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Kirk, Hanno W - Restoring The Brain - Neurofeedback As An Integrative Approach To health-CRC Press (2016) PDF
Kirk, Hanno W - Restoring The Brain - Neurofeedback As An Integrative Approach To health-CRC Press (2016) PDF
the Brain
Neurofeedback as an
Integrative Approach to Health
Edited by
Hanno W. Kirk
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Foreword vii
Acknowledgments xi
Editor xiii
Contributorsxv
Introduction xxi
v
vi Contents
vii
viii Foreword
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
neurosciences.
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
patient.
xi
Editor
xiii
Contributors
xv
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
therapeutics.
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.
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.
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.
xxi
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.
SHORT SUMMARY
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.
* 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.
1
Part
HANNO W. KIRK
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.
3
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
* 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
* 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
Neurotransmitter
Synaptic
vesicle
Neurotransmitter Axon
Voltage- transporter terminal
gated Ca2+
channel
Receptor
Synaptic
Post-synaptic
cleft
density
Dendrite
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).
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
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.
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
reluctantly.
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
century.
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
Arousal regulation
Affect regulation
Autonomic set-point and balance
Interoception
Motor system excitability
Attentional repertoire
Executive function
Working memory
Sensorium
Cognitive processes
* 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 http://www.humanconnectomeproject.org/informatics/
relationship-viewer/.
16 Changing the paradigm from neurochemical to neuroelectrical models
1.6 CONCLUSION
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
denigrated.
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.
REFERENCES
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of Developmental Trauma: Changing the Fear-Driven Brain. New York:
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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:
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5. Sherrington CS. 1906. The Integrative Action of the Nervous System.
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6. Bennett M. 2001. The History of the Synapse. Australia: Harwood
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7. Loewi cited in Clarke E, O’Malley CD. 1968. The Human Brain and the
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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
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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.
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July 14, Vol. 58, 12.
21. Shepherd. 2010. Chapter 15—Neuropsychiatry: The breakthrough in
psychopharmacology.
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 http://www.humanconnectomeproject.org/. Accessed on May 15, 2015.
25. Garey LJ. 2006. Brodmann’s Localisation in the Cerebral Cortex. New
York: Springer, retrieved from Wikipedia http://en.wikipedia.org/wiki/
Brodmann_area#References on July 8, 2014.
26. Relationship Viewer at http://www.humanconnectomeproject.org/data/
relationship-viewer/. February 2014.
27. Zimmer, C. Secrets of the Brain, National Geographic, http://ngm.
nationalgeographic.com/2014/02/brain/zimmer-text. 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). http://www.dana.org/Cerebrum/2001/Mastering_Our_
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
Publications.
2
History of neurofeedback
SIEGFRIED OTHMER
23
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.
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
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
improvement.
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
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.
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
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
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.
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.
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.
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.
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.
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.
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.
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.
2.6 SUMMARY
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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3
The role of glia and astrocytes
in brain functioning
DAVID A. KAISER
3.1 Introduction 51
3.2 Scientific findings on astroglial activity 51
3.3 Rhythmicity of the brain and energy cycles 53
References 56
3.1 INTRODUCTION
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.
51
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
hemodynamics.13,14
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
Subcortical concentration
0.60
5–7 Hz
0.55
Eyes open rest-parietal
7–9 Hz
Magnitude µV (Pz)
0.50 9–11 Hz
11–13 Hz
0.45
0.40
0.35 8 AM Noon 6 PM
0.30
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
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2. Cauli B, Hamel E. 2010. Revisiting the role of neurons in neurovascular
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References 57
MEIKE WIEDEMANN
59
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.
Front
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
Back
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.
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?
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.
4.1.4.1 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.
4.1.4.2 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.
4.1.4.3 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.
4.1.4.4 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.
4.1.4.5 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
4.1.4.6 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
session.
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.
4.2.1.1 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 (www.eegexpert.net). 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
4.2.1.2 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 (www.beemedic.com) 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.
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.
Arousal
Figure 4.2 (See color insert.) The arousal performance curve shows different
states depending on the arousal level.
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.
4.2.2.2 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.
4.2.2.3 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
behavior/thinking.
Table 4.3 Training on left and right hemispheres for different issues
4.2.2.4.5 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–right (T3–T4)
Stabilizing of instabilities (e.g., migraine, headache, seizures, panic, mood swings)
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.
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.
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:
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.
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.
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
followed.20,21
●● 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
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.
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.
