent pos-
research. Investigation of the role of the default network in
itive relationships have been observed with several inter-
neuropsychiatric disorders is providing novel findings and
nal thought processes such as stimulus independent
a new framework within which to interpret them. Clinical
thoughts, daydreaming, mind wandering, imagining an-
research on the default network remains limited; however,
other persons perspective, imagining the future, self-
this direction is very likely to grow rapidly.
referential thought, and retrieving memories. At rest
and during externally focused cognitive challenges, de-
fault network activity has been found to be inversely References and Readings
correlated with another set of brain regions that are
recruited during externally focused goal-directed proces- Buckner, R. L., Andrews-Hanna, J. R., & Schacter, D. L. (2008). The
sing (i.e., task-positive network). Therefore, the default brains default network: Anatomy, function, and relevance to disease.
network may represent one component of an opponent Annals of the New York Academy of Sciences, 1124, 138.
process system that is responsible for introspection, while Fox, M. D., Snyder, A. Z., Vincent, J. L., Corbetta, M., Van Essen, D. C., &
the task-positive network may be related to processing Raichle, M. E. (2005). The human brain is intrinsically organized
into dynamic, anticorrelated functional networks. Proceedings of the
with external attentional focus. It has been suggested National Academy of Sciences USA, 102(27), 96739678.
that the general function of the default network is flexi- Raichle, M. E., MacLeod, A. M., Snyder, A. Z., Powers, W. J., Gusnard,
ble mental simulation. Cognitive subprocesses may also D. A., et al. (2001). A default mode of brain function. Proceedings of
be mapped onto different subsystems of the default the National Academy of Sciences USA, 98, 676682.
network. For instance, areas in the medial temporal Shulman, G. L., Fiez, J. A., Corbetta, M., Buckner, R. L., Miezin, F. M.,
et al. (1997). Common blood flow changes across visual tasks: II.:
lobes appear to be recruited during memory contribu- Decreases in cerebral cortex. Journal of Cognitive Neurosciences, 9,
tions to default processing, while increased activity in 648663.
the medial frontal cortices has been associated with
evaluation of self-relevant situations. Altered default net-
work activity has been reported among older adults and
several clinical populations, including patients with Defective Visual Localization
autism, Alzheimers disease, depression, anxiety disor-
ders, and schizophrenia. Optic Ataxia
Future Directions
Defensiveness
There has been rapid growth in research on the default
network since it was first recognized as more than simply K Scale
Dejerine, Joseph Jules (18491917) D 787
Cross References
Deficit Measurement
Best Performance Method
S ANDRA B ANKS Individual Comparison Standards
Allegheny General Hospital National Adult Reading Test
Pittsburgh, PA, USA Premorbid Functioning
Wechsler Test of Adult Reading D
Definition
Deficit measurement is the measurement of impairment
Knapp, S. J., & VandeCreek, L. D. (2006). Assessment. Washington, DC:
when an examinees performance is significantly below an
American Psychological Association.
actual or estimated previous level of functioning. Lezak, M. D., Howieson, D. B., Loring, D. W., Hannay, H. J., &
Fischer, J. S. (2004). Neuropsychological Assessment. New York:
Snyder, P. J., Nussbaum, P. D., & Robins, D. L. (2006). Clinical neuro-
Current Knowledge psychology: A pocket handbook for assessment. Washington, DC:
American Psychological Association.
In neuropsychology, deficit measurement can be achieved
by assessing cognitive functioning as separate domains or
as a composite of domains. For instance, cognitive deficits
in a particular ability domain, such as list-learning ability, Degenerative
can be measured via the administration of a list-learning
task during which the examinee must recall a list of words Atrophy
both immediately and after a specified time delay. If the
examinee performs poorly, the score on this subtest pro-
vides information about deficits associated with the Deglutition Disorder
examinees list-learning ability. In the case of using com-
posite scores, several subtests are combined to generate a Dysphagia
composite score that represents performance in a general
domain of functioning, such as auditory memory. This
could include several separate aspects of functioning, such
as list-learning, narrative memory, encoding of abstract
Dejerine, Joseph Jules (1849
concepts, etc. 1917)
The level of deficit is determined by comparing the
examinees subtest or composite score with that of the J ACKIE L. M ICKLEWRIGHT, T RICIA Z. K ING
normative group (the group of individuals in the popula- Georgia State University
tion who have been examined with the same test) or with Atlanta, GA, USA
the examinees previous level of functioning. Deficit mea-
surement thus highlights the concept of normality,
given that a particular level of performance to represent Education and Training
a deficit when the level of performance falls below the
level most commonly observed (also called the criterion 1868 and 1870: Academie de Geneve (Bachelors of
level) in the population at large is considered. Deficit Science in Biology and Comparative Anatomy)
measurement is often captured indirectly, by estimating 1875: Hospital de la Pitie (Internship)
the examinees premorbid ability level, ideally by clinical 1879: Faculty of Medicine of Paris (Doctor of Medicine)
interview with the examinee and others, behavior rating
scales, and premorbid test results, and comparing the Major Appointments
examinees present performance with this estimate.
More direct comparison can be challenging because ob- Head of Clinic, Hospital Bicetre (18791886)
jective measures of an examinees previous level of func- Professor of Neurology and Chief Consultant,
tioning may be unavailable. Hospital Bicetre (18871894)
788 D Dejerine, Joseph Jules (18491917)
Professor of Neurology, Salpetriere (18951911) Charcot was planning to block his candidacy; Dejerine
Clinical Chair in Diseases of the Nervous System, confronted Charcot and demanded an explanation. After
Salpetriere (19111917) a heated discussion, Jean Martin Charcot conceded and
promised Dejerine his vote. Dejrine was appointed Profes-
sor Agrege and Chief Consultant for Hospital Bicetre in
Major Honors and Awards 1887. During his 8-year tenure he began his seminal work
on cerebral localization, outlining the somatotopy of pyra-
Vice-President Societe de Biologie (1895) midal tracks, ascending sensory tracts, and thalamo-corti-
Founding member of the French Neurological Society cal connections. Dejerine also published widely on
(1899) acquired disorders of spoken and written language. His
Moxon Gold Medal of the Royal College of Physicians first publication on writing disorders in aphasia patients
of London (1914) (1891) provided an outline of the neural architecture
necessary for reading, writing, and pronunciation. He
went on to provide detailed clinical and organic descrip-
Landmark Clinical, Scientific, and tions of progressive aphasia and pure alexia. Dejerine was
Professional Contributions the first to demonstrate that pure alexia resulted from the
disconnection of the angular gyrus from both visual
French neurologist J. Jules Dejerine earned acclaim for cortices.
his localizationist approach to the study of the ner- In 1895, Dejerine joined the faculty of the famed
vous system by combining the anatomical approach of Salpetriere as a Professor of Neurology. In the years to
Charcot with the experimental approach of Vulpian. follow, his collaborations yielded numerous publications
Dejerines early research focused on the pathophysiol- and clinical descriptions of disorders of the nervous
ogy of sensation and acquired disorders of spoken and system, including peripheral and central ataxia, sensory
written language. His body of work yielded detailed parietal syndrome, and thalamic syndrome. His body of
clinical and anatomical descriptions of a number of work culminated in the publication of Anatomie des
cognitive disorders, including pure alexia, aphasia, centres nerveux in 1895 and Semiologie des affections du
tactile agnosia, and thalamic syndrome. systeme nerveux in 1914. Akin to many of the French
neurologists before him, Dejerine developed an interest
in the therapeutic treatment of mental disorders. Dejerine
Short Biography believed that rational and theoretical aspects of psycho-
therapy are secondary to the emotional elements; he
J. Jules Dejerine was born into a modest family in 1849, in emphasized nonspecific contributors to therapeutic
Geneva, Switzerland. As a young man during the Franco- change such as support, empathy, and understanding.
Prussian war, Dejerine cared for wounded soldiers in a In 1915, he published. The psychoneuroses and their
Geneva hospital. After earning degrees in biology and com- treatment by psychotherapy.
parative anatomy from the Academie de Geneve, he depart- In addition to his prolific research career, Dejerine
ed for Paris in 1871 to pursue medical studies. Under the served as a founding member of the French Neurological
mentorship of Edme Felix Alfred Vulpian at Hospital de la Society. He also was actively involved with the Academie
Pitie, Dejerine published numerous papers on pathologies de Medicine and Societe de Biologie, which elected him
of the peripheral nervous system. In 1879, after completing Vice-President in 1895. Dejerines final contributions
his dissertation on acute ascending paralysis, Dejerine came during the First World War when he worked
received a Doctor of Medicine degree from the Faculty of endlessly to care for the neurologically wounded in a
Medicine of Paris. In 1888, Dejerine found both a partner military hospital. After many years of service, Dejerine
and collaborator when he wed American Augusta Marie died of uremia in 1917 at the age of 67.
Klumpke, the first female medical intern in Paris.
Dejerines hard-working reputation preceded him, and
upon completion of his degree, he was offered the Head of Cross References
Clinic position under Professor Alfred Hardy at the Hospi-
tal Bicetre in Paris. He remained in this position until 1886 Agraphia
when he was nominated Professor Agrege. Shortly follow- Alexia
ing his nomination Dejerine learned that Jean Martin DejerineRoussy Syndrome
Delayed Response Tasks D 789

Delayed Alternation
Bassetti, C. L., & Jagella, E. C. (2006). Joseph Jules Dejerine (18491917).
Journal of Neurology, 253, 823824. Delayed Response Tasks
Bub, D. N., Arguin, M., & Roch Lecours, A. (1993). Jules Dejerine and his
interpretation of pure alexia. Brain and Language, 45, 531559.
Dejerine, J. J. (1891). Sur un cas de cecite verbale avec agraphie suivi
dautopsie. Memoires Societe Biologique, 3, 197201. D
Dejerine, J. J. (1914). Semiologie des affections du systeme nerveux. Paris:
Masson.
Dejerine, J. J., & Dejerine-Klumpke, A. M. (1895). Anatomie des centres Delayed Matching-to-Sample
nerveux. Paris: Masson.
Dejerine, J. J., & Gauckler, E. (1915). The psychoneuroses and their Delayed Response Tasks
treatment by psychotherapy (S. E. Jelliffe, Trans.). Oxford, England:
Lippincott.
Dejerine, J. J., & Roussy, G. (1906). Le syndrome thalamique. Review of
Neurology (Paris), 12, 521532.
Gauckler, E. (1922). Le Professeur Dejerine (18491917). Paris: Masson.
Miller, M. (1967). Three great neurologists. Proceedings of the Royal
Society of Medicine, 60, 399405. Delayed Nonmatching-to-Sample
Schurch, B., & Dollfus, P. (1998). The Dejerines: An historical review
and homage to two pioneers in the field of neurology and their Delayed Response Tasks
contribution to the understanding of spinal cord pathology. Spinal
Cord, 36, 7886.
DejerineRoussy Syndrome Delayed Object Alternation

J OHN E. M ENDOZA
Delayed Response Tasks
Synonyms
Delayed Prompting
Thalamic pain syndrome
Errorless Learning
Definition
Contralateral loss of or diminished somatosensory

sensation, particularly proprioception or position sense
following a thalamic lesion. The syndrome most com- Delayed Response Tasks
monly results from a vascular lesion affecting the ventral
posterior nucleus. Most notable in this syndrome is the PAUL M ALLOY
concomitant presence of diffuse, lingering pain which Alpert Medical School of Brown University
may be produced by relatively minor and even noncuta- Providence, RI, USA
neous stimuli, while the response to actual painful-type
stimuli may be diminished.
Synonyms
Cross References Delayed alternation; Delayed matching-to-sample;
Delayed nonmatching-to-sample; Delayed object alterna-
Thalamic Pain Syndrome tion; Delayed spatial alternation
790 D Delayed Response Tasks
Description fixate on a central location during the delay interval, to

prevent the use of body posture (rather than working
Delayed response (DR) tasks represent the classic para- memory), and to cue them for the correct response.
digm for studying working memory in both animals and In feature-oriented DR tasks, the location of the re-
humans. Working memory refers to the temporary stor- ward is randomized, and instead some feature of the
age of information in a buffer for rehearsal and organi- response choice is the critical cue to correct responding.
zation of new information, and frontal systems are For example, a cube-shaped cover may be placed over the
thought to subserve this process. Frontal working-memory food dish containing the reward, and a dome-shaped
systems are also involved in the active retrieval of cover may be placed over the other dish. After the delay,
previously stored information through temporal tagging the subject must choose the cube-shaped dish, regardless
and organization of retrieval strategies. The hippocampus of whether it is on the left or right. That is, the features of
and other posterior brain regions, in contrast, are thought the choice, rather than spatial location, are the cue for
to be more involved in memory consolidation and per- correct responding. The delayed object alternation (DOA)
manent storage. Studies utilizing DR tasks have been used task is a two-choice task in which the monkey needs to
to elucidate the neuroanatomical organization of memory correctly select an object that alternates between trials. For
systems in the brain through behavioral, lesion, and delayed matching-to-sample (DMTS) tasks, the subject is
electrophysiological studies. presented with a stimulus array with multiple alternatives
In DR tasks, information is presented to a subject, then (e.g., squares containing different visual patterns), and
withdrawn, and a relatively brief delay interval ensues. The must choose the correct pattern after the delay. Delayed
subject is then presented with a choice of two or more nonmatching-to-sample (DNMTS) tasks are similar to
response alternatives and is required to choose the one DMTS paradigms, except that the subject is required
presented previously to obtain reinforcement. While intact to choose the stimulus that does not match the stimulus
animals can perform these tasks easily, animals with frontal that was presented before the recall delay.
lesions often have trouble performing correctly with delay
intervals as brief as 520 s. DR tasks must be made more
difficult to detect deficits in human patients. This can be Historical Background
accomplished by increasing the delay interval, interpolat-
ing a cognitive distraction task during the delay, and/or Most early DR studies were conducted using the Wiscon-
increasing the number of choices after the delay. sin General Test Apparatus (WGTA). In the WGTA, a
There are several variations of DR tasks, which can be monkey sat in a cage in front of a tray that contained
divided into spatial- and feature-oriented tasks. In general, recessed food wells. The experimenter baited one of the
spatial DR tasks are thought to depend on more dorsal wells with food, covered it, and then lowered a screen to
frontal systems, whereas feature DR tasks are more depen- block the wells from the monkeys view. After the delay
dent on ventral frontal systems. interval, the screen was raised and the monkey made a
Delayed spatial alternation (DA) is the simplest spatial choice of food wells. The WGTA was used for both spatial-
DR task. In a typical animal DA experiment, the subject is and feature-oriented DR tasks.
presented with two food dishes, and a food reward is placed Currently, most animal and human experiments are
in one of the dishes in view of the animal. The dishes are conducted using computerized response panels and auto-
covered and hidden for a delay period and then the animal mated reinforcement devices. These devices provide
is required to choose the correct dish to obtain the food greater precision in timing of responses, and can accom-
reward. After a correct response on one side, the correct modate a much wider variety of stimuli and response
side is switched (alternation), another delay interval ensues devices. Computerized DR tasks are also amenable to
and the subject must choose the other side to obtain the data collection in functional imaging studies, although
reward. Frontal animals have trouble making the switch to some adaptation of the tasks is typically necessary to
the new side, instead tending to perseverate on the previ- limit subject movement.
ously rewarded side. This mirrors the tendency of frontally
lesioned patients to perseverate on habitual or recently
reinforced behavior, even when it is inappropriate to Clinical Uses
current environmental circumstances. Spatial DR tasks
can be made more complex by adding multiple spatial Delayed response deficits have been demonstrated in a
choice locations. Animals can be restrained and trained to variety of diseases affecting frontal systems, including
Delirium D 791
traumatic brain injury, anterior communicating artery

aneurysm, Korsakoff syndrome, degenerative disorders Delirium
(Oscar-Berman, McNamara, & Freedman, 1991), and
schizophrenia. Many studies have investigated the effects R OBERT J. B OLAND
of pharmacological challenges on DR tasks in order to The Warren Alpert School of Medicine at Brown
study the role of various neurotransmitters in working University
memory. However, most versions of DR tasks remain Providence, RI, USA
D
experimental methods for cognitive neuroscience
experiments.
There are a few standardized DR tasks suitable for Synonyms
clinical use. The CANTAB (Cambridge Neuropsychological
Test Automated Battery) consists of computerized tests of Acute brain failure; Acute confusional state; Acute
memory, attention, and executive function. It includes a encephalopathy; Intensive care unit (ICU) psychosis;
DMTS task for the assessment of working memory. Toxic-metabolic encephalopathy

Cross References
Delirium describes a wide variety of confusional states.
CANTAB Generally, it includes several features that are central to
Examiner the disorder: it is acute, has a fluctuating course, and has a
Working Memory gross effect on brain functioning. Most typically, delirium
affects a persons level of consciousness; that is, the per-
sons ability to focus, sustain, and shift attention. In addi-
References and Readings tion, it affects a persons level of arousal, and a delirious
persons behavior can range from lethargic to agitated;
Freedman, M., & Oscar-Berman, M. (1986). Bilateral frontal lobe disease often it will fluctuate between the two states within rela-
and selective delayed response deficits in humans. Behavioral Neuro-
tively brief intervals of time (e.g., several hours). In addi-
science, 100, 433435.
Fuster, J. M. (1989). The prefrontal cortex (2nd ed., p. 255). New York:
tion, it can affect any area of cognitive functioning:
Raven. delirious persons are confused and disoriented (i.e., un-
Goldman-Rakic, P. S. (1987). Circuitry of the prefrontal cortex and the aware of their surroundings). Their thoughts are often
regulation of behavior by representational knowledge. In F. Plum, & disorganized, and may include loose associations, circum-
V. Mountcastle (Eds.), Handbook of physiology (pp. 373417).
stantial or tangential thought, perseverations, or thought
Bethesda: American Physiological Society.
Goldman-Rakic, P. S. (1995). Cellular basis of working memory. Neuron,
blocking. Delirious persons may have disturbances of
14, 477485 perceptions and thought content and they may experience
Oscar-Berman, M., McNamara, P., & Freedman, M. (1991). Delayed- hallucinations or delusions. Higher intellectual functions
response tasks: Parallels between experimental ablation studies and such as the ability to make decisions are usually impaired
findings in patients with frontal lesions. In H. S. Levin, H. M.
because of disorders in these more basic cognitive
Eisenberg, & A. L. Benton (Eds.), Frontal lobe function and dysfunc-
tion. New York: Oxford University Press.
functions.
Rodriguez, J. S., & Paule, M. G. (2009). Working memory delayed
response tasks in monkeys. In J. J. Buccafusco (Ed.), Methods of
behavior analysis in neuroscience. Boca Raton: CRC Press/Taylor & Categorization
Francis Group. http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?
book=frbehav&part=ch12 Delirium is not a disorder, per se, but a syndrome describ-
Rosenkilde, C. E. (1979). Functional heterogeneity of the prefrontal ing the neuropsychiatric expression of gross dysfunctions in
cortex in the monkey. Behavioral and Neural Biology, 25, 301345.
brain physiology, and as such, it is quite heterogeneous.
Typically, delirium is categorized based on a persons level
of arousal and is usually divided into hyperactive and
hypoactive types. This distinction dates back to the ancient
Delayed Spatial Alternation Greeks, who called the two types as phrenitis and lethar-
gus. The delirium associated with complicated alcohol
Delayed Response Tasks withdrawal (delirium tremens) is sometimes included as
792 D Delirium
an example of a hyperactive delirium; however, the condi- days. It may be preceded by a subsyndromal period of
tion, along with the withdrawal caused by other sedatives, more subtle cognitive deficits. The level of confusion and
may represent a distinct condition with unique pathophys- degree of arousal generally fluctuates throughout the day.
iology. Hypoactive delirium, although also common is The following vignette illustrates a typical presentation of
under recognized given its subtler phenomenology, and it delirium:
is sometimes called quiet delirium. That the hyperactive An 82-year-old man was transferred from a nursing
and hypoactive states can co-occur in a mixed state (which home to a general medical hospital for a change in mental
may be more common than either state alone) lends sup- status. Usually quiet and pleasant, he became increasingly
port to the idea that the two types are not distinct entities, suspicious and annoyed at the nursing home staff. He had a
but rather two expressions of the same syndrome. history of Alzheimers disease, which was considered moder-
It should be noted that in the neurology literature, the ate in severity. On admission to the hospital, he was lethar-
word delirium is sometimes used to describe only the gic and slept for most of the morning. Later in the day, he
hyperactive type, and the hypoactive category is referred was seen by the attending physician; at that time, he was
to terms such as acute encephalopathy. However, as awake, alert, and only mildly confused and the physician
discussed above, there is little evidence to suggest that questioned the appropriateness of the patients admission to
the two categories represent meaningful distinctions, the hospital. However, later that evening the patient became
and in the psychiatric literature, delirium refers to argumentative with staff, demanding to leave the hospital.
both the hyperactive and hypoactive types. He seemed to believe he was in fact locked up in a prison,
Delirium is also occasionally categorized by the site in and worried that people were trying to break in through his
which it takes place: thus, the term Intensive Care Unit window in order to harm him. He was given haloperidol,
(ICU) Psychosis is sometimes used in the medical litera- which helped calm him; however, he continued to be para-
ture to describe a particularly troublesome example of a noid and confused. On medical evaluation, a urinary tract
hyperactive delirium seen in the intensive care setting. infection was discovered, and appropriate antibiotics were
Again, such categorizations are of little heuristic or diag- initiated. His periods of belligerence slowly decreased over
nostic value and there is no reason to suspect that the the next several days, and within a week, although still more
delirium occurring in that setting differs from that seen confused than normal, he was able to return to his nursing
elsewhere. home.
This vignette illustrates several typical aspects of de-
lirium, most notably the fluctuating course, which can
Epidemiology
confuse the treating team. The patients dementia can be
seen as a predisposing factor, while the infection was the
Delirium is likely the most common syndrome affecting
likely precipitant. Although treating the precipitants is the
patients in general hospitals. Accurate prevalence figures
mainstay of treatment, it is typical that cognitive improve-
are difficult to obtain given the methodological limita-
ment lags behind treatment of the underlying medical
tions of the various investigations into the disorder. Epi-
condition.
demiological and clinical studies suggest that 1020% of
The prognosis and outcome of delirium is under-
all hospitalized adults, 3040% of elderly hospitalized
standably variable, and dependent on the actual preci-
patients and up to 80% of patients in intensive care
pitants. Although much literature including the
units experience delirium at some time during their hos-
DSM-IV-Text Revision (DSM-IV-TR) (American
pitalization. Delirium is most likely underreported in any
Psychiatric Association, 2000) describes delirium as a
setting; the hypoactive type in particular is often not
transient and reversible state, more recent work suggests
noticed by clinical teams, or misdiagnosed as another
that there are often permanent cognitive deficits following
disorder. The development of validated instruments
an episode of delirium. The syndrome is a poor prognos-
designed to detect delirium (see below) has improved
tic indicator that is associated with high morbidity and
the detection of delirium.
mortality. That this is so may simply reflect the many
serious illnesses than can precipitate a delirium, however
Natural History, Prognostic Factors, some investigators have suggested that the syndrome itself
Outcomes can have a deleterious effect on the course of an illness,
perhaps through the damaging effects of the abnormal
By definition, delirium is an acute syndrome, meaning neurochemical activity that occurs during a delirious
that it comes on rapidly, often in the course of hours to episode.
Delirium D 793
Neuropsychology and Psychology Rating Scale (Trzepacz, Mittal, Torres, Kanary, Norton,
of Delirium & Jimerson, 2001), the Memorial Delirium Assessment
Scale (Breitbart et al., 1997), and the Confusion Assess-
Delirium is a neuropsychological syndrome that can ment Method (Inouye, VanDyck, Alessi, Balkin, Siegal, &
affect any area of cognitive functioning. Its effect on the Horwitz, 1990).
most primitive of functions (attention, concentration, Many disorders can mimic the symptoms of delirium,
and arousal) clearly has effects on more complex func- and the differential diagnosis can be difficult in the acute D
tions such as abstract thinking, judgment, and insight. setting. One of the more challenging distinctions is be-
Decision-making capacity is generally impaired, and tween delirium and the dementias. Although both are
patients (and their families) are encouraged to postpone defined by their cognitive effects, patients with dementia
important decisions until the delirium can be treated. generally have an intact level of consciousness, and the
Many delirious patients, once recovered, do not recourse of dementia (particularly the common ones such
member the episode. In one study, of those who were able as Alzheimers disease) is more chronic and less fluctuat-
to recall it, at least half experienced their delirious episode ing. However, the two disorders frequently co-occur, and
as highly distressing (Breitbart, Gibson, & Tremblay, comorbid delirium including subsyndromal delirium
2002). This is true even for those patients who appeared should be suspected in cases where patients with dementia
calm or sedated at the time they were delirious. have perceptual disturbances or sudden changes in their
mental state (Meagher & Trzepacz, 2007).
Both delirious and psychotic patients can have hallu-
Evaluation cinations and delusions; however, patients with primary
psychotic disorders such as schizophrenia tend to experi-
The provocative behavioral effects of delirium (such as ence their symptoms in the setting of a clear sensorium:
agitated and violent behavior) usually bring patients to they feel alert, awake, and aware of their surroundings.
clinical attention. When these symptoms are lacking, de- Schizophrenic patients generally lack the profound con-
lirium is often missed; thus, the most important part of fusion and general cognitive deficits seen with delirious
the evaluation is maintaining a high level of suspicion for patients. In addition, the delusions and hallucinations
delirium in the clinical setting. Delirium should be sus- experienced in schizophrenia tend to be more elaborate
pected in individuals who have factors that predispose and fixed than with delirious patients.
them to the syndrome. These include preexisting cogni- Delirium, particularly hypoactive delirium, can be
tive disorders, such as any dementia, substance use dis- mistaken for depression, and the psychosomatic medicine
orders (particularly alcoholism), neurological disorders, literature suggests that this misdiagnosis is common in
and the presence of any collection of chronic medical the general hospital setting. Although the two share some
disorders and/or the use of multiple therapeutic medica- features such as impairments in concentration and atten-
tions. Psychiatric disorders alone, apart from the demen- tion, depression has a more gradual onset and a less
tias and substance use disorders do not significantly fluctuating course. Delirious patients may look sad at
increase the risk of a delirium. times, even tearful, however their mood tends to be
When delirium is suspected, the evaluation should more labile than with depressed patients.
focus on the cognitive examination. Evidence of impaired Similarly, mania, particularly severe mania can mimic
attention, disorientation to date and place, and gross the confusion and agitation associated with delirium.
confusion all make delirium a likely explanation. General Again, the course can help distinguish the two, with
cognitive testing such as that used for the Mini-Mental mania usually having a history of a more progressive course
State Exam can show evidence of the gross cognitive leading to the current symptoms. In addition, although
impairment found in delirious patients; however, the severely manic patients can be confused, they tend not to
test is not specific for delirium. It can be useful to include have the gross cognitive changes seen with delirium.
tasks that focus on the attentional deficits seen in deliri- In cases where the clinical exam cannot distinguish
um, and such as Clock Drawing and the Trail Making Test. between delirium and other psychiatric disorders, an
These tests, although limited in scope have the advantage electroencephalography (EEG) may help: the EEG shows
of being simple to use and require little training. diffuse slowing, whereas the EEG is normal in most other
A number of tests specifically designed to detect delir- psychiatric disorders.
ium have been developed; these require specific training Once convinced of the presence of a delirium, the
in their use, and include such tests as the Delirium major evaluative task becomes one of discovering the
794 D Delirium
underlying etiology. Essentially, any process that can cause simple exercises, and sleep hygiene protocols. Most of
a disruption in the normal functioning of the brain can these behavioral strategies have limited support in the liter-
cause a delirium. The most common causes are infections ature, and many have never been tested in the acute setting;
and the toxic effects of drugs and other substances. There however, they have anecdotal support, face validity, and are
are a number of useful mnemonics meant to help one unlikely to harm the patient. There is some methodologi-
remember the potential precipitants: one popular mne- cally sound data to support behavioral interventions for the
monic is the acronym I WATCH DEATH (a potent prevention of delirium in predisposed individuals (Inouye
reminder of the morbidity associated with delirium): et al., 1999) as well as for the efficacy of staff education to
Infections recognize delirium early (Lundstrom, Edlund, Karlsson,
Withdrawal (Alcohol and other substances) Brannstrom, Bucht, & Gustafson, 2005).
Acute Metabolic At times, symptomatic pharmacological treatment of
Trauma delirium becomes necessary. Such treatment is usually
Central nervous system pathology initiated when the behavioral manifestations of delirium,
Hypoxia particularly aggressive or violent behaviors, make it im-
Deficiencies (vitamin, other nutritional) practical or dangerous to wait for the natural improve-
Endocrinopathies ment that will follow the successful treatment of the
Acute vascular disorders underlying precipitants. Alternately, no clear underlying
Toxins/drugs disorder may be found, and yet palliative care may be
Heavy metals indicated to relieve the delirious patients distress.
It is apt to consider these as precipitants than Most commonly, sedating medications are given to
causes. In reality, the cause is usually multifactorial, calm the delirious patient. Most of the evidence for such
combining predisposing factors with acute precipitants treatment is anecdotal or derived from uncontrolled stud-
that upset an already tenuous cognitive balance. It can ies. Historically, the most common medications used in
be argued that neither is a direct cause, but that the the acute setting were narcotics, benzodiazepines, and
combination initiates a cascade of events in the patients antipsychotics. Narcotics are rarely used now except in
brain. A number of experts have used the term acute cases where pain or dyspnea is thought to play a role in
brain failure to describe delirium: the term is meant to the patients general distress. Benzodiazepines are still
imply an analogy to heart failure, in which an already commonly used, however should not be considered a
impaired organ can suddenly and rapidly malfunction first-line medication given their capacity to confuse
after the onset of a seemingly minor insult. patients further. Although this side effect is sometimes
labeled as a paradoxical effect of the drug, it is in fact a
common side effect of all sedative-hypnotic medications.
Treatment Antipsychotics are most commonly used, both typi-
cal antipsychotics such as haloperidol, and the atypical
The most important step in the treatment of delirium is agents such as risperidone, olanzapine, quetiapine, and
recognition of the syndrome. Once recognized, treatment newer agents. All antipsychotics seem to carry the benefit
primarily focuses on discovering and treating the under- of having a calming effect without causing the level of
lying precipitants, and the particular treatment is specific sedation and confusion seen with benzodiazepines. It is
to the medical or neurological disorder. thought that the antipsychotic effect of these agents can
A number of behavioral strategies have been suggested help organize a patients thoughts; this latter supposition is
to minimize the confusion of the delirious patient. These not as well supported, and seems counter to the under-
strategies include indirect environmental interventions, for standing of the pharmacodynamic effects of a group of
example introducing lighting variations (or windows) into drugs that often take weeks to treat psychosis. Anecdotally,
intensive care settings to help orient patients to the time of however, patients do seem less confused and psychotic
day, and the minimization of unnecessary noise. Objects after only a short term of antipsychotics; it may simply
from the patients home may be placed in a hospital room to be that patients can organize their thoughts better once
increase the familiarity of the surroundings or family mem- they are calmer.
bers may be encouraged to remain with the patient when- Many of the side effects that limit the use of antipsy-
ever possible. Direct behavioral interventions include chotics, such as parkinsonian symptoms or tardive dyski-
frequent reorientation of the patient, minimization of nesia, are less relevant in the acute care setting. When
restraints, use of sensory aids (eyeglasses, hearing aids) using antipsychotics, once should watch for the rare but
Delirium D 795
serious adverse effects that could occur, such as an acute Chlorpromazine

