International Handbook of Psychiatry PDF

International Handbook of
A Concise Guide for Medical Students,

Residents, and Medical Practitioners
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B1405 International Handbook of Psychiatry
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International Handbook of
A Concise Guide for Medical Students,

Residents, and Medical Practitioners
Editors
Laura Weiss Roberts

Stanford University School of Medicine, USA
Joseph B Layde
Medical College of Wisconsin, USA
Richard Balon
Wayne State University, USA
World Scientific
NEW JERSEY • LONDON • SINGAPORE • BEIJING • SHANGHAI • HONG KONG • TA I P E I • CHENNAI
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Published by
World Scientific Publishing Co. Pte. Ltd.
5 Toh Tuck Link, Singapore 596224
USA office: 27 Warren Street, Suite 401-402, Hackensack, NJ 07601
UK office: 57 Shelton Street, Covent Garden, London WC2H 9HE
Library of Congress Cataloging-in-Publication Data

International handbook of psychiatry : a concise guide for medical students, residents,
and medical practitioners / editors, Laura Weiss Roberts, Joseph B. Layde, Richard Balon.
p. ; cm.
Includes bibliographical references.
ISBN 978-9814405607 (hardcover : alk. paper)
I. Roberts, Laura Weiss, 1960– II. Layde, Joseph B. III. Balon, Richard.
[DNLM: 1. Mental Disorders--diagnosis. 2. Mental Disorders--therapy. WM 141]
616.89--dc23
2012051672
British Library Cataloguing-in-Publication Data

A catalogue record for this book is available from the British Library.
Copyright © 2013 by World Scientific Publishing Co. Pte. Ltd.

All rights reserved. This book, or parts thereof, may not be reproduced in any form or by any means,
electronic or mechanical, including photocopying, recording or any information storage and retrieval
system now known or to be invented, without written permission from the Publisher.
For photocopying of material in this volume, please pay a copying fee through the Copyright
Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, USA. In this case permission to
photocopy is not required from the publisher.
In-house Editor: Veronica Low
Typeset by Stallion Press

Email: enquiries@stallionpress.com
Printed in Singapore.
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Contents
Abbreviations List ix
Contributors List xix
Chapter 1 Impact of Mental Illness 1

Laura Weiss Roberts, Richard Balon
and Joseph B. Layde
Chapter 2 International Issues in Psychiatry 9
Richard Balon and Cyril Höschl
Chapter 3 Psychiatric Diagnosis 28
Stephanie Bagby-Stone, Jessica Nittler
and John Lauriello
Chapter 4 Psychiatric Genetics 59
Bhanu Prakash Kolla and David Mrazek
Chapter 5 Psychiatric Interviewing: What to Do,
What Not to Do 78
Mara Pheister
Chapter 6 Psychological and Neuropsychological Testing 102
Jennifer Niskala Apps and Jonathan E. Romain
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vi Contents
Chapter 7 Psychiatric Disorders in Childhood

and Adolescence 137
Michael Koelch and Joerg M. Fegert
Chapter 8 Schizophrenia and Other Psychotic Disorders 184
Peter F. Buckley, Adriana Foster
and Scott Van Sant
Chapter 9 Mood Disorders 204
Sandra Rackley and J. Michael Bostwick
Chapter 10 Anxiety Disorders 227
Leanne Parasram and Dan J. Stein
Chapter 11 Substance Use Disorders 260
Nidal Moukaddam and Pedro Ruiz
Chapter 12 Cognitive Disorders 291
Alana Iglewicz, Ipsit V. Vahia and Dilip V. Jeste
Chapter 13 Somatoform Disorders 317
Christina L. Wichman
Chapter 14 The Dissociative Disorders 337
Jean M. Goodwin
Chapter 15 Sleep Disorders in Psychiatry 352
Oludamilola A. Salami
Chapter 16 Eating Disorders 379
Athena Robinson and W. Stewart Agras
Chapter 17 Sexual Disorders 409
Richard Balon
Chapter 18 Adjustment Disorder 443
Mauro Giovanni Carta, Maria Carolina Hardoy
and Matteo Balestrieri
Chapter 19 Personality Disorders 461
Joel Paris
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Contents vii
Chapter 20 Geriatrics 478

Randall Espinoza
Chapter 21 Emergency Psychiatry 524
Divy Ravindranath, Mark Newman
and Michelle Riba
Chapter 22 Outpatient Psychiatry 554
Ondria Gleason, Aaron Pierce and Bryan Touchet
Chapter 23 General Hospital Psychiatry 572
Jen Alt McDonald and Mark T. Wright
Chapter 24 Psychiatric Education 606
Linda Gask and Michelle B. Riba
Chapter 25 Residency Training 642
Sanjai Rao and Sidney Zisook
Chapter 26 Methods of Psychiatric Research 669
Elizabeth Burgess, Nicolas Ramoz
and Philip Gorwood
Chapter 27 World Suicide 690
Morton M. Silverman
Chapter 28 AIDS Psychiatry 723
Mary Ann Cohen
Chapter 29 Pharmacogenomic Variability Associated with
Psychotropic Medication Response 746
David Mrazek and Bhanu Prakash Kolla
Chapter 30 Ethics in Psychiatry 768
Kristi Estabrook
Chapter 31 The Culturally Competent Psychiatric Assessment 794
Ajoy Thachil and Dinesh Bhugra
Chapter 32 Traditional Healing for Psychiatric Disorders 823
Roger M. K. Ng, Zhang-Jin Zhang and Wendy Wong
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viii Contents
Chapter 33 International Perspective on Homelessness 841

Belinda Bandstra, Anthony Mascola
and Daryn Reicherter
Chapter 34 Mental Health Consequences of War
and Political Conflict 865
Daryn Reicherter and Rena Sugarbaker
Chapter 35 Stigma 886
Travis Fisher
Chapter 36 Legal Aspects of Psychiatry 904
Joseph B. Layde
Index 915
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Abbreviations List
rGE Gene–Environment Correlation

AAMI Age-Associated Memory Impairment
AAPL American Academy of Psychiatry and the Law
ABA Applied Behavior Analysis
ABMS American Board of Medical Specialists
ABPN American Board of Psychiatry and Neurology
ACNP American College of Neuropsychopharmacology
ACT Assertive Community Treatment
AD Alzheimer’s Disease
ADHD Attention Deficit Hyperactivity Disorder
ADLs Activities of Daily Living
ADPAT Adolescent Depression Antidepressant
and Psychotherapy
AIMS Abnormal Involuntary Movement Scale
ALDH1A1 Aldehyde Dehydrogenase 1 Family, Member A1 gene
ANK3 Ankyrin-G gene
ANKK1 Ankyrin repeat Kinase Domain containing 1 gene
ANT Attention Network Test
APA American Psychiatric Association
APM Academy of Psychosomatic Medicine
APP Amyloid Precursor Protein gene
ix
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x Abbreviations List
ARNTL Aryl Hydrocarbon Receptor Nuclear Translocation-

like gene
ASDs Autistic Spectrum Disorders
ATP6V1B2 Lysosomal 56/58kDa, V1 subunit B2 gene
AUDIT Alcohol Use Disorders Identification Test
AUDs Alcohol Use Disorders
BAL Blood Alcohol Level
BDI Beck Depression Inventory
BDNF Brain-Derived Neurotrophic Factor gene
BDS Behavior Disturbance Scale
BED Binge Eating Disorder
BFT-BN Behavioural Family Therapy for Adolescent
Bulimia Nervosa
BOLD Blood-Oxygenation-Level-Dependent
BPRS Brief Psychiatric Rating Scale
BRIEF Behavior Rating Inventory of Executive Functions
BUN Blood Urea Nitrogen
BWL Behavioural Weight Loss Therapy
CACNA1C Alpha 1C subunit of the L-type Voltage-Gated
Calcium Channel gene
CATIE Clinical Antipsychotic Trials of Intervention
Effectiveness
CBC Complete Blood Count
CBT Cognitive–Behavioural Therapy
CBT-BN Cognitive Behavioural Therapy for Bulimia Nervosa
CCMD Chinese Classification of Mental Disorder
CCRCs Continuing Care Retirement Communities
CD Conduct Disorder
CDCV Common Disease/Common Variant
CDH10 Cadherin 10, type 2 gene
CDH13 Cadherin 13, H-Cadherin, Heart gene
CDH9 Cadherin 9, type 2 gene
CDR Clinical Dementia Rating
CDT Carbohydrate-Deficient-Transferrin
CDT Clock Drawing Test
CGA Anterior Cingulus
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Abbreviations List xi
CIDI Composite International Diagnostic Interview

CINP Collegium Internationale Neuro-
Psychopharmacologicum
CIS-R Clinical Interview Schedule-Revised
CIWA Clinical Institute of Withdrawal Assessment
CK Clinical Knowledge
CLAS Culturally and Linguistically Appropriate Services
CLOCK Circadian Rhythm gene
CME Continuing Medical Education
CMP Comprehensive Metabolic Profile
CMV Cytomegalovirus
CNR1 Cannabinoid Receptor 1, Brain gene
CNS Central Nervous System
CNV Copy Number Variation
COMT Catechol-O-Methyltransferase gene
COPD Chronic Obstructive Pulmonary Disease
CPAP Continuous Positive Airway Pressure
CPD Continuous Professional Development
CPE Continuous Professional Education
Cr Creatinine
CSAS Central Sleep Apnoea Syndrome
CSE Clinical Skills Examinations
CSP Chinese Society of Psychiatry
CSTC Corticostriatalthalamocortical
CSV Clinical Skills Verification
CT Computed Tomography
CT Computerized Tomography
CXR Chest X-Ray
DA Dopamine
DALY Disability-Adjusted Life Year
DAOA D-Amino Acid Oxidase Inhibitor gene
DBH Dopamine Hydroxylase gene
DBS Deep Brain Stimulation
DBT Dialectical Behaviour Therapy
DID Dissociative Identity Disorder
DISC1 Disrupted in Schizophrenia gene
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xii Abbreviations List
DLB Dementia with Lewy Bodies

DLPFC Dorsolateral Prefrontal Cortex
DMHDS Dunedin Multidisciplinary Health
and Development Study
DOSMeD Determinants of the Outcome of Severe Mental
Disorders
DRD2 Dopamine-2 Receptor gene
DRD4 Dopamine D4 Receptor gene
DRD5 Dopamine D5 Receptor gene
DSM Diagnostic and Statistical Manual
of Mental Disorders
DSM-IV-TR Diagnostic and Statistical Manual, Fourth Edition,
Text Revision
DTI Diffusion Tensor Imaging
DTNBP1 Dysbindin gene
EACLPP European Association for Consultation Liaison
Psychiatry and Psychosomatics
ECFMG Educational Commission for Foreign Medical
Graduates
ECHO Elder Cottage Housing Opportunity
ECNP European College of Neuro-Psychopharmacology
ECT Electroconvulsive Therapy
EE Expressed Emotion
EEGs Electroencephalograms
EKG Electrocardiogram
EKG Electrocardiography
EKGs or ECGs Electrocardiograms
EMCDDA European Monitoring Centre for Drugs
and Drug Addiction
EMG Electromyography
EOG Electrooculography
EOS Early-onset schizophrenia
EPA European Psychiatric Association
ERAS Electronic Residency Application Service
ESR Erythrocyte Sedimentation Rate
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Abbreviations List xiii
EUFAMI European Federation of Associations of Families

of People with Mental Illness
FAST Functional Assessment Staging Tool
FFT Family Focused Therapy
FGA First Generation Antipsychotics
fMRI Functional Magnetic Resonance Imaging
FOD Female Orgasmic Disorder
FOXP2 Forkhead Box P2 gene
FSAD Female Sexual Arousal Disorder
FTD Frontotemporal Degeneration
GAB2 GRB2-Associated Binding Protein 2 gene
GABA Gamma-Aminobutyric Acid
GABA1 Gamma-Aminobutyric Acid Receptor, alpha 1 gene
GABA6 Gamma-Aminobutyric Acid Receptor, alpha 6 gene
GAD Generalized Anxiety Disorder
GAF Global Assessment of Functioning
GALP Galanin-like Peptide gene
GAMIAN Global Alliance of Mental Illness Advocacy Networks
GBV Gender based violence
GC Cuban Glossary
GDS Global Deterioration Scale
GID Gender Identity Disorder
GLDP Latin American Guide for Psychiatric Diagnosis
GMEC Graduate Medical Education Committee
GPCOG General Practitioner Assessment of Cognition
GRIN2B Subunit 2B gene
GRM3 Glutamate Receptor 3 gene
GRM7 Glutamate Receptor, Metabotropic 7 gene
GWAS Genome Wide Association Studies
GxE Gene–Environment Interaction
HAM-D or Hamilton Rating Scale for Depression or Anxiety
HAM-A
HAND HIV-Associated Neurocognitive Disorder
HI Haemophilus Influenzae
HIV Human Immunodeficiency Virus
HPA Hypothalamus-Pituitary-Adrenal
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xiv Abbreviations List
HRT Habit Reversal Training

HSDD Hypoactive Sexual Desire Disorder
HTR1B Serotonin 1B Receptor gene
I-ADLs Instrumental Activities of Daily Living
IBS Irritable Bowel Syndrome
ICD International Classification of Diseases
ICD-10 International Classification of Diseases, Tenth Edition
ICM Intensive case management
IDPs Internally Displaced Persons
IM Intramuscular
IMGs International Medical Graduates
IPSRT Interpersonal Social Rhythms Therapy
IPSS International Pilot Study of Schizophrenia
IPT Interpersonal Psychotherapy
IRIS Immune reconstitution inflammatory syndrome
IV Intravenous
JSIDCP Japanese Society for International Diagnostic
Criteria in Psychiatry
KLF12 Kruppel-like Factor 12 gene
LAI Long-Acting Injection
LFTs Liver Function Tests
LSA d-Lysergic Acid Amide
MAC Mycobacterium avium intracellulare
MAO-Is Non-Reversible Monoamine Oxidase Inhibitors
MBT Mentalization-Based Treatment
MCI Mild Cognitive Impairment
MCQs Multiple Choice Questions
MDA Methylenedioxyamphetamine
MDD Major Depressive Disorder
MDEA Methylenedioxyethylamphetamine
MDMA 3,4-Methylenedioxymethamphetamine
MED Male Erectile Disorder
MEO Microsomal Ethanol Oxidizing System
METH Methamphetamine
MGH Massachusetts General Hospital
MINI Mini-International Neuropsychiatric Interview
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Abbreviations List xv
MMSE Mini-Mental Status Examination

MOCA Montreal Cognitive Assessment
MOD Male Orgasmic Disorder
mPFC Medial Prefrontal Cortex
MRI Magnetic Resonance Imaging
MRV Multiple Rare Variant
MTA Multimodal Treatment Study of ADHD
MTBIC Moderate Traumatic Brain Injury Clinic
MUPS Medically Unexplained Physical Symptoms
NE Norepinephrine
NHS National Health Service
NOS1 Nitric Oxide Synthase 1, Neuronal gene
NREM Non-Rapid Eye Movement
NRG1 Neuregulin 1gene
NRMP National Residency Match Program
NSSI Non-Suicidal Self-Injury
OCD Obsessive-Compulsive Disorder
ODD Oppositional Defiant Disorder
ODIN Outcome of Depression International Network
ODT Orally Dissolving Tablet
OI Opportunistic Infection
OSCE Observed Structured Clinical Examinations
OSLER Objective Structured Long Examination Record
OTC Over-The-Counter
OVC Orphans and Vulnerable Children
PANDAS Pediatric Autoimmune Neuropsychiatric
Disorders Associated with Streptococcal Infection
PBL Problem-Based Learning
PCPs Primary Care Physicians
PD Parkinson’s Disease
PE Premature Ejaculation
PET Positron Emission Tomography
PGY-1 First Postgraduate Year
PGY-2 Second Postgraduate Year
PGY-3 Postgraduate Year
PGY-4 Fourth Postgraduate Year
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xvi Abbreviations List
PLMD Periodic Limb Movement Disorder

POMC Pro-Opio-Melanocortin
PRITE Psychiatry Resident-In-Training Examinations
PRS Psychosis Risk Syndrome
PSEN1 Presenilin 1 gene
PSEN2 Presenilin 2 gene
PSG Polysomnogram
PTPRZ1 Protein Tyrosine Phosphatase, Receptor-type,
Z Polypeptide 1 gene
PTSD Posttraumatic Stress Disorder
PUD Period of Untreated Disorder
RCTs Randomized Clinical Trials
RELN Reelin gene
REM Rapid Eye Movement
RGS4 Regulator of G Protein Signaling 4 gene
RLS Restless Legs Syndrome
RPR Rapid Plasmin Reagin
RRC Residency Review Committee
RUDAS Rowland Universal Dementia Assessment Scale
RUUP Research Units on Pediatric Psychopharmacology
SAQs Short Answers Questions
SAR Special Administrative Region
SCAN Schedules for Clinical Assessment in Neuropsychiatry
SCID Structured Clinical Interview for DSM-IV
SD Standard Deviation
SGA Second Generation Antipsychotics
SIB Self-Injuring Behavior
SLC6A3 Dopamine Transporter gene
SLC6A4 Serotonin Transporter gene
SLC9A9 Solute Carrier family 9, Sodium/Hydrogen
Exchanger, Member 9 gene
SMD Severe Mood Dysregulation
SMR Standardized Mortality Ratios
SNAP-35 Synaptosomal-Associated Protein gene
SNPs Single-Nucleotide Polymorphisms
SNRIs Serotonin and Noradrenaline Reuptake Inhibitors
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Abbreviations List xvii
SP4 Sp4 Transcription Factor gene

SPECT Single Photon Emission Computed Tomography
SPMSQ Short Portable Mental Status Questionnaire
SRC Stimulus-Response Compatibility
SSRIs Selective Serotonin Reuptake Inhibitors
T.O.V.A Test of Variables of Attention
TADS Treatment for Adolescents With Depression Study
TCAs Tricyclic Antidepressants
TCM Traditional Chinese Medicine
TD Time Duration Discrimination
TEACH Treatment and Education of Autistic and Related
Communication-Handicapped Children
TEOSS Treatment of Early Onset Schizophrenia Study
THC Tetrahydrocannabinol
TMS Transcranial Magnetic Stimulation
TNK1 Tyrosine Kinase, Non-Receptor, 1 gene
TOEFL Test of English as a Foreign Language
TS Tourette Syndrome
TSH Thyroid Stimulating Hormone
UNICEF United Nation’s Infant Children’s Emergency Fund
USMLE United States Medical Licensing Exam
VCF Velo-Cardio-Facial
VEOS Very-Early-Onset
WFME World Federation of Medical Education
WHO World Health Organization
WHO-DDS WHO-Disability Diagnostic Scale
WPA World Psychiatric Association
YBOCS Yale-Brown Obsessive-Compulsive Scale
YGTSS Yale Global Tic Severity Scale
YLD Years Lived with Disability
Y-MRS Young Mania Rating Scale
YTSSL Yale Tourette Syndrome Symptom List
ZNF804A Zinc Finger Protein 804A gene
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Contributors List
Laura Weiss Roberts, MD, MA

Stanford University
Chairman and Katharine Dexter McCormick
and Stanley McCormick Memorial Professor
Department of Psychiatry and Behavorial Sciences
Stanford University School of Medicine
401 Quarry Road, C3215
Stanford, CA 94305-5717, USA
Email: RobertsL@Stanford.edu
Joseph B. Layde, MD, JD

Professor of Psychiatry
Department of Psychiatry
Medical College of Wisconsin
8701 Watertown Plank Road
Milwaukee, WI 53226, USA
Email: jlayde@mcw.edu
xix
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xx Contributors List
Richard Balon, MD
Department of Psychiatry and Behavioral Neurosciences
Wayne State University, Detroit, MI, USA
Email: rbalon@wayne.edu
Cyril Höschl, MD
Professor of Psychiatry and Chair
Third School of Medicine, Charles University and
Director, Psychiatric Center Prague
Prague, Czech Republic
Email: hoschl@pcp.lf3.cuni.cz
Stephanie Bagby-Stone, MD
Assistant Professor of Clinical Psychiatry
University Missouri Medical Centre
1 Hospital Drive, Columbia, MO 65201, USA
Email: BagbyStoneS@health.missouri.edu
Jessica R. Nittler, MD
Assistant Professor of Clinical Psychiatry
Department of Psychiatry, University of Missouri
1 Hospital Drive, Columbia, MO 65212, USA
Email: NittlerJ@health.missouri.edu
John Lauriello, MD
Professor and Chairman
Chancellor’s Chair of Excellence in Psychiatry
University of Missouri Department of Psychiatry
1 Hospital Drive, DC067.00, Columbia, MO 65212, USA
Email: laurielloj@health.missouri.edu
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Contributors List xxi
Bhanu Prakash Kolla, MBBS, MRCPsych.

Assistant Professor
Department of Psychiatry and Psychology
Mayo Clinic, 200 First Street, SW
Rochester, MN 55905, USA
Email: bhanuprakash.kolla@gmail.com
David Mrazek, MD, FRCPsych.

Director of the SC Johnson Genomics
of Addictions Program
Chair of Department of Psychiatry and Psychology
Department of Psychiatry and Psychology
Mayo Clinic, 200 First Street, SW
Rochester, MN 55905, USA
Email: Mrazek.David@mayo.edu
Mara Pheister, MD
Assistant Professor, Director of Residency Education
Department of Psychiatry and Behavioral Medicine
8701 Watertown Plank Road, Milwaukee, WI 53226, USA
Email: mpheister@mcw.edu
Jennifer Niskala Apps, PhD

Associate Professor and the Assistant Director
of Research for the Child and Adolescent Division
Children’s Hospital of Wisconsin
Email: japps@chw.org
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xxii Contributors List
Jonathan E. Romain, PhD, ABPP

Assistant Clinical Professor of Neurology
Assistant Clinical Professor of Physical Medicine and Rehabilitation
Children’s Hospital of Wisconsin
Email: JRomain@chw.org
Michael Koelch, MD
Assistant Professor, Department of Child and
Adolescent Psychiatry and Psychotherapy
University Hospital of Ulm, Germany and
Medical Director, Department of Child
and Adolescent Psychiatry and Psychotherapy, Vivantes
Berlin, Germany
Email: michael.koelch@uniklinik-ulm.de
Joerg M. Fegert, MD
Professor for Child and Adolescent Psychiatry and Psychotherapy
Medical Director, Department of Child and
Adolescent Psychiatry and Psychotherapy
University Hospital of Ulm, Germany
Email: joerg.fegert@uniklinik-ulm.de
Peter F. Buckley, MD
Dean, Medical College of Georgia and Professor
Department of Psychiatry and Health Behavior
Medical College of Georgia, Georgia Health Sciences University
1120 15th St, Augusta, GA 30912, USA
Email: pbuckley@georgiahealth.edu
Adriana Foster, MD
Associate Professor
Medical College of Georgia, Georgia Health Sciences University
997 St Sebastian Way, Augusta, GA 30912, USA
Email: afoster@georgiahealth.edu
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Contributors List xxiii
Scott Van Sant, MD

Assistant Professor
Medical College of Georgia
Georgia Health Sciences University
1120 15th St, Augusta, GA 30912, USA
Email: svansant@georgiahealth.edu
Sandra Rackley, MD
Program Director, Child and Adolescent Psychiatry Fellowship,
Director, Psychiatry Consultation-Liaison and Emergency
Department Services, Children’s National Medical Center,
Assistant Professor of Psychiatry and of Pediatrics, and
The George Washington University School of Medicine
111 Michigan Ave, NW, Washington, DC 20010, USA
Email: srackley@childrensnational.org
J. Michael Bostwick, MD
Assistant Dean of Student Support Services and
Director of Medical School Education in Psychiatry
Mayo Clinic College of Medicine
200 First Street, SW, Rochester, MN 55905, USA
Email: Bostwick.John@mayo.edu
Leanne Parasram, MBBCh, DMH

Resident in Psychiatry
Department of Psychiatry and Mental Health
University of Cape Town, Rondebosch 770, South Africa
Email: leanneparasram@yahoo.com
Dan J. Stein, MD, PhD

Professor and Chair of the Department of
Psychiatry and Mental Health
University of Cape Town, Rondebosch 770, South Africa
Email: dan.stein@uct.ac.za
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xxiv Contributors List
Nidal Moukaddam, MD, PhD

Professor of Psychiatry, Universiy of Texas Medical School
at Houston, USA
Email: nmoukaddam@yahoo.com
Pedro Ruiz, MD
Professor and Executive Vice Chair
Department of Psychiatry and Behavioral Sciences
School of Medicine, University of Miami, USA
Email: PRuiz2@med.miami.edu
Alana Iglewicz, MD
Assistant Clinical Professor
University of California, San Diego
9500 Gilman Drive #0664 San Diego, CA 92122, USA
Email: aiglewicz@ucsd.edu
Ipsit V. Vahia, MD
Assistant Clinical Professor
Stein Institute for Research on Aging
9500 Gilman Drive #0664 San Diego, CA 92122, USA
Email: ivahia@ucsd.edu
Dilip V. Jeste, MD
Estelle and Edgar Levi Clair in Aging
Director, Sam and Rose Stein Institute
for Research on Aging
Distinguished Professor of Psychiatry and Neurosciences
9500 Gilman Drive #0664
La Jolla, CA 92093-0664, USA
Email: djeste@ucsd.edu
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Contributors List xxv
Christina L. Wichman, DO
Assistant Professor
Email: cwichman@mcw.edu
Jean M. Goodwin, MD
Clinical Professor of Psychiatry
The University of Texas Medical Branch, Galveston, TX, USA
Email: jmgoodwin@aol.com
Oludamilola A. Salami, MD
Assistant Professor
Department of Psychiatry and Behavorial Sciences
The Medical College of Wisconsin
1155 N. Mayfair Road, Milwaukee, WI 53226, USA
Email: damisal@gmail.com
Athena Robinson, PhD

Instructor
Stanford University, School of Medicine
Email: athenar@stanford.edu
W. Stewart Agras, MD
Professor
Stanford University, School of Medicine
Email: sagras@stanford.edu
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xxvi Contributors List
Mauro Giovanni Carta, MD

Professor of Psychiatry, Head of Graduate Courses
on Rehabilitation Techniques
Department of Public Health and Clinic
and Molecular Medicine
University of Cagliari, Cagliari, Italy
Email: mgcarta@tiscali.it
Maria Carolina Hardoy, MD

Centro per la Ricerca e la Terapia in Salute Mentale
Department of Public Health
University of Cagliari, Cagliari, Italy
Email: carolinahardoy@tiscali.it
Matteo Balestrieri, MD
Professor of Psychiatry, University of Udine
Director, Department of Psychiatry, Teaching Hospital of Udine
P. le S. M. Misericordia 15
33100 Udine, Italy
Email: matteo.balestrieri@uniud.it
Joel Paris, MD
McGill University
845 Sherbrooke Street West
Montréal, Québec, Canada
Email: joel.paris@mcgill.ca
Randall Espinoza, MD, MPH

Clinical Professor of Psychiatry,
Associate Director, UCLA Center on Aging, and
Director, UCLA Multi-campus Geriatric
Psychiatry Fellowship Training Program
Department of Psychiatry and Biobehavioral Sciences
Geffen School of Medicine at UCLA, USA
Email: REspinoza@mednet.ucla.edu
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Contributors List xxvii
Divy Ravindranath, MD, MS

Clinical Assistant Professor
Department of Medical Education
University of Michigan Medical School
Ann Arbor, MI 48109, USA
Email: divyr@med.umich.edu
Mark Newman, MD
University of Michigan House Officer
University of Michigan Health System
1500 E. Medical Center Drive
Ann Arbor, MI 48109, USA
Email: marknewm@med.umich.edu
Michelle Riba, MD, MS

Clinical Professor
Associate Chair for Integrated Medical
and Psychiatric Services
University of Michigan, Ann Arbor, MI 48109, USA
Email: mriba@umich.edu
Ondria Gleason, MD
University of Oklahoma
Professor and Chair
University of Oklahoma School of Community Medicine
4502 E. 41st Street
Tulsa, OK 74135-2512, USA
Email: Ondria-Gleason@ouhsc.edu
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xxviii Contributors List
Aaron Pierce, DO
Assistant Professor
4502 E. 41st Street, Tulsa, OK 74135, USA
Email: Aaron-pierce@ouhsc.edu
Bryan Touchet, MD
Associate Professor
4502 E. 41st Street, Tulsa, OK 74135, USA
Email: bryan-touchet@ouhsc.edu
Jen Alt McDonald, MD

Addiction Psychiatry Fellow
University of Wisconsin Hospital
and Clinics, Madison, WI 53719, USA
Email: jenmariealt@gmail.com
Mark T. Wright, MD
Associate Professor
Departments of Psychiatry and Behavioral
Medicine and Neurology
Milwaukee, WI 53226, USA
Email: mwright@mcw.edu
Linda Gask, MB ChB, PhD, FRCPsych, FRCGP

Professor of Primary Care Psychiatry
School of Community Based Medicine
5th Floor Williamson Building
University of Manchester, Oxford Road
Manchester, M13 9PL, UK
Email: linda.gask@manchester.ac.uk
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Contributors List xxix
Michelle B. Riba, MD, MS

Associate Chair for Integrated Medicine and Psychiatric
Services Department of Psychiatry University
of Michigan Room F6236 MCHC/Box 0295 1500 E.
Medical Center Drive, Ann Arbor, MI 48109-0295, USA
Email: mriba@umich.edu
Sanjai Rao, MD
Associate Training Director
UCSD Department of Psychiatry
University of California, San Diego, USA
Email: sdrao@ucsd.edu
Sidney Zisook, MD
Professor
UCSD Department of Psychiatry
University of California, San Diego, USA
Email: szisook@ucsd.edu
Elizabeth Burgess, MD
Hospital Psychiatrist, INSERM U894 Team 1
Centre de Psychiatrie et de Neurosciences
2ter rue d’Alésia, 75014 Paris, France
Email: elizabeth_burgess@yahoo.com
Nicolas Ramoz, PhD

Neurogeneticist, INSERM U894 Team 1
Email: Nicolas.ramoz@inserm.fr
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xxx Contributors List
Philip Gorwood, MD, PhD

Professor of Psychiatry and Head of the Research Unit
Hospital Sainte-Anne (CMME) and Paris Descartes University
ISERM U894 Team 1
Email: P.GORWOOD@ch-sainte-anne.fr
Morton M. Silverman, MD
Clinical Associate Professor of Psychiatry
Department of Psychiatry and Behaviorial Neuroscience
The University of Chicago Pritzker School of Medicine
4858 S. Dorchester Ave Chicago, IL 60615-2012, USA
Email: msilverman@suicidology.org
Mary Ann Cohen, MD

Clinical Professor of Psychiatry
Mount Sinai School of Medicine
350 Central Park West
New York City, NY 10025, USA
Email: macohen@nyc.rr.com
Kristi Estabrook, MD
General Practice Physician
Email: kestabrook@mcw.edu
Ajoy Thachil, MRCPsych

Walport Academic Clinical Fellow
Section of Cultural Psychiatry
Health Service and Population Research Department
Institute of Psychiatry, King’s College, London, UK
Email: athachil@sgul.ac.uk
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Contributors List xxxi
Dinesh Bhugra, PhD FRCPsych

Professor of Mental Health and Cultural Diversity
Section of Cultural Psychiatry Health Services
and Population Research Department
Institute of Psychiatry, King’s College London, UK
Email: d.bhugra@iop.kcl.ac.uk
Roger MK Ng MSc (Oxon), FRCPsych (UK),

FHKAM(Psychiatry)
Consultant Psychiatrist and Chief of Service
Department of Psychiatry, Kowloon Hospital
Hong Kong SAR, People’s Republic of China
Email: ngmk@ha.org.hk
Zhang-Jin Zhang, BMed, MMed, PhD

Associate Professor
School of Chinese Medicine
The University of Hong Kong, Hong Kong SAR
People’s Republic of China
Email: zhangzj@hku.hk
Wendy Wong, BCM, BMed, PhD

Post-doctoral Fellow
Department of Family Medicine and Primary Care
The University of Hong Kong
3/F., Ap Lei Chau Clinic, 161 Main Street
Ap Lei Chau, Hong Kong SAR, People’s Republic of China
Email: wwongllo@hku.hk
Belinda Bandstra, MD
Clinical Instructor
Department of Psychiatry and Behavioral Science
Stanford University, 450 Serra Mall
Email: bandstra@stanford.edu
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xxxii Contributors List
Anthony Mascola, MD
Department of Psychiatry and Behavioral Science
Email: amascola@stanford.edu
Daryn Reicherter, MD
Department of Psychiatry & Behavioral Science
Email: reichertermd@yahoo.com
Rena Sugarbaker, MD
Psychiatry Resident
Email: rena1@stanford.edu
Travis Fisher, MD
Assistant Professor
Email: tfisher@mcw.edu
B1405_FM.indd xxxii 1/31/2013 2:44:42 PM

Chapter 1
Impact of Mental Illness
Laura Weiss Roberts, Richard Balon

and Joseph B. Layde
1. INTRODUCTION
The suffering associated with neuropsychiatric diseases is severe and yet
remains poorly understood. Most of these conditions emerge relatively
early in life, or have clear antecedents, and recent advances in neurosci-
ence make the biological contributions to neuropsychiatric disease
increasingly evident. The personal experience of mental illness redefines
the lives of those affected by these diseases as well as all who love and
care for them. People with mental illness, by definition, have deficits in
the spheres of life that bring fulfillment and social good. These deficits
affect personal and family relationships and employment or other forms
of meaningful work. Beyond the effects on individuals, families, and com-
munities, it is clear that the burden of disease — as measured in death,
disability, lost productivity, and direct and indirect societal costs —
throughout the world is devastating.
Understanding and providing care for people living with neuropsychiatric
diseases involve a special set of professional attitudes and expertise. This
work entails a respectful, empathic, and compassionate approach to indi-
viduals who have serious, disabling, and stigmatizing conditions. This work
also requires foundational knowledge of the biomedical and social sciences,
of clinical therapeutics, and of different models and systems of care.
B1405_Ch-01.indd 1 1/31/2013 2:29:22 PM

2 L. W. Roberts, R. Balon and J. B. Layde
It involves attention to prevention, early identification, effective and time-

sensitive interventions, and, when necessary, chronic disease management.
It also involves being well informed about legal considerations that influ-
ence mental health care practices and financial resources that may be of help
to ill individuals who often start with, or end up with, disproportionate
economic difficulties. Ideally, and most excitingly, being prepared to work
with people with mental illness involves an eye to the future — being aware
of emerging discoveries at the basic science level as well as innovations at
the community and national levels.
In this book we have endeavored to provide a balanced introduction
that touches upon all of these topics in order to help prepare early career
clinicians for their work with people with neuropsychiatric diseases. We
have organized the book so that it will have value for generalists in pri-
mary care, medical specialists and subspecialists, including in psychia-
try, and psychologists and mental health clinicians in diverse international
settings. The book is informed by psychiatry in the United States, but
seeks to encompass perspectives and approaches that are multinational
and international in context. Special attention has been given to educa-
tional issues, such as how psychiatry residency training is organized in
the United States, as well as special topics of importance such as suicide,
HIV, homelessness, and legal issues. This book has been written at a time
of heightened awareness of the impact of neuropsychiatric disease
globally and rapid change in the diagnostic system and interventional
methods of psychiatry. As psychiatry evolves, we have sought to help the
early career clinician with this transition by incorporating the insights of
the past with what we expect to occur in the near future in this robust
field. In this introductory chapter, we will characterize the societal/
global impact of mental illness, and we will supplement an overview of
the evolving understanding of phenomenology in the field of psychiatry
to provide valuable context for understanding its significance and
complexity.
2. SOCIETAL IMPACT OF MENTAL ILLNESS

Societies around the world deal with the extraordinary consequences of
mental illness. The personal suffering of individuals with psychiatric
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Impact of Mental Illness 3
diseases and the public health ramifications of their disorders place a

heavy burden on all cultures in all countries. The role of psychiatrists in
ameliorating mental illness is a crucial part of the overall role of physi-
cians in decreasing the burden of disease around the globe.
2.1. Illness burden

The World Health Organization (WHO) calculates the disability-adjusted
life year (DALY) burden of diseases globally. The DALY is a measure that
combines the years of life lost due to premature mortality and the years
lived in less-than-good health by people suffering from illnesses. In 2004,
unipolar depressive disorders ranked behind only lower respiratory infec-
tions and diarrheal diseases as a leading cause of the burden of disease in
the world. The WHO estimates that as improved sanitation decreases the
incidence of infectious disease in the developing world, unipolar depres-
sive disorders will be ranked as the leading cause of the burden of disease
globally by 2030.4
Another reflection of the burden of disease is years lived with disabil-
ity (YLD), a measure of the number of years of healthy life lost by those
who suffer from chronic illnesses. Because so many psychiatric condi-
tions are long-lasting, and because they do not necessarily cause the
immediate death of those individuals suffering from them, the statistics
collected by the WHO on YLD due to mental diseases are even more
impressive than those on DALY. In 2004 among men globally, unipolar
depressive disorders was ranked first among disease in years of healthy
life lost due to disability, alcohol use disorders was second, and schizo-
phrenia and bipolar disorder were also ranked in the top seven diseases.
Among women globally, unipolar depressive disorders as a group were
also ranked first in terms of YLD, while schizophrenia, bipolar disorder,
and Alzheimer and other dementias were also listed among the top 10
diseases in 2004.4
No country is spared of the illness burden associated with neuropsychi-
atric disease. The WHO also reports that in 2004, people living in low-
and middle-income countries suffered enormously from psychiatric
illness, as did those living in high-income countries. Unipolar depressive
disorders were noted to be the leading cause of YLD in both low- and
B1405_Ch-01.indd 3 1/31/2013 2:29:23 PM

middle-income countries and high-income countries, while alcohol use

disorders, schizophrenia, and bipolar disorder were also among the top ten
diseases in terms of YLD in low- and middle-income countries, and alco-
hol use disorders, Alzheimer and other dementias, and drug use disorders
were among the top ten diseases in terms of YLD in high-income coun-
tries. What is more, neuropsychiatric disorders are the most important
causes of disability in all regions, accounting for about a third of YLD in
adults aged 15 and older globally.4
Alcohol and drug use disorders are also a significant problem world-
wide. For example, in the United States, recent data indicated that 32%
of adults had five or more alcoholic drinks on one day in the past year;
23 million people in the United States currently use illegal drugs.5 The
effects of drug abuse carry over to the workplace, with significant eco-
nomic fallout. Roughly 14% of workers in the United States report hav-
ing used at least one illicit drug in the past year, and 3% reported having
done so at work.1
2.2. Economic burden

The economic cost of mental illness globally is a huge, although poorly
recognized, problem. The economic costs of mental illness include both
the direct costs associated with treating mental illness and the indirect
costs associated with the disability from mental illness — including, for
instance, lost employment. The direct cost of mental illness is a small
percentage of its total economic cost; a recent study estimated that the
direct medical cost of mental illness in Canada represents only 9.8% of
the total economic burden of mental illness in that country.3
The WHO reports that although good data are not available for all
countries, estimates of the cost of mental illness in the United States and
the European Union range from 2.5% to 4% of the Gross National Product
(GNP) in those countries. Psychosis was estimated in 1996 to be the sin-
gle most expensive chronic condition treated by the National Health
Service (NHS) of the United Kingdom, followed by neurosis.6 Although
the economic costs of psychiatric disorders are tremendous in all coun-
tries, developing nations are least able to pay the huge costs of mental
disease.
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2.3. Unmet need

The treatment of mental disorders globally is complicated by the shortage
of mental health workers, especially psychiatrists, and by their uneven
distribution in the world. According to the WHO, the median number of
psychiatrists per 100,000 population in low income countries is 0.05, ris-
ing to 0.54 in lower-middle income countries, 2.03 in upper-middle
income countries, and 8.59 in high income countries. Almost half the
people in the world live in countries with less than one psychiatrist per
200,000 residents.7 The availability of psychiatric hospital beds and of
psychiatric medication also varies tremendously throughout the world,
with lower income countries having substantially fewer such resources
available than higher income countries. Even in high income countries,
the uneven distribution of mental health resources often means that some
mentally ill patients have very poor access to care; the unmet need for
caring mental health care is truly a global one.
Psychiatrists around the world spend their professional lives dealing
with the suffering of people with mental illness. The illness and cost bur-
dens of neuropsychiatric disease are immense, and the world is poorly
positioned to respond to the problem of unmet need for psychiatric ser-
vices. This handbook places the diagnosis and treatment of psychiatric
illness in a global perspective, recognizing the ubiquity of the problem of
mental disorders and the variety of approaches to the problem used by
psychiatrists around the world in their attempts to improve the lives of
their patients with mental illness.
3. EVOLVING APPROACHES TO PHENOMENOLOGY

IN PSYCHIATRY
The first step in recognizing and addressing neuropsychiatric disease is
appreciating the nature of mental illness as distinct from other medical
conditions and other sources of burden in society. This first step is not an
easy one to take, however, given that mental illness has not been well
understood across time or nations. Indeed, throughout history, the nature
of mental illness has been the focus of interest, exploration, and debate of
B1405_Ch-01.indd 5 1/31/2013 2:29:23 PM

psychiatrists, psychologists, philosophers, anthropologists, sociologists,

and many others, including people suffering from mental illness and their
families. In different societies and cultures, even at the present time, men-
tal illness has been understood in terms of magic, curse, God’s punish-
ment for a sin, and other supranatural forces. Contemporary science views
mental illness in terms of disorder of the brain.
In the past, attempts to classify mental disorders have been based in
various theoretical models of mental illness and in presumable etiology of
mental illness. These models included psychosocial (JCA Heinroth), psy-
chodynamic (S. Freud and followers, with the emphasis on presumed
etiology in form of a psychological conflict), behavioral (IP Pavlov, JB
Watson and BF Skinner), and organic (W. Griesinger). As none of these
models was satisfying, psychiatry gradually accepted the pragmatic,
atheoretical, clinical approach to classification, based on the observations
and work of a German psychiatrist, Emil Kraepelin. He recognized that
psychoses, for example, could be observed to fit into certain common
patterns, and, further, that the unfolding course of psychotic illnesses
across the lives of affected individuals fit into certain common patterns.
While he believed that eventually the underlying roots of all mental ill-
nesses will be discovered, Kraepelin strongly advanced a non-etiology-
based classification of mental illness. This descriptive, phenomenological,
and atheoretical approach has been reluctantly embraced in the modern,
global society that prefers causally based or etiologically driven explana-
tions for disease.
The work of psychiatry is certainly not finished and our diagnostic
system is far from perfect. As Kendler et al.2 wrote, “… the task of devel-
oping reliable and valid psychiatric diagnosis, will…remain central to the
clinical and research mission of psychiatry for the foreseeable future.” The
Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,
represents a substantial advancement in characterizing the patterns of
neuropsychiatric diseases and related conditions. This iteration in the
evolving effort to accurately characterize and classify mental disorders
differs from past work in that it seeks to incorporate insights from genet-
ics and emerging neurosciences, to be of practical utility in widely vary-
ing settings, to enhance the recognition of different developmental
pathways in neuropsychiatric disease, and to illuminate how gender and
B1405_Ch-01.indd 6 1/31/2013 2:29:23 PM

sociocultural factors may shape the experience and manifestation of

illness. These efforts reaffirm what the father of psychiatric phenomenol-
ogy, Karl Jaspers, suggested long ago: studying the patient’s symptoms and
signs should help us understand the patient’s inner experience. Moreover,
the terms we use to characterize this experience should have meaning and
serve as the basis for clinically astute and compassionate treatment.
In sum, mental illnesses are the source of immense suffering and give
rise to poorly recognized but nearly overwhelming health burden through-
out the world. These diseases emerge through a complex interplay of
biological, psychological, social, and cultural factors, and we are only
beginning to understand the nature of these factors and their relationships
and interactions. Contemporary science sees mental illness as brain dis-
ease or dysfunction, and yet that is an overly simplistic view of the ful-
some experience and contributors to mental illness and related conditions.
It is our sense that, in time, improved understanding of the biological,
developmental, psychological, social, and cultural features and influences
that shape mental illness will help us better categorize mental disorders
and, ultimately, improve and refine their treatment. Also in time, the
capacity to better categorize mental disorders as they become manifest in
large populations will lead to better systemic interventions and diminished
burdens and costs of disease.
On the road to developing a reliable and valid approach to diagnosis in
psychiatry, it is nevertheless valuable to remember Kendler’s caution that
“our… criteria, however detailed, never contain all the important features
of psychiatric illness that we should care about.” In other words, the
abstract conceptualization and classification of neuropsychiatric diseases
should never blind us to the reality of what it is like to endure each day
with these devastating conditions.
4. HANDBOOK ORGANIZATION
This handbook is organized around several core knowledge domains:
approaching the field of psychiatry, the initial assessment of the patient,
psychiatric disorders, treatment settings, psychiatric education and
research, and special topics. It is our hope that this handbook will help the
clinician to progress from the starting point of recognizing the possible or
B1405_Ch-01.indd 7 1/31/2013 2:29:23 PM

likely diagnosis to the more important insights that come with understand-
ing of their patients’ experiences of living with disease and helping them
to bear and alleviate their suffering.
ACKNOWLEDGEMENT
Foremost and most importantly, we would like to express our gratitude to
Ann Tennier for her hard work on this book. She has done a marvelous job
to keep us on target and on time. Her editing has been flawless. This book
would not exist without her.
REFERENCES
1. Center for Substance Abuse Prevention. (2008) Substance abuse and mental
health services administration.
2. Kendler et al. (2010) The development of the Feighner criteria: A historical
perspective. Am J Psychiatry 167: 134–142.
3. Lim et al. (2008) A new population-based measure of the economic burden
of mental illness in Canada. Chronic Dis Can 28(3): 92–98.
4. Mathers C, Boerma T, Fat DM. (2004) The Global Burden of Disease: 2004
Update, Available at: http://www.searo.who.int/LinkFiles/Reports_GBD_
report_2004update_full.pdf
5. U.S. Department of Health and Human Services, Substance Abuse and
Mental Health Services Administration. (2010) Results from the 2010
National Survey on Drug Use and Health: Summary of National Findings,
Center for Behavioral Health Statistics and Quality.
6. World Health Organization. (2003) Investing in mental health. Available at:
http://www.who.int/mental-health/media/investing_mnh.pdf
7. World Health Organization. (2011) WHO Mental Health Atlas. Available at:
whqlibdoc.who.int/publications/2011/9799241564359_eng.pdf
B1405_Ch-01.indd 8 1/31/2013 2:29:23 PM

Chapter 2
International Issues in Psychiatry
Richard Balon and Cyril Höschl
1. INTRODUCTION
Why address international issues in psychiatry? There are multiple
reasons for addressing international issues on the pages of this textbook,
but foremost, as Melvin Sabshin14 aptly wrote, “Whether it is recognized
or not, all psychiatrists are internationalists, and the field of psychiatry is
international.” For a long time, the main international issue in psychiatry
was the abuse of psychiatry in various countries around the world (nota-
bly, in the past, the USSR, Chile under Pinochet, Cuba, South Africa dur-
ing apartheid) in particular and ethical and human rights issues in general.
However, as the world has become more interconnected and many areas
of human activities have globalized, it has become obvious that many
other issues addressing modern-era psychiatry are global, international,
and that Sabshin14 is correct in calling the field of psychiatry an interna-
tional one.
Psychiatry, much more than other medical disciplines, is connected
with many other fields and societal and social issues. As psychiatry inves-
tigates the brain and its relationship to the human experience and behav-
ior, it is frequently asked to help to understand various undesirable social
phenomena (e.g. addictive behaviors, cults, terrorism, and violence).4 One
of the branches of psychiatry, social psychiatry, actually focuses on the
relationship between manifestation, course, and outcome of mental illness
B1405_Ch-02.indd 9 1/31/2013 2:29:34 PM

10 R. Balon and C. Höschl
and social factors. It may provide partial explanation for some psychiatric
phenomena and their relationship to social issues. However, “. . . it cannot
provide psychiatric explanations for social phenomena. Psychiatry is not
a social service. It does not provide expertise in taking care of the helpless
people if the helplessness is the effect of social factors rather than a dis-
ease process. Psychiatry is not a psychological counselling service for the
unhappy, unfortunate, weary and dissatisfied. It may tell them that their
plight is not a disease but a human condition.”4 It is important to under-
stand that the limits of psychiatry were frequently obscured and
misunderstood during the last century. Thus, psychiatry frequently either
overpromised its abilities to solve societal phenomena or was abused for
the purpose of solving some societal (or even political) phenomena. Some
of the areas discussed in this chapter are connected to social and societal
issues but should be viewed and understood within the limits of psychiatry
as a medical discipline.
2. DIAGNOSTIC CLASSIFICATION
Our understanding of mental disorders is limited. Sartorius13 notes,
“Biological and other sciences have produced a lot of new facts in recent
years but no unifying theory that would help to put them in meaningful
relationships.” He is also correct in stating that there is very little evidence
about the nosological status of psychiatric disorders. However, diagnosis
is an extremely important issue in everything that physicians do. It is
important to realize that a diagnosis has meaning not only for physicians
but also for patients. It allows us to label what is wrong — and that iden-
tification provides a great relief to patients in any country or culture. The
fact that the physician is able to identify “what is wrong” means, in the
patient’s mind, that the doctor knows what he or she is doing. It is a start-
ing point and a cornerstone of the treatment process. From a physician’s
point of view, a diagnosis means several related things. It is a short scien-
tific description for taxonomic classification and/or a process of deciding
the nature of a diseased condition by examining the symptoms. Diagnosis
is also a careful examination and analysis of the facts in an attempt to
understand and explain something. Finally, it is a decision and an opinion
based on such an examination.
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International Issues in Psychiatry 11
Because the knowledge of the etiology of psychiatric disorders is

limited and the expression of these disorders in different cultures varies,
there is a great need for a common defining “language” or “terminology.”
Physicians from different countries and cultures should be able to under-
stand each other when discussing mental disorders and their treatment.
Two widely accepted diagnostic classification systems have been created
and modified over the last several decades — the International Classification
of Diseases (ICD) by the World Health Organization and the Diagnostic
and Statistical Manual of Mental Disorders (DSM) by the American
Psychiatric Association. The emphasis and focus of these systems, espe-
cially the DSM, has been shifting from the validity of the diagnosis to its
reliability and now possibly back to validity (by validity we mean that the
diagnosis really describes what one means it describes, and by reliability
we mean that in using the diagnostic criteria of the particular classifica-
tion, physicians all over the world would be able to describe a similar
entity).
There are other approaches to diagnosing mental illness in various
cultures (e.g. the Chinese Classification of Mental Disorders; Cuban
Glossary of Psychiatry; the Japanese Clinical Modification of ICD-10; the
Latin American Guide for Psychiatric Diagnosis — all discussed in
Chapter 3). However, the DSM and ICD systems (similar and, in a way,
merging) dominate the approach to the diagnosis of mental illness around
the world. It is important to realize that some syndromes or diagnoses are
culture bound (e.g. koro — a sudden and intense fear that the penis or, in
women, vulva and nipples will recede into the body seen in East and
South Asia; piblokto — an abrupt dissociative episode associated with
irrational or dangerous attacks and, at times, followed by convulsive sei-
zures and coma, seen in Eskimos; or latah — hypersensitivity and then
sudden fright often associated with dissociative state with echopraxia,
echolalia, and command obedience observed originally in South East Asia
but described under different names in other cultures) and that the
expression of mental illness may be partially influenced by the standing
diagnostic system (e.g. the changing picture of anorexia nervosa
symptomatology in East Asia).
From the international point of view, the future of psychiatric classifi-
cation should focus on two issues: creating a truly widely accepted,
B1405_Ch-02.indd 11 1/31/2013 2:29:35 PM

reliable, and valid diagnostic system through international collaboration,

and a valid translation of this system to various languages. The newest
revisions of both the ICD and DSM classification systems are expected by
2013, with translations to follow.
3. EDUCATION
Many aspects of medicine in general and psychiatry and mental health in
particular10 are becoming global. With globalization and the movement of
the workforce around the globe, medical education, including psychiatric
education, needs to become truly international.1 In fact, the process of
internationalizing clinical care and medical education has been gradually
happening over the last several decades. Examples of globalization and
international exchange of medical education and clinical care include
the opening of US medical school campuses in other countries (e.g. the
Cornell University Medical Campus in Doha, Qatar, or the Duke University
Medical Campus in Singapore), clinical rotations of medical students from
Caribbean and some Israeli medical schools in the United States, interpre-
tation of imaging studies overseas during the night-time in the United
States, special tracks for students from various countries in some European
countries (e.g. Greek and Norwegian students in the Czech Republic),
medical “tourism” (traveling abroad to get cheaper or better medical care,
which occurs among citizens of many nations), and the Joint Commission
(a US agency which ensures through an accreditation process that hospi-
tals meets certain standards of care) accreditation of some hospitals in
India and Thailand.
The education of medical students in psychiatry has, on the international
level, focused mostly on student exchange at various levels (mostly elective
psychiatry rotations abroad) and on teaching students about transcultural
psychiatry. The opportunity to experience different systems of delivery of
care, different approaches to mental illness, and of course, different
cultures has always been attractive to some students. However, arranging
rotations abroad has not always been easy for various reasons, including
student safety and malpractice coverage. The recent integration of Europe
allows much easier movement of medical students among European coun-
tries, and thus the exchange of medical students interested in psychiatry
B1405_Ch-02.indd 12 1/31/2013 2:29:35 PM

rotations abroad will probably increase significantly, at least in the coun-

tries of the European Union. Teaching medical students about transcultural
psychiatry does not necessarily need to take the form of international
exchange. Telemedicine has been frequently used for providing consulta-
tions and long-distance assessment of patients when various services and/
or expertise are difficult to obtain. Interestingly, Ekblad and colleagues3
reported on using videoconferencing to allow students in Sweden to access
international teachers in refugee mental health in situations in which teach-
ers would not otherwise be accessible. International teachers from
Australia, Sweden, and the United States interviewed an actual and a simu-
lated patient at the Australian and US sites. The interviews were followed
by discussions involving those two sites with students and their supervisors
in Sweden. As the authors noted, videoconferencing may still be out of
reach in many developing countries, but with the increasing availability of
technology and decreasing prices, videoconferencing and the streamlining
of various teaching activities may be a very useful method of teaching
psychiatry to medical students and other trainees at the international level.
Actually, some places already offer various lectures for trainees and mental
health specialists free via the Internet. An example is the Carter-Jenkins
Center at the University of South Florida in Tampa that makes numerous
lectures available to an international audience for free at its website (www.
thecjc.org/slp.htm).
International postgraduate or psychiatry specialty training (called
“residency training” in the United States) may also take the form of a rota-
tion abroad. Some international medical graduates in training in the
United States take rotations in their native countries. Arranging postgrad-
uate training rotations in the United States for trainees from other coun-
tries is usually difficult for the same reasons as it is for medical students,
i.e. medico-legal and, to some extent, economical issues. It is important to
note that there is considerable variation in postgraduate training require-
ments and quality around the world. Postgraduate training for young
psychiatrists can occur in forms or activities other than rotating abroad.
One example is the existence of various summer schools, e.g. the Berlin
Summer School. This “school” or summer course was established to edu-
cate Central and Eastern European young psychiatrists on a yearly basis.9
This school inspired other schools and courses at national and
B1405_Ch-02.indd 13 1/31/2013 2:29:35 PM

international levels. One of the areas of education for young psychiatrists

is research. Many organizations (e.g. American Psychiatric Association
(APA), American College of Neuropsychopharmacology (ACNP),
Collegium Internationale Neuro-Psychopharmacologicum (CINP),
European College of Neuropsychopharmacology (ECNP), European
Psychiatric Association (EPA), and Society of Biological Psychiatry) offer
various “fellowships” for young psychiatrists during their annual meet-
ings. In this case, the “fellowship” means participation in a research-
focused course or mentorship with some financial support. One of the
longest existing research educational activities for students and residents
is the APA Research Colloquium for Young Investigators, organized
yearly and available to international participants (http://psych.org/Main
Menu/Research/ ResearchTrainingandFunding/ResearchColloquium for-
JuniorInvestigators.aspx). The Colloquium is organized yearly during the
APA annual meeting. It provides young investigators with a review of
their projects and career advice and allows them to establish contact with
well-established researchers.
Continuing Medical Education (CME) is another area that is becoming
gradually internationalized. There are multiple opportunities for continu-
ing medical education during meetings of organizations such as the APA,
EPA, and World Psychiatric Association (WPA). Psychiatric organizations
sponsor other educational activities that do not necessarily result in CME
credits. For instance, the WPA has created an educational program on per-
sonality disorders,16 available free over the internet (at www.wpanet.org).
Numerous other institutions foster international education, for instance,
the Lundbeck International Psychiatric Institute in Skodsborg, Denmark.
This institute was founded as an independent forum for international discus-
sions on improving the treatment of mood disorders and schizophrenia. The
Massachusetts General Hospital (MGH) Department of Psychiatry has estab-
lished a division of international psychiatry.2 This division outlined three
general initiatives: educational (to help train MGH residents in public mental
health and international psychiatry, to help establish psychiatry training pro-
grams in developing countries, and to sponsor scholars from abroad seeking
assistance with specific projects aimed at furthering educational activities at
their countries of origin); clinical (to provide consultations to clinical pro-
grams in the developing world); and research (to train skilled clinical
B1405_Ch-02.indd 14 2/6/2013 4:11:45 PM

researchers and to collaborate in the study of effective interventions for

disorders as they appear in the developing countries). It is hoped that more
educational activities, such as those of MGH and the Lundbeck Institute or
that of King’s College of London Maudsley Forum courses, will be devel-
oped around the globe, with these existing programs serving as a template.
International education activities in psychiatry may take the form of “on
site” consultation with focus on training young psychiatrists in countries
where there are almost no mental health services available, such as
Cambodia.15 Some of the international psychiatric organizations (e.g. WPA
and EPA) may help in arranging these consultations. These activities will
certainly increase with the widespread use of various social media,
increased networking, instant messaging, voice-over-Internet protocol, and
free online courses.
Finally, one important caveat: Psychiatric education should play an
important role in the critical evaluation of information flowing from one
part of the world to another. Examples include educating psychiatrists in
developing countries about the uncritical acceptance of new antipsychotic
medications, with their risks of development of obesity and diabetes
mellitus, or warning about the “export” of unhealthy lifestyles and habits
from developed countries into developing countries.
Psychiatric education is slowly moving toward becoming, if not truly
international, then at least more internationalized. Five of the top ten con-
tributing factors to years lived with disability globally are mental disor-
ders, so we need to pay more attention to global mental health, as pointed
out by Patel and Prince,10 who also emphasize that knowledge can and
must flow in both directions between high-income countries and low- or
middle-income countries. International psychiatric education has to be
more sophisticated and organized to play a crucial role in this actually
multidirectional flow of knowledge to help us in our efforts to improve
global mental health. Psychiatric educators around the world should also
play a crucial role in raising mental health awareness. As Prince and col-
leagues11 wrote, “Mental health awareness needs to be integrated into all
elements of health and social policy, health-system planning, and health-
care delivery.” There is an increased need for a common international
platform for exchanging information about education in psychiatry, edu-
cational experiences in various countries, novel educational programs,
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and results of educational research in psychiatry. The journal Academic

Psychiatry is rapidly becoming such an international platform.
4. RESEARCH
Psychiatric research is also gradually spreading around the globe in the
form of international studies. Some of the original international studies
yielded quite interesting and important results — for instance, the study
pointing out the overdiagnosing of schizophrenia and underdiagnosing of
bipolar disorder in the United States as compared to in the United Kingdom.
The WHO has organized various studies on schizophrenia (e.g. the WHO
International Pilot Study of Schizophrenia (IPSS)). The unexpected find-
ings of the early WHO studies were that patients with schizophrenia in the
developing countries (Nigeria, India) had a considerably better course and
outcome than patients with schizophrenia in the developed countries. The
outcome of patients in developing countries was not uniformly better.6
However, patients from the developing countries in some WHO studies
had higher rates of complete clinical remission than those from the devel-
oped countries, and they experienced significantly longer periods of unim-
paired functioning in the community (while only 16% of them were on
antipsychotic medication versus 61% in the developed countries). The
results of these studies underscored the variety of factors involved in the
course and outcome of mental disorders and were very important in modi-
fying our thinking about chronic mental illness. Some of the conclusions
of these studies were later criticized as overreaching and not uniform.
However, as Jablensky and Sartorius6 wrote,
The erosion of social support systems, likely to be associated with the pro-
cesses of globalization, should be a matter of grave concern. The sobering
experience of high rates of chronic disability and dependency associated
with schizophrenia in high-income countries, despite access to costly bio-
medical treatment, suggests that something essential to recovery is missing
in the social fabric. Thus the existence of outcome differentials between
populations and cultures is not ‘presumed wisdom’ but a real complex issue
which should be addressed with standards of precision and rigor that are
customary in scientific research and discourse.
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International studies have not been limited to schizophrenia or other

severe mental illnesses or to the collection of purely epidemiological data.
A study by Laumann and colleagues8 surveyed various aspects of sex and
relationships among adults aged 40–80 years in 29 countries. They found
that sexual problems tend to be more associated with physical health and
aging among men than women, thus basically confirming findings from
other studies. Interestingly, they also found that the reported prevalence of
sexual problems was higher in East Asia and Southeast Asia than in other
regions of the world (e.g. prevalence of erectile difficulties among men
and lubrication difficulties among women were approximately double
those reported in other regions). The reasons for the regional differences
are not clear but certainly worth further exploration. Other international
studies have addressed issues such as recovery and the different ways of
using this term; the naturalistic course of bipolar disorder (under the aus-
pices of the Stanley Foundation Bipolar Network); differences in recogni-
tion and treatment of depression in various countries; or the expertise of
general practitioners in assessing early psychosis and the risk of it.
An important emerging area deserving special attention is the spread of
international clinical trials organized by the pharmaceutical industry. As
the conduct of clinical trials in the developed countries is becoming more
costly and more complicated (e.g. regulations, population less interested
in participation in research trials without clear-cut benefits), the industry
has been moving clinical trials into the developing countries. As Jeglic
and colleagues7 pointed out, these global studies pose unique challenges
in training and calibrating raters due to language and cultural differences,
but certainly these are not the only challenges. The ethical standards of
conducting clinical research in the developing countries may be much
lower. Patient participation in research studies may be unduly enhanced,
if not coerced by Western standards, by relatively small rewards more
valuable than in Western countries. Similarly, the evaluation of efficacy
and reporting of side effects could be compromised by the combination of
a relatively large amount of money for the investigators (though still low
according to developed countries’ standards), looser regulations, and dif-
ferent ethical views and rules. The views on what constitutes mental ill-
ness, what is major stress, and what defines recovery (e.g. symptom relief
versus return to functioning) may also differ. Patients in the developing
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countries may also, for cultural and other reasons, attempt to please the
investigators and thus report a better outcome than it actually is. These
insights are supported by the fact that in some Eastern-European coun-
tries, the placebo-verum signal is usually more pronounced than, for
instance, in the United States. All these factors make the interpretation of
international studies difficult at times.
Psychiatric research will certainly become more international. The
internationalization of research brings advantages in combining financial
resources, exchanging different ideas and approaches to various problems,
and accessing different subject populations. However, we have to be care-
ful about its negative aspects, such as the possible exploitation of research
subjects in the developing countries or questionable reliability of the data.
5. ETHICS
Ethical and various other issues discussed in this chapter are certainly
interconnected on all levels. However, ethics is probably most connected
to human rights in general and to the mentally ill in particular, as well as
to the previously discussed issues on international research studies.
Different countries have different ethical standards for care and for
research. Some authors from the developed countries would even question
whether the lack of implementation of comprehensive mental health care
is ethical — an attitude barely comprehensible to a psychiatrist from a
country without any financial resources for mental health and with wide-
spread sexual abuse of women and torture of members of minority ethnic
groups.
Participation of psychiatrists in torture or assistance in execution would
probably be considered unethical all over the world at the present time.
However, forcible commitment of dissidents to mental institutions and
questionable experimentation by psychiatrists in the former Soviet Union
is a well-known fact.
The most important area of international ethics is probably the partici-
pation of patients with severe mental illness in clinical trials. The issues
involve the evaluation of patients’ capacity to participate in a research
study, their ability to give informed consent to participate in research, and
B1405_Ch-02.indd 18 1/31/2013 2:29:35 PM

the issue of possible coercion to participate (either direct or indirect due

to a relatively large monetary compensation). Other areas in need of
special ethics attention include the treatment of mentally ill prisoners (and
their participation in research studies) and, in some countries, evaluation
of prisoners on death row.
The standard ethical principles discussed in Chapter 30 are probably
not known, recognized, appreciated, or taught all over the world. This is
another area for future expansion with the help of the WHO and other
international organizations. The advent of new technologies such as tele-
medicine or electronic medical records will bring new ethical questions
(e.g. responsibility of the supervisor in telemedicine supervision of medi-
cal students seeing mentally ill violent patients in another country; trans-
fer of medical and research data between countries and interaction with
local and international legal restrictions, such as the US Patriot Act; and
neuro-imaging and genetic international databases).
6. CULTURE AND CULTURAL PSYCHIATRY

The major aspects of cultural psychiatry are addressed in Chapter 31 of
this textbook. We would like to emphasize that the cultural issues could
be “national” (e.g. differences between various cultures or groups of dif-
ferent ethnic origin in the United States; differences between different
ethnic groups in various African or Middle Eastern countries whose colo-
nial past led to creation of entities including groups or areas with large
differences, if not enmities) but are largely “international.”
As pointed out in many texts, culture and cultural psychiatry is not just
listing differences and naming culture-bound syndromes. We have dis-
cussed the effect of culture and economic development on the outcome of
one of the serious mental illnesses, schizophrenia. Another mental health
phenomenon profoundly affected by culture is suicide. Some countries
report almost no suicide (e.g. some Muslim countries), some report very
low rates (e.g. Georgia, Greece), and some report very high rates (e.g.
Hungary, Sri Lanka, Baltic Countries). Psychiatrists and psychologists in
most developed countries believe that almost all people who committed
suicide were mentally ill, while psychiatrists in some developing countries
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do not fully accept the high association between suicide and mental ill-
ness. Some cultures and religions (e.g. Catholicism, Islam) significantly
stigmatize suicide. Studying these differences and cultural influences may
help us to understand some aspects of suicide. Interestingly, two major
studies on possible treatment of suicidality and prevention of suicide had
elements of international research studies. The first study on the antisui-
cidal effect of lithium was a collaborative effort between US and Italian
researchers conducted in Sardinia. The InterSePT study examining the
antisuicidal effect of clozapine was a truly international effort conducted
in centers in several countries.
The increased migration between countries also brings culture and
cultural issues into the international spotlight. Some of the mentioned
culture-bound syndromes could suddenly appear in a country where these
syndromes have never been seen before, such as cases of koro syndrome
in Western Europe. Another example is the practice of so-called folk
healers from developing countries in major urban areas of developed
countries.
7. PSYCHIATRIC CARE FOR VICTIMS OF MAJOR

DISASTERS, VICTIMS OF TORTURE,
AND REFUGEES
Major psychiatric disasters like the 2010 earthquake in Haiti or the 2004
Indian Ocean earthquake and tsunami present a major stressor for the
entire population of a country or region. Most of the international help
to the victims of these natural disasters has been limited to acute surgi-
cal and other emergency medical interventions. Unfortunately, psychi-
atric help addressing possible posttraumatic stress disorder and other
sequelae of stress is usually not involved. After the 2004 tsunami, the
Department of Psychiatry at the University of Indonesia in Jakarta
organized an intensive training program for practitioners in the province
of Aceh, Sumatra, a unique and successful endeavor. Interestingly, some
psychiatrists have taken into “their own hands” the help to victims of
major trauma due to war and siege. S. Arshad Husain, M.D., from the
University of Missouri with his colleagues from the International
Center for Psychosocial Trauma has conducted training for teachers and
B1405_Ch-02.indd 20 1/31/2013 2:29:35 PM

other laypeople to help children with the stress of war or major disasters
in various places around the world (e.g. Sarajevo, Bosnia; Caucasus;
Pakistan).5
Haiti’s mental health system (previously almost non-existent) collapsed
during the 2010 earthquake there. As many as one in five Haitian earth-
quake victims are estimated to have suffered serious psychological trauma
for which professional help is needed. Various international and national
psychiatric organizations have offered and arranged some professional
help (e.g. volunteers, medications), but to this date we are not aware of
any systematic effort to rebuild the previous mental health system or to
build something more effective.
Similarly, there has been no systematic effort to address the psycho-
logical traumas and mental health of refugees. The psychological issues
of victims of torture (e.g. anxiety, depression, survivor guilt, and loss
of dignity, family, possessions, and trust) have been addressed in a non-
systematic way. Studying these issues in an organized fashion is impos-
sible for logistical reasons.
These issues definitely warrant the attention and efforts of various
international and national psychiatric associations, such as the WHO,
APA, or EPA.
8. MISCELLANEOUS
A host of international issues may or do require involvement of psychiatry
and psychiatrists, such as international adoptions (e.g. evaluation of chil-
dren to be adopted; post-adoption adjustment); airline passenger miscon-
duct (e.g. intoxication, exacerbation of mental illness) and its handling
within the medico–legal context; estimates of global mental health burden
associated with alcohol and drug abuse; and urbanization of developing
countries and its association with mental health issues and services.
9. THE ROLE OF INTERNATIONAL/NATIONAL

ORGANIZATIONS
Various international non-governmental organizations (besides charities)
have attempted to address some of the international issues discussed in
B1405_Ch-02.indd 21 2/6/2013 10:55:22 AM

this chapter. The most prominent is the World Health Organization

(WHO) with its Division of Mental Health. The WHO has organized
numerous studies of mental illness and mental health (mostly epidemio-
logical and descriptive), international meetings, educational programs
(e.g. for early-career psychiatrists), and research fellowships. Other inter-
national associations that may be helpful in addressing some of the inter-
national problems and even disasters include the World Psychiatric
Association (WPA), the Global Alliance of Mental Illness Advocacy
Networks (GAMIAN), European Federation of Associations of Families
of People with Mental Illness (EUFAMI), Collegium Internationale
Neuro-Psychopharmacologicum (CINP), European College of Neuro-
Psychopharmacology (ECNP), and Doctors Without Borders. Europe
seems to be the best organized and integrated continent with regard to
collaborative efforts in mental health, under the leadership of the European
Psychiatric Association (EPA). EPA is an organization that includes indi-
vidual members from all over Europe (and the world) and also national
psychiatric organizations of European countries. Other continents do not
have well-functioning international psychiatric organizations and rely
more on the WHO.
In the future, the role of various international organizations should not
be limited to organizing scientific meetings, studies on epidemiology and
diagnosis, or educational programs for psychiatrists. Rather, international
organizations should increase their role in areas such as psychological
help after major disasters, treating refugees, helping to organize large
treatment trials, or providing information and psychoeducational materi-
als for patients in developing countries.
10. CONCLUSION
Psychiatry certainly is an international discipline connected to many inter-
national problems and issues. As a discipline, psychiatry at the interna-
tional level needs to establish an active global network for collaboration
in mental health research and policy, to map the needs and structures for
providing them, to define a minimum standard of care, to harmonize edu-
cational efforts in psychiatric education, and to establish international
B1405_Ch-02.indd 22 1/31/2013 2:29:35 PM

ethical rules and treatment guidelines. The rest of medicine is developing

and “getting internationalized” very rapidly, and psychiatry should follow
this trend.
11. KEY POINTS

• Historically, the most prominent international issue in psychiatry used
to be the abuse of psychiatry for various political reasons and abuse
of human rights of the mentally ill.
• With growing globalization of all aspects of life, psychiatry is
increasingly more international, and other issues are becoming more
prominent.
• Establishing a truly international, valid, and reliable diagnostic
classification system accepted by all countries around the globe is a
crucial element for the future of psychiatry.
• Psychiatric education has to play a key role in the exchange of knowl-
edge and information about the latest developments among psychia-
trists internationally.
• International, multicenter research studies in all areas of psychiatry
(epidemiology, psychopathology, treatment, education) are becoming
more frequent.
• The growing presence of international research in psychiatry brings
various old and new ethical issues to the forefront.
• Increased use of various information technologies (e.g. videoconfer-
encing, telemedicine in supervision) is becoming more frequent and
increases the “internationalization” of psychiatry.
• Numerous international psychiatric organizations have been active
mostly in organizing conferences, exchanging information, and help-
ing young psychiatrists in the form of various fellowships.
• There seems to be an increased need for international psychiatric
organizations to become more involved in helping the victims of
disasters and torture; harmonizing the standard of care among coun-
tries; promulgating and distributing educational materials, ethical
principles, and public health principles; and preventing mental
illness.
B1405_Ch-02.indd 23 1/31/2013 2:29:35 PM

12. SELF-ASSESSMENT
12.1. Clinical trials conducted by pharmaceutical companies
in the developing countries may face which of the
following difficulties?
(A) Poor training of local raters in using rating instruments.
(B) Different concepts of mental illness.
(C) Looser ethical standards.
(D) Possible economic coercion.
(E) All of the above.
Clinical trials are frequently conducted in the developing countries for

economic reasons — the expenses are lower. However, the financial
incentives may border on economic coercion (that may happen in the
developed countries, too) as the payments per patient may be much
higher than a patient’s daily or even monthly salary and the payment to
the investigator could be fairly high, too. The ethical standards could be
looser, not every country has adopted the stringent ethical regulations
of many developed countries and some countries have not had ethical
committees or Internal Review Boards/Human Investigation Committees
till recently (plus, these committees may be less regulated than commit-
tees in the developed countries). As has been discussed elsewhere in
this book, various cultures and countries may have a more or less dif-
ferent concept of mental illness (e.g. depression in East Asia). The
training of local rater may be less stringent and these raters may not
necessarily attend training session organized in the developed
countries.
Answer: E
12.2. International educational activities include all

of the following except:
(A) International conferences.
(B) Exchange of medical students.
(C) Use of videoconferencing for therapy training.
B1405_Ch-02.indd 24 1/31/2013 2:29:35 PM

(D) Evaluation of children for international adoption.

(E) Use of telemedicine for supervision.
Evaluation of children for international adoption is not an educational

activity for psychiatrists. The other four options — international confer-
ences, exchange of medical students, use of videoconferencing for therapy
training, and use of telemedicine — are clearly international educational
activities.
Answer: D
13. CASE STUDIES

13.1. Development of psychiatric service and training
in Cambodia
Dr. Savin15 describes the development of psychiatric service and training
in Cambodia after the Khmer Rouge rule (between 1979 and 1992, no
mental health services were available in Cambodia). The training started
with several months of English language study, followed by three years of
didactic instruction and on-the-job training. Three Norwegian psychia-
trists (the Cambodian Mental Health Development program was Norwegian
funded) each spent one full year providing training and supervision for the
residents. Trainees also spent two months learning inpatient psychiatry in
Thailand. Several times a year, consultant psychiatrists conducted two-
week teaching blocks on specific subjects. The program graduated a num-
ber of psychiatrists who then helped train new groups of residents with
some help of expatriate psychiatrists.
13.2. An American training Chinese psychoanalysts

Ms. S., an American psychoanalyst, provides training to Chinese psychoana-
lysts-in-training through voice over Internet protocol and a videoconferencing
service (International Herald Tribune, October 29, 2010). So far, 31 Chinese
analysts graduated from her program. Ms. S. believes that the past violent
political campaigns and control of freedom and political expression left a
significant legacy of trauma, and, to her, the Chinese resemble Holocaust
B1405_Ch-02.indd 25 1/31/2013 2:29:35 PM

survivors and their children. She thus uses her experience of analytical work
with US. Holocaust survivors and their children in her telesupervision of
Chinese analysts in training.
13.3. Concepts of mental illness

The concept of mental illness could be different even among the young
supposedly well-informed and technologically savvy population of medi-
cal students. In a study by Rong and colleagues.12 comparing Australian
and Chinese medical students’ level of awareness of depression, Chinese
students were far less likely to consider mental health conditions and
depression as major public health problems than their Australian counter-
parts. Interestingly, Chinese medical students were more likely to consider
some psychological symptoms, such as “thinking life is not worth living,”
but less likely to consider some somatic features, such as “sleep distur-
bance,” as typical for people with depression.
REFERENCES
1. Balon R, Roberts LW, Coverdale J, Louie A, Beresin E. (2008) Globalization
of medical and psychiatric education and the focus of Academic Psychiatry
on the success of “international” authors. Acad Psychiatry 32: 151–153.
2. Belkin GS, Fricchione GL. (2005) Internationalism and the future of aca-
demic psychiatry. Acad Psychiatry 29: 240–243.
3. Ekblad S, Manicavasagar V, Silove D, Baarnhielm S, Reczycki M, Mollica R,
Coello M. (2004) The use of international videoconferencing as a strategy
for teaching medical students about transcultural psychiatry. Transcult
Psychiatry 41: 120–129.
4. Höschl C. (2009) European psychiatry: Needs, challenges and structures.
Eur Arch Psychiatry Clin Neurosci 259 (Suppl 2): S119–S122.
5. Husain SS, Nair J, Holcomb W, Reid JC, Vargas V, Nair SS. (1998) Stress
reactions of children and adolescents in war and siege. Am J Psychiatry 155:
1718–1719.
6. Jablensky A, Sartorius N. (2008). What did the WHO studies really find?
Schizophr Bull 34: 253–255.
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7. Jeglic E, Kobak KA, Engelhardt N, Williams JB, Lipsitz JD, Salvucci D,

Bryson H, Bellew K. (2007) A novel approach to rater training and certifica-
tion in multinational trials. Int Clin Psychopharmacol 22: 187–191.
8. Laumann EO., Nicolosi A, Glasser DB, Paik A, Gingell C, Moreira E, Want T.
for the GSSAB Investigators’ Group. (2005) Sexual problems among women
and men aged 40–80 y: Prevalence and correlates identified in the Global
Study of Sexual Attitudes and Behaviors. Int J Impot Res 17: 39–57.
9. Mihai A, Strohle A, Maric N, Heinz A, Helmchen H, Sartorius N. (2006)
Postgraduate training for young psychiatrists — experience of the Berlin
summer school. Eur Psychiatry 21: 509–515.
10. Patel V, Prince M. (2010). Global mental health. A new global health field
comes of age. JAMA 303: 1976–1977.
11. Prince M, Patel V, Saxena S, Maselko J, Phillips MR, Rahman A. (2010)
Global mental health 1. No health without mental health. Lancet 370: 859–877.
12. Rong Y, Luscombe GM, Davenport TA, Huang Y, Glozier N, Hickle IB.
(2009) Recognition and treatment of depression. A comparison of Australian
and Chinese medical students. Soc Psychiatry Psychiatr Epidemiol 44:
636–642.
13. Sartorius N. (2002) Fighting for Mental Health. A Personal View, pp. 202,
Cambridge University Press, NY.
14. Sabshin M. (2008) International affairs. In: Changing American Psychiatry.
A Personal Perspective, Chapter 7, pp. 83–99, American Psychiatric
Publishing, Inc., Arlington, VA.
15. Savin D. (2000) Developing psychiatric training and services in Cambodia.
Psychiatric Serv 21: 935.
16. Simonsen E, Ronnigstam E, Millon T. (2008) A synopsis of the WPA
educational program on personality disorders. World Psychiatry 7: 119–125.
B1405_Ch-02.indd 27 1/31/2013 2:29:35 PM

Chapter 3
Psychiatric Diagnosis
Stephanie Bagby-Stone, Jessica Nittler

and John Lauriello
1. INTRODUCTION
As in other medical specialties, psychiatrists make a diagnosis by observing
signs and symptoms; collecting data from the patient and family, friends,
and former medical care providers; and utilizing appropriate diagnostic
procedures. At this time, most psychiatric diagnoses are made by using lists
of signs and symptoms organized into diagnostic criteria, which do not
refer to the etiology of the ailment. A few psychiatric diagnoses do refer-
ence etiology in their diagnostic criteria, including mental disorders due to
a general medical condition, trauma-related disorders, and adjustment dis-
orders. However, due to our current deficit in etiological understanding of
most mental illnesses, nearly all psychiatric conditions are considered dis-
orders of functioning or syndromes composed of patterns of signs and
symptoms, but not diseases with specific causes. We are in an exciting time
of advancement in the understanding of molecular biology, genetics, neuro-
chemistry, neuroanatomy, neurophysiology, and cognitive neuroscience.
In the near future much will be learned regarding the etiology of psychiatric
disorders as the technologies to study the brain, the body, and the mind
expands. In psychiatric diagnosis, context also matters. As our biological
knowledge expands, our diagnoses and diagnostic systems will have to
grow to embrace these new insights alongside cultural diversity.
28
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Psychiatric Diagnosis 29
1.1. What is a psychiatric diagnosis?

1.1.1. Significance of psychiatric diagnosis
When confronted with new information, our brain first begins a simple yet
elaborate process of searching for known patterns. If none is found, then
new naming and categorizing of the novel information ensues. Much like
the workings of the brain, psychiatry has sought to label the signs and
symptoms of mental illness to begin to sort them into diagnostic catego-
ries. Such simplification and organization attempt to aid in the diagnosis
and treatment of our patients and our understanding of mental disorders.
A psychiatric diagnosis functions as much more than just a “name,” a
“label,” or a “pattern”; it serves many purposes by providing useful and
concise information and facilitating communication in clinical, educa-
tional, and research practices.5
In clinical settings, a psychiatric diagnosis allows for efficient commu-
nication among health care providers across specialties regarding a
patient’s medical condition. A psychiatric diagnosis summarizes suc-
cinctly a large amount of information about a patient, which can then be
conveyed quickly among treatment providers. A diagnosis also helps to
guide clinicians to the appropriate treatment and therapeutic management
for the patient. A diagnosis can provide information regarding course of
illness, risk of comorbidities and complications, and prognosis. It also
provides a way to communicate to insurance companies regarding cover-
age for illnesses, medications, and other therapies. A diagnosis may open
or close doors to other mental health care services and resources. Because
a psychiatric diagnosis is used to communicate to multiple medical and
non-medical entities and can determine treatment, it is very important to
make thorough evaluations and accurate diagnoses.5
A psychiatric diagnosis can also play a very important role for patients
because it brings words to express their experience. For people struggling
with mental illness, a psychiatric diagnosis can provide validation of their
symptoms and their suffering. It can also help them to feel less isolated or
ashamed and give them comfort that they are not alone in their disease. It
can dispel the belief that the illness is “all in their heads” by appropriately
defining their symptoms as a medical illness. A psychiatric diagnosis can
give hope to a patient by identifying an illness that has treatment options.
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30 S. Bagby-Stone, J. Nittler and J. Lauriello
A diagnosis can be the “answer” for which some patients and their
families are looking to understand themselves and their loved ones.
However, for some patients, a psychiatric diagnosis may feel shameful,
devastating, and inconsistent with their experience, e.g. delusional, con-
version, or somatoform disorders. Talking with patients about how they
feel regarding their diagnosis as well as educating patients and the impor-
tant people in their lives regarding the nature of psychiatric illness is
necessary to decrease stigma and promote understanding of these complex
biologic disorders.
Psychiatric diagnosis allows a means of communication to educate
future health care providers across disciplines. A psychiatric diagnosis
provides an international common language around which learning, train-
ing, and discussions can occur. Psychiatric patients are not isolated to
mental health clinics and often suffer from multiple co-occurring medical
conditions. It is important for all health care providers to have an under-
standing of and sensitivity to mental health diagnoses. Education regard-
ing psychiatric diagnoses helps to facilitate this understanding. Moreover,
the value of a psychiatric diagnosis in education is not limited to academic
medical settings; public education of the signs and symptoms of mental
illness can bring hope and understanding to those in need and their com-
munity, reduce stigma regarding psychiatric conditions, and facilitate
treatment.
In research, a psychiatric diagnosis provides a standardized means to
reduce heterogeneity by specifically defining conditions for study. This
categorization is vital for crafting research to further our knowledge of
mental illness, etiology, epidemiology, and treatment.5
2. SIGNS AND SYMPTOMS IN PSYCHIATRIC ILLNESS

The signs and symptoms of mental illness are complex and varied and
provide the “clues,” the data, upon which a psychiatric diagnosis is made.
If you conceptualize psychiatry as a language, our basic vocabulary is
built around these signs and symptoms, which provide the foundation for
psychiatric diagnosis. A psychiatric diagnosis attempts to bring order to
the complex and, at times, disjointed psychiatric phenomena by structur-
ing and organizing the signs and symptoms to make them easier to com-
municate, understand, and use.
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Psychiatric signs and symptoms can be found along a spectrum of

behavior ranging from normal to abnormal. The characterizations of psy-
chiatric signs and symptoms have remained constant over time. However,
some terms have fallen out of favor. For example, recent revisions of the
American Psychiatric Association’s Diagnostic and Statistical Manual of
Mental Disorders1 and the World Health Organization’s International
Classification of Diseases31 have tended towards terms that emphasize the
biological basis of all forms of mental illness rather than more psychody-
namic interpretations.16
Signs are the objective clinical findings observed by clinicians, whereas
symptoms are the subjective experiences described by patients. For exam-
ple in depression, a patient’s reported symptoms might include anhedonia,
feelings of worthlessness and guilt, and suicidal thoughts, and the
observed signs may include weight loss or gain, psychomotor agitation or
retardation, and objective data regarding sleep disturbances. In a patient
with anorexia nervosa, the symptoms could include body image distortion,
fear of weight gain, and refusal to maintain weight, and the signs could be
weight loss, amenorrhea, downy lanugo, hypotension, and bradycardia.
2.1. Specificity, sensitivity, and predictive value of signs

and symptoms
Unlike diagnoses in many other medical fields, which have cardinal signs
or symptoms that are pathognomonic for a specific illness, in psychiatry
it is atypical to find a single sign or symptom that defines a specific psy-
chiatric disorder. For example, visual hallucinations are found in multiple
diagnoses, including depression, mania, schizophrenia, substance intoxi-
cation, or delirium related to a medical illness. Psychiatric diagnoses are
made on the basis of patterns of signs and symptoms that often need to be
observed over a period of time, not just by the presence or solitary occur-
rence of a single sign or symptom.
2.2. What information is useful in making a psychiatric

diagnosis?
A psychiatrist often can use multiple resources to gather the needed infor-
mation regarding a patient’s signs and symptoms in order to make an
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accurate psychiatric diagnosis. The psychiatric clinician attempts to

look at the “whole picture,” which includes the biological, psychological,
social, and cultural aspects of the patient’s condition.
2.2.1. Psychiatric interview

The psychiatric interview is a skilful blend of science and art — and as
such, mental health practitioners must combine the scientific knowledge
we currently have with experience, intuition, creativity, and the ability to
navigate uncertainty. The psychiatric interview is the prime opportunity
for the mental health clinician to engage in a conversation with the patient
regarding his or her mental and physical concerns and the effect on the
patient’s functioning. The interview reviews the chief complaint, history
of present illness, psychiatric history, medical history, family history,
social and cultural history, substance use history, review of symptoms, and
mental status examination. This process allows the patient the opportunity
to tell his or her story. The interviewer generally begins with open-ended
questions. A skilled interviewer will establish rapport, convey empathy
and cultural sensitivity, create an atmosphere of trust, and encourage hope
during an interview. In addition to listening attentively to what the patient
is saying, the clinician is also acutely aware of the patient’s non-verbal
communications, including his or her body posture and movements, tone
and volume of voice, personal hygiene, and eye contact.2 When interview-
ing patients from other cultures, the clinician should consider allowing for
more interview time and requesting a bilingual, bicultural interpreter if
necessary.29 Because a psychiatric interview relies so heavily upon patient
self-report and few objective tests, a clinician’s intuition can be very use-
ful in patient assessment, but it is not infallible and cannot substitute for a
thorough evaluation. Nevertheless, an interviewer’s experience or “feel”
of the patient may suggest, guide, or modify diagnosis.28 More details on
this topic can be found in Chapter 5.
2.2.2. Collateral information

Unfortunately, patient self-report and insight is not always adequate or
sufficiently reliable to make an accurate psychiatric diagnosis. Additional
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history can be provided through reports from family or other important

people in the patient’s life regarding the patient’s moods, behaviors, and
history. Collateral information can be invaluable information to the psy-
chiatrist and provide a better view of the patient’s world outside the clinic
or hospital. Records of previous psychiatric and medical treatment, hospi-
talization, and psychological testing can confirm the accuracy of self-
report and provide critical information when the patient is a poor historian
or cannot recall details of past treatment or assessment.2
It is important to respect patient confidentiality and to gain permission
to contact, give information to, and request records from collateral
sources of information. In non-emergent situations, health care providers
may listen to information offered by collateral sources, but they are pro-
hibited from giving out patient information without the patient’s
expressed permission. In emergent medical situations, when safety con-
cerns are present, exceptions to confidentiality can be made to protect the
patient and others. Such concerns would include if the patient is in immi-
nent danger to self or others or if there is evidence of child or elder
abuse.2
2.2.3. Physical examination

Although most psychiatrists do not routinely conduct a physical examina-
tion of their patients, a standard medical and neurologic examination may
be helpful in the diagnosis and management of a psychiatric patient.
Weight and vitals are useful in the monitoring and diagnosis of many dis-
orders and critical in eating disorders. They are also important in the
monitoring of patients who have metabolic issues or who are prescribed
medications that have side effects of weight gain or affect blood pressure
or heart rate. In some situations, referral to an appropriate medical special-
ist may be indicated, for example, a gynecologist, endocrinologist, or
neurologist. The physical examination may reveal findings consist with
organic causes of psychiatric signs and symptoms. The examination may
also reveal evidence of current or previous self-harm or abuse. It is a good
practice when performing a physical examination on a patient of the oppo-
site sex or with any patient who has been abused that a chaperone always
be present.2,16
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2.2.4. Laboratory testing

In general, psychiatrists rely more upon clinical signs and symptoms for
diagnosis than objective laboratory testing; however, laboratory testing
can still play an important role in psychiatric diagnosis and clinical man-
agement. Many organic causes of psychiatric symptoms can be evaluated
through laboratory testing, and blood work may be necessary in medica-
tion monitoring.
Basic laboratory studies, including a complete blood count (CBC) with
information regarding white blood cell count, hematocrit, and platelet
count, as well as a comprehensive metabolic profile (CMP) with informa-
tion regarding blood glucose, electrolytes, and liver and kidney functioning,
can provide baseline treatment information and clues to underlying medical
conditions. Endocrine studies including thyroid profiles can be useful in the
evaluation of mood, anxiety, and psychotic disorders. Patients with demen-
tia or delirium may need additional blood workup, including vitamin B12
and folate levels, urinalysis, or other imaging studies. In some cases, a
Lyme serology, syphilis serology, or HIV testing can be useful to test for
infectious diseases that could present with psychiatric symptoms. A urine
drug screen and blood alcohol level (BAL) can also offer valuable informa-
tion regarding current substance use. A toxicology screen may reveal illicit
drugs or other ingested substances. In women of reproductive age, a preg-
nancy test may be indicated before initiating or continuing treatment.2,16
Drug levels and other laboratory monitoring are necessary for many
psychotropic medications. Many of the mood stabilizers require baseline
laboratory testing and then periodic testing of drug levels and other labo-
ratory parameters. Lithium, carbamazepine, valproate, and also the antip-
sychotic medication clozapine require this level of laboratory monitoring.
Blood levels of tricyclic antidepressants are also important to maintain
doses within the therapeutic window and avoid toxic blood levels. Toxic
blood levels may by themselves have psychiatric manifestations. For
instance, a patient with bipolar disorder may present with visual halluci-
nations that are related to a delirium induced by toxic levels of lithium, or
a patient with depression may appear with manic symptoms. For patients
being prescribed atypical antipsychotics, baseline and regular monitoring
of fasting blood glucose and lipid profile are recommended.2,16
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In the future, neurogenetic testing may play a larger role in psychiatric

diagnosis and treatment planning. Currently, testing for genetic markers is
available for some syndromes and inborn errors of metabolism that
can often present with psychiatric symptoms, such as Down syndrome
(trisomy 21), Fragile X syndrome (increased triplet repeats in the FMRI
region of Xq27.30), Huntington’s disease (triplet repeats on chromosome
4p16), DiGeorge Syndrome (CATCH-22 syndrome, 22q11.2 deletion),
and Alzheimer’s disease (apoplipoprotein E ε4 allele). Genetic testing
may also become useful in the medication management of psychiatric ill-
ness. Testing done on variations in drug metabolism may provide clini-
cians information regarding a patient’s response or sensitivity to a
medication. Although there is variation amongst individuals, testing of the
CYP isoenzymes may explain ethnic trends found in the pharmacokinetics
of psychotropic medications in Asians, Hispanics, and African Americans.29
Future advances in neurogenetic research may provide improved
understanding of the biological mechanism of psychiatric disease and the
role of environment in psychiatric disease. Genetic testing could provide
for early diagnosis, improved treatment, and possibly prevention. However,
along with this improved understanding, ethical and social issues may
arise concerning the emotional and financial effect on individuals who
have been found to be genetically susceptible to psychiatric illness and its
sequelae.2,29
2.2.5. Neuro-imaging and other studies

Neuro-imaging studies are rarely used alone in making a psychiatric diag-
nosis. However, computerized tomography (CT) and nuclear magnetic reso-
nance imaging (MRI) can reveal structural brain abnormalities and lesions,
including evidence of infection, cerebrovascular events, trauma, malig-
nancy, or multiple sclerosis. Newer technology such as positron emission
tomography (PET), functional MRI (fMRI), and single photon emission
computed tomography (SPECT) are most useful in research but are not used
diagnostically at this time. Further research will likely allow these neuro-
imaging studies to be of greater use diagnostically and in clinical settings.2
Polysomnography may be useful diagnosis for patients in whom a cli-
nician suspects sleep disorders such as obstructive sleep apnoea or
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narcolepsy. Certain seizure disorders, like temporal lobe epilepsy and

partial complex seizures, may present with psychiatric symptoms.
Electroencephalograms (EEGs) may be indicated if a seizure disorder is
suspected or can be useful in distinguishing delirium from dementia.
Electrocardiograms (EKGs or ECGs) may be indicated for some patients
when there are concerns regarding cardiac condition status or cardiac side
effects of medications including tricyclic antidepressants and antipsychot-
ics. A lumbar puncture may be necessary to investigate the possibility of
a central nervous system (CNS) infection. A chest X-ray may be useful to
evaluate cardiopulmonary problems in delirium.2,16
2.2.6. Psychological testing

Psychological testing is best employed when it complements a thorough
psychiatric interview and appropriate history taking. The role of psycho-
logical testing in psychiatric diagnosis includes evaluation of intelligence,
personality, psychopathology, and psychological and neuropsychological
functioning. Such psychological testing can be objective or projective.
Objective tests are self-report and are generally designed to quantify and
clarify. Projective testing is much less structured than objective psycho-
logical testing and much more open to interpretation.29 When to request
psychological testing and which tests to recommend is based on clinical
judgment. More details on this type of testing can be found in Chapter 6.
2.2.7. Psychiatric rating scales and diagnostic interviews

Psychiatric rating scales are most commonly used in research; however,
they can also aid clinicians in making a diagnosis, measuring a patient’s
social or occupational functioning, and monitoring changes in symptoms
or side effects of medications over the course of treatment. Rating scales
can provide a means to quantify severity of symptoms and response to
treatment. Rating scales vary in their reliability and validity and can have
biases. As such, rating scales can augment diagnosis or treatment plan-
ning, but should not be used alone.2
Rating scales used in psychiatry can be self-rated or clinician-rated.
Clinician-rated scales that are given by the clinician are generally more
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reliable than self-rated scales, which are completed by the patient. Self-rated
scales can be efficient screening tools. Examples of commonly used clinician
rating scales include the Mini-Mental Status Examination (MMSE), Brief
Psychiatric Rating Scale (BPRS), Hamilton Rating Scale for Depression or
Anxiety (HAM-D or HAM-A), Yale-Brown Obsessive-Compulsive Scale
(YBOCS), Young Mania Rating Scale (Y-MRS), Global Assessment of
Functioning (GAF), and the Abnormal Involuntary Movement Scale (AIMS).
Examples of commonly used self-rating scales include the Beck Depression
Inventory (BDI) and the CAGE Questionnaire to assess alcohol problems.29
Structured clinical interviews were developed due to concerns regard-
ing the unreliability of psychiatric diagnosis and the different conceptual-
izations of mental disorders from different cultures. Structured clinical
interviews greatly increase inter-rater reliability and are of great use in
research.17,29
The Structured Clinical Interview for DSM-IV (SCID) is the most
commonly used structured diagnostic interview in psychiatry. It is a semi-
structured interview that applies the DSM-IV criteria to the patient. The
SCID can take upto two hours to complete and is used almost exclusively
in research. The Mini-International Neuropsychiatric Interview (MINI) is
a shorter, focused diagnostic interview for psychiatric diagnosis included
in the DSM-IV and ICD-10. The MINI can be administered in 15–30 min
and is used in research, clinical trials, and epidemiologic studies and may
be of use in clinical settings.29
3. HOW ARE PSYCHIATRIC DIAGNOSES CLASSIFIED?

Psychiatry is the only medical specialty that has so meticulously ordered,
formalized, and manualized its diagnostic processes and criteria. Because
psychiatric diagnosis relies so heavily upon patient presentation and
history and because we lack full understanding of the underlying etiolo-
gies of most mental disorders, this structure and formality are necessary.
3.1. Categorical versus etiological

Current psychiatric diagnostic systems, including the DSM and ICD
(which will be discussed in detail in the following pages), are constructs
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based on expert opinion derived from collective clinical experiences and

not necessarily pathophysiology or cause. A diagnosis is made by match-
ing a patient’s presentation with the diagnostic criteria, which are com-
posed of these categorized collections of signs and symptoms that have
been gathered together as a disorder.
3.2. Reliability and validity in psychiatric diagnosis

Our current classification systems were designed for improved diagnostic
reliability. Reliability refers to the consistency and repeatability in clini-
cians making the same diagnosis on the same patient. On the basis of
measures of inter-rater reliability, the diagnosis of several major psychiat-
ric disorders is generally on a par with diagnosis in other medical special-
ties and considered to be very good.5,24 Structured clinical interviews have
also greatly improved the reliability of psychiatric diagnosis.17
Because our current classification systems are based on subjective,
consensus categorizations, they are diagnostically reliable but lack valid-
ity. Defining validity can be complicated. In psychiatry, the concept of
diagnostic validity can be applied to our ability to predict prognosis,
outcome, response to treatment, and etiology.5
Attempts to improve diagnostic validity can be traced back to Robins
and Guze’s criteria for establishing validity in psychiatric diagnosis in
1970. These criteria included (1) distinct clinical description (including
symptom profiles, demographic characteristics, and typical precipitants);
(2) laboratory studies (including psychological tests, radiology, and post-
mortem findings); (3) delimitation from other disorders (by means of
exclusion criteria); (4) follow-up studies showing a characteristic course
(including evidence of diagnostic stability); and (5) family studies show-
ing familial clustering. These criteria were highly influential in forming
the basis of the DSM and ICD classification systems.17 Kendler in 1980
elaborated on psychiatric diagnostic validity criteria by differentiating
antecedent validators (comprising familial aggregation, premorbid per-
sonality, and precipitating factors), concurrent validators (which includes
psychological tests), and predictive validators (including diagnostic
consistency over time, rates of relapse and recovery, and response to
treatment).17
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A distinct challenge in using diagnostic stability and consistency longi-

tudinally to test the validity of psychiatric diagnosis is that many psychi-
atric diagnoses change in presentation and evolve over time.6 For example,
what may appear as a major depressive disorder proves to be bipolar dis-
order over the years. Likewise, an acute stress reaction can become post-
traumatic stress disorder, schizophreniform disorder can evolve into
schizophrenia, and bereavement may become a major depressive episode.
In regards to substances, patients may move diagnostically in the realms
of intoxication to abuse to withdrawal to dependence. The difficulty is that
often as diagnosticians we are provided with “freeze frame” signs and
symptoms and we instead need the “movie” that is a patient’s life to truly
see the full picture and nature of the mental illness in order to make an
accurate diagnosis.
In 1995, Nancy Andreasen suggested several additional diagnostic
validators including molecular genetics and molecular biology, neuro-
chemistry, neuroanatomy, neurophysiology, and cognitive neuroscience.
These validators are all potentially capable of relating symptoms and
diagnoses to their biologic basis.17 In time, such biologic validators could
make the limitations regarding diagnostic validity on the basis of diag-
nostic stability obsolete. Future editions of the DSM and ICD will con-
tinue to evolve and incorporate new knowledge to improve diagnostic
validity.
4. CURRENT CLASSIFICATION SYSTEMS

The two most commonly utilized psychiatric diagnostic classification
systems in existence currently are the International Classification of
Diseases, Tenth Edition (ICD-10) and the Diagnostic and Statistical
Manual, Fourth Edition, Text Revision (DSM-IV-TR). Both systems will
be discussed in detail to better understand their historical inception and
evolution, as well as how they are used in making psychiatric diagnoses.
Other classification systems include the Chinese Classification of Mental
Disorder (CCMD-2-R and CCMD-3), the Latin American Guide for
Psychiatric Diagnosis, the Japanese Clinical Modification of ICD-10 and
other Asian developments, and the Cuban Glossary of Psychiatry (GC-3).
Many of these systems are based on cultural distinctions.
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4.1. The international classification of diseases (ICD)

The International Classification of Diseases (ICD) has become a system
developed collaboratively between the World Health Organization (WHO)
and 10 international centers so that medical terms reported by physicians,
medical examiners, and coroners on death certificates can be grouped
together for statistical purposes.10 The ICD provides diagnostic codes and
descriptions for the classification of diseases and other health problems. It
is used in epidemiological studies and clinical settings and for health man-
agement purposes. The origins of the ICD can be traced back to the 1700s.
Since 1900, the ICD has been modified about once every 10 years. The
last interval, however, between the revision of ICD-9 and ICD-10, was
20 years.
In 1785, William Cullen (1710–1790) helped write and establish a clas-
sification of disease titled Synopsis Nosologiae Methodicae. This classifi-
cation system attempted to estimate the proportion of causes of mortality
during that era. Despite its crudity, it appeared to be statistically relevant.
In 1837, William Farr, the first medical statistician in the General Register
Office of England and Wales, found the Synopsis to be a helpful resource
and wanted to improve medical classification to make it more universal
and usable internationally. Farr noticed that the Synopsis Nosologiae
Methodicae had not been revised since Cullen had originally implemented
it, so in 1853 he convened the first International Statistical Congress in
Brussels, Belgium. The Congress wanted to create a system that could be
used internationally for classification of diseases and deaths. It met again
in 1855, 1864, 1874, 1880, and 1886. Eventually, a classification origi-
nated on the basis of Farr’s proposal of classifying diseases by anatomical
site. The classification was named the International List of Causes of
Death.31
In 1891, the International Statistical Institute, originally known as the
International Statistical Congress, held its meeting in Vienna. A commit-
tee led by Jacques Bertillon, Chief of Statistical Services of the City of
Paris, was formed to prepare a uniform classification of the causes of
death to present to the International Statistical Institute in Chicago in
1893. The Bertillon Classification of Causes of Death was adopted
by several countries and cities and was revised every 10 years thereafter.
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The first International Conference for the Revision of the Bertillon or

International List of Causes of Death was convened in 1900 in Paris.
Revisions followed in 1909, 1920, 1929, and 1938.31
Jacques Bertillon died in 1923, and with his death the conference was
left without a leader. Recognizing that the classification was left without
a guiding force, an international commission, known as the Mixed
Commission, was created to continue the work on the revisions and drafts
of the International List of Causes of Death. This Commission helped
draft the proposals for the fourth (1929) and the fifth (1938) revisions.31
In July 1946 in New York City, the International Health Conference
was held. A new committee was appointed by the Interim Commission of
the World Health Organization, called the Expert Committee for the
Preparation of the Sixth Decennial Revision of the International Lists of
Diseases and Causes of Death. The Committee reviewed all previous clas-
sifications, including a proposal set forth by the United States Committee
on Joint Causes of Death. It determined that a resulting classification
system was justified, and in April 1948 the International Conference for
the sixth revision of the International Lists of Diseases and Causes of
Death was convened. The Conference adopted the classification system.
This was an important watershed for international health. For the first
time, the conference linked national statistical institutions and the World
Health Organization to cooperate on further endeavors. It was also a
milestone in psychiatry, because the sixth revision of the International
Statistical Classification of Diseases included a section on mental disor-
ders for the first time.31
The seventh and eighth revisions were held in 1955 and 1965 in Paris
and Geneva. During these years, the acceptance and integration of the
International Classification of Diseases grew rapidly worldwide.31
In 1975 in Geneva, the International Conference for the ninth revision
of the International Classification of Diseases was convened by the World
Health Organization. Although major revisions were suggested, previous
changes had shown that each time revisions were needed, expensive sys-
tems also needed to be implemented to help with the revisions. Therefore,
the final proposals encouraged acceptance of the basic structure of the
ICD, but with additional details at the level of the four-digit subcategories
and even some optional five-digit subdivisions.31
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In 1999 the objectives for development of the tenth version were to

develop a new procedure coding system, improve accuracy and efficiency
of coding, reduce training efforts, and improve communication with phy-
sicians. Other essential characteristics included completeness, a unique
code for all substantially different procedures, expandability, a system
structure that allowed incorporation of new procedures as unique codes,
standard terminology, and the adoption of a multiaxial system.21 Besides
these objectives and characteristics, ICD-10 distinguishes itself from
ICD-9 by its diagnostic detail comprising about 8,000 categories in com-
parison to the ICD-9’s 4,000 categories.31
The most relevant chapter used by psychiatrists and mental health pro-
viders internationally is ICD-10, Chapter V: Mental and Behavioral
Disorders. When making a psychiatric diagnosis using the ICD system, a
multiaxial approach consisting of three axes is utilized: Axis I, Clinical
diagnosis; Axis II, Disabilities; and Axis III, Contextual factors.
Clinical diagnosis on Axis I incorporates all possible considerations for
psychiatric diagnosis from ICD-10, Chapter V (see Table 1). Disabilities
on Axis II are rated according to the “WHO-Disability Diagnostic Scale”
(WHO-DDS) (see Table 2). Contextual factors on Axis III comprise
“Environmental/Circumstantial and Personal Lifestyle/Life Management
Factors” that are selected from a prepared list, which consists of 11 cate-
gories with a total of 85 items related to childhood and upbringing, educa-
tion, family support, social and economic circumstances, lifestyle, life
management difficulties, and physical disabilities.22
4.2. The Diagnostic and Statistical Manual of Mental Disorders

The first Diagnostic and Statistical Manual of Mental Disorders was pub-
lished in 1952 by the American Psychiatric Association and is used pri-
marily in the United States as a classification system of mental disorders.
There have been five major revisions (I, II, III, IIIR, and IV). Similar to
the International Classification of Diseases, the DSM was first established
to collect statistical information for mental disorders.13
In 1840, an attempt was made by the US census to collect statistical
data regarding individuals classified with “idiocy/insanity,” which was the
single category used at that time. In 1880, during the annual census, the
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Table 1. Diagnostic categories.
ICD-10
F00–F09 Organic, including symptomatic, mental disorders.
F10–F19 Mental and behavioral disorders due to psychoactive substance use.
F20–F29 Schizophrenia, schizotypal, and delusional disorders.
F30–F39 Mood (affective) disorders.
F40–F48 Neurotic, stress-related, and somatoform disorders.
F50–F59 Behavioral syndromes associated with physiological disturbances and physical
factors.
F60–F69 Disorders of adult personality and behavior.
F70–F79 Mental retardation.
F80–F89 Disorders of psychological development.
F90–F98 Behavioral and emotional disorders with onset usually occurring in childhood
and adolescence.
F99 Unspecified mental disorder.
DSM-IV-TR
1. Disorders usually first diagnosed in infancy, childhood, or adolescence.
2. Delirium, dementia, and amnestic and other cognitive disorders.
3. Mental disorder due to general medical condition.
4. Substance-related disorders.
5. Schizophrenia and other psychotic disorders.
6. Mood disorders.
7. Anxiety disorders.
8. Somatoform disorders, factitious disorders, dissociative disorders.
9. Sexual and Gender Identify Disorders.
10. Eating disorders.
11. Sleep disorders.
12. Impulse — control disorders not elsewhere classified, adjustment disorders.
13. Personality disorders.
14. Other conditions that maybe a focus of clinical attention.
categories were expanded to include mania, melancholia, monomania,

paresis, dementia, dipsomania, and epilepsy. In 1917, a Committee on
Statistics, from what is now known as the American Psychiatric Association
(APA), together with the National Commission on Mental Hygiene, devel-
oped a new guide for mental hospitals called the Statistical Manual for the
Use of Institutions for the Insane, which included 22 diagnoses.13 In 1943,
a new classification system was developed called Medical 203 and issued
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Table 2. WHO Disability Diagnostic Scale (WHO-DDS) for Axis II of ICD-10.
1) Global rating
This rating should represent the best estimate of the degree of dysfunction-in relation
to the maximum level of expected functioning in the sociocultural context of the
patient. The rating should be made regardless of whether the dysfunction is due to
somatic or psychiatric conditions, but the main reason for dysfunction should also
be indicated, i.e. mainly psychiatric, mainly somatic, both somatic and psychiatric.
2) Ratings of specific areas of functioning
A. Personal care and survival.
B. Occupational functioning: performance of expected role as remunerated workers,
student, or homemaker.
C. Functioning with family: interaction with spouse, parents, children, and other
relatives.
D. Broader social behavior (functioning in other roles and activities): interaction
with other individuals and the community at large, leisure activities.
Please use all available information (case notes, reports from relatives or staff, observation,
and interview of patient) in making global and specific ratings of dysfunction.
Rating Scale
Rate global and specific areas of functioning (A–D) using any of the values from 00–99,
including intermediate values. The following anchor values and definitions are
provided to facilitate rating:
00 No dysfunction: The patient’s functioning conforms to the norms of his/her reference
group or sociocultural context.
20 Minimum dysfunction: Deviation from the norm in one or more activities/roles is
present. The disturbances are minor but persist over the time period. More conspicuous
dysfunctions may appear for very short periods. E.g. one or two days.
40 Obvious dysfunction: The deviation from the norm is conspicuous, and dysfunctions
interfere with social adjustment. Dysfunction in at least one activities/role persists nearly
all the time. More severe dysfunction may appear only for a few days.
60 Serious dysfunction: Deviations from the norm are marked in most activities/roles
and persist more than half the time.
80 Very serious dysfunction: Deviation in all areas is very severe and persists nearly all
the time. Action by others to remedy or control the dysfunction might be required
(according to the rater’s judgment), but it does not need to have taken place in order
to make this rating.
99 Maximum dysfunction: Deviation from the norm has reached a crisis point. A clear
element of danger to the patient’s own existence or social life and/or to the lives of
others may be present. Some form of action or social intervention is necessary.
XX Not applicable (please state reason on coding sheet).
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as a “War Department Technical Bulletin.” It was used primarily by the

Armed Forces and Veterans Administration as a classification system for
mental illnesses that were seen during World War II. In 1950, an APA
Committee on Nomenclature and Statistics reviewed Medical 203, the VA
system, and the Standard’s Nomenclature. It disbursed these documents to
approximately 10% of APA members, of which 46% replied. Of these
46%, 93% approved the documents, which became the Diagnostic
and Statistical Manual first published in 1952.15 The original manual was
130 pages and listed 106 mental disorders.14
In 1968 both the ICD and the DSM were revised, and the APA was
closely involved in both revisions. This second version of the DSM listed
182 disorders and was 134 pages long.19 A diagnostic debate evolved
regarding DSM-II’s classification of homosexuality as a mental disorder.
This controversy led to protests by gay activists at the APA annual confer-
ences from 1970 to 1973. When the seventh printing of the DSM-II was
completed in 1974, homosexuality by itself was removed as a disorder and
replaced with Sexual Orientation Disturbance. The third edition of DSM
defined Sexual Orientation Disturbance as homosexual persons who were
disturbed by, in conflict with, or wishing to change their sexual orientation
and who were seeking help to be heterosexual. This controversial
diagnosis was later renamed and is presently referred to as Gender Identity
Disorder (GID).27
In 1974, it was decided to create a DSM whose nomenclature was more
consistent with the International Statistical Classification of Diseases.
Thus, DSM-III sparked international interest and was eventually trans-
lated into 13 languages.27 The decision was made to also make it less
psychodynamically oriented and more research based. Research showed
that psychiatric diagnoses differed significantly between Europe and the
United States; thus the impetus was to create diagnoses that were more
standard in practice, uniform, and valid across cultures.26 The DSM-III
was considered to be much more reliable than previous versions in diag-
nosing psychiatric disorders. The final draft of the DSM-III was published
in 1980. It was 494 pages long and had 265 diagnostic categories.19
Included in the DSM-III revision was the creation of a “multiaxial”
system. The DSM organizes psychiatric diagnosis into five axes, whereas
the ICD organizes categories into three axes (see Tables 1, 3, and 4).
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Table 3. Contributing psychosocial and environmental problems for Axis IV of the

DSM-IV-TR.
Problems with primary support group: e.g. death of a family member, health problems
in family, disruption of family by separation, divorce, or estrangement; removal from
the home; remarriage of parent; sexual or physical abuse; parental overprotection;
neglect of child; inadequate discipline; discord with siblings; birth of a sibling.
Problems related to the social environment: e.g. death or loss of a friend; inadequate
social support; living alone; difficulty with acculturation; discrimination; adjustment
to life-cycle transition (such as retirement).
Educational problems: e.g. illiteracy; academic problems; discord with teachers or
classmates; inadequate school environment.
Occupational problems: e.g. unemployment; threat of job loss; stressful work schedule;
difficult work conditions; job dissatisfaction; job change; discord with boss or
co-workers.
Housing problems: e.g. homelessness; inadequate housing; unsafe neighborhood; discord
with neighbors or landlord.
Economic problems: e.g. extreme poverty; inadequate finances; insufficient welfare
support.
Problems with access to health care services: e.g. inadequate health care services;
transportation to health care facilities unavailable; inadequate health insurance.
Problems related to interaction with the legal system/crime: e.g. arrest; incarceration;
litigation; victim of crime.
Other psychosocial and environmental problems: e.g. exposure to disasters, war, or other
hostilities; discord with non-family caregivers such as counselor, social worker, or
physician; unavailability of social services agencies.
Unlike the ICD, the DSM separates mental disorders, personality disor-
ders, mental retardation, and medical conditions into distinct axes: Axis I:
Clinical disorders, including major mental disorders and learning
disorders; Axis II: Personality disorders and mental retardation; Axis III:
Acute medical conditions and physical disorders; Axis IV: Psychosocial
and environmental factors contributing to the disorder; Axis V: Global
Assessment of Functioning.
DSM-IV was published in 1994, had 886 pages, and listed 297 disor-
ders. To develop DSM-IV, the APA appointed a task force to significantly
revise the DSM-III. The committee of 27 individuals created 13 work
groups of 5–16 members each. Each work group had approximately
20 advisors and underwent a three-step process. First, they would conduct
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Table 4. Global assessment of functioning (GAF) rating scale for Axis V of the
DSM-IV-TR.
100–91: Superior functioning in a wide range of activities, life’s problems never seem to
get out of hand, is sought out by others because of his or her many positive
qualities. No symptoms.
90–81: Absent or minimal symptoms (e.g. mild anxiety before an examination), good
functioning in all areas, interested and involved in a wide range of activities,
socially effective, generally satisfied with life, no more than everyday problems
or concerns (e.g. an occasional argument with family members).
71–80: If symptoms are present, they are transient and expectable reactions to
psychosocial stressors (e.g. difficulty concentrating after family argument);
no more than slight impairment in social, occupational, or school functioning
(e.g. temporarily falling behind in schoolwork).
61–70: Some mild symptoms (e.g. depressed mood and mild insomnia) OR some
difficulty in social, occupational, or school functioning (e.g., occasional
truancy, or theft within the household), but generally functioning pretty well,
has some meaningful interpersonal relationships.
51–60: Moderate symptoms (e.g. flat affect and circumstantial speech, occasional
panic attacks) OR moderate difficulty in social, occupational, or school
functioning (e.g. few friends, conflicts with peers or co-workers).
41–50: Serious symptoms (e.g. suicidal ideation, severe obsessional rituals, frequent
shoplifting) OR any serious impairment in social, occupational, or school
functioning (e.g. no friends, unable to keep a job).
31–40: Some impairment in reality testing or communication (e.g. speech is at times
illogical, obscure, or irrelevant) OR major impairment in several areas, such as
work or school, family relations, judgment, thinking, or mood (e.g. patient with
depression avoids friends, neglects family, and is unable to work; a child
frequently beats up younger children, is defiant at home, and is failing at
school).
21–30: Behavior is considerably influenced by delusions or hallucinations OR serious
impairment in communication or judgment (e.g. sometimes incoherent, acts
grossly inappropriate, suicidal preoccupation) OR inability to function in
almost all areas (e.g. stays in bed all day; no job, home, or friends).
11–20: Some danger of hurting self or others (e.g. suicide attempts without clear
expectation of death; frequently violent; manic excitement) OR occasionally
fails to maintain minimal personal hygiene (e.g. smears feces) OR gross
impairment in communication (e.g. largely incoherent or mute).
10–1: Persistent danger of severely hurting self or others (e.g. recurrent violence) OR
persistent inability to maintain minimal personal hygiene OR serious suicidal
act with clear expectation of death.
(Note: Use intermediate codes when appropriate, e.g. 45, 68, 72.).
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an extensive literature review of their diagnosis, then request data from

researchers, and finally conduct multicenter field trials relating the diag-
nosis to clinical practice. Major changes included the addition of the
phrase “clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning” to almost half of all cate-
gories. Also, Attention Deficit Hyperactive Disorder was characterized
and added to the DSM.12,25
In 2000, the DSM-IV was further revised and known as DSM-IV-TR,
“Text Revision.” Most of the information was unchanged, but sections
were updated to give extra information on each diagnosis and some of the
diagnostic codes were changed to maintain consistency with the ICD.4
The DSM is now undergoing major revisions, and the DSM-5 has an
expected release date of May 2013.3 Similar to the process of revisions from
the DSM-III, there are 13 work groups, representing different categories of
psychiatric diagnoses. They are reviewing the scientific research, consulting
with expert advisors, and conducting three phases of field trials to test some
of the proposed diagnostic criteria in real-world clinical settings. The fol-
lowing are examples of the draft revisions currently being entertained:
• A single category of “autism spectrum disorder” is recommended to

incorporate the current diagnoses of autistic disorder, Asperger’s dis-
order, childhood disintegrative disorder, and pervasive developmental
disorder.
• Another recommendation is to change the diagnostic term “mental
retardation” to “intellectual disability,” which is more compatible with
terminology used by other disciplines.
• Revisions are suggested to eliminate the current categories of sub-
stance abuse and dependence and replace them with a new category,
“addiction and related disorders.”
• A new category of “behavioral addictions” is proposed, in which gam-
bling will be the sole disorder.
• New suicide scales for adults and adolescents will be added.
• Binge eating disorder will be recognized as a specific diagnosis and
the criteria for anorexia nervosa and bulimia nervosa will be improved.
• A new diagnostic category of temper dysregulation with dysphoria
(TDD) will be made within the Mood Disorders section to help
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clinicians better differentiate children with these symptoms from

those with bipolar disorder or oppositional defiant disorder.3
• Because the five axes of DSM are not validated, they will be changed
in DSM-5 to use the multiaxial system of ICD-10.
5. CULTURAL ISSUES REGARDING PSYCHIATRIC

DIAGNOSIS
Psychiatric disorders are globally pervasive, and all societies have evolved
knowledge and practices to respond to the problems related to mental ill-
ness. Culture includes the entirety of the arts, customs, behaviors, sym-
bols, and beliefs transferred from generation to generation in a society.
Just as one’s cultural background can play a profound role in guiding an
individual’s thoughts, actions, and way of life, culture can also greatly
influence a patient’s psychiatric presentation, diagnosis, treatment, and
prognosis. The field of cultural psychiatry seeks to understand psychiatric
disorders from the perspective of these societal systems of meanings and
values.11,20,29
Although the field of psychiatry has been strongly influenced by its
Anglo–European history, current diagnostic systems acknowledge cul-
ture-bound syndromes which are found in specific settings and have a
special relationship to the setting. A few examples of such syndromes
include amok (sudden mass assault) among Malaysians, koro (genital
retraction) among Chinese, or susto (fright or soul loss) among Latinos.29
The DSM-IV attempts to acknowledge that a patient’s ethic and cultural
context must be considered in any evaluation for psychiatric illness. The
process, which is termed “cultural formulation,” includes (1) cultural
identity of the individual; (2) cultural explanations of the individual’s ill-
ness; (3) cultural factors related to psychosocial functioning; (4) cultural
elements of the relationship between the individual and the clinician; and
(5) overall cultural assessment for diagnosis care.20,29
6. OTHER PSYCHIATRIC CLASSIFICATION SYSTEMS

In light of limitations in the cultural competency of the ICD and DSM
systems, some countries have created their own systems of psychiatric
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diagnostic classification to better identify mental health concerns within

their specific cultural contexts. Just as the DSM could be considered the
US version of mental health classification, a few other countries have ver-
sions of classification systems that vary from the ICD and DSM. The four
most common adaptations include the Chinese Classification of Mental
Disorders (CCMD-2-R8 and CCMD-39), the Japanese Clinical Modi-
fication of ICD-10 and other Asian developments, the Cuban Glossary of
Psychiatry (CG-3), and the Latin American Guide for Psychiatric Diagnosis.
The Chinese Classification of Mental Disorders (CCMD) is published
by the Chinese Society of Psychiatry (CSP) and used in China for the
diagnosis of mental disorders. It is currently in its third revision and is
written in both Chinese and English.7 The first Chinese classification sys-
tem appeared in 1979, with the CCMD-1 first being published in 1981. It
was modified, and another version was released in 1984 (CCMD-2-R). The
latest version, CCMD-3, was published in 2001. A major difference
between the CCMD and the DSM and ICD includes the CCMD diagnosis
of neurasthenia as a more central diagnosis. Neurasthenia focuses on
somatic complaints in conjunction with fatigue or depressed feelings.
Neurasthenia is less stigmatizing than a diagnosis of depression in China
and fits well with the Chinese concept of disharmony of vital organs and
imbalance of qi as the causation of diseases. The CCMD also replaces
borderline personality disorder (DSM), or emotionally unstable personal-
ity disorder (ICD), with impulsive personality disorder. Diagnoses included
in the CCMD that are more specific to Chinese classification are mental
disorder due to qigong (a Chinese method of meditation, posture, and exer-
cise that has been linked to psychosis), koro (excessive fear of the genitals
shrinking), and mental disorders due to superstition or witchcraft.7,18,23,32
The Japanese Society for International Diagnostic Criteria in
Psychiatry (JSIDCP) also has a version of the ICD, labeled the
Japanese Clinical Modification of ICD-10 and other Asian develop-
ments. Similar to the Chinese system, there is a focus on neurosis that
is connected to predisposing personality traits and life events rather
than depression or mood disorders. Also, the term somatoform disorder
is avoided.20
The Cuban Glossary (GC) of Psychiatry, developed under the guiding
force of Havana University and the Havana Psychiatric Hospital, is in its
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third revision. The basic principles of ICD-10 are followed, as is the same
coding system. However, the GC-3 encourages diagnostic formulations
that are based on the use of all information available and allows experi-
enced clinicians to formulate diagnoses without strictly adhering to stand-
ard diagnostic criteria.20
The Latin American Guide for Psychiatric Diagnosis (GLDP) helps
clinicians from Latin America diagnose individuals that share a common
history, language, and way of dealing with life. These cultural differences
are felt to not be reflected in any other classification system, and thus the
GLDP was created for better psychiatric diagnosis in this particular subset
of individuals.20
7. FINAL THOUGHTS ON PSYCHIATRIC DIAGNOSIS

AND ITS FUTURE
As we have seen from the beginning of psychiatric diagnosis, immense
time, deliberation, and care have gone into the development and progression
of our current psychiatric diagnostic systems; likewise, time, consideration,
and compassion enter into the diagnosis and treatment of patients. We have
also seen that in psychiatric diagnosis, both content and context matters, and
as our neurobiological knowledge expands, our diagnoses and diagnostic
systems will have to grow to embrace these new insights in the framework
of our culturally diverse world. The current and future challenge for psychi-
atric diagnosis will be to not only incorporate all of our cultural, clinical,
and scientific understandings but also to be able to bring these insights to
our patients in diagnostically, therapeutically, and culturally sensitive ways.
8. KEY POINTS
• Due to our current lack of etiological understanding of most mental
illnesses, nearly all psychiatric conditions are considered disorders of
functioning or syndromes composed of patterns of signs and symp-
toms, and not diseases with specific causes.
• In psychiatry, it is atypical to find a single sign (observed objective
clinical finding) or symptom (subjective patient experience) that is
pathognomonic for a specific psychiatric disorder.
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• A psychiatric diagnosis functions as much more than just a “name” or

a “label.” It provides useful, concise information and facilitates com-
munication in clinical, educational, and research settings.
• When making a psychiatric diagnosis, the clinician needs to look at
the “complete picture,” which includes the biological, psychological,
social, and cultural aspects of the patient’s experience.
• Psychiatric interview, collateral information, laboratory testing,
neuro-imaging and other medical studies, psychological testing, psy-
chiatric rating scales, and diagnostic interviews can all provide vital
information for psychiatric diagnosis and patient care.
• Because our current classification systems are based on subjective,
consensus categorizations, they have good diagnostic reliability
(ability to make consistent and repeatable diagnoses) but not-so-good
diagnostic validity (ability to predict prognosis, outcome, response to
treatment, and etiology).
• The two most commonly utilized psychiatric diagnostic classification
systems currently in existence are the ICD-10 (International
Classification of Diseases, Tenth Edition) and the DSM-IV-TR
(Diagnostic and Statistical Manual, Fourth Edition, Text Revision).
• In light of limitations in the cultural competency of the ICD and DSM
systems, some cultures (including China, Japan, Cuba, and Latin
America) have created their own systems of psychiatric diagnostic
classification to better identify mental health concerns within their
specific cultural contexts.
9. SELF-ASSESSMENT
9.1. Which of the following would be important
in the evaluation of a 55-year-old woman who was
brought to a hospital by her family with new onset
manic and psychotic symptoms?
(A) Patient interview.
(B) Collateral information.
(C) A complete physical and neurologic examination.
(D) Structural neuro-imaging.
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New onset mania or psychosis in a 55-year-old is an atypical presentation

and raises concern for an underlying organic cause to her symptoms. She
requires a full medical workup, including a complete physical examina-
tion, laboratory testing (including, but not limited to, a CBC, CMP, thy-
roid studies, toxicology, and drug screens), and neuro-imaging, in addition
to the standard psychiatric interview and collection of information from
family members and previous medical or psychiatric treatment.
Answer: E
9.2. Which of the following is false regarding our current

psychiatric diagnostic classification systems — the
DSM-IV-TR and the ICD-10?
(A) They are considered reliable and valid.
(B) The diagnostic systems are based on expert opinion derived from col-
lective clinical experiences and not necessarily pathophysiology or
cause.
(C) They are works in progress and have undergone many revisions.
(D) Their cultural competency is questioned by some, and their diagnoses
may not generalize across all cultures.
(E) None of the above.
The DSM and ICD were designed to be diagnostically reliable; however,

they lack validity. Clinicians do their best with current knowledge, and as
pathophysiological understanding of psychiatric disorders increases, so
will clinicians’ ability to predict etiology, outcome, and response. Further
revisions of the DSM and ICD will incorporate these understandings to
improve the validity of the diagnostic systems.
Answer: A
9.3. Which of the following are true statements regarding

the function and meaning of a psychiatric diagnosis?
(A) A psychiatric diagnosis can feel validating to patients because the
construct can bring words to a patient’s experience.
(B) A psychiatric diagnosis can feel shameful to patients because of
cultural stigmas about mental illness.
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(C) A psychiatric diagnosis helps to improve communication and under-

standing in clinical, research, and educational environments.
(D) A psychiatric diagnosis can change over time.
Patients can have varied reactions to receiving a psychiatric diagnosis,

including relief, validation, hope, embarrassment, fear, or shame. Talking
to patients about their reactions is an important part of good psychiatric
care. Communication is a key role of any diagnosis and improves under-
standing across all settings. Due to changes in patient presentation, medi-
cal conditions, psychosocial situations, and classification systems, an
individual’s diagnosis may change over the course of time.
Answer: E
10. CASE STUDIES

10.1. Seeing patient and diagnosis in context
A 20-year-old male college student is brought to the hospital by the police
after he came to their station very agitated and reporting that he was being
“spied upon” and “manipulated” by his neighbors, who were trying to
control his thoughts with their video gaming system. He reports hearing
his neighbors commenting on his daily activities, laughing at him, and
saying he should be dead. These voices have been worse lately, but started
nine months ago. They are very upsetting, following him everywhere he
goes and making it difficult for him to sleep. He has used cannabis multi-
ple times daily for the past few months to calm down. He also admits that
he recently “borrowed” his roommate’s methylphenidate to study. He was
recently fired from his food service job because he got into a verbal fight
with a customer who he thought was talking about him. Collateral infor-
mation from family reveals that he was a “good kid” and excellent student
in high school. His grades have been progressively worsening in college,
and he has been increasingly withdrawn from friends and family. His par-
ents moved to the United States from the Caribbean nine years ago and he
feels isolated from their family back home. They were concerned about
his sadness and withdrawal, but because of financial difficulties and lack
of health care insurance they did not take him to a doctor sooner. Physical
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examination, blood work, and neuro-imaging were all within normal

limits. UDS was positive for cannabis and amphetamines.
This case illustrates how a multiaxial diagnostic system can help clini-
cians see the patient and his diagnosis in context. Using the DSM system, the
most likely diagnosis on Axis I is Schizophrenia — Paranoid Type as well as
possible Cannabis and Amphetamine Abuse. The onset of symptoms before
substance use makes Substance Induced Psychosis less likely; however, the
recent abuse of methylphenidate may be exacerbating his symptoms. He has
no diagnoses on Axis II or III. Numerous psychosocial and environmental
issues would be found on Axis IV, including educational, occupational, and
economic problems and problems related to social environment and access
to health care. On Axis V, his GAF would be 25. He was hospitalized on a
psychiatric unit and started on risperidone with good response.
10.2. Diagnosis changes over time

A 35-year-old single, unemployed woman comes to clinic, encouraged by
her parents, for advice on how to keep a job. She recently was fired as a
legal secretary because of difficulty working with the public and her co-
workers. She enjoyed filing and paperwork but found chatting with the
customers or making any change to her routine very difficult. Her co-work-
ers accused her of being aloof and rigid. When work would become over-
whelming, she would hide in a closet. She was treated for social anxiety as
a child. She stayed at home during college and completed a bachelor’s
degree by taking online classes. Now she lives alone with her cat. She is
content to have few friends but eats dinner with her family every weekend.
She has had a lifelong interest in trains and likes to memorize the schedules
of transit systems in cities she wants to visit. She has Type I Diabetes and
checks her blood sugars and takes her medication “precisely” as her doctor
tells her to. When telling her life story in chronological order, she is calm
but has poor eye contact, twirls her hair, and uses very proper grammar.
Using the DSM multiaxial system, the most likely Axis I diagnosis
is Asperger’s Syndrome. Her previous childhood diagnosis of Social
Anxiety is better accounted for by this diagnosis. No diagnosis would be
given on Axis II. Axis III contains Type I Diabetes. On Axis IV, she is
having difficulty with social and occupational issues. On Axis V, her cur-
rent GAF is 50, with the highest GAF in the previous year being 60. She
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was referred to vocational rehabilitation and given education on her diag-

nosis as well as local and online support groups.
10.3. A complete perspective of mental illness

A 40-year-old married computer programmer presents to clinic with
sadness, poor sleep, guilt, worthlessness, decreased appetite, poor concen-
tration, low motivation, and decreased energy that have been worsening
over the past eight months. He reports occasional, fleeting, passive death
wish but has strong religious beliefs and no wish to make his wife and
children suffer for his “mistakes.” His symptoms are causing him diffi-
culty in getting work done and being irritable at home. He denies any
manic episodes. He denies a specific trigger for the onset of his symp-
toms. Recent stressors include rumors of layoffs at work, his parents’
health issues, and debt. He had a similar episode after college and
responded well to a selective serotonin reuptake inhibitor. Several of his
siblings have depression, and his aunt has bipolar disorder. He has hyper-
tension, high cholesterol, and type II diabetes. Since he has been down, it
has been more difficult to exercise and maintain the diet his physician
recommended. He resumed his previous antidepressant with a good
response. His work performance improved, and he was promoted. His
blood pressure and glucose also improved.
This case illustrates how a multiaxial diagnostic system can help clini-
cians see a patient’s mental health from a complete perspective. Using the
DSM system, the diagnosis on Axis I is Major Depressive Disorder,
recurrent. He has no diagnoses on Axis II. Axis III contains hypertension,
hypercholesterolemia, and DM II. Psychosocial and environmental issues
found on Axis IV would be occupational and economic problems and
problems related to primary support due to the ailing health of his par-
ents. On Avis V, his GAF at the initial encounter was 60 and improved to
75 after treatment.
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Chapter 4
Psychiatric Genetics
Bhanu Prakash Kolla and David Mrazek
1. INTRODUCTION
There has long been an appreciation that psychiatric illnesses are herita-
ble. A century ago, Emil Kraepelin studied the family histories of patients
with schizophrenia and concluded that the siblings of patients with schiz-
ophrenia were at a greater risk of developing schizophrenia than the gen-
eral population. Early investigations in psychiatric genetics focused on
twin studies by comparing the concordance rates of illnesses between
monozygotic and dizygotic twins. Adoption studies explored the relative
contributions of genetic influences and the influence of family environ-
ment. As it became possible to identify specific genetic variations, linkage
and association studies were conducted. More recently, genome wide
association studies (GWAS) have become possible. The goal of these
genetic studies is to increase our understanding of psychiatric disorders in
order to enhance diagnosis, treatment, and prevention.
Reliably defining psychiatric diagnoses has been a major challenge.
The diagnostic criteria used to identify a case must include a clinically
relevant threshold that defines the diagnosis. A common example of the
problems that clinicians have in establishing a diagnosis is illustrated
in their difficulty in reliably defining a threshold of mania and hypoma-
nia that consistently differentiates bipolar disorder type I from bipolar
disorder type II.
59
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60 B. P. Kolla and D. Mrazek
1.1. Endophenotypes and intermediate phenotypes

Complex psychiatric disorders are the result of multiple genetic varia-
tions. The considerable heterogeneity of phenotypic features that are all
included within a broad diagnostic category further complicates the inter-
pretation of genetic studies.
One strategy for more reliably defining diagnostic phenotypes is to
define a subset of patients within a specific broad diagnostic category by
identifying an endophenotype. An endophenotype is a heritable, state
independent marker that is associated with an illness in the population.
The patients who are defined by having one of these markers are some-
times referred to as having an intermediate phenotype associate with a
broader phenotype. Endophenotypes or intermediate phenotypes can be
defined by their having a heritable behavioral trait such as neuroticism.
Alternatively, they may be defined by having a quantitative physiological
trait such as increased P300 event potential amplitude.
1.2. Heritability
Heritability is a measure of the genetic underpinnings of a disease and is
defined as the proportion of disease risk that can be attributed to genetic
factors. The establishment of the heritability of a condition provides a
measure of the degree to which a disorder is genetically determined. For
virtually all psychiatric illnesses, phenotypic expression depends on both
genetic vulnerability and environmental influences.
A common method used to calculate the heritability of a specific illness
is to determine the difference between the concordance rates in monozy-
gotic and dizygotic twin samples and then multiply this difference by 2.
For example, if the concordance rate in monozygotic twins is 50% and
the concordance rate in dizygotic twins is 20%, the heritability is 60%
(i.e. (50 − 20) × 2 = 60).
Alternatively, heritability can be mathematically calculated using
analysis of variance to determine a restricted maximum likelihood statistic
(REML). Given that heritability is an estimate of the genetic nature of an
illness at the level of a given population, a heritability estimate for one
population cannot be assumed to be correct for a different population.
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Psychiatric Genetics 61
1.3. Twin studies

The comparison of phenotypes between twin pairs provides a strategy
to assess the effects of the environment. Monozygotic twins share virtu-
ally all of their genes. In contrast, dizygotic twin pairs share approxi-
mately half of their genes. Although both types of twins share a similar
rearing environment, it has been demonstrated that parents treat
monozygotic twins in a somewhat more similar manner than they do
dizygotic twins.
Twin studies have shown that monozygotic concordance rates for all
psychiatric disorders are greater than dizygotic concordance rates.
However, both types of twins are more likely to have a more compromised
intrauterine environment and experience more delivery-related complica-
tions than singletons. Moreover, monozygotic male twins are more likely
to be more similar to each other than monozygotic female twins are to
each other because of the potential inactivation of different X chromo-
somes in the two female monozygotic twins.
1.4. Adoption studies

Adoption studies of the children of patients with psychiatric illnesses who
have been “adopted away” provide another method of evaluating the
influence of genetics and environment on the expression of phenotypes.
The children of parents with a psychiatric illness have a different, and in
all likelihood, less stressful family environment if they are adopted by
parents who do not have a psychiatric illness. If the rate of illness in these
adopted children is higher than that of similar controls, the inference
is that the expression of the illness is influenced by their genetic
vulnerability.
1.5. Linkage studies

Linkage analysis involves the study of families with one or more
affected children and is designed to identify specific gene variants that
are more frequently associated with a given phenotype. Once a chromo-
somal location has been detected by linkage analysis, the region
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adjacent to the marker can be examined to identify one or more possible

candidate genes.
Linkage studies are most useful when a disease is highly penetrant and
is the consequence of a variant in a single gene. Given that most psychi-
atric disorders have low penetrance and involve multiple genes, linkage
analyses have been less informative.
1.6. Association studies and genome wide association studies

Association studies are case-control studies that are designed to identify
genetic variations between patients with a specific illness and controls
without the illness. Single nucleotide polymorphisms (SNPs) are polymor-
phisms that are the result of a single nucleotide which is replaced by a
different nucleotide. The resulting variation may have functional implica-
tions. If a SNP occurs in the coding region of a gene, these polymorphisms
can lead to the substitution of an amino acid in the sequence (a missense
mutation), a premature termination of coding (a nonsense mutation), or no
change in the amino acid sequence (a silent mutation). A SNP can occur
in a non-coding region and still have functional implications.
A copy number variation (CNV) is defined as a variation that is at least
one kilobase in size (i.e. 1,000 nucleotides). A smaller deletion or inser-
tion of nucleotides is often referred to as an indel. A CNV can consist of
a large deletion, duplication, or insertion in one or more loci. CNVs can
disrupt structure, disrupt regulation, or have no effect. Like all genetic
variations, a CNV can be inherited or created “de novo” in an individual.
Some CNVs have been recognized for many years and are known to be
associated with behavioral phenotypes.
With the decrease in the cost of genotyping, genome wide association
studies (GWAS) have become a realistic method for investigating the
genetic basis of psychiatric disorders. Given that multiple comparisons are
made, a large patient and control sample must be analyzed to avoid
“chance findings.” The most basic objective of a GWAS is to identify
genetic variations that occur more frequently in patients than in controls.
The significance required has been calculated to be 5 × 10−8 in order to
account for multiple testing, given that more than one million SNPs and
CNVs are assessed in the analysis.
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2. THE GENETICS OF PREVALENT PSYCHIATRIC

ILLNESS
Virtually all psychiatric illnesses have a heritable component. In the case
of nearly every psychiatric illness, multiple genes contribute to the indi-
vidual’s overall genetic vulnerability. Therefore, it is relevant to define the
specific gene variants that play a role in the expression of symptoms. The
most well-studied genetic variants associated with the most prevalent psy-
chiatric illnesses will systematically be described in the following review.
Our evolving understanding of the function of these genes will be briefly
highlighted.
2.1. Alzheimer’s disease

Two major categories of Alzheimer’s disease (AD) have been described.
The early-onset form occurs in patients under the age of 65 years. The
early-onset form progresses rapidly and is associated with a strong family
history. This early-onset form may be the result of Mendelian autosomal
dominant variants in one of three genes that affect the metabolism of beta
amyloid precursor proteins. These three genes are the amyloid precursor
protein gene (APP), the presenilin 1 gene (PSEN1), and the presenilin 2
gene (PSEN2).
The late-onset form occurs after 65 years of age and progresses more
slowly. The late-onset form accounts for over 90% of the cases of AD. The
APOE gene codes for apolipoprotein E, which is a carrier protein that is
involved in the metabolism of amyloid precursor protein. The APOE gene
occurs in three forms: APOE2, APOE3, and APOE4. The APOE4 variant
is associated with an increased risk of developing AD.
Ten GWAS have identified additional genetic variations conferring an
increased risk for developing AD. One of the major candidate genes that
have been implicated on the basis of a GWAS is the GRB2-associated
binding protein 2 gene (GAB2). GAB2 codes for a scaffolding protein that
plays a role in various signaling pathways. Other candidates include the
galanin-like peptide gene (GALP) and the tyrosine kinase, non-receptor,
1 gene (TNK1). GALP codes for a galanin-like peptide that is overex-
pressed in patients with AD and reduces cholinergic neurotransmission.
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Current treatments try to improve cholinergic neurotransmission by

inhibiting acetylcholinesterase. TNK1 codes for a protein involved in
apoptosis.3
2.2. Alcohol use disorders

Alcohol Use Disorders (AUDs) include alcohol abuse and alcohol depend-
ence. Current diagnostic criteria result in patients with quite different
patterns of problematic drinking receiving the same diagnosis. This pro-
vides a clear challenge to defining a homogenous phenotype. Consequently,
studying endophenotypes such as patients with delirium tremens or with-
drawal seizures increases the possibility of identifying genes that influ-
ence the development of AUDs. Two well-studied clinical endophenotypes
defined by clinical characteristics are a flushing reaction after the con-
sumption of alcohol and having a high tolerance for alcohol. However, as
in all psychiatric diagnoses, strong cultural and environmental influences
affect the rates of alcohol consumption and alcohol addiction within a
given population.
Twin and adoption studies have demonstrated a genetic vulnerability
for the development of AUDs. The heritability of AUDs is estimated to be
between 40% and 60%.
A polymorphism in the acetaldehyde dehydrogenase 2 family gene
(ALDH2), which codes for acetaldehyde dehydrogenase, renders the
enzyme less functional and results in increased levels of aldehyde when
these individuals consume alcohol. The accumulation of aldehyde results
in unpleasant sensations and flushing, which is a deterrent to drinking
alcohol. In Asian populations, there is a higher incidence of ALDH2
alleles that produce less functional enzyme.
A decreased response to alcohol consumption is influenced by poly-
morphisms in genes involved in GABA transmission. Two of these genes,
the gamma-aminobutyric acid receptor, alpha 1 gene (GABA1) and the
gamma-aminobutyric acid receptor, alpha 6 gene (GABA6), are located
on chromosome 5. The more active long allele of the serotonin transporter
gene (SLC6A4) is also associated with a higher degree of response to
alcohol, which, in turn, is protective as a low level of response to alcohol
and is associated with an increased risk of developing AUDs. The Taq1A1
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allele (i.e. rs18004970), which historically has been thought to be within

the dopamine-2 receptor gene (DRD2), has recently been shown to be
located in the nearby ankyrin repeat kinase domain containing 1 gene
(ANKK1). The A1 allele of the Taq1A polymorphism has consistently
been associated with externalizing behaviors and increased risk for drug
and alcohol dependence.16
A recent genome wide association study of men who developed AUDs
at an early age identified two markers located on chromosome 2 at 2q35.
This region has been previously identified in a linkage study to be associ-
ated with low response to alcohol.20
2.3. Autism and other pervasive development disorders

Autistic spectrum disorders (ASDs) are characterized by problems in
three broad areas. Affected individuals exhibit deficiencies in social inter-
action; show repetitive, stereotyped behaviors; and have impairments in
communication.
The prevalence of autism is estimated to be 0.5%–1%. Boys are affected
4–5 times more frequently than girls. Autism is considered to be one of the
most heritable psychiatric disorders, with heritability rates reported to be
between 80% and 90%. The concordance rate in monozygotic twins
has been estimated to be as high as 90%, and the dizygotic twin concord-
ance rates have been reported to be between 23% and 37%. If parents
have one affected child, the risk of having another child with autism is
about 10%.4
Children with more severe autism are also more likely to have mental
retardation. Fragile X Syndrome occurs in 3% of patients with autistic
disorders. Autistic traits have been described in a number of single gene
disorders, such as tuberous sclerosis (20%), fragile X syndrome (25%),
phenylketonuria (10%), and Smith–Lemli–Opitz syndrome (50%). The
genetic abnormalities in these patients are hypothesized to result in some
of the feature characteristics of autism. However, the presence of severe
mental retardation and the presence of dysmorphic features differentiate
these patients from other patients with autism.
Many of the genes that have been associated with ASD are involved in
cell-to-cell communication, neuronal migration, and neurotransmission.
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A meta-analysis of linkage studies in autism has confirmed 7q31–36 to

be a region of interest. This region is close to three genes that could
potentially be involved with the phenotypic features of autism. The first is
a polymorphism of the forkhead box P2 gene (FOXP2) associated with
speech and language impairment, which is one of the cardinal features
of autism. The second is the reelin gene (RELN), which is involved in
neuronal migration and synaptogenesis. The third is the protein tyrosine
phosphatase, receptor-type, Z polypeptide 1 gene (PTPRZ1), which is
involved in embryogenesis.
A GWAS reported genetic variants at 5p14.1 and 5p15. Two genes, the
cadherin 9, type 2 gene (CDH9) and the cadherin 10, type 2 gene
(CDH10), are located close to 5p14.1 and are involved in calcium-
dependent, cell-to-cell junctions in the nervous system. The sema domain,
seven thrombospondin repeat, transmembrane domain, and short cytoplas-
mic domain, 5A gene (SEMA5A) is involved in axonal guidance and is
located near 5p15.8
Maternal duplications at 15q13 are found in up to 1% of patients with
autism. These copy number variations may result in an increased risk
for ASD.
2.4. Anxiety disorders

Anxiety disorders represent a broad class of illnesses that are defined by
the pattern of anxiety symptoms that result in impaired function.
Obsessive-compulsive disorder (OCD) and posttraumatic stress disorder
(PTSD) are also classified as anxiety disorders.
Anxiety disorders have a relatively low degree of heritability of 20%–
40%. Twin studies have revealed that the concordance rates for anxiety
disorders in monozygotic pairs are between 12% and 26%, and for dizy-
gotic pairs they are between 4% and 15%.
The short allele of the indel polymorphism of the serotonin transporter
gene (SLC6A4) has decreased activity due to a decrease in the production
of the serotonin transporter protein. This short allele has been associated
with harm avoidance as well as social phobias, PTSD, and OCD.
The OCD was associated with the val allele (i.e. guanine allele) of the
rs4680 variant of the catechol-O-methyltransferase gene (COMT). The
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COMT gene produces the COMT enzyme, which metabolizes dopamine,

epinephrine, and norepinephrine.
PTSD has been associated with the A1 allele of ANKK1, which is
located adjacent to DRD2 and is believed to modify the function of the
dopamine 2 receptor. PTSD is also associated with the rs380073 variant
of the FKBP5 gene, which regulates the glucocorticoid receptor.18
2.5. Schizophrenia
Schizophrenia is characterized by positive symptoms such as delusions
and hallucinations as well as negative symptoms such as apathy, abulia,
and lack of social interactions. Abnormalities in smooth pursuit eye move-
ments represent an endophenotype of schizophrenia that has been demon-
strated in both patients with schizophrenia and some of their family
members. Other endophenotypes of schizophrenia include reduced inhibi-
tion of P50 auditory-evoked potentials and P300 event-related potentials.
Schizophrenia has rates of heritability that have been estimated to be
between 73% and 90%. However, only a third of patients with schizophre-
nia have a positive family history. The rate of concordance between
monozygotic twins is approximately 50%, and the rate of concordance in
dizygotic twins is approximately 17%. Interestingly, the risk of an off-
spring of an unaffected twin developing schizophrenia is the same as the
risk of the offspring of the affected twin.
Several candidate genes have been associated with schizophrenia, and
some of these have also been associated with bipolar disorder (see
Table 1). A linkage study of a Scottish family with multiple members who
were diagnosed with schizophrenia identified a linkage site near the “dis-
rupted in schizophrenia” gene (DISC1). This finding was replicated in a
Finnish cohort and is a balanced translocation between chromosomes 1
and 11. DISC1 is involved in neurodevelopment and cAMP signaling.14
Association studies have identified the neuregulin 1 gene (NRG1) and
D-amino acid oxidase inhibitor gene (DAOA) as potential candidate
genes. Neuregulin regulates synaptic transmission, especially at the
excitatory glutamatergic system and inhibitory GABAergic system.
DAOA activates D amino acid oxidase, which oxidizes D-Serine, which,
in turn, is a co-agonist at NMDA glutamate receptors. This association
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Table 1. Genes that have been associated with schizophrenia and bipolar disease.
Associated Associated
with with Bipolar
Gene Abbreviation Schizophrenia Disorder
Disrupted in schizophrenia 1 DISC1 √ √
D-amino acid oxidase activator DAOA √ √
Neuregulin 1 NRG1 √ √
Zinc finger protein 804A ZNF804A √
Catechol-O-methyltransferase COMT √
Dystrobrevin binding protein 1 DTNBP1 √
Regulator of G-protein signalling 4 RGS4 √
Glutamate receptor, metabotropic 3 GRM3 √
Solute carrier family 6 SLC6A3 √
Brain-derived neurotrophic factor BDNF √
Glutamate receptor, ionotropic,
GRIN2B √
N-methyl D-aspartate 2B
Clock homolog CLOCK √
Glutamate receptor, ionotropic,
GRIK4 √
kainate 4
Calcium channel, voltage-dependent,
CACNA1C √
L type, alpha 1C subunit
Ankyrin 3, node of Ranvier
ANK3 √
(ankyrin G)
Aryl hydrocarbon receptor nuclear
ARNTL √
translocator-like
Aldehyde dehydrogenase 1 family,
ALDH1A1 √
member A1
Kruppel-like factor 12 KLF12 √
lends support to the glutamate hypothesis of schizophrenia. New pharma-

ceutical agents acting on the glutamatergic system are being explored to
treat schizophrenia.21
Other studies have reported variations of the dysbindin gene (DTNBP1),
the regulator of G protein signaling 4 gene (RGS4), and the glutamate
receptor 3 gene (GRM3) to be associated with schizophrenia. DTNBP1
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codes for a protein that is a component of the dystrophin associated pro-

tein complex. RGS4 codes for a GTPase activator that modulates trans-
mission at dopaminergic, glutamatergic, and muscarinic receptors. GRM3
is a metabotropic glutamate receptor that also modulates serotonergic and
dopaminergic transmission.9
A genome wide association study of patients with schizophrenia
reported an association with the zinc finger protein 804A gene (ZNF804A).
ZNF804A maps to chromosome 2 and is believed to have a role as a regu-
lator of gene expression.13
Evaluation of copy number variations in GWAS demonstrated an
increase in de novo CNVs in patients with schizophrenia. There appears
to be a 1.15 fold increase in low frequency CNVs (CNVs occurring in less
than 1% of the population) and a 1.6 fold increase in deletions of 500 kb
or more in patients with schizophrenia.22
Deletions in the 22q11 region that result in velo-cardio-facial syndrome
(VCF syndrome) are associated with an increased risk of developing
schizophrenia and bipolar disorder.2 VCF syndrome is associated with
cardiac and craniofacial abnormalities, as well as mental retardation. The
COMT gene and the proline dehydrogenase gene are located in the area
that is deleted.
Deletions at 1q21.1 and 15q13.3 are associated with an increased
odds ratio of developing schizophrenia of about 10. CNVs close to
the neurexin gene (NXRN1) have also been associated with a tenfold
increase in the risk of developing schizophrenia. Neurexin acts as a
receptor for neureglin and facilitates glutamatergic and GABAergic
neurotransmission.19
2.6. Bipolar disorder

Bipolar type I disorder has a heritability that is estimated to be between
79% and 90%. The concordance rate of monozygotic twins is about 40%,
and the concordance rate in dizygotic twins is about 5%. Family members
of patients are at a tenfold increased risk of developing bipolar disorder
than the general population. Family members are also at a threefold
increased risk of developing depressive disorders, which illustrates that
these two affective disorders share risk factors.
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A meta-analysis of linkage studies found evidence of linkage at 6q for

bipolar type I, and association studies of families have identified many
other possible candidate genes for bipolar disorders. Some of the genes
identified are similar to those identified in schizophrenia and point to a
shared genetic etiology. The disrupted in schizophrenia gene (DISC) iden-
tified in studies of families with schizophrenia is also associated with
bipolar disorder. This gene is involved in neurodevelopment and cAMP
signaling. Other genes associated with both bipolar disorder and schizo-
phrenia include the DAOA and the NRG1.
Other potential candidate genes that have been associated with bipolar
disorder include the dopamine transporter gene (SLC6A3), the brain-
derived neurotrophic factor gene (BDNF), and the NMDA glutamate
receptor, subunit 2B gene (GRIN2B). These candidate genes implicate
both dopamine and glutamate in the pathogenesis of bipolar disorder.
Recent evidence has pointed to the involvement of circadian rhythm
genes in bipolar disorder. Sleep deprivation is commonly associated with
relapse in bipolar disorder. A murine model characterized by frenetic
behavior can be created by the inactivation of the circadian rhythm gene
(CLOCK), which is involved in the maintenance of a normal circadian
rhythm. A variation of CLOCK has been shown to be associated with
bipolar disorder.17
A deletion on the kainite class ionotropic glutamate receptor gene
(GRIK4) on chromosome 11 has been found to reduce the risk of develop-
ing bipolar disorder. Post-mortem studies have found an increased expres-
sion of this glutamate receptor in the hippocampi of patients with a
deletion of GRIK4.1
A meta-analysis of the GWAS of bipolar disorder have indicated that
the alpha 1C subunit of the L-type voltage-gated calcium channel gene
(CACNA1C) and ankyrin-G gene (ANK3) are associated with bipolar
disorder. ANK3 codes for ankyrin-G, which codes for components of volt-
age gated sodium channels.6
Convergent functional genomic analysis combines data obtained from
GWAS, post-mortem studies of gene expression in brains of patients, and
animal models. Using this analytic strategy, four candidate genes were
shown to have a role in the pathogenesis of bipolar disorder. The first
gene was the aryl hydrocarbon receptor nuclear translocation-like gene
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(ARNTL), which is involved in the regulation of circadian rhythm gene.

The second gene was the brain-derived neurotrophic factor gene (BDNF),
which codes for a growth factor. The third gene is the aldehyde dehydro-
genase 1 family, member A1 gene (ALDH1A1), which is implicated in
brain development. The fourth gene is the Kruppel-like factor 12 gene
(KLF12), which is a zinc finger protein transcription repressor in mice.12
2.7. Attention deficit hyperactivity disorder

Attention deficit hyperactivity disorder (ADHD) is characterized by dis-
ruptions in attention, hyperactivity, and impulsivity. ADHD is also associ-
ated with a disruption in executive function. About a third of children with
ADHD continue to have symptoms into adult life. Hyperactivity appears
to subside, but inattentive symptoms are more likely to continue.
Rates of ADHD have been estimated to be as high as 9% in the United
States, and in Europe the rates are estimated to be around 1%. This dispar-
ity has been suggested to reflect differences in diagnostic practices. ADHD
is a highly heritable disorder, with heritability estimates of 70%–80%. The
heritability rate of hyperactivity and impulsive symptoms are higher than
the heritability of inattention symptoms. A meta-analysis of linkage studies
has identified a region on chromosome 16 to be associated with ADHD.23
Candidate gene studies have identified individual genetic variations
that are associated with an increased risk for the development of ADHD.
Four dopamine-related genes associated with ADHD are the dopamine D4
receptor gene (DRD4), the dopamine D5 receptor gene (DRD5), the dopa-
mine transporter gene (SLC6A3), and the dopamine hydroxylase gene
(DBH). Additionally, two serotonin-related genes, the serotonin trans-
porter gene (SLC6A4) and the serotonin 1B receptor gene (HTR1B),
have repeatedly been associated with ADHD. Finally, the synaptosomal-
associated protein gene (SNAP-35) has been reported to be associated
with ADHD and comorbid depression.5
The GWA studies in ADHD have identified four additional candidate
genes. The first gene is the cadherin 13, H-cadherin, heart gene (CDH13),
which codes for a protein involved with cell-to-cell adhesion. The second
gene is the solute carrier family 9, sodium/hydrogen exchanger, member
9 gene (SLC9A9), which codes for a sodium and hydrogen exchanger.
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The third gene is the nitric oxide synthase 1, neuronal gene (NOS1),
which is involved in nitric acid synthesis and has been associated with
aggression and impulsivity. Nitric oxide is a second messenger that is
involved in both dopaminergic and serotoninergic neurotransmission. The
fourth gene is the cannabinoid receptor 1, brain gene (CNR1), which
codes for the endogenous cannabinoid receptor.7
2.8. Anorexia nervosa

Anorexia nervosa (AN) is characterized by weight at least 15% below the
norm, body image disturbances, and hormonal sequelae. Patients with
anorexia have significant morbidity and mortality.
Anorexia nervosa has a significant degree of heritability, although there
is considerable variability in the estimates of this heritability. AN with an
onset between ages 14 to 18 years appears to be more heritable than AN
developing before age 14.
Anorexia nervosa has been linked to many gene variations. The
1438G-A (i.e. rs6311) polymorphism of the 5-HT2A receptor gene, which
is associated with increased serotonergic function, has been linked to an
increased risk of developing AN. Similarly, a repeat polymorphism of the
norepinephrine transporter gene (SLC6A2) in the promoter region has
been reported to double the risk of the restricting type of AN.15 Finally, the
66 Met variant of the brain-derived neurotrophic factor gene (BDNF)
has been associated with an increased risk of developing the restricting
type AN.
2.9. Major depressive disorder

Major depressive disorder occurs in 10%–25% of women and 5%–12% of
men. It is characterized by negative cognitions, neuro-vegetative symp-
toms, and suicidal thoughts and behavior.
Heritability rates for major depression vary by the age at the time of
onset of depressive symptoms. The heritability rates are highest for
depression that begins during adolescence. The rates for depressive disor-
ders that arise in this age group are between 30% and 40%. The heritabil-
ity rates for depressive disorders that arise in childhood are lower.
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The short allele polymorphism of the indel promoter polymorphism of

SLC6A4 has been associated with reduced function of the transporter
that is believed to increase levels of serotonin in the synapse. Although
stressful life events have been associated with an increased risk of devel-
oping depressive disorders, such risk may primarily be true for individu-
als with the less active polymorphism of the serotonin transporter gene.
A developmental cohort study has shown an increased predisposition to
developing depressive disorders following exposure to trauma primarily
in children with the short allele. Some studies have also shown a dose
response relationship between the short allele and the severity of depres-
sion. Those with two copies of the short allele were at a greater risk than
those with one copy. Individuals with two copies of the long allele
appear to be least at risk. A large meta-analysis has confirmed this
association.10
Polymorphisms of the brain-derived neurotrophic factor gene (BDNF)
are also associated with depression. BDNF supports neuronal survival and
promotes growth and differentiation. The met allele at codon 66 is associ-
ated with reduced secretion of BDNF and higher symptom scores for
depression.
A GWAS of the STAR*D sample identified some genes that reached
modest significance, including the ATPase, H+ transporting, lysosomal
56/58kDa, V1 subunit B2 gene (ATP6V1B2), the Sp4 transcription factor
gene (SP4), and glutamate receptor, metabotropic 7 gene (GRM7).
ATP6V1B2 codes for a protein that is part of a proton pump ATPase.
This protein performs receptor mediated endocytosis and maintains a pro-
ton gradient across synaptic membrane vesicles. SP4 encodes for zinc
finger transcription factor. GRM7 codes for glutamate receptor 7. Glutamate
is an excitatory neurotransmitter, and glutamate receptor 7 agonists have
antidepressant-like effects in murine models. GRM7 gene was also found
to be associated with affective disorders in other GWAS.11
3. CONCLUSION
The ability to obtain extensive genotypic information and the expansion
of international collaborations of researchers has resulted in a rapid
advance in our understanding of psychiatric genetics. These advances
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have brought the possibility of genetic testing of patients to ascertain risk

and prognosis closer to practical applications. Genetic studies also have
the potential to contribute to evolution of the nosology of psychiatric dis-
orders. The field of psychiatric genetics will continue to progress even
more rapidly as entire genomes of informative patients are sequenced.
With the evolution of our understanding of the genetic basis of psychiatric
disorders, more effective treatments will be developed that will ultimately
result in better clinical care.
4. SELF-ASSESSMENT
4.1. The parents of a four-year-old boy who was recently
diagnosed with autism want to have another child and are
worried about the next child also having autism. There
is no family history of autism of which they are aware.
The chromosomal analysis of their first child did not reveal
any abnormalities. What is the best estimate of the
likelihood that their second child will develop autism?
(A) 1%.
(B) 10%.
(C) 25%.
(D) 50%.
(E) 66%.
Autism has heritability rates reportedly between 80% and 90% and is one
of the most heritable psychiatric disorders. Parents with one affected child
have about a 10% risk of having another child with autism.4
Answer: B
4.2. Which of the below genes is implicated in both

schizophrenia and bipolar disorder?
(A) DAOA.
(B) ZNF804A.
(C) CLOCK.
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(D) GRIK4.
(E) COMT.
One gene associated with both bipolar disorder and schizophrenia is

DAOA. ZNF804A is associated with schizophrenia, whereas a variation
of CLOCK has been shown to be associated with bipolar disorder.16
A deletion on GRIK4 on chromosome 11 has been found to reduce the
risk of developing bipolar disorder. COMT is associated with obsessive
compulsive disorder.
Answer: A
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Holmans PA, Blackwood DH, Gurling HM, Owen MJ, Purcell SM, Sklar P,
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9. Harrison P, Weinberger D. (2005) Schizophrenia genes, gene expression, and
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10. Karg K, Burmeister M, Shedden K, Sen S. (2011) The serotonin transporter
promoter variant (5-HTTLPR), stress, and depression meta-analysis revis-
ited: Evidence of genetic moderation. Arch Gen Psychiatry 68(5): 444–454.
11. Lau JY, Eley TC. (2009) The genetics of mood disorders. Annu Rev Clin
Psychol 6: 313–337.
12. Le-Niculescu H, Patel SD, Bhat M, Kuczenski R, Faraone SV, Tsuang MT,
Mcmahon FJ, Schork NJ, Nurnberger JI, Jr., Niculescu AB, III. (2008)
Convergent functional genomics of genome-wide association data for bipolar
disorder: Comprehensive identification of candidate genes, pathways and
mechanisms. Am J Med Genet Part B 150B: 155–181.
13. O’ Donovan MC, Craddock N, Norton N, Williams H, Peirce T, Moskvina V,
Nikolov I, Hamshere M, Carroll L, Georgieva L, Dwyer S, Holmans P,
Marchini JL, Spencer CC, Howie B, Leung HT, Hartmann AM, Moller HJ,
Morris DW, Shi Y, Feng G, Hoffmann P, Propping P, Vasilescu C, Maier W,
Rietschel M, Zammit S, Schumacher J, Quinn EM, Schulze TG, Williams NM,
Giegling I, Iwata N, Ikeda M, Darvasi A, Shifman S, He L, Duan J,
Sanders AR, Levinson DF, Gejman PV, Cichon S, Nothen MM, Gill M,
Corvin A, Rujescu D, Kirov G, Owen MJ, Buccola NG, Mowry BJ,
Freedman R, Amin F, Black DW, Silverman JM, Byerley WF, Cloninger CR.
(2008) Identification of loci associated with schizophrenia by genome-wide
association and follow-up. Nat Genet 40: 1053–1055.
14. Ross CA, Margolis RL, Reading SA, Pletnikov M, Coyle JT. (2006)
Neurobiology of schizophrenia. Neuron 52: 139–153.
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tus of molecular genetic research. Eur Child Adolesc Psychiatry 19: 211–226.
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16. Schuckit MA. (2009) An overview of genetic influences in alcoholism.

J Subst Abuse Treat 36: S5–14.
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Mcmahon FJ, Gershon ES, Liu C. (2008) Clock genes may influence bipolar
disorder susceptibility and dysfunctional circadian rhythm. Am J Med Gen B
Neuropsychiatr Genet 147B: 1047–1055.
18. Smoller JW, Block SR, Young MM. (2009) Genetics of anxiety disorders:
The complex road from DSM to DNA. Depress Anxiety 26: 965–975.
19. Tam GW, Redon R, Carter NP, Grant SG. (2009) The role of DNA copy
number variation in schizophrenia. Biol Psychiatry 66: 1005–1012.
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Moessner R, Gaebel W, Dahmen N, Fehr C, Scherbaum N, Steffens M,
Ludwig KU, Frank J, Wichmann HE, Schreiber S, Dragano N, Sommer WH,
Leonardi-Essmann F, Lourdusamy A, Gebicke-Haerter P, Wienker TF,
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(2009) Genome-wide association study of alcohol dependence. Arch Gen
21. Williams H.J., Owen, M.J. and O’ Donovan M.C. (2009). Schizophrenia
genetics: New insights from new approaches. Br Med Bull 91, pp. 61–74.
22. Xu B, Roos JL, Levy S, Van Rensburg EJ, Gogos JA, Karayiorgou M. (2008)
Strong association of de novo copy number mutations with sporadic schizo-
phrenia. Nat Genet 40: 880–885.
23. Zhou K, Dempfle A, Arcos-Burgos M, Bakker SC, Banaschewski T,
Biederman J, Buitelaar J, Castellanos FX, Doyle A, Ebstein RP, Ekholm J,
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Jacob C, Lesch KP, Loo SK, Lopera F, Mccracken JT, Mcgough JJ, Meyer J,
Mick E, Miranda A, Muenke M, Mulas F, Nelson SF, Nguyen TT, Oades RD,
Ogdie MN, Palacio JD, Pineda D, Reif A, Renner TJ, Roeyers H,
Romanos M, Rothenberger A, Schafer H, Sergeant J, Sinke RJ, Smalley SL,
Sonuga-Barke E, Steinhausen HC, Van Der Meulen E, Walitza S, Warnke A,
Lewis CM, Faraone SV, Asherson P. (2008) Meta-analysis of genome-wide
linkage scans of attention deficit hyperactivity disorder. Am J Med Genet B
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Chapter 5
Psychiatric Interviewing: What to Do,

What Not to Do
Mara Pheister
“If there is any single mark of a successful interview, it is the degree

to which the patient and clinician develop a shared feeling of
understanding.”7
Despite evolving technology, the interview remains the psychiatrist’s
primary tool for diagnosis and treatment.6 It is a skill to be practiced,
developing slightly with each interview. A seasoned interviewer can make
an initial psychiatric interview seem like a conversation yet is able to
obtain a wealth of information. The key is maintaining a balance between
building rapport and gathering data, while recognizing that the two tasks
are interdependent.
1. PURPOSE AND CONTEXT

Every psychiatric interview has four goals — each more or less critical,
depending on the setting and the situation. The psychiatrist seeks to
(1) establish rapport, (2) obtain data, (3) formulate a diagnosis and assess
risk, and (4) negotiate a treatment plan.
Which goal takes priority depends on the time frame and the setting.
The interviewer should ask himself or herself what questions need to be
answered by the end of the interview. The approach might be different if
78
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Psychiatric Interviewing: What to Do, What Not to Do 79
this is a one-time consultation than if it is the start of a long-term

therapeutic relationship. Are 15 min allotted or 90? For example, when
interviewing a patient with depression in a hospital, while 15 others are
waiting, assessing risk might be the main priority. This needs to be bal-
anced, however, with the fact that someone revealing information may
depend on the psychiatrist’s ability to establish rapport. In an outpatient
therapy interview with a depressed patient, the focus may be more on
social history and development, while broaching the treatment plan during
a later session.
To some extent, every interview should provide some therapeutic value
as well. Less experienced interviewers sometimes feel insecure in this
respect, thinking they do not know enough to be therapeutic, not recogniz-
ing that just developing a rapport with a patient can have therapeutic value.
Sadock and Sadock11 define “rapport” as “the spontaneous, conscious feel-
ing of harmonious responsiveness that promotes the development of a
constructive therapeutic alliance.” [p. 1] Stern et al.13 linked the physician–
patient relationship to the attachment relationship of a parent and child. As
with an early childhood attachment, development of rapport involves
mutual respect, communication, empathy, correction of miscommunica-
tions and misunderstandings, and the establishment of a “safe place.”
Perhaps one of the biggest obstacles in building rapport is using the
computer or writing excessively while asking questions. Often taking
notes is useful and necessary. However, it should not interfere with eye
contact with the patient. Jotting down key words, rather than whole sen-
tences, can help. Also, using a note-taking sheet that is blocked off with
color or shading can help the interviewer organize the information without
looking directly at the paper. In the same vein, it is difficult to build a rap-
port when asking questions in a checklist form. Patients sometimes
respond to this by closing down, answering only the close-ended ques-
tions. Often clinics or hospitals have checklists that need to be filled out,
but they should be used as a tool to interview rather than a script.
2. PSYCHOTHERAPEUTIC TECHNIQUES
It is beyond the scope of this chapter to discuss psychotherapy. However,
it may be useful to touch on some of the basic therapeutic tools that might
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80 M. Pheister
be used in a patient interaction. These include the concepts of empathic

validation, reflection, clarification, containment, confrontation, interpreta-
tion, and education.
2.1. Process versus content

MacKinnon et al.7 describe the content of the interview as the factual
information, both verbal and non-verbal, that is exchanged between
interviewer and patient. The process of the interview is defined by
MacKinnon as “the developing relationship between interviewer and
patient.” Stern et al.13 challenge the interviewer to facilitate “the patient’s
narrative,” recognizing that “narratives, like all stories, are co-created by
the teller and the listener.” This requires interviewers to be self-reflective
and to recognize how their own story may influence their perception.
2.2. Empathic validation

There is a significant therapeutic value in validating a patient’s feelings
and experience. Sometimes this just naturally happens with sharing an
experience and not being judged. Other times, such validation takes the
form of empathy — an expression, a word, or a sentence that lets the lis-
tener know that he or she is heard. For example, “It must be really fright-
ening to feel as if everyone is watching you.”
2.3. Reflection
Reflection is a similar technique to empathic validation. The interviewer
repeats back what has been said in a supportive way. For example, for a
teenager who presents with superficial cuts to her wrists after a breakup
with a boyfriend, a statement of support, “You must have felt very alone,”
has two purposes. First, it checks with the patient to be sure that her story
is being understood, and it allows for correction if it is not. Second, it
names an emotion related to a behavior. Although this reflection may not
entirely accurately portray what the patient is feeling, it invites the patient
to put a name to the emotion. It also implies that others in the same
situation might also feel “alone.”
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2.4. Containment
For some patients, the most therapeutic aspect of the interview can be
setting a boundary, or acting as a “container,” for their overwhelming
feelings. For a patient who is overwhelmed by powerful emotions, sharing
them with someone who will sit with him or her, without judgment or
reaction, can alleviate some of the pain.
2.5. Confrontation
Confrontation is a way to bring the patient’s attention to something that he
or she may be consciously avoiding. Done in a respectful way, it can be a
powerful tool to improve insight. For instance, a patient who says he is angry
that his girlfriend called for an ambulance after he took an overdose might
be confronted with the statement, “I wonder if there is a part of you that did
not want to die, and that is why you told your girlfriend what you did.”
2.6. Interpretation
Interpretation is a therapeutic technique usually reserved for later on in
treatment because it relies on a solid therapeutic relationship and under-
standing of the patient’s conscious and unconscious issues. Gabbard4 says,
“The intent is to make patients aware of things that are currently outside
of their awareness.” For instance, a patient who misses two appointments
after the psychiatrist’s vacation might be expressing anger toward the
therapist for the perceived “abandonment.” A partial interpretation might
start with, “I missed you at our last couple of sessions. I wonder if you had
any feelings about my vacation.” In a patient who has progressed further,
an interpretation might be, “I missed you at our last couple of sessions.
We have talked about how it feels for you when people leave. I wonder if
you are feeling angry with me for being away on vacation.”
2.7. Education
Finally, providing education to a patient can be extremely therapeutic. This
may involve explaining a diagnosis, normalizing a feeling, or reassuring
the patient (if appropriate) that something more serious is not going on.
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82 M. Pheister
3. ASKING QUESTIONS
3.1. Open versus closed questions
In gathering information, it is important to recognize that the way in
which questions are asked will influence the answers. The inquiry “tell me
about your family,” is open ended, inviting the patient to explain in his or
her own words. How the patient answers tells a great deal. It allows the
patient to prioritize the importance of the information. For instance, does
the patient begin with his or her family of origin or with his or her own
children? Notice the patient’s body language and whether it matches the
patient’s words. Notice the thought process.
“Do you have brothers and sisters?” is an example of a closed ques-
tion, one which allows the patient to answer with one word. This pro-
vides factual information — for example, he has a sister — but less in the
way of his emotion, attachment, and so on. In some circumstances,
closed questions might be appropriate. For example, “Are you having
thoughts of killing yourself?” “Do you ever hear things that other people
do not hear?” Using closed questions like this helps to fill in important
details.
3.2. Transitions
Maintaining balance between listening to someone’s story and getting
some of the critical information that is needed can be difficult. Transitions
can be an effective way to get the needed information without being rude
or isolating the patient. Carlat3 refers to several kinds of transitions that
can help guide the patient. For example, the “smooth transition” [p. 30] is
a way of gently guiding the interview in a different direction.
• It sounds as if your father has had some trouble with alcohol (family
history or social history). Is that something with which you have ever
struggled? (moving into the substance abuse history).
A “referred transition” [p. 31] picks up on something that the patient
said earlier. It is useful to get more details from something mentioned
in another part of the interview or as a way to shift topics. It also lets
the patient know that you have been listening.
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• Earlier you mentioned that you feel as if you are “going crazy” (open-
ing, chief complaint). What did you mean by that? (open question
expanding on the history of present illness).
The “introduced transition” [p. 31] lets the patient know that you are
changing course.
• Now I want to ask you some questions about your memory.
3.3. Focusing a talkative patient

One of the most challenging things, at the beginning, an interviewer will
face is the verbose patient who has trouble staying on track. This might
bring up conflicting feelings in the interviewer. Impatience and irritability
are not uncommon, especially when many other patients are waiting or the
interviewer is running late. It also may feel difficult to interrupt someone
who is talking about something deeply personal.
A few things to keep in mind: the interviewer considers what questions
need to be answered that day and how much time is available. This allows
the interviewer to find a balance between listening and obtaining informa-
tion. It is also helpful to keep in mind that the ultimate task is to assess and
treat the patient. Although there is some value in hearing all of the details
of a patient’s story, it does not serve the patient to know all about his or her
family but not to know that the patient is having command hallucinations.
In the case of a talkative, disorganized, or manic patient, moving
toward close-ended questions will help focus the interview. The inter-
viewer will likely have to use multiple transitions in order to stay on task.
Making an empathic statement or summarizing before the transition can
clue the patient into the behavior and help focus his or her attention.
• It sounds as if this has been a very difficult time for you. (empathic
statement) Has the stress gotten in the way of your sleep? (smooth
transition)
• It sounds as if it was very difficult growing up. (empathic statement)
I would like to talk more about that when we have the chance. First,
however, I want to make sure that I understand what has been happen-
ing over these last few weeks. (introduced transition back to history
of present illness)
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84 M. Pheister
• We do not have too much time left and there are a few things I want
to make sure we cover. (introduced transition) I am going to ask you
a few yes/no questions to see if I can fill in the blanks a little bit.
(focusing the patient, letting the patient know that you only need a
yes/no answer, which is especially helpful for disorganized patients
and also lets the clinician know if the patient has the capacity to
organize his or her thoughts for a short time).
An anxious or tangential patient may need even more direction.

Depending on the type of information needed, multiple-choice questions
may be helpful. For example, please see Table 1.
Table 1. An example of using multiple-choice questions in the interview.

Interviewer Patient
How long did you take the fluoxetine? It seems as if I have been on medicine
forever. None of it works. My last
doctor kept on changing things
because I never got better. I do not
know why you want to know about the
fluoxetine — I am not taking it.
It is helpful for me to know how you I do not know, a few months maybe. It did
responded to other medications, even not work.
if you did not do well with them (short,
definitive explanation that does not
invite debate). Were you on it for a few
days, weeks, months? (multiple-choice
options, letting the patient know the
extent of detail needed)
Do you remember if you refilled the No, that stuff did not do anything (unlikely
prescription? (a useful question in that the patient took the medication for
assessing whether the patient had an a full month, despite saying she had
adequate medication trial) been on it “a few months.” Recall of an
uncommon event — refilling meds — is
more reliable than recalling the length
of an everyday task — taking meds. This
one month mark is important because it
can guide the clinician as to whether
this was an adequate medication trial)
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3.4. Eliciting information from a guarded patient

Some patients are not very forthcoming. Perhaps they are nervous, do
not want to be there, feel paranoid, feel shy, and so on. In this “pulling
teeth” interview, it is common for the clinician to get caught up in the
patient’s nervousness, which tends to lead to more discomfort and less
interaction. Thus it is helpful for the clinician to take a breath, step back
mentally, and think about the strategy. To begin, the interviewer should
employ mostly open-ended questions. The difference can be seen in
Table 2.
When someone is not talking, the interviewer can make an attempt at
interpreting what is going on, because the patient is not revealing any-
thing. If the clinician offers a correct assessment, the patient may agree or
elaborate on what the clinician has said. If the assessment is incorrect, the
patient’s response may clarify things or add information.
• Interviewer: It is not easy to talk about (empathic statement in an
attempt to interpret what is going on, because the patient is not
saying).
• Patient: It is not that I cannot talk about it. I just do not want to be
here! (provides information — the patient has affect, is not interested
in being with the clinician, and has some energy).
Interviewers should feel free to use their own personalities. This
includes using humor or stating the obvious if such expression is done
with the intention of helping the patient.3
• Patient: It is not that I cannot talk about it. I just do not want to be
here!
• Interviewer: I hear you. But listen, your mom is paying for this. Why
don’t we humor her? We have an hour; what would you like to talk
about?
Anxiety can get in the way of starting, especially for someone
who has never seen a mental health professional. If the patient has
trouble, acknowledge the difficult, possibly overwhelming, nature of
the situation.
• Interviewer: So, tell me what is going on.
• Patient: I do not know where to start (appearing anxious,
overwhelmed).
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86 M. Pheister
Table 2. Examples of closed and open question style when interviewing a withdrawn
patient.
Closed Open
Interviewer Tell me what’s going Interviewer Tell me what’s going on.
on. (open ended (open ended question/
question/statement) statement)
Patient I don’t know. I’m Patient I don’t know. I’m depressed.
depressed.
Interviewer How long have you Interviewer Describe what you mean by
been depressed? (closed “depressed.” (open ended)
question)
Patient Forever Patient I do not know, sad.
Interviewer Since you were a child? Interviewer Anything else? (staying with
( frustrated, turning to open-ended question, pressing
“20 questions” style of further)
interviewing to get
information)
Patient Yeah Patient I do not have any energy; I do
not really care about things.
(a little more information)
Interviewer Nothing? (minimal talking,
invites patient to fill in the
blanks)
Patient Well, not nothing, I mean I
still worry about my kids and
stuff. ( patient brought up
“kids,” indicating this might
be a more comfortable topic)
Interviewer Tell me about your kids.
(open ended and, in this case,
a more neutral subject).
• Interviewer: Yes, that is a pretty big question. Would it help if I asked

you some more specific questions? (narrows scope, more directed,
decreases anxiety).
• Patient: I think so.
• Interviewer: What made you decide to see a psychiatrist? (still open,
not leading, but more directed).
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In some circumstances, the psychiatrist might choose to move on.

Knowing what the priorities are for a particular interview is necessary
to make such a decision. For instance, if a potential psychotherapy
patient begins to cry and looks away in a first interview when asked
whether anyone has ever tried to hurt her, the clinician could reassure
the patient that it does not need to be discussed right away, change to a
less threatening topic, and wait for the patient to bring it up at another
time.
3.5. Cultural considerations in asking questions

Both the physician and the patient bring their cultural values to the inter-
view.8 It is important to be aware of cultural differences, while recogniz-
ing and understanding each person’s experience. Culturally competent
therapists recognize their own biases, seek knowledge about other cul-
tures, and feel comfortable with differences in race, ethnicity, culture,
and beliefs.2,15 Such therapists also recognize the influence of culture on
a patient’s life, illness, and relationship with the medical system.
Questions about culture, religion, race, ethnicity, migration, oppression,
and so on should be included as part of the social history. If the patient
uses cultural references or slang terms with which the interviewer is
unfamiliar, the clinician should ask the patient for more information. A
less experienced interviewer may avoid asking such questions and
instead think that he or she should already know this information, but
asking helps to understand the patient and avoids misunderstanding later.
It also allows a patient to educate the physician, which can be empower-
ing for a patient who may feel vulnerable in the situation of the psychi-
atric interview.
If there is any question about communicating effectively with the
patient in the same language, the clinician should use a professional
interpreter. It is important for the interpreter to have experience in medi-
cal translation, cultural expertise, and understanding of the confidential
nature of the interview. At times, a family member or other staff mem-
ber may be available to translate. Despite the convenience of this situa-
tion, it should be avoided. Using a family member to translate interferes
with confidentiality and possibly with the information the patient (or
family member) is willing to disclose. Using a patient’s child as a
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88 M. Pheister
translator is difficult for both the parent, who may not want the child to
know some personal details, and the child, who is put into a parentified
role. Telephone services may allow for easy, effective, immediate, con-
fidential translation if a professional interpreter is not physically
available.
A translator’s cultural expertise allows for some explanation when
needed, rather than direct, word-for-word translation. However, because
the interviewer is also assessing the presence or absence of a thought
disorder, it is important for the interpreter to note if the patient is not
speaking comprehensibly. When using an interpreter, begin with an
introduction. Face the patient and speak to the patient directly, rather
than to the interpreter; for example, “Tell me how you are feeling,” not
“Ask him how he feels.” Pause frequently to allow the interpreter to
translate.
4. STRUCTURE OF THE INTERVIEW

Although a seasoned interviewer may make an interview seem like a natu-
ral conversation, the discussion has an underlying structure. A diagnostic
interview is divided into an opening (3–5 min), middle (20–30 min), and
closing (5–10 min).3 Maintaining this structure helps to organize the inter-
view and to keep track of time, without missing crucial sections.
4.1. Opening
According to MacKinnon et al.,7 “The most important technique in
obtaining the psychiatric history is to allow the patient to tell his story in
his own words and in the order he chooses” [p. 41].
The purpose of the opening is twofold — to begin hearing the patient’s
concerns and to start building rapport. Let the patient know what to
expect. Many people may have seen a psychiatrist only on television.
They may not know what is expected of them. Most of the time, patients
have been in significant distress for some time before they finally ask for
help.13 For the anxious patient, this leaves plenty of time to build up an
idea of what a first visit might be like. Such patients may feel afraid that
the psychiatrist will think they are “crazy” or hospitalize them. Letting
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patients know what to expect can create a more comfortable environment

and helps build rapport. For example, “We will take the next 30 min or so
to talk about what has been going on, and then we will decide where to go
from there.”
Begin with an open-ended question and let the patient talk, uninter-
rupted, for several minutes. The opening question should elicit the
patient’s chief complaint, without being overly directive, such as “So, tell
me what is going on.” “What brings you here?” “With what can I help
you?” According to Sandifer12 [p. 92], about half of the patient’s symp-
toms are revealed or observed in the first 3 min of the interview. Is the
patient tangential, direct, disorganized, or paranoid? Letting a person talk
without interruption allows the interviewer to note the person’s thought
process and can also provide some direction as to how to adjust the inter-
view, for example, with more closed questions or more direction.
As the patient talks, the clinician must take note of a few things. With
what does the person start? Something that may be offered as an aside
may be more crucial than initially appears. Initial words might be some-
thing to come back to after more context has been gathered.
• “My wife says she will leave me if I do not get help, but my ADHD
is not that big a deal.” (going back to the man’s first words gives the
clinician an idea of the effect the ADHD is having on his functioning
and relationship).
• “I am looking for a new psychiatrist because the last one never lis-
tened to me.” (such a statement may indicate that the patient has dif-
ficulty in relationships and that the clinician may be the next one who
“does not listen”).
Transitioning to the questioning part of the interview will depend on

the patient. With a very disorganized, manic patient, only a couple of
minutes may be needed to note the thought pattern and then it may make
sense to move to close-ended questions. However, in patients with some
subtle delusions or in patients who have the insight to hide such thought
patterns, allowing uninterrupted free speech is important in identifying
evidence of thought disorder. With someone who is able to describe the
situation clearly, the interviewer might wait until the natural “end of the
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story” to begin clarifying symptoms with some close-ended questions.

This change in questioning leads to the middle section of the interview.
4.2. Middle
The middle section is the bulk of the interview, what most might think of
as a psychiatric interview. This is the time to obtain data, test the differen-
tial diagnosis, perform a mental status examination, observe responses,
determine safety, and decide what else is needed to make treatment deci-
sions. Again, some therapeutic value to the interview should be balanced
with the need to gather information. It is helpful to keep in mind what is
needed to determine the treatment plan — how much detail is needed for
this particular interview? To some extent, all interviews need to cover the
history of present illness, the psychiatric history, the psychiatric review of
systems, substance abuse history, family history, medical history, social
history, and mental status examination. Knowing this allows the inter-
viewer to follow the patient’s lead as different topics come up but to recall
what topics still need to be covered. A useful pneumonic is “History of
psychiatry reviews family drug abuse, medical and mental.”
4.2.1. Presenting problem (history of present illness)

In the opening, the patient started to describe his or her concerns and
likely gave several symptoms. The interviewer needs to clarify the details
and answer the fundamental question of “why now?” Specifically, why is
the patient presenting at this time? For many patients, the symptoms have
been chronic. The “why now” tells the interviewer more about the
patient’s functioning, motivation, strengths, and so on. Consider the dif-
ferences in motivation, function, and insight among the following reasons
for entering treatment: “My boss suggested I come.” “My regular psychia-
trist was in an accident.” “I never thought about suicide before; it really
scared me.”
By this point, a differential diagnosis has likely started to form. Testing
the differential with specific questions about severity, timing, associated
symptoms, and pertinent negatives allows the interviewer to rule in or rule
out a diagnosis.
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4.2.2. Psychiatric review of systems

After clarifying most of the current symptoms, the interviewer needs to
explore other symptom clusters in a psychiatric review of systems. Screening
questions probe for symptoms of mania, psychosis, depression, anxiety, and
so on that may not have been addressed in the history of present illness
(Table 3). The phrasing of screening questions will affect the answer. On one
hand, “Have you ever had a time when you felt overly happy?” is a sensitive
question, but not very specific for symptoms of mania. On the other hand, a
very specific question, “Have you ever had a time when you had a lot of
energy, did not need to sleep, spent a lot of money, had an increased sex
drive, and talked a lot and really loud for more than 4 days?” will not pick
up many of the patients who have manic or hypomanic symptoms.
An efficient and valid screening question balances both sensitivity and
specificity. For instance, “Have you ever had a time when you felt the
opposite of depressed, when you felt really happy, had a lot of energy, and
did not need to sleep much?” “How about a time when you had a lot of
Table 3. Psychiatric review of systems — screening questions.
Depression — “Have you ever had a time where you felt depressed? More than just sad,
but where it felt like you couldn’t get out of it, it affected your sleep, your appetite,
your energy?”
Mania — “Have you ever had a time where you felt the opposite of depressed? Where
you felt great, had a ton of energy, didn’t need as much sleep, spent more money or
did things that are unusual for you?” “How about when you had a lot of energy, but
felt really irritable, maybe yelling, screaming.” “Did others notice the change in your
mood?”
Psychotic — “Have you ever heard things other people don’t hear, seen things other
people don’t see?” “Ever feel like people are talking about you, following you?”
Cognitive — “Do you often lose things?” “Does your family every comment on your
memory?”
Anxiety — “Have you ever had a panic attack?” “Are there thoughts that you have
trouble getting out of your head?” “Do you ever need to check things, like the locks
or the stove, or need to do things in a certain order?”
Suicidal or Homicidal Ideation — Start with safest, most sensitive, before getting more
specific — “Have you ever felt like life wasn’t worth living?” “Do you ever think
about killing yourself?”
Somatoform/Eating — “How do you feel about your body?”
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energy but were really irritable, yelling, throwing things…?” These ques-
tions are specific enough to distinguish from “just a regular mood.” If the
patient offers any hesitation, the clinician can ask more specific questions
to clarify the situation.
4.2.3. Psychiatric history

Learning the psychiatric history is important in determining the risks,
prognosis and course of treatment. The doctor needs to inquire about pre-
vious psychiatric hospitalizations, suicide attempts, medications used,
side effects and response to medication, and psychotherapy. Depending on
the goal of the interview, specific details may be useful.
For instance, a patient with Major Depressive Disorder, with a remote
history of suicide attempt is seen for evaluation in an outpatient clinic. He
denies any suicidal ideation. He was treated in the past with sertraline, but
says that medication did not work for him. In this case, it would be impor-
tant to know whether he had an adequate trial of medication, before deter-
mining that he hadn’t responded. It is a rare patient who has details on
dosing and length of medication trials. However, the person might remem-
ber the color of the pill, whether there were one or two and whether they
refilled the prescription. Pill pictures are available in the PDR or certain
smart phone applications to help a patient identify a medication or dose.
If this same patient were being seen in the emergency room for suicidal
ideation, details about the remote suicide attempt would be more useful
than details about previous medication trials. In this setting, where the
primary question is to determine safety, specific details about previous
suicide attempts help stratify risk.
4.2.4. Substance abuse history

Approach substance abuse questions without judgment. Asking as if you
expect that they drink (normalizing)10 may increase the likelihood that
someone will be honest about their use. Depending on the situation, the
question might be worded, “How much do you drink?” rather than “Do you
drink?” Being overly inclusive in questioning, “Ever use marijuana,
cocaine, heroin, pills, ecstasy,… ?” gives permission for someone to admit
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to their use. This technique also avoids the checklist way of asking them
one a time. “Have you ever used marijuana?” “Have you ever used
cocaine?” Etc. Include questions about tobacco and caffeine, both because
of the health risks and the effects they might have on potential treatments.
A positive response to screening questions should prompt further
inquiry. Clinically relevant details include questions about last use,
longest period of sobriety, history of detox or withdrawal. Some patients
may minimize use, so asking questions about consequences — history of
a DUI, of withdrawal seizures — is a way to obtain more reliable
information.
4.2.5. Family history

Again, a screening question can be useful. “Has anyone in your family
ever had problems with depression, bipolar, drugs, alcohol, suicide,
schizophrenia…?” “Anyone you think might have been undiagnosed?” It
is important to get details about suicide attempts, hospitalizations, and
specific medications, if relevant. Given the side effect profile of many
psychotropic medications, it is helpful to know if there is a family history
of diabetes or of sudden unexplained death.
4.2.6. Medical history

In addition to any medical or surgical problems, the interview should
elicit any medications the patient is taking and any medication intoler-
ance. Ask the patient to explain whether previous reactions are allergies or
side effects. Knowing all of the patient’s medications, including any over-
the-counter medications, herbs or supplements, is critical when consider-
ing the treatment plan as many psychiatric medications have drug–drug
interactions. Also, many non-psychiatric medications can cause or worsen
psychiatric symptoms.
4.2.7. Social history

The social history includes the patient’s developmental history, education
and work history, living situation, family, spiritual beliefs, relationship
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history, sexual history, history of trauma, and legal history. Knowing some
of the social history can be helpful at the beginning of the interview to
help put the presenting problem in some context. It’s important also to
assess a patient’s cultural values. This may include level of acculturation,
economic issues, language, migration history, history of oppression, war,
racism.
4.2.8. Mental status examination

The mental status examination is sometimes described as the psychiatric
equivalent of a physical examination. (Although, depending on the
circumstance, a physical examination might be performed as well.)
Assessing a patient’s mental status begins with the interaction, or sooner
in the case of hearing someone yelling or smelling an odor. Certain infor-
mation needs to be elicited, but much of the MSE is assessed through
observation.
• Appearance (observed) — Despite the adage, “you can’t judge a book

by its cover”, appearance is important to consider. Notice their dress
(professional, revealing, sloppy), their habitus (obese, cachectic,
thin), their dentition, their cleanliness, their fingernails, makeup, tat-
toos, piercings, etc. This may or may not have any bearing on the
diagnosis or treatment, but it can be important on subsequent visits
when a woman who is usually professionally dressed and made up
arrives in sweatpants with no makeup. Notice also if they are sweat-
ing, have exophthalmos, are malodorous, etc.
• Behavior (observed) — This includes the process of the relationship
that was discussed earlier. Notice the patient’s body language. Are
they cooperative? Do they have clenched fists with a paranoid stare or
are they hunched over with little or no eye contact?
• Psychomotor Activity (observed, sometimes elicited) — Notice the
patient’s general movements. A depressed patient may have very slow
movements — psychomotor retardation. Describe any restlessness,
abnormal movements, increased or decreased blinking, agitation.
In a patient on antipsychotics, the psychiatrist may perform an
abnormal involuntary movement scale (AIMS) assessment to elicit
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abnormal movements. A targeted neurologic examination might

check for the presence and character of tremor, rigidity, waxy flexibil-
ity, cogwheeling, ataxia, etc.
• Speech (observed) — The interviewer should note the volume,
prosody, and rate of speech.
• Mood & Affect — Mood (elicited) is the patient’s subjective state,
often reported in the patient’s words (“fine”, “depressed”), while
Affect (observed) refers to the patient’s expression. Note the range
and appropriateness of their affect.
• Thought process (observed) — Thought process takes note of the
patient’s way of talking or thinking. For instance, is there a long pause
before answering (thought blocking)? Do they get sidetracked in
answering the question, but return to the answer eventually (circum-
stantial)? A patient, who gets distracted, might talk excessively and
never answer the question asked (tangential).
• Thought content (observed and elicited) — Delusions can be sponta-
neously revealed during the course of the interview, but direct ques-
tions are usually needed to elicit ideas of reference or thought
broadcasting. The same is true of suicidal and homicidal ideation.
Patients typically need to be asked directly about perceptual distur-
bances like hallucinations or illusions, but the clinician may also
observe that a patient is internally preoccupied.
• Insight & Judgment (observed, sometimes elicited) — Insight
describes a patient’s understanding of their illness. It can be inferred
by how a patient talks about her illness, and judgment from some of
their recent decisions, actions, and statements. There are some stand-
ard questions used to assess judgment, the classical being “what
would you do if you found a stamped, sealed addressed envelope?” I
lost faith in this question (and humanity), however, when a man asked
for a small fee after finding the stamped, sealed addressed envelope
that I had lost.
• Cognition (observed and elicited) — The patient’s level of alertness is
observed by the psychiatrist. General cognitive function can also be
observed in the patient’s telling of their history and understanding of
why they are consulting a psychiatrist. The interviewer would further
elicit cognitive issues by asking questions about orientation (time,
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place, person), recent memory (what they had for breakfast), immedi-
ate memory (repeating three words or a series of numbers), recall
(recalling the three words). Level of concentration is tested by having
the patient count backwards from 100 by 7 or saying the alphabet
backwards. Calculations, writing, fund of knowledge, repetition, and
abstract reasoning can also be tested.
4.3. Closing
The closing part of the interview is reserved for presenting and negotiating
a treatment plan. While interviewers may be tempted to ask questions up
until the last minute, this discussion is crucial to maintaining rapport.13
Eliciting a patient’s concerns, providing education and demonstrating
empathy have a direct effect on patient compliance.5
In lay terms, explain to the patient what may be causing their symp-
toms, including the biological, psychological, and social influences.13
This may include a diagnosis or an explanation of the differential diagno-
sis and what further information needs to be obtained. Finding out what
the patient knows about the diagnosis or what he/she thinks about the
formulation will allow the interviewer to clarify any misinformation and
address any issues that may interfere with treatment.
A useful way to discuss treatment is to approach it in a similar biopsy-
chosocial way: “Like depression, which involves biology, stress and the
way you cope with things, we need to approach treatment in the same
way.” Eliciting a patient’s thoughts and feelings about treatment can be
helpful. If someone is very apprehensive about taking medication, dis-
cussing the reasons behind this or addressing any myths can be useful. It
can also help the psychiatrist tailor the treatment plan.
“If you had a magic wand, and could make three symptoms disappear,
which would they be?” The answer to this question is sometimes surpris-
ing as the things the physician is concerned about may be very different
from the patient’s primary concerns. It allows one to further tailor the
treatment plan to address the patient’s primary concerns. For instance, a
depressed patient whose most concerning symptoms are concentration,
energy and motivation might be started on a different medication from
another depressed patient who is most troubled by lack of sleep,
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ruminating thoughts and anhedonia. The clinician should also invite any
questions from the patient.
5. CONCLUSION
The psychiatric interview is a skill that will continue to develop over
time.1 Crucial is maintaining a balance between developing rapport and
gathering information, keeping in mind the context and purpose of this
particular interview. Ideally, in each patient interaction, there will be some
therapeutic value in an exchange of information between patient and
doctor.
6. KEY POINTS
• The purpose of the psychiatric interview is to establish rapport, obtain
data, formulate diagnoses, assess risk, and negotiate a treatment plan.
• Ideally, each interview should provide some therapeutic value.
• Create structure by dividing the interview into the opening, middle,
and closing.
• Avoid using a computer, taking copious notes, or asking lists of
questions.
• “History of Psychiatry Reviews Family Drug Abuse, Medical and
Mental”
7. SELF-ASSESSMENT
7.1. “It seems like you are concerned about being a burden
on your family” is an example of:
(A) Confrontation.
(B) Validation.
(C) Interpretation.
(D) Reflection.
(E) Education.
Answer: D, it is reflecting back a patient’s feeling or concern.
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7.2. Which is an example of a good screening question?