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References 91
An Integrative Approach
to Health
DOREEN E. McMAHON
95
96 Neurofeedback in an integrative medical practice
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
5.3 BRAIN–GUT CONNECTION
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
5.5 SLEEP MANAGEMENT
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
5.6 BEHAVIOR MANAGEMENT
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
5.8 CASE PRESENTATIONS
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
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.
5.9 CONCLUSION
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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NORA T. GEDGAUDAS
117
118 Nutrition and the brain
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
powerfully—complementary.
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.
6.2 A PREMISE
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
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
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).
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:
“Hungry.”
If the client asks: “How am I supposed to feel after I eat?,” answer:
“Not hungry.”
Insulin le r level
ga
ve
Su
l
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
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
Alzheimer’s/dementia
Memory impairment
Attentional disorders
Schizophrenia
Autism/Asperger’s syndrome
Anxiety spectrum issues
Depression
Insomnia
Bipolar disorder
Wheat
Protein Lectins
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
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.
6.10 ANEMIA
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
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
stressful.
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
Genetic
susceptibility
AI
Increased Environmental
intestinal triggers
permeability to • Dietary components
macromolecules • Toxic chemicals
• Infections
Autoimmune progression
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.
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.
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.
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References 143
KURT N. WOELLER
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,
147
148 Biomedical factors that impact brain functioning
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:
Methionine
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
Homocysteine
synthase.
P-5-P
Glutathione
(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.
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.
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 (www.stopcallingitautism.org) 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:
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.
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:
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.
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
listed:
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.
●● 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.
●● 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:
Testing:
●● 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
high).
Treatment:
Treatment outcome:
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Part 3
Neurofeedback and
Integrative Medicine
in Practice
KELLEY E. FOUST
8.1 INTRODUCTION
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
169
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.
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
R L R L
Amy
STS
FG
FG
FG
x = 34 y = –55 z = –14
Normal
R L R L
Amy
STS
FG
FG
FG
x = 34 y = –55 z = –14
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
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.
8.3.2.1 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.
8.3.2.2 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:
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.
8.3.2.3 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.
8.3.2.4 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.
8.3.2.5 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.
8.3.2.6 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.)
8.3.2.7 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.
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.
8.4 CONCLUSION
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
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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
Touch. http://www.nationalautismresources.com/wilbarger-protocol.html.
9
The use of neurofeedback for
combat veterans with post-
traumatic stress
9.1 INTRODUCTION
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).
181
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.
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
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 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)
9.7 PROTOCOL
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
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.
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)
9.10 VIGNETTES
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!”
9.11 SUMMARY
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
9.12 DISCLAIMER
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.
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moduation at infralow frequencies. Semin Pediatr Neurol 20(4):246–257.
33. Othmer SF. 2013. Protocol Guide for Neurofeedback Clinicians (fourth
edition). Los Angeles: EEG Info Publications.
34. Othmer SF. 2013. Protocol Guide for Neurofeedback Clinicians (fourth
edition). Woodland Hills: EEG Info Publications.
35. Youngner CG, Gerardi M, Rothbaum B. 2013. PTSD: Evidence-based psy‑
chotherapy and emerging treatment approaches. FOCUS 11(3):307–314.
10
PTSD symptom reduction with
neurofeedback
MONICA G. DAHL
10.1 INTRODUCTION
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
201
202 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
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
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.
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
activities.
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.
* 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
25
20
September 11, 2012
September 21, 2012
15
October 4, 2012
10 December 6, 2012
March 8, 2013
5 July 26, 2013
November 8, 2013
0 March 24, 2014
April 16, 2014
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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.
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
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:
* 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
Front
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
Back
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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;
(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).
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
training.
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.
10.7 QUESTIONS
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:
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?
10.8 CONCLUSION
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 homecoming4veterans.org
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
Snoring
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
conversations
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
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)
symptoms
Poor balance Poor fine motor coordination
Poor gross motor Reflux
coordination
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
Other:
_______ __________________________________________________
_______ __________________________________________________
_______ __________________________________________________
_______ __________________________________________________
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230 PTSD symptom reduction with neurofeedback
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)
231
232 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.
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 https://www.crcpress.com/product/isbn/9781482258776.)
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 https://www.crcpress.com/product/
isbn/9781482258776.)
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 https://www.crcpress.com/product/isbn/9781482258776.)
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 https://www.crcpress.com/product/
isbn/9781482258776.)
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 https://www.crcpress.com/product/isbn/9781482258776.)
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 https://www.crcpress.com/product/
isbn/9781482258776.)