dystonia, cardiac dysfunction, or the neuroleptic malig- Clock Drawing
nant syndrome; of these, the latter two are life threatening Dementia
and require immediate discontinuation of the offending Dystonia
agent, close monitoring, and intense general medical sup- Electroencephalography
port. Other side effects, such as akathisia can be difficult Haloperidol
to distinguish from the agitation associated with delirium, Metabolic Encephalopathy D
but should be suspected in cases where the addition of an Mini-Mental State Exam
antipsychotic seems to make the patient more restless. Olanzapine
Many antipsychotics are anticholinergic and thus can Parkinsonism
cause confusion, and the agents with a higher anticholin- Quetiapine
ergic profile should be avoided; these included many of Risperidone
the lower potency antipsychotics such as chlorpromazine Schizotypal Personality Disorder
and thioridazine. Among the newer agents, clozapine and Tardive Dyskinesia
olanzapine are the most anticholinergic. Despite these Thioridazine
concerns, in the majority of cases antipsychotics appear Trail Making Test
to be a safe and at least moderately effective approach.
Despite the reported safety of these agents in the
treatment of delirium, concern has been raised in the References and Readings
wake of the US Food and Drug Administrations (FDA,
2005) warnings about the increased risk of mortality American Psychiatric Association (1999). Practice guideline for the treat-
found in elderly patients with dementia who are treated ment of patients with delirium. American Journal of Psychiatry, 156
(Supplement), 120.
with antipsychotics. The debate on the appropriate risk
American Psychiatric Association (2000). Diagnostic and statistical man-
and benefit balance continues, and specific data on the ual of mental disorders, (4th edn., Text Revision). Washington, DC:
safety in elderly patients with delirium is lacking. Until American Psychiatric Association.
more guidance is available, delirious patients who are Breitbart, W., Gibson, C., & Tremblay, A. (2002). The delirium experi-
elderly, or who have predisposing cardiac conditions ence: Delirium recall and delirium-related distress in hospitalized
patients with cancer, their spouses/caregivers, and their nurses. Psy-
should be monitored closely if an antipsychotic is used.
chosomatics, 43, 183194.
The particular agent to choose is largely a clinical Breitbart, W., Rosenfeld, B., Roth, A., Smith, M. J., Cohen, K., & Passik, S.
decision based on an assessment of likely side effects and (1997). The memorial delirium assessment scale. Journal of Pain and
any history of prior response to a particular drug. Both the Symptom Management, 13, 128137.
American Psychiatric Association (1999) and the Society Inouye, S. K., Bogardus, S. T., Charpentier, P. A., et al. (1999). A multi-
component intervention to prevent delirium in hospitalized older
of Critical Care Medicine (Pandharipande, Jackson, &
patients. New England Journal of Medicine, 340, 669676.
Ely, 2005) recommend the use of haloperidol for the Inouye S. K., VanDyck, C. H., Alessi, C. A., Balkin, S., Siegal, A. P., &
treatment of delirium. Newer agents are likely to be help- Horwitz, R. I. (1990). Clarifying confusion: The confusion assess-
ful, but currently lack sufficient data to support any par- ment method: a new method for detection of delirium. Annals of
ticular agent. Available routes of administration can be Internal Medicine, 113, 941948.
Lundstrom, M., Edlund, A., Karlsson, S., Brannstrom, B., Bucht, G., &
important in choosing an agent as well: haloperidol is
Gustafson Y. (2005). A multifactorial intervention program reduces
available in a short-acting injectable formulation as is the duration of delirium, length of hospitalization, and mortality in
olanzapine; most of the other agents are not. delirious patients. Journal of the American Geriatrics Society, 53,
622628.
Meagher, D., & Trzepacz, P. T. (2007). Phenomenological distinctions
needed in DSM-V: Delirium, subsyndromal delirium, and demen-
Cross References
tias. The Journal of Neuropsychiatry and Clinical Neurosciences, 19,
468470.
Akathisia Pandharipande, P., Jackson, J., & Ely, E. W. (2005). Delirium: Acute
Alzheimers Disease cognitive dysfunction in the critically ill. Current Opinion in Critical
Anticholinergic Care, 11, 360368.
Trzepacz, P. T., Mittal, D., Torres, R., Kanary, K., Norton, J., &
Antipsychotics
Jimerson, N. (2001). Validation of delirium rating scale revised-98:
Arousal Comparison to the delirium rating scale and cognitive test for
Benzodiazepines delirium. The Journal of Neuropsychiatry and Clinical Neurosciences,
Capacity 13, 229242.
796 D Delirium Tremens
U.S. Food and Drug Administration. (2005). FDA public health advisory: The single-score method is particularly problematic for
Deaths with antipsychotics in elderly patients with behavioral distur-
executive-function tests because these tasks typically
bances. Rockville, MD: U.S. Food and Drug Administration.
require both more fundamental cognitive skills (e.g.,
language, visuoperception, and fine motor skills)
and higher-level executive functions for successful perfor-
mance. The D-KEFS was developed to provide measures
Delirium Tremens that assess (a) both fundamental and higher-level skills in
order to evaluate if a patients poor performance on a task
Alcoholic Brain Syndrome is due to an executive-function deficit or to an im-
pairment in a more fundamental cognitive skill and (b)
strategies and error types in order to more precisely char-
acterize the nature of the executive dysfunction.
DelisKaplan Executive Another objective of the D-KEFS was the development
of test-design features that enhanced the instruments
Functioning System sensitivity to mild executive dysfunction or mild frontal-
lobe injury. For instance, switching conditions were added
E RIC M. F INE 1, D EAN C. D ELIS 2 to several traditional executive-function tasks that previ-
1
San Diego, CA, USA ously did not require cognitive flexibility. As an example,
2
University of California, San Diego, School of Medicine in addition to the three standard Stroop conditions
La Jolla, CA, USA (color naming, word reading, and inhibition; Stroop
Color Word Test, Adult), a new Stroop condition was
developed for the D-KEFS Color-Word Interference Test
Synonyms that requires examinees to switch back and forth between
naming the dissonant ink color and reading the dissonant
D-KEFS word. Cognitive switching, or the ability to abandon a
previous response in order to generate a novel or compli-
mentary response (Delis et al., 2001a), is considered one
Description of the hallmarks of executive functions and is particularly
dependent on the integrity of frontal-lobe functioning. In
The DelisKaplan Executive Function system (D-KEFS) is addition, certain D-KEFS tests were designed to contain
the first battery of tests designed exclusively for the assess- capture stimuli that pull for concrete or stimulus-
ment of executive functions in children and adults that bound responding in patients who are vulnerable to this
has been normed on a large national sample representa- tendency due to frontal-lobe injury.
tive of the demographic characteristics of the U.S. popu-
lation (Delis, Kaplan, & Kramer, 2001a). Key objectives in
the development of D-KEFS measures were to provide Descriptions of the D-KEFS Tests
psychologists a comprehensive tool for assessing a wide
array of executive functions, including cognitive flexibili- The D-KEFS consists of nine tests measuring a wide spec-
ty, problem-solving, conceptual reasoning, inhibition, trum of verbal and nonverbal executive functions. These
multitasking, and nonverbal and verbal creativity. tests were either (a) modifications of existing clinical tests of
The D-KEFS can be distinguished from most other executive functions (e.g., Stroop Color-Word Interference
executive-function tests by its embrace of the cognitive Test and Trail-Making Test) in order to increase their sensi-
process approach in which multiple measures are gener- tivity to frontal-lobe dysfunction, (b) or modifications of
ated to isolate the mechanism of a patients poor score on tasks used in past experimental studies of executive func-
a particular task (Delis, Kramer, Kaplan, & Ober, 2000; tions but that had not been developed into standardized
Kaplan, Fein, Kramer, Delis, & Morris, 1999). With the clinical instruments, or (c) relatively new tests that Delis
exception of the Wisconsin Card Sorting Test (Heaton, and colleagues developed.
Chelune, Talley, Kay, & Curtiss, 1993), the majority of
existing clinical measures of higher-level cognitive func- D-KEFS Trail-Making Test
tions yield a single achievement score for each task (e.g., The D-KEFS Trail-Making Test is a modification of the
the Category Test and the traditional Trail-Making Test). traditional Trail-Making Test that was first developed by
DelisKaplan Executive Functioning System D 797
Partington (Partington & Leiter, 1949), modified by army and empty dots. The switching condition, which is novel
psychologists, and then included in the HalsteadReitan to the D-KEFS, has been found to be particularly sensi-
battery. It is one of the most commonly used neuropsy- tive to frontal-lobe dysfunction (e.g., Cato, Delis, Ailds-
chological measures for assessing executive functions. kov, & Bigler, 2004; Kramer et al., 2007).
While the traditional version offers two conditions Part
A (number sequencing) and Part B (numberletter D-KEFS Color-Word Interference Test
switching) the D-KEFS version offers five conditions: The D-KEFS Color-Word Interference Test is a variant of D
visual scanning, motor speed, number sequencing, letter the Stroop Test (Stroop, 1935; Stroop Color Word Test,
sequencing, and numberletter switching. The four base- Adult), a commonly used measure of response inhibition.
line conditions enable the clinician to assess empirically if The D-KEFS version includes two baseline conditions
a patients poor performance on the switching condition is naming of color squares (Condition 1) and reading of
due to a deficit in cognitive flexibility or to impairment in color words printed in black ink (Condition 2) and the
one or more of the underlying component skills needed to traditional interference condition (Condition 3) in which
perform the switching task (i.e., motor speed, visual scan- the examinee must inhibit reading the words in order to
ning, number sequencing, or letter sequencing). name the incongruent ink colors in which these words are
printed in. The D-KEFS version differs from other Stroop
D-KEFS Verbal Fluency Test tasks by the inclusion of a fourth condition that requires
Verbal fluency tasks are among the most commonly admi- the examinee to switch back and forth between naming
nistered neuropsychological measures ( Verbal Fluency). the dissonant ink colors and reading the conflicting
The D-KEFS Verbal Fluency Test is a timed measure that words. This condition has been shown to be particularly
includes (a) a letter fluency condition that requires exam- sensitive to frontal-lobe dysfunction (e.g., Cato et al.,
inees to generate as many words as possible that start with a 2004).
particular letter, (b) a category fluency condition that
requires examinees to generate as many words as possible D-KEFS Sorting Test
from designated semantic categories, and (c) a category The D-KEFS Sorting Test (formerly called the California
switching condition that requires examinees to alternate Card Sorting Test; Delis, Squire, Bihrle, & Massman,
between generating words from two different semantic cate- 1992) was designed to provide a standardized measure of
gories. In general, patients with predominately frontal-lobe conceptualreasoning skills. Specifically, Condition 1, free
damage tend to have more difficulty on the letter fluency sorting, requires examinees to sort cards according to eight
task relative to the category fluency task, whereas patients possible target rules, including five primarily perceptual or
with early Alzheimers disease often show the opposite nonverbal rules (e.g., straight versus curved outer edges),
pattern due to a breakdown in semantic knowledge and three primarily verbal rules (e.g., clothing versus body
(Delis et al., 2001b). parts). In Condition 2 (sort recognition), the examiner
sorts the same sets of cards into two groups according to
D-KEFS Design Fluency Test the eight target sorts and, after each sort, asks the examinee
Design fluency measures, developed as a nonverbal analog to identify and describe the correct rules used to generate
of verbal fluency measures (Jones-Gotman & Milner, the sort. Performance is evaluated both in terms of the
1977; Design Fluency), require examinees to produce total number of correct target concepts reflected in the
as many different designs as possible that meet a particu- examinees sorts, as well as the accuracy and level of ab-
lar criterion (e.g., the designs must always contain four straction of the examinees sort descriptions. This measure
lines) within a time interval. The D-KEFS Design Fluency has been found to be sensitive to frontal-lobe dysfunction
Test is a modified version of traditional procedures. For (e.g., Huey et al., 2009; Fine et al., 2009).
each condition, the examinee is presented rows of boxes
that contain an array of dots and is instructed to draw as D-KEFS Twenty Questions Test
many different designs as possible using only four straight The D-KEFS Twenty Questions Test is a modification of a
lines. The three conditions of the test vary in difficulty, popular, informal game played by children and adults, and
with Condition 1 (filled dots) assessing basic design assesses categorical processing, hypothesis testing, and
fluency, Condition 2 (empty dots only) requiring exam- concept formation. For this task, the examinee is presented
inees to inhibit connecting the filled dots while connect- with a stimulus page depicting pictures of 30 common
ing only the empty dots, and Condition 3 (switching) objects. The examinee tries to ask the fewest number of
requiring examinees to switch between connecting filled yes/no questions in order to identify the unknown target
798 D DelisKaplan Executive Functioning System
object. Multiple process measures are scored, including clearly displayed to the examiner in the stimulus booklet
level of abstract thinking, error types, and response stra- and the response form.
tegies (e.g., verbal versus nonverbal). This test has been Each D-KEFS test is a stand-alone instrument that
found to be sensitive to focal frontal lesions (Baldo, Delis, can be administered individually or with other D-KEFS
Wilkins, & Shimamura, 2004). tests. For all of the primary measures and many of the
optional measures, the raw scores are converted to scaled
D-KEFS Word Context Test scores, with a mean of 10 and a standard deviation of 3, for
The D-KEFS Word Context Test is an adaptation of a test each of the following 16 age groups: 8, 9, 10, 11, 12, 13, 14,
developed originally for studying how children acquire 15, 1619, 2029, 3039, 4049, 5059, 6069, 7079, and
word meanings (Werner & Kaplan, 1952). The examinee 8089. Raw scores for several of the optional measures
is asked to discover the meaning of mystery words based have limited ranges in normative (nonclinical) popula-
on clues given in sentences. For each mystery word, the tions, and therefore they are corrected using cumulative
examinee is shown five sentences (clues) that assist with percentile ranks for each of the 16 age groups. The D-KEFS
decoding the meaning of the words. This test is a measure scoring software is available, which automatically com-
of deductive reasoning and verbal abstract thinking and putes many of the scoring formulas and converts raw
patients with focal frontal lesion exhibit deficits on this scores into standardized scores. Most traditional execu-
measure (Keil, Baldo, Kaplan, Kramer, & Delis, 2005). tive-function tests do not provide alternate forms, which
can be problematic for repeat examinations. However, the
D-KEFS Towers Test D-KEFS provides alternate forms for three of the tests that
The D-KEFS Towers Test is a modified version of other are particularly prone to practice effects (i.e., Sorting Test,
tower tasks that have been used in experimental studies. Twenty Questions Test, and Verbal Fluency Test).
The examinee is asked to build target towers by moving
two to five disks of different sizes across three pegs in as
few moves as possible while adhering to two rules: (a) Normative Sample
move only one disk at a time and (b) never placing a
larger disk over a smaller disk. The D-KEFS Tower Test The D-KEFS was standardized on a nationally representa-
assesses several aspects of executive functioning, including tive, stratified sample of 1750 children, adolescents, and
spatial planning, rule violations, and inhibition. This test adults, aged 889 years. Stratification was based on age,
has been found to be sensitive to focal frontal lesions sex, race/ethnicity, years of education, and geographic re-
(Yochim, Baldo, Kane, & Delis, 2009). gion. The 2000 U.S. census figures were used as target values
for the composition of the D-KEFS normative sample.
D-KEFS Proverb Test There were 75 175 people in each of the 16 age groups.
The D-KEFS Proverb Test was modeled after a prov- The D-KEFS sample was comprised of approximately equal
erb interpretation measure developed in the 1950s by proportions of men and women for most of the age groups;
Gorham (1956). For the D-KEFS version, an examinee is however, the older age groups had more women than men,
asked to interpret proverbs in two conditions: (a) free which is consistent with the census data. The D-KEFS
inquiry where the examinee generates his or her own sample was divided into five major educational groups
interpretations of the proverbs and (b) multiple choice used by the U.S. Census: less than or equal to 8 years,
where the examinee selects the best interpretation from 911 years, 12 years, 1315 years, and greater than or
among four alternatives. This task measures metaphorical equal to 16 years. For examinees between the ages of
thinking and provides a means for comparing generation 8 and 19, the mean parental education was substituted.
versus comprehension of abstract verbal information.
This test has been found to be sensitive to frontal-lobe
dysfunction (McDonald, Delis, Norman, Tecoma, &
Iragui-Madozi, 2008)
Most of the D-KEFS tests were developed in the late 1980s
and early 1990s by Delis and colleagues, with the entire set
Administration and Scoring of D-KEFS instruments assembled in 1994. The prelimi-
nary measures underwent a try-out study of approxi-
Instructions for administration are given in the stimulus mately 300 normative subjects and 50 mixed neurological
booklet or record form. The required materials, discon- patients, and modifications were made to improve the
tinued rules, time limits, and standardized prompts are reliability and validity of the measures.
DelisKaplan Executive Functioning System D 799
Psychometric Data performance on a number of D-KEFS measures. The test

manual includes correlations between the CVLT-II (Delis
Reliability and Validity et al., 2000), a measure of verbal learning and memory
( California Verbal Learning Test), and the D-KEFS in a
Evidence of the reliability and validity of the D-KEFS is sample of 292 adults. Correlations between the tests were
discussed in detail in the technical manual (Delis, Kaplan, for the most part not significant, which supports the
& Kramer, 2001b; also see, Delis, Kramer, Kaplan, & discriminate validity of the D-KEFS (for additional dis- D
Holdnak, 2004; Homack, Lee, & Riccio, 2005). Internal cussion of validity studies of the D-KEFS, see Delis et al.,
consistency (split-half coefficients), testretest reliability, 2001b; Delis et al., 2004; Homack et al., 2005).
standard errors of measurement, and confidence intervals
were estimated for each D-KEFS test. The split-half reliabil-
ity estimates varied across measure and across age group, Clinical Uses
and the majority of tests had moderate or better reliability
estimates (Delis et al., 2001b; Homack et al., 2005). Simi- Consistent with a stated aim of the D-KEFS, numerous
larly, testretest reliability estimates varied considerably studies have demonstrated that the D-KEFS is sensitive to
across task and age group, and most of the testretest frontal-lobe dysfunction and executive-function deficits
coefficients were adequate (Delis et al., 2001b; Homack associated with a variety of neurological, developmental,
et al., 2005). Alternate forms reliability was provided for and psychiatric disorders.
the D-KEFS Verbal Fluency Test, Sorting Test, and Twenty A series of studies by Baldo and colleagues have demon-
Questions Test. Most of the measures possessed adequate strated that patients with focal frontal-lobe injury have def-
alternate forms reliability, although the reliability coeffi- icits on a variety of D-KEFS measures, including the D-KEFS
cients for some measures from the Twenty Questions Test Towers Test (Yochim et al., 2009), the D-KEFS Trail-Making
were relatively low (Delis et al., 2001b). Test (Yochim, Baldo, Nelson, & Delis, 2007), the Twenty
The technical manual includes evidence of validity Questions Test (Baldo et al., 2004), and the Word Context
in the form of correlations between D-KEFS measures, Test (Keil et al., 2005). Further evidence of the D-KEFS
between the D-KEFS and other tasks (i.e., California Verbal sensitivity to frontal-lobe dysfunction is found in a series
Learning Test-II (CVLT-II); Delis et al., 2000; and the of studies by McDonald and colleagues examining D-
Wisconsin Card Sorting Test; Heaton et al., 1993), and KEFS performance in patients with frontal-lobe epilepsy.
findings from clinical populations (see clinical uses below). Results from these studies indicate that frontal-lobe epilep-
Many of the validity studies of the D-KEFS have been sy is associated with deficits on D-KEFS measures that
published in refereed scientific journals rather than in emphasize cognitive switching (i.e., the numberletter
the test manual, with scientific journals often requiring switching from the Trail-Making Test, design fluency
more rigorous methodology than the validity studies switching, inhibition/switching from the Color-Word
often reported in test manuals (Delis et al., 2004). Interference Test; McDonald, Delis, Norman, Tecoma, &
In general, primary measures from the same test were Iragui, 2005a, b, c) and verbal abstraction (i.e., the Prov-
more highly correlated, and the strength and association erbs Test; McDonald, Delis, Kramer, Tecoma, & Iragui,
between variables varied considerably across the age groups. 2008). In addition, recent studies utilizing quantitative
The correlations between optional (process) measures magnetic resonance imaging (MRI) to elucidate the
tended to be low, which was expected given that normative brain regions underlying performance on the D-KEFS
(nonclinical) populations often have reduced ranges of have provided further support for the utility of particular
these scores (e.g., error measures are typically low in nor- D-KEFS measures (i.e., Design Fluency Test, Towers Test,
mative populations but significantly elevated in certain and Sorting Test) in assessing frontal-lobe functions (see
clinical populations). As evidence of convergent validity, Kramer et al., 2007; Carey et al., 2008; Fine et al., 2009).
the manual reports that the D-KEFS Sorting Test and the In addition, the clinical utility of various D-KEFS subt-
Wisconsin Card Sorting Test were moderately correlated ests has been demonstrated in studies of clinical popula-
in a small sample of participants (n = 23). In addition, tions, including multiple sclerosis (Parmenter et al., 2007),
a recent study by Floyd, McCormack, Ingram, Davis, cardiovascular disease (Jefferson, Poppas, Paul, & Cohen,
Bergeron, and Hamilton (2006) demonstrated that partic- 2007; Kramer, Reed, Mungas, Weiner, & Chui, 2002),
ular clinical clusters from the WoodcockJohnson-III autistic spectrum disorders (Kleinhans, Akshoomoff, &
Tests of Cognitive Abilities that draw upon aspects of Delis, 2005), Parkinsons disease (Beatty & Monson,
executive functions were significantly correlated with 1990), schizophrenia (Lysaker, Whitney, & Davis, 2006;
800 D DelisKaplan Executive Functioning System
Kiang, Light, Prugh, Coulson, Braff, & Kutas, 2007), and Kaplan executive function system sorting test. Journal of Clinical and
in children with heavy prenatal alcohol exposure (Matt-
Floyd, R. G., McCormack, A. C., Ingram, E. L., Davis, A. E., Bergeron, R.,
son, Goodman, Caine, Delis, & Riley, 1999; Schonfield, & Hamilton, G. (2006). Relations between the Woodcock-Johnson
Mattson, Lang, Delis, & Riley, 2001). III clinical clusters and measures of executive functions from the
Delis-Kaplan executive function system. Journal of Psychoeducational
Assessment, 24, 303317.
Cross References Gorham, D. R. (1956). Use of the proverbs test for differentiating schizo-
phrenics from normals. Journal of Consulting Psychology, 20(6),
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Learning Test-II) Wisconsin card sorting test manual - Revised and expanded. Odessa,
Category Test FL: Psychological Assessment Resources.
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function system (test review). Journal of Clinical and Experimental
Frontal Lobe Syndrome Huey, E. D., Goveia, E. N., Paviol, S., Pardini, M., Krueger, F.,
Stroop Color Word Test, Adult Zamboni, G., et al. (2009). Executive dysfunction in frontotemporal
Trail Making Test dementia and corticobasal syndrome. Neurology, 72(5), 453459.
Verbal Fluency Jefferson, A. L., Poppas, A., Paul, R. H., & Cohen, R. A. (2007). Systemic
hypoperfusion is associated with executive dysfunction in geriatric
Wisconsin Card Sorting Test
cardiac patients. Neurobiology of Aging, 28, 477483.
Jones-Gotman, M., & Milner, B. (1977). Design fluency: The invention of
nonsense drawings after focal cortical lesions. Neuropsychologia, 155
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Kaplan, E., Fein, D., Kramer, J., Delis, D., & Morris, R. (1999). WISC-III
Baldo, J. V., Delis, D. C., Wilkins, D. P., & Shimamura, A. P. (2004). Is it as a process instrument. San Antonio, TX: The Psychological
bigger than a breadbox? Performance of patients with prefrontal Corporation.
lesions on a new executive function test. Archives of Clinical Neuro- Keil, K., Baldo, J., Kaplan, E., Kramer, J., & Delis, D. C. (2005). The role of
psychology, 19(3), 407419. the frontal cortex in inferential reasoning: Evidence from the word
Beatty, W. W., & Monson, N. (1990). Problem solving in Parkinsons context test. Journal of the International Neuropsychological Society,
disease: Comparison of performance on The Wisconsin and 11, 426433.
California card sorting tests. Journal of Geriatric Psychiatry & Neu- Kiang, M., Light, G. A., Prugh, J., Coulson, S., Braff, D. L., & Kutas, M.
rology, 3, 163171. (2007). Cognitive, neurophysiological, and functional correlates of
Carey, C. L., Woods, S. P., Damon, J., Halabi, C., Dean, D., Delis, D. C. proverb interpretation abnormalities in schizophrenia. Journal of the
et al. (2008). Discriminant validity and neuroanatomical correlates International Neuropsychological Society, 13, 653663.
of rule monitoring in frontotemporal dementia in Alzheimers dis- Kleinhans, N., Akshoomoff, N., & Delis, D. C. (2005). Executive func-
ease. Neuropsychologia, 46(4), 10811087. tions in autism and Aspergers disorder: Flexibility, fluency, and
Cato, M. A., Delis, D. C., Aildskov, T. J., & Bigler, E. (2004). Assessing the inhibition. Developmental Neuropsychology, 27(3), 379401.
elusive cognitive deficits associated with ventromedial prefrontal Kramer, J. H., Reed, B. R., Mungas, D., Weiner, M. W., & Chui, H. C.
damage: A case of a modern-day Phineas Gage. Journal of Interna- (2002). Executive dysfunction in subcortical ischemic vascular disease.
tional Neuropsychological Society, 10(3), 453465. Journal of Neurology, Neurosurgery, & Psychiatry, 72, 217220.
Delis, D. C., Squire, L. R., Bihrle, A., & Massman, P. (1992). Componen- Kramer, J. H., Quitania, L., Dean, D., Heuhaus, J., Rosen, H. J., Halabi, C.,
tial analysis of problem-solving ability: Performance of patients with et al. (2007). Magnetic resonance imaging correlates of set shifting.
frontal lobe damage and amnesic patients on a new sorting test. Journal of the International Neuropsychological Society, 13(3),
Neuropsychologia, 30, 683697. 386392.
Delis, D. C., Kramer, J., Kaplan, E., & Ober, B. A. (2000). California verbal Lysaker, P. H., Whitney, K. A., & Davis, L. W. (2006). Awareness of illness
learning test - Second Edition. San Antonio, TX: The Psychological in schizophrenia: Associations with multiple assessments of executive
Corporation. functions. Journal of Neuropsychiatry & Clinical Neurosciences, 18,
Delis, D. C., Kaplan, E., & Kramer, J. H. (2001a). Delis-Kaplan executive 516520.
function system: Examiners manual. San Antonio, TX: The Psycho- Mattson, S. N., Goodman, A. M., Caine, C., Delis, D. C., & Riley, E. P.
logical Corporation. (1999). Executive functioning in children with heavy prenatal alco-
Delis, D. C., Kaplan, E., & Kramer, J. H. (2001b). Delis-Kaplan executive hol exposure. Alcoholism: Clinical and Experimental Research, 23
function system: Technical manual. San Antonio, TX: The Psycholog- (11), 18081815.
ical Corporation. McDonald, C. R., Delis, D. C., Norman, M. A., Tecoma, E. S., & Iragui-
Delis, D. C., Kramer, J. H., Kaplan, E., & Holdnak, J. (2004). Reliability Madozi, V. J. (2005a). Is impairment in set-shifting specific to fron-
and validity of the Delis-Kaplan executive function system: An update. tal lobe dysfunction? Evidence from patients with frontal lobe or
Journal of the International Neuropsychological Society, 10, 301303. temporal-lobe epilepsy. Journal of the International Neuropsychologi-
Fine, E. M., Delis, D. C., Dean, D., Beckman, V., Miller, B. L., Rosen, H. J., cal Society, 11(4), 477481.
& Kramer, J. H. (2009). Left frontal lobe contributions to concept McDonald, C. R., Delis, D. C., Norman, M. A., Tecoma, E. S., & Iragui,
formation: A quantitative MRI study of performance on the Delis- V. J. (2005b). Discriminating patients with frontal lobe epilepsy and
Delusion D 801
temporal lobe epilepsy: Utility of a multi-level design fluency test. beliefs are sustained despite incontrovertible evidence to
the contrary. Delusions can occur in the context of a wide
McDonald, C. R., Delis, D. C., Norman, M. A., Wetter, S. R., Tecoma,
E. S., & Iragui, V. J. (2005c). Response inhibition and set-shifting in
variety of psychiatric and medical conditions (for a review
patients with frontal lobe epilepsy or temporal-lobe epilepsy. Epilepsy see Fenning et al., 2005) including the following:
& Behavior, 7, 438446.
McDonald, C. R., Delis, D. C., Kramer, J. H., Tecoma, E. S., & Iragui, V. J.
Psychiatric disorders including psychotic disorders
(2008). A componential analysis of proverb interpretation in (schizophrenia, schizoaffective disorder, and delusional
patients with frontal lobe epilepsy and temporal lobe epilepsy: rela- disorder), mood disorders (bipolar disorder and de- D
tionships with disease-related factors. The Clinical Neuropsychologist, pression), and substance-related disorders (ampheta-
22(3), 480496.
mines, cocaine, alcohol, cannabis, and hallucinogen).
Parmenter, B. A., Zivadinov, R., Kerenyi, L., Gavett, R., Weinstock-
Guttman, B., Dwyer, M. G., et al. (2007). Validity of the Wisconsin
Neurodegenerative disorders such as Alzheimers dis-
Card sorting and Delis-Kaplan executive function system (D-KEFS) ease, frontotemporal dementia, dementia with Lewy
sorting tests in multiple sclerosis. Journal of Clinical and Experimen- bodies, Huntingtons disease, basal ganglia calcifica-
tal Neuropsychology, 29, 215223. tion, and multiple sclerosis.
Partington, J. E., & Leiter, R. G. (1949). Partingtons pathway test. The Other central nervous system disorders including
Psychological Service Center Bulletin, 1, 920.
Reitan, R. M., & Wolfson, D. (1993). Halstead-Reitan neuropsychological
brain tumors, particularly temporal lobe and deep
battery. Tuscon, AZ: Neuropsychology Press. hemispheric tumors, epilepsy, subdural hematomas,
Schonfield, A. M., Mattson, S. N., Lang, A. R., Delis, D. C., & Riley, E. P. anoxic brain injuries, and fat embolism.
(2001). Verbal and nonverbal fluency in children with heavy prenatal Metabolic conditions including hypercalcemia, hypo-
alcohol exposure. Journal of Studies on Alcohol, 62, 239246.
natremia, hypoglycemia, uremia, hepatic encephalop-
Stroop, J. R. (1935). Studies of interference in serial verbal reaction.
Journal of Experimental Psychology, 18, 643662.
athy, and porphyria.
Werner, H., & Kaplan, E. (1952). The acquisition of word meanings: A Vascular conditions such as atherosclerotic vascular
developmental study. Monographs of the Society for Research in Child disease, especially when associated with diffuse, tem-
Development,15 (Serial No. 51). United Kingdom: Blackwell poroparietal or subcortical lesions, hypertensive en-
Publishing.
cephalopathy, subarachnoid hemorrhage, and
Yochim, B., Baldo, J., Nelson, A., & Delis, D. C. (2007). D-KEFS Trail
Making Test performance in patients with lateral prefrontal cortex
temporal arteritis.
lesions. Journal of the International Neuropsychological Society, 13, Infectious diseases such as human immuno-
704709. deficiency virus/acquired immune deficiency syn-
Yochim, B. P., Baldo, J. V., Kane, K. D., & Delis, D. C. (2009). D-KEFS drome, CreutzfeldtJakob disease, syphilis, malaria,
Tower Test performance in patients with lateral prefrontal cortex
and acute viral encephalitis.
lesion: The importance of error monitoring. Journal of Clinical and
Endocrinopathies such as Addison disease, Cushing
syndrome, hyperthyroidism or hypothyroidism, and
panhypopituitarism.
Vitamin deficiencies including vitamin B-12 deficiency,
Delusion folate deficiency, thiamine deficiency, and niacin
deficiency.
A NTHONY C. RUOCCO 1, FARZIN I RANI 2 Medications including adrenocorticotropic hor-
1 mones, anabolic steroids, corticosteroids, cimetidine,
University of Illinois at Chicago
Chicago, IL, USA antibiotics (cephalosporins, penicillin), disulfiram,
2 and anticholinergic agents.
University of Pennsylvania
Philadelphia, PA, USA Toxins such as mercury, arsenic, manganese, and
thallium.
Synonyms Categorization
Psychotic misconception
Delusions are usually categorized according to the follow-
ing themes:
Description Other delusions may involve themes of guilt, jealousy,
or religion. Delusions may also be classified as bizarre or
A delusion is an erroneous belief typically associated with non-bizarre. Bizarre delusions are implausible beliefs,
misinterpretation of perceptions or experiences. These which are incomprehensible and are not associated with
802 D Delusion
typical life experiences (e.g., person believes tiny robots psychotic features, as they have a longer time to recovery
are recording his or her conversations by installing micro- and are more likely to be treated with antipsychotic med-
phones in his or her teeth). Bizarre delusions are asso- ication (Maj, Pirozzi, Magliano, Fiorillo, & Bartoli, 2007).
ciated with schizophrenia and its spectrum disorders.
Non-bizarre delusions are plausible, understandable, and
consistent with a persons daily experiences (e.g., person Neuropsychology of Delusion
believes his or her spouse is unfaithful). Delusions can
be systematized or organized around a common theme. A delusion is a symptom of psychosis, which may be
Delusions may be congruent with the persons mood (e.g., present in a variety of neuropsychiatric disorders, including
person believes he or she can walk on water during the delirium, dementia, brain injury, and psychiatric disorders.
course of a manic episode) or the content of the delusion One prominent theory of the neuropathogenesis of delu-
can also be incongruent with the persons mood (e.g., sions and hallucinations in schizophrenia is a reactive
person believes he or she is dead but is not depressed). synaptic regeneration in brain regions, such as the frontal
cortex, which receive degenerating temporal lobe connec-
tions (Stevens, 1992). These connections might result in
Epidemiology spontaneous, stimulus-independent retrieval of episodic
memories that resemble delusions. Positive symptoms of
A World Health Organization survey of first-contact inci- schizophrenia, including delusions, share minimal rela-
dence of schizophrenia in 10 countries found the incidence tions with neuropsychological function, whereas cogni-
of referential and persecutory delusions to be the most tive deficit is more commonly associated with negative
common (Sartorius et al., 1986). Delusional thinking symptoms (e.g., deficiencies in emotional responsiveness,
may be quasidimensional in nature (i.e., both continuous spontaneous speech, and volition) (OLeary et al., 2002).
and dichotomous), ranging from overvalued ideas on one Several brain structures have been associated with delu-
hand to frank psychosis on the other. The prevalence of sions in a variety of neuropsychiatric disorders. Delusions
delusional beliefs in nonclinical samples is estimated at in Alzheimers disease are correlated with lower gray mat-
between 1 and 3 percent, which may vary depending on ter density in the left frontal lobe, right frontoparietal
the content of the delusion and the demographic charac- cortex, and left claustrum (Bruen, McGeown, Shanks, &
teristics of the sample (for a review, see Freeman, 2007). Venneri, 2008). Lower prefrontal cortex volumes are
related to delusions in older adults with depression
(Kim et al., 1999). In patients with schizophrenia, de-
Natural History, Prognostic Factors, lusional symptoms have been associated with smaller
Outcomes right planum temporale volumes (Yamasaki et al., 2007).
Karl Jaspers, a German philosopher and physician, was