(A) “Have you ever felt hopeless?”
(B) “Have you ever attempted suicide?”
(C) “Have you ever felt as though life wasn’t worth living?”
(D) “Do you have a plan on how you would hurt yourself?
(E) “How close have you gotten to hurting yourself?”
Answer: C, it is specific enough but sensitive enough to pick up most true

positives. “Have you ever felt hopeless?” is too broad to be a screen for
suicide. The other three are too detailed and specific. As a screening ques-
tion, they would miss many true positives.
8. CASE STUDY
A 57-year-old woman, previously diagnosed with “manic-depression”,
comes in after not seeing a psychiatrist for 10 years because “I need help.”
She is currently depressed and irritable, spends most days in a bathrobe,
thinks of suicide daily, but denies any intention. In the past, she has had
episodes of increased energy and decreased need for sleep, with racing
thoughts, irritability, paranoia, and talking loud and fast, lasting for “hours to
weeks.” “My family doctor does not think it is bipolar — I think that is what
I need to find out first.” She currently takes sertraline 50 mg, diazepam, and
zolpidem. The following is an example of how to negotiate a treatment plan:
Interviewer: Okay, here’s what I think is going on. First of all, I do think
this is bipolar disorder and let me tell you why. Like you
said, “bipolar disorder” is another name for “manic
depression”. I think you know what depression is — more
than just feeling sad, having trouble thinking, not enjoying
things, not functioning, having thoughts of hurting your-
self. And the manic part is when you have high energy, are
sleeping less, are more irritable, doing things that are un-
usual for you. And then there are times, like now, where you
have all of those symptoms together. It’s caused by a few
things — genetics for one (from what you described with
your dad, I think he may have been struggling with
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something similar), stressors going on (like not working)

and then the way you cope with things. I think the first thing
we need to do is figure out your medication because the
way you’re feeling right now, it’ll be hard to change some
of the other things. What do you think about that?”(diagnosis,
minilecture, eliciting patient’s understanding and feelings)
Patient: Okay. I just want to feel better.
Interviewer: Alright. So you’re taking the Zoloft, the Ambien, and the
Valium. I think the first thing we need to do is get you on
what’s called a mood stabilizer — something to calm the
ups and the downs and get you on an even keel.
Patient: Yeah, that’s what I need.
Interviewer: So there are a few different kinds of mood stabilizers —
1. Lithium, 2. Some anti-seizure meds like depakote and
tegretol, and then 3. Atypical antipsychotics like aripipra-
zole, quetiepine, olanzapine. Have you heard of any of
those? (eliciting patient’s fantasies, fears, understanding)
Patient: I met someone on a chat room who was on Lithium for
30 years and then her kidney’s failed. They never told her
about that. (Note — he wants to know about side effects)
Interviewer: Yes, Lithium is a very effective medication, but it can cause
problems with your thyroid and kidneys. So if we did some-
thing like that, we would monitor you very closely. All of
the medications can have side effects, but you in particular
may not have any. (psychoeducation, dispelling myths).
So, if there were three symptoms that you could make
magically disappear, which would they be? (eliciting target
symptoms)
Patient: Only three? Well, the irritability, the hopelessness, and the
feeling of not wanting to do anything.
Interviewer: I would like to start off with Depakote. It’s used for a few
things — seizures, bipolar, and headaches, so it may even
help your migraines. Depakote is something that we need
to make sure stays within a certain level in your blood, so
initially, we’d have to do a few blood draws. (explain use,
monitoring).
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Patient: What’s a few?

Interviewer: Well, we’d start with 500 mg and then I’d like to check a
level to see where you’re at. For some people, that can be
a lot, for some, it’s nothing. Once I have a level, I’ll have
a better idea of how fast to go up. At that time, we’ll also
check your liver and blood count because rarely, it can
affect this in people. Aside from those, some people can
have weight gain, dizziness, nausea, tiredness. So we’ll
keep an eye on it and if those are an issue, we can go from
there. (explanation of risks and benefits).
Patient: Okay.
Interviewer: I want you to get your blood drawn next week, and then
we can meet back in about a week and a half or two. If
you have any issues, give me a call. (when/how to reach
doctor)
Patient: (nod)
Interviewer: Do you have any questions for me? (eliciting questions)
Patient: No, I think I’m good.
Spouse: Me too.
REFERENCES
1. American Association of Directors of Psychiatric Residency Training.
(2008) AADPRT Clinical Skills Verification Examination Form CSV.3.
Available at: http://www.academicpsychiatry.org/htdocs/Fidlerdocs/
Education/Clinical_Skills_Assessment/AADPRT_CSV_3b.pdf
2. American Psychological Association, Joint Task Force of Counseling
Psychology and The Society for the Psychological Study of Ethnic Minority
Issues (2002) Guidelines on Multicultural Education, Training, Research,
Practice and Organizational Change for Psychologists (Approved as APA
Policy thy the APA Council of Representatives, August 2002).
3. Carlat DJ. (2005) The Psychiatric Interview, 2nd ed. Lippincott Williams &
Wilkins, Philadelphia, PA.
4. Gabbard GO. (2009) Textbook of Psychotherapeutic Treatments. American
Psychiatric Publishing, Inc., Arlington, VA.
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5. Griffith S. (1990) A review of the factors associated with patient compliance

and the taking of prescribed medications. Br J Gen Practice 40: 114–116.
6. Hales RE, Yudofsky SC, Gabbard GO. (2010) The psychiatric interview and
mental status examination. In: Andrews LB (ed.), The American Psychiatric
Publishing Textbook of Clinical Psychiatry, 5th ed. Chapter 1, American
7. MacKinnon RA, Michaels R, Buckley PJ. (2006) The Psychiatric
Interview in Clinical Practice, 2nd ed. American Psychiatric Publishing,
Inc., Arlington, VA.
8. Marx JA. (2009) Marx: Rosen’s Emergency Medicine — Concepts and
Clinical Practice, 7th ed. Mosby (Elsevier), Philadelphia, PA.
9. Othmer E, Othmer JP, Othmer SC. (2007) Our favorite tips for “getting in”
with difficult patients. Psychiatr Clin N Am 30(2): 261–268.
10. Roberts LW, Hoop JG, Heinrich TW. (2010) The psychiatric interview. In:
Anderson DL, Hoop JG, Roberts LW (eds.), Clinical Psychiatry Essentials,
Chapter 3, pp. 23–38, Lippincott Williams & Wilkins, Philadelphia, PA.
11. Sadock BJ, Sadock VA. (2007) The patient-doctor relationship. In: Kaplan
and Sadock’s Synopsis of Psychiatry, 10th ed. Chapter 1, pp. 1–11, Lippincott
Williams & Wilkins, Philadelphia, PA.
12. Sandifer MG, Hordern A, Green L. (1970). The psychiatric interview: The
impact of the first three minutes. Am J Psychiatry 126(7): 92–97.
13. Stern TA, Rosenbaum JF, Fava M, Biederman J, Rauch SL. (2008) The psychi-
atric interview. In: Beresin EV, Gordon C (eds.), Massachusetts General
Hospital Comprehensive Clinical Psychiatry, Chapter 2, Mosby (Elsevier),
Philadelphia, PA.
14. Stern TA, Rosenbaum JF, Fava M, Biederman J, Rauch SL. (2008) Culture
and psychiatry. In: Henderson DC, Yeung A, Fan X, Fricchione GL (eds.),
Massachusetts General Hospital Comprehensive Clinical Psychiatry,
Chapter 66, Mosby (Elsevier), Philadelphia, PA.
15. Sue DW, Arredondo P, McDavis RJ. (1992) Multicultural counseling compe-
tencies and standards: A call to the profession. J Couns Dev 70: 477–486.
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Chapter 6
Psychological and Neuropsychological

Testing
Jennifer Niskala Apps and Jonathan E. Romain
1. INTRODUCTION
The modern-day physician has myriad medical and laboratory tests at his
or her disposal to aid in the diagnosis of physical disease, and it is this
diagnostic clarity that ultimately leads to comprehensive treatment plan-
ning intended to substantively improve or restore normal function. Mental
health providers seek similar goals. Unfortunately, mental illness can cre-
ate greater obstacles for the clinician than traditional physical disease
states because the symptoms and underlying pathology are often far more
elusive. For example, helping a parent to understand that her child has
Attention Deficit Hyperactivity Disorder (ADHD) and, moreover, that a
stimulant medication might be indicated on the basis of a set of intangible
symptoms is arguably more complicated than explaining why a course of
antibiotics is needed in the presence of a positive strep culture. The assess-
ment of human behavior can be daunting. Often, subjective measures are
relied upon when assessing human behavior, relying on our behavioral
descriptions of illness and clinical attempts to subjectively identify behav-
iors that meet symptom criteria. This chapter is written with the hopes of
increasing the reader’s familiarity and comfort level with the utility (and
limitations) of more objective psychological and neuropsychological tests
in diagnosis and treatment. Objective testing relies on scientific theory
102
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Psychological and Neuropsychological Testing 103
and data to support the findings and conclusions drawn from an evalua-
tion. Issues related to the reliability and validity of standardized tests, test
selection, and cultural differences will be explored systematically to aid in
expanding the resources available to the practicing physician in the man-
agement of mental health disorders.
2. HISTORY OF TESTING
Human behavior encompasses a complex network of emotions and cogni-
tions working in concert to produce thoughts, feelings, and ideas. The
measurement of human thought poses many challenges and is fundamen-
tally obscured by the reality that we are using the very thing that we are
trying to measure (our own cognitions) to understand the behaviors,
beliefs, and intentions of others. With this in mind, it becomes essential
to use tools rooted in the scientific method as a framework to more
objectively evaluate and assess psychological processes. Psychometric
testing represents our attempts at quantifying and systematically explor-
ing behavior and has been used in the laboratory since the 19th century,
initially in measuring perception and other psycho–physiological pro-
cesses (e.g. Weber’s Law). As the research and tools evolved, the study of
human emotions and, later, human intelligence began to predominate.
Theories and developments in quantifying intelligence were the first focus
of testing. Developments were worldwide, including significant theoreti-
cal contributions from Sir Francis Galton in England, who proposed sta-
tistical concepts core to psychometrics; James Cattell in the United States,
who measured sensory and motor skills; Wilhelm Wundt and Emil
Kraepelin in Germany, who measured memory, perception, motor skills,
and perceptions; Carl Wernicke in Poland and Germany, who studied
brain localization to measure mental retardation; and importantly, Alfred
Binet and others in France, who developed formal methods of intellectual
measurement, leading to the Binet–Simon Scale in 1905.15
The first “clinical” application of psychological tests seen in the United
States was during World War I, where paper-and-pencil tasks aided in
classifying recruits for the military. Analysis of the scores obtained on
these “intelligence measures” formed the basis for the Intelligence
Quotient (IQ), which was represented by the equation Mental Age divided
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104 J. N. Apps and J. E. Romain
by Chronological Age multiplied by 100. A score of 100 would suggest

that Mental Age and Chronological Age are equivalent; thus, the partici-
pant would be considered functioning solidly within the average range.
Intelligence tests have increased in sophistication over the years and
are no longer based on a quotient model, but the mean standard score of
100 remains. A Standard Deviation (SD) is applied to represent variability
(typically SD = 15), and together this information can help the examiner
make population-based comparisons.
2.1. Classical test theory

Much of the science behind current test construction is based on classical
test theory.13,14 Classical test theory maintains that the Obtained Score
(X) on any given test represents the True Score (T) and Error (E). The
True Score is a hypothetical construct and reflects the average score one
would obtain after an infinite number of administrations of a given test.
Error reflects the contribution of extraneous variables on performance
and can negatively or positively affect the outcome on a test. Positive
error might be guessing correctly on a multiple-choice test question.
Negative external influences might include taking a final examination on
little or no sleep in a noisy gymnasium. Other examples might include
being administered a test in English when English is not the primary
language of origin or being presented with test questions that are inher-
ently culturally biased. Error can also be found within the tests them-
selves. For example, an anxiety rating scale with several questions
devoted to increased activity and motor restlessness might be tapping
into symptoms that are more commonly associated with ADHD. Another
example might be assuming that an oral math test is measuring math
skills when it could arguably be measuring memory span just as much as,
if not more than, math aptitude. Whether a given measure is actually
measuring what it was designed to measure is known as test validity and
will be discussed in greater detail below. How well a test measures a
particular trait or how consistently it distinguishes between performances
on the attribute being measured is equally as, if not more, important and
is termed reliability. Validity and reliability serve as the foundation for
discerning whether a test is useful.
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2.2. Reliability & validity

Validity studies during test development and construction are intended to
answer fundamentally whether the test is measuring what it is purported
to measure.
Content validity specifically looks at whether a test is effectively sam-
pling the domain being assessed and is usually addressed at the onset of
test construction by researchers charged with designing the measure. In
simplest terms, is the test measuring what it says that it is measuring?
For example, if we intend to measure weight and step on a scale, are we
indeed measuring weight? Face validity is a related term and refers to
whether most people would believe on the surface that the measure is
assessing what it is supposed to assess and is an important consideration
in test construction, because low face validity can affect motivation and
effort.
Additional validity studies relate to whether the measure is adequately
sampling the correct trait or construct, as opposed to another trait, and is
termed construct validity. In other words, determining if a test is ade-
quately measuring academic achievement is harder than saying it has
content validity, because this is a broader construct. Therefore, the extent
to which a measure has a strong correlation with other known measures
assessing the same trait is referred to as convergent validity, whereas dis-
criminant validity addresses whether a measure is able to discriminate
between traits. For example, if an oral math test correlates well with
paper-and-pencil math tests, then the oral test would have good conver-
gent validity in assessing math skills. However, if the oral math test also
has a high correlation with memory span tests, then it would have poor
discriminant validity, and thus test results would be difficult to interpret.
Lastly, measures are often designed to draw conclusions about perfor-
mance or aptitude. Standardized entrance examinations often given in
high school rely on strong predictive validity, in this case the ability to
determine whether a student will be successful in a university setting. In
the classroom, final examinations are routinely given to measure the stu-
dent’s ability to have adequately acquired information presented through-
out the semester. If the test has strong concurrent validity, it will accurately
reflect current knowledge of the subject material.
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As discussed in the Classical Test Theory section, an obtained score

reflects the true score and an error component. Whereas measurement
error is the amount of random error inadvertently captured by a test, reli-
ability is an estimate of the proportion of variability that can be explained
by true differences and speaks to the consistency of test performance. For
example, a thermometer that reads boiling water at 100°C at time one,
103°C at time two, and 95°C at time three would be considered
unreliable.
Several procedures can be employed to assist the researcher in deter-
mining a test’s reliability, but it should be borne in mind that there will
always be sources of error; reliability is an estimate and not absolute.
Test–retest reliability refers to the estimates of reliability that can be
obtained by repeat administrations of a measure at different time points.
Tests also can be given during a single administration and responses can
be scored, compared, and correlated amongst each other to provide an
assessment of internal consistency reliability. The Cronbach’s Alpha3 is a
formula used to determine inter-item correlations by estimating the relia-
bility of a test on the basis of all possible comparisons among items.
Occasionally, researchers have the luxury of administering equivalent or
parallel forms to the same examinee, which forms the basis of alternate
forms reliability. This is often done with tests that have multiple forms due
to a need for retesting at close time intervals, such as the Woodcock–
Johnson Tests of Achievement, academic tests that offer versions A and B.
Finally, variability can occur as a result of different examiners giving the
test, and inter-rater reliability looks at the consistency of test performance
in this context.
In general, the intent of reliability studies is to obtain a reliability
coefficient, which is the proportion of variability in obtained test
scores that can be attributed to true differences. The reliability coeffi-
cient (r) ranges from 0 to 1, where 0 suggests test results are entirely
attributable to error and 1 reflects variability fully attributed to true
differences. An r = .30 would mean that 30% of the variability is due
to true score and 70% is due to error variability. In general, a value at
or above .70 is considered acceptable. Most psychological and neu-
ropsychological measures should have published data regarding relia-
bility and validity.
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3. STANDARDIZATION AND INTERPRETATION

3.1. Standardization processes
Tests can be used for many purposes, but to make test data useful they are
converted into a comparison result or score. Published tests are standard-
ized. Standardization involves formalizing the administrative methods of
a measure. Often this means writing out every aspect of administration,
including the standard instructions given to each participant, to ensure that
administrations are consistent across occurrences and to remove as much
error due to administration as possible. Error in administration, whether
inadvertent or due to bias, adds a statistical anomaly to the outcome, as
mentioned above, making interpretation of a person’s performance uncer-
tain. Standard administration, much like the formal methods in a research
study, attempt to hold constant as many extraneous variables as possible.
Formalized tests are administered to large groups of populations in order
to determine the normative data. The test constructors determine what their
population should be and then attempt random selection from that population.
Often this process involves administering the test to hundreds or even thou-
sands of individuals. This provides the numerical data required to statistically
analyze the test, develop factor scores or scores indicative of the attribute
being measured by the test, and provides normative data for comparisons.
3.2. Normative groups

During test development, the creators must determine the appropriate
normative group or groups. It is equally important that any clinician
administering a standardized test knows and understands what the norma-
tive or standardization group consisted of and how that group compares to
the individual who is taking the test. An individual taking a standardized
test measure should match the general characteristics of the normative
group used in the test’s development.
3.2.1. Age
Many tests are developed for specific age ranges. The content of a test is
often designed to appeal to or be most appropriate for the age range
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targeted. For example, a language measure will vary greatly if it is being

used to assess language development in a toddler with limited language
skills and a short attention span, a school-aged child, or an adult. Clearly
the stimuli used to evaluate that person’s language skills would need to be
age-appropriate in appearance, content, and amount. It would be obviously
inappropriate to assess an adult’s language skills with a pre-school meas-
ure or vice versa. Often, age bands, or comparative normative groups,
become narrower in age at either end of the age spectrum. Because chil-
dren develop and change quickly, normative groups often include children
within ages approximately 1–3 months of one another. As individuals age,
many tests include normative groups of a wider range. Some adult meas-
ures offer only one normative group, collapsing the full range of partici-
pants into one. Careful analysis of the test’s manual should reveal what
statistical analyses the test developers completed in order to ensure that
the test would be appropriate.
Interpretation of a person’s performance on a standardized test measure
should include a review of the normative data to ensure that the age com-
parisons are appropriate. Interpretation of test outcomes is extremely
limited if the person varies greatly from the standardization population.
For example, a 65-year-old man may have been evaluated using a test
normed on individuals aged 18–65. Although he appears to fall within the
appropriate normative group, a more careful analysis of the standardiza-
tion sample will reveal what percentage of that group was close to the
upper age range. If only 1% of the overall standardization sample was
over the age of 50 years, the test might not truly be appropriate for use
with this individual.
3.2.2. Gender
Many tests are developed without specific attention to gender, and norma-
tive data is analyzed post-collection to determine if gender is a significant
factor. However, some measures must account for gender from the begin-
ning of test development. Obviously if a test is being developed to address
a characteristic, a factor, or a quality belonging only to one sex, then it will
be normed for use with that sex and would be inappropriate to administer
otherwise. Some measures will require different administration methods
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or normative groups that are based on gender. For example, due to the
differences in physiology of the sexes, many motor measures require
separate normative groups. Additionally, attitude measures will often
require separate normative groups. Although the questions asked on the
measures may be the same, the interpretation of how a person responds
may be directly influenced by gender and thus must be analyzed using
specific normative data.
Interpretation of test data should consider the possible interaction of
gender with other factors in the evaluation process. Even if all the tests
administered have accounted for sex differences within their normative
data, a person’s gender can also affect his or her engagement in the test
process itself. Rapport with the examiner, engagement, and effort should
always be considered in interpretation. Cultural differences may play a
significant role, interacting with gender to affect how a person responds to
the testing process and the individual examiner, a topic covered in more
detail later.
3.2.3. Education
Educational experiences can significantly affect a person’s interaction
with the testing process, as well as performance on a test. In the standardi-
zation process, educational levels can be quantified within a culture and
then treated as an extraneous variable if necessary. Many times, however,
educational experiences can vary so much, even within one country, for
example, that test developers rely on larger numbers in their sample size
to “average out” any extraneous effects of education.
Educational level becomes far more important to the normative process
in measures intended to quantify academic skills, however. Measures of
academic achievement can often be scored on age- or grade-based norma-
tive data. An examiner must understand the differences between these
normative groups and clinically determine which method of score inter-
pretation is appropriate in each clinical setting.
Most often, educational experience is considered a factor affecting the
reliability of test outcomes in an individual situation. In other words, a
clinician will need to think very differently about what tests to use and
how to interpret the results when working with a patient who has attended
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organized school for only four years in comparison to testing a patient

with a similar referral question who completed 12 years of public school.
Further, a person’s culture significantly influences educational experi-
ences. The clinician must determine what differences may exist in the
educational experiences of someone raised in another culture and how
those differences may affect responses to testing.
3.3. Standardized scores

Once a test is administered and scored on the basis of normative data,
standardized scores are derived. Statistically, if a test is administered to a
large number of individuals, or sample, the performances will fall into a
normal distribution or normal curve (Fig. 1). Raw scores represent the
actual performance of a person on a test. It is important to understand the
maximum and minimum levels of performance available on any given
2.2% 6.7% 16.1% 50% 16.1% 6.7% 2.2%
Low High Very

Borderline
Average Average Superior
70 80 90 100 110 120 130

Standard Score
Mean 100 (10) 2nd%ile 9th%ile 25th%ile 50th%ile 75th%ile 91stile 98th%ile
IQ100(15)
T-score 30 37 43 50 57 63 70
Mean 50 (10)
Fig. 1. The normal curve and visual representation of standardized scores.
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test, in order to best understand how those levels can affect standard
scores. For example, if a test is designed in such a way that items for very
young children become difficult quickly and few items are assessed, lead-
ing to very small raw scores, only one or two questions may make very
large differences in that child’s standard score in comparison to results
from older children who may answer more questions.
Raw scores do not inform how a person compares to the larger popula-
tion. Therefore, raw scores are transformed statistically into “standardized
scores,” which place that raw performance onto the normal curve illus-
trated in Fig. 1.
Many options are available for reporting statistical scores. These
include the most basic of transformations, which numerically change
every score into a z-score, with a mean of zero and a standard deviation
of one. This is a cumbersome method for describing data, however, so
most measures further transform performances into either t-scores (with
a mean of 50 and a standard deviation of 10) or standard scores (with a
mean of 100 and standard deviation of either 10 or 15). Almost all tests
described in this chapter and used in most psychological and neuropsy-
chological testing utilize standard scores. Many test performances are also
described using percentile ranks, which can be best described as placing a
person’s performance at a rank out of 100. In other words, a performance
score at the 75th percentile means that the examinee performed better than
75 out of 100 other individuals. Labels are also often used to describe
performances, with the greatest number of people in the normative group
performing at what becomes “average,” and then modified labels being
used at each standard deviation either above or below average.
3.4. Sensitivity and specificity

The concepts of sensitivity and specificity are often subconsciously con-
sidered when making decisions in medicine. It is essential for clinicians
to know whether a given laboratory test is indeed sensitive at identifying
a disorder so that the results can be correctly interpreted. Sensitivity is a
statistical concept that reflects the percentage of individuals who have a
particular disease and is often referred to as the True Positive Rate.
Specificity speaks to the rate of individuals who truly do not have a
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particular disease and is referred to as the True Negative Rate. It is optimal

for a test to have both high sensitivity and specificity; however, the prob-
ability that an individual truly has a disease is also dependent upon the
incidence or base rate of the disease in question. If the disorder is consid-
ered rare, it will be difficult to predict the presence of the disease state
even if the test is sensitive and specific. Ideally, predictive power of a test
is best attained with high prevalence of the disease state and high
specificity.
4. INTERNATIONAL CONSIDERATIONS
The ethical use of standardized psychological tests across cultures and
languages has been addressed by a variety of organizations (Table 1).
Ultimately, psychologists are bound by law and the professional ethics of
their licensing organization to consider, use, administer, and interpret
measures in an appropriate and ethical manner at all times. This begins
with a constant evaluation of the psychologists’ own level of competency.
When considering testing someone of a different culture or nationality,
considering one’s own level of knowledge about that culture helps deter-
mine if one is able to adequately judge the appropriateness of a measure.
The level of acculturation a patient of a different culture has to the psy-
chologist’s culture is also an important factor. A psychologist practicing
Table 1. Resources for international testing considerations.
The Ethical Principles of Psychologists and Code of Conduct (American Psychological

Association, 2002).
The American Psychological Association’s (APA) “Guidelines for Providers of
Psychological Services to Ethnic, Linguistic, and Culturally Diverse Populations”
(American Psychological Association, 1993).
The APA Guidelines on Multicultural Education, Training, Research, Practice, and
Organization Change for Psychologists, (American Psychological Association, 2003).
The International Test Commission (ITC) Test Adaptation Guidelines (International Test
Commission, 2002).
The Office of Minority Health of HHS National Standards for Culturally and
Linguistically Appropriate Services (CLAS) in Health Care (Office of Minority
Health, 2001).
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in the United States who is referred a German-born patient, who was

raised from the age of one year in the United States, may still need to
consider the cultural impact of the immediate family on that patient.
However, it is more likely that US-normed tests will be appropriate to use
with that individual than with another patient born and raised in Germany
who has only moved to the United States in the past year.
4.1. Cultural differences

Cross-cultural testing is becoming increasingly common. The development
of alternate versions and alternate use instructions for tests should stem from
test theory, and that development should be carefully analyzed by any pro-
fessional considering the test’s use. Multiple questions arise, not the least of
which is whether or not the construct in question is consistent across cul-
tures. Test theory discusses the conceptualization of constructs as being
either universal or specific. Some theorists argue that there are universal
constructs and that the individual expression of a universal construct is influ-
enced by an individual’s culture. As a result, some tests have been re-created
across different cultures, and each culture generally utilizes tests normed in
that culture. Each test used in a multicultural examination must be carefully
considered for bias and equivalence across cultural populations.4
Bias can be introduced through the construct. Constructs can be defined
very differently across cultures. Even intelligence, one of the most widely
examined constructs, would be defined disparately in a western culture
versus an agrarian third-world culture. Similarly, behaviors may not carry
the same meanings across cultures. Therefore, it becomes extremely
important to utilize tests that focus on construct-specific approaches but
not culturally impacted items.
Individual items can also introduce bias into the test process. Item
analysis should have been carefully completed on any cross-cultural test
in order to ensure appropriate meaning across cultural groups, transla-
tions, connotations, and applicability. The methods by which the test was
constructed for use in other cultures are important on a holistic level as
well. The normative group should be considered. Not only should norms
be available for that person’s expressed culture, but those recruited in the
normative group should have similar educational and test experiences.
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The International Test Commission has stated that in order for a test to be
translated or adapted for use in other cultures, four domains must be
addressed, including the context of the test, the construction, the test adminis-
tration, and the documentation and score interpretation [www.intestcom.org].
4.1.1. Context
The context with which any test is used across cultures must account for
fundamental cultural differences, which can be quite broad. Educational
differences across cultures are primary. Western culture has a dominant
educational style that has significantly affected the development of many
standardized tests. Different cultures may have not only different educa-
tional styles but also different levels of item knowledge and format expo-
sures. Some cultures may not be familiar with multiple-choice formats,
for example. Religion, social practices, and psychological influences
can also significantly affect how a person responds to specific tests.
It becomes most important for the psychologist to consider what infor-
mation the test results will contribute and to ensure that any risks of test
bias are significantly lower than the benefits the results may provide.
4.1.2. Administration
The administration of a test has a significant impact on the person taking
the test in cross-cultural testing or any form of testing and is why stand-
ardization of the test administration process is so important. However, just
such standardization may negatively affect certain cross-cultural situa-
tions. A psychologist’s test administration style may be more or less palat-
able to other cultures for a variety of reasons interacting with sex,
personality, tone and volume of voice, and even personal appearance. The
development of rapport is vital to reliable and valid test administration.
If cultural difference causes problems with the development of rapport,
not even the most appropriate test will yield valid results. Further, at times
psychologists might use other professionals during the testing process,
which can further complicate cross-cultural issues.
Many psychologists utilize psychometrists, test administration profession-
als with advanced training in test administration. The test administrator must
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be as aware of and attentive to cross-cultural issues as the psychologist super-

vising the case, much the same as a resident physician working with an
attending physician to evaluate an ill patient. In some cases, interpreters may
be used in the testing process. This is more common during the interview por-
tion of an evaluation session and unusual in actual testing situations, because
the use of an interpreter violates the standardized methods of most formal
psychological measures. In order for an interpreter to ensure that he or she is
following all testing protocols succinctly enough for the administration to be
valid, the interpreter would in essence have to administer a translated test, and
translating a test into an alternate version is a long scientific process.
To create a version of a test in another language, various approaches can
be used, ranging from two-way translations to committees. Often, problems
arise during attempts to directly translate a measure. Many languages do
not have direct word translations for colloquial sayings, and connotations
of questions are easily lost in the change of language. By the time a test has
been translated, it may no longer measure what it was originally designed
to measure. Therefore, often a complete re-analysis and re-norming of the
measure must be completed in order to ensure validity. In other words,
translating a test into another language actually means redesigning and
re-creating a new test. Using a translator to simply change the language dur-
ing test administration severely jeopardizes the ability to interpret results.5
Test selection in a cross-cultural setting, therefore, becomes extremely
important. If tests are not available with normative data appropriate to a
person’s cultural background, serious consideration must be given to what
constructs should be evaluated. Tests should be selected that avoid lan-
guage all together, if possible, and focus only on specific constructs that
will be useful to treatment planning. For example, if a Spanish-speaking
person is being evaluated to estimate English proficiency as part of a voca-
tional assessment, the use of English-language tests would be appropriate.
However, if a Spanish-speaking person were referred for assessment of
intellectual skills to assist with treatment planning for rehabilitation after
a stroke, the clinician would need to be able to provide either non-
language or Spanish-instruction assessment instruments only. Further, if
the clinician did not have the competency to administer tests with Spanish
instructions, that clinician may need to consider referring the patient to
another testing professional with appropriate experience.8
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4.1.3. Interpretation
The interpretation of test results in a cross-cultural setting is heavily influ-
enced by the issues discussed above regarding test creation and selection.
The use of appropriately normed measures should allow the clinician to
make appropriate interpretations about the patient’s skills. If measures have
been used that do not have similar normative groups as the patient, interpre-
tation becomes more difficult. Attempts must be made to account for cultural
influence in the person’s performance. For example, if a bilingual patient
from a primarily African culture was administered an English-normed intel-
lectual measure, the interpretation would need to explain that lower scores
would be expected on verbal measures due to cross-cultural impact.
Psychologists do not rely on one measure to make a definitive
diagnosis. During an evaluation process, each measure’s interpretation is
either supported or refuted by collaborating data, such as interview,
behavioral observations, or other test data. Interpretation in a cross-cul-
tural setting is no different. Particularly in situations where cultural influ-
ence may affect a patient’s performance, corroborating information
should be obtained to support any reported findings.
The documentation of the evaluation session should also carefully out-
line cultural considerations, including a thorough discussion of behavioral
observations and the rapport developed with the examiner. Effort and abil-
ity to engage in the testing process should be clearly explained. The
choice of tests should be outlined, along with rationale, and the findings
should include discussions of the cultural impact on the testing session.
5. CLINICAL TESTING AND NEUROPSYCHOLOGY

Neuropsychology is the study of brain and behavior relationships, and
neuropsychologists comprise approximately 2% of clinical psychologists,
collectively defined as those who have advanced training in neuroscience,
neurobehavioral disorders, and psychological principles. Unfortunately,
there is presently no uniform regulating body for the practice of neuropsy-
chology in the United States, such that any US psychologist can proclaim
that he or she does “neuropsychological testing.” There further appears to
be inconsistency in how the term neuropsychologist is used in other coun-
tries. Perhaps a universally helpful litmus test for the referring clinician is
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whether the neuropsychologist has undergone a formal, typically two-plus

year, postdoctoral fellowship in neuropsychology, which is considered the
gold standard of training.
Several neurocognitive domains of function are assessed as part of the
comprehensive evaluation, which is perhaps the most substantial way
neuropsychological evaluations differ from psychological or psychoedu-
cational assessments (Table 2). In the past, formal batteries were
Table 2. Examples of psychological/neuropsychological measures by Realm.
Intelligence
Wechsler Intelligence Scales (preschool, child, adult, abbreviated, non-verbal)
Stanford–Binet Intelligence Scales
Leiter International Performance Scales-Revised
Kaufman Brief Intelligence Test-Second Edition
Memory
Wechsler Memory Scale-Third Edition
Wide Range Assessment of Memory and Learning-Second Edition
Language
Boston Naming Test
Clinical Evaluation of Language Fundamentals-Fourth Edition
Visual and Motor
Grooved Pegboard Task
Attention and Executive Functions
Conners’ Continuous Performance Test-Second Edition
Delis–Kaplan Executive Function System
Personality
Minnesota Multiphasic Personality Inventory (Adolescent, Second
Edition Restructured)
Beck Inventories (Depression, Anxiety)
Rorschach Inkblot Test
Thematic Apperception Survey
Sentence Completion Survey
Academic
Woodcock–Johnson Tests of Achievement-Third Edition
Wechsler Individual Achievement Test-Third Edition
Wide Range Achievement Test-Fourth Edition
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developed for neuropsychological assessment, but the use of standardized

batteries is limited now, with the majority of clinicians electing a more
eclectic choice of test administration. In the 1940s, the Halstead–Reitan
Battery was created to identify specific areas of brain damage. In the
1980s, the Luria–Nebraska Neuropsychological Battery was formalized
by Golden to discriminate between patients with and without neurological
impairment. Although portions of these well-known neuropsychological
batteries are often still used, other similar batteries have been developed.
Particularly for specific conditions, a wider range of individual measures
is available across domains.12
6. COGNITIVE OR ATTRIBUTE TESTING

6.1. Intellectual
The study of human cognition can be traced back several centuries, but
modern assessment techniques owe a great deal to early statistical concepts
pioneered by Sir Frances Galton (1822–1911). Statistical analyses provide
a foundation for which meaningful comparisons can be made between an
individual’s performance and that of a sample population and can be used
further to track performance of an individual over time. The term intelli-
gence represents a multifaceted theoretical concept to encompass various
analytic, novel learning, and mental processing skills necessary to navigate
the greater social world. Multifactorial theories of intelligence abound, and
a detailed exploration of these theories would deviate well beyond the
scope of this chapter, which instead presents a practical understanding of
intelligence tests and their place in clinical practice.
As noted earlier, Intelligence Quotient (IQ) is a term reflecting a sum-
mary score of an individual’s performance on a standardized measure rela-
tive to a sample of age-matched peers. Three essential points are made here:
(1) An IQ score is a measure of aptitude, and although it is correlated

with academic and vocational success, it does not determine success,
nor should it be used as an absolute ceiling of one’s potentials.
(2) An IQ score is a sample data point and thus some error and variability
is inherent. It is therefore most appropriate to view a particular score
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as representing functioning within a band of scores. Some clinicians

will include a range of scores based on a 90% or 95% confidence
interval. For example, a Full Scale IQ of 95 would indicate that the True
score falls between 90 and 100 with a 95% degree of confidence.
(3) An IQ score is a summary score on a particular test relative to a sam-
ple obtained from the population. If the sample is skewed or otherwise
insufficient or if the “IQ test” is flawed in validity, the obtained
score is useless. Keep this in mind the next time a friend touts the
robust 138 IQ he or she recently obtained on an Internet-based
“What’s your IQ?” test.
Intelligence testing is often indicated in clinical settings where cognitive

disabilities are suspected but is also utilized within the school setting to
establish special education needs and school placement. Intelligence test-
ing also is frequently incorporated into a larger battery of tests used by
neuropsychologists to evaluate cognitive functioning in the context of
neurological dysfunction or suspected neurological changes secondary to
disease state directly or indirectly impacting the central nervous system.
Often in cases of brain injury in which no previous testing is available,
measures of reading decoding can provide estimates of premorbid intel-
ligence, as long as that person has no history of reading disability.
Repeated intellectual evaluations can help track changes in cognition
secondary to a stroke or brain injury but can also be used to assess for and
monitor changes that may be reflective of the beginning stages of a
dementia. A word of caution though: it would not be surprising for an
individual to perform substantially better on a test with repeated expo-
sures, particularly if the measure were given relatively shortly after the
initial administration. This phenomenon refers to practice effects, which
is simply defined as an improvement in performance with repeat exposure
of a test. There is substantial debate as to what constitutes a sufficient
amount of time to have elapsed between repeat testing, and much depends
on the patient population and the actual subtests being administered.
Convention would suggest that a span of at least 12 months since prior
testing will help limit practice effects. Unlike most of the intelligence
tests, some neuropsychological measures should be repeated only in
extenuating circumstances.
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The most commonly administered intellectual measures for English-

speaking cultures would likely be considered the Wechsler measures.17
Different versions of Wechsler’s intelligence tests exist for different age
ranges (e.g. preschool, child, and adult). In addition, specialized versions
of these tests have been developed for short (abbreviated) administrations
and non-verbal administrations. Also, the Stanford–Binet Intelligence
Scales, which are based on an originally internationally developed scale,
are still strongly in use. Additional intellectual measures are used for
specific populations, including the Leiter International Performance
Scales-Revised, which are specifically designed to be used in an entirely
non-verbal environment, eliminating the confounds of testing someone
with significant language problems, non-English speaking patients, or
other forms of impairment that might interfere with more traditional
forms of intellectual testing.
Approximately half the population will fall within the average range
on an IQ test, or demonstrate a performance range between 90 and 110,
on the normal curve. The upper 25% of the population will score between
110 and 160, depending on the instrument administered. It is important to
note that a score >120 is considered the Superior range and many schools
use a score of 130 (among other factors) in determining gifted and talented
placement.
Perhaps of greatest clinical interest is the population representing the
lower 25%, which includes the low average range through the profoundly
cognitively disabled range. According to the Diagnostic and Statistical
Manual of Mental Disorders-Fourth Edition (DSM-IV) and historical
conventions, an IQ between 80 and 90 is considered to be in the low aver-
age range, and an IQ between 70 and 80 is considered to be in the border-
line cognitively disabled range. The borderline range represents
approximately 6% of the general population. What has historically been
termed mental retardation refers to intellectual functioning (and commen-
surate adaptive skills) falling within the extremely low range and repre-
senting the lowest 2% of the population. Degrees of severity include mild,
moderate, severe, and profound mental retardation, and each of these
levels requires a unique approach when managing school, treatment, and
community functioning. The reader is encouraged to review the DSM-IV
and current texts such as Mental Retardation: Historical Perspectives,
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Current Practices, and Future Directions by Ronald Taylor et al.16 for a

more in-depth discussion of the various levels of cognitive disability and
its management.
We have discussed several of the benefits and cautions when consider-
ing the use of intellectual measures, and it should be apparent that an IQ
summary score can provide a wealth of knowledge about a patient’s level
of functioning, which in turn can be used with other data to facilitate the
most appropriate level of care for an individual. At this point, making the
clinical diagnosis of mental retardation warrants a bit further discussion.
As mentioned, a diagnosis of mental retardation includes a subaverage
level of intelligence on formal testing and adaptive functioning (e.g. social
skills, daily living skills) at a similar level. The reason for this is that most,
if not all, IQ measures incorporate multiple sub-domains that are often
equally weighted. An individual with significant language impairment
might perform poorly on measures of verbal reasoning but might be low
average or even average range in visual-spatial skills and processing
speed, but the aggregate score (Full Scale IQ) might very well yield a
borderline or lower score. This is an unfortunate consequence of statistical
averaging and illustrates how caution should be used when interpreting an
IQ score and test scores in general. The reason that an associated deficit
in adaptive behaviors is necessary in the diagnosis of mental retardation
should now be evident; it is to minimize the likelihood of attributing an
isolated deficit as reflective of global cognitive dysfunction. In cases
of known or suspected isolated deficits or markedly variable levels of
performance, more comprehensive neuropsychological testing is often
indicated.
6.2. Additional attributes

6.2.1. Learning and memory
Memory and learning represent a vast construct in clinical neuropsychology,
and an entire section could be devoted to the subject. The most essential
concepts are discussed here.
Memory includes the complex process of acquisition, encoding, stor-
ing, and retrieval, and disruption at any point can result in memory
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disturbance. Therefore, close examination and scrutiny of various test

results is essential in addressing a referral for memory complaints, par-
ticularly when a diagnosis of dementia is at stake. At the acquisition end
of memory, attention and working memory serve as the basis for learning,
often assessed utilizing working memory measures such as those from the
Wechsler intelligence scales. After information enters conscious aware-
ness, it is processed through the working memory system, which serves as
a scratch pad for temporary recall of information under process. At this
point, memory is rehearsed, encoded, and ultimately stored for retrieval at
a later time. The assessment of encoding, storage, and retrieval is accom-
plished through the use of measures such as the Wechsler Memory Scale,
Third Edition and Wide Range Assessment of Memory and Learning,
Second Edition. These two measures offer verbal and visual memory
measures of structured and unstructured formats.
Explicit or declarative memory refers to memory for what one can
bring to mind or declared. Memory can also be explicit and episodic,
referring to memory for events (e.g. a recent trip to the zoo). Finally,
memory can be implicit, which includes the ability to perform actions and
tasks or to produce a specific type of response (e.g. a golf swing). Implicit
memories cannot be consciously recalled or remembered to be used for
reasoning. Often, implicit memory capacity remains intact in all but the
most profound neurological disruption. Even the late bilateral hip-
pocampectomy patient H. M., whose amnesia served as the basis for many
theoretical models of memory, was able to demonstrate implicit learning
despite profound anterograde amnesia.
6.2.2. Memory loss

Anterograde memory loss prevents a patient from establishing new perma-
nent memories from the time of illness. Importantly, the recall burden
must exceed the immediate memory span, because true memory impair-
ment is a failure to encode and retrieve the information that has been
learned. Duration of anterograde memory loss subsequent to injury is
often a stronger predictor of recovery than retrograde symptoms.
Retrograde amnesia is the loss of ability to recall events occurring before
the illness. In most cases, this impairment is worse for relatively recent
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events than for events that occurred in the remote past. Many amnesiac
patients show preservation of certain cognitive abilities, and the presence
of intact global cognition can help define the syndrome. For example, mild
cognitive impairment by definition consists of normal global cognitive
abilities in the context of circumscribed deficits in aspects of memory.
Not surprisingly, a variety of measures exist to help the clinician evalu-
ate memory functions in patients ranging from early childhood through
senescence. Some measures assess span memory for auditory information
(e.g. Digit Span from the Wechsler scales) or visual span (e.g. Knox’s
Cube Test). In-depth measures also exist to assess memory for informa-
tion in context, often assessed through story memory. Rote verbal memory
can be assessed through list learning activities (e.g. Hopkins Verbal
Learning Test, Rey Auditory Verbal Learning Test). Although an inher-
ently more challenging prospect, measures have been designed to assess
visual memory and learning by having the examinee remember patterns,
draw objects from memory, recall faces, and recall information from pic-
tures. Again, the keen examiner will evaluate performance on various
memory measures in the context of the entire battery to determine where
the deficit truly lies. For example, a patient may present with unusual
symptoms of loss of autobiographical information with a lack of addi-
tional memory loss, as illustrated by testing. Such a presentation is often
more indicative of a conversion disorder or memory issues related to
emotional problems rather than neurological sequelae.
6.2.3. Language
Language is a necessary component in communication and is essential in
classroom and occupational success. The discipline of speech and lan-
guage pathology places a major emphasis on evaluating and treating
expressive and receptive language disorders in children and adults.
Psychologists and, more typically, neuropsychologists incorporate lan-
guage measures as a part of broader testing batteries to provide assess-
ment for specific referral questions, such as determining the type and
degree of aphasia, as well as to help answer questions related to develop-
mental language delays in the context of neurobehavioral syndromes
(e.g. autism spectrum disorders). Language tests can be brief and include
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simple naming or word generation activities (e.g. word fluency), or they

can have a more linguistic focus, emphasizing syntax, grammar, and
morphology (e.g. Clinical Evaluation of Language Fundamentals-
Preschool, Second Edition or Fourth Edition). Another important aspect
of language assessment is pragmatic language, essentially those aspects
of language that address communicative intent. These include voice
inflection, idioms, inference, and implied meaning (e.g. Comprehensive
Assessment of Spoken Language). Testing in this realm can be difficult
in the clinic setting but useful for children when there is a strong suspi-
cion for an autistic spectrum disorder, such as Asperger’s syndrome.
6.2.4. Visual–spatial abilities

Several measures are available to the neuropsychologist to assess
non-verbal abilities, and this type of evaluation is often helpful in the
assessment of visual neglect and forms of agnosia, such as a line bisection
task. These measures are of course not designed to take the place of an
ophthalmological vision examination, and it needs to be assured that basic
vision functions are intact before proceeding with assessment of higher
order visual-spatial abilities. The contribution of motor control and coor-
dination, as well as general speed, needs to be considered when evaluating
non-verbal functions and can be assessed with measures such as the
Beery–Buktenika Developmental Test of Visual–Motor Integration. Select
measures are available to the examiner that are non-motor-dependent and/
or are untimed, which can help to control for some of the variance
(e.g. Motor-Free Visual Perception Test, Third Edition [MVPT-3]).
However, measures that are novel and have a motor and planning compo-
nent are often incorporated into a battery because they may be helpful
adjuncts in the assessment of executive functions, including the Trail
Making Test. Taken together, these factors illustrate some of the com-
plexities in evaluating visual-spatial abilities.
6.2.5. Motor and sensory examination

Motor and sensory examination is commonplace in the adult practice of
neuropsychology and is frequently employed to assess lateralization of
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hemisphere dysfunction. Motor examination is also helpful for returning

to job and day-to-day functions following injury and, in the pediatric set-
ting, aids in understanding supports and accommodations that might be
necessary in the context of cerebral trauma. Commonly used measures
include assessment of dexterity (e.g. Grooved Pegboard and Purdue
Pegboard), motor fluency (e.g. Finger Tapping), and grip strength as
assessed via hand dynamometer. Tactile examination is steeped in the
tradition of the neurological examination and includes an assessment of
finger gnosis and graphaethesia, which also is helpful in lateralizing
deficits.
6.2.6. Attention and executive skills

Attention refers to the cognitive processes of sustaining, selecting, disen-
gaging, and dividing attention. This is often an area of interest in patients
referred for the neurobehavioral syndrome of ADHD but is also important
to evaluate in patients suffering focal and diffuse brain injury and
dementias. Neuropsychologists have at their disposal a variety of meas-
ures designed to tease out overt and even subtle problems with the atten-
tion system. Continuous performance tests, such as Conners’ Continuous
Performance Test-Second Edition, Gordon Diagnostic Systems Vigilance
Task, and Test of Variables of Attention (T.O.V.A.) are perhaps the most
frequently employed measures and assess sustained mental effort. They
have the added benefit of assessing for disinhibition and impulse control.
Although these tests have not been proven to be diagnostic of ADHD, they
can be used with other clinical information to discern whether a clinically
significant attention problem exists. Other more specialized measures of
attention exist to complement the referral question and might include an
exploration of whether there is a problem related to visual versus auditory
attention or determining whether other neurocognitive processes are exac-
erbating attention problems (e.g. Test of Everyday Attention for Children,
Paced Auditory Serial Addition Test).
Methods of assessing abstract reasoning ability and the shifting of
thought processes, called cognitive flexibility, have existed for many
years. The Wisconsin Card Sorting Test, originally designed in the 1940s,
is one example that continues to be used extensively.7 “Executive
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functions” are higher order processes that govern cognition and include
the abilities necessary to plan, organize, and generate goal-directed behav-
iors. This multidimensional construct has been conceptualized for some
time and has been more fully explored in the last few decades.11 Research
on executive functions continues to build momentum. It has long been
established through head injury research that executive deficits are a pre-
dictable consequence of damage to the prefrontal cortex; however, there
is mounting evidence that the frontal lobes may help with the recruiting
process of different brain regions to initiate a given task but that executive
dysfunction can be seen in a variety of lesions, including damage to sub-
cortical structures and the cerebellum.10 Due in part to the vast and com-
plex nature of executive functions, it should be no surprise that tests
designed to assess higher order cognition in the laboratory or clinic setting
remain far from perfect. At present, measures exist to reasonably assess
working memory, logical problem-solving, abstract reasoning, sequencing
and planning, and reactive flexibility, such as the Delis–Kaplan Executive
Function System [2001]. As a word of caution, it is essential to explore
and elicit examples of “real world” problem solving skills in the clinical
interview over relying too heavily on standardized measures of higher
order cognition. The Behavior Rating Inventory of Executive Functions
(BRIEF)6 is a rating questionnaire for children aged 5 through 18 designed
to assess behavioral regulation and metacognition on a day-to-day basis.
6.2.7. Developmental and functional abilities

As we have discussed, several psychological and neuropsychological
measures exist to aid in the evaluation of patients through the life span;
however, many of these clinical instruments provide only a sliver of
insight into the daily living situation at home and in the community.
Adaptive behavior scales are designed to complement in-clinic testing
measures by collecting collateral information from caregivers, teachers,
and other informants as to how the patient functions in various capacities.
Examples of adaptive behaviors in younger children include washing,
dressing, and peer development skills. Activities of managing finances
and medication and the ability to plan or engage in a routine are necessary
skills to be assessed in adults. Historically, adaptive behavior scales have
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been used when a diagnosis of mental retardation or cognitive disability

is being considered. Indeed, the Diagnostic and Statistical Manual of
Mental Disorders, Fourth Edition, Text Revision1 explicitly defines Mental
Retardation as subaverage general intellectual functioning that is accom-
panied by significant limitation in adaptive behaviors in various skill
areas. Although the scope of adaptive behavior assessment continues to
increase, particularly in the assessment of children with disabilities other
than mental retardation, measures such as the Vineland Adaptive Behavior
Scales, Second Edition, continue to represent the standard in the evalua-
tion of suspected cognitive disability. Gaining a clear picture of cognitive
strengths and weaknesses by way of standardized testing as well as quan-
titative level of current day-to-day functioning can prove extremely useful
in treatment planning and prognosticating.
6.2.8. Effort
Individuals may have many reasons for not engaging adequately in the
testing process. Unlike medical tests that objectively measure aspects of a
person’s body without the person’s overt involvement, psychological test-
ing requires that a person put forth appropriate effort and remain moti-
vated for the process. At times, that motivation can be impacted by
secondary gain or less conscious, non-malicious psychological issues. In
order to evaluate whether a person is being impacted by subconscious
emotional issues, negativistic attitudes, or more overt secondary gain,
personality measures are often incorporated as part of an evaluation where
motivation is at question. Many self-report measures, such as the Behavior
Rating Inventory of Executive Function6 mentioned earlier, offer scoring
opportunities to determine how consistent the person’s responding has
been and indicators of how extreme the person’s responses may be in the
negative direction. More lengthy self-report personality measures, such as
the Minnesota Multiphasic Personality Inventory-2,2 offer more formal
validity scales, meant to help the clinician interpret the person’s motiva-
tion and engagement in the task. Additionally, more formal “malingering”
measures have been created and are available commercially. However,
poor performances on these measures can be complex to interpret. If a
person was not believed to be completely engaged or motivated toward
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performing as well or as honestly as they could during the testing process,

then interpretation of the entire testing session outcomes should be called
into question. At times, some aspects of testing can still be informative,
particularly with regards to trying to determine what the persons other
motivations may be. However, overall interpretation becomes extremely
complex. Many times these types of evaluations involve some form of
legal arbitration, such as determining the extent or permanency of cogni-
tive injuries or impairment. Although poor effort can negatively impact a
psychological or neuropsychological evaluation at any time.
6.2.9. Competency
Psychologists are often called upon to perform evaluations of a person’s
competency in various settings. A common area in which competency is
questioned is in legal settings, where a defendant must be shown to be
competent to stand trial. Individuals not competent to stand trial often
participate in training and re-evaluations until they are shown to be able
to understand and discuss the legal process. However, several other areas
of competency are often evaluated by psychologists as well and range
throughout the lifespan. Parenting, self-care, and the care of others are
often questions of concern. Functional independence can involve compe-
tency issues, including requests to evaluate individuals for competency to
drive, manage finances, and make medical decisions for themselves and
for others. A psychologist would not rely on one singular or specific
evaluation measure to make such decisions. Recommendations for com-
petency would be made based on a cumulative decision inclusive of a
broad approach to evaluation.
6.2.10. Personality and emotional

Many medical and clinical personnel refer to psychological testing as
being synonymous with an emotional evaluation. While we have clearly
outlined in this chapter that psychological testing can actually be multi-
factorial, emotional assessments are often an important component of an
evaluation. This can include personality assessment, which is often based
more strongly in theoretical approaches such as psychodynamics, or more
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overt emotional assessments, which tend to focus on more quantifiable

aspects of diagnostic emotional dysfunction. The approach a psychologist
chooses to use to assess personality and emotional functioning will be
strongly impacted by their training and theoretical approach. Assessment
can include rating scales, which are standardized questionnaires that gen-
erally result in several standard scores in various areas of functioning.
These can be completed by the person being evaluated, self-rating scales,
or others involved in that person’s care, teachers and parents. Structured
and semi-structured interviews can also be used, generally to assess the
quantifiable number of symptoms of emotional dysfunction based on the
diagnostic symptoms of emotional disorders. Projective measures are also
available and require specific training on the part of the clinician.
Projective measures assess the patient’s ability to respond to relatively
ambiguous stimuli, with the theory being that without overt structure a
person will “project” their personality and emotional structure onto the
stimuli. This is generally expressed by the patient sharing stories, finish-
ing sentences, or interpreting vague visual stimuli. Once completed, a
thorough emotional evaluation should inform a patient’s view of them-
selves, others, their overall emotional state, reality testing, and coping
skills. Personality structure is often discussed as part of the evaluation of
adults, or if there is a specific diagnostic personality issue.
7. ACADEMIC ACHIEVEMENT
Academic achievement testing is extremely useful in psychological, psy-
choeducational, and neuropsychological assessment, particularly when
evaluating children and adolescents. After all, much of the early feedback
we receive about our successes and failures germinates in the classroom.
Therefore, it is often important to address academic skill development as
part of more comprehensive testing, particularly to rule out specific learn-
ing disabilities that might have a greater chance of remediation if
addressed earlier along the academic path. Achievement measures tend to
be grouped into two categories: screening tools and broad-based assess-
ment. The former consists of brief measures of reading in isolation or
single-word decoding, spelling, and papers/pencil math as is the case for
the Wide Range Achievement Test (WRAT-4). More elaborate academic
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achievement measures such as the Woodcock–Johnson III Tests of

Achievement and the Wechsler Individual Achievement Test-III address
multiple facets of reading, math, and written language, and scores on
these measures are widely accepted by college and post graduate entrance
examination boards when petitioning for extra time or other testing
accommodations. More fine grained assessment of academic skills can be
achieved with specialized instruments. For example, assessment of funda-
mental phonological processing skills necessary for successful reading
decoding is essential in addressing concerns for developmental dyslexia.
8. OCCUPATIONAL TESTING
Occupational or vocational testing is available from psychologists with
specialized training and focus of practice. An individual’s functional level
may be of particular interest in an occupational evaluation, and this could
also include quantifying handicaps or specific needs of individuals seek-
ing employment. However, specific and unique approaches to occupa-
tional testing include the development of individualized batteries for a
company, who then utilizes that battery to provide similar assessment
measures for all prospective employees. In particular this can allow for the
assessment of skills required for individual jobs, such as typing speed for
an administrative assistant or knowledge of medical terminology for a
transcriptionist. Occupational assessments are often used to try and pre-
dict who will perform best when placed in certain positions. Vocational
assessments more often refer to assessments used by an individual to help
ascertain where their skills would be best suited in the job market. This
can assist in planning for future vocational training, and treatment plan-
ning in rehabilitation facilities.
9. KEY POINTS
• Reading decoding often provides an accurate estimate of premorbid
intelligence in individuals with CNS dysfunction who have no prior
history of reading disability.
• Duration of anterograde memory loss is a far better predictor of brain
injury recovery than degree of retrograde memory impairment.
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• Dissociative amnesia is a fairly common presentation in conversion

disorders. Close examination of the pattern of memory loss (e.g. is
there a preference for losing autobiographical information) as well as
a detailed history of the events leading up to the symptoms will often
elucidate the true etiology.
• Whether a given measure is actually measuring what it was designed
to measure is known as test validity. How well a test measures a par-
ticular trait or how consistently it distinguishes between performances
on the attribute being measured is equally, if not more, important and
is termed reliability.
• An individual taking a standardized test measure should match the
general characteristics of the normative group used in the test’s
development.
• Sensitivity is a statistical concept that reflects the percentage of indi-
viduals who have a particular disease and is often referred to as the
True Positive Rate. Specificity speaks to the rate of individuals who
truly do not have a particular disease and is referred to as the True
Negative Rate.
• During an evaluation process, each measures’ interpretation is either
supported or refuted by collaborating data, either from interview,
behavioral observations, or other test data.
10. SELF-ASSESSMENT
10.1. Intellectual measures yield standard scores. For the most
part, when considering a standard score, the score
is based on:
(A) Mean of 10 and a standard deviation of 3.
(B) Mean of 50 and a standard deviation of 10.
(C) Mean of 100 and a standard deviation of 15.
(D) Mean of 100 and a standard deviation of 10.
Most neuropsychological measures are based on a mean of 100 and a

standard deviation of 15. T-scores can be converted from standard scores
and have a mean of 50 and a standard deviation of 10. Scale scores, which
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are often represented as subtest scores on particular measures have a mean

of 10 and a standard deviation of 3.
Answer: C15
10.2. You have been given a rating scale to review that measures
apathy and notice several of the items appear more related
to self-esteem and social anxiety. Concern for whether
patients would believe this measure actually taps into
apathy relates to:
(A) Discriminate Validity.
(B) Convergent Validity.
(C) Predictive Validity.
(D) Face Validity.
(E) Internal Consistency.
Discriminate and convergent validity have to do with how a measure

relates to similar measures. Predictive validity as the name implies relates
to how well the measure can predict future behavior/performance. Internal
consistency is a type of reliability looking at how well items on a given
measure are related to each other. Face validity addresses whether on the
surface a measure appears to be measuring the construct it is intended to
measure.
Answer: D15
10.3. An adolescent female presents at the hospital with

“memory problems” of an unknown etiology. Which
of the following would raise the greatest suspicion
for dissociative amnesia:
(A) An inability to recall the names of her treating professionals despite
frequent repetition.
(B) Difficulty remembering that she is in a hospital.
(C) Progressive loss of information occurring in the days leading up to
the hospitalization.
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(D) Intact novel learning with spotty recollection for autobiographical

information, such as the names of close friends and family.
Differentially impaired autobiographical information is a common theme

in conversion disorder presenting as memory impairment. Although some-
what rare in children outside of traumatic brain injury, individuals can
have temporally graded memory loss where they can remember remote
information (e.g. where they grew up) but struggle with more recent infor-
mation/events. Deficits in novel learning can also be seen in various neu-
rological disruptions.
Answer: D9
11. CASE STUDIES

11.1. Neuropsychological assessment in a traumatic brain
injury clinic
A 37-year-old Hispanic male presented for neuropsychological assess-
ment as part of his participation in the Moderate Traumatic Brain Injury
Clinic (MTBIC). The patient was born in Juarez, Mexico and immigrated
to a Midwestern state in the United States at 30 years of age. Since mov-
ing he has been working on a construction crew, where he was injured by
falling from scaffolding. Reports indicate a 10 min loss of consciousness
with negative cranial CT. Immediate symptoms included disorientation to
place and time for at least 4 hrs and 24 hrs retrograde amnesia. Symptoms
continuing two weeks post-injury include headache, dizziness, fatigue,
sensitivity to light and noise, problems with memory and concentration,
and increased irritability. Standard MTBIC protocol includes assessment
by a psychometrist utilizing IQ, memory, attention and executive function,
and self-report emotional measures. Upon reviewing the intake informa-
tion, the supervising neuropsychologist changed the assigned case to a
graduate student technician who speaks Spanish and has two years of
experience living in Mexico. Measures were changed to include the
Kaufman Brief Intelligence Scale-Second Edition, which can be adminis-
tered according to standardization in Spanish. Additional measures were
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administered per protocol. Findings suggested average IQ, with verbal

and visual memory scores falling in the borderline impaired range and
attention and executive skills results ranging from low average to average.
Significant levels of anxiety and depression were endorsed. Results were
felt to indicate Post-Concussion Syndrome, with continued memory defi-
cits. Treatment planning included work and cognitive activity restrictions,
as well as referral to therapy and psychiatric treatment of emotional
symptoms.
11.2. School failure

An eight-year-old girl presented for evaluation due to school failure.
While the child was born in the United States, her parents were both
born and raised in Germany, learned English as a second language, and
spoke German at home. No additional major medical or psychiatric his-
tory was reported. Assessment included administration of standard
intelligence, academic, language, and attention and executive skills
measures. Results indicated a slightly stronger, high average, perfor-
mance on visual intelligence measures than the average results on ver-
bal intellectual measures. Such a split between verbal and visual skills
is often observed in bilingual children tested utilizing English meas-
ures. Academic skills acquisition was in the borderline impaired range
for word reading, comprehension, spelling, and written language skills.
Mathematics skills were in the above average range. Overall language
comprehension abilities, even on English-normed measures, were in
the average range, with the exception of a borderline impaired perfor-
mance on a task of phonemic awareness. Attention and executive skills
were in the average to above average range. Results indicated dyslexia,
a reading disability in which the brain is unable to appropriately pro-
cess the phonemes or individual sounds corresponding with letters.
Recommendations included special education assistance through
school as a child with a learning disability. Specifically, participation
in alphabetic-phonics instruction was encouraged, as well as a skills
appropriate (rather than grade appropriate) curriculum and individual
tutoring.
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Chapter 7
Psychiatric Disorders in Childhood

and Adolescence
Michael Koelch and Joerg M. Fegert
1. INTRODUCTION
Child and adolescent psychiatry involves the assessment and treatment of
disorders from birth up to the threshold of adulthood. Psychological
development plays a special role in child and adolescent psychiatry. Just
as the physiological behavior of children differ from that of adults, psy-
chopathologies may differ markedly from those in adults as well. Behavior
may have different functions at various ages and may be either normal or
abnormal at different stages. For example, fear of strangers is normal in
toddlers but is considered abnormal in adolescents, and toddlers naturally
exhibit more motor activity and motor restlessness than older children. In
other words, the frame of reference for what is normal and what is symp-
tomatic is strongly dependent on the developmental stage. In addition,
some phenomena that would represent a qualitative change in experience
in adults are completely normal variants of experience in childhood.
These include imaginary friends or conversations with such friends,
which are not at all rare in prepubescent children and are in no way to be
viewed as hallucinatory symptoms or signs of schizophrenia.
Developmental transitions (starting school, puberty, etc) are particularly
associated with the development of psychiatric disorders. The various
137
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138 M. Koelch and J. M. Fegert
transitions from infancy to young adulthood present many such situations

in which adaptation to new challenges may succeed — or fail, giving rise
to disorders.
1.1. Development
The development of child and adolescent psychiatry as an autonomous
discipline has been influenced by many other disciplines, including edu-
cation, pediatric medicine, social work, and psychiatry. These have all had
an effect on the day-to-day practice as well as on research areas in child
and adolescent psychiatry. Today, child and adolescent psychiatry is an
autonomous discipline informed by a broad spectrum of research, but it
is also characterized by a particular multidisciplinarity. Collaborative
research projects involve fields such as pediatrics, neurology, neurobiol-
ogy, psychology, psychiatry, the social sciences, education, and the law.
1.2. Specific aspects of treatment

Whereas the autonomy of the patient is central to the therapeutic process
in adult psychiatry, the therapeutic focus in the treatment of child and
adolescent disorders is always the patient’s family. Treating only the child
or adolescent is rarely successful. At the same time, the treatment of chil-
dren and adolescents involves particular ethical issues. Given their
increasing sense of autonomy, minors’ right to participate must be bal-
anced against the rights and needs of their parents. Therapeutic interven-
tions must be carefully explained to the parents and to the child. The
child’s cooperation and motivation must consistently be elicited in treat-
ment. Many children suffering from child and adolescent psychiatric dis-
orders, particularly externalizing disorders (e.g. ADHD, conduct disorder)
but also some internalizing disorders (e.g. anorexia nervosa), are not
motivated to receive treatment. Often, the parents are eager to treat the
symptoms. Critical therapeutic situations occasionally arise, such as when
an adolescent is endangered and treatment is medically indicated but he
simply refuses treatment. In such cases, treatment must be administered
against the adolescent’s will in cooperation with the parents. An even
more problematic situation arises when treatment reveals that the parents
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Psychiatric Disorders in Childhood and Adolescence 139
themselves are endangering their child (e.g. as a result of maltreatment or

abuse). In these cases, the protection of the child and the developmental
prognoses for the child under the given circumstances are paramount. The
legal framework of child protection differs very much between different
countries. Some countries require the notification of youth services, while
other countries consider child abuse and the sexual abuse of children pri-
marily as criminal offenses and rely on the criminal law system with
prosecution. In many other countries, child psychiatrists, like pediatri-
cians or family doctors, are bound by medical confidentiality, and this
confidentiality can only be broken in cases where the child in question is
in imminent danger. Child protection is the subject of on-going debate in
modern societies. Critical reports like the Lord Laming recommendations
in the United Kingdom led to legal changes and changes in practice.18
Therefore, experts in child and adolescent psychiatry always have to keep
up to date about the legal conditions and the practical network of child
protection in their local area.
Because child and adolescent psychiatric disorders affect mostly the
family and social contacts of a child, assessment includes evaluation of
parents, teachers, and further relevant persons. For most of the disorders,
standardized check-lists for parents or teachers are available (CBCL, TRF,
Conners, SNAP, etc). Especially in disorders, for which diagnostic criteria
require a pervasive presence of symptoms in more than one situation,
e.g. for ADHD, the evaluation of teachers is of importance.
Evaluation of children and adolescents can be hard. Sometimes chil-
dren or adolescents dissimulate their problems, or children may lack
insight into their disorders. Building a therapeutic relationship with the
child is essential, as the child sometimes views the psychiatrist as allied
with his or her parents. This can complicate diagnostic evaluation and
therapy, especially when parents and child differ or when interaction prob-
lems between child and parents are the cause of seeking help. A separate
interview with the child is necessary.
1.3. Psychopharmacotherapy
The use of psychotropic drugs in children and adolescents has increased
over the past several decades. Findings about patterns of use (age,
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psychotropic drug classes, sex) and the implications of changes in these

patterns over time are heterogeneous and differ between countries,
especially between European countries and the United States, where
antidepressants are more widely prescribed and are as much as 15 times
more frequently used than in Germany, for example. The most fre-
quently prescribed psychotropic medications to children and adolescents
are stimulants, antidepressants, and antipsychotics — and in some
countries herbal preparations such as valerian and St. John’s wort.
The off-label use of psychotropic drugs in children and adolescents is
widespread and global. Over the past several years, some preparations
have been approved for use in young people in some countries. These
include fluoxetine for depression in children older than 8 years of age in
the United States and most European countries, aripiprazole or risperi-
done for use in schizophrenic patients older than 14 years, and aripipra-
zole used to treat bipolar disorder in the United States. Statutory incentives
in the United States and Europe will likely result in an increasing number
of preparations being studied in children and then being approved if they
prove efficacious.17
There are few long-term safety studies of drugs used in children. The
safety of many drugs, but particularly of antidepressants, antipsychotics,
and stimulants, has been the subject of vigorous discussion for many years.
Therefore, the child and adolescent psychiatrist must inform the parents as
well as the children and adolescents about the benefits and risks of pro-
posed medications. The patient must be informed of the risk of activation
syndrome, possibly with suicidal ideation, when commencing and discon-
tinuing treatment with selective serotonin reuptake inhibitors (SSRIs) and
serotonin and noradrenaline reuptake inhibitors (SNRIs) like atomoxetine.
1.4. Access to care

In world-wide comparisons, access to child and adolescent psychiatric
care differs widely, and inequalities in medical care resulting from the
living standards in the various countries are frequently also reflected in
access to child and adolescent psychiatric care. The modalities of treat-
ment also differ among industrialized countries. Some countries have a
broad spectrum of inpatient treatment facilities, whereas other countries
have a denser outpatient care network. In developing countries, on the
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other hand, child and adolescent psychiatric care is sparse, and accessing
care for children is more difficult. It should be noted, however, that care
may be difficult to access in industrialized countries as well if, for exam-
ple, the health care system is not affordable by all the citizens.
1.5. An international debate: Childhood bipolar disorder

or combined ADHD with conduct disorder?
Childhood bipolar disorder is a new diagnosis that has been the subject
of scientific debate for about the past decade. There has been a dramatic
increase in the diagnosis of this disorder in the United States, but not in
Europe. Some authors postulate that this difference might be influenced
by issues related to reimbursement and access to care, which both may be
easier in the United States for this type of diagnosis. Debate has centered
on whether this diagnosis represents the same phenotype as adult bipolar
disorder or whether it represents a severe case of ADHD with combined
conduct disorder and emotional problems.28 A reanalysis of data derived
from typical diagnostic screening tools has revealed that so-called child-
hood bipolar disorder is generally diagnosed as ADHD with a conduct
disorder (CD) in Europe.9 A further important question in pediatric bipo-
lar research is whether marked non-episodic irritability is a manifestation
of bipolar disorder in adolescents. Leibenluft and co-workers have dem-
onstrated that young people with severe mood dysregulation (SMD), a
category created for the purpose of studying children presenting with
severe non-episodic irritability, are significantly less likely to develop
(hypo-) manic or mixed episodes over time than those with true bipolar
disorder (BD).36 To date, there seems to be no evidence that childhood
bipolar disorder is correlated with a higher risk for bipolar disorder in
adulthood. Interestingly, treatment is similar for ADHD combined with
CD and childhood bipolar disorder: for severe cases, stimulants and
atypical antipsychotics are generally prescribed in clinical practice.
1.6. Categorical classification versus clinical entities

Whereas classification systems currently generally describe categorical
manifestations, symptom complexes would seem to be better suited for
describing patient pathology. DSM-5, which is currently under
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development, seems to take cognizance of this fact and will, to the extent
foreseeable, orient itself to symptom complexes. Finally, the definition
of symptom complexes also more closely reflects the reality of child
and adolescent psychiatric clinical entities, which tend to develop out
of normal behavior and only become pathological as a result of their
intensity or a particular pervasiveness. This can be seen, for example, in
ADHD and in anxiety disorders. Fidgety, hypermotor, and impulsive
behavior are not generally abnormal in children; only the severity and
consistency of the behavior characterize it as a disorder. The same
applies to fear, shyness, and reticence toward strangers, which are not
per se pathological. However, these physiological fears become
pathological — a disorder — when they extend to important areas of life
such as school, where they impose limitations, including refusal to go to
school, inability to cooperate in school, and the like. Therefore, symptom
complexes and the resultant child and adolescent psychiatric disorders
will be described here. Because the disorders that occur most frequently
are not necessarily also the most severe, we will describe here the most
frequent and the most severe disorders typically found during childhood
and adolescence. The most frequent disorders are ADHD, conduct disor-
ders, depressive disorders, and anxiety disorders. Attachment disorders,
autistic disorders, and schizophrenic disorders are frequently among the
most severe. Typical disorders that initially manifest in childhood and
early adolescence include tic disorders and eating disorders. After
describing the epidemiology and etiology of these disorders as well as
risk and resilience factors, we will then chronologically describe the
symptom complexes as they occur during the development of the child.
2. EPIDEMIOLOGY
According to a variety of international studies, 6%–8% of all children
and adolescents manifest a psychiatric disorder. Psychopathological phe-
nomena, which may be symptomatic but do not yet fulfill the diagnostic
criteria for a psychiatric disorder according to the classifications estab-
lished in ICD-10 or DSM-IV, are far more frequent: approximately 20%
of all children and adolescents across the age spectrum exhibit such symp-
toms.14,18,23 Overall, psychiatric disorders in children appear to be
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increasing. Cultural differences in the prevalence of certain disorders have

to date been inadequately studied; the published prevalence figures mostly
come from industrialized countries. The prevalence of these disorders
appears to be similar in these countries. Individual studies do indicate that
certain disorders and symptoms of a psychiatric disorder occur more or
less frequently in different cultural contexts. However, further research is
required in this area.
In general, specific child and adolescent disorders typically first appear
at certain ages. For example, ADHD usually manifests in early school-
age; the same applies to tic disorders and emotional disorders with separa-
tion anxiety. By contrast, eating disorders and self-harming behavior tend
to arise more often at the onset of puberty, and depression becomes more
frequent in adolescence as well. Schizophrenic disorders, by contrast,
manifest more frequently in early adulthood. There are also diseases that
tend to be more frequent in one sex. Externalizing disorders are more
frequent in boys, whereas internalizing disorders affect girls more often,
even though there has been a partial shift over the past several years.
However, among female adolescents, the criteria for diagnosing a conduct
disorder are met in 5% of those between the ages of 11 and 16 and in
barely 3% of those between the ages of 5 and 10.
Prevalence rates for the individual disorders vary greatly, the most
common disorders being ADHD, with a prevalence of 4%–8%, and con-
duct disorder, with a prevalence of 4%–16%.27 Two peculiarities are of
note. First, these disorders are clearly more common in boys, occurring up
to five times more frequently in boys than in girls. Second, the criteria for
ADHD according to ICD-10 and DSM-IV differ markedly; for example,
DSM-IV distinguishes between two subtypes that are not present in this
form in ICD-10. Therefore the diagnostic criteria are less stringent, so that
the prevalence rate is higher according to the DSM.
Anxiety disorders, by contrast, more frequently affect girls; this is par-
ticularly true for phobias, panic disorders, agoraphobia, and separation
anxiety. Overall, the prevalence of anxiety in children is said to be
6%–20%, although the percentage of anxieties that conforms to a diagno-
sis is lower. As with anxiety disorders, eating disorders are more frequent
in girls; the lifetime prevalence of anorexia nervosa is 0.5%–1%, that of
bulimia nervosa 0.3%–1%. The most frequent somatoform symptoms are
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functional pain disorders, particularly headache and abdominal pain, with

a frequency of approximately 10% each. Whereas no sex difference has
been reported during early childhood, the frequency and number of
somatoform symptoms increase in adolescence, and with increasing age.
A rising percentage of those affected are girls and young women rather
than boys and young men. The prevalence of obsessive-compulsive disor-
der in children and adolescents is estimated at 1%–3.6%. Whereas more
boys than girls become symptomatic during early childhood, this tendency
is cancelled out with increasing age. Chronic tic disorders or Tourette
syndrome (TS), the combined development of chronic motor and phonetic
(vocal) tics, used to be considered rare diseases. Over the past several
years, several school-based international studies have, however, estab-
lished a prevalence of TS of 1% (0.4%–3.8%). Males are 3–4 times more
frequently affected by tic disorders. Nocturnal enuresis is reported to
affect up to 10% of all 10-year-olds (spontaneous remission rate, approxi-
mately 14% per year), but only 2% of all children are reported to wet
themselves during the day two or more times per week. As reported by
epidemiological studies, the prevalence of autism spectrum disorders has
been rising over the past several years. In the United States and other
countries, overall estimates of prevalence of typical autism were 3 per
10,000 in the 1970s and increased to more than 30 per 10,000 in the 1990s.
3. ETIOLOGY OF PSYCHIATRIC DISORDERS

IN CHILDHOOD AND ADOLESCENCE: NATURE,
NURTURE, OR GENE–ENVIRONMENT
INTERACTIONS?
Complex patterns of interaction between genetic factors, environmental
factors, and social aspects are generally responsible for increasing the risk
that a psychological disorder will lead to the development of disease. The
influence of attachment and social and environmental factors has been
confirmed in numerous studies. For example, genetic variants combining
with environmental factors contribute strongly to the development of post-
traumatic stress disorder (PTSD) in children and to the development of a
psychiatric disorder.15 In major depression, the underlying neurobiology is
also likely to represent an interaction between genetic susceptibility and
environmental factors such as stress. Frodl et al.5 have found that
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childhood stress also predicts further changes in the white matter of the
hippocampus independently of the genotype and that subjects with both
environmental and genetic risk factors are susceptible to stress-related
hippocampal changes. Structural brain changes due to stress represent part
of the mechanism by which the illness risk and outcome might be geneti-
cally mediated. These epigenetic effects of environmental factors have
been of special interest in research on psychiatric disorders, but to date,
few of these gene-environment interactions (G × E) have been sufficiently
replicated. Indeed, meta-analyses have raised doubts about the robustness
of even the most well-studied findings.39
The biopsychosocial model can today be viewed as an integral explana-
tory model for the development of psychiatric disorders in childhood and
adolescence. In this model, the overall risk results from biological factors
(such as underlying genetic risk factors), psychological factors (such as
negative, distorted, and learned thoughts patterns such as “I can’t do any-
thing”), and social factors (such as loss of a loving relationship, unem-
ployment). Of course, the weighting of these individual factors differs
from person to person in the development of the disorder. In fact, the
genesis of a psychiatric disorder is frequently the result of an interaction
between risk factors and resilience factors, so that a one-sided focus on
risk factors neglects the protective factors that may prevent that disorder
despite existing risk factors.
3.1. Neurobiological aspects and risks of psychiatric

disorders in childhood and adolescence
A child’s brain is subject to rapid and global development comprising
developmental, transformational, and degradation processes.33,37 This
extremely dynamic complex of events provides many areas where aber-
rant development is more likely to occur, but also great potential for
repairing such aberrations. In this respect, neurobiology is of great impor-
tance for our understanding of the genesis and treatment of child and
adolescent psychiatric disorders. The genetic and neurobiological aspects
of many symptoms and disorders have been clarified; often, however, the
findings only explain some aspects of the disorders, so that although there
has been a rapid growth in our understanding of the fundamentals, com-
prehensive explanations are frequently still lacking.
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The dynamics of brain development are exemplified by the prefrontal

cortex, which is crucial for many executive functions, planning, and
impulse control. In adolescents, whose brains exhibit higher myelination
than adult brains, we find decreasing synaptic density (“synaptic prun-
ing”), a decreasing volume of grey matter (“use it or lose it”), and
increased prefrontal activation.21 Animal experiments on rats have shown
that between the age of 35 days (adolescence) and 90 days (early adult-
hood), the number of neuronal cells decrease in the medial prefrontal
cortex (mPFC), but not in the dorso-prefrontal cortex. A “late wave” of
apoptotic processes occurs during the transition to adulthood, which may
explain the particular susceptibility to environmental influences during
adolescence. Substantial changes occur not only in the prefrontal cortex,
but especially in the limbic areas. Developmentally controlled alterations
include the shift in the balance between the mesocortical and mesolimbic
dopaminergic system, which evidently contributes to the unique charac-
teristics of adolescent behavior, which are reflected in their more intense
emotionality, elevated impulsivity, and increased risk behavior (“sensation
seeking”). In this respect, adolescents differ from both adults and children
in terms of brain maturity.
The etiology of autism seems to have a genetic aspect.4 Immunological
dysfunctions such as chronic inflammatory processes, prenatal exposure
to viruses like cytomegalovirus or rubella, exposure to antibiotics and vac-
cines in early childhood, or exposure to neurotoxins, especially to sulphur
or polychlorobiphenyls, have been discussed as etiopathological factors in
the development of autistic disorders. Some researchers hold that the real
increase in this disorder may be caused by environmental factors. To date,
most of these non-genetic hypotheses have not been verified by studies. In
affective disorders, the serotonin transporter gene is of greatest interest.
Investigations of gene-environment interaction in depression have impli-
cated a polymorphism in the promoter region of the serotonin transporter
gene (5-HTTLPR) as a moderator of the stress-depression relationship.
For panic disorder (PD), the most common anxiety disorder, studies have
consistently shown that genetic factors explain approximately 48% of
the variance. Polymorphisms of the serotonin transporter gene SLC6A4
have been found to be involved, but this finding has not yet been suffi-
ciently replicated. There is also strong evidence of genetic involvement in
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the pathogenesis of tic disorder even though no definitive locus has been
found. Genetic factors play a role in ADHD; twin studies have demon-
strated that the twin effect is greater than the influence of environmental
conditions. Alcohol and nicotine abuse by mothers during pregnancy are
also well-known risk factors. The dopaminergic system, especially the
striatum, is involved in the pathomechanism of ADHD, which is a striato-
frontal disorder. Polymorphisms that correlate with ADHD include the
10-repeat allele for the dopamine transporter (DAT 1) and the DRD 4
promoter (7-repeat allele for the DRD 4 and DRD 5 receptors). Furthermore,
SNAP25 seems to be involved in the development of ADHD. Functional
magnetic resonance imaging (fMRI) studies have found abnormalities in
the dorsolateral prefrontal cortex (DLPFC) and in the anterior cingulus
(CGA) in subjects with ADHD. Individuals with ADHD, as compared
with unaffected subjects, had distinct activation of brain regions under
medication with methylphenidate. Executive functions and time percep-
tion are typically impaired in subjects with ADHD. In an fMRI study
conducted while subjects performed a combined spatial stimulus-response
compatibility (SRC) and time duration discrimination (TD) paradigm,
subjects with ADHD showed significantly reduced neuronal activity in the
left putamen during SRC testing and reduced fronto-cerebellar activation
during TD testing.38
3.2. Social risk factors

Copious research efforts have confirmed the various social and environ-
mental risk factors involved in psychiatric disorders in children. Failure to
form a secure attachment to primary caregivers in early childhood,
trauma, inconsistent child-rearing styles on the part of primary caregivers,
social factors such as belonging to disadvantaged social classes, and psy-
chiatric disorders or delinquency in the parents are strong risk factors for
children and adolescents, predisposing them to develop psychiatric disor-
ders (see also figure on risk factors). Several representative studies have
shown that children of single parents or of parents with a low level of
education and income are at elevated risk for psychiatric disorders.8,22
The following relationships were found regarding social classes: Those
in the lowest social class are at 3.2 times greater risk of developing
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hyperactivity, 4.7 times greater risk of antisocial behavior, and 1.7 times
higher risk of anxieties than those in the highest social class. It should be
noted that the cumulative effect of several risk factors (such as current
family conflict, dissatisfaction of parents in marriage, and social prob-
lems) leads to a dramatic increase in risk. In the presence of all three risks,
30.7% of children exhibit symptoms; if there are four risk factors, that
figure climbs to 47.7%. The recognition of high-risk groups is important
in terms of both prevention and timely intervention. In this respect, it has
been shown over the past several years that children receiving institution-
alized care (in foster care, youth service institutions, or an orphanage) are
at high risk, with markedly higher prevalence than the normal popula-
tion.34 Whereas fewer than 1% of children who grew up with their birth
mother suffer from an attachment disorder, according to ICD-10 criteria,
one study of a clinical population found that more than 25% of all children
from foster families and more than 10% of children in orphanages, who
have a higher average age, met one of the two diagnostic criteria for an
attachment disorder according to ICD-10.
3.3. Resilience
Since Emmy Werner’s Kauai study, which followed the 1955 birth cohort
on the island of Kauai, it has been known that resilience factors have a
crucial effect in balancing out risk factors and determining whether a child
develops in a positive direction in spite of the presence of many risk fac-
tors. In the Kauai study, approximately one-third of the children with risk
factors developed no disorders and was even happier and more contented
than low-risk peers. Numerous twin and adoption studies have confirmed
the importance of resilience. Resilience is the process of biopsychosocial
adaptation and the resultant emotional resilience of children to biological
and psychosocial developmental risks.30 Resilience is best recognized by
a high level of functioning and/or disorders that are either absent or mild
in persons in whom the opposite might be expected. Resilience factors
may be inherent to the child in the form of personality traits such as curi-
osity, extroversion, and the like, or be the result of family traits. The qual-
ity of interaction in terms of child-rearing behavior or warmth in the
parent–child relationship plays a major role here. Factors in the social
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Genetic predisposition
Attachment experiences
Other socialization
conditions
Fig. 1. Risk factors.
environment may also foster resilience, including inclusion in a peer

group, educational systems, and the like (see Fig. 1).
4. SPECIAL DISORDERS
4.1. Attachment disorders
4.1.1. Phenomenology
According to ICD-10 (F94) and DSM-IV (313.89, Reactive Attachment
Disorder of Infancy or Early Childhood), attachment disorder describes
children’s behavior that greatly deviates from attachment behavior
that would be expected according to the attachment theory paradigm. In
most social contexts, children with early childhood attachment disorders
exhibit developmentally inappropriate behavior. For example, they fail to
seek contact with their attachment figure in situations of uncertainty and
stress, or they fail to respond with what may be a tentative, though none-
theless organized, strategy, by means of which they may to some extent
regulate their internal stress. Rather, though clearly stressed in such situ-
ations, they do not seek out comfort and reassurance from their attach-
ment figure, or they remain not merely distanced but may even seek out a
strange person rather than their trusted primary caregiver (Table 1). There
are two types of attachment disorders: “Reactive attachment disorder of
childhood” (F94.1) and “Disinhibited attachment disorder of childhood”
(F94.2).
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Table 1. ICD-10: Attachment disorders.

Reactive attachment disorder Disinhibited attachment disorder
Begins before age 5. Diffuse attachments.
Contradictory, ambivalent reactions Lack of socially selective social attachment
in various situations. Indiscriminate seeking of comfort or closeness.
No or little social or emotional Relatively unmodulated social interaction with
responsiveness, aggressive or others.
anxious or oversensitive Generally clingy behavior or undifferentiated
behavior. friendly behavior towards both primary
Social reciprocity is possible in caregivers and strangers or uninhibited,
principle (DD deep-seated inappropriate interactions with strangers;
developmental disorder). the behavior is not situation-specific.
The criteria for reactive attachment disorder of childhood (ICD-10

F94.1) include excessively fearful and wary behavior and contradictory or
ambivalent reactions in various social situations. Emotional symptoms
manifest in decreased responsiveness, fearfulness, withdrawal behavior,
and aggressive behavior toward themselves or toward others as a reaction
to their own distress. Children with reactive attachment disorders exhibit
ambivalent reactions toward their attachment figures, such as alternating
between seeking closeness and avoiding physical contact or parental com-
forting, even (or even particularly) in situations that are stressful for the
child. They also exhibit equally aggressive and restrained behavior
towards their attachment figures. Nonetheless, social reciprocity and
responsiveness may be observed in their interaction with adequately
responsive primary caregivers. Interaction such as social play with peers
is limited.
In clinical practice, we frequently see children who have been subjected
to pronounced neglect or emotional and physical abuse and who are clas-
sified as having a reactive attachment disorder. Insufficient or grossly
inadequate parental behavior cannot, however, be used as a sufficient diag-
nostic criterion on its own. Symptoms of the child and inadequate parental
behavior are both necessary for a diagnosis of attachment disorder.
In disinhibited attachment disorder of childhood (ICD-10 F94.2)
we see less emotional or absent personal attachments, less modulated and
inhibited interactions with strangers (no age-appropriate distance,
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indiscriminate friendliness) in many situations, as well as clingy behavior

or attention seeking. Diffuse attachments with primary caregivers mani-
fest in that attachment needs in particular, such as the need for comfort
and closeness, are expressed without differentiating between primary
caregivers and strangers. Disinhibited attachment disorder of childhood is
also characterized by aggressive behavior (towards themselves or others)
and limited interaction with peers and limited social play.
According to attachment theory, infants and toddlers have an innate
social need to form one or several close relationships with emotionally
close primary caregivers.3 The attachment system describes the organiza-
tion of behavior by which the child creates closeness and (physical) con-
tact with one or several primary caregivers when under stress. When
activated, the physical effects of this system may be observed in terms of
an elevated heart rate in the child, which subsides only with closeness or
physical contact with the primary caregiver. Mary Ainsworth speaks of the
“safe base” that parents create as a precondition for the child’s ability to
explore the environment with interest and in a care-free manner. The basic
need to explore complements the need for attachment. Accordingly, a
good balance between the needs for safety and attachment on the one hand
and exploration and autonomy on the other may be equated with secure
attachment. The insecure attachment patterns (insecure-avoidant and
insecure-ambivalent) are normal variants of secure attachment in which,
however, the balance between attachment and exploration is skewed.
Although they must be clearly differentiated from attachment disorders as
defined in the classification systems, they may be preliminary stages
thereof. The disorganized attachment type most closely resembles an
attachment disorder in the clinical sense.
Diagnostically, it is important to obtain a detailed history, including
evidence of deprivation, and to observe behavior. (Mis-)behavior in chil-
dren under five years of age that is relevant to attachment may be observed
(e.g. limited exchange of affect in various social situations or unlimited
positive affect towards a relatively strange adult, lack of comfort-seeking
in stressful situations, excessive clinging or inability to seek out and use
the primary caregiver’s help, lack of cooperation with the primary car-
egiver, consistent disobedience when requested or required to do some-
thing, or “compulsive compliance” along with a failure to seek reassurance
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from the primary caregiver when exploring, or a failure to explore because

of the inability to detach from the primary caregiver). Often the most
conspicuous symptom is the inappropriate, uninhibited behavior towards
strangers (the children immediately engage without any initial reticence,
enter into extensive physical contact, and may even leave their primary
caregiver with a stranger without protest).
4.1.2. Treatments
Pharmacotherapy
In severe cases of hyperkinetic behavior, an off-label medication with
stimulants may be beneficial.
Psychotherapy
No therapeutic treatment has to date proved adequately effective in treat-
ing children with attachment disorders. However, it is indisputable that the
presence of an emotionally reliable and constant attachment figure is
indispensable to the success of any treatment. Therefore, it is important to
promote parent–child interaction, if possible with standardized programs,
while simultaneously working with the parents. More advanced psycho-
therapy should be considered only after emotional stabilization has been
achieved through the establishment of a stable relationship and concurrent
work with the parents.
In fact, a child with an attachment disorder places increased require-
ments on the (foster) parents’ child rearing and relational skills. As a
result, outpatient therapeutic support services should be considered in
addition to regular consultation sessions.
Children with a diagnosis of attachment disorder have a rather unfa-
vorable prognosis. Many of the children originally diagnosed with a dis-
inhibited attachment disorder are diagnosed with personality disorders in
adolescence or early adulthood.40 Children have age-dependent ways of
reacting to traumatic events and neglect. Children with repeated trauma
and a background of early neglect often do not show the full characteris-
tics of adult posttraumatic stress disorder (PTSD) but show a
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developmental phenomenological heterotopy with a severe case of dis-

turbed impulse regulation and emotional imbalance in relationships. In the
on-going process of the introduction of a new classification system, DSM-
5, some authors proposed the introduction of a so-called developmental
trauma disorder to distinguish these age-dependent phenomena and the
severe developmental causes from adult PTSD.
4.2. Autistic syndromes

Signs and symptoms
Autistic disorders are accompanied by a permanent and pervasive quali-
tative impairment in development and, at the worst, with a chronic and
severe disability in social functioning. Core symptoms relate to social
interaction, qualitative impairment in communication, and behavioral
abnormalities such as restricted, repetitive, and stereotyped patterns of
behavior, interests, and activities (Table 2). According to psychiatric
classification systems, several types of autism exist, and autism can be
described along a spectrum with varying degrees of pervasive impair-
ment: mild forms that are often called autism spectrum disorders with
less impairment and few symptoms, through Asperger syndrome, to
severe forms of typical pervasive developmental disorders with extremely
limited or non-existent communication skills, persistent repetitive
behaviors, and self-mutilation. ICD-10 distinguishes between typical
autistic disorders (Kanner autism with onset of symptoms before the age
of three years), atypical autism (atypical onset, symptoms, etc), Asperger
syndrome (with no clinically significant delay in development of speech
and early development similar to that of a normal child), Rett syndrome,
which mainly affects girls (with arrested development and an on-going
decrease in functions), and not otherwise specified forms. For diagnosis,
it is necessary to understand the child’s social behavior, the development
of language, and her use of language in social communication and play
(imaginative, symbolic play) before the age of three. Parents often real-
ize that their early interaction with the child was strange (no responsive
smile, no desire to kiss or cuddle with the mother, etc). Diagnosis may
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Table 2. Core symptoms of autistic disorders according to ICD-10.

Social interaction Difficulties with and little interest in developing social
relationships.
Unawareness of the importance of facial expressions,
eye contact, gestures, body language, intonation, and
social gestures that convey meaning and regulate
social interaction.
Limited ability to imagine the thinking (“theory of
mind”) and feelings (“empathy”) of others.
Language as used in Language deficits lead to delayed or reduced speech,
social communication including complete silence or the inability to start or
carry on a conversation with others.
Stereotyped and repetitive use of language that may be
very literal, idiosyncratic, or excessively formal:
Such language may be used to express needs and
information, but may not serve for social interaction.
Difficulties understanding metaphorical language,
including ironic or sarcastic language and lies.
Limited interests and Rigid and repetitive behavior patterns, including
repetitive behavior dysfunctional routines or rituals (such as touching
walls or steel parts of something).
Resistance to changing or interrupting routines.
Stereotyped and repetitive motor mannerisms such as
clapping when excited or behaviors that are
experienced as pleasant such as repeated viewing of a
video or stereotyped oral movements such as
humming or incessant questioning.
Narrowing of the range of interests such as a focus on
bus schedules, or single-minded, unusually intense
preoccupation with certain objects Inflexibility in
thinking.
No imaginary activities (plays etc).
Typical autism Onset before the age of three, impairment in atleast one
of the following areas: Development of receptive/
expressive speech, selective/reciprocal social
interactions, functional or imaginative play.
Several symptoms from among the symptoms above.
Atypical autism Onset after the age of three and/or atypical number of
symptoms.
(Continued)
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Table 2. (Continued )
Rett syndrome Normal psychomotor development within first five
months.
Between five months and the age of four years: Loss of
targeted hand movements, communication disorder,
disorder of social interaction, barely coordinated,
impaired gait.
Psychomotor slowing and speech disorder (expressive
and receptive).
Asperger syndrome Similar symptoms as with typical autism; but
No speech development disorder/cognitive
developmental delay.
be difficult, and several diagnostic interviews such as ADOS and ADI

are available to confirm symptoms and verify the diagnosis.
Differential diagnoses may include Angelman syndrome, fragile X
syndrome, intellectual disability, and deprivation.
4.2.2. Treatment
Pharmacotherapy
Drugs are administered mainly to treat (auto-)aggressive behavior and
impulsivity, and in some cases mood and hyperactivity. Antipsychotics,
SSRIs, and methylphenidate can be efficacious, even if most pharmaco-
therapy will be used off-label. The Autism Network of the Research Units
on Pediatric Psychopharmacology (RUUP) studied risperidone for core
symptoms of autism. Risperidone led to significant improvements in the
restricted, repetitive, and stereotyped patterns of behavior, interests, and
activities of autistic children but did not significantly change their deficit
in social interaction and communication.22
Psychotherapies
Treatment includes counseling of parents, which is essential to provide
them with information and afford them relief. Knowing what is the matter
with their child is very important to parents because they may have felt for
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a long time that something was wrong. In US studies, the median age at
diagnosis ranged between 3 and 7; it normally takes about three years
from the time the parents first notice the problem to the final medical
diagnosis. Behavioral interventions such as “Treatment and Education of
Autistic and related Communication-handicapped Children” (TEACH),
the Applied Behavior Analysis (ABA) of Lovaas, and other treatments are
very expensive and resource and time intensive. A review of the effective-
ness of therapies is provided in Ospina et al.26
4.2.3. Prognostic factors

Even though several treatment strategies are available, patients may
remain impaired for their entire lifetime, although patients with mild
forms may be successful if they find a niche that works for their special
abilities.
4.3. Attention deficit/hyperactivity disorder (ADHD)

Signs and symptoms
Core symptoms of Attention Deficit/Hyperactivity Disorder (ADHD)
include lack of attention, hyperactivity, and increased impulsivity (Table 3).
DSM-IV distinguishes between three types of ADHD: a combined type
with hyperactivity/impulsivity and inattention (314.01); a predominantly
inattentive type (314.0); and a predominantly hyperactive type (314.01).
By contrast, the ICD-10 criteria are more rigid comprising only one type
that requires the presence of all core symptoms. Additionally, a combined
disorder of ADHD and CD may be diagnosed under ICD-10 (F90.1).
These differences in the classification systems account for the varying
prevalence in different studies (Fig. 2).
Boys more often exhibit externalizing behavior and are more likely to
be diagnosed (in clinical samples: 4–8 boys to 1 girl), although the ratio
is smaller in school-based studies (2–4 boys to 1 girl). For the diagnosis,
symptoms should be present before the age of six years, be pervasive in at
least two settings, not be present only in school or in the family, and be
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Table 3. ICD-10 ADHD.

Impulsivity Burst out with answers
Cannot wait for their turn
Interrupt or disturb others
Talk excessively
Inattention Inattentive to details
Make careless mistakes
Cannot maintain concentration
Do not listen
Poor structuring skills
Easily distracted
Very forgetful
Hyperactivity Cannot stay in their seats
Constantly fidget and squirm (with
fingers, legs etc)
Constantly run and climb around
(gross motor agitation)
Very loud during play
Lasts longer than six months
Begins before the age of seven
Consistent in many situations
Leads to impairment
stable for more than six months. Children with ADHD are likely to have
problems in school and with peer relationships even though they have
average or above-average IQs. Hyperkinetic behavior is generally reduced
in adolescents, disorganization being more dominant in adolescents and
young adults.
4.3.2. Treatment
Pharmacotherapy
Stimulant medication is the treatment of choice for ADHD (level of evi-
dence I). In cases of severe symptoms and essential impairment of the
child by its symptoms, pharmacotherapy is effective. According to most
guidelines, pharmacotherapy of ADHD should be embedded in a multi-
modal treatment setting, which also includes parent trainings and so on.
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Classification according to Classification according to DSM-IV

ICD -10 and frequency of and frequency of needed symptoms for
needed symptoms for diagnosis:
diagnosis:
a) Disturbances of activity and a) Predominantly inattentive type
attention (F90.0) 314.0
Inattention + Hyperactivity+ Inattention +
Impulsivity Hyperactivity/Impulsivity
6/9 + 3/5 + 1/4 ≥6<6
b) Hyperkinetic conduct b) Predominantly hyperactive-

disorder (F90.1); impulsive type 314.01
to meet the definition, both Inattention +
criteria for a hyperkinetic Hyperactivity/Impulsivity
disorder and for a conduct <6≥6
disorder/ oppositional defiant
disorder must be present.
c) Attention deficit disorder c) Combined type 314.01
without hyperactivity (F 98.8) Inattention +
needed symptoms not classified Hyperactivity/Impulsivity
≥6≥6
Fig. 2. Different classification systems and its meaning for prevalence.
Medication without counseling parents would be inappropriate. Stimulants

increase the levels of dopamine (and norepinephrine) in the brain via
reuptake inhibition. Additionally, stimulants can release catecholamine.
The Multimodal Treatment Study of ADHD (MTA) produced the most
comprehensive results concerning treatment effects, long-term outcome,
and side effects of stimulant medication.10 This multicentre study exam-
ined 579 children in the United States who were 7–9 years old at onset,
using four study arms: medication only, behavioral therapy only, a combi-
nation of medication and behavioral therapy, and conventional treatment
by a child and adolescent psychiatrist. Analysis of data revealed that
stimulants were best used to treat hyperkinetic disorder and attention
problems in school, while combined treatment was found to be best in
ADHD patients with concurrent emotional problems and those with con-
current CD.31 Long-acting preparations are currently available that opti-
mize therapy. These preparations are titrated with non-retard stimulants to
find the lowest effective dosage. In the United States, amphetamines (and
salts) are more frequently used to treat ADHD than in Europe, where
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methylphenidate is the most frequently used substance. Possible side-

effects are loss of appetite, (temporary) loss of weight and retardation in
growth (about 1–2 cm). Sleep can be disturbed, especially if the child
receives medication late or the extended release preparation acts too long.
Stomach-ache, nervousness, and irritability are mostly temporary at
starting of medication. In some cases a tic-disorder can be triggered by
stimulants. Further, therapy with atomoxetine, a selective noradrenalin-
reuptake-inhibitor, is possible, but this medication is slightly less effective
than stimulants. Therefore stimulants remain the first-line pharmacothera-
peutic intervention for the majority of patients. Atomoxetine may be a
useful alternative in cases of concurrent tic disorder or substance abuse
and reluctance of parents against the use of stimulants.
Psychotherapy
Therapeutic options may be family-, school-, or child-oriented. Training
parents in parenting skills is effective but shows a high degree of variabil-
ity from parent to parent. The programs are focused on improving parent–
child interaction and contingency management. Interventions in school
also show immediate effects, particularly when they implement routines
in school, encourage physical activity that focuses the child’s attention,
and improve environmental conditions (“do not place a child with ADHD
in the last row”). Cognitive behavioual treatment (CBT) programs are the
most effective child-oriented psychotherapeutic option for treating
ADHD, the most effective elements of CBT in ADHD being contingency
management in pre-schoolers. Parent-training should be the first-line
intervention and seems to be most effective, while these CBT interven-
tions are aimed at improving impulsivity control and attention to relevant
stimuli. Psychotherapy generally requires adjuvant medication to work.
Neuro-feedback is another promising psychotherapeutic option whose
effectiveness is currently being studied.

ADHD that is detected early and treated consistently in the context of
a caring parental environment that focuses on school and skills for
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self-control generally has a favorable outcome. High-risk children and those

with concurrent ODD or CD have a much less favourable prognosis with a
high risk for delinquent behavior. Untreated ADHD can lead to further
emotional problems and the well-known social risks of school failure,
delinquent behavior, substance abuse, and on-going externalizing behavior
problems.1
4.4. Conduct disorder and oppositional defiant disorder

Signs and symptoms
The high comorbidity of ADHD and conduct disorder (CD) and opposi-
tional defiant disorder (ODD) may be the result of reduced impulsivity
control. Symptoms of conduct disorder (DSM-IV: 312.8x) are heteroge-
neous, with a pattern of antisocial, aggressive, or oppositional behavior
to expectations appropriate for the developmental age of the patient
(Table 4). Symptoms present before the age of 10 years are coded accord-
ing to DSM IV 312.81; if symptoms are present after this age, 312.82
should be coded. This different coding has relevance for prognosis (see
further). Leading symptoms of ODD (DSM-IV: 313.81) include loss of
temper, frequent severe anger, frequent arguments with adults, and fre-
quent overt defiance or refusal to comply with adults’ requests or rules.
CD is characterized by aggressive conduct that causes or threatens physi-
cal harm to other people or animals, non-aggressive conduct that causes
property loss or damage, deceitfulness or theft, and serious rule viola-
tions. The behavior must be repetitive or persistent for the diagnosis to be
made. ICD-10 describes CD and OCD together in one entity with sub-
diagnoses of CD only present in the family (F91.0), without or with social
relationships (F91.1/F91.2), for children with oppositional behavior
against caregivers (F91.3) and not otherwise specified symptoms (F91.9).
Differential diagnosis
Because symptoms are clear and unambiguous, differential diagnosis is
straightforward. Comorbid diagnoses of ADHD, emotional or affective
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Table 4. ICD-10 Conduct disorder.

Presence of a persistent pattern of violating social norms over at least six months with
Intense or violent outbreaks of anger Use of weapons (knives, bottles, guns)
Fighting with adults Physical violence against people and animals
Breaking rules, disregarding prohibitions Intentional destruction of property
Intentionally antagonizing others Stealing
Spitefulness and vindictiveness Running away
Constantly starting physical fights Sexual violence
Skipping school
disorders, and underlying post-traumatic disorders should be considered.

In conduct disorder, it is important to distinguish the type of aggression.
In terms of prognosis and therapy, it is relevant whether the subject
exhibits so-called hot or cold aggression. Hot aggression is characterized
by reactive, affective-defensive, and impulsive behavior, whereas cold
aggression is planned, instrumental, and proactive.35 This concept is also
based on neurobiological facts. Hot aggression is more common, and the
loss of control demonstrates its kinship with ADHD.
4.4.2. Treatment
i. Pharmacotherapy
In cases of increased impulsivity, treatment with atypical antipsychotics
can help the patients gain some control over their impulses (in case of low
intelligence, level of evidence II). Serotonergic medication (SSRI) is used
both to reduce impulsivity and, in the case of comorbid affective disorders,
to improve mood and thereby to reduce bad temper. No real pharmaco-
therapeutic options are available to treat conduct disorder causally or
totally.
ii. Psychotherapy
Although CD and ODD are common disorders, no strong comparative
clinical trial literature exists. Therapeutic interventions are mainly
family-based (modification of parenting style, implementation of
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adequate and consistent rules in the family, etc; level of evidence I).12
Multisystemic therapy is one approach; it is very challenging, but with
first results both on its efficacy and limits of effectiveness.7 The patient-
centered approach is similar to that used to treat ADHD with token
systems and self-management elements (level of evidence II). Approaches
to conduct disorder often require involvement of the youth welfare sys-
tem with long-term intervention. In severe cases with high impulsivity,
treatment with atypical antipsychotics may be beneficial to improve
impulsivity, even though these interventions are currently approved only
for low-IQ patients.

Onset in childhood (before the age of 10) is assumed to be associated
with persistent conduct disorders, and patients with childhood onset are
more likely to develop adult antisocial personality disorder. These
patients are usually male, and they frequently display physical aggres-
sion. They often have disturbed peer relationships and may have had
symptoms of ODD early in childhood. Later onset in adolescence is
associated with less aggressive behavior. Patients with adolescent-onset
CD present with a less pervasive disturbance than those with child-
hood-onset CD, but the course of disease is still difficult for many
of them.
4.5. Tic disorder and Tourette syndrome

4.5.1. Phenomenology: Signs and symptoms
ICD-10 and DSM-IV define chronic tic disorders and Tourette syndrome
virtually identically. The occurrence of multiple motor tics and at least
one phonetic tic is classified as Tourette syndrome (ICD-10 F95.2; DSM
IV 307.23) if the tics occur frequently during the day, last longer than a
year, and if there are no asymptomatic phases lasting for more than two
months. Motor and phonetic tics need not occur at the same time. Onset
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of the disorder should be before the age of 18. The same is true for
chronic motor or vocal tic disorder (ICD-10 F95.1; DSM IV 307.22).
Simple motor tics include eye blinking or winking, grimacing and
frowning, as well as headshaking and shoulder shrugging. Convulsive
contractions of the diaphragm, stomach, or trunk muscles are also con-
sidered a simple motor tic. Complex motor tics, by contrast, include
hopping, treading, jumping, scratching, and hitting. Simple vocal or
phonetic tics include throat clearing, coughing, spitting, and grunting
and may include excessively loud inspiratory and expiratory breath
sounds. Palilalia (repetition of one’s own words), echolalia (repetition of
another person’s words), and rarely coprolalia (obscene and socially
unacceptable words) are examples of complex vocal tics. The cardinal
symptoms of Tourette syndrome include motor and phonetic tics
(because not all sounds made by patients with Tourette syndrome are
actually vocalized, the term “vocal tic” has been largely abandoned). The
extent of the tics may be highly variable. Days may go by without symp-
toms, followed by more severe tic episodes. Motor tics are understood to
mean sudden, rapid, explosive movements, often involving several mus-
cle groups. These movements may appear to be stereotypic, but they
often are non-rhythmic and repeat in series. Phonetic tics are associated
with a sound (Table 5).
Many patients report a premonitory urge before the tic. This urge
becomes so unbearable that the tic must be expressed overtly. Patients
can sometimes suppress the tic for a limited period of time, which is
why some children with tics are not diagnosed. Once at home, however,
the tics may become all the more pronounced. Some are well
Table 5. ICD-10 Tic disorder.

An involuntary, rapid, recurrent, non-rhythmic stereotyped movement or vocalization
Chronic motor/vocal Motor/vocal tics most days of the year, most hours of the day.
tic disorder No remission lasting longer than two months.
Onset prior to age of 18.
Combined tic disorder Multiple motor tics and one/several local techs.
(Tourette) Several times each day, almost each day for more than a year.
Onset prior to age of 18.
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able to suppress their tics when doing tasks that require a high level of
concentration, but the tics may be much more pronounced in stressful
situations. The extent of inter-individual differences is illustrated by the
fact that for some people, the tics may subside almost completely when
they are on vacation or relaxing, while for others, tics increase in these
situations.
In chronic tic disorders, motor tics may develop as early as kinder-
garten age. Phonetic tics often start several years later. The disease
becomes manifested in 96% of affected children before the age of 11.
It is often most severe between the ages of 12 and 14. Data about com-
plete remission during adolescence differ widely. Tic symptoms seem
to disappear in approximately a third of adolescent patients, regress
markedly in another third, and remain constant in the remaining
patients.
Complex motor tics are difficult to distinguish from obsessive-com-
pulsive behavior. The transitions between the two are sometimes poorly
defined. Checklists like the Yale Tourette Syndrome Symptom List
(YTSSL) or the Yale Global Tic Severity Scale (YGTSS) can be helpful
in the differential diagnosis. It is important to rule out chorea minor
(Sydenham) as well as post-infection autoimmune processes (“Pediatric
autoimmune neuropsychiatric disorders associated with streptococcal
infection,” PANDAS). Stereotypic movement disorders in severe devel-
opmental disorders are easy to distinguish, because tics seem arrhyth-
mic in comparison. If the disorder develops after the age of 18, rare
causes, such as drug-induced tic disorder, neuroacanthocytosis, and
Wilson’s disease, should be considered. There is a high comorbidity (up
to 90%) with ADHD and obsessive-compulsive disorders (the dysregu-
lation of dopaminergic neurotransmission in the cortiko-striato-
thalamokortical circuit can be assumed as the pathway). Further relevant
comorbid psychiatric disorders are anxiety and mood disorders, which
can be the consequence of the social stigma caused by the symptoms of
tic disorder. For disruptive disorders, which also frequently occur with
tic disorder, the lack of control over impulsivity can be seen as a
pathway.
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4.5.2. Treatments
i Pharmacotherapy
Several drug treatments are currently available if the tic symptoms lead to
considerable impairment in terms of psychosocial functioning or if, for
example, loud noises make participation in school difficult. Haloperidol
has shown evidence of efficacy (level of evidence I), but it cannot be con-
sidered a first-line medication because of its side effects. In Europe,
tiaprid (level of evidence II; selective dopamine D2 and D3 antagonist) is
frequently used to treat tics. Other substances include risperidone (level of
evidence II; potent 5HT2A receptor and dopamine D2 receptor antago-
nist). Initial studies are available for aripiprazole (partial agonist D2 and
5HT1A receptor). Atomoxetine (inhibition of presynaptic noradrenalin
transporters; evidence level II-III) may be helpful in concurrent ADHD.
Occasionally, atomoxetine may exacerbate tic disorders (stimulant effect).
Serotonergic drugs can be helpful in OCD, the common comorbidity in
tics, but no RCT about effects is available.
ii. Psychotherapy
If symptoms are mild or moderate, psychoeducation may lessen the tic
disorder. Therapeutically, it is important to educate the patients, their par-
ents, and other relevant school personnel, because this helps to minimize
stigmatization and correct wrong ideas, such as that tics are voluntary.
Behavioral therapy programs such as “habit reversal training” (HRT) and
“comprehensive behavioural intervention for tics” (CBIT) may be quite
effective according to study data. Relaxation programs such as progres-
sive muscle relaxation are also applied in tic disorders. In younger chil-
dren, psychotherapy programs are hardly applicable because the patients
are seldom motivated to take part in such elaborate techniques.

Tourette syndrome is usually diagnosed very late (normally five years
after onset of symptoms). No causal therapy is available. Therefore
patients have to learn to cope with the disorder as a chronic condition. The
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fluctuating course of the disorder allows reducing the medication during

times with fewer symptoms.
4.6. Stuttering
4.6.1. Phenomenology: Signs and symptoms
Stuttering (ICD-10: F98.5; DSM IV: 307.0) is a disorder affecting coor-
dination of speech. Symptoms are syllable repetition and blockades of
speech (involuntary). A high genetic aspect of this disorder can be
assumed, because stuttering appears at a higher frequency within fami-
lies of affected patients. However, in addition to a genetic component,
further aspects have an influence on the risk of stuttering: In homozy-
gote twins one may be affected, not the other. Subjects affected by stut-
tering have often a delayed development of speech; auditory, other
sensory, and word motor deficits may be connected with stuttering. No
mono-causal etiology of stuttering has been found. Prevalence of stutter-
ing shall be about 5% (2:1 boys: girls). Mostly the symptoms are present
before the age of six years (50% already between the age of three and
five years).
Typical symptoms of stutterers are sound and syllable repetitions,
prolongation of sound, interjections, pauses within a word (broken
words), audible or silent blocking (filled or unfilled pauses in speech),
circumlocutions (word substitutions to avoid problematic words), words
produced with an excess of physical tension and monosyllabic whole-
word repetitions.
DSM-IV considers in the diagnostic criteria the disability caused by
stuttering: “Disturbance in fluency interferes with academic or occupa-
tional achievement or with social communication.” DSM-IV also requires
coding stuttering on Axis III, if a speech-motor or sensory deficit or a
neurological condition is present.
4.6.2. Differential diagnoses

Tic disorder has to be considered as a differential diagnosis. If tic-
disorder repetition is involuntary, without sense and suddenly starting,
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obsessive-compulsive disorder may imitate stuttering symptoms, but

differences (obsessive thoughts, etc) can normally be detected easily.
Another speech disorder is tachyphasia (pressured speech, ICD-10:
F98.6) with abnormally fast speech, few pauses, and difficult to interrupt.
No blocks or prolongation are present in this disorder.
4.6.3. Treatment
i. Pharmacotherapy
Pharmacotherapy is not very successful in stuttering, even if haloperidol
or second generation antipsychotics and botulinum (i.m.) have been used
for treatment. Long-term efficacy of these substances is not proven.
ii. Psychotherapies
Psychotherapeutic interventions are complex and show no fast or easy
success. A metronome as aid for the rhythm of speech can be helpful
and can be used as an exercise for prolongation. Modification of stutter-
ing aims at changing secondary reaction on stuttering as anxiety.
Fluency shaping wants to modify speech (learning new patterns of
speech), which is adapted step by step to normal speech. Combined
treatment approaches shall be most efficacious. Evidence for fluency
shaping is level III for children; combined therapy has evidence levels
between Ib-III. The best evaluated therapy program (for preschool chil-
dren) is the Lidcombe program.11,25 It is a behavioral treatment with
contingencies.

Within growing up, most of the children lose the symptoms of stuttering
and present a normal speech. Treatment should start at pre-school age due
to social impact of stuttering and lower effectiveness of therapies in older
children than in pre-schoolers. Although the rate of remission is high,
relapse can occur and in cases of severe stuttering, a refreshing of therapy
is necessary.
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4.7. Further relevant disorders and symptoms

in childhood and adolescence
4.7.1. Elimination disorders: enuresis and encopresis
Enuresis nocturna is defined as nocturnal bedwetting with a frequency of
atleast two nights per month in children who are older than five years.
DSM-IV (307.6) and ICD-10 (F98.0) are quite similar in their diagnostic
criteria. According to DSM-IV, urination can be involuntary or inten-
tional, but according to ICD-10, urination shall be involuntary. ICD-10
states that below the age of seven years, a frequency of twice per month
and in older children once per month with a minimum duration of three
months is required for diagnosis. Enuresis may occur at night (nocturnal,
most common), during the day (diurnal), or at day and night (diurnal and
nocturnal). It is diagnostically important to determine whether the enure-
sis is primary (the child has never been dry) or secondary (the child had
been dry for more than six months when bedwetting suddenly recurred).
In 60% of cases, relatives of children with enuresis experienced similar
problems (genetic component).
Drug-induced urinary disorders must be ruled out as well as malforma-
tion of the urinary tract and chronic urinary tract infection. Other reasons
for wetting during the day may include psychogenic urinary retention
(retention of urine and postponement of urination) and idiopathic urge
incontinence (involuntary urination with excessive urinary urge in patients
with decreased bladder capacity). Relevant differential diagnoses include
detrusor-sphincter dyscoordination, stress and laughing incontinence, and
lazy bladder syndrome (underactive bladder) in the sense of detrusor
decompensation with infrequent, irregular urination and large residual
volumes of urine.
The recommended first step is keeping a calendar for approximately
one month, which may be designed as a “sun and clouds” calendar in
which dry days, days with wetting, and the frequency of wetting are
entered (e.g. “twice during the night”). Occasionally, keeping a calendar
may in and of itself decrease wetting. However, if there is no reduction in
wetting using this method, a wireless bedwetting treatment alarm in the
form of underwear or a mattress may be helpful. The goal should be
complete dryness, not just a decrease in wetting frequency.
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Pharmacotherapeutic intervention should remain the exception, even if

parents may prefer this “easy” option of treatment (antidepressants: imi-
pramine; ADH-analogs: Desmopressin Acetate (DDVAP) tablets are
approved by FDA for treatment of primary nocturnal enuresis, but there
are strict safety warnings for hyponatremia (edema) and seizures. Note:
intranasal application is not licensed anymore for this indication).
Encopresis (ICD-10 F98.1) is the “repeated, voluntary or involuntary
passage of feces, usually of normal or near-normal consistency, in places
not appropriate for that purpose in the individual’s own sociocultural set-
ting.” According to ICD-10, the diagnosis of encopresis can be made if the
passage of feces occurs at least once per month over a period of at least
half a year and the child has a mental age of at least four. DSM-IV uses a
different time criterion (three months) and also distinguishes forms of
encopresis more precisely: encopresis with constipation and overflow
incontinence (787.6) are differentiated from these forms without constipa-
tion and overflow incontinence (307.7). The child may never have been
clean, or the child may have been clean over a longer period of time and
then begun passing feces again. Children with encopresis show a high
frequency of concurrent psychiatric disorders, especially ADHD, conduct
disorder, and depression. Organic causes must be ruled out, and collabora-
tion with pediatricians is mandatory. Behavioral therapy is the most effec-
tive treatment option (psychoeducation, toilet training with tokens, etc).
4.7.2. Anxiety disorders

Anxiety is a physiological state that can become an established trait.
Beginning with increased shyness in early childhood, children may not
leave home to go to school out of fear that something may happen to their
parents. Separation anxiety is the typical type of anxiety disorders in child-
hood. Panic attacks and general anxiety may become manifested in adoles-
cence, and phobia (social, agoraphobia, etc) may develop. Developmentally,
social phobia and general anxiety represent mature forms of anxious
behavior.
Physiological anxiety in early childhood may be triggered by loud
noises (thunder, etc) or by strangers. Children may be afraid of the dark,
of monsters, or of losing or becoming detached from their family. Children
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going to school may be anxious about natural disasters or bodily harm. In

adolescence, social anxiety and worries about school achievement and
health are normal. If such anxiety persists and impairs the child’s func-
tioning, a threshold has been passed, and a disorder may be diagnosed.
Families of patients often show a pattern of elevated levels of worry or
anxiety. Selective mutism can be seen as a severe type of anxiety disorder:
the child does not communicate, either with non-family members or even
with anybody at all. Even though anxiety disorders are treated separately
in ICD-10 and in DSM-IV, anxiety plays a dominant role in the etiology
and persistence of selective mutism as well.
Psychotherapy with cognitive behavior therapy and, in severe cases
(high-level impairment and/or chronicity), psychopharmacotherapy with
SSRIs may be useful in treating anxiety disorders. Several evaluated and
efficacious therapy (behavioral or cognitive-behavioral) programs for
treating anxiety disorders in childhood and adolescence have been devel-
oped, including Coping CAT, FRIENDS, and Cool Kids, some of which
have been evaluated in non-English versions. Basic elements of all these
programs include psychoeducation, cognitive elements, stimulus confron-
tation, and adjunct training in social skills. Children shall recognize and
analyze their fears (including physical reaction of anxiety) and then
develop strategies to cope with situations that provoke the anxiety (e.g.
self-talk to reduce anxiety). Coping CAT uses 16 sessions to treat anxi-
ety.13 FRIENDS is a school-based prevention program (10 sessions plus 2
booster sessions) run by teachers in normal class times. The teacher has to
be trained, and workbooks for children and adolescents are used.
Information and material is available online (www.friendsinfo.net/). It is
used in the United States, Europe, and Canada. The Cool Kids Anxiety
Program is a group program (10 sessions, 2 parent sessions) for adoles-
cents (originally developed also for children) and parents. It teaches
how to better manage anxiety by teaching clear and practical skills and is
available in Chinese, Turkish, and Spanish).
4.7.3. Eating disorders

Whereas the frequency of anorexia nervosa (AN) has scarcely changed
during the 20th century, the frequency of bulimia nervosa (BN) reached a
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peak in 1996, after which it remained relatively stable or decreased

slightly. The incidence is highest among girls between the ages of 10 and
19 at 34.6 (AN) and 35.8 (BN) per 100,000 (all females: 8.6 and 12.4 per
100,000, respectively). The disorders are more common in females at
gender ratios of 12:1 and 18:1, respectively.
For general criteria, see Chapter 16. To date, SSRIs have not proved
effective for adolescents with acute anorexia nervosa. If a patient shows
symptoms of a severe depression, pharmacotherapeutic intervention with
an SSRI might be, nevertheless, helpful to reduce symptoms of depres-
sion. In bulimia SSRI are to reduce the frequency of bulimic attacks. In
severe cases with manifest obsessive-compulsive disorder or distorted
thinking, atypical antipsychotics may help patients for a defined period of
time until they reach a more acceptable weight level. If the onset takes
place during childhood and adolescence, it is important that therapy be
mostly family-based with a core focus on the development of autonomy,
expressing feelings, showing attachment between family members, and
the like. Family-based psychotherapy combined with elements of behav-
ioral therapy has shown good efficacy.
4.7.4. Non-suicidal self-injury

Non-suicidal self-injury (NSSI) is the direct, repetitive, intentional,
socially unacceptable injury of one’s own body tissue (mostly cutting,
scratching, or hitting oneself), without suicidal intent.19 NSSI seems to
represent a global behavioral phenomenon that occurs in adolescence
and is not necessarily associated with a psychiatric disorder; it seems to
disappear in early adulthood, except in those patients who suffer from a
severe personality disorder.29 Up to 20% of adolescents report having
injured themselves at least once. Self-injuring behaviour (SIB) under-
taken without suicidal intent must be differentiated from suicidal behav-
ior undertaken with the intent to die.24 The relationship between these
entities is still subject to on-going research, and both sets of behaviors
must be fully understood as a worldwide phenomenon. Rates of NSSI
have been positively correlated with the risk of suicidal behavior. To
date, research results show that those who injure themselves repeatedly
are at increased risk of attempting suicide.24 Girls injure themselves
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more frequently than boys. Currently, NSSI must be handled in clinical

practice at least as a signal that the individual engaging in NSSI is under
psychological stress, which may increase the risk of attempted suicide.
It can occur within many psychiatric disorders such as depression, eat-
ing disorders, and early development of personality disorders, but also
as an independent psychopathological phenomenon without further psy-
chopathology. Because NSSI may become a habit, especially when it is
reinforced by peer-group behavior in Internet communities, treatment
will be difficult, and therapy, mostly consisting of elements of DBT or
other CBT programs, must continue until the frequency of NSSI is
reduced.
4.7.5. Depressive disorder

The symptoms of depressive disorder in children and adolescents are fre-
quently different from those seen in adults, although diagnostic codes
both in DSM-IV and ICD-10 are the same as in adults (DSM-IV: 296.xx;
ICD-10: F32.x/F33.x). Younger patients tend to more frequently exhibit
anger, hostility, and rapid changes in mood and temper. Social withdrawal
is more hidden, less overt, than in adults. Often, symptoms are misdiag-
nosed as “normal” behavior in puberty (loss of interest in activities, hob-
bies, and peers). Because 6%–16% of children will be affected by
depression during adolescence, awareness of symptoms is essential. In
mild to moderate depression, counseling of the patient, involvement of the
patient in activities, and encouragement of an active lifestyle seem to be
effective in most cases. If after a certain time (or about three to four vis-
its), no improvement in depression is observed, intensified psychotherapy,
including in combination with an SSRI, is recommended. In severe cases,
fluoxetine, which is the only approved SSRI in Europe and the United
States, has been shown to be effective (in the Treatment for Adolescents
With Depression Study (TADS) and the Adolescent Depression
Antidepressant and Psychotherapy (ADPAT) study.)6,20 (Es-)citalopram
also seems to be effective, while tricyclic and tetracyclic antidepressants
have not been shown to be effective and may be associated with intolera-
ble side effects. Children and adolescents under antidepressant medication
and their parents must be educated about the risk of behavioral activation
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syndrome (suicidal ideation/thoughts), which usually starts at the begin-

ning or end of pharmacotherapy. Behavioral activation syndrome seems to
be more frequent in children and adolescents than in adults. Patients have
to be carefully monitored, but the potential for activation syndrome does
not justify avoiding pharmacotherapy when patients need it. Close moni-
toring is then required, however.
4.7.6. Schizophrenia
Early-onset schizophrenia (EOS) is defined as psychosis with onset
before the age of 18, and very-early-onset (VEOS) as schizophrenia with
onset before the age of 14. VEOS is very rare and EOS is also rare in
comparison to adult onset. Onset in childhood and adolescence causes the
most severe impairment, which can be explained both by neurobiological
factors that affect the developing brain and by social factors, because
these patients have generally not yet finished their education and often
have no stable peer relations, friends, and the like. Symptoms are the
same as in adults; the hebephrenic form of psychosis is more frequent
than in adults.
On the basis of the recognition that the period of untreated disorder
(PUD) is relevant to the outcome, research has in recent years focused
on psychosis risk syndrome (PRS) for the early detection of prodromal
symptoms.3 Results were initially encouraging with regard to the predic-
tive validity of PRS criteria, but they were too variable over long-term
examination. As a result, there are to date no clear-cut recommendations
for the pharmacological treatment of these (insufficiently predictive)
symptoms, even though they have been treated with atypical antipsy-
chotics in several studies. Atypical antipsychotics should be used to
treat EOS, even though first-generation antipsychotics are also effective.
Until the Treatment of Early Onset Schizophrenia Study (TEOSS) was
published, there was hope that second generation antipsychotics (SGA)
would cause fewer side effects; however, rates of side effects are also
high under SGA, although the types of side effects are different from
those under first generation antipsychotics (FGA).34 According to
TEOSS, there is no difference in treatment compliance under SGA
or FGA.
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4.7.7. Sleep problems and sleep disorders

The classification of sleep disorders is (i) dyssomnias: insomnia with
problems falling asleep, hypersomnia with extensive sleep and distur-
bance of the sleep-wake-rhythm and (ii) parasomnias (somnambulism,
ICD-10, F51.3; DSM-IV, 307.46; pavor nocturnus/ sleep terror disorder,
ICD-10, F51.4; DSM-IV, 307.46; and nightmares, ICD-10, F51.5; DSM-IV,
307.47). Sleep problems have to be differentiated into sleep problems
accompanied by other psychiatric disorders (e.g. depression or schizophre-
nia) and mono-symptomatic sleep problems. In childhood sleep problems
are often accompanied with anxiety disorders and problems in school or
family. Diagnosis must consider whether the sleep problems are temporar-
ily or chronically present. Parents have to be asked for the history of the
problems and the conditions of taking the child to bed. What does the child
do before going to bed, does he or she drink anything (e.g. drinks with caf-
feine), is the child watching TV before going to bed, etc. In most cases of
dyssomnias/temporarily sleep problems, the simple counseling of parents
and modification of the situation around sleep (adequate environment with
darkness and silence, rituals such as stories for falling asleep, etc) help.
A typical but rare sleep disorder of the age of 3–5 years is the pavor
nocturnes: The child is sitting in bed, cries, and seems to be anxious. For
parents the child seems to be awake. The child is not awake and after
being awake the child is disorientated and unable to remember the pavor.
After minutes the child sleeps again. Sleep terror disorder happens typi-
cally after one to two hours after falling asleep (during transition of
NREM phase III-IV to REM phase). Nightmares happen typically in the
mid of the night or the second half of the sleep and they disrupt sleep.
Children remember normally the nightmare, are awake or easy to awake,
and are orientated. Contents of nightmares are horrible, dangerous stories.
Nightmares can produce conditioning patterns similar to classic psycho-
physiological insomnia. Especially a specific complaint of fear of going
to sleep may be the consequence. Somnambulism (typically more fre-
quent in early adolescence) is characterized by walking around (going to
toilet, in another room, etc) while being asleep. Duration of somnambu-
lism attacks is normally short (within minutes). Next day, patients do not
remember their somnambulism attack.
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In adolescence, sleep problems are mostly symptoms of other psychi-

atric disorders. Treating the underlying condition also helps to improve
sleep problems.
The evidence of treatment is limited. Aside from counseling and modi-
fication of stimuli that prevent the child from falling asleep, especially the
analysis of the behavior which can cause sleep problems, therapy is lim-
ited. In somnambulism and sleep terror disorder, it is recommended to
sleep for 30–60 min in the afternoon (reduction of NREM phases at night)
and to avoid fatigue and stress. In somnambulism mechanisms to protect
the patient (e.g. bedrails) can be useful. In nightmares it is important to
avoid an expectation of fear. Therefore writing or talking about the con-
tents of nightmares (desensitization) can be helpful. Imagery rehearsal
therapy (learning about nightmares as dysfunctional behavior, changing
the view on the nightmare into positive, new imagery) was proven to be
efficacious in adults. A modified version of this therapy might also help
children with chronic nightmares.
The use of medication can be justified for a short period of time, espe-
cially if the sleep disorder is a consequence of other psychiatric disor-
ders. Low-potent antipsychotics, histamine, or melatonin can be helpful
in these cases — for short term use. Benzodiazepine can cause depend-
ency, therefore its use for sleep disorders should be extremely restricted
(and it should only be used in inpatients). Medication that suppresses
REM sleep will be effective in somnambulism and sleep terror disorder.
Sleep terror disorder will be improved by the use of imipramine, diaze-
pam, and methylphenidate.
5. CONCLUSION AND FURTHER DIRECTION

Child and adolescent psychiatric disorders affect the patient during vulner-
able periods of development. Early detection of symptoms is crucial; in
clinical practice, however, symptoms are often present a long time before
the child is seen by a child and adolescent psychiatrist. A careful anamnes-
tic examination, including the parents’ and patient’s motivation for treat-
ment, is essential to the diagnostic process and treatment planning. In most
cases, obtaining information from the parents alone will not be effective;
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further assessments in school, kindergarten, and the like are necessary to

meet diagnostic guidelines and criteria. In case of internalizing symptoms,
the patient tends to be a much better source of information than the primary
caregivers. Structured interviews, such as K-SADS or Mini-KID, may be
helpful in the comprehensive diagnostic assessment, even if they are not
usually used in clinical routine. There are many self-assessments for
patients and parents that are well evaluated and provide additional informa-
tion for diagnosis according to the ICD-10 or DSM-IV classification sys-
tems. Most treatments in child and adolescent psychiatry are based on
multimodal interventions, including psychotherapy, pharmacotherapy, and
parent-training, as well as home-treatment to guarantee transfer of thera-
peutic effects to the real world of the patients. Because of the limited num-
ber of randomized and well-designed psychotherapy studies, the evidence
for psychotherapy is unfortunately generally not as good as for pharmaco-
therapeutic approaches. Information on the long-term safety of medication
is not available for all substances, although the situation is improving as
more and more substances are studied in children, and networks of hospi-
tals and clinics for child and adolescent psychiatry have been built all over
the world to assess long-term safety data of medications.
The future will bring more studies similar to the MTA and TADS stud-
ies that examine the effects of combined treatments. Therefore, knowledge
about best practice treatments, mediators, and moderators of effectiveness
of the treatments will be gained, and choosing evidence-based approaches
will become easier. Psychotherapeutic interventions have to be adapted to
the needs of migrant patients in most developed countries, and they have
to be modified for underdeveloped countries so that treatment can be
offered in these health care systems with special needs.
Despite all the improvements in evidence-based treatments, the most
severely ill patients often face the burden of cumulative risks and disor-
ders. Identifying groups of high-risk patients and providing prevention
programs for them will be another challenge for the future. High-risk
patients include those with histories of trauma, sexual abuse, or neglect;
patients in the youth welfare system; and children whose fathers or moth-
ers suffer from psychiatric disorders. Adherence to guidelines and evi-
dence-based practice is one side of the coin; the choice of the best therapy
strategy for the individual patient and the patient’s family is the other.
These should not be viewed as opposites, however, because
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individualized treatment based on the available evidence is the best

approach to treatment. This approach is of the utmost importance, as
there is a trend toward individualized medicine, where individual phar-
macogenetic profiles will be used in the future to select the best treat-
ments. Individual factors that promote or hinder the success of certain
types of therapy must be considered in order to meet the needs of patients
and to treat them in an ethical manner. The publication of the new ver-
sions of the DSM-5 and the ICD-11 will present another challenge in the
next decade. It currently seems that fundamental changes will be made,
among other things involving a new entity called “psychosis at risk,”
which will occasion critical debate, in part to determine whether such an
entity even exists. Another area might be the introduction of a new diag-
nosis of self-harming behavior. The prevalence of psychiatric disorders in
adolescence would increase markedly if this common phenomenon was
upgraded to a disorder.
6. KEY POINTS
• In the clinical examination, information about the disorder should be
obtained from several sources (parents, teachers, etc).
• It is crucially important to talk with the child or adolescent separately
from the parents during clinical examination.
• Cognitive behavioral therapy is the most effective therapeutic approach
in both externalizing and internalizing disorders in children.
• Family therapy will be helpful in many cases, especially in family-
related disorders such as eating disorders.
• It is of the utmost importance to inform parents and patients about the
approval status of proposed medications.
• Distinguishing between self-harming behavior and suicidal behavior
is essential for treatment planning, despite the fact that self-harming
behavior increases the risk of suicide attempts.
• Screening patients with externalizing disorders for internalizing
symptoms (depression, traumatic experience) is important to deter-
mine comorbidities and ensure that they are appropriately treated.
• Individualized, evidence-based multimodal treatment plans should be
provided to each patient and discussed with both the parents and the
patient.
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7. CASE STUDIES
7.1. ADHD
An eight-year-old boy at the time of presentation already had to repeat
a class. He lags behind in school. He has a long history of problems in
school, including forgetting homework, disciplinary problems, and dis-
ruptive talking in the classroom. He is extremely impulsive, and he is
unable to wait his turn when playing with friends. He always wants to
be first. As a result, only a few children are willing to play with him; he
is seldom invited by others to take part in activities. His soccer coach
has replaced him on the team because he drags down the team and
argues constantly. His mother tells the doctor that he concentrates
intently for hours when playing computer games but ignores her when
she tries to get him to do homework. He jumps out of his seat at meal-
times. He lost several tote bags, watches, and a fair amount of money
last year.
Stimulant medication was prescribed after he was diagnosed with
ADHD (initially a short-acting preparation for titration, then a long-
acting preparation after it was determined that a dosage of 0.8 mg per
kg body weight was appropriate), and he and his parents attended par-
enting training. Although his IQ was 113, he was an underachiever. His
performance in school improved under medication. He was able to listen
to the teacher and was less impulsive (even though he sometimes con-
tinued to talk loudly out of turn). He joined a swimming team where he
made some new friends who did not know him when he was untreated.
They invite him regularly to their birthday parties and other activities.
In the afternoon, hypermotor behavior recurs, but because it was not
clinically significant, he and his parents decided not to increase the
dosage.
7.2. Autism
A six-year-old boy is presented after he tried to push another kindergarten
student down a set of stairs. He had not done this in the course of a strug-
gle or argument. He stated that he merely wanted to see what would
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happen when the boy fell. The parents reported a long history of abnormal
behavior with hypermotor behavior and a lack of responsiveness to praise
or punishment. He was never interested in snuggling with the mother or
having any intimacy with the parents. The child was never separated from
parents in early childhood. He has always lived with his family. The par-
ents have another child (girl + four years) whose behavior is completely
normal. The father was 42 and the mother 39 when the boy was born.
Speech development was slightly delayed. He is especially interested in
buses and trains (particularly streetcars). He has no friends, but this does
not seem to bother him.
In the clinical examination, he never looked directly at the examiner,
even when spoken to. His voice was elevated and monotonous. He did not
respond in conversation, instead repeating the examiner’s questions. He
exhibited extreme hypermotor and impulsive behavior (running in and out
of the room several times and the like). His IQ, 83, was somewhat subav-
erage, and his motor development was slightly delayed.
7.3. Self-harming behavior

A 15-year-old girl is presented by the surgery unit of the hospital
because she had been admitted several times previously for wound treat-
ment. She has multiple wounds from cutting herself, mostly on her
forearms (left more than right), but also on her thighs. She reports that
she always cuts herself when she feels tension that she cannot deal with
in other ways. After cutting herself, she feels better and calmer. She
often thinks about committing suicide and has chatted on the Internet
with unknown other adolescents about cutting and killing themselves.
On questioning, she denies that she has ever thought about killing her-
self or that she plans to do so. Her cutting, she states, has nothing to do
with a wish to die.
She has several friends, but no close ones. She consistently terminates
relationships with boys after two or three months because she feels that
they bother her. If she goes to a party on weekends, she may drink as much
as a bottle of hard liquor. She has had several periods of depression but
has never sought treatment.
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tions for autism spectrum disorder: A clinical systematic review. PLoS One
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27. Parens E, Johnston J. (2009) Facts, values, and attention-deficit hyperactivity
disorder (ADHD): An update on the controversies. Child Adolesc Psychiatry
Ment Health 3(1): 1.
28. Parens E, Johnston J. (2010) Controversies concerning the diagnosis and
treatment of bipolar disorder in children. Child Adolesc Psychiatry Ment
Health 4(9).
29. Plener PL, Libal G, Keller F, Fegert JM, Muehlenkamp JJ. (2009) An inter-
national comparison of adolescent non-suicidal self-injury (NSSI) and
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30. Rutter M. (2006) Implications of resilience concepts for scientific under-
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31. Santosh PJ, Taylor E, Swanson J, Wigal T, Chuang T, Davies M, et al. (2005)
Refining the diagnoses of inattention and overactivity syndromes: A reanaly-
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32. Schmid M, Goldbeck L, Nuetzel J, Fegert JM. (2008) Prevalence of mental
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28(14): 3586–3594.
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Lieberman JA. (2008) Double-blind comparison of first- and second-
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disorder versus severe mood dysregulation: Risk for manic episodes on
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37. Tau GZ, Peterson BS. (2010) Normal development of brain circuits.
Neuropsychopharmacology 35: 147–168.
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Konrad K. (2010) Neural mechanisms of interference control and time dis-
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Frühkindliche Bindungsstörung, pp. 875–890, Springer, Heidelberg.
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Chapter 8
Schizophrenia and Other Psychotic

Disorders
Peter F. Buckley, Adriana Foster and Scott Van Sant
1. INTRODUCTION
Schizophrenia is arguably the most severe and least well understood of all
mental disorders. It is a highly debilitating condition. It is also a highly
stigmatizing condition. In one recent survey of over 700 people with
schizophrenia spanning across 27 countries, 70% of patients indicated that
they would not declare their illness in public. Moreover, 29% of patients
felt as if they had been discriminated against when applying for a job.20
Schizophrenia is largely considered a disorder of the brain, in the sense
that there are demonstrable — albeit remarkably subtle — brain changes
that are seen in large patient-control comparisons (but not evident on an
individual patient’s brain scan). Although the frontal and temporal lobes
are perhaps most frequently implicated in the pathology of schizophrenia,
in truth, studies over time have found changes of some sort in virtually
every area of the brain.9,17,18 Macroscopically, these appear as loss of
tissue — either failure of the brain tissue to develop or, alternatively, a
progressive loss of tissue overtime. Microscopically, there are aberrant
brain cells as well as abnormal structures (e.g. lack of spines on synaptic
neurons) in discrete brain cells. Collectively these features point to
schizophrenia being a disorder of faulty brain development — i.e. a
184
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Schizophrenia and Other Psychotic Disorders 185
neurodevelopmental disorder. On the other hand, patients can run a dete-

riorative clinical course, and it has now been shown that those patients
who relapse frequently have a progressive (‘neurodegenerative’) loss
of brain tissue. The relationship of pathogenic course to etiology is still
unclear.9 A host of neurochemical abnormalities — especially dysregula-
tion of the dopamine system — have been documented. To some
extent, these abnormalities have guided our development of drugs —
antipsychotic medications — to treat the core features of schizophrenia.
Most people believe that drug treatment is a ‘necessary but not sufficient’
component of an overall comprehensive care plan for helping people
recover (i.e. helping them to minimize their disability and maximize their
ability) from schizophrenia.5 It is appreciated that the outcome of schizo-
phrenia is far better in developing countries than developed countries.
This chapter will focus on key clinical aspects of schizophrenia, illumi-
nating points of relevance to those trainees and clinicians who are seeking
international perspectives on this enigmatic condition. To augment this,
the reader is recommended to consult several authoritative journal review
articles and books on schizophrenia that are co-authored by international
experts on schizophrenia.6,9,16–19
2. EPIDEMIOLOGY
Worldwide, the occurrence of schizophrenia is just under 1% of the
population. However, higher rates of psychosis are observed among
British of an African–Caribbean descent, among those from Croatia, and
those from Southern India.18 There is also a curious winter birth excess of
schizophrenia — that is, people with schizophrenia from the northern
hemisphere are more likely to be born in the first three months of the
year; the reverse is true for the Southern hemisphere. Another highly
reducible finding is that about 1 in 5 people with schizophrenia have
experienced some complication at birth — that is, preterm labor, fetal
distress, anoxia, head trauma during delivery, or prenatal infections.
Although none of these effects are either specific to schizophrenia or of
themselves (alone) are powerful enough to explain why schizophrenia
occurs, collectively they point to events in early fetal life as powerful
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186 P. F. Buckley, A. Foster and S. Van Sant
determinants of a condition that later emerges in later adolescent/early

adulthood.5,9,11,17 Males and females are equally affected by schizophre-
nia, although the onset in males is some five years earlier typically than
in females. Also, females typically have a less severe course of illness —
it is considered that this is due to some moderating effect in females of
estrogen on dopamine sensitivity and dysregulation. Collectively, these
epidemiological findings inform the search for clues to the etiology of
schizophrenia.11
3. ETIOLOGY
One very clear observation on the etiology of schizophrenia is that it runs
in families. Monozygotic twins have a 47% risk of both twins developing
schizophrenia, while this risk drops to 27% among dizygotic twins.
A child born to a parent with schizophrenia has a 14% morbid risk,
whereas a child of parents who both carry a diagnosis of schizophrenia
has a 46% morbid risk of developing schizophrenia. Thus, genetic influ-
ences are powerful, but they do not tell the whole story. Other factors —
acting alone or in some (gene-environmental) combination — are also
important.16 As an example, it is estimated that people who smoke can-
nabis are between 2 and 4.5 times more likely than non-smokers to
develop schizophrenia. It remains unclear whether cannabis is simply a
trigger — that is, bringing on schizophrenia in somebody who is already
(perhaps genetically) vulnerable — or whether it can actually cause
schizophrenia. Additionally, there is on-going debate as to whether schiz-
ophrenia and mood disorder, especially bipolar disorder, are similar dis-
orders, with an overlap in heritability and genetic findings between the
conditions.6
3.1. Diagnosis and phenomenology

Schizophrenia is characterized by a prolonged course of positive symp-
toms, negative symptoms, cognitive impairment, and decline in premorbid
function (see Table 1). The point of ‘onset’ of schizophrenia is often
demarcated by the emergence of florid ‘positive’ psychotic symptoms —
delusions, hallucinations, bizarre behavior. Clearly, if symptoms are gross
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Table 1. Typical phenomenological features of schizophrenia.

• Positive symptoms
— delusions
— hallucinations
— thought disorganization
• Negative symptoms
— apathy
— avolition
— ahedonia
• Cognitive symptoms
— impaired attention and concentration
— memory loss
— cognitive shift inflexibility
• Prodromal features (that antedate the onset of florid positive
symptoms and obvious decline in functioning)
— odd or idiosyncratic ideas
— mild paranoia
— depressed mood
— occasional muffled or indistinct sounds
and result in disruption to society (e.g. urination in public as a bizarre

behavior associated with hearing voices), then the presentation will come
to the attention of medical personnel via family, police, or others bringing
the disturbed individual to a point of care (e.g. an emergency room). The
first clinical vignette illustrates that scenario. But less pronounced fea-
tures of psychosis — especially negative symptoms — can persist for
years before coming to the attention of medical personnel. In some
instances the delay of untreated psychosis can be even up to one year.
Often people may become depressed at or before the time they have a
psychotic episode — this is another diagnostic complication. The second
clinical vignette illustrates this more gradual deteriorative course, as well
as the real clinical dilemma of distinguishing depression from psychosis
early on in the course of the illness. This dilemma is particularly evident
when there is an onset of serious mental illness in childhood.
It is crucial to appreciate that there are no symptoms that are ‘pathog-
nomonic’ of schizophrenia. The pattern and duration of symptoms, com-
plete with an absence of ‘organic’ explanation or prominence of mood
features, are used to arrive at a diagnosis of schizophrenia. The ICD-10
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Table 2. The International Classification of Diseases 10th edition (ICD-10) criteria for
the diagnosis of schizophrenia.
A minimum of one very clear symptom (and usually ≥2 if less clear-cut) from groups
(a)–(d) below, or symptoms from ≥2 of the groups (e)–(h), which have been present
for most of the time during a period of one month or more:
Thought echo, insertion, withdrawal, broadcasting.
Delusions of control, influence, passivity; delusional perception.
Hallucinatory voices of running commentary, third-person discussion, or other types
of voices coming from some part of the body.
Persistent delusions of other kinds that are culturally inappropriate and completely
impossible.
Persistent hallucinations in any modality; daily for weeks/months, or accompanied
by half-formed non-affective delusions, or with persistent overvalued ideas.
Breaks in thought fluency, i.e. incoherence, irrelevant speech, neologisms.
Catatonic behavior; excitement, stupor, Mutism, posturing, waxy flexibility, negativism.
Negative symptoms; apathy, paucity of speech, blunted emotions, social withdrawal;
not due to depression or neuroleptic medication.
A significant and consistent change in the overall quality of some aspects of personal
behavior (loss of interest, social withdrawal, aimlessness).
Subtypes: paranoid, hebephrenic, catatonic, undifferentiated, post-schizophrenic
depression, residual, simple schizophrenia.
criteria for schizophrenia are given in Table 2. ICD-10 groups together

schizophrenia, schizotypal states, and delusional disorder. Only one
month’s illness duration is required for diagnosis — which differs from
the six-month duration required by DSM. The most current DSM nomen-
clature is DSM-IV-TR.1 ICD-10 also recognizes the category of post-
schizophrenic depression. Both ICD-10 and the DSM system are currently
under revision. Two major changes are at least under consideration: the
removal of the diagnosis of schizoaffective disorder (which has probably
become too broad to be meaningful) and the inclusion of an ‘at risk for
psychosis’ category. The latter change reflects the impact of burgeoning
research on prodromal phase of schizophrenia — that is, the period (usu-
ally weeks to months in duration) where there are attenuated features of
perceptual and thinking disturbances but functioning remains relatively
unimpaired and there is an absence of frank psychotic symptoms. The
idea is that intervening earlier might result in either averting a transition
to psychosis or at least minimizing the potentially toxic effect of
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prolonged, untreated psychosis. Although this seems intuitive, it is not

proven, yet. Moreover, early intervention for ‘prepsychotic states’ could
be a ‘hit or miss’ strategy, thereby exposing (and stigmatizing) individuals
who will not develop schizophrenia to the harmful effects of antipsychotic
medications. At the very least, we should make every effort to configure
our services so as to optimize access to care for people who experience
their first psychotic break. In some US programs — but more so in
Europe and (particularly) in Australia, there are dedicated first-episode
clinics that are tailored toward adolescents. The more progressive pro-
grams are also using social network Internet sites as a source of informa-
tion and early care referral for psychosis.14
It is important to observe that the diagnosis of schizophrenia requires
the exclusion of other organic conditions that could have caused the psy-
chosis (Table 3). Although many of these conditions are far less common
than schizophrenia in this adolescent — early adult stage, these conditions
merit consideration. There is an on-going debate as to the value of doing
brain scans and related diagnostic works when a person presents with a
typical psychotic episode. Because they will have a low yield, exhaustive
testing does not make pragmatic or economic sense. However, prudent
testing (including a brain scan, preferably MRI) does make sense because
Table 3. Conditions that can mimic Schizophrenia.

• Bipolar disorder
• Psychotic depression
• Brain tumours
• Metabolic disturbances
— e.g., hyponatremia
• Endocrine disorders
— e.g. hyperthyroidism
• Cardiovascular disorders
— e.g. stroke
• Congenital brain disorders
— e.g. velocardiofacial syndrome
• Toxic disturbances
— e.g. metallic poisoning
• Drug-induced psychosis
— e.g. illicit drugs (cannabis as an example)licit drugs
(steroids as an example)
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it provides the patient and family with clarity about the diagnosis and it
reassures them that the condition has been thoroughly assessed. The fre-
quent co-occurrence of illicit drug abuse around the time of the first psy-
chotic episode is another consideration that is very complex. Family
members are often left confused as to ‘the chick and the egg’ effect: did
the drug abuse bring on the psychosis or did the psychosis lead to the drug
abuse? It is best clinically to remain circumspect, to acknowledge the
potential deleterious effects of drug abuse, and to revisit the diagnosis
months later.
4. TREATMENT
4.1. General considerations
Schizophrenia is a difficult condition to treat and should be treated by
specialists.5,16 Because lack of insight into psychosis is so common —
even in the face of the serious personal consequences (e.g. incarceration)
of untreated psychosis and bizarre behavior — it is really hard to keep
people engaged in treatment. On one hand, many people discontinue treat-
ment over time because they do not believe they are ill. On the other hand,
it has been observed that people who gain insight directly following their
first psychotic episode are at risk of harming themselves because they
become demoralized about their plight.
The burden and emotional toll of this condition on family members is
enormous. Families need a lot of support. The range of services available
to support patients and their families differ substantially from country to
country. In China, for instance, people are usually hospitalized for months
during their first psychotic episode. The condition is highly stigmatizing,
and families have great difficulty supporting their loved one. In many
developing countries, families provide great support — even to the point
of (inadvertently) delaying the person’s access to care because psychotic
symptoms are well tolerated by family members. In many countries with
socialized medicine, people get access to a range of services for free and
they are afforded benefits (including housing support) for their illness.
In the United States, services are fragmented and the extent of social sup-
port across the continuum of illness needs (clinical, housing, vocational,
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Table 4. Elements of a recovery-based approach

to the care of persons with schizophrenia.
• Medications — but with a different focus:
— ‘Alliance — non-compliance’
— Shared — Decision making medications
seen as a means to a goal
• Abilities driven
• Hope affirmed
• Personal strengths and resilience affirmed
• Role of spirituality
• Wellness recovery action plan
• Peer support services
social) are more limited than they should be.8 Services also differ in the
extent to which they view the person with schizophrenia as a patient who
is a recipient of services versus a person who is able to use services to take
more personal charge of the illness. The latter is a more patient-focused,
recovery-based perspective. Some countries are more recovery-based in
their mental health services than others, which remain traditional in their
service orientation and delivery.5 There is growing interest in recovery-
based approaches to care (Table 4), including the involvement of people
who are themselves recovering (called peer support specialists) as part
of the multidisciplinary team that helps the person maximize his or her
abilities and minimize disabilities.
4.2. Medication treatments

Medications are the bedrock of the treatment of schizophrenia. Having
said that, medications alone are not sufficient, and as clinicians, we often
convey the message to people that medications are the only component of
care — this contributes to people stopping their medications.4 Additionally,
people stop taking their medications for a host of other reasons — the
drugs are ineffective, the drugs cost too much, the drugs have distressing
side effects (e.g. weight gain or muscle movements), people (and/or their
family) have a natural disinclination toward taking drugs, people are
deluded and consider that they are being poisoned by these medications
(in which instance, side effects often constitute ‘proof’ for patients that
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they are being harmed). Whatever the reason, it is hard to treat schizophre-
nia when the person either refuses medication treatment and/or goes off
the medications. Giving medication in the form of a long-acting injection
(LAI) — which is typically effective for 2–4 weeks — is an alternative. In
the United States, approximately 12% of patients are receiving an LAI of
antipsychotic medication, whereas in Europe the rates of use may be as
high as 50% of patients.
The pharmacology of antipsychotic medications is complex.16 Virtually
every antipsychotic has in common an affinity for dopamine (D2) recep-
tors, with most drugs having a strong antagonism of D2 receptors.
Classical receptor occupancy theory posits that at least a 60% D2 occu-
pancy is required for antipsychotic efficacy but that motor side effects
(extrapyramidal side effects such as restlessness) will occur at occupancy
rates of 75% and above. On the other hand, newer antipsychotics seem to
belie this theory because they have low D2 occupancy rates (e.g. 28% for
clozapine, 48% for quetiapine) and yet these drugs are clearly effective
antipsychotics. This observation challenges our field to look for other
explanations for antipsychotic activity — perhaps some balance between
D2 and other dopamine receptor classes, perhaps some moderating effect
of glutamatergic receptor agonism, or perhaps even the gestalt of multiple
receptor occupancy effects involving dopamine, serotonin, nonadrenergic,
cholinergic, and histaminergic receptors. All currently available antipsy-
chotics share an affinity for D2 receptors (although this affinity also differs
widely across drugs), yet they are also quite disparate in their effects on
these other receptors. The drugs have merely, for convenience, been clas-
sified into first generation antipsychotic (FGA) and second generation
antipsychotic medications (SGAs). SGAs were originally conceived as
clinically superior to FGAs. Apart from clozapine, this distinction has
become less clear overtime. In the United States, SGAs are the predomi-
nant choice of drugs. In European countries, there is a greater balance
of use between FGAs and SGAs. The relative merits of these two
classes — and of each drug — remains hotly debated by our field.10,16
FGAs are considered to have more motor side effects and to have limited
beneficial effect upon negative or cognitive features of schizophrenia.
SGAs were considered to have more therapeutic benefit beyond amelio-
rating positive symptoms, including reducing negative symptoms and
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improving cognition. However, these latter effects now appear to be pretty

small for any given patient. Additionally, although on balance SGAs have
less motor effects than FGAs, they have more metabolic and weight-
related side effects. These generalizations are helpful for an overall under-
standing of the array and profile of drugs. However, it cannot be stressed
enough that the efficacy and tolerability of any given drug in a patient is
highly individualized. Unfortunately, the current pharmacologic treatment
of schizophrenia is more of a sequential ‘trial and error’ process than any-
body would like.3
Although in a general sense these drugs are comparable in efficacy,
they will differ for any given patient. Similarly, although the drug’s
side effect profile is more predictable, it is still a matter of ‘trial and
error’ to determine whether or not a patient will experience a given
side effect and how significant it might be for that patient. Moreover,
both efficacy and drug tolerability are powerfully influenced by the
dosing of the antipsychotic. Unfortunately, the evidence-base as to
what is the most effective dose and how high a clinician should raise
the dose of a drug to optimize efficacy is poorly understood.3 Often,
clinicians and patients agree to switch medications, hoping that the
next drug will be a better fit. However, while switching medication
offers an opportunity it can also be a risky time for relapse (most clini-
cians now recommend ‘cross tapering’ gradually between the current
and new antipsychotic). The patient will not know for weeks/months
whether the new drug is a better fit. Clozapine currently represents the
drug of choice ‘when all else fails,’3 although many clinicians are con-
cerned that this drug is underutilized and should be used much earlier
in the algorithm (Fig. 1).
4.3. Non-medication treatments

There is much that can — and should — be done beyond medications.
People need an immense amount of personal and family support to cope
with this disabling and demoralizing condition.5 People need counseling.
People often need social skills and vocational training.21 Vocational train-
ing includes preparing people to acquire the skills (both specific job-
specific competencies and social skills repetitive) to obtain and then
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SGA or FGA
Inadequate response
Trial of a different SGA or

FGA monotherapy
Inadequate response
Subsequent SGA or FGA Trials

with/without polypharmacy
FGA = First generation antipsychotic Inadequate response

SGA = Second generation antipsychotic
ECT = Electroconvulsive therapy
Inadequate response
CLOZAPINE + ECT Clozapine with

FGA SGA rTMS
SGAs/FGAs
Fig. 1. Typical approach to the pharmacotherapy of schizophrenia.
sustain employment. Employment rates for people with schizophrenia are

low and more often than not people who gain work do so through shel-
tered work opportunities rather than in the competitive work market. It is
also very difficult for people to remain in employment, both due to the
strain of daily coping with the others as well as the inevitable setbacks that
occur when there is a relapse of illness. There are specific cognitive
behavioral therapies that can be helpful for people with schizophrenia,
especially if they have persistent voices.21 These services are more readily
available in Europe than in the United States. Elements of comprehensive
care for people with schizophrenia are given in Table 5.
5. PSYCHOTIC CONDITIONS OTHER THAN

SCHIZOPHRENIA
Although the terms psychosis and schizophrenia are often used interchange-
ably, there are several conditions in psychosis that are distinct from schizo-
phrenia. These are highlighted in Table 6. Additionally, the conditions listed
in Table 3 are different from schizophrenia yet can mimic schizophrenia.
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Table 5. Elements of comprehensive care for people

with schizophrenia.
Supportive relatives
A peer support specialist and/or individual counselor
Social support
Vocational rehabilitation
Housing support
Financial and disability services support
Transportation support to and from outpatient visits
Outpatient visits
Day — rehabilitative care
Hospitalization
Outreach teams (Assertive Community Treatment ACT)
Involuntary commitment services
Legal support
Medications
Table 6. Other psychotic disorders beyond schizophrenia.

Psychoses related to mood disorders
Schizoaffective disorder
Delusional disorder
Shared delusional disorder [‘Folie Au deux’]
Brief psychotic disorder
Culture-bound syndromes e.g. Koro
Psychoses related to mood disorder — either mania or depression —

are common. The pattern of relationship to mood and the course over time
help distinguish these psychoses from schizophrenia. Schizoaffective
disorder is another common condition. Schizoaffective disorder closely
resembles schizophrenia and is the recorded diagnosis in approximately
30% of outpatient populations with chronic psychoses in the United
States. It is a poorly understood condition, occupying a position seem-
ingly midway between schizophrenia and mood disorder. Treatment prin-
ciples are similar to schizophrenia, including also close attention to mood
stabilization. In general, the outcome appears more similar to schizophrenia
than to other disorders.
Delusional disorder is considerably less common than schizophrenia.
Several varieties are described and these inevitably run an untreatable
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course. Patients with delusional disorder rarely comply with treatment.

Some patients, for example those with erotomanic delusions, may pose a
risk of harm to others.
Historically, we recognize brief psychotic disorders as separate entities.
In practice, it is difficult to distinguish a brief psychotic disorder from a
schizophrenic form of psychosis or from a drug- or organic substance-
induced psychosis of short duration.
Other, rare, psychotic conditions, may be culture-bound conditions.
6. PROGNOSIS
Schizophrenia is a life-shortening condition, either by suicide or by
comorbid physical illness, which is now a major consideration for treat-
ment, especially given the higher liability to weight gain and metabolic
disturbances during treatment with SGAs.15 Although some patients
recover over time, many/most patients remain to some extent sympto-
matic and/or with impaired functioning. Approximately 4% of people who
develop schizophrenia end up committing suicide — most often, early on
in their illness. The outcome is better in developing countries.11 Our field
remains optimistic that intervening earlier — and with more effective
treatments — might result in an attenuated illness course and improved
overall prognosis. Selecting treatments that target key components of the
illness, like cognition, remains another promising approach.7 Clinicians
also look forward to improved, newer medications that might offer better
efficacy and lower side effects.2 Psychiatry is also poised to embrace per-
sonalized medicine. Initial pharmacogenetic studies in schizophrenia give
cause for cautious optimism that over time we will be better able to match
‘drug to patient.’
7. KEY POINTS
• Schizophrenia, although its onset is typically demarcated by florid
psychotic symptoms, appears to have its origins early in life, and
many patients may manifest (in retrospect) very subtle signs of neuro-
logical-cognitive-social impairment (so called ‘pandysmaturation’).
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• Drug abuse is common in people with schizophrenia. It definitely

worsens the course of illness, and it may even be — of itself — a
cause of schizophrenia for some patients.
• Physical comorbidities (diabetes, respiratory conditions, etc.) are com-
mon and potentially life-shortening in people with schizophrenia.
Recognition of the metabolic effect of antipsychotic medications is
prompting a move (albeit slowly) toward integrated medical-psychiatric
care for schizophrenia.
• Medications are the bedrock of treatment. However, non-adherence
with medications wreaks havoc with the maintenance treatment of
schizophrenia.
• Despite pharmacological differences between antipsychotics in neu-
rotransmitter receptor profiles, the matching of ‘the right drug’ to ‘the
right patient’ is still a ‘trial-and-error’ process.
• Polypharmacy — the simultaneous use of two or more antipsychotics
and/or the use of different classes of psychotropic medications (mood
stabilizers, hypnotics, anxiolytics) in association with antipsychotic
therapy — is common in clinical practice.
• Promoting self-resilience and hope is essential to the recovery journey
of people with schizophrenia.
• Family members need — and deserve — on-going support.
8. SELF-ASSESSMENT
8.1. Available information on the efficacy of antipsychotic
medications suggests that:
(A) Most patients respond well to treatment, no matter which medication
is prescribed.
(B) All of the drugs have the same response in this patient group.
(C) Switching of antipsychotic medications is a common clinical
practice.
(D) All of the above.
Switching antipsychotic medications is a common clinical practice, the

most common reason being for inadequate efficacy of the original drug.
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Side effects are another major reason. Often switching medication occurs
before treatment and dosing with the previous antipsychotic has been
optimized.
Answer: C
8.2. In attempting to understand the relative efficacy

of antipsychotic medications, which of the following
is most pertinent:
(A) All drugs work the same.
(B) Clozapine works the best.
(C) FGAs are better than SGAs.
(D) SGAs are better than FGAs.
The relative efficacy of antipsychotics remains a hotly debated topic.

However, few people will dispute the superior efficacy of clozapine. This
has been well demonstrated in a variety of studies from across the world.
Answer: B
8.3. In attempting to understand the relative tolerability

of antipsychotic medications, which of the following
is most pertinent concerning the risk of tardive
dyskinesia and the rates across antipsychotic classes:
(A) Similar between FGAs and SGAs.
(B) Lower with FGAs.
(C) Higher with FGAs.
(D) Increased now as compared with 10 years ago.
Current information now suggests that the rate of tardive dyskinesia is

about 10 times lower with SGAs compared with FGAs. It is important to
put in context the relative tolerability of FGAs versus SGAs. Although
tardive dyskinesia is less common, it is still possible during treatment with
SGAs.
Answer: C
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8.4. Optimizing the dose of an antipsychotic is a reasonable

(first) alternative to switching medications once:
(A) There are good case management services.
(B) The medication is well tolerated and there is an absence of or mini-
mal dose-related adverse effects.
(C) The patient has been tested for pharmacogenetic analysis of drug
metabolism.
(D) The dose is less than 20% of bioavailability index.
The optimum dose for a given antipsychotic is still poorly understood.

Once tolerability is not a major consideration, it is appropriate to increase
the dose of a given antipsychotic to the upper limit of its FDA dosing
indications in advance of switching to another antipsychotic medication.
Answer: B
9. CASE STUDIES
9.1. Psychotic break complicated by substance abuse
A 21-year-old woman presents for the first time to the hospital with a nine-
month history of fear that her college roommates are spying on her. She
believes that they are plotting to get her thrown out of school. She believes
that on several occasions she has overheard them say, “Let’s tell the
Provost she is a terrorist.” She is distressed and agitated when interviewed.
Her speech is unelaborated, and she barely answers questions. She appears
to be preoccupied. Occasionally, she is observed to whisper to herself. The
police who brought her to the hospital confirmed that her college room
was a mess and that it looked as if she had been not caring for herself for
months. The patient tests positive for marijuana and for the use of cocaine.
9.2. Depression or prodromal state?

An 18-year-old man was brought to an outpatient clinic by his mother, who
is concerned that he is ‘not making his grades’. He has missed classes and
appears generally disinterested in life. This has been going on for a long
time but has become more pronounced in recent months. On one occasion
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recently, he said to his brother that ‘life is a drag’. His mother reports that
he was always a shy kid and socially withdrawn. She describes that he was
more upset than his siblings at the divorce of his parents 10 years ago.
When seen in the clinic, he was unkempt in appearance. He made poor
eye contact and was clearly unhappy to be there. He did not engage in the
interview. His answers to questions were brief and unelaborated. He was
mildly disorganized in his speech. He denied being depressed or paranoid.
He said he had never heard voices or seen unusual things. His urinary drug
screen and other tests were all normal.
The clinician determined to monitor the patient over time: perhaps he
is depressed or perhaps he is experiencing some prodromal state. Time
will tell.
9.3. Schizophrenia and suicide

A 28-year-old man with schizophrenia is brought to the hospital by family
due to refusal to eat and to leave his room, agitation, and paranoia. He is
treated in the hospital and placed in a personal care home. His antipsy-
chotic medication is changed within the month after discharge from the
hospital due to side effects. Within the same week, he completes suicide
by hanging.
9.4. Schizophrenia and pharmacology

A 26-year-old woman is brought to the hospital because she was found
wandering the streets in the early morning hours and when questioned by
the police, she said she was ‘looking for aliens’. She then told the doctor
that aliens had implanted a device in her brain three years ago, that space
monitors were watching her every move, and that two ‘super aliens’ were
talking constantly to her. She denied drug abuse or physical illnesses, and
her work-up was normal. She was admitted to a psychiatric care unit.
Although initially calm on the unit, she became agitated after watching a
news report, and she ran up and down the hall shouting, ‘Aliens are com-
ing! Aliens are coming!’ She could not be calmed. She refused medication
and was eventually given ziprasidone 10 mg intramuscularly. The next day,
she agreed to take ziprasidone orally, and the ziprasidone was gradually
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titrated to a therapeutic dose. The voices she was hearing receded, but she
continued to have bizarre ideas. Upon discharge from the hospital, she
could not afford ziprasidone. This medication was denied by her insurance
company in favor of oral risperidone, which was available in a less costly
form. She agreed to switch to risperidone. It worked better, but three
months later she stopped it completely because she believed it had harmed
her by obliterating her menstrual cycle (risperidone is known to cause
hyperprolactinemia). She subsequently relapsed and was committed to the
hospital against her will. Her symptoms were stabilized well on olanzap-
ine, but she gained 30 lbs within six weeks. Her cholesterol level also rose
to an almost abnormal level. Efforts to help her with dietary restriction and
with a weight loss and exercise program were ineffective. The addition of
metformin to her treatment regimen did not have much effect on her
weight and elevated cholesterol. The patient again stopped her medication.
Months went by until she was brought to the hospital by the fire brigade,
this time having set fire to her apartment in an effort to ‘shine a light for the
aliens to land their ship.’ She refused to take any medication and eventually
agreed to take a long-acting injection of monthly paliperidone palmitate,
which helped. Nine months later, her ideas are less pronounced and her
behavior is less erratic. However, she remains deluded. Her psychiatrist is
considering starting her on clozapine. The psychiatrist is concerned as to
whether she will take this medication, given her history of non-adherence
with other oral medications. He wonders whether she might be better off
to stay on the long-acting injection, even though it is only partially effec-
tive. The patient is scared about taking clozapine. She says that if she
‘blacks out’ with a seizure, she might lose contact altogether with the
aliens, who might then land and attack China. She is also very worried
about gaining weight on clozapine. As a compromise, the patient and her
doctor agree to add a small dose of quetiapine to her current regimen.
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2. Biedermann F, Fleischhacker WW. (2009) Antipsychotics in the early stage
of development. Curr Opin Psychiatry 22: 326–330.
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3. Buchanan RW, Kreyenbuhl J, Kelly DL, et al. (2010) The 2009 schizophre-
nia PORT psychopharmacological treatment recommendations and summary
statements. Schizophr Bull 36: 71–93.
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Disorders, National Academies Press, Rockville, MD.
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facts’: What we know in 2008 — part 3. Neurobiology. Schizophr Res 106:
89–107.
10. Leucht S, Corves C, Arbter D, et al. (2009) Second-generation versus first-
generation antipsychotic drugs for schizophrenia: A meta-analysis. Lancet
373: 31–41.
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American Psychiatric Press, Washington, DC.
12. Lieberman JA, Stroup TS, McEvoy JP, et al. (2005) Effectiveness of antipsy-
chotic drugs in patients with chronic schizophrenia. N Engl J Med 353:
1209–1223.
13. McEvoy JP, Lieberman JA, Stroup TS, et al. (2006) Effectiveness of clozap-
ine versus olanzapine, quetiapine, and risperidone in patients with chronic
schizophrenia who did not respond to prior atypical antipsychotic treatment.
Am J Psychiatry 163: 600–610.
14. McGorry PD, Tanti C, Stokes R, et al. (2007) Headspace: Australia’s
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What we know in 2008 — part 1. Overview. Schizophr Res 100: 4–19.
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and anticipated discrimination against people with schizophrenia: A cross-
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Schizophr Bull 34: 523–537.
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Chapter 9
Mood Disorders
Sandra Rackley and J. Michael Bostwick
1. INTRODUCTION
Patients with mood disorders are ubiquitous in general medical practice.
These illnesses can cause substantial suffering for patients, but with
appropriate recognition and management, patients with mood disorders
can have significant relief from their symptoms and live productive lives.
Thus all clinicians must be able to recognize symptoms of these disorders
and know how to initiate treatment. In this chapter we review the epide-
miology of these disorders, new frontiers in understanding the biological
and psychological underpinnings of mood symptoms, typical clinical
features, and evidence-based approaches to treatment.
2. EPIDEMIOLOGY OF MOOD DISORDERS

Mood disorders are common. Lifetime prevalence of Major Depressive
Disorder is 10%–25% in women and 5%–12% in men, and Dysthymia has
a prevalence of about 5% in the general population, with women 2–3
times more likely than men to develop the disorder. Bipolar-spectrum
disorders have a prevalence of about 1%–2% in both men and women, and
another 2%–5% meet criteria for cyclothymia. Onset of the first episode
of either disorder commonly occurs in early adulthood, but initial depres-
sive episodes can present at any age. Onset of bipolar disorder is rare after
204
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Mood Disorders 205
age 50, and if mania happens for the first time in an older adult, causative
conditions such as medical illness, prescription drug side effects, or
substance abuse should be ruled out.
Mood disorders appear in all socioeconomic and cultural groups,
leading to significant morbidity and mortality worldwide. The World
Health Organization listed unipolar depressive disorder as the world’s
third most frequent cause of burden of disease in 2004, behind only lower
respiratory infections and diarrheal illnesses. Projections suggest that
by 2030 unipolar depression will move into the # 1 spot. Mood disorders
are associated with such substantial morbidity because they tend to have
onset early in life and be a chronic, if intermittent, presence throughout
the working and reproductive years, substantially impacting course of life.
Mortality is also a serious concern in mood disorders, because they are the
primary risk factor for completed suicide. In 2005, the most recent year
for which data are available, suicide was the # 2 cause of death in
15–19-year-old girls in the United States, and the # 3 cause of death for
boys in the same age group. It was also the 8th leading cause of death for
men of any age. Thus, both disability and suicide associated with mood
disorders are major public health concerns.
3. ETIOLOGY OF MOOD DISORDERS

Like most psychiatric illnesses, mood disorders are likely caused by the
interplay of genetic and neurodevelopmental vulnerability with the envi-
ronment. Numerous biological factors have been linked to depression.
First-degree relatives of depressed patients are 2–3 times more likely than
controls to also have depression, and identical twins have approximately
a 50% concordance rate for major depression. Heritability studies for
bipolar disorder are even stronger, suggesting a 10-fold higher likelihood
of bipolar disorder in first-degree relatives of bipolar patients and a con-
cordance rate of 33%–90% for monozygotic twins. Recent genetic studies
have proposed a number of genes that may influence the presence or
course of mood disorders, including functional polymorphisms in the
serotonin transporter gene, the serotonin receptor gene, the glucocorticoid
receptor gene, and the gene encoding BDNF. Multiple neurotransmitter
systems are putatively involved in mood disorder etiology and treatment,
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206 S. Rackley and J. M. Bostwick
including the monoamines (serotonin, norepinephrine, and dopamine), the

cholinergic system, GABA, glutamate, CRF and the HPA axis, neuropep-
tides like substance P and neuropeptide Y, and neurotropic factors such as
BDNF. Many brain regions are linked to mood disorders, including mul-
tiple areas of the prefrontal cortex, the anterior cingulate, and the amyg-
dala. Growing capacities for genetic sequencing and structural and
functional neuro-imaging are likely to continue providing important infor-
mation to better clarify the biological underpinnings of these disorders
and potential treatment targets.
Psychological and social factors also play a prominent role in mood disor-
der etiology. Numerous studies have shown a link between early life trauma
and later development of depression, and stressors also often occur shortly
before a mood episode. Patients with certain personality disorders —
especially borderline, histrionic, and obsessive-compulsive — may be more
prone to develop depression. Aaron Beck suggested that depression arises
out of a classic cognitive triad of negative beliefs about the self, the world,
and the future, and proposed that depression treatment should focus on
modifying these negative beliefs.
4. DEPRESSIVE DISORDERS
4.1. Phenomenology of depressive disorders
A depressive episode is more than just a passing mood or an acute reaction
to immediate circumstances. Depression robs patients of their vitality and
saps the psychic energy that would otherwise motivate emotional, cogni-
tive, and physical activity. Particularly with prolonged symptoms, patients
with major depression often struggle to maintain work or school function-
ing. They may significantly curtail their leisure activities or experience
strain in significant relationships. A depressive episode is also persistent:
DSM-IV-TR requires symptoms of at least two weeks’ duration in order
to diagnose a major depressive episode, and while ICD-10 does not
specify a minimum amount of time, it does note that episodes, at least in
recurrent depression, tend to last a few weeks to several months.
Prominent emotional symptoms required to diagnose a depressive
episode include a lowered mood and a reduced capacity for enjoyment of
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Mood Disorders 207
normally pleasurable activities. Patients will sometimes notice feeling at

their worst in the morning and improving throughout the day, a cycle
referred to as a “diurnal” variation in mood. Overall, however, most
patients describe their mood as persistently down. In addition to sadness,
patients often also exhibit irritability, and indeed in children and adoles-
cents, DSM-IV allows a diagnosis of major depressive disorder to be
made if the mood is mostly irritable, rather than depressed. Anhedonia, or
reduction in the capacity for enjoyment, frequently manifests as a loss
of interest in normally pleasurable activities, diminished libido, or —
particularly in adolescents — a sense of “boredom.” Cognitive symptoms
are also quite common in depressive episodes and can include inattentive-
ness, indecisiveness, ruminative thinking, excessive guilt, and lowered
self-esteem or self-confidence. Physical symptoms are also clues to a
depression diagnosis. Depressed patients commonly complain of reduced
energy or stamina. Sleep is frequently disrupted. Some patients describe
spending most of the day in bed, despite the rest not being restorative.
Others report reduced quantity and quality of sleep. A classic pattern of
sleep disruption is early morning awakening with difficulty returning to
sleep (referred to as “terminal insomnia”), though any phase of the sleep
cycle may be affected. Appetite may significantly increase or decrease,
and a weight change of 10% or more is not uncommon. Depressed
patients may endorse feeling extremely fidgety or restless (“psychomotor
agitation”) or, conversely, quite slowed and heavy (“psychomotor retarda-
tion”). These alterations of activity level are often more obvious to the
patient’s physicians or friends and relatives than to the patient.
A small proportion of severely ill patients develop psychotic symptoms
during the course of a depressive episode. Delusions in such patients typi-
cally have a negative cast and can range from somatic preoccupations,
such as the belief of having a horrible disease or of rotting inside, to para-
noid beliefs of being rejected by spouse or family, to religiously based
convictions of going to hell. Hallucinations, most often auditory, can also
be present and may take the form of taunting voices saying the patient is
worthless and deserves to die or commanding the patient to commit
suicide.
Age, personality style, and cultural factors can all influence how
depressive illness presents. In cultures or families in which a depression
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diagnosis carries significant stigma, the disorder may take the form of a
panoply of vague somatic symptoms such as increased headaches, pain, or
gastrointestinal distress underlain by typical depressive symptoms that are
often only elicited on specific questioning. Patients who struggle to iden-
tify or directly communicate emotional distress may also present with
prominent physical symptoms. Somatic symptoms may dominate the
depressive presentations of geriatric patients, who may also display
significant memory and cognitive impairment, often referred to as “pseu-
dodementia.” Finally, women in their reproductive years can have fluctu-
ating mood symptoms coinciding with their menstrual cycles, with the
peripartum period a particularly high-risk time for developing full-blown
mood disorders.
In terms of morbidity and mortality, suicidal behavior is the most
significant concern in depressed patients. Although numbers vary, studies
suggest 2% of patients with affective disorders die by suicide, a number
that increases to more than 8% in patients ever hospitalized for suicidality.
Suicide risk factors include a past history of suicide attempts, social isola-
tion, and a family history of suicide. Potentially modifiable factors include
significant agitation and/or insomnia, substance misuse, and access to
such lethal means of suicide as firearms. All depressed patients should be
questioned about desire for death, plans for self-injury, access to means of
self-injury, and intent to act upon these plans. When a patient has active
thoughts of self-harm, the treatment plan should include interventions to
reduce suicide risk, including instructing patient and family to remove
firearms from the home, prescribing medications to reduce agitation and
insomnia, and referring the patient for chemical dependency treatment
when indicated. If these risks cannot be modified or if a patient presents
significant risk of self-harm, immediate hospitalization can help reduce
distress and lower acute suicide risk.
4.2. Differential diagnosis of depressive symptoms

When considering the diagnosis of a patient who appears sad, withdrawn,
and indecisive, it is important to consider a differential of alternate psy-
chiatric illnesses whose symptoms overlap with depression. Perhaps the
most significant of these is bipolar illness, as discussed later, but certain
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Mood Disorders 209
anxiety disorders, personality disorders, and the negative symptoms of

schizophrenia can also lead to a depressed appearance. Certain medical
illnesses and substance use disorders can have physical effects on the
brain and body that lead to depression or resemble depression (see discus-
sion in “Other Mood Disorders” section in this chapter). Finally, bereave-
ment and adjustment disorders, in which a loss or stressor provokes
symptoms, can be difficult to distinguish from depression.
Patients with bereavement or adjustment disorders often complain of
tearfulness, difficulties with sleep and appetite, feelings of guilt or preoc-
cupation with the loss, and at times even fleeting thoughts of wanting to
die and join the loved one who was lost. Their symptoms do not reach the
severity threshold of a depressive episode, however. These patients often
continue to enjoy pleasurable activities, look to the future with hope, and
find satisfaction in their achievements and relationships. Their mood
symptoms improve as time passes and they accommodate to the loss or
stressor. Symptoms more highly suggestive of depression in the setting of
grief and stress include a change in self-concept (feeling like a bad per-
son), hopelessness, pervasive sadness, anhedonia, or symptom persistence
several months beyond the loss or stressor. It is important to remember that
bereavement behaviors and responses to stressors can be highly culturally
determined, and distinction between these and depressive illness generally
require obtaining a careful history from the patient, including weighing the
influence of behavioral norms within her family or culture. If a grieving
patient does have symptoms meeting criteria for a depressive episode, then
the depressive episode supersedes the bereavement diagnosis.
One way of remembering the broad differential for patients with
depressive symptoms is the “Eight Ds”:
• Depressed (unipolar or bipolar)

• Demoralized (adjustment disorder)
• Disaffiliated (bereavement)
• Difficult (personality disorders)
• Delusional (primary psychotic disorder)
• Delirious (effects of medical illness or medications)
• Drugged (chemical dependency or intoxication)
• Dulled (cognitive impairment)
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These include biological disturbances like Drugged, Delirious, or

Dulled, in which treatment of the mood disturbance should focus on
eliminating or managing the underlying cause of the mental status change
that resembles depression, psychological crises like Depressed and
Delusional, in which disease-specific treatment should be implemented,
and challenges related to disruption of the social network or communica-
tion like Demoralized, Disaffiliated, and Difficult, in which support of the
patient through psychotherapy or efforts to improve the patient-physician
alliance are most helpful.
4.3. Treatments for depressive disorders

Because depressive episodes can be driven by biological, psychological,
or social contributors, treatments for depression should ideally incorpo-
rate somatic, psychotherapeutic, and social/environmental components.
Several short-term (10–16-session) psychotherapies have been shown
to be helpful for depressive episodes, and in patients with mild to moder-
ate symptoms, these may be as effective as medications in treating symp-
toms and preventing relapse. In cognitive behavioral therapy (CBT),
patient and therapist examine patterns of thoughts and behaviors that
perpetuate depressive symptoms and work on strategies to change them.
CBT can be delivered in individual or group formats, and some patients
even find benefit from book- or computer-based self-help resources based
on CBT principles. CBT for depression emphasizes “behavioral activa-
tion,” encouraging the patient to establish a regular day–night cycle,
gradually return to higher activity levels, and schedule pleasant events
during the day and week. The targeted cognitions are the helplessness
and worthlessness depressed patients often experience. Patient and
therapist collaborate in setting goals that often include between-session
homework.
Interpersonal psychotherapy (IPT) is an individual psychotherapy that
emphasizes four factors commonly perpetuating depression: role transi-
tions, role disputes, interpersonal conflicts, and social skills deficits.
Patient and therapist collaborate to help the patient adapt to life changes,
develop strategies for resolving interpersonal conflicts, and improve
social skills.
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Mood Disorders 211
Both CBT and IPT have been shown to be effective at treating depres-
sive symptoms in patients and, in some studies, have been shown to be as
effective as medications. Several studies also demonstrate a protective
effect of therapy in preventing future episodes even after therapy is
discontinued, an effect not demonstrated after discontinuation of
medications.
Psychodynamic therapies, based on the psychoanalytic treatments
developed by Freud and his successors, suggest that depression results
from buried internal conflicts stemming from earlier experiences. The
goals of therapy include bringing these conflicts into conscious awareness
and gaining insight into old patterns of thinking and relating that interfere
with optimal mental health. Psychodynamic therapies have classically
involved sessions 1–4 times a week over years, but brief psychodynamic
therapies similar to CBT and IPT in duration and frequency demonstrate
good efficacy in improving depressive symptoms.
Most psychotherapies for depressive episodes incorporate psychoedu-
cation that aims to improve the patient’s understanding of depression and
its treatment; reduce stigma, guilt, and shame; and promote wellness-
enhancing behaviors such as exercise.
The most commonly used somatic treatments for depressive episodes
are the antidepressant medications. These come in several classes,
including the Selective Serotonin Reuptake Inhibitors (SSRIs),
Serotonin–Norepinephrine Reuptake Inhibitors (SNRIs), tricyclic anti-
depressants (TCAs), and non-reversible Monoamine Oxidase Inhibitors
(MAO-Is). Other antidepressant medications include mirtazapine,
bupropion, trazodone, and nefazodone. Given that all antidepressant
medications achieve similar efficacy against the core symptoms of
depression, the best antidepressant for a particular patient maximizes
salubrious side effects and minimizes noxious ones. For example, a
sedating antidepressant such as a TCA may help with sleep distur-
bances, while an activating medication like bupropion may combat low
energy and motivation.
Most antidepressant treatment algorithms, such as those suggested
in the STAR*D trial1 or in the NICE clinical guidelines, follow a simi-
lar pattern. Given the favorable risk–benefit ratio, they recommend
starting with SSRIs. They emphasize the importance of the patient
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understanding that beneficial antidepressant effects are often not appar-

ent for at least 3–4 weeks, and that lack of earlier improvement does not
mean the medication will not work. They recommend initially adminis-
tering medication at the lowest known effective dose. After 3–4 weeks,
if adherence has been confirmed and a patient’s symptoms have not
improved, the dose should be increased and the response reassessed
after another 3–4 weeks. At that point, if response still remains mini-
mal, the medication should be changed, either to a different medication
in the same class or to one in another class. Augmentation strategies in
which more than one antidepressant is prescribed simultaneously or
agents such as lithium, stimulants, or triiodothryonine are added are
typically reserved for the most treatment-resistant patients.
Antipsychotic medications should be employed, at least in the short
term, for depressed patients with psychotic symptoms. Limited data
suggest that an atypical antipsychotic added to an antidepressant may
constitute a successful augmentation strategy even in patients without
psychotic symptoms.
About 60%–70% of patients respond to the first medication tried. This
percentage decreases with each subsequent medication trial. Response
rates in clinical trials clearly are higher when medications and psycho-
therapy are combined, and if a patient has not responded to medication
alone, concurrent psychotherapy should be implemented. Medications are
often continued for 6–12 months after recovery has been achieved in order
to prevent relapse, but for some patients with recurrent depressive
episodes, medications are continued indefinitely to help forestall the
development of future episodes.
Additional somatic therapies for depression include phototherapy, elec-
troconvulsive therapy, transcranial magnetic stimulation, and deep brain
stimulation. Particularly helpful in patients with seasonal depression,
phototherapy (light therapy) is thought to exert its effect through the mela-
tonin system and resultant impact on the circadian cycle. Treatment con-
sists of sitting in front of a light box for a prescribed length of time each
morning.
Electroconvulsive therapy (ECT) involves inducing a seizure by appli-
cation of brief electrical stimulation while the patient is under general
anesthesia. Treatments are usually repeated three times weekly, with a
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Mood Disorders 213
total of 6–12 treatments in an acute series. Although the mechanism of

therapeutic action is not understood, ECT has proven to be the most rapid
and efficacious therapy available for severe depression, with patients often
noticing substantial improvement after 3–4 treatments. The most bother-
some side effect of ECT is memory impairment; most patients will have
short-term memory impairments during the acute course of ECT that
leave them somewhat amnestic for the treatment course and limit their
ability to work or to drive safely. This amnesia typically resolves within a
couple of weeks of completing a treatment course. However, a small sub-
set of patients experience on-going memory impairment, some with retro-
grade amnesia for events preceding ECT and others with on-going
complaints of short-term memory loss. Modifications in ECT technique,
such as unilateral electrode placement, can reduce the incidence of
cognitive side effects.
Transcranial Magnetic Stimulation (TMS) involves induction of a
small current in the brain by an external electromagnet. TMS does not
induce seizures and does not require anesthesia. It is typically adminis-
tered in daily sessions over a several-week period. TMS has shown some
promise in patients who have responded poorly to medications, and seems
to have fewer cognitive side effects than ECT.
Deep brain stimulation involves surgically placing, in the brain,
electrodes connected to a stimulator implanted in the chest wall. It has
shown promise in treating severe, otherwise unresponsive depres-
sion, but is currently available in the United States only in research
settings.
4.4. Prognostic factors

Up to 50% of untreated depressed patients will experience complete
remission after six months. However, a substantial minority have longer
episodes despite treatment. Up to 20% of patients will continue to have
depressive symptoms two years after diagnosis, and 12% of patients will
remain symptomatic five years after initial diagnosis. Even upon full
remission, 50% of patients who have one depressive episode will have
another. The recurrence rate rises to 70% after a second episode, and
90% after a third. Thus, for many patients Recurrent Depressive
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Disorder is best thought of as a chronic condition with intermittent

relapses, and treatment planning for these patients should include a
focus on medications and/or therapies that may help prevent future
mood episodes.
Up to 10% of patients who experience a depressive episode will
eventually develop bipolar disorder. Clues that an individual may be at
higher risk for eventual bipolar disorder include exceptionally severe
depressive symptoms or simultaneous psychotic symptoms. Women with
postpartum depression also seem to carry a higher risk of later manic
episodes.
5. BIPOLAR DISORDER
5.1. Phenomenology of bipolar disorder
If depressive illness can be viewed as a deficit of psychic energy, manic
and hypomanic episodes involve an excess of such energy. As with
depressive illness, these mood changes are more than a passing reaction
to circumstances, and are typically prolonged and significantly impairing.
ICD-10 does not specify a length of time, but DSM-IV requires symptoms
to be present for at least four days to diagnose hypomania and a week to
diagnose mania.
The sense of well-being often extends to self-aggrandizement, with
manic patients developing exalted ideas about their worth and achieve-
ments, even to the extent of believing themselves to be a celebrity or deity.
This overconfidence drives a tendency to underestimate risk: manic
patients engage in reckless behaviors such as promiscuous sex, excessive
gambling, or fast driving. Excess energy manifests in increased physical
activity, extreme talkativeness, decreased or absent need for sleep, and
difficulty sustaining attention or focus. Psychotic symptoms can also
develop and can take the form of delusions, typically of a grandiose
nature, or auditory or visual hallucinations.
The euphoria of mania can prove contagious to those around the
patient, and many a treatment team has walked out of a manic patient’s
hospital room with the entire team chuckling at what has just transpired!
No matter how amusing, manic behaviors are a dramatic departure
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Mood Disorders 215
from a patient’s euthymic or dysthymic baseline and can precipi-

tate tremendous difficulty in school, at work, and in important
relationships.
Hypomania possesses less euphoria and energy increase than mania
and usually does not affect the profound disruption of a patient’s life that
a manic episode does. Hypomanic episodes cannot, by definition, include
psychotic symptoms. Hypomania, nevertheless, does represent a departure
from normal and can result in relationship and work problems.
Although a pervasive sense of well-being, euphoria, and elevated mood
characterize a typical manic episode, for some patients the corresponding
effect is irritability, with rapidly oscillating emotional state shifts consti-
tuting what is termed “affective lability.” Some patients even meet criteria
for simultaneous depressive and manic episodes, a particularly dangerous
phenomenon referred to as a “mixed” episode because of coexisting
manic pressure and dysphoric — even suicidal — affect.
For some bipolar patients, manic episodes occur unprovoked. Others
come to discover over time triggers for their mood changes. A common
instigator of mania is lack of sleep or disruption in the circadian cycle,
such as occurs with travel across time zones. If they have a propensity
toward mania, sleep-deprived students during exam periods or soldiers
during combat may be particularly vulnerable to mania. Use of sub-
stances, particularly stimulants, can induce mania, and treatment with
antidepressants in a vulnerable depressed or anxious patient can cause a
manic switch. Some women notice a pattern of symptom onset coinciding
with their menstrual cycles. Finally, the peripartum period is a high-risk
time for women with bipolar disorder. Such women should be monitored
closely during pregnancy and after delivery, and they and members of
their support system should be counseled to seek help emergently if mood
symptoms arise.
In order to diagnose bipolar affective disorder, ICD-10 requires at least
two mood episodes, one of which must be mania or hypomania. DSM-IV
assigns a diagnosis of Bipolar I Disorder after a single manic episode,
regardless of whether there have been other mood episodes, and Bipolar
II disorder after a hypomanic episode and a major depressive episode.
After the initial episode, most bipolar patients experience recurrent mood
episodes, interspersed with euthymic periods. Untreated manic episodes
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last an average of four months, and untreated depressive episodes at least

six months. Most bipolar patients experience primarily depressive epi-
sodes, with studies suggesting anywhere between 4 and 32 depressive
episodes occurring for each manic or hypomanic episode. Thus, it is
important to screen for bipolar disorder in any patient presenting with
depression and to monitor closely for emergence of hypomanic or manic
symptoms during treatment.
Bipolar disorder has one of the highest rates of suicide of any diagnos-
tic group. Suicide can occur in any mood phase but is more likely to hap-
pen during mixed or depressed episodes. All patients presenting with
bipolar symptoms should be evaluated for suicidality, with therapeutic
interventions as needed.
5.2. Differential diagnosis of manic symptoms

As with depression, medical conditions and substance use can mimic bipolar
disorder and should be ruled out before settling on a primary bipolar diag-
nosis. Substance use disorders in particular may confound the diagnosis,
because intoxication and other substance-induced states can resemble mania
and hypomania in the absence of bipolar disorder, even as patients with true
bipolar disorder also have a high rate of comorbid substance misuse.
The distinction between a manic episode with psychotic features and
schizophrenia can be difficult to make at times. Symptoms more sugges-
tive of mania than schizophrenia include an elevated mood, pressured
speech, and hyperactivity. Schizophrenia tends to commence insidiously
and become pervasive, as contrasted with the intermittent, abrupt-onset
bouts that characterize mania.
Mood instability is a core feature of certain personality types,
particularly borderline personality disorder. However, in personality
disorders, mood can fluctuate over minutes to hours, whereas in bipolar
disorder the fluctuations usually occur over days to weeks or longer.
Finally, particularly in younger patients, the distractibility, inattention,
hyperactivity, and talkativeness of ADHD can resemble mania. Age of
onset and time course can distinguish the two. Bipolar episodes com-
monly begin in the teen or young adult years and wax and wane through-
out life, while ADHD typically emerges in early childhood, becoming a
constant presence if untreated.
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Mood Disorders 217
5.3. Treatment of bipolar disorder

Treatment for bipolar disorder falls into two categories: acute manage-
ment of mood episodes (depressed or manic), and maintenance treatment
to sustain euthymia and prevent relapse into another mood episode. When
mood episodes, either manic or depressed, are severe, inpatient treatment
may be indicated at least initially to maintain the patient’s safety in the
face of suicidality and/or high-risk behaviors.
Several agents have good effect as mood stabilizers, including lithium,
various anticonvulsants, and atypical antipsychotic agents. Available since
the late 1960s, lithium has remained the gold standard treatment for
treating mania and forestalling further mood episodes. Patients often
experience anti-manic effects within days of starting lithium. Lithium is
also one of the only psychotropic medications proven to mitigate suicide
risk. Its narrow therapeutic index is problematic, requiring frequent blood-
level monitoring, particularly in the early stages of therapy. Anticonvulsants
including valproic acid, carbamazepine, oxcarbazepine, and lamotrigine,
also demonstrate good anti-manic effect, and may be more effective than
lithium in stabilizing patients with rapid-cycling versions of bipolar disor-
der. These drugs have wider therapeutic indices than lithium but can be
associated with severe and idiosyncratic side effects that also require care-
ful monitoring early in treatment.
More recently, several atypical antipsychotics have demonstrated effi-
cacy in treating manic episodes, whether or not psychotic symptoms are
present. Their long-term tendency to induce Metabolic Syndrome may
make them less desirable as first-line agents for mania. However, if psy-
chotic features are present, antipsychotic medications can be quite helpful
as either single agents or as adjunctive treatments with lithium or an anti-
convulsant. Benzodiazepines can be helpful adjuncts in acute manic
episodes, as they can rapidly curtail the physical activation and agitation
associated with mania and improve sleep.
Treatment of bipolar depressive episodes requires particular care,
because patients are at high risk of switching to a manic episode when
treated with an antidepressant. Because lithium may have antidepressant
effects above and beyond its mood stabilization qualities, a trial can be
considered when treating bipolar depression. Lamotrigine has also been
demonstrated to effectively treat the depressed phase of bipolar disorder,
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and several of the atypical antipsychotics have shown promise as well.

