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Theodore Wasserman

Lori Drucker Wasserman

Depathologizing
Psychopathology
The Neuroscience of Mental Illness and
Its Treatment
Depathologizing Psychopathology
Theodore Wasserman • Lori Drucker Wasserman

Depathologizing
Psychopathology
The Neuroscience of Mental Illness
and Its Treatment
Theodore Wasserman Lori Drucker Wasserman
Wasserman and Drucker PA Wasserman and Drucker PA
Powerline Road, FL, USA Boca Raton, FL, USA

ISBN 978-3-319-30908-8 ISBN 978-3-319-30910-1 (eBook)


DOI 10.1007/978-3-319-30910-1

Library of Congress Control Number: 2016933671

© Springer International Publishing Switzerland 2016


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Preface

Recently, we were sitting in a workshop that was describing the effects of toxic
stress on the development of young children. As you can imagine, these effects were
not good. The presenter did an impressive job of detailing the neurophysiological
reaction of developing brain networks to continuous stress. Problems with both con-
nectivity and recruitment of white matter connections in brain networks and the
deleterious impact that stress has on their development were discussed. There was a
clear and convincing demonstration of the interaction of an environmentally based
stressful experience (learning) and neural physiology detailing how the damage was
caused and what the long-term cognitive and emotional sequelae were.
After the presenter finished the formal presentation and called for questions, the
inevitable question arrived, “What can we do to fix this damage once it occurs?”
“Therapy” came as the answer. Just therapy. Nothing else was provided. While
some examples of things such as play therapy or even swaddling were shown, there
was no discussion as to why a particular technique should be selected or what
changes in an individual’s neural network functioning could be expected from its
utilization. There was no review of the science and discussion of a model behind a
particular intervention practice. Apparently all therapies were equal and valuable
and all were OK.
In almost any other branch of science that involves itself in the clinical treatment
of people, this answer would be wholly unacceptable. Imagine yourself confronted
with any of a number of medical issues. In those situations, we would all ask why a
particular treatment was being suggested and what the reasonable expectations of
success were.
This discussion highlighted a lack of symmetry in the field of mental health
today. Why is it that, in the mental health arena, the cause of an issue is usually
unrelated to its treatment? It is apparent that while our knowledge concerning the
neurophysiological presentation of many disorders of mental health is increasing
exponentially, we know far less about the impact of therapy on these same neural
networks. This is in large part true because the existing therapy models were devel-
oped independently of the issues they were designed to address. They were also
developed without an integrated understanding of the etiology of mental disorders.

v
vi Preface

They were developed in response to questions regarding why people became


dysfunctional, but developed within a universe that was in many respects free of the
constraint of the physical sciences, and in some cases represent philosophical posi-
tions as opposed to empirically verifiable facts.
To us, it appears that the sciences exploring the development and operation of the
human connectome advanced by recognizing the epigenetic interaction between the
individual and the environment in a manner that respected the neurophysiology of
the laws of learning, while in many respects, the field of therapy continued to
develop without recognizing these same facts. The current situation results in us
being certain in our recommendation for therapy as a general construct, while pro-
fessional courtesy and the lack of solid empirical proof as to a particular form of
therapeutic efficacy demand that many types of treatment are treated as if they all
have the same functional outcomes.
We recognize that there are numerous clinical outcome studies that show efficacy
for particular forms of treatment. These are often aggregate in nature. Groups of
people receive varying treatments for a particular disorder, and one group of people
does statistically better than another. While this has enabled practitioners to offer
treatment that is statistically better than chance, it does not tell us why a particular
technique is effective or how it changes the neural architecture of the individual to
whom it is provided. In particular, it does not specify how the person’s neural net-
work for learning, processing information, and behavior has been altered by the
intervention.
There are other problems as well. Ofttimes, varying forms of highly differenti-
ated treatment approaches can claim outcome studies supporting their efficacy for
the same types of difficulties. This is true even though within the statistically signifi-
cant samples there are those individuals that do not improve and individuals within
the nonsignificant samples that do. Finally, even though there might be data sug-
gesting that one therapeutic technique is superior to the others in the treatment of
specific mental health issues, there remains constituencies of practitioners that con-
tinue to utilize scientifically unsupported models based on case studies or their own
philosophical positions.
The result of this is that within the existing therapeutic paradigms, therapists still
have wide latitude, often free of empirical justification, in deciding what technique
they will use to address an issue. The zeitgeist of the field in general expects that all
of these choices must be respected. In fact it is true that training programs still train
therapeutic models that do not have and never had robust empirical justification for
their use. This would make some sense if all models of therapy were all equally
effective, but there is considerable research that suggests that this is not the case. To
us this situation is no longer acceptable.
We will show that this state of affairs was brought about because the research
into the etiology of most disorders of mental health was clearly not able to clarify
causation, and as a result, a system for classifying disorders based upon what behav-
iors they were comprised of was developed. As a result of this phenotypical type of
clustering of symptoms, physiologically heterogeneous problems were grouped
together solely because they produced the same or similar overt behavior. For exam-
Preface vii

ple, any child that failed to pay attention had a form of attention deficit hyperactivity
disorder. This less than perfect solution caused difficulties that continue to persist
and handicap the ability of the science to move forward.
One of the ongoing consequences for the failure to develop unifying models of
causation is the continuing absence of an underlying metric of causation against
which to compare the efficacy of various treatment models. Treatments were able to
be relatively nonspecific because they were targeting behaviorally defined criteria
as opposed to an integrated whole. For example, there are many ways to get a child
with attention deficit hyperactivity disorder to stop fidgeting, and if they all worked,
they would all be valid. There continues to be no central conceptualization for
developing treatment protocols.
We believe that it is time that this changed and that there is now sufficient infor-
mation available that will allow us to posit an underlying neurophysiologically
based learning model that accounts for a significant portion of those things currently
called disorders of mental health. We believe that many of the issues that confront
individuals in the mental health arena represent the interaction between the indi-
vidual neural network that regulates learning and the environment and that the
results of this interaction represent learned behavior. While it is true that each indi-
vidual brings to the situation a uniquely variable (as defined by patterns of connec-
tivity) neural network, it is also very true that each of these individualized networks
processes information according to the same rules. It would be possible then to
demonstrate how this learning occurs over an individual’s neural networks and
develop ways of impacting these networks that correct for faulty learning and estab-
lishing more adaptive patterns of association.
Simply stated, the laws of learning are not suspended for issues related to mental
health. If that is true, then it is possible to develop a system of learning that should
explain the etiology of mental health issues while at the same time underpinning all
therapeutic endeavors. In other words, a unifying model is now possible. It would
take the fusion of several fields to accomplish this. Contributions from psychology,
neurology, physiology, and epigenetics are all required.
This book represents the fruition of 10 years of discussion, learning, and research.
These discussions were not just between ourselves. They included colleagues in
many areas of academic study including the aforementioned neuropsychology, neu-
rophysiology, genetics, and neurology. Writing this book meant challenging many
of the foundational beliefs about what we had been told were the core pillars of
psychology as it pertains to the treatment of issues related to mental health. As we
developed our thinking and our model, we grew in the recognition that there was
something seriously wrong with the current concept of mental illness, and because
of that, treatment for individuals who were experiencing difficulty in adjusting to
the world around them was not as effective as it should be.
Without a fundamental redesign in our conceptualization regarding mental health
research, meaningful advancement in the field would not occur. That is largely
because, when we seek to investigate the etiology of heterogeneous disorders,
results get obscured. The same can be said for investigating effective treatment
approaches. Is it possible that the same intervention will be effective for a youngster
viii Preface

who fails to sustain attention and one who fails to pay attention to one stimulus
because his attention is captured by another? Even though they both might be
labeled with attention deficit disorder under the current system, we believe we could
answer that above question in the negative. Yet, in an aggregate treatment design, a
successful treatment intervention for one of the possibilities might be lost.
Although not the subject of this book, it should suffice to say that there has been
sustained criticism of the research on mental health. Much of the early work con-
cerned itself with methods that compared treatments to untreated control groups.
One major criticism is that, when you have just a treatment and a control group and
the treatment group shows greater improvement, you do not know why that occurred.
Something happened but just what it was is not articulated. Another of the major
criticisms is that the major method of investigation, controlled trials, has also failed
to be informed sufficiently by theory. This is largely because no integrated theory of
the factors related to the development and maintenance of mental health is univer-
sally accepted.
So, we arrive at last to the reason we wrote this book. We wrote this book to
propose a new model to conceptualize the neuropsychological nature of mental
health, its development, and its treatment when things go awry. The model we pro-
pose is based on the recognition that all human learning, even the learning involved
in development of skills related to mental health, is based on the epigenetic interac-
tion between the individual’s neural architecture and the environment that impinges
upon and shapes it. The model recognizes that there are clear principles that govern
how humans learn. These principles are not suspended and should not be ignored,
when the learning to be done is in the context of gaining skills related to mental
health or changing skills in the context of the therapeutic treatment of mental
illness.
When the mental health of the individual is compromised and treatment becomes
necessary, the implications of this model are clear. These principles effect learning
regardless of the therapeutic model being utilized or the therapeutic orientation of
the therapist. We believe therefore that it is incumbent for every therapist to be cog-
nizant of these principles and know how to incorporate them into their work. It is
incumbent on every therapist to understand how the learning experiences provided
as part of therapy interact with an individual’s neural architecture to create new con-
nections associated with, and supportive of, adaptive behavior. Finally it is incum-
bent on every therapist to understand the principles by which the connectionist
networks that lead to maladaptive behavior are reengineered. Without this knowl-
edge and its infusion into the everyday practice of treatment for mental health-
related issues, therapeutic practice will remain open to, and increasingly susceptible
to, scientific scrutiny and perhaps relegation to the judgment of history.

Boca Raton, FL, USA Theodore Wasserman


Lori Drucker Wasserman
Contents

1 Paradigm Shifts ....................................................................................... 1


2 Pathologizing Everyday Life .................................................................. 7
3 How We Learn: Models of Learning and Cognition............................ 13
4 A Proposed Learning Model for Therapy ............................................ 23
5 The Effect of Learning on the Development of the Connectome ........ 33
6 The Connectome and Emotion .............................................................. 45
7 Biologically Based Disorders of Mental Illness .................................... 57
8 Automaticity and Unconsciousness: What Are They
and What’s the Difference? .................................................................... 67
9 Mental Illness .......................................................................................... 79
10 Therapy .................................................................................................... 91
11 Historical Principles of Therapy and Information Exchange............. 101
12 New Principles of Therapy ..................................................................... 107
13 Tell Me How You Feel ............................................................................. 129
14 Case Studies ............................................................................................. 135
15 The Takeaway .......................................................................................... 149

Neurocognitive Learning Therapy: Clinical Teaching Guide ..................... 157

Index ................................................................................................................. 177

ix
Chapter 1
Paradigm Shifts

Q. Oh, oh, I’m sorry, you testified earlier that the boys went into the store and you had just
begun to make breakfast, you were just ready to eat and you heard a gunshot, so obvi-
ously it takes you five minutes to make breakfast.
A. That’s right
Q. So you knew that. Do you remember what you had?
A. Eggs and grits.
Q. Eggs and grits. I like grits too. How do you cook your grits? You like ‘em regular,
creamy, or al dente?
A. Just regular, I guess.
Q. Regular? Hmm. Instant grits?
A. No self-respecting southerner uses instant grits. I take pride in my grits.
Q. So, Mr. Tipton, how could it take you five minutes to cook your grits, when it takes the
entire grit-eating world twenty minutes?
A. I don’t know. I’m a fast cook I guess.
Q. I’m sorry, I was all the way over here, I couldn’t here you. Are we to believe that boiling
water soaks into a grit faster in your kitchen than in any place on the face of the earth?
A. I don’t know.
Q. Perhaps the laws of physics cease to exist on your stove? Were these magic grits? Did
you buy them from the same guy who sold Jack his beanstalk beans?
(My Cousin Vinny, 1990)

All of us, at one time or another, want to believe things that we were taught to be
true, or wish were true, would always remain true. Oftentimes these very same
things are in fact not true. They were never true, but they were in fact things that we
merely thought were true based on the science and understanding of the times.
Science and spiritual beliefs are replete with such examples. The homunculus, the
belief that the world is flat, or that the sun orbits the earth are examples of erroneous
beliefs consistent with knowledge available at the time. The belief that the sun was
carried by a chariot is now recognized as a myth. In a world of turmoil and uncer-
tainty, it is certainly comforting to have reasons and answers to things, even if the
particular set of answers are wrong. People tend to hold onto their beliefs with a
passion reserved for few things. In fact, research suggests that misinformed people

© Springer International Publishing Switzerland 2016 1


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_1
2 1 Paradigm Shifts

rarely change their minds when presented with the contravening facts and, in the
alternative, often become even more attached to their beliefs as they are threatened
(National Public Radio, 2010). As in the grits example above, even though we know
the laws of physics preclude certain possibilities, we hold onto our explanations and
attempt to mold new facts into our preexisting schema or data. This is true even in
the circumstance when our ability to explain the new phenomena requires us to
rethink some of our basic and passionately held premises. Ofttimes we save the
premise and throw out that inconvenient fact.
The science of mental illness and its treatment has had its fair share of beliefs that
were once popular, but later found to be inaccurate or just plain wrong. The idea that
autism was caused by “refrigerator mothers” is one example. Homosexuality was
only declassified as a mental disorder in 1973. While not an example of a specific
diagnosis, this book, in part, addresses several beliefs about mental illness that have
outlived their usefulness. One such belief is that disorders of mental health might be
meaningfully classified based on co-occurring behaviors or that that classification
would lead to a productive science of understanding the etiology of issues related to
mental health. A second belief is that consistently effective and predictable treatment
can be developed for disorders that were created using such a system. Still another is
that issues related to mental health occurred in a universe somehow independent of
the laws of learning and neurophysiology. The final belief that might have outlived its
usefulness, or at least overextended its reach, is the idea that medicalization of issues
related to mental health would lead to the most efficacious treatment interventions.

When Paradigms Shift

It is usually the case that in the fullness of time, science progresses, and the truth, or
something closer to the truth about a particular issue, presents itself. When this
occurs, these new ideas are not always easily embraced, and they are in many cases
resisted. We believe that just such a circumstance currently presents itself in our
understanding of mental health and mental disorders. We, among others (Insel,
2013), believe that the older models and understandings of the construct called
“mental Illness” are no longer sufficient and no longer match the available research
and should no longer serve as the basis of future research.
We believe that this opportunity of fundamental change in conception was cre-
ated when the worlds of neuroscience, genetics, mental health, and mental health
treatment, long separated by scientific custom, finally and appropriately began to
merge. By merging we do not mean just the recognition that altering certain neu-
rotransmitters can produce altered mood states. Although this was a tremendous
advancement in the field of treatment of issues related to mental health, the under-
standing that “brain chemistry” played a role in addressing mental health concerns
for some people did not bring about a fundamental paradigm shift. What we are
referring to is the idea that neurophysiology, genetics, and environment all operate
together to affect the individualized development of neural network architecture,
The Mind–Body Problem for Psychology 3

and the behavior that is based upon it and that the concept of mental health should
be understood from this perspective. Understanding mental health, and the genesis
of mental disorders in this way, requires a fundamental paradigm shift in the way we
conceptualize the construct of “mental illness.”
We believe 1. that there exists sufficient evidence, from a variety of fields that
demands that this existing therapy paradigm has seen its day and should be changed.
2. That there are rules of learning that govern all learning: emotional, physiological,
and biological. Every therapeutic technique should be cognizant of these rules in
order to understand how the neurophysiology of learning is being affected.
We wrote this book to outline the thinking required of this paradigm shift and
discuss what it would mean for the concepts of mental health and mental illness. It
is no small matter.

The Mind–Body Problem for Psychology

As we have suggested, paradigm shifts are a slow process as old beliefs tend to
remain quite vibrant. This is very true in the field of mental health treatment. Giving
testimony to this statement is the fact that for many people in the world of mental
health, treatment and research, the mind–body problem is alive and well. Stated
simply, the mind–body problem (Radner, 1971) is a philosophical one, asking how
we understand the relationship between the mind and the body. The mind is about
mental processes, thought, and consciousness. The body is about the physical
aspects of the neural architecture and how the brain is structured. The mind–body
problem is about understanding how these two interact. Historically, they were con-
sidered different and separate constructs that either operated independently or inter-
dependently. The mind was where emotions resided, and when these emotions
became disrupted somehow, many mental health problems resulted. While it is clear
that the two are closely related, mental processes often were conceptualized as dis-
tinct from physical processes and somehow independent of the physiology where
they nevertheless resided. Some philosophers held that mental properties involving
conscious experience had fundamental properties that were not governed by the
laws of physics, while the body had fundamental properties identified by a com-
pleted physics. We do not intend to examine the complexities of the mind–body
problem. What we would like to emphasize is that this separation has persisted and
has allowed mental health professionals to develop treatment strategies that ignored
the neurophysiology of learning and the neurology that underpins it. This, in ours
and others’ opinion, resulted in inefficient treatment approaches and compromised
therapeutic outcomes that did not stand the scrutiny of outcome-based verification
(National Institute of Mental Health, 2015).
Finally and appropriately, according to the National Institute for Mental Health,
the landscape for mental health intervention is now changing rapidly. New tools and
discoveries from genomics, neuroscience, and cognitive science have led to emerging
and quite different ideas about mental health in general and treatment targets across
4 1 Paradigm Shifts

mental illnesses in specific. Although it could be said that we are in the golden years
of psychopharmacology, the pharmacology industry has begun to back away from
investing in research and development for new medications. At the same time, insur-
ance companies have increasingly raised questions about the evidence base for non-
pharmacological treatments. Indicative of this increasing recognition of the
inadequacy of investigational models based on the existing mental health paradigm,
the National Institute of Mental Health (NIMH) has begun shifting its clinical trial
portfolio toward studies with defined targets and milestones in contrast to previous
studies that looked only for statistical differences in efficacy. This new NIMH exper-
imental medicine approach seeks trials that will also reveal more about the actual
neurophysiological or epigenetic mechanisms of disorders of mental health. There is
then increasing awareness that the mind–body distinction is a barrier to understand-
ing mental health, rather than a necessary precondition to understanding it. This is
because it has become increasingly clear that the dichotomy is a false one. Whatever
the monitoring and executive processes are that constitute the mind, they are con-
ducted over the same neural circuitry as everything else that is learned and processed
in the human brain (Bremner, 2002). It is surprising that it took so long to get to this
point. The paradigm is beginning to shift. What will replace it?