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 https://www.crcpress.com/product/
isbn/9781482258776.)
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
helpful.
11.3 Clinical case studies 245
Figure 11.8 Pre-post graphs, Case #1. (Full-color version of figure available at
https://www.crcpress.com/product/isbn/9781482258776.)
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 https://www.crcpress.com/product/isbn/9781482258776.)
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.
11.3.3.1 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 https://www.crcpress.com/product/isbn/9781482258776.)
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.
11.3.3.2 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 https://www.crcpress.com/product/isbn/9781482258776.)
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 https://www.crcpress.com/product/isbn/9781482258776.)
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 https://www.crcpress.com/product/
isbn/9781482258776.)
11.3 Clinical case studies 251
Figure 11.14 Results summary QIK test 2, Case #4. (Full-color version of figure
available at https://www.crcpress.com/product/isbn/9781482258776.)
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 https://www.crcpress.com/product/isbn/9781482258776.)
252 Neurofeedback in application to the ADHD spectrum
Figure 11.16 Pre-post graphs, Case #4. (Full-color version of figure available at
https://www.crcpress.com/product/isbn/9781482258776.)
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 https://www.crcpress.com/product/isbn/9781482258776.)
254 Neurofeedback in application to the ADHD spectrum
Figure 11.18 Results summary QIK test 2, Case #5. (Full-color version of figure
available at https://www.crcpress.com/product/isbn/9781482258776.)
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
https://www.crcpress.com/product/isbn/9781482258776.)
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.
of the mean or better, and nearly half of these scored above the norm. The median
score of 77 pre-training (sixth percentile) moved to a median score of 93 (32nd
percentile). This improvement is by more than one standard deviation, which
indicates a large effect size. Significantly, the pool of those who started in deepest
deficit saw substantial depletion. The second percentile cohort declined from 20%
to 5%. It is a commonly observed feature of neurofeedback that those who are in
greatest deficit benefit preferentially. These data are shown in Graph 11.2.
The 20-session retest data cannot tell us what is ultimately achievable in the
absence of constraints. It is already known that those in significant deficit tend to
benefit from additional training, so the results given here should be considered a
floor for what is intrinsically achievable with this method. Another consideration
is that the data compiled in these figures were accumulated from over 200 practi-
tioners, reflecting differing levels of clinical skills. They also reflect a period of 6
years, a time of significant evolution of the method, with each step along the way
involving a learning curve for all concerned.
Similar data from the EEG Institute, where this method was developed,
show even better results, albeit with a smaller sample size (n = 350). These data
258 Neurofeedback in application to the ADHD spectrum
were analyzed with TOVA norms, and thus are not directly comparable. On
the impulsivity scale, 75% of those who scored below 85 at the outset ended up
scoring above 85 after 20 sessions (versus 68% for the larger sample). The cohort
scoring within the second percentile dropped to 14% of its pre-training value
(versus 25% for the larger sample), and the first percentile cohort was depleted
by 90%.
In yet another compilation, the question was addressed as to the degree to
which normality is approached in the training population if so-called non-
responders are removed, as is conventional in medication studies. Referring
again to the results from the EEG Institute for the deficited cohort (pre-train-
ing score <85), the pre-training mean standard score for impulsivity was 63
(first percentile) and the post-training mean score was 96 (39th percentile).
Removing the non-responders (who amounted to 8% of the pool) yielded
a score of 99.5 (49th percentile). As expected, the test scores are effectively
normalized among the responders. Comparable values for the inattention
References 259
scale were as follows: the pre-training mean score was 53 (0th percentile) and
the post-training mean score was 81 (tenth percentile). Removing the non-
responders (who amounted to 24% of the pool) yielded a post-training value
of 93 (32nd percentile).
The difference in outcomes between the two tracked variables is likely to be
attributable to several factors. First, organicity is reflected more in the inatten-
tion measure than in the impulsivity measure. There are many reasons why a
particular brain may not be able to rise to the challenge, a prominent one being
minor traumatic brain injury, including birth injury. Impulsivity, by contrast,
can only be observed in brains with a certain level of functionality. Impulsivity
is deemed to lie almost purely in the functional domain. Almost any nervous
system capable of demonstrating impulsivity should also be capable of normal
behavior. The clinical evidence is increasingly bearing this out, as clinical skills
and methods improve. It has also been generally observed that inattention nor-
malizes more slowly than impulsivity. This helps to account for the fairly general
recommendation of 40 training sessions for the ADHD spectrum.