Typical antidepressant medications can be gingerly prescribed, but
patients should ideally take a mood stabilizer in conjunction with the anti-
depressant, and the prescriber should monitor closely for signs of rough-
ening of mood or emergence of frank mania.
Once acute mood episodes have resolved, fewer or lower doses of
medications may be required, but most patients should remain on mood
stabilizers to prevent relapse. Lithium, valproate, and carbamazepine are
first-line choices for maintenance therapy, but some have advocated using
atypical antipsychotics for this purpose as well.
Psychotherapy has not been demonstrated to be of benefit in treating
acute manic episodes, but has shown promise in relapse prevention.
Psychoeducation of patient and family, emphasizing understanding of
bipolar illness, adherence to treatment recommendations, and mainte-
nance of healthy habits including good sleep hygiene, is a typical compo-
nent of most psychotherapies for bipolar disorder. Specific therapies have
been developed to incorporate psychoeducation and interventions targeted
specifically at situations that threaten euthymia, including modifications
of CBT and IPT; a specific form of IPT called interpersonal social
rhythms therapy (IPSRT), which adds sleep hygiene and activity schedul-
ing to IPT; and an adaptation of Family Focused Therapy (FFT), which
focuses on lowering expressed criticism and mobilizing support for the
patient within the family. Each of these therapies has shown promise in
relapse prevention in bipolar disorders, and many studies point to positive
effects on depressive symptoms as well.
5.4. Prognostic factors in bipolar disorder

For most patients, bipolar affective disorder is a lifelong illness. Mood epi-
sodes are often most frequent and severe in the early years after diagnosis,
but patients remain vulnerable to recurrences throughout the lifespan.
Prognosis for meaningful functioning at work or in relationships for patients
with both manic and depressive episodes tends to be worse than the prognosis
for those with depressive episodes only, but better than that for patients with
schizophrenia. Patients who are male or have poor premorbid functioning,
earlier onset of illness, or substance dependence fare worse in the long run.
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Mood Disorders 219
6. PERSISTENT MOOD DISORDERS

6.1. Phenomenology of persistent mood disorders
Dysthymia and cyclothymia are disorders in which patients have many
years of nearly continuous low-grade mood symptoms that do not rise to
the level of either recurrent depressive disorder or bipolar disorder.
Dysthymic patients have depressed mood, accompanied by other depres-
sive symptoms insufficient to meet criteria for a depressive episode. For
cyclothymic patients, mood alternates between mild depression and hypo-
mania, with the symptoms expected of each state but never of sufficient
severity or duration to constitute a major depressive or manic episode.
DSM-IV-TR criteria for both disorders requires symptoms to be present
for at least two years (one year in children), with no periods of euthymia
lasting longer than two months during that time, while ICD-10 simply
describes symptoms lasting “many years.” For many patients, however,
the symptoms have lasted so long that they will simply describe them as
“the way I have always been.”
The lower intensity of symptoms notwithstanding, patients with dys-
thymia and cyclothymia still experience significant social and occupa-
tional difficulties. The long-term symptoms have a cumulative effect on
relationships and work that interferes with optimal functioning in both
arenas. The persistent pessimism and sadness in dysthymics and the
unpredictable and frequent mood shifts in cyclothymics may repel col-
leagues, friends, and romantic partners and compromise even simple day-
to-day functioning. Once these disorders have become patients’ baselines
rather than changes from baseline, they may fail to recognize there being
something wrong and therefore not seek treatment.
6.2. Treatment of persistent mood disorders

Given the long-term nature of dysthymia and cyclothymia, treatments are
long-term as well. In general, recommended treatments for dysthymia
resemble those for depressive episodes, and cyclothymia treatments
mirror those for bipolar affective disorder.
In dysthymia, psychotherapy is often recommended as a first step
because of the pre-eminence of cognitive and functional symptoms over
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somatic symptoms. Indeed, longer-term psychodynamic therapy is often

recommended for dysthymia. However, CBT and IPT have also shown
good evidence for efficacy in dysthymia. Many of the antidepressant
medications have been used for patients with dysthymia with good effect,
and combining an antidepressant with therapy can reduce symptoms and
improve function more quickly than using psychotherapy alone.
Medications are more frequently first-line treatment in cyclothymia, a
forme fruste of bipolar disorder, than in dysthymia. With its antidepressant
and anti-manic properties, lithium is a reasonable first step, but such
anticonvulsants as valproate and carbamazepine can be tried as well.
Antidepressants should be used with caution in cyclothymic patients
because of the risk of triggering a full-blown manic episode. Psychotherapy
of various forms can aid in managing symptoms and mitigating the
disorder’s effect on social and occupational functioning.
6.3. Prognosis of persistent mood disorders

Both cyclothymia and dysthymia may reflect an underlying vulnerability to
developing a major mood disorder: up to 75% of patients diagnosed with
dysthymia will eventually develop a superimposed depressive episode
(often referred to as “double depression”) or bipolar affective disorder, and
15%–50% of cyclothymic patients will eventually meet criteria for bipolar
affective disorder. Patients with these mood disorders also have a high rate
of comorbid personality disorders that can worsen prognosis and compro-
mise treatment response. Even in the absence of comorbid illnesses, patients
with dysthymia have limited spontaneous remission, perhaps only 10% per
year, and patients with “double depression” often return to a dysthymic
rather than euthymic baseline after remission of a depressive episode.
7. OTHER MOOD DISORDERS

Many medical conditions can produce symptoms suggestive of depres-
sion or mania. Thyroid dysfunction; CNS disease such as stroke,
demyelination, neoplasm, or infection; and metabolic disturbances such
as renal or hepatic failure are all associated with changes in mood. In
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Mood Disorders 221
some conditions, notably pancreatic cancer, mood change can be the first
sign of an otherwise asymptomatic process. Medications can also induce
mood changes. Prednisone and other corticosteroids, interferon alpha,
antiparkinsonian medications, and beta blockers are commonly impli-
cated, but almost any pharmacologic agent has the potential for causing
mood changes. Long-term opiate or benzodiazepine use may create the
equivalent of a depressive syndrome. Whenever a patient complains of
mood symptoms, the physician should always conduct a medical review
of systems and review all current medications, including over-the-
counter and complementary preparations. Targeted physical examination
and laboratory and imaging investigations should be performed as
indicated.
Substance abuse is almost universally associated with mood changes,
and indeed many patients use substances precisely because of their mood
effects. The colloquial terms “uppers” and “downers,” for stimulants and
sedatives respectively, invoke the desired effects of ingestion. Intoxication
with stimulating substances such as cocaine, methamphetamine, and hal-
lucinogens can at times be indistinguishable from mania, while alcohol,
narcotics, marijuana, and other sedatives can induce a depressed appear-
ance. Chronic use of many substances such as amphetamines or cannabis
can result in persistent mood changes even when a user is not acutely
intoxicated. Deciding whether mood disorders are secondary to substance
use or comorbid with substance use (“dual diagnosis”) can be challenging,
particularly because patients with mood disorders have a high rate of co-
occurring substance use. Timing of mood symptoms can be helpful in
making this distinction: if mood symptoms resolve during extended
periods of sobriety, they are much more likely to be secondary to substance
use than if they predate substance use and/or persist during extended
sobriety.
Treatment of secondary mood disorders focuses on managing or elimi-
nating the provoking condition, along with educating patient and family
about the symptoms’ presumed etiology. However, if the condition is
anticipated to become chronic, such as with cancer or stroke, treatment
recommendations for secondary mood disorders generally parallel those
for primary mood disorders.
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8. CONCLUSIONS AND FUTURE DIRECTIONS

Mood disorders are common and disabling illnesses. Although good treat-
ments for both depression and bipolar disorder are available, many
patients with these disorders do not seek treatment, and when they do,
treatments may be poorly tolerated or unsuccessful in restoring a premor-
bid level of functioning. Moreover, when patients have comorbid physical
illnesses, physicians and patients alike may consider depression as the
inevitable companion of serious disease, disregarding effective treatments
for secondary mood disorders. Improving recognition of both primary and
secondary mood disorders and continuing development of effective treat-
ments are the primary goals of on-going research into depressive and
bipolar disorders.
9. KEY POINTS
• Mood disorders are common and disabling illnesses, and present at all
ages and in all cultures and socioeconomic strata.
• Mood changes are the defining symptom of mood disorders, but these
illnesses also affect physical energy, cognitive abilities, sleep and
appetite, and self-concept.
• Consider the “Eight D” differential for mood symptoms — Depressed
(unipolar or bipolar), Demoralized, Drugged, Difficult, Delirious,
Delusional, Dulled, and Disaffiliated.
• Patients presenting with mood symptoms should be screened for
suicide, including desire for death, plans for suicide, intent to act, and
access to lethal means.
• The most effective mood disorder treatments combine biological and
psychosocial approaches.
• Although mood disorders are treatable, they are characterized in
many patients by recurrent episodes and long-term vulnerability to
relapse.
• Mood symptoms in dysthymia and cyclothymia may have a lower
intensity than those of major depressive disorder or bipolar disorder,
but patients with these disorders still experience significant dysfunc-
tion in work and relationships.
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Mood Disorders 223
10. SELF-ASSESSMENT
10.1. Mrs Jones, a 62-year-old recently-widowed woman, sees
her family physician with complaints of on-going sadness
after her husband’s death a month ago. Which of the
following symptoms is most suggestive of a depressive
episode rather than bereavement?
(A) Difficulty focusing.
(B) Feeling like a bad person.
(C) Fleeting suicidal thoughts.
(D) Problems sleeping.
(E) Frequent tearfulness.
Patients who are grieving often have difficulties with sleep and appe-
tite, problems with focusing, and can even occasionally wish to die
and join their lost loved one. Changes in self-concept, however, are
uncommon in simple bereavement and much more suggestive of
depression.
Answer: B
10.2. In a patient with bipolar disorder, all of the following

are associated with an increased risk of death
by suicide except
(A) Mixed mood episode.
(B) Access to a shotgun.
(C) Use of lithium.
(D) Active alcohol use.
(E) History of suicide attempts.
Lithium has been shown to decrease death by suicide in patients with

depression or bipolar disorder.
Answer: C
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10.3. Which of the following would not be considered first-line

treatment for a patient with a diagnosis of a recurrent
depressive disorder?
(A) Interpersonal psychotherapy (IPT) alone.
(B) Sertraline.
(C) Cognitive behavioral therapy (CBT) plus citalopram.
(D) Fluoxetine.
(E) Transcranial magnetic stimulation (TMS).
SSRIs, psychotherapy, or the two in combination are most commonly

recommended as the first step in treating patients with depressive disorders.
TMS, ECT, and deep brain stimulation are typically reserved for the most
treatment-resistant patients.
Answer: E
11. CASE STUDIES

11.1. A depressive episode
Mr H is a 19-year-old first-year university student brought to his family
physician by his mother during the winter holidays. He reports that he
struggled with the transition from home to his university and has had on-
going conflicts with a roommate that has been quite difficult to manage.
Starting sometime in the late fall, he began feeling “not like myself” and
noticed that he was feeling numb most of the time but occasionally sad
and tearful without provocation. He had difficulty falling asleep at night,
often finding himself worrying about his classes and his grades when try-
ing to fall asleep, and would wake up frequently overnight. He was so
exhausted from lack of sleep that he would doze off during his classes but
could only toss and turn if he tried to take a nap when back in his dorm.
He had difficulty staying focused when trying to read or study. An A
student in secondary school, he barely passed three of his classes this
semester, and has an incomplete grade in the fourth because he has not yet
finished the term paper. Once home, his mother has noticed that he is not
interested in spending time with his friends or with the family, despite
previously being very close with his younger brother and school friends.
He spends most of his time either watching television or in his room
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Mood Disorders 225
listening to music with the lights off. She reports that he eats very little,
and all of the trousers she purchased for him before his leaving home are
now too loose.
On examination, Mr H is mildly dishevelled. He stares at the floor
during most of the conversation, moving very little. He speaks so softly
that it is difficult to hear him at times, but his answers make sense. His
facial reactions are almost non-existent, although he does shed a couple of
tears when talking about his poor grades. He acknowledges having had
passive thoughts that it might be easier to be dead than to continue to face
all of his stresses, and says that he feels that he is so stupid he will never
be able to graduate from university, “so why bother.” However, he says
that he has no actual desire to be dead and has not thought of any plans to
try to kill himself.
11.2. A manic episode

Mr H receives a combination of citalopram and interpersonal psycho-
therapy and experiences significant improvement in his mood symptoms
over the course of his second term at school. He discontinues his medica-
tion on his own over the summer holiday and has an uneventful second
year. In his third year of university, he chooses to study abroad. However,
within three weeks of his arrival, his advisor sends him back home
because of concerns about his behavior. Upon his arrival at home, his
mother brings him straight to the Emergency Department from the airport
because of her concerns.
In the Emergency Department, Mr H paces in his examination room
and, when addressed, begins speaking loudly and so quickly that it is
difficult to follow his train of thought. He becomes irritated if the examiner
attempts to interrupt his story, and says that after arriving overseas, he
realized he did not need to be a student any longer because he had been
given “natural gifts” that his professors did not possess. He says that he
spent several nights in a row designing a new invention on his computer,
but when he tried to introduce it to his professors they jealously tried to
suppress his ideas. He says he intends to contact the President while he is
home, “because this will be the end of all of the security problems.”
During the evaluation, he seems unable to sit still, frequently standing up
and performing calisthenics “because you can never be too healthy!” He
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makes frequent verbal puns and jokes, and on several occasions flirts with
the female resident. When asked about suicidality, he shouts, “Die? Me?
I cannot die! I will never die!”
REFERENCES
1. Gaynes BN, Warden D, Trivedi MH, Wisniewski SR, Fava M, Rush AJ.
(2009) What did STAR*D teach us? Results from a large-scale, practical,
clinical trial for patients with depression. Psychiat Serv 60: 1439–1445.
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Chapter 10
Anxiety Disorders
Leanne Parasram and Dan J. Stein
1. INTRODUCTION
Anxiety disorders are amongst the most prevalent of the psychiatric disor-
ders. Epidemiological studies indicate that anxiety disorders are, in fact,
more prevalent than mood disorders among the general population.1
Approximately 25% of individuals will meet criteria for an anxiety disor-
der in their lifetime, with females being affected more commonly than
males (female to male lifetime prevalence ratio is 3:2). In addition, anxi-
ety disorders are associated with significant morbidity, comorbidity, and
economic costs. Part of the costs of anxiety disorders are unfortunately
still due to underdiagnosis and undertreatment.
The World Health Organization’s 10th revision of the International
Statistical Classification of Diseases and Related Health Problems (ICD-
10) lists the main anxiety disorders as (1) phobic anxiety disorders, which
include agoraphobia, social phobia, and specific phobia; (2) other anxiety
disorders, which include panic disorder and generalized anxiety disorder;
and (3) obsessive-compulsive disorder. ICD-10 groups reactions to severe
stress (acute stress reaction and posttraumatic stress disorder) together
with adjustment disorders as stress-related disorders, but for the purpose
of this handbook, acute stress reaction and posttraumatic stress disorder
will be discussed in this chapter.
The Diagnostic and Statistical Manual of Mental Disorders (DSM-
IV-TR) published by the American Psychiatric Association, classifies
227
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228 L. Parasram and D. J. Stein
anxiety disorders slightly differently. DSM-IV-TR defines criteria for

a panic attack, which is a collection of symptoms that may be present
in a variety of anxiety disorders but is not by itself a codable disorder.
It also recognizes the following disorders: panic disorder without
agoraphobia; panic disorder with agoraphobia; agoraphobia without
history of panic disorder; specific phobia; social phobia; obsessive-
compulsive disorder; posttraumatic stress disorder; acute stress disor-
der; generalized anxiety disorder; anxiety disorder due to a general
medical condition; substance-induced anxiety disorder; and anxiety
disorder not otherwise specified. It is likely that DSM-5 will divide the
anxiety disorders into three separate chapters; anxiety disorders, obses-
sive compulsive and related disorders, and trauma and stress-related
disorders.
The neurobiological basis of anxiety disorders is increasingly under-
stood. Advances in basic and clinical research have led to the hypothesis
that each of the anxiety disorders is mediated by specific neural circuits.
Abnormality in these circuits activates “false alarms” that have cognitive,
affective, and behavioral manifestations. The alarms triggered in individu-
als with anxiety disorders may serve an evolutionary purpose in healthy
individuals. Family studies have shown that anxiety disorders have a herit-
able component; relatives of individuals with anxiety disorders are at
significantly increased risk of developing an anxiety disorder themselves,
as compared to the general population. Life experiences further modify
that risk.
Advances in psychopharmacology and psychotherapy have led to the
development of treatments for anxiety disorders that are effective, safe to
use, and easily accessible. Selective serotonin reuptake inhibitors (SSRIs)
and cognitive behavior therapy (CBT), which are first line treatments for
the anxiety disorders, have been found to normalize abnormal neurocir-
cuitry associated with the pathophysiology of anxiety disorders. Other
classes of antidepressants used in the treatment of anxiety disorders
include serotonin–noradrenaline reuptake inhibitors (SNRIs), tricyclic
antidepressants (TCAs), and monoamine oxidase inhibitors (MAOIs.)
Benzodiazepines, which are anxiolytic agents, are highly effective in
treating acute anxiety. A major limitation of their use, however, is that
these agents carry a risk of dependency.
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Anxiety Disorders 229
This chapter will review each of the major anxiety disorders. Sections
will cover phenomenology (e.g. diagnostic criteria, epidemiology, clinical
presentation, and assessment), psychobiology, and management.
2. PANIC DISORDER AND AGORAPHOBIA

Although ICD-10 classifies panic disorder under “other anxiety disorders”
and agoraphobia under “phobic anxiety disorders,” they will be discussed
together here because they are commonly comorbid.
2.1. Diagnostic criteria

A panic attack is a discrete period of intense fear. Onset of symptoms is
rapid; symptoms then crescendo and last a further 10–20 mins before
quickly or gradually dissipating. Very rarely do symptoms last longer than
an hour. Diagnosis necessitates four of 14 possible symptoms to be pre-
sent simultaneously, which may be cardiovascular, respiratory, abdominal,
psychological, or general, with at least one of the four symptoms being of
autonomic arousal.
Panic disorder is characterized by the presence of recurrent panic
attacks that occur spontaneously (as opposed to being triggered by a spe-
cific stimulus, as would be the case in specific phobia, for example). In
order for the diagnosis of panic disorder to be made, the panic attacks
experienced cannot be secondary to a physical condition or another psy-
chiatric disorder. ICD-10 makes allowance for two grades of panic disor-
der: moderate or severe.
The word agoraphobia is of Greek origin and literally means “fear of
the marketplace.” Patients with agoraphobia are markedly fearful of,
and often avoid, public places with crowds of people — shopping malls,
airports, bus and train stations, gatherings, and even being outside their
own homes alone. If made to endure such situations, they experience at
least two symptoms of panic attacks, at least one of which must be of
autonomic arousal. They may experience a full-blown panic attack, but
unlike the panic attacks of panic disorder, panic attacks of agoraphobia
are restricted to occurring in the fearful situation, or sometimes even on
contemplation of the fearful situation. The individual is aware that his
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or her distress is excessive. Avoidance behaviors and panic-like symp-

toms experienced are not a result of a psychotic or mood or obsessive
disorder. Agoraphobia is classified as occurring with or without
panic disorder, and severity can be rated by the extent of avoidance
behaviors.
2.2. Clinical presentation

Patients often present to their primary care physician or a hospital, fearful
that they have just had a heart attack or are suffering from another serious
medical illness. Symptoms experienced vary widely and are not character-
istic of dysfunction of only one organ system. The most common symp-
toms experienced include tachycardia, a pounding heart, shortness of
breath, and sweating. Between panic attacks, function may be impaired by
worry about the next attack. Patients may worry that they are “going
crazy.”
Initial panic attacks of panic disorder are spontaneous, but over time
panic attacks may be triggered by external cues (e.g. walking past a
store in which a panic attack has previously occurred) or internal cues
(e.g. interpretation of mild light-headedness as the onset of a panic
attack).
Many patients with panic disorder go on to develop agoraphobia as a
result of their panic attacks, and consequent fear and avoidance behaviors.
Patients with agoraphobia may be forced to seek help by concerned rela-
tives whose own activities are being curtailed because affected individuals
refuse to leave home or travel or engage in any activities outside of the
home if unaccompanied. Although patients with panic disorder may lose
work days, patients with agoraphobia may not be able to leave home to
attend work at all.
Comorbid depressive or substance-related problems (usually involving
alcohol) may also be presenting symptoms for patients with panic disor-
der and/or agoraphobia. Other anxiety disorders — specific and social
phobia, generalized anxiety disorder, obsessive-compulsive disorder, and
posttraumatic stress disorder — can all occur comorbidly, as can hypo-
chondriasis and personality disorders.
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2.3. Differential diagnosis

The diagnosis of panic disorder requires exclusion of a physical disorder
that may account for symptoms experienced. For this reason it is impor-
tant to know the physical disorders in which panic-like symptoms
commonly occur (Table 1) and to investigate appropriately if a physical
disorder is suspected.
A patient is more likely to be suffering from a physical disorder if
symptoms experienced are atypical and limited in number, if onset of
symptoms is after age 35, and if the patient has no family history of an
anxiety disorder, does not exhibit phobic avoidance, and does not respond
to anxiolytics (benzodiazepines).
2.4. Epidemiology
Studies have revealed that lifetime prevalence for panic disorder ranges
between 1.5% and 3.5%. The female to male ratio is approximately 2–3:1.
Onset of panic disorder is usually between late adolescence and age 30,
but panic disorder has been diagnosed in childhood and early adolescence,
as well as in later life.
2.5. Pathogenesis
As with the other anxiety disorders, the exact cause of panic disorder
remains uncertain. Specific neural circuits, genetic contributions, and
psychosocial stressors have all been implicated in the development of
panic disorder.
2.6. Neurocircuitry — the “fear network”

and “false suffocation alarm”
Panic disorder comprises three components — the acute panic attack,
anticipatory anxiety between panic attacks, and the development of pho-
bic avoidance. These three components may be mediated by specific sites
within the brain. The acute panic attack may involve brainstem and hypo-
thalamic activation. The emotion of fear, its perception and expression,
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Table 1. Physical disorders in which panic-like

symptoms commonly occur.
• Cardiovascular Disease
Ischaemic heart disease
Cardiac arrhythmias
Congestive cardiac failure
Hypertension
Anaemia
• Respiratory Disease
Pulmonary embolus
Asthma
Chronic obstructive airways disease
• Metabolic Disease
Acidosis
Hyperthermia
Hypocalcaemia
• Endocrine Disease
Hyperthyroidism
Hyper- and hypoglycaemia
Hyper- and hypoparathyroidism
Cushing’s syndrome
Pheochromocytoma
Menopause
• Neurological Disease
Cerebrovascular disease
Seizures, especially complex partial seizures
Syncopal attacks
Vestibular dysfunction
Intracranial tumors
• Drug Intoxication
Cocaine
Cannabis
Amphetamines
Caffeine
Nicotine
Sympathomimetics
Theophylline
• Drug Withdrawal
Alcohol
Anxiolytics especially benzodiazepines
Opioids
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and the anticipatory anxiety associated with panic disorder may be medi-
ated by the amygdala and its afferent and efferent projections. The devel-
opment of phobic avoidance may be mediated by the prefrontal cortex.
Reception of threatening information may in part lead to amygdalar
activation. Amygdalar efferents project to various brainstem and hypotha-
lamic nuclei eliciting the autonomic and behavioral responses associated
with panic; these include (1) an increased respiratory rate, (2) sympathetic
nervous system activity, (3) increased heart rate and blood pressure,
(4) release of adrenaline from the adrenal glands, and (5) defensive behav-
iors and postural freezing. The prefrontal cortex receives and evaluates
sensory information and is able to inhibit the amygdala, thereby modulat-
ing amygdalar fear reactions. The development of phobic avoidance may
involve hippocampal and prefrontal cortical activity; patients remember
the context in which panic attacks have occurred in the past; this is known
as contextual learning.
Neurotransmitters associated with the above neural circuits include
serotonin, noradrenaline, and gamma-aminobutyric acid (GABA).
Psychotropics that target symptoms of panic attacks typically act on these
three receptors.
Panic attacks in panic disorder can also be understood in terms of
neurocircuitry triggering a false alarm. In panic disorder this may be a
false suffocation alarm; it has been postulated that everyone has a suffoca-
tion alarm, which is an evolutionary response to increased levels of carbon
dioxide. In individuals with panic disorder, this alarm is falsely triggered
at a lower threshold than normal, or more frequently than normal.
2.7. Genetic contribution

Studies indicate that panic disorder tends to run in families. The risk of
developing panic disorder is 4–8 times higher among first-degree relatives
of those affected than among the general population. Twin studies reveal
higher concordance rates for panic disorder among monozygotic twins
than dizygotic twins. What seems most likely is that a susceptibility to
developing panic disorder is inherited and this risk is modified by psycho-
social factors.
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2.8. Psychosocial factors

Several traumatic childhood experiences have been identified as increas-
ing the risk of developing panic disorder. These include early parental
death, more so of the mother and before age 10, and parental divorce or
separation before age 10. The prevalence of panic disorder has also been
found to be greater among survivors of childhood physical and sexual
abuse. In adulthood, those who develop panic disorder have been found to
have experienced a higher incidence of stressful life events, most often
loss in the year preceding onset of the disorder.
Learned behavioral responses may also contribute to the development
of panic disorder; responses may be acquired by modeling the behavior of
anxious family members.
2.9. Course and prognosis

Panic disorder is a chronic condition, and its course is variable. Even
though effective treatments do exist, high rates of relapse are associated
with discontinuation of psychotropics following successful therapy.
Good premorbid functioning and short duration of symptoms before
seeking treatment have been associated with a better outcome. Patients
may, however, experience fluctuations in the intensity and frequency of
attacks, as well as variation in the symptoms experienced over time. An
increase in symptoms may occur during periods of stress. As discussed
earlier, comorbid psychiatric disorders are common and often compli-
cate the course of panic disorder. Patients commonly self-medicate with
alcohol; however, rebound anxiety, tolerance, and withdrawal can exac-
erbate symptoms. Patients with panic disorder are at higher risk of sui-
cide than the general population, and this risk must be monitored as
appropriate.
2.10. Assessment
It is of prime importance to exclude panic-like symptoms that may be due
to a general medical condition or exacerbated by a poorly controlled con-
dition or due to the effects of drug treatments or substances of abuse. Once
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a medical disorder has been excluded as a cause of panic attacks, the clini-
cian should enquire about the characteristics of attacks with the aim of
clarifying the diagnosis, establishing severity, and identifying comorbid
psychiatric disorders.
Patients should be asked to list the symptoms experienced during a
panic attack. The intensity and frequency of panic attacks is also impor-
tant to note. Patients may experience several attacks a day or less than one
attack per month. The level of impairment in social, occupational (or
academic), and leisure functioning should be noted, as well as the level of
premorbid functioning in these areas.
Psychosocial stressors need to be identified. The clinician should try to
establish a link between panic attacks and preceding thoughts, activities,
and situations. Panic disorder and agoraphobia can occur in isolation but
are commonly comorbid. Clarity is needed as to whether the patient meets
criteria for one or both disorders. Patients should be screened for the pres-
ence of comorbid psychiatric disorders and suicidal ideation and intent.
2.11. Management
As with other psychiatric disorders, patients should be managed within a
biopsychosocial framework to achieve optimal results. Decisions regard-
ing management should be made in conjunction with patients after they
have been educated about their disorder and treatment options and should
be tailored to address patients’ particular difficulties and concerns, while
drawing on support from the protective factors in their lives.
Biological management comprises optimal control of comorbid
medical disorders; the initiation, monitoring, and adjustment of psycho-
tropic medication; and education of patients about panic disorder,
including available treatments and treatment side effects. Psychotropics
found to be effective in the treatment of panic disorder include antide-
pressants and anxiolytics, principally benzodiazepines. B-adrenergic
receptor antagonists are not effective in treating panic disorder.
Antidepressants used include selective serotonin reuptake inhibitors
(SSRIs) as first-line agents, and serotonin-noradrenaline reuptake inhib-
itors (SNRIs), tricyclic antidepressants (TCAs), and monoamine oxi-
dase inhibitors (MAOIs).
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All SSRIs (e.g. paroxetine, fluoxetine, sertraline, citalopram, escit-

alopram, and fluvoxamine) can be used to treat panic disorder.
Paroxetine in particular has been approved by the US Food and Drug
Administration (FDA) for the treatment of panic disorder. Some patients
experience an increase in the number of panic attacks on initiation of
SSRIs. Although this adverse effect is transient, it may affect adherence.
For this reason SSRIs are initiated at half their usual dosages, for exam-
ple, paroxetine at 10 mg daily for 1–2 weeks before increasing to 20 mg
daily.
In patients with severe panic disorder or those who are anxious about
initiation of pharmacotherapy, a short course of benzodiazepines can be
prescribed. Alprazolam is FDA-approved for the treatment of panic disor-
der, and dosages of 0.25–0.5 mg two to three times daily may be pre-
scribed for 2–3 weeks. Patients should be forewarned of the potential for
dependency and the possible cognitive impairment that these agents pro-
duce with continued use, as well as the rebound anxiety they may cause.
Tapering of these agents must be performed slowly in order to prevent
rebound anxiety on withdrawal.
Monitoring of therapy should include reassessment of panic-like symp-
toms experienced and the frequency and intensity of attacks. Occupational,
social, and leisure functioning should also be monitored. Although some
patients achieve remission of symptoms at low therapeutic dosages, others
will require an increase in dosage. Most patients with panic disorder expe-
rience less anxiety and a decrease in the frequency and intensity of panic
attacks by four weeks of treatment.
Recommended treatment doses for SSRIs are as follows: paroxetine
20–60 mg; fluoxetine 20–60 mg; sertraline 50–200 mg; fluvoxamine
100–150 mg; citalopram 20–40 mg; and escitalopram 10–20 mg. The
doses of antidepressants may be increased in increments of the dosage at
which agents were initiated, at 1–2 week intervals after the first two weeks
of treatment.
If one SSRI is ineffective, it may be worthwhile to try another SSRI
before switching to another class of antidepressants. Options other than
SSRIs include using an SNRI, TCA, or MAOI. As a general prescribing
guide, all antidepressants prescribed should be started at the lowest
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possible doses to prevent them precipitating jitteriness and possibly

panic attacks on the initiation of the psychotropic agent. If patients are
non-responsive to treatment, the clinician should review the diagnosis,
possible comorbidity, and patient adherence to medication.
Once successful pharmacological therapy has been found, psychotropic
treatment should continue for a further 8–12 months. The decision to
withdraw psychotropics should be made in conjunction with the patient
and awareness of the risk of relapse. Medication should be tapered
gradually.
Psychosocial management can be used in combination with pharmaco-
logical intervention or alone. When used in combination, it may be most
beneficial to commence with psychotropics to reduce the frequency and
intensity of panic attacks before addressing the anticipatory anxiety and
phobic avoidance with psychosocial intervention. Several studies have
found that cognitive and behavioral therapies are successful in inducing
long lasting remission of symptoms.
Numerous psychosocial interventions exist. These include psychoedu-
cation for patients and their families; referral to support groups; cognitive
behavior therapy (CBT), which can include cognitive restructuring,
relaxation techniques, breathing training, and desensitization; identifying
stressors; and including family in the management plan.
CBT, apart from being educative, aims to teach patients to realistically
evaluate and modify faulty thinking. Cognitive restructuring seeks to
teach patients not to misinterpret bodily sensations as signals of an
impending panic attack. Relaxation techniques taught include muscle
relaxation and the imagining of relaxing situations, which patients can use
to help them get through a panic attack, as well as breathing techniques,
which aim to control the hyperventilation that often occurs in panic
attacks. Desensitization involves the gradual exposure of patients to the
situations which they fear and/or avoid, until they become desensitized.
Irrespective of the type of management chosen, every attempt should be
made to identify and address stressors that may be precipitating or aggra-
vating the disorder.
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Referral to a psychiatrist should be considered in cases of severe panic

disorder and/or agoraphobia, non-response to treatment, and the presence
of comorbid severe major depressive disorder or substance-related disor-
ders, which may complicate treatment.
3. SOCIAL AND SPECIFIC PHOBIAS

Phobias may well be the most prevalent psychiatric disorders and are
associated with significant distress and impairment.

Phobias are excessive and unreasonable fears of specific objects or situa-
tions. Exposure to the feared object or situation induces panic-like symp-
toms, which the individual typically recognizes is excessive. Most phobic
individuals with phobia avoid the anxiety-provoking stimulus. ICD-10
groups specific (isolated) phobias and social phobias together with agora-
phobia in the category of Phobic Anxiety Disorders.
Specific phobias can be subdivided into animal type (which is the most
common); nature-forces type (e.g. heights and water); blood, injection,
and injury type; situation type (e.g. aeroplanes and enclosed spaces); and
other type (e.g. fear of clowns).
The fear in social phobias is of being a focus of attention or of behaving
in an embarrassing or humiliating manner. This fear may be restricted
only to having to eat in public, speak in public, or urinate in public toilets
or may be more generalized. Although shortness of breath, tachycardia,
palpitations, and sweating are the predominant symptoms of panic attacks
in agoraphobia and specific phobias, the predominant symptoms of anxi-
ety in social phobia may be blushing6 and trembling. Panic attacks in
social phobia may or may not be overtly evident to those present, even
though the subjective distress is marked.

Many individuals affected by social phobia simply consider themselves as
shy. More often than not, they do not seek help for the symptoms they
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experience. For this reason social phobia may go unrecognized and

untreated. Clinicians should suspect a diagnosis of social phobia in indi-
viduals who admit to experiencing difficulty in social interactions. On
questioning, patients may admit to remaining quiet in groups and with-
drawn and uncomfortable in new social situations, despite wishing for the
acceptance of others. They are distressed by their symptoms or avoidance
behavior, and their functioning is impaired. They may be soft spoken,
largely avoid eye contact, be highly self-critical, have low self-esteem,
and have difficulty asserting themselves.
It is not uncommon for these individuals to present with symptoms of
comorbid disorders. Major depressive disorder and substance-related dis-
orders, particularly alcohol-related disorders, are most commonly comor-
bid. Other comorbidities include bipolar disorder, other anxiety disorders,
and eating disorders. Of those with social phobia, 50%–70% also meet
criteria for avoidant personality disorder. At present, avoidant personality
disorder may be considered as an especially severe form of social phobia.
In children affected by social phobia, school refusal may be a common
presenting symptom.
Those affected by specific phobia of the blood, injection, and injury
type may be unable to comply with necessary physical investigations.
3.3. Epidemiology
Social phobia is one of the most prevalent anxiety disorders. Lifetime
prevalence estimates of 12.1% have been found by the US National
Comorbidity Survey-Replication. Similar prevalence rates have been
found in a number of countries. Lifetime prevalence of specific phobias is
approximately 11%. Although community studies find that specific and
social phobias are more prevalent among women than men, a greater pro-
portion of males to females is seen in clinical settings.
Age of onset for social phobia is during adolescence. The more severe
generalized type may begin even earlier. The disorder manifests in about
80% of those affected by age 20.
Age of onset for specific phobias vary according to the subtype. Nature
forces and blood, injection, and injury type usually begin in childhood.
The situational type tends to begin in the mid-20s.
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3.4. Pathogenesis
The underlying pathogenesis of social phobia is uncertain. Advances in
basic and clinical research have, however, implicated abnormalities in
specific neural circuits as contributory to its development. Neuro-imaging
studies, for example, have found increased activation of the amygdala
(involved in fear processing), the anterior cingulate cortex, and the insular
cortex in social phobia. Neurotransmitters involved in the functioning of
these structures include serotonin, noradrenaline, and dopamine.
Pharmacotherapy with SSRIs has been found to normalize functional
neuroanatomy in social phobia.
It is possible that both genetic and environmental factors contribute to
disruption of this neurocircuitry. Family and twin studies have found
social phobia to be of moderate heritability, with first-degree relatives of
those affected having increased risk of developing the disorder as com-
pared with the general population. Specific phobias have also been found
to run in families. It is possible that those affected by the blood, injection,
and injury type of specific phobia inherit a particularly sensitive vasovagal
reflex. Studies have also shown that specific phobias can be induced by
classical conditioning, with some individuals able to link their phobia to a
preceding traumatic experience. Learning may play a role in the develop-
ment of phobias, with children modeling their responses after adults in
their environment.
A typical symptom of anxiety in individuals with social phobia is
blushing. It has been hypothesized that blushing is representative of an
appeasement display, the function of which is to lessen the negative reac-
tion of others. Individuals with social phobia may misperceive the need
for social appeasement, perhaps because of overestimating threat from
others or by having an exaggerated opinion of their low status.5 Humans
also appear to be predisposed to developing certain phobias more easily
than others, for example, a phobia of spiders rather than of squirrels. This
may serve a survival function.

Both specific and social phobias tend to be chronic disorders if left
untreated. Social phobia in particular, with its early age of onset, tends to
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be a rather disabling condition. It has consistently been associated with

disruption in scholastic performance. Disruptions in social, leisure, and
occupational functioning are also common. The course of social phobia
is often complicated by the development of major depressive disorder
and/or substance-related disorders, which may be an attempt to
self-medicate.
Data reveal that only 50% of those with the disorder seek help, and
when they do, it is often after 15–20 years of symptoms.7 With treatment,
improvement is seen in many of those affected.
3.6. Management
Both pharmacotherapy and CBT are effective in the treatment of social
phobia. The decision regarding which treatment modality to use is often
dependant on patient profile and preference. All patients should be edu-
cated about their disorder and treatment options to help inform their deci-
sions. Pharmacotherapeutic agents often show quicker response times and
should be considered instead of psychotherapy in patients with severe
social phobia who are too anxious to engage in therapy. Pharmacotherapy
may also be a better option for those with comorbid depressive disorder
or patients in whom suicidality is a concern. CBT may have longer-lasting
effects than pharmacotherapy and may be the treatment of choice for
patients who are highly motivated and not open to pharmacotherapy.
A combination of pharmacotherapy and CBT is often used; however,
definitive evidence supporting the use of combination therapy over treat-
ment with a single modality is lacking. Irrespective of the treatment
modality adopted, all patients should be educated about their disorder.
With regards to pharmacotherapeutic agents in the treatment of social
phobia, selective serotonin reuptake inhibitors (SSRIs) are first-line
agents and are effective, tolerable, and easily accessible. Response may
take up to 8–12 weeks. A serotonin–noradrenaline reuptake inhibitor,
venlafaxine, has also been shown to be effective. Irreversible monoamine
oxidase inhibitors are especially efficacious in the treatment of general-
ized social phobia; however, their use remains limited because of the pos-
sibility of serious adverse effects (hypersensitive crisis) and the need for
strict dietary restrictions to prevent this. Social phobia does not respond to
treatment with most tricyclic antidepressants.
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For individuals with performance anxiety, B-adrenergic receptor antag-

onists can be used, for example, propranolol 20 mg one hour before expo-
sure to the anxiety-provoking situation. Patients should experiment with
propranolol beforehand. Short- or intermediate-acting benzodiazepines
(alprazolam or lorazepam, respectively), can be used as an alternative to
propranolol in these situations.
Small studies suggest that SSRIs may have a role in the treatment of
specific phobia.
Fluvoxamine and paroxetine have been used in the treatment of social
phobia in children and adolescents with good effect. The use of SSRIs in
individuals younger than 21 years of age, however, does require careful
monitoring for suicidal ideation and intent.
CBT for patients with social and specific phobia focuses on psychoedu-
cation, cognitive restructuring, desensitization, and relaxation techniques.
Cognitive restructuring aims to modify dysfunctional thoughts about
humiliation and embarrassment through the use of realistic appraisal
of social situations. Desensitization involves gradual exposure to a prede-
termined list of anxiety-provoking stimuli in order of least anxiety-
provoking to most anxiety-provoking.
4. OBSESSIVE-COMPULSIVE DISORDER
Obsessive-compulsive disorder (OCD) is a common and disabling disorder.
In the Epidemiological Catchment Area study, it was found to be the fourth
most prevalent psychiatric disorder, following phobias, substance-related
disorders, and major depressive disorder. Morbidity and mortality studies
conducted under the auspices of the World Health Organization have found
OCD to be among the most disabling of all medical conditions.

ICD-10 requires the presence of either obsessions or compulsions for a
period of at least two weeks in order for the diagnosis of OCD to be made.
Obsessions may take the form of thoughts, images, or impulses and are
repetitive, intrusive, and anxiogenic. Compulsions are repetitive behaviors
or mental acts that the individual feels compelled to carry out, often in a
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rigid manner. Although compulsions may result in anxiety being tempo-

rarily abated, they are unpleasurable to carry out. Both obsessions and
compulsions are recognized as being the product of the individual’s own
mind and not imposed on the individual from an external source, as may
be the case in schizophrenia. Although some individuals with OCD have
poor insight into their disorder, there must have been recognition (at some
point) of at least one obsession or compulsion being excessive, irrational,
or unreasonable.
Affected individuals are distressed by their symptoms and attempt to
resist them; however, functioning in the areas of social, occupational, and
leisure activities is often compromised by time-consuming behaviors.
For the diagnosis of OCD to be made, obsessions and compulsions can-
not be the result of another psychiatric disorder, for example, a preoccupa-
tion with food in an individual with bulimia nervosa or rumination about
past behaviors in an individual with major depressive disorder.
ICD-10 allows for OCD to be further specified as occurring with a
predominance of obsessions, compulsions, or mixed obsessions and com-
pulsive acts.

Even though OCD is a common and disabling condition, many of those
affected by the disorder do not openly disclose their symptoms. Reasons
for this may include shame and guilt about the content of obsessions and
compulsions; a lack of awareness of having a treatable disorder; and poor
insight, where the individual fails to recognize that symptoms are exces-
sive or unreasonable. Those with OCD may well present to physicians in
fields other than psychiatry, for example, pediatricians, when parents of
children are concerned about the child’s behaviors, or dermatologists or
primary care physicians, when seeking treatment for dermatitis as a result
of excessive hand washing.
The majority of patients with OCD experience both obsessions and
compulsions. Both of these phenomena are experienced as ego-dystonic.
Patients may report that carrying out a compulsive act brings a temporary
relief of anxiety, until the next obsessive thought or image raises anxiety
once more.
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There appears to be remarkable consistency of themes between patients

of different cultures and times. The most common theme is a fear of con-
tamination. Patients may be plagued by obsessions about contracting
infections from other people or germs from surrounding objects and may
bathe or wash their hands excessively in an effort to prevent this. Other
common themes include concerns about danger (e.g. fears for one’s safety
or that of loved ones, with subsequent checking); symmetry concerns
(e.g. needing to arrange objects in a particular manner); religious, sexual,
or aggressive concerns (e.g. thoughts of murdering friends or family);
and hoarding concerns (e.g. a need not to throw objects away). A system-
atic analysis2 has outlined five predominant symptom dimensions in
OCD: (1) contamination/cleaning; (2) aggressive/checking; (3) symmetry/
ordering; (4) hoarding; and (5) sexual/religious themes.
As with panic disorder, agoraphobia, and social and specific phobias,
patients with OCD are commonly affected by comorbid psychiatric disor-
ders. Especially common are major depressive disorder, other anxiety
disorders, and OCD-spectrum disorders. Because patients may present
with symptoms of these disorders rather than symptoms of OCD, all
patients presenting with these conditions should be screened for OCD.
On physical examination, patients with OCD may have tics or soft
neurological signs and may even have comorbid Tourette’s disorder or
Sydenham’s chorea.
4.3. Epidemiology
Epidemiological studies conducted in many countries around the world
have found lifetime prevalence of OCD to be 2%–3%. In adults, the male
to female ratio is approximately 1:1. Although average age of onset of the
disorder is 20 years, some patients are able to track ritualistic behavior
back to childhood. Onset tends to occur slightly earlier in males than
females. Later onset of the disorder may be precipitated by neurohormonal
changes, in particular, pregnancy and the postpartum period in females.
4.4. Pathogenesis
Advances in basic and clinical research have led to an emphasis on the
role of cortico–striatal circuitry in OCD.
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The first indication that OCD was related to basal ganglia pathology
was data from research on patients with post-influenza encephalitis who
developed symptoms of OCD. Subsequently, OCD has also been noted to
occur in other neurological disorders associated with basal ganglia dam-
age. These include Tourette’s disorder, Huntington’s disease, Parkinson’s
disease, and Sydenham’s chorea. Cortico-striatal-thalamo-cortical (CSTC)
circuitry impacted by these disorders may be responsible for mediating a
range of processes involved in OCD (e.g. disgust, procedural control).
Neuro-imaging findings support evidence of CSTC circuit dysfunction.
MRI studies have found a decrease in volume of the caudate nucleus in
some individuals with OCD, while functional MRI studies have found
hyperactivity in the caudate nucleus, orbitofrontal cortex, and anterior
cingulate cortex (Fig. 1). It has been speculated that hyperactivity in corti-
cal areas is an attempt to dampen a basal ganglia “false alarm.”
Pharmacotherapeutic and psychotherapeutic interventions that success-
fully treat OCD result in normalization of hyperactivity in the CSTC
circuit (Fig. 2).
Fig. 1. Increased activity in the orbitofrontal cortex and caudate nucleus in individuals
with untreated OCD.4
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Fig. 2. Normalization of activity in the CSTC circuit following pharmacotherapeutic or

psychotherapeutic intervention; yellow lines represent serotonergic pathways originating
in the raphe nucleus that project to the CSTC circuitry and other areas of the cortex.4
Neurotransmitters associated with CSTC circuitry include serotonin

and dopamine. A serotonin hypothesis of OCD is supported by the selec-
tive response of OCD symptoms to clomipramine (a predominantly sero-
tonergic tricyclic) and SSRIs. Dopamine agonists have been found to
worsen obsessive-compulsive symptoms and tics in individuals with
OCD, while dopamine antagonists are used to treat tics in individuals with
Tourette’s disorder and have been found useful in augmenting SSRIs in
treatment-refractory OCD. Genetic variants in these neurotransmitter sys-
tems may contribute to the development of OCD.

OCD is a chronic condition with a variable course. Although some
patients experience constant symptoms, others may have a fluctuating
course. Symptom themes may overlap and change with time. With treat-
ment, many individuals show improvement.
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Indicators of poor prognosis include childhood onset, hoarding,2 and

comorbid personality disorder.
4.6. Assessment
The severity of symptoms and extent of impairment should be ascertained
before initiating therapy. Because comorbid psychiatric disorders occur
with high frequency, all patients with OCD should be screened for comor-
bid disorders.
On physical examination, the clinician should search for medical seque-
lae of symptoms (e.g. dermatitis secondary to excessive hand washing)
as well as evidence of comorbid neurological disorders (e.g. Tourette’s
disorder, Sydenham’s chorea).
Presentation of the disorder after age 35 is unusual, and if this is the
case, the need for more rigorous investigation should be considered.
4.7. Management
Research has found that OCD is responsive to pharmacotherapy and
CBT. As with the other anxiety disorders, psychoeducation for the
patient and family is an important component in treatment. Families may
collude with patients in an attempt to ease their distress or may them-
selves require support to help them better understand the patient and the
disorder. Effective pharmacotherapeutic agents in the treatment of OCD
include the tricyclic antidepressant clomipramine and the SSRIs.
Clomipramine has more adverse effects (e.g. anticholinergic, alpha adr-
energic, and antihistaminergic) than the SSRIs. SSRIs as a group are
safe to use and well tolerated. Symptoms of OCD may take 10–12 weeks
to respond to treatment, and symptom reduction is often achieved at
higher dosages than those used to treat depression and other anxiety
disorders. Dosages may be increased at 2–4 weekly intervals up to
60 mg for fluoxetine and citalopram, 60 mg for paroxetine, 300 mg for
fluvoxamine, 200 mg for sertraline, and 250 mg for clomipramine.
Following non-response to one agent, another serotonin reuptake inhibi-
tor should be tried. Augmentation with a low dose atypical antipsychotic
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(e.g. risperidone) can be considered in treatment-refractory individuals.

Once adequate response has been achieved, pharmacotherapy should
continue for at least 12 months.
CBT is effective and may induce longer-lasting effects than treatment
with psychotropics. CBT for the treatment of OCD employs exposure and
response prevention. A graded hierarchy is used, with gradual exposure to
situations that the patient fears or usually avoids. Patients can also be
taught thought-stopping techniques and relaxation techniques. Family
members can be enlisted to encourage patients while they begin to employ
therapy techniques.
For patients who are severely treatment-refractory with debilitating
symptoms, deep brain stimulation or other neurosurgical procedures may
be considered. Deep brain stimulation involves the placement of elec-
trodes into various subcortical structures. Other neurosurgical procedures
involve disruption of the CSTC pathways that are implicated in the patho-
genesis of OCD.
5. POSTTRAUMATIC STRESS DISORDER

AND ACUTE STRESS REACTION
Symptoms of posttraumatic stress disorder (PTSD) have been described
for centuries in soldiers exposed to war; however, PTSD was only intro-
duced into the official nomenclature in DSM-III. Because only a small
percentage of individuals exposed to trauma develop PTSD, the disorder
is increasingly viewed as an abnormal psychobiological response to trau-
matic exposure. It is “normal” for any individual exposed to a trauma to
have some alteration in mental state; however, this normal response
includes adaptation and an acceptance of what has occurred with a time-
ous return to functionality.

Individuals diagnosed with PTSD must have experienced a traumatic
event that almost anyone would find stressful. Following exposure, indi-
viduals develop symptoms of three symptom clusters, including re-
experiencing, avoidance symptoms, and hyperarousal. These symptoms
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must be experienced within six months of exposure to the trauma or else

be specified as manifesting with delayed onset.
ICD-10 also describes an acute stress reaction, which differs from PTSD
in that symptoms begin developing within an hour of exposure to the trauma
and begin diminishing within 48 hrs of the trauma having ended. Patients
with an acute stress reaction do not necessarily go on to develop PTSD.

Although patients may present complaining of symptoms of the three
symptom clusters of PTSD, many do not readily disclose that they have
had a traumatic experience. Reasons for this may include survivor guilt
(that is, guilt at having survived while others did not); a sense of personal
failure or inadequacy; shame about the nature of the trauma (e.g. being the
victim of rape); or avoidance of engaging in conversation or thinking
about the trauma. Clinicians may be reluctant to enquire about traumatic
experiences because of worry about causing distress or discomfort.
However, because PTSD is prevalent and misdiagnosis can readily occur,
they should be encouraged to do so.
Difficulty in making the diagnosis of PTSD may be due to the high
frequency of somatic complaints with which patients often present or
complaints of symptoms of comorbid psychiatric disorders rather than of
PTSD itself. Somatic complaints are often non-specific and include head-
aches, dizziness, gastro–intestinal symptoms, and various bodily aches
and pains. Comorbidity is common in patients with PTSD; commonly
occurring comorbid disorders include major depressive disorder (comor-
bid in approximately 50% of those with PTSD), other anxiety disorders,
substance-related disorders (particularly alcohol-related), and personality
disorders. Diagnosis may be further complicated given that some patients
with PTSD may experience hallucinations and illusions, panic attacks,
and mood swings.
5.3. Epidemiology
The majority of the population is exposed to a traumatic event severe
enough to result in PTSD. However, only a relatively small proportion of
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these go on to develop PTSD. Although any traumatic event can lead to

the development of PTSD, risk is higher for less common and more severe
events, for example, rape and war. Risk factors predisposing to the devel-
opment of PTSD include pre-trauma factors (e.g. female gender, having
experienced a childhood trauma, genetic factors, pre-existing psychiatric
disorder, lower intelligence); peri-trauma factors (e.g. unexpected and
severe nature of the trauma, interpersonal violence, dissociation during
the trauma); and post-trauma factors (e.g. poor social support following
the trauma).
5.4. Pathogenesis
A key precipitant in the development of PTSD is exposure to a traumatic
event. Not every individual exposed to a sufficiently stressful situation
goes on to develop PTSD, indicating the importance of other risk factors.
Basic and clinical research has contributed to our understanding of the
psychobiology of PTSD.
Clinical studies implicate dysfunction in numerous molecular systems
in PTSD. These include disruption in the hypothalamus-pituitary-adrenal
(HPA) axis, serotonin and noradrenaline systems, glutamate-GABA, and
opiate systems. There have been various attempts to link such distur-
bances with particular symptoms; for example, it has been suggested that
noradrenergic disturbances contribute to physiological arousal, while
opioid disturbances contribute to numbing symptoms.
Neuro-imaging studies have found decreased hippocampal volume in
those affected by PTSD. This may account in part for the disturbance in
memory and learning that these individuals experience. Decreased hip-
pocampal volume may be due to the neurotoxic effect of HPA axis dys-
function or may be a pre-existing risk factor for the development of PTSD.

The course of PTSD is variable. The disorder usually manifests soon after
traumatic exposure. Approximately half of those affected will recover
after one year. Up to 30% of those diagnosed may develop a lifelong ill-
ness. For those with chronic PTSD, symptom frequency and intensity
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fluctuates, usually worsening during periods of stress. PTSD with delayed

onset may develop decades after traumatic exposure; however, these
individuals often experience a more recent precipitating trauma that bears
resemblance to the original trauma in some manner.
5.6. Assessment
Assessment should include ensuring that the current environment is a
safe one; evaluating the intensity and frequency of symptoms experienced
and their impact on level of functioning; screening for comorbid major
depressive disorder, substance-related disorders, anxiety disorders, and
personality disorders and exploring suicidal ideation and intent; identify-
ing on-going social stressors and supports; and assessing the patient’s
view of his or her symptoms and of optimal intervention.
5.7. Management
Psychoeducation for patients and their families is an important tool in de-
stigmatizing the illness. Patients may be encouraged to accept that they
are experiencing a common psychobiological reaction to an extreme
stressor and should be educated about available treatment options.
A growing body of research supports the use of both pharmacotherapy
and psychotherapy as optimal treatments for PTSD.
As with other anxiety disorders, SSRIs are first-line pharmacothera-
peutic agents in the treatment of PTSD.9 Paroxetine and sertraline in par-
ticular are. FDA approved for the treatment of PTSD. SSRIs are safe and
effective agents that target all three symptom clusters of PTSD.
Tricyclic antidepressants, monoamine oxidase inhibitors, and the
serotonin-noradrenaline reuptake inhibitor venlafaxine have all been used
to treat PTSD with good effect and may be considered in SSRI non-
responders. A range of agents can also be used to augment SSRIs, includ-
ing antipsychotic agents and mood stabilizers. Once treatment response
has been achieved, pharmacotherapy should continue for at least one year
before considering withdrawal of the drug.
There is good evidence for the efficacy of CBT in PTSD. CBT may be
provided in an individual or group setting and incorporates
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psycho-education; anxiety management techniques (relaxation techniques,

breathing exercises, and thought-stopping techniques); exposure therapy;
and cognitive therapy. Exposure therapy involves detailed repeated imag-
ining of the traumatic event in the safety of a controlled and supportive
environment in order to gain mastery over the overwhelming emotions
evoked during the traumatic experience. Cognitive therapy aims to address
cognitive distortions that the individual may hold (e.g. thinking “I will
never be safe again”).
There is a growing literature on evidence-based responses to disasters
and other traumas. Of note, critical incident stress debriefing, which has
been advocated in the past, is now thought to be associated with worse
outcomes.
Referral to a psychiatrist is indicated in cases of treatment non-
response, for assessment of complicating or severe major depressive dis-
order, and in addressing suicidality.
6. GENERALIZED ANXIETY DISORDER

Generalized Anxiety Disorder (GAD) was introduced into the diagnostic
nomenclature with DSM-III. GAD is a chronic and highly prevalent con-
dition that is associated with significant morbidity and economic burden.

The diagnosis of GAD requires at least a six month history of excessive
and persistent worry, tension, and apprehension relating to a number of
everyday events. These are not purely related to real worries that would
cause anxiety to most individuals. The World Health Organization’s ICD-
10 criteria focus on the somatic and psychological symptoms that stem
from the patient’s anxiety. Diagnosis necessitates that at least one of four
symptoms of anxiety is of autonomic arousal. Because the symptoms of
GAD are not always specific to the disorder, diagnosis necessitates that
symptoms experienced are not as a result of the presence of another anxi-
ety disorder. Symptoms should also not be due to a general medical condi-
tion or a substance-related disorder.
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Individuals with GAD frequently seek treatment for their somatic com-
plaints. This may lead to their presentation to primary care physicians,
cardiologists, pulmonologists, neurologists, endocrinologists, and gastro-
enterologists, who may undertake unnecessary investigations.
On mental state examination, patients may be visibly anxious. They
may sit on the edge of their seat, tremble, clench muscles, wring their
hands, or show other signs of psychomotor agitation.
Patients with GAD typically experience significant distress and impair-
ment in social, occupational, and leisure functioning. Impairment is worse
in individuals affected by comorbid psychiatric disorders.
Comorbidity is the norm rather than the exception in those with GAD.
Comorbid major depressive disorder is present in three out of five of those
affected.8 Other commonly comorbid disorders include dysthymia, other
anxiety disorders, and substance-related disorders. These disorders should
therefore be screened for in individuals with suspected GAD.
6.3. Epidemiology
As with the other anxiety disorders, GAD is highly prevalent. It is the
most common anxiety disorder in primary care practice. The lifetime
prevalence of GAD, as suggested by US and European studies, is in the
region of 5%. The female to male ratio is 2:1. Onset of the disorder may
be as early as adolescence, although it often begins somewhat later than
this. Less than 40% of those affected seek treatment for their disorder, and
when they do, it is often much later in life.
6.4. Pathogenesis
The etiological factors that give rise to GAD remain uncertain. Both
biological and psychosocial factors have been implicated in its pathogen-
esis. Research thus far has focused on dysfunction in the glutamate-
GABAergic systems, and serotonergic and noradrenergic systems. Various
psychosocial factors may also play a role.
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GAD is a chronic disorder. It may manifest early in life, and it is often
exacerbated during periods of stress. GAD is a risk factor for the subsequent
development of comorbid mood, anxiety, and substance-related disorders.
6.6. Assessment
Assessment requires an evaluation not only of GAD symptom severity
and functional impairment but also of comorbid psychiatric and medical
disorders. The Hamilton Anxiety Disorder rating scale is widely used as a
symptom severity measure in GAD.
6.7. Management
Both pharmacotherapy and psychotherapy have been found to be effective
in the short- and medium-term treatment of GAD. SSRIs are first-line
agents in the treatment of GAD. Some patients report improvement in
symptoms as early as two weeks following initiation of medication.
Treatment should be continued for at least a year, given that early discon-
tinuation often leads to relapse.
Benzodiazepines have been widely used in the treatment of GAD.
However, limiting factors include impaired memory, increased risk of
accidents, and rebound anxiety on withdrawal. A range of other agents are
available, including serotonin–noradrenaline reuptake inhibitors (venla-
faxine, duloxetine), tricyclic antidepressants (TCAs), and buspirone.
The psychotherapy that is best supported by controlled trials in GAD is
CBT. CBT focuses on psychoeducation, relaxation techniques, identifying
and addressing precipitating stressors, cognitive restructuring to address
cognitive distortions, and the behavioral techniques of worry exposure
and worry behavior control.
7. KEY POINTS
• Anxiety disorders are highly prevalent and disabling psychiatric
disorders.
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• Pathological anxiety is persistent and distressing to the individual and

impairs function.
• Thorough history taking, physical examination, and appropriate
investigation are important before making a diagnosis of an anxiety
disorder.
• Comorbid major depressive disorder, substance-related disorders
(particularly alcohol-related), and other anxiety disorders are com-
mon and must be screened for on initial assessment and at follow up.
• Management plans should be devised in collaboration with the patient
to best address his or her unique needs and situation.
• Psychoeducation for patients and their families is key.
• SSRIs are safe, efficacious, and tolerable first-line pharmacotherapeu-
tic agents.
• Benzodiazepines produce rapid relief of anxiety but should only be
prescribed as a short course of treatment.
• CBT is effective and can be used to treat the major anxiety
disorders.
• Precipitating stressors should be identified and addressed.
• Optimize each patient’s social support system.
• Refer patients and their families to local support groups.
8. SELF-ASSESSMENT
8.1. With regard to anxiety disorders, please state which
statement is true:
(A) Males are more commonly affected by anxiety disorders than
females.
(B) Mood disorders are more prevalent than anxiety disorders.
(C) Tricyclic antidepressants are first-line pharmacotherapeutic agents in
the treatment of anxiety disorders.
(D) Both pharmacotherapeutic agents and cognitive behavioral therapy
are effective in the treatment of anxiety disorders.
(E) Anxiety disorders do not have a heritable component.
Answer: D
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8.2. With regard to panic disorder, please state which statement

is true:
(A) Initial panic attacks are usually in response to an identifiable trigger.
(B) A thorough physical examination is not always necessary if panic
attacks are most likely due to psychiatric pathology.
(C) No association exists between psychosocial stressors and the devel-
opment of panic disorder.
(D) On initiating an SSRI, a patient may report an increase in the number
of panic attacks experienced.
(E) The amygdala is not involved in the perception and expression of
fear.
Answer: D
9. CASE STUDIES
9.1. Panic attack
Mrs K, a 29-year-old married woman, was driving over a bridge one even-
ing when she had her first panic attack. Her heart began to race, and she
felt short of breath. Within minutes she was sweating profusely, nauseous,
and afraid that she was dying. About 10 mins later, the symptoms sub-
sided. Convinced that she had a heart attack, she drove to the closest
hospital for investigation. Physical examination, electrocardiogram, and
blood tests undertaken by the emergency room doctor were all within
normal range, and she diagnosed a panic attack.
9.2. Social phobia

Ms A, a 19-year-old college student, recently began to consider dropping
out of college. She had always considered herself a shy individual and was
only completely comfortable around her family and a few close friends.
Before beginning college she was excited at the thought of meeting new
people and perhaps even dating. However, during her first year, she started
to become increasingly self-conscious when surrounded by fellow stu-
dents whom she did not know. The thought of having to answer questions
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during lectures made her sweat and her stomach churn, and she was cer-
tain she would say something humiliating. She stopped writing notes dur-
ing lectures because of her fear of others noticing that her hands trembled,
and she avoided conversations with acquaintances between classes.
Recently she began skipping classes altogether and, as a result, was now
failing three of her courses.
9.3. OCD
Mrs T, a 24-year-old woman, was happily married for one year before she
and her husband were delighted to find out that she was pregnant with
their first child. Three months after the birth of a healthy baby boy, she
presented to her primary care physician requesting “something to boost
energy levels.” On questioning, she disclosed difficulty coping with the
demands of taking care of her baby because of repetitive checking behav-
iors that she was unable to resist carrying out. She checked the plug points
in her home several times a day to ensure they were switched off unless
in absolute need of being used. She also continuously made sure that the
stove was switched off and that the iron, lighters, and boxes of matches
were stored away. She spent approximately two hours a day carrying out
these activities and had difficulty falling asleep at night because of the
worry that she had not checked properly. Her primary care physician dis-
covered that these behaviors were in response to intrusive and recurrent
images of her baby and house being burned down and that Mrs T
had begun experiencing these symptoms of OCD soon after the birth of
her baby.
9.4. PTSD
Mr D, a 50-year-old businessman, was locking up his store one evening
when he was approached by three masked men, one of whom held a gun
to his head and threatened to kill him if he did not comply with their
demands. After he had given them all the money he earned that day, he
was gagged, physically restrained, and assaulted. Mr D was convinced he
would be killed, but the assailants fled after assaulting and verbally
abused him for 20 min. Mr D was found by his son later that evening. Six
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weeks after the traumatic event, Mr D’s son insisted that he consult their
primary care physician, because Mr D was experiencing nightmares and
flashbacks of the trauma. He also avoided speaking about the trauma,
expressed no interest in previously pleasurable activities, and felt unable
to emotionally engage with others. While at work he was hypervigilant
and had difficulty concentrating on daily tasks.
9.5. Generalized anxiety disorder

Mrs S, a 50-year-old married mother of two, was referred to a psychiatrist
by her primary physician three months after her youngest child moved
away from home. During the initial consultation, she described herself as
a “worrier.” She reported anxiety dating back to her school days. She often
consulted medical doctors for numerous somatic complaints — palpita-
tions, muscle spasms, headaches, and abdominal discomfort, to name a
few. Since her daughter had moved away from home, she began experi-
encing more irritability and insomnia than usual. Try as she might, she
could not concentrate at work. She worried about everything — how her
daughter was managing on her own, whether her husband would enjoy the
dinner she prepared, whether she would have enough time to do the gro-
cery shopping, whether her friends thought she was supportive enough.
Her psychiatrist diagnosed generalized anxiety disorder.
REFERENCES
1. Kessler RC, Chui WT, Demler O, Walters EE. (2005) Prevalence, severity,
and comorbidity of 12-month DSM-IV disorders in the National Comorbidity
Survey Replication. Arch Gen Psychiatry 62: 617–627.
2. Mataix-Cols D, Rauch SL, Manzo PA, Jenike MA, Baer L. (1999) Use of
factor-analyzed symptom dimensions to predict outcome with serotonin
reuptake inhibitors and placebo in the treatment of obsessive-compulsive
disorder. Am J Psychiatry 156: 1409–1416.
3. Sadock BJ, Sadock MD. (2007) Kaplan and Sadock’s Synopsis of Psychiatry:
Behavioral Sciences/Clinical Psychiatry, 10th ed. Lippincott Williams &
Wilkins, Philadelphia, PA.
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4. Stein DJ. (2002) Obsessive-compulsive disorder. Lancet 360: 397–405.

5. Stein DJ. (2006) Advances in understanding the anxiety disorders: The cog-
nitive-affective neuroscience of ‘false alarms.’ Ann Clin Psychiatry 18(3):
173–182.
6. Stein DJ, Vythilingum B. (2007) Social anxiety disorder: Psychobiological
and evolutionary underpinnings. CNS Spectr 12(11): 1–4.
7. Stein MB, Stein DJ. (2008) Social anxiety disorder. Lancet 371: 1115–1125.
8. Tyrer P, Baldwin D. (2006) Generalised anxiety disorder. Lancet 368:
2156–2166.
9. Yehuda R. (2002) Post-traumatic stress disorder. N Engl J Med 346(2):
108–114.
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Chapter 11
Substance Use Disorders
Nidal Moukaddam and Pedro Ruiz
1. INTRODUCTION
Drugs have been used since the dawn of humanity, whether for religious
or recreational purposes. References to drug use date back thousands of
years;14 drug consumption for religious and recreational purposes, as well
as the negative consequences associated with excessive use, have been
mentioned in Greek history and that of other early civilizations.
Substance use disorders are mental and behavioral disorders attributed
to substances, whether prescribed or not. Excessive use of alcohol or
drugs has been referred to as addiction, addictive disorders, abuse or
dependence, or SUDs, although many cultural and social considerations
color those terms. Designations such as “alcoholic” or “cokehead” hold
no agreed-upon scientific meaning and are often regarded as pejorative.
This chapter presents general considerations about drugs and alcohol, fol-
lowed by brief descriptions of each of these drug categories and special
considerations that apply to each drug category, as well as guidelines for
treatment.
Substance use disorders carry a tremendous societal cost, stemming
from lost productivity, trauma, medical problems, and crime expenditures,
and finally, non-financial welfare costs, which refer to pain, suffering, and
lost life. Users of illicit drugs or alcohol are more likely to be involved in
260
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Substance Use Disorders 261
violence and criminal behavior, traumatic injuries, and significantly more

likely to abuse their spouses physically and sexually.22
The simplest definition of drug dependence, given by WHO in its
Lexicon of alcohol and drug terms [1994], is “a need for repeated doses
of the drug to feel good or to avoid feeling bad.” In fact, alcohol and
substance use occurs along a continuum that starts with socially accepta-
ble use, a usage pattern carrying little to no adverse consequences on the
user’s life, but that might eventually worsen into dependence. The
hallmark of substance dependence is impaired control over the use of
the substance, with ensuing behavioral, cognitive, medical, or legal
difficulties.
The ICD-10 specifies two diagnostic categories for problematic
psychoactive substance use: harmful use and the dependence syndrome.
Harmful use is a “pattern of psychoactive substance use that is causing
damage to health. The damage may be physical (as in cases of hepatitis
from the self-administration of injected psychoactive substances) or men-
tal (e.g. episodes of depressive disorder secondary to heavy consumption
of alcohol.” The dependence syndrome, on the other hand, is a “cluster of
behavioral, cognitive, and physiological phenomena that develop after
repeated substance use and that typically include a strong desire to take the
drug, difficulties in controlling its use, persisting in its use despite harmful
consequences, a higher priority given to drug use than to other activities
and obligations, increased tolerance, and sometimes a physical withdrawal
state.” The ICD also allows for the fact that the dependence syndrome may
be present for a “specific psychoactive substance (e.g. tobacco, alcohol, or
diazepam), for a class of substances (e.g. opioid drugs), or for a wider
range of pharmacologically different psychoactive substances.” All diag-
noses related to psychoactive substance use are listed under the rubric of
mental and behavioral disorders due to psychoactive substance use (F10-
F19), a wide variety of disorders that differ in severity and clinical form
but that are all attributable to the use of one or more psychoactive sub-
stances, which may or may not have been medically prescribed. These
include intoxication states, withdrawal (with or without delirium), demen-
tia, amnestic disorders, psychotic disorders, mood disorders, and anxiety
disorders, as well as sexual dysfunction and sleep problems. All drugs of
abuse can mimic psychiatric diagnoses, and the only way to determine that
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262 N. Moukaddam and P. Ruiz
symptoms are substance-induced is via careful history taking, emphasiz-

ing timeline, cyclical symptom patterns, and symptom abatement during
periods of drug abstinence. Drug testing and collateral information are
also extremely helpful. Treatment planning often depends on a clear dis-
tinction between primary and substance-induced symptomatology, with
the ever-present possibility that the patient could have two primary diag-
noses. For patients with a primary SUD, care must be taken not to over-
prescribe addictive medications. However, assuming all psychiatric
symptomatology occurring within the context of substance use is exclu-
sively substance-induced can lead to under-treatment of both conditions
and increased risk of relapse.
2. CONSIDERATIONS REGARDING DRUG

USE EPIDEMIOLOGY
Illicit drug use activity is a rapidly changing field, with new chemical
compounds being generated frequently. Most of these compounds are
merely trendy and do not gain widespread popularity. Conversely, com-
pounds that generate user interest and positive experiences tend to become
widely used and well known. Such recognition is dependent on many fac-
tors, including supply and demand as well as price. “Successful” drugs
subsequently become a target for law enforcement and other regulatory
entities. Such efforts vary per country and world region, as do drug use
patterns. Sadly, drug-related regulations often lag behind, and many sub-
stances remain legal for a while after harmful use has become evident.
Additionally, drug testing methods do not evolve as fast as drugs become
available, limiting accurate detection. Further hindrances are caused by
the common practice of adulteration.
An example of the interplay between social and legal factors is seen in
the increasingly popular synthetic cannabinoid use (see subsequent text).
Synthetic cannabinoids sales have flourished over the Internet and remain
legal in some countries.
Knowledge of the epidemiology of drug use is subject to the above
limitations, as well as funding limitations. This chapter will present an
overview of worldwide use, with notations of variations applicable to
certain areas or countries as warranted. Global data are mainly obtained
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from the World Health Organization (WHO), whereas data pertaining to

the European Union is widely available from the European Monitoring
Centre for Drugs and Drug Addiction (EMCDDA). Data related to US use
patterns is mentioned as well from sources such as the National Institute
of Drug Abuse.
3. NEUROBIOLOGICAL CONSIDERATIONS
IN SUBSTANCE USE DISORDERS
Powerful myths and misconceptions about the nature of addiction persist.
For the longest time, according to what is termed the moral model, indi-
viduals suffering from substance use disorders were thought to be morally
flawed, lacking willpower, and these views continue to shape society’s
responses to drug abuse. Thus, most societies still consider, and treat, drug
and alcohol related problems as a moral failing rather than a health
problem. This is evident in the preponderance of punitive rather than
therapeutic or preventive actions.
Considering substance use disorders as a brain disease allows a more
objective and scientific approach to this issue. Thus, an SUD is a chronic,
relapsing disorder characterized by:20
(i) compulsion to seek and take the drug,

(ii) loss of control in limiting intake, and
(iii) emergence of a negative emotional state (e.g. dysphoria, anxiety,
irritability) when access to the drug is prevented.
The extent to which a drug is sought compulsively is thought of as its

reinforcing effect, a concept which can be evaluated using multiple para-
digms such as conditioned place preference or self-administration (oral or
intravenous). A substance with no reinforcing effect simply does not
become popular. Thus, the concept of reinforcing roughly correlates into
how addictive a substance is, although this translation requires major
oversimplification.
Ultimately, all drugs, regardless of acute mechanism of action, activate
the brain’s reward circuitry, the mesolimbic dopamine system, an area
consisting of the ventral tegmental area and the nucleus accumbens. The
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crucial role of dopamine in acute reinforcing properties of drugs of abuse

has been instrumental in shaping the addiction research field for decades,
but other neurotransmitters are also involved as effectors, mediating
reward (opioids, GABA), or as modulators (serotonin and endocannabi-
noids). Hence, although the acute effects of a drug might be heavily
mediated by a dopaminergic reward, chronic drug use recruits other neu-
rotransmitter systems. The promising results of using N-acetylcysteine
in cocaine dependence illustrate how treatment might be successfully
targeted to non-dopaminergic systems.
Decreased reward system function is a common result of chronic drug
use. This decreased function may persist in the form of long-term bio-
chemical changes, which clinically manifests as protracted abstinence and
vulnerability to relapse. Clinically, this may manifest as lack of interest in
daily life and its rewards, which the typical substance-dependent individ-
ual finds less than interesting. Additionally, neurochemical systems other
than those involved in positive rewarding effects of drugs of abuse are
recruited or dysregulated by chronic activation of the reward system,
resulting in emotional dysregulation and negative affects during
withdrawal.7,8
4. NICOTINE
Nicotine is an alkaloid extracted from the Solanaceae plant genus, which
includes the tobacco plant, containing the highest concentration of
nicotine in comparison to other plants in that family. Nicotine was purified
in 1828 and initially considered as a pesticide. It can be smoked (e.g. ciga-
rettes) or used orally (by chewing tobacco leaves) or otherwise inhaled
(e.g. flavored tobacco smoked in a hookah). Cigarettes, the most com-
monly used of those methods, contain hundreds of other substances that
carry high potential for adverse medical consequences. The WHO
estimates that about 1.22 billion people are smokers worldwide. In adoles-
cents, there is little gender gap, but in adults, men are found to have a
higher prevalence than women. Smoking prevalence generally decreases
with increasing education, thus the health sequelae of smoking tend to
disproportionately affect the economically disadvantaged classes and
individuals with mental illness. Certain groups, such as individuals with
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psychiatric pathology, are at particularly high risk for nicotine depend-

ence. Further, anxiety, attention-deficit, mood, and other substance use
disorders are more common among current smokers than among people
who have never smoked or are ex-smokers.
Factors leading to increased popularity of smoking in the 1900s include
the use of cigarette-making machines and the availability of non-poisonous
matches. Further, the use of acidifying agents, allowing nicotine to enter
the lungs, contributes to rapid spread in the bloodstream and thus rapid
effects on the brain reward system. Cigarette smoking was long consid-
ered popular, and risks associated with smoking have only been high-
lighted in the past few decades. Bans on smoking in public places have
become widespread in many countries. That led to a sharp decrease in
smoking since the mid-1990s, although the number of smokers remains
staggering.
Medical complications of smoking include lung cancer, chronic
obstructive pulmonary disease (COPD), cardiovascular disease, low birth
weight in offspring of females smoking during pregnancy, and perinatal
complications. Smokers have twice the mortality rate of non-smokers, and
it is estimated that 50% of smokers die of a smoking-related illness.
However, smoking cessation almost eliminates the risk of heart disease in
5 years post-cessation and the risk of lung cancer in 20 years.
Nicotine is very widely used and is a legal drug. Nicotine is known to
be addictive but, unlike other drugs of abuse, causes mood-altering effects
without behavioral effects. When smoked, nicotine has a half-life of about
two hours. The majority of nicotine (up to 80%) is metabolized to cotinine
(an anagram of the word nicotine). Cotinine, the main metabolite of nico-
tine, has similar, albeit less potent, effects on the nicotinic acetylcholine
receptors and has a half-life of about 16–20 hours. The main pathway for
nicotine metabolism is the cytochrome P450 system (mainly CYP2A6,
less CYP2B6). Genetic polymorphisms in those genes can affect this pro-
cess, thereby affecting individual susceptibility to nicotine addiction and
side effects. The second step is catalysed by aldehyde oxidase. Nicotine
and cotinine clearance is higher in women than men. Clearance is
decreased in the elderly as well.
Nicotine exerts its functions through α4/β2 nicotinic Acetylcholine
receptors (the most common nicotine receptor subtype in the mammalian
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brain) in the ventral tegmental area of the midbrain, leading to dopamine

release. Additionally, it causes release of GABA and glutamate and
inhibits monoamine oxidase A and B.
Close to half the population of smokers attempt to quit each year, with
most smokers making 5–10 attempts before reaching a successful
outcome. Around 5–10% stop permanently, and relapse is exceedingly
common. Withdrawal symptoms include mood changes (irritability,
depression), insomnia (potentially with intense vivid dreams, waking up
frequently at night), concentration difficulties, and increased appetite
accompanied by weight gain. Withdrawal symptoms peak at 1–3 days
post-cessation and last for a few weeks. However, craving and weight gain
can persist for 6 months or more and enhance the risk of relapse.
Smoking cessation usually requires lengthy or repeated treatments
because of the high risk of relapse. Heavy tobacco use and other comor-
bidities may require longer courses of treatment. These measures are cost-
effective, given the health benefits of quitting smoking. First-line
treatments include nicotine replacement therapies, bupropion SR,
Varenicline HC, group or individual psychotherapy, and combination
treatments. Psychosocial measures focus on education about addiction,
health consequences, and withdrawal. Teaching patients how to monitor
smoking behavior, recognize triggers causing relapse, and help setting a
target quit date can be very helpful. Therapy can also be helpful in reduc-
ing overall stress and teaching relaxation techniques, as well as avoiding
trigger situations.
About one third of all quit attempts are accompanied by medication use.
Medications designed for smoking cessation double the quit rate.
Replacement therapies, including nicotine gum, spray, inhaler, or patch, are
easy to use and convenient and can be customized to patients’ dose needs.
Bupropion is effective for smoking cessation in both depressed and
non-depressed patients at a dose of 300 mg per day. At this dose, seizures
are rare, and main side effects include anxiety, insomnia, headache, and
dry mouth. Bupropion is an antidepressant with dopaminergic actions,
which decreases withdrawal symptoms as well as urges to use cigarettes.
Full effect may take 2–4 weeks. Varenicline is a partial agonist of the
nicotinic receptor. It is thought to exert its effects by reducing crav-
ing and blunting the pleasurable effects of cigarettes and other tobacco
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products. It is superior to other smoking cessation measures efficacy-wise

but carries some risk of mood instability and other adverse effects (poten-
tial worsening of suicidal thoughts). These adverse effects may be more
common in patients with comorbid psychiatric conditions. A typical treat-
ment course with Varenicline is 12–24 weeks. Varenicline can be com-
bined with bupropion but not nicotine replacement therapies.
Second-line pharmacological treatments include nortiptyline and
clonidine. For patients with comorbid psychotic illnesses, atypical antip-
sychotics, particularly clozapine, are helpful with nicotine dependence.
Novel and experimental treatments that might be available in the future
include the nicotine vaccine, nicotine receptor antagonists such as meca-
mylamine, glutamate antagonists, and opioid antagonists.
5. CAFFEINE
Caffeine is 1,3,7-trimethylxanthine, belonging to the methylxanthine class
of alkaloids. Other members of that family include theobromine (found in
chocolate) and theophylline. Caffeine is structurally similar to adenosine,
an endogenous neuromodulator. Caffeine is an antagonist of A2A and A1
receptors. Additionally, it increases dopamine release in the shell of the
nucleus accumbens (reward circuitry). Adenosine is beyond the scope of
this chapter; however, it is worth noting that it may have a role in agonist
treatment of cocaine and stimulant addictions.
Caffeine is metabolized by the liver cytochrome P450 1A2 and has a half-
life of 4–6 hrs. The rate of caffeine elimination can be increased by smoking
or concomitant use of medications such as cimetidine or fluvoxamine,
whereas oral contraceptives slow its metabolism. Caffeine metabolism is
also slower during the second and third trimesters of pregnancy. Caffeine
may inhibit the metabolism of clozapine and theophylline.
Caffeine is contained in beverages (e.g. coffee, tea, soft drinks, energy
drinks), foods (e.g. chocolate, coffee-flavored items), and medications (both
prescription and over-the-counter drugs, particularly weight loss products
and energy-touting compounds). Whereas coffee is the primary source of
caffeine among adults, soft drinks are the primary source of caffeine among
children and adolescents. Soft drink consumption has more than doubled
over the past 30 years and is a factor to be explored during health assessments.
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Because caffeine is widely used, its contribution to anxiety, sleep, sexual

disorders, and other health issues is challenging to diagnose. Caffeine
causes an intoxication syndrome that can be characterized by restlessness,
nervousness, excitement, insomnia, flushed face, dieresis, gastrointestinal
disturbance, muscle twitching, rambling flow of thought and speech,
tachycardia or cardiac arrhythmia, periods of inexhaustibility (subjective),
psychomotor agitation, and withdrawal symptoms. Dependence to the
effects of caffeine develops quickly. Physiological effects of caffeine
include bronchodilation, modest increases in blood pressure, increase in
gastric acid secretion, plasma epinephrine, norepinephrine, renin, and free
fatty acids. Peak plasma concentrations typically occur within 45–60 min
after ingestion. Subjective reactions to caffeine are dose dependent and
vary from individual differences in sensitivity and caffeine tolerance.
Polymorphisms in the adenosine A2A receptor gene are associated with
individual differences in caffeine consumption and the effects of caffeine
on sleep and anxiety. It is noteworthy that caffeine use, cigarette smoking,
and alcohol use may share a common genetic predisposing factor.
In most cases, pleasurable subjective effects are noted with low to
moderate doses (20–200 mg). Such positive effects can include well-being,
alertness, energy, improved concentration, and sociability. Decreases in
ratings of feeling sleepy or tired are also noted, although performance
ratings do not necessarily show an improvement that parallels subjective
feelings. High doses of caffeine (e.g. 400–800 mg) can produce anxiety,
nervousness, jitteriness, and insomnia.
Withdrawal symptoms, including sleepiness, headache, and decreased
ability to concentrate, among other symptoms, are very common, especially
on weekends for individuals who drink coffee in the work setting. Education
about the adverse effect of caffeine and recommendations to decrease caffeine
use to combat anxiety and insomnia symptoms should be part of symptomatic
management and precede medication managements of these conditions.
6. ALCOHOL
Alcohol use disorders are the most common substance use ailment in the
world, with a lifetime prevalence of dependence in 15%–20% of men and
10% of women. The WHO estimates that 3.8% of mortality worldwide
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can be attributed to alcohol use and its complications.22 Additionally,

10%–20% of the average physician’s patients are estimated to suffer from
alcohol use disorders. Behavioral and cognitive differences between
alcohol-dependent individuals and non-dependent individuals may start
appearing in the early 20s. Excessive alcohol consumption is related to
premature death and is a major contributor for cardiovascular diseases,
cirrhosis of the liver and cancer, as well as infectious diseases such as
HIV/AIDS and tuberculosis. Additionally, injuries, accidents, and sui-
cides are increased in the context of alcohol intake. Alcohol consumption
in women of childbearing age is concerning because of negative effects on
the fetus, including higher abortion rate, limb malformation, mental retar-
dation, and low birth weight. With heavy alcohol consumption during
pregnancy, fetal alcohol syndrome may result, including low weight, cen-
tral nervous system abnormalities, and facial malformations.4
Ethyl alcohol, or ethanol, is produced by the fermentation of yeast, sug-
ars, and starches. Ethanol is a simple molecule that distributes quickly into
highly perfused tissues, such as the brain, and is fat soluble. It is absorbed
throughout the lining of the GI tract, mostly in the small intestine, and is
metabolized by the enzymes alcohol dehydrogenase and aldehyde dehy-
drogenase. In addition to those enzymal metabolism processes, the micro-
somal ethanol oxidizing system (MEO) might be involved at higher blood
alcohol levels. Alcohol metabolism transforms ethanol into carbon dioxide
and water molecules. Metabolism follows zero-order kinetics.
A typical alcoholic drink consists of 0.6 ounces of pure ethanol, or 12
ounces of beer; 8 ounces of malt liquor; 5 ounces of wine; or 1.5 ounces
(a “shot”) of 80-proof distilled spirits or liquor (e.g. gin, rum, vodka, or
whiskey). Alcoholic drinks also contain congeners (e.g. tannins, flavo-
noids, and other substances that confer taste or smell to the beverage).
Touted benefits of alcoholic drinks, such as the cardiac benefits of red
wine, are due to the effect of its congeners, not ethanol. Peak blood
alcohol levels are reached about 30 min after ingestion.
6.1. Genetic contributions in alcohol use disorders

Vulnerability to alcohol use involves a heavy genetic component (up to
∼60% genetic). Increased risk of alcohol dependence is demonstrated in
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close relatives of alcoholic patients; monozygotic twins, as compared to

dizygotic twins; and offspring of alcoholics (even if adopted at birth).17
Certain genetically-influenced characteristics could predispose individu-
als to alcohol use or to a rapid progression from social use to severe
dependence. Conversely, genetic characteristics could protect an indi-
vidual from developing alcoholism, as in the case of aldehyde dehydro-
genase mutations prevalent in persons of Asian ethnicity. These
characteristics can help define intermediate phenotypes of alcohol use.
A higher risk for alcoholism is shown for individuals with impulsivity
and disinhibition, who typically display lower harm avoidance and
higher novelty seeking personality traits. Higher alcoholism risk is also
seen in individuals with low levels of response to alcohol, a feature
found in a significant percentage of sons and daughters of alcoholic
individuals. In comparison to their peers, users then need to consume
large amounts of alcohol to obtain the desired effect. Lowered sensitivity
is mediated by genetic variability in the serotonin gene system as well
as others.
6.2. Mechanism of action

Alcohol primarily affects the GABA system but also has effects on
serotonin, glutamate, and opioid systems. Ethanol causes a biphasic
effect with a rapid stimulatory phase, associated with an increase in
blood ethanol concentrations, followed by a depressant phase. Craving,
intoxication, and other phenomena associate with ethanol intake have
different mechanisms, which are beginning to be better understood, pav-
ing the road to targeted, effective treatments of alcoholism. As an exam-
ple, craving alcohol could be related to stress “obsessive craving,” and be
associated with serotonin dsyregulation, craving a reward, perhaps more
dopamine related or due to subclinical withdrawal symptoms, in which
case GABA and glutamate systems are more prominently activated.
Although this is an oversimplification of actual mechanisms, it is helpful
for the clinician to assess symptoms in light of this understanding, and it
is hoped that this will guide more sophisticated treatment choices in the
future.
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6.3. Identification in clinic settings

Identification of alcohol use disorders relies on the clinician having a high
index of suspicion with medical and psychiatric issues, because most
alcohol-dependent individuals do not develop delirium tremens or liver
cirrhosis and are able to maintain jobs and families, albeit at a high cost
to themselves and their relationships. Using screening instruments can be
helpful and time-effective in the context of emergency or routine care, and
some biological markers of heavy drinking can elicit suspicion. Most
markers are suggestive, but fairly non-specific for heavy alcohol use, with
the exception of carbohydrate-deficient-transferrin (CDT). Such biologi-
cal markers may include CDT, elevated liver function tests (gamma gluta-
myl transferase, GGT, elevated typically after binge drinking), elevated
MCV (> 91 µm3), other liver function tests: AST, ALT, or elevated uric
acid. Additionally, chronic heavy alcohol use can lead to severe cognitive
and memory deficits that may become irreversible, known as Wernicke–
Korsakoff syndrome, due to mammillary body degeneration. In its most
severe form, this can manifest as frank dementia, with confabulation as a
hallmark clinical sign. Thus, screening for alcohol use disorders in the
clinical setting should always include inquiring about memory
difficulties.
6.4. Alcohol withdrawal

Alcohol withdrawal syndrome is fairly common and represents a spec-
trum of disease manifesting in a variety of ways, including autonomic
hyperactivity (e.g. sweating, elevated pulse rate); increased hand tremor;
insomnia; nausea or vomiting; transient visual, tactile, or auditory hallu-
cinations or illusions; psychomotor agitation; anxiety; or grand mal sei-
zures. Withdrawal symptoms can last up to six months (protracted
withdrawal) in the form of insomnia or subclinical anxiety, dysphoria.
In its most severe form, alcohol withdrawal can become delirium tremens
(DTs), or agitated delirium, occurring in up to 5% of alcohol-dependent
individuals. Mortality from untreated DTs can reach up to 20%. Risk fac-
tors include advanced age, concomitant medical problems, and larger
amounts of alcohol/longer dependence duration.21 DTs can occur as late
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as 14 days after the last alcohol ingestion, although a more typical

presentation is seen about 48 hrs after last drink. Withdrawal seizures,
which typically occur in the context of a clear sensorium, peak at 24 hrs
after the last alcohol intake.
Treatment of alcohol withdrawal symptomatology must be individual-
ized, with some patients necessitating inpatient hospitalizations. A good
rule of thumb is to assume that an alcoholic individual is malnourished,
because alcohol could easily account for half of an alcohol-dependent
individual’s caloric intake. Administering thiamine (before intravenous
glucose) is essential to avoid Wernicke–Korsakoff syndrome, and treat-
ment should ideally include folate and multivitamins.
In acute management of alcohol withdrawal, benzodiazepines remain
the mainstay of treatment, with advantages including prevention of
seizures, minimal respiratory, cardiac depression, and ease of dosing.
Benzodiazepines reduce withdrawal symptoms by stabilizing the patient’s
GABA receptors and are all equally efficacious for seizure prophylaxis.
Earlier studies suggest that longer-acting benzodiazepines (chlordiaze-
poxide, diazepam) may be better than ones with a shorter-acting profile
(oxazepam, lorazepam) for seizure prophylaxis, but the latter, having no
active metabolites, and not being subject to hepatic oxidation are indicated
in elderly patients and those with liver impairment.
Anti-epileptics (carbamazepine, phenytoin, etc.) also have solid
research backing for treatment of alcohol withdrawal, particularly for
seizure prophylaxis, but do not present many advantages over benzodiaz-
epines.11 Anti-epileptics are particularly useful in patients with co-morbid
alcoholism and seizure disorders, although it should be noted that long-
term treatment of alcohol-related seizures is not recommended. Some
anti-epileptics (e.g. topiramate) may be useful in long-term alcohol treat-
ment, as detailed in the following text.
6.5. Long-term management of alcohol use disorders

Alcohol use disorders treatment includes detoxification: acute-treating
withdrawal, versus chronic rehabilitation: education, cognitive behav-
ioral approaches, increasing motivation, and help people rebuild
their lives. Behavioral treatments, such as Alcoholics Anonymous, or
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cognitive behavioral therapies, should continue for 6–12 months. The

current perspective on alcohol use disorders as a chronic, relapsing medi-
cal disorder allows for less confrontational, moralizing approaches. This
perspective also helps with defining treatment targets: although tolerance
and withdrawal are common, they are not necessarily the core symptoms
of alcoholism and may not be as prominent in relapse prevention as
craving alcohol and the inability to handle daily life stressors. Thus,
ideally, treatment should combine psychosocial measures and pharmaco-
logical ones. Treatment should also take into account comorbidities, such
as mood, anxiety, or psychotic disorders. If treatment is to incorporate
anti-craving medications, these can improve outcome by prolonging time
to relapse and decreasing the number of “heavy drinking days.”
6.5.1. Medications to prevent alcoholism relapse

Medications that can be used to prevent alcoholism relapse include the
following.
Disulfiram, which blocks aldehyde dehydrogenase, causes acetalde-
hyde accumulation, flushing, nausea, shortness of breath, tachycardia, and
headache. Disulfiram treatment is an example of aversive conditioning but
faces major issues with adherence and has scant data for efficacy.
Acamprosate, available since the 1980s, is a functional glutamate
antagonist normalizes the hyperglutamatergic state associated with
repeated heavy alcohol consumption and targets relief craving. Acamprosate
modulates glutamatergic activity via NMDA receptor modulation and may
have a role in helping alleviate alcohol withdrawal symptomatology. Most
common side effects include diarrhea, headache, dizziness, and pruritus.
Naltrexone is an opioid receptor antagonist that is relatively selective
for µ-opioid receptor at lower doses. By modulating mesolimbic dopa-
mine release, naltrexone blunts the acute positive reinforcing effects of
alcohol. Naltrexone is available orally for daily dosing and in an intramus-
cular form for monthly dosing, which can help circumvent adherence
issues. A mu-opioid receptor polymorphism affects the response to
naltrexone.
Other promising medications in the long-term treatment of alcohol
dependence include topiramate, quetiapine, and baclofen.
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7. CANNABIS
Cannabis, whose active psychoactive ingredient is ∆9-tetrahydrocannabinol
(THC), is extracted from the plant Cannabis sativa and has been used for
more than 8,000 years. The flowers have higher drug concentration than
the stem and leaves. Cannabis is typically smoked, although it can also be
used orally or vaporized. Most commonly, cannabis, consisting of a mix-
ture of dried leaves and flowers of the Cannabis sativa plant is smoked in
“joints,” which resemble cigarettes in size and shape. Joints can be
smoked alone, dipped in formaldehyde (then referred to as fry or water),
or adulterated with PCP. “Blunts” are larger than joints, are similar to
cigars in size, and have become more common in recent years. Other
preparations extracted from the cannabis plant include hashish (literally
meaning “grass” in Arabic), a paste-like substance consisting of the plant
resin, and higher in THC concentration than the leaf/flower mixture. Hash
oil, an evaporated solution of solvent-extracted cannabis from resin, is not
to be confused with hashish.
Cannabis is considered an illicit substance in most countries. However,
per WHO statistics, it remains the most widely used drug globally, with
use ranging from around 2% of the population aged 15–64 in Asia to 15%
in the Oceania region. Around 75 million European adults have used can-
nabis at least once in their life (lifetime prevalence), with an estimate of
around 23 million European adults having used it in the last year. In the
United States, cannabis is the fourth most commonly used drug in the
United States after caffeine, alcohol, and nicotine. Use by young people is
concerning, because cannabis is considered a gateway drug. Further, can-
nabis has an addictive potential, although most users consider it as a
benign drug, a deep-rooted misconception. More attention has been given
recently to the fact that cannabis use can lead to dependence and that can-
nabis withdrawal (manifested mostly by intense craving, insomnia, irrita-
bility, decreased appetite, aggression, and anger) is problematic and may
lead to repeated relapses. Additionally, cannabis can exacerbate psychotic
symptoms and may precipitate psychosis in susceptible individuals.12
Cannabis intoxication can manifest with mild euphoria, relaxation,
perceptual alterations, time distortion, intensification of ordinary experi-
ences, laughter, and sociability but may also carry negative consequences
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such as increased impulsivity, impaired short-term memory and attention,

difficulty sustaining mental activities, and impairment in motor skills,
reaction time, and motor coordination. Delirium has also been reported
upon intoxication. Cannabis use can also lead to postural hypotension,
light-headedness, and increased heart rate, and those acute effects may be
life-threatening in middle-aged adults with pre-existing heart disease.
THC is fat soluble, remaining in the body for up to 28 days. It is detect-
able in hair, urine, blood, or saliva testing. THC is a cannabinoid receptor
agonist. Cannabinoid receptors include CB1 (identified in 1990) and CB2
(identified in 1993). Those receptors are G-protein coupled receptors,
activated by the central nervous system’s endocannabinoids (e.g. ananda-
mide, 2-arachidonoyl glycerol). CB1 is mainly found at nerve terminals,
and CB2 is preferentially found on immune cells. The main function of
cannabinoid receptors is modulation of neurotransmitter release (CB1)
and regulation of cytokine release (CB2). Therapeutic effects of cannabi-
noids can include analgesia, anti-emesis, appetite stimulation (HIV/
AIDS), and appetite regulation. Cannabinoid receptors antagonists (e.g.
rimonabant, taranabant) have been tried for weight loss and smoking
cessation but are associated with significant adverse effects of mood
depression and worsening suicidal thoughts.
Cannabis joints include multiple other substances, akin to cigarettes,
and can have adverse reactions, including respiratory effects, symptoms of
chronic bronchitis, increase in risk of lung cancer, ovulation irregularities,
decreased sperm count, possible increase in risk of head and neck cancers,
and impairment in cell-mediated and humoral immunity.
No specific pharmacological treatments for cannabis dependence exist,
and general psychosocial treatments, such as 12-step programs, are the
most commonly used.
8. OPIOIDS
Opiates are naturally-occurring substances with potent psychoactive prop-
erties, widely used for analgesia and also in illicit fashion. Opium has
been used for more than 3,000 years, whereas morphine and codeine were
isolated in the 1940s. “Opioids” is an all-inclusive term referring to both
natural and synthetic substances in that family. The main therapeutic use
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for opioids remains management of chronic and severe pain, and oral
prescription opioids used for that purposes are frequently diverted for
illicit use. That aspect of opioid use is on the rise worldwide. However,
injecting opioids remains a significant health problem that figures dispro-
portionately among treatment admission in both the United States and
Europe.2 For instance, although estimates of lifetime heroin use in the
United States hovers around 1.5%, heroin is responsible for at least 15%
of drug-related admissions. Opioid users constitute a heterogeneous popu-
lation, from offspring of disadvantaged families with extensive childhood
trauma to well-off teenagers with no psychiatric comorbidities.
The problem of prescription drug abuse is getting worldwide attention
because of its rapid expansion. Adolescents appear to be the prime source
of that increase, because prescription drugs are widely available and can
be easily diverted from family and acquaintances. There is a concern that
prescription drugs might play the role as a gateway drug once held by
cannabis. Death rates caused by unintentional overdoses of painkillers
used for recreational purposes have increased at least fourfold since 2000.
Prescription drug abuse consists mostly of opioid pain killer use but also
includes muscle relaxants and tranquillizers such as benzodiazepines.
Multiple substance use is common, exacerbating medical complications
and withdrawal symptoms. Of particular risk is, of course, withdrawal in
the context of benzodiazepine/opioid use, as well as withdrawal from
muscle relaxants such as carisoprodol, which is metabolized into
mepobromate.
Heritability estimates for opioids dependence are ∼50%–60%, but that
component seems to represent specific vulnerability rather than a general
predisposition to drug use via the impulsivity/disinhibition endopheno-
type discussed in the alcohol use disorder subsection. Roughly 23% of
individuals who try opioids become dependent on them, as compared to
∼16% for cocaine. Users who ultimately become dependent on opioids are
more likely to report euphoria rather than dysphoria or mental clouding
upon use.
Opioids act on the endogenous opioids receptor system, a complex
modulatory system with far-reaching effects in the human body. The
system is activated by endogenous peptides, which are genetically distinct
families of precursors that can be processed to different peptides.
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Endogenous opioids can be the precursors for non-opioid substances as

well, such as melanocyte stimulating hormone and ACTH. Endogenous
opioid peptide families include pro-enkephalin, pro-dynorphin, pro-opio-
melanocortin (POMC), Endomorphin, and pro-OFQ/N à OFQ/N. There
are four subtypes of opioid receptors: µ, κ, δ, and OFQ/N (orphan-opioid-
like receptor); all have seven trans-membrane helices, coupled to
G-proteins. Variability among individuals in response to opioids can be
due to receptor dimerization, formation of receptor complexes, or genetic
differences in expression levels.
Opioid receptor agonists include heroin (diacetylmorphine), morphine,
hydromorphone, fentanyl, methadone, L-α-acetylmethadol (LAAM), and
oxycodone. Receptor antagonists include naloxone, naltrexone, and
nalmefene, whereas buprenophine is a partial agonist (that is, has agonist
action until effects reach a “ceiling”). There are also lesser known opioids
with mixed agonists/antagonist actions: pentazocine, nalbuphine, butor-
phanol, and dezocine. Subjective effects differ among opioids, and
“experienced” users can differentiate between opioids following blind
administration. Most clinically available drugs, particularly those abused,
are µ-receptor agonists, as agonism of the µ-opioid receptor produces
analgesia, altered mood, and decreased anxiety. It also produces cough
suppression, miosis, nausea, and vomiting and suppresses corticotropin
releasing factor and adrenocorticotropic hormone release. κ opioid
agonists are typically not abused because of dysphoria, rather than relaxa-
tion, produced by their intake. Longer-lasting effects of opioid abuse
include decreased responsiveness to pleasurable stimuli and increased
sensitivity to stress, two factors that place opioid-dependent individuals at
high risk for relapse.
Opioids cause QT prolongation, constipation, and, in the context of
intravenous use, cardiac or pulmonary emboli, and septicaemia (when
non-opioid substances are used accidentally). Increased mortality has
been reported, with deaths due to drug overdose, drug-related infections,
HIV/AIDS, and suicide.1
Opioid withdrawal, though not a life-threatening condition, poses a
difficult management quandary and makes abstinence difficult for most
users. Withdrawal occurs upon cessation of (or reduction in) opioid use
that has been heavy and prolonged (several weeks or longer) or in the case
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of inadvertent administration of an opioid antagonist after a period of

opioid use. Withdrawal can be characterized by dysphoric mood, nausea
or vomiting, muscle aches, lacrimation or rhinorrhea, pupillary dilation,
piloerection, or sweating, diarrhoea, yawning, fever, or insomnia.
Symptoms can occur minutes to days following opioid use, and detoxifi-
cation consists primarily of symptom management. The widely used
expression “kicking the habit” came to be used because of the leg jerking
movement frequently observed during opioid withdrawal, which is due to
spinal hypereflexia. Severity of withdrawal can be easily assessed during
brief clinical examinations by monitoring for signs such as dilated pupils,
lacrimation, rhinorrhea, or piloerection.
In addition to, or in parallel with, detoxification, agonist therapies for
opioids are a viable modality. Agonist therapy, also called maintenance,
has a twofold purpose: Administering a legal, carefully dosed, long-acting
opioid in a structured setting blocks withdrawal symptoms, decreases
craving and allows patients to continue with a normal life, avoiding legal
problems. Maintenance treatments are meant to be long term, or unlimited
in time, and are administered in specialized clinics (in the case of metha-
done) versus outpatient physician offices (e.g. buprenorphine). Methadone
maintenance treatment has been in existence since 1965 with tremendous
success, although efforts to use LAAM have failed because of QT prolon-
gation leading to torsades de pointe. Buprenorphine represents an excel-
lent alternative and has been gaining in popularity. However, the long-term
prospect of agonist therapy as a concept is a deterrent to some individuals
and policy-makers.
9. STIMULANTS
Stimulants represent a broad category including cocaine, methampheta-
mine (METH), methcathinone, phentermine, methylenedioxyamphetamine
(MDA), 3,4-methylenedioxymethamphetamine (MDMA), and methylen-
edioxyethylamphetamine (MDEA), although the latter three are often
considered under the “club drug” category.
Amphetamine (phenylisopropylamine) was first synthesized in
Germany in 1887, and methamphetamine was manufactured in Japan in
1918. The early twentieth century saw multiple clinical uses for
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amphetamines, including treatment for migraine, alcoholism, epilepsy,

nasal congestion, asthma, and hay fever. At the current time, ampheta-
mines continue to be the mainstay of pharmacological treatment for nar-
colepsy and attention deficit hyperactivity disorder (ADHD). Lifetime
prevalence of the use of amphetamines in Europe varies between countries
from 0%–12.3% of all adults (15–64 years), and about 10.4 million
Americans age 12 and older (4.3% of the population) had tried METH at
least once in their lifetimes.19
Stimulants cause their actions by releasing monoamines, such as dopa-
mine (DA) and norepinephrine (NE), from dopaminergic and noradrener-
gic nerve endings, leading to the shared behavioral and psychological
effects noted in users.16 However, the precise mechanism of action differs
according to the substance use. Thus, while cocaine blocks the reuptake
of the above-mentioned neurotransmitters by the dopamine transporter,
the norepinephrine transporter, and the serotonin transporter, ampheta-
mines can also reverse the direction of transport of dopamine and, at high
doses, norepinephrine.
9.1. Cocaine
Cocaine, also a potent stimulant, is the product of the leaves of the plant
Erythroxylon coca, indigenous to the high mountain ranges of South
America. Cocaine can be smoked, chewed, or injected. Coca leaves have
been chewed for at least 15 centuries in countries such as Peru. The tradi-
tional practice of chewing coca leaves is associated with addictive issues
less frequently than other modes of administration. This is thought to be
due to the lower bioavailability of oral cocaine. Use of smoked or intrave-
nous forms of cocaine is associated with faster progression to the more
serious cocaine-related problems characteristic of cocaine dependence.
Crack cocaine is inexpensive, ready-to-smoke cocaine alkaloid, which
leads to a powerful “high” because of its rapid onset of action. As with
amphetamines, cocaine was also touted as an effective treatment for
multiple diseases until its addictive potential was emphasized.
Stimulants can be smoked or injected to achieve peak plasma concen-
trations more quickly than oral ingestion. They are popular because of
their subjective effects, including euphoria; an enhanced sense of
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well-being, power, and confidence; decreased appetite; decreased need for

sleep; and increased energy and concentration. Stimulant intoxication can
also cause hypervigilance, pupillary dilation, perspiration, chills, nausea
or vomiting, and psychomotor agitation or retardation.
Stimulant use is associated with the undesirable effect of paranoia and
even frank psychosis. The duration of cocaine- or amphetamine-induced
paranoia is generally brief (minutes to hours) but is reported by up to
50%–70% of users. Delusions of being the target of police or legal pursuit,
or of persecution in general, may persist beyond peak plasma stimulant
levels and last hours, and even 1–2 days in the case of high-dose metham-
phetamine. These can be accompanied by perceptual disturbances and
misinterpretations of existing stimuli. However, bizarre delusions and
frank hallucinations are rare in the context of stimulant use and may
indicate the presence of an underlying psychotic disorder.
Stimulants, being potent sympathomimetic drugs, cause adrenergic
stimulation and lead to vasoconstriction, increased heart rate, and elevated
blood pressure. This, in turn, increases the risk of angina pectoris and even
myocardial infarction. Strokes or aortic dissection, as well as damage to
other end organs, including the brain, kidneys, or intestines, can result
from vasoconstriction. Decreased blood flow to the nasal mucosa fre-
quently causes nasal symptoms like rhinorrhea and nosebleeds, frequently
reported with cocaine snorting. Grand mal seizures are common with
cocaine overdose and may occur with routine cocaine use.
Problematic use of stimulants remains a challenge to treatment teams,3
because rates of progression to full dependence are faster with stimulants
than with cannabis or alcohol. Further, rates of relapse are very high. The
success of psychosocial measures is reasonable, but limited. A promising
option in the treatment of stimulant dependence, particularly cocaine, is
the use of agonist substitution therapy,6 akin to methadone therapy in
opioid addiction.
9.2. Inhalants
As the name indicates, inhalants are volatile solvents inhaled through the
nose or mouth with the purpose of intoxication. The process can be
referred to as sniffing, huffing, glading, dusting, bagging, or other names.
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Peak age of use is 14–15 years of age, although use has been reported in
children as young as five years old. Inhalants are readily-available con-
sumer products, such as whipped cream cans, deodorants, keyboard clean-
ers, or “poppers” (amyl nitrites) diverted from medical practices. They are
broadly classified into three categories: (1) Volatile alkyl nitrites;
(2) Volatile solvents, fuels; and (3) nitrous oxide. Inhalant use has a high
comorbidity with mood, anxiety, and personality disorders and is associ-
ated with impoverished living conditions, rurality and isolation, delin-
quency, criminal behavior, incarceration, family disorganization, conflict,
a history of abuse and violence, and other drug use, including intravenous
drug use.10
The high provided by inhalants consists of a sense of euphoria and
inebriation, with minimal hangover symptoms. Because inhalants are
readily absorbed by the lungs, their effects are immediate and brief. Rush,
light-headedness, and disinhibition are reported but with a risk of diplo-
pia, ataxia, dizziness, disorientation, slurred speech, and visual hallucina-
tions. Nausea, vomiting, diarrhea, abdominal cramps, and wheezing are
among the adverse effects related to inhalant use. “Sudden sniffing death
syndrome” is the leading cause of inhalant-related mortality (∼56%), but
other medical complications (e.g. arrhythmias, suffocation, aspiration,
renal toxicity, and trauma) can also occur. Most feared is long-term,
persisting neurological damage (“toluene dementia”) and brainstem dys-
function, neuropathy, that occur with sustained use, because most inhal-
ants are lipophilic and will be stored in myelin, gradually releasing over
time and exerting toxic effects. Inhalation of nitrites cause vasodilation
and floating, increased tactile sensations, thus leading to enhanced sexual
feelings, penile engorgement, and anal sphincter relaxation, albeit with a
risk of hypotension and syncope. The demographics of nitrite use differ
somewhat from the other two classes of inhalants. Methhemoglobinemia
is a possible adverse effect of nitrite use and can lead to cyanosis and
lethargy.
Mucous membrane irritation, “huffer’s rash,” can be noted sometimes
on physical examination. As with other drug use, inhalant use can lead to
exacerbation of existing psychological, family, and school problems.
Standard psychosocial treatments for substance use disorders are useful
for treatment, although no specific treatment modality has been identified
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to be of help with inhalant dependence. Addressing underlying issues with

family or individual psychotherapy or pharmacological treatment might
also be of value for youths with other psychiatric comorbidities.
10. HALLUCINOGENS
Hallucinogens are agents that cause alterations in perception, cognition,
and mood in the presence of a clear sensorium. They are traditionally
divided into three groups: indolealkylamines (psilocybin, DMT), ergo-
lines (LSD), and phenethylamines (ecstasy, mescaline). They all act via
serotonin system activation. Contrary to common belief that hallucino-
gens are non-addictive, physiological tolerance develops easily.13
Acute effects of hallucinogen use include psychological symptoms,
such as visual, auditory, olfactory, gustatory, and tactile, and somatic illu-
sions, hallucinations, and synesthesias (combinations of two sensory
modalities). In general, hallucinogens intensify the mood and exaggerate
the emotional state existing at the time of drug ingestion, unlike other
drugs, such as stimulants or alcohol, whose effects are more predictable.
The possibility of negative “trips” could explain the lack of popularity of
hallucinogens as compared to other substances. Adverse physical effects
include nausea, vomiting, autonomic activation, dilated pupils, hyperther-
mia, incoordination, and possible liver enzyme elevation.
Acute hallucinogen intoxication can be a highly aversive experience
with paranoia, confusion, and some dissociative symptoms (e.g. deperson-
alization, derealization) that last a few days following ingestion. It is
noteworthy that hallucinogens (e.g. LSD) can induce persistent psychosis
(0.8%–4% prevalence) that resembles schizophrenia and has been
reported to last up to a month following use.
11. CLUB DRUGS

As the name suggests, club drugs are thought to be mostly used in club/
party or rave social settings, although that is not always accurate. They
may include designer drugs such as 2C-B, 2C-I, 2C-T (phenethylamine),
and DMT (dimethyltryptamine). Some classification of club drugs divide
them by effect into categories like “dissociatives,” hallucinogens, and
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“deliriants”; however, most club drugs are usually substances with mixed
pharmacological profiles, as in the case of ecstasy, which has both
stimulant and hallucinogen properties, or phencyclidine (PCP). Club drugs
represent a constantly changing field, and it is thought that successful club
drugs may become mainstream.18 Ecstasy, an amphetamine derivative with
both stimulant and hallucinogenic properties, is a classical club drug
example. Ecstasy use can cause severe acute adverse effects such as hyper-
thermia, hyponatremia, bruxism, rhabdomyolysis, and seizures, but those
risks are not widely recognized. Long-term use could exacerbate depres-
sive and anxiety symptoms insusceptible individuals. Additionally, there is
a possibility of ecstasy-induced neurotoxicity to serotonin neurons that has
been proven in animal studies and now is being studied in human users.
Club drugs include dissociative anesthetics such as ketamine, which is
typically diverted from veterinary clinics, and gamma hydroxybutyrate
(GHB), a naturally occurring, short-chain fatty acid in the CNS with high
addictive potential. GHB, as well as flunitrazepam, have been used as
“date rape” drugs.
Risks of club drugs include the fact that they are poorly characterized
and often used in a pattern of polysubstance consumption, which is par-
ticularly concerning because toxic effects can be exacerbated by certain
mixtures. A typical example would be the possibility of neurotoxicity fol-
lowing ecstasy use, which can be amplified by amphetamines, alcohol, or
cannabis.5 Another concern is the popular perception that club drugs are
not addictive, whereas in fact evidence exists concerning the potential of
developing dependence with GHB, ecstasy, and others.
12. NEW DRUGS

Designer drugs are synthetic substances created with the purpose of
enhancing the pharmalogical properties of already existing ones. More
than 90 new substances have been reported through the EMCDDA early-
warning system since its establishment in 1997, with most new synthetic
substances being characterized by stimulant properties. Per EMCDDA,
designer drugs are usually produced in waves, “based on fentanyl in the
1980s; to ring-substituted phenethylamines in the late 1980s and
tryptamines in 1990s; to piperazines and cathinone derivatives in the
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2000s.” JWH-018, a synthetic cannabinoid, was the first ever to be

reported. JWH-018 is more potent than THC and may be an active com-
ponent in what is known as “spice,” a mixture widely sold on the Internet
and consisting of at least three synthetic cannabinoids.
Plant-derived products are typically not under monitoring by the Food
and Drug Administration in the United States or its counterparts in
EU-member countries but are notable nonetheless, because they can have
dangerous drug–drug interactions when mixed with other substances and
might become regulated if harm is proven, as in the case of ecstasy in the
1980s and of “bath salts”9 more recently. Among newer drugs, two have
gained notoriety: synthetic cannabinoids and “bath salts.” JWH-018, a
synthetic cannabinoid, was the first reported though a host of other syn-
thetic cannabinoids are now known. They are sold in incense-like mix-
tures that are smoked. More potent than THC, these compounds can cause
a wide range of effects including triggering psychotic symptoms in users.
“Bath salts” refer to stimulant (cathinone)15 derivatives, chemically
related to amphetamines. Bath salts are not detectable on standard urine
drug tests. They can be smoked, injected, or snorted. Users can develop
severe, schizophrenic-like psychosis. The base compounds in bath salts,
e.g. mephedrone, are now regulated substances. Below are other plant-
based compounds that can be of some concern though their use has not
attained epidemic proportions yet.
(i) Kava (Piper methysticum) is used for anti-anxiety effects but is of

concern because of potential liver damage. Active priniciple of kava
are kavalactones.
(ii) Khat, derived from Catha edulis, has mild stimulant properties due
to its active components, cathinone and cathin. Those are chemically
related to amphetamine. Khat is regulated in several countries.
(iii) Kratom (Mitragyna speciosa), also has mild stimulant properties at
low doses but appears to have opioid-like effects at higher doses.
(iv) Salvia divinorum, a perennial herb native to southern Mexico, has
hallucinogenic properties. The main active chemical in Salvia, salvi-
norin-A, is a potent kappa opioid receptor agonist. Salvia divinorum
is the only known hallucinogenic drug whose mechanism of action is
not serotonin based.
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(v) Hawaiian baby woodrose (Argyreia nervosa) seeds contain d-lysergic

acid amide (LSA, also known as d-lysergamide), which is a sub-
stance closely related to LSD. LSA can produce mild hallucinogenic
effects and is considered a controlled substance in Ireland and the
United Kingdom.
13. TREATMENT CONSIDERATIONS IN SUBSTANCE

USE DISORDERS
Substance use results in associative learning between environmental cues
and the expected reward of drug use. Substance use also occurs frequently
in the presence of a narrow behavioral repertoire and an inability to deal
with daily stressors. Further, substance use sometimes masks, yet wors-
ens, psychiatric symptomatology such as flashbacks, mood dysregulation,
or psychotic symptoms.
Most treatment modalities for SUD rely on psychosocial interventions
that aim to help the substance dependent individual refashion his or her
life and learn how to deal with the temptations of drug use without yield-
ing to them. One of the most popular frameworks, 12-step programs, is
based on a book, Alcoholics Anonymous: The Story of How More Than
One Hundred Men Have Recovered From Alcoholism. Twelve-step pro-
grams apply to alcohol use disorders but also to cocaine and narcotics, as
well as non-substance addictions, such as pathological gambling or even
excessive Internet use and gaming. The guiding principles of 12-step pro-
grams emphasize resisting compulsions to use substances, regaining con-
trol of one’s life, and making amends to victims of that problematic use.
Individuals are paired with sponsors who can provide round-the-clock
support, and sharing experiences is encouraged within group meetings.
Other therapeutic modalities useful for substance use disorders focus on
the neurobiological basis for those disorders and often view addictive dis-
orders as behaviors to be changed. Thus, modalities that are useful include
cognitive-behavioural therapy (CBT), where the role of thoughts (cogni-
tion) and feelings is emphasized with respect to choices individuals make
(behaviors). The CBT seeks to attenuate or eliminate certain thinking pat-
terns (cognitive distortions) that may perpetuate negative decision making
and other behaviors related to the SUD. Motivational interviewing, a
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client-centered technique, focuses on exploring ambivalence an individual

might have about abstinence. By exploring this ambivalence, the therapist
tries to help resolve resistance to change and bring about behavioral modi-
fication. Motivational interviewing is more focused and goal-directed than
other therapies. Contingency management (based on behavioral therapy
and applied behavior analysis), is effective for substance use disorders. In
contingency management abstinence from drugs is “rewarded” via
voucher programs or other incentives.
Pharmacological treatment of SUD is still limited in use as compared
to psychosocial treatments. As detailed in the alcohol, stimulant, and
opioid sections, pharmacological treatments either consist of agonist sub-
stitution, as in the case of methadone or buprenorphine for opioid depend-
ence and the promising prospect of stimulants for cocaine dependence, or
anti-craving medications, such as naltrexone or Acamprosate for alcohol
dependence. In general, pharmacological treatments have small to moder-
ate effect sizes and are best used in conjunction with therapy or other
psychosocial interventions.
14. KEY POINTS

• SUD are serious illnesses related directly to the use of licit or illicit
substances that can manifest as cognitive, behavioral, or mental dis-
turbances and lead to legal, medical, and interpersonal difficulties.
• Substance use disorders represent chronic, relapsing brain disorders
characterized by compulsive drug taking, negative emotional states in
the absence of drug consumption, and loss of control over drug
intake.
• All drugs of abuse and alcohol activate the brain’s reward circuitry,
a phenomenon that is dopamine-mediated. Acute mechanisms of
action may differ.
• Other neurotransmitters are involved in drug use as well. Acute and
chronic use patterns lead to different neuro-adaptations within the
central nervous system.
• Alcohol can lead to severe fetal malformations, cognitive deficits, and
potentially dementia in heavy users.
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• Alcohol withdrawal, or delirium tremens, can be a life-threatening

clinical entity and needs prophylaxis and aggressive treatment.
• Cannabis is one of the most commonly used substances in the world,
and heavy cannabis use is associated with severe psychosocial
impairment and a high risk of exacerbating or triggering psychosis in
susceptible individuals.
• Stimulant dependence, cocaine and amphetamines, presents with
myriad of problems — cardiac, neurological, paranoia, and even frank
psychosis — that outlast initial drug use.
• Opioid use is on the rise, with several distinct patterns of use corre-
sponding to different subgroups of drug users e.g. intravenous heroin
drug users versus young users of oral prescription opioids diverted
from medical practice.
• Opioid withdrawal is not life threatening but may require detoxifica-
tion in an inpatient setting.
• Club drugs are poorly regulated substances with mixed pharmacologi-
cal profiles and potentially severe adverse consequences.
• Inhalant dependence can lead to severe persisting neurological
dysfunction, including the possibility of dementia.
15. CASE STUDIES

15.1. A complaint of anxiety
A 23-year-old male presents to a clinic complaining of anxiety. He states
that he needs help for his “nerves,” because he gets very anxious before
exams and has failed several times even when well prepared. He also feels
anxious in social situations and has had difficulty making friends and dating.
No medical, psychiatric, or other alcohol/drug use history is elicited. His
family history is significant for alcoholism in his father and uncle. He is
started on an antidepressant and clonazepam at a low dose, with explana-
tions about the addictive potential of benzodiazepines. Within a week, he
complains that his antidepressant causes too many side effects and stops it
but remains on clonazepam. A month later, he requests some opioid pain-
killers because of back pain from a previous injury. Within a year, despite
marginally regular attendance in psychotherapy, he has “failed” trials of
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five antidepressants, never having reached a full therapeutic duration on

any, and insisted that his clonazepam dose be increased. Fourteen months
after starting treatment, he calls and requests a new prescription about two
weeks before renewal of his medications is due, pretexting that he lost his
script accidentally. A month later, he decides to drop out of college and
stop therapy. For the next two months, he comes to the clinic once a month
for medications only and refuses further trials of antidepressants. This is
followed by a frantic phone call requesting further medications. During
that call, the patient has slurred speech and rambling, illogical thoughts.
He had escalated his intake of clonazepam but, more important, has been
drinking alcohol daily and using cocaine and painkillers. Additionally, he
was arrested for driving under the influence about six months prior, and
that was the reason he dropped out of college.
15.2. An overdose
A 24-year-old female with no formal past psychiatric history is admitted
to an inpatient psychiatric unit after an overdose on several over-the-
counter medications (vitamins and other supplements). The overdose
occurred one day after the death of her mother. A few hours after admis-
sion to the psychiatric unit, she appeared increasingly anxious, respond-
ing to internal stimuli, and reporting vivid visual hallucinations. About
20 hrs into her hospital course, she was delirious, with waxing and wan-
ing awareness. She was not oriented to person, place, or time and was
not able to hold a coherent conversation. The patient was transferred to
the medical wing, where she received intravenous hydration. She was
found to have a potassium of 2.8, with other electrolytes being within
normal limits. She had tachycardia (110 beats per minute) but normal
temperature and blood pressure. She was combative and needed to be
physically restrained. Emergency medications were also administered.
Within 5 hrs, the patient had received three doses of haloperidol (total
10 mg) and lorazepam (total 4 mg). She remained delirious and was
writhing in bed. Another dose of lorazepam (6 mg) was given, after
which the patient improved noticeably, becoming oriented to person and
place (but not to date or time), and was able to say that she took 10
tablets of alprazolam “to forget about it all.” She further reported that for
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the past two months, she had used alprazolam frequently, in doses up
to 16 mg per day. She was diagnosed with benzodiazepine withdrawal/
delirium tremens.
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Chapter 12
Cognitive Disorders
Alana Iglewicz, Ipsit V. Vahia and Dilip V. Jeste
1. INTRODUCTION
Cognitive domains include memory, problem solving, judgment, lan-
guage, orientation, and performance of actions (praxis). Cognitive disor-
ders, which include dementia and delirium, are defined by dysfunction in
one or more of these domains. In the ICD-10, dementia and delirium are
categorized as organic, including symptomatic, mental disorders. They
result from etiologies that lead to cerebral dysfunction, such as brain
injury or cerebral disease. This terminology can occasionally be confus-
ing, however, because multiple etiologies exist for both delirium and
dementia. In this chapter, we first describe delirium and then the dementia
syndromes. Although the chapter is organized on the basis of the diagnos-
tic classification of ICD-10, we describe clinical entities that are well
recognized in the literature but not currently included in either the ICD-10
or the most recent edition of the Diagnostic and Statistical Manual
(DSM-IV-TR).
2. DELIRIUM
In ICD-10 delirium is described as an etiologically non-specific syndrome
characterized by disturbances of consciousness and attention, perception,
thinking, memory, psychomotor behavior, emotion, and the sleep–wake
291
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292 A. Iglewicz, I. V. Vahia and D. V. Jeste
cycle. It is considered possible at any age but is most common after the
age of 60 years. The ICD-10 also describes delirium as transient and of
fluctuating intensity, with recovery frequently observed within four weeks
or less. Yet, delirium is known to persist for longer periods in some cases
of chronic medical conditions, such as chronic liver disease, carcinoma,
or sub-acute bacterial endocarditis. The ICD-10 further notes that delir-
ium may not be diagnosed if the clinical symptoms are a direct result of
abuse of psychoactive substances. Delirium can, however, be superim-
posed on dementia and several other general medical conditions.
2.1. Epidemiology
The point prevalence of delirium in the general population is 0.4% for
people aged 18 years and older, whereas it is 1.1% for people aged
55 years and older. The rates of delirium are much higher for medically ill
individuals. Delirium is seen in approximately 10%–30% of hospitalized
medically ill patients. Higher rates are seen in intensive care unit patients,
patients recovering from surgical repair of hip fractures, and especially in
postcardiotomy patients. In one study conducted in a sample of termi-
nally-ill persons receiving palliative care, delirium was found in 80% of
the sample, suggesting the possibility of a subtype of delirium called
“terminal delirium.”5
Delirium is a common disorder, and the rates of delirium increase
with age. Delirium is found in 14%–56% of hospitalized older adults,
30% of older adults presenting to the emergency department, and up to
80% of older adults in intensive care units. Delirium is present in over
50% of older adults in skilled nursing facilities or post-acute care
settings.
2.2. Etiology
The major causes of delirium are systemic disease, central nervous system
disease, intoxication or withdrawal from substances, and medication side
effects and/or interactions. The exact underlying mechanism of delirium
is not well elucidated but is thought to be multi-factorial. Pathogenic
mechanisms include inflammation, chronic stress, and neurotransmission
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Cognitive Disorders 293
imbalances. Dysfunction in the cholinergic system is frequently consid-

ered. All medications, especially any newly prescribed medications,
should be considered as possible etiologic factors to any delirium.2,13
Notably, anticholinergic medications (e.g. tricyclic antidepressants,
diphenhydramine, benztropine, and low-potency antipsychotics), medica-
tions with histamine-2 blockade (e.g. ranitidine, cimetidine), and medica-
tions with narcotic properties are especially likely to cause delirium.
Risk factors are numerous and include cognitive impairment, dementia,
underlying illness, number and severity of comorbid conditions, older age,
dehydration, sensory impairments, malnutrition, male gender, functional
dependence, and alcohol abuse or dependence. An underlying dementia
increases the risk of developing delirium two- to five-fold. In addition to
medications, recent surgery, infections (especially urinary tract infections
in the elderly), metabolic abnormalities, anemia, pain, admission to an
intensive care unit, primary neurological disease, and immobility are also
common precipitating factors for delirium.
2.3. Phenomenology
Core features of delirium include acute or sub-acute onset, alteration in
consciousness and attention, and fluctuating course. Perceptual distur-
bances, disorganization of thought processes, sleep–wake cycle disrup-
tion, emotional lability, and psychomotor abnormalities are frequently
observed clinical features of delirium. Mood alterations range from subtle
irritability to severe anxiety, depression, or even euphoria. Psychotic
symptoms can also occur and include delusions, visual hallucinations
(e.g. lilliputian, in which people, animals, or things seem smaller than
they would in real life), and visual illusions. Restlessness and fearfulness
can occur as prodromal symptoms to a delirium.8 Diffuse slowing of back-
ground activity is typically seen on the electroencephalogram in
delirium.
Delirium can be categorized as hyperactive, hypoactive, or mixed. In the
hyperactive form, agitation, perceptual disturbances, and hyper-vigilance
are common. In contrast, lethargy and psychomotor retardation predomi-
nate in the hypoactive sub-type. Hypoactive delirium is more common in
older adults, often unrecognized or misdiagnosed, and associated with a
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worse prognosis than the hyperactive form. In the mixed subtype, patients
fluctuate between the hyperactive and hypoactive presentations of
delirium.
It is relatively important to differentiate a delirium from a dementia.
Dementias tend to have a gradual onset, extended duration, non-fluctuating
course (except in Lewy Body Dementia), and comparatively intact atten-
tion. In contrast, the onset of a delirium is usually sudden, the duration
often (but not always) brief, the course fluctuating, and the attention
impaired. Although delirium was traditionally thought to be brief in
nature, newer studies demonstrate that symptoms of delirium may persist
for months to years.
2.4. Treatments
The primary goal of treating a delirium is to treat the underlying contribut-
ing etiology/etiologies.1 This involves discontinuing offending medica-
tions, addressing underlying infections, and reversing any metabolic
abnormalities. Psychiatrists often are involved in managing the neuropsy-
chiatric symptoms of the delirium while the underlying causes are being
addressed. Non-pharmacologic approaches to managing a delirium should
be initiated before pharmacologic intervention. These include limiting the
number of different people caring for an individual, encouraging family
members to visit, reorientation, minimizing use of physical restraints, and
correcting sensory deficits. Ensuring adequate exposure to daylight during
the day and a quiet, dark environment at night in addition to ensuring that
a clock, calendar, and familiar decorations are visible to the patient can
also help with the management of a delirium.1
Agitation, psychosis, and insomnia often require pharmacologic inter-
ventions. When pharmacologic agents are used, they should be used at the
lowest doses and for the shortest period of time required. Ironically, the
drugs used to help manage a delirium may actually contribute to it by
worsening confusion. Neuroleptics are the first-line of medication ther-
apy, despite their numerous potential side effects, including extrapyrami-
dal symptoms (especially tardive dyskinesia with typical antipsychotics),
weight gain, metabolic symptoms, orthostatic hypotension, and an
increased risk for cerebrovascular events and mortality in individuals with
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dementia. Of the neuroleptics, haloperidol has the most data supporting its
use for addressing the agitation associated with delirium. Benzodiazepines
are the treatment of choice for managing alcohol withdrawal but should
be avoided when possible in the management of other forms of delirium
in light of their sedative and confusion-inducing effects. When benzodiaz-
epines are used to address the insomnia associated with delirium, short- or
intermediate-acting ones (e.g. lorazepam) should be chosen.1
2.5. Prognostic factors

Delirium carries a poor prognosis and is associated with a high mortality
rate. Even though the definition of delirium implies reversibility, approxi-
mately 30% of patients diagnosed with a delirium are expected to die
within three months, and the one-year mortality rate is as high as 50%.
These rates are worse for older adults who experience delirium. Elderly
patients diagnosed with a delirium during a hospitalization carry a high
mortality rate (up to 75%) during that hospitalization. Patients with delir-
ium are at increased risk for developing cognitive and functional decline,
even after their delirium resolves. Because delirium is such a poor prog-
nostic sign, clinicians should be vigilant in preventing, diagnosing, and
treating this important condition.
3. DEMENTIAS
According to ICD-10, dementia is a progressive syndrome secondary to
disease of the brain in which there is a disturbance of multiple higher corti-
cal functions (i.e. memory, thinking, orientation, comprehension, lan-
guage, judgment, calculation). Consciousness remains unaffected.
Problems with social interactions, emotional control, and motivation often
accompany the cognitive impairments in dementia. According to ICD-10,
there are three broad categories of dementias — Alzheimer’s disease,
Vascular dementia (including multi-infarct dementia), and Other demen-
tias. The term ‘Other dementias’ refers to symptoms of dementia seen in
conjunction with other specific neuropsychiatric conditions. The ICD-10
specifically recognizes dementia in Pick’s disease, dementia in Creutzfeldt–
Jakob disease, dementia in Huntington’s disease, dementia in Parkinson’s
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disease (PD), and dementia in HIV disease. In the past decade, much
attention has been given in the scientific literature to the continuum from
normal aging to dementia, in terms of loss of cognitive function. While not
recognized as distinct entities by either ICD-10 or DSM-IV-TR, there is a
large body of literature addressing Age-Associated Memory Impairment
(AAMI) and Mild Cognitive Impairment (MCI). Here we briefly summa-
rize AAMI and MCI and then we will discuss in more detail Alzheimer’s
disease, vascular dementia, and the other forms of dementia.2,13
3.1. Age-associated memory impairment

Certain cognitive changes are normal for aging. Oftentimes, as people
age, they report difficulty remembering appointments or names. It is also
common for older adults to report difficulty solving complex problems.
Although older adults may require more time and practice to learn new
material, the overall ability to learn new material is maintained with nor-
mal aging. When older adults present with these complaints but have no
functional impairment and the cognitive impairment is not attributable to
a mental or neurological disorder, they may be considered as meeting
criteria for AAMI. In general, however, the definition and criteria for
AAMI have not gained widespread acceptance, and this term is unlikely
to be included in forthcoming editions of the ICD or the DSM.
3.2. Mild cognitive impairment

The MCI is a term used to describe a heterogeneous group of individuals
who have modest cognitive symptoms but no clear functional impairment.
MCI is often conceived of as a transitional state between normal aging and
dementia. However, not all individuals with MCI will progress to develop
dementia. Approximately one third of individuals who meet criteria for
MCI will remain stable, one third will return to normal, and one third will
develop dementia. Overall, the degree of cognitive impairment in MCI is
more severe than that for AAMI. MCI encompasses individuals who may
demonstrate cognitive deficits resulting from a variety of medical or neu-
rological conditions (e.g. traumatic brain injury, HIV, substance-use-
related brain disorders, diabetes, and early/mild stages of cerebrovascular
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disease or neurodegenerative disorders like Alzheimer’s disease). MCI is

an important entity for the purposes of research. It is considered a focus
of early intervention, which may enable the use of treatments that are not
effective at more severe levels of impairment. Potentially, research on
MCI can lead to the development of preventative or progression-slowing
interventions for Alzheimer’s disease. For the forthcoming DSM-5, a
change in the nomenclature has been proposed. Under the new nomencla-
ture, MCI will be termed as Minor Neurocognitive Disorder (and demen-
tia will be termed Major Neurocognitive Disorder).6 The criteria, as
currently proposed, define this condition as minor levels of decline in
memory, language, cognitive motor activity, naming/recognition, or
executive function, involving greater difficulty performing these tasks or
the use of compensatory strategies. The criteria also require presence of
mild deficits on objective cognitive assessment. In addition, the criteria
require that symptoms are not severe enough to interfere with Instrumental
Activities of Daily Living, do not occur exclusively in the context of a
delirium, and are not wholly or primarily attributable to another major
psychiatric disorder.
There is a lack of consensus on treatment recommendations for MCI.4
Pharmacological interventions are not indicated unless there is clear
evidence of progression to Alzheimer’s disease or other forms of demen-
tia. Management centers around close monitoring of cognitive status,
encouragement of lifestyle choices that promote healthier living (including
diet and physical activity interventions), and treatment of vascular risk
factors.
4. DEMENTIA DUE TO ALZHEIMER’S DISEASE

4.1. Epidemiology
Of the different types of dementia described in the following text,
Alzheimer’s disease is the most common type of dementia in most coun-
tries, accounting for 50%–75% of cases of dementia. However, exceptions
exist. For example, vascular dementia is more common in Japan. In India,
there is a lower rate of Alzheimer’s disease. In Spain, there are regional
differences in the prevalence of various types of dementia. Ethnic differ-
ences also exist. For example, in the United States, African–Americans
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have higher rates of vascular dementia and lower rates of Parkinson’s

disease than do Caucasians. Overall, the prevalence of dementia increases
as people age. The prevalence of Alzheimer’s disease is approximately 1%
at age 60, and the rate doubles every five years. The rate is approximately
4% at age 70, 8% at age 75, 16% at age 80, and 30% or higher at age 85.
A critical issue, however, is the startling fact that only 10% of the
research on dementia has focused on developing and low income coun-
tries, whose populations comprise approximately two-thirds of the world
population at potential risk for dementia. Addressing this gap in the
research is a global priority. Currently, there are good prevalence data
from Europe, North America, and developed Asia-Pacific nations (Japan,
South Korea, Taiwan, and Australia). Meanwhile, some studies have
examined prevalence rates of dementia in India and China. Yet, because of
the large size and diversity of these countries’ populations, general esti-
mates are unreliable. There is a major need for research on the epidemiol-
ogy of dementia in Latin America, Africa, Russia, the Middle East, and
South East Asia.
4.2. Etiology
Neurofibrillary tangles and beta-amyloid plaques are evident on the histo-
pathology of Alzheimer’s disease. Neurofibrillary tangles are intracellular
aggregates of hyperphosphorylated tau proteins. Normally, tau proteins
help stabilize microtubules. However, in their hyperphosphorylated state
(pTau), microtubule stability and assembly is disrupted, with the resultant
formation of neurofibrillary tangles. Beta-amyloid plaques are extracellular
deposits of a 42-amino acid peptide called Abeta42 or beta-amyloid.
Neurofibrillary tangles are seen in several conditions (e.g. Pick’s disease,
progressive supranuclear palsy, dementia pugilistica) and are thus non-
specific. Also, beta-amyloid plaques predate the development of tangles
and dementia. Yet, tangle density correlates better than does amyloid plaque
density with the severity of dementia. A loss of neurons in the cholinergic,
serotonergic, and dopaminergic systems is also present. Synapse loss cor-
relates even better than do plaques or tangles with disease progression.
Although most persons with Alzheimer’s disease do not have a known
genetic determinant, genetic determinants do exist. The ApoE4 allele on
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chromosome 19 is correlated with an increased risk of developing

Alzheimer’s for individuals older than 50 years of age. Meanwhile, the
presenilin 1 gene on chromosome 14, the amyloid precursor protein gene
on chromosome 21, and the presenilin 2 gene on chromosome 1 are also
genetic determinants of Alzheimer’s disease.
4.2.1. Risk factors

A wide range of risk factors for Alzheimer’s disease has been described in
the literature.3 Genetic risk factors (described earlier in the ‘etiology’
section) may be the best known. Additional risk factors and predictors of
worse prognosis include earlier age at onset (although prevalence
increases at later ages), higher body mass index, female gender, and his-
tory of smoking. Higher education, alcohol consumption in moderation,
and cognitively stimulating activities may be protective. The role of
lifestyle and environmental factors is less well understood. Existing
evidence for the role of lifestyle and environmental factors suggests a
more complex picture. Metals such as iron, copper, aluminum, and zinc
have all been associated with dementia, but the nature of these associa-
tions is not well understood. Dietary factors such as increased glucose,
protein, and polyunsaturated fat intake have all been associated with
cognitive changes. Broadly, the role of environmental factors needs to be
studied in greater detail, especially from the perspective of understanding
how gene-environment interactions impact dementias.
4.3. Phenomenology
The diagnosis of dementia remains clinical. Several screening tests are
commonly used. The Mini-Mental Status Exam (MMSE) is one of the
most commonly used tests. However, it has several limitations. It does not
assess for executive functioning or praxis. Also, it has a poor sensitivity
and specificity, especially for highly educated or intelligent patients.
Adding a clock-draw and a test of praxis (e.g. “show me how you would
use a comb”) can improve its use. The Rowland Universal Dementia
Assessment Scale (RUDAS) has less cultural and educational biases than
does the MMSE. The Clinical Dementia Rating (CDR), Global
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Deterioration Scale (GDS), and Functional Assessment Staging Tool

(FAST) are frequently utilized dementia staging scales.
Alzheimer’s disease progresses over time. Typically, the average dura-
tion is 8–10 years. However, there is a wide range of variation based on
individuals’ general health, age of onset, and culture. Individuals with
“mild” dementia typically have MMSE scores >18 and CDR scores of 1
and are categorized as stage 4 on FAST. They often misplace items, forget
names, become socially withdrawn, and develop impairments in their
IADLs (instrumental activities of daily living, such as shopping, manag-
ing finances). In this manner, “mild dementia” differs from MCI in that
persons with mild dementia have functional impairments for which they
cannot adequately compensate. People with “mild” dementia often have
difficulty managing complex medication schedules. With “moderate”
dementia, individuals typically have MMSE scores of 10–18 and CDR
scores of 2 and are categorized as stage 5 or 6 on FAST. Individuals with
“moderate” impairment develop problems with their ADLs (activities of
daily living, such as dressing, bathing, toileting). As a result, they may
require assistance with aspects of self-care (e.g. picking out appropriate
clothing). They also often develop neuropsychiatric and behavioral distur-
bances (i.e. anxiety, wandering, suspiciousness). As these individuals
become more impaired, they usually require increased supervision for
their safety. They are more at risk for having accidents related to
forgetfulness, such as starting a fire by accidentally leaving the stove on
while cooking. Those who have “severe” dementia often have MMSE
scores <10 and CDR scores of 3 and are categorized as FAST stage 6 or 7.
Individuals with “severe” dementia require considerable or total assis-
tance with their ADLs and full-time care-giving. At this stage of their
dementia, individuals are severely incapacitated and are dependent on
others for most, if not all, aspects of their self-care, including feeding,
dressing, toileting, and bathing. At the latest stages of dementia, “termi-
nal” dementia, patients become bedbound and require constant care. They
are often susceptible to the development of bed sores, contractures, and
infections.
Behavioral and neuropsychiatric symptoms are common with dementia
(see Table 1). Behavioural symptoms include agitation, aggression, and
uncooperativeness. In Western countries, the behavioral disturbances are
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Cognitive Disorders
Table 1. Other behavioral and psychological symptoms of dementia.
Symptom Clinical presentation Etiology Management and prognosis
Agitation/ Refers to vocal or physical behaviors Heterogeneous groups of Behavioral/Psychological: Monitoring level of
Aggressiveness14 whose origins are not understood behavior that do not stimulation, identifying and eliminating
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and which are not explained by represent a single triggers for agitation.
patients’ needs. The range of syndrome, so likely to Pharmacology: Atypical antipsychotics are used.
have multiple
International Handbook of Psychiatry

observed behavioral disturbances Typical antipsychotics are also effective.
includes combativeness, etiologies Minor tranquilizers have also been used but
threatening behavior, disinhibition, are less effective in comparison. Propensity
physical aggression, and for side effects is high. Risks and existing
psychomotor hyperactivity. black box warnings must be considered during
clinical decision making.
Anxiety Usually experienced early in No consensus on Psychosocial: Non-confrontational approach.
dementia. Related to recognition precise etiopathology Identification of early signs of distress and
of loss of cognitive abilities. Often of anxiety in dementia. preventative approach.
replaced by agitation as illness Pharmacology: Benzodiazepines are the drug of
progresses. Usually manifests as choice. Buspirone was found effective in one
generalized anxiety rather than clinical trial. SSRIs may also be considered.
panic attacks or phobia.
(Continued)
301
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302
Table 1. (Continued)
Symptom Clinical presentation Etiology Management and prognosis
Apathy/ Social withdrawal may be the Possibly associated with Psychosocial: Educating caregivers is a major
Withdrawal earliest sign of dementia. As such, degenerative or component of managing apathy. May be
the term ‘apathy’ indicates loss of disruptive processes in beneficial to involve patients in activities —
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motivation, feeling, interest, and the frontotemporal initially as spectators and gradually as
emotion. The motor component is lobes. Seen in most participants.

termed ‘abulia’. Apathy is forms of dementia. Pharmacology: Psychostimulants have been tried
commonly observed in nursing with success for motor apathy. Methylphenidate
homes. and dextroamphetamine have been shown as
effective in clinical trials. Paradoxically, risk
of side effects with these medications may
be lower.
A. Iglewicz, I. V. Vahia and D. V. Jeste

Sleep Common phenomena, often the Alterations in melatonin Psychosocial: Establishing sleep hygiene and
Disturbances16 reason for institutionalization. levels may be maintaining a regular daily routine. Use of
Presentations include insomnia, responsible. light sources may help with disturbances of
hypersomnia, and reversal of sleep–wake cycle.
sleep–wake cycle. Pharmacology: Monitor drug regimen to check
for medications (e.g. stimulants) that may
interfere with sleep patterns. To induce sleep,
short-acting benzodiazepines or zolpidem or
zaleplon may be used.
1/31/2013 2:33:47 PM
the primary precipitant for placement in a skilled nursing facility. The

neuropsychiatric symptoms include anxiety, depression, and psychosis. In
contrast to the psychosis seen in schizophrenia, the psychosis of
Alzheimer’s dementia only occurs in 30%–50% of patients, caregiver
misidentification is frequent, delusions tend to be simple and influenced
by memory deficits (i.e. theft), hallucinations tend to be visual rather than
auditory, and the psychosis oftentimes remits.
Cultural differences influence families’ perceptions and reports of cog-
nitive symptoms. Similarly, cultural differences affect care-giving styles,
perspectives on skilled nursing facility placement, and interpretation and
acceptance of neuropsychiatric symptoms. Clinicians should remain sen-
sitive to these cultural influences.
4.4. Clinical syndromes associated with Alzheimer’s disease

In recent literature, three distinct syndromes associated with Alzheimer’s
disease have been described. These are under consideration for inclusion
in forthcoming editions of DSM and ICD and have relevance for clini-
cians as targets for prompt clinical intervention.
4.4.1. Psychosis of Alzheimer’s disease (and other dementias)7

Psychotic symptoms have been commonly reported in dementia patients,
including in the first patient described by Alzheimer himself (hallucina-
tions and delusions). This form of psychosis differs from schizophrenia in
that incidence is high (30%–50%), bizarre symptoms are rare, visual hal-
lucinations are far more common than auditory, suicidal ideation and past
history of psychotic symptoms are rare, and spontaneous remission is
common without long term antipsychotic use. Proposed criteria for this
syndrome include presence of either hallucinations or delusions or both,
meeting criteria for Alzheimer’s disease, presence of symptoms for one
month or longer, and disruption of functioning as a result of these symp-
toms. Proposed criteria also require that psychotic symptoms are not
present before the onset of dementia symptoms and are not better
explained by delirium or other major psychiatric disorders.
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4.4.2. Depression of Alzheimer’s disease11

Prevalence of depression in Alzheimer’s disease is estimated to range
from 15%–40% across studies. Commonly, it manifests as subsyndromal
symptoms, which rarely meet criteria for a Major Depressive Episode.
Hence, it is often unrecognized and therefore untreated, with resultant
increased morbidity and worsened functioning. Depression of Alzheimer’s
disease is different from Major Depression in that it can be diagnosed by
presence of only three depressive symptoms (as opposed to five for Major
Depression). Symptoms to consider are depressed mood, anhedonia, dis-
ruption in appetite and/or sleep, psychomotor changes, fatigue/loss of
energy, feelings of worthlessness or guilt, thoughts of death/suicidal idea-
tion, social isolation, and irritability. As with psychosis criteria, meeting
criteria for Alzheimer’s disease and significant functional impairment are
also required. In addition, for the diagnosis of depression of Alzheimer
disease to be made, depressive symptoms should not be present before
onset of symptoms of dementia. Depressive symptoms should not be bet-
ter explained by delirium or other major psychiatric disorder.
Other behavioral and psychological symptoms associated with demen-
tia are outlined in Table 1.9
4.5. Treatments
The main pharmacological interventions for the cognitive symptoms of
dementia are cholinesterase inhibitors (donepezil, rivastigmine, galan-
tamine) and NMDA antagonists (memantine). International debate exists
over the effectiveness of these treatment modalities and when and if these
treatments should be initiated and discontinued. Clinical trials have shown
modest benefit of cholinesterase inhibitors in 30%–40% of patients with
mild to moderate dementia. The American Psychiatric Association (APA)
2007 Practice Guideline for the Treatment of Patients with Alzheimer’s
disease and Other Dementias recommends that clinicians offer their
patients with mild to moderate dementia a trial on a cholinesterase inhibi-
tor, but only after the risks and benefits are thoroughly discussed. Vitamin
E is no longer recommended for the treatment of the cognitive symptoms
of dementia due to its limited efficacy and safety concerns. Similarly,
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statin medications, non-steroidal anti-inflammatory agents (NSAIDS),

and estrogen supplementation with conjugated equine estrogens are not
recommended in light of their lack of efficacy and safety in clinical trials.
Promising treatments on the horizon target beta-amyloid and its
pathways.1
Although the neuropsychiatric symptoms associated with dementia are
nearly universal, there is much uncertainty about how to manage these
symptoms. It is critical to consider the safety of patients and those around
them when determining if treatment is warranted. Because there are often
multiple contributing causes of neuropsychiatric symptoms, it is impor-
tant to first determine and address the underlying contributing etiology(ies)
before initiating a medication if possible and safe. Contributing causes are
numerous and include underlying medical conditions, delirium, comorbid
psychiatric conditions, environmental stressors, suboptimal care-giving,
medication side effects, and unmet needs. If the neuropsychiatric symp-
toms persist despite addressing the contributing causes, but the symptoms
do not cause significant distress or danger, these symptoms are best man-
aged with reassurance and redirection. However, if these symptoms are
dangerous or distressing, pharmacological interventions are indicated.
When pharmacological interventions are used, the focus should be symp-
tom oriented.
Antidepressants are used to treat depressive and sometimes anxiety
symptoms. Atypical antipsychotics are often used to treat the psychotic
symptoms. The treatment of agitation in dementia is not well understood.
Wide-variation exists in its treatment, and there is some evidence to sup-
port the use of antipsychotics, SSRIs, trazodone, and cholinesterase
inhibitors. Notably, there is an increased risk of cerebrovascular or cardio-
vascular events and mortality when older adults with dementia are treated
with atypical antipsychotics. The United States Food and Drug
Administration issued a ‘Black Box’ advisory warning indicating that use
of atypical antipsychotics in older adults with dementia may increase
mortality risk. Because lithium, beta-blockers, and anti-convulsants have
significant associated side effects and have limited evidence for efficacy,
they are generally not recommended unless patients have not responded to
other treatments. It is important to avoid anticholinergic medications and
sedative-hypnotic agents when possible. Side effects of benzodiazepines
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include sedation, delirium, worsening cognition, increased fall risk, and

worsening of respiratory disorders. If benzodiazepines are used, loraze-
pam and oxazepam are preferable to benzodiazepines with longer half-
lives and active metabolites. When medications are used, they should have
defined targets, be used cautiously, and monitored closely.
Non-pharmacologic treatments are important. Maintaining safety is a
priority, especially in regards to driving, medications, falls, and living
arrangements. Assessing driving and placing restrictions on driving when
necessary is an important, yet challenging, aspect of care for patients with
dementia. Clinicians should inquire about any history of traffic accidents,
near accidents, or getting lost and explore patients’ current driving pat-
terns and transportation needs. Meanwhile, wandering behaviors are com-
mon in dementia. Wandering is associated with dementia severity and
duration. Ensuring adequate supervision is important for preventing
patients from wandering. However, it is important to provide for safe
access to supervised walks when possible, because walking is beneficial
for exercise and stimulation. Use of identity bracelets can help ensure
safety when wandering behaviors occur. Behavioral interventions also
exist to help individuals have structure and remain engaged during the
day. These interventions are commonly used at day programs.
Specific psychosocial treatments, which reflect a person-centered phi-
losophy of care, exist. They focus on maximizing function and improving
quality of life. These psychosocial treatments can be divided into four sub-
groups: behavior oriented (e.g. scheduled toileting times), cognition ori-
ented (e.g. reality orientation), stimulation oriented (e.g. art, music, and pet
therapy), and emotion oriented (e.g. supportive and reminiscent therapy).
Family members of individuals with dementia often feel overwhelmed
by their care-giving requirements. Caregiver burnout and depression is
very common. Importantly, caregivers are often the lifelines of the patients
for whom they are caring. As such, assessing, treating, educating, and sup-
porting caregivers remains a crucial component of the care of individuals
with dementia. Various interventions aimed at supporting caregivers are
available, although cultural differences exist. These include psychother-
apy focused on improving coping skills and alleviating depressive or
anxiety symptoms, psychoeducational programs, stress management
workshops, and support groups.1
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4.6. International policy implications

At this time, there is a lack of strong public policy initiatives directed at
the impending crisis in dementia care. This crisis will result from the
expected large increase in the elderly population, combined with an
absence of a corresponding growth in the number of providers who can
care for this population. This planning will require great resources, which
may not be available easily in all countries. To address this impending
crisis, Alzheimer’s disease International issued a Kyoto Declaration at its
20th annual meeting in Kyoto, Japan, in 2004. This declaration, which
was based on the 2001 WHO World Health Report, lays out 10 recom-
mendations for dementia care based on availability of resources (Table 2).
5. VASCULAR DEMENTIA
Vascular dementia is the world’s second most common type of dementia,
although it is the most common type of dementia in certain Asian coun-
tries, such as Japan. In its pure form, it accounts for 5%–20% of demen-
tias. In its mixed form, it accounts for another 5%–20% of dementias. The
regional variations in incidence of vascular dementia found in the world
probably reflect differences in risks for cardiovascular and cerebrovascu-
lar disease, which, in turn, may reflect dietary and lifestyle differences
across cultures.
Vascular dementia is best understood as a heterogeneous group of
dementias resulting from infarction of the brain. The infarcts are typically
small but cumulative in effect.
Classically, vascular dementia has a step-wise progression, in which a
temporal relationship can be found between cognitive changes and wors-
ening brain vascular disease. These step-wise cognitive declines may cor-
relate with the development of focal neurological signs.
Vascular dementia can be further categorized as vascular dementia of
acute onset, multi-infarct dementia, and subcortical vascular dementia.
Vascular dementia of acute onset typically develops shortly after a suc-
cession of strokes from thromboses, emboli, or hemorrhage. Rarely, it
may result from a single large infarction. In contrast, multi-infarct
dementia is gradual in onset and results from an accumulation of infarcts
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308
Table 2. Alzheimer’s disease international Kyoto declaration recommendations (Adapted from Prince et al.12)
Recommendation Nations with low resources Nations with medium resources Nations with high resources
Treatment in primary care Include dementia recognition Create training materials that are Improve efficiency of dementia
and treatment in training relevant locally. management.
curricula of health personnel. Refresher training for PCPs. Establish referral systems.
Refresher training to primary
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care physicians (PCPs).
Make treatments available Increase availability of Ensure availability of Create access to newer
medications. medications. medications.

Basic education for caregivers. Create effective caregiver
interventions.
Care in the community Establish awareness of home- Pilot integration of dementia care Develop alternate residential
based treatments. into primary care. facilities.
Pilot community care teams, day Provide community facilities. 100% coverage community care.
A. Iglewicz, I. V. Vahia and D. V. Jeste

care, and short-term respite Develop residential facilities and Develop individualized care.
settings. staff training.
Develop needs assessments.
Public education Support NGOS and focus on Use mass media to promote Public campaigns for early help
removing stigma. awareness and prevention. seeking, recognition, and
management.
Involvement of consumers, Promote self-help groups. Involve consumers and Advocacy initiatives.
families, and communities Funding for NGOs. communities in policy making
and service development.
(Continued)
1/31/2013 2:33:47 PM
B1405_Ch-12.indd 309
Cognitive Disorders
Table 2. (Continued )
Recommendation Nations with low resources Nations with medium resources Nations with high resources
National policy, programs, Update national policy on the Dementia care policies at national Ensure fair access to primary,
and legislation basis of the latest international and subnational levels. secondary, and tertiary care
recommendation and human Appropriate budgets for mental and social welfare programs
rights laws. health care. and benefits.
Dementia care programs to
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include persons with dementia
in entitlement plans.

Human resources Training for primary health Network of national training Train specialists in advanced
workers. centers for advanced healthcare treatment and management
Training for doctors and nurses professionals. skills.
in old age psychiatry and
medicine.
Link with other sectors Community, school, and Strengthen and support Occupational health services for
workplace programs. community programs. dementia. Special workplace
facilities for caregivers.
Mental health promotion
cross-sectorally.
Monitor community health Include dementia in basic health Surveillance in the community. Advanced monitoring systems,
systems and survey high-risk including monitoring for
populations. effectiveness of programs.
Research Studies in primary care settings Effectiveness and cost- Research on causes of dementia,
on prevalence, course, and effectiveness studies. service delivery, and
309
impact of dementia. preventive measures.
1/31/2013 2:33:47 PM
in the cerebral parenchyma. Unlike multi-infarct dementia, which tends

to be cortical, subcortical vascular dementia usually spares the cerebral
cortex. Rather, it occurs in people with a history of poorly controlled
hypertension and ischemic disease in the deep white matter of the cere-
bral hemispheres. The underlying types of tissue injury accounting for
the cognitive deficits in these different categories of vascular dementia
are usually the result of atherosclerotic disease or amyloid angiopathy.
Much less commonly, they are the result of autoimmune mechanisms.
Although no specific cognitive profile for vascular dementia exists,
executive dysfunction and attentional deficits are usually more prominent
than short-term memory deficits. The progression of vascular dementia is
variable and ranges from a precipitous decline to a non-progressive
course for years until another stroke to a slow, progressive course. The
best treatment to slow the course of the disease is to address the cardio-
vascular and cerebrovascular risk factors contributing to the disease
progression.
6. DEMENTIA IN PICK’S DISEASE

(FRONTOTEMPORAL DEGENERATION)
What is referred to as Pick’s Disease in the ICD-10 is now referred to as
Dementia due to Frontotemporal degeneration (FTD) in many parts of the
world. FTD is now commonly viewed as a condition under the overarch-
ing category of FTD spectrum disorders. FTD spectrum disorders also
include progressive supranuclear palsy, corticobasal ganglionic degenera-
tion, hippocampal sclerosis, and amyotrophic lateral sclerosis with
dementia. FTD is the second most common dementia in people younger
than 65 years of age. It is a progressive dementia, typically commences in
patients aged 50–60 years, and contrasts with the clinical syndrome seen
in Alzheimer’s disease. The course is typically more rapidly progressive
than that of Alzheimer’s, although significant heterogeneity is seen. FTD
is characterized by early changes in affect, personality, and behavior.
These changes often result in socially inappropriate behaviors, disinhibi-
tion, and hyperorality. The development of language disturbances and
apathy typically follow. Cognitive impairments in intellect, memory, and
praxis usually arrive later in the course of the dementia. Executive
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dysfunction is common, whereas visuospatial skills are often preserved.

As compared to Alzheimer’s disease, FTD can be a greater burden to car-
egivers in light of the characteristic disinhibition. Because individuals
with FTD spectrum disorders often present with psychiatric symptoms,
including personality changes, apathy, disinhibition, and substance abuse,
rather than with cognitive impairments, it is important that psychiatrists
are cognizant of and screen for this group of disorders. Otherwise, there
is often a delay in the correct diagnosis.
7. DEMENTIA IN PARKINSON’S DISEASE

AND DEMENTIA WITH LEWY BODIES
Dementia in PD and dementia with Lewy bodies (DLB) can both be
categorized under the umbrella term ‘Lewy body disorders’. These con-
ditions share a common pathology involving impairments in alpha
synuclein metabolism, resulting in an abundance of Lewy inclusion
bodies in cortical and subcortical brain regions. DLB is found in
7%–26% of dementia cases. The dementia of both PD and DLB has an
insidious onset and is slowly progressive. It is often characterized by
executive dysfunction, impairments in memory retrieval, cognitive
inflexibility, and cognitive slowing. The clinical presentations of
dementia in PD and DLB are often similar and involve progressive cog-
nitive impairments, motor Parkinsonism, gait imbalance, and visual
hallucinations. The relationship between the onset of motor distur-
bances and cognitive disturbances can help differentiate PD and DLB.
In PD, the dementia typically does not become evident until many years
after the motor deficits occur. With DLB, the Parkinsonism (which
tends to be more symmetric than that in PD) often develops at the same
time as the cognitive impairments. DLB is also associated with a fluc-
tuating course with significant variations in attention and alertness,
vivid well-formed visual hallucinations, delusions (e.g. Capgras syn-
drome), REM sleep behavior disorder, and neuroleptic sensitivity.10
Because patients with LBD are markedly sensitive to the extrapyrami-
dal side effects of neuroleptics, caution should be taken when prescrib-
ing this class of medication. Low potency agents, such as quetiapine,
are preferred when antipsychotics are required.
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8. CONCLUSION
Cognitive disorders, including delirium and dementia, are common in
late life. With the exponential aging of the world population, the number
of older adults experiencing cognitive disorders will likewise expand.
As outlined in this chapter, dementia and delirium are associated with
numerous neuropsychiatric symptoms and incur enormous costs to soci-
ety, affected individuals, and their caregivers. Furthermore, delirium is
associated with a poor prognosis, including increased mortality. It is
thus imperative that we monitor for and treat these important conditions.
Future research into the recognition and treatment of cognitive disor-
ders, especially in developing countries, is warranted.15
9. KEY POINTS
• Delirium is often under-recognized, under-diagnosed, and
under-treated.
• Delirium carries a poor prognosis.
• The best treatment for delirium is the treatment of its underlying
etiology(ies).
• Urinary tract infections are a common infectious etiology of delirium
in older adults.
• When evaluating for underlying etiologies of a delirium, always con-
sider medications (side effects, anticholinergic properties, and medi-
cation interactions).
• Dementia is a common neurocognitive disorder with large social,
economic, and medical implications.
• The rate of dementia will increase substantially as the world popula-
tion ages.
• Alzheimer’s disease is the most common dementia, although cultural
differences exist in dementia prevalence rates.
• Neuropsychiatric symptoms commonly occur with dementias.
• Caregiver burnout is common and should be carefully monitored and
treated.
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10. SELF-ASSESSMENT
10.1. Which of the following features best help distinguish
a delirium from a dementia?
(A) Memory changes.
(B) Agitation.
(C) Visual hallucinations.
(D) Acute onset.
In contrast to most types of dementia, which have a slow, gradual onset,

the onset of delirium is typically acute. Fluctuation in consciousness and
alertness is another key feature of a delirium but can also be seen in Lewy
Body Dementia.
Answer: D
10.2. Individuals with which type of dementia are especially

sensitive to antipsychotic medications?
(A) Alzheimer’s dementia.
(B) Lewy body dementia.
(C) Frontotemporal dementia.
(D) Vascular dementia.
Individuals with Lewy Body Dementia are sensitive to the side effects of
neuroleptics, especially to the extrapyramidal side effects.
Answer: B
11. CASE STUDIES

11.1. Delirium
An 85-year-old Indian woman was brought to the hospital by her family
for an evaluation of her acute onset of confusion, visual hallucinations,
and sleep–wake cycle disturbance. Her family reports that her current
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presentation is an acute change from her baseline mild memory impair-

ments. They explain that she was started on an Ayurvedic treatment (con-
taining Datura metel — a shrub-like herb with anticholinergic properties
used in Ayurvedic and traditional Chinese medicine for the treatment of
wheezing) for her asthma three days before the development of her acute
mental status changes.
The patient was unable to provide a coherent history, because she was
unable to sustain or shift attention during the interview. She sat on her
hospital bed, picking at the sheets and the air in a distracted fashion.
On physical examination, the patient had normal vital signs, and no
abnormalities of her heart, abdomen, or extremities were found. However,
there were mild, diffuse, expiratory wheezes on her lung exam. She was
disoriented to time and place, believing that it was 1957 and that she was
on a train rather than in the hospital. The laboratory evaluation demon-
strated an elevated white blood count. Her urinalysis indicated a urinary
tract infection.
The patient was given a diagnosis of delirium. She was started on an
antibiotic to address her urinary tract infection and an inhaler to address
her asthma. Meanwhile, her Ayurvedic treatment was discontinued,
because there were concerns that the anticholinergic properties of Datura
were contributing to her delirium. Over the next week, her delirium
resolved and she returned to her previous level of functioning.
11.2. Dementia due to Alzheimer’s disease

The family of an 81-year-old English man reported a six-year history of
progressively worsening cognitive impairment. He tended to rapidly forget
the details of conversations and television programs and had been forgetting
names of common objects. The patient recently got lost walking around his
neighborhood, where he had lived for the past 20 years. He had been unable
to manage his finances for the past three years. For several weeks, he had
been hiding his belongings in drawers and socks, forgetting where he
placed his items, and accusing his family members of stealing from him.
On office cognitive testing, he had marked short-term memory deficits,
word finding difficulties, paraphasic errors, difficulty copying intersecting
pentagons, but intact attention span. Neuropsychological testing
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confirmed significant deficits in these same cognitive domains. Basic

laboratory studies were essentially unremarkable. A head CT demon-
strated atrophy slightly out of proportion for age.
The patient was given a diagnosis of dementia due to Alzheimer’s
disease.
A family session was scheduled, where the possible use, benefits, and
risks of medications and both course and prognosis of the disorder were
explained. Caregiver issues, the need for safety precautions, and the impor-
tance of settling the patient’s affairs were also highlighted. Regular outpa-
tient follow-up sessions were scheduled with the patient and caregivers.
REFERENCES
1. American Psychiatric Association. (2006) American Psychiatric Association
Practice Guidelines for the Treatment of Psychiatric Disorders, Compendium
2006, American Psychiatric Publishing, Inc., Arlington, VA.
2. Blazer D, Steffens D. (2009) American Psychiatric Press Textbook of Geriatric
Psychiatry, 4th ed. American Psychiatric Publishing, Inc., Arlington, VA
3. Chen JH, Lin KP, Chen YC. (2009) Risk factors for dementia. J Formos Med
Assoc 108: 754–764.
4. Chertkow H, Massoud F, Nasreddine Z, et al. (2008) Diagnosis and treat-
ment of dementia: 3. Mild cognitive impairment and cognitive impairment
without dementia. CMAJ 178: 1273–1285.
5. Fainsinger RL, De Moissac D, Mancini I, Oneschuk D. (2000) Sedation for
delirium and other symptoms in terminally ill patients in Edmonton. J Palliat
Care 16: 5–10.
6. Jeste DV, Blacker D, Blazer D, et al. (2010) Proposal from the Neurocognitive
Disorders Work Group. Available at: http://www.dsm5.org/Proposed%20
Revision%20Attachments/APA%20Neurocognitive%20Disorders%20
Proposal%20for%20DSM-5.pdf
7. Jeste DV, Finkel SI. (2000) Psychosis of Alzheimer’s disease and related
dementias: Diagnostic criteria for a distinct syndrome. Am J Geriatr
8. Meagher DJ, Maclullich AM, Laurila JV. (2008) Defining delirium for the
international classification of diseases, 11th Revision. J Psychosom Res 65:
207–214.
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9. Meeks TW, Ropacki SA, Jeste DV. (2006) The neurobiology of neuropsychi-
atric syndromes in dementia. Curr Opin Psychiatry 19: 581–586.
10. McKeith IG, Dickson DW, Lowe J, et al. (2005) Consortium on DLB.
Diagnosis and management of dementia with Lewy bodies: Third report of
the DLB consortium. Neurology 65:1863–1872.
11. Olin JT, Schneider LS, Katz IR, et al. (2003) Provisional diagnostic criteria
for depression of Alzheimer disease: Description and review. Expert Rev
Neurother 3: 99–106.
12. Prince M, Acosta D, Albanese E, et al. (2008) Ageing and dementia in low
and middle income countries — using research to engage with public and
policy makers. Int Rev Psychiatry 20: 332–343.
13. Sadock BJ, Sadock VA, Ruiz P. (2009) In: Sadock BJ, Sadock VA (eds.),
Kaplan & Sadock’s Comprehensive Textbook of Psychiatry, 9th ed. Lippincott
14. Salzman C, Jeste DV, Meyer RE, et al. (2008) Elderly patients with demen-
tia-related symptoms of severe agitation and aggression: Consensus statement
on treatment options, clinical trials methodology, and policy. J Clin
Psychiatry 69(6): 889–898.
15. Vahia IV, Cain A, Depp CA. (2010) Cognitive interventions: Traditional and
novel approaches. In: Depp CA, Jeste DV (eds.), Handbook of Successful
Cognitive and Emotional Aging, pp. 325–349, American Psychiatric
16. Yesavage JA, Friedman L, Ancoli-Israel S, et al. (2003) Development of
diagnostic criteria for defining sleep disturbance in Alzheimer’s disease.
J Geriatr Psychiatry Neurol 16: 131–139.
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Chapter 13
Somatoform Disorders
Christina L. Wichman
1. INTRODUCTION
There are several types of somatoform disorders, as classified in the ICD-
10, which will be discussed here, including somatization disorder, undif-
ferentiated somatoform disorder, hypochondriacal disorder, dissociative
(conversion) disorder, and persistent somatoform pain disorder. We will
also review factitious disorder and malingering, although they are not
classified as somatoform disorders.
There are several shared generalizations of the class of somatoform
disorders. These patients have the presence of physical symptoms that
suggest a general medical condition but are not explained by a medical
condition. Medically unexplained physical symptoms (MUPS) are
physical symptoms that prompt the sufferer to seek health care but remain
unexplained even after an appropriate medical evaluation.20 Some authors
have suggested that the precise diagnosis of MUPS depends more on the
diagnosing physician’s specialty than on any actual difference between
the syndromes.20 MUPS are typically classified by either psychiatric
syndromes or hypothetical syndromes on the basis of the diagnostic
criteria.
Several consequences may occur when a patient is diagnosed with
MUPS. First and foremost, there typically is an impaired physician–
patient relationship. Studies have demonstrated physician frustration
317
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318 C. L. Wichman
in this patient population, with one in six primary care visits considered
difficult. Furthermore, there seems to be a “dose–response” relationship
between the number of symptoms and level of physician frustration. For
example, among patients presented with 0–1 symptoms, only 6% of
patient interactions were labeled as “difficult” by providers, but these
increased dramatically to 36% when patients presented with 10 or more
symptoms.8 As expected, patients with MUPS have higher levels of dis-
satisfaction with their health care providers and demonstrate increased
psychosocial distress, decreased quality of life, and increased rates of
depression and anxiety. Patients suffering with somatoform disorders
often demonstrate alexithymia, the inability to articulate their internal
feeling states in words. They may therefore express their feelings through
somatic (or physical) complaints. Alexithymia correlates positively with
depression, somatization, and hypochodriasis.22 Patients with MUPS also
have increased rates of health care utilization. Unfortunately, higher rates
of utilization often lead to more harm and patient dissatisfaction than to
medical benefits. Studies have demonstrated that this patient population
has to up nine times higher medical costs.
Patients with somatoform disorders are often convinced that their
suffering comes from an undetected and untreated physical disease state.
Their bodies are demonstrating their psychosocial stress as physical stress
and patients often misinterpret normal physiological functions as prob-
lematic. For the class of somatoform disorders, these symptoms are not
consciously produced or feigned.
The ICD-10 category of somatoform disorders (Table 1) differs from
the DSM-IV class1 in that it requires “persistent requests for medical
investigations” and resistance to consideration of “psychological causa-
tion” despite “repeated negative findings and reassurance by doctors that
the symptoms have no physical basis.” As described later in this chapter,
DSM-IV only requires these elements in hypochondriasis and body
dysmorphic disorder. Additionally, the ICD-10 grouping encompasses
different disorders: somatization disorder, undifferentiated somatoform
disorder, hypochondrical disorder (of which body dysmorphic disorder is
a subset), somatoform autonomic disorder (a disorder not included in
DSM-IV), persistent somatoform pain disorder, other somatoform disor-
ders, and somatoform disorders unspecified. Conversion disorder is not
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Somatoform Disorders 319
Table 1. ICD-10 criteria of somatization disorder.
• History of at least two years’ complaints of multiple and variable physical symptoms
that cannot be explained by any detectable physical disorders.
• Preoccupation with the symptoms causes persistent distress and leads the patient to
seek repeated (three or more) consultation or sets of investigation with either primary
care specialist doctors. In the absence of medical services within either the financial or
physical reach of the patient, there must be persistent self-medication of multiple
consultations with local healers.
• Persistent refusal to accept medical reassurance that there is no adequate physical
cause for the physical symptoms.
• There must be a total of six or more symptoms from the following list, with symptoms
occurring in at least two separate groups:
{ Gastrointestinal Symptoms
• Abdominal pain
• Nausea
• Feeling bloated or full of gas
• Bad taste in mouth or excessively coated tongue
• Complaints of vomiting or regurgitation of food
• Complaints of frequent and loose bowel movement or discharge of fluids
from anus
{ Cardiovascular Symptoms
• Breathlessness without exertion
• Chest pains
{ Genitourinary Symptoms
• Dysuria or complaints of frequency or micturition
• Unpleasant sensation in or around the genitals
• Complaints of unusual or copious vaginal discharge
{ Skin and pain symptoms
• Blotchiness or discoloration of the skin
• Pain in the limbs, extremities or joints
• Unpleasant numbness or tingling sensations
• Most commonly used exclusion cause: Symptoms do not occur only during any of the
schizophrenic or related disorders (F20–F29), any of the mood (affective) disorders
(F30–F39), or panic disorder (F41.0).
included as a distinct somatoform disorder in ICD-10 but is classified

under dissociative (conversion) disorder. Also of note, there is no ICD-10
condition corresponding to pain disorders specified as acute in DSM-IV;
ICD-10 considers only persistent pain disorders.
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320 C. L. Wichman
2. SOMATIZATION DISORDER
Somatization disorder is the prototype somatoform disorder. It is charac-
terized by symptoms in multiple physical domains that continue for many
years, often leading to impairment of functioning. Medical investigation
does not reveal an underlying cause to these symptoms. In order to diag-
nose somatization disorder, multiple, recurrent, and frequently changing
physical symptoms of at least two years’ duration must be present.
A detailed history, as well as review of medical and psychiatric records, is
often warranted to uncover a somatization disorder. Patients are not inten-
tionally producing or lying about their symptoms, as in factitious or
malingering disorders.
Patients typically present for medical care before the age of 30 years.
Many patients will describe themselves as sickly most of their lives.
Common presenting symptoms vary but may include back pain, head-
aches, abdominal pain, pelvic pain, nausea, vomiting, dizziness, fainting,
seizures, weakness, paralysis, or painful sexual intercourse. Histories are
often vague, circumstantial, and inconsistent, but patients take the time to
relate their distress, often in a dramatic, emotional, and exaggerated
fashion. Oftentimes, patients will have had a large number of outpatient
visits, frequent hospitalization, and repetitive subspecialty referrals, as
well as multiple unnecessary tests and procedures that are usually unre-
vealing. Patients are often frustrated and disappointed with their care
providers when further medical tests are deemed inappropriate. Patients
may experience iatrogenic disease or injury secondary to diagnostic inves-
tigations, polypharmacy, or multiple surgeries. These patients tend to be
at a higher risk for abuse or dependence on drugs designed for symptom
control (i.e. pain medications, sedatives).
Somatization disorder is found predominately in women, with a
female to male ratio of approximately 10:1 in the United States popula-
tion. However, this ratio is not as high as in some other cultures, for
example, in Greeks and Puerto Ricans. Therefore, gender and culture
specific rates are more meaningful than generalized figures. The lifetime
risk of somatization disorders has been estimated to be 2% in US
women, 0.5% in US men,3 however slightly lower at 0.5%–1% in the
United Kingdom.2
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Patients often have comorbid psychiatric illness, including mood,

anxiety, personality, and substance use disorders. Patients often have a
history of childhood abuse or neglect and may describe multiple social
problems and chaotic lifestyles characterized by poor interpersonal rela-
tionships and difficult behavior.
The Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition (DSM-IV), defines somatization disorder (300.81) very differ-
ently than does ICD-10. DSM-IV requires a history of physical com-
plaints beginning before the age of 30 years that occur over a period of
several years and result in treatment being sought or significant impair-
ment in social, occupational, or other areas of functioning. Additionally,
the DSM-IV requires a certain number of individual symptoms occurring
at any time during the course of the illness, including four pain symptoms,
two gastrointestinal symptoms (not pain-related), one sexual symptom,
and one pseudo neurological symptom. Symptoms cannot fully be
explained by a known general medical condition or substance; if a general
medical condition does exist, the resulting physical complaints or level of
impairment would be in excess of what would be expected.1
The most important consideration in the differential diagnosis of soma-
tization disorder is an undiagnosed physical illness. Even in patients with
a diagnosis of somatization disorder, each new physical complaint should
be fully medically evaluated. Patients with occult medical illness typically
look chronically ill and usually have abnormal physical examinations or
laboratory studies. Clinicians must look closely at medical conditions
with transient, vague, and non-specific symptoms. This can include mul-
tiple sclerosis, myasthenia gravis, systematic lupus erythematous, AIDS,
acute intermittent porphyria, hyperparathyroidism, and chronic systemic
infections. Furthermore, patients with multiple somatic complaints begin-
ning after the age of 40 years should be presumed to have a non-psychiatric
cause until an exhaustive medical work-up has been completed.
Other psychiatric disorders, such as mood or anxiety disorders, may
have physical symptoms as part of their presentation, such as physical
pain or fatigue. However, these symptoms tend to have a temporal rela-
tionship to the onset of the other signs of the disorder and remit when
psychiatrically treated. Patients with a primary thought disorder may also
have somatic concerns or delusions; however, these are typically bizarre
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322 C. L. Wichman
and in the context of other false beliefs. By definition, somatization

disorder differs from factitious disorder and malingering by the lack of
internal symptom production.
Three classic features suggest the diagnosis of a somatization disorder
instead of a medical disorder: multiple organ system involvement, early
onset and chronic course without development of physical signs or struc-
tural abnormalities, and absence of laboratory abnormalities that are
characteristic of a specific medical condition.
From a primary care standpoint, once patients have been diagnosed
with somatization disorder, regular medical follow-up visits should be
scheduled regardless of medical complaints. Limitation should be set on
contacting the physician outside of regularly scheduled appointment
times. Each physical exam should be focused on the area of discomfort for
that visit. Physicians should look at objective signs of disease rather than
taking patients’ symptoms at “face value.” Avoidance of unnecessary tests,
invasive treatments, referrals, and hospitalizations is key in order to avoid
more harm to the patient. Physicians should avoid insulting explanations
such as “the symptoms are all in your head” and instead explain that stress
can manifest as physical symptoms. Perhaps the best long-term goal is to
increase patients’ awareness of the possibility that psychological factors
are involved in the patient’s symptoms and continue to encourage psychi-
atric involvement. Psychiatric consultation is only helpful when it is
acceptable to the patient.18
Somatization disorder has not been shown to be responsive to long-
term, insight-oriented psychotherapy. Short-term dynamic therapy has
shown to have some efficacy, as has cognitive behavioral therapy. Within
therapy, patients and clinicians should work to pinpoint the visceral sensa-
tions, the thoughts that were elicited by the discomfort, and the context in
which the discomfort occurred. Ideally, patients learn to cope with their
symptoms, express their underlying emotions, and develop alternative
strategies for expressing their emotions. Additionally, psychotherapy has
been shown to decrease patients’ health care expenditures by up to 50%,
largely by decreasing the rate of hospitalizations.
Unfortunately, there is little evidence to support the use of pharmaco-
logic agents in patients with somatoform disorders. Antidepressants have
shown inconsistent results and tend to show a partial response rather than
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remission of symptoms. Patients with somatization disorder also tend to

have higher rates of discontinuation and tend to be more sensitive to side
effects. Additionally, these patients often continue to believe that there is
an underlying medical cause for their symptoms, whereas agreement in
taking an antidepressant medication signifies a psychiatric component.
There is unknown efficacy of psychotropic agents in this patient
population.
There are several non-specific treatments, of which some have demon-
strated usefulness in patients with somatization disorder. Kathol has
shown that ending a patient visit in a positive and reassuring manner is
beneficial.9 Broadening the agenda to include both physical and psycho-
logical factors has also demonstrated efficacy.5 Normalization of patients’
symptoms (e.g. “test results are normal” or “everything is fine”) is not
effective. These patients need to have their concerns addressed.13
Somatization disorder tends to be waxing, waning, and chronic.
Patients rarely achieve full remission but can have a decrease in symptom
frequency and medical visits. The greatest risks come from iatrogenic
harm, which can be reduced by diagnosis of the condition and avoidance
of unnecessary medical studies.
3. HYPOCHONDRIACAL DISORDER
Hypochondriacal disorder is the preoccupation with fear of having a
serious illness that does not respond to reassurance after appropriate medi-
cal work-up. The prevalence of hypochondriacal disorder in the general
population is unknown but has been estimated at 3%–10% in the outpa-
tient medical clinic population4 and 3% in medical students. A 1965 study
reported prevalence figures ranging from 3%–13% in different cultures,10
but it is unclear whether this represents a syndrome comparable to the
current definition of hypochondriacal symptoms. It does appear that
hypochondriacal disorder is equally common in males and females.
Similar to somatization disorder, hypochondriacal disorder is charac-
terized by the presence of unexplained symptoms and sensations (Table 2).
However, patients with hypochondriacal disorder take these symptoms
one step further by leaping to a catastrophic cognitive misinterpretation of
the significant of these symptoms, thereby convincing themselves that
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324 C. L. Wichman
Table 2. ICD-10 criteria of hypochondriacal disorder (F45.2).
Either of the following must be present:

— A persistent belief, of at least six months duration, of the presence of a maximum
of two serious physical diseases (of which at least one must be specifically named
by the patient).
— A persistent preoccupation with a presumed deformity or disfigurement (body
dysmorphic disorder).
Preoccupation with the belief and the symptoms causes persistent distress or interference
with personal functioning in daily living, and leads the patient to seek medical treatment
or investigations.
There is persistent refusal to accept medical reassurance that there is no physical
cause for the symptoms or physical abnormality.
Most commonly used exclusion clause: The symptoms do not occur only during any
of the schizophrenic and related disorders (F20–F29) or any of the mood (affective)
disorders (F30–F39).
they have a physical disease.14 The belief of their disease state, however,
cannot have the intensity of a delusion; such a condition would be more
appropriately diagnosed as a delusional disorder.
Hypochondriacal disorder may have a chronic course, with waxing and
waning of symptoms. When the course is chronic, hypochondriacal disor-
der may appear similar to lifetime obsessive-compulsive disorder or as a
personality disorder. When the course is intermittent or of new onset, the
physician should search for predisposing stressful life events as the cause.
There are several general aspects to treatment of hypochondriacal dis-
order. Patients should have regularly scheduled physical examinations in
order to aid with reassurance that their physicians are not abandoning
them and that their complaints are being taken seriously. Thorough history
taking should occur during initial consultation, and clinicians should aid
patients with the identification of their stressors. Education about hypo-
chondriacal disorder, as well as about how stressors may be playing a role
in physical symptoms, is also quite useful. Cognitive behavioural therapy7
and supportive therapy, in an attempt to reduce stressors and identify a
relationship between stressors and physical symptoms, has proven to be
beneficial. From a pharmacologic standpoint, serotonergic medications,
such as selective serotonin reuptake inhibitors, appear to have the most
benefit in this patient population.7
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3.1. Body dysmorphic disorder

Body dysmorphic disorder is defined as a pervasive feeling of ugliness
with some aspects of one’s appearance, despite having a normal or near-
normal appearance. It is classified as a hypochondriacal disorder under
ICD-10 criteria. Body dysmorphic disorder is very poorly studied. In
dermatologic settings, studies have identified up to 12% of a practice with
this diagnosis, while other studies looking at a cosmetic surgery sub-
population have ranged from 6%–15% of a practice.12 The epidemiology
of body dysmorphic disorder in the general population is unclear.
Onset of body dysmorphic disorder typically occurs between 15 and 30
years of age. Although the body part in which the patient has the preoc-
cupation may be any part, the preoccupation most often involves the face
or head. Gender differences are also noted; women tend to focus on their
hips and breasts, while men may tend to focus on their body build, geni-
tals, or thinning hair. Typically, these patients think about their flaws
several hours daily. Nearly all individuals with body dysmorphic disorder
perform repetitive, time-consuming, and compulsive behaviors, which can
include comparing one’s appearance to that of others, excessively check-
ing the perceived flaw, excessive grooming, and seeking reassurance
about the perceived flaw. If patients receive treatment or a procedure on
the area of concern, they often shift their focus to another area.
Unfortunately, patients with body dysmorphic disorder often undergo
medical or surgical treatments in order to correct their perceived flaws.
They tend to have a higher rate of complications from these treatments.
Patients diagnosed with body dysmorphic disorder also have high rates
of psychiatric comorbidities, including major depressive disorder, social
phobia, substance use, obsessive-compulsive disorder, and personality
disorder, with avoidant personality being the most prevalent. As many
as 25% of patients with body dysmorphic disorder attempt suicide.16,17
Some consider body dysmorphic disorder to be part of an
obsessive-compulsive disorder spectrum; however, rituals seen in body
dysmorphic disorder are less likely to decrease anxiety.
Treatment of body dysmorphic disorder primarily is to avoid iatrogenic
harm. Cognitive behavioural therapy,17 including systematic desensitiza-
tion, response prevention, and preventing avoidance behaviors, have been
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326 C. L. Wichman
shown to be helpful in this patient population. In terms of pharmacologic

management, serotonin-specific medications, especially in high doses,
have been beneficial. SSRIs have shown to reduce symptoms in about
50% of patients suffering from body dysmorphic disorder.19 Often a
delayed response has been noted, and higher doses of SSRIs are often
needed to achieve response.15 Long-term treatment is typically warranted.
Surgery to “correct” the perceived deformity is not helpful, almost invari-
ably unsuccessful, and may be a potential cause of litigation by these
patients, because they do not perceive that their “deformity” has been
corrected.
4. PERSISTENT SOMATOFORM PAIN DISORDER

In persistent somatoform pain disorder, pain is the predominant focus of
clinical attention, and complaints of pain are significantly affected by
psychological factors. Psychological factors are required in the genesis,
severity, and maintenance of the pain. Pain disorder is likely the most
common of all of the somatoform disorders; lifetime prevalence has been
estimated as high as 12%.21
Clinically, patients with persistent somatoform pain disorder describe
severe and constant pain that may take on various forms (Table 3). Pain is
typically disproportionate to the underlying medical condition, if one
exists. Unfortunately, pain is often the main focus of the patient’s life.
Other diagnoses to consider in patients presenting with predominate pain
symptoms include purely physical pain, depression, other somatoform
disorders, substance use disorder, factitious disorder, or malingering.
Table 3. ICD-10 criteria for persistent somatoform pain disorder (F45.4).
There is a persistent severe and distressing pain (for at least six months, and
continuously on most days), in any part of the body, which cannot be explained
adequately by evidence of a physiological process or a physical disorder, and which is
consistently the main focus of the patient’s attention.
Most commonly used exclusion clause. This disorder does not occur in the presence of
schizophrenia or related disorders (F20–29), or only during any of the mood [affective]
disorder (F30–39), somatization disorder (F45.0), undifferentiated somatization disorder
(F45.1) or hypochondrical disorder (45.2).
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In treating patients with persistent somatoform pain disorder, it is

imperative that patients believe that their medical providers believe that
their pain is real. The goal is often to improve functioning, rather than to
have complete resolution of pain. Clinicians should discuss the issue of
psychological factors early in treatment and should frankly tell patients
that such factors are important in the cause and consequences of both
physical and psychological pain. Cognitive behavioural therapy, with spe-
cific focus on relaxation and biofeedback, is useful, as is hypnosis.
Antidepressants are the most effective pharmacological agents. Those
with action at both serotonin and norepinephrine, such as venlafaxine and
duloxetine, have been demonstrated to have benefit.11 Poor prognostic fac-
tors in the treatment of persistent somatoform pain disorder include a
pre-existing character pathology, pending litigation, use of addictive sub-
stances, and prolonged history of pain complaints, while those who have
prompt treatment and resolution of any litigation have markedly improved
prognosis.
5. DISSOCIATIVE (CONVERSION) DISORDERS

Dissociative (conversion) disorders are generally defined as having one or
more symptoms involving voluntary motor or sensory function that sug-
gest a medical condition (Table 4). Psychological factors are judged to be
associated with the symptoms. Importantly, these symptoms are not inten-
tionally produced or feigned, unlike factitious disorder or malingering,
which are discussed later in this chapter.
Conversion disorder has a prevalence rate of 0.1% in the general
population but is much more common in the psychiatric and neurologic
populations,21 with estimates of 5%–24% of psychiatric outpatients,
5%–14% of general hospital patients, and 1%–3% of outpatient
Table 4. ICD-10 criteria for dissociative (conversion) disorders (F44).
G1. There must be no evidence of a physical disorder that can explain the characteristic
symptoms of this disorder (although physical disorders may be present that give rise
to other symptoms).
G2. There are convincing associations in time between the onset of symptoms of the
disorder and stressful events, problems or needs.
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328 C. L. Wichman
psychiatric referrals reporting a history of conversion symptoms. It is far

more common in women; however, this may be due to the fact that
women tend to seek medical evaluation more often than men do.
Dissociative disorders are much more common in patients with low levels
of education, as well as those in rural areas and developing countries.
Consistent with this, conversion symptoms have higher rates of outpatient
psychiatric referrals in developing countries, with estimates near 10%.23
There may be a declining incidence as countries develop, which may
relate to increasing levels of education, as well as medical and psychological
sophistication.
There are several clinical subtypes of dissociative (conversion) disor-
ders. Each requires that the general criteria of dissociative disorder (G1
and G2 in Table 4) must be met, in addition to its own specific criteria.
• Dissociative Amnesia (F44.0)

• Dissociative Fugue (F44.1)
• Dissociative Stupor (F44.2)
• Trance and Possession disorders (F44.3)
• Dissociative Motor disorders (F44.4)
• Dissociative Convulsions (F44.5)
• Dissociative Anesthesia and Sensory Loss (F44.6)
• Mixed Dissociative (conversion) disorders (F44.7)
• Other Dissociative (conversion) disorders (F44.8)
• Dissociate (conversion) disorder, unspecified (F44.9)
From a psychoanalytic standpoint, a conversion disorder is caused by

repression of unconscious intrapsychic conflict and conversion of anxiety
into physical symptoms. The symptom allows partial expression of the
forbidden wish or urge but disguises it, so the patient can avoid con-
sciously confronting the unacceptable impulses. There are several clinical
features of dissociative disorders. Often, patients will exhibit “la belle
indifference,” seemingly undistressed by the physical symptoms they are
experiencing.
Symptoms tend to conform to the patient’s understanding of neurology
and do not have a consistent physical examination. Common symptoms
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have a rapid onset in the face of psychological stress and include non-
eliptiform seizures (pseudoseizures), blindness, deafness, paralysis, mut-
ism, falling, and psychogenic vomiting. Gait problems are also common;
astasia-abasia describes a dramatically unbalanced gait that could not
result from weakness or loss of balance without falls. Patients with asta-
sia-abasia do not fall but continue to walk in an unbalanced manner, with
writhing of the torso and often thrusting of limbs.
Treatment of dissociative disorders is generally quite conservative.
Providing patients with reassurance that the appropriate work-up has been
performed and that full recovery is expected is beneficial, as is addressing
identified stressors. Physical and occupational therapy are also key in
resolution of symptoms; initial symptoms of most patients resolve typi-
cally within a month with use of therapy. If the symptom can be resolved
by suggestion, hypnosis, or parenteral amobarbital24 it is probably the
result of a conversion disorder.
Patients with good prognostic factors are those who have onset of
symptoms following clear stressors and receive prompt treatment as com-
pared to those who have delayed treatment. Patients with symptoms of
paralysis, aphonia, or blindness have a better prognosis than those who
present with seizures or tremor.
6. FACTITIOUS DISORDER
Factitious disorder is defined as intentional exaggeration or induction of
signs and symptoms of illness in order to assume the sick role (Table 5).
For a diagnosis of factitious disorder, one must be able to establish the
Table 5. ICD-10 criteria for intentional production of feigning of symptoms or disabili-

ties, either physical or psychological [factitious disorder] (F68.1).
The individual exhibits a persistent pattern of intentional production of feigning of
symptoms and/or self-infliction of wounds in order to produce symptoms.
No evidence can be found for an external motivation such as financial compensation,
escape from danger, or more medical care.
Most commonly used exclusion clause. There is no confirmed physical or mental disorder
that could explain the symptoms.
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330 C. L. Wichman
intentional and conscious production of symptoms in oneself or others.

Other incentives to induce the illness, such as drug use, litigation, or
avoidance of work or military responsibilities, are absent.
The nature of factitious disorder makes it difficult to determine how
common it is; therefore, the prevalence in the general population is
unknown. Factitious disorder is diagnosed in about 1% of patients seen
in psychiatric consultation services in general medical hospitals.
Prevalence is similar in studies that have been performed in Toronto,
Berlin, and Belgium. Patients who work in the health care field, such as
nurses, often have elevated rates. Very little data are available on patients
with factitious disorder because these patients often resist psychiatric
evaluation. What is known is that these patients have typically suffered
from childhood abuse, which may have resulted in frequent hospitaliza-
tions, and hospitals are generally viewed as safe by these patients.
Patients frequently have comorbid personality, substance use, or mood
disorders.
A typical hospital admission for a patient with factitious disorder will
occur on a weekend or late at night. The patient often praises hospital staff
but quickly begins making demands of the medical team, which leads to
anger from the treatment team. Once discharged (either by the medical
team or against medical advice), the patient often is quickly readmitted to
another hospital.
Munchausen syndrome is defined as severe and chronic factitious
disorder; this encompasses approximately 10% of patients diagnosed
with factitious disorder. Pseudological fantastica is often seen in
Munchausen syndrome; it is defined as patients telling grand lies about
their educational or military credentials, past exploits, social or politi-
cal connections, and so forth. Limited factual material is mixed with
extensive and colorful fantasies, and the listener’s interest pleases the
patient and thus reinforces the symptom. Munchausen’s by proxy
occurs when a person intentionally produces physical signs or symp-
toms in another person who is under the first person’s care. Most com-
monly, it is perpetrated by mothers against infants or young children.
It occurs rarely or may be unrecognized; it accounts for approximately
1,100 of three million cases of child abuse reported in the United States
each year.
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Ganser’s Syndrome is characterized by the use of approximate answers.