An Old Idea Reimagined

Adopting a paradigm shift inevitably means reevaluating long-held beliefs as they


relate to the new model. Historically, therapeutic intervention for mental health
problems placed great emphasis on the clearly established fact that the nature of the
relationship between the client and their therapist is an essential element to the
therapeutic process. Some (Rogers, Client Centered Therapy, 2003) argue that it is
the only thing that is meaningful. We do not seek to take issue with the value of the
therapeutic relationship. We do seek to point out that what occurs in the context of
this relationship is governed by the same laws of learning as any other interaction
between an individual and their environment. We believe that in the therapeutic
relationship as it exists, it is the role of the therapist to choose which ideas and
behaviors are, or are not, reinforced. This occurs in all therapeutic relationships,
although in some the therapist is quite directive and in others the therapist is less
overt about the activity. Even in nondirective treatments, the questions we ask, or
the client phrases that the therapist seizes upon to explore, shape through the pro-
cess of reinforcement (using the approval earned in the relationship) the direction of
the conversation. All learning is learning, and learning is governed by the same
principles whether it is learning how to drive an automobile, learning about the his-
tory of our country, or learning about ourselves.
In addition to introducing the reader to the new paradigm shift and outlining the
physiologically based principles of learning, this book is designed to teach both
therapists and their clients how these principles govern the way we learn and, by
extension, learn about our behavior and our mental health. Regardless of the type of
References 5

therapeutic relationship one prefers, all learning that occurs is over brain networks
that are recruited for specific tasks, but the connective properties of these networks
are always the same. Learning about ourselves in therapy is not different than any
other kind of learning in this regard. It is a synthesis of our neurophysiologically
based learning networks and the environment in which it operates.

References

Bremner, D. (2002). Does stress damage the brain. New York: W.W. Norton and Company.
Insel, T. (2013, April). Director’s blog: Transforming diagnosis. National Institute of Mental
Health. http://www.nimh.nih.gov/about/director/2013/transforming-diagnosis.shtml
Lynn, J. (Director). (1992). My cousin Vinny [Motion Picture]. Retrieved from Indiana School of
Law: http://www.law.indiana.edu/instruction/tanford/web/movies/MyCousinVinny.htm.
National Institute of Mental Health. (2015). NIMH strategic plan for research. Retrieved from
National Institute of Mental Health: http://www.nimh.nih.gov/about/strategic-planning-
reports/index.shtml.
National Public Radio. (2010). In politics, sometimes the facts don’t matter. Retrieved from
National Public Radio: http://www.npr.org/templates/story/story.php?storyId=128490874.
Radner, D. (1971). Descartes’ Notion of the Union of Mind and Body. Journal of the History of
Philosophy, 9, 159–170.
Rogers, C. (2003). Client centered therapy. London: Robinson Publishing.
Chapter 2
Pathologizing Everyday Life

In chaos, there is fertility.


Anaïs Nin

The world of mental health is in chaos. Ok, maybe not major chaos just yet, but
maybe it should be. So let’s call it impending chaos. Akin to the beginning of an
earthquake tremor, or the dark clouds of a hurricane on the horizon, the recent pub-
lication of the American Psychiatric Association Diagnostic and Statistical Manual
(Diagnostic and Statistical Manual of Mental Disorders, 2013) has in many ways
crystallized a growing chorus of criticism not only of the DSM system itself, but on
the science on which it stands and the definition of mental health that devolves from
it. This criticism raises questions about the very nature of what we define as mental
illness. For example, recently, there has been a number of works that challenge
existing assumptions about psychopathology. From Crazy Like Us (Watters, 2010)
which speaks about the spread of the American interpretation of mental illness over-
taking the views of other societies often with disastrous consequences to What Is
Mental Illness? (McNally, 2011), which directly questions the diagnostic systems
we use to identify problems with mental health, scientists are increasingly challeng-
ing the status quo concerning how we as a society define mental illness.

The Medicalization of Mental Health

In What Is Mental Illness? McNally highlights the increasing difficulty in distin-


guishing the concept of “mental disorder” and all that the classification includes,
from the differing degrees of what he termed “mental distress” in response to the
emotional enmeshments, breaks, or situational predicaments of everyday life.
Increasingly, he points out, these everyday problems that cause stress are being
made into medical disorders which then require a form of medical intervention to
resolve. The issues of the over-medicalization of mental illness have been the

© Springer International Publishing Switzerland 2016 7


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_2
8 2 Pathologizing Everyday Life

subject of numerous articles and books. McNally also points out the deleterious
consequences of being classified with a disorder. He identifies certain mental ill-
nesses, like multiple personality disorder, as representatives of an “interactive kind.”
These are disorders where psychiatric classification has a feedback effect on the
behavior of the people being classified, as well as beliefs, institutions, and practices.
His book, as well as others, decries the increasing medicalization of the concept
mental health or, more specifically, mental illness. Medicalization is not necessarily
a positive term. It describes the practice by which medical knowledge and perspec-
tive are applied to human conditions and problems which become increasingly
defined and treated as medical conditions, and thus become the subject of medical
study, diagnosis, prevention, or treatment. In its most pernicious form, it has been
described as disease mongering (Payer, 1992), which is a pejorative term describing
the practice of incessantly widening the diagnostic boundaries of illnesses and
encouraging public awareness of these new diseases. This is done in order to expand
the markets for those who sell and deliver treatments, which may include pharma-
ceutical companies, physicians, and other professional or consumer organizations.

The Boom in the Number of Mental Disorders

The effect of the medicalization is that there are increasing numbers of mental ill-
nesses and increasing numbers of individuals being diagnosed with medically
defined mental illnesses. For example, the most recent iteration of the DSM nosology
(DSM 5) added 15 new diagnoses to the 297 disorders in the DSM IV. In contrast, the
original DSM listed only 106 disorders. With the increased number of disorders
comes the natural consequence of increased number of people reaching criteria for
diagnosis. Whitaker (2010) points out that the number of people disabled by mental
illness in the United States tripled over the past two decades. In 2010, when his book
Anatomy of an Epidemic was published, 1100 adults and children were being added
to the government disability rolls because they had become newly disabled by mental
illness. Angell (2011) reports that a large survey of randomly selected adults, spon-
sored by the National Institute of Mental Health (NIMH) between 2001 and 2003,
found that an astronomical 46 % of them met established DSM criteria for having
had at least one mental illness within four major categories at some point in their
lives. The categories were “anxiety disorders,” including, among other subcatego-
ries, phobias and post-traumatic stress disorder (PTSD); “mood disorders,” including
major depression and bipolar disorders; “impulse-control disorders,” including vari-
ous behavioral problems and attention deficit/hyperactivity disorder (ADHD); and
“substance use disorders,” including alcohol and drug abuse. Most met criteria for
more than one diagnosis. Other studies have not yielded as high a percentage, but still
indicate that more than 25 % of the American public could be identified with a men-
tal illness (McLean, 2012). This study by Substance Abuse and Mental Health
Services Administration (SAMHSA), which did not include individuals with pri-
mary drug or alcohol problems, reported an overall rate of 20 % with individuals
Does Something Have to Be Broken in Order to Improve It? 9

between the ages of 18 and 25 experiencing the greatest number of instances of men-
tal illness, at 29.9 %. Twenty-two percent of adults ages 26–49 and 14.3 % of adults
50 and older experienced mental illness. McNally identifies the problem that many
of us see when we realize that perhaps nearly 50 % of the American population is
classified or classifiable as having a mental disorder when he talks about “pathologiz-
ing everyday life.” Wakefield (2007) described the problem thusly; “What do we
mean when we say that a problematic mental condition, such as adolescent antisocial
behavior, a child’s defiant behavior toward a parent, intense sadness, intense worry,
intense shyness, failure to learn to read, or heavy use of illicit drugs, is not merely a
form of normal, albeit undesirable and painful, human functioning, but indicative of
psychiatric disorder?” (p. 149). We would add the following; is it necessary to concep-
tualize all of these issues of everyday life as reflective of an illness in order to devise
effective treatment approaches? To that question we will answer with a resounding
“No.” For example, recent research supports the idea that disorders, such as obses-
sive–compulsive disorder, are the result of learned behavior and cognitive labeling as
opposed to a disease process (Gillan & Robbins, 2014). Gilliam and Robbins con-
clude that research evidence suggests that rather than goal-directed avoidance behav-
iors, compulsions in OCD may derive from manifestations of excessive habit
formation. They proposed that the irrational threat beliefs (obsessions) characteristic
of OCD may be a consequence, rather than an instigator, of compulsive behavior.

Does Something Have to Be Broken in Order to Improve It?

While it arguably can be true that nearly 46 % of Americans are mentally ill, a coun-
terargument is also possible. As we have indicated, this counterargument would
state that we have incorrectly made everyday distress and stress into a medically
defined mental illness. This counterargument states that we have overreached and
extended the idea of diagnosis too far. This counterargument would begin with cor-
recting a definitional problem in that everything labeled as a mental illness would be
considered as being caused by a medical condition. This does not have to be so, but
in practice, it is what is done. It is important to note that the diagnostic nomenclature
systems, either the DSM or the International Statistical Classification of Diseases
and Related Health Problems (ICD), are etiologically silent as they make no state-
ment as to causality in the field of mental health. Historically, the ICD was devel-
oped to provide physicians with uniformity in the description of diseases for
statistical purposes (Moriyama, Loy, Robb-Smith, & Robb-Smith 2011). The
assumption that mental health disorders identified through these systems represent
medical conditions are then made by the users once the diagnosis has been made.
We in fact assume that we are looking for a type of illness when we commence the
diagnostic process by collecting symptoms to compare to the criteria of the diagnos-
tic system. We diagnose mental illness by the use of observable behavior or by
verbal report. In medicine this would be akin to diagnosing all individuals with a
pattern of red bumps on their chest as having measles.
10 2 Pathologizing Everyday Life

While we do not for a minute doubt or dispute that there are certain conditions of
mental disturbance that represent medical conditions requiring medical interven-
tion, we do seriously doubt that the majority of individuals diagnosed as ill under
the current system are indeed ill as a result of a medically determined disease pro-
cess. While we do not doubt that individuals experience stress, distress, and discom-
fort in their everyday lives, we would point out that there is increasing evidence that
these problems do not require a medical procedure to correct them. What is more,
the process by which these behaviors have become problematic had nothing to do
with disease progression, but rather reflected a predictable pattern of learned inter-
action between the individual and the environment.

Medicalization Is Not the Only Way to Understand Problems


with Mental Health

While we would add our voices to those who believe that the current system which
understands that problems with adjustment as medical issues is outdated, we also recog-
nize that it is not sufficient or productive to carp. If our current models of mental illness
and the treatments that are based on them are in part in error, then it is the obligation of
science to develop better models. This is because there remains societal need for a uni-
form language that describes mental illness. Until a new system is created, the old one
will have to do (Jabr, 2013). While we do not pretend to be able to replace the entire
system, we are prepared to offer what we believe to be an effective alternative to under-
standing the genesis of mental problems, the diagnostic system used to describe them,
and the treatments that devolve from the system. The model we propose is based on an
understanding of neural networks and their interaction with the environment based on
connectionist learning theory (Thorndike, 1932). Our model integrates genetic predis-
position and the development of integrated neural networks from a vertical brain per-
spective (Koziol & Budding, 2009). For example, it is now well understood that genetic
programming in utero can interact with the uterine environment in an epigenetic manner
to produce adverse neuropsychiatric outcomes (Bale & Erperson, 2015). Further under-
standing regarding how these areas work together to produce behavior would contribute
to a reconceptualization of the concept of mental illness.
While we will raise many issues, one thing is central to our discussion. Stated
simply, it is that the concept of an illness is not required to understand the etiology
of a large number of problems currently considered to represent some form of ill-
ness, nor to formulate effective treatment options for many of the issues that present
themselves for treatment.

Elements of Another Way

There are many elements that will be recognizable in the work. In some senses our
model has elements of a diathesis (vulnerability)-stress model (Ingram & Luxton,
2005) in that we will explain certain elements of behavior as occurring because of a
Questions 11

predispositional neurobiological vulnerability that interacts with life experiences


which are in some instances stressful (Lazarus, 1993). Diatheses include a wide
variety of vulnerabilities including biological, cognitive, genetic, and physiological
factors. They have even been conceptualized to include temperamental or
personality-related factors. Interestingly enough, diatheses include early life experi-
ences such as the loss of a parent and situational factors, such as low socioeconomic
status or having a parent with depression. All of these represent the potential for the
development, through learned experiences, of difficulties. We will argue that these
vulnerabilities in and of themselves do not represent illness per se, but rather the
potential for the development of problematic behavior depending on the learned
environmental interaction with the environment. Our model also includes elements
of what have been termed biomedical models in that we will describe the systems
that support and maintain the behaviors as brain-based neural connectivity systems
that work in a highly integrated vertical brain orientation (Koziol & Budding, 2009).
We will argue that for the most part, these connections are the result of learned
experiences and are neither permanent nor unchangeable. We will further posit that
it is the epigenetic interaction between the environment, what is learned from it, and
the genetic predisposition that produce many adverse conditions of mental health.
We will also, of course, review neurodevelopmental disorders as those that are
based on a fundamental defect in the connectome and discuss why a separate nosol-
ogy might be necessary to understand these problems.

Questions

What do we mean when we talk about an individual’s mental health or mental


illness? Is mental health status just the accumulation of our learning experiences
as they interact with the environment, or are there structural abnormalities in the
learning system that produces deficient learning? Might the field be better served
by delineating three types of mental health issues (those caused by faulty learn-
ing, those caused by faulty physiology, or those caused by a combination of the
two)? We recognize that we cannot definitively answer these questions at the
current time, but there are rapidly clarifying suggestions that can be made. The
most basic is that learning is a process, and mental health is the result of this
process and in some instances our neurophysiological integrity. This book is an
attempt to help the reader integrate the two in a therapeutic, and by extension,
mental health context. While we do not have all the answers, research from our
field, in conjunction with associated fields, is yielding sufficient information to
allow us, with a good deal of certainty, to better direct our therapeutic efforts.
Information will allow us to discuss how specific interventions might work to
repair those same networks that have been negatively impacted or the kind of
experience that would predictably provide the learning that the system needed to
restore better functioning.
12 2 Pathologizing Everyday Life

References

Bale, T., & Epperson, N. (2015). Sex differences and stress across the lifespan. Nature Neuroscience,
18(10).
Diagnostic and statistical manual of mental disorders (5th ed.). (2013). Washington, DC: American
Psychiatric Association.
Gillan, C., & Robbins, T. (2014, November 5). Goal-directed learning and obsessive-compulsive dis-
order. Philosophical Transactions of the Royal Society B, 369(1655), 20130475. doi:10.1098/
rstb.2013.0475. Retrieved from http://rstb.royalsocietypublishing.org/content/369/1655/20130475.
full.pdf+html
Ingram, R., & Luxton, D. (2005). Vulnerability-stress models. In B. Hankin & J. Abela (Eds.),
Development of psychopathology: A vulnerability stress perspective (pp. 32–46). Thousand
Oaks, CA: Sage.
Jabr, F. (2013, May 7). No one is abandoning the DSM, but it is almost time to transform it.
Retrieved from Scientific American: http://blogs.scientificamerican.com/brainwaves/2013/
05/07/no-one-is-rejecting-the-dsm-but-it-is-almost-time-to-transform-it/
Koziol, L. F., & Budding, D. E. (2009). Subcortical structures and cognition: Implications for
neuropsychological assessment. New York: Springer.
Lazarus, R. S. (1993). From psychological stress to the emotions: A history of changing outlooks.
Annual Review of Psychology, 44, 1–21. doi:10.1146/annurev.ps.44.020193.000245.
Lynn, J. (1992). My cousin Vinny (motion picture). Retrieved from Indiana School of law: http://
www.law.indiana.edu/instruction/tanford/web/movies/MyCousinVinny.htm
McLean, B. (2012). Survey finds many living with mental illness go without treatment. Retrieved
from National Alliance on Mental Illness (NAMI): http://www.nami.org/Template.cfm?
Section=top_story&template=/contentmanagement/contentdisplay.cfm&ContentID=138381
&title=Survey%20Finds%20Many%20Living%20with%20Mental%20Illnes
McNally, R. (2011). What is mental illness? Boston, MA: Belknap.
Moriyama, I., Loy, R., & Robb-Smith, A. (2011). A history of the statistical classification of dis-
eases and causes of death. Bethesda, Maryland: National Center for Health Statistics.
Payer, L. (1992). Disease-mongers: How doctors, drug companies, and insurers are making you
feel sick. New York: Wiley. ISBN 978-0471543855.
Thorndike, E. (1932). The fundamentals of learning. New York: AMS Press. ISBN
0-404-06429-9.
Wakefield, J. (2007). The concept of mental disorder: diagnostic implications of the harmful dys-
function analysis. World Psychiatry. 6(3): 149–156.
Watters, E. (2010). Crazy like us: The globalization of the American psyche. New York: Free Press.
Whitaker, R. (Spring 2005). Anatomy of an epidemic: Psychiatric drugs and the astonishing rise of
mental illness in America (PDF). Ethical Human Psychology and Psychiatry (Springer) 7 (I): 1.
Retrieved October 11, 2010.
Chapter 3
How We Learn: Models of Learning
and Cognition

In the animal kingdom, the rule is, eat or be eaten; in the human kingdom, define or be
defined.
Thomas Szasz

The Mind–Body Problem

The mind–body problem has bedeviled psychology for over a century (Psychological
Wiki, 2014). The mind–body problem is a historical issue rooted in philosophy that
concerns itself with how to understand the relationship between the construct of the
mind and the physical body. At the outset let us point out that the mind is a construct
rather than a physical entity. “In a word “Mind” as we actually find it, contains all
sorts of laws—those of fancy, of wit, of taste, decorum, beauty, morals and so forth
as well as perception of fact (James, 1878, p. 3).” In brief the mind was there to do
the thinking while the body was there to do the physical reacting. While historically
most everyone acknowledges that mind and body are closely interconnected, mental
phenomena are often seen as distinct from physical phenomena and therefore gov-
erned perhaps by different fundamental laws. Early experimental psychologists of
the nineteenth century worked within departments of philosophy, and they consid-
ered themselves as “scientific philosophers” (Reed, 1997). Their goal was to study,
in a scientific manner, the fundamental nature of the conscious mind. Given their
placement within departments of philosophy however, it is not surprising that philo-
sophical constructs were introduced into their thinking. As a result, what we now
know as academic psychology originated in a blending of the experimental methods
of physiology with the speculative theories of philosophy. This leads to some inter-
esting considerations. For example, Murphy (1949) proposed that this type of think-
ing had a long history suggesting that early humans thought that a “detachable soul”
contained our fundamental human nature. It would follow that if this soul could
detach from the body, it could survive the body’s death, supporting the idea that the

© Springer International Publishing Switzerland 2016 13


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_3
14 3 How We Learn: Models of Learning and Cognition

soul’s essence must differ from the body’s essence. Therefore, if the human mind is
located within the nonphysical soul, then the mind’s essence also must differ from
the body’s essence.

