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the Brain
Neurofeedback as an
Integrative Approach to Health

Edited by Hanno W. Kirk

the Brain
Neurofeedback as an
Integrative Approach to Health

Edited by
Hanno W. Kirk

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To Sue Othmer—
Whose journey into neurofeedback began as a mother seeking effective and
appropriate care for her child, and who has continued as a tireless pioneer in
the quest for optimizing clinical outcomes. Through your years of collecting
clinical data as a teacher and trainer, you have been one of the most significant
contributors to the field, turning neurofeedback into a tool whose effects are
powerful and specific. Your guidance and mentoring have been an invaluable
help to so many of us.
We offer a collective Thank You!

Foreword vii
Acknowledgments xi
Editor xiii
Introduction xxi


History and overview of neurofeedback 1

1 Changing the paradigm from neurochemical to

neuroelectrical models 3
Hanno W. Kirk
2 History of neurofeedback 23
Siegfried Othmer
3 The role of glia and astrocytes in brain functioning 51
David A. Kaiser
4 The evolution of clinical neurofeedback practice 59
Meike Wiedemann


5 Neurofeedback in an integrative medical practice 95

Doreen E. McMahon
6 Nutrition and the brain 117
Nora T. Gedgaudas
7 Biomedical factors that impact brain functioning 147
Kurt N. Woeller

vi Contents



8 Applying neurofeedback to autism spectrum disorders

and other developmental disorders 169
Kelley E. Foust
9 The use of neurofeedback for combat veterans with
post‑traumatic stress 181
Anna Benson and Tamsen W. LaDou
10 PTSD symptom reduction with neurofeedback 201
Monica G. Dahl
11 Neurofeedback in application to the ADHD spectrum 231
Roxana Sasu and Siegfried Othmer

Conclusion: The future of neurofeedback 261

Siegfried Othmer

The book Restoring the Brain: Neurofeedback as an Integrative Approach to Health

is a unique volume whose publication by a major, highly respected scientific pub-
lisher is long overdue. Since its inception, neurofeedback has been received by
the health care community with a mixture of great enthusiasm and considerable
skepticism. Neurofeedback holds out the promise of treating serious neurologi-
cal and psychiatric disorders without resorting to traditional tools of medicine,
such as pharmacology or surgery. Considering, let alone embracing, this general
premise requires a genuine paradigm shift and an open mind, since its implica-
tions are profound both scientifically and clinically.
Scientifically, neurofeedback entails direct manipulation of the variables that
more traditional treatment modalities could affect only indirectly. That bioelec-
tric processes are central both to brain normal function and to its dysfunction
has been known for decades. Electroencephalogram (EEG), event-related poten-
tial (ERP), and contingent negative variation (CNV) recordings are important
and unchallenged methods of neuroscience research as well as tools of the diag-
nostic tool kit in neurology and psychiatry, but impacting these variables directly
as a treatment modality is an altogether different matter. Yet by recognizing the
relevance, even centrality of electrophysiological processes to brain function,
we recognize the validity and appeal of impacting these processing as a form of
treatment, at least in principle. As an unbiased outside observer who does not
practice neurofeedback himself and has no dog in the neurofeedback debate
fights, I believe that it has proven its legitimate place in the therapeutic arsenal
at the “proof-of-concept” level. There is a difference between embracing a novel
approach in principle and accepting its specific applications, and it is the latter
challenge that neurofeedback as a clinical genre is facing now. A body of rigorous
research into the efficacy of neurofeedback exists and is growing, but for a variety
of reasons, the results of this research are published in major high-profile clini-
cal journals relatively infrequently. This is why the publication of this volume by
Taylor & Francis, a world leader in scientific publishing, is such an important
milestone in introducing neurofeedback to the broad biomedical community.
Clinically, any promise of therapeutic effect without the potential downside of
side effects unavoidable in pharmacological approaches is inherently appealing.
Yet the often-made assumption that direct manipulation of brain electric activity

viii Foreword

is free of long-term side effects, while reasonably plausible on a priori grounds,

must nevertheless be tested directly for every specific application of neurofeed-
back. This effort is currently underway. The practice of neurofeedback does not
require a medical degree; in fact, most neurofeedback practitioners are not phy-
sicians or psychiatrists. This challenges some of the most entrenched societal
biases, that a medical degree is the requisite qualification for participating in the
provision of health care. The notion is patently incorrect; a wide array of clini-
cal psychologists, neuropsychologists, nurses, physical therapists, occupational
therapists, music therapists, social workers, biochemists, biophysicists, and oth-
ers have been indispensable and highly respected members of the biomedical
community in direct patient contact, yet the prejudice endures. Overcoming this
prejudice is among the challenges facing neurofeedback in its quest for becoming
fully embraced by the health care community and the general public alike.
Practically, neurofeedback equipment ranges from very sophisticated to rela-
tively basic and inexpensive, and access to this equipment is not rigorously regu-
lated. This makes it easier to integrate neurofeedback into clinical practices and
to combine it with other therapies. But it is also a mixed blessing because the
easy affordability of such equipment may make it appealing to ill-qualified prac-
titioners and may blur the boundary between serious therapies and “new-age”
gimmicks. The qualifications for practicing neurofeedback have yet to be clearly
defined, let alone enforced, and this will have to take place for neurofeedback to
be fully embraced and any lingering concerns to be alleviated.
Therefore, neurofeedback as a clinical discipline is clearly in the midst of its
growth pains but the process is exciting, infused with a great deal of creativity
and promise. It has evolved and expanded since Barry Sterman’s pioneering work
with sensorimotor rhythm (SMR) training and its rigid specification of electrode
scalp placement, to an integration with quantitative EEG (qEEG) and a great deal
of neuroanatomical specificity tailored to individual clients. The review of the
history and continuing refinement of neurofeedback in the book is comprehen-
sive and insightful; it clarifies the philosophy behind the approach and its devel-
opment. The discussion of new directions, such as infra-low-frequency training
and the putative mechanisms behind it is particularly interesting.
Restoring the Brain makes a forceful case for neurofeedback. The contributors
are acknowledged experts in the field, some of them with national and interna-
tional reputations. One of the book’s strengths is placing neurofeedback in a broad
neuroscientific context. These include neurochemistry, neural development, neu-
roplasticity, neurogenesis, as well as nutrition and the brain. Another strength
is a broad panorama of clinical applications of neurofeedback to a wide range
of clinical conditions offered in the book. These include autism spectrum disor-
ders, post-traumatic stress disorder, and attention-deficit hyperactivity disorder.
General discussions of each of these applications are interspersed with clinical
case reviews and every chapter is accompanied by comprehensive reference lists.
The volume culminates in a section on the future of neurofeedback across
a wide range of applications, from biomedical to educational to forensic. On
the whole, the volume is an invaluable source for the practitioners of neuro-
feedback; as well as for the broader clinical neuroscientific and mental health
Foreword ix

community aiming to understand its potential in clinical use. Restoring the Brain
will help reinforce the enthusiasm about, and the belief in the promise of, this
evolving clinical discipline in the process of finding its proper place in clinical

Elkhonon Goldberg, PhD, ABPP

Luria Neuroscience Institute and NYU School of Medicine

This book would not have been possible without the help and support of many.
I want to especially compliment each of the expert contributors, who labored
under pressure from me to produce manuscripts on time.
My thanks to Siegfried Othmer, who immediately endorsed the project, com-
mitted to writing two chapters, and suggested possible co-contributors. As some-
one deeply steeped in the history of the theory and practice of neurofeedback,
and possessing a great wealth of technical knowledge, I entrusted him with read-
ing, editing, and sometimes fleshing out points by other contributors.
I also want to thank Daniela Gutierrez, who provided an outside eye for the
project. Her editorial skills in cutting excess verbiage and turning awkward or
convoluted sentences into elegant and readable prose are much appreciated.
The professionals at Taylor & Francis also deserve my thanks. Lance Wobus,
the acquisitions editor, first approached me to suggest writing this book, and
then played a supportive role through the process of producing the detailed book
proposal. He stayed involved, even after the manuscript was received and sent
from department to department within the publishing company. Kyle Meyer in
the production department helped keep track of “what else” was needed. Nick
Barber directed the typesetting, and was patient when late changes arrived.
Finally, I want to thank my wife Jo Weisbrod, who was encouraging, and very


Hanno W. Kirk, PhD, LICSW, has been a lec-

turer/trainer for the past 35 years at various
universities. He has taught abnormal psychol-
ogy, sociology, social work, and p ­ sychosocial
and behavioral issues in medicine. From  2003
to 2007, Dr. Kirk gave all-day seminars
throughout the United States on “Is It ADHD
or Pediatric Bipolar: Differential Diagnosis
and Effective Treatment.” From 2008 to 2011,
he gave nationwide seminars on “End of Life
Care: Best Practices and Applied Ethics.” He
has presented “Creating Sacred Space at the
End of Life” at numerous conferences. Dr. Kirk
is the principal author of Psychosocial and Behavioral Aspects of Medicine. After
retiring from active teaching and touring in 2011, he is now in private practice
in Lewisburg, West Virginia. His practice specializations include children and
adolescents with behavioral and autistic spectrum disorders, as well as persons
with trauma issues, including veterans with PTSD and TBI. He has been using
neurofeedback in his practice since 2006.


Anna Benson, PhD, is a licensed clinical psy-

chologist having been in private practice in
Southern California for over 25 years, along
with six and a half years at Camp Pendleton
with service members returning from Iraq and
Afghanistan. Her trauma specialty became even
more of an emphasis as she worked increasingly
with the active-duty and veteran military popu-
lation. She is highly skilled with utilizing stan-
dard care therapeutic strategies, but has found
neurofeedback to be one of the most effec-
tive interventions for treating trauma, having
received about 300 hours of additional training
in this modality. Her professional background
has included intensive work in substance abuse,
along with work with couples and families. Throughout her career, she has taught
periodically at Alliant International University and the University of California,
San Diego in the humanities.

Monica G. Dahl, EdD, has been in private prac-

tice in Key West, Florida, since 1985, with a spe-
cial interest in veterans. From 1985 to 1995, she
taught Mind Power classes for human develop-
ment and peak performance. Using hypnosis on
patients under medical supervision, she devel-
oped a hypnotherapy training manual, which
was accepted in 1994 for certification train-
ing with the International Medical and Dental
Hypnotherapy Association. She was awarded
Educator of the Year (2010) by the organization.
In 2003, by invitation, Dr. Dahl taught stress
reduction for family members of staff working at
the American Interest Section in Havana, Cuba.

xvi Contributors

In 2008, she integrated neurofeedback into her private practice, and then used
neurofeedback in research for a doctorate in counseling psychology from Argosy
University, Sarasota, Florida. Her dissertation was a qualitative case study with
quantitative subunits on the effects of neurofeedback training for PTSD symptom
reduction. As a volunteer member of the Homecoming4Veterans program, she
provides pro bono neurofeedback training for service men and women.
Aside from PTSD and trauma, her clinical interests include ADD/ADHD,
autism/Asperger’s syndrome, gay/lesbian bisexual/transgender issues, pain man-
agement/elimination, peak performance, phobias, spiritual emergence, stress
reduction, stroke recovery, surgical preparation, and post-surgical suggestive

Kelley Foust, OTR, has been practicing occupa-

tional therapy in El Paso, Texas, for the past 21
years. For the first 15 years, she worked in inpa-
tient rehabilitation with a focus on brain inju-
ries and upper extremity rehabilitation, as well
as in outpatient and home health. After her son
experienced alarming side effects while being
treated with multiple medications for ADHD,
she went on a search for non-pharmacological
alternatives. After finding out about neuro-
feedback and receiving training in this area,
she founded Focus NeuroRehab and is now the
owner/operator of two clinics in El Paso. She
has worked collaboratively with a physician and
a speech therapist to establish an Integrative
Medicine Treatment Center that provides multiple therapies and biomedical ser-
vices for children with autism and other developmental disorders. Laser Focus
Nutrition will provide nutritional products to support the needs of patients. Since
2009, she has used neurofeedback with over 1000 children (aged 4–18 years) with
autism, ADHD, and other disorders. She has had extensive training and experi-
ence with the Othmer method of neurofeedback.

Nora T. Gedgaudas, CNS, CNT, is the author

of the groundbreaking, international best-
selling book: Primal Body, Primal Mind:
Beyond the Paleo Diet for Total Health and a
Longer Life. Her subsequent book is Rethinking
Fatigue: What Your Adrenals Are Really Telling
You and What You Can Do about It. Her work
has been endorsed and promoted by numer-
ous respected medical and scientific experts
and allied health care practitioners. Her popu-
lar articles on diet and health have appeared
Contributors xvii

in magazines and the press. She has given numerous educational talks, semi-
nars, courses, and workshops nationally and internationally, and has lectured
by invitation at many universities, both in the United States and abroad. She
has appeared internationally on radio and television and in documentary films.
She hosts her own radio program on Voice of America Radio’s “Health and
Wellness” channel, and her Primal Body, Primal Mind Radio podcasts are cur-
rently available on iTunes.
Ms. Gedgaudas has conducted training on nutrition’s impact on mental
health for health care workers for the State of Washington Institute of Mental
Health. Ms. Gedgaudas is in private practice as a board-certified neurofeedback
specialist, as well as a board-certified holistic nutritional consultant in Portland,
Oregon. Ms. Gedgaudas serves on the advisory board for Paleo Magazine.

David A. Kaiser, MFA, PhD, is a neuroscientist

with 25 years of military, clinical, entrepreneur-
ial, and academic experience. He has pub-
lished numerous scientific papers and articles,
as well as presented at dozens of major scien-
tific conferences. He was editor of the Journal
of Neurotherapy for 11 years, a fellow of the
International Society for Neurofeedback and
Research, past president of the Neurofeedback
Division of the Association for Applied
Psychophysiology and Biofeedback, founding
member and technical director of the Society
for Advancement of Brain Analysis, and pub-
lisher of Brain and Cosmos (an interdisciplin-
ary journal). He is the founder of the American
Neurotherapy Association and Kaiser Academy,
through which he trains professionals in func-
tional EEG and evidence-based neurotherapy. He teaches a range of psychol-
ogy, neuropsychology, and neuroscience courses, including the world’s first EEG
course at the Rochester Institute of Technology. His research interests include
functional EEG, clinical neuroscience, family neurodynamics, and neurocosmol-
ogy, a field he created to study the relationships between cosmology, the Earth,
and brain function.
xviii Contributors

Tamsen W. LaDou, PhD, is a licensed psychol-

ogist currently in private practice in Oceanside
and Temecula, California. While working at
Camp Pendleton, she specialized in treating
both active-duty marines and sailors, as well
as combat veterans, using CBT, eye movement
desensitization reprocessing (EMDR), cognitive
processing therapies, and other training tech-
niques. She finds neurofeedback to be the most
effective technique to reduce physiological as
well as emotional dysregulation for individuals
suffering from PTSD, traumatic brain injury, and acute stress. Prior to her work
with combat veterans, her focus was on treating children and families to address
trauma and its effects on adaptation.

Doreen E. McMahon, MD, trained with

Sue Othmer, BCIAC, and Siegfried Othmer,
PhD, two of the world’s leading neurofeed-
back experts. She has been through the
Neurofeedback in Clinical Practice and Alpha/
Theta courses offered by EEG Spectrum
International. She completed her neurother-
apy internship with Deborah Stokes, PhD,
BCIA-EEG, of Neurofeedback Consultants of
Northern Virginia, with whom she continues to
be active as a medical consultant.
Prior to her neurotherapy training,
Dr.  McMahon served as a medical advisor
and treasurer to the Oundle Special Children’s
Asso­ciation, an organization in Northamptonshire, United Kingdom, charged
with helping families and their special-needs children. Dr. McMahon practiced
at Annandale Family Medicine in Annandale, Virginia, from 1989 to 2001,
where she was responsible for full-time patient care and managing a primary
care office. During that period, she was affiliated with INOVA Fairfax Hospital.
Dr. McMahon received her board certification from the American Board of
Family Practice in 1989. Her internship and residency were completed at
INOVA Fairfax Hospital and Virginia Commonwealth University. She is a grad-
uate of the University of Maryland School of Medicine in Baltimore. A mem-
ber of the American Academy of Family Physicians and Virginia Academy  of
Family Physicians, Dr. McMahon is also a member of the EEG Associates and
the International Society for Neuronal Regulation.
Contributors xix

Siegfried Othmer earned his PhD in physics at

Cornell University in 1970. He has been active
in the development of EEG neurofeedback for
some 28 years, along with his wife Susan. After
an initial focus on ADHD children, their work
has increasingly encompassed the more seri-
ous childhood afflictions, such as the autism
spectrum, epilepsy, pediatric bipolar disorder,
Tourette syndrome, trauma conditions, and
developmental delay. Another key focus of the
work has been on PTSD, traumatic brain injury,
and addictions in the adult population. An addi-
tional focus has been on educational perfor-
mance in children and optimum performance in
adults. Dr. Othmer has been active in all aspects
of the field: instrumentation development, pro-
fessional training, clinical service delivery, clinical research, and publication in
both professional and popular media. The Othmers have built a large practitioner
network that now extends to many countries around the world. They have over
6000 professionals in ten countries since 1990. The Othmers have also initiated
a non-profit venture, the Brian Othmer Foundation, which provides neurofeed-
back services to veterans. Siegfried Othmer is the author of two books: ADD: The
Twenty-Hour Solution (with co-author Mark Steinberg) and Brian’s Legacy, the
remarkable story of their son who was struggling with epilepsy.

Roxana Sasu, MD, RN, earned her MD from

the Carol Davila Faculty for General Medicine
and Pharmacy, Bucharest, Romania, in 1998
and became licensed in 1999. She completed
her internship at Fundeni Clinical Hospital in
Bucharest. Subsequently, she became involved
in nutritional research and used nutritional sup-
plements in conjunction with standard Western
medical care. During this time (2004–2006),
she earned a master’s degree in marketing and
business communication from the Academy of
Economic Studies, Bucharest.
Dr. Sasu was introduced to the neurofeed-
back field by a friend, and after training in the
Othmer method, joined the clinical staff of
the EEG Institute in May 2008, where she practices under a registered nursing
license. Her clinical interests include developmental and autism spectrum dis-
orders, eating disorders, and physiological dysregulation related to anxiety and
depression. She divides her time between clinical work and teaching professional
xx Contributors

training courses at the EEG Institute and in Europe. She is also part of ongoing
research and data collection for improving the efficacy of neurofeedback.

Meike Wiedemann, PhD, is a neurobiologist

and associate professor for membrane physiol-
ogy at the University of Hohenheim, Germany,
where she teaches self-organization in biologi-
cal systems and neurofeedback. In research, her
interest in earlier days was in the development
of pre-clinical screening models for the devel-
opment of neuro-active drugs. Later on, she
studied the effects of micro-gravity on the cen-
tral nervous system. In this context, she led sev-
eral projects in cooperation with the German
Space Agency and the European Space Agency.
Since 2002, she has directed a private practice
for biofeedback and hypnosis with an empha-
sis on neurofeedback in Stuttgart, Germany. In
2011, she became chief scientist at EEG Info Europe. She has been teaching the
German version of infra-low frequency (ILF)–neurofeedback professional train-
ing courses since 2009.

Kurt N. Woeller, DO, is an internationally

respected autism biomedical specialist and
integrative medicine physician. He is an author,
international speaker, and clinical practitioner
with years of experience working with individ-
uals with complex health conditions including
autism, mental health disorders, chronic fatigue
syndrome, and autoimmune conditions such as
rheumatoid arthritis and inflammatory bowel
disease, as well as neurological diseases such as
multiple sclerosis.
Dr. Woeller also serves as a clinical con-
sultant for Great Plains and BioHealth
Laboratories—two integrative medicine labo-
ratory companies offering specialized testing
for individuals with complex medical condi-
tions. He also maintains extensive online edu-
cational resources for parents with autistic children and health practitioners
working with complex patients at, and through
monthly educational webinars hosted at

As I was reading the chapters of the other contributors to this book, I was struck
by their accounts of epiphanies when they recognized that neurofeedback train-
ing was making a positive change either in their own lives or in the lives of some-
one dear to them. So it was with me. After years of teaching, I decided to focus
my energy on private practice. I started treating mostly children and adolescents,
many of whom came to me already labeled and medicated for attention-deficit/
hyperactivity disorder (ADHD). I quickly realized that this catch-all diagnosis
frequently was a convenient cover for a number of other conditions. Convinced
that too many kids with other issues were misdiagnosed and medicated for
ADHD, in 2004 I created a professional training program on differential diagno-
sis and effective treatment for children with behavioral disorders. It was during
a nationwide tour for this program that I first learned about neurofeedback. The
stories I heard from other working health care professionals, who had success-
fully remediated the behaviors of kids like the ones I was talking about by train-
ing their brains, set me on a new course.
To find out more, I invited myself to the EGG Institute on my next trip to
Southern California in 2005. Siegfried Othmer and his wife Sue Othmer were
gracious in their welcome, and patiently explained how and why neurofeed-
back works. They invited me to experience a 30-minute sample session. I was
impressed, and upon my return to Lewisburg, West Virginia, my adopted home-
town, I explored how I could integrate neurofeedback into my psychotherapy
practice. I took the basic professional training at the EEG Institute in 2006, and
under supervision, started to use neurofeedback to train the brains of my youth-
ful clients. It certainly seemed to work better and faster than doing psychotherapy
with often recalcitrant or mute teens. After successfully working with a number
of children with autistic spectrum disorders (ASD), I had two cases that I con-
sidered spectacular failures. Each of the teenage girls had close to 100 sessions,
including home training, with little effect on their severe autistic behaviors. I was
searching for answers.
When I attended the 2012 Integrative Medicine and Mental Health Confer­
ence in Santa Fe with some neurofeedback colleagues, I found the answers I was
looking for.

xxii Introduction

I learned that while neurofeedback is a powerful tool for training the brain, it
needs to be considered in the larger context of other biological and environmen-
tal influences on the workings of the brain, whether they be chronic infections or
inflammation, molds or toxins, or nutritional deficits or food sensitivities.
With this new perspective firmly in hand, I realized that biological conditions,
unless addressed, could weaken or render ineffective even an intensive course of
neurofeedback training. It turned out that this is what happened with the two
female clients with ASD. They both had chronic biomedical issues. Once these
conditions were identified and addressed, both clients improved rapidly, and at
the time of this writing were excelling academically in their college work.
My experience as a practitioner is not a unique one. The critical understand-
ing that neurofeedback can work best within the framework of integrative health
is one that many of my colleagues have come to as well, and I feel fortunate to
have been able to work with a number of them in the production of this book.
In 2014, Kelly Foust and I gave a presentation at the annual IMMH Conference,
which led to an invitation from the publisher to put together this book.
The experiences of neurofeedback practitioners are not the only basis for this
work. A large body of published evidence now exists for the proposition that
neurofeedback, in general, and the infra-low training, in particular, is effective
for a broad range of mental disorders. In developing this book, we made a choice
to focus on a few common categories of dysfunction that are representative of
the classes of conditions that are accessible to neurofeedback. Clinical ADHD
(Chapter 11) is an example of conditions that heavily involve left-hemisphere
executive function, and is representative of a number of common but less severe
dysregulations. Autism spectrum disorders (Chapter 8) and post-traumatic stress
disorder (Chapters 9 and 10) on the other hand, have been chosen because they
represent more severe brain dysregulation, and are also representative of condi-
tions that afflict primarily the right hemisphere and the limbic system.
Some common conditions such as depression, migraines, or sleep disorders,
while not specifically the focus of any one chapter, do get mentioned by several
authors as they describe either their own experiences or those of their clients.
This touches upon an important principle of neurofeedback: Due to the amazing
interconnectivity of neural networks in the brain, improvements in one aspect
of functioning will generally produce global improvement in effective self-reg-
ulation. Thus, while addressing a targeted issue, we find most clients reporting
that other symptoms, which were not their primary concern when they came for
neurofeedback training, had improved or disappeared altogether.

The book is divided into three parts, which aim to introduce the reader to the
history of neurofeedback, to explain the integrative approach to health, and to
discuss how these two work together in practice.
In Part 1, I trace the evolution of the concepts of brain functioning, culmi-
nating in the “War of the Soups and Sparks,” followed by the dominance of the
neurochemical paradigm. Siegfried Othmer takes us from the simple beginnings
Introduction xxiii

of measuring brain waves, and the early operant conditioning experiments with
animals and the application to humans, to the development of quantitative elec-
tro encephalography (qEEG)-guided neurofeedback, and the split between those
committed to prescriptive qEEG-based neurofeedback and the non-prescriptive,
patient-centered approach of the more recently developed infra-low frequency
(ILF) training. David A. Kaiser’s chapter on astrocytes provides us with the sci-
entific basis for why ILF is so effective, citing startling new findings of how these
ultra-slow oscillations of the astrocytes are the dominant features in state regula-
tion of the brain, including the timing of circadian rhythms and the instanta-
neous allocation of blood to activate critical brain networks. Rounding out this
section, Meike Wiedemann gives us a comprehensive description of how neuro-
feedback is done in clinical practice.
Part 2 looks at neurofeedback in the context of integrative medicine. Doreen
E. McMahon describes how she has incorporated neurofeedback into her medical
practice, and provides a template for how other physicians can do the same. Nora
T. Gedgaudas, in her chapter on nutrition and diet, talks about how the presence
or absence of specific nutrients in our bodies can either nourish or harm our
brains. She also presents evidence on how nutritional deficits or toxic influences
can trigger disease and autoimmune conditions. Kurt N. Woeller discusses how
biomedical factors, such as infections in the lower intestines, or malfunctioning
in key metabolic processes, can interfere with brain functioning, causing symp-
toms such as autism spectrum disorders, as well as a number of other physical
and mental health conditions.
Part 3 of the book gives examples of how neurofeedback is applied to spe-
cific brain dysfunctions. Kelley E. Foust describes her success in using neuro-
feedback for the treatment of children in the autism spectrum. Anna Benson
and Tamsen W. LaDou describe their use of neurofeedback in the treatment of
combat stress with nearly 1000 active-duty military service personnel.* Monica
G. Dahl presents several case studies to provide an in-depth look at and analysis
of PTSD (posttraumatic stress disorder) when comorbid with other serious psy-
chological conditions. Roxana Sasu and Siegfried Othmer review representative
samples of the data collected over the years on the application of neurofeedback
to attention-deficit disorder. The final chapter, by Siegfried Othmer, looks at the
promises and pitfalls of the road ahead.
The aim of this book has been to present the case for the application of neu-
rofeedback within the framework of the integrative health model. It is my belief,
and the belief of the other contributing authors to this text, that neurofeedback, a
powerful tool in its own right, can be made even more effective and be maximally
beneficial with consideration for the context in which it is being applied.

Hanno W. Kirk, Editor

* By claiming that the information was proprietary, the military command structure pro‑
hibited the authors from presenting their extensive data collection, statistical analysis,
and graphs of PTSD symptom reduction.

From the Beginning:

History and overview of

1 Changing the paradigm from neurochemical to

neuroelectrical models 3
Hanno W. Kirk
2 History of neurofeedback 23
Siegfried Othmer
3 The role of glia and astrocytes in brain functioning 51
David A. Kaiser
4 The evolution of clinical neurofeedback practice 59
Meike Wiedemann
Changing the paradigm
from neurochemical to
neuroelectrical models


1.1 The early days of speculation 3

1.2 The soups and the sparks 6
1.3 The neurochemical paradigm 8
1.4 Neuropsychiatry: The pharmacological breakthroughs 11
1.5 Moving to a new paradigm 12
1.6 Conclusion 18
References 19

Communication patterns in the brain are mediated by chemical and electrical signals.
Because of the enormous clinical and commercial potential of psychiatric medications
thus far, only the chemical paradigm has received significant interest from the scien-
tific community. The electric patterns in the brain have been almost entirely ignored.

Bessel A. van der Kolk, MD1


Our understanding of how the brain functions has changed dramatically over the
centuries. Through much of time, the heart was celebrated as the central locus of
thought, emotions, and even the soul. The contents of the skull were regarded as
an undifferentiated biomass. While an ancient Egyptian papyrus—attributed to a
battlefield surgeon—noted that head trauma affected physical function, there was
no anatomical knowledge of the brain. In the first century BC, Greek philosophers

4  Changing the paradigm from neurochemical to neuroelectrical models

theorized that the brain was where the mind was located and that it might be
the seat of sensations. In the second century AD, the great Roman physician and
anatomist Galen used dissection and produced detailed hand-drawn maps of the
brain and the spinal cord. Galen believed that the soul and mind consisted of
pneumo, or spirits emanating from the heart, and that the role of the brain was to
ennoble these spirits in human beings. Galen’s “hydraulic” view of spirits moving
around the body like fluids was to dominate thinking into the Renaissance.2
The intensely curious Renaissance genius Leonardo da Vinci used anatomi-
cal dissection to study all parts of the body, including the brain. He left behind
beautifully detailed and accurate anatomical drawings of the brain, including the
­cavities, or ventricles. Da Vinci’s slight departure from the heart-centered spirits
view was his belief that perception and cognition resided not in the brain “sub-
stance” itself, but in these cavities. But without modern tools, he and others could
only speculate. A radical departure from this spirit-dominated view of the body
came in the 17th century, when Rene Descartes declared that the mind and the
body were distinct. This dualistic view has largely dominated Western medical
thinking to this day. Even today, it seems to inform how the brain is seen as an
organ driven by biochemical actions, yet somehow separate from the myriad of
mental activities sparked by electrical networks. Brain surgeons and neurologists
look at neurological dysfunction in terms of a physical pathology, but only mini-
mally concern themselves with mental health issues deriving from the condition.
Psychiatrists tend to look at mental dysfunctions with little understanding of how
they are impacted by dysregulation of the neural networks in the brain, as well
as biomedical issues in other parts of the body, like the gut (see Chapter 7). Part
of the effort of this book is to move away from this arbitrary dualistic view and
instead take an integrative view of mind and body, one that recognizes that seam-
less interplay between physical and mental health can be used for enhancing over-
all functioning.
Modern understanding of the nervous system and later of brain functions had
to await the technological advances of the 19th and 20th centuries. In succession,
they were the invention of the microscope, the development of the Golgi staining
method for nerve tissue, the development of a refined sensitive galvanometer for
measuring the electrical action potentials in the nerves, the invention of micro-
pipettes and, ultimately, the appearance of the electron microscope in 1950. Each
of these breakthroughs allowed for more detailed examinations of theories and
assumptions that had previously been based on speculation.
In the 1880s, Italian scientist Camillo Golgi invented a silver chromate stain-
ing solution that made possible the study and identification of neural tissue in
the spinal cord and in muscular tissue under the microscope for the first time.
However, because he was limited by the low amplification of microscopes in the
1890s, Golgi made a critical inaccurate assumption. He believed that the nerve
tissue he was identifying with his staining technique was comprised of a seamless
network (reticulum) through which nerve impulses could travel in either direc-
tion. This became known as the Reticular Theory.3
At about the same time, Spanish pathologist Santiago Ramon y Cajal, using
Golgi’s new staining technique, came to a completely different conclusion. He was
1.1  The early days of speculation  5

able to identify and follow individual long axons to their termination. Through
this, he demonstrated that the neuron was the principal structural and functional
unit of the nervous system. This became known as the Neuron Doctrine.4 This
doctrine states that each nerve cell is separate and individual, bounded like all
other cells in the body by its plasma membrane. He argued that the junction (or
synaptic gap) between neurons was essential for regulating the transmission of
signals in the nervous system. From his discovery of the axonal growth cone, he
experimentally demonstrated that the relationship between nerve cells was con-
tiguous, rather than continuous as Golgi had supposed.* The Neuron Doctrine
initially was very controversial and was opposed by Golgi and other histologists,
who continued to defend the Reticular Theory past the turn of the 20th century.4†
However, Cajal’s discoveries, including his detailed drawings and lucid prose
explanations, had a major influence on the work of British physiologist Charles
Sherrington. After meeting Cajal in Spain, Sherrington turned his attention to
the connection between the brain and the spinal cord. He observed that signal
conduction in the long nerve trunks of the spinal cord was much faster than
in the gray matter of the brain. To explain the differential in the speed of con-
duction, Sherrington hypothesized that neurons had to have gaps between them,
to which he gave the term “synapse” in 1897. He argued that the synaptic gap
between neurons was essential to the regulation of the transmission of signals
in the nervous system.5,6 If a synaptic gap existed, then the burning question
became: what was happening at this gap?
In 1921, the Austrian pharmacologist Otto Loewi, inspired by a dream, con-
ducted experiments on the vagus nerve of frog hearts. He found that during the
stimulation of the vagus nerve, a substance was formed. From these experiments,
he concluded that neurohumoral substances were critical in nerve transmission.
But it was difficult to identify this vagus-stimulating neurohumoral substance,
which turned out to be acetylcholine (ACH). As Loewi later realized, the difficulty
was that “acetylcholine produces only a very short lasting effect [and] is speed-
ily metabolized.” This is why other scientists had trouble replicating his studies.7
The problem of proving the existence and function of these seemingly ephemeral
substances, which later became known as neurotransmitters (NTs), turned into a
40-year scientific quest to determine what role these chemical substances played
in neurotransmission.
Another group of scientists believed that the transmission of the nerve
impulses was accomplished simply by electrical “sparks” flying across the syn-
aptic gaps from one neuron to another. The idea of electrical transmission was
seemingly substantiated by the work of German physiologist Emil du Bois-
Reymond. After inventing a highly refined and sensitive galvanometer, he was
able to observe that nerve impulses were accompanied by electrical discharges.

* Acrimony developed between the two men, as Golgi refused to acknowledge the valid‑
ity of Cajal’s research. Ironically, both men were awarded the Nobel Prize in 1906 for
their contributions.
† Golgi evidently was so upset over having to share the 1906 Nobel Prize with Cajal that

he used his acceptance speech to attack Cajal’s neuron doctrine.

6  Changing the paradigm from neurochemical to neuroelectrical models

He identified that there could be fluctuations of these discharges from negative

to positive, and back again. He found that this corresponded to a variation in the
action potential as nerve impulses traveled from the brain through the spinal
cord to cause muscle contractions. With only low-amplification microscopes and
crude measuring tools, du Bois-Reymond could only speculate on the mystery
of how this nerve transmission was accomplished. In a textbook of the time, he

Of known natural processes that might pass on excitation, only two

are, in my opinion, worth talking about—either there exists at the
boundary of the contractile substance—a stimulating secretion…
or the phenomenon is electrical in nature.8

Even though du Bois-Reymond considered that chemical change was part of

muscle contraction, he did not consider that the transmission between nerve and
muscle was chemical. Based on his observations with the galvanometer, du Bois-
Reymond tended to place more emphasis on the concept of electrical transmis-
sion. Indeed, he became known as the father of the field of electrophysiology.9


Du Bois-Reymond’s speculation that the process might be either chemical or
electrical had defined the debate over the nature of neural transmission that was
to continue over the next 60 years. Elliott Valenstein called the debate between
the two scientific camps The War of the Soups and the Sparks (2005). The chemists
and pharmacologists argued for the primacy of neurohumoral secretions in trig-
gering neurotransmission.* The physiologists proposed that nerve conduction
was achieved primarily by electrical impulses traveling along neural pathways
and then into the muscles.
At the beginning of the 20th century, the intensive study of the nervous system
by various eminent scientists produced exciting speculation and debate about
which side was right. The research on the autonomic nervous system c­ onducted
between 1890 and 1920 laid the foundations for later studies on the role of chemi-
cals. Two eminent anatomists, Walter Haskell and John Langley, conducted
research at Cambridge University that led to the discovery of the sympathetic and
parasympathetic nervous systems. Their studies and those of Wilhelm Feldberg
led to the positive identification of ACH at the junction of motor neurons and
muscle when the muscle contracted.
Much of the systematic search for evidence to support the chemical trans-
mission of nerve impulses was conducted under the leadership of Henry Dale at

* We may regard some of the early terms, such as “neurohumoral substances,” as quaint.
It needs to be remembered that modern terms such as neuroscience, neurophysiology,
and even neurotransmitters did not come into regular use until the 1950s.
1.2  The soups and the sparks  7

the Institute of Medical Research outside London.* A spirited debate developed

between the Soups group, headed by Dale, and the Sparks group, whose most
prominent proponent was the Australian physiologist John Eccles. Eccles did not
believe that the “ACH hypothesis” derived from Feldberg’s work with parasym-
pathetic ganglia applied to the central nervous system. The neurophysiologists,
who recorded electrical impulses with a multistage vacuum tube that displayed
on fast-responding cathode ray oscilloscopes, were sure that their impressive
visual data proved that neurotransmission was electrical. As Valenstein records,
there was “also a tendency of the neurophysiologists to look down on the phar-
macologists, who spent their time investigating ‘spit, sweat, snot and urine’.”10
The principal flaw in the Sparks hypothesis was that neurotransmission did not
occur at the speed of electrical transport. To account for this discrepancy, Eccles
came up with various explanations that seemed plausible at the time. He cleverly
proposed that “wave interference” slowed the transmission. He also attempted
to explain that the excitation and inhibition phenomena were caused by “eddy
currents” of different polarities. Then, in 1947, he posited a new theory based
on a dream. He claimed that interneurons (previously identified with the Golgi
staining method) were responsible for producing inhibition at the synapse level.
Four years later, it was Eccles who disproved his own theory and confirmed
the chemical neurotransmission theory. Two technological advances allowed for
the change. In 1950, magnification provided by the electron microscope brought
into view individual cells and even their constituent parts. The second innova-
tion, coming in 1951, was the micropipette, the glass microelectrode filled with
saline solution capable of penetrating the outer membrane of single neurons.
This allowed for the precise measurement of the voltage changes that character-
ized inhibitory and excitatory states. Using these two innovations, Eccles and
two colleagues conducted an all-day experiment in August 1951 in his Australian
laboratory. The results produced were contrary to his expectations. He was quick
to admit that he had been wrong. He acknowledged that the “large post-synaptic
potential” evoked could not be accounted for by a “trans-synaptic flow of cur-
rent,” but could only be accounted for by “the chemical transmitter mechanism.”
The riddle of the change in charge had been explained by the discovery of the dif-
ference in polarity between the core of the neuron and its outer membrane. With
this breakthrough and its publication in a prominent journal in 1952,11 the War
of the Soups and the Sparks had come to an end.†
The use of the electron microscope and micropipettes spurred almost fever-
ish research in a number of prestigious institutions and made the study of neuron

* Dale had met many of the leading German Jewish scientists working at the cutting
edge of neurotransmission at international conferences in Europe prior to the rise of
Hitler. When the Nazis took over and they lost their jobs, he, with the assistance of
the Rockefeller Foundation, brought some of them, including Otto Loewi and Wilhelm
Feldberg, to work with his group in Britain.
† Eccles, after his “conversion,” became an active proponent and researcher of neuro‑

chemical transmission. He was knighted by the Queen in 1958 and received the Nobel
Prize in 1963.
8  Changing the paradigm from neurochemical to neuroelectrical models

Structure of a typical chemical synapse


Neurotransmitter Axon
Voltage- transporter terminal
gated Ca2+


Figure 1.1  (See color insert.) This image identifies the synaptic vesicles on
the presynaptic side which release their NT via voltage gated channels into
the synaptic cleft, where they need to connect almost instantaneously to the
­special key hole receptors on the surface of post-synaptic dendrite before
being reabsorbed into the pre-synaptic axon terminal.

function the new frontier of science. The 1950s was a heady time for these research-
ers, as they came up with one discovery after another. Neuroscience was acknowl-
edged to be a separate field of study with its own publications.12 The new tools
for the investigation of the nervous system at the electron microscope level also
allowed for exploration of the staggering complexity of the human brain. There are
some 100 billion neurons in the brain, composed of 150 different cell types. They
vary in size from a robust 100 microns in diameter for the long motor neurons
extending down the spinal cord to 4 microns for the interneurons. In addition,
there are trillions of glial cells, including astrocytes, which jointly make up 90%
of the volume of the cortex.13 (The critical functions of astrocytes are explained
in Chapter 3.) While one area of research focused on the identification and differ-
ences of the functions of the various neurons, or clusters thereof, another segment
focused on the neurochemical mechanisms operating at the synapse level of axons
(Figure 1.1).


Once chemical substances had been confirmed as initiating electrical action
potentials, the attention of much research turned to the identification and role
of NTs in every facet of functioning of the brain and the nervous system. Indeed,
once the primacy of NTs had been established, the reigning paradigm for under-
standing the brain was from the perspective of these neurochemical agents and
1.3  The neurochemical paradigm  9

their action upon physiological function, as well as behavior. With the empha-
sis on the role of neurochemicals from the 1950s onward, we also see the entry
of the then-nascent pharmaceutical industry into the research field. With the
enormous profit potential of marketing drugs to correct neurochemical “imbal-
ances” in the brain, the study of how the timing and organization of the brain
was related to the patterns of neuroelectrical currents, measured in waves with
specific bandwidths and amplitudes, fell into relative neglect.
There was much excitement as neuroscientists, with their new technological
tools, deciphered the detailed mechanisms by which NTs fulfilled their roles at
the synapse level. One of the first accomplishments of the new field of neurosci-
ence was to identify the chemical substances in the mechanisms of excitation and
inhibition at the synapse of individual neurons. The first two to be identified were
ACH and gamma-aminobutyric acid (GABA). The excitatory substance is ACH,
a complex organic molecule. The inhibitory organic molecule is GABA.
When a neuron is in the resting state, the inside of the cell membrane is nega-
tively charged and the outside surface is positively charged. If an activating mes-
sage from an adjoining axon is received at the synaptic junction, the cell body
(soma) of the neuron responds to the cholinergic action of ACH. Immediately,
the charge of the neuron changes as the interior core becomes positive and the
outside becomes negative. This is called depolarization. (The change of charge
is accomplished by cellular ion pumps embedded in the neuronal membranes.)
This triggers the creation of an action potential, a wave front of chemical inter-
action and, equivalently, an electric pulse traveling at great speed from one
myelin hillock to the next down the axon to the next synapse. There, the pro-
cess is repeated as the activating signal gets passed along.14 This happens in the
brain, in the spinal cord, and in the motor neurons connecting to our muscles.
Depending on where it occurs and for how long the excitation cycle lasts, the
neurons will be firing before returning to the resting state. Meanwhile, the ACH
in the synaptic cleft has a short lifespan. It is available only long enough to bind to
the post-synaptic receptors before deactivation occurs. Deactivation comes about
either by the removal of the NT by re-uptake into the pre-synaptic terminal or
via degradative enzymes in the synaptic cleft. However, short-term exposure of
the receptor to ACH is usually sufficient for setting off a post-synaptic response
to release the action potential in the next neuron.15
GABA is the chief inhibitory NT and plays a key role in regulating neuro-
nal activity in the nervous system. It is also directly responsible for regulating
muscle tone via the motor neurons.16 GABA acts at inhibitory synapses in the
brain by binding to specific receptors in both pre- and post-synaptic neuronal
processes. This binding causes the opening of ion channels to enable the flow of
either negatively charged chloride ions into the cell or positively charged potas-
sium ions out of the cell. This action results in a negative charge in the trans-
membrane potential, called hyperpolarization. The key role of GABA, both in the
brain and in muscle tone, was recognized early by the pharmaceutical industry,
which led to the development of a host of GABAergic drugs. The earliest of these
were the barbiturates and benzodiazepines. Later, a wide range of GABA agonist
and antagonist medications were developed, ranging from sedative–hypnotic
10  Changing the paradigm from neurochemical to neuroelectrical models

drugs (methaqualone) to anti-seizure medications (phenytoin, valproate, and

In addition to ACH and GABA, it is estimated that there are close to 100 other
NTs or neuromodulators, each with different functions. In the category of neu-
romodulators, we find the biogenic amines or monoamines, such as dopamine,
norepinephrine, and serotonin. Although relatively small in quantity (as compared
to other NTs), they are distributed throughout the brain in small clusters of cells.
They are found in key nuclei that have massive axonal connections to the cortex.
These neuromodulators are responsible for regulating some of the highest-order
functions we have as human beings. Their effects on mood, alertness and attention,
cognitive processing and executive functioning, among others, were also recog-
nized by the pharmaceutical industry, which developed drugs to target those areas.
Another category of NTs are the enkephalins and endorphins, which are found
in the areas of the brain that process pain. They act as natural morphine-like
substances to decrease the transmission of pain in the nervous system. They are
also found in areas of the brain associated with well-being. Endorphins are often
touted in popular self-help and sports literature as causing the “runner’s high,”
in which increased exercise releases more endorphins, allowing for a heightened
sense of good feelings. Since various types of pain are widespread and most people
want to avoid pain, it is not surprising that the pharmaceutical industry zeroed in
on producing and marketing analgesics as a very profitable line of drugs.
An excitatory NT system worth mentioning in this brief overview is the hista-
mines. Histamines respond to the presence of irritating or pathogenic substances
introduced into the body either via ingestion, inhalation, or injury. Their main
function appears to be to increase blood supply, especially white blood cells, to the
affected area to fight or neutralize the alien substance. The problem is that this is an
inflammatory response that is usually experienced as unpleasant (as in congested
sinuses or bronchial areas, watery eyes, sneezing, etc.). Here, again, the pharma-
ceutical industry came to the rescue with a wide range of anti-histamines and non-
steroidal anti-inflammatory drugs, which suppress the inflammatory histamine
action. One of the problems with anti-histamines is that they not only suppress
allergy symptoms in the body, but also have a systemic inhibitory effect in the brain,
which is experienced as drowsiness, fuzzy thinking, and delayed motor action.
One of the curious aspects of the endogenous neurochemical substances in
the brain is that not all of them are found exclusively within the cellular bodies of
neurons, dendrites, or the synaptic terminals. Indeed, some are found operating
outside the neural membranes in the vast sea of astrocytes. The most important
of these extra-cellular substances is adenosine triphosphate (ATP). ATP is often
called the “molecular unit of currency” of intracellular energy transfer.17 ATP
is instrumental in the activation of blood flow to neural networks. As we will
see in detail in Chapter 3, the ebb and flow of ATP is central to regulating the
ultradian rhythms of the brain. In that fashion, it has a systemic effect on the
awake/rest/sleep cycle, not only of the brain, but also of the various systems of
the body. Because astrocytes play such a critical role in the regulatory regime of
critical neural networks, they become the target for neurofeedback when there is
1.4  Neuropsychiatry: The pharmacological breakthroughs  11


Prior to the 1950s, psychiatry often had to rely on psychoanalysis, h ­ ospitalization,
or psychosurgery for mental illness conditions. There were only a few medica-
tions available and those were for severe conditions like schizophrenia and
bipolar disorder. “All prototypes of modern psycho pharmaceuticals (lithium,
chlorpromazine, meprobamate, imipramine, and chlordiazepoxide) were dis-
covered in a period of about 10 years” from 1948 to 1958.18
Part of the excitement of that period in the new field of neurophysiology was the
discovery and identification of the function of the growing numbers of the c­ hemical
NTs. With that came intensive research on how either over- or under-production
of specific NTs, or dysfunctions at the synapse level, could negatively impact brain
functioning. For example, norepinephrine (noradrenalin), an ­excitatory NT, is
produced in the locus coeruleus in the pons of the brain. In response to arousal
stimuli, the locus coeruleus distributes norepinephrine to various centers in the
brain to regulate the body’s physiological arousal response via long axon connec-
tions.13 One of the conditions associated with over-production of norepinephrine
is post-traumatic stress disorder (PTSD), in which the limbic system is in a con-
stant state of over-arousal due to hypervigilance. On the other hand, if too little
norepinephrine reaches the key cortical areas involved in cognitive processing and
emotions, then attention, motivation, decision-making, learning, and memory are
likely to be degraded or depressed (as in ADHD). For over-production, the phar-
maceutical industry came up with anxiolytics; for under-production, the answer
became stimulant medication.
A dysfunction common at the synapse level is re-uptake. Generally, NTs only
stay in the synaptic gap for a fraction of a second before being reabsorbed into
the pre-synaptic axon terminal, in what is known as re-uptake. When a mood-
regulating NT like serotonin is released into the synaptic gap, it needs to connect
to the post-synaptic serotonin receptor sites instantly before being reabsorbed
into the pre-synaptic axon terminal. However, if there are too few post-synaptic
receptors, or they are not functioning well, the serotonin may be reabsorbed into
the pre-synaptic vessel before it can pass on its neuromodulating message. Low
serotonin levels are associated with depression, and once this mechanism was
discovered, the major pharmaceutical companies raced to produce a solution.
Each came up with its own formulation of selective serotonin re-uptake inhibi-
tors, designed to keep the serotonin in the synaptic cleft for longer to force itself
into whatever post-synaptic receptors are functioning.
The seeming great success of the early psychopharmaceuticals like the benzo-
diazepines, the monoamine inhibitors, and the tricyclics for depression—and later
meprobamate (Miltown) and again the benzodiazepines (Librium and Valium)
for anxiety—spurred the pharmaceutical industry to devote major resources to
exploring what other neurochemical brain dysfunctions could be solved with
A major problem with most psychoactive drugs is that they lack specificity in tar-
geting (i.e., they often have effects in other parts of the brain or the central nervous
12  Changing the paradigm from neurochemical to neuroelectrical models

system where their effects are either not needed or they produce negative effects).
For example, the main target of stimulant medication is to raise the norepinephrine
level in the prefrontal cortex of a person with ADHD. However, the stimulant action
affects the whole central nervous system and may produce heart palpitations, high
blood pressure, and dizziness (as well as inhibiting appetite). Another point is that
most mood-modulating drugs are only slightly more effective than placebos.19,20
The psychiatric profession, for the most part, welcomed and embraced the
appearance of pharmaceutical “solutions” to the problems of psychiatric disor-
ders. The profession adopted the “neurochemical paradigm” of functioning of the
brain and became the purveyors of the drugs designed to correct the neurochemi-
cal imbalances that were said to be at the root of most psychiatric disorders.21 The
pharmaceutical industry had a strong vested interest in promoting the prescribing
of psychoactive medications not only by psychiatrists, but also by general medical
practitioners. Towards this end, the industry spent hundreds of billions of dollars
on advertising, and used a system of direct marketing to doctors by “drug reps,”
who gave away free samples. Big Pharma has profited enormously and there-
fore has a strong incentive in upholding the neurochemical paradigm, and thus
maintaining its influence over the treatment of mental and physical health condi-
tions. The health insurance industry also embraced the neurochemical paradigm,
because treatment of symptoms with psychoactive drugs tends to be cheaper in
the short run than the long-term face-to-face talk therapy that might be under-
taken to resolve the underlying causes of mental health problems.


The preceding review was designed to show how we arrived at seeing brain func-
tioning through the lens of the neurochemical paradigm. As we have seen, the
neurochemical paradigm was deeply rooted in the discovery process of the physi-
cal components and functions of the nervous system and the brain. It led to a focus
on the neurochemical interactions at the synaptic cleft between neurons at the
microscopic level. It was a mechanistic view of functioning at the micro level. Less
attention was paid to the functioning of the brain at the macro level.
The neuroelectrical paradigm sees the whole brain as a self-organizing system.
Neurons organize into functional assemblies and execute their functions through
collective action, all the while also retaining their individuality of expression. This
complementary perspective is absolutely necessary in order to understand brain
function. This has been recognized as far back as the turn of the 20th century,
when Camillo Golgi described in his 1906 Nobel Prize acceptance speech:22

Far from being able to accept the idea of the individuality and
independence of each nerve element, I have never had reason,
up  to now, to give up the concept which I have always stressed,
that nerve cells, instead of working individually, act together…
However opposed it may seem to the popular tendency to individu‑
alize the elements, I cannot abandon the idea of a unitary action of
the nervous system. (Golgi, 1906)
1.5  Moving to a new paradigm  13

It is apparent that Golgi was standing apart from the views prevailing at the
time, and in fact that split stayed with us longer than the controversy about the
Soups and the Sparks. In his autobiography, titled In Search of Memory,23 Eric
Kandel recalls accepting the mandate of his mentor, Harry Grundfest: “Study
the brain one neuron at a time.” This absolutely needed to be done and it was the
right time to do it, but this was not the key to understanding brain function that
had been hoped for. It did not yield the “neural code” by means of which brain
encodes “information.”
Observe that the collective action of neurons was understood as a necessity by
Golgi even before the discovery of the electroencephalogram (EEG) in the 1920s.
Once the EEG was understood as reflecting the electrical activity of neurons, of
course, their collective mode of action was immediately apparent, even if the func-
tional implications were not yet understood. However, this did not make much
difference at the time. First of all, these two perspectives on the brain remained
largely invisible to each other. When looking at the EEG, the action of individual
neurons is no longer apparent, and when looking at the action of individual neu-
rons, their participation in group activity is not evident. It is as if one only got to
hear the timpani instead of the whole orchestra. Worse than that, neurons can be
part of several different choruses at the same time, and each of these choruses is
non-local, involving the whole brain. In short, the brain yielded its secrets only
In the absence of a formal theoretical model for self-organizing systems, the
approach to the EEG was predominantly phenomenological for most of the 20th
The brain’s neuroelectrical function was described in terms of a rhythmic
activity whose ebb and flow reflected the self-regulatory activity of the neuronal
network. This electrical activity takes place in distinct wavebands that are distin-
guishable in terms of their temporal properties and spatial distributions, reflect-
ing their distinct functional roles. In the 1960s, the availability of the first digital
signal averagers gave impetus to the study of evoked potentials, which turned
out to be a mere perturbation on the passive baseline EEG. It was apparent that
the bulk of brain electrical activity related to the brain’s self-regulation of states,
which was only marginally affected by interaction with the outside world. As it
happens, the evoked potential research bore only limited fruit at the time. The
brain really had to be understood in terms of its organization in baseline.
The mathematical formalism for the understanding of networks did not
become available until the 1990s. The brain is perhaps the most elaborate exem-
plar in the known universe of what is known as the “small-world” model of
networks. This is a combination of high local connectivity—composed of the
dendritic tree on the input site and the axonal branching network on the output
side—and of high distal connectivity. The latter follows from the fact that every
cortical pyramidal cell participates in the communication with distal networks
by means of axons that jointly constitute the cortical white matter. By virtue
of the globally connected network of pyramidal cells, the brain is drawn into
a unitary functional entity, with every part communicating with every other
part more or less directly. As the National Institute of Health (NIH)-sponsored
14  Changing the paradigm from neurochemical to neuroelectrical models

Human Connectome Project has shown, our brain is so interconnected that any
synapse in the cortex is no more than three synapses away from any other syn-
apse in the cortex.24
Because long-distance communication is mediated by the action potential,
the entire communication scheme is subject to very specific timing constraints.
This is where we find the nexus between the microcosm of the individual neuron
and the behavior of the neural assembly. The initiation of an action potential is
dependent on the coincidence of synaptic firing events at the receptor neuron.
This makes neuronal action contingent on cooperativity, and that imposes a fun-
damental timing constraint. By virtue of distal communication, the timing con-
straint ultimately applies to the entire nervous system. Coincidence at the neuron
level translates into simultaneity at the level of the neuronal assembly, which in
turn is observable as local synchrony in the EEG. In this manner, the exquisite
timing control exercised by the brain at every frequency becomes directly visible
to us in the EEG. By the same token, deviations in appropriate timing and net-
work synchronization become evident as well.
Given the dependence of good brain function on universal timing integrity
throughout the brain, we have identified a potential failure mode that could, in
principle, account for mental dysfunctions, either directly or indirectly. A vari-
ety of internal and external factors, like stroke, brain injury, or toxins, can dis-
rupt or inactivate normal patterns of communication among neural networks
through structural disruption of neural integrity. Others, like emotional or phys-
ical trauma or various mental deficiencies, can emerge out of chronic patterns
of electrical instability and/or over- and under-activation in parts of the brain.
The dysregulation of brain timing would be expected to yield what we call soft
failures, rather than the hard failures we might see in a stroke. The functional
deficits are on a continuum, and they exhibit variability and dependencies on a
variety of factors. This is just what we observe.
We can measure or document these patterns of dysregulation by way of quanti-
tative encephalograms (QEEG), functional magnetic resonance imaging (fMRI),
or single-photon emission computerized tomography (SPECT). The QEEG is
most closely identified with measuring the actual patterns of the distinct wave-
bands in various regions of the brain, whereas fMRI and SPECT measure activity
by blood flow patterns, which correspond to neuroelectrical activation.
So let us take a look at the individual elements of this neuroelectrical paradigm.
The 19th century German anatomist Korbinian Brodmann divided the cerebral
cortex into 47 distinct regions, based entirely on differences in cellular structure.
As study of the brain shifted from purely structural classification to functional
classification, it was found that the areas Brodmann had identified, by mere inspec-
tion of differences in appearance and texture of brain tissue, corresponded almost
exactly to specific brain functions.25 For example, Brodmann areas 17–19, located
at the occipital pole, contain the visual cortex. The strip of gray matter that runs
across the brain from ear to ear—Brodmann area 4—is known as the motor cor-
tex. It controls our muscular movements and our sense of where we are in space.
None of the 47 areas performs its specific function in isolation. All rely on heavy
neural interconnectivity with other regions of the brain. This interconnectivity has
1.5  Moving to a new paradigm  15

The brain’s self-regulatory functions

Arousal regulation
Affect regulation
Autonomic set-point and balance
Motor system excitability
Attentional repertoire
Executive function
Working memory
Cognitive processes

been graphically demonstrated with the stunning images from NIH-sponsored

studies at various research centers and collectively called the Human Connectome
Project.26,27 The color-coded renderings show axonal connections running verti-
cally from the cortex down into the brainstem and laterally from one side of the
brain to the other, as well as from front to back and back to front. One of the precepts
of the neuroelectrical paradigm is that this vast net of interconnectivity between
different functional networks is achieved through patterns of signaling that are
near instantaneous. Neurofeedback practitioners using the infra-low-frequency
(ILF) approach have learned that this interconnectivity often produces surprisingly
global effects. Clinical experience has shown that by targeting a specific Brodmann
area with electrode placement on the scalp produces a spillover effect* into more
distal parts. Thus, for example, calming over-arousal in the right hemisphere also
tends to move the whole brain towards balance and optimal self-regulation via this
inter-connectivity (see Chapter 4 for details on how this is done clinically).
This interconnectivity also explains how different regions of the brain interact
to perform self-regulatory functions. To help us understand how these self-regu-
latory functions can become dysregulated and how we can apply neurofeedback
to restore the balance, we can use a simple model of the central nervous system.
The basic building blocks from the bottom up are the spinal cord, the brainstem,
the subcortical nuclei and, sitting on top of that, the cortex.28 The spinal cord
provides input and output to the body and coordinates some reflexive functions.
The brainstem is involved in core physiological functions vital to life. It relays
information to and from the spinal cord and also controls our basic sleep/wake
cycle. Between the brainstem and the cortex are many functional groups of cells,
also known as subcortical nuclei. There are fluid-filled ventricles and a sea of

* This point is illustrated beautifully by the NIH Connectome Project, which shows
that when we train one location (e.g., the temporal pole), there are multiple connec‑
tions across the brain from front to back and from one hemisphere to the other. See
the relationship viewer at
16  Changing the paradigm from neurochemical to neuroelectrical models

astrocytes among the subcortical nuclei, as well as many vertical connections

up to the cortex and down through the brainstem. The limbic system, as part of
the subcortical areas, manages and drives emotions. This is where we assess and
react to internal and external dangers. It is where our learned fears and reactions
to trauma reside. It is also where our priorities and motivations are embedded in
our reward centers.
The cortex mediates detailed analysis of sensory input from the structures
below and then selects and modulates behavioral output. The cortex, as the most
developed part of the brain, also exercises inhibitory control over the subcorti-
cal areas and emotional impulses from the limbic area. Indeed, inhibitory con-
trol is an important factor in how different levels of the central nervous system
work together. Cortical areas process and filter incoming information in the
associational areas of the hindbrain and then send that information forward
for decisional output by the frontal parts of the cortex. Of specific importance
in this process is the prefrontal cortex, the most highly developed region of
our brain. The prefrontal cortex moderates (inhibits) impulses from the lower
regions of the central nervous system and the automatic and reflexive reactions
originating there.
In the ideal of a well-functioning brain, this model is descriptive of what
happens. But what if this top-down hierarchy of control is upset or even turned
upside down? The neurofeedback model considers several types of dysregulation.
The first is physiological arousal, which is under brainstem control, where the
reticular formation can activate a total body alarm response. Shifts in arousal
levels have specific impacts on the brain’s overall level of functioning. In tempo-
rary emergencies, high arousal is useful, as we need to react reflexively for safety
and survival. But chronic stress or trauma can lead to an impairment of the pre-
frontal cortex’s inhibitory control, as the limbic system and brainstem keep us in
a state of hypervigilance and arousal. For example, for persons with PTSD, novel
incoming stimuli, instead of being handed off by the thalamus to the hindbrain
for processing, are routed into the limbic system and brain stem for survival
mode.29 In this switch from thalamo–cortical processing to thalamo–limbic pro-
cessing, the top-down inhibitory control gets hijacked by the activation of over-
powering emotions, like fear, anger, rage, and disinhibited fight–flight–freeze
behaviors. At the other side of the arousal curve is under-arousal. This may
manifest as depression, low physical energy, and lack of interest. It may slow and
impair our decision-making and dull our responses to stimuli.
The brain may also experience state instabilities, which manifest as symptoms
that arise chaotically or with shifts in arousal. Hyper-excitability leads to par-
oxysmal symptoms as the brain flies out of control.28 An electroencephalogram
would show that, in the case of extreme instabilities, whole regions of electrical
circuits are firing at the same time (in phase), indicating a seizure. At a slightly
lesser intensity, we can see that instabilities indicate a loss of internal control, as
in mood swings (think bipolar disorder). In the practice of neurofeedback, we
use a 149-item symptom rating form to ascertain the type and severity of the
above types of dysregulation and then adjust our training strategy accordingly
(see Chapter 4).
1.5  Moving to a new paradigm  17

Let us examine another macro element of neuroelectrical functioning. In the

neurochemical “Soup” paradigm, we saw that chemical changes in charge build
up an electrical charge that travels down the neuron through to the next synaptic
gap. We know that the electric potential generated by an individual neuron is far
too small to be picked up by an electroencephalogram.29 EEG activity therefore
always reflects the summation of the synchronous activity of thousands or mil-
lions of neurons distributed over networks of neurons.30 Measurable scalp EEG
activity shows that these synchronous activities oscillate in wavebands of specific
frequency ranges and spatial distributions across the brain. Certain frequency
bands are associated with different states of brain functioning (e.g., waking and
the various rest or sleep stages). The oscillations of these frequencies are measured
in Hertz (Hz) (i.e., how often an electrical wave crosses a midline in one second).
In the United States, we tend to be familiar with the 60-Hz cycle of our standard
110-volt household current. In the brain, we have a wide range of frequencies that
are usually measured in wavebands of about 4-Hz bandwidths from 0.5 to 40 Hz.
Until recently, the lowest of these we could measure or work with was about 1 Hz.
However (as will be elaborated in Chapter 2), with new instrumentation, we
now can measure and target frequencies as low as 0.01 milli-Hz (now called ILF).
This is indeed a very slow wave and is found primarily in the realm of the astro-
cytes. As explained in Chapter 3, these ILF oscillations are the dominant features
in state regulation of the brain, meaning that they are critical in managing the
functional connectivity of our resting-state networks, as well as managing the
hemodynamics of activation. They are highly responsive at the micro level, while
being resistant to disruption on a larger scale. This is why they have become the
target for the ILF approach to neurofeedback work.31
The first traditional 4-Hz band is the delta frequency from 0.5 to 4 Hz. Delta
waves are predominant during sleep, which is a restorative rest state for the brain,
but if excessively present during wake states, delta can interfere with cognitive
and emotional processing. The theta frequency band extends from 5 to 8 Hz. It
is dominant when we enter into the pre-sleep hypnogogic, dream-like state. We
can also enter into this trance-like state while daydreaming or undergoing hyp-
notherapy. It is the default resting frequency for the prefrontal cortex. Problems
arise when there is too much theta (and delta) prefrontally—recall the discussion
above on too much dopamine and not enough norepinephrine. This condition
would produce distractibility, an inability to focus or pay attention, and poor
inhibitory control—all characteristics most often associated with attention defi-
cit disorder (ADD) and attention deficit disorder with hyperactivity (ADHD).
The next frequency band, alpha (8–12 Hz), is associated with being awake but
relaxed and not processing much information. It is the default resting frequency
for the occipital area. It should be noted that as soon as we close our eyes and cut
off input to the visual cortex (Brodmann areas 12–17), we tend to automatically
generate alpha as that area goes into its default resting mode.
Our sensory motor cortex (Brodmann area 4) runs in a band from one ear
across the top of the cortex to the other. It operates primarily in the 12–15 Hz
range. This band is called either low beta or the sensory motor rhythm (SMR)
band. Activity in this frequency range is associated with monitoring our body in
18  Changing the paradigm from neurochemical to neuroelectrical models

space and movement (proprioception) and also activating or inhibiting muscle

actions. It is involved in regulating emotional stability, energy levels, attentive-
ness, concentration, and impulsivity.
Mid-range beta waves (15–18 or 20 Hz) are noticeable during focused cogni-
tive processing. They usually indicate alert external attention and are critical in
executive functions. In the right hemisphere, the processing of new stimuli and
social–emotional issues are done in this mid-range beta waveband. Activation of
high-level mental processing is usually done in the high beta range. Depending
who is defining it, high beta at the low end starts at either 18 or 20 Hz and extends
up to 22–27 Hz. High beta can also be present when there is chronic over-arousal
from emotional trauma, which prevents key areas in the brain from returning to
their default resting mode (see Chapters 9 and 10).
More fascinating are the gamma waves (40 Hz and up), though what we know
of their function is based on relatively scant research evidence.32 The 40 Hz fre-
quency is said to be associated with neural consciousness via a wave that, origi-
nating in the thalamus, sweeps the brain from front to back, 40 times per second,
drawing different neuronal circuits—including the associational cortices in the
hindbrain, the memory areas of the hippocampus and the cerebellum—into
synch with specific mental constructs, and thereby bringing them into the atten-
tional and decisional frontal area of the brain.33 The hypothesis is that when these
neuronal clusters oscillate together during these transient periods of synchro-
nized firing, they help bring up memories and associations to create new synthe-
ses of ideas and notions, and possibly a changed self-awareness.34 As we learn in
Chapter 8, in autism spectrum children where this associational function of the
gamma waveband seems not to be functioning, we see an inability to generalize
from one social situation to the next. Thus, gamma waves play a critical role in
the acquisition of knowledge from experience and applying it to new situations.
Indeed, we can speculate that this integrative function of gamma waves is critical
to the concept of the brain as a complex self-regulating system.35
As award-winning neuroscientist Nancy Andreasen has shown in her imaging
studies, high levels of activation of these associational areas via the gamma waves
are seen in persons of unusually high creativity.36 Another curious aspect of high-
amplitude gamma waves is that they have been observed in experienced Buddhist
monks in deep meditative states.37 It has been proposed that the activities in the
gamma frequency may be a bridge into the very essence of our own spiritual
self.36 Gamma training has been used by some neurotherapists in the prescriptive
training mode for ADHD and other conditions, but in general, gamma training
has not been utilized widely in neurofeedback. This may be changing, as syn-
chrony training is being explored by some prominent researchers.38

The 60-year-long debate between the Soups and Sparks was resolved by break-
throughs in technology that allowed identification of the action of neurotrans-
mitters at the synaptic cleft in the 1950s. This launched the drive to uncover the
biochemical regulation of human behavior, mood, thought, and functioning. For
References 19

the 60 years since then, a period as long as the Soups and Sparks debate, the
neurochemical paradigm has reigned supreme, while the bioelectrical regulation
of human behavior, mood, thought, and functioning has been either ignored or
Today, breakthroughs in technology, comparable to the invention of the
micropipette and the electron microscope, are bringing the bioelectrical proper-
ties of brain functioning greater scientific awareness. Stunning advances in both
hardware and computer software have given us the capability to use neurofeed-
back to influence the brain’s self-regulatory functions at the very foundational
level of the brain’s self-organizing activities. With current computerized capaci-
ties that were unimaginable even 20 years ago, scientific interest has turned once
again to an investigation of practical applications for a bioelectrical method of
re-establishing healthy currents of electrical activity in the human brain and
body, as one whole functioning bioelectrical being. Years of documented clini-
cal experience by neurofeedback practitioners have established beyond a doubt
that our knowledge of the neuroelectrical properties of the brain can be used
to train the brain into balanced self-regulation (see Part 3: Neurofeedback and
Integrative Medicine in Practice). When the scientific community accepts this
new paradigm for understanding the neuroelectrical functioning of the brain, we
can make another leap in human health. We will be able to use neurofeedback as
a supplement or alternative modality to current efforts for addressing a number
of pressing mental health concerns facing our society.