REFERENCES
1. Othmer S, Othmer SF, Kaiser D. 1999. EEG biofeedback: An emerging
model for its global efficacy. In Introduction to Quantitative EEG and
Neurofeedback. Evans JR, Abarbanel A, eds. San Diego: Academic Press,
243–310.
260 Neurofeedback in application to the ADHD spectrum
SIEGFRIED OTHMER
261
262 Conclusion
state to the level that the functional brain must ultimately do so. Whereas they
are sufficient to affect recovery broadly for mental dysfunctions, they are largely
deficit focused and have much less to offer the brain that is largely functional.
These methods are also prescriptive, falling into the standard medical approach
of “doing what we know is best,” in this case for the brain.
There is one instrumentally aided method currently in existence that allows
the brain to enhance its self-regulatory skills entirely without external direction
and at the level of discrimination at which the system actually needs to oper-
ate. That is the method of infra-low-frequency (ILF) neurofeedback, in which the
brain simply interacts with a correlate of its own activity. There is no externally
imposed challenge at all, and hence no intrusion into the regulatory process by
external inputs. There is no interrupt for the brain to contend with and fold into
its schema. This is the realm of skill learning at the very limit of the brain’s regu-
latory competence. The challenge of correction evoked in this process is entirely
endogenous. It is a matter of the brain reacting to its own appraisal of its regula-
tory status. The external signal becomes internalized, effectively, and fused into
one integrated regulatory response. This is a case of the brain encountering itself
more directly than it does in the course of life itself. In conventional skill learn-
ing, the brain refines its skills on the basis of feedback on its actions from the
external environment. In ILF training, that feedback loop is both shortened and
directed toward the process of regulation itself. If history is any guide, we are
only at the beginning of the exploration of the full potential of this method.
The second major concern is that the official description of ADHD appears to
have been shaped to match what stimulant medication is capable of remediating.
This does not match what parents are necessarily the most concerned about. There
is, for example, 60% comorbidity with oppositional/defiant disorder, a substan-
tial comorbidity with conduct disorder, and a large overlap with pediatric bipolar
disorder, as well as with Tourette syndrome. There is a substantial comorbidity
with the anxiety/depression spectrum. In addition, a majority of ADHD children
report sleep irregularities, and a large minority complain of chronic stomach and
head pain.
In the population seeking the benefit of neurofeedback for ADHD, there
is unsurprisingly a dearth of children who respond in classic fashion to stimu-
lants, and correspondingly a preponderance of children whose problems cannot
be resolved with stimulant medication. Hence, the neurofeedback practitioner is
typically contending with various comorbidities as well as with the cardinal mark-
ers of ADHD. Here is where neurofeedback truly distinguishes itself with respect
to the standard medical remedies. Neurofeedback is able to address multiple dys-
functions simultaneously, while stimulant medications are not. Furthermore, a
substantial fraction of children diagnosed with ADHD have a history of closed
head injury in early childhood. Stimulants do not help such cases, by and large.
Neurofeedback is the only known remedy for such cases. An even larger fraction
of ADHD children is afflicted with a specific learning disability or a sensory pro-
cessing deficit. In these cases, the resolution of ADHD symptoms with stimulants
is likely to be elusive, because these conditions can give rise to such symptoms.
Yet neurofeedback may well resolve both the learning disability and the sensory
processing deficits along with the ADHD.
If ADHD children are evaluated comprehensively, then it will be observed
that their dysregulation does not just manifest in executive function and in
motor function, but rather is observable broadly in their physiology. Autonomic
regulation is likely to be disturbed, for example. Emotional regulation is likely
to be deficient. In sum, it seems appropriate to think of ADHD as a founding
member of the class we are labeling “disorder of dysregulation.” Here, dysregula-
tion of neural networks is the defining issue. Brain function is not well-regulated,
and the consequences of that are observable variously in regulatory systems. This
model of ADHD receives further support when it is found that a strategy that
restricts itself to re-normalizing brain function is capable of remediating the
whole spectrum of symptoms that has been associated with ADHD, albeit some
more readily than others. If this model of ADHD is valid, then it should also
explain the effectiveness of stimulant medication. In this new frame, these are
seen as also re-regulating system status, albeit not as comprehensively and not as
organically as is the case with feedback.
Lines of argument similar to the above can be constructed for the anxiety/
depression spectrum, for pain syndromes, for sleep disorders, for minor trau-
matic brain injury (mTBI), and for other clinical conditions. These should all be
regarded in the frame of a disorder of dysregulation. This does not exclude from
consideration organic causation at some level, but it focuses matters on the core
deficit at issue and the aspect of the problem where resolution is likely to be found.