The Psychological Sequelae of the Bifurcation of Reality

This bifurcation of the laws of reality has had its consequences on the development
and operation of psychological science. One of these consequences is that the failure
to resolve the mind–body problem has enabled the development of clinical treatments
designed to address the properties of the mind that are able to ignore the body’s physi-
ologically based fundamental laws of human learning. It was as if the mind was gov-
erned by a different set of factors that governed its functions, and humans apart from
every other animal species operated with a different and fundamentally separate group
of learning principles that controlled their emotional lives. Humans were governed by
ids, egos, and superegos or personality types that could be identified through the out-
flow of information or judging and perceiving. These drives or forces had little to do
with how people academically or physiologically learned, areas that were historically
assumed to involve nonemotional engagement, or how that new learning resulted in
improved functioning in those “cool” areas of dispassionate learning. These forces
only governed learning of emotionally related behaviors and were only concerned
with the learning of emotionally regulated adaptive or maladaptive behavior. This
separation and creation of an alternative learning universe for emotionally based stim-
uli have persisted to the present moment. This situation is no longer acceptable. We
are not alone in this belief. Others have begun to identify the same issue and call for
change. For example, Karlsson (2011), in summarizing existing research, stated that
it has become clear that all mental processes derive from changes in the brain and that
the traditional dichotomy of psychotherapy being for “psychologically based” disor-
ders, while medication is for “biologically based” disorders, was “unfortunate.”

The Laws of Learning Are Never Suspended

We posit and believe that the science will show that the laws of learning are not
suspended for the human emotional realm and are not unique to humans although,
humans are able to exponentially use these laws to produce functioning that far
exceeds any other animal. We will demonstrate that there are networks of the brain
that are devoted to both reward recognition and attentional arousal that do a per-
fectly acceptable job of explaining emotional engagement. Then we will take pains
to point out that anyone seeking to work with people in order to have them under-
stand both how their response patterns are either adaptive or maladaptive, and then
how to change them, will have to understand how those patterns of behavior are
acquired and maintained. Anyone seeking to alter maladaptive behavior or thought
Learning Models: A Very Brief Tour of the Landscape 15

will have to become adept in creating learning environments and situations that
effectively facilitate the learning of new behaviors. It is equally important for their
clients to understand these same laws. As we shall see, effective learning requires
active and engaged learners.

We Are Always Learning

From the moment you arrive in the world, you are learning. It is unavoidable. The
human brain is receiving stimulation and processing data constantly. That is what it was
designed to do. Its activities are initially centered on making analyses related to the fol-
lowing simple questions. Can I eat it? Does it represent a threat? Did I like it in the past?
If, for learning to occur, all that was necessary was to receive and record data,
everything would be simple, and learning across all people would be rather uniform.
We would just have to present information and people would, sponge like, absorb it.
That is however, not what happens. We learn in context to both where we are and
what we have previously learned. The initial three analyses become vastly more
complex and intuitive. These analyses and classifications color how the information
is learned. For example, a housewife in New York typically would be repulsed by
the site of scores of dead cockroaches in her kitchen, unless she was from, for
example, Thailand and had just brought home a pint of fried cockroaches from the
delicacy store. One of Thailand’s most popular snacks is Jing Leed, a deep-fried
cricket seasoned with a soy sauce derivative and pepper. Other favorites include
grasshopper, woodworm, bamboo worm, and Maeng Da, or 3.5 inch-long water
beetles. Clearly, edible sources of protein accepted or rejected from our diets based
upon what we have learned to eat.
Learning new material also requires effort and attentional focus. Learning is an
active, not a passive, process. Learning is such an extremely complex process that
no one theory or model has been developed that is able to explain it exhaustively,
and describing the process remains a subject of considerable debate.
We want to be clear that the following is merely the briefest of summaries and is
designed to acquaint the reader with some of the basics. The volume of scientific
knowledge on human learning is enormous and increasing exponentially. The inter-
ested reader is directed to Guadagnoli (2008) or Ormrod (2014) to begin their review.
We will first look at models of learning and then look at models that discuss how
information is transmitted over the neural networks that subserve these models.

Learning Models: A Very Brief Tour of the Landscape

Learning is a complex construct. The complexity and depth of the topic have
resulted in the lack of a universally accepted definition. One reasonable psychologi-
cal/physiological definition is that learning is a more or less permanent change in
16 3 How We Learn: Models of Learning and Cognition

behavior (action) potential that occurs as a result of practice. It is not, therefore, a


change due to motivational factors, sensory adaptation, fatigue, maturation, senes-
cence, or stimulus change. This implies that learning refers to relatively stable
changes within the organism, as opposed to more transient states such as moods
(Mikulas, 1977). This definition makes a clear distinction between learning as a
physiological process and the factors that affect learning such as motivation. It also
makes a distinction between learning as a physiological process and the processes
that support learning such as attention. Defining learning as a change in behavior
potential distinguishes between the concepts of performance and learning. Learning
has a hypothetical limit; it partially determines what the organism is capable of
doing. Performance is what the organism actually does. According to Mikulas
(1977), it is often motivational variables that keep performance below potential.
Reinforcement history, the determinant of motivation, is a crucial determiner of
what gets remembered and what does not. In other words, motivation (reinforce-
ment history) gates learning. We will discuss this later in more detail.
In therapy, as in all other areas, learning is about creating new connections between
bodies and elements of knowledge. One vector for this learning is the connection
between new information and existing information, but that is not the only one.
Another vector is the connections created between elements or bodies of existing
knowledge. This is the basis of creativity, looking at things from new and differing
perspectives. Still another vector is looking at existing information and creating infer-
ential constructs. In addition to focusing on expanding connections between elements
of knowledge, therapy should also concern itself with identifying and/or establishing
key learning concepts or schemata that form the basis for future learning.

The Components of a Learning Model for Therapy

The model that we will propose has its feet firmly embedded on two traditional
learning schools, constructivism (Bruner, 1966; Piaget & Inhelder, 1972), and con-
nectionism (Thorndike, 1932). It is reflective of the Unified Learning Model (Shell
et al., 2010), which represents an attempt to integrate these two schools.

Constructivism

Constructivism posits that a basic principle of human learning is pattern matching.


These patterns are essentially groups of related objects (spoons) or things (animals).
These patterns/groups are called schemas. Humans generate knowledge, meaning, and
emotional responsivity from an interaction between their existing schemata (themes),
experiences, and their analysis of the results of that interaction. In short, learners build
knowledge out of their own experiences, which helps explain why each learner builds
a unique body of knowledge. Constructivism requires an active learner. The
Constructivism 17

constructionist model posits that learning is not a continual stimulus response process,
but rather a process of building self-regulated conceptual structures through reflection
and abstraction (Von Glasersfeld, 1995). We would add that both reinforcement history
and experience are critical in determining the content of these schemas. There is a
specific role for the therapist within a constructivist model. Constructivism’s core tenet
is that knowledge is not transmitted from a mentor to a mentee. Constructivism posits
that knowledge is actively constructed in the mind of the learner.
Constructivism differs from many other learning theories in that it is not a purely
cognitive model. It provides an essential place for emotional engagement (motiva-
tion). Constructivism proposes that learning takes place when learners are engaged
in purposefully meaningful activities (Kafai & Resnick, 1996). We would interpret
this statement as meaning that in constructivism, forming a relationship with the
material that engages an individual’s reward circuitry is a crucial step in the process
of constructing or creating new knowledge.
Hein (1991) described two outcomes important for a therapist who was trying to
impart knowledge to an individual, both of which are related to the core idea that
constructing meaning is learning; there is no other kind. The implications for a
therapist were as follows:
1. The therapist must focus on the learner (client) and how they will incorporate the
new knowledge, not on the subject/lesson to be taught.
2. There is no knowledge independent of the meaning attributed to experience
(constructed) by the learner (client).
The above implies a number of constructivist learning principles which impact
and should guide key processes in therapy. Based on the work of Hein (1991)
expanded to describe their implications within a neurocognitive learning model,
they can be described as follows:
1. Learning in therapy is an active process in which the client (learner) gates sen-
sory input and constructs meaning out of it. It is not a passive acceptance of
knowledge which exists, but involves the learner (client) actively engaging with
the material in a purposeful way.
2. Clients learn to learn as they learn: they construct systematically more advanced
and complex schema. Learning in therapy consists both of constructing mean-
ing and constructing systems of meaning. Because human learning consists of
pattern matching, each meaning we construct makes us better able to give
meaning to other sensations which can fit a similar pattern.
3. The crucial action of constructing meaning is neurophysiologically based and
involves brain circuitry dedicated to learning and reinforcement recognition.
4. The language we use influences learning. Language and learning are inextrica-
bly intertwined.
5. Learning in therapy is a social activity involving an analysis of our relationships
with other important human beings in our lives. To be useful, knowledge
acquired in therapy must be applied and practiced within the context of our new
and existing relationships.
18 3 How We Learn: Models of Learning and Cognition

6. Learning in therapy is contextual. We learn in relationship to what else we


already know and what we already believe. In therapy we cannot append adap-
tive knowledge to a set of maladaptive preexisting knowledge. New skill sets
must be developed and practiced.
7. It is not possible to assimilate new knowledge without having some structure
developed from previous knowledge upon which to build. The more we know,
the more we can learn. Therefore, any effort to teach must be connected to the
state of the client and must provide an unambiguous path into the subject for the
learner that emanates from the learner’s (client’s) previous knowledge.
8. Learning is not instantaneous. Significant learning requires the revisiting of
ideas in many contrasts and situations. Clients must recognize old ideas as mal-
adaptive and actively seek to replace them with new ideas based upon a founda-
tion of new learning and successful application.
9. Motivation is a key component in learning. Not only is it the case that motiva-
tion helps learning, it is essential for learning. The reward recognition circuit is
the essential gating in selecting knowledge to be learned.
10. Maladaptive behavior and thought are based upon automaticity. The adaption
of new schema implies that the old schemas are no longer automatically
selected. This at first is a conscious and planned process of selection.

The Role of a Therapist Within a Constructivist Model

The primary role of the therapist within a constructivist model is to support the
client and facilitate knowledge acquisition as opposed to didactically imparting it.
We would add that helping the learner incorporate new knowledge is not a passive
or haphazard process. The therapist would be required to have some clear under-
standing about where they wished to go. Another essential task of the therapist is
to insure that the client is actively involved and engaged in the learning process.
The therapist in a constructivist model asks, rather than tells, questions and chal-
lenges causing the client to think through their answers as opposed to relying on
automatically produced responses. The therapist provides guidelines and creates
the environment for the learner to arrive at his or her own conclusions. A therapist
is a facilitator that is in continuous dialogue with the learners. The therapist should
also be able to adapt the learning experience “in mid-air” by “taking the initiative
to steer the learning experience to where the learners want to create value.”
(Rhodes & Bellamy, 1999).
All of this does not imply that the therapist is nondirective. Much to the contrary,
the therapist must be aware of how humans learn and help guide the client to struc-
ture and view experiences to facilitate new learning. As our model stresses, the
recognition that reward circuitry plays an essential part in the direction and alloca-
tion of attentional and working memory resources to learning a specific task, it is
often dependent on the therapist to highlight the potential rewards and benefits of
new behaviors to clients who may be predisposed not to see them.
Blended Connectionist Models 19

Historical Connectionism

For Thorndike, one of the founders of the connectionist model, learning resulted
from associations forming between stimuli and responses. These associations or
“habits” become strengthened or weakened by the nature, intensity, and frequency
of the S–R pairings. The paradigm for S–R theory was trial-and-error learning in
which certain responses come to dominate others due to rewards. In Thorndike’s
model, there were four essential principles that covered learning:
1. Laws of effect/exercise: Learning requires both practice and rewards.
2. Law of readiness: A series of S–R connections can be chained together if they
belong to the same action sequence.
3. Transfer of learning occurs because of previously encountered situations.
4. Intelligence is a function of the number of connections learned.
The neurocognitive learning model we propose also integrates a connectionist
model that recognizes that neuropsychologically and neurophysiologically classical
S–R pairings as described by Thorndike are represented neurophysiologically by
white matter connections in integrated neural circuits. The above principles govern
the development of these circuits.

The Role of the Therapist in a Connectionist Model

The therapist plays a more active and, in many respects, directive role in a connection-
ist system. The primary objective in a connectionist model is to engage in processes
that result in classification, generalization, and schema formation of adaptive response
patterns (Parkins, 2013). This means arranging, planning, and implementing thera-
peutic activities designed to strengthen the adaptive associations between behaviors
and positive emotional responses and decreasing the strength of connections between
behavior and maladaptive emotional responses. This goal can be achieved by focus-
ing on either the classically conditioned maladaptive responses or on the operant rein-
forcement patterns that are assessed as maintaining the inappropriate target behavior
or emotional response. More specifically, the classically conditioned maladaptive
response can be addressed either through extinction or counterconditioning proce-
dures; the operant responses can be targeted through contingency management or
coping skills training (National Center for Biotechnology, 2015).

Blended Connectionist Models

The classic connectionism of Thorndike has been developed and expanded in many
ways. There are blended models such as trimodal learning theory (Rumelhart &
Norman, 1978). Rumelhart and Norman postulated three modes (stages) of
20 3 How We Learn: Models of Learning and Cognition

learning: accretion, structuring, and tuning. Accretion is the addition of new


knowledge to existing memory. Structuring is the application or relating that knowl-
edge to a task. Tuning is the adjustment (or fine tuning) of knowledge to a specific
task usually through practice. Accretion is the most common form of learning;
structuring occurs much less frequently and requires considerable effort; tuning or
practice is the slowest form of learning and results in expert performance. Accretion
is similar to the notion of schema (Piaget & Inhelder, 1972) and clearly constructiv-
ist in origin. Structuring and tuning are more connectionist in origin.
While connectionist neurophysiologically, ours is a blended model when it comes to
understanding the processes of learning within a therapeutic environment. That is
because it recognizes the importance of central themes (schemas) and understands the
connectionist relationships of these schemas. As we will see later, these relationships are
best represented by brain organization networking models known as small-world hubs.

References

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Ormrod, J. (2014). Human learning (6th ed.). New York: Pearson.
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practices. New York: Springer.
Thorndike, E. (1932). The fundamentals of learning. New York: Teachers College Press.
Von Glasersfeld, E. (1995). Constructivism in edcuation. In T. Husen & N. Postlewaite (Eds.),
International Encyclopedia of Edcuation (p. 10). Oxford: Pergamon Press.
Chapter 4
A Proposed Learning Model for Therapy

Conjecture implies that information is incomplete, and so it surely is with human learning.
On the other hand, we assert that more than enough is known to sustain a “scientific” model
of learning.
(Shell et al., 2010)

All of what we have just discussed allows for the development of a learning model that
would apply to all types of therapy for mental health problems. Whatever the technique
or model being used, these principles would govern how knowledge is generated and
retained. The model that we developed is heavily indebted to the Unified Learning Model
(ULM) (Shell et al., 2010) and combines elements from constructivist, but especially
connectionist cognitive learning models, neuropsychology, and basic learning theory.

What Is the Unified Learning Model?

The Unified Learning Model (ULM) was proposed as a model that integrated
current theory and research in learning, and applied this integrated model to issues
in teaching and instruction. The ULM integrates three aspects of cognition: (a) crys-
tallized intelligence (knowledge) as represented by accumulated knowledge stored
in long-term memory, (b) fluid intelligence as represented by working memory
capacity, and (c) motivation which is considered to be a product of working mem-
ory allocation. The ULM is a blended connectionist model. It also has constructs
like core flexible networks and understands that there are knowledge chunks that
constitute the indispensable building blocks of knowledge. For example, one has to
learn the constructs of addition, subtraction, and multiplication in order to do math.
These core constructs are found in all later and complex forms of mathematics.
Similarly, the construct of government is core to any discussion of forms of govern-
ment, ethics, or human rights. Our model understands these core constructs as con-
structionist schemata that are connected and reconnected in connectionist networks
based on small-world hub models.