among the first to describe the nature of delusions. In his Evaluation
book General Psychopathology, originally published in
1913, he outlined three classic criteria for a delusion: In evaluating the presence of delusions, a distinction
conviction, incorrigibility, and impossibility. These should be drawn between delusions and overvalued
notions remain visible in modern descriptions of delu- ideas, which may be held with less conviction, particularly
sion, such as in the American Psychiatric Associations in the face of clear contradictory evidence regarding the
Diagnostic and Statistical Manual of Mental Disorders. truthfulness of the belief. In neuropsychological evalua-
Current attempts at understanding the nature of delu- tion, the presence of delusions may aid in differential
sions examine the contributions of life experiences (e.g., diagnosis. For example, Alzheimers disease and dementia
paranoia-inducing events), perceptual and attentional with Lewy bodies are more likely to present with delusions
factors (e.g., selective attention to threat-related informa- as a component of the neuropsychiatric disorder. Certain
tion), and inferential processes (e.g., attributions of nega- delusions are sometimes present in specific neuropsychia-
tive events) to the development and maintenance of tric disturbances. For example, Capgras delusion, or the
delusions. Over the lifespan, delusions tend to decrease in belief that impostors have replaced persons familiar to
severity in patients with schizophrenia (Mancevski et al., the individual, is sometimes observed in patients with
2007). Outcomes for delusional patients with major de- Alzheimers disease, dementia with Lewy bodies, and
pressive disorder tend to be worse than those without schizophrenia.
Delusion D 803
Delusion. Table 1
Theme Description
Persecutory Belief of being tormented, followed, tricked, spied on, or ridiculed
Referential Belief that certain gestures, comments, passages from books, newspapers, song lyrics, or other
environmental cues are specifically directed at the patient
Grandiose Belief about exaggerated power, knowledge, importance, or a special relationship to a deity or famous person D
Somatic Belief that there is a change or disturbance in ones body appearance or functioning
Control Belief that ones feelings, impulses, thoughts, or actions are under the control of some external force
Thought Belief that ones thoughts are audible to others
broadcasting
Thought insertion Belief that thoughts which are not ones own have been inserted into his or her mind
Thought Belief that ones thoughts have been removed from his or her mind
withdrawal
Erotomanic Belief that another person is in love with him or her
Treatment Dementia with Lewy Bodies

Psychotherapy
Antipsychotics are the drugs of choice for treating delu-
sions. The strong connection between neuropsychological
function and functional disability makes improving cog-
nitive abilities a primary target of pharmacologic treat-
Bruen, P. D., McGeown, W. J., Shanks, M. F., & Venneri, A. (2008).
ment in schizophrenia. Antipsychotic drugs, however, Neuroanatomical correlates of neuropsychiatric symptoms in Alz-
appear to have variable effects on neuropsychological heimers disease. Brain, 131, 24552463.
function (Jerrell & Ramirez, 2008). Conventional antipsy- Fennig, S., Fochtmann, L. J., & Bromet, E. J. (2005). Delusional and
chotics have several adverse side effects, including neuro- shared psychotic disorder. Kaplan & Sadocks comprehensive textbook
of psychiatry (8th ed., pp. 15251533). Philadelphia, PA: Lippincott
logic (extrapyramidal reactions, tardive dyskinesia, and
Williams & Wilkins.
miscellaneous neurologic effects), cardiovascular (ortho- Freeman, D. (2007). Suspicious minds: The psychology of persecutory
static hypotension, tachycardia, and electrical conduction delusions. Clinical Psychology Review, 27, 425457.
delays), and anticholinergic (both peripheral and central Jerrell, J. M., & Ramirez, P. M. (2008). Changes in neuropsychological
manifestations). Atypical antipsychotics tend to have functioning following treatment with risperidone, olanzapine, and
conventional antipsychotic medications. Human Psychopharmacolo-
comparatively fewer side effects than conventional anti-
gy, 23, 595604.
psychotics, but notable risks include extrapyramidal side Kim, D. K., Kim, B. L., Sohn, S. E., Lim, S. W., Na, D. G., et al. (1999).
effects and metabolic syndrome. Caution must be taken in Candidate neuroanatomic substrates of psychosis in old-aged de-
prescribing antipsychotic drugs to older adults with psy- pression. Progress in Neuro-psychopharmacology & Biological Psychi-
chosis. In 2005, the Food and Drug Administration issued atry, 23, 793807.
Maj, M., Pirozzi, R., Magliano, L., Fiorillo, A., & Bartoli, L. (2007).
a black-box warning because atypical antipsychotics
Phenomenology and prognostic significance of delusions in major
were associated with increased risk of death in dementia depressive disorder: A 10-year prospective follow-up study. Journal
patients. The conventional antipsychotics may also in- of Clinical Psychiatry, 68, 14111417.
crease dementia patients risk of death. Cognitive-behav- Mancevski, B., Keilp, J., Kurzon, M., Berman, R. M., Ortakov, V., et al.
ioral psychotherapy has also demonstrated efficacy for the (2007). Lifelong course of positive and negative symptoms in chron-
ically institutionalized patients with schizophrenia. Psychopathology,
treatment of delusions in medication-resistant schizo-
40, 8392.
phrenia (Rathod, Kingdon, Weiden, & Turkington, 2008). OLeary, D. S., Flaum, M., Kesler, M. L., Flashman, L. A., Arndt, S., et al.
(2000). Cognitive correlates of the negative, disorganized, and psy-
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Rathod, S., Kingdon, D., Weiden, P., & Turkington, D. (2008). Cognitive-
behavioral therapy for medication-resistant schizophrenia: A review.
Alzheimers Dementia Journal of Psychiatric Practice, 14, 2233.
Capgras Syndrome Sartorius, N., Jablensky, A., Korten, A., Ernberg, G., Anker, M., et al.
Delirium (1986). Early manifestations and first-contact incidence of
804 D Dementia
schizophrenia in different cultures. A preliminary report on the initial 1. Multiple cognitive deficits are present, including the
evaluation phase of the WHO Collaborative Study on determinants of
following:
outcome of severe mental disorders. Psychological Medicine, 16,
909928.
(a) Memory impairment (new learning or recall)
Stevens, J. R. (1992). Abnormal reinnervation as a basis for schizophre- (b) One or more of aphasia, apraxia, agnosia, or
nia: A hypothesis. Archives of General Psychiatry, 49, 238243. executive dysfunction
Yamasaki, S., Yamasue, H., Abe, O., Yamada, H., Iwanami, A., et al. 2. Cognitive deficits significantly impair social or occu-
(2007). Reduced planum temporale volume and delusional beha-
pational functioning and reflect a significant decline
viour in patients with schizophrenia. European Archives of Psychiatry
and Clinical Neuroscience, 257, 318324.
from a previous level of higher functioning
3. Cognitive deficits are not exclusively present during a
delirium
4. Cognitive deficits cannot be better attributed to
another Axis I disorder, such as depression or schizo-
Dementia phrenia (Rabin, Wishart, Fields, & Saykin, 2006)
While the etiology of every type of dementia is not
K ATHRYN V. PAPP
fully understood, there are a wide variety of causes
The University of Connecticut
including vascular changes, inherited genes, vitamin
Storrs, CT, USA
deficiencies, prions, and viruses. The causes of demen-
tia may not be mutually exclusive, with a number of
pathologies contributing to a patients symptoms. Mul-
Synonyms
tiple types of dementia have been described, which
roughly fall into two groups that exemplify the initial
Senility
area of degeneration: Cortical versus subcortical.
Dementias are more easily distinguished from one an-
other in early stages but become increasingly difficult
to differentiate as pathology becomes more global. The
time period from diagnosis to death involves interindi-
Dementia is characterized by a progressive decline in mul-
vidual variation and variation based on the dementias
tiple domains of cognitive functioning which ultimately
etiology. Mortality can be as short as 2 months after
interferes with independent daily living and results in a
symptom onset in AIDS dementia and Creutzfeldt
shortened lifespan. It is not a disease or a disorder in itself
Jakob disease and as long as 20 years in Alzheimers
but a descriptive symptom complex with a number of
disease (AD).
potential underlying pathologies and/or traumas which
result in deficits in multiple domains. It is largely a diagno-
sis of the elderly, but certain forms such as Multiple sclero- Categorization
sis and Huntingtons disease can appear in middle age.
Variations such as CreutzfeldtJakob disease and head Dementia can be broadly characterized as Cortical (origi-
trauma, which results in a nonprogressive dementia, can nating in cortical areas; characterized by intellectual and
occur at any age. In progressive dementia, early symptoms memory dysfunction, aphasia, agnosia, and apraxia) ver-
can include memory complaints (forgetting names and sus Subcortical (originating in frontosubcortical systems
appointments) and difficulty in learning new material. As such as brainstem, thalamus, and basal ganglia; initial
dementia progresses, complaints may include difficulties motor dysfunction and cognitive slowing, with language
with expressive and receptive language, impairments in and memory the last faculties affected). These distinctions
executive function (poor judgment, difficulty planning), are not necessarily mutually exclusive and there is much
an inability to remember already learned information overlap (Table 1).
(such as names of family members), and changes in per- Until approximately 1015 years ago, dementia was
sonality. Dementia patients ultimately require full nursing largely subdivided into nonspecific atrophy, Parkinsons
care in the last stages of disease; they suffer from inconti- disease, dementia with Lewy bodies, AD, and Picks
nence, motor inability, echolalia, paraolia, and the return of disease. Since then, an explosion in both research and
primitive reflexes. A common cause of death is infection. imaging techniques as well as a more thorough study of
The general characteristics of dementias (as outlined in the cognitive deficits earlier in the disease course has
detail for specific dementias in the DSM-IV-TR) are: shown that these categorizations may oversimplify the
Dementia D 805
Dementia. Table 1 Types of dementias
Cortical dementias Subcortical dementias Other dementias

Alzheimers disease (AD) Parkinsons disease Multiple sclerosis
Lewy body dementia Huntingtons disease AIDS dementia
Frontotemporal dementia Wilsons disease WernickeKorsakoffs disease
Picks disease Normal pressure hydrocephalous CreutzfeldtJakob disease D
Semantic dementia/primary progressive aphasia Progressive supranuclear palsy Head trauma
Vascular dementia/multi-infarct dementia
differential etiology and neuropathology of dementia. Ott, Breteler, Bots, & Slooter, 1997); high stress (Pope,
Further research may parse out further categories and Shue, & Beck, 2003); exposure to aluminum, copper, and
stages of dementia in the future. iron in the water supply (Christen, 2000); and occupa-
tional exposure to fumigants and/or defoliants (Tyas,
Manfreda, Strain, & Montgomery, 2001).
Epidemiology Several protective factors have also been explored,
with varying degrees of empirical support, including
AD is the most common form of dementia with estimates high educational attainment (Ott, Van Rossum, Van
that account for 5080% of dementia cases. Other com- Harskamp, Van de Mheen, Hofman, & Breteler, 1999),
mon forms include Vascular dementia, which accounts strong social networks (Fratiglioni, Paillard-Borg, &
for 15% of cases, and dementia with Lewy Bodies which, Winbald, 2004), participation in leisure activities
accounts for 20% of all incidence (McKeith, Galasko, (Scarmeas, Levy, Tang, Manly, & Stern, 2001; Verghese,
Kosaka, Perry, Dickson, & Hansen, 1996). Less prevalent Lipton, Katz, Hall, Derby, & Kuslansky, 2003), exercise
are Parkinsons disease, progressive supranuclear palsy (Colcombe & Kramer, 2003), the use of nonsteroidal anti-
(PSP), Picks disease, frontotemporal dementia, normal inflammatory drugs, the use of antioxidants (Fotuhi et al.,
pressure hydrocephalus, and Wernicke-Korsakoff s syn- 2008), and diets with high levels of vitamins B6, B12, and
drome. Relatively rare dementias are prion diseases such folate (Tyas et al., 2001).
as CreutzfeldtJakob disease which occurs in one in one
million (Kapur, Abbott, Lowman, & Will, 2003).
Vascular dementia is more common in Japan versus Natural History, Prognostic Factors,
AD although the overall dementia rates are equal (Otsuka, Outcomes
1994; Seno, Ishino, Inagaki, Iijima, Kaku, & Inata, 1999).
It is unclear if this difference occurs because of different Dementia was long considered a natural part of aging
diagnostic trends or environmental and/or gene pool dif- (Berchtold & Cotman, 1998). The term was first used in
ferences. AD is particularly prevalent in Israeli Arabs a clinical context by Pinel and Esquirol in the eighteenth
(Wertman, Brodsky, King, Bentur, & Chekhmir, 2007) century (Berchtold & Cotman; Cummings & Benson,
and less prevalent in China (Liu, Guo, Zhou, & Xia, 1992); however, the link between neuropathology and
2003) and India (Ferri et al., 2005). dementia was not made until 1907 by Alois Alzheimer.
The prevalence of dementia in developed countries is A date considered as the beginning of the modern study of
1.5% in people aged 65. The incidence of dementia dementia is 1968 which marks the publication by Blessed
increases dramatically with age, doubling every 5 years et al. of an article linking cognition with histopathology.
after age 65 (Kukull & Ganguli, 2000). The largest risk The general prognosis for dementia is poor, although
factors are increasing age and familial history. Those if caught early, WernickeKorsakoff s dementia, Normal
diagnosed with mild cognitive impairment (MCI) or Pressure Hydrocephalous, and Wilsons dementia can be
Downs syndrome and those with a history of traumatic treated with relative success. The disease course from
brain injury, stroke, or migraine are at greater risk. A diagnosis to death is quite variable with Creutzfeldt
variety of lifestyle risk factors have been studied and Jakob disease, resulting in death within a few weeks for
variably implicated, including vascular symptoms asso- some patients; Lewy body dementia averaging 3 years to
ciated with hypertension, obesity, and diabetes (Hofman, mortality; and AD from 5 to 20 years.
806 D Dementia
Cortical Dementias 40 and 50; however, there is juvenile onset in 510% of

cases. Neurotransmitters GABA and acetylcholine are de-
AD involves a slowly progressive, prominent memory pleted. Degeneration begins in striatum, but is also seen in
disturbance. It extends into other cognitive domains and globus pallidus, hypothalamus, subthalamic nucleus, sub-
leads to behavioral and personality alterations. It is de- stantia nigra, and thalamus. The majority of patients
generative and ultimately leads to death within 520 experience early difficulties in attention, executive func-
years. AD results in the reduction in size of temporal tion, and spatial abilities.
and frontal lobes, the brain regions involved in learning Wilsons disease results from a genetic metabolic disor-
and memory processes. The classic, neuronalpathologi- der which results in the accumulation of copper in the
cal features seen in autopsy sections are neuritic plaques basal ganglia. About 40% of patients present with a liver
and neurofibrillary tangles. Definitive diagnosis is still disorder, another 40% exhibit motor problems, and the
only available post mortem and is indicated by a sufficient remaining 20% suffer from psychiatric symptoms which
number of plaques and tangles. present as mania or schizophrenia-like symptoms. Diag-
Lewy body dementia is characterized by parkinsonian nosis can be confirmed by looking for a buildup of copper
pathology with early dementia as well as visual hallucina- in the eyes.
tions. Duration is relatively short with the average diag- Normal pressure hydrocephalous results from a block-
nosis to death lasting 3 years. age of cerebral spinal fluid (CSF). It is characterized by
Frontotemporal dementia is characterized by cerebral progressive gait ataxia, incontinence, and amnesia. How-
atrophy which begins in the frontal regions and progresses ever, these symptoms are reversible if caught early and
from anterior to posterior regions. Plaques and tangles treated with a shunt to drain CSF.
are not present but postmortem pathology may reveal Progressive supranuclear palsy results in cell loss in the
Picks bodies. brainstem, cerebellum, and basal ganglia. It is character-
Picks disease presents similarly to frontotemporal de- ized by difficulty in moving the eyes and gait disturbance.
mentia. It is characterized by frontal and temporal atro-
phy and Picks bodies. In its first stages, it is characterized
by disinhibition, loss of judgment/insight, and utilization Other Dementias
behavior. The second stage involves echolalia, agnosia,
and intellectual dysfunction with relatively preserved Multiple sclerosis is a disorder of myelin which follows a
memory. The final stage resembles the end-stage AD. pattern of relapse and remission. Effective treatments can
Mortality occurs in approximately 612 years with onset slow the progression of the disease, but once cognitive
earlier than most other dementias (from age 40 to 60). deficits which include attention, language, memory, and
Semantic dementia/Primary progressive aphasia usual- executive function difficulties are present, there are
ly involves 2 years of progressive aphasia before other fewer and shorter periods of remission.
symptoms present themselves. It is considered a subtype AIDS dementia results from HIV replication in the
of frontotemporal dementia; it is defined by its symptoms central nervous system, producing a progressive enceph-
as the exact pathology is not yet understood. alopathy. It is associated with increasing age, increased
Vascular dementia/Multi-infarct dementia is character- viral load, and decreased CD4 cell count. Once AIDS
ized by an abrupt onset. It originates in the blood vessels patients become demented, time to death averages
with a series of small strokes and can progress in a step- 2 months.
wise fashion if more infarcts occur. The neuropsychology WernickeKorsakoff s disease results from thiamine
of this type of dementia is dependent on the locations of deficiency (vitamin B1) and is most often seen in chronic
the infarcts. alcoholics. It is characterized by anterograde and retro-
grade amnesia, confabulation, apathy, and lack of insight.
CreutzfeldtJakob disease is the most common human
Subcortical Dementias prion disease. It involves a rapidly progressive dementia,
with memory loss, personality changes, hallucinations,
Parkinsons disease is characterized by a loss of dopamine speech impairment, myoclonus, ataxia, and changes in
cells in the substantia nigra. Up to 90% of patients exhibit gait and seizures.
cognitive impairments. Head trauma can produce nonprogressive dementia
Huntingtons disease is a genetic dominant disorder and also confer greater risk for developing other
whose symptoms typically begin in people between ages dementias.
Dementia D 807
Neuropsychology and Psychology of (Kelley & Petersen, 2007). Petersen et al. (2001) divided
Dementia MCI into categories to reflect a subgroup of patients with
episodic memory complaints who convert to AD at a
Differential Diagnosis greater rate: Amnestic (primary memory complaint) ver-
sus nonamnestic (complaints can include language, atten-
Memory impairment is necessary for a diagnosis of tion/executive function, and visuospatial skills). Those
dementia; however, it must be accompanied by an diagnosed with Amnestic MCI (MCIa) progress to AD D
impairment in at least one more cognitive domain, to be at a rate of 1015% per year in comparison with a rate of
distinguished from Amnestic Disorder. It must also be 12% per year in healthy elderly (Petersen et al).
distinguished from Delirium which can include deficits Presentations typical of cortical and subcortical
in multiple cognitive domains including memory; dementias are outlined in Table 2.
however, delirium primarily presents with decreased The ability to distinguish between dementias is greatest
awareness and altered consciousness. Delirium is also at the early stages of the disease. Late stages of dementia
characterized by abrupt onset and fluctuating course present similarly as deterioration becomes profuse. These
whereas dementia onset is usually insipid and progressive. mid- and late-stage dementia symptoms can include per-
Depression is comorbid in the early stages of a number of sonality changes with delusions of persecution, comabtive-
dementias, but because Depression itself can present as ness, agitation (especially at night which is termed
cognitive impairment, it must be ruled out as the primary sundowning effect), gait disturbances, and delirium.
diagnosis. Depression can also be a predictor of later
dementia; following the cognitive changes of an individu-
al will enable the practitioner to make the most accurate Evaluation
diagnosis (Cummings, 2003).
Dementia must also be distinguished from the cogni- The goals of a neuropsychological evaluation for dementia
tive changes (such as lowered speed of processing and are obtaining baseline measures of functioning to provide a
changes in attention) which are seen in normal aging. benchmark of change over time, determining areas of
Recent research has also outlined the state between nor- strength and weakness, assisting in making a diagnosis
mal aging and dementia. The criteria for diagnosis of MCI and providing treatment recommendations, and determin-
include (1) cognitive complaint (usually memory), pref- ing the validity of a prior diagnosis or the effectiveness of a
erably corroborated by an informant; (2) cognitive im- treatment/intervention. Diagnosis of dementia involves a
pairment (usually memory), for age and education; (3) detailed patient history, a clinical exam, and radiology to
essentially normal general cognitive function; (4) largely detect structural or electrical abnormalities in the brain.
preserved activities of daily living and (5) no dementia The clinical exam covers the following domains: (1) general
Dementia. Table 2 Presentations of typical cortical and subcortical dementias
Cortical dementia Subcortical dementia