Conclusion 265
regulation was already in the model, so the impact on the bottom of the regula-
tory hierarchy was already seen as key to success in the training. Significantly, the
regulatory hierarchy outlined above also matches the developmental hierarchy.
One can therefore understand the arc of development of the ILF neurofeedback
protocols over the years as a progression (regression?) toward the early devel-
opmental stages as a training priority. This has meant a migration toward right
hemisphere training as a first concern, as well as a migration toward the lower
frequencies.
Yet another hierarchy is in play, namely that of the EEG spectrum. The lower
frequencies index the more basic, more persistent, and more broadly distributed
regulatory functions. The higher frequencies index progressively more transient
and more localizable functions as one moves up in the frequency spectrum. The
lower frequencies establish the context for the higher-frequency activity.
at the personal level, but systematically at the population level, just as in the case
of vaccines.
The above assumes that neurofeedback can in fact be helpful in staving off the
ravages of dementia. For that, we already have good evidence in case reports. In
numerous cases, clear cases of dementia have been reduced to below the level of
clinical significance by means of brain training, and the benefit has been sus-
tained for years with maintenance training. In the case of Alzheimer’s disease, it
is reasonable to estimate that symptom progression may be delayed on average by
2 years or more. That alone would be worth $50 billion to the American economy,
at a cost–benefit ratio of some 25 to 1.
NEUROFEEDBACK IN SOCIETY
If we elevate our gaze at this point to the problems faced not just within the health
care field, but in society at large, then we confront a number of critical concerns
to which neurofeedback is relevant. There is firstly the problem of school failure.
This in turn propagates to become a problem of criminality. Allied with that is
the general problem of substance abuse and drug dependency. Among the gen-
eral population, there exists an extreme level of stress that impinges negatively on
performance, quality of life, and success in parenting. It also leads to a worsening
of any propensity toward dysregulation that may have pre-existed, and thus to
the emergence of stress-related diseases. Finally, we then come to the dysfunc-
tions associated with aging. Already about 10% of the U.S. population is engaged
with the care of an elderly person at home. The stress of such situations leads to a
decline in life expectancy of caregivers, who now tragically sometimes even pre-
decease the person being cared for.
When surveying the field of education, one is struck by the complete absence
of any concern that is at all related to brain function. The entire field of education
272 Conclusion
model regards addiction first and foremost as a moral failing, and proceeds
from there. The predominant modality is individual and group psychotherapy,
delivered largely by non-professionals who were themselves addicts, and success
rests mostly upon the ongoing group experience of the 12-step program. One is
reminded of the time when society left lepers in the care of other lepers. Long-
term success rates are abominable.
The most startling statistic in the field of addictions treatment is that the
majority of those who recover do so on their own. The same phenomenon is
reflected in the observation that treatment success is greatest if the person took
the initiative to seek help. So who are the people who repeatedly fail to succeed
in treatment? It is of course predominantly the same group that has already been
identified, namely those with a developmental trauma history. These are typi-
cally now labeled “dual diagnosis.” These are not people who should be left to the
tender mercies of quasi-professionals. They should all have the opportunity to do
neurofeedback in the course of their therapy.
So where are we with neurofeedback in application to addictions? In the one
large-scale study in which standard treatment plus neurofeedback was com-
pared to standard treatment alone, outcomes in terms of sobriety were a factor
of three better than the controls after 1 year (nominally 75% versus 25%), but
the ratio kept rising over the years as the control group continued to attrition
through relapse. Clearly, something significant had been accomplished with the
neurofeedback training. When these people were asked about what accounted
for their success in maintaining sobriety, however, they uniformly credited their
group participation, not the neurofeedback they had done years before. These
people were still mostly craving their drugs, but group participation sustained
them in sobriety.
With the addition of ILF training, we have a much better chance to remedi-
ate the drug craving as well. The subsidence of drug craving was certainly part
of our experience in the earlier study, but it is more commonplace now. The
ILF training is impinging on the mechanism that sustains the dependency to
a greater degree than before. That is what a truly effective remedy must accom-
plish, and we appear to be well on our way to that goal. Another element may,
however, be needed.
Alcoholism treatment is unusual in that it sets an unrealistic goal for itself.