© Springer International Publishing Switzerland 2016 23


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_4
24 4 A Proposed Learning Model for Therapy

As indicated, the ULM is based on a rather simple premise that three


components underlie all of human learning. These are working memory, knowl-
edge, and motivation. Working memory is defined as temporary storage and
processing of information. The way in which working memory is constructed
and operated determines how things are learned. Working memory stores infor-
mation in identifiable patterns or schemas that are pulled out when new infor-
mation is encountered. This is an important construct for our therapy model as
it recognizes that working memory is based on knowledge, which is in turn
based on the network’s response to the stimuli it receives. The second core
component, knowledge, essentially is defined as every piece of information we
have stored within long-term memory. Knowledge, within the ULM, has a two-
fold role. First and foremost is that the purpose of learning is to increase the
data in long-term storage (increase or change knowledge). Knowledge then is
what results from the proper functioning of working memory. Knowledge has
a second function in that it influences the functioning of working memory. The
way working memory encodes new information is directly constrained by the
existing knowledge base in long-term memory. This is because new knowledge
is constantly being compared to, and appended upon, old knowledge. New and
old knowledge meet in memory store. The result of this meeting is that each
works upon the other and produces new knowledge which is then returned to
long-term memory. This is an important construct within our neurocognitive
learning model because it indicates that no two sets of knowledge stores are
identical. It accounts for the individuality and uniqueness of each person who
creates knowledge. The third component of the ULM is motivation. While
there are many definitions and models of motivation, the ULM defines motiva-
tion quite specifically as the impetus for directing working memory, and atten-
tion, to a particular task. It is therefore, along with attention, an essential
component of working memory.
The interplay of the components results in the three basic principles of learning
for the ULM which have their implications for therapeutic learning. They are:
1. Learning is a product of working memory allocation.
2. Working memory’s capacity for allocation is affected by prior knowledge.
3. Working memory allocation is directed by motivation.
In direct terms, people only learn what they pay attention to, and what they
pay attention to is directed by what they already know and what they find rein-
forcing. Clinically speaking, this means that if I have a tendency to pattern
match a new incoming stimulus as reinforcing, I will allocate my working
memory to it and learn it. For example, I may love to debate issues and now
want to learn strategies for public speaking. It also means, however, that if I
perceive a threat, because historically my threat centers were easily engaged,
then I will feel anxious and threatened in most new situations. Ultimately, I
won’t enroll in anything new or perhaps, in the extreme, not even go near social
events.
A Word About the Neurophysiology of Learning 25

General Rules of Learning

The ULM develops additional principles of learning that are based upon the
neurobiology of learning and are incorporated into the therapeutic interaction for a
vertical brain model. These are as follows:
1. New learning requires attention. Only those items that are being attended to will
be candidates for working memory store.
2. Learning requires repetition. Learning is pattern recognition. Those patterns that
are recognized and routinely retrieved from store are utilized and generalized.
We would add that those patterns are associated by repetition and reinforcement
to the arousal centers located in the limbic system. Any new learning is attached
to existing schemas, and each set of these existing schemas (represented neuro-
anatomically and neurophysiologically as small-world hubs) has a motivational
and emotional response associated with it.
3. Learning is about connections, in that what is stored together stays together in
memory. Appropriate or socially acceptable responses can be stored with socially
unacceptable responses should that association be reinforced. Given the right set
of motivational circumstances, inappropriate responses can be stored.
4. Some learning is effortless and some requires effort. The goal of learning is
automaticity. That is, the goal of learning is to have some complex connections
between elements of data available to the learner without effort. People will
automatically associate and continue to associate emotional states with events
without cognitive effort to change those associations. The goal of therapy is to
make new, essential connections as efficient and automatic as possible.
5. Learning is learning. While all neurons learn in exactly the same way, people uti-
lize these processes idiosyncratically. Motivation is particular to the individual.

A Word About the Neurophysiology of Learning

Recent research has made it increasingly clear that learning is based on changes in syn-
aptic connections, and these changes in synaptic connections are affected by the products
of specific genes which are expressed under specific conditions. Learning, therefore, is
the product of a consistent and ongoing interaction between the individual’s experiences
and their genetically derived predispositions. This interaction has been termed epigenetics
(Elman et al., 1996). Epigenetics basically posits that behaviors and experience interact
with physiological, cognitive, and emotional predispositions to produce current behavior
(Atzaba-Poria, Pike, & Deater-Deckard, 2004; Buehler & Gerard, 2013). Available
research suggests that current behavior reflects the accumulation of all these interactive
events. Rutter (2002) points out that a number of factors including susceptibility genes,
environmentally mediated causal risk processes, nature-nurture interplay, the effects of
psychosocial adversity on the organism, the causal processes responsible for group dif-
ferences in rates of disorder, and age-related changes in psychopathological characteris-
tics all play a part in the development of complex adaptive and maladaptive behavior.
26 4 A Proposed Learning Model for Therapy

Competence

The term competence has been used to refer to the result of these accumulated
experiences when a pattern of effective adaptation within an environment is achieved.
Competence results from complex interactions between a child and their environ-
ment (Marsten & Coatsworth, 1998). In the context used herein, it implies that the
individual has (or lacking competence does not have) the capability to perform well
in the future. An individual who lacks competence in an environment becomes self-
aware and engages in negative self-appraisals. These negative self-appraisals are
reinforced and reproduced regularly until they are automatically associated with a
class of behaviors. These automatically associated appraisals are experienced as
affect states such as depression and anxiety. That is, in part, because the physiologi-
cal responses associated with these affect states are also associated, through the same
principles of learning, to the cognitions associated with the appraisals.
While it is clear that there are numerous complex and interactive factors that
influence development of adaptive or maladaptive behavior, it is also clear that
these influences must be processed through the human learning system. There is
only one such system composed of specific circuitry recruited as necessary. All
human learning is the result of the operation of this system. Information travels
over the same networks and is encoded by the same memory, goal seeking, and
reinforcement identifying systems. This system processes all sort of informa-
tion, both positive and negative. Specific learning experiences govern the devel-
opment of the neural architecture to be sure, but the system’s properties and
functioning are governed by a constant and unchanging set of operational rules.
In more direct terms, all learning is learned in the same way and there are ways
to make that learning efficient. Research has identified numerous neural struc-
tures that are involved in this network (McClure, York, & Montague, 2004).
Essentially this network governs reward processing and reward-dependent
learning. McClure et al. identified a set of reward-related brain structures linked
together in a small-work connectionist system including the orbitofrontal cor-
tex, amygdala, ventral striatum, and medial prefrontal cortex. How information
is transmitted over the networks is increasingly being elucidated. What is
important here for us to understand is that environmental experiences are evalu-
ated in terms of their reward potential, and it is this determination that is the
basis of what is learned and what isn’t.

Knowledge

At the neurophysiological level, knowledge is what is stored in long-term


memory. It results when groups of interconnected neurons, whose connections
have been repeatedly strengthened, fire together. There are several types of
knowledge.
Semantic Knowledge 27

Episodic Knowledge

Episodic memory is memory of the significant moments of our lives. It can be


acquired effortlessly; it just happens to us or through considerable effort. It can be
very general, but is oft times quite detailed. An important feature of episodic
knowledge is that it is attended to automatically. Most episodic memory is not
relatively long lasting. While it is true that significant events are retained, usually
because we replay these events and talk about them, most of the things that hap-
pen to us are not retained. For example, you might remember where and when you
went shopping yesterday, but can you remember where and when you went shop-
ping last month or last year? This is because most episodes in our lives are rela-
tively unimportant from a learning standpoint and are not connected with other
learning events and are not rehearsed. Simply put, they are attended to (the first
rule of learning), but are not repeated (the second rule of learning). As a result of
their lack of connectedness, they are often not recalled and connected with new
information. After a while, these memory bits fade. On the other hand, some
events are highly arousing and therefore motivational. These events are frequently
recalled and related to new knowledge as it is attended to. They become major,
automatically produced themes, and are appended in working memory to many
events. Some of these themes may be socially approved of and societally appro-
priate, and even encouraged. Some of these motivational themes may be societally
sanctioned or clinically inappropriate. These central themes are the basis of many
of the disorders that present to a therapist.

Semantic Knowledge

Semantic knowledge refers to knowledge about things other than our own personal
life experiences. Semantic knowledge can exist within episodic contexts, but it
does not require those contexts. The life courses of episodic and semantic knowl-
edge differ greatly. Episodic knowledge starts out as chunks, rich in detail and
emotional overlay, and, as the associations decline from lack of continued use,
becomes smaller and smaller, ultimately becoming merged within an overall life
script. Semantic knowledge starts out as a single unassociated chunk and over time
merges with other chunks by being associated and integrated into a network of
information. Semantic knowledge acquisition requires effort to both process and
encode. Interestingly, most cognitive therapeutic approaches are heavily semantic,
while many analytic and humanistic approaches tend to focus on the importance of
episodic memory. We propose a blended model incorporating both episodic and
semantic elements stressing the important interplay between the two to allow for
the client to alter automatically accessed schemata. We recognize, for example,
that episodic knowledge can, and is included within semantic knowledge as an
example of a specific theme or idea.
28 4 A Proposed Learning Model for Therapy

Declarative Knowledge

Declarative knowledge is usually thought of as fact and figures. Declarative


knowledge is usually split into two categories: objective knowledge defined as
knowledge of objects and actions in the outside world and symbolic knowledge
that includes the meaning of words, moral codes, and laws. Both objective and
symbolic knowledge are learned through the allocation of working memory by the
first three rules of learning: attention, repetition, and connection. The base unit of
declarative knowledge is the chunk.

Procedural Knowledge

Declarative knowledge does not produce any action that is the domain of procedural
knowledge. Procedural knowledge produces action. It directs motor output. While
declarative knowledge exists as a memory to be activated, procedural knowledge is
goal directed. It directs both cognitive and motor behavior. Procedural knowledge is
easily thought of as if–then knowledge; if something is happening, then do this.
Procedural memory and the actions related to it have received increasing attention
and, in many ways, serve as the raison d’etre for vertical brain models of cognition
(Koziol & Budding, 2009).

Automaticity

The goal of procedural knowledge, which often contains a declarative element, is


automaticity. Active working memory and transfer of information involve effort,
and the amount of effort that people can expend in this area is physiologically lim-
ited (Callicott et al., 1999). In addition, there are many situations where active, or
controlled, working memory is not adaptive. For example, imagine playing catch
and someone throws a ball at you. If you had to think about the entire process, the
ball would hit you before you could raise your arms. Controlled processing is rela-
tively slow and laborious. The more we practice a procedural event however, the
less we have to think about it and the quicker we become. The goal is to make the
thought and motor response chain automatic, that is, to perform the action instantly
upon recognition. A procedure that has achieved automaticity can run itself. What
occurs is that the initial sensory input to working memory pattern matches and
retrieves the first declarative condition chunk. The entire chain in the procedure then
fires without additional monitoring or involvement from working memory. This
process is termed a habit. When these automatic response chains produce maladap-
tive procedures and we must change an automated process, we must de-automatize
it. This is the process of therapy. Our model recognizes that to de-automatize a
Chunking to Learn 29

maladaptive procedure and create a new adaptive procedural chain, specific-directed


allocation of attentional resources is required. This concept is important as it implies
a more directed and targeted process than what is used in many nondirective
approaches. Without directed allocation of working memory, nondirective
approaches result in many false starts and allocation of working memory to proce-
dures that would not, in the end, result in adaption.

Chunking to Learn

A memory chunk can be considered as an interconnected unit of knowledge, stored


in long-term memory, and retrieved into working memory as a unit. As human
memory is limited, chunking is the strategy we use to correct for this problem. The
easiest example is the following. Read the following numbers only once and then
try to repeat them:
5-0-2-3-7-5-7-9-8

Most people cannot successfully repeat the series because of the limits of their
working memory. Now try it again like this: 501-237-5798. It is easier because yes,
it occurs in the familiar pattern of a telephone number. There are now three chunks,
each of which is a small enough amount to be efficiently handled by available work-
ing memory. Our therapy model considers chunked knowledge to potentially repre-
sent thematically based schema. Human knowledge expansion is based upon
constantly reviewing and modifying schematically based information. To demon-
strate this we will use the example of a schema of a car. At the first encounter, when
we are young, with the term car and its real-world representative, our knowledge is
quite limited. We may remember a car as something having wheels and being able
to move about. Likely, we identify a car as the type of vehicle our parents owned.
This initial chunk is stored in memory and retrieved the very next time the knowl-
edge of car is retrieved from long-term memory store. Perhaps on this next retrieval,
we modify the chunk by adding color or a steering wheel or radio. The modified
chunk is then returned to working memory. This process of identification, retrieval
modification, and return to storage happens every time the knowledge of car is
accessed from long-term memory to working memory. The chunk (schema) is con-
stantly modified, expanded, and refined until it can be quite complex and refined.
This process is how humans continually learn. If, along the way, we were involved
in a car accident and were injured, negative arousal states would become associated
with this chunk (schema). As a result, every time we see a car, we might become
anxious. This becomes the basis of a maladaptive response.
The learning rules governing chunks of information are the same as the rules
governing single units of knowledge. Any chunk that is not retrieved and modified
begins to fade because connectivity is not maintained. This is why repetition
and review are essential to learning. This is also why not merely accessing the
same concept repeatedly in exactly the same way is a productive learning strategy.
30 4 A Proposed Learning Model for Therapy

Only by using the concept in different ways and in different circumstances are new
connections created and learning taking place. Piaget and Inhelder (1972) effec-
tively describe this process using the terms equilibration and accommodation, and
the interested reader is directed to his work for a thorough review of constructivist
learning theory.
Connecting declarative and procedural knowledge into larger overlapping
networks that associate specific chunks together in different ways is the goal of
complex learning. One can think of the schema of a car as a mechanic would, or
as the owner would or a designer, city planner, environmentalist, engineer, or a
banker would. What’s more, people who are both owners and road designers,
and maybe environmentalists, would be able to think of the chunk or schema
cars in various ways depending upon the circumstance. The viability of these
connections does not seem to be solely based on the strength of connections
based on repetition. There seems to be an active, motivational, and volitional
component involved.

Hierarchies

Declarative knowledge is structured in hierarchies (groups of overlapping and


increasing embedded schema) that allow for more efficient storage and access. This
also allows various elements of hierarchies to be pulled together and their similari-
ties compared and contrasted. Think about the concept of hierarchy of “animal” and
the schemas of dogs and cats, for example. Dogs and cats share similar elements
that are together in the “animal” hierarchy and can also be separated in their indi-
vidual respective hierarchies. If all of this were completely automatic, the compari-
sons would be impossible to make. These linkages between hierarchies are called
networks, and the ability to make connections between various networks is a com-
ponent of complex learning.

Critical Thinking

Critical thinking can be defined as the ability to retrieve knowledge in situations


that have never been encountered before and use the retrieved information to
help resolve the problem currently being encountered. We engage this activity by
recognizing pattern matches between the new situation and networks recruited to
solve similar problems and then associating those existing networks with the new
situation. This is why, upon encountering an unspoiled lake full of fish, an envi-
ronmentalist might think of protection, a fisherman might think of food, and a
real estate developer might think of resort. Critical thinking happens in working
memory. Newly encountered situations are rapidly compared with existing
Critical Thinking 31

hierarchical networks looking for points of similarities. When a pattern match is


found, a new connection is made, and the new information stored as part of a
newly configured network. Obviously, a new situation can create pattern match
with several networks at once, thereby creating a bridge between networks or
even a newly integrated network consisting of previously unrelated ideas.
Something like that happened in the game of American football which was ini-
tially a running-only game. The rules were changed in 1906, and the previously
illegal forward pass was now legal. A new schema was created overnight, and the
modern game of football was born. Prior to that moment, the running/football
network was unconnected with any concept of throwing catching and then run-
ning the ball. Once the connection was made, it caused a network change and
continued to develop.
We can, therefore, summarize knowledge acquisition into a set of basic
knowledge-related processes that govern the process of therapy. We will list them
here, but go into more detail later:
1. If knowledge in long-term memory is retrieved, the strength of association
between these items in working memory is increased. How things are presented
and grouped in working memory determine what procedures will be developed.
2. If a knowledge chunk is retrieved, all other chunks to which it is connected are
retrieved, and all connections between these retrieved chunks are strengthened
(small-world hubs).
3. If parts of retrieved knowledge match to working memory contents, they are
strengthened. If parts of retrieved knowledge do not match to contents in work-
ing memory, they are weakened and inhibited. Therefore, establishing new pat-
tern matches (schemata) is an essential component in therapy.
4. Episodic learning is easy. Semantic knowledge is difficult.
5. If an action is successful, its connection to the knowledge of the situation in
which it occurred is strengthened. If an action is unsuccessful, its connection to
the knowledge of the situation in which it occurred is weakened or inhibited.
New procedures must be understood and conscientiously practiced.
6. If knowledge has been retrieved, new information in working memory will be
connected to this knowledge. This is the basis of establishing new adaptive
procedures.
7. Any active knowledge in long-term memory is accessible to working memory.
In our model, as in many theories of learning, one major goal is to create core
flexible networks that can be readily adapted to newly encountered situations.
The core flexible networks (schemata) constitute the building blocks for future
interaction and adjustment to the environment. Our model postulates that these
networks can be targeted, modified and/or efficiently created through direct
instruction, thereby compensating for past learning deficiencies. That is not the
entire goal of learning. What is also critical is that we assist in the production of
a response tendency in the individual that would encourage that person to bring
these networks to bear on new situations.
32 4 A Proposed Learning Model for Therapy

References

Atzaba-Poria, N., Pike, A., & Deater-Deckard, K. (2004). Do risk factors for problem behaviour
act in a cumulative manner? An examination of ethnic minority and majority children through
an ecological perspective. Journal of Child Psychology and Psychiatry, 45(4), 707–718.
doi:10.1111/j.1469-7610.2004.00265.x.
Buehler, C., & Gerard, G. (2013). Cumulative family risk predicts increases in adjustment difficul-
ties across early adolescence. Journal of Youth and Adolescence, 42(6), 905–920.
Callicott, J., Mattay, V., Bertolino, A., Finn, A., Coppola, R., Frank, J., et al. (1999). Physiological
characteristics of capacity constraints in working memory as revealed by functional MRI.
Cerebral Cortex, 9(1), 20–26.
Elman, J., Bates, E., Johnson, M., Karmiloff-Smith, A., Parisi, D., & Plunkett, K. (1996).
Rethinking innateness: A connectionist perspective on development. Cambridge, MA: MIT.
Koziol, K., & Budding, D. (2009). Subcortical structures and cognition. New York: Springer.
Marsten, A., & Coatsworth, J. (1998). The development of competence in favorable and unfavor-
able environments. American Psychologist, 53, 205–220.
McClure, S., York, M., & Montague, P. (2004). The neural substrates of reward processing in humans:
The modern role of FMRI. Neuroscientist, 10(3), 260–268. doi:10.1177/1073858404263526.
Piaget, J., & Inhelder, B. (1972). The psychology of the child. London: Routledge.
Rutter, M. (2002). Nature, nurture and development: From evangelism through science toward
policy and practice. Child Development, 73(1), 1–21.
Shell, D., Brooks, D., Trainin, G., Wilson, K., Kauffman, D., & Herr, L. (2010). The unified learn-
ing model. New York: Springer.
Chapter 5
The Effect of Learning on the Development
of the Connectome

People often say that this or that person has not yet found himself.
But the self is not something one finds,
it is something one creates.
Thomas Szasz

What Is a Connectome?