Intellect Aphasia, amnesia, visuospatial disorder, poor Psychomotor retardation, forgetfulness, impaired
abstraction, acalculia, apraxia, agnosia insight, poor strategy formulation
Personality Indifference, depression Depression or mania, apathy
Speech Normal Dysarthria
Language Anomia, paraphasia Normal
Memory Unable to learn Retrieval problems
Motor Normal Abnormal (parkinsonian, chorea, dystonia, tremor)
system
Stance Normal Stooped
Gait Normal or pacing Dancing, unsteady, festinating, ataxic
Activity Normal Slow
Appearance Normal Inform, disheveled, perplexed
Visuospatial Construction problems Sloppy because of movement
808 D Dementia
awareness and cooperativeness; (2) function of cranial status is equivocal. Side effects include mild psychotic
nerves; (3) motor function; (4) reflexes; (5) sensory func- symptoms such as visual hallucinations, paranoid delu-
tion; and (6) mental status. sions, vivid dreams, confusional states, and dyskinesias.
Selegiline, a monoamine oxidase (MAO) inhibitor has
been used to extend the efficacy of L-Dopa (Nutt, Ham-
Treatment
merstad, & Gancher, 1992). Anticholinergic medications
have been used to treat motor effects, but they tend
Cortical Dementia
to have adverse effects on some executive functions
(Glatt & Koller, 1992). Deep brain stimulation or lesion-
Current treatments for cortical dementias are symptom-
ing in the globus pallidus, subthalamic nucleus, or ventral
atic. Cholinesterase inhibitors are used to treat AD and
intermediate thalamic nucleus has been used in patients
Lewy body dementia as they enhance cholinergic function
with no sign of cognitive symptoms and difficulty in
early in disease course (often up to 4 years). However, this
managing medication (Eskandar, Cosgrove, & Sinobu,
class of drug confers less benefit on cognition as choliner-
2001). When successful, these treatments result in im-
gic cell death increases throughout the disease progres-
proved motor function as well as increased psychomotor
sion. Currently used anticholinesterase inhibitors include
speed and working memory (Pillon, Ardouin, & Damier,
Reminyl (galantamine), Aricept (Donepezil), and Exelon
2000).
(rivastigmine). Side effects include gastrointestinal diffi-
Treatment options for Huntingtons are limited to
culties, particularly anorexia, nausea, and vomiting, and
palliative care. Neuroleptic drugs have been used to relieve
serious side effects which occur in 1% of patients are
choreic movements, however, they tend to promote
gastrointestinal ulceration, gastrointestinal hemorrhage,
Parkinson-like symptoms (Lerner & Whitehouse, 2002).
and mild pancreatitis. Also reported are diarrhea, vivid
PSP does not respond to dopamanergic or anticholin-
dreams, cramps, and dizziness. Cholinesterase inhibitors
ergic drugs despite its shared features with Parkinsons
may decrease heart rate and increase shortness of breath
disease (Kompoliti, Goetz, & Litvan et al., 1998). Anti-
in patients with asthma. Patients who respond with im-
depressants have been used to treat its emotional
provement in both cognitive and behavioral symptoms,
symptoms.
while taking a cholinesterase inhibitor are more likely to
have dementia with Lewy bodies rather than AD
(McKeith, 2002). Disease-modifying drugs, some of Cross References
which are in human trials, continue to be investigated
(Cummings, Vinters, Cole, & Khachaturian, 1998). Alzheimers Dementia
Patients with comorbid depression are also treated with Alzheimers Disease
antidepressants, and those with psychotic symptoms such Subcortical Dementia
as frequent hallucinations and delusions are treated with Vascular Dementia
antipsychotic agents. In the earlier stages of dementia,
patients might benefit from supportive therapy or group
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810 D Dementia Rating Scale-2
Dementia Rating Scale-2
The original version of the DRS was developed by Mattis in
S TEPHANIE G RIFFITHS 1, E LISABETH M. S. S HERMAN 2 the early to mid-1970s so that clinicians and researchers
E STHER S TRAUSS 3 could evaluate patients who suffered from organic mental
1
Simon Fraser University syndromes. Although the initial descriptions of the de-
Burnaby, British Columbia, Canada mentia rating scale included relatively small samples of
2
University of Calgary cognitive impaired patients, considerable psychometric ev-
Calgary, Alberta, Canada idence supporting its utility as a dementia-screening tool
3
University of Victoria has accumulated in the intervening decades (e.g., Strauss
Victoria, British Columbia, Canada et al., 2006). The test revision (DRS-2) has not changed
any of the original DRS items, but the clarity of scoring
instructions has improved and extensive new normative
Synonyms data are available. An alternate version (DRS-2: Alternate
Form) with a new item content has also been developed
DRS-2; Mattis dementia rating scale (Schmidt & Mattis, 2004) for use in serial assessments.
Psychometric Data
Description
Estimates of internal consistency (Cronbachs alpha) vary
The Dementia Rating Scale-2 (DRS-2) is the most recent by subscale, with total score, construction, conceptualiza-
edition (2001) of a battery-style assessment of mental tion, and memory falling above 0.70, attention falling
status in older patients with suspected dementia. The above 0.65, and initiation/perseveration at approximately
DRS-2 consists of 24 brief subtests whose scores are com- 0.45 (Smith et al., 1994). The estimated alternate form
bined into five subscales of attention, initiation/persever- reliability for the DRS-2 total score falls above 0.80, and
ation, construction, conceptualization, and memory (for ranges from 0.66 (initiation/perseveration) to 0.80 (Mem-
details, see Strauss, Sherman & Spreen, 2006). In addition ory) for subscale scores (Schmidt et al., 2005). Practice
to quantifying impairment in these specific cognitive effects appear to be reduced when the alternate form
domains, the sum of all five subscale scores (out of a is given. Numerous studies report strong correlations
possible total of 144 points) yields an estimate of overall between DRS total scores and other mental status evalua-
dementia severity. As subtest items are arranged and tions, such as the Mini Mental State Exam (MMSE),
administered in order of decreasing difficulty, patients and the DRS has demonstrated adequate sensitivity and
who successfully complete the initial items on any sub- specificity for cognitive impairment in a variety of sam-
scale can be given credit for adequate performance on the ples (Strauss et al., 2006). However, the validity of specific
entire subscale. subscales is not as consistently supported (especially for
Historically, clinical cutoff scores were used to construction, attention, and initiation/ perseveration)
identify individuals with cognitive impairment. More and subscale scores should be interpreted with caution.
recently, normative data for the DRS were collected
through the Mayo Older Americans Normative Study Clinical Uses
(MOANS; Lucas et al., 1998). As the DRS-2 items and
subscales are identical to those of the DRS, the MOANS Like the original version, the DRS-2 provides screening
normative data can be used to calculate age-corrected information regarding mental status. As such, it does not
scaled scores (M = 10, SD = 3) and percentile rank provide a comprehensive evaluation of cognitive func-
equivalents for subscale and total scores (see also Strauss tioning and, if impairment is evident, patients should be
et al., 2006). Administration time for the entire battery referred for a full neuropsychological evaluation. The
ranges from 10 to 15 minutes for healthy older individuals DRS-2 has the advantage of removing floor effects for
to 3045 minutes for those with dementia. This instru- some lower functioning patients who would be difficult
ment facilitates comprehensive screening of mental status to test using other cognitive batteries. A corresponding
in patients whose cognitive impairments preclude the use disadvantage is its potential insensitivity to cognitive def-
of more demanding tests. icits, or ceiling effects, in high-functioning individuals.
Dementia with Lewy Bodies D 811
As a screening instrument, the DRS accurately differ- Jurica, P. J., Leitten, C. L., & Mattis, S. (2001). Dementia Rating Scale-2.
Odessa, FL: Psychological Assessment Resources.
entiates individuals with probable Alzheimers dementia
Knox, M. R., Lacritz, L. H., Chandler, M. J., & Cullum, C. M. (2003).
from cognitively normal elderly adults, and is capable of Association between Dementia Rating Scale performance and neu-
detecting both early signs of dementia (Knox et al., 2003) rocognitive domains in Alzheimers disease. The Clinical Neuropsy-
and cognitive impairment in low-functioning samples chologist, 17(2), 216219.
(Das et al., 1995). The DRS also allows clinicians to assess Lucas, J. A., Ivnik, R. J., Smith, G. E., Bohac, D. L., Tangalos, E. G.,
Kokmen, E., Graff-Radford, N. R., & Petersen, R. C. (1998). Norma-
the initial severity of cognitive impairment in the elderly D
tive data for the Mattis Dementia Rating Scale. Journal of Clinical
and, particularly with its alternate version, can be used to and Experimental Neuropsychology, 20(4), 536547.
track the progression of dementia over time. There is Plehn, K., Marcopulos, B. A., & McLain, C. A. (2004). The relationship
evidence that patterns of performance on the subscales between neuropsychological test performance, social functioning,
of the DRS permit clinicians to discriminate between and instrumental activities of daily living in a sample of rural older
adults. The Clinical Neuropsychologist, 18(1), 101113.
common forms of dementia such as AD, Huntingtons
Rilling, L. M., Lucas, J. A., Ivnik, R. J., Smith, G. E., Willis, F. B., Ferman,
disease (HD), Parkinsons disease (PD), and vascular de- T. J., Petersen, R. C., & Graff-Radford, N. R. (2005). Mayos Older
mentia (e.g., Cahn-Weiner et al., 2002). Further, DRS African American Normative Studies: Norms for the Mattis Demen-
total scores appear to predict adaptive functioning in tia Rating Scale. The Clinical Neuropsychologist, 19(2), 229242.
community-dwelling elderly (e.g., Plehn et al., 2004) Schmidt, K., & Mattis, S. (2004). Dementia Rating Scale-2: Alternate form.
Lutz, FL: Psychological Assessment Resources.
and are related to objective indicators (MRI) of cortical
Schmidt, K. S., Mattis, P. J., Adams, J., & Nestor, P. (2005). Alternate-form
atrophy (Fama et al., 1997). reliability of the Dementia Rating Scale-2. Archives of Clinical Neu-
The MOANS DRS-2 normative data has been criti- ropsychology, 20(4), 435441.
cized for over-sampling highly educated Caucasians living Smith, G. E., Ivnik, R. J., Malec, J. F., Kokmen, E., Tangalos, E. G., &
in urban areas, thus, underestimating the abilities of indi- Petersen, R. C. (1994). Psychometric properties of the Mattis
Dementia Rating Scale. Assessment, 1(2), 123131.
viduals with lower education and socioeconomic status or
of minority ethnicities. To address this concern, new age- neuropsychological tests. New York: Oxford University Press.
and education-corrected data from a large group of
AfricanAmerican community volunteers (Mayo African
American Normative Studies, MOAANS) have been
provided by Rilling and colleagues (2005). Like the Dementia Scale (DS)
MOANS data, these DRS norms may be extended to
the DRS-2. Blessed Dementia Scale
Cross References
Dementia Syndrome of
Alzheimers Dementia
Depression
Mental Status Examination
Subcortical Dementia
Vascular Dementia
References and Readings Dementia with Lewy Bodies

Cahn-Weiner, D. A., Grace, J., Ott, B. R., Fernandez, H. H., & Friedman, M ATTHEW K RAYBILL , YANA S UCHY
J. H. (2002). Cognitive and behavioural features discriminate be-
University of Utah
tween Alzheimers and Parkinsons disease. Neuropsychiatry, Neuro-
psychology & Behavioural Neurology, 15(2), 7987.
Salt Lake City, UT, USA
Das, J. P., Mishra, R. K., Davison, M., & Naglieri, J. A. (1995). Measure-
ment of dementia in individuals with mental retardation: Compari-
son based on PPVT and Dementia Rating Scale. The Clinical Synonyms
Fama, R., Sullivan, E. V., Shear, P. K., Marsh, L., Yesavage, J., Tinklenberg,
J. R., Lim, K. O., & Pfefferbaum, A. (1997). Selective cortical and
Cortical lewy body disease (CLBD); Diffuse lewy body
hippocampal volume correlates of Mattis Dementia Rating Scale in disease (DLBD); Lewy body dementia (LBD); Senile de-
Alzheimer disease. Archives of Neurology, 54(6), 719728. mentia of lewy type
812 D Dementia with Lewy Bodies
Definition motor functions, including subcortical and brainstem nu-

clei (e.g., substantia nigra, basal forebrain, and locus cer-
Dementia with Lewy bodies (DLB) is a degenerative dis- uleus), limbic structures (e.g., hippocampus, amygdala,
order characterized by progressive cognitive decline and nucleus basalis of Meynert), and cortical areas. There
combined with three additional defining features: (1) pro- are at least two subtypes of DLB. The most common form
nounced fluctuations in alertness and attention (e.g., fre- consists of coexistent Lewy bodies and Alzheimers pathol-
quent drowsiness, lethargy, and disorganized speech), ogy, while the other form is believed to overlap with Par-
(2) visual hallucinations, and (3) parkinsonian motor kinsons disease dementia (PDD). Although DLB usually
symptoms (e.g., resting tremor, muscle rigidity, bradyki- occurs sporadically with no family history of the disease,
nesia, and/or postural instability) (McKeith et al., 1996). rare familial cases have been reported.
The most recent consensus criteria have been modified to
include additional features that may be suggestive of
possible DLB (McKeith et al., 2005) (See Table 1). Historical Background
DLB is believed to account for 1520% of all autopsy-
confirmed cases of dementia and as such may be the second In 1912, Friedrich Lewy first described the neuronal inclu-
most common type of degenerative dementia in older sions that were found in the substantia nigra of patients
adults (after Alzheimers disease). The symptoms of DLB diagnosed with Parkinsons disease. In 1923, Lewy pub-
are believed to be caused by Lewy body (LB) pathology, lished a detailed account of 43 patients with Parkinsonism
which is an abnormal aggregation of alpha-synuclein pro- (including 21 with dementia), integrating neurological,
tein inside the nuclei of neurons. LBs accumulate in areas psychiatric, and neuropathological data. The DLB syn-
of the brain that control particular aspects of memory and drome continued to be clarified by researchers, and by
Dementia with Lewy Bodies. Table 1 Revised criteria for the clinical diagnosis of probable or possible DLB (Adapted from
McKeith et al., 2005)
Suggestive
Central features Core features features Supportive features
Cognitive Progressive dementia Fluctuating cognition
with impairments in with pronounced
(a) memory (b) attention changes in attention
(c) executive functioning and alertness
(d) visuospatial ability
Psychiatric Recurrent, detailed Neuroleptic (a) Nonvisual hallucinations
visual hallucinations sensitivity (b) delusions (c) depression
Behavioral/ Parkinsonism REM sleep (a) Autonomic dysfunction
somatic disturbance (e.g., orthostatic hypotension, urinary
incontinence) (b) repeated falls and
syncope (c) transient, unexplained
loss of consciousness
Neuroimaging SPECT/PET: Low (a) CT/MRI: Relative preservation of
dopamine medial temporal lobe (b) SPECT/PET:
transporter Generalized low uptake with reduced
uptake in basal occipital activity (c) EEG: Prominent
ganglia slow wave activity with temporal lobe
transient sharp waves (d) MIBG
myocardial scintigraphy: Abnormally
low uptake
Note: Central features are essential for DLB diagnosis. Two or more core features are needed for probable DLB diagnosis, and one for possible DLB
diagnosis. One or more suggestive feature in addition to one or more core feature are needed for probable DLB diagnosis, and one or more
suggestive features with no core feature is sufficient for possible DLB diagnosis. Suggestive features are commonly present but not proven to have
diagnostic specificity
Dementia with Lewy Bodies D 813
the early 1970s, the term incidental Lewy body disease whether it lies on the same disease spectrum as PDD. The
began to be used. Clinical and pathological features of current guidelines regarding clinical diagnosis consider
demented patients with Lewy bodies were subsequently whether cognitive or motor symptoms are present first
detailed by a number of Japanese neuropathologists. By (McKeith et al., 2005). If cognitive symptoms appear prior
the late 1980s, it came to be recognized that DLB occurred to, or concurrently with, motor symptoms, then a diag-
much more commonly than previously suspected, as it was nosis of DLB can be made.
reported to be the second most common type of dementia Although there is also considerable similarity between D
among the elderly. With advances in histological techni- the cognitive symptoms and clinical course of DLB and
ques, LBs and Lewy neurites were identified outside of the AD, retrospective clinical assessments of pathologically
substantia nigra, including limbic and cortical areas. In confirmed DLB have revealed distinct cognitive and psy-
October of 1995, an international workshop in Newcastle, chiatric features of the disorder, with the presence of visual
England was organized to establish clinical diagnostic cri- hallucinations and visuospatial or constructional dysfunc-
teria and pathological protocols for DLB, the results of tion suggesting DLB. There is increasing consensus that the
which were published by McKeith et al. (1996). These DLB syndrome can be identified and can be differentiated
criteria were reviewed again at a 1999 international work- from other dementia syndromes in routine clinical prac-
shop (McKeith, Perry and Perry, 1999) and then most tice, prior to pathological confirmation (Lennox & Lowe,
recently revised in 2005 (see above) (McKeith et al., 2005). 1996). Differentiating between brainstem predominant,
limbic and diffuse neocortical LB pathology may also be
relevant to the clinical syndrome (McKeith et al., 2005).
Current Knowledge
Clinical Symptoms Neuropathology
A description of DLB symptoms can be found in Table 1. The original neuropathologic criteria for DLB only re-
In addition to the more typical signs of dementia, com- quired the presence of LBs somewhere in the brain of a
plex visual hallucinations accompanied by a fluctuating patient who was clinically diagnosed with dementia
course are often viewed as the tell tale indicators of DLB (McKeith et al., 1996). Other coexistent pathological fea-
(McKeith et al., 2005). Hallucinations are often accompa- tures such as amyloid plaques, neurofibrillary tangles, and
nied by delusions, anxiety, and behavioral disturbances. neuronal loss were neither inclusive nor exclusive for a
Additionally, patients with DLB often suffer from sleep diagnosis of DLB. Although this liberal definition had the
disturbances and a disruption of the day/night cycle, advantage of including many cases, the development of
which may be the result of vivid, frightening dreams that more sensitive methods for detecting LBs has lead to
occur during REM sleep. It is not uncommon for patients many neuropathologically positive cases being identified
to appear to act out their dreams by vocalizing or violently as DLB even without the clinical syndrome. The most
moving around in bed. Therefore, when assessing for DLB, recent consensus guidelines regarding neuropathological
screening questions that address sleep issues should always criteria for DLB recommend a semiquantitative grading
be utilized. With respect to the extrapyramidal motor scale (e.g., mild, moderate, severe, and very severe) for
features, patients with DLB may exhibit similar, but some- lesion density, as opposed to simply identifying the pres-
what more severe, difficulties as compared to patients with ence or absence of LB pathology (McKeith et al., 2005).
PD. These include action tremor (resting tremor is less The density of LB pathology can be highly variable, and
common in DLB), slowness of movement, postural insta- LBs can be frequently found in brainstem nuclei, as well as
bility, gait difficulty, facial immobility, and muscle rigidity. various limbic, and neocortical regions.
However, the assessment of motor features can be compli-
cated by the presence of cognitive impairment. Fluctua-
tions may be one of the most difficult clinical symptoms to Treatment
assess and inter-rater reliability is often low.
Because DLB appears to have motor symptoms, cog- The clinical management of patients with DLB can be
nitive profiles, neuropathological features, and a clinical complex and includes (a) efforts to detect and appropri-
course that are comparable to those of Parkinson disease ately diagnose cognitive impairment early on in the dis-
dementia (PDD), there is an ongoing debate in the cur- ease process, (b) assessment and management of
rent literature about whether DLB is a distinct entity or neuropsychiatric and/or behavioral symptoms, (c)
814 D Demographically-Adjusted T Score
treatment of the movement disorder, and (d) monitoring Lennox, G., & Lowe, J. (1996). The clinical diagnosis and misdignosis of
Lewy body dementia, In R. Perry, I. McKeith, & E. Perry (Eds.),
and management of autonomic dysfunction and sleep
Dementia with Lewy bodies: Clinical, pathological, and treatment
disorder. Non-pharmacologic interventions have not issues (pp. 920). Cambridge, UK: Cambridge University Press.
been systematically evaluated, but may include strategies McKeith, I. G., Dickson, D. W., Lowe, J., Emre, M., OBrien, J. T.,
that increase social interactions and increase levels of Feldman, H. et al. (2005). Diagnosis and management of dementia
arousal as a way of reducing the presence and impact of with Lewy bodies: third report of the DLB Consortium. Neurology,
65(12), 18631872.
visual hallucinations (McKeith et al., 2005). Pharmaco-
McKeith, I. G., Galasko, D., Kosaka, K., Perry, E. K., Dickson, D. W.,
logic treatments such as Levodopa can be used to help Hansen, L. A. et al. (1996). Consensus guidelines for the clinical and
alleviate the parkinsonian motor disorder associated with pathologic diagnosis of dementia with Lewy bodies (DLB): report of
DLB. However, dopaminergic medications may exacer- the consortium on DLB international workshop. Neurology, 47(5),
bate psychiatric symptoms, and as such should be started 11131124.
McKeith, I. G., Perry, E. K., & Perry, R. H. (1999). Report of the second
at low doses and increased only gradually (McKeith et al.,
dementia with Lewy body international workshop: diagnosis and
2005). Other pharmacologic interventions may include treatment. Consortium on Dementia with Lewy Bodies. Neurology,
cholinesterase inhibitors or atypical antipsychotic medi- 53(5), 902905.
cations. Cholinesterase inhibitors may specifically be use-
ful for the fluctuating cognitive impairments that are
associated with DLB, and may improve global functioning
as well as activities of daily living. Although selective Demographically-Adjusted T
serotonin reuptake inhibitors (SSRIs) or serotonin-nor-
epinephrine reuptake inhibitors (SNRIs) have been
Score
reported as the preferred pharmacologic intervention for
T Scores
depression in DLB, there have been no systematic studies
of the treatment of depression in patients with this
disorder.
Demyelination
Future Directions K ATHLEEN L. F UCHS
University of Virginia Health System
Efforts to find new ways of treating DLB have begun to Charlottesville, VA, USA
focus on early detection in hopes of finding ways of
potentially slowing the progression of the disease. For
example, practical biomarkers or disease modifying stra- Definition
tegies that target alpha-synuclein deposition would be
significant developments that hopefully will occur in the Demyelination is the process in which myelin, the protec-
near future (Goldmann Gross, Siderowf, & Hurtig, 2008). tive protein and lipid sheath around a nerve fiber, is
broken down. This impacts the efficiency of nerve con-
duction and leaves the axon vulnerable to damage and
Cross References degeneration. In multiple sclerosis, demyelination in the
central nervous system is presumed to result from im-
Alzheimers Disease
mune system activation of inflammatory processes that
Lewy Bodies (Alpha-Synuclein Inclusions)
attack myelin and inhibit repair (remyelination) by
Metabolic Encephalopathy
oligodendrocytes. Axonal damage and loss are thought
Parkinsons Dementia
to produce some of the symptoms of multiple sclerosis,
Parkinsons Disease
especially in myelin-rich fibers such as the optic nerve.
Goldmann Gross, R., Siderowf, A., & Hurtig, H. I. (2008). Cognitive

Multiple Sclerosis
impairment in Parkinsons disease and dementia with lewy bodies: A Myelin
spectrum of disease. Neurosignals, 16(1), 2434. Neuron
Dentate Gyrus D 815
Compston, A., Lassmann, H., & Smith, K. (2006). The neurobiology American Psychiatric Association (1994). Diagnostic and statistical
of multiple sclerosis. In A. Compston et al. (Eds.), McAlpines manual of mental disorders (4th edn.). Washington, DC: American
multiple sclerosis (4th ed., pp. 449490). Philadelphia, PA: Elsevier. Psychiatric Association.
Caplan, B. (2010). Rehabilitation psychology and neuropsychology with
stroke survivors. In R. G. Frank, M. Rosenthal, & B. Caplan (Eds.),
Handbook of rehabilitation psychology (2nd edn., pp. 6394). D
Washington DC: American Psychological Association.
Prigatano, G. P., & Klonoff, P. S. (1998). A clinicians rating scale for
evaluating impaired self-awareness and denial of disability after
brain injury. The Clinical Neuropsychologist, 12(1), 5667.
Denial
DAWN E. B OUMAN
Drake Center Dentate Gyrus
Cincinnati, OH, USA
S EVERN B. C HURN
Definition Richmond, VA, USA
A psychological coping mechanism used to protect

against stressful events. Early conceptualizations by Synonyms
Freud, as well as recent references such as DSM-IV
describe this automatic psychological process that Gyrus dentata
protects the individual against anxiety and from
awareness of internal or external stressors or dangers.
(American Psychiatric Association, 1994). Denial can be Definition
adaptive or maladaptive, depending upon the context
and extent to which it is used. In neurological impair- One of the two stratified folds of gray matter comprising
ments, denial of disability is contrasted with anosog- the hippocampus, the dentate gyrus is situated between
nosia and unawareness. Simplified conceptualizations the major cortical connection to the hippocampus, the
view denial as a psychological process that occurs inde- entorhinal cortex, and the other hippocampal regions
pendently of cognitive impairment, while anosognosia CA1, CA2, and CA3. Granule cells of the dentate granular
is viewed as a problem of insight that is neurologically layer receive one of the two major entorhinal outputs, the
and cognitively mediated. More comprehensive concep- perforant pathway, and their excitatory axons (mossy
tualizations consider both denial and impaired self- fibers) relay mostly to interneurons but also to CA3 and
awareness as continuous variables which may interact possibly CA2. Neural progenitor cells of the subgranular
in a given individual following brain damage (Priga- layer enable neurogenesis, a perpetual process believed to
tano & Klonoff, 1998). One scale used to tease apart support learning and memory, be enhanced by exercise
and describe the constructs of denial of disability and and negatively influenced by stress, depression, and aging.
impaired self-awareness is described by Prigatano and
Klonoff (1998).
Cross References
Hippocampus
Cross References
Anosognosia
Anosodiaphoria
Scharfman, H. E. (Ed.). (2007). The dentate gyrus: A comprehensive guide
Coping to structure, function, and clinical implications: Vol. 163. Progress in
Insight, Effects on Rehabilitation brain research. Amsterdam: Springer.
816 D Deoxyribonucleic Acid (DNA)
specific protein. A gene may also include regulatory

Deoxyribonucleic Acid (DNA) elements that determine when expression occurs. Within
a cell, DNA is organized into structures called chromo-
R OHAN PALMER 1, M ARTIN H AHN 2 somes that are located within the nucleus of the cell.
1
University of Colorado Human somatic cells contain 23 pairs of homologous
Boulder, CO, USA chromosomes and one pair of sex chromosomes. The
2
William Paterson University DNA within a cell is accessed by unfolding the double
Wayne, NJ, USA helix. Once unfolded, depending on the process at hand,
DNA can either be replicated by a process called DNA
replication, or genes may be expressed by the cooperation
Synonyms of two process, transcription and translation. DNA
replication is the reproduction of DNA to create a copy.
Allele; Chromosome; Gene For gene expression to occur, DNA is first transcribed into
messenger RNA (ribonucleic acid; mRNA). From each
gene, mRNA comprises exons that specify the amino
Definition acid sequence. Once complete, mRNA is transported
into the cytoplasm of the cell where it is translated to
Deoxyribonucleic acid (DNA) is a double-stranded create an amino acid chain.
polynucleotide chain that encodes genetic information Both DNA replication and gene expression are built
responsible for the development and functioning of around the complimentary base-pair sequencing of the
organisms. nucleotide. DNA replication is simplified by the phenom-
enon of complimentary-base pairing because only one
strand of the molecule needs to be read. Gene expression
is simplified since the mRNA sequence indicates the
Current Knowledge specific amino acid.
DNA Structure
A DNA molecule consists of two polynucleotide chains

Application in Neuropsychology
held together in the shape of a double helix by weak
hydrogen bonds (Fig. 1). The polynucleotide strands run
Twin and adoption studies indicate that most psychiatric
in alternate directions. Nucleotides within DNA contain a
disorders, such as schizophrenia and bipolar disorder
50 deoxyribose sugar, a phosphate molecule, and one of
(Bestelmeyer, Phillips, Crombie, Benson, & St Clair,
the four bases (adenine (A), guanine (G), cytosine (C),
2009) are heritable. Neuropsychiatric genetics attempts
and thymine (T)). As a result, DNA is made up of
to understand individual differences in disorder risk by
sequences of combinations of the four possible nucleo-
examining differences in genetic risk factors. The ultimate
tides. The four DNA nucleotides have specific pairings:
goal of these studies is the development of new drugs to
adenine pairs with thymine and guanine pairs with
treat the genetic basis of a disorder. For instance, using
cytosine. The number of adenine bases in a DNA mole-
high-angular resolution diffusion imaging on a sample of
cule is equal to the number of thymine bases; the number
young adult twins, Chiang et al. (2009) demonstrated that
of cytosine bases equals the number of guanine
common genes influence brain fiber architecture and IQ.
bases. Within the helix, nucleotides are stacked upon
A future goal of the project is to identify genes involved in
each other.
the myelination of brain circuits in order to preclude
diseases such as multiple sclerosis.
Gene expression profiling using high throughput
DNA Function methods is an affordable method used to correlate the
expression of genes in specific brain regions with specific
DNA is referred to as the blueprint of an organism disorders. For example, microarray studies of bipolar
because it codes for the makeup of the entire organism, disorder have implicated several genes (e.g., CASP8,
such as cell components and proteins. A gene is a segment ERBB2, and neuropeptide Y) that influence the risk for
of DNA that determines the amino acid sequence for a bipolar disorder (Bezchlibnyk, Wang, McQueen, &
Deposition D 817
Base pairs
Adenine Thymine D
Guanine Cytosine
Sugar phosphate
backbone
U.S. National Librany of Medicine
Deoxyribonucleic Acid (DNA). Figure 1 Structure of DNA. (This figure is the property of the US National Library of
Medicine (2009))
Young, 2001; Konradi et al., 2004; Kuromitsu et al., 2001), U.S. National Library of Medicine. Structure of DNA. Accessible at:
http://ghr.nlm.nih.gov/handbook/basics/dna. Accessed 23 Sep 2009.
as well as the risk for schizophrenia (Tkachev et al., 2003).