Patients with this disorder respond to simple questions with astonishingly
incorrect answers (e.g. 1 + 2 = 4).
There are several methods of inducing signs and symptoms of factitious
illness, including exaggeration or lying about symptoms, tampering with
tests to produce positive results, or doing something that may cause actual
physical harm (e.g. injecting oneself with insulin or taking unprescribed
medications).
Factitious disorder by proxy is defined as a person who intentionally
produces signs or symptoms in another person who is under the first per-
son’s care (i.e. a child or vulnerable adult). Direct evidence is necessary,
as is exclusion of other causes. Other diagnoses to consider include medi-
cal illnesses, somatoform disorders, or malingering. There are several
factors that may predispose an individual to development of a factitious
disorder, including true physical illnesses in childhood that leads to exten-
sive medical treatment, employment (either currently or in the past) in the
medical profession, or a severe personality disorder.
Management of factitious disorder is difficult. Prognosis is poor. No
specific treatment has been shown to be effective in this patient popula-
tion. Early identification is most important, in order to prevent iatrogen-
esis from medical testing, followed by being mindful of negative
countertransference, as well as legal and ethical issues that may arise. By
explaining to medical staff that the patient likely has a serious psychologi-
cal disturbance, staff members are more likely to treat the patient with
respect after the diagnosis is made. Addressing any underlying psychiatric
diagnoses may be beneficial but are rarely allowed by the patient.
Nonetheless, patients should be offered the option of inpatient psychiatric
care or outpatient follow-up.
7. MALINGERING
Malingering (Z76.5) is the intentional production of illness; it is
distinguished from factitious disorder by the clarity of the motivation.
Patients who are malingering are motivated to obtain the sick role to gain
external incentives. The most common motives for malingering include
evading criminal prosecution, obtaining illicit drugs, avoiding military
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332 C. L. Wichman
conscription or dangerous military duty, and obtaining sickness benefits

or improvements in housing conditions. Patients in medico–legal set-
tings, such as prisoners or those involved with litigation, are more likely
to be malingering than those seen in a general psychiatric clinic.6
Detection of malingering can be difficult but should be attempted to
optimize patient care.
Malingering is rare in the general population but increases in psychiatric
populations and even more in the military and criminal populations.21
Common comorbid diagnoses include antisocial and borderline personality
disorders.
Malingering should be suspected when there is a discrepancy between
complaints and findings, patients are uncooperative with evaluation of
symptoms, external gains are obvious, or there is a concurrent antisocial
personality disorder.
There is no specific treatment for malingering. Once the diagnosis has
been made, the treatment team involved in the patient’s care should be
made aware so that they can respond appropriately to patient requests and
set suitable limits. Patients often leave once their deception has been dis-
covered. Because patients often have comorbid psychiatric disorders, they
may benefit from on-going treatment and decrease these behaviors over
time. Unfortunately, patients with a history of malingering are at risk for
repeated episodes. Generally, behaviors decrease as the potential to gain
is lost.
8. KEY POINTS
• The majority of patients with somatization disorder respond best to a
stable relationship with a primary care provider who provides on-
going, consistent care.
• Patients with somatization disorders have high rates of iatrogenic
morbidity and mortality; once diagnosed, patients should have proce-
dures and surgeries on the basis of objective findings, not subjective
symptoms described by the patient.
• Patients who do not meet full criteria for somatization disorder con-
tinue to have similar risks of complications and are likely to benefit
from the same treatment.
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• Conversion disorder may respond well to suggestion, hypnosis, or

amobarbital interview.
• Hypochondriasis is the only somatoform disorder that is as common
in men as it is in women.
• A typical hospital admission for a patient with factitious disorder
often occurs after-hours, with the patient initially praising hospital
staff but quickly becoming demanding of the medical team, which
leads to anger from the staff. Once confronted with the diagnosis, the
patient often becomes angry, leaves the hospital quickly, and is often
readmitted to another hospital.
• Although malingering is rare in the general population, its prevalence
increases in criminal and military populations.
9. SELF-ASSESSMENT
9.1. A 50-year-old woman admitted to the hospital from
the neurology clinic complains in a dramatic fashion
of bilateral ankle pain that she suffered while at work.
Multiple physicians have been involved. Legal action for
worker’s compensation is pending, but the patient does
not want the medical staff to confirm this chain of events.
A thorough outpatient evaluation has not revealed a clear
etiology for the pain complaints. Psychiatry has been asked
to evaluate for depression contributing to her pain, which
was felt to be disproportionate to the injury. She denies any
depression, psychosis, or anxiety symptoms or family history
of psychiatric issues. Testing is negative, and she becomes
increasing labile and irritable and begins to demand a more
aggressive work-up to find out what is wrong. She continues
to complain of 10/10 pain without appearing subjectively
distressed. Given these facts, the correct diagnosis is:
(A) Somatization disorder.
(B) Conversion disorder.
(C) Factitious disorder.
(D) Malingering.
(E) Hypochondriacal disorder.
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334 C. L. Wichman
The patient is likely exaggerating her pain symptoms secondary to her

pending legal action from her injury.6 This is evidenced by negative
outpatient and inpatient work-ups, as well as not appearing subjectively
distressed while complaining of significant pain.
Answer: D
9.2. A 26-year-old woman presents to a plastic surgeon’s office

requesting a rhinoplasty. She has had several other cosmetic
procedures by other surgeons. She describes her nares as
“too large” and the bridge of her nose as “too wide.” She
states that she thinks about her nose several hours daily
and has become more isolated lately because she fears
that others are focused on the appearance of her nose. No
deformity is noted by the surgeon. Which of the following
issues should be addressed during the consultation?
(A) Suicide risk.
(B) Ability to pay for procedure.
(C) Paranoia and suspiciousness.
(D) Plans for further cosmetic procedures.
(E) Previous psychiatric contacts.
This patient likely suffers from body dysmorphic disorder because she has
excessive concern about her appearance, without any identified defect by
a third party, and spends a significant amount of time preoccupied with
this concern. Patients with body dysmorphic disorder have an elevated
risk of suicide.16
Answer: A
REFERENCES
of Mental Disorders, 4th ed. Washington, DC.
2. Bass C, Peveler R, House A. (2001) Somatoform disorders: Severe psychiat-
ric illnesses neglected by psychiatrists. Br J Psych 879: 11–14.
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3. Cloninger CR, Reich T and Guza SB. (1975) The multifactorial model of
disease transmission. III. Familial relationship between sociopathy and
hysteria. Br J Psych 127: 23–32.
4. Eschobar JI, Gara M, Waitzkin H, et al. (1998) DSN-IV hypochrondriasis in
primary care. Gen Hops Psych 20: 155–159.
5. Fink P, Rosendal M, Toft T. (2002) Assessment and treatment of functional
disorders in general practice: The extended reattribution and management
model — an advanced educational program for nonpsychiatric doctors.
Psychosomatics 43(2): 93–131.
6. Ford CV. (2005) Deception syndromes: Factitious disorders and malingering.
In: Levenson JL (ed.), Textbook of Psychosomatic Medicine, American
7. Greeven A, van Balkom AJLM, Visswe S, et al. (2007) Cognitive behavior
therapy and paroxetine in the treatment of hypochondriasis: A randomized
controlled trial. Am J Psych 164: 91–99.
8. Hahn SR. (2001) Physical symptoms and physician-experienced difficulty in
the physician-patient relationship. Ann Intern Med 134(9 Pt 2): 897–904.
9. Kathol RG. (1997) Reassurance therapy: What to say to symptomatic
patients with benign or non-existent medical disease. Int J Psychiatry Med
27(2): 173–180.
10. Kenyon FE. (1965) Hypochondriasis: A surgery of some historical, clinical
and social aspects. Br J Psych 129: 1–14.
11. Kroenke K, Messina 3rd N, Benattia I, et al. (2006) Venlafaxine extended
release in the short-term treatment of depressed and anxious primary care
patients with multisomatoform disorder. J Clin Psych 67: 72–80.
12. Jakubietz M, Jakubietz RJ, Kloss DF, et al. (2007) Body dysmorphic
disorder: Diagnosis and approach. Plast Reconstr Surg 199: 1924–1930.
13. Knipschild P, Arntz A. (2005) Pain patients in a randomized trial did not
show a significant effect of a positive consultation. J Clin Epidemiol 58(7):
708–713.
14. Noyles Jr R, Stuart S, Watson DB, et al. (2006) Distinguishing between
hypochondriasis and somatization disorder: A review of the existing
literature. Psychother Psychosom 75: 270–281.
15. Phillips KA. (1998) Body dysmorphic disorder: Clinical aspects and
treatment strategies. Bull Menninger Clin Fall 62(4 Suppl A): A33–48.
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336 C. L. Wichman
16. Phillips KA, Menard W. (2006) Suicidality in body dysmorphic disorder:

A prospective study. Am J Psych 163: 1280–1282.
17. Phillips KA, Pagano ME, Menard W, et al. (2006) A 12-month follow-up
study of the course of body dysmorphic disorder. Am J Psych 163: 907–912.
18. Quill TE. (1985) Somatization disorder. One of medicine’s blind spots.
JAMA 254(21): 3075–3079.
19. Ravindran AV, da Silva TL, Ravindran LN, Richter MA, Rector NA. (2009)
Obsessive-compulsive spectrum disorders: A review of the evidence-based
treatments. Can J Psychiatry 54(5): 331–343.
20. Richardson RD, Engel CC. (2004) Evaluation and management of medically
unexplained physical symptoms. Neurologist 10(1): 18–30.
21. Sadock BJ, Sadock VA. (2007) Kaplan & Sadock’s Synopsis of Psychiatry,
10th ed. Lippincott Williams & Wilkins, Philadelphia, PA.
22. Sifneos PE. (1973) The prevalence of ‘alexithymic’ characteristics in psy-
chosomatic patients. Psychother Psychosom 22(2): 255–262.
23. Stefanis C, Markidis M, Christodoulou G. (1976) Observations on the evolu-
tion of the hysterical symptomatology. Br J Psych 128: 269–275.
24. Stonnington CM, Barry JJ, Fisher RS. (2006) Conversion disorder. Am J
Psych 163: 1510–1517.
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Chapter 14
The Dissociative Disorders
Jean M. Goodwin
1. INTRODUCTION
Dissociation is defined as disruption in the normally integrated functions
of consciousness, memory, identity, and perception.1 Severe dissociation
almost always occurs in a context of multiple, severe, and often sadistic
traumatic experiences beginning in early childhood.
The dissociative disorders mark the severe end of a spectrum of
trauma responses, which involve both anxiety and dissociation, a spec-
trum that begins with the disorders involving acute responses to stress
and continues in intensity to posttraumatic stress disorder (PTSD). At the
most severe end of this spectrum, individuals with major dissociative
disorders often report extreme and multiple past trauma, as well as
describing severe anxiety and dissociation; they often meet criteria for
other trauma-related conditions and other dissociative disorders.
Comorbidities, listed in Table 1, co-occur more frequently in these more
severe cases.
This discussion begins with an overview of the spectrum and then
focuses on the most complex condition, Dissociative Identity Disorder
(DID, formerly known as Multiple Personality Disorder).
337
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338 J. M. Goodwin
Table 1. Spectrum of trauma-dissociative disorders with frequent comorbidities (ICD

codes in parentheses).
Trauma-related disorders Comorbidities
Acute Reaction to Stress (308) Anxiety Disorders (300.0; 300.2; 300.3)
emotions predominate (.0) Hysteria, unspecified (300.10)
consciousness disturbed (.1) Conversion Disorder (300.11)
psychomotor disturbance (.2) Somatoform Disorder (300.8)
other disturbance (.3)
mixed (.4) unspecified (.9)
Post-Traumatic Stress Disorder (309.81) Substance Use Disorders (303; 304; 305)
Borderline Personality (301.83)
Depersonalization Disorder (300.6) Affective Disorders (296)
Dissociative Amnesia (300.12) Eating Disorders (307)
Dissociative Fugue (300.13) Impulse Control Disorders (312)
Dissociative Identity Disorder (300.14) Sexual Disorders (302)
Dissociative Disorder, Unspecified (300.12) Re-victimization
2. TRAUMATIC ANXIETY AND DISSOCIATION:

A SPECTRUM OF RESPONSE
All forms of anxiety — phobias, hyper alert scanning, sleep disturbance,
panic, compulsions — have long been understood as expectable responses
to life-threatening attack. We now understand that dissociative splitting of
consciousness is just as fundamental, allowing the individual total immer-
sion with one part of the mind in fight, flight, and other emergency
responses to threat, while pre-attack coping skills are kept separated in
another part of the mind. This mechanism preserves the everyday person-
ality, relationships, and coping skills that the individual will return to once
the attack is survived.
The acute reactions to stress can be understood as conditions in which
bits of traumatic experience have crossed the dissociative barrier and are
disrupting the everyday world. Pat Barker’s trilogy of historical novels2
about shell shock victims in World War I provides vivid illustrations of
these disorders. One soldier struggles with a stammer (psychomotor type),
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The Dissociative Disorders 339
another with outbursts of weeping (emotional type), another with hyper-

alertness that prevents sleep (disturbance of consciousness), and another
with constant nausea and vomiting (other acute reactions).
This de-linking of Behavior, Affect, Sensation, and Knowledge (the
“BASK” self-functions) is another aspect of the dissociative fragmenta-
tion of usually integrated functions.3 It is as if the mind protects itself from
overwhelming experience by allowing only isolated fragments to surface
deprived of context. Intrusive traumatic experiences may impact BASK
functions in the direction of either functional loss or hyper-function.12
Table 2 gives examples of both types of symptoms. The oscillation in
PTSD between inhibiting and activating symptoms stems in part from this
kaleidoscope of disparate BASK intrusions.
More fundamentally, it reflects the individual’s efforts to avoid disman-
tle and to deny the explosive emotions that characterize unprocessed
traumatic experiences; these nonetheless intrude episodically into every-
day life.
Like PTSD (covered in Chapter 11), the dissociative disorders include
both functional losses and intrusive states of activation. Dissociative
fugue (300.13) is characterized by the intrusion of traumatic flight
behaviors with loss of recent memory and the knowledge of one’s own
identity. Depersonalization disorder (300.6) involves a loss of affective
connection to one’s own body, identity, and relational world, with, at
times, traumatic intrusions, including the capacity to leave the body and
to see it from afar. Psychogenic amnesia (300.12) is defined as loss of
the knowledge of important events, usually distressing events, in the
individual’s life.
Table 2. Intrusive BASK fragments of traumatic memory lead both to

functional loss and disruptive hyper-functioning.
BASK element Functional loss Intrusive hyper-function
Behavior Paralysis Re-enactments
Affect Emotional Numbing Emotional Flashbacks
Sensation Anesthesia Somatic Flashbacks
Knowledge Amnesia Traumatic Abreactions
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340 J. M. Goodwin
3. DISSOCIATIVE IDENTITY DISORDER

DID (ICD 300.14) is the best studied of the dissociative disorders. It is
defined as the presence of two or more distinct personality states that
recurrently take control of the person’s behavior; some evidence of mem-
ory gaps or lost time is also required. DID often involves elements of
fugue (finding oneself somewhere and not knowing how one got there and
having lost memory for some time), of depersonalization (feeling a stran-
ger both to one’s environment and to one’s own body), and of psychogenic
amnesia (having no recollection for important past events, encountering
belongings or acquaintances that one cannot account for). This chapter
will focus on the diagnosis and treatment of DID and related complex and
severe atypical dissociative disorders (DDNOS; ICD 300.15).
3.1. Epidemiology
Nineteenth-century Anglo–European physicians encountered dissociative
symptoms in their explorations of hysteria and hypnosis.12 Hysterical sub-
jects manifested BASK symptoms in varying combinations; they tended
to be highly hypnotizable; they often described tragic and chaotic
childhoods.7
The first reported case of DID in North America was a British immi-
grant, Mary Reynolds, who was in her early twenties when she fell ill in
1811.6 At that time Shawnees were raiding settlements near her frontier
home and the War of 1812 was threatening to break out. Mary’s family
had fled religious persecution in England in the 1790s; Mary and her
brother had crossed the Atlantic on their own when they were both still
children; two of Mary’s closest sisters had died of infections. None of
these traumatic circumstances was noted by nineteenth-century commen-
tators. They focused instead on the phenomenology of her illness. Mary A,
the “original” personality was dour, staid, depressed, and often in ill
health. Mary A suffered periodic fainting spells. After a particularly
prolonged trance state, Mary B appeared, requiring to be spoon fed and
re-taught to speak and read and seeming to the family like a new-born
identity. Mary B was playful, irrepressible, and funny. She had no access
to Mary A’s litany of tragic memories and, like some patients with
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psychogenic fugue, seemed prepared to start life anew with a new identity.
Mary A and Mary B were mutually amnestic and switched back and forth
for over a decade. At last, Mary seemed to stabilize in a state that she
described as a combination of both A and B. A close relationship with her
brother and with the local country doctor seemed to facilitate her
recovery.
Two hundred years later, we know that DID has been described in over
25 different countries, including Argentina, Turkey, Israel, Oman, Iran,
Australia, the Philippines, and Japan. It is difficult to estimate the preva-
lence of this disorder. It must be persistently under-diagnosed, because
many studies show that the average patient spends 5–13 years in the men-
tal health system before the diagnosis is made.8
3.2. Etiology of dissociative disorders

As indicated above, nineteenth-century observers documented BASK
functional losses and hyper-functioning in hysterical patients and linked
these to hypnotisability. Research in the twentieth century has made the
link to childhood trauma.7
Some trauma theorists understand hypnosis as part of a trauma response
system that humans share with most animals and birds.20 Table 3 lists
qualities of the trance state and indicates how each can contribute to the
survival of an individual attacked by a predator.
In the typical urban, Western case of childhood trauma, the predator is
likely to be a family member. Issues of secrecy and betrayal make it even
more necessary for the child to keep the attack as separate as possible from
the everyday world of school, play, and positive attachments. The dissocia-
tive barrier, conceptualized as overlapping with hypnotic capacity, protects
this everyday, here and now world from vivid and disruptive memories.
This barrier also protects the everyday self (termed by van der Hart
et al.19 as “the apparently normal personality”) against other aspects of the
internal world of trauma (which they call “the emotional personality”).
Animals under attack (see Table 4) resort to a well-described arsenal of
emergency reactions: fight, flight, freeze, surrender, repeated distress
calls, and the reparative behaviors also called “tend and befriend.”13,18
These behavioral states, although life-saving during a predatory attack,
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342 J. M. Goodwin
Table 3. How trance capacity might facilitate survival of an individual

under attack.
Quality of trance state Survival adaptation
Deep Relaxation, Stillness Hiding from predator
Focused Attention Monitoring, predicting predator behavior
Enhanced Suggestibility Rapid response to threat signals
Capacity for Vivid Perceiving and planning escape routes
and Visual Imagery
Anesthesia Continued fight/flight even if injured
Amnesia Prevention of post-attack avoidance that
might functionally reduce territory
Table 4. Characteristics of the trauma world (“emotional personality”). The “apparently

normal personality” protects itself from these disruptive contents with a dissociative
barrier and by active avoidance.
Living in the “there and then” of traumatic experience.
Traumatic memories experienced vividly as if taking place right now in real time.
Impulses to:
Fight for one’s life
Flight
Freeze in hyper-alert watchfulness
Surrender, “play dead”
Emit repeated distress signals
Engage in reparative “Tend and Befriend” activities
(Self-grooming, Binge eating, Tending to co-victims)
Victim/Perpetrator/Rescuer fantasies
can be disruptive if they emerge into everyday life. The capacity to fight
to the death, so necessary in combat, can lead, if re-enacted back home, to
criminal charges. The swift, compulsive eating that provides necessary
re-fuelling under attack can, if it becomes chronic, turn into a life-threat-
ening eating disorder.
As dissociation escalates to keep at bay both traumatic memories and
emergency protective mechanisms, dissociation itself becomes a problem,
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with “trancing out,” “lost time,” and other trance-like disturbances of con-
sciousness intruding into the everyday world, as well as fragments of
traumatic experience.
3.3. Phenomenology of dissociative identity disorder

Like other trauma-dissociative disorders, DID is characterized by disrup-
tive intrusions: (a) from BASK memory fragments (Table 2); (b) from
trancelike dissociative elements (Table 3); and (c) from the self-protective
impulses that are part of the world of trauma (Table 4).
What makes DID more complex is that in this condition some trau-
matic intrusions become personified. Instead of a flashback to an over-
whelming experience of child abuse, there is the emergence of a
personification of the hurt and needy child experiencing the abuse as if it
were happening in the here and now, a “child alter.” Instead of the inter-
mittent avoidance and emotional numbing that one sees in PTSD, this set
of symptoms may be personified as a depleted and restricted “host alter,”
perhaps phobic of and antagonistic to the “child alter.” A personification
encompassing many intrusive trance phenomena might describe itself as a
disembodied, pain-free “observer.” A personification constructed around
the “fight” response might be viewed by the “child” as a protector but seen
by the “host” as a persecutor. The repeated distress call might be personi-
fied as a “self-harming alter,” and “tend and befriend” impulses could be
personified as a compulsive “helper” who persists in trying to please and
appease others, even abusers.
How does this happen? Kluft9 hypothesizes that when extreme and
chronic traumatic experience coincides with extreme and chronic absence
of secure attachment or other refuges, the young child’s only protection is
to escape into fantasy. Table 5 gives examples of how fantasized narratives
of rescue can be personified and then internalized.10 Intermediate steps in
this process might emerge as the experience of a comforting imaginary
companion or as extreme over-idealization of a potential external rescuer.
Unfortunately, these personified subsystems of the personality become
yet another source of disruptive intrusions, most commonly in the form of
“voices inside the head.” When rescue plans are quite disparate and even
mutually incompatible, this can be experienced as a species of internal
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344 J. M. Goodwin
Table 5. How survival impulses and fantasies in a sexually abused girl might lead to the
formation of internalized personified rescuers.
Survival impulse Internalized personified rescuer
“I wish I were somewhere else” “Space Alien” lives on another planet
“I wish it would be over” “Sexual Expert” brings her partners to climax
swiftly
“I’d feel better if I could throw up” “Queasy” is always nauseated
“I wish my mother would help” “Mommy” tries to protect younger siblings
“I wish he were dead” “Killer” is always hostile and threatening
warfare. Each subsystem is subject to BASK disruptions from “the

others” — sudden impulses, overwhelming affects, inexplicable bodily
sensations, or intrusive thoughts.
Less frequently, the disruption takes the form of a “switch,” with an
alternate personality suddenly “taking over.” However, switching is
detectable in only about 15% of individuals with DID; thus, to require a
witnessed “switch” is an overly conservative way to make the diagnosis.
Identifying a lifelong pattern of subjective intrusions is the more sensitive
and specific diagnostic strategy.8 Evidence of such a pattern can be found
at times in childhood diaries or school records.9,10
In most cases, the fragmented internal self-system is kept hidden and
struggled against in the same way as are the traumatic memories, trance
elements, and emergency protective states. Given this intensely subjective
phenomenology, it is important for clinicians to screen systematically
when they suspect DID. Intrusions that might trigger screening11 include
voices inside the head, spontaneous age regression, unremembered behav-
iors, repeated self-harm with anesthesia and amnesia, trancing out, lost
time, out-of-body experiences, repeated fugues, pseudo-seizures, pro-
longed psychotic flashbacks, and unremitting somatic or emotional
flashbacks.
The most widely used screening instrument is the Dissociative
Experiences Scale (DES), a 28-item self-test, with each item scored 0 to
100.4 An overall average score of 30 or above is highly suggestive of the
presence of a disorder. The DES is available at no cost on the Internet
(www.isst-d.org). Ross and co-workers16 have developed a simple
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structured interview, The Dissociative Disorders Interview Schedule,

which is also available on the Internet (www.empty-memories.nl/dis_89/
Ross_structured interviews). Diagnosis of more difficult cases may
require the Structured Clinical Interview for DSM-IV Dissociative
Disorders, but training is necessary for optimal use of this instrument.8
The clinician working with complex traumatic dissociation for the first
time needs allies and resources. The website of the International Society
for the Study of Traumatic Dissociation (www.isst-d.org) offers (1) list-
ings of members who can be called upon to consult or render second
opinions; (2) detailed clinical guidelines describing additional diagnostic
instruments and treatment techniques; (3) information about an intensive
introductory curriculum for clinicians, which can be taken online or in
person at various international sites; and (4) information about member-
ship, annual meetings, the society’s journal, the society’s newsletter, and
other educational resources.
3.4. Treatment of DID: timing and techniques

As in other trauma-dissociative disorders, the treatment of DID is best
approached in a phase-specific way.17 In Stage One, safety is achieved, as
well as control of the most disruptive symptoms. Traumatic experiences
are processed and integrated in Stage Two. In Stage Three, normal devel-
opmental tasks — derailed first by traumatic experience and subsequently
by symptoms — are resumed and completed.
The DID patient may present with on-going abuse, multiple comorbidi-
ties, and global threats to basic needs. This state of un-safety, which I have
termed Stage Zero, precludes all but the most basic interventions — find-
ing shelter, making a police report, achieving sobriety, getting a physical
examination.14 Even when Stage One work can be started, this must often
begin by addressing the multiple comorbidities — affective disorders,
anxiety disorders, addictions, chronic self-harm. Months and years may
elapse before work can begin on the traumatic intrusions, and even then,
work on the personifications may have to give place to containment of
more disabling symptoms.
Although medication is helpful in managing comorbidities, psycho-
therapy is the only treatment specific for dissociation.15 The therapist
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346 J. M. Goodwin
treating these cases works within a narrow and paradoxical space, which
requires both firm boundaries and flexible emotional accessibility, both
comfortable expertise and utter respect for the patient’s autonomy. This
kind of psychotherapy requires a rare combination of expertise in psycho-
dynamic psychotherapy, skills in trauma therapy, and basic familiarity
with specific techniques for working with the internal system.
The clinical case gives examples of specific interventions in Stage One
work as well as sources for further study.10,15 The case, although illustra-
tive, is atypical in many ways: (a) male gender and diagnosis in middle
rather than early adulthood; (b) absence of significant comorbidities;
(c) presence of a relatively crisis-free present-day life with optimal access
to allies, resources, and treatment; and (d) an unusually free and creative
capacity for the use of imagery. In the more typical, more difficult case,
this stage might not be reached for many years, and when reached, the
work toward co-consciousness and cooperation might consume many
more years.10
Stage Two psychotherapy moves the treatment from stabilizing the
everyday life to the more painful and frightening zone of unprocessed
trauma memories and reactions. The clinician relies on the strong thera-
peutic alliance and emotional attunement achieved during Stage One.
Patients skilled in dissociation are quite capable of describing traumatic
experiences and then becoming so anxious that they re-dissociate every-
thing. This is to be avoided. All the anti-anxiety techniques learned in
Stage One are required here and more. Lifelong reliance on dissociation
may have left the patient bereft of other strategies for coping with anxiety.
Psycho-education, Dialectical Behavioural Therapy and other systematic
interventions to teach emotional containment may be required.
Some of the special techniques used in PTSD can be useful, such as
written trauma narratives or eye movement desensitization retraining.8
Imagery remains important. The traumatic episode can be put onto an
imaginary storage disc with many options for replay: (a) with certain
sections visually blocked; (b) without sound; (c) with restricted viewing
for child alters; (d) with the option to stop play after only a few seconds;
and so forth. Anxiety can be imagined as draining into an ocean of calm.
An anxiety alarm can be created in imagery that signals the system when
to close down processing and initiate calming measures. Managing the
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group dynamics of the system remains important. Those alters who did
not experience a particular traumatic memory can sometimes comfort the
overwhelmed alter who is abreacting it.
Stage Three therapy is similar to psychodynamic work with other
adults who have grown up in chaotic environments. Unification and post-
unification strategies are the unique elements here.10 Stable fusions often
benefit from a special session in which relaxation and imagery are used to
consolidate the process. An example would be imaging the previous per-
sonalities as streams that have now flowed into one another. Post-
unification work involves careful exploration to ascertain that all the
BASK elements contained in the previously separate alters are represented
in the new configuration — skills, emotional capacities, bodily sensations,
motor functions, memories, and ways of thinking.
4. SPECIAL ISSUES IN DISSOCIATION

Individuals with dissociative disorders, because of the frequent history of
victimization and re-victimization and because of dissociated behaviors,
may find themselves in legal difficulty. Nowhere is the general recom-
mendation more important that forensic planning and evaluation should
be kept separate from the clinical treatment plan. Dissociation is a disor-
der of memory; it affects memory registration, rehearsal, and storage.
Sequencing, sourcing, contexting, and dating memories may be very dif-
ficult. Despite this, many clinicians, starting with Sigmund Freud, have
found external validation for the fragmented accounts of their patients.
Nonetheless, the question of capacity to witness in these cases is a diffi-
cult one, which should be dealt with by an outside expert, not by the treat-
ing clinician.
Access to treatment is another difficulty in these cases. In many
countries, including the United States, the individual who requires dec-
ades of psychotherapy confronts a dearth of resources. This can be miti-
gated somewhat by a stage-based approach that addresses Stage Zero
problems and the comorbidities before proceeding to the traumatic dis-
sociative symptoms that require more specific psychotherapy approaches.
A team approach is also helpful. Such a team might include a primary
care physician, a twelve-step group, a medicating psychiatrist, an
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348 J. M. Goodwin
inpatient or day treatment facility, a marital therapist, and an individual

therapist. This team approach is much less vulnerable to disruption by
a caregiver vacation or retirement and much less burdensome to each
team member.
Difficulties arise as well when a dissociative patient encounters a clini-
cian who asserts that DID does not exist. In a condition defined by identity
confusion, this can be confusing. It is useful in these situations to try to
explain the clinician to the patient, as well as trying to educate the clini-
cian about dissociation. Dissociative individuals have lifelong experience
in avoiding trauma and can understand that other individuals and groups
tend to use the same strategy. Biological psychiatrists prefer to understand
symptoms in terms of disorders for which effective medications exist.
Psychodynamic clinicians tend to see symptoms in terms of object rela-
tions, disturbed attachment, repetitive personality patterns, and deficits in
self-soothing. Hypnotherapists are concerned about suggestibility in
highly hypnotizable individuals. Family therapists understand trauma dis-
closures in the context of on-going family conflict. All these viewpoints
have merit, and none is incompatible with the recommendations of this
chapter. Disbelieving clinicians can at times work productively with the
treatment team, especially within a defined focus on a comorbid condi-
tion. Even today, many training programs do not cover traumatic dissocia-
tion systematically; often practitioners must find their own way to relevant
information while grappling with their first case.
Clinician exhaustion, counter-transference, and enactment have
spawned an entire sub-literature in the trauma field. Most dissociative
systems include alters capable of engaging the clinician’s grandiosity as
well as other alters adept at triggering victimization fantasies and/or
vengeful rage. Especially for the neophyte clinician, consultation is
almost always indicated.8
In summary, meaningful therapy in these cases depends on a therapeu-
tic alliance that offers enough connection and reliability to support the
disclosure of previously hidden subjective intrusions; an understanding of
these phenomena as expectable and essentially human responses to life-
threatening experiences; and the step-by-step co-creation of new coping
tactics to decrease anxiety and process traumatic mental contents so that
the need for dissociation is diminished.
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5. CASE STUDY
A 40-year-old married Italian–American professional was referred by his
marital therapist, who had observed that Frank responded in sessions in
widely disparate ways. He could be harshly accusatory of his wife,
extremely solicitous, coldly intellectual, or briskly business-like. At times,
he would simply walk out. Frank was relieved by the referral and eager to
talk for the first time about the 12 different “channels” that governed his
life.
“Husband” and “Papa” were the personalities most involved in the mar-
riage. “Husband” felt injured and misunderstood when his wife saw him
as over-controlling; he saw himself as a protector, not a perpetrator. He
explained that when he became angry, harsher personalities, like
“Enforcer,” would “jump in.” The abandoning alter, “Lefty,” was based on
his own childhood experience with a rejecting father. Mapping of the sys-
tem indicated that “Teenager,” “Intellectual,” and “Financial Guy” also
interacted with the wife. The clinician, talking through to all involved
personalities, planned appointments with each and suggested they form a
committee to improve the marriage. This committee began to meet at an
imagined table in an imaginary meeting place5 and soon reported that
other alters were “hanging out” nearby. They noted that together they
could block sudden takeovers by alters who were too young or too upset
to handle situations at an adult level. They were now managing switches
more smoothly; previously, switches had been accompanied by severe
headaches and confusion. Now the two involved alters simply touched the
“table” when they were ready to exchange places. “Enforcer” agreed to
change jobs and, instead of trying to limit the wife’s activities, took a
more backstage role in designing a security system for the home; he
warned that an angrier alter, “Bruiser,” was not yet ready to join the com-
mittee and helped design a glass booth using this imagery to contain the
threatening alter. “Papa” became involved in caring for the child alters and
built an imaginary playhouse near the table so that they could have a safe
place. He also helped the most traumatized child begin to draw pictures of
his abuse in an imaginary sketchbook. In the reality sphere, the adult alters
kept a daily journal, which they used to reconstruct lost time when that
occurred and to post questions that other alters might be able to address.
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350 J. M. Goodwin
On subsequent maps, “Husband” and “Papa” were drawn as almost over-

lapping; they began to practice temporary fusions and chose a name for
the unified entity they would become.
REFERENCES
of Mental Disorders, 4th ed. Text Revision, American Psychiatric Association,
Washington, DC.
2. Barker P. (1991) Regeneration, Penguin, London.
3. Braun B. (1988) The BASK model of dissociation. Dissociation 1: 4–23.
4. Carlson EB. (1997) Trauma Assessments: A Clinician’s Guide, Guilford
Press, NY.
5. Fraser GA. (2003) Fraser’s “Dissociative table technique” revisited, revised.
J Traumatic Dissociation 4: 5–28.
6. Goodwin J. (1987) Mary Reynolds: Post-traumatic factors in the first
reported case of multiple personality disorder. Hillside J Clin Psychiatry 9:
89–99.
7. Goodwin J. (1993) Rediscovering Childhood Trauma. American Psychiatric
8. International Society for Study of Traumatic Dissociation. (2010) Guidelines
for Treating Dissociative Identity Disorder in Adults.
9. Kluft RP. (1999) Body-ego integration in dissociative identity disorder. In:
Goodwin J, Attias R (eds), Splintered Reflections: Images of the Body in
Trauma, Chapter 11, pp. 239–255, Basic Books, NY.
10. Kluft RP. (1999) Current issues in dissociative identity disorder, J Pract
Psychiatr Behav Health 5: 3–19.
11. Loewenstein RJ. (1991) An office mental status examination for complex
chronic dissociative symptoms and multiple personality disorder. Psychiatr
Clin N Am 14: 567–604.
12. Nijenhuis ERS, van der Hart O. (1999) Somatoform dissociative phenomena:
A Janetian perspective. In: Goodwin J, Attias R (eds.), Splintered Reflections:
Images of the Body in Trauma, Chapter 4, pp. 89–128, Basic Books, NY.
13. Nijenhuis ERS, van der Hart O. (1999) Forgetting and re-experiencing
trauma. In: Goodwin J, Atttias R (eds.), Splintered Reflections: Images of the
Body in Trauma, Chapter 2, pp. 39–65, Basic Books, NY.
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14. Nykiel SA, Baldessarini RJ, Bower MC, Goodwin J, Salvatore P. (2008)
Psychosis NOS: Search for diagnostic clarity. Harv Rev Psychiatry 16: 55–65.
15. Putnam FW. (1989) The Diagnosis and Treatment of Multiple Personality
Disorder, American Psychiatric Publishing, Inc., Arlington, VA.
16. Ross CA, Heber S, Norton GR, Anderson D, Anderson G, Barchet P. (1989)
The dissociative disorders interview schedule: A structured interview.
Dissociation 2: 169–218.
17. Steele K, van der Hart O, Nijenhuis ERS. (2005) Phase-oriented treatment of
structural dissociation in complex traumatization: Overcoming trauma-
related phobias. J Trauma & Dissociation 6: 11–54.
18. Taylor SE. (2002) The Tending Instinct, Henry Holt (Macmillan), NY.
19. van der Hart O, Nijenhuis ERS, Steele K. (2006) The Haunted Self,
WW Norton, NY.
20. Volgyesi FA. (1963) Hypnosis of Man and Animals, Lippincott Williams &
Wilkins, NY.
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Chapter 15
Sleep Disorders in Psychiatry
Oludamilola A. Salami
1. INTRODUCTION
Sleep is an integral part of normal physiological functioning in humans
and is critical for good health. The lack of sleep produces significant
direct and indirect morbidity and mortality. The yearly prevalence of sleep
disorders varies from 20%–40% of adults. The wide range could be due
to the classification systems used in the diagnosis of sleep disorders. The
scope of sleep medicine is quite broad and has garnered multidisciplinary
interest from medical specialties including psychiatry, neurology, internal
medicine, and surgery. In this chapter, we will focus on the normal physi-
ology of sleep as well as the psychiatric aspects of its patho-physiology.
The clinical features and management of common sleep disorders will
also be discussed.
2. PHYSIOLOGY OF NORMAL SLEEP

Normal sleep is a complex brain process regulated by endogenous and
exogenous mechanisms, including the circadian rhythms, homeostatic
mechanisms, and influences from the autonomic nervous system.3,4
Homeostatic sleep mechanisms are similar to the normal physiological
states that drive goal-directed behaviors (e.g. sex, hunger, and thirst). This
is evidenced by the increasing desire to sleep, the longer one stays awake
culminating in an irresistible urge to sleep after a protracted period
352
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Sleep Disorders in Psychiatry 353
without sleep. However, as one may have noticed after remaining awake
for about 24 hrs, a burst of wakefulness often occurs, which would be
unexpected solely on the basis of homeostatic sleep mechanisms. This
process is due to the circadian rhythm. The circadian rhythm is based
roughly on a 24-hour sleep-wake cycle that is regulated by neurobiologi-
cal mechanisms and exogenous cues. Exogenous regulation is via
“zeitgeber,” which is a German term for “time giver.” “Zeitgeber” is
believed to synchronize the internal sleep mechanisms with the 24-hour
light/dark cycle. The suprachiasmatic nucleus (SCN) is thought to be the
pacemaker of the circadian rhythm and is a key component in its regula-
tion. The SCN functions are modulated via the retino–hypothalamic tract,
where ambient light stimulates the melanopsin-containing retinal gan-
glion cells to aid in wakefulness during the day, and the pineal gland,
which secretes melatonin in response to diminished ambient light in the
evenings, promoting sleepiness. There are also neurotransmitter-based
systems that promote wakefulness through effects mediated via the
ascending reticular activating system located in areas of the midbrain and
brainstem. The key neurotransmitters thus identified include norepineph-
rine, serotonin, acetylcholine, glutamate, and dopamine.
3. STAGES OF SLEEP
There are two primary types of normal sleep: Rapid eye movement (REM)
sleep and Non-rapid eye movement (NREM) sleep. NREM sleep is
further subdivided into NREM-1 and NREM-2 (formerly designated as
Stages 1 and 2) and NREM-3 (formerly Stages 3 and 4). NREM-1 and
NREM-2 are light stages of sleep, while NREM-3 encompasses deeper
sleep, with its characteristic slow wave sleep. The stages of sleep are
determined with the aid of a polysomnogram (PSG). The PSG involves
monitoring brain activity with electroencephalography (EEG), heart
rhythm with electrocardiography (EKG), skeletal muscle activity with
electromyography (EMG), eye movements with electrooculography
(EOG), nasal and oral airflow with pressure transducers, and blood oxy-
gen levels with pulse oximetry.
During periods of wakefulness, the EEG shows high-frequency waves
with low-amplitude, and the EMG reveals presence of muscle tone,
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354 O. A. Salami
particularly in the skeletal muscles. NREM-1 occurs at sleep onset and is

characterized by the disappearance of alpha (8–12 Hz) and appearance of
theta waves (4–7 Hz) on EEG. NREM-2 has characteristic sleep spindles
(short bursts of 12–14 Hz waves) and K-complexes (high amplitude
waves) on the EEG. NREM-3 is defined by 20% or more delta waves
(1–4 HZ with high amplitude). The hallmarks of REM sleep are the pres-
ence of low-amplitude, high-frequency waves, reduction or absence of
muscle tone, and rapid eye movements on the EOG.
The characteristic progression of sleep stages during the night features
NREM sleep at onset, which alternates with REM approximately every
60–90 mins (see Fig. 1). NREM-3 density is higher in the initial third of the
sleep cycle, and REM sleep increases over the course of sleep becoming
more prevalent in the latter third of the sleep cycle with increasing density.
REM latency is the time from sleep onset to the first REM sleep period. It
is important to note that there are normal changes in sleep patterns that
occur with age; the total sleep time diminishes, REM sleep portion of over-
all sleep, which is initially high following birth, gradually declines to about
20%–25% by adolescence; and NREM-3 gradually declines beginning at
adolescence and completely disappears in some elderly individuals.
Fig. 1. Sleep stages.
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4. CLASSIFICATION OF SLEEP DISORDERS

There are two major classifications for sleep disorders. These are the
DSM-IV-TR and ICSD. The scope of the DSM-IV-TR classification sys-
tem was developed by the American Psychiatric Association (APA) and
is geared towards mental health providers. The ICSD is a comprehensive
classification system developed by the American Academy of Sleep
Medicine in association with several regional sleep societies as a diag-
nostic and coding manual for sleep disorders. The ICD-10 is a compre-
hensive coding manual of all diseases, with a sub-section on sleep
disorders, based on the World Health Organization (WHO) classification
of diseases.
The DSM-IV-TR groups sleep disorders into three broad categories and
several sub-categories:2
(1) Primary sleep disorders

(a) Dyssomnias; Primary insomnia, primary hypersomnia, narco-
lepsy, breathing related sleep disorder, circadian rhythm sleep
disorder, and dyssomnia not otherwise specified
(b) Parasomnia; Nightmare disorder, sleep terror disorder, sleepwalk-
ing disorder, parasomnia not otherwise specified
(2) Sleep disorders related to another mental disorder
(a) Insomnia due to an Axis I or II disorder
(b) Hypersomnia due to an Axis I or II disorder
(3) Other sleep disorders
(a) Sleep disorder due to a general medical condition
(b) Substance induced sleep disorder.
The International Classification of Sleep Disorders divides sleep dis-

orders into four major categories:1
(4) Dyssomnias
(a) Intrinsic Sleep Disorders
(b) Extrinsic Sleep Disorders
(c) Circadian Rhythm Sleep Disorders
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356 O. A. Salami
(5) Parasomnias
(a) Arousal Disorders
(b) Sleep–Wake Transition Disorders
(c) Parasomnias Usually Associated with REM Sleep
(d) Other Parasomnias
(6) Sleep Disorders Associated with Mental, Neurologic, or Other
Medical Disorders
(a) Associated with Mental Disorders
(b) Associated with Neurologic Disorders
(c) Associated with Other Medical Disorders
(7) Proposed Sleep Disorders
(a) Short Sleeper
(b) Long Sleeper
(c) Sub-wakefulness Syndrome
(d) Fragmentary Myoclonus
(e) Sleep Hyperhidrosis
(f) Menstrual-Associated Sleep Disorder
(g) Pregnancy-Associated Sleep Disorder
(h) Terrifying Hypnagogic Hallucinations
(i) Sleep-Related Neurogenic Tachypnea
(j) Sleep-Related Laryngospasm
(k) Sleep Choking Syndrome
ICD-10 describes sleep impairment as either a symptom of an underlying

organic disorder or as a non-organic sleep disorder. The non-organic sleep
disorders of the ICD-10 include the following:
(1) Non-organic insomnia

(2) Non-organic hypersomnia
(3) Non-organic disorder of the sleep-wake schedule
(4) Sleepwalking [somnambulism]
(5) Sleep terrors [night terrors]
(6) Nightmares
(7) Other non-organic sleep disorders
(8) Non-organic sleep disorder, unspecified
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Due to the limited descriptive scope of the ICD-10 classification of sleep

disorders, we will discuss the disorders of sleep primarily on the basis of
the classification outlined in the DSM-IV-TR, with some references to the
ICSD.
5. PRIMARY SLEEP DISORDERS

The primary sleep disorders are those that originate as a primary abnor-
mality in physiology or pathology that is not secondary to another patho-
logic process such as mental illness, medical illness, or substance use.7
Both dyssomnias and parasomnias are included in this category. Some
disorders produce symptoms of insomnia, such as psychophysiological
insomnia, sleep state misperception, restless legs syndrome, and idiopathic
insomnia. Others, like narcolepsy, recurrent hypersomnia, idiopathic
hypersomnia, and posttraumatic hypersomnia, are primarily disorders of
excessive sleepiness, whereas obstructive sleep apnoea syndrome, central
sleep apnoea syndrome, central alveolar hypoventilation syndrome, and
periodic limb movement disorder can produce a complaint of either
insomnia or excessive sleepiness.
Idiopathic insomnia can be defined as a lifelong inability to obtain
adequate sleep. It is suspected that the etiology is from a defect in the
neurological systems that modulate sleep function. The prevalence and
gender differences are not known, but idiopathic insomnia is rare and
often begins at birth. Characteristics include complaints of unremitting
difficulty initiating or maintaining sleep or non-restorative sleep begin-
ning in early childhood or birth. Polysomnography may show evidence of
an increase in sleep latency, a reduction in sleep efficiency, or an increase
in number and duration of nocturnal awakenings.
Psycho–physiological insomnia occurs in individuals who have an
underlying unacknowledged or unknown stressor and have developed a
conditioned arousal response to sleep. Patients complain of insomnia and
decreased functioning during wakefulness. They often try unsuccessfully
to sleep at home or when desired but may easily fall asleep when away
from their bedroom or at other times, such as when watching television or
reading. Polysomnography shows an increase in sleep latency and number
and duration of awakenings, as well as a reduction in sleep efficiency.
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358 O. A. Salami
Sleep-state misperception is characterized by complaints of insomnia

with objective evidence of normal sleep duration and quality on
Polysomnography.
5.1. Dyssomnias
Dyssomnias are primary sleep disorders that are characterized by impair-
ment in the quantity, quality, or timing of sleep. Persons with the various
types of dyssomnias have difficulty initiating or maintaining sleep and
may also have complaints of excessive sleepiness.
Primary insomnia (Table 1) can be defined as sleep impairment that is
not directly attributable to a medical, psychiatric, or environmental cause.8
This category also loosely correlates to the ICD-10 classification for non-
organic insomnia. Primary insomnia affects up to 25% of patients with
chronic insomnia and can be regarded as a disorder of hyperarousal. Using
the ICSD classification, there are three types of primary insomnia: idio-
pathic insomnia, psycho–physiologic insomnia, and paradoxical insomnia
(formerly sleep-state misperception).
5.2. Management
The management of primary insomnia follows the same principles as other
medical disorders.6,10 It is important to take a good history and perform a
physical exam, guided by pertinent positives in the history. Elements of
Table 1. DSM-IV-TR classification of primary insomnias.
(A) The predominant complaint is difficulty initiating or maintaining sleep, or

non-restorative sleep, for at least one month.
(B) The sleep disturbance (or associated daytime fatigue) causes clinically significant
distress or impairment in social, occupational, or other important areas of functioning.
(C) The sleep disturbance does not occur exclusively during the course of narcolepsy,
breathing-related sleep disorder, circadian rhythm sleep disorder, or a parasomnia.
(D) The disturbance does not exclusively occur during the course of another mental
disorder (e.g. major depressive disorder, generalized anxiety disorder, a delirium).
(E) The disturbance is not due to the direct physiological effects of a substance
(e.g. a drug of abuse, a medication) or a general medical condition.
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good sleep history include the sleep symptoms causing distress and pattern
of sleep, including time to bed, awakening time, sleep latency, awakenings
during the night, and frequency of daytime naps. In addition, associated
symptoms should also be elicited: respiratory symptoms, including snoring
and apnoeic episodes; headaches and memory changes; gastrointestinal
symptoms; and cardiovascular, pulmonary, and mood symptoms. Questions
pertaining to sleep hygiene should also be asked and should include activi-
ties around bedtime, such as snacking, exercise, alcohol consumption,
ambient temperature in the room, and other environmental factors.
Further investigations may be warranted, if there is ambiguity regard-
ing the diagnosis. Patients are asked to keep a sleep diary or chart to
accurately monitor sleep habits. Other investigations include a sleep study.
The sleep study may either be a polysomnography, multiple sleep latency
test, or actigraphy. The multiple sleep latency test, which is an important
diagnostic tool, follows a polysomnography the night before and consists
of four or five 20-minute nap opportunities that are scheduled about two
hours apart. Actigraphy is a non-invasive method of monitoring human
rest/activity cycles by measuring gross skeletal motor activity.
5.3. Treatment
Non-pharmacological strategies aimed at ameliorating insomnia are based
on cognitive behavior therapy and include attention to sleep hygiene,
patient education, stimulus control, behavioral interventions, sleep restric-
tion therapy, and relaxation therapy.
(a) Sleep hygiene and education involves maintaining healthy and regular
sleep habits (e.g. avoiding exercise shortly before bed, no alcohol
before bed, consistent time to bed).
(b) Stimulus control includes creating a quiet and comfortable sleep
environment.
(c) Sleep restriction is a strategy used in regulating the timing of sleep by
staying awake even when sleepy in order to fall asleep within a desir-
able period of time.
(d) Relaxation therapy incorporates strategies for unwinding and distrac-
tion to achieve a cognitive state suitable for sleep.
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Cognitive behavior therapy is an effective non-pharmacological strat-

egy. It involves correcting the cognitive distortions and learning skills to
improve their sleep function. Non-pharmacological treatments are effec-
tive interventions and are recommended as a first-line and long-term
strategy of managing primary insomnia.
Pharmacological interventions may be used in treating insomnia.
Classes of medications used to treat insomnia include
(a) Benzodiazepines (diazepam, lorazepam, temazepam, etc.)

(b) Non-benzodiazepine sedatives (eszoplicone, zaleplon, zolpidem, and
zoplicone)
(c) Antidepressants, such as amitriptyline, doxepin, mirtazapine, and
trazodone, can also be used but are not approved for this purpose
(d) Other agents used are circadian rhythm modulators, such as melatonin
or ramelteon
The benzodiazepines and, to some extent, non-benzodiazepine seda-

tives have an addictive potential, and patients may develop tolerance and
dependence on these agents. These effects limit the benefits of using them
long-term. In addition, benzodiazepines may alter sleep architecture by
decreasing NREM-3 and REM sleep and abnormally increasing NREM-2
sleep. The result is poorer quality and often non-restorative sleep.
5.4. Primary or recurrent hypersomnia

Primary hypersomnia (Table 2) usually occurs before the age of 25 years,
and polysomnography may show normal or prolonged sleep duration,
shortened sleep latency, normal REM sleep latency, and less than two
sleep-onset REM periods. It is recurrent if there are periods of excessive
sleepiness of three days or more occurring several times a year for at least
two years. Primary hypersomnia can be a very debilitating disease with
impairments in occupational and social function. Patients often have dif-
ficulty maintaining their academic performance or employment. The eti-
ology is largely unknown, and the goal of treatment is to improve quality
of life. Treatment approaches include both behavioral intervention (good
sleep hygiene, scheduled naps, etc.) and mostly stimulant medications
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Table 2. DSM IV-TR classification of primary hypersomnia.
(A) The predominant complaint is excessive sleepiness for at least one month (or less if
recurrent) as evidenced by either prolonged sleep episodes or daytime sleep
episodes that occur almost daily.
(B) The excessive sleepiness causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
(C) The excessive sleepiness is not better accounted for by insomnia and does not occur
exclusively during the course of another sleep disorder (e.g. narcolepsy, breathing-
related sleep disorder, circadian rhythm sleep disorder, or a parasomnia) and cannot
be accounted for by an inadequate amount of sleep.
(D) The disturbance does not occur exclusively during the course of another mental
disorder.
(E) The disturbance is not due to the direct physiological effects of a substance
such as modafinil, amphetamine, methamphetamine, dextroamphetamine,

and methylphenidate.
Kleine–Levin syndrome is a well-known form of recurrent hypersom-
nia. Patients are more likely to be male. They may have voracious eating
and exhibit hypersexuality and disinhibited behaviors, such as irritability
and aggression. They may appear disoriented or confused and may have
hallucinations.
5.5. Narcolepsy
Patients with narcolepsy (Table 3) report excessive sleepiness with recur-
rent daytime napping. They also report sudden muscle weakness or bilat-
eral loss of postural muscle tone occurring in the context of intense
emotion. Other clinical features include sleep paralysis, hypnagogic hal-
lucinations, and polysomnographic evidence of short overall and REM
sleep latency and two or more sleep-onset REM periods. Patients may be
DQB1or DR2 positive on HLA typing.
As with most sleep disorders, treatments include both non-pharmaco-
logical and pharmacological strategies. Non-pharmacological interven-
tions involve good sleep hygiene and modulating the environment to
optimize conditions suitable for sleep, with limitation of sleep-inhibiting
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362 O. A. Salami
Table 3. DSM IV-TR classification of narcolepsy.
(A) Irresistible attacks of refreshing sleep that occurs daily over at least three months.
(B) The presence of one or both of the following:
(1) Cataplexy (i.e. brief episodes of sudden bilateral loss of muscle tone, most often
in association with intense emotion).
(2) Recurrent intrusions of elements of REM sleep into the transition between sleep
and wakefulness, as manifested by either hypnopompic or hypnagogic
hallucinations or sleep paralysis at the beginning or end of sleep episodes.
(C) The disturbance is not due to the direct physiological effects of a substance
(e.g. a drug of abuse, a medication) or another general medical condition.
stimuli. Scheduled naps during the day help to reduce excessive daytime
somnolence and improve function. Patients should also exercise good
judgment and avoid driving and other activities that require a high level of
concentration and focus when they feel sleepy.
Pharmacological treatments include agents targeting excessive sedation
and cataplexy. CNS stimulants such as methylphenidate and ampheta-
mines and their derivatives have been the mainstay medications for pro-
moting wakefulness. Modafinil is a relatively new agent with a poorly
understood mechanism of action, which is being used with increasing
frequency to promote alertness. Modafinil has a favorable side effect pro-
file in comparison to methylphenidate and other stimulants. Sodium oxy-
bate (Xyrem) is a CNS depressant that is approved by the US Food and
Drug Administration for the treatment of cataplexy.
5.6. Breathing related sleep disorder

Obstructive sleep apnoea (OSA) is the most common breathing-related
sleep disorder (Table 4) and is estimated to affect up to 4% of men and 2%
of women, commonly between the ages of 40 to 60 years. There is a male
predominance in adulthood. Symptoms occur as a result of upper airway
narrowing secondary to an increase in the craniofacial or oropharyngeal
soft tissue. Clinical features include excessive sleepiness or insomnia and
frequent episodes of obstructed breathing occurring during sleep. Patients
may snore loudly and often complain of headaches in the morning and dry
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Table 4. DSM IV-TR classification of breathing related sleep disorder.
(A) Sleep disruption, leading to excessive sleepiness or insomnia that is judged to be due
to a sleep-related breathing condition (e.g. obstructive or central sleep apnoea
syndrome or central alveolar hypoventilation syndrome).
(B) The disturbance is not better accounted for by another mental disorder and is not due
to the direct physiological effects of a substance (e.g. a drug of abuse, a medication)
or another general medical condition (other than a breathing-related disorder).
mouth. PSG shows over five apnoeic episodes per hour of greater than
10 secs in duration in addition to frequent arousals from sleep or arterial
oxygen desaturations associated with the episodes of apnoea. OSA is
associated with several medical and psychiatric disorders including
GERD; mood disorders (particularly depression); cognitive impairment
with impaired attention, concentration and memory; hypertension; and
cardiac arrhythmias. Management involves mitigating the risk factors,
including weight loss and treatment via mechanically maintaining airway
patency with use of continuous positive airway pressure (CPAP). Other
treatment options include use of a dental appliance to anchor the lower
jaw and/or surgical intervention.
Central sleep apnoea syndrome (CSAS) is characterized by a cessa-
tion or reduction of ventilatory effort during sleep and is often associ-
ated with oxygen desaturations. Patients report either insomnia or
excessive sleepiness with frequent episodes of shallow or absent breath-
ing during sleep. Other clinical features include complaints of frequent
motor activity, with gasping, grunting, or choking during sleep often
reported by their partners. Polysomnography demonstrates central
apnoeic pauses more than 10 secs in adults in addition to frequent arous-
als from sleep and oxygen desaturations associated with the apnoea.
CSAS is often associated with systemic and pulmonary hypertension,
cardiac arrhythmias, cardiac failure, cognitive impairment, and depres-
sive symptoms.
Central alveolar hypoventilation syndrome is characterized by ventila-
tory impairment, resulting in sleep-related arterial oxygen desaturations
that occur in patients with normal mechanical properties of the lung.
There is diminished physiological response to hypercapnia or hypoxia
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364 O. A. Salami
during wakefulness and sleep despite normal lung functioning. Cardiac

arrhythmias may occur from severe hypoxemia and hypercapnia.
For overweight patients, weight loss and good sleep hygiene measures
are recommended first line strategies for treating mild forms of breathing-
related sleep disorders. These strategies can also be used in combination
with other treatment modalities for more severe forms. More intrusive
strategies include delivering positive airway pressure to maintain a patent
airway and improve airflow via CPAP. This is done via a CPAP machine,
which administers a positive pressure through a sealed nasal mask or face-
mask to maintain the patency of the airway. This involves either fixed
continuous pressure regardless of inhalation or exhalation or automatic
titration of the pressure to that required per breath. Due to the discomfort
of breathing against resistance, non-adherence rates are as high as 20% or
more. Other strategies are more invasive and include the use of oral appli-
ances that work to facilitate airflow either by advancing the tongue, the
jaw, or the soft palate. Oral appliances are most useful in patients with
retrognathia or micrognathia who are not overweight and have mild dis-
ease. Surgical interventions include procedures aimed at increasing the
size of the upper airway.
5.7. Circadian rhythm sleep disorders

Circadian rhythm disorders (Table 5) are characterized by incongruence
between the patient’s actual sleep pattern and the pattern of sleep desired.
In other words, patients find it difficult to sleep when sleep is wanted,
Table 5. DSM IV-TR classification of circadian rhythm sleep disorder.
(A) A persistent or recurrent pattern of sleep disruption leading to excessive sleepiness

or insomnia that is due to a mismatch between the sleep–wake schedule required by
a person’s environment and his or her circadian sleep–wake pattern.
(B) The sleep disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
(C) The disturbance does not occur exclusively during the course of another sleep
disorder or other mental disorder.
(D) The disturbance is not due to the direct physiological effects of a substance
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needed, or expected. The cycle of normal sleep may be disrupted, result-

ing in sleeping and being awake at inappropriate or undesired times. In
contrast to inadequate sleep hygiene, the timing of sleep is the predomi-
nant cause of the sleep disturbance in circadian rhythm disorders.
5.7.1. Delayed sleep-phase syndrome

Delayed sleep-phase syndrome is a disorder in which sleep is delayed
relative to the desired time reserved for sleep. This results in initial insom-
nia with prolonged sleep latency and persistence of sleep beyond the tar-
geted awakening time. Other features include consistently delayed sleep
onset with minimal to no sleep fragmentation or awakenings following
sleep onset and difficulty advancing sleep onset to an earlier time.
Repeated efforts to regulate the sleep cycle via timing of sleep, relaxation
techniques, and sedative hypnotic medications have limited long-term
success. The prevalence in the general population is unknown. Some
patients report that the onset of their symptoms correlates with staying up
late to study or party or following a period of night shift work.
5.7.2. Time zone change syndrome

Time zone change ( jet lag) syndrome occurs as a result of rapid travel
across multiple time zones. Patients develop difficulty regulating their
sleep cycle and exhibit problems with initiating or maintaining sleep.
Patients may also report excessive sleepiness and diminished alertness and
often complain of mostly gastrointestinal somatic symptoms. The course
of the syndrome is self-limiting, with most symptoms resolving by the
third day after the flight. The dysfunction from jet lag syndrome varies
from an occasional minor inconvenience to severe impairment with
diminished alertness and excessive sleepiness.
5.7.3. Shift work disorder

Shift work disorder is characterized by complaints of insomnia or exces-
sive sleepiness that is temporally related to a work period, commonly the
night shift. Polysomnography and the MSLT show a disruption of the
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366 O. A. Salami
normal sleep–wake pattern. Other associated features include reduced

alertness with subsequent impairment in social, interpersonal, and occu-
pational function. Mood symptoms may also occur with increased irrita-
bility or depression.
5.7.4. Treatment
Treatment options are aimed at resetting the circadian rhythm and
include bright light therapy at over 5,000 Lux for 30–60 mins, chrono-
therapy, and stimulus control. Bright light therapy should be adminis-
tered on the basis of the disruption to the circadian rhythm. If the sleep
phase is advanced, bright light should be administered later in the day to
delay sleep onset and vice versa for a delay in the sleep phase.
Chronotherapy involves shifting the sleep time gradually to the desired
sleep period.
5.8. Dyssomnia not otherwise specified

The dyssomnia not otherwise specified group of sleep disorders consists
of disorders with impairments in the quantity, quality, or timing of sleep
that do not meet the criteria for the other categories of dyssomnia. These
include environmentally triggered insomnia or hypersomnia due to noise,
sleep deprivation, or interruptions or other factors. Sleep-related move-
ment disorders may also be categorized under dyssomnia not otherwise
specified and include restless legs syndrome and periodic limb movement
disorder.
5.8.1. Restless legs syndrome

Restless legs syndrome (RLS) may be described as a neurologic move-
ment disorder of the extremities associated with a disturbance with sleep.
The prevalence of RLS in the general population is 2%–10% and increases
with age. There is a familial association in 50%–90% of patients.
Diagnosis is based on the presence of an urge to move the legs or arms,
associated with uncomfortable paresthesia or dysesthesia. Symptoms are
worse or occur exclusively when the individual is at rest and worsen in the
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evening or night. Movement or activity relieves symptoms temporarily.

Other features, which are not required for diagnosis, include a positive
response to dopaminergic medications, insomnia, daytime somnolence,
and involuntary, repetitive, periodic, jerking limb movements that can
occur at rest or during sleep, akin to periodic limb movements. RLS can
be classified as primary or secondary. In primary RLS, the cause is
unknown, but there is strong family association. Secondary RLS can result
from iron deficiency and peripheral neuropathy and also from pregnancy,
medications (tricyclic antidepressants, dopamine antagonists, SSRIs,
lithium, etc), and other medical conditions, including vitamin deficiencies
(B12, foliate) and autoimmune diseases. Management involves limiting
precipitating factors in secondary RLS in addition to medication therapy
with dopamine agonists, benzodiazepines, opioids, and anticonvulsants
(gabapentin and pregabalin).
5.8.2. Periodic limb movement disorder

Periodic limb movement disorder (PLMD) is often comorbid with RLS
and is characterized by stereotyped periodic limb movements that cause
sleep fragmentation and nocturnal awakenings. The movements com-
monly affect the legs but may occur in the upper limbs. Patients complain
of sleep that is not refreshing. Mood symptoms of anxiety and depression
may be present with chronic sleep impairment. Polysomnography may
show onset of symptoms in NREM-1 sleep, with increased frequency dur-
ing NREM-2 sleep, and less in NREM-3 sleep. The periodic limb move-
ments are rarely seen during REM sleep. Medications used in treating
PLMD include benzodiazepines, dopamine agonists, anticonvulsants, and
skeletal muscle relaxants.
5.9. Parasomnias
The parasomnias are disorders of arousal or partial arousal from central
nervous system activation with motor and verbal manifestation. Parasomnias
occur during specific stages of sleep or during sleep-stage and sleep–wake
transitions. These disorders can be categorized into four groups using the
DSM-IV-TR classification system.
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368 O. A. Salami
5.9.1. Nightmare disorder

The onset of nightmare disorder (Table 6) is typically in childhood, usu-
ally between the ages of three and six years. The disorder may continue
into adulthood, with up to 50% of previously diagnosed adults reporting
at least an intermittent nightmare and 1% reporting recurrent nightmares.
Synonyms for nightmare disorder include dream anxiety attacks, terrify-
ing dreams, and REM nightmare. Nightmares usually occur during REM
sleep. There may be emotional and autonomic arousal with anger, fear,
tachycardia, tachypnea, and diaphoresis, but there are rarely associated
motor or verbal manifestations. Polysomnography shows a sudden awak-
ening from REM sleep.
5.9.2. Sleep terror disorder

Sleep terrors (Table 7) are characterized by a sudden awakening during
NREM-3 and -4 sleep with verbal manifestations of a loud scream that is
accompanied by autonomic and behavioral manifestations of intense fear,
tachycardia, tachypnea, and diaphoresis. Onset is usually in children, with
prevalence rates of about 3% of children and less than 1% in adults. There
is a male predominance.
Table 6. DSM IV-TR classification of nightmare disorder.
(A) Repeated awakenings from the major sleep period or naps with detailed recall of
extended and extremely frightening dreams, usually involving threats to survival,
security, or self-esteem. The awakenings generally occur during the second half of
the sleep period.
(B) On awakening from the frightening dreams, the person rapidly becomes oriented
and alert (in contrast to the confusion and disorientation seen in sleep terror disorder
and some forms of epilepsy).
(C) The dream experience, or the sleep disturbance resulting from the awakening, causes
clinically significant distress or impairment in social, occupational, or other
important areas of functioning.
(D) The nightmares do not occur exclusively during the course of another mental
disorder (e.g. a delirium, posttraumatic stress disorder) and are not due to the direct
physiological effects of a substance (e.g. a drug of abuse, a medication) or a general
medical condition.
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Table 7. DSM-IV-TR classification of sleep terror disorder.
(A) Recurrent episodes of abrupt awakening from sleep, usually occurring

during the first third of the major sleep episode and beginning with
a panicky scream.
(B) Intense fear and signs of autonomic arousal, such as tachycardia,
rapid breathing, and sweating, during each episode.
(C) Relative unresponsiveness to efforts of others to comfort the person
during the episode.
(D) No detailed dream is recalled and there is amnesia for the episode.
(E) The episodes cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
(F) The disturbance is not due to the direct physiological effects of a
substance (e.g. a drug of abuse, a medication) or a general medical
condition.
5.9.3. Sleepwalking disorder

Sleepwalking disorder (Table 8) features a complex series of behaviors
with onset during NREM-3 and -4 sleep in the early third of the night and
results in motor activity during sleep. Sleepwalking may vary from simple
activities such as sitting up in bed to walking. The incidence rate is
between 1% and 15% of the general population, and sleepwalking is more
common in children than in adults.
5.9.4. Parasomnia not otherwise specified

The parasomnia not otherwise specified category is for disturbances that
are characterized by abnormal emotional, motor, verbal, or physiological
events during sleep or sleep–wake transitions that do not meet specific
criteria for the other parasomnias. These include the following:
(a) Confusional arousals: These present as disorientation during and fol-

lowing arousals from sleep. This often occurs in the first part of the
night following awakening from deep sleep.
(b) Rhythmic movement disorder: This is characterized by stereotyped
and repetitive movements of large skeletal muscles just before sleep
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370 O. A. Salami
Table 8. DSM IV-TR classification of sleepwalking disorder.
(A) Repeated episodes of rising from bed during sleep and walking about,
usually occurring during the first third of the major sleep episode.
(B) While sleepwalking, the person has a blank, staring face, is relatively
unresponsive to the efforts of others to communicate with him or her,
and can be awakened only with great difficulty.
(C) On awakening (either from the sleepwalking episode or the next
morning), the person has amnesia for the episode.
(D) Within several minutes after awakening from the sleepwalking episode,
there is no impairment of mental activity or behavior (although there
may initially be a short period of confusion or disorientation).
(E) The sleepwalking causes clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
(F) The disturbance is not due to the direct physiological effects of a
substance (e.g. a drug of abuse, a medication) or a general medical
condition.
onset and are sustained into light sleep, in contrast to sleep starts,
which are sudden, brief and non-stereotyped leg, arm, or neck con-
tractions that occur at the onset of sleep.
(c) Sleeptalking: This phenomenon involves the production of sounds or
comprehensible speech during sleep without simultaneous subjective
detailed awareness of the event.
(d) Nocturnal leg cramps: These are painful sensations of muscular tight-
ness or tension, usually in the calf but occasionally in the foot that
occur during the sleep episode.
(e) Sleep paralysis: Sleep paralysis consists of a period of inability to
perform voluntary movements at sleep onset (hypnagogic form) or
upon awakening, either during the night or in the morning (hypnop-
ompic form).
(f) REM sleep behavior disorder: This is characterized by the intermit-
tent loss of REM sleep, electromyographic (EMG) atonia, and the
appearance of elaborate motor activity associated with dream
mentation.
REM sleep behavior disorder can be treated with low dose clonazepam.
The treatment of the parasomnias involves supportive management.
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6. SPECIFIC PSYCHIATRIC SYNDROMES

Disturbances with sleep, including insomnia and hypersomnia, can occur
as a consequence of underlying medical, neurological, or psychiatric dis-
orders.5 The management of sleep symptoms in this context should be
based on identifying and treating the underlying disorder.
6.1. Sleep and schizophrenia

Sleep disturbance presenting often as insomnia is common in schizophrenia
and can be a feature of the prodromal phase of the syndrome or can occur
with relapse of psychotic symptoms. A common sleep architecture finding
on polysomnography of patients with schizophrenia is a shortened REM
sleep latency with compensatory reduction in NREM-3 sleep, particularly in
the early part of the night. There appears to be an association between the
changes in sleep architecture described above and the negative and cognitive
symptoms found in schizophrenia. Medications used in treating schizophre-
nia also produce an effect on sleep. The effects of antipsychotic medications
on both the sleep architecture and function are mediated via the changes in
neurotransmitter systems. The neurotransmitters commonly involved
include dopamine, histamine, and acetylcholine. Both first- and second-
generation antipsychotics have varying effects on these newer transmitter
systems. In addition, the second-generation antipsychotic medications also
modulate serotonin function. These effects are mostly inhibitory. These
medications also influence sleep function in the primary sleep disorders.
Examples include obstructive sleep apnoea, where weight gain mediated by
the anti-histaminic properties may worsen cognitive and mood disturbance.
In addition, the anti-dopaminergic properties of antipsychotic medications
may worsen clinical symptoms of restless legs syndrome and periodic limb
movement syndrome. The effects of these medications on sleep architecture
include suppression of REM sleep and increase in NREM-3 sleep via their
effects on 5-HT 1A agonism and 5-HT 2 antagonism.
6.2. Sleep and anxiety disorders

Insomnia is the most common sleep symptom seen in anxiety disor-
ders, and this often manifests as difficulty falling asleep and frequent
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372 O. A. Salami
awakenings. Prevalence rates can be as high as 61% in certain anxiety

disorders, particularly panic disorder. Anxiety disorders are also fre-
quently associated with several underlying primary sleep disorders.
Polysomnography findings in generalized anxiety disorder include
increased sleep latency and reduced sleep efficiency. The sleep archi-
tecture changes have been inconsistent in generalized anxiety disorder.
Panic disorder has been shown to be closely associated with restless
legs syndrome. Sleep disturbance frequently occurs in panic disorders.
In certain instances, up to 77% of patients report a sleep symptom.
This is commonly sleep fragmentation. Sleep fragmentation and
frequent nocturnal arousals are also common features of sleep distur-
bance in posttraumatic stress disorder (PTSD) in addition to frequent
nightmares. The changes in sleep architecture in posttraumatic
stress disorder include an increase in NREM-1 sleep and decreasing
NREM-3 sleep, increased REM sleep latency and increased REM
sleep density. One theory underlying this mechanism is hyperactivity
of the adrenergic system in these patients, with likely involvement of
the amygdala, medial prefrontal cortex, and other limbic system
structures.
6.3. Sleep and depressive disorders

Insomnia is a core symptom of depressive disorders. Patients with depres-
sion commonly report frequent awakenings during the night with sleep
fragmentation as well as early morning awakening with difficulty falling
back to sleep. Hypersomnia may also occur in depression, as an atypical
symptom, and is less frequent than insomnia. Changes in sleep architec-
ture seen in depression include a shortened REM latency. It is important
to note that sleep symptoms may arise from co-occurring medical disor-
ders and psychiatric disorders. An example is major depression and
obstructive sleep apnoea. It is difficult to discern in these cases which of
the underlying disorders is the primary cause of the sleep disturbance.
Treatments will involve the same approaches discussed earlier, with both
pharmacological and non-pharmacological treatments. Antidepressants
are the recommended medication treatments and major classes include
selective serotonin re-uptake inhibitors (SSRI), serotonin–norepinephrine
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re-uptake inhibitors (SNRI), dopamine-norepinephrine re-uptake inhibi-

tors (DNRI), tricyclic antidepressants (TCA), monoamine oxidase inhibi-
tors (MAO inhibitors), and others. Mirtazapine and trazodone have
sedating properties and may be useful in depressed patients with insom-
nia. Bupropion is a DNRI with activating properties and aids in promot-
ing alertness in patients with atypical depressive symptoms with
hypersomnia.
6.4. Sleep and dementia

Alzheimer’s dementia is the most common form of dementia, and sleep
disturbance affects over 40% of patients with dementia. Sleep fragmen-
tation with frequent nocturnal awakenings, daytime somnolence, and
napping are common symptoms of sleep disturbance in this population.9
Polysomnography may show increased sleep latency, increased REM
latency, less sleep efficiency, increased NREM-1, and decreased REM
sleep. Alzheimer’s dementia may be comorbid with other primary sleep
disorders, including movement-related sleep disorders and breathing-
related sleep disorders. The principles of treatment are similar to those
of other sleep disorders and involve both pharmacological and non-
pharmacological treatments. However, managing sleep disturbance in
patients with Alzheimer’s dementia can be particularly challenging due
to the memory decline, executive dysfunction, and other cognitive
impairments in the patient population. The difficulty with managing
sleep disturbance is a common factor associated with institutionalization
of patients with Alzheimer’s dementia. Behavioral and multifaceted
interventions have been shown to be effective in some patients. These
include decreasing the time spent in bed during the day, increased daily
sunlight exposure, increased physical activity, structured bedtime rou-
tine, decreased night-time noise and light, and exposure to bright light
for a period of time.
6.5. Substance-induced sleep disorders

Sleep disturbance can occur as a result of intoxication or withdrawal
from various substances. Insomnia can result from withdrawal from CNS
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374 O. A. Salami
suppressants like alcohol and sedative-hypnotic medications like benzodi-

azepines, barbiturates, and chloral hydrate. Use or intoxication with CNS
stimulants can also cause insomnia. Hypersomnia or somnolence may
result from withdrawal from CNS stimulants and use of sedative-hypnotic
drugs. These effects on sleep may be desired initially; however, with con-
tinued use, tolerance often develops, and increasing quantities are ingested
to achieve the desired effects on sleep.
The effects of alcohol on sleep function vary with duration of alcohol
use. Acute alcohol consumption is associated with decreased sleep latency
and reduction in REM sleep, particularly in the early part of the night. The
shortened sleep latency may be why individuals who imbibe alcohol
report falling asleep easily following alcohol consumption. There, how-
ever, is a compensatory rebound in REM sleep function in the latter part
of the night, which is often associated with dreams and nightmares, often
resulting in sleep fragmentation and diminished sleep efficiency. With
chronic alcohol consumption, tolerance develops, and the effects on sleep
function changes. These changes include increased sleep latency, decreased
sleep efficiency, decreased NREM-3 sleep, and decreased REM sleep. In
addition, the total sleep time is decreased. It is important to note that the
changes in sleep function may persist for several months after cessation of
alcohol. Alcohol consumption may also worsen sleep symptoms associ-
ated with other primary sleep disorders, including obstructive sleep
apnoea, periodic limb movement syndrome and restless leg syndrome.
Other disorders that may be exacerbated include the parasomnias and
REM sleep behavior disorder.
Opioids affect sleep function in varying degrees by duration of use.
Acute changes to sleep from opioids include decreases in REM sleep,
NREM-3, and total sleep time. Chronic opioid use is associated with an
attenuation of the changes seen with acute use and directly linked with
central sleep apnoea, a primary sleep disorder via chronic suppression of
ventilatory drive.
Marijuana has varying effects on sleep function due to the numerous
psychoactive agents found in commercial marijuana. The active ingredi-
ent in marijuana, delta-9 tetrahydrocannabinol, causes decreases in
sleep latency. Withdrawal from marijuana has been associated with
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sleep disturbance, particularly vivid dreams and nightmares, and also

increased sleep latency. Suffice to say that marijuana withdrawal may
worsen sleep symptoms seen in posttraumatic stress disorder and the
parasomnias.
7. KEY POINTS
• Insomnia and hypersomnia are the main characteristics of sleep
disturbance.
• Sleep disturbance occurs as a symptom of primary sleep disorders and
also as a common feature of medical, psychiatric, and neurologic
disorders.
• Sleep disorders can be classified under two major classification
systems: DSM-IV and ICSD.
• Sleep disturbance varies in severity from mild to severe and can pro-
duce a profound impairment with social and occupational function.
• Treatment of sleep disturbance involves both non-pharmacological
and pharmacological interventions.
8. SELF-ASSESSMENT
8.1. Mr J, a 27-year-old construction worker, is diagnosed
with major depression. His most distressing symptom
is insomnia. A polysomnogram in this patient would
most likely show which of the following?
(A) Decreased REM sleep.
(B) Increased REM latency.
(C) Increased REM sleep density.
(D) Increased NREM-3 sleep.
The changes in sleep architecture associated with depression include

increased REM sleep, decreased REM latency, increased REM sleep
density, and decreased non-REM 3 sleep.
Answer: C
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376 O. A. Salami
8.2. Michael, a 34-year-old schoolteacher, has had difficulty

falling asleep and was prescribed diazepam by his family
doctor. Benzodiazepine medications are associated with
which of the following?
(A) Decreased REM sleep.
(B) Severe insomnia upon stopping the medication.
(C) Decreased NREM-3 sleep.
(D) All of the above.
Benzodiazepines may cause tolerance and dependence, resulting in

rebound insomnia upon discontinuing. Benzodiazepines can also alter
sleep architecture by decreasing NREM-3 and REM sleep and abnormally
increasing NREM-2 sleep.
Answer: D
9. CASE STUDIES
9.1. Primary sleep disorder
Julia, a 20-year-old college student, presents with complaints of difficulty
falling asleep and waking up several times over the course of the night for
six months. She feels tired in the morning and often turns off her alarm
clock to get more sleep. In addition, her roommate snores loudly. She
states that she is frequently arriving late for her morning classes and is
having difficulty concentrating, sleeping through most of the morning,
and struggling to stay awake. She reports that her symptoms began shortly
after her final examinations. During her exams, she would stay up late
studying and had irregular sleeping hours. She has since had difficulty
with sleep. Her grades have declined due to impaired attention at school.
She also reports difficulty with short-term memory and feelings of
depressed mood.
Julie was diagnosed with a primary sleep disorder. She was educated
on good sleep hygiene measures, and a non-pharmacological regimen of
was designed aimed at improving sleep function.
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9.2. Circadian rhythm disorder

John, a 42-year-old married male, was referred by his company’s occu-
pational health service following a near accident at work after falling
asleep. He had been on the night shift for years, and due to downsizing
at work, he was transferred to the day shift a week earlier. He reports
difficulty staying awake at work since the shift change. In addition, he
reports difficulty concentrating, culminating in impaired functioning
at work, and a decline in his previously stellar work performance. He
reports that he has difficulty falling asleep when he is supposed to,
because his new sleep time correlates to when he would have been at
work just a week earlier.
John was diagnosed with circadian rhythm disorder. Chronotherapy
was devised to aid in resetting his sleep cycle. After four days, he was able
to resume sleep at an appropriate time, and his function at work returned
to normal.
9.3. Parasomnia
Marie, a 32-year-old social worker who is accompanied by her husband,
presents with complaints of early morning fatigue. She states that her
husband has asked her to sleep in a different room due to several instances
of striking him while she is asleep. She has no recollection of the events
but states that she does not feel rested upon awakening. She adds that she
has been dreaming more frequently than usual. Her husband reports that
she speaks in her sleep and also appears as if she is in trance. He describes
her as often acting out in her sleep, and she has struck out at him several
times. She reports that she recalls a similar family history in her paternal
grandfather, as reported by her grandmother. Marie had a sleep study
done with video monitoring and was noted getting up several times over
the course of the night. She initially walked around the bed, then stood
on the bed and imitated changing a light bulb. Following the sleep study,
she reported no recollection of the events. She was diagnosed with a
parasomnia and prescribed clonazepam, with complete resolution of
symptoms.
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378 O. A. Salami
REFERENCES
1. American Academy of Sleep Medicine. (2001) International Classification
of Sleep Disorders, revised. American Academy of Sleep Medicine Diag-
nostic and Coding Manual, Chicago, IL.
2. American Psychiatric Association. (2000) Diagnostic and Statistical
Manual of Mental Disorders, 4th ed. Text Revision, American Psychiatric
Association, Washington, DC.
3. Datta S, Maclean RR. (2007) Neurobiological mechanisms for the regulation
of mammalian sleep wake behavior: Reinterpretation of historical evidence
and inclusion of contemporary cellular and molecular evidence. Neuroscience
and biobehavioral reviews 31(5): 775–824.
4. Kaplan HI, Sadock BJ, Grebb JA. (1994) Normal sleep and sleep disorders.
In: Sadock BJ, Sadock VA (eds.), Kaplan and Sadock’s Synopsis of
Psychiatry, 7th ed. pp. 699–716, Lippincott Williams & Wilkins, Baltimore,
MD.
5. Kyung LE, Douglass AB. (2010) Sleep in psychiatric disorders: Where
are we now? Can J Psychiatry, Revue Canadienne de Psychiatri 55(7):
403–412.
6. Loewy DH, Black JE. (2000) Effective management of transient and
chronic insomnia. In: CNS News, pp. 19–22, McMahon Publishing Group,
NY.
7. Richert AC, Baran AS. (2003) A review of common sleep disorders. CNS
Spectr 8(2): 102–109.
8. Roth T, Roehrs T. (2003) Insomnia: Epidemiology, characteristics, and con-
sequences. Clin Cornerstone 5(3): 5–15.
9. Salami O, Lyketsos C, Rao V. (2011) Treatment of sleep disturbance in
Alzheimer’s dementia. Int J Geriatr Psychiatry 26(8): 771–782.
10. Schenck CH, Mahowald MW, Sack RL. (2003) Assessment and management
of insomnia. JAMA 289(19): 2475–2479.
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Chapter 16
Eating Disorders
Athena Robinson and W. Stewart Agras
1. INTRODUCTION
The three major eating disorders are anorexia nervosa, bulimia nervosa,
and binge eating disorder. The diagnostic criteria for the International
Statistical Classification of Diseases and Related Health Problems25 and
Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition3
for each of these major disorders are listed in Table 1. The eating disorders
may occur in sub-clinical forms, classified as eating disorder not other-
wise specified, and, as such, form the largest category. Other potentially
distinct syndromes, for which there is not enough evidence to form a
diagnostic classification, are incorporated within the eating disorder not
otherwise specified category and include night eating syndrome and vom-
iting disorder. Less common disorders, at least in developed countries,
include pica. In addition, there are specific childhood eating disorders,
including selective eating, comprising neophobia and picky eating, and
food avoidance emotional disorder. Often neglected by clinicians as
“trivial,” the eating disorders are frequently comorbid with other psychi-
atric illnesses, including mood, anxiety, impulse-control, and substance-
use disorders. In addition, these disorders may significantly affect health
and well-being. For example, anorexia nervosa is characterized by marked
weight loss and associated with disorders secondary to malnutrition, such
as osteoporosis, compromised cardiovascular functioning, and numerous
379
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380 A. Robinson and W. S. Agras
Table 1. International Statistical Classification of Diseases and Related Health

Problems-10 and Diagnostic and Statistical Manual of Mental Disorders-IV criteria for
anorexia nervosa, bulimia nervosa, and binge eating disorder.
International Statistical
Classification of Diseases
and Related Health Diagnostic and Statistical Manual of Mental
Disorder Problems 10 Criteria Disorders IV criteria
Anorexia Deliberate weight loss, Refusal to maintain body weight at or above
Nervosa induced and sustained a minimally normal weight for age and
by the patient. height (e.g. weight loss leading to
Dread of fatness and maintenance of body weight less than
flabbiness of body 85% of that expected; or failure to make
contour persists as an expected weight gain during period of
intrusive overvalued growth, leading to body weight less than
idea. 85% of that expected).
Usually under nutrition Intense fear of gaining weight or becoming
of varying severity with fat, even though underweight.
secondary endocrine Disturbance in the way in which one’s body
and metabolic changes weight or shape is experienced, undue
and disturbances of influence of body weight or shape on self-
bodily function. evaluation, or denial of the seriousness of
Symptoms include the low body weight.
restricted dietary choice, In post menarcheal females, amenorrhea
excessive exercise, (i.e. absence of at least three consecutive
induced vomiting and menstrual cycles).
purgation, and use of Specify type:
appetite suppressants Restricting type: no binge-eating or purging
and diuretics. behavior during episode.
Binge-eating/Purging type: during the
current episode of Anorexia, person
regularly engages in binge-eating/purging
behavior.
Bulimia Repeated bouts of Recurrent episodes of binge eating which is
Nervosa overeating followed by characterized by the following:
vomiting or use of Eating, in a discrete period of time,
purgatives. (e.g. within any two hour period), an amount
Excessive preoccupation of food that is definitely larger than most
with the control of body people would eat during a similar period
weight. of time and under similar circumstances.
(Continued)
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Eating Disorders 381
International Statistical
Classification of Diseases
and Related Health Diagnostic and Statistical Manual of Mental
Disorder Problems 10 Criteria Disorders IV criteria
Over concern with body A sense of lack of control over eating during
shape and weight. the episode (e.g. a feeling that one cannot
Repeated vomiting is stop eating or control what or how much
likely to give rise to one is eating).
disturbances of body Recurrent inappropriate compensatory
electrolytes and physical behavior in order to prevent weight gain,
complications. such as self-induced vomiting; misuse of
May be preceded by an laxatives, diuretics, enemas, or other
episode of anorexia medications; fasting; or excessive
nervosa. exercise.
The binge eating and inappropriate
compensatory behaviors both occur, on
average, at least twice a week for three
months.
Binge Recurrent episodes of binge eating.
Eating Associated features of binge eating:
Disorder Eating much more rapidly than normal.
Eating until uncomfortably full.
Eating in the absence of hunger.
Eating alone because of embarrassment over
the amount eaten.
Feelings of disgust, depression, or guilt after
overeating.
Binge eating occurs at least two days per
week, on average, for a six-month period.
Note: See the International Statistical Classification of Diseases and Related Health Problems 1025 and
Diagnostic and Statistical Manual of Mental Disorders IV3 for additional details.
electrolyte changes. Moreover, anorexia nervosa has the highest death

rates of any psychiatric disorder and is as costly to the health services as
schizophrenia. Another example is that obesity, often associated with
binge eating disorder, includes elevated risk for many serious medical
conditions including diabetes, hypertension, cardiovascular disease, and
stroke. Females are far more likely than males to develop an eating
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disorder, although males may be more prone to develop particular eating

disorders. For example, of those individuals diagnosed with anorexia
nervosa or bulimia nervosa, only an estimated 5%–15% are male, while
35% of those with binge eating disorder are male.
2. EPIDEMIOLOGY
Eating disorders are prevalent across the world, both in developed and
developing countries. Data from various studies suggest a 1% lifetime
prevalence of anorexia nervosa in adults, 1.5% for bulimia nervosa, and
2%–3% for binge eating disorder. The total prevalence of eating disorders,
including eating disorder not otherwise specified, would approximate
6%–8%.
Historically, epidemiological studies of eating disorders have focused
on white women and girls, and relatively little research has been con-
ducted with participants from racial and ethnic minority groups.
Consequently, research before the mid-1990s typically reported that
eating disorders affected primarily white women of high socioeconomic
classes and were less common among specific minority groups. However,
more recent empirical studies suggest that minority populations are sub-
stantially affected by disordered eating behaviors. Table 2 outlines the
prevalence rates for anorexia nervosa, bulimia nervosa, and binge eating
disorder and the presence of any binge eating within the United States and
various countries abroad.
Preliminary conclusions regarding the prevalence of eating disorders
among ethnic minorities within the United States are that anorexia ner-
vosa is rare among blacks, data are mixed on whether rates of bulimia
nervosa among ethnic minority and white females differ, and rates of
binge eating among ethnic minorities are higher than other forms of dis-
ordered eating. Available global data suggest a lifetime prevalence pattern
comparable to those found within the United States; anorexia nervosa is
the least frequently occurring disorder, followed by bulimia nervosa, and
a significant per cent of individuals endorse any binge eating and/or meet
sub threshold diagnostic criteria.
Erroneous assumptions about eating disorder prevalence, cultural influ-
ence, course of illness, and access to treatment among minority persons can
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B1405_Ch-16.indd 383
Eating Disorders
Table 2. Prevalence rates of anorexia nervosa, bulimia nervosa, binge eating disorder, and any binge eating.
Lifetime prevalence
n (%)
Binge Sub-
Anorexia Bulimia eating Any Binge threshold
Reference Sample Nervosa nervosa disorder eating syndrome
Streigel-Moore et al.19 (United States 985 white women 15 (1.5) 23 (2.3) 27 (2.7) — —
B1405
sample)
1061 black women 0 4 (.4) 15 (1.4) — —

20
Taylor et al. (United States sample) 5191 African American & 7 (.17) 79 (1.49) 88 (1.66) 245 (5.08) —
Caribbean Black adults
Adolescents* 2 (.07) 5 (.40) 4 (.28) 18 (1.56) —
Alegria et al.1 (United States sample) 2554 Latino adults 2 (.08) 41 (1.61) 49 (1.92) 143 (5.61) —
Nicado et al.14 (United States sample) 2095 Asian American adults 2 (.08) 23 (1.09) 43 (2.04) 91 (4.35) —
Nobakht and Dezhkam15 (Iranian sample) 3100 Iranian adolescent girls 27 (.9) 99 (3.2) — — 204 (6.6)
Hay, 19988 (Austrailian sample) 3001 South Austrialian — 8 (.3) 30 (1.0) 96 (3.2)
individuals (>15 years)
Morande et al.13 (Spainsh sample) 1314 Spanish adolescents in 5 (.69) 11 (.8) — — 23 (1.79)
Madrid, Spain
Chen et al.5 (Chinese sample) 509 Chinese college freshman 0 5 (1.1) — — —
Note: List of lifetime prevalence rates of anorexia nervosa, bulimia nervosa, binge eating disorder, any binge eating, and subthreshold disorder as reported
by recent studies.
— data not provided by study.
* only 12 month prevalence rates for adolescents provided by original paper.
Rates for Alegria et al.,1 Nicado et al.,14 Nobakht & Dezhkam,15 Chen et al.,5 were calculated by A. Robinson using percentage data provided in original
383
1/31/2013 2:39:48 PM
manuscripts. See original manuscripts for further detail.

create referral biases and differences in service availability and access and,
consequently, make it more difficult to estimate the true prevalence of eating
disorders among men, women, children, and adolescents across the world.
Data are needed to further our understanding about disordered eating behav-
iors among all ethnic and racial groups in order to prevent bias in assess-
ment, prevention, and intervention endeavors. Primary care physicians are
often the first viable line of eating disorder assessment and referral. It is
therefore imperative that primary care physicians are aware of disordered
eating presentations in order to provide needed evaluation and intervention.
3. ETIOLOGY OF EATING DISORDERS

As with many complex disorders, the etiology of the eating disorders is
unknown. However, their complex underpinnings are likely determined by
genetic, interpersonal, intrapersonal, and environmental factors that inter-
act in a variety of ways. Genetic factors account for some 50% of the vari-
ance for each of the three major eating disorders, although the nature of
the genetic contribution is unknown at present. A known risk factor for
eating disorders is gender, with females at higher risk than males, although
whether the increased risk is biological or environmental is unknown.
In addition, social pressure to attain a thin body profile spurs body dis-
satisfaction and excessive dieting, which, in turn, may fuel binge eating
and purging. Overweight may increase the risk for this pathway. Modeling
of a thin body profile, for example, via the media, and family and peer
pressures to be thin are also risk factors. Negative affect also appears to be
a risk factor for eating disorders and may work by increasing body dis-
satisfaction. Disturbances of the various biologic mechanisms underlying
eating may also occur, but at present, no clear picture has emerged.
4. ANOREXIA NERVOSA
Anorexia nervosa is a serious psychiatric illness characterized by purpose-
ful and sustained weight loss, refusal to gain weight, intense fear of weight
gain, overvaluation of body weight and shape, and intrusive and pathologi-
cal thoughts and behaviors surrounding food and weight (see Table 1 for
diagnostic criteria). The disorder may include episodes of binge eating,
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purging, and excessive exercise. The point prevalence of anorexia nervosa

is estimated to be 0.1% of adults. The disorder typically onsets during
adolescence and most commonly occurs in adolescent girls and young
women (prevalence in girls aged 15–19 is 0.48% and is 9–10 times more
common in girls than boys). The mortality rate among individuals with
anorexia nervosa is estimated at 0.56% annually, which is approximately
12 times greater than the annual death rate due to all causes of death
among girls and women aged 15–24 years in the general population.
4.1. Medical complications

Because of the profound nutritional disturbances associated with anorexia
nervosa, there are a number of medical complications specific to the
disorder seen both in adolescents and adults. Most complications are
reversible with weight gain, although if prolonged, some may be irrevers-
ible. Physical examination reveals marked emaciation; dry skin that may
be covered with fine body hair (lanugo), and cold, cyanotic extremities
often accompanied by peripheral edema, bradycardia, and hypotension.
Among the most common complications are osteopenia and osteoporosis,
affecting about half of all anorexics, for which the best treatment appears
to be weight regain. Electrolyte abnormalities may include low levels of
potassium, phosphorous, and magnesium, all of which require attention
usually in an inpatient setting. Low potassium levels combined with the
effects of poor nutrition on the heart may lead to ventricular fibrillation
and death. Malnutrition leads to a number of hormonal abnormalities.
Plasma gonadotropin levels are decreased, and the 24-hour luteinizing
hormone pattern resembles that found in prepubertal girls. Follicle-
stimulating hormone, estrogen levels, total serum thyroxine, and triiodo-
thyronine levels are usually low, and growth hormone levels are elevated.
Resting plasma cortisol levels are also elevated and the metabolic
clearance of cortisol is decreased.
4.2. Problems with anorexia nervosa treatment research

There has been remarkably little change in our ability to treat anorexia
nervosa over the past 25 years despite the research that has been
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accomplished. Several problems plague research investigating efficacious

anorexia nervosa treatment. Such problems need to be considered before
substantial headway in research is made. First, recruitment of individuals
with anorexia nervosa into clinical trials is difficult. Individuals with ano-
rexia nervosa are often resistant to treatment and thus are reluctant to
volunteer for treatment. This, combined with the relative rarity of anorexia
nervosa, makes recruitment of a sufficient number of individuals to clini-
cal trials difficult. Studies suggest that it is easier to recruit adolescent
anorexics than adults, although the low sample sizes of many adolescent
studies suggests otherwise. Nonetheless, the involvement of parents who
are anxious about their child’s illness is likely to help in recruiting and
retaining adolescent participants. Second, insufficient sample size due to
low prevalence rates and/or difficulty in recruitment yields inadequate
statistical power for reliable and valid statistical analyses, although some
studies have reported results despite low and unreliable power. Third,
participant dropout rates of up to 40% reflect the reluctance of such indi-
viduals to engage in treatment that may lead to weight gain and compound
the aforementioned issue of insufficient sample size and statistical analy-
sis complications. A fourth concern is that, given the high rates of medical
complications and death from anorexia nervosa, ethical considerations
limit the use of a no-treatment comparison or placebo control group in
randomized clinical trials. Thus, the specificity of any particular treatment
is difficult to assess. Because of these problems, relatively few adequate
trials have been reported in the literature.
4.3. Treatments for anorexia nervosa

A summary of evidence based treatment(s) for anorexia nervosa, bulimia
nervosa, and binge eating disorder is presented in Table 3.
4.3.1. Cognitive behavioral therapy for anorexia nervosa

The central tenet of CBT for anorexia nervosa (CBT-AN) is that the
symptoms are maintained by a reciprocal interaction between cognitive
disturbances, such as prominent concerns regarding food, eating, shape,
and weight, and behavioral disturbances, which directly influence eating
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Table 3. Review of evidence-based practices for eating disorders.
Evidence Type Anorexia nervosa Bulimia nervosa Binge eating disorder

High evidence None CBT, IPT, CBT, IPT, GSH
antidepressants. antidepressants,
anti-epileptics.
Moderate BFT for adolescent BFT for adolescent DBT-BED
evidence AN BN
Further CBT Treatment Algorithms Treatment Algorithms
research needed Treatment Algorithms
Note: High evidence=at least one adequately sized outcome study that has been replicated; Moderate
evidence=at least one adequately sized outcome study with no replication to date; Further research
needed=no adequately sized outcome study to date.
AN=anorexia nervosa; BN=bulimia nervosa; BED=binge eating disorder; BFT=behavioral family
therapy; CBT=cognitive behavioral therapy; IPT=interpersonal psychotherapy; DBT=dialectical
behavior therapy; GSH=guided self-help.
and weight control behaviors. Treatment involves addressing behavioral

disturbances via working towards normalized eating patterns (e.g. eating
three meals and two snacks daily, reincorporating previously feared foods)
and using cognitive challenging strategies to address and reframe thought
disturbances.
Of five randomized trails published to date investigating CBT-AN for
anorexia nervosa, none provide evidence that CBT-AN was superior to
comparison treatments including behavior therapy, treatment-as-usual,
nutritional counseling, behavioral family therapy, and interpersonal psy-
chotherapy.16 It is noteworthy, however, that these five studies were lim-
ited by high attrition rates, small sample sizes, short treatment duration,
and other methodological concerns. Two studies investigating CBT-AN’s
effectiveness among weight restored anorexia nervosa patients demon-
strated preliminary evidence in preventing relapse and improving recovery
rates following weight restoration.
4.3.2. Behavioral family therapy for adolescent anorexia nervosa

Behavioral family therapy (BFT) is a manualized treatment that is based
on the approach developed at the Maudsley Hospital in the 1980s. The
approach empowers the patient’s parents to undertake the responsibility of
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restoring their child’s weight and provides a collaborative environment for

teaching and generating behavioral and psychological strategies to facili-
tate weight restoration. Treatment leverages parental understanding and
concern to promote changes in eating and weight control behaviors. BFT
is currently the best-established treatment for adolescents with anorexia
nervosa. Small-scale studies and two larger studies suggest that a particu-
lar type of family therapy is effective both at the end of treatment and at
follow-up. Recent data indicate that BFT is superior to an adolescent-
focused individual therapy at six- and 12-month follow-up.10 However,
only small-scale comparisons with another form of family therapy have
been published to date. Hence, it is important to investigate the specificity
of this form of family therapy by comparing it with another type of family
therapy.
4.3.3. Inpatient and day hospitalization for anorexia nervosa

The use of inpatient and day hospitalization varies widely from country to
country. In some countries, the initial treatment of anorexia nervosa
occurs exclusively in an inpatient setting, with relatively long stays and
then referral to day care. In other countries, outpatient care is the primary
mode of treatment, with inpatient care used only for medical stabilization,
with correspondingly short stays. The goals of inpatient and day hospitali-
zation programs may include medical stabilization, weight gain, symptom
control, normalized eating, identification and management of underlying
symptom-maintaining factors, and social and vocational rehabilitation.
A recent study of 71 patients with anorexia nervosa demonstrated that
after a mean of five weeks of inpatient treatment plus three weeks of day
hospitalization treatment, 35.2% had excellent outcome, 26.8% had good,
14.1% below average, and 23.9% had poor outcome.21 Case series results
of inpatient treatment for anorexia nervosa also consistently show effec-
tiveness in weight restoration. However, there are several shortcomings of
such programs. First, drop out is substantial, ranging from 20%–51% for
inpatient treatment and 13%–19% for day hospitalization treatment, with
available evidence suggesting that those who drop out from such intensive
treatments appear to be more severely ill. Second, relapse rates following
inpatient hospitalization range from 9%–42%, and no data are presently
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available on relapse rates following day hospitalization programs. Some

data suggest that the first year following discharge appears to be the high-
est for relapse. Given that there is some evidence to suggest that those
treated with a multimodal outpatient treatment were not significantly
different than those who received inpatient care at the end of a year of
treatment, coupled with concerns regarding significant drop out, refusal to
participate, relapse, readmission rates, and cost, it appears that, at least for
those anorexics who are physiologically stable, outpatient treatment
represents an effective alternative to inpatient and day hospitalization
programs.
4.3.4. Pharmacotherapy for anorexia nervosa

Anorexia nervosa remains largely resistant to pharmacological interven-
tions, and there is limited empirical support for the range of treatments
used. Most controlled trials have found no clinically relevant effect for
medication. A recent large-scale study compared fluoxetine and placebo
in weight-restored, mostly adult patients, finding no difference between
groups in the proportions of patients who maintained their weight over a
one-year trial. However, over half the patients had dropped out by the end
of treatment. Similarly, no differences were found between fluoxetine and
placebo in an inpatient trial in which patients were being treated with
other modalities.4 Although the atypical antipsychotics, such as olanzap-
ine and risperidol, are associated with weight gain, there have been no
satisfactory studies of these agents in anorexia nervosa because of diffi-
culty recruiting sufficient participants. Given the lack of evidence for
effectiveness, the use of medication in anorexia nervosa should be
restricted to the treatment of comorbid psychopathology.
4.3.5. Summary of evidence for the treatment of anorexia nervosa

The broad and profound psychiatric, medical, and nutritional consequences
of anorexia nervosa clearly indicate that treatment is complex and requires
a comprehensive approach to all aspects of the illness. Despite the need
for comprehensive and effective treatment, there is only weak evidence
for the effectiveness of both psychotherapeutic and pharmacologic studies
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for either adolescent or adult patients with anorexia nervosa. BFT for
adolescent anorexia nervosa appears promising and should be regarded as
the treatment of choice at this point but awaits the results of further
studies.
5. BULIMIA NERVOSA
Bulimia nervosa is a disabling disorder that has a profound impact on the
lives of those affected. Bulimia nervosa typically arises in adolescence,
with a peak onset at 18 years of age. Core features of the disorder include
repeated episodes of binge eating accompanied by a sense of loss of con-
trol, guilt, and remorse. There is an intense fear of fatness and purposeful
attempts to control weight through dieting and/or compensatory behaviors
such as self-induced vomiting, excessive exercise, or abuse of laxatives,
diuretics, diet pills (see Table 1). About a quarter of individuals with
bulimia nervosa report a previous history of anorexia nervosa.
5.1. Medical complications

There are relatively few medical complications associated with bulimia
nervosa. Dental and periodontal disease is common, due to binge eating
and purging, and may require extensive treatment. Some 5% of individu-
als with the illness have low potassium levels that require remediation.
Other uncommon problems include esophageal bleeding due to purging
and, very rarely, gastric dilatation or rupture.
5.2. Treatments for bulimia nervosa

5.2.1. Cognitive behavioral therapy and interpersonal
psychotherapy
The CBT-BN is based on the restraint model of binge eating, which pos-
tulates that severe dietary restriction places the individual at risk for binge
eating. Compensatory behaviors (i.e. vomiting, excessive exercise, dietary
restriction) are used to minimize the potential weight gain caused by the
binge eating. CBT also postulates that the pervasive and persistent preoc-
cupation with and undue self-evaluation based on shape and weight spur
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and maintain weight loss pursuing behaviors. Thus, CBT intervenes via
behavioral techniques to replace restrained eating with more regular
eating patterns and cognitive techniques to restructure problematic
thoughts that over-evaluate shape and weight.
Interpersonal psychotherapy (IPT) is based on the observation that
interpersonal issues frequently trigger binge eating and purging.
Interpersonal issues are conceptualized within one of four domains (grief,
interpersonal role disputes, role transitions, and interpersonal deficits) and
works to decrease binge eating and purging by directly addressing these
social and interpersonal deficits. Both treatments are administered in
18–20 sessions over a six-month period in either individual or group
mode.
When compared to IPT, CBT yields significantly higher rates of absti-
nence from binge eating and lower rates of purging at post treatment.2
By 8- and 12-month follow-up, however, the two treatments were no
longer significantly different from one another. Interestingly, participants
in the IPT condition rated their treatment as more suitable and expected
greater success than did CBT participants. At present, CBT is regarded as
the treatment of choice because of its quicker action, and thus IPT is indi-
cated as a second-level treatment. A more complex version of CBT, trans-
diagnostic CBT, may be more effective than standard CBT for individuals
with more complex psychopathology. Neither CBT nor IPT for bulimia
nervosa have been explored with adolescents.
5.2.2. Behavioral family therapy for adolescent

bulimia nervosa
Like BFT for adolescent anorexia nervosa, behavioral family therapy for
adolescent bulimia nervosa (BFT-BN) views parents and siblings as
resources to help the patient overcome bulimia nervosa. Treatment is
divided into three phases. During phase one, parents are asked to disrupt
and challenge dysfunctional eating, purging, exercise, and excessive diet-
ing behaviors. Phase two focuses on returning control of eating back to the
adolescent, and phase three involves supporting the patient and his or her
family as general adolescent and family issues come to the fore during
treatment. A randomized clinical trial compared BFT-BN to individual
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supportive psychotherapy and found that significantly more patients in

BFT-BN than in supportive therapy were binge and purge abstinent at
posttreatment (39% versus 18%) and six-month follow-up (29% versus
10%).9 In addition, BFT-BN participants yielded significantly greater
improvements in behavioral and attitudinal features of eating disorder
psychopathology and demonstrated a more rapid rate of improvement in
core bulimic symptoms. Additional data regarding on BFT-BN’s effective-
ness in the treatment of adolescent bulimia nervosa is warranted before
firm conclusions can be drawn.
5.2.3. Pharmacotherapy for bulimia nervosa

Both the tricyclic antidepressants and serotonin reuptake inhibitors
(SSRIs) have been shown to be more effective than placebo in the treat-
ment of bulimia nervosa. CBT however, is more effective than either the
tricyclics or SSRIs in controlled comparisons. This suggests that CBT
should remain the first choice for the treatment of bulimia nervosa.
Nonetheless some patients may opt for less expensive pharmacologic
treatment before attempting CBT. Patients with concurrent major depres-
sion should probably be treated for the depression before beginning
psychotherapy.
5.2.4. Summary of evidence for the treatment of bulimia nervosa

The CBT is presently the recommended treatment for bulimia nervosa
although only about half of all treated cases respond sufficiently to such
intervention. While IPT has demonstrated long-term equivalence to
CBT, the latter is recommended given its ability to decrease binge eat-
ing and purging symptoms more quickly than IPT. Pharmacotherapy
is an established treatment for bulimia nervosa but less effective
than CBT.
6. BINGE EATING DISORDER

Binge eating disorder (BED), a diagnostic research category in the
Diagnostic and Statistical Manual of Mental Disorders-IV,3 is a chronic
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disorder characterized by recurrent episodes of binge eating without the

compensatory behaviors seen in bulimia nervosa (Table 1). Binge eating
disorder impacts approximately 2%–5% of the general population and up
to 30% of weight control program participants. Findings from clinic, com-
munity, and population-based studies note that binge eating disorder is
associated with overweight and obesity, and the prevalence of binge eating
increases with body mass index. Through its association with overweight
and obesity, binge eating disorder includes a greater risk for many serious
medical conditions. In addition, when compared to overweight persons
without binge eating disorder, overweight persons with binge eating dis-
order have increased rates of Diagnostic and Statistical Manual of Mental
Disorders-IV Axis I and Axis II psychopathology and increased rates of
interpersonal and work impairments due to weight and eating concerns.
6.1. Treatments for binge eating disorder

6.1.1. Cognitive behavioral therapy and interpersonal
psychotherapy for binge eating disorder
CBT and IPT, the two most studied treatments for binge eating disorder,
have shown equivalent immediate and longer term binge abstinence
rates.23 The most recent trial comparing CBT and IPT verified that there
were no significant differences in binge eating abstinence (defined as no
objective binge episodes over the past 28 days) between CBT and IPT at
post treatment (79% versus 73%) or at one year follow-up (59% versus
62%).23 Previous research has indicated that CBT yields an average of
50% of patients abstinent at the end of the usual course of treatment. Thus,
both approaches have empirical support for the treatment of binge eating
disorder.
6.1.2. Dialectical behavior therapy for binge eating disorder

Recently, DBT for binge eating disorder (DBT-BED) was compared to a
carefully designed, active comparison group therapy in a randomized
clinical trial of 101 men and women with binge eating disorder.18 Results
indicated that although DBT-BED participants had significantly higher
abstinence rates at 20 weeks post-treatment (intention-to-treat results
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of 64% for DBT-BED versus 33.3% for the active comparison group
therapy), there were no significant group differences in abstinence rates at
any other follow-up assessment point through 12 months. DBT-BED
yields low drop-out rates suggesting that it is a highly acceptable treat-
ment for most participants and superior to supportive therapy in maintain-
ing engagement in treatment.18 Additional empirical evidence of
DBT-BED’s effectiveness compared to CBT and IPT is now needed.
6.1.3. Self-help approaches for binge eating disorder

Research on binge eating disorder self-help has varied in terms of meth-
odological quality (e.g. sample size, pathology assessment), settings, and
intervention implementation details. Consequently, strikingly different
outcomes have been reported. Reviews of the literature investigating
guided self-help (GSH) and pure self-help (PSH) for binge eating disorder
and bulimia nervosa agree on the utility of GSH and PSH and recommend
further investigation of self-help approaches. A recent large-scale study
compared behavioral weight loss therapy (BWL), IPT, and GSH based on
CBT.24 At initial outcome, there were no differences between groups, but
at the two-year follow-up, both IPT and GSH were superior to BWL,
which had shown relapse. Evidence suggested that GSH, because of its
lower costs, could be considered a first-line treatment for binge eating
disorder, with IPT being reserved for patients with greater comorbid
psychopathology.
6.1.4. Pharmacotherapy for binge eating disorder

A recent review found that pharmacological treatments yielded 48.7%
remission from binge eating, as compared with 28.5% from placebo over
the short-term (post-treatment assessments ranged from 6–24 weeks).17
This review also concluded that antiepileptic (topiramate) medication may
be preferable to selective serotonin reuptake inhibitors, given the latter’s
smaller effects on binge eating and absent impact on weight. McElroy and
colleagues12 reported results of a longer-term extension trial of topiramate
in treating binge eating disorder among obese subjects (N = 10) and found
significant reductions in binge eating (mean reduction of 5.0, p = .002) at
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56 weeks post-treatment. However, the authors note that treatment with

topiramate was associated with a high medication discontinuation rate.
Although previous research indicated significantly higher binge eating
remission rates among patients receiving pharmacotherapy than placebo,
data are limited and long-term studies are needed.
6.1.5. Summary of evidence for the treatment

of binge eating disorder
The CBT, IPT, and GSH have empirical support for the treatment of binge
eating disorder. GSH represents an alternative that is potentially more
cost-effective and readily accessible and disseminable to the clinical com-
munity as compared to specialty therapies such as CBT and IPT. It is also
less time intensive than CBT and IPT, which may make it an attractive
alternative to patients and managed care and insurance companies. Further
research on GSH, including its viability within a treatment algorithm for
binge eating disorder, is warranted. DBT-BED needs additional empirical
evidence before firm conclusions of its effectiveness can be drawn.
Topiramate appears useful because it leads to weight loss in addition to
reductions in binge eating, despite substantial dropout rates.
7. OBESITY
Some of the eating disorders, most frequently binge eating disorder and
more rarely bulimia nervosa, are associated with overweight and obesity.
Overweight and obesity increase risk for many diseases, including hyper-
tension, cardiovascular disease, stroke, gallbladder disease, osteoarthritis,
sleep apnoea, and endometrial, breast, prostate, and colon cancers.
Overweight is defined as a body mass index of 25.0 to 29.9 kg/m2, and
obesity is defined as ≥ 30 kg/m2. The World Health Organization estimates
that there are approximately 180 million obese adults worldwide and at least
twice as many overweight adults. However, many Asian experts consider
lower body mass index cut-off points appropriate for their populations,
given that medical conditions associated with overweight (e.g., glucose
intolerance, hypertension, diabetes) emerge at body mass indices above
23.0, with few of the overall population having indices greater than 30.
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7.1. Treatments for obesity

7.1.1. Behavioral weight loss, cognitive behavioral
therapy, low calorie diets, and bariatric surgery
The most common treatments for obesity are behavioral weight loss, CBT,
very low calorie diets, low calorie diets, and bariatric surgery.
Behavioral weight loss treatment is aimed primarily at weight loss by
decreasing caloric intake, increasing physical activity, and use of self-
regulation strategies to limit overeating (e.g. stimulus control). These
programs induce an average weight loss of 7%–10% of initial body
weight during the active phase of treatment. However, this weight loss is
not well maintained, because individuals regain an average of 1/3 of
treatment-induced weight loss at one-year follow-up.
Recent research investigating the impact of longer-term (e.g. three
year) CBT for obesity found that the great majority of participants
regained nearly all initial weight loss over the three-year follow-up period,
and surmised that obesity may be resistant to psychological methods of
treatment in terms of sustained, longer-term effects.6
Very low calorie diets are defined as those providing < 800 kcals per
day and low calorie diets as providing 800–1,200 kcals per day. On aver-
age, those treated with a very low calorie diet regain 35%–50% of their
lost weight within one year following treatment. Six randomized con-
trolled trials found that long-term weight losses (greater than one year)
attained with very low calorie diets were not significantly greater than
those produced by 1,000–1,500 kcal per day balanced deficit diets, due
to the greater weight gain associated with the very low calorie diet.22
Low calorie diets or balanced deficit diets accompanied by physician
monitoring and appropriate lifestyle modification (e.g. increase physical
activity) are preferred to very low calorie diets, given the latter’s associ-
ated rate of weight regain.
Surgical intervention is reserved for individuals with morbid obesity,
defined as a body mass index (BMI) that exceeds 40 kg/m2, or those with
a BMI greater than 35 kg/m2 who also present with significant associated
comorbidities (hypertension, diabetes, endocrine disorders, etc). Obesity
surgery can be divided into the following broad categories: (1) restrictive
procedures, which limit the stomach’s capacity for food; (2) malabsorptive
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procedures, which interfere with digestion; and (3) a combination of the

former two. Surgery typically yields sustained (greater than 10 years) and
significant (greater than 15%) weight loss among the obese. Thorough
medical and psychological evaluation is recommended before surgery to
ascertain if any contraindications for surgery are present and to determine
if the candidate is appropriate for this intensive intervention.
Although there are various potential medical and psychological bene-
fits for those who successfully follow pre-operative and post-operative
medical and behavioral recommendations, considerable side-effects are
possible. A common and significant postsurgical concern is lack of adher-
ence to dietary recommendations. Such non-compliance may lead to
physically adverse and damaging side-effects such as cramping, vomiting,
diarrhea, dehydration, ultimate weight regain, and dumping. Dumping, or
a rapid emptying of stomach contents into the small intestine, may occur
in up to 85% of patients who undergo procedures that combine gastric
restriction and malabsorption. The onset of frank eating disorders post-
surgery appears uncommon. In addition, data on the impact of pre-morbid
binge eating, binge eating disorder, and depressive, anxiety, and/or sub-
stance-use disorders on postsurgical outcome are mixed.11 Thus, postsur-
gical monitoring of disordered eating and psychological and psychosocial
functioning, with adjunctive psychotherapeutic and/or pharmacologic
intervention as needed, is recommended. Further research investigating
the potential impact of premorbid psychiatric conditions on postsurgical
outcomes is warranted.
7.1.2. Pharmacotherapy for obesity

There are relatively few pharmacologic agents available for the treatment
of obesity. Sibutramine has been removed from the market by the US
Food and Drug Administration for the treatment of obesity, joining fenflu-
ramine and other medications that, although effective, have caused serious
side effects. Medication approaches to the treatment of obesity should be
limited to patients with a BMI of 30 kg/m2 or above or those with a BMI
between 27 and 30 kg/m2 and a concurrent condition such as diabetes or
hypertension. Medication should always be prescribed in conjunction
with a diet leading to moderate caloric restriction and with exercise.
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The two most common medications presently in use are orlistat, now sold
over the counter as “Alli,” and phentermine.
Orlistat inhibits gastrointestinal lipase, thus preventing fat absorption,
leading to effects such as oily stools, diarrhea, and fecal spotting. These
side effects can be eliminated by reducing fat intake. The dose of orlistat
is 60 mg three times daily. If taken regularly, orlistat leads to weight
loss, with differences between placebo and drug, of between 3 and 5 kg.
Beneficial effects on blood pressure, serum lipid profiles, and carbohy-
drate metabolism have been found. Orlistat has been approved for longer-
term weight loss. Some concern has arisen about cases of severe liver
damage that have been reported with Orlistat use. It should also be
remembered that the activity of fat soluble drugs such as warfarin, thyrox-
ine, and cyclosporine, as well as fat soluble vitamins, is affected by orl-
istat. Hence, orlistat is contraindicated in patients taking such drugs, and
patients should also take multivitamins.
Phentermine, the second most common medication used for weight
loss, is a noradrenergic sympathomimetic amine approved for short-term
(e.g. a few weeks) treatment. Side effects include raised blood pressure
and heart rate with central nervous system stimulation and insomnia. The
dosage of phentermine is 37.5 mg daily, usually taken in the morning
because of stimulant effects, and weight losses are modest.
7.1.3. Summary of evidence for the treatment of obesity

In regard to behavior modification treatments of obesity, low calorie diets
or balanced deficit diets (providing 800–1,200 kcals per day) accompa-
nied by physician monitoring and appropriate lifestyle modification (e.g.
increase physical activity) are preferred to very low calorie diets (provid-
ing < 800 kcals per day), given the latter’s associated rate of weight regain.
Surgical interventions for obesity yield significant weight loss; however,
surgical candidates should be well informed on the risks and benefits
associated with such procedures, including, but not limited to, the strict
dietary recommendations accompanying surgical interventions, devia-
tions from which can cause uncomfortable and potentially deleterious side
effects. Thus, thorough psychological evaluation before undergoing obe-
sity surgery and regular follow-up with a surgical team member and/or
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psychologist post-surgery is recommended. Last, limited available phar-

macological interventions for obesity have demonstrated weight loss;
however, longer-term data on sustained weight losses, including after the
medication is withdrawn, are warranted.
8. PICA
Pica is defined as craving for, and consuming, substances such as earth,
clay, ash, and charcoal, first described by Hippocrates in the 4th century
BC. Pica is seen most frequently in less developed countries or in sub-
populations in developed countries, for example, in institutions for the
mentally ill or in poverty-stricken rural areas. In some African countries
pica occurs in almost three quarters of pregnant women. Both children and
adults may be affected. The etiology of the disorder is unknown. The three
principal hypotheses concerning etiology are that (1) the behavior is
driven by hunger caused by malnutrition; (2) the behavior is driven by
micronutrient deficiencies that could be remedied by the ingested materi-
als; or (3) the ingestion of these substances protects against pathogens and
toxins in the gut. All three of these mechanisms have been observed in
different populations. Animal experiments have shown that ingestion of
some earths does protect against toxins. Pica may lead to anemia by
competing with nutritive foods, particularly in pregnant women.
Cases of pica should be evaluated carefully because this condition may
be associated with celiac or renal disease. In addition, pica may lead to
anemia or other disorders of inadequate nutrition. Little is known about
the treatment of this disorder. Antidepressants have been used successfully
in some cases that have been conceptualized as an obsessive-compulsive
(OCD) spectrum disorder with other evidence of OCD. Some behavioral
procedures have also been used in children and institutionalized adults.
9. DISORDERS OF CHILDHOOD
Childhood eating disorders have not been well defined into separate
syndromes at this point, and there are very few treatment studies. Hence,
no evidence-based treatments are available for these disorders, which
include selective eating (neophobia and picky eating), food phobias, and
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food avoidance emotional disorder. There is considerable overlap between

these categories.
9.1. Selective eating

Selective eating comprises two syndromes, neophobia and picky eating,
which overlap. Neophobia is defined as avoidance of newly introduced
foods, particularly fruits, vegetables, and proteins, but may extend to other
foods. One hypothesis is that this syndrome is an adaptive evolutionary
response that protects against the ingestion of poisonous foods. These
children are often more sensitive to the sensory aspects of food, including
taste and texture. Sensitivity to bitter taste, for example, is genetically
endowed and observable in infancy and leads to avoidance of certain veg-
etables. Neophobia may also be associated with temperamental distur-
bances such as shyness and with autistic spectrum disorders. The most
extreme forms of neophobia may be associated with underweight some-
times diagnosed as infantile anorexia. Picky eating is common in child-
hood, affecting about a quarter of all children at some time in infancy and
early childhood. It is characterized by avoidance of fruits and vegetables
and may cause parents considerable anxiety. Picky eaters may also be
underweight, at least in infancy and early childhood. Picky eating may
persist into adolescence. One prospective study suggested that picky
eating is a risk factor for anorexia nervosa.
The usual treatment for picky eating is watchful waiting, because most
cases resolve in a year or two. Otherwise the treatment for picky eating is
to serve the child the same foods as served at family meals, to avoid pre-
paring special meals for the child, and to refrain from putting undue pres-
sure on the child to eat. Treatment for neophobia involves gradual
introduction of small amounts of avoided foods. However, at this point,
there is no evidence-based approach to the treatment of either of these
disorders.
9.2. Food phobias

Food phobias are usually seen in school-aged children and may be associ-
ated with a fear of swallowing. These phobias may have a sudden onset
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triggered by some event, for example, after nausea has been paired with a
specific food during an illness or after choking on some food. Because a
food phobia is usually specific to one type of food, treatment is usually
unnecessary. However, food phobia associated with a fear of choking
should be treated as any other phobia, with graduated exposure to the
feared foods, often all solid foods. Hence, a gradient from liquid foods to
solid foods is required.
9.3. Food avoidance emotional disorder

Food avoidance emotional disorder, usually seen in later childhood or
adolescence, is associated with much reduced food intake, weight loss,
and possibly growth retardation. The disorder is accompanied by marked
anxiety over eating. Because such cases may resemble early cases of ano-
rexia nervosa, it is important to differentiate the two syndromes. Patients
with food avoidance emotional disorder are not concerned with their
weight and shape and recognize that they are thin and need to put on
weight, as distinct from anorexia nervosa. Treatment of this disorder
involves individual and parent counseling focusing on the details of the
particular child’s problems and using various behavior change procedures
as applicable.
10. CONCLUSIONS AND FUTURE DIRECTIONS

Eating disorders are psychiatric illnesses that involve intense and persis-
tent concern regarding weight, shape, and food combined with behavioral
manifestations that attempt to control or otherwise alter intake, weight,
and shape. These disorders are frequently comorbid with other psychiatric
illnesses and often incur severe repercussions on physical health, self-
esteem, interpersonal and social functioning, and quality of life. To date,
empirical research on effective treatments for eating disorders indicates
that there are a few treatments with a high evidence base for bulimia ner-
vosa and binge eating disorder (including CBT and IPT). No treatment has
yet established a high evidence base for anorexia nervosa, although BFT
for adolescents has demonstrated strong preliminary evidence. Research
needs to be an on-going effort that incorporates a comprehensive focus on
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etiology, prevention, and treatment combined with culturally sensitive and

appropriate assessment and intervention. Specific areas for further inves-
tigation include global incidence, variations in clinical presentations,
generalizability of empirically supported treatments to community set-
tings, cost-effectiveness of treatments, accessibility of treatments to vari-
ous ethnic and minority groups, effective treatment of chronic anorexia
nervosa in adults, the efficacy of treatments for children and adolescents,
and the impact of ethnicity and race on assessment, provider assumptions,
and access to treatment.
11. KEY POINTS
• A thorough medical evaluation of patients presenting with eating

disorder is warranted. Vital checks may include electrolytes, specific
gravity, pulse, heart rate, blood pressure, bone density, and
temperature.
• Binge eating, purging, and ‘water loading’ can lead to dramatic
weight fluctuation and weight instability. Look for steady trends in
weight gain to ensure that the patient is gaining “real” weight. (‘Water
loading’ is a phrase used to describe the ingestion of large amounts of
fluids, typically water, to give the appearance of increased weight.
It may be used by anorexia nervosa patients trying to gain weight as
measured in their doctor’s office. Specific gravity measures may indi-
cate water loading. Water loading is highly dangerous and can lead to
seizure.)
• The use of appropriate assessments in ascertaining the severity and
duration of eating disorder are strongly recommended. For example,
the Eating Disorder Examination7 is a widely used and well-validated
measure of the spectrum of disordered eating.
• Despite likely obvious manifestations, symptom minimization is not
infrequent in anorexia nervosa, particularly with recent onset in ado-
lescence (e.g. before the disorder becomes chronic). Clinicians, par-
ticularly primary care physicians and pediatricians, are encouraged to
be highly attuned to this presentation and to a patient’s efforts to
‘rationalize’ or ‘normalize’ their eating behaviors.
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• Bulimia nervosa may present in individuals with comorbid and/or

pre-existing impulse control concerns. Thus, it is often helpful to
assess for other manifestations of impulse dysregulation, including,
but not limited to, substance abuse, self-harm, shoplifting, gambling,
spending above ones’ means, and frequent interpersonal dysfunction.
12. SELF-ASSESSMENT
12.1. On the basis of the current empirical literature, which
of the following is presently the recommended treatment
of choice for bulimia nervosa?
(A) Dialectical behavior therapy.
(B) Interpersonal psychotherapy.
(C) Cognitive behavioral therapy.
(D) Behavioral family therapy.
(E) The available empirical data is insufficient to support a particular
therapy.
Answer: C2
12.2. Which of the following refers to the international statistical

classification of diseases and related health problems-10
and diagnostic and statistical manual of mental
disorders-IV criteria for anorexia nervosa?
(A) A dread of fatness and flabbiness of body contour persists as an intrusive
overvalued idea when weight loss is induced and sustained by the patient.
(B) Usually accompanied by under nutrition of varying severity with sec-
ondary endocrine and metabolic changes.
(C) Includes preoccupation with the control of body weight, which may
lead to a subjective or objective episodes of overeating.
(D) Symptoms include deliberate, restricted dietary choice, excessive
exercise, induced vomiting and purgation, and use of appetite sup-
pressants and diuretics.
(E) Anorexia nervosa could include all of the above.
Answer: E3,25
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13. CASE STUDIES

13.1. Anorexia nervosa
Claire, aged 16 years, was brought in for treatment by her parents, who
were worried about their daughter’s recent weight loss. Her mother
explained that Claire had always been a fairly lean girl but that over the
past five months, she had dropped 20 lbs astonishingly quickly. Three
weeks ago, Claire’s mother and father took Claire to her pediatrician’s
office and then to an eating disorder specialty inpatient unit, where Claire
was hospitalized for two weeks. The physicians on the eating disorder unit
stated that Claire had anorexia nervosa and were particularly concerned
about her severely low weight (she was 70% of her ideal body weight
upon admission) and significantly below normal pulse rate and tempera-
ture. Claire gained 5 lbs in the hospital, and now her family was interested
in receiving outpatient treatment to ensure her further recovery and pre-
vent future hospitalizations. Claire did not want to be in therapy; she
believed that the 5 lbs she gained in the hospital were enough to allow her
to return to school and soccer, even though the doctors strongly disagreed.
Claire continued to refuse the food her mother prepared for her, and meals
often ended in chaos and frustration. Claire’s mother and father reported
that she gradually but steadily limited the types of foods she would allow
herself to eat until she was eating only 1,000 calories per day. They did
not understand why Claire, a straight-A student, president of the yearbook
committee, and stellar soccer player, refused to regain enough weight to
be healthy. Claire just did not seem to care about the medical, psychologi-
cal, or social consequences of being at such a low-weight.
13.2. Bulimia nervosa

Lucy, a single 24-year-old woman, came to therapy expressing great
concern over her eating behaviors. She stated that she alternates between
very light eating to large, out-of-control overeating episodes, which are
regularly followed by self-inducing vomiting. A typical binge episode for
Lucy may include half a gallon of ice-cream, 3–4 bowls of cereal, 4–5
slices of bread with cheese, and 2–4 pieces of fruit. Lucy states that she
has been binging and purging for approximately three years but has been
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worried about her weight and shape since high school. Early in college,
she began limiting the types of foods she allowed herself to have and
began intensely exercising as a means of influencing her weight and
shape. She continues to use intense exercise as a means of weight control,
even though her weight has never been out of the healthy range for her
height. Presently, she binges and purges about once per day which is down
from three daily binges and purges last year. Lucy reports that many
things appear to trigger her binge episodes, including hunger and/or feel-
ing lonely, sad, or bored. Lucy has a number of “food rules,” which
demand a diet very limited in fat and carbohydrates and specify off-limit
foods (such as sweets, cereal, breads, and red meat). On her “good days”
she reports eating fruits, vegetables, non-fat yogurt, and lean pieces of
chicken. During binge episodes, however, Lucy noticed that she tends to
overeat foods that she otherwise forbids herself. Lucy reports that she
feels ashamed about her eating and often suffers from intense worry and
sadness over the financial position her binging has left her in. Although
she maintains a steady job, her social life has suffered, because of the time
dedicated to shopping for binge foods and binging and purging rather than
being with friends and family. A recent visit to the dentist, where the
doctor informed her of the extensive and severe dental enamel decay and
erosion that the purging has caused, prompted Lucy to come to therapy.
13.3. Binge eating disorder

Tony is a 40-year-old, overweight, married man who is fed up with his
eating patterns. He told his therapist that he has episodes of intense over-
eating, during which he eats quickly until all the food is gone. Tony said
that he eats everything he can get his hands on until he is too full and
uncomfortable to eat any more. He reflected that during his most recent
episode, he ate various foods from a fast food restaurant, including
four cheeseburgers, two large orders of French fries, and two pieces of
apple pie. He noted that while eating he feels numb, as if he were in a zone
in which the sole focus is food. Tony said that he eats when his family is
not at home, because he does not want them to see how much he is eating,
and that he often eats without feeling truly hungry. After the eating epi-
sodes are over, Tony berates himself for having eaten so much food and
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calories and feels guilty and disgusted. Tony noted that he has these eating
episodes about three or four times per week, depending upon how stressed
out he is. Outside of the binge eating episodes, Tony eats regularly and has
three meals and a couple of snacks daily. Sometimes he goes through
phases where he will try to eat “healthfully” and cut down on calorie and
fat intake, but he generally does not restrict his intake. Tony noted that
these “healthy” eating periods do not last very long. In addition, he
reported that he has some marital concerns but is mainly very distressed
about his weight and eating problems. Tony said that his wife knows that
he “overeats” now and then but that she does not know the extent of the
problem or how much it bothers him.
REFERENCES
1. Alegria M, Woo M, Cao Z, Torres M, Meng X, Striegel-Moore R. (2007)
Prevalence and correlates of eating disorders in Latinos in the United States.
Int J Eat Disord 40: S15–S21.
2. Agras WS, Walsh BT, Fairburn CG, Wilson GT, Kramer HC. (2000) A
multicenter comparison of cognitive-behavioral therapy and interpersonal
psychotherapy for bulimia nervosa. Arch Gen Psychiatry 57: 459–466.
of Mental Disorders, 4th ed. American Psychiatric Association, Washington,
DC.
4. Attia E, Haiman C, Walsh BT, Flater SR. (1998) Does fluoxetine augment
the inpatient treatment of anorexia nervosa? Am J Psychiatry 155: 548–551.
5. Chen ZF, Mitchell JE, Li K, Yu WM, Lan YD, Jun Z, et al. (2006) The
prevalence of anorexia nervosa and bulimia nervosa among freshman
medical college students in China. Int Eat Disord 12(2): 209–214.
6. Cooper Z, Doll HA, Hawker DM, Byrne S, Bonner G, Eeley E, et al. (2010)
Testing a new cognitive behavioral treatment for obesity: A randomized
controlled trial with three-year follow-up. Behav Res Ther 48: 706–713.
7. Fairburn CG, Cooper Z. (1993) The eating disorder examination. In: Fairburn
CG, Wilson GT (eds.), Binge Eating: Nature, Assessment and Treatment,
12th ed. pp. 317–360, Guilford Press, NY.
8. Hay P. (1998) The epidemiology of eating disorder behaviors: An Australian
community-based survey. Int J Eat Disord 23(4): 371–382.
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9. LeGrange D, Lock J, Dymek M. (2003) Family-based therapy for adoles-

cents with bulimia nervosa. Am J Psychother 67: 237–251.
10. Lock J, LeGrange D, Agras WS, Moye A, Bryson SW, Jo B. (2010)
Randomized clinical trial comparing family-based treatment with adoles-
cent-focused individual therapy for adolescents with anorexia nervosa. Arch
Gen Psychiatry 67(10): 1025–1032.
11. Marcus MD, Kalarchian MA, Courcoulas AP. (2009) Psychiatric evaluation
and follow-up of bariatric surgery patients. Am J Psychiatry 166: 285–291.
12. McElroy SL, Shapria NA, Arnold LM, Keck PE, Rosenthal NR, Wu SC,
et al. (2004) Topiramate in the long-term treatment of binge-eating disorder
associated with obesity. J Clin Psychiatry 65(11): 1463–1469.
13. Morande G, Celada J, Casas J. (1999) Prevalence of eating disorders in a
Spanish school-age population. J Adolesc Health 24(3): 212–219.
14. Nicado EG, Hong S, Takeuchi DT. (2007) Prevalence and correlates of eating
disorders among Asian Americans: Results from the National Latino and
Asian American Study. Int J Eat Disord 40: S22–S26.
15. Nobakht M, Dezhkam M. (2000) An epidemiological study of eating disor-
der in Iran. Int J Eat Disord 28(3): 265–271.
16. Pike, Carter, Olmsted. (2010) Cognitive behavioral therapy for anorexia ner-
vosa. In: Grilo CM, Mitchell JM (eds.), The Treatment of Eating Disorders:
A Clinical Handbook, Guilford Press, NY.
17. Reas DL, Grilo CM. (2008) Review and meta-analysis of pharmacotherapy
for binge-eating disorder. Obesity 16(9): 2024–2038.
18. Safer D, Robinson AH, Jo B. (2010) Outcomes from a randomized controlled
trial of group therapy for binge eating disorder: Comparing dialectical behav-
ior therapy and an active comparison group therapy. Behav Ther 41(1):
160–120.
19. Striegel-Moore R, Dohm FA, Kraemer HC, Taylor CB, Daniels S, Crawford
PB, et al. (2003) Eating disorders in black and white women. Am J Psychiatry
160: 1326–1331.
20. Taylor JY, Caldwell CH, Baser RE, Faison N, Jackson JS. (2007) Prevalence
of eating disorders among blacks in the national survey of American Life. Int
J Eat Disord 40(S3): S10–S14.
21. Treat, Gaskill, McCabe, Marcus. (2005) Short-term outcome of psychiatric
inpatients with anorexia nervosa in the current care environment. Int J Eat
Disord 38(2): 123–133.
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22. Wadden TA, Berkowitz RI. (2002) Very-low calorie diets. In: Fairbun CG,
Brownell KD (eds.), Eating Disorders and Obesity: A Comprehensive
Handbook, 2nd ed. pp. 534–538, Guilford Press, NY.
23. Wilfley DE, Welch R, Stein RI, Spurrell EB, Cohen LR, Saelens BE, et al.
(2002) A randomized comparison of group cognitive-behavioral therapy and
group interpersonal psychotherapy for the treatment of overweight
individuals with binge eating disorder. Arch Gen Psychiatry 59(8): 713–721.
24. Wilson GT, Wilfley DE, Agras WS, Bryson S. (2010) Psychological treat-
ments of binge eating disorder. Arch Gen Psychiatry 67: 94–101.
25. World Health Organization. (2007) International Statistical Classification of
Diseases and Related Health Problems, 10th Revision, World Health
Organization, Geneva.
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Chapter 17
Sexual Disorders
Richard Balon
1. INTRODUCTION
Sex is one of the three basic drives, the other ones being sleeping and eat-
ing. Although the underlying basic role of sex is reproduction, sex plays
other important roles, such as providing pleasure, satisfaction, and feel-
ings of well-being. Human sexuality is a complex affair regulated at vari-
ous levels. Seemingly simple sexual events, e.g. erection, are regulated
by multiple systems — central nervous system, peripheral nervous sys-
tem, vascular system, endocrine glands — and influenced by many fac-
tors, such as previous experience, childhood trauma, stage of development,
interpersonal relationship, life circumstances, culture, and medications.
Age is also an important factor — sexuality usually peaks in early
adulthood and then gradually declines.
It is important to realize that sex, like the other basic drives, could be
impacted by various mental and physical illnesses. Impairment of basic
drives could be part of the symptomatology of an underlying illness — for
instance, decreased libido, inability to maintain sleep, and decreased
appetite could be all part of major depressive disorder symptomatology;
or impaired erectile function and changes of appetite could be part of
diabetes mellitus symptomatology. One should bear this in mind during
the evaluation of any patient complaining of impairment of any of the
basic drives. Discerning between the basic drive dysfunction due to
409
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410 R. Balon
mental/physical illness and true disorder/dysfunction plays an important

role in treatment planning. Impairment of sexual functioning is more com-
plicated than impairment of other functions or other mental disorders,
because it usually involves more than one person — the patient’s partner.
What may be stressful for the patient may not be stressful for the partner
and vice versa.
Impairments in the area of human sexuality could be conceptually
divided into impairment of “normal” sexual functioning (sexual dysfunc-
tions), impairment of the focus of sexual behavior (paraphilias), and
impairment of sexual identity (gender identity disorders — GID).
A number of medical, social, and legal issues, such as sexually trans-
mitted diseases, abortion, and sex-related crimes, involve human sexuality.
This chapter, however, addresses only impairment or changes of sexual
functioning, focus, and identity.
2. GENERAL CONSIDERATIONS
2.1. Epidemiology
Although sexual dysfunctions/disorders are thought to occur frequently,
the exact incidence and prevalence are difficult to establish for various
reasons. In the case of sexual dysfunctions, the patient may not be forth-
right in reporting sexual difficulties because he or she may be ashamed,
may feel the issue of sexual functioning is too private to talk about, or,
incorrectly, may feel that his or her way of sexual functioning is “normal.”
Various studies on sexual dysfunctions associated with antidepressants
illustrate the difficulties in estimating the frequency of sexual dysfunc-
tions. In these studies the patients filled out questionnaires about sexual
dysfunctions first and were subsequently interviewed by experienced cli-
nicians. Invariably, the estimates of sexual dysfunctions’ frequency were
significantly higher when patients were interviewed by clinicians. These
findings warn us that we need to interpret the results of epidemiological
studies with some caution. The reporting of paraphilias is even more com-
plicated — paraphilias are relatively rare and not socially acceptable; thus
patients usually do not seek help and do not report their difficulties unless
they are seriously distressed. In addition, comorbidity with other disorders
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Sexual Disorders 411
is high. Finally, studies in paraphilias are difficult to conduct for ethical

and medico–legal considerations.
Nevertheless, some well-conducted epidemiological studies point out
that sexual dysfunctions are frequent (again, one needs to take the results
with some reservation, considering epidemiological versus other studies).
Laumann, Paik, and Rosen11 studied the prevalence of sexual dysfunction
in the United States. They analyzed data from the National Health and
Social Life Survey and found that sexual dysfunction is more prevalent in
women (43%) than in men (31%) and is associated with various demo-
graphic characteristics, such as age (increasing with age, especially erec-
tile dysfunction) and education (usually lower education is associated
with higher frequency of sexual dysfunction). The most frequent dysfunc-
tion among men was premature ejaculation (31%; erectile dysfunction and
low desire both 5%). Among women it was low sexual desire (22%), fol-
lowed by impaired arousal (14%), and sexual pain (7%). Importantly,
sexual dysfunction was more likely among women and men with poor
emotional and physical health and was associated with negative experi-
ences in sexual relationships and overall well-being. Laumann and col-
leagues10 later studied sexual dysfunction among adults aged 40–80 years
in 29 countries. There were some similarities between the results of this
study and the results of the study conducted in the United States. In
women, lack of interest in sex and inability to reach orgasm were the most
common, ranging from 26% to 43% and 18% to 41% respectively,
depending on the region. In men, early ejaculation was most common,
ranging from 12% to 31%. Interestingly, in most cases, the reported preva-
lence of sexual problems was higher or highest in East and Southeast Asia
(e.g. erectile dysfunction and lubrication problems were double the rates
in other regions). Again, sexual problems tended to be more associated
with declining physical health and aging.
The frequency of paraphilias in the general population is unknown.
There are no solid data available. Most paraphilias (with probably the
exception of sexual masochism) are thought to be more frequent among
men. Gender identity disorders are rare — according to data from some
European countries with access to total population statistics and referrals,2
roughly 1 in 30,000 adult males and 1 in 100,000 adult females seek
sex-reassignment surgery.
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412 R. Balon
Besides the differences in prevalence of sexual dysfunctions in various

parts of the world, there are numerous other issues that differ between
countries and cultures. The acceptance of homosexuality varies widely
across cultures and religions, with some tolerating and accepting it
almost fully and some still criminalizing it. Interestingly, some ancient,
“pre-Christianity” cultures were more tolerant of homosexuality (e.g.
Roman and old Hindu cultures). Some paraphilias are also viewed and
tolerated differently in various cultures (e.g. transgendered individuals
are tolerated in India and may be invited to dance at weddings; sex with
adolescent boys was accepted in ancient Rome). Some cultures and coun-
tries are more permissible and tolerant of expressing one’s sexuality and
sexual interest. There is clearly a lot that needs to be addressed in the area
of human sexuality regarding international issues, starting with proper
sexual education across cultures.
2.2. Etiology
The etiology of sexual dysfunctions is frequently multifactorial, involving
biological, psychological, interpersonal, and, at times, cultural factors.
In some cases, such as erectile dysfunction in a man suffering from diabetes
mellitus and atherosclerosis, the etiology is obvious. In other cases, such as
lifelong male orgasmic disorder, the cause is mostly unknown. Biological
factors possibly involved in sexual dysfunction include endocrinopathies,
cardiovascular diseases, injury, urological diseases, medications, and sub-
stance abuse. Psychological factors include stress, clinical depression, vari-
ous other mental disorders, anxiety, and sexual abuse, while interpersonal
factors include marital conflict, partner’s sexual dysfunction, extramarital
affair, homosexual conflict, religious differences and conflict, cultural dif-
ferences, childbearing demands, and others.
The etiology of paraphilias and gender identity disorders has been
a subject of various psychological theories but is basically unknown. Men
with paraphilias, in general, have difficulties with attachment and inti-
macy, high levels of neuroticism, lower agreeableness, and lower consci-
entiousness. There have been attempts to explain some paraphilias (e.g.
voyeurism, exhibitionism, and frotteurism) in terms of courtship disorder
theory9 — impairment of one of the four sequential phases of a normal
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sexual relationship: finding a partner (voyeurism); non-physical interac-

tion (exhibitionism); physical non-sexual contact (frotteurism); and sexual
intercourse (rape).
2.3. Genetics
No data are available on the genetics of low sexual desire, sexual aversion,
and arousal dysfunction. According to Australian female twin studies,
genetics may account for some variance of orgasm during coitus (31%)
and masturbation (51%). Premature ejaculation may have a familiar
pattern. No solid data from genetic studies of paraphilias are available.
Similarly, no solid genetic studies of gender identity disorders are
available.
2.4. Diagnosis and classification

Classification of sexual dysfunctions is anchored in the sexual response
cycle (Masters and Johnson, 1966). Masters and Johnson divided the
sexual response cycle into four parts: desire (libido), excitement (arousal),
orgasm, and resolution. Sexual dysfunctions according to the DSM-IV12
and the International Classification of Diseases (ICD-10)20 are summa-
rized in Table 1. In general, the DSM criteria are more structured and
detailed and thus are used in the descriptions of different diagnoses
through this chapter.
The DSM and ICD classification systems differ slightly in classifying
sexual disorders but basically cover the same areas (Table 1). The ICD
classification does not place all sexual disorders into one group —
sexual dysfunctions are subsumed into the category of “Behavioral
syndromes associated with physiological disturbances and physical fac-
tors,” while paraphilias and gender identity disorders are subsumed into
the broad category of “Disorders of adult personality and behavior.”
Beyond this, the main difference is the inclusion of psychological and
behavioral disorders associated with sexual development and orientation
in the ICD, while these are not considered disorders in the DSM clas-
sification. There are three main entities in this category — sexual matu-
ration disorder (the individual suffers from uncertainty about his or her
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414 R. Balon
Table 1. Sexual disorders — DSM and ICD classifications.
ICD — Sexual dysfunctions not caused

DSM — Sexual dysfunctions by organic disorder or disease
Sexual desire disorders Lack or loss of sexual desire (F52.0)

Hypoactive sexual desire disorder (includes frigidity, hypoactive sexual
(302.71) desire disorder)
Sexual aversion disorder (302.79) Sexual aversion and lack of sexual enjoyment
(F52.1)
Lack of sexual enjoyment (F52.11) (includes
anhedonia, sexual)
Sexual arousal disorders Failure of genital response (F52.2)
Female sexual arousal disorder (includes female sexual arousal disorder,
(302.72) male disorder, psychogenic impotence)
Male erectile disorder (302.72)
Orgasmic disorders Orgasmic dysfunction (F52.3)
Female orgasmic disorder (302.73) (includes inhibited orgasm, male, female;
psychogenic anorgasmia)
Male orgasmic disorder (302.74)
Premature ejaculation (302.75) Premature ejaculation (F52.4)
Sexual pain disorders Non-organic vaginismus (F52.5)
Dyspareunia (302.76) (includes psychogenic vaginismus)
Vaginismus (306.51) Non-organic dyspareunia (F52.6)
(includes psychogenic dyspareunia)
Excessive sexual drive (F52.7)
(includes nymphomania, satyriasis)
Sexual dysfunction due to a general
medical condition (specify type,
general medical condition)
Substance-induced sexual dysfunction
(specify substance, subtype, whether
onset during intoxication)
Sexual dysfunction not otherwise Other sexual dysfunction, not caused by
specified (302.70) organic disorder or disease (F52.8)
Unspecified sexual dysfunction, not caused by
organic disorder or disease (F52.9)
DSM Paraphilias ICD Disorders of sexual preference
Exhibitionism (302.4) Fetishism (F65.0)
(Continued)
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ICD — Sexual dysfunctions not caused

DSM — Sexual dysfunctions by organic disorder or disease
Fetishism (302.81) Fetishistic transvestitism (F65.1) (includes

transvestic fetishism)
Frotteurism (302.89) Exhibitionism (F65.2)
Pedophilia (302.2) Voyeurism (F65.3)
Sexual masochism (302.83) Pedophilia(F65.4)
Sexual sadism (302.84) Sadomasochism ((F65.5) (includes
masochism, sadism)
Transvestic fetishism (302.3) Multiple disorders of sexual preference (65.6)
Voyeurism (302.82) Other disorders of sexual preference (F65.8)
(includes frotteurism, necrophilia)
Paraphilias not otherwise specified Disorders of sexual preference, unspecified (F65.9)
(302.9) (includes sexual deviation NOS)
DSM Gender identity disorders ICD Gender identity disorders
Gender identity disorder (in child Transsexualism (F64.0)
coded 302.6; in adolescent or adult
302.85)
Gender identity disorder not otherwise Dual-role transvestism (F64.1) (includes GID of
specified (302.6) adolescence or adulthood, non-transsexual type;
excludes fetishistic transvestism)
Sexual disorder not otherwise specified Gender identity disorder of childhood (F64.2)
(302.9) (excludes: egodystonic sexual orientation, sexual
maturation disorder)
Other gender identity disorders (F64.8)
Gender identity disorder, unspecified (F64.9)
(includes gender-role disorder NOS)
ICD Psychological and behavioral disorders
associated with sexual development and
orientation (sexual orientation alone is not
regarded as a disorder)
Sexual maturation disorder (F66.0) (specify
heterosexual, homosexual, bisexual, other
including prepubertal)
Egodystonic sexual orientation (F66.1)
Sexual relationship disorder (F66.2)
Other psychosexual development disorders (F66.8)
Psychosexual development disorder, unspecified
(F66.9)
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416 R. Balon
gender identity or sexual orientation, which causes anxiety or depres-

sion; this occurs mostly in adolescents); ego dystonic sexual orientation
(the gender identity or sexual preference is not in doubt but the indi-
vidual wishes it were different because of associated psychological and
behavioral disorders); and sexual relationship disorder (the gender iden-
tity or sexual preference abnormality is responsible for difficulties in
forming or maintaining a relationship with a sexual partner). The ICD
classification defines sexual response as a psychosomatic process and
emphasizes that both psychological and somatic processes are usually
involved in the causation of sexual dysfunction. ICD-10 classification
also suggests that women tend to present more commonly with the sub-
jective quality of the sexual experience rather than a failure of specific
response. ICD specifically states, “The complaint of orgasmic dysfunc-
tion is not unusual, but when one aspect of a women’s sexual response
is affected, others are also likely to be impaired. For example, if a
woman is unable to experience orgasm, she will often find herself una-
ble to enjoy other aspects of lovemaking and will thus lose much of her
sexual appetite. Men, on the other hand, though complaining of failure
of a specific response such as erection or ejaculation, often report a
continuing sexual appetite.”
The diagnoses of sexual dysfunctions, paraphilias, and gender identity
disorder are descriptive. Similar to the rest of psychiatric diagnoses,
there are no specific tests or examinations available, although, at times,
some tests may help to clarify the diagnosis (e.g. testosterone level in
male hypoactive sexual desire disorder or phaloplethysmography in
pedophilia).
2.5. Evaluation of sexual functioning in clinical practice

Evaluation of sexual functioning should be part of every comprehensive
patient evaluation. Patients are usually comfortable with questions about
sexual functioning, and the evaluator needs to be comfortable too. Inquiry
into sexual functioning should be specific, not vague and general.
The basic components of evaluation include clinical interview, psycho-
metric assessment, physical examination, and laboratory testing (not all
components are always applicable or done).
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2.5.1. Clinical interview

Clinical interview is the primary source of information. It could be done
with or without previous screening. The previous screening information
source could be previous examination, data bank (electronic medical
records), referral information, or previously filled questionnaires or
scales. Previously obtained information about sexual functioning should
always be discussed with the patient — it should not be accepted at its
face value. Clinicians should always bear in mind that not all sexual prob-
lems meet the criteria for sexual dysfunction but, rather, may be classified
as sexual difficulties. The multifactorial origin of sexual dysfunctions
should be considered and addressed in every evaluation.
The questioning about sexual functioning should be very specific;
vague questions, such as “How is your sex life?” are not very helpful. An
example of detailed questioning about sexual dysfunction is the following
set of questions to be clarified with the patient: Is it sexual dysfunction or
difficulty? What dysfunction is it? Do all parts of the sexual response
cycle occur? Which one is impaired? What is the course, duration, inten-
sity, severity? Is there any associated distress? How frequently does the
dysfunction occur? Does it occur just in a specific situation? Has there
been any change time? Does the person masturbate, and does the
dysfunction occur during masturbation? (For detailed outline of clinical
interview/evaluation, see Derogatis and Balon6) The interview should be
semi-structured yet tailored to the specific patient’s needs. The questions
should be asked in a serious manner, and the interviewer should be com-
fortable with them. Interviewing the partner can be an invaluable addition
to the patient interview. Some recommendations for specific questioning
are summarized in Table 2.
During evaluation of sexual function/dysfunction, one should realize/
think that there is a variety and a difference in what patients and their
evaluators consider “normal” and “acceptable” sexual functioning and
orientation. The clinician should be respectful and tolerant of patients’
personal, cultural, and religious feelings and/or “norms” of human sexual-
ity and should definitely not bring in his or her own views of sexuality.
The interview should be conducted in a serious and courteous manner;
patients should not feel that they are being judged in any way.
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418 R. Balon
Table 2. Specific, clinically oriented questions about sexual function/dysfunction.*
General/introductory questions
The questioning should start with an introductory statement such as, “Let me ask you a
few questions about your sex life I ask all patients, as I consider sex life to be an
important part of a person’s life.”
1. Can you tell me whether you are satisfied with your sexual functioning and if not,
why not?
2. Is your partner satisfied with the frequency and quality of your sexual encounters?
3. How often do you have sex?
4. Who starts sex, you or your partner?
5. Are there any differences in sexual interest/demand between you and your partner?
Questions about sexual desire/libido
1. Do think about sex often?

2. Do you feel like having sex often?
3. Have there been any changes in your desire to have sex?
4. Are there any situations or things that increase/change your desire to have sex?
Questions about arousal/erection
1. Do you get easily aroused by your partner or anybody else?

2. Have you noticed any change in being aroused lately?
For women:
1. Do you get wet easily?

2. Have you had any problems with lubrication lately?
3. Do you need more stimulation lately to get aroused?
For men:
1. Have you observed any changes in getting hard or having an erection lately?
2. Are you getting hard during intercourse?
3. Are you having erections when you wake up?
4. Any problems with getting hard during masturbation?
Questions about orgasm
1. Do you have any difficulties reaching orgasm?
2. Do you need additional stimulation to reach orgasm/to ejaculate?
3. Do you reach orgasm every time when having sexual intercourse?
4. Does it take you too long to reach orgasm?
Additional questions may ask about masturbation, sexual abuse, sexual orientation, sex
outside the permanent relationship etc.
*Adapted in part from Derogatis and Balon.6
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2.5.2. Psychometric assessment

The psychometric assessment of sexual functioning is usually used in a
more specialized clinical or research practice. No diagnostic instruments
are available for sexual disorders; however, many instruments (e.g. self-
reported questionnaires, clinical rating scales, structured interviews) are
available to help the evaluator to quantify the patient’s response.
Unfortunately, most of the instruments in this area are not validated. Some
of the better known and widely used instruments are The Arizona Sexual
Experience Scale,13 The Derogatis Interview for Sexual Functioning,7
Changes of Sexual Functioning Questionnaire,5 The International Index of
Erectile Function,17 and Sexual Function Questionnaire.16

The physical examination should include a review of systems and a
general physical examination with a special focus on cardiovascular,
endocrine, neurological, and sexual systems/organs. Pelvic examination
and evaluation of the genitalia should be done by a specialist (e.g.
gynecologist for women, urologist for men).
2.5.4. Laboratory testing

The selection of laboratory testing should always be guided by the clinical
context (e.g. testosterone level should be ordered in a middle-aged male
who lost desire but not in a young male with sudden onset erectile dys-
function). Recommended tests include plasma estradiol, total testoster-
one, free testosterone, sex-hormone binding globulin, thyroid stimulating
hormone, and prolactin. Optional tests include lipid profile, dihydroepian-
drosterone, fasting glucose, thyroid panel, glycosylated hemoglobin
A1C, and complete blood count. Some specialized tests evaluate the vas-
cular status of the penis, such as Doppler sonography, phaloplethysmog-
raphy, and RigiScan for evaluation of nocturnal penile tumescence.
However, the use of these tests almost ceased with the arrival of new
medications for erectile dysfunction, the phosphodiesterase-5 inhibitors.
There are also some specialized tests for the evaluation of paraphilias,
namely pedophilia, such as phaloplethysmography and Viewing Time.1
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420 R. Balon
2.6. General management recommendations

As Balon3 pointed out, several general issues should be considered before
the treatment of each specific sexual disorder.
First, the treating clinician should be aware of the fact that sexual
dysfunctions and disorders frequently overlap and more than one sexual
dysfunction/disorder could be identified in a single patient. The clinician
should identify the primary dysfunction and start treating it, while
addressing the associated or overlapping entity too.
Second, causal factors and treatment should not be framed only in the
traditional biology-vs.-psychology dichotomy, but other factors, such as
culture and value system, should also be considered and included in treat-
ment planning.
Third, the differential diagnostic process should carefully untangle
various organic and psychological factors and underlying causes (e.g.
diabetes mellitus). Treatment of the underlying cause may or may not
relieve the sexual dysfunction. One should not forget the possible
adverse effects of numerous medications (e.g. antidepressants,
antipsychotics, and some cardiovascular medications) on sexual
functioning.
Fourth, various multidimensional perspectives, such as the four
perspectives (disease perspective, dimension perspective, behavior
perspective, and life story perspective) suggested by Fagan,8 could be
implemented to assist in the organization of clinical information.
Fifth, although we have seen significant advances in what is called
sexual pharmacology,18 all treatment modalities should always be con-
sidered for various sexual dysfunctions. Frequently, clinicians do not
pay attention to psychological issues but focus on possible “medical”
reasons and in prescribing medications for them. Nevertheless, combin-
ing medication and psychotherapy or sex therapy clearly makes clinical
sense (although there are no good studies of medication(s) and psycho-
therapy/sex therapy for sexual dysfunction) and thus it is strongly
recommended.
Last, but not least, the treatment approaches to sexual disorders and
dysfunctions are continuously developing and the clinician should
incorporate the newest developments into his or her armamentarium.
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3. SEXUAL DYSFUNCTIONS
Sexual dysfunctions in the DSM classification system are divided into
sexual desire disorders (hypoactive sexual desire disorder and sexual
aversion disorder), sexual arousal disorders (female sexual arousal disor-
der and male erectile disorder), orgasmic disorders (female orgasmic
disorder, male orgasmic disorder, and premature ejaculation), sexual pain
disorders (dyspareunia and vaginismus), sexual dysfunction due to vari-
ous general medical conditions (e.g. diabetes mellitus), substance-induced
sexual dysfunction, and sexual dysfunction not otherwise specified. Hyper
sexuality is not classified as a sexual dysfunction in the current DSM
diagnostic system because it is not clearly conceptualized and defined.
However, the ICD classification includes the diagnosis of excessive sexual
drive, and hyper sexuality disorder is being considered for the next edition
of the DSM.
According to the DSM-IV classification, all primary sexual dysfunc-
tions have specific subtypes. These subtypes may be used to help to delin-
eate the nature of the onset, context of sexual dysfunction, and possible
etiology. The lifelong subtype indicates whether the sexual dysfunction
has been present since the onset of sexual functioning; the acquired
subtype indicates whether the dysfunction developed only after a period
of normal functioning. The situational and generalized subtypes indicate
whether the sexual dysfunction is or is not limited to certain types of
stimulation, situations, or partners (in some cases it may be appropriate to
mention whether the dysfunction occurs during masturbation). Finally, the
“due to psychological factors” subtype is used when psychological factors
are judged to have a major role in the onset and the severity, exacerbation,
or maintenance of the dysfunction and general medical conditions and
substances play no role in the etiology of dysfunction. The “due to
combined factors” subtype is used when both psychological factors and a
general medical condition or a substance have a role in the etiology but
the general medical condition or the substance’s contribution is not
sufficient to account for the dysfunction. If a general medical condition or
substance use is sufficient to account for the dysfunction, the diagnoses of
sexual dysfunction due to general medical condition or substance-induced
sexual dysfunction are used.
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422 R. Balon
All sexual dysfunctions discussed are diagnosed in the DSM classifica-

tion system using three essential diagnostic criteria (A, B, C). Criterion A
is specific for each dysfunction, while the other two criteria are basically
the same for all sexual dysfunctions: B. The disturbance causes marked
distress or interpersonal difficulty; and C. The dysfunction is not better
accounted for by another Axis I diagnosis (except for another sexual
dysfunction) and is not due exclusively to the direct physiological effect
of a substance (e.g. a drug of abuse, a medication) or a general medical
condition.
3.1. Sexual desire disorders

3.1.1. Hypoactive sexual desire disorder
The diagnosis of hypoactive sexual desire disorder (HSDD), especially in
women, has been a subject of controversy. Some experts are proposing a
new diagnosis for DSM-5 by merging the desire and arousal diagnosis
into one entity — sexual interest arousal disorder.
Essential diagnostic features of HSDD are persistently or recurrently
deficient (or absent) sexual fantasies and desire for sexual activity. The
judgment of deficiency or absence is made by the clinician, taking into
account factors that affect sexual functioning, such as age and the context
of the person’s life. In addition, the above-mentioned criteria B and C
have to be met.
The differential diagnosis of low sexual desire includes numerous
mental disorders (e.g. mood disorders, anxiety disorders, schizophrenia,
other sexual disorders, and pain disorder); physical illnesses (e.g. hypog-
onadism, hypothyroidism); use of substances of abuse (e.g. alcohol,
opiates); use of various medications (e.g. antipsychotics, some antidepres-
sants); and interpersonal/relationship problems.
The lifelong subtype of HSDD may start in puberty but usually starts
in early adulthood. The course of HSDD (especially of the subtypes
other than lifelong) may be continuous or episodic, depending on various
psychosocial and relationship factors.
A thorough differential diagnosis is a prerequisite for the appropriate
management of HSDD. Subtyping of HSDD may serve as guidance for
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selecting treatment (e.g. the lifelong subtype would be approached

differently than an acquired one; similarly, generalized and situational
subtypes would require a different approach).
Hormonal therapy (e.g. testosterone), mostly in men, is indicated if
hypogonadism (low testosterone level) is detected. It is important to note
that normal physiological testosterone levels in men should be the
treatment target and that supraphysiological levels of testosterone are not
helpful. Administration of testosterone in postmenopausal women may
increase libido but is usually accompanied by side effects, and its
long-term effects are unknown.
Bupropion (an antidepressant) has been reported to improve sexual
desire in non-depressed females. No data for males are available.
Sex therapy (including sensate focus therapy) and modifications of
CBT are probably the most frequently used treatments in HSDD of
unknown etiology. Their efficacy is widely claimed yet not well tested.
3.1.2. Sexual aversion disorder

Sexual aversion disorder is a very rare entity. It may not be included in the
next version of the DSM. Essential diagnostic features of sexual aversion
disorder are persistent or recurrent extreme aversion to and avoidance of
all (or almost all) genital sexual contacts with a sexual partner. In addition,
the above-mentioned criteria B and C have to be met.
The differential diagnosis includes anxiety disorders (namely, panic
disorder and specific phobia), mood disorders, and other sexual disor-
ders (e.g. dyspareunia). The course of sexual aversion disorder is usu-
ally chronic. Treatment modalities found useful in sexual aversion
disorder include individual (psychodynamic) psychotherapy and in vivo
desensitization.
3.2. Sexual arousal disorders

A merge of HSDD and arousal disorder into one entity, that is, sexual
interest arousal disorder, is considered for the next edition of the DSM.
The lack of sexual desire and impaired arousal are intertwined on many
levels, especially in women.
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424 R. Balon
3.2.1. Female sexual arousal disorder

Essential diagnostic features of female sexual arousal disorder (FSAD)
are persistent or recurrent inability to attain, or to maintain until
completion of sexual activity, an adequate lubrication-swelling response
of sexual excitement. In addition, the above-mentioned criteria B and C
have to be met.
The differential diagnosis of FSAD includes other sexual dysfunctions,
various mental disorders (e.g. major depressive disorder, posttraumatic
stress disorder), substance-induced sexual dysfunction, somatic illness
(diabetes mellitus, atrophic vaginitis), and, in postmenopausal women,
hypogonadism.
The course of FSAD has not been studied. However, it is assumed that
many problems in sexually inexperienced women may improve over time
during a stable sexual relationship.
The treatment of FSAD should start by addressing some lifestyle
changes, if appropriate (e.g. smoking cessation, decrease of alcohol
intake, exercise) and psychoeducation. Psychological modalities include
sex therapy (sensate focus exercises), CBT, and masturbation exercises.
Numerous lubricants are commercially available to alleviate lack of lubri-
cation. Estrogen replacement, either locally (vaginal rings or creams) or
systemically (orally, transdermally) may be useful, especially in post-
menopausal women. Various pharmaceutical agents have been tried in the
treatment of FSAD (e.g. apomorphine, phentolamine, L-arginine, phos-
phodiesterase-5 inhibitors), but none of them has been found very effec-
tive in all patients. Phosphodiesterase-5 inhibitors may be helpful in some
subgroups of women with FSAD, such as FSAD associated with antide-
pressants. Finally, mechanical devices may be useful in addressing FSAD,
either vibrators or the EROS Clitoral Therapy Device,4 a small battery-
operated device applied to the clitoris (basically a vacuum pump).
3.2.2. Male erectile disorder

Essential diagnostic features of male erectile disorder (MED) are persis-
tent or recurrent inability to attain, or to maintain until completion of the
sexual activity, an adequate erection. In addition, the above-mentioned
criteria B and C have to be met.
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The differential diagnosis of MED includes various medical conditions

(e.g. diabetes mellitus, other endocrinopathies, atherosclerosis, trauma,
Peyronie’s disease), use of substances and medications (e.g. tricyclic
antidepressants or antipsychotics), some mental disorders (e.g. major
depressive disorder), and interpersonal/relationship problems.
The course of untreated acquired MED is usually chronic, especially in
cases of underlying physical illness. Some cases of psychogenic erections
(especially brief failures to achieve an erection due to performance
anxiety) may resolve spontaneously.
The treatment of MED should start by assessing and addressing
possible psychological issues related to the lack of erection (individual
and/or couples therapy) and introducing lifestyle changes (smoking cessa-
tion, substance abuse cessation, exercise, diet — e.g. Mediterranean, and
psychoeducation). Individual and sex therapy should address issues such
as earlier trauma, stress, premature ejaculation, and possible performance
therapy. Genital sensate-focus work could be also used.
Pharmacotherapy and surgical or mechanical approaches are the
mainstay of MED management. These approaches could be divided into
three lines of treatment. The first line, less invasive, includes oral medica-
tions, androgen replacement (in case of hypogonadism), and vacuum
erectile devices. The most frequently used oral erectogenic agents are
phosphidiesterase-5 inhibitor sildenafil (50–100 mg about an hour before
coitus; effect may last up to four hours), tadalafil (10–20 mg about an hour
before coitus; effect may last up to 36 hrs, and vardenafil (about half an
hour before coitus; effect may last about four hours). There is plenty of
evidence that these agents work in 60%–80% of MED of various etiolo-
gies. They all have similar mild side effects (headaches, flushing, blue-
tinged vision) and contraindications (concomitant use of nitrates; known
hypersensitivity to a particular phosphodiesterase-5 inhibitor). Several
other phosphodiesterase-5 inhibitors (udenafil, mirodenafil) are being
developed. Other oral agents such as apomorphine, phentolamine, and
yohimbine have been used in MED, but their efficacy and safety are either
not fully established or problematic, and they have not been approved as
widely as phosphodiesterase-5 inhibitors. Hormonal replacement —
testosterone — is most efficiently applied transdermally (gel, patches).
Vacuum erectile pumps (i.e. glass cylinder over the penis; air is pumped
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426 R. Balon
out, a rubber band laced at the base of the erected penis, and the tube
removed) are safe but cumbersome to use.
Second line treatments include intraurethral alprostadil and intracaver-
nosal injections of alprostadil and various other substances.
Third line treatment may also involve vacuum erectile devices but
usually means much more invasive approaches, such as penile prosthesis
and microvascular surgery of the penis.
3.3. Orgasmic disorders

3.3.1. Female orgasmic disorder
Essential diagnostic features of female orgasmic disorder (FOD) (also
inhibited female orgasm) are persistent or recurrent delay in, or absence
of, orgasm following a normal sexual excitement phase. Women exhibit
wide variability in the type or intensity of stimulation that triggers
orgasm. The diagnosis of FOD should be based on the clinician’s
judgment that the woman’s orgasmic capacity is less than would be rea-
sonable for her age, sexual experience, and the adequacy of sexual stimu-
lation she receives. In addition, the earlier mentioned criteria B and C
have to be met.
The differential diagnosis of acquired FOD includes the effect of
various medications (e.g. serotonergic antidepressants, antipsychotics),
general medical conditions (e.g. spinal cord injury), other sexual dysfunc-
tions, and interpersonal problems. The differential diagnosis of lifelong
FOD includes various psychological issues. Situational FOD suggests
psychological issues; generalized impairment may be suggestive of a
medical condition.
The course of FOD is usually chronic, although orgasmic capacity may
improve with increased sexual experience.
Psychotherapy, sex therapy, and CBT constitute the mainstay of FOD
management. Directed masturbation homework assignment may be used
too. There is no solid evidence of efficacy of any pharmacotherapy in
FOD, although some studies suggested the usefulness of sildenafil. FOD
associated with medications and substances responds best to the discon-
tinuation of the offending agent, or if not possible, various antidotes may
be applied.18
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3.3.2. Male orgasmic disorder

Essential diagnostic features of male orgasmic disorder (MOD) (also
Inhibited male orgasm) are persistent or recurrent delay in, or absence of,
orgasm following a normal sexual excitement phase during sexual activity
that the clinician, taking into account the person’s age, judges to be ade-
quate in focus, intensity, and duration. In addition, the above mentioned
The differential diagnosis includes medical conditions (e.g. multiple
sclerosis or diabetes mellitus), substances of abuse and medications, other
sexual dysfunctions, and some mental disorders. Subtyping may help in a
fashion similar fashion to FOD.
The course of MOD is unknown because this dysfunction is rare in
clinical settings and has not been well studied.
If an underlying etiology can be established, the treatment should focus
on dealing with the underlying illness. MOD is notoriously difficult to
treat; there is no effective pharmacological agent. Most clinicians would
use psychotherapy and sex therapy, although no evidence demonstrates
their efficacy.
3.3.3. Premature ejaculation

Essential diagnostic features of premature ejaculation (PE) (also rapid
ejaculation) are: persistent or recurrent ejaculation with minimal sexual
stimulation before, on, or shortly after penetration and before the person
wishes it. The clinician must take into account factors that affect duration
of the excitement phase, such as age, novelty of the sexual partner or situ-
ation, and frequency of sexual activity. Additionally, the disturbance
causes marked distress or interpersonal difficulty, and the premature
ejaculation is not due exclusively to the direct effect of a substance
(e.g. withdrawal from opioids).
The differential diagnosis of PE includes anxiety disorders, such as panic
disorder and social anxiety disorder; substance-induced PE; and relation-
ship-related problems. The course of untreated PE is chronic, lifelong.
Two main behavioral approaches to PE are the start-stop technique and
the squeeze technique. Both techniques require partner cooperation and
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428 R. Balon
are widely recommended, although the evidence of their efficacy from

controlled studies is weak.
Pharmacotherapy using serotonergic antidepressants is the most widely
used management approach to PE. Agents such as clomipramine, fluoxe-
tine, paroxetine, and sertraline could be used on a daily basis or on-demand
several hours before coitus. The doses are usually the same as or lower than
for the treatment of depression. The success rate of serotonergic antidepres-
sants in PE is high, up to 100%, and partners are usually also quite satisfied.
These agents are not approved in this indication by regulatory agencies.
Clinicians should be aware of potential risks of these agents and their side
effects and should discuss them with their patients up front. Topical
application of lidocaine or prilocaine to the penis may also be useful.
3.4. Sexual pain disorders

Some experts advocate moving sexual pain disorders to the group of
somatoform/pain disorders, but at the present time these disorders are still
classified as sexual pain disorders.
3.4.1. Dyspareunia (not due to general medical condition)

Essential diagnostic features of dyspareunia are recurrent or persistent
genital pain associated with genital intercourse in either a male or a
female. In addition, the above mentioned criteria B and C have to be met.
Dyspareunia may include syndromes such as vulvar vestibulitis
syndrome, vulvodynia, or postmenopausal dyspareunia.14
The differential diagnosis of dyspareunia could be complicated. The
clinician should focus on a possible organic, treatable underlying
condition (e.g. sexual dysfunction due to a general medical condition).
Other sexual dysfunctions (e.g. vaginismus) and a substance-induced
sexual problem (e.g. painful orgasm due to some medications, such as
antipsychotics) should also be ruled out.
The course of dyspareunia is not well known and is usually considered
chronic and unremitting.
The treatment of vulvar vestibulitis syndrome may include medical
interventions progressing from conservative, non-invasive ones to more
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invasives ones, such as sitz baths, topical lidocaine or corticosteroids,

systemic corticosteroids, antifungals, injected interferon, and biofeed-
back. Antidepressants (amitriptyline, duloxetine) may be helpful if
comorbid depression is present. The CBTs, including cognitive behav-
ioural pain management, sex therapy, and pelvic floor biofeedback, have
been frequently used. Some advocate using alternative methods such as
acupuncture and hypnotherapy. There is little information about the treat-
ment of vulvodynia, but a multidisciplinary approach, including psycho-
therapy, pelvic floor muscle rehabilitation, and possibly amitriptyline for
pain has been suggested.
3.4.2. Vaginismus (not due to general medical condition)

Essential diagnostic features of vaginismus are recurrent or persistent
involuntary spasm of the musculature of the outer third of the vagina that
interferes with sexual intercourse. In addition, the above-mentioned
The differential diagnosis includes pain during coitus for various physi-
cal/medication/substance reasons and sexual dysfunction due to general
medical condition.
The course is unknown. Spontaneous remission in long-term sexual
relationship is possible.
Behavioral therapy intervention is the preferred approach for treatment.
Various elements include systemic desensitization (also using benzodiaz-
epines), relaxation training, inserting fingers or dilators of gradually
increasing size into the vagina, gradual involvement of the partner, and
finally engaging in coitus.
3.5. Other categories

3.5.1. Sexual dysfunction due to general medical condition
For sexual dysfunction due to general medical condition (specific con-
dition should be indicated), diagnostic criteria are clinically signifi-
cant sexual dysfunction (any of the above) that results in marked
distress or interpersonal difficulty predominates in the clinical picture.
There is evidence from the history, physical examination, or laboratory
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430 R. Balon
findings that the sexual dysfunction is fully explained by the direct

physiological effects of a general medical condition. The disturbance
is not better accounted for by another mental disorder (e.g. major
depression).
The management should include treatment of the underlying medical
condition and, if treatment of this condition not possible or sexual dys-
function remains, treatment according to approaches described above.
3.5.2. Substance-induced sexual dysfunction

The diagnostic criteria for substance-induced sexual dysfunction are
clinically significant sexual dysfunction (any of the above) that results in
marked distress or interpersonal difficulty predominates in the clinical
picture (criterion A). There is evidence from the history, physical exami-
nation, or laboratory findings that the sexual dysfunction is fully explained
by substance use as manifested by either (1) the symptoms in criterion
A developed during, or within a month of, substance intoxication or (2)
medication use is etiologically related to the disturbance (criterion B). The
disturbance is not better accounted for by a sexual dysfunction that is not
substance induced (criterion C).
Management should include discontinuation of the offending substance
and treatment of substance abuse. If cessation/treatment is not possible,
the sexual dysfunction should be approached as mentioned above.
3.5.3. Sexual dysfunction not otherwise specified

As noted in DSM IV, the category sexual dysfunction not otherwise speci-
fied includes sexual dysfunctions that do not meet the criteria for any
specific sexual dysfunction discussed previously, such as no subjective
erotic feelings, despite otherwise normal arousal and orgasm, or when
dysfunction is present but the clinician cannot determine whether it is
primary or due to a general medical condition or a substance.
The treatment of sexual dysfunction not otherwise specified is basically
an uncharted territory. Psychotherapy or sex therapy should probably be
used, and at times, no treatment may be necessary.
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4. PARAPHILIAS
The diagnostic criteria of paraphilias are descriptive and also a bit vague
and arbitrary. The reliability of the diagnostic criteria is not well studied
and thus is unknown. There are three basic types of paraphilias: those
involving non-human objects, those involving suffering of oneself or
one’s partner, and those involving children or other non-consenting per-
sons. One should realize that there are cultural aspects of paraphilias and
that there are cultural underpinnings of the efforts to define normal and
abnormal sexual behavior. The concept of what is and what is not accept-
able sexual behavior has also been changing through history. Paraphilias
are difficult to study because they are rare and socially not acceptable
(thus help is rarely sought).
The differential diagnosis of paraphilias includes other paraphilias;
non-pathological use of sexual fantasies, behaviors, or objects as a stimu-
lus for sexual excitement;2 mental retardation; dementia; personality
changes due to a general medical condition; substance abuse; manic
episode; and schizophrenia.
The course of paraphilias is usually chronic. Some fantasies and
behaviors may begin in childhood or adolescence and some may diminish
with advancing age. Paraphilic behavior may increase in response to
stress.2 Some paraphilias are relatively harmless (fetishism), and some
have serious consequences (pedophilia).
Newer issues, not fully addressed by psychiatry and medicine, include
online sexual offending (especially the child pornography trade) and
increase of sexual deviances in females. This section will review the
diagnostic criteria of individual paraphilias. The treatment of all para-
philias will be discussed together, because there are many similarities in
treatment recommendations (and scarce evidence).
4.1. Diagnostic criteria of individual paraphilias

All paraphilias include the following criterion B: the fantasies, sexual
urges, or behaviors cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.2
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432 R. Balon
4.1.1. Exhibitionism
Essential diagnostic criteria of exhibitionism are, over a period of at least
six months, recurrent, intense, sexually arousing fantasies, sexual urges,
or behaviors involving the exposure of one’s genitals to an unsuspecting
stranger. Exhibitionism should be distinguished from public urination and
nudism.
4.1.2. Fetishism
Essential diagnostic criteria of fetishism are, over a period of at least six
months, recurrent, intense, sexually arousing fantasies, sexual urges, or
behaviors involving the use of non-living objects (e.g. female undergar-
ments). The fetish objects are not limited to articles of female clothing
used in cross-dressing (as in Transvestic Fetishism) or devices designed
for the purpose of tactile genital stimulation (e.g. vibrator); however,
fetishism is usually ego syntonic and rarely causes distress (in contrast to
the DSM diagnostic criteria).
4.1.3. Frotteurism
Essential diagnostic criteria of frotteurism are, over a period of at least six
months, recurrent, intense sexually arousing fantasies, sexual urges, or
behaviors involving touching and rubbing against a non-consenting person.
4.1.4. Pedophilia
Essential diagnostic criteria of pedophilia are, over a period of at least six
months, recurrent, intense sexually arousing fantasies, sexual urges, or
behaviors involving sexual activity with a prepubescent child or children
(generally age 13 or younger). The person also is at least age 16 years and
at least five years older than the child or children. (Individuals in late
adolescence involved in an on-going sexual relationship with a 12- or
13-year-old should not be included).
The diagnostic description of pedophilia should also specify whether
the individual is sexually attracted to males, females or both; whether the
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sexual relationship is limited to incest; and whether this is the exclusive

type (attracted only to children) or non-exclusive type of pedophilia.
4.1.5. Sexual masochism

Essential diagnostic criteria of sexual masochism are, over a period of at
least six months, recurrent, intense, sexually arousing fantasies, sexual
urges, or behaviors involving the act (real, not simulated) of being humili-
ated, beaten, bound, or otherwise made to suffer.
4.1.6. Sexual sadism

Essential diagnostic criteria of sexual sadism are, over a period of at least
six months, recurrent, intense sexually arousing fantasies, sexual urges, or
behaviors involving acts (real, not simulated) in which the psychological
or physical suffering (including humiliation) of the victim is sexually
exciting to the person.
4.1.7. Transvestic fetishism

Essential diagnostic criteria of transvestic fetishism are, over a period of
at least six months, recurrent, intense, sexually arousing fantasies, sexual
urges, or behaviors involving cross-dressing. It should be specified
whether transvestic fetishism is associated with gender dysphoria (i.e. if
the person has persistent discomfort with gender role or identity).
4.1.8. Voyeurism
The essential diagnostic criteria of voyerism are, over a period of at least
six months, recurrent, intense, sexually arousing fantasies, sexual urges,
or behaviors involving the act of observing an unsuspecting person who is
naked, in the process of disrobing, or engaging in sexual activity.
4.1.9. Paraphilias not otherwise specified

The category paraphilias not otherwise specified includes other paraphilic
sexual behaviors that do not meet any of the discussed criteria. This category
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434 R. Balon
includes, for instance, coprophilia (feces), klismaphilia (enemas), necro-

philia (corpses), partialism (exclusive focus on part of the body), tele-
phone scatophilia (obscene phone calls), urophilia (urine), and zoophilia
(animals).
4.2. Treatment of paraphilias

Treatment of paraphilias is a complicated and difficult affair. Most of the
time, treatment should be started with various forms of psychotherapy or
combinations of psychotherapeutic modalities and pharmacotherapy. The
treatment is usually forced by law enforcement agencies. The data on
treatment efficacy are not very good. There is no evidence as to whether
pharmacotherapy or psychotherapy works better than the other. The treat-
ment should progress form modalities associated with fewer side effects
and complications, such as CBT and relapse prevention and later antide-
pressants, to treatments with a higher risk of complications, such as anti-
androgens and other hormones. Osborne and Wise15 state that paraphilias
are mostly chronic, incurable, but highly manageable.
Psychotherapies used in the treatment of paraphilias include individual
psychodynamic psychotherapy, CBT, psychoeducation, covert sensitiza-
tion and imaginal desensitization (in pedophilia), and occasionally marital
therapy in case of marital discord. Most reports on the usefulness of vari-
ous psychotherapy modalities are based on individual cases, because stud-
ies of psychotherapy efficacy in paraphilias would be extremely difficult
to conduct. As Osborne and Wise15 point out, “Psychotherapy is essential
to foster compliance with medication, ameliorate attitudinal problems,
and to develop cognitive skills in resisting and managing paraphilic fanta-
sies and urges.” Cognitive behavioral strategies are used in modifying
paraphilic sexual arousal and relapse prevention.
Pharmacotherapy of paraphilias includes treatment with selective
serotonin reuptake inhibitors (SSRIs) and clomipramine, treatment with
hormonal preparations (mostly anti-androgens), treatment with antipsy-
chotics, treatment with mood stabilizers, and, occasionally, treatment with
other psychotropic medications, such as buspirone. It is important to note
that these medications are not approved for treatment of paraphilias by
any regulatory agency. The use of SSRIs and clomipramine in paraphilias
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is based on certain phenomenological similarities between paraphilias and

obsessive-compulsive disorder and between paraphilias and impulse con-
trol disorder. However, the side effects of antidepressants, such as
decreased libido and delayed orgasm/anorgasmia, may also contribute to
the usefulness of these medications in paraphilias. Various SSRIs and
other antidepressants were found useful in paraphilias in various small
scale studies. The doses of antidepressants are usually relatively high (e.g.
up to 80 mg of fluoxetine, up to 250 mg of sertraline, up to 400 mg of
clomipramine). The use of hormones in paraphilias is based on an
assumption that the reduction of sex drive will also reduce paraphilic
behavior and that this could be achieved by decreasing or blocking andro-
gens. Because estrogens have quite unpleasant side effects, anti-androgens
are usually used. These include medroxyprogesterone acetate and cypro-
terone acetate. Other hormonal preparations, such as luteinizing hormone-
releasing hormone agonist (leuprolide acetate) and pure anti-androgen
(flutamide) have also been used. The use of hormonal preparations in
paraphilias should be reserved for facilities specializing in the treatment
of these disorders. Various antipsychotics (e.g. fluphenazine and fluphen-
azine decanoate) have been used in the past, because they reduce the sex
drive, performance, and sexual fantasies. However, their use has been
restricted lately due to their side effects. Lithium, buspirone, and other
agents have been occasionally reported as effective.
Surgical castration and stereotactic surgery have been used in cases of
repeated sexual offenders (pedophilia, sexual sadism) outside of the
United States.
The treatment of paraphilias should be multidisciplinary, and if medi-
cations are used, they should always be combined with various forms of
psychotherapeutic intervention.
5. GENDER INDENTITY DISORDERS

Gender identity disorders are very rare. Some suggest that they should not
be included in the next edition of the DSM. The onset of cross-gender
interest and activities is usually between ages two and four years2;
however, only a small number of children with gender identity disorder
(GID) will continue to have symptoms of this disorder into adolescence
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436 R. Balon
and adulthood.2 The course of GID in those who continue to have

symptoms into adulthood is usually chronic and may be fluctuating.
The differential diagnosis of GID includes nonconformity to stereo-
typical sex role behavior, transvestic fetishism, concurrent congenital
intersex conditions, and schizophrenia.
5.1. Gender identity disorder

Essential DSM diagnostic criteria of GID are a strong and persistent
cross-gender identification (not merely a desire for any perceived cultural
advantages of being the other sex).
In children, the disturbance is manifested by four (or more) of the
following:
(1) Repeated stated desire to be, or insistence that he or she is, the other
sex.
(2) In boys, preference for cross-dressing or stimulating female attire; in
girls, insistence on wearing only stereotypical masculine clothing.
(3) Strong and persistent preference for cross-sex roles in make-believe
play or persistent fantasies of being the other sex.
(4) Intense desire to participate in the stereotypical games and pastimes
of the other sex.
(5) Strong preference for playmates of the other sex.
In adolescents and adults, the disturbance is manifested by symptoms

such as a stated desire to be the other sex, frequent passing as the other
sex, desire to live or be treated as the other sex, or the conviction that one
has the typical feelings and reactions of the other sex.
Diagnostic criteria further include persistent discomfort with one’s
sex or sense of inappropriateness in the gender role of that sex. In chil-
dren, examples include a boy’s disgust with his penis or a girl’s asser-
tion that she does not want to grow breasts or menstruate. In adolescents
and adults, the disturbance is manifested by symptoms such as preoc-
cupation with getting rid of primary and secondary sex characteristics
(e.g. requesting hormones, surgery) or belief that one was born the
wrong sex.
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The disturbance is not concurrent with a physical intersex condition,

and the disturbance causes clinically significant distress or impairment in
social, occupational, nor other important areas of functioning.
It should be specified whether the GID is in children or in adolescents
or adults and (for sexually mature individuals) whether one is sexually
attracted to males, females, both, or neither.
5.2. GID not otherwise specified

The category GID not otherwise specified is for gender identity disorders
that are not classified as specific. Examples, according to DSM IV,2
include:
(1) Intersex conditions (e.g. androgen insensitivity) and accompanying

gender dysphoria.
(2) Transient, stress-related cross-dressing behavior.
(3) Persistent preoccupation with castration or penectomy without a
desire to acquire the sex characteristics of the other sex.
5.3. Sexual disorder not otherwise specified

The category sexual disorder not otherwise specified includes sexual
disturbances not meeting the criteria for any specific sexual disorder that
are neither a sexual dysfunction nor paraphilia. Examples include marked
feelings of inadequacy concerning sexual performance; distress about a
pattern of repeated sexual relationships involving a succession of lovers
who are experienced by the individual only as things to be used; or
persistent or marked distress about sexual orientation.
5.4. Treatment of GIDs

The treatment of GID should be conducted by specialists in the treatment
of these disorders or at special facilities. The treatment includes various
forms of therapy (CBT, individual psychotherapy) and may end by
sex-reassignment surgery. Psychotherapy for the parents of a child or
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438 R. Balon
adolescent with GID should be part of the management plan. Psychotherapy

should address the underlying psychopathology and accompanying
distress and should also address coping skills with the social ostracism
that individuals with GID frequently face.
6. CONCLUSION
Sexual disorders are unique in being at the intersection of many
disciplines — psychiatry, psychology, biology, sexology, urology, obstet-
rics, gynecology, and others. Unfortunately, sexual disorders, especially
paraphilias, have not been well studied. Sexual functioning can be pro-
foundly influenced by various biological, psychological, interpersonal,
cultural, religious, and other factors. The diagnostic classification of sex-
ual disorders is undergoing important changes. The etiology of sexual
disorders is mostly unknown. There have been tremendous developments
in the pharmacological management of some sexual disorders, such as
male erectile disorder, premature ejaculation, and paraphilias. Good clini-
cal management of sexual disorders requires a multidisciplinary approach,
usually combining pharmacotherapy and psychotherapy and, at times,
other management approaches.
7. KEY POINTS
• Sexual dysfunctions are fairly frequent in the general population.
Their incidence increases with age and with comorbid mental and/or
physical illness.
• Sexual dysfunctions are associated with the use of various medica-
tions such as antidepressants, antipsychotics, and antihypertensives
and also with some substances of abuse.
• There have been important developments in the area of “sexual phar-
macology” — efficacious medications are available for male erectile
disorder and for premature ejaculation.
• Sexual desire impairment may be amenable to administration of
bupropion or, in the case of hypogonadism, testosterone.
• There are no efficacious medications available for orgasmic disorders
and sexual pain disorders.
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• Treatment of sexual dysfunctions should be multidisciplinary, com-

bining sex therapy, various psychotherapies (namely, CBT) and, when
indicated, medications.
• Paraphilias are rare and difficult to treat.
• Paraphilias may be amenable to medications such as serotonergic anti-
depressants, some hormones (anti-androgens), and antipsychotics.
• Gender identity disorders are very difficult to treat and should be
referred to facilities specializing in their treatment.
8. SELF-ASSESSMENT
8.1. Which of the following sexual disorders is not classified as
paraphilia?
(A) Exhibitionism.
(B) Fetishism.
(C) Vaginismus.
(D) Voyeurism.
Vaginismus is classified in both the DSM and ICD systems as sexual

dysfunction, not as paraphilia.
Answer: C
8.2. Bupropion may be useful in the treatment of which of the

following sexual disorders?
(A) Exhibitionism.
(B) Female hypoactive sexual desire disorder.
(C) Gender identity disorder.
(D) Masochism.
(E) Premature ejaculation.
Two small studies (e.g. Segraves et al.19) suggest the usefulness of bupro-
pion in female hypoactive sexual desire disorder. There are no solid phar-
macotherapy studies of exhibitionism, masochism, and gender identity
disorder. Treatment of premature ejaculation may include some SSRIs
(e.g. fluoxetine, paroxetine, sertraline)
Answer: B
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440 R. Balon
9. CASE STUDIES
9.1. Female hypoactive sexual desire disorder
A 40-year-old woman was evaluated for chronic depression, social with-
drawal, and lack of energy. She reported some difficulties in social situa-
tions and low interest in pleasurable activities, including sex. She was
started on citalopram 20 mg/day. At her return visit three weeks later, she
reported improved mood; however, she complained that she had a com-
plete lack of sexual desire and that it took her “forever, if at all” to reach
orgasm. Because citalopram was suspected as the agent causing the lack
of libido and delayed orgasm, it was discontinued, and she was started on
bupropion 150 mg/day. About a month later, she reported improved mood
and energy and also increased libido. Her orgasmic capacity returned to
her usual level.
9.2. Difficulty to ejaculate

A 65-year-old man reported a gradual onset of sexual difficulties. His main
complaint was the difficulty to ejaculate. He stated that at times he was able
to ejaculate only during “endless” masturbation. Detailed questioning
revealed that he had gained some weight lately and had undergone minor
prostatic surgery. Subsequently, his erections have become “softer.” He was
started on sildenafil 100 mg an hour before intercourse and was advised to
start to exercise daily. At his follow-up visit, he reported an improved qual-
ity of erection and occasional ejaculation as he “used to have before.”
9.3. Exhibitionism
A 25-year-old man was arrested by the police and referred for treatment.
After ordering food, he drove to a restaurant’s drive-through window, and
when the female employee was handing him his order, he opened his coat
and flashed his naked body and genitals at her. When she started to
scream, he quickly drove away. However, the woman was able to catch his
license plate number in the mirror at the drive-through window and called
the police, who arrested him within minutes. During his evaluation, he
admitted flashing his genitals at several unsuspecting women with
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subsequent masturbation. He stated that he had not been able to date and
that he had been a bit depressed over it. He responded well to individual
therapy and paroxetine.
REFERENCES
1. Abel GG, Huffman J, Warberg B, Holland CL. (1998) Visual reaction time
and plethysmography as measures of sexual interest in child molesters. Sex
Abuse 10: 81–95.
D.C.
3. Balon R. (2007) Sexual dysfunctions. In: Gabbard GO (ed.), Gabbard’s
Treatment of Psychiatric Disorders, 4th ed. Chapter 42, pp. 641–655,
American Psychiatric Publishing, Inc., Arlington, VA.
4. Billups KL, Berman J, Berman L, Metz ME, Glennon ME, Goldstein I.
(2001) A new nonpharmacological vacuum therapy for female sexual
dysfunction. J Sex Marital Ther 27: 435–441.
5. Clayton AH, McGravey EL, Clavet GJ, Piazza L. (1997) Comparison of
sexual functioning in clinical and nonclinical populations using the Changes
of Sexual Functioning Questionnaire (CSFQ). Psychopharmacol Bull 33:
747–753.
6. Derogatis LR, Balon R. (2009) Clinical evaluation of sexual dysfunctions.
In: Balon R, Segraves RT (eds.), Clinical Manual of Sexual Disorders,
Chapter 2, pp. 23–57, American Psychiatric Publishing, Inc., Arlington, VA.
7. Derogatis LR. (1997) The Derogatis interview for sexual functioning (DISF/
DISF-SR): An introductory report. J Sex Marital Ther 23: 291–304.
8. Fagan PJ. (2004) Sexual Disorders: Perspectives on Diagnosis and Treatment.
Johns Hopkins University Press, Baltimore, MD.
9. Freund K, Blanchard R. (1986) The concept of courtship theory. J Sex
Marital Ther 12: 79–92.
10. Laumann EO, Nicolosi A, Glasser DB, Paik A, Gingell C, Moreira E,
Want T, for the GSSAB Investigators’ Group. (2005) Sexual problems among
women and men aged 40–80y: Prevalence and correlates identified in the
global study of sexual attitudes and behaviors. Int J Impot Res 17: 39–57.
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11. Laumann EO, Paik A, Rosen RC. (1999) Sexual dysfunction in the United
States. Prevalence and predictors. JAMA 281: 537–544.
12. Masters WH, Johnson V. (1966) Human Sexual Response, Little Brown,
Boston, MA.
13. McGahuey CA, Gelenberg AJ, Laukes CA, Moreno FA, Delgado PL,
McKnight KM, Manber R. (2000) The Arizona sexual experience scale
(ASEX): Reliability and validity. J Sex Marital Ther 26: 25–40.
14. Pukall CF, Payne KA, Kao A, Khalife S, Binik YM. (2005) Dyspareunia.
In: Balon R, Segraves RT (eds.), Handbook of Sexual Dysfunction, Chapter
1, pp. 249–272, Taylor & Francis, NY.
15. Osborne CS, Wise TN. (2005) Paraphilia. In: Balon R, Segraves RT (eds),
Handbook of Sexual Dysfunction, Chapter 12, pp. 293–330, Taylor &
Francis, NY.
16. Quirk FH, Heiman J, Rosen RC, Laan E, Smith MD, Boolell M. (2002)
Development of a sexual function questionnaire for clinical trials of female
sexual function. J Womens Health Gender Based Med 11: 277–285.
17. Rosen RC, Riley A, Wagner G, Osteloh IH, Kirkpatrick J, Mishra A. (1997)
The international index of erectile function (IIEF): A multidimensional scale
for assessment of sexual dysfunction. Urology 49: 822–830.
18. Segraves RT, Balon R. (2003) Sexual Pharmacology: Fast Facts, WW Norton,
NY.
19. Segraves RT, Clayton A, Croft H, Wolf A, Warnock J. (2004) Bupropion
sustained release for the treatment of hypoactive sexual desire disorder in
premenopausal women. J Clin Psychopharmacol 24: 339–342.
20. World Health Organization. (1992) The ICD-10 Classification of Mental and
Behavioural Disorders: Clinical Description and Diagnostic Guidelines.
World Health Organization, Geneva.
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Chapter 18
Adjustment Disorder
Mauro Giovanni Carta, Maria Carolina Hardoy

and Matteo Balestrieri
1. INTRODUCTION
Stressful life events, even if brief, may influence one’s health. These
events may even lead to psychopathological alterations. ICD-10 classifi-
cation divides disorders that are strongly related to stressful life events
into two main categories: post-traumatic stress disorder (PTSD) and
adjustment disorder. The former comes as a consequence of life-events
such as life-threatening menaces, injury menaces, or great physical or
psychological distress. The latter are conditions of subjective and emo-
tional distress triggered as consequences of a meaningful change in life.
2. EPIDEMIOLOGY
2.1. Prevalence
The only large epidemiological survey which included adjustment disor-
der is the Outcome of Depression International Network (ODIN) pro-
ject,11 which investigated depressive disorders in five European countries.
By using a two-step screening method, researchers quite surprisingly
diagnosed adjustment disorder in less than 1% of population affected by
a depressive-like disorder. The low prevalence of adjustment disorder
may be due to the exclusion of patients with adjustment disorder as a
443
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444 M. G. Carta, M. C. Hardoy and M. Balestrieri
consequence of too high cut-off scores used to identify depression with

the rating scale. Moreover, the reliability and accuracy of the diagnostic
tools are unknown, because they were not tested against a golden standard
instrument for diagnosis of adjustment disorder.
Adjustment disorder is a problem among military personnel. Solders
showed a diagnosis of adjustment disorder in 37.6% and other diagnoses
in 22.1% of cases during the first six months in the theatre of the recent
Operation Enduring Freedom and Operation Iraqi Freedom.26 Among vet-
erans, the low accuracy in the diagnosis of adjustment disorder, together
with the frequent presence of more serious mental health problems, can
explain why other diagnoses — such as PTSD, substance abuse, pain, and
chronic fatigue syndrome — are more frequently reported.
A consensus exists that adjustment disorder is most typically seen in
primary care settings and frequently used in liaison psychiatry, where it is
purported to have an estimated incidence of 5%–21% in psychiatric con-
sultation services for adults.
Still, in the hospital setting there also is a paucity of data. Probably the
main factor is the advent of easily managed antidepressants that render
psychiatrists more prone to use the Major Depression Disorder (MDD)
diagnosis and treat adjustment disorder as such. In fact, an observational
study of referrals to consultation-liaison psychiatric units conducted in the
United States over the course of 10 years found that from 1988 to 1997
the percentage of diagnosis of MDD in patients with concomitant medical
illness increased from 6.4% to 14.7%, while in the same period the
diagnosis of adjustment disorder with depressed mood decreased from
28% to 14.7%.10
When considering particularly stressing situations, like patients with a
painful serious illness or an illness with serious impairment, other inves-
tigators report similar proportions6: in children with chronic renal failure
or end-stage renal disease on hemodialysis, adjustment disorder is the
most common diagnosis (18.4%), with a higher prevalence in dialysis
patients than in predialysis patients; in breast cancer patients adjustment
disorder is also the most common diagnosis (7.1%), followed by general
anxiety disorder (6.3%), and MDD (4.7%).
The concern has also been expressed that in the context of the emo-
tional response of cancer the diagnosis of adjustment disorder risks to
be inappropriate, because of the difficulty to define the level of what
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Adjustment Disorder 445
represents an “excessive” response. Consequently, it would be better to

consider a sub-threshold depression or a full or partial presentation of
PTSD. In fact, according to the review of Ronson25 an average of 10% of
cancer patients has been shown to meet criteria for PTSD.
Notwithstanding these assertions, the diagnosis continues to be used in
consultation-liaison psychiatry. Proportions of adjustment disorder rang-
ing between about 10% and 20% have been found in the general hospital
population and among psychiatric consultations. Adjustment disorder
with depressed mood, anxious mood, or mixed emotions are the common-
est subcategories used, while in about one third of cases, this diagnosis is
assigned in comorbidity with other diagnoses, more frequently personality
disorders and organic mental disorders.
2.2. Outcome
In the definition of adjustment disorder, there is an expectation of a good
outcome after the removal of the precipitating stressor. Follow-up studies
of subjects with adjustment disorder showed that after five years only
13%–17% had a diagnosis of MDD and/or alcoholism, and 8% met the
criteria for antisocial personality disorder.1,3
By studying consecutive patients in a hospital emergency department
during the first six months after a serious accident, Kuhn et al.19 found an
incidence of adjustment disorder of 1.5%. Six months after the accident,
10% of the subjects met criteria for MDD, 6% for PTSD, 4% for subsyn-
dromal PTSD, and 1.5% for specific phobia.
Greenberg et al.16 studied the outcome of inpatients who were given a
diagnosis of adjustment disorder at admission in hospitals. Adolescents
and adults with adjustment disorder had a significantly shorter index of
hospitalizations and more suicidality than the comparison subjects. Two
years after discharge, as compared with control subjects, adults — but not
adolescents — with adjustment disorder had significantly fewer psychiat-
ric re-admissions, fewer re-hospitalization days, and higher rates of
comorbid substance use disorder. A careful observation during hospitali-
zation caused about 40% of the patients admitted with the diagnosis of
adjustment disorder being discharged with different diagnoses. Only 18%
of the inpatients with adjustment disorder who were hospitalized were
diagnosed as such at re-admission.
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Although there is an increased risk of suicide and suicide attempts in

patients with adjustment disorder, the suicide ratio is lower than in other
Axis I disorders. The risk of suicide in adjustment disorder is about
2%–4%, even though psychological autopsy investigations state that the
diagnosis of adjustment disorder may be applied in about 25% of the cases
of adults and of male adolescent suicides. Suicide in adjustment disorder
is bound to alcohol abuse and is more frequently of impulsive than of
planned type. The suicidal process (from first indications of suicidal idea-
tion to completed suicide) is short and rapidly evolving, with few previous
indications of emotional or behavioral problems. This underlines the
importance of assessing suicide risk in patients with adjustment disorder.
Other factors precipitating a suicidal behavior in adjustment disorder are
the occurrence of a suicide of a significant other, a previous psychiatric
treatment, a poor psychosocial functioning, a dysphoric mood, and a psy-
chomotor restlessness. It has been also reported that in males with adjust-
ment disorder, suicidal behavior is associated with school-related stressors
and problems with the law, whereas in females, suicidal behavior is asso-
ciated with parental illness and internalized symptoms.22
3. ETIOLOGY
Stressors causing adjustment disorder may be of different types and
different weights. Individual reactions to stressors may be influenced
by individual variables (e.g. age, gender), health variables, factors
related to instruction, ethics, political and religious beliefs, and other
factors. Other variables may be found within the family environment:
the presence or absence of an affective support, the relational strength,
the economic status. It has been also reported that biological markers —
such as regional brain metabolic changes at 18-F-fluoro-deoxy-glucose
positron emission tomography (18-F-FDG PET) can identify sub-
jects with adjustment disorder, because they are present in cancer
patients who later develop MDD or adjustment disorder, while cancer
patients who do not show such changes do not develop psychiatric
disorders.20
Brown and Harris4 introduced the concept of subjectivity in stress
evaluation, which means that the same event (e.g. the death of a pet)
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may be traumatic for one person and not relevant for another person.
The research into personal predisposition to a depressive reaction to
stress and into attachment style during childhood suggests that these
factors may influence stress vulnerability. Mildly depressed individuals
who report a dismissing attachment style (higher levels of avoidant
attachment and lower levels of anxious attachment) or preoccupied style
(lower levels of avoidant attachment and higher levels of anxious attach-
ment) experience higher levels of stress associated with sociotropic
events. These effects are not present among more severely depressed
patients.
Troisi et al.28 reported alexithymic traits more pronounced in patients
with adjustment disorder who had patterns of insecure attachment and
who reported more severe symptoms of separation anxiety during
childhood, independently of the severity of their current anxiety and
depressive symptoms. These data imply a role for early developmental
factors in the etiology of alexithymia and suggest that alexithymia may
be associated with insecure attachment when adjustment disorder
occurs.
Another line of research regards the concept of sensitization. Some find-
ings show that in non-melancholic depressed patients, severe stressful life
events are more likely to occur before the first depressive episode rather
than after subsequent ones. This suggests an enhanced sensitization of
depressed patients to subsequent episodes of non-melancholic depression.
Finally, a few studies on military personnel showed that solders with
higher neuroticism, lower extroversion, separation anxiety symptoms,
maternal overprotection, and parental abuse style have an increased risk
of suffering from adjustment disorder.12,14
4. DIAGNOSIS
The main problems with the diagnosis of adjustment disorder are its insta-
bility and its vague boundaries with depression and PTSD from one side
and with normal reactions to stress from the other side.
In fact, clinicians run the risk to start unnecessary drug treatments
or, on the contrary, to consider the emotional response as an inevitable
consequence of the illness. To contrast this risk, clinicians should avoid
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disputing diagnostic labels, while, in the spirit of the biopsychosocial

model, they should be able to use in the same patient antidepressants for
anhedonia, psycho-educational or cognitive approaches to deal with mala-
daptive adjustment, and behavioral activation for poor motivation and
learned helplessness.
Adjustment disorder entered the DSM-II nomenclature in 1968 and
was recognized in ICD-9 in 1978. Before then, the term ‘transient situa-
tional disturbance’ was applied to such conditions. The addition of adjust-
ment disorder to the ICD classification was in response to the confusion
generated by the older concepts of reactive and endogenous depression
(Table 1). ICD-10 places adjustment disorder in a category of its own,
separate from acute stress reactions and defined as follows:
Table 1. Diagnostic criteria for adjustment disorder according with the WHO International
Classification of Diseases (ICD-10).
Chapter V. Mental and behavioral disorders (F00-F99)