The connectome is a term used to describe a comprehensive map of the neural white
matter connections in the brain. The human brain is believed to have between 86 billion
and 100 billion individual neurons, each making on average about 10,000 connections.
Approximately 100,000 miles of axons serve as information highways between the inter-
connected neurons (Lent, Azevedo, Andrade‐Moraes, & Pinto, 2012). The connectome is
then a wiring diagram of the white matter connections between and among structures in
an individual’s brain. It is important to note that these connections are not hard wired.
There are pathways and routes that are traveled, but there are neurochemical intersections
that allow pieces of the pathway to be used for different routes. These neurochemical
intersections are called synapses. There is then a related term, the synaptome—the set of
all synapses in a brain region. Synapses themselves are highly complex, consisting of up
to 1000 diverse protein molecules. Each of these may act independently, as a “switch” for
cellular signaling. The synaptome is believed to be the site of learning, memory, and
retrieval occurring at molecular states at each synapse of the connectome. A human brain
is an amazingly complex organ containing some 700 trillion synaptic connections (What
is the connectome, 2014). What is important for us to understand, is that this complexity
is also its beauty. Connections of the human connectome are in large part, but not abso-
lutely, due to the experiences that that connectome has with the environment. The con-
nectome is being continually shaped, formed, and altered by learning.
Any discussion of the connectome includes a discussion of a second type of
brain matter, gray matter, which are the regions connected in the system by the

© Springer International Publishing Switzerland 2016 33


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_5
34 5 The Effect of Learning on the Development of the Connectome

white matter. This gray matter is responsible for higher-order cognition and
information analysis. The white matter connects various gray matter areas (the
locations of nerve cell bodies) of the brain to each other and carries nerve impulses
between neurons. White matter, long ignored or dismissed by research scientists,
has taken on increasing importance in the last 10 years as it is now recognized that
it actively affects how the brain learns and functions. While gray matter is primarily
associated with processing and cognition, white matter modulates the distribution
of action potentials, acting as a relay and coordinating communication between
different brain regions. An action potential is the change in the electric potential of
an individual neuron when it fires. White matter, which lies beneath the gray matter
cortex, is composed of millions of bundles of axons (nerve fibers) that connect
neurons in different brain regions into functional circuits (Fields, 2010). White
matter neurons are coated with a fatty myelin sheath which acts as an insulator,
increasing the speed of transmission of all nerve signals (Fields, 2008a). White
matter tracts are the structural highways of our brain, enabling information to travel
quickly from one brain region to another region (van den Heuvel, Mandl, &
Hulshoff-Pol, 2009). There is evidence that spontaneous and automatic (not in reac-
tion to a stimulus) activity of these large-scale neural systems of the brain is not
random, but orderly and organized based on the resting-state operation of specific
functional networks that maintain, at all times, a high level of coherence. What is
critical to understand is that these networks of spontaneous activity (resting-state
networks or RSN) are closely related to the underlying anatomical connectivity, but
their topography is also gated by the history of prior task activation. Therefore,
network coherence does not only depend on covert cognitive activity, but its strength
and integrity relates to behavioral performance and learning as well (Deco &
Corbetta, 2011). The base system performance reflects anatomical preconditions
and learning, and the operational result is the indivisible product of the two.

The Development of the Connectome and Psychopathology

The human connectome is the result of a complex developmental trajectory (van den
Heuvel et al., 2014). The purpose of the development of these networks is to insure
the development of key neural networks that govern all aspects of cognition (Menon,
2013). Aberrations in the development of any of the networks contribute to psycho-
pathology. Humans are born with a functional but rudimentary connectome, orga-
nized in a stable, small-world fashion, which integrates key networks to insure initial
survival and support future learning. van den Heuvel et al. (2014) examined the
architecture of the human neonatal anatomical brain network and found clear evi-
dence of small-world modular organization (more on that later) before term birth and
that this network was available for environmental interaction and modification.
Specifically, their analysis of functional neonatal connectivity (FC) showed the early
formation of resting-state networks and that developmental changes to this network
involved an increase in integration capacity and complexity. Research also demon-
strates that the early structure and developmental iterations of these networks are
Small-World Hubs 35

essential for the development of higher-order skills such as language (Elman, 1993).
Just as critical is the research that demonstrates the heterogeneous pattern of changes
across developing functional systems that map the external world onto the brain’s
attentional, sensory, emotional, and motivational subsystems (Menon, 2013).
One of the subcortical nodes that feature prominently in the development of
these functional networks is the basal ganglia, which plays a prominent role in both
reward saliency and habit formation (automaticity). Therefore, environmental
interaction and experience plays a role in the development of the networks, and this
can lead to poor outcomes that we label as psychopathology. For example, depending
on the pattern of reward and habit formation, issues can arise in nodes being hypo-
or hyper-connected to each other. Hypo-connected nodes involving the posterior
cingulate cortex have been identified in children with autism, while hyper-connected
nodes involving the substantia nigra or the ventral tegmental area with limbic reward
regions have been demonstrated in children with attention deficit hyperactivity
disorder (Tomasi & Volkow, 2012). To sum this up, we are born with a rudimentary
connectome designed to allow us to function at a very basic level and with
considerable support, outside the womb, and this connectome has the capability to
expand and adapt to the environment in which it finds itself.

How Does the Connectome Organize Itself in Response


to Learning?

Research has shown a high level of functional connectivity within resting-state net-
works of the brain, which suggests the existence of direct neuroanatomical connections
between these functionally linked brain regions that subserve ongoing interregional
neuronal communication (van den Heuvel et al., 2009). These resting-state networks
represent what the brain is doing when it isn’t directed to any specific task.
Research has shown that clearly identifiable white matter tracts interconnect at
least eight of the nine commonly found resting-state networks, including the default
mode network, the core network, primary motor and visual network, and two
lateralized parietal-frontal networks. As we have seen, we are born with these
networks in rather fundamental form, and they are developed through a process of
interaction with the environment. It is these networks that are recruited as needed
when we are asked to perform a specific task.

Small-World Hubs

One way to represent these networks is called graphical analysis. Graphical analysis is
basically a statistically driven graph of the relationship between variables, in this case
brain regions. In a review of graphical analysis of connectionist models of cognition,
Bullmore and Sporns (2009) suggest that complex cognitive functioning is best repre-
sented by a connectionist small-world hub model of neural networks. Small-world neu-
ral network models are based on the concept of nodes which represent the confluence or
36 5 The Effect of Learning on the Development of the Connectome

connectivity points of neurons. Research has demonstrated that brain networks have
characteristically small-world properties of dense or clustered local connectivity (nodes)
with relatively few long-range connections to other similarly dense nodes. Nodes cluster
together in small networks and vary to the degree of how central they are to the connec-
tions to other small clustered networks within the system. These nodes are complex
networks containing billions of nerve cells interconnected to other nodes by trillions of
fibers. The nodes of a small-world network have greater local interconnectivity or
“cliquishness” than a random network, but the minimum path length between any pair
of nodes is smaller than would be expected in a regular network.
Small-world networks are valuable models to use when evaluating the connectivity
of nervous systems because the combination of high clustering and short path length
between nodes provides a capability for the network to perform both specialized and
modular processing in local neighborhoods and distributed or integrated processing
over the entire network (Achard, Salvador, Witcher, Suckling, & Bullmore, 2006).

Integrated Brain Circuitry

a b

Central module Parieto-frontal module Medial occipital module

Lateral occipital module Fronto-temporal module

Reprinted with permission (Meunier, Achard, Morcom, & Bullmore, 2009).


Small-World Organization of the Brain 37

Small-World Organization of the Brain

Reprinted with Permission (Hagmann et al., 2008).

In the current learning model, we propose that a particular small-world hub is the
neurophysiological representation of a constructivist schema where the connections
between the elements of the hub have been strengthened over time by connectionist
principles. These nodes and small-world networks, integrated with clusters of other
networks, represent schemas interacting with other schemas, which are all related to
central themes. Increasing data from connectionist models (Chaytor & Schmitter-
Edgecombe, 2007) and from connectionist vertical brain models suggest that this
view is supported and that cognitive functioning is best represented by integrated
small-world hub-based networks with specific brain regions being recruited by a num-
ber of cognitive systems and activities. For example, Simões-Franklin, Hester,
Shpaner, Foxe, and Garavan (2010) found that the dorsal anterior cingulate cortex
(ACC) played a crucial role in executive function, while Menon and Uddin (2010)
found evidence from network analysis suggesting a critical role for the insula, particu-
larly the anterior division, in high-level cognitive control and attentional processes.
38 5 The Effect of Learning on the Development of the Connectome

Vandewalle et al. (2009) found that under conditions of sleep deprivation, individuals
recruited supplemental anterior frontal, temporal, and subcortical regions in order to
maintain executive regulation over activities.
Following the historical model of studying damaged areas, most research looking
at the role of white matter in relation to mental health concerned itself with damage
to the white matter or structural deficiencies of the white matter. And research had
demonstrated the association between psychiatric disorders and damage or disease
affecting the myelin sheath on nerve fibers. For example, inferior frontal white mat-
ter microstructure has been associated with impulsivity and aggression in men with
schizophrenia (Hoptman et al., 2002). More recently, white matter defects have also
been associated with a wide range of psychiatric and neurological disorders (Fields,
2008a, b). Schizophrenia, chronic depression, bipolar disorder, obsessive–compul-
sive disorder, and post-traumatic stress disorder have all been recently associated
with white matter defects. Similarly, neurodevelopmental cognitive and emotional
disorders including autism, dyslexia, and attention deficit hyperactivity disorder
have been associated with white matter changes. Both bipolar disorder and major
depressive disorder involve alterations in white matter tracts or myelin genes. Finally,
microstructural abnormalities in prefrontal white matter have been found to occur
early in the course of major depressive disorder and may be related to the neuropa-
thology of depression throughout adulthood (Li et al., 2007).

Neural Networks and Mental Health

More recently, research has begun to focus on and demonstrate how neural networks
play a role in mental health issues. For example, mental health status is generally
associated with appropriate physiological responses to environmental and
homeostatic challenges. In particular, the reestablishment and maintenance of
physiological homeostasis, and the related control of anxiety responses, entail the
coordinated activation and control of neuroendocrine and autonomic stress systems.
Recent research demonstrates that stress responses are mediated by largely
overlapping white matter circuits in the limbic forebrain, the hypothalamus, and the
brainstem. This permits respective contributions of the neuroendocrine and auto-
nomic systems to the fine tuning of stressor modality and intensity. In addition, the
limbic circuits that are responsible for regulating stress responses intersect with
circuits that are responsible for memory and reward, providing a means to
demonstrate learning of the stress response with respect to prior experience and
anticipated outcomes (Ulrich-Lay & Herman, 2009).
Studies of psychopathology are increasingly focused on how connectivity-based
disturbances involving distributed brain areas operating within large-scale brain net-
works contribute to emotional dysregulation (Menon, 2011). For example, Fornito,
Zalesky, and Breakspear (2015) found that pathological disruptions of brain circuitry
are rarely confined to a single locus. Rather, they often spread via axonal pathways to
influence other regions. They postulated that patterns of disease propagation are
constrained by the extraordinarily complex, yet highly organized, topology of the
The Effects of Therapy on the Connectome 39

underlying neural architecture, the so-called connectome. They concluded that network
organization fundamentally influences brain disease, “and a connectomic approach
grounded in network science is integral to understanding neuropathology” (p. 159).
Highlighting this connectome model, which features increased activation and network
recruitment, the work of Thiel et al. (2014) has demonstrated that individuals with
obsessive–compulsive disorder processed stimuli associated with a hand washing com-
pulsion in a manner different than that of normal controls (Thiel et al., 2014). They
found that when viewing aggressive pictures compared to neutral stimuli, OCD patients
demonstrated greater activation than controls in the right frontal gyrus, posterior cingu-
late cortex, insula, claustrum, and in parietal areas of the left hemisphere. There was no
structural deficiency noted. There was only increased activity suggestive of increased
connectivity. While there are several ways for this to have occurred, one logical way
was to propose that the connections were strengthened by practice and eventually auto-
maticity. Simply stated, the increased activation was the result of learning. That leads
us to the question of whether there are white matter changes that occur in response to
learning. The answer is a resounding “yes.” Recent research has substantiated the effect
of therapy on the human connectome.

The Effects of Therapy on the Connectome

Learning involves changes in strength of synapses, the connections between certain


neurons arrayed in hubs in gray matter. Human brain imaging using magnetic
resonance imaging (MRI) has revealed structural changes in white matter after
learning complex tasks. This has raised the question of whether white matter
responds to experience in a manner that affects neuron function under normal
circumstances, thereby affecting information processing and performance (Fields,
2010). Fields (2010, p. 769) speculates “perhaps white matter differences that
correlate with scoring on intelligence quotient tests (Schmithorst, Wilke, Dardzinski,
& Holland, 2005) and certain psychiatric conditions can be attributed in part to a
direct role for white matter in learning and cognitive function.” This hypothesis has
been confirmed in many studies which show that learning a new skill is associated
with altered white matter structure in the mature brain. Recent research has begun
to identify particular white matter tracts that are associated with different learning
skills such as mathematics (Matejko & Ansari, 2014). They identify an expanding
body of research that uses diffusor tensor imaging to explore how individual
differences in brain microstructures relate to different numerical and mathematical
abilities. This research has identified several tracts associated with numerical and
mathematical abilities such as the superior longitudinal fasciculus, the posterior
segment of the corpus callosum, inferior longitudinal fasciculus, corona radiata, and
the corticospinal tract. They also report that impairments in mathematics tend to be
associated with atypical white matter structures within similar regions, especially in
inferior parietal and temporal tracts. Similarly, Schmithorst et al. (2005) in an earlier
work found a positive correlation of fiber density, axonal diameter, and myelination
in white matter in a left temporoparietal area which was associated with higher
40 5 The Effect of Learning on the Development of the Connectome

reading skills. Reading is a task that heavily relies on highly specialized brain areas
in frontal, temporoparietal, and occipitotemporal regions and their fast and efficient
connection. While it could be argued that these denser fiber areas existed from birth
and made these people better readers, the opposite can also be true, and it is in fact
more likely that these associations were strengthened over time through learning
and that the changes seen represented a positive and adaptive process. New research
in the development of reading disorders suggests just this possibility, stating that
parents confer liability for reading difficulties via intertwined genetic and
environmental pathways (van Bergen, van der Leij, & de Jong, 2014). Recent
research has even identified the mechanism by which particular neurons are selected
for recruitment (Helie, Ell, & Ashby, 2014). They found that one role among many
for the basal ganglia (BG) is to train connections between posterior cortical areas
and frontal cortical regions that are responsible for automatic behavior. This model
suggests that one effect of BG trial-and-error learning is to activate the correct
frontal areas shortly after posterior associative cortex activation, thus allowing for
learning of robust, fast, and efficient cortico-cortical processing.

The Effect of Learning on the Connectome and Its


Implications for Mental Health

As far as a discussion of mental health is concerned, this leads us to think about


mental health from a vastly different perspective. It allows us to think about the
human development of the connectome with consideration of multiple factors which
can ultimately affect how we think about mental disorders. There are others who are
thinking about mental health in connectomic terms. Consider the etiology and
potential resulting outcome of where in the process of the development of the con-
nectome the damage occurs. For example, Menon (2013) stated that dysfunctional
brain networks can arise from damage to individual nodes or to the edges (white
matter) that link them. In that regard, problems can be related to a structurally
deficient initial and largely genetically determined base connectome or those
associated with later occurring structural damage to the connectome. Recently,
models have been developed that attempt to describe the operation of these brain
networks. For example, computational connectomics (Deco & Kringelbach, 2014)
models the spontaneous dynamics of brain connectivity networks during rest and
also task-related dynamics in health and disease. The related field of computational
neuropsychiatry describes the whole or partial breakdown of these task-related
network dynamics in mechanistic terms.
Disruption or damage to the connectome is not the only way for a network to
function poorly. Dysfunctional networks can also develop as a result of epigenetic
and learning-based changes to the connectome. For example, Fields (2008a, 2008b)
cited research that identified potentially 89 abnormally regulated genes in the pre-
frontal cortex alone that were related to schizophrenia, the expression of each one
potentially related to epigenetic influences. In these dysfunctional networks, there
The Effect of Learning on the Connectome and Its Implications for Mental Health 41

would be no detectible structural abnormality or lesion, but rather differing patterns


of connectivity leading to inefficient processing of information (Schmithorst et al.,
2005) or differing patterns of network activation (Thiel et al., 2014). For example,
there is recent research that demonstrates that infants with autism actually have supe-
rior object-related visual perceptual skills (Gliga, Bedford, Charman, & Johnson,
2015) which may later contribute to atypical development in that there are other stud-
ies that have hypothesized or identified deficiencies in the ability of young autistic
children to attend to social movement cues, thereby failing to engage key identifica-
tion and reward recognition circuits with early social behavior (Klin, Shultz, & Jones,
2015). In sum, “local circuit abnormalities can contribute to abnormal signaling and
temporal interactions between brain regions even in the presence of normal structural
connectivity” (Menon, 2013, p. 337).
In addition to the damage/no damage dimension, Menon (2013) identified prob-
lems with the operation of specific coherent large networks as contributory to prob-
lems with emotional regulation. The function of the networks naturally imposes
strong functional constraints on the development of information processing capacity.
The networks were identified as task-positive and task-negative networks that create
bottlenecks to network access and allocation of network resources, a default mode
network that plays an executive monitoring role, and a salience network that is
responsible for attentional capture of biologically, emotionally, and cognitively
relevant events. Disruption of the functioning of any of these three networks can
lead to a reduction of synchronized neuronal activity.
It is important to note that a problem in a particular area of connectivity can have
significant downstream effects both in the specific networks and to other nodes in
networks which are recruited in a task-specific manner to accomplish specific
behaviors. In addition, to these large-scale networks, research has begun to identify
neurocognitive networks, each of which is dedicated to a specific cognitive function.
Monitoring the interaction of these networks is the central executive system, which
is intimately involved with actively maintaining and manipulating information in
working memory, rule-based problem solving, and decision-making.
Menon (2013) proposes that a deficit of either engagement or disengagement of
any of these three networks plays a key role in many psychiatric or neurological
disorders. What is important for our discussion is that these networks are integrated
in relation to a task as a result of the epigenetic interaction between their constitutional
characteristics and the interaction of that system with the environment. By increasing
or decreasing reward potential, the likelihood of these systems operating in concert
in the future in relation to a particular environmentally presented task, is either
increased or decreased. Learning determines the direction of interaction. Menon
proposes that learning-based (among other reasons) aberrant saliency filtering,
detection, and mapping result in deviant signaling into and out of the saliency
network (SN), and this deviant signaling is the basis for most psychopathology. Two
subcortical nodes of the SN system are highlighted as essential for this process.
These are the amygdala which is essential for the detection of biologically salient
affective cues, and the nucleus accumbens which is crucial for reward prediction.
Finally, the insula is identified as essential because it sits at the interface of the cog-
42 5 The Effect of Learning on the Development of the Connectome

nitive, homeostatic, and affective systems for the brain, and is responsible for
switching and gating between them. A disease concept is not required to understand
the development of these connectionistically determined signaling patterns, nor is a
disease concept necessary when describing how to effect change in the operation of
the system. While it is clear that there are diseases, such as Alzheimer’s disease, that
affect the operation of the connectome, it is also clear that there are many problems
that affect emotional regulation that represent learned and automatized response.