Deposition
Bestelmeyer, P. E., Phillips, L. H., Crombie, C., Benson, P., & St Clair, D.
(2009). The P300 as a possible endophenotype for schizophrenia and
bipolar disorder: Evidence from twin and patient studies. Psychiatry Chicago Neuropsychology Group
Research, 169, 212219. Chicago, IL, USA
Bezchlibnyk, Y. B., Wang, J. F., McQueen, G. M., & Young, L. T. (2001).
Gene expression differences in bipolar disorder revealed by
cDNA array analysis of postmortem frontal cortex. Journal of
Neurochemistry, 79, 826834.
Definition
Chiang, M. C., Barysheva, M., Shattuck, D. W., Lee, A. D., Madsen, S. K.,
Avedissian, C., et al. (2009). Genetics of brain fiber architecture and In cases where forensic neuropsychology is involved, a
intellectual performance. Journal of Neuroscience, 29, 22122224. deposition occurs following the determination that the
Konradi, C., Eaton, M., MacDonald, M. L., Walsh, J., Benes, F. M., &
specific psychological or neuropsychological methods are
Heckers, S. (2004). Molecular evidence for mitochondrial
dysfunction in bipolar disorder. Archives of General Psychiatry, 61,
admissible. Written opinions or oral opinions are
300308. provided by the expert witness under oath. Such opinions
Kuromitsu, J., Yokoi, A., Kawai, T., Nagasu, T., Aizawa, T., Haga, S., et al. are scrutinized by the opposing counsel and by the trier of
(2001). Reduced neuropeptide Y mRNA levels in the frontal cortex fact (e.g., judge or jury). The sworn testimony can be
of people with schizophrenia and bipolar disorder. Brain Research.
delivered in several ways. First, it can be presented in
Gene Expression Patterns, 1, 1721.
Tkachev, D., Mimmack, M. L., Ryan, M. M., Wayland, M., Freeman, T.,
written form (e.g., affidavit) or orally via a deposition
Jones, P. B., et al. (2003). Oligodendrocyte dysfunction in or in the courtroom. A deposition is considered a form
schizophrenia and bipolar disorder. Lancet, 362, 798805. of legal discovery and allows for litigants (e.g., their
818 D Depressed Skull Fracture
attorneys) to question fact or expert witnesses to make cerebral blood vessels. Individuals with depressed skull
decisions regarding the testimony to be presented at the fracture may develop raccoon eyes, or a battle sign that
trial. During a deposition, both attorneys and a court tips the clinician off about the presence of a skull fracture.
recorder are present, but no judge or jury is in attendance. Depressed skull fracture is common after blunt trauma to
Everything asked and answered during the deposition is the head (i.e., direct blow with a hammer or any other
transcribed by a court reporter. hard object).
There are essentially two types of depositions: Individuals with depressed skull fracture are at the
discovery deposition and trial deposition. A discovery increased risk of developing brain infection, as the brain
deposition is held by the opposing counsel and is tissue may be directly exposed to the outside environ-
intended to extract information about an experts ment. As such, emergent management of the skull frac-
opinions, refine the dispute by focusing on the most ture, with removal of bone fragment and appropriate
relevant issues, and to gain a sense of the expert witness dressing of the skull wound, is pursued, typically with
demeanor. A trial deposition (de bene esse) serves to surgical intervention.
preserve an expert witness testimony if he/she is not
able to appear at trial. A trial deposition and live trial
testimony consist of two parts: direct examination and Cross References
cross-examination. For further details on direct and cross-
examinations please see each respective entry. Battle Sign
Raccoon Eyes
Cross References Skull Fracture
Cross-Examination
Direct Examination References and Readings
Braakman, R. (1972). Depressed skull fracture: Data, treatment, and
References and Readings follow-up in 225 consecutive cases. Journal of Neurology, Neurosur-
gery, & Psychiatry, 35, 395402.
Greiffenstein, M. F. (2009). Basics of forensic neuropsychology. In Graham, D. I., Saatman, K. E., Marklund, N., Conte, V., Morales, D.,
J. Morgan, & J. Ricker (Eds.), Textbook of clinical neuropsychology. Royo, N., & McIntosh, T. K. (2006). The neuropathology of trauma.
New York: Psychology Press. In R. W. Evans (Eds.), Neurology and trauma (2nd ed., pp. 4594).
Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C. (2007). New York: Oxford University Press.
Psychological evaluations for the courts (3rd ed.). New York: Guilford Victor, M., & Ropper, A. H. (2001). Principles of neurology (7th ed., pp.
Press. 925953). New York: McGraw-Hill.
Depressed Skull Fracture

Depression
B ETH R USH
Mayo Clinic Depressive Disorder
Jacksonville, FL, USA Dysphoria
Definition
Depression Equivalent
Depressed skull fracture is a fracture or break of the
cranial bone that results in depression of the bone frag- Masked Depression
ment into the underlying brain tissue.
Current Knowledge
Depression Without a Depression
This may result in bruising because of compression of the
underlying brain tissue, or disruption to the underlying Masked Depression
Depressive Pseudodementia D 819
Treatment
Depressive Disorder
Treatment of depression includes pharmacological and
R OBERT G. F RANK psychotherapeutic interventions. A wide range of antide-
Kent State University pressant medications thought to modify the level of neu-
Kent, OH, USA rotransmitters in the postsynaptic cleft. In particular, the
neurotransmitters serotonin, norepinephrine, and doma- D
nine have been identified as associated with depression.
Synonyms Combined treatment providing psychopharmacological
antidepressants and psychotherapy has been shown to be
Affective disorder; Depression; Emotional disorder; effective (Thase et al., 1997).
Mood disorder In the National Comorbidity Study (Kessler et al.,
2003), 51.65 of those with 12 month in major depressive
episode treatment was adequate in only 41.9% of the
cases, resulting in only 21.7% of those with major depres-
sive disorder being treated adequately.
A depressive disorder refers to the presence of sad or
irritable mood that lasts for more than 2 weeks. In addi-
tion, the individual must experience lack or increase in
appetite with decrease or increase in weight, insomnia or References and Readings
hypersomnia, feelings of worthlessness, despair, suicidal
ideation or intent, guilt, and impaired social and occupa- American Psychiatric Association (1994). Diagnostic and statistical man-
ual of mental disorders (4th ed.). Washington, DC: American Psychi-
tional functioning. In the USA in DSM-IV, depressive
atric Association.
disorders are divided by severity and duration into American Psychiatric Association (2000). Diagnostic and statistical man-
major depressive episode and dysthymic disorder. ual of mental disorders (4th ed., text revision). Washington, DC:
Kessler, R. C., Berglund, P., Demler, O., Jin, R., Koretz, D., Merikangas,
Epidemiology K. R., et al. (2003). The epidemiology of major depressive disorder:
Results from the National Comorbidity Survey Replication (NCS-
R). The Journal of the American Medical Association, 289, 30953105.
The National Comorbidity Study (Kessler et al., 1994)
Kessler, R. G., McGonagle, K. A., Zhao, S., Nelson, C. B., Hughes, M.,
reported a prevalence of 17.1% for depressive disorders. Eshleman, S., et al. (1994). Lifetime and 12 month prevalence of
Males were less affected (12.7%) than females (21.3%). DSM-III-R psychiatric disorders in the United States: Results from
Dysthymic disorder is less common, affecting 4.8% the National Comorbidity Study. Archives of General Psychiatry, 51,
of men, 8% of women, and 6.4% of the population 819.
Thase, M. E., Greenhouse, J. B., Frank, E., Reynolds, C. F., Pilkonis, P. A.,
overall. A more recent replication of the National Comor-
Hurley, K., et al. (1997). Treatment of major depression with psy-
bidity Study focusing on major depressive disorder chotherapy or psychotherapy-pharmcotherapy combinations.
(Kesser et al., 2003) found a month prevalence of 6.6% Archives of General Psychiatry, 54(11), 10091015.
of the population, or about 13.114.2 million adult
Americans. The majority (59%) of individuals with
major depressive episode had significant or very severe
role impairment.
Depressive Disorder Not
Otherwise Specified
Evaluation
Minor Depressive Disorder
The assessment and treatment of depressive disorders
relies upon clinical evaluation or self-report instruments.
Many self-report inventories allow patients to assess their
own symptoms. Also, structured clinical interviews based
on DSM-IV exist. The majority of these tools focus on Depressive Pseudodementia
major depressive episode, though some provide a blended
rating that does not equate to DSM-IV diagnoses. Pseudodementia
820 D Dermatome
Definition
Dermatome
Dermatome is the area of the skin supplied by a spinal
J OHN E. M ENDOZA sensory nerve root. Since the nerve roots come in pairs,
Tulane University Medical Center the dermatome on one side of the body is a mirror image
New Orleans, LA, USA of the other (see Fig. 1). The numbers in figure refer to the
level at which the nerve roots enter the spinal vertebrae.
Dermatome. Figure 1 Approximate distribution of the segments of the skin represented by the various dorsal roots of the
spinal cord
Design Fluency Test D 821
sum of all perseverations and errors (e.g., drawing with

Desensitization the wrong number of lines or nameable by participant as
representative of object). The original scoring criteria
Tachyphylaxis yielded interrater reliabilities that were marginal to ade-
quate. However, with more refined criteria, the interrater
reliability has improved (Jones-Gotman, 1991; Harter,
Hart, & Harter, 1999). Nonetheless, the scoring of D
this test is challenging. The standardized samples are
Design Fluency Test relatively small for the adults, with 45 adults ranging in
age between 14 and 54 years and 10 elderly between 58
R ONALD RUFF
and 72 years; however, the pediatric sample of 256 chil-
San Francisco Clinical Neurosciences & University
dren is larger and ranges between the ages of 5 and 14
of California San Francisco
(Strauss, Sherman, & Spreen, 2006).
San Francisco, CA, USA
Synonyms Psychometric Data
DFT In a sample of college students, the retest reliability fol-

lowing a 1-month interval was r = 0.56 for the total
number of drawings in the free condition and r = 0.70
Historical Background in the fixed condition. As expected, the correlation coeffi-
cients were lower for the error scores (Ross, Axelrod,
Dr. Brenda Milner is one of the most prominent pioneers Hank, Kotasek, & Whitman, 1996). Harter, Hart, and
for advancing the discipline in neuropsychology. In par- Harter (1999), in a different college sample that was tested
ticular, her seminal research established the neuropsycho- again 1 month apart, found a slightly higher retest reli-
logical assessment of frontal lobe functioning. In ability of r = 0.69 for the free condition. As to the concur-
collaboration with Dr. Jones-Gotman, Dr. Milner rent validity, according to Demakis and Harrison (1997),
designed the design fluency test (DFT) measure analo- the fixed condition of the DFT is modestly correlated with
gous to the Thurston verbal fluency test. Their seminal Ruff Figural Fluency Test (r = 0.38), whereas the correla-
study (Jones-Gotman & Milner, 1977) documented pre- tion with free condition is minimal (r = 0.25).
frontal lobe involvement in both verbal and design fluen-
cy. Initially, the DFT was introduced as an experimental
measure, and over the years, a number of neuropsychol- Clinical Uses
ogists have contributed toward establishing the DFT as a
psychometric tool. As a research measure, the DFT has contributed to
the understanding of frontal lobe functioning. Research
studies have shown that patients with right frontal lobe
Description damage are more impaired compared to patients with
lesions in other brain regions. There are a variety of
In the first part of the DFT, the participant is asked to neurological conditions that have also demonstrated
invent drawings that are neither scribbles nor nameable the DFTs sensitivity and these include frontal lobe
objects or forms (e.g., geometrical shapes). During 5 min, dementias and traumatic brain injuries. However, the
as many different designs as possible are to be drawn on DFT has not yet been developed into a solid psychometric
a blank piece of paper. During the second part, the partic- test. There is no published test manual available. Review-
ipant is given examples and instructions to limit the ing the clinical uses of the DFT, Strauss, Sherman, and
drawings to four straight or curved lines. Over a period Spreen (2006) stated: One of the common criticisms of
of 4 min, the participants are asked to generate as many this test. . .has been that the scoring criteria are difficult to
different four-line drawings as possible. interpret and overly subjective. Although more detailed
For each condition, there is a novel output score which administration and scoring criteria have been advanced,
consists of the total number of unique drawings minus the the interrater agreement remains suboptimal, especially
822 D Desipramine
for nameable errors and designs that are drawn with the
wrong number of lines. Moreover, Strauss, Sherman, and Desipramine
Spreen, (2006) concluded: . . .the norms for older adults
are based on a very small sample of individuals and J OHN C. C OURTNEY
should be used with considerable caution. Thus, the Childrens Hospital of New Orleans
DFT is a sensitive measure, but it is difficult to score New Orleans, LA, USA
and the available normative data for adults are
suboptimal.
Generic Name
Cross References Desipramine
Delis-Kaplan Executive Function System (D-KEFS)

Brand Name
Figural Fluency Test
Norpramin

Class
Boone, K. B., Miller, B. L., Lee, A., Berman, N., Sherman, D., & Stuss, D. T.
(1999). Neuropsychological patterns in right versus left frontotem- Tricyclic Antidepressant
poral dementia. Journal of the International Neuropsychological Soci-
ety, 5, 612622.
Carter, S. L., Shore, D., Harnadek, M. S., & Kubu, C. S. (1998). Normal-
tive data and interrater reliability of the Design Fluency Test. The
Demankis, G. J., & Harrison, D. W. (1997). Relationships between verbal Desipramine acts primarily as an inhibitor of the norepi-
and nonverbal fluency measures: Implications for assessment of nephrine reuptake pump. This results in a boost in neu-
executive functioning. Psychological Reports, 81, 443448. rotransmitter availability in the cleft and, since dopamine
Elfgren, C. I., & Risberg, J. (1998). Lateralized frontal blood flow increases
is inactivated by norepinephrine reuptake in the prefron-
during fluency tasks: Influence of cognitive strategy. Neuropsycholo-
gia, 36, 505512.
tal cortex, it is hypothesized that desipramine also
Harter, S. L., Hart, C. C., & Harter, G. W. (1999). Expanded scoring increases to total ambient availability of dopamine as
criteria for the Design Fluency Test: Reliability and validity in neu- well. At higher doses, it appears to boost presynaptic
ropsychological and college samples. Archives of Clinical Neuropsy- serotonin production and release.
chology, 14, 419432.
Jones-Gotman, M. (1991). Localization of lesions by neuropsychological
testing. Epilepsia, 32, S41S52.
Jones-Gotman, M., & Milner, B. (1977). Design fluency: The invention of Indication
nonsense drawings after focal cortical lesions. Neuropsychologia, 15,
653674. Depression.
Levin, H. S., Culhane, K. A., Hartmann, J., Harword, H., Ringholtz, G.,
Ewing-Cobbs, L., & Fletcher, J. M. (1991). Developmental changes in
performance on tests of purported frontal lobe functioning. Devel-
opmental Neuropsychology, 7, 377395. Off Label Use
Ross, T. P., Axelrod, B. N., Hanks, R. A., Kotasek, R. S., & Whitman, R. D.
(1996). The interrater and test-retest reliability of the Design Fluency Anxiety, insomnia, neuropathic pain, and treatment resis-
and Ruff Figural Fluency Tests. Paper presented to the 24th meeting
tant depression.
of the International Neuropsychological Society, Chicago.
Strauss, E., Sherman, E., & Spreen, O. (2006). A compendium of neuro-
psychological tests (3rd ed.). New York: Oxford University Press.
Varney, N. R., Roberts, R. J., Struchen, M. A., Hanson, T. V., Franzen, Side Effects
K. M., & Connell, S. K. (1996). Design fluency among normals and
patients with closed head injury. Archives of Clinical Neuropsychol-
Serious
ogy, 11, 345353.
Woodward, J. L., Axelrod, B. N., & Henry, R. R. (1992). Interrater
reliability of scoring parameters for the Design Fluency Test. Neuro- Paralytic ileus, hyperthermia, lowered seizure threshold,
psychology, 6, 173178. sudden death, cardiac arrhythmias, tachycardia, QT
Detroit Edison v. NLRB (1979) D 823
prolongation, hepatic failure, mania, and potential for thought to originate in multipotential cells found in
activation of suicidal ideation. the neural plate in the embryonic stage of human
development. In patients younger than 2 years, the des-
moplastic ganglioglioma presents as a large, cystic, often
Common dura-attached mass. Although it is usually of low grade,
the desmoplastic ganglioglioma can be slow-growing,
Blurred vision, constipation, urinary retention, increased infiltrating, and become fatal in its progression. Surgery D
appetite, dry mouth, diarrhea, heartburn, weight gain, is the treatment of choice, with no complimentary
fatigue, weakness, dizziness, anxiety, sexual dysfunction, treatment needed in cases of complete tumor resection.
sweating, rash, and itching.
Cross References
Brain Tumor
Ganglioglioma
PDR. Glioma
Stahl, S. M. (2007). Essential psychopharmacology: The prescribers guide Neoplasms

Keating, R. F., Goodrich, J. T., & Packer, R. J. (2001). Tumors of the
pediatric central nervous system. New York: Thieme.
Drug Interaction Effects: http://www.drugs.com/drug_interactions.html Pizzo, P. A., & Poplack, D. G. (2005). Principles and practice of pediatric
Drug Molecule Images: http://www.worldofmolecules.com/drugs/ oncology (5th ed.). New York: Lippincott.
com:8080/cgi bin/ddiD4?ver = 4&task = getDrugList
Desmoplastic Ganglioglioma
Desmoplastic Gangliocytoma
Desmoplastic Gangliocytoma
J ACQUELINE L. C UNNINGHAM Detroit Edison v. NLRB (1979)
Philadelphia, PA, USA R OBERT H EILBRONNER
Chicago, IL, USA
Synonyms
Desmoplastic ganglioglioma Synonyms
Disclosure of tests and raw data; Release of psychological

Definition test materials; Test security
A variant of gangliogliomas, the desmoplastic ganglio-

glioma, is a rare intracranial tumor of mixed cell type, Historical Background
containing properties of both glial cells and neuronal cells.
It is further characterized by the fibrosis forming in the Petitioner employer (Detroit Edison), in response to a
vascular stroma (framework) of the tumor. The origin request made by a Union (National Labor Relations
and cellular makeup of a desmoplastic gangliocytoma is Board: NLRB) in connection with arbitration of a griev-
incompletely understood. However, its derivation is ance filed on behalf of employees in a bargaining unit,
824 D Detroit Edison v. NLRB (1979)
supplied the Union with certain information pertaining NLRB decisions (NLRB v. Pfizer, 1985; NLRB v. U.S. Postal
to petitioners employee psychological aptitude testing Service, 1994) uniformly recognize that discovery of psy-
program under which certain unit employees had been chological tests is restricted under Detroit Edison v. NLRB
rejected for certain job openings because of their failure to and essentially amounts to an implied federal common
receive acceptable test scores. However, petitioner re- law psychologist nondisclosure privilege. However, in
fused to release the actual test questions, the actual em- another case (Chiperas v. Rubin, 1998), the Court did
ployee answer sheets, and the scores linked with the not agree that a psychologist had no standing to quash a
names of the employees who received them, maintaining subpoena (for records) issued to someone who is not
that complete confidentiality of these materials was nec- a party to the action, unless that party (e.g., the psychol-
essary to insure the future integrity of the tests and to ogist) claims some personal right or privilege with regards
protect the examinees privacy interests. Petitioner offered to the documents sought. In other words, if the psychol-
to turn over the scores of any employee who signed a ogist does not assert a privilege, then there is no basis to
waiver releasing petitioners psychologist from his pledge object to the release of psychological test materials.
of confidentiality, but the Union declined to seek such Kaufmann (2009) provides a comprehensive review
releases. In unfair labor practice proceedings against of the issues surrounding psychological and neuropsy-
petitioner based on the Unions charge that petitioner chological test security and recommended practices and
had violated its duty to bargain collectively under 8(a)(5) legal arguments against disclosure of test materials.
of the National Labor Relations Act by refusing to pro- Some of the recommended practices include: (1) infor-
vide relevant information needed by the Union for the mal negotiation and agreement among the parties, (2)
proper performance of its duties as the employees bar- file a motion to quash the subpoena, (3) file a motion to
gaining representative the NLRB contended that all intervene as a right, and (4) consider contempt citations
the requested items were relevant to the grievance and carefully. Legal arguments include: (1) assertion of psy-
ordered petitioner to turn over all of the materials directly chological nondisclosure privilege based on state and
to the Union, subject to certain restrictions on the Unions federal law and (2) assertion of intellectual property
use of the information. The Board rejected petitioners restrictions and contractual obligations. Other proce-
request that, in order to preserve test secrecy, the tests dures include: (1) move for protective orders and (2)
and answer sheets be turned over to a psychologist select- seeking an in camera review. This elaborates upon previ-
ed by the Union. The Board and the Court of Appeals, in ous position papers from neuropsychological organiza-
its decision enforcing the Boards order, rejected peti- tions (NAN, 2000; 2003; AACN, 2003; 2007) related to
tioners claim that employee privacy and the professional issues of test security and disclosure of tests and raw
obligations of petitioners industrial psychologists should test data.
outweigh the Unions request for the employee-linked
scores. In its decision, the High Court held that the
NLRB abused its discretion when it ordered the consult- Cross References
ing I/O psychologists to release to the union standardized
test questions, answers, and results from psychological Confidentiality
aptitude tests. In Camera Review
Privilege
Current Knowledge
According to Kaufmann (2009), there are no U.S.
Supreme Court holdings directly addressing whether or
American Academy of Clinical Neuropsychology (2003). Official position
not psychologists must release test materials to nonpsy- of the American Academy of Clinical Neuropsychology on ethical
chologists or may refuse to release those materials. How- complaints made against clinical neuropsychologists during adver-
ever, in Detroit Edison v. NLRB, the Court spoke of the sarial proceedings. The Clinical Neuropsychologist, 17, 443445.
public policy of test security for standardized psychologi- American Academy of Clinical Neuropsychology (2007). AACN practice
guidelines for neuropsychological assessment and consultation. The
cal instruments. The Court determined that the right
of the psychologists to refuse release of test materials American Psychological Association (2002). Ethical principles of
superseded the rights of a Union to discovery of such psychologists and code of conduct. American Psychologist, 57,
information. Additional federal appellate cases and 10601073.
Developmental Delay D 825
Bush, S. S., & Martin, T. A. (2006). The ethical and clinical practice of Current Knowledge
disclosing raw test data: Addressing the ongoing debate. Applied
Detroit Edison Co. v. NLRB, 440 U.S. 301, (U.S. 1979).
A developmental delay in a specific domain may occur in
Freides, D. (1993). Proposed standard of professional practice: Neuro- isolation or in conjunction with delays in other domains. To
psychological reports display all quantitative data. The Clinical Neu- recognize a delay and to select an appropriate intervention,
ropsychologist, 7, 234235. clinicians must first have an understanding of developmen-
Grote, C. (2005). Ethical practice of forensic neuropsychology. In
tal norms (Schroeder & Gordon, 2002). It is important to D
G. Larrabee (Ed.), Forensic neuropsychology: A scientific approach.
consider that patients may present with a developmental
Jaffe v. Redmond, 518 U.S. 1 (1996). delay as their primary or secondary area of concern, and
Kaufman, P. M. (2009). Protecting raw data and psychological tests from clinicians should be able to evaluate and recognize such a
wrongful disclosure: A primer on the law and other persuasive delay in both contexts. This is especially important in med-
strategies. The Clinical Neuropsychologist, 23, 11301159.
ical settings where a developmental delay may be secondary
National Academy of Neuropsychology (2000). Test security: Official
statement of the National Academy of Neuropsychology. Archives
to a medical condition (Stone, MacLean, & Hogan, 1995).
of Clinical Neuropsychology, 15, 383386. Assessing for the presence of developmental delays is critical
National Academy of Neuropsychology Policy and Planning Committee in making accurate diagnoses of developmental disorders
(2003). Test security: An update. Official statement of the National and formulating subsequent treatment plans. The following
Academy of Neuropsychology. See http://www.nanonline.org/NAN/
chart provides examples of developmental disorders, devel-
Files/PAIC/PDFs/NANTestSecurityUpdate.pdf.
NLRB v. Pfizer, Inc., 763 F.2d 887 (7th Cir., 1985).
opmental delays associated with them, and the age para-
NLRB v. U.S. Postal Service, 17 F. 3d 1434 (4th Cir., 1994). meters based on the DSM-IV-TR criteria (American
Psychiatric Association, 2000).
To better understand the role of developmental delays
within the context of a developmental disorder, a closer look
at a specific diagnosis is warranted. For example, as Table 1
Developmental Coordination depicts, developmental delays in the intellectual and
Disorder
Developmental Delay. Table 1
Soft Signs Developmental Developmental
disorder delays observed Age of onset
Mental Intellectual Prior to age 18
Retardation Adaptive
(MR)
Developmental Delay
Autistic Disorder Social Prior to age 3
L AURA C RAMER-B ERNESS Emotional
William Paterson University Communication/
Wayne, NJ, USA Language
Aspergers Social No age specified
Disorder Emotional
Synonyms Retts Disorder Social Typical development
Communication/ followed by onset of
Developmental retardation Language delays that may begin
as early as 5 months of
Physical
age
Motor
Definition Childhood Social Typical development
Disintegrative Emotional until at least age 2 and
Developmental delay is the failure to achieve certain Disorder loss of skills prior to
Communication/
developmental milestones at the appropriate age. Such Language
age 10
delays may occur in one or more of the following areas:
Physical
intellectual, emotional, social, motor, physical, language/
Motor
communication, and adaptive skills.
826 D Developmental Dyslexia
adaptive domains are necessary for a diagnosis of mental Short Description or Definition
retardation. As currently defined in the DSM-IV-TR
(American Psychiatric Association, 2000), an intellectual Developmental Gerstmann syndrome (Gerstmanns syn-
quotient (IQ) of less than 70 indicates an intellectual drome) is a rare disorder that has been infrequently de-
delay. The criteria for delayed adaptive skills are a signifi- scribed in the literature. The descriptions focus on four
cant impairment in two or more of the following areas: classic deficits: difficulty writing (dysgraphia or agraph-
communication, self-care/home living, social/interper- ia), difficulty with arithmetic (dyscalculia or acalculia), an
sonal skills, use of community resources, self-direction, inability to distinguish left from right, and difficulty
functional academic skills, work, leisure, health, and safe- identifying fingers (finger agnosia). Constructional dys-
ty. If this combination of developmental delays is present praxia, an inability to copy simple figures, is often includ-
prior to the age of 18, then a diagnosis of mental retarda- ed as a fifth symptom. The cause is not known, but over
tion may be made. It is important to note that there may the last 10 years, studies using advanced imaging techni-
be an overlap in certain diagnoses. For instance, a patient ques have reported the deficits to be associated with
may be diagnosed with mental retardation and autistic posterior inferior parietal lesions located on the left side
disorder. This comorbidity of disorders would then need of the brain (Miller & Hynd, 2004).
to be considered in how to best address the developmental
delays associated with each.
Characterization
Cross References
Fewer than 25 cases have been reported in the literature
Disability and, in the last 15 years, fewer than five appear to have
Intellectual Disability been described. As a result, there is not yet a consensus
about how to define the syndrome.
References and Readings It was first described as a discrete syndrome by Kins-
bourne and Warrington (Kinsbourne & Warrington,
American Psychiatric Association (2000). Diagnostic and statistical man- 1963) who reported on seven children. All presented
ual of mental disorders (4th ed., text revision). Washington, DC: with left-right confusion, finger agnosia, and construc-
American Psychiatric Association. tional dyspraxia, and about half also presented with dys-
Schroeder, C. S., & Gordon, B. N. (2002). Assessment & treatment of
calculia and dysgraphia. As that description suggests,
childhood problems (2nd ed.). New York: Guilford.
Stone, W. L., MacLean, W. E., & Hogan, K. L. (1995). Autism and mental there is some disagreement in the literature as to whether
retardation. In M. C. Roberts (Ed.), Handbook of pediatric psychology all four classic deficits must occur for a diagnosis to be
(pp. 655675). New York: Guilford Press. reached. (A similar lack of consensus applies to adult cases
as well.) At least one author has theorized that the disor-
der may present in a partial form if a child has simply
Developmental Dyslexia learned to compensate to some degree in a deficit area of
the syndrome (PeBenito, 1987).
Dyslexia
Epidemiology
Developmental Gerstmann
Syndrome No epidemiological studies of the syndrome have been
reported and some authors have stated that there is no
B ONNY J. F ORREST clear basis for considering it to be a unique syndrome
San Diego Center for Children (Miller & Hynd, 2004).
San Diego, CA, USA
Synonyms Natural History, Prognostic Factors, and

Outcomes of Gerstmanns Syndrome
Developmental right parietal syndrome; Nonverbal dis-
orders of learning; Nonverbal learning disability; Right Almost all reported cases involve symptoms that could
hemisphere Impairment/Disorder be attributed to other diagnoses, including fragile
Developmental Milestones, Stages D 827
X syndrome, Williams syndrome, nonverbal or right References and Readings

hemisphere learning disabilities, or autism spectrum dis-
orders. Most cases are identified when children reach Kinsbourne, M, & Warrington, E. K. (1963). The developmental Gerst-
school age, a time when they are challenged with writing mann syndrome. Archives of Neurology, 8(5), 490501.
Miller, C. J., & Hynd, G. W. (2004). What ever happened to developmen-
and math exercises. Although it has been suggested that
tal Gerstmanns syndrome? Links to other pediatric, genetic, and
childrens symptoms may diminish over time, it appears neurodevelopmental syndromes. Journal of Child Neurology, 19
likely that most children probably do not overcome their (4):282289. D
deficits, but rather learn to adjust to them. PeBenito, R. (1987). Developmental Gerstmann syndrome: Case report
and review of the literature. Developmental Behavioral Pediatrics,
8(4), 229232.
Semrud-Clikeman, M., & Hynd, G. W. (1990). Right hemispheric dys-
Neuropsychology and Psychology of function in nonverbal learning disabilities: Social, academic, and
adaptive functioning in adults and children. Psychological Bulletin,
Developmental Gerstmann Syndrome
107, 198209.
Shaley, R. S., & Gross-Tsur, V. (1993). Developmental dyscalculia and
As noted above, the cluster of neuropsychological fea- medical assessment. Journal of Learning Disabilities, 26, 134137.
tures described in Gerstmann syndrome may represent
soft neurological signs associated with a number of
neurodevelopmental disorders. In addition to the four
classic deficits previously described and constructional
dyspraxia, other symptoms frequently co-occur with Developmental Milestones,
Gerstmanns syndrome. These include average or better Stages
intelligence, elevated verbal skills, average or better
reading abilities, negative family history for learning L EESA V. H UANG 1, S ARAH F REEMAN 2
disabilities, lack of clinically significant delays in language, 1
California State University
and no history of a head injury. Chico, CA, USA
A number of theories have been put forth to account 2
San Jose Unified School District
for the cluster of symptoms observed in the syndrome. San Jose, CA, USA
Kinsbourne and Warrington, referencing adult cases with
lesions in the parietal lobes of the left hemisphere, postu-
lated that in children the symptoms were likely the result Synonyms
of a developmental learning disorder (Kinsbourne & War-
rington, 1963). Other authors have speculated that the Developmental stages
syndrome occurs as a result of a neurological abnormality
(Shaley & Gross-Tsur, 1993), or abnormal developmental
processes (Semrud-Clikeman & Hynd, 1990). Given the
Definition
lack of consensus about the definition, and the resulting
paucity of cases, there has been no clear explanation of the
Developmental milestones are a set of functional skills
syndromes cause although, as Kinsbourne and War-
that a majority of children have acquired during a certain
rington hypothesized, the deficits appear to be associated
age range. Infants and children develop skills in five main
with left-sided posterior inferior parietal lesions (Miller &
areas: cognition, social and emotional, speech and
Hynd, 2004).
language, fine motor, and gross motor. All milestones
develop sequentially; that is, a child will need to develop
some basic skills before developing more advanced skills.
Treatment Although each stage has a specific time frame, the
actual age at which an individual child may successfully
There is no cure for Gerstmanns syndrome. Treatment is demonstrate a skill varies widely. Therefore, developmen-
symptomatic and supportive. Occupational and speech tal milestones should be viewed as guidelines for the
therapies may help diminish the dysgraphia and apraxia. development of age-appropriate skills. These age-specific
In addition, calculators and word processors may tasks allow educational and medical professionals to
help school children cope with the symptoms of the determine how a child is progressing and what areas
disorder. may need additional support or intervention.
828 D Developmental Psychology
In relation to neuropsychology, development involves

two main phases of neurological organization. The first Developmental Test of Visual
stage commences at the time of conception and consists of Motor Integration
neurulation, proliferation, migration, and differentiation.
The second phase is characterized by the reorganization Beery Developmental Test of Visual-Motor Integration
of the cortex, which begins during gestation and may (VMI)
continue through young adulthood (second decade of
life). Dendritic and axonal growth, synapse production,
neuronal and synaptic pruning, and changes in neuro-
transmitter sensitivity occur. Due to the rapid growth of
the brain during the first several years, developmental
Dexamethasone
milestones assist practitioners in the prediction of when
DAVID J. L IBON
certain skills develop in infants and children.