Neurotic, stress-related, and somatoform disorders (F40-F48)
F43.2 Adjustment disorders
States of subjective distress and emotional disturbance, usually interfering with social
functioning and performance, arising in the period of adaptation to a significant life change
or a stressful life event. The stressor may have affected the integrity of an individual’s
social network (bereavement, separation experiences) or the wider system of social
supports and values (migration, refugee status), or represented a major developmental
transition or crisis (going to school, becoming a parent, failure to attain a cherished
personal goal, retirement).
Individual predisposition or vulnerability plays an important role in the risk of
occurrence and the shaping of the manifestations of adjustment disorders, but it is
nevertheless assumed that the condition would not have arisen without the stressor.
The manifestations vary and include depressed mood, anxiety or worry (or mixture of
these), a feeling of inability to cope, plan ahead, or continue in the present situation, as
well as some degree of disability in the performance of daily routine. Conduct disorders
may be an associated feature, particularly in adolescents. The predominant feature may be
a brief or prolonged depressive reaction, or a disturbance of other emotions and conduct.
Includes: –Culture shock
–Grief reaction
–Hospitalisation in children
Excludes:–Separation anxiety disorder of childhood (F93.0)
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• Occurring within one month of a psychosocial stressor that is not of

an unusual or catastrophic type.
• The duration of symptoms does not usually exceed six months except
for prolonged depressive reaction (in response to prolonged exposure
to a stressful situation); if the symptoms persist beyond this period,
the diagnosis should be changed according to the clinical picture
present.
• The symptoms or behavior disturbances are of a type found in any of
the affective disorders, but the criteria for an individual disorder are
not fulfilled.
• Symptoms vary in severity and form (see Table 2).
The World Health Organization (WHO) classification specifies that

predisposition or individual vulnerability plays a greater role in
Table 2. Predominant feature of the symptoms according to ICD-10 classification.
F43.20 Brief depressive reaction. A transient mild depressive state of a duration not
exceeding one month.
F43.21 Prolonged depressive reaction. A mild depressive state occurring in response to
a prolonged exposure to a stressful situation but of a duration not exceeding two
years.
F43.22 Mixed anxiety and depressive reaction. Both anxiety and depressive symptoms
are prominent, but at levels no greater than specified in mixed anxiety and
depressive disorder (F41.2) or other mixed anxiety disorders (F41.3).
F43.23 With predominant disturbance of other emotions. The symptoms are usually of
several types of emotion, such as anxiety, depression, worry, tensions, and anger.
Symptoms of anxiety and depression may meet the criteria for mixed anxiety and
depressive disorder (F41.2) or other mixed anxiety disorders (F41.3), but they are
not so predominant that other more specific depressive or anxiety disorders can
be diagnosed. This category should also be used for reactions in children in
which regressive behavior such as bedwetting or thumb-sucking are also present.
F43.24 With predominant disturbance of conduct. The main disturbance is one involving
conduct, e.g. an adolescent grief reaction resulting in aggressive or dissocial
behavior.
F43.25 With mixed disturbance of emotions and conduct. Both emotional symptoms and
disturbances of conduct are prominent features.
F43.28 With other specified predominant symptoms.
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conditioning the onset and symptoms of adjustment disorder than in other

disorders of the same cluster (Neurotic Syndromes, F43), and that the
disorder would not start without the stressor. This implies a sort of “stress
vulnerability syndrome,” even if it does not correspond to a diagnostic
group. Essentially, the core feature in the diagnosis of adjustment disorder
(using either WHO or APA criteria) is the presence of clinically significant
emotional or behavioral symptoms, often depressive in nature, that
develop after an identifiable stressor. The two main classifications differ in
terms of the severity of impairment: ICD-10 points to “usually interfering
with social functioning and performance” and “some degree of disability
in the performance of daily routines”, whereas DSM-IV points to “marked
distress that is in excess of what would be expected given the nature of the
stressor by significant impairment in social or occupational functioning.”
This type of diagnosis, in some ways, contradicts the principles that
have guided modern psychiatric classifications. The DSM and ICD
classifications were designed conceptually within an anti-theoretical
framework to encourage psychiatric diagnoses to be derived on phe-
nomenological grounds with an avowed dismissal of pathogenesis or
etiology as diagnostic imperatives. In direct contradiction to this anti-
theoretical approach, adjustment disorder and the stress-induced disor-
ders require the inclusion of an etiologic significance to a stressor and
the need to relate the stressor’s effect on the patient in clinical terms.
On a strictly descriptive level, the diagnostic features of the adjustment
disorder (specifically, (a) reaction to a significant stressor; (b) maladap-
tation to the stressor with dysfunction in social and work activities; (c)
disturbance in mood, anxiety and conduct) are not given quantifiable
criteria, and this omission may obfuscate reliability and validity. One of
the risks is to include among the symptoms of adjustment disorder a set
of ailments, perhaps “treatable with psychotherapy,” in contrast to those
“threshold-based diagnosis” disorders that, with their more rigid diag-
nostic criteria and their better-characterized patho-physiologic targets,
can be treated pharmacologically.
Indeed, this premise could well help to explain why the diagnosis of
adjustment disorder has been eclipsed by the focus on mood disorders
among researchers and policy makers. Nevertheless, these concepts bring
up some unresolved dilemmas. In the first place, the proportion to which
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affective disturbances are triggered by stressful events is unknown. Brief

recurrent depression is not postulated to have any triggering event, and
even for the major depressions or anxiety disorders it has never been
shown, nor even hypothesized, that a stressful event is always necessary
for disease occurrence or evolution.5
Even those works that have put forth and validated diagnosis criteria for
adjustment disorder have not resolved the questions, because patients with
adjustment disorder differ from those with no diagnosis and those with
mood disorders on a number of parameters, including differences in the
nature of the stressors, outcome, and quality of life. Furthermore, the pro-
posed criteria do not resolve if the parameters are merely related to the
severity of symptoms or if they are related to specific differences between
adjustment disorder and depressive or anxious disorders. For example, a
national survey carried out in Italy by Balestrieri et al.2 showed that
patients with major depressive disorders experienced more life events in
the last six months than patients with sub threshold mixed anxiety depres-
sion disorder.
There are two border disputes concerning the diagnosis of adjustment
disorder. One is the indistinct separation between the varied manifesta-
tions of adjustment disorder from normal adaptive reactions. Casey8 stated
that the conceptual problem lies in the following statement: “the border
between adjustment disorder and ordinary problems of life may be clari-
fied by the notion that adjustment disorder implies that the severity of the
disturbance is sufficient to justify clinical attention or treatment.” The
application of the diagnosis on the basis of not just objective criteria but
on search of a treatment opens up a deontological problem and points out
the limits of resolution in detecting psychiatric morbidity.
The second dispute is the problem of overlap with other disorders. Both
ICD-10 and DSM-IV attempt to overcome this problem by specifying that
if criteria for another disorder are met, then the diagnosis of adjustment
disorder should not be made; in essence, the diagnosis is one of default.
Given this, at the present, most diagnoses of adjustment disorder are
essentially descriptive; it is not known if there are clear neurological or
behavioral differences among patients in the course of developing, say
MDD, from those who suffer from adjustment disorder. Overall, the most
that we can say of the current situation is that the efforts to identify
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hallmark differences between adjustment disorder and more serious disor-

ders have not yielded certain results.
Casey et al.,7 working on the ODIN study database, failed to identify
any variables, even robust ones, such as BDI severity, that independently
differentiated adjustment disorder from depressive episode. Adjustment
disorder may consist of either mild symptoms for a prolonged period or
severe symptoms for a short period. In either case, the condition needs
careful evaluation and intervention as required.
At the moment, biological data do not differentiate adjustment disor-
der from major depressive disorder: Kumano et al.,20 as mentioned
before, found that cancer patients who later developed major depressive
disorder or adjustment disorder showed regional brain metabolic
changes. Although this study is interesting, it does not allow the distinc-
tion between those disorders. Furthermore, it does not permit an accurate
prognosis between episodes that are self-limiting and those that are not
and, therefore, require specific intervention.
Given this unclear situation, it is no surprise that the most common
diagnostic tools may substantially be divided between those which pay no
attention and those which pay little attention to adjustment disorder.
Many studies use as the gold standard a diagnosis derived from clinical
structured or semi-structured interview using tools like SCID, or the
Clinical Interview Schedule-Revised (CIS-R), which was used in the
British National Psychiatric Morbidity Survey, or the Composite
International Diagnostic Interview (CIDI), which was used in the US
National Comorbidity Study. All these instruments failed to incorporate
adjustment disorder in their assessments. Casey8 noted that in Schedules
for Clinical Assessment in Neuropsychiatry (SCAN), the disposal of the
adjustment disorder items at the end of the interview, after all other sec-
tions have been completed, sends a clear message that this section is not
as important as others. The effects of this on the diagnosis of adjustment
disorder in epidemiological studies would be an underestimation.
Kirsh et al.,17 in a survey about the prevalence of adjustment disorder
in a population of cancer patients, asserted that there is little accuracy in
using existing scales for detecting adjustment disorder in cancer patients
undergoing bone marrow transplantation and that other tools for identify-
ing patients with adjustment disorder who might benefit from counseling
are needed. Later, the same author tried to assess the diagnosis of
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adjustment disorder by the use of a new tool, the CFlex (Coping Flexibility
Scale for Cancer), but he could not succeed in developing a specific scale.
This may be because of problems with the scale or for the heterogeneous
nature of the adjustment disorder category.
The difficulties in differentiating between adjustment disorder and
major depressive disorder were underscored by Malt et al.,21 who
examined the diagnostic reliability among the components of the
European Consultation Liaison Workgroup. The study design required
that each consultant had to complete a training program for reliable use of
the ICD-10. Even if 76% of consultants reached a high reliability rate
(kappa of at least 0.70), the study underlined some problems in the
differentiation between adjustment disorder and depressive disorders.
5. TREATMENTS
The fact that episodes of adjustment disorder are short-lived and that
patients recover with the passage of time may explain the paucity of stud-
ies, especially randomized controlled trials, on the therapy of these disor-
ders. This no longer justifies the idea that no specific intervention is
required unless the individual is acutely suicidal.
It is a shared opinion that currently psychotherapy remains the treat-
ment of choice for adjustment disorder, while we lack major pharmaco-
therapy studies to support antidepressant treatment.9 Unfortunately,
psychotherapy is not always viable, because adjustment disorder is often
diagnosed in the primary care setting. Moreover, the problem of which
psychotherapy may be useful in adjustment disorder cannot find a certain
answer. The clinical characteristics of adjustment disorder (a short-term
difficulty, related to a stressor, that rarely goes beyond six months) suggest
a solution-focused therapy, like interpersonal psychotherapy (IPT) or
problem solving therapy, that helps the individual to deal more effectively
with the specific life problem. A study on adolescents with major depres-
sion or other depressive disorders (among them adjustment disorder)
showed that psychosocial functioning improved in all subjects, whether
their treatment involved only psychotherapeutic treatments or additional
psychotropic medication.23
Unfortunately, data on efficacy of brief psychotherapies in adjustment
disorder are scarce.6 IPT was found to be effective in HIV-positive
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inpatients with depressive symptoms. Also, autogenic training showed to

be helpful in decreasing the levels of physiological indicators of adjust-
ment disorder (blood pressure, pulse rate, concentration of cholesterol and
cortisol) and in diminishing the effects of stress, thus helping patients to
cope with stress. Among other psychotherapies, “ego-enhancing therapy”
was proposed for the treatment of adjustment disorder in the elderly, with
the aim of promoting coping strategy and helping patients to acknowledge
the stressors.
A study by Gonzales-Jaimes and Turnbull-Plaza15 compared three
different treatments (Gestalt psychotherapy, medical conversation, and
a control group without emotional support) for the treatment of adjust-
ment disorder in patients with acute myocardial infarction. They found
that patients not receiving emotional support treatment in conjunction
with medical treatment continued to experience emotional disorders
and showed greater apprehension with regard to medical treatments.
The only randomized control trial that evaluated the efficacy of
psychotherapy in adjustment disorder was the study of van der Klink
et al.18 that compared the “activating intervention” with “care as usual”
(control group) for the guidance of employees on sickness leave
because of an adjustment disorder. It was hypothesized that the inter-
vention would be more effective than care as usual in lowering the
intensity of symptoms, increasing psychological resources, and
decreasing sickness leave duration. At 12 months all patients had
returned to work, but sickness leave was shorter in the intervention
group than in the control group. The recurrence rate was also lower in
the intervention group. There were no differences between the two
study groups with regard to the decrease of symptoms. The authors
concluded that the experimental intervention for adjustment disorder
was successful in shortening sick leave duration, mainly by decreasing
long-term problems. The “activating intervention” was based on a
three stage model, resembling stress inoculation training, a highly
effective CBT approach. In the first stage, there was emphasis on infor-
mation: understanding the origin and cause of the loss of control.
Patients were also stimulated to do more non-demanding daily activi-
ties. In the second stage, patients were asked to draw up an inventory
of stressors and to develop problem-solving strategies for these causes
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of stress. In the third stage, patients put these problem-solving strate-

gies into practice and extended their activities to include more demand-
ing ones.
Psychotropic drug treatments show promising results in the treatment
of depression secondary to medical illness. A systematic review on this
topic concluded that antidepressants, significantly more frequently than
either placebo or no treatment, cause improvement in depression in
patients with a wide range of physical diseases.13 On the contrary, there is
limited evidence for the effectiveness of pharmacological treatments in
the treatment of cancer patients with depressive disorders.24 Finally, in a
systematic review on the adjuvant use of herbal therapies (gingko biloba,
kava-kava) with antidepressants and other psychotropic drugs, Sarris
et al.,27 concluded that those therapies have not been sufficiently studied
to warrant standard clinical application.
6. CONCLUSION
Adjustment disorder is a very common diagnosis in clinical practice, but
we still lack data about its rightful clinical entity. This may be caused by
a difficulty in facing, with purely descriptive methods, a “pathogenic
label,” based on a stressful event, to which a subjective impact has to be
considered. We lack efficacy data concerning treatment of adjustment
disorders. The use of psychotropic drugs such as antidepressants, in
adjustment disorder with anxious or depressed mood is not properly
founded and should be avoided in less severe forms of this disorder. More
solid evidence has been produced about the usefulness of psychothera-
pies. Data from randomized-controlled trials would be particularly inter-
esting, also in resistant forms, even with combined use of drugs and
psychotherapies.
7. KEY POINTS
• A mood disturbance must be investigated for previous episodes of
depression or hypomania, in order to assign a correct diagnosis.
• The diagnosis remains essentially clinical and not statistical, that is,
the treatment must be guided more by a clinical evaluation of the
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actual severity and duration of the affective disturbance or of the con-

duct disorder and less by the preoccupation of a well-defined diagnos-
tic label.
• Consider that the type and severity of emotional reactions in patients
with cancer or other severe diseases can vary greatly and that the
range of what can be considered as normal is quite wide. Nevertheless,
be prepared to offer professional support and expertise to allow an
adequate elaboration of the affective breakdown.
• When a stressful event is recognizable in patients presenting a mood
disturbance, always explore the presence of suicidal ideation.
• It is important to ask about the occurrence of a recent suicide of a
significant other or of a suicide in the family history to assess appro-
priately the actual risk for the patient.
• Take in consideration the possibility to start a multifaceted treatment,
with antidepressants aimed to control anhedonia and depressed mood
or enduring anxiety symptoms, combined with psychoeducational or
cognitive-behavioral treatments to deal with maladaptive adjustment
and learned helplessness.
8. SELF-ASSESSMENT
8.1. The onset of an adjustment disorder is usually
(A) Independent from the occurrence of a stressful event or life change.
(B) Within a few days of the occurrence of a stressful event or life change.
(C) Within one month of the occurrence of a stressful event or life change.
(D) Within three months of the occurrence of a stressful event or life
change.
(E) Within six months of the occurrence of a stressful event or life change.
Although DSM-IV-TR states that the development of emotional or behav-

ioral symptoms in response to an identifiable stressor should occur within
three months of the onset of a stressor, according to ICD-10 the experi-
ence of an identifiable psychosocial stressor should occur within one
month of the onset of symptoms.
Answer: C
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8.2. Which of the following manifestations are not included in

the ICD-10 diagnostic description of adjustment disorder?
(A) Depressed mood, anxiety, or worry.
(B) Bad dreams and frightening thoughts.
(C) Inability to cope.
(D) Disability in the performance of daily routine.
(E) Conduct disturbance.
The presence of bad dreams, frightening thoughts, intrusive flash backs,

and vivid memories should orient toward a diagnosis of post-traumatic
stress disorder.
Answer: B
9. CASE STUDIES
9.1. Adjustment disorder with mixed anxiety and conduct
disturbances
A 59-year-old transportation businessman, married to a secretary at the
company where he works, started to have financial problems. As a conse-
quence of increasing worrying, he demonstrated some administrative
irregularities, which alerted his wife and caused some arguments between
the two spouses.
Three weeks later he began to show irritability, psychomotor agitation,
disruption of his sleep–wake cycle, hopelessness, emotional lability, and
mood disturbances. His general practitioner referred him to psychiatry
after a severe aggressive episode with menace with a handgun against
his wife.
His premorbid character was reflexive and calm, with no history of
psychiatric disorders. Physical examination revealed normal vital signs
and a normal heart, lungs, and abdomen. The laboratory evaluation and
EGC were normal. Mental status evaluation revealed impaired attention
and concentration, without language, perception, or ideative disorders.
The patient received a diagnosis of adjustment disorder with mixed
anxiety and conduct disturbances and was prescribed escitalopram and
lorazepam at night.
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Over the next few weeks, his symptoms resolved and he returned to his
previous level of functioning.
9.2. Adjustment disorder with mixed anxiety and depression

A 47-year-old math teacher in an important school of aeronautics is mar-
ried to a commanding pilot with one son. Five months ago, she received a
diagnosis of benign ovarian neoplasm, which was treated with surgery.
Over the next few weeks, the patient began to show irritability, psycho-
motor agitation, hopelessness, anxiety, and disruption of her sleep–wake
cycle. Her husband brought her for consultation for progressively worsen-
ing irritability and isolation.
Physical examination and laboratory evaluation were normal. At the
clinical examination, her current mental state represented an acute change
from the previous condition. She appeared fatigued and gloomy and had
suspended her normal occupations. Her family reported that the symp-
toms were worse at night.
She was diagnosed with adjustment disorder with mixed anxiety and
depression. She started to take paroxetine and alprazolam, with good effi-
cacy over the next few days and a progressive recovery in the following
two months.
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Assessing mixed anxiety-depressive disorder. A national primary care sur-
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spective follow-up of former patients in a crisis intervention ward. Acta
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Carpiniello B, Angst J. (2003) Is recurrent brief depression an expression of
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mood spectrum disorders in young people? Results of a large community

sample. Eur Arch Psychiatry Clin Neurosci 253: 149–153.
6. Carta MG, Balestrieri M, Hardoy MC. (2009) Adjustment disorder: Epide-
miology, diagnosis and treatment. Clin Pract Epidemol Ment Health 5: 15.
7. Casey P, Maracy M, Kelly BD, Lehtinen V, Ayuso-Mateos JL, Dalgard OS,
Dowrick C. (2006) Can adjustment disorder and depressive episode be dis-
tinguished? Results from ODIN. J Affect Disord 92: 291–297.
8. Casey P. (2001) Adult adjustment disorder: A review of its current diagnostic
status. J Psichiatr Pract 7: 32–40.
9. De Leo D. (1989) Treatment of adjustment disorders: A comparative evalua-
tion. Psychol Rep 64: 51–54.
10. Diefenbacher A, Strain JJ. (2002) Consultation-liaison psychiatry: Stability
and change over a 10-year period. Gen Hosp Psychiatry 24: 249–256.
11. Dowrick C, Casey P, Dalgard O, Hosman C, Lehtinen V, Vazquez-Barquero
JL, Wilkinson G. (1998) Outcomes of depression international network
(ODIN). Background, methods and field trials. ODIN Group. Br J Psychiatry
172: 359–363.
12. For-Wey L, Fei-Yin L, Bih-Ching S. (2002) The relationship between life
adjustment and parental bonding in military personnel with adjustment dis-
order in Taiwan. Mil Med 167: 678–682.
13. Gill D, Hatcher S. (2000) Antidepressants for depression in medical illness.
Cochrane Database Syst Rev 4: CD001312.
14. Giotakos O, Konstantakopoulos G. (2002) Parenting received in childhood
and early separation anxiety in male conscripts with adjustment disorder. Mil
Med 167: 28–33.
15. Gonzales-Jaimes EI, Turnbull-Plaza B. (2003) Selection of psychotherapeu-
tic treatment for adjustment disorder with depressive mood due to acute
myocardial infarction. Arch Med Res 34: 298–304.
16. Greenberg WM, Rosenfeld DN, Ortega EA. (1995) Adjustment disorder as
an admission diagnosis. Am J Psychiatry 152: 459–461.
17. Kirsh KL, McGrew JH, Dugan M, Passik SD. (2004) Difficulties in screening
for adjustment disorder, Part I: Use of existing screening instruments in cancer
patients undergoing bone marrow transplantation. Palliat Support Care 2: 23–31.
18. van der Klink JJ, Schene AH, van Dijk FG. (2003) Reducing long term sick-
ness absence by an activating intervention in adjustment disorders: A cluster
randomized controlled design. Occup Environ Med 60: 429–437.
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19. Kuhn M, Ehlert U, Rumpf HJ, Backhaus J, Hohagen F, Broocks A. (2006)

Onset and maintenance of psychiatric disorders after serious accidents. Eur
Arch Psychiatry Clin Neurosci 256: 497–503.
20. Kumano H, Ida I, Oshima A, Takahashi K, Yuuki N, Amanuma M, Oriuchi N,
Endo K, Matsuda H, Mikuni M. (2007) Brain metabolic changes associated
with predispotion to onset of major depressive disorder and adjustment disorder
in cancer patients — A preliminary PET study. J Psychiatr Res 41: 591–599.
21. Malt UF, Huyse FJ, Herzog T, Lobo A, Rijssenbeek AJ, the ECLW
Collaborative Study III. (1996) Training and reliability of ICD-10 psychiatric
diagnoses in the general hospital setting — an investigation of 220 consul-
tants from 14 European countries. J Psychosom Res 41: 451–463.
22. Pelkonen M, Marttunen M, Henriksson M, Lönnqvist J. (2007) Adolescent
adjustment disorder: Precipitant stressors and distress symptoms of 89 out-
patients. Eur Psychiatry 22: 288–295.
23. Pelkonen M, Marttunen M. (2005) Adolescent outpatients with depressive
disorders: Clinical characteristics and treatment received. Nord J Psychiatry
59: 127–133.
24. Rodin G, Lloyd N, Katz M, Green E, Mackay JA, Wong RK, Supportive Care
Guidelines Group of Cancer Care Ontario Program in Evidence-Based Care.
(2007) The treatment of depression in cancer patients: A systematic review.
Support Care Cancer 15: 123–136.
25. Ronson A. (2005) Adjustment disorders in oncology: A conceptual frame-
work to be refined. L’Encéphale 31: 118–126.
26. Rundell JR. (2006) Demographics of and diagnoses in Operation Enduring
Freedom and Operation Iraqi Freedom personnel who were psychiatri-
cally evacuated from the theater of operations. Gen Hosp Psychiatry 28:
352–356.
27. Sarris J, Kavanagh DJ, Byrne G. (2010) Adjuvant use of nutritional and
herbal medicines with antidepressants, mood stabilizers and benzodiaze-
pines. Psychiatr Res 44: 32–41.
28. Troisi A, D’Argenio A, Peracchio F, Petti P. (2001) Insecure attachment and
alexithymia in young men with mood symptoms. J Nerv Ment Dis 189:
311–316.
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Chapter 19
Personality Disorders
Joel Paris
1. INTRODUCTION
Everyone has a personality. It can be difficult to determine a boundary of
dysfunction that would define a personality disorder. By and large, the
threshold for diagnosing a personality disorder should be kept high.
Diagnosis requires clinically significant (i.e. seriously problematic)
dysfunction in work and/or relationships. Using current criteria, research
shows that patients with personality disorder are often disabled on a
similar level as those with most chronic mental disorders.18
Personality disorders usually present clinically with maladaptive and
problematic interpersonal relationships. Many of the problems seen in
personality disorders are “ego-syntonic,” in that patients view the outside
world and other people (rather than themselves) as the problem. But many
patients have symptomatic features not seen in community populations.
Examples include the chronic criminality associated with dissocial
personality disorder and the repeated suicidal behaviors associated with
borderline personality disorder. Thus personality disorders are not just
normal variants but are disorders with definite consequences for an ability
to establish stable intimacy and/or a satisfying occupation.
Personality disorders have an important cultural context. Although
personality traits are universal, their frequency varies somewhat from one
society to another. For example, one has to be careful not to interpret
the emotional expressiveness that is encouraged in some cultures, or the
461
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462 J. Paris
emotional reserve that is encouraged in other cultures, as in any way

pathological. However patients with personality disorders have personal-
ity characteristics that are in strong conflict with social and cultural expec-
tations. Most developed countries have a culture that encourages high
levels of autonomy and individualism. In contrast, traditional societies
expect individuals to be closely attached to family and community. For
this reason, externalizing symptoms (associated with impulsive personal-
ity disorders) are more common in developed countries, while internaliz-
ing symptoms (associated with anxious personality disorders) are more
common in traditional settings (Table 1).14
Research shows that a third to a half of patients meet general criteria
for a personality disorder but do not fit into any category, leading to a
Table 1. ICD-10 general criteria for a personality disorder (World Health Organization,
1993).
The diagnosis of a personality disorder must satisfy the following general criteria, in addition
to the specific criteria listed under the specific personality disorder under consideration:
1. There is evidence that the individual’s characteristic and enduring patterns of inner
experience and behavior as a whole deviate markedly from the culturally expected and
accepted range (or “norm”). Such deviation must be manifested in more than one of the
following areas:
i. cognition (i.e. ways of perceiving and interpreting things, people, and events;
forming attitudes and images of self and others);
ii. affectivity (range, intensity, and appropriateness of emotional arousal and response);
iii. control over impulses and gratification of needs;
iv. manner of relating to others and of handling interpersonal situations.
2. The deviation must manifest itself pervasively as behavior that is inflexible, maladaptive,
or otherwise dysfunctional across a broad range of personal and social situations
(i.e. not being limited to one specific “triggering” stimulus or situation).
3. There is personal distress, or adverse impact on the social environment, or both, clearly
attributable to the behavior referred to in criterion 2.
4. There must be evidence that the deviation is stable and of long duration, having its onset
in late childhood or adolescence.
5. The deviation cannot be explained as a manifestation or consequence of other adult
mental disorders, although episodic or chronic conditions may coexist with, or be
superimposed upon, the deviation. Organic brain disease, injury, or dysfunction must
be excluded as the possible cause of the deviation.
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Personality Disorders 463
diagnosis of what DSM-IV-TR1 calls “personality disorder, not otherwise

specified,”21 or what ICD-10 calls “unspecified personality disorder.”
The underlying problem is that personality disorder does not fit neatly
into categories. ICD-1020 lists eight types of personality disorder:
paranoid, schizoid, dissocial, emotionally unstable (divided into two
sub-categories: impulsive and borderline), histrionic, anankastic, anxious
(or avoidant), and dependent. This classification is similar to DSM-IV-TR,
with a few differences. What DSM-IV-TR calls “schizotypal” personality
disorder is classified in ICD-10 as simple schizophrenia. DSM-IV has a
category of narcissistic personality disorder that is absent in ICD-10. The
ICD-10 category of emotionally unstable personality disorder is divided
into an unstable subtype (close to the DSM-IV-TR diagnosis of intermit-
tent explosive disorder) and a borderline type (similar to DSM-IV-TR).
Some DSM-IV-TR categories use different names (e.g. antisocial instead
of dissocial, obsessive-compulsive instead of anankastic), although the
constructs are basically equivalent. Because many categories tend to over-
lap, DSM-IV-TR, unlike ICD-10, has organized its 10 categories into
three clusters: A (related to the schizophrenic spectrum), B (dysregulated
and/or impulsive), and C (anxious) (Table 2).
Table 2. Personality disorder classification in ICD-9,

DSM-IV-TR, and DSM-5.
ICD-10 DSM-IV-TR and DSM-5
Paranoid Paranoid
Schizoid Schizoid
Schizotypal
Dissocial Antisocial
Emotionally unstable Borderline
Histrionic Histrionic
Narcissistic
Anankastic Obsessive-compulsive
Anxious/avoidant Avoidant
Dependent Dependent
Not otherwise specified Unspecified
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464 J. Paris
About 90% of empirical research has been conducted on only two

of these categories: dissocial (antisocial) personality disorder and bor-
derline personality disorder. The other categories have a clinical tradi-
tion behind them, but validity has not been established by research.
Many of these diagnoses are likely to disappear in future
classifications.19
Although some patients neatly fit prototypes, many more do not. The
problem is that a categorical system favors a yes–no decision rather than
a quantitative assessment. For this reason, personality disorders could be
defined in terms of underlying trait dimensions rather than rigid diagnos-
tic categories. Trait profiles could provide more information about an
individual than a standard diagnosis. For example, patients with border-
line personality disorder have high levels of affective instability and
impulsivity. The combination of these traits helps explain many of their
clinical features (emotional storms, unstable relationships, and
suicidality).
DSM-5 had considered, but not adopted, a dimensional measure of
personality traits to the assessment of personality disorders, while allow-
ing for categorical diagnosis only when the clinical picture closely fits a
defined prototype. It is possible that ICD-11, due in 2015, may adopt
some aspects of this system.
In spite of their clinical importance, personality disorders are not
always recognized. One reason is their high “comorbidity,” in that most
patients with personality disorders meet criteria for other diagnoses,
particularly mood disorders, anxiety disorders, and substance abuse.
However, this overlap should not be understood as the presence of multi-
ple disorders but, rather, as a reflection of how patients can meet multiple
criteria in an imprecise system.
Making a diagnosis of personality disorder places other symptoms in a
broader context. For example, in patients with borderline personality dis-
order, depressed mood is less stable than in mood disorders, mood swings
do not show the same picture as in hypomanic episodes, and micro
psychotic phenomena do not resemble true psychosis. Thus, in each case,
one is looking at symptoms that should not lead to multiple, separate
diagnoses but that can be better understood as part of a larger picture of
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personality disorder. These differences help to understand the limited role

of psychopharmacology in these disorders.
2. EPIDEMIOLOGY OF PERSONALITY DISORDERS

Epidemiological studies conducted in the United States8 and in the United
Kingdom4 show that personality disorders, as defined by DSM criteria,
have an overall community prevalence of about 10%. However, these rates
vary significantly across cultures. A recent international study5 (examin-
ing DSM-IV-TR clusters rather than specific categories) found the mean
prevalence of personality disorders over 13 countries to be 6.1%, but with
overall rates ranging from 2.4% to 7.9% and with large variations across
countries and regions.
Thus while personality disorders have been identified in psychiatric
clinics all over the world, community prevalence can vary a great deal. For
example, antisocial personality disorder as defined by DSM-IV-TR is
much less common in traditional societies such as Taiwan than in North
America and Europe.6 Similarly, although cases of borderline personality
disorder have been described in societies such as India and China,
this diagnosis also shows cross-cultural variation, given that many of its
symptoms (particularly parasuicide) are more common in developed
countries.12
Although some cultural variations could be due to difficulty in diagno-
sis, personality disorders are “socially sensitive” — that is, their preva-
lence depends on social forces and cultural context.12 The reason is that
different societies place different demands on individuals. Thus, external-
izing symptoms are more common in developed countries, probably
because societies undergoing rapid social change reduce the threshold for
personality disorders in DSM-IV-TR’s Cluster B.
Personality disorder prevalence studies also demonstrate some gender
differences. In both clinical and community populations, dissocial per-
sonality usually affects males.2 But borderline personality disorder,
although mainly seen in females in clinical settings, is found in an equal
number of males in community studies.4 The explanation is that men with
the disorder are less likely to seek help. Thus psychological autopsy stud-
ies of completed suicide in young adults have found that borderline
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466 J. Paris
personality disorder accounts for nearly a third of cases, and most cases
are male.10
3. ETIOLOGY OF PERSONALITY DISORDERS

As with many mental disorders, the causes of personality disorders remain
largely unknown. Because these conditions begin early in life, one might
expect that temperamental variations would have effects in early develop-
ment and that precursors could be identified in late childhood or adoles-
cence. However, the childhood precursors of most categories are unknown,
although dissocial personality disorder is always preceded by conduct
disorder in childhood. Abnormal aggressiveness can be measured as early
as age three years, and an early onset of conduct disorder predicts a
personality disorder in adulthood.3
When disorders begin in childhood, they are likely to be influenced by
genetic factors. Behavior genetic research has established that close to
half the variance in both normal personality and in personality disorders,
is heritable.7 The nature of this genetic vulnerability is unclear. In border-
line personality disorder, some research suggests that impulsivity is asso-
ciated with abnormalities in central serotonergic activity and in frontal
lobe sites affecting executive function.15 However, no specific biological
or genetic markers for any category of personality disorder have been
identified.
Research on the environmental influences on personality disorders
yields a very complex picture. Given that these conditions start early
in life, it is also possible that childhood adversity is a major risk factor.
In fact, many patients with dissocial or borderline personality disorders
come from dysfunctional families.13 However, such relationships
could reflect both genetic and environmental influences. Moreover,
some patients will develop disorders without experiencing notable
adversities, while most people with childhood adversities never develop
disorders.
The most likely explanation is that the pathways to personality
disorders depend on interactions between temperamental vulnerability
and life adversity. Thus, biological diatheses are expressed under stressful
circumstances. This stress-diathesis model is widely applicable to mental
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disorders, and for personality disorders, etiological models also need to

take into account social contexts that amplify personality traits to the point
of dysfunction.12
4. DISSOCIAL PERSONALITY DISORDER

Dissocial personality disorder (Table 3) has been the subject of a large body
of research. However, much of the literature has made use of the similar (but
not identical) construct of “psychopathy,” for which researchers have devel-
oped a widely used clinical checklist and which can be factor analyzed into
two trait dimensions: aggressive narcissism and a socially deviant lifestyle.
5. EMOTIONALLY UNSTABLE (BORDERLINE)

PERSONALITY DISORDER
There is a very large body of research on borderline personality disorder14
(Table 4). The etiology of the disorder is complex and multifactorial. No
specific biological markers are known, but the traits that most characterize
patients with borderline personality disorder are affective instability (also
called emotion dysregulation) and impulsivity. Many have histories of
severe family dysfunction, which can contribute to the development of
psychopathology. Many patients with borderline personality disorder also
suffer from social stress and are in some kind of cultural transition.
Table 3. ICD-10 criteria for dissocial personality disorder.
Characterized by at least three of the following:

1. Callous unconcern for the feelings of others and lack of the capacity for empathy.
2. Gross and persistent attitude of irresponsibility and disregard for social norms, rules,
and obligations.
3. Incapacity to maintain enduring relationships.
4. Very low tolerance to frustration and a low threshold for discharge of aggression,
including violence.
5. Incapacity to experience guilt and to profit from experience, particularly punishment.
6. Markedly prone to blame others or to offer plausible rationalizations for the behavior
bringing the subject into conflict.
7. Persistent irritability.
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468 J. Paris
Table 4. ICD-10 criteria for emotionally unstable personality disorder.
Impulsive type
At least three of the following must be present, one of which must be:
1. marked tendency to act unexpectedly and without consideration of the consequences.

2. marked tendency to quarrelsome behavior and to conflicts with others, especially when
impulsive acts are thwarted or criticized.
3. liability to outbursts of anger or violence, with inability to control the resulting
behavioral explosions.
4. difficulty in maintaining any course of action that offers no immediate reward.
5. unstable and capricious mood.
Borderline type
At least three of the symptoms mentioned in F60.30 Impulsive type must be present, with
at least two of the following in addition:
1. disturbances in and uncertainty about self-image, aims, and internal preferences
(including sexual).
2. liability to become involved in intense and unstable relationships, often leading to
emotional crisis.
3. excessive efforts to avoid abandonment.
4. recurrent threats or acts of self-harm.
5. chronic feelings of emptiness.
6. OTHER PERSONALITY DISORDERS

Paranoid personality disorder (Table 5) and schizoid personality disorder
(Table 6) lie in the schizophrenic spectrum, as shown by family history
studies. A more severe disorder, the DSM-IV category of schizotypal per-
sonality disorder, is characterized by negative symptoms without positive
symptoms and shares biological markers with psychosis. In ICD-10 these
patients are considered to have a form of schizophrenia, even though most
schizotypal patients never become overtly psychotic.
Anankastic personality disorder (Table 7), avoidant (anxious) personal-
ity disorder (Table 8), and dependent personality disorder (Table 9) all fall
within the C (anxious) Cluster described in DSM-IV-TR. Research is very
sparse on any of these categories. Anankastic personality disorder has
been described by psychotherapists, but has never been studied systemati-
cally in research. The avoidant category overlaps with social phobia. In
contrast, the dependent category describes an extreme level of a trait.
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Table 5. ICD-10 criteria for paranoid personality disorder.

1. excessive sensitivity to setbacks and rebuffs.
2. tendency to bear grudges persistently, i.e. refusal to forgive insults and injuries or slights.
3. suspiciousness and a pervasive tendency to distort experience by misconstruing the
neutral or friendly actions of others as hostile or contemptuous.
4. a combative and tenacious sense of personal rights out of keeping with the actual situation.
5. recurrent suspicions, without justification, regarding sexual fidelity of spouse or sexual
partner.
6. tendency to experience excessive self-importance, manifest in a persistent self-referential
attitude.
7. preoccupation with unsubstantiated “conspiratorial” explanations of events both immediate
to the patient and in the world at large.
Table 6. ICD-10 criteria for schizoid personality disorder.

1. few, if any, activities, provide pleasure.
2. emotional coldness, detachment, or flattened affectivity.
3. limited capacity to express either warm, tender feelings or anger towards others.
4. apparent indifference to either praise or criticism.
5. little interest in having sexual experiences with another person (taking into account age).
6. almost invariable preference for solitary activities.
7. excessive preoccupation with fantasy and introspection.
8. lack of close friends or confiding relationships (or having only one) and of desire for
such relationships.
9. marked insensitivity to prevailing social norms and conventions.
Table 7. ICD-10 criteria for Anankastic personality disorder.

1. feelings of excessive doubt and caution.
2. preoccupation with details, rules, lists, order, organization, or schedule.
3. perfectionism that interferes with task completion.
4. excessive conscientiousness, scrupulousness, and undue preoccupation with productivity
to the exclusion of pleasure and interpersonal relationships.
5. excessive pedantry and adherence to social conventions.
6. rigidity and stubbornness.
7. unreasonable insistence by the patient that others submit to exactly his or her way of
doing things, or unreasonable reluctance to allow others to do things.
8. intrusion of insistent and unwelcome thoughts or impulses.
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470 J. Paris
Table 8. ICD-10 criteria for avoidant (anxious) personality disorder.

1. persistent and pervasive feelings of tension and apprehension.
2. belief that one is socially inept, personally unappealing, or inferior to others.
3. excessive preoccupation with being criticized or rejected in social situations.
4. unwillingness to become involved with people unless certain of being liked.
5. restrictions in lifestyle because of need to have physical security.
6. avoidance of social or occupational activities that involve significant interpersonal
contact because of fear of criticism.
Table 9. ICD-10 criteria for dependent personality disorder.
Characterized by at least three of the following

1. encouraging or allowing others to make most of one’s important life decisions.
2. subordination of one’s own needs to those of others on whom one is dependent, and
undue compliance with their wishes.
3. unwillingness to make even reasonable demands on the people one depends on.
4. feeling uncomfortable or helpless when alone, because of exaggerated fears of inability
to care for oneself.
5. preoccupation with fears of being abandoned by a person with whom one has a close
relationship, and of being left to care for oneself.
6. limited capacity to make everyday decisions without an excessive amount of advice and
reassurance from others.
Table 10. ICD-10 criteria for histrionic personality disorder.

1. self-dramatization, theatricality, exaggerated expression of emotions.
2. suggestibility, easily influenced by others or by circumstances.
3. shallow and labile affectivity.
4. continual seeking for excitement and activities in which the patient is the center of
attention.
5. inappropriate seductiveness in appearance or behavior.
6. over-concern with physical attractiveness.
The histrionic category (Table 10) has a long clinical tradition and
reflects problematic traits that psychotherapists see in practice, but it has
not been the subject of research.
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7. TREATMENT
Treatment of personality disorders should be seen in light of their unique
course. By definition, personality disorders start early in life and, once
they emerge, continue to produce dysfunction for years. However, it does
not follow that personality disorders rarely remit or improve. On the con-
trary, large-scale prospective research has shown that most patients remit
symptomatically within a few years, even though improvement in func-
tional impairment is more sluggish.18 Even in antisocial personality disor-
der, patients are less likely to be involved with the law as they age.2
Recovery is particularly striking in borderline personality disorder.13
These patients may be suicidal for years, but only a minority die by their
own hand. By the age of 50 years, most find a niche in society and are no
longer in contact with the mental health system.
A diagnosis of personality disorder can help guide management. For
example, there is no evidence that patients with dissocial personality
disorder benefit from psychological or pharmacological treatment. In con-
trast, there is a large body of evidence that patients with borderline
personality disorder can benefit from mental health interventions.
However, extensive research on the treatment of borderline personality
disorder suggests that pharmacotherapy has only weak evidence for effec-
tiveness, while specific forms of psychotherapy have been more
successful.16 Unfortunately, these findings have not prevented physicians
from prescribing patients a wide variety of pharmacological treatments,
while access to evidence-based psychotherapy remains limited.
Some comorbid diagnoses affect treatment. Although patients with
personality disorders are often depressed, they do not greatly benefit from
antidepressants, and they sometimes have severe substance abuse that has
to be managed first.
The strongest evidence base in borderline personality disorder concerns
the effectiveness of dialectical behaviour therapy (DBT), and there is also
fairly good evidence for mentalization-based therapy (MBT).17 Both
methods use primarily cognitive methods that help patients to overcome
affective instability and impulsivity.
Unfortunately, evidence-based psychological treatment is resource-
intensive and not widely available. Access to psychotherapists with
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472 J. Paris
specialized skills is quite uneven. Nevertheless, the data supporting the

efficacy of specifically targeted treatments has supported an increasing
climate of hopefulness for patients with borderline personality
disorder.
One of the main clinical problems with management of borderline
personality disorder concerns patients who are often chronically suicidal
and are hospitalized recurrently for suicidal actions and threats.
Follow-up studies show that somewhere between 4% and 10% of patients
with borderline personality disorder do eventually commit suicide.13
However, death is most likely to occur later in the course of illness, in
patients who fail to recover by the age of 30 years. The common presen-
tation around the age of 20 years, in which young patients come to a
hospital with suicidal threats or actions, is less dangerous than many
clinicians think. And although hospitalizing suicidal patients with per-
sonality disorders is common, there is no evidence that doing so has any
preventive effect. It is also important to understand that self-harm (such
as wrist-cutting) is not a suicidal behavior, but an attempt by patients to
regulate their unstable emotions. One should not hospitalize patients for
that symptom.
Research on the treatment of other personality disorders is very thin.
There is some evidence for the efficacy of CBT in avoidant personality
disorder, but little on other categories. Although clinical experience sug-
gests that not every patient does well with psychotherapy, psychological
treatment has long been the mainstay of management for personality dis-
orders. And these patients, even if they have had long-term problems, do
not have to be treated for years on end, but can benefit from brief and
intermittent interventions.
8. CONCLUSION AND FUTURE DIRECTIONS

Personality disorders, though often seen in clinical practice, have been,
until recently, neglected by researchers. Much remains to be learned about
these interesting conditions. Recognition of personality disorders is
important for management. Otherwise, patients who have had serious
problems for many years will be offered treatment for an episodic disorder
rather than for long-term problems.
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9. KEY POINTS
• Personality disorders are defined by problems in behavior, emotion,
and thinking patterns that begin early in life and that lead to dysfunc-
tion over many years in many contexts. Personality disorders are not
episodic conditions, but enduring patterns.
• To make a diagnosis of personality disorder, one should first deter-
mine that overall criteria are met and then see if the patient fits a
specific category.
• Individuals with dissocial personality disorder are commonly found in
the prison system or in the community living off petty crime. These
patients may only appear in the mental health system when advised to
do so by a third party. Recognizing the clinical picture is important
because it guides clinicians to avoid offering interventions to patients
who lack sufficient motivation for change.
• Borderline personality disorder is very commonly seen in emergency
settings, psychiatric clinics, and primary care. The chronic suicidality
and emotional instability that characterize the disorder present unique
clinical challenges. Most patients get better with time, and no more
than 10% will kill themselves.
• Although clinical trials of antidepressants, neuroleptics, and mood
stabilizers show some symptomatic benefit, one never sees full remis-
sion, and even though personality disorders are often comorbid with
depression, antidepressants are much less effective in these patients.
• Clinical trials show that psychological treatment specifically adapted to
borderline personality disorder is effective, most particularly DBT and
MBT. Successful therapies for borderline personality disorder are designed
to combat affective instability and impulsivity by teaching skills in self-
observation and emotion regulation.
10. SELF-ASSESSMENT
10.1. The following are defining criteria for dissocial
personality disorder, except for
(A) Callousness.
(B) Self-harm.
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474 J. Paris
(C) Poor frustration tolerance.

(D) Irresponsibility.
(E) Absence of guilt.
Self-harm is not a defining criteria for dissocial personality disorder.20
Answer: B
10.2. The following are defining criteria for borderline

personality disorder, except for:
(A) Affective instability.
(B) Impulsivity.
(C) Micro psychotic reactions.
(D) Self-harm.
(E) Hypomanic episodes.
Hypomanic episodes are not defining criteria for borderline personality
disorder.1
Answer: E
10.3. Etiological factors in personality disorders are reflected in

(A) Characteristic findings on brain scan.
(B) Changes in monoamine activity.
(C) Abnormal limbic functioning.
(D) History of family dysfunction.
(E) Family history of personality disorder.
Etiological factors in personality disorders are reflected in a history of
family dysfunction.11
Answer: D
10.4. The long-term outcome of most personality disorders

demonstrates
(A) Gradual decline.
(B) Gradual recovery.
(C) Increasing suicide with age.
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(D) Increasing use of substances over time.

The long-term outcome of most personality disorders demonstrates grad-
ual recovery.13
Answer: B
10.5. Which form of psychological treatment for personality

disorders has been supported by randomized clinical trials?
(A) DBT.
(B) MBT.
(C) both DBT and MBT.
(D) Neither DBT nor MBT.
(E) Standard supportive therapy.
Both DBT and MBT have been supported by randomized clinical trials.15
Answer: C
11. CASE STUDIES

11.1. Borderline personality disorder
Colleen was a 22-year-old student who had recently taken an overdose of
pills after a break-up with a boyfriend. However, she had a history of mul-
tiple suicide attempts since age 14. Colleen experienced daily mood swings
from depression to intense anger and often cut herself on the wrists and arms
to relieve her dysphoria. When stressed, she would experience feelings of
unreality, sometimes hearing a voice telling her to kill herself. Colleen had
tumultuous relationships, falling quickly in and out of love with men and
feeling that her life depended on them, even when they behaved abusively.
11.2. Dissocial personality disorder

A 27-year-old man was referred to a clinic by a lawyer after facing a
charge of credit card fraud. He had behavior problems since early child-
hood and had dropped out of high school, after which he was arrested
several times for breaking and entering and for passing forged cheques.
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476 J. Paris
He also had a long history of alcohol and cocaine abuse. His parents, now
estranged, had been unable to control him. There was always a woman in
his life, but he never stayed with anyone for long. He had never held a job
for more than few months.
REFERENCES
DC.
2. Black DW, Baumgard CH, Bell SE. (1995) A 16–45 year follow-up of 71
men with antisocial personality disorder. Compr Psychiatry 36: 130–140.
3. Caspi A, Moffitt TE, Newman DL, Silva PA. (1996) Behavioral observations
at age three predict adult psychiatric disorders: Longitudinal evidence from
a birth cohort. Arch Gen Psychiatry 53: 1033–1039.
4. Coid J, Yang M, Tyrer P, Roberts A, Ullrich S. (2006) Prevalence and corre-
lates of personality disorder in Great Britain. Br J Psychiatry 188: 423–431.
5. Huang Y, Kotov R, de Girolamo G, Preti A, Angermeyer M, Benjet C,
Demyttenaere K, Graaf R, Gureje O, Nasser Karam A, Lee S, Lépine JP,
Matschinger H, Posada-Villa J, Suliman S, Vilagut S, Kessler RC. (2009)
DSM–IV personality disorders in the WHO world mental health surveys. Br
J Psychiatry 195: 46–53 .
6. Hwu HG, Yeh EK, Change LY. (1989) Prevalence of psychiatric disorders in
Taiwan defined by the Chinese diagnostic interview schedule. Acta Psychiatr
Scand 79: 136–147.
7. Kendler KS, Aggen SH, Czjaikowski N, Roysamb E, Tambs K, Torgersen S,
Neale MC, Reichborn-Kjennerud T. (2008) The structure of genetic and
environmental risk factors for DSM-IV personality disorders. A multivariate
twin study. Arch Gen Psychiatry 65: 1438–1446.
8. Lenzenweger MF, Lane MC, Loranger AW, Kessler RC. (2007) DSM-IV
personality disorders in the National Comorbidity/Survey Replication. Biol
9. DSM-IV Personality Disorders in the National Comorbidity Survey
Replication. (2007) Biol Psychiatry 62: 553–556.
10. McGirr A, Paris J, Lesage A, Renaud J, Turecki G. (2007) Risk factors for
suicide completion in borderline personality disorder: A case-control study of
cluster B comorbidity and impulsive aggression. J Clin Psychiatry 68: 721–729.
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11. Oldham J, Skodol A, Bender D (eds.) (2005) Textbook of Personality Disorders,

12. Paris J. (1996) Social Factors in the Personality Disorders: A Biopsycho-
social Approach to Etiology and Treatment, Cambridge University Press,
Cambridge.
13. Paris J. (2003) Personality Disorders Over Time, American Psychiatric Press,
Washington, DC.
14. Paris J. (2004) Sociocultural factors in the treatment of personality disorders.
In: Magnavita J (ed.), Handbook of Personality Disorders: Theory and
Practice, pp. 135–147, John Wiley & Sons, NY.
15. Paris J. (2008a) Treatment of Borderline Personality Disorder: A Guide to
Evidence-Based Practice, Guilford Press, NY.
16. Paris J. (2008b) Clinical trials in personality disorders. Psychiatr Clin N Am
31: 517–326.
17. Paris J. (2010) Effectiveness of differing psychotheraphy approaches in
the treatment of borderline personality disorders. Curr Psychiatry Rep 12:
56–60.
18. Skodol AE, Gunderson JG, Shea MT, McGlashan TH, Morey LC, Sanislow
CA, et al. (2005) The collaborative longitudinal personality disorders study
(CLPS): Overview and implications. J Pers Disord 19: 487–450.
19. Skodol AE, Clark LA, Bender D. Krueger RF, Livesley WJ, Morey LC,
Verheul R, Siever LJ, Oldham JM. Proposed changes in personality and per-
sonality disorder assessment and diagnosis for DSM-5. Part I. Description
and Rationale. J Pers Disord 2: 4–22.
20. World Health Organization. (l993) International Classification of Diseases,
l0th ed, Mental Disorders, World Health Organization, Geneva.
21. Zimmerman M, Rothschild L, Chelminski I. (2005) The prevalence of
DSM-IV personality disorders in psychiatric outpatients. Am J Psychiatry
162: 1911–1918.
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Chapter 20
Geriatrics
Randall Espinoza
1. INTRODUCTION
The world is aging. Advances in control of childhood deaths and improve-
ments in public health, especially in developing countries, coupled with
drops in fertility and increases in life expectancy have led to a gradual
aging of the global population. Sometime within the next decade, and for
the first time in history, there will be more people older than age 65 years
than there are children younger than five years of age. As shown on the
map (Fig. 1), these increases in the geriatric population are occurring all
over the world but most rapidly in Europe and Japan, followed by North
America, Australia, and New Zealand.4 Developing countries, however,
are also experiencing a rise in older inhabitants. Although currently only
5% of their residents, by 2050 the percent of older persons will more than
triple, to 18% in Asia and to 19% in Latin America, and while smaller, the
rise in Africa will more than double from 3% today to 7% in just 40 years.22
The field of medicine concerned with the mental health care and treat-
ment of the older person is geriatric psychiatry. The assessment and man-
agement of psychiatric disorders in later life is grounded on the principles
of geriatrics, which recognizes that older persons have unique life histo-
ries, must be treated with respect and dignity, and have needs that should
be coordinated across multiple providers and domains of care.1,3
Additionally, because aging is not synonymous with disease, psychiatric
478
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Geriatrics 479
Fig. 1. Population age 65 and older, by Country.

4
Source: Haub World Population Data Sheet.
conditions cannot be viewed as the usual consequences of growing old.

Efforts, therefore, must be directed at seeking out treatable or reversible
causes of mental impairment. Another important feature in the care of the
older person is the value placed on optimizing function, enhancing quality
of life, and fostering social integration in the community. Living life to the
fullest extent possible is the goal of successful aging.1,3
Although the field of Old Age Psychiatry is well established in high-
income countries as manifested by the various national and international
organizations devoted to the profession, little is known about the status of
geriatric psychiatry or of mental health services for the elderly in lower-
and middle-income countries. A survey in 1998 by Reifler and Cohen of
members of the International Psychogeriatric Association found that the
majority of high-income countries had begun to establish training
programs in geriatric psychiatry and to train leaders in the field.13
However, in lower- and middle-income countries, the status of geriatric
psychiatry was relatively nascent, with very limited to non-existent train-
ing programs. Here most practitioners of geriatric psychiatry were self-
designated. The same situation held for health services for the mentally ill
elderly. Developed countries were beginning or had established separate
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480 R. Espinoza
or specialized geriatric programs in community, hospital-based, and long-

term care settings. However, developing countries were more likely to
have only very basic services and usually only in general psychiatric
facilities. Whether there has been substantial change in any of the above
for either the developed or developing world over the last 10 years has not
been re-examined. Importantly, since this seminal survey, the World
Health Organization working with the World Psychiatric Association has
sought to articulate statements of need, care, training, and practice to
address the concerns of the older person with mental illness.7 Yet, although
frameworks exist outlining Human Rights Principles for Older People
(United Nations, 1991 and 2011) and for people with mental illness
(World Health Organization, 2005), there is still no international docu-
ment specific to the needs and concerns of older persons with mental ill-
ness, which is a serious deficiency given the special vulnerability of the
older person due to societal ageism, stigmatization from mental illness,
and dependency as the result of illness and infirmity of old age.7,23
Also, with differing cultural attitudes toward aging that occur across
the world, the experience of growing older varies considerably. In Western
countries, the prevailing ethos values youth and vigor, and so the elderly
are often relegated to the background, if seen at all. Older persons are
often mocked and demeaned, depicted as intransigent or dim-witted in
popular culture, and seen as a drain on resources as they languish alone in
nursing homes away from family. The value of the older person to society
is diminished and their contributions forgotten. However, with the arrival
of the baby boomers, a youth-oriented generation born between 1946 and
1964 and now just entering the early stages of older age, these negative
attitudes toward older persons are likely to change. This cohort appears
deeply invested in maintaining good health, a positive physical image, and
high levels of activity and independence. Results now show positive
images of older persons becoming more prevalent in western societies. In
contrast, in most Asian and developing countries, the elderly are valued
for their wisdom, resilience, and experience and are accorded places of
honor and high visibility throughout their lives. Extended family networks
are more common, and intergenerational contact is more frequent and
rewarding. The older person often spends his or her remaining years in the
home of a son or daughter, in contrast to being placed in a nursing home.
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Geriatrics 481
While often underappreciated, the later stages of life can be positive

and fulfilling, replete with rich experiences, fond memories, and expres-
sions of gratitude, happiness, and love. Relationships spanning decades
alongside new connections add to the vibrancy and color of the lives of
older persons. Yet, myths and misconceptions about the aging process still
abound. In contrast to the common belief that a person’s later years are
uniformly fraught with disease and decline, in fact the vast majority of
older persons continue to function proficiently and sufficiently. Indeed,
the heterogeneity of individuals increases with aging, due not only to
intrinsic genetic and biologic variation, but also as a result of the variety
and multitude of experiences, exposures, and challenges encountered
throughout a lifetime. Changes in culture and sociological mores have
also evolved over time so that expectations of living into one’s later years
healthier, still capable, and independent are more common. This chapter
discusses the assessment and management of major psychiatric disorders
in later life in this context.
2. AN OVERVIEW OF GROWING OLDER

2.1. Who is old
Although the world population is aging, the elderly are not a monolithic
group. There are significant changes in the size and growth rate among the
young-old (persons between 65–74 years), the middle-old (persons
between 75–84 years), and the oldest-old (persons 85 years and greater).
For example, comparing US Census data over the last 100 years, the
young-old group is now 8 times larger, the middle-old group 16 times
larger, and the oldest-old group an astonishing 31 times larger. In fact, the
oldest-old group is growing the fastest (see Fig. 2). By 2050, there will be
over 800,000 individuals in the United States older than 100 years of age.
This trend in growth of the oldest-old appears to hold internationally.
The increases in life expectancy are due to gains both at birth and at age
of 65 years. Additionally, death rates are at a record low according to the
most recent report from the US Centers for Disease Control and
Prevention. A child born in 2007 could expect to live 77.9 years, or about
30 years longer than a child born in 1900. The gains in life expectancy at
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482 R. Espinoza
800,000
thousands)
Number
600,000
(in
400,000
200,000
0
1980 1995 2030 2050
Year
Fig. 2. Growth of the oldest-old (2000 US Census Data).
age 65 are even more remarkable. Between 1900 and 1960, life expec-
tancy at age 65 increased by 2.4 years, but since 1960, life expectancy
increased by 3.4 years, or by 140% in less than 40 years. Greater changes
in the percentage of the older population are also noted in many European
countries and Japan.
Generally, gender differences internationally show that women outlive
men, and this difference begins in middle age and is most pronounced
after age 80. For example, in the US women maintain a slight advantage
in life expectancy earlier in life, but by the age of 50 the differences in life
expectancy begin to more noticeably diverge and rapidly accelerate in
the 8th and 9th decades of life, so that by age 85 or greater there are only
40 men for every 100 women. Much of the difference is due to higher
male mortality from heart disease, lung cancer, industrial and motor
vehicle accidents, and violence.
2.2. Cognitive and psychological aging

Accumulating research has not only continued to debunk many myths
about brain function in later life in general but has also uncovered new
findings about improvements in well-being and psychological health
with age. Areas of study (Table 1) have focused on a variety of abilities
and perceptions, and for the most part, these show that our later years
can be replete with happiness, greater satisfaction, and overall
well-being.11,14,15,20,21
While there is a smaller tendency for an increase in positive thinking
with age, there is a much larger decrease in focus on negativity or
recall of negatively emotionally charged material. Indeed, new research
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Geriatrics 483
Table 1. Emotional and cognitive areas of strength in aging.

Wisdom Ability to make decisions that provide greatest benefit to greatest
number of people; pragmatic, not idealistic. Begins to rise in middle
ages and continues to rise through 80s
Happiness Begins to drop in young adulthood, nadir at middle age, but then
begins to rise through 80s
Stress and worry Follows a similar U-shaped curve
Life satisfaction Continually increases from 60s through 80s
Well-being Begins to rise in 50s and 60s and continues to rise through 80s
Emotional control Less cognitive efforts expended compared to younger cohorts
Peace and calm Increase with age
illustrates that older persons are much more efficient than younger per-
sons at emotional control, resulting in improved memory performance
and efficiency. Thus, contrary to general cultural perceptions, growing
older confers some benefits, to wit, emotional and cognitive stability.
Further, the “well-being paradox” describes that, although adults over 65
face challenges to both brain and body, as we reach our 70s and 80s we
also harbor an abundance of social and emotional knowledge. Over time,
older adults, in general, acquire a greater sense of knowing right from
wrong, which enhances the ability to make more sound and dispassion-
ate decisions. This growth in wisdom may partially explain why older
age appears to correlate with greater happiness. Indeed, a recent study
found a U-shaped relationship between happiness and age. While we
begin life with very high levels of happiness, we reach a nadir in middle
age, but then experience a continuing rise through our 70s and into our
80s. This increase in happiness was true for both sexes. As shown in a
recent study, perception of stress over time also decreases. Stress is high-
est in adulthood, begins to drop in middle age, and continues to drop
through later life.
2.3. Adjustment to growing older

As noted, research in the psychology of aging has shown that, contrary
to long-held notions, life in our later years can be a time of satisfaction,
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484 R. Espinoza
Table 2. Major transitions or losses in later-life.

Changing family/support systems Driving
Retirement Death
Relocation Parents
Loss of Independence Siblings
Financial Friends
Physical Spouse
Cognitive
well-being, and positivity. The reasons for this positive outlook are only
recently being understood but include fundamental psychological pro-
cesses attributable to aging that are distinct from the ways of coping and
interpreting the world of our earlier years.
Notwithstanding, the elderly inevitably must face multiple changes and
losses that impact self-image and must also confront ideas of how they
function and live in the world. The main challenges confronted in later life
are shown in Table 2. An individual’s course through life is an interaction
between sociocultural biases and internal cumulative life experiences.
Thus, physiologic changes of aging are accompanied by transitions in
roles that an older person has in society, family, and work and by altera-
tions in interpersonal relationships. Western cultures are focused on
youth, athleticism, and vigor, so that society often diminishes the older
person. Perceived as useless, the elderly are not valued for their sagacity
and wisdom. Ageism is discrimination against a person on the basis of
age, which for the older individual means that negative attitudes and
stereotypes of aging are likely. Ageism permeates contemporary Western
culture, creating a constant barrage of negative views and depictions of
aging.
In contrast, in most developing countries and Asian societies, the
elderly are often revered and highly respected.10 A long view of life is
taken, and wisdom and experience are more readily incorporated in both
personal and broader social contexts such as politics, economics, and cul-
ture. The journey is valued and family history exalted. Extended families
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Geriatrics 485
are often headed by a grandparent who can hold much sway over daily
decisions or long-term plans. Part of the reason for the difference in relat-
ing may lie in the way that death and dying are viewed. While dying and
death are avoided or delayed in Western society, in other parts of the world
these passages are seen as vital stages of the life cycle meant to be shared,
supported, and experienced among the living. Thus, when inevitable life
changes and decline do occur, the older person remains an integral part of
society until the end.
2.3.1. Retirement
Longevity has changed retirement patterns, and today an individual in the
developed world can expect to live one quarter or more of life in retire-
ment. Planning and preparation for retirement can facilitate a successful
transition to a new life stage, but a lack of such planning can create hard-
ships across generations. Beginning new hobbies and cultivating new
interests should not be left until retirement. Some elderly continue to work
as a source of enjoyment or of supplemental income, while many are
forced to retire or are subtly eased out of their careers. Retirement can
bring a focus on one’s health and financial status. Not all countries plan
financial support for their elderly population, however, and in many parts
of the world families must assume primary responsibility for the care and
housing of an older parent. Without a pension, many elderly are living in
or near poverty. Sadly, a financially safe and comfortable retirement may
not be an option for many. Mounting financial pressures leave low-income
elderly having to choose between medications, other essential medical
treatments, food, or shelter. Not surprisingly, a higher economic status at
retirement is associated with more positive health outcomes and more life
satisfaction.
Successful retirements are not totally dependent on health and financial
matters, however. Making creative use of time influences quality of life to
a great degree. There are many physiological and psychological benefits
that retirees gain from leisure activities and volunteer work. Leisure
activities such as gardening, dancing, and traveling bring a sense of fun
and entertainment. Membership in volunteer associations and volunteer
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486 R. Espinoza
work allow the elderly to share their expertise and skills while continuing
to contribute to society. It has been estimated that 40% of the elderly per-
form volunteer work, with elderly women being more likely to volunteer
their time. Other types of volunteer work include tutoring, helping reli-
gious organizations, raising money for charities or for social and political
causes, handiwork, and assisting in an office or hospital. Helping others
in need provides a way of achieving and maintaining a sense of purpose,
which is essential to sustaining a positive sense of self.
2.3.2. Relocation and housing

Our homes provide a refuge of security and safety, and for the elderly, the
form and structure of their living situations may change significantly.
There are many types of housing arrangements for the elderly (Table 3).
In the United States, more than 21 million people over the age of 65
live in their own homes. Nearly 80% of the elderly own their homes, and
about 50% have owned their homes for more than 25 years. Moving to a
smaller residence after a spouse’s death or as a result of financial need can
be very difficult. On the other hand, voluntarily downsizing to a smaller
Table 3. Spectrum of living arrangements.

Level of assistance Type of housing Comments
Low Independent Living Home/Apt/Condo: full freedom; person
maintains all or most I-ADLs and B-ADLs;
low cost
In-home help Needs some minor assistance; formal or
informal caregivers; variable cost
Assisted living Mainly facility-based; provides housing,
meal preparation, transportation; more cost
Board and care Housing in community; small home or large
apartment-style building with communal
areas; more cost
High Nursing home/ Institutional care; persons with acute or
Long term care chronic medical problems, often cognitive
decline; most cost
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Geriatrics 487
residence can bring a sense of relief by lessening financial obligations and

reducing worry about the physical burden of the upkeep in an aging house.
Most elderly prefer independent living with options ranging from condo-
miniums to cooperative apartments. Elder Cottage Housing Opportunity
(ECHO), Accessory Units, and “Granny Flats” refer to housing arrange-
ments where seniors share a single family home, a separate apartment, or
a rental unit on a single family lot with another person or family. There
are also age-segregated retirement communities, senior housing develop-
ments and retirement hotels, and mobile homes and recreation vehicles
that are available at various costs. For those anticipating a future need in
assistance, Continuing Care Retirement Communities (CCRCs) allow
individuals and couples to enjoy independent living in apartments until
they are ready for further help or a change in the level or intensity of care.
Short- and long-term nursing care is often available on site in CCRCs.
Assisted living is for those elderly who do not need nursing home care but
who desire a facility where housing and meals are provided along with
help with everyday living activities and transportation. Board and care
homes are usually located in a community setting where rooms, meals,
and supervision are provided for a monthly fee.
2.3.3. Institutionalization
The majority of those over the age of 65 do not live in nursing homes, and
according to the 2000 US Census Bureau, only 5% of elderly above age
65 do. However, the rates of admission to nursing homes go up with age;
for example, almost 50% of those elderly older than the age of 95 live in
nursing homes. Entering a nursing home has many ramifications. Families
and spouses often feel as though they have failed their loved one, and fam-
ily dynamic issues surrounding the decision for nursing home placement
can be difficult and painful. However, caregivers who attempt to provide
total care for their family members have high rates of morbidity and
mortality, as they often neglect their own health and succumb to stress.
The transition to a nursing home is difficult, but the care received in this
setting is usually more successful and less stressful for both patient and
family. The nursing home can never be the same as home, nor can the care
delivered be the same as that from a devoted family member. However,
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488 R. Espinoza
now an entire cadre of nursing home staff provides the care formerly
delivered by one or two family members, which results in an enhanced
quality of life for all. Concerns about abuse, neglect, or exploitation by
nursing home personnel are real, but sometimes overblown. State and
federal regulations and guidelines help ensure the safety and quality of
care.
There are high rates of psychiatric disorders in nursing homes.
Although healthy community-dwelling elderly have lower rates of depres-
sion, between 25% and 50% of the elderly residing in nursing homes have
or will develop clinical depression. Nearly two thirds of elderly patients
in long-term care exhibit some element of dementia. One of the most dif-
ficult issues confronting any society is where the demented patient exhib-
iting problematic neurobehavioral symptoms should be placed. These
patients are not appropriate for acute adult psychiatric units, where they
are at risk of being abused or injured, yet they remain a danger to them-
selves and/or to others in a conventional nursing home. Currently, there
are not enough dedicated or locked dementia facilities capable of manag-
ing this growing population of often physically robust individuals who
require a safe and caring environment.
Finally, for terminally ill patients, hospices and palliative care pro-
grams are now increasingly available for use by patients and families to
help them through the final days, weeks, or months of life. These pro-
grams aim to maintain dignity and compassion in the experience of death
and in the dying process. In 2000, about 2.4 million Americans died but
only 600,000 received hospice care. About 80% of these patients were
over the age of 65. Hospice programs promote comprehensive and com-
passionate care in hopes of avoiding another acute but futile hospitaliza-
tion, another abrupt change of surroundings, introduction of new providers
who are not familiar with the patient and family, or additional traumatic
and stressful experiences.
2.3.4. Driving
Driving represents independence, freedom, and personal power in many soci-
eties but especially in the United States, where public transportation in most
cities is less developed than in parts of Europe or Asia. Curtailing or
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Geriatrics 489
discontinuing unfettered access to an automobile can represent a significant

social and psychological loss for an older person. Compounding the difficulty
of this transition, older persons with cognitive deficits and impaired reality
testing often cannot make an accurate assessment of their driving compe-
tence. The challenge of identifying and removing the impaired and incompe-
tent older driver before a tragedy strikes confronts many localities, and there
is no national standard or law for evaluating or reporting an older individual
who is no longer fit to operate an automobile. The role of the physician or
healthcare provider is not to determine driving competency, which is the
purview and obligation of the state or provincial licensing agency, but is to
identify those persons who may be unsafe to drive as the result of a physical,
mental, or cognitive disorder that hinders safe operation of a vehicle. Tactics
employed by legislatures and licensing departments to standardize evaluation
of the older drivers include more frequent evaluations beyond a certain age
and more comprehensive physical, visual, and cognitive assessments.
2.3.5. Sexuality
Physiological and psychological changes may affect sexuality in the later
stages of life. These changes occur in the context of societies that do not
promote or accept sexuality in the elderly, and sexual expression in later
years is either ignored or, more often, ridiculed. This bias is reflected in the
paucity of studies addressing sexuality in the elderly. Physiological changes
may make sex less spontaneous or carefree for the older person, but clearly,
the yearning for closeness, sexual pleasure, and sexual release continues to
be part of the life of an older person. Issues of love and intimacy, sexual
attractiveness, partner availability, safe-sex, homosexuality, and masturba-
tion remain important aspects of the daily lives of older people. Increasingly,
research in the area of human sexuality supports the notion of “use it or
lose it,” meaning that those who maintain active sex lives as they age can
expect to remain sexually active and to derive pleasure from sexual activity
into the latter stages of life. An unusual but possible concern is sexual
exploitation of the cognitively impaired individual in an institutional
setting. These problems are often not addressed or discussed, although
there is increasing evidence for their occurrence as more people become
cognitively impaired while remaining physically and sexually robust.
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490 R. Espinoza
2.3.6. Coping with loss and decline

i. Psychological challenges
A series of changes and losses accompanies aging. Erik Erikson, a noted
psychologist, wrote of eight stages of personality development from birth
to death. Each life stage had a conflict that had to be resolved for success-
ful completion. Postulated to occur in the last decades of life, the final
stage of development involves the struggle between ego integrity and
despair in the face of death. Integrity occurs when a person accepts life’s
accomplishments and accepts death as inevitable. Those persons who
have the ability to accept life’s joys and pains in perspective and with
resolve have an easier time accepting death. Those living in despair view
life as misspent and are full of regrets. They fear death as an unacceptable
aspect of life. More recently, these views have been challenged and newer
psychological milestones proposed. Social theories of aging that incorpo-
rate cultural and societal influences are further updating conceptualiza-
tions of what drives behavior and thinking in later life.
For example, shame is a universal human emotion that occurs through-
out the life cycle and that may become more pronounced in the aged.
Shame is a painful emotion resulting from an awareness of inadequacy
or guilt. The stigma of ageism and existential issues inherent in the aging
process form the basis of shame in the elderly. Thus, shame in later life
is the reaction felt to multiple losses and deviations in appearance, status,
role, and ability from the idealized youthful, healthy, and powerful “self.”
Society also shames individuals about diseases and frailty, both of which
happen more commonly in older age. Shame in these circumstances
becomes more intense when the older person feels invisible or is treated
with rejection, impatience, disrespect, and derision. Patients may experi-
ence physical or psychological limitations as defects or inadequacies that
threaten treasured ideals of the self, such as youth, beauty, strength,
stamina, dexterity, self-control, independence, and mental competence.
Some conditions and treatments may further jeopardize self-image. For
example, loss of hair and weight, mastectomies, and erectile dysfunction
from cancer interventions can be degrading to patients. Reactions to
shame may take many forms and are often masked by anger, sadness,
depression, or non-compliance.
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Geriatrics 491
ii. Physical challenges

Many people over time will develop a chronic illness, which often begins
in middle age. Most elderly patients learn to live with one or more chronic
illnesses for the rest of their lives. Degenerative musculoskeletal diseases;
loss or decline in primary sensory function (vision/hearing/taste); gastro-
intestinal conditions like ulcers or acid reflux; cardiovascular diseases;
endocrinologic disorders like diabetes and hypothyroidism; genitourinary
problems like incontinence, urgency, or prostate enlargement; and several
cancers, some benign and some not, commonly present in older age.
These changes and decrements in function, while common, may precipi-
tate a psychiatric disorder as the elderly person attempts to cope with
these losses and signs of degeneration. In addition, chronic health neglect
and poor hygiene begin to show detrimental cumulative effects as the
person ages. Lifelong smoking, drinking, substance abuse, lack of exer-
cise, poor dental hygiene, and poor eating habits often take years to affect
gross health, and with the onset of older age, these behaviors begin to
harm the physical and mental condition of an older person. Unfortunately,
making significant changes in poor lifelong habits is frequently difficult
to achieve.
iii. Cognitive challenges
The world burden of dementia is well known, and many elderly are
understandably concerned and afraid of losing their cognitive abilities.
Dementia spares no one, from everyday people to former world leaders,
such as US President Ronald Reagan, who announced he had Alzheimer's
disease, and British Prime Minister Margaret Thatcher, who after several
strokes developed vascular dementia. The disclosure of their ailments
brought media coverage highlighting the ravages of these conditions. The
fear of developing dementia when an occasional memory lapse occurs,
such as misplacing keys or being unable to remember a person’s name,
can lead to increased anxiety and depression. A single or occasional lapse
rarely signifies a dementia process, and without other evidence, the older
individual should be reassured and counseled about some of the natural
but normal cognitive changes with aging. Conversely, anxiety and depres-
sive disorders may affect an older person’s abilities, and clearly, these
need to be addressed and effectively treated. Perhaps surprisingly, many
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492 R. Espinoza
elderly are reluctant to participate in a cognitive assessment. Some may

even become insulted when asked to answer questions about their cogni-
tive state. Others may fear that their deficits will be exposed or that they
will be ridiculed for appearing stupid or dumb. Finally, some elderly are
concerned that poor test results will have some adverse effect on their
ability to remain independent. Therefore, evaluation of cognition should
be performed with sensitivity to the potential issues uncovered and
involved. If diagnosed with a cognitive disorder, an individual may
respond in a variety of ways. Common responses are denial that test
results are correct or that memory problems are significant, and projec-
tion that others are mistaken or that others are having difficulties coping.
Confrontation of denial is often met with further resistance due to impair-
ment of insight, termed anosognosia, and lack of judgment, both of which
may accompany cognitive loss. On the other hand, some elderly are
keenly aware of their problems and cognitive struggles, and become anx-
ious and depressed. Approximately 25% of patients with early stage
Alzheimer’s disease present with symptoms of depression that should
and can be treated. A cognitive disorder in the elder head of household
will impact all family members. The necessary changes in family struc-
ture and responsibilities for decisions will create new challenges as shifts
in family dynamics and power differentials add to caregiver burden and
stress.
iv. Competency
Independence and the ability to make decisions are important and defining
characteristics of being an adult. Losing the ability to make decisions
about one’s health care, finances, and legal matters is a serious infringe-
ment of the basic rights of an adult individual. The task of assessing
whether to deny a person of his or her rights cannot be taken lightly.
Confusion surrounds the difference between the terms capacity and com-
petency, which are often used interchangeably, if imprecisely. Capacity
refers to the ability of an individual to make decisions about medical,
financial, or legal matters of estate or of person and is a conclusion
reached usually after a medical or clinical evaluation. Competency, on the
other hand, is usually a legal definition and reflects an adjudicated court
decision about the state of a person after a court or judge hears evidence
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Geriatrics 493
concerning the proposed question and incorporates the findings of a pro-

fessional evaluator such as a physician, psychologist, religious arbiter, or
attorney. Thus, the terms are not entirely synonymous.
Competency assessments should focus on the specific decision or task
that is being questioned, because incompetence or competence in one area
may not predict or correlate with ability in another. Typical concerns arise
when an older adult with a possible cognitive, medical or psychiatric ill-
ness that impacts decision-making is changing or writing a will, signing a
contract, distributing property, or considering a potentially dangerous or
experimental medical treatment. In truth, any time an older patient is mak-
ing or considering a choice on any matter, competency is a factor.
Legal authorities and forensic experts use several processes for deter-
mining competency. Essentially, to be legally valid, any decision made by
an individual must be voluntary, informed, and competent. Voluntary deci-
sions are freely given and not the result of coercion, threat, or undue influ-
ence. Additionally, the person must evidence a choice either explicitly in
writing or by speech or implicitly by actions and behaviors. The decision
must also be informed, which entails, for medical decisions, disclosure of
the condition being treated and indication(s) for treatment; discussion and
description of the recommended intervention or treatment; review of the
risks, benefits and side effects of the recommended treatment; disclosure
of alternative therapies, including doing nothing at all; and the conse-
quences of those choices. The clinician should assess for understanding of
information presented and ask the patient to repeat and describe the dis-
cussion in his or her own words. In short, the clinician must determine if
the older person has the ability to assimilate relevant facts and if the per-
son appreciates or rationally understands his or her own situation as it
relates to medical circumstances. For older patients with cognitive impair-
ment or serious medical or psychiatric illness, information may have to be
presented multiple times or in multiple formats. Importantly, the state of
competency can vary over time, such as during delirium or during a period
of grave illness in which a patient was not able to make decisions or to
participate in discussion. Conversely, with dementia, other cognitive dis-
orders, and pervasive unremitting psychiatric conditions, cognitive abili-
ties may be so impaired that competency will never be regained, a
situation that may lead to guardianship or conservatorship, where a court
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494 R. Espinoza
formally appoints and charges another person with the responsibility and
authority to make all medical, financial, and/or legal decisions.
Standardized tools may help facilitate the evaluation of competency,
but these need to be used in conjunction with a thorough clinical evalua-
tion that entails a complete medical history, review of medications, physi-
cal and psychiatric evaluations, and laboratory tests. A diagnosis, if
established, may impact the determination of the decision-making ability
and guide further work-up. Finally, evaluation of family structure and
social network and, frequently, interviews of family members, caregivers,
and friends are necessary for a complete competency assessment.
v. Ethics and Elder Abuse
Related to the issue of competency is the ethical care of the older adult with
mental illness. As highlighted previously, the older person experiences a
double jeopardy due to ageism and stigma from mental illness. At times, an
older person may be infantilized, be treated in an undignified manner, or
lack access to appropriate care. Indeed, many studies show that older per-
sons are typically both under-treated and less intensely treated for similar
conditions of equal severity, thereby leading to avoidable distress. To
address these concerns, recently the World Psychiatric Association Section
on Old Age Psychiatry in 2009 issued a consensus statement on ethics and
capacity in older people with mental disorders.7 In this statement they note
values that should inform a care framework for this population. In particu-
lar, they note the importance of striving for independence and self-
determination where possible, of attending to safety and dignity, and of
enhancing care and treatment. Moreover, poverty and female sex may place
additional risks and obstacles, especially in underdeveloped, religiously-
conservative or male-dominated societies. Finally, from a public health
perspective, older age should not place a limitation on resource utilization,
just as resource shortage does not justify discrimination on the basis of age.
Elder abuse remains a hidden and unspoken problem and is perpetrated
by family, caregivers, and even professionals. The true scope of the prob-
lem is unknown because elder abuse is often underreported. Sadly, older
persons with mental illness are among the most vulnerable and are at high
risk of elder abuse. Forms of elder abuse are listed in Table 4. Most juris-
dictions have laws protecting the elderly and the mentally impaired.
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Geriatrics 495
Table 4. Forms of elder abuse.
Psychological Verbal abuse, threats, manipulation, intimidation, humiliation, scapegoating
Physical Non-accidental use of force against an elderly person that results in

physical pain, injury, or impairment; includes not only assaults but
inappropriate restraints, drugging, and confinement
Sexual Sexual contact without consent; ranges from sexual acts to showing an
unwilling person pornography, and forcing a person to watch sex acts or
to undress
Financial Misuse of funds, stealing, misappropriation of property, self-enrichment
Healthcare Charging for care not provided; submitting false claims; fraudulent practice
Social Public ridicule, demeaning behaviors, deprivation of visits
Neglect Lack of provision of food, shelter, clothing, housing, medication
Abandonment Failure to fulfil a caretaking obligation in a dependent senior
Whatever might be proffered as a mitigating circumstance is never an

excuse for abuse of any type. It is important to keep in mind that behavior
or actions that are not considered abusive towards a healthy and competent
person could be abusive when applied to a vulnerable older adult.
vi. Separation and Death
Loss of a loved one, especially of a spouse or child, is devastating for most
people. There are often changes in the survivor’s social and financial situ-
ation. The death of a spouse is associated with high rates of morbidity and
mortality in previously healthy people. Depression, anxiety, and insomnia
are common psychiatric features of bereavement. Studies suggest that the
stress of bereavement produces changes in the body’s immune system,
creating negative health outcomes. Women generally adjust better than
men do to the loss of a spouse, and males are much more likely to die
within a year after being widowed. Widowhood is difficult, but in many
cases, after the period of grief passes, survivors adjust and find that they
can regain a sense of normalcy, if not enjoy a new sense of independence.
Some elderly find new experiences and new relationships in the aftermath
of a death of a spouse or partner. The losses of parents and adult children
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496 R. Espinoza
can be extremely painful for the elderly. Having a strong social network
of close and valued relationships with friends and family provides the best
means of coping with these losses. Early psychological treatment of com-
plicated bereavement may prevent the development of clinical depression.
Grief support groups available through pastoral counseling, hospice pro-
grams, or community organizations are helpful in providing or creating a
sense of security and of sharing and are sources for new relationships. The
role of spirituality and religion, for those who subscribe to these tenets
and hold these beliefs, cannot be underestimated as a source of comfort,
strength, and solace.
3. GENERAL APPROACH TO THE OLDER PATIENT

3.1. Psychiatric interview
The psychiatric interview remains the most important diagnostic tool in
the assessment of the older person. Psychiatric assessment of an older
individual entails an evaluation and analysis of a person’s thoughts, emo-
tions, behaviors, and cognition. The presenting psychiatric symptoms
must be analyzed comprehensively and placed in the appropriate medical
and psychosocial frameworks. Importantly, psychiatric evaluation of the
older individual must balance respect for personal autonomy, dignity, and
privacy with the need to gather information from a variety of collateral
sources, including spouses, partners, adult children, extended family and
friends, and usually multiple providers. The older person is considered
competent until proven otherwise, and except in an emergency, his or her
permission must be sought to discuss care and treatment with others.
However, there may be cultural differences and sensitivities to observe,
and ideally, the clinician should be aware of these at the outset. For exam-
ple, in some cultures it is common for adult children to attend medical
appointments with an elderly parent and to provide not just history, but to
remain actively involved in treatment decisions or discussion of manage-
ment options. The older person may defer substantially to the adult child
and may not want to know any of the details of the evaluation or care
recommendations. Conversely, while adult children may be present during
appointments, they may not wish to contradict or seem to upset an older
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Geriatrics 497
parent in front of an authority figure, and they either may avoid making
any comments during the evaluation or may seek out separate or discreet
ways of conveying information in order to preserve the elder’s respect.
Lastly, some older persons may shun psychiatric evaluation due to the
stigma of mental illness or to a tendency to express psychological difficul-
ties as somatic complaints as a means to avoid the perception of character
flaws or weaknesses. In some cultures, emotional or behavioral problems
are handled not by a medical provider but by a local elder, spiritual healer,
or shaman. With the above in mind, a careful systematic and comprehen-
sive approach includes query for past medical and neurologic conditions,
review of medication and supplement lists, family medical and psychiatric
history, social history, and review of systems.
3.2. Medical history

Medical or neurologic comorbidity often complicates the psychiatric
evaluation of an older individual. Psychiatric symptoms by themselves are
relatively non-specific and may develop in practically any medical disor-
der. That is, medical conditions may present with psychiatric symptoms,
such as pancreatic cancer or hypothyroidism presenting with depressed
mood, and conversely, psychiatric disorders may present with medical
symptoms, such as clinical depression presenting with weight loss or
panic disorder with chest pain.
When performing a psychiatric evaluation on an older patient with on-
going medical problems, it is useful to try to get a timeline that details the
development of psychiatric symptoms with illness. Acute or new presenta-
tions of psychiatric illness in patients with known medical disease but absent
psychiatric histories should prompt for a thorough evaluation of recurrent
illness. Atypical, mixed, or incomplete presentations of common psychiatric
disorders should also raise concern for a medical disorder, as should unusual
vital sign changes and new or focal neurological deficits. However, it is criti-
cal to keep in mind that even patients with psychiatric histories can get ill or
develop new medical problems, so it should not be assumed that somatic
presentations are manifestations solely of recurrent psychiatric disorders.
As further clues to aid in distinguishing medical from most psychiatric
illness, medical complaints that are usual for the medical problem, vary
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498 R. Espinoza
with the severity of illness, and respond in a typical manner to common

medical remedies likely indicate that psychological symptoms are
expected reactions to illness and not a separate primary psychiatric disor-
der. Conversely, when symptoms do not match the usual expected course
of illness or do not respond to accepted treatments despite compliance, a
psychiatric disorder may be involved. Asking the patient what he or she
thinks is the cause of the problem may also be helpful in distinguishing
between a medical or psychiatric disorder. A medical disorder is more
probable if the patient points to a reasonable cause for the complaint, such
as insomnia arising from a noisy room or cold temperature. However, a
patient who rejects help despite presenting for evaluation of a medical
complaint may be manifesting a psychiatric problem.
3.3. Medication and supplement history

The issues and problems of medication use in the elderly are several and
are related to the increasing numbers of older adults, the heterogeneity of
this population, the increasing prevalence and number of both acute and
chronic conditions, and the consequent increasing number of medications
or supplements used to treat those conditions. All of these issues make the
medication and supplement history essential. Elderly patients use more
medications than younger groups overall. For example, in the United States,
patients over 65 years old fill an average of 13 prescriptions per year,
which is twice the national average and three times the average for
younger individuals. Additionally, the number of prescribed and over-the-
counter (OTC) medications and supplements increases with age. With the
heterogeneity of the population, decrements in physiologic function do
not develop at the same rate or extent across all tissues or organ systems,
and moreover, chronological and physiologic ages are poorly correlated.
Further, the increasing numbers of medical problems experienced make
patients less responsive to treatment and less tolerant to treatment. In
some cultures, it is common to seek out home remedies for common
psychological ailments or to ingest herbs or teas as a means of dealing
with emotional distress. Older recent immigrants to a new country may
feel more comfortable with this approach as well. At times, older persons
may have an aversion to taking psychotropic drugs but may readily ingest
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Geriatrics 499
supplements purported to have a psychological or cognitive benefit, only to

suffer from an untoward reaction. Finally, the increasing number of medi-
cations used makes medication errors more likely, often leads to or reflects
inappropriate drug prescribing, heightens the likelihood of drug–drug or
drug–supplement interaction, or hampers medication compliance due to
complex drug schedules or cost. Thus, for the reasons given, medications,
OTC drugs, and supplements can easily cause an alteration in thinking or
behavior as the result of an adverse interaction.
Despite these concerns, obstacles to obtaining an accurate medication
and OTC history include poor recall, sincere confusion, benign omission,
not keeping an up-to-date list, medication hoarding, recent hospitaliza-
tion, presence of multiple providers, deception, shame, or guilt. Persons
who no longer manage their own medications, whether due to cognitive
impairment or delegation, may not care to keep close track. In situations
like these, a caregiver or primary care provider may be able to corroborate
the medication and supplement list.
3.4. Family history

Just as in younger populations, it is helpful to query the older person about
other family members with mental illness. The basics should be covered,
including diagnosis, type of treatment, and course of illness, including
need for hospitalization. However, it is important to keep in mind that
diagnostic nomenclature likely has changed over the decades, and past
descriptions or diagnoses will not usually follow current schema. In the
past, mental illness was not openly discussed and was highly stigmatized,
so complete knowledge of illness or treatment course may be shrouded in
mystery or come only in fragments. With no contemporaries available,
corroboration can be difficult. Family members with dementia or other
cognitive disorders were often overlooked or labeled senile, which years
ago was considered a normal part of aging. Some relatives may have been
committed to asylums, but the reasons for these admissions may not be
known and were likely based on different standards of care from today.
Many forms of treatment, like hydrotherapy, insulin coma, and frontal
lobotomy, are now discredited, and others, like electroconvulsive therapy
(ECT), were used indiscriminately. Nonetheless, for a treatment like ECT,
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500 R. Espinoza
a positive response can be quite informative, whether in the individual or

family member.
Although accurate assessment of the past may be challenging, it is
important not to overlook asking about the mental health history of cur-
rent family members, from siblings to children and grandchildren. Several
disorders tend to run in families or increase the risk of other psychiatric
disorders. Finally, specific inquiry should be made about any family sui-
cides in first-degree relatives. Here again, stigma may shroud details and
deaths reported as accidents.
3.5. Past psychiatric history

As above, it is useful to ask about past psychiatric treatment, including
possible diagnosis and use of, response to, and tolerance of psychotropic
agents, engagement in psychotherapy, and hospitalization. Provider his-
tory should also be ascertained. If the patient engaged in psychotherapy,
the type, duration, and perceived benefit, if any, should be explored. If a
patient was hospitalized, the circumstances leading to inpatient treatment
and duration of inpatient stay should be clarified. Specific inquiry about
suicide ideation, attempts, and outcomes is also critical.
Another issue to consider is that an older person may be experiencing
an exacerbation of a pre-existing psychiatric disorder, present since earlier
in life, or may be developing a psychiatric disorder for the first time only
later in life. The former group is said to have an early-onset disorder and
the latter to have a late-onset disorder. The age cut-off for various disor-
ders is not firmly settled, but an episode starting after age 60–65 is usually
considered late-onset.
Patients with early-onset disorders have positive psychiatric histories,
although details may be sketchy or hard to corroborate, as well as higher
genetic or biological load with positive family histories of mental disor-
ders. In general, patients with early-onset psychiatric disorders tend to
have in later life overall poorer physical health than their peers without
any previous psychiatric history. In contrast, patients with most late-
onset disorders typically have negative past and family psychiatric histo-
ries and carry a lower genetic load. Late-onset psychiatric disorders
appear to be associated with the development or worsening of an
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Geriatrics 501
underlying medical or neurological condition. Thus, in older patients

who present with a psychiatric disorder for the first time only in later-life,
a thorough medical and neurological work-up is warranted, which would
include comprehensive laboratory review, neuro-imaging, and likely for-
mal neuropsychological testing, among other studies. Notwithstanding,
many of the same conditions found earlier in life can develop later in life,
although the likelihood, risk, and prevalence of disorders are different.
For example, de novo presentation of bipolar mania in later life is rare.
Presently, diagnostic schemes do not distinguish most major psychiatric
disorders according to age at presentation of illness during adulthood
because the dimensions of illness appear to be constant over age.
However, in the older adult it is critical to take into account the effects of
concurrent medical illness on symptom expression, which can often be
challenging.
3.6. Social history

The social history covers background, like where the person was born and
raised, highest level of education attained, marital or relationship status,
and availability and extent of involvement of a spouse or significant other,
children, siblings, friends, and formal or informal caregivers. For persons
married, involved, or otherwise socially engaged, a brief sexual history
can also be included. Continuing sexual intimacy and close physical con-
tact remain important throughout much of adulthood. However, older
persons may be unaware of the risks of sexually transmitted diseases or
how to engage in safe sex practices. If the subject is broached, this line of
inquiry should be done privately, to avoid uncomfortable feelings or unto-
ward reactions, especially from adult children, who may be unaware of a
parent’s continuing sexual activity. If available, the caregiver(s) can be
asked about any stress burden experienced in caring for the older person.
Work history and retirement status are also helpful to know, and learning
how this transition occurred, whether successful or not, can be insightful.
Knowing about participation in social or religious groups, hobbies, and
leisure activities is similarly useful. Asking about losses, difficult
transitions, or declines in function further enriches understanding of the
older adult. Performing an assessment of function includes determining
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502 R. Espinoza
Table 5. Activities of daily living.
Function Independent Needs help Dependent Does not do

Instrumental ADL
Shopping
Cooking
Managing meds
Using the phone
Housework
Doing laundry
Managing finances
Driving
Basic ADL
Bathing
Dressing
Grooming
Oral care
Toileting
Transferring
Walking
Climbing stairs
Eating
independence in activities of daily living (Table 5). As implied, it can also

be informative to know how often the elder actually engages in the activ-
ity. For many, the goal is to remain independent in one’s home, but this
often requires being able to manage a variety of affairs, including driving,
use of public transportation, or being able to climb stairs. It is also critical
not to overlook specific queries about alcohol, recreational drugs, or inap-
propriate use of pain or sleeping remedies, some of which are found over
the counter or may be prescribed but not closely managed.
Finally, an assessment about short- and long-term care goals, health
and family values, and health care proxy arrangements, such as living
wills, advanced life directives, and durable powers of attorney for health
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Geriatrics 503
care, is critical to include. Copies of executed instruments should be

placed in the patient chart and readily available for future need. If appro-
priate, discussion about end-of-life care wishes or options might also be
preliminarily addressed.
3.7. Review of systems

There is no substantial difference between the review of systems for the
younger and older adult. Standard questions about constitutional status
and all the major body systems are appropriate to pose even into advanced
age. However, it is useful to keep in mind that many medical conditions
will either manifest with associated behavioral changes or increase the
risk for development of a psychiatric disorder. The following outlines
some of the considerations to keep in mind (Table 6).

Data parameters to assess include basic vital signs (temperature, blood
pressure, heart rate, respiratory rate, pain, and if appropriate, pulse
oximetry); hearing and vision abilities; height, weight, and nutritional
status; and coordination of gait and balance. Primary sensory loss can
Table 6. Review of systems in the older mentally ill adult.

Body area Potential concern
Constitutional Energy, fever, night sweats, diaphoresis, sleep
Cardiovascular Shortness of breath, exertional dyspnea, fatigue, chest pain, palpitations
Pulmonary Cough, sputum production, wheezing, SOB
Gastrointestinal Weight changes, dyspepsia, reflux, abdominal pain, stool change
Genitourinary Urinary frequency, retention, pain, blood
Endocrine Hot or cold intolerance, malaise, skin or hair changes
Musculoskeletal Joint pain or swelling, weakness, muscle pain, poor healing sores
Neurologic Vision or hearing loss or changes, pins and needles, dizziness, LOC,
trauma
Psychiatric Sadness, worries, fears, panic, suspicions, personality changes
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504 R. Espinoza
have a significant impact on the daily functioning and cognitive ability

of an older person and may be easily correctable. Weight should be
followed periodically, especially when initiating medications with
known appetite suppressing or stimulating effects. Weight loss of more
than 10% over three months without dieting merits further investigation.
Older adults may not mount significant fevers due to temperature
dysregulation, so elevated temperature may not be a reliable marker of
infection. The physical examination focuses on acute processes and
must include at least an elemental neurologic examination (cranial
nerves, reflexes, and motor examinations). Patients on antipsychotic
medications should periodically be followed for development of tardive
dyskinesia or Parkinsonism. An Abnormal Involuntary Movement Scale
(AIMS) is a useful assessment to perform before initiating neuroleptic
drugs and every 3–6 months.
3.7.2. Mental status examination

The mental status examination, which starts when the patient enters the
room, continues throughout the interview, and incorporates observation of
the interaction between the patient and interviewer as well as between the
patient and environment, should specifically assess for suicidality, psy-
chosis, and impaired thinking. As during the interview, the patient should
be approached with respect and dignity, being called by his or her last
name, unless instructed otherwise. Walk alongside or lead the patient to
the room, being ready to give assistance for those who are frail or gait
unstable or have difficulty navigating a narrow passage. The area from the
lobby to the office should be well lit and throw carpets avoided. Rapport
should be established and the patient placed at ease, while clarifying his
or her understanding of the purpose of the interview. The patient, if capa-
ble and competent, should be offered an interview alone, in private, unless
he or she explicitly gives permission for others to attend the session or the
appropriate documentation is provided giving legal authority for others to
participate. In emergency matters or questions about safety, clinical judg-
ment must prevail.
When conducting the interview, questions should be directed to the
patient and ample time given for response. If a person has a hearing
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Geriatrics 505
problem, either ask for the patient to adjust his or her hearing aids if these
are worn or speak directly in front of the patient in a clear and loud, but
not shouting, voice. Should others try to interject, respectfully ask that the
patient first be given a chance to respond and say that their input will be
sought out separately or later. The standard areas covering appearance,
behavior, mood, affect, speech, thought process, thought content, and
insight and judgment should be covered over the course of the meeting
and then detailed during the testing portion. In the appropriate clinical
situation, be sure to specifically ask about psychotic thinking or suicidal
ideation. The former can be easily overlooked and often is in the older
individual. The elderly have the highest suicide rates of any population;
thus, suicide is a serious concern in the older age group and should be
carefully investigated. However, some individuals may find direct ques-
tioning uncomfortable or embarrassing, especially in front of family
members, so starting from a general question, such as “Is life still worth
living?” may be a way to sensitively open the subject for further explora-
tion, after which the standard suicide assessment can follow.
Various psychopathology screens can also be deployed during the
interview, and numerous instruments exist, some of which have been
translated into several languages, such as the Geriatric Depression Scale.
Long and short versions of many of these scales are available for use in
different settings and by different providers. Although not replacing a
clinical interview, which remains the gold standard for diagnosing a
mental disorder, screening instruments can help quantify the degree of
impairment or severity of illness and may be used to follow change to
treatment.
The cognitive portion of the mental status examination is one of the
most essential components, but it is important to keep in mind that clinical
judgment should direct the extent of cognitive testing. Some patients who
show minimal cognitive difficulty during the interview may not merit
more than a few additional questions assessing their understanding of
general affairs, gross orientation, and judgment. As clinical suspicion
rises, additional cognitive screening tools of varying complexity may be
utilized. Additionally, it can be helpful to ask the informant to rate the
patient because the patient may have a lack of awareness of deficits or
denial of illness, or while patients may state a capability, in reality he or
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Table 7. Comparison of cognitive screening tools for detection of dementia in older

patients.
Informant
Screening or patient Sensitivity/ Cut-off
tool* administered Specificity score comment
2-Questions Informant 97% / 61% 2 or 1 Useful since incorporates
from BDS caregiver input
4-Items from Informant or 60%/98% Varies Correlates well with
I-ADLs patient dementia probability
AD8 Informant or 84%/80% ≥2 Preferentially given to
patient informant; easy to use
CDT Patient 75%/76% ≤3 Correlates well with
driving ability
GPCOG Patient 85%/86% <5 Easy to use in primary care
settings
Mini-Cog Patient 97%/95% 3 Easy to use but not
sensitive to change
MOCA Patient 89%/87% 26 Improves upon MMSE; not
copyrighted
MMSE Patient 65%/94% 24 Copyrighted; misses early
dementia, frontal deficits
SPMSQ Patient 72%/87% 3–4 Easy to use in primary care
settings
*BDS: Behavior Disturbance Scale; CDT: Clock Drawing Test; GPCOG: General Practitioner
Assessment of Cognition; I-ADLs: Instrumental Activities of Daily Living (data for all 4-items);
MOCA: Montreal Cognitive Assessment; MMSE: Mini-Mental State Examination; SPMSQ: Short
Portable Mental Status Questionnaire.
she is not performing the activity regularly, if at all. Some of the most
commonly available screening tools and their characteristics are shown in
Table 7.
Ultimately, the cognitive screen is an aid to deciding if additional or
more formal neuropsychological testing is needed.17 The latter should be
reserved for patients with more pervasive cognitive deficits that are out of
proportion to what was expected, to help differentiate between a medical
or psychiatric etiology, to help in the differential diagnosis of an unusual
or atypical presentation, to better delineate the extent and pattern of cognitive
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Geriatrics 507
deficits and then to follow for change or stabilization of deficits after treat-
ment, to provide medico–legal documentation, or to establish a cognitive
baseline. It is important to keep in mind that appropriate timing of testing
is essential in order to achieve the best use and interpretation of neuropsy-
chological assessment. When the patient’s current condition would pre-
vent obtaining reliable testing information, such as during a delirious
state, or when stabilization of a temporary condition unrelated to the test-
ing question has not yet occurred, formal testing is not indicated.
3.7.3 Laboratory studies

Proper laboratory investigation must be comprehensive and judicious but
not necessarily exhaustive, at least not initially (Table 8). These tests are
best done in collaboration with the primary care or referring physician but
can be ordered directly, especially when the patient is hospitalized.
Patients with known medical illness presenting with new psychiatric
symptoms should have those studies appropriately directed at ruling out
recurrent medical illness. Acute and new psychiatric presentations merit a
more thorough review but should first be directed at the most commonly
occurring medical or neurological conditions and include screens for alco-
hol or other drug toxicities. A patient on a drug with a narrow therapeutic
index such as digoxin, lithium, or warfarin should have a drug level deter-
mined. In addition to standard medical care, a patient presenting after
overdose, especially if altered and uncommunicative, should have a urine
drug screen and blood studies for acetaminophen, aspirin, cardiac
troponin, liver function, coagulation, and ingested drug sent, in addition
to a 12-lead EKG, which should be done serially in the case of overdose
on tricyclic antidepressants, although ideally the patient may better be
monitored on continuous cardiac telemetry for the first 24 hrs. A patient
with head trauma, history of relevant neurologic condition, altered level of
consciousness, or new or focal neurological change merits a brain scan,
either a CT of the head (if presenting within 24 hrs of event or if an MRI
is contraindicated, such as with cardiac pacemakers) or an MRI of the
brain. However, even in patients with seemingly only minor attention or
confusion changes, a high suspicion for an intracranial process should
be held if the presentation or course appears otherwise psychiatrically
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508 R. Espinoza
Table 8. Laboratory considerations in the initial evaluation of the older psychiatric

patient.
Condition
New onset
Lab test* Anxiety Psychosis AMS Mood disorder Illness
Routine
• Electrolytes x x x x x
• Calcium x x x x x
• Magnesium x x
• CBC x x x x x
• BUN/Cr x x x x x
• LFTs x x x x
• TSH x x x x x
• ESR x x x x x
• Urinalysis x x x x x
• Pulse Oximetry x x x x x
• EKG x x x x x
• CXR x x x x
• CT/MRI x x x x x
Special
• Toxicology x x x x x
• Drug levels x x x x x
• RPR x x x
• HIV x
• Ammonia x x x
*CBC: complete blood count; BUN: blood urea nitrogen; Cr: creatinine; LFTs: liver function tests;
TSH: thyroid stimulating hormone; ESR: erythrocyte sedimentation rate; EKG: electrocardiogram;
CXR: chest x-ray; CT: computed tomography; MRI: magnetic resonance imaging; RPR: rapid
plasmin reagin; HIV: human immunodeficiency virus.
atypical. Patients with dementia are not immune from developing new
medical problems and should not receive substandard care. These patients
merit the same careful and thorough evaluation given their limited or
unreliable histories.
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Geriatrics 509
Should the first pass of investigation yield no evidence of an abnormal-

ity and the patient’s condition persist despite usual treatment or worsen,
then additional studies as listed may be needed. HIV infection, while not
a huge concern in the older population, nonetheless should not be over-
looked, especially because many people are now living longer with the
advent of effective antiviral regimens. With the aging of the baby boomers
along with iatrogenesis, older persons are now abusing controlled
substances to a greater degree, so that toxicology may have a role. Other
laboratories of potential benefit include Vitamin D 25-hydroxy level,
24-hour urine cortisol collection, cortrosyn stimulation testing, heavy
metal urine screen, ceruloplasmin level, and CSF studies. Other investiga-
tions might include EEG or functional brain imaging.
4. MAJOR PSYCHIATRIC DISORDERS

Each of the major psychiatric disorders reviewed in this section has been
more fully described in earlier sections. Here discussion is limited to spe-
cific issues that pertain to presentation, assessment, and management in
older adults.5 Unfortunately, specific information pertaining to ethnic
minority elderly remains sparse.16 Specific treatments are also discussed
separately in other chapters of this text.
4.1. Geriatric psychopharmacology

Before discussing each category of psychiatric disorders, it is useful to
consider some general principles of psychopharmacological management
of the older adult with mental illness. In addition to the concerns about
concurrent medical illness affecting presentation of a psychiatric disorder,
there are also separate age-related changes of pharmacokinetics and phar-
macodynamics to keep in mind, given the higher likelihood of use of
multiple medications in a large portion of the older population. The most
well-described and relevant pharmacokinetic and pharmacodynamic
issues are shown in Tables 9 and 10. Pharmacokinetics refers to the
absorption, distribution, metabolism, and excretion of a drug, while phar-
macodynamics refers to drug actions on the body and is responsible for
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510 R. Espinoza
Table 9. Relevant pharmacokinetic changes due to aging.

Age Effect Disease Effect Management Consideration
Absorption Usually unaffected Concurrent meds Drug–drug and drug–food/
in most may alter supplement may alter
absorption
Distribution Increase in fat: Increase fluid states Fat-soluble drugs have a larger
water ratio; like CHF, ascites volume of distribution; highly
decrease in plasma will increase body protein-bound drugs have a
protein, especially water greater free concentration
albumin
Metabolism Decreased liver Other conditions May account for use of lower
mass or blood like genotype, doses reaching same
flow slows drug alcohol, cigarette use therapeutic effect (can
metabolism have more effect confirm with blood levels)
Excretion Mainly a renal Decreased renal Watch closely, especially for
concern given age- clearance leads to water-soluble medications and
related decrease in longer half-life drugs with narrow therapeutic
GFR and steady-state index, e.g. lithium
concentrations
Table 10. Aging and pharmacodynamics.

CNS: sedation, confusion, disorientation, memory impairment, delirium
CV: hypotension, orthostasis, cardiac conduction abnormalities (arrhythmias, QTc
prolongation)
Peripheral anticholinergic effects: constipation, dry mouth, blurred vision, urinary
retention
Motor effects: EPS, tremor, impaired gait, increased body sway, falling
Other: agitation; mood and perceptual disturbances; headache; sexual dysfunction; GI
(N/V, anorexia, appetite changes, bowel habits); metabolic, endocrinologic, and electrolyte
changes
side effects, toxicity, and withdrawal reactions. Pharmacodynamic effects

are further a reflection of alterations in brain and body receptor sensitivity
and availability due to the changes of aging.
With the above in mind, general principles are that complete review of
medical status and of medications and supplements being used
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Geriatrics 511
is necessary; medications can be safely used in older persons but more

frequent monitoring is needed; a good strategy to follow is slow introduc-
tion of a medication but to continue adjustments every 3–5 days or as
tolerated until the usual therapeutic range is reached; side effects may not
be immediately evident; and a new illness or introduction of a new medi-
cation may make a previously tolerated medication intolerable.
4.2. Psychotherapy and other behavioral treatments

Despite the availability of effective and safe, if used appropriately, psy-
chopharmacological agents, it is critical not to overlook the utility and
benefit of non-pharmacologic approaches for many disorders afflicting
the older population. This is useful because some patients will have biases
against psychotropics, fear the notion of “mind-altering” effects of drugs,
may feel stigmatized if taking a psychotropic, may be medication sensi-
tive or intolerant, may prefer talk or behavior therapy over medications, or
may have different values or cultural beliefs that make drugs less desira-
ble, at least initially. Further, not all medications have the same demon-
strated efficacy in all older age groups; there remains a dearth of research
in use of psychotropics in the oldest-old; and some research shows that
some minor or mildly impairing conditions respond just as well or better
to non-pharmacological intervention, making psychotropics unnecessary.
Practically all psychotherapies have been investigated in the older popula-
tion, with most showing consistent benefit and acceptance. Of particular use
are manualized psychotherapies like CBT, Interpersonal Psychotherapy,
Grief Therapy, Problem-Solving Therapy, and Mindful Awareness Training,
as well as traditional supportive and psychodynamic therapies. These differ-
ent types can be applied across individual, couple, family, or group arrange-
ments and also across different practice settings, from office and hospital to
long-term care or home. In a related manner, day treatment or intensive
outpatient therapy programs can also be considered as viable options for the
older adult. A critical element is to ensure that the therapist has the requisite
background, training, and inclination to work with the older age group and
recognizes the special needs or accommodations due to illness or disability.
Recently, more research has also shown the benefits of socialization
groups and exercise regimens on a variety of conditions ranging from
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512 R. Espinoza
cognitive impairment to mood and anxiety disorders to general behavioral

disturbances. Benefits are seen not just on specific symptom and illness
measures but also on broader measures of stress, general well-being, con-
tentment, and happiness. These set-ups are particularly useful in providing
respite for over-stressed caregivers, mitigating against social isolation,
and fostering a sense of belonging. Many group programs are community-
based and provide transportation to the facility and can be government,
private, or religiously organized and run. Most provide programming
through the work week over the course of a standard business hour day
and according to the individual needs of the client. Nourishment is usually
provided, and sometimes medication monitoring or simple medical care
can be arranged.
4.3. Mood disorders

Mood disorders are common in the elderly population, albeit at a lower
prevalence than generally thought. Mood disorders include unipolar and
bipolar depression, dysthymia, subsyndromal depression, substance-
induced depression, and mood disorder due to general medical conditions.
In fact, in community-dwelling, healthy elderly the prevalence of clinical
depression is only about 1/3 the rate of the general adult population.
A recent study undertook to determine the 12-month prevalence rate of
depression across all ages in an international sample of 17 countries,
10 of which were classified by the World Bank as developed and seven
as developing.8 Abbreviated results are shown in Table 11.
Although, as expected, prevalence rates of depression in the over-65
group were lower and about half of that of younger groups in developed
countries, a surprising finding was that the exact opposite was true in
developing countries overall, but not uniformly. On closer look, a similar
lack of uniformity was also seen in developed countries. Prevalence rates
of depression in the older age group for Israel, Italy, and Spain did not
follow the overall combined prevalence rate comparison, and neither did
Brazil, Lebanon, or South Africa. The precise reasons for this variability
are unknown but likely reflect underlying cultural and sociological factors
and cannot be explained by increased confounding of depression symp-
toms with symptoms of chronic physical conditions. Another finding was
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Geriatrics 513
Table 11. Twelve-month prevalence of DSM-IV/CIDI major

depression by country, all ages and 65+.
Percentage %
Developed countries All 65+
Belgium 5.0 2.4
France 5.9 2.5
Germany 3.0 1.3
Israel 6.1 6.0
Italy 3.0 3.3
Japan 2.2 1.0
Netherlands 4.9 2.4
New Zealand 6.6 1.8
Spain 4.0 3.6
United States 8.3 2.6
Combined 5.5 2.6
Brazil 10.4 3.9
Columbia 6.2 5.9
India 4.5 5.2
Lebanon 5.5 3.1
Mexico 4.0 5.2
South Africa 4.9 3.5
Ukraine 8.4 13.0
Combined 5.9 7.5
8
Data from Kessler et al.
that in both developed and developing countries, duration of depression

increased with age; however, the severity of depression declined with age
in developed but not in developing countries. Unfortunately, this same
study found that for all groups with mental disorders, depression treat-
ment was lowest among the elderly in both developed and developing
countries. Thus, in developed countries community prevalence rates of
depression are generally lower, and although severity may decrease with
age, duration appears to increase. This latter situation may explain the
higher prevalence of subsyndromal depressive states in older adults.
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514 R. Espinoza
Nonetheless, even subsyndromal or minor depression places a burden on

an individual and increases the risk for subsequent conversion to major
depression.
While depression prevalence is low in community-dwelling, healthy
elderly, depression rates increase across more medically ill populations
and in various medical settings, although this has not been rigorously
studied in all international samples. Depression should be recognized
because it is a diagnosable and treatable condition.
Unfortunately, studies continue to show that depression in the elderly
remains under recognized, misdiagnosed, and both poorly and less
intensely treated. Many older persons, their families, or healthcare provid-
ers may also show therapeutic nihilism and attempt to explain away the
reasons for depression. However, an untreated mood disorder is associated
with poorer medical and psychiatric outcomes. Depression in later life is
associated with lower quality of life, prolonged suffering, more disability,
increased healthcare utilization and costs, and increased morbidity and
mortality. Psychiatric consequences of late-life depression include mental
health-related disability, increased risk of substance abuse, and increased
risk of suicide.6
Diagnosis of depression or any mood disorder in the medically ill
elderly patient may be particularly difficult due to the overlap of many
physical complaints with the symptoms of depression. Evaluation for the
psychological symptoms of depression such as depressed mood or sad-
ness, anhedonia, or loss of interests, feelings of guilt or worthlessness, or
suicidal ideation, or of behavioral equivalents such as crying, social
regression, or withdrawal can increase the specificity of diagnosis.
Neurovegetative symptoms like sleep disturbance, loss of appetite or
weight, psychomotor retardation, or fatigue are less specific for depres-
sion in medically ill elderly but may be considered attributable to depres-
sion if these worsen or co-vary with mood. An older person with
depression may develop severe cognitive impairment and appear demented.
These patients may be either in the prodrome of a dementia syndrome or
at higher risk of subsequently converting to a dementia syndrome and, in
any case, merit particular close attention. Screening instruments are avail-
able for use in the elderly population and include the Geriatric Depression
Scale, which is available in several item and language versions and is
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Geriatrics 515
validated across different settings; the Patient Health Questionnaire 9,

which has been validated in various older patient groups and settings; and
the Cornell Scale for Depression in Dementia. However, the gold standard
for diagnosis of depression remains a thorough clinical interview.

Anxiety disorders are among the most common yet poorly recognized and
diagnosed mental conditions in later life. While de novo anxiety disorders
are relatively rare in elderly persons, many patients live decades without
accurate identification. These patients in particular are at high risk for
self-medication with or abuse of alcohol, prescription drugs such as ben-
zodiazepines or opiates, or over-the-counter sedatives and pain relievers.
Often, these patients are only identified because of an alcohol-related or
medication-induced medical problem or withdrawal syndrome. However,
it is important to appreciate that anxiety may be a normal response to a
stressful life event or serious medical problem. Only when anxiety symp-
toms become too overwhelming, interfere with daily functioning, or
impair health or safety is psychiatric evaluation or intervention needed.
Finally, anxiety may be a component of a variety of medical conditions or
a manifestation of drug side effect or drug toxicity.
Another anxiety spectrum condition to consider in the older adult that
often is overlooked and remains poorly studied is PTSD, which can arise
from a multitude of experiences, including having a terrible or disfiguring
illness and dealing with the effects of treatment or difficult interventions;
surviving natural disasters like earthquakes, floods, and famine; contend-
ing with extreme social conditions like abject poverty; or living amidst
war and terrorism.9,12,18,19 Recent studies have shown both that PTSD is not
rare in the elderly population and that a lifetime diagnosis of PTSD is
associated with symptoms of depression and anxiety. Another study found
that Holocaust survivors of World War II still displayed significant psy-
chosocial and functional impairment throughout their later years.19 Only
recently have the effects of rape committed by soldiers on German women
at the end of World War II come to light, showing that even over 50 years
later, nearly a third met criteria for partial PTSD and carried a significant
psychological burden for decades.9 For veterans of World War II, a
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516 R. Espinoza
50-year prospective study of the psychological sequelae of combat found

premorbid vulnerability predicted subsequent psychopathology, though
not necessarily PTSD. Finally, a study in five countries of mental disor-
ders following war in the Balkans found that older age, female sex, and
having more traumatic experiences during and after the war were associ-
ated with higher rates of anxiety and mood disorders.12 Clearly, the effects
of trauma are profound and affect the elderly both acutely and chronically,
with imposition of lifelong burdens of distress and increased risk of later
life psychopathology.
4.5. Substance abuse disorders

Substance abuse and dependence disorders in the elderly remain poorly
understood, appreciated, and studied. The elderly may abuse alcohol, pre-
scription drugs like opiates and benzodiazepines, or over-the-counter
drugs and supplements. Like in younger populations, substance abuse in
the elderly significantly increases the risk for medical and psychiatric
morbidity and mortality. Prevalence estimates of the extent of substance
abuse in older populations are difficult to ascertain for a variety of rea-
sons. For example, identification of problem drinking in older patients is
challenging because alcoholism may be a hidden condition, diagnostic
criteria developed for younger populations may not apply to older groups,
and physicians may be reluctant to make a diagnosis in an older adult.2
While most problem drinkers began in early life, about 1/3 to 1/2 of older
people developed a problem with alcohol only later in life. Periods of high
risk include time around the death of a spouse or companion; stresses
around illness, loss of function, or life transitions; and development of
clinical depression. Additionally, many elderly may minimize or conceal
their extent of alcohol or drug use. Elderly patients with multiple condi-
tions may visit multiple providers and obtain multiple prescriptions. A
recent systematic review of screening instruments in the elderly found that
the Alcohol Use Disorders Identification Test (AUDIT) was useful for
detecting harmful and hazardous drinking, and the CAGE questionnaire
was valuable when screening for dependence.2
The elderly are more prone to the toxic effects of alcohol and drugs.
Due to physiologic changes of aging, older people have higher blood
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Geriatrics 517
levels of alcohol and drugs and manifest toxic effects more readily, such
as confusion, disorientation, memory loss, poor motor coordination,
unsteady gait, and more falls. Chronic alcohol use is associated with poor
nutritional status and with vitamin and protein deficiencies, which may
lead to peripheral and central nervous system disorders like motor palsies,
neuropathies, Wernicke’s encephalopathy, or Korsakoff’s psychosis.
Finally, consequences of alcoholism and unsupervised or inappropriate
drug use are serious, leading possibly to early deaths. In the elderly, drug-
alcohol interactions and withdrawal syndromes from central nervous
system depressants can be lethal.
4.6. Psychotic disorders

Primary psychotic disorders in the elderly include schizophrenia, schiz-
oaffective disorder, and delusional disorder. However, symptoms of
psychosis may manifest in other psychiatric conditions such as major
depression, substance-induced intoxication and withdrawal states, and
cognitive disorders such as dementia or delirium. Since DSM-IV, there is
no longer an age specification for schizophrenia onset, although interest-
ingly, it appears that older women may be at higher risk. Elderly patients
with late-onset schizophrenia, whose illness typically begins after age 60,
tend to have positive symptoms like paranoid delusions or hallucinations,
while negative symptoms, like alogia and apathy, and disorganized states
occur, in general, less frequently in older groups than in younger adults
and those elderly with early-onset disorder. The original assumption that
all patients with early-onset schizophrenia suffered unrelenting cognitive
deterioration (i.e. dementia praecox) is likely wrong, and some patients
remain remarkably stable over a lifetime. Late-onset schizophrenia, also
termed paraphrenia, may be more common in women and in patients with
primary sensory (vision and hearing) impairment and is marked by pre-
dominance of paranoid symptoms and less bizarre ideation. De novo
psychotic symptoms in later life may be a manifestation of underlying
central nervous system disease such as dementia, other neurodegenera-
tive disorders like Parkinson’s or Huntington’s diseases, stroke, inflam-
matory processes, infection, primary or metastatic cancer, seizure
disorder, or trauma.
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518 R. Espinoza
5. CONCLUSION
The older population is vast and heterogeneous, presenting a variety of
unmatched challenges, enormous complexity, and pressing needs within
limited resources. Soon in this coming decade, for the first time in history,
there will be more people in the world over the age of 65 than there are
younger than five years. The experience of aging across the globe varies
considerably, and psychological, sociocultural, and economic determi-
nants impact upon the quality of life in later years. Maintaining dignity,
respecting autonomy, and promoting self-determination, where culturally
and clinically indicated, are major goals in the care of the elderly, who are
particularly prone to ageism and stigmatization. Psychiatric disorders in
later life often must be evaluated in the context of on-going medical prob-
lems or complex social situations, so that comprehensive but judicious
care is warranted. Nonetheless, providing care for this population can be
a very intellectually satisfying and personally rewarding experience.
6. KEY POINTS
• Heterogeneity among individuals increases as they grow older, con-
tributing to unique life and medical histories and varied presentations
of illness.
• Aging is not synonymous with disease.
• Across the world, different cultures place different values on the lives
and care of the elderly.
• Common goals of healthy aging include optimizing function, enhanc-
ing quality of life, and remaining socially integrated in one’s home
and community.
• The essentials of care of the older adult include a thorough psychiatric
history, detailed medical and medication review, and comprehensive
mental status exam.
• Medical comorbidity affects the presentation, assessment, and man-
agement of psychiatric illness.
• The inappropriate use of medications and polypharmacy contribute
significantly to poor health and functional outcomes in the geriatric
population.
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Geriatrics 519
• Due to age-related changes, an older person may be more sensitive but

not necessarily less responsive to psychopharmacologic treatment.
• Psychotherapy, behavioral, and other non-pharmacologic approaches
should not be overlooked in the management of psychiatric disorders
in the older adult.
• Frequent communication and coordination of care among the older
patient, family, caregivers, and other healthcare providers are vital to
attaining the best healthcare outcomes.
7. SELF-ASSESSMENT
7.1. Which of the following is true?
(A) An inverted U-curve typifies the course of happiness over a lifetime.
(B) Because the perception of stress uniformly increases as we age, our
risk for mental disorders also uniformly increases.
(C) Older persons are less effective than younger persons at controlling
negative emotions, which explains the higher risk for depression in
later life.
(D) Because older adults cannot control negative emotions, their efficiency
performance on memory tasks declines.
(E) Older adults have a greater sense of well-being starting about middle-
age and continuing through their later years.
Recent research11,14,20,21 shows that our sense of well-being starts to rise in

our 50s and continues to rise through at least our 80s. The Happiness
curve is U-shaped, not inverted. Our perception of stress actually dimin-
ishes in later life despite our risk for increased health problems. Older
adults are much more efficient than younger adults at controlling negative
emotion, resulting in improved efficiency on memory tasks.
Answer: E
7.2. General true statements about the aging world population

include all the following except:
(A) The rate of increase in the aging population will be highest in devel-
oped countries in 2050.
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520 R. Espinoza
(B) Lower infant mortality rates account for some of the increase in the
older population worldwide.
(C) Across the world, women tend to outnumber men in later life.
(D) Differences in cultural attitudes toward aging explain some of the
variable experiences of growing older.
(E) Increased rates of death in men due to heart disease, lung cancer,
and violence account for the differences in gender longevity in later
life.
The rate of increase at double or triple will actually be highest in develop-

ing countries by 2050, although developed countries will still have a
higher overall percentage of the older population.4,22
Answer: A
8. CASE STUDIES
8.1. Depression in an older adult
A 78-year-old woman is brought in for consultation by her children
because she is more nervous, refuses to leave her house, and no longer is
cooking, cleaning, or marketing. During the interview the patient says life
is hopeless and she has no future. About an year ago her husband died, and
six months ago her closest sister also passed away unexpectedly. She feels
guilty about both deaths, thinking she could have saved them if she had
paid closer attention to their ailments. She is worried about finances,
becoming impoverished, and having no home, despite reassurances from
her children that her house is paid for and she has ample funds. While
denying suicidal ideation, she adds, “If I do not wake up tomorrow, it
would be okay. I am done.” She denied frank hallucinations.
Physical exam shows normal vital signs except for mild temperature
elevation. She appears undernourished and unkempt and has dry mucus
membranes. She has lost 10 pounds in one month. The remainder of her
physical and neurological exam is unremarkable. Mental status exam
reveals psychomotor slowing with increased speech latency. No parapha-
sic errors are noted. Her Montreal Cognitive Exam score is 25, but she
extends minimal effort. She has poor attention and missed items on recall
but did better with cueing. She refused to draw a clock or copy a cube. Her
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Geriatrics 521
mood is “terrible” and affect is congruent and constricted. Insight into her
illness is poor because she denies being depressed, and judgment is also
poor, because she refuses help and support.
Laboratory studies were normal except for elevated BUN and Cr and a
slightly elevated albumin but low normal prealbumin. TSH and urinalysis
were also normal.
The patient is given a diagnosis of Major Depression, severe with psy-
chosis, and admitted to hospital due to her dehydration and nutritional
compromise. Given the relative urgency, ECT is recommended, and she
agrees. After eight sessions, she is remarkably improved, no longer fixated
on finances, and feels as if life with her children and grandchildren will
keep her quite busy. She is discharged to continue outpatient psychiatric
care and will enroll in a day treatment program.
8.2. Adjustment disorder in an older adult

A 66-year-old man is referred by his primary care provider for evaluation
of mood. He notes that the man had usually been in good spirits and rela-
tively healthy, but for the last two months, he has called his office every
couple of weeks asking about minor ailments and requesting more fre-
quent visits. While his physician thought he might be depressed, the
patient denied feeling sad or hopeless, so his physician wonders whether
treatment is needed, and if so, what type.
On evaluation, he speaks of all his free time since his retirement three
months ago but admits to being bored and having no hobbies. Although
his wife is supportive, she maintains her own schedule and encourages
him to get out more on his own. He notes no changes in energy, appetite,
or memory. However, recently he has found himself more restless and
disquieted about seemingly minor matters. For the past month, he has had
trouble with sleep and does not feel rested the next day. He now wonders
whether he should have retired or waited until he was older. In retrospect,
he did not feel ready to let go of work.
A diagnosis of adjustment disorder, anxious type, is made. The patient
is interested in a short-course of psychotherapy to help him through this
period of adjustment, so the clinician recommends interpersonal psycho-
therapy, prescribe an exercise regimen, and counsels him on sleep
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522 R. Espinoza
hygiene, as well as screens for alcohol abuse. In eight visits the man’s
symptoms have resolved and he enrolls in a sculpting class.
REFERENCES
1. Agronin ME, Maletta GJ. (2006) Principles and Practice of Geriatric
Psychiatry. Lippincott Williams & Wilkins, New York.
2. Berks J, McCormick R. (2008) Screening for alcohol misuse in elderly
primary care patients: A systematic literature review. Int Psychogeriatr
20(6): 1090–1103.
3. Blazer DG, Steffens DC. (2009) Textbook of Geriatric Psychiatry, 4th ed.
American Psychiatric Publishing, Inc., Washington, DC.
4. Haub C. (2007) The 2007 world population data sheet. In: Population
Reference Bureau. Available at: http://www.prb.org/publications/datasheets/
2007/2007worldpopulationdatasheet.aspx. Accessed on May 12, 2010.
5. Jimenez DE, Alegría M, Chen CN, et al. (2010) Prevalence of psychiatric
illnesses in older ethnic minority adults. J Am Geriatr Soc 58(2): 256–264.
6. Juurlink DN, Herrmann N, Szalai JP, et al. (2004) Medical illness and the
risk of suicide in the elderly. Arch Intern Med 164(11): 1179–1184.
7. Katona C, Chiu E, Adelman S, et al. (2009) World psychiatric association sec-
tion of old age psychiatry consensus statement on ethics and capacity in older
people with mental disorders. Int J Geriatr Psychiatry 24(12): 1319–1324.
8. Kessler RC, Birnbaum HG, Shahly V, et al. (2010) Age differences in the
prevalence and co-morbidity of DSM-IV major depressive episodes: Results
from the WHO world mental health survey initiative. Depress Anxiety 27(4):
351–364.
9. Kuwert P, Klauer T, Eichhorn S, et al. (2010) Trauma and current posttrau-
matic stress symptoms in elderly German women who experienced wartime
rapes in 1945. J Nerv Ment Dis 198(6): 450–451.
10. Lai DW. (2009) Older Chinese’ attitudes toward aging and the relationship to
mental health: An international comparison. Soc Work Health Care 48(3):
243–259.
11. Mickley KR, Kensinger EA. (2009) Phenomenological characteristics of
emotional memories in younger and older adults. Memory 17(5): 528–543.
12. Priebe S, Bogic M, Ajdukovic D, et al. (2010) Mental disorders following war
in the Balkans: A study in 5 countries. Arch Gen Psychiatry 67(5): 518–528.
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13. Reifler BV, Cohen W. (1998) Practice of geriatric psychiatry and mental
health services for the elderly: Results of an international survey. Int
Psychogeriatr 10(4): 351–357.
14. Ross CE, Mirowsky J. (2008) Age and the balance of emotions. Soc Sci Med
66(12): 2391–2400.
15. Scheibe S, Blanchard-Fields F. (2009) Effects of regulating emotions on
cognitive performance: What is costly for young adults is not so costly for
older adults. Psychol Aging 24(1): 217–223.
16. Shah A, Doe P, Deverill K. (2008) Ethnic minority elders: Are they neglected in
published geriatric psychiatry literature? Int Psychogeriatr 20(5): 1041–1045.
17. Shulman KI, Herrmann N, Brodaty H, et al. IPA survey of brief cognitive
screening instruments. Int Psychogeriatr 18(2): 281–294.
18. Spitzer C, Barnow S, Völzke H, et al. (2008) Trauma and posttraumatic stress
disorder in the elderly: Findings from a German community study. J Clin
Psychiatry 69(5): 693–700.
19. Stessman J, Cohen A, Hammerman-Rozenberg R, et al. (2008) Holocaust
survivors in old age: The Jerusalem longitudinal study. J Am Geriatr Soc
56(3): 470–477.
20. Stone AA, Schwartz JE, Broderick JE, Deaton A. (2010) A snapshot of the
age distribution of psychological well-being in the United States. Proc Natl
Acad Sci USA 107(22): 9985–9990.
21. Sullivan SJ, Mikels JA, Carstensen LL. (2010) You never lose the ages
you’ve been: Affective perspective taking in older adults. Psychol Aging
25(1): 229–234.
22. United Nations (UN), World Population Ageing: 1950–2050. Available at:
www.un.org/esa/population/publications/worldageing19502050. Accessed
on November 22, 2010.
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Chapter 21
Emergency Psychiatry
Divy Ravindranath, Mark Newman and Michelle Riba
1. INTRODUCTION
Psychiatric emergencies are acute clinical situations that demand immedi-
ate assessment, evaluation, and treatment. Psychiatric emergencies may
occur at any time, at any place, and really, to any person. They can arise
after a long period of observation or over a very short duration. When psy-
chiatric emergencies are perceived by the identified patient, the patient’s
family or friends, clinicians, police, bystanders, or others, a response is
invoked that usually includes a referral for emergency psychiatric
evaluation.
Common psychiatric emergencies include suicidal ideation or suicidal
behavior; danger to others based on psychiatric problems; inability to care
for oneself related to a mental condition; or acute mental status changes.
These may be due to an underlying medical condition (metabolic abnor-
mality, infections, cerebrovascular condition, etc.); new onset psychotic
disorder; substance use; depression or bipolar disorder; anxiety; dementia;
and/or adjustment issues.
The goals for psychiatric emergency care are to provide access to care;
deliver timely care; assure safety and stabilization; and provide appropri-
ate treatment and continuity of care.4 The type of psychiatric emergency,
settings, nature of the problem, and availability of resources will all drive
how to best provide the evaluation and management. Triaging to another
524
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Emergency Psychiatry 525
facility, waiting to get more information from family or treating clinicians,

referral for further diagnostic or medical services may all impact what is
often one of the most complex clinical situations in psychiatry.
Emergencies can occur in medical offices, on the street, in places of
worship, in schools, in nursing homes, and so on. While psychiatric emer-
gency services or medical emergency departments are the places for
optimal triage, it is important to recognize that all clinicians must be ready
to quickly determine if there is a psychiatric emergency and then how to
stabilize the patient and get to the next level of appropriate care.
This chapter will serve to provide an overview on the approach to the
evaluation and management of a patient in the context of a psychiatric
emergency. The key element is to develop rapport with the patient. This is
essential — that the patient is able to have hope and trust that there can be
safe resolution to the current problems by working with the clinician. The
astute clinician must quickly assess current issues, what predisposing
conditions might be impacting the current problems, and determine best
ways to engage the patient. The clinician must identify important treat-
ment interfering problems, such as agitation, that must be addressed first,
for they risk inhibiting construction of rapport. Through careful and delib-
erate evaluation, assessment of mental status, evaluation of other medical
problems, and attention to safety, the clinician is building a database that
can be used to make a thorough differential diagnosis, treatment plan, and
disposition.
For purposes of simplicity, the chapter is written from the perspective
of an evaluation in an emergency department — the intersection between
outpatient and inpatient care. However, we ask that the reader keep in
mind the setting of their particular emergencies with application of prin-
ciples from this chapter as appropriate.
2. APPROACH TO THE PATIENT

2.1. Building rapport
As with any psychiatric intervention, establishing rapport is critical to
evaluation and management of a psychiatric emergency. In contrast to
patients in other settings, these patients are perhaps more likely to be
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526 D. Ravindranath, M. Newman and M. Riba
opposed to the interaction with mental health providers. Patients who are
actively psychotic may be paranoid about the treatment team. Manic
patients may be unaware of the danger of their mental condition. Severely
depressed patients may be bent on suicide or near catatonic, each of which
presents a different challenge. Moreover, the provider attempting the
interaction is generally under significant time pressure and this provider
will rarely have a longitudinal relationship with the patient to draw upon
in attempting to get the patient to tell their story. In all, attempting to build
rapport in the emergency department can be challenging and yet it is
essential to eliciting the history needed to stabilize the patient.
Patients in distress do want to have their situation understood by
another person. As such, the task of establishing rapport is not insur-
mountable. The patient should be addressed with respect and in a non-
threatening manner. The history should be initially elicited using open
ended questions so that the patient can relate their experience in a narra-
tive fashion and generate a framework for the patient’s history of present
illness. The use of active listening and empathetic reflection can help the
patient feel heard and may promote additional detail. Any issues of physi-
cal comfort, such as the need for food or water, can be addressed to the
degree possible while maintaining safety. Providing for these needs may
also help build the patient’s trust in the treatment team. Closed ended
questions can then be used to fill in the details of the history of present
illness.
At times, the examiner may feel compelled to challenge the patient’s
statements. However, this is not done without cost. For example, a psy-
chotic patient may express fear that a secret government organization is
out to get him, prompting the provider to reassure the patient that there is
no such government organization. However, a challenge of this sort may
make the patient feel that they are not being believed and, in turn, may
rupture the fragile therapeutic relationship. The patient may even incorpo-
rate the examiner into their paranoid delusions. In this circumstance,
it may be a better idea to empathize with the patient’s fear rather than
reassure the patient of the facts of his situation. However, if the rapport
is judged to be strong enough, a gingerly delivered challenge may provide
critical diagnostic information. For example, if the patient in this example
agrees with the challenge and questions the thoughts about the government
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organization, then those thoughts may come from a cognitive distortion,

perhaps driven by anxiety, rather than a paranoid delusion.
As the rapport builds, then the patient can be asked to participate
in more intrusive aspects of the evaluation. Examples include performing
a physical examination, obtaining blood or urine for laboratory testing, or
requesting contact information for friends or family members who may be
helpful in resolving the emergency.
2.2. Management of agitation

Patients may become agitated in the course of their evaluation. As detailed
in Table 1, a number of behaviors may be considered evidence of agitation.
A mildly agitated patient may exhibit only one or two of these behaviors,
though a severely agitated patient will exhibit many of these behaviors.
Apatient may be agitated before the evaluation even begins. For example,
a patient brought forcibly or under false pretences for the emergency
evaluation may be agitated simply by the fact that their freedom has been
curtailed. Alternatively, the patient may become agitated in the waiting
area before seeing the examiner. As such, all individuals who work with
psychiatric patients, including physicians, nurses, psychologists, social
workers, and even office staff, should be trained in the recognition of agi-
tation, and every work setting should have a plan for communicating that
there is an agitated patient and for initial management of the situation.18
Table 1. Signs of agitation.
Verbal Behavioral
Increased volume Increased muscle tension
Tense or sarcastic tone of voice Glaring eye contact
Coarsening of vocabulary Clenching fist or jaw
Demanding content Pacing
Insults or personal attacks Inability to sit still
Threats Pointing
Pushing
Striking
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Recognition of agitation is important for two reasons. First, agitation

may be an outward representation of crumbling rapport. Second, an
agitated patient is at greater risk of violence, including violence towards
the treatment team.
Agitation should first be addressed verbally. For example, the examiner
may simply point out to patients that they are engaging in an agitated
behavior, such as pacing or yelling. Alternatively, the examiner may inter-
pret this behavior as evidence of internal unrest and then point this out to
the patient; for example, the examiner may say “Your pacing makes me
think that you are upset about something.” This will hopefully open a
dialog with patients about the reason for their unrest, revealing needs that
can be addressed to reduce the agitation. As discussed above, this should
be done with compassion and in a non-threatening and non-judgmental
manner.14
The patient may be offered medications to help with the agitation at any
time. If the patient and the treatment provider continue to hold a good rap-
port, then the patient may be willing to take a medication orally or via
orally dissolving tablet.23 Orally dissolving tablets carry an advantage over
oral tablets or capsules because they cannot be “cheeked.” They dissolve
in the patient’s saliva and are swallowed along with oral secretions. If the
patient is not cooperative enough to take an oral medication, then one of
many medications may be administered parenterally. Parenteral medica-
tions are advantageous in that they manifest a clinical effect in shorter time
and require less patient cooperation for administration, but do risk injury
or infection to the patient if improperly administered or injury to the treat-
ment team, for example, a needle stick injury. Table 2 details medications
commonly used in the management of agitation, including available routes
of administration. Dosages listed assume that the agitated individual is an
otherwise healthy non-delirious adult. Children, the elderly, and patients
with medical illness should receive lower doses of medication.
Despite best efforts, agitated patients may become acutely dangerous
to themselves or to others, such as members of the treatment team.
Patients who cannot refrain from hurting themselves or others may
warrant seclusion in a safe area or the use of restraints. It is important to
note that regulations governing these interventions vary from locality to
locality.
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Table 2. Medications used in the management of agitation.
Medication name Routes of administration

Aripiprazole 5–10 mg PO, ODT, IM
Chlorpromazine 10–25 mg PO, IM, IV
Haloperidol 2–5 mg PO, IM, IV
Olanzapine 5–10 mg PO, ODT, IM
Risperidone 1–2 mg PO, ODT
Ziprasidone 10–20 mg PO, IM
Alprazolam 0.25–1 mg PO
Diazepam 5–10 mg PO, IM, IV, PR
Lorazepam 0.5–2 mg PO, IM, IV
Promethazine 25–50 mg PO, IM, IV
Benztropine 0.5–1 mg PO, IM, IV
Diphenhydramine 25–50 mg PO, IM, IV
(PO: oral, ODT: orally dissolving tablet, IM: intramuscular, IV: intra-
venous, PR: rectal).
These interventions are also not without their cost. Secluded patients
experience a dramatic transgression of their right to free movement.
Moreover, secluded patients can still injure themselves by throwing them-
selves against the walls or by striking themselves, and, as such, this may
be an insufficient intervention when addressing a patient at acute risk of
self-injury. Restrained patients may injure themselves when fighting
against the restraints.11 As such, these patients need to be closely moni-
tored, including regular medical monitoring, for prevention of morbidity
or mortality. Finally, administration of seclusion and/or restraint carries a
very high risk for injury to the treatment team. This should only be done
by trained individuals and should only be done when there are a sufficient
number of trained individuals present to execute the intervention.
As discussed previously, agitated patients are at risk of committing
violence against their examiners. Aside from recognition of agitation, risk
of violence against an examiner can be reduced in a number of ways. First,
the physical environment in which the evaluation is taking place can be
designed in a manner that prevents violence. For example, the patient could
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be interviewed in a room without small objects, such as desk lamps, that

could be used as weapons. Second, the physical environment could afford
easy escape for both the patient and the examiner in the event of escalating
agitation. Agitated patients may prefer to flee rather than fight, and easy
egress allows for this. Third, when a potentially agitated patient is identi-
fied, the examiner may elect to conduct the interview with another person
present. Agitated patients are agitated but not necessarily so grandiose that
they think they can overwhelm a numerical advantage; the presence of
strength in numbers may dissuade the agitated patient from enacting vio-
lence. For this very reason, the examiner should also have a low threshold
to leave an escalating situation to get help for de-escalation.18
2.3. Evaluation
The critical assessment question in any psychiatric emergency is
whether or not the patient experiencing an emergency that can be
resolved in the current setting of care or whether the patient will need a
higher level of care. For example, a crying patient encountered in a
clinic may be effectively consoled there, but a suicidal patient in the
same setting may need further evaluation in an emergency department.
Additionally, patients who are newly psychotic and unable to care for
themselves may warrant psychiatric hospitalization until the reason for
the psychosis can be identified and resolved and until social supports
can be established to prevent relapse of the psychosis after discharge.
The examination of the patient should be conducted with this critical
assessment question in mind.
It is important to note that critical elements of the history and examina-
tion will be obtained during the process of generating rapport and address-
ing agitation. As such, the examination should not be conceptualized as an
independent or secondary phase of the interaction.
The exact criteria for psychiatric hospitalization will vary from emer-
gency to emergency. However, the guiding concept is that hospitalization is
warranted for patients who cannot protect themselves without this level of
supervision or for patients who would be too much of a threat to the society
at large if they were not hospitalized. The following section of this chapter
goes into additional detail regarding common psychiatric emergencies.
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2.3.1. General medical evaluation

It is important to note that a behavioral aberration may have at its root an
uncontrolled medical condition. For example, a patient may be severely
depressed secondary to an endocrine abnormality, like hypothyroidism.
Alternatively, a patient may be experiencing chest pain and anxiety sec-
ondary to a progressing myocardial infarction, rather than due to a panic
attack. Therefore, the complete examination of a patient in a psychiatric
emergency must include at least a basic medical examination.
The examiner should elicit the patient’s past medical history, any medi-
cations used for chronic medical conditions, and, if these symptoms are not
incidentally discovered, a physical review of systems focusing on concern-
ing symptoms. Concerning symptoms may include fevers, chills, rapid
weight loss, headaches, sudden onset vision or hearing changes, cough,
shortness of breath, chest pains, palpitations, abdominal pain, nausea, vom-
iting, anorexia, hemoptysis, blood per rectum, changes in bowel or bladder
pattern or control, sudden onset weakness or numbness, or sudden onset
changes in speech pattern. The patient’s vital signs, such as temperature,
heart rate, blood pressure, respiratory rate, and pulse oxymetry (if availa-
ble), should be checked and a screening physical examination should be
performed. Depending on local practice patterns and index of suspicion,
the provider may also elect to obtain screening laboratory tests, such as a
complete blood count, basic metabolic panel, or thyroid stimulating hor-
mone level. The examiner may also elect to obtain a urine or serum drug
or alcohol screen to evaluate for a behavioral aberration secondary to sub-
stance ingestion or withdrawal. Medical specialists may need to become
involved in the case to adequately evaluate the patient along these lines.
2.3.2. Psychiatric evaluation

The psychiatric evaluation should focus on the presenting complaint and
associated symptoms. This includes the time course and changes in sever-
ity of these symptoms, and any exacerbating or relieving factors. The
patient’s past psychiatric history should be elicited, including any prior or
current diagnoses, prior attempts at self-harm or harm to others, prior
psychiatric hospitalizations, and the names of prior and current treatment
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providers. The patient should be asked whether they currently or in the

past use any substances of abuse or alcohol. A family history for psychi-
atric conditions, including a history of suicide attempts, should be
obtained. Moreover, the patient’s should be asked whether they work, with
whom they live, and who they consider to be in their support network.
A mental status examination can help the examiner refine the assess-
ment. It should focus on the patient’s overall insight, demeanor, and atti-
tude towards the examiner; any psychomotor aberrations; the patient’s
mood and affect; the patient’s thought process and thought content, with
special attention to any obsessional or perseverative thoughts such as sui-
cidal or homicidal thoughts, or thoughts reflective of psychosis such as
paranoid or grandiose delusions or sensory hallucinations. If a cognitive
disturbance is suspected, then the examiner may also elect to perform a
standardized screening cognitive examination, such as the Folstein Mini-
Mental Status Examination8 or the Montreal Cognitive Assessment.17
Given that the patient’s mental state may obscure their capacity to pro-
vide a complete history, the use of collateral informants is critical. These
collateral informants may include any individuals who accompanied the
patient to the evaluation, the patient’s current treatment providers, or
friends and family. These individuals can confirm or refute the patient’s
reports, fill in absent details, and may even be able to provide a longitudi-
nal sense of the patient and take responsibility for the patient after they
leave the evaluation. The issue of patient privacy is an important one to
consider when contacting collateral informants, and some countries have
laws that prevent sharing confidential patient information with others
without the patient’s consent. However, in an emergency situation, the
need for information to safely treat the patient may outweigh the patient’s
privacy concerns. Regardless, collateral information should be sought
with the patient’s consent if possible and with protection of the patient’s
privacy in mind by revealing as little of the patient’s information as
possible.15
2.3.3. Culture-bound syndromes

Culture-bound syndromes are clusters of symptoms that are considered
an illness within a particular ethnic group, but seen infrequently outside
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of that group.1 Some of these syndromes may constitute psychiatric

emergencies.
Amok refers to an outburst of violent, aggressive, or homicidal behav-
ior, followed by a return to the premorbid state. Dissociative symptoms
and amnesia may be present. This phenomenon was originally described
in Malaysia and the Philippines, though similar behavior is seen in other
cultures.19
Ataque de nervios describes a constellation of symptoms that resemble
panic attacks in some ways. Episodes typically occur in the context of
stressful life events. Patients describe uncontrollable crying, trembling,
shouting, and a sensation of heat in the chest. A sensation of fear and
impending doom are typically absent, however. This syndrome is associ-
ated with individuals of Hispanic descent, particularly from the Caribbean
region.
Koro is a sudden episode of anxiety in which the patient believes their
genitals have receded into their body. This has been described primarily
in China and Southeast Asia.16
Another culture-bound syndrome seen primarily in China is the qi gong
psychotic reaction, which consists of acute, self-limited episodes of
dissociative or psychotic symptoms that are associated with qi gong, a
Chinese folk health practice.
As with any psychiatric emergency, assurance of safety and stabiliza-
tion of acute symptoms, in the current care setting if possible, are the
primary goals. Diagnostically, it is important to determine whether the
patient’s presentation is consistent with cultural norms. For providers with
different cultural backgrounds, collateral informants can also be cultural
informants to aid with this task.
3. RISK MANAGEMENT FOR COMMON PSYCHIATRIC

EMERGENCIES
3.1. Dangerousness to self
3.1.1. Definition
Suicidality encompasses a broad spectrum of thought and behavior. An
individual may simply wish they could go to sleep and not wake up the
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next day, they may fantasize about various ways to die, they may develop
a specific plan to end their life, and they may then carry out that plan.
3.1.2. Risk factors

An individual’s risk for suicide at a given time depends on multiple fac-
tors, interacting in a synergistic rather than summative fashion. In the
emergency setting, the primary task is to identify individuals with acutely
elevated risk. This group includes patients in major depression with
comorbid alcohol abuse, anxiety, and/or hopelessness; patients with bipo-
lar disorder especially in a mixed episode; and patients with schizophrenia
or schizoaffective disorder who have recently been hospitalized. These
and other significant risk factors are delineated in Table 3.
Management decisions depend largely on the results of a thorough suicide
inquiry. Important elements include the frequency and intensity of suicidal
ideation. An obsessive quality and presence of a considered plan suggest
higher intensity and therefore risk. In addition, a plan involving highly lethal
means and access to these means, or one that the patient has rehearsed sug-
gests greater risk. The details of a patient’s suicide history are also critical;
in addition to number of attempts, the severity of prior attempts is important
to assess. Markers of severity include admission to a medical unit, loss of
consciousness, and lasting tissue damage. When considering a patient’s
Table 3. Static and dynamic risk factors for suicide.

Static Dynamic
Demographic (male gender, older in age) Hopelessness
Prior suicide attempt Impulsivity
Family history of suicide Personal loss
Chronic physical illness Interpersonal conflicts or social isolation
History of physical or sexual abuse Active alcohol or drug abuse
Major psychiatric illness (e.g. major Active psychiatric illness (e.g. major
depression, bipolar disorder, depressive or mixed episode,
schizophrenia, etc.) uncontrolled psychosis, etc.)
Access to firearms
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suicide risk, these factors should be weighed against protective factors

including positive social support, life satisfaction, and religious prohibitions.
3.1.3. Management
Determining the appropriate treatment setting is the most important
decision in the emergency setting. The options available to clinicians vary
between nations, as do the criteria for involuntary and voluntary hospitali-
zation. However, inpatient treatment is indicated for high risk suicidal
patients. A 2005 study of clinical decision making at a psychiatric emer-
gency unit in Madrid, Spain found six variables associated with hospitali-
zation: intention to repeat the attempt, a highly lethal method, low
psychosocial functioning, previous hospitalization, previous suicide
attempt, and belief that nobody would try to save their life.3 For lower risk
patients, issues such as availability of outpatient follow-up and social sup-
port often determine disposition. These also depend heavily on specific
treatment setting and healthcare services that vary between countries.7
Since the advent of dialectical behavioral therapy (DBT), emergency
management of patients with acute suicidality superimposed on chronic
suicidal ideation has changed. Outpatient management of these patients may
be in their best interests in the long term, though the emergency psychiatrist
is still responsible for at least ameliorating the acute exacerbation in suicidal
ideation. A DBT-informed approach may be useful in this situation. Please
see Chapter 27 for further guidance regarding suicidal ideation.
3.2. Dangerousness to others

3.2.1. Definition
While all physicians have a shared responsibility to protect the safety of
their patient, psychiatrists frequently face the additional burden of protect-
ing individuals whom they have never met. These may be specific indi-
viduals at the focus of a patient’s homicidal ideation, or they may be
hypothetical members of the public, in the case of an impulsive and dis-
organized patient. However, despite common perceptions of psychiatric
patients as frequently violent or predatory, there is little evidence that
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psychiatric disorders themselves are major risk factors for violence

toward others.13 In fact, patients with mental illness are more likely to be
the victims of violence.2
3.2.2. Risk factors

There are both unchangeable and changeable risk factors for dangerous-
ness to others. The most important static risk factor is a history of violent
behavior. Certain characteristics of that behavior, i.e. whether it was pre-
meditated or impulsive, or directed toward family or strangers, can be
valuable information. Another major static factor is a history of substance
addiction, which elevates an individual’s risk of violence more than either
psychotic or mood disorders.21
Dynamic risk factors are temporary, often modifiable, factors that
increase acute risk of violence. The most important dynamic risk factor is
access to firearms. Others static and dynamic risk factors are listed in
Table 4.
3.2.3. Management
The risk assessment for violence toward others is similar to that for sui-
cidal risk. The immediate concern is ensuring a safe environment for the
patient, staff, and any others in the area. This includes a thorough search
of their person for potential weapons and treatment of agitation.
Table 4. Static and dynamic risk factors for homicide.

Static Dynamic
History of violent behavior Access to firearms
History of substance abuse or dependence Social isolation
History of abuse as a child Inability to meet housing and financial needs
Multiple psychiatric hospitalizations Delusions of paranoia or thought control
(over ten)
Previous military service Medication non-compliance
Male gender Unemployment
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The psychiatric interview should focus on the content and characteris-

tics of on-going homicidal ideation and identification and reduction of
any present risk factors. Unlike suicidal ideation, a patient with homicidal
ideation may not identify this ideation as their chief complaint. Instead,
the possibility of homicidal ideation may need to be inferred based on
risk factors identified above combined with hostile or aggressive com-
ments or behaviors. As with suicide, the presence of a considered plan is
cause for greater concern. The presence of multiple risk factors should
also weigh into the decision about the level of care needed for any given
patient.
While there are standardized models to estimate lifetime risk of vio-
lence toward others, predicting acute risk remains a difficult clinical
decision involving the balancing of protective and risk factors.
4. PSYCHOSIS
4.1. Definition
Psychosis refers to disordered thought and behavior, often manifesting as
hallucinations, delusions, and thought process disturbances. Hallucina-
tions, the perception of something when there is no clear stimulus, can be
in any sensory domain — auditory, visual, tactile, gustatory, and olfactory.
Moreover, patients may have illusions, defined as the misinterpretation of
a sensory stimulus; for example, a delirious patient may see an IV pole as
a long lost relative. Delusions are fixed false beliefs that are incongruous
with the patient’s culture. Common delusions fall into paranoid, grandi-
ose, hyper-religious, or somatic themes. In contrast to distortions that may
be driven by mood or anxiety conditions, delusions tend to get stronger
when they are challenged with logic. Thoughts may be tangential, loosely
associated, circumferential, concrete, derailed, or some combination of
these features.
Psychosis is a symptom that may result from several primary psychiat-
ric disorders, general medical conditions, and substance use. Rapidity of
onset tends to point towards a general medical or substance related etiol-
ogy to the psychosis. This is a particularly important consideration in the
emergency setting.
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4.2. Risk factors

In the United States, psychosis is a common reason for presentation to
emergency departments, representing about one per cent of all ER visits
and one-fifth of psychiatric related visits.10 There is some evidence that
similar figures are seen in other developed countries.6
This high incidence is partly due to the numerous disease entities that
present with acute psychosis. These include schizophrenia, mania in bipo-
lar disorder, major depression with psychosis, schizoaffective disorder,
dementia, and substance-induced psychosis. Medical conditions such as
CNS infections, electrolyte abnormalities, or endocrine dysfunction may
cause delirium, a syndrome that can feature psychotic symptoms.
In addition, the incidence of psychosis is elevated by the fact that indi-
viduals with primary psychotic disorders tend to suffer multiple exacerba-
tions over time. Medication non-compliance is a major reason for this, and
is itself correlated with risk factors such as poor insight, substance abuse,
negative subjective response to medication, and poor therapeutic alliance.
Stressful life events also appear to be associated with acute decompensa-
tions, particularly early in the illness course.
4.3. Management
One of the earliest decisions to make, prior to a full psychiatric assess-
ment, is whether a patient is medically stable. The somatic complaints of
psychotic patients should not be dismissed lightly, as there is significant
evidence that patients with primary psychotic disorders have higher rates
of medical comorbidity than the general population.22 Moreover, a serious
medical illness may present first with psychosis, especially in an other-
wise mentally well individual. Concern for serious illness should result in
referral for appropriate medical evaluation, with the mental health profes-
sional clearly articulating their concerns to medical staff.
A full psychiatric evaluation is often difficult to complete in frankly
psychotic individuals; however it is important to gather as much informa-
tion as possible about the patient’s current symptoms. When auditory hal-
lucinations are present, important points include the number of voices,
whether they speak directly to the patient, and whether they command the
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patient toward certain actions. Any of these features indicate more serious
psychotic symptoms, and therefore higher risk. Patient’s actions prior to
the encounter and in response to challenges of suspected delusions as well
as the content of their hallucinations may inform the assessment, even
when the patient denies having delusions. When the patient is unwilling
or unable to provide relevant history, gaining collateral information from
medical records, outpatient providers, and family members is critical.
Psychotic patients are at higher risk of being agitated and, due to their
psychosis, they may be less amenable to verbal redirection. As such, treat-
ment providers should have a low threshold for use of medications, espe-
cially antipsychotic medications, in the management of agitation as
discussed above.
After full evaluation, the primary management decision is whether the
patient requires admission. This decision is based not only on careful risk
assessment, but also on the patient’s likely compliance and the level of
services available in the community. Thus, a patient who is too psychotic
to be able to care for themselves or receive care in the community should
be considered for inpatient treatment. However, a patient with good
capacity to access social supports, e.g. treatment providers who are trusted
even when the patient is paranoid, and with rapid access to outpatient
appointments may be safely treated in the community. Moreover, medica-
tion adjustments based on the ER evaluation may help keep the patient’s
psychosis under control until they can meet with their customary treat-
ment providers. For further discussion, please see the chapter on psychotic
disorders.
5. MANIA
5.1. Definition
Mania refers to state of abnormally elevated, expansive, or irritable mood.
Common causes include bipolar disorder, intoxication with cocaine or
other stimulants, and schizoaffective disorder. The differential also
includes medical conditions such as hyperthyroidism, as well as the
effects of prescription medications such as corticosteroids. To meet ICD-10
criteria, the mood alteration must persist for at least one week, and be
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accompanied by at least three symptoms of increased physical activity,

pressured speech, flight of ideas, loss of normal social inhibitions,
decreased need for sleep, grandiosity, distractibility, reckless behavior, or
increased sexual energy.
5.2. Risk factors

Patients may become manic for many reasons. Use of illicit substances,
non-compliance with prescribed medications, or medication changes,
such as initiation of a new antidepressant or corticosteroids, commonly
result in mania. Certain laboratory tests, such as liver function tests, thy-
roid stimulating hormone levels, and serum levels of mood stabilizers, are
usually indicated as well, given that some medical conditions may present
with mania. Risk for illness exacerbation is also higher earlier in the
course of illness, particularly the first year after diagnosis.5
5.3. Management
While they often present in a euphoric, affable state, manic patients may
quickly become irritated and agitated, or even manifest psychosis, when
bothered by questioning during evaluation or by other patients in the
emergency department. Having security staff on hand for these situations
is advisable. As with psychotic patients, obtaining appropriate medical
evaluation is absolutely necessary, as is maintaining a low threshold for
use of medications, especially antipsychotic medications, in the manage-
ment of agitation.
Interviewing manic patients can be challenging, even when they are not
irritable. It helps to keep questions as close-ended as possible to avoid
long-winded and tangential responses. In the emergency setting, eliciting
a history of high-risk activities and functional impairment is a more
immediate concern than eliciting a lifetime history of episodes in order to
make a firm diagnosis. Relevant topics include promiscuous sexual activ-
ity, excessive spending, and run-ins with law enforcement.
The decision to hospitalize should be made based on careful safety
assessment. The primary reason to admit manic patients is when they
represent a danger to themselves or others, such as when their risky
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behavior inadvertently puts their life in danger. While suicide is relatively

rare in acute mania, patients with bipolar disorder are at drastically
elevated risk, with suicide completion around 1% annually,9 and, as
above, patients in a mixed episode are also at higher risk. Moreover, the
manic patient’s grandiosity may cause them to be less attentive to per-
sonal safety. Other considerations include symptom severity, symptom
trajectory, i.e. whether the episode just began or appears to be winding
down, and the extent of the patient’s outpatient support system. Even
when patients do not represent an acute safety risk, they may lack appro-
priate follow-up care and so require admission for stabilization and to
ensure that follow-up is arranged. Unfortunately, manic patients rarely
have insight into their condition and often must be hospitalized against
their will.
Patients who are experiencing an energy and/or mood elevation but are
not functionally impaired may be in a hypomanic state. This state can be
unstable, and medication adjustments from the ER, e.g. increased dose of
mood stabilizer or augmentation with an antipsychotic medication, may
be appropriate in order to keep the patient stable until they can reach their
usual outpatient psychiatrist. Please see Chapter 9 for additional details on
bipolar disorder.
6. ANXIETY
6.1. Definition
The ICD-10 identifies multiple categories of anxiety disorders, including
disorders with periodic elevation in anxiety (such as phobic anxiety disor-
ders), disorders with more sustained elevation in anxiety (such as general-
ized anxiety disorder and hypochondriasis), and conversion disorders.
Patients may present to the emergency department with symptoms of any
of these conditions. Indeed, many patients have a tendency towards anxi-
ety that manifests itself through multiple anxiety disorders. Because of the
somatic nature of anxiety symptoms, many of these patients will initially
present with a somatic chief complaint that will later be discovered to be
driven by anxiety. Details regarding the anxiety disorders are provided
elsewhere in this book.
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6.2. Risk factors

Patients with anxiety disorders have presumably compensated to their
anxious tendencies until something happens to cause their anxiety to ele-
vate beyond the usual baseline. Relevant risk factors for worsening anxi-
ety include a recent traumatic experience or appearance of new social
stressors. Because anxiety is controlled through cognitive mechanisms,
subtle cognitive impairments may present with anxiety. These include
cognitive impairments from delirium, worsening dementia, or depression.
Many substances can induce anxiety, such as stimulants, cocaine, or even
SSRIs shortly after initiation or dose adjustment. Akathisia can be misin-
terpreted by the patient as anxiety. Many medical conditions can also
present with anxiety, including thyroid illness, COPD, and cardiopulmo-
nary illness.
6.3. Management
As with other presenting complaints, the first responsibility of the emer-
gency psychiatrist is to ensure that the patient does not have an indication
for hospitalization, either medical or psychiatric. Some providers are too
quick to ascribe a physical symptom with an atypical presentation to a
psychiatric diagnosis, like anxiety. Thus, the evaluating mental health
professional should be especially certain that the patient’s physical com-
plaint has not been prematurely dismissed. Chest pain, for example, is a
common complaint in a panic attack. A 2003 meta-analysis found that the
following five variables correlate with panic disorder in patients present-
ing to the emergency room with chest pain: younger age, female sex,
higher self-reported anxiety, atypical character to the chest pain, and
absence of known coronary artery disease.12
Once cleared for outpatient management, the management approach
for patients with sustained anxiety is different from that for patients with
non-sustained periodic anxiety, i.e. panic attacks. In either circumstance,
if a risk factor for worsening anxiety is identified, a strategy for ameliorat-
ing this risk factor should also be established.
Patients with panic attacks can be reassured that their attacks are emo-
tional in nature and not in and of themselves dangerous to their health.
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Moreover, these patients can be taught behaviors to calm themselves in the

midst of a panic attack, such as diaphragmatic breathing and use of imagery.
While positive cognitions and behaviors can also be recommended to
patients with sustained anxiety to help them manage any superimposed
periodic elevations in anxiety, these patients also maintain a tonic level of
somatic arousal that may best be managed with medications. Benzodiazepines
are the usual first choice for immediate symptomatic relief, though these
medications carry a risk of dependency and also serious consequences in
overdose. SSRIs may also be used and are considered more definitive treat-
ment, though these medications may induce anxiety during the initial titra-
tion. It may be best to defer initiation of SSRIs to an outpatient provider
with whom the patient has a good treatment relationship.
Patients with dissociative symptoms or somatoform disorders are not as
well studied in emergency settings as patients with other types of anxiety
disorders. Please refer to Chapters 13 and 14 in this book for further
information.
7. DISPOSITION
Based on the facts of the case at hand, a patient may be deemed appropriate
for inpatient or outpatient psychiatric treatment, including treatment in a
partial hospital or other day treatment program. This section details the steps
needed to complete a safe discharge from the emergency department.
7.1. Inpatient
At the moment that the patient is determined to be appropriate for inpa-
tient psychiatric treatment, the objective of the patient’s care in the emer-
gency department shifts towards maintenance of stability until the patient
can be safely transferred to an inpatient facility. This includes administra-
tion of medications or other interventions to help the patient remain calm
and ensuring that the patient does not leave the supervision of the
emergency personnel. Depending on how long the patient remains in the
emergency department, the patient may also need their regularly sched-
uled psychiatric and non-psychiatric medications, meals, a place to sleep,
and perhaps even means of grooming.
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The evaluating team is also responsible for identifying an inpatient

psychiatric facility to which to discharge the patient. Different inpatient
facilities have different expertise and capacities. Moreover, in countries
with multiple payers for medical care (e.g. insurance companies, the gov-
ernment, etc), some facilities may be allied with some payers but not with
others. These factors should be considered when determining to which
facility to transfer the patient.
The selected hospital should be contacted directly and at least one
member of the evaluating team should gain agreement from an authorized
representative of the hospital for admission of the patient. This may
require the hospital’s review of available records, including documenta-
tion of the patient’s medical stability and lack of need for a medical hos-
pitalization prior to a psychiatric hospitalization. A member of the
treatment team should also take responsibility for contacting any paying
organization to ensure that the hospital will be paid.
The patient’s preferences should also be taken into account, though
patients in the middle of a psychiatric emergency have variable capacities
to consent to inpatient psychiatric treatment. As such, if the patient does
not have capacity to consent for their treatment, then their wishes may
need to be overridden. Different communities have different legal stand-
ards for how this should be done.
Once the necessary medical, financial, and legal steps have been taken,
transportation to the hospital should be arranged and the patient trans-
ferred. Transportation by a family member is not acceptable because
psychiatric admission implies that the patient is too ill to be outside of the
view of trained professionals. Of course, if the patient has not yet been
searched for weapons and other contraband, then this should be done
before departure from the emergency department.
7.2. Outpatient
If the patient is not appropriate for inpatient treatment, then the treatment
team should develop a plan to ensure that the patient does not have to return
to the emergency department due to an exacerbation of their presenting
complaint. The patient may only require a psychopharmacologic or psy-
chotherapeutic intervention in the emergency department, for example, an
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injection of a long acting antipsychotic medication or psychoeducation

about the nature of anxiety. Impromptu family meetings may also be
important in resolving severe psychiatric symptoms that appear as a result
of conflicts within the family.
The patient may require ongoing administration of medications, and, as
such, the patient should be provided with a means to obtain the needed
medications. This may be as simple as furnishing a prescription to the
patient. However, for other patients, it may be simpler to discharge the
patient from the emergency department with a small supply of medica-
tions. Moreover, for patients who are cognitively impaired or paranoid
about the medications, a family member or friend may need to agree to
ensure that the patient continues to take the medication after discharge.
Most patients, especially potentially suicidal patients, should not be
discharged from the emergency department with an excess of medica-
tions. A supply to cover them until their next outpatient appointment
should suffice.
The patient should have a clear means of follow-up with a provider who
can help them improve their psychiatric status. For patients in chronic
treatment, this may be as easy as setting up a follow-up appointment with
their usual outpatient treatment provider. However, some patients may
require services they are not currently receiving, such as CBT or sub-
stance abuse treatment. These patients should be given the necessary
information to receive the services they need, such as phone numbers for
the relevant programs.
At times, a high risk patient may be discharged from the emergency
department without a clear follow-up plan. This may happen because the
patient arrived after hours and an appointment could not be set, for exam-
ple. Some emergency departments have taken to making “bridging
appointments” in the emergency department available for these patients.
Other emergency departments have allied themselves with more compre-
hensive psychiatric emergency services for these patients.20
7.3. Liaison with other providers

Whether the patient is discharged to inpatient or outpatient treatment, the
receiving treatment provider will need information about the patient’s
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course of care in the emergency department. This may be done by sending

a copy of the patient’s treatment record to the relevant provider. However,
if the record will not reach the inpatient or outpatient treatment provider
in a timely manner, then the needed information should be communicated
by telephone. In some countries, the patient’s written consent for waiver
of privacy rights is necessary to ensure continuity of care.
8. CONCLUSION
Psychiatric emergencies are defined as any change in a patient’s mental
status that may lead to intentional or unintentional dangerousness to them-
selves or other people or a general inability to care for themselves in their
current social setting. These emergencies can be challenging, though can
certainly be managed by maintaining empathy in establishing rapport and
by being attentive to any treatment interfering behavior by the patient,
such as agitation or acute violence. Specific psychiatric emergencies have
different features, though their management generally involves identifica-
tion of present risk factors, reduction of these risk factors in the patient’s
current setting to the degree possible, and referral to a higher level of care
if complete reduction of risk factors cannot be completed in the current
treatment setting.
9. KEY POINTS
• Psychiatric emergencies are situations in which a patient cannot maintain
their safety or refrain from endangering others as a result of their mental
illness. Common emergencies include severe suicidal ideation, severe
homicidal ideation, severe psychosis, mania, and severe anxiety.
• Patients in crisis are at risk of agitation, disrupting rapport with their
treatment providers, and further putting themselves and their treat-
ment providers at risk of injury. Agitation should be recognized and
addressed verbally first, then with medications and other more restric-
tive measures if needed.
• If the crisis can be addressed in the current treatment setting and
changes to the patient’s treatment plan can be made to prevent reap-
pearance of the crisis, then hospitalization can be avoided. If these
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tasks cannot be completed, then the patient will need to be hospital-

ized, even if it is against the patient’s wishes.
• Use of collateral informants and collaboration with outpatient and
inpatient treatment providers is an essential step in complete assess-
ment and management of any psychiatric emergency.
10. SELF-ASSESSMENT
10.1. According to a 2005 study, which of the following risk
factors closely correlates with the decision to pursue
inpatient hospitalization of a suicidal patient?
(A) Presence of a plan.
(B) Available social supports.
(C) Prior suicide attempt.
(D) Male gender.
(E) Family history of suicide.
Prior suicide attempt greatly increases the risk of repeat suicide attempt,
and closely correlates with the decision to admit a suicidal patient.3
Answer: C
10.2. All of the following characteristics correlate with an

anxiety aetiology, rather than a cardiac etiology,
for chest pain, except:
(A) Atypical character to the chest pain.
(B) Female sex.
(C) High self-reported anxiety.
(D) Family history of early myocardial infarction.
(E) Younger age.
Family history of early myocardial infarction is a key factor in stratifying

risk for patients experiencing an acute coronary syndrome, whereas the
other four characteristics correlate with chest pain caused by anxiety.12
Answer: D
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11. CASE STUDIES

11.1. At risk of self-harm
Ms R is a 31-year-old divorced, unemployed female who was brought to the
Emergency Department by her sister after stating that she planned to cut her
wrists. Over the past month, Ms R has wished that she were dead at least
once a day. Five days ago she began thinking about cutting her wrists with
a kitchen knife. She is able to redirect her thoughts and has not rehearsed the
act. She recently divorced her husband and moved to stay with her sister in
another city. She was diagnosed with major depression three years ago, after
a suicide attempt in which she purposely took 15 tablets of alprazolam.
After a brief hospitalization, she saw an outpatient psychiatrist for two
years, during which time she was treated with an SSRI to good effect. She
is not currently seeing any mental health provider. She states she only drinks
on special occasions and denies other drug use. She has a family history of
bipolar disorder but not suicide. She has not found a job since moving.
During the course of the interview, Ms R states that she has “nothing to
look forward to.” Her sister is highly concerned since the patient is home
alone when she is at work. The emergency department psychiatrist feels
that Ms R’s risk is high enough to warrant inpatient treatment, and the
patient agrees to admission.
11.2. A danger to others

Mr B is a 62-year-old military veteran with post-traumatic stress disorder
who brought himself to the Emergency Room because he has been having
urges to kill his wife.
He states that his wife has become increasingly difficult to live with
since she had a stroke one year ago. Her personality has become more
negative and critical, even as he has taken on greater responsibility to
care for her. They have been arguing frequently, and he complains of
“constant stress, I just can’t take it.” This has occurred on top of his
chronic PTSD symptoms, which include inability to control his own
anger outbursts, persistent anxiety, and difficulty sleeping due to night-
mares. In the past month, during their fights, he began to have urges to
shoot her with his handgun. Since then he has become progressively
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preoccupied with this idea, and presents today because he is worried he

will “snap” and harm her. He has shared his concerns with his wife. He
denied thoughts of harming other people and gets along well with other
members of his family.
He denies any history of domestic violence, but reports a long history
of “getting into bar fights” while intoxicated and has been arrested several
times for this behavior. He continues to drink about six beers daily. He has
never been hospitalized for psychiatric reasons, but does see an outpatient
provider on a bi-weekly basis.
During the interview, Mr B appears highly anxious but his affect is
stable. There is no evidence of psychosis. His blood alcohol is 0.06 g/L.
Collateral information is sought with the patient’s permission. Mr B’s
brother agrees to let Mr B stay with him for a few days until Mr B’s next
appointment with his outpatient provider. Mr B agrees to stay away from
his wife and his firearm during that time. The patient’s outpatient provider
and his wife were also contacted. They expressed comfort with this plan.
Mr B was discharged to his brother’s home.
11.3. A patient with paranoid schizophrenia

Mr G is a 43-year-old divorced, unemployed man with a long history of
paranoid schizophrenia who was brought to the Emergency Room by
police. They were called after the patient reportedly became combative
toward staff at the group home where he lives. He came willingly with the
officers, and he is currently in a locked observation room, pacing and
speaking to an unknown audience. After the physician enters the room
with a nurse and a security staff member, the patient states “the princes of
this world, they control me like a game, they want to corrupt me. I have
to get to the monastery.” He does not make any threatening statements or
gestures, and he sits when asked to do so.
On further evaluation, Mr G endorses derogatory and command audi-
tory hallucinations. His thought process is tangential and he is preoccupied
with religious and persecutory delusions. His vital signs are within normal
limits. The physician contacts his outpatient psychiatrist and finds that she
had changed his antipsychotic regimen in the past three weeks, as he had
gained 15 lbs on the prior regimen. Mr G has also been drinking an
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increasing amount of alcohol over the past two months, though he is not
intoxicated currently.
While collateral information was being obtained, Mr G becomes agi-
tated, shouting “I need sanctuary!” repeatedly. He receives a single dose
of olanzapine and subsequently calms. Due to his recurrent agitation, he
is admitted to the inpatient unit for further stabilization.
11.4. A patient with bipolar disorder

Mr F is a 48-year-old man with bipolar disorder who was brought to the
Emergency Department by police. He had been found walking on the side
of the road in a rural area wearing only a plastic trash bag. He has not been
sleeping. He was shown to a bed in the emergency room, however he was
unable to lay down and staff has already had to escort him back several
times. He is now pacing by the bed. At the start of the interview, he inter-
jects, stating “Hi Doc, those cops were nice guys. They were helping me
out because my feet hurt. Thanks! I’m Dennis the menace who plays
tennis.” He continues speaking without interruption for several minutes.
He continues to pace and gesticulate throughout the interview. His
speech is fast and uninterruptible, and he frequently changes topics with-
out apparent connection. Urine drug screen is negative for cocaine,
amphetamines, and alcohol. His liver function tests are within normal
limits, and serum levels of lithium and valproic acid are undetectable.
He is unable to provide contact information for family members or
outpatient providers. Based on his current inability to care for himself, he
is admitted to the inpatient psychiatric unit for mood stabilization.
11.5. Sudden-onset chest pain

Ms N is a 16-year-old girl who experienced sudden onset chest pain, pal-
pitations, and near syncope at school just before starting a final examina-
tion. She received a cursory medical evaluation, including only a history
and physical examination and screening laboratory tests. She received a
diagnosis of panic attack and a psychiatric consultation was called.
Ms N reports that she has been feeling these symptoms from time to
time for the past few months and usually without clear triggers, but has not
reported them to anyone yet. She was hoping that they would just go away
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and was not terribly worried about them. She denied having symptoms like
this prior to other examinations, and is not upset at having missed the
examination today. Because of her outstanding performance in class
through the semester, the examination was not going to change her final
grade in the course. The patient does appear calm and denied any depres-
sion, anhedonia, psychotic symptoms, or suicidal/homicidal ideation.
The psychiatrist talked with the patient’s mother in private, who con-
firms that the patient is generally calm and collected. The patient did not
have significant separation anxiety when she started in school. There is no
family history of anxiety disorders.
The psychiatrist insisted that the patient receive a more thorough evalu-
ation for causes of pre-syncope. The remainder of the patient’s evaluation
was deferred to the ER physician. On outpatient arrhythmia monitoring,
the patient was found to have a paroxysmal arrhythmia.
ACKNOWLEDGEMENT
The authors would like to thank Rockafeller Oteng, MD for his thoughtful
comments in preparing this chapter.
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Mental Disorders, 4th ed. Text Revision, American Psychiatric Publishing, Inc.,
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de Leon J. (2004) Variables associated with hospitalization decisions by emer-
gency psychiatrists after a patient’s suicide attempt. Psychiatr Ser 55(7): 792–797.
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6. Fiseković S, Burnazović L. (2005) Clinical features in emergency psychiatric

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Vijayakumar L, Malakouti K, Schlebusch L, De Silva D, Nguyen VT,
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8. Folstein MF, Robins LN, Helzer JE. (1983) The mini-mental state examina-
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of adult psychiatric visits to US emergency departments. Acad Emerg Med
11(2): 193–195.
11. Huckshorn KA. (2006) Re-designing state mental health policy to prevent
the use of seclusion and restraint. Adm Policy Ment Health 33(4): 482–491.
12. Huffman JC, Pollack MH. (2003) Predicting panic disorder among patients
with chest pain: An analysis of the literature. Psychosomatics 44: 222–236.
13. Krug EG, Dahlberg LL, Mercy JA, Zwi A, Lozano R (eds.) (2002) World
Report on Violence and Health. World Health Organization, Geneva.
14. Marder SR. (2006) A review of agitation in mental illness: Treatment guide-
lines and current therapies. J Clin Psychiatry 67 (Suppl 10): 13–21.
15. Mermelstein HT, Wallack JJ. (2008) Confidentiality in the age of HIPAA:
A challenge for psychosomatic medicine. Psychosomatics 49: 97–103.
16. Mattelaer JJ, Jilek W. (2007) Koro — the psychological disappearance of the
penis. J Sex Med 4: 1509–1515.
17. Nasreddine ZS, Phillips NA, Bedirian V, Charbonneau S, Whitehead V,
Collin I, Cummings JL, Chertkow H. (2005) The Montreal cognitive assess-
ment (MoCA): A brief screening tool for mild cognitive impairment. J Am
Geriatr Soc 53: 695–699.
18. Petit JR. (2005) Management of the acutely violent patient. Psychiatr Clin N
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21. Swanson JW, Holzer CE, Ganju VK, Jono RT. (1990) Violence and psychi-
atric disorder in the community: Evidence from epidemiologic catchement
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agitation in emergency settings. Emerg Med J 20(4): 339–346.
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Chapter 22
Outpatient Psychiatry
Ondria Gleason, Aaron Pierce and Bryan Touchet
1. INTRODUCTION
Psychiatric services provided in the outpatient clinic include psychiatric
evaluation, medication management, and individual psychotherapy. Other
services may include group, couples, and family therapy, neuropsychologi-
cal testing, social services, and vocational counseling for patients. Outpatient
services may be provided in a variety of settings including solo or group
practice. Group practice may include collaborative care models, where the
psychiatrist sees patients in primary care or other (non-psychiatric)
specialty clinics.
This chapter will provide a broad overview of pertinent aspects of
psychiatric practice in the outpatient setting. Topics to be covered include
professional and ethical considerations, the format of the psychiatric
interview and mental status examination, and attention to safety in the
outpatient clinic. The development of the differential diagnosis and case
formulation will also be discussed along with outpatient treatments.
Patients may present independently for psychiatric evaluation and treat-
ment but are often referred from another health care provider. The referral
process is an important step in initiating treatment for the patient. If the
patient is being referred from another health care provider, it is important to
know what prompted the referral and if the referring provider would like the
psychiatrist to assume psychiatric care of the patient or to simply answer a
554
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Outpatient Psychiatry 555
consultation question. As with other medical specialists, the more informa-

tion the outpatient psychiatrist has about the referral, the better equipped he
or she will be to provide the patient with high quality care. After the patient
is evaluated, it is important to provide the referring provider with the
psychiatrist’s initial impressions and treatment plan for the patient.
Psychiatric consultations may be conducted in the outpatient setting.
A consultation is requested when the patient is referred by another physi-
cian who requests assistance with the patient’s care but who intends to
continue to treat the patient for that condition after the consultation. The
collaborative care model, where the psychiatrist sees patients in other clin-
ics, improves patient access to psychiatric care by increasing convenience
and, for some patients, reducing the fear of stigma by avoiding attending
a “psychiatric clinic.” This also enhances communication between care
providers, enhancing knowledge sharing and improving all providers’
understanding of the care the patient is receiving.
Before considering the elements of psychiatric evaluation and treat-
ment, it is important to consider the ethical framework upon which
patients should receive care.
2. PROFESSIONALISM AND ETHICAL

CONSIDERATIONS
Professionalism and ethics are foundational to the understanding of what
motivates and defines compassionate, meaningful, and sound psychiatric
practice. In psychiatric care, as in all of medicine, ethical obligations are
incurred because of society’s trust in, and place of privilege and power for,
the professional. These obligations include respect for persons as autono-
mous, dignified beings, the duty to do good for the patient and for society,
and the responsibility to avoid harm.
Professionalism manifests itself in the psychiatric outpatient setting
much as it does in other settings, although with its own expression appro-
priate to an office-based venue. Some key attributes of professionalism
include the following:
• Sensitivity to and respect for diversity.

• Serving patients’ and society’s interests above one’s own.
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556 O. Gleason, A. Pierce and B. Touchet
• Practicing within one’s scope of practice.

• Acquisition and maintenance of competence.
• Ensuring continuity of care for patients through collaborative cover-
age arrangements in which psychiatric colleagues provide care when
the primary psychiatrist is not available.
Key ethical considerations particularly pertinent to outpatient psychiatry

may be summarized as follows:
• Confidentiality: Protecting privacy of patient information within lim-

its imposed by other principles such as non-maleficence.
• Boundaries: Avoiding competing relationships, which reduce the pri-
mary importance of the doctor-patient relationship; avoiding exploita-
tion of patients.
• Informed consent: Continually ensuring that the patient is provided
every opportunity to fully exercise his or her autonomy in decisions
regarding his or her own psychiatric care.
Understanding and resolving ethical dilemmas, when possible, are impor-

tant skills of the physician. The astute psychiatrist or trainee recognizes
the conflict that may arise between honoring the patient’s autonomy and
preventing harm to the patient and others. In this case, the highest ethical
duty is to protect the patient and others from harm, especially given the
fact that the patient’s judgment is impaired by mental illness. With an ethi-
cal and professional framework in mind, one proceeds to evaluate the
patient, beginning with the psychiatric interview.
3. THE PSYCHIATRIC INTERVIEW

There are two main purposes to the initial psychiatric interview. The first
is to form a differential diagnosis and biopsychosocial formulation for the
patient, which drive the treatment plan and give the patient knowledge of
the diagnosis and prognosis. The second main purpose of the interview is
to begin to establish rapport: an empathic, trusting, relationship with the
patient. This is important to the patient’s outcome. Without a strong thera-
peutic alliance, the patient may not share personal information as readily,
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and patient compliance with treatment could also suffer. The psychiatrist
strengthens this alliance through professional conduct and with attitudes
of caring, concern, and respect.4 The interview should take place in a pri-
vate, comfortable, and quiet setting, and interruption of the interview must
only occur during an emergency. There should be no barrier between the
interviewer and the patient that would obstruct the complete view of the
patient. The patient’s general appearance, facial expressions, posture, and
movements may reveal information that otherwise would be lost if the
psychiatrist were unable to view the patient completely. Chairs or couches
must be comfortable enough for the patient to sit for the entirety of the
interview, and extra chairs should be available for the patient’s family or
friends.
Often, the patient will be accompanied by family or friends who wish
to be present during the interview. In Western culture, it is common to
interview the patient privately initially and invite family or friends in
afterwards, if the patient gives permission to do so. When patients are
interviewed alone, they may provide information they otherwise would
not share in the presence of others. In some other cultures, the family
may expect to stay with the patient during the entire interview. Family
members or friends might be the only reliable source of information
about the patient, particularly when the patient displays gross disorgani-
zation of thought, severe dementia, and so on. When interviewing a
patient who speaks a different language, it is preferable to use a profes-
sional interpreter. Family members or friends may be uncomfortable
asking the patient particular questions or may ask questions in a way the
interviewer did not intend. Conversely, the family member or friend may
subtly edit the patient’s response, altering its meaning to the
psychiatrist.
It is important to have a basic understanding of the patient’s cultural
background and the environment in which the patient lives. Culture may
be defined as the values, beliefs, and customs of a group of people with
whom the patient identifies. Knowledge of the patient’s culture and social
environment (e.g. exposure to war or political unrest) is essential to
understanding the patient and the symptoms and experience the patient
reports.
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3.1. Interview format

It is important that the psychiatrist perform the psychiatric evaluation in
the same manner every time. This will help ensure that all important infor-
mation is gathered and nothing is left out. The format is divided into nine
parts and is very similar to a medical history, with additional emphasis on
the patient’s past psychiatric history and the mental status examination.
See Tables 1 and 2 for a summary and Chapter 5 for more details.
Table 1. Elements of the psychiatric interview.
Patient identification
Chief complaint and reason for referral, if appropriate
History of the present illness
Past psychiatric treatment history
Medical history
Current medications and allergies
Family history (medical and psychiatric)
Social history
Mental status examination
Table 2. Components of the mental status examination.
Appearance
Level of consciousness
Cooperation
Behavior
Speech
Orientation
Concentration
Mood and affect
Thought content (including suicidal and homicidal ideation)
Perceptual disturbances (such as visual and auditory hallucinations)
Thought processing
Memory
Abstract thinking
Fund of knowledge
Estimation of intelligence
Insight and judgment
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The psychiatric interview and mental exam are the fundamental compo-
nents of the psychiatric evaluation. The process of the evaluation offers the
first opportunity to establish rapport and an effective working relationship
with the patient that will aid in the successful management of their psychiat-
ric issues. Due to the nature of some psychiatric illnesses, there is a potential
for impulsive, even dangerous behavior. It is paramount that the psychiatric
examiner understands basic safety concerns in the outpatient setting.
4. SAFETY IN THE OUTPATIENT SETTING

One of the most important aspects of psychiatric practice is safety, not only
for the patient, but also for the providers. Safety issues are more likely to
be encountered in situations where the psychiatric condition is more acute,
such as in the emergency room, psychiatric inpatient unit and in the general
hospital consultation setting. However, acute psychiatric events that may
pose a danger to the clinician or the patient are certainly possible in the
outpatient setting. Examples include patients with active psychosis, patients
under the influence of illicit substances or medications with central nervous
system effects, patients experiencing substance withdrawal, patients with
delirium related psychosis, delusions or disorientation as a result of an
underlying medical condition, and patients who are actively suicidal.
In the psychiatric outpatient clinic, one begins by being actively aware
of his or her surroundings. The practitioner’s chair should be closest to the
door. Ideally, a “panic button” should be in place for the practitioner to
activate to call for assistance. The panic button may be wired to alert secu-
rity staff or the front office staff, who would call for help. During the
examination, it is important to remain alert for clues that the patient is
agitated or becoming agitated. Use a calm voice and maintain view of the
patient during the examination. Be careful to avoid further agitating a
psychotic or angry patient. For example, avoid challenging delusions in an
angry psychotic patient. In all settings, an agreed-upon plan for handling
emergencies in the outpatient setting should be in place.
Whenever concern arises for the psychiatrist’s or the patient’s safety, it
is appropriate to summon security to stand near the examination room or
to accompany the psychiatrist in the examination room. This provides an
extra layer of protection for the psychiatrist and the patient, who may be
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an elopement risk (e.g. a suicidal patient who tries to flee to avoid hospi-
talization). Many countries have laws pertaining to involuntary treatment
of mental illness. These laws vary across nations and may vary between
states and jurisdictions, so a clinician must be familiar with the involun-
tary commitment laws governing his or her state or region. In most juris-
dictions in the United States, clinic and hospital security staff will not
detain a patient against his or her will, without a written affidavit indicat-
ing that the clinician has evidence or reason to suspect that the patient
poses an immediate danger to self or others as a result of a psychiatric
condition requiring treatment. Access to required forms or other proce-
dures should be readily available to the clinician. An understanding of the
process for involuntary commitment is important before seeing patients.
5. SUICIDE RISK ASSESSMENT

A critical task in any psychiatric evaluation or treatment setting is to assess
a patient’s risk for suicide. This assessment may begin with a question
such as, “Have you ever thought that life is not worth living?” Follow-up
questions will vary depending upon the patient’s initial response. If the
patient answers affirmatively, the clinician will need to engage the patient
in a conversation that further explores the severity of the patient’s self-
harm thoughts; determining the frequency of such thoughts, when the
patient last had such thoughts, if the patient ever thought of a possible plan
to end his or her life, and how close the patient actually was to caring out
the plan. A question as straightforward as “Do you have any thoughts of
suicide now?” must be asked at the time of the examination and followed
up with an assessment of plan and intent to carry out such a plan. It is
important to remember that asking a patient about suicidal thoughts does
not increase a patient’s chances of attempting suicide; in fact, it can be
life-saving in that it allows the patient an opportunity to express his or her
feelings and to obtain needed help.
6. SUBSTANCE ABUSE SCREENING

It is important to screen patients in the outpatient setting for substance
use. Symptoms attributed to psychiatric disorders such as depression,
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anxiety, and psychosis may, in fact, be the manifestation of substance

use or withdrawal. It is helpful to preface such an inquiry with a state-
ment such as, “The following questions that I am going to ask you are
very important. Answering them as honestly as you can will help me to
make the best diagnosis possible and allow me to help you the most.”
Asking questions that assume the patient uses substances in large
quantities, a technique known as symptom amplification may have the
greatest yield.8 For example, in assessing alcohol use, rather than
asking, “Do you drink alcohol?” or “How much alcohol do you drink?”
ask, “Do you drink a case or more of beer per week?” This question
allows the patient who may consume large amounts of alcohol to “save
face” and provide an answer that more accurately reflects their actual
consumption, rather than underreporting with the open ended
question.
The possibility that the patient may be abusing prescription medica-
tions must also be considered. Opiate preparations and benzodiazepines
are particularly prone to abuse, and the effects of these substances can
mimic a number of psychiatric conditions, including mood disorders,
anxiety disorders, and psychosis. Questions similar to those utilized to
screen for alcohol abuse can be used in assessing prescription substance
abuse, although the focus will be on the patient’s reason for using the
medications. For example, patients who are prescribed opiate pain
medication for a chronic pain condition should be asked whether or not
they find themselves using the medication not only for pain control but
also to improve their mood, reduce anxiety, or “get through the day.” It
is important to provide information to patients about the potential con-
tribution of these medications to their presenting psychiatric symptoms;
however, patients are often reluctant to endorse that they are taking
these medications for reasons other than that for which they are
prescribed.
Valuable information can often be obtained from collateral sources,
such as the patient’s family members, who can provide an accounting of
what they observe at home. Ordering a urine drug screen as part of the
initial psychiatric workup and as indicated throughout the course of out-
patient treatment is prudent in many cases; understand that the screen will
be positive for substances that the patient is prescribed.
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7. EFFECT OF MEDICAL ILLNESS ON PSYCHIATRIC

DISORDERS
Just as substance use can result in symptoms that mimic psychiatric ill-
ness, medical conditions can also be associated with symptoms that
mimic psychiatric disorders. It is important to consider the possibility that
an underlying medical condition may be causing or exacerbating the
patient’s psychiatric presentation. It is particularly important to consider
this when evaluating a patient with new onset of psychiatric symptoms or
when a patient with a pre-existing psychiatric disorder has a sudden onset
of psychiatric symptoms that are unlike the typical psychiatric presenta-
tion and when a patient does not respond to psychiatric treatment as
expected. For example, patients with chronic pain syndromes are often on
opioid pain preparations. Opiates are known to cause sedation, which can
add to the sedative effect of some psychotropics. This can pose a poten-
tially dangerous situation, particularly if the patient has built up a toler-
ance to the effects of the opiates and is on high doses of the pain
medication. Furthermore, the opiate medications act as central nervous
system depressants. These effects can mimic symptoms of depression,
making it difficult to accurately assess the effects of antidepressant
pharmacotherapy.
Other common medical problems that can present with psychiatric
symptoms include infection, anemia, electrolyte disturbances, glucose
abnormalities, thyroid abnormalities, liver and kidney dysfunction, pul-
monary disorders, and vitamin deficiencies. As discussed above, pre-
scribed medications, over-the-counter medications, and illicit substances
must also be considered as potential causes of the patient’s psychiatric
presentation.
Psychiatric conditions and their treatments can also adversely affect
comorbid medical conditions. Obtaining a complete medical history and
a current list of medications is important. This information must be
reviewed and taken into consideration as psychiatric diagnoses are consid-
ered and treatment decisions made.
Examples of common medical conditions that can be affected by psy-
chiatric conditions and treatments include asthma, chronic obstructive
pulmonary disease, hypertension, diabetes, and chronic pain syndromes.
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For example, anxiety disorders and depression are more common in

patients with asthma, and asthmatic attacks can be induced by psychologi-
cal stress.6 Conversely, respiratory distress can be mistaken as anxiety.
Psychotropic medications can have adverse effects on underlying medi-
cal conditions. An example is the negative effect that antipsychotic medica-
tions can have on a patient’s lipid profile. This is of particular concern in
patients who are at risk for, or who have pre-existing, hyperlipidemia,
obesity, diabetes, and cardiac disease. Potential interactions between psy-
chotropic medications and other medications must also be considered. For
example, warfarin is a common anticoagulant whose metabolism can be
adversely affected by almost any psychotropic medication due to its high
degree of protein binding and involvement of several cytochrome p 450
isoenzymes, also utilized by most psychotropics in its metabolism.11
Regular monitoring of prothrombin time and international normalized ratio
(INR) is important for patients receiving warfarin, with additional monitor-
ing necessitated whenever a psychotropic medication is added or dosage
adjusted. Particular attention should be paid to patients receiving both
antihypertensives and lithium. Some antihypertensives are excreted through
the kidneys or may alter sodium levels, which may, in turn, alter lithium
levels, resulting in lithium toxicity. Patients on diuretics are at increased
risk for dehydration and also lithium toxicity. An electronic database or
updated drug reference book are invaluable tools for identifying adverse
drug reactions and potential drug–drug interactions. After obtaining a com-
plete history and performing the mental status examination and taking into
consideration underlying social and medical problems, the psychiatrist is
ready to begin considering possible psychiatric diagnoses and treatments.
8. DIFFERENTIAL DIAGNOSIS AND FORMULATION

After the psychiatric interview and mental status examination are com-
plete, the psychiatrist then develops a differential diagnosis, formulates
the patient using a biopsychosocial model, and develops a treatment plan.
A biopsychosocial model can help guide further investigation such as
laboratory testing, neuro-imaging, neuropsychological testing, and the
gathering of collateral information from others who are familiar with the
patient. In addition, it will guide the psychiatrist’s treatment plan, such as
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the need for pharmacotherapy, psychotherapy, or referral to social ser-

vices. As described by Campbell and Rohrbaugh,2 the biological compo-
nent of the formulation addresses the effects of genetics, physical
illnesses, medications, and substances on the patient’s illness. The psy-
chological component involves establishing a “psychological theme” for
the patient that usually deals with control, trust, or self-esteem. Stressors,
their consequences, and how the patient copes with them are also
addressed. The social component, while having much overlap with the
psychological component, addresses social stressors and support that
influence the patient. At this point, the clinician is ready to develop a treat-
ment plan.
9. MANAGEMENT OF THE PSYCHIATRIC

PHARMACOLOGICAL MANAGEMENT VISIT
Increasingly, psychiatrists are practicing more pharmacotherapy and less
formal psychotherapy in their office-based practices.7 Cost constraints
have made effectively managing pharmacotherapy visits increasingly
important, and psychotherapeutic techniques can be very helpful in
accomplishing this. Supporting this idea is research demonstrating that
clinical management skills, most importantly the ability to establish and
maintain a strong therapeutic alliance, appear to be more important than
medication selection in contributing to clinical outcomes in pharmaco-
therapy.5 The duration of a psychopharmacologic visit should be sufficient
to address the needs of the patient. The visit may be shorter for an estab-
lished patient with a stable psychiatric condition or longer for a patient
with several psychiatric problems or for a patient in crisis. Typically, visits
range from 15–30 mins. Essential elements of a pharmacotherapy visit
have been proposed by experts and are listed below.12
• Performs a focused interval history.