Summary

We believe that a great portion of what is currently considered mental illness is reflective
of learned responses. While we do not question that for the smaller subset of biologi-
cally expressed disorders medical intervention is necessary, we would argue that the
majority of issues that present, and are considered mental illness, are in fact disorders of
maladaptive learning resulting in an inefficient or differently activated connectome. And
that even when acting in unison with psychotherapy, medication is insufficient as a treat-
ment as it does not alter the trajectory of the maladaptive patterns which continue to
reinforce the maladaptive development or structure of the connectome.

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Chapter 6
The Connectome and Emotion

Based on our scientific knowledge of physics, neurology, and behavior, our actions are
predetermined rather than dictated by some ghost in our brains. We would do better by
sussing out the consequences of that conclusion and applying them to society.
(Jerry A Coyne)

Wait one second, what about emotion? Isn’t the main manifestation of a mental
health problem dysfunctional emotional regulation and the behavioral problems
dysfunctional regulation causes? Isn’t the treatment for mental health problems,
therapy, supposed to be about emotion? Don’t people go to therapy to talk about
how they feel? After all, isn’t the regulation of emotional states vital for adaptive
behavior in a social environment? The short answer to all these questions is that of
course emotion plays an important part in both etiology and treatment. The longer
and more scientifically accurate answer isn’t that clear. That’s because the longer
answer examines the neurophysiology and nature of emotion and its operation
within a network model. It is to that issue that we now turn our attention.

Defining Emotion

When we talk about an emotion, just what specifically are we talking about? While it
goes without saying that when we say humans have emotions, we can get agreement
that they do, and we can get people to name a few for us. But asked to define emotion,
things get rapidly quite murky and scientifically vague. That is because, as we have
discovered with many things in psychology, a precise and agreed-upon definition of
emotion does not exist. Look at this statement from the field of product design, for
example, “The study of user emotions is hindered by the absence of a clear overview
of what positive emotions can be experienced in human-product interactions. Existing
typologies are either too concise or too comprehensive, including less than five or
hundreds of positive emotions, respectively” (Desmet, 2012). This paper went on to
identify a basic set of 25 positive emotion types that represented the general repertoire

© Springer International Publishing Switzerland 2016 45


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_6
46 6 The Connectome and Emotion

of positive human emotions when relating to design elements. Gross (1998) took an
evolutionary perspective and characterized emotion in terms of response tendencies.
In this model emotion regulation was not only defined, it was distinguished from cop-
ing, mood regulation, defense, and affect regulation. Obviously, these response ten-
dencies were in part a reflection of learned behavior.
The ephemeral nature of the definition of emotion was captured by Kemper
(1987) when he said “Fundamental to the field of emotions is the question of how
many emotions there can or cannot be. The answer proposed here is that the number
of possible emotions is limitless. As long as society differentiates new social situa-
tions, labels them and socializes individuals to experience them, new emotions will
continue to emerge” (p. 263). Scherer (2005) summarized the problem succinctly
when he stated “defining ‘emotion’ is a notorious problem. Without consensual
conceptualization and operationalization of exactly what phenomenon is to be stud-
ied, progress in theory and research is difficult to achieve and fruitless debates are
likely to proliferate.” That was probably an understatement.
In addition to the difficulties surrounding the definition of emotion and the iden-
tification of a specific number of emotions, researchers also differ on the exact num-
ber of emotional response types from among four factor models (anger, fear,
sadness, happiness) to seven factor models (neutrality, joy, boredom, sadness, anger,
indignation, fear) and everything in between (Nicholson, Takahashi, & Nakatsu,
2000). These groupings are often made based on a subjective appraisal of the authors
as opposed to an understanding of their neural basis.

Neural Networks and Emotion

Despite potentially hundreds of emotional response types all being grouped under
the term ‘emotion’, it is clear that differing neural networks (defined as recruited
elements) are in play for differing emotional states (Blaira et al., 2007). As we have
seen, all stress responses are mediated by largely overlapping white matter circuits
in the limbic forebrain, the hypothalamus, and the brainstem (Ulrich-Lay & Herman,
2009). The limbic circuits that are responsible for regulating stress responses inter-
sect with circuits that are responsible for memory and reward, providing a means to
demonstrate learning of the stress response with respect to prior experience and
anticipated outcomes. This implies that the underlying physiology of classes of
stress-related states is the same, but that experience and reward value determine the
label we put on these reactions. This hypothesis is supported by data that suggest
that both common and distinct neural systems support various forms of emotional
appraisal and that particular prefrontal systems modulate the amygdala in different
ways depending on the regulatory goal and strategy employed (Ochsner et al.,
2004). Recent research has in fact discovered brain circuitry for encoding positive
and negative learned associations in mice. After finding that two circuits showed
opposite activity following fear and reward learning, these researchers demonstrated
What Is an Emotion? 47

that this divergent activity causes either avoidance or reward-driven behaviors


(National Institute of Health, 2015). So we have the circumstance wherein a key
psychological construct is essentially undefinable and exists without empirical
foundation in human brain networking or physiology. In fact, the existing network
studies suggest entirely different modeling may be appropriate when defining what
physiologically goes on when a human emotionally responds.

What Is an Emotion?

For the purposes of our discussion, we will identify emotions as the cognitive labels
and the learned response tendencies associated with them, assigned to physiological
changes resulting from the appraisal of threats, stress, or potential reward in the
immediate environment. We are not alone in considering emotions in this manner.
There is a robust literature on what has been termed appraisal theory (Roseman &
Smith, 2001). Appraisal theory at its most basic is a model that emotions are the
result of evaluations (appraisals) of events and situations. We would extend these
appraisals to the contextually based cognitive labeling of an individual’s physiologi-
cal responses and related cognitively labeling operations. In appraisal theory it is
important to recognize that emotions can be regarded both as experiences of forms
of cognitive appraisal (initially flight or fight responses) and as states of action read-
iness related to the appraisal (Scherer, 2005). Appraisal theory was developed to
address a number of issues that demonstrate the interconnectivity of neural net-
works in various issues related to mental health. Among these are how to explain
individual and temporal differences in individual responses to the same event, how
to account for the highly differentiated nature of most responses in general, and
finally how to account for the vast amount of emotional response possibilities pro-
duced by the same environmental situation. Other areas addressed by appraisal
theory include the appropriateness or inappropriateness of the situationally specific
(and individual specific) emotional response. Appraisal theory discusses both the
potentially integrated nature of the networks underpinning the ultimate emotional
response and that facts that these emotional labels are acquired through the interac-
tion between the physiological response and the cognitive label. In our view, that
implies that appraisal theory understands that emotional responses are based in part
on learned reactions. We should stress that, in our view, this model is not at odds
with other theories, such as behavioral models, that proffer that emotions can be
elicited without the benefit of an appraisal. We would offer that with learning
appraised emotional responses can, like any other form of learning, become auto-
matic and no longer require each component step. For example, if you live in the
southwest United States and see a rattlesnake, you do not have to go through all of
the appraisal steps. You have done so many times before, and your complicated
response to the visual presentation of the snake into your immediate stimulus field
occurs without cognitive threat assessment.
48 6 The Connectome and Emotion

The Regulation of Emotional States

The regulation of emotional states is recognized as an important developmental


priority (Diamond & Aspinwall, 2003). The regulation of emotion is crucial for
adaptive behavior leading to an “optimal developmental outcome with respect to
emotion regulation that is not affective homeostasis, but rather a dynamic flexibility
in emotional experience, the ability to pursue and prioritize different goals, and the
capacity to selectively and proactively mobilize emotions and cognitions in the ser-
vice of context-specific and developmentally specific goals” (p. 125). Studies have
clearly demonstrated that individuals differ in their use of emotion regulation strate-
gies; these individual differences have implications for affect, well-being, and social
relationships (Gross & Oliver, 2003). The repair of faulty emotion regulation strate-
gies that do not achieve this optimal outcome is the goal of most therapeutic mental
health encounters (Gross & Munoz, 1995).
According to the process model of emotional regulation (Gross, 1998), emotion
may be regulated at five points in the emotion-generative process: (a) selection of
the situation, (b) modification of the situation, (c) deployment of attention, (d)
change of cognitions, and (e) modulation of responses. Different strategies have
been postulated to achieve successful emotion regulation, ranging from suppression
and attentional control which encompass the strategy of distraction (relaxation,
mindfulness techniques) to cognitive change incorporating the strategy of reap-
praisal (cognitive behavior therapy) (Kanske, Heissler, Shoenfelder, & Wesa, 2010).
Distraction is an antecedent-focused strategy of emotional regulation, indicating
that it is implemented before the generation of the emotion. Distraction involves the
redirecting attention away from a negative aspect of a situation to a neutral or posi-
tive aspect. Attention can be deployed externally (e.g., focus on the size of a stimu-
lus) or internally (e.g., focus on neutral, other, or positive thoughts).
Reappraisal is also an antecedent-focused strategy. As an antecedent strategy, it
is implemented later than distraction during the time course of emotional regulation.
It can also be used as a post-emotional response strategy when evaluating how a
particular emotional response determined a course of action. Reappraisal consti-
tutes a cognitive change of the meaning of an emotion eliciting situation, in order to
reduce negative feelings.
Suppression comes later in the emotion-generative process and consists of inhib-
iting the outward signs of inner feelings. Both experimental and individual-
difference studies find reappraisal is often more effective than suppression.
Reappraisal decreases the emotional valence of the experience and behavioral
expression and has no impact on memory. By contrast, suppression decreases behav-
ioral expression, but fails to decrease the emotionality of the experience, and actually
impairs memory. Suppression also increases physiological responding for suppressors
and their social partners (Gross, 2002). In general suppressive strategies are less effec-
tive than reappraisal strategies.
There is limited research identifying the different regulation strategies with
respect to their neural mechanisms and their effects on emotional experience.
Network Recruitment and Emotional Response 49

One study (Kanske et al., 2010) compared reappraisal and distraction strategies
in a functional magnetic resonance imaging study. Both strategies were deemed
successful in reducing subjective emotional state ratings and were related to
lowered activity in the bilateral amygdala. There was a stronger decrease in
amygdala activity for distraction when compared with reappraisal. Both strate-
gies had common network components in the medial and dorsolateral prefron-
tal and inferior parietal cortex. Each strategy also had unique network
components. The orbitofrontal cortex was activated for reappraisal, while the
dorsal anterior cingulate and large clusters in the parietal cortex were active in
the distraction condition. Finally functional connectivity patterns of amygdala
activation confirmed the roles of these specific activations for the two emotion
regulation strategies.

Network Recruitment and Emotional Response

What is clear from both the modeling and the research is that there is neural net-
work capacity devoted to, in response to a stimulus, generating certain physiolog-
ical responses, “feeling states,” which are then cognitively appraised with an
environmentally contextual label. As part of this process, humans do a number of
things with these states and their antecedent stimuli. We first determine if they are
related to a threat or a reward, and then secondly, we determine whether they are
internally mediated or externally occurring. Research suggests that there are dif-
fering brain networks involved in these separate operations (Ochsner et al., 2004).
There are both shared elements and unique elements of the networks charged with
emotional regulation. For example, Ochsner et al.’s research indicated that both
upregulating (enhancement—increase in cellular response) and downregulating
(reduction in cellular response) negative emotion recruited prefrontal and anterior
cingulate regions which are implicated in cognitive control and that amygdala
activation was modulated up or down in accord with the regulatory goal. There
were differences associated in recruited networks for negative emotion.
Upregulation uniquely recruited regions of left rostromedial prefrontal cortex
(PFC) where they are implicated in the retrieval of emotion knowledge, whereas
downregulation uniquely recruited regions of right lateral and orbital PFC which
are implicated in behavioral inhibition. Most importantly for the current discus-
sion, their research indicated that self-focused regulation recruited medial pre-
frontal regions implicated in internally focused processing, whereas
situation-focused regulation recruited lateral prefrontal regions which were impli-
cated in externally focused processing. In sum, once it is determined whether the
threat is internal or external, we then determine whether we will upregulate or
downregulate it. This determination is based upon environmentally learning in
relationship to the particular stimuli currently perceived as a threat.
50 6 The Connectome and Emotion

Downregulating Emotion Is Essentially the Provenance


of Therapy

The goal of much, but not all of therapy, is the downregulation of emotional states.
In general, we want people to become calmer, to become better focused, and to be
able to handle perceived threats in a more mindful manner. Functional neuroimag-
ing studies examining the neural bases of the cognitive control of emotion have
found increased prefrontal and decreased amygdala activation for the reduction or
downregulation of negative emotion (Ochsner et al., 2004). As we have seen, there
are varying networks involved directly in the downregulation of emotional
responses. Their research suggests that both common and distinct neural systems
support various forms of the same strategy such as reappraisal, and that particular
prefrontal systems modulate the amygdala in different ways depending on the regu-
latory goal and strategy employed.

Neural Networks Are Uniquely Recruited Depending


on the Strategy Employed to Modify the Emotional State
and the Circumstances Related to the Arousal of That
Emotion

There has been a research that demonstrates both a core set of networks and a
strategy-specific network depending on the strategy used to deal with the emo-
tional appraisal. For example, Schiller and Delgado (2010) investigated three
adaptive strategies of learned fear; reaction extinction, reversal, and regulation of
fear and reviewed their underlying neural mechanisms. They found overlapping
brain structures that comprise a general circuitry in the human brain which
potentially enables the flexible control of fear, regardless of the particular task
demands. Ochsner, Silvers, and Buhle (2012) demonstrated that “prefrontal and
cingulate control systems modulate activity in perceptual, semantic, and affect
systems as a function of one’s regulatory goals, tactics, and the nature of the
stimuli and emotions being regulated” (p. E1). Finally, Beauregard (2007) in a
review demonstrated that metacognition and cognitive reappraisal selectively
alters the way the brain processes and reacts to emotional stimuli and that mental
functions and processes involved in diverse forms of psychotherapy exerted a
significant influence on brain activity. In sum, he indicated that the findings of
“the reviewed neuroimaging studies strongly support the view that the subjective
nature and the intentional content (what they are ‘about’ from a first-person per-
spective) of mental processes (e.g., thoughts, feelings, beliefs, volition) signifi-
cantly influence the various levels of brain functioning (e.g., molecular, cellular,
neural circuit) and brain plasticity” (p. 218). In other words, learned response
alters the way that the brain physiologically responds to potential stimuli and that
these responses include emotions.
Symptoms of Psychiatric Dysfunction Are the Partial Result of an Individual’s… 51

There are a number of implications for the practicing therapist, the most important
of which is that the selection of a particular treatment strategy involves the selection
of the underlying circuitry as well. Clearly then, it would behoove the practicing
therapist to be aware of these processes and be knowledgeable in the strategies that
would optimally utilize an individual’s resources. Just as clearly in our opinion, is
that it would be productive for the client to understand how the process works so
that they may effectively participate in the process of its utilization.

Upregulated Threats and Working Memory

There are, of course, perceived threats that require some action be taken. These
responses, consisting of elevated activity, are termed upregulated. Upregulated
threats are gated to attention and allocated working memory. This requires the
recruitment of networks that control the gating of attention.
Studies have suggested that there are two different attention networks: the dorsal
attention network (DAN) and the ventral attention network (VAN). These have been
shown to interact with various emotion networks. Each attention network has a
specific role. The dorsal attention network controls goal-oriented top-down deploy-
ment of attention. The ventral attention network controls stimulus-driven bottom-up
deployment of attention. These interact with the emotion network that feeds back
the stimulus, especially fearful expressions from the environment (Liu, Kong, Jin,
& Lin, 2014). The research of Liu et al. (2014) demonstrated that there is interaction
within the three networks, the triad of two attention networks, and the specifically
recruited emotion network. Specifically, they suggested that the ventral attention
network may distract the dorsal attention network and that the emotion network
may influence both attention networks. In other words, the presentation of a stimu-
lus that is determined to be a threat (fearful) into the environment activates the
ventral attentional network (gates the fearful stimulus into working memory), which
in turn recruits the dorsal attention network to deploy more active attention to the
threat. The engagement of the attentional networks also occurs in the presence of
highly rewarding stimuli.

Symptoms of Psychiatric Dysfunction Are the Partial Result


of an Individual’s Reward Valuation of Perceived Threat

Much of the above would lead to the assumption that the underlying basis of many
negative emotional responses is the perception of a threat (stress) to the person. Studies
have indicated that this is likely the case in that stress is a significant risk factor for the
development of psychopathology, due largely to symptoms related to reward process-
ing history. Specifically, individuals display marked variation in how they perceive and
cope with events they determine to be stressful, and such differences are strongly
52 6 The Connectome and Emotion

linked to risk for developing psychiatric symptoms following stress exposure


(Treadway, Buckholtz, & Zald, 2013). Treadway et al. (2013) found that stressors
deemed uncontrollable and overwhelming were related to blunted neural responses in
medial prefrontal cortex (mPFC). These blunted responses reflect changes in the valu-
ation of reward value. They hypothesized that changes in reward-seeking and goal-
directed behavior are a common symptom of mental illness, usually reflecting a shift in
how different options in the environment are valued and pursued, resulting in either
reduced motivation for experiences (Treadway & Zald, 2011) that were previously
found to be rewarding, or a heightened desire for certain rewards (i.e., drug cravings).
Clinically, this model would offer some guidance to those clinicians seeking to under-
stand how a teenager may be chronically under-aroused with regard to school and
school-related work. Stress is also a central risk factor in the development of psychiat-
ric conditions characterized by prominent abnormalities in reward-related processes,
such as depression, schizophrenia, and substance use (Treadway et al., 2013).