Definition
Berk, L. E. (2006). Child development (7th ed.) New York: Pearson/Allyn
and Bacon. Dexamethasone is a medication used to diagnose and
Webb, S. J., Monk, C. S., & Nelson, C. A. (2001). Mechanisms of postnatal
treat medical as well as psychiatric conditions. Dexameth-
neurobiological development: Implications for human develop-
ment. Developmental Neuropsychology, 19, 147171. asone is often used to block inflammation. As such dexa-
methasone can be used as an anti-inflammatory agent to
treat a number of medical conditions including a wide
array of auto-immune disorders. Dexamethasone can also
be used to assess for negative feedback regarding the
Developmental Psychology ability of the pituitary gland to suppress adrenocortical
activity.
Normal Aging
Current Knowledge
As such, the dexamethasone suppression test (DST) was

Developmental Retardation developed to diagnosis medical conditions such as Cush-
ing disease. However, the DST has also been used to
Developmental Delay
diagnose major depression (Carroll, Martin, & Davies,
1968). The rationale for the diagnostic use of the DST
to treat major depression was initially based on observa-
tions of increased adrenocortical activity in depression.
Developmental Right Parietal The inability to suppress adrenocortical activity has been
used as a means to diagnose depression and related psy-
Syndrome chiatric illnesses. Data on the efficacy of the DST has been
mixed; however, recent data provided by Fountoulakis
Developmental Gerstmann Syndrome
et al. (2008) suggests that under certain circumstances
Nonverbal Learning Disabilities
the DST may be helpful to better characterize patients
with major depression.
Developmental Stages Cross References
Developmental Milestones, Stages Hypothalamus

DFT D 829
References and Readings Off Label Use
Carroll, B. J., Martin, F. I., & Davies, B. (1968). Resistance to suppression Narcolepsy and depression (treatment-resistant).
by dexamethasone of plasma 11-O.H.C.S. levels in severe depressive
illness. British Medical Journal, 3, 285287.
Fountoulakis, K. N., Gonda, X., Rihmer, Z., Fokas, C., & Iacovides, A.
(2008). Revisiting the Dexamethasone Suppression Test in unipolar Side Effects
major depression: an exploratory study. Annals of General Psychiatry, D
7, 2231.
Serious
Psychotic episodes, seizures, neuroleptic malignant syn-

drome, hypomania, mania, and possible suicidal ideation.
Dexedrine
Amphetamine
D-Amphetamine Common
Insomnia, irritability, tremor, anxiety, and tics (exacerba-

tion, dizziness, anorexia, blurred vision).
Dexmethylphenidate
J OHN C. C OURTNEY 1, C RISTY A KINS 2 References and Readings
1
New Orleans, LA, USA Physicians Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson
2
Mercy Family Center PDR.
Metarie, LA, USA Stahl, S. M. (2007). Essential psychopharmacology: The prescribers guide
Generic Name
Dexmethylphenidate
Brand Name Free Drug Online and PDA Software: www.epocrates.com
Focalin, Focalin XR com:8080/cgi bin/ddiD4?ver = 4&task = getDrugList
Class
Stimulant
Dextroamphetamine
Proposed Mechanism(s) of Action Amphetamine
D-Amphetamine
Dexmethylphenidate facilitates the release and blocks the
reuptake of both norepinephrine and dopamine.
Indication DFT
Attention-deficit hyperactivity disorder. Design Fluency Test
830 D Diabetes Mellitus
include stroke, cardiovascular disease and hypertension,

Diabetes Mellitus nephropathy, retinopathy, neuropathy, and foot difficulties.
Considerable research has also evaluated the effect of
G EORGE D EMAKIS diabetes on cognitive functioning. This research is
University of North Carolina Charlotte characterized by considerable variety in the samples age,
Charlotte, NC, USA gender, duration of diabetes and comorbid conditions,
methodological approaches including cross-section and
longitudinal designs, and neuropsychological measures
Synonyms employed (Ryan, 2001). In a review of many studies
with children and adolescents with Type 1 diabetes,
Type 1 diabetes, previously termed juvenile-onset or in- Desrocher and Rovet (2004) concluded that a variety of
sulin-dependent diabetes; Type 2 diabetes, previously cognitive deficits were associated with an early onset
termed non-insulin-dependent diabetes or adult-onset (prior to 5 years of age), recurrent episodes of hypoglyce-
diabetes mia, and longer duration of illness. Though not observed
in all studies, cognitive deficits tended to be observed in
Short Description or Definition areas such as motor functioning, attention, memory, and
set-shifting, and in general, were judged to be rather
Diabetes mellitus is a complex set of metabolic disorders small. Awad, Gagnon, and Messier (2004) conducted a
involving chronically high levels of blood glucose (hypergly- meta-analytic review of studies that compared adults with
cemia) secondary to the impaired production of the treated Type 2 diabetes with controls. Across the various
hormone, insulin. Classic symptoms include polyuria studies, the diabetic groups tended to perform somewhat
(excessive urine), polydipsia (intense thirst), polyphagia worse on measures of verbal memory and processing speed.
(intense hunger), and fatigue. There were either minimal or no differences across the
studies on measures of verbal and nonverbal memory, at-
tention, visuospatial functioning, and executive function-
Categorization ing. Worse performance by diabetic samples was associated
with older age, poorer glycemic control, and insulin treat-
There are two main types of diabetes: Type 1 diabetes is ment as opposed to oral hypoglycemic treatment or diet. A
much less common, accounting for about 10% of all diag- meta-analysis of the effect of Type 1 diabetes on cognition in
nosed cases, and is characterized by an inability to secrete adults (Brands, Biessels, de Haan, Kappelle, & Kessels, 2005)
insulin due to destruction of the beta cells of the pancreas. found that individuals with diabetes scored significantly
This type of diabetes usually is diagnosed before the age 20. lower than non-diabetic controls on a variety of cognitive
The more common Type 2 typically occurs in adulthood measures. Poorer cognitive performance was associated
and results from the development of insulin resistance, with microvascular complications (neuropathy or retinop-
which can result in chronic hyperglycemia. Risk factors for athy), but not with the occurrence of severe hypoglycemic
Type 2 diabetes include heredity, age, and obesity. episodes or poor metabolic control. Despite these findings,
it is important to note that some studies have not found
Epidemiology cognitive differences between diabetics and non-diabetes (e.
g., Jacobson et al., 2007), and that if cognitive impairment
Diabetes affects over 20 million individuals in the United does exist, it usually tends to be relatively minor.
States. Men, individuals older than 60, and ethnic mino- What is the cause or mechanism of these neuropsycho-
rities are more likely to be affected. logical deficits? Glucose is the primary energy substrate of
the brain and normal brain structure and function are
dependent on its metabolic control. Hypoglycemia, if left
Natural History, Prognostic untreated, can lead to seizures, loss of consciousness, brain
Factors, Outcomes: Emphasis damage, and even death. Hyperglycemia, if left untreated,
on Neuropsychological and can be associated with vascular damage, leading to a variety
Psychological Issues of complications including stroke, heart attack, and hyper-
tension. As an example of research in this area, Jongen, van
Acute complications of diabetes may include hypoglycemia der Grond, Kappelle, Biessels, Viergever, and Pluim (2007),
and ketoacidosis, whereas chronic complications may using magnetic resonance imaging (MRI) of the brain,
Diagnosis D 831
found that Type 2 diabetics had smaller volume gray References and Readings
matter, larger lateral ventricle volume, and a larger white
matter lesion volume than those in the controls. This Anderson, R. J., Clouse, R. E., Freedland, K. E., & Lustman, P. J. (2001).
same research group found that cognitive functioning, The prevalence of comorbid depression in adults with diabetes:
A meta-analysis. Diabetes Care, 24, 10691078.
particularly attention/executive functioning and informa-
Awad, N., Gagnon, M., & Messier, C. (2004). The relationship
tion processing speed, was inversely related to white mat- between impaired glucose tolerance, Type 2 diabetes, and cognitive
ter lesions, brain atrophy, and the presence of infarcts function. Journal of Clinical and Experimental Neuropsychology, 26, D
(Manschot et al., 2006). 10441080.
In addition to these neuropsychological issues, it is not Brands, A. M. A., Biessels, G. J., de Haan, E. H. F., Kappelle, L. J., &
Kessels, R. P. C. (2005). The effects of Type 1 diabetes on cognitive
surprising that diabetes is associated with higher levels of
performance: A meta-analysis. Diabetes Care, 28, 726735.
psychological distress than in controls (Ryan, 2001). For Brands, A. M. A., van den Berg, E., Manschot, S. M., Biessels, G. J.,
instance, in a meta-analysis, Anderson, Clouse, Freedland, Kappelle, L. J., de Haan, E. H. F., & Kessels, R. P. C. (2007). A detailed
and Lustman (2001) found that prevalence rates of depres- profile of cognitive dysfunction and its relation to psychological
sion varied widely across studies (360%, but with most distress in patients with type 2 diabetes mellitus. Journal of the
studies around 20%), and that Type 1 and Type 2 diabetics
Desrocher, M., & Rovet, J. (2004). Neurocognitive correlates of Type I
were twice as likely to be depressed as the controls. The diabetes mellitus in childhood. Child Neuropsychology, 10, 3652.
prevalence of comorbid depression was higher in women Jacobson, A. M., Musen, G., Ryan, C. M., Silvers, N., Cleary, P,
than in men, in clinical versus community samples, and Waberski, B., Burwod, A., Weinger, K., Bayless, M., Dahms, W.,
when assessed via self-report versus standardized diagnos- Harth, J., & The Diabetes Control and Complications Trial/Epide-
miology of Diabetes Interventions and Complications Study Re-
tic interviews. When depression has been evaluated in
search Group. (2007). Long-term effect of diabetes and its
diabetes populations, Watari et al. (2006) found that de- treatment on cognitive function. The New England Journal of Medi-
pressed Type 2 diabetics performed more poorly than cine, 356, 18421852.
non-depressed diabetes and controls in cognitive domains Jongen, C., van der Grond, J. V. D., Kappelle, L. J., Biessels, G. J.,
of attention and executive functioning. In contrast, Viergever, M. A., & Pluim, J. P. W. (2007). Automated measurement
of brain and white matter lesion volume in type 2 diabetes mellitus.
Brands et al. (2007) found no relationship between self-
Diabetologia, 50, 15091516.
report measures of psychological distress and cognition in Manschot, S. M., Brands, A. M. A., van der Grond, J., Kessels, R. P. C.,
individuals with type 2 diabetes. Algra, A., Kappelle, L. J., & Biessels, G. J. (2006). Brain magnetic
resonance imaging correlates of impaired cognition in patients with
type 2 diabetes. Diabetes, 55, 11061113.
Ryan, C. M. (2001). Neurobehavioral disturbances associated with dis-
Evaluation orders of the pancreas. In R. E. Tarter, M. Butters, & S. R. Beers
(Eds.), Medical neuropsychology (2nd ed., pp. 127162). New York:
A variety of relatively minor cognitive deficits can be asso- Kluwer Academic/Plenum.
Watari, K., Letamendi, A., Elderkin-Thompson, V., Haroon, E., Miller, J.,
ciated with diabetes and, as such, any neuropsychological
Darwin, C., & Kumer, A. (2006). Cognitive function in adults with
measure used in this population should be quite sensitive to type 2 diabetes and major depression. Archives of Clinical Neuropsy-
cognitive impairment. Domains to be assessed by the chology, 21, 787796.
neuropsychologist should include, at minimum, verbal
memory and learning, processing speed, attention, set-
shifting, and motor functioning.
Treatment Diabetic Retinopathy

Retinopathy
Treatment for Type 1 includes insulin injections, whereas
for Type 2 exercise and diet, oral hypoglycemic agents,
and, if necessary, insulin is prescribed.
Cross References Diagnosis

Hypoglycemia Behavior Assessment System for Children (BASC)
832 D Diagnostic Dyspraxia
Originally coined by von Monakow in 1914, the term

Diagnostic Dyspraxia diaschisis currently is used to describe a depression of
regional neuronal metabolism and cerebral blood flow
Alien Hand Syndrome caused by dysfunction in an anatomically separate but
functionally related region of the brain. It is important to
note that diaschisis is a dysfunction of tissue that is not
damaged but for which the blood supply has been reduced
Diagnostic Interview because of interruption of neurons that are connected to it.
Clinical Interview
Cross References
Diaschisis Cerebral Blood Flow
Ischemic Penumbra
E LLIOT J. R OTH Ischemic Stroke
Chicago, IL, USA
Definition Finger, S., Koehler, P. J., & Jagell, C. (2004). The Monakow concept of
diaschisis: Origins and perspectives. Archives of Neurology, 61,
Diaschisis is a sudden loss of function in a portion of the 283288.
brain connected to, but at a remote distance away from, Infeld, B., Davis, S. M., Lichtenstein, M., Mitchell, P. J., & Hopper, J. L.
(1995). Crossed cerebellar diaschisis and brain recovery after stroke.
a damaged area.
Stroke, 26, 9095.
Komaba, Y., Mishina, M., Utsumi, K., Katayama, Y., Kobayashi, S., &
Mori, O. (2004). Crossed cerebellar diaschisis in patients with
Current Knowledge cortical infarction: Logistic regression analysis to control for con-
founding effects. Stroke, 35, 472476.
The site of the area that has been injured by an acute focal
disturbance such as stroke or penetrating brain injury,
and the site of the diaschisis are connected to each other
by neurons. The loss of the damaged structure disrupts
the function of the remaining intact systems and causes
Diazepam
a physiological imbalance. These changes are most
J OHN C. C OURTNEY
pronounced during the first few days following cerebral
infarction or injury. Some function may be restored with
a gradual readjustment of the otherwise intact but
suppressed areas.
Diaschisis can be classified according to the connecting
neuronal fibers involved. When the connecting fibers are
Generic Name
intra-hemispheric, the phenomenon of ipsilateral thalamic
Diazepam
or subcortical-cortical diaschisis may be seen; when they
are interhemispheric, there is transcallosal diaschisis, and if
they are cerebellar, the diaschisis is of the contralateral Brand Name
cerebellum or crossed cerebellar diaschisis. Ipsilateral tha-
lamic and crossed cerebellar diaschisis are frequently ob- Valium, Diastat
served, but have no clinical significance.
Reversal of the effects of the subcortical-cortical and
transcallosal diaschisis might explain the neuropsychologi- Class
cal and functional neuroimaging changes observed over the
first few months after the cerebrovascular incident. Anxiolytic
Dichotic Listening D 833

Dichotic Listening
Binds to benzodiazepine receptors at the GABA-A ligand-
gated channel, thus allowing for neuronal hyperpolariza- M ELISSA A MICK
tion. Benzodiazepines enhance the inhibitory action of VA Boston Healthcare System
GABA via boosted chloride conductance. Diazepam also Boston, MA, USA
produces inhibitory action in the spinal cord and may D
provide therapeutic benefits for muscle spasms.
Description
Indication In the dichotic listening words test (Hayden & Spellacy,
1978), the participant hears three pairs of one-syllable
Anxiety disorder, symptoms of anxiety, acute agitation, words (one presented to each ear simultaneously).
muscle spasm, spasticity caused by upper motor neuron Each word pair begins with the same consonant (see
disorders, athetosis, stiff-man syndrome, convulsive dis- Strauss, Sherman, & Spreen, 2006, for examples). The
orders (adjunctive), preoperative anxiety, and initial audiotape is played through a cassette recorder and head-
treatment of status epilepticus. phones. The stimuli presented to the left ear are recorded
on the left channel of the tape, and played through the left
headphone. The reverse arrangement is used for the right
Off Label Use ear. According to Strauss et al. (2006), the earphones
should be calibrated to ensure that each is producing
Insomnia
approximately 6570 dB for each ear. It is also recom-
mended that the earphones be reversed halfway through
testing, to avoid the possible effect of poor earphone
Side Effects
calibration. Discrepancies in hearing between ears would
create an advantage for the intact ear, and if hearing
Serious
differs significantly between ears, the test should not be
administered.
There are other versions of the dichotic listening task.
dysfunction and blood dyscrasias, Grand mal seizures
Another common procedure is to use stop consonant
vowel syllable pairs (e.g., /ba/, /da/, /ga/) rather than
Common words. The participants task is to identify the one syllable
heard clearly (Hugdahl, Carlsson, Uvebrant, & Lunder-
Sedation, fatigue, depression, dizziness, memory pro- vold, 1997). Dichotic listening has also been examined
blems, disinhibition, confusion, ataxia, slurred speech using the Fused Dichotic Word Test (Hiscock, Cole,
Benthall, Carlson, & Ricketts, 2000). The stimuli
employed for this dichotic listening task are rhyming
References and Readings consonant vowel consonant pairs (e.g., hearfear, cage
gage). A forced choice response is required from four
Physicians Desk Reference (62nd ed.). (2007). Montvale, NJ: Thomson possible options. Attention can also be manipulated in
PDR.
dichotic listening tasks. In forced attention conditions,
(2nd ed.). New York, NY: Cambridge University Press. the participant is instructed to report stimuli presented
to a specified ear, while in the unforced condition, parti-
cipants are not directed to attend to either ear (Gadea
Additional Information et al., 2002).