1. Cited from Foreword to Fisher S. 2014. Neurofeedback in the Treatment
of Developmental Trauma: Changing the Fear-Driven Brain. New York:
Norton. p. xvi.
2. Norden J. 2007. Historical underpinnings of neuroscience. Understanding
the Brain. The Great Courses Six disk Video DVD. Chantilly, VA: The
Teaching Company.
3. Mazzarello P. 1999. The Hidden Structure: A Scientific Biography of
Camillo Colgi. Oxford University Press.
4. Shepherd GM. 1991. Foundations of the Neuron Doctrine. New York:
Oxford University Press.
5. Sherrington CS. 1906. The Integrative Action of the Nervous System.
New Haven: Yale University Press.
6. Bennett M. 2001. The History of the Synapse. Australia: Harwood
Academic Publishers.
7. Loewi cited in Clarke E, O’Malley CD. 1968. The Human Brain and the
Spinal Cord. Oakland, CA: University of California Press, p. 252.
8. Dubois-Reymond cited in Valenstein ES. 2005. The War of the Soups and
the Sparks: The Discovery of Neurotransmitters and the Dispute Over
How Nerves Communicate. New York: Columbia University Press, p. 6.
9. Ibid., p. 6.
10. Ibid., p. 122.
20  Changing the paradigm from neurochemical to neuroelectrical models

11. Brock LG, Coombs JS, Eccles JC. 1952. The recording of potential from
motor neurons with an intracellular electrode. J Physiol 117:431–460.
12. Shepherd GM. 2010. Creating Modern Neuroscience: The Revolutionary
1950s. New York: Oxford Press.
13. Norden J. 2007. Neurotransmitters. In Understanding the Brain. Disc 2,
Section 10.
14. Nunez PL, Srinivasan R. 2006. Electric Fields of the Brain: The
Neurophysics of EEG (second edition). New York: Oxford University
Press, pp. 228–232.
15. Norden 2007. Pathways and synapses. In Understanding the Brain. Disk 2,
Section 9.
16. Watanabe M, Maemura K, Kanbara K, Tamayama T, Hayasaki H. 2002.
GABA and GABA receptors in the central nervous system and other
organs. J Internat Rev Cytol 213:1–47.
17. Knowles JR. 1980. Enzyme-catalyzed phosphoryl transfer reactions. Annu
Rev Biochem 49:877–919.
18. Spiegel R. 1996. Psychopharmacology. An Introduction (third edition).
Somerset, NJ: John Wiley and Sons, p. 45.
19. Kirsch I. 2010. The Emperor’s New Drugs: Exploding the Antidepressant
Myth. New York: Basic Books.
20. Angell M. 2011. The illusions of psychiatry. New York Review of Books
July 14, Vol. 58, 12.
21. Shepherd. 2010. Chapter 15—Neuropsychiatry: The breakthrough in
22. Golgi C. 1967. The Neuron Doctrine-Theory and Facts’, Nobel Lecture 11
Dec 1906. In Nobel Lectures: Physiology or Medicine 1901–1921. p. 216
Elsevier, London, UK.
23. Kandel E. 2006. In Search of Memory: The Emergence of a New Science
of Mind. New York: W. W. Norton & Company.
24. See Accessed on May 15, 2015.
25. Garey LJ. 2006. Brodmann’s Localisation in the Cerebral Cortex. New
York: Springer, retrieved from Wikipedia
Brodmann_area#References on July 8, 2014.
26. Relationship Viewer at
relationship-viewer/. February 2014.
27. Zimmer, C. Secrets of the Brain, National Geographic, http://ngm.
national­ Accessed on May
26, 2015.
28. Othmer SF. 2013. Protocol Guide for Neurofeedback Clinicians (fourth
edition). Woodland Hills, CA: EEG Institute. p. 22.
29. Nunez PL, Srinivasan R. 2006. Electric Fields of the Brain: The
Neurophysics of EEG (second edition). New York: Oxford University
Press, pp. 518–523.
30. Fehmi L, Robbins J. 2001. Mastering our brain’s electrical rhythms.
Cerebrum 3(3).
Brain’s_Electrical_Rhythms/ (retrieved on March 19, 2015).
References 21

31. Othmer S. 2013. The Role of Infra Slow Oscillations in Infra Low
Frequency Training. PowerPoint presentation of April 2013. Woodland
Hills, CA.
32. Bird BL, Newton FA et al. 1978. Biofeedback training of 40-Hz EEG in
humans. Biofeedback Self Regul 3(1):1–12.
33. Melloni L, Molina C, Pena M, Torres D, Singer W, Rodriguez E. 2007.
Synchronization of neural activity across cortical areas correlates with
conscious perception. J Neurosci 27(11):2858–2865.
34. Buzsaki, G. 2006. Cycle 9, the gamma buzz. In Rhythms of the Brain.
Oxford. Retrieved from the web June 27, 2014.
35. Nunez PL, Srinivasan R. 2006. Electric Fields of the Brain: The
Neurophysics of EEG (second edition). New York: Oxford University
Press, p. 458.
36. Andreasen NC. 2014. The secrets of the creative brain. The Atlantic, July/
August. pp. 62–75.
37. Lutz A, Greischar L, Rawlings NB, Ricard M, Davidson RJ. 2004. Long-
term meditators self-induce high-amplitude gamma synchrony during
mental practice. Proc Natl Acad Sci USA 101:16369–16373.
38. Fehmi L, Robbins J. 2008. The Open Focus Brain: Harnessing the
Power of Attention to Heal the Body and the Mind. Boston: Shambala
History of neurofeedback


2.1 The scientific antecedents of neurofeedback 23

2.2 The foundations of neurofeedback in animal studies 24
2.3 Evaluation of SMR reinforcement with human subjects 26
2.3.1 Seizure disorder 26
2.3.2 Attention deficit hyperactivity disorder 28
2.3.3 Learning disabilities and IQ 29
2.3.4 Comparison of SMR training with stimulant medication 29
2.4 Neurofeedback in application to addictions 31
2.4.1 Slow cortical potential training (SCP) 33
2.5 New departures in neurofeedback 33
2.5.1 The beginnings of quantitative EEG-informed training 33
2.5.2 The evolution of mechanisms-based training 35
2.5.3 The migration to lower frequencies 36
2.5.4 Status of the principal approaches to neurofeedback 37
2.5.5 Toward a new departure in feedback 39
2.5.6 The development of infra-low-frequency training 40
2.5.7 The search for a mechanism 42
2.5.8 Understanding infra-low-frequency training 43
2.5.9 Exploiting infra-low-frequency training 44
2.6 Summary 46
References 47


The discovery of electroencephalography (EEG) biofeedback in the 1960s was
dependent on three principal antecedents. These were the discovery of the EEG
by Hans Berger, the development of classical conditioning by Ivan Pavlov, and the
establishment of operant conditioning under B.F. Skinner. The original discovery

24  History of neurofeedback

of the EEG was the result of determined efforts by Hans Berger over the course
of nearly two decades. He was set upon this path by a personal experience of
mental telepathy, which redirected his career into medicine, where he was deter-
mined to find a physiological basis for the phenomenon. In this enduring side
project, undertaken while serving as clinical director of a neurology and psychia-
try clinic, he failed. But despite the limitations of primitive electronics, he was
able to find the miniscule EEG signal. In the face of his own uncertainties, it took
another 5 years for him to publish his findings, which occurred in 1929, and then
it was his colleagues’ turn to be skeptical. It took another 5 years before Adrian
and Matthews replicated his work in England, which served to change the con-
versation. These authors were also the first to observe the effects of synchronous
visual stimulation on alpha band activity in the EEG. Berger had first identified
this prominent EEG rhythmic bursting pattern, which subsequently came to be
labeled the Berger rhythm.
Berger must be considered one of the pioneers of the nascent discipline of psy-
chophysiology, and he is credited with coining the term. Although he did observe
EEG phenomenology in epilepsy, he was not oriented toward the medical utili-
zation of the EEG. For decades, as a matter of fact, the principal utility of the
EEG in neurology remained with those features that were obvious on mere visual
inspection of the clinical EEG. This had the effect of consolidating a rather mod-
est appraisal of the utility of the EEG, one that would prove difficult to dislodge.
The usefulness of the EEG in psychophysiology remained modest as well. The full
exploitation of the EEG would have to await the availability of new tools of both
measurement and of analysis.
Ivan Pavlov received his Nobel Prize for his work on the digestive system of
dogs rather than for his work in classical conditioning, but one set the stage for
the other. In studying salivation, he observed that it often occurred well before
the food arrived. The classical conditioning experimental design placed these
observations in a rigorous framework. He called the anticipatory salivation the
conditional response. Pavlov also studied the anticipatory reaction to aversive
stimuli such as foot shocks, and in one design combined both food reward, sig-
naled by one frequency with the occasional delivery of a foot shock, indexed by
another frequency. When the two frequencies were slowly brought together so
that the dogs could no longer reliably distinguish between them, the dogs tended
to give up on the whole experiment. Some of them even went to sleep.


Six decades later, Pavlov’s study inspired M. Barry Sterman, a research psychol-
ogist and sleep researcher at the University of California, Los Angeles School
of Medicine and the Sepulveda Veterans’ Administration Hospital, in his own
investigations of sleep onset. Pavlov’s dogs had absented themselves from the task
even in the face of the aversive foot shocks. Sterman took this as a paradigm for
the voluntary withdrawal of behavioral responding that we all undertake once
the head hits the pillow with the intention to fall asleep.
2.2  The foundations of neurofeedback in animal studies  25

An operant conditioning design was set up in which cats were trained to

expect a food reward upon a bar press whenever a light came on in their experi-
mental chamber. The trained cats were then taught that whenever a tone was
present, food would not be available. They would simply have to bide their time
until the tone stopped. A behavioral state had thus been induced in which cats
had to withhold their natural tendency to pounce on the bar whenever the light
came on.
The cats had all been fully instrumented for EEG measurements, with elec-
trodes surgically implanted beneath the skull but external to the dura. These
measurements now revealed a bursting rhythm in the sensorimotor cortex that
Sterman named the sensorimotor rhythm (SMR). It was present only during
periods of motoric stillness, and bore a strong resemblance to the sleep spindle
that characterizes stage II sleep in both cats and humans.1 Just as the alpha spin-
dle tends to occur during eyes-closed conditions, the SMR spindle occurred only
during periods of deactivation of the motor system. It was centered at the slightly
higher frequency of nominally 13 Hz.
Once this association was firmly established, Sterman made the food reward
conditional on the appearance of such an SMR burst. All the cat had to do was
to compose itself in a state of quiet anticipation. As hunters, this comes naturally
to them. Beautiful learning curves were acquired over a period of some weeks to
months. Reinforcement on the waking SMR spindles was found to increase sleep
spindle density and improve sleep efficiency.2 Controlled experiments followed,
with both a balanced reversal design and an extinction design, to prove unam-
biguously that operant conditioning of the SMR bursting pattern had occurred.
The reversal design was the first to demonstrate that suppression of the SMR
bursting response could also be trained. This must necessarily occur by an indi-
rect pathway. The cat is fed at regular, brief intervals as long as SMR bursts are not
observable. Even this task could be readily learned. The behavioral response to
the training was that the cats became physically restless and twitchy, indicating a
heightened level of motoric excitability, in contrast to the SMR-conditioned cats,
who exhibited a general calming. The sleep of the SMR-trained cats also changed:
it became more efficient, and the sleep spindle density increased with the train-
ing. In fact, the experiments relied upon the sleep spindle density as the salient
index of change, simply because there was no chance that it might be affected by
the cat’s mood of the moment.
The extinction design made it clear that the conditioned SMR response had
to be understood as a brain response rather than as a volitional response on the
part of the cat. All the cat could contribute to the project of obtaining food was
its motoric stillness, which was not sufficient by itself. This observation is founda-
tional to the entire field of neurofeedback. The process must be understood in the
perspective of the brain and of its engagement with the sensory environment, one
that now also includes the feedback signal that bears directly on its own activity.
Subsequently, Sterman had the opportunity to research the low-level effects of
the toxic rocket fuel monomethylhydrazine (MMH), for which his instrumented
and well-characterized cats were highly suitable. MMH effected the depletion
of gamma-aminobutyric acid, the primary inhibitory neurotransmitter, over
26  History of neurofeedback

the course of about an hour, after which the cats went into seizure. The animals
responded with a high degree of uniformity until the end stage, at which point
the population bifurcated, with a subpopulation showing substantially delayed
seizure onset.
The seizure susceptibility was completely predicted by their assignment to
cohort in the reversal design that had taken place many months earlier. Those
who had received the SMR reinforcement last were selectively resistant to seizure
onset. There must have been a carryover effect from the earlier training. Learning
must have occurred that was not subject to the usual extinction that attends
operant conditioning designs after reinforcement ceases. This experiment, which
was quite unambiguous in its implications, was the signal experiment that estab-
lished the direction and thrust of development in the field of neurofeedback.
Quite unintentionally, the above experiment met all the criteria one would
impose on a fully controlled design. For their part, the cats were not subject to a
placebo response, and the researchers were obviously not biased in that they were
totally blindsided by the outcome. The bifurcation of the response was problem-
atic with respect to the objectives of the research. The experiment had been of a
totally placebo-controlled and fully blinded design, and the implications of the
findings were not equivocal. In follow-up experiments, cats could be character-
ized in terms of their native seizure susceptibility, trained in the SMR paradigm
and then re-tested to evaluate their newly heightened tolerance. Two of the eight
experimental cats from the study remained entirely seizure free despite having
shown all of the prodromal symptoms.3 These results were subsequently con-
firmed by studies on rhesus monkeys as well.4


2.3.1  Seizure disorder
Sterman turned his attention to human trials. An employee in his laboratory suf-
fered from nocturnal seizures and offered to be the first trainee. During training
for only 34 sessions over 4 months, a near elimination of seizures was observed,
which promptly led to a publication.5 It took several years of training to render the
person entirely seizure free, to the point where she qualified for a California driv-
er’s license. An exploratory outcome study on four participants, all of whom ben-
efited from the training, was published in 1974.6 By 1972, Sterman’s research had
attracted the interest of Joel Lubar, Professor of Psychology at the University of
Tennessee in Knoxville. His research group published an outcome study on eight
participants, seven of whom benefited from the training.7,8 Controlled studies fol-
lowed, using either the reversal design or sham training as an ostensibly neutral
control condition. All participants in this research were medically refractory sei-
zure patients whose conditions were stable. Whereas the initial target was motor
seizures, the scope eventually encompassed complex partial seizures as well.
The first study utilizing an A–B–A design involved eight participants.9 Two
reinforcement bands were evaluated: 12–15 Hz and 18–23 Hz. For the reversal
2.3  Evaluation of SMR reinforcement with human subjects  27

phase, Sterman used reinforcements in the 6–9 Hz band. This avoided the lower
EEG frequencies that, if reinforced, could potentially aggravate seizures. The
results were remarkable: six of eight improved significantly in their seizure inci-
dence, with an overall improvement of 74%. This was despite the fact that half the
time had been spent training in the wrong direction, where seizure incidence did
indeed mostly get worse. One of the eight became entirely seizure free, another
very nearly so.
A second such A–B–A study was published by Lubar’s group.10 This was the
first to use a double-blind design. This study also involved eight participants. The
reversal phase utilized a 3–8 Hz band pass. As feared, seizure incidence could
be exacerbated in this manner, and indeed one participant had to be withdrawn
from this phase of the training for that reason. The average reduction in seizure
incidence in the cohort was only 35%. In terms of the five of eight who were
considered “responders,” the mean reduction was 49%, a clinically significant
In Sterman’s sham-controlled study, 24 participants with complex–­partial
­seizures were divided into three groups: a passive seizure-tracking group, a
sham-training group, and a veridical feedback group. After an initial 6-week
training program at a rate of three sessions per week, the two control groups were
given the chance to train for another 6 weeks. All were weaned off the training
over the course of 4 weeks, and a 6-week follow-up period was allowed for. An
overall improvement in seizure incidence of 60% was found in post-testing.11 The
study also included extensive neuropsychological and neurocognitive evaluation,
and these results were published subsequently.12 Those who improved the most in
terms of seizure incidence also tended to improve more on the mental skills test-
ing, as well as on the Minnesota Multiphasic Personality Inventory. The results
also correlated with observed improvements in the clinical EEG. Of the 17 who
exhibited typically abnormal EEG patterns, nine normalized their EEGs, and of
this subset, three brought their seizures fully under control.
In this same time frame, replications were also undertaken as far away as
Scandinavia and Italy. There appeared to be a groundswell of interest in the
method for a time. The results of all the early studies were reviewed by Sterman
in 2000.13 Some 24 studies were evaluated, and these collectively involved some
243 participants. Twenty of these were group studies, and 13 of those included
competent controls. Collectively, 82% of all the participants improved their sei-
zure incidence by at least 30%, with the average improvement being greater than
50%. A more recent reflection on the status of this clinical approach was pub-
lished in 2006.14
A meta-analysis of the epilepsy studies has brought the appraisal up to date.15
Some 63 studies were evaluated for inclusion, but only ten survived the screen.
These involved some 87 participants. The analysis confirmed a “significant”
reduction in seizure incidence. The review included one study that trained par-
ticipants only on the slow cortical potential.16 Strictly speaking, then, the review
consolidated the case for the use of EEG-derived cues in a behavioral strategy
of seizure reduction. This relatively recent meta-analysis reflects the diversity of
approaches that came to characterize the field. This is described further below.
28  History of neurofeedback

2.3.2  Attention deficit hyperactivity disorder

After seizure disorder, the second principal area of clinical interest developed
early around what is now called attention deficit hyperactivity disorder (ADHD),
but at the time was still thought of mainly in terms of hyperkinesis. This thrust
was led throughout by Joel Lubar. This interest was initially kindled by the obser-
vation that a child undergoing training of seizure control also experienced a sub-
sidence of their hyperactivity.7 This observation was confirmed with other such
cases. Since the training was targeting the motor strip, it seemed reasonable to
assume that hyperactivity was being tamed as well. Formal evaluation followed
with children who were not afflicted with a seizure condition.
The first case study was soon published.17 It was postulated that EEG training
would be helpful for those children who were responsive to Ritalin, in which case
the training would be expected to yield additive benefits. The study involved a
14-year-old who was placed on 10 mg of Ritalin for the duration. Six no-drug
and six drug-only baselines were obtained on behavioral and EEG assessments.
A training sequence of 78 sessions of SMR reinforcement, combined with inhibi-
tion on excessive 4–7 Hz activity, was followed by 36 sessions of reversal-phase
training, which in turn was followed by another 28 sessions of the design proto-
col. Placement was bipolar on the left hemisphere sensorimotor strip.
Learning curves were acquired for the incidence of rewards relative to base-
line conditions, and electromyographic (EMG) activity at the chin was tracked as
an index of muscular tone. Both reward incidence and EMG trends reflected the
prevailing protocol to a statistically significant degree. Over the sessions, reward
incidence increased by factors of up to three or four over baseline. It regressed
equally strongly during the reversal phase. Regression was also noted during a
2-week break in the training.
Some 13 behavioral categories were tracked by two independent observers
monitoring classroom behavior. Eight of these were found to be responsive to the
training. Six of these categories had already shown improvement with Ritalin, but
further improvements were observed with the EEG training, and countertrends
were observed during the reversal phase. Five additional categories included four
social behaviors plus self-talk, and these showed no improvement with the SMR
training. In fact, benefits that had been observed with Ritalin were reversed with
the training.
The above was the first of four cases that were treated using the same study
design.18 Two children responded much like the first, and one was non-responsive
to Ritalin as well as the EEG training. In a final phase added to the program, the
three children were successfully weaned off the Ritalin while continuing to train,
and behavioral gains were maintained. Years later, Lubar revisited a number of
clients whom he trained during those early years, and found that the gains had
been retained over the longer term.19
Other studies followed. Tansey was successful in remediating a case of hyper-
activity, developmental reading disorder, and ocular instability with a sequential
combination of EMG and SMR training.20 He utilized a placement on the mid-
line. Normalization of highly elevated EMG levels was achieved, and substantial
2.3  Evaluation of SMR reinforcement with human subjects  29

increases in SMR amplitudes were observed over the course of 20 training ses-
sions. Success was achieved with respect to all three symptoms, and this status
was maintained over a 2-year follow-up period.

2.3.3  Learning disabilities and IQ

Lubar pursued the growing interest in the applications to learning disabilities
with extended training of six boys.21 In this work, beta1 training (16–20 Hz) was
added for enhanced focus of attention and arousal regulation. All of the boys
improved in their academic performance, and all exhibited learning curves with
respect to SMR and beta amplitudes, EMG levels, theta band amplitudes, and
gross movement indicators.
The promise of benefit for learning disabilities eventuated in an investiga-
tion of SMR training of eight mildly neurologically impaired children.22 The
average improvement in Full-Score Wechsler IQ (WISC-R) score was found to
be 19 points. If either verbal or performance IQ lagged the other by more than
14 points, the lagging variable improved by an average of 40% more than the
other. This epoch-making study was followed by one on 24 comparably impaired
children. The average improvement in WISC-R score was found to be 19.75.23,24
Moreover, this was achieved with an average of 27 training sessions, delivered at
the rate of one per week. Both the number of sessions and the pace of training
would now be considered suboptimal, and yet the results were stunning.
Tansey’s extraordinary findings led to a replication in our own clinic using
a left-lateralized protocol and reinforcement at beta1 frequencies (15–18 Hz),
rather than at 14 Hz on the midline. Fifteen children with attention deficit disor-
der (ADD) features and/or learning disabilities were trained just as if they had
been in ordinary clinical practice. Independent testing and evaluation was relied
upon exclusively.25 The average improvement in WISC-R score was found to be
23 points. The profile of average change scores for the subtests of the WISC-R
bore a remarkable similarity in the two studies. Strong improvements in perfor-
mance were also registered on the Benton Visual Retention Test, the Wide Range
Achievement Test, and the tapping subtest of the Harris Tests of Laterality. Not
subject to quantitative assessment were the subsidence of oppositionality, general
improvement in sleep quality among those where it was deficient, and the relief
from persistent stomach and head pain.

2.3.4 Comparison of SMR training with

stimulant medication
Since stimulant medication was already recognized as a treatment for ADHD,
the practical question faced by the medical practitioner consisted of whether
neurofeedback was in fact comparably effective. This essential question was
answered in a study comparing 23 children in each arm.26 Comparison of out-
comes was by means of the TOVA® (Test of Variables of Attention), a continuous
performance test. The results were comparable in both arms, with both methods
showing essential normalization of inattention and impulsivity, accompanied
30  History of neurofeedback

by more modest improvements in mean reaction times, but with substantial

improvements in variability.
Rossiter repeated the same design some 9 years later, with 30 participants in
each arm of the study. The results were better than they had been in 1995.27,28
Both medication management and neurofeedback protocols had improved in
the interim, and the two approaches were now even more closely matched. Most
likely, the neurofeedback strategies benefited from adding pre-frontal place-
ments to the standard protocol. By now, six such studies have been done, all
showing essentially comparable outcomes for pharmacotherapy and SMR/beta
The largest such study involved 100 participants.30 It used the Lubar protocol.
By 1991, Lubar had adopted the “theta–beta ratio” as a criterion of functioning
in the ADHD population, based on the observation that the most prominent
change observed in the EEGs of these children with training was a decline in
theta band amplitudes. An increase in SMR/beta amplitudes was not observed
as consistently.33 Lubar had also adopted the vertex Cz as a standard placement
for the SMR training, on the basis that the theta–beta ratio was typically largest
at this site.
Study participants were selected on the basis of the theta–beta criterion,
among others. All were medicated to a level at which performance on the TOVA
was optimized, with the result that both groups normalized their TOVA subtest
scores. EEG training was undertaken with the neurofeedback cohort until the
theta–beta ratio normalized. This required an average of 43 sessions. Over the
course of training, behavioral variables normalized for the EEG training cohort,
whereas they remained in the clinical range for the medication-only comparison
After a year of the above regimen, medication was discontinued for a week to
allow the children to be evaluated under no-medication conditions. The neuro-
feedback contingent held gains on both the TOVA and the parent/teacher rat-
ings, while the comparison group fell back into the clinical range on the TOVA
and remained in the clinical range on behavioral ratings. A clear advantage had
been demonstrated for the neurofeedback approach using multiple independent
criteria, and medication was not required to sustain the gains.
In 2009, a meta-analysis was published that reviewed the research status of
neurofeedback in its application to the ADHD spectrum.34 The unsurprising
conclusion was that neurofeedback treatment for ADHD can be considered “effi-
cacious and specific,” with large effect sizes for inattention (0.81) and impulsiv-
ity (0.69), and a medium effect size for hyperactivity (0.4). Fifteen studies were
included in the evaluation, and these comprised some 476 participants in the
controlled studies and some 718 in the pre/post-evaluation.35
Ironically, the Monastra study was excluded from the above compilation
because the effect size was so large (2.22) that it failed the test for homogeneity of
the sample of studies. Of course, it did so for the best of reasons. The participants
had been picked on the basis of an EEG criterion, the theta–beta ratio, which no
doubt selected for those most likely to do well with a protocol tailored to that
2.4  Neurofeedback in application to addictions  31

By 2009, then, meta-analyses had confirmed the efficacy of SMR/beta neuro-

feedback in application to epilepsy and ADHD, respectively. Both reviews had
also included studies employing slow cortical potential training.


A third major clinical interest emerged in the late 1980s around neurofeedback
in application to alcohol dependency. This topic also takes us back to the very
beginnings of the field. The original discovery of EEG biofeedback had in fact
been made by Joe Kamiya in the course of his research on the alpha rhythm
of the EEG. Kamiya had originally intended to investigate the relationship of
the EEG to psychophysiological states, and in that quest was testing whether an
individual was able to discriminate the presence of an alpha burst in his occiput
at a given moment. Fortuitously, he had in his chair someone who was able to
learn that task perfectly in just four sessions, over which Kamiya gave him simple
verbal feedback on whether or not he was correct whenever he was prompted by
an occasional tone. By the fourth session, the trainee had an unbroken run of
400 successful trials. Kamiya never again had such a good subject, but the field
was launched. This work took place in 1958 at the University of Chicago.
Within a few years, operant conditioning of the alpha rhythm was undertaken
in Kamiya’s laboratory.36 Its application to anxiety reduction followed.37 Just as
happened with the work of Sterman on epilepsy, as soon as therapeutic benefit
of the training experience was insinuated, the whole procedure was subjected to
heightened scrutiny. It did not help that the alpha training had been brought to
broad public awareness through an interview with Kamiya that was published
in Psychology Today in 1968. This resonated with the zeitgeist of the psychedelic
age, and alpha training became popular in certain circles as a way of inducing
an LSD-like experience without the attendant risks. In the same time frame,
Barbara Brown worked diligently to bring alpha training to broader awareness
within the culture through her books and lectures.38,39
Several replications by teams of academics failed to support Kamiya’s find-
ings, and suddenly the nascent field of biofeedback, which had organized itself
formally in 1989 around this new method of promoting self-regulation, found
itself on the defensive. In particular, one controlled study used alpha down-train-
ing as a control condition, and found that both conditions resulted in improved
anxiety control.40 As the original hypothesis was not supported, alpha training
was deemed a nullity. This is understandable in terms of the theories of the day.
A more modern perspective would hold that both kinds of training can lead to
learned self-regulation. Indeed, bi-directional training has become common-
place in biofeedback.
A second blow was struck with the report that subjects sitting in subdued
lighting under eyes-open conditions were unable to increase their alpha ampli-
tude with training above their own eyes-closed baseline.41 Since this served as a
replication of an earlier finding, the issue was considered settled, and this caused
academics to abandon the research into alpha training. It was soon pointed out
that the negative-outcome studies had been riddled with methodological flaws.
32  History of neurofeedback

For example, Lynch et al. based their negative findings on the basis of a single
training session. But by the time of the sober reappraisal by Kamiya and Ancoli,42
it was too late.
The biofeedback community reconstituted itself around the use of periph-
eral physiology to affect improved self-regulation. Fortunately, the work con-
tinued among a variety of independent groups that included, in particular, one
at the Menninger Foundation that was organized originally by Elmer Green, at
the invitation of Karl Menninger himself. The interests of this group lay with the
study of the dimensions of the human experience, not with the amelioration of
mental disorders. However, their work did inspire such pursuits by others. One
early study yielded promising outcomes in application to alcoholism, and this
kindled a new focus for the field.43
This initial study of the application of alpha training to addictions, among
other influences, led Eugene Peniston to apply the method to his alcoholic vet-
erans at the Fort Lyon Veterans Administration Medical Center in Colorado.44
His first study involved ten Vietnam-era veterans who had had a minimum of
four prior treatment failures. The control participants received only the regular
VA treatment. The experimental participants received some initial exposure to
temperature training, which was then followed up with 30 sessions of what is
now called Alpha–Theta training. This training utilizes reinforcements in both
the alpha and theta bands. The results were stunning. Initially, eight of the exper-
imental participants sustained abstinence after release from the program. The
remaining two, having contemptuously dismissed the EEG training as a mean-
ingless exercise, soon found out that they had lost their tolerance for alcohol, and
perforce became abstinent as well. All the controls stayed true to their prior pat-
terns, and all were readmitted to treatment within 18 months. The experimental
participants were followed up for more than 8 years. All retained their sobriety.
This intriguing research was not welcomed by the biofeedback community
when it was presented in 1990 because it threatened to rekindle the controversy
about alpha training. Nevertheless, Peniston followed with several successful
replications, and other groups did so as well. He summarized his research in
1995,45 and described his method in a book chapter.46 One major criticism was
the limited sizes of the studies, even though they were clearly sufficient in light
of the strong results.
A large-scale study was undertaken in 1994 at an addictions treatment center
in Los Angeles. A total of 121 participants were entered into a controlled study
in which the control was the regular Minnesota Model inpatient treatment pro-
gram.47 An SMR/beta protocol was inserted in place of the temperature training,
but the emphasis again remained on the Alpha–Theta component. At 1 year post-
treatment, it was established that the experimental participants were sustaining
sobriety at a rate three times that of the controls, nominally at 75%. After 3 years,
the control group had mostly relapsed, while the experimental participants had
largely maintained sobriety—albeit with maintenance of group participation
that was a key part of the 12-step-based program. Ongoing sobriety was highly
correlated with continued participation in the group, which in turn was highly
correlated with the prior EEG training experience.
2.5  New departures in neurofeedback  33

What came to be known as the Peniston Protocol was then also evaluated in
a multi-faceted program in Houston to rehabilitate homeless crack users. This
program was large scale and it was extraordinarily effective, with success in plac-
ing participants back into housing and into either an educational setting or a job
in excess of 80%. While it is not possible to parse just how much the neurofeed-
back contributed to this outcome, those involved clearly saw it as the heart of the
therapeutic dimension of this comprehensive program.48

2.4.1  Slow cortical potential training (SCP)

Whereas all of the above developments took place in the United States, a very dif-
ferent method of neurofeedback was being developed by a research group under
Niels Birbaumer in Tübingen, Germany. The discovery in 1964 of the contingent
negative variation (CNV), a transient negative excursion of the surface potential
in preparation for a response, soon led to further observation that the CNV could
be subjected to voluntary control. That in turn led to successful control of the
baseline SCP through operant conditioning techniques.49 As the SCP appeared to
reflect cortical excitability directly, the method was applied to the management of
medically uncontrolled seizures, migraines, and even schizophrenia. The empha-
sis in research, however, has been on ADHD, as in the case of EEG band training.50
The clinical claims were not welcomed in Europe any more than they had been
in the United States, so research focused increasingly on the use of this method
in order to give locked-in patients the capability to communicate. Voluntary con-
trol of excursions in the SCP could be used in a selection scheme for letters of
the alphabet. At a minimum, the success in this application proved the method
to be quite capable of yielding real-time control of the SCP. Given the cognitive
demand, the training could not be done with very young children, but in other
respects, the method was straightforward. A single placement at Cz was univer-
sally used, and there are not many nuances to the protocol. Bi-directional train-
ing of the SCP has been adopted in order to train for better regulation in general.
At each trial during the session, the trainee is given the direction in which the
SCP is to be moved.


2.5.1  The beginnings of quantitative EEG-informed training
Up to the early 1990s, all of the principal neurofeedback protocols were grounded
in physiological models, and hence could be referred to as mechanisms based.
SMR up-training was targeting the down-regulation of motoric excitability. The
accompanying theta band down-training was targeting the improvement of
thalamocortical regulatory control. Alpha band training moved trainees to lower
arousal levels and to residence in calmer states. SCP training reduced cortical
excitability directly.
However, the beneficial consequences could be observed over a variety of clini-
cal conditions, ranging from migraines to insomnia to pain syndromes, which had
34  History of neurofeedback

not been specifically targeted. Cognitive function was often enhanced as well. The
­generality of effects could be best seen in applications to minor traumatic brain
injury (mTBI), where benefits could be seen for the entire range of symptoms char-
acteristic of such injury. At the same time, there was no reason to assume that a
physically injured brain should necessarily respond in the same way as other brains.
In the early 1990s, it became practical and affordable to acquire a 19-channel
digital EEG capability even in a private clinic, and to subject it to quantitative
analysis for comparison against norms. This made it possible to tailor the train-
ing to the specific conditions prevailing in a particular brain. That in turn would,
for the first time, yield the kind of protocol specificity that researchers would be
looking for to validate the technique. Finally, this new capability would give neu-
rofeedback the same “deficit focus” that characterizes psychiatry and psychology.
This need was keenly felt, because neurofeedback still lacked general acceptance
within the health professions.
One consequence of this orientation to the quantitative EEG (QEEG) is that
it placed clinical considerations into the background. Deviation from norms
provided the rationale for the protocol, rather than any specific symptom or
diagnosis. In practice, the observed deviations were often arbitrarily attrib-
uted to whatever diagnosis the person came in with, in order to make the case
for neurofeedback to the client. Effectively, the target was the deviation from
norms. Training could now be done at any site and at any EEG frequency, and
this resulted in a ramp-up of the collective body of experience and of the learn-
ing curve within the practitioner community. Aiding this endeavor further was
the fact that this exploration was taking place in hundreds of individual clinics,
without any central direction. The downside was that this collective effort would
not yield the kind of research that would be persuasive to academia. Hence, neu-
rofeedback would retain its outsider status even in the face of this aspiration to a
scientifically grounded procedure.
There was yet another problem. Neither the field of neurology nor that of psy-
chiatry had yet adopted digital EEG analysis to guide therapies, so the neurofeed-
back field had just multiplied its challenges of persuading the mainstream, rather
than reduced them. It did not help that individual neurofeedback clinicians were
typically not credentialed in EEG diagnostics. Hence, there was the messenger
problem. Further, in its early days, the whole field of digital EEG analysis was
riven with controversies because many issues had simply not yet been resolved.
Expert analysis of clinical cases rarely corresponded between experts. There was
also a fundamental problem lying at the root of the whole enterprise, namely that
EEG deviations sometimes reflect accommodations rather than deficits, which
complicates targeting. Finally, EEG deviations were often so numerous that
clinical judgment was required to establish the appropriate hierarchy of targets.
Meanwhile, the promise of professional guidance toward reliable prescriptions
for training protocols served to attract weak players into the field.
It also transpired that in the new regime, in which the normalization of EEG
parameters became the objective, the up-training of presumptive deficits in the
EEG band amplitudes was found to be much more problematic than the inhibition
of excesses. The latter either worked or it did not, but it rarely caused a problem.
2.5  New departures in neurofeedback  35

The promotion of higher EEG amplitudes, on the other hand, often led trainees
into further distress. In consequence, QEEG-based training came to be focused
largely on inhibiting excesses. For the reward-based training, clinicians typically
defaulted back to the standard protocols that had carried the field to its initial
success. In this manner, the information yielded up from the full-head EEG was
more clearly additive to what could be done with only single-channel derivation.
How is this differential effectiveness of reward- and inhibit-based training to be
understood? The inhibit-based training is typically accomplished with threshold-
based withholding of the rewards. Nothing is actually being inhibited. This
kind of cueing elicits a rather non-specific response on the part of the brain. The
reward-based training, on the other hand, is much more specific in its appeal
to the brain, and the specifics matter. In our own implementation of the SMR/
beta protocols, for example, we consistently observed a preference for higher-­
frequency training in the left hemisphere over the right. This finding came about
in an interesting way. We had started out with left-hemisphere training in the
beta1 band (15–18 Hz), following Margaret Ayers, who had been a graduate stu-
dent of Barry Sterman.
Ayers had found the higher band to be more consistently helpful for her head
injury and stroke patients.51 We then added SMR band training at Cz, following
Tansey and Lubar, for ADHD children. A move from Cz to C4 then led to much
more hemisphere-specific effects. Thus, our standard protocol became a combi-
nation of “C3beta and C4SMR,” with the two protocols titrated as needed. This
approach became broadly popular within the field, and was adopted by several
thousand practitioners over the years. This was the protocol employed in our
large practitioner survey on ADHD.35

2.5.2  The evolution of mechanisms-based training

By the mid-1990s, even our standard mechanisms-informed, protocol-based
training was subjected to evolution. It was observed that trainees who happened
to be particularly sensitive to the training responded in a highly frequency-
specific manner. The training needed to be individualized with respect to the
rewards as well as the inhibits. First, the intermediate frequency of 15 Hz was
provided. Then, adjustment in 0.5-Hz steps was provided for. Eventually, even
finer frequency divisions turned out to be advantageous. Such a high frequency
specificity has never been adequately explained.
This surprising finding led to our adoption of an optimization strategy for
each client, one in which the best reward frequency needed to be determined
through sequential A/B comparisons. The optimization had to be accomplished
by tracking the sometimes-subtle responses of the client through the sessions
and from session to session. It could not be done by merely inspecting the EEG.
This finding sheds light on the difficulties that had been encountered earlier with
the QEEG-based training, because the requisite discrimination of the optimum
target frequency is just not possible on the basis of the EEG.
The discovery of the frequency specificity of reward-based training gave per-
mission for the migration of the reward frequency beyond the standard bands
36  History of neurofeedback

in pursuit of the optimum training frequency. In fact, for many individuals, this
became mandatory. This, together with the liberation from the standard train-
ing sites that had already been accomplished with the adoption of digital EEG
analysis, led to yet another period of rapid clinical progress. Looking back on
this period, however, it is apparent that every step into the unknown was under-
taken cautiously. Every incremental step forward was thoroughly consolidated in
empirical support before additional steps were taken.
With the availability of 19-channel data for the display of spatial maps, atten-
tion shifted to site-specific data and away from the bipolar derivation that had
been customary in clinical EEGs. Furthermore, in the conceptual frame of tar-
geting EEG anomalies, it had also become obligatory to undertake single-site
training. This is referred to as referential placement, which means that only a
single active electrode is placed over the cortex, with the other active electrode—
referred to as the reference—placed on a quasi-neutral site, such as an ear lobe.
This meant the abandonment of the bipolar montage that had been standard for
Sterman and Lubar—even for the standard Sterman and Lubar protocols. We
had found the Sterman and Lubar protocols to be quite adequate for our pur-
poses, and with the impetus to move beyond the sensorimotor strip, we later
returned to bipolar montage so that we could at once explore new sites while
keeping one foot planted, so to speak, on the familiar turf of the sensorimotor
strip. As Sterman felt the need to point out, the sensorimotor rhythm is only
observable on the sensorimotor strip. By moving the other electrode off the strip,
we were training the relationship between the two sites. The training effect was
enhanced nicely by virtue of the incorporation of frontal and prefrontal sites, but
possibly also by virtue of the return to bipolar montage.
The increase in sensitivity of the training that was purchased with bipolar
montage brought about a heightened awareness of the frequency specificity. This
was particularly an issue with those who responded very sensitively to the train-
ing, such as migraineurs and fibromyalgia patients. It was the challenge of sensi-
tive responders that led us progressively to new placements and new regions of
the EEG spectrum. Over the course of some years, the entire conventional EEG
spectrum, from 0.5 to 40 Hz, was eventually encompassed. During this initial
exploration, we found the distribution of optimum target frequencies to cover
the entire spectrum.

2.5.3  The migration to lower frequencies

The greatest challenge we confronted in that time frame (1999–2004) was the
progression to ever-lower frequencies. We proceeded into this terrain with some
trepidation because of the known hazards of training at low EEG frequencies that
Lubar and Sterman had already exposed. The difference was that we were now
armed with the knowledge that training had to take place under very specific con-
ditions. We therefore actually had complete consistency between the new and the
old findings. The problem that had been identified by Lubar was that up-­training
toward greater EEG synchrony was potentially a risk, particularly in conditions
such as epilepsy, where excess synchrony is a known hazard. Under specific
2.5  New departures in neurofeedback  37

conditions, however, this could now be managed. The use of bipolar montage
biases the training toward de-synchronization of the target frequency between
the two active sites.52,53 Lubar had used bipolar montage as well, but that was not
enough to render the training benign in his early study on seizure disorder. With
careful adjustment of the training frequency, however, the effects were not only
favorable, but rather more powerful than we had been accustomed to. This led to
breakthroughs with clinical conditions that had not yielded to the earlier higher-
frequency training. These positive developments encouraged further exploration,
and that led eventually to the exploration of the infra-low-frequency regime, the
clinical approach that is featured in many of the chapters of this book.

2.5.4  Status of the principal approaches to neurofeedback

Before that topic is taken up, however, a perspective on the context in which this
development took place is in order. Progress was being made in all of the princi-
pal ways of doing neurofeedback that have been described. QEEG-based training
evolved in the direction of targeting the coherence between two sites, rather than
amplitudes at a single site. This made for more dynamic and impactful training,
just as we had found when moving from referential back to bipolar training in
our own approach. Representative studies that reflect the state of the art of this
approach exist for migraine,54,55 TBI56,57 and schizophrenia.58,59
Site-specific targeting also evolved further. This approach could be aided with
the use of LORETA, a program that constructs a source distribution of virtual
dipoles that is consistent with the prevailing EEG at the 19 sites. With the appli-
cation of physically realistic constraints, the infinity of such solutions that exists
in principle can be reduced to just one. This procedure can be used to refine tar-
geting and to focus on sources at depth within the cerebrum. It can also be useful
in the pre/post-evaluation of training procedures.
Inhibit-based training also matured as a standalone approach in two princi-
pal manifestations. In the first, the brain is regarded as a non-linear dynamical
system, and the EEG is seen to reflect those properties. This means that the EEG
cannot be properly analyzed in terms of Gaussian distributions. On the contrary,
EEG parameters are known to exhibit scale-free statistics, or very broad distribu-
tions that may be well approximated by power laws. In the Gaussian perspective
that we continue to press into service, it would be said that there are long tails.
In essence, stationarity of the EEG cannot be assumed. What is measured at one
moment is not necessarily replicable at another moment. Hence, fixed thresholds
are contra-indicated. Excursions into dysregulation are detected dynamically at
two bilateral sites (C3 and C4) on the sensorimotor strip, and the brain is cued
with respect to these excursions. All the drama that attends reward-based train-
ing because of the decision-making involved is avoided. Since no clean boundary
between function and dysfunction is discernible in the EEG, the tactical choice
is made to inhibit only the extrema in the tracked variables. This increases the
likelihood that the fouls being called on the brain are indeed episodes of dys-
regulation. A study was recently published in which this method was used in the
recovery from “chemo-fog.”53
38  History of neurofeedback

The second approach seeks to enhance the reliability in the discrimination of

dysregulation by force of large numbers. By tracking a number of EEG param-
eters (band amplitudes and site-to-site coherences) for several sites over time,
advantage is taken of the fact that correlation between the measures increases
as the brain enters a state of dysregulation. Superposition of all the measures
then yields a collective index to the instantaneous state of dysregulation of the
whole system. The reliability of this index increases further as the brain reaches
extremes of dysregulation. In practice, the trainee is simply exposed to the time
course of this index, which serves as an incremental guide to more regulated
states and, ultimately, to clinical success. Since this method is typically based on
deviations from normative behavior, it is referred to as Z-score training.
The bulk of the work in the clinical realm is still being done with variations on
the standard SMR/beta protocols, combined with one inhibit strategy or another.
Placement is either on the midline at Cz, straddling Cz on the midline in bipo-
lar montage, or using the traditional lateralized placements such as “C3beta/
C4SMR,” which likely remains the most common choice.
Alpha–Theta training has also been adopted quite broadly as a complement to
the SMR/beta training. The thrust here is very different. Whereas the intellectual
frontier in this field has all along been the challenge of functional normaliza-
tion, there has remained a persistent need to redress the psychological residue
of prior traumatic experiences or of a traumatic early childhood. This can be
accomplished with Alpha–Theta training, and more effectively after a measure
of physiological stabilization has been achieved. The Alpha–Theta training qui-
etens the outer-directed faculties that keep one rooted in the present moment and
calms the fear-driven self. Hence, it allows a journey to the interior realm, where
historical traumas can be resolved while the person is resident in a perceived
calm and safe place. The intent in this training is entirely experiential.
For many who encounter this training, the effect is transformational. In par-
ticular, it is those who come with a trauma history who find this experience
healing. This can go a long way toward explaining the early reports of dramatic
spiritual experiences with alpha training that were so off-putting to the aca-
demic community originally. Having fled their families, those youngsters who
were drawn to Haight-Ashbury and the drug experience were likely also those
who would respond powerfully to Alpha–Theta training. By the same token,
those same experiences would not easily be replicated with research subjects
plucked from among engineering students. In retrospect, it is apparent that all
the early “magical” claims for alpha training have since been validated in clini-
cal experience.
Alpha training has also played a large role in training toward functional nor-
malization and the enhancement of our attentional capacities. This is the work of
Lester Fehmi, which also had its origins in the early days of discovery of alpha train-
ing. Fehmi relies heavily on the language of attention, thus recruiting the individ-
ual actively into the task of self-regulation practice. The objective is to move from a
narrow and objective focus to a broader, more inclusive focus, and from a separate
to an immersive presence. This shift is accompanied by a lowering in arousal level,
albeit with the maintenance of alertness. Reinforcement on alpha band activity
2.5  New departures in neurofeedback  39

supports this shift, and it does so even more strongly when the training promotes
whole-brain synchrony (read: coherence) of the alpha signal explicitly.53
Jim Hardt has also relied on the promotion of alpha synchrony for most of his
work. His engagement with this field extends all the way back to his days as a grad-
uate student of Joe Kamiya, given impetus by his own impactful first alpha training
experience. He had also been an engineer. Hardt offers intensive programs in alpha
training that also incorporate group therapy to support personal transformation.
More advanced training is offered with an emphasis on the theta band.57
Yet another approach that had an early start is one that emphasizes 40-Hz
training. This training was first investigated by Sheer, targeting cortical func-
tion.59 The 40-Hz region is one where EEG synchrony is commonly observed in
the engaged brain, meaning that bursts of such narrow-band activity are readily
discernible above the background. As with other synchrony training, the train-
ing is experienced as both calming and alerting. But the subjective response is
typically distinct for each of these frequencies, in that different network configu-
rations are being appealed to in each case.

2.5.5  Toward a new departure in feedback

The range of clinical conditions that are presently addressed with one or more
of these methods now extends to nearly the entire spectrum of psychiatric con-
ditions, plus many neurological conditions. The best evidence indicates that
neurofeedback can be far more effective than pharmacotherapy alone or psycho-
therapy alone. The best evidence in this case is to be found in the clinical realm,
where clients typically come to neurofeedback late in their clinical trajectory and
are already getting treatment to current standards.
The implications are clear. Psychiatric and neurological conditions involve
learned brain behavior that cannot readily be undone by means of pharmaco-
therapy or talk therapy alone. Yet this learned behavior is accessible to us through
methods of relearning. It is appropriate, therefore, to think of neurofeedback as
a modality of rehabilitation, by analogy to physical rehabilitation. Just as there
is a complete continuum between physical therapy and training for optimum
functioning in the athletic realm, there is complete continuity between feedback-
based rehabilitation and optimal mental capability—not only in the cognitive
realm, but the affective realm as well.
This core reality has been somewhat obscured by the fact that neurofeedback
has had to find its place within the framework of our disease- and disorder-
focused health care model. Within that model, problems need to rise to a given
level of severity before they get any attention. Inline with that model, neurofeed-
back strategies have been favored that maximally emulate the prevailing focus on
the discrete disorders. This becomes obvious in the focus on features of the EEG
that manifest the dysregulation status. The immediate target is not the disorder
itself, but rather the landmarks of disorder, implicitly the dysregulation status
per se. Without question, this approach has borne abundant fruit, and therefore
its validity is not in question, but the approach remains incomplete. Alas, some
of the most disturbing and intractable mental disorders cannot be discerned in
40  History of neurofeedback

the EEG at all by current methods. The personality disorders are a case in point.
These are also the conditions that first take root in the course of early develop-
ment. Dysregulation status is not reducible to what can be readily detected in the
EEG. A different approach is needed to complement what we already have.
Throughout our quarter century of work with neurofeedback, we had always
stymied by the most intractable end of the distribution of severity, irrespective
of the particular diagnosis involved. This might involve migraines, fibromyalgia,
depression, anxiety, Tourette syndrome, obsessive compulsive disorder (OCD), or
substance dependency. Then there were the conditions that had remained relatively
intractable to remediation, such as chronic pain syndromes, the developmental dis-
orders of childhood, borderline personality disorder, dissociative identity disorder,
and addictions. Almost all of these most challenging and even intractable cases had
a problematic early childhood history in common, with a preponderance of emo-
tional trauma. We were confronting dysfunctions that had had a whole lifetime to
be elaborated and consolidated. In other cases, a vulnerability appears to have been
created that was later exposed through further physical or emotional traumas.
Since 2006, inroads have been made with a new clinical approach that allows
us to address even the most challenging cases that are seen in psychiatry out-
side of institutional settings. This method is a radical departure from all existing
approaches. It cannot be understood in terms of the existing models. It is not
deficit focused and it is not prescriptive. It is not a close-order drill to micro-
manage the brain and teach it how to behave. This method allows the brain to
acquire new capacities for self-regulation in the same way that it learns other
skills. Even in the face of all that has already been accomplished with various
methods of neurofeedback, this new approach is deserving of special treatment,
and for that reason, this book is largely devoted to this one approach. We now
turn to the further elaboration of the development of this method.

2.5.6  The development of infra-low-frequency training

By 2004, we had explored the EEG spectrum across the entire “conventional”
range, from 0.5 to 40 Hz, and found individuals who were optimized in all regions
of this spectrum. We were constrained, however, by our software, which limited
us to a 3-Hz bandwidth. This meant that the lowest center frequency we could dial
in was 1.5 Hz. Over time, client data piled up to the point where it was obvious that
the lowest frequency was preferred by more clients than any other. This motivated
the investigation of yet-lower frequencies. This transpired in 2006.
We found software that allowed us to extend the range to 0.1 Hz, expecting
of course that those who had been optimized at 1.5 Hz would now distribute
themselves over this wider range. Instead, we observed that the new distribution
was even more strongly skewed toward the new lowest value than had been the
case before. In fact, some two-thirds of all our clients exhibited a preference for
the lowest frequency of 0.1 Hz. This frequency was too low for our conventional
methods of signal handling, and accommodations had to be made.
In the conventional frequency range, the narrow-band signal was rectified and
smoothed in order to yield the magnitude of the EEG in the particular frequency
2.5  New departures in neurofeedback  41

band. At 0.1 Hz, that process is too slow for good feedback, so instead we simply
had the trainee watch the EEG signal go up and down with its periodicity of ten
seconds. This actually worked quite well. That was not entirely unexpected, how-
ever, because we had already been feeding the continuous band magnitude back
to the client over all these years to accompany the discrete rewards. The intent
all along had been to promote engagement of the client with the process. But
the brain was clearly also deriving information from the ongoing signal stream,
so it was more engaged with the process for that reason as well. The continuous
signal was information-rich by comparison to the discrete rewards, and as such
was responsible for the exquisite frequency sensitivity of the training that we had
observed. The same thing was now happening with the actual signal. The brain
got all the information it needed for the low-frequency training from the time
course of the continuous signal. This struck us as remarkable on first encounter,
but at another level, it was also not unexpected. After all, we had undertaken this
initiative in the expectation of success.
In the low-frequency region, the simple expedient of tracking the actual sig-
nal instead of the amplitude envelope meant that the discrete rewards no longer
made sense. Thresholds had lost their meaning in this new context. We would
have threshold crossings once every cycle, and they would not convey signifi-
cance. With the abandonment of discrete rewards, it also became clear that we
had entirely cut our moorings to the operant conditioning model that had been
a central pillar of the entire development of neurofeedback. The operant con-
ditioning model had been our lodestone. Indeed, Sterman’s cat data stand as
elegant exemplars of that kind of learning. Now, another explanation was clearly
needed. We will return to this conundrum later.
In the clinic, the path was clear. With clients piling up at the lowest frequency,
the range obviously needed to be extended further. It was extended another order
of magnitude, to 0.01 Hz, early in 2008. We were now dealing with a rather slowly
changing signal, and yet the brain seemed to handle it much as it had before. Over
time, the same pattern we had observed before was once again repeated. About
two-thirds of the clients were optimized at the lowest frequency. The range was
hastily extended yet another order of magnitude to 1 milli-Hz, or 1 mHz, later in
2008. Yet the same pattern emerged over time as we became acquainted with this
new regime: cases piled up at the lowest frequency available. Finally, as the range
was extended in 2010 to 0.1 mHz, a similar pattern once again developed. Some
two-thirds of clients eventually ended up preferring the lowest target frequency.
A frequency of 0.1 mHz implies a period of 10,000 seconds, or a period of 2.8
hours. We did not have to be told that training a frequency this low is an absur-
dity. Yet the brain was responding as promptly as ever. In fact, the overall train-
ing process was more demanding than it had been before, quite simply because it
was stronger in its impact. It needed to be done right, which meant in particular
that the choice of target frequency was critical. But just how did the frequency
enter the picture? In the conventional view, an outside observer would have to
track the signal for a good part of a whole cycle in order to know the precise
frequency being represented. And yet the brain was responding quickly, and in a
way that was very frequency specific. On top of everything else, the signal did not
42  History of neurofeedback

even appear very sinusoidal, which meant that the signal unfolding on the screen
was not necessarily the target frequency; that is, the center frequency of the filter.
The laws of nature—or at least the principles of signal processing—appeared to
be violated.

2.5.7  The search for a mechanism

At this point, I would hate to deprive a certain kind of reader of the challenge of
figuring this out, so for these people, it is recommended that they stop reading at
this point and see if they can puzzle this out on their own. For everyone else, and
for those who gave up trying to figure this out, what follows is the explanation of
what is happening in this process. It is best to start with an anecdote that makes
matters concrete: at a professional training course, an attendee had just been
wired up to experience the training for the first time. After just a few minutes
of training, she found herself feeling distinctly different from before, but had no
idea why. She was urged to report how she felt, because this was the beginning of
the process of hunting for the optimum response frequency. Everything was hap-
pening as expected, except of course for the specifics that related to this person.
But a psychologist in the audience who was thoroughly steeped in the operant
conditioning model leapt out of his chair and blurted out with finality: “This is
not operant conditioning.”
Indeed it is not, but we do have something to explain here. The brain had gone
into action on the basis of the information that was being provided, and we had
nothing to do with the specifics of that. To understand this process, matters have
to be regarded from the perspective of the engaged brain, not that of an outside
observer. The low-frequency filter shapes the information going back to the brain
about the EEG so that it contains only low-frequency information. This would
appear to preclude a rapid response on the part of the client. But even though the
frequency response is slow, the transient response is not. The transient response
is merely attenuated by the filter, but it is still present. Most significantly, it is still
present in real time. Even slow brain rhythms must respond to environmental
demands, both internal and external, and they must do so promptly. The signal
processing does not obliterate that information. It does not delay the signal, it
merely attenuates it.
The brain is able to detect the subtle changes in the signal because it is expect-
ing them, and therefore is looking for them. As soon as the brain recognizes
that the signal on the screen is somehow reflecting an aspect of its own activity,
it ceases to be the naïve observer of an innocuous signal. The brain then relates
to the signal as its own output, but the particulars of the relationship remain
obscure, at least at the outset. The brain goes into a hypothesis-testing mode. It
assumes command of the situation, if you will, and attempts to anticipate, con-
trol, and manipulate the signal. This is just how the brain deals with information
about its more direct interactions with the world through movement. Movement
that the brain cares about is always the execution of an intention, and then the
brain renders an ongoing judgment about whether its intentions are being suc-
cessfully executed. Finally, it takes corrective action, such as a fine adjustment of
2.5  New departures in neurofeedback  43

the activity. All the elements are there: prediction, comparison to a template, and
correction. The “movement” of the EEG signal is treated analogously to the man-
ner in which the brain treats actual movements of the body.
A fruitful way to regard brain function is to see it as being organized for the
regulation of movement. Clearly, this has become a highly refined skill on the
part of our brain. All that is required to understand infra-low-frequency neuro-
feedback is to realize that this entire repertoire of refined regulatory control can
now also be applied to the brain’s internal activity, as reflected in the EEG. This
capability extends to every function that is subject to regulatory control by the
brain and can be made “visible” to the brain through its EEG. The brain relates to
the outside world as an agent, and the feedback allows the brain to encounter its
own EEG also as an agent.
The EEG is a correlate of brain activity, and so is the dance reflected in the
mirror in the dance studio. The brain is directly in charge only of its own neuro-
nal activity, but it adjusts its responses on the basis of the correlates that imple-
ment or reflect that intrinsic activity. Nearly all of the brain’s activity with respect
to its axonal communication is regulatory in nature, and that is distilled for us
in the EEG in large measure. Finally, the refinement of the regulatory role that
results from the brain attending to itself then plays through the entire hierarchy
of regulation.
Infra-low-frequency training has shown us that the brain can enhance its
own self-regulatory capacities through conventional skill learning. It is not nec-
essary to install an operant conditioning paradigm. This also means that voli-
tional engagement is not required, nor does the process impose high cognitive
demands. This makes the training available even for working with infants. Even
the infant brain is doing its best to come to terms with its environment, and is
quite capable of becoming entranced with its own EEG. When it comes right
down to it, if we have given the method an appropriate interpretation, should that
same explanation not also serve to explain operant conditioning? Indeed, it does.
With the point of departure that the brain is to be understood in the first
instance by its role as agent rather than in its role as observer, we can also view
the operant conditioning paradigm in that perspective. Once the brain is exposed
to a sequence of discrete rewards that begins to look like a pattern, it will simul-
taneously register those events that are correlated with it. These can be external
events, internal activity or external events that reflect internal activity. The brain
will then resort to its predictive algorithm to do hypothesis testing on the various
correlations. Eventually, only a single correlation will survive the screening, but
the hypothesis testing continues. This explains both the extinction phenomenon
and the observation that a program of partial reinforcement is most resistant to
extinction. Under the latter, it is most difficult to be certain that circumstances
have indeed changed.

2.5.8  Understanding infra-low-frequency training

On the one hand, we have the well-established operant conditioning model, and
on the other we have what we call the prediction model, one in which the brain
44  History of neurofeedback

reacts to the ongoing signal on the basis of its own interpretation of the signal, and
the resulting projecting of the signal into the future. If an equivalence between the
two methods can be drawn, what then is the advantage conferred by the infra-low-
frequency training? First of all, there is the matter of information density. In the
infra-low-frequency training, the signal is continuous rather than discrete. There
is more information per unit of time, first of all, and secondly, the continuous sig-
nal offers greater traceability to the underlying activity that the brain is trying to
regulate. There is more subtlety and precision, which leads to finer control.
But it has already been said that we have had the continuous signal as part of the
feedback all along, so there must be yet another advantage to training in the infra-
low-frequency regime to compensate for the fact that there is less “information”
forthcoming per unit of time than at higher frequencies. This may have to do with
the fact that, in this region, the signal reflects more purely what the brain is trying
to manage—cortical activation. At higher frequencies, the EEG signal is much more
complex, and reflects many influences, only one of which is local cortical activation.
Once the advantages of training at infra-low frequencies are apparent, it is also
clear that, at these frequencies, there is very little choice about how the training
must take place. We know of no viable alternative to the “waveform-tracking”
approach to training. But even if that is accepted, there remains the question as to
why there is such a strong preference for the extreme low-frequency training. What
advantage do we derive from training at such a specific frequency? At this point, we
are reduced to mere speculation. The most common target frequency of nominally
0.1 mHz falls into the range of our basic rest–activity cycle (BRAC) of 90–120 min-
utes. This may be the lowest periodicity governing our cerebral activation that is
dynamically managed. The circadian rhythm, by contrast, is under tighter control
by a number of clock genes. This topic is given further consideration in Chapter 3.
It seems only too likely that we are interacting with the mechanisms that gov-
ern this periodicity of tonic cortical activation. The periodicity of the BRAC sug-
gests that the governing mechanisms are organized as a resonant system and act
to maintain the system in resonance status. If that is the case, then we would
expect to encounter some of the properties of a resonant system.60 One feature
is that the behavior of the system is most strongly frequency dependent within
the vicinity of the resonance frequency. Another is that the system behaves most
benignly at the resonance frequency. A third is that the behavior can be very dif-
ferent in the near neighborhood of the resonance frequency. All these observa-
tions hold true for this kind of training.

2.5.9  Exploiting infra-low-frequency training

The direct engagement with the regulation of cortical activity ties us directly into
arousal regulation governed by the brainstem. This in turn can be seen as the
foundation of our entire regulatory hierarchy. By suitable site selection, the train-
ing can then be focused on higher rungs of the regulatory hierarchy, with auto-
nomic regulation and affect regulation being the first among them. Surprisingly,
perhaps, a wide variety of rather intractable symptoms fall away with just one or
two key placements that address the bottom of the regulatory hierarchy.
2.5  New departures in neurofeedback  45

The early work with SMR/beta protocols had already given evidence of sys-
tem-wide impacts that appeared to have no particular connection to what was
going on at the sensorimotor strip. The conclusion that we are interacting with
a highly integrated regulatory regime was already inescapable at the time. With
infra-low-frequency training, this system was being engaged at its most foun-
dational level, and that yielded immediate clinical benefits. One is tempted to
draw the conclusion that the principal problems in brain regulation lie at the
foundations rather than—to pick an example—in the specifics of higher cogni-
tive function and the subtleties of attentional failure. By facing the problems of
learning disabilities early on, we were tackling the issues in the wrong order. We
were starting at the wrong end of the regulatory hierarchy.
Infra-low-frequency training has now given us access to the infant brain in its
age-appropriate stages of development. By the same token, it has given us access to
all those disorders that could be traced to early childhood developmental lacunae
or misdirections: traumas of neglect and abuse; physical injury to the brain; birth
trauma; high fevers and brain infections; and emotional crises in early childhood,
for example. It has been clear for a long time that the most intractable disorders
encountered in psychiatry are traceable to disruptions in the normal developmen-
tal trajectory for one reason or another, or because the psyche had simply been
under prolonged siege during its formative stages. We finally have a way of effec-
tively reaching back into those early developmental years and redressing the mal-
formations of regulatory networks. The success of infra-low-frequency training
made it unambiguously apparent that even though the behavioral consequences
appeared therapeutically intractable, the causal chain lay largely in the functional
realm and was therefore accessible to us for remediation.
Indeed, we know that “structure follows function,” but we can take that in
both directions. We can understand the intractable disorders in terms of the
equivalent dictum, “structure follows dysfunction,” but with a persistent appeal
to function, the process can now be substantially walked back. Having finally
“discovered” brain plasticity in the mid-1990s, neuroscientists came to see it
mainly in positive terms. However, one can also understand mental disorders in
terms of brain plasticity mediating accommodations under duress. In the case of
shock trauma, for example, such accommodations can even be appropriate in the
immediate context, and yet be detrimental over the longer term. The term “plas-
ticity diseases” has been invoked to classify this phenomenology.
In conventional therapies, the dysfunctional network status is the point of
departure (irrespective of whether that is part of the operative model). If the par-
ticular therapy does not resolve the core dysregulation, however, then the resolu-
tion can only be partial. Symptom relief may be obtained, but the core dysfunction
remains, and may even be further consolidated. With infra-low-­ frequency
­training, the appeal is made directly to the core issue of the regulation of corti-
cal activation and of central and autonomic arousal. Once it is firmly established
that this is possible, it also follows that it is obligatory for the therapeutic com-
munity. The ineluctable reality of the domain of mental disorders is that the most
intractable among them are trauma-based. If the potential exists to remediate the
consequences of physical and emotional traumas of early childhood, then that
46  History of neurofeedback

must become the therapeutic priority. We know by now that these calamities can
be remediated even in very young children, and they can also be remediated later
in the adult stage. It is for this reason that a relatively new therapeutic approach,
arriving late upon the scene, deserves to be treated as its own entity in this book.
Over the last decade, new findings in the realm of brain functional imaging
have provided new theoretical support for the above claims. This is the discovery
of our “resting state networks.” The term has its basis in the historical develop-
ment of functional magnetic resonance imaging (fMRI). For years, comparisons
were being made between activated states and the baseline state, when at some
point it was realized that the baseline state was itself active. In fact, its activity
totally dominates what the brain does at any moment. Engagement with the out-
side world is never more than a perturbation of baseline activity.
It seems reasonable to propose, therefore, that our good function hinges largely
upon the organization of our baseline state, which is called the default mode net-
work.61,62 A secondary concern is then the smooth integration of the task-negative
network with the task-positive networks. This coordination is mediated by the
salience network.63 In a groundbreaking paper, Menon made the case that much
of psychopathology is traceable to dysregulation in the coordination of the default
mode and the central executive networks, as mediated by the salience network.64
As it happens, the empirically derived electrode placements of our key proto-
cols match up with those key nodes of the default mode network that are accessible
to us at the cortical surface. It appears that our primary pathway of intervention
is to restore the internal functional connectivity of the default mode network.
Subsidiary protocols then address the smooth integration with the central execu-
tive network, the key task-positive control network and the salience network that
mediates between them. Recently, evidence derived from fMRI measurements has
documented the up-regulation of the salience network with neurofeedback.65
With infra-low-frequency training, we restore the proper hierarchy to the ther-
apeutic agenda. This hierarchy recapitulates the original developmental sequenc-
ing. This sets the stage for other therapies to follow, if necessary. Surprisingly,
however, if the proper hierarchy is respected, a lot gets done with as few as four
basic protocols. This statement is given substance in the remainder of this book.