Hijacking Attention and Emotional Regulation

There is increasing evidence that problems other than downregulation are involved in
those activities identified as disorders of emotional regulation. For example, the conse-
quences of hijacking attention (a survival mechanism designed to respond to true envi-
ronmental stressors or threats) are just beginning to be appreciated by the clinical
community in generating newer models of impulsivity, emotional response, and anti-
social behavior. There is evidence that for some people, the presence of an individual-
ized, highly salient reward will capture the dorsal attentional stream to such an extent
that they will hyper-focus on the reward and stop forward predicting any outcome
(Goldberg, 2014). Essentially this indicates that these people will strive for the goal
without considering the consequences. It also means that they will not consider alterna-
tives and are unlikely to be distracted from their pursuit. This might be seen in the clini-
cal setting wherein a child who has been diagnosed with attention deficit disorder
insists on playing computer games rather than complete a homework assignment. This
is true, even though in a more reflective moment outside the presence of the game
(perhaps in the therapist’s office), the child can articulate the reason why they should
not play the game. It is not that they don’t know the reason or can dispassionately state
the reward probabilities of each choice. It is that the presence of the reward (the game)
captures all of their attention, blocking out executive forward planning or analysis.

Strategies to Regulate Emotion

Therapies have adopted different models to aid in the regulation of emotion ranging
from attentional control (e.g., distraction) to cognitive change (reappraisal, redefini-
tion, and re-categorization). To date there is only scarce evidence comparing the
Summary 53

different regulation strategies with respect to their neural mechanisms and their effects
on emotional experience (Kanske et al., 2010). While both aforementioned models
were effective in reducing emotional responsivity, different neural components form-
ing differing neural networks were involved in each strategy. For example, Ochsner,
Silvia, Bunge, Gross, and Gabrieli (2002) employed functional magnetic resonance
imaging to examine the neural systems used to reappraise highly negative scenes in
unemotional terms. Reappraisal of highly negative scenes reduced subjective experi-
ence of negative affect. Neural correlates of reappraisal showed increased activation
of the lateral and medial prefrontal regions and decreased activation of the amygdala
and medial orbitofrontal cortex. While both strategies relied on common areas in the
medial and dorsolateral prefrontal and inferior parietal cortex, the orbitofrontal cortex
was selectively activated for reappraisal. In contrast, the dorsal anterior cingulate and
large clusters in the parietal cortex were active in distraction only (Kanske et al.,
2010). This in retrospect should not be surprising as one strategy necessitates the real-
location of attention and the other a redefinition of context.

Summary

Overall, the research data clearly suggest that processes involved in emotional regulation
are recruited during task performance in the context of emotional disorders (Blaira et al.,
2007). What this means is that there are environmentally learned and contextual
responses that are a part of every disorder of mental health. As we have seen, a purely
biological or genetic model is not serviceable; Learning must be included in any effec-
tive model that hopes to describe the etiology of mental health issues.
This clearly places an additional burden on the therapist, as it appears that one
would need to understand the constraints of the recruited network in order to maxi-
mize functionality for the client. Identifying neurobiological mechanisms underlying
psychiatric symptoms and understanding how the brain processes the information
related to emotions through recruited networks in an effort to find more effective treat-
ments for psychiatric symptoms have been pointed out by the National Institute of
Mental Health as key areas of investigation (Insel, 2009). This of course implies that
the current interventions, which continue to largely ignore the complex epigenetic
interactions involved in emotional respondency, are not up to the task. This idea has
found increasing support. Insel (2010) writes regarding schizophrenia “After a cen-
tury of studying schizophrenia, the cause of the disorder remains unknown. Treatments,
especially pharmacological treatments, have been in wide use for nearly half a cen-
tury, yet there is little evidence that these treatments have substantially improved out-
comes for most people with schizophrenia. These current unsatisfactory outcomes
may change as we approach schizophrenia as a neurodevelopmental disorder with
psychosis as a late, potentially preventable stage of the illness. This ‘rethinking’ of
schizophrenia as a neurodevelopmental disorder, which is profoundly different from
the way we have seen this illness for the past century, yields new hope for prevention
and cure over the next two decades” (p. 187). Similarly, McGorry, Purcell, Goldstone,
54 6 The Connectome and Emotion

and Amminger (2011) point out, “although the onset of most mental disorders usually
occurs during the first three decades of life, effective treatment is typically not initi-
ated until a number of years later. Although there is increasing evidence to suggest
that intervention during the early stages of a disorder may help reduce the severity
and/or the persistence of the initial or primary disorder and prevent secondary disor-
ders, additional research is needed into appropriate treatment for early stage cases as
well as the long-term effects of early intervention, and to appropriate service design
for those in the early stages of a mental illness. This will mean not only the strengthen-
ing and re-engineering of existing systems but also, crucially, the construction of new
streams of care for young people in transition to adulthood” (p. 301). Finally reflect-
ing on how learning and therapy might interplay with the connectome (March, 2009)
offers the following “driven largely by scientific advances in molecular, cellular and
systems neuroscience, psychotherapy in the future will focus less on personal narra-
tives and more on the developing brain. In place of disorders as intervention targets,
modularized psychosocial treatment components derived from current cognitive
behavior therapies will target corresponding central nervous system (CNS) informa-
tion processes and their functional behavioral consequences. Either preventive or
rehabilitative, the goal of psychotherapy will be to promote development along typi-
cal developmental trajectories” (p. 170). Clearly understanding how the connectome
learns will be essential for the conduct of psychotherapy.

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Chapter 7
Biologically Based Disorders of Mental Illness

A group of scientists told you that my genes were damaged, that there was something wrong
with me – they showed you the test results that proved it. And even I started to believe it.
“You never believed it,” he says. “Not for a second. You always insisted I was… I don't
know, whole.”
Veronica Roth, 2012, Allegiant

Are there disorders of mental health that have as their basis purely biological/
genetic-based dysfunction? It would be easy to assume that there were. Certainly
there is emerging evidence that there are disorders of mental health that have, at
least, a very strong biological/genetic contribution to their etiology. In particular
disorders such as schizophrenia, bipolar disorder, and autism fit a biological model
very well (McNally, 2011). That is, there are disorders of mental health that are
based on brain-based dysfunction that an individual is born with and then manifest
themselves either at birth or soon after (e.g., autism) or at a point later in an indi-
vidual’s development (e.g., manic depressive disorder, psychosis). According to the
biological model, these disorders can all be adequately described utilizing biologi-
cally based phenomena. Learning, socialization, acculturation, and other environ-
mental influences need not apply. As we have seen this idea is changing.

Biological Underpinning of Mental Illness

Certainly there is rapidly increasing evidence for the biological underpinnings of


many metal disorders. In recent years researchers have made many groundbreaking
discoveries about the function and dysfunction of the human brain. Research has iden-
tified genes linked to schizophrenia and also discovered that certain brain abnormali-
ties escalate an individual’s risk of developing post-traumatic stress disorder. Similar
findings have been recognized with anomalies associated with autism, including
abnormal brain growth and under-connectivity among brain regions (Weir, 2012).

© Springer International Publishing Switzerland 2016 57


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_7
58 7 Biologically Based Disorders of Mental Illness

The emergence of techniques that allow imaging of active brain function in humans
and genetic engineering in rodents has demonstrated the impact of serotonin (5-HT),
an important modulator of emotional behavior, on neural systems subserving anx-
iety and depression. A key finding from the research has been the discovery of
genetic variations in critical regulatory molecules within the 5-HT system, the 5HT
transporter (5-HTT), and its influence on emotional traits (Hariri & Holmes, 2006).
Deficits in access, engagement, and disengagement of large-scale neurocognitive
networks are shown to play a prominent role in several disorders including schizo-
phrenia, depression, anxiety, dementia, and autism (Menon, 2011).

Damaged Connectome Models

There are models that posit that a damaged connectome is the etiological foundation
of most mental illness. The study of human brain networks with in vivo neuroimag-
ing techniques coupled with advances in both network science and graph theory has
given rise to the field of connectomics. Connectomics focuses on how whole-brain
computational models can help generate and predict the dynamic interactions and
consequences of brain networks. These models propose that whole-brain modeling
and computational connectomics may provide a starting point for understanding
brain disorders at a causal mechanistic level and that computational neuropsychia-
try can ultimately be used to provide innovative and more effective therapeutic
interventions (Deco & Kringlrbach, 2014).

Basic Assumptions of Fixed Models

Both biological and preexisting damaged connectome models would argue that for all
disorders, the outcome was inevitable. The patterns of connections would be fixed and
immutable and unerringly lead to a specific mental disease. In short, everybody that
had a particular pattern of connectivity at birth, or that everyone with a particular pat-
tern of genome, would go on to develop a particular mental disorder. Secondly, it
would argue that environmentally based learned experiences would have no effect on
the outcome. The eventual architecture of the developed connectome would be predict-
able from the outset. There are examples of such models. Menon (2011) described the
triple action network model to describe how aberrant structures with a neural network
would lead to certain mental illnesses. In particular, schizophrenia and major depres-
sive disorder were found to be characterized by aberrant intrinsic functional connectiv-
ity (iFC) within intrinsic connectivity networks (ICNs), including the default mode,
salience, and central executive network (DMN, SN, CEN). The “triple network model
of psychopathology” suggests that anterior insular (AI) dysfunction within the SN
might contribute to aberrant modulation between DMN-mediated, self-related/inter-
nally oriented and CEN-mediated, goal-directed/externally oriented cognitive activity,
Biology Does Not Hold All the Answers 59

giving rise to distinct disease-specific symptom dimensions such as hallucinations


(“heightened salience of internal speech”) in schizophrenia and depressive ruminations
(“heightened salience of self-referential thoughts”) in major depressive disorder.
Van den Heuveland and Fornito (2014) described the dysconnectivity hypothe-
ses, which links schizophrenia to abnormal structural and functional connectivity in
the brain. This model posits that brain disorders such as schizophrenia emanate
from abnormal brain network wiring and dynamics.
By extension, if one held this view, then one could conclude that all mental
disorders are based on neurophysiologically based damage to the connectome
and that science just has not found the evidence yet for those disorders that have
not had the connectome issues identified. There are proponents for this view.
Eric Kandel, MD, a Nobel Prize laureate and professor of brain science at
Columbia University, believes it’s all about biology. “All mental processes are
brain processes, and therefore all disorders of mental functioning are biological
diseases,” he says. “The brain is the organ of the mind. Where else could [mental
illness] be if not in the brain?” (Weir, 2012).

Biology Does Not Hold All the Answers

At first glance the existence of this research on a group of disorders that appears
biologically determined would appear to argue persuasively against a learning-
based model as an etiological component for most mental disorders. On careful
analysis however, it does nothing of the sort.
The first question that might be asked is whether there is evidence to suggest that
such a model is supported by the research. As we have seen, there is some. There is
however, a number of confounds with the existing research. For example, Mayberg
and In Weir (2012) point out that one of the biggest problems with mental health
research is that mental illness diagnoses are often catch-all categories that include
many different underlying malfunctions. Mental illnesses have traditionally been
described by their outward symptoms, both out of necessity and convenience. But
just as cancer patients are a wildly diverse group marked by many different disease
pathways, a depression diagnosis is likely to encompass people with many unique
underlying problems. That presents challenges for defining the disease in biological
terms. “Depression does have patterns. The caveat is different cohorts of patients
clearly have different patterns and likely the need for different specific interven-
tions.” In addition while it is true that certain disorders have a clear biological con-
tribution, there are other conditions, such as depression or anxiety, where the
biological foundation is far more nebulous.
In a review article, Sullivan, Neale, and Kendler (2000) concluded that while
major depression is a familial disorder and its familiarity mostly or entirely results
from genetic influences, environmental influences specific to an individual are also
etiologically significant. Major depression is a complex disorder that does not result
from either genetic or environmental influences alone but rather from both.
60 7 Biologically Based Disorders of Mental Illness

Example of the Paradigm Shift: The Serotonin Hypothesis


of Depression

A similar course of development was established concerning the biological/genetic-


based models. The serotonin model of depression provides an instructive example.
The serotonin hypothesis of depression originally postulated that a reduction in
serotonin leads to increased predisposition to depression. This was initially based
on therapeutic strategies that affect serotonin activity which found that alterations in
serotonin may not only predispose to depression, but also to aggressive behavior,
impulsivity, obsessive–compulsive behavior, and suicide (Albert & Benkelfat, 2013).
This hypothesis has increasingly found little research support, and now it is gen-
erally accepted that recurring mood disorders are brain diseases resulting from the
combination, to various degrees, of genetic and other biological as well as environ-
mental factors, evolving through the life span (Albert, Benkelfat, & Descarries,
2012). Emblematic of this position, Berton et al. (2006) using a viral-mediated,
mesolimbic dopamine pathway-specific knockdown of brain-derived neurotrophic
factor (BDNF) showed that BDNF is required for the development of experience-
dependent social aversion that resulted in aggressive behavior.
As a result of this and other research, the original serotonin-only hypothesis has
been modified to include many influences including the environment (Young, 2013)
and one’s own learned perceptual set (Harmer & Cowen, 2013). The importance of
psychosocial environment in combination with serotonin is actually postulated to
enhance the response to selective serotonin reuptake inhibitors (SSRI) treatment
(Young, 2013). Young noted that an important problem with most current antidepres-
sant treatments including SSRI treatment is that several weeks of treatment are
required before clinical improvement is observed. Harmer and Cowen proposed a
neuropsychological framework to explain this delay, suggesting that it represents the
time for the emergence of a conscious positive bias in emotional processing. They
argue that the progressive awareness of the positive effects of SSRI treatment on the
emotional balance is central to the antidepressant effect. This time period was consid-
ered consistent with SSRI-induced changes in neurogenesis and synaptic plasticity, as
well as a greater desensitization of 5-HT1A (5-hydroxytryptamine) autoreceptors.
All of the above highlights the second issue with connectivity-only and/or
genetically-only hypotheses. Both assume that the current state of the system was
that way from the beginning. The possibility that there are outside influences that
affect the development of the connectome or the genome is not considered.

Genetic Contributions to Mental Health Disorders

As you can imagine, there has been extensive research into the genetic contributions
of many types of mental disorders. Much has been speculated, but to date, there
exists strong evidence that nine clusters of disorders have strong genetic
Searching for the Cause of Mental Health 61

components. These are Alzheimer’s disease, attention deficit hyperactivity disorder,


alcohol dependence, anorexia nervosa, autism spectrum disorder, bipolar disorder,
major depressive disorder, nicotine dependence, and schizophrenia (Sullivan, Daly,
& O’Donovan, 2012). We would rush to point out here that findings from family and
twin studies suggest that genetic contributions to psychiatric disorders do not in all
cases map to present diagnostic categories (Cross-Disorder Group of the Psychiatric
Genomics Consortium, 2013a). In fact, several of these disorders share common
loci. Genetic correlations are high between schizophrenia and bipolar disorder,
moderate between schizophrenia and major depressive disorder, bipolar disorder
and major depressive disorder, and ADHD and major depressive disorder. They are
low between schizophrenia and ASD and nonsignificant for other pairs of disorders
(Cross-Disorder Group of the Psychiatric Genomics Consortium, 2013b). These
data have pointed to significant problems in nosology and classification that we
have discussed in detail elsewhere (Wasserman & Wasserman, 2015). Nevertheless,
it is fair to say that there are genetic markers for a group of mental health problems.
In addition, the available research demonstrates that by and large, these factors con-
tribute to, not absolutely cause, the development of a particular disorder.
The disorders of greatest medical, research, and policy concern today, particularly in psy-
chiatry, are likely to be complex. Such disorders may have not a single cause but a causal
chain, or multiple such causal chains. These chains may involve genetic, environmental,
social, and biological risk factors. The effect of no one of these risk factors can be fully
understood except in the context of all the others (Kraemer, Stice, Kazdin, & Kupfer, 2001,
p. 848).

So overall, mental illnesses are likely to have multiple causes, including genetic,
biological, and environmental factors. As we now know, that is true for many other
chronic diseases such as heart disease and diabetes. In the case of mental illnesses,
we’re a particularly long way from understanding the interplay among those factors.
What should be clear by now is that these environmental factors have to have a
mechanism of operation. There must be a way that they impact the connectome and
contribute to the outcome. That way is learning.

Searching for the Cause of Mental Health

Searching for the causes of mental disorders is analogous to piecing together sec-
tions of a jigsaw puzzle whose solution changes depending on the theme. It is excit-
ing as it is complex. The relationship between pathophysiology and its overt
manifestations of healthy or unhealthy behavior is exceedingly intricate, and often
the causes of a disorder are elusive at best (Susser et al., 2006). For example,
Peedicayil (2007) asserts that there are two major categories of mental illness. One
comprises idiopathic mental disorders like schizophrenia, bipolar disorder, and
major depressive disorder (MDD) where there are no definitive structural changes
in the brain. The other class comprises the neuropsychiatric disorders like
Alzheimer’s disease and Huntington’s disease which are characterized by definitive
62 7 Biologically Based Disorders of Mental Illness

structural changes in the brain. Peedicavil indicates that family, twin, and adoption
studies indicate that both of these categories of disorders have a genetic basis. The
major point is that the idiopathic mental disorders have complex inheritance pat-
terns involving many genes and environmental factors, while the neuropsychiatric
disorders have simpler patterns of inheritance.
So, the problem with the damaged connectome model is not that problems with
the operation of the connectome are associated with problems of mental health. The
problem is that the models presuppose some sort of structural damage. The possibil-
ity that learning through interaction with the environment can lead to alterations in
the connectome and resulting faulty operation is not considered. Despite evidence
of poorly integrated neural networks associated with certain mental health issues,
that evidence does not necessarily imply that those mental health issues were caused
by the neural network problems. It could just as easily be that the neural networks
were the result of a system and its interaction with the environment. That is learning
produced or contributed to the network pattern reflective of the dysfunctional behav-
ior or emotional reaction. There is some evidence that, at least in the instance of
post-traumatic stress disorder, that is exactly what happened. Hull (2002) studied of
a group of individuals who first assessed prior to the development of post-traumatic
symptoms as having no discernable brain dysfunction. Evidence from their study
indicated areas of the brain that appeared to be damaged by psychological trauma.
Specifically, they found volume reduction in the hippocampus, which had the effect
of limiting the typical evaluation and categorization of experience. Localized func-
tional changes included increased activation of the amygdala after symptom provo-
cation (which was conjectured to reflect its role in emotional memory) and decreased
activity of Broca’s area at the same time (which was thought to explain the difficulty
patients have in labeling their experiences). In sum, experiential learning produced
changes in the brain, not the other way around.