Drug Molecule Images: http://www.worldofmolecules.com/drugs/ Historical Background
com:8080/cgi bin/ddiD4?ver=4&task=getDrugList Early studies with the dichotic listening task revealed a
Pill Identification: http://www.drugs.com/pill_identification.html right ear advantage (REA, inferred left hemisphere
834 D Dichotic Listening
advantage) for spoken words (digits). Kimura (1961a, b, patients with complete hemispherectomy are able to pro-
1967) observed that patients with damage to the left cess auditory material presented monaurally but are
temporal lobe performed more poorly than patients impaired under dichotic presentation. Specifically, these
with right temporal lobe damage as well as adult control patients are able (7489% accuracy) to detect dichotic
participants. These findings were expected as patients information in the ear contralateral to the hemispherec-
with damage to the left hemisphere should have more tomy but accuracy was extremely poor (312%) for the
difficulty performing language-based tasks relative to the ear ipsilateral to the lesion (de Bode, Sininger, Healy,
other groups. Surprisingly, all groups demonstrated better Mathern, & Zaidel, 2007).
detection for information presented to the right relative to An attentional model has also been proposed to ex-
the left ear. The REA was initially unexpected because each plain the REA observed on dichotic word listening tasks.
ear projects to the contralateral and ipsilateral hemi- Kinsbourne (1975) proposed that a REA occurs because
sphere. Based on these redundant connections, each ear attention is shifted toward the contralateral side of space
should have access to the language center. Kimura rea- following engagement of a hemisphere. For example, a
soned that a REA occurred because the ipsilateral pathway REA occurs during dichotic word listening because the
is suppressed during dichotic but not monaural stimuli left hemisphere is engaged for processing verbal material,
presentation. According to her model, in patients with and the activation of the left hemisphere leads to a shift of
speech localized to the left hemisphere, information from attention toward information presented to the right side
the left ear is sent to the right hemisphere and then of space (see Springer & Deutsch, 1985 for review). In
through the cerebral commissures before gaining access support of the attentional model, a double dissociation
to the left hemisphere for processing of the verbal mate- was found in dichotic listening depending upon the type
rial. By contrast, the right ear projects to the left hemi- of material (verbal or melodic) that had to be remem-
sphere (without the additional step of crossing over the bered across trials. That is, a REA was found when parti-
cerebral commissure) that results in a REA (see Kimura, cipants had to remember a sentence across dichotic trials
1967 for review). Further support for Kimuras model of and a modest LEA (as measured by reaction time) oc-
dichotic listening comes from work done with patients curred when subjects compared melodies presented just
who have undergone the intracarotid sodium amytal pro- before and immediately following dichotic syllable pairs
cedure (Wada test) to determine which hemisphere med- (Morais & Landercy, 1977). According to the attentional
iates language. Unlike patients with language lateralized model, activation of the right hemisphere during melodic
to the left hemisphere with the typical REA, patients who processing would focus attention to the left side of space
have language lateralized to the right hemisphere showed creating the LEA.
a left ear advantage (LEA, Kimura, 1961b, 1967).
Data from patients with complete disconnection of
the hemispheres via commissurotomy have also been Psychometric Data
cited as support for Kimuras model. Split-brain patients
are able to identify spoken words presented monaurally, Strauss et al. (2006) report normative data for children
indicating that the ipsilateral pathway is intact in the (age 2 through grade 6) as well as mean scores for right-
absence of competing information. However, under dich- handed adults. The authors caution that the adult norms
otic presentation, an exaggerated REA occurs. In fact, are based upon university students and therefore are only
seven out of ten patients with a commissurotomy detected applicable for younger adults. Normative data for older
no information presented to the left ear (Milner, Taylor, & adults is not available for this particular task. There are
Sperry, 1968), and this extinction of information was also published means and standard deviations for adults rang-
described in two patients with complete disconnection of ing in age from 16 to 79, split into decades (Meyers,
the hemispheres (Springer & Gazzaniga, 1975). According Roberts, Bayless, Volkert, & Evitts, 2002) using a similar
to Kimuras model, the extinction of information occurs task with more word pairs (Dichotic Word Listening Test,
because information presented to the left ear is projected Roberts et al., 1994). Generally, normative data for dich-
to the disconnected right hemisphere. The right hemi- otic listening tasks are not presented separately for men
sphere is not specialized to process this type of verbal and women, as it is thought that gender does not signifi-
material, and this information cannot be projected to cantly influence dichotic listening performance. A recent
the left hemisphere because the corpus callosum is cut. meta-analysis of 12 studies involving a total of 3,822
Consequently, split-brain patients are not able to report subjects concluded that there were no significant differ-
hearing information presented to the left ear. Similarly, ences between sexes in terms of dichotic listening
Dichotic Listening D 835
performance (Sommer, Aleman, Somers, Boks, & Kahn, and psychiatric populations. Patients with multiple scle-
2008). rosis (MS) also show abnormal dichotic listening perfor-
Testretest reliability for dichotic listening word pairs mance. For example, relative to control participants,
is variable. Hiscock and colleagues (2000) report a reli- patients with MS have been observed to demonstrate a
ability of 0.45 with a 1 week interval between testing. This greater REA in unforced and right ear forced attention
was conducted with a sample of 340 right- and left-hand- conditions. By contrast, in the left ear forced attention
ed college students. Reliability did improve when more condition, the control group demonstrated the expected D
trials were added (0.76). Testretest reliability has been LEA, while the MS group persisted in demonstrating a
reportedly higher (0.760.92) when testing was per- REA (Gadea et al., 2002). Patients with other neurode-
formed in the same day with a smaller sample of epileptic generative diseases can also show an exaggerated REA
patients (Strauss, Gaddes, & Wada, 1987). relative to a neurologically normal comparison group.
According to Kimuras model, the ear advantage on This has been observed in patients with very mild and
dichotic word listening tasks should indicate which hemi- mild Alzheimers disease (Duchek & Balota, 2005;
sphere is dominant for language. Test validity data is Gootjes et al., 2006, Claus & Mohr, 1996). Additionally,
derived from patients who have completed both the dich- patients with Alzheimers disease and Huntingtons dis-
otic listening task and undergone the Wada test to deter- ease have been found to demonstrate a REA even under
mine which hemisphere mediates language. Hugdahl and left ear forced attention conditions, whereas demented
colleagues (1997) reported a REA for 8/10 participants and non-demented patients with Parkinsons disease are
who demonstrated left hemisphere language dominance, able to shift attention to the left ear and show the
whereas all three patients with right hemisphere language expected LEA (Claus & Mohr, 1996). Dichotic listening
dominance showed a LEA. Similarly, in a larger sample of has also been examined in patients with depression and
epileptic patients, a REA was found in the patient group schizophrenia, disorders often associated with right
with left hemisphere language dominance, whereas hemisphere dysfunction. An exaggerated REA in de-
patients with right hemisphere language dominance pressed individuals has been associated with response
reported words presented to the left ear more accurately to antidepressant treatment (see, Bruder et al., 1999 for
than patients with left or bilateral hemisphere language review), and patients with schizophrenia also show a
dominance (Strauss et al., 1987). These findings are also REA even under left ear forced attention conditions
consistent with the original studies reported by Kimura (Hugdahl et al., 2003).
(1961b, 1967) described above. High concordance has
also been found for fused dichotic word listening and Cross References
lateralized fMRI activation during a verb generation task
performed by children with epilepsy. All eight patients Auditory Cortex
with greater left than right hemisphere activation during Auditory Pathway
the verb generation task showed a REA, whereas bilateral Auditory Processing
activation was associated with a REA in three of the Auditory System
patients and no ear advantage in the other three (Fer- Intracarotid Sodium Amobarbital Test
nandes, Smith, Logan, Crawley, & McAndrews, 2006). As Split-Brain
seen above, dichotic listening performance is not always Wada Test
predictive of the hemisphere that mediates language. A
significant factor to consider is that patients who undergo
Wada testing have epilepsy or other brain abnormalities, References and Readings
which can effect brain organization and the lateralization
Bruder, G. E., Tenke, C. E., Stewart, J. W., McGrath, P. J., & Quitkin, F. M.
of different cognitive abilities.
(1999). Predictors of therapeutic response to treatments for depres-
sion: A review of electrophysiologic and dichotic listening studies.
CNS Spectrums, 4, 3036.
Clinical Uses de Bode, S., Sininger, Y., Healy, E. W., Mathern, G. W., & Zaidel, E.
(2007). Dichotic listening after cerebral hemispherectomy: Method-
ological and theoretical observations. Neuropsychologia, 18,
Dichotic listening is used frequently with patients who
24612466.
have epilepsy or focal brain tumors, as described above Claus, J. J., & Mohr, E. (1996). Attentional deficits in Alzheimers,
(see Historical Background and Psychometric Data). Parkinsons, and Huntingtons diseases. Acta Neurologica Scandina-
This task also has clinical utility with other neurological vica, 93(5), 346351.
836 D Diencephalic Seizures
Duchek, J. M., & Balota D. A. (2005). Failure to control prepotent path- Strauss, E., Gaddes, W. H., & Wada, J. (1987). Performance on a free-
ways in early stage dementia of the Alzheimers type: Evidence from recall verbal dichotic listening task and cerebral dominance deter-
dichotic listening. Neuropsychology, 19, 687695. mined by the carotid amytal test. Neuropsychologia, 25, 747753.
Fernandes, M. A., Smith, M. L., Logan, W., Crawley, A., & McAndrews, Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A compendium of
M. P. (2006). Comparing language lateralization determined by neuropsychological tests (3rd ed.). New York: Oxford University Press.
dichotic listening and fMRI activation in frontal and temporal
lobes in children with epilepsy. Brain and Language, 96, 106114.
Gadea, M., Marti-Bonmat, L., Arana, E., Espert, R., Casanova, V., &
Pascual, A. (2002). Dichotic listening and corpus callosum magnetic
resonance imaging in relapsing-remitting multiple sclerosis with
emphasis on sex differences. Neuropsychology, 16, 275281.
Diencephalic Seizures
Gootjes, L., Bouma, A., Van Strien, J. W., Van Schijndel, R., Barkhof, F., &
Scheltens, P. (2006). Corpus callosum size correlates with asymmet- Hemodynamic Response
ric performance on a dichotic listening task in healthy aging but not
in Alzheimers disease. Neuropsychologia, 44, 208217.
Hayden, S., & Spellacy, F. (1978). Dichotic word listening test. Neuropsy-
chology Laboratory, Department of Psychology, University of
Victoria. Diencephalon
Hiscock, M., Cole, L. C., Benthall, J. G., Carlson, V. L., & Ricketts, J. M.
(2000). Toward solving the inferential problem in laterality research:
Effects of increased reliability on the validity of the dichotic listening
L INDA L. P HILLIPS
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Hugdahl, K., Carlsson, G., Uvebrant, P., & Lundervold, A. J. (1997).
Dichotic-listening performance and intracarotid injections of amo-
barbital in children and adolescents. Preoperative and postoperative
comparisons. Archive of Neurology, 54, 14941500.
Synonyms
Hugdahl, K., Rund, B. R., Lund, A., Asbjrnsen, A., Egeland, J.,
Landr, N. I., et al. (2003). Attentional and executive dysfunctions Epithalamus-pineal gland, habenular nuclei; Subthalamus-
in schizophrenia and depression: evidence from dichotic listening Subthalamic nucleus, zona incerta
performance. Biological Psychiatry, 53, 609616.
Kimura, D. (1961a). Some effects of temporal-lobe damage on auditory
perception. Canadian Journal of Psychology, 15, 156165.
Kimura, D. (1961b). Cerebral dominance of the perception of verbal
Structure
stimuli. Canadian Journal of Psychology, 15, 166171.
Kimura, D. (1967). Functional asymmetry of the brain in dichotic listen- The diencephalon can be divided into four regions:
ing. Cortex, 3, 163178. epithalamus, thalamus, subthalamus, and hypothalamus.
Kinsbourne, M. (1975). The mechanism of hemispheric control of the The epithalamus constitutes a small area of the dienceph-
lateral gradient of attention. In P. M. A. Rabbitt, & S. Dornic (Eds.),
Attention and performance V (pp. 8197). London: Academic Press.
alon, located dorsally above the thalamus. It contains the
Meyers, J. E., Roberts, R. J., Bayless, J. D., Volkert, K., & Evitts, P. E. pineal, a lobular midline structure, just rostral to the
(2002). Dichotic listening: Expanded norms and clinical application. superior colliculi. Historically thought to be the seat of
Archives of Clinical Neuropsychology, 17, 7990. the soul, neurons in this single midline structure are
Milner, B., Taylor, L., & Sperry, R. W. (1968). Lateralized suppression called pinealocytes, which secrete melatonin and are
of dichotically presented digits after commissural section in man.
Science, 161, 184186.
linked with the retina through a circuitous path via the
Morais, J., & Landercy, M. (1977). Listening to speech while retaining sympathetic chain. At the base of the pineal, a stalk con-
music: What happens to the right-ear advantage? Brain and Lan- nects the structure to the remainder of the diencephalon.
guage, 4, 295308. The bilateral habenula is the other component of the
Roberts, M. A., Persinger, M. A., Grote, C., Evertowski, L. M., Springer, epithalamus, positioned rostral to the pineal and posteri-
J. A., & Tuten, T., et al. (1994). The dichotic word listening test:
Preliminary observations in American and Canadian samples.
or commissure. The two habenular nuclei are joined by a
Applied Neuropsychology, 1, 4556. commissure, and receive input from the dorsal thalamus
Sommer, I. E., Aleman, A., Somers, M., Boks, M. P., & Kahn, R. S. (2008). via the stria medullaris fibers. Output from the habenula
Sex differences in handedness, asymmetry of the planum tempor- targets the midbrain reticular formation.
ale and functional language lateralization. Brain Research, 1206, The largest portion of the diencephalon is the dorsal
7688.
Springer, S. P., & Deutsch, G. (1985). Left brain, right brain (Rev. ed.).
thalamus. It extends rostrally to the interventricular fora-
New York: W.H. Freeman. men, superiorally to the transverse cerebral fissure and the
Springer, S. P., & Gazzaniga, M. S. (1975). Dichotic testing of partial and floor of the lateral ventricles, inferiorly to the hypotha-
complete split brain subjects. Neuropsychologia, 13, 341346. lamic sulcus, and posteriorly it overlaps the midbrain.
Diencephalon D 837
Topographically, the thalamus is divided into nuclear the pituitary. The hypothalamus has three sets of nuclear
groups, designated medial or lateral based upon their groups based upon their rostrocaudal position. As with
relationship to an interposed sheet of axons called the the dorsal thalamus, both medial and lateral areas are
internal medullary lamina. Largely rostral to this lamina identified. The anterior group, arranged above the optic
is an anterior set of nuclei, collectively grouped into one chiasm, includes medially the preoptic, paraventricular,
entity and bordering the interventricular foramen. The anterior, and supraoptic nuclei. Laterally, an anterior pre-
medial division of the dorsal thalamus contains a single optic group is also identified and a broadly dispersed D
dorsomedial nucleus. Laterally, the nuclei are divided into lateral nucleus. In dorsoventral alignment with the tuber
dorsal and ventral layers. Dorsally, they include lateral cinereum (pituitary stalk) is the tuberal group of nuclei.
dorsal, lateral posterior, and pulvinar groups. Ventrally, a These include dorsomedial, ventromedial, and arcuate
more complex arrangement exists forming the ventral nuclei in the medial area. In the lateral tuberal zone, the
anterior and lateral nuclei, with the posterior group having rostral lateral nucleus extends more caudally, accompa-
a posteriolateral and posteriomedial region. More laterally nied by the lateral tuberal nuclei and tuberomammillary
arranged are the geniculate bodies, made up of a medial nuclei. Finally, the posterior nuclear group of the hypo-
auditory and lateral visual nuclear group. In one region the thalamus is formed primarily of the mammillary bodies
internal medullary lamina splits to surround two centrally and the posterior nuclear groups. Laterally, this region
embedded nuclei, the centromedian and parafascicular contains the most caudal extension of the lateral nucleus.
groups. Finally, the thalamus has two more thinly The hypothalamic nuclei are traversed by major fiber
distributed nuclear groups: the thalamic reticular nucleus bundles, including the fornix, stria terminalis, median
surrounding portions of the thalamic perimeter and the forebrain bundle, dorsal longitudinal fasciculus, and
midline nuclei, which are essentially a sheet of cells that the two major mammillary body connections, the mam-
extend from the periaqueductal gray zone to cover the millothalamic tract and mammillotegmental tract. These
midline surface of the thalamus. Major thalamic input is pathways interconnect the hypothalamic nuclei and
derived from ascending sensory and motor pathways, as represent their major input (e.g., fornix stria terminalis,
well as limbic inputs, information that is processed within median forebrain bundle)/output (e.g., mammillothala-
the thalamus. A subset of this input is routed as relay mic, mammillotegmental tracts, median forebrain
connections to specific areas of functional cortex or to bundle, and dorsal longitudinal fasciculus) routes to in-
more broadly integrative regions of association cortex. terface with other brain regions. A unique relationship
Fiber routes for input include the mammillothalamic exists between the hypothalamus and the pituitary.
tract, fornix, medial lemniscus, central tegmental tract, Through two different mechanisms, the hypothalamus
inferior colliculi, optic tract, and the white matter tracts interacts with the pituitary gland: either via direct axonal
of the prefrontal, parietal, occipital, and temporal lobes. In projections to the posterior pituitary (neurohypophysis)
this way, the thalamus acts as a gateway to influence output or through the secretion of regulatory factors at a portal
from a wide range of cortical and subcortical circuits. vein interface in the pituitary stalk (adenohypophysis).
A part of the midbrain gray matter is wedged rostrally
between the hypothalamus and internal capsule to form
the subthalamus. It lies inferior to the dorsal thalamus and Function
contains nuclear extensions from the midbrain red nucle-
us and substantia nigra as they project to the thalamus. The primary function associated with the epithalamus is
Specific cellular groups in the subthalamus include the regulation of circadian rhythm through the pineal gland.
subthalamic nucleus and the zona incerta. The subthala- The pineal is an endocrine gland, secreting high levels of
mic group is the largest and has extensive connections melatonin hormone during darkness. Melatonin provides
with the basal ganglia. Dorsal to the subthalamic nucleus a rhythm for setting the sleepwake cycle, and can affect
is the thinner zona incerta, which represents an extension gonadotrophic hormone production as a function of day-
of midbrain reticular formation. light period. It is thought that hormonally stimulated
Most ventral in the diencephalon is the hypothalamus. reproductive behavior may be optimized by linking longer
It extends along the descending portion of the third day length with sexual cycles. Although the specific func-
ventricle, rostrally to the lamina terminalis, superiorly to tion of the habenular nucleus is not fully understood, it
the hypothalamic sulcus at its border with the dorsal receives input from the stria medullaris and projects to the
thalamus; inferiorly it forms the most ventral diencepha- midbrain reticular formation, potentially mediating lim-
lic tissue, a portion extending into the posterior lobe of bic influence on brainstem output.
838 D Diencephalon
The thalamus is generally thought to function as a diencephalon. In the epithalamus, the primary target of
gateway for information transfer to the cerebral cortex. pathology is the pineal gland. Both tumor and cyst for-
The physiological firing of thalamic neurons can occur in mation can occur in the pineal. Tumors often alter the
either a tonic or bursting mode. Tonic firing permits production and release of melatonin, affecting sleepwake
point-to-point information transfer, where signals from cycle patterns and, in some cases, are correlated with
the lower levels of the CNS can pass directly to the cortex. ocular dysfunction. Since melatonin also has gonadotro-
Thalamic neurons also have a burst mode of signaling, phic effects, shifts in its production may change reproduc-
which conveys longer, rhythmic waves of depolarization, tive behavior. Non-neoplastic parenchymal cysts can
critical to functional patterns of activation such as those occur within the pineal. Although a rare occurrence,
that occur during sleep/wake cycles. Different thalamic these may reach a size that compresses the adjacent cere-
nuclear groups target specific brain regions to affect bral aqueduct and tectal plate. Such compression could
motor coordination (cortex, basal ganglia, and cerebel- restrict CSF flow, with the potential for producing
lum), autonomic integration (midbrain), hormonal regu- hydrocephaly.
lation (hypothalamus), hearing, vision, cognition, and Within the dorsal thalamus, pathology is usually
emotion (auditory, visual, and limbic cortices). linked to neuronal loss, astrocytosis, or myelin break-
Of all the diencephalic divisions, least is known about down. These can occur due to metabolic dysfunction, as
subthalamic function. The subthalamic nucleus is in WernickeKorsakoff syndrome or Parkinsons disease,
interconnected with the basal ganglia, and is part of the in the prion-induced plaque pathology of Creutzfeldt
indirect pathway between that region and the cerebral Jakob disease and sporadic fatal insomnia, or with the
cortex. At this position, the subthalamic nucleus may act characteristic spongy white matter condition generated in
to regulate inhibitory output from the basal ganglia. KearnsSayre syndrome. With the loss of neurons and
Much less is known about the zona incerta, its function axonal degeneration, abnormal thalamocortical integra-
most likely related to its continuity with the midbrain tion affects motor function and may generate spasticity,
reticular formation. epileptic seizure activity, or dementia.
Hypothalamic function is mediated by two types of Functional change in the subthalamus is thought to
interface: reciprocal connections with regions providing contribute to the muscular rigidity of Parkinsons disease.
its major afferent pathways (thalamus, septum, and brain- In that case, over activity of neurons in the subthalamic
stem), which influence the behavioral output directed by nucleus and the related globus pallidus leads to increased
those regions, and projections to brainstem autonomic inhibition of the thalamus, with reduced cortical motor
nuclei (midbrain, medulla, and spinal cord), which di- activation. Focal vascular lesions of the subthalamus can
rectly regulate visceral functions such as circadian cycles, also produce the violent involuntary limb movement seen
osmoregulation, appetite, body temperature, and fight/ with hemiballismus.
flight response. These systemic responses are also influ- Pathology in the hypothalamus/pituitary is most
enced by hypothalamic connections to the limbic system extensively described, due to the significant role of these
(via the mammillothalamic tract, fornix, and stria termi- regions in autonomic nervous system regulation and their
nalis). Two other major functions of the hypothalamus are interface with a variety of peripheral organs. For example,
the regulation of growth and reproductive cycles, con- lesions within specific hypothalamic nuclei controlling vis-
trolled through broad feedback loops, utilizing receptor- ceral functions of appetite, thirst, sleepwake cycle, regula-
mediated monitoring in both the hypothalamus and the tion of body temperature, or emotional state often result in
affected peripheral organs. Growth and reproduction are extreme shifts within the normal range of these functions.
particularly dependent upon interaction with the pituitary Many of the human responses to such hypothalamic
lobes, either via secretion of hypothalamic-generated lesions can be replicated in animal models. Functional
hormones within the lobe (neurohypophysis), or release disorders of the hypothalamus/pituitary axis can also be
of hypothalamic regulatory factors into the hypothalamic driven by abnormal metabolism. One of the best-known
hypophyseal portal system for control of pituitary hor- examples is thiamine deficiency, where microvascular
mone production (adenohypophysis). lesions occur in the mammillary bodies. These lesions
underlie WernickeKorsakoff syndrome encephalopathy,
Illness which presents as a variety of ophthalmic abnormalities
and cognitive deficits. A wide range of tumors, including
Illness resulting from structural and metabolic pathology gliomas and adenomas, are also common in the hypothal-
has been documented for all subregions of the amus and pituitary. They selectively affect the secretion of
Differential Ability Scales (DAS and DAS-II) D 839
pituitary hormones, producing syndromes ranging from

gigantism and infertility to the more complex cortisol- Differential Ability Scales
related abnormalities of Cushings disease. (DAS and DAS-II)
K ELLY C ROTTY, I DA S UE B ARON
Cross References Inova Fairfax Hospital for Children
Falls Church, VA, USA D
Associational Cortex
Basal Forebrain
Cerebral Cortex Synonyms
Fornix DAS-II
Hypothalamic Glioma
Korsakoff s Syndrome
Mediodorsal Nucleus of Thalamus
Parkinsons Disease Description
Pineal Tumors
Pituitary Adenoma The Differential Ability Scales-II (DAS-II; Elliott, 2007) is
Pituitary Mass an individually administered, comprehensive cognitive
Thalamus ability battery. It consists of 20 subtests for children and
adolescents, aged 2 years 6 months to 17 years 11
months. Results of the DAS-II yield a General Concep-
tual Ability (GCA) score (consisting of Verbal Compre-
References and Readings hension, Naming Vocabulary, Picture Similarities,
Matrices, Pattern Construction, and Copying), diagnos-
Felten, D. L., & Jozefowicz, R. F. (2003). Netters atlas of human neuro-
tic scores (consisting of Early Number Concepts, Recall
science, Teterboro, NJ: MediMedia.
Haines, D. E. (2006). Fundamental neuroscience for basic and clinical of Digits Forward, and Recognition of Pictures), and a
applications (3rd ed.). Philadelphia, PA: Elsevier. Special Nonverbal Composite (SNC) score (consisting
Horvath, E., Scheithauer, B. W., Kovacs, K., & Lloyd, R. V. (2002). of Picture Similarities, Pattern Construction, Matrices,
Hypothalamus and pituitary. In D. I. Graham & P. L. Lantos and Copying). Core subtests are used to estimate a
(Eds.), Greenfields neuropathology (Vol. I, pp. 9831062). London:
childs GCA score, which is derived from verbal, non-
Arnold.
Kandel, E. R., Schwartz, J. H., & Jessell, T. M. (2000). Principles of neural verbal, and spatial cluster scores. GCA focuses on a
science (4th ed.). New York: McGraw-Hill. childs overall reasoning and conceptual abilities. The
Lantos, P. L., Louis, D. N., Rosenblum, M. K., & Kleihues, P. (2002). SNC score is derived only from the nonverbal and
Tumours of the nervous system. In D. I. Graham & P. L. Lantos spatial clusters and provides a valid comprehensive
(Eds.), Greenfields neuropathology, (Vol. II, pp. 7671052). London:
score for children whose oral responses may not be
Arnold.
Lowe, J. S., & Leigh, N. (2002). Disorders of movement and system valid (see Riccio, Ross, Boan, Jemison, & Houston,
degenerations. In D. I. Graham & P. L. Lantos (Eds.), Greenfields 1997). Diagnostic subtests do not contribute to GCA,
neuropathology, (Vol. II, pp. 325430). London: Arnold. but instead, measure aspects of memory, processing
Netter, F. H. (1974). The hypothalamus. In F. H. Netter (Ed.), The Ciba speed, and foundational abilities for early school learning
collections of medical Illustrations, (Vol. I, pp. 147168). New York:
(Elliott, 1990).
CaseHoyt.
Notle, J. (2002). The human brain: An introduction to its functional The DAS-II battery is divided into Early Years for
anatomy (5th ed.). St. Louis, MO: Mosby (Harcourt Health children 2:66:11, and School-Age for children 7:0
Sciences). 17:11. The Early Years battery is further divided into
Lower Level (2:63:5) and Upper Level (3:66:11).
Upper Level yields six core subtests and 11 diagnostic
subtests, while the Lower Level yields four core subtests
and three diagnostic subtests. The Early Years and School-
Diener Life Satisfaction Scale Age batteries are normed on an overlapping sample of
children 5:08:11 to accommodate children who may
Satisfaction with Life Scale possess strengths or weaknesses above or below their
840 D Differential Ability Scales (DAS and DAS-II)
age-matched peers. This flexibility in test administration recall of digits backward, phonological processing, and
allows for the assessment of children based on ability rapid naming.
rather than age.
Administration time for the core battery is 2565 min
for Early Years, and 4565 min for School-Age. Diagnostic Psychometric Data
subtests average an additional 1530 min of testing time.
Each subtest offers predetermined starting points based The manual states that the internal reliability for GCA is 0.90
on the childs age that eliminates items likely to be too for lower-level preschool, 0.94 for upper-level preschool, and
easy or too difficult for a child. Discontinuation rules are .95 for school-age. Internal reliabilities of subtests vary be-
based on decision points, stopping points, and basal and tween 0.70 and 0.95. Testretest reliability was reported to be
ceiling guidelines. Raw scores are converted to T-scores quite strong with GCA score reliability ranging from 0.89 to
that are then converted into standard scores. Verbal, non- 0.94. The DAS handbook includes a number of studies
verbal, and spatial cluster scores can be derived from reporting consistently high correlations of the DAS GCA
subtest standard scores. score with overall composite scores of other cognitive bat-
The DAS-II manual suggests that qualifications to teries, such as the Wechsler Preschool and Primary Scale
administer the test battery include formal graduate or of Intelligence, StanfordBinet, WoodcockJohnson, and
professional training in psychological assessment and in- Wechsler Intelligence Scale for Children.
terpretation of results. A trained technician can adminis-
ter and score the battery, but should not be involved in the
Clinical Uses
interpretation.
The DAS-II is designed to provide an understanding of
a childs definable strengths and weaknesses within a wide
Historical Background range of cognitive abilities. The DAS-II helps determine
why a child is not learning and targets the specific nature
The original DAS (1990) was designed as a revision and
of the problem. Interpretation of the DAS-II allows for
extension of the British Ability Scales (BAS), published
intervention strategies to be identified and implemented.
in 1979. The BAS is a cognitive ability battery devel-
Results can assist in placement decisions for educational
oped to meet the need of British psychologists and
settings, and provide useful clinical information for neu-
educators for an assessment similar to the Wechsler
ropsychological evaluation and research purposes.
Intelligence Scale for Children (WISC), but valid for
The DAS-II is not considered an intelligence test.
British culture and standardized on a British popula-
The aim of the DAS-II is to provide a summary of mean-
tion. The BAS also aimed to resolve weaknesses of the
ingful and distinct subtest scores, with IQ assessment as a
available ability and IQ tests such as ethnic and social
secondary function. Interpretation of the DAS-II is
class bias within measures and minimal focus on
intended to identify specific strengths and weaknesses.
diagnostic subtests. A further aim was to incorporate
A unique aspect of the DAS-II is that the diagnostic
findings of emerging research of early cognitive devel-
subtests are fairly independent of composite scores.
opment that were not measured by existing ability-test
Therefore, these subtests are capable of providing unique
batteries.
information beyond that provided by composite scores
The development of the DAS began in 1984 by obtain-
(Elliott, 2007).
ing reviews, opinions, and feedback of the BASs perceived
Minimal research is currently available on the DAS-II
strengths and weaknesses from educators and clinical
because of its recent publication date; however, the origi-
psychologists. Based on this feedback, six subtests were
nal DAS has proven useful in differentiating children with
dropped and four subtests were added. Other revisions
learning disability from control children as well as
included reconstruction of existing subtests to increase
providing distinct profiles for various subtypes of learning
efficiency and reliability. Standardization of the DAS
disability (McIntosh & Gridley, 1993).
was performed during 19871989 in 70 cities across the
USA.
The DAS-II was published in 2007, and offers new and Cross References
updated artwork and materials, revised subtests, and
updated standardized norms. Four new subtests were Kaufman Assessment Battery for Children (K-ABC)
added to the second edition: recall of sequential order, NEPSY-2nd Edition
Diffuse Axonal Injury D 841
StanfordBinet 5 consideration the possible organic sources of the presenta-

Wechsler Intelligence Scale for Children tion (e.g., congenital brain anomaly or event, HIV status,
Wechsler Preschool and Primary Scale of Intelligence- brain tumor, neuronal demyelination, etc.), psychiatric
III (WPPSI-III) concerns (psychosis, severe depression), medical interven-
tions (e.g., pharmaceuticals), and substance use. In addi-
tion, age of onset of dysfunction, change over time in
functioning, neurological findings, and cultural beliefs D
and rituals may assist in differentiating a diagnosis. For
example, in differentiating dementia from memory deficits
Elliott, C. D. (1990). Differential ability scales: Introductory and technical
handbook. San Antonio, TX: The Psychological Corporation.
occurring secondary to a severe mood disorder, one must
Elliott, C. D. (2007). Differential ability scales second edition: Adminis- consider age of onset of difficulties, change in functioning
tration and scoring manual. San Antonio, TX: Harcourt Assessment, across time, medical conditions associated with memory
Inc. difficulties and mood symptoms, brain injury, acute and
McIntosh, D. E., & Gridley, B. E. (1993). Differential ability scales:
long-term substance use, developmental history, present-
Profiles of learning-disabled subtypes. Psychology in the Schools, 30,
11024.
life circumstances and any previous treatment. Assessment
Riccio, C., Ross, C., Boan, C., Jemison, S., & Houston, F. (1997). Use of over time is also very likely to contribute to differentiating a
the differential ability scales (CAS) special nonverbal composite dementing disorder from cognitive difficulties occurring
among young children with linguistic differences. Journal of Psychoe- secondary to psychiatric disturbance.
ducational Assessment, 15(3), 196204.
Diffuse Astrocytoma
Differential Diagnosis Fibrillary Astrocytoma
S ANDRA B ANKS
Pittsburgh, PA, USA
Diffuse Axonal Injury
Definition B ETH R USH
Mayo Clinic
Differential diagnosis refers to the process of differentiat- Jacksonville, FL, USA
ing one diagnosis from another, and in turn, providing
the most fitting diagnosis based on an individuals pre-
sentation. The Diagnostic and Statistical Manual of Synonyms
Mental Disorders, for instance, has historically defined
diagnoses from a categorical perspective, with many DAI
diagnoses having features in common with one another.
This requires careful consideration of all features of
an individuals presentation and the fine details of the
Definition
diagnosis itself.
One of the major types of traumatic brain injury that
results from accelerationdeceleration effects rather than
direct impact on the brain. Typically, the injury is the
Current Knowledge result of high-speed situations such as motor vehicle
accidents or violent shaking of the head from side to
In neuropsychology, the process of providing the most side. The forceful motion of injury disturbs the delicate
fitting diagnosis for a patient involves assessment of the underlying white matter tracts of the brain that are re-
possible causes of the patients current condition as well as sponsible for connecting the functional areas controlling
a consideration of characteristics of the cognitive and neu- motor skills, cognitive skills, language skills, and behavior.
robehavioral presentation. This process must take into Because each neural cell or vessel has a fixed length and is
842 D Diffuse Axonal Injury
held in position along its path by other cells, there is simple terms, DWI makes it possible to see the disruption
limited elasticity in any cell or vessel. Thus, acceleration of cortical and subcortical connections throughout the
deceleration forces can disrupt cells and vessels despite an brain that may appear normal on a structural image
absence of direct trauma to the cell or vessel. Damage may of the brain such as a standard brain MRI or head CT.
result from stretching, twisting, or rotation. Diffuse axonal With DWI techniques, the understanding of DAI and the
injury (DAI) is more likely to occur with lateral movements implications of such damage have exploded. For example,
of the brain and least likely to occur with sagittal move- DWI images can now demonstrate structural abnormal-
ments of the brain. ities in traumatic brain injury patients even when DAI
cannot be visualized using standard imaging techniques
(Hou et al., 2007). DWI images have also been used as
Historical Background prognostic indicators to determine the length of coma
following traumatic brain injury (Zheng et al., 2007).
The first detailed pathological and histological account of Cognitive studies show that the greater the white matter
diffuse white matter damage following traumatic brain damage in diffuse axonal injury, the greater the cognitive
injury occurred in 1956 (Strich, 1956). In 1982, the first deficits observed in traumatic brain injury survivors
paper using the term diffuse axonal injury was pub- (Kraus et al., 2007). These improved methods for study-
lished (Gennarelli et al., 1982). Since that time, the idea of ing DAI will most likely expand the knowledge of the
DAI has further evolved and it is now clear that axons are heterogeneity of clinical presentation and outcome in
not affected in isolation, but rather there is injury to the the so-called mild traumatic brain injury, suggesting that
functional areas of the brain that are disconnected from mild traumatic brain injury may not be mild at all.
one another as a result of axonal damage. There is also DAI disturbs white matter tracts that are responsible
secondary damage to brain areas resulting from biochem- for efficient and coordinated communication between
ical changes and edema that evolve following disruption functional areas of the brain. Consequently, patients
of the axons. It has been suggested that diffuse axonal with DAI undergoing neuropsychological evaluation typ-
injury is therefore a misnomer and that it may be more ically demonstrate diffuse cognitive impairment most
appropriate to describe this type of injury as diffuse brain prominently characterized by markedly slowed cognitive
injury, a term that would include DAI. processing speed, poor attention, and difficulties with
executive functions like frontal lobe connections to
other functional brain areas are disturbed.
Current Knowledge
DAI may manifest as transient biochemical change, or Future Directions

permanent injury to the axons of neurons. Three levels of
DAI have been suggested (Gennarelli et al., 1982). Grade I As neuroimaging techniques continue to advance, it
accounts for widespread axonal damage with no focal will be possible to study recovery from DAI and to
abnormalities observed on the brain imaging. Grade II understand the time course of recovery for such an
involves the presence of Grade I damage, with additional injury. These improved methods open up the horizon
focal abnormalities often in the corpus callosum. Grade III for further research studies. For example, using DWI,
injury involves the presence of Grade I and II injuries, with it may be possible to describe detailed effects of early
additional injury observed in the brainstem. Studies have rehabilitation interventions or pharmacological treat-
shown that the earliest that DAI can be detected is within ments that can enhance recovery and limit the extent
1 h of the onset of injury. The full spectrum of patholog- of long-term brain damage that evolves following the
ical change may take place over the first 2472 h following onset of DAI.
the onset of injury. Total brain volume may be affected in
the acute stages of recovery and may continue to reduce in
response to injury, up to 3 years following injury. Cross References
The advent of new neuroimaging methods have
allowed further understanding of diffuse axonal injury. AccelerationDeceleration Injury
Diffusion-weighted images (DWIs) allow clinicians to Diffusion-Weighted Imaging
more precisely measure the extent of white matter and Shearing Injury, Shear Strain
parenchymal damage following traumatic brain injury. In Traumatic Brain Injury
Diffusion Tensor Imaging D 843
Bigler, E. D. (2001). Distinguished Neuropsychologist Award Lecture Diffusion tensor imaging (DTI) is a magnetic resonance
1999. The lesion(s) in traumatic brain injury: Implications for imaging (MRI) technique that reveals the integrity of white
clinical neuropsychology. Archives of Clinical Neuropsychology, 16,
matter tracts that link regions of the brain to each other.
95131.
Gennarelli, T. A., Thibault, L. E., Adams, J. H., Graham, D. I., Thompson,
DTI exploits the characteristic that water molecules
C. J., & Marcincin, R. P. (1982). Diffuse axonal injury and traumatic are in constant motion. In regions such as the ventricles, D
coma in the primate. Annals of Neurology, 12, 564574. which offer little physical constraint, movement occurs
Hou, D. J., Tong, K. A., Ashwal, S., Oyoyo, U., Joo, E., Shutter, L., & randomly in every direction. In contrast, water molecules
Obenaus, A. (2007). Diffusion-weighted magnetic resonance imag-
in white matter fibers are constrained by the physical
ing improves outcome prediction in adult traumatic brain injury.
Journal of Neurotrauma, 24, 15581569.
boundaries of the axon sheath, which cause greater
Kraus, M. F., Susmaras, T., Caughlin, B. P., Walker, C. J., Sweeney, J. A., & movement along the long axis of the fiber than across it.
Little, D. M. (2007). White matter integrity and cognition in chronic The diffusion properties of water molecules are
traumatic brain injury: A diffusion-tensor imaging study. Brain, 130, studied within and between three dimensional elements
25082519.
called voxels. The technique is called diffusion tensor
Strich, S. J. (1956). Diffuse degeneration of the cerebral white matter
in severe dementia following head injury. Journal of Neurology,
imaging because a tensor, a mathematical description of
Neurosurgery, and Psychiatry, 19, 163185. the orientation and magnitude of diffusion, is computed
Zheng, W. B., Liu, G. R., Li, L. P., & Wu, R. H. (2007). Prediction of for each voxel. Images acquired in different planes will
recovery from a post-traumatic coma state by diffusion-weighted highlight different white matter tracts or provide different
imaging (DWI) in patients with diffuse axonal injury. Neuroradiology,
views of them. Within a uniformly oriented tract,
49, 271279.
anything that disrupts the regular structure of white
matter, such as loss of the protective myelin sheath or
deterioration of the axons, might allow the water mole-
Diffuse Cerebral Gliomatosis cules to move more freely, resulting in an altered image.
Gliomatosis Cerebri
Current Knowledge
DTI has demonstrated white matter abnormalities in
Diffuse Lewy Body Disease Alzheimers disease, schizophrenia, AIDS, depression,
(DLBD) and normal aging. DTI has also been used to examine
brain white matter microstructural integrity in alcoholism
Dementia with Lewy Bodies and in the corticospinal tracts after stroke. It can reveal
microstructural abnormalities in white matter, such as
myelin loss, enlargement of microtubules, and degrada-
tion of membranes, even when that region appears
Diffuse Plaques normal on structural MRI.
In the area of traumatic brain injury, there is early
Amyloid Plaques evidence to suggest that DTI may be of value in assessing
diffuse axonal injury, which is typically difficult to image
with other available techniques.
Diffusion Tensor Imaging
Cross References
S USAN L ADLEY-OB RIEN
Denver Health Medical Center Magnetic Resonance Imaging
Denver, CO, USA
Synonyms Bigler, E. D. (2007). Neuroimaging correlates of functional outcome.
In N. D. Zasler (Ed.), Brain injury medicine (pp. 202). New York:
DTI Demos.
844 D Diffusion-Weighted Imaging
Rosenbloom, M. (2003). Using magnetic resonance imaging and infarction core, which usually progresses to full infarc-
diffusion tensor imaging to assess brain damage in alcoholics.
tion unless there is early reperfusion. The initial DWI
Alcohol Research and Health, 27, 146.
Xu, J., et al. (2007). Diffuse axonal injury in severe traumatic brain injury
lesion volume and ADC values correlate with infarction
visualized using high-resolution diffusion tensor imaging. Journal of volume and with neurologic assessment tests. ADC values
Neurotrauma, 24(5), 75365. may be useful in differentiating tissue destined to infarct
from that potentially salvageable with reperfusion thera-
py. With improvements in MR software and hardware,
diffusion MR will continue to improve the management
Diffusion-Weighted Imaging of patients with acute stroke.
E LLIOT J. R OTH
Northwestern University Cross References
Chicago, IL, USA
Ischemic Penumbra
Perfusion-Weighted Imaging
Synonyms
DWI References and Readings
Schaefer, P. W., Grant, P. E., & Gonzalez, R. G. (2000). Diffusion-weighted

Definition MR imaging of the brain. Radiology, 217, 331345.
Gonzalez, R. G., Schaefer, P. W., Buonanno, F. S., et al. (1999).
Diffusion-weighted imaging (DWI) produces magnetic Diffusion-weighted MR imaging: Diagnostic accuracy in patients
resonance images of biological tissues weighted with the imaged within 6 hours of stroke symptom onset. Radiology, 210,
155162.
local characteristics of water diffusion. Acquisition of
images using regular MRI utilizes the behavior of protons
in water to generate contrasting appearances between
features of the different tissues being studied. This ability
to produce contrast across tissues is called weighting,
Digit Memory Test
and is stimulated by imposing a strong magnetic field that
Hiscock Forced-Choice Test
makes the protons in water molecules move differently
depending on their specific tissue environment. In certain
clinical situations, this can generate contrast between an
area of pathology and the surrounding healthy tissue. In Digit Span
DWI, the specific magnetic field used causes the protons
to behave in a particular manner that varies depending on D ENENE WAMBACH 1, M ELISSA L AMAR 2, R OD S WENSON 3,
the characteristics of the tissue. Each section of the image DANA L. P ENNEY 4, E DITH K APLAN 5, DAVID J. L IBON 1
that is produced has a unique apparent diffusion coeffi- 1
Drexel University College of Medicine
cient (ADC), and each section can then be mapped as an Philadelphia, PA, USA
image illustrating diffusion levels at each section as the 2
Kings College London
contrast marker. London, UK
3
University of North Dakota Medical School
Current Knowledge Fargo, ND, USA
4
The Lahey Clinic
Although DWI is now used for a variety of clinical Burlington, MA, USA
5
conditions, it was first applied to imaging of the brain Suffolk University
following stroke. Injured areas show up darker on an Boston, MA, USA
ADC map compared to healthy tissue. As a consequence,
diffusion-weighted MR images are useful to diagnose
acute ischemic strokes. DWI more accurately detects Synonyms
early-onset pathophysiologic changes of infarction than
does traditional MRI or CT. It also may detect the Backward digit task; Digit span test
Digit Span D 845
Historical Background magical number seven, plus or minus two: Some limits on
our capacity for processing information, the basic para-
The term digit span encompasses several important digm of span as a psychological method had already been
constructs and names of tests designed to measure these examined.
constructs. First and foremost digit span, along with The second and more frequently used meaning of
reaction time, may be viewed as one of the two original the term digit span is as the name of psychological
paradigms used by experimental psychologists to investi- tests to assess working memory and/or the ability to D
gate cognition. The origins of digit span as a psychological retain and keep in mind a circumscribed amount of
construct date from the work Gottfried Leibniz information for a short period of time (Wechsler, 1997).
(16461716). Leibniz suggested that individuals have a As a psychological test, digit span and other techniques
finite capacity to prospectively process or hold in mind to measure span of apperception have long history.
the information from the environment. He termed this James McKeen Cattell (18601944; 1890), who worked
capacity the span of apperception. (Much of the historical in Wilhelm Wundts laboratory in Leipzig, included a
information reviewed in this essay is drawn from JTE test of span for consonants in his compendium of mental
Richardsons paper: Measurements of short-term mem- tests. (After being fired from Columbia University for his
ory: A historical review. Cortex, 43, 635650, 2007.) opposition to World War I, Cattell, along with Robert
In the nineteenth century, Herman Ebbinghaus Woodward and Edward Lee Thorndike, founded the
(18501909; 1885/1964 cited in Richardson, 2007) was Psychological Corporation in 1921 in New York City. In
the first cognitive scientist to show how span could be 1939, Woodwards former student, David Wechsler, pub-
used as an experimental paradigm to investigate memory lished the first version of the intelligence test that has so
and learning. In America, Oliver Wendell Homes pater very much influenced the science and practice of psychol-
(18091894; 1871 cited in Richardson, 2007) made ogy.) In addition, span was included as part of the intelli-
cogent observations on the parameters of digit span as a gence tests devised by Binet and Simon (1905; cited in
method to assess span of apperception, i.e., in uttering Richardson, 2007). In this version, up to three trials
distinctly a series of unconnected numbers or letters were administered for each digit sequence. Terman
before a succession of careful listeners, I have been (1916) also included a digit span test in the Stanford
surprised to find how generally they break down, in trying revision of the BinetSimon scales, but in Termans ver-
to repeat them, between seven and ten figures or letters sion, digit sequences both forward and backward were
(Holmes, 1871, cited in Richardson, 2007). (Oliver Wen- administered.
dell Holmes, Sr., M.D., a resident of Cambridge,
Massachusetts, was a very influential nineteenth century
physician. In addition to his achievements as Dean of
Harvard Medical School, Dr. Holmes popularized the use Psychometric Data: Digits Forward/
of the stethoscope as medical instrument. Equally impres- Digits Backward
sive were Dr. Holmes literary achievements. Admired by
Edgar Allan Poe, Dr. Holmes was a member of an illustri- From the beginning, a digit span subtest has been at least
ous group of Boston literati and could count as his friends included in virtually all Wechsler intelligence and memory
such individuals as Ralph Waldo Emerson and Henry scales for both children and adults. Wechsler combined
Wadsworth Longfellow. Known for his essays and poetry, performance on the digits forward and digits backward
Dr. Holmes was a founder of the Atlantic Monthly tasks into a single score on the basis of psychometric
magazine. In addition to his other achievements Dr. considerations. However, clinical observations have long
Holmes is credited for naming the city of Boston The demonstrated the value of treating each procedure as a
Hub of the Universe. Holmes son, Oliver Wendell Holmes, separate test as combining forward and backward test
Jr., was a well known jurist and was appointed Associate performance potentially obscures the value of each test
Justice to the Supreme Court by President Theodore Roo- condition to measure related, but separate psychological
sevelt.) Several years later, Ebbinghaus made a similar constructs.
observation commenting, the question can be asked, A lively debate has centered on the cognitive con-
what number or syllables can be correctly recited after structs that underlie successful performance for both
only one reading. . . for me the number is usually seven, digits forward and backward test conditions. Indeed,
(1885, cited in Richardson, 2007). Thus, more than 80 Kaplan and colleagues (1991) tend to view the digits
years before George Millers seminal paper (1956) The forward test condition as a means for measuring span or
846 D Digit Span
how many bits of information can be held in mind, where- where the examinee is asked to repeat increasing spans of
as the digits backwards test condition is viewed as a test of digits in the order they were presented; and digits back-
mental manipulation. In this context, the observations of wards, where the examinee is asked to repeat increasing
Kaplan and colleagues (1991) are consistent with the con- spans of digits in reverse order. In both test conditions,
structs put forth by Baddeley and Hitch (1974) regarding two trials are administered for each span length. Each
working memory. Other researchers have made similar condition is discontinued when the examinee fails both
observations. For example, Ramsey and Reynolds (1995) trials for a given span. The raw score is the sum of trials
and Reynolds (1997) studied large samples of children correctly repeated. This raw score is converted into an
and adolescents using a protocol of tests requiring the age-corrected scale score. Developed as part of the origi-
repetition of sequences of digits and letters both forwards nal Bellevue Intelligence Tests (Wechsler, 1939), Wechsler
and backwards. An analysis of forward and backward test writes there is perhaps no test that has been so universally
scores using principal component analysis found that used in scales of intelligence as that of Memory Span for
forward and backward span loaded on different factors. Digits (Wechsler, 1944). Wechsler acknowledges that
These researchers therefore concluded that the forward low scores on the Memory Span for Digits Test are
and backward span should not be combined and reflect frequently associated with attention deficits (Wechsler,
distinct underlying cognitive processes. 1944). He further states that the problems with attention
Weinberg, Diller, Gerstman, and Schulman (1972) and concentration as measured with his Memory Span for
studied patients with visual scanning deficits associated Digits Test are often associated with differentially poor
with right hemisphere pathology and noted differential repetition for digits backward, writing this deficiency is
impairment on digits backwards versus digits forward. often referred to by psychologists as a lack of mental
These researchers advanced the notion that repeating digits control (Wechsler, 1944). Wechslers use of the term
backward may rely on a capacity to form and keep in mind mental control is consistent with what is now understood
a visual image of the digit sequence. Successful perfor- as working memory. Thus, although Wechsler combined
mance on digits backward may be viewed in terms of the forward and backward digit test performance, he was
ability to keep this visual image in mind while peeling certainly cognizant that his combined scale score could
numbers off in reverse order. Rudel and Denckla (1974) be fractionated to measure a variety of cognitive
retrospectively studied digit forward and backwards test functions.
performance in children with learning disabilities. Children Kaplan and colleagues (1991) have suggested a num-
with evidence of left hemisphere dysfunction produced ber of additional administration and scoring techniques
particularly reduced scores on digits forward. Children to complement the traditional administration of the
with evidence of right hemisphere dysfunction appeared Wechsler Digit Span Test. First, Kaplan and colleagues
disadvantaged when asked to repeat digits backward. Rudel (1991) suggest the investigator administer test trials
and Denckla (1974) believed that their data suggested the until the examinee fails to repeat the exact number of
successful performance for digits forward is governed by a digits that were administered, rather than discontinuing
left hemisphere-mediated cognitive construct involving after failure within a pair of trials within a particular span,
auditory storage/ rehearsal while successful performance regardless of whether the examinees response is correct or
for digit backwards is governed by a right hemisphere not. By following this procedure, particularly for the
mediated construct involving visual imagery operations. digits forward test condition, one is able to assess the
The value of separating forward from backwards test con- patients span of apperception, or the number of bits of
ditions is acknowledged in the latest version of Wechslers information the patient is able to keep in mind. Moreover,
IQ test (WAIS-IV) wherein separate scale scores are now for some brain damaged patients where attention, con-
provided for digits forward and backward. centration, and working memory may be compromised
or fluctuate it is possible that despite, say, failing both
5-span test trials, a patient could be successful on one or
Clinical Uses more 6-span test trials or on even longer span lengths.
Kaplan (personal communication) has also said that a
Wechslers Digit Span Task better scoring procedure for the Digit Span Test would
be to tally the number of digits correctly recalled, rather
This task is most often associated with the corpus of than the number of successful trials. (Dr. Kaplan is well
intelligence tests authored by David Wechsler. Wechslers known for saying: If they want numbers, give them
Digit Span subtest comprises of two parts digits forward, numbers that are meaningful.) The interpretation of a
Digit Span D 847
juxtaposition of two digits in the middle of a trial could be 5-digit span lengths for a total of 21 trials. All 4 and
very different compared to instances of omissions or 5-span trials were constructed so that contiguous
obvious perseverations. The idea of tallying the number numbers were placed in strategic positions. For example,
of digits correctly recalled was the impetus for the in 4-span trials contiguous numbers were placed in either
creation of The Backwards Digits Test (BDT; Lamar & the first and third or second and fourth digit positions,
colleagues, 2007, 2008) described below. e.g., 5269 or 1493. In 5-span trials contiguous numbers
Kaplan (1988) and Kaplan and colleagues (1991) also were placed in the three middle digits positions, e.g., D
call the attention to the variety of errors patients make on 16579. Three-span test trials were not constructed in this
the digit span test. fashion because of the primacy and recency effects. This
Omission Refers to responses characterized by a miss- placement strategy was devised to examine the capacity of
ing digit. On the digits forwards task, an omission error patients to resist the temptation to produce capture errors
occurs if a four-digit response of 6-8-2-1 is given to the or to erroneously group contiguous numbers together,
five-digit stimulus 6-8-2-5-1. Interpretation of omission e.g., 15679 incorrectly reported backward as 96751.
errors typically considers the length of the number se- The BDT is administered using standardized Wechsler
quence: whether this kind of error occurs on shorter (4- procedures except that there is no discontinuation.
span) versus longer (7 or 8-span) digit sequences. All 21 trials are administered. The two major indices
Addition Refers to responses characterized by added derived from this test are percent of digits recalled in
digits. On the digits forward task, an addition error ANY ORDER and percent of digits recalled in SERIAL
occurs if a five-digit response for 4-7-2-3-1 is given to the ORDER.
four-digit stimulus 4-7-2-3. One type of addition error is Percent Correct ANY-ORDER This score reflects the
an automatized addition error. An automatized addition sum total of digits correctly recalled regardless of their
error occurs when the added number is sequential, i.e., serial position, divided by the total possible correct, mul-
7-4-5-3 repeated as 7-3-4-5-6. Automatized addition errors tiplied by 100, [(total number of correct digits ANY-
suggest an executive control or frontal system problem. ORDER)/ (total possible correct)] 100. By eliminating
Perseveration A perseveration refers to a number the importance of serial position, this measure is believed
duplication error. Perseveration errors occur within to reflect less complex aspects of working memory char-
and/or between trials. When noting a perseveration, one acterized mainly by short term or immediate storage and
should observe whether the perseverated responses were rehearsal mechanisms.
captured within or between test trials. Percent Correct SERIAL-ORDER This score reflects
Substitution A substitution error refers to a unique the total number of digits correctly recalled in exact
number that is contained in the digit response string serial position, divided by the total possible correct,
that replaces an original number and does not change multiplied by 100, [(total number correct digits SERI-
the original digit string length. This differs from the AL-ORDER)/ (total possible correct)] 100. This mea-
addition errors described previously, because addition sure is believed to assess the more executively demanding
errors change the digit string length. This is coded when aspects of working memory that are associated with
any digit is given instead of a digit contain on the mental manipulation, such as disengagement and tem-
stimulus. poral reordering.
Sequence Error A sequence error refers to a correctly In addition to ANY and SERIAL ORDER recall, the
repeated digit that is simply misordered, but does not BDT affords an opportunity to examine for capture errors
change the number string length. or the tendency of patients to erroneously group contigu-
Capture Error A type of sequence error that is ous numbers together. Two major types of capture errors
characterized by the grouping of contiguous numbers are scored (see Kaplan, Fein, Morris, & Delis, 1991).
together. Within Trial Capture Errors This error is coded on
4 and 5-span trials when the capture error is confined
to digits within the trial at hand, i.e., 14933491;
The Backwards Digit Test (BDT) 1657995671.
Between Trial Capture Errors This error is coded on
Lamar and colleagues (2007, 2008) devised The Backward 3, 4 and 5-span test trials when participants pull down or
Digits Test (BDT), a digit backward paradigm designed incorporate a digit or digits from an immediately preced-
specifically to assess for working memory deficits in ing test trial. In a larger sense, both types of capture errors
dementia. This test consists of seven trials of 3, 4, and could be viewed as perseverations.
848 D Digit Span
Lamar and colleagues (2007) studied two groups of References and Readings
dementia patients where the onset of the illness was insid-
ious and the overall severity of the dementia was mild. Baddeley, A. D., & Hitch, G. J. (1974). Working memory. In (Ed.),
The severity of periventricular and deep white disease was G. H. Bower, The psychology of learning and motivation: Advances
in research and theory (vol. 8). New York: Academic Press.
measured using MRI scans, and patients were categorized
Cattell, J. M. (1890). Mental tests and measurements. Mind, 15, 373381.
as presenting with either mild versus moderate/severe Cosentino, S., Jefferson, A. J., Chute, D. L., Kaplan, E., & Libon, D. L.
white matter disease. No difference was found for ANY (2004). Clock drawing errors in dementia: Neuropsychological and
ORDER recall, suggesting that span, storage, and rehearsal neuroanatomic considerations. Cognitive and Behavioral Neurology,
mechanisms did not differ between these dementia 17, 7483.
Ebbinghaus, H. (1964). Memory: A contribution to experimental psycho-
groups. However, significant differences were found for
logy (Ruger HA and Bussenius CE, Trans) (Original work published
SERIAL ORDER recall suggesting differential working in 1885). New York: Dover.
memory impairment for dementia patients who had Holmes, O. W. (1871). Mechanism in thought and morals: An address
significant subcortical white matter disease, a finding delivered before the Phi Beta Kappa Society of Harvard University, June
well documented in the literature (see Lamar et al., in 29, 1870, with notes and afterthoughts. Boston: Osgood.
Kaplan, E. (1988). A process approach to neuropsychological assessment.
press; Libon, Price, Garrett, & Giovannetti, 2004 for
In T. Boll, & B. R. Bryant (Eds.), Clinical neuropsychology and brain
reviews). A series of step-wise regression analyses found function: Research, measurement, and practice: Master lectures.
that ANY ORDER recall was primarily related to perfor- Washington, DC: The American Psychological Association.
mance on the MMSE or dementia severity. By contrast, Kaplan, E., Fein, D., Morris, R., & Delis, D. (1991). The WAIS-R as a
SERIAL RECALL was related to performance on wide neuropsychological instrument. San Antonio, TX: The Psychological
Corporation.
number of other executive tests including letter fluency,
Lamar, M., Catani, M., Heilman, K. M., & Libon, D. J. (2008). The impact
The Boston Revision of the Wechsler Memory Scale Men- of region-specific leukoaraiosis on working memory deficits in de-
tal Control Test (Lamar et al., 2002), and clock drawing mentia. Neuropsychologia, 46, 25972601.
errors (Cosentino, Jefferson, Chute, Kaplan, & Libon, Lamar, M., Price, C., Davis, K. L., Kaplan, E., & Libon, D. J. (2002).
2004). In a follow-up study, Lamar and colleagues Capacity to maintain mental set in dementia. Neuropsychologia, 40,
435445.
(2008) examined regional MRI white disease and perfor-
Lamar, M., Price, C. C., Libon, D. J., Penney, D. L., Kaplan, E., Grossman,
mance on ANY and SERIAL order recall and found that M., et al. (2007). Alterations in working memory as a function of
reduced SERIAL ORDER recall was related to left inferior leukoaraiosis in dementia. Neuropsychologia, 2007; 45, 245254.
parietal white matter disease. These data are consistent Libon, D. J., Price, C., Garrett, K. D., & Giovannetti, T. (2004). From
with ideas put forth by Rudel and Denckla (1974), sug- Binswangers disease to Leukoaraiosis: What we have learned about
subcortical vascular dementia. The Clinical Neuropsychologist
gesting that a visual imagery mechanism may underlie
Vascular Dementia Special Edition, 18, 83100.
successful backward digit span performance. The impor- Miller, G. A. (1956). The magical number seven, plus or minus two: Some
tance of number sequencing is acknowledged in the latest limits on our capacity for processing information. Psychological
version of Wechslers IQ test (WAIS-IV) wherein a sepa- Review, 63, 8197.
rate score is now calculated for the longest digit string Ramsey, M. C., & Reynolds, C. R. (1995). Separate digits tests: A brief
history, a literature review, and a reexamination of the factor
correctly sequenced.
structure of the Test of Memory and Learning (TOMAL). Neuropsy-
Digit span is one of the original paradigms used chology Review, 5, 151171.
to investigate cognitive psychology. Attention to Reynolds, C. R. (1997). Forward and backward memory span should not
error type, i.e., the act of focusing on the process be combined for clinical analysis. Archives of Clinical Neuropsy-
by which the scaled score is obtained (Kaplan, 1988), chology, 12, 2940.
Richardson, J. T. E. (2007). Measurements of short-term memory:
particularly where errors occur and differential perfor-
A historical review. Cortex, 43, 635650.
mance on forward versus backward recall, can yield a Rudel, R. G., & Denckla, M. B. (1974). Relation of forward and backward
wealth of information about cognitive disorders in digit repetition to neurological impairment in children with learning
brain-injured patients. After more than a century, a disabilities. Neuropsychologia, 12, 109118.
seemingly simple task of digit repetition remains an Terman, L. M. (1916). The measurement of intelligence: An explanation of
and a complete guide for the use of the Stanford revision and extension
important construct in the understanding and assessment
of the Binet-Simon intelligence scale. Boston: Houghton Mifflin.
of cognition. Wechsler, D. (1939). The measurement and appraisal of adult intelligence
(1st ed.). Baltimore: Williams and Wilkins Corporation.
Wechsler, D. (1944). The measurement and appraisal of adult intelligence
Cross References (3rd ed.). Baltimore: Williams and Wilkins Corporation.
Wechsler, D. (1997). The Wechsler adult intelligence scale-III. San Antonio,
Serial Recall TX: Psychological Corporation.
Digit Symbol Substitution Test D 849
Weinberg, J., Diller, L., Gerstman, L., & Schulman, L. (1972). Digit corresponding geometric symbol. The examinee is then
span in right and left hemiplegics. Journal of Clinical Psychology,
shown a series of boxes containing numbers in the top
28, 361.
boxes, and blank boxes below them. After a short practice
trial, they are then asked to copy the corresponding
geometric symbol under each number. The raw score is
the number of correct items completed within the pre-
Digit Span Test scribed time limit. D
The Symbol Digit Modalities Test (SDMT; Smith,
Digit Span
1982): This test is very similar to Wechslers DS test,
except that rather than transposing symbols to numbers,
the examinee is asked to transpose numbers to symbols.
An advantage of the SDMT is that there are both written
Digit Supraspan and oral administrations. Smith (1984) suggests the
administration of both the written and oral versions of
Serial Digit Learning the test, with the written version being administered first.
In addition, the SDMT provides the additional advantage
of allowing the examinee to write familiar numbers (19)
rather than geometric symbols (Lezak, Howieson, &
Digit Symbol Substitution Test Loring, 2004). Smith (1984) reported greater sensitivity
of the SDMT compared to the DS subtest in detecting
B RIANNE M AGOUIRK B ETTCHER 1, DAVID J. L IBON 2 brain damage.
E DITH K APLAN 3, R OD S WENSON 4, DANA L. P ENNEY 5 Both the DS and SDMT are well known to be highly
1
Temple University sensitive to the presence of cognitive impairment (see
Philadelphia, PA, USA Lezak et al. (2004) for a review). The general sensitivity
2
Drexel University College of Medicine of these tests stems from the fact that multiple cognitive
Philadelphia, PA, USA skills are necessary for optimum performance. For
3
Suffolk University example, at a minimum the examinee must be able to
Boston, MA, USA produce written output (graphomotor skills); visually
4
University of North Dakota Medical School track back and forth from the test key to the test form
Fargo, ND, USA (visual scanning); and locate the test items (visuospatial
5
The Lahey Clinic Burlington ability). Performance improves to the extent the examinee
MA, USA learns the symbol/number pairs without referring to
the test key for each test item (incidental memory). In
addition to norms provided in the Wechsler test manuals,
Synonyms additional adult norms for DS can be found in DElia,
Boone, and Mitrushina (1995); Heaton, Grant, and
Coding; Digit symbol subtest Matthews (2004); and Ivnick, Malec, and Smith, (1992).
DS performance is highly sensitive to the effects of age
(Lezak et al., 2004). Wechsler (1981) reported low correla-
Description tions between DS and many of his other subtests. Since
the addition of the Symbol Search subtest to the Wechsler
The Digit Symbol substitution test (DS): This is a subtest corpus, factor analysis suggests that DS and Symbol
from the corpus of intelligence tests authored by David Search comprise a general processing speed factor.
Wechsler. Since Wechslers publication of the Bellevue In order to disambiguate the specific brain-behavior
Intelligence Scale (BIS; Wechsler, 1939), the basic format relationships that underlie impaired performance on the
and concept of this test has changed very little. The test is DS test, Kaplan and colleagues (Kaplan, 1988; Kaplan,
timed. Various versions from the Wechsler corpus allow Fein, Morris, & Delis, 1991) have developed additional
90 or 120 s. The test requires the examinee to transcribe a test procedures (see WAIS-R-NI; Kaplan et al., 1991) as
unique geometric symbol with its corresponding Arabic described below.
number. The examinee is initially shown a key containing Symbol Copy Test Condition: The symbol copy test
the numbers from 1 to 9. Under each number there is a condition of DS test involves the direct copying of
850 D Digit Symbol Substitution Test
geometric symbols without the burden of visual scanning indicating that the tests share 50% of variance. This fur-
or incidental memory. The purpose of this measure is ther reiterated the integral role of processing speed in DS
to assess the contribution of both motor speed and performance. Joy, Kaplan, and Fein (2004) also examined
graphomotor ability to DS performance. It is also data (n = 1167) from the WAIS-III/WMS-III standardiza-
suggested that the examiner keep track of the output tion sample for individuals who completed at least one DS
produced in each 30 s epoch (Kaplan et al., 1991). Kaplan supplemental procedure. Consistent with previous find-
et al. (1991) noted that the output produced by some ings, results suggested that speed (i.e., Symbol Copy)
patients, particularly with subcortical disease, may decline accounted for approximately 50% of the variance in DS.
on the latter portion of the test. Using the incidental memory learning indices, memory
Incidental Learning: This test condition involves two accounted for only 57% of DS variance. However, per-
procedures. After the DS test is concluded the examinee formance on the pairing and free recall tests provided
may be asked to recall and write the symbols that were incremental explanatory power, authenticating a second-
coupled with each number (pairing). This is followed by ary (albeit small) role of memory in DS performance.
asking the examinee to recall and write as many of the Contributory role of incidental memory: The incidental
symbols as possible without any visual cues (free recall). memory measures (pairing and free recall) have been
Part of the rationale for this procedure is that, although previously used as supplementary indices of memory
examinees are not instructed to memorize the number/ without extensive research regarding their construct
symbol pairs, some degree of incidental learning can validity and without normative data. Joy, Kaplan, and
reasonably be expected to occur. Fein (2003) examined the performance of WAIS-III/

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Encycl in Neuro Psy

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Encyclopedia of Clinical Neuropsychology

John DeLuca, PhD, ABPP

ISBN 978-0-387-79947-6 e-ISBN 978-0-387-79948-3

Library of Congress Control Number: 2010933970

Springer ScienceBusiness Media, LLC 2011

Printed on acid-free paper

Springer is part of Springer ScienceBusiness Media (www.springer.com)

Jeffrey S. Kreutzer, PhD, ABPP, FACRM

John DeLuca, PhD, ABPP

Bruce Caplan, PhD, ABPP

Cristy Akins Ronald A. Cohen

Robert G. Frank James F. Malec

Robert L. Heilbronner John E. Mendoza

Elliot J. Roth Lyn Turkstra

HEATHER ANDERSON AMY J. ARMSTRONG

SAMANTHA BACKHAUS ERIKA M. BARON

IDA SUE BARON

STACY BELKONEN JOHN BIGBEE

BRIAN D. BELL ERIN D. BIGLER

ANDREW BELL NATALIE C. BLEVINS

ROBERT BOLAND ISABELLE BOURDEAU

DAWN E. BOUMAN SARAH S. CHRISTMAN BUCKINGHAM

HUGH W. BUCKINGHAM MERYL A. BUTTERS

JEFFREY M. BURNS DEBORAH A. CAHN-WEINER

DOMINIC A. CARONE COLBY CHLEBOWSKI

JESSICA CHAIKEN ANGELA HEIN CICCIA

MARY CLARK ADAM CONLEY

JOHN C. COURTNEY ANTHONY CUVO

RIK CARL DAMATO

JACQUELINE L. CUNNINGHAM SCOTT L. DECKER

SEAN CUNNINGHAM NICK A. DEFILIPPIS

KATHLEEN DEIDRICK BRUCE J. DIAMOND

KERRY DONNELLY JEFF DUPREE

LINDSEY DUCA NATASHA K. EADDY

KARI DUNNING ERIN E. EMERY

ALLISON S. EVANS AMANDA FAULHABER

JULIE TESTA FLAADA Winthrop University Hospital

JENNIFER FLEMING HELENE FORGET

MICHAEL FRANZEN PAMELA G. GARN-NUNN

KELLI WILLIAMS GARY

TERISA GABRIELSON HELEN M. GENOVA

FRANK J. GALLO GERARD A. GIOIA

ELIZABETH LOUISE GLISKY BRAM GOLDSTEIN

MYRON GOLDBERG ROBERT M. GORDON

CHARLES J. GOLDEN JANET GRACE

MARTIN R. GRAF AUDREY H. GUTHERIE

LORI GRAFTON KARL HABERLANDT

WILLIAM GUIDO FLORA HAMMOND

BENJAMIN M. HAMPSTEAD KENNETH M. HEILMAN

AMY HEFFELFINGER MERRILL HISCOCK

ANNA DEPOLD HOHLER BRADLEY J. HUFFORD

TRACEY HOLLINGSWORTH JOEL W. HUGHES

SUMMER IBARRA MATTHEW JACOBS

KIMBERLE M. JACOBS CHASMAN JESSE

AMITABH JHA KRISTIN L. JOHNSON

EDITH KAPLAN SALLY L. KEMP

JENNIFER SUE KLEINER

BONITA P. KLEIN-TASMAN KATE KRIVAL

STEPHANIE A. KOLAKOWSKY-HAYNER LAUREN B. KRUPP

DAVID LACHAR GUDRUN LANGE

RAEL T. LANGE RONALD M. LAZAR

VICTORIA M. LEAVITT GEORGE LEICHNETZ

SING LEE JEANNIE LENGENFELDER

MARCUS PONCE DE LEON