• Uses validated symptom scales.
• Assesses patient adherence to treatment and side effects.
• Makes evidence-based modifications in the treatment plan when indi-
cated, both psychopharmacologic and psychosocial-behavioral.
• Provides support and reassurance as needed.
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• Communicates optimism.
• Collaborates with the patient and other treatment team members in
treatment planning.
The above components form the basis for an effective psychopharmaco-

logic treatment session and also contribute to successful psychotherapy
management.
10. PSYCHOTHERAPY IN THE OUTPATIENT SETTING

Despite the remarkable advances made in psychopharmacology in the past
few decades, psychotherapy remains a powerful therapeutic tool for
addressing the suffering of mental illness. Psychotherapy is the process by
which the patient and psychiatrist engage in a dialogue that assists the
patient in developing new understandings and behaviors. As a result of
this process, patients experience a new freedom to engage their own lives
with greater meaning and fewer symptoms of illness. Psychotherapy in the
outpatient setting is represented by a multitude of therapy models, a sur-
vey of which is well beyond the scope of this chapter. Despite the features
that distinguish these models from each other, the various psychotherapies
share common features, many of which are related to the practical aspects
of how outpatient psychotherapy is practiced effectively and ethically.
Two major features are the treatment frame and boundary issues.
The treatment frame is analogous to the structural frame of a house,
which promotes a safe and secure environment for its occupants. The
treatment frame encompasses agreed-upon structures such as the location,
duration, and frequency of sessions. It also governs fee arrangements and
informs structural issues such as office arrangement. Particulars of the
treatment frame may vary by therapy modality, treatment goals, and
patient needs and resources. The “psychotherapy hour” typically lasts
45–50 mins with a few minutes left at the end of the hour to complete
charting and to prepare for the next patient. The frequency of visits may
range from several visits per week in psychoanalysis to visits once per
month in more supportive therapies.
The location of outpatient psychotherapy is typically office-based. The
psychotherapy office should be professionally appointed, suitably
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comfortable, and reasonably quiet and allow for seating for the patient and
psychiatrist unobstructed by desks or other furniture. The chairs should be
arranged to avoid a confrontational “head on” stance, which could pro-
duce unnecessary anxiety in the patient. A clock should be positioned so
that the psychiatrist may monitor the time unobtrusively.
Fee arrangements for psychotherapy should be established by agree-
ment before the beginning of formal treatment, and it should be made
clear that timely payment for services is a requirement for on-going treat-
ment. A patient’s avoidance of or failure to pay for services may be a
behavior that can be explored and resolved in the therapy process, but if
such behaviors are resistant to change, then the therapy process becomes
untenable.
Observing appropriate professional boundaries is particularly impor-
tant in psychotherapy because psychotherapeutic work between the
patient and psychiatrist involves engagement at a level of emotional inti-
macy and vulnerability that can arouse powerful affinitive or even sexual
feelings. Such feelings are not in themselves considered to be unethical or
unprofessional, but if indulged, they change the professional nature of the
relationship between doctor and patient to a social and personal one.
Because of the inherent power differential between doctor and patient, the
development of a sexual relationship with a patient or former patient is
recognized always to be unethical, even in cases in which the patient may
offer consent. The psychiatrist must avoid exploiting the patient for his or
her own gratification. In avoiding such boundary violations, the psychia-
trist maintains as the top priority the safety and well-being of the patient.3
Observing professional boundaries also means avoiding dual relation-
ships, which compromise the psychiatrist’s primary commitment to clini-
cally benefiting the patient.
11. TREATMENT ADHERENCE

Even when the best and most appropriate treatment psychopharmacologic
and psychotherapeutic regimens are prescribed, they are unlikely to be
effective if the patient does not adhere to treatment. It is important to
assess the patient’s expectations of treatment before prescribing medica-
tion or recommending psychotherapy. At the time of the initial psychiatric
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evaluation, it is wise to inquire if the patient is anticipating a particular

form or type of treatment. Beginning with a question such as, “In psychia-
try we use a variety of treatment modalities, including medications and
individual and group psychotherapy; is there a particular form of treat-
ment that you prefer or were hoping I would use?” may be informative.
Likewise, if medications are being considered, it is useful to ask patients
if there is a particular medication they think may be helpful. For example,
if the patient says he or she has a family member that responded well to
sertraline and thinks it may be helpful for his or her depression; sertraline
may be a good choice for that patient because the patient will be begin-
ning therapy with hope and the expectation that the treatment will be
effective. Remember, placebo is “effective” for a large percentage of
patients in clinical drug trials.
Some dosing strategies will create an environment conducive to maxi-
mum treatment adherence. Basic strategies include the following:
• Utilize once-daily dosing whenever possible.

• Use the fewest number of medications necessary. Adherence to the
treatment regimen declines exponentially with each additional medi-
cation and dose prescribed. In a recent study of patients receiving
antihypertensive and lipid-lowering medications, adherence declined
as the number of prescriptions increased.1
• Carefully and thoughtfully prescribe medications. For example,
before adding a medication to address a reported symptom, consider
all potential causes of the symptom, including the possibility of an
adverse reaction from another medication that may need to be reduced
or discontinued and the possibility that the problem may be better
addressed through other treatment methods, such as individual
psychotherapy.
It is important to inquire about medication adherence throughout the

course of treatment with patients. Some patients will desire to please their
psychiatrist or other physician and will not inform them that they have
missed doses or are no longer taking the medication prescribed. Some
patients may even allow the doctor to continue to write prescriptions for
them that they do not fill, rather than disappoint their doctor. Possessing
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accurate information about the patient’s medication usage is important

because clinical decisions will be based on this information. An environ-
ment that encourages honest disclosures will increase the odds of obtain-
ing meaningful information regarding treatment response. Starting with
non-judgmental statements, such as “Sometimes people have difficulty
taking medication every day and especially several times a day,” followed
by a face-saving question that assumes the patient has missed doses, such
as, “How many doses in the last week do you estimate that you missed?”
will provide an environment where the patient feels safe in accurately
describing medication usage.
Patients may also have difficulty adhering to psychotherapeutic regi-
mens. Missed appointments, coming late to appointments, and not paying
for sessions are all signs of non-adherence in psychotherapy. In CBT,
homework is routinely assigned to the patient for completion between ses-
sions. When a patient presents to a therapy appointment without having
completed the homework assignment, this should be explored.
12. KEY POINTS

• Professionalism and ethics build the foundation of sound psychiatric
patient care.
• Perform and record the psychiatric evaluation in the same manner
every time, to avoid omissions.
• Safety is one of the most important aspects of psychiatric practice, not
only for the patient, but also for providers.
• Any psychiatric evaluation must assess a patient’s risk for suicide.
• It is important to screen patients for substance use.
• It is important to consider the possibility that an underlying medical
condition may be causing or exacerbating the patient’s psychiatric
presentation.
• A psychiatric formulation using the biopsychosocial model will guide
the comprehensive psychiatric treatment plan.
• The ability to establish and maintain a strong therapeutic alliance
contributes to positive clinical outcomes in psychiatry.
• Psychotherapy remains a powerful and therapeutic tool.
• Attention to treatment adherence is important.
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13. SELF-ASSESSMENT
13.1. Rapport is
(A) A brief form of psychotherapy.
(B) A type of music popular with young people.
(C) The psychiatric write-up after the interview.
(D) A relationship characterized by mutual trust.
Answer: D10
13.2. A 45-year-old man is brought to the psychiatric clinic

after being found wandering on the street. Initial
management includes which of the following:
(A) Admit the man to a psychiatric inpatient unit.
(B) Instruct police to take the man to jail on “public intoxication” charges
because of suspicion that alcohol intoxication is the cause of his
presentation.
(C) Place the patient in a safe environment and obtain additional history
and laboratory evaluation.
(D) Begin psychotherapy.
The patient was found wandering, suggesting mental confusion. The

workup for this patient includes assessing for common causes of mental
confusion including substance intoxication, medical conditions, and
medications. One cannot assume that the patient’s presentation is due to a
primary psychiatric illness without ruling out the possibility that his pres-
entation is due to an underlying medical problem or substance. Although
alcohol intoxication is a common cause of confusion, assuming this with-
out engaging in additional workup to rule out medical causes (e.g. diabetic
ketoacidosis can present in the same way) places the patient at risk for not
receiving appropriate medical or psychiatric treatment. Although psycho-
therapy may be an appropriate long-term treatment for this patient, the
clinician must first establish the diagnosis.
Answer: C9
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14. CASE STUDIES

14.1. A case emphasizing ethical dilemmas
in outpatient practice
A 24-year-old young man is seen by his outpatient psychiatrist for man-
agement of schizophrenia. Since the onset of his illness in his late teenage
years, the patient has suffered frequent auditory hallucinations, which
have been incompletely suppressed by antipsychotic medications. On
presenting to his psychiatrist’s office for a scheduled visit, he tells his
physician that the voices he hears are commanding him to kill a family
member with whom he lives and that he cannot resist the commands any-
more. The psychiatrist asks the patient to consider hospitalization, but the
patient refuses and conveys his plan to leave the office and return home
immediately to carry out the plan. The psychiatrist delays the patient
while calling the police, who then take the person into protective custody,
pending a commitment hearing at a local psychiatric hospital.
REFERENCES
1. Brenner JS. (2009) Association between prescription burden and medication
adherence in patients initiating antihypertensive and lipid-lowering therapy.
Am J Health Syst Pharm 66(16): 1471–1477.
2. Campbell WH, Rohrbaugh RM. (2006) The Biopsychosocial Formulation
Manual A Guide for Mental Health Professionals, pp. 17–70, Routledge, NY.
3. Gutheil TG, Gabbard GO. (1998) Misuses and misunderstandings of bound-
ary theory in clinical and regulatory settings. Am J Psychiatry 155: 409–414.
4. Hales RE, Yudofsky SC. (eds.) (1996) Synopsis of Psychiatry, pp. 188,
5. Krupnick JL, Sotsky SM, Simmens S, Moyer J, Elkin I, Watkins J, Pilkonis
PA. (1996) The role of the therapeutic alliance in psychotherapy and pharma-
cotherapy outcome: Findings in the national institute of mental health
treatment of depression collaborative research program. J Consult Clin
Psychol 64(3): 532–539.
6. Lehrer P, et al. (2002) Psychological aspects of asthma. J Consult Clin
Psychol 70(3): 691–711.
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7. Mojtabai R, Olfson M. (2008) National trends in psychotherapy by office-

based psychiatrists. Arch Gen Psychiatry 65(8): 962–970.
8. Shea SC. (2004) The delicate art of eliciting suicidal ideation. Psychiatr Ann
34(5): 385–400.
9. Sood TR, Mcstay CM. (2009) Evaluation of the psychiatric patient. Emerg
Med Clin North Am 27(4): 669–683.
10. American Heritage. (1997) The American Heritage College Dictionary, 3rd
ed. pp. 1132, Houghton Mifflin, Boston, MA.
11. Williams S. (2007) Cardiovascular medications. Psychosomatics 48(6):
537–547.
12. Young J, Nelson J. (2009) Reconceptualizing medication management:
Implications for training and clinical practice. J Clin Psychiatry 70(12):
1722–1723.
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Chapter 23
General Hospital Psychiatry
Jen Alt McDonald and Mark T. Wright
1. INTRODUCTION
In the United States, recognition of the need for psychiatric services in the
general hospital setting dates back to the early 20th century.9 Over the last
several decades, an extensive body of knowledge pertaining to the care of
people with complex medical/psychiatric illnesses has developed. In the
United States, this led in 2003 to the establishment of “psychosomatic
medicine” as a formal subspecialty of psychiatry.6 Psychosomatic medi-
cine, or “consultation-liaison psychiatry,” services are now integral parts
of many US academic hospitals. In Europe, psychiatrists and psychoso-
maticists are likewise engaged in work at the medicine/psychiatry inter-
face, and in 1997 the European Association for Consultation Liaison
Psychiatry and Psychosomatics (EACLPP) was formed to facilitate clini-
cal, educational, and research growth in this area as well as international
collaboration. Psychiatrists and other health care practitioners in other
parts of the world are actively involved hospital consultation and liaison
work as well.11 Consultation work usually involves a psychiatrist or other
mental health professional responding to a request from a non-psychiatric
colleague to evaluate a patient who is believed to be mentally ill. Liaison
work can involve psychiatric consultations on individual patients, but it is
broader in scope in that it also involves work with patients and caregivers
572
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B1405 International Handbook of Psychiatry FA
General Hospital Psychiatry 573
on a systems level (e.g. educating non-psychiatric caregivers on psychiat-

ric subjects, incorporating psychiatric principles into the treatment of all
patients in a given unit/system, etc). Consultants usually offer advice to
medical/surgical teams on the treatment of patients selected by the team,
whereas the liaison psychiatrist is an integral member of the medical/
surgical team who, either directly or indirectly, works with all of the
patients cared for by the team.26
2. PSYCHIATRIC DISORDERS IN THE GENERAL

HOSPITAL POPULATION
Psychopathology is common among general hospital inpatients, and this
fact has been a major catalyst in the development of general hospital psy-
chiatric services. It has been estimated that up to 50% of medical inpa-
tients have a psychiatric disorder.15 Hospitalized patients can have primary
psychiatric disorders that coexist with medical illness, psychiatric disor-
ders caused by medical illness or medications (i.e., secondary psychiatric
disorders), or both. Variables such as the age distribution and gender ratio
of the hospital population and disease prevalence and severity influence
the prevalence of psychopathology.
Psychiatrists working in general hospitals must be competent to address
the full range of psychopathology but will encounter certain psychiatric
disorders more commonly than others. Delirium is a frequent concomitant
of severe medical illness and is probably the psychiatric disorder most
commonly found in the medical inpatient population. It has been esti-
mated that about 20% of hospital inpatients have delirium at some point
during their hospitalization, and the prevalence of delirium may be much
higher in certain vulnerable populations such as the elderly. Depressive
disorders may be present in up to 15% of the medical hospital population.
Alcohol abuse or dependence may be present in up to 20% of general
hospital inpatients15 and carries with it a significant rate of psychiatric and
medical comorbidity. Anxiety disorders are common in medical inpatients
and are particularly common in certain medical subpopulations (e.g. up to
a quarter of patients presenting with chest pain may suffer from panic
disorder). Approximately 2%–5% of hospitalized patients may suffer
from a somatoform disorder.15
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FA B1405 International Handbook of Psychiatry
574 J. A. McDonald and M. T. Wright
It is important to recognize and address psychiatric illness in general hos-

pital inpatients so that patients’ suffering can be minimized. Numerous
research studies have also shown that, left untreated, psychiatric illness
can increase morbidity and mortality associated with medical illnesses
and have a negative impact on hospital lengths of stay and health care
costs.12,16 Unfortunately, non-psychiatric caregivers frequently fail to
recognize psychiatric illness in medical inpatients, and psychiatric consul-
tation rates rarely exceed 5% worldwide.11
3. THE WORK OF GENERAL HOSPITAL

PSYCHIATRISTS
The focus of general hospital psychiatry is the complex interplay between
psychosocial issues, psychiatric illness, and medical illness. The patients
general hospital psychiatrists are asked to evaluate and treat often have a
range of problems that cannot be adequately addressed by a single medi-
cal specialty or health care profession. Psychiatrists practicing in the
general hospital therefore need a wide range of knowledge and should be
skilled in inter-professional communication and collaboration. Many gen-
eral hospital psychiatry services are now comprised of psychologists,
nurses, and other professionals in addition to psychiatrists.
Psychiatrists practicing in general hospitals face a number of chal-
lenges. Because psychiatrists rarely spend all of their professional time on
general hospital consultations and usually have other responsibilities,
practitioners’ attention and energy may be divided between the hospital
and other practice sites. The distribution of health services across a num-
ber of facilities also leads to general hospital psychiatrists spending a
significant amount of time obtaining information from, and coordinating
care with, other facilities such as freestanding psychiatric hospitals. The
general hospital environment is often not conducive to psychiatric care
since the privacy and time needed for psychiatric assessment and treat-
ment are difficult to come by when patients are frequently getting medical
tests and treatments. The focus on crisis stabilization and rapid pace of
care in many hospitals can exert pressure on general hospital psychiatrists
whose work is fairly labor-intensive (e.g. getting good histories from
medical records, collateral informants, etc. can be very time-consuming).
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Finally, psychiatrists caring for general hospital patients are often required
to balance the needs of patients, patients’ significant others and caregivers,
and the health care system, and these needs can sometimes be at odds with
one another. Given the economic pressures facing most health care sys-
tems, general hospital psychiatrists also need to demonstrate the economic
benefits of their work to system administrators.10,16
Various authors have reviewed the ingredients necessary for an effec-
tive consultation.7 Early clarification of the reasons and goals for psychi-
atric consultation is of paramount importance. In clarifying these issues, a
psychiatrist should keep in mind the possibility of conflicting agendas, as
discussed above. Once a goal for consultation is established, a thorough
review of the available information is undertaken. Given the frequent
inability of patients, and particularly those who are severely medically ill,
to give accurate historical information, it is imperative that collateral
information such as medical records and information from family mem-
bers, friends, and other caregivers be reviewed. Doing this review before
seeing the patient can put the patient’s statements in the proper context.
Finally, clear and concise communication with the patient, treatment
team, and others involved in the case is essential.
4. AGITATION AND AGGRESSION IN THE GENERAL

HOSPITAL
General hospital psychiatrists frequently assess and treat patients with
agitation and aggression. Agitation can be defined as pathologically
intense emotional arousal and motor restlessness. Aggression has been
defined as hostile, threatening, and violent behaviors directed at another
person or objects, usually out of proportion to any provocation.22
Agitation and aggression in hospitalized patients can be related to a
number of common triggers as well as several neuropsychiatric condi-
tions. Physical discomfort caused by things such as hunger or pain can
lead to agitation. Hospitalized patients, and especially those in teaching
hospitals, have a number of caregivers, and interpersonal conflict can
sometimes lead to agitation. In terms of psychopathology, agitation and
aggression are most commonly associated with delirium, dementia, sub-
stance intoxication and withdrawal, mood disorders, psychotic disorders,
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impulse control disorders, and personality disorders. Possible shared

pathogenic factors underlying the agitation/aggression in these different
conditions include dysfunction of the orbitofrontal cortex, amygdala, and
posterolateral and ventromedial hypothalamus, and decreased serotoner-
gic activity.
When a hospitalized patient becomes agitated or aggressive acutely, the
urgent nature of this situation often leads caregivers to first consider psy-
chopharmacological management options while paying little or no atten-
tion to immediate safety concerns or possible causes of the agitation/
aggression. In those patients with more severe acute agitation or aggres-
sion, the first order of business is ensuring the safety of the patient and
others. Mechanical restraints such as limb restraints must sometimes be
used to do this. In many places, hospital rules and local laws place limita-
tions on use of mechanical restraints. Once the safety of the patient and
others is ensured, possible causes of the agitation/aggression should be
sought. A good review of the history and examination may reveal triggers
such as hunger, mild pain, and situational anxiety that are easily elimi-
nated or minimized with non-pharmacological interventions. When medi-
cation is needed to calm agitated or aggressive patients, medication
selection is guided by the cause(s) of the agitation/aggression. In the
general hospital setting, the medications most commonly used by psychia-
trists for “rapid tranquilization” are benzodiazepines and antipsychotics.
These medications are often chosen because of they can be given via
multiple routes (orally, intramuscularly, intravenously) and have a rapid
onset of action. In using these medications, the hospital psychiatrist
should keep in mind the fact that medically ill individuals may be particu-
larly susceptible to some side effects (e.g. patients with severe pulmonary
disease are at increased risk for respiratory depression with benzodiaz-
epines; antipsychotic medications may prolong cardiac repolarization in
patients with severe cardiac disease).
5. ANXIETY IN THE GENERAL HOSPITAL

Anxiety disorders are the most common psychiatric disorders in the gen-
eral population, with approximately one in five people having an anxiety
disorder. In medically ill patients and in patients presenting to primary
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care physicians, the prevalence of anxiety disorders is similarly high.

These patients often have significant somatic symptoms, comorbid psy-
chiatric illnesses, and functional impairments and tend to utilize more
medical care than patients without anxiety disorders.
Anxiety is a normal response to stress, and some level of anxiety is to
be expected in hospitalized patients. A normal amount of anxiety can
motivate patients to seek treatment for their illness and comply with medi-
cal recommendations. Excessive or pathological anxiety, however must be
addressed as high levels of anxiety can interfere with a patient’s care.
Patients with significant anxiety may refuse evaluations or treatments
because of fear or, conversely, they may limit their engagement with treat-
ment due to denial of the seriousness of their condition.
Hospitalized patients encounter a number of “threats,” all of which can
be anxiety provoking. One of the most prominent fears faced by hospital-
ized patients is the fear of death. Although normal coping mechanisms
including rationalization, denial, social support, and religious faith typi-
cally aid patients in dealing with this fear, the significance of a hospital
stay can overwhelm patient’s coping strategies, leaving them feeling
scared and vulnerable. Hospitalized patients may also fear pain, loss of
control, and being abandoned by their family or care team. Addressing a
patient’s underlying concerns can often be as effective as pharmacological
treatment for anxiety.
Anxiety disorders can be difficult to diagnose in a medical setting.
Some patients presenting with somatic complaints actually have anxiety,
while a significant number of patients presenting with anxiety actually
have a medical illness. Although the core symptoms of anxiety disorders
are fear, obsessions, worry, and nervousness, physical symptoms are also
prominent in anxiety disorders. These somatic symptoms, including palpi-
tations, nausea, sweating, numbness, and gastrointestinal problems, can
confound the diagnosis of anxiety (Table 1). Further, many patients only
describe their somatic symptoms and do not mention they are also feeling
nervous or worried. In cases where patients present with only somatic
symptoms, up to 50% of anxiety disorders may go undiagnosed. Difficulties
diagnosing anxiety can be detrimental to the patient and expensive for
society as patients often undergo unnecessary tests and receive ineffective
treatments before their anxiety disorder is eventually discovered.
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Table 1. Somatic signs and symptoms of anxiety.
Dizziness, light-headedness, fainting

Nausea, diarrhea, abdominal pain
Feeling short of breath, sensation of choking
Chest pain, rapid heartbeat, palpitations
Numbness, tingling
Sweating, chills
Restlessness, tremors
Insomnia
Table 2. Medical disorders and substances associated with anxiety.

Endocrine disorders: Cushing’s disease/syndrome, Addison’s disease, hyperthyroidism,
pancreatic tumors, pituitary tumors, diabetes/hypoglycaemia
Drugs and substances: Antidepressants, thyroid hormone, steroids, antihypertensives,
caffeine, beta adrenergic agonists
Cardiovascular diseases: Anemia, congestive heart failure, myocardial infarction
Respiratory diseases: Asthma, pneumonia, pulmonary edema, pulmonary embolus
Metabolic problems: Acidosis and electrolyte abnormalities
Neurologic disorders: Brain tumors, encephalopathy, epilepsy, migraines, Parkinson’s
disease, Alzheimer’s disease
Although some patients presenting with somatic complaints actually

have an underlying anxiety disorder, it is important to remember that
between 5% and 42% of patients presenting with anxiety symptoms actu-
ally have an underlying medical illness. Several medical illnesses can
present as anxiety, with the most common being neurologic and endocrine
disorders. Additionally, both prescribed medications and street drugs can
precipitate anxiety. Withdrawal from alcohol, nicotine, barbiturates, or
benzodiazepines and intoxication or use of cocaine, caffeine, and amphet-
amines are commonly overlooked causes of anxiety (Table 2).
The following factors should be considered when trying to determine
the cause of anxiety:
• Epidemiological factors should be considered. A medical cause of

anxiety should be sought in patients with anxiety beginning after the
age of 35, no family history of anxiety, no significant life events
preceding the anxiety, or a poor response to anti-anxiety agents.
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• Some particular medical and substance issues should always be

considered as a possible source of the anxiety. For example, in a
patient with chronic obstructive pulmonary disease (COPD), is
anxiety caused by respiratory distress or beta adrenergic agonist bron-
chodilator treatment? How much caffeine does the patient use?
In the hospital setting, rapid interventions are often favored as patients are
typically hospitalized for only a brief time. Medications are often the first
line treatment for anxiety in inpatients. However, a complete assessment of
the cause of a patient’s anxiety may lead to interventions other than medi-
cation management. Cognitive and behavioral therapies are effective treat-
ments for anxiety disorders and may be especially useful in patients with
severe comorbid medical conditions in whom pharmacotherapy may be
contraindicated. The SSRIs are the most common treatment for anxiety
disorders because of their efficacy and favorable side-effect profile.
However, SSRIs may take six or more weeks to become effective and may
initially increase anxiety. Because of this, SSRIs are sometimes started in
conjunction with a benzodiazepine for more immediate relief. Serotonin–
norepinephrine reuptake inhibitors (SNRIs) are also generally effective in
treating anxiety but, like SSRIs, they can take weeks to work and may
increase anxiety early in treatment. Benzodiazepines are effective in treat-
ing anxiety, reasonably safe, and have a fast onset of action, making them
popular in an acute setting. However, there are risks to using these medica-
tions as well. In the hospital, the largest risk of using a benzodiazepine is
the sedative effect of these medications and patients must often be started
at a low dose to keep them from being over-sedated. Patients with liver
disease and elderly patients can find benzodiazepines to be particularly
sedating. Patients with respiratory problems, including COPD and sleep
apnea, are at risk of significant respiratory impairment with benzodiaz-
epines. Additionally, concerns about abuse and dependence prevent use of
these medications with some patients. Finally, although all benzodiaz-
epines are effective in treating anxiety, the pharmacokinetics of each medi-
cation must be taken into consideration when choosing a treatment. In
general, the risk of rebound anxiety is greater with the short-acting benzo-
diazepines, although the clinical effect of these drugs is more rapid.
Longer-acting medications have a slower onset of action and will clear less
quickly, but there are fewer problems with abrupt onset of sedation and
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confusion with the long acting benzodiazepines. In addition to benzodiaz-

epines, several other classes of medication are also used to treat anxiety in
the inpatient setting. Anticonvulsants, especially gabapentin and pregaba-
lin, are sometimes used to treat anxiety. Because these medications are
renally excreted, they are an appropriate choice for patients with liver dis-
ease. Atypical antipsychotics, especially the more sedating drugs such as
quetiapine, are also used. Beta blockers, most notably propranolol, can be
used to decrease some of the autonomic symptoms of anxiety. However,
side effects including fatigue, hypotension, and dysphoria can make these
mediations difficult to use with medically ill patients. Finally, buspirone
may be used in anxiety disorders, although its gradual onset of action
(4–6 weeks, similar to antidepressants) makes it ineffective for acute use.25
6. DEPRESSION IN THE GENERAL HOSPITAL

Depression is a common problem in medically ill patients. It is thought
that between 10% and 20% of medical inpatients and patients with
chronic diseases have major depression.8 Certain subsets of the medically
ill may have even higher rates of depression with up to 27% of patients
with cardiac disease, 29% of patients with cancer, and 75% of patients
with Parkinson’s disease meeting diagnostic criteria for depression.3
Patients with depression and a comorbid medical illness often struggle
with apathy and amotivation and can have serious problems adhering to a
treatment regimen for their medical condition. Depressed patients may
also have other difficulties such as poor hygiene or poor nutrition that can
further complicate their medical problems. In patients with medical ill-
nesses, depression has been associated with poor quality of life as well as
increased mortality from the medical illnesses.4
Despite the frequency with which it occurs in medically ill patients,
depression is often overlooked in the hospital. When a patient with a
severe medical illness develops depression, it is often seen as an inevitable
consequence of their illness. Many physicians feel that patients have a
“reason” to be depressed if they are ill, and this often prevents accurate
diagnosis and early treatment. Further, many non-psychiatric profession-
als do not feel competent to treat depression, leading them to under-
diagnose this disorder in their patients. It is important to remember that,
although transient feelings of sadness, helplessness, and anger are normal
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responses to a stressful situation, full-blown depression is never a normal

reaction to a medical illness.
The diagnosis of depression in a hospitalized patient can be a chal-
lenge. Four of the nine cardinal symptoms of depression-insomnia, ano-
rexia, fatigue, and decreased concentration-can accompany medical
illness or medical treatments. Some patients may feel more comfortable
reporting these physical symptoms rather than mood changes or anhedo-
nia, and this can confuse the diagnostic picture. Many medical illnesses
can present with symptoms of depression, and many medications can
contribute to depression as well (Table 3).
In evaluating a hospitalized patient for depression it is important to ask
the following questions:
(1) What are the epidemiological factors at play? In an older patient with
no personal or family history of depression, medical causes of depres-
sion must be carefully sought.
Table 3. Medical disorders and substances associated with depression.
Neurologic: Stroke, Parkinson’s disease, sleep apnea, multiple sclerosis, Huntington’s

disease, epilepsy, Alzheimer’s disease, traumatic brain injury
Endocrine: Cushing’s disease/syndrome, Addison’s disease, hypothyroidism
Infectious:
— CNS infections, including HIV
— Systemic infections, including sepsis, urinary tract infection, pneumonia
Cancer
Cardiac: Congestive heart failure, myocardial infarction
Nutritional: B12 deficiency, foliate deficiency
Metabolic: Diabetes mellitus
Drugs and substances:
— Alcohol
— Sedative/hypnotics
— Opioids
— Metoclopramide, H2 receptor blockers
— Antihypertensives, especially beta blockers, methyldopa, clonidine, reserpine
— Sex steroids including oral contraceptives and anabolic steroids
— Glucocorticoids
Substance withdrawal: Nicotine, amphetamines, cocaine
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(2) Are the patient’s symptoms due to a medical condition? If so, will treat-
ment of this condition relieve the symptoms? In diseases such as hypo-
thyroidism where treatment of the medical condition will relieve the
depression, this should be done prior to considering other treatments
such as antidepressant medication. If the patient’s depression is due to
a medical condition but treatment of this condition will not relieve the
depression (e.g. post-myocardial infarction or post-stroke depression),
consideration should be given to starting an antidepressant medication.
(3) Are the patient’s symptoms due to a medication?
Depression occurring in the hospital setting can be difficult to treat.

Most interventions for depression are slow to produce results, and inpa-
tient teams often need a patient’s depression to clear rapidly so that the
patient can participate fully in their care. Although not as commonly used
as medications, psychotherapy is often key to improving the health status
of depressed, medically ill patients. Many hospitalized patients are strug-
gling with grief, fear, and loss of autonomy and independence. Even brief
psychotherapy interventions can help patients deal with these issues and
improve their coping ability. In general, therapy for depressed hospital-
ized patients focuses on enhancing social support, helping patients express
their emotions, increasing coping skills, and teaching cognitive restructur-
ing techniques. In selecting a medication to treat a hospitalized patient
with depression it is important to consider (1) the patient’s previous medi-
cation trials and responses, (2) the side effect profile of the medication,
and (3) medication interactions. The greatest issue when using antidepres-
sants in the inpatient setting is the length of time it takes for them to
become efficacious (several weeks to full effect). SSRIs are generally the
first line treatment for medically ill patients. These agents have a fairly
benign side effect profile and minimal drug–drug interactions. Side effects
that are common with all SSRIs include nausea, sexual dysfunction, and
CNS activation. Paroxetine and fluvoxamine can also have sedative
effects. SSRIs have the potential to affect cytochrome P450 activity and
this must be taken into consideration when using these medications. In
specific inpatient groups, SSRIs may carry additional risks. The GI side
effects of SSRIs can be problematic in patients with cancer who are under-
going chemotherapy or in post-surgical patients who are attempting to
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return to a regular diet. Additionally, SSRIs can increase the risk of GI

bleeding, especially when combined with NSAIDs. Since many hospital-
ized patients are on antiplatelet medications or have platelet abnormali-
ties, the risk of bleeding must be carefully weighed. SNRIs have many of
the same side effects as the SSRIs. Additionally, both venlafaxine and
duloxetine carry a risk of increased blood pressure which may be con-
traindicated in some hospitalized patients. Duloxetine however can be a
useful first line agent in patients with chronic pain syndromes as it is
known to treat neuropathic pain. When prescribing bupropion to medi-
cally ill patients, it is important to remember that this medication also
carries a risk of hypertension and can lower the seizure threshold.
Therefore it is typically not used in patients with a history of head trauma
or a seizure disorder. Tricyclic antidepressants (TCAs) are rarely used in
hospitalized patients. The anticholinergic side effects (dry mouth, consti-
pation, urinary retention, tachycardia, and confusion) coupled with the
fatigue, orthostatic hypotension, and cardiac conduction changes that can
result from these medications have limited their use. However, in select
populations, these medications may prove helpful. Patients with irritable
bowel syndrome (IBS) may see some improvement in their symptoms
with a TCA, and patients with Parkinson’s disease may be prescribed
TCAs as they tend to gain some physical benefit from the anticholinergic
activity of these medications.24 Psychostimulants such as methylphenidate
are also used in treating depression in hospitalized patients. Stimulants
can rapidly improve depression, apathy, and fatigue and allow patients to
better engage in their care while hospitalized. The rapid onset of action of
stimulants (3–5 days) makes them useful in an acute setting. Evidence
supporting the use of stimulants is limited, however and patients must be
carefully monitored for hypertension, cardiac arrhythmias, and psychotic
symptoms while on stimulants.
7. SUICIDALITY IN THE GENERAL HOSPITAL

Assessment of suicidality is a staple of general hospital psychiatry. In the
United States, there are approximately 12–25 non-fatal suicide attempts
for every completed suicide, and many attempt survivors will be admitted
to a general hospital. In some places, psychiatric evaluation of suicide
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attempters is required, and in others it is not.11 In addition to patients who

have attempted suicide, hospital psychiatrists are also often asked to
evaluate patients with suicidal ideation who have not harmed themselves,
and patients who have harmed themselves without a clear expectation of
death (i.e. suicide gesture, or parasuicide, patients). In dealing with hospi-
talized patients with suicidal ideation and behaviors, psychiatrists should
do a systematic assessment while considering the known risk factors for
suicide, use this information to make a common-sense estimation of the
patient’s suicide risk, and take reasonable steps to minimize these risks.
Suicide risk is assessed by doing a thorough general psychiatric exami-
nation while paying special attention to factors that may increase or
decrease risk of suicide. Since a significant minority of patients with
suicidal ideation will deny it, it is important to review any available his-
torical information before interviewing a patient. Suicidal ideation and
intent may have been revealed in earlier interactions with law enforce-
ment officers, paramedics, emergency department caregivers, and hospi-
tal caregivers. When interviewing a potentially suicidal patient, it is
important to first establish a calm and accepting milieu in which patients
can feel free to express their thoughts at their own pace; establishing such
a milieu in the often frenzied hospital setting can be difficult, though. In
discussing suicide with a patient, it is imperative that the examiner clarify
the patient’s thoughts as much as possible. This is especially a concern in
cultures in which terminology related to suicide can be vague (e.g. some
patients will express a desire to die by saying “I just want to go to sleep”)
or suicide is taboo. In working with patients who have harmed them-
selves, it is important to ask about immediate antecedents (i.e. why
now?). It is also useful to ask suicidal patients what might lead them to
harm themselves, and what might prevent them from harming them-
selves, in the future. Again, because the veracity of suicidal patients’
reports is sometimes called into question, it is imperative that a hospital
psychiatrist obtain collateral information from sources such as family,
friends, and outpatient caregivers. In deciding whether or not to obtain
such information, concerns about patient safety often trump concerns
about releasing confidential information. It should also be kept in mind
that one can gather information while releasing little or no information
about the patient.
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A number of factors may increase or decrease an individual’s risk of

suicide.20 In evaluating patients who have made a suicide attempt, any
evidence of forethought (e.g. recent talk of, or writing about, suicide; giv-
ing away belongings, or making a will; extensively planning a suicidal
act) is worrisome. Losses, whether threatened, real, or perceived, fre-
quently precede suicidal ideation and behavior, and taking an inventory of
patient losses is an important aspect of the psychiatric evaluation. Patients
with histories of suicidal or any other violent behavior are at increased risk
for completed suicide. In terms of specific psychiatric disorders, patients
with mood, psychotic, eating, or substance use disorders are at particu-
larly increased risk for suicide. Certain factors that cross psychiatric diag-
noses such as turmoil, anxiety, hopelessness, pessimism, impulsivity,
psychosis (especially auditory hallucinations commanding a patient to
harm themselves), and insomnia are especially worrisome and should be
considered in every suicide evaluation. Certain medical conditions such as
HIV infection, epilepsy, cancer, traumatic brain injury, spinal cord injury,
and Huntington’s disease are associated with an increased risk of suicide.
Any medical condition associated with chronic pain, immobility, disfig-
urement, depression, impulsivity, or a poor prognosis is especially con-
cerning when considering suicide risk. Limited social support, whether
perceived or real, also increases suicide risk and is important to ask about
in the psychiatric evaluation. When working with suicidal patients, disen-
gagement and poor cooperation with care should be regarded as worri-
some signs. In keeping with these factors that elevate suicide risk, a
number of factors have been found to decrease suicide risk including good
problem-solving skills, belief in a religion that forbids suicide, good
social support, and ready access to health care.
After a comprehensive evaluation, a hospital psychiatrist’s first task is
to make a common-sense judgment about the patient’s current suicide
risk. In assessing suicidal patients, psychiatrists and other caregivers
should remember that estimation of suicide risk, even after the most thor-
ough clinical assessment, is difficult and that factors that increase and
decrease suicide risk change over time. All the most competent practi-
tioner can do in a suicide evaluation is estimate the chances that a patient
will attempt self-harm in the near future. After a suicidal patient has been
assessed, taking steps to ensure their safety is the first order of business.
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Safety measures can be tailored to the degree of the patient’s suicidality.

With hospital patients who are felt to be at significantly increased risk for
suicide, it is important to first make the patient’s environment safe by
removing means for easy self-harm such as medications, sharp objects,
electrical cords, belts, and shoelaces. In US medical/surgical hospitals,
patients felt to be at high risk for self-harm are usually placed under
continuous observation by a staff member (a “sitter”), and patients at
lower levels of risk are often evaluated by staff at intervals ranging from
15–30 mins. Once immediate safety issues are addressed, a psychiatrist
can begin to minimize suicide risk factors and bolster protections against
suicide. Psychotherapeutic and/or pharmacological treatments aimed at
anxiety, depression, hopelessness, psychosis, impulsivity, insomnia, and
pain are often employed in the early treatment of suicidal patients, and
supports are maximized. Disposition planning should begin as early as
possible so that when a patient is medically stable enough for hospital
discharge an appropriate psychiatric treatment plan is in place. Post hos-
pital psychiatric care should be given in the “least restrictive” setting that
is appropriate for the patient’s level of suicide risk. Most patients felt to
be at significantly increased risk for suicide will need to be transferred to
an inpatient psychiatric unit for further stabilization. For patients at lower
levels of suicide risk (including patients with chronic suicidal ideation and
parasuicidal acts17), discharge home with a plan for continued mental
health care is sometimes appropriate. Before discharging a patient home,
the hospital staff should work with the patient’s significant others to make
the home environment as safe as possible. Hospital psychiatrists usually
emphasize the importance of removing firearms and unnecessary medica-
tions from the home. Post hospital psychiatric care can be given in a par-
tial hospitalization program or outpatient setting as appropriate and
should begin promptly after hospital discharge.
8. SOMATOFORM DISORDERS, FACTITIOUS

DISORDERS, AND MALINGERING
IN THE GENERAL HOSPITAL
Hospital psychiatrists are frequently asked to evaluate patients whose
physical signs and symptoms are not substantiated by, or are inconsistent
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with, findings on examinations and tests. In evaluating patients for possi-

ble “psychogenic” illness, it is important to consider somatoform disor-
ders, factitious disorders, and malingering in the differential diagnosis. It
is important to remember, though that patients thought to have a psycho-
genic illness may actually have an undiagnosed medical condition. Only
after ruling out a medical basis for the patient’s complaints should a soma-
toform or factitious disorder be considered.
As discussed in Chapter 13, the somatoform disorders are a group of
disorders in which individuals unconsciously/unintentionally transform
stress and conflict into physical signs and/or symptoms.14 These disorders
are differentiated from the factitious disorders and malingering in which
illness signs and symptoms are consciously/intentionally produced.
Physical symptoms and a lack of insight into their true nature often lead
patients with somatoform disorders to consult non-psychiatric physicians,
and psychiatrists usually see these patients when they are referred by a
non-psychiatric colleague. The specific somatoform disorders include
somatization disorder and conversion disorder. Patients with somatization
disorder develop multiple “psychogenic” physical symptoms by early
adulthood that last a number of years and often lead to extensive medical
consultation. Unrevealing medical evaluations and unsuccessful somatic
treatments often lead to patients with this disorder seeing hospital
psychiatrists as do their comorbid anxiety, mood, substance use, and per-
sonality disorders. Poor insight into the nature of the illness may lead
somatization patients to reject psychiatric care and sometimes makes fol-
low up with a primary care physician the only treatment option. A primary
physician can support the patient and try to link the idea of psychosocial
stress with physical symptoms while minimizing unnecessary tests and
treatments that may result in iatrogenic harm. There are some suggestions
in the literature that CBT and antidepressant medications may be helpful
in somatization disorder. Conversion disorder involves unconscious con-
version of stress or conflict into “pseudoneurological” symptoms such as
blindness, paralysis, and seizures. Neurological evaluation of such
patients often yields unusual physical examination findings and unreveal-
ing neuro-imaging studies, and hospital psychiatrists are often called in to
help solve the puzzle. Conversion episodes often resolve with reassurance,
but a significant number of patients will have further episodes, and
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repeated episodes can become a chronic problem in some individuals. The

CBT may be helpful with episodes that do not resolve with reassurance,
and with chronic illness.
The factitious disorders are a group of disorders characterized by con-
scious/intentional feigning or exaggeration of physical and/or mental ill-
nesses. Patients with these disorders are primarily motivated by the
satisfaction they get from being in the sick role (“primary gain”). Common
factitious physical complaints and findings include pain, abnormal bleed-
ing, fever, hypoglycaemia, hyperthyroidism, and non-healing wounds.
Factitious mental illnesses can be seen as well and range from bereave-
ment, depression, posttraumatic stress disorder, and eating disorders to
cognitive disorders or psychosis. The initial presentation of factitious
disorder patients can sometimes be dramatic. On questioning, these
patients will typically give histories of extensive medical evaluations and
diagnoses. Some individuals produce signs and symptoms of illnesses, or
true illnesses, in dependent children or elders, and this disorder has been
called “factitious disorder by proxy.” Factitious disorder patients often
have comorbid depressive disorders, substance use disorders, and person-
ality disorders (typically borderline and antisocial personality disorders).
The disorder can be episodic or chronic. Patients with factitious disorder
are often demanding and angry and “split” their caregivers. These prob-
lems, and the tendency of factitious patients to want to leave the hospital
against medical advice when their needs are not met, often lead to requests
from caregivers for psychiatric consultation. In evaluating a patient sus-
pected of having a factitious disorder, gathering as much collateral infor-
mation as possible is of paramount importance since fabrication is a
hallmark of the illness. Once a psychiatrist establishes a diagnosis of facti-
tious disorder, the first order of business is usually speaking to the
patient’s care team. In this meeting, the diagnosis should be discussed and
any anger or desire to confront the patient should be diffused. It should
also be emphasized that patients with factitious disorder often have self-
induced, or iatrogenic, “real” medical concerns and that complaints
offered by the patient should not be immediately presumed to be facti-
tious. At the same time, it is important to minimize diagnostic tests and
treatments related to signs and symptoms that are likely factitious in
nature. Patients diagnosed with factitious disorder will usually not admit
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the true nature of their illness nor will they accept a referral for outpatient
mental health care.13 If patients are willing to accept treatment, it should
be some form of insight-oriented psychotherapy designed to explore why
the patient seeks attention through feigning medical illness. Psychotropic
medication treatment is primarily aimed at addressing comorbid illnesses
and is not the first line of treatment in these patients.
Malingering, like the factitious disorders, involves conscious/inten-
tional feigning or exaggeration of physical and/or mental illnesses. Unlike
factitious illness, though, malingering is motivated primarily by tangible
incentives such as medications of abuse, disability payments, and lawsuit
awards (i.e. “secondary gain”). Unlike factitious disorder patients who
often cooperate with tests and treatments in order to remain in the patient
role, malingerers are generally uncooperative with any medical care that
is not closely related to the gain they are seeking.
9. SUBSTANCE WITHDRAWAL IN THE GENERAL

HOSPITAL
Substance abuse and dependence are prevalent and costly problems
worldwide. Patients who abuse alcohol are commonly seen in general
hospital settings as these patients are at greater risk of heart disease, liver
problems, cancer, and infectious diseases. Additionally, alcohol dependent
patients usually stop drinking at the time of admission, thus increasing
their risk of developing alcohol withdrawal while in the hospital. For most
alcohol dependent patients, withdrawal from alcohol begins 6–8 hrs after
their last drink, peaks within a day, and resolves within one week.
Although only 5% of alcohol dependent patients develop more than mild
to moderate withdrawal symptoms (Table 4), patients withdrawing from
alcohol can be at risk of life-threatening complications including grand
mal seizures and delirium tremens. In the case of delirium tremens, this is
a medical and psychiatric emergency as up to 20% of patients will die
without adequate treatment.21
All patients being treated for alcohol withdrawal need to have electro-
lyte and nutritional problems corrected. They also need a thorough evalu-
ation for possible medical conditions such as cardiac, liver, or pancreatic
disease, GI bleeding, infections, and neurological problems. In terms of
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Table 4. Signs and symptoms of withdrawal.
Alcohol withdrawal
— Autonomic hyperactivity
— Hand tremor
— Insomnia
— Nausea or vomiting
— Visual, tactile, or auditory hallucinations
— Psychomotor agitation
— Anxiety
— Seizures
Opioid withdrawal
— Anorexia, abdominal cramps, nausea and vomiting
— Anxiety, insomnia, irritability, restlessness
— Opioid cravings
— Dysphoria, fatigue
— Increased blood pressure, pulse, and respiratory rate;
hot and cold flashes; low grade fever
— Headache
— Muscle and bone pain; muscle spasms
— Mydriasis
— Lacrimation, perspiration, piloerection, rhinorrhea
— Yawning
Cocaine withdrawal
— Dysphoria, depression
— Psychomotor agitation or slowing
— Fatigue
— Insomnia or hypersomnia
— Vivid dreams, nightmares
— Appetite increase
electrolyte and vitamin replacement, many patients with chronic alcohol

use have hypomagnesemia, hypophosphatemia, and hypokalemia as well
as a thiamine deficiency. Any patient being treated for alcohol withdrawal
should be given 100 mg of thiamine daily while they are in withdrawal.
Patients with thiamine deficiency, and particularly patients who are given
glucose prior to administration of thiamine, are at risk of developing
Wernicke’s encephalopathy. Patients with this condition typically have a
change in their level of consciousness, ophthalmoplegia, and ataxia.
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Episodes of Wernicke’s encephalopathy can lead to Wernicke–Korsakoff

syndrome, an irreversible amnestic disorder.
After comorbid physical conditions are addressed, the question of
when and where to detoxify a patient from alcohol must be considered.
Patients can complete alcohol detoxification safely in either the inpatient
or outpatient setting, depending on their particular needs. In general,
patients with a history of significant withdrawal symptoms including
seizures or delirium tremens, patients with very high levels of alcohol
consumption, and those with serious comorbid medical or psychiatric
illnesses are better served in an inpatient setting while most other patients
can tolerate an outpatient detoxification.
Patients in alcohol withdrawal are typically treated with benzodiaz-
epines and/or anticonvulsants to help ameliorate withdrawal symptoms
and prevent advanced stages of withdrawal. Benzodiazepines reduce with-
drawal severity as well as the incidence of delirium and seizures.
Anticonvulsants have been shown to reduce withdrawal severity although
it is unclear if they have significant effects on delirium and seizures.
Patients in withdrawal who are treated with benzodiazepines may be
treated with a fixed dosing schedule or a symptom triggered schedule. In
the fixed dosing schedule, a patient is first given a benzodiazepine every
hour until symptoms resolve or they develop mild sedation. Patients are
then kept on a scheduled dose of this medication for 1–2 days and then it
is either discontinued or rapidly tapered. Symptom-triggered treatment
uses the Clinical Institute of Withdrawal Assessment for Alcohol Scale
(CIWA) to measure withdrawal symptoms, and benzodiazepine dosing is
based on the CIWA score. The advantage of this approach is that patients
typically require lower doses of benzodiazepines and are therefore less
sedated than with a fixed dosing schedule. No benzodiazepine has been
shown to be more efficacious than any other for treatment of alcohol with-
drawal. Therefore, the selection of a specific benzodiazepine should be
made based on the patient’s medical history and the half-life and liver
metabolism of the medication.1
Another common withdrawal syndrome encountered in the hospital
setting is that of opioid withdrawal (Table 4). Both heroin users and
patients who abuse prescription narcotics are at risk of withdrawal when
admitted to the hospital. Some opioid dependent patients are admitted to
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medical/surgical hospitals for detoxification prior to beginning outpatient

addictions treatment programs. The onset and duration of withdrawal var-
ies with the type of opioid used. Patients who abuse oxycodone develop
withdrawal symptoms 8–12 hrs after stopping use, and the withdrawal
syndrome lasts approximately one week. Methadone, on the other hand,
has withdrawal symptoms that appear 36–72 hrs after cessation of use and
has a withdrawal syndrome that lasts 14–21 days. These differences are
important to remember when attempting to detoxify a patient from opi-
oids as the type of drug used will affect the duration of the withdrawal
treatment. As with alcohol withdrawal, opioid detoxification can take
place in inpatient or outpatient settings. Unlike withdrawal from alcohol,
opioid withdrawal generally does not have any life threatening symptoms
and does not necessitate inpatient treatment. Some medically compro-
mised individuals, though, may be at risk of exacerbation of their medical
illnesses by withdrawal phenomena (e.g. vomiting). Many patients prefer
an inpatient withdrawal as their withdrawal symptoms can be treated more
efficaciously and they can complete their withdrawal more rapidly.
There are several different methods of managing opioid withdrawal:
opioid agonist substitution and taper, the use of alpha adrenergic agents,
and rapid detoxification procedures. Methadone and buprenorphine are
the most common agents used to prevent withdrawal and gradually detox-
ify opioid dependent patients. Determining the exact dose of medication
to start for detoxification is complicated since quantifying patients’ nar-
cotic abuse can be difficult. The purity of illicitly obtained narcotics can
vary greatly. In using methadone as an opioid substitution agent, the start-
ing dose should be less than 40 mg a day in order to prevent respiratory
suppression. Dosage adjustments can be made over several days until the
patient is stable and not exhibiting any withdrawal symptoms. At that
point, the patient’s methadone can then be tapered over 5–7 days.23 With
buprenorphine, the patient must be in some opioid withdrawal before this
medication is started in order to prevent precipitating further withdrawal.
Typically, patients are given doses of 2–4 mg of sublingual buprenorphine
every hour until they are not in withdrawal or until they have had a total
of 8–12 mg. As with methadone, dose adjustments can be made over the
next several days and then the buprenorphine can be tapered over one
week. It is important to remember that when using either buprenorphine
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or methadone these medications may not completely control withdrawal

symptoms and other medications (such as NSAIDS for aches or antiemet-
ics for nausea and vomiting) may also be needed. Alpha adrenergic agents
are also used to detoxify patients from opioids. Clonidine is the most com-
monly used alpha-adrenergic agent and is useful for treating many of the
autonomic symptoms of opioid withdrawal. Heart rate and blood pressure
must be carefully monitored when using higher doses of clonidine as
patients on this medication are at risk of hypotension and syncope.
Clonidine is usually given in divided doses, typically every 4–6 hrs, for
four days and then gradually tapered. Clonidine does not treat insomnia,
muscle aches, cravings, or lethargy and additional medication may be
needed to address these symptoms. Clonidine may also be combined with
naltrexone for a more rapid withdrawal. Patients are given naltrexone to
induce withdrawal and are simultaneously given clonidine to provide
relief from the withdrawal symptoms. Patients need to be monitored
closely during this type of withdrawal as they can develop delirium from
their opioid withdrawal or hypotension from the clonidine.
10. OTHER ISSUES IN THE GENERAL HOSPITAL

10.1. Informed consent
Obtaining informed consent shows respect for the autonomy, dignity, and
self-determination of patients. Patients may give or withhold consent for
testing or treatment when (1) they have received adequate information
about the test or treatment, (2) they possess the mental capacity to make a
decision, and (3) the decision is made without coercion. In the hospital
setting, a patent’s capacity to make medical decisions sometimes comes
into question and this can lead to psychiatric consultation. The ability to
give or withhold informed consent is called competence and is a legal
term, not a clinical one. A psychiatrist assessing a patient’s capacity may
be called on to make a recommendation as to whether or not a patient’s
competence should be formally determined by a court. Evaluation of four
skills is required to determine if a patient has the mental capacity to make
their own medical decisions. First, and most basically, patients should
have the ability to express a clear choice regarding their care and to
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maintain this choice long enough for it to be implemented. Secondly,

patients must have the cognitive capacity to understand the options avail-
able to them. After being educated by their treatment team, they should be
able to describe their treatment options and the potential risks and benefits
of each. Next, patients need to be able to apply the information about their
treatment choice to themselves and understand the possible effects that
each treatment option could have on their lives. Finally, patients must be
able to rationally process the information presented to them. This does not
mean that patients must make a decision that appears ‘rational’ to an out-
side observer, but rather they must be able to analyze information in a
rational and logical way. This involves actually weighting the risks and
benefits (as opposed to just understanding the risks) of their treatment
options and being able to identify factors that are important to them in the
decision making process. A good assessment of competence should com-
ment on all four of these areas.2 Decision-making capacity is often
impaired by delirium, dementia, paranoia, depression, or denial. For
patients who lack capacity, the right to consent to or refuse therapy is
transferred to a surrogate decision maker who is given the authority to
consent or refuse on the patient’s behalf.
10.2. Conflicts within the treatment team

Hospitals are a high-stress environment for patients, families, and treat-
ment teams. In modern hospitals, different professional groups (physi-
cians, nurses, medical assistants, physician’s assistants, respiratory
therapists, nutritionists, etc.) all work together to advance patient care.
Although it is clear that inter-professional teams provide the best out-
comes, any time a group of professionals work together there can be
issues with power dynamics, poor communication, confusion over roles
and responsibilities, and differences in the approach to patient care. Just
as a well-functioning team can advance patient care, a poorly functioning
team can have adverse effects on patient care, service, and safety.
Psychiatrists in consultant and liaison roles may find themselves observ-
ing or embroiled in team conflict. It is important to remember that, in gen-
eral, problems within a treatment team are not a result of hostility between
team members, but rather a result of poor communication. Psychiatrists can
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have a unique role in teaching and promoting skills that lead to conflict reso-
lution, healthy communication, and role definition for team members. Often
a ‘team meeting’ that allows participants to discuss communication break-
downs and role confusion and then re-focus on patient care can be helpful.
10.3. Conflicts with families

The stress of having a loved one in the hospital can lead families to
become very demanding. This often results from a feeling of loss of con-
trol. Demanding families can increase the stress on the treatment team and
lead the team to shut down in the face of difficult questions and requests.
When psychiatrists become involved in these situations they can serve as
a mediator between the family and the treatment team. Reminding teams
that demanding families are usually acting out of fear and that their goal
is to be heard and understood can go a long way toward helping team
members be more accommodating.
As when mediating conflict within treatment teams, medicating con-
flict between families and treatment teams can be facilitated by a family-
team meeting. In general, families find these conferences to be more
helpful if they are held in a private location, and if clinicians spend more
time listening as opposed to talking. A pre-conference meeting of the
treatment team may be useful in order to assure that all members agree on
the goal of the family conference, the patient’s prognosis, and the treat-
ments to be recommended. This helps facilitate consistent communication
from all members of the treatment team and decreases the confusion
family members can feel when they hear different things from different
people. After explaining the prognosis and treatment recommendations,
the focus of a family meeting should turn to answering family members’
questions and acknowledging and addressing their emotions.
10.4. Patient refusal to speak or eat

Refusal of a hospitalized patient to speak is fairly uncommon. However,
when it occurs, an inability to speak due to a psychiatric or medical condi-
tion must be ruled out. These conditions include neurological problems
such as stroke and epilepsy as well as psychiatric issues such as catatonia.
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In addition to mutism, catatonia is often associated with catalepsy, pur-

poseless motor activity, negativism, posturing, and mimicry. In general,
patients with catatonia are immobile, mute, withdrawn, and refuse to eat
or drink. Other psychiatric conditions that may lead to an inability or
refusal to speak include acute stress disorder/posttraumatic stress disor-
der, autism, and personality disorders. In children, the diagnosis of selec-
tive mutism must also be considered.
As opposed to patients who refuse to speak, hospitalized patients who
refuse to eat are fairly common. Although food refusal is more common
in children and the elderly, any patient can refuse to eat while in the hos-
pital. The first task of any psychiatrist called to assess a patient who is not
eating is to determine if the patient is actually refusing to eat or if they
instead lack the ability to eat (as with patients who are too delirious to
attend to eating, or patients who develop dysphagia after a stroke).
Psychiatric conditions to consider in patients who are not eating also
include dementia, depression, paranoia, anorexia/bulimia, and self-harm-
ing or suicidal behavior. Medical causes of anorexia including cancer and
medication side effects should also be considered. Social and environmen-
tal factors such as lack of social connections, religious or ethnic prefer-
ences, and the presentation of the food also can play a role in a patient’s
refusal to take in food.18 In children, gastroesophageal reflux, food aller-
gies, anatomical anomalies, and delayed gastric emptying are common
causes of food refusal. After evaluating and treating underlying psychiat-
ric and medical conditions, environmental and behavioral interventions
can be started. These include providing favored foods, enhancing the
taste, appearance, and presentation of food, providing companionship dur-
ing meals, and serving ethnically appropriate foods. Appetite stimulant
medications may sometimes be used. For some patients, particularly chil-
dren, more intensive behavioral interventions may be needed. Starting
enteral feeding by nasogastric or gastric tube is a last resort in patients
who refuse to eat.
10.5. Privacy and stigma

Privacy, or freedom from intrusion, can be quickly and significantly com-
promised when a person requires health care. Medical care, from history
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taking to physical examination to testing and treatment, is inherently

intrusive. Privacy can be particularly difficult to maintain in hospitals
where patients are often treated in close proximity to one another (e.g.
emergency departments, hemodialysis units) and have a number of car-
egivers. It is important to respect patients’ autonomy and earn their trust
by minimizing the impact of care on their privacy, and it is particularly
important to keep their health care information confidential. Maintenance
of confidentiality is very important for hospital psychiatrists who, by the
nature of their work, become privy to information about sexual function-
ing, substance use, mental illness, and other highly sensitive issues.
Hospital psychiatrists must weigh concerns about confidentiality against
the need to share clinical information with the patient’s other caregivers,
though, and particularly with the caregiver who initiated the psychiatric
consultation. This conflict of duties is usually resolved by the psychiatrist
disclosing only the minimum information necessary to deal with the clini-
cal problem at hand. Doing this usually means omitting things like exten-
sive discussions of social issues, psychodynamic formulations, and
speculations about personality problems from psychiatric notes. Hospital
psychiatrists must also frequently weigh patients’ rights to privacy and
confidentiality against issues of safety. In working with suicidal patients,
for example, it is often necessary to obtain collateral history from family
members, friends, and other outside sources despite patients’ requests that
this not be done. In this situation, care must be taken while obtaining his-
tory to not release information about the patient. Hospitalized patients felt
by psychiatrists to be at high risk for suicide are usually placed on con-
stant observation for their own safety, and in doing so psychiatrists tem-
porarily curtail the right to privacy for the patient’s benefit. A hospital
psychiatrist may similarly have to violate the confidentiality of a patient
who is felt to pose a significant danger to others (e.g. due to homicidal
ideation, abuse of a spouse or child) in order to protect those threatened.
Certain legal situations (e.g. competency and civil commitment proceed-
ings) also dictate that clinical information that is normally kept confiden-
tial be disclosed.19
Mental illness can be highly stigmatizing in many societies. Caregivers
on medical and surgical units in general hospitals, though they have
often had some training in psychiatry, are often wary of people with
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significant mental illness. A number of factors, including past difficult

experiences with patients with severe mental illness and feelings that
they are not responsible for mental health care, probably contribute to
this discomfort. Hospital psychiatrists sometimes need to diffuse the
discomfort of caregivers dealing with odd, uncooperative, suicidal, agi-
tated, and other difficult patients and make sure their patients receive
excellent medical care.
11. CONCLUSION
Psychopathology is highly prevalent in the general hospital population.
As the number of elderly people in society increases, the general hospital
population will become older and more medically complex and the psy-
chopathology burden will increase. This fact and the association of cer-
tain forms of psychopathology with poor medical outcomes suggest
psychiatric services are greatly needed in the general hospital setting.
Obstacles to the delivery of these much-needed services include a lack of
recognition of mental illness by non-psychiatric caregivers, a hospital
environment not well suited to psychiatric work, and difficulty demon-
strating the financial benefits of psychiatric care to administrators.
Hospital psychiatrists must be particularly knowledgeable in the areas of
delirium, agitation and aggression, depression, addictions, suicidality,
and “psychogenic” medical illnesses. Many general hospital mental
health services are now using a multidisciplinary team approach to these
problems.
12. KEY POINTS

• Psychopathology is common among general hospital inpatients, and
some forms of psychopathology are associated with poor medical
outcomes.
• The reason for a general hospital psychiatric consultation should be
clarified with the requesting professional before the patient is seen.
Requests for psychiatric consultation may arise from a number of
stated and unstated reasons.
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• In evaluating most general hospital patients, it is important to gather

collateral information from sources such as the medical records and
not rely solely on information obtained from the patient.
• The first step in the evaluation of an agitated or aggressive general
hospital inpatient is to diagnose the particular psychiatric or medical
condition(s) causing the agitation. Rational treatment of an agitated/
aggressive patient is guided by this diagnosis.
• Patients perceived to be anxious, depressed, or psychotic by non-
psychiatric caregivers are often found on psychiatric evaluation to be
delirious.
• Even thorough diagnostic evaluations will not enable psychiatrists to
predict with great certainty which suicidal patients will harm them-
selves and which will not. Psychiatrists use patients’ histories and
examinations to make reasonable, common-sense assessments of
suicide risk and use these assessments to guide treatment.
• Patients with somatoform disorders produce physical signs and symp-
toms and concerns about illness unconsciously, whereas patients with
factitious disorders and malingering patients consciously feign illness.
Somatoform and factitious disorder patients seek relief from uncon-
scious conflict (“primary gain”) whereas malingering patients seek
tangible rewards (“secondary gain”).
• Anxiety and depressive disorders seen in general hospital inpatients
frequently result from interplay between primary psychiatric illness
and general medical factors.
• General hospital inpatients thought to be at high risk for suicide must
be observed by hospital staff at all times.
• Anxiety, depression, hopelessness, psychosis, impulsivity, recent loss,
limited support, insomnia, physical pain, and a history of suicide
attempts are particularly worrisome in suicidal patients.
13. SELF-ASSESSMENT
13.1. Which of the following factors is associated with
a decrease in suicide risk?
(A) Advanced age.
(B) Anxiety.
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(C) Insomnia.
(D) Being married.
(E) Impulsivity.
The support of a marital relationship probably confers some protection

against suicide. The other factors have been associated with an increase in
suicide risk.
Answer: D20
13.2. A hospital ward nurse calls you to report a patient is

agitated. The best response to this is:
(A) An order for haloperidol 5 mg intravenously.
(B) Brief questions about the safety of the patient and others, followed by
brief questions about the patient’s medical and psychiatric histories.
(C) Questions about the nurse’s feelings toward the patient and the
quality of their working relationship.
(D) An order for lorazepam 1 mg intravenously.
(E) Calm reassurance that agitation is usually short lived and
insignificant.
Since agitation is non-specific and can be caused by a variety of psy-

chiatric and general medical conditions, it is important to try to estab-
lish the etiology of a patient’s agitation before treating it. A brief
discussion of safety factors should precede this discussion. Agitated
and aggressive patients should never be blindly treated with psycho-
tropic medications.
Answer: B22
14. CASE STUDIES

14.1. Agitation in a general hospital patient
A 31-year-old man with schizoaffective disorder, bipolar type was trans-
ferred from a psychiatric hospital to a general hospital after falling and
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sustaining rib fractures. An emergency psychiatric consultation is sought

soon after hospital admission for “severe psychosis and agitation.”
Examination reveals a thin man with poor hygiene and grooming. His
level of consciousness varies between alertness and lethargy. When alert,
the patient yells loudly and thrashes against his limb restraints. His coop-
eration with the examination is poor. The patient’s speech is not clearly
pressured. His comments are suggestive of confusion and are not clearly
delusional in nature. He appears inattentive.
The attending psychiatrist at the psychiatric hospital said the patient
was manic and delusional (thought the police were chasing him) on
admission. Soon after admission, divalproex sodium was added to the
aripiprazole the patient was taking at home. When the general hospital
psychiatrist found the patient delirious rather than manic or psychotic, a
delirium evaluation revealed marked hyperammonemia probably associ-
ated with divalproex sodium treatment. The patient’s divalproex sodium
was held and he was treated with L-carnitine and as-needed doses of
intravenous haloperidol. After a few days, he returned to his cognitive
baseline and was transferred back to the psychiatric hospital.
14.2. Depression in a general hospital patient

A 68-year-old woman with a history of hypertension, diabetes mellitus
with diabetic gastroparesis, and major depression presented to a general
hospital with a several-hour history of effortful speech and right hemipa-
resis. Evaluation including a cranial MRI scan revealed evidence of an
acute ischemic stroke in the left frontal lobe. The patient’s family history
is positive for stroke as well as depression. Ten days after hospital admis-
sion, a psychiatric consultation is requested for depression because crying
has been noted and the patient has not been fully cooperative with early
rehabilitation efforts.
On examination, the patient is alert but her cooperation is limited.
Tearfulness is noted on occasion, and the patient says her mood is “low.”
Speech is sparse. Some pessimism and loss of hope are acknowledged
with questioning. On cognitive examination, signs suggestive of a mem-
ory retrieval deficit and executive dysfunction are noted but are unclear
due to suboptimal patient cooperation and residual aphasia.
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The patient is given a diagnosis of depression. Possible contributing

factors include recurrent major depression, stroke, and treatment with
metoclopramide for diabetic gastroparesis. The patient’s metoclopramide
dose is decreased and she is started on escitalopram 10 mg per day.
14.3. Parasuicidal behavior

A 29-year-old woman with a history of major depression, alcohol
abuse, and borderline personality disorder with multiple suicide
gestures was admitted to the hospital after taking an overdose of aceta-
minophen. When medical monitoring does not reveal significant hepa-
totoxicity or other acute medical concerns, a psychiatric evaluation is
requested.
On interview, the patient tells the consulting psychiatrist that, after
learning her psychotherapist was about to go on a long vacation, she
became very upset, drank a large amount of alcohol, and impulsively took
an overdose. She said she called emergency medical services herself after
taking the overdose. The patient said that prior to this she had been doing
relatively well: she said she had been experiencing some “mood swings”
but denied anxiety, hopelessness, hallucinations, and insomnia. She said
that after her overdose her thoughts of self-harm abated. On examination,
the patient was cooperative, had a full affect, and showed no psychotic
signs, and she clearly denied any desire or plan to harm herself. She asked
when she could go home.
A call to the patient’s therapist corroborated the patient’s history. The
therapist did not feel the patient was currently at high risk for suicide and
hoped she would be discharged soon so she could keep her upcoming
therapy appointments. In the hospital, the patient was initially put on
standard suicide precautions and continuous observation by a sitter. Over
the following few days, as the patient remained calm and continued to
deny suicidal ideation, her observation parameters were decreased. After
the patient’s parents removed the unnecessary medications from the
patient’s home and the patient was given appointments to see her psycho-
therapist’s practice partner until her therapist returned from vacation, the
patient was discharged home.
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14.4. Alcohol withdrawal

A 45-year-old man was brought to the emergency room by paramedics
after suffering a generalized tonic-clonic seizure. On interview, the patient
said he had a 30 year history of heavy alcohol abuse. He typically con-
sumes a fifth of vodka and 10–12 12-oz beers each day. He smokes 1 pack
of cigarettes a day but denied other substance use. He has been hospital-
ized five times for alcohol detoxification and had one seizure in the past
when withdrawing from alcohol. He was recently arrested for his second
drunk driving violation and decided to stop drinking prior to his court date
tomorrow. It has been about 36 hrs since his last drink.
On exam, the patient was hypertensive and tachycardic as well as
tremulous and somewhat anxious. He was alert and oriented to person,
place, and time.
In the emergency room the patient was started on a CIWA and given
2 mg of lorazepam IV as well as 100 mg of thiamine. His blood pressure
and heart rate decrease with the administration of the benzodiazepine. He
is then admitted to the hospital for general medical observation and main-
tained on a CIWA for the next three days. His withdrawal is controlled
with lorazepam alone.
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Chapter 24
Psychiatric Education
Linda Gask and Michelle B. Riba
1. INTRODUCTION: TEACHING AND LEARNING

Teaching and learning should be at the core of what we do as psychiatrists
in our everyday work. Even an experienced psychiatrist has much to learn,
not only in terms of knowledge, to keep up with the latest developments
in her field, but in other ways too. Both of the authors of this chapter can
acknowledge how much they still learn each year from their students, and
above all from their patients. We have both undergone training in different
parts of the world, in very different health care systems; one a publicly
funded health care system (the National Health Service in the United
Kingdom) and the other a much more diverse system funded through
health insurance and private payment (the United States). We are also both
teachers and have been extensively involved in educating students to work
within these healthcare systems; not only to become psychiatrists but also
as future physicians in all specialties, sensitive to the mental health needs
of their patients. So we perhaps bring to this chapter some differing views
of the everyday role of a ‘psychiatrist,’ because our training differed in
many ways and we work in contrasting settings. However ours are only
two perspectives of a much more varied experience of psychiatry both at
medical school and in residency training across the world and we would
suspect that our experiences, and those of others who have trained in Asia,
or Eastern Europe for example, may have quite a deal in common. There
may also be important ways that we can learn from each other. Our aims
606
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Psychiatric Education 607
are thus twofold. To try and give the reader a comprehensive overview of
the importance of and key elements of education as it relates to psychiatry,
while at the same time ensuring that the reader has a view of key interna-
tional perspectives and innovations in psychiatric education — not just
from our own experiences, but also from the published literature.
2. PSYCHIATRY AND MENTAL HEALTH

Psychiatry is the medical specialty devoted to the study and treatment of
mental disorders. Psychiatrists are only one subset of a wider professional
group of mental health specialists which may also include (amongst oth-
ers) psychologists, mental health nurses, and social workers. Psychiatry is
also unique in medical specialties in that it should, by default, incorporate
a broad range of perspectives (social, psychological, biological, religious,
and cultural) into devising, with the patient or service user, the most
appropriate way of providing treatment. The medical training of psychia-
trists, their ability to make psychiatric diagnoses and prescribe medication
distinguish them (although not entirely because in some countries nurses
and psychologists may have prescribing rights) from their fellow workers
— but they also have many skills in common — particularly in relation to
these broader socio–psychological–cultural aspects of carrying out assess-
ments and planning care. In some places the role of the psychiatrist as the
traditional medically qualified ‘leader’ of the mental health team remains
unchallenged, in others this is far from the case, for example the team
leader role in the United Kingdom may be taken by any of the above pro-
fessionals but this would be considered to be quite odd in many other
places (for example in Africa or Asia) where doctors retain clear leader-
ship of healthcare. This is important to acknowledge because if the profes-
sional culture in which a person has trained is very different from where
they work, then they may face difficulties, as have some internationally
trained doctors who move across continents to work within a specialty for
which they have trained elsewhere. Some educational systems have
sought to break down the differences between professional roles (and
challenge (mis-)perceptions) for example by facilitating inter-profes-
sional learning in basic training,9 although this approach not been widely
adopted internationally.
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608 L. Gask and M. B. Riba
3. EDUCATION AND RECRUITMENT

The quality of psychiatric education provided to students in their basic
medical training, (which in many countries is called ‘undergraduate’ as,
unlike in the United States, medicine may be studied in some places as
first degree (and therefore ‘psychiatric residency may be called ‘post-
graduate’ training)), is considered to be central to the issue of recruitment
into the specialty. Recruitment into psychiatry is declining in many places
in the world, but reports of a ‘crisis’ need to be considered in an interna-
tional context. In 1994, only 3.2% of US medical school graduates chose
psychiatry, the lowest proportion since 1929.19 The World Health
Organization recommends that there should be approximately one psy-
chiatrist per 10,000 population but the survey of 192 countries carried out
for the Mental Health Atlas in 2005 revealed a distribution across regions
ranged from 9.8 in Europe to just 0.04 in Africa. In 47.6% of countries
covering 46.5% of the world’s population, there is less than one psychia-
trist per 100,000 population. Recruitment in developing nations is also
undermined by medical immigration of potential psychiatrists to devel-
oped nations; a considerable proportion of the psychiatric trainees in
developed countries are ‘international medical graduates.’ There are many
possible reasons for the decline in recruitment, but negative attitudes to
psychiatry among medical students have been widely observed interna-
tionally. The psychiatry departments that have high recruitment rates give
considerable priority and resources for medical student psychiatric
education.
4. MEDICAL SCHOOL TEACHING IN PSYCHIATRY:

AN INTERNATIONAL PERSPECTIVE
It is important to understand something about how medical training varies
across the world. All of us should, as clinicians, be involved in teaching
students as part of our responsibility to recruiting interested and imagina-
tive young people into our specialty in the future. However, with the
increasing mobility of medical graduates in search of specialty training, it
is essential to recognize how training, and experience in psychiatry, may
differ from one country to another when international graduates seek
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psychiatric training in another healthcare system. Medical education is

still far from being standardized, and that is probably most pronounced in
relation to psychiatry, where apparent exposure to people with mental
health problems in some countries may still unfortunately only be in the
setting of a visit by students to a large mental hospital to talk to patients
who are overtly psychotic (although students may see many people in
general medical clinics where these problems remain unacknowledged by
their teachers).
The length of time that it takes to train in medicine varies between dif-
ferent countries. As we have noted above, in some places, such as the
United States and Canada, medicine is embarked upon after taking an
initial ‘pre-med’ degree, which may not necessarily be in one of the basic
sciences. This is then followed by a four year period at medical school.
This route is now also open to some students in Australia and in the United
Kingdom, but the norm in both of those countries is to take medicine as
the first undergraduate degree, leading to a Bachelor’s degree rather than
an MD. This can cause some confusion, as some countries in the world do
award an MD after graduation from medical school — as in the United
States, but others (like the United Kingdom) do not. One of us (Linda
Gask) has a Bachelor of Medicine degree awarded after five years of study
from the age of 18 years. Medical school is then followed up by a period
as an intern which may or may not contain some psychiatric experience.
5. EXPERIENCE OF PSYCHIATRY
IN MEDICAL SCHOOLS
Additionally, there is considerable international (and even intra-national)
variation in the length of time devoted to psychiatry during the medical
school psychiatry curriculum. In 1994, the World Psychiatric Association
collaborated with the World Federation of Medical Education (WFME)
to devise a core curriculum for undergraduates in psychiatry.23 Prior to its
development, a survey was conducted in medical schools about the
existing curricula for undergraduates in psychiatry which is reviewed by
Dogra and her colleagues.4 Out of a list of 1,305 medical schools pro-
vided by the WFME, the questionnaire was sent to 500 faculties of medi-
cine. Responses came from 124 departments of psychiatry belonging to
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40 different countries; only 113 responses were usable. Around 77 depart-

ments were from high income countries and 44 from low–middle income
countries. Almost half (47.8%) of these departments had a national cur-
riculum for undergraduates in psychiatry, and more than half (53%) were
dissatisfied with their teaching. There was no relationship between the
availability of a national core curriculum and satisfaction with the teach-
ing of psychiatry to undergraduates. The most frequently taught topics
were: mental state assessment, psychopathology, personality disorders,
affective disorders, schizophrenic disorders, alcoholism and drug depend-
ence, psychosexual disorders, organic psychosis, psychiatric aspects of
medical disorders and psychosomatic medicine, mental handicap, and
treatment in psychiatry. The mean duration of theoretical teaching
psychiatry was 46.4 ± 24 hrs. Most of it was lectures (34.9%) or lectures
and discussions (24.8%). Rotations or practical training varied from
1–32 weeks (mean: 6.2 ± 4 weeks). The teaching was done through clini-
cal cases (70%), presentation of patients (79%), writing case reports by
medical students (56.9%). Only 46.9% of the responders mentioned that
undergraduates were involved in emergency rooms by being on duty.
The suggested topics for inclusion in the core curriculum were:
Psychiatric disorders (63.5%), especially depression (25.4%), substance
abuse (22.2%), anxiety disorders (22.2%), and organic mental syndrome
(19%), but also: psychopharmacology (39.7%), psychotherapy (28.6%),
interviewing skills (28.6%), and patient–doctor relationship (17.5%).
There was no expectation that curricula would be different between high
and low–middle income countries.
The main outcomes were that there was a need to sensitize other spe-
cialties to the importance of psychiatric teaching, to stress the importance
of mental health in the community, to improve teaching of behavioral sci-
ences and psychotherapy, and to emphasize the importance of an interna-
tionally coordinated education for undergraduates in psychiatry.
A survey of teaching undergraduate psychiatry in UK and Irish medical
schools in 200510 found that the content of programs even within the
British Isles remain highly variable with a range of teaching and assess-
ment methods applied. The variation of time allocated for the clinical
discipline also somewhat surprisingly varied between two and twelve
weeks! Teachers generally felt that education was undervalued in relation
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to research in medical schools and it was unclear how the differences in

exposure of students to psychiatry impacted on their competence in the
specialty at graduation. This situation is probably similar in many other
countries — for example a survey of medical schools in Turkey carried
out in 2006 found a lack of standardization of undergraduate training in
psychiatry across the 29 medical schools which responded to the survey
and three medical schools did not offer a period of psychiatric clinical
attachment.2 The survey carried out in the United Kingdom led to the
development within the Royal College of Psychiatrists of a core curricu-
lum for medical students in psychiatry (see Table 1).
Table 1. The Royal College of Psychiatrists’ core curriculum for undergraduate educa-
tion in psychiatry (UK).
Specific to teaching in clinical psychiatry, the principal aims of the undergraduate medical
course should be:
• To provide students with knowledge of the main psychiatric disorders, the principles
underlying modern psychiatric theory, commonly used treatments, and a basis on
which to continue to develop this knowledge.
• To assist students to develop the necessary skills to apply this knowledge in clinical
situations.
• To encourage students to develop the appropriate attitudes necessary to respond
empathically to psychological distress in all medical settings.
The Learning Outcomes are:

Knowledge
On completion of undergraduate training the successful student will be able to:
1. Describe the prevalence and clinical presentation of common psychiatric conditions

and how these may differ according to age and developmental stage.
2. Summarize the major categories of psychiatric disorders, for example using ICD-10.
3. Explain the biological, psychological, and sociocultural factors which may predispose
to, precipitate or maintain psychiatric illness and describe multi-factorial etiology.
4. Describe the current, common psychological and physical treatments for psychiatric
conditions, including the indications for their use, their method of action, and any
unwanted effects.
5. State the doctor’s duties and the patient’s rights under the appropriate mental health
legislation and mental capacity legislation.
(Continued)
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6. Describe what may constitute risk to self (suicide, self harm and/or neglect, engaging
in high risk behavior) and risk to and from others (including knowledge of child,
adults with learning disabilities, and elder protection requirements).
7. Describe how to assess and manage psychiatric emergencies, which may occur in
psychiatric, general medical, or other settings. In particular be able to describe the
elements of a risk assessment and the management of behavioral disturbance.
8. Describe the basic range of services and professionals involved in the care of people
with mental illness and the role of self help, service user, and carer groups in providing
support to them. As part of this students should be able to describe when psychiatrists
should intervene and when other clinicians should retain responsibility.
Skills
On completion of the course the successful student will be able to:
1. Take a full psychiatric history, assess the mental state (including a cognitive
assessment) and write up a case. This includes being able to describe symptoms and
mental state features, etiological factors, differential diagnoses, a plan of management,
and assessment of prognosis.
2. Screen empathically for common mental health problems in non-psychiatric settings
and recognize where medically unexplained physical symptoms may have
psychological origins.
3. Evaluate and describe patients presenting with abnormal fears/anxieties, pathological
mood states, and problematic, challenging, or unusual behaviors.
4. Summarize and present a psychiatric case in an organized and coherent way to
another professional and be able to discuss management with doctors or other staff
involved in a patient’s care.
5. Recognize the differences between mental health problems and the range of normal
responses to stress and life events.
6. Evaluate information about family relationships and their impact on an individual
patient, which may involve gaining information from other sources.
7. Assess a patient’s potential risk to themselves and others, at any stage of their illness,
and in particular be able to assess a patient following an episode of deliberate
self-harm.
8. Evaluate the impact of psychiatric illness on the individual and their family and those
around them.
9. Find, appraise, and apply information and evidence gained from in depth reading
relating to a specific clinical case.
10. Discuss with patients and relatives the nature of their illness, management options,
and prognosis.
(Continued)
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Attitudes
On completion of the course the successful student will be able to:
1. Utilize an empathic interviewing style, which is suitable for eliciting information from
disturbed and distressed patients.
2. Recognize the importance of the development of a therapeutic relationship with
patients, including the need for their active involvement in decisions about their care.
3. Demonstrate sensitivity to the concerns of patients and their families about the
stigmatization of psychiatric illness.
4. Recognize the importance of multidisciplinary teamwork in the field of mental illness
in psychiatric, community, and general medical settings, primary care settings, and
some non-medical settings.
5. Demonstrate awareness of capacity, consent, and confidentiality issues as they apply
in psychiatry.
6. Reflect on their own attitudes to patients with mental health problems and how these
might influence their approach to such patients.
7. Reflect on how working in mental health settings may impact upon their own health
and that of colleagues.
The challenge in designing curricula for medical school settings is to

provide students with the experience that they will need; not to become
specialists in psychiatry, but competent generalists, given that the majority
of mental health problems in the community are in fact treated not by
psychiatrists but primary care doctors. Unfortunately, however, this has
not always been apparent in the way that undergraduate education is deliv-
ered, with an emphasis on teaching in the hospital setting, with patients
who are experiencing psychotic symptoms, rather than in the liaison-
psychiatry setting where students will see the kind of patients that they
will meet throughout their working career-people who have common
chronic physical conditions such as diabetes, arthritis and coronary heart
disease, and who also may be suffering from comorbid anxiety and or
depression. This is as much a problem in low and middle income coun-
tries, where chronic physical health problems are becoming more com-
mon, as it is in the high income countries of North America and Western
Europe. The challenge is to ensure that medical students have a good
knowledge of how to recognize and manage common mental health
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disorders such that they will be competent in basic mental health care
whatever specialty they ultimately choose.
5.1. Behavioral science teaching

In the World Psychiatric Association (WPA) survey cited above, 86% of
respondent medical schools reported that psychiatrists were engaged in
teaching behavioral science to students. In a traditional approach to
designing the medical curriculum, behavioral science is taught alongside
the other ‘basic sciences’ (such as anatomy, physiology, biochemistry) in
the pre-clinical years, often at a time when it seems to have very little
relevance to real patient experiences.
The Institute of Medicine reviewed behavioral science teaching in
US medical schools and defined it as consisting of six priority topics:
(1) Mind–Body Interactions; (2) Patient Behavior; (3) Physician Role and
Behavior; (4) Physician–Patient Interactions; (5) Social and Cultural
Issues; and (6) Health Policy and Economics. However a recent interna-
tional review of the teaching of behavioral science carried out by a group
of psychologists from the United States, the United Kingdom, Australia,
Thailand, Mexico, and Saudi Arabia1 noted some common themes emerg-
ing across these quite different settings:
• A lack of suitable professionals to fulfill the role of teaching behavio-

ral science, combined with poor awareness of the potential role of
psychologists (particularly health psychologists) in fulfilling this
shortage.
• The need to defend the importance of behavioral sciences as a valid
and important area of medicine and to justify its inclusion in curricula
to both colleagues and to students.
• Disappearance of psychologists with replacement by other profes-
sionals such as primary care doctors and psychiatrists in teaching
behavioral science.
• The increasing domination of the biomedical model in the
curriculum — a factor which they considered is promoted rather than
discouraged by problem-based learning (PBL) approaches to curricu-
lum design.
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The contributor from Saudi Arabia noted that psychological teaching

was sometimes viewed as a ‘luxury’ because it was not seen as entirely
relevant to medicine. However the response from the Thai correspondent
will be familiar to many:
The general attitude of students toward behavioral sciences may range

from “irrelevant” to “interesting” with the majority seeming to regard it as
a necessary inconvenience. A typical situation near the end of each semes-
ter, when the final exam is on the mind of most students, is that many
students may stop attending behavioral sciences classes in order to cram
for other “more serious” subjects. Even among those who attend, a number
of them may be observed reviewing materials from other courses while
sitting in the behavioral sciences class.
Certainly there is a shortage internationally of skilled social and behav-

ioral scientists to fulfill this role in medical education and in many coun-
tries it will fall, by default, for psychiatrists to lead in developing and
improving the delivery of behavioral science education. Nevertheless, this
does require appropriate skills, knowledge, and preparation. What
psychiatrists can bring to behavioral science teaching that often many
other professionals cannot is the opportunity to really make the teaching
seem clinically relevant with examples of cases to discuss, class visits,
visiting speakers who can engage the group in talking about their work in
real community settings, and use of popular media such as television and
film and the internet to stimulate discussion. These approaches have been
utilized, for example, by our colleague Bulent Coskun at the Kocaeli
Medical School in Turkey with considerable success.
5.2. Communication skills training

Basic training in talking to people who may have emotional problems is
sometimes viewed as part of behavioral science teaching, but is probably
most effectively delivered by clinicians working in collaboration with
behavioral scientists in order to ensure that students do fully understand
the clinical relevance of what they are doing. Often this is taught during
psychiatry, and psychiatrists may take a particular role, often with primary
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physicians, in teaching this within the curriculum. It is important that this

is however not seen as a ‘psychiatric’ skill (with emphasis only on its
application during history taking in psychiatry) but as an important skill
regardless of which specialty students will be entering after qualification.
Various methods can be employed, some of them quite “high tech” involv-
ing recording of interviews and observing in a group setting; other, such
as role-play and working with ‘standardized patients’ (a person, usually a
layperson, who has been trained to portray, in a realistic, disciplined, and
standardized manner, a patient for the purpose of training or assessing
medical professionals). Standardized patients are commonly involved in
Observed Structured Clinical Examinations (OSCE) in both medical stu-
dent and psychiatric postgraduate examinations.
5.3. Integrated curricula and problem-based learning

In 1993, the General Medical Council in the United Kingdom recom-
mended new medical curricula that integrate preclinical and clinical
courses more and devote more time to communication skills, PBL, and
practical clinical tasks. Most medical schools in the United Kingdom
(with the exception of Oxford, Cambridge, and St. Andrews) have radi-
cally redesigned their approach to teaching over the last few years. This
approach is also being adopted around the world although some medical
schools still favor the traditional approach of two to three years prior to
any clinical content to cover all the basic sciences. Psychiatry teaching
(and behavioral science instruction) can therefore be incorporated from
earlier on in teaching, particularly in relation to physical health problems,
than would traditionally be the case.
The PBL is particularly utilized in integrated curricula. The PBL is a
“student-centered” approach in which students collaboratively solve prob-
lems in small group work, usually based on a clinical ‘problem case’ and
reflect on their experiences, generating questions and bringing the results
of their reading and research back to the group in order to jointly learn
about the nature and approach to managing the problems presented by the
“patient.” It was pioneered and used extensively at McMaster University
in Canada but has now been adopted worldwide. From the point of view
of teaching about mental health issues, PBL provides an opportunity to
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build mental health topics into cases at the curriculum design stage so that
these issues are addressed by the students as they learn.
As noted earlier, behavioral science teachers may feel that PBL pro-
vides paradoxically fewer rather than more opportunities to teach to stu-
dents given that most PBL tutors have a limited grounding in and
understanding of behavioral sciences. In integrated curricula, students will
have less protected time (for example in terms of a specific block of
weeks) within one specialty exclusively and unless psychiatrists in the
medical school are very determined and fight for their place within the
faculty, it is not unusual for time spent with psychiatry to decrease rather
than increase. The assumption is of course that more time is now provided
across the whole curriculum, but this requires psychiatric teachers who
are willing to be very flexible and take every opportunity, for example, to
get involved in joint facilitation of a group, to be an ‘expert resource’ to
group members who may come and interview him or her, and provide
support and input wherever possible. Exposure to psychiatry as practiced
more formally in the outpatient clinic or inpatient ward will be less. This
may be a good thing in that psychiatry becomes seen as more widely rel-
evant to medicine as a whole, but it may also mean, on the downside, that
there are fewer opportunities to identify with teachers, get to know
patients with mental health problems over time and break down barriers
and stigma. This will be even more of the case if psychiatric teachers
themselves fail to take the opportunities afforded by redesign so that stu-
dents see very little of them at all.
The question of which educational system is better is still in debate.
Some people say that integrated courses allow students to put knowledge
in context that in traditional courses, and that they prepare students better
for clinical problems in the first years of practice. Supporters of the tradi-
tional method, however, say longer preclinical components give students
a more comprehensive foundation and more thorough grounding of scien-
tific knowledge on which to build an understanding of clinical medicine.
6. RESIDENCY AND POSTGRADUATE TRAINING

IN PSYCHIATRY ACROSS THE WORLD
In some countries this is known as ‘residency’ training, in others as ‘post-
graduate’ coming as it does after the undergraduate experience at medical
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school. Information about how psychiatrists are trained in different coun-

tries has only become more widely available in recent years.
6.1. Purpose and overview

Training in psychiatric evolved in the early 19th century with the lec-
tures for doctors with an interest in this (then) developing field. For
more than a century, training developed more as a loose form of appren-
ticeship, with little formal organization, and it is only in relatively recent
years, (during the last half century) that it has become more organized
even in Western countries. In the United States, the Accreditation
Council on Graduate Medical Education (www.acgme.org) oversees
psychiatric residency education while the American Board of Psychiatry
and Neurology (www.abpn.com) determine specialty board certification
upon the completion of training. In the United Kingdom, the Royal
College of Psychiatrists (www.rcpsych.ac.uk) provides both functions
although training is formally overseen now by the General Medical
Council (www.gmc-uk.org). The Royal College of Physicians and
Surgeons of Canada (http://rcpsc.medical.org/) is the Canadian equiva-
lent. Across Europe, the European Board of Medical Specialties
(UEMS) and its European Board of Psychiatry (www.uemspsychiatry.
org) is now highly influential in determining the content of psychiatric
training curricula (although there is still considerable variation (see fur-
ther)) and the latest European Framework for Competencies can be
accessed at http://www.uemspsychiatry.org/board/reports/2009-Oct-
EFCP.pdf. The WPA has meanwhile taken a particular interest in fur-
thering the quality of training (both undergraduate and postgraduate)
since it was founded in the 1950s and has published its own version of
an international curriculum for psychiatric training,21 which is now
being updated. Throughout the world, psychiatric training is become
more structured with increasing oversight being applied to its imple-
mentation and evaluation.
In the United States, the ACGME has outlined six core competencies,
consisting of (1) Patient care, (2) Medical knowledge, (3) Practice-based
learning and improvement, (4) Interpersonal and communication skills,
(5) Professionalism, and (6) Systems-based practice. These six core
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competencies are held for all medical specialties, including psychiatry.

Each specialty has additional guidelines which then specify the knowledge
necessary for their own specialties within this framework. In contrast, the
Royal College of Physicians and Surgeons of Canada is organized around
seven specific roles of the medical professional known as CanMeds. These
seven roles include: (1) Medical expert, (2) Scholar, (3) Communicator,
(4) Health advocate, (5) Manager, (6) Collaborator, and (7) Professional.
Recently, the European Board of Psychiatry (a part of the UEMS
Section of Psychiatry) has adopted a framework similar to the Canadian
system by outlining the following roles of the psychiatrist: (1) Psychiatric
expert/clinical decision-maker, (2) Communicator, (3) Collaborator,
(4) Manager, (5) Health advocate, (6) Scholar, and (7) Professional.
The adoption of required competencies by these organizations provides
a theoretical framework in which one can approach formulating and moni-
toring a curriculum. The key principles behind the development of a post-
graduate curriculum are extensively detailed in a recent chapter by
Mackey and Tasman.12 There is not, however, a specified course which the
curriculum must follow. Ideally, a fully trained psychiatrist is capable of
serving as a medical expert with the clinical ability to diagnose and treat
mental illnesses within given systems in a professional manner that
further improves the quality of practice.
6.2. International comparisons

Selection criteria for entry into psychiatric training differ from country to
country and training may be part of a national program, be university-
based, or be locally organized.
The organizations mentioned above, although highly influential in
determining the content of psychiatric training worldwide, do not oversee
training outside Europe and North America. A large number of other
organizations across many different countries have developed in recent
years to oversee training across the world. However, as Zisook and his
colleagues have commented “… surprisingly little work has been done to
gather and disseminate information about psychiatric training around the
world, including understanding how various countries meet the challenges
of providing adequate training appropriate to unique regional needs.”
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The ATLAS project22 has been the first major attempt to try and map
the form and content of Psychiatric training across the world. The project
arose out of collaboration between the WPA and the World Health
Organization. The WPA sent questionnaires to the 143 National Member
Societies from 121 countries. The major limitation of the study was the
low response rates from the countries. Information on aspects of psychi-
atric training was only available from 74 countries and one WHO
Territory. The reasons for this might have been: absence of a training
program; inability to provide aggregated information when the country is
large with a lot of diversity in the quality of individual programs; absence
of any functioning psychiatric organization in the country or the absence
of any known key person with the ability to respond to the questionnaire.
Even when countries did respond the completion rate was poor. In view of
these limitations, the WHO and WPA then used other sources to gather
more information.
Eventually, it was found that 122 (68.2%) countries had a psychiatric
training program. This varied from 47.4% countries in the WHO Africa
Region to 94.1% countries in the European Region. When analyzed
according to World Bank income group psychiatric training facilities were
present in 54.5% of low income countries compared to 77.1% of high
income countries.
However, clearly the mere presence of a training facility neither pro-
vides sufficient information regarding the quality of training provided nor
the uniformity of training across the country. More detailed information
on aspects of psychiatric training was only available from 74 countries as
indicated above. About half reported having an accredited diploma or a
Master’s degree in psychiatry. Super-specialization in specific areas of
psychiatry or a doctoral program in psychiatry was reported by fewer
countries. Interestingly, while more than 10 teachers for psychiatry were
reported by 32 countries, less than 15 had more than 10 teachers in the
area of clinical psychology, psychiatric social work, and psychiatric nurs-
ing. The minimum duration of training varied to a great degree among
countries. While 22 countries out of 74 reported 3–4 years training for
diplomas, 28 countries reported the same time frame for completing a
Master’s program. Sub-specialization required a further 1–2 years in
18 out of the 35 countries reporting on it. This information must be
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viewed in the context of differing opportunities that doctors training in

psychiatry will have had to achieve basic competencies in psychiatry at
medical school (such as taking a psychiatric history and carrying out a
mental state examination) before even entering specialist training. This
will also have been very varied.
Zisook and his colleagues24 collated information across 10 countries
(the United States, Canada, Chile Brazil, the United Kingdom, Sweden,
Korea, China, India, and the Czech Republic) and reported that while
training in none of these countries lasted less than three years, in some it
could be much longer (in China training last five years and in the United
Kingdom training now last six years). Oakley and Malik14 recently sur-
veyed informants from 22 European countries and reported a variation in
duration of training from 4–6 years except in Belarus (one year).
It is impossible to do justice to the immensely detailed findings from
the ATLAS project here, and the reader is directed to the results which are
freely available via the web. We will try and summarize some key findings
from the literature on variation in training experiences across the world.
6.3. International variation in the content of training schemes

The quality of psychiatric training varies to a large extent across countries.
Even within Europe there are still considerable differences in the length,
content and structure of postgraduate psychiatric training and training is
not formally standardized even in some Western European countries
(Austria, Bosnia, France, Italy, and the Netherlands).14 These differences
are particularly important in terms of the establishment of the right of
professionals to move across national borders in the European Union in
order to work.
Within countries there are some specific areas of training which may be
weaker than others. For example, ATLAS reported Turkey had ‘good’
training opportunities in biological psychiatry, psychopharmacology, and
psychiatric nosology but training opportunities in psychotherapy, commu-
nity psychiatry, forensic psychiatry, and cultural and administrative issues
are relatively less. Bolivia was reported as having particular strength in
teaching epistemology, statistics, community care, epidemiology, and
methodology of scientific research as a part of psychiatric training.
B1405_Ch-24.indd 621 1/31/2013 2:41:41 PM

In some countries, specific training is only in the early stages of devel-

opment. Psychiatric training in Syria only started in the late 1990s. The
trainees are (according to ATLAS) based in two mental asylums and the
curriculum is under-developed. There were also no facilities for psycho-
therapy, social work, and quality research in 2005 according to ATLAS.
The quality of training was ‘poorly monitored’ and there were no licensing
laws. There is no specific program devoted solely to psychiatry in Kuwait.
However, the Kuwait Institute for Medical Specialization (www.kims.org.
kw/training.html) runs a specialist program, for which the native Kuwaiti
doctors involved do rotation in the psychiatric hospital. Okasha and
Karam reported a wide variation in length of specialist training in psychia-
try across the Arab world during the 1990s from one year for specialization
in Jordan and the United Arab Emirates to four years in Egypt.15
In contrast, postgraduate psychiatric training in Australia and New Zealand
is essentially an apprenticeship model, with great emphasis placed on a
particular set of clinical rotations and careful clinical supervision as in
North America and Europe. The Royal Australian and New Zealand College
of Psychiatry (www.ranzcp.org) maintains an accreditation process and
oversight of all of those clinical placements and the documented supervi-
sion. In addition, there are formal, more academic programs which usually
occupy one or two half days per academic year, for 3–5 years.
In Africa, the M. Med Psychiatry course in Tanzania consists of six
semesters and includes basic sciences courses and theoretical and skill
modules specific to the discipline of psychiatry and mental health. Basic
science courses include physiology and clinical pharmacology, biochemis-
try, microbiology/immunology, epidemiology, and biostatistics. Apart from
clinical psychiatry, medical, sociological, anthropological, and psychological
disciplines are part of the course. A structured supervised dissertation is an
essential part of the curriculum. In Tunisia, the curriculum lasts four years
during which residents are encouraged to spend a six-month training period
in child psychiatry and in neurology. Many residents are offered a one-year
training period abroad, mainly in France (as Tunisia is one of the strong
network of francophone countries) to increase their knowledge in an areas
of training not available in Tunisia e.g. CBT or neuro-imaging.
There is considerable variation in training experience too across Asia.
Basic psychiatric training in China lasts for three years with a doctoral
program extending for 5–6 years. Much of the time over the first few years
B1405_Ch-24.indd 622 1/31/2013 2:41:41 PM

is spent in inpatient settings.24 Korea was the first country in Asia to adopt
an America style training program and has a highly structured and stand-
ardized pathway to Board certification, similar to that in North America,
and extensive experience available in psychotherapy. In contrast, the expe-
rience available to trainees in India is much more varied. Training takes
three years leading to an MD for which the completion of a research
project is compulsory. Further training after the MD degree as a senior
registrar for a period of three years leads to eligibility for consultancy.
Many doctors do not opt for senior registrar training, but go into private
practice or work as a psychiatrist in a district hospital. In some hospitals,
it is not deemed necessary to complete senior registrar training to become
a consultant. However, senior registrar training is essential if the trainee
plans a career in academia or plans to join a teaching institution. A signifi-
cant number of trainees from India go abroad to the United Kingdom or
United States for further training and experience.3
In terms of psychiatry residency subspecialty training, in the United
States, there are additional opportunities for training in child and adolescent
psychiatry, addiction, forensics, psychosomatic medicine, and geriatrics.
Further, there are areas such as sleep medicine, pain, and palliative care, to
highlight several where psychiatrists, as well as other types of specialists,
can apply to receive additional training. These programs are accredited by
the American Board of Medical Specialties and there are Board examina-
tions for those who successfully complete their training. The importance of
this increased focused training is seen in enhanced research and scholar-
ship, improved ways to teach, train, and supervise students in these areas,
and opportunities for medical students to choose elective experiences.
It is important to recognize that training across countries will vary
according to the specific sociocultural and economic factors pertaining to
that nation and the prevailing health care system. Zisook et al.24 note that
for Brazil … perhaps the main challenge for residency training … is put-
ting into practice in such a dissimilar reality the knowledge and theories
learned from mainstream American textbooks and recent scientific arti-
cles. Despite marked regional variations, infrastructure is more precari-
ous, funding for research not as accessible, and the salary is extremely
low, even after accounting for cost-of-living. Training in psychiatry in the
United Kingdom is focused towards working in the National Health
Service, with no specific education on aspects relating to private practice.
B1405_Ch-24.indd 623 1/31/2013 2:41:41 PM

Training psychiatrists on issues related to cultural sensitivity are part of

the training in some countries e.g. Switzerland and Denmark. In the latter,
there are both introductory courses and a few lectures focusing on the
cultural issues relevant to psychopathology and treatment. Uganda trains
its psychiatrists in different culture-bound syndromes and provides some
idea about the treatment methods followed by traditional healers.
6.4. Psychiatry, neurology and biological psychiatry

In the United States, all residents in psychiatry must complete a mini-
mum of two months of training in neurology. The emphasis is often on
both the common neurological disorders likely to be seen in psychiatry
practice, and issues at the intersection of the two disciplines, such as
presentations of neurological disorders with mental status changes, and
of psychiatric disorders with neurological symptoms. In the United
States, there is also a requirement for training in internal medicine or
primary care. Many European countries also retain a strong tradition of
neurological experience as part of psychiatric training; for example in
Germany, one of five years in training is usually spent in studying
neurology.8 In the United Kingdom, in contrast, neurology not considered
to be part of psychiatric training. In many countries, training in neuro-
imaging is becoming more common, but in some places this is simply
limited by the number of research centers in the country providing access
to facilities for teaching.
6.5. Training in psychotherapy

Psychotherapy has a traditional place in psychiatry as a key skill to be
acquired. Students need opportunities to acquire not only knowledge
about the different models of psychotherapy (psychoanalytic, cognitive–
behavioral, etc.) but also have opportunities to acquire and practice the
skills under regular and competent supervision.
Despite the heavy psychoanalytic emphasis in psychiatric training in
the mid 20th century, the United States has recently focused on biological
psychiatry with only some centers having a greater focus on psychother-
apy. There is scope for imparting different forms of psychotherapy to
B1405_Ch-24.indd 624 2/6/2013 11:06:16 AM

those interested. In Europe, there is considerable variation. Mihai et al.13

while exploring psychotherapy training across Europe found four catego-
ries of training systems:
• Training in psychotherapy is compulsory, and after completing train-

ing in psychiatry trainees are accredited as “psychiatrist and psycho-
therapist” (Netherlands, Denmark, France, Germany, and Italy).
• Basic training in psychotherapy is compulsory. After completing
training in psychiatry trainees are not accredited as specialist
psychotherapists. If a trainee wants to work as a psychotherapist he or
she has to complete a specialist course in the chosen therapy (the
United Kingdom, Denmark, Sweden, Estonia, Romania, and Austria).
• Psychotherapy is a recommended but not a compulsory part of train-
ing (Bosnia, Herzegovina, Finland, and Turkey).
• Training in psychotherapy is not recommended or compulsory. If
trainees wish to become trained in psychotherapy then they to pay for
it and complete the training in their own time (Albania, Greece,
Moldavia, and Russia).
In some countries across the world psychotherapy retains a powerful

position in training. Zisook et al.24 note that this is the case in Chile, for
example. In others, particular in African countries, there is a shortage of
clinicians to provide practical training and supervision so opportunities
for training are much more limited.
6.6. Involvement of service user/patients and carers

in psychiatric training
Involvement of people who are in receipt of psychiatric services, and
those who care for them, is now mandatory in the United Kingdom but
not well developed in most part of the world (it indeed receives no men-
tion in the ATLAS report). Fadden et al.5 suggest the following possible
roles in:
• Planning of training.
• Sharing experiences and perspectives.
B1405_Ch-24.indd 625 1/31/2013 2:41:41 PM

• More detailed training, e.g. interview skills training.

• Helping junior staff to learn about the experience of mental health or car-
ing issues by being willing to be interviewed about their experiences.
• Commenting on assignments.
• Supervision and consultancy with service users and carers while on
placement.
• Feedback from those who receive services from a trainee about capa-
bility, attitudes and skills (although it must be acknowledged that this
can be tricky to manage if the person is still receiving services from
the doctor in training).
• Involvement in the selection of trainees for training schemes.
• Involvement in selection of tutors and others responsible for training.
Finally in this section, cases studies of training in Uganda and

Switzerland adapted from the ATLAS project can be found in Table 2
highlighting the differences (and increasing similarities-at least in aspira-
tion if not always possible in delivery) between training schemes across
the world.
7. ASSESSMENT OF PSYCHIATRIC EDUCATION

Assessment of psychiatric education has been an issue for debate due to
difficulties in checking knowledge, skills in diagnosis and treatment, deci-
sion making in real life conditions, leadership skills within therapeutic
teams and research abilities. Different methods of evaluation have been
discussed and criticized over time11 and in the following section we have
drawn on the recent review carried out by Lunn and his colleagues.11
7.1. Assessing knowledge

Methods of knowledge assessment vary between:
• An oral presentation of one or more specified topics — this may be

formal presentation and/or a viva examination with questions asked
by examiners.
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Table 2. A comparison between training programmes in Switzerland (high income) and

Uganda (low income) adapted from the ATLAS study (2005).
Switzerland Uganda
Current resources 2,229 psychiatrists for 18 psychiatrists for
(as of 2004) 7.2 million population. 25.8 million population.
Psychiatric training Years residency, standardized Three years residency.
curricula, stringent
accreditation policies.
Biological psychiatry Standardized and fixed 1st year of postgraduate
period of training in training imparts skills in
different aspects of biological psychiatry.
biological psychiatry. This is hampered by lack of
modern laboratories.
Psychotherapy Three years training in Mainly theoretical knowledge
analytical or CBT. with some practical training
in CBT over one semester.
Psychology and Basic theoretical knowledge Basic theoretical background
social science about psychology, sociology, in social sciences is taught.
and anthropology is provided. Interpretation and application
Interpretation of psychological of psychological tests in
assessments are taught. diagnosis is also provided.
Neurology and Provision of a one year Neurological skills are taught
neuro-imaging rotation in somatic therapy during the training. Exposure
and neurology could be an to modern neuro-imaging
option during that period. and neurophysiological tests
Adequate exposure to is limited by the lack of
different neuro-imaging and resources across all centers
neurophysiological tests are in the country.
provided.
Rational prescription Evidence-based practice is Molecular pharmacology
encouraged and taught. and psychopharmacology
is taught during the course
rational prescription
practices are imparted.
(Continued)
B1405_Ch-24.indd 627 1/31/2013 2:41:41 PM

Switzerland Uganda
Research Epidemiological and statistical Basic research skills in statistics
training is provided as a and epidemiology are taught
course requirement. as part of the compulsory
Individual skills and research dissertation submitted by all
interests can be gained students as part of their
through an optional one-year course requirement.
posting in a research center.
Public health and Public health principles and Basic principles in public health
health economics health economics as applied and macroeconomics as
to mental health are taught. applied to financing of mental
health systems are provided.
Law and ethics Provision for stipulated period Mental health legislation and
of training in laws and its relevance to practice are
principles of ethics as taught as part of forensic
applied to the country. psychiatry principles.
Cultural sensitivity Aspects of transcultural Knowledge about culture-
psychiatry and social bound syndromes and
psychology are emphasized traditional healing practices
during training to improve are imparted during the
the communication skills training period.
and psychiatric understanding
of multi-ethnic clients.
Others Migration of psychiatrists is Uganda is severely affected my
not a major issue. migration of its limited
number of psychiatrists to
high income countries.
• Written examination with multiple choice questions.

• A written dissertation on a case.
• Essay(s) about a particular theme or question drawn from the psychi-
atric literature.
Essays have some theoretical advantages in assessing integrated knowl-

edge but they do pose logistical problems as they are very labor intensive
to mark. The reliability of examiners in consistently marking work is poor.
Even the same examiner remarking the same essay after a six-month gap
B1405_Ch-24.indd 628 2/6/2013 11:06:16 AM

has been shown in one study to only have a correlation of 0.35. Short
answers questions (SAQs) are theoretically easier to focus but there are
still issues as to how candidates interpret what is asked. However, improv-
ing reliability of marking in SAQs is easier than with essays. Some exami-
nation boards have therefore chosen to reject essays and SAQs in favor of
other assessments of knowledge. However, this is not without risk. Unless
assessed in the workplace, the skill of writing, which is core to specialized
psychiatric practice, can be missed out. This is apparent in the letters writ-
ten by some of our own trainees.
Multiple choice questions (MCQs) have been a core feature of medical
examination in many countries for some years but there has been debate
over the best design. Recently the shift has been to single item questions
with an adjusted mark to take into account guessing. Extended matching
items/questions (EMIs or EMQs) have also been developed with the aim
of better assessing knowledge application than with MCQs but with a
higher reliability than can be had with SAQs and essays.
The assessment of knowledge should correlate with those items speci-
fied as core to the curriculum in each specific training system.
7.2. Skills assessment

Traditionally this has included at least one “long case” i.e. the assessment
of a doctor in a setting as close to clinical practice as is possible and this
is probably still the most widely used assessment of skill of psychiatrists
across the world (see next section).
7.3. The long case

The traditional clinical assessment involves a meeting, usually lasting an
hour, between candidate and patient in which the candidate is required to
carry out an assessment interview, from which they derive a diagnosis and
management plan, upon which the candidate is then examined during a
viva. Typically, the candidate is not observed during the assessment inter-
view, although they may be asked subsequently to demonstrate a portion
of the assessment, usually a specific part of the mental state examination,
in front of the examiners.
B1405_Ch-24.indd 629 1/31/2013 2:41:41 PM

This mode of assessment has apparent high face validity in that it simu-
lates the clinical encounter, involves the assessment of real patients, and
requires the demonstration of “higher order” clinical skills such as the
integration of clinical findings and knowledge. However, key clinical
skills are actually rarely observed and their assessment is largely by infer-
ences drawn post-hoc in the following viva.
There are also a number of other potential problems. Luck has a signifi-
cant role to play in candidates’ experiences as the (usually single) case
allocated may play of course to their strengths or weaknesses. Patients
may be helpful, or possibly even hostile, regardless of how a candidate
performs. The symptoms and signs that the patient exhibits on the day of
the examination may vary considerably from that in the summary pre-
pared (sometimes a day or two before) by the organizers for the examin-
ers, and case selection will depend on the local services from which
patients are recruited. Finally, the examiners own skills and prejudices
may play a part in how a candidate is judged to have performed. Wass and
Jolly20 showed that that reliability from a single long case of an hour is
around 0.60 rising to 0.86 after 4 hrs of testing and 0.90 only after 8 hrs,
which would be impossible in most examination centers and still does not
take into account the variation in viva examinations carried out by differ-
ing examiners.
7.4. Modified long cases

Concerns about the reliability and validity of the viva component led to
the development of the Objective Structured Long Examination Record
(OSLER) which structures the process in such a way that there is a focus
on the candidate both carrying out observed clinical skills, whether his-
tory taking or examination, and presenting their conclusions and recom-
mendations in response to a structured oral examination. This has however
still not eradicated all the concerns about reliability and validity.
7.5. The objective structured clinical examination (OSCE)

In an OSCE, the candidate moves round a series of “stations” in which a
variety of different clinical skills are assessed. The reliability of this form
B1405_Ch-24.indd 630 1/31/2013 2:41:41 PM

of examination is much higher than the long case as each candidate can be
given a similar experience through the use of standardized patients per-
forming defined roles. The candidates are also assessed against clear
objectives, which can be designed to match an examination “blueprint”
that enables assessment of a broad range of different skills. The OSCE is
now becoming more widely used in both undergraduate and postgraduate
settings in many countries as it allows examination of a greater range of
skills, in a more reliable manner, than a single clinical examination.
7.6. Assessment methods used internationally

In the light of our comments above on the background to assessment
methods utilized in psychiatry, it is interesting to review the findings of
the ATLAS project in this regard.
The ATLAS project22 countries reported that knowledge, skills, atti-
tude, and clinical acumen were evaluated by written and oral examina-
tions as part of on-going and end of training evaluation. On-going or end
of training evaluation of knowledge by oral methods was the most pre-
ferred mode of evaluation in 39 and 46 countries, respectively. Managerial,
teaching, and research skills were evaluated during some point of training
in about 40%, 55%, and 70% of countries, respectively. Research was the
only skill that was evaluated more through written format. This was most
likely due to the fact that the assessment was often based on a dissertation
submitted by the trainee.
The commonest assessment methods for examinations as recommended
by national bodies were clinical examination (73.0%), essays (66.2%),
patient interviews (66.2%), MCQs (63.5%), and dissertation (55.4%).
While 33 (44.6%) countries used a combination of internal and external
examiners to evaluate the trainees, 25 (33.8%) countries used only internal
examiners. An independent or accrediting body to evaluate the trainees was
used by 20.3% and 21.6% of countries, respectively.
7.7. Life-long learning

The concept of the “reflective practitioner” was introduced by Schon17 in
the 1980s in his book The Reflective Practitioner (1983). Reflective
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practice can be defined in a number of different ways, but all the defini-
tions encapsulate a range of activities associated with both learning and
thinking about the process of learning. Essentially it is a continuous pro-
cess from a personal perspective, informed by considering critical inci-
dents within your life’s experiences. As defined by Schon, reflective
practice involves thoughtfully considering one’s own experiences in
applying knowledge to practice while being coached by professionals in
the discipline.
After qualification as a psychiatrist, there are many opportunities for
engaging in reflective practice. Some will choose to become full-time
clinicians, others may wish to do research, many will be involved in teach-
ing and all of these will be involved in updating their knowledge and skills
from time to time and in doing this will be reflecting on what they have
learned and what they identify as their on-going educational priorities
while taking the opportunity to reflect on their daily clinical practice and
work. All should be also concerned about ensuring that they take care of
their own health and well-being in order to ensure that they are able to
continue to practice safely and competently.
7.8. Developing research and teaching skills

Increasingly, in some high income countries, young doctors are encour-
aged to make decisions about which direction they wish to go in their
careers, and will develop an interest in research by carrying out small
research projects at medical school and intercalating a specialist area of
interest for one year into their degree course in medicine in the United
Kingdom, for example, this is most commonly a year of extra study in
psychology for those who are interested in psychiatry and possibly fol-
lowing an academic career track. However in many countries, such oppor-
tunities will necessarily be more ad hoc and opportunities to learn about
research skills and carry out projects will come through involvement in a
Master’s or PhD program during their psychiatric training, and application
for Fellowships to study in particular centers of excellence for research,
often overseas.
Most universities through departments of education offer some instruc-
tion on “how to teach” but in many medical schools there is now specific
B1405_Ch-24.indd 632 1/31/2013 2:41:41 PM

expertise in medical education where psychiatrists who are interested in

learning how to teach can acquire a range of skills such as learning how
to give a lecture in an engaging and interactive way, small group work,
and how to facilitate PBL. If psychiatrists wish to become involved in
teaching beyond psychiatry in settings such as primary care, it is advisable
that they make close links with primary care teachers in order to ensure
that they develop a teaching experience that is going to be both specifi-
cally relevant and of interest to doctors working in that setting. Many
psychiatrists provide training in this setting across the world, but provide
lectures and seminars that are more suited to the needs of trainee psychia-
trists that primary care physicians. Lectures for primary care settings must
be brief and practically focused and there should be specific attention to
addressing skills needed to recognize and manage emotional problems in
primary care, as well as importing knowledge.6
The WPA, as part of its Action Plan 2008–2011, has launched a pro-
gram of research fellowships for early-career psychiatrists from low or
lower–middle income countries, in collaboration with internationally
recognized Centers of Excellence in Psychiatry: Institute of Psychiatry,
King’s College, London; Case Western Reserve School of Medicine,
Cleveland, Ohio, USA; and the University of Maryland School of
Medicine, Baltimore, Maryland, USA. It also runs a highly successful
(and competitive) program of courses for early career psychiatrists
covering such topics as improving skills in making oral and poster
presentations, preparing papers, writing project proposals, preparing
resumes, conducting meetings, writing meeting reports, producing good
titles, selecting research subjects, and deciding on priorities for study.
Further information about all of these initiatives is available from the
WPA website at www.wpanet.org.
7.9. Continuous professional development and education

All clinicians should be engaged in “life-long learning” and this has been
formalized in medical education under the concept of continuous profes-
sional development (CPD). This differs from continuous professional
education (CPE) in that it is not a passive activity simply turning up at
lectures and getting points for attending, but involves actively determining
B1405_Ch-24.indd 633 1/31/2013 2:41:41 PM

what are one’s own particular educational needs, usually in consultation

with a peer group or mentor, and then planning a program of activities for
specifically meeting those needs in a manner in which achievement can be
measured and audited. It can be defined as any learning activity that
enhances knowledge, skills, and competencies required for professional prac-
tice. CPD encompasses clinical education, practice management, ethical
decision-making, evidence-based care, managed care principles, etc. CPD
can include a variety of learning formats that are focused on relevant out-
comes and practice applications. Over the last five years, the Royal College
of Psychiatrists has, for example, developed CPD as its key contribution
to promoting life-long learning. At its core, engagement in CPD requires
psychiatrists to maintain, develop, and remedy any deficits in the knowl-
edge and skills relevant to their professional work.
7.10. CPD and the pharmaceutical industry

As a previous President of the Royal College of Psychiatrists commented
five years ago:
I had just spoken to a meeting of one of our users’ and carers’ organiza-
tions. Mingling at coffee time, I lapped up congratulations on how
approachable the College had become, when I was brought up short by a
long-term patient with a scowl on his face. ‘The trouble with you psychia-
trists’, he said, ‘is that you’re all pill-pushers. You’re all in the pocket of the
drug companies’.
As a child psychiatrist by trade, and as a President who has fought
hard to tighten the College guidelines on sponsorship, I bridled at such
stereotypes. But unfair though they may seem, the charges are persistent
and deserve to be tackled head-on….
The sponsorship of CPD events for physicians by the pharmaceutical

industry is a highly contentious issue within medicine.18 In some countries
that we have visited, there is clearly more of a presence from the pharma-
ceutical industry than is now the case at the annual meetings of both of our
national associations, where speakers have to be full and frank
B1405_Ch-24.indd 634 1/31/2013 2:41:41 PM

with disclosures at the beginning of their lectures and in anything they

publish — although this has not always been the case; service users and
carers’ perceptions of our relationships with pharmaceutical companies
are often understandably suspicious.
There have been major changes. In the United Kingdom, the level of
industrial sponsorship of College activities has been steadily and deliber-
ately reduced, but we must all be aware of the role that we may be playing,
both in attending industry sponsored events, and in speaking at them
and be quite clear about what we are, and are not, prepared to say or do.
As Dr Shooter concluded, “I think, is that psychiatry as a whole is not for
sale, but certain psychiatrists regrettably are.”
7.11. Re-licensing
In some countries (though not yet in the United Kingdom which is a
notable exception here in high income countries although change is cur-
rently on the horizon), CPD policy is intimately involved with the pro-
cess of maintaining one’s license to practice as a psychiatrist. It is
interesting to note that in the ATLAS survey while 40 countries report-
edly had permanent licensing, 19 countries said that they had licensing
for a limited duration only. Continued medical education was cited as a
requirement for maintaining a license in 12 out of the 16 countries
responding to that question. In some countries, such as the United
States, maintaining a license requires not only attending CME but
undergoing formal recertification every 10 years.
7.12. Self-care
As health professionals, we have a duty to ensure that we are fit to prac-
tice. As a group within society, the health care of doctors is problematic:
we have a higher than average risk of succumbing to the four ‘Ds’ —
depression, drink, drugs, and divorce. Several cross-sectional studies have
reported higher rates of depression and burnout among psychiatrists than
among doctors from other specialties. The higher depression scores
among psychiatrists have been mirrored by higher suicide rates over some
B1405_Ch-24.indd 635 1/31/2013 2:41:41 PM

decades, both in the United States16 and in the United Kingdom,7 but it is
not clear whether these findings are translated internationally. The main
sources of stress for all doctors seem to be excessive workloads, organi-
zational changes, poor management, and insufficient resources, dealing
with patients’ suffering and mistakes, complaints and litigation, and pres-
sure of work. However, psychiatrists face particular pressures in addition
to these, given the relatively low status of psychiatry as a profession in
many countries, the stigma often experienced by psychiatrists and the low
numbers of psychiatrists practicing in some settings internationally.
Psychiatrists also have to deal with the suicide of patients during their
career.
As doctors, we need to do several things. Ensuring that we do have and
maintain a satisfactory work–life balance, honestly reviewing alcohol
intake (where alcohol is culturally acceptable doctors have a reputation,
supported by evidence, for using it to excess as a coping strategy); ensur-
ing that we keep up with regular health checks and put into practice at
least some on the advice on diet and exercise that we expect others to
follow each day; keep up our support systems with friends and family, and
ensure that if we do experience problems that we seek help early. In our
experience this is often a major barrier for doctors who will continue to
work when they should have sought help. In some countries, licensing
authorities will also expect medical professionals to report colleagues who
are unfit to practice — this is the case in the United Kingdom for the
General Medical Council.
As teachers and supervisors, we have a responsibility to do a number
of things to help prevent mental health problems in our trainees.
At an individual level:
• Teach better coping strategies for stress at undergraduate level.
• Problem-solving skills.
• Coping with self-criticism and conflict.
• Substance misuse.
• Importance of home–work balance.
• Ensure early detection and treatment of problems through close super-
vision and mentoring.
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• Recognition of the wide range of opportunities/work patterns for pro-

fessionals who develop mental health difficulties and provision of
support through career counseling.
At an organizational level:
• Ensuring professionals have proper personal health care arrangements.

• Adequate sleep patterns.
• Challenging the ‘macho’ culture of medicine and bullying and
harassment.
• Attention to working environment to manage workload.
• Challenging stigma of discrimination against mental illness in health
professionals.
• Setting up support networks.
• Confidential and accessible treatment programs for health professionals.
• Challenge the willingness of organizations to employ professionals
with mental health problems.
• Supportive and flexible working environments.
8. KEY POINTS
• Psychiatry departments that have high recruitment rates give consid-
erable priority and resources for medical student psychiatric
education.
• The challenge in designing medical school curriculum, whether for
low or middle income countries, is to ensure that medical students
have a good knowledge of how to recognize and manage common
mental health disorders such that they will be competent in basic
mental health care whatever specialty they ultimately choose.
• PBL provides an opportunity to build mental health topics into cases
at the curriculum design stage so that these issues are addressed by the
students as they learn.
• It is important that training in Communication Skills is not seen as a
‘psychiatric’ skill, but as an important skill regardless of which
specialty students will be entering after qualification.
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• All clinicians should be engaged in “life-long learning” and this has

been formalized in medical education under the concept of CPD.
9. SELF-ASSESSMENT
9.1. In the United States, the accreditation council
of graduate medical education has determined
six competencies for all medical specialties,
including psychiatry:
(A) Patient knowledge practice-based teaching, medical skills, interper-
sonal and communication technology, professional billing, and
evidence in practice.
(B) Patient care; medical knowledge, practice-based learning and
improvement; interpersonal and communication skills; professional-
ism and system-based practice.
(C) Patient competency; medical professionalism; medical skills; inter-
personal and communication skills; evidence of professional billing;
evidence in practice.
(D) Primary care competency; practice-based teaching; patient communi-
cation; medical professionalism; medical skills; medical knowledge.
(E) Office-based billing practices; medical skills; professionalism; com-
munication skills; internet skills; evidence in practice.
Answer: B
9.2. The Royal College of Physicians and Surgeons

of Canada organized competencies around seven
specific roles of the medical professional:
(A) Medical scholar; health care promoter; investigator; business
manager; teacher; preacher; health-care provider.
(B) Decision-maker; ethicist; translator; manager; teacher; professional;
expert.
(C) Medical expert; scholar; communicator; health advocate; manager;
collaborator; professional.
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(D) Medical expert; medical promoter; investigator; teacher; health-care

provider; business manager; ethicist.
(E) Health advocate; scholar; psychiatrist; decision-maker; ethicist;
translator; business manager.
Answer: C
10. CASE STUDY

A woman of 45 years of age with a breast lump becomes extremely anx-
ious during her examination and while undergoing assessment for surgery
and radiotherapy. Later on, after treatment she is very unhappy with her
body image after surgery. She is unable to let her husband see her scar after
the operation. She is unable to sleep, has no energy, and has persisting pain.
This case provides opportunities for students to work on topics, for
example, relating to common mental health problems — anxiety and
depression — as they occur in people who are facing life threatening ill-
ness, issues of post-operative mental health problems in cancer treatment,
body image, grief and relationships etc. If facilitated effectively, a PBL
group will address a range of psychosocial learning outcomes in addition
to the more obvious surgical and oncological issues in this case. However,
there does remain the risk that a tutor with a particular view of the impor-
tance or otherwise of addressing psychosocial problems in medicine will
skip over the psychological and social cues that have been carefully writ-
ten in to the case (by the case-writing group which will ideally be multi-
disciplinary), and stick to a more biomedical theme, such as the
management of post-operative pain or the pros and cons of reconstructive
surgery. This may sometimes be more likely to happen when tutors are
drawn from a particular specialty and do not view their remit in teaching
to address the broader issues demanded by the PBL case.
REFERENCES
1. Chur-Hansen A, Carr JE, Bundy C, et al. (2008) An international perspective
on behavioral science education in medical schools. J Clin Psychol Med
Settings 15: 45–53.
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2. Cıngı Başterzi AD, Tükel R, Uluşahin A, Coşkun B, Alkın T, Murat Demet M,

Konuk N, Taşdelen B. (2010) Undergraduate psychiatric training in Turkey.
Turk Psikiyatri Derg 21: 195–202.
3. Das M, Gupta N, Gupta K. (2002) Psychiatric training in India. Psychiatric
Bull 26: 70–72.
4. Dogra N, Hoschl C, Moussaoui D. (2011) Developing a medical student
curriculum in psychiatry. In: Gask L, Coskun B, Baron D (eds.), Teaching
Psychiatry: Turning Theory into Practice, Chapter 4, pp. 27–46, Wiley, Bristol.
5. Fadden G, Shooter M, Holsgrove G. (2005) Involving carers and service
users in the training of psychiatrists. Psychiatric Bull 29: 270–274.
6. Gask L, Lewis B, Goldberg D. (2009) Teaching and learning about mental
health. In: Gask L, Lester L, Kendrick T, Peveler R (eds.), Primary Care
Mental Health, pp. 423–438, Gaskell, London.
7. Hawton K, Clements A, Sakarovitch C, et al. (2001) Suicide in doctors:
A study of risk according to gender, seniority and specialty in medical prac-
titioners in England and Wales, 1979–1995. J Epidemiol Community Health
55: 296–301.
8. Hohagen F, Treichel S, Berger M. (1997) Psychiatric training in Germany.
Eur Arch Psychiatry Clin Neurosci 247: S15–S17.
9. Illingworth P, Chelvanayagam S. (2007) Benefits of interprofessional educa-
tion in health care. Br J Nurs 16: 21–24.
10. Karim K, Edwards R, Dogra N, et al. (2009) A survey of the teaching and
assessment of undergraduate psychiatry in the medical schools of the United
Kingdom and Ireland. Undergraduate psychiatry: What’s going on? Med
Teach 31: 1024–1029.
11. Lunn B, Corral M, Mihai A. (2011) Assessment in psychiatric education. In:
Gask L, Coskun B, Baron D (eds), Teaching Psychiatry: Turning Theory into
Practice, Chapter 17, pp. 213–230, Wiley, Bristol.
12. Mackey AB, Tasman A. (2011) Psychiatric residency curriculum: Development
and evaluation. In: Gask L, Coskun B, Baron D (eds), Teaching Psychiatry:
Turning Theory into Practice, Chapter 7, pp. 77–96, Wiley, Bristol.
13. Mihai A, Weiss E, Beezhold J, et al. (2009) Psychotherapy training across
Europe: Status quo. Die Psychiatrie 6: 84–88.
14. Oakley C, Malik A. (2010) Psychiatric training in Europe Psychiatrist 34:
447–450.
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15. Okasha A, Karam E. (1998) Mental health services and research in the Arab
world. Acta Psychiatr Scand 98: 406–413.
16. Rich CL, Pitts FN Jr. (1980) Suicide by psychiatrists: A study of medical
specialists among 18,730 consecutive physician deaths during a five-year
period, 1967–72. J Clin Psychiatry 41: 261–263.
17. Schön DA. (1983) The Reflective Practitioner: How Professionals Think in
Action, Temple Smith, London.
18. Shooter M. (2005) Dancing with the devil? A personal view of psychiatry’s
relationships with the pharmaceutical industry. Psychiatr Bull 29: 81–83.
19. Sierles FS, Taylor MA. (1995) Decline of U.S. medical student career choice
of psychiatry and what to do about it. Am J Psychiatry 152: 1416–1426.
20. Wass V, Jolly B. (2001) Does observation add to the validity of the long case?
Med Educ 35: 729–734.
21. World Psychiatric Association. (2002) World Psychiatric Association
Institutional Program on the Core Training Curriculum for Psychiatry,
Available at: http://www.panet.org/detail.php?section_id=8&content_id=112.
Accessed December 26, 2010.
22. World Health Organization. (2005) ATLAS: Psychiatric Education and
Training Across the World 2005, World Health Organization, Geneva.
23. World Psychiatric Association and the World Federation of Medical
Education. (1999) Core curriculum in psychiatry for medical students. Med
Educ 33: 204–211.
24. Zisook S, et al. (2007) Psychiatry residency training around the world. Acad
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Chapter 25
Residency Training
Sanjai Rao and Sidney Zisook
1. INTRODUCTION
Psychiatric residency training is one step in the trajectory from novice to
expert as a psychiatric physician. This chapter will describe the longitudinal
process, from the application, through training, and then into practice for
psychiatric specialists. We begin by briefly describing the typical path a
student in the United States takes to enter residency, followed by a discus-
sion of the admissions process, with special emphasis on features relevant to
International Medical Graduates (IMGs). An overview of a typical psychia-
try residency training program is provided, including the structure and over-
sight, regulatory issues, curriculum, and clinical experiences. Where useful,
the authors will amplify general principles with specific examples from the
training program with which they are affiliated. The chapter will conclude
with a brief discussion of post-residency issues, including fellowships,
board certification, maintenance of licensure, and employment options.
2. THE PATHWAY TO PSYCHIATRY RESIDENCY

IN THE US
2.1. Undergraduate education
Before entering medical school, students are required to have at least a
Bachelor’s degree (some will also have Master’s, and a few will have
642
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Residency Training 643
PhDs) and also to fulfill a number of prerequisites in subjects such as biol-

ogy, chemistry, and physics. However, there is no standard “pre-medical”
major. Therefore, although most pre-med students major in related fields
such as biology or chemistry, many also choose less-related fields, such as
history, English, or political science, and complete the premedical require-
ments outside their major. Generally, an undergraduate Bachelor’s degree
takes four years (although many students will choose to take longer) but
can be completed in as few as three.
2.2. Medical school

Medical school in the United States is generally four years. Traditionally, the
first two “pre-clinical” years are classroom-based, and the last two “clinical”
years take place in the hospital and in outpatient clinics. However, many
medical schools are now integrating more clinical exposure into the first two
years of their curriculum. In addition, some schools are recommending one
year of independent study, either as part of the four-year curriculum or in
addition to it. Finally, a relatively small number of students pursue joint MD/
PhD degrees, which take at least seven years and often longer.
2.3. Psychiatry residency

Historically, psychiatry residency in the United States consisted of an
internship year in a “primary care” specialty, such as internal medicine or
pediatrics, followed by three years of psychiatry training. Today, most
training programs provide a full four-year curriculum, which includes two
months of neurology and at least four months of primary care in the first
year (sometimes still referred to as the “internship” year). However, many
programs will also accept a small number of residents who have com-
pleted an internship in another discipline (such as internal medicine) into
their second year of training, as space allows.
3. THE ADMISSIONS PROCESS

In general, the residency application and admissions process for IMGs is
similar to that for US medical students. All medical students (US and
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644 S. Rao and S. Zisook
international) apply to residency through the Electronic Residency

Application Service (ERAS) and are assigned to a training program
through the National Residency Match Program. However, before apply-
ing, IMGs must also be certified by the Educational Commission for
Foreign Medical Graduates (ECFMG), which requires them to fulfill
additional requirements that are described below.
Because the admissions process can change in small ways from year to
year, it is vitally important that applicants review the websites of these
organizations thoroughly in order to understand the latest procedures.
Failure to do so can result in an application being delayed or even
rejected. Table 1 contains a summary of these organizations and lists their
websites.
3.1. Applications
3.1.1. Electronic Residency Application Service
The ERAS is an electronic service that gathers application documents,
such as personal statements, letters of recommendation, and medical
school transcripts, and then transmits them to residency training programs
Table 1. Important organizations and their websites.
Electronic Residency Application Service (ERAS): Electronic application service that

gathers application documents and transmits them to residency training programs.
http://www.aamc.org/students/eras/
Educational Commission for Foreign Medical Graduates (ECFMG): Certifies the
academic credentials of IMGs and allows them to access the ERAS application
system. http://www.ecfmg.org/
National Residency Match Program (NRMP): Gathers rank lists from applicants and
training programs and matches applicants to the highest program on their list that
can accommodate them. http://www.nrmp.org/
American Association of Directors of Psychiatry Residency Training (AADPRT):
Professional organization dedicated to the education and training of future
psychiatrists. http://www.aadprt.org/
American Psychiatric Association (APA): Professional organization for psychiatrists
practicing in the United States and Canada. http://www.psych.org/
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across the United States. Nearly all residency training programs partici-
pate in ERAS, so applicants need to become familiar with this service.
The ERAS website4 provides applicants and programs detailed informa-
tion on the entire application process. Students also find the MYERAS
section of the ERAS website to be a “friendly” user guide. US medical
students gain access to the ERAS website through the Dean’s office of
their medical school, which registers with ERAS and provides each stu-
dent with an electronic “token” that allows access.
3.1.2. Educational Commission for Foreign Medical Graduates

The IMGs must first apply for and receive certification from the ECFMG
before they are able to access the ERAS application system. Essentially,
the ECFMG acts as their Dean’s office and issues ERAS tokens. The most
current requirements for certification are published on the ECFMG
website.3
As of this writing, applicants must be an international medical student
or graduate in good standing with at least four academic credit years
(ECFMG will verify all credentials directly with the medical school).
They must also satisfy examination requirement in medical science and
clinical skills. These requirements are currently met by passing the United
States Medical Licensing Exam (USMLE) Step 1 and Step 2 Clinical
Knowledge (CK), as well as USMLE Step 2 Clinical Skills. The Test of
English as a Foreign Language (TOEFL) is no longer required.
Once IMGs have received ECFMG certification, they can begin prepar-
ing their ERAS application. The ERAS application consists of three key
areas:
(1) The Common Application Form: This is where applicants can enter
demographic information and their curriculum vitae (CV). This form
will be seen by every program to which the applicant applies.
Applicants might find it useful to try to provide brief, informative
descriptions of various activities they enter on their CV to demonstrate
how that activity has contributed to their unique skills and mastery.
(2) The Personal Statement: A large number of websites and services
assist applicants with personal statements. Those will not be reviewed
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Table 2. Tips for the personal statement.
1. Keep it relatively short: The people reviewing applications typically read dozens
(or even hundreds) of them. Personal statements that go much beyond a page are
more likely to be skimmed rather than carefully read.
2. Tailor it to the program: ERAS allows applicants to upload multiple personal
statements, which can be assigned to different programs. Applicants may want to
consider modifying their personal statement to make it more appealing to different
programs on their list.
3. Proofread: Fairly or not, programs may question English proficiency. The personal
statement is an opportunity to demonstrate fluency, so make sure it contains no
grammatical errors.
here, but a few recommendations that apply to most IMG applicants

are highlighted in Table 2.
(3) Letters of Recommendation: Most programs require three letters of
recommendation from faculty or chief residents. Although these can
be from any specialty, many programs like to see at least two letters
from psychiatry faculty familiar with the applicant’s work and at least
one from a non-psychiatric physician. IMGs who are applying for
residency in California will also need a Postgraduate Training
Authorization Letter, formerly known as a “California Letter.” This
letter will be filed with ERAS and be available to all California resi-
dency programs to which the applicant applies. Some California pro-
grams will not invite the applicant for an interview until the California
Letter is posted.
3.1.3. Maximizing the odds

The IMGs can be at a disadvantage when applying for a residency, espe-
cially at more competitive programs, which often have an abundance of
US medical graduates from which to choose. Because of this, it is impor-
tant to practice good strategy in selecting to which (and to how many)
programs to apply. Typically, even very well-qualified IMGs would be
well advised to apply to a fairly large number of programs. At least a few
of these should be less competitive, “safety” programs. In addition, a lit-
tle research may yield valuable information on a program’s historical
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rates of accepting IMGs and guide the decision about whether or not to
apply there.
3.2. Interviews
Because interviews are typically the only face-to-face contact between
applicants and training programs, they usually play a significant role in
each program’s selection process. Although the criteria for being offered
an interview varies with each program, in general, interviews are offered
after the program has reviewed the applicant’s ERAS application and
determined that he or she meets the program’s criteria. Typically, some
combination of the applicant’s grades, examination scores, accomplish-
ments, personal statement, and letters of recommendation are used to
make this determination. Most programs begin issuing invitations for
interviews before the Dean’s Letters are available, so it is important to
complete as much of the rest of the application by late summer to early
fall. Proactive applicants are likely to place themselves at an advantage.
Many programs screen hundreds of applications, with each one reading
more alike than different. Therefore, programs often make arbitrary, best
estimates of who they invite first, knowing full well that they may be miss-
ing several outstanding applicants. If an applicant does not hear from a
program in which he or she is interested, a call or an e-mail to the Program
Director may make all the difference. There may be a fine line between
healthy assertiveness and intrusive aggressiveness, but it often is benefi-
cial for an applicant to let a program know of his or her interest.
3.2.1. Scheduling and preparation

Once an applicant is offered an interview, the next step is to contact the
program directly and schedule the interview. Although most programs
have multiple interview days, it is important to do schedule the interview
as soon as possible, because many dates may not be available later in the
interview season. It is important to be flexible in scheduling an interview
day, especially at the more competitive programs.
Before an interview, it is advantageous to learn as much about the pro-
gram as possible. Consider reviewing the program website to get a better
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sense of the unique features of the program and what is desired in appli-
cants. Friends or colleagues who have applied to (or attend) this program
can often be a valuable source of information as well.
Applicants who are anxious or who struggle with interview situations
may benefit from practice interviews. These can be with colleagues or
faculty at their own medical school. However, it would be most beneficial
to practice with someone who administers (or at the very least has gone
through) interviews at a US medical school. Many websites also list ques-
tions that are commonly asked during residency interviews.
3.2.2. The interview day

Although the structure of the interview day can vary widely across differ-
ent programs, a typical interview day at most programs will consist of a
combination of different experiences. These may include several individ-
ual interviews with faculty and residents, a tour of the program’s training
sites and other facilities, and lunch with residents and/or faculty. Some
programs will also incorporate group interviews and team problem-
solving exercises. Programs in particularly nice locations may offer a tour
of their surrounding area. Some will also have an evening activity, such as
dinner.
If the program provides the names of individual interviewers in
advance, it may be helpful to look them up on the program website.
Knowing their interests in advance may allow applicants to share relevant
parts of their own experience.
It is important for applicants to dress and conduct themselves profes-
sionally during the entire interview experience. Standard attire for men is
a suit and tie or at least a sport jacket. Women will usually also wear a suit,
and both pant and skirt suits are acceptable according to individual prefer-
ence. Casual clothes such as jeans and polo shirts are frowned upon.
During a typical interview day, applicants will receive a great deal of
information about the program. For most applicants, it will be difficult to
recall this information weeks or months later. Therefore, it is advanta-
geous to take notes on various aspects of the program, such as overall
structure, rotation schedule, call schedule, pros and cons, and impressions
B1405_Ch-25.indd 648 1/31/2013 2:41:53 PM

of residents and faculty. This can also help when doing post-interview
follow up (see next section).
3.2.3. After the interview

After the interview, it is generally considered good form to send a card or
an e-mail to each interviewer. If a program is particularly appealing, it
may be a good idea to write to the training director, letting him or her
know that the experience was enjoyable and the program liked. If a pro-
gram is particularly interested in an applicant, it may also contact the
applicant to express that interest. However, it is important to be aware that
the National Residency Match Program (NRMP) has guidelines on com-
munication between applicants and programs. Excessive amounts of com-
munication are discouraged, and programs are prohibited from asking
applicants where they will rank them (although applicants may volunteer
this information if they wish). Applicants may ask programs where they
will be ranked, but programs are under no obligation to answer (although
some will).
3.3. The match

Once all interviews have been completed, applicants will need to create a
rank list, in which they list the programs they would like to attend, in order
of preference. Programs will also create a rank list of applicants. These
rank lists are submitted to the NRMP, which uses a computer algorithm to
match applicants to the highest program on their list that can accommo-
date them. The NRMP website5 has more information on the precise way
in which this match is conducted.
It is important for applicants to realize that by participating in the
NRMP match, they are agreeing to attend the program to which they are
assigned. If an applicant chooses to decline the match assignment, he or
she will not be able to attend any other program that participates in the
NRMP (almost all US programs) that year. Unless there is a legitimate
reason for declining a matched position, most programs will be hesitant to
match an applicant very highly should the applicant reapply in subsequent
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years. For this reason, applicants are advised to rank only programs that
they are willing to attend. In addition, while programs were previously
able to offer some of their positions outside the match, NRMP now man-
dates that any program participating in the match has to list all its PGY-1
and -2 open positions in the match (often known as the “all in” rule).
Rank lists for both applicants and programs are usually due in mid-
February, with the Match results typically being published one month
later. Most medical schools hold a “Match Day” celebration, in which
applicants find out where they have matched. Match information is also
available on the NRMP website.
3.4. The Supplemental Offer and Acceptance Program

Applicants who do not match and programs that do not fill will learn this
information shortly before Match day. For these applicants and programs,
there is still an opportunity for placement known as the Supplemental Offer
and Acceptance Program (SOAP). This process consists of a series of
“rounds” in which programs with available positions can offer them to
applicants who have not matched. More detailed information on SOAP is
available on the NRMP website.
4. ADMINISTRATIVE HIERARCHY FOR RESIDENCY

TRAINING
Besides the NRMP, which oversees the admission process described above,
there are many additional levels of governance and quality assurance
responsible for oversight of training programs (e.g. the Accreditation
Council for Graduate Medical Education and Residency Review Committee
for Psychiatry) and trainees (e.g. the American Board of Psychiatry and
Neurology, Graduate Medical Education Committees, Training Committees).
4.1. Oversight of programs

4.1.1. Accreditation Council for Graduate Medical Education
In most of the United States, graduation from an accredited residency
program is a prerequisite for obtaining a medical license. Residency
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programs are accredited by the Accreditation Council for Graduate

Medical Education (ACGME).2 The ACGME was established in 1981
from a consensus in the academic medical community for an independent
accrediting organization. Its forerunner was the Liaison Committee for
Graduate Medical Education, established in 1972. The mission of the
ACGME is to improve health care by assessing and advancing the quality
of resident physicians’ education through exemplary accreditation. In
recent years, the ACGME has instituted an ambitious Outcomes Project
that emphasizes a program’s “actual accomplishments” through a series of
multidimensional, comprehensive assessments of several competency-
based outcomes (see section on evaluations).
4.1.2. Residency Review Committee for Psychiatry

Each residency specialty (psychiatry, medicine, surgery, etc.) has a
Residency Review Committee (RRC) that decides the minimum require-
ments a program must fulfil in order to be accredited. These requirements
involve not just the didactic and practical curriculum but also the process
and criteria by which residents are evaluated, as well as work hours and
other structural elements.
4.2. Oversight of residents

4.2.1. American Board of Psychiatry and Neurology
The key certifying body for individual psychiatrists and neurologists, the
American Board of Psychiatry and Neurology (ABPN), is the organiza-
tion responsible for board certification of psychiatry residency graduates.1
Board certification requires residents to demonstrate both their knowledge
base and their clinical skills. Knowledge base is tested by the ABPN cre-
dentialing examination, which residents are eligible to take late in the fall
after residency. As of the graduating class of 2011, the training program
itself is responsible for verifying clinical skills by administering Clinical
Skills Verification (CSV), given by ABPN-certified psychiatrists, through-
out resident training. In this exam, residents perform an observed patient
interview followed by a presentation of the history and mental status
B1405_Ch-25.indd 651 1/31/2013 2:41:53 PM

exam. Residents are required to successfully pass three of these examina-

tions to be eligible for the post-residency credentialing exam.
4.2.2. Local Graduate Medical Education Committee

Each medical school (of which residency programs are a part) also
typically has a local Graduate Medical Education Committee (GMEC),
which assists residency programs in meeting all RRC and ACGME
guidelines.
4.2.3. Residency Training Committee

Each residency program typically has a Residency Training Committee,
which is responsible for guiding program development, program evalua-
tion, and resident and faculty evaluation and monitoring. The committee
usually consists of the Program Director, one or more Associate Program
Directors, key faculty members, and one or more residents.
4.2.4. Program director and associate program directors

The Program Director is the faculty member responsible for the overall
operation of the residency training program. The Program Director’s
duties include (but are not limited to) overseeing didactic and clinical
education, overseeing and evaluating program faculty, monitoring resident
performance and providing regular feedback, and ensuring that the pro-
gram is in compliance with all departmental and ACGME requirements.
Many programs also have at least one Associate Program Director, who
assists the Program Director in the oversight of the residency program.
The ACGME has guidelines on the minimum amount of time that should
be allocated to Program Director and Associate Program Director, on the
basis of the size of the residency program. In addition, each clinical train-
ing site is required to have a “Site Director,” who is responsible for the
day-to-day activity, teaching, and well-being of the residents working at
that site. In some programs, the Site Directors will also serve as Associate
Training Directors.
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5. RESIDENCY TRAINING
Different residency programs have wide variability in curriculum and
organization. However, they also share many common elements. In this
section, we will describe ACGME requirements for residency training and
describe how a typical program may meet the requirements for clinical
rotations, didactic curriculum, and supervision.
5.1. Clinical rotations

The ACGME and the Psychiatry RRC mandate at least four months of
primary care (internal medicine, pediatrics, or family practice) and
two months of neurology, ideally completed in postgraduate year one
(PGY-1), 6–16 months of inpatient psychiatry, 12 months of continuous
and supervised outpatient psychiatry, two months of child and adolescent
psychiatry, two months of consultation-liaison psychiatry, one month of
geriatric psychiatry, one month of addiction psychiatry, and experiences
in forensic, emergency, and community psychiatry.
There is wide variation in the way clinical rotations are managed across
different residency programs. However, most programs share some ele-
ments in common (summarized in Table 3), beginning with a combination
of primary care, neurology, and psychiatry in the first year, a large bolus
of inpatient psychiatry in the second year, mostly outpatient psychiatry in
the third year, and great variability in leadership positions and elective
opportunities in the fourth year. In addition, most programs set up their
rotations so that the requirements can be completed by the end of the third
year, allowing residents who wish to “fast track” into child and adolescent
specialty training in postgraduate year four to do so. The best source of
information about a program’s curriculum is usually the program
website.
5.2. Postgraduate year one

The typical curriculum in PGY-1 consists of a combination of psychiatry,
neurology, and primary care. Most programs will split the year evenly
between psychiatry and non-psychiatry months, although not necessarily
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Table 3. Typical clinical rotations.

PGY-1 Four months primary Two months neurology Six months inpatient
care (internal medicine, psychiatry
family medicine and/or
pediatrics
PGY-2* 4–6 months Two Two months 1–2 months One One
inpatient months consultation- alcohol month month
psychiatry child and liaison and drug geriatric emergency
adolescent treatment psychiatry psychiatry
PGY-3** Outpatient psychiatry
PGY-4*** Chief and senior resident positions
Long-term outpatients and/or psychotherapy patients
Specialty electives research
*Some programs include about half-day per week for a specialty and/or continuity clinic, and many
provide time for a few on-going psychotherapy outpatients.
**Some programs provide opportunities for specialty outpatient clinics (geriatrics, anxiety, student
health, women’s health), and or research electives.
***Some programs feature extensive elective opportunities, while others have more structures leader-
ship positions; in most programs, residents interested in child and adolescent psychiatry are able to
begin their child fellowship as PGY-4s.
in six-month blocks. The Psychiatry RRC requires at least two months of

neurology and four months of primary care, typically a mix of inpatient
and outpatient internal medicine. Many programs allow residents to elect
pediatrics or family practice months as part of their primary care require-
ment. If a program has multiple training sites, residents will often split
their time between these sites.
5.3. Postgraduate year two

Usually, the second postgraduate year (PGY-2) is focused on inpatient and
acute care psychiatry, although most programs will also incorporate out-
patient and psychotherapy experiences. Table 4 shows a sample break-
down of these experiences.
In addition, many programs will have an outpatient continuity clinic
that runs for the entire year. Many programs have similar experiences and
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Table 4. Sample didactic curriculum.

PGY-1 1. Crash course
2. Introduction to psychiatry
3. Psychiatric interviewing and inpatient supportive psychotherapy
PGY-2 1. Psychopathology/therapeutics
2. Introduction to psychotherapy
a. Foundations of dynamic psychotherapy
b. Cognitive-behavioral psychotherapy
3. Neurology
PGY-3 1. Advanced dynamic psychotherapy
2. Other evidence-based psychotherapies
3. Advanced pharmacotherapy
4. Ethics
5. Forensics
6. Teaching skills
7. Marital and family therapy
8. Cross-cultural and diversity psychiatry
9. Human sexuality
PGY-4 1. Certification examination preparation
2. Transition to practice
3. Neurology review
4. Intensive short-term dynamic psychotherapy
5. History of psychiatry
6. History of psychoanalytic thought
7. Foundations of neuroscience
All 1. Grand rounds
2. Case conferences
3. Journal clubs
4. Many programs provide unique curricular activities, such as process
groups, movie nights, psychiatry in literature, and/or no-cost
psychotherapy electives
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will often offer residents a choice of clinics through which they can rotate.
For example, residents may be able to choose clinics focusing on mood
disorders, anxiety disorders, or psychotic disorders. Some programs have
a combination psychiatric and primary care clinic, in which residents treat
both psychiatric and medical issues and receive supervision from both a
psychiatry attending and a medicine attending.
PGY-2 is also often the year in which residents begin their psycho-
therapy experience. Many programs will require residents to carry a mini-
mum number of psychotherapy patients, with appropriate supervision.
5.4. Postgraduate year three

At most programs, the third postgraduate year (PGY-3) is an immersive
outpatient experience. Typically, residents serve as the primary psychia-
trist for their own caseload of patients, with extensive supervision from
on-site faculty, and also provide backup medication coverage for patients
treated by other mental health staff or trainees. In some programs, they
also have the opportunity to rotate through various specialty clinics, such
as those focused on anxiety, obsessive-compulsive disorder, bipolar disor-
der, schizophrenia, substance dependence, and forensics. PGY-3 residents
may also have some elective time, during which they can pursue inde-
pendent academic and research interests.
PGY-3 is also often the time in which residents learn about and practice
various forms of psychotherapy. The Psychiatry RRC requires that resi-
dents develop competence in “applying supportive, psychodynamic, and
cognitive-behavioral psychotherapies to both brief and long-term indi-
vidual practice, as well as to assuring exposure to family, couples, group,
and other individual evidence-based psychotherapies.” Residents will
typically study multiple modalities of individual psychotherapy (e.g. CBT,
dynamic, interpersonal), as well as group and family therapy. They are
typically expected to carry multiple psychotherapy patients in different
modalities and to receive supervision from individual psychotherapy
supervisors who specialize in those modalities. Many programs encourage
residents to keep one or more of their individual psychotherapy patients
from PGY-2 and extend at least a few into PGY-4 to enhance the continu-
ity experience. Some programs will also offer residents the opportunity to
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co-lead an on-going psychotherapy group with an experienced facilitator.

Family and couples therapy experiences may also be available.
5.5. Postgraduate year four

Some of the greatest variation between training programs is often seen
during the fourth postgraduate year (PGY-4). Some residents will use this
year to begin fellowships in Child and Adolescent Psychiatry. Residents in
a “research track” may spend most of their time on their research interests,
and many programs also provide teaching, community, or other academic
tracks to enrich training for residents with special interests and skills.
At some programs, PGY-4 is an almost entirely elective year, in which
residents may rotate through multiple clinics or subspecialty experiences
or conduct research. At other programs, PGY-4 is geared toward placing
residents in leadership and teaching positions, in part to mentor them
toward faculty positions. Most programs will select at least one “Chief
Resident,” whose job description varies but typically involves teaching
and administrative responsibilities. Some programs have multiple Chief
Residents, each responsible for a particular class (PGY-1, -2, or -3) or
training site. In many programs, the Chief Residents are viewed as junior
faculty members and are invested with large amounts of responsibility for
clinical supervision, teaching, scheduling, problem solving, and conflict
resolution.
Many programs also require a scholarly project, to be completed by the
end of residency. This project may involve basic research, clinical
research, a literature review, an educational innovation, or other appropri-
ate scholarly pursuit. Although residents are free to work on this project
during any part of their residency, the more flexible nature of the fourth
year means that most of the work usually takes place then. At some pro-
grams, residents are also given the opportunity to present their work to the
faculty and other residents during a departmental Grand Rounds.
5.6. Didactic Curriculum

Psychiatry residency programs in the United States are required to have
an integrated curriculum of didactics that provides formal instruction on
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the major types of psychopathology and biological, psychological, and

psychosocial treatment modalities. The didactic sessions must be sched-
uled to ensure a minimum of 70% of resident attendance while adhering
to program duty-hour policy. Specifically, the ACGME requires that
didactics cover the following areas:2 listed below are major theoretical
approaches to understanding the patient–doctor relationship:
(1) Biological, genetic, psychological, sociocultural, economic, ethnic,

gender, religious/spiritual, sexual orientation, and family factors that
significantly influence physical and psychological development
throughout the life cycle;
(2) Fundamental principles of the epidemiology, etiologies, diagnosis,
treatment, and prevention of all major psychiatric disorders in the
current standard diagnostic statistical manual, including the biologi-
cal, psychological, sociocultural, and iatrogenic factors that affect
the prevention, incidence, prevalence, and long-term course and
treatment of psychiatric disorders and conditions;
(3) Comprehensive discussions of the diagnosis and treatment of neuro-
logic disorders commonly encountered in psychiatric practice, such
as neoplasm, dementia, headaches, traumatic brain injury, infectious
diseases, movement disorders, multiple sclerosis, seizure disorders,
stroke, intractable pain, and other related disorders;
(4) Use, reliability, and validity of the generally accepted diagnostic
techniques, including physical examination of the patient, labora-
tory testing, imaging, neurophysiologic and neuropsychological
testing, and psychological testing;
(5) Use and interpretation of psychological testing (under the supervi-
sion and guidance of a qualified clinical psychologist, residents
should have experience with the interpretation of the psychological
tests most commonly used, some experience of which should be
with their own patients);
(6) History of psychiatry and its relationship to the evolution of
medicine;
(7) Legal aspects of psychiatric practice, and when and how to refer;
(8) Understanding US culture and subcultures, particularly those found
in the patient community associated with the educational program,
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with specific focus for residents with cultural backgrounds that are
different from those of their patients;
(9) Case formulation that includes neurobiological, phenomenological,
psychological, and sociocultural issues involved in the diagnosis and
management of cases;
(10) Instruction in research methods in the clinical, biological, and
behavioral sciences related to psychiatry, including techniques to
appraise the professional and scientific literature and to apply evi-
dence-based findings to patient care. Each program must provide the
following:
(a) All residents must be educated in research literacy. Research
literacy is the ability to critically appraise and understand the
relevant research literature and to apply research findings appro-
priately to clinical practice. The concepts and process of
Evidence Based Clinical Practice include skill development in
question formulation, information searching, critical appraisal,
and medical decision-making, thus providing the structure for
teaching research literacy to psychiatry residents. The program
must promote an atmosphere of scholarly inquiry, including the
access to on-going research activity in psychiatry. Residents
must be taught the design and interpretation of data.
(b) The program must provide residents with research opportunities
and the opportunity for development of research skills for resi-
dents interested in conducting research in psychiatry or related
fields. The program must provide interested residents access to
and the opportunity to participate actively in on-going research
under a mentor. If unavailable in the local program, efforts to
establish such mentoring programs are encouraged.
(c) The program must ensure the participation of residents and fac-
ulty in journal clubs, research conferences, didactics, and/or
other activities that address critical appraisal of the literature
and understanding of the research process.
Ideally, programs will meet these requirements using a didactic curricu-

lum that spans all four years, in which each year builds on what is learned
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the previous year. For example, one US program uses the following
framework:
5.6.1. PGY-1
First-year residents receive a “Crash Course” in psychiatry that covers
essential information they will need to know in order to capably treat
patients in the emergency department and wards. Following the Crash
Course, the core curriculum occurs during a half-day period of “protected
time,” when the PGY-1 residents are kept free of all routine clinical
responsibilities and expected to attend seminars. This half-day period
includes two weekly seminars and departmental Grand Rounds. The first
seminar focuses on Adult Psychopathology and the second on Inter-
viewing, Communication Skills, and Supportive Psychotherapy.
5.6.2. PGY-2
Second-year residents also have a half-day of protected time, during
which they continue to attend the seminar series and departmental Ground
Rounds. The PGY-2 seminar series expands on topics that were first
presented in PGY-1. Additional topics include therapeutic interventions,
geriatric psychiatry, consultation-liaison, child development and psycho-
pathology, behavioral neurology, cross-cultural psychiatry, marital and
family therapy, and reading the literature. In addition, there are two
weekly seminars on psychotherapy: one on CBT and another on the
“Foundation of Dynamic Psychotherapy.”
5.6.3. PGY-3
Third-year residents attend seminars, conferences, or rounds five mornings
a week. This comprehensive and sophisticated series includes in-depth
exposure to all contemporary forms of psychotherapy (supportive, group
milieu, hypnotherapy, insight-oriented, marital and family, short-term
dynamic, cognitive and integrative psychotherapy), outpatient psychophar-
macology, Axis II disorders, ethics, forensic psychiatry, board preparation,
teaching skills, cross-cultural/diversity issues, and human sexuality.
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5.6.4. PGY-4
Fourth-year residents attend advanced-level seminars in transition to pri-
vate practice, history of psychiatry, neurology review, and an advanced
workshop on short-term dynamic psychotherapy. In recent years, an
extensive Part 1 Board Review Course has overshadowed all others in
terms of time, focus, and energy, because residents face the prospects of
passing their examinations in May of their senior year. Senior residents
are also invited to participate with departmental fellows in the advanced
psychopharmacology seminar. Each year, senior residents help develop
their own modification and additions to their senior seminars on the basis
of the recognized needs and unique interests of each class.
5.7. Other common seminars

In addition to didactics, psychiatry training departments also commonly
hold the following:
(1) Grand rounds: A department-wide educational activity featuring pres-

entations by residents, as well as local and visiting faculty.
(2) Specialty rounds/case conferences: A forum for residents to present
interesting or complicated cases to faculty and resident colleagues.
(3) Journal clubs: A discussion of current and classic psychiatric and
medical literature.
5.8. Supervision
Psychiatry residents are typically supervised by many different attendings
during their training. In general, the level of supervision is greatest at the
beginning of the residency and gradually decreases as the resident gains
more knowledge and experience. In many programs, PGY-4 residents will
often supervise their junior colleagues, while still receiving supervision
themselves. Residents at all training levels are required to have at least
2 hrs per week of faculty-level supervision.
On most rotations, clinical supervision is provided by the attending
physicians who work at that clinical site. Usually, those attendings are
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ultimately responsible for the care of the patients at that site (medically
and legally). Therefore, they will often work side by side with the resi-
dents at the site and should provide frequent, timely feedback. However,
residents will also typically have “continuity” supervisors, who meet with
them on a weekly basis for several months in a row or even the entire year.
These are often psychiatrists in the community with voluntary faculty
appointments. Most programs will strive to provide residents with well-
balanced outside supervision, such that each resident’s supervisors have
complementary areas of expertise. For example, as resources allow, each
resident may have outside supervisors who are skilled in medication man-
agement and different psychotherapy modalities.
In addition to formal supervision, residents at many programs will be
exposed to psychotherapy in a more experiential manner. For example,
many programs have a resident “process group,” facilitated by a faculty
member, in which residents learn about group process by participating in
a group themselves. Some programs also give residents the opportunity to
receive individual psychotherapy, either at no cost or at significantly
reduced rates.
5.9. Evaluation
Throughout their training, residents undergo frequent, comprehensive
evaluation of their clinical ability and knowledge base. The Psychiatry
RRC guidelines specify that residents must receive formative evaluation
on a regular basis, after each rotation or educational experience. Upon
completion of the program, they must also receive a summative evalua-
tion, summarizing their performance and verifying their competency. The
summative evaluation is maintained in the resident’s permanent file. In
addition, residents themselves are regularly asked to evaluate the program
and individual faculty.
5.10. Core competencies

All programs are required to evaluate their residents on a set of core com-
petencies. Typically, the supervising faculty at each clinical site will be
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responsible for completing these evaluations after each rotation. Although

the exact evaluation criteria vary somewhat between programs, the fol-
lowing elements are required by the RRC.2
(1) Patient care: “Residents must be able to provide patient care that is
compassionate, appropriate, and effective for the treatment of health
problems and the promotion of health.”
(2) Medical knowledge: “Residents must demonstrate knowledge of
established and evolving biomedical, clinical, epidemiological, and
social-behavioral sciences, as well as the application of this knowl-
edge to patient care.”
(3) Practice based learning and improvement: “Residents must demon-
strate the ability to investigate and evaluate their care of patients, to
appraise and assimilate scientific evidence, and to continuously
improve patient care based on constant self-evaluation and life-long
learning.”
(4) Interpersonal and communication skills: “Residents must demonstrate
interpersonal and communication skills that result in the effective
exchange of information and collaboration with patients, their fami-
lies, and health professionals.”
(5) Professionalism: “Residents must demonstrate a commitment to car-
rying out professional responsibilities and an adherence to ethical
principles.”
(6) System’s based practice: “Residents must demonstrate an awareness
of and responsiveness to the larger context and system of health care,
as well as the ability to call effectively on other resources in the sys-
tem to provide optimal health care.”
5.11. Psychotherapy
Among the clinical skills psychiatry residents must be competent to pro-
vide are supportive, psychodynamic, and cognitive-behavioral psycho-
therapies to both brief and long-term individual patients. In addition, they
must have exposure to family, couples, group, and other individual evi-
dence-based psychotherapies.
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5.12. Resident evaluations

Most training programs must give residents the opportunity to confiden-
tially and anonymously evaluate various aspects of the program, such as
their rotations, didactics, faculty, and resident colleagues. In addition, the
ACGME conducts an annual, independent survey of residents across pro-
grams, addressing many of the same elements.
5.13. Standardized exams

One of the key methods by which training programs assess clinical skills
is the Clinical Skills Examinations (CSE) given throughout resident train-
ing. In this exam, residents perform an observed patient interview fol-
lowed by a presentation of the history and mental status exam. The
Clinical Skills Verification (CSV) process requires residents to pass three
CSEs conducted by board-certified examiners in order to be eligible for
board certification. In addition, although not required for ABPN certifica-
tion, many programs supplement these evaluation instruments by also
asking for case formulations, differential diagnoses, and treatment plans.
In most programs, residents prepare for the Part 1 ABPN examinations
in board review courses and by taking the annual National Psychiatry
Resident-In-Training Examinations (PRITE), a standardized self-assess-
ment test. This examination is modeled after the ABPN exam and is
designed as a self-assessment and to prepare residents for the written por-
tion of the psychiatry and neurology boards. Some programs use these
examinations as one of the measures of trainees’ knowledge and may plan
remedial courses or supervision for residents falling below a certain
threshold.
6. AFTER RESIDENCY
Graduating psychiatry residents have a number of options as they begin
their career. Some will opt for further training in a subspecialty field.
Others may choose to remain in an academic setting, either teaching
or conducting research. Most, however, will go into practice in the com-
munity. Here, we present a brief (and by no means comprehensive) look
at several of the options.
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6.1. Specialty training/fellowships

Some residents will opt for further training in a subspecialty field of psy-
chiatry. This typically involves a “fellowship,” a postgraduate training
program in which residents spend one or more additional years. The
ABPN recognizes and provides board certification for several such areas,
including the following.1
• Addiction psychiatry: Psychiatry that focuses on evaluation and treat-

ment of individuals with alcohol, drug, or other substance-related
disorders and of individuals with dual diagnosis of substance-related
and other psychiatric disorders.
• Child and adolescent psychiatry: Psychiatry with additional skills and
training in the diagnosis and treatment of developmental, behavioral,
emotional, and mental disorders of childhood and adolescence.
• Forensic psychiatry: Psychiatric focus on interrelationships with civil,
criminal, and administrative law; evaluation and specialized treatment
of individuals involved with the legal system, incarcerated in jails,
prisons, and forensic psychiatry hospitals.
• Geriatric psychiatry: Psychiatric expertise in prevention, evaluation,
diagnosis, and treatment of mental and emotional disorders in the
elderly, and improvement of psychiatric care for healthy and ill
elderly patients.
• Hospice and palliative medicine: Psychiatry, neurology, or child neu-
rology specialists with special knowledge and skills to prevent
and relieve the suffering experienced by patients with life-limiting
illnesses. This specialist works with an interdisciplinary hospice or
palliative care team to maximize quality of life while addressing
physical, psychological, social, and spiritual needs of both patient and
family throughout the course of the disease, through the dying
process, and beyond for the family. This specialist has expertise in
the assessment of patients with advanced disease; the relief of dis-
tressing symptoms; the coordination of interdisciplinary patient and
family-centered care in diverse venues; the use of specialized care
systems including hospice; the management of the imminently dying
patient; and legal and ethical decision-making in end-of-life care.
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• Psychosomatic medicine: Subspecialization in the diagnosis and treat-

ment of psychiatric disorders and symptoms in complex medically ill
patients. This subspecialty includes treatment of patients with acute or
chronic medical, neurological, obstetrical, or surgical illness in which
psychiatric illness is affecting their medical care and/or quality of life,
such as HIV infection, organ transplantation, heart disease, renal fail-
ure, cancer, stroke, traumatic brain injury, high-risk pregnancy, and
COPD, among others. Patients also may be those who have a psychiat-
ric disorder that is the direct consequence of a primary medical condi-
tion or a somatoform disorder or psychological factors affecting a
general medical condition. Psychiatrists specializing in psychosomatic
medicine provide consultation-liaison services in general medical hos-
pitals, attend on medical psychiatry inpatient units, and provide col-
laborative care in primary care and other outpatient settings.
Many programs offer their own, non-certified “fellowships,” such as

special training in academic psychiatry or teaching excellence, public or
community psychiatry, or clinical trials.
6.2. Academic psychiatry

Some residents will choose to stay in academics and accept teaching or
research positions with a university. Usually, this involves a career in basic
science research, clinical research, clinical education, or some combina-
tion of the three.
6.3. Community and/or private practice psychiatry

Most graduating residents will go into practice in the community, in a
wide variety of settings. Some of these may include the following:
• Solo practice: Work alone and handle all needs of their patients.
• Small group practice: Similar to solo practice but with colleagues who
will typically share on-call duties.
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• Large group practice: A larger group of colleagues, which typically

has an administrative structure that handles scheduling, billing, etc. in
exchange for a percentage of revenue.
• Inpatient: Focusing on patients who have been admitted to an inpa-
tient facility.
Many psychiatrists will practice in more than one of these settings (for
example, splitting time between inpatient and solo practice).
7. CONCLUSIONS
The direction that psychiatry residency training will take in the next dec-
ade and beyond is something of an open question. Psychoanalytic and
psychodynamic thinking dominated the field until the 1980s, and although
these disciplines are still important, the amount of time most training
programs devote to them has decreased dramatically over the last
20 years. In the 1990s, the “Decade of the Brain” gave rise to major
advances in psychopharmacology, genomics, neuroscience, and func-
tional neuro-imaging, all of which continue today and have helped rede-
fine mental illnesses as brain disorders. In line with this explosion of new
understanding, there has been a shift from expert-based psychiatry to
evidence-based psychiatry. Some argue that future psychiatrists will need
a much stronger background in neuroscience and genomics. Yet, even in
an era of technologically driven care (or perhaps because of it), it will be
essential for future psychiatrists to continue to acquire a deep understand-
ing of human behavior and emotion and the interpersonal skills to apply
this knowledge.
REFERENCES
1. ABPN. (2010) American Board of Psychiatry and Neurology, Available at:
http://www.abpn.com/. Accessed on June 6, 2010.
2. ACGME. (2010) Accredication Council for Graduate Medical Education,
Available at: http://www.acgme.org. Accessed on June 6, 2010.
B1405_Ch-25.indd 667 1/31/2013 2:41:54 PM

3. ECFMG. (2010) Educational Commission for Foreign Medical Graduates,

Available at: http://www.ecfmg.org/. Accessed on June 6, 2010.
4. ERAS. (2010) Electronic Residency Application Service. Available at: http://
www.aamc.org/students/eras/. Accessed on June 6, 2010.
5. NRMP. (2010) National Residency Match Program. Available at: http://
www.nrmp.org/. Accessed on June 6, 2010.
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Chapter 26
Methods of Psychiatric Research
Elizabeth Burgess, Nicolas Ramoz and Philip Gorwood
1. INTRODUCTION
Neurosciences and psychiatric researches are progressing quickly. On one
hand, this sentence was written so frequently before, raising new hopes
each time a technique was invented providing new possibilities on under-
standing how the brain functions, that scepticism is understandable. On
the other hand, the interest of major neuroscientists around the world, the
increase of funds devoted to this specific topic (although largely below
what is spent in less damaging disorders such as cardiovascular disease
or cancer) and new studies dedicated to psychiatric researches published
in major journals are positive signs. Some of the main lines of progress in
recent years are:
(1) Creation of consensual cognitive tasks that are assessed on the com-
puter (such as with MATRICS).
(2) GWAS technique (genetic studies testing the whole genome in a
single procedure).
(3) Diffusion tensor imaging (imagery devoted to white fibres therefore
tracking the connection between different brain areas).
(4) Nearly lifetime cohorts (such as the Dunedin cohort).
(5) Development of new pharmacological approaches closer to treatment
settings (‘mega trials’) or treatments aiming at specific symptoms and
669
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670 E. Burgess, N. Ramoz and P. Gorwood
not only at global syndromes (such as negative symptoms in

schizophrenia).
Although all these techniques are paving the way toward progress, the
main advance might be none of these. It might, rather, be using at least
two of these techniques together in the same research and shifting from
translational to integrative biological systems in medicine and research for
psychiatry. Looking with one versus two eyes means a lot, especially
when we still have no biological marker that is clearly differentiating
patients with versus without a psychiatric disorder. This chapter will
present many types of experiences where the use of two techniques clearly
helped to further understand, even a little, the complex functions of the
brain.
2. IMAGERY
Neuro-imaging has helped better understand psychiatric disorders,
especially during development, and better assess drug treatment response.
Brain structures, including volume and organization of grey and white
matters, can be deciphered in a more detailed and precise fashion thanks
to anatomic magnetic resonance imaging (MRI) using a high field of 3
Teslas. Furthermore, direction changes of white fibres can now be
detected with diffusion tensor imaging (DTI). Functional brain imaging
studies have also revolutionized the way of exploring neural response in
cognitive tasks or in experimental symptom induced situations.
Positron emission tomography (PET) which uses tracers that label
specific molecules, and functional MRI which analyses blood oxygenation
level-dependent (BOLD) signals, have helped to further understand some
of the biological rules of psychiatric disorders, including metabolism and
pharmacological proprieties. A nice example of the importance of this
approach was a research devoted to the complex phenomenon of ‘craving.’
Patients with alcohol dependence who have been through rehabilitation
have indeed acute and dramatic urges to drink alcohol at specific moments.
The exact mechanism of such a relapse risk factor is not well understood,
although craving is usually triggered by moments, situations, or stimuli
previously associated with past drinking habits. One of the treatments that
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Methods of Psychiatric Research 671
has helped patients maintain abstinence is naltrexone, a mu-opioid

receptor blocker that is supposed to reduce the risk of craving. Heinz
et al.12 analyzed the availability of central mu-opiate receptors in vivo
with PET in the ventral striatum and compared it with the severity of
alcohol craving. The authors demonstrated that abstinent alcoholic
patients displayed an increase in mu-opiate receptors in the ventral stria-
tum (compared to healthy controls) which correlated with the severity of
alcohol craving. Hence, this PET study helped to link the complex clinical
feature of “craving” to the density of a specific receptor (OPMR1) in a
brain region that is known to play a major role in the reward system (the
nucleus accumbens), and gave further explanation of the mechanisms
involved in one of the treatments that helps patients with alcohol
dependence.
Functional MRI (fMRI) increased the understanding, for example, of
how executive cognitive functions are nearly systematically impaired in
patients with schizophrenia. While trying to respond to a cognitive task
that solicited executive functions, healthy controls and patients activated
a similarly distributed cortical–subcortical network (including the dorso-
lateral and ventrolateral prefrontal cortex, the anterior cingulate cortex,
and the thalamus), but the patients showed, on the one hand, a reduced
activation of some structures (the left dorsolateral rostral/dorsal anterior
cingulate cortex, left thalamus, and inferior/posterior cortical areas) and,
on the other hand, an increased activation of several midline cortical areas.
The conclusions of the author was that patients with schizophrenia show
altered cognitive activities, with some deficits in core regions dealing with
executive functions, but also with increases in other areas, which could be
compensatory in nature, explaining delayed and poorer performances.19
2.1. Mixing fMRI and PET

A recent and exciting development is the use of both instruments in the
same procedure. It is now possible to use PET imaging (for example
analyzing psychostimulant-induced DA release), in concert with a fMRI
probe (implicated in the reward system for example). Using these
techniques together, Buckholtz et al.3 could demonstrate that impul-
sive antisocial psychopathic traits selectively predicted nucleus accumbens
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dopamine release and reward anticipation-related neural activity in

response to both pharmacological and monetary reinforcers.3 The fact that
the reward system (both dopamine and ventral striatum are involved in this
study) is a core mechanism not only in addictive disorders but also in anti-
social personality disorder has not been demonstrated as clearly before
with just a single approach.
2.2. Mixing fMRI and genetics

If a genetic polymorphism constitutes a risk factor for a specific disorder,
then the involved allele should give sense to some of the findings related
to imagery studies. Hariri et al.11 analyzed the impact of carrying the short
allele (“s” allele) of the serotonin transporter (5-HTT) promoter polymor-
phism, which has been associated with reduced 5-HTT expression and
function, and increased fear and anxiety-related temperament and behav-
iors. They demonstrated that subjects with this vulnerability allele exhibit
greater amygdala neuronal activity, as assessed by fMRI, in response to
fearful stimuli compared with individuals homozygous for the long allele.
Using genetics and fMRI is very rich as it helps to add a missing link
between an unspecific risk factor (the short allele of the 5-HTT gene) and
a complex disorder (anxiety). Analyzing how the brain is functioning in
controls while dealing with some potentially anxious probes, and accord-
ing to the presence or not of some risk factors, might increase insights on
the involved mechanisms.
Another example of coupling fMRI and genetics was the study from
Esslinger et al.8 A genome-wide association study (GWAS, see the
definition later in this chapter) detected a significant role of one gene
(ZNF804A) in a very large sample of patients with schizophrenia, but the
role of this gene was not really known, neither its potential impact in
schizophrenia. The authors showed that healthy carriers of the risk geno-
types, while having to perform a task requiring attention and memory,
exhibit pronounced alterations in functional coupling (correlated activity)
of dorsolateral prefrontal cortex (DLPFC) across hemispheres and with
hippocampus, mirroring findings in patients, and abnormal coupling of
amygdala.
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3. GENETICS
Psychiatric disorders are known to be genetically influenced. This obser-
vation is provided from epidemiological works on monozygotic and dizy-
gotic twins but also adoption and family studies. However, the assumption
that there might be a direct path between genes and complex psychiatric
disorders has not been successful. Genes are shown to have an impact on
most aspects of psychiatric disorders as the effects of heredity are substan-
tial and are estimated to represent 30%–70% of total variation. Nevertheless,
reality in psycho-pathogenesis is probably much more complex involving
the combined action of many environmental factors and gene networks
impacting on brain development and function.10
Association studies test in two populations (the cases, i.e. subjects with
the disease or trait, and the controls, i.e. subjects without the disease or
trait) whether a genetic variant is associated with a disease or trait. An
association is present if a particular allele or genotype is of a frequency
greater than expected on the basis of chance alone in an individual carry-
ing the disease or trait. When a combination of alleles or genetic markers
occurs more or less frequently in a population than expected, this is
known as linkage disequilibrium.24 Association studies may be case-
control based (unrelated subjects) or family-based association designs and
are used in genetics in order to search either the involvement or the locali-
zation of a gene in the risk of certain disorders.
The GWAS use highly efficient genotyping technologies in order to
assay hundreds of thousands single-nucleotide polymorphisms (SNPs)
spread across the whole genome in a large set of individuals and relate
them to observable traits. Results in GWAS depend on the ability to detect
an association of a SNP that is in linkage disequilibrium with a predispos-
ing gene variant. This implies that variants need to be in great enough
frequency for detection.4 GWAS have rapidly become a “disease gene
discovery method,” provide precious preliminary genetic information, and
they increase the chances of identifying genes, alleles (and therefore
pathophysiologic mechanisms) for deeper investigations.4,22,23
GWAS require sufficiently large samples from populations in order to
provide sufficient statistical power to identify associations in common
variants. Large study samples have been made possible thanks to productive
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international collaborations and data sharing, thus increasing the power to

detect positive effects.6,29 The rate of false positives is, nevertheless, an
issue and varies little relatively to sample size, as it is largely depending
on the significance level that is used. GWAS analyses are complex due in
part to multiple testing. A conventional p-value below 0.05 level of
significance would statistically, and mostly out of chance, associate
50,000 if one million of SNPs are studied in a disease. This issue has been
addressed by carrying out the Bonferroni correction in which the conven-
tional p-value is divided by the number of tests performed, thus reducing
the false positive rate. Studying a million SNPs necessitates a p-value
lower than 5 × 10−8 in order to identify non-random associations. However,
this correction has been described as overly cautious as it considers each
SNP as independent, thus not taking under account the fact that the
informativity of neighboring SNPs is partially redundant (i.e. they are in
linkage disequilibrium).
There are two genetic models that explain how each locus in our
genetic architecture can impact on phenotypic risk of complex diseases
including psychiatric disorders. These models are called common disease/
common variant (CDCV) and multiple rare variant (MRV). Together they
form the allelic spectrum. The CDCV model puts forward common (≥5%)
genetic variants that confer modest (≤1.5) genetic relative risk toward
developing a complex trait. The MRV model proposes that many different
rare (≤1%) genetic variants confer a very strong genetic relative risk (≥10)
toward developing a complex trait.
The GWAS have shown great potential in many diseases including
asthma, rheumatoid arthritis, and breast cancer. Whether or not psychiat-
ric disorders may also benefit from this new research method is still a
matter of debate. Many major psychiatric diseases are amongst the most
genetically influenced. There is no evidence that the genetic mechanisms
in cause for developing psychiatric illnesses should be any different from
those in cause for non-psychiatric diseases. However, severe social
impairment due to psychiatric disorders may strongly limit gene transmis-
sion to future generations, thus losing high risk variants. The genetic
epidemiological consideration would favor the CDCV hypothesis, which
implies higher difficulty to find the genes (as many would be involved,
with little frequency differences between patients and controls).
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Phenotype in psychiatry is another issue as it is not relying on

unambiguous biological markers. Descriptive systems have designed diag-
nostic categories between which overlaps are very likely, and for which
genetic validity has yet to be confirmed. Although such descriptive systems
are necessary to guide research, they have limitations such as being discon-
nected from specific biological mechanisms and even epidemiological find-
ings, clinical common sense being the main factor driving these international
criteria. A good example is the strict difference between schizophrenia and
bipolar disorder in the international manuals (such as the ICD-10 and DSM-
IV-TR), which is in contradiction with the frequent difficulty clinicians have
to differentiate these two disorders, and with the large overlaps of research
findings (mainly in imagery and genetics). Moskvina et al.20 undertook the
analysis of two GWAS data sets: schizophrenia and bipolar disorder. The
authors found evidence for association across disorders, in favor of an
overlap between schizophrenia and bipolar disorder in genetic risk.
4. COGNITIVE FUNCTIONS
There are many standardized evaluation tools of cognitive impairment
in psychiatric disorders. Although there is no golden standard in neuro-
cognitive evaluation, constant scientific evaluations of measures try to deter-
mine which tests (among more than 90) are the most test–retest reliable,
valid when used as a repeated measure, practical and tolerable for patients.21
Tasks evaluate several cognitive domains such as speed of processing,
attention and vigilance, working memory, verbal learning and memory, vis-
ual learning and memory, motor response, inhibition, reasoning and problem
solving, and social cognition. Such tests are of particular interest in nearly all
psychiatric diseases, as constituting potential intermediate phenotypes
(sometimes entitled endophenotypes) between the initial biological defect
and the resulting complex phenotype known as a psychiatric disease).
Experts recommend the use in schizophrenia of a battery of tests
including the Trail Making Test, the Hopkins Verbal Learning Test, the
Wechsler Memory Scale, or the Brief Visuospatial Memory Test. The
MATRICS Consensus Cognitive Battery is the result of thorough exami-
nation, and is now considered as a standard, at least for schizophrenia,
helping studies to spread comparable results in the scientific community.
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4.1. Cognitive functions as endophenotypes

Cognitive tests are also of interest in order to identify potential candidate
disease endophenotypes for biological, imagery, and genetic investiga-
tions. Executive performance, working memory, and sustained attention
are thought to be central aspects of schizophrenia for example, and defi-
cits in these cognitive areas have a high heritability and a number of
potentially related candidate genes. For example, the Attention Network
Test (ANT) is a test in which participants must respond to a leftward or
rightward pointing central arrowhead visual stimulus. This central stimu-
lus is flanked by a neutral stimulus (blank lines) or lateral arrows that may
be congruent or incongruent to central arrow. Participants must respond
accordingly to direction of central arrow as fast and accurately as possible.
The ANT has been shown suitable to identify potential endophenotypes in
view of the fact that efficiency of the executive attention network shows
sufficient heritability. There is also evidence for genetic origin in many
psychiatric disorders involving attention deficit. Studies using discordant
twins affected with schizophrenia have shown that spatial working mem-
ory, choice reaction time, selective attention, attentional set-shifting, and
divided attention are also thought to be caused by inherited factors. Thus,
endophenotypes studies may help to link genetic variations with cognitive
performance involving anatomical attention networks.
5. EPIDEMIOLOGICAL COHORT STUDIES

A cohort is a designated group of subjects followed or traced over a period
of time. Cohort studies are epidemiological studies in which subsets of a
particular population can be defined who are, have been, or in the future
may be exposed, or not exposed, or exposed in different degrees, to a fac-
tor or factors hypothesized to influence the probability of occurrence of a
given disease, or a specific outcome. For example, a cohort study could
compare the occurrence of depression in the subjects exposed to child
abuse versus those who were not exposed. There are several types of
cohort studies.
Retrospective cohort studies or historic cohort studies are medical
researches in which the investigator collects data from the medical records
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of individuals who are alike in many ways but differ by a certain charac-
teristic. These medical records are compared for a particular outcome.
Two groups are established: exposed (1) versus non-exposed (2). Exposure,
latent period, and subsequent development of disease have already
occurred. These researches are greatly less time-consuming and less
costly, but are exposed to a large series of biases such as retrospective
assessments (less accurate), selection biases (patients are usually recruited
through care systems to which all patients do not have access), survival
rates of the disorder (surviving patients of a disorder with a high mortality
rate are not representative).
A prospective cohort study is a medical research in which the
investigator follows over time groups of individuals, assessing at baseline
the subjects with versus without the analyzed risk factor. Follow-up looks
for the occurrence of a disease in the different subgroups in relation to the
exposition to a particular risk. This kind of study is time-consuming and
costly, but it is more scientifically valued.
Many questions arise when considering recruitment of control, or unex-
posed, subjects. Should controls be chosen in a restricted fashion, thus
pushing away from real life conditions? In order to allow comparison, a
reference group must come from a source population from which cases
originate. This allows a possible representativity of the source population,
thus permitting analysis of data. Controls should share similar exclusion
and restriction criteria as cases do, be identified as non-cases and have
been susceptible to have been exposed or developed disease. At best, con-
trol patients should be a random sample of source population. However,
this is not always feasible and often controls are matched according to
several important criteria (such as age and sex), or originate from a spe-
cific subpopulation of the source population (such as friends or
neighborhoods).
5.1. Mixing cohort studies and genetics

Genes have different effects in different environmental backgrounds, and
conversely an environment exposure has different effects on people with
different genotypes. In the past, the goal of behavioral genetics has been to
explain individual differences, such as the way people behave, through
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variations of their genetic constitution. Indeed, the impact of genes on

personality, social behavior, cognitive function, and mental disease has
been largely shown.7 Heritability represents between 30% and 70% of the
inter-individual variations of the majority of psychiatric disorders. Animal
studies are also being used, for example analyzing mice lacking a specific
gene, known as “knock out” models, in order to determine the gene’s
impact on behavior can constitute grounds for further exploration or cor-
roborate findings in human studies. However, findings have been inconsist-
ent and results often disappointing. A potential explanation for these
inconclusive researches consists in their reducing to simple linear relation
individual genes to emotions and thoughts, far from the rich complexity of
the human mind. Behavioral genetics have also tried to separate all the
genetic from the environmental constituents in order to explain the variance
of a population for a particular disease or characteristic. Such
oversimplifications are often deceptive as they ignore the fact that having a
specific gene and being exposed to a specific environmental factor
might not always be independent. There are two main types of gene-
environment interplay. Gene–environment interaction (GxE) refers to
genetic differences in susceptibility to particular environmental factors
(partly explaining why all exposed subjects do not develop the disorder).
Gene–environment correlation (rGE) reflects the fact that genes can influ-
ence individual variations in exposure to risky or protective environments.
Twin studies are good models to determine the effects of the environ-
ment and have showed that for almost all traits environment is responsible
for a considerable proportion of the population variance. Nonetheless
there is a considerable heterogeneity in the response to negative life
events. Such heterogeneity may be at least partially the result of genetic
influence on environmental susceptibility.
In schizophrenia for example, similarly to Knudson’s two-hit model in
cancer genetics, the two-hit hypothesis advocates that first a genetic
mutation or variant involved in neurogenesis or neuroplasticity is trans-
mitted and then, secondarily, an environmental factor reveals this latent
abnormality, leading to a late development of the psychiatric disorder.16
A good example to illustrate this GxE method is the research on the
gene associated with major depressive disorder and antidepressant
response (the gene coding for the serotonin transporter, 5-HTT) and
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the exposure to stressful life events14 to explain the occurrence of new

depressive episodes in the ‘Dunedin’ cohort.
The Dunedin Multidisciplinary Health and Development Study
(DMHDS) members are the 1,037 babies born between 1 April 1972 and
31 March 1973 in Dunedin, New Zealand and followed up in a longitudi-
nal investigation of health, development and behavior. Children included
in the cohort were followed up at the age of 3, and then at 5, 7, 9, 11, 13,
15, 18, 21, 26, and 32. The sample is considered to be comparable to those
of New Zealand, although Maori and Pacific populations are under-
represented, and those from other English-speaking Western cultures. The
Dunedin cohort has generated more than 1,100 publications.
The serotonin system is the source of candidate genes, as it is a major
drug target for SSRI drugs. The short allele of the 5-HTT gene has been
shown to enhance the risk of suicidal behavior.1,18 The 5-HTTLPR locus
is located in the promoter region and modifies the expression of the
5-HTT gene. The s allele is associated with lower transcription efficiency
compared with the l allele.
In their research, Caspi et al.5 studied phenotype (depression) in relation
to genotype, environmental factors, and their interaction. Subjects were
divided into three groups according to their serotonin transporter gene-
linked polymorphic region (5-HTTLPR) genotype: 17% of homozygotes
for the short (s) allele (s/s), 31% of homozygotes for the long (l) allele (l/l)
and 51% of heterozygotes (s/l). This cohort was assessed for stressful life
events, as well as, for past-year depression. The authors found that stress-
ful life events in the immediate preceding five years predicted a diagnosis
of major depression in a cause-effect order among carriers of an s allele
but not among l/l homozygotes. The authors also found that history of
child maltreatment predicted adult depression only among individuals car-
rying an s allele but not among l/l homozygotes. This study pushes toward
a model where high prevalence genetic variants (i.e. l/l homozygotes) may
enable resistance against environmental pathogens and, to a larger extent,
life stressors. However, compelling results may seem much precaution
must be taken. What may seem as environmental factors may in fact be
linked to genetic factors, i.e. individuals may have a tendency to put them-
selves in situations where they are bound to encounter stressful life events.
Also, the onset of complex multifactorial psychiatric disorders cannot be
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reduced to genetic pathways only and is probably also explained by the

genetic influenced variability conditioned by environmental risk expo-
sure.27,28 Replication of these findings has been an issue. In a recent meta-
analysis, no evidence was found that the serotonin transporter genotype
alone or in interaction with stressful life events is associated with an ele-
vated risk of depression.25 On the other hand, in their review Uher et al.31
showed that all studies using objective measures or structured interviews
replicated gene-environment interaction wholly or partially whereas non-
replications were all based on self-report measures of environmental
adversity. They also suggested that gene–environment interplay may be
stronger in early life. This may be in favor of multiple life events only
being a risk marker for depression whereas child maltreatment could be
the true feature involved in the actual risk process leading to depression.
6. VIRUSES AND PARASITES AS ENVIRONMENTAL

FACTORS
The concept that microbial agents may cause mental illness such as
schizophrenia has been an attractive theory for etiopathogeny ever since
Kraeplin in the 1890s. Recent hypotheses analyzed microbial agents such
as Toxoplasma gondii (T. gondii), Haemophilus influenzae (HI), and the
cytomegalovirus (CMV).32 Rationale for this theory is based on mental
illness onset after having undergone microbial disease, modest seasonal birth
predominance in winter and spring months and probable increase in psy-
chotic disorder incidence in offspring after maternal infection. Further
grounds for the exploration of non-genetic factors that may provide
understanding in mental illness onset is the fact that these environmental fac-
tors may actually reveal underlying genetic factors and thus enabling the
diminution of population heterogeneity through proper factor identification.
T. gondii, a coccidian protozoan of the apicomplexa family, hosted by
felines, has a peak of seroconversion at ages between 15 and 35 in
humans, which is of interest in relationship to schizophrenia as is earlier
infection in adolescent males compared to females and suggestion of sea-
sonal occurrence. A recent meta-analysis published an odd ratio of 2.73
(95% confidence interval of 2.10–3.60) associating risk for schizophrenia
and T. gondii infection supporting evidence of etiopathogenesis.30 Although
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neurobiological mechanisms by which T. gondii may contribute in psy-

chosis onset is unknown, several hypotheses have been suggested such as
increased levels of antibodies in individuals who would later develop
schizophrenia or activation of specific protein kinases responsible for
altering signal transduction which may in turn be responsible of humoral
immune function modulation.
Another example of a microbial agent that has been connected to a
particular mental disease is CMV and schizophrenia. In the central
nervous system, CMV is known to provoke a strong glial response as well
as producing cytokines and chemokines. Several studies have shown that
patients with a more recent onset of schizophrenia reveal higher rates of
CMV seropositivity compared to controls. Similarly, it has been shown
that patients with untreated schizophrenia have significantly higher CMV
serum and cerebrospinal fluid immunoglobin G antibody levels com-
pared to unaffected controls. It has also been reported that some antipsy-
chotic treatments suppress the replication of some infectious agents, such
as CMV. However, the replication of these findings has not always been
conclusive, and although link is plausible, evidence is debatable.
Despite the fact that certain genes implicated in schizophrenia appear to be
involved in the life cycles of microbial agents such as CMV, T. gondii as well
as influenza and herpes simplex viruses, it appears that power to show asso-
ciation in genetic studies is inadequate as pathogen presence varies with popu-
lation and season, a cause for heterogeneity leading to inconclusive results.
7. PHARMACOLOGY
Clinical trials can be classified in observational studies in which there is
no active investigator management and interventional studies in which the
investigators actively compare two treatments (usually a new treatment is
compared to a standard treatment or placebo).
Randomized clinical trials (RCTs), which are interventional studies,
have been the gold standard in the evaluation of psychiatric treatments.
These studies are designed as randomized, double blind, and placebo-
controlled and provide information concerning treatment efficacy of a
given treatment under best possible control of all other involved parame-
ters apart from the presence of a product with known biological activity.
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Randomization is the process that involves randomly allocating the

new drug or the standard drug to each patient included in the study. This
process reduces selection biases and separates patients into two treatment
groups in which distribution of known and unknown factors are similar.
Randomization provides a respectable statistical basis for the evaluation
of the evidence related to treatment effects.
Blinding is the process that prevents identification of the treatments
allocated. A double-blind trial is one in which neither the subject nor the
investigator are aware of the treatment received. The purpose of blinding
is limiting biases due to the influence of treatment knowledge in recruit-
ment and allocation of subjects, their further care, their assessment, etc.
Clinical trials may have several kinds of designs. The most common
design is the parallel group design in which subjects are randomized to
one of two (or more) arms, an arm implying one or another treatment
allocation. Another possible design is the crossover design in which each
subject is randomized to a sequence of two or more treatments, implying
that each subject acts as his own control for treatment comparison.
Factorial designs are of lower statistical power as they evaluate simultane-
ously two or more treatments through the administration of different
combinations of the treatments. However, this type of trial can examine
drug interaction, which the others cannot.
Multicenter trials are preferred as they evaluate a new drug more
efficiently as subject recruitment is from a wider population which is basis
for subsequent generalization of findings. Trials can be designed to show
superiority. Efficacy of a new treatment is established by showing superi-
ority to placebo or even better to a standard active treatment or by showing
a dose-response relationship. In some cases, trials are designed to show
equivalence or non-inferiority, implying that the response to the new drug
does not statistically differ or is not clinically inferior to the standard
active treatment or placebo.
7.1. Access to the protocol before it starts

(www.clinicaltrial.gov)
RCTs are the golden rule in order to demonstrate that a new product
should be available for the patients, as giving advantages compared to the
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others, either for a better efficacy (sometimes) or, more frequently in

psychiatry up to now, for better tolerance or safety with the same efficacy.
Demonstrating superior efficacy than placebo is usually required by the
agencies (e.g. Food and Drug Administration, FDA, in the United States,
EMEA in Europe), as is the demonstration that the proposed product has
at least no difference regarding efficacy as compared to a standard treat-
ment. These studies are extremely expensive, and have been criticized as
exposed to the financial capacity of the industry. Indeed, a worldwide
leading company could afford four or five pivotal studies and, if they pub-
lish only the most favorable ones (positive studies are always easier to
publish), be able to present a file with more than one positive study.
An important and recent progress dealt with these limits, proposing that
all RCTs be detailed on the web, especially giving the number of patients
to be recruited for the conclusion, inclusion and exclusion criteria, loca-
tions of the participating centers, statistical plan, and, last but not least, the
endpoint of the study. The website where this information is available at
www.clinicaltrial.gov, and is accessible to everyone, including the agen-
cies and editors of journals. This approach has probably increased a lot the
transparency of controlled studies and might explain that in the files more
recently proposed to the agencies, it seems that more failed and negative
studies are being included.
7.2. The use of ‘mega trials’

Another limit is that RCTs cannot (and are not intended to) reflect the
reality of the day-to-day practice. Selective recruitment in clinical trials
reduces generalizability of the findings (exclusion of comorbid, resistant,
suicidal patients), study protocols are therefore not supposed to have the
flexibility of prescriptions and follow-ups as in the real-world clinical
practice. A recent research progress dealing with these difficulties are the
development of mega trials, proposing strict but multiple choices guide-
lines, and allowing the recruitment of many types of patients, even the
ones that are usually not selected in RCTs.
The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE)
study is the largest outcome schizophrenia study performed up to now,
with 1,493 patient inclusions in 57 sites and more than 200 subsequent
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publications.15,17 CATIE’s study outline was ambitious and complex,

comparing five antipsychotics (including a first generation, typical neuro-
leptic) with multiple secondary outcomes, the endpoint being the “time
before discontinuation.” An unbalanced randomization process assigned
treatments to chronic schizophrenic patients within four stratified popula-
tions. Stratification was established according to dyskinesia status and
date of inclusion before or after ziprasidone was added to study drug
selection. Although the CATIE study suffered from an unbalanced design
and underwent criticism, it serves as a model to improve future clinical
trials. Choice of population sample which was very unrestrictive con-
curred to better generalizability of potential results. Multisite clinical tri-
als such as CATIE take into consideration side effects and site-by-treatment
interactions, thus reducing the risk of false positives and false negatives in
final analyses.
Practical clinical mega-trials such as STAR*D have challenged the
golden standard of randomized controlled clinical trials to a whole new
level and have adapted psychiatric research to real-world settings in major
depressive disorder as well.26 In the multisite, prospective, randomized,
multistep STAR∗D study, Rush et al. compared various antidepressant
treatment options for depressed outpatients who did not attain a satisfac-
tory response with citalopram, a classic first-step antidepressant treatment.
Novelty consisted in taking in consideration the treatment options enrolled
patients considered acceptable with the use of equipoise-stratified rand-
omization. This procedure allowed patients to refuse randomization
toward treatments they considered unacceptable. Change in treatment
(switch or augmentation) was decided by the clinician based on symptom
severity and side effect status. Treatment assignment resembled real-world
practice as the clinician and the patient shared the decision making.
Studies in children and adolescent populations are the object of many
debates as these populations are particularly vulnerable, research may be
invasive and cause unnecessary pain or anxiety and child consent is con-
testable. However, clinical studies in these particular populations are
necessary as children are not “small adults.” There are in fact many phar-
macokinetic and pharmacodynamic differences in children compared to
adults and diseases in these populations are specific and differ from adult
pathologies.
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7.3. Mixing pharmacology and cognitive analyses

The mega trial CATIE was also used to analyse the differential impact of
five antipsychotics on cognitive functions of patients with schizophrenia.13
At week 12, each of the treatments significantly improved the composite
score on the CATIE neurocognitive battery compared with baseline
(p < 0.01 for olanzapine, and p < 0.001 for quetiapine and risperidone).
Specifically analysing the impact of pharmacological treatment on cognitive
functions in schizophrenia is particularly interesting as we known, for
example, that cognitive functions are much more able to predict functional
remission compared to level of severity of crude schizophrenic symptoms.
7.4. Mixing pharmacology and genetics

Data collected in mega trials such as CATIE or STAR*D may have wider
uses, such as giving the material for GWAS. The search for genes that
should help clinicians predict which genetic variants might be tested in
order to foresee positive or negative response to a specific psychotropic
treatment or the occurrence of side effects, defines the field of
psychopharmacogenetics.9
Psychopharmacogenetics determine the inherited component of varia-
bility in drug response with hopes of giving the right drug at the right dose
to the right patient at the right time.9 As progress is made in investigating
and understanding the genetic variations between individuals thanks to the
sequencing of the human genome and the use of genetic markers, novel
approaches such as genotyping are coming into use concerning drug
prescription as well as drug development.
Psychiatry is a medical specialty in which the pharmacogenetic approach
would be of the utmost importance. Although considerable advances such
as third generation antipsychotics have been made toward improving
effectiveness of psychotropic treatments and diminishing undesirable
side-effects, still too many patients do not obtain a complete response to
medication and may have poor compliance due to impairing side effects.
Prescription strategies in psychiatry are based on symptomatic evalua-
tion (such as described in ICD-10) which may not reflect underlying
neurobiological etiologies, but rather the psychiatrists’ subjective
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experience. Experience often proves that patients with the same diagnosis
respond in an uncertain fashion to a given treatment.
The FKBP5 gene, a gene coding for a glucocorticoid receptor-regulating
co-chaperone protein, could be one of the first genes useful to predict
antidepressant response. Initially, this gene was found associated with
treatment response in two independent German samples of depressed
inpatients.2 Individuals carrying the associated genotypes had less HPA-
axis hyperactivity during the depressive episode, which implies that the
studied SNP might have functional impact. As the association has now
been replicated at least three times to this day, including in the large
STAR*D sample, then testing this gene might be helpful for clinicians.
For such use, many gaps have to be fulfilled. What type of prediction is
related to the knowledge of these genotypes? How can this information be
used, regarding the numerous other factors that are involved, such as
presence of co-prescription, heterogeneity of the disorder, and social
background specificities? But complexity does not mean that it is impos-
sible to clearly demonstrate, it only implies that many factors are involved.
Research has yet to be pursued, and its pursuit will now have more
possibilities to decipher the involved mechanisms thanks to the use of
more complex approaches, i.e. using different types of techniques.
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increased recurrence of depressive episodes and rapid response to antidepres-
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3. Buckholtz J, Treadway MT, Cowan RL, Woodward ND, Benning SD, Li R,
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a polymorphism in the 5-HTT. Gene Science 301(5631): 386–389.
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studies in psychiatry: Lessons from early studies of non-psychiatric and psy-
chiatric phenotypes. Mol Psychiatry 13: 649–653.
7. Ebstein RP, Israel S, Chew SH, Zhong S, Knafo A. (2010) Genetics of human
social behavior. Neuron 65: 831–844.
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Mier D, Opitz von Boberfeld C, Raab K, Witt SH, Rietschel M, Cichon S,
Meyer-Lindenberg A. (2009) Neural mechanisms of a genome-wide sup-
ported psychosis variant. Science 324: 605.
9. Gorwood P, Hamon M. (2006) Psychopharmacogenetics, Springer, Inc.,
NY.
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11. Hariri AR, Mattay VS, Tessitore A, Kolachana B, Fera F, Goldman D,
Egan MF, Weinberger DR. (2002) Serotonin transporter genetic variation and
the response of the human amygdala. Science 297: 400–403.
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(2005) Correlation of stable elevations in striatal mu-opioid receptor avail-
ability in detoxified alcoholic patients with alcohol craving: A positron
emission tomography study using carbon 11-labeled carfentanil. Arch Gen
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Lieberman JA. (2007) Effects of olanzapine, quetiapine, and risperidone on
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52-week comparison. Am J Psychiatry 164: 1061–1071.
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an episode of major depression in women. Am J Psych 152: 883–42.
15. Kraemer HC, et al. (2009) Clinical trials design lessons from the CATIE
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with chronic schizophrenia. N Engl J Med 353: 1209–1223.
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18. Lin PY, Tsai G. (2004) Association between serotonin transporter gene
promoter polymorphism and suicide: Results of a meta-analysis. Biol
Psychiatry 15: 1023.
19. Minzenberg MJ, Laird AR, Thelen S, Carter CS, Glahn DC. (2009) Meta-
analysis of 41 functional neuroimaging studies of executive function in
schizophrenia. Arch Gen Psychiatry 66: 811–822.
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Wellcome Trust Case Control Consortium, Owen MJ, O’Donovan MC.
(2009) Gene-wide analyses of genome-wide association data sets: Evidence
for multiple common risk alleles for schizophrenia and bipolar disorder and
for overlap in genetic risk. Mol Psychiatry 14: 252–260.
21. Nuechterlein KH, et al. (2008) The matrics consensus cognitive battery, part
1: Test selection, reliability and validity. Am J Psychiatry 165: 203–213.
22. O’Donovan MC, et al. (2008) Identification of loci associated with schizo-
phrenia by genome-wide association and follow-up. Nat Genetics 9:
1053–1055.
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study. JAMA 299: 35–50.
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ciation studies in psychiatric disorders. In: Jones B, Mormède P (eds.),
Neurobehavioral Genetics: Methods and Applications. pp. 169–182, CRC
Press.
25. Risch N, et al. (2009) Interaction between the serotonin transporter gene
(5-HTTLPR), stressful life events and risk of depression. Meta-analysis.
JAMA 301: 2462–2474.
26. Rush AJ, et al. Sequenced treatment alternatives to relieve depression
(STAR*D): Rationale and design. Controlled Clin Trials 25: 119–142.
27. Rutter M. (2010) Gene-environment interplay. Depression Anxiety 27: 1–4.
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186: 4–6.
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31. Uher R, McGuffin P. (2010) The moderation by the serotonin transporter

gene of environmental adversity in the etiology of depression: 2009 update.
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microbial agents? A review of evidence. Mol Psychiatry 13: 470–479.
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Chapter 27
World Suicide
Morton M. Silverman
1. INTRODUCTION
Every year, a million individuals die by suicide and at least twenty times
as many attempt suicide, making suicide and suicidal behaviors a major
international public health problem and challenge. This toll is higher than
the total number of world deaths each year from war and homicide com-
bined. On average, almost 3,000 people die by suicide every day. Every
30 secs, the loss of a loved one to suicide shatters the lives of family and
friends. For family and friends affected by suicide or attempted suicide,
the emotional impact may last for many years.
According to the World Health Organization (WHO), in 1998, suicide
represented 1.8% of the global burden of disease, and it is expected to
increase to 2.4% by the year 2020. Suicide is presently among the ten
leading causes of death for all ages in most countries, and in some coun-
tries, it is among the top three causes of death for those aged 15–34 years.
In the last 45 years, suicide rates have increased by 6% worldwide.
Suicide is among the three leading causes of death among those aged
15–44 years in some countries, and the second leading cause of death in
the 10–24 years age group; these figures do not include suicide attempts,
which are up to 20 times more frequent than completed suicide.
Substantial economic costs are associated with suicide. These costs
arise from the loss of economic potential due to lives lost to suicide, from
690
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the often devastating effects of symptoms of bereavement due to suicide,

from the medical and mental health costs associated with suicide attempts,
and from the burden of care for those who have made suicide attempts.
Internationally the annual economic cost of suicidal behavior is estimated
to be in the billions of dollars.33
Worldwide, the prevention of suicide has not been adequately addressed
due to basically a lack of awareness of suicide as a major problem and the
taboo and stigma in many societies that prevent suicide from being openly
discussed. In fact, only a few countries have included the prevention of
suicide among their national priorities.
Many believe that we can lessen the burden of suicide and suicidal
behaviors through enhanced surveillance, identification of at-risk indi-
viduals or populations, better and more efficient/effective assessment
tools, interventions, management, monitoring, and, of course, prevention.
The twin goals of health (and mental health) promotion and disease
(mental illnesses and their causes) prevention are especially critical
because suicide and suicidal behaviors are just that — behaviors — and
all behaviors are multi-determined and multi-faceted. Hence, there are
multiple risk and protective factors that contribute to this behavior. The
challenges are to enhance the protective factors and reduce, eliminate,
attenuate, and/or disengage the risk factors.
2. RISK FACTORS
Understanding risk and protective factors at the individual, family, com-
munity, societal, and national levels is necessary in order to identify
those at most risk, intervene in a timely and effective manner, and
implement preventive interventions. Many different populations are at
risk for suicide and suicidal behaviors, highlighting the diversity of
biopsychosocial factors that contribute to self-destructive behaviors:
age, gender, race/ethnicity, geographical location, socioeconomic
upheavals, presence of physical illness, presence of mental disorders
(especially affective disorders, substance abuse disorders, anxiety
disorders, psychotic disorders, and certain personality disorders), and
ruptures in interpersonal relationships leading to isolation, loneliness,
and rejection.
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692 M. M. Silverman
Major risk factors include gender, race, ethnicity, culture, access and
availability of lethal means, physical and sexual abuse, sexual orienta-
tion, violence, and loss. Mental disorders (particularly depression and
alcohol use disorders) are a major risk factor for suicide in Europe and
North America; however, in Asian countries, impulsiveness plays an
important role.
Risk for suicide is only partly dependent upon the presence of a psychi-
atric disorder and/or physical illness, because the majority of individuals
suffering from psychiatric and physical illnesses do not kill themselves as
a result of their illnesses. Apart from demographic factors (such as gender
and age, which will be discussed separately below), significant risk factors
consist of a combination and interaction between and among psychiatric,
biological, social, cultural, and environmental factors, as well as factors
related to an individual’s life history.
Certain life events may serve as precipitating factors for suicidal
behavior. Such events include personal loss, interpersonal conflict, social
isolation, a broken or disturbed relationship, and legal or work-related
difficulties.25
Within countries, the prevalence of suicide among Caucasians is
approximately twice that observed in other races, although an increasing
rate among African Americans has recently been reported in the United
States.23
One of the challenges is not only to identify the presence of risk factors
but also to develop and appropriately implement preventive interventions.
Knowing which individuals possess a predisposition to suicide, and also
possibly face a combination of risk factors, can help identify those most
in need of therapeutic and preventive interventions.
It is clear that suicide prevention requires intervention also from
outside the health sector and calls for an innovative, comprehensive
approach, including both health and non-health sectors, such as education,
labor, police, justice, religion, law, politics, and the media.
3. PROTECTIVE FACTORS
Compared to our knowledge about predisposing and precipitating risk
factors, we know relatively little about protective factors, especially on a
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global level. Generally, the following factors have been identified: strong
religious orientation, social support and connectedness (including
marriage), parenthood, self-esteem, emotional well-being, and economic
stability.
4. SUICIDE ATTEMPTS
Internationally, the ratio of suicide attempts to death by suicide is
generally estimated at 20–30 to 1 in adolescents and young adults and 3
or less to 1 in the elderly population. Suicide attempts range in intent and
medical severity from mild to very severe, often resulting in the individual
being disabled by the psychological, physical, social, and interpersonal
consequences of their self-injurious behavior.
Suicide and suicide attempts have serious emotional consequences as
well for families, peers, and significant others. The families of those who
attempt suicide are often especially anxious and concerned about the risk
of further suicidal behavior and about their responsibilities in trying to
prevent further attempts.
Very few countries in the world have systematic data registration of
attempted suicide, which makes it impossible to relate national trends of
suicide to national trends of attempted suicide. In fact, very few states
within the United States collect such data. Two of the very real obstacles
to collecting such data are that the majority of suicide attempters never
come to the attention of medical facilities, and there is no uniform defini-
tion for suicide attempts within countries, let alone across the globe. In
addition, in many developing countries, attempted suicide remains a
punishable offense; therefore many hospitals do not register cases.
Furthermore, in many locales, injuries do not need to be officially
reported, so information on injuries is consequently not collected at any
level of government. Hence, reported cases of attempted suicide are only
the “tip of the iceberg,” resulting in the large majority of suicidal people
remaining uncounted.16
What is known is that non-fatal suicidal behavior is more prevalent
among younger people than among older people. The ratio of fatal to non-
fatal self-injurious behavior (with and without suicidal intent) in those
over the age of 65 years is usually estimated to be 1:2–3, while in young
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694 M. M. Silverman
people under the age of 25 years the ratio may approach 1:100–200.26
Although suicidal behavior is less frequent in the elderly, the probability
of a fatal outcome is much higher. As a general trend, rates of non-fatal
suicidal behavior tend to be 2–3 times higher in women than in men.
Results from the WHO/EURO Multicentre Study of Parasuicide indicate
that the most common method of suicide attempts used by men and
women is poisoning, followed by cutting. More than half of those
attempting suicide made more than one attempt, with nearly 20% of
second attempts being made within 12 months of the first.30
One approach to understanding why individuals choose to end their
own lives is to construct a chain of causation and study each element’s
contribution to the suicidal process. It is generally accepted that, in most
cases, but not all, a suicidal act is preceded by some form of suicidal plan-
ning and that planning is the result of a thinking process that involves a
desire or intent to die. The sequence usually begins with a suicidal thought
(ideation), followed by suicidal intent, suicidal planning, and finally a
self-injurious act, which may result in a fatal or non-fatal outcome.7
However, and most important, the majority of suicidal thoughts will never
end in a suicidal act.
Three lines of research have dominated the suicide field: retrospective
studies of those who have died by suicide, retrospective (and subsequent
prospective) studies of those who attempt suicide, and studies of those
who have suicidal thoughts. Many researchers have looked upon suicide
attempts as the best available “proxy measure” for suicide completions,
although there is not a one-to-one relationship between these two behav-
iors. Inasmuch as we cannot interview the dead, many believe that
studying suicide attempters will provide a window into the suicidal mind,
inasmuch as about 10%–20% of those who attempt suicide will eventually
die by suicide and an even higher percent will repeat suicidal attempts.
5. A PUBLIC HEALTH PERSPECTIVE

Much has been written about applying a public health approach to under-
standing suicide and suicidal behaviors, as well as applying a public
health model to designing and implementing interventions for at-risk
populations and individuals — both therapeutic and preventive.
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By definition, public health research and findings are at the population-

level, not at the individual or clinical level. Hence, there are major differ-
ences between data collected in general population surveys and data
collected as part of a clinical interview (or, for that matter, data collected
by self-report instruments). Bias in reporting can occur in many different
ways, including how critically important terms are understood by the
respondent (e.g. suicide attempt) and how memory affects timeframes
(e.g. remembering whether an event occurred in the last two weeks, last
12 months, or in a lifetime).19
Figures on suicide mortality made available to the WHO by its Member
States are based on death certificates signed by legally authorized person-
nel, usually doctors and, to a lesser degree, police officers. Nevertheless,
it is a well-known fact that underreporting of suicide attempts and deaths
by suicide occurs.14 Hence, the actual number of deaths by suicide is
higher than what is recorded or estimated, as is the respective calculated
suicide rate. It is assumed that, because the bias in reporting is, more or
less, occurring to equal degrees amongst all of the reporting countries, the
relative relationships in the suicide rates remain comparable over time. So,
although there is underreporting of suicidal behaviors, that underreporting
is equally distributed amongst all the countries, so it remains possible to
compare numbers and rates across countries contemporaneously and over
time.
6. WORLD HEALTH ORGANIZATION STATISTICS

After its creation in 1948, the WHO began to compile and disseminate
data on mortality as reported by its Member States, using the
International Classification of Diseases and Causes of Death (ICD).
Most countries include information on mortality associated with sui-
cide, the category name and code of which remained relatively stable
through successive editions of the ICD, from ICD-6 to ICD-10.
Currently, however, only a portion of the more than 130 Member States
report on a regular basis. Data from developed countries (e.g. Europe,
North America, and a few countries in the western Pacific Region) are
received on a regular basis. Most developing countries (in Latin
America, Asia, and in the eastern Mediterranean Region) report on a
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696 M. M. Silverman
less regular basis, while very few countries in Africa report mortality
regularly.6 Some of the 70 least developed countries (mostly in Africa,
but also in South East Asia) do not maintain vital registration systems
due to the lack of means to collect and process data related to births and
deaths in the general population.
Using both reported and estimated data (for countries that do not report
to the WHO on mortality), the estimated number of individual cases of
suicide in 2002 (the last year for which there are reliable reported data)
was about 877,000 cases, of which 549,000 were males and 328,000
females, which gives a proportion of 1.7:1 (Table 1).6 According to WHO
estimates for the year 2020, approximately 1.53 million people will die by
suicide, and 10–20 times more people than this will attempt suicide
worldwide. This represents, on average, one death every 20 secs and one
attempt every 1–2 secs.5
However, total numbers do not tell the whole story, because national
suicide rates provide a better measure of the suicide activity within a
country. The WHO estimates that the global suicide rate is 14/100,000, of
which 18/100,000 is the male rate and 11/100,000 is the female rate.
Based on the most recent data sent to the WHO, the highest suicide rates
for both males and females are found in Europe, predominantly in Eastern
Europe (i.e. Lithuania, the Russian Federation, Belarus, and, to a lesser
extent, Finland, Hungary, and Latvia), among a group of countries that
share similar historical, genetic, and sociocultural characteristics. However,
some countries that are quite distinct in relation to each other also have
some similarly high suicide rates, i.e. Cuba, Japan, and Sri Lanka.
During the 20th century, Finland, Ireland, the Netherlands, Norway,
Scotland, Spain, and Sweden experienced a significant increase in
suicides, while England and Wales (combined data), Italy, New Zealand,
and Switzerland experienced a significant decrease.24 During the period
between 1960 and 1990, at least 28 countries or territories had rising sui-
cide rates, including Bulgaria, China, Costa Rica, Mauritius, and
Singapore, while eight had declining rates, including Australia and
England and Wales (combined data). In the last 45 years, suicide rates
have increased by 60% in some countries.
Interestingly, when the data are separated into WHO geographical
regions, the highest rates in each region (with the exception of Europe) are
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World Suicide 697
Table 1. Suicide rates by country year, and sex(2).