Where else in the treatment of major mental disorders is there the expectation
that a single treatment program over a set duration should yield success to the
end of life? Undoubtedly, this high expectation follows from the centrality of
the “decision to change,” the presumed life-altering aspect of the therapy. This
fails to give due respect to the primacy of the brain, and of its propensity to have
its way when its own imperatives are involved. Addiction remains a chronically
relapsing condition. Our triumphs in brain training are not always permanent.
In response to this baleful reality, the treatment program must be a per-
petual resource for the person. Whenever they see themselves at risk of relapse,
help must be immediately available. At best, the training would be available
to them on their home computer or even on their mobile phone, where their
personal training protocol would be installed. But a more personal therapeutic
274 Conclusion
process restores access to the emotional core, the self immediately assumes
occupancy, and what is true for sociopathy holds equally well for the intractable
conditions we see under many other designations. The healing of this rupture is
the essence of what ILF training can do for our collective mental health. Nearly
everything else is a grace note by comparison.
We are witnessing the emergence of a culture of estrangement in our society.
At the top, the ascendancy of the sociopathic mind installs an extreme individ-
ualism as the cultural ideal, whereas at the bottom, we see the propagation of
attachment-deprived child-raising from one generation to the next. In between,
we increasingly see individuals leading solitary lives that cultivate no abiding
bonds of affection. The first priority must be the restoration of the integrity of
the self, which can restore the capacity for developing healthy bonds and lasting
relationships. This is the agenda for a pathway back to mental health, and neuro-
feedback is the key to this societal transformation.
NEUROFEEDBACK IN EDUCATION
Brain training for school children will assume a place in the minds of parents
analogous to gym class. If a child might benefit from neurofeedback, then it is
in our society’s interest to provide the opportunity. Once again, the cost–benefit
ratio is substantial. Just as a solid case can be made for providing pre-school
opportunities to children, an even stronger case can be made for neurofeedback.
That is principally because this intervention works with even the most chal-
lenged children. School systems collectively expend 20% on special education
services, with a cost factor of 1.9 with respect to regular students. The addition of
neurofeedback to the special education curriculum would substantially decrease
the residence time in special education settings for most of these children. This
can be accomplished for less than the cost of 1 year of special services. The real
payoff to society, though, comes from the fact that the trained individual is much
more functional than would have been the case otherwise.
is breaking the boundaries on left hemisphere thinking that has constrained our
sense of self and shaped our modern institutions.
The right hemisphere is our experiencing self, and ILF feedback facilitates the
brain’s intimate communion with itself. When we invite the right hemisphere
to encounter itself in this manner, we build the capacity for nurturing the self
and fostering strong relationships. The promise of the future of neurofeedback
is a deepening of our understanding of the brain’s capacity for both healing and
optimal function. A future in which all may live up to their full potential is one
in which we should all want to live.
Structure of a typical chemical synapse
Neurotransmitter
Synaptic
vesicle
Neurotransmitter Axon
Voltage- transporter terminal
gated Ca2+
channel
Receptor
Post-synaptic Synaptic
density cleft
Dendrite
Figure 1.1 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.
Arousal
Figure 4.2 The arousal performance curve shows different states depending
on the arousal level.
Insulin le r level
ga
ve
Su
l
Normal blood sugar range
Hunger Hunger
Morning Evening
Wheat
Protein Lectins
Genetic
susceptibility
AI
Increased Environmental
intestinal triggers
permeability to • Dietary components
macromolecules • Toxic chemicals
• Infections
Autism
R L R L
Amy
STS
FG
FG
FG
x = 34 y = –55 z = –14
Normal
R L R L
Amy
STS
FG
FG
FG
x = 34 y = –55 z = –14
The book is written in an accessible style for easy understanding and application to classification
and treatment. It shares the clinical experiences of practitioners working with specific symptom
constellations generally categorized by a DSM diagnostic label. It examines the brain as a
self-regulating communications system and discusses how much of mental dysfunction can
be understood as acquired brain behavior that can be redirected with the help of EEG-based
neurofeedback. It describes principles and practices of integrating neurofeedback that make
redirection possible.
Recent discoveries on the neuroelectrical properties of the brain illuminate the possibilities of
combining innovative neurotherapy techniques with integrative medicine to achieve optimal
brain function. Case studies of clinical applications highlight the effectiveness of neurofeedback
in treating autism, ADHD, and trauma, particularly PTSD. Integrative approaches are the
future of health care, and neurofeedback will play an increasingly significant role. Restoring the
Brain: Neurofeedback as an Integrative Approach to Health is an essential reference for all
mental health professionals and those with an interest in the use and practice of neurofeedback.
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