By virtue of all the research and clinical work that has been done over the last
40 years, the following propositions have been established beyond doubt among
reasonable people: (1) the brain is responsive to information about its own EEG;
(2) the brain is capable of utilizing this information to enhance self-regulatory
control; and (3) the new capability is a learned response that is then reinforced
through ongoing activities of living. The evidence alluded to in the remainder
of this volume testifies to the utility of infra-low-frequency training in address-
ing the physiological basis of mental disorders in considerable generality. In this
chapter, it is proposed that the benefits of infra-low-frequency training can be
explained in terms of the altered functional connectivity of our intrinsic con-
nectivity networks. The information made available to the brain on cortical
References 47

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The role of glia and astrocytes
in brain functioning


3.1 Introduction 51
3.2 Scientific findings on astroglial activity 51
3.3 Rhythmicity of the brain and energy cycles 53
References 56

Recent brain research has uncovered a myriad of functions for astrocytes, show-
ing that these cellular multiplicities are critical to the regulation of the brain’s
daily and hourly rhythms and blood flow. This chapter briefly enumerates astro-
cytic processes and posits that well-functioning astroglia are essential to mental
health, and that damaged astrocytes produce dysfunctions in brain regulation. It
goes on to explain that these cells exhibit vital fluctuations that lie in the infra-
low-frequency (ILF) range, and it is reasonable to propose that ILF neurofeed-
back engages mechanisms managed by our astrocytic networks.


With trillions of organisms dedicated to getting along, our brain is an arena of
cosmic politics, one organized around neurons, as agents of communication, and
astroglia, as regulators of the blood supply. Partners in movement, neocortical
astroglia (astrocytes) and pyramidal neurons create our goal-directed mental
processes.1–6 Early neuroscientists speculated about the role of astrocytes and
other elaborate cells in our nervous system, and named this class glia—Greek
for glue—interwoven as they are throughout the brain. The consensus for many
years was that these star-shaped cells did little more than fill the empty spaces
between neurons, providing passive structural support for the billions of neurons

52  The role of glia and astrocytes in brain functioning

and axons embedded around them.7 The primary function of glial cells appeared
to be insulation for the axons and neurons as they transmit electrical impulses
across axonal pathways and synapses.
However, research within the past dozen years has identified a variety
of functions of astroglia that are far more numerous and more complex than
expected. Among many duties, astroglia facilitate the creation of new synapses
(synaptogenesis), a necessity for neuronal survival and vital to cortical network
integration.4,8–12 Astroglia also manage network excitability through capillary
blood flow, allocating blood flow to active networks, a process that is known as
It is estimated that the human central nervous system contains 500 billion
neurons, of which 70 billion are pyramidal—those neurons with high dendritic
branching across the neocortex, amygdala, and hippocampus. By virtue of the
fact that pyramidal neurons mediate long-distance communication between cor-
tices, they play a key role in organizing, coordinating, and regulating a variety
of functions, which are themselves regulatory in character.15 Our brain also con-
tains four trillion glia and 30,000 miles of capillaries, astronomical numbers in
a three-pound brain.
Animal brains generally consist of more neurons than glia; for example, there
is one glia for every 25 neurons in the leech, one glia for every six neurons in the
round worm, and one glia for every three neurons in rats and mice.16 But the
human neocortex possesses seven astrocytes for every neuron. When one con-
siders the differences in gross neuronal organization between us and our animal
relatives, they are modest, and most of the general cerebral architecture is the
same. Neurons are doing for us what they are doing for mice. By contrast, con-
siderable novelty has emerged within our glial networks.
When oligodendrocytes (white matter) and microglia are factored in, glia
make up 90% of the volume of our cortex.17 Oligodendrocytes are glia that
wrap around axons, insulating them electrically and speeding electrochemical
exchange by a factor of 3000 by maturity, by virtue of their higher propagation
velocity and faster refractory phases.18–21 Microglia are a first line of defense for
our central nervous system. Through the release of glutathione and ascorbate,
they protect neurons from oxidative damage and they are critical in the devel-
opment and/or maintenance of our protective blood–brain barrier.9,22 Through
phagocytosis, they clean up the inter-cellular space, disposing of neuronal waste
products, as well as toxins that make it across the blood–brain barrier.9,23,24
The messaging performed by astrocytes is of primary interest. Human astro-
cytes are larger and signal other glia ten-times faster than is standard in other
mammals (e.g., rats).16 When healthy, they send different messages to different
neurons, laying the ground for a well-regulated brain. However, when imma-
ture or diseased, they send the same signals to all of the neurons they attend.12,25
Hence, it is no surprise that functional disturbances in astrocytic networks are
common to many mental health conditions, including attention deficit hyperac-
tivity disorder (ADHD), depression, bipolar disorder, autism, and schizophrenia,
as well neurological disorders, including epilepsy, Alzheimer’s, Parkinson’s, and
multiple sclerosis.26–28
3.3 Rhythmicity of the brain and energy cycles  53


Far from being passive structural supports that sheath axons or fill space
between different elements of the brain, we now know that astroglial cells
have a variety of complex regulatory functions that are essential to the health
and smooth functioning of the brain. One of these functions is that neurons
and glia interact dynamically at the molecular level to process information.
Astrocytes modulate the tone of neuronal activity through capillary manage-
ment, as well as timed releases of adenosine triphosphate (ATP).29–33 Tone refers
to the general level of activity (or inactivity) of neuronal assemblies subject to
internal and external demands, as well as to our daily rhythmic cycles of rest
and engagement. In this regard, astroglia regulate cortical excitability and plas-
ticity via both short-term and long-term rhythmic fluctuations in ATP release,
which in turn affects glutamate and calcium availability, vital to neuronal fir-
ing capability.34,35
A synapse is an interplay between two neurons and an astrocyte.19,20,21,36
Astrocytes provide a feedback loop on synaptic transmission, integrating the
activity of connected neurons,10,11,35 which are the grassroots organizations of
the regulatory hierarchy. This affects regulation on a spatial scale comparable to
pyramidal neurons, but on a significantly longer time scale. Astrocytes release
vasoconstrictors and vasodilators into capillaries via “foot processes” so as to
manage blood flow to each neuron, controlling the local energy supply.4,8,9
Another key role played by astroglia lies in the regulation of our sleep/wake
cycles. Astrocytic networks manage sleep pressure accumulation across the cir-
cadian sleep/wake cycle.37,38 They are also implicated in our hourly (ultradian)
cycles of rest and activity.39–41 Finally, astrocytes separate cortical groups into
functional networks, which is another echelon in the hierarchy of regulation.
Network organizations and cycles of arousal are optimizations across time and
space in the brain, enabling the highest functionality possible.42,43
On the largest spatial scale, the corticolimbic system divides into competing
networks centered around our resting-state network, also known as the default
mode network. These core networks organize cortical activity in response to
engagement. Cortical networks are highly active at all times, including during
sleep and anesthesia. The default mode network is most active during rest and
self-referential tasks, including mind wandering, self-judgments, empathy, and
envisioning our future. This network deactivates when outward-directed atten-
tion is needed, in which case task-positive networks engage, including the dorsal
attention and central executive networks. A salience network mediates among
these networks.
Our primary target in ILF neurofeedback is usually the default mode network,
as all cognition—all coordinated network action and response systems—work
in relation to this grouping. Of course, the impact of neurofeedback extends
beyond the immediate target to the brain as a whole. Our default mode network
includes the medial prefrontal cortex, posterior cingulate cortex, lateral and
medial temporal lobes, and posterior inferior parietal lobule; when it is active,
we are at rest, and when other networks are active, such as the dorsal attention
54  The role of glia and astrocytes in brain functioning

or central executive networks, we are at work.44–47 The principal protocols cur-

rently employed in ILF training typically target regions of the default mode or
of the salience network, where these are accessible to us at the cortical surface.
Ultradian rhythms can be described as a trough (reduction or insensitivity) in
sensory processing, followed by a peak (receptivity) every two hours, represent-
ing periods of less activity, followed by more. They are a signature of life, and our
brain is replete with them.48 What is of interest to neurofeedback practitioners is
that they operate at an ILF of around 0.14 mHz (see Figure 3.1).
In healthy individuals, ultradian rhythms are phase-locked to the circadian
rhythm, so that of the number of cycles of peaks and troughs within a 24-hour
cycle is an integer, or approximately so (10 or 12, as opposed to 13.6 or 8.38 cycles
per day). The number of ultradian cycles ranges from 10 to 12 per day. As stated
above, this activity is interesting to neurofeedback practitioners because it falls
into the ILF range. ILFs correspond to multiple minute periods or rhythms.
A frequency of 1 mHz corresponds to a 17-minute ultradian rhythm, 0.18 mHz
to a 90-minute cycle, and 0.14 mHz to 2 hours. The latter two periods encompass
our basic rest–activity cycle (BRAC) (i.e., how we tend to rest and work in near-
2-hour increments).48,49
This cycle of cortical excitability is controlled by astroglia. In cases where
astroglia are affected by internal genetic anomalies or biomedical factors
(described in Chapters 6 and 7) or damaged by direct injury (e.g., traumatic brain
injury), the regulation of these cycles is disturbed. Brain functioning degrades,
due to regulatory loss or the mismanagement of energy. This is where neuro-
feedback in the ILF domain is used effectively to restore the healthy functioning

Time of day changes in posterior alpha activity

Subcortical concentration
5–7 Hz
Eyes open rest-parietal

7–9 Hz
Magnitude µV (Pz)

0.50 9–11 Hz
11–13 Hz


0.35 8 AM Noon 6 PM


Cortical concentration

Figure 3.1  Theta and alpha activity for 130 adults during eyes-open rest
recorded between 8 am and 6 pm. Most individuals provided three recordings
an hour apart, and scatter points are smoothed (20 individuals per point), to
site Pz.
3.3 Rhythmicity of the brain and energy cycles  55

of astrocytic networks, leading to improved brain efficiency.50 Much of ILF

training is presently conducted in the vicinity of 0.14 mHz, strongly suggesting
that we engage and adjust a person’s BRAC with ILF training.
The tight regulation of ultradian rhythms makes neurofeedback in this fre-
quency range possible and accounts for the particularity of the conditions under
which it needs to take place. Since feedback engages a specific rhythmic process,
we observe frequency sensitivity or optimization, reflecting a high dependence
of the response based on the frequency we train. It is in this precise regulation
of ultradian rhythms that the mechanisms of neuronal activation are available
for our engagement through the external feedback mechanism we provide with
By targeting basic regulatory functions associated with astrocytes and pyra-
midal neurons, neurofeedback improves brain functioning locally and glob-
ally. This may be understood by regarding brain function at a systems level.
First of all, feedback at a single electrode placement on the cortex has a global
impact on the management of overall cortical excitability. Second, feedback on
a single extremely slow frequency impinges on the timing of neuronal networks
throughout the EEG spectrum. This is comprehensible when we recognize that
the brain is a highly integrated, unitary functional entity, with exquisite aware-
ness of the forces engaging it. The brain is particularly alert to any information
available from the environment that correlates with its own internal activ-
ity—its own signature of agency. Neurofeedback in general, and ILF training
in particular, takes advantage of the fact that the brain constantly seeks out
activity in parallel or in opposition to its actions, and acts as a hyperactive
agency detector.
By virtue of the fact that the response to neurofeedback is usually a non-
specific (whole-brain) response, albeit with occasional focal presentations of
change, we are wise not to focus too much attention on specific mechanisms
of efficacy for any form of neurotherapy. The ultradian rhythms are targeted
not because we have determined that they are behaving badly, but because
our central nervous system is organized (regulated) around these rhythms
and responds strongly to this information. The brain responds irrespective of
whether the information we provide relates to its hemodynamics (blood flow),
electrodynamics (slow cortical potentials), or moment-to-moment fluctuations
in activity (as seen in functional magnetic resonance imaging). All of these
measures correlate with local cortical excitability, and such signals engage our
brain as it seeks out environmental information that parallels and confirms its
own agency.
Cerebral plasticity, which is vital to mental health and intelligence, is largely
served by astrocyte networks, which explains the clinical efficiency of ILF neuro-
feedback for numerous conditions. Whereas neurofeedback in the corticolimbic
rhythm (conventional) range of EEG frequencies (1–100 Hz) engages neuronal
assemblies in all of their complexity, ILF neurofeedback simplifies the focus to
regulatory dynamics, focusing on astrocytic mechanisms with a minimum of
other influences. This is currently the best explanation for why the brain is able to
accomplish so much reorganization on the basis of so little information.
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44. Yates FE, Yates LB. 2008. Ultradian rhythms as the dynamic signature of
life. In Ultradian Rhythms from Molecules to Mind. Lloyd D, Rossi EL, eds.
London: Springer, 249–260.
45. Leopold DA, Murayama Y, Logothetis NK. 2003. Very slow activity fluctu‑
ations in monkey visual cortex: Implications for functional brain imaging.
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46. Staba RJ, Wilson CL, Bragin A et al. 2002. Sleep states differentiate
single neuron activity recorded from human epileptic hippocampus,
entorhinal cortex, and subiculum. J Neurosci 22(13):5694–5704.
47. Steriade M, McComick DA, Sejnowski TJ. 1993. Thalamocortical oscilla‑
tions in the sleeping and aroused brain. Science 262(5134):679–685.
48. Rossi E, Kleitman N. 1992. The basic rest–activity cycle—32 years later:
An interview with Nathaniel Kleitman. In Ultradian Rhythms in Life
Processes: A Fundamental Inquiry into Chronobiology and Psychobiology.
Lloyd D, Rossi E, eds. New York: Springer, 303–306.
49. Kleitman N. 1982. Basic rest–activity cycle—22 years later. J Sleep Res
Sleep Med 5:311–317.
50. Othmer S, Othmer SF, Legarda SB. 2011. Clinical neurofeedback: Training
brain behavior: Treatment strategies. Pediatr Neurol Psychiatry 2:67–73.
The evolution of clinical
neurofeedback practice


4.1 History and placement of the “ILF training” in the neurofeedback

universe 60
4.1.1 Lessons from earlier days and the very beginning
of neurofeedback 60
4.1.2 Evolution from conventional beta/SMR training 61
4.1.3 The logic of moving towards lower frequencies 63
4.1.4 Differentiating the ILF method from other neurofeedback
approaches 65
4.2 ILF neurofeedback: A process-oriented training approach—
Overview of the clinical process and the development of individual
treatment plans 68
4.2.1 Assessment and reassessment: Type of intake information
needed from the client 69
4.2.2 Protocol decision tree: The art and science of how and
where to train 72
4.2.3 Interaction with the client: Importance of in-session
communication and reports from between-session effects
for adjusting training protocols 80
4.3 Combining the ILF approach with proven older neurofeedback
methods 85
4.3.1 Reasons for doing this 85
4.3.2 Combining with Alpha–Theta training 85
4.3.3 How is Alpha–Theta training performed? 86
4.3.4 Combination with two-channel sum training 88
4.4 Closing remarks for neurofeedback clinicians 89
References 90

60  The evolution of clinical neurofeedback practice

This chapter shows how clinical neurofeedback evolved over the last 30 years and
focuses on modern individualized neurofeedback training methods as contrasted
with prescriptive protocols derived from normative-based interpretations of the
quantitative electroencephalogram (QEEG). It focuses on practical and clini-
cal aspects. It will explain the infra-low-frequency (ILF) neurofeedback training
below 0.1 Hz, which initially evolved out of the pioneering clinical work at the
EEG Institute in Los Angeles, under the clinical guidance of Sue Othmer.


4.1.1 Lessons from earlier days and the very beginning
of neurofeedback
Since the beginning of neurofeedback in the late 1960s and early 1970s (as recounted
in Chapter 2), several different approaches have evolved. Early in the history of
neurofeedback, there were mainly two different branches. In the United States, cli-
nicians and scientists were focused on amplitude-based reinforcement of the tradi-
tional frequency bands between 1 and 30 Hz.1–3 The early EEG amplifiers excluded
the lower range of the EEG via high-pass filters. They cut off everything nominally
below 0.5 Hz, because the large amplitude fluctuations in the lower ranges would
otherwise have dominated the signal. They were also regarded as artifacts, in the
sense that they were not expected to yield information that would be useful to the
electroencephalographer. Meanwhile, in Europe, specifically in Germany, scientists
worked on that lower end of the EEG spectrum. They used amplifiers with much
lower cut-off frequencies and focused on the modulation of slow baseline shifts (also
known as slow cortical potentials [SCPs]) that reflect episodes of cortical activation
and deactivation through negative and positive excursions in the surface potential,
respectively.4,5 In the early days, both methods mainly recorded EEG signals that
were on the central strip (Cz, C3, and C4 in the international 10–20 system) (Figure
4.1) of the cortex. In the case of SCP training, this was followed because the objective
was to train the contingent negative variation (CNV), and the largest amplitudes of
the CNV are found at the central sites.6 The frequency band training, specifically
the sensory motor rhythm (SMR) training, began with the work on motor seizures.7
Therefore, the sensory–motor cortex was the obvious target for the training.
Over the years, the question arose again and again as to whether a “one-size-
fits-all” approach or individualized training strategies should be preferred. The
strength of each model is obvious: the “one-size-fits-all” approach is especially
suitable for research, because there is no large variability of the training param-
eters and the results do not depend on the therapeutic skills and the experience of
the clinician. The individualized approach is more attractive for the seasoned cli-
nician because the training effects are quicker and more specific and the training
can be adapted to the individual needs of each client. Still, the question is then
how to adapt the training to the individual needs of the client. Can the treatment
plan be derived from the norm-based interpretation of QEEG data8,9 or should
the change of the client’s symptoms guide one through the training?10 In theory,
4.1  History and placement of the “ILF training” in the neurofeedback universe  61


Fp Fp
1 2

F7 F8
F3 FZ F4

Left T3 C3 CZ C4 T4 Right
side side
A1 A2
P3 PZ P4
T5 T6

O1 O2


Figure 4.1  International 10-20 System: The neurofeedback community has a

standardized model for placing electrodes on the scalp. This provides uniform
reference points in research and training.

it might be an attractive idea to collect actual data and then train the client’s
brain to a nominal value by rewarding amplitudes in frequency bands where the
amplitude is too low compared to reference values, and inhibiting amplitudes in
frequency bands where the amplitude is too high. Juri Kropotov, a specialist in
the QEEG field, calls this the “bulldozer” method: to cut whatever is too high and
fill up whatever is too low.9 Nevertheless, daily clinical work shows that brains
react idiosyncratically to any type of training protocol and this individual reac-
tion is not readily predictable from the EEG. If we understand the brain’s neural
circuits as excitable media, this is of course what we would expect, due to the
intrinsic properties of excitable media.

4.1.2 Evolution from conventional beta/SMR training

ILF training was not suddenly born de novo; it was empirically developed from
conventional beta/SMR training to optimize clinical results. The Othmer group
that developed ILF training started with beta/SMR training on the central strip in
the 1980s. In the beta/SMR era, clients were more or less divided into two groups:
clients who were stuck in over-arousal and those who were stuck in under-arousal.
Over-arousal clients were trained with SMR reward and theta and high beta inhibit
on the right side (T4–C4). Clients with symptoms of under-arousal were trained
with beta reward and theta and high beta inhibit on the left side (T3–C3).11 Clients
with symptoms of both over-arousal and under-arousal were trained on both sides.
At that time, neurofeedback was explained in terms of the operant condition-
ing model. One could track the amplitudes and reward an increase or decrease in
62  The evolution of clinical neurofeedback practice

certain frequency bands and train this over several sessions. There was no thought
that the client might feel the effects of the training during the session. This old
model was intuitively attractive and therefore still exists in many schools: see what
is wrong and then train up the “good” waves and train down the “bad” waves.
Into these categories fall the beta/SMR training for awake-state training and the
Alpha–Theta training (for more details, see Section 4.3.2) for what is called deep-
state training. Whereas the beta/SMR training was used for physiological regu-
lation, the Alpha–Theta training (rewarding alpha and theta amplitudes, while
inhibiting delta and high beta) was designed more for psychological resolution.
In the beginning, there was no expectation that people would feel different
with different kinds of awake-state training. Some people even stated that it was
ridiculous to ask the client how they felt, as we had all these data to rely on. But if
the clinician or the researcher is alert to the possibility that the immediate state
shift induced with the training is discernible by the trainee, it becomes obvious
just how specific the training can be. It turned out that SMR training on the right
side had a more calming effect, whereas beta training on the left side was more
activating, at least for most of the clients. From then on, the question was which
clients fit into which categories.
Over time, the question of how the clinical effects could be improved when
the reward frequencies are adapted individually for each client according to
the client’s symptoms and reaction to the training during the session, as well as
after the session, was systematically investigated. If during or after the neuro-
feedback training the client showed symptoms of high arousal, then the reward
frequency needed to be shifted to lower frequencies. For clients that showed low
arousal symptoms after the training, the reward frequency needed adjustment to
higher frequencies.11 It turned out that people do have very individual arousal–
performance curves and not, as assumed before, that the “good” frequencies are
always in the beta/SMR range, and below and above are the “bad” frequencies
for the awake state and optimal function. This means that the optimal response
frequency (ORF) needs to be found individually for each client. Already, people
were reacting very differently—and reproducibly so—in this higher frequency
range, even if the reward was shifted up or down by a mere 0.5-Hz step.
The more the training was extended to the lower frequencies, the easier, faster,
and better certain clients reacted to the training. Also, the symptoms could be
interpreted as low- or high-arousal symptoms more specifically, and therefore it
became easier to optimize the training parameters for each client. The under-
standing of neurofeedback changed gradually when the training range was
extended to lower reward frequencies. Over the years, the immediate effects of
the lower frequencies also led to a better understanding of the different electrode
placements over the different cortical areas.
The immediate effects of neurofeedback training—sometimes resulting in
state shifts within mere minutes—also called for another theoretical understand-
ing than the operant conditioning model that had been accepted without chal-
lenge at that time. It seems that the training of the ILF brain waves below 0.1 Hz
engages directly with the core regulatory functions of the central nervous sys-
tem (CNS). Today, we understand neurofeedback as a brain exercise in which the
4.1  History and placement of the “ILF training” in the neurofeedback universe  63

brain uses the feedback on its own activity as an additional information channel
to regulate its own physiology.12 This seems to be reasonable, as the brain needs
to make sense of all the internal and external information it gets and has to adapt
its own activity according to this information. Therefore, the brain is optimized
for learning to use any information from the inside and the outside to its own
advantage. As soon as the brain realizes that it has a causal connection with the
presented signal, it will try to affect and manipulate the signal. The famous neu-
roscientist Paul Bach-y-Rita summarized his decades of research: “Give the brain
the information and it will figure it out.”13 The clinical development of neuro-
feedback over the last 30 years has always been driven by the question: what EEG
signals should be employed and how should the signal be presented to the brain
of each client to get the most beneficial clinical outcome?

4.1.3 The logic of moving towards lower frequencies

As the first objective of the training is always the promotion of CNS stability,
clients with unstable brains, who are very common in daily practice work, have
always driven the evolution of ILF neurofeedback. They can be easily destabilized
with very small deviations from their own ORF. These sometimes very strong
reactions to small changes in the response frequency were especially obvious
with bipolar electrode placements at T3–T4 by comparison, for example, with
C3–C4 placement, which had been used previously. This is why T3–T4 remains
the starting electrode placement for many clients when seeking to find the ORF.
The ORF cannot be predicted from either the EEG or the diagnosis. This
means that the ORF needs to be found individually for each client through the
actual training experience. This could be compared with the process of adapting
glasses at the optometrist. The ORF is found according to the described worsen-
ing or reducing of symptoms during and after ILF training at a certain frequency,
and then adjusting the frequency accordingly.
During the evolution of ILF training, this was a big challenge to the clinician,
since the options where quite numerous, especially once it became possible to
choose the increments in 0.1-Hz steps. Even more challenging for the existing
theoretical model of good and bad frequencies was that the best clinical results
were not obtained in the beta/SMR range as might be expected, with most cases
experiencing the greatest benefit at much lower frequencies.
In the years from 2001 to 2006, there was a distinct trend towards lower
reward frequencies. At that time, there was a technical limitation. The normal
EEG amplifiers that were used in clinical work and research had their lowest
limit typically at 0.5 Hz. This is probably the reason that, throughout this period,
the ILF frequencies never got any attention either in research or in clinical work.
An exception was of course the slow cortical potentials (SCPs) that were inves-
tigated at German universities. They worked with the tonic SCP signals and for
that purpose cut off anything that fell above 0.5 Hz.
Cumulative historical data from the neurofeedback clinic of the Othmer
group show that after adapting the reward frequencies to the individual needs
of the clients, only a small fraction of clients were still trained in the beta range
64  The evolution of clinical neurofeedback practice

of 15–18 Hz. On the other hand, there was a flat distribution from 0 to 15 Hz.14
At that time, 3-Hz band pass filters were still standard, a legacy of the classical
frequency band training. This meant that the reward frequency bands ranged
from 0–3 to 27–30 Hz in 0.5-Hz steps. The data motivated the extension of the
frequency range to even lower frequencies, and the decision to move on from the
classical frequency bands.
It became technically possible to extend the frequency range to 0.05 Hz in
2006. At that time, the nomenclature also changed. In the search for the ORF, it
was now more appropriate to cite the center frequency of the filter than the range
(e.g., a reward band from 1 to 4 Hz was called 2.5 Hz, a reward band from 12.5
to 14.5 Hz was called 13 Hz, and so on). The progress to ever-lower reward fre-
quencies happened over a number of years and involved more than 1000 patients
at the EEG Institute that spearheaded this development. When the extension to
0.05 Hz occurred in 2006, within only a few months, 66% of the clients were
training at the lowest frequencies. More than 250 clients were involved in this
phase. Clinical outcome was mainly measured in continuous performance tests
(CPTs) and symptom tracking, which will be explained in more detail in Section
4.2.1. Of course, these data motivated the development of further techniques to
venture to even lower frequency ranges. This was done successively to 0.01 Hz
and even 0.001 Hz, and finally to 0.0001 Hz, or 0.1 milli-Hz (mHz). The latter
change was introduced in 2010.
Searching for the ORF became even more challenging for the clinician, since
the frequency range was being increasingly extended and the possible increments
in the reward frequency were getting smaller and smaller. Therefore, the starting
frequencies, where the search for the ORF routinely begins, had to be reasonably
adapted with every step down in the frequency range. This entire development
took place with an amplifier that had initially been designed for the conventional
EEG range and provided for a flat band pass nominally only down to 0.1 Hz.
Since the training had migrated so totally down to the extremely low frequencies,
it was appropriate to develop special hardware and software modules tailored to
the special needs of ILF training. At present, the frequency range for ILF train-
ing extends from 0.1 to 100 mHz, and most people train in the range from 0.1 to
1.5 mHz, with a clear preponderance for the lower end of the range (unpublished
data from the EEG Institute).
From a technical point of view, it does not make sense to talk about reward
frequencies any longer when we are operating in the mHz range. Of course, we
cannot reward the amplitude of a wave with a periodicity of over an hour in a
30–50-min training session. These terms only reflect the evolution of the method
that is described above. By the same token, it would not make sense to use Fast
Fourier Transfer (FFT) analysis, as is routinely used in the beta/SMR training.
Even the term “reward” does not fit anymore, as we no longer ask the brain to
produce a higher amplitude within a certain frequency band. With respect to the
EEG signal, we are operating in the range of slow potential shifts. If one were to
track this signal over the course of hours, it would indeed reveal the whole cycle
of activity at 0.1 or 0.2 mHz, but this is obviously not the issue in this training.
4.1  History and placement of the “ILF training” in the neurofeedback universe  65

The matter of interest is the real-time behavior of the direct current (DC)
potential from moment to moment. The observed potential in this case selectively
reflects the activity of a particular brain rhythm. In particular, if one realizes
that adjustments in the response frequency can be felt almost immediately (i.e.,
within a few minutes), it is apparent that even such a slow rhythm reflects the
activities of life in real time. One might relate this observation to velocity and
acceleration. If you sit in a car, you might not feel the difference if the car drives
at 50 or 100 mph, but you would definitely feel a sudden acceleration at either
speed. The brain is particularly sensitive to change, and especially to change that
it has itself produced.

4.1.4 Differentiating the ILF method from other

neurofeedback approaches
The main difference between the ILF method and other approaches is that the
operant conditioning model no longer applies as an explanation for the neuro-
feedback effects. Clients feel state shifts in accordance to very small frequency
shifts (e.g., from 0.1 to 0.2 mHz) within minutes. This does not fit into the oper-
ant conditioning model. We rather think that we show the brain what it needs to
regulate itself, just as the brain always uses internal as well as external feedback to
self-regulate. We cannot predict the training parameters from EEG data, but we
learn them from the client’s reaction to the training, as will be discussed in more
detail in Section 4.2. As mentioned above, the objective is not to consciously raise
or lower the amplitude of certain frequencies. We rather understand the chosen
“reward” frequency as a target frequency that we observe, like zooming in with
a magnifier to extract this frequency from the whole spectrum. In the feedback,
we show back to the client the subtle fluctuations of this target signal, but we do
so without asking the client to react in any particular way. As the brain responds
automatically to this target signal, the chosen frequency is called the response
frequency in the rest of this chapter.
However, one might well ask: what should cause the brain to be interested? This
might be best explained with a situation from daily life. Think of the display win-
dow of an electronics store. To draw attention, they may have installed cameras
that record the area in front of the store for display on one of the monitors. Even if
you are not consciously looking at the shop window at all, as soon as you appear
on one of the screens, your attention will automatically be drawn to that display.
If you linger, you may even start to observe yourself and to adjust things like your
posture, your hair or your clothes, perhaps even largely unconsciously. You will
automatically focus on the image of yourself on the screen and start a self-correct-
ing process. The same, of course, holds true for a mirror. As you walk by, it will
catch your attention and you will start to self-correct, often without realizing it.
Let us have a look at what exactly is shown to the client in this ILF “mirror.” ELECTRODE MONTAGE
How is the signal picked up on the scalp? In the early days of neurofeedback, cli-
nicians used mainly bipolar electrode montages. This changed in the early 1990s
66  The evolution of clinical neurofeedback practice

when QEEG came into the picture. Since that time, most people have used uni-
polar (referential) placements. This means that one electrode is mounted over an
electrically active area of the head, whereas a reference electrode is mounted on a
relatively inactive area (e.g., ear lobes or mastoid). EEG signals are measured with
differential amplifiers, meaning that one input is subtracted from the other, and
the measured signal reflects the difference in the potentials that prevail at the two
electrode sites. With the referential or unipolar recording, the result is the differ-
ence between an active placement and the “quasi”-passive reference site, yielding
a net signal that is dominated by the potential at the active electrode.
By contrast, for ILF training, we use a bipolar electrode montage, which
means that both electrodes are positioned on active areas (e.g., T3–T4). The result
in the signal reflects the difference between the two electrode sites. The ground
can be anywhere on the head and does not contribute directly to the difference
signal. This creates a paradox: on the one hand, we get better clinical results with
the bipolar montage; on the other hand, it is useless to try to interpret amplitude
changes in the signal during the training, because we cannot assign them to their
origin. If we have a large amplitude in a given frequency band, there might be
at least three reasons for this in a bipolar montage: (1) the amplitude at the (+)
electrode is much higher than the amplitude at the (−) electrode; (2) it might be
the other way around, with the amplitude at the (+) electrode being much lower
than at the (−) electrode; or (3) the amplitudes at both electrode sites are more or
less the same, but they differ in the time domain, meaning they are phase shifted
with respect to each other. In ILF training, electrode montages for training the left
hemisphere always have one electrode on T3 (e.g., T3–Fp1, T3–P3, T3–T5, or T3–
F7). Training on the right hemisphere always includes T4 (e.g., T4–P4, T4–Fp2,
T4–T6, or T4–F8). Inter-hemispheric training could be T3–T4, P3–P4, or Fp1–
Fp2. Other inter-hemispheric pairs see much less usage. ELECTRODE POSITIONS
Different training sites have different and very specific training effects. ILF train-
ing usually starts with one bipolar training site, with the initial goal of optimiz-
ing the reward frequency (for more on clinical decision-making, see Section
4.2). This process might need several sessions. The reward frequency relates to
balancing the arousal level, which is the most important objective for optimal
brain function. Years of clinical experience have shown that very basic electrode
positions used at the optimal reward frequency can bring about reductions of a
surprising variety of symptoms. If more specific symptoms need to be addressed,
different areas of the cortex need to be taken into account. In Section 4.2—and in
more detail in Sue Othmer’s Protocol Guide10—the process is described by which
different training sites might be added systematically in the individualized train-
ing process. REWARD
As described already in Section 4.1.3, the “reward” frequency, which should now
be better termed the response frequency, lies in the ILF range somewhere between
0.1 and 100 mHz and needs to be discovered individually for each client. There is
4.1  History and placement of the “ILF training” in the neurofeedback universe  67

no basis for instructing the client to make more of the “reward” signal. The client
only tracks the undulations of the signal, without the need to pass judgment on
it. There is no threshold that needs to be exceeded. For working in these very low
frequency ranges, special electrodes need to be used that minimize the drifts that
quite normally occur in the potential between the skin and the electrode mate-
rial. These drifts can continue for more than 10 or 15 minutes and, of course, will
be picked up in the ILF band pass filter. Therefore, sintered silver/silver chloride
electrodes that minimize these drifts need to be used exclusively. INHIBIT
Inhibition of large excursions in EEG amplitudes has been a part of neurofeed-
back strategies since the very beginning. This activity might be artifactual or it
might indicate the brain’s entry into a state of greater dysregulation. In either case,
the reward signal chain needs to be shielded from contamination. Artifact detec-
tion is a standard part of the signal processing chain. For the episodic descent
into dysregulation, the signal can also serve as a cue to the brain to restore better
regulatory status, hence the inhibit strategy.
How does one manage sudden sharp amplitude increases in the spectrum
in practice? Whereas the classical frequency band training uses inhibits in cer-
tain unwanted frequency bands like theta, delta, or high beta, which are most
likely to reflect the dysregulation status, ILF training uses multiple inhibits to
cover the whole spectrum from 2 to 40 Hz. The inhibits are subdivided into eight
different frequency bands to detect sharp increases in amplitude in any part of
the spectrum. In ILF training, the inhibit function is fully automated, making
no demands upon the clinician. Thresholds are adaptive in order to track the
prevailing ambient band amplitudes. The point is to detect excursions in band
amplitude that substantially exceed the ambient background levels. FEEDBACK
Conventionally, the amplitude changes of the reward band drive the dynamic
feedback, punctuated at times by the intrusion of an inhibit. However, ILF train-
ing demands management of the feedback that is different from the classical fre-
quency band training. Feedback is given continuously on the slowly undulating
potential. Since clients are not asked to interact with the signal volitionally, the
feedback can be delivered in a subtle way, effectively beneath notice. Alternatively,
feedback parameters may be very obvious. For example, they may be linked to
the speed of different vehicles (cars, rockets, planes, jet skis, or trains) in a com-
puter animation. This introduces sufficient dynamism into the scene to keep cli-
ents engaged with the feedback. But if someone is too competitive and is always
thinking: “Why is this stupid car not going faster?,” then the feedback needs to be
changed to a more subtle mode.
This might involve the showing of a movie, where the client is then asked to
simply enjoy the movie. Of course, there is still feedback involved (e.g., black
borders may intrude into the frame or the screen size shrinks in a manner gov-
erned by the “reward” signal; the picture gets more or less foggy according to the
inhibit signal; or the music changes volume in a manner that tracks the EEG).
68  The evolution of clinical neurofeedback practice

In some feedback animations, there are up to 17 parameters that can change

according to the client’s EEG. The changes in the lower range of the EEG band
are slower; therefore, the feedback has to be adapted in order not to frustrate or
bore the client.
As the signal is ultimately cyclical, there can be no preferred direction of
change. The instruction for the client is only to enjoy the feedback. Just as the
response frequency and the electrode positions might be different for each client,
there needs to be a variety of choices of different kinds of feedback. Some clients
are not used to the concept that they have the choice and they want the therapist
to choose the “best” or clinically most effective feedback for them. What is best
ultimately depends on the client’s reaction. We need to choose the most comfort-
able feedback for the client and allow the brain unconsciously to get the feedback.
For some people, the feedback needs to be activating and engaging with a lot of
input. Others might need very relaxing feedback with as little stimulation as pos-
sible. Some clients retain the same feedback mode for 40 sessions while others
might change the feedback mode every few sessions. INDIVIDUALIZED TRAINING
ILF training is a very process-oriented type of training. There is no one formula
for how to conduct ILF training. Even after a very intensive assessment (for more
details, see Section 4.2), we do not know the exact treatment plan in advance.
Of course, with all the information of the assessment, we will have several ideas
about where to train and how to train. A training strategy is shaped, yielding
hypotheses to be confirmed. The most important information the therapist
needs in order to optimize the training is the reaction of the client to the train-
ing parameters utilized. The training procedure has to be built up step by step,
based on all the information received from the assessment, together with all the
information that the client gives us during the session, as well as from session to
The information from the assessment only gives the therapist enough infor-
mation for an initial hypothesis of where and how to train. The training itself
then either verifies the hypothesis or points in a different direction. The biggest
challenge for the therapist is to find out what the individual brain needs at a given
moment to self-regulate. This can only be done in cooperation with the client
and their family. In the following section, the clinical decision-making process is
described in more detail.


A clinician who decides to work with an individualized neurofeedback approach
like ILF training definitely needs sufficient education and preparation for this
specific method. This is best obtained in adequate professional training courses
with a lot of practicum work, self-training, and discussion time for the training
4.2  ILF Neurofeedback: A process-oriented training approach  69

effects of all attendees. As Director of Training for Neurofeedback Practitioners

in Europe, the author has found it continually fascinating to observe how people
react so variously to the same kind of training. ILF training induces shifts in
physiological state. Sometimes, these state shifts arise unexpectedly rapidly. In
clients with unstable nervous systems, these sudden state shifts might lead to
unwanted training effects that need to be dealt with by the clinician. This can
only be done if the clinician knows how to interpret the symptoms and how to
react to them in terms of neurofeedback. Fortunately, these adverse effects are
usually transient and can be quickly reversed. The following section will give a
short summary of the clinical process and the related decision-making. A more
comprehensive overview is given in the Protocol Guide by Sue Othmer.10 The fol-
lowing is a distillation of some of that material.

4.2.1 Assessment and reassessment: Type of intake

information needed from the client
Before we start training someone with neurofeedback, a detailed client inter-
view and assessment is performed. As in any other kind of treatment, it has to
be decided whether neurofeedback is a promising tool for the issues and goals
of the client. It has to be checked whether the client needs to be referred for fur-
ther medical work-up, and how neurofeedback can be integrated into the overall
treatment plan of the client (e.g., medication and other medical or psychological
treatments). The client should be comprehensively informed about the training
process, about the commitment of time and money, and especially about their
responsibility to report training effects—negative as well as positive—to the
The client must be told how often and how long the training should be. ILF
training is a very effective neurofeedback approach, so it is not unusual for clients
to feel state shifts and symptom changes during or after the first session, and to
observe noticeable symptom reductions after only very few sessions. Nevertheless,
we are talking about a training and a learning process that needs time and repeti-
tion. Unless the training process is reinforced by repetition, the brain will tend
to fall back into its old patterns. If the training is terminated too early because
of initial positive results, symptoms may well return over time. Therefore, it is
necessary to explain to the client that at least 20 sessions of training are needed to
solidly embed the gains. Generally, after 20 sessions, a reassessment is performed
to compare the results obtained so far with the initial assessment and in light of
the established goals.
The clinician and client should then decide together whether the training goal
has been reached or whether it would be useful to continue the training and reas-
sess again after another 10 or 20 sessions. This is more easily said than done.
Quite commonly, expectations escalate during the training process as progress
is experienced. After all, clients usually come to the training with quite modest
expectations and clinicians, for their part, do not wish to overpromise. During
the initial assessment, the client must also be informed that the training needs to
be done intensively, at a rate of at least two or three sessions per week for the first
70  The evolution of clinical neurofeedback practice

10 or 20 sessions. If good progress is made during the intensive training phase,

the frequency of the training sessions can be lowered to build upon and consoli-
date the changes. If all symptoms are reduced sufficiently or even resolved, the
frequency of the training sessions can be further reduced to ascertain whether
the changes are stable and persist over longer time periods.
To understand the patterns of dysregulation of each client, the clinician needs
as much information as possible about the client’s function and dysfunction,
strengths and weaknesses. We use specific symptom rating lists to look at indi-
cators for different modes of dysregulation. It is not enough to know whether a
certain symptom exists or not. Symptoms need not only to be rated in severity,
but we also need to know the typical patterns of occurrence to gauge the effects
of the specific training parameter. For example, it is not enough to know that
the client has sleep problems and that they got better after the training session.
To decide which training parameters might be useful, we need to distinguish
between problems of falling asleep, waking up frequently, inability to return to
sleep after waking, waking up too early in the morning, sleeping too long but not
feeling rested, and so on.
Besides the medical interview and other possible tests and questionnaires
(according to the clinician’s background), there are two very valuable tools for
assessing symptoms and judging neurofeedback training success in the reassess-
ment: symptom tracking and CPTs. SYMPTOM TRACKING
Most symptoms that clients present with are not measurable objectively.
Nevertheless, we need the symptom profile in order to decide where and how to
train, and also as a progress indicator of training effects. For ILF training, it is
important to track as many symptoms as possible in order to form a comprehen-
sive perspective of the client. Reporting all of the symptoms can help determine
whether the self-regulation of the trained brain is being enhanced with the train-
ing. Often, clients would choose to describe only a few key symptoms at their own
initiative. The symptom tracking system helps to fill in the whole picture. The
symptom tracking system contains a list of 150 symptoms that can be addressed
with neurofeedback. The list is printed out for the assessment and every symptom
needs to be rated on a scale from 0 to 10 (0 = no issue, 10 = biggest issue the client
can imagine). The symptoms are allotted to seven different symptom categories
(sleep, attention and learning, sensory, behavioral, emotional, physical, and pain).
We use specific symptoms as indicators for different modes of dysregulation. That
does not mean that we target symptoms directly; rather, we use symptom status
to guide us through the training towards better function, which is the real objec-
tive. This understanding has great import for our work. For example, if a client
suffers from a migraine and has no other symptoms to track, the training might
seem like a kind of blind flight in its initial stages, especially if the migraine is
irregular and only appears every 3–5 weeks. If the migraine itself was the only
indicator of training success, one might need to train for many sessions before
one knew whether the training was on the right track. Since the objective is really
the enhancement of regulatory status, there are always many indicators. At a more
4.2  ILF Neurofeedback: A process-oriented training approach  71

subtle level, there are usually other symptoms to focus on, such as problems of fall-
ing asleep, feeling groggy during the day, muscle tension, tension headache, and
so forth. In the absence of even such minor issues, one enquires into the perceived
level of functionality: alertness, mental sharpness, vigilance, energy level, motiva-
tion, and susceptibility to fatigue. By all these means collectively, it is possible to
discern whether self-regulatory capacities are being enhanced.
Another reason to use comprehensive symptom tracking is to create aware-
ness in the client about what symptoms can be influenced with neurofeedback to
motivate them to talk about a variety of symptoms and to report changes after
the training sessions. Clients often start neurofeedback training because they are
seeking relief from very specific symptoms. Typically, they are not inclined to
think about what else could be influenced by the training, and therefore they may
not talk about other symptom changes. In consequence, the clinician might miss
something or not be able to interpret the training effect due to missing informa-
tion. It is a well-known phenomenon that we are only aware of things that we
focus on. The client who comes complaining of concentration problems would
not necessarily mention his muscle tension or digestion problems unless such
information is explicitly sought. Filling out and discussing the symptom track-
ing list helps to motivate the client to observe and report all different kinds of
symptoms during and after the training sessions. Since good reporting by the
client is so critical to the success of the training, an essential part of the process
is educating the client in the role of being a good reporter. Hence, there are really
two kinds of training going on: that of the brain and that of the client, with the
latter focusing on the skills of awareness of self and self-appraisal.
In the assessment and the reassessment, all 150 symptoms, as well as other indi-
vidual symptoms that are not contained in the symptom tracking forms, are recorded
and filled in a table. This can be done either in custom software or in an online plat-
form like EEGexpert ( The online platform has the advantage
that access can be given to the client and the client can then type in their own ratings
via the internet. Graphs of the time course of the severity of all symptoms are created
automatically, all of which can be shown in one combined graph or also in graphs of
individual symptoms. Other people, such as parents, partners, teachers, etc., can also
get symptom tracking forms or online access to judge the training effects.
We have learned from experience that, due to limited self-awareness, one can-
not expect that positive training effects will always be noticed by the client or
their family, or that they will always be reported. As for adverse effects, they
are frequently not recognized as being connected with the training, particularly
since in most cases such states are not novel in the client’s experience. Often,
we learn about some of the client’s positive changes haphazardly. Therefore, it is
sometimes good to chat for a while and listen very closely. It is also common for
symptoms to be forgotten once they subside, so careful probing is called for.
An example may be useful here: in the training of a long-term bulimic woman,
she failed to report that she had not binged and purged the day before, a first in
about 18 years. She did not feel that it was worth reporting because “I had not felt
like binging, so not doing so didn’t seem like a big deal.” Of course, “not feeling
like binging” was the whole point.
72  The evolution of clinical neurofeedback practice CPTs
Symptom tracking suffers from the limitation of being a subjective rating.
However, CPTs such as the TOVA® (Test of Variables of Attention) or the QIK
test ( are possibilities for quantifying training results objec-
tively. Whereas the TOVA needs to be done at the computer, the QIK test is a
standalone, hand-held device that allows for the data to be transferred to the
computer after testing. The CPTs measure impulsivity, sustained attention, reac-
tion time, and consistency of reaction time. Not only do the results give useful
hints as to where and how to train, but any improvements in the measured vari-
ables, which can be impressive, furnish objective evidence of progress.  CONTRA-INDICATIONS AND REFERRALS

After the assessment, the clinician needs to judge whether any contraindica-
tions are present. Although there are almost no contraindications with respect
to neurofeedback itself, there are still clients who should not be trained by just
any clinician and in just any setting. Clients with severe psychiatric indications
should only be treated by clinicians who are experienced with these clinical pre-
sentations. At a minimum, the clinician needs to work within an adequately sup-
portive network environment. It may be that such high-risk clients can only be
treated in a safe inpatient environment. Of course, this caution is not specific to
neurofeedback, but rather applies for any kind of impactful treatment. Still, one
should be aware that neurofeedback is a particularly efficient clinical tool that
needs adequate education, experience, care, and attention in its utilization. There
is also the issue of prioritization. In some cases, other interventions from integra-
tive medicine should precede or at least accompany the utilization of neurofeed-
back if it is to be the most productive.

4.2.2 Protocol decision tree: The art and science of how

and where to train
With neurofeedback, the brain is able to witness its own brain activity and use
this information for better self-regulation. Better self-regulation promotes better
function. We are not treating disorders, nor are we repairing brain wave patterns.
Our goal as neurofeedback clinicians is to help the client’s brain to find its own
path to better self-regulation and consequently better function.10
With ILF neurofeedback, we get strong and specific effects. This means that
it makes a significant difference where we put the electrodes and what frequen-
cies we feed back to the brain. Therefore, we need a model of brain function to
understand categories of regulation and dysregulation. From these patterns, we
derive where to train and how to train. We can use a very simplified model to
understand basic categories of brain regulation and dysregulation. In this model,
it helps to look at the CNS in three axes:

●● Top-down and bottom-up axis ↔ cortical–subcortical axis

●● Front–back axis ↔ prefrontal and parietal cortex
●● Left–right axis ↔ left and right hemispheres
4.2  ILF Neurofeedback: A process-oriented training approach  73

Table 4.1  Five training categories of the working model

No. Category Relation to training process

1 Arousal indicators Response frequency
2 Instabilities Paroxysmal symptoms that need
inter-hemispheric stabilization
3 Disinhibition Loss of control that needs calming and
prefrontal control
4 Localized dysfunction Electrode placements
5 Learned fears and habits Alpha–Theta

Good balance in all three axes is the basis for good brain function. We will
come back to the three axes when we discuss the five training categories. The
three-axis model of the CNS together with the five training categories is a work-
ing model that will support our decision-making during the whole training pro-
cess. The model is shaped by clinical neurofeedback experience over many years,
mainly from the group of Sue Othmer. Finally, modern neuroscience is providing
us with theoretical models that might explain why the training sites and frequen-
cies that have been found empirically are as effective and specific as they are in
clinical practice (see Chapters 2 and 3).
Table 4.1 gives an overview of the five training categories that we have to keep
in mind when finding our path through the training process. These basic train-
ing categories will correlate with how and where to train with ILF training and
Alpha–Theta training. They play a key role in understanding the assessment and
the results of each training session. They help the clinician to find the best start-
ing point after the assessment, and also to optimize the training step by step and
from session to session.
Let us take a closer look at the different categories. CATEGORY 1: AROUSAL INDICATORS

The arousal indicators help us to adjust the response frequency during the train-
ing and from session to session. We use symptoms that are related to shifts in
arousal to adjust the response frequency for each client.
Physiological arousal is the most basic component of brain state regulation
and is related to the cortical–subcortical axis. The core arousal is managed by
brainstem nuclei that project widely throughout the CNS. It is the so-called
reticular activating system that manages the different states of wakefulness and
alertness. No matter where we place the electrodes on the scalp, we will always
interact with this system; therefore, it is always an issue in the training.
The brainstem sets the tone of the arousal system; this is about how awake the
person is, but it is not very specific. On the other hand, it is very specific in how
individual persons react to shifts in arousal level. This might affect attention,
mood, or physical tension, which involve other more specific brain functions.
The individual shifts in arousal level guide us to find the optimal, comfortable
response frequency for the client.
74  The evolution of clinical neurofeedback practice

Arousal and performance curve

Low arousal High arousal

Sedation Agitation
Sleep Normal Emergency mode


Figure 4.2  (See color insert.) The arousal performance curve shows different
states depending on the arousal level.

Arousal has a crucial influence on the overall level of functioning, which is

reflected in the individual arousal performance curve (Figure 4.2). It is normal
that everyone will move up and down along their own arousal curve during the
course of the day. Good self-regulation means flexibility and stability on the
arousal curve. This enables us to stay in the middle range for good function,
go to the lower end at the close of the day when we need to sleep, and use the
higher end of the curve when we need to react quickly to emergencies without
freezing and without taking time to stop and analyze the situation. However,
getting stuck in a state of high arousal without the presence of an emergency
can lead to significant problems. In an emergency situation, we hyper-focus on
the emergency and ignore our body and future plans; this can lead to chronic
dysregulation in the long run. Low arousal states, on the other hand, are essen-
tial for rest and sleep, but are not helpful for good alert function during the day.
The first objective with neurofeedback training is to improve the flexibility and
stability of state regulation. In neurofeedback training, we use symptoms that
indicate arousal shifts to adapt the response frequency. Increasing the response
frequency leads to symptoms of high arousal, and decreasing the response fre-
quency leads to symptoms of low arousal. It is remarkable how sensitive the
brain is to even minute shifts in response frequency, which therefore need to
be adapted carefully for each client. When the response frequency is too high,
the brain responds with feelings of increased agitation—physical, emotional,
­mental, or physiological. Training too high might produce increased muscle
tension or spasms, hyperactivity or impulsivity, tics or obsessive compulsive
disorder (OCD) symptoms, increased heart rate or heart palpations. Emotional
agitation might show up as increased anxiety, anger, fear, despair, or emotional
reactivity. Sleep could be disturbed by nightmares or difficulties falling asleep.
Constipation is a common symptom for people who live in emergency mode.
Hence, increased constipation could be a sign of training too high. Decreased
constipation is often a sign of training in the right direction.
Training with a response frequency that is too low leads to brain responses
of feeling slowed down or sedated. This can be uncomfortable for the client.
Training too low might result in feeling dizzy, heavy, nauseated, groggy, or sad.
4.2  ILF Neurofeedback: A process-oriented training approach  75

Table 4.2  High- and low-arousal symptoms

Training too low: Increase Training too high: Decrease response

response frequency frequency
Sedated, slowed down Agitated, speeded up
Dizziness, nausea Physical tension, muscle spasms
Groggy, lethargic Hyperactivity, impulsivity
Heaviness Tics, obsessive compulsive behavior
Sadness, crying Heart palpations, tachycardia
Emotional sensitivity Emotional reactivity
Lack of deep sleep Difficulty falling asleep
Difficulty waking Nightmares
Low blood sugar symptoms Constipation
Aggressive behavior
Anxiety, fear, anger, despair

It can also lead to being emotionally sensitive, which is very different from being
emotionally reactive, which is normally related to training too high. Another
sign of training too low can be a heaviness in the chest that might make it dif-
ficult to inhale deeply. (This has to be differentiated from training too high and
producing chest tension with increased anxiety.) Also, symptoms similar to low
blood sugar might arise from training too low. With respect to sleep issues, train-
ing too low can result in extreme sleepiness and also a lack of deep sleep. This
might show up in falling asleep easily, but then waking up frequently and not
feeling rested in the morning, despite sleeping for long enough. Sleepiness dur-
ing and after training always needs to be looked at closely and is very helpful
for finding the right response frequency. Relaxation often leads to comfortable
sleepiness and, in this case, is probably a sign of a good response frequency. With
neurofeedback, we want to calm the brain, but not sedate it. If people feel groggy,
sedated, slowed down or uncomfortable during the session, this is often a sign
of training too low. On the other hand, this has to be differentiated from feeling
uncomfortably exhausted when training too high, eventually leading to difficulty
keeping the eyes open. Table 4.2 shows an overview of arousal indicators when
training too high or too low. CATEGORY 2: INSTABILITIES
Instabilities result in paroxysmal symptoms as the brain loses control, like in
migraines, seizures, panic attacks, bipolar disorders, narcolepsy, etc. The presence
of instabilities at any time in a person’s life implies a vulnerability that indicates
inter-hemispheric training for stabilization, with T3–T4 as a part of the training.
At a physiological level, instabilities might be explained as hyper-excitability
due to deficient local inhibitory control. Incoming excitation can then set off an
escalation of nerve activity that destabilizes the brain. People with instabilities
often react very sensitively and reproducibly to changes in response frequency,
so for these persons, the response frequency has to be adapted very carefully
76  The evolution of clinical neurofeedback practice

without too many changes in frequency in one session, because rapid shifts in
arousal state, as well as shifting up and down on the arousal curve, can also trig-
ger instabilities. Medically, instabilities are often treated with anticonvulsants, so
if clients depend on anticonvulsants for any condition, that would be an indica-
tion for inter-hemispheric training.
In terms of neurofeedback, we have to differentiate between hyper-excitability,
high arousal, and reactivity. Hyper-excitability leads to instabilities with parox-
ysmal symptoms that need inter-hemispheric training, such as T3–T4. Symptoms
of high arousal need to be addressed with the response frequency (see Category
1), and reactivity in terms of neurofeedback is better understood in terms of dis-
inhibition, as is explained in Category 3. CATEGORY 3: DISINHIBITION
Disinhibition relates to a loss of self-control with stress or boredom, as with tics
or impulsivity. This needs prefrontal training for better inhibitory control.
The prefrontal cortex is the most highly developed part of the brain. It
develops last, both phylogenetically and ontogenetically. Good brain function
depends on sufficient inhibitory control from the highest level of the CNS: the
prefrontal cortex. Due to its complexity, the prefrontal cortex is vulnerable to
loss of function. If we lose good inhibitory top-down control due to injury, ill-
ness, or sedating substances, this might result in disinhibition, with the release
of immature and primitive behaviors. With ILF neurofeedback, we can improve
prefrontal control substantially, most commonly in combination with parietal
training for physical calming. Training the right prefrontal quadrant (T4–Fp2)
increases the control of emotional reactivity and helps with aggressive, oppo-
sitional, and fearful behavior. Left prefrontal training (T3–Fp1) increases con-
trol of thinking and acting, especially in cases of impulsivity and compulsive

Localized dysfunction might be indicated by reported symptoms, brain injury,
by testing or by brain imaging, all of which is information that suggests useful
training sites.
ILF training has very specific effects depending on frequency as well as on
electrode placement. With ILF training, it becomes increasingly important
where to place the electrodes: left or right, front or back, or intra-hemispheric
or inter-hemispheric. The clinician needs to decide whether sensory processing
in the back of the brain needs to be trained or whether circuits creating output
in the front need to be involved. Does the right side need to be targeted for big-
picture awareness or the left side for the processing of details? Or is there a need
to target limbic areas to impact drives and emotions? It is remarkable how rapidly
shifts in brain state can occur in response to changes in electrode placements.
The changes can be observable in mere minutes. If a new electrode position is
incorporated into the training procedure to address specific functions, it is nor-
mally obvious within one or two sessions whether or not this new site will be
useful further in the training process.
4.2  ILF Neurofeedback: A process-oriented training approach  77 Left and right

The division of the brain into left and right is something neuroscientists do not
like to discuss anymore, as a result of its oversimplification in popular science,
whereby certain skills have been attributed to only one hemisphere (e.g., one
hemisphere for reason and one for emotion, or attributing language function
exclusively to the left). Indeed, our cerebral architecture supports the view that
we effectively have two brains in our head with quite different functions, but it is
critical that they communicate and cooperate with each other, so key functions
such as language cannot be assigned to one hemisphere. Nevertheless, the effects
of left-side and right-side ILF training are very different and these need to be
taken into account throughout (Table 4.3).
We have to consider all of the information that we obtain from the assessment
about life history and symptoms to sort out indicators for left- and right-side
training. For neurofeedback training, it is important to be aware of the fact that
things that are newly learned are mainly processed on the right side, and later,
when they have become routine, they are processed mainly on the left side. This
has implications especially for developmental disorders that normally call for a
lot of right-side training. The foundations of our regulatory hierarchy are pre-
dominantly organized on the right side, and that generally gives priority to right-
hemisphere training as the point of departure. Front and back

Besides the left/right decision, the clinician also needs to figure out whether
training in the back, training in the front, or both is needed. Generally, it could
be said that training in the back of the head improves sensory processing and
training in the front improves executive function. The back of the brain processes
input, which means all kinds of sensory information from outside the body as
well as from inside. In clinical experience, training the back of the brain has an
impact on sensory processing and integration. It improves body awareness and
spatial attention to our environment. The frontal region processes output such
as moving, speaking, planning, thinking, etc. Training over the frontal part of
the brain improves executive function and self-control. Training over the frontal
sites, especially the prefrontal areas, has impacts on impulsivity, as well as on
immature and reactive behaviors. It enhances inhibitory control to give the client
the possibility of considering how to respond prior to acting.

Table 4.3  Training on left and right hemispheres for different issues

Left hemisphere Right hemisphere

Cognitive routine Novelty and flexibility
Self-motivated behavior Environmentally motivated behavior
Top-down control Bottom-up control
Knowledge and skills Sensing danger
Competence Creativity
Later development Early development
78  The evolution of clinical neurofeedback practice Multi-modal association areas

The highest levels of input and output processing in the CNS are the multi-modal
association areas. In these areas, all sensory input from all different modal-
ity-specific areas (visual, auditory, somatosensory, and premotor) and output
modalities is integrated. This is the basis for making sense of all the different
inputs that finally results in adequate feeling, acting, and behavior, a process
that principally involves the right insula and hippocampus. The multi-modal
association areas mainly involve inferior parietal, mid-temporal, and prefrontal
cortical regions. Basic training sites

The multi-modal association areas lead to the basic training sites. As described
in the beginning of this chapter, the training sites were found empirically, but
of course not without knowledge about neurophysiology. The multi-modal asso-
ciation areas correspond to the basic ILF training sites (T3–T4, T4–P4, T4–Fp2,
T3–Fp1, and T3–P3). For most of the clients in ILF training, only a subset of the
basic sites are needed to reach the training goals. To encompass Categories 2–4
in terms of where to train, it is useful to simplify the possible training sites into
a picture of four quadrants plus inter-hemispheric (left–right) training and their
prospective training effects. This places the understanding of front versus back
and left versus right training effects in a simplified model (Table 4.4). Inter-hemispheric
Training in one hemisphere (left side or right side) normally has strong and spe-
cific effects. In some people with instabilities, training in only one hemisphere
might even trigger instabilities. Therefore, a gentler way of training—namely the
reliance on inter-hemispheric placements—can be used alternatively for people

Table 4.4  The four training quadrants plus inter-hemispheric training sites

Left frontal (T3–Fp1) Right frontal (T4–Fp2)

Mental calming Calming of emotional reactivity
Planning and organization Emotional comfort and security
Verbal and written expression Emotional expression
Logical thinking Common sense

Left–right (T3–T4)
Stabilizing of instabilities (e.g., migraine, headache, seizures, panic, mood swings)

Left back (T3–P3) Right back (T4–P4)

Awareness and processing of detail Physical calming
Symbolic processing Body and spatial awareness
Stored knowledge and skills Sensory integration
Orientation to time and space
4.2  ILF Neurofeedback: A process-oriented training approach  79

with instabilities, and particularly for those who do not tolerate left- or right-side
training. This process normally starts with T3–T4 to adjust for the ORF. More specific training sites

More specific training sites are only used after training with the basic sites, which
is often specific enough for most clients. Only in some cases (e.g., in rehabilita-
tion after brain injury or specific learning disabilities) might one take other sites
into account to address specific functions. On the left side, this may be T3–F7 for
word finding and verbal articulation, or T3–T5 for decoding words when read-
ing. On the right side, this may be T4–F8 for the acquisition of language and
emotional expression. T4–T6 might be used to enhance the ability to read facial
expressions and the body language of others, which is useful with clients on the
autistic spectrum. T4–O2 is sometimes an emotionally calming electrode posi-
tion with traumatized clients. Localization theory versus network theory

The most useful training sites have been developed empirically over the years upon
observation of the clinical training effects, as well as on the available knowledge
of functional neuroanatomy, such as the functional differentiation of Brodmann
areas. However, we should not go back to the localization theory. Rather, we should
keep in mind that billions of neurons are working together in complex networks.
This is presently being investigated on the structural level (e.g., in the big human
connectome project [www.humanconnectomeproject .net]). On a functional level,
it is interesting that the key electrode montages that were empirically found in ILF
training target nodes in the default mode network, salience networks, and central
executive network.12 It has been proposed that a number of psychiatric disorders
are characterized by significant deviations in the functional connectivity of these
control networks.15,16 The list includes autism, attention deficit hyperactivity dis-
order (ADHD), and post traumatic stress disorder (PTSD). Interestingly, these are
conditions we are treating very well with ILF training. CATEGORY 5: ALPHA–THETA TRAINING

Alpha–Theta training is not ILF training, but is often a necessary complement to
the work in the ILF domain. Alpha–Theta training is not even primarily a brain
training procedure. It addresses learned fears and habits, and it does so largely
experientially. After physiological calming and stabilizing with ILF training,
the Alpha–Theta procedure can then enable needed processing and resolution
of traumatic experiences, while the client resides in a safe and relaxed state. The
role of reinforcements in the alpha and theta bands is to serve as cues to the brain,
to facilitate state shifts into deeply relaxed, disengaged, and internally directed
states. As a deep-state training, it is only indicated after enough awake-state
training with ILF has been done to provide a stable foundation for the subsequent
experience. Alpha–Theta training is one of the older training protocols that can
fruitfully complement the ILF training process. It is discussed in more detail in
Section 4.3.1, together with other older, but still useful protocols.
80  The evolution of clinical neurofeedback practice

4.2.3 Interaction with the client: Importance of in-session

communication and reports from between-session
effects for adjusting training protocols
All the above categories help us to design a treatment plan and form a hypothesis
of what kind of training sites might be helpful for the client. Training the client can
then rather quickly either confirm or invalidate the hypothesis. Training needs
then to be adjusted step by step based on the response. The client’s response to the
training within the session, and even more importantly after the session, guides us
through the different training categories above. There is no fixed rule about what
to do for how many sessions and when to change parameters, change frequency, or
change or add electrode positions. With some clients, changes can occur in quick
succession, while in other cases, multiple changes in short order might lead to out-
comes that are difficult to interpret in terms of cause-and-effect relationships.
Because ILF training is client oriented, it is a challenge for the clinician and
demands close attention. A burden is also placed on the client. This is why it is
critically important to have good client–clinician interaction and a good under-
standing of the complexity of the training process to be able to recognize and
interpret the training responses. This is not an easy job, neither for the client nor
for the clinician. Most of the clients are not used to reporting on how they feel
and may not be aware of their own state shifts unless they become very uncom-
fortable. Yet for the optimization process, we do need to know about the small
changes in the client’s state and we need to interpret them with the help of the
client as symptoms of under-arousal and over-arousal, or as other indications for
changing or adding electrode sites. So how do we accomplish this, and how do
we proceed in the first session? We have to start somewhere in terms of electrode
position and response frequency and then go from there.
First session: for the starting protocol, we need to decide between two elec-
trode positions according to the assessment, either T4–P4 or T3–T4. Again, we
have to start somewhere, and only after we get the results of the initial training
session do we know whether we made the right decision. Fortunately, it is not as
difficult and uncertain as it seems, because we have clear indications for each of
the two positions that help with the decision. So, if we follow the indications, they
will fit most clients. We start with one electrode position in the first session and
adjust the response frequency as needed.
Indications for starting positions (the given starting frequencies are valid for
the Cygnet® HD-application):
●● T4–P4 is used as a starting position for clients with early development or
attachment issues, chronic disorders, a lack of resilience, or a trauma his-
tory. People with chronic pain, chronic mood disorders, chronic insomnia,
chronic addictions, etc., generally respond best to T4–P4 as a starting posi-
tion for physical calming. With T4–P4, we start with a response frequency of
0.5 mHz and optimize the frequency from there.
●● T3–T4 is used as a starting position for clients for whom right-side train-
ing alone might trigger instabilities. This particularly refers to clients with
4.2  ILF Neurofeedback: A process-oriented training approach  81

instabilities (like migraine, seizure, bipolar disorders, etc.) and no indica-

tions for T4–P4, or in cases where too much right-side calming without
inter-hemispheric stabilization can leave people unbalanced in their func-
tion. This might be an issue, for example, with some attention deficit disor-
der (ADD) clients with no strong indications for T4–P4 training. At T3–T4,
we start with a response frequency of 0.5 mHz and optimize the frequency
from there.
●● If there are indications for both placements, then training is begun at T4–P4
at 0.5 mHz.

If the decision is made for the starting position, we need to know the symptom
baseline for that day, so the client needs to describe their current state concerning
their symptoms and level of arousal. Most people are not well versed in describ-
ing their own state, so in most of the cases they will need some coaching from the
clinician. It is best to ask simple questions, starting with general questions and
then getting more specific. The questions are always open ended, and the inquiry
is conducted in a non-judgmental manner.

●● How does your body feel today?

●● Are you tense or relaxed?
●● How do you feel mentally?
●● Are you tired or awake?
●● Do you have any pain or tension at the moment?
●● Where do you have this pain/tension, can you show the area?
●● Is the pain sharp or dull?
●● On a scale from 0 to 10, where would you judge your pain/tension now?
●● From which situation do you know this symptom?
●● Do you feel this when you are stressed or when you are relaxed or tired?