Country Year Males Females
Albania 03 4.7 3.3
Antigua and Barbuda 95 0.0 0.0
Argentina 05 12.7 3.4
Armenia 06 3.9 1.0
Australia 04 16.7 4.4
Austria 07 23.8 7.4
Azerbaijan 07 1.0 0.3
Bahamas 02 1.9 0.0
Bahrain 88 4.9 0.5
Barbados 01 1.4 0.0
Belarus 03 63.3 10.3
Belgium 99 27.2 9.5
Belize 01 13.4 1.6
Bosnia and
Herzegovina 91 20.3 3.3
Brazil 05 7.3 1.9
Bulgaria 04 19.7 6.7
Canada 04 17.3 5.4
Chile 05 17.4 3.4
China (selected rural
and urban areas) 99 13.0 14.8
China (Hong Kong SAR) 06 19.3 11.5
Colombia 05 7.8 2.1
Costa Rica 06 13.2 2.5
Croatia 06 26.9 9.7
Cuba 06 19.6 4.9
Cyprus 06 3.2 1.8
Czech Republic 07 22.7 4.3
Denmark 06 17.5 6.4
Dominican Republic 04 2.6 0.6
Ecuador 06 9.1 4.5
Egypt 87 0.1 0.0
El Salvador 06 10.2 3.7
Estonia 05 35.5 7.3
Finland 07 28.9 9.0
(Continued)
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698 M. M. Silverman
France 06 25.5 9.0
Georgia 01 3.4 1.1
Germany 06 17.9 6.0
Greece 06 5.9 1.2
Grenada 05 9.8 1.9
Guatemala 06 3.6 1.1
Guyana 05 33.8 11.6
Haiti 03 0.0 0.0
Honduras 78 0.0 0.0
Hungary 05 42.3 11.2
Iceland 07 18.9 4.6
India 98 12.2 9.1
Iran 91 0.3 0.1
Ireland 07 17.4 3.8
Israel 05 8.7 3.3
Italy 06 9.9 2.8
Jamaica 90 0.3 0.0
Japan 07 35.8 13.7
Jordan 79 0.0 0.0
Kazakhstan 07 46.2 9.0
Kuwait 02 2.5 1.4
Kyrgyzstan 06 14.4 3.7
Latvia 07 34.1 7.7
Lithuania 07 53.9 9.8
Luxembourg 05 17.7 4.3
Maldives 05 0.7 0.0
Malta 07 12.3 0.5
Mauritius 07 16.0 4.8
Mexico 06 6.8 1.3
Netherlands 07 11.6 5.0
New Zealand 05 18.9 6.3
Nicaragua 05 11.1 3.3
Norway 06 16.8 6.0
Panama 06 10.4 0.8
Paraguay 04 5.5 2.7
Peru 00 1.1 0.6
(Continued)
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World Suicide 699
Philippines 93 2.5 1.7
Poland 06 26.8 4.4
Portugal 04 17.9 5.5
Puerto Rico 05 13.2 2.0
Republic of Korea 06 29.6 14.1
Republic of Moldova 07 28.0 4.3
Romania 07 18.9 4.0
Russian Federation 06 53.9 9.5
Saint Kitts and Nevis 95 0.0 0.0
Saint Lucia 02 10.4 5.0
Saint Vincent and the
Grenadines 04 7.3 0.0
Sao Tome and Principe 87 0.0 1.8
Serbia 06 28.4 11.1
Seychelles 87 9.1 0.0
Singapore 06 12.9 7.7
Slovakia 05 22.3 3.4
Slovenia 07 33.7 9.7
Spain 05 12.0 3.8
Sri Lanka 91 44.6 16.8
Suriname 05 23.9 4.8
Sweden 06 18.1 8.3
Switzerland 06 23.5 11.7
Syrian Arab Republic 85 0.2 0.0
Tajikistan 01 2.9 2.3
Thailand 02 12.0 3.8
Tfyr Macedonia 03 9.5 4.0
Trinidad and Tobago 02 20.4 4.0
Turkmenistan 98 13.8 3.5
Ukraine 05 40.9 7.0
United Kingdom 07 10.1 2.8
United States of America 05 17.7 4.5
Uruguay 04 26.0 6.3
Uzbekistan 05 7.0 2.3
Venezuela 05 6.1 1.4
Zimbabwe 90 10.6 5.2
Suicide rates per 100,000 by country, year, and sex Most recent year available; as of 2009.
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700 M. M. Silverman
found in island countries, such as Cuba, Japan, Mauritius, and Sri Lanka.
The lowest suicide rates are found in countries that primarily follow
Islamic traditions and in some Central Asian republics that had formerly
been integrated into the Soviet Union.6 A cautionary note is that it is
difficult to compare rates across regions and countries because of impor-
tant differences in ethnic and sociopolitical features. For example,
although the highest suicide rates are currently found in Eastern Europe,
the largest number of suicides occurs in Asia. Of the total number of sui-
cides worldwide, approximately 46% take place in the top 13 countries
listed in Table 2, while the top 13 countries in terms of suicide rates
(Table 3) represent less than 14% of worldwide suicides. Only two
countries — the Russian Federation and Sri Lanka — are among the top
13 countries for both suicide rate and number of cases of suicide.
Of particular note is that almost one-third of all suicides worldwide
occur in China and India. By way of comparison, the number of suicides
in China alone is 30% greater than the total number of suicides in the
whole of Europe, and the number of suicides in India is equivalent to
Table 2. Ranking of top 13 countries by the number of suicides.
Country Number of suicides Rate per 100,000 Ranking by suicide rate

China 170,000 13.9 26
India 105,000 10.7 38
Russian Federation 55,000 38.7 2
USA 31,000 10.7 39
Japan 30,000 23.8 11
Ukraine 13,000 26.1 9
Germany 11,000 13.5 27
France 10,000 17.6 19
Rep. Korea 9,000 17.9 18
Brazil 7,000 4.1 71
Poland 6,000 15.5 22
Sri Lanka 5,000 21.6 11
Thailand 5,000 7.8 52
Ranking of the top 13 countries, number of suicides (estimated for the year 2000).
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World Suicide 701
Table 3. Ranking of top 13 countries by suicide rates.
Number of Ranking by number

Country suicides Rate per 100,000 of suicides
Lithuania 1,500 42.1 28
Russian Federation 55,000 38.7 3
Belarus 3,500 35.1 16
Kazakhstan 4,500 28.8 14
Slovenia 600 28.1 44
Hungary 3,000 27.7 18
Estonia 400 27.3 56
Ukraine 13,000 26.1 6
Latvia 600 26 43
Japan 30,000 23.8 5
Sri Lanka 5,000 21.6 12
Belgium 2,000 21.1 24
Finland 1,100 20.6 36
those in the four European countries, with the highest number of suicides
together (Russia, Germany, France, and Ukraine). Yet, the suicide rate in
China almost parallels the global average rate, and that of India is almost
half of the global suicide rate.
7. ACCESS TO MEANS
Our knowledge of the methods used and their variation across countries
and world regions is very limited. Ajdacic-Gross et al.,1 using ICD-10
data, were able to identify typical patterns of suicide methods in different
countries. Hanging was the predominant method of suicide in most coun-
tries. The highest proportion was around 90% in men and 80% in women,
as observed in Eastern Europe (i.e. Estonia, Latvia, Lithuania, Poland, and
Romania). Poisoning by pesticide, especially among women, was com-
mon in many Asian countries (e.g. the Republic of Korea and Thailand)
and in rural Latin American countries (e.g. El Salvador, Nicaragua, and
Peru), as well as in Portugal. Poisoning by drugs was common in women
and men in Canada, the Nordic countries, and the United Kingdom.
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702 M. M. Silverman
Firearm suicide was the most common method in the United States but
was also prevalent in Argentina, Switzerland, and Uruguay. Jumping from
a high place in cities and urban societies was the most common method in
Hong Kong Special Administrative Region (SAR), China, Luxembourg,
and Malta. In addition, there has been an emergence of a new method,
charcoal-burning suicide, in Hong Kong SAR, China, and urban Taiwan,
China.12
Adjacic-Gross et al.’s analyses showed that pesticide suicide and
firearm suicide have replaced more traditional methods in many countries.
Violent and highly lethal methods such as firearm suicide and hanging are
more frequent among men, whereas poisoning or drowning are more fre-
quent among women. The lethality of firearm suicide and hanging
approaches 80%–90%, but lethality is markedly lower for poisoning.32
Three methods — hanging, pesticide suicide, and firearm suicide —
dominate country-specific suicide patterns. Jumping from a height and
non-pesticide poisoning (i.e. mainly poisoning by drugs) occasionally
appear as important alternative methods. Hanging is the main suicide
method when no other major method is available. The proportion of
hangings typically decreases as either pesticide suicide or firearm suicide
increases.
With regard to poisoning and firearm suicide, Adjacic-Gross et al.’s
analyses suggest that preventive efforts are likely to have the greatest
impact on the subgroup that carry out unplanned impulsive acts. Perhaps
20%–30% of all suicides in industrialized countries belong to this
subgroup, and their deaths might be preventable. They concluded that
although numerous factors contributed to the choice of a suicide method,
societal patterns of suicide could be understood from basic concepts such
as the social acceptability of the method (i.e. culture and tradition) and its
availability (i.e. opportunity). This suggests that restricting access to the
means of suicide would be a major form of suicide prevention globally.
8. GENDER AS A RISK FACTOR

Pesticide suicides have been recognized by the WHO as a major public
health problem in developing Asian countries and may account for as
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World Suicide 703
many as 300,000 deaths each year.9 It is the major method of suicide and
suicide attempts among young rural women in China.29 Preventive actions
undertaken by the WHO, in collaboration with other international health
and public health organizations, include changing attitudes, knowledge,
and beliefs about pesticides; controlling access to pesticides (including
developing secure storage practices); and training primary health care
personnel (including doctors and nursing staff at emergency care units) in
the clinical management of such intoxications.10
On average, there are about three male suicides for every female
suicide, and this is so more or less consistently for different age groups,
with the exception of advanced age groups, when men tend to have even
higher rates. An increase of approximately 49% for suicide rates for males
and 33% for suicide rates for females occurred between 1950 (when the
first worldwide suicide rate calculations were done, with 21 countries
reporting) and 1995 (the last year of full data collection, with 105 coun-
tries reporting). There is a relatively constant predominance of male
suicide rates over female suicide rates over the last 60 years: 3.2:1 in
1950; 3.6:1 in 1995; and projected to be 3.9:1 in 2020. China is the only
exception to this finding, where female suicide rates are slightly higher
than male suicide rates.
9. AGE AS A RISK FACTOR

Globally, there is a clear tendency for suicide rates to increase with age.
In 2000, the male rates for specific age groups started at 1.4/100,000 (in
the youngest age groups) and gradually increased up to 52.1/100,000 (in
the age group 75 years and older). For females, the rates increased from
0.4/100,000 (in the youngest age group) to 15.9/100,000 (in the oldest age
group). Although suicide rates can be 6–8 times higher among the elderly
than among the youth, currently more young people die from suicide than
elderly people. As of 2000, with 53 countries reporting, more suicides
(55%) occurred in the 5–44 year old group than in those aged 45 years and
older (45%). Of particular note is that the age group in which most
suicides are currently occurring is the 35–44 year old group for both males
and females.
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704 M. M. Silverman
Suicide rates among young people have been increasing, and they are
currently the group with the highest risk in one third of all countries
(developed and developing). At least 100,000 adolescents die by suicide
every year. This is a remarkable change from just 50 years ago, when the
absolute number of cases of suicide roughly increased with age. It is not
explained in terms of the overall aging of the global population; in fact, it
runs counter to this demographic trend. Although the proportion of the
elderly in the total global population is increasing at a greater pace than
that of younger people, the suicide rate in young people is increasing at a
greater rate than it is in the elderly. This phenomenon appears to exist in
all continents and is not correlated to levels of industrialization or wealth.23
10. INTERNATIONAL ACTIVITIES

In 1993, the WHO presented six broad approaches to the prevention of
suicidal behavior.37 These were:
(1) The treatment of those with mental disorders.

(2) Gun possession control.
(3) Detoxification of domestic gas.
(4) Detoxification of car emissions.
(5) Control of availability of toxic substances.
(6) A toning down of reports of suicide in the press.
In 1996, the United Nations Department for Policy Coordination and

Sustainable Development, in collaboration with the WHO, published a
document highlighting the importance of a guiding policy for the
formulation and implementation of national strategies.36 The WHO subse-
quently issued a series of documents on the prevention of suicide and two
publications on mental, neurological, and psychosocial disorders. Other
reports on suicide prevention have resulted in more than 20 nations
developing and enacting national suicide prevention programs, in part
based on the guidance provided by these documents.
In 2002, the WHO Department of Violence and Injury Prevention
published the World Report on Violence and Health,23 which highlighted
the significance of self-directed violence as a global public health
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World Suicide 705
problem. This document also led to the inception of World Suicide

Prevention Day, beginning in 2003 on 10 September.
As part of its global suicide prevention program, the WHO launched
Suicide Prevention: Multisite Intervention Study on Suicidal Behaviors
(SUPRE-MISS) in 2002.8 The study pertained to three different areas of
investigation:
(1) A transcultural description of the communities participating in the

study;
(2) A community survey of suicidal ideation and behavior on a repre-
sentative sample of subjects from each community; and
(3) A randomized controlled trial of treatment as usual (TAU) of suicide
attempters at health facilities versus TAU plus a brief form of contact
and intervention (BIC) with suicide attempters. The assumption on
this specific part of the study was that a necessarily simple interven-
tion performed with some continuity (nine follow-ups in an 18-month
trial) could elicit different results from routine forms of treatment.15
The community survey component of SUPRE-MISS consisted of interviews

conducted with subjects in the general population in nine cities/towns on
the five continents. Overall approximately 20,000 individuals were
engaged in face-to-face interviews by trained interviewers. Three key
questions were asked:
(1) Have you ever seriously thought about committing suicide?

(2) Have you ever made a plan for committing suicide?
(3) Have you ever attempted suicide?
If any of the questions received a “yes” as the answer, then further

questions were asked according to the established survey protocol.
The proportion of subjects in the general population who admitted to
having had suicidal thoughts in their lifetime varied from 2.6% (Chennai,
India) to 25.4% (Durban, South Africa). Those having planned a suicidal
act varied from 1.1% (Hanoi, Vietnam) to 15.6% (Durban, South Africa).
The proportion of suicide attempts ranged from 0.4% (Hanoi, Vietnam)
to 4.2% (Brisbane, Australia and Karaj, Iran). At all sites there was a
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706 M. M. Silverman
decreasing gradient between ideation and planning, as well as between

planning and attempts.
One striking finding was the great disparity across sites in the enact-
ment of the suicidal process. For instance, in Brisbane, 96% of those who
thought about suicide also planned it and 38% of those attempted it,
whereas in Hanoi, the corresponding figures were 13% and 5%. When
comparing suicide ideation rates to suicide attempt rates across these nine
cities, it became clear that there were great discrepancies overall. In addi-
tion, there was a virtually complete lack of relationship between the rate
of suicidal ideation and the clinical severity of the subsequent suicide
attempts, measured in terms of the nature and intensity of medical
attention required after the attempt.
The most relevant results of the SUPRE-MISS are those related to the
randomized controlled trial involved in the pooling of all data of the TAU
versus TAU + BIC on suicide attempters in all centers. In the group that
received the series of planned follow-ups, mortality for cases of suicide
was significantly reduced (p <. 0001) as compared to the TAU-only sub-
jects. At the 18-month follow-up, there were only two suicidal deaths in
the first group as compared to 18 suicidal deaths in the group that received
the routine care only. Furthermore, even the mortality for all other causes
was higher in the group that received only TAU.18
The findings from the WHO SUPRE-MISS community survey suggest
that a universal preventive intervention that is based on suicide ideation
only will have quite distinct and different cost-effectiveness from one
culture to another. Furthermore, there is a strong cultural underpinning
behind the whole spectrum of suicidal behaviors. Without a clear under-
standing of the local meaning and implications of suicidal ideation, any
further action, including prevention and clinical care for suicidal people,
becomes challenged.6 There is compelling evidence indicating that ade-
quate prevention and treatment of depression and alcohol and substance
abuse can reduce suicide rates, as well as follow-up contact with those
who have attempted suicide.
The WHO subsequently revised its effective strategies for suicide
prevention to include restriction of access to means of suicide (such as
toxic substances, medications, and firearms), identification and manage-
ment of persons suffering from mental disorders (particularly those with
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World Suicide 707
depression, alcoholism, and schizophrenia), improved access to health

and social services, following up people who made suicide attempts, train-
ing primary care health care workers to identify those at most risk, and
responsible reporting of suicide by the media. Probably of paramount
importance is the emphasis on the restriction of access to methods of
self-injury (prescription medications, over-the-counter drugs, pesticides,
firearms).9,10
Although the risk factors for suicide are universal, their importance and
nature differ across countries and cultures. Whereas there might be more
focus on early identification and treatment of mental disorders in
developed countries, restricting access to pesticides may have a more
significant effect in agricultural communities in low and middle income
countries. Strategies involving restriction of access to common methods
of suicide, such as firearms or toxic substances like pesticides, have
proved to be effective in reducing suicide rates; however, there is a need
to adopt approaches involving many levels of intervention and activities.
Currently, the WHO is undertaking demonstration projects for safer
access to pesticides by safer storage and education in communities in
China, India, and Sri Lanka.
11. INTERNATIONAL STUDIES ON INCREASED

RISK FOR SUICIDE
Numerous international studies have demonstrated that psychiatrically
ill individuals are at increased risk for the expression of self-destructive
behaviors, ranging from deliberate self-harm21 to suicide attempts4 to
death by suicide.20 Although almost all major psychiatric illnesses are
associated with suicidal behaviors, the following disorders have consist-
ently been found in most large-scale epidemiological studies to infer a
considerably increased risk for suicide: substance disorders (including
alcohol abuse), psychotic disorders (including the schizophrenias),
affective disorders (including bipolar disorders and depressive disor-
ders), anxiety disorders (including panic disorder and posttraumatic
stress disorder), borderline personality disorder, and impulse-control
disorders (including conduct disorder). However, because mental disor-
ders are highly comorbid, it is possible that many of the observed
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708 M. M. Silverman
associations are due to the true effects of only a smaller number of

disorders.28
The best predictor of future behavior is past behavior. Hence, the best
predictor of future suicidal behavior is a history of previous suicidal
behavior. Mental disorders are only one factor that contributes to the
development and expression of suicidal ideation and suicidal behaviors.
Several recent studies suggest that although mental disorders are strongly
predictive of suicidal ideation, they are less useful in predicting which
individuals with suicidal ideation will go on to make suicide plans and
suicide attempts.11 Nevertheless, a recent cross-national analysis of the
associations among mental disorders and suicidal behavior showed that
each lifetime disorder examined in the study significantly predicted the
subsequent first onset of suicide attempt. Overall, mental disorders were
equally predictive in developed and developing countries, with a key dif-
ference being that the strongest predictors of suicide attempts in devel-
oped countries were mood disorders, whereas in developing countries
impulse-control, substance use, and posttraumatic stress disorders were
most predictive. Of note is that the findings also showed that only half of
the people who have seriously considered killing themselves have a men-
tal disorder. Thus, although future suicide prevention efforts should focus
on screening and treating those with mental disorders, approaches must
also be found to identify those without mental disorders who also are at
risk for suicidal behaviors.28
12. INTERNATIONAL STUDIES ON

PSYCHOPHARMACOLOGICAL INTERVENTIONS
FOR MENTAL ILLNESSES ASSOCIATED WITH
SUICIDAL BEHAVIORS
Inasmuch as suicide is a behavior and is therefore multi-determined, there
does not exist a specific intervention to treat or prevent suicidal behaviors
per se. To date, the most efficacious and effective approach has been to
identify predisposing and precipitating factors that have been statistically
shown to be associated with the onset and expression of suicidal behav-
iors. Inasmuch as certain specific mental disorders, such as schizophrenia,
bipolar disorder, and major affective disorder, have been associated with
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World Suicide 709
the expression of suicidal behaviors, the reasoning has been that the
successful treatment of these disorders should result in the reduction of
suicidal behaviors among those with these disorders. In theory this is quite
reasonable and eminently testable. However, there are many obstacles to
showing a cause-and-effect relationship. Among them are the following:
(1) Suicide and suicidal behaviors are low base-rate behaviors, even
amongst those with psychiatric illnesses.
(2) Patients do not always comply with medication regimens as pre-
scribed, so it is not uncommon for patients to have sub-threshold or
sub-therapeutic blood levels of medications.
(3) Even when patients take medications at prescribed therapeutic levels,
they may not have relief of symptoms.
(4) Psychotropic medications are prescribed for multiple disorders and
dysfunctions, so inferring diagnoses and prescribing patterns from
national, regional, or large pharmaceutical data bases may not be true
indications of their use.
(5) It is difficult to extrapolate findings from a clinical population to a
general population.
Nevertheless, over the last five years, there have been an increasing
number of international studies that have suggested that the use of specific
medications for the treatment of specific mental disorders is associated
with a reduction in suicidal behaviors in those clinical populations receiv-
ing certain medications. Space precludes me from reviewing the literature
here; however, definitive studies exist for the use of clozapine to prevent
suicide attempts in the treatment of schizophrenia27 and the use of lithium
to prevent suicide in the treatment of bipolar disorder.2
13. SUICIDE RISK ASSESSMENT FROM

A CULTURAL PERSPECTIVE
There is suggestive evidence that anti-anxiety medications may be of
therapeutic benefit in lowering agitation, aggression, impulsivity, and
psychic anxiety often associated with acute suicidal states.17 Controversy
remains as to whether antidepressants, specifically the selective serotonin
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710 M. M. Silverman
reuptake inhibitors, have resulted in a decline in the suicide rate in

large-scale studies.3,22 Because of the widespread use of antidepressants in
the treatment of multiple disorders, including those not usually associated
with suicidal behaviors, it is difficult to determine in large-scale studies
the exact role that these drugs may play in effecting rates of suicide in a
given population.35
The WHO study mentioned above, as well as other international
studies, have underscored the importance of conducting a comprehensive
suicide risk assessment as a necessary part of a mental status examination
for all psychiatric patients, inasmuch as most, if not all, acutely ill psychi-
atrically ill patients are at increased risk for the development and expres-
sion of suicidal ideation and suicidal behaviors during an acute psychiatric
episode. In fact, for many seriously and chronically mentally ill patients,
suicidal ideation can be a fairly constant component of their illness. Hence
it is incumbent upon the diagnostician and the clinician to accurately
assess and monitor the presence and level of suicidal ideation, the severity
of the suicidal intent, and the degree of suicidal planning and to fully
explore all aspects of a current suicide attempt (the “who, what, when,
where, why, and how” of the behavior) as well as the history of any prior
suicidal behaviors, in order to arrive at a determination of current suicidal
risk and to develop a suicide safety plan.
The debate amongst suicidologists is what constitutes an adequate
screening question or brief set of screening questions regarding suicidal
ideation, intent, planning, and behaviors, such that a negative answer(s) will
suffice to indicate that a more comprehensive suicidal risk assessment need
not be undertaken. What short set of easily and quickly administered ques-
tions can assure the clinician that the patient is not suicidal? Unfortunately,
no short set of questions exists that has been shown to have the reliability
and validity that is required to assure the clinician that a patient is not poten-
tially suicidal, especially if the patient is acutely psychiatrically ill at the
time of the examination. Hence, in order to determine the level of suicide
risk of an individual, we then must rely on the education and clinical train-
ing of the clinician, the degree to which he or she explored and weighed the
individual’s risk and protective factors, and the extent to which the compo-
nents of a suicide risk assessment were investigated. See Table 3 for a list
of the components of a comprehensive suicide risk assessment.
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World Suicide 711
Once a suicide risk assessment is completed, a level of suicide risk —

low, medium, or high — can be determined. The next step is for a safety
plan to be developed on the basis of the level of suicide risk, level of
cognitive functioning, degree of available coping skills, severity of current
psychiatric illness, extent of the support network, degree of therapeutic
alliance, and history of previous treatment compliance.
What potentially complicates completing a comprehensive suicide risk
assessment is that in different cultures the concept of self-destructive
behaviors or self-killing has different meanings in different contexts.
Hence, there is no one question, or no set of standardized screening ques-
tions, that can be used to ensure that an individual is not potentially suicidal
or self-destructive. The assessment must be culturally sensitive and must be
context-specific, while at the same time recognizing the role that an active
psychiatric illness can play in facilitating the onset and expression of sui-
cidal thoughts and behaviors. Furthermore, an acute or chronic psychiatric
illness, such as psychosis, depression, or substance abuse, can interfere with
an individual’s ability to accurately process and respond to the clinician’s
questioning and investigation of past or current suicidal ideation, intent,
motivation, and plans. Hence, it is incumbent upon the clinician to seek out
as much collateral information as is available from medical sources,
friends, family, and significant others before arriving at a determination as
to whether an individual is at on-going risk for suicide in the near future.
14. RECOMMENDATIONS
Several important recommendations for reducing both fatal and non-fatal
suicidal behavior were developed at an international conference on violence
and health sponsored by the WHO in 2002, and although progress has
been made on some of these recommendations, they remain as relevant
today as they were when they were initially formulated.23
14.1. Better data

There is an urgent need for more complete information on the causes of
suicide, nationally and internationally, particularly among minority
groups. Cross-cultural studies should be encouraged. They can lead to a
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712 M. M. Silverman
better understanding of the causative and protective factors and conse-

quently can help improve prevention efforts. The following are some
specific recommendations for better information on suicide:
• Governments should be encouraged to collect data on both fatal

and non-fatal suicidal behavior and to make such data available to
the WHO. Hospitals and other social and medical services should
be strongly encouraged to keep records of non-fatal suicidal
behavior.
• Data on suicide and attempted suicide should be valid and up to date.
There should be a set of uniform criteria and definitions and — once
established — these should be consistently applied and continually
reviewed.
• Data collection should be easily accessible for researchers conducting
analytical and epidemiological surveys.
• Efforts should be made to improve data linkage across a variety of
agencies, including hospitals, coroners, and police departments.
• All health professionals and officials in relevant agencies should be
trained to detect and refer people at risk of suicidal behavior and to
code such cases appropriately in data collection systems.
• There is a need to collect information on social indicators — such as
quality-of-life indicators, divorce rates, and social and demographic
changes — in tandem with data on suicidal behavior, in order to
improve the current understanding of the problem.
14.2. Further research

More research should be conducted to examine the relative contribution
of psychosocial and biological factors in suicidal behavior. A greater
coupling of the two types of factors in research programs would allow for
major advances in the current knowledge on suicide. One particularly
promising area is the rapidly expanding research in molecular genetics,
where, among other things, there is now greater knowledge relating to the
control of serotonin metabolism.
More clinical research should be carried out on the causative role of
comorbid conditions, for example, the interaction between depression and
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World Suicide 713
alcohol abuse. There should also be a greater focus on subgroups of the

population by age (because suicide among the elderly has different
features from that in young people), personality, and temperament. Brain
imaging is another area that calls for more research effort. Finally, there
should be more research on the role of hostility, aggression, and
impulsivity in suicidal behavior.
14.3. Better psychiatric treatment

The considerable contribution that psychiatric factors make towards
suicidal behavior suggests that improving treatment for those with psychi-
atric disturbances is important in preventing suicide. In this respect, the
following steps should be taken:
• Pharmaceutical companies should be urged to develop more medica-

tions that are effective for psychiatric disorders.
• Research funding should be directed towards devising more effective
techniques of psychotherapy and counseling for suicidal individuals.
• Many more people need to be made aware of the signs and symptoms
of suicidal behavior and of where help, if needed, can be obtained —
whether from family and friends, doctors, social workers, religious
leaders, employers, or teachers and other school staff. Doctors and
other health care providers, in particular, should be educated and
trained to recognize, refer, and treat those with psychiatric disorders,
especially affective disorders.
• An urgent priority for governments and their health care planning
departments is the early identification and treatment of individuals
suffering not only from mental disorders, but also from drug and
alcohol abuse and dependence.
14.4. Environmental changes

A range of environmental changes are suggested for restricting access to
methods of suicide, including:
• Fencing in high bridges.

• Limiting access to the roofs and high exteriors of tall buildings.
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714 M. M. Silverman
• Obliging car manufacturers to change the shape of exhaust pipes of

vehicles and to introduce a mechanism by which the engine automati-
cally turns off after running idle for a specified duration.
• Restricting access by people other than farmers to pesticides and
fertilizers.
• Where potentially lethal medications are concerned:
— requiring strict monitoring of prescriptions by doctors and
pharmacists;
— reducing the maximum size of prescriptions;
— packaging medications in plastic blister packs; and
— where possible, prescribing medication in the form of suppositories.
• Reducing easy access to guns.
14.5. Strengthening community-based efforts

Local communities are important settings for existing suicide prevention
activities, though much more can be done to strengthen community-based
efforts. In particular, attention should be given to the following:
• Developing and evaluating community-based programs.

• Improving the quality of services for existing programs.
• Greater government funding and more professional support by gov-
ernments for activities such as the following:
— suicide prevention centers;
— support groups for people who have experienced the suicide of
someone very close to them (such as a child, an intimate partner,
or a parent) and who may thus themselves be at a heightened risk
for suicide; and
— reducing social isolation, by promoting community-based pro-
grams such as youth centers and centers for older people.
• Establishing partnerships and improving collaboration between the
relevant agencies.
• Devising educational programs to prevent suicidal behavior, not only
for schools, as is mainly the case at present, but also for workplaces
and other settings in communities.
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World Suicide 715
15. CONCLUSIONS
Suicide is one of the leading causes of death worldwide and is recognized
as a major public health problem. Suicide and attempted suicide are com-
plex phenomena that arise, in very individualistic ways, from the interplay
of biological, psychological, psychiatric, and social factors. The complex-
ity of causes necessarily requires a multifaceted approach to prevention
that takes into account cultural context. Cultural factors play a major role
in suicidal behavior,13 producing large differences in the characteristics of
this problem around the world.30 Given these differences, what has a
positive effect in preventing suicide in one location may be ineffective or
even counterproductive in another cultural setting.
Global figures and statistics about suicide and suicide attempts provide
a broad view of the scope of the problem, especially as it relates to other
causes of morbidity and mortality. However, these numbers and rates
mask important regional, national, and local characteristics. Therefore,
although we need to think globally to prevent suicide, we must act locally.
If governments commit to defining national responses to prevent suicide
among all ages, huge progress can be made. If we build networks and alli-
ances to promote common approaches that support governments in plan-
ning and implementing their national responses, we will find that suicide
is a huge but largely preventable public health problem.
Major investment is needed, both for research and for preventive
efforts. While short-term efforts contribute to an understanding of why
suicide occurs and what can be done to prevent it, longitudinal research
studies are necessary to fully understand the role of biological, psychoso-
cial, and environmental factors in suicide. There is also a great need for
rigorous and long-term evaluations of interventions. To date, most pro-
jects have been of short duration with little, if any, evaluation. Finally,
suicide prevention efforts will be ineffective if they are not set within the
framework of large-scale plans developed by multidisciplinary teams,
comprising government officials, health care planners and health care
workers, and researchers and practitioners from a variety of disciplines
and sectors. Major investments in planning, resources, and collaboration
between these groups will go a long way toward reducing this important
international public health problem.
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716 M. M. Silverman
16. KEY POINTS

• Suicide is a behavior, not a diagnosis, and must be understood as a
consequence of multiple factors and determinants, often interpersonal
in nature and often related to perceived losses.
• Suicidal behaviors can be impulsive and secondary to acute losses, so
always ask about a history of impulsive behaviors and the previous
management of unanticipated losses.
• Suicide is often associated with psychiatric illnesses, especially in
their acute phases and especially when a patient is actively psychotic,
depressed, or under the influence of alcohol or other drugs.
• Just because a patient does not have a significant number of suicidal
risk factors it does not mean that the patient is not potentially suicidal.
• Never accept “No” to the question “Are you currently having thoughts
of killing yourself?” as indicating that an individual is not potentially
suicidal. Suicidal ideation and suicidal intent waxes and wanes
throughout the course of a day or over a few days, so if there is any
indication at all of the potential for suicidal risk, explore the risk
beyond asking about current ideation.
• If the clinician is not comfortable with discussing suicide openly and
frankly with the patient, the patient will not feel comfortable discuss-
ing his or her suicidal ideation, intent, planning, or past suicidal
behaviors.
• Placing a psychiatrically ill patient on an antidepressant or antipsy-
chotic may not in the short term decrease the risk for suicide.
Immediately addressing the level of anxiety and agitation may be
more protective.
17. SELF-ASSESSMENT
17.1. You have just been asked to serve as a medical consultant
to the new Deputy Minister of Health for a developing
country whose major economic resource is agriculture.
You have been asked to consult on the suicide problem
in this country. The Deputy Minister of Health wants a
solution to the problem as fast as possible and has asked
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World Suicide 717
you for your best advice as to how to lower the suicide rates
in the next 12 months.
Before you agree to accept this consultation, you ask the
Deputy Minister of Health for which of the following
information:
(A) Suicide rates by age, gender, race, and geographical location by year
for the last 10 years.
(B) Death rates by all causes by year for the last 10 years.
(C) The manner of death by suicide by year for the last 10 years.
(D) The number and location of hospitals throughout the country.
(E) The number, level of training, and location of medical personnel
throughout the country.
Answer: All of the above. In order to begin to understand the extent of a

national suicide problem, you must first look at the problem from a public
health perspective and identify the risk and protective factors that are
associated with the disorder. In this case, you would want to know how big is
the problem (Increasing over time? Decreasing?), how big is the problem as
compared to other related problems (Are suicidal deaths disproportionately
high?), for whom is it a problem (Men? Women? Natives? Migrants? Youth?
Elderly?), where is it a problem (Urban? Rural?), when is it a problem
(Fall? Spring?), how are people dying by suicide (What methods are they
using? Do they have easy access to lethal means of suicide? Are pesticides
the problem?), are people dying by suicide because no medical intervention
is readily available (Is access to medical care scarce in locations where
suicide rates are high? Are hospitals ill-equipped or ill-prepared to treat
suicide attempters?), and are medical personnel appropriately trained to
assess, diagnose, and treat those disorders and dysfunctions associated with
increased risk for suicidal behaviors (Is it a problem of lack of awareness
by medical personnel or is it a lack of public education about identifying
warning signs of increased risk for suicide? Or is it both?).
In order to advise the Deputy Minister of Health about the likelihood
of significantly reducing the suicide rate in 12 months, or in 12 years, you
must first determine what are the most likely predisposing and precipitating
factors contributing to the suicide rates and which ones are most amenable
to interventions at the local, regional, and national levels. You also might
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718 M. M. Silverman
want to develop a “map” or causal chain of events that lead to a typical

suicidal death in this population and look for points where you can
develop and insert interventions to prevent that fatal outcome.34
17.2. A 28-year-old, recently separated, intoxicated male is

brought into the Emergency Department following an
apparent overdose of sleeping pills after a verbal fight on
the telephone with his estranged wife. He told her on the
telephone that he would continue to swallow sleeping pills
until she agreed to come back to live with him. Instead she
hung up and called the police, who went to his apartment
and brought him to the emergency room. The first course
of action was to medically stabilize the patient and to
ensure that he had not ingested a lethal amount of sleeping
pills. The next step was to wait until he was no longer
inebriated before conducting a standard mental status
examination. When asked if he was thinking of killing
himself, he replied, “No, I did not want to kill myself. I was
only trying to get my wife’s attention.”
As the examining clinician, your next step, after
completing the rest of the mental status examination, is to:
(A) Educate the patient about his drinking, and refer him to a substance
abuse counselor for a follow-up appointment.
(B) Educate the patient about his drinking, and refer him to a marital
therapy counselor for a follow-up appointment.
(C) Ask the patient if he has ever had any similar episodes such as this one
in his past.
(D) Ask the patient if he would voluntarily sign in to the inpatient psychi-
atric unit.
(E) Ask the patient if there is anyone he could stay with for the next few
days.
Answer: C. Until a complete suicide risk assessment is completed, it remains

unclear whether this individual was suicidal when he was threatening his
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World Suicide 719
wife by swallowing sleeping pills and whether he is at increased risk for

another self-destructive episode when he is under the influence of alcohol.
We do not know whether this is a behavioral pattern that occurs while
intoxicated (and possibly prompted his wife to leave him in the first place)
or whether this episode represents an escalation of a depression secondary
to his marital separation or a depression secondary to alcohol abuse. We
need to know whether he has a history of suicide attempts, suicidal ideation,
or exposure to suicidal behaviors (family history). Is his alcohol abuse
recent or long-standing? The fact that he has lethal means of self-injury
readily available to him (alcohol plus sleeping pills) is reason to be con-
cerned enough to warrant a full suicide risk assessment. One obvious ques-
tion is what would have happened if his wife had not hung up and called the
police. Would he have continued to swallow the sleeping pills? Did he count
out the pills before calling her? Did he know how many pills he had swal-
lowed? Does he know how much alcohol and pills it would take to kill
himself? Before discharging him from the emergency room, we have to be
sure that he does not have enough sleeping pills at home to kill himself and
that he has a safety plan in place if he should become depressed, despond-
ent, or suicidal again about his marital situation.31
REFERENCES
1. Adjacic-Gross V, Weiss MG, Ring M, Hepp U, Bopp M, Gutzwiller F,
Rossler W. (2008) Methods of suicide: International suicide patterns derived
from the WHO mortality database. Bull WHO 86(9): 726–732.
2. Baldessarini RJ, Tondo L, Davis P, Pompili M, Goodwin FK, Hennen J.
(2006) Decreased suicidal risk during long-term lithium treatment: Meta-
analysis. Bipolar Disord 8: 625–639.
3. Baldesssari RJ, Pompilli M, Tondo L. (2006) Suicidal risk in antidepressant
trials. Arch Gen Psychiatry 63: 246–248.
4. Beautrais AL, Joyce PR, Mulder RT, Fergusson DM, Deavoll BJ, et al. (1996)
Prevalence and comorbidity of mental disorders in persons making serious
suicide attempts: A case-control study. Am J Psychiatry 153: 1009–1014.
5. Bertolote JM. (2001) Suicide in the world: An epidemiological overview,
11995–2000. In: Wasserman D (ed.), Suicide: An Unnecessary Death,
pp. 3–10, Martin Dunitz, London.
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6. Bertolote JM, Fleischmann A. (2009) A global perspective on the magnitude

of suicide mortality. In: Wasserman D, Wasserman C (eds.), Oxford Textbook
of Suicidology and Suicide Prevention: A Global Perspective, pp. 91–98.
Oxford University Press, Oxford.
7. Bertolote JM, Fleischmann A, De Leo D, Wasserman D. (2009) Suicidal
thoughts, suicide plans and attempts in the general population on different
continents. In: Wasserman D, Wasserman C (eds.), Oxford Textbook of
Suicidology and Suicide Prevention: A Global Perspective, pp. 99–104,
Oxford University Press, Oxford.
8. Bertolote JM, Fleischmann A, De Leo D, Bolhari J, Botega N, De Silva D,
Thanh HTT, Phillips M, Schlebusch L, Varnik A, Vijayakumar L,
Wasserman D. (2005) Suicide attempts, plans, and ideation in culturally
diverse sites: The WHO SUPRE-MIISS community survey. Psychol Med
35: 1457–1465.
9. Bertolote JM, Fleischmann A, Eddleston M, Gunnell D. (2006) Deaths from
pesticide poisoning: A global response. Br J Psychiatry 189: 201–203.
10. Bertolote JM, Fleischmann A, Butchart A, Besbelli N. (2006) Suicide,
suicide attempts and pesticides: A major hidden public health problem. Bull
WHO 84(4): 260–261.
11. Borges G, Angst J, Nock MK, Ruscio AM, Kessler RC. (2008) Risk factors
for the incidence and persistence of suicide-related outcomes: A 10-year
follow-up study using the National Comorbidity Surveys. J Affect Disord
105: 25–33.
12. Chan KP, Yip PS, Au J, Lee DT. (2005) Charcoal-burning suicide in post-
transition Hong Kong. Br J Psychiatry 186: 67–73.
13. De Leo D. (1999) Cultural issues in suicide and old age. Crisis 20: 53–55.
14. De Leo D, Bertolote JM, Lester D. (2002) Self-directed violence. In: Krug
E, Dahlberg L, Mercy J, et al. (eds.), World Report on Violence and Health,
pp. 183–212, World Health Organization, Geneva.
15. De Leo D, Evans R. (2004) International Suicide Rates and Prevention
Strategies. Hogrefe & Huber, Gottingen.
16. Diekstra RF, Garnefski N. (1995) On the nature, magnitude, and causality of
suicidal behaviors: An international perspective. Suicide Life Threat Behav
25: 36–57.
17. Fawcett J. (2001) Treating impulsivity and anxiety in the suicidal patient.
Ann N Y Acad Sci 932: 94–102.
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World Suicide 721
18. Fleischmann A, Bertolote JM, Wasserman D, De Leo D, Bolhari J, Botega NJ,

et al. (2008) Effectiveness of brief intervention and contact for suicide
attempters: A randomized controlled trial in five countries. Bull WHO 86:
703–709.
19. Goldney RD, Smith S, Winefield AH, et al. (1990) Suicidal ideation:
Its enduring nature and associated morbidity. Acta Psychiatr Scand 83:
115–120.
20. Harris EC, Barraclough B. (1997) Suicide as an outcome for mental disor-
ders. A meta-analysis. Br J Psychiatry 170: 205–228.
21. Hawton K, Houston K, Haw C, Townsend E, Harriss L. (2003) Comorbidity
of axis I and axis II disorders in patients who attempted suicide. Am J
Psychiatry 160: 1494–1500.
22. Henriksson S, Isacsson G. (2006) Increased antidepressant use and fewer
suicides in Jamtland county, Sweden, after a primary care educational pro-
gramme on the treatment of depression. Acta Psychiatr Scand 114: 159–167.
23. Krug EG, Dahlberg LL, Mercy JA, Zwi AB, Lozano R. (2002) Self-directed
violence. In: World Report on Violence and Health, Chapter 7, pp. 183–212,
World Health Organization, Geneva.
24. Lester D, Yang B. (1998) Suicide and Homicide in the in 20th Century. Nova
Science, Commack, NY.
25. Maris RW, Berman AL, Silverman MM. (2000) Comprehensive Textbook of
Suicidology, Guilford Publications, NY.
26. McIntosh JL, Santos JF, Hubbard RW, Overholser JC. (1994) Elder Suicide:
Research, Theory, and Treatment, American Psychological Association,
Washington, DC.
27. Meltzer HY, Alphs L, Green AI, Altamura AC, Anand R, Bertoldi A, et al.
(2003) International suicide prevention trial study group. Clozapine treat-
ment for suicidality in schizophrenia: International suicide prevention trial
(InterSePT). Arch Gen Psychiatry 60: 82–91.
28. Nock MK, Hwang I, Sampson N, Kessler RC, Angermeyer M, Beautrais A,
Borges G, Bromet E, Bruffaerts R, de Girolamo G, de Graaf R, Florescu S,
Gureje O, Haro JM, et al. (2009) Cross-national analysis of the associations
among mental disorders and suicidal behavior: Findings from the WHO
world mental health surveys. PLoS Med 6(8): e1000123.
29. Phillips MR, Yang, GH. (2004) Suicide and attempted suicide in China,
1990–2002. Morb Mortal Wkly Rep 53(22): 481–484.
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722 M. M. Silverman
30. Schmidtke A, Weinackera B, Apter A, Batt A, Berman AL, Bille-Brahe U,

et al. (1999) Suicide rates in the world: An update. Arch Suicide Res 5:
81–89.
31. Shea SC. (1999) The Practical Art of Suicide Assessment: A Guide
for Mental Health Professionals and Substance Abuse Counselors.
John Wiley & Sons, Inc., NY.
32. Shenassa ED, Catlin SN, Buka SL. (2003) Lethality of firearms relative to
other suicide methods: A population based study. J Epidemiol Community
Health 57, 120–124.
33. Stoudemire A, Frank R, Hedemark N, Kamlet M, Blazer D, et al. (1986) The
economic burden of depression. Gen Hosp Psychiatry 8: 387–394.
34. Taylor SJ, Kingdom D, Jenkins R. (1997) How are nations trying to prevent
suicide? An analysis of national suicide prevention strategies. Acta Pychiatr
Scand 95: 457–463.
35. Tondo L, Baldessarini RJ. (2006) Trends in suicide rates: An international
perspective (abstract). Ital J Psychopathol 12(Suppl. 2): 202–203.
36. United Nations. (1996) Prevention of Suicide: Guidelines for the Formulation
and Implementation of National Strategies, United Nations (document
ST/SEA/245), NY.
37. World Health Organization. (1993) Guidelines for the Primary Prevention of
Mental, Neurological and Psychological Disorders, World Health
Organization, Geneva.
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Chapter 28
AIDS Psychiatry
Mary Ann Cohen
1. THE SCOPE OF THE AIDS PANDEMIC

AND RELEVANCE TO PSYCHIATRY
In the modern world, few medical illnesses are as stigmatized as acquired
immune deficiency syndrome (AIDS) has been over the past 30 years
since the first previously healthy young men and women presented with
the mysterious symptoms of immune deficiency, pneumonia, and severe
respiratory distress and died of respiratory failure. Gradually, as the mys-
teries of transmission, cause, and course of the illness were solved and an
human immunodeficiency virus (HIV) subspecialty of infectious disease
medicine was developed, HIV clinicians and scientists helped transform
AIDS from an inevitably fatal illness into a chronic illness for many per-
sons in areas of the world where there is access to competent medical care
and antiretroviral medications. Although amazing strides have catalyzed
this transformation, three unsolved HIV mysteries remain throughout the
world. These are the mysteries of continuing transmission of HIV from
seropositive to seronegative individuals, continuing transmission of HIV-
associated stigma, and the lack of access to early diagnosis of HIV and to
competent medical care and treatment with antiretroviral medications.
According to global estimates from the UNAIDS 2009 AIDS Epidemic
Update, 33.4 million adults and children are living with HIV, with 2.7
million newly infected annually and two million dying of AIDS each year.
723
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724 M. A. Cohen
More than 25 million people have died of AIDS since 1981. Around
half of persons with HIV are women and half become infected before
age 25 years of age making AIDS the second most common cause of death
among 20–24 year olds. As of 2008, the AIDS pandemic had left behind
15 million AIDS orphans throughout the world. Ironically, while the
global rate of new HIV infections has decreased from 5.3 million in 2002
to 2.7 million in 2008, in the United States, the incidence of new infec-
tions rose from 40,000 in 2002 to 55,000 in 2008. The majority of persons
living with HIV and AIDS are living in developing countries where access
to medical care and antiretroviral therapy is inadequate. While sub-
Saharan Africa has only 10% of the world’s population, it has 67% of all
persons living with HIV. Asia and Eastern Europe also have rapidly grow-
ing AIDS epidemics. Global estimates suggest that while 9.5 million
persons with AIDS need antiretroviral therapy, only 4 million or 42% have
access to treatment. AIDS is unique among severe and complex illnesses
in that it is entirely preventable. The primary mode of HIV transmission
throughout the world is sexual transmission and is preventable with bar-
rier contraception. The second most common mode of transmission is
from injecting drug use although use of other substances can lead to sex-
ual coercion and unprotected sex. Gender-based violence throughout
the world results in rape, sexual coercion, and childhood sexual abuse.
The “Virgin Cure” myth of AIDS prevention and treatment is likely to be
responsible for the rape of infants and babies in very few areas of the
world. However, incest, childhood sexual enslavement, and childhood
sexual abuse are responsible for severe trauma as well as HIV transmis-
sion in many areas of the world. Disparities in the prevention, diagnosis,
and treatment of HIV infection are tragic and multidimensional. These
disparities are based on social, cultural, economic, and political as well as
psychiatric factors.
Substance use disorders as well as many other psychiatric disorders are
major vectors of HIV transmission worldwide. Injecting drug use and sex
work complicate and perpetuate the HIV pandemic. Alcohol and other
drug use lead to intoxication, inappropriate partner choice, violent and
coercive sexual behaviors, and lack of use of barrier contraception.
Sharing of needles and other drug paraphernalia are also instrumental in
direct HIV transmission. The exchange of sex for drugs leads to HIV
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AIDS Psychiatry 725
transmission and also intimate partner violence and coercive sexual

activity. The indirect impact of alcohol and other substance abuse may be
almost immeasurable when accounting for the impact of intimate partner
violence, child abuse, neglect, abandonment, as well as future develop-
ment of posttraumatic stress disorder in adults with early childhood
trauma leading to repeating their own history or lack of self-care and
unhealthy partner choices and use of drugs and alcohol to numb the pain
associated with trauma. In developing countries, lack of access to psychia-
trists and other mental health combines with lack of access to antiretroviral
therapy to further perpetuate the AIDS pandemic.
Psychiatric factors play an important role in perpetuating transmission
of HIV as well as HIV stigma. Psychiatric disorders and distress play a
significant role in the transmission of, exposure to, and infection with
HIV. They are relevant to prevention, clinical care, and adherence through-
out every aspect of illness from the initial risk behavior to death. They
result in considerable suffering from diagnosis to end-stage illness. This
chapter will provide the reader with clues to help solve the mysteries
involved with prevention of HIV and HIV stigma, improvement in access
to diagnosis and treatment, and amelioration of suffering, morbidity, and
mortality in the care of persons with HIV and AIDS.
2. A BIOPSYCHOSOCIAL APPROACH TO PSYCHIATRIC

DIAGNOSIS IN PERSONS WITH HIV AND AIDS
Since the evolution of antiretroviral therapy from a single medication
(zidovudine) into the treatment with combinations of antiretroviral
medications (antiretroviral therapy or ART) in 1995, persons with HIV
and access to medical care and ART are no longer dying of AIDS but are
dying of other multimorbid and severe medical illnesses as are compa-
rable populations without HIV infection. However, when psychiatric
disorders interfere with adherence to care, persons with HIV and AIDS
are dying as they did in early in the pandemic prior to the development
of antiretrovirals.10,11 Psychiatric disorders can limit access to HIV care
from before birth to the end of life. Perinatal HIV transmission is pre-
ventable with antiretroviral treatment but women who are pregnant and
HIV positive may lack prenatal care if severe mental illness is not
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726 M. A. Cohen
recognized and treated. Throughout the lifecycle, non-adherence can

result in transmission of infection or progression of illness in persons
with HIV. This is especially significant in persons of older age who are
not often thought of as vulnerable to HIV and are often recognized late
and progress more rapidly to death.17 At any age, risky behaviors such
as having sexual intercourse without a condom or sharing of parapher-
nalia in injecting drug use can result in transmission of HIV as well as
other blood borne infections. Progression of illness can occur when
children with AIDS transition from adolescence to adulthood and rebel
against following a carefully prescribed regimen, to persons with sub-
stance dependence who prioritize cocaine, crystal methamphetamine, or
heroin over medical care, or to persons with depression, mania, post-
traumatic stress disorder (PTSD), psychosis, or cognitive disorders.
Some individuals with HIV or AIDS and no psychiatric disorder may
become non-adherent to antiretrovirals because of side effects such as
lipodystrophy resulting in disfigurement (sunken cheeks from lipoatro-
phy of the face, buffalo hump, deposition of abdominal fat or “protease
paunch”) that may be perceived as stigma or an obvious sign and invol-
untary disclosure of HIV infection. AIDS is a paradigm for psychoso-
matic medicine and the need for a biopsychosocial approach to
care.7,10–12
Figure 1 provides a graphic representation of AIDS as multimorbid,
complex, and severe illness.
AIDS psychiatry has become a subspecialty of psychosomatic medi-
cine similar to psychonephrology, psychooncology, and transplant
psychiatry. A body of AIDS psychiatry literature includes a textbook
one edited by Cohen and Gorman,11 a handbook by Cohen and col-
leagues,10 and many thousands of articles and chapters. The Academy
of Psychosomatic Medicine AIDS Psychiatry Special Interest Group
has a growing membership of national and international members.
Founded as a Special Interest Group of the Academy of Psychosomatic
Medicine (APM) in 2004, the group meets annually and is dedicated to
providing a network and forum for AIDS psychiatrists and other men-
tal health clinicians. It can be accessed on the Web.2 While AIDS is
similar to other severe and complex medical illnesses, AIDS presents
special challenges, such as its public health implications and stigma,
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AIDS Psychiatry 727
Multimorbid Severe and Complex

Tabo
Multisystem Illness Cardiac
Topics Hepatitis C HIV-Nephropathy Dermatological
Sex Endocrinological
Drugs Depression Dementia Delirium
GI
Infection Psychosis Injecting Drug Use Infectious
Death PTSD PCP CMV PML Neurological
Prevention Oncological
Ophthalmological
Alcohol treatment
Barrier contraception
Drug treatment
AIDS Psychiatric
Pulmonary
Safe sex
Sterile works
Psychiatry Renal
Lethality
Adherence to Prevention and Treatment
Women African Latino- Men who
have sex Addicts Children Elderly
American American with men
Vulnerable Populations
Fig. 1. AIDS psychiatry as a psychosomatic medicine paradigm.
that make it a very different illness. These differences are summarized

in Table 1.
AIDS stigma and discrimination against persons with HIV and AIDS
was described in 19895 as “AIDSism.” AIDSism results from a multiplicity
of prejudicial and discriminatory factors and is built on a foundation of
racism, homophobia, ageism, addictophobia, misogyny, and discomfort
with mental and medical illness, poverty, and sexuality as well as fears of
contagion and death in many communities throughout the world as well as
in the United States. Although the medical profession has made great
strides against discrimination and stigma, AIDSism still exists. In May
2009, Lambda Legal filed suit in United States federal court (Franke
versus Parkstone Living Center, Inc.) on behalf of a 75-year-old university
provost who fulfilled all criteria for admission to an Arkansas assisted
living facility but was forced to leave the facility on the day after arrival
when detailed review of his medical records indicated HIV seropositivity.15
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728 M. A. Cohen
Table 1. How AIDS differs from most other severe and complex medical illnesses.
Pathophysiology
Infectious etiology
Modes of transmission: unsafe sex, sharing of needles in injecting drug use, perinatal
Public Health Implications
AIDS is preventable and contagious
Disinhibition induced by HIV-associated dementia, substance use, or other psychiatric
disorders can lead to HIV, HBV, HCV, and STD transmission
Recognition and treatment of psychiatric disorders can prevent HIV transmission as well
as AIDS progression and ameliorate suffering throughout the course of illness
Unique Issues
AIDS stigma and discrimination or AIDSism5
Age of onset from birth to old age
Treatment, stabilization, or prevention with antiretrovirals is possible
Exacerbation by treatment with antiretrovirals can occur — IRIS4
Multiple infections and complex medical multimorbidities
Complex psychiatric multimorbidities
High prevalence of psychiatric disorders including substance use and its consequences
High prevalence of delirium due to infectious, respiratory, cardiac, metabolic illnesses
High prevalence of delirium due to end-stage renal and liver disease
High prevalence of HIV-associated dementia
HIV is the most frequent cause of treatable dementia in persons under 501
Unique neurological deficits, paresis, paralysis, pain, and behavioral manifestations
3. DIAGNOSIS AND TREATMENT IN AIDS

PSYCHIATRY
The psychiatric aspects of AIDS psychiatry are best illustrated with clini-
cal examples. These case vignettes represent the gamut of painful and
complex medical, psychiatric, and psychosocial issues that result in severe
distress and non-adherence to medical care and ART as well as to reduc-
tion in the risk behaviors that lead to HIV transmission. These illustrative
examples provide clinicians with some of the most frequent, salient, and
potentially risky presenting problems in AIDS psychiatry in different
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AIDS Psychiatry 729
medical settings. Persons with HIV and AIDS at different stages of illness
and different ages are represented.
4. COGNITIVE DISORDERS IN HIV AND AIDS

One of the most complicated aspects of caring for persons with HIV and
AIDS is the high prevalence of cognitive disorders at any age and at any
stage of HIV infection. As we enter the 30th year of the AIDS pandemic,
it is important to understand how to recognize and care for persons
with HIV-associated neurocognitive impairment and other cognitive
disorders.
Three clinical vignettes will illustrate the important clues to look for
and how to distinguish cognitive disorders in persons with HIV and
AIDS.
4.1. HIV-associated neurocognitive disorder

Significant clues to diagnosis and treatment of HAND:
• HIV-associated neurocognitive disorder (HAND) is prevalent AIDS

long-term-care settings.
• This vignette illustrates that although CART has had a major impact
on both morbidity and mortality in persons with AIDS, HAND is still
prevalent and is the most common treatable cause of dementia in
persons under 50 years of age.1
• It is important to diagnose HIV infection early and begin CART, since
there is evidence that HIV begins to damage the brain within months
of infection.
• Every person with HIV infection needs a comprehensive evaluation
for cognitive impairment at baseline and at least twice yearly to
ensure early diagnosis and of HAND. For a description of a
comprehensive psychiatric assessment for HAND and other psychiat-
ric disorders in persons with HIV and AIDS, see the relevant
references.9,11
• HAND is a prevalent diagnosis young persons as well as in elderly
persons with HIV and AIDS.
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730 M. A. Cohen
Table 2. Differential diagnosis of visual hallucinations in late-stage AIDS.
Medical causes
Infectious
• Cytomegalovirus (CMV) retinopathy
• Sepsis
• Fungemia
• Immune reconstitution inflammatory syndrome (IRIS)
Neurologic causes
• Space-occupying lesions of brain: CNS lymphomas, toxoplasmosis, PML
• Seizures: Ictal, interictal, and postictal states
Psychiatric causes
Substance use disorders
• Alcohol withdrawal
• Benzodiazepine withdrawal
• Hallucinogens
• Amphetamine and other stimulants
Delirium
Toxic or drug-induced delirium
• Intoxication: Sedative-hypnotics, alcoholic hallucinosis, opiates
• Drugs: Antibiotics, anticholinergics, anticonvulsants, antineoplastic drugs,
antiretrovirals, ketamine, lithium, narcotic analgesics
• Withdrawal: Alcohol, sedative-hypnotics
Metabolic encephalopathy
• Hypoxia
• Hepatic, renal, pulmonary, pancreatic insufficiency
• Hypoglycemia
Disorders of fluid, electrolyte, and acid-base balance
• Dehydration
• Lactic acidosis (secondary to antiretroviral treatment)
• Hypernatremia, hypokalemia, hypocalcemia, hypercalcemia, alkalosis, acidosis
Endocrine disorders
• Hypothyroidism
• Pancreatitis and diabetes mellitus
Infections
• Systemic: Bacteremia, septicemia, infective endocarditis, bacterial pneumonia,
Pneumocystis jerovici pneumonia, cryptococcal pneumonia
(Continued)
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AIDS Psychiatry 731
• Herpes zoster
• Disseminated Mycobacterium avium-intracellulare complex
• Disseminated candidiasis
• Intracranial: Cryptococcal meningitis, HIV encephalitis, tuberculous meningitis,
toxoplasmosis
Malnutrition and Vitamin deficiency
• Protein energy undernutrition
• Vitamin B12 deficiency
• Thiamine deficiency and Wernicke’s encephalopathy
• Wasting and failure to thrive
Neoplastic
• Space-occupying lesions: CNS lymphoma, CNS metastases, cryptococoma,
toxoplasmosis
• Paraneoplastic syndromes associated with lung and other neoplasms
Neurologic
• Seizures: Ictal, interictal, postictal states
• Head trauma
• Space-occupying lesions of brain: CNS lymphomas, toxoplasmosis, CMV infection,
abscesses, cryptococcoma
Hypoxia
• Pneumocystis jerovici pneumonia
• Pulmonary hypertension
• Cardiomyopathy
• Coronary artery disease
• End-stage pulmonary disease
• Anemia
Psychotic Disorders
• Schizophrenia
• Schizoaffective disorder
Mood Disorders
• Major depressive disorder with psychotic features
• Mania
Anxiety Disorders
• Posttraumatic Stress Disorder with Psychotic Features
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732 M. A. Cohen
• CART reduces the severity and slows progression of HAND. The

CART that reduces the CSF viral load, can induce full recovery in
some persons with HAND.
• HAND leads to non-adherence if patients are not supervised and
cannot remember to take medication or to keep appointments. Direct
observation therapy in the nursing home setting led to a full reversal
of Mr C’s dementia.
• This vignette illustrates the reversibility of HAND as well as role of
AIDS psychiatrists in its prevention and treatment.
4.2. Delirium
Delirium is prevalent in acute as well as long-term care settings and is
also a highly prevalent diagnosis in persons with HIV and AIDS.
Establishing the cause of delirium is complicated by both HIV-related
medical conditions as well as multimorbid medical conditions and their
treatments.
• Delirium is rarely recognized by HIV clinicians and is rarely men-

tioned in reasons for consultation although it is the most common
reason for consultation in the inpatient medical setting.
• Hypoactive delirium is prevalent in persons with HIV and AIDS, can
masquerade as depression, and is easily resolved when the underlying
cause is identified and treated.
• It is often possible to identify a specific cause in persons with HIV and
AIDS (see Table 2 for the differential diagnosis of delirium in AIDS).
• Delirium may be overlooked in persons with HIV and AIDS since it
can be prevalent in any age group, while in other illnesses it is more
prevalent in older individuals.
• Delirium is a prevalent diagnosis in the inpatient medical setting in
persons with AIDS and may be overlooked because it often mimics
other psychiatric disorders. Hypoactive delirium often masquerades
as depression while hyperactive or agitated delirium often masquer-
ades as mania or psychosis.
• Delirium may be superimposed on HIV-associated neurocognitive
disorder.
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AIDS Psychiatry 733
5. MOOD DISORDERS IN HIV AND AIDS

Depression is prevalent in persons with HIV and AIDS. Depression and
other mood disorders are multifactorial and may be related to stigma
as well as to biological, psychological, and genetic factors. Both
depression and suicide are prevalent in persons with HIV and
AIDS.9–11
Suicide is a tragic, prevalent, and risky complication of depression and
of HIV and its stigma, AIDSism. Every person with HIV should be evalu-
ated depression and suicidal ideation. Suicide is preventable if depression
is diagnosed and adequately treated.
6. ANXIETY DISORDERS IN HIV AND AIDS:

POSTTRAUMATIC STRESS DISORDER
PTSD is a prevalent and risky diagnosis in persons with HIV.10 Intimate
partner violence, history of childhood trauma and childhood sexual
trauma, are all risk factors for HIV infection as well as for PTSD. The
severity of HIV-related PTSD symptoms is associated with a greater
number of HIV-related physical symptoms, extensive history of pre-
HIV trauma, decreased social support, increased perception of stigma,
and negative life events. PTSD is often a multimorbid with other psychi-
atric and medical disorders, pain, and depressive symptoms. PTSD is
associated with non-adherence to risk reduction and medical care.8 It is
often difficult to diagnose PTSD in persons with HIV since its symp-
toms may be overshadowed by associated psychiatric disorders includ-
ing substance use disorder, mood disorders, and HIV-associated
dementia, and delirium. Diagnosis is further complicated by repression
or retrograde amnesia for traumatic events, difficulties with in forming
trusting relationships and disclosing trauma if it is recalled, and non-
adherence to care.
PTSD is often overlooked in persons with HIV and AIDS since it may
be overshadowed by other psychiatric diagnoses. A biopsychosocial
approach and integrated psychiatric and medical care are essential in
AIDS psychiatry and are necessary in prevention of perinatal transmission
of HIV infection.
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734 M. A. Cohen
7. CLINICAL DECISION-MAKING AND TREATMENT

IN AIDS PSYCHIATRY
7.1. Clinical decision-making
Clinical decision-making in persons living with HIV and AIDS takes into
account not only the multimorbid medical and psychiatric illnesses but
also the need for prevention of HIV transmission and the alleviation of the
distress and suffering of persons infected and affected by the illness.
Psychiatric illness is prevalent in persons with HIV infection and HIV
infection is prevalent in persons with severe mental illness. The most
important factors in clinical decision-making are:
7.1.1. Psychosomatic medicine and prevention

of HIV transmission
• Prevention of early childhood trauma through prenatal and parenting
education.
• Designing educational programs for children and adolescents to
prevent unsafe sex and substance abuse and other risky behaviors.
• Recognition of, education about, and treatment of risky behaviors and
their causes.
• Need to address prevention and diagnosis issues in all age ranges:
Childhood to older age.
• Education of clinicians.
• Encouraging availability of condoms in inpatient and outpatient
settings.
• Education of staff about offering testing for HIV.
• Education about reduction of risk behavior, harm reduction.
• Training about sexual and drug history-taking.
7.1.2. Recognition and treatment of psychiatric

disorders — diagnostic mnemonic A, B, C, D
• Anxiety and PTSD.
• Bereavement.
• Bipolar disorder and mania secondary to HIV.
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AIDS Psychiatry 735
• Cognitive disorders — delirium and HIV-associated neurocognitive

disorders.
• Drug and alcohol dependence.
• Depression.
• Demoralization.
7.1.3. Comprehensive psychiatric evaluation

Each person with AIDS who is referred for psychiatric treatment should be
carefully evaluated at baseline and periodically evaluated for the following:
• Risk behaviors and histories — relational patterns, sexual behaviors,

and drug use.
• Depression.
• Suicidal ideation and history.
• Cognitive impairment.
8. TREATMENT ISSUES
8.1. Psychotherapeutic modalities
AIDS is a severe and complex medical and psychiatric illness that responds
best to psychotherapeutic treatments. The pill burden imposed by multi-
morbid medical conditions in addition those associated with HIV mitigates
against adding additional medications and can complicate the regimen by
altering levels of antiretrovirals. There is a growing evidence base that
illustrates the importance of these modalities including support groups,16,18
and psychotherapy.3 Choice of therapy from cognitive behavioral to
psychoanalytic and psychodynamic psychotherapy needs to be tailored to
the needs of individuals, couples, and families coping with AIDS.
The full range of psychotherapeutic and other therapeutic modalities
are relevant in persons with HIV and AIDS:
• Individual, couple, family, and group psychotherapy.

• Crisis intervention.
• Palliative psychiatry.
• Bereavement therapy.
B1405_Ch-28.indd 735 1/31/2013 2:42:34 PM

736 M. A. Cohen
• Spiritual support.
• Relaxation response.
Wellness interventions including exercise, yoga, keeping a journal or

writing a life narrative, reading, artwork, movement therapy, and listening
to music or books on tape.
8.2. Psychopharmacology and AIDS psychiatry

8.2.1. General principles
Accurate diagnosis and awareness of drug–drug and drug-illness interac-
tions are of primary importance in AIDS psychiatry and it is important to
become familiar with resources in the literature as well as those online
that are updated regularly.13,14
The principle of geriatric psychopharmacology is even more significant
in AIDS psychiatry: START VERY LOW and GO VERY SLOW.
Persons with AIDS are exquisitely vulnerable to extrapyramidal and
anticholinergic side effects of psychotropic medications.
8.2.2. Psychopharmacology and addictive disorders10,11

Become familiar with medications that are cytochrome P450 3A4 induc-
ers since these medications can lower levels of methadone in persons on
agonist treatment and will lead to opioid withdrawal symptoms discon-
tinuation of antiretrovirals or relapse to heroin.
Cytochrome P450 3A4 inducers include carbamazepine, efavirenz,
nevirapine, ritonavir, and St. John’s wort.
When a person with AIDS and pain is maintained on a standing dose of
methadone or treated with methadone for heroin withdrawal, pain should be
treated as a separate problem with additional opioids including methadone.
The patient’s methadone maintenance dose cannot be thought of as
analgesia, but rather as agonist therapy for relapse and withdrawal
prevention. Methadone for relapse prevention will target opioid tolerance
needs and prevent withdrawal but will not provide analgesia for pain.
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AIDS Psychiatry 737
8.2.3. Psychopharmacology and other psychiatric

disorders — examples of medicines
and doses are listed
• Citalopram 10–40 mg or escitalopram 10–20 mg.
• Bupropion 150–300 mg.
• Venlafaxine 150 mg.
• Quetiepine 25–100 mg, aripiprazole 5–10 mg, or olanzapine
2.5–10 mg.
• Clonazepam 0.5–2 mg bid.
9. CONCLUSION
Understanding AIDS psychiatry can help HIV clinicians prevent transmis-
sion of HIV and AIDSism, can improve adherence to medical care, and
diminish suffering, morbidity and mortality in persons with HIV and
AIDS.
10. KEY POINTS

• AIDS is a multimorbid, severe, complex medical and psychiatric
illness.
• While AIDS is similar to other severe and complex medical illnesses,
AIDS presents special challenges, such as its public health implica-
tions, that make it a very different illness.
• AIDS is a highly stigmatized illness.
• There is a need for a comprehensive biopsychosocial approach6,7,10–12
to psychiatric symptom evaluation in persons with HIV and AIDS.
• This comprehensive approach to differential diagnosis includes
exploring clues for infectious, neurologic, and psychiatric causes and
requires complete medical, psychiatric, and psychosocial assessments
as well as ancillary evaluations and consultations.
• Each person with HIV and AIDS should have a complete cognitive
assessment at baseline and on at least a semi-annual or annual basis.
• Cognitive impairment can cause non-adherence at any stage of HIV
infection.
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738 M. A. Cohen
• Antiretroviral therapy may prevent progression or reverse cognitive

impairment.
• HAND is still prevalent and is the most common treatable cause of
dementia in persons under 50 years of age.1
• Hypoactive delirium is prevalent in persons with HIV and AIDS, can
masquerade as depression, and is easily resolved when the underlying
cause is identified and treated.
• Depression and suicide are prevalent in persons with HIV and AIDS
• It is extremely important to take a suicide history in every person with
HIV and AIDS.9
• It is also important to incorporate smoking cessation as well as
nutrition, relaxation, and exercise as part of an effort to maximize life
potential in persons with HIV and AIDS.
• Psychotherapy, crisis intervention, family therapy, and medication can
alleviate depression and prevent the tragic complication of suicide in
persons with HIV and AIDS.
• PTSD is often overlooked in persons with HIV and AIDS since it may
be overshadowed by other psychiatric diagnoses such as substance
dependence and depression that are often multimorbid with PTSD.
Furthermore, early trauma may lead to substance dependence to numb
the anguish of traumatic memories and to escape from intrusive thoughts.
• In AIDS, diagnosis of PTSD has been associated with risky behavior
and non-adherence to risk reduction and medical care.
• Early childhood trauma-induced PTSD prevalent in persons with HIV
and responds well to psychodynamic psychotherapy and medication.
• Psychiatric care and an integrated multidisciplinary team approach to
prenatal and other care of persons with HIV and AIDS can make a
difference in prevention of perinatal, sexual, and injection drug-related
HIV transmission as well as illness progression and the morbidity and
mortality of AIDS.
• Prevention starts with early childhood trauma prevention through
parent education.
• Risk prevention and HIV diagnosis is relevant at every age through
older age.
• Treatment needs to be comprehensive and tailored to meet patient
needs.
• No “one size fits all” in the treatment of persons with HIV and AIDS.
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AIDS Psychiatry 739
• If medications are indicated START VERY LOW and GO VERY

SLOW.
11. SELF-ASSESSMENT
11.1. What is the differential diagnosis of new-onset visual
hallucinations in a person with late-stage AIDS?
(A) Delirium.
(B) Substance use disorder.
(C) Psychosis.
(D) Medical conditions or their treatments.
There is no more obvious need for a biopsychosocial approach to AIDS

than in the differential diagnosis of presenting psychiatric symptoms.
Persons with late-stage AIDS are vulnerable to every psychiatric diagno-
sis as well as to opportunistic infections, multimorbid medical conditions,
and side effects of medications. The differential diagnosis of visual hal-
lucinations includes all of the above, delirium, substance use disorder,
psychosis, medical conditions (such as an opportunistic infection with
CMV retinitis), or their treatments.
Answer: E
11.2. What is the most common cause of dementia

in persons under 50 years of age?
(A) Attention deficit disorder.
(B) Central nervous system lymphoma.
(C) Cerebrovascular disease.
(D) HIV-associated neurocognitive disorder.
(E) Early dementia of the Alzheimer’s type.
HIV-associated neurocognitive disorder is the most common cause of

dementia in persons under 50 years of age.1 While it may be subtle in
presentation and unexpected in a person who is 20, 30, or 40 years old, it
is important to assess for HAND in persons with HIV.
Answer: D
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740 M. A. Cohen
12. CASE STUDIES

12.1. Differential diagnosis of visual hallucinations
Mr A is a 41-year-old construction worker who was not diagnosed with
HIV until his first hospital admission for odynophagia, weakness, wasting,
and weight loss. He was found to have esophageal candida, an opportun-
istic infection (OI) and AIDS-defining illness, and late-stage AIDS (CD4
count of 2 and an elevated viral load), treated for esophageal candida, and
transferred to a long-term care facility for nutritional resuscitation and
reconditioning as well as antiretroviral medication (ART). One month
later Mr A was transferred back to the hospital with a fever and abnormal
chest X-ray and diagnosed with Mycobacterium avium intracellulare
(MAC). When he reported that he was seeing frightening faces, his HIV
clinician requested a psychiatric consultation.
These are some clues that can lead us to a diagnosis.
Mr A was not diagnosed with HIV or treated with CART until he had
late-stage AIDS. New-onset visual hallucinations in a person with HIV or
AIDS are rarely caused by underlying psychiatric disorders and most
often caused by delirium or other medical conditions.
Mr A may have been more vulnerable to both MAC when he was
started on ART in late-stage AIDS shortly after his first opportunistic
infection with esophageal candida. New CDC recommendations report
that beginning ART in a treatment-naïve individual within weeks
following a first opportunistic infection may unmask another subclinical
opportunistic infection (such as toxoplasmosis, MAC, or cryptococcosis)
by causing an immune reconstitution inflammatory syndrome (IRIS).4
Mr A denied previous experience of visual hallucinations.
He described the hallucinations as “seeing faces” that he realized were
not really there.
The differential diagnosis of visual hallucinations in late-stage AIDS is
summarized in Table 2.
Psychiatric assessment revealed no psychiatric symptoms or signs to
suggest delirium or an underlying thought, mood, substance dependence,
or anxiety disorder that could account for his visual hallucinations. Since
Mr A also complained of decreased visual acuity, I recommended ophthal-
mologic consultation. This revealed a diagnosis of a third OI,
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AIDS Psychiatry 741
cytomegalovirus (CMV) retinitis. Mr A’s visual hallucinations resolved on

gancylovir although his visual acuity was not fully restored.
Mr A’s visual hallucinations were due to CMV retinitis, an opportunistic
infection that could have been prevented.
His visual loss was also preventable.
12.2. Nonadherence due to subtle cognitive impairment

Ms B is a 31-year-old with HIV who is the mother of two healthy children.
Her CD4 decreased from 1,240 to 516 and viral load increased from <48
to 14,600 over the course of two years. Her HIV physician has known her
for five years and reports that she is adherent to care. Her virus is sensitive
to the antiretroviral medication regimen that was prescribed but her viral
load is no longer undetectable. Ms B’s HIV clinician refers her for a psy-
chiatric consultation concerned that depression might be contributing to
her gradual change in immune system function.
These are clues that can lead us to a diagnosis:
Ms B had no evidence of mood, anxiety, psychotic, or substance use
disorder.
She was able to manage ADLs, IADLs, and the care of her two
children.
On cognitive assessment, her memory was good for remote events and
she was able to give an adequate history. On formal assessment of her
cognition, Ms B was able to register four words but she was unable to
recall four words in 5 mins despite three rehearsals. She had evidence of
impaired executive function on clock-drawing. She was unable to provide
the names of her medications. Although she stated that she was able to
take them and took them as directed, she did not know the doses and fre-
quency of administration. She was diagnosed with HAND. Recommendation
was for directly observed antiretroviral therapy. With the help of visiting
nurse services, Ms B was adherent to medications. Her cognitive impair-
ment gradually improved and her immune parameters improved.
Ms B’s non-adherence was a result of relatively subtle cognitive
impairment.
Diagnosis of HAND requires a complete cognitive assessment.
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742 M. A. Cohen
12.3. A young man AIDS and severe cognitive impairment

Mr C is a 37-year-old disabled investment banker with AIDS (CD4 112
and elevated viral load) who was admitted to a nursing home when he was
no longer able to care for himself in the community or perform activities
of daily living (ADLs). On initial psychiatric consultation, Mr C denied
being ill or needing care and wanted to return home. He had impaired
memory, abstract thinking, and executive function as well as anosognosia,
and constructional apraxia on clock and Bender drawings, psychomotor
retardation, and profoundly diminished intellectual functioning relative to
his educational and occupational levels. He was incontinent of urine and
feces. His diagnosis was HAND.
Over the course of a year in an AIDS nursing home, Mr C responded
well to treatment with combination antiretroviral therapy and gradually
regained cognitive function. After two years of directly observed antiret-
roviral therapy in the structured and supportive setting, he was fully aware
of his illness, kept track of his immune function and viral load, and was
able to live independently and resume his work as an investment banker.
12.4. Delirium
Mr D is a 68-year-old married disabled attorney admitted with chest pain,
who has diabetes mellitus, hypertension, coronary artery disease, HIV
(CD4 1100, viral load undetectable), and hepatitis C and was referred for
depression. Psychiatric consultation revealed psychomotor slowing,
confusion, disorientation to time and place, fluctuating levels of con-
sciousness, emotional incontinence, and no evidence of depression.
Diagnosis diagnosed was hypoactive delirium. A comprehensive medical
evaluation, including urine and blood cultures, was recommended and
revealed a urinary tract infection with E. coli sepsis.
Mr D had multimorbid medical illness and was found to have hypoac-
tive delirium due to urosepsis.
12.5. Depression, suicide, and HIV infection

Mr E is a 58-year-old married grandfather and disabled chef who is a
long-term non-progressor with HIV, CD4 of 1,382, and undetectable
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AIDS Psychiatry 743
viral load (never treated with antiretroviral medications) and has been
depressed and suicidal since his HIV diagnosis. He has multimorbid
medical illnesses as well as a prior history of depression. Mr E is fol-
lowed in an ambulatory AIDS center and has oxygen-dependent chronic
obstructive pulmonary disease with mild cyanosis and severe emphy-
sema, pulmonary hypertension, rheumatic heart disease, untreated hepa-
titis C, Paget’s disease, and benign prostatic hypertrophy. He is addicted
to cigarette-smoking although dependent on oxygen. He has a long-
standing history of major depressive disorder, recurrent, and suicidal
ideation. Mr E’s suicidal thoughts rarely leave him and are related to
HIV stigma.
Mr E was diagnosed with major depressive disorder recurrent, severe,
with chronic suicidal ideation, active nicotine cigarette dependence. He
engaged easily in weekly psychotherapy and agreed to attempt smoking
cessation. He responded well to dynamic psychotherapy, family therapy,
and medication with venlafaxine XR, 150 mg hs and quetiepine, 25 mg at
bedtime for augmentation. Bupropion XL, 150 mg was added for smoking
cessation as well as augmentation. He responded to a recommendation to
use jigsaw puzzles to keep occupied and prevent cigarette cravings but
refused nicotine substitution. After two years of smoking cessation, he
almost acyanotic and has convinced other family members to give up
smoking as well.
Mr E was able, in individual and family therapy, to accept that he was
not a burden to his family but a beloved, productive, valued member, and
a reliable caregiver to his grandchildren. Although he remains intermit-
tently suicidal, he is gradually working on the development of a sense of
meaning and purpose and is less depressed and is adherent to medical and
psychiatric care.
12.6. PTSD and non-adherence to care

Ms F is a 38-year-old divorced unemployed woman with HIV who is
pregnant and actively using cocaine. She was found to have PTSD due to
early childhood trauma and intimate partner violence and responded
well to twice weekly psychodynamic psychotherapy and placement in
a structured residential drug treatment facility for pregnant and addicted
women and their children. She was escorted to her psychotherapy,
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744 M. A. Cohen
discontinued cocaine use, received antiretrovirals in direct observation

therapy, and delivered a healthy HIV negative baby. She continued in
psychotherapy for a total of three years and began to attain her goals
before relapsing to cocaine after discharge to the community and
becoming non-adherent to medical and psychiatric care.
ACKNOWLEDGEMENT
This chapter was adapted in part from the following chapter with permis-
sion of Cambridge University Press: Cohen MA. (2010) Psychiatric
aspects of AIDS. In: JJ Amos and RG Robinson (eds.) Psychosomatic
Medicine: An Introduction to Consultation-Liaison Psychiatry, pp. 170–
180, Cambridge University Press, Cambridge.
REFERENCES
1. Ances BM, Ellis R. (2007) Dementia and neurocognitive disorders due to
HIV-1 infection. Semin Neurol 27: 86–92.
2. APM. (2010) Available at: http://www.apm.org/sigs/oap/. Accessed on 7 July
2010.
3. Blanco C, Weissman MM. (2007) Interpersonal psychotherapy. In: Gabbard
GO, Beck JS, Holmes J (eds.), Oxford Textbook of Psychotherapy, pp. 23–34,
Oxford University Press, NY.
4. CDC. (2009) Guidelines for prevention and treatment of opportunistic
infections in HIV-infected adults and adolescents. Recommendations from
CDC, the NIH and the HIV medicine association of the infectious diseases
society of America. Morb Mortal Wkly Rep 58:1–5.
5. Cohen MA. (1989) AIDSism, a new form of discrimination. Am Med News
32: 43.
6. Cohen MA. (2008) History of AIDS psychiatry — A biopsychosocial
approach — Paradigm and paradox. In: Cohen MA, Gorman JM (eds.),
Comprehensive Textbook of AIDS Psychiatry, pp. 3–14, Oxford University
Press, NY.
7. Cohen MA, Alfonso CA. (2004) AIDS psychiatry: Psychiatric and palliative
care, and pain management. In: Wormser GP (ed.), AIDS and Other
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Manifestations of HIV Infection, 4th ed. pp. 537–576, Elsevier Academic

Press, San Diego, CA.
8. Cohen MA, Alfonso CA, Hoffman RG, Milau V, Carrera G. (2001) The
impact of PTSD on treatment adherence in persons with HIV infection. Gen
Hosp Psychiatry 23: 294–296.
9. Cohen MA, Batista SM, Lux JZ. (2010) A biopsychosocial approach to
psychiatric consultation in persons with HIV and AIDS. In: Cohen MA,
Goforth HW, Lux JZ, Batista SM, Khalife S, Cozza KL, Soffer J (eds.),
Handbook of AIDS Psychiatry, pp. 33–60, Oxford University Press, NY.
10. Cohen MA, Goforth HW, Lux JZ, Batista SM, Khalife S, Cozza KL,
Soffer J. (2010) Handbook of AIDS Psychiatry, Oxford University Press,
NY.
11. Cohen MA, Gorman JM. (2008) Comprehensive Textbook of AIDS Psychiatry,
12. Cohen MA, Weisman H. (1986) A biopsychosocial approach to AIDS.
Psychosomatics 27: 245–249.
13. UCSF Center for HIV Information. (2012) Drug Interactions. Available at:
http://hivinsite.ucsf.edu
14. University of Liverpool. (2012) Drug Interactions. Available at: http://www.
hiv-druginteractions.org
15. Lambda Legal, Franke V. Parkstone Living Center, Inc. (2009) Available at:
http://www.lambdalegal.org/publications/articles/protecting-our-seniors.
html. Accessed on 7 July 2010.
16. Sikkema KJ, Hansen NB, Kochman A, et al. (2004) Outcomes from a
randomized controlled trial of a group intervention for HIV positive men and
women coping with AIDS-related loss and bereavement. Death Stud 28:
187–209.
17. Smith RD, Delpech VC, Brown AE, Rice BD. (2010) HIV transmission and
high rates of late diagnoses among adults aged 50 years and over. AIDS 24:
2109–2115.
18. Weiss JJ, Mulder CL, Antoni MH, de Vroome EM, Garssen B, Goodkin K.
(2003) Effects of a supportive-expressive group intervention on long-term
psychosocial adjustment in HIV-infected gay men. Psychother Psychosom
72: 132–140.
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Chapter 29
Pharmacogenomic Variability Associated

with Psychotropic Medication Response
David Mrazek and Bhanu Prakash Kolla
1. INTRODUCTION
Pharmacogenomics is the study of gene variation that predicts medication
response. Psychiatric pharmacogenomics is the application of genetic
testing to provide guidance in selecting and dosing psychotropic
medication.25 While hundreds of associations between gene variations and
medication responses have been reported, this chapter will only review the
most well-known and widely recognized gene variants that are associated
with the responses of antidepressant medications, antipsychotic medica-
tions, and medications used to treat attention deficit hyperactive disorder.
These variants will be identified by their rs number (i.e. reference SNP
number). A list of key variants is listed in Table 1.
At this stage in the evolution of psychiatric pharmacogenomics, the
primary emphasis of clinical testing is primarily to avoid adverse reactions
to psychotropic medications. This has been demonstrated most clearly by
the identification of patients who have impaired metabolic capacity as a
consequence of variations in their drug metabolizing genes that influence
their pharmacokinetic response to specific medications. Increasingly it is
possible to identify genes that influence the pharmacodynamic response
of a patient to specific psychotropic medications. By assessing a panel of
genes that influence medication response, it has become increasingly
746
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B1405_Ch-29.indd 747
Pharmacogenomic Variability Associated with Psychotropic Medication Response

Table 1. Key genes with specific variants and clinical implications.
Gene Nucleotide Nucleotide
Gene name abbreviation rs Number location change Clinical implications
Catecholamine-O- COMT rs737865 −19847 C/T Predicts response to bupropion
methyltransferase
rs4680 427 G/A Predicts response to bupropion and
B1405
antipsychotic medications
rs165599 1338 G/A Predicts response to bupropion

Norepinephrine SLC6A2 rs2242446 −182 T/C Predicts response to antipsychotic
transporter medications
rs17841329 275 G/A May predict response to methylphenidate
rs192303 275 C/G May predict response to methylphenidate
rs5569 1287 G/A Predicts response to nortriptyline,
antipsychotic medications, and
methylphenidate
Dopamine SLC6A3 rs28363170 Exon 15 VNTR Predicts response to methylphenidate
transporter
Serotonin SLC6A4 rs25531 Promoter region A/G Predicts occurrence of side effects for
transporter escitalopram
rs4795541 −2063– 44 bp Del Predicts response to SSRIs and
−1714 methylphenidate
rs57098334 2nd Intron VNTR Predicts response to citalopram
747
1/31/2013 2:42:47 PM
(Continued)
B1405_Ch-29.indd 748
748
Gene Nucleotide Nucleotide
Gene name abbreviation rs Number location change Clinical implications
Serotonin 1A HTR1A rs6295 −1019 C/G Predicts response to fluvoxamine,
receptor escitalopram, risperidone, and olanzapine
Serotonin 2A HTR2A rs6311 −1438 G/A Predicts response to antidepressants,
B1405
receptor clozapine, and olanzapine
rs6313 102 T/C Predicts response to clozapine and the

occurrence of side effects for paroxetine
rs7997012 1178 G/A Predicts response to citalopram
rs6314 1354 T/C Predicts response to clozapine
Serotonin 2C HTR2C rs6318 69 G/C Predicts response to clozapine
receptor
D2 dopamine DRD2 rs1799978 −241 A/G Predicts response to risperidone
receptor
rs1799732 −141 Ins/Del C Predicts response to chlorpromazine
D. Mrazek and B. P. Kolla

rs1801028 932 C/G Predicts response to risperidone
D3 dopamine DRD3 rs# unknown −205 A/G Predicts response to olanzapine
receptor
rs6280 27 C/T Predicts response to antipsychotic
medications
D4 dopamine DRD4 rs# unknown Exon 3 VNTR Predicts response to antipsychotic
1/31/2013 2:42:47 PM
receptor medications
Pharmacogenomic Variability Associated with Psychotropic Medication Response 749
possible to select the right drug for the right patient at the right dose.
However, given that many other factors effect medication response
beyond these gene variations, the result of clinical testing will always be
a greater prediction of the probability of an effective response rather than
an absolute certainty that a medication will be effective.
2. ANTIDEPRESSANT MEDICATIONS
Variations in both drug metabolizing enzyme genes and genes that influ-
ence neurotransmission have been associated with antidepressant response.
The most significant and consistent associations will be reviewed.
2.1. Cytochrome P450 drug metabolizing enzyme genes

There are several cytochrome P450 enzymes that play major roles in the
metabolism of antidepressants.
2.1.1. The cytochrome P450 2D6 gene (CYP2D6)

The CYP2D6 enzyme is involved in the metabolism of 17 commonly
prescribed antidepressants. Six antidepressants are metabolized primarily
by the 2D6 enzyme. A substrate is usually designated as being ‘‘primar-
ily’’ metabolized by the 2D6 enzyme if there are no other enzymes that
would normally be involved in metabolism of the drug if an adequate
concentration of the 2D6 enzyme were present. Desipramine, doxepin,
fluoxetine, nortriptyline, paroxetine, and venlafaxine are all primarily 2D6
substrates.
Six other antidepressants have substantial, but not exclusive, 2D6 sub-
strate metabolic clearance. The designation that the substrate is ‘‘substan-
tially but not exclusively” a 2D6 substrate refers to the fact that other
enzymes are normally involved in the metabolism of the substrate.
Amitriptyline, bupropion, duloxetine, imipramine, mirtazapine, and trazo-
done are all metabolized by the 2D6 enzyme, but are also metabolized by
other cytochrome P450 enzymes.
The 2D6 enzyme plays a relatively minor role in the metabolic clear-
ance of citalopram, escitalopram, fluvoxamine, and sertraline. However,
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750 D. Mrazek and B. P. Kolla
the 2D6 enzyme is designated as providing a secondary metabolic path-

way for these drugs which may become clinically relevant if the primary
pathway is impaired.
The cytochrome P450 2B6 enzyme is primarily responsible for the
metabolism of bupropion to hydroxybupropion. However, hydroxybupro-
pion is primarily metabolized by the 2D6 enzyme. As a result, patients
with no 2D6 activity may develop high serum concentrations of hydroxy-
bupropion which provides a plausible explanation for the occurrence of
severe adverse reactions to bupropion in some patients.
2.1.2. The cytochrome P450 (CYP2C19)

Amitriptyline, citalopram, clomipramine, and escitalopram are metabo-
lized primarily by 2C19.16 Additionally, doxepin, imipramine, moclobe-
mide, nortriptyline, and sertraline have substantial 2C19 substrate metabolic
clearance. Venlafaxine is minimally metabolized by the 2C19 enzyme.
Sertraline is an SSRI (selective serotonin reuptake inhibitor) that is
purportedly metabolized by five cytochrome P450 enzymes (i.e.
CYP2C19, CYP2B6, CYP2C9, CYP3A4, and CYP2D6). Consequently,
the inhibition of any single enzyme should conceptually not result in a
major change in the pharmacokinetics of sertraline. However, poor
CYP2C19 metabolizers have been shown to have higher serum levels of
sertraline than do normal metabolizers. Similarly, poor 2B6 metabolizers
also have higher serum levels of sertraline. The contributions of
CYP2C9, CYP3A4, and CYP2D6 to sertraline metabolism appear to be
minimal unless there is impaired CYP2C19 and CYP2B6 metabolism
capacity.
2.1.3. The cytochrome P450 2C9 gene (CYP2C9)

Amitriptyline is a tricyclic antidepressant that is demethylated by
CYP2C19, CYP2C9, and CYP3A4 to produce an active metabolite, nor-
triptyline. Amitriptyline is hydroxylated by CYP2D6.
Fluoxetine is an SSRI that is metabolized primarily by CYP2D6 to pro-
duce the biologically active metabolite, norfluoxetine. Fluoxetine is metabo-
lized secondarily by CYP2C9. Given the slow elimination of fluoxetine and
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the subsequent required secondary clearance of norfluoxetine, fluoxetine

has the longest functional half-life of any SSRI antidepressant.
2.1.4. The cytochrome P450 1A2 gene (CYP1A2)

Fluvoxamine is the only antidepressant that is metabolized primarily by
the CYP1A2 enzyme. Additionally, duloxetine, clomipramine, and imi-
pramine are substantially metabolized by the CYP1A2 enzyme and the
CYP1A2 genotype may be important for their metabolism if their primary
enzymes are inactive. Mirtazapine and amitriptyline are minimally metab-
olized by CYP1A2.
2.2. Target genes that affect antidepressant response

2.2.1. The catechol-O-methyltransferase enzyme gene (COMT)
Bupropion is an antidepressant which inhibits the reuptake of both norepi-
nephrine and dopamine. Bupropion is also a nicotinic antagonist.
Although bupropion was initially developed as an antidepressant, it is now
used to facilitate smoking cessation. Given that nicotine plays a role in the
release of dopamine, patients with the higher activity allele (i.e. the Val or
guanine allele) of the rs4680 (i.e. the well-known Val158Met polymor-
phism) may be at a greater risk for smoking relapse when treated with
bupropion.4
A haplotype is defined as a specific combination of genetic variations
that occur within a defined region of a gene. COMT haplotypes which are
composed of two identified single nucleotide polymorphisms (i.e. rs737865
and rs165599) have been reported to predict the efficacy of bupropion
when compared with placebo. Subjects of European ancestry who had a
guanine allele at both rs737865 and rs165599 did not benefit as much
from bupropion treatment as did subjects with other haplotypes.4
2.2.2. The norepinephrine transporter gene (SLC6A2)

Nortriptyline inhibits the function of the norepinephrine transporter mol-
ecule. Transporter molecules have been demonstrated to facilitate the
B1405_Ch-29.indd 751 1/31/2013 2:42:47 PM

reuptake of neurotransmitters into the neuron. In a Korean sample, a nor-

epinephrine response rate of 83% was reported in patients who were
homozygous for the more common guanine allele of rs5569 polymor-
phism (i.e. 1287G/A) of the norepinepherine transporter gene (SLC6A2).
In contrast, only 43% of patients with a copy of the adenine allele
responded to nortriptyline.15 In patients who were homozygous for the
guanine allele of rs5569 and who were also homozygous for the short
allele of the indel promoter polymorphism of the serotonin transporter
gene, the response rate was 89%.
2.2.3. The serotonin transporter gene (SLC6A4)

The indel promoter variant of SLC6A4, rs4795541, is often referred to as
5HTTR or SERTPR. This promoter variant has been repeatedly associated
with SSRI response in samples of European ancestry. This genetic varia-
tion also predicts responses to other antidepressant medications that influ-
ence availability of serotonin.
In a study of Italian inpatients with depression that included patients
with psychotic symptoms, patients who were homozygous for the short
allele of the indel promoter polymorphism of SLC6A4 responded less
well to treatment with fluvoxamine than did patients who were heterozy-
gous for the long allele and short allele or those who were homozygous
for the long allele. In a second study of depressed Italian patients, patients
who were homozygous for the short allele of the indel promoter polymor-
phism of SLC6A4 responded less well to treatment with fluvoxamine.39
In a large cohort of patients with major depression, those patients who
defined their ancestry as being ‘‘white’’ and ‘‘not Hispanic’’ and who were
treated with citalopram using a standard protocol were more likely to
respond to citalopram if they were homozygous for the long allele of
rs4795541.26 A different analysis of this data set that pooled white
Hispanics with white non-Hispanics failed to demonstrate a statistically
significant association between remission and having the homozygous
long allele genotype.18
In Spanish patients with a major depressive disorder, there was not an
association between the indel promoter variant and response to treatment
with escitalopram. However, patients who were homozygous for the more
active long indel polymorphism genotype and were also homozygous for
B1405_Ch-29.indd 752 1/31/2013 2:42:47 PM

the cytosine allele of rs6295 (i.e. −1019C/G) in the serotonin receptor 1A

gene (HTR1A) did respond better than patients who were homozygous for
the short allele of the indel promoter polymorphism genotype in SLC6A4
and who were also homozygous for the guanine allele of rs6295 in
HTR1A.1
It has been observed that in patients of Asian ancestry, there may be
epistatic interactions that influence the effect of the indel polymorphism.
Epistasis is a mechanism by which a gene at one locus influences the
effect of another gene at a different locus. For example, 76% of the sub-
jects who were homozygous for the short form of the indel promoter poly-
morphism and were treated with nortriptyline responded. In comparison,
the response rate of patients who were homozygous for the long polymor-
phism was 30%.15 As described above, an interaction between the guanine
allele of rs5569 of the norepinephrine transporter gene and the short allele
of the indel promoter polymorphism of the serotonin transporter gene was
also found. A similar association between a better response rate with ser-
traline and fluoxetine in Korean patients who were homozygous for the
short allele of the indel polymorphism has also been reported.
A review of 15 studies examining the implications of variations in the
indel promoter polymorphism of SLC6A4 concluded that patients of
European ancestry who had at least one copy of the more active long indel
allele consistently had a better response to treatment with SSRIs than did
patients who were homozygous for the short allele of the indel promoter
polymorphism.32 Additionally, patients who were homozygous for the
short allele of the indel promoter polymorphism were less likely to show
improvement in core symptoms of depression and somatic anxiety.
A relationship between the indel promoter genotype and the develop-
ment of gastrointestinal side effects, including diarrhea, has been reported.
Subjects who identified themselves as white and who had at least one
copy of the long allele of the indel promoter genotype were divided into
two separate groups based on their rs25531 genotype. White subjects who
were homozygous for the long allele of SLC6A4 and who also had one or
more copies of the adenine allele of rs25531 were less likely to report
gastrointestinal side effects.11
A study of German inpatients with the diagnosis of depression reported
associations between side effects and two genetic variants of SLC6A4.28
Those patients who were treated with selective serotonin reuptake inhibitor
B1405_Ch-29.indd 753 1/31/2013 2:42:48 PM

antidepressants who had one or more copies of the short allele of the indel
promoter polymorphism experienced more side effects than patients who
were homozygous for the long allele. Those patients who were homozygous
for the 10-repeat VNTR in the second intron of SLC6A4 had more side
effects when compared to other VNTR genotypes. In this study, 63% of
patients who were both homozygous for the short indel genotype and
homozygous for the 10-repeat allele of the VNTR variant reported having
side effects. No patients who were both homozygous for the long indel allele
and had one or more copies of the 12-repeat allele experienced side effects.
Depressed geriatric patients who were treated with paroxetine and had
at least one active copy of the active long allele of the indel promoter poly-
morphism were less likely to have side effects than those who were
homozygous for the short allele.27 Specifically, patients who did not have
a copy of the active allele were more likely to discontinue participation in
the study and reported more gastrointestinal symptoms, fatigue, agitation,
sweating, and dizziness.
A study of Spanish patients with depression reported they were less
likely to experience antidepressant-induced mania if they had at least one
copy of the long allele of the indel promoter polymorphism. Most of the
patients had been treated with tricyclic antidepressants, although treat-
ment with selective serotonin reuptake inhibitors, monoamine oxidase
inhibitors, and venlafaxine were also associated with the induction of
manic symptoms.
2.2.4. The serotonin 1A receptor gene (HTR1A)

Generally, depressed patients who are homozygous for the cytosine allele
of rs6295 (i.e. −1019C/G) have been reported to have a better response to
antidepressant medications than patients with a copy of the guanine allele.
A positive response to fluvoxamine has also been reported in patients with
bipolar disorder who were homozygous for the cytosine allele of rs6295
(i.e., −1019C/G).31
An interaction between variants of HTR1A and SLC6A4 in patients
with major depression treated with citalopram has been demonstrated.
Patients with a copy of the long allele of the indel promoter long variant
of SLC6A4 who also had a copy of the cytosine allele of rs6295 did
B1405_Ch-29.indd 754 1/31/2013 2:42:48 PM

better than patients who were homozygous for the less active indel pro-
moter short allele of SLC6A4 and who were homozygous for the gua-
nine allele of rs6295.1 Patients who were homozygous for both the short
allele of SLC6A4 and the guanine allele of rs6295 had a remission rate
of only 17%.

Variations in HTR2A have been associated with response to antidepres-
sant medication. In a sample of depressed Korean patients treated with
citalopram, those patients who were homozygous for the guanine allele of
rs6311 (i.e. −1438G/A) were more likely to respond than patients who had
a copy of the adenine allele.6 Specifically, 48% of the subjects who were
homozygous for the guanine allele fully remitted compared to 30% of the
subjects who had one or two copies of the adenine allele.
In a sample of North American patients who were treated with citalo-
pram, 80% of the white patients who were homozygous for the adenine
allele of rs7997012 (i.e. 1178G/A) were classified as responders. Only
64% of subjects who were homozygous for the guanine allele responded.21
Discontinuation of treatment with paroxetine has been associated with
having two copies of the cytosine allele of rs6313 (i.e. 102T/C). About
40% of the homozygous cytosine allele subjects discontinued paroxetine,
while only about 16% of patients with the other genotypes stopped their
treatment.
3. ANTIPSYCHOTIC MEDICATIONS
Four cytochrome P450 drug metabolizing enzyme genes are involved in
the metabolism of antipsychotic medications.
3.1. Drug metabolizing genes associated with antipsychotic

response
3.1.1. The cytochrome P450 2D6 gene (CYP2D6)
Risperidone is an atypical antipsychotic medication that is primarily
metabolized by the 2D6 enzyme. Poor CYP2D6 metabolizers have been
B1405_Ch-29.indd 755 1/31/2013 2:42:48 PM

shown to have an increased frequency of side effects when taking stand-

ard doses of this medication.8 Patients who are poor 2D6 metabolizers
have also been shown to have an increased probability for hyperprol-
actinemia, which may be related to high levels of the metabolite,
9-hydroxyrisperidone.
Aripiprazole is an atypical antipsychotic medication that is metabolized
by both the 2D6 enzyme and the 3A4 enzyme. Consequently, CYP2D6
poor-metabolizing patients can usually tolerate aripiprazole at a reduced
dose if they have adequate CYP3A4 capacity. CYP2D6 provides an alter-
native pathway for olanzapine metabolism.
3.1.2. The cytochrome P450 2C19 gene (CYP2C19)

The 2C19 enzyme is substantially involved in the metabolism of clozapine
and has a secondary role in the metabolism of thioridazine.

While CYP1A2 is primarily responsible for clozapine metabolism,
CYP2C19, CYP2D6, CYP2E1, CYP3A4, and CYP3A5 can provide alter-
native metabolic pathways. Olanzapine is primarily metabolized by
CYP1A2 and secondarily metabolized by CYP2D6. Chlorpromazine is
also metabolized by both CYP1A2 and CYP2D6.

Quetiapine is extensively metabolized by CYP3A4. CYP3A4 provides an
alternative pathway for ziprasidone metabolism.
3.2. Target genes that affect antipsychotic response

COMT variation may be related to the severity of psychotic symptomatol-
ogy of schizophrenia as well as influencing the response of patients to
neuroleptic treatment. In a Finnish study, patients were classified
B1405_Ch-29.indd 756 1/31/2013 2:42:48 PM

as having low COMT activity or high COMT activity based on rs4680

genotypes.12 Patients who were homozygous for the less active adenine
allele (i.e. Met allele) were compared to patients who had at least one
copy of the guanine allele (i.e. Val allele). Patients with the higher COMT
activity also responded more positively to typical antipsychotic medica-
tions as those with lower COMT activity.
COMT genotype may predict treatment with olanzapine in patients
with schizophrenia. Patients who were homozygous for the Met allele
have shown more improvements than patients who were homozygous for
the Val allele.5

In a French study, patients with schizophrenia who had at least one copy
of the thymine allele of rs2242446 (i.e. −182T/C) had greater improve-
ment in their positive symptoms than did patients who were homozygous
for the cytosine allele.22 Similarly, patients who were homozygous for the
adenine allele of rs5569 (i.e. 1287G/A) demonstrated better improvement
of positive symptoms than did patients who had at least one copy of the
guanine allele.

Patients with schizophrenia who were homozygous for the cytosine allele
of rs6295 responded better to risperidone and olanzapine than those with
a copy of the guanine allele.29 This improvement was the result of resolu-
tion of negative symptoms as opposed to positive symptoms.

In patients of European ancestry, the adenine allele of rs6311
(i.e. −1438G/A) and the thymine allele of rs6313 (i.e. 102T/C) are
associated with a better response to clozapine than the guanine allele
of rs6311 or the cytosine allele of rs6313. An initial report docu-
mented a response rate of 72% in patients who had one copy of the
thymine allele of rs6313 that was in complete linkage disequilibrium
B1405_Ch-29.indd 757 1/31/2013 2:42:48 PM

with the adenine allele of rs6311, as compared to a response rate of

43% in patients who were homozygous for the cytosine allele of
rs6313.
The polymorphism rs6314 (i.e. 1354T/C) is another variant of HTR2A
that has been linked to clozapine response and is not in strong linkage
disequilibrium with either rs6311 or rs6313. Patients who had one or
more copies of the thymine allele (i.e. histidine allele) had a response
rate of 66%, whereas patients who were homozygous for the relatively
rare cytosine allele (i.e. tyrosine allele) of rs6314 had a response rate of
only 25%.2
A European study of patients with schizophrenia reported that those
who were homozygous for the adenine allele of rs6311 (i.e. −1438G/A)
experienced a 45% improvement in their negative symptoms with olan-
zapine. Patients with other rs6311 genotypes experienced only a 19%
improvement in negative symptoms.9 A study of French patients with
schizophrenia also reported that subjects with the adenine allele of rs6311
had more improvement in their negative symptoms when treated with
antipsychotic medications.10
3.2.5. The serotonin 2C receptor gene (HTR2C)

Clozapine is an antipsychotic medication for which variability in HTR2C
has been associated with treatment response. Patients with one or two cop-
ies of the cytosine allele (i.e. serine allele) of rs6318 were more likely to
have a positive response to clozapine. However, a study examining the
association of variability in rs6318 and response to clozapine in an
American sample reported only a trend between the cytosine allele of
rs6318 and clozapine response. The combination of two variants in
HTR1A and three variants of HTR2A has been reported to have a positive
predictive value of 76%.3
3.2.6. The dopamine 2 receptor gene (DRD2)

Patients with the adenine allele of rs1799978 (i.e. −241A/G) of DRD2
have been reported to respond more rapidly to risperidone than patients
B1405_Ch-29.indd 758 1/31/2013 2:42:48 PM

with the guanine allele.37 Patients with a copy of the guanine allele of
rs1801028 (i.e. 932C/G) also have responded more rapidly to risperi-
done when compared to patients who were homozygous for the cyto-
sine allele.19 Furthermore, patients without the cytosine allele of
rs1799732 (i.e. −141 Ins/Del C) have responded to chlorpromazine
more rapidly than did patients who carried an allele with a deleted
cytosine.36

The cytosine allele (i.e. serine allele) of rs6280 has been associated with
a more positive response to typical antipsychotic medication.30 In contrast,
the thymine allele (i.e. glycine allele) has been associated with a more
positive response to atypical antipsychotic medication.35
An interaction between rs6280 and the promoter variant −205A/G has
been reported. Subjects with schizophrenia who were treated with olan-
zapine and who had both the thymine allele (i.e. the glycine allele) of
rs6280 and the glycine allele of −205A/G were most likely to have an
improvement in their positive symptoms.33 Korean patients with schizo-
phrenia who were homozygous for the thymine allele (i.e. the glycine
allele) of rs6280 and treated with risperidone had better symptom relief
than did patients who had at least one copy of the cytosine allele (i.e. the
serine allele). In contrast, patients who had at least one copy of the cyto-
sine allele (i.e. the serine allele) and who were also homozygous for the
cytosine allele of rs6313 (i.e. 102T/C) of the HTR2A gene were the least
likely to respond.14

A study of patients of European ancestry who had either the 4-repeat
allele or shorter repeat alleles of the 48-bp VNTR in the third exon were
more likely to respond to typical antipsychotic medication than were sub-
jects with the 7-repeat allele.7
In Taiwan, patients with schizophrenia who were homozygous for the
4-repeat allele were more likely to respond to typical antipsychotic
B1405_Ch-29.indd 759 1/31/2013 2:42:48 PM

medication than were subjects with copies of the 2-repeat allele. No

patients in this study had a copy of the 7-repeat allele.
4. MEDICATIONS USED TO TREAT ADHD

4.1. Drug metabolizing enzyme associated with response
to ADHD treatment
Atomoxetine is a non-stimulant medication that is used to treat patients
with ADHD. Poor CYP2D6 metabolizers may develop adverse reactions,
including severe sedation which is believed to be related to higher serum
levels. However, poor CYP2D6 metabolizers who are able to tolerate ato-
moxetine may have a positive therapeutic response, which may be medi-
ated by their sustaining higher serum levels.23
4.2. Target genes that affect response to ADHD treatment

About 87% of children who were homozygous for the more active gua-
nine allele (i.e. the Val allele) of rs4680 responded to methylphenidate. In
contrast, only about 58% of children who were homozygous for the ade-
nine allele (i.e. Met allele) responded.13 Patients who are homozygous for
the guanine allele (i.e., Val allele) of rs4680 have also been more likely to
respond favorably to amphetamines.20

Han Chinese patients with ADHD who had one or two copies of the
guanine allele of rs5569 (i.e. 1287G/A) had a symptom score reduction of
7% when treated with methylphenidate, whereas subjects who
were homozygous for the adenine allele had a symptom score reduction
of only 2% (e.g. A/A).38 In American children with ADHD, variants of
rs17841329 (i.e. 275G/A) and rs192303 (i.e. 275C/G) were associated
with methylphenidate response. Given the multiple comparisons that were
conducted in this study, these associations were considered to be prelimi-
nary until they could be replicated in an independent sample.24
B1405_Ch-29.indd 760 1/31/2013 2:42:48 PM

4.2.3. The dopamine transporter gene (SLC6A3)

The 9-repeat and the 10-repeat alleles of rs28363170 (i.e. 40-bp VNTR in
the 3’ UTR) have been associated with differential responses to methyl-
phenidate. An early report based on 16 children who responded to meth-
ylphenidate and 14 children who did not respond found that subjects who
were homozygous for the 10-repeat allele were less likely to respond
to methylphenidate than those with one or more copies of the 9-repeat
allele. However, more recent studies of children with ADHD have
reported that the 10-repeat allele was associated with better response to
methylphenidate.34
In a study of adult patients with ADHD who were treated with methyl-
phenidate, the 10-repeat allele had an allele frequency of 70%, and 43%
of the sample were homozygous for the 10-repeat allele.17 Only 22% of
subjects who were homozygous for the 10-repeat allele responded to
methylphenidate, while 52% of all of the heterozygous subjects
responded.17
4.2.4. The serotonin transporter gene (SLC6A4)

In a German study, hospitalized children with ADHD were treated with
methylphenidate. Subjects who were homozygous for the long indel allele
of SLC6A4 and also had one or two copies of the 7-repeat allele of the
DRD4 VNTR were less likely to respond to methylphenidate when com-
pared to children with other genotypes. Children who were homozygous
for the short allele of the indel promoter polymorphism and who also had
one or more copies of the 7-repeat allele of DRD4 VNTR had the best
response to methylphenidate.
5. CONCLUSION
The field of psychiatric pharmacogenomics is expanding rapidly. While it
is now possible to improve the probability of selecting an effective psy-
chotropic medication for a patient, the accuracy of these predictions will
increase as more genes are identified that affect the individual pharma-
cokinetic and pharmacodynamic responses of each patient.
B1405_Ch-29.indd 761 1/31/2013 2:42:48 PM

Already hundreds of reports of statistically significant associations

between specific gene variants and the response of psychotropic medica-
tions have been published. A continuing challenge for clinicians will be to
integrate contradictory findings in a manner that will more consistently
lead to the improvement of treatment outcomes.
At this stage in the development of our use of pharmacogenomic test-
ing, the primary organizing principle is to increase the safety of the use of
psychotropic medications. A classic example has been the determination
of impaired metabolic capacity so that clinicians can use caution in pre-
scribing for these patients. With the increasing capacity to identify varia-
tions in “target gene” variants, clinicians will have to integrate multiple
emerging pharmacogenomic findings in order to make fully informed
treatment decisions.
One compelling reason to consider pharmacogenomic testing is that
there are many psychotropic agents available to treat depression, psychosis,
and problems with attention. Consequently, if a particular medication is
identified as having a more problematic likelihood of tolerance, many alter-
native choices exist. Consequently, clinicians can be guided to select from
medications that are identified as having the lowest probability of adverse
effects. With the increasing integration of new research findings, these pre-
dictions will become increasingly precise and pharmacogenomic testing
will be routinely used to insure the safe management of psychiatric patients.
6. SELF-ASSESSMENT
6.1. A patient is a poor metabolizer of CYP2D6 and CYP2C9,
but has normal metabolic capacity for CYP2C19 and
CYP1A2. Which antidepressant would be the best choice
as an initial medication to treat a major depression?
(A) Fluoxetine.
(B) Venlafaxine.
(C) Desipramine.
(D) Paroxetine.
(E) Escitalopram.
Answer: E
B1405_Ch-29.indd 762 1/31/2013 2:42:48 PM

6.2. A patient is hospitalized with a psychotic illness and

successfully treated with olanzapine. It is determined
that he has an inducible form of CYP1A2. Which
of the following discharge instructions is not necessary?
(A) Instructions not to smoke.
(B) Instructions to limit the ingestion of cruciferous vegetables.
(C) Instructions to limit ingestion of charcoal cooked meats.
(D) Instructions to avoid taking medications that inhibit CYP1A2.
(E) Instructions to limit his intake of grapefruit juice.
Answer: E
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O-methyltransferase val158-met genotype and individual variation in the
brain response to amphetamine. Proc Natl Acad Sci USA 100: 6186–6191.
21. McMahon FJ, Buervenich S, Charney D, Lipsky R, Rush AJ, Wilson AF,
Sorant AJM, Papanicolau GJ, Laje G, Fava M, Trivedi MH, Wisniewski SR,
Manji H. (2006) Variation in the gene encoding the serotonin 2A receptor is
associated with outcome of antidepressant treatment. Am J Hum Genet 78:
804–814.
22. Meary A, Brousse G, Jamain S, Schmitt A, Szoke A, Schurhoff F, Gavaudan
G, Lancon C, Macquin-Mavier I, Leboyer M, Llorca PM. (2008)
Pharmacogenetic study of atypical antipsychotic drug response: Involvement
of the norepinephrine transporter gene. Am J Med Genet 147B: 491–494.
23. Michelson D, Read HA, Ruff DD, Witcher J, Zhang S, McCracken J. (2007)
CYP2D6 and clinical response to atomoxetine in children and adolescents
with ADHD. J Am Acad Child Adolesc Psychiatry 46: 242–251.
24. Mick E, Neale B, Middleton FA, McGough JJ, Faraone SV. (2008) Genome-
wide association study of response to methylphenidate in 187 children with
attention-deficit/hyperactivity disorder. Am J Med Genet B Neuropsychiatr
Genet 147: 1412–1418.
25. Mrazek DA. (2010) Psychiatric Pharmacogenomics, Oxford University
Press, NY.
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26. Mrazek DA, Rush AJ, Biernacka JM, O’Kane DJ, Cunningham JM, Wieben
ED, Schaid DJ, Drews MS, Courson VL, Snyder KA, Black JL, Weinshilboum
RM. (2009) SLC6A4 variation and citalopram response. Am J Med Genet B
Neuropsychiatr Genet, 150B: 341–351.
27. Murphy GM, Hollander SB, Rodrigues HE, Kremer C, Schatzberg AF.
(2004) Effects of the serotonin transporter gene promoter polymorphism on
mirtazapine and paroxetine efficacy and adverse events in geriatric major
depression. Arch Gen Psychiatry 61: 1163–1169.
28. Popp J, Leucht S, Heres S, Steimer W. (2006) Serotonin transporter polymor-
phisms and side effects in antidepressant therapy — a pilot study.
Pharmacogenomics 7: 159–166.
29. Reynolds GP, Arranz B, Templeman LA, Fertuzinhos S, San L. (2006) Effect
of 5-HT1A receptor gene polymorphism on negative and depressive symp-
tom response to antipsychotic treatment of drug-naive psychotic patients. Am
J Psychiatry 163: 1826–1829.
30. Scharfetter J. (2004) Pharmacogenetics of dopamine receptors and response
to antipsychotic drugs in schizophrenia — an update. Pharmacogenomics 5:
691–698.
31. Serretti A, Artioli P, Lorenzi C, Pirovano A, Tubazio V, Zanardi R. (2004) The
C (-1019) G polymorphism of the 5-HT1A gene promoter and antidepressant
response in mood disorders: Preliminary findings. Int J Neuropsychophogy
7: 453–460.
32. Serretti A, Kato M, De Ronchi D, Kinoshita T. (2007) Meta-analysis of sero-
tonin transporter gene promoter polymorphism (5-HTTLPR) association
with selective serotonin reuptake inhibitor efficacy in depressed patients.
Mol Psychiatry 12: 247–257.
33. Staddon S, Arranz MJ, Mancama D, Mata I, Kerwin RW. (2002) Clinical
applications of pharmacogenetics in psychiatry. Psychopharmacology 162:
18–23.
34. Stein MA, Waldman ID, Sarampote CS, Seymour KE, Robb AS, Conlon C,
Kim SJ, Cook EH. (2005) Dopamine transporter genotype and methylpheni-
date dose response in children with ADHD. Neuropsychopharmacology 30:
1374–1382.
35. Szekeres G, Keri S, Juhasz A, Rimanoczy A, Szendi I, Czimmer C, Janka, Z.
(2004). Role of dopamine D3 receptor (DRD3) and dopamine transporter
(DAT) polymorphism in cognitive dysfunctions and therapeutic response to
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atypical antipsychotics in patients with schizophrenia. Am J Med Genet B

36. Wu S, Xing Q, Gao R, Li X, Gu N, Feng G, He L. (2005) Response to chlor-
promazine treatment may be associated with polymorphisms of the DRD2
gene in Chinese schizophrenic patients. Neurosci Lett 376: 1–4.
37. Xing Q, Qian X, Li H, Wong S, Wu S, Feng G, Duan S, Xu M, Gao R, Qin
W, Gao J, Meng J, He L. (2007) The relationship between the therapeutic
response to risperidone and the dopamine D2 receptor polymorphism in
Chinese schizophrenia patients. Int J Neuropsychopharmacol 10: 631–637.
38. Yang L, Wang YF, Li J, Faraone SV. (2004) Association of norepinephrine
transporter gene with methylphenidate response. J Am Acad Child Adolesc
39. Zanardi R, Serretti A, Rossini D, Franchini L, Cusin C, Lattuada E, Dotoli
D, Smeraldi E. (2001) Factors affecting fluvoxamine antidepressant activity:
Influence of pindolol and 5-HTTLPR in delusional and nondelusional
depression. Biol Psychiatry 50: 323–30.
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Chapter 30
Ethics in Psychiatry
Kristi Estabrook
1. INTRODUCTION
A medical student refers to himself as “doctor” when he calls a family
member of a patient because he feels it is too complicated to explain his
role in the patient’s care and wants to ensure he is taken seriously.
A chronically mentally ill woman with schizophrenia gives a hand-knit
scarf as a thank-you gift to a graduating psychiatry resident who has man-
aged her medications for a number of years.
A forensic psychiatrist is asked to perform a competency evaluation for
a prisoner sentenced to the death penalty. The prisoner will only be
executed if he is found to be competent on evaluation.
Ethical situations occur at all levels of experience and training, but the
field of ethics can at times feel far removed from the pressures of clinical
patient work. It may seem, to the busy medical student or clinical psychia-
trist, to be better left to the academician. Yet, in all fields in medicine,
particularly psychiatry, ethical dilemmas are a near-daily part of the grind
and grit of clinical work. How, then, can a topic that flavors daily clinical
work feel so distant? It is because ethics is subtle. It is nuanced in a way
that one may not see the ethical dilemmas unless a foundation of ethical
knowledge has been set. Thus, it is unlike many other medical practices
where a “you will know it when you see it” mentality can often be applied
(think first encounter with a manic patient). Rather, ethics is more “you
768
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Ethics in Psychiatry 769
will see it when you know it.” That is what makes studying and learning
the core principles of ethics so important, because trying to be an ethical
physician is of no use if one is unable to spot an ethical dilemma when it
occurs. This chapter will give a foundation of basic ethical principles and
review the most salient ethical topics in psychiatry in a practical and
internationally focused manner. The goal is to provide a beginning foun-
dation of psychiatric ethical knowledge so that ethics can be more readily
seen in, and thus more easily applied to, everyday practice.
2. HISTORY OF INTERNATIONAL
PSYCHIATRIC ETHICS
Ethics has been an international focus in psychiatry in part due to past
atrocities that have been uncovered in which psychiatrists played a cen-
tral role. In Nazi Germany psychiatrists were involved in passing laws
allowing the forced sterilization of people with “defective genes,”
including mentally ill patients, in the name of “racial hygiene.” A few
years later, psychiatrists were involved in carrying out the “Euthanasia
Programme” in Germany in which thousands of mentally ill people were
killed in psychiatric hospitalizations just before the Holocaust. In the
Soviet Union from the 1960s to 1980s, psychiatrists were involved in
labeling political dissenters with psychiatric illnesses to justify impris-
oning them against their will, at times for many years.11 Although this
may seem like a problem of the distant past, psychiatrists in the last
several years have been involved in religious repression in China and
in aiding and participating in interrogations in military prisons in the
United States.11
Ethics in psychiatry is imperative not just because of past atrocities on
the part of psychiatrists but also because of the susceptibility of the psy-
chiatric patient to be treated unethically. Mentally ill persons are inher-
ently vulnerable because of the nature of their illness. Throughout history
they have been a victimized population. The mentally ill have been tar-
geted as witches, burned at the stake, and killed in the name of ethnic
cleansing.11 Even what was offered as treatment for mental illness was
often painful and baseless in science. Previous “treatments” of the men-
tally ill include bleeding, beating, isolation, and lobotomies.14 Because the
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770 K. Estabrook
mentally ill do have special vulnerability from the very nature of their
illness, which can impair judgment and reason, extra precautions must be
taken to protect them.
In an attempt to protect patients and to construct an international stand-
ard for ethics in psychiatry, the World Psychiatric Association (WPA) met
in 1977 and passed the Hawaii Declaration.16 The Hawaii Declaration was
the first formal international code of ethics for psychiatry and focused on
acting in the patient’s best interest and respecting patient autonomy.14,16 A
major revision, the Declaration of Madrid, now serves as the overriding
international standard for psychiatric ethics. The Declaration of Madrid
gives general guidelines for basic ethical concepts but also takes specific
stances on certain issues such as euthanasia, torture, the death penalty,
selection of sex, and organ transplantation, among others.16,25
3. CURRENT BIOETHICAL PRINCIPLES

Understanding the basic principles of bioethics in general sets a founda-
tion for applying ethics to specialty areas like psychiatry. The four main
principles in bioethics are autonomy, non-maleficence, beneficence, and
justice (Table 1).3 These philosophical concepts are now widely accepted
as the frame for which bioethics looks at ethical problems. Solving more
complex ethical problems can be viewed and analyzed through these
principles.
3.1. Autonomy
Autonomy in the field of medical ethics refers to the concept of self-
determination and self-rule. It is the right on the patient’s part to choose.
Table 1. Basic bioethical principles.

Foundational principles Autonomy: Self rule
Non-maleficence: Do no harm
Beneficence: Do good
Justice: Fair and equitable
Professionalism principles Fidelity: Loyalty
Veracity: Truthfulness
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Autonomy is an ethical principle that places the patient at the center of

health care and gives a patient the right to make informed decisions about
his or her own body and mind. However, it is important not to confuse this
ethical right as a duty, and require the patient to be involved in all choices.
In some cultures, patients prefer that family members make medical deci-
sions in their stead or would rather not know information on, for example,
a terminal prognosis. The right to allow others to make decisions and to
refuse information is a central part, in and of itself, of patients’ autonomy.
Thus, autonomy gives patients the ethical right to self-determine their own
health care decisions or to self-determine that they prefer to have family
or the physician make those decisions.3 However, autonomy can be lim-
ited in cases of incompetence or incapacity or in situations where allowing
patients to make certain health care decisions will harm others or them-
selves. In psychiatry, many ill patients are too sick or incapacitated by
mental illness to exercise full autonomy, yet it should be respected to the
greatest extent possible. Thus, for psychiatrists and other mental health
care providers, the ability to achieve true self-determination can be seen
as an ideal to work towards.19
3.2. Non-maleficence
Non-maleficence is a single word to encompass the Hippocratic oath’s
mantra “first, do no harm.” It is an ethical ideal that is central to all physi-
cian–patient interactions. It is the principle used when weighing the risk
and benefits of a medication or potential procedure. It is also the main
ethical consideration concerning the participant in medical research.
Because research is meant for advancing the greater good, and generally
not for the benefit of an individual participant, the lack of any harm to
participants is the most important value of ethical medical research.23
3.3. Beneficence
Beneficence refers to doing good for the patient. Like the root of the word
implies, it is the ethical principle of benefiting others. However, unlike
non-maleficence, which is a hard-and-fast principle with potential legal
consequences in cases of patient harm, beneficence can be thought of as a
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772 K. Estabrook
guiding ideal.3 For example, although physicians can strive to help a

patient to the best of their abilities, they have no ethical obligation to pro-
vide free psychotherapy sessions to an indigent patient. Beneficence is an
ideal that can be followed on the basis of an individual physician’s moral
ideals and goals. However, it is obligatory that physicians and health care
providers have an overriding goal of benefiting patients and working
toward overall wellness, health, and safety when providing specific
services to patients.
3.4. Justice
Justice in biomedical ethics deals with fair and equitable, but not neces-
sarily equal, distribution of resources and access to care. Whether this
includes equal access to care and globalization of finite health care
resources (such as organs for organ transplant) is hotly debated. The con-
cept of justice is also interpreted and implemented differently throughout
the globe, with some nations having universal access to health care and
others with a fee-for-service model or third-party-payer system that does
not ensure equal levels of care. Regardless, the ethical principle of justice
works to bring in a larger societal perspective into what is otherwise an
ethical discussion about individuals, specifically patients and providers.
The concept of justice, then, serves as a balance between individual
autonomy and beneficence, the interests of all of society, and the good of
other individuals.
It is important to note that none of these basic ethical principles trumps
another principle. Although some cultures may place heavier value on
certain principles than others, in general each principle should be initially
given equal weight. Thus, the core ethical principles must be applied to an
individual circumstance and then priority given to certain principles,
depending on the context and issues at hand.3
3.5. Professionalism
The concept of professionalism adds two additional ethical values that
must be considered: veracity and fidelity. However, to understand how
these values play into the ethical framework for medical ethics, the idea
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of professionalism itself must first be explored. What constitutes a

professional can vary widely in definition, but broadly, professionals per-
form services of which they have specific, expertise knowledge. They
generally have special training and attain certification. Professionals are
often bound by their own ethical codes and standards of behavior and
values. In medicine, there are codes of conduct and ethics on many levels
of organization (e.g. county, state, country, and world) and also for most
specialties. Thus, it is the combination of service, expertise, and self-
governance of acceptable standards and behaviors that define a profes-
sional.3,19 Medical professionals are further defined by their focus on the
patient, which necessitates that above all else, the patient’s best interest
must be at the centre of all interactions.
Veracity is an ideal that deals with truth and honesty. In professional
interactions, it entails being forthright with the knowledge and under-
standing of facts that non-professionals may not know. In medicine, verac-
ity encompasses being comprehensive, accurate, and forthcoming with
information regarding diagnosis, prognosis, and plan. In a professional
relationship, a certain level of blind trust is put in the professional by the
nature of the level of expertise the professional has that the patient does
not. So then, veracity is essentially respect for that trust. In professional
relationships, an agreement is informally formed implying that in
exchange for the patient’s trust, the professional will be honest and forth-
right with the patient. Thus, it brings the overall medical ideals of respect
for autonomy and beneficence to the professional relationship.
In medicine, fidelity is the concept of loyalty to the patient. A health
care provider, once in a professional relationship with a patient, has an
obligation to support and be faithful to the patient. This is often referred
to in medical literature as the concept of non-abandonment.21 In other
words, the professional is available to the patient unless an agreement is
made that the professional relationship will be terminated. Furthermore,
when the professional relationship is ended, fidelity calls for some level
of an arrangement for further care with another professional. However,
fidelity is more than just non-abandonment. In today’s world of third-
party payers and public health care, loyalty is often split between the
patient and government agencies, insurance payers, and the general pub-
lic, for example. Fidelity, then, is the recognition that in these situations
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774 K. Estabrook
of dual obligations, the physician’s first loyalty is to the patient. However,

full and complete loyalty to a patient is not always possible. For example,
a physician has an ethical and legal responsibility to be truthful when fill-
ing out disability paperwork for the government and should not exagger-
ate the truth of a patient’s condition, even if it would benefit the patient.
The overarching ethical principles that guide fidelity in the professional
relationship are non-maleficence and beneficence, where the real goal is
to benefit the patient and protect the patient from harm as much as
possible, especially when divided loyalties occur.
4. CULTURAL THEMES AND INTERNATIONAL

PERSPECTIVES IN ETHICS
The aforementioned ethical principles can be used as a starting point for
all ethical discussions in psychiatry. However, how much weight each
individual principle is given is often determined in part by cultural and
societal values. The principles of non-maleficence and beneficence tend to
be highly valued near equally universally, but the practical application of
the principles of autonomy and veracity vary widely among cultures.3 It
must be mentioned that although cultural groups do tend to have their own
unique set of values and tendencies, these are generalizations and should
not be applied to individuals in clinical encounters but, rather, should
increase awareness of possible cultural influences. Patients should be
assessed as individuals, and their cultural values and views ought to be
explored as part of the clinical relationship.
Veracity, as described previously, can be thought of as truthfulness and
forthrightness in the patient–physician relationship. Veracity as a value
and expectation in that relationship varies greatly between cultures.
Cultures that place less value on the individual and more emphasis on the
core cultural group, like family, tend to differ in terms of veracity from
more individually oriented cultures.15 For example, a 1990 Japanese study
found that 90% of physicians did not disclose the diagnosis of cancer to a
patient, because this information is perceived as a burden for the patient.13
In Arab cultures, there is a strong sense that at times not knowing the true
diagnosis allows the patient to have more hope. Thus, in that culture, it is
the norm to convey medical information to the family first and allow the
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family to decide how much to disclose to the patient.17 In contrast, in

1979, 98% of US physicians disclosed a diagnosis of cancer to a patient,
and a 1995 study in the United States found that 87% of European
Americans and 88% of African Americans felt that the patient should be
told about a diagnosis of metastatic cancer.4
Even within Western cultures, however, emphasis on veracity in medi-
cine has been an evolving process. In the United States and many other
Western cultures, full disclosure with patients has been a recent trend
with the decreasing popularity of the paternalistic view of medicine that
took place in the 1970s and 1980s.3,19 Paternalism in medicine refers to
the idea that the physician has superior knowledge and training and, as
such, is in a position of authority to make decisions for the patient in the
patient’s best interest.3 In most Western cultures today, veracity, or truth
telling, is highly valued in the physician–patient relationship, with full
disclosure of diagnosis, treatment options, and prognosis an expectation
on the part of the patient. In fact, in many Western countries, patients
have full access to all medical records, and this right is often exercised in
countries like Denmark, where a strong tradition of veracity and auton-
omy prevail.10 The move in Western cultures away from paternalism in
medicine has also coincided with an increased focus on autonomy of the
individual. Some cultures, such as in Scandinavia, view lack of auton-
omy as the greatest unhappiness of the modern person, and therefore
helping patients move toward autonomy is the ultimate goal of psychia-
try in those countries.10 In these cultures, the current trend is to give
patients all necessary information about diagnosis, and then treatment is
decided together by the physician and patient with the patient being
given all options, risks, and benefits. In fact, the WPA Madrid Declaration
states that it is a duty to provide patients with all relevant information so
that patients themselves can make informed decisions about the thera-
peutic process.25
This is in contrast to more family-centered cultures like the Arab cul-
ture, where family harmony can often be of greater value than individual
autonomy.17 In sub-Saharan Africa, the family frequently decides the form
of treatment, and women often get the permission of their husbands to
follow a physician’s advice.18 In fact, in these cultures some feel that
insisting on patient autonomy can run counter to the deepest held values
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776 K. Estabrook
of that ethnic group and can in fact turn into another form of modern-day
paternalism.17 A different way to view autonomy in a family-centered
culture would be to see the patient’s choice to allow family to be the pri-
mary communicators and decision makers as a form of autonomy in and
of itself, permitting it is actually the choice of the patient.3
5. ESSENTIAL ETHICAL SKILLS

Once an understanding of the basic principles in ethics has been obtained,
it has been proposed that certain skills are needed to apply ethics to daily
clinical practice.19,20 The ethical skills in Table 2 can be organized into
skills that work to prevent ethical problems from arising and skills that are
employed to identify and manage ethical dilemmas once they do arise.
Being familiar with these skills and applying them to clinical situations in
a pragmatic manner serves as a bridge from ethical theory to the daily
application of ethics. Although working knowledge of these concepts is
important to all medical professionals, those in mental health have the
advantage of already incorporating many of these skills, such as self-
awareness and supervision, into psychiatric practice and training. Perhaps
this is why psychiatrists and mental health professionals are well suited,
and often called upon by others, to interpret and give opinions on ethical
dilemmas.
Some ethical dilemmas can be prevented through deliberate steps on
the part of the mental health professional. For example, a psychiatrist who
prescribes a patient an antibiotic for a supposed urinary tract infection that
turns out to be a sexually transmitted disease could have easily avoided
this mishap, and ethically questionable decision, by being more careful to
Table 2. Practical skills for prevention, identification, and management of ethical

dilemmas.20
Prevention Identification and management
Stay within the scope of one’s knowledge Recognize ethical issues as they arise
Maintain self-awareness of personal biases Seek out supervision and ethics consults
Build ethical safeguards
Anticipate ethically problematic situations
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stay within the scope of one’s practice. Continually engaging in internal

examination of one’s biases, opinions, and values is another skill that can
prevent possible ethical dilemmas. This can be done by simply acknowl-
edging and being aware of personal discomfort and then examining what
may be the source of that discomfort. It could also be a more conscious
act when clinicians are involved in a situation in which they know they
hold strong opinions. For example, a strictly pro-life, religious psychia-
trist who works with a young, unmarried pregnant woman considering
abortion would be best served by acknowledging internally the bias that
exists and carefully consider this bias in all interactions with this patient,
as to maintain the highest ethical standards. Ethical safeguards can be
built into practice, as well, to decrease potential ethical problems. For
example, patients should be informed up front about the limits of confi-
dentiality. Anticipating situations that tend to bring up ethical dilemmas
and how they might be addressed before the situation arises is also useful.
For example, placing a patient in restraints is a high-risk ethical situation
that a psychiatrist is likely to encounter, so a clear understanding of the
local law and ethical opinions regarding restraints is helpful and will aid
in making good ethical decisions regarding this issue when it does arise.
Inevitably, ethical issues will arise even with strict attention to the ethi-
cal skills aimed at prevention. Thus, it is also important to gain compe-
tence in identification and management of ethical issues. It is obvious that
an ethical issue cannot be dealt with and examined without first acknowl-
edging that in fact an ethical situation has arisen. However, this is possibly
one of the most difficult skills to acquire because it so often requires close
scrutiny, or a “second look” at an issue that in a busy clinical practice
could easily be missed or glossed over. A clear understanding of areas of
common ethical difficulties in mental health is helpful to ensure that these
issues are identified when they arise. Careful attention to what some might
call “gut feelings,” or a feeling of unease, also can serve as a flag to con-
sider if that unease is being triggered by an unidentified ethical situation.
Lastly, once an ethical dilemma is identified, it is a skill unto itself to
know when an ethical problem has reached a level that a second opinion
or an ethics committee should be consulted. In many developed countries
today, ethics committees are available in hospitals for consultation, and
serve a sole purpose of examining medically oriented ethical situations
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778 K. Estabrook
and giving opinions on them. However, even when an ethics committee is

not an option, informally consulting with a more experienced clinician
can be extremely helpful. In fact, becoming comfortable with discussing
difficult cases and situations with a more senior clinician can not only help
to resolve ethical dilemmas, but aid in identifying, and even preventing,
some ethical situations from arising.
6. ETHICS IN PSYCHIATRY
Psychiatry as a specialty deals with people’s most personal emotions,
thoughts, and past experiences. Psychiatry is also a field around which
there continues to be much stigma, particularly in some areas of the world.
The intensely private nature of the work makes ethics and maintaining
professionalism in psychiatry of utmost importance. It also brings unique
ethical situations and challenges to the table. To be able to practically
apply ethical principles and acquired ethical skills, background knowl-
edge in some of the most salient of these unique issues in psychiatric
ethics is required.
6.1. Boundaries
The concept of boundaries is of particular importance in psychiatry
because of the close relationship and intimate details that the patient
shares. Also, the healing in psychiatry, particularly psychotherapy, is often
a result of a positive therapeutic relationship itself rather than a procedure
or prescription.19 It is because of the more intense nature of the relation-
ship that psychiatrists have to pay even more careful attention to bounda-
ries between themselves and patients than other areas of medicine.
Boundaries can be thought of as a frame around the therapeutic rela-
tionship that serves as the limit of appropriate behavior in a clinical set-
ting.7,9 Ideally, appropriate boundaries create a safe and predictable
therapeutic relationship in which the patient can explore their issues with-
out concern of being taken advantage of or exploited. The Madrid
Declaration by the WPA emphasizes that psychiatrists should not use the
psychiatrist–patient relationship to benefit themselves in any way or vio-
late the boundaries of the professional relationship.25 However, this ethical
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guideline does not specify what, exactly, the boundaries of a professional

relationship are. One major and clear boundary is that sexual relationships
with patients are never appropriate. Some psychiatric societies, like the
American Psychiatric Association, have extended the policies to include
prohibiting sexual relationships with all former patients, as well, and this
is widely accepted thinking in psychiatry.1
However, most other boundaries are not hard and fast but, rather,
dependent on the patient, relationship, and nature of the psychiatric work.
For example, a hug from a patient with borderline personality disorder in
long-term psychodynamic psychotherapy is likely outside the boundaries
of a professional relationship, but a hug from a developmentally delayed
young child in a medication management clinic in most cases would be
considered benign. This illustrates that boundaries can be fluid in nature.
In psychiatry this concept has been further expanded to differentiate what
have been labeled boundary crossings from boundary violations. A bound-
ary crossing is a mild over-stepping of the boundaries that does not harm
the patient or the therapeutic relationship and can even be beneficial for
the patient.7,9 An example of a boundary crossing would be in the opening
vignette of the chapter in which a woman with paranoid schizophrenia
gives a handmade gift to a resident psychiatrist who is soon graduating.
Accepting gifts in psychiatry, particularly when the treatment modality is
psychotherapy, is commonly thought to be outside of the professional
boundaries. However, in this case, the gift is of nominal value because it
was homemade, and not accepting the gift could worsen the patient’s para-
noia or self-esteem. Thus, graciously accepting the gift in this instance
may actually be more beneficial to the patient than refusing it.
Contrast this to a wealthy patient who, one year into weekly therapy for
mild depression, offers the psychiatrist a weekend at his oceanfront home
as a thank-you for his service. This would be more consistent with a
boundary violation, which involves transgression of boundaries with
potential harm to the patient. If accepted, the patient may later in therapy
begin to feel taken advantage of or start to expect favors like extra session
time in exchange for such an extravagant gift, and therapeutic and profes-
sional relationship could be damaged. Again, the distinction lies in not
only the boundary itself, but also the patient and the situation.
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780 K. Estabrook
The overriding ethical principles that should be applied to practical

questions of boundaries are beneficence and non-maleficence. That is,
ensuring that in all clinical encounters, the commitment to “do good” for
the patient and to not cause harm to the patient needs to be above the
therapist’s own personal motivations and wishes. Boundary crossings can
quickly progress to boundary violations; thus, the clinician must be vigi-
lant and aware of possible boundary issues.9 In the case of boundaries, a
conscious commitment to beneficence at all times helps to safeguard one
against boundary violations. Additionally, the mental health professional
must be familiar with ethical standards and opinions on boundary issues,
pay close attention to and examine feelings of uneasiness in any clinical
encounter, and have access to an honest, trustworthy supervisor with
whom to discuss these situations.20
6.2. Confidentiality: An Evolving Ethical Challenge

Confidentiality is central to building and maintaining the therapeutic rela-
tionship; however, absolute privacy is not a reality in medical care today.
Health care at present involves many individuals who need access to
patient charts, like nurses and medical assistants, as well as multiple non-
clinical staff, like secretaries and billing personal. Thus, what is written in
a patient’s chart is not completely private, and patients should be informed
of that fact. However, a patient can expect confidentiality, which can be
thought of as protection from any unnecessary or non-patient-care-
directed breach of privacy without consent from a patient. However, in an
era of third-party payers and the easy access to patient records afforded by
the advancement of electronic medical records, the ability to maintain
confidentiality is continually being threatened.19
The guiding ethical principles in confidentiality are autonomy and non-
maleficence. Autonomy is central to confidentiality. Namely, patients
have a right to know who and why people may need or have access to their
medical information. They also ethically should be able to make informed
decisions about who gets that information. Nonmaleficence is also a cen-
tral theme in confidentiality and ethical dilemmas involving privacy
issues, especially when breaching confidentiality is necessary. In those
cases it is in the interest of doing no harm to both the patient and the
general public that guides when, and if, to break confidentiality.
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From an international guideline perspective, the WPA’s Madrid

Declaration states that psychiatrists must do everything possible to ensure
that patient’s medical information is kept confidential.25 However, it is
acknowledged that there are times when such confidentiality could be
breached.25 It is widely accepted, and in many countries mandated, that
knowledge of child or elder abuse, for example, must be reported to
authorities and thus patient confidentiality must be broken. It is also
broadly acknowledged that if patients are a threat to themselves or a third
party that confidentiality must be breached for the safety of those involved.
In some countries, such as the United States, it is also mandated that the
mental health provider warn the third party at whom the threat was tar-
geted. However, it is important to note that in any case of breaking confi-
dentiality, no more than the minimum information needed to protect
should be given.21
Although there are some direct guidelines to confidentiality, much of
this area of ethics is subject to ongoing debate and influenced greatly by
culture. Expectations regarding confidentiality vary widely from country
to country given each country’s system of pay, rules and regulations about
mandatory reporting, and family dynamics within the culture. For exam-
ple, in Western cultures, it is an expectation, and in many countries a legal
obligation, to get consent before discussing a patient’s medical or psychi-
atric issues with family members. However, in Arab culture, for example,
the expectation often is to tell the family first about a major diagnosis or
treatment, and the family will then decide whether to inform the patient.17
Thus, the expectation of confidentiality amongst families may be different
in different cultures. Regardless of culture, however, patients have an ethi-
cal right to decide who receives their healthcare information, even if they
decide themselves that they would like to have their family receive that
information first.
Psychiatry in particular is a field where treatment is based on trust and
the patient feeling safe to freely disclose personal information to the phy-
sician. Thus, patients should be able to expect confidentiality be main-
tained, and therefore patients should be informed of the limits of
confidentiality. Explaining to patients in a clear and direct manner the
nature of confidentiality and the safeguards in place to protect their confi-
dentiality, such as written consent forms, will encourage open and honest
communication and likely result in more effective psychiatric care.
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782 K. Estabrook
6.3. Informed consent

Informed consent is the formal medical-legal process by which a patient
agrees, or does not agree, to a particular treatment intervention. It is more
than just a signed sheet of paper; it is a free exchange of information,
values, and goals of treatment between the patient and health care pro-
vider that results in an agreed-upon action of care with full understanding
and knowledge of the risks and potential benefits of that choice. However,
the ability or capacity of a patient to give consent is not always clear-cut.
Take, for example, a chronically ill man with major depression who
refuses a blood transfusion in the setting of an acute gastrointestinal bleed,
stating that he no longer has the will to fight, or a young woman with
schizophrenia who refuses antibiotics for a kidney infection because she
believes that drugs are the “devil’s work.”
Psychiatrists are often called on to assess difficult cases of informed
consent, such as these, and give opinions about the patient’s decision-
making capacity. Thus a complete understanding of what truly is informed
consent and how to decide if a patient has decisional capacity, which is
only one part of informed consent, is integral to mental health care
training.
Informed consent has three components that must all be met in order
for true informed consent to occur (Fig. 1).19,20 The first component of
informed consent is the exchange of information to the patient about diag-
nosis, the proposed treatment, and its risks and benefits. This includes the
risk of refusing the suggested treatment and discussion of alternative treat-
ments. The second component of informed consent is decisional capacity.
Decisional capacity is the patient’s ability to fully assess and understand
the medical decision at hand and to apply meaning and comprehension of
that understanding to his or her own value system and situation.
Volunteerism is the third component of informed consent. It involves the
patient’s ability to decide on a course of action that is consistent with his
or her own sense of self and is, therefore, inherently free of coercion or
outside influencing factors. For example, the patient described above with
depression would likely be found to lack the volunteerism component of
informed consent because his major depression is an external influence
that affects his ability to think clearly.
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Fig. 1. Three vital components to informed consent.20
Decisional capacity can be further broken down into four components:

communication, understanding, reasoning, and appreciation (Fig. 1). All
four must be intact in order for a patient to have decisional capacity.2,20
Communication is literally the ability to communicate choice. Thus,
someone in a catatonic state who refuses to speak or write does not have
the ability to give informed consent because he or she lacks that compo-
nent of capacity. Understanding is the capability to comprehend the fac-
tual information involved, such as the nature of one’s illness, the risks and
benefits of a certain medication, and alternatives. Reasoning refers to the
ability to use the factual information in an objective and logical way. For
example, a reasonable person with new-onset mild depression would
choose a selective serotonin reuptake inhibitor (SSRI) over an experimen-
tal and invasive treatment like deep brain stimulation (DBS) as a first
option for treatment. Appreciation is the subtlest of the requirements for
decisional capacity and involves the patient synthesizing all of the above
components and applying them to his or her situation given his or her
personal values, beliefs, and emotions.
An evaluation for capacity often begins by having patients explain in
their own words the medical situation at hand. Further evaluation
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784 K. Estabrook
of reasoning and appreciation can be obtained by asking the patient to

envision the outcome for all given options in detail, as well as a full mental
status examination to examine for abnormalities, like psychosis or delu-
sions, that often make full appreciation of the medical situation difficult.
It is important to note that decisional capacity is neither permanent nor
legally binding. Competence is the legal terminology for people who are
not able to make decisions for themselves and reflects a more permanent
state of incapacity. Decisional capacity, in contrast, can change day by day.
For example, a patient with a severe delirium would generally lack the
capacity to refuse a blood draw for routine laboratories, but when the
delirium clears, the same patient may meet all the standards for decisional
capacity and could not be forced to have laboratories done.
The level of capacity, and therefore requirements for informed consent
necessary for different decisions, also varies. Decisions that are low risk,
whether refusing or accepting treatment, do not require the same level of
decisional capacity as high-risk situations. For example, a delusional
woman with schizophrenia who refuses to have a routine lipid panel
drawn does not need to meet the same criteria for decisional capacity and
informed consent as if she were to refuse antibiotics for a kidney infec-
tion. Capacity should not just be scrutinized when someone refuses the
recommended treatment, but in all high-stakes settings. For instance, a
person seeking an organ transplant should meet rigorous criteria for
informed consent and capacity as well. This has been labeled the “slid-
ing scale” of informed consent, to illustrate that the risk–benefit ratio
involved is directly proportional to the stringency of informed consent
and capacity.20
6.4. Dual roles

Mental health professionals, by nature of their expertise, are often asked
to assume additional roles besides patient care. For example, a psychiatrist
may be asked to be on an expert panel by a pharmaceutical company or a
political committee advising mental health care law. These types of situa-
tions can be a source of ethical conflict by adversely affecting a mental
health care professional’s ability to be unbiased in patient care.
Relationships with pharmaceutical companies or the medical supply
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industry is a major point of ethical focus recently. The concern is that

financial incentives or gifts may affect patient care. In a large meta-
analysis, it was in fact found that funding of conferences, medication
samples, and continuing medication education sponsored by industry does
affect prescribing practices.22 While the actual effect on patient care is
unclear, it is important that clinicians appreciate, and attempt to minimize,
possible influence to patients that comes from dual roles. Awareness of the
ethical conflict and commitment to providing unbiased patient care and to
minimizing unnecessary dual roles can be a starting point for managing
these situations.
Another form of a dual role is often described as dual agency, in which
the health care professional is asked to perform professional duties outside
of the normal role of a physician.21 An example of this is the chapter’s
opening vignette in which a forensic psychiatrist is asked to perform a
competency evaluation on a death row inmate. Another example would be
psychiatrists involvement in guiding military interrogations, as has
occurred recently in the United States.12 Being involved in decisions on
capital punishment and interrogation is normally outside the role of a
physician by the ethical principle of non-maleficence, yet forensic psy-
chiatrists are often asked by governments to perform such evaluations.
Although the WPA’s ethical guidelines oppose physician involvement in
interrogation or capital punishment evaluations, these particular examples
of dual agency continue to be controversial.8,25 However, it is illustrative
of the fact that a professional at times plays multiple potentially conflict-
ing roles involving patients. In these situations, it is important that there is
full disclosure of the role the physician is playing in the patient’s care, the
extent of confidentiality, and potential ramifications of any information
obtained in situations of dual agency.19
6.5. Ethics in training

Psychiatry and psychology trainees as well as medical students often find
themselves in ethical dilemmas simply by being in training. It is, in many
ways, another form of dual agency, in which a trainee is attempting to be
a learner and to fulfill patient care obligations.6,19 Being in training inher-
ently means having a lack of experience and knowledge that overall can
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786 K. Estabrook
place the trainee in uncomfortable positions. For example, does a patient

need to be informed that the psychiatry resident performing electrocon-
vulsive therapy has never been involved in that procedure before, provided
there is appropriate supervision? Should a psychiatry resident bypass the
sometimes confusing explanation of being a training doctor in psychiatry
when the patient is paranoid and acutely psychotic?
Often the questions involving inexperienced training clinicians can be
thought of as a balance between beneficence to the society as a whole
(which is clearly benefited by continued training of mental health profes-
sionals) and ensuring that patients are not in any way harmed or receive
lesser care because of a trainee’s involvement. Faculty members play a
role in achieving this with close supervision and adequate support of the
students and trainees. In regard to the examples above, it is always best
that a professional in training explain his or her role and level of experi-
ence to a patient and allow the patient to address specific concerns related
to that explanation. Trainees themselves can ensure that patients are pro-
tected from errors that are based on lack of knowledge or inexperience by
seeking out supervision and asking questions when one begins to feel
discomfort in clinical situations. However, time constraints and possibly
embarrassment or pride in having to seek out faculty guidance often
prevents this from happening in the “real world” of patient care. It is
important for the trainee to remember, though, that seeking out ade-
quate supervision and guidance is an ethical obligation to protect patients
from harm.
6.6. Research
Research in psychiatry using human subjects is a necessary part of the
advancement of treatment for the mentally ill to relieve suffering.
However, the psychiatric population has special risks and considerations
involving research due to the fact that the nature of their illness can impact
cognitive processes and thus can affect the ability to receive truly informed
consent.21 For example, can a man with schizophrenia who believes that
joining a research study will guarantee him safety from the military
police, who he thinks are out to get him, be admitted to a research study
for antipsychotic medication? This illustrates how impaired thinking can
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be both the issue that possibly limits ability to true informed consent (in
this case psychosis) but also can be the very illness that the researching
team is attempting to study. This can make research in psychiatry a
complicated undertaking.
The overarching ethical framework for psychiatric research involves
the principles of beneficence, justice, and non-maleficence. The concept
of beneficence in research concerns the broader sense of providing benefit
to society and decreased suffering through advances in treatment and
diagnosis of disease. Thus, the concept of beneficence does not always, in
the area of research, mean direct benefit for the subject enrolled in the
study. At times, research subjects can get direct clinical benefit, such as
when they are enrolled in drug trials in the treatment arm, but at other
times a subject is placed in the placebo arm of a study, and thus does not
garner any direct benefit from the trial. In this case, then, the ethical prin-
ciple of beneficence in research is broadened to include the general public
and those individuals who suffer from the illness that is being researched.
Thus non-maleficence is the balancing and protective ethical principle for
the individual subjects enrolled in research studies. Non-maleficence to
the clinical subjects enrolled in research is the most important overriding
ethical principle, and must be carefully built into each research study and
continually monitored throughout the clinical investigation. The principle
of justice in research guides recruitment of subjects and works to ensure
equal opportunity and access to research. Justice also ensures that no
population, specifically vulnerable populations, carries an overwhelming
burden of involvement in research.
Specific worldwide ethical guidelines are also in place to protect
patients and guide researchers on the ethical use of human subjects in
medical research. The World Medical Association’s Declaration of
Helsinki is the worldwide standard for medical research ethics and serves
as an international guide on how to conduct ethical medical research with
human subjects.24 Some of the basic principles of the Declaration of
Helsinki state that it is the physician’s duty to protect the dignity, health,
and privacy of human subjects, that human subject welfare in research
should be placed at all times above advancement of knowledge and inter-
ests of society, and that research protocols should be carefully considered
and submitted to review boards for approval to minimize potential harm.24
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788 K. Estabrook
The Declaration also discusses the idea of risk versus benefit, which has
now been widely accepted as a basic standard in human research, which
is guided by the moral principles of societal beneficence and individual
non-maleficence as described earlier.23
Informed consent is a basic premise of human research as well and
has been an area of contention in psychiatric research due to the inherent
vulnerability of the mentally ill and the concern that informed consent is
more difficult to obtain in the setting of serious mental illness.2 However,
it is also ethically concerning to make general policies or special
requirements that restrict the mentally ill from being involved in
research. Studies in this area suggest that subjects with serious psychi-
atric illness are generally able to give informed consent for research and
that their motivations for enrolling in psychiatric research are generally
similar to those of people enrolling in other medical research.5 Those
who do have difficulty with informed consent often can have improved
understanding of the research process with educational interventions.21
Thus, serious mental illness alone does not ethically exclude individuals
from participating in research. Overall, it is important that individuals
with mental illness neither carry the burden of research nor be limited by
blanket policy from participating in research because of their mental
illness.
7. CONCLUSION
Ethics is an important endeavor in all fields of medicine, but because of
the increased vulnerability of the mentally ill, it is an essential part of the
field of psychiatry. This chapter served as a brief overview of basic ethical
principles, the history of international psychiatric ethics, and special top-
ics in psychiatric ethics with an international perspective. Laws and cus-
toms in individual countries and regions should be reviewed, particularly
in regard to confidentiality, informed consent, and involuntary treatment,
to gain a more complete understanding of local rules and regulations.
Ethics in psychiatry has evolved over the last century from a minor con-
sideration to a key component of competency. The future of ethics in
psychiatry will need to adapt to new issues and the challenges of advanc-
ing technology. Although the details of ethical discussions may evolve and
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change over time, the most important consideration — protection and

ethical treatment for those suffering with mental illness — should remain
at the center of each patient interaction and in the foreground of day-to-
day clinical work.
8. KEY POINTS
• Be cognizant of potential ethical dilemmas in order to spot them when
they arise.
• Use basic ethical principles as a guide to solving ethical dilemmas.
• Consider an ethics consult for particularly difficult cases.
• Keep cultural norms in mind but evaluate each individual’s personal
beliefs and values.
• Discuss with a supervisor all ethical cases with which you feel uneasy.
• Decisional capacity is fluid in nature and distinct from competence,
which is court determined.
• Be honest with patients about your level of training and experience.
• Be familiar with local laws surrounding confidentiality and its
exceptions.
• Do not engage in sexual relationships with any current or former
patient.
9. SELF-ASSESSMENT
9.1. A 35-year-old woman dies from an intentional overdose.
Her husband approaches her psychiatrist of the last
10 years, devastated about her death and looking for
answers as to why she might have killed herself. The
patient did not sign a release of information before her
death. What should the psychiatrist say to the husband?
(A) The psychiatrist should tell the husband everything that is known
about the patient, because now that the patient is dead, confidentiality
is no longer needed.
(B) The psychiatrist should not tell the husband anything because of
possible legal action against the psychiatrist for the patient’s death.
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790 K. Estabrook
(C) The psychiatrist should explain that he or she is not able to reveal any
information about the patient because of confidentiality
requirements.
(D) The psychiatrist should tell the husband only the minimal amount of
information needed to answer his questions, if the psychiatrist thinks
that the patient would have been okay with that.
Confidentiality rules apply even after a patient’s death. In this case, the
patient did not sign a release of information form, and thus the psychiatrist
is ethically, and in many countries legally, bound to continue to uphold
standards of confidentiality. In some countries verbal consent before death
on the part of the patient may suffice; however, many require a written
consent to release medical information, even to families. This is based on
the ethical principle of autonomy and fidelity.
Answer: C
9.2. A 19-year-old man is found wandering the street, confused

and clothed only in underwear, on a very cold night. On
evaluation he denies thoughts of harming himself or
wanting to harm others. He insists that he was on his
way to church, and he is religiously preoccupied and
psychotic. The patient declines inpatient treatment
and requests a cab home. The psychiatrist should:
(A) Try to reach a family member to pick up the patient to ensure that he
gets home safely.
(B) Admit the patient against his will to a psychiatric unit.
(C) Convince the patient that he needs to be admitted to a medical unit
for observation of possible frostbite and then treat his psychosis
while on the medical unit.
(D) Send the patient home in a cab. Because he is not homicidal or
suicidal, he cannot be admitted against his will.
Although the patient is not suicidal or homicidal, his mental illness still
caused him to take actions that placed him in danger of bodily harm. This
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is generally accepted as a reason for treatment against one’s will because,

given the patient’s actions, he is not able to safely care for himself. It is
unnecessary to attempt to convince him to be admitted to a medical bed,
and given the extent of his psychosis, that is not the best treatment
environment for him. This is based on the ethical principles of both
beneficence and non-maleficence.
Answer: B
REFERENCES
1. American Psychiatric Association. (2009) The Principles of Medical Ethics
with Annotations Especially Applicable to Psychiatry, American Psychiatric
Association, Arlington, VA.
2. Appelbaum P, Grisso T. (1995) The MacArthur competence study I, II, III.
Law and Hum. Behav 19: 105–174.
3. Beauchamp TL, Childress JF. (2009) Principles of Biomedical Ethics, 6th ed.
4. Blackhall LJ, Murphy ST, Frank G, Michel V, Azen S. (1995) Ethnicity and
attitudes toward patient autonomy. JAMA 274: 820–825.
5. Dunn LB, Candilis PJ, Roberts LW. (2006) Emerging empirical evidence on
the ethics of schizophrenia research. Schizophr Bull 32: 111–119.
6. Hoop JG. (2004) Hidden ethical dilemmas in psychiatric residency training:
The psychiatry resident as dual agent. Acad Psychiatry 28: 183–189.
7. Gabbard GO. (1999) Boundary violations. In: Bloch S, Chodoff P, Green SA
(eds.), Psychiatric Ethics, 3rd ed. Chapter 8, pp. 141–160, Oxford University
Press, NY.
8. Gutheil, T.H. (1999) Ethics and forensic psychiatry. In: Bloch S, Chodoff P,
Green SA (eds.), Psychiatric Ethics, 3rd ed. Chapter 16, pp. 345−362,
9. Gutheil TH, Gabbard GO. (1993) The concept of boundaries in clinical prac-
tice: Theoretical and risk-management dimensions. Am J Psychiatry 150:
188–196.
10. Kastrup M. (2000) Scandinavian approaches. In: Okash A, Arboleda-Florez J,
Sartorius N (eds.), Ethics Culture and Psychiatry, pp. 65−82, American
Psychiatric Press, Washington, DC.
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11. López-Muñoz F, Almo C, Dudley M, Rubio G, Garcia-Garcia P, Molina JD,

Okasha A. (2007) Psychiatry and political-institutional abuse from the his-
torical perspective: The ethical lessons of the Nuremberg trial on their 60th
anniversary. Prog Neuro-Psychoph 31: 791−806.
12. Marks JH, Bloche MG. (2008) The ethics of interrogation — the U.S. mili-
tary’s ongoing use of psychiatrists. JAMA 359(11): 1090−1092.
13. Mizushima Y, Kashii T, Hoshino K. (1990) A survey regarding the disclosure
of the diagnosis of cancer in Toyama prefecture, Japan. JPN J Med 29:
146–155.
14. Musto DF. (1999) A historical perspective. In: Bloch S, Chodoff P, Green SA
(eds.), Psychiatric Ethics, 3rd ed. Chapter 1, pp. 7–23, Oxford University
Press, NY.
15. Nakane Y, Radford M. (2000) Intersubjectivity and its influence on psy-
chiatry in Japan. In: Okasha A, Arboleda-Florez J, Sartorius N (eds.),
Ethics Culture and Psychiatry, pp. 133−146, American Psychiatric Press,
Washington, DC.
16. Okasha HH. (2000) From the Hawaii declaration to the declaration of
Madrid. Acta Psychiatr Scand 101: 20−23.
17. Okasha A. (2000) The impact of Arab culture on psychiatric ethics. In:
Okasha A, Arboleda-Florez J, Sartorius N (eds.), Ethics Culture and
Psychiatry, pp. 15−28. American Psychiatric Press, Washington, DC.
18. Olatawura MO. (2000) Ethics in sub-Saharan Africa. In: Okasha A,
Arboleda-Florez J, Sartorius N (eds.), Ethics Culture and Psychiatry
pp. 103−108. American Psychiatric Press, Washington, DC.
19. Roberts LW, Dyer AR. (2004) Concise Guide to Ethics in Mental Health
Care, American Psychiatric Publishing, Washington, DC.
20. Roberts LW, Geppert CM, Bailey R. (2002) Ethics in psychiatric practice:
Essential ethics skills, informed consent, the therapeutic relationship, and
confidentiality, J Psychiatr Pract 8: 290–305.
21. Roberts LW, Hoop JG, Dunn LB. (2008) Ethical aspects of psychiatry. In:
Hales RE, Yudofsky SC, Gabbard GO (eds.), The American Psychiatric
Publishing Textbook of Psychiatry, 5th ed. Chapter 42, pp. 1601−1636,
American Psychiatric Publishing, Washington, DC.
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23. Wing J. (1999) Ethics and psychiatric research. In: Bloch S, Chodoff P,
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24. World Medical Association. (2004) Declaration of Helsinki. Available at:
http://ohsr.od.nih.gov/guidelines/helsinki.html. Accessed 22 June 2010.
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http://www.wpanet.org/detail.php?section_id=5&category_id=9&content_
id=48. Accessed 16 June 2010.
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Chapter 31
The Culturally Competent Psychiatric

Assessment
Ajoy Thachil and Dinesh Bhugra
1. INTRODUCTION
Contemporary psychiatry is practised in a globalizing, multicultural
environment. Clinicians increasingly assess and manage patients with
cultural backgrounds different from their own.3 In this environment, a key
task is to assess the patient and formulate their problems in the context of
their culture. Patients may not present with classic ICD or DSM symp-
toms. Presenting symptoms are influenced by cultural conceptions of
illness and the way cultures allow idioms of distress to be expressed.
They are modified by the way in which idioms are presented. Patients
may use culturally familiar metaphors to express their distress.15 The
clinical interaction itself is influenced by the personal history, training,
socioeconomic status and culture of the clinician, and the personal his-
tory, education, socioeconomic status, and culture of the patient. Their
beliefs and values may differ.15 Cultural differences can lead to misinter-
pretation triggered by linguistic difficulties, and differing styles of non-
verbal communication and codes of etiquette. Members of non-western
ethnic groups often view mental health services with mistrust because
they may be seen to represent dominant Western cultural values and
implicit racism, and rely on formulations that ignore non-Western cul-
tural values.9 However, blanket cultural assumptions about the ‘other’
794
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The Culturally Competent Psychiatric Assessment 795
may themselves be misconceived and lead to misleading conclusions.

Equally, it is important to remember that persons sharing the same ethnic-
ity can differ in their cultural backgrounds, as ethnic groups are socially
and culturally heterogeneous.
2. CULTURAL PSYCHIATRY
Cultural psychiatry deals with the impact of social and cultural differences
on mental illness: its occurrence, manifestations, management, and out-
comes. From the perspective of cultural psychiatry, culture influences the
sources, the symptoms, and idioms of distress, the individuals’ explana-
tory models, their coping mechanisms, and help-seeking behavior as well
as the social response to distress and disability.14 Thus, cultural differences
can translate into distinct manifestations and treatment expectations of
illness.
In order to provide care that is appropriate and acceptable to people
from different cultural backgrounds, clinicians need to take these factors
into account. This chapter aims to introduce a culturally sensitive frame-
work for the clinical assessment of psychiatric disorders. The sequential
aspects of this framework are sensitivity, awareness, knowledge, and
competence.9 It can be adapted to individual patients’ social and cultural
contexts.
3. DEFINITIONS OF KEY TERMS

The language used to describe cultural issues can be imprecise and con-
fusing. Table 1 offers some useful definitions. They are not comprehen-
sive and may differ from that used by other practitioners working in the
area of culture.
4. THE EPIDEMIOLOGY OF MENTAL ILLNESS

ACROSS CULTURES
International surveys of mental disorders reveal major differences in rates.
The largest so far, the World Health Organization (WHO) study of common
psychological disorders in primary health care, was based in 14 countries.26
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796 A. Thachil and D. Bhugra
Table 1. Key definitions in cross-cultural psychiatric assessment.
Culture: Culture is the learned, shared beliefs, values, attitudes, and behaviors characteristic
of a society or population that guides its thinking, decisions, and actions.17 It refers to
patterns of perceiving and adapting to the world. From a psychiatric perspective, culture
influences the causes, symptoms, and idioms of distress, the patient’s explanatory models,
coping mechanisms, and help-seeking behavior, and the social response to illness.
Ethnicity: A subjective or social description of belonging to a group whose common
heritage distinguishes its members from other groups. This can be based on subjective
identification, a shared culture, common geographic origins, race, religion, or an appraisal
of physical appearance.
Race: An inconsistently defined term that has varied by culture and over time. In
anthropology, it refers to a social construct independent of biological or genetic variation.
In legal usage, it refers to a group of people defined by their skin color, nationality
(including citizenship), or ethnic or national origins.
Identity: A person’s internal self-concept and external expression of his/her individuality
or sense of group affiliation. This can be based on social, cultural, ethnic, economic,
religious, and personal factors.
Acculturation: The process of adapting to another culture while attempting to retain
aspects of ones’ original culture. This may involve physical, psychological, social, cultural,
and biological changes that occur in response to pressure to conform to and accommodate
the dominant cultural lifestyle. Berry2 defines four states of acculturation: integration (both
the individual’s original culture and the dominant culture are valued); separation (the
individual’s culture is valued and the dominant culture is devalued); assimilation (the
dominant culture is valued but the individual’s culture is devalued; and marginalization
(both the individual’s culture and the dominant culture are devalued). Awareness of one’s
cultural history and being bicultural (social competence in host culture without losing the
same competence in the culture of origin) is associated with increased resilience and better
mental health.
Emic and etic: The emic perspective refers to a description of a belief or behavior by a
person within the culture. This insider’s perspective provides a culturally contextualized
interpretation that is culturally specific. The etic perspective refers to a description of a
belief or behavior by an external observer. This outsider’s perspective provides a culturally
neutral interpretation that than can be universally applied to other cultures.
The terms are derived from cultural anthropology.
Cultural competence: The set of congruent attitudes, behaviors, skills, and procedures that
enable the clinician to work effectively and efficiently in cross-cultural situations.
Its key domains are empathy, cultural sensitivity, cultural knowledge, and cultural skills.
Its approach is pragmatic, context driven, and result-oriented.
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Of primary care attendees worldwide, 24% received an ICD-10 psychiatric

diagnosis: the most common being ‘current depressive episode’ (10.4%).
Other common diagnoses were generalized anxiety disorder, neurasthenia
and problems with alcohol. The relatively high rates of neurasthenia were
due to the diagnosis being allowed to stand in the presence of depression
or anxiety. If the ICD-10 exclusion rule is enforced, its prevalence falls to
1.7 % and alcohol problems become the third most common disorder. The
most frequent comorbid disorders were depression and anxiety. Overall,
Asian sites showed the lowest prevalence rates, European and South
American centers the highest. In addition to overall differences in preva-
lence, centres showed significant differences in the relative prevalence of
specific disorders. For instance, anxiety was much more common than
depression in Rio de Janeiro, Nagasaki, and Athens, while the reverse was
true for Groningen and Ankara.
These differences in prevalence may have several causes.26 They may
reflect true variations in population prevalence e.g. lower rates of alcohol
use disorders at a site where there were many Muslims among the popula-
tion accessing the service. They may reflect differences in the selection of
patients into primary care e.g. weakness and non-specific pains may have
been seen as ‘Jibyo’ in Japan or ‘Shin Qua’ in China, conditions typically
managed by traditional healers. Here, culture-specific concepts of illness
prompt those with illness to seek help from non-medical practitioners.
Other factors like differences in clinicians’ recognition and management
of psychological distress and health systems could have contributed to the
variation (the Ibadan Centre, which charges user fees, had one of the low-
est rates of depression).
Two international studies were conducted by the WHO: the International
Pilot Study of Schizophrenia (IPSS),27 based on prevalence samples and
the subsequent Determinants of the Outcome of Severe Mental Disorders
(DOSMeD).13 DOSMeD investigated incidence using active clinical and
community case-finding at 12 research sites in Colombia, Czechoslovakia,
Denmark, India, Ireland, Japan, Nigeria, Russia, the United Kingdom, and
the United States. Both studies found similar rates across centers, for
schizophrenia defined by narrow (stringent) diagnostic criteria. Rates
were divergent across centers when schizophrenia was defined by broader
(less stringent) diagnostic criteria. It has been hypothesized that this may
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indicate a wider range of correlates that are culturally influenced or fur-

ther, a different subtype of schizophrenia. Replications of the DOSMeD
design have been carried out with similar results by investigators in India,
the Caribbean, and the United Kingdom. The IPSS found a significantly
better overall outcome for schizophrenia in India and Nigeria at 2 and 5
year follow-up. The epidemiologically designed DOSMeD showed a
more complex picture. High rates of complete remission were signifi-
cantly more common in developing countries (37%) than in developed
ones (15.5%). However, the proportions of continuous unremitting illness
(11.1% and 17.4%) did not differ significantly between the two settings.
Patients in developing countries experienced significantly longer periods
of unimpaired functioning in the community, although only 16% of them
were on continuous antipsychotic medication (compared with 61% in the
developed countries). Family environments may explain variations in
prognosis; expressed emotion (EE) is a key culturally influenced variable
that could explain this. An international comparison has shown that the
prevalence of high EE households is greatest among the most industrial-
ized and urbanized societies and least among rural agrarian societies.16
Systematic reviews indicate that prevalence estimates of schizophrenia
from ‘least developed’ countries are significantly lower than those from
both ‘emerging’ and ‘developed’ sites ( p = 0.04).22
Studies of the global occurrence of schizophrenia reveal higher rates of
both incidence and prevalence in migrants compared to native-born indi-
viduals. Incidence rates in migrants are significantly higher.20,22 The
excess risk differs according to ethnic origin; it is significantly higher in
black migrants than in their white or non-white non-black counterparts.
Rates in countries of origin are not particularly high, strongly suggesting
that the increased risk in migrant groups is related to environmentally
mediated exposures. The stress of migration, social defeat, stigma and
discrimination, and Vitamin D deficiency (in dark skinned migrants to
northern latitudes) have all been proposed as likely factors. Increased risk
among migrants have been observed in affective and other psychoses, and
in neurodevelopmental disorders such as autism in children born to
migrant parents.7 Again, the excess risk of neurodevelopmental disorders
is significantly higher in children born to black migrants, than to their
white or non-white non-black counterparts. Very low rates of autism were
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reported by the first study on autism in Africa and the rates were even
lower in African children of African parents who had not left Africa.19 No
increased risk has been found for other mental disorders. Differences in
the prevalence of anxiety and depression between migrant and native-born
communities are inconsistent internationally. International studies of
depression have found more comorbid personality disorders in Western
centers.
The observed epidemiological differences may be true or influenced by
methodological problems related to insufficient cross-cultural validation
of instruments and methods. Such problems can artificially exaggerate or
reduce rates. Ideally, data should be collected using research questions
and instruments that have been validated both qualitatively and quantita-
tively, using a mixture of emic and etic approaches. It should then be
interpreted within the cultural i.e. emic context of symptoms, illness
experience, and disease.6
5. CULTURE-RELATED SPECIFIC SYNDROMES

These are mental and behavioral syndromes whose occurrence or mani-
festations are closely related to cultural factors, and which thus warrant
understanding and management from a cultural perspective.23 Over the
last hundred years, the term has evolved from the colonial “peculiar psy-
chiatric disorders,” to the West-centric “culture-bound syndromes” and
recently, to the epidemiologically neutral “culture-related specific syn-
dromes.”23 They often cut across diagnostic categories.
The ICD-10 and DSM-IV list a large number of such syndromes
including Dhat syndrome reported from India, Nepal, Sri Lanka,
Bangladesh, Pakistan, and Taiwan (anxiety, depression, and hypochon-
driacal complaints associated with undue concern about the debilitating
effects of the passage of semen), Koro reported from China, Malaysia,
Indonesia, Thailand, and India (anxiety and fear that the penis, vulva, or
nipples will retract into the body and cause death), and Ataque de nervios
reported from Latin Caribbean, American, and Mediterranean groups
(loss of control triggered by a stressful familial event resulting in shout-
ing, crying, trembling, heat rising to the head, aggression, dissociative
experiences, and suicidal gestures). Western culture-related specific
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syndromes include anorexia and bulimia nervosa,18 Type A behavior,11 and

Multiple Personality Disorder.21
Attempts to force these syndromes into descriptive classification sys-
tems risk the loss of their unique cultural meaning.23 It is also necessary
to be cautious while labeling “peculiar behavior” as a “disorder” and
“culture-bound” simply because it is unfamiliar. A classic example is pro-
vided by the phenomenon of latah, first described by W. Gilmore Ellis, the
medical superintendent of the Government Asylum in Singapore in the
Journal of Mental Science in the late 19th century.8 Latah, a term of
Malaysian and Indonesian origin, refers to a condition where, startled by
sudden fright, victims fall into a trance in which they engage in repetitive
speech or movements, including echolalia, echopraxia, and command
obedience. Anthropologists now view latah as a social behavior and not a
“disorder,” even though some psychiatrists have considered it a psycho-
pathological condition and offered clinical diagnoses ranging from hys-
terical dissociation to hysterical psychosis.
Years later, a similar behavior was reported by the Japanese psychiatrist
Uchimura25 among the Ainu, an aboriginal minority ethnic group living in
the Eastern Siberian island of Sakhalin and the northern Japanese island
of Hokkaido. This was an entirely different ethnocultural group from the
Malays and the behavior was called imu (literally, possessed). These phe-
nomena are rarely observed today, except among older people who have
known about it from when they were young. A similar pattern has been
observed with amok (mass, indiscriminate homicidal acts that tend to be
precipitated by a perceived slight or insult) reported originally among the
Malays, then from New Guinea, Laos, Thailand, and the Philippines.
Terrifying episodes of amok behavior have recently and frequently
occurred on school campuses and in workplaces in the United States.23
Globalization and subsequent “Westernization” has also seen the spread
of eating disorders and Type A behavior to societies where these were
hitherto unknown.
Once cultural considerations are incorporated into all descriptive diag-
nostic categories, it will no longer be necessary to group culturally deter-
mined behavioral patterns into the disconnected categories of “other
specific neurotic disorders” in ICD-1028 and “culture-bound syndromes”
in DSM-IV.1 It is more important to focus on the cultural context of each
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individual’s distress and that of every disorder, rather than being con-
cerned with finding room for specific syndromes in current classification
systems.23
6. PREPARING FOR A CROSS-CULTURAL

PSYCHIATRIC ASSESSMENT
Before commencing the assessment, it is important to ascertain key fea-
tures of the culture relevant to the assessment. These include first and
preferred language, cultural norms, taboos, rites of passage, and religious
values. It is useful to ascertain the preferred mode of help seeking
(e.g. prayer, rituals, and traditional healing) and the reasons for seeking
psychiatric help at this instance. It is particularly important to understand
patients’ notions of intimacy and the clinician–patient encounter, and
cultural expectations of what a doctor, nurse, social worker, or therapist
are supposed to do. Gender may influence these perceptions, and this
aspect has to be explored beforehand.
If the clinician is not fluent in the patient’s preferred language of com-
munication, an appropriate interpreter must be identified. Interpreters
have different levels of linguistic proficiency and understanding of idioms
of distress and emotional states. It is important to ascertain the extent
of the interpreter’s cultural knowledge and identify areas of difference
e.g. dialect, tribe, caste, social status, and religion. A preliminary discus-
sion with the interpreter regarding the importance of gestures, smiles, and
non-verbal behavior, and the identification of idioms of distress and
emotion-laden phrases is crucial to developing a useful partnership.
However, emotional communication across cultures is complex and sub-
ject to distortion, more so when a third person is involved. Organizational
policies that ensure the recruitment and training of specialized interpreters
to meet the mental health needs of the local population can address this
problem to a great extent.
This should be followed by an unstructured 10-minute period of cul-
tural familiarization with the patient where idioms of distress and
emotion-laden phrases can be identified to orient the clinician (and inter-
preter) to the patient’s style of communication. If informants or family
members are present, this time could also be used to familiarize oneself
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Table 2. Setting up a cross-cultural psychiatric assessment.9
1. Obtain maximum pre-assessment information.