The Mind–Body Problem Once Again

In the end you are forced to the conclusion that trying to identify mental disorders
for which the cause is strictly genetic is a reflection of the mind–body problem. As
Rutter (2006) states,
“for far too long, behavioral genetics and socialization theory have been viewed as neces-
sarily in opposition to one another. Researchers in both “camps” have very rarely referred
to studies from the other “camp,” other than to attack their concepts and findings. The result
has been much fruitless dispute and serious misunderstandings of what each body of
research has to contribute” (Rutter, 2006).

Both Rutter (2006) and Sutter et al. (2006) encourage us to think about the contribu-
tions of various factors, nature and nurture being two of several factors. In the end, a
far more nuanced position has evolved that has necessitated a rethinking of how we
understand mental disorder. Unlike common physical disorders, mental illness usually
has its beginnings early in the reproductive stage and is therefore associated with
substantial reproductive disadvantage. Logically, genetic variations associated with
Epigenetic Models Integrate All Factors 63

vulnerability to mental illness should be under strong negative selection pressure and
be eliminated from the genetic pool through natural selection. Nevertheless, mental
disorders are common, and twin studies indicate a strong genetic contribution to their
etiology. While several theories have been advanced to explain the paradox of high
heritability and reproductive disadvantage associated with the same common pheno-
type, none offers a satisfactory explanation for all types of mental illness. Identification
of the molecular substrate underlying the large genetic contribution to the etiology of
mental illness is proving more difficult than expected. Uher (2009) postulates that this
is because the search for genetic variants associated with vulnerability to mental illness
is predicated upon the common disease/common variant (CDCV) hypothesis. This
hypothesis predicts that common disease-causing alleles, or variants, will be found in
all human populations which manifest a given disease. Uher (2009) concludes that a
summary of evidence demonstrates that the CDCV hypothesis is untenable for most
types of mental illness. He proposes an alternative evolution-informed framework
which suggests that gene–environment interactions and rare genetic variants constitute
most of the genetic contribution to mental illness. This model posits that common
mental illness with mild reproductive disadvantage is likely to have a large contribu-
tion from interactions between common genetic variants and environmental exposures.
Severe mental illness that confers strong reproductive disadvantage is likely to have a
large and pleiotropic contribution from rare variants of recent origin. Uher points out
that this new framework requires a paradigm change in genetic research to enable
major progress in elucidating the etiology of mental illness (Uher, 2009).
So, perhaps it is no longer pragmatic to ask if there are groups of mental disorders
that have an identifiable genetic (physiological) contribution to their development and
groups of disorders that do not. It appears that all mental health issues both positive
and negative have genetic and environmentally based learning contributions. While at
the current time it appears that there might be groups of disorders that do not have a
clear genetic predisposition, is this state of affairs temporary? Will their genetic con-
tribution be identified in the fullness of time? Finally, the question becomes for the
disorders with clear generic contribution, what is the role of environmentally based
learning on the expression of the disorder? If the outcome is not predetermined, what
experience would encourage healthy development and which would not?

Epigenetic Models Integrate All Factors

Epigenetics refers to the study of heritable changes in gene expression that occur with-
out a change in DNA sequence (Wolffe & Matzke, 1999). Heritable defects in gene
expression not involving DNA sequence changes have been referred to as epimutations
(Petronis, 2000). It has been clearly established that many common diseases involve
interactions between genes and the environment, and epigenetic mechanisms are
thought to be an interface between genes and the environment in these diseases
(Chakravarti & Little, 2003). The physiology of the various epigenetic mechanisms is
beyond the scope of this book, but there is clear evidence of pathways that permit
environmental factors to influence genetic expression (Jones & Takai, 2001). As an
64 7 Biologically Based Disorders of Mental Illness

example of epigenetic interactions we provide the following: de Kloet, Joëls, and


Holsboer (2005) found that in response to stress, the brain activates several neuropeptide-
secreting systems which led to the release of adrenal corticosteroid hormones. These
hormones feedback on the brain by binding two types of nuclear receptor that act as
transcriptional regulators. This affects many genes. They conclude that corticosteroids
functioned in a binary fashion, serving as a master switch in the control of neuronal and
network responses that underlie behavioral adaptation. For those individuals that are
genetically predisposed, an imbalance in this binary control mechanism can introduce
a bias toward stress-related brain disease after adverse (read as learned) experiences.
Psychosocial factors have been identified as important environmental factors
involved in the pathogenesis of mental disorders (Crow, 2003; Kato, 2001). Random
factors are thought to be involved in epigenetics, and hence they may also contribute to
the epigenetic defects underlying mental disorders. Recent experimental evidence sug-
gests that genetic, epigenetic, and environmental factors can interact with each other in
determining gene expression in mammals (Pritchard, Coil, Hawley, Hsu, & Nelson,
2006). There are numerous environmental/psychological factors that have been postu-
lated including toxic stress, and early prenatal care (Shonkoff & Garner, 2012) could
impact epigenetic patterns, with important implications for mental health in humans.
In summary, we do not mean to either ignore or make light of the contribution of
genetic or other factors in the development of mental disorders. Quite the contrary,
they are there and they are significant. They form the backdrop or beginning scaf-
fold of what become disordered behaviors associated with poor mental health.
These contributions will by themselves form a workable basis as part of a model of
how disorders of mental health finally develop in an individual.
We do mean to highlight how learning and the connectome interact and contrib-
ute to the overall result. As a therapist, or a client, you can do little about the fact
that the network architecture has been determined by a number of factors. You can,
however, do a lot about learning how to influence and modify the operation of that
connectome in the future.

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Chapter 8
Automaticity and Unconsciousness: What
Are They and What’s the Difference?

Our life is composed greatly from dreams, from the unconscious, and they must be brought
into connection with action. They must be woven together (Anais Nin).

It has long been recognized both in the professional literature and popular folklore
that people do things without thinking about them. For about as long as people rec-
ognized that they do things without conscious thought, they have devised explana-
tions for why these phenomena occurred. Early explanations have included peckish
gods, demon possession, and witch’s spells. Early mental health science posited ids
and personality archetypes to name but a few. As you are likely aware, entire theo-
ries regarding mental health have based themselves around the idea that certain
things are unconscious, and provided reasons for why this should be so. Many of the
reasons that were offered postulated that those things that were unconscious were
uncomfortable for the person.

Therapeutically Oriented Views of the Unconscious

Even today, the Freudian model of the unconscious is still with us. Freud considered
the unconscious as the primary guiding influence over daily life. Freud’s uncon-
scious is more specific and richly detailed than any to be found in contemporary
cognitive or social psychology (Bargh & Morsella, 2008). Freud, for example,
divided the mind into the conscious mind (or the ego) and the unconscious mind.
The unconscious mind was divided into the id (or instincts and drive) and the super-
ego (or conscience). In Freud’s theory, the unconscious refers to the mental pro-
cesses of which individuals make themselves unaware. These processes occur in
response to specific stimuli, but the relationship between stimulus and response is
below the level of conscious awareness. In other words, individuals exert cognitive
effort in order to suppress their awareness of certain thoughts (Mannoni, 1971).
Contemporary perspectives on the unconscious mind are quite different and
remarkably varied. For cognitive psychology, unconscious information processing

© Springer International Publishing Switzerland 2016 67


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_8
68 8 Automaticity and Unconsciousness: What Are They and What’s the Difference?

has been equated with subliminal information processing. For cognitive psycholo-
gists the question of how good is the mind at extracting meaning from stimuli of
which one is not consciously aware is fundamentally important. Social psycholo-
gy’s traditional focus has been on mental processes of which the individual is
unaware, not on stimuli of which one is unaware (Bargh & Morsella, 2008).

Contemporary Models of the Role of the Unconscious

More modern theories such as unconscious thought theory (UTT) (Dijksterhuis &
Nordgren, 2006) seek to demystify the role of the unconscious and describe its function-
ing as a specific type of cognitive processing that operates without the benefit of con-
scious control. It distinguishes between two modes of thought: unconscious and
conscious. Unconscious thought and conscious thought are posited to have different
characteristics, and these different characteristics make each mode of thought useful
under different circumstances. For instance, decisions about simple issues can be better
tackled by conscious thought, whereas decisions about complex matters can be better
approached with unconscious thought. More recently Bos, Dijksterhuis, and van Barren
(2011) demonstrated how unconscious thought might operate. They demonstrated that
unconscious thought involves an automatic weighting process, whereby important deci-
sion attributes receive more weight and unimportant decision attributes receive less
weight. This weighting depended upon reinforcement saliency as determined by history.
This automatic process is ongoing, operating behind the scenes as it were all the time.
All such explanations attempt to describe and explain what appear to be univer-
sally occurring cognitive processes. It appears certain that there are neurophysiolog-
ical processes that occur either below the level of conscious awareness or without
the benefit of conscious awareness and effort. That distinction is an important one.
If one says “below the level of conscious awareness,” it is almost implied that con-
scious processing of information is the default and desirable human state. If one
says “without the benefit,” it is implied that there is a reason for such processing that
serves an adaptive function. As we shall see there are some very good reasons why
human have to process information without the benefit of conscious processing, and
in fact conscious processing may not, in all instances, provide a clear benefit at all.

Why We Need Automatic Processing

Humans, despite all of the wonderful things we do with our brains, have, in fact,
somewhat limited cognitive capacity with which to do everything we want to do
(Callicott et al., 1999). There are several components of cognitive capacity; the first
is termed working memory.
What Is Automaticity? 69

Working Memory

Working memory is defined as the part of short-term memory that is concerned with
the immediate conscious processing of information required to carry out complex
cognitive tasks such as learning, reasoning, and comprehension. Working memory
as we have implied is very limited. For example, research suggests that a person can
retain about 2 seconds’ worth of speech through silent rehearsal. If you think about
listening to a person and trying to remember what was said, you can readily see that
isn’t very much. According to Cowan (2010), in order to understand the nature of
working memory capacity limits, two distinctions matter. While working memory
ability is usually discussed in a processing-related, inclusive way, it instead takes
storage-specific, central measures to observe capacity limits that are similar across
materials and tasks. Storage models suggest that working memory ability varies
widely depending on what processes can be applied to the task but that typical
humans can handle between three and five items at any one time. Individuals not
only differ in working memory ability in terms of how much can be stored. They
also differ in their use of cognitive processes that aid working memory and influ-
ence how effectively working memory is used. One important example is in the use
of attention to fill working memory with the items one should be remembering (say,
the concepts being explained in a class) as opposed to filling it with distractions.
This last issue is important when assessing the issues related to attention deficit
disorder, for example (Wasserman & Wasserman, 2015).

Cognitive Load

A related concept is the concept of cognitive load which is defined as the total
amount of mental effort required to use working memory (Sweller, van Merrienboer,
& Paas, 1998). Human cognitive capacity is actually quite small when compared to
the amount of information we must process and act upon at any one time. Humans
must carefully select what activities to devote their limited capacity to. At any one
time there may be more action required than there is cognitive capacity available.
As a result humans have had to develop a system that permits them to engage in
well-learned behavior that does not require utilizing limited active/conscious pro-
cessing capacity. We call the operation of this system automaticity.

What Is Automaticity?

As is true of many of the constructs commonly used in psychology, the construct of


automaticity has multiple definitions and no consensus as to how the state of auto-
maticity is achieved. For our purposes, automaticity is an outcome of learning.
70 8 Automaticity and Unconsciousness: What Are They and What’s the Difference?

When it works right, the outcome is desirable and allows us to complete many
common everyday tasks without depleting cognitive resources. When the outcome
is less desirable, it means that we sometimes engage in undesirable behaviors with-
out thinking. Of course it also means that we engage in undesirable emotional
responses without thinking.
The basic concept of automaticity is historically rooted in operant/instrumental con-
ditioning models, wherein reinforcement is made contingent on the occurrence of a
response. When a particular behavior is rewarded enough times, it becomes automatic.
That is, the individual does the behavior in the presence of the reward without thinking
about it.
This instrumental learning can be divided into two types: goal directed and habit-
ual (Braunlich & Seger, 2013). These two types really describe the state of the
relationship between the stimulus and the reward. Goal-directed behavior assesses
the contingencies (probabilities) between our behavior and potential outcomes. It is
a conscious process guiding our behavior and therefore costly in terms of cognitive
resources. Once a particular choice is made and repeated and has become suffi-
ciently practiced, it becomes habitual. That is, it enters a state of automaticity. It can
then be expressed without the requirement of the prior analysis of probabilities and
can be produced more quickly and efficiently. For our purposes then, automaticity
is defined by the broader definition of a behavior or emotion that is so practiced, it
emerges without conscious effort.

Why Is Understanding Automaticity Necessary?

As Braunlich and Seger point out, habitual behavior (automatic) is elicited by envi-
ronmental stimuli without conscious consideration of outcome. It is a behavior that
has become so practiced; it is automatic. As we have pointed out, the purpose of this
automaticity is to free the individual of the need to expend executive management
resources in the performance of a particular task. This is necessary because working
memory and executive resources are limited, and this process of automatization frees
the cognitive resources of an individual for processing novel tasks. The point of this
all is, as a result of practice and experience, we engage in many behaviors and feel
many emotions without actively thinking about them. In our view, an understanding
of automaticity is therefore essential for both understanding the development of what
is termed mental dysfunction and the system of intervention required to address it.
This is so because at the beginning therapy requires and is conducted by using con-
scious mental effort. Therapy requires making implicit knowledge temporarily
explicit for the purposes of exploration analysis and potential change. Research has
demonstrated that we have two primary memory and learning systems which function
in the brain: the first for facts and ideas (i.e., the declarative or explicit system) and the
other for habits and behaviors (i.e., the procedural or implicit system). Broadly speak-
ing these two memory systems can operate either in concert or entirely independently
of one another during the performance and learning of skilled motor and cognitive
behaviors (Vidoni & Boyd, 2007). When you are seeking to change the relationship,
Maladaptive Behaviors and Emotions Can Be Automatic 71

you need to examine those previously learned and now habitual behaviors. In order to
be successful you must make those implicit relationships and behaviors explicit
(Talvite & Ihanus, 2002).

Automaticity Is Not Only About Behavior

Automaticity is not necessarily limited to observable behaviors. It also refers to the


learning of cognitive processing routines which require attention, focus, and work-
ing memory. Koziol and Budding (2009) discuss how humans require a system
which will allow them to “know” what to do: a “habit” or automatic system for
dealing with the well rehearsed or routine and a problem solving system for unfa-
miliar or novel circumstances. These two systems have fused into the fronto-striatal
system and allow and collectively enable the organism to “know what to do.” These
rehearsed/automatized responses to stimuli can become quite complex. All that is
required for their expression is a stimulus to initiate the response sequence. This
initiation is referred to as priming.
According to Bargh (2006), research on priming, defined as nonconscious acti-
vation of social knowledge structures, has produced a plethora of rather dramatic
findings. Priming a single social concept such as aggression can have multiple
effects across a wide array of psychological systems, such as perception, motiva-
tion, behavior, and evaluation. Priming and automaticity have been demonstrated in
the development and expression of social norms, cultural ideology, performance
goals, interpersonal relations, complex social behavior, and understanding ambigu-
ous social behavior.

Maladaptive Behaviors and Emotions Can Be Automatic

Is should be obvious by now that both positive and negative maladaptive behavior
and emotional states can become automatic as well. It all depends on what is learned
and processed as a result of the individual’s interaction with the environment.
Research demonstrates that the regulation of emotions is in many aspects highly
automatized (Mauss, Bunge, & Gross, 2007). Defining this process as automatic
emotional regulation (AER), Mauss, Bunge, and Gross describe it as goal-driven
change to any aspect of one’s emotions without making a conscious decision to do
so, without paying attention to the process of regulating one’s emotions, and with-
out engaging in deliberate control. In other words, “AER is based on the automatic
pursuit of the goal to alter the emotion trajectory” (p. 147). The concept of AER can
be applied to a plethora of maladaptive emotional strategies such as repression and
defense mechanisms. For example, Shaver and Mikulincer (2007) describe how
individuals with avoidant attachment styles (individuals who habitually avoid close
emotional relationships) would have learned as children, that the expression of neg-
ative emotion is ineffective or counterproductive with respect to certain attachment
72 8 Automaticity and Unconsciousness: What Are They and What’s the Difference?

figures. This process becomes both automatized and generalized to other people as
the individual practices this maladaptive avoidance.
Brain networks associated with AER have been identified. Studies suggest the
involvement of the orbitofrontal cortex (OFC), especially lateral and medial por-
tions, lateral and ventromedial portions of the prefrontal cortex (lPFC and vmPFC),
the basal ganglia (BG), and the cerebellum. All of these regions have been implicated
in emotion regulation, cognition–emotion interactions, top-down direction of atten-
tion in response to negative emotional stimuli, and encoding affective expectations
in relation to conditioned stimuli (Beer, Heerey, Keltner, Scabini, & Knight, 2003;
Davidson, 2002; Elliott, Dolan, & Frith, 2000; Gottfried, O’Doherty, & Dolan,
2003; Hamann, Ely, Hoffman, & Kilts, 2002).

Automaticity and Mental Health

We propose that much of what is currently defined as constituting mental disorders


reflects (a) the development of maladaptive behaviors which have become auto-
matic and (b) the inappropriate application of these habitual or automatic behaviors
onto novel situations. This creates a cycle in which there is strengthening of the
automaticity of the habitualized behaviors, which, in turn, results in outcomes
which cause emotional and mental distress because of misapplication.

Automatization and Therapy

How does this conceptualization alter the application of therapy? Historically, behav-
ior which resulted in internal distress was conceptualized as a function of the uncon-
scious. Entire therapeutic systems are constructed on the basis of definition and
understanding of the unconscious. Like much else in the world of psychology, the
construct of the unconscious also has multiple meaning and usages. One can even
initially think that automaticity as used in learning theory and the principles of verti-
cal brain-driven therapy is classic analytic unconscious (Freud, 1913) disguised in
sheep’s clothing. In truth, the concepts share many things in common, but have major
definitional differences that render them completely distinct constructs. In psycho-
analytic theory of personality, the unconscious mind is a reservoir of feelings,
thoughts, urges, and memories that are outside of our conscious awareness. So far
that sounds the same. What distinguishes this