Why do we need to ask all these questions? We expect to induce state shifts
with the training. To interpret in which direction we shifted the state, we need
to know where we started from. Since we must rely on the client to indicate what
change has occurred, it is important to benchmark their status at the outset of the
session and to place these matters within the conscious awareness of the client.
The next step is to find an appropriate feedback application for the client. For
the first session, this should be a more or less neutral and comfortable one. Why
comfortable? Because if the client feels comfortable with the feedback, it is easier
for their brain to engage with the training. Why neutral? Because state shifts
should be induced by the brain’s response to the signal and not because the client
is suddenly agitated or depressed due to the movie or a car race that is too acti-
vating. What is comfortable and neutral could be very different for each client.
Therefore, it is important to have a variety of options from which to choose.
After the state of the client has been appraised, they are hooked up to elec-
trodes, impedance is checked, feedback is chosen, and then the training ses-
sion can start. The client should be instructed that they need to tell the clinician
immediately if they do not feel good. Otherwise, the session can be run with the
82  The evolution of clinical neurofeedback practice

starting frequency for a few minutes, and then the clinician can begin to query
the client with regard to state shifts. The interview starts again with general open
questions to give the client the chance to describe the experience in their own
words. In a few cases, this might be a detailed description, but most of the time
this will be something like “good,” “I feel fine,” or “no difference.” The clinician
may need to help with some more detailed questions about the symptoms or the
states that were described at the beginning of the session. The questions should
be specific, but not suggestive or tendentious. For example, we might ask: “In the
beginning, you described a pain above your right eye with an intensity of 4. Is
this still the same or did it change during the training?” Further useful questions
might be:

●● Do you feel more alert, less alert, or the same?

●● Is the tension you described in the beginning more, less, or the same?
●● Did your relaxation change? More, less, same, or different?
●● How do you feel mentally?
●● How do you feel emotionally?

In addition to the questions, the clinician of course needs to observe the client
and look for changes in physiology, facial expression, voice, posture and so on.
According to the answers of the client and the observations of the clinician, the cli-
nician needs to interpret the results primarily in terms of under- and over-arousal,
which speaks to the issue of response frequency and also the criteria that bear on
site selection. Low-arousal symptoms are typically obvious and uncomfortable for
the client. Clients might feel groggy, sedated, nauseous, dizzy, or sad. If the client
feels symptoms of under-arousal, the response frequency needs to be increased to
relieve symptoms. If high-arousal symptoms are induced by the training, the client
might feel agitated or physically tense, and the response frequency will need to be
decreased to relieve symptoms. Response frequency always needs to be adjusted
carefully, and usually slowly and incrementally guided by the symptoms reported
by the client.
In clinical practice, it is not always easy to interpret the reported symptoms
correctly; therefore, it is always worthwhile to bring the reported symptoms
into the context of the individual client, and not only to use Tables 4.2 and 4.4
like a cookbook. If we misinterpret the symptoms and change the frequency in
the wrong direction, the client might feel worse after the session. This might be
explained best with the example of how we interpret sleepiness during the ses-
sion. Does sleepiness mean we trained too high, too low, or are going in the right
direction? It could be any of the three depending on the whole picture of the cli-
ent. It could be absolutely fine if somebody feels comfortably sleepy and relaxed.
A lot of people do experience relaxation as a comfortable sleepiness. If people feel
sedated or groggy and uncomfortable, the training frequency was likely too low.
But this is often difficult to differentiate from training too high and bringing the
client to exhaustion, sometimes in combination with eye strain. Therefore, we
need to probe further. A key question is: “Do you know this feeling from certain
situations in your life?” If the answer is something like, “Yes, I normally feel that
4.2  ILF Neurofeedback: A process-oriented training approach  83

way when I am sitting outside in the garden and relaxing,” then one would not
be concerned. If, on the other hand, the client reports to this question with: “Yes,
I know this from when I am very exhausted after sleeping only 2–3 hours for
several days or nights,” then the clinician can be sure that the response frequency
was too high. In this case, if the clinician misinterprets the sleepiness as too low
and raises the response frequency, the client might indeed feel more awake dur-
ing the session, but might have more trouble falling asleep that night. In some
cases, one can only be sure about the interpretation of sleepiness in consideration
of the effect after the session. If the client feels sleepy during the session, refreshed
after the session, and sleeps well at night, this is a confirming sign. If instead the
client feels sedated, heavy, and groggy after the session and sometimes even the
next day, this is a definite sign of having trained too low. As such, one should not
rush to judgment prior to having all the information.
Normally, we stay with the starting site for a few sessions because we want to
be sure of the ORF and the specific effect of the training site. It becomes the base
from which we move in the ongoing training process. Sometimes, there might be
a need to change the starting position in or after the first session. Indications to
change the starting site and rethink the original hypothesis might be

●● It is not possible to find a comfortable response frequency at the first site. For
example, if even the lowest response frequency is too agitating at T3–T4, the
electrodes need to be changed to T4–P4 for a more calming effect. Even at
the lowest frequency, T3–T4 can be too activating for some people.
●● If instabilities are triggered by training at T4–P4, then T3–T4 needs to be
added or even replace T4–P4 entirely for a more stabilizing effect.
●● If there are indications for T4–P4 and headaches are not impacted with the
training, this might be an indication for T3–T4.
●● In some cases, T4–Fp2 needs to be added for more emotional self-control.
T4–P4 is a very calming training, but might lead to right/left or back/front
imbalances for some people. If there is a loss of emotional control due to
T4–P4 training, this is an indication for adding T4–Fp2, while keeping
T4–P4 in the mix. If there is more ADHD-like immaturity and impulsivity,
one needs to move to T3–T4 as a first step on the way to T3–Fp1.

One big advantage of the modern ILF neurofeedback is that clients feel state
shifts and the changing of symptoms very quickly, often after only a few minutes
of training. This makes the process of optimizing response frequency easy. Still,
there are some clients who do not feel any difference during the session. This is
not a reason to panic or shift the response frequency up and down in search of
something better. Even if people do not feel anything during the session, they
might have strong and specific effects after the session. If the clinician’s hypothesis
about the starting position is verified by the client’s response to the training, it
sometimes still takes a few sessions to optimize the response frequency. As such, if
lowering the response frequencies yielded a positive result, even lower frequencies
should be evaluated. If the response frequency has been optimized at the starting
electrode site, but after a few sessions has not impacted all of the symptoms, then
84  The evolution of clinical neurofeedback practice

the next electrode position can be added according to the pattern of dysregulation
indicated. In this case, several frequency rules have to be considered:

●● Response frequencies for basic sites: All right-side sites train with the same
response frequency and the same frequency as T3–T4. The left side, in
most cases, needs to be trained higher, normally two times as high as the
right side and T3–T4. For example, if the response frequency is optimized
on T4–P4 at 0.4 mHz, then T4–Fp2 and T3–T4 should also be trained at
0.4 mHz, whereas training on the left side, like T3–Fp1 or T3–P3, should be
at 0.8 mHz. An exception is that if T3–T4 or T4–P4 is already being trained
at the lowest frequency (0.1 mHz), it might be that left-side sites are also
trained best at frequencies less than the expected 0.2 mHz.
●● Response frequencies for inter-hemispheric sites: The response frequency for
inter-hemispheric training at Fp1–Fp2 needs to be divided by 2 from the
response frequency at T3–T4. The response frequency for inter-hemispheric
training at P3–P4 needs to be divided by 4 from the response frequency at
T3–T4. For example, if the response frequency for T3–T4 is optimized at
0.8 mHz, the training frequency for Fp1–Fp2 would be 0.4 mHz and for P3–P4
would be 0.2 mHz. An exception is that if T3–T4 is already trained at the
lowest frequency (0.1 mHz), the other inter-hemispheric sites might also be
trained best with 0.1 mHz.

Besides these rules, response frequency is always an issue in further training.

For some people, the optimal response frequencies can be kept constant during
the whole training process; for others, they need to be adjusted repeatedly. It has
to be considered that if the response frequency needs to be adjusted at one site,
then all other sites likely have to be adjusted accordingly.
In building up the training process step by step, the clinician must be very
clear about the rationale for changing training parameters and what effects are
expected due to the change. Of course, the expected effects then need to be veri-
fied during the training session and, even more importantly, with the results after
the session. For the interpretation of training effects, it is absolutely essential that
only one parameter be changed at a time, either frequency or electrode position.
Too many steps in frequency within a session can make for difficulties in the
interpretation of what effects can be attributed to a particular cause. The training
parameters and changes need to be documented accurately in order to keep the
training process comprehensible. This cannot be emphasized enough. The train-
ing process needs to be as disciplined as is possible within a clinical setting. At
each step, we have to document what was changed and why. Did the change of
training parameters result in the expected training effects? If so, it could be con-
tinued, but if not, the hypothesis of the clinician needs to be rethought. However,
the clients do not react like machines, of course. Sometimes, this is obvious after
one session and sometimes it needs a few sessions to become apparent.
As the training process continues, we have to determine which training sites
are useful and which can be dropped. Useful sites are kept in the mix, and sites
that bring negative effects or no effects can be skipped. Normally, the training
4.3  Combining the ILF approach with proven older neurofeedback methods  85

will end up with two to four useful sites and the training time should be divided
equally among all sites. The addition of Alpha–Theta training is described in
Sections 4.3.2 and 4.3.3.
The training progress should be assessed regularly with adequate tools like
the symptom tracking system, CPTs, or whatever is appropriate in each case. In
most cases, successful completion of the training can be achieved in 20, 30, or 40
sessions. If the training goals are reached or sometimes even exceeded early, the
training should not be ended too abruptly. Instead, it is suggested that training
sessions be spaced further apart to verify that the effects are long lasting. There
is no risk of training too much; on the contrary, there is always room for the
improvement of function and quality of life.


4.3.1 Reasons for doing this
If we talk about the ILF approach as formalized in the Othmer method, the
awake-state training over all the years has been usefully complemented with
Alpha–Theta training. Alpha–Theta training is one of the most impressive train-
ing methods from the early days of neurofeedback. One important principle of
ILF training concerning electrode position is to keep useful sites and skip train-
ing sites that are not useful. The same principle holds true more generally for the
different neurofeedback approaches. Alpha–Theta training is one neurofeedback
method that has always been useful and obvious in its effect. It is not alone in
that regard. There is ongoing investigation into how other methods that train for
enhanced synchrony of the resting rhythm EEG frequencies can also effectively
support ILF training.

4.3.2 Combining with Alpha–Theta training

Alpha–Theta training addresses the resolution of learned fears and adverse pat-
terns of habitual responding. This training is incorporated after physiological
stabilization is achieved with the awake-state training in the ILF range. Alpha–
Theta training has a long history. As early as 1966, Joe Kamiya17 successfully
reinforced the alpha rhythm in the EEG of his subjects by ringing a soft bell every
time he observed alpha spindles in the EEG. As a result, the trainees learned to
produce more alpha activity. Elmer and Alyce Green from the Menninger Clinic
in Topeka, Kansas, worked with alpha training as well as with Alpha–Theta
training. They saw the theta component of the experience as the entry portal
for transformation. For more than 20 years, they travelled all over the world to
teach biofeedback and self-regulation techniques and investigate the brain waves
and other bio-signals from meditators, shamans, and healers. Some experiences
of their fascinating journey were published in the book Beyond Biofeedback in
1977.18 Another pioneer in this field is Les Fehmi, who, in the late 1960s, started
with alpha synchrony training. Later, he combined the EEG training with other
86  The evolution of clinical neurofeedback practice

techniques like mindfulness training for mental and physical health. His more
than 30 years of research and professional experience are summarized in his very
absorbing book “The Open Focus Brain,” published in 2007,19 in a perfect combi-
nation of theoretical background, practical exercises, and first-hand experiences.
As already described in Chapter 2 of this book, several studies in which Alpha–
Theta training was successfully used in the treatment of addiction and PTSD

4.3.3 How is Alpha–Theta training performed?

Alpha–theta can be trained with one or more EEG channels. In the single-chan-
nel mode, training a unipolar montage is used. One active electrode is positioned
on Pz and the reference is behind one ear (mastoid). The ground can go anywhere
on the head, but normally the other mastoid is used for the ground. Alpha as well
as theta frequencies are rewarded to allow the client to shift to a relaxed alpha
state, and from there to a hypnagogic state, alternating between alpha and theta
dominance. Delta is inhibited to prevent a shift into sleep states. Beta and high
beta are inhibited to allow the brain to calm down. Traditionally, the training is
done under eyes-closed conditions. This is because the unloading of the visual
system increases the incidence of alpha spindles in the EEG. However, eyes-open
training has also had a long history. Modern neurofeedback systems allow the
client to choose from a variety of calming, peaceful scenes, like a forest, beach,
fireplace, etc. For some people, a pre-recorded guided imagery routine can be
used to help shift attention away from the outside to the inner realm. Of course,
clinicians can also use their own personalized imagery scripts that are adapted
to the client’s needs.
Sensory deprivation can be used to facilitate entry into deep states. The cli-
ent should sit or lie comfortably and with closed eyes (perhaps aided with eye
shades), with auditory feedback delivered via headphones, and cocooned in pil-
lows and a blanket. Training time is normally 20–30 minutes. There is no special
introduction to the client, except something like, “Allow yourself to relax with-
out falling asleep.” There is no need for the client to try to influence the differ-
ent noises and tones from the feedback. Instead, the client should simply accept
whatever happens and yield to the sounds. Some clients are already acquainted
with special relaxation or meditation techniques, but these should not be used
during the Alpha–Theta training. Instead, the brain should be allowed to inter-
act with the feedback signal by itself, without guidance or direction. Normally,
if people close their eyes and fall into a light trance, the alpha amplitude in the
posterior region rises almost immediately. After a while, for most people, the
alpha drops down within a few minutes, sometimes below the theta amplitudes,
and theta might even rise a little bit, indicating a deeper state. Still, the client’s
experience can never be judged by the trend lines, and if the client had wonderful
experiences during the session and positive effects after the session, there is no
need to be concerned about producing higher alpha or theta amplitudes! These
are mere indices of residence in particular states, and that is what matters, rather
than the particulars of the waveform.
4.3  Combining the ILF approach with proven older neurofeedback methods  87

In alpha–theta states, cortical control is loosened and dream-like pictures might

emerge. It is a state somewhere at the edge of sleep, which is a state of high suggest-
ibility that is optimal for the self-regulation of psychological processes in a manner
that is once again totally self-directed. Actually, this is a very natural state, but
unfortunately not very supported in our culture. We all go through these states at
a minimum on our way to sleep or back again to wakefulness. In Western cultures,
these states are too brief for many people to really enjoy or benefit from them. A lot
of clients report feeling that their brain only knows two states: a busy awake state
and sleep. They definitely miss the variety of states in-between these two states.
The Alpha–Theta training is very helpful for facilitating residence in this
undefended state that allows the resolution of traumatic experiences, the finding
of solutions to personal crises, and the working out of relationship issues from a
position of feeling safe and intact. This is the venue in which the core self finds
expression through imagery and visual narrative. The experience can be pro-
foundly healing to the traumatized self in a way that is difficult for the persons
themselves to verbalize.
An Alpha–Theta training session should not be stopped abruptly. Instead, it
should be brought to closure gently by fading out the feedback and giving the cli-
ent sufficient time to come back and reorient. Some clients like to talk about their
experience at that time, so there should be enough time given for that. Others
may need a few minutes of awake-state training to reorient.
For most people, Alpha–Theta training is a very comfortable and useful form
of training, not only for psychological issues, but also in terms of peak perfor-
mance and the visualization of goals and the ideal self, or to deepen mindfulness
training. Nevertheless, if Alpha–Theta training is used too early in the training
process, there might be some uncomfortable reactions. Therefore, it needs to be
handled with care and should only be used after enough awake-state training has
been done. There are a few indications that show the clinician that the client is not
ready for Alpha–Theta training that we have to keep in mind:

●● Persons who are still anxious and hypervigilant and unable to relax will not
benefit from Alpha–Theta training. They report not enjoying the session and
might actually feel more anxious. These clients normally need more sessions
of awake-state calming or stabilization training before they can benefit from
Alpha–Theta training later on in the training process.
●● If people are still anxious and hypervigilant, it might be that they are unable
to relax and benefit from Alpha–Theta training. After an Alpha–Theta train-
ing session, they normally report that they were not able to relax and did not
enjoy the training. These clients normally need more sessions of awake-state
training and might benefit from Alpha–Theta training later on in the train-
ing process.
●● Some ADD clients and people who are very exhausted fall immediately
asleep when they relax. They also need more awake-state training until they
are able to relax without falling asleep.
●● Alpha–Theta training might trigger instabilities in unstable brains, because
Alpha–Theta training enhances synchronous EEG activity. If this happens
88  The evolution of clinical neurofeedback practice

within the Alpha–Theta training session, this can usually be corrected

immediately with a few minutes of stabilizing training on T3–T4, if this was
tolerated before, or else with their primary awake-state training protocol.
Alpha–Theta training should only be tried again later on in the training
process, after more awake-state training focused on stabilization has been
conducted. For some clients, Alpha–Theta training can be done only if it is
balanced with a few minutes of stabilizing ILF training after the Alpha–Theta
training session. For others with instabilities, it is enough if they alternate
Alpha–Theta training and awake-state sessions.
●● In clients with a trauma history, Alpha–Theta training is an important part
of the recovery process, but it could lead to abreactions if it is used too early
in the training. Although abreaction might be a useful aspect in several
kinds of psychotherapy, it is not an intentional part of the Alpha–Theta
training. If an abreaction happens during the Alpha–Theta training, there
is no need to panic. The clinician should keep calm, stop the feedback, and
let the client report what is happening. The next steps depend on the clini-
cal background of the clinician. If the clinician is trained in working with
abreactions, they might want to seize this opportunity. In other cases, and
in terms of neurofeedback, the client could be stabilized with awake-state

The above list makes it very clear that the clinician should always know the
“parachute” for each client before Alpha–Theta training. What does that mean?
The clinician should always know for each client which ILF training position and
frequency leads to which effect. If a new training site or a new kind of training,
like Alpha–Theta training, is added to the treatment plan, the basic stabilizing
positions and the ORF need to be known to have the possibility for correction
if changing of the training parameters leads to negative effects. Without know-
ing this parachute, it is not advisable to experiment with new training param-
eters. Neurofeedback effects are strong and specific and need to be handled with
care and responsibility. There is no one-size-fits-all protocol in the ILF training
approach, and also Alpha–Theta training might not be suitable for everyone, but
it is always worth a try.

4.3.4 Combination with two-channel sum training

In two-channel sum training, two EEG channels, each with a unipolar elec-
trode montage, are summed to yield the feedback signal. This type of training,
which has been done up to now only within the conventional EEG spectrum,
promotes common-phase or synchronous activity in the reinforced frequency
band. Historically, it has typically been used with the primary cortical resting
frequency, the famous alpha band. The most commonly used two-channel sum
training is probably two-channel Alpha–Theta training, which can therefore be
considered paradigmatic for two-channel sum training in general.
The EEG for one-channel Alpha–Theta training, which was discussed above,
is normally recorded at Pz, and increases in alpha and theta amplitudes are
4.4  Closing remarks for neurofeedback clinicians  89

rewarded. Increases of amplitudes in the reward bands correlate with locally syn-
chronous activity in the reward band underneath the active electrode. In two-
channel Alpha–Theta training, normally one channel picks up the EEG at P3 and
the other channel at the homotopic site P4 on the other hemisphere. This means
that the training promotes synchrony in the reward frequency band simultane-
ously at two distal sites (P3 and P4). This results in an even greater degree of syn-
chrony of neuronal network activity between the two hemispheres. In work with
clients, it is advisable to start with one-channel Alpha–Theta training, to be sure
that synchrony training is tolerated by the client, especially in clients with insta-
bilities. Then, two-channel sum training can be implemented as the next step.
For most people, this has a stronger and deeper effect than one-channel training.
There are special two-channel neurofeedback applications available that not
only reward the sum of signals in the reward band, but also explicitly reward
synchrony, or phase correspondence, in the reward band at the two training
sites. Compared to the traditional two-channel amplitude reward mode, people
trained in this way report that they sometimes reach completely new and com-
fortable resting states faster and deeper than before.
The fact that EEG training is being done fruitfully with such a variety of
immediate objectives, some of them even mutually inconsistent, compellingly
demonstrates that the objective is not the attainment of specific states, but rather
the enhancement of the control of state. Alpha–Theta training complements this
kind of training by using these same capabilities for experiential purposes that
are clinically relevant and promote the fuller human experience.


Please work respectfully with the client’s brain and only use neurofeedback
methods that you are sufficiently trained in! This chapter can only provide a short
overview to give an impression of the ILF neurofeedback approach and how it
could be combined effectively with older approaches to get the most beneficial
effects for clients. It can never replace a training course with its practicum exer-
cises, self-training experience with neurofeedback under competent supervision,
and live discussion of training results among peers.
In the meantime, neurofeedback is a very rapidly developing field due to
increasingly technically advanced and user-friendly medically approved prod-
ucts. Neurofeedback is not a mechanical instrument that displaces one’s thera-
peutic work. It is a very effective tool that supports one’s work. To use this tool
in the most beneficial way for one’s clients, it needs to be emphasized that the
paradigm of the symptom-driven ILF approach demands a high level of thera-
peutic skills, as well as sensitive clinical decision-making and astute interpret-
ing of training results in order to use this capability in the most beneficial way
for the client. Because of the complexity of this work, and because this method
is still in its early stages of maturation, neurofeedback practitioners using this
method should be in contact with colleagues and mentors to refine their work,
and always work respectfully within the scope of their professional expertise and
90  The evolution of clinical neurofeedback practice

support networks. In neurofeedback, we interact with a complex self-organized

system that is daunting in its complexity. We are still very far away from under-
standing it completely, but at least we have learned to understand the reactions
to the applied neurofeedback training sufficiently in order to adapt the training

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An Integrative Approach
to Health

5 Neurofeedback in an integrative medical practice 95

Doreen E. McMahon
6 Nutrition and the brain 117
Nora T. Gedgaudas
7 Biomedical factors that impact brain functioning 147
Kurt N. Woeller
Neurofeedback in an
integrative medical practice


5.1 Assessment and screening 96

5.2 Diet and nutrition 96
5.3 Brain–gut connection 98
5.4 Physical exercise and the brain 98
5.5 Sleep management 99
5.6 Behavior management 100
5.7 Medications and neurofeedback 101
5.8 Case presentations 101
5.9 Conclusion 111
References 112

Neurofeedback has been successfully applied to patients with a variety of men-

tal health issues by professionals in the psychology and social work communi-
ties. However, neurofeedback is recognized by few practitioners in the allopathic
(mainstream) medical community, even though biofeedback received the
highest level of efficacy rating for the treatment of attention deficit disorder by
PracticeWise, a research service acting on behalf of the American Academy of
Pediatrics (AAP).1 This may be due to a paucity of published studies of neurofeed-
back in major medical journals and because neurofeedback is associated with the
treatment of non-medical issues.
However, numerous studies have been published that show the efficacy of
neurofeedback in the treatment of sleep issues,2 migraine headaches,3–5 seizure
disorders,6–10 fibromyalgia,11 chronic fatigue syndrome,12 autistic spectrum dis-
order,13 and traumatic brain injury.14 Despite this evidence, many in the scientific
community have difficulty accepting the efficacy of a treatment modality that
does not lend itself to the supposed gold standard of a double-blind study. An
experiment has not yet been designed in which it would not be readily apparent

96  Neurofeedback in an integrative medical practice

to experimental subjects as well as the personnel administering neurofeedback

when a sham neurofeedback treatment is being given.
Neurofeedback can be viewed as carefully applied brain fitness by exploit-
ing latent brain plasticity.15 Just as body fitness is desirable in maintaining good
health and helping to overcome the symptoms of many health and mental health
conditions, neurofeedback can similarly improve functionality, both physical
and psychologically, for “medical” issues.16
I was introduced to neurofeedback when I was exploring alternative tech-
niques to help my then 10-year-old son with autistic spectrum disorder.
Medications, behavioral therapy, speech therapy, occupational therapy, and
social skills training provided little or only temporary relief from his symp-
toms. Electroencephalographic (EEG) neurofeedback slowly, but surely,
enabled him to benefit from his therapies and be weaned from medications. He
is now successfully studying to become a teacher at a major state university.17
In this chapter, I am presenting recent case studies from my practice as a
solo physician in a “neurointegrative” practice. In all cases, EEG neurofeedback,
using the equipment and training protocols18 of the EEG Institute of Woodland
Hills, California, was the primary therapeutic modality, even as other treatments
were integrated into patient care.


The initial visit for a neurofeedback patient begins with a thorough history and
physical examination. At a minimum, this should include a detailed description
and history of the presenting issues, past medical and mental health histories,
medications, non-prescription medications and dietary supplements, aller-
gies and intolerances towards medications and foods, family health and mental
health history, health habits (smoking, drinking, recreational drug use, caf-
feine use, exercise, and diet), and a review of the major body systems. A physical
examination should be performed with especial emphasis on areas of complaint,
the nervous system, and brain function. Review of previous laboratory work and
studies can be very helpful. The clinician should analyze these results and form
a treatment plan.
As in regular medical practice, many patients presenting for neurofeedback
have the need for instruction and ongoing coaching in basic health maintenance.
Areas that frequently require attention include: diet and nutrition, physical activ-
ity, sleep, and the development of healthy brain behaviors.


A lack of basic vitamins, minerals, and other essential nutrients can adversely
affect the function of many body systems, including the brain.19 Therefore,
patients’ dietary proclivities are important in ensuring the effectiveness of neu-
rofeedback. Underlying medical conditions that can cause nutritional deficien-
cies should be identified and adequately treated. Many patients have diets that are
5.2  Diet and nutrition  97

restricted in basic nutrients due to food flavors and/or textures, poor nutritional
knowledge, unhealthy ingrained habits of eating, and neurological or gastroin-
testinal difficulties. Consultation and treatment by a dietician, nutritionist, or
speech therapist may be an essential part of treatment for complicated or difficult
patients. However, many patients can be treated with reminders to follow healthy
dietary guidelines20 with increased use of whole foods and decreased consump-
tion of prepared, fatty, and sugary foods.19
There may be indications for special diets based on dietary history, special-
ized testing, and observation. These may include: Feingold diet,21 elimination/
reintroduction diet, 22 gluten-free/casein-free diet, 23 specific carbohydrate diet, 24
and gut and psychology syndrome (GAPS) diet.25 Since patients may already
utilize specific diet plans, clinicians should familiarize themselves with the
basic guidelines of these diets, even if they are not comfortable prescribing and
helping patients adopt them.
Supplementation of commonly deficient nutrients is frequently indicated in
those receiving neurofeedback. Caution must be taken to carefully evaluate each
patient who is receiving supplements for contra-indications or complications
from dietary supplements. A multivitamin can be recommended for those who
are unable to get adequate nutrition via a healthy diet.26 While supplementation
must be carefully individualized, omega-3 fatty acids, vitamin D3, and magne-
sium are commonly used in my neurofeedback practice.
Neurofeedback induces changes in the architecture of both gray and white
matter in the brain.27,28 Essential fatty acids, in particular omega-3 fatty acids, are
generally agreed to be vital to brain health, since they must be present to form the
myelin sheaths that make up about 60% of brain volume.29,30 Omega-3 fatty acids
via dietary and supplemental sources can ensure adequate molecular building
blocks for the brain remodeling process31 induced by neurofeedback training.
Omega-3 fatty acids are generally quite safe, but they should not be mistaken for
fish liver oil that contains vitamin A, which can be toxic at large doses.32
Vitamin D deficiency is estimated to be at around 70% in white and 95% in
African-American populations in the United States.33 Manifestations of vitamin
D deficiency can include chronic fatigue, fibromyalgia, weakness, and mood dis-
orders,33,34 symptoms that are seen in many patients who present for neurofeed-
back. Vitamin D3 levels can be measured with blood work. However, empiric
supplementation of vitamin D3 of 1000–2000 IU daily is felt to be safe in those
without obvious risk factors for over-supplementation.34
Magnesium is another vital nutrient to nervous system function that is often
deficient due to depleted farming soils and removal from municipal water sup-
plies. Adequate levels of magnesium have been shown to treat depression, anxi-
ety, headaches, seizures, psychosis, and irritability.35 Magnesium supplements
can interact with a number of medications including digoxin, oral anticoagulants
and quinolone and tetracycline antibiotics. Kidney function should be normal.
Magnesium doses of 200–350 mg daily are usually well tolerated. For those who
experience loose stools or cannot take oral supplements, Epsom salt baths (1–2
cups of Epsom salts and half a cup of baking soda in at least 6 inches of water) are
an excellent and calming alternative.35
98  Neurofeedback in an integrative medical practice

The interconnected nature of the brain and the digestive system has been studied
for over a century. Recent advances in functional brain imaging techniques have
enabled scientific inquiry into central nervous system interactions with the human
gut to flourish and shown that their relationship is far more intimate than previously
supposed.36 For example, the limbic system of the brain, which plays a central role in
emotional regulation, is the area most concerned with gut control. Some neurotrans-
mitters have been demonstrated to be more plentiful in the gut than a­ nywhere else
in the body, including the brain.37 The integrated nature of the function of these
systems has been exhaustively demonstrated and may explain the emotional influ-
ence on the control of insulin and blood pressure regulation.38,39 Thus, ensuring the
optimal function of both should be prioritized in a neurofeedback practice.
Eliciting good patient history data that go beyond the usual review of sys-
tems is imperative. Dietary history should include information about patient
intake and reactions to potentially neuroactive substances such as coffee, tea,
sodas, spices, and other foods and food additives. A functional history of chew-
ing, swallowing, satiety, gastro-esophageal reflux, belching, nausea, vomiting,
abdominal cramping, flatulence, bowel movements, and pain patterns may help
guide treatment modalities in addition to neurofeedback.
Of particular interest to practitioners of neurofeedback are the influences of
food allergies and intolerances on brain function. Sensitivity to the wheat pro-
tein, gluten, and the milk protein, casein, in the form of elevated antibody lev-
els, have been clearly linked to neurological dysfunctions of unknown cause.40,41
National Institute of Allergy and Infectious Diseases Food Allergy Guidelines
can steer the investigation of food allergies.42,43
Dysbiosis—abnormal microbial flora—can also contribute to immunological
and physiological disruption of digestive and neurological function.44,45 A cycle
of inflammation and abnormal function of intestinal and blood–brain barriers
is thought to allow incompletely digested neuroactive substances, such as caso-
morphins (from milk) and gluteomorphins (from wheat), to cause neurological
symptoms.46–48 Implications for treatment include removing offending foods
from the diet, improving digestion function via enzyme supplements, and cor-
recting dysbiosis.39,49–51


Lack of adequate physical activity is a frequent finding in the patient popula-
tion presenting for neurofeedback. Regular aerobic exercise has been proven
to increase physical and mental health.52 Exercise, along with prudent dietary
habits, promotes the activity of the brain-derived neurotrophic factor (BDNF)
system, which plays a critical role in the interface between metabolism and cog-
nition.53 Exercise has been shown to increase the effects of the BDNF system in
conjunction with omega-3 fatty acids.31 Treatment of anxiety and depression
with exercise and yoga has been shown to be as efficacious as cognitive behav-
ior therapy and medication.54 Experiments have demonstrated that exercise for
5.5 Sleep management 99

5 hours a week at 80% of estimated aerobic capacity shows significant protec-

tive effects against neurotoxins in monkeys.55 Exercise guidelines for children,
adolescents, adults, and older adults are available at

Chronic lack of adequate sleep has been linked to many health and mental health
issues that include obesity, poor dietary choices, heart disease, hypertension,
elevated cholesterol levels, diabetes, cancer, Alzheimer’s, depression, increase in
inflammation, deterioration of performance of daily activities, substance abuse,
and shorter lifespan.57 Sleep disorders are estimated to be as prominent as 50% in
children in the United States and are felt to contribute to daytime sleepiness, irri-
tability, behavioral problems, learning difficulties, poor academic performance
and, in teenagers, to motor vehicle accidents.58 The average American adult gets
less than the recommended 7–9 hours of sleep a night.59

Sleep hygiene rules

●● Keep the same wake time 7 days a week.

●● The bed should be used for sleep only (no TV, no radio, no reading,
●● Sleep nowhere else except in bed.
●● Leave the bedroom if you awaken and cannot get back to sleep within
15 minutes.
●● Return to bed only when you are sleepy. Leave again if you cannot get
to sleep within 15 minutes. Repeat as necessary.
●● Do not time watch. Clocks should not be visible from the bed.
●● Keep the sleeping area quiet, dark, and cool. Use earplugs, eyeshades,
and other aids as necessary to accomplish this.
●● Activity levels for 30–60 minutes prior to bedtime should be very lei‑
surely and unimportant (not TV, especially news programs).
●● Maintain a regular bedtime.
●● Cut down on or eliminate caffeine.
●● Cut down on or eliminate tobacco products.
●● No alcohol consumption within 4 hours of bedtime.
●● Do not go to bed hungry, but no snacks with sugar or refined carbohy‑
drates near bedtime.
●● Use exposure to bright sunlight or artificial sunlight early in the day to
awaken and reset light-reactive hormone cycles.
●● School-aged children need a minimum of 8 hours—preferably at least 9
hours—of sleep per night.
●● Adults need a minimum of 7 hours—preferably 8 hours—of sleep
per night.57–60,68
100  Neurofeedback in an integrative medical practice

A thorough sleep history includes sleep initiation, sleep duration, arousals

during the sleep period, ability to awaken, daytime sleepiness, bruxism, move-
ments during sleep, dreaming patterns, snoring, apneic breathing patterns,
enuresis, sleeping positions, sleep environment, and sleep timing.58 Overnight
polysomnography (sleep study) can be used to help identify sleep problems that
are not readily distinguished by history. Neurofeedback can help with the man-
agement of many sleep issues in conjunction with specific therapies58,59 and pris-
tine sleep hygiene.60
Even with effective neurofeedback and strict adherence to good sleep hygiene,
sleep normalization can take weeks or months. Practitioner coaching and focus-
ing on maximizing daytime functioning can help patients maintain patience
while striving for the goal of satisfactory sleep.

A psychological and physical environment that supports positive changes in
behavior is vital to the success of neurofeedback. Even as neurofeedback therapy
changes arousal levels of the brain and strengthens cortical tracts, the behaviors
that allow improved function need to be strengthened. Just as sending an addict
from a recovery program back to their “using” environment seems to correlate
with relapse, having a neurofeedback patient stay in a setting that helped pro-
mote or did not prevent their symptoms can slow or confound progress towards
wellness. History-taking during initial and follow-up encounters should be used
to form impressions about psychosocial conditions that could be modified to
encourage healthy functioning.
Among the environmental issues that can complicate neurofeedback treat-
ment are poor or disrupted personal relationships. Mental health professionals
and community resources can be utilized to guide patients and their significant
others to more useful modes of conduct and better cognitive states. Parent–child
interaction problems can be especially troublesome, since parenting skills are
usually acquired “on the job” and reflect the parents’ upbringing, rather than the
specific needs of an individual child. Parent–child relationships can get stuck in
maladaptive ruts of unrealistic expectations and negative emotions. Carefully
delineated behavioral incentive systems can foster improved behaviors, codify
accountability between adults and children, and enable positive cognition.61
Practitioner support in the development, adaptation, and implementation of a
behavioral system is often vital in making it a successful intervention.
The overuse of electronic media, including television, computers, and video
games, is another concern for the general population, as well as in patients
receiving neurofeedback. The American Academy of Pediatrics has determined
that the average child spends 7 hours per day using entertainment media and
recommends that children under the age of two use no media and that older
children and teenagers use only 1–2 hours per day.62 Media exposure is linked to
drug use, alcohol use, low academic achievement, earlier initiation of risky sex-
ual behaviors,63 eating disorders, obesity, sleep disorders, and attention issues.64
Functional magnetic resonance imaging (MRI) has shown that playing violent
5.8 Case presentations 101

video games is directly connected with lasting changes in the brain regions
associated with cognitive function and emotional control.65,66 A small percent-
age of child and teenager video game players show multiple signs of behavioral
addiction, including academic problems, increased lying, and inability to cut
back on gaming.67
Practitioners need to be aware that it can be difficult to cut the electronic
umbilical cords, since media are used as safe and affordable distractions, as well
as parents’ modeling of heavy media use, the incorporation of media—especially
TV—in household routines and a need to fill leisure time. Frank and frequent
discussions with health care providers on ways to limit electronic media use to
recommended levels may help households implement rules on media consump-
tion. These should include paying attention to the amount of entertainment
media utilized, not placing a television in a bedroom, eliminating background
television, limiting television viewing especially on “school days,” identifying
non-screen, in-home activities that are pleasurable, and disconnecting television
use from eating.68


Medications must be closely monitored and adjusted in someone receiving neu-
rofeedback. As the brain becomes better self-regulated, symptoms may arise that
look like medication overdose. For instance, a patient on a seizure medication
may have an increase in lethargy and fatigue. This effect is not limited to medica-
tions that are generally considered to be brain specific. For example, blood pres-
sure medications might become overly effective. Careful vigilance throughout
the course of therapy is important. For many patients, decreasing or eliminating
medications is a desirable goal of neurofeedback.

Patient 1: 38-year-old man presented with functional difficulties and constant,
chronic pain from multilevel spinal injuries. Failed therapies included surgeries,
an implanted neural stimulator, and epidural medication. Therapies with lim-
ited effectiveness were: acupuncture, chiropractic manipulation, massage, physi-
cal therapy, cranio–sacral therapy, meditation, transcutaneous electrical nerve
stimulation (TENS), antidepressant medication, neuromodulator medications,
anti-inflammatory medications, muscle relaxers, and narcotic medications. He
took Ultram, Flexeril, Dilaudid, Tylenol, and Advil on an as-needed basis, which
was usually multiple doses per day. Pain caused him problems with sleep initia-
tion and maintenance. Physical and mental stresses led to pain crises approxi-
mately weekly that confined him to bed for 2–4 days at a time. He was anxious
about being able to provide for his family and his mood was depressed. He had
heartburn 80% of the time. His ability to function at work and be available to his
family was severely limited.
Neurofeedback was started based on Othmer protocols at T4–P4 for physi-
cal calming and sensory integration. Reward was optimized at 0.1 mHz before
102  Neurofeedback in an integrative medical practice

gradually adding Fp2–T4, T3–T4, and Fp1–T3 sites over ten sessions. Medication
use was altered so that the patient took his most effective medications on a regu-
lar basis, and he used a set protocol at the onset of more significant discomfort.
Education in sleep hygiene was undertaken and reinforced at each visit. Physical
activity types and levels were reviewed. Regular low-stress, better-tolerated exer-
cise was initiated.
After approximately 25 sessions of neurofeedback, pain levels were reduced to
manageable levels most days. The patient was aware of discomfort, but felt like he
was able to push it to the back of his mind and control it. Ultram was used on a
daily basis. Dilaudid and Flexeril were needed for moderate pain flares every 7–10
days. Heartburn was resolved. He rarely missed work due to back issues. Sleep
was longer and more restful, even though compliance with sleep rules was loose.
Energy levels were significantly increased and mood was vastly improved. Activity
tolerance was up. The patient felt much more involved with family activities. He
saw his chiropractor infrequently. Over 50 sessions of neurofeedback were com-
pleted and the patient comes back for a “recalibration” session every few months.
Patient 2: 56-year-old woman was recently retired on disability for fibromyalgia.
Her physical activity was severely limited due to pain and stiffness every day. Pain
and restless legs disrupted sleep initiation and maintenance. She never felt rested
and had problems with focus and memory. She had been diagnosed with attention
deficit disorder (ADD) in the past. Her mood was depressed, and she was anxious
about dealing with and providing for her teenage son as a single mother. Her house
and yard were “a mess” because she had neither the energy nor the strength to orga-
nize or clean. Her past medical history was significant for psoriasis with arthritis
and osteoporosis. Medications were numerous and included Concerta, Cymbalta,
Lamotrigine, Voltaren, Etodolac, Seroquel, and medications specific for psoriasis.
Dietary supplements included: multivitamins, Coenzyme Q10 (CoQ10), curcumin,
S-adenosyl methionine (SAM-e), vitamin D3, zinc, and krill oil. Family history
revealed attention disorders and alcoholism. The patient was a non-smoker and
non-drinker who avoided caffeine because it made her “jittery.” She saw a mental
health counselor on a twice-a-week basis. The physical examination was significant
for sad affect with occasional crying. The patient moved slowly and with obvious
discomfort. TOVA• (Test of Variables of Attention) showed a significantly dysfunc-
tional score of –7.43.
The patient was started on a course of neurofeedback per Othmer protocols at
T4–P4 for the calming of physical sensations and anxiety. Reward frequency was
optimized to 0.1 mHz before gradually adding Fp2–T4, T3–T4, and Fp1–T3 sites
over 12 sessions. Discussions about establishing daily routines and good sleep
hygiene were initiated at each therapy session. By her tenth session, she was expe-
riencing better moods and increased energy to the point that she started swim-
ming laps at the local pool 3–4 days per week. She was starting to tackle household
chores for an hour or two a day. Episodes of depression, low energy, and physical
discomfort still occurred every few days. By session 40, TOVA had normalized to
+0.57. Weaning the patient from Concerta, Cymbalta, Lamotrigine, and Seroquel
was initiated. By session 50, she was no longer taking any of these medications.
As long as she was following good sleep hygiene and swimming 4–5 days a week,
5.8 Case presentations 103

her energy levels and moods were good, even though her teenage son was having
behavioral issues and she was caring for her terminally ill mother. A behavioral
incentive program was set up for son. Counseling about realistic expectations for
dealing with the dying process of her mother was included in each session, and
the patient coped well when her mother died.
The patient found that she rarely experienced any inappropriate physical dis-
comfort or mood problems as long as she had a neurofeedback session every 1–2
months. She also found that when she practiced good sleep hygiene, her energy
levels were appropriate. She became reasonably organized in her household and
developed a normal relationship with her teenage son. She volunteered several
days a week at an animal shelter, where she tolerated mild-to-moderate physical
effort. Friends and family told her that she was a “new person.”
Patient 3: 9-year-old girl with a history of traumatic head injury at 7 years of
age in the left fronto–temporal head areas, resulting in a seizure disorder. Multiple
left-sided seizure foci were observed with EEG studies. Three different types of
seizures had been diagnosed, including absence seizures, myoclonic seizures, and
rare generalized tonic–clonic seizures. The mother noted multiple, daily episodes
of unresponsiveness followed by decreased alertness, focus problems, and inabil-
ity to learn academic material. During the night, the child had one to three epi-
sodes of limb and body jerking, as well as enuresis. She complained of almost
constant feelings of “electricity” in her legs and sometimes in her arms. Her per-
sonality had gone from sunny and outgoing to introverted and fearful. She was
unable to attend school because of her seizures. She was home schooled, but was
behind grade level due to an inability to retain knowledge. Social interactions
were fairly normal within her family, but severely compromised by her social iso-
lation and her worries of having seizures in front of peers. She had been minimally
responsive to multiple trials of anti-epileptics including Lamictal, Topiramate,
and Vimpat. Current medications were Lamictal, Topiramate, Pulmicort inhaler,
Albuterol inhaler, Singulair, and vitamin B12 injections.
Her medical history was significant for recurrent ear and sinus infections
until tonsillectomy and adenoidectomy at 3 years of age, pernicious anemia due
to intrinsic factor antibodies, and celiac disease. Asthma was poorly controlled
with frequent daily use of rescue inhalers. Known allergies were to penicillin,
pollen, animal dander, and dust mites. Bowel function tended toward constipa-
tion with some complaints of bloating. Her diet was gluten and sugar free, with
an emphasis on vegetable and fruit consumption with healthy fats and complex
carbohydrates. She participated in a number of physical activities, including Tae
Kwon Do and well-supervised swimming. Sleep routines were well enforced for
a total of 11–12 hours of sleep per day. However, bedtime was compromised by
anxiety, and sleep maintenance was always interrupted by seizures and bedwet-
ting. She slept with her mother for comfort and supervision of her seizures. The
mother had a history of thyroiditis and environmental allergies. The patient saw
a counselor, a speech therapist and an occupational therapist.
Physical examination showed swollen, pale nasal turbinates with copious clear
nasal discharge. The lungs were clear. The abdomen showed increased tympani
to percussion with minimal generalized tenderness. Mild weakness was noted
104  Neurofeedback in an integrative medical practice

in the muscles of the right arm and leg. The patient walked with a mild limp.
She could not cooperate to test deep tendon reflexes. Several episodes of staring,
mouth movements with speech-like sounds, and random, small movements of
the arms and legs lasting 10–20 seconds were observed. The patient appeared
unfocused, fidgeted, and had little spontaneous speech.
Neurofeedback using Othmer protocols was started at T3–T4 to stabilize the
seizures. Reward was optimized to 0.1 mHz. After eight sessions, additional sites
were added after tolerance for each new site was established over three to four
sessions: T4–P4 for control of physical sensations, Fp2–T4 for emotional trauma,
and Fp1–T3 for attention issues. By session 30, the patient was having many fewer
obvious daytime seizures. Nocturnal seizure activity decreased to none at all or
once nightly, except for an increase that obviously correlated with the patient
visiting a relative who exercised no dietary restrictions. Because of the patient’s
strong history of atopy, food allergy testing was undertaken and multiple strong
positive reactions were noted. Testing for casein sensitivity showed significant
levels of casomorphins. Nutritionist consultation was obtained to design and
institute a diet that accommodated the patient’s medical conditions and sensi-
tivities. Sleep hygiene and daily routines were modified as the patient’s function-
ality improved. Melatonin seemed to help the patient fall asleep. The counselor
and speech therapist emphasized social skill training.
The patient completed over 60 sessions of neurofeedback. She no longer had
generalized tonic–clinic seizures and absence seizures were rare. Nocturnal
myoclonic seizures occurred only when there was dietary non-compliance or
other major stressors, such as getting off routines. When she felt stressed, she
still got the feeling of “electricity” in her legs. She was on a single anti-convul-
sant. Her asthma was under excellent control with no need for any medications
other than her prophylactic ones. Anxiety was decreased to appropriate levels,
and the patient was thriving in public schools with an individualized education
plan (IEP) geared to specific residual learning disabilities from her head trauma.
She had many friends and participated fully and enjoyed many social activities
with groups of peers.
Patient 4: 6-year-old girl with high-functioning autistic spectrum disorder who
was having violent meltdowns with such frequency that her specialty school for
children with developmental disorders wanted to expel her. She had already been
asked to leave two previous preschools. There were problems getting her to focus
unless she was interested in something, and then it was difficult to get her to break
away. She was described as “wiggly” and impulsive. Extreme anxiety was caus-
ing issues with getting her to bed at night. Her pediatrician put her on omega-3
fatty acids and Metadate. Her anxiety and expressions of frustration seemed to
increase. So she was switched to Vyvanse with no obvious changes in behavior.
The patient was born at 36 weeks’ gestation and had been diagnosed with cho-
lestasis. However, early milestones were generally within the normal range. She
disliked loud sounds and noisy crowds. Daily bowel movements were described
as hard and chunky. She had an unusually high pain tolerance with little or no
crying after injuries, yet would not wear shoes until her socks were arranged to
her satisfaction. She was a good consumer of a nutritious diet and exercised for
5.8 Case presentations 105

hours a day in her school program that emphasized physical activity. She used
media entertainment for 3 hours a day watching Public Broadcasting System
(PBS) children’s shows and playing “Cool Math” and “Fun Brain” video games.
The patient saw a child counselor weekly and seemed to have good rapport with
her. The physical examination was significant for the child’s unwillingness to
speak in front of the examiner.
The parents were willing to institute good sleep hygiene measures with an
emphasis on a quiet, calm bedtime routine that included Epsom salt baths. There
was little interest in laboratory testing, resuming omega-3 fatty acids, or cutting
down on media exposure. Neurofeedback treatment per Othmer protocols was
initiated at T4–P4 for calming of anxiety and sensory integration issues. T4–T6
for social integration and Fp2–T4 for emotional regulation were added after sev-
eral sessions. By session 12, the patient was consistently getting to bed with mini-
mal drama and sleeping well through the night. She was able to show acceptable
behaviors at school for at least 3–4 hours. The patient became consistently com-
fortable and talkative with the clinician. The pediatrician stopped Vyvanse and
started Intuniv. Within 1 week, the patient experienced volatile emotions, fatigue,
and decreased appetite. The pediatrician added Prozac with a possible decrease in
behavioral issues. The parents insisted on continuing medications, but agreed to
get organic acid testing, as well as an assessment of casein and gluten sensitivity.
Laboratory tests showed sensitivity to both casein and gluten. She also had ele-
vated markers for gut dysbiosis of both yeast and bacteria. After a 10-day course
of antifungal medication (Nystatin), she was started on a casein-free, gluten-free,
anti-yeast diet with daily probiotics. The patient had a dramatic reduction in her
symptoms over the next month. She was now considered to be the best-behaved
and a promising student in her school and plans were underway to transfer her to
a school with a normal curriculum. The parents continued to insist that she take
psychiatric medications. Follow-up at 5 months after finishing neurofeedback
showed persistent positive behaviors and development.
Patient 5: 18-year-old woman with Type 1 diabetes and hypertrophic cardio-
myopathy who suffered a cardiac arrest at 16 years of age in front of her father
and a nurse. Resuscitation efforts were begun immediately. Subsequent events
are uncertain due to misunderstandings between health care providers and the
patient’s family, who originate from a foreign culture and were legally excluded
from her care. She suffered anoxic brain injury and was in a coma for several
months. She had been in a hospital and residential rehabilitation for over a year,
but had stopped making any progress for over 6 months. She was discharged from
further formal health care to her family. Speech was unintelligible except to some
family members. She could not chew food. She was wheelchair bound because of
spastic arms, legs, and body. Her balance was poor, and her mood was anxious
and depressed. She felt trapped in an uncooperative body and upset that she was
totally dependent on her family for everything, including activities of daily living.
Feelings of social isolation were prominent. Her premorbid condition was that of
a high-achieving, well-focused, musical and social high-school student.
Type 1 diabetes mellitus had been diagnosed at 3 years of age and was reason-
ably well controlled on insulin injections until her cardiac arrest. An automatic
106  Neurofeedback in an integrative medical practice

implantable cardioverter defibrillator had been surgically placed after her car-
diac arrest. Medications included insulin, birth control pills for menstrual man-
agement, and clonazepam as needed for anxiety. She was sensitive to sodium
benzoate, soy, and food dyes. She slept well for 8–9 hours per night. She rarely
consumed caffeine. Her bowel function tended towards constipation. Her diet
was a high-fiber diabetic diet. Mouth articulation problems made eating difficult
and the patient was significantly underweight.
The physical examination was commensurate with the described handicaps.
The neurological examination showed slow, unintelligible speech, spasticity in
both legs and the right arm, profound weakness in the left arm, and a lack of
intentional movement. She could balance for a couple of seconds on her feet when
pulled up to a standing position, but could not move her legs or feet in any mean-
ingful way.
A course of neurofeedback per Othmer protocols was started at T3–T4 and
optimized to a reward of 0.1 mHz. The patient and her family were unwilling to see
speech, occupational, or physical therapists because of previous adverse encoun-
ters during residential rehabilitation. However, the family was willing to institute
any measures thought necessary at home. Detailed instruction for home therapy
was given at each neurofeedback session. Bowel care measures were implemented.
Improvements in the patient’s functioning were rapid and dramatic over
three to four sessions at T3–T4. Neurofeedback sites were added at T4–P4 for
body awareness, Fp2–T4 for emotional stability, and Fp1–T3 for focus. Within
3 months, the patient’s speech was intelligible, eating was easier, and body weight
had risen to more appropriate levels. Diabetes control was more consistent and
bowel function normalized. She was able to use a computer keyboard and write
slowly. She could get to sitting and standing positions with minimal help. She
could ambulate with a walker. Frustrations with physical limitations contributed
to ongoing feelings of depression and anxiety. However, the patient successfully
applied, was admitted, and went to a pre-medical university program, where she
received straight As.
Patient 6: 20-year-old woman who presented with a 5-month history of nausea
and vomiting spells that occurred at least daily. Associated symptoms included
chronic fatigue, palpitations, flushing, diaphoresis, urgent need to defecate, syn-
cope or near-syncope, anorexia, and 20-lb weight loss. Medical work-up included
normal pelvic ultrasound, normal head and abdominal computerized tomogra-
phy (CT) scans, normal colonoscopy, and unremarkable stool analysis. Upper
endoscopy showed “reactive gastropathy.” The gastric emptying test was signifi-
cant for markedly prolonged gastric emptying time and established a diagnosis of
gastroparesis. Dynamic defecography demonstrated pelvic floor laxity with cys-
tocele and rectocele. Blood work confirmed mild malnutrition with low albumin
and vitamin D levels, but had no signs of inflammation, hormonal dysfunction,
or liver problems.
The past medical history was significant for chronic yeast infections, eczema,
and food intolerances controlled with the avoidance of milk products, wheat, and
sugar. A history of abdominal bloating, constipation, and encopresis dated to tod-
dlerhood. Medications included Prozac, Xanax, Promethazine, and Zofran. She
5.8 Case presentations 107

considered Xanax to be the most effective for treating her symptoms. Dietary
­supplements consisted of vitamin D and probiotics. She was a non-smoker who
avoided caffeine and recreational drugs. She drank occasionally to “numb” her
stomach, but would later get nauseated. She described herself as needing at least
10 hours of sleep to feel rested. She felt dependent on Xanax to initiate sleep. A his-
tory of hypersensitivity to sounds, touch, smell, and taste was elicited. Anxiety and
depressed moods were prominent. She was unable to exercise or go to school. Family
history was significant for anxiety, depression, and syncope due to “hypotension.”
The physical examination was significant for an increased heart rate of 93, with
an otherwise normal cardiac examination. Her abdomen demonstrated general-
ized tenderness with no other findings. Her skin showed livedo reticularis.
A course of neurofeedback per Othmer protocols was initiated at T4–P4 for
physiological and psychological calming. Reward was optimized to 0.1 mHz.
Several additional sites were added one at a time over the next several sessions:
Fp2–T4 for anxiety control, T3–T4 for physiological stabilization, and Fp1–T3 for
depressed mood. The patient was overwhelmed with medical recommendations
and wanted to avoid any further consultations, testing, or therapies. By her fifth
session of neurofeedback, she was having some symptom-free days and was start-
ing to increase the quality and quantity of her food. A schedule to taper bedtime
Xanax was established, with melatonin to be used instead. The patient was will-
ing to use stool softeners for constipation. Her energy levels were increasing. By
session 15, the patient was contemplating re-enrolling in college. Reviewing the
practical and cognitive issues with symptom management at school was incor-
porated into each session. Her moods improved and anxiety decreased as she
met with success in her classes. A Prozac taper was initiated and well tolerated.
By session 30, further increases in food amounts and diversity, including eating
in restaurants, was noted. Omega-3 fatty acid and vitamin D supplements were
added. By session 40, she was feeling well enough that she was testing her toler-
ances for food types and quantities. She was also breaking sleep routines. Mild
recurrences of symptoms were associated with these. Neurotherapy sessions were
gradually tapered. At her last check-up, she was able to eat a carefully selected
diet and regained all the weight she had lost. She was able to eliminate all medi-
cines. She was at college full time, exercising regularly, socializing, and thriving.
Patient 7: 16-year-old boy with Tourette syndrome, ADD, and social anxi-
ety presented with constant, debilitating nausea and exacerbation of his tics
that began 5 months prior during a stressful time at school. He had a multi-
year history of anxiety about going to school that would crescendo at the end
of a weekend and thus had a record of poor school attendance. On one Sunday
evening, he had an episode of extreme agitation and violence in which he physi-
cally tore apart portions of the house. He was hospitalized and medicated with
Haldol for a “psychotic” episode. He had not attended school since that time. He
spent all his time either in bed or in front of electronic media. He rarely left the
house unless physically forced. Nausea was moderate and vaguely located in the
abdomen. He had vomited twice since symptoms began. His appetite was rarely
compromised, and the patient had gained about 40 lbs. Bowel movements were
formed and occurred daily to every other day. Anti-nausea medications had been
108  Neurofeedback in an integrative medical practice

ineffective, including Zofran. At presentation, his only medicine was Prilosec

40 mg daily. His Tourette syndrome had been diagnosed at 4 years of age. The
patient expressed much embarrassment and distress about his tic disorder: “On
a scale of 1–10, it is a 13.”
The patient had undergone exhaustive medical work-up. Upper endoscopy
showed only minimal esophagitis and negative testing for Helicobacter pylori.
Food allergy testing revealed multiple mild reactions to foods that the patient
was unwilling to forego. Blood analyses showed borderline low vitamin D, high
triglycerides, low high density lipoprotein (HDL) cholesterol, normal metabolic
profile, normal blood counts, normal thyroid function, normal adrenal function,
normal androgens, normal inflammatory parameters, negative Epstein–Barr
virus profile, negative Lyme disease profile, and negative Babesia microti and
Ehrlichia chaffeensis testing. Brain magnetic resonance imaging (MRI), electro-
cardiogram (EKG), sleep-deprived EEG, and overnight polysomnogram were
normal. Two neuropsychological work-ups had been performed. One concluded
that the patient had encephalopathy, tic disorder, learning disabilities, sleep dis-
order, and mood disturbance; the other found autistic spectrum disorder, high
functioning, cognitive disorder, learning disorders, mood disorder, bipolar type,
and Tourette syndrome. The patient was tried on multiple treatments, includ-
ing Vyvanse, Strattera, clonidine, Topamax, Risperdal, Seroquel, Haldol, Xanax,
Ativan, Zoloft, Effexor, chlorpromazine, omeprazole, omega-3 fatty acids, vita-
min D, and probiotics. For a couple of months prior to consultation for neuro-
feedback, he refused to take any further medications.
The past medical history was significant for neuropsychological issues going
back to 4 years of age. A recurring theme involved altercations with his father who
had bipolar disorder with a predominantly hypomanic affect, and disengagement
of his ADD-diagnosed mother. The patient reported nearly daily headaches con-
sisting of intense pressure in random locations around his head that would last up
to a day. However, he “ignored most pain.” His sleep schedule was chaotic, with
the patient sleeping any time of the day or night. His diet included few vegetables
and fruits. He did not exercise. Family history was significant for the father with
bipolar disorder, mother with ADD and obsessive compulsive disorder (OCD),
and paternal relatives with bipolar disorder and addiction problems.
The physical examination showed a shoddily dressed, overweight, poorly
groomed, slouching teenage boy with moderate acne and acne scars on his face.
Tics were observed in the face, especially the forehead, with variable occurrence
from constant to up to 10 minutes tic free. He argued repeatedly with his father,
who was emotionally volatile and provocative.
A course of Othmer protocol neurofeedback was started with T4–P4 elec-
trode placement that was optimized to a reward of 0.1 mHz to initiate physi-
ological ­calming. Every couple of sessions, additional sites were added: Fp2–T4,
T3–T4, and Fp1–T3. Much of each session was spent establishing a rapport with
the t­ herapist as a reliable adult who would advocate for his best interests. He also
started sessions with a psychiatrist who specialized in adolescents with somatic
disorders. Parenting skills training was undertaken with inconsistent effect.
Further m ­ edical consultations were discouraged to break the constant distraction
5.8 Case presentations 109

of multiple appointments, the psychological trauma of looking for something

“wrong” with the patient, and the physical disruption of testing and invasive treat-
ment. As the patient calmed, sleep hygiene was introduced with melatonin use to
help regulate sleep onset. A personal trainer came to the home every morning to
help patient get out of bed at a regular time and then do aerobic and strengthening
exercises. The patient started and did well with a remote curriculum from his high
school. The patient was successfully weaned from excessive entertainment media.
By session 20, nausea-free periods lasted for a day or two at a time. The patient was
able to consume a healthier diet. By session 30, sleep routines were well established
and fatigue had abated. Tics and nausea were well controlled, except for confronta-
tions with parents and the prospect of returning to school classrooms. By session
40, the patient had lost 40 lbs and completely altered his physical appearance, with
improved posture, good personal hygiene, and appropriate clothing.
After consultation with his psychiatrist, it was felt that the patient would be
able to move on in his personal growth in a setting that emphasized stability and
routine with consistent positive behavioral reinforcement. The parents were unable
to provide this in their home, even with extensive family therapy. The patient was
enrolled in and attended a boarding school with a reputation for providing a con-
structive environment for special needs students. He became a top student at this
school, and he coped well with visits and vacations with his family. The parents
became more relaxed and positive in their interactions with him. Tics were rare
events and somatic symptoms were resolved. He was off all medicines.
Patient 8: 9-year-old boy who presented with a 2-year history of generalized
tonic–clonic seizures and nocturnal rolandic seizures that occurred at least weekly
while on medications. EEG showed multifocal sharp-wave discharges in multiple
brain areas, including mid-central, mid-parietal, right temporal, and left pari-
etal regions. MRI showed right hippocampal sclerosis. For religious reasons, the
family wanted to have the patient off medications, but they agreed to start medi-
cine after an episode of status epilepticus that resulted in hospitalization about 6
months prior to presentation for neurofeedback treatment. The mother observed
that medications (Trileptal and Lamictal) caused side effects of slurred speech,
tremors, poor motor coordination, decreased processing speed, and fatigue.
The past medical history was significant for prolonged labor and fetal distress
during the birth process. As a baby, he was diagnosed with reflux. As he matured,
he continued to have daily upper abdominal discomfort with belching and regur-
gitation. As a toddler, he met most developmental milestones, except for issues of
low neurological tone causing some delay in gross motor skills. Iron supplements
were prescribed for mild anemia. The mother noted ongoing issues with anxiety
and obsessive thoughts about bad things happening to him or his family. He was
worried about various body sensations representing significant disease. He was
prone to getting generalized tightness around his head for an hour or so after
using electronic media. He was under the care of a naturopath and receiving a
large number of supplements, including vitamin B complex, magnesium, zinc,
vitamin A, vitamin C, vitamin D, taurine, probiotics, and digestive enzymes.
The patient was on a diet that was based on the GAPS plan. He used no caf-
feine. He took part in daily exercise routines that included running, cycling,
110  Neurofeedback in an integrative medical practice

and bouncing on a trampoline. He was homeschooled because of seizures and

fatigue. He was at grade level even though he worked very slowly and had trouble
with focus. Screen time was strictly limited to academic purposes. Days were
very scheduled with predictable routines, including sleep. Bedtime was 8 pm, but
the patient was often awake for hours with physical restlessness and obsessive
thoughts. He usually slept through his nocturnal seizures and was sluggish and
slow to arise at around 7 am. A year-old overnight sleep study showed mild apnea
and restless sleep.
The physical examination was significant for a pale and very slender boy with
speech that was so slurred that it was often unintelligible. Muscular tone and
strength was generally decreased. A mild tremor of the hands was observed. He
was unable to balance on one foot. The patient brought up his anxieties about his
physical well-being frequently and at length.
A course of neurofeedback using Othmer protocols was undertaken, begin-
ning at T3–T4 for seizure stabilization. Reward was optimized to 0.1 mHz. T4–P4
for calming of somatization, Fp2–T4 for anxiety, and Fp1–T3 for OCD and focus
were gradually added over ten sessions. The patient was slowly weaned off medi-
cations over 11 months and 50 neurofeedback sessions. His seizures decreased
in frequency to one every 1–2 months. All seizures were about 30 seconds or less
and occurred at around waking time. The seizures did not interfere with get-
ting up promptly, being alert, and having a productive day. Speech intelligibility
issues cleared up completely. Some mild tiredness during the daytime persisted,
but tremors and balance issues resolved. Melatonin and Epsom salt baths were
used successfully to decrease sleep onset time. School achievement rose to above
grade level, except for in math and physical sciences, which remained at grade
level. Cognitive counseling techniques were used at each session to allow for cor-
rect interpretation of body sensations. Expressions of anxiety and obsessive wor-
ries normalized. Headaches and gastric reflux symptoms were rare.
Patient 9: 63-year-old woman with a lifelong history of headaches presented
with crescendo and complex migraines. She was hospitalized twice in 2 months
to rule out cerebrovascular accident (CVA) when she presented with left facial
droop, confusion, and left arm weakness and paresthesias, in addition to a left-
sided throbbing headache. Headaches were preceded with auras of huge blue and
yellow splatters in all visual fields for about 20 minutes. MRI showed supraten-
torial bright spots that were thought to be commensurate with the history of
migraines. Other testing was negative for CVA. She also had a history of chronic
daily headaches that also involved discomfort in the left side of her head and
heaviness in her left eye that prevented her from opening it fully. Her headaches
caused difficulties with memory, reasoning, and organization. She typically
tried treating her migraines with caffeine as a first step. If caffeine did not help,
she took Tylenol #3, which did not help with the recent, more severe headaches.
Amitriptyline prophylaxis had been unsuccessful.
The past medical history was significant for decreased renal function second-
ary to childhood streptococcal infection, generalized osteoarthritis, hiatal hernia
with Nissen repair, environmental allergies, and lifelong chronic depression and
anxiety. In the past, the patient tried a number of antidepressant and anxiolytic
5.9 Conclusion 111

medicines and had side effects including decreased alertness, palpitations, trem-
ors, and flushing. Taking Adderall on an as-needed basis was considered effective
and reasonably comfortable. Feeling of sadness increased in the fall and win-
ter, but improved in the spring when she could resume gardening. Medications
included Tylenol #3, Excedrin, Adderall, and nasal corticosteroids. Glucosamine
was the sole dietary supplement. The family history was significant for a “seven-
generation” history of migraines. She was a non-smoker who had about one alco-
holic drink a week and up to a liter of Diet Coke daily. Sleep time was scheduled
for 6 hours per night. The patient fell asleep quickly because of exhaustion, but
then awoke every couple of hours. She felt minimally refreshed in the morning
and experienced chronic fatigue. Her diet was nutritious with an emphasis on
green vegetables, but she had recent carbohydrate cravings that she indulged. She
worked long hours as a nurse treating brittle diabetic patients. Her husband was
retired and had recently been diagnosed with a blood dyscrasia. He and a mildly
disabled adult son living at home were completely dependent on her for all house-
hold chores. The house was disorganized and filled with clutter. She repeatedly
expressed anxiety, anger, and frustration about her work and family situations.
The physical examination was significant for left eyelid drooping. She cried
easily and had problems with word retrieval when she was emotional.
A course of neurofeedback was started per Othmer protocols with an initial
site of T3–T4 for headache stabilization at an optimal reward of 0.1 mHz. Good
sleep hygiene was reviewed and begun. Omega-3 fatty acids and vitamin D3 2000
IU per day were started. 5-hydroxytryptophan (5-HTP) supplements, full-spec-
trum lights in the morning, and the need for ongoing mental health counseling
were discussed, but the patient did not “get around” to trying them. A house-
hold chore chart was concocted for the patient’s husband and son. Severe head-
aches abated within ten sessions of neurofeedback. Facial droop cleared except
for times of extreme stress. Additional neurofeedback sites included T4–P4 for
physical and emotional calming, Fp2–T4 for anxiety, and Fp1–T3 for focus issues.
By 30 sessions, chronic daily headaches were resolved and the patient had only
mild headaches every week or two. Fatigue was still an issue at the end of a long
working day, but the patient rarely used Adderall to get through the day. The
patient continued to be unhappy about aspects of her home and work life, but felt
like things were considerably less stressful.

Neurofeedback is a vital tool in an integrative medical practice that emphasizes
good brain regulation and fitness as the basis for improved function in patients
with a wide variety of presenting complaints and symptoms. Even medical condi-
tions like asthma, diabetes, and gastrointestinal problems, which are not normally
considered to be brain based, can be better controlled. Potentially harmful or poorly
effective treatments can be scaled back or eliminated. Twice-weekly neurofeedback
sessions give the practitioner a platform to communicate frequently with patients.
This enables rapport to be established that can be used to educate patients and help
them implement better lifestyle habits and management of health conditions.
112  Neurofeedback in an integrative medical practice

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Nutrition and the brain


6.1 My own journey 117

6.2 A premise 119
6.3 Going back to our evolutionary beginnings 120
6.4 Primal fat-heads 121
6.5 Primal mind 123
6.6 What clinicians need to know 124
6.7 The glucose myths 127
6.8 The problem with gluten 128
6.9 “Adrenal exhaustion” 131
6.10 Anemia 131
6.11 The autism explosion 132
6.12 Modern threats to human health and brain function 136
6.13 Emotional dysregulation and nutrients 136
6.14 Other nutrients 138
6.15 Your aging brain 139
6.16 Concluding remarks 140
References 141


I came to the field of neurofeedback by way of my own suffering. I had spent
more  than 30 years battling intractable depression, together with anxiety and
panic attacks that had remained unresponsive despite trying a myriad of approaches
over the years. Suicidal ideation and social paralysis were near-­constant compan-
ions for me through the better part of my early childhood into my adult life.
Back in those days, depression was essentially seen as largely a psychological
disorder: if you felt down and depressed, the remedy was professional talk ther-
apy to sort out the psychological variables and provide an integrative resolution.
Over the years, I flitted like a hummingbird to various counselors, psychologists,

118  Nutrition and the brain

psychotherapists, and psychiatrists in my search for what I believed might be a

foundational psychologically driven impasse blocking my potential. As it turned
out (and what eventually came to light), I did in fact have an early history that
would readily lead many people toward some manner of potentially long-term
psychological distress and dysfunction.
Around the time that the very first selective serotonin reuptake inhibitor (SSRI)
medication for depression, Prozac•, entered the public sphere of awareness, there
was a paradigm shift in the minds of professionals and the public: if you hap-
pened to feel depressed, it was not really because you had “bad toilet training” or
got smacked around as a child, but instead it was “simply” about an underlying
“biochemical imbalance.” All one needed in order to deal with this biochemical
imbalance was to take this prescribed “magic pill” in order to restore everything to
normal. Today, we understand that the studies used to approve Prozac and other
SSRIs as the “gold standard” in treating depression found these medications to
be only slightly more effective than a placebo (just about 13% more effective).1
Of those who were actually helped, roughly 40% found diminishing returns over
time through lost effectiveness, potentially requiring changes of prescription. The
neurotransmitter model and theory of depression was flawed from its outset and
is currently being replaced by independent researchers by what is called “the cyto-
kine model of depression.”2 In other words, depression is being viewed by these
researchers as an inflammatory disorder, rather than any sort of underlying “neu-
rotransmitter deficiency.”
Years later, after a seemingly endless struggle with deepening bouts of severe
paralyzing depressive episodes (complete with almost daily suicidal ideation)
and intermingled with lesser states of chronic dysthymia, I came upon an article
in the early 1990s in Omni Magazine. The article discussed an emerging new
paradigm in science that viewed the brain as something beyond mere psycho-
logical constructs or some sort of vessel of “chemical soup.” It talked about a
newly emerging field called “neurotechnology,” which described the brain as
fundamentally bioelectric. If the bioelectric functioning of the brain was “off,” it
was likely that the functioning of the underlying biochemistry and psychological
state of a given individual would be as well.
As explained in Chapter 1, biochemical reactions in the nervous system and
brain are preceded by “an electrical depolarization of the cell,” and this electri-
cal depolarization is intimately dependent upon accurate timing mechanisms to
accurately and effectively drive it. If these timing mechanisms are fundamentally
off, the resulting biochemistry will be as well. Anything that can serve to restore
or improve healthy timing mechanisms (and their interactive phase relation-
ships) can normalize the functioning of any brain—as long as that brain has the
appropriate raw materials to work with. With these realizations, I knew there had
to be something to this, and I was determined to learn more.
I spent a couple of years exploring the various emerging realms of neurotechnol-
ogy. After a chance meeting with Dr. Siegfried Othmer in Santa Fe, New Mexico,
during which I became acquainted with neurofeedback, a new chapter of my life
began to unfold. I returned to Minneapolis, Minnesota, and started a course of
training my brain with neurofeedback with John Anderson of the Minnesota
6.2 A premise 119

Neurotherapy Institute. After a mere couple of sessions, what had been more than
30 years of persistent feelings of helplessness and hopelessness, frequently colored
with varying shades of suicidal ideation, simply vanished. I completed the then-
customary 40 sessions of neurofeedback training (together with some Alpha–Theta
training) to better secure its long-term persistence. To say that this was a miracle
for me is understating the obvious. I became fully determined to become a part of
this field, so that others within my reach might also benefit from this tool for self-
empowerment. It has been just over 17 years now since my liberation from chronic
suffering due to depression and frequent anxiety and panic attacks.
At about the same time that I was undergoing my neurofeedback training
process, my core passion for nutritional science had reached a particular epiph-
any: I had begun recognizing the need for an underlying cohesive foundation
in my understanding of fundamental nutritional requirements. In my readings,
I had stumbled upon the logic of an evolutionary-based approach to this subject.
I proceeded to make major changes to my diet that added noticeably to the posi-
tive changes I was experiencing with neurofeedback. There was a distinct differ-
ence in the way that the two approaches (nutrition and neurofeedback) that I was
implementing affected me, but it was clear that they were decidedly—and very
From my intense research, I have come to understand that diet and nutrition
are essential to the good functioning of the brain. I have seen this approach—
combined with neurofeedback training—affect profound recoveries in countless
clients over many years. Among neurofeedback practitioners, there seems to be
a growing awareness of the importance of diet and nutrition as needed elements
toward helping facilitate better outcomes. I personally have been astonished
at the capacity for neurofeedback alone to seemingly override what were obvi-
ous nutritional/dietary shortcomings. There is no question that taking diet and
nutritional principles into account can lead to better and more lasting outcomes,
regardless of any other interventions. Considering the effectiveness of each of
these approaches alone, I believe this combined approach is clearly indicated in
the pursuit of the best possible outcomes.

We all see the world through a lens shaped by our biochemistry—our hormones,
our neurotransmitters, and (to the degree to which we choose to be dependent
upon it) our blood sugar. These factors, working jointly with the quality of our
brain regulation in the bioelectrical domain, shape our interpretation of the
world around us. It is apparent that all of these factors are inter-related. This is
what “colors” our perceptions and the meanings we attach to our perceptions.
Every physiological process in the human body is wholly dependent upon the
nutrients in our diets and other (perhaps less than nutritive) substances we supply
to these processes. Recent research says that our genes are partially controlled by
epigenetic factors (i.e., dietary and other environmental influences).3,4 Therefore,
the functioning of our brain is very powerfully influenced by what nutrients we
supply or fail to supply to our body.
120  Nutrition and the brain

Unfortunately, this reality has been poorly acknowledged by mainstream

medicine. Only within that neurochemical paradigm would one assert that the
quality of the materials you make use of to construct your physical and mental
health has no bearing whatever on the quality of the end product. In effect, this
has been the attitude and bias of conventional medicine toward the subject of
nutrition. We are told that, regardless of our symptoms, what we eat is not par-
ticularly consequential in symptom presentation. Of the top 300 most prescribed
medications (many of the top 10 medications are mood-related), none actually
serve to support natural physiological functioning. This is simply not the role of
medications. With reference to brain function, medications artificially manipu-
late synaptic activity and/or receptor site properties as a way of temporarily ame-
liorating symptoms, while the underlying cause behind the symptom remains
essentially unaddressed. Claims about the benefits of nutritional intervention are
viewed by mainstream medicine as peripheral to core interests at best, and as
inconsequential pseudoscience or even quackery at worst. This rigid and hostile
position has led generations of suffering people into feelings of helplessness and
confusion about the essentials of nutrition for achieving health, frequently at a
devastating price.
Understanding the foundational requirements behind our fundamental
design and where things might be lacking is essential to optimum functioning.
We must begin with the assumption that every biochemical process in the body
and brain is wholly dependent upon the nutrients we supply to it.


Our long evolutionary history as a distinct lineage began roughly 3 million years
ago, but it was only about 200,000 years ago that we emerged as Homo sapiens,
genetically the same as we are today. The selection pressures that our ancestors
faced over 100,000 generations, together with the foods available to us in our
natural environment, have shaped our underlying physiological makeup and
basic nutritional requirements. Some 99.99% of our genes were formed before the
development of agriculture, according to medical anthropologist S. Boyd Eaton.5
When it comes to understanding what an optimal human diet should consist of,
this consideration is an essential starting place.
As the wild hominids we once were, resources and food availability would
have been uncertain, therefore nutrient density would have been of paramount
importance and highly coveted. As understood by most paleoanthropologists
today, it was likely our dependence on the meat and especially the fat of the ani-
mals we hunted not only allowed us to survive, but also consequently resulted in
the very rapid enlargement of the human brain.6
Weston A. Price, a well-recognized and respected researcher and author,
spent more than 10 years studying the diets and health of primitive and tradi-
tional peoples all over the world in the 1930s. In his now-classic book, Nutrition
and Physical Degeneration (once required reading for Harvard Anthropology
students),7 he estimated that the intake of fat-soluble nutrients by primitive and
traditional societies, which consistently exhibited exceptional health, easily
6.4 Primal fat-heads 121

exceeded modern-day intake by ten times throughout virtually all of these

diverse cultures. Price attributed much of their extraordinary health and vital-
ity to this particular class of nutrients. He contrasted these findings with the
study of many individuals from these various cultures that had become “mod-
ernized.” They had adopted a diet of “foods of modern commerce” (i.e., a diet
high in refined, processed foods and vegetable oils). His photographs and metic-
ulously collected data clearly demonstrated the severe deterioration in physical
and mental health of these individuals.


Compared to large-bodied apes, humans have an enhanced capacity to digest
and metabolize higher-fat diets and indeed tend to consume far higher levels of
it than other primates. Our gastrointestinal tract, with its significantly expanded
small intestine and reduced colon, is quite different from that of chimpanzees
and gorillas and is consistent with the consumption of what anthropologists
term “a high-quality diet” with large amounts of animal-source foods.8,9 We also
evolved as a species consuming much higher levels of key long-chain polyun-
saturated fatty acids that are critical to brain development. These were obtained
directly from the wild (grass-fed) meat, organs, and tissues of the animals we
hunted.10,11 The available evidence indicates that humans are in fact designed to
consume significantly high levels of dietary fat.
Roughly half of the fat in the human brain is actually saturated fat, and indeed
brain growth is dependent on dietary fats (i.e., dietary animal-source fats), par-
ticularly 20- and 22-carbon fatty acids docosahexaenoic acid (DHA) and amino
acids, which play a critical role in the protection and utilization of the delicate
omega-3 fatty acids. Saturated fat is also by its very nature rather resistant to
oxidation, which is protective in effect (seeing as our brains are not refrigerated).
The human brain makes up about 2%–5% of our total body weight, but it
uses 20%–25% of our total caloric energy demands. Humans clearly allocate a
substantially larger share of their daily energy budget to their brains than do
other primates or other mammals. The brains of great apes use only about 8% of
their caloric demands.12 This makes our human brain very expensive in terms
of energy consumption, and this fundamentally demands a diet rich in nutrient
density. What has been termed “the expensive tissue hypothesis” is now widely
accepted in the field of paleoanthropology.

Without this metabolic adaptation, Homo sapiens could not have

evolved such a large brain.13

By contrast, if during early evolution our ancestors would have tried to get
energy from starchy roots and tubers, they would have had to do extensive cook-
ing. It would also have required a different digestive system from the one tuned to
dietary fats. Even if we had been able to make use of starch calories in any significant
way, it still would have amounted to substantially fewer meaningful calories than
would have come from the richly complex nature of dietary fat from the animals we
122  Nutrition and the brain

hunted. Dietary fat (in its great variety of functionally useful forms, including criti-
cal essential fatty acids such as omega-3 fatty acids/DHA) would really have been
our primary and only truly viable source of nutrient density for brain development.6
Following the adoption of a more agricultural lifestyle about 10,000 years ago,
humans have lost just over 10% of their total brain volume by (in significant part)
sacrificing some of this nutrient density in favor of a starch-dense, highly anti-
genic and inflammatory grain/legume-rich diet.
In 2011, Marta Lahr from the Leverhulme Centre for Human Evolutionary
Studies at Cambridge University explained this documented decrease in human
brain volume by stating:

The brain is a fatty organ, and two forms of fat that play an inte‑
gral part in its development are arachidonic acid and docosahexae‑
noic acid. Arachidonic acid is found in, among other things, meat.
Docosahexaenoic acid is also found in fish, seafood and meat, as well
as bone marrow and, perhaps not surprisingly, brain (there is good
evidence that our early ancestors used stone tools to break open
skulls and bones to gain access to brains and bone marrow respec‑
tively). In some respects, therefore, the diet we ate as hunter–gath‑
erers, rich in animal foods as it was, provided an abundance of brain
food. Of course our move to grains as a staple food would have seen
a fall in our intake of crucial brain-building fats.14 [Emphasis added]

Lahr also stated, “When modern humans, Homo sapiens, first appeared
around 200,000 years ago they were tall and muscular. The fossil evidence for
the next 190,000 years is patchy, but shows that humans remained tall and robust
until about 10,000 years ago when many populations show reduced stature and
brain size. It is a striking change.”14
Not everyone agreed with these findings and there has been fierce scholarly
debate as to what our Paleolithic ancestors may have actually eaten along the
way. Early paleoanthropology research used human coprolite studies to ascertain
what our most ancient ancestors ate throughout our prehistory. More recently,
modern technology has helped put this sometimes emotional debate to rest.
A new, more precise method of analysis of the content of prehistoric human
and animal diets is called stable isotope analysis of bone collagen of human and
animal skeletal remains. From hundreds of samples spanning many periods of
our ancient hominid history, Michael Richards at the Max Planck Institute for
Evolutionary Anthropology concluded that early humans were not just carni-
vores but truly high-level carnivores. In fact, not only were we high-level car-
nivores, but we were actually higher-level carnivores than wolves, foxes, bears,
or other known carnivores of these time periods. What helps explain this in
part is the fact that we were cunning enough to be able to successfully hunt
Pleistocene megafauna throughout most of our evolutionary history (the era of
massive Pleistocene megafauna spanned from roughly 2.5 million years ago to
about 11,500 years ago). Those large animals (such as woolly mammoths, giant
aurochs, woolly rhinos, giant sloths and others) would have posed a considerable
6.5 Primal mind 123

challenge to wolves, bears, or foxes. Megaherbivores frequently attained a body

mass of over 10,000 kg. Once you take down a fat-and-sassy woolly mammoth,
you have a family barbecue that can easily last over a week. The megafauna would
have come with copious amounts of fat (woolly mammoths having had an esti-
mated 4 inches of subcutaneous fat on them). One thing is clear from these iso-
tope analysis studies: plant foods did not play much of a practical dietary role
until the advent of more universally adopted cooking practices (which would
have allowed for better nutrient availability through the thermal breakdown of
cellulose and the neutralization of certain toxic compounds).15 What is also obvi-
ous from the data is that we were never even close to being vegetarians.16–20
When the megafauna disappeared by the end of the last Ice Age, humans were
left with much smaller animals to hunt and subsist upon. Animal species surviv-
ing into the Holocene would have been proportionally leaner. This led certain
paleo-diet advocates to assume that our ancestors were designed to eat a diet
rich in lean meat. However, the anthropological evidence consistently shows a
decided preference in even post-Ice Age primitive and traditional societies for
animal fats. Fat was always both venerated and coveted for its considerable value
as a nutrient-dense source of critical nourishment.
The bottom line is that the earliest anatomically modern humans got nearly all of
their dietary protein from land-based animals in our pre-agricultural days. None of
the studies to date has found evidence suggesting any meaningful source of protein
from the consumption of grains or legumes. Therefore, it is clear that these kinds of
foods did not play a significant role in our diets. By logical inference, we may assume
that our digestive system was less adapted to them, in part because we lacked the
genes for producing the enzymes (i.e., amylase) necessary to digest them.


The relevance of this review of our prehistoric ancestors and their eating habits
is that fat and ketones (the energy units of fat), play central roles in the optimal
development, composition, and functioning of the human brain. Fat in general
makes up roughly 70%–80% of the human brain and nervous system by dry
weight. Roughly 50% of this is saturated fat, 11% of which is made up of arachi-
donic acid. About 25% of the fatty acids making up the human brain are DHA, an
omega-3 fatty acid found almost exclusively in animal-source foods. Fully 25%
of your body’s entire repository of cholesterol exists in your brain. Indeed, cho-
lesterol is essential for optimal cognitive and neurological functioning. In sup-
port of this, it may be observed that a common side effect of cholesterol-lowering
statin drugs is memory dysfunction and dementia-like symptoms.
Human infants are literally born in a state of effective ketosis (fully reliant on
fat as their primary source of physical and brain-based fuel). One researcher states:
“Once the onset of suckling takes place … ketone bodies become the major fuel
for brain development.”21 The authors of the textbook Basic Neurochemistry state:
“Significant utilization of ketone bodies by the brain is normal in the neonatal
period. The newborn infant tends to be hypoglycemic but becomes ketotic when it
begins to nurse because of the high fat content of mother’s milk”22 [emphasis added].
124  Nutrition and the brain

The richest natural source of the medium-chain fats essential to early brain devel-
opment—the most ready source of ketones—is human breast milk. Sugars add to
subcutaneous fat stores and this may be the role for the sugars found in human
breast milk. Babies, lacking the insulating fur of most other mammals, must rely
instead on a thicker layer of subcutaneous fat for protective insulation.
In fact, infants up to 5 months of age have literally negligible levels of salivary
alpha-amylase needed for the pre-digestion of starch into maltose and glucose
during chewing. Thus, they have a minimal ability to digest any form of dietary
starch at all. This human infant dietary limitation had been clearly demonstrated
in research published in 1984.23
When compared to ketones, glucose as a primary source of fuel is a volatile
and unreliable source of energy and requires frequent replenishment, as well as
constant management for its stability. The tidal waves of insulin generated to
remove excess blood sugar created by the standard American diet are a strictly
modern phenomenon to which we as human beings are ill suited. A significant
percentage of physical, cognitive, and mental health-related problems can be
traced to this modern-day abnormality (for more detail, see my book, Primal
Body, Primal Mind).24
There has been increasing acceptance that sugar and starch-based diets can
cause endocrine disruption, cumulative glycation and the generation of advanced
glycation end-products, inflammation, free radical production, mutagenic/carci-
nogenic effects, adverse effects on triglycerides, lipoproteins and cardiovascular
changes, premature aging, neuroinflammatory and neurodegenerative changes,
and nutrient depletion (particularly B-vitamins and magnesium).


First, hypoglycemia and reactive hypoglycemia are relatively common in the
population today, and especially among those with mood lability, irritability, and
anxiety-related issues. Many individuals deal quite poorly with a predominantly
carbohydrate-based diet. In fact, there is nothing more destabilizing to the brain
and nervous system than a diet based on carbohydrates, particularly processed
and refined carbohydrates. This is why I ask several questions about a person’s
dietary tendencies, along with the rest of their history, prior to embarking on a
neurofeedback protocol (See Inset 6.1). The answers to these questions provide
direct insight into their particular form of neurological or mood-related dys-
regulation. Blood sugar dysregulation is as American as apple pie and frequently
manifests in ways that compromise normal cognitive functioning, energy, and
moods. In addition, if the blood sugar-dependent client who walks through the
door has not eaten in several hours, their brain may have little energy during your
time with them in-session, and this may lead to less-than-optimal results. In the
early stages of working with clients who seem to exhibit symptoms of unstable
blood sugar, I always ask them or their parents to be sure that they eat some
form of protein/fat-rich food, but avoid a sugar-based snack or drink prior to
their appointments with me. If a client is unwilling to consider a more fat-based
ketogenic approach to diet for the health and stability of their brain and nervous
6.6  What clinicians need to know  125

system, then at the very least they will need to be diligent and highly disciplined
in managing their blood sugar through more frequent snacking on low-glycemic
foods to maintain better blood sugar stability (See Figure 6.1). For some, par-
ticularly those who have autoimmune disorders (especially autoimmune thyroid
issues) and bipolar conditions, this can be especially challenging.

INSET 6.1: Q
 uestions to determine whether your client has
blood sugar-related problems

1. How do you feel before you eat (especially if you have not eaten in a
few hours)?
a. Do you feel fatigued?
b. Out of it?
c. Jittery?
d. Irritable?
e. Moody?
Do you experience carbohydrate cravings or crave caffeine?
2. How do you feel immediately after you eat?
a. Do you feel somewhat better?
b. Do you feel more energized?
c. Or do you feel perhaps more drowsy or fatigued (preferring a nap
after meals)?
Do you crave something sweet at the end of a meal?
If you answered “yes” to the first set of questions and the last two, you
have a blood sugar problem.
If the client asks: “How am I supposed to feel before meals?,” answer:
If the client asks: “How am I supposed to feel after I eat?,” answer:
“Not hungry.”

Source: Nora Gedgaudas

Insulin le r level


Normal blood sugar range

Hunger Hunger

Morning Evening

Figure 6.1  (See color insert.) Circadian blood sugar–insulin cycles. Adopting
a fat-based ketogenic metabolism may be your best approach to getting off
the blood sugar mood, cognitive function and energy roller coaster! Life in the
“green” zone (depicted in the figure) becomes more constant and blood sugar
becomes effectively irrelevant when adopting this approach.
126  Nutrition and the brain

Cultivating more of a fat-based, ketogenic metabolism may be the single

most effective means of both optimally feeding and stabilizing any brain or
nervous system. It is the ideal natural fuel for neurological tissue. This is why
ketogenic diets have been used in the treatment of epilepsy. Those of us that
understand the general approach to neurological instability as applied to epi-
lepsy from the perspective of neurofeedback protocols will also appreciate the
correlation with other forms of neurological instability. Evidence suggests that
the ketogenic diet “has neuroprotective properties in diverse models of neuro-
degenerative disease (See Inset 6.2).”25
According to a study published in 1996, “A ketogenic state results in a sub-
stantial (39%) increase in cerebral blood flow, and appears to reduce cogni-
tive dysfunction associated with systemic hypoglycemia in normal humans”26
[emphasis added]. A study from 2010 in the journal The Neurobiology of Aging
shows that a ketogenically adapted diet is effective and shows promise for far
more than just seizures. It also has neuroprotective and neuroregenerative
potential, as well as improving IQ and memory. Indeed, ketone bodies are
profound memory-enhancing agents. In keeping with American medicine’s
neglect of dietary factors, little attention has been given to using ketogenic
diets for Alzheimer’s and Parkinson’s diseases or other brain conditions.
Awareness of these critical foundational concepts can directly enhance the
clinician’s ability to facilitate better health outcomes for patients. Effectively
applied, they can greatly accelerate the speed of and enhance the effective
response of appropriate neurofeedback protocols, and lead to results that will
be maintained.

INSET 6.2: B
 rain-based conditions shown to benefit
significantly from ketogenic diets

Parkinson’s disease
Amyotrophic lateral sclerosis (ALS) (and other neurologically related auto‑
immune conditions)
Epilepsy/seizure disorders
Memory impairment
Attentional disorders
Autism/Asperger’s syndrome
Anxiety spectrum issues
Bipolar disorder

Source: Information compiled from various sources by Nora Gedgaudas.

6.7  The glucose myths  127


The mantra of mainstream medicine and conventional dieticians/nutritionists
commonly taught and blindly accepted as an “absolute truth” is the idea that
glucose is required by all tissues, including the brain, for everyday energy. This
would only be true if we had metabolically adapted ourselves to dependence
on glucose as our primary source of fuel by chronic consumption of sugar and
starch, but the human brain is designed to make use of more than just one pri-
mary form of fuel. Ketones, the energy units of fat, are the alternative source
for our brains, other organs and tissues, for which we are by far better adapted
through eons of evolutionary selective pressure. Indeed, recent studies have
shown that d-beta-hydroxybutyrate, the principal “ketone,” is not just a fuel,
but a “superfuel” that more efficiently produces adenosine triphosphate energy
than glucose or fatty acids.12
Unfortunately, most food advertising is designed to steer us toward carbo-
hydrate consumption. The consequence is the metabolic equivalent of running
our bodies and brains on metabolic “kindling” (starch and sugars) versus a more
stable and long-burning “log-like” substrate such as fat (ketones and free fatty
acids). About 90 cents out of every food dollar spent today in the United States is
spent on processed foods—most of which are carbohydrate based. Taste and con-
venience have become the primary appeal when grocery shopping or eating out.
While this is highly profitable to the big food companies (carbohydrate-based
foods are less costly to produce but have a substantially higher mark-up), it is
demonstrably detrimental to our health. It keeps most people more or less con-
stantly hungry and preoccupied with where their next handful of “kindling” is
coming from. These processed foods with their high sugar content and chemical
additives keep most people prioritizing food as a source of strictly taste and/or
entertainment rather than a source of substantive nourishment. The nutrient-
devoid nature of these “food-like substances” contributes to constant cravings
while people literally “starve their way toward obesity.” The brain also releases
opioids and dopamine in response to sugar, impacting limbic (pleasure) centers
in the brain. This is why this type of diet is so addictive.
The food industry has been successful in demonizing the detrimental
effects of dietary fat because most epidemiological studies measured dietary
fat in combination with high carbohydrate intake. Yet we know that dietary
fat behaves very differently within the human body and brain in the absence
of dietary carbohydrate (sugar and starch). Interestingly, of the three major
macronutrients (proteins, fats, and carbohydrates), the only one for which
there is no established human dietary requirement (in any medical textbook)
is carbohydrate. We can manufacture all the glucose we need under nearly all
circumstances by relying on glycogenolysis and gluconeogenesis from a com-
bination of protein and fat in our diets. This, coupled with the fact that sugars
are so inherently damaging to the body and brain, while also being linked to
destructive/dysregulating processes, makes eliminating these foods a critical
step towards overall health.
128  Nutrition and the brain

As a neurofeedback practitioner, I know that chronic dietary carbohydrate

(sugars and starch) consumption has a direct impact on moods, cognitive func-
tion, memory, and neurological stability. I recognize that dietary factors can
dramatically impact training outcomes. In my own practice, I use functional
evaluation of expanded basic blood chemistries as a means of identifying imbal-
ances in these areas. Those less well acquainted with this type of evaluation
would do well to seek the help of an integrative or functional medicine specialist.


Sugar is far from the only culprit when it comes to the deleterious impact of
post-agricultural foods on the dysregulation of the human brain. A review paper
published in The New England Journal of Medicine in 2002 listed 55 medical
conditions potentially associated with eating gluten.27 Today, this number easily
exceeds 20028 and includes virtually all autoimmune diseases (currently number-
ing close to 100, with 40 additional diseases that are thought to have an autoim-
mune component). According to the American Autoimmune Related Diseases
Association, as many as 53 million Americans currently suffer from some form
of autoimmune disease, as compared to cancer (9 million) or cardiovascular dis-
ease (22 million) (See Inset 6.3). Gluten is known to potentially initiate or exacer-
bate essentially all autoimmune processes (even though it is not the sole culprit)
and its consumption poses a very high risk in many cases (See Figure 6.2).
The presence of chronic symptoms should motivate us to rule out gluten
immune reactivity through accurate testing (many standard laboratory tests
are inadequate). Among other conditions one might not necessarily think of as
being  associated with autoimmunity are various psychiatric disorders29–31 and
cognitive issues.32,33 Autoimmunity today is considered to be the third leading
cause of morbidity and mortality in the industrialized world, but it is as-yet
poorly recognized by mainstream medicine, which is ill equipped to deal with
this burgeoning problem.


Protein Lectins

Gluten Wheat germ agglutinin

Gliadin Gluteomorphin/ Glutenin


Figure 6.2  (See color insert.) Components of gluten associated with immune
reactivity. (Courtesy of Nora T. Gedgaudas.)
6.8  The problem with gluten  129

INSET 6.3: Facts on autoimmune disorders

●● An estimated 54.1% of people with depression may have autoimmunity

against their own serotonin receptors.31,34,35
●● More than 80% and quite possibly more than 90% of all low-function‑
ing thyroid cases are actually autoimmune in nature. Thyroid autoim‑
munity (Hashimoto’s disease) can have symptoms that may seem very
similar at times to bipolar disorder.36,37
●● Up to 40% of those with Parkinson’s disease exhibit antibodies to their
own dopamine.38–41
●● Up to 30% of those people with schizophrenia may be producing anti‑
bodies to their own neurotransmitters.42
●● Bipolar disorder is found to be highly correlated with autoimmune
thyroid conditions.36,37,42
●● Alzheimer’s disease is also believed to frequently have an autoimmune

Part of the reason for this involves the inherent disconnect between the field of
medicine and the field of immunology. There really is no such thing as a “medical
immunologist.” Instead, there are rheumatologists, concerned mainly with prescrib-
ing pharmacologic agents, and allergists, focused on immunoglobulin E reactions to
antigens that induce anaphylactic responses or seasonal allergies. The immunologists
who are pioneering autoimmune research are PhD researchers and only rarely medi-
cal doctors. Even though there is a rapidly emerging literature in the field of clinical
research immunology, mainstream medicine seems to be paying little attention so far.
This discrepancy is partly due to the elevated diagnostic thresholds that are
often applied to autoimmune disorders, as well as the lamentable reality of hav-
ing few if any remedies to offer anyone suffering from autoimmune disorders.
When offered at all, treatments typically involve the use of cortisone therapy
(with its well-known negative side effects). Low-dose naltrexone is an experimen-
tal therapy, but there is little else available from allopathic medicine to address
the underlying mechanisms that initiate or drive these devastating disorders.
To be producing inappropriate levels of antibodies against one’s own adrenal
tissue, for instance, is not all that uncommon. According to medical diagnostic
criteria, Addison’s disease (chronic adrenal insufficiency) is not diagnosable
until a minimum of 90% tissue destruction has already occurred. If you are only
halfway there, you will most certainly notice this in the way you feel and func-
tion, but you will have no substantial answers or help for this from mainstream
medicine. In another example, it is estimated that between 80% and 95% of all
low-functioning thyroid cases are autoimmune in nature, often producing sub-
stantial inflammatory effects and gastrointestinal and neuropsychiatric issues.
These symptoms frequently confront many neurofeedback providers through
their clients’ symptom profiles, yet the presence of autoimmunity and all it
implies is rarely acknowledged by most medical practitioners. Most people
130  Nutrition and the brain

(usually women—at a rate of roughly 24:1 versus men) suffering from an auto-
immune thyroid condition are not even aware that they have one, even if they
have been diagnosed with “low thyroid function.” There is rarely any follow-
up thyroid antibody testing. Autoimmune thyroid conditions are usually not
treated differently from primary hypothyroidism, which merely involves the
prescription of exogenous thyroid hormone. Due to the nature of this particular
autoimmune disorder, supplemental thyroid hormone may actually have little
positive effect on anything (except blood chemistry numbers), since the associ-
ated inflammatory cytokines may be blocking thyroid receptor sites. In the case
of autoimmune thyroid disorders, the primary issue is not thyroid gland related,
but is instead immune in nature. Furthermore, 98% of all thyroid autoimmunity
is directly correlated with gluten immune reactivity. Without any understand-
ing of this, it is no surprise that mainstream medicine has little to offer for this
condition. Neurofeedback providers can have an enormous impact on the out-
comes of their protocols by taking this type of awareness into practical account
through encouraging accurate testing and appropriate dietary management.
According to current autoimmune research in this area, thyroid hormone is in
fact critical for dampening neuroinflammation, which is why this brand of autoim-
munity (the second most common form of autoimmunity behind gluten immune
reactivity/celiac disease) is especially damaging to the brain. An inflamed brain
is also typically an anxious and/or depressed brain. The “inflammatory cytokine
storms” caused by Hashimoto’s disease flare-ups increase microglial activity,
while low thyroid hormone status fails to adequately dampen the microglial cells.
The result can readily amount to accelerated neurodegeneration.46 The person is
left feeling agitated, anxious, depressed, and spiritually broken.
A little-discussed genetic condition known as pyroluria also seems to affect
a significant number of individuals presenting with mental, emotional, and
cognitive-related issues. It is thought to affect roughly 11% of the population.
Individuals identified with pyroluria produce excess amounts of a byprod-
uct from hemoglobin synthesis called hydroxyhemopyrrolin-2-one (also called
OHHPL), which is an otherwise-unimportant waste product. In the case of pyro-
luria, excess levels of this metabolite will bind to both zinc and vitamin B6 and
can lead to potentially severe deficiencies of these critical nutrients. The condi-
tion is diagnosed through the presence of elevated kryptopyrroles in the urine.47
The condition is recognized within the field of orthomolecular medicine and
orthomolecular psychiatry, but is seldom recognized or acknowledged within
conventional medical circles. At this time, there are no medications for treating
it and it is only manageable with nutritional protocols.
The condition has profound implications for various aspects of mental and
physical health, including neurotransmitter production, immune functioning,
cognitive functioning, digestion, and any other functions impacted by critical
nutrients such as zinc and vitamin B6. The symptoms can be anywhere from
mild to severe and tend to be worsened by increased stress. Nutritional manage-
ment of pyroluria generally involves relatively large doses of zinc and vitamin B6
(in the form of pyridoxal-5-phosphate [P-5-P]), as well as added gamma-linolenic
acid supplementation (i.e., blackcurrant seed oil) and diets higher in arachidonic
6.10 Anemia 131

acid and omega-6 fatty acids in general. Dietary omega-3 fatty acids tend to be
less well tolerated by this particular population.


Neurofeedback providers may encounter clients complaining of “adrenal
fatigue,” “adrenal exhaustion,” or “adrenal burnout.” This perception is know-
ingly or unknowingly based upon a theory of “progressive adrenal glandular
exhaustion” proposed by Hans Selye in the 1950s. It turns out that Selye’s theo-
ries were never actually confirmed as accurate and have since been dismissed by
many modern-day researchers in the field of stress physiology.
It is more fruitful to regard adrenal function as one element of the system of
neuro-endocrine regulation. It turns out that brain dysregulation is often at the
core of the majority of “adrenal”-related complaints. The amount of cortisol,
its circadian rhythms and amplitude of response are all fully managed by the
brain—and these are many of the primary areas of “adrenal dysregulation”-
related complaints. Conventional adrenal supplements are severely limited in
their ability to substantially impact these issues. Neurofeedback can be very
effective here, especially so when it is coupled with appropriate nutritional sup-
port. Neurofeedback providers are aware that optimizing brain self-regulation is
the central goal of our training strategies. However, most are not attuned to the
obvious adrenal connection.
When it comes to adrenal dysregulation, diet definitely matters, but often in
different ways from what is traditionally considered. Supplements, too, can have a
positive impact, but they need to be paired with the particular manner of adrenal
dysregulation at hand (which must first be more clearly identified through screen-
ing and/or testing). Salivary hormone panels such as the Adrenal Stress Index can
provide a far more accurate and comprehensive picture of actual cortisol load and
its circadian rhythms throughout the day than any available blood test “snapshot”
of serum levels ever could. My most recent book Rethinking Fatigue: What Your
Adrenals are Really Telling You and What You Can Do About it outlines these
issues and helpful approaches to addressing them in considerable, practical detail.

Symptoms of neurological over-arousal or anxiety are common with any form of
anemia. The basal ganglia of the brain are particularly oxygen-dependent brain
structures that serve to inhibit excess thalamic activity in the brain. Even mild
depression of hemoglobin levels can serve to prevent normal inhibitory function
in the basal ganglia and result in thalamic over-arousal. This may commonly
translate to symptoms of anxiety or obsessive-compulsive symptoms in some
individuals. The presence of glutamic acid decarboxylase antibodies can also lead
to similar symptoms (and can be tested for using the Cyrex Labs Array 5 test).
Low ferritin levels may also increase the risk of fibromyalgia and restless legs syn-
drome. Ferritin levels ideally should be between 80 and 110 ng/mL.48 Women will
routinely complain of hair loss at levels of between 40 and 60 ng/mL and fatigue
132  Nutrition and the brain

INSET 6.4: Common causes of low ferritin levels

Excessive consumption of antacids, milk thistle, tea, alcohol, caffeine,

anti-inflammatory medications and dairy products (including whey pro‑
tein), excessive calcium supplementation, high doses of zinc, depressed
hydrochloric acid levels, malabsorption illnesses such as ulcerative colitis,
irritable bowl syndrome, Crohn’s disease, celiac disease, gastrointesti‑
nal ulcers, colon cancer, blood loss from heavy menstruation, surgery or
blood donation, endurance exercise, and vegetarian and vegan diets are
common causes of low ferritin levels.

and lightheadedness at levels between 20 and 40 ng/mL, and levels of 20 ng/mL

or lower can manifest in heart arrhythmias, breathlessness, irritability, and nerve
pain. Iron is also needed for the conversion of T4 to active T3 thyroid hormones
and for the production of our primary stress hormone, cortisol. Generally, when
you measure low in ferritin levels, it means that you have been in a biologically
iron-deficient state for quite a while (See Inset 6.4).
However, iron excess/overload is also serious, as it can produce fatigue symp-
toms, sometimes mimicking the symptoms of depressed thyroid function. It
needs to be ruled out as a possible cause when the symptoms appear. Excess levels
of iron/ferritin are associated with profound levels of inflammation, free radi-
cal activity, and neurodegenerative tendencies. Remedies for excess iron include
eliminating excess dietary sources of inorganic, non-heme iron and periodic
donation of blood.


Autistic spectrum disorders are increasing at a blinding rate—a greater than
600% increase over the last two decades. In 1970, the rate of autistic spectrum
disorders was one in 10,000. Close to 10 years ago, this number was one in 166.
Today, it is one in every 50 children. In the immunology literature, autism is
considered an autoimmune brain disease that begins to develop during preg-
nancy.49–51 An important Danish study looked at the amniotic fluids of 700,000
fetuses. It was observed that the risk of a child developing autism was signifi-
cantly impacted by the mother’s health during pregnancy. Mothers who had
rheumatoid arthritis elevated a child’s risk by 35%, and those with celiac disease
increased it 350%.52 Other studies show that a mother’s diagnosis of asthma or
allergies during the second trimester of pregnancy increases her child’s risk of
autism, as does metabolic syndrome, a disorder associated with insulin resis-
tance, obesity and, crucially, low-grade inflammation. The theme here is mater-
nal immune dysregulation. The take-away message here seems to be: control
inflammation during pregnancy and it will not be as likely to interfere with fetal
brain development.53
6.11  The autism explosion  133

Genetic studies tell a similar tale. Gene variants associated with autoimmune
disease also increase the risk of autism, especially when they occur in the mother.
It has been shown that there is often a presence of antibodies to the fetus’s brain in
the mother’s blood and also elevated neurological antibodies in autistic children.
These are dramatic and important findings that lend us clues as to the origins of
the autoimmunity epidemic and what might offer the most rational approach to
averting new cases.
Due to a combination of hormonal and sex differences in the mucosal immune
and microbiome systems, women are at higher risk for many autoimmune dis-
eases, such as Sjogren’s syndrome, lupus, autoimmune thyroid disorders, sclero-
derma, myasthenia gravis, rheumatoid arthritis, multiple sclerosis, and a few
others. This greater female susceptibility makes it critical and urgent that all
women planning to become pregnant are tested for both gluten immune reac-
tivity and inappropriately elevated antibody production. They can then be put
on an appropriate management program to quiet their immune system as much
as possible during the course of the pregnancy. Removing any known autoim-
mune triggers and bringing inflammation under control are critical for a safer
pregnancy, as well as for lowering the chance that the child will develop autism.
Neurofeedback can serve to wind down excitatory activity in the brain and ner-
vous system and lead to raising the bar of what is perceived or experienced as
The autoimmune sensitivity of the mother also seems to be passed on to
their autistic children. A 2013 article on the link between pediatric autism and
celiac disease states: “Children with autism had significantly higher levels of
IgG antibody to gliadin compared with unrelated healthy controls.”54 It has
been found that their immune system identified gliadin (gluten) as “other,” and
that their digestive system was not able to process it and often entered into
the circulatory  system through a “leaky” gut. In Chapter 7, Kurt N. Woeller
details research by William Shaw that describes the role of acetaminophen in
the autism epidemic. He posits that in genetically vulnerable children, a toxic
metabolite N-acetyl-p-benzoquinone imine [NAPQI]) is formed that destroys
glutathione, which is the mainstay of the body’s immune modulatory system.55
Autoimmune-driven inflammation is inherently depleting of critical gluta-
thione as well, leading to a chronically impaired TH-3 immune response. An
immune system thus weakened is much more susceptible to sensitivity to glu-
ten, casein, or environmental pathogens.55
Neurofeedback can have a profound effect on functionality and affect regula-
tion in these populations. However, experience has shown that autism is best
addressed in a multi-modal approach that includes diet, immune modulation,
gut health, and neurofeedback training.
Autoimmunity in general emerges from the intersection of a “triad” of genetic
susceptibility, increased intestinal permeability to macromolecules, and envi-
ronmental triggers (which may include dietary components, toxic chemicals, and
various types of infections) (See Figure 6.3). The single most prevalent dietary
component associated with all forms of autoimmunity is gluten. Since 1974, the
prevalence of celiac disease has increased five-fold overall. This increase is not
134  Nutrition and the brain


Increased Environmental
intestinal triggers
permeability to • Dietary components
macromolecules • Toxic chemicals
• Infections

Figure 6.3  (See color insert.) The “triad of autoimmunity.”

due to increased sensitivity of testing, but rather due to an increasing number of

subjects that have lost the immunological tolerance to gluten in their adulthood.56
I have often referred to gluten as somewhat of a “gateway food sensitivity,”
as it quite uniquely generates an enzyme known as zonulin, which has been
shown to influence intestinal permeability (as well as blood–brain barrier per-
meability). This literally opens up the floodgates to other dietary antigens and
substances that may then trigger inappropriate immune reactivity, leading to
both autoimmune and polyautoimmune conditions. It should be noted that this
effect occurs with gluten ingestion whether or not one might happen to have an
immune reactivity to it. Also, polyautoimmunity (where there is inappropriate
autoantibody production involving more than one issue) is rapidly becoming
the norm. This drives the need for greater reliance on explicit testing for auto-
immune susceptibility, for which I have come to rely on Cyrex Labs (www.
Neurofeedback providers routinely see instances where many of the stress-
related symptoms associated with autoimmune conditions may be positively
mitigated by appropriate brain training protocols. Since stress is a major factor
in the etiology and progression of all autoimmune diseases, the neurofeedback
clinician is well positioned to have a positive effect on individuals who are know-
ingly or unknowingly struggling with autoimmune-related symptoms. Still, it is
critical to understand some of these underlying mechanisms as a means of better
serving these populations.
The mechanisms that initiate and drive autoimmunity can be mitigated
through the systematic application of immunologic testing results and natural
immune modulation. Diet and supplementation can have a significantly benefi-
cial (if not pivotal) role to play here, if applied systematically and carefully using
currently understood mechanisms. The combination of diet and neurofeedback
can be truly profound and unmatched by any other combination of approaches
(Illustration 6.1 and Diagram 6.1).
6.11  The autism explosion  135

Diet and environmental factors

Imbalanced microbiota 
Release of endotoxins
Loss of immune tolerance
Gut inflammation
Loss of gut integrity
Entry into circulation of lipopolysaccharides/LPS
and/or undigested dietary components)

Loss of blood-brain barrier integrity

Humoral and cell-mediated immune response

Cross reaction with various tissue antigens

Multi-organ tissue inflammation and autoimmunity

Physical, cognitive and/or neuropsychiatric symptoms

Illustration 6.1  Initiation and progression of autoimmunity. (Special thanks to

Aristo Vojdani, PhD, for identifying and detailing this sequence.)

Autoimmune progression

Trigger Varying Typical

symptoms diagnosis
Dietary threshold

Healthy Autoimmune Silent stage Symptomatic/ Advanced/

activation autoimmune end-stage
reactivity stage

Diagram 6.1  (See color insert.) Typical pattern of autoimmune progression.

(Courtesy of Nora T. Gedgaudas.)
136  Nutrition and the brain


As a species, we are facing unprecedented stressors from our environment, mod-
ern lifestyle, and deteriorating water and food supply (See Inset 6.5). We have had
less than 500 generations now (out of approximately 100,000) of human evolu-
tionary history in terms of eating grains and increasing amounts of starchy, sug-
ary, and refined carbohydrates. At this point, we have had roughly 13 generations
with exposure to an industrialized food supply.

INSET 6.5: Negative modern-day environmental influences

●● Depleted soils and diets leading to nutrient deficiencies of the foods

grown in them
●● Nutrient-deficient diets from highly processed foods
●● Dietary antigens (especially gluten, casein, etc.)
●● Genetically modified organisms (GMOs) and glyphosate
●● Electromagnetic fields (EMF) pollution
●● Dysbiosis/infections (due to the overuse of antibiotics)
●● Vaccines
●● Radiation contamination in the air, water, and soil
●● Neurotoxic additives in processed foods and soft drinks
●● Environmental haptens and heavy metals

Source: Compiled by Nora Gedgaudas from various sources.

As each subsequent generation is exposed to these things, the health of our

genome is being progressively put under pressure. The expression of our genes is
controlled by regulatory genes, and those are largely influenced by nutrients and
other environmental conditions. In other words, a gene will not express itself
unless the environment is favorable to its expression. Although there is a rec-
ognized genetic component to autoimmune thyroid disorders, for instance, epi-
genetic modulation is emerging as a major mechanism by which environmental
factors interact with autoimmune thyroid disease (AITD)-susceptibility genes.57
AITD-susceptibility genes are far from alone in this respect.
There is evidence that inflammation/neuroinflammation can, by its very
nature, trigger “fight-or-flight” pathways and generate or exacerbate cognitive
processing problems, anxiety-related issues, and cognitive compromise, as well
as depression. These mental health reactions can be further exacerbated when
food sensitivity impacts blood sugar and insulin.


We can view emotional dysregulation as a biochemical storm in the body and
neuroelectrical instability or over-arousal in the brain. It stands to reason: the
6.13  Emotional dysregulation and nutrients  137

healthier a person’s underlying biochemistry, the better the emotional forecast.

The brain needs most of the following macro- and micro-nutrients for optimal
functioning and enhanced ability for emotional self-regulation:

●● Vitamin B12 (its enemies include birth-control pills, hormone replacement

therapy (HRT), and acid-blocking medications). The best source of the
vitamin is meat, particularly liver. If taken as a supplement, methylcobala-
min and/or hydroxocobalamin (hydroxy-B12) and/or adenosylcobalamin
(adenosyl-B12) appear to be most effective.

One particularly interesting study looked at the effects of vitamin B12 defi-
ciency on brain shrinkage.58 Those with the lowest levels of vitamin B12 intake
were six times more likely to have brain shrinkage. Vegetarians and vegans, who
of course avoid most/all foods of animal origin, suffered the most brain shrinkage.
A troubling aspect of the study was that all participants had vitamin B12 levels
that were considered to be within the “normal” range. In another study, vitamin
B12 deficiency was clearly associated with cognitive deficits in the elderly, even
though subjects had concentrations of vitamin B12 above the conventional cut-
offs for deficiency.49,59 This suggests that the “normal” range is simply too low—
and by quite a large margin. The authors’ conclusion in the study was that the
elderly in particular should be encouraged to maintain a good, rather than just
an adequate, vitamin B12 status by dietary means. From my perspective, these
findings suggest that we need to eat more animal-source foods, supplemented
with sublingual methyl/hydroxo/adenosyl-cobalamin.

●● 5-MTHF–MTHFR genetic defects are a common cause of deficits, also

leading to potentially elevated (i.e., neurodegenerative) homocysteine levels.
(More information about MTHFR genetic defects is available at www.
●● Omega-3 fatty acids (e.g., DHA): Apart from being essential to neurological
and visual development in infants, DHA can be adjunctively helpful for staving
off psychiatric and neurological ailments such as depression, post-traumatic
stress disorder, and even Alzheimer’s disease. DHA may also help to modulate
the damaging effects of excess cortisol in the brain (commonly responsible for
the neurodegenerative changes seen increasingly in younger persons today).
●● Arachidonic acid (found in organ meats) is essential for normal cognitive
●● CoQ10 (or ubiquinol) is critical for neurological energy production, mito-
chondrial health, and antioxidant protection, and is readily found in animal-
source foods.
●● Vitamin D3, which is anti-inflammatory and protective of omega-3 fatty
acids. Animal fats are the best dietary source of vitamin B3.
●● Magnesium, which is critical for roughly 400 biochemical reactions in the body.
It displaces excess aluminum and is essential for a calm parasympathetic state
and quality sleep. It assists in liver detoxification. It is often deficient in indi-
viduals presenting with mood- and cognitive-related disorders. Magnesium is
138  Nutrition and the brain

typically low in the brains of those with Alzheimer’s disease and dementia and
is readily lost as a result of blood sugar surges. Optimum levels of magnesium
in the brain promote synaptic density and plasticity in the hippocampus (the
structural basis of learning and memory).60 Loss of magnesium as a result of
chronic blood sugar surges leave binding sites vulnerable to accumulations
of aluminum (and other toxic metals). It can also result in electrochemical
gradient changes, allowing more calcium into the cell, with subsequent hyper-
excitability, N-methyl-D-aspartate (NMDA) receptor activation, and cell death.
The dietary importance of magnesium is presently underappreciated. Common
symptoms of magnesium deficiency include leg and foot cramps, muscle
twitches and muscle tension/pain with insomnia, feelings of chest tightness,
backaches, neck pain, tension headaches, constipation, anxiety, panic attacks,
depression, mitral valve prolapse, high blood pressure, premenstrual syndrome
(PMS) menstrual cramps, and even heart palpitations, numbness, tingling
or temporomandibular joint (TMJ) symptoms. People who are magnesium
deficient sigh a lot and may have low tolerance to daily stress. They may seem
“uptight” or irritable. In terms of hydration, adequate liquid intake is essential
for effective cognitive functioning and stable mood. It is vastly under-rated,
and inadequate hydration can lead to strokes, especially in the elderly. The best
sources for magnesium are ionic or transdermal forms, with intravenous Myer’s
cocktails being the most rapid and reliable source of intracellular repletion.
●● Cholesterol: There is a changing perception of the importance of adequate
levels of cholesterol in the brain for good brain functioning. Low levels and
statin use have been associated with a wide range of issues, which include
dementia-like symptoms, endocrine problems, mood disorders, and atten-
tion and cognitive disorders, as well as susceptibility to seizures.


●● Vitamin B6 is essential for normal neurotransmitter functioning, particu-

larly when it comes to converting l-tryptophan into serotonin. Vitamin B6 is
dependent on the presence of zinc and riboflavin for these roles. Vitamin B6
(pyridoxine) needs to be first converted to an active form called P-5-P by a
zinc-containing enzyme, pyridoxine kinase.61 Since serotonin is the forerun-
ner of melatonin, this can also affect a person’s sleeping patterns (one of the
common symptoms associated with vitamin B6 deficiency is a lack of dream
recall).62 Vitamin B6 is involved also with detoxification. A primary culprit
in depleting vitamin B6 is alcohol use, but a close second is SSRI medica-
tion. As such, if a person is using drugs or medications—or is exposed to
any xenobiotic substance, pollutant, or toxin—the body may lack one of the
essential coenzymes for the effective production of serotonin. Taking vita-
min B6 as a supplement in its coenzymated P-5-P form can help get around
this issue.
●● Zinc is an essential ingredient in our system. It is predominantly found in
its most utilizable form in animal-source foods. It provides an important
6.15  Your aging brain  139

coenzyme in about 80 or more enzymes, which, together with vitamin B6,

vitamin D3, and magnesium, are essential for serotonin production. Zinc is
also needed for the healthy production of hydrochloric acid and the digestive
enzyme gastrin, the production of which is dependent on the presence of com-
plete dietary protein. Depressed thyroid function usually means poor hydro-
chloric acid production and consequently poor digestion and nutrient/mineral
absorption. Zinc deficiency also leads to an imbalance of the zinc/copper ratio
and may lead to cerebral hypoglycemia, even where actual serum blood sugar
levels may appear to be within a normal range.63 Zinc deficiency (See Inset 6.6)
can open the gates to undesirable heavy metal retention, particularly cadmium
and mercury, both of which have an affinity for unoccupied zinc receptors.
On the mental/behavioral level, zinc deficiency has been identified as playing
a key role in depression, anxiety, attention deficity disorder with hyperactivity
(ADHD), learning disabilities, emotional lability, delinquent behaviors, and
eating disorders, as well as various forms of cognitive decline or dysfunction.

INSET 6.6: Causes of low zinc levels

●● High consumption of grains and legumes, especially soy, or non-

soaked/sprouted/activated nuts and seeds rich in phytic acid can gen‑
erate significant zinc deficiencies. Vegetarian/vegan diets are decidedly
problematic. Depressed zinc levels can also be brought on by acute
and/or chronic stress, chronic infections, eating disorders, pernicious
anemia, alcoholism, renal disease, pyroluria, cardiovascular disease,
some malignancies, and protein calorie malnutrition.

Effective zinc supplementation is best achieved through liquid, ionic supple-

ments. They can rapidly replenish deficiencies because they can be readily uti-
lized and can obviate the need for supplemental digestive enzymes. The best
dietary sources of zinc are essentially zinc-rich animal foods like oysters, her-
ring, meat, and egg yolks. As little as 3 ounces of red meat daily can help signifi-
cantly to improve zinc sufficiency (coupled with at least temporary hydrochloric
acid supplementation).


How our brain ages under prevailing conditions of threat remains substantially
under our control. Emerging findings suggest that dietary factors play major
roles in determining whether the brain ages successfully or experiences neuro-
degenerative disease.64
Some stunning research demonstrated that older persons with low total cho-
lesterol (under 200 mg) perform worse on tests of mental function than those
with high cholesterol (over 240 mg).65 Indeed, some studies support the notion
that restricting caloric intake may also improve memory function. The single
140  Nutrition and the brain

most critical rate-limiting factor in aging appears to be a decreased need for insu-
lin, which may be readily accomplished through the implementation of a low-
carbohydrate, moderate-protein and higher-quality natural-fat diet.
Increasing dietary protein levels so that they meet (but do not exceed) one’s
daily needs stimulates cellular maintenance and repair, leading to an anti-aging
effect. While limiting total caloric intake (especially from carbohydrates) is
essential, we find that dietary fat is a “free fuel.” We can eat as much of it as
we need to satisfy our hunger without any adverse effects related to aging. Such
findings may lead to new prevention and treatment strategies for maintaining
cognitive health into old age. The bottom line is that one does not need to count/
overly restrict calories in order to benefit from the effects of caloric restriction. A
well-adapted, fat-based ketogenic diet mimics all of the benefits of caloric restric-
tion without any feelings of hunger or deprivation.
Neurofeedback can play a vital role in maintaining good brain function, stress
management, and improved self-regulation, but in some instances, neurofeed-
back may not achieve optimal results. Initial short-term success with neurofeed-
back may even result in not taking notice or neglecting underlying dietary and
environmental factors. Appropriate assessment and testing should be included in
a comprehensive program to restore and maintain optimal functioning.

INSET 6.7: Nine steps to minimizing neurodegeneration

Eliminate blood sugar issues.

Avoid grains, soy, and gluten-containing foods.
Consume sufficient healthy natural fats and cholesterol (plus sufficient DHA).
Improve methylation, using methyl supplements such as vitamin B6 and
B12, folic acid, dimethylglycine (DMG), TMG, S-adenosylmethionine
(SAMe), and dimethylaminoethanol (DMAE).
Carry out detoxification, especially if exposed to toxic contaminants.
Maintain gastrointestinal health to support a healthy microbiome and gut
barrier integrity.
Optimize glutathione levels (sulfur-based amino acids, selenium/E, and
natural sulfur-containing foods).
Use modified caloric restriction/a ketogenic approach to eating.
Take regular physical exercise.

Source: Developed by Nora Gedgaudas.


In this chapter, I have attempted to touch upon some of the more common nutri-
tionally related issues surrounding emotional, neurological, cognitive, and other
brain-based deficits frequently addressed through neurofeedback training. Due
to the limitations of space in a book of such broad reach, I have not been able to
go into the amount of detail required to cover the topic exhaustively. The purpose
References 141

was to sensitize my colleagues and others to these issues. In my book Primal

Body, Primal Mind,24 I cover the nutritional basis for mental, emotional, and
brain health in much greater detail than was possible here. It may be an excellent
follow-up reference.
Evidence from the clinical realm suggests that there exists no more powerful
combination than a comprehensive dietary approach coupled with neurofeed-
back training in terms of applications to functional deficits. The organizing prin-
ciple of the dietary approach is an alignment with the developmental hierarchy
of our primate brain. The two approaches are complementary and synergistic.
When the two approaches are effectively combined, the client has been well
served from both a biochemical and bioelectrical perspective.

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31. Benros ME, Berit L, Waltoft M et al. 2013. Autoimmune diseases and
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32. Hu WT, Murray JA, Greenaway MC et al. 2006. Cognitive impairment and
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33. Bushara KO. 2005. Neurologic presentation of celiac disease.
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35. Olga JG, Schiepers MC, Wichers MM. 2005. Cytokines and major
depression. Prog Neuropsychopharmacol Biol Psychiatry 29(2):201–217.
36. Carta MG, Loviselli A, Hardoy MC et al. 2004. The link between thyroid
autoimmunity (antithyroid peroxidase autoantibodies) with anxiety and
mood disorders in the community: A field of interest for public health in
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37. Chang KD, Keck PE Jr, Stanton SP et al. 1998. Differences in thyroid function
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38. Huber VC, Mondal T, Factor SA et al. 2006. Serum antibodies from
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Biomedical factors that impact
brain functioning


7.1 Methylation and brain function 148

7.1.1 Methylation (or re-methylation) 149
7.1.2 Transsulfuration 149
7.2 B-Vitamins and dementia 150
7.3 Role of methylation defects in brain function 151
7.4 What is MB-12? 152
7.5 Brain inflammation and microglial activation 152
7.6 Clostridia bacteria and the link to autism and certain
mental disorders 154
7.7 Acetaminophen and the link to autism, attention deficit, and
hyperactivity disorder and asthma 156
7.8 What should happen with acetaminophen? 157
7.9 Therapy suggestions 158
7.10 Oxytocin: An intervention for social and generalized anxiety,
bonding issues, and facial recognition problems 158
7.11 Cholesterol and oxytocin 159
7.12 Two case studies 160
7.12.1 Case #1: The benefits of methylation therapy (MB-12) 160
7.12.2 Case #2: Behavioral issues related to Clostridia bacteria
and improvement from low total cholesterol 161
7.13 Final thoughts 163
References 164

The goal of this chapter is to outline common biological factors seen in clini-
cal p
­ ractice  that negatively impact brain function. Some emphasis will be given
to autism spectrum disorders, but the following information can pertain to
Alzheimer’s disease, dementia, and other disorders such as mental health problems,

148  Biomedical factors that impact brain functioning

including depression, anxiety, and even schizophrenia. Even individuals with trau-

matic brain injury have underlying problems with inflammation from microglial
activation that negatively impacts brain function. The reality is there are many bio-
chemical similarities between these disorders that are often triggered by various
nutritional deficiencies, metabolic problems, digestive infections, and the endog-
enous accumulation of toxins. The goal is not to get lost in the diagnostic label per se,
but to look deeper into the pathophysiology of how common biological factors cross
over into various health and mental health disorders—all of which influence brain
function. This is the key to integrative medicine, where the goal is to search out the
root cause of someone’s illness and provide interventions that address the underly-
ing biochemical and neurochemical imbalances by using biomedical therapies such
as targeted nutritional supplementation, antioxidants, specialized medications, non-
invasive diagnostic testing, and therapeutic interventions such as neurofeedback.
In this chapter, I will refer to these interventions as “biomedical” to mean “bio-
logical” imbalances that are addressed with integrative medicine, which has now
expanded to allied fields such as allergies and immunology, epigenetics, toxicology
and nutrition, as well as various somatic therapies, exercise physiology, and bio-
feedback and neurofeedback. Often, new research about a particular condition in
one or more of these disciplines brings to light new factors that impact the etiology
or maintenance of that disorder. This is certainly the case with abnormal brain
function and the wide-ranging research that has come to light in the last few years.
This chapter focuses on some areas that have been under scientific scrutiny
for many years, as well as a few exciting new areas of research that are just now
reaching publication. While it is not possible to cover all aspects of biomedical
medicine in one chapter, my clinical experience informs me that the following
topics play significant roles in this discussion about biomedical impacts on neu-
rological health for many people:

1. Methylation dysfunction, glutathione deficits, and the use of methylcobala-

min and l-methyl-folate as therapeutic options.
2. Microglial activation and brain inflammation and the positive impact of a
common over-the-counter remedy called ibuprofen.
3. The neurochemical imbalance of dopamine metabolism brought on by an
overgrowth of Clostridia bacterial species in the digestive system and the
link to mental disorders.
4. The detrimental effects of acetaminophen on brain function.
5. The link between oxytocin, cholesterol, and the negative consequence of low
total cholesterol.


Methylation is a vital biochemical reaction that supports the neurological,
cardiovascular, hormone, immune and detoxification systems, DNA/RNA
structure and function and other key metabolic systems.1 There are many nutri-
ents that support this biochemical process, including methylcobalamin (also
known as methyl-B12 [MB-12]), dimethylglycine, and trimethylglycine (TMG).
7.1  Methylation and brain function  149

l-methyl-folate (the active form of folic acid) is important in supporting the

methylation pathway as well, and is one of the nutrients that is often needed to
maintain the proper balance of nutritional support at the cellular level. There are
two key biochemical pathways related to methylation that need to be discussed.
The balance between these processes is critical in order to maintain the normal
balance of cofactors related to brain health. These two pathways are called meth-
ylation (also known as re-methylation) and transsulfuration.

7.1.1  Methylation (or re-methylation)

This pathway involves the conversion of homocysteine to methionine. Production
of methionine, an amino acid, is the rate-limiting step for the conversion of other
necessary chemicals that affect the heart and blood vessels, muscle tissue, and
immune and nervous systems. The conversion of homocysteine to methionine
can occur by direct transference of a methyl (CH3) group from methylcobala-
min (B12) or betaine (TMG). Homocysteine sits at the junction of two different
biochemical reactions. Because of its position in this biochemical matrix, it has
the capacity to impact methylation and sulfur group transference processes in the
body. The most recognized impact of homocysteine is an increased risk for cardio-
vascular disease. However, in individuals with Alzheimer’s disease or dementia, a
faulty methylation system can affect other functions as well, specifically concen-
tration, attention, and memory.

7.1.2 Transsulfuration
This pathway involves degrading homocysteine to two different amino acids—
taurine and cysteine. Taurine is most commonly known for its cardiac and liver
support, detoxification, bile acid formation, and cholesterol excretion. Cysteine
has direct influence on glutathione production.
Glutathione is a potent antioxidant and has protective effects against DNA/
RNA damage, as well as being involved in heavy metal and chemical detoxifica-
tion and immune function.
The chart listed here is an outline of the methylation and transsulfuration
pathways in general:

The cycle constantly
spins from
DMG homocysteine to
Methyl-B12 SAM-e methionine. Methyl-
(Methionine TMG B12 has the greatest
synthase) influence through the
enzyme complex
called methionine


(Potent antioxidant)
150  Biomedical factors that impact brain functioning

There are many intermediary steps involved in these two biochemical reac-
tions. What is important is to keep the big picture in mind when referencing these
pathways. Visualize a wheel that is constantly spinning in a clockwise direction.
Homocysteine is at 6 o’clock and methionine is at 12 o’clock. The goal is to get
from 6 o’clock to 12 o’clock, and then from 12 o’clock back to 6 o’clock. If any
one of these intermediary steps is blocked, then the wheel slows down, causing
biochemical imbalances. This causes a backlog of chemical information that has
deleterious effects on other dependent systems (i.e., immune, hormone, detoxifi-
cation, and DNA/RNA structure and function). Nutrients such as methylcobala-
min, l-methyl-folate, and betaine (TMG) are responsible for taking homocysteine
from 6 o’clock to methionine at 12 o’clock. S-adenosylmethionine, the body’s
“universal methyl donor,” helps take methionine from 12 o’clock to homocysteine
at 6 o’clock. Along the way, other important chemicals are being spun off in dif-
ferent directions to support the many dependent biochemical reactions that are
required by the immune, cardiovascular, hormone, and detoxification systems.


Vitamin B12 and folate deficiencies have long been known to be associated with
cognitive problems, including dementia.2 In fact, there are a number of well-
established medical disorders that are linked specifically to certain B-vitamin
deficiencies: vitamin B1 (thiamine deficiency), seen as Wernicke–Korsakoff syn-
drome; vitamin B3 (niacin), seen as pellagra; and vitamin B12, seen as psychosis,
depression, mania, and neuropathy.
Back in the 1980s, blood measurements of homocysteine were introduced to
assist in diagnosing the deficiencies of vitamin B12 and folate. Homocysteine gets
recycled through the methylation cycle via an enzyme called methionine syn-
thase (MS), which is dependent on a particular type of vitamin B12 called meth-
ylcobalamin. Another enzyme called methylenetetrahydrofolate (MTHFR) helps
the recycling activity in association with the MS enzyme and plays an important
role itself in helping cellular metabolism. One of the important links to diseases
like Alzheimer’s and various dementias is that blood homocysteine levels can be
elevated when there are inadequate amounts of vitamin B6, vitamin B12, and
nutritional folate (also known as l-methyl-folate). These increased levels are also
associated with aging, smoking, environmental exposures, male gender, and var-
ious medications such as methotrexate, metformin, and levodopa.3
Homocysteine has been found to be highly prevalent in the elderly in various
studies.4,5 This has led some researchers and clinicians to speculate that elevated
homocysteine in the elderly may contribute to dementia in general, including
Alzheimer’s disease (AD).5–7 Elevated homocysteine implies an impaired meth-
ylation cycle (also called hypomethylation), which predicts negative effects on
neurochemistry production and regulation, as well as other dependent chemical
reactions that support antioxidants and corresponding adverse chemical reac-
tions in the brain that are often seen with Alzheimer’s disease pathology. One
associated problem is that elevated homocysteine is correlated with blood vessel
disease,8 which is also a risk factor for dementia.9
7.3 Role of methylation defects in brain function  151


In addition to problems with B-vitamins, particularly vitamin B12 (most spe-
cifically methylcobalamin) and folate, there are many other common issues that
explain the neuropathology of AD, dementias, and autism spectrum disorders,
as well as other mental disorders.

Brain inflammation—Brain inflammation through brain immune cells, called

microglia, has been shown to be chronically activated, leading to cell damage
and death.10
Oxidative damage—A number of studies have documented generalized oxi-
dative stress in the brains of individuals with AD from oxidative damage
attributable to various causes, such as environmental toxins.11
Oxidative stress leading to methylation problems—Oxidative damage, often
from multiple environmental factors, creates dysfunction in the methylation
Decrease in glutathione production—Glutathione is a critical antioxidant in our
cells.13 Decreased methylation function from oxidative stress often leads to
glutathione depletion. The depletion of glutathione is highly correlated with
autoimmune dysfunction.
Mitochondrial dysfunction and damage—This is often seen in people with
chronic illnesses, including AD.14
Neurofibrillary tangle formation—Neurofibrillary tangles are a hallmark of AD.
They are a derangement of microtubules within brain cells (neurons) that
lead to poor brain cell function.15
Amyloid plaque formation—Amyloid plaques are another source of cell dys-
function seen in AD.16,17 They are an accumulation of inappropriately folded
cellular proteins.
Glutamate receptor hypersensitivity—Glutamate is an excitatory amino acid in
the brain, and at normal levels and without increased N-methyl-D-aspartate
(NMDA) receptor (glutamate receptor) sensitivity, things are fine. However,
in AD, glutamate receptor activity is often a problem, leading to cell damage
and premature death.18
Cholinergic nervous system problems—Acetylcholine is an important
neurochemical in the brain. Some of its primary functions are in
memory formation, learning, and attention. In Alzheimer’s disease,
its production and availability for normal chemical influence is often
Premature nerve cell death and DNA damage—This is often brought on by poor
methylation chemistry, decreased glutathione production, increased oxida-
tive stress, and glutamate receptor hypersensitivity.19,20
Blood–brain barrier (BBB) problems—The BBB is the protective mechanism
for the brain. Oxidative stress and inflammation can damage or weaken
the BBB. Once the BBB is breached, brain cells in general become more
vulnerable to dysfunction. For example, in some cases of autism, as well as
152  Biomedical factors that impact brain functioning

a condition called Landau–Kleffner syndrome (characterized by language

problems and seizures), areas in the temporal lobe of the brain are negatively
influenced, leading to speech and language difficulties.21

All of the well-researched problems listed above either directly or indirectly

link back in part to the overall positive influence of methylcobalamin and folate
metabolism. This is not to claim that methylcobalamin (also known as MB-12)
is a panacea for some brain disorders like AD, dementia, autism, attention defi-
cit hyperactivity disorder (ADHD), and anxiety disorders. However, from the
author’s clinical experience, I have found supplementation with methyl-B12 and
supportive nutrients to be very useful when I want to make a positive impact on a
person’s overall health. Therefore, let me explain in more detail what methyl-B12
is and how it works.

7.4  WHAT IS MB-12?

MB-12 stands for methylcobalamin—a particular form of vitamin B12. Like its
counterparts—hydroxocobalamin, adenosylcobalamin, and cyanocobalamin—
methylcobalamin has specific biomedical influences on the human body. MB-12
influences the positive changes often seen with individuals on the autism spec-
trum or with improving attention,22 awareness, mental and emotional stability,
language, and social interaction. In fact, the biomarker model of oxidative stress
and brain inflammation linked to methylation defects and autism is very similar
to that being described here with respect to AD and dementia.23 However, MB-12
with respect to Alzheimer’s disease points to the fact that methylcobalamin is
responsible for stimulting the regeneraton of neurons and for protecting against
neurodegenerative processes. The research in the field of MB-12 therapy emcom-
passes a wide range of biochemical pathways through “methylation.”
Even though traumatic brain injury is not discussed in detail in this chap-
ter, there is an entire area of research literature describing brain inflammation,
microglial activation (see the next section), and methylation defects for individ-
uals with traumatic brain injury (TBI). A general search online for “traumatic
brain injury, microglial activation and/or methylation defects” will produce a
number of research abstracts. My clinical experience has been that the biomedi-
cal approach using nutrient therapy such as methylcobalamin and other inter-
ventions for mental health issues (AD, autism, etc.) can be applied to individuals
with TBI as well, because many of the underlying chronic inflammatory problems
that negatively impact methylation and brain function are the same or similar.


A groundbreaking article titled “Neuroglial activation and neuroinflammation
in the brain of patients with autism” from Johns Hopkins University in 200524
paved the way for greater understanding and recognition within the medical
7.5  Brain inflammation and microglial activation  153

community that many individuals on the autism spectrum are dealing with
brain inflammation as a causative or contributing factor to their disorder. The
article also started a discussion about biological factors in the etiology of autism.
As we saw in the previous discussion about AD, dementia, and TBI, this informa-
tion applies to other disorders too. In summary, here is what the Johns Hopkins
research team did in the study:

●● They examined tissues from three different regions of the brains of 11 deceased
individuals with autism aged 5–44 years (who died of accidents or injuries).
●● They measured cytokines and chemokines from cerebrospinal fluid in six
living individuals with autism aged 5–12 years.

Their findings were

●● There were active neuroinflammatory processes in the cerebral cortex, white

matter and, notably, in the cerebellum of autistic patients.
●● There was marked activation of microglia and astroglia.
●● There was elevated macrophage chemoattractant protein 1 (MCP-1) and
tumor growth factor-beta1, derived from neuroglia.
●● The cerebrospinal fluid analysis showed a unique pro-inflammatory profile
of cytokines, including a marked increase in MCP-1 (a pro-inflammatory

The authors concluded that the findings “indicate that innate neuroimmune
reactions play a pathogenic role in an undefined proportion of autistic patients,
suggesting that future therapies might involve modifying neuroglial responses in
the brain.”
In 2010, two parents of an autistic child named Daniel founded an orga-
nization called Stop Calling It Autism ( based
on the concept that autism for some people is a medical disorder versus just
being a neurodevelopmental problem. The focus for their son’s treatment and
the research they gathered to support their approach was based on the conclu-
sions from the Johns Hopkins study in 2005, as well as other research regard-
ing brain inflammation and microglial activation. After the implementation of
various therapies (i.e., dietary changes and supplements), they found that their
son responded quite favorably to ibuprofen, with improvements in his language,
becoming more aware and interactive with his surroundings and being less
hyperactive and anxious overall. Following this lead, they began to delve deeper
into the pharmacology of ibuprofen and its role on microglia activation.
It turns out that ibuprofen has multiple influences on the brain in helping to
reduce inflammation. In fact, there is ample research that supports the findings
of the Vargas team from Johns Hopkins University that activated microglia and
its role in brain inflammation can be helped with common ibuprofen as a poten-
tial targeted therapy. Here is a short list of research to support this hypothesis:

●● Microglia appear to be the main target of non-steroidal anti-inflammatory

drugs (NSAIDs) such as ibuprofen.25
154  Biomedical factors that impact brain functioning

●● NSAIDs appear to reduce the number of activated microglia. NSAID use in

humans has been associated with decreased numbers of activated microglia.26

The implications for this are significant as it not only shows the role of the
immune system in brain dysfunction, but also how inflammation and its cor-
responding impact on disorders such as autism, Alzheimer’s, dementia, TBI
and potentially others may be remedied in part by anti-inflammatory thera-
pies. Chapter 3 explained that well-functioning astroglial cells are essential to
good brain health and that damaged astrocytes usually produce dysfunction
in brain regulation. The chapter also posits that the astrocytic networks neuro-
electrically operate in the infra-low-frequency range. Other chapters show that
neurofeedback can be used to tap into the regulatory functions of astroglia to
restore healthy functioning, whether it be from autism spectrum disorder (ASD)
(Chapter 8), post-traumatic stress disorder, ADHD (Chapter 11), or others.


In 2010, William Shaw published a paper in Nutritional Neuroscience titled
“Increased urinary excretion of 3-(3-hydroxy-phenyl)-3-hydroxypropionic acid
(HPHPA), an abnormal phenylalanine metabolite of Clostridia spp. in the gastro-
intestinal tract, in urine samples from patients with autism and schizophrenia.”27
This important paper discusses the fact that this toxic compound called HPHPA
was found in very high concentrations in urine samples of children with autism
compared to age and gender controls, and in adults with recurrent diarrhea due
to Clostridium difficile infections. In fact, the highest value was 7500 mmol/mL of
creatinine—a value 300-times the median normal value for an adult—was found
in an individual with acute schizophrenia. In this particular patient with schizo-
phrenia, their psychosis remitted after a treatment course with oral vancomycin.
For years, I have been advocating my patients to perform organic acid test-
ing from Dr. Shaw’s Great Plains Laboratory for the evaluation of HPHPA and
other metabolic markers known to negatively influence body and brain chem-
istry. The role of Clostridia infections in neurological health had been poorly
understood until Dr. Shaw’s paper in 2010. From years of clinical experience,
many integrative medicine doctors had recognized digestive pathogens and their
role in negative health outcomes in special needs and mental health patients. Dr.
Shaw’s contribution was to explain the connection between the infections and
the formation of the toxic metabolite HPHPA.
The major impact I see clinically in patients with elevated HPHPA, particu-
larly in individuals on the autism spectrum, is erratic, aggressive, and self-inju-
rious behavior. However, knowing that HPHPA can be elevated in other mental
health disorders, especially disorders related to attention and cognitive process-
ing, suggests a greater overall role for this neurotoxic endogenous chemical.
Biochemically, HPHPA seems to specifically interfere with a converting dopa-
mine enzyme called dopamine beta-hydroxylase. This enzyme is responsible for
converting dopamine into the neurotransmitter norepinephrine. Norepinephrine
7.6  Clostridia bacteria and the link to autism and certain mental disorders  155

is the neurochemical that is most responsible for vigilant concentration, whereas

one of the roles of dopamine is in raising alertness.28 One of the major problems
recognized with the accumulation of dopamine, and the negative effects it has on
brain function, has to do with neurodegeneration (associated with oxidative stress).
A research article in 2008 titled “Unregulated cytosolic dopamine causes
neurodegeneration associated with oxidative stress in mice”29 discusses the bio-
chemical consequences of excess dopamine:

●● Dopamine is a very reactive molecule compared with other neurotransmit-

ters, and dopamine degradation naturally produces oxidative stress.
●● More than 90% of dopamine in dopamine neurons is stored in abundant
terminal vesicles and is protected from degradation.
●● A small fraction of dopamine is cytosolic, and this is the major source of
dopamine metabolism and presumed toxicity.
●● Cytosolic dopamine undergoes degradation to form a compound called
3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid, as well as
hydrogen peroxide, via the monoamine oxidase pathway.
●● Dopamine also undergoes oxidation to form superoxide, hydrogen peroxide,
and o-quinone and reacts with cysteine residues on glutathione, thus render-
ing glutathione ineffective.
●● Dopamine oxidation can also form cysteinyl-dopamine and cysteinyl-
DOPAC conjugates, which are neurotoxic.
●● These biochemical abnormalities caused by excess dopamine may cause the
severe neurodegeneration of neural pathways that utilize dopamine as a

Prior to this research article, a paper in 2000 titled “Short-term benefit from
oral vancomycin treatment of regressive-onset autism”30 discussed the benefits of
such treatment to a group of autistic children:

●● Eleven children with regressive-onset autism were recruited for an interven-

tion trial using a minimally absorbed oral antibiotic.
●● Entry criteria included antecedent broad-spectrum antimicrobial expo-
sure followed by chronic persistent diarrhea, deterioration of previously
acquired skills and then autistic features. Short-term improvement was
noted using multiple pre- and post-therapy evaluations. These included
coded, paired videotapes scored by a clinical psychologist blinded to treat-
ment status.
●● There were noted improvements in eight of ten children studied.
Unfortunately, these gains had largely waned at follow-up.

The authors summarized their research with the following statement:

“Although the protocol used is not suggested as useful therapy, these results indi-
cate that a possible gut flora–brain connection warrants further investigation, as
it might lead to greater pathophysiologic insight and meaningful prevention or
treatment in a subset of children with autism.”
156  Biomedical factors that impact brain functioning

Note:  I remind the reader that it is important not to get lost in the diagnostic
label of an individual and assume that just because an example of pathophysiol-
ogy of brain function was discussed with autism, it does not apply to another
individual with a different brain disorder. Work to widen your view biochemi-
cally by understanding that many of these dysfunctions with the neuroimmune
and methylation systems are similar or the same across multiple subgroups of
individuals, whether they are suffering from the complications of traumatic
brain injury, Alzheimer’s disease, various mental health issues, or autism. The
pathophysiology can be similar, but the patient’s disorder may present differently
depending on what part of the brain is being affected, as well as the age of the
individual and other individual health factors.


On May 23, 2012, an article titled “Fever during pregnancy more than doubles
the risk of autism or development delay”31 was published in Science Daily. This
article was based on research from a team at the University of California at Davis
who found that mothers who had fevers during their pregnancies were more
than twice as likely to have a child with autism or developmental delay than were
mothers of typically developing children, and that taking medication to treat
fever countered the effect of the fever.
The article discusses the notion that various cytokines generated by the
mother’s immune system during infection may cross the placenta and disrupt
the developing brain of the newborn. In doing so, what is likely happening is
that microglia—the immune glia cells in the brain—become over-stimulated,
thus causing disruption of synaptic development. One area in the brain that
could be affected is the oxytocin system, which is critical for bonding, social
interest, and facial expression recognition. Social problems are a major issue
in autism.32 Thus, the information that can be derived from this article again
relates to the role of microglial activation and its negative impact on brain func-
tion. However, the recommendation to take antipyretics during pregnancy to
control fever needs to be countered with what we know now about a specific
Acetaminophen is known to alter glutathione levels in the body, according
to research from 2008 linking acetaminophen use, the measles, mumps, rubella
(MMR) vaccine, and autism.33 Glutathione, being a major cellular antioxidant, is
critical for controlling toxicity reactions within the cell and oxidative stress. The
research team from the University of California, San Diego found that acetamin-
ophen use following an MMR vaccine in children less than 5 years of age was
associated with the development of autism spectrum disorder.33 One could argue
that the MMR vaccine, particularly the measles component, could be enough to
trigger problems, but the compounded influence of acetaminophen on glutathi-
one could certainly increase the potential for neurological problems as well.
7.8  What should happen with acetaminophen?  157

In 2013, William Shaw released a paper in the Journal of Restorative Medicine

titled “Evidence that increased acetaminophen use in genetically vulnerable chil-
dren appears to be a major cause of epidemics of autism, attention deficit with
hyperactivity, and asthma.”34 He presented strong evidence for a myriad of issues
with past acetaminophen use and the correlation with biochemical problems seen
in autism and other spectrum disorders. Here are some highlights of Dr. Shaw’s
findings (references for each listing below are found within the article itself):

●● It is well known that acetaminophen has a narrow range of toxicity, specifi-

cally with respect to liver disease and damage. However, there are additional
concerns for acetaminophen use.
●● Acetaminophen can deplete glutathione levels, which compromises a
­person’s ability to combat oxidative stress.
●● Acetaminophen has the ability to overload a detoxification pathway called
phenol-sulfotransferase, which leads to an increase in the toxic byproduct
called N-acetyl-p-benzoquinone (NAPQI).
●● NAPQI reduces the ability to detoxify toxic environmental chemicals, which
leads to further oxidative stress and damage, protein and DNA damage and
potentially subsequent inflammation.
●● NAPQI reacts similar to mercury in that it binds to the sulfhydryl groups in
body and brain proteins, thus further preventing detoxification.
●● Increases in autism rates coincide strongly with the increased use of acet-
aminophen starting in the early 1980s.
●● Countries throughout the world that use acetaminophen as a primary agent for
pain control prior to and after circumcision in boys and in conjunction with
childhood vaccination have seen the highest rates of autism, similar to the U.S.
●● The one country where this has not occurred is Cuba, where acetaminophen
is not available over the counter and is used infrequently, despite their vac-
cination rates being one of the highest in the world. The percentage of autism
cases in the U.S. is 298-times that in Cuba.


Dr. Shaw’s article is so alarming that I believe steps need to be taken to regu-
late acetaminophen use to prevent a further acceleration of the autism epidemic.
Unfortunately, for many individuals, this information comes too late. One
recommendation to both parents and members in the health care professions,
including nurses, is to avoid acetaminophen use in the future.
However, what can be done about past exposure and the potential toxicity
that may have occurred from byproducts like NAPQI? At the time of this writ-
ing, there is no established treatment for NAPQI exposure, nor a commercially
available test to measure for the presence of it. There are blood tests that are
used for suspected acetaminophen toxicity from large-scale, acute exposure, but
these are not relevant for over-the-counter recommended dosing that occurred
over time prior to or in association with vaccinations, circumcision, fevers, etc.
158  Biomedical factors that impact brain functioning


Since we know that acetaminophen has the ability to deplete glutathione levels,
supplementation for glutathione may be worthwhile. Also, the use of N-acetyl-
cysteine, which is a glutathione precursor, may support the restoration of normal
glutathione levels.
Glutathione as a supplement comes in many forms (i.e., oral capsule, liquid,
or transdermal). The oral capsule form is not very effective, based on per-
sonal experience, as absorption is poor and most of it is degraded in the diges-
tive system. An oral liquid called liposomal (lipoceutical glutathione) shows
good absorption and a higher clinical effect than oral capsules. Glutathione
administered via the transdermal route is favorable for special-needs children
or adults who do not tolerate the liposomal liquid. Finally, glutathione can be
administered intravenously by a licensed physician. This is by far the most
potent way of taking glutathione, but needs to be done through a doctor’s
office. There is some clinical use of various whey protein powders that con-
tain glutathione precursor amino acids—cysteine, glutamic acid, and glycine.
Whey protein can be taken as a daily supplement, but often to correct truly
long-standing deficiencies of glutathione, a person needs to supplement with
actual glutathione for a while. Neurofeedback, in conjunction with the above
named suggestions, has proven to be quite successful in restoring functioning
in the key areas in the brain that have been damaged by the toxic breakdown
products of acetaminophen.


Oxytocin, a hormone involved in social bonding that is commonly administered
as a sublingual tablet or nasal spray, can have beneficial effects as a biomedical
treatment for individuals with an autism spectrum disorder.35
Autism can involve a wide range of problems, not all of which may be found
in any one individual. Some typical ones are speech/language problems (com-
munication issues), lack of social bonding or interest in peers, inability to pro-
cess emotional expressions by others, repetitive and odd behaviors, and sensory
problems (taste, touch, and sound sensitivities). (How these issues are related to
brain dysregulation will be covered in Chapter 8.) Many autistic individuals have
severe anxiety and trust issues. In some cases, their anxiety can contribute to
aggressive or defensive behavior. The anxiety—particularly social anxiety—can
be a hindrance for one-on-one relationships and in group settings. Obviously,
aggressive behavior is problematic for everyone involved.
A natural hormone called oxytocin helps with improved social interaction.36
It acts to decrease nerve signaling from an area in the brain called the amygdala.
The amygdala transmits impulses that are connected to a perceived threat. One
function of oxytocin is to silence fear from this area in the brain, hence diminish-
ing the behaviors of anxiety and apprehension.36
7.11  Cholesterol and oxytocin  159

Researchers at Mt. Sinai School of Medicine, New York, believe that oxy-
tocin could be a useful therapy for autism because the physiological function
of oxytocin fits with those characteristics commonly seen in ASD individu-
als.37 “Studies with animals have found that oxytocin is involved in a variety of
behaviors, including adult-to-adult and parent–child bonding, social memory
and cognition, reduction of anxiety and repetitive behaviors,” states researcher
Jennifer Bartz.
The Mt. Sinai research team did an infusion study with a group of autistic and
Asperger’s syndrome adults. What they found was both a “reduction of repetitive
behaviors and anxiety. No reduction occurred in the placebo group,” reported
Eric Hollander.
The research group also evaluated the positive effects of oxytocin on social
cognition (the ability to detect facial or vocal emotional cues). Each participant
listened to pre-recorded speech patterns with various intonations such as hap-
piness, frustration, anger, etc. Each member of the study then had to try and
identify the emotion they were hearing. The participants who received oxytocin
were able to retain their ability for emotional cue recognition up to 2 weeks after,
whereas those who received a placebo had no change.
Each researcher at Mt. Sinai acknowledged that more research is needed, par-
ticularly with oxytocin use in children. However, the results of this study are
promising because they show that a hormone can have wide-ranging effects for
many of the behavioral and cognitive challenges seen in autism.
For a more comprehensive picture of oxytocin, some additional benefits are

●● Reduces blood pressure and regulates abnormal cortisol levels

●● Decreases anxiety, social anxiety, and fear
●● Increases bonding and feelings of love
●● Improves social interactions and feelings of trust
●● Improves pain thresholds, as well as promotes growth and healing
●● Involved in milk production and “let-down” during breast-feeding and plays
a major role in mother-to-baby bonding


Low cholesterol has been an area of research in the special-needs community
over the past several years. In a variety of papers, William Shaw discusses the
health consequences of low cholesterol in autism and other chronic illnesses.
Information about the negative health consequences regarding low cholesterol in
part comes from research supported by the National Institutes of Health show-
ing that total cholesterol of less than 160 mg/dL is correlated with a vast array
of diseases and disorders such as cancer, Parkinson’s disease, bipolar disorder,
depression, violent behavior, and premature death.38
Relating this information more specifically to the wider community, we can
see certain behaviors that are the same or similar to individuals with a specific
cholesterol deficit disorder called Smith-Lemli-Opitz syndrome (SLOS).39 It
160  Biomedical factors that impact brain functioning

turns out that many individuals with SLOS show improvements in the following
areas when they are given large dosages of cholesterol:

●● Increased alertness
●● Head banging stops
●● Decreased tactile defensiveness
●● Increased sociability
●● Behavior improves
●● Some adults begin to speak who previously were not talking
●● Decreased irritability
●● Many improvements in only a few days after supplementation

Finally, what is the relationship between low cholesterol and oxytocin? It turns
out that cholesterol has a role in oxytocin function. Not only does cholesterol
help to stabilize the function of oxytocin receptors,40 but it also improves the effi-
ciency of oxytocin receptor function.41 Therefore, some of the benefits that may
be seen with the short-term application of cholesterol supplementation could
in part be coming from an improvement in the function of oxytocin already in
the brain.


7.12.1 Case #1: The benefits of methylation
therapy (MB-12)
This case highlights the typical presentation of an individual with a special-
needs diagnosis who, like many, has communication issues and inattentiveness
to their surroundings. The subject showed marked improvement with the imple-
mentation of the primary agent in methylation therapy—MB-12.
Diagnosis: Pervasive development disorder.
Age: 9 years old (at time of first visit).
Development/medical history:

●● Appeared deaf
●● No spontaneous conversation
●● Poor eye contact
●● Poor social skills
●● High-pitched screaming
●● Inattentive to surroundings
●● TV/video obsession
●● Echolalia

Medical history: A few ear infections as a young child and periodic digestive
upset. Otherwise, the medical history throughout life was unremarkable.
7.12  Two case studies  161

Biomedical intervention:

●● Gluten- and casein-free diet—Parents began this diet when the child was
approximately 4 years of age and recognized a slight improvement in sponta-
neous verbal output and increased conversational interactions, increased eye
contact, and increased awareness of his environment.
●● Multivitamin/mineral supplement—This was started shortly after starting
the gluten- and casein-free diet. A major change was increased attention, but
still experienced learning delays and social engagement issues.
●● MB-12—Positive changes happened quickly, within 5–7 days. The following
is a short list of positive changes that were observed:
●● Greatly improved eye contact
●● Increased awareness of surroundings
●● More engaged socially, especially with family members
●● Greatly improved conversation capacity
●● More cooperative, following commands appropriately and more willing
to assist around the house (i.e., chores and cleaning-up after meals)

This particular therapy was used for over 3 years with great improvement and
maintenance of social and cognitive skills gain.

7.12.2 Case #2: Behavioral issues related to Clostridia

bacteria and improvement from low total
This case highlights the sometimes-complicated presentation of behavioral
issues related to digestive infections, as well as the importance of checking total
cholesterol levels.
Diagnosis: Autism.
Age: 5 years old (at time of first visit).

●● Typical development up to 10 months, but parents did report that the child
seemed to lack a lot of need for physical contact.
●● Eye contact satisfactory up to 10–11 months of age.
●● Physical milestones appeared fine.
●● Was babbling, but never any real-word development.
●● Language development noticed to be delayed after 15 months.
●● Was playful and happy overall and engaged with sibling.

Medical history:

●● Breastfed for one year, then began cow dairy.

●● Started solid foods at around 6 months of age.
162  Biomedical factors that impact brain functioning

●● Multiple ear infections (with corresponding antibiotics)—Parents reported

“it always seemed like he was on antibiotics for ear problems.”
●● Digestion—Hard stools even in first and second years, parents needed to use
periodic suppositories.
●● Vaccines—Began at 2 months up through 2 years, then stopped.
●● Fevers after each series of vaccines.
●● Parents remembered that at 8 months of age, the child seemed excessively
irritable after vaccine series.
●● No noticeable immediate regression pattern.
●● MMR, chicken pox, and influenza vaccines given at 15 months of age—Loose
stools for 3 days, fever (told by pediatrician’s clinic to give the child Tylenol;
i.e., acetaminophen), irritable and sleepy.
●● Within 1 month, the child started acting “really silly” and waking at night
“hyper and laughing” (from my clinical experience over the years, this type
of behavior is often seen with Candida reactions coming from the digestive
system secondary to multiple antibiotics).
●● By 20 months of age, these symptoms seemed to disappear, according to the
●● No expressive language, poor social interaction, and not interested in sibling
or neighbor kids.
●● Became easily agitated and irritable.
●● Side-glancing while standing close to TV screen and increased self-stimula-
tory behavior.
●● Hand-flapping and finger-twisting.
●● Finally diagnosed as autistic at 3 years of age.

Pediatrician: Child referred to neurologist for evaluation.

Neurologist: Performed fragile X test (normal). Stated there was nothing else
he could do. Parents requested a magnetic resonance imaging scan, which was
Biomedical Intervention: Started shortly after diagnosis:

●● Casein-free diet—Improved eye contact, began to sleep through the night.

●● Gluten-free diet—No noticeable changes observed.
●● Started multivitamins/minerals—Made the child hyper and agitated, so the
parents stopped this after 3 weeks.
●● At 4 years of age, the child developed an upper respiratory infection—Given
antibiotic treatment.
●● Within the week of completing the treatment, the child became unusually
agitated and aggressive—Hitting, screaming, scratching, and biting and was
not consolable.
●● Behavior “off and on” for 2 weeks, but never fully went away.
●● Parents implemented various herbal remedies and supplements to try and
help (suspected Candida problem), which initially helped with eye contact
and focusing issues and lessoned aggressive behavior.
7.13 Final thoughts 163


●● Urinary peptide: High levels of gliadin and casein peptides (despite claiming
to be on gluten- and casein-free diet)—diet was adjusted.
●● Organic acid test (from Great Plains Laboratory): HPHPA over 700 (very


●● Flagyl (antibiotic against Clostridia bacteria) for 10 days

●● Nystatin (antifungal medication to help against Candida overgrowth second-
ary to antibiotics)
●● Probiotics

Treatment outcome:

●● Five days into Flagyl treatment, aggression and irritability disappeared

●● Within 3 weeks, the child was happy, content, and playful.
●● Continued treatment with Nystatin, diet and implemented low-sugar diet—
the child continued to progress.
●● Overall gains in sleep, attention and behavior were improved, but still suf-
fered from low-level anxiety and social engagement issues.
●● Further assessment revealed low total cholesterol in the low 100s, which was
believed to be compromising healthy brain function.
●● Initiated cholesterol supplementation, and within 3 weeks, the parents
reported marked improvements in terms of the child being more calm, and
over the ensuing months, there were positive changes with respects to social


Whether your specialty is working with individuals with special needs (i.e.,
autism) or patients with various dementias, traumatic brain injuries, or mental
health challenges, it is important to take a comprehensive approach to their over-
all health. Not every biochemical mechanism is going to be the same for every
individual, but there are enough similarities that cross over to various brain dis-
orders that learning how to implement biomedical interventions such as those
discussed in this chapter can go a long way in helping people with their health
challenges. The brain is an incredibly complex organ that has multiple layers of
functionality and influence. When viewed not as an isolated system within the
body impervious to outside influences, but as an integral component that is con-
nected to all other body systems, we can see how biological factors from various
sources, such as the environment, diet, and other endogenous factors, can impact
its function.
164  Biomedical factors that impact brain functioning

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Part     3
Neurofeedback and
Integrative Medicine
in Practice

8 Applying neurofeedback to autism spectrum disorders and other

developmental disorders 169
Kelley E. Foust
9 The use of neurofeedback for combat veterans with
post-traumatic stress 181
Anna Benson and Tamsen W. LaDou
10 PTSD symptom reduction with neurofeedback 201
Monica G. Dahl
11 Neurofeedback in application to the ADHD spectrum 231
Roxana Sasu and Siegfried Othmer
Applying neurofeedback to
autism spectrum disorders
and other developmental


8.1 Introduction 169

8.2 The multiple aspects of autism 170
8.3 Autism as brain dysregulation 171
8.3.1 Evaluations and test instruments 173
8.3.2 Treatments and case studies 175
8.3.3 Comments on case studies 178
8.4 Conclusion 179
References 180

In this chapter, I briefly review how autism manifests as functional deficits in the
brain. I explain what kinds of before-and-after tests I use for screening children
for the wide range of symptoms that children with autism spectrum disorders
(ASDs) usually present with. After a discussion of symptomology, I summarize
seven case studies from my clinical practice. These were chosen from about 500
ASD children I have treated over the past 5 years because they illustrate the wide
range of symptomology that is typically present in the autistic spectrum.
Let me recount how I came into this work. After obtaining a degree in occu-
pational therapy from Texas Tech University Health Sciences Center in Lubbock,
Texas, I moved to El Paso, Texas. Although I wanted to work with children and
was drawn to kids with autism and attention deficit disorder with hyperactivity

170  Applying neurofeedback to autism spectrum disorders

(ADHD), there were no jobs in that specialty field for occupational therapists.
Instead, I ended up in inpatient rehabilitation. I struggled for years to fit into that
environment, but it just was not for me. When my second son started school, he
was found to be quite active and inattentive. He was a sensory-seeking child. He
could attend to the instruction, but he would be doing so while upside down in
his chair. I can laugh about it now, but back then, I just did not understand, and it
was upsetting to me as a parent. Believing that all boys are more hyper than girls,
he seemed like a normal child to me. After all, my first son was a non-stop mover.
But as time went on, I had to accept that both boys were more active than the
“norm.” After attending an all-day seminar on childhood behavioral ­disorders
given by Dr. Hanno Kirk, I decided to learn how to become a neurofeedback
therapist, primarily because I wanted to treat my own children. The appeal was
that neurofeedback is non-pharmacological and non-invasive. Indeed, as the
“Patrick” case study will show, I was pleased with the results. From the perspec-
tive of the children on the autism spectrum I am working with now, “normal” is
often what I used to regard as hyperactive.
When I first started neurofeedback, my only direct experience with autism
had been during a student internship. I had worked intensively (without neu-
rofeedback) with a little autistic boy for about 2 weeks. At the completion of my
time with him, I felt like we had finally connected, and were communicating!
I was excited and knew that I was destined to work with kids like him.
Starting my own private practice in occupational therapy with a focus on
treating children with neurofeedback was a bit scary. I had learned a lot from
being the mother of two sons with sensory integration problems and hyperactiv-
ity, but I had no professional training for working with children, and especially
children with ASDs. However, during my training at the EEG Institute, I had met
Sue Othmer, who had done years of research and clinical work with ASD chil-
dren and had published the good results she had obtained.1 She had developed a
Protocol Guide for neurofeedback practitioners, which became my “bible.” With
Sue Othmer’s active support and frequent mentoring, I slowly gained confidence.
I was also buoyed and much encouraged by some of my stunning early successes.


Many parents ask me, “What is autism, and what causes it?” When I first started
working with autistic children, I had only vague notions about those questions.
All I knew was that autism is a conglomerate of a wide variety of symptoms col-
lected into one Diagnostic and Statistical Manual (DSM) diagnostic label. From
my years of clinical experience with about 500 autistic patients, I found that they
were characterized more by their differences than their similarities. Indeed, it is
a puzzle how some of the disparate behavioral, developmental, and sensory issues
all fit into one category. That seems to be why the logo for the Autism Society is
a few puzzle pieces in different colors. The problem is that a child with severe
ADHD or a seizure disorder could present with similar symptoms, as could a
child with deafness or a severe visual disorder. For me, autism is very much a
puzzle, and we have to figure out each puzzle piece as we learn more about each
8.3  Autism as brain dysregulation  171

individual child. Add to this complex diagnostic picture that persons with ASDs
usually also have some comorbid biomedical issues including major immune
system deficits or sensitivities (e.g., gluten/casein intolerance), and it becomes
evident that creating a treatment protocol to help each individual achieve better
functioning can be very challenging. There is certainly no single cure-all solution
(like applied behavioral analysis) that will work for all kids with ASDs. Given the
difficulty in finding solutions for these children, it is clear why there is a shortage
of professionals working with autistic children.


Autism has been termed a developmental disorder characterized by a triad of
deficits, including impairments in reciprocal social interaction, delays in early
language and communication, and the presence of restrictive, repetitive, and ste-
reotyped behaviors. Most of these characteristics are noticeable by the end of the
second year of life.2 Clearly, each of these major categories is indicative of major
neurological dysfunction. Indeed, much research has focused on finding how
and where in the brain these deficits manifest.3–5
The two regions in the brain of most interest are the amygdala6 and lateral
aspect of the fusiform gyrus (FG), which contains the fusiform face area (FFA).7
It has been established that, in autistic children, the amygdala is smaller and has
fewer neural connections to key regions that process social information than in
normal children. The reduced size and lesser activity of the amygdala has a cas-
cading influence on the development of cortical areas that mediate social percep-
tion in the visual domain, specifically the FFA of the ventral temporal lobe.8
Some recent research using sophisticated measuring techniques posits that
there is a quantitative link between the number of “facial recognition neurons” in
the FFA and face discrimination deficits (i.e., the fewer of these specialized neu-
rons are available, the more severe the deficits).9 This deficit was clearly demon-
strated in a study that showed differential activation of brain areas when autistic
and normal children reacted to faces.5,8 As shown in Figure 8.1 (taken from this
study), in normal children, the FG, the amygdala (Amy) and the right superior
temporal sulcus (STS) are activated. In the autistic children, these areas are silent.
Instead, the autistic child uses object recognition areas to decipher the stimulus
presented by the face. Without the associational input from the amygdala and
the associational node at the STS to interpret facial expression or gestures, the
autistic child, using object recognition only, tends to “see” only minor changes
in facial muscles.10
The right lobe processes new social stimuli, which in normal brains are dis­
tributed by the amygdala into memory in the associational areas in the hind
brain.11 This is done via the associational function of the gamma wave band.12
This allows for social learning. However, in autistic children, the paucity of
gamma wave action, combined with the almost total lack of activation in the
amygdala, the FG, and the STS, means that there is little or no learning or ability
to generalize from social experiences. This explains why ASD children often have
strong adverse reactions even to social situations that are similar. Every social
172  Applying neurofeedback to autism spectrum disorders



x = 34 y = –55 z = –14



x = 34 y = –55 z = –14

Figure 8.1  (See color insert.) Functional resonance images of differences in

facial recognition between autistic and normal children. Orange shows activa‑
tion, blue shows deactivation. Abbreviations: Amy, amygdala; STS, superior
temporal sulcus; FG, fusiform gyrus.

situation is treated as a new stimulus and may be routed via the thalamus to the
reticular activating system in the brain stem. This can then produce the outsized
alarm reactions often seen in ASD children when presented with change.
In Chapter 7, Dr. Kurt N. Woeller explored the various biomedical conditions,
including neurotoxins, and oxidative damage that can lead to the inflammation
of the neuroglia, as well as neurodegenerative damage, which can disrupt neuro-
electrical functions in various parts of the brain. Those disruptions can manifest
as ASDs, as well as a number of other mental disorders. In Chapter 6, Nora T.
Gedgaudas showed that genetic and epigenetic factors, autoimmune issues, and
nutritional factors can play major roles in major brain dysfunctions like autism,
Alzheimer’s disease, schizophrenia, and a host of other disorders. In this chap-
ter, we look at the electrophysiological dysfunction in autism spectrum disorders
and how neurofeedback can be used to restore better functioning.
Siegfried and Sue Othmer have provided a model for how autism affects brain
behavior.1 According to that model, the “most obvious shortcoming in autism
lies at the level of integration of function.” There is a wide range of deficits that
affect the emotional core of how we interact in socially connected ways. In the
ASD child, there are developmental flaws in the neural networks processing emo-
tional functioning. This makes it difficult for these children to connect to those
around them. In this regard, the life experience of an autistic child, who is not
8.3  Autism as brain dysregulation  173

emotionally connected, is similar to children with reactive attachment disorder.

Handicapped by an impaired ability to process emotional cues, the autistic child
is likely to perceive the world as uncertain or, at worst, as constantly threatening.
Instead of most social stimuli being perceived as routine by the cortical process-
ing areas of the left lobe, we see many stimuli, which should be familiar, being
processed thalamo-limbically from the right side. As a consequence, the brain as
a whole tends to be in a constant state of activation and arousal: “Even if a child
presents as shut down, the internal state of that system is invariably one of high
arousal.”1 When the brain is chronically highly activated, brain function suffers.
Top-down or inhibitory control is impaired or absent.
From the perspective of neurofeedback, the most significant point of this
model is the over-arousal. Indeed, the first priority is to move the child’s brain
out of emergency mode. “Calm the stressed and agitated nervous system” is the
operative principle. Since the autistic child tends to see even repetitive situations
as new, the right lobe of the brain is in a constant state of vigilance and over-
arousal. Hence, with ASD children, we usually focus first and foremost on calm-
ing the right lobe of the brain, so the preferred placements would be T4–P4 for
physiological and emotional calming, followed by T4–Fp2 for anxiety and con-
trolling (inhibiting) emotional reactivity.

8.3.1  Evaluations and test instruments

As an occupational therapist, I treat the whole person. In order to evaluate
­children with autism, I had to find tools that covered all aspects of functioning.
They had to be informative and professional, but also fast and easy to administer.
It took several years to assemble the following combination of test instruments
that I felt could adequately provide useful before-and-after measures of abilities
and developmental issues.
The QIK test is a computerized continuous performance test that is standard-
ized for ages 6 years and above. I usually do not use it for 6-year-olds, because
most 6-year-olds I treat cannot maintain their attention for more than a minute.
It is a 21-minute test and has three sections: low demand, high demand, and
then low demand again. It is different from the TOVA® (Test of Variables of
Attention), in that it has the third low-demand part at the end of the test. For
children with attention deficits, the QIK is quite demanding. For children with
autism, it may not be a viable test option, depending on the type and severity of
symptoms. Most kids with Asperger’s syndrome can perform the test. Because
the QIK is a separate handheld device, from which the data can be downloaded
onto a computer, it is also more kid friendly than the TOVA, which uses a com-
puter keyboard.
The Short Sensory Profile is a quick form that is easily filled out by the parent.
There is a longer form available, but I have found the short form to be adequate.
Most children with autism have sensory integration problems, for which neuro-
feedback does wonders. This tool supplies metrics to sensory functioning in the
following areas: tactile sensitivity, taste/smell sensitivity, movement sensitivity,
174  Applying neurofeedback to autism spectrum disorders

under-responsive/seeks sensations, auditory filtering, low energy/weak, and

visual/auditory sensitivity. A Likert scale is used for responses in each section
with the following key: 1 = always, 2 = frequently, 3  =  occasionally, 4  =  sel-
dom, and 5  =  never. After adding up all the sections, the test summarizes each
area as typical performance, probable difference, or definite difference. I use this
tool to record the positive changes in sensory functioning brought about by the
The Vineland II Adaptive Behavior Scale is an excellent scale that is standard-
ized for ages 6 months and up. I started to use this scale because the insurance
companies wanted age equivalencies. I ended up appreciating it because it is a
good before-and-after assessment tool for most areas of occupational therapy,
as well as developmental life skills/behaviors. It gives age equivalencies in the
following areas: receptive, expressive, and written communication; personal,
domestic, and community daily living skills; interpersonal relationships, play
and leisure skills and coping skills; and gross and fine motor skills. It also has a
section for maladaptive behaviors, and it rates them as average, elevated, or clini-
cally significant.
The Brown ADHD scale states that a score of 55 or higher on the symptom
rating scale indicates a high probability that the child has ADHD. I do not use
this for diagnosing (that is not my job), but I use it as a before-and-after treat-
ment baseline so that I can see whether the neurofeedback is affecting the child’s
ADHD symptoms. It also helps me to know the severity of the child’s symptoms,
and it is useful in cases where a parent is not good at providing answers on the
symptom tracker form.
The Focus NeuroRehab Symptom Tracker is one that I formulated for congru-
ence with neurofeedback protocols. This is a crucial part of my evaluation, and I
usually review it with the parents during the interview part of the evaluation. It
has five sections, which correspond to the brain areas we train with neurofeed-
back. Using the Othmer Protocol Guide, I formulated the symptom tracker in the
order of the progression of treatment with most ASD children (i.e., right parietal,
right frontal/prefrontal, left frontal/prefrontal, left parietal, and temporal inter-
hemispheric). Based on the symptoms recorded on this assessment tool, I form a
treatment plan. As distinct from the EEG Institute Symptom Tracker, my form
does not have ratings for the severity of symptoms or problems. I assign those
from my own observations and interviews with parents and/or teachers.
Before I see a child, I ask the parents to pick up copies of these instruments,
fill them out at home, and bring them to the first session. This shortens the time
needed for the intake evaluation. After analyzing the information, I develop an
assessment. Based on that assessment, I formulate a hypothesis on where the dys-
functions that I want to target are in the brain, which indicates where I might
place the electrodes on the scalp. Due to the wide variance in symptoms in ASDs,
the dysfunctions in the brain are highly individual. Cookie-cutter solutions do
not work for ASD children because treatment needs to be tailored to each child’s
specific constellation of symptoms. For some therapists, this may be frustrating
or even confusing. However, I love the challenge of optimizing the neurofeed-
back training protocol for the patient in front of me.
8.3  Autism as brain dysregulation  175

In addition, I also need to consider the biomedical pieces of the puzzle. From
attending several Integrative Medicine and Mental Health conferences, I have
learned that there is a wide range of biomedical issues that are either causal to or
arise with ASDs (see Chapters 7 and 8). So if I see evidence from my intake evalu-
ation and interviews with the parents that there is a probable gut issue, gluten
intolerance, or any of the other factors mentioned in Chapters 7 and 8, I will refer
the patient to an integrative medicine physician, if they are not already work-
ing with one. I do not order tests, but when compiling intake information, I ask
whether certain tests have been done. I leave the medical testing up to the medi-
cal doctor who is specialized in that field.

8.3.2  Treatments and case studies

Starting treatment with an anxious and hyper-aroused autistic child with severe
sensory issues can be challenging and requires improvisation. Over the years,
I  have learned some techniques for dealing with sensory symptoms. Taking a
cue from Temple Grandin’s own experience with the soothing effect of a body
“squeeze box,” I may use a weighted blanket to help a child feel more secure and
grounded.13 We have had some kids bring their body pressure garments to help
with proprioceptive input. We also utilize the Wilbarger protocol for brush-
ing, and joint compressions to help normalize the supersensitive system of an
ASD child.14 ELAINE
Elaine was the first patient I had for neurofeedback. She was a 6-year-old girl with
autism who was highly suspicious of new people and new environments. I offered
her family ten free sessions, primarily so that I could get my feet wet with neu-
rofeedback. Initially, she was so hyperactive that the only way she would sit long
enough for a treatment was to allow her to eat a corndog—her afternoon “snack.”
We started with only 8 minutes of neurofeedback in the first session, but this
increased in duration so that by the time we reached ten sessions, she was sitting
still for 30 minutes. By that time, her hyperactivity had calmed enough that she
no longer had to eat while getting a treatment.
Elaine was a so-called fast responder. To my delighted surprise, she went
from a one-word vocabulary (“NO!”) to speaking full sentences within ten ses-
sions! Unfortunately, I was only able to treat her for ten sessions, because despite
her fast progress, her father did not approve of her coming for therapy. It was
immensely gratifying to be able to connect with this ASD child and to observe
her rapid response to neurofeedback. The experience reinforced my commitment
to continue to work with this population. After realizing the power of neurofeed-
back, I dedicated my practice to treating children like Elaine. RICHARD
Richard was a 6.5-year-old boy. I was flabbergasted when I compiled the results
of his first re-evaluation. After 18 sessions, this patient showed noticeable
176  Applying neurofeedback to autism spectrum disorders

improvements in most areas of the Vineland II. The following are his pre- and
post-scores after 18 sessions of neurofeedback:

Receptive language Pre: 3:5 Post: 11:0

Expressive language Pre: 2:10 Post: 3:5
Written language Pre: 5:11 Post: 6:9
Personal daily living Pre: 3:6 Post: 4:10
Domestic daily living Pre: 6:6 Post: 9:10
Community daily living Pre: 4:6 Post: 4:10
Interpersonal relationships Pre: 4:11 Post: 6:6
Play and leisure Pre: 4:8 Post: 6:7
Coping skills Pre: 6:6 Post: 7:6
Gross motor skills Pre: 3:2 Post: 4:5
Fine motor skills Pre: 5:2 Post: 5:10

Given that neurofeedback was the only treatment he was receiving, I was con-
vinced that I could not have achieved these results with traditional occupational
therapy strategies. It reinforced my commitment to use neurofeedback, because
I became convinced that it produced quick and lasting effects. Traditional thera-
pies using sensory integration and applied behavioral analysis can work, but they
require much time and intense effort. Seeing the startling and rapid improve-
ments in this child motivated me to solicit support from within the occupational
therapist (OT) community and academic world to conduct studies using neuro-
feedback with ASD children and measuring outcomes with the Vineland II and
the Short Sensory Profile. ALEXA
Alexa was diagnosed with moderate–severe autism at a very young age, but came
to me at the age of 8 years. Her symptoms were severe meltdowns with an inability
to be calmed; screaming when she did not get her way; minimal verbalization; bed-
wetting two- to three-times per night; and being unable to follow instructions. Her
parents did not opt for biomedical treatments. After 3 weeks of two sessions per
week, her mom came to me saying, “Thank you for what you’ve done, Kelley. Our
daughter hasn’t wet the bed since she started here!” For her multiple other issues,
Alexa was a slow responder, and she continued with weekly sessions for 4 years,
doing hundreds of sessions. At the time of this writing, she still comes in for rein-
forcement sessions. However, she went from being in special education to being
fully integrated into regular middle-school classrooms, receiving special education
services only for reading. Her parents expressed gratitude that instead of having
to go through years of trying medications, she was able to get a fast therapeutic
intervention that has helped her to become academically and socially successful. LESLIE
Leslie was a 5-year-old girl with mixed issues, but no clear diagnostic label. She
was another super-fast responder. Within 13 sessions, she went from a score of
8.3  Autism as brain dysregulation  177

102 on the Brown ADHD scale to 45. Her Short Sensory Profile overall score
went from “Definite difference” to “Typical performance.” On the Vineland II,
almost all her scores improved to within her chronological age equivalencies.
Her parents were very pleased with the strides she made in such a short time. In
fact, they found it hard to believe, and when we did the re-evaluation, they were
having flashbacks of her uncontrollable behavior prior to neurofeedback. At the
time of writing this their daughter is within the norms in all areas tested. She will
continue to receive treatment until she reaches 40 sessions to make sure her brain
has fully learned to self-regulate. PATRICK
I started working with Patrick, my own son, when he was 10 years old. He is the
reason I started doing neurofeedback. He suffered from severe anxiety and had
many ADHD symptoms. In addition, he had some unusual sensory issues, or
“talents.” One is a photographic memory and another is apraxia. The latter meant
he had great difficulty putting his thoughts on paper. (I later learned that it was
because his brain was very busy, so he could not organize his thoughts.) He was
so distractible that it used to take him a good hour to write 30 spelling words.
Patrick also has what I call “supersonic” hearing (i.e., any noise would distract
him). His hearing was so acute that he could hear the dialog of a movie playing in
another part of the house even with several closed doors between his room and
the TV. This had made studying a challenge, because he would begin to recite the
words of what he heard.
After my own professional training in neurofeedback, and as soon as I
received my equipment, I started training Patrick. We did sessions 5 days a
week, and we completed 20 hours of training in 1 month. By summer, he was
weaned from his attention deficit disorder (ADD) medication (Daytrana Patch),
and in the fall, he was able to go back to school without medication. Patrick was
a moderate-to-fast responder. Shortly after he started training, his personal-
ity changed noticeably for the better. Considering his previous apraxia, I was
amazed when he started to enjoy drama and writing. Patrick also developed
the self-awareness to realize that he needed occasional booster sessions to keep
his anxiety in check when things got stressful and overwhelming for him. After
these calming sessions, he would say, “Thank God for neurofeedback!” There
was one other significant change: during the time he had been on various psy-
chotropic medications, his mood had usually been negative and irritable, and
he had no sense of humor. Shortly after starting neurofeedback, Patrick began
cracking jokes and looking for humor in everything he did. Whereas before he
would get very upset by teasing from his older brothers, he now cracks jokes
and teases right back. He has become a talented young man whose creative and
expressive talents have been unleashed by the neurofeedback training. He is
thriving socially and academically in high school as I write this. MARK
Mark was a 12-year-old boy who came to my office via a referral from a new
neurologist in town. He had been having severe migraines for 2–3 years, which
178  Applying neurofeedback to autism spectrum disorders

seemed to become more intense with increased stress of any kind. This boy, who
loved to play baseball, had been told by a previous neurologist that he would
never be able to play ball again, but would have to learn to live with his migraines
because there was no medication that could stop them. Upon hearing this, the
boy told his mother he would rather die than not be able to play ball. On his
intake day, he reported a migraine at 5 out of 10 in intensity. It was obvious that
he was not feeling well. I looked straight into his eyes and asked, “Are you ready
to get rid of your headache?” He nodded his head with tears in his eyes. Within
5–10 minutes of his first session, his headache was gone. I knew he was going to
be a successful, fast-responder case. Within 25 sessions, we were able to wean him
from neurofeedback. He no longer needed it because he no longer had migraines.
Now he is an active young man, no longer suicidal but doing what he loves most:
playing baseball. (His old neurologist still does not believe in neurofeedback, or
any other integrative therapy for that matter. Given that sometimes families of
children with ASDs often live with the fear of suicide or another type of inexpli-
cable violence, it is sad that so few health professionals are willing to refer such
children for neurofeedback.) GLENN
Glenn came to me as a junior in high school. He had been diagnosed with
Asperger’s syndrome at around 8 years of age. His mother, who was a kinder-
garten teacher, had always supported him and done her best to help him with
his challenges. Glenn did not believe that neurofeedback was helping him, and
one time his paranoia overcame him and he accused us of “brain-washing” him.
He thought that we should not be trying to “alter his brain.” Instead of belit-
tling his illogical statements, we patiently explained in detail how neurofeedback
works; that it would not change him as a person, but help him to calm his anxiety.
Reassured by our caring attitude, he began to trust us and agreed to continue
training. After finishing his initial intensive phase, he still comes in once or twice
a month because he is more of a slow, steady responder. He went on to enroll as a
full-time college student at the University of Texas, El Paso, supporting himself
by working in the technical department of the university. He has become more
social, grooms himself appropriately (which was a serious issue before) and really
enjoys school and work. In short, he is thriving. Watching this transformation
was very gratifying for all concerned.

8.3.3  Comments on case studies

My hope in presenting these snapshots of diverse cases is to demonstrate the
efficacy of neurofeedback for treating ASDs. Developing a protocol to fit the idio-
syncratic symptoms of brain dysregulation for each of these cases was both excit-
ing and challenging. I sometimes face a different kind of challenge when, after a
course of treatment, a mother comes to me and asks if there is an “off switch” on a
previously non-verbal child, or when I hear a complaint about a previously intro-
verted, soft-spoken child who suddenly becomes outspoken and a bit argumenta-
tive. I have to explain to the parent that this child is now in a normal teenager
8.4 Conclusion 179

development phase and that they need to adjust their parenting accordingly. It
has been very rewarding to work with these ASD children and their parents.

In my practice of using neurofeedback with children in general, and ASD chil-
dren in particular, my guiding principle has been that the results are what matter
most. That is why I have chosen the measuring instruments described above.
They provided me with good pre- and post-training metrics of efficacy. In the
process, I have been able to learn how to improve my techniques.
Second, I have adopted and adhered to the Othmer approach of symptom-
based neurofeedback therapy (as contrasted with quantitative electro encephalo-
gram [QEEG]-based therapy). Client-oriented neurofeedback was developed by
Sue Othmer from her 30 years of clinical experience. It requires flexibility and
adapting the protocol to the individual patient in front of me. I am grateful that
she has always been helpful and made herself available via phone consultations.
Through frequent remote supervision, Sue has become an integral part of my
learning and practice.
A word about equipment: I was attracted to the Othmers’ pioneering philoso-
phy and constant drive to make their instrumentation better, and so I have used
Cygnet equipment and software from the beginning.
I currently utilize infra-low-frequency neurofeedback, described in Chapters
2 and 4. This is quite a change from the early years of QEEG-based prescriptive
neurofeedback. With the higher frequencies then in use, autistic children some-
times were over-stimulated, leading to a worsening of symptom severity. As a
consequence, working with ASD children was abandoned for a while.1 However,
with the advent of the infra-low frequencies and individualized training proto-
cols, most autistic children have been trained with good to excellent effect. Due
to the high incidence of comorbid biomedical conditions in the ASD population,
the additional variable for efficacy here is that biomedical factors, as well as psy-
chosocial/environmental issues, need to be addressed to ensure that the brain
training is not being neutralized. This also applies to children who are either
on medication or undergoing some biomedical treatment. Neurofeedback can
be used concurrently to calm an over-aroused brain and stabilize a neurological
system while other treatments are in progress.
A word about training: I have alluded above to the challenge of individualizing
treatments for each person. This takes skill and keen perception. It also requires
training and supervision. Technical breakthroughs in software and instrumenta-
tion have allowed treatment techniques to evolve rapidly over the past 10 years.
It is essential that neurofeedback practitioners continue to get ongoing training
and supervision. This is especially critical for those who venture into the field
of treating ASD children. For me personally, this has meant going to all of the
new training courses and practicum sessions offered by the EEG Institute. I also
attend their annual Clinical Summit training for advanced practitioners. In
addition, I am an active participant of the EEG listserve, a closed forum where
practitioners can share questions and experience.
180  Applying neurofeedback to autism spectrum disorders

1. Othmer S, Othmer SF. 2014. Neurofeedback for the Autism Spectrum.
2. Tager-Flusberg H. 2010. The origins of social impairments in autism spec‑
trum disorder: Studies of infants at risk. Neural Netw 23(8–9):1072–1076.
3. Lewis JD, Evans AC, Pruett JR et al. 2014. Network inefficiencies in
autism spectrum disorder at 24 months. Transl Psychiatry 4:388.
4. Ernst M, Zametkin AJ, Matochik JA et al. 1997. Low medial prefrontal
dopaminergic activity in autistic children. Lancet 350(9078):638.
5. Critchley HD, Daly EM, Bullmore ET et al. 2000. The functional neu‑
roanatomy of social behaviour: Changes in cerebral blood flow
when people with autistic disorder process facial expressions. Brain
6. Schultz RT. 2005. Developmental deficits in social perception in autism:
The role of the amygdala and fusiform face area. Int J Dev Neurosci
7. Schultz RT, Grelotti DJ, Klin A et al. 2003. The role of the fusiform face
area in social cognition: Implications for the pathobiology of autism.
Philos Trans R Soc Lond B Biol Sci 358(1430):415–427.
8. Pierce K, Müller RA, Ambrose J et al. 2001. Face processing occurs
outside the fusiform “face area” in autism: Evidence from functional MRI.
Brain 124(10):2059–2073.
9. Xiong J, Bollic A, Cox B et al. 2013. A quantitative link between face
discrimination deficits and neuronal selectivity for faces in autism.
Neuroimage Clin 2:320–331.
10. Hobson RP, Ouston J, Lee A. 1988. Emotion recognition in autism:
Coordinating faces and voices. Psychol Med 18(4):911–923.
11. McGaugh JL. 2004. The amygdala modulates the consolidation of memo‑
ries of emotionally arousing experiences. Ann Rev Neurosci 17:1–28.
12. Sun L, Gruetzner S, Bölte S et al. 2009. Impaired gamma-band activity
during perceptual organization in adults with autism spectrum disorders:
Evidence for dysfunctional network activity in frontal–posterior cortices.
J Neurosci 32(28):9563–9573.
13. Grandin T. 2008. The Way I See It: A Personal Look at Autism and
Asperger’s. Arlington: Future Horizons Press.
14. Wilbarger P. 2014. The Wilbarger Protocol: Helping People Sensitive to
The use of neurofeedback for
combat veterans with post-
traumatic stress


9.1 Introduction 181

9.2 Qualitative differences between civilians and combat veterans
who have post-traumatic stress 182
9.3 PTSD defined 184
9.4 Physiological markers of PTSD 186
9.5 Why neurofeedback? 187
9.6 Beginning the process 189
9.7 Protocol 189
9.8 Barriers to treatment 192
9.9 Evidence-based treatments utilized to treat PTSD and their
limitations 193
9.10 Vignettes 195
9.11 Summary 197
9.12 Disclaimer 198
References 198

Although only those warriors who have lived through combat understand the
impact this experience has on their lives, we can gain insight into the psychiatric
casualties by the devastating symptoms these veterans report and the stories they
tell. In this chapter, we will recount our experience in treating the psychiatric
wounds of combat veterans from Iraq and Afghanistan. We will reveal the prom-
ise that neurofeedback holds as a method to ameliorate the symptoms associated
with post-traumatic stress disorder (PTSD).

182  The use of neurofeedback for combat veterans with post-traumatic stress

The authors of this chapter have over 13 years of combined experience treat-
ing hundreds of combat veterans, both with evidence-based psychotherapy as
well as alternative treatment strategies. Twelve of those years were spent utilizing
neurofeedback as an adjunctive training to reduce the symptoms associated with
PTSD, combat and operational stress, anxiety, depression, and mild traumatic
brain injury (mTBI). The qualitative changes and self-reports from these combat
veterans are impressive and warrant further research.
Statistical findings differ; however, it is estimated that nearly 17%–42% of indi-
viduals who have deployed to Iraq and Afghanistan become psychiatric casual-
ties.1,2 More recent statistics from a Congressional Budget Office report published
by the Office of Naval Research estimate that 21% of military personnel returning
from overseas operations suffer from PTSD.3 The Rand study predicted in 2006
that the 2-year post-deployment cost to society from PTSD and depression alone
ranged from $4 to $6.2 billion.4 Once the costs of treating the combat injured are
combined with costs for treating traumatic brain injury, substance abuse, and
other psychiatric disorders, these numbers will continue to climb. The hidden
costs of unemployment, marital separation, divorce, and chronic physical health
consequences will be formidable and impact this generation and their families
for years to come. As mental health clinicians, we can no longer minimize the
psychological consequences for this generation. We will benefit from learning a
variety of therapeutic strategies to treat our nation’s warriors.

We were watching as most of our squad ran across an open field.

One at a time, each attempted to avoid the rain of incoming bul‑
lets from enemy fire. As squad leader I was going last, my friend
not wanting to leave me behind held back. We pulled out of cover
and began to run, with the weight of our packs some 60 pounds
or more. Out of the corner of my eye, I saw my buddy’s head snap
back as we ran… he was hit. (Deployment in Iraq, 2006)


Trauma of any severity in an individual can cause acute stress disorder.
However, in combat, there are events or situations that may increase the inten-
sity of trauma, which in turn impacts the nervous system in deleterious ways.
In assessing post-traumatic stress, a veteran may recount a single event that
precipitated their symptoms. However, more commonly, these combat warriors
have numerous exposures to life-threatening or traumatic events. The risk of
being diagnosed with PTSD rises in direct proportion to the level of combat
exposure.5 Additionally, concerns about being ambushed while out on a routine
patrol, taking small arms fire, engaging the enemy over a prolonged period, or
going out on patrol in areas riddled with improvised explosive devices (IEDs)
can create conditions of chronic stress.
9.2  Qualitative differences between civilians and combat veterans  183

What causes symptoms to be intractable can be associated with the num-

ber of combat traumas, the severity and the personal nature of a given trauma,
such as witnessing a friend killed, an unexpected twist to an event that makes it
more difficult to grasp, or even the sensitivity of an individual’s nervous system.
Countless times, we have heard stories of trauma created by what did not hap-
pen, such as a weapon jam preventing discharge in the heat of combat, a foot
step and the audible “click” signaling the warrior had stepped on an IED that
does not detonate, or the whistle of a rocket or mortar careening by an ear. The
fact that those events did not result in death or harm does not negate the sig-
naling to the nervous system of immediate danger, and the pump of adrenaline
to the body.

I was doing security while waiting for the ordinance guys to com‑
plete their post-blast analysis. I was clearing a path to the post-blast
scene. As I threw a clod of dirt, while it was airborne, I saw two
orange wires sticking out. Everything went slow-motion as I waited
for the explosion. It never came. But now I have nightmares not of
all my combat experiences but of the IED. In my dream it detonates
and I die or lose part of my body. All the time I was in combat I never
had nightmares or symptoms, but this one thing got to me… the
explosion that didn’t kill me. (Deployment in Iraq, 2005)

When our body begins its signaling of a threat, this physiological arousal can
be experienced as yet another trauma exposure. During a nightmare with abrupt
awakening, heart-racing, sweating, trembling, and violent intrusive images, the
body experiences this as yet another life-threatening event. The difficulty in
treating PTSD symptoms can be a result of the pervasive or chronic re-exposures
to perceived threat by ongoing internal and external cues.
As Grossman identified in his landmark book On Combat (2008), many civil-
ians who suffer from PTSD report a trauma that happened to them. They did
not seek out the event that resulted in their trauma diagnosis. Natural disasters,
a home invasion, even terrorist attacks or rape came to them, devastating their
lives as they knew them. In combat, our warriors are trained to go towards that
life-threatening event.6 In the book On Killing, Grossman (2009) reviewed earlier
research that supports an overwhelming instinct not to kill another human.7 He
cites earlier research that reports 80%–85% of infantrymen did not discharge
their weapons during World War II, even when it came to saving the lives of
a buddy or themselves. When this was understood, it led to a change in com-
bat conditioning, which included training warriors through physical and men-
tal conditioning and desensitization. With this change in combat training, the
number of warriors who did not discharge their weapons dropped to nearly 5%
during the Vietnam War. Then, when psychologically shaken by their killing
experiences in combat, the dialogue changed to not only regrets of killing, but
also regrets of not killing. When one veteran infantryman was asked if he had
regrets, he paused and said, “Yes. I had an enemy combatant in my sight and I
didn’t get the shot off. I regret that.”
184  The use of neurofeedback for combat veterans with post-traumatic stress


In the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5), the American Psychiatric Association revised the criteria for the diag-
nosis of PTSD.8 In this section, we will discuss how a PTSD diagnosis is derived
using the DSM-5 criteria. Although the Clinician-Administered PTSD Scale
(CAPS-5)9 is considered the standard in diagnosing PTSD, the Post Traumatic
Stress Check List (PCL-5)10 is the revised evaluation tool used as a provisional
indicator for PTSD and the tool we utilize in combination with the diagnostic
clinical interview in assessing combat veterans who we see for neurofeedback
(see Figure 9.1).
PTSD is assessed after an individual either witnesses or experiences a life-
threatening event, serious injury, or violence. Additional criteria need to be
met. By using the PCL-5 or CAPS-5, these criteria can be identified. The PCL-5
was based on the DSM-IV8 diagnostic criteria. It contained three clusters: re-
experience, avoidance, and hyper-arousal. Re-experience refers to the intrusion
of images, sounds, or smells associated with combat while in a waking state or
during sleep (nocturnal flashbacks), or unwanted and untimely recollections of
combat. Avoidance is defined as efforts to avoid internal memories, thoughts, or
reminders of the trauma, or avoidance of external reminders (individuals, places,
or situations) of the traumatic event. Hyper-arousal includes symptoms such as
irritability, sleep disruption, startle effects, or jumpiness.
With the DSM-5, a fourth cluster was added. It is referred to as “negative
mood and cognitions” and includes: inability to remember important aspects
of the trauma; persistent negative beliefs or expectations about oneself or the
world (i.e., “no one is safe; the world is dangerous”); distorted cognitions about
the cause or results of the traumatic event; persistent negative emotional state;
guilt or shame (i.e., “if I had only looked over my shoulder I would have pre-
vented the death”); persistent inability to experience positive emotions; feelings
of detachment or estrangement; and/or diminished interest in things they used
to enjoy.
Significant factors were found in those individuals who met the criteria for
PTSD. The two that were identified as the most significant factors contributing to
a positive PTSD diagnosis were service members who experienced deployment-
related stress and combat exposure. Two other factors that increased the likeli-
hood of developing PTSD included marital status (those single or divorced) and
educational background.5 A recent study of combat experiences found that those
individuals who endorsed all 15 items on the Combat Experience Scale (CES) had
PTSD.11 They also found that personally witnessing the death or serious injury of
a friend in combat and exposure to friendly fire were independent predictors of
PTSD in Iraq and Afghanistan veterans. Those most closely exposed to a trauma
event in real time had the highest levels of PTSD.12 Adverse childhood events also
increase the likelihood of developing PTSD in adulthood. Bessel van der Kolk
has referred to this as developmental trauma disorder.13 High levels of family
and life stress, in addition to combat exposure, also increased the likelihood of
developing PTSD.14
9.3 PTSD Defined 185

Figure 9.1  (See color insert.) Pre-post SPECT scan data are shown for a
veteran treated at the EEG Institute Clinic, comparing pre-training conditions
with those prevailing after 24 sessions. Classic signs associated with PTSD
include elevations in activity at the anterior cingulate, the basal ganglia, and
the thalamus. In post-training data, the activity level at the anterior cingulate
and basal ganglia are reduced. Additionally, the high activation of the cerebel‑
lum has been reduced. (Courtesy of Daniel Amen, MD, Orange County Amen
Clinic, Costa Mesa, CA.)

Even more sobering, one expert posited, “Forty percent of those who develop
PTSD will likely not recover whether or not they have ever received treatment.”15
Although this statistic was written prior to the decade of engagement in the
Middle East, if that percentage holds true today, further strategies need to be
explored to address not only the psychological sequelae of the trauma experience,
but also the physiological responses that signal its presence.
186  The use of neurofeedback for combat veterans with post-traumatic stress

I made a deal after my first combat deployment. I was willing to

lose my left leg … I don’t know why I thought it had to be my
left leg, but that was the deal I made with God. (Deployment in
Afghanistan, second tour, 2011)


To understand how neurofeedback can reduce the symptoms of PTSD, we need
to understand its physiological markers. As far back as Hans Selye’s recogni-
tion of the hypothalamus–pituitary–adrenocortical axis’ response to stress, we
began to understand the impact of PTSD on the structure and functioning of
the brain.16
As van der Kolk17 so clearly described, the three general areas of our brain
with interdependent action are the brainstem and hypothalamus, which regulate
involuntary actions such as heart rate and the regulatory system of homeostasis;
the limbic system, which monitors our internal experience with some translation
to outer cues; and the neocortex, which is the processing-intensive part of the
brain that mediates interactions with the outside world. Initially, it was thought
that trauma would have the greatest impact on the part of the brain that interacts
with the environment or experiences the trauma. However, research has not sup-
ported this. All of our neurophysiology is impacted by trauma.18–20 Therefore,
to help readers understand the physiological changes that occur with combat
trauma, we will briefly review the basic response systems, neurochemical and
structural changes that take place as a result of stress, in particular combat stress.
Our nervous system contains both the sympathetic nervous system, which
governs the fight-or-flight response, and the parasympathetic nervous system,
which is the vegetative, homeostatically regulated system. These systems operate
to not only protect us under threat, but also restore our bodies to their resting
and recuperative state. However, during intense combat stress, the sympathetic
system is highly activated. Adrenaline is released and a hyper-alert state is estab-
lished. After sustained activation, when the battle is over, the parasympathetic
system is activated, leaving the service member with exhaustion, perhaps to a
degree they have not known before. The intensity of combat can result in a let-
down of such magnitude that emotional numbing, isolation, and fatigue ensue.6
As stress increases, so do cortisol levels, and dehydroepiandrosterone levels
decrease, causing the ratio to get out of balance. The chemical reactions transmit
signals that mediate the fight, flight, or freeze response known as the adrenergic
response, causing the release of noradrenaline (norepinephrine) and adrenalin
(epinephrine). As the threat pattern is activated, there is blood flow to the mus-
cles and away from the periphery,21 and an increase in energy caused by raising
blood glucose levels, which leads to a decrease in the immune response. If this
status persists and is left unchecked, it can lead to illness and disease.21
Two structures—the amygdala and hippocampus—help us to understand the
effect trauma has on the brain. The amygdala is the first structure to activate in
response to stress, before conscious perception is made. Its response bypasses
the prefrontal cortex, considered the rational part of the brain.21 The amygdala
9.5 Why neurofeedback? 187

is involved with attachment, emotion, fear processing, assessing the environ-

ment, and appraisal of danger and safety. Post-trauma brain imaging reveals
that exposure to traumatic incidents results in elevated activity in the amygdala,
insula, and prefrontal cortex.22–24 The activation and neuronal firing continue
post-trauma, unlike in other areas of the brain. The physiological effects from
trauma are heightened and fix the traumatic memory by the release of norepi-
nephrine.23 The amygdala is implicated in the experience of negative emotion.
The persistence of activity in the amygdala post-trauma may indicate that newly
formed fear memories are being consolidated into stable long-term memories in
this part of the brain.25
While the role of the amygdala is to generalize sensory information when
danger is imminent, the hippocampus helps us differentiate the severity of the
danger.26 The hippocampus is involved in the conversion of short-term memory
into long-term memory.27 It helps store past experiences and newly learned infor-
mation, and thus initiates the formation of narrative memory. The release of nor-
epinephrine and glucocorticol, which occurs in the hippocampus, plays a role in
memory conversion. Under traumatic stress, the hippocampus atrophies, thus
compromising information processing and learning.28 Under prolonged stress,
such as combat exposure, hippocampal cell loss correlates with deficits in encod-
ing short-term memory into long-term memory.29 Glucocorticols such as cor-
tisol are used for immediate energy in times of need, overriding other systems,
and are not meant to be activated for more than immediate danger. Cortisol also
damages the prefrontal cortex, which is responsible for attention, impulse con-
trol, and emotional regulation.30


We became interested in neurofeedback after seeing the unique challenges in
treating PTSD and anxiety disorder. Often veterans would be unwilling to dis-
close the highly disturbing memories or recollections that plagued them. Some
reported unwillingness to disclose their accounts, while others felt unable to
describe or recall the events precipitating the trauma response. Alexithymia,
which is commonly experienced post-trauma, refers to the difficulty translat-
ing experience into words. Broca’s area is compromised in the trauma response,
making articulation more difficult, in addition to impairments in semantic
memory.31 Additionally, some warriors report no single event precipitated the
trauma they experienced. Without a distinct “narrative” that some therapies rely
on, treatment can become difficult. Neurofeedback does not rely on verbal dis-
closure of combat experience. It bypasses the usual resistance encountered in the
therapeutic process that occurs in these highly traumatized individuals. We have
found that once the body is calm, the veteran may willingly enter into discussions
about combat at their own pace.
One of the key benefits of neurofeedback is that it is a non-intrusive method
that can impact the nervous system in positive ways. Although medication can
have a positive effect on symptom reduction, combat veterans complain about
the side effects. There is resistance to taking any medication, as this could impact
188  The use of neurofeedback for combat veterans with post-traumatic stress

their deployable status or ability to handle firearms or explosives. Some do

not want to take medication for other reasons. Medication for sleep, mood, or
anxiety can be somewhat effective, but few traditional therapies are effective in
improving sleep dramatically or decreasing anxiety in a timely manner. In our
experience, neurofeedback has showed marked effectiveness in addressing the
physiological symptoms that other therapies cannot.
With psychological trauma and mTBI, there is deterioration in the brain’s
ability to self-regulate. This failure to regulate is observable broadly in behav-
ioral, autonomic, cognitive and affective domains. These failures are also observ-
able in the behavior of neural networks. Through neurofeedback, we allow the
brain to be a witness to its own behavior. The brain utilizes this information for
its own benefit. The information available to us in the electroencephalography
(EEG) relates entirely to the brain’s attempt to regulate its own activities. By act-
ing upon that information, the brain is able to improve its own self-regulatory
Recent findings in the neurosciences have brought us the understanding that
the brain lives predominantly in its resting states. The ability to interact with the
world is contingent on good resting-state function. Seen in this frame, PTSD and
mTBI can be understood as disturbances in resting-state organization and as
losses of access to good resting-state activity. Through neurofeedback, the brain
requires access to its own resting states, and it is capable of restoring good rest-
ing-state function. The process is as follows: the witnessing of its own behavior
causes the brain to alter its own state, and then the brain reacts to that altered
state. This is effectively an exercise of the brain’s own control mechanisms, and
by these means, control is enhanced. This is a learning process, consolidated by
the mechanisms of brain plasticity.32 By the same token, we can understand per-
sistent PTSD as a manifestation of brain plasticity, by means of which the brain
is sustained in an activated “alarm state,” even when it is no longer needed. This
chronic condition leads to a dysregulated status. Neurofeedback may be the most
efficient way to walk this process back toward regulatory competence.
Few traditional therapies have the advantage of increasing self-regulatory
competence, and fewer still make this the explicit objective. Significantly, both
the objective and the means in neurofeedback consist of the promotion of good
brain function. Dysfunction diminishes as a consequence of the restoration of
regulatory competence. The symptoms of PTSD are not the target here, although
their diminution is a marker of success in the effort. The point is that the process
does exhaust itself once dysfunction is no longer observable. Good function is not
merely the absence of debilitating symptoms. With neurofeedback, the ongoing
objective is optimum functioning under the prevailing physiological constraints.
The training process can be fruitfully continued until the trainee reaches his/her
own plateau of good function.
The integrated or self-regulated brain can produce the experience of well-
being. The final outcome for the combat veteran receiving neurofeedback train-
ing is calm alertness, which develops from an improved flexibility and stability of
the state regulation. There seems to be no extinction effects with neurofeedback,
but rather a cumulative learning effect from the training.
9.7 Protocol 189

I can’t explain it, I can’t handle the horrific image in my own head.
I know you’re a therapist, but I can’t risk having that image in any‑
one’s head, not even yours. (Deployment in Iraq, 2004)


Recognizing the unique benefits of a noninvasive training technique that might
improve overall well-being and functioning, we began to incorporate neurofeed-
back as an adjunct to evidence-based therapies. We would suggest this training
technique to those interested in or avoidant of talk therapies. The potential of
neurofeedback is to help regulate a nervous system in ways in which other thera-
pies are unable.

When working with combat trauma, certain symptoms are common in most cli-
ents seeking treatment. Almost all symptoms reported correlated with the stan-
dard PTSD test instruments (PCL-5 or CES). About 90% of the clients report
sleep disturbance, whether that be sleep onset problems, sleep maintenance,
nightmares, night sweats, or restless sleep. Additionally, flashbacks are often cor-
related with the sleep state. Other problems present as anxiety, being keyed up,
having undifferentiated dread, panic attacks, fears, nightmares, muscle tension,
and obsessive compulsive behaviors.
The initial session is a thorough assessment of the presenting symptoms.
Although we are not treating symptoms, we are using the symptoms to guide
us in the training protocol. In this manner, we can understand how the system
is dysregulated and chose placements of the electrodes for observing brain wave
activity within the training session. There is no diagnosing involved in the neu-
rofeedback assessment, but rather there is a noting of the pattern of dysregulation
from symptoms disclosed. A list of those symptoms is compiled and used to track
changes throughout the training.
Each patient is viewed as an individual with their unique symptom picture;
however, symptoms included and monitored are those correlated with PTSD.
Although it is harder to elicit disclosure with respect to substance abuse, we
found alcohol abuse or a history of this in at least 50% of our clients. Those that
do admit to alcohol abuse often claim that they drink to initiate sleep. Others
say it reduces feelings of anxiety that permeate their daily life. Yet some would
report that they could not drink, fearing they would “lose control” or “be over-
whelmed” with images and thoughts of combat.
We are first-and-foremost clinicians, so as we began our work, we tracked the
individual progress through a reduction in self-reported symptoms, along with
validated measures, but not within the framework of a research design. There
were, of course, individual differences. Instead of tracking a mixture of over 60
different symptoms, we honed down our list to 17 core symptoms. Those corre-
lated with post-traumatic stress. These include but are not limited to: sleep distur-
bances, low motivation, poor concentration, poor short-term memory, headache,
190  The use of neurofeedback for combat veterans with post-traumatic stress

panic attacks, anxiety, agitation, irritability, anger, rages, mood swings, lack of
pleasure, obsessive negative thoughts and worries, and depression. Irritability and
aggressive behaviors usually accompany sleep disturbances, as well as being key
symptoms of PTSD.33 In addition, every individual reported anxiety, the hall-
mark of the PTSD diagnosis. We learned that nearly all symptoms could be
viewed as a product of brain dysregulation.
Headaches were another common—and critical—symptom that was reported.
There are many reasons why a large number of combat veterans reported head-
aches. Some reported muscle tension headaches, others attributed their head-
aches to exposure to burn pits while deployed and most reported headaches from
blast exposure (IEDs, grenades, or mortars). Some individuals could not identify
where their headaches came from, but they knew they were related to deployment.
Headache is the most ubiquitous symptom of mTBI. Headache is also synonymous
with brain dysregulation. In neurofeedback terminology, headaches are under-
stood as instabilities. We addressed brain instabilities in almost all of our protocols.
With neurofeedback training, we are inviting the brain to engage with infor-
mation derived from the EEG. Typically, the signal is presented to the veteran
in the form of a video display, has an auditory component, and can be accom-
panied by tactile feedback. Our focus is balance, stability, self-regulation, and
cognitive–emotional integration. We attempt to train the person twice weekly
for the first 2 weeks, then continue with one session a week thereafter, which is
adequate to retain what is learned from the previous sessions. After a period of
stabilization that can occur within the first three to five sessions, a missed session
is not detrimental to the continuity of training. The effects of neurofeedback tend
to be gradual and cumulative, hence the necessity for regular symptom track-
ing. Trainees often do not recall the intensity of the symptoms they endorsed at
the onset of training. One veteran was asked (after about ten sessions) how she
would rate her nightmares. She said she did not have that problem, completely
forgetting that it was rated as eight out of ten on her initial assessment. Another
service member was asked about headache frequency, and he replied he did not
have headaches, forgetting that many sessions earlier he was having headaches
three to four times a week. Therefore, symptom tracking is critical not only as a
baseline to record immediate response changes but also note improvements as
they unfold gradually.
In the population of combat veterans, trauma is the focus of our treatment. We
begin at T4–P4 (see International 10-20 diagram of placements in color section)
to determine the optimal response frequency. Placement of the electrodes requires
knowledge of functional neuroanatomy. Trauma-related symptoms appear to be
associated with functions that are predominantly managed by the right hemi-
sphere, which informs our choice of neurofeedback training at T4–P4 (the right
parietal region). We learned through experience that our first goal was to calm
the individual both physically and mentally, which is accomplished through
right-side training. This has become the foundation for all state-regulation train-
ing. The trainees often notice the calming immediately within the session.
We place the electrodes on the scalp so we can monitor the person’s brain
waves. The individual is seated in front of the monitor screen, where the feedback
9.7 Protocol 191

is presented; this feedback is responsive to the real-time brain activity. Since imple-
menting the high-definition (HD) amplifier, which is optimized for low-frequency
applications, we begin at 0.5 mHz and slowly move down every 2–5 minutes, and
prior to making any frequency change. We ask the client to report any changes in
their perceived internal state. If our target frequency is too high, they may report
agitation, muscle tension, or headache. If the target frequency is too low, they may
report a feeling of heaviness, grogginess, or pressure. The responses differ, but for
the most part, sensory changes consist of being more relaxed or more tense (often
in the shoulders), more or less agitated, feeling tired or more alert, a decrease or
increase in an existing headache, or other physiological changes. The frequency
is adjusted for optimal comfort within the session. If there are any problems that
cannot be accommodated by means of frequency adjustment, we can move the
electrodes to T3–T4, the other primary site for the initiation of this kind of train-
ing. Each session is about 30 minutes. The subtle changes in the feedback are just
enough for the trainee to note, but not to be distracted by.
The training process is noninvasive and free of lasting adverse effects. Any
discomforts that do occur during the training process are not considered to be
side effects in the usual sense. They are effects of the training process or exercis-
ing the brain as presently constituted, and they call for adjustment of the training
parameters. These adverse effects can be corrected in the session within minutes,
or in the next session if they arise between sessions. Throughout the session, the
sensory state of the individual is constantly monitored. Presenting symptoms,
the targets of our training, are also monitored between sessions for additional
information. Questions commonly asked by the clinician include: how was your
sleep throughout the week? Did you have any headaches? How was your mood
or level of anxiety? In the inquiry of headache events, the number, intensity, and
duration are assessed.
When the clinician is able to determine the individual’s optimal frequency,
we then proceed to an extended training plan. Once the frequency is established
and solidified (usually within two to three sessions), all symptoms are taken into
account and the full treatment plan is implemented. The Protocol Guide34 gives
us most of the information used in directing our progress; however, we remain
vigilant to individual differences and sensitivities. The client’s reactions and
reports during the session and post-session guide our course of future training,
rather than the norms that have been established.
The brain responds immediately to the feedback, particularly with the HD
program, but it generally takes approximately 20 sessions—usually spaced no
longer than a week apart—for the brain to finally maintain and incorporate its
new learned behavior. The brain’s behavior is shaped so that the ability to self-
regulate on its own is restored. There are circumstances where the training goes
beyond the 20-session minimum; however, we typically plan on 20 sessions to
complete the training. During the training protocol, after approximately ten ses-
sions, Alpha–Theta training can be introduced. Alpha–Theta training provides
deep relaxation, calming, and inward focus. There is a quieting of cortical func-
tioning, and hence a relinquishing of executive control and a diminution of self-
criticism. It is here we believe that the trauma can be diffused and integrated with
192  The use of neurofeedback for combat veterans with post-traumatic stress

what we call the psychodynamics of healing. This Alpha–Theta training process

can consolidate and solidify the training, reducing the likelihood that future
exposures will be re-traumatizing.34
For example, F.K. had a complete remission in his obsessive compulsive
dressing ritual, which included a time-consuming pattern of repeatedly putting
on his shoes and socks, sometimes up to eight times each morning. Within five
sessions, this ritual was eliminated. This change came before any measurable
change of symptoms related to his combat stress occurred. There was a brief
interruption in the neurofeedback training and this ritual resumed. It became
obvious to us then that the 20-session protocol was a “best practice” to guide us
with combat veterans, suggesting that some individuals may need more than 20
sessions. The brain has to relearn how to simply “be,” which we now understand
as the resting-state organization or default mode network.32 When one realizes
the incredible job the entire body does in maintaining homeostasis, one begins
to honor that relearning and trust it will bring about if we merely provide it with
the opportunity. After an additional three sessions, the ritual dressing behavior
again subsided, but the 20-session protocol continued in order to resolve other
On average, there was a 50% decrease in symptom severity over the course
of 20 sessions, as reported by combat veterans, with sleep disturbance decreases
being most notable. There were many individuals who had a complete remission
in certain symptoms, and others with modest but helpful reductions in sever-
ity. Improvements in sleep included faster sleep onset, better sleep maintenance
(reduction in the frequency and duration of nighttime waking), and fewer night-
mares. There was also a noted decrease in anxiety, irritability, mood swings,
and depression. Obsessive compulsive behavior and thrill-seeking behavior
decreased. We also found that neurofeedback improved working memory and
general cognitive functioning.
Many pleasurable activities were resumed, hobbies re-established, and family
activities increased. Educational goals were pursued as motivation, concentra-
tion, and memory improved. The overall sense of well-being was the most subtle
but also the most life-altering response reported. The renewal of the capacity to
feel joy, pleasure, and love for others was commonly reported. With a focus on
symptoms, however, the more overtly positive features of the training were not
tracked as assiduously although they were proffered by the participants anecdot-
ally with surprising frequency.


Stigma is still likely the greatest barrier to the access of care. There is a common
belief in military settings that a problem or symptoms are considered mental
weaknesses. A service member revealing these symptoms is perceived as having
the potential to jeopardize their career. We have heard countless veterans share
that “they tell you to take care of yourself, get the care you need,” yet report see-
ing others being treated as “different” if they do seek care. Once, when a combat
veteran was scheduling his appointment, he wrote “Wizard” in his phone after
9.9  Evidence-based treatments utilized to treat PTSD and their limitations  193

the phone number. When asked about this, he said, “When I was active, that
term meant once someone sees a therapist, they would disappear.” A clinician
on a military base may deem the service member be placed on medical disability
due to the severity of their symptoms, or temporarily assigned to an Intensive
Outpatient Program, thus the service member “disappears.” These recommenda-
tions could lead to a move to a different unit where the impact of having a non-
deployable member would be lessened. Commands need to be operational and
“combat ready.” Even though all commands support their troops in obtaining
needed treatment, they also carry the burden of keeping a unit battle ready. The
challenge to leadership intensifies when so many troops are attending medical
or mental health appointments. In a private practice setting, these challenges are
lessened, although service members are encouraged to use the base resources.
Great strides have been made to improve access to care both in and out of mili-
tary settings; however, the barrier of stigma still exists.


As we clinicians know, evidence-based treatments are those treatments that
have been substantiated through empirical research to reveal significant
improvements in symptoms through valid and reliable measures. Having
received training in all of the evidence-based therapies and using three of
them frequently, we are familiar with the advantages but also the limitations
of these techniques. In this section, we will share our experiences with using
these therapies and reveal the advantages of using neurofeedback as an adjunc-
tive training to treat PTSD.
Those treatments endorsed by many military service branches to treat PTSD
include cognitive processing therapy (CPT), exposure therapies (such as pro-
longed exposure and virtual reality therapies), adaptive disclosure, trauma-
focused cognitive–behavioral therapy, eye-movement desensitization and
reprocessing (EMDR) therapies, and psychopharmacology. In a recent meta-
analysis of evidence-based therapies for PTSD, many therapies revealed efficacy
for treating trauma; however, trauma-focused cognitive–behavioral therapy alone
emerged as a type 1 treatment for PTSD.35 The advantages are many; however, the
limitations of these therapies include time, retention rates, emotional disclosure,
and physiological arousal. There is an increase in attempts to provide adjunctive
therapies (acupuncture, heart rate variability biofeedback, hyperbaric chamber
treatment, and neurofeedback) that may reveal greater improvements in some of
the most intractable symptoms. Once research is conducted in the population of
Operation Iraqi Freedom and Operation Enduring Freedom service members,
other therapies may also emerge as effective in treating combat stress.
CPT, when executed correctly, takes time (1 hour in therapy for 12 weeks),
consistency (reading the narrative daily), and written exercises. Active-duty
military personnel rarely have a period of 3 months that is not interrupted by
field operations, range training, assigned overnight duties, or leave. Veterans
may be employed full time or have family and social demands that interfere
194  The use of neurofeedback for combat veterans with post-traumatic stress

with regular sessions. In our experience, when evidence-based therapies are

completed, service members report a sharp decrease in symptoms; however, we
found the retention rate of this technique and compliance with assignments in
our population to be very low. Fear of putting down onto paper an experience
that was devastating, chaotic, or challenged their moral fiber may elicit tremen-
dous anxiety. As referenced in the section on physiological correlates in PTSD,
alexithymia—or the inability to generate words to attach to an internal experi-
ence—can interfere with the ability to speak or even write about trauma.32 Some
group CPT treatments, in an effort at modification, will ask service members to
write for 5–7 minutes to initiate the narrative of an experience. We have heard
comments such as, “I’ll do anything, just don’t make me write,” or, “If it requires
homework, it just won’t happen.” Modifications such as dictating their experi-
ences into their phone or iPod can improve compliance when writing proves
difficult, but the exposure to their narrative requires moments each day for lis-
tening or re-reading. Avoidance of reminders of combat, people, or places is a
primary feature of PTSD. Breaking that avoidance is the key to many treatment
strategies; however, it takes great effort and compliance by the veteran to achieve
those gains.
EMDR has also shown promise with traumatic experiences and is used often
within the military population. However, in using EMDR, the veteran will often
briefly experience an increase in emotional and physiological distress as the pro-
cess unfolds. The ability of the brain to continue the processing (through dreams)
can support the service member who is willing to recount their experience. Yet
experiencing intrusive nightmares immediately following these events can be
overwhelming. One service member reported, “I’m not sure I can risk it; I fear
going to sleep as it is.” Even though he knew this technique would likely dra-
matically reduce his symptoms, he was unwilling to try it. He reported it was
like opening Pandora’s Box, where several excruciating experiences could flood
him without adequate coping to manage the events. Unlike some people with
trauma, combat veterans often experience multiple traumas even within a single
combat experience. When offered this treatment, some veterans refused, stat-
ing that they could not “talk through it” or refused to think about their com-
bat experiences. Alternative methods, such as asking them to just imagine the
event without c­ ommunicating it, proved helpful to a few; however, for most, this
proved difficult to maintain.
Although we use evidence-based treatments daily in treating combat veter-
ans and do not dismiss the value of these treatments, neurofeedback has become
an effective training for the restoration of normal physiological regulation in
the traumatized nervous system. This includes the reduction of physiological
arousal, the restoration of appropriate autonomic regulation, and the subsidence
of PTSD symptoms that are grounded in physiological dysregulation. Its benefits
and outcomes continually amaze us.

We were ambushed from two sides, RPGs, small arms fire, mortars
… the dust, noise and chaos was everywhere … we had to move.
I knew the gunfire was raining down on me, and I could hear the
9.10 Vignettes 195

bullets hitting the dirt around me … but with each step … I wasn’t
worried about those bullets … all I could think of was hitting an IED
and losing my legs… (Deployment in Afghanistan, 2010)

A.T. was a 38-year-old retired Gunnery Sergeant who presented with sleep prob-
lems and both marital and family problems. There had been four deployments
over his career and all had been very stressful and kinetic in high-combat areas.
He had alienated both of his teenage children with his erratic moods, short
temper, and high expectations of them. Fights with his wife occurred over how
he treated the children, which further alienated them. No one was pleased to
have him at home more often now that he had retired. There were no physical
problems except for a back injury sustained when he was active duty. He was in
physical therapy and felt he was getting better. Once neurofeedback was initiated,
almost immediately he noted a change in mood. The stories he presented in the
session became much less about the conflict with his sons and more about family
activities. By the time the training was completed, 20 sessions later, the conflicts
and discord at home were well within the range of a normal family with teen-
age children. Discussing the family problems at home was the norm, rather than
screaming and demanding perfection of the children. He was enjoying his family
and it appeared they were enjoying him too.
K.R. was a medically retired marine who had been on three combat deploy-
ments. He was involved in many combat mounted and dismounted patrols and
had experienced three injuries, with the last one being the worst. He was in a
convoy in the lead vehicle. The Humvee was hit by an IED. Although no one was
killed, all occupants of the vehicle were medically evacuated with injuries. K.R.
had shrapnel wounds to his legs and had lost consciousness for about a minute
after he hit his head. Pain was now chronic, with nerve pain from his leg injuries
and daily headaches that could last for hours with a pain intensity identified “of
about a six out of ten.” There was a resistance to talking about his combat events.
In his opinion, it was just something he did, and no one could understand unless
they had been there. He had been through all the standard treatments for mTBI
with no success. His friend had received some relief from neurofeedback, so with
prompting from his wife, he decided to try it. When he came to his initial session,
he presented as a depressed man with flat affect. He and his wife had three young
children; she was not comfortable leaving the children alone with him because he
was forgetful, had terrible mood swings, and was irritable much of the time from
chronic insomnia and pain.
Because of the mTBI, it became evident after about ten sessions that this train-
ing would probably go beyond the normal 20 sessions. On the symptom ratings,
there were no changes noted, except for perhaps an hour or two more sleep, but
he still awakened throughout the night. A noticeable change was reported after
about 15 sessions. At this point, he became more animated and began talking
about day-to-day events in his life. Once in a while, he would discuss combat
memories, but they were typically superficial events. His wife noticed changes
196  The use of neurofeedback for combat veterans with post-traumatic stress

and began insisting he not miss any appointments, which he was prone to do. She
began leaving him with the children for brief periods of time that grew in length
over the training. Future plans were being discussed. At the end of 42 sessions,
he was ready to return to school, his headaches had decreased to a manageable
level, and sleep was normal. The most significant change was in his personality
and outlook on life. He had hopes, opinions, and good recall. This all occurred
very gradually and would not have been noticed if we had not kept records of the
intensity, frequency, and duration of his headaches and overall functioning.
Another combat veteran, T.K., after ten neurofeedback sessions mentioned
that his 10-year-old daughter asked, “Daddy, how come you are being so nice
to me now?” He was so shaken by this comment that he made a stronger com-
mitment to neurofeedback training. Isolation, irritability, anger, and occasional
rages were commonplace in his home. His wife had told him she was consider-
ing leaving, not so much for her sake but for the sake of their two children. She
felt her role was buffering their children from the critical, angry stance of their
father. The marital relationship was suffering too, with little physical or emo-
tional intimacy. A referral was made for marital therapy during the 24 neuro-
feedback sessions, which he said was helpful. After completion of the training,
he reported family functioning had improved markedly and family cohesiveness
was restored.
L.F. came for his first session stating that his anger scared him, and that he
could find no joy in daily living. There was no reluctance to discuss combat
events. He had spent weeks at a time outside the base with no showers and mini-
mal food. He was still dealing with foot fungus, which is commonplace with ser-
vice members not able to manage basic hygiene. Beds were in holes that they dug
as they moved through the harsh countryside. There were five casualties in the
course of a long patrol outside the wire by IEDs. Two lost legs, one lost his arm,
and two were killed. The one factor that kept them going was the bond they felt
for each other. They were no longer fighting a war for the American people, but
fighting to keep one another alive. One of their assignments was to interact with
the locals as they encountered them in what was called “winning the hearts and
minds.” The problem was knowing which people to trust: even small children
could attack them. As such, they were not only fearful of every step they took,
but also fearful of any local they met. When L.F. came for treatment, his identi-
fied problem was anxiety that interfered in all aspects of his life. Leaving his
home was a challenge; he resisted in any way he could. His fiancée was growing
weary of having no social life, and his unwillingness to accompany her to any
store or restaurant. Sleep was only possible with heavy medication; their sexual
life was deteriorating, which she took personally. He said that he knew he loved
her but could not feel it. Like so many veterans, he had hoped to attend college
once he left the military, but found he could not relate to the other students and
hated being in the classroom with all those people. Concentration and short-
term memory issues made studying difficult. He dropped out after a semester. He
was adamant that suicide was not an option, yet stated living a life like this made
him think it would be acceptable to die. Neurofeedback was initiated with two
sessions a week for a total of 28 sessions. He immediately found it relaxing during
9.11 Summary 197

the sessions, which gradually extended beyond the sessions to the next day and
then 2 days after the session, and finally from session to session. Toward the end
of the 14 weeks, he had cut back to only occasional use of his sleep medication.
An increase in confidence had helped him venture back to school, beginning
with one class, with a goal of resuming full-time studies.
S.R. was a “boots-on-the-ground” combat veteran. He was fearful of seek-
ing mental health care on-base and avoided therapy, not wanting to have “any-
thing in my medical record.” He postponed therapy until he was 6 weeks out
from a second deployment to the same region where he had deployed the first
time. The region was riddled with IEDs, combat was frequent, and he admit-
ted to apprehension about the deployment. He presented as anhedonic, flat,
and stoic. He reported his marriage was tenuous, and when asked what moti-
vated him to obtain needed services, he said, “Well, my wife said she would
leave me if I didn’t.” We agreed that due to the brief time remaining, we would
complete as many sessions of neurofeedback as possible prior to his departure
to Afghanistan. After the first session, he reported, “It was weird, I felt almost
euphoric and had a sense of calm.” He revealed a sharp improvement in anxiety,
sleep, and agitation. His initially pervasive anhedonia also sharply decreased.
He revealed an approximately 50% improvement in all self-reported symptoms.
More strikingly, he came back to this provider 9 months later, once he returned
from the deployment, stating: “I know it’s amazing, but I’m good. I just wanted
to thank you for your help. I still sleep, rarely have a nightmare, but more impor-
tant, I’m happy, my wife is happy, we’re good!”

When I came back, I knew I had PTSD. I checked out therapists,

and chose the one I thought who could “do it all.” I am back! The
only thing I would do different is that I would have done neuro‑
feedback first. I was given EMDR first but it was so overwhelming.
There were days when I could barely get through. But the neuro‑
feedback helped me feel grounded and allowed sleep for the first
time in years. (Deployments in Iraq, 2004, 2006, and 2007)

Combat veterans have many challenges. Having developed skills for com-
bat, many will return to their families and face an even greater adjustment.
Attempting to integrate a traumatic experience into their now peaceful life, or
trying to manage severe insomnia or physiological arousal, pose great demands
on our warriors. Neurofeedback shows great promise in regulating somatic
responses. Our experience in offering neurofeedback as an adjunctive treatment
to standard care revealed greater improvements than we could have imagined.
It often decreased or eliminated nightmares, created a sense of calm, lessened
reactivity, and ushered in restful sleep. Some reported a sharp decline in head-
aches or migraines, while others reported improved focus. Research needs to be
initiated to empirically support what we have come to believe and know: that
neurofeedback is a powerful tool to help treat PTSD in our nation’s warriors.
198  The use of neurofeedback for combat veterans with post-traumatic stress

All details described in the vignettes have been altered to mask any identifying
details of the veterans we served. The quotes are fictional but reflect the com-
mon combat experiences shared with us over the years. Symptom reports and
improvements are accurate and reflect the many improvements that we observed.

1. Booth-Kewley S, Larson GD, Highfill RM, Garland CF, Gaskin TA. 2010.
Correlates of posttraumatic stress disorder symptoms in marines back
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2. Hoge CW, Castro CA, Messer SC, McGurck D, Cotting DI, Koffman RI.
2004. Combat duty in Iraq and Afghanistan, mental health problems and
the barriers to care. N Engl J Med 351(1):13–22.
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4. Tanielian T, Jaycox LH, eds. 2008. Invisible Wounds of War: Psychological
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15. Committee on Treatment of Posttraumatic Stress Disorder, Institute
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PTSD symptom reduction with


10.1 Introduction 201

10.2 War’s impact on human life 202
10.3 Human biology and the stress response 202
10.4 Development of PTSD 205
10.5 History of neurofeedback in veteran care 206
10.5.1 A/T training 207
10.5.2 Behavioral conditioning 208
10.5.3 Neurofeedback training schedule 208
10.5.4 Post-traumatic life 208
10.5.5 PTSD summary 209
10.6 Case studies 210
10.6.1 The case of Rand: “The white noise in my head is gone” 210
10.6.2 Case summary: Rand 215
10.6.3 The case of Jackie O.: An outcome report of a combat medic 216
10.6.4 Case summary: Jackie O. 222
10.6.5 Case presentation summary 222
10.7 Questions 223
10.8 Conclusion 224
Appendix: (Modified) Othmer symptom tracking report (+2 behavior
category symptoms: Hypervigilance and exaggerated startle) 225
References 227

This chapter looks at the impact of trauma on the human nervous system in
terms of a bioelectric arousal theory and describes how neurofeedback training
can elicit a relaxed state sufficient to restore a greater sense of well-being and

202  PTSD symptom reduction with neurofeedback

quality of life. It includes a discussion of how neurofeedback training impacts

symptoms presented by humans diagnosed with post-traumatic stress disorder
(PTSD). Two representative case studies are presented to illustrate the type of
outcomes veterans report using the Othmer method of neurofeedback.


Military men and woman are trained and expected to respond with lethal efficacy
when called upon to kill other humans, or be killed, without the civilian aspect of
criminal punishment for the killing. Most people are not natural killers of other
people; the killing has to be taught.1 With enough exposure to this kind of experi-
ence, most humans will be wounded, killed, or driven insane. The experience of
war changes human biochemical and neurological activity, disrupting cerebral,
biological, spiritual, interpersonal, and environmental functions.2 The warrior
ideal is a state of self-control that is focused and calm under adverse conditions.3
“Part of the grace of the nervous system is that it is constantly self-regulating.”4


The human autonomic nervous system has two parts: sympathetic and parasym-
pathetic. The sympathetic nervous system is only intended to function in times
of threat. When the emergency situation is done, the parasympathetic system is
supposed to restore a more natural state of functioning.5 Hans Selye coined the
term general adaptation syndrome (GAS).6 Selye proposed that humans “suffer
from chronic activation of the sympathetic nervous system,” with a three-phase
stress-induced systemic response.7
The first part of GAS is an alarm phase in which the body prepares for fight or
flight, activating the sympathetic nervous system, adrenals, and hypothalamus–
pituitary–adrenal (HPA) axis. A burst of energy for fight or flight occurs as stress
hormones are released consisting of adrenaline, noradrenalin, and cortisol. The
second part of GAS is a resistance phase with adaptation of the body to a resolved
stressful situation, or to stress without the nervous system returning to a healthy
idling speed. The body experiences diminished energy, as it is in need of rest and
recovery. If there is sufficient time for renewal, the body has a homeostatic ten-
dency to restore itself. Even when the stress hormones decrease, the human may
experience a time of reduced adaptive capacities while the human energetic sys-
tems rebuild their energy reserves. If the stressors are not reduced or eliminated,
the system may continue functioning in a state of hyper-arousal. With unre-
lenting stress and insufficient time to rest and restore the body, the third stage
is exhaustion. Symptoms of nervous system exhaustion include pain, asthma,
cold extremities, gastrointestinal trouble, depression, headaches, anxiety, cardio-
vascular problems, and inflammatory, autoimmune, and endocrine problems of
glucose tolerance, insulin resistance, and obesity.6,8
An organism’s response to threat is a threefold unified defense system: fight,
flee, or freeze. When fight or flight is thwarted, an organism instinctively moves
10.3  Human biology and the stress response  203

toward its last option: immobility. Trauma is a result of a “frozen residue of

energy that has not been resolved and discharged … trapped in the nervous
system.”9 Biologically, PTSD indicates that a fulcrum point that shifted to the
arousal needed for survival of a war fighter has failed to reset to its pre-stress
position. The old balance is gone, and a new balance is needed for life in a civilian
setting where the battle-setting dangers are no longer present.10,11
Biological development is a pragmatic process of dynamic change between
an individual’s inherited biology and environmental experiences.12 The kindling
model of development proposes that environmental stressors can influence a per-
son’s biological development. The kindling model of pathology proposes that an
initial event sets the stage for the next, with repeating occurrences resulting in pro-
gressive deterioration of adaptive functioning.13 Neurobiology examines adaptive
capacities that, in PTSD, appears to have a HPA pattern that is unique. Inactivation
of Broca’s area and over-activation of the amygdala also appears to be part of the
biology of trauma processing in PTSD development.12 One reason PTSD is intrac-
table to talk therapy is the unitary experience of PTSD memories found in the
limbic structures, making those memories unavailable for processing through the
neocortex. The under-activation of Broca’s area creates difficulty in articulation.
When the sympathetic nervous system is aroused, Broca’s area of the brain
stops functioning effectively.14 Broca’s area is the language center of the brain.
Psychotherapy usually asks a person to talk about their experiences in order
to gain access to the emotional load and work through thoughts and feelings.
With an impaired Broca’s area, talking about and telling a story are difficult.
Trauma stories tend to be non-linear, fragmented, and unprocessed. The declara-
tive or explicit memory is different from the implicit, unspoken memory.15 Self-
regulation is needed to restore parasympathetic nervous system activity and
re-engage Broca’s area.14
Structural magnetic resonance imaging used to examine PTSD indicates that
the hippocampus, frontal limbic system, anterior cingulate cortex, and amygdala
are involved. The amygdala in PTSD subjects is more active than in controls, and
there is less activity in the medial prefrontal cortex. Smaller hippocampal vol-
ume is common, but it is unknown if this is an attribute or precursor.16 Memory
acquisition is mediated by the hippocampus, a horseshoe-shaped aspect of the
limbic system connected to the hypothalamus, thalamus, amygdala, and brain
stem nuclei through groups of neural connections. Memories of trauma have so
much survival value that they are firmly and comprehensively encoded by the
hippocampus, becoming “frozen in time.”17 These memories appear to be stored
in the parietal, temporal, or central regions of the cortex.18 They are “even more
generally in peripheral physiology” (personal conversation with Siegfried Othmer
in 2009). Single-photon emission computerized tomography (SPECT), examining
brain activity in PTSD commonly reveals a diamond pattern of elevated activa-
tion in the anterior cingulate cortex, basal ganglia, and thalamus (Figure 10.1).
Humans have natural, healthy biological rhythms. Circadian rhythms are
indications of human behavior in synchrony with the light and dark influence
of our planet’s rotation in relation to the sun. “Ultradian means many times a
day … Ultradian rhythms are observed in our daily behavior and in the brain.”19
204  PTSD symptom reduction with neurofeedback

Figure 10.1  (See color insert.) Pre-post SPECT scan data are shown for a
veteran treated at the EEG Institute Clinic, comparing pre-training conditions
with those prevailing after 24 sessions. Classic signs associated with PTSD
include elevations in activity at the anterior cingulate, the basal ganglia, and
the thalamus. In post-training data, the activity level at the anterior cingulate
and basal ganglia are reduced. Additionally, the high activation of the cerebel‑
lum has been reduced. (Courtesy of Daniel Amen, MD, Orange County Amen
Clinic, Costa Mesa, CA.)

One ultradian rhythm is a basic cycle of rest and arousal activity that is evi-
dent in a normal human cortical arousal cycle of 90–120 minutes. This cycle
­corresponds with the challenges of metabolism in response to perceived envi-
ronmental demands. Neuronal integration facilitates effective human thinking
activities, feelings, perceptions, sensory motor capacities, and behaviors. Optimal
­functioning requires neuronal network coordination. Exposure to traumatic
10.4  Development of PTSD  205

stress and neurotoxins can impact the functions of neuronal assemblies through
dysregulation of n­ euronal networks. Disruptions in neuronal functioning can
cause serious impairment in cognitive performance, omission of needed activi-
ties, and commission of errors.20,21 This can have potentially disrupting effects
during a military mission and when carried back into civilian life.
The human brain is flooded with sensory cues about the environment and
prioritizes incoming data demands according to internal and external pressures
and resources. Biological, mental, emotional, spiritual, creative, social, and pro-
fessional processes of adaptation, assimilation, and accommodation occur in an
ongoing dialogue of engagement with, and disengagement from, the inner and
outer worlds. Healthy connections with the self and with the environment are
ongoing developmental activities of living. The homeodynamic nature of the
human nervous system shifts between a default mode of rest, in which it disen-
gages from external demands, and a central executive active mode of engaging in
the external world, a cycle modulated by a salience network. Salience refers to the
personal relevance of incoming sensory input and the order an individual places
on any need for action or response to the incoming information. In order to per-
form optimally over time, a brain needs rest and healthy oscillations between
activity and relaxation. Traumatized people tend to be hyper-vigilant, inflexible,
and cannot relax.22–26


PTSD may develop in those exposed to natural disasters, assault, rape, moles-
tation or child abuse, motor vehicle accidents, war, torture or genocide.27–30
Traumatic stress can be viewed as a continuum with differing break points for
different people.31,32 Unexpressed losses and the impact of grief can over-arouse
the autonomic nervous and endocrine systems.33 Trauma begins with an acute
phase through exposure to an event or series of events that create excessive
fatigue, autonomic arousal, and perhaps feelings of being overwhelmed, helpless,
and horrified. Acute trauma tends to resolve itself, while chronic trauma is more
complicated.29,34,35 War fighters may have a different, more complex PTSD due
to repeated or prolonged exposure to traumatic events, or having had to commit
violent acts that violate their personal values.30 Neuroses of war have three forms:
acute, transitional, and stabilized. It can take up to 6 months for a war neurosis
to move from an acute to a stabilized form; most occur in 2–3 weeks. The most
rapidly stabilizing are disturbed sensory motor activity.35
There are three causal perspectives on why some war fighters develop PTSD
and others do not. The dispositional model assumes a pre-existing personality
or history that leaves a person more vulnerable to the disorder than their peers.
The situational attributional model assumes that an event or series of events can
push someone to break down. The interactional model suggests that it takes both
an existing disposition and the event(s) to trigger PTSD.36 The entire body main-
tains explicit and state memories as a survival process known clinically as PTSD.
The key to resolving this survival mechanism is provoking the body and mind to
remember how it feels to be calm, and maintaining that visceral relaxation until
206  PTSD symptom reduction with neurofeedback

the body is able to sustain it. The sense of being safe in the world is influenced by
the arousal level of the limbic system.10,11
Trauma can cause a loss of interest in previously enjoyed activities and a nar-
rowing range of emotional responses.37,38 As Victor Frankl pointed out, survival
after severe stress often involves emotional death; one cannot care anymore.39
Traumatic stress reactions can act as an emotional contagion that can adversely
impact family members and caregivers.1,34,40,41 Family members are at risk for
secondary trauma due to decreased intimacy and life satisfaction, increased iso-
lation, loneliness, conflict, and marital distress.42
PTSD is a “soft trauma,”43 meaning that it is not a result of physical dam-
age to the head; it is an emotional damage that comes from bearing witness to
or knowing something that is traumatic or wounding. PTSD is a disorder that
begins with bioelectric encoding of trauma in the central nervous system (CNS).
Neuronal dysregulations can be intractable in talk therapy, as cognitive interven-
tions are not able to impact the nervous system in the same manner as neurofeed-
back.44 With veterans, there are often trust issues, as the hyper-arousal has been
a tool of protection. One reason why neurofeedback can be such an effective tool
is that it slips “under the radar” of the hyper-vigilance, helping modify the exces-
sive arousal issue without having to talk about it.23,45


The existing system of categories for diagnosing psychopathology uses a bio-
chemical and behavioral frame of reference that fails to effectively address the
issues and challenges of multiple diagnoses and comorbidity. Pharmaceutical
treatment tinkers with a variety of medications in the search for the right cock-
tail or chemical soup to help a veteran—and sometimes their family members—
adjust to post-war life. Pharmaceutical crutches may be what some veterans need
and want. Other veterans prefer to use their crutches until they are strong enough
to exercise, walk, run, and move with limberness in that peak performance ideal
of these military-trained athletes.
Using a bioelectrical network and behavioral frame of reference, the quirks
of multiple diagnoses are reframed as issues of physiological arousal, optimal
arousal, brain instability, timing, phase, localized dysregulation, disinhibition,
and learned fears/habits.46 The goal of neurofeedback training is stress reduc-
tion and relaxation. Instead of a pathological model of tinkering to modify the
biochemical soup within the human, neurofeedback is a non-invasive, behav-
ioral, peak performance model of training the brain to relax. As one veteran
said, “I didn’t know it was possible to be so awake, so alert, so relaxed all at the
same time.”47
Neurofeedback immediately targets the hyper-arousal criteria of PTSD that
prevent a person from sleeping deeply without drugs. Sleep is a naturally restor-
ative process of rest, rejuvenation, and healing. Each person has an innate, biolog-
ical wisdom and healing capacity. Neurofeedback appears to positively influence
an underlying common factor in the CNS that addresses a broad range of symp-
tom reduction, including the hyper-arousal criteria of PTSD, and comorbidities
10.5  History of neurofeedback in veteran care  207

such as traumatic brain injury (TBI), attention and learning disorders, emotional
reactivity, and addictions (see Chapters 1 and 4).
Between 1989 and 1991, researchers in the Veteran’s Administration (VA)
tested Alpha–Theta (A/T) brainwave neurotherapy after observing alpha
absence in the brainwaves of alcoholics. A/T was integrated into VA standard
care (SC) in experimental treatments for alcoholism, PTSD nightmares and
flashbacks, reducing the use of psychotropic pharmaceuticals, and to discover
its impact on established measures of personality. Their replicated findings
demonstrated that the veterans who received neurofeedback treatment inte-
grated into their VA SC decreased their medications more than those in con-
trol groups.48–51 Veterans in treatment for alcoholism who received brainwave
training had higher rates of abstinence and relapse prevention in 13 months
following treatment than SC controls.52 Use of the Millon Clinical Multiaxial
Inventory50 and Minnesota Multiphasic Personality Inventory51 revealed that
veterans who received brainwave training integrated into their existing SC had
greater reductions in their symptom severity on different personality scales
than controls.

10.5.1  A/T training

The A/T training done by Peniston and Kukolsky in their 1989 experiments
used an active lead on the occipital lobe (O1). (By contrast current A/T training
uses parietal placements at Pz for single channel or P3+P4 for two channel sum
­t raining.) Integrating neurofeedback training into VA SC resulted in a signifi-
cant reduction of nightmares, flashbacks, and psychotropic medications. The
SC veterans who received individual therapy, psychodynamic therapy, group
therapy, and rap groups did not have reductions in nightmares, flashbacks, or
psychotropic medications, and had minimal reductions in symptom severity
on personality scales. The results indicated that A/T neurofeedback was useful
in the “long-term prevention of PTSD relapse,”53 and superior to SC for combat
A/T training was found to be an effective intervention for cocaine abuse, buli-
mia nervosa, alcoholism, stress disorders, and Vietnam combat veterans with
chronic PTSD.50 Whether PTSD aggravates vulnerability to addiction or whether
existing neurophysiological vulnerabilities to addiction promote the develop-
ment and maintenance of PTSD is unclear. What is clear is that comorbidity cre-
ates complications in treatment. There are currently no effective pharmacological
treatments for methamphetamine or cocaine addiction. Cognitive behavior ther-
apy, eye-movement desensitization reprogramming, imagery rehearsal, and drug
therapies are considered to be effective treatments for PTSD. However, they are
costly in terms of time and professional resources. Neurofeedback is a type of
behavioral conditioning that has demonstrated efficacy in both addiction and
PTSD treatment. A/T training in particular appears to be able to open a window
into traumatic memories that allows them to be released and processed without
re-traumatization or the emotional abreaction common to cathartic release in
talk therapies.18,54
208  PTSD symptom reduction with neurofeedback

10.5.2  Behavioral conditioning

SC using behavioral treatments for combat stress injuries involves exposure-
based treatments or stress management. The operant conditioning of learning
theory uses stress inoculation, exposure, virtual reality, and systematic desensi-
tization. All of these require a strong motivation for an individual to be willing to
relive his or her experiences of trauma. Dredging up memories and re-vivifying
the emotions can be re-traumatizing.10 Emotional numbness and avoidance can
interfere with exposure therapy.38 Neurofeedback is a behavioral stress reduc-
tion/relaxation training technology that rapidly guides the human nervous sys-
tem to remember and restore a natural, healthful state of relaxed well-being. The
A/T aspect of neurofeedback training is unique in that it saves the client from
exposure to further emotional stress; a collateral benefit is the reduced risk of
secondary trauma for the clinician.

10.5.3  Neurofeedback training schedule

A 20-session neurofeedback training schedule appears to be effective with many
veterans; there are generally progressive, residual effects that unfold with time
following a series of training sessions. For those who live at a distance, have
ongoing training needs, and have completed a training series with a clinician,
home training systems are available.
In a matched group (n = 135) drug rehabilitation study, 40–50 neurofeedback
sessions were integrated into existing client services.55 Reports from standard
rehabilitation programs from across the nation indicate that 20%–30% absti-
nence is a common finding. By contrast the experimental group demonstrated
a 50% abstinence rate at 1 year post-neurofeedback training. In addition, at 45
days into the treatment, there were fewer dropouts from the experimental group
(6%) as compared to the control group (30%). Graap and Freides suggested that
a 30-session neurofeedback structure might be considered an effective interven-
tion if no other modalities are available or work faster.56 In some cases of neuro-
feedback, changes are noticed in the first session.13
The question about the length of time needed for effective treatment does not
appear to be raised when discussing how long a person will be taking medication
for a specific category of diagnosed disease or disorder. Some medications need
time for a rise in blood serum levels to be sufficient to create effective treatment
results. Neurofeedback is a behavioral, non-invasive learning strategy that tends
to improve retention in existing programs, reduce recidivism, and promote absti-
nence in PTSD/substance abuse comorbid veterans.

10.5.4  Post-traumatic life

If recovery is taken to mean a full restoration of what was lost, recovery may not
be possible with a PTSD-damaged nervous system. Post-traumatic health may
not mean a full restoration of what was normal prior to the traumatizing event(s)
10.5  History of neurofeedback in veteran care  209

because the human who has been through traumatic experiences may be forever
changed. A path of accommodation has been worn into the brain as a useful sur-
vival strategy. The best some individuals will achieve is rehabilitation, an adapta-
tion to something different or an accommodation that may require ongoing care.
This means that the individual has a need for more flexibility in cognitive and
behavioral responses to the world and their thoughts, feelings, and behaviors.28
Human self-regulation requires ongoing, intentional reflection intended to bring
awareness to one’s inner state.14 Neurofeedback is an effective tool for achieving
the gestalt of the self in context.
Some people who have been through trauma report finding that those trau-
matic experiences ground them down, while some report finding that those trau-
matic experiences revealed a healing crisis that polished them into a different
form of competence and creative expression. It is a creative human capacity to
transcend difficulties and achieve positive breakthroughs in personal growth
and development. Positive post-traumatic growth includes re-connection with
the civilian community, a restored sense of humor, and of self intra and inter-
personally. The peak performance and fitness benefits of neurofeedback training
often result in the re-emergence of interests in art, photography, playing music,
cultivating relationships, fishing trips, attending community events, going out
dancing, and dining with friends. The individual’s creative sense of well-being
elicits an improved quality of life and the resumption of personally meaningful

10.5.5  PTSD summary

It has been a quarter of a century since research in a VA setting found neurofeed-
back to be effective in reducing the adverse symptoms of PTSD and a common
comorbidity, alcoholism. Neurofeedback training yields systemic benefits that
exceed the expectations of simply reducing/eliminating target symptoms and
problematic issues of comorbidity. When veterans were freed from the exhaus-
tion of not getting enough sleep, which often occurred rapidly in the first few
sessions of neurofeedback training, the uptick in energy levels was often redi-
rected toward a resumption of interest in creative endeavors, social activities,
and intimate relations. The behavioral conditioning of neurofeedback allows the
human nervous system to reboot and reactivate parasympathetic functioning
and Broca’s area. Thus, after the hyper-arousal symptoms of PTSD are reduced
or eliminated, neurofeedback can restore the foundation for integrating more
effective talk therapy into existing services. Ongoing research by private clini-
cians replicate good findings in PTSD symptom reduction using neurofeedback
training, yet in 2014, as this chapter is being written, most veterans are unaware
that neurofeedback, a peak performance technology, is useful in reducing the
symptoms of the human suffering known as PTSD.
In a discussion with Cpt. Hammer of the U.S. Navy at the end of the 2011
Combat Operational Stress Conference in San Diego, California, he told me that
funding for research into the use of neurofeedback had been approved by him. Yet
it seems odd and counterproductive that the Navy would fail to make the results
210  PTSD symptom reduction with neurofeedback

public, given the pressing need for relief from PTSD suffering for our service
members and veterans. The ethics statement of the World Medical Association
holds doctors accountable to serving others: “The health of my patient shall be
my first consideration.”57 One could argue that withholding a method known
to reduce the PTSD-related suffering of veterans and failing to make taxpayer-
funded research findings available to other researchers does not meet the bench-
mark of open discourse in treatment evaluation, or in terms of patient health
being the first consideration.
Currently veterans with PTSD are all too often canalized into pharmaceuti-
cal strategies. The findings by private researchers and therapists of neurofeed-
back training for PTSD symptom reduction indicate a potential for reducing the
lifelong taxpayer costs of pharmaceutical treatment for PTSD-afflicted veterans.
At the same time these findings have produced reports from veterans of drug-
free improved sleep hygiene, mood, and family and social relations. The focus on
drug interventions for treating the symptoms of PTSD are counter to the inher-
ent military model of peak physical performance training, while neurofeedback
training fits the peak performance training model.
From my first hand experience of having seen the suffering of veterans and
active duty service members with PTSD, I know the importance of being fully
reintegrated into their families and social lives. My hope is that our military lead-
ers in the Pentagon and the VA will embrace this technology and move to initi-
ate a broad research approach examining the effects of neurofeedback on service
members’ health and well-being. Publication of findings of such trials, followed by
open peer review may be the only way to overcome the current resistance to the
demonstrated benefits of neurofeedback in the upper echelons of the VA and mili-
tary establishment. Neurofeedback could then be used to reduce or eliminate the
severity of symptoms for service members who are struggling to cope with PTSD.


10.6.1 The case of Rand: “The white noise
in my head is gone”
Rand* was a 52-year-old Irish-American male. His military background was in the
security police of U.S. Air Force (USAF) for 46 months. Rand reported to have no
VA benefits and that his PTSD was not military related. He said he separated from
the military early, with a general discharge, because “The USAF claimed I would
have a great way of life when I enlisted for 6 years. The reality was that their rules
treated the dogs better than the men. When the temperature reached a certain
point outside, the dogs got to go inside…” When a junior officer gave him orders
he felt he could not follow, Rand realized that he was never going to re-enlist, and
needed to bail early on his 6-year contract: “I refused to follow a wrong order, and
I refuse to work for someone who demonstrates so little regard for me.”

* Rand (2012–2014) insisted on being known by his own first name. He refused to let his
information be released under a pseudonym, and signed a release to that effect.
10.6  Case studies   211

I was recruiting veterans in 2009 for my doctoral research project when Rand’s
brother brought me to meet Rand in a bar.47 Rand was living off the grid, on the
street, with no identification, job, or cell phone. I asked Rand if he would partici-
pate in my study and he declined. As a member of the Homecoming for Veterans
organization,58 I offered Rand pro bono neurofeedback if he ever changed his mind
after my study was done. I maintained contact with him over the next few years in
a small military town, sometimes conversing with him informally. I learned that
he had lived through a tornado at 13 years of age that blew away his home and all
his personal effects, and that his stepfather was violent. He was managing over 40
employees in a restaurant when he received the call that his father was hospitalized
with emergency heart surgery and needed round-the-clock care. Rand walked off
the job and took care of his father for a year and a half. As his father got closer to
dying, his father moved in with a girlfriend, and Rand was on his way to living on
the street. He did not want to drive a car and contribute to pollution, so he moved
to a small island community where he could get around by walking or riding a
bike. His plan was to earn a living playing music.
Over time, I observed Rand repeatedly demonstrate an inability to form and sus-
tain close relationships. He had a lack of eye contact, repetitive body movements, lack
of insight into other people, lack of social or emotional reciprocity, social isolation,
emotional reactivity when routines were disrupted. He demonstrated enhanced pat-
tern recognition skills in music and environmental cues. His behaviors were indica-
tive of a high-functioning autistic disorder. His attempted communication patterns
with other people revolved around one perceived loss after another. Attempts at
simple conversation would devolve into an angry rant about some loss or some abuse
from the past through the immediate present. He had a long line of complaints of
mistreatment. We had a breakthrough in trust development when he asked if I would
help him get a copy of his birth certificate so that he could get an identification card
and a job. We went online and got him a copy of his birth certificate. At the same time,
another veteran he knew was completing a 20-­session neurofeedback PTSD proto-
col with me. Rand confronted me, “What did you do to that guy? … I know I’m all
fucked up. That doesn’t help when I’m living on the street and someone says I have a
problem. I know I have a problem. I need solutions. Talking about my problem is just
whining. I don’t need whining, I need solutions” (see Figure 10.2).
Rand’s original plan with me was to do the intensive schedule of 20 neurofeed-
back sessions in 2 weeks, two sessions a day, with the weekend off. My plan with
him was to collect symptom tracking data of 151 symptoms (Appendix A) every
five sessions, targeting the lead placement based on the most severe symptoms using
existing protocol guides.46,59 A/T training was planned for after ten sessions of sin-
gle-channel difference training. The first ten sessions are intended to strengthen and
stabilize the human nervous system before an emotional cleansing of A/T training.
Measure #1—September 11, 2012. The baseline measure of the 151 forced-
choice symptoms was used to steer the neurofeedback process and gathered
Rand’s self-report of 95 symptoms ranging from 1 to 10 in severity, with 0 mean-
ing no problem and 10 meaning a big problem.
Rand found that he could not stay awake after a neurofeedback training ses-
sion: he had to immediately lay down, had no problem falling asleep, and slept
212  PTSD symptom reduction with neurofeedback


September 11, 2012
September 21, 2012
October 4, 2012
10 December 6, 2012
March 8, 2013
5 July 26, 2013
November 8, 2013
0 March 24, 2014
April 16, 2014















Figure 10.2  Summary of Rand’s self-reported symptom tracking: September

2012–April 2014. y axis = number of symptoms reported; x axis = 8 categories
of symptom tracking summaries, earliest measure on the left. #1, September
11, 2012, 95 symptoms. #2, September 21, 2012, 36 symptoms. #3, October 4,
2012, 24 symptoms. #4, December 6, 2012, 37 symptoms. #5, March 8, 2013,
41 symptoms. #6, July 26, 2013, 24 symptoms. #7, November 8, 2013, 15 symp‑
toms. #8, March 24, 2014, 64 symptoms. #9, April 16, 2014, 38 symptoms.

for several hours before waking naturally. He informed me that he could not do
that twice a day, he had other things to do in his life. The first five sessions were
completed in 10 days.
Measure #2—September 21, 2012, 36 symptoms (95 → 36 = −62%) ranging
from 1 to 10 in severity. A falling away of 59 symptoms in 10 days was observed.
The next five sessions were completed in 2 weeks for a total of ten sessions in
3.5 weeks. Rand requested A/T training on the seventh session, insisting he was
ready for it. His response at the end of A/T was that he felt “quietly confident.”
Over 3.5 weeks, just prior to his tenth session, symptom tracking revealed that
three-quarters of Rand’s baseline symptoms had fallen away.
Measure #3—October 4, 2012, 24 symptoms (95 → 24 = −75%) ranging from 1
to 4 in severity. Another 12 symptoms fell away and there was a decrease in reported
symptom severity. “It was so subtle in the beginning. Now I’m no longer so preoc-
cupied with bad memories from 20 years ago. It reminds me of Carly Simon’s song,
‘I Haven’t Got Time for the Pain.’ The white noise in my head is gone.”
Of the remaining symptoms, all showed reduced reported severity. At this
point in the training schedule, Rand described his life as “just peachy … I’m busy.”
He had a job, was enjoying life, and showed no inclination to complete the 20 sessions
we had planned. This was concerning to me as the stability of neurofeedback train-
ing in sustaining a relaxed sense of well-being is reportedly is best with a minimum
of 20 sessions. After 2 months without neurofeedback, Rand offered measure #4.
Measure #4—December 6, 2012, 37 symptoms (95 → 37 = −61%) ranging
from 1 to 4 in severity. An increase of 13 symptoms in 2 months was observed.
10.6  Case studies   213

Rand did three neurofeedback sessions in 2 weeks of December, and did not
show up again until March 8, 2013, when he provided data for measure #5.
Measure #5—March 8, 2013, 41 symptoms (95 → 41 = −51%) ranging from
1 to 5 in severity. An increase of 4 symptoms from measure #4 was observed, as
well as an increase in symptom severity.
On July 26, after approximately 3.5 months without additional neurofeedback
training, he provided measure #6: “What’s going on in my life? Things are going
my way. Making money.”
Measure #6—July 26, 2013, 24 symptoms (95 → 24 = −75%) ranging from 1 to
2 in severity. A decrease of 17 symptoms from measure #5 was observed, as well
as a decrease in symptom severity.
Rand’s life and attitudes were positive until one night when he walked home
from the bar to pick up his Scrabble board and rode his bike back to the bar instead
of walking back. He came out after playing Scrabble to discover someone had sto-
len his bike. That meant he had to walk to and from work during the time before he
had enough funds to buy a new bike, a total of 43 miles. Some of the behaviors that
had gone away with neurofeedback training—rocking and angry stories—came
back after losing his bike to theft. The difference was that he was no longer twisting
his hands together and avoiding eye contact as he rocked on his feet—he was now
stabbing his index finger toward people and making eye contact as he told angry
stories. His jaw grinding did not resume; instead, his jaw remained relaxed. After
Rand bought a new bike, his rocking behavior did not lessen, nor did his angry
stories and finger stabbing. We discussed whether it might be helpful to do another
round of neurofeedback training, but he was not inclined to at that time.
Two months later, Rand was accosted while leaving a bar. A man attempted to
grab his new bike, insisting it was his own bike. The assailant called the police,
and Rand waited quietly for the officers to arrive. When the police came around
the corner, the assailant escalated the assault on Rand. Rand called me at around
11 p.m. that night, rousing me from a deep sleep, saying, “I think I am about to be
arrested.” He gave me a brief summary of what was occurring.

Myself: What do you want me to do, come down and bail you out?
Rand: No. If you don’t see me tomorrow, I want someone to know
where I am. I’m going to speak with the police now.

Rand came by the next day. The local police who witnessed the assault escalate
checked Rand’s bike serial number with the serial number on the assailant’s bike
purchase receipt, which did not match. Responsibility for the incident was rightly
placed on the man being loaded into the ambulance and Rand was released with
his bike. Rand was pleased that it was only a hospitalization run, rather than a trip
to the morgue.

Neurofeedback training gave me the clarity of thought to put down

my bike lock before counter-punching, otherwise I would have
killed him with the lock in my right hand. Instead, I had enough
time and forethought to avoid killing the man. My left arm blocked
214  PTSD symptom reduction with neurofeedback

the man’s assault, I simultaneously dropped the lock in my right

hand before laying him out on the ground.

A week later, Rand was wearing a wrist wrap. He said it took several days to
realize his left wrist was broken. He had to think back to how he had broken it:
“My attention was with the right hand counter-punch so that I didn’t notice the
left arm swing block connect with my own handle bar.”
In October of 2013, Rand lost his job due to the restaurant closing for renova-
tions. He asked me when there would be time in my schedule to resume neuro-
feedback training: “My brain is going foggy. Now that I know how much better
I can feel, I need a tune up.” My schedule for pro bono work was full until March,
2014. Rand had not received neurofeedback sessions for 7 months when he pro-
vided measure #7.
Measure #7—November 8, 2013, 15 symptoms (95 → 15 = −84%), ranging
from 1 to 4 in severity. A decrease of nine symptoms was observed, as well as
an increase in symptom severity from measure #6: “My brain has gotten fuzzy
again. The PTSD is gone, thank you very much. Now that those severely disrup-
tive symptoms have receded, like the rage, sleep problems, nightmares, flash-
backs, hypervigilance, depression, anxiety, I can notice the little things, things
that weren’t so severe compared to the PTSD symptoms. I know that these are
just nitpicking little things.”
In December, Rand contracted a severe, lingering upper respiratory infec-
tion and was ill for an extended period of time. He provided measure #8 prior
to resuming neurofeedback training in March, 2014, after 11 months without
neurofeedback training. He reported that he has felt different since contracting
the respiratory infection: he was not as strong, experienced less stamina, and
fatigued more easily. He was most interested in improving his musical compre-
hension and composition capacity.
Measure #8—March 24, 2014, 64 symptoms (95 → 64 = −33%), ranging from
1 to 4 in severity. An increase of 49 symptoms from measure #7 was observed.
Rand completed seven sessions in 3 weeks and provided measure #9.
Measure #9—April 16, 2014, 38 symptoms (95 → 38 = −60%) ranging from 1
to 3 in severity. A falling away of 26 symptoms was observed, as well as a decrease
of reported symptom severity.
Rand also read about Asperger’s syndrome and reported back:

I know that you have been talking to me about Asperger’s for some
time, so I finally looked it up and found myself reading about myself
and all my little quirks. I have a lot of little quirks. I didn’t know there
were other people like me dealing with what I have to deal with every
day. I do have a hard time making and keeping friends. I don’t inter‑
view well, I get jobs because I know someone who knows my skills …
I didn’t believe that anything could change my PTSD, I’m still amazed
that those problems are gone. I don’t know if it is possible to change
a personality disorder (sic) through neurofeedback, but I’m back to
find out.
10.6  Case studies   215

10.6.2  Case summary: Rand

Rand’s self-report of symptoms reflects the typical response of veterans to neuro-
feedback training in the rapid reduction or elimination of post-traumatic stress
symptoms and reconnection in the community. This case is representative of
PTSD behavior with avoidance, isolation, and intrusive thoughts. Being vulner-
able in a military setting can mean death, but in an endearing civilian setting, it
can mean intimacy and being cared for and loved. When a veteran rejects help
for their obvious distress due to not wanting to appear weak or vulnerable, that
person is stuck in feelings of isolation and of having to do it all alone. These
veterans reject offers for help, avoiding their problems and isolating themselves.
Veterans may intend to follow through on a schedule, but not show up because of
the avoidance aspect of PTSD. Intrusive thoughts interfere with being fully pres-
ent, disrupting healthy interactions with others and the obtaining of a relaxed
sense of well-being in oneself. Gaining the trust of a veteran with PTSD can be
slow and intermittent. Rand became interested in neurofeedback only after he
observed rapid, positive changes in another veteran.
The challenges of comorbidity appear in Rand’s case with an interactional
model of PTSD development: childhood trauma (tornado destroying his home
and a violent stepfather) and military activities (poor treatment from his own
team and erroneous orders from a junior officer) taking him to a breaking point
where he could not complete his military contract. He then put aside his own self-
support to become his father’s caregiver for a year and a half until shortly before
his father’s death. With previously undiagnosed Asperger’s syndrome and exces-
sive alcohol consumption, Rand’s life experiences and biological heritage com-
bined to create difficulties in maintaining a sense that the world is a safe place in
which he will be cared for or in which he can enjoy a relaxed sense of safety and
well-being. Rand’s flashbacks were not primarily military related; they stemmed
from the tornado, the violent stepfather, and repeating patterns of betrayal by
people he needed to be able to trust, including but not limited to the junior offi-
cer in the military. The undiagnosed Asperger’s syndrome likely were a part of
Rand’s problem in coping with military life. All humans have a breaking point.
Rand’s nervous system reached a breaking point while he was in the military, but
he has no VA benefits to address his disabilities.
Prior to neurofeedback training, Rand’s intrusive negative thoughts of
unpleasant past experiences were interfering with his ability to form and sustain
healthy interactions with himself and other people in the present. The intrusive
thoughts were of the many instances of his life history that had not turned out
well. Unwanted distressing thoughts automatically began looping around to
unpleasant memories with the slightest provocation. His energy and time were
consumed with unwanted, repetitive thoughts about very unpleasant past expe-
riences. He was unable to be fully present while obsessively ruminating on how
things could have turned out differently and what he could have done differ-
ently. Rand’s rapid positive response to neurofeedback demonstrates the speed
with which a human brain can respond to the challenge of relaxing using neu-
rofeedback, creating improvements in the overall quality of life. Rand’s case also
216  PTSD symptom reduction with neurofeedback

demonstrates how the sensitivity of some human nervous systems may benefit
from ongoing brain training to sustain optimal functioning as evident in expe-
riencing mental clarity, pleasant wakefulness/alertness, physical relaxation, and
feeling ready to tackle anything.
The changes in Rand were not limited to the reduction in the number and
severity of the symptoms we tracked. Human performance improves when the
individual is able to restore the self through the natural processes of rest. As Rand
learned to rest and relax, he unfolded from a tightly wound, loud, insensitive musi-
cian stepping on other musicians’ time at open mic sessions to hosting an open
mic session every other week, creating a sacred space for musicians to play and
jam together. As Rand’s symptoms of PTSD were reduced sufficiently, he was able
to turn his attention to other little “quirks” of behavior that had been problematic
for years, but were not as severe as the issue of PTSD. Even with the comorbidity
of Rand’s situation, 20 neurofeedback sessions were sufficient for achieving some
sustained results over time in terms of reducing the number and severity of his
symptoms. He has agreed to participate in another 20 sessions of neurofeedback
training. We will be using the cutting-edge high-definition (HD) version of the
software and latest release of Neuroamp II, for targeting his remaining symptoms.
There are anomalies in Rand’s case: (1) his drinking did not stop, although he
reported that his alcohol tolerance had decreased and his consumption was down
by two thirds; and (2) his reward frequency was not consistently stable, being
transient instead. Rand asked:

How come this technology is not available in the library so that

people like me can get a tune up when I need it?

10.6.3 The case of Jackie O.: An outcome report

of a combat medic
Jackie O.,* a female in her early fifties, had two decades of combined active duty
and reserves as an Army Special Ops medic. She had 100% disability: 70% PTSD,
30% combined minor traumatic brain injury (mTBI, aka concussion), and surgi-
cal reconstruction of her knee and foot, a corpse heel, corpse navicular and part
of her own calf for the instep. A unique aspect of Jackie O.’s data is the pre/post-
symptom tracking of VA SC for PTSD prior to starting the neurofeedback train-
ing. When she returned to initiate a neurofeedback PTSD protocol, she said, “I’ve
been attending PTSD groups for almost a year …The average ­veteran with PTSD
is on ten meds…” When Jackie O. left Ft. Bragg, she was on 18 medications. She
was down to ten medications with VA SC. These veterans are actively seeking to
comply with VA SC for improved health and quality of life.
The method of neurofeedback training used was a replication of existing neuro-
feedback protocol guides.46,59 We gathered a pre/post-QIK test.60 Jackie O. agreed to
use the established symptom tracking report (see Appendix) and to pay attention

* The pseudonym, Jackie O. (2012–2014), was selected by the client for publication of her
clinical outcomes, and she signed a release to that effect.
10.6  Case studies   217

to and describe any perceived efficacy or detrimental effects, any progressive or

regressive impacts, and any surprise outcomes or unintended consequences.
The initial, intention in our clinical research together was to track symptoms
every five sessions, ideally once a week for the first month post-training, then once
a month for the next year, then quarterly for another year. In this fashion, if there
were any issues of relapse, Jackie O. would be aware that booster sessions were
needed promptly. Unfortunately Jackie O. clashed with me over my desire to col-
lect data. She had a strong aversion to repeatedly answering the same questions
over time. She was not the first combat veteran to tell me how odious the Likert-
like scales for 151 forced-choice symptoms was. “Worst part of this whole process,”
she wrote after putting it in the “other” category of symptoms, with a 10 in severity
during the #7 iteration of symptom tracking. Another combat veteran had snarled
at me, “How many times are you going to have me answer those same questions?!
… What?! No way. I already answered them once. I don’t want to answer them
again … I like my opiates, thanks. Bye.” Veterans who drop out tend to do so
between the sixth and the tenth sessions.
In order to guide the neurofeedback lead placement and monitor the efficacy
of the training, I want to obtain a Likert-like scale from 0 (no problem) to 10 (the
worst) of 151 forced-choice symptoms, as well as anything else that the individual
finds bothersome that is not on the list, every five sessions. Veterans , on the other
hand, would rather track only a few symptoms—the ones most bothersome to that
individual—and often will not bother to report pain if not directly asked about it.
I want to obtain as broad a sweep of data as is possible for a peek into that individ-
ual’s self-perceived nervous system performance capacities at that time. I use the
data to create bar charts allowing a quick visual assessment of symptom reporting,
and select lead placement sites using the 10–20 International System (see Figure
10.3) to target the symptoms with the highest reported severity, starting with the
sleep symptoms. I then look at the attention and learning symptoms, and so on,
in the forced-choice symptom tracking categories. When looking at a case with a
high number of reported symptoms, I tally the sites from all eight categories (sleep,
attention and learning, sensory, emotional, behavioral, physical, pain, and other)
and use the lead placement sites with the highest numbers of symptoms reported. It
is not uncommon for the symptoms of greatest interest to the individual to show a
slower response to training than other symptoms. Yet it is the early falling away of
or increase in symptoms seemingly unrelated to the target symptoms that are the
most useful indicators of how successful we are in our training strategies.
In deference to Jackie O.’s aversion to my data collection, we waited until
Jackie O. felt that she could tolerate another iteration of the same questions (see
Figure 10.4).
There were two pre-neurofeedback measures:
#1—August 13, 2012, was the baseline measure, with 62 symptoms prior to 11
months of VA SC for PTSD (ranging from 1 to 9 in severity).
The second measure was taken after 11 months of compliance with existing
VA SC, before starting neurofeedback training.
#2—July 5, 2013, 113 symptoms, with an increase of 51 symptoms from mea-
sure #1 being observed (ranging from 1 to 10 in severity).
218  PTSD symptom reduction with neurofeedback


Fp Fp
1 2

F7 F8
F3 FZ F4

Left T3 C3 CZ C4 T4 Right
side side
A1 A2
P3 PZ P4
T5 T6

O1 O2


Figure 10.3  International 10-20 System: The neurofeedback community has a

standardized model for placing electrodes on the scalp. This provides uniform
reference points in research and training.



August 13, 2012

15 July 5, 2013
July 10, 2013
10 July 14, 2013
July 22, 2013
5 August 8, 2013
November 29, 2013
0 April 5, 2014















Figure 10.4  Summary of Jackie O.’s self-reported symptom tracking: August

2012–April 2014. y axis = number of symptoms reported; x axis = 8 catego‑
ries of symptom tracking summaries, earliest measure on the left. #1, August
13, 2012, 62 symptoms. #2, July 5, 2013, 113 symptoms. #3, July 10, 2013, 41
symptoms. #4, July 14, 2013, 28 symptoms. #5, July 22, 2013, 40 symptoms.
#6, August 8, 2013, 18 symptoms. #7, November 29, 2013, 80 symptoms. #8,
April 5, 2014, 65 symptoms.
10.6  Case studies   219

Jackie O. received three-lead, one-channel difference training with infra-low-

frequency (ILF) rewards for the first ten sessions. She optimized at 0.45 mHz on
the right and 0.9 mHz on the left, meeting the standard math used in determin-
ing neurofeedback training in the ILF range. She had a relatively stable state of
training, with a little fluctuation around her optimal reward frequency over the
course of 20 sessions. She was eager to proceed with an intensive schedule of 2
weeks, twice a day with the weekend off. Initially, she could do no more than
one session a day, and expressed an immediate need to sleep after the first few
neurofeedback training sessions. Within the first five sessions, she was reporting
falling asleep as soon as her head hit the pillow with no medications. This was not
something we planned or discussed in advance; it happened spontaneously. She
slept deeply and woke rested. She then noticed that she did not need to take all of
her medications every day to stay calm.
When Jackie O. stopped taking her medications, this was outside of my domain
of knowledge. As a trained Department of Defense (DoD) medic, Jackie O. is
uniquely qualified to assess the impact of pharmaceutical interventions on her own
mental, physical, and emotional well-being. I have a medical field supervisor for case
management of cross-domain issues.* I asked him to evaluate this aspect of Jackie
O.’s rehabilitative strategy. They met, he reviewed the findings, was pleased with her
progress and surprised by the difference in effectiveness between neurofeedback
training and VA SC. He told Jackie O. that since she lived hours away from me by car,
if the clinical outcomes indicated a need for further sessions, he would write her a
prescription for a neurofeedback home training system to continue with her rehabil-
itative progress. His terms were that I was responsible for directing her in the practi-
cal application of a home training plan to specifically target her symptoms, so that
he could stay in the loop as to her progress. He supported her decisions to reduce or
eliminate her medications based on her own medically educated observations.
After Jackie O. had built up sufficient stamina for a more intensive training
schedule, there were days when she was willing to train for three sessions, with
an hour off in between, seeking to complete the training in the 2 weeks she had
originally planned to be in town. The first in-training measure was July 10, after
eight neurofeedback sessions.
#3—July 10, 2013, 41 symptoms (from 1 to 8 in severity); 20 fewer symptoms
were observed from measure #1, and 71 fewer symptoms observed from measure #2.
We took 2 days off after ten sessions, before three A/T (at Pz) sessions (sessions
11–13). The preset 7 and 10 Hz of the existing software did not get much A/T
cross-over until we lowered the theta reward, and then we got the A/T cross-over.
There was a cross-over of delta/theta amplitude trend lines that dominated one of
the A/T sessions, in contrast to the expected A/T cross-over. Symptom tracking
was gathered July 14, after the 14th neurofeedback session.
#4—July 14, 2013, 28 symptoms (from 2 to 8 in severity), 13 fewer symptoms were
observed from measure #3, and 34 fewer symptoms were observed from measure #1.
After A/T training with veterans reporting residual or emergent depression,
I  may raise the reward from ILF training to a higher frequency, often 14 Hz.

* McKnight RE. Allied Health Associates, Key West, FL.

220  PTSD symptom reduction with neurofeedback

Jackie O. reported no residual/emergent depression after the A/T training, so she

completed the remaining sessions receiving three-lead, single-channel difference
training with her optimized ILF reward.
We gathered two in-training symptom tracking data sets, instead of four as
originally planned. Normally, a data set is obtained immediately following the
20th session; Jackie O. was reluctant to sit through another iteration of symptom
tracking after completing her post-QIK test. I had a travel schedule and could
not wait for her to be ready. The first post-training symptom tracking data were
gathered 6 days later, on July 22, before her re-entry into VA SC.
#5—July 22, 2013, 40 symptoms (from 1 to 5 in severity), 12 more symptoms were
observed from measure #4, and 22 fewer symptoms were observed from measure #1.
Of the symptoms reported in measure #1, all had reduced severity, so it was
surprising to see the report of 16 new symptoms. Did this mean that neurofeed-
back training elicited new symptoms/adverse responses? Neurofeedback has few
adverse side effects.61 Jackie O. said that as she was more comfortable with and
aware of herself, the symptoms may have been present before, but were not as
severe as the other symptoms so they may not have been noticeable. “All side
effects seem to be related to stress at some point in life, and they may be indi-
cators of residual thoughts, feelings, emotions, physiological sensations, and/or
behaviors that have been repressed as a defense mechanism when the individual
did not have the resources to deal with an event when it occurred.”62
After Jackie O. completed the 20-session PTSD protocol, she agreed to stay in
touch for post-training data collection and to pay attention to any reoccurrence of
symptoms, new symptoms, odd phenomena, unexpected emergent events, indica-
tors of distress, and pleasant surprises. An uptick in her symptoms in the first week
following an intensive training schedule is not uncommon; there is often a report of
a rise in symptoms in the first week following an intensive training schedule. This
is commonly followed by reports of residual, progressive benefits in which remain-
ing symptoms continue to melt away without additional neurofeedback training. A
slower pace of training twice a week over 10 weeks provides a more gradual decon-
struction of hyper-arousal and a reconstruction of a relaxed state.
Research into the impact of neurofeedback training with mTBI reports that
from 47–75 sessions are helpful with some mTBI patients.63 With Jackie O.,
20 sessions may have been insufficient to address the diagnosed mTBI. Jackie O.
provided symptom tracking data over the phone on August 8, at 3 weeks post-
training, after re-integrating into VA SC.
#6—August 8, 2013, 18 symptoms (from 1 to 2 in severity); 22 fewer symptoms
were observed from measure #5, and 44 fewer symptoms were observed from
measure #1.
Jackie O.’s integration of neurofeedback training into her rehabilitation strategy
with the VA indicates that it works effectively with VA SC, showing good results in
symptom and severity reduction. My concern was an uptick in sleep symptoms for
Jackie O. following an external anxiety-provoking trigger. She was driving on the
highway and noticed the smell of smoke, visually located a plume of dark smoke
and experienced a flashback to the dangers of driving in a war zone. She was able
to calm herself by recognizing that the smoke plume was in a civilian setting and at
10.6  Case studies   221

sufficient distance to be of no immediate threat to her. That night, she had her first
nightmare since neurofeedback training. This indicated for me that her nervous
system was not yet able to easily self-regulate into or sustain a relaxed state auto-
matically. My medical field supervisor* reviewed the findings during our August
16, 2013, meeting, and as promised, issued a prescription for a neurofeedback home
training system and introductory technical training to support Jackie O.’s self-
directed, post-traumatic, rehabilitative growth. On November 29, 4.5 months post-
training with only VA SC, Jackie O. provided symptom tracking data by phone.
#7—November 29, 2013, 80 symptoms (from 1 to 10 in severity), an increase of
62 symptoms was observed from measure #6, as well as an 18-symptom increase
over measure #1. The only rating of 10 in severity was for answering the symptom
tracking list; the others ranged from 1 to 8.
Jackie O. reported that the VA was non-responsive to a civilian doctor’s pre-
scription for a neurofeedback home training system; no one in the VA was will-
ing to discuss the use of or showed interested in the gains neurofeedback had
elicited in her ongoing rehabilitative goals. While attending a 2013 Veterans’ Day
event, Jackie O. heard a helicopter in the distance and automatically jumped out
of her seat to get her medic bag. Re-embedded in VA SC without neurofeedback
booster sessions, she had experienced olfactory- and auditory-triggered flash-
backs, as well as an increase in adverse symptoms and symptom severity.
In measure #7, the behavioral symptoms showed the worst increases in
reported severity from measure #6. Hyperactivity had increased (severity: 1 → 8),
as well as hyper-vigilance (1 → 6). There was a re-emergence of rage, exagger-
ated startle, oppositional defiance (0 → 2), poor social or emotional reciprocity
and poor speech articulation (0 → 4), aggressive behavior (0 → 5), and a lack of
social interest (0 → 6). Excessive talking (severity: 5) emerged as a new symp-
tom. The other categories showed an overall reduction in symptom severity. Sleep
symptoms ranged in severity from 1 to 3, while the initial measure had been
1–9. Attention and learning symptoms ranged in severity from 1 to 2, while the
initial measure had been 5–7. Sensory symptoms ranged in severity from 1 to 3,
while the initial measure had been 7–8. Emotional symptoms ranged in severity
from 1 to 3, while the initial measure had been 6–9. Physical symptoms ranged
in severity from 1 to 5, while the initial measure had been 5–8. Pain symptoms
ranged in severity from 1 to 4, while the initial measure had been 7–9. The uptick
in symptoms along with her self-report of sobriety indicated to me that Jackie O’s
nervous system was not able to sustain a relaxed state or adequately self-soothe;
without booster sessions of neurofeedback, her nervous system was slipping back
into maladaptive behavior. During a field visit to collect data on April 5, 2014,
Jackie O. revealed that she had relapsed into self-medicating with alcohol. The
number of symptoms had gone down and their severity decreased.
#8—April 5, 2014, 65 symptoms (1–5 severity), showing a 15-symptom decrease
from measure #7, and three more symptoms were observed from measure #1.
Surprise findings reported by Jackie O. included: (1) nightmares were gone
during the time of neurofeedback training and for almost 1 month post-training;

* McKnight RE. Allied Health Associates, Key West, FL.

222  PTSD symptom reduction with neurofeedback

(2) a reduction in pain; (3) her family interactions were less tense; (4) she was
able to socialize and go fishing with friends; and (5) the VA was not interested in
helping her obtain a medical device that she had found helpful for rehabilitation
in reducing the adverse effects of being a combat veteran. Unsurprisingly, due to
Jackie O.’s aversive response to my repeated requests for in-training data collec-
tion, instead of obtaining the nine planned post-training data sets over 1 year, we
gathered only four data sets (July 2013–2014).

10.6.4  Case summary: Jackie O.

The speed of clinical outcomes in Jackie O.’s neurofeedback training is represen-
tative of other veterans and of reports by other researchers using neurofeedback.
When she left Ft. Bragg on 18 medications, VA SC was able to taper her down to
ten medications. With neurofeedback, Jackie O. stated: “I don’t need any meds.”
She was no longer using Ambien and Trazodone to fall asleep and stay asleep. Five
neurofeedback training sessions were sufficient to eliminate Jackie O.’s problems
falling asleep; she now wakes refreshed, and that symptom has not rebounded. In
addition to improved sleep hygiene, there were improvements in her learning and
attention capacities, social skills, physical/behavioral/emotional self-regulation,
pain management strategies, and peacetime driving habits. She no longer loses
her temper over small things with her family, which has created a more relaxed
family life. She is overtly more social and less isolating.
Jackie O. received ILF training throughout the training process, other than
the A/T portion (sessions 11–13). The generalized reduction in symptom severity
over time post-training reflects a residual, progressive effect of neurofeedback
on the adaptive, assimilating, and accommodating aspects of the CNS. Without
access to neurofeedback, at 8 months after re-integration into VA SC, there was
an increase in the number of reported symptoms. The rise in symptom severity
with external triggers and relapse into self-medicating with alcohol indicates that
Jackie O. is not self-regulating as effectively as she is able. Weekly preventive ses-
sions, or as needed, following a 20-session neurofeedback protocol can be antici-
pated to restore, sustain, and maybe even further improve Jackie O.’s ability to
self-regulate into a relaxed state, improving her overall quality of life.

10.6.5  Case presentation summary

Both cases presented in this chapter are representative of the speed with which
neurofeedback reduces the symptoms known as PTSD. Comorbidity creates
challenges that may require ongoing care to sustain or even improve the relief for
our suffering veterans. A home training system, like other medical devices, could
be provided through the VA system of veteran care. This approach to war after-
care could allow technology-savvy veterans to gain a sense of empowerment in
being able to sleep without medications. It is effective in targeting reactive ner-
vous system activity when an external trigger stirs something up that is suffi-
cient to elicit a rise in adverse symptoms. Such booster sessions are anticipated to
restore a more relaxed state.
10.7 Questions 223

I was surprised at both cases having ongoing alcohol issues, as most veterans
I have worked with report that their alcohol and tobacco tolerances decrease with
neurofeedback training. The research done with A/T training in a VA setting
included 15 sessions of autogenic training prior to 15 sessions of neurotherapy.
Neither case in this chapter received 30 sessions of training, nor a specific proto-
col targeting alcoholism; we were targeting PTSD symptom reduction with ILF
Both Rand and Jackie O. reported surprise in identifying new symptoms with
smaller severity toward the end of their training concerning issues that they had not
paid much attention to prior to neurofeedback. The severity with which a human
nervous system is disrupted with PTSD can mask other issues, pushing smaller-
severity symptoms into the background of awareness. The repetitive questions of
symptom tracking tend to create an increase in self-observation and awareness,
bringing issues from the background to the foreground, which can be difficult for a
person experiencing emotional numbness and ­avoidance. The ­ongoing processes of
neurofeedback training reawakens/restores an ­intrapersonal capacity for relation
with self, and an interpersonal capacity for relation with others.
Without booster sessions, there were increases in the number of adverse symp-
toms and rises in the levels of severity for both Rand and Jackie O. With the mTBI
portion of Jackie O.’s diagnosis and the Asperger’s syndrome aspect of Rand’s
development, 20 neurofeedback sessions were a good start for sustaining results
in symptom reduction or elimination. These findings were achieved with the pre-
HD iteration of Cygnet software, computers, and Neuroamp of 2008 vintage. The
next iteration of neurofeedback training with Rand and Jackie O. will use the lat-
est HD software and the breakthrough Neuroamp II, which was released in 2013.

Can a resumption of neurofeedback training in the form of booster sessions or
a home training system reduce or eliminate symptom relapse/slippage? Can it
modify a neurodevelopmental disorder so that those little quirks fall away or
transmute into some marvelous creative outlet? The lack of resolution of some
of the symptoms and the rebound of other symptoms, such as drinking for both
cases, indicates the possibility that:

1. Some symptoms need more than 20 sessions for a reduction in severity or

2. Additional A/T training is indicated to address the alcohol issue.
3. The optimal reward may not have been adequately identified.
4. There may be other issues such as the biomedical and environmental factors
discussed in Chapters 5, 6, 7 which may need to be addressed by Integrative
Medicine specialists.

When a veteran separates from the military without receiving care for a break
in functional capacity during military service, the cost of recovery or rehabilita-
tion is shifted to the individual, family, friends, and civilian community, who
224  PTSD symptom reduction with neurofeedback

may lack the professional skills that the veteran needs. How many veterans or
reservists have separated from the military with no VA benefits, even though
they broke while in military service? How many people living on the street are
veterans without benefits? How many veterans would prefer to be off many of the
pills they are provided with through VA SC to cope with the symptoms of PTSD?

When a problem ceases to be a problem, the individual often remembers to forget
that it was ever a problem; it is gone, so they do not have to think about it or lose
sleep over it. Regular symptom tracking allows for a more precise targeting of
lead placement sites, reward frequencies, and the creation of trend lines or bar
charts to view the individual’s progressive response to neurofeedback training.
By using 151 symptoms to track the individual’s progress and seeing symptoms
that were seemingly irrelevant to the client’s concerns decrease in severity and
fall away, we obtain indications of our progress in restoring a more relaxed state,
even when the individual’s preferred target symptoms are still problematic. It
has been my experience that a broad sweep of symptom tracking is needed to
accurately steer the process for each unique individual and to track our progress.
The human brain and CNS are constantly self-regulating, using what works
and putting aside what does not work. Like timing a motorcycle or tuning an
instrument for smooth performance, neurofeedback helps the brain in timing
itself and tuning it up for peak performance. Neurofeedback promotes stress
reduction through timing nervous system activities to restore the body’s ability
to remember, restore, and sustain a relaxed state. A self-regulating, non-anxious
presence yields better-sustained performance over time.14,44,64 “Between stimulus
and response there is a space. In that space is our power to choose our response.
In our response lies our growth and freedom.”65
A 20-session neurofeedback training strategy intended to teach the nervous sys-
tem to sustain more habitual parasympathetic functioning was effective in restoring
a more relaxed state with the veterans who agreed to have their clinical outcomes
presented in this chapter. This is evident in the elimination of some symptoms and
the reduced severities of the remaining symptoms. Both veterans demonstrated the
speed of response to neurofeedback. These two cases are representative of approxi-
mately two-thirds of the veterans who accept from me a
offer of pro bono training.58 I lose a third to attrition, usually between the sixth and
tenth sessions, as they notice changes and clarify how much they like their opiates.
Rehabilitation using a bioelectric strategy may require ongoing neurofeedback
care in the same way that the biochemical strategy requires ongoing pharmaceuti-
cal care for stabilization over time. Integrating neurofeedback into standard care
has been shown to improve outcomes for combat veterans. It has been found to
be better than SC alone for combat veterans. Neurofeedback has the potential to
improve the quality of life of humans who are suffering from the symptoms known
clinically as PTSD. It is common to observe that as the individual’s nervous system
explores, attains, and practices being awake, clear, and relaxed, many other seem-
ingly intractable symptoms melt away also.
Appendix 225



Date: _____________________
Time: Start_____ Complete____
Name: _____________________
Data provided by: ___________
Symptom tracking: (0 = No problem, 10 = The worst)
1. Category: Sleep
 Bruxism   Difficulty falling asleep
  Difficulty maintaining sleep   Difficulty waking
  Dysregulated sleep cycles  Narcolepsy
  Night sweats   Night terrors
  Nightmares or vivid dreams   Nocturnal enuresis
  Periodic leg movements  Restless leg
 Restless sleep   Sleep apnea
  Sleep walking   Talking during sleep
2. Category: Attention and Learning
  Difficulty completing tasks  Difficulty following instructions
  Difficulty making decisions  Difficulty organizing personal
 Difficulty remembering names time or space
  Difficulty shifting tasks   Difficulty shifting attention
 Difficulty understanding   Difficulty thinking clearly
  Lack of alertness  Distractibility
  Messy handwriting   Lacking common sense
  Poor concentration   Not listening
  Poor math   Poor drawing ability
  Poor sustained attention   Poor short-term memory
  Poor vocabulary   Poor verbal expression
 Reading difficulty   Poor word finding
 Unmotivated   Slow thinking
3. Category: Sensory
  Auditory hypersensitivity   Chemical sensitivities
  Motion sickness   Poor body awareness
  Somatosensory deficits   Tactile hypersensitivity
 Tinnitus  Vertigo
  Visual deficits   Visual hypersensitivity
4. Category: Behavioral
  Addictive behaviors   Aggressive behavior
 Anorexia   Autistic stimming
226  PTSD symptom reduction with neurofeedback

  Binging and purging   Class clown

  Compulsive behaviors   Compulsive eating
 Crying  Exaggerated startle response
  Excessive talking  Hyperactivity
 Hypervigilance  Impulsivity
 Inflexibility   Lack of appetite awareness
  Lack of sense of humor   Lack of social interest
  Manipulative behavior   Motor or vocal tics
  Nail biting  Oppositional or defiant behavior
  Poor eye contact   Poor grooming
 Poor social or emotional   Poor speech articulation
 Rages   Self-injurious behavior

5. Category: Emotional
 Agitation  Anger
 Anxiety  Depression
  Difficult to soothe   Dissociative episodes
  Easily embarrassed   Emotional reactivity
 Fears   Feelings of unreality
  Flashbacks of trauma  Impatience
 Irritability   Lack of emotional awareness
  Lack of pleasure   Lack of social awareness
  Low self-esteem  Mania
  Mood swings   Obsessive negative thoughts
  Obsessive worries   Panic attacks
 Paranoia   Suicidal thoughts

6. Category: Physical
 Allergies  Asthma
  Chronic constipation  Clumsiness
  Difficulty walking or moving   Difficult working
  Effort fatigue  Encopresis
 Fatigue   Heart palpitations
  High blood pressure   Hot flashes
  Immune deficiency   Irritable bowel
  Low muscle tone   Muscle tension
  Muscle twitches   Muscle weakness
 Nausea  Premenstrual syndrome (PMS)
  Poor balance   Poor fine motor coordination
 Poor gross motor  Reflux
 Rigidity  Seizures
  Skin rashes  Spasticity
  Stress incontinence   Sugar craving and reactivity
 Sweating  Tachicardia
 Tremor   Urge incontinence
References 227

7. Category: Pain
  Abdominal pain   Chronic aching pain
  Chronic nerve pain   Fibromyalgia pain
  Jaw pain   Joint pain
  Muscle pain   Muscle tension headaches
 Sciatica   Sinus headaches
  Stomach aches   Trigeminal neuralgia
_______ __________________________________________________
_______ __________________________________________________
_______ __________________________________________________
_______ __________________________________________________

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Neurofeedback in application
to the ADHD spectrum


11.1 Why diagnosis is not important from a neurofeedback perspective 233

11.2 The ADHD spectrum in the clinical perspective 234
11.3 Clinical case studies 237
11.3.1 Case #1 237
11.3.2 Case #2 244
11.3.3 Case #3 247
11.3.4 Case #4 248
11.3.5 Case #5 252
11.4 Statistical appraisal of neurofeedback for attentional deficits 256
11.5  Summary and conclusion 259
References 259

In Chapter 2, the review of early research history established that the traditional
sensorimotor rhythm (SMR)/beta protocols of electroencephalogram (EEG)
biofeedback were quite effective in managing the canonical symptoms of atten-
tion deficit hyperactivity disorder (ADHD). Our own role in that development is
covered in detail in two book chapters.1,2 Six comparison studies have now been
done that unanimously found an essential equivalence between EEG training in
the classical manner and state-of-the art pharmacological management. These
comparisons typically relied strongly on the results of continuous performance
tests (CPTs) of attention. These tests do not give us a handle on the hyperactivity
component, for which one needs to rely on the observations of parents, teachers,
or trained observers. These have their obvious shortcomings. Nevertheless, the
essential findings are no longer in any doubt. Neurofeedback is competitive with
standard medical treatment in the management of ADHD.
In recognition of this substantial body of evidence, in 2013 PracticeWise, a
research service acting on behalf of the American Academy of Pediatrics (AAP)

232  Neurofeedback in application to the ADHD spectrum

has rated neurofeedback as having Level 1 efficacy in application to ADHD.3 This

recognition subsequently became controversial, and in 2014 the AAP clarified
that its prior position had not in fact changed. Since 2010 biofeedback had been
recognized as having “Good” evidence.3 Notably the supportive documentation
was not challenged by the AAP. Recent brain imaging research had been cited in
addition to the clinical studies.4 This research documents the impact of neuro-
feedback training on the functional connectivity of neuronal networks. In view
of the above, the existing behavioral model of ADHD remains in place essentially
without alteration. The more groundbreaking implications of the effectiveness
of neurofeedback in application to ADHD have yet to be recognized formally
within the medical community.
The clinical reality as experienced by neurofeedback practitioners cannot be
accommodated within the prevailing model of ADHD. By and large, the clientele
that seeks out neurofeedback for ADHD is not looking merely to replace medica-
tion in their therapy. Neurofeedback is sought out because the medications are
not resolving the issues that are actually compromising the child’s life, or the
side effects are not tolerated, or because the impetus is a related symptom such
as bed-wetting, nocturnal bruxism, or scary dreams. Yet these are clearly ADHD
children that have been medically diagnosed. The case can be made that the very
success of the medical remedies has resulted in a co-development of the concep-
tion of ADHD as being whatever is successfully treated with the medical arsenal,
most typically stimulants. ADHD is what the medications treat.
This has resulted in a kind of diagnostic tunnel vision that is unlikely to be
called into question because it is working as intended. The synergy between the
model and the remedy has led to ever more elaborate efforts to shore up the model
rather than to move beyond it. Developmental precursors of ADHD are not given
the attention they deserve. The complex etiology is not taken into account. The
emotional context of attentional deficits has been completely ignored. There is no
nexus between the behavioral model and emerging neurophysiological models
of brain regulation. This has not been an issue just for ADHD. With the devel-
opment of the Diagnostic Statistical Manual, Fifth Edition (DSM-V), the initial
objective was to seek more congruence with emerging neurophysiological mod-
els, as well as to increase reliance on biomarkers for diagnostic specificity. This
nobly motivated effort failed, however, because the DSM model was hopelessly
paradigm bound. Plainly, the phenomenological basis of the DSM formalism
“does not carve nature at its joints.” The diagnostic partitioning does not line up
with any biologically based organizational schema.
The clinical experience of the neurofeedback practitioner mandates a more
inclusive conception. This is the dysregulation model. In this model, ADHD is
seen as a disorder of cerebral dysregulation that crosses diagnostic boundaries
and affects multiple systems. In this model, attentional dysfunction becomes a
mere observable for the core dysregulation, and is one among many such observ-
ables. The issue can be illustrated with the following example: within the classic
DSM framework, oppositional defiant disorder is comorbid with ADHD in some
60% of cases.5 Since stimulants do not address this comorbidity, the dichotomous
view is likely to be sustained. The more organic view would have it that emotional
11.1  Why diagnosis is not important from a neurofeedback perspective  233

dysregulation clearly cohabits quite commonly with attentional dysregulation.

One clearly impinges on the other. Emotionally based disorders often lie at the
core of attentional disorders, and in such cases should have priority in therapeu-
tic attention. A common mechanism may even underlie both. Alternatively, sen-
sory processing disorders or specific learning disabilities may lie at the root of the
apparent attentional deficit. Conversely, the attentional deficits seen in ADHD
are ubiquitous in other clinical conditions.
The need clearly exists for us to move beyond a purely behavioral and phe-
nomenological model. Since neurofeedback engages neural network organiza-
tion directly, the impetus exists to understand the canonical disorders in that
new framework. At the same time, the clinical decision-making by the neuro-
feedback practitioner remains based largely on behavioral and phenomenologi-
cal observations. The difference is that a more physiologically grounded model
allows the clinical phenomenology to be appraised differently. A simple refram-
ing is called for, the principal feature of which is that a more inclusive perspective
is called for, one that is no respecter of diagnostic boundaries.
As described in Chapter 4, the clinical model is informed by considerations of
functional neuroanatomy and is subject to selection through empirical findings.
The results are consistent with current understanding of our intrinsic connectiv-
ity networks (ICNs), or resting state networks. The quality of brain function is
contingent on the steady-state functional connectivity of our ICNs, as well as on
their dynamical interaction.6 This is discussed further in Chapter 2.
The study of intra-individual variability of reaction time performance
under various challenge conditions has revealed fluctuations in the range of
0.01–0.1 Hz.7 Another such study found correlations between responses on the
time­scale of 1 second.8 The study of event-related potentials (ERPs) under such
challenges has shown differences on the timescale of 10 milliseconds.9 Each of
these time domains can be targeted with a neuromodulation strategy. However, it
has been empirically found that the broadest impact can be achieved by targeting
the steady-state behavior of functional connectivity in the infra-low-frequency
range. The case histories presented below are intended to illustrate the method in
application to the ADHD spectrum.


Neurofeedback exercises the brain into self-regulation and improved function.
With proper training, improvements in performance should be achievable irre-
spective of baseline performance when initiating neurofeedback. There is usually
a set of symptoms to work with that cues us with respect to self-regulatory status,
and that set of symptoms might or might not fit into the diagnostic criteria for
a particular condition. Even if nothing rises to the level of symptoms, there are
relative strengths and weaknesses that may be discerned. Parents are often con-
cerned that their children will not get the training because they don’t have a for-
mal diagnosis, and we quickly lay those concerns to rest. From a neurofeedback
perspective, the more important aspect is “who is this person that is presenting
234  Neurofeedback in application to the ADHD spectrum

with these symptoms? How is that unique brain affected and constrained, given
those specific symptoms? How is it dysfunctional and dysregulated?” The symp-
toms are the observable manifestations of the dysregulation status that we need
to learn about and impact with the training.
A symptom is necessarily subjective, observed, and appraised by the patient,
and typically it cannot be measured directly or with much accuracy. Therefore,
the same symptom is going to be perceived differently by any two affected indi-
viduals. This is not, however, a lamentable limitation. On the contrary, the specif-
ics of how this symptom manifests in one brain or another is the information we
need in order to decide how to train. The particularity and the context of symp-
tom presentation are keys to the underlying pattern of dysregulation.
Having a diagnosis merely orients us towards one set of symptoms or another,
but does not give us any specifics on how those symptoms are related at a deeper
level, that of the pattern of dysregulation that is affecting that brain and body. At
the same time, not having a diagnosis simply means we get the information we
need in the form of a list of symptoms the client will describe during the intake.
We then map those symptom patterns to our training sites and design a training
protocol that will target the areas in the brain that are involved in controlling the
symptoms. The client will experience the training and will be able to notice and
report on changes in symptoms. These changes help us understand in what way
the training is affecting brain function, and we make continual adjustments to
the training protocol to optimize results. Such adjustments may be made several
times during one of the early sessions, before the training protocol settles down
to a more predictable pattern.


The clinical model distinguishes between two principal subtypes of ADHD for
the purposes of structuring a neurofeedback protocol: the simple subtype and the
complicated subtype. The simple ADHD subtype is well described by the cardinal
symptoms of ADHD: inattention and distractibility on the one hand; impulsiv-
ity and hyperactivity on the other. This pattern indicates the need to train two
main areas in the brain: the left prefrontal cortex and the right parietal cortex.
This bi-hemispheric strategy has served us well for many years, going back to
the mid-1990s. It is traceable back to the model of ADHD of Malone, Kershner,
and Swanson,10 which in turn is based on the model of Tucker and Williamson.11
Representative clinical results obtained with the earlier SMR/beta training pro-
tocols at some 32 clinical practices are covered by Kaiser and Othmer.12
The left prefrontal cortex is a critical part of the executive system that refers to
directed attention, planning, reasoning, and judgment. It is involved in voluntary
behaviors such as decision-making, planning, internally motivated attention and
the inhibition of impulsive and compulsive behaviors. Good prefrontal function
allows us to memorize information while planning and executing appropriate
sequences of actions to achieve concrete goals. It is also crucial to good self-
regulation by inhibiting primitive and immature reactions while time is allocated
11.2  The ADHD spectrum in the clinical perspective  235

to considering possible outcomes and consequences of alternative courses of

action. Whenever there is a lack of appropriate prefrontal control, the person may
have difficulty completing tasks, focusing for a long period of time and hewing to
longer-term goals; the person may also exhibit poor organization skills and may
even be unaware of their own behavior and unable to consider consequences of
behavioral alternatives.
The right parietal cortex plays an important role in integrating information
from our senses to build a coherent picture of the world around us. It is involved
in visual–spatial processing, spatial and body awareness, orientation of the body
in space, and motor coordination on the macro-scale. Impaired function of the
right parietal cortex can lead to a lack of self-awareness and spatial awareness,
and it can result in the inability of the subject to control body movement, leading
to hyperactivity.
The complicated subtype of ADHD includes the above mentioned symptoms
as a result of poor function of the left prefrontal cortex and right parietal cortex,
but adds physiological dysregulation and emotional symptoms to the picture.
(Strictly speaking, ADHD is a disorder of exclusion, and thus the more compli-
cated presentations should not be labeled ADHD. But in the real world, this is
what often happens, and that leads to the diagnostic tunnel vision already alluded
to. The more complicated aspects may not be attended to because they do not fit
the template.) The lack of emotional control resulting in oppositional or aggres-
sive behavior requires training the right prefrontal cortex, while the symptoms
of instability, including headaches, mood swings, asthma, etc., require left–right
(i.e., inter-hemispheric) temporal stabilization. It is tempting to surmise that it is
easier to work with the uncomplicated subtype. The problem is that the lack of
self-awareness in ADHD makes it difficult for clients to report on changes occur-
ring with the training. For the neurofeedback clinician, this presents a chal-
lenge in making clinical decisions regarding training protocols. The complicated
subtype, on the other hand, involves sensitive, touchy nervous systems with an
abundance of symptoms that are easy to report on and easy to track. These people
are well aware of what is bothering them. Our clinical adjustments to the training
protocols are perceived promptly by the client and this helps the process of find-
ing what is optimal. Fortunately, these clients are plentiful in our clinic.
In a clinical setting like ours, people who seek help have typically already tried
numerous other modalities to resolve their issues, and that explains why we tend
to see the complex cases, where ADHD-related symptoms are part of a bigger
picture. For those with uncomplicated ADHD, modern medicine addresses the
problem sufficiently well such that further help with neurofeedback is unlikely
to be sought. It is mostly when clients really want to avoid medication altogether
that we get to see people in this category.
There are a few major differences between traditional treatment options and
neurofeedback for ADHD. The most important one is the fact that neurofeedback
is non-invasive and does not put anything into the system, while medication is
invasive and has potentially significant, troublesome, and even lasting side effects.
The other difference is that while medication administration is limited by age,
neurofeedback can be done at any age. Last but not least, allopathic medicine will
236  Neurofeedback in application to the ADHD spectrum

consider the severity of the presenting symptoms when deciding on a treatment

plan and a certain dose of medication to be administered. With neurofeedback,
the severity of a symptom is not important in establishing how to train that brain.
We also have the ability to be very specific in terms of which areas in the brain
we target with the training and exactly how to fine-tune the frequency in order
to obtain the best results. Medication effects wear off in hours, while the changes
promoted by neurofeedback can last a lifetime if sufficient training has been done.
In our assessment process, we include a CPT called the QIK test,13 which char-
acterizes aspects of brain performance that are directly relevant to our clinical
objectives. Since symptoms are subjective and self-reporting is sometimes diffi-
cult, having measurable data before and after we train a brain for a certain num-
ber of sessions is essential. The test provides information on accuracy, speed, and
consistency under a pressured-choice reaction time challenge of a 21-minute
duration. The QIK  test emulates the TOVA® (Test of Variables of Attention),14
which is perhaps the best-known CPT within the ADHD community.
This Go/No-Go test involves two periods of stimulus-sparse challenge, fol-
lowed by two periods of stimulus-frequent challenge, and this is followed (only
in the case of the QIK test) by a return to a single period of stimulus-sparse chal-
lenge. The inter-stimulus interval is invariant at 2 seconds in order to maintain
uniformly boring conditions. This challenges the maintenance of vigilance.
The QIK test differs from the TOVA mainly in the analysis of the data. Explicit
account is taken of response time outliers, and the threshold of an anticipatory
error has been shortened from 200 to 150 milliseconds. In addition, the QIK test
analysis relies on up-to-date norms. Non-parametric analysis is used for the vari-
ables that are not Gaussian distributed.
This is a grueling test for the young ADHD child. It is administered at 6 years
of age and up, provided that the client can understand and follow instructions
and is able to stay with the task. The baseline test is a consistency check on what
we learn about that brain’s way of functioning during the intake. The client
should also “recognize themselves” in the test results as they are explained to
them. The conditions under which the baseline test is taken (e.g., with or without
any medication) will typically be replicated during the comparison test that is
done 20 sessions later. It is expected that the second test will show improvements
in most areas, with significant improvements expected in areas of initial deficit.
Adverse outcomes in one aspect or another compel the training strategy to be
redirected. Statistical results are reviewed later in this chapter.
Often, attention and impulse control issues are part of a more complex sce-
nario that can present under a different name: post-traumatic stress disorder,
attachment issues, developmental disorder, addiction, depression, or anxiety.
Our understanding of brain function allows us to interpret symptoms of inat-
tention, impulsivity, or hyperactivity in the context of a certain layered and more
complicated picture. The CPT has historically been associated with the charac-
terization of the ADHD brain, but we have put it to use much more universally.
It is a test of nervous system status that is very revealing of the capacity for self-
regulation. Whereas it is not prescriptive of training protocols, it is a truth test
of sorts to index our approach to the goal of improved self-regulatory capacity.
11.3  Clinical case studies  237


11.3.1  Case #1
Christine, a 20-year-old woman, sought help for symptoms related to her ADHD
diagnosis. During the intake interview, a much more complicated picture was
disclosed, a picture that included trauma and a history of addiction. Adopted as
an infant, she had a normal early life. Her adoptive parents divorced when she
was 12 years old and she was raised by her mother, with whom she never really
got along. The relationship with her sister, who was also adopted, was not close
until later in life. As her family life became increasingly more stressful, her aca-
demic performance suffered. She had been in several car accidents, and had pain
in her upper back and muscle tension in her neck and shoulders as a result. She
had a history of multiple drug addictions that she was able to overcome—she had
been sober for 2 years when she came to us. She described how anything she put
into her system had the power to get her hooked—she had abused cocaine and
marijuana, and would even use Adderall to get high. Currently, she was strug-
gling with new addictions: food and cigarettes. She had suffered one seizure-like
episode with a drug overdose. She complained of poor balance and motor coor-
dination and her sense of direction was not good either. She described having dif-
ficulties falling asleep and found it impossible to wake up in the morning despite
setting several alarms. She also had a history of sleepwalking.
Between the addictive behaviors, immense anxiety, her terrible sleep hygiene
and thus disrupted sleep patterns, the obsessive fears of failure or becoming over-
weight and the migraines and headaches and severe pre-menstrual syndrome
(PMS), the fact that she came in with the diagnosis of ADHD seemed beside the
point. She did have difficulties concentrating and had a hard time staying on task;
she would often zone out and was both hyperactive and impulsive. However, given
the fact that her brain had been through so much, could we understand the latter
symptoms as consequences of all the different traumas her brain had suffered, or
were they just another set of separate issues that happened to be experienced by
the same brain? Furthermore, did this distinction really matter?
Our improved understanding of brain organization and function has helped
us refine our methods of training the brain. It is a well-known fact that trauma to
the brain means disruption in early development and interference with self-regu-
latory processes, particularly those affecting regulation and autonomic function.
When core self-regulation is deficient, a person will be unable to feel safe or com-
fortable within themselves and in the world. An unmodulated fear response radi-
ates throughout the regulatory regime, affecting regulatory status quite broadly.
The right hemisphere is responsible for acquiring this skill, and when things do
not go as planned for whatever reason, this puts the brain in emergency mode
and makes it work overtime to try and keep the person safe and connected. The
more urgent issue is the lack of core self-regulation and its consequences, which
can emerge immediately or later in life in the form of anxiety or hyper-vigilance,
attachment deficits or reactivity, or aggressive or paranoid behaviors, all serving
the same purpose of preserving life and ensuring personal safety.
238  Neurofeedback in application to the ADHD spectrum

With the client described above, not only had she experienced trauma as an
infant when she was adopted at 4 months of age, but then her sense of safety and
bonding was shattered yet again when her adoptive family broke up. The self-
destructive, addictive behaviors can be easily explained by her lacking a sense of
core self and needing external stimuli to cope with life.
During her first QIK test, she found it quite challenging to stay awake, missed
one target and almost missed 19 others (reaction time outliers), while also push-
ing the button for the non-target four times. She was slow and variable in her
response times and her accuracy suffered as well, as shown in Figure 11.1.
On more detailed analysis, as shown in Figure 11.2, we can see which parts
of the test were more challenging to her. She started the first period with a low-
demand task and did quite well, with only one outlier and no other errors, and
she was fairly fast and consistent. As we kept boring her in the second period,
she remained accurate but slowed down and became significantly more variable
in her responses. Entering the third period of the test with the faster pace, she
started making more mistakes, missed the target once, and also had two commis-
sion errors. Maintaining the high-demand task was an even bigger challenge for
her, as she slowed down and became very inconsistent, and also had a significant
number of outliers. Just as she described during the intake, she had a hard time
staying on task, which is obvious when we look at how her performance degraded
as she needed to maintain a boring or challenging task. With increased perfor-
mance pressure, her anxiety level increased, and thus when making mistakes in

Figure 11.1  Results summary QIK baseline test, Case #1. (Full-color version of
figure available at
11.3  Clinical case studies  239

Figure 11.2  Raw data and Standard scores, QIK baseline test, Case #1.
(Full-color version of figure available at

the test she sped up instead of taking her time to consider before acting. Recovery
in the fifth period was difficult, with three outliers and one commission error,
and she was both slow and variable.
The response time graphs in Figure 11.3 allow us to see the time course of
events, where she made the mistakes, and the parts of the test in which her per-
formance was better or worse. Clearly, this client was able to perform fairly well
when under pressure, as long as the stress was of a short duration. When the
pressure continued, her performance declined, and with increased stress, her
nervous system tended to shut down. She almost fell asleep during the test.
Compared to a normal distribution of response times for age group and gen-
der, the distribution of her response times in Figure 11.4 is much more spread
out, with the mean of her test at 423 milliseconds compared to 362 milliseconds
for the norm. When looking at the different parts of the test, it is evident that the
performance decrement increased during the second high-demand task, which
was the most difficult for her to perform.
She had been medicated in the past, but her sensitive nervous system did not
tolerate the different medications well, or she ended up abusing them, so eventu-
ally she just stopped taking them. The only medication still being used when we
started our sessions was melatonin to help her sleep.
We started training and, one by one, we added all the training sites needed
to target her symptoms. Given her traumatic early life and addiction history,
240  Neurofeedback in application to the ADHD spectrum

Figure 11.3  Response time graphs, QIK baseline test, Case #1. (Full-color version
of figure available at

right parietal training for calming was crucial. At the same time, several insta-
bility symptoms indicated a great need for bilateral training at mid-temporal
sites to enhance stability. Later on, right prefrontal placement was introduced to
address her attachment issues, as well as to impact on her addictive behaviors.
Finally, when her system settled down, she had fewer headaches and her sleep had
11.3  Clinical case studies  241

Figure 11.4  Response time histograms, QIK baseline test, Case #1. (Full-
color version of figure available at

improved, we introduced left prefrontal training to specifically target concentra-

tion, distractibility, and impulse control.
The re-evaluation revealed that most symptoms had greatly improved: con-
centration was much better and her ability to stay on task for prolonged periods
had dramatically improved. She was no longer zoning out while reading. Her
anxiety was gone and her sleep had normalized. She had also stopped taking
242  Neurofeedback in application to the ADHD spectrum

melatonin. Her sense of direction had greatly improved, but she continued to
have difficulties getting to appointments on time. She rarely had any nightmares
now and waking up in the morning had become easier. Her obsessive worries
had moderated and she was less hyperactive. The headaches and migraines had
vanished, and her PMS symptoms were less intense after the training. After suc-
cessfully reducing her smoking before training, she felt less of an urge to abuse
substances of any kind, and switched to electronic cigarettes to help her quit.
Concerns related to weight gain and being successful in life remained, but she felt
like she was more in control of her thoughts and emotions.
If we look at the comparison between the first and the second QIK test (Figure
11.5), it is easy to notice the significant changes in her performance. At the sec-
ond QIK test, there are no omissions or outliers, but interestingly, she had seven
commission errors, compared to just four earlier. One variable on the day of her
second QIK test was her coffee intake: she had not had any before the test, which
was different from the previous time. Coffee acted like a stimulant for her, wak-
ing her mind up and helping her focus, so the fact that she had not consumed any
probably influenced her performance. Speed and consistency were significantly
improved from the first test.
The greatest difficulty was still her performing under the pressure of the
high-demand task, especially when maintaining that task (Figure 11.6). She had
similar difficulties during the first test, but this time she was faster and more

Figure 11.5  Results summary QIK test 2, Case #1. (Full-color version of figure
available at
11.3  Clinical case studies  243

Figure 11.6  Raw data and standard Scores, QIK test 2, Case #1. (Full-
color version of figure available at

consistent during that part of the test, and this might have caused her to make
more commission errors. With a mean reaction time of more than one standard
deviation above the norm (i.e. faster), she was performing at greater risk of com-
mission errors. It is only at the very end, during the recovery period, that she sped
up instead of becoming more careful after the one commission error she made,
but overall, her performance had significantly improved, which is consistent with
the perceived changes in her symptoms, which were all reduced in severity to
allow for better performance in everyday life (Figure 11.7).
With such a complex case, 20 sessions is typically enough to see significant
favorable change, but not enough to be able to say “we are done training.” In fact,
because of her complicated early life and addictive behaviors, further training
was recommended, and other training modalities were needed to work on the
resolution of her learned habits (Figure 11.8).
244  Neurofeedback in application to the ADHD spectrum

Figure 11.7  Response time yistograms, QIK test 2, Case #1. (Full-
color version of figure available at

11.3.2  Case #2
George, a 33-year-old man, sought help for his attention deficit disorder (ADD)
symptoms when the medication he was taking created new issues for him, such as
rebound headaches and palpitations. In other respects, the medications had been
11.3  Clinical case studies  245

Figure 11.8  Pre-post graphs, Case #1. (Full-color version of figure available at

In his developmental history, there was nothing exceptional except for his
parents’ divorce when he was still an infant. He was raised by his mother and
stepfather. In his family history, he mentioned ADHD, along with autoimmune
disorders, insomnia, depression, anxiety, obesity, alcohol addiction, and conduct
problems. He was taking Adderall 10 mg/day and up to 20 mg occasionally when
he had to undergo some testing in school.
His main concerns before we started training were difficulties concentrating,
getting on task, completing tasks, and impulsivity. About once a week, he would
have a hard time falling back to sleep once he woke up at around 2 am. He would
experience anxiety as tension in his body and obsessive worries. He sometimes
246  Neurofeedback in application to the ADHD spectrum

had neck tension and ground his teeth. He would overeat with stress and was
sensitive to sugar—he would have a sugar-fueled high and then crash later. He
had frequent headaches when not drinking coffee or not taking Adderall.
His only QIK  test was taken before we started training him, and he com-
plained that it had been difficult to perform because he was getting distracted
by the ticking of the clock on the wall. He missed the target three times during
the test, twice in the recovery part of the test in period 5 and once during the
high-demand task, which is consistent with what we already knew about his dif-
ficulties performing under pressure and staying on task for long periods of time
(Figure 11.9). His overall performance and accuracy were average; he had not
taken Adderall on the day of the test and did not take it for the most part while
doing the sessions in the clinic.
He started noticing positive changes in his distractibility early on with the
training, and was able to track the results as he was studying for examinations. It
took a while to find the optimal protocol for him; he had a very sensitive nervous
system, and because of the Adderall and caffeine variables, it was at times chal-
lenging to figure out what each was contributing to the reported shifts. He clearly
benefited from the sessions and would report improvements in concentration
and the ability to deal with stress and deadlines he had to meet, but usually the
results faded a day or two after the sessions. He did not finish his 20 treatments
and we did not get to take a second QIK test, so there are no measurable data to
gauge brain performance. Given his inability to maintain the gains, it was clear
that a lot more training would have been needed before his brain would have suc-
cessfully stayed on track and performed optimally on its own. One hypothesis for

Figure 11.9  Results summary QIK baseline test, Case #2. (Full-color version of
figure available at
11.3  Clinical case studies  247

the failure to maintain gains is that, as an infant, he had in fact been traumatized
by his parents’ divorce, and that the resulting impact on nervous system func-
tioning had not yet fully resolved. This case also illustrates what can frequently
happen as the client comes to terms with this novel method. An initial healthy
skepticism may well transition to its opposite of heightened expectations as the
first good effects are felt. When the training procedure then fails to live up to
those new expectations, the effort is abandoned.

11.3.3  Case #3
Aidan, a 16-year-old young man with a dual diagnosis of ADHD and dyslexia,
received intensive neurofeedback training at our clinic. Over a 2-week span, he
received 20 neurofeedback sessions, at a rate of two sessions a day, and he contin-
ued with home training.
The main concerns described during the intake with us were hyperactivity
and distractibility, anxiety as worries, some frustration, and compulsive organi-
zation, as well as difficulty with academic classes. Words would move on the page
when he tried to read. This problem was helped considerably with Irlen lenses. He
had headaches with reading or when dehydrated and had some difficulties falling
asleep. In the past, he had been sleepwalking and had night terrors as well. Sugar
sensitivity was also described.
He was born through emergency C-section with his umbilical cord around
his neck and was described as a stressed baby. He walked early and talked late,
and was not much of a talker even later on in life. He was accident prone and
had a few falls and stitches growing up, and even had a finger reattached at 11
months. Around the time he was 4 years old, his parents separated for a year.
In his genetic history, insomnia, post-partum depression, anxiety, obsessive-­
compulsive ­disorder (OCD), dyslexia, and Asperger’s syndrome were present.
Prior to the neurofeedback, he had been on 54 mg of Concerta® per day,
which he stopped taking while undergoing neurofeedback. His pre-training
QIK test (Figure 11.10) revealed an average performance index and an accuracy
index well below average, with impulsivity scores in the first percentile, as well
as a high number of commission errors and also a significant number of omis-
sions. The part that he found to be the most difficult was the high-demand sec-
tion, where his performance dropped significantly. After the first two sessions,
he reported falling asleep faster, and one session later, improvements in read-
ing comprehension were noted, although at the time the protocol was not yet
focusing on reading issues. His mother also noticed him becoming less hyperac-
tive, even though he was off his medication for the duration of the neurofeed-
back training. By session 10, his behavioral issues had subsided to the level they
would have been when he was on medication. His reading continued to improve,
and he actually started reading more with—or even without—his Irlen lenses. QIK test #1
During reassessment, the progress made by Aidan was reported: he had better
understanding while reading and was more able to visualize what he read. He
248  Neurofeedback in application to the ADHD spectrum

Figure 11.10  Results summary QIK baseline test, Case #3. (Full-color version of
figure available at

described more immediate and detailed imagery and was less fidgety and dis-
tracted. His sleep had gotten better with fewer nightmares, and he experienced
less anxiety or obsessive worries. He also noticed being more comfortable when
having to deal with traffic. QIK test #2
The second QIK test (Figure 11.11) showed some improvement in the performance
index, with a significant shift in speed and consistency. His speed of response
decreased somewhat, which allowed for higher consistency of responses and also
improved accuracy. In fact, his accuracy went from a score of 55 to a score of 100
(i.e., from the first percentile to the 50th). This kind of spectacular improvement
becomes even more relevant in the prevailing context, since he had stopped tak-
ing his medication before undergoing treatments in the clinic.
He was transitioned to training at home, receiving four to five sessions a week,
while continuing to stay of his medications. One month into his home training,
his mother reported further improvements in concentration and in his ability to
make good choices, and he was better able to manage usual day-to-day events.

11.3.4  Case #4
Michael, an 11-year-old boy, was having a hard time in school. He did not have a
formal diagnosis, but exhibited some of the classic symptoms of ADHD. He had
11.3  Clinical case studies  249

Figure 11.11  Results summary QIK test 2, Case #3. (Full-color version of figure
available at

a short attention span, was easily distracted, was impulsive and disorganized,
and could not sit still in school. Among the presenting symptoms, there were
some learning difficulties, like understanding math concepts and calculation,
and also writing problems. He was described as being clumsy. He was inflexible
and defiant mostly in a school setting; frustration and anger were issues as well.
Occasional headaches and stomachaches as well as teeth-grinding and sugar
cravings completed the picture. After being adopted at birth, his early life was
unremarkable, except for some chronic ear infections that required tubes at 1
year of age until 2 years of age. As a result, he was sensitive to sound, especially
to loud noise.
Taking the QIK test (Figure 11.12) the first time proved to be quite a challenge
for Michael. He scored below average for speed, consistency, and inattention
with only one score, impulsivity, within the normal range. This indicates that
he was slow and very variable, and unable to stay on task. The response time
histogram (Figure 11.13) reveals a broad distribution of response times with lots
of outliers.
His training protocol targeted areas in the brain to promote physical, emo-
tional, and mental calming, as well as stabilization. T3–P3 was added for the
learning difficulties. Over a 5-month span, he completed 20 sessions of neuro-
feedback. His statement at the end—“I’m not stupid anymore”—conveys his own
sense of the progress he had made in just 20 sessions. The child was thrilled about
his new way of relating to his peers. This sheds some light on how difficult it can
250  Neurofeedback in application to the ADHD spectrum

Figure 11.12  Results summary QIK baseline test, Case #4. (Full-color version of
figure available at

be for people with these symptoms to fit in, how much harder they feel they need
to work to keep pace in school or at work, and how much their dysregulated ner-
vous system can hinder function. During his re-evaluation, his mother reported
improvements in most initial symptoms, and his second QIK test supported that
with measurable data.
He was enjoying school and was more optimistic now that his attention and
impulse control had significantly improved. In place of his earlier defiance, he
was less frustrated and angry, and much more flexible and cooperative. He was
much more organized, and improved his writing and math skills. He did not
have any headaches or stomachaches and was not grinding his teeth anymore. He
was less clumsy and was now able to sit still in school, so he was not distracting
others as he had been before.
His first test reflected the above described difficulties mostly in attention and,
to a certain degree, in impulse control. Twenty sessions later, a second test showed
significantly improved overall scores, with a superb leap towards the upper limit
of normal accuracy index scores (Figure 11.14). Both sustained attention and

Figure 11.13  Response time histogram—total, QIK baseline test, Case #4.
(Full-color version of figure available at
11.3  Clinical case studies  251

Figure 11.14  Results summary QIK test 2, Case #4. (Full-color version of figure
available at

impulse control were much better, and the performance index greatly improved
as well.
In light of these impressive gains, we suggested retesting Michael after 3
months to see whether the results were holding. This is not always assured after
training for only 20 sessions. Although the impulse control continued to improve,
the performance index dropped back to the level that had been measured prior to
the neurofeedback. The need for additional sessions is indicated by these results
(Figures 11.15 and 11.16). Since the brain showed itself capable of operating at

Figure 11.15  Results summary QIK test 3, Case #4. (Full-color version of figure
available at
252  Neurofeedback in application to the ADHD spectrum

Figure 11.16  Pre-post graphs, Case #4. (Full-color version of figure available at

the higher performance level, it should be able to do so again. Other factors that
could explain the failure to hold gains should also be looked for.

11.3.5  Case #5
Nicky, an 8-year-old boy, had been diagnosed 3 years prior to coming to see us
for ADHD symptoms. His mother described him as a very smart child who was
highly impulsive and hyperactive, had poor self-control, and a short attention
span. He had difficulties organizing, was distractible and forgetful, and was
11.3  Clinical case studies  253

impatient and easily frustrated. He was always rushing through tasks, which led
to making mistakes, and had some difficulties with math and spelling. He always
wanted to do as little as possible to get by and had poor self-confidence. He was
playing the class clown in order to feel accepted, and would manipulate anyone
to get his way by lying and cheating, about which he never exhibited remorse. He
was fearless, selfish, and careless, and felt he was never personally at fault. Most
recently, he had gotten into trouble in school for aggressive behaviors. He was
also biting his nails, mostly when under pressure. He had stomachaches with
constipation, and sugar cravings were an issue as well. Bedwetting had been a
problem in the past, but had stopped a few months back.
Noteworthy was the fact that the birth process had been a breach presentation
that required an emergency C-section, and Nicky was born with the umbilical
cord around his neck. All developmental milestones were reached on time. His
mother described herself as a perfectionist, and would push him just as hard as she
pushed herself. In consequence, Nicky blamed her for wanting him to be perfect.
The genetic history revealed addiction problems, thyroid disorders, and bipo-
lar disorder, as well as ADHD. When we started training, he was on 10 mg of
Adderall a day, which had been doubled 3 months prior to the start of neurofeed-
back treatments, due to a lack of improvement in symptoms. Despite the increase
in the medication, his symptoms were not controlled, and his parents were con-
cerned that he would have to take more and more of it until, eventually, it would
not work for him at all.
During the first QIK  test (Figure 11.17), Nicky had a difficult time staying
on task and had to be prompted several times to continue, as he was becoming
increasingly restless and bored. At the end, he was able to report on the number of
mistakes he had made. The test report revealed all scores to be within the normal
range, with high scores in sustained attention and consistency of response times,
while the speed of response was normal. Whereas his impulse control score was
high, he clearly struggled with stopping himself from impulsively pressing the but-
ton for the non-target.
In designing his training protocol, we considered basic placements to target
most of the described symptoms: stabilization for the sugar cravings; physical
calming for anxiety, hyperactivity, self-awareness and constipation; emotional
control for self-confidence, frustration, anger, and aggressive and manipulative

Figure 11.17  Results summary QIK baseline test, Case #5. (Full-color version of
figure available at
254  Neurofeedback in application to the ADHD spectrum

behaviors, as well as social–emotional awareness; and mental calming to address

impulse control, organization, attention, and forgetfulness, and also attention to
detail to help with math and spelling. We did a total of 21 neurofeedback sessions
in the clinic, and after the re-evaluation, they continued with home training for
another 2 months.
He responded quickly to the training and subtle changes in symptoms were
noticed early on. By session 4, he was mellower, less easily frustrated and not get-
ting into trouble as much in school, something that the teacher had commented
on. He was less impatient and also less forgetful, and he was no longer rushing
through tasks all the time. He also did not need to be told to stop misbehaving
very often. He was even able to report feeling calmer and felt good about not get-
ting into trouble in school very often anymore.
Nicky was still taking his medication on school days, but his parents decided
to try to stop it on the weekends to observe his behavior without it. While before
doing neurofeedback, going off the medication on the weekends was impossible
due to his being really “out of control,” after just six sessions, he did quite well
with the drug holiday. Soon, his math improved and he became more thoughtful
and calm, while remaining well behaved without medication during the week-
ends. During his treatments, we adjusted the protocol as needed, according to his
response to the training, and took on more areas to work on as we continued to
calm and stabilize his nervous system.
The re-evaluation revealed significantly improved performance with the
QIK test (Figure 11.18) and, according to his parents, the following changes in
symptoms: he was less hyperactive, less impulsive, and less easily frustrated.
He had not displayed any aggressive behaviors in weeks, was biting his nails
less, and his math performance had improved considerably. He had been off the
medication during the weekends and was observed to maintain good behavior
without  it. He  was doing much better in school both with performance and
behavior—a change that his parents and his teachers had noticed. Several
symptoms had not changed significantly: he was still rushing through tasks
and was still using manipulative behaviors to get his way. Spelling was still
problematic and he needed repetitions and prompts to follow instructions.
These concerns, along with the goal of helping lower his medications while
supporting brain function with neurofeedback, were the reasons we recom-
mended home training.

Figure 11.18  Results summary QIK test 2, Case #5. (Full-color version of figure
available at
11.3  Clinical case studies  255

All the scores in the second test were significantly better than the scores in
his first test, and interestingly, he did not have any anticipatory responses or
outliers in the retest. This reflects a readiness of his nervous system to attend to
the task at hand and respond appropriately. Also noteworthy was the fact that
although his performance during the first test scored within the normal range,
he improved it during the second test in all of the tested areas (Figures 11.17
through 11.19).
Home training allows for frequent and also longer sessions, utilizing the pro-
tocols that were established in the clinic. By reinforcing the training further on
an almost daily basis, the expectations are to see further significant gains and to

Figure 11.19  Pre-post graphs, Case #5. (Full-color version of figure available at
256  Neurofeedback in application to the ADHD spectrum

help the brain to hold onto those gains. They did about four sessions a week in
the 2 months following the treatments in the clinic before returning the system,
to a total of 32 sessions in addition to the 21 we had completed here. While doing
the home training, Nicky was only taking half of his 10 mg of Adderall and he
continued to improve. His teacher was impressed with his good behavior, and he
even got an award for his creative writing. The teacher pointed out that his spell-
ing had improved, and that he had taken a lot of time and put a lot of effort into
this project, something he would have not been able to do before neurofeedback.
He continued to benefit from the sessions at home, and when they returned the
system 2 months later, he was a different child, according to his mother. During
the summertime, while on vacation, he went off the medication and continued
to do well without it.
With all the clinical cases described above, as well as with all the other cli-
ents we continue to help with neurofeedback, the individuality and specificity
of our method, as well as the individual responses of each person we train,
become ever more obvious. It is within the brain’s scope to enhance its own
functional capacity if it is merely given information on its own behavior, to
which it is normally blind. By facilitating this process, we allow enhanced self-
regulation to emerge and to consolidate. Beyond the diagnostic label, what
needs to be fully understood is the uniqueness of each case and the many vari-
ables that come with it.


The presentation of case histories illustrates the individualization of the
approach to remediation that is infra-low-frequency neurofeedback. To com-
plement such a perspective, it is also useful to have some statistical measures
that give one a better sense of what one might expect in the general case. Such
an appraisal necessarily needs to be done with measures that can easily be quan-
tified, and that brings us back to the cardinal symptoms of ADHD, namely inat-
tention and impulsivity. We have recently surveyed all of the pre–post data that
have been accumulated over the past 6 years using infra-low-frequency training
and evaluated these data with the contemporary QIK test norms. Nearly all of
these data refer to nominally 20-session retests.
To make the data maximally useful, the sample was restricted to those who
scored below 85 in the standard score, equivalently below the 16th percentile.
This yielded a sample size of some 800 in the case of the inattention measure
(out of a total sample of more than 5000). This sample includes not only ADHD
children, but also everyone who was given the QIK test. In our practice, we ask
everyone who is capable of managing the task to take the test. Data for the inat-
tention measure (based on errors of omission and on outliers in reaction time)
are shown in Graph 11.1.
On the attention scale, nearly ha