2. Clarify patient’s pathway into care, preferred mode of help-seeking, and reasons for
psychiatric consultation at this instance.
3. Identify key features of culture relevant to the assessment. These include cultural
norms, taboos, religious values, rites of passage, appropriate physical distance and eye
contact, appropriateness of physical contact, appropriate means of exploring sensitive
issues, and impact of gender.
4. Clarify patients’ and their families’ sense of urgency and expectations of the
consultation.
5. Clarify patients’ and their families’ explanations of causes, likely outcome, and
treatment of illness, and perceptions of illness, disability, and stigma.
6. Identify common and culturally acceptable idioms of distress.
7. Be aware of your own culture and how it can influence your perceptions and
assessment technique.
8. Be aware of patients’ and families’ skills and strengths. Their coping strategies,
support systems, resilience, and financial capabilities may be crucial to outcome.
9. Know the interpreter’s role, skills, and limitations. Discuss the importance of non-
verbal communication, idioms of distress, and emotion-laden phrases beforehand.
Clarify their level of cultural knowledge and its limits e.g. dialect, tribe, caste, class,
religion, and region.
10. Agree to work collaboratively with all participants: stress on literal translation,
clarification of the cultural context of symptoms, and patients’ and families’ views on
interpretations.
with patterns of communication between the patient and those accompa-

nying, as well as their interpersonal dynamics. Table 2 lists the prelimi-
nary steps in preparing for an optimal cross-cultural assessment.
Be aware that reaching a clinical diagnosis represents only the first step
in cross-cultural psychiatric assessment. It lays the foundation for under-
standing the patient’s distress in its sociocultural context and developing
a collaborative therapeutic relationship.
7. ELICITING THE PSYCHIATRIC HISTORY

Interviewing the patient (and informants) to collect historical data follows
conventional patterns. However, some areas of information are crucial to
the cross-cultural assessment.
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7.1. Identity and worldview

The patient’s sense of identity influences the distress that led to the con-
sultation and their perspective of the clinical encounter. Identity has
social, cultural, ethnic and religious, as well as personal components. It is
important to resist stereotyping and recognize that there can be incongru-
ence between a person’s individual identity and the collective identity of
their ethnocultural group. This incongruence, as well as any incongruence
between individual identity and that of the dominant ethnocultural group
can both generate distress. Identity is also the prism through with patients
view the world. This view of stressors, illness, consultation, outcome,
work, money, play, children, parents, friends, sex, and social role can be
ascertained only after several meetings with the patient, family, advocates,
religious figures, and community representatives as nominated by the
patient. Though necessarily time-consuming, the information thus gained
will provide individually contextualized insights that are crucial to
outcome.12
7.2. Idioms of distress

Patients may use culturally familiar metaphors and emotion-laden phrases
to express their distress. These may be unfamiliar to the clinician and may
not fit classic ICD and DSM presentations. Diverse somatic presentations
have been found across cultures and represent between a quarter and half
of all presentations to all types of doctors in primary and secondary care.
If present, they should be described in terms of location, intensity, fluctua-
tion, and relation to psychological symptoms. The metaphors used as
idioms of distress, the types of somatic presentation, and the reasons for
their deployment vary widely. Nonetheless, it is important to attempt to
understand and contextualize the meaning of such metaphors and emo-
tion-laden phrases through patient enquiry and if necessary, consultation
with informants. They often represent the sole gateway to assessing dis-
tress, psychopathology, and disability. Although core depressive and psy-
chotic symptoms are regarded as universal, many behavioral scientists
(mainly anthropologists) and psychiatrists have argued that they reflect
Western formulations of illness that lack universal validity.
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7.3. Life events

Life events can have a far greater impact on an individual than that
described in the literature. The separation of families due to migration,
even for relatively short periods, can have an adverse impact on mental
health in collectivist societies, where measures of individual wellbeing
are correlated with family wellbeing. The processes of migration and
acculturation are themselves complex clusters of life events that can
include separation, loss, change of status, unemployment, culture shock,
racial discrimination, and rejection. For instance, a marriage into another
culture or country can be stressful for both the individual and family
members. Admission to a psychiatric hospital and separation from chil-
dren and family can itself constitute a traumatic life event for all parties,
with culturally unacceptable consequences. Empathic and flexible inquiry
is necessary to adequately assess the true impact of the patient’s life
experiences.
7.4. Migration and acculturation

Migration can be stressful due to loss, language barriers, social skills defi-
cits, immigration status, change of employment, dislocation, alienation,
isolation from people with common experiences, marriage into another
culture, and acculturation. Losses can include family separation, and loss
of status and social networks. Table 3 provides a framework for assessing
the impact of migration.
Acculturation is a multidimensional phenomenon. Its domains include
language, religion, entertainment, food and shopping habits, attitudes to
traditional patterns of behavior in the community, and changing cognitive
styles and behavioral patterns. It is not identical at every level and degrees
of acculturation may vary across members of the family. For the clinician,
it is important to understand the patient’s degree and perception of accul-
turation to contextualize the patient’s distress in terms of their change in
cultural identity. As discussed in Table 1, the state of acculturation has an
impact on mental health. Table 4 provides a framework for assessing
acculturation and the impact of changes in identity.
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Table 3. Assessment of the impact of migration.9
1. How long ago did the patient migrate? How old were they at the time?
2. Was the migration internal or international?
3. Reasons for migration (e.g. occupational, educational, economic,
political)?
4. Was migration forced or voluntary? Have they experienced violence
or natural disasters?
5. Were they prepared for migration?
6. Did the patient migrate alone or with family? Who was left behind
and how does the patient feel about this?
7. Difficulties in migration?
8. Differences between expectations and outcomes of migration?
9. Perceptions of the new region/country and culture?
10. Social supports? Contact with family and people with common
migratory experiences and a shared heritage?
11. Is this migration temporary or permanent? Previous experiences
of migration and outcomes?
7.5. Discriminatory experiences

Members of minority groups (including but not only ethnic minorities)
may have experienced discrimination in one or more fields of daily activ-
ity. These include major, acute events of discrimination as well as less
obvious, chronic experiences of perceived discrimination. The discrimina-
tion may be based on physical appearance, race, religion, language, gen-
der, sexual orientation, and social class among other factors. Discrimination
can have a profound impact on people’s lives and is associated with both
psychological distress and specific mental disorders. Such experiences
should be carefully investigated in a tactful, respectful, and sensitive man-
ner. Even if such experiences have not contributed to the psychiatric pres-
entation, they should be treated with empathy and respect. If a patient
sensitized by discriminatory experiences feels that you are not paying
sufficient attention and respect to such experiences, they may perceive the
consultation itself as unsatisfactory and discriminatory. They may thereaf-
ter find it difficult to trust you with sensitive information, thereby compro-
mising the therapeutic relationship.9
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Table 4. Assessment of the impact of acculturation.
Language
First language? Others?
With what degree of fluency?
Spoken in what contexts?
Food and attire

What kind at home and outside?
Where do they shop for food/clothes?
Family and relationships

Nuclear, extended, or joint family?
Responsibilities and roles (including gender roles)?
Attitudes to relationships and marriage? Arranged marriage?
Work and education

Education in new country?
Relationships at education and work?
Ethnocultural group of fellow students and co-workers?
Entertainment and leisure

What do they do?
What do they prefer e.g. food, music, movies? Of what type?
Social interaction
Socialize with other ethnocultural groups?
Supports from members of other ethnocultural groups?
Religion
Do they consider themselves religious?
With what belief and frequency? Taboos and rituals?
Where do they practice and with whom?
Culture shock and conflict

Sense of loss and feelings of deprivation?
Persistent feelings of surprise, confusion, anxiety, and
irritability?
Have they experienced discrimination and rejection?
Differences between aspired identity and real identity?
Loss of self-esteem?
Culture conflicts within the family?
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7.6. Personal history

Attitudes towards childhood, adolescence, and parenting are culturally
determined. Equally, attitudes towards sexual development and sex, mar-
riage and relationships, pre and extramarital sex are strongly influenced
by cultural and religious values. In some cultures, it is regarded as inap-
propriate to discuss sexual issues with a member of the opposite sex.
Directly questioning a patient of the opposite sex about such issues may
be perceived as insensitive or threatening. This could disrupt a budding
therapeutic alliance. Under such circumstances, use an interlocutor of the
same sex to put the patient at ease and facilitate trust. Ask about these
issues in a careful, paced, and sensitive manner so that the patient may
respond accordingly.
The phrasing of questions is important when eliciting personal history.
For instance, the question ‘What sort of birth control do you use?’ assumes
that the person uses birth control. This may be inappropriate if the
patient’s religious beliefs preclude this, or if the patient is lesbian.
The assumptions implicit in the question i.e. that the patient does use
some form of birth control or that she is heterosexual, may lead the patient
to surmise that the clinician will not understand or respect her religious
beliefs or sexual orientation. A more helpful question would be ‘Do you
need to use birth control as part of your sex life?’
7.7. Explanatory model of illness

The explanatory model of illness is an internal framework that is the result
of the patient’s efforts to make sense of their symptoms and suffering. It
is shaped by culture. It includes ideas about the nature of the problem, its
cause, severity, prognosis, the preferred mode of help-seeking, and treat-
ment preferences. Patients may attribute symptoms to psychological,
somatic/physical, or social problems. They may be attributed to combina-
tions of the above. They may be even regarded as part of the normal ups
and downs of everyday living. Incongruence between models used by
doctor and patient can affect both diagnosis and management. Eliciting
the model of symptom attribution not only improves outcomes but also
helps ascertain patients’ ability to relate their symptoms in certain styles
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of communication. This helps judge whether physical or psychological

treatments will be more acceptable.
7.8. Previous experience of services and treatment

Previous adverse experiences with services and treatment in any country
can affect engagement. Ethnic minorities in many countries have dispro-
portionately more adverse experiences with psychiatric services and may
view such services as part of an institutional power structure that is
skewed against them and treats them differently. Exploring such experi-
ences is useful in any psychiatric assessment.
8. THE MENTAL STATE EXAMINATION

Cultural factors influence every aspect of psychopathology to some
extent. The symptom and signs elicited during the mental state examina-
tion need to be contextualized within the patient’s culture and reappraised
critically if new information emerges later. It is important not to accept
findings at face value or make judgments based on stereotyped views of
the patient’s culture, for instance while judging attire and behavior.
Although clinicians’ formats for structuring the mental state vary to some
extent internationally, its content is almost always the same. Needless to
say, it must be thorough and detailed, even if the patient is mute, incoher-
ent, or un-cooperative.
8.1. Appearance and behavior

Appearances and behavior that appear unusual to the assessing clinician
may be ethnoculturally appropriate or sanctioned. A common error is to
categorize body type using terms like “short” and “tall” according to the
standards of the clinician’s ethnocultural group. Describing attire as
“colorful,” “conservative,” or “traditional” using a similar approach can be
misleading. The appropriateness of maintaining eye contact is again cul-
turally determined. In such circumstances, it is best to record the appear-
ance objectively, and seek clarifications from the patient, family, and
cultural community about norms and variations from them.
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Behaviors like trance possession, speaking in tongues, religiosity,

reluctance to express emotion, facetiousness, and social physical contact
may be culturally sanctioned. The concept of “personal space” is itself
culturally determined and subject to wide variation across cultures.
Another important component of behavior is patients’ attitudes towards
clinicians. These attitudes, which can range from co-operative and
friendly through guarded to indifferent, ingratiating, or downright hostile,
is influenced both by cultural perceptions of the doctor–patient relation-
ship and past experiences with services, people in authority and intercul-
tural interactions.
These behaviors should be evaluated by recording the behavior objec-
tively, clarifying the patient’s explanation for it, and seeking the response
of the family and cultural community to both the behavior and the expla-
nation. Unfamiliar behaviors that are not contextualized culturally run the
risk of being labeled as psychotic, when they may actually represent cul-
turally sanctioned adaptive coping. Understanding changes in appearance
and behavior is crucial to relapse prevention, since they are often the earli-
est signs by which patients, families, and communities can identify
relapse.
8.2. Impulse control and aggression

Impulse control is usually described as part of behavior, but merits sepa-
rate discussion as a sensitive aspect of cross-cultural assessment. It is a
measure of the patient’s awareness of socially appropriate behavior, risks
to self and others. Is the patient able to control emotional, aggressive,
sexual, and other impulses? A person’s biology interacts with their cultur-
ally shaped experiences to produce frustration and a variety of responses
to it. Anger and aggression are two such responses. Since patients may be
unable to control impulses secondary to psychosis, personality disorders,
and cognitive deficits, anger and aggression are often labeled as manifes-
tations of these. This can be misleading. There may be cultural norms of
frustration, conflict resolution, and acceptability of anger and aggression.
Potentially aggressive situations have to be managed without jeopardizing
trust and the therapeutic relationship. Ensure safety at all costs, but in a
culturally sensitive way. Ensure that you are accompanied by someone
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trained in control and restraint, as well as a relative or friend of the patient.

Evaluate anger and verbal aggression against pre-morbid personality and
cultural norms. Discussion with an accompanying relative or friend is
useful in this regard.
8.3. Mood
People use adjectives like depressed, sad, fed up, empty, fine, happy, and
scared, among others, to describe their mood. However, in everyday life,
especially in Western societies, the expression “I feel depressed” can
mean something figurative, rather than literal. Additionally, it can denote
a normal or abnormal state, and if abnormal either an individual symp-
tom or a full-blown disorder. Clarifications, if sought, can range from
“I feel a bit depressed,” through “I sometimes feel depressed,” to “I have
always felt depressed.” These clarifications, and the impact of the
reported “depressed” mood on functioning, are crucial in the assessment
of mood in the cross-cultural encounter, particularly between the non-
Western clinician and the Western patient. Affect is the external expres-
sion of mood. In many cultures e.g. British culture, it can be colored by
cultural conditioning towards a less expressive, stoic “need to put up a
brave face” in adversity. “Flat affect” has been observed to be a norma-
tive component of mourning in some Native American cultures.15 Again,
investigation is the key to accurate assessment. People in certain cultures
may perceive the impact of stressful circumstances in situational, collec-
tive, moral, or physical/somatic terms. In such circumstances, the level of
impairment is a better measure of the degree of distress than either mood
or affect.
8.4. Depressive cognitions

Religious beliefs and cultural values (e.g. an emphasis on family obliga-
tions over individual rights), act as powerful barriers to suicidal ideation
in certain societies. Death wishes are more salient markers of severity than
suicidal ideas in such contexts. Ideas of guilt also vary across cultures, and
may be less commonly associated with depression in non-Western
patients.
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8.5. Delusions
Delusions, by definition, need to be established as inappropriate to the
persons’ cultural context. A clinician unfamiliar with a patient’s culture
may misattribute such beliefs, either as pathological or normative.
Religious ideas, and cosmic, spiritual and culturally unfamiliar explana-
tions, should be recorded verbatim. Clarify the patient’s explanation for it,
and seek the response of the family and cultural community to the expla-
nation. Record this clearly. Life events with discriminatory or persecutory
elements are a part of everyday reality for some people e.g. ethnic minori-
ties and refugees. These can become internal representations that can
emerge in their mental life, fantasy, and beliefs. However, if a culturally
unfamiliar belief is accompanied by functional impairment and behavior
inappropriate to the culture of origin, it is likely to be pathological.
8.6. Perception
Perceptual disturbances such as illusions, hallucinations, depersonaliza-
tion and derealization are experienced in reference to the self and the
environment. The circumstances of occurrence of an unusual perceptual
experience are important. For instance, auditory experiences of the voice
of a dead relative calling the living to join them in the afterworld are part
of normal bereavement in many Native American cultures.15 Normative
(and often therapeutic) trance and possession states in many cultures can
include hearing and seeing spiritual beings. Dissociative experiences can
also cause perceptual abnormalities. Such experiences do not indicate
complicated grief reactions or psychoses. Document exact experiences,
consistency and clarify differences between illusions, hallucinations and
suggestibility states. Visual phenomena can be particularly difficult to
place within the mental state examination. Investigate and discuss with
informants to avoid erroneous labeling.
8.7. First rank symptoms

First rank symptoms can occur in other disorders, particularly bipolar
mania. They can also occur as part of culturally appropriate methods of
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resolving distress e.g. trance, possession, and exorcism. Beliefs of being

controlled or influenced by others can be part of these states.
8.8. Cognitive assessment

Standard cognitive assessments, if used rigidly across languages and cul-
tures, would yield few valid inferences. Excellent culturally validated
schedules for cognitive assessment are available in many languages, but
their use is hindered by two problems: poor international availability and
linguistic barriers between clinician and patient. In the latter situation, the
help of a team member or advocate who speaks the patient’s first language
can address difficulties to a great extent. If a formal assessment is not pos-
sible, information about memory problems and intellectual decline should
be sought from family and friends. Such information would also help
contextualize any future formal assessment.
9. CULTURAL FORMULATION AND DIAGNOSIS

Tseng24 describes six different ways in which culture can influence mental
disorders:
(1) Pathogenic effect (where cultural ideas and beliefs generate particular
types of stress and lead to a disorder e.g. Type A behavior).
(2) Pathoselective effect (where culturally selected reaction and coping
patterns are deployed when faced with stress e.g. amok attacks).
(3) Pathoplastic effect (where culture shapes the content of psychopathol-
ogy e.g. delusions).
(4) Pathoelaborating effect (where culture supports the exaggeration of
stress reactions into unique patterns e.g. ritual suicide in Japan).
(5) Pathofacilitating effect (where cultural attitudes promote the fre-
quency of occurrence of particular disorders e.g. eating disorders).
(6) Pathoreactive effect (where culture influences communal responses to
distress, disorder, and disability e.g. interpreting and labeling distress,
consulting a traditional healer etc.).
This provides a useful framework for understanding the factors relevant

to a culturally contextualized formulation. A patient’s cultural context is
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influenced by the intersection of multiple factors, including those of gen-

der, ethnicity, sexual orientation, and socioeconomic status; therefore, it
would need to be described in individual rather than collective terms
in order to avoid stereotyping. The cultural formulation model in
Appendix 1 of the DSM-IV (the penultimate section of the manual) offers
a systematic method to arrive at such a diagnosis.1 Its content includes
most, but not all the factors and concepts discussed in this chapter.
The cultural formulation model is intended to supplement the standard
biopsychosocial formulation. It provides both a checklist and a succinct
description of the effects of culture on the patient’s worldview, symptoms,
explanatory models of illness, help-seeking behavior and expectations of
outcome, as well as the therapeutic relationship. A summary is outlined in
Table 5.
The final section of the Cultural Formulation (Sec. 5) summarizes the
information from the previous sections, focusing on the cultural factors
that have contributed to diagnosis and management. However, the overall
emphasis on culture in DSM IV is limited. In addition to the formulation,
it mentions ‘cultural,’ along with ‘age’ and ‘gender’ considerations, as part
of the text in some groups of disorders. Appendix 1 also lists an incom-
plete glossary of “culture-bound syndromes.” This has contributed to a
lack of attention to these crucial concepts in training and practice.
Mention of the cultural aspects of psychiatric diagnosis in Chapter 5 of
the ICD-10 is even more limited. The ICD-10 is a product of collaboration
across countries, conducted on behalf of the WHO, which serves all
nations. The WHO is concerned with the public health impact of disease,
which makes the consideration of culture central. In addition, the ICD-10
aims to “provide a useful stimulus for clinical teaching, since they serve
as a reminder for points of clinical practice.”28 Despite this, the presenta-
tion of cultural aspects lacks both focus and structure. Nonetheless, the
inclusion of categories like neurasthenia, mixed anxiety and depressive
disorder, trance and possession disorder, and conduct disorder confined to
the family context reflect a global cultural inclusiveness. However, a dis-
cussion of cultural variants within categories, a list of culture-specific
psychiatric syndromes, and recommendations for culturally competent
interviewing styles and approaches are notably lacking. The Cuban
Glossary of Psychiatry, the Chinese Classification of Mental Disorders
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Table 5. Components of the cultural formulation.1

Section Sub-section
1. Cultural identity of the • The individual’s self-defined cultural and ethnic
individual. reference group.
• The individual’s degree of involvement with their
culture of origin and the host culture.
• The individual’s language abilities, use, and
preferences (including multilingualism).
2. Cultural explanations of the • Predominant idioms of distress through which
individual’s illness. symptoms or the need for support are
communicated.
• Meaning and perceived severity of the individual’s
symptoms in relation to the norms of the cultural
reference group.
• Local illness categories used by the family and
community to identify the condition.
• Perceived causes and explanatory models used by
the individual and the reference group to make
sense of the condition.
• Current preferences for and past experiences with
professional and popular sources of care.
3. Cultural factors related to • Culturally relevant interpretations of stressors,
psychosocial environment available social supports, and levels of functioning
and levels of functioning. and disability.
• Stressors in the local social environment.
• Role of religion and kin networks in providing
emotional, instrumental, and informational
support.
4. Cultural elements of the • Individual differences in culture and social status
relationship between the between the individual and the clinician.
individual and the clinician. • Problems that these differences may cause in
diagnosis and treatment (e.g. in eliciting
symptoms and understanding their cultural
significance, in determining whether a behavior
is normal or pathological etc.)
5. Overall cultural assessment • Formulation concluded with a discussion of how
for diagnosis and care. cultural considerations specifically influence
comprehensive diagnosis and care.
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and the Latin American Guide for Psychiatric Diagnosis represent cultur-
ally competent diagnostic systems developed to address specific local
requirements.
10. MANAGEMENT
The formulation of a culturally competent management plan needs to take
the patient’s wishes and explanatory model of illness into account.
However, this needs to be balanced with the risk assessment. This is par-
ticularly relevant if the clinical decision is based on inadequate informa-
tion. Arrange for a further assessment if the problem is not urgent. This
will allow you time to think about the presentation, consult senior col-
leagues, obtain information from past records, other professionals, family
members and relevant members of the community, and gather more infor-
mation about the patient’s problem within its cultural context. Let the
patient and family know that you will be doing this. This is important
since your formulation needs to agree as much as possible with their
explanatory models of illness and perceptions of acceptable management.
In case of disagreement, arrange to meet them to discuss the risk assess-
ment. Treatment adherence is especially low in cross-cultural settings.
Family and community support is crucial to adherence and overall out-
come, so do not alienate them.
There are ethnic variations in response to psychotropic medication as a
result of both pharmacodynamic and pharmacokinetic differences.
Interactions resulting from the concomitant use of traditional medicines,
differing levels of stress and other environmental and social factors may
affect the pharmacodynamics and pharmacokinetics of psychotropic
medications.4 For instance, African Americans may respond faster and
more favorably to tricyclic antidepressants, but are also more sensitive to
their side effects.5 Such factors need to be taken into consideration while
prescribing. Do not prescribe symptomatically if the diagnosis remains
unclear. This may expose the patient to needless adverse effects and make
them less likely to adhere to treatment and attend follow-up. Evidence
based psychotherapies can be adapted to be appropriate for people from
different backgrounds. In addition to being open to individual flexibility
within a framework of fidelity, practitioners have proposed systematic
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adaptations to manuals and protocols such that culture, language, and

socioeconomic contexts are explicitly considered.10
11. CONCLUSION
Human beings are guided by their values. Their thinking and behavior are
powerfully influenced by attitudes, norms, peer values, and upbringing
derived from the culture of which they are a part. These values affect the
way they seek help, and where they seek help. It also affects the way
health services are delivered. Help-seeking is also influenced by educa-
tion, socioeconomic status, previous experiences of help seeking, and
explanatory models of illness. Explanatory models of illness, in turn, are
influenced by familial, social, religious, and folk constructs. Clinicians
bring into the clinical encounter their own values, training, experience,
and cultural and other prejudices which may or may not promote the
therapeutic alliance. Thus, it is of paramount importance that clinicians
are aware of the personal cultural perspectives, strengths, and weaknesses
they bring into the clinical encounter. Equally, they should try and learn
as much as they can about the patient’s cultural perspectives, strengths,
and weaknesses. A therapeutic alliance that results from a mutually cultur-
ally sensitive and respectful clinical encounter is very likely to be a good
one. A good therapeutic alliance is crucial to effective diagnosis and
good clinical outcomes. In a globalizing world, cultural psychiatry is good
clinical psychiatry.
The structure and content of current international diagnostic and clas-
sificatory systems are marked by an uneven and inadequate recognition of
culture. In a changing, multicultural clinical milieu, this jeopardizes
accurate diagnosis, the central step in the clinical encounter.
12. KEY POINTS

12.1. Preparing for cross-cultural assessments
• Know the main ethnocultural groups represented in your catchment
area.
• Cultivate a genuine curiosity in their cultures.
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• Read about other cultures, and travel if you can.

• Be patient. Some patients, irrespective of their ethnocultural status,
require longer periods of interaction to be understood within their
sociocultural contexts.
12.2. Eliciting the psychiatric history

• Explore unfamiliar metaphors of distress thoroughly; seek assistance
from informants if necessary.
• Take somatic complaints seriously; they can be the gateway to assess-
ing distress, psychopathology, and disability.
• Do not underestimate the subjective impact of life events; this may be
more than expected.
• Establish the state of acculturation and its impact on distress.
12.3. Good practice points9

• Elicit first and preferred language, self-defined ethnicity, culture and
religion, for each party involved in the consultation.
• Do not get family members to interpret, unless in a psychiatric
emergency.
• Be sensitive to cultural taboos and accommodate them as much as is
practical.
• Be sensitive to aspects of the pathway to care, the setting and your
actions that may compromise trust e.g. referral through the legal sys-
tem. Ensure that the patient is interviewed in a preferred setting that
is comfortable and non-threatening e.g. with family, friends, or alone.
Communicate confidentiality.
• Identify and clarify idioms of distress and emotion-laden phrases to
develop a shared vocabulary.
• Clarify terms used by you and the patient to develop a shared under-
standing of problems.
• Clarify unusual symptoms and signs with help from all parties
involved in the consultation.
• Discuss your findings and conclusions with an independent profes-
sional familiar with the culture, within the bounds of confidentiality.
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13. SELF-ASSESSMENT
13.1. The WHO conducted two international studies,
the IPSS and the DOSMeD. These studies
(A) Compared the incidence of schizophrenia across countries.
(B) Demonstrated that the overall course and outcome of schizophrenia
was uniformly better in developing countries.
(C) Showed a better overall outcome for schizophrenia in India and
Nigeria in the IPSS, and significantly higher rates of complete remis-
sion but similar rates of continuous illness in developing countries
compared to developed, in DOSMeD.
(D) Showed that Standardized Mortality Ratios (SMR) for schizophrenia
cohorts were significantly higher in developing countries.
(E) Compared the diagnosis of schizophrenia across countries.
Answer: C. The IPSS was a preliminary study conducted by the WHO

between 1968 and 1973 to assess the prevalence, characteristics, symptoms,
diagnosis, and clinical course of schizophrenia across seven participating
countries. These countries were Colombia, Czechoslovakia, Denmark,
India, Nigeria, Taiwan, and the United Kingdom. An unexpected finding
in its follow-up stage was a significantly better overall outcome of schizo-
phrenia in India and Nigeria at two-year and five-year follow-up. The
epidemiologically designed DOSMeD used active case finding to identify
incidence cohorts across 12 countries viz. Colombia, Czechoslovakia,
Denmark, India, Ireland, Japan, Nigeria, Russia, the United Kingdom, and
the United States. It showed significantly higher rates of complete remis-
sion but similar rates of continuous illness in developing countries com-
pared to developed countries. Patients in developing countries experienced
significantly longer periods of unimpaired functioning in the community.
Commentators have ascribed this to better social support systems and
lower rates of Expressed Emotion among families in developing coun-
tries. Neither study examined mortality rates in schizophrenia cohorts.
13.2. Somatic idioms of distress include

(A) “My heart suddenly wants to fly out” and “biting sensation all over
my body” in Nigeria.
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(B) “Something is blocking my throat” and “My heart is poisoning me”

in the United Arab Emirates (UAE).
(C) “My brain is aching,” “My brain is uncontrollable,” and “My brain is
exploding” among Mexican Americans.
(D) “My nerves are weak” in China, and “My heart is sinking” and
“I have gas” in India.
Answer: E. All the above are culturally sanctioned metaphors from the
respective cultures. Other somatic metaphors include: “Blood jumps from
the veins of the heart to my head, my feet, and hands” in Ecuador, “My body
is broken” and “My body is aching, fatigued” in Dubai, “I feel as if there is
hot water on my back” in the UAE, “Feeling hot” in India, and “Heat in the
head” in Nigeria. For an overview, read Bhugra and Mastrogianni.3
14. CASE STUDIES

14.1. Overdose
A 15-year-old Tamil girl presented to the Accident and Emergency
Department of a busy General Hospital in London, having taken a third
overdose of aspirin tablets in six months. Her father was semi-literate and
worked in a shop; her mother was illiterate, and worked in a factory. The
patient was ‘forced’ to change into traditional clothes as soon as she walked
in through the door after school. Her British peers were going out, making
friends, and going to clubs, concerts, and parties, while she was not allowed
out. She had no psychiatric symptoms and she acknowledged that taking an
overdose meant that she would be admitted to hospital for a few days,
which allowed her “time out” from a difficult family environment. Here, the
culture conflict between the traditional attitudes of the parents and the more
modern views of their teenaged daughter culminated in repeated overdoses
and hospital admissions. This conflict, if not addressed, could potentially
have adverse consequences on the mental health of all family members.
14.2. Cognitive decline

A 58-year-old Englishman with cognitive difficulties was referred to a
Neuropsychiatry service by his General Practitioner, who suspected a
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dementia of early onset. He had held senior management positions in the

entertainment industry, before deciding to quit and start his own consul-
tancy. This enterprise, set up just before the worldwide financial crisis,
ended in bankruptcy. The General Practitioner had noted a gradual cogni-
tive decline over the previous two years, but felt that he was managing
well despite this. On initial assessment, he presented as an expensively
dressed, well-groomed, seemingly confident, and engaging gentleman,
whose reminiscences about his past was peppered with humorous stories
of encounters with a number of celebrities. However, when questioned
closely about his current circumstances, he unexpectedly broke down in
tears and described constant feelings of guilt, hopelessness, and despair.
He was now working as a retail assistant at a department store, so that he
had “something to go out and do every day.” He felt that he was “too old
to start over.” He had lost contact with his friends and could no longer
afford the leisure activities they pursued. His partner had a job and was
just about able to support the family. He acknowledged that he had stead-
fastly maintained “a stiff upper lip” throughout and had refused to admit
to feeling low since it would have been “like admitting I had failed
completely.”
REFERENCES
1. American Psychiatric Association. (1994) Diagnostic and Statistical Manual,
4th ed. American Psychiatric Association, Washington, DC.
2. Berry JW. (2004) Psychology of group relations: Cultural and social
dimensions. Aviat Space Environ Med 75(Suppl 1): C52–C57.
3. Bhugra D, Mastrogianni A. (2004) Globalisation and mental disorders:
Overview with relation to depression. Br J Psychiatry 184(1): 10–20.
4. Bhugra D, Bhui K. (1999) Ethnic and cultural factors in psychopharmacol-
ogy. Adv Psychiatr Treatment 5: 89–95.
5. Brown C, Schulberg HC, Sacco D, Perel JM, Houck PR. (1999) Effectiveness
of treatments for major depression in primary medical care practice: A
post hoc analysis of outcomes for African American and white patients.
J Affect Disord 53: 185–192.
6. De Jong JTVM, Van Ommeren M. (2002) Toward a culture-informed epide-
miology: Combining qualitative and quantitative research in transcultural
contexts. Transcult Psychiatry 39: 422–433.
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7. Dealberto M-J. (2010) Ethnic origin and increased risk for schizophrenia in
immigrants to countries of recent and longstanding immigration. Acta
Psychiatr Scand 1–15.
8. Ellis WG. (1897) Latah: A mental malady of the Malays. J Men Sci. 43:
33–40.
9. Goldberg D, Murray R (eds.) (2002) Special assessments with adults. In: The
Maudsley Handbook of Practical Psychiatry, 4th ed. Oxford University
Press, Oxford.
10. Hall, GCN. (2001) Psychotherapy research with ethnic minorities: Empirical,
ethical, and conceptual issues. J Consult Clin Psychol 69(3): 502–510.
11. Helman GG. (1987) Heart disease and the cultural construction of time: The
type A behaviour pattern as a western culture-bound syndrome. Soc Sci Med
25(9): 969–979.
12. Hogg M, Abrams D. (1988) Social Identifications: A Social Psychology of
Intergroup Relations and Group Processes. Routledge, London.
13. Jablensky A, Sartorius N, Ernberg G, et al. (1992) Schizophrenia:
Manifestations, incidence and course in different cultures. A World Health
Organization ten-country study. Psychol Med Monogr. 20(Suppl): 1–97.
14. Kirmayer LJ. (2001) Cultural variations in the clinical presentation of
depression and anxiety: Implications for diagnosis and treatment. J Clin
Psychiatry 62(Suppl 13): 22–28.
15. Kleinman A. (1988) Rethinking Psychiatry: From Cultural Category to
Personal Experience, Macmillan/Free Press, NY.
16. Leff J, Warner R. (2006) Social Inclusion of People with Mental Illness,
pp. 12–13, Cambridge University Press, Cambridge.
17. Leininger M. (1991) Culture Care Diversity and Universality: A Theory of
Nursing, National League for Nursing Press, NY.
18. Littlewood R. (1995) Psychopathology and personal agency: Modernity,
culture change and eating disorders in South Asian Societies. Br J Med
Psychol 68(1): 45–63.
19. Lotter V. (1978) Childhood autism in Africa. J Child Psychol Psychiatry
19(3): 231–244.
20. McGrath J, Saha S, Welham J, El Saadi O, McCauley C, Chant D. (2004)
A systematic review of the incidence of schizophrenia: The distribution of
rates and the influence of sex, urbanicity, migrant status and methodology.
BMC Med 2: 13.
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21. Paniagua FA. (2000) Culture-bound syndromes, culture variations, and psy-
chopathology. In: Cuéllar I, Paniagua FA (eds.), Handbook of Multicultural
Mental Health: Assessment and Treatment of Diverse Populations,
pp. 140–141, Academic Press, NY.
22. Saha S, Chant D, Welham J, McGrath J. (2005) A systematic review of the
prevalence of schizophrenia. PLoS Medicine 2(5): e141.
23. Tseng WS. (2006) From peculiar psychiatric disorders through culture bound
syndromes to culture related specific syndromes. Transcult Psychiatry 43:
554–576.
24. Tseng WS. (2001) Handbook of Cultural Psychiatry, Academic Press, San
Diego, CA.
25. Uchimura VY, Akimoto, Ishibash. (1938) The syndrome of imu in the Ainu
race (Comment). Am J Psychiatry 94: 1467–1469.
26. Üstün TB, Sartorius N (eds.) (1995) Mental Illness in General Health Care.
An International Study, John Wiley & Sons, Chichester.
27. World Health Organization. (1979) Schizophrenia: An International
Follow-up Study, John Wiley & Sons, Chichester.
28. World Health Organization. (1992) International Classification of Diseases,
10th ed. World Health Organization, Geneva.
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Chapter 32
Traditional Healing for Psychiatric

Disorders
Roger M. K. Ng, Zhang-Jin Zhang and Wendy Wong
1. SHOULD WE CARE OR SHOULD WE NOT?

Mental health problems are highly prevalent conditions in modern society,
with over 450 million people worldwide diagnosed with various psychiatric
disorders, mainly including psychosis, mood, and behavioral disorders.26
It will become the third most common illness globally by year 2020
following ischemic cardiovascular disease.26
Although pharmacotherapy has become the mainstay in contemporary
psychiatry practice since the 1950s, various approaches of traditional
healing have also been widely adopted into prevention and treatment of
mental health problems for many centuries. Traditional healing, com-
monly labeled as “complementary medicine,” poses a great challenge to
medical practitioners. Practitioners may feel that their patients need con-
ventional psychiatric treatments but find themselves embarrassed about
their relative lack of knowledge on traditional healing practices. The
extent of use of these alternative or complementary treatments is not to be
underestimated; as research has consistently found that 8%–57% of
patients with mental health problems turn to complementary medicine for
treatment.24
Depressive disorders and anxiety disorders seem to be the most
common indications for traditional methods of healing.24 Globalization is
823
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824 R. M. K. Ng, Z.-J. Zhang and W. Wong
sped up by immigration, increased flux of international travelers, and, not

the least, the boom of internet communication. Many immigrants to the
West seek traditional healers as their first point of contact in the pathway
of care, understandably out of language barrier, religious beliefs, and
incongruence of explanatory models of illness with Western medical
practitioners.6
Medical practitioners and psychiatric residents often hear statements
such as “My son is not psychotic. I would like to take him to a priest for
consultation. Do you believe that my son is being possessed by ghosts?”
and “I read about acupuncture for the treatment of obsessive-compulsive
disorder from a website. Will I benefit from this treatment? Will there
be any side effects from combining therapies?” There are endless varie-
ties of questions that could be asked by a patient in this age of globaliza-
tion and free information flow. Indeed, it is impossible to keep up with
the rich knowledge base on traditional healing and alternative medicine.
Yet lack of awareness of patients’ use of such alternative medicine might
not only miss significant drug–drug interaction but also a potentially
rewarding opportunity of establishing a more trusting doctor–patient
relationship.
This chapter is not meant to be exhaustive in discussing traditional
healing but attempts to provide a glimpse about common traditional
healing practices in the world (Table 1).
Table 1. Types of traditional healing.

Region of practice Types of traditional healing
Indian sub-continent Unani medicine
Ayurvedic medicine
China Traditional Chinese medicine including
acupuncture and herbal treatments
Afro-Caribbeans Obeah
African Continent Ubunta
Mexican/Peruvian Americans Curanderas
American Indians Shamanism
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Traditional Healing for Psychiatric Disorders 825
2. ANCIENT WISDOM ON MANAGEMENT

OF MENTAL HEALTH PROBLEMS
2.1. Unani medicine in Indian sub-continent culture
The Muslim population in Pakistan, the United Kingdom, and the United
States frequently consult Hakims, who are practitioners practicing Unani
medicine. Unani is a form of medicine commonly practiced in the Indian
sub-continent. The word Unani means “Ionian.” Unani medicine was
originally practiced by the Nestorian Christians in the Byzantine Empire,
who were forced to go into exile in Sassanid Persia to escape purging as
a heretic cult. The secret knowledge was eventually absorbed into Arabic
medicine during the Islamic conquest of the Middle East in the 9th
century. Unani became a more sophisticated system of medical knowl-
edge, thanks to the cross-fertilization of medical knowledge derived from
the vast Islamic Empire spanning across Egypt, Sumeria, Assyria, and
Babylon.
Unani Tibbia was eventually codified into a system of medical knowl-
edge by the Arab scholar Ibn Sina (Avicenna). Unani Tibbia was formally
adopted as a university curriculum in the Central Asian universities of
Samarkhand and Tashkent. Unani eventually arrived in the Indian sub-
continent with Islamic refugees fleeing from the Mongolian invasion in
the 13th century.4
Unani focuses on holism, which takes into account physical, psycho-
logical, and spiritual well-being. This approach was guided by the concep-
tual view of illness as an interaction of temperament and hereditary
factors. Assessment requires understanding of presenting complaints,
clinical observation, and examination of pulse (Nubz), urine, and stool.
Treatment consists of dietary modification, pharmacotherapy, climato-
therapy, and regimental therapy. Regimental therapy refers to venesection,
diaphoresis, diuresis, Turkish bath, massage, cauterization, purging, and
emesis.
In a British study investigating the use of Unani among British South
Asians, Healy and Aslam10 found that most subjects consulted the
Hakims for psychosexual problems and depressive disorder. Apart from
the above manipulations, amulets incorporating holy words from the
Koran (ta’wiz) are used to treat illness resulting from the jealous glance
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of another person (the evil eye or nazar). Mullah will be referred if the
patient is suspected of suffering from a supernatural illness such as a dis-
sociative state. Healy and Aslam10 suggested that hakims are preferred to
Western medical practitioners for their holistic view of illness and family
orientations in assessment and treatment, as well as their ample time
dedicated for consultation. Later studies also confirmed that many
South Asian immigrants in the United Kingdom consulted hakims for
their ailments.
2.2. Ayurvedic medicine in Indian sub-continent culture

Ayurvedic medicine, like Unani, is an ancient system of medicine that has
been widely practiced in the Indian sub-continent for more than 5,000
years. It is based on three major texts (Charaka Samhita, Sushruta
Samhita, and Ashtanga Hridayam), which elaborate illness as originating
from an imbalance of three humors (doshas) in the body. The three
humors are wind (vata), bile (pitta), and phlegm (kapha). An Ayurvedic
practitioner ascertains the specific humor constitution (prakriti) of each
patient and identifies the presence and magnitude of any humor imbalance
(vikriti) through detailed history taking and performing an eight-point
physical examination (pulse, urine, stool, tongue appearance, eyes, skin,
quality of speech, and general appearance).3
Ayurvedic texts conceptualize disease as arising from the dynamic inter-
action between the individual and the environment. Treatment involves
changes in diet and lifestyle, meditation, and use of herbal medicine.
Ayurvedic medicine developed a special branch called Graha Chikitsa
for the treatment of mental health problems, which evolved more than
4,500 years before the development of psychiatry as a medical sub-spe-
cialty. It is noteworthy that its popularity has grown not only in the Indian
sub-continent but also in the Western world. Patients use such traditional
remedies in tandem with standard psychiatric treatments.1
2.3. Traditional Chinese medicine in oriental culture

The first Chinese encyclopedia of medicine that founded the disease
concepts of Traditional Chinese Medicine (TCM), the Medical Principles
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of the Yellow Emperor, was written over 2,000 years ago. The founding
principle of TCM rests on the assumption that there exists a balance
between a variety of opposing hypothetical constructs, the most promi-
nent of which is the yin and the yang. Maintaining a balance (or har-
mony) between such opposing forces has far-reaching implications on
the wellness of the bodily system, which is conceptually divided into
the five organs: the heart, the liver, the spleen, the lungs, and the kid-
neys. Interestingly these organs do not correspond to the current ana-
tomical definition of corresponding organs as defined by Western
anatomy. By direct translation, the yin literally means “dark” but has the
connotation of being gentle, slender, weak, and feminine, epitomized by
the moon. The yang, on the other hand, literally means “bright” and has
the connotation of being forceful, virile, strong, and masculine, epito-
mised by the sun. Achieving harmony between the yin and the yang is
essential for the synchronization of the five organs, and the synergy
helps to maintain normal functioning and hence physical health.
Illnesses are construed as a disharmony between these two opposing
constructs. The corollary of this thesis is that in the event of any
malfunctioning in the bodily organs, the cure would be to restore the
yin–yang balance.
The TCM principle also views physical ailment as the result of the
body being inflicted by excessive internal “fire,” versus excessive internal
“coldness.” Moreover, the unwanted presence of “wetness” and other
body “toxins” will result in ill health. The practice of TCM, therefore, is
to have a correct diagnosis of such internal states and to skillfully manipu-
late a cocktail of herbal preparation to restore harmony and to rid the body
of unwanted toxins. The internal bodily states are also regulated by the
forces of xie, which literally means “blood”; and qi (pronounced “chi”),
which is a word meaning “air” but connotes “internal spirit.” To ensure
good health, both the xie and the qi need to be active and regulated.
Stimulation, and thus regulation, of the xie and the qi can be effected by
TCM herbals or the stimulation of the acupuncture points located with
some precision on the bodily meridians plotted out in the Medical
Principles of the Yellow Emperor. If so-wished, the xie can also be
enhanced by physical exercise; the qi can be enhanced by practicing qi
gong, which literally means “qi exercises.” The positive effects of qi gong
B1405_Ch-32.indd 827 1/31/2013 2:43:30 PM

have been reported in a few studies, but some clinicians have cautioned
against untoward psychological disorders and other problems resulting
from misuse of qi gong.19
What has transpired from this washed-down exposition of TCM princi-
ples is the basic assumption that all bodily ailments (illnesses and diseases
included) can be traced to an imbalance between a number of coexisting
but opposing hypothetical constructs such as the yin versus the yang, fire
versus coldness, and so on. TCM prescriptions and other physical forms
of treatment were initiated with the aim of restoring the balance between
these constructs and enhancing the xie and the qi activities. When these
are achieved, harmony will be restored, symptoms will vanish, and the
patient will become well.
TCM holds the viewpoint that mentality is a psychological capacity of
regulating a reciprocal balance of physiological and emotional activities.
Excessive and prolonged emotional activities may result in the imbalance
of both and then develop as an important pathogenesis, which is widely
involved in the development of various psychological and physical
impairments. For example, if one is in prolonged sorrow, his or her mind
will be restless, resulting in uneasiness of the internal organs.27 Clinically,
TCM diagnoses of mental–emotional conditions could be made on the
basis of TCM diagnostic principles and syndrome differentiations
through the Four Diagnostic Approaches, consisting of inspection, aus-
cultation and olfaction, inquiry, and palpation. An apparent therapeutic
advantage of TCM for mental–emotional conditions is individualized
treatment strategy, in which formulation of herbal medicine and acupunc-
ture points is based on the individual diagnosis made and the different
stages of condition development. For example, for those who are diag-
nosed as excessive emotional activities with anxiousness, herbal medi-
cines and acupoints that could reduce emotional excessiveness and calm
down anxious mood are applied. For those who manifest depressive mood
with low energy, fatigue, and poor concentration, herbal medicines and
acupoints that could heighten mood status and reinforce the energy may
be used.
Because excessive worries and anxiousness are the most common
emotional responses to extremely rapid and radical social changes in
today’s society, three mental–emotional syndromes are frequently observed
B1405_Ch-32.indd 828 1/31/2013 2:43:30 PM

in TCM clinical practice. The clinical manifestation, diagnosis, herbal,

and acupuncture treatment of these three syndromes are introduced below.
2.3.1. Stagnation of liver qi

Major clinical manifestations include anxious or depressed mood, inter-
costal muscle pain with tight pulse, and pale tongue, which are found in
syndrome differentiation of stagnation of liver qi. This syndrome is often
observed in patients with major depression and during the withdrawal
period of drug dependence. The treatment principle of the stagnation of
liver qi is to move qi and pacify the liver, settle the ethereal soul and calm
the mind. Chai Hu Shu Gan Tang (柴胡疏肝湯) could be used as an initial
formula. With acupuncture treatment, acupoints used may be mainly cho-
sen from the meridians of liver, heart, and spleen, such as Baihui (DU 20),
Yintang (EX-HN3), Neiguan (PC6), Waiguan (SJ5), Shenmen (HT7),
Hegu (LI4), Taichong (LR3), Zusanli (ST36), Fenglong (ST40), Sanyinjiao
(SP6), and Taiyuan (LU9). Some ear acupoints could be also used. The
therapeutic effect of acupuncture may be associated with a composite
sensation termed “deqi” which manifests as numbness, heaviness, disten-
sion, and soreness as the insertion of needles are manipulated manually or
electrically. Numerous clinical studies have shown beneficial effects of
herbal and acupuncture treatment for this.28
2.3.2. Stagnation of liver qi with spleen deficiencies

In addition to depressed mood, patients also present with obvious gastroin-
testinal upset with poor appetite and pale and tooth mark on the tongue.
This syndrome is often found in patients with moderate to severe depres-
sive disorder or with substance dependence syndrome. The treatment prin-
ciple of the stagnation of liver qi with spleen deficiencies is to move qi and
reinforce the spleen. Xiao Yao San (逍遙散), in the form of tablets or
decoction, is most commonly used for this syndrome differentiation.
2.3.3. Disturbed shen (神) with phlegm

Insomnia, productive coughing with a strong, tight pulse, and reddish
tongue with white or yellow thickening are typical presentations of this
B1405_Ch-32.indd 829 1/31/2013 2:43:30 PM

syndrome. Treatment principle of the disturbed shen caused by phlegm is

to clear the mind by removing phlegm. To treat this, Wen Dan Tang (溫膽湯),
a decoction, is commonly used.
Apart from TCM use in emotional disorders, studies have shown clinical
efficacy of both Chinese herbal medicine and acupuncture on opiate and
alcohol withdrawal. Radix Puerariae shows the most promising efficacy
for alcoholism by acting through daidzin, which inhibits mitocochondrial
aldehyde dehydrogenase 2 and leads to disulfiram-like alcohol reactions.
Peyote also has some evidence for alcoholism treatment among Native
Americans.12 There is also evidence of TCM for relieving anxiety in regu-
lating corticotrophin-releasing factor in the amygdala during withdrawal
from opiate dependence syndrome.2
2.4. Curanderas in Mexican and Peruvian Americans

Shamanism has been practiced by the Native Americans for hundreds of
years as a major traditional healing practice. A particular type of Shamanic
practice in Peru, Curanderas, involves the ingestion of psychoactive sub-
stances (San Pedro Cactus Plant) during all-night shamanic rituals (Mesos).
The purpose of the ritual is to facilitate the Shamanic practitioners in
accessing the unseen worlds of ghosts and magical landscapes. Glass-
Coffin8 describes in her anthropological account of personal experience
with Curanderas that the unusual experience induces a feeling of tranquil-
lity and sense of unison of the self with the surroundings, leading to a radi-
cal shift in her perception about the relation between self, others, and the
world. Such positive transformative experience leads to a personal sense of
relief from suffering. Indeed, research has found that excessive self-focus
in the form of rumination may lead to depressive and anxiety disorders.16
Decentring from excessive self-focus by means of various strategies,
including attention-control strategies,23 mindfulness-based techniques,25
and acceptance-based techniques,9 have been associated with benefits in
the alleviation of psychological disorders. Research conducted in the
United States has also confirmed that older US-dwelling Mexicans and
Native Americans regard traditional healing practices like Curanderas and
herbal treatment as more acceptable and affordable than conventional
medical treatment.17 More importantly, traditional healing practices were
B1405_Ch-32.indd 830 1/31/2013 2:43:30 PM

considered by the subjects as more acceptable to their family members and

local communities at large. Seeking culturally and socially acceptable
means of alleviation, like religious faith, has been regarded social capital
to explain health inequalities among different nations.21
2.5. Obeah in Afro-Caribbean culture

Due to colonialism in the West Indies, Afro-Caribbean religion has been
an amalgamation of two predominant religious traditions: native African
religion and European Christianity. Obeah is a term used in the West
Indies to describe a form of witchcraft containing elements of Christianity,
animism, folk medicine, mysticism, and personal malevolence. It is asso-
ciated with both benign and malign magic. In some Caribbean nations,
Obeah encompasses religious practices derived from Central and West
African slave religions and rituals adopted from Hindu labor immigrants.
In other parts of the Caribbean, Christians absorbed elements of Obeah
into their religion or vice versa. Obeah is now widely practiced in the
West Indies. Patients of Afro-Caribbean origin suffering from “posses-
sion states” might attribute the illness to Obeah curse, so that an Obeah
man (a traditional healer specializing in the removal of an Obeah curse)
will be consulted to counter the curse.5 “Possession state” indicates the
takeover of mind and body by an external force such as a spirit, a deity,
or an ancestor, so that the possessed victims are usually absolved from
the responsibility of any thoughts and actions expressed during a posses-
sion state. It has been widely believed that such a possession state is an
expression used by disadvantaged members in a social group to gain
otherwise unattainable goals.5 Patients in such a possession state are fre-
quently misdiagnosed as suffering from psychosis, followed by prescrip-
tion of anti-psychotics. Dein5 has argued that the exorcism ritual
performed by an Obeah man might lead to a more satisfactory outcome,
possibly allowing patients to “have an honorable way out from the stale-
mate.” Afro-Caribbeans who believe in Christianity tend to attend
churches with members of similar ethnic origin. In the United Kingdom,
the most popular faiths are Pentecostal and Charismatic Christianity and
Seventh Day Adventism.11 The culture of these churches emphasizes
enthusiastic praying with speaking in tongues, dance, and trance-like
B1405_Ch-32.indd 831 1/31/2013 2:43:30 PM

possession states. The very nature of such culture renders the church
leader a pivotal position in the pathway to mental health care. Mutual
respect, communication, and collaboration with the church leaders and
the traditional healers are therefore extremely important in early
intervention of mental health problems and promoting acceptance of
mainstream mental health care.
2.6. Ubunta in African culture

The emphasis on harmony and balance between the body and the environ-
ment is not unique to Indian and Asian cultures. In fact, in African culture,
the human being (umuntu) is regarded not only as the representative of
God in creation but also shares in the divine being. The human being is
considered as a special creation by the Creator (Tixo) and is the center-
piece of existence and the primary concern of the Creator God in all
creations.
Umuntu is composed of eight essential elements: (1) umzimba (body,
flesh, form); (2) umoya (breath, air, life); (3) umphefomulo (shadow, spirit,
soul); (4) amandla (vitality, strength, force, energy); (5) inhliziyo (heart as
the seat of emotions); (6) umgrondo (head or brain, intellect); (7) ubuvime
(language, speaking); and (8) ubuntu (humanness). Ubuntu is considered
the most important quality of umuntu.15 Ubuntu is based on the philosophy
and world view that emphasize collectiveness and interdependence.
Human nature is defined as an interdependent and inseparable whole.
Mbiti14 pointed out the strong emphasis within this worldview on
kinship — it controls relationships and regulates and determines interper-
sonal behavior. He defined this kinship as taking place horizontally, to
include all the living in society, as well as vertically, to include all the dead
and those not yet born. The living spirits of the dead (ancestors) are seen
as possessing the power to invoke good health, wealth, illness, and mis-
fortune to the living. This leads to a sense of oneness between the visible
and the invisible, among human beings, nature, and God.
Ubuntu, as a philosophical concept, contains three dimensions. First,
God is conceived and perceived as the uncreated Creator who breathed
life in all people, thus giving to people their humanity. Ancestors are
B1405_Ch-32.indd 832 1/31/2013 2:43:30 PM

also perceived as capable of providing people with their humanity.

The philosophy can contribute to an awareness of the purpose and
meaning of life. Second, on a psychological level, ubuntu is not merely
positive human qualities, but the very human essence itself, which ena-
bles human beings to become abantu, humanized beings. The absence of
ubuntu leads to tension, conflicts, frustration, and disintegration of basic
human relationships. Third, on an interpersonal level, the ideal person
has the virtues of sharing and compassion. Ubuntu is therefore a very
powerful source of healing for the people in Africa. Traditional healers
typically facilitate the sufferers to tell their story from their own perspec-
tive. Dancing, art, and music are used to facilitate the sufferers’ expres-
sion of emotion and enhance their acceptance of their negative emotions.
Family members and community leaders are often invited to join the
sufferers to facilitate restoration of harmony and therefore restore
ubuntu. It is worthy to note that the interpersonal focus is not restricted
to the treatment of emotional problems. In Ethiopia, when a patient con-
tracts malaria, the traditional healer would invite the patient’s spouse and
family to come with the patient. The healer would facilitate the patient
and relatives to air out their grievances about each other and facilitate
negotiation. Although such treatment may sound unscientific to most
medical practitioners in the West, there is indeed some wisdom in this
approach. In regions where malaria is prevalent, most Africans are par-
tially immune against malaria through genetic predisposition (sickle-cell
alleles). Yet immune defense against malaria drops during periods of
stress. As interpersonal harmony is considered as ubuntu in every human
being, conflicts within the family or the community understandably cre-
ate an immense source of stress. The traditional approach of restoring
harmony exactly aims to resolve stress and restore such immune
competence.
3. CONCLUSION
Some of the reasons cited for the use of traditional healing include
lower incidence of side effects, perceived effectiveness, a desire for
egalitarian relationships with medical practitioners, a holistic approach
B1405_Ch-32.indd 833 1/31/2013 2:43:30 PM

to an individual’s problems, and dissatisfaction with conventional

healthcare.7 Other reasons include an emphasis on the overall experi-
ence of illness, simple language of communication, lay explanations of
illness, and provision of a cause for illness that is not offered by conven-
tional health care.22
In the era of evidence-based medicine, there are many concerns and
criticisms about the value of traditional healing. One major concern is the
relative lack of evidence of efficacy of traditional healing and alterna-
tive medicine in the treatment of psychiatric disorders, although there
are some isolated meta-analyses of TCM on psychiatric disorders.28
Understandably, it is extremely difficult to standardize the skills and tech-
niques of individual practitioners, let alone the identification of effective
components of traditional healing in dismantling studies.20 Furthermore,
measures developed for Western illness concepts may not capture tradi-
tional concepts laid down in ancient medical approaches. For example, as
Chinese people tend to present with somatic symptoms in the face of
emotional difficulties, outcome measures of TCM should be coherent with
its underlying philosophy and theory so that they could be sensitive and
responsive to the changes brought about by TCM treatments.13 The issue
of appropriate measures to capture the process and outcome of changes
delivered by a particular traditional approach requires more in-depth
research. In the past few years, there have been some encouraging signs
along this direction. Several TCM condition-specific HRQOL measures
have been developed. The Emotion Scale for Ganzangxiang of TCM was
developed to measure HRQOL specific to the anxiety and depression
syndromes that are classified under the liver-syndrome by the TCM the-
ory. PiWei syndrome differentiation measure “脾胃病辨證量表” and the
Liver Fire Ascending Syndrome Scale “肝火上炎證候量表” were devel-
oped with similar principles to capture specific physical symptoms and
psychological state changes related to a specific TCM diagnosis.
Understandably there is still a lot of concern about the safety of herbal
medicine and the potential drug–drug interaction with other herbal medi-
cines and Western medicine. In Hong Kong, a database has been set up by
the Department of Health to facilitate reporting of adverse events associ-
ated with herbal medicine and their potential drug interactions with
Western medicine.
B1405_Ch-32.indd 834 1/31/2013 2:43:31 PM

One might argue that traditional healing is not evidence-based practice

and therefore should not be discussed or encouraged in our clinical
practice. However, if one reads the book Evidence-based Medicine: How
to Practice and Teach EBM, David Sackett18 defines evidence-based
medicine as having three distinct elements: (1) best research practice;
(2) experience and skills of practitioners; and (3) patient’s values. By
“patient’s values,” Sackett et al. continue, “we mean the unique prefer-
ences, concerns and expectations each patient brings to a clinical encoun-
ter and which must be integrated into clinical decisions if they are to serve
the patient.” They then conclude, it is only “when these three elements
(best research evidence, clinician’s experience, and patients’ values) are
integrated, clinicians and patients form a diagnostic and therapeutic alli-
ance which optimizes clinical outcome and quality of life.” Through
understanding the current evidence base about traditional healing, updat-
ing our knowledge about different traditional practices, and exploring and
respecting patients’ preferences about traditional healing, medical practi-
tioners are in fact striving toward evidence-based care.
4. KEY POINTS
• High percentage of patients with mental health problems resort to

complementary medicine for treatment, due to their perceived bene-
fits for chronic health problems, accessibility, and acceptability by the
patients.
• Lack of awareness of use of alternative medicine will possibly miss
significant drug–drug interactions and possible chance of establishing
better rapport and understanding of the patients.
• Traditional healing emphasizes holistic approaches that take into
account physical, psychological, and spiritual dimensions of the per-
son, as well as the dynamic interactions between the person and the
environment.
• Evidence-based medicine should also take into consideration the
patient’s unique treatment preference, meaning that selection and recom-
mendation of an evidence-based traditional healing practice to patients
will become an important yet challenging task for all clinicians.
B1405_Ch-32.indd 835 1/31/2013 2:43:31 PM

5. SELF-ASSESSMENT
5.1. What are the three essential components of evidence-based
medicine as suggested by Sackett?18
Answer: Best research practice, experience and skills of practitioners, and
patients’ values.
5.2. What are the major criticisms of the practice

of traditional healing practices?
Answer: Lack of research evidence of treatment efficacy; lack of
standardization of the skills and competence of the individual practitioners;
variation in practice and treatment components of the healing practice; lack
of systematic documentation of the associated risks and side effects of such
traditional healing practices; and association of such healing practices with
the notion of barbarism, due to historical reason of colonialism.
6. CASE STUDIES
6.1. Obeah
A 21-year-old male patient was admitted through the casualty depart-
ment into the psychiatric ward. According to the report of his mother,
the patient had complained about being haunted by ghosts for the past
three months. He felt that his thoughts and actions were under the con-
trol of the evil spirits. His experience of hearing a male voice threaten-
ing him at night confirmed his belief that he was being possessed. The
attending psychiatrist conducted a thorough psychiatric interview and
made a diagnosis of paranoid schizophrenia on the basis of the presence
of bizarre delusions and second-person auditory hallucinations. The
attending psychiatrist explained the diagnosis, the dopamine theory of
psychosis, and the treatment plan to the patient and his mother. The
patient’s mother immediately demanded he be discharged, because she
believed that those abnormal phenomena were due to ghosts and would
prefer exorcism by Obeah. The attending psychiatrist was trained in
Western medicine and dismissed Obeah as some kind of witchcraft;
B1405_Ch-32.indd 836 1/31/2013 2:43:31 PM

thus, the patient and his mother were eventually discharged against
medical advice.
The patient underwent a ritual of exorcism, leading to a reduction in
anxiety and in severity of abnormal experience. However, a few days later,
the symptoms recurred to such an extent that the patient followed the
voice, which commanded him to slash his wrist. During the second
admission, the attending psychiatrist took a more thorough psychosocial
history, which revealed that before the onset of psychosis, the patient’s
mother had just driven away his father’s mistress from the home. His
mother believed that his illness was related to magical spells cast upon
him by the mistress. She therefore believed that exorcism was the best
method to drive away the evil spirits. The attending psychiatrist then spent
time to explain to the patient’s mother about the relation between occur-
rence of the life event (family discord) with the onset of such psychotic
symptoms, the effect of anxiety upon the severity of the symptoms, as
well as affirming the anxiety-reducing value of Obeah. Both the patient
and his mother became more accepting of the stress-related hypothesis of
his illness. There was also improvement in mutual rapport with associated
acceptance of medication in reducing his anxiety and psychotic
symptoms.
6.2. Traditional Chinese medicine

Ms X is a 56-year-old teacher who complained of feeling anxious and
depressed for the past two years before treatment. She consulted her
primary care doctor and was diagnosed as suffering from depressive
disorder. She was prescribed with antidepressants and sedatives for
symptomatic relief, but there was limited improvement. During consulta-
tion with a Chinese Medicine Practitioner, her complexion was observed
to be pale and sallow, her tongue color being purple with a thin yellow
coating, and her pulse being fast and wiry. The Chinese Medicine diag-
nosis made was “Stagnation of Liver Qi” while her Chinese Medicine
Syndrome differentiation was “Stagnation of Liver Qi with Spleen defi-
ciencies.” The therapeutic principle applied to such conditions was to
relieve liver stagnation and tonify the spleen and to nourish the blood.
The treatment prescribed according to this principle was a combination
B1405_Ch-32.indd 837 1/31/2013 2:43:31 PM

of Chai Hu Shu Gan Tang (柴胡疏肝湯) and Xiao Yao San (逍遙散) and
Dan Sen (丹蔘), Yu Jin (郁金), Chao Zao Ren (炒棗仁). By her next fol-
low up after taking the Chinese herbal decoction for nine days, her
depressive condition had greatly improved with better sleep quality and
improved appetite. With further counseling and reassurance from the
Practitioner, the patient had gained more confidence in Chinese Medicine.
With an additional prescription of 15 days of 30 g of Huang Zhe (北茋)
and 15 g of Wu Wei Zi (五味子) to reinforce the qi and Blood, the patient
called the clinic and reported significant improvement in her depressive
symptoms. With further emphasis on cultivating good mental health and
continuous intake of Xiao Yao San (逍遙散), the patient eventually recov-
ered without any recurrence.
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17. Rogers TA. (2010) Exploring health beliefs and care seeking behavior of the
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Medicine: How to Practice and Teach EBM, Churchill Livingstone,
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19. San HH, Yan WW, Yan HQ. (1990) Mental hygiene problems of QiGong. Inf
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B1405_Ch-32.indd 840 1/31/2013 2:43:31 PM

Chapter 33
International Perspective on Homelessness
Belinda Bandstra, Anthony Mascola

and Daryn Reicherter
1. INTRODUCTION
Homelessness is a social issue present in all nations. It is not a diagnosis,
nor is it necessarily correlated with any single diagnosis. Rather, it is a
social situation with multifactorial causes and correlations. Because this
complicated societal issue is so often correlated with mental illnesses and
substance abuse disorders, it warrants special mention in this volume.
Homelessness is a social justice issue often related to poverty, unem-
ployment, and the lack of affordable health/mental health care. It is also
highly correlated with political issues like war, family system issues like
orphanhood and domestic violence, and legal issues such as the reentry of
prisoners into society. Social systems issues are often an overarching fac-
tor predicating the condition of homelessness. Mental illness alone does
not cause an individual to be homeless. Mental illness and substance
abuse are major risk factors for homelessness. The burden of mental ill-
ness often will be the key issue, when added to other social risk factors,
leading to chronic homelessness. The correlation between homelessness
and mental illness is staggering. With all other variables equal, people
with mental illness are hugely vulnerable to the condition of homelessness
relative to those without mental illness.
841
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842 B. Bandstra, A. Mascola and D. Reicherter
2. DEFINITIONS
The United Nations discusses housing in the Universal Declaration of
Human Rights as a basic Human Right, thus defining homelessness as an
international social justice issue: “Everyone has the right to a standard of
living adequate for the health and well-being of himself and of his family,
including food, clothing, housing and medical care and necessary social
services, and the right to security in the event of unemployment, sickness,
disability, widowhood, old age, or other lack of livelihood in circum-
stances beyond his control.”
But the definition of homelessness remains a topic of debate.
Socioeconomic and political realities will challenge definitions for the
homeless problem from one country situation to another. “Homelessness”
defined in post-earthquake Port-au-Prince may place emphasis on differ-
ent factors when compared to “homelessness” in Paris or New York City.
Likewise, a schizophrenic “street person” in Los Angeles will have a dif-
ferent set of definitions as compared to a “street orphan” in Zimbabwe,
though both will satisfy most definitions of “homelessness.”
There are many different definitions for homelessness, and there is no
internationally recognized absolute standard definition. Rather, a spec-
trum of definitions exists between narrow and wide concepts for home-
lessness. At one end of this continuum, homeless is defined as simply the
absence of shelter in the literal sense. Many feel that this is too restrictive
of a definition and that a broader context of social situations must be
intrinsic to any meaningful definition.
The United States Department of Housing and Urban Development
defines a “chronically homeless” person as “an unaccompanied homeless
individual with a disabling condition who has either been continuously
homeless for a year or more, or has had at least four episodes of home-
lessness in the past three years.” Many other systems use a similar
definition.
The lack of clarity around the definition can make consensus in epide-
miology ambiguous. Nevertheless, it seems that the conceptual framework
of the problem seems to be more similar between nations with similar
political and socioeconomic situations.
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International Perspective on Homelessness 843
3. EPIDEMIOLOGY
Because the valence of homelessness varies with socioeconomic situa-
tion, and because homelessness is a sensitive issue in some cultures, the
degree to which the topic has been studied and documented differs widely
from country to country. The greatest volume of research on homeless-
ness comes from the United States, Canada, the United Kingdom, France,
and Australia.44 Few credible estimates exist regarding the size of the
homeless population in different countries. In general, studies suggest
that 6%–8% of Americans can expect to be homeless at some point in
their lives, 1% in any given year.44 The number is comparable in the
United Kingdom, and lower in Italy (4% lifetime prevalence per Toro44),
Belgium (3.4% in the same study), and Germany (2.4% in the same
study). In many developing countries, the numbers are much higher —
sometimes too high to reliably quantify. A study in Brazil suggests
that nearly one-third of the population lives in conditions that fall under
a loose definition of homelessness described as “miserable living
conditions.”18 In some cities in sub-Saharan Africa, it is estimated that as
much as 60% of the population lives in crowded, informal, and often
illegal slum or squatter settlements, without water, sanitation, waste dis-
posal, or job opportunities.34
Homeless people fall into three key groups: homeless families, home-
less youths, and homeless single adults. These groups have largely distinct
social services and research literatures.
Homeless families are typically single mothers with one or more young
children, often under the age of five. They tend to be homeless for reasons
of extreme poverty, loss of benefits, eviction, or domestic violence. They
are rarely found on the streets and are mostly housed in shelters or dou-
bled up with friends or family. In the past, among developed countries,
this has been noted to be a predominantly American phenomenon, dispro-
portionate among African Americans or other ethnic minorities. However,
the number of homeless families may be on the rise in Europe, especially
in nations with immigration from conflict-torn or poverty-stricken nearby
regions.44 Families made homeless by forced eviction are also documented
in major urban areas in Africa.34
B1405_Ch-33.indd 843 1/31/2013 2:43:44 PM

Homeless youths in developed countries are typically “runaways”

(youths who have left home without parental permission) or “throwa-
ways” (youths who have been forced to leave home by their parents);
these are more common in the United States than in other countries,
although perhaps less rare than homeless families. Their numbers are also
noted to be on the rise. This group is distinct from “street children,”
defined as children living on the street most of the time, maintaining
varying degrees of contact with their family. Worldwide, there are over
30 million of these children living in urban areas throughout the develop-
ing world.34 They are usually victims of abuse, the girls are often sexually
assaulted, and many engage in drug abuse.
Homeless adults are the group most heavily studied internationally.
Across countries, they are predominantly male, unmarried, and not work-
ing at a regular job. They are usually from poor backgrounds, and groups
that have traditionally been discriminated against are generally overrepre-
sented. In the United States, Western Europe, and Brazil, the vast majority
are between the ages of 18 and 50,18,37,44 although in Japan over 70% are
above the age of 60.35
Among homeless adults, high rates of substance use disorders and
other mental health problems are consistently observed. In general, the
emergence of mental health problems in an individual tends to precede
homelessness. However, the association between homelessness and psy-
chiatric disorders is not unidirectional — significant increases in rates of
substance use and mood disorders have been noted among homeless
cohorts over time. Some researchers have noted that multiple indirect
effects related to having a psychiatric disorder may not only increase an
individual’s chance of becoming homeless, but also create barriers to exit-
ing homelessness.13,31,36 Some research has suggested that the demo-
graphic composition of the homeless population varies with economic
conditions: the better the economic conditions, the more people benefit
from employment opportunities and are able to exit homeless-
ness. Consequently, in times of extended economic growth or prosperity,
healthy, younger poor people are able to exit homelessness, and the home-
less population reflects a more distressed population: those with less
social networks, more physical health symptoms, and a higher rate of
severe mental illness.21
B1405_Ch-33.indd 844 1/31/2013 2:43:44 PM

4. MENTAL HEALTH AND HOMELESSNESS

4.1. Substance use disorders
Across international borders, substance use disorders account for the vast
majority of lifetime psychiatric disorders among homeless people. The
lifetime prevalence exceeds 2/3 of homeless people in most studies, reach-
ing as high as an estimated 97% for alcohol abuse or dependence among
homeless people in London.13 The prevalence of illicit substance abuse
varies widely on cultural grounds and availability of substances. In Korea,
where illicit substances are very difficult to obtain, prohibitively expensive,
and associated with strong social taboos, reports of illicit substance abuse
run as low as 1.2%,17 whereas rates near, and sometimes exceed, 50% in
the United States, Canada, and parts of Western Europe.1,37,39 Illicit
substance users are younger on average than alcohol users and enter home-
lessness at an earlier age. In the United States, lifetime prevalence of IV
drug use was noted at 22%.39 Other countries also note significant amounts
of IV drug use, without specific statistics.
4.2. Mood disorder

Among non-substance use psychiatric disorders, major depressive disor-
der is most commonly noted, with lifetime prevalence in the 30%–50%
range. One study done in the United States demonstrated that men were
more likely to meet criteria for major depressive disorder on days when
it was cold and wet, suggesting that major depressive disorder can be
difficult to distinguish from “the miseries of homelessness.”32 No differ-
ence was noted for women, however.
Rates of bipolar disorder range from comparable to that of the general
population (in Korea, for example, per Han et al.17) to elevated relative to
the general population in countries such as the United States (7%–10%)39
and Germany (4.8%).11

In Western Europe, a high prevalence of generalized anxiety disorder is
noted,37 although Pollio et al.39 note in their discussion of anxiety
B1405_Ch-33.indd 845 1/31/2013 2:43:44 PM

disorders among homeless people in the United States that situational

anxiety can be difficult to distinguish from symptoms of anxiety disorder
in this population. They do note a 20% lifetime prevalence of PTSD
among homeless people in the United States.
4.4. Psychotic disorders

In the United States, schizophrenia is relatively common among homeless
adults (4%–17%,39 and 8% among men seeking shelter for the first time).
The Brazilian study gives a comparable rate, about 10%.18 However, in
both Western Europe and in Korea, rates of schizophrenia are very low
among homeless people. Differences in social welfare and national health
systems are postulated to account for this difference,17,37 because most
Western European countries have an extensive health care system and sup-
port for individuals with severe chronic mental illness, and deinstitution-
alization has not occurred in Korea, so patients with psychotic disorders
are rarely seen on the streets there.
4.5. Personality disorders

In general, personality disorders are noted to be more common among
homeless persons than among age-matched controls in the general popu-
lation.10 In the United States, a 16%–20% lifetime prevalence of antisocial
personality disorder has been noted among homeless people,39 compara-
ble to the 25% found in a Munich sample.11 Some have argued that meet-
ing criteria for antisocial personality disorder is functional or adaptive on
the street, and thus the use of the diagnosis is “culturally insensitive,”9 but
others note that the onset of the personality disorder almost always pre-
cedes homelessness, and thus is not a result of street life.33
4.6. Traumatic brain injury

Among a representative sample of homeless people in Toronto, Canada,
53% were found to have a history of traumatic brain injury, defined as any
self-reported head injury that left the individual dazed, confused, disori-
ented, or unconscious. About 12% had moderate or severe brain injury, in
B1405_Ch-33.indd 846 1/31/2013 2:43:44 PM

which they had been unconscious for 30 mins or longer. Around 70% of
these injuries had occurred before homelessness.20 A number of studies
in the United States also suggest high levels of traumatic brain injury,
48%–82%, among homeless people.27 Moderate or severe traumatic brain
injury is associated with higher likelihood of poor mental and physical
health, as well as more drug problems.
4.7. Cognitive dysfunction

There is growing evidence of cognitive dysfunction in homeless people
across international borders. A review including North American, South
American, Australian, and European studies suggests that about 4%–7%
of homeless people exhibit deficits on the Folstein mini mental status
examination.3 Other studies, however, suggest significantly higher levels
of cognitive dysfunction, reaching 80% in some homeless cohorts.
Additionally, focal deficits in verbal and visual memory, attention, speed
of cognitive processing, and executive function are observed. There may
be multiple reasons for cognitive dysfunction, including primary mental
illness, traumatic brain injury, substance use, poverty, social disability,
and malnutrition. Although no causative links have been made, cognitive
dysfunction is likely a risk factor both for becoming homeless as well as
for poor social outcomes once homeless.
4.8. Comorbidities
Comorbidity is a common finding across countries among homeless
individuals with mental illness. In general, the most common combi-
nation is alcohol dependence with other substance use and/or mood
disorders.
4.9. Mortality and general medical health

Homelessness has been shown across international studies to be associ-
ated with significantly increased mortality compared to the general popu-
lation.30 The increased mortality is often related to illicit substance use.
Additionally, it is often difficult for homeless people to obtain adequate
B1405_Ch-33.indd 847 1/31/2013 2:43:44 PM

health care. In a study done in Los Angeles County, California, homeless

people were found to have an increased prevalence of most cancer risk
factors, but lower cancer screening rates than the general public.5 This
finding also holds in countries with more extensive health care systems.
In a German study, 90% of homeless men with hypertension were receiv-
ing no treatment for their hypertension.41
4.10. Criminal justice systems

There is an overwhelming correlation between incarceration and home-
lessness for mentally ill people. Behaviors resulting from mental health
disorders are often criminalized. Therefore, it is common for people with
mental health disorders to become connected with the criminal justice
system rather than mental health treatment. This is especially true for
people with substance dependence disorders. Recognition and treatment
of mental health disorders is limited within the criminal justice system, so
often the mentally ill person becomes identified as criminal rather than
mentally ill.
There is a general correlation between incarceration and homelessness.
It was demonstrated in one study that recent homelessness was 7.5–11.3
times more common among jail inmates than the general population. But
the major contributing variables associated with this statistic were mental
illness and substance abuse.16 The correlation between mental illness and
homelessness is already high. When mentally ill people are associated
with the criminal justice system, treatment becomes less likely and a
vicious cycle of homelessness and incarceration is promoted.
5. TREATMENT INTERVENTIONS PROPOSED

TO ASSIST HOMELESS PERSONS
AND THEIR EFFECTIVENESS
5.1. Historical context
Throughout much of recorded history, various groups of disadvantaged
persons including the mentally ill have been socially outcast and vulner-
able to the ravages of extreme poverty and homelessness. In the late
B1405_Ch-33.indd 848 1/31/2013 2:43:44 PM

1800s, the efforts of Chiarugi and Pinel15,29 propelled the “moral move-
ment” in psychiatry urging more humanitarian care for those suffering
from mental illnesses. By the end of the 19th century, institutional systems
and asylums began to develop on a more widespread basis for these pur-
poses.19 Severely mentally ill persons who otherwise would have been
homeless, jailed, or in the poorhouses of the day began instead to be
directed into such facilities. Multiple factors, however, including lack of
public investment and resources, segregation from society and lack of
oversight caused these systems to deteriorate, leading to inhumane condi-
tions, and human rights violations, and humanitarian calls began to swing
back against institutionalization as a result.19 Deinstitutionalization efforts
increased and began to peak in the mid-20th century and have dominated
the policies of most Western countries since. Circumstances in the devel-
oping world may crudely mirror these historical patterns.42 As the deinsti-
tutionalization movement has proceeded, however, it has not been without
much controversy. Many of the more vulnerable appear again to be “fall-
ing through the cracks” as many communities have been poorly equipped
to deal with the needs of the severely mentally ill who comprise a large
percentage of homeless persons. Intense and vigorous debate occurs
between proponents of autonomy and paternalism.8,19,23
As cultural conceptualizations of the causes of homelessness and men-
tal illness have shifted over time, these persons’ places in competition for
scarce societal resources and considerations for humanitarian assistance
have shifted. Causal conceptual models have ranged from moral depravity
to more complex social, psychological, and biological models in which
disadvantage results from many factors, not all within the control of the
consciousness and will of the affected person. Conceptual models of
moral depravity have resulted in isolation and shunning of disadvantaged
persons. Deterministic environmental and biological models have caused
such persons to be viewed as objects of compassion and pity rather than
of evil or laziness. These models however may run the risk of over objec-
tification and may foster an unhealthy paternalism, lack of personal
agency, and cause harm. Other contemporary models may view disadvan-
taged persons as equals deserving of social and environmental opportuni-
ties to practice autonomy and responsibility. These models may under
appreciate the unique vulnerabilities of persons with biological conditions
B1405_Ch-33.indd 849 1/31/2013 2:43:44 PM

such as schizophrenia which may make these persons exposed to severe

disadvantage in competition for scarce resources. Tensions between such
warring conceptualizations and their various calls for autonomy, respon-
sibility, and benevolent paternalism are violently colliding in any discus-
sion considering assistance for persons who experience homelessness.
5.2. Contemporary treatment interventions proposed

for homeless persons with various health conditions
Multiple challenges exist in determining how best to assist persons who
experience homelessness today. Homelessness is an extremely broad
social problem and definitions of what it is, its causes, estimates of the
needs of, and resources to assist homeless persons vary widely within
and between geographic areas and epochs of time. Research is chal-
lenging to conduct and interpret due to the diverse and heterogeneous
likely causes and groups of persons who may end up homeless across
these spans, the diverse needs of these persons, the challenges of con-
ducting research among transient persons including loss of follow up of
participants and many other challenges which make conclusive inter-
pretation and generalization of findings extremely difficult. Interventions
found effective in one time, in one specific sociocultural domain are not
likely to generalize to the unique circumstances and needs of other
domains.22
In this chapter, we are limited to reviewing the research published in
English language journals, with a conceptual model of homelessness
heavily influenced by the Western construction and experience. Far fewer
writings are available from developing nations unfortunately. Most of the
published research has had a focus on assisting those with severe mental
illness and substance use disorders in the era of deinstitutionalization. We
review interventions performed by medical systems and professionals
which attempt to assist homeless adults and children with various health
related diagnoses including mental health and substance-related concerns.
We have preferentially sought information which has been tested in rand-
omized controlled trials, though the literature in many areas is lacking
such rigorous study designs. Unfortunately, there are no comparisons of
outcomes between institutional treatments versus non-institutional
B1405_Ch-33.indd 850 1/31/2013 2:43:44 PM

treatments. Two related continua are frequently compared against each

other in the current deinstitutionalized context. In the first group of com-
parisons we find intensive ongoing outpatient case management approaches
being compared with less intensive case management approaches.
Comparisons also are beginning to appear in the literature in which con-
tingency based programs requiring compliance with mental health or
substance use treatment prior to providing assistance with housing are
being tested against programs without such stringent compliance
requirements.
5.2.1. Intensive case management versus other forms of care

The largest amount of research published appears in the treatment of
severe mental illness and the subsequent impact upon homelessness.
A smaller literature exists in looking at substance use and other chronic
medical conditions.
i. Adult homeless persons with severe mental illnesses

The results of comparisons between intensive case management (ICM)
and other models of treatment differing in the number of managed clients
per case manager (non-ICM and other less well defined forms of com-
munity care termed “standard care”) have been summarized in a recent
high quality systematic review.7 Intensive case management is defined in
this review as a health care model which provides ongoing, organized
outpatient supportive resources for the mental health, rehabilitative and
social needs of an eligible person, over an indefinite period of time, by a
multi-disciplinary team of mental health professionals, coordinated by a
single case manager, usually a social worker, who has a fairly small group
of clients (less than 20). ICM typically offers 24-hour help and often con-
ducts consultations in non-clinical settings. It aggressively attempts out-
reach to persons who traditionally have been difficult to engage with.
Assertive Community Treatment (ACT)43 is a well defined and validated
example of intensive case management. More information can be found at
the Assertive Community Treatment Association website (http://www.
actassociation.org/).
B1405_Ch-33.indd 851 1/31/2013 2:43:44 PM

Intensive case management via ACT for persons with severe mental
illness appeared to have significant advantages over standard care in this
systematic review of previous trials.7 When intensive case management
was compared to standard care, those in the intensive case management
group were significantly more likely to stay with the service, have
improved general functioning, get a job, not be homeless, and have shorter
stays in the hospital (especially when they had had very long hospitaliza-
tions previously). There was also a suggestion that it reduced the risk of
death and suicide. If intensive case management was compared to other
case management with >20 clients per case manager (non-intensive case
management), the only clear difference was that those in the intensive case
management group were more likely to remain in care. There were no tri-
als comparing non-intensive case management with standard care or insti-
tutional care. It remains uncertain if intensive case management is
significantly better than other models of case management with a higher
caseload per case manager or institutional care and thus these remain top-
ics for further investigation. Another meta-analysis6 found advantages
for ACT over standard case management. In the randomized trials
included in this meta-analysis, ACT treatment subjects demonstrated a
greater reduction in homelessness and greater improvement in psychiatric
symptom severity compared with standard case management treatments.
Hospitalization outcomes were not found to be significantly different
between the two groups in the studies included in this review however.
ii. Adult homeless persons with substance

use and other health related diagnoses
A recent moderate quality systematic review included comparisons
between various interventions including various forms of case manage-
ment and standard care practices for a broader range of health related
diagnoses.20 For homeless people with mental illness, case management
linked to other services was found effective in improving psychiatric
symptoms, and intensive case management was found effective in
decreasing psychiatric hospitalizations and increasing outpatient contacts
similar to the findings reported in the above reviews. For homeless people
with substance abuse problems, case management was found to result in
B1405_Ch-33.indd 852 1/31/2013 2:43:44 PM

greater decreases in substance use than usual care. For homeless people
with latent tuberculosis, monetary incentives were found to have improved
adherence rates with treatment. The authors noted that although a number
of studies comparing an intervention to usual care were positive, studies
comparing two interventions frequently found no significant difference in
outcomes. The authors concluded overall that coordinated treatment pro-
grams for homeless adults with mental illness or substance abuse usually
resulted in better health outcomes than usual care and felt that health care
for homeless people should be provided through such programs whenever
possible. They found that research was lacking on interventions for
youths, families, and conditions other than mental illness or substance
abuse.
5.2.2. “High threshold interventions,” requiring substance use

and mental health stabilization first before providing
further assistance to homeless persons versus “low
threshold, harm reduction” strategies
Many programs for homeless persons include provisions to ensure com-
pliance with abstinence and mental health treatment prior to offering fur-
ther efforts in providing shelter. These are referred to as “high threshold”
treatment models, in that there is a higher level of adherence to risk reduc-
tion behaviors demanded of participants (i.e. abstinence) prior to provid-
ing additional assistive resources. Recent trends have begun to examine
whether such efforts to provide access to housing should be made less
contingently as per the tenets of the Harm Reduction model.26 Proponents
of “low threshold, harm reduction” models argue that ongoing treatment
and engagement with persons who exhibit risk behaviors may result in
reduction or stabilization of some risks and be better than no treatment at
all. The long-term goals of the high threshold models are retained and
encouraged, but assistive resources are provided to persons who continue
to be engaged in risk behaviors. In substance abuse treatment, needle
exchange programs are examples of low threshold harm reduction types
of interventions.
Housing First is an example of a low threshold, harm reduction pro-
gram which has begun to be studied in addressing the specific needs of
B1405_Ch-33.indd 853 1/31/2013 2:43:44 PM

homeless persons.24,38,40,45 It encourages providing housing with less

contingent requirements upon compliance with treatment for mental
health, medical illness, or substance dependence in the hopes that
access to stable housing will reduce some of the harmful exposures
present during homelessness. Critics of harm reduction approaches
raise concerns that such programs may encourage persons to remain at
intermediate levels of risk exposure for longer periods of time or that
more permissive attitudes toward risk exposure will encourage or
reward persons to take such risks. Research efforts though have shown
promise in some outcomes in two randomized controlled trials.
Homeless, mentally ill persons with high rates of substance abuse were
randomly assigned to receive housing contingent on treatment and
sobriety (control) or to receive immediate housing without treatment
prerequisites (experimental condition). Those in the experimental con-
dition obtained housing earlier, remained stably housed and reported
higher perceived choice. Utilization of substance abuse treatment was
significantly higher for the control group, but no differences were found
in substance use or psychiatric symptoms. The authors concluded that
participants in the Housing First program were able to obtain and main-
tain independent housing without compromising psychiatric or sub-
stance abuse symptoms.
Offering housing and case management to a population of chroni-
cally homeless adults with chronic medical illnesses who were frequent
users of medical resources resulted in fewer hospital days and emer-
gency department visits, compared with usual care.40 Medical outcomes
were not significantly different between groups. A non-randomized trial
of the Housing First intervention for chronically homeless individuals
with severe alcohol problems found reduced health care and public ser-
vice costs relative to usual care.24 Another small non-randomized trial
found that shelter-based alcohol administration to chronically homeless
people addicted to alcohol decreased hospital visits and police encoun-
ters with no significant changes in blood alcohol levels.38 Overall, such
approaches may show some promise, although additional randomized
controlled trials are needed and many complex issues are raised which
are deserving of careful attention before firm conclusions can be
reached.22
B1405_Ch-33.indd 854 1/31/2013 2:43:44 PM

5.2.3. Effective interventions for homeless youth

Not much has been done, unfortunately, for this population in recent sys-
tematic review,2 and research is especially needed to address this vulner-
able population.
6. SUMMARY
Assessing the effectiveness of efforts to conceptualize and assist home-
less persons internationally is challenging. There are varying conceptual
models of what homelessness is, there are varying social, political, and
historical contexts in which homelessness occurs which may shift dra-
matically over short periods of time even in the same geographic locale.
Homelessness is likely to have multiple diverse causative factors.
Conceptualizations of the needs of homeless persons may vary greatly
depending upon these factors. How to measure the need of homeless per-
sons is not universally agreed upon, and there are varying intervention
models which have been proposed which may not easily generalize out-
side of the unique circumstances where they have been implemented.
Resources for gathering information, developing interventions, and track-
ing outcomes vary substantially from region to region. The homeless
population by its very nature is difficult to study as a result of factors such
as loss of follow-up making strong inferences from research challenging.
Only a limited number of interventions and outcomes have been tested
rigorously and few non-Western cultures have been represented in this
literature.
Future research should include prospective studies to elucidate the risk
factors into and out of homelessness and suggest targets for randomized
controlled trials to support the many needs of homeless persons. The inter-
ventions literature from Western populations does seem to support the
effectiveness of ACT versus usual care for those with severe mental illness
in the context of deinstitutionalization. Current usual care community and
hospital service delivery models do not meet the needs of many homeless
people who suffer from high prevalence rates of mental illness, personal-
ity disorders, and alcohol and drug dependence. Integrated approaches to
treatment which incorporate intensive case management to support mental
B1405_Ch-33.indd 855 1/31/2013 2:43:44 PM

health, alcohol and drug abuse, welfare, and housing needs may be benefi-
cial. Harm reduction approaches may offer promise and randomized con-
trolled trials may assist in further delineating the risks and benefits of
these approaches and for whom they are most likely to be favorable.
Children and adolescents are understudied vulnerable populations.
Research may be particularly important in non-Western populations
where there appears to be very limited information. The broadest context
of history must be considered carefully as the tension between autonomy,
responsibility and paternalism results in a potential for pendular swings in
policy.
7. SOCIAL VARIABLES AND HOMELESSNESS

There is a matrix of overlapping social system and cultural variables that
affect the issue of homelessness. Political and socioeconomic climates
are important factors, but there are other social system variables that have
heavy bearing on the issue. These variables include, but are not limited
to, government policies around homelessness, access to care, and access
to public welfare as well as cultural attitudes around homelessness, men-
tal illness, and substance abuse (Table 1). These variables are intermixed
in a complicated web and sum to create a context for the problem from
country to country and place to place. As the variables change, so do the
rates of homelessness, and also the conditions and outcomes for those
affected.
Table 1. Cultural factors and homelessness.

Cultural attitudes may determine largely what is acceptable and unacceptable
with regard to the society’s handling of homelessness.
Cultural risk factors
Stigma against mental illness
Acceptance of homelessness as part of the human condition
Protective cultural factors
Expectation that the family/extended family is responsible for the mentally ill
persons
Cultural attitudes promoting social welfare
B1405_Ch-33.indd 856 1/31/2013 2:43:44 PM

7.1. Government
From the standpoint of government, a policy on homelessness (or lack
thereof ) is a critical variable. The stated, official stance on this social issue
may predict for the pragmatic supports (or lack of supports) of money and
social resource connections that will make the phenomena more or less
common and will change likely outcomes for those affected. After policy,
the amount of available real resources for homeless and at risk for home-
lessness will predict the epidemiology and the outcomes.
How governments handle the issue of access to public health, mental
health, and substance abuse treatment will have critical bearing on the
possibilities and outcomes for many persons affected by homelessness.
Without access to care, a core risk factor for homelessness like mental
illness remains unabated. Also, social welfare access and public policy
around disabilities will have huge relevant relation over outcome.
Another governmental factor that is important affecting homelessness
among mentally ill populations is the laws around involuntary commit-
ment and state conservatorship. Each country has its own set of laws that
attempt to make a reasonable balance between the autonomy of mentally
ill persons and insurance of the protection of their wellness. The nature
of these laws may result in more or less state oversight of the chroni-
cally mentally ill and therefore more or less mentally ill persons
institutionalized.
A prime example of the complex nature of how these systems interface
to predict rates of homelessness is seen in the recent history of deinstitu-
tionalization movements in Western countries. The deinstitutionalization
movement provides insight into the level of complexity with which the
social variables interact to predict rates of homelessness. In this move-
ment toward community-based treatment of mental illness, commitment
laws were challenged as well as public attitudes around mental illness and
its proposed social solutions. In the United States, the movement began
in the context of a larger Civil Rights push and it emphasized the auton-
omy and basic rights of mentally ill persons and criticized the poor condi-
tions in institutional settings at the time. But deinstitutionalization was
(and still is) also an economic reaction to shrinking financial resources
for mental health treatment. There is financial incentive and, therefore,
political motivation in reducing institutions. So the outcomes from the
B1405_Ch-33.indd 857 1/31/2013 2:43:44 PM

movement also highlight the very real correlations between reduced over-
all financial services for mentally ill persons and increased rates of
homelessness.14
8. KEY POINTS
• Definitions of homelessness vary across countries, as does the degree

to which the topic has been studied.
• High rates of substance use disorders and other mental health prob-
lems are seen among homeless adults.
• Substance use disorders account for the majority of psychiatric disor-
ders among homeless people. The prevalence of illicit substance
abuse varies from country to country.
• Among non-substance use disorders, major depressive disorder is
most common.
• Differences in social welfare and national health systems may account
for some variance in the amount of psychotic disorders seen among
homeless people.
• There is growing evidence of traumatic brain injury and cognitive
dysfunction among homeless people.
• Homelessness is associated with increasing mortality, often related to
substance use or difficulty obtaining health care.
• Treatment settings for homeless persons have shifted from institu-
tional settings to outpatient community settings in recent years in
developed nations.
• Many communities are poorly equipped to deal with the needs of the
severely mentally ill who comprise a large percentage of the homeless
in Western countries.
• The interventions literature from Western populations supports the
effectiveness of ICM models such as ACM versus usual care for
adults with severe mental illness in the context of
deinstitutionalization.
• Harm reduction approaches may offer promise in treating chronically
homeless persons with comorbid substance use, medical illness, and
mental health concerns. Randomized controlled trials are needed to
B1405_Ch-33.indd 858 1/31/2013 2:43:44 PM

assist in further delineating the risks and benefits of these approaches

and for whom they are most likely to be favorable.
• Homeless children and adolescents as well as those from non-Western
populations are understudied vulnerable populations.
9. SELF-ASSESSMENT
9.1. What diagnoses account for the majority of psychiatric
disorders among homeless people?
(A) Substance use disorders.
(B) Psychotic disorders.
(C) Mood disorders.
(D) Traumatic brain injury.
(E) Antisocial personality disorder.
Answer: A
9.2. A harm reduction intervention is characterized by a:

(A) High treatment entry threshold.
(B) Low treatment entry threshold.
(C) High ratio of clients to case managers.
(D) Low ratio of clients to case managers.
(E) None of the above.
Answer: B
10. CASE STUDIES

10.1. Chronic psychiatric symptoms
DG is a 25-year-old homeless African American male with a chronic and
continuous history of psychotic symptoms present since he turned 18. He
reports being fearful that he is being followed by a vague network of per-
sons who he believes are plotting to kill him. He hears voices and believes
that various health care providers, family members or law enforcement
personnel are imposters posing as themselves in order to gain access to
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him. He sees cars on the street that he believes are following him. He
exhibits limited coping skills with stressors and has been unemployed and
low functioning since age eighteen, markedly below his previous level of
function. He has been in and out of various shelters despite multiple fam-
ily efforts toward assistance. When his family has attempted to assist him
he has become fearful, impulsive, erratic, and becomes very hostile and
threatening toward them. He then elopes from their care. He has been
homeless for several years now despite their repeated efforts at obtaining
assistance for him via multiple hospital admissions and appeals to various
government health agencies. He has had extreme difficulty in providing
for self care after hospital discharge and his function has never returned to
levels achieved prior to the age of 18. He does not remain in any particular
shelter for any prolonged period of time, nor does he follow up with out-
patient clinical appointments for either medical or psychiatric care. He is
not compliant with medications. He has had periods of depressive symp-
toms, suicidal ideation and attempts during active psychotic periods how-
ever the total duration of depressive symptoms has been brief relative to
the active and residual periods of psychosis. He has had no known manic
symptoms. He has a well-established diagnosis of polysubstance depend-
ence (alcohol, marijuana, crack cocaine, and amphetamine) likely exacer-
bating his symptoms. His psychotic symptoms do not appear to remit even
in several month-to-two month long periods of prolonged abstinence from
illicit substances during observed inpatient hospitalizations. He has a sei-
zure disorder and has been poorly compliant with his anti-epileptic regi-
men. His psychotic symptoms appear independent of his seizures which
are not considered causative for his mental status changes per neurologi-
cal consultation and his symptoms are most consistent with a DSM-IVTR
diagnosis of chronic paranoid schizophrenia.
10.2. Multiple hospital admissions

Mr G has been admitted on dozens of occasions to various private and public
inpatient hospitals in several adjacent counties in Northern California. His
mother states he has been homeless wandering the streets and that he is
unable to hold a job. He has been unable to obtain consistent medical, psy-
chiatric care, or housing. She and the patient’s grandmother have pursued
multiple attempts at conservatorship with little success unfortunately as a
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result of various legal challenges raised in establishing the patient’s county

of residence with officials from several counties stating that he is not consid-
ered a resident of their county and determining that he is therefore ineligible
for public assistance in their locale as a result of his transientness. Without
conservatorship, he is ineligible for secured treatment facilities and the
patient has had dozens of hospitalizations for various medical and psychiat-
ric reasons. He has had multiple encounters with law enforcement officials.
He cannot provide the name of any outpatient doctor despite having been
referred on multiple occasions and has had multiple failures at various low
fee outpatient treatment clinics with serious consequences including multi-
ple suicide attempts and recurrent hospitalizations for mental health decom-
pensation as well as his poorly controlled seizure disorder and substance use.
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16. Greenberg G, Rosenheck R. (2008) Jail, incarcaration, homelessness,
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17. Han O, Lee HB, Ahn J, Park J, Cho M, Hong J, Hahm B, Kim C. (2003)
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18. Heckert U, Andrade L, Alves MJM, Martins C. (1999) Lifetime prevalence
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Kaplan and Sadock’s Comprehensive Textbook of Psychiatry, Lippincott
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Redelmeier DA, Levinson W. (2008) The effect of traumatic brain injury on
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homeless population: 1992–2002. Am J Community Psychol 46: 49–59.
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(2004) Self-reported changes in drug and alcohol use after becoming home-
less. Am J Public Health 94(5): 830–883.
37. Philippot P, Lecocq C, Sempoux F, Nachtergael H, Galand B. (2007)
Psychological research on homelessness in Western Europe: A review from
1970 to 2001. J Soc Issues 63: 483–504.
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39. Pollio DE, Eyrich-Garg KM, North CS. (2010) The homeless. In: Johnson
BA (ed.), Addiction Medicine: Science and Practice, pp. 1487–1504,
Springer, NY.
40. Sadowski LS, Kee RA et al. (2009) Effect of a housing and case management
program on emergency department visits and hospitalizations among chron-
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41. Salkow K, Fichter M. (2003) Homelessness and mental illness. Curr Opin
42. Sontag D. (2010) In Haiti, mental health system is in collapse. The New York
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43. Stein LI, Test MA. (1980) Alternative to mental hospital treatment: I. concep-
tual model, treatment program, and clinical evaluation. Arch Gen Psychiatry
37(4): 392–397.
44. Toro PA. (2007) Toward an international understanding of homelessness.
J Soc Issues 63: 461–481.
45. Tsemberis S, Gulcur L, et al. (2004) Housing first, consumer choice, and
harm reduction for homeless individuals with a dual diagnosis. Am J Public
Health 94(4): 651–656.
B1405_Ch-33.indd 864 1/31/2013 2:43:45 PM

Chapter 34
Mental Health Consequences of War

and Political Conflict
Daryn Reicherter and Rena Sugarbaker
1. INTRODUCTION
Armed conflicts occur today in many countries, resulting in death and
disability. They also have far-reaching mental health consequences for
everyone involved, from soldiers to civilians. Armed conflicts can include
wars, terrorism, and other violent political conflicts or violence perpe-
trated by the state such as genocide, torture, kidnapping, or other human
rights abuses.13
The destruction from wars is usually measured by the number of lives
lost, by statistics around the number of people crippled, or by monetary
values of property damaged. Beyond the physical and structural damage
calculated in the reported statistics, there is an ever-increasing understand-
ing of the consequences on individual and mass psychology.3 The psycho-
logical consequences are often misunderstood and often overlooked. But
they are present, important, and destructive.
Mental health consequence of war is an internationally important issue
because the number of conflicts in the latter part of the 20th century
increased, especially in developing countries. These conflicts also tended
to be within states rather than between them. Frequently these are coun-
tries whose social services, infrastructure, and political systems are
865
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866 D. Reicherter and R. Sugarbaker
undeveloped.8 A common result of war is the destruction of existing

social, economic, health, and education structures, and the displacement
of large numbers of civilians from their homes due to physical destruction
or occupation. In the last 30 years, 80 million people have been forced to
leave their homes, communities, and even their countries due to conflict.6
The mental health effects on traumatized people create problems on an
enormous public health scale.
The psychological pathology resulting from war is amplified to a
societal level when the prevalence of trauma-related mental health
problems become very high.9 The burden on the society is difficult to
measure or even to estimate because there is a gap between understand-
ing the psychological deficits and measuring their consequences on the
behaviors of whole societies. But this gap may be theoretically bridged
by understanding the mental health effects on individuals and the
behavioral risks to them in the context of real statistics for the observed
social consequences in post conflict societies. Post-conflict societies
have high burdens of mental suffering, mental health disorders, and
social dysfunction.
The dysfunction from psychological problems causes systemic prob-
lems that starts at the individual level and is multiplied by the effect size
of the magnitude of the conflict. From individual to family to kinship to
village to society, the ripples of mental suffering disrupt functioning on
multiple levels. Furthermore, there is a tendency to create a multigenera-
tional transfer of maladaptive functioning. Cultural nuances around the
interpretation of mental health vary from culture to culture, but grave
outcomes and dysfunction are the rule worldwide.
Wars and conflicts have lead to massive immigrations of people from
conflict areas, creating a refugee crisis internationally. At the end of
2009, there were an estimated 43.3 million forcibly displaced people
worldwide, the highest number since the mid-1990s. Of these, 15.2 million
were refugees and 27.1 million internally displaced persons (IDPs).30
The mental health impact on the growing number of refugees is
overwhelming and contributes greatly to the public health emergency
that wars cause. Specialized treatments have been developed to address
the issue, but the growing needs for mental health services are vastly
unmet.
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Mental Health Consequences of War and Political Conflict 867
2. WAR AND TRAUMA-RELATED MENTAL

HEALTH DISORDERS
In the past, international health organizations tended to focus only on
physical disabilities as a consequence of war and the resulting morbidity.
More recently, the growing numbers of conflicts and increasing evidence
of the debilitating mental health consequences of trauma has led major
international health organizations to focus on the psychological impact of
conflicts. The consequences of mental health disorders on human health
and social function has come to the attention of the world’s health organi-
zations as a major, worldwide problem.
In recent years, major multilateral international health agencies such
as the United Nations’ World Health Organization (WHO) and Infant
Children’s Emergency Fund (UNICEF), as well as the United Nations
itself, and the World Bank have placed more emphasis on addressing men-
tal health issues in general. These as well as other non-governmental
organizations (NGOs) have begun to recognize the impact of war on the
psychological health of adults and children, and the need to systematically
and proactively address mental health challenges created by wars.
In 2001, the WHO’s yearly world health report was for the first time
dedicated to the mental health. The report recognized that that mental health
is essential to the well-being of individuals, societies, and countries and that
conflict takes a heavy toll on the mental health of people involved. Most of
those involved in recent conflicts live in developing countries, which have
a limited capacity to address such problems. They reported that between a
third and a half of people affected by conflict suffer mental distress.
The most well-known major mental health disorder associated with war
trauma is post-traumatic stress disorder (PTSD). But PTSD is not the only
mental health disorder expected to see an increase in a population as a
consequence of war. Other disorders, such as anxiety disorders, somato-
form disorders, and depression are also seen at higher frequencies after
war.18 While many of those affected by war do meet the criteria for estab-
lished disorders such as PTSD or major depression, most individuals
report troubling and even disabling psychological symptoms that are not
necessarily defined as a disorder.33 The comorbidities of maladaptive reac-
tions to war trauma are grave. Alcohol and other substance related disor-
ders increase after war. Alcohol abuse is frequently related to mental
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health disorders like PTSD and depression. People with PTSD are also
more likely to have and develop alcohol abuse problems. Women who
have experienced trauma have a higher risk of developing alcohol depend-
ence whether or not they have PTSD.24 Other major, problematic social
issues like domestic violence increase after war.32 It is also known that the
perpetration of violence is more common for persons affected by PTSD.
While there is not necessarily a causal link between the violence of war
and these outcomes, the correlation is clear and the connection is not dif-
ficult to understand.
3. PTSD IN WAR SETTINGS

While PTSD is only one of many mental health problems seen after
conflict, it is a major topic of study in war settings. It was officially
recognized as an emotional disorder in 1980 when the American
Psychiatric Association added it to the Diagnostic and Statistical Manual
of Mental Disorders III (DSM-III). The syndrome had been observed in
soldiers returning from the battlefields having faced life-threatening
events over the last several hundred years. It also describes the symptoms
seen in non-veterans as the result of interpersonal violence as well as
events such as natural disasters, and led to the study of the diagnosis in
other populations. While most people who are exposed to trauma do not
develop PTSD, a significant fraction will, and there are wide but signifi-
cantly increased prevalence rates reported in studies.28
In the United States, the 12-month prevalence of the disorder is 3.4%,
according to the NIMH. Statistics from other developed countries without
war are similar. In addition to people who meet the full criteria for the
disorder, there may be as many as one to two times with severe subsyn-
dromal PTSD as those with full PTSD.26 The prevalence of PTSD
dramatically increases in war and post-conflict settings.
War settings often create a confluence of risk factors for exposure to
trauma and the later development of PTSD symptoms. It creates an envi-
ronment where safety cannot be taken for granted. In wartime, death
looms and can occur at any time. The breakdown of social and political
order, as well as increased targeting of civilian populations as a tool of war
create environments full of risks for massive numbers of people to
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Table 1. Risk factors for PTSD.
Risk factors for PTSD

Individual characteristics
Presence of childhood trauma
Being female
Previous psychiatric history
Dissociation at the time of the trauma
Younger age
Lower socioeconomic status
Lower education
Lower intelligence
Racial minority status
Trauma-related
Severity of the event and extent to which life was threatened
Number of traumas experienced
Post-trauma environment related
Inadequate family or peer support system
Recent stressful life changes
experience traumas.6 People find themselves not only at risk for death but
for other traumatic experiences such as witnessing death, rape, torture,
displacement, and kidnapping.
Risk factors for development of PTSD are many, and in general the
effect sizes reported in the literature for various factors are modest.5 PTSD
is a heterogeneous disorder and no one factor results in development of the
illness. Psychosocial risk factors for developing PTSD include those related
to the individual’s susceptibility, the traumatic event itself, and the circum-
stances that surround the individual afterwards. War promotes these risk
factors by increasing likelihood of exposure to traumas, including the pos-
sibility of repeated exposures. It also creates an environment of chaos that
negatively impacts the stability of the environment in which victims find
themselves in afterwards. Table 1 lists several common risk factors.
4. MENTAL HEALTH CONSEQUENCES

OF CURRENT AND RECENT CONFLICTS
Much data has been generated examining the statistics around mental
health problems that have arisen after various conflicts around the world.
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Data may suggest differing rates of symptoms and diagnosable disorders.

As discussed in relation to the development of PTSD, there are many
different variables that may predict for greater or lesser rates of trauma-
related mental health disorders. The following review of findings of
differing rates from different countries is less important for the purposes
of this chapter than the fact of grossly increased rates of mental health
disorders generally seen in post-conflict societies.
De Jong and colleagues9 found high population rates of lifetime PTSD
in their study of four post-conflict settings (see Table 2), including 15.8%
in Ethiopia, 17.8% in Gaza, 28.4% in Cambodia, and 37.4% in Algeria.
Mollica et al.15 studied 1,000 Cambodian refugees living in camps along
the Thai–Cambodia border, and found a 17% rate of PTSD in persons
with four or less trauma events. This statistic increased to 80% among
refugees who had experienced 25 or more traumatic events.
4.1. Afghanistan
Afghanistan is a country that has experienced conflict for over two
decades, resulting in the displacement of a large segment of the popula-
tion, loss of life, and loss of security for surviving civilians. Two recent
studies found high rates of experience of multiple traumas and high levels
of psychiatric symptoms. The first study found a rate of PTSD of 42% and
that men and the disabled had a poorer mental health status.7 A second
study found the rate of PTSD to be about 20.4%. High rates of symptoms
were associated with higher numbers of traumatic events experienced.
Table 2. Rates of DSM disorders (%) in people both with and without
exposure to armed conflict associated violence.9
PTSD Mood d/o Anxiety d/o Somatoform d/o
Algeria 37.4 22.7 37.2 8.3
Cambodia 28.4 11.5 40.0 1.6
Ethiopia 15.8 9.4 13.5 5.3
Gaza Strip 17.8 9.4 13.5 5.3
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Women had higher rates than men. The main sources of emotional support
were religion and family.25
4.2. The Balkans

In the vicious and deadly ethnic wars in the Balkans in the 1990s, the use
of torture, mass rape, and ethnic cleansing shocked the world. Several of
the involved groups have been studied. PTSD symptoms were found in
17.1% of Kosovar Albanians and a linear decrease in mental health and
functioning was noted with increased exposure to traumatic events in
those over age 65, who had previous psychiatric illness or a chronic
health condition.15 Another study among Bosnian refugees showed an
association between psychiatric disorders and disability, including
depression and PTSD. Three years later, a follow-up study on the same
group showed that they still exhibited psychiatric disorders and
disability.17
4.3. Chechnya
The human rights abuses that took place in the recent conflict between
Russian and Chechnya deeply affected Chechen population and troubled
human rights groups around the world. Several studies have evaluated
asylum seekers as well as internally displaced people. In one recent study,
a survey was given to displaced people living in settlements, and revealed
that two-thirds experienced emotional disturbance and upset and almost
all reportedly had non-specific complaints such as somatic complaints,
anxiety, insomnia, depressive feelings, or social dysfunction.10
4.4. Iraq
There have been many conflicts in Iraq in the last 50 years, but few studies
have been conducted on their impact on mental health. One small study of
45 internally displaced Kurdish families living in camps in northern Iraq
five years after attacks in 1988 found that 87% of children and 60% of
their caregivers had PTSD.1
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4.5. Israel
In the context of the longstanding ongoing conflicts within the country,
Israel has experienced bouts of violence for many years. A study in 2003
found that of subjects who have had exposure to conflict-related trauma,
76.7% had at least one traumatic stress-related symptom and 9.4% met the
criteria for acute stress disorder.4
4.6. Lebanon
A civil war lasting from 1975 to 1990 as well as several invasions by Israel
has led to several studies evaluating mental health outcomes of war in this
country. In one 1998 study of 658 people exposed to war, the lifetime
prevalence of major depression ranged from 16.3–41.9%. Predictors of
depression included prior history of depression and exposure to war.12
4.7. The Gaza strip

The violence in the Israeli–Gaza conflict has been severe and long lasting.
Gaza has been one of the areas mainly affected by much of the violence.
A series of studies have come from the Gaza Community Mental Health
Centre, revealing that among children living in the area of heavy bom-
bardments, 54% suffered from severe PTSD, 33.5% moderate, and 11%
of mild PTSD.21
4.8. Rwanda
Survivors of the Rwandan genocide in 1994 have contended with severe
mental and physical health consequences. A community-based study of
2,091 subjects found that about 24.8% met the criteria for PTSD, with the
odds of meeting the PTSD criteria increasing by 1.43 for each additional
traumatic event experienced.20
4.9. Sri Lanka

In May of 2010, the United Nations estimated that between 80,000 and
100,000 people have been killed in the war between the government and
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the Tamil minority population that has persisted over the last several dec-
ades. In addition, the conflict has recently left thousands of civilians dis-
placed. One epidemiological survey in Sri Lanka looking at the
psychological effects on civilians found that in the population, PTSD was
present in 27%, somatization in 41%, anxiety disorder in 26%, and major
depression in 25%. Drug and alcohol misuse was found in 15% and func-
tional disability in 18% of the population. They also found that only 6%
of the population had not experienced any war stresses.27
4.10. Somalia
Since 1991 the Somali civil war has resulted in millions of civilian deaths
and civilian displacement. A study from UNICEF investigated 10,000
children and found a high proportion of them experienced psychological
effects from the prolonged conflict.31
Each in this short list of examples of countries with recent or current
political conflict demonstrates several similarities. War and conflict
increases risks for negative mental health outcomes. Mental health disor-
ders are grossly exaggerated in these countries compared to countries
without the war related risks. These examples also expose varying degrees
of the limits of access to mental health resources.
5. UNMEASURED MENTAL SUFFERING FROM WAR

In most studies on psychiatry and psychology in post-conflict settings,
statistics are generated based on specific diagnostic ideas and rating scales
designed to capture specific symptoms. This method of data collection
leaves much of the psychological suffering and cultural idioms of distress
that do not fall into the narrow categories defined in the concept of PTSD,
undocumented. As Duncan Pendersen writes, “The PTSD model has
important limitations in capturing the complex ways in which individuals,
communities, and larger groups experience massive trauma, socialize
their grief, and reconstitute a meaningful existence.”19 Therefore, it is
likely that much of the psychological distress that is a consequence of war
violence and loss is poorly captured in the studies that examine the mental
health statistics of post-conflict populations. Falling outside the inclusion
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criteria for PTSD does not make the stress or suffering or the risks for its
consequences on human behavior any less real. It is difficult to quantify
the suffering from victimization or from having to establish a new life and
sense of normalcy after losing most or all of one’s family members,
having to flee from home and community, frequently into a foreign land,
and facing years of life in refugee camps.
The consequences of war can create different outcomes for different
people. Grief and loss are internalized psychologically in different ways,
but usually result in suffering and anguish. Specific violations and
personal injuries from war can cause intense anger, hatred, and resentment
or disillusionment and the inability to trust. These psychological changes
are difficult to measure and report on, but negatively affect people’s lives,
relationships, and behaviors.
“The health impact of political violence and wars should be examined not
only along the lines of sheer number of casualties and trauma-related dis-
orders among survivors, but also on the individual and collective levels.
Indirect effects such as disintegration of the family and social networks,
disruption of the local economies, dislocation of food production systems
and exodus of the work force have profound implications in the health and
well-being of survivors.”19
As with the disorder states described above, these psychological problems

are increased greatly in a whole population, amplifying all the sequela of
behavioral disturbance in the society. While they are harder to quantify, it
is not difficult to understand how these issues cause dysfunction in fami-
lies, relationships, and work life, and will have a more profound effect
across the society when prevalence is so high. Greater numbers of persons
with a debilitating psychological effect lead to a greater magnitude of the
sociological effect.
The psychological and behavioral effects of war have a multigenera-
tional element as well. Parenting styles can be disturbed by exposure to
violence and trauma and personal psychological dysfunction can create
dysregulation in parenting. This way, the psychological insults of war on
one generation can lead to difficulties in the next, as is exemplified in
studies of second-generation Holocaust survivors.22
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6. HUMAN RIGHTS VIOLATIONS PROMOTED

IN CONFLICT SETTINGS
Survivors of violence from war and political conflicts are at great risk for
mental health disorders. They may be survivors of unspeakable human
rights violations. Clinicians who work with clients exposed to war vio-
lence must be aware of specific situations that have specific psychological
targets. The following human rights violations may be promoted in war
zones and certainly increase the risk for mental health problems. It is
important to understand the amount of exposure that a population may
have had to these particularly concerning factors in assessing risk for
trauma-related mental health disorders.
6.1. Genocide
Genocide has become an international concern that has occurred with fre-
quency throughout the 20th century and into the 21st. Genocide includes a
primary terrorization of a targeted group. That group usually suffers from a
general violent oppression during the violence. Survivors of genocide have
been targets of murder and usually have been heavily exposed to violence.
They carry a heavy burden of trauma exposure and multiple losses. They
also tend to have among the highest incidences of mental health disorders.
6.2. Torture
Torture is a widely practiced weapon used in war and state-sponsored
political violence. Torture is generally used as a mechanism of terror. As
such, victims’ psychology is a major target of the violence in torture. In
fact, torture is often designed specifically to fit an individual or a particu-
lar ethnic group to maximize the psychological impact. Torture is among
the most highly correlated to the development of PTSD and other mental
health disorders.
6.3. Gender-based violence

Gender-based violence (GBV) is a commonly seen in the context of war
and political violence. Politically motivated campaigns of mass rape have
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become more common as state-supported terror mechanisms. Mass rape

has intentional psychological targets intended for terror of a population.
Rape is a primary cause of traumatization and among the most common
causes worldwide for the development of PTSD.
7. HIGH RISK CONDITIONS CREATED

BY CONFLICT
There are human population displacement conditions that are promoted
during war which lead to great suffering and the increased risk for mental
health disorders.
7.1. International issues linked to increased

mental health problems
The massive displacement of people as a result of war and conflict has a
huge, negative bearing on mental health. There are now 43.3 million peo-
ple forcibly displaced around the world including 27.1 million IDPs and
15.2 million refugees.28 The world’s conflicts have created massive immi-
gration issues particularly in Africa, Asia, and the Middle East, and the
exposure to trauma among the refugee populations is staggering. The risks
for mental health related illness is increased. Human trafficking/sex traffic
has become another major issue that has come of the massive movements
of disenfranchised people as a result of war. Estimates vary widely for the
rates of PTSD and other mental health disorders in these two populations,
but the risk of mental health pathology is greatly increased.
7.2. Internal issues linked to increased

mental health problems
In-country situations also develop during war that create high risk of
traumatization, and increase risk for mental health disorders. Human trade
and sex traffic are internal (as well as international) problems amplified
by mass internal displacement. IDPs are “refugees within their own
country.” They have the displacement problem and traumatization of refu-
gee populations without the protection of UN laws for refugees. These
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groups have very high rates of traumatization and increased rates of

mental health disorders.
8. DEMOGRAPHICS OF POPULATIONS
AT RISK IN WAR SETTINGS
Wars disproportionately affect certain populations, placing them at greater
risk of experiencing trauma and poor mental health outcomes. Some
special populations are described below.
8.1. Veterans
An obvious at-risk population are soldiers involved in fighting on the front
lines. Studies of American veterans from the “Vietnam Conflict” con-
ducted between 1986 and 1988 estimated a prevalence of PTSD of 30.9%
for men and 26.9% for women. At the time of the study, 15.2% of males
and 8.1% of females were diagnosed with active PTSD. Of American Gulf
War veterans, PTSD was found at a prevalence of 12.1% in a population-
based sample of 11,441 veterans.14 An estimated overall prevalence of
PTSD in the “Gulf War” population was 10.1%.11 In the more recent
American wars with Iraq and Afghanistan, a 2008 study of veterans of
previously deployed “Operation Enduring Freedom” and “Operation Iraqi
Freedom” reported a prevalence of PTSD of 13.8%.29
8.2. Civilians
More frequently during the late 20th and early 21st centuries, civilian
populations have suffered a major impact of war. An estimated 191 mil-
lion people have died as a result of wars and conflicts in the 20th century,
with more than 60% of total war deaths occurring among civilians.23
Particularly troubling have been uses of “ethnic cleansing” and genocide
as weapons of war, targeting civilians and placing them at great risk of
terror, harm, and death. In the 1994 genocide in Rwanda, at least 800,000
civilians were systematically killed over the course of 100 days. In the
months that followed, other devastating consequences, including lack of
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food and sanitation, also result in staggering numbers of civilian deaths.

In the war in Congo, 5.4 million people died over a five-year period from
1998 to 2003, most of them civilians and most of them dying from starva-
tion and disease. These conditions create risks for poor mental health
outcomes among large populations of civilians. In addition, individuals
living in poverty are at increased risk for poor mental health outcomes
during war compared to the general civilian population.33
8.3. Women
The use of GBV as a weapon of war has also become more common and
has gained more attention in recent years. It had previously been consid-
ered an unfortunate co-occurrence during wartimes, but is now being rec-
ognized as a weapon of war. In 2008, the United Nations Security Council
passed a resolution naming sexual violence as a war crime, a crime against
humanity, a form of torture, and a constituent act of genocide.
Estimates of rapes of women during the 1994 genocide in Rwanda are
between 250,000 and 500,000. During the civil war in Sierra Leone, at
least 50,000 women were victims of gender-based sexual violence. During
the conflict in Bosnia and Herzegovina between 1992 and 1995, an
estimated 10,000 and 60,000 women were raped.2 In the Congo, approxi-
mately 200,000 women and girls have been raped. Rape is used as a
method of destabilizing, terrorizing, and controlling civilian populations.
In all of these conflicts, perpetration of rape as a weapon of war has had
devastating effects on the social fabric of societies and the mental health
of women. It is used also as a method of humiliation of women as well as
their families. The consequences, including unwanted pregnancies and
children, diseases, and social stigmatization and rejection, frequently
result in a near complete breakdown of the fabric of society.
8.4. Children
Children are very often victims of war. They may be injured or killed, or
enter into one of the high-risk conditions listed above. However, there are
two other specific conditions that children may find themselves in. The
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Orphans and Vulnerable Children (OVC) category is one in which a child

loses parent or guardian figures. There are incredibly high numbers of
OVC currently in post-conflict settings. The UNICEF has highlighted
OVC as one of the most concerning issues for children in the modern age.
Also, a new trend increasing the use of children as soldiers has become
common in Africa and Asia. OVC and child soldier circumstances are
highly correlated with childhood trauma and subsequent serious mental
health pathology.
9. SPECIAL CLINICAL ISSUES IN TREATING

SURVIVORS OF CONFLICT
In 2007, the Interagency Standing Committee, established in 1992 to
increase coordination of humanitarian assistance organizations, published
the Guidelines on Mental Health and Psychosocial Support in Emergency
Settings. The goal was to create a consensus on how to coordinate
agencies and establish an integrated approach to address urgent psychoso-
cial needs in emergency situations. They now have a standing committee
dedicated to implementing these guidelines.
9.1. Rebuilding public mental health in post conflict settings

A major challenge for dealing with the increased burden of trauma-related
mental health disorders seen after conflict is that many post-conflict coun-
tries have a very limited public mental health system and that the system
is often crippled by the country’s infrastructure changes from war. Often,
public health systems will be decimated along with other government
services during the course of conflict. Mental health is often marginalized
in the restructuring of those systems even though the burden of mental
health disorders is greatly increased.
In rebuilding mental health systems, trauma-related mental health
disorders are not necessarily prioritized. Particularly in developing
countries, the scope of mental health programs may be limited mostly to
the treatment of psychotic disorders. As these programs are reconstituted
after conflict the increased prevalence of trauma-related mental health
disorders is not reciprocated with increased resources for them.
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9.2. Refugee mental health for influx of traumatized people

The massive migration of people from conflict areas has created a new public
mental health crisis globally. Refugees have incredible exposure to violence
and trauma prior to and during their flight. Furthermore, mental health disor-
ders are predicted at very high rates within this population. Often, host states
are unprepared to deal with the public health needs of refugees and even less
equipped for dealing with the complicated mental health issues of refugees.
Many developed countries have mental health programs that specialize
in refugee trauma. However, this resource is scarce and the vast majority
of the refugee population will never have access to such resources. Such
resources are limited or non-existent in developing countries.
9.3. Cultural variables in mental health of diverse

traumatized populations
Trauma-related mental health symptoms might be interpreted differently
by different persons and in different cultural contexts. It is very common
that symptoms of anxiety (that may be interpreted as PTSD in the West)
will be understood otherwise in a different cultural context. Depending on
the context, trauma-related mental health disorders are often interpreted as
physical problems or as spiritual problems. Moreover, mental health dis-
orders are also highly stigmatized over the world. For these reasons, the
presentation of symptoms is likely to occur somewhere other than in men-
tal health treatment. Often, psychiatric symptoms will present to primary
care physicians, to spiritual leaders, or to traditional healers rather than to
mental health professionals.
Once connected with mental health resources, there are many different
treatment approaches to traumatized people that should take into account
culturally sensitive issues. Western mental health programs that work with
refugees have to take these cultural factors into account as standard mental
health approaches might lack cultural relevance.
9.4. Centers for torture rehabilitation

There is an international network of programs that provide mental health
treatment services specifically for survivors of torture. Political
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persecution and state-sponsored terror campaigns have created a necessity

for this international niche in mental health treatment. If survivors have
access to this resource, they can align themselves with specialized treat-
ment tailored to survivors of torture.
9.5. Veterans’ mental health services

In many countries, mental health services are available for veterans.
Soldiers are exposed to exorbitant levels of traumatic stress in war and
therefore are at high risk for developing trauma-related mental health
disorders and maladaptive behaviors. Most developed countries and some
developing countries acknowledge this reality and have screening mecha-
nisms and services specifically devoted to these issues.
10. KEY POINTS

• War and political conflict have deleterious mental health conse-
quences on all populations involved, from soldiers on the frontlines to
civilians threatened or assaulted, to children left as OVC from parental
loss.
• The mental health consequences of war may be definable mental
health “disorders” like PTSD or major depressive disorder. Outcomes
may be more difficult to categorize, but result in serious outcomes like
loss and suffering leading to social dysfunction such like domestic
violence and substance abuse.
• War creates enormous populations of persons exposed to violence
(like refugees and internally displaced people) who will be at
extremely high risk for poor mental health outcomes and maladaptive
behaviors, with very poor resources for detection and/or treatment.
• War creates greatly increased risk for human rights crimes like geno-
cide, torture, and GBV that increase exposure to extremes of violence
and increase risk for trauma-related mental health disorders and other
negative psychological outcomes.
• Resources for mental health treatment for post conflict populations
are poorly prioritized and usually unavailable for those that need
it most.
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11. SELF-ASSESSMENT
11.1. Aside from soldiers, which populations are at risk
for trauma related mental health problems
in the context of war/conflict?
All people exposed to extremes of violence and traumatic experience in war
settings are at high risk of developing trauma-related mental health problems.
Civilians are at high risk in conflict settings. Women and children exposed to
violence are at very high risk. In addition, victims of torture and GBV are at
very high risk of developing mental health symptoms or full syndromes.
11.2. Will PTSD from war/conflict always present

in an identical fashion, independent of culture,
gender, or nationality?
Similar characteristics of trauma-related mental health disorders might be
identified irrespective of culture or gender, especially if Western notions
of PTSD are applied in assessment. However, expressions of trauma-
related psychological suffering may vary greatly based on gender and
culture and may not present as a classic case of PTSD. It is important to
have a sense of how symptoms may be expressed within a certain cultural
context in order to assess an individual’s suffering and make an accurate
assessment (or diagnosis). It is important to understand culturally sensi-
tive issues in order to arrange an appropriate treatment plan.
12. CASE STUDIES

Sarosa Chhim is a 65-year-old monolingual, illiterate Cambodian female
immigrant to the United States. She complained of frequent “head aches,”
“dizziness,” and “thinking too much.” She initially presented these symp-
toms to Buddhist monks at a local Khmer temple. The monks blessed her
and recommended traditional methods of relaxing her mind with Buddhist
meditation that were somewhat helpful. She was fortunate enough to have
access to public insurance that will pay for her medical treatment. She told
her primary care doctor that she “thinks too much” and that her sleep was
poor. After negative medical work-up, she was referred to psychiatry for
assessment of anxiety. It was reported that Ms. Chhim survived the Khmer
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Rouge genocide in the late 1970s prior to living in a Thai refugee camp
for five years. She sustained multiple losses including watching the execu-
tion of family members and her own multiple violations including sexual
assault, forced labor, and severe beatings. Since that time, she has devel-
oped intrusive memories of the “Killing Fields” that she thinks about
much of the time. She also relives traumatic events in nightmares almost
every night. She avoids situations or conversations that might remind her
of Cambodia or Thailand and will not listen to the Khmer news reporting
on the Khmer Rouge Tribunal. She is easily startled and has episodes
consistent with the Western notion of “panic attack” almost every time she
goes into a public place.
Ms Chhim’s diagnosis can likely be thought about as a chronic form of
PTSD. Treatment for her may be multifactorial and include (among other
things) social support, psychotropic medication, and culturally sensitive
forms of counseling or behavioral therapy. These treatment approaches
may reduce her suffering and improve her quality of life, but they are
unlikely to eliminate symptoms completely.
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9. de Jong JTVM, Komproe IH, Van Ommeren M. (2003) Common mental
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D, et al. (2007) The trauma of ongoing conflict and displacement in
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traumatic stress disorder and chronic fatigue syndrome-like illness among
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Epidemiol 157(2): 141–148.
12. Karam EG, Howard DB, Karam AN, et al. (1998) Major depression and
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13. Krug E, et al. (eds.) (2002) World Report on Violence and Health, World
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14. Kulka RA, Schlenger WA, Fairbanks JA, Hough RL, Jordan BK, Marmar CR,
et al. (1990) Trauma and the Vietnam War generation: Report of findings from
the National Vietnam Veterans Readjustment Study, Brunner/Mazel, NY.
15. Lopes-Cardozo B, Vergara A, Agani F. (2000) Mental health, social function-
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20. Pham PN, Weinstein HM, Longman T. (2004) Trauma and PTSD symptoms
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Experience. Vrije Universiteit, Amsterdam. Doctoral Dissertation.
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following war and repression in Eastern Afghanistan. JAMA 292, 585–593.
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Chapter 35
Stigma
Travis Fisher
1. INTRODUCTION
Stigma — the word itself has a hard, harsh sound. Given the destruction
and pain that can be wrought upon those afflicted with it, there is a certain
aptness in that. The origins of the word date back to ancient Greece, when
criminals and other social undesirables would be tattooed, cut, or other-
wise given a permanent mark representing their offence. In the modern
era, the definition has broadened, though some debate exists as to the
extent of these new boundaries.5 This chapter will discuss that broadened
definition, the historical consequences of mental health stigma, various
theories which attempt to explain why it develops, and close with broad
categories of “treatment” for it.
Throughout this chapter, there will be instances where families or
individuals living with the symptoms or the diagnosis of mental illness
are mentioned. The term “patient” will be used when describing those
individuals relationship to the mental health system, rather than
“client,” “consumer,” or “service user.” We prefer the term “patient” for
its invocation of the great moral responsibility owed to those seeking
treatment, as it brings to mind traditions of care as ancient as
Hippocrates and as modern as the unique laws governing doctor–patient
relationships.
886
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Stigma 887
2. DEFINITION
Most modern discussions of the stigma of mental illness begin with
Goffman’s8 classic definition of stigma: “the view that an attribute such as
having a mental illness is deeply discrediting and justifies a hostile
response from society.” His definition was intended for all categories of
disability, but has special resonance for mental illness. Since then, various
philosophical camps have argued that stigma is simply another term for
prejudice based on negative stereotypes, that it is the negative effect of the
label itself, or that it is when one aspect of a person becomes the explana-
tion for all they do.5 This chapter will follow the leads of Corrigan7 and
Hinshaw9 who view stigma as the stereotypes, prejudices, and discrimina-
tion that give rise to negative reactions from the so-called “normal” major-
ity. This is a cognitive and social model that will assist us in maintaining
a practical focus on not just how we academically define stigma but what
it does — impairs the life of those affected by it.
2.1. Stereotype
Stereotypes are the cognitive component of stigma. They are negative ver-
sions of the structures or “schemas” that all individuals use to categorize
information. The presence of these schemas, even the presence of negative
ones, does not in and of itself constitute stigma. An individual may be able
to endorse knowledge of the stereotype about mental illness indicating
dangerousness, incompetence, and character weakness without agreeing
with them.7 However, they may support the development of prejudice and
discrimination.
2.2. Prejudice
Prejudice is the affective component of stigma. The difference from the
previous category is that those stereotypes have now become unreasoning,
unjustifiable, and prejudged.9 Knowledge of those cognitive schemas has
now hardened into belief, with no or little allowance for exceptions to be
made. Anger, fear, or other negative emotions are generated as a result,
and may support behavioral reactions.
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888 T. Fisher
2.3. Discrimination
Behavioral reactions are the discrimination of stigma, built upon justifica-
tions provided by prejudice and stereotypes. This category certainly
includes violence by members of the public toward those perceived as
mentally ill, but denying opportunities and other subtle forms of stigma
can be targeted at the stigmatized individual or their family.
It should be noted that stigma does not always come only from mem-
bers of the public; the receiver of public stigma can perceive truth and
validity in the stigma, a process often called “self-stigma” (Table 1),
adapted from Corrigan.7 While self-stigma is defined in a very similar way
as public stigma, the “symptoms” are not always the same, and require
different interventions.
3. THE SIGNS OF STIGMA

As mentioned in the previous section, stigma can be commonly seen in the
denial of opportunities to those who otherwise would be fully entitled to
them, for no other reason than their mental illness or symptoms. These can
be thought of as the “signs” that the “disease” of stigma is present. We
divide these into three general categories: restrictions on personal liberty,
social opportunities, and access to healthcare.
3.1. Personal liberty

Restrictions on personal liberties are perhaps the most universal of all
forms of stigma. In all societies, there are circumstances in which a person
Table 1. Comparison of the definitions of public and self-stigma.

Public stigma Self-stigma
Stereotype Negative schemas about a group Negative thought about oneself,
e.g. I am incompetent.
Prejudice Belief in the stereotype Agreement with that belief
associated with negative emotion leading to a negative self-image.
Discrimination Behavior in response to the Change in behavior in response,
prejudice e.g. not pursuing work.
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Stigma 889
will be stripped of the basic right of free movement. In the case of mentally
ill persons in westernized nations, free movement may be restricted though
a bureaucratic civil commitment process that involves the courts, locked
hospital wards, and involuntary medication. Patients lose the ability to
choose whom they congregate with, and what and when they eat; they may
spend periods of time under direct physical restraint. In resource-poor
regions like sub-Saharan Africa, rural India, or rural China, there may be
fewer options for treatment. Simple chains may be used to restrain indi-
viduals for prolonged periods, especially if the individual is perceived to
be otherwise uncontrollable. This may occur at home, in healing temples,
or in hospitals. The World Health Organization (WHO) has targeted this
practice for elimination, noting that if chained to a bed or wall, individuals
lose the ability to flee danger and may be denied basic sanitation.18
As the world was reminded in 2001, this danger is more than mere
hyperbole. The small town of Erwadi, in the Tamil Nadu state of India, is
home to a Muslim shrine that many believe cures mental illness. On
6 August 2001, a fire swept through one of the town’s 16 asylums, killing
28 mentally ill patients who were chained to stone pillars. The patients
had no opportunity to escape; the fire spread too quickly for anyone to free
them from their shackles. Much like the justification for physical restraint
in psychiatric hospitals in the West, the justification for chaining patients
in shrines hinges on the danger that these men and woman pose to them-
selves or others if freed. The individual details of the confinement vary but
the loss of free movement is the same. Also similar is that mentally ill
people may face stigma coming from their “treatment providers.”
It is initially tempting to overlook the potential for stigma inside this
process. After all, doesn’t society have a right to “defend itself” from the
dangers of unpredictable, violent mentally ill patients? If treatment pro-
viders share the stereotype that all mentally ill patients are violent, they
can also become fearful for their safety. They may restrain patients for
potential violence who do not actually represent any threat, “just to be
safe.” In regions and countries where long-term restraint is an option, such
thinking may lead to not recognizing improvement or recovery soon
enough to remove the chains from a now passive individual. A stereotype,
prejudice, and discriminatory action have then come together to create
stigma.
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890 T. Fisher
Though formal studies into the psychological effect of enduring

restraint are relatively new, they have occurred in the United States,
Europe, and Australia.3 The body of research points to significant emo-
tional distress, feelings of betrayal by the mental health system, and resist-
ance to future involvement or treatment by that system. “Ex-patients” and
other consumer advocates have added to this evidence, and spurred the
research to begin with, by telling their stories.
3.2. Social opportunities

Most patients and individuals with symptoms of mental illness are not
inpatients, so restraint is not a day-to-day reality for them. Instead, there
are barriers to various social opportunities to contend with. Legal treat-
ment, housing, employment, and marriage are four such opportunities that
can be affected.
3.2.1. Housing
Independent housing is desired by many mental health patients for a vari-
ety of reasons: as a sign of recovery, as an indication of increased wealth
and status, or simply out of a desire for independence, privacy, and the
ability to raise a family. Multiple studies have demonstrated landlords’
decreased willingness to rent to individuals with a diagnosis of mental
illness.7 Landlords wield great power in their role as “gatekeepers,” and
any prejudice they demonstrate can be disproportionately damaging to
mentally ill persons seeking housing. Many communities in Western
nations have proven unwillingness to allow low-cost housing for the men-
tally ill to be built in “their” neighborhoods.
In regions with emphasis in an extended rather than a nuclear family
structure, there is less pressure for independent housing for mentally ill
people. Traditional Indian, Chinese, and Japanese cultures are such exam-
ples. Many individuals with symptoms of mental illness utilize the family
unit as their primary source of treatment and support.13 However, they do
not necessarily avoid stigma. Ng13 points out that this same familial orienta-
tion can lead to strong intra-family shame and guilt, culminating in a desire
to conceal the mentally ill family member as a “disgrace.” There may be
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active discouragement of the mentally ill family member’s leaving the

home or seeking outside services to maintain the family secret. Activists in
such communities seek creative means to bypass these barriers.
In an effort to identify individuals with long-term health needs who had
instead been confined to home, Susie Kim gathered 20 South Korean
nurse practitioners to work in a door-to-door community mental health
campaign during the 1990s. In a single poor district of South Korea, they
found 204 such people.2
3.2.2. Employment
The difficulties faced by mentally ill patients seeking employment extend
beyond prejudice and discrimination by employers; they may encounter
such attitudes in their co-workers as well. This may lead to mentally ill
workers not only overtly keeping “the secret” of their diagnosis or symp-
toms from their employer, but also withdrawing from workplace socializa-
tion or relationships out of fear that their secret may be discovered.7 Kay
Redfield Jamison writes in her book “An Unquiet Mind” that even as a
mental health academic, she herself encountered stigma regarding her
bipolar disorder — one of her colleagues expressed disappointment with
her after discovering her history of illness and a suicide attempt.
Wahl’s16 work with patients demonstrated that, at some point, 72% had
not mentioned their illness on an application, 53% felt they had lost a job
by disclosing their illness, and only 33% felt that co-workers were at least
“often” understanding of their status as patients. Similar results have been
found in eastern cultures as well; more than 50% of surveyed patients in
China and Singapore also indicated that they concealed their diagnosis
from their co-workers.19
Some authors have questioned whether the level of industrialization of
a region influences psychiatric prognosis, especially in the case of schizo-
phrenia. The “industrialization hypothesis” posits that family support and
roles in manual labor in developing regions allow individuals to avoid the
intolerance, isolation, and marginalization faced by their counterparts in
the industrialized world.17 Taking India as an example, some studies have
demonstrated less stigma in rural areas than urban ones, but other studies
are mixed, or show the reverse.10
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892 T. Fisher
3.2.3. Treatment by the legal system

The “criminalization” of mental illness in the United States is a trend
identified by many researchers and authors over the last 40 years.7
Individuals identified as having mental illness are more likely to be
arrested and to spend longer periods incarcerated than others; they consti-
tute a disproportionate percentage of the incarcerated.7
There are many other ways in which the law affects citizens that can
also be avenues of stigma. Hinshaw9 points out that the right to vote, hold
office, marry, obtain child custody, and serve on a jury can all be consid-
ered social opportunities that are regulated to some degree by the law. As
of 2005, half of the states in the United States had legal restrictions affect-
ing at least one of those rights, specifically singling out those individuals
diagnosed as being mentally ill.
Some nations are targeting their legal systems to decrease stigma for
mentally ill persons. In 2008, the European Union launched its “European
Pact for Mental Health and Well-Being” that included explicit goals of
reducing stigma and considering patient rights in policy decisions. In
1990, the Caracas Declaration triggered a wave of mental health reforms
in Central and South America, including measures specifically aimed at
protecting the legal rights of persons with disabilities.
3.2.4. Marriage
Along with the structural stigma mentioned above, marriage and other
romantic relationships can uncover powerful stigma from individuals who
are asked to accept mental illness “into the family.” Many patients can tell
of the anxiety involved in considering whether and when to discuss a
diagnosis or symptoms with a potential partner. There may be concerns
about passing “defective” genes onto any children, or about future epi-
sodes of the illness being disruptive to the marriage or family. In cultures
where marriage has additional social status implications, a person with a
history of mental illness to be considered a “poor match.” This discrimina-
tion has been described in several Asian cultures,13 but is by no means
exclusive to them. When assessing stigma, one of the first questions asked
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by Littlewood et al.12 after presenting a vignette of a man with schizophre-

nia was “Would you be happy if he married your sister?”
3.3. Health care

3.3.1. General medical care
Stigma can present itself internally in mentally ill patients, in their
family members, and in the public at large. It is present in the health-
care system as well. Research has in fact shown that mental health
patients are likely to receive fewer insurance options and fewer medi-
cal services than individuals without this label.7 The consequences for
this may be not simply worsened health, but greater mortality as well.
In a study across eight US states, public mental health patients had a
mortality rate that was 1.2–4.9 times higher than expected.6 The major
causes of death were cardiac disease, cancer, and cerebrovascular dis-
ease — the same profile as the general population. Public mental health
patients often find themselves at a lower socioeconomic level as well,
which itself could cause a higher mortality rate. Research such as
Adewuya and Oguntade’s1 help confront this variable directly by meas-
uring physician’s attitudes rather than actions. In a survey of 312
Nigerian physicians, they were able to demonstrate prevalent beliefs in
supernatural causes for mental illness similar to those held by the cul-
ture at large.
3.3.2. Mental health care

Patients’ psychiatric care is no guaranteed haven from stigma either. There
have been several studies that demonstrate such “iatrogenic” stigma in
psychiatric care itself, which have shown that these attitudes are present
early in students entering training and are little changed by their training.15
Patients’ reports of stigma within the mental health system are some of the
most powerful evidence for its presence, and since the 1970s, organized
efforts have helped draw providers’ attention to ways in which their good
intentions can become paternalistic, coercive, dehumanizing, and
pessimistic.
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4. EXPLANATORY MODELS
Why does stigma exist? Is inflicting pain and marginalizing others simply
woven into our design, or is stigma a by-product of some otherwise adap-
tive or positive process? An understanding of the origins of the stigma
against the mentally ill may help in efforts to confront it.
Sociologists and psychologists have developed multiple theories to explain
the existence and “purpose” of stigma. At times, such models can seem very
esoteric or clinically irrelevant, but they share the common goal of trying to
better understand the phenomenon in order to change it. We will explore
several models here, though what follows is by no means an exhaustive list.
4.1. Classical conditioning

Classical conditioning is a hypothesis which highlights the role of affect,
or negative emotional responses, in the development of stigma. This
model assumes that stigma toward the mentally ill is developed by the
repeated pairing of an aversive stimulus with that group.7 This is classi-
cally conceived as occurring during childhood, but later life experiences
can be influential as well. Imagine a scenario in which a parent and child
are walking past an individual who is exhibiting signs of mental illness.
The parent frowns as they pass. The person is the conditioned stimulus;
the frown the unconditioned stimulus. The child’s feeling of discomfort
at seeing his parent frown is an unconditioned response. After multiple
similar events, the child will now associate their discomfort directly with
the mentally ill individual — it is now a conditioned response. Parents
and others can therefore “pass on” their stereotypes, prejudices, and
discrimination. Within this model, stigma can be thought of as “bad hab-
its” taught through a neutral technique, whether consciously or
unconsciously.
Charlene Zunkel, a development worker in Johannesburg, South Africa
illustrated this well when discussing her mental illness. Her family’s reac-
tion to the symptoms of her schizophrenia and to the side effects of her
medication, initially led her to adopt their prejudice that she could “pull
herself together” and it was “all in her head.” It took years before she was
able to break this belief and accept treatment.20
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4.2. “Just world” hypothesis

The “just world” hypothesis is an explanatory model which proposes that
an emotional need is met in individuals who stigmatize others, and that
this need provides the motivation to continue an otherwise negative prac-
tice. This theory proposes that in order to feel safe and secure, most peo-
ple assume that they have some measure of control over negative life
events affecting them. When we are hit by illness, accident, or seemingly
random destruction, we consciously or unconsciously blame the victims
for “getting themselves into trouble,” in order to avoid facing our own
vulnerability to such pain and suffering.7 “Just world” beliefs are often
present in religious and spiritual traditions, where mental illness may be
associated with family or personal sin, broken taboos, evil forces testing
or possessing an individual, or moral weakness.
4.3. Social identity theory

The social identity argues that the desire to maintain a positive social iden-
tity is the motivation behind stigma. Individuals are motivated to develop a
positive social identity, and this fosters a tendency to have less favorable
attitudes toward those out of our group than those in it.7 This creates stereo-
typed attitudes. This theory further goes on to posit that it is difficult for any
“out-group” member to challenge the stereotype because positive actions by
the “out-group” may be interpreted as transitory in nature, but as stable and
intrinsic in the “in-group.” The converse is also true; any negative behavior
is viewed as evidence supporting the individual’s “out-group” status.
4.4. Categorization
Categorization is a theory that characterizes prejudice and stereotypes as
extensions of the cognitive “schemas” that humans have developed to
organize our worlds. The physical world is complicated enough that we
need to “lump” objects and events into categories so that we can accu-
rately and quickly respond appropriately to our environment.9 These sche-
mas can be benign and even helpful, for instance, seeing someone behind
the counter of a store instantly brings to mind general assumptions about
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896 T. Fisher
how much he will know about the products within it, and preparation for
interacting with them in a certain way to make purchases. This nearly
automatic process helps reduces our mental “work load” by using past
experience to inform future behavior. In this view, prejudice and discrimi-
nation can develop either when individual differences are ignored in order
to “fit” someone into a pre-existing category, or when the category itself
is invalid.
4.5. Modified labeling theory

The modified labeling theory is a sociologic model which argues that
stigma develops due to interactions between individuals with mental
health symptoms and society.9 First, generally held stereotypes become
known to individuals who have been given the label of mental illness.
This knowledge leads them to believe they will be discriminated against,
and such individuals then withdraw or use secrecy to cope. This raises
their stress levels and decreases social support, perpetuating their symp-
toms which, when seen publicly, generate discriminatory actions from
society. The individual’s fears become a self-fulfilling prophecy. Past
iterations of this theory — now discredited — took the even stronger
stance that the label of “mental illness” caused patients to stay ill because
they saw battling against stigma as futile; this led society to feel that their
stereotype of mental illness was “proven.” The stereotype becomes more
entrenched, making it even harder to overcome in the future, and more
likely that future patients will give up, and a vicious cycle is created.
Link11 proposed a more modern modified labeling theory recognizing
some role for stigma in the perpetuation of symptom of mental illness
after demonstrating that when controlled for other variables, “patient
status” had twice as large of an effect on job and financial statuses as
actually symptoms did.
5. INTERVENTIONS
What can we do about stigma? As current or future doctors, is there a
special role for us in challenging and quashing stigma, or is it left to
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Stigma 897
patients and society to work it out among themselves? The latter choice
seems ridiculous, but in practice it is exactly how many psychiatrists have
approached the issue over the years. In the midst of a busy practice and
life, it is often very easy to want that time for other things, or fool our-
selves into thinking that we do “more good” by treating patients and leav-
ing everything else for someone else to do. Norman Sartorius,14 former
president of the World Psychiatric Association and anti-stigma advocate,
has posed the following broad categories.
5.1. Examination of our own attitudes

Efforts to increase our own tolerance and empathy, and those of our col-
leagues, constitute an easily accomplished first step in reducing stigma.
Negative and disparaging remarks may represent a defense against the
stresses and stigma faced by mental health service providers, but it is not
an adaptive or excusable one. It is also important to recognize how past
schools of thought and theory within psychiatry have contributed to
current misconceptions of mental illness. The theory that lunacy is caused
by the cycling of the moon, lobotomy, “treating away” homosexuality, and
even eugenics all had adherents within the world of psychiatry, and this is
not an exhaustive list.4 Byrne also points out stereotypes around certain
diagnoses may actually be quite prevalent in the field.
5.2. Be active advocates

Protest, education, and contact are the broad approaches used by existing
anti-stigma campaigns, and we can not only support our patients in these
endeavors but participate ourselves.7 We can aid in protests against media
and societal discrimination by providing expert commentary that chal-
lenges stereotype with fact. We can support efforts to connect patients with
the community, and facilitate it by helping ensure that patients have a “seat
at the table” within our hospitals and clinics. Even small steps, like efforts
to remove “crazy” and “nuts” from the everyday vocabulary, can have last-
ing benefit. Most importantly, there is no group of people better able than
physicians to advocate for a patient’s ability to access quality services.
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898 T. Fisher
5.3. Increased focus on patients quality of life

Current clinical and research focus is dominated by an attention on clini-
cal symptoms and their treatment, reducing many patients to “maniacs” or
“schizophrenics” — their diagnoses rather than their persons. Obtaining
true informed consent from patients for psychiatric treatment, setting
goals and treatment plans collaboratively, and not equating disagreement
with a particular contemplated treatment with non-compliance are all
ways to put greater emphasis on the person in front of us and not on the
pathology. Greater professional collaboration with providers of voca-
tional, education, and social rehabilitation will also help move our profes-
sion beyond offering a biopsychosocial assessment to offering actual
biopsychosocial treatment.
6. CONCLUSIONS
This introduction to the current study and understanding of stigma has
introduced the reader to the complexities underlying this pervasive phe-
nomenon. Though there may be debate about the exact definition of
stigma, or the etiological theory that best explains it, there is agreement
on the fact that stigma impedes our patients in multiple realms of their
lives. Seek out and remember your patients’ stories, and join your patients
as they work to gain from society the simplest of dignities — equality.
7. SELF-ASSESSMENT
7.1. The just world hypothesis argues that:
(A) Pairing of an aversive reaction with mental illness leads to fear of it.
(B) Being labeled as mentally ill leads patients to behave in ways that fit
society’s negative stereotypes.
(C) Fear of one’s own vulnerability leads to blaming the patient for part
or all of their difficulties.
(D) Stigma results when the mind groups an individual into a broad cat-
egory based on faulty information or ignoring evidence challenging
the fit.
Answer: C
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7.2. Which of the following is not a component

of the sociologic definition of stigma?
(A) Prejudice.
(B) Discrimination.
(C) Stereotype.
(D) Deviancy.
Answer: D
8. CASE STUDIES
8.1. Mr A
I remember going into the hospital the first time. I wasn’t ready for the
police to show up after I called the crisis line to tell someone about my
hallucinations. They put me in the back of a squad car and drove me to the
hospital. I was so scared when we finally got there that the first thing I did
was try to run. But they caught me right away.
I was roughly lifted up and tied down. It was terrifying, painful torture.
I didn’t know when it was going to stop. No one was talking to me, as if
they didn’t even see me, only the threat I represented to them. With the
straps came the shot. No one told me what it was, or asked me about it.
Instead they told me I was “getting medicine” as I felt my pants pulled
down and the needle pierce my skin.
Not only were the restraints biting into my limbs, but now fire was
coursing through my veins. In my paranoid mind, I was certain that I had
just been poisoned. No one was left in the room to comfort me as I cried,
only an unnamed staff member outside the door. The newspaper in her
hands never even twitched.
8.2. Ms B
I guess the trouble really started in the hospital. I had been attending the
university, and found out that I would no longer be welcome to return
because of my “mental disorder.” They thoughtfully sent all my belong-
ings to my family’s home. I thought about trying to stay in the city, but no
one seemed very interested in renting to me. Even if I didn’t tell them
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900 T. Fisher
where I was, they knew as soon as they returned my phone calls and a
nurse picked up. The staff kept “encouraging” me to return home, where
it would be less stressful, and my family could care for me.
At home it is as if I died instead of got sick. Mother goes to the market
alone, never asking if I want to come. One night at dinner I said one sentence
about possibly going back to school — one sentence! — and I thought my
brother would have a stroke. He spent a half-hour talking about how bad it
would be for him if my “next episode” was more public than this one. Part
of me thinks it was pointless to get better, if this is all there is.
8.3. Mrs C
My lawyer warned me, but I still felt violated. My husband’s lawyer
started talking about my hospitalization, and it all fell apart. I was “crazy,”
and therefore not fit to raise the children. His history of drugs didn’t mat-
ter, or all the hours he worked now. He had even been arrested once! I take
my medicine, I pray, and I’ve been doing great, but it didn’t matter.
I barely see them [the kids] now. I can’t take it. All I ever was [sic] was
a mother; what am I now?
8.4. Mr F
I told D about E this morning. She didn’t even know I had a brother. I
didn’t want to lie to her any longer, but I was so nervous about how she
was going to react. We’re pretty westernized now (and good thing too, or
I’d really never get matched up), but her family is still really traditional.
She seemed to take it pretty well, at least at first.
She just called me a minute ago, saying she couldn’t see me anymore.
I could still hear people talking about me, and speculating about E, in the
background. She had a bunch of other reasons, but I knew. It’s not my
fault! Why does he keep getting pulled into my life — we never had any-
thing to do with each other, even when he lived here! Why wasn’t he just
born dead instead of defective?
8.5. Mr G
I don’t think a single person remembered my name today. The other nuts,
I guess, but hey, we don’t count, right? The doc didn’t remember my name
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Stigma 901
and I overheard the nurses call me “the tall schizo.” Nice, huh? You can
confront them, but it doesn’t do any good: you are just “difficult,” couldn’t
possibly have a valid point.
And the social worker? Refuses to help me find my own place. She
figures that I couldn’t handle it, or something. Keeps pushing and pushing
me to let someone else take care of my money, like I should be a kid wait-
ing for an allowance. I got pissed, and let her know. Now “anger manage-
ment” is part of my treatment plan, and if I don’t “work on it” they cut my
OWPs (off ward privileges).
Oh, I almost forgot the best part — when the doc was talking to his med
students and not me, he drops that “these patients have very poor out-
comes.” How about focusing on THIS patient?
8.6. Mrs H
So this guy came into my store the other day, one of those crazy guys from
the hospital up the road, you know? He was dressed nice, didn’t act weird,
but he was staying out at The Inn — only nuts live there. He wanted to
apply for the assistant manager’s job. I wanted to say “no way,” but I had
to take his application just like anybody else. The last time we hired some-
one like that they kept showing up late, missing shifts, could not follow
directions, violated the dress code; probably the worst employee I ever
had. I never hired another one after that experience.
But I am not the only one. When I first moved the shop here all the
other businesses told me their horror stories; it was good to learn from
them, not have to make the same mistakes. Sure enough, over the next
week he got all pushy, calling a couple of times “inquiring about the job;”
made me glad we got someone else.
REFERENCES
1. Adewuya A, Oguntade A. (2007) Doctors’ attitude towards people with men-
tal illness in Western Nigeria. Soc Psychiatry Psychiatr Epidemiol 42(11):
931–936.
2. American Psychiatric Association. (2001) Nurse battles to erase Korea’s
entrenched stigma problem. Psychiatric News 36(17): 11–32.
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3. Ashcraft L, Anthony W. (2008) Eliminating seclusion and restraint in

recovery-oriented crisis services. Psychiatr Serv 59(10): 1198–1202.
4. Byrne P. (2000) Stigma of mental illness and ways of diminishing it. Adv
Psychiatr Treatment 6: 65–72.
5. Byrne P. (2001) Psychiatric stigma. Br J Psychiatry 178: 281–284.
6. Colton CW, Manderscheid RW. (2006) Congruencies in increased mortality
rates, years of potential life lost, and causes of death among public mental
health patients in eight states. Prev Chronic Dis 3(2): 1–14.
7. Corrigan P. (2005) On the Stigma of Mental Illness: Practical Strategies for
Research and Social Change, American Psychological Association,
Washington, DC.
8. Goffman E. (1963) Stigma: Notes on the Management of Spoiled Identity,
Prentice Hall Inc., NY.
9. Hinshaw S. (2007) The Mark of Shame: Stigma of Mental Illness and An
Agenda for Social Change Oxford University Press, USA.
10. Jadhav S, Littlewood R, Ryder AG, Chakraborty A, Jain S, Barua M. (2007)
Stigmatization of severe mental illness in India: Against the simple industri-
alization hypothesis. Indian J Psychiatry 49: 189–194.
11. Link BG. (1982) Mental patient status, work, and income: Ann examination
of the effects of a psychiatric label. Am Sociol Rev 47: 202–215.
12. Littlewood R, Jadhav S, Ryder A. (2007) A cross-national study of the stig-
matization of severe psychiatric illness: Historical review, methodological
considerations, and development of the questionnaire. Transcult Psychiatry
44: 171–202.
13. Ng CH. (1997) The stigma of mental illness in Asian cultures. Aust NZ J
14. Sartorius N. (1998) Stigma: What can psychiatrists do about it? Lancet 352:
1058–1059.
15. Tsao CIP, Tummala A, Roberts LW. (2008) Stigma in mental health care.
Acad Psychiatry 32(2): 70–71.
16. Wahl O. (1999) Mental health consumers experience of stigma. Schizophrenia
Bull 25(3): 467–478.
17. Warner R. (1994) Recovery from Schizophrenia: Psychiatry and Political
Economy. Routledge, New York.
18. World Health Organization. (2010) World Health Organization (WHO)
Regional Office for the Eastern Mediterranean (EMRO) website. Available
at: http://www.emro.who.int/mnh/cfi_about.htm. Accessed on 3 April 2010.
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19. Yang LH. (2007) Application of mental illness stigma theory to Chinese
societies: Synthesis and new directions. Singapore Med J 48(11): 977–985.
20. Yeni A. (2010). All Africa Global Media Website. Available at: http://
allafrica.com/stories/201007130428.html. Accessed on 8 May 2010.
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Chapter 36
Legal Aspects of Psychiatry
Joseph B. Layde
1. INTRODUCTION
The relationship between psychiatry and the law varies tremendously
from country to country and even from jurisdiction to jurisdiction in
federal systems like the United States, Canada, and India. Additionally,
nations or parts of nations have judicial systems with varying histories —
systems based on English common law, Roman civil law, and Islamic
Sharia being a few noteworthy examples (Table 1). Different legal systems
handle the practice of psychiatry and the application of psychiatric opin-
ion to legal issues in various ways, but certain core areas of interaction of
psychiatry and the law are universally important, although the details
of that interaction may be very different in different jurisdictions. This
chapter examines several of those core areas of interaction and briefly
discusses some of the variation found in the relationship of psychiatry and
law around the world.
2. LEGAL REGULATION OF PSYCHIATRIC PRACTICE

Medical practice in general is subject to legal regulation in all countries
and in all jurisdictions. Before anyone can obtain a license to practice
medicine, he or she needs to obtain a degree from a medical school and
complete a prescribed program of general medical clinical training, which
904
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Legal Aspects of Psychiatry 905
Table 1. Representative nations using major systems of law.

Common law system
Australia
Canada (except Quebec)
Ghana
India
Ireland
Nigeria (Southern states)
South Africa
United States
United Kingdom
Roman–Germanic law system
Argentina
Austria
Brazil
Canada (Quebec) — hybrid system
Colombia
France
Germany
Italy
Mexico
Portugal
Spain
Sweden
Islamic law system
Algeria
Iran
Nigeria (Northern states — hybrid system)
Saudi Arabia
United Arab Emirates
Yemen
(Adapted from Abdalla-Filho and Bertolote1).
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906 J. B. Layde
varies substantially from country to country. Before a doctor can practice

the medical specialty of psychiatry, he or she needs to complete a program
of training in the treatment of people with mental illness. A practicing
psychiatrist is subject to rules promulgated by legislatures and administra-
tive bodies in his or her jurisdiction that define the scope of psychiatric
practice and the nature of the health care system in which the psychiatrist
operates.
Health care systems vary widely from country to country in their meth-
ods of allocating resources to psychiatric clinics and to inpatient hospitals
and in their mechanisms of reimbursement for physicians. The practice of
psychiatry is additionally subject to regulation of the use of therapies,
including psychotherapy, medication, and electroconvulsive therapy
(ECT), as well as regulation of the means of providing involuntary treat-
ment in the care of severely mentally ill patients.
European Union (EU) nations and other European countries are cur-
rently attempting to find some common ground in the regulation of psy-
chiatric practice, which has varied widely in Europe in the past. ECT, for
example, has previously been very frequently used in the United Kingdom
as a treatment for depression, while its use in other European countries,
such as Germany and the Netherlands, has been much more circumscribed
and subject to severe restrictions.5 In the 1990s, 36 nations in the World
Health Organization’s European Region signed the “Declaration on the
Promotion of Patients’ Rights in Europe,” attempting to find a common
European ground for regulation of the doctor–patient relationship in medi-
cine, including psychiatry.
In some jurisdictions, governments share responsibility for regulating
psychiatric practice with non-governmental entities. In the United States,
licensure of physicians is handled by the governments of the individual
states, while certification of the professional qualifications of medical
specialists is conducted by the private American Board of Medical
Specialties (ABMS). One of the constituent boards of ABMS, the
American Board of Psychiatry and Neurology (ABPN), certifies the com-
petence of US psychiatrists.
Given the wide variety among systems of legal regulation of psychiatric
practice, it is important that clinicians make themselves familiar with the
rules in place in the jurisdiction in which they plan to practice.
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3. APPLICATION OF PSYCHIATRY TO CRIMINAL LAW

Psychiatry plays a role in the handling of mentally ill individuals who
violate the criminal law codes of every country, but the specifics of the
relationship of psychiatry to systems of criminal law vary tremendously.
In countries following the common law tradition originated in Great
Britain, including the United States and most Commonwealth nations,
expert psychiatric testimony is often required in criminal cases in which
there is a question of a defendant’s competency to stand trial for an
offense on the basis of mental illness or defect.
Criminal responsibility is also an area in which psychiatric testimony is
permitted in most common law jurisdictions, although four states in the
United States have abolished the insanity defense. The legal tests for insan-
ity vary considerably among common law jurisdictions, with many relying
on the cognitive test enunciated in the M’Naughten test formulated by the
British House of Lords in 1843. The M’Naughten test excuses a defendant
from criminal responsibility for his actions if, on the basis of his mental
condition, he either did not know the nature and quality of his actions or did
not know the actions were wrong. Some other common law jurisdictions
utilize a legal test for insanity that considers both cognitive and volitional
issues, considering whether or not a defendant could control his actions.
In Brazil, a representative example of a country which follows the legal
tradition based originally on the system of the Roman Empire, by way of
contrast with common law jurisdictions, defendants in criminal proceed-
ings are relatively passive in the context of their trials, with their lawyers
taking the active role in their defense. Accordingly, the issue of compe-
tency to stand trial is not as important in Brazil as in common law
jurisdictions.1
Forensic psychiatrists in Brazil, like those in most common law juris-
dictions, may be called upon to address the issue of whether or not a crimi-
nal defendant meets the criteria for unaccountability, or lack of criminal
responsibility, for his actions. The legal standard for unaccountability of
defendants in Brazil includes both cognitive and volitional elements.
Before becoming involved as a consultant or an evaluator in criminal
legal proceedings, a psychiatrist should become familiar with the role of
mental health experts in criminal law in his or her jurisdiction and should
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908 J. B. Layde
learn the legal standard that possible testimony in a criminal case would
address.
4. APPLICATION OF PSYCHIATRY TO CIVIL LAW

Psychiatrists may be involved in many different sorts of legal disputes that
are not criminal in nature. Psychiatrists may be asked to evaluate their
patients’ disabilities and eligibility for compensation from the state or
from private disability insurers; they may be asked to testify regarding the
psychological aspects of injuries individuals received in a motor vehicle
collision, or they may be involved in lawsuits contesting the transfer of
property by an individual with dementia. There is tremendous variability
around the globe in the way these issues are handled in different legal
systems, but certain principles of proper psychiatric practice in dealing
with these legal concerns are universal.
Psychiatrists involved in the evaluation of patients in civil proceedings
should attempt to simultaneously uphold both the best interests of their
patients and the truth. Psychiatric disability evaluations should be con-
ducted in a way that truthfully explains patients’ psychiatric conditions
and neither understates nor exaggerates the degree of patients’ impairment
in social and occupational realms. Psychiatric evaluations of individuals
who are involved in litigation involving, for instance, alleged posttrau-
matic stress disorder following an automobile collision should be simi-
larly dispassionate.
“Independent medical evaluations” may be conducted by psychiatrists
as part of legal proceedings in some jurisdictions. Such evaluations are
performed not by treating psychiatrists but, rather, by psychiatrists who
may be retained by lawyers for the specific purpose of the evaluations. It
is imperative that a psychiatrist conducting an evaluation for such a pur-
pose explain to the evaluee the nature of the examination and the fact that
the psychiatrist is acting not as the evaluee’s agent but, rather, as an agent
of a lawyer whose interests may be very much contrary to those of the
person undergoing the examination. Such evaluations should be con-
ducted fairly, with the greatest possible degree of medical impartiality;
hiring attorneys must sometimes be given news as a result of such an
evaluation which they would rather not hear.
B1405_Ch-36.indd 908 1/31/2013 2:44:25 PM

Psychiatrists who are asked to be involved in civil litigation must famil-

iarize themselves with the relevant legal standards. In the case of a lawsuit
filed by a young woman alleging that her uncle suffers from dementia and
is being unduly influenced to transfer a large home to a young lover, for
instance, a psychiatrist retained to evaluate the uncle must become famil-
iar with the relevant jurisdiction’s requirements for validly transferring
property.
Psychiatrists who are asked to testify as expert witnesses in civil cases
or in criminal cases should consider the ethical ramifications of acting in
that role. The American Academy of Psychiatry and the Law (AAPL), the
US professional organization of forensic psychiatrists (psychiatrists who
apply their training to legal issues), has promulgated guidelines for ethical
behavior for expert psychiatric witnesses.2 The guidelines highlight the
importance of honesty and objectivity on the part of the psychiatrist acting
as an expert witness. They also emphasize the importance of basing clini-
cal opinions in legal cases on clinical examinations whenever possible. In
some circumstances, as, for instance, when a psychiatrist is asked to give
an opinion on the basis of a medical record review about whether a
deceased person was capable of rationally issuing a will during a final ill-
ness, the psychiatrist should make it clear that his or her opinion is based
on a review of records, because personal examination of the deceased is
impossible.
5. PSYCHIATRIC MALPRACTICE
As is the case in all fields of medicine, legal recourse is available to
patients who are injured by psychiatrists practicing substandard care. In
some societies, medical (including psychiatric) malpractice suits are quite
rare, while in others (such as the United States), they occur frequently.
Patients who have had a bad outcome due to the improper diagnosis
and treatment of their psychiatric disorder may sue because they received
the wrong medication; family members of a patient who committed sui-
cide while a psychiatric inpatient may sue the hospital and the patient’s
psychiatrist for failing to keep the patient safe. Forensic psychiatrists
may be involved in evaluating whether or not the psychiatrist’s practice
has met the appropriate standard of medical care. Malpractice insurance
B1405_Ch-36.indd 909 1/31/2013 2:44:25 PM

910 J. B. Layde
is a significant professional expense for psychiatrists practicing in some

jurisdictions, including many US states.
Various factors influence the likelihood of a psychiatrist being sued.
Even in countries like the United States, where medical malpractice suits
are common when patients or their families are dissatisfied with their care,
physicians who have a good personal relationship with their patients are less
likely to be sued. Psychiatrists practicing in countries where adverse patient
outcomes more rarely lead to malpractice suits are, of course, less likely to
be sued. However, even in societies such as Japan, where patient trust of
physicians has historically been high and where rates of malpractice suits
have been low, trust in physicians is eroding, and the frequency of malprac-
tice suits is rising; Japan instituted specialized medical courts in 2001 to
handle the increasing number of malpractice cases there.4 As it becomes
more difficult for physicians to maintain close relationships with their
patients in an increasingly fragmented world, other societies may see a rise
in legal suits for medical malpractice, including psychiatric malpractice.
6. PSYCHIATRY AS AGENCY OF SOCIAL CONTROL

Historically, psychiatry has sometimes been inappropriately used to pro-
mote governmental control over society. Physicians, including psychia-
trists, have been involved in torture. In the former Soviet Union, political
dissidents were involuntarily hospitalized in psychiatric institutions and
treated for non-illnesses such as so-called “sluggish schizophrenia.”8 In
recent decades, psychiatrists have been reported to have been involved in
inappropriate interrogation techniques in places as far-flung as apartheid-
era South Africa, Northern Ireland, and Guantanamo Bay.
Psychiatric involvement in torture is always unethical. The World
Medical Association made that clear in 1975 when it adopted the Tokyo
Declaration (Table 2). The United Nations reaffirmed it in 1982 when it
adopted the Principles of Medical Ethics. Psychiatric participation in
involuntary treatment that is not for the benefit of the patient but, rather,
for the perpetuation of a system of government is also unethical. The
World Psychiatric Association (WPA) promulgated the Declaration of
Hawaii in 1977 (reaffirmed and amended in 1963) to make it clear that
psychiatrists’ primary ethical duties are to their patients.6
B1405_Ch-36.indd 910 1/31/2013 2:44:25 PM

Table 2. Major international declarations on misuse of medicine and psychiatry.

1975 Tokyo Declaration of World Medical Forbids physician participation in
Association torture
1977 Declaration of Hawaii of World States psychiatrists’ primary duties are
Psychiatric Association to patients
1981 Islamic Code of Medical Ethics States health is a basic human necessity
1982 Principles of Medical Ethics of Reiterates prohibition on physician
United Nations participation in torture
1983 Declaration of Hawaii of World States mentally ill persons shall be
Psychiatric Association (revised) protected from abuse and
exploitation
1996 Declaration of Madrid of World Forbids psychiatrists’ participation
Psychiatric Association in execution
1999 Enhancement of Declaration of Madrid States psychiatrists’ discrimination on
of World Psychiatric Association in ethnic or cultural grounds is
Hamburg unethical
2002 Enhancement of Declaration of Madrid Addresses psychiatrists’ interactions
of World Psychiatric Association in with pharmaceutical industry
Yokahama
2005 Enhancement of Declaration of Madrid Addresses dual agency situations for
of World Psychiatric Association in Cairo psychiatrists
(Adapted with additions from Vesti and Lavik16).
The ultimate means of social control is the execution of individuals by

the state. Psychiatrists may not ethically be directly involved in execu-
tions. Many would go further and forbid psychiatric involvement in the
legal evaluation of individuals whose competence to be executed is ques-
tioned. At the World Psychiatric Association Congress in Madrid in
August 1996, the General Assembly unanimously passed the Declaration
of Madrid, which included the statement “Under no circumstances should
psychiatrists participate in legally authorized executions nor participate in
assessments of competency to be executed.”7 Because governmental inter-
ests will continue at times to be adverse to personal liberty, psychiatrists
around the globe must remain vigilant against the misuse of their profes-
sion for political purposes.
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912 J. B. Layde
7. KEY POINTS
• Differing legal systems around the world handle the regulation of
psychiatric practice substantially differently.
• Psychiatrists must be familiar with the laws in their own jurisdictions
regarding psychiatric practice.
• Psychiatric testimony is used in many jurisdictions in handling issues
in criminal law, including criminal responsibility.
• Psychiatric evaluations may be important in dealing with issues in
civil law, including questions of psychological injuries.
• The subject of a psychiatric legal evaluation must be informed of the
purpose of the evaluation.
• Psychiatric involvement in torture is always unethical.
8. SELF-ASSESSMENT
8.1. A psychiatrist is asked by a patient, a 28-year-old man
who suffers from dysthymia, to fill out a form requesting
medical disability insurance payments for his illness.
The patient says, “You can exaggerate my symptoms
a little bit, just for my sake.” Which of the following
is the most appropriate response by the psychiatrist?
(A) “I cannot say anything useful about your clinical condition.”
(B) “We will just make sure the disability insurance company gives you
some money.”
(C) “I can tell them how you are doing — no more and no less.”
(D) “You deserve whatever you can get.”
(E) “Your clinical condition is not the business of the insurance
company.”
Answer: C3
8.2. Which of the following is most accurate in describing

the role of psychiatrists in torture?
(A) Psychiatric participation in torture is ethically permissible as part of
the interrogation of suspected terrorists if it is likely to save lives.
(B) Psychiatric participation in torture is always unethical.
B1405_Ch-36.indd 912 1/31/2013 2:44:25 PM

(C) The ethical permissibility of psychiatric participation in torture

depends on whether a torture subject has been convicted of a crime.
(D) Psychiatric participation in torture is ethically permissible if it is
limited to monitoring the degree of lasting ill effects on the torture
subject.
(E) Psychiatric participation in torture is ethically permissible only in the
case of “soft” torture techniques such as waterboarding.
Answer: B6
9. CASE STUDY
A psychiatrist practicing in California is contacted by a defense attorney
with the request that she examine a 25-year-old man who suffered third-
degree burns on his leg in a collision between the motorcycle he was rid-
ing and a truck. The young man complains of nightmares and flashbacks
related to the crash and is suing for damages related to both the burn injury
and psychological injuries. The defense attorney represents the driver of
the truck, who was at fault in the collision.
The psychiatrist agrees to see the injured man in her office for an “inde-
pendent medical evaluation.” She explains to the injured man that she is
not his treating psychiatrist but, rather, has been retained by the truck
driver’s lawyer to conduct the examination. The young man says that
he understands the circumstances of the evaluation and is willing to
continue.
In the course of examining the injured young man, the psychiatrist
finds that he in fact suffers from moderately severe posttraumatic stress
disorder as a result of the collision. She informs the lawyer who hired her
of her opinion. Although the defense lawyer is unhappy with the psychia-
trist’s findings, she clearly explains to him the medical reasons for her
conclusions. He recognizes that the validity of the injured man’s claim
would be evident if the case were to go forward to trial. Partly on the basis
of the psychiatrist’s evaluation, the defense attorney recommends to the
truck driver that he offer a generous settlement to the motorcycle rider for
both his burn injuries and for his resultant psychological injuries.
B1405_Ch-36.indd 913 1/31/2013 2:44:25 PM

914 J. B. Layde
REFERENCES
1. Abdalla-Filho E, Bertolote JM. (2006) Forensic psychiatric systems of the
world. Rev Bras Psiquiatr 28(Supl II): S56–S61.
2. AAPL — American Academy of Psychiatry and the Law. (2005) Ethics
Guidelines for the Practice of Forensic Psychiatry, adopted May 2005.
Available at: http://www.aapl.org/ethics.htm. Accessed on 6 November 2010.
3. Appelbaum PS. (1997) A theory of ethics for forensic psychiatry. J Am Acad
Psychiatry Law 25(3): 233–247.
4. Feldman EA. (2009) Why patients sue: The Japanese experience. J Law Med
Ethics 37(4): 792–799.
5. Neeleman J, Van Os J. (1996) Ethical issues in European psychiatry. Eur
6. Vesti P, Lavik NJ. (1991) Torture and the medical profession: A review.
J Med Ethics 17: 4–8.
7. WPA — World Psychiatric Association. (1996) Madrid Declaration on Ethical
Standards for Psychiatric Practice, Approved 25 August 1996. Available at:
http://www.wpanet.org/detail.php?section_id=5&content_id=48.
Accessed on 6 November 2010.
8. Young-Anawaty A. (1977) International human rights norms and Soviet
abuse of psychiatry. Case West Reserve J Int Law 10(3): 785–816.
B1405_Ch-36.indd 914 1/31/2013 2:44:25 PM

Index
Abnormal Involuntary Movement depression of Alzheimer’s

Scale (AIMS) 504 disease 304
abuse 488, 491, 494, 495, 514 psychosis of Alzheimer’s disease
academic achievement 105, 109, 129 303
access to means 701, 706 American Academy of Psychiatry
acculturation 796, 804, 806, 817 and the Law (AAPL) 909
ACGME 651–653, 658, 664 American Board of Psychiatry and
activities of daily living 502, 506 Neurology (ABPN) 651, 664, 665,
acupuncture 824, 827–830 906
admissions 642–644 amnesia 338–340, 342, 344
adolescents 137–144, 146, 147, 157, amyloid precursor protein gene 63
170–173, 179, 384–386, 388, 390, anorexia nervosa 379, 381, 382,
392, 401, 402 384–387
adoption studies 59, 61 anti-craving medications 273, 286
aggression 575, 576, 799, 809, 810 antidepressant medications 211,
agitation 525, 527–530, 536, 539, 218, 220
540, 546, 550, 575, 576, 598, 599, antipsychotic 185, 189, 192, 193,
600, 601 197–200
agoraphobia 227–230, 235, 238, 244 antiretroviral therapy 724, 725, 738,
AIDS 723–729, 732–740, 742–744 741, 742
alcohol antisocial personality disorder 465,
alcohol withdrawal 271–273, 471
287 anxiety 367, 368, 371, 372, 524,
alexithymia 318 527, 531, 533, 534, 537, 541–543,
alters 346–349 545–548, 551, 573, 576–580, 586,
Alzheimer’s disease 295–300, 303, 587, 599, 602
304, 307, 310–312, 314, 315 anxiety disorder 845, 846
915
B1405_Index.indd 915 1/31/2013 2:29:10 PM

916 Index
anxiety in children 143 boundaries 556, 566, 778–780

asking questions 79 brain-derived neurotrophic
Assertive Community Treatment factor gene 70
(ACT) 195, 851 bulimia nervosa 379, 380, 382, 386,
association studies 62 390–395, 401, 403, 404
astasia-abasia 329 burden of disease 1–4
ATLAS project 620, 621, 626, 631
attachment disorders 142, 149–152 CanMeds 619
attention 102, 108, 122, 125, 133, cannabis 274–276, 280, 283, 287
134 capacity 492, 494, 593, 594
atypical antipsychotics 217, 218 caregivers 306, 311, 312, 315
autism 144, 146, 153, 155, 178 catechol-O-methyltransferase enzyme
autonomy 770–772, 774–776, 780, gene (COMT) 751, 756, 760
790 categorization explanatory model in
avoidant personality disorder 472 stigma 895
avolition 187 child soldier 879
Ayurvedic 826 childhood 379, 399–401
childhood bipolar disorder 141
bariatric surgery 396 children 137–144, 146–152,
BASK 339–341, 343, 344, 347 155–158, 160, 163–170, 172–178
behavioral science teaching 614, Chinese Classification of Mental
615 Disorders 813
behavioral family therapy 391, 403 chronotherapy 366, 377
behavioral weight loss 394 circadian 352, 353, 355, 360,
beneficence 770–774, 780, 786–788, 364–366, 377
791 civil law 904, 908, 912
benzodiazepines 228, 231, 232, 235, clarification 80
236, 242, 254, 255, 360, 367, 374, 376 classical conditioning explanatory
bereavement 209, 223, 691 model in stigma 894
beta-amyloid plaques 298 Classical Test Theory
binge eating disorder 381, 382, 386, clinical assessment 629
392–395, 397, 401, 405 closed and open question 86
bipolar disorder 204, 205, 214–220, clozapine 192, 193, 198, 201
222, 223 cocaine 264, 267, 276, 278–280,
body dysmorphic disorder 318, 325, 285–288
326, 334 cognition 675
borderline personality disorder 461, cognitive 186, 192, 194, 196, 512,
464–467, 471–475 514, 517, 520
B1405_Index.indd 916 2/1/2013 9:16:41 AM

Index 917
cognitive behavior therapy (CBT) cross-cultural testing 113, 114

210, 228, 237, 386, 390, 393, 403 Cuban Glossary of Psychiatry 813
cognitive disorders 726, 729, 735 cultural competence 796
cognitive domains 291, 315 cultural differences 87
cognitive dysfunction 847, 858 cultural formulation 49, 812–814
cohort 669, 676, 677, 679 cultural psychiatry 19, 20, 795, 816
collateral information 32, 33, 52, 54, cultural themes 774
532, 539, 549, 550 cultural values 794, 810
collectivist societies 804 culturally competent management
common law 904, 905, 907 plan 815
communication skills training 615 culturally familiar metaphors
comorbid disorders 239, 247, 249, 253 794, 803
comorbidities 337, 345, 346, 347 culture 557
competency 112, 115, 128, 489, culture-bound syndromes 532, 799
492–494, 597 culture shock and conflict 806
conduct disorder 138, 141–143, Curanderas 830
160–162, 169 curriculum 642, 643, 645, 651, 653,
confidentiality 556, 777, 780, 781, 657, 659, 660
785, 788–790 cyclothymia 204, 219, 220, 222
confrontation 80, 81 CYP2C19 750
construct validity 105 CYP2D6 749
consultation 555, 559, 572, 574, 575, cytochrome P450 749
587, 593, 598, 601 cytochrome P450 1A2 gene
consultation-liaison psychiatry 445, (CYP1A2) 751, 756
572 cytochrome P450 2B6 750
containment psychotherapeutic cytochrome P450 2C19 gene
technique 80, 81 (CYP2C19) 756
content validity 105 cytochrome P450 2C9 gene
continuous professional development (CYP2C9) 750
(CPD) 633 cytochrome P450 2D6 749
convergent functional genomic cytochrome P450 2D6 gene
analysis 70 (CYP2D6) 755
conversion disorder 318, 327–329, cytochrome P450 3A4 gene
333 (CYP3A4) 756
copy number variation 62 cytomegalovirus 680
core competencies 618, 662, 663
core curriculum 609–611 death 478, 481, 484–486, 488, 490,
criminal justice system 848 495, 500, 516, 517, 520
criminal law 907, 912 decisional capacity 782–784
B1405_Index.indd 917 2/6/2013 11:07:44 AM

918 Index
Declaration of Hawaii 770, 910, 911 differential diagnosis 554, 556, 563
Declaration of Madrid 770 diffusion tensor imaging (DTI) 670
deep brain stimulation 212, 221, 224 disability-adjusted life year (DALY)
deinstitutionalization 846, 849, 850, 3
855, 857, 858 discrimination 727, 728, 798,
delirium 291–295, 303–306, 804–806, 887, 888, 891, 892, 894,
312–314, 573, 575, 589, 591, 593, 896, 897, 899
594, 598, 601, 732, 733, 735, 738, disease 28, 29, 31, 34, 35, 39–41, 45,
739, 740, 742 50, 51, 52
delusions 186–188, 196, 811, 812 disrupted in schizophrenia 67, 70
dementia 291, 292, 295–300, dissociation 337, 338, 342, 345–348
303–307, 310, 311–315, 488, 491, dissociative amnesia 328
493, 499, 506, 508, 514, 515, 517, dissociative disorder 328, 329, 337,
729, 732, 733, 738, 739 339–341, 343, 345, 347
dementia with Lewy bodies (DLB) dissociative fugue 328
311 dissociative identity disorder 337,
demoralization 735 340, 343
dependence 260, 261, 264, 265, dissociative stupor 328
267–271, 273–276, 279, 280, 282, disturbed shen (神) with phlegm 829
283, 286, 287 dopamine 185, 186, 192
dependent personality disorder 468, dopamine 2 receptor gene (DRD2)
470 758
depersonalization 338–340 dopamine 3 receptor gene (DRD3)
depression 488, 490–492, 495–497, 759
505, 576, 580, 581–583, 585, 588, dopamine 4 receptor gene (DRD4)
594, 596, 598, 599, 601, 602, 726, 759
732, 733, 735, 738, 741–743 dopamine transporter gene (SLC6A3)
Determinants of the Outcome 761
of Severe Mental Disorders driving 484, 488, 489, 502, 506
(DOSMeD) 797 dual roles 784, 785
Diagnostic and Statistical Manual of dyspareunia 414, 421, 423, 428
Mental Disorders (DSM) 31, 42 dyssomnia 355, 357, 358, 366
diagnostic classification 10, 11 dysthymia 204, 219, 220, 222
diagnostic criteria 28, 38, 48, 50, 51
diagnostic reliability 38, 52 early childhood trauma 725, 734,
diagnostic validity 38, 39, 52 738, 743
dialectical behavior therapy 393, 403 early-career psychiatrists 633
didactics 657–659, 661, 664 early-onset schizophrenia 173
B1405_Index.indd 918 2/1/2013 9:16:41 AM

Index 919
eating disorders 142, 143, 170, 172, factitious disorder by proxy 331
177 family 492, 494, 496, 497, 499,
ECFMG 644, 645 500
education 12–16, 80, 96, 642, 644, fellowships 642, 657, 665, 666
645, 650–652, 657, 658, 661, 666 female sexual arousal disorder 414,
Eight Ds 209 421, 424
elder abuse 494, 495 fidelity 772–774, 790
electrocardiography 353 fight 338, 341–343
electroconvulsive therapy (ECT) formulation 554, 556, 563, 564, 568
212, 906 frontotemporal degeneration (FTD)
electroencephalography 353 310
electromyography 353 fugue 339, 340, 341, 344
electrooculography 353 fusion 347, 350
elimination disorders: enuresis and
encopresis 168 Ganser’s Syndrome 331
emic and etic 796, 799 gender identity disorder 410–413,
empathic validation 80 415, 416, 435, 436, 437, 439
employment 890, 891 gene variations 746
endophenotypes 60 gene–environment interaction (GxE)
epistasis 753 680
ERAS 644–647 generalized anxiety disorder (GAD)
erectile disorder 421 252
error 104, 106, 107, 118 genetic determinants of Alzheimer’s
Erwadi 889 disease 299
ethical skills 776, 777, 778 genetics 59
ethics 18, 19, 555, 568, 768–770, genocide 865, 872, 875, 877, 878,
772–774, 776–778, 781, 785, 787, 881, 883
788, 789 genome wide association studies 59,
ethnic minorities 805, 808, 811 62
ethnicity global assessment of functioning
ethnocultural group 800, 803, (GAF) rating scale 47
808, 816 glutamatergic 192
evaluation of sexual functioning 416
execution 911 Haemophilus influenzae 680
explanatory model of illness 807, 815 hallucinations 186–188
expressed emotion 798, 818 haplotype 751
harm reduction 734, 853, 854, 856,
factitious disorder 317, 322, 326, 327, 858, 859
329, 330, 331, 333, 586–589, 599 heritability 60
B1405_Index.indd 919 2/6/2013 11:07:44 AM

920 Index
histrionic personality disorder 470 intensive case management 851,

HIV 723–729, 732–735, 737–739 852, 855
HIV-associated neurocognitive intermediate phenotypes 60
disorder (HAND) 729, 732, 739, internally displaced person 866
741 International Classification of
homeless 841–844 Diseases (ICD) 40
homeostatic 352, 353 ICD-10 695, 701
homicidal ideation 535, 537, 546, International Pilot Study of
551 Schizophrenia (IPSS) 797
hospice 488, 496 international psychiatric
hospitalization 388, 389, 404 organizations 14, 15, 21, 22
housing 485–487, 890 interpersonal psychotherapy (IPT)
Housing First 853, 854 210, 224, 387, 390, 391, 393, 403
human rights abuses 865, 871 interpretation 80, 81
human sexuality 409, 410, 412, 417 interpreter 87, 88
hypersomnia 355–357, 360, 361, interview 78, 79, 81, 85, 554,
366, 371–375 556–558, 563, 569, 647–649
hypnosis 340, 341 involuntary commitment 195, 857
hypoactive delirium 293 Islamic law 905
hypoactive sexual desire disorder
416, 421, 422, 439, 440 just world hypothesis 895
hypochondriacal disorder 317, justice 770, 772, 787
323–325, 333
la belle indifference 328
identity 796, 803, 804, 806, 814 laboratory studies 507, 521
illicit substances 286 laboratory testing 34, 35, 52, 53
imagery 346, 347, 349 language 795, 801, 804–806, 812,
incarcerated 892 814, 816, 817
indel 62 language disorders 123
independent medical evaluations later life 478, 481–484, 490, 500,
908 501, 514–518
informed consent 556, 782–784, Latin American Guide for Psychiatric
786–788 Diagnosis 815
inhalants 280, 281 legal issues 904, 909
insight 190 liaison 572, 573, 594
insomnia 355–360, 363, 365–367, life change 448, 456
371–376 life events 804, 811, 817
Intelligence Quotient (IQ) 103, life-long learning 631, 633, 634, 638
118 linkage analysis 61
B1405_Index.indd 920 2/6/2013 11:07:44 AM

Index 921
major depressive disorder neurexin 69

(MDD) 204, 207, 222, 444 neurobiological basis 228
major disasters 20, 21, 22 neurofibrillary tangles 298
malingering 317, 320, 322, 326, 327, neuro-imaging 35, 36, 52, 53, 55
331–333, 586, 587, 589, 599 neuropsychology 116, 117, 121, 124
malpractice 909, 910 nicotine 264–267, 274
mania 205, 214–221, 538–541, 546 non-maleficence 770, 771, 774, 785,
Mary Reynolds 340 787, 788, 791
match 644, 649, 650 nonsense mutation 62
matrics 669, 675 non-suicidal self-injury 171
medical causes 581, 596 non-verbal communication 794, 802
medical complications 385, 386, 390 norepinephrine transporter gene
medical conditions 216, 220 (SLC6A2) 751, 757, 760
medically unexplained physical normative groups 107–109, 116
symptoms (MUPS) 317 NREM 353, 354, 360, 367–369,
medication 554, 559, 561–570 371–376
medication use 498 NRMP 649, 650
memory 483, 491, 492, 510, 517 nursing home 480, 486–488
memory loss 122, 123, 130, 131, 133
mental retardation 103, 120, 121, 127 Obeah 831, 836, 837
mental status examination 94, 554, obesity 381, 393, 395–398
558, 563 objective structured clinical
migration 798, 804, 805 examination (OSCE) 630
mild cognitive impairment objective structured long examination
(MCI) 296 record (OSLER) 630
military personnel 444, 447 obsessive-compulsive disorder 227,
missense mutation 62 228, 230, 242
M’Naughten test 907 occupational testing 130
modified labeling theory 896 open-ended questions 85, 86, 89
mood disorder 844, 845, 847, 859 open versus closed questions 82
motor and sensory examination 124 oppositional defiant disorder 160
multiple choice questions orgasmic disorders 414, 421, 426,
(MCQs) 628, 629 438
orphans and vulnerable children
narcissistic personality disorder 463 (OVC) 879
narcolepsy 355, 357, 358, 361, 362 Outcome of Depression International
negotiate a treatment plan 78 Network (ODIN) 443
neural circuits 228, 231, 233, 240 outpatient 554–556, 559–561, 565,
neurasthenia 797, 813 570
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922 Index
pain 561, 562 premature ejaculation 411, 413, 414,

palliative care 488 421, 425, 427, 438, 439
panic attacks 229–231, 233, presenilin 1 gene 63
235–238, 249, 256 presenilin 2 63
panic disorder 227–231, 233–236, prevention 724, 725, 732, 733, 734,
238, 244, 256 736, 738
paranoid personality disorder 468, Principles of Medical Ethics 910,
469 911
paraphilias 410–413, 416, 419, 431 privacy 574, 596, 597
434, 435, 438, 439 problem-based learning 614, 616
parasomnias 356, 357, 367, 369, prodromal 188, 199, 200
370, 374, 375 professionalism 555, 568, 770, 772,
peer 191, 195 773, 778
personal space 809 psychiatric classification 36–39, 49
personal statement 644–647 psychiatric diagnosis 28–32, 34–39,
personality 114, 127, 128, 129 42, 45, 49–54
personality disorder 461, 462, psychiatric education 12, 15, 22,
464–468, 471–475, 846, 855, 859 23
personality traits 461, 464, 467 psychiatric hospitalization 530, 531,
pharmacogenomic testing 762 536, 544
pharmacogenomics 746 psychiatric interview 32, 36, 52, 53,
pharmacotherapy 389, 392, 394, 90, 496
395, 397 psychodynamic therapies 211
phenomenology 5–7 psychoeducation 99, 211, 218
phobias 238–240, 242, 244 psychological testing 33, 36, 52
physical examination 33, 53, 54 psychopharmacogenetics 685
Pick’s disease 295, 298, 310 psychopharmacological
political conflict 865, 873, 875, 881 interventions 708
polypharmacy 197 psychopharmacology 509
polysomnography 357–360, 363, psychosis 185, 187–190, 194, 196,
365, 367, 368, 371–373 530, 532, 537–540, 546, 549
Positron emission tomography psychosocial stressors 231, 235,
(PET) 670 256
posttraumatic stress disorder (PTSD) psychosomatic medicine 572
248, 337, 339, 343, 443, 346, 725, psychotherapy 450, 453, 454, 500,
726, 731, 733, 734, 738, 743 511, 519, 521, 554, 564–569, 713
prejudice 887, 888, 889, 890, 891, psychotherapy training 625
894, 896 public health approach 694
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Index 923
racism 794 serotonin 2A receptor gene

randomized clinical trials (RCTs) 681 (HTR2A) 755, 757
rape 869, 871, 875, 876, 878 serotonin 2C receptor gene
rapport 78, 79, 525–528, 530, 546 (HTR2C) 758
rating scales 36, 37, 52 serotonin transporter gene
referral 554, 555, 564 (SLC6A4) 752, 761
reflection 80 sexual pain disorders 414, 421, 428,
refugee 866, 870, 871, 874, 876, 880, 438
881, 883 sexuality 489
reliability 103–106, 109, 131, 132 signs and symptoms 28, 29, 30, 31,
re-licensing 635 33, 34, 38, 39, 51
religion 801, 802, 804–806, 814, 817 silent mutation 62
REM 353, 354, 356, 360, 361, 367 single-nucleotide polymorphisms
research 771, 786, 787, 788 (SNPs) 62, 673
residency 606, 608, 617, 618, 623, sleep 352–359
642–646, 648–653, 657, 661, 664, 667 social control 910, 911
resilience 142, 145, 148, 149 social identity theory 895
retirement 485, 487, 501, 521 social phobia 227, 228, 230, 238–242,
reward circuitry 263, 267, 286 256
risk behaviors 728, 735 social physical contact 809
risk reduction 733, 738 somatic presentations 803
rotations 653, 654, 661, 664 somatization disorder 317, 318,
320–323, 326, 331–333
safety 554, 559, 566, 568 somatoform disorders 318, 322, 326,
schizoid personality disorder 468, 331, 586, 587, 599
469 specificity 111, 112, 131
schizophrenia 184–197, 200, 846, stagnation of liver qi 829, 837
850, 860 stagnation of liver qi with spleen
schizotypal personality disorder 468 deficiencies 829, 837
screening questions 91 standardization 107–109, 114,
sedatives 360 133
selective serotonin reuptake inhibitors stereotype 887–889, 894–899
(SSRIs) 228, 235, 241 stigma 723, 725–727, 733, 743
self-care 635 stressful event 451, 455, 456
self-help approaches 394 stuttering 166, 167
sensitivity 111, 112, 131, 133 substance 575, 579, 585, 587, 588,
serotonin 1A receptor gene 589, 597, 603
(HTR1A) 754, 757 substance abuse 205, 221, 560, 561
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924 Index
substance use disorder (SUD) 260, treatment plan 90, 96

263, 265, 281, 285, 286, 724, 730, true score 104, 106, 119
733, 739, 741, 844, 845, 850, 858, 859 twin studies 59, 61
suicidal behavior 208
suicidal ideation 524, 534, 535, 537, Ubunta 824, 832
546 Unani 825, 826
suicide 446, 456, 500, 505, 514, undergraduate 608–611, 613, 617,
583–586, 599, 600, 602 618, 631, 636
suicide attempts 690, 691, 693–695, United States Department of Housing
703, 706–709, 715, 719 and Urban Development 842
suicide prevention 691, 704 Universal Declaration of Human
suicide rates 690, 695, 696, 700, 703, Rights 842
704, 706, 707, 717 USMLE 645
suicide risk 709, 710, 711, 718, 719
suicide risk assessment 560, 709, vaginismus 414, 421, 429, 439
710, 711 validity 103–106, 115, 119, 127, 131,
supervision 653, 656–658, 661, 662, 132
664 vascular dementia 295–298, 307,
SUPRE-MISS 705, 706 310, 313
switching 344 velo-cardio-facial syndrome 69
veracity 772–775
therapeutic relationship 81 veteran 868, 877, 881
Tokyo Declaration 910, 911 visual–spatial abilities 124
torture 865, 869, 871, 875, 878, vocational 190, 193
880–882
Toxoplasma gondii 680 war 865–869, 872–876, 881, 877–879,
Traditional Chinese Medicine 881, 882
(TCM) 826 WHO-Disability Diagnostic Scale
trainees 785, 786 (WHO-DDS) 42
training 642–654 withdrawal 575, 578, 589–593, 603
trance and possession 811, 813 World Health Organization
transcranial magnetic stimulation (WHO) 889, 690
(TMS) 213, 224 World Psychiatric Association
transitions 82 (WPA) 910
trauma 337, 341, 343, 346, 348
traumatic dissociation 345, 348 years lived with disability (YLD) 3, 4
treatment 228, 234, 235, 251, 382,
385–396, 398–403 zeitgeber 353
treatment of paraphilias 434, 435 zinc finger protein 69
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International Handbook of

A Concise Guide for Medical Students,

8472hc_9789814405607_tp.indd 1 14/12/12 8:41 AM

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A Concise Guide for Medical Students,

Laura Weiss Roberts

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Library of Congress Cataloging-in-Publication Data

British Library Cataloguing-in-Publication Data

Copyright © 2013 by World Scientific Publishing Co. Pte. Ltd.

In-house Editor: Veronica Low

Typeset by Stallion Press

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Chapter 1 Impact of Mental Illness 1

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Chapter 7 Psychiatric Disorders in Childhood

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Chapter 20 Geriatrics 478

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Chapter 33 International Perspective on Homelessness 841

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rGE Gene–Environment Correlation

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ARNTL Aryl Hydrocarbon Receptor Nuclear Translocation-

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CIDI Composite International Diagnostic Interview

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xii Abbreviations List

DLB Dementia with Lewy Bodies

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Abbreviations List xiii

EUFAMI European Federation of Associations of Families

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xiv Abbreviations List

HRT Habit Reversal Training

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MMSE Mini-Mental Status Examination

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xvi Abbreviations List

PLMD Periodic Limb Movement Disorder

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Abbreviations List xvii

SP4 Sp4 Transcription Factor gene

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Laura Weiss Roberts, MD, MA

Joseph B. Layde, MD, JD

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Contributors List xxi

Bhanu Prakash Kolla, MBBS, MRCPsych.

David Mrazek, MD, FRCPsych.

Jennifer Niskala Apps, PhD

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xxii Contributors List

Jonathan E. Romain, PhD, ABPP

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Contributors List xxiii

Scott Van Sant, MD

Leanne Parasram, MBBCh, DMH

Dan J. Stein, MD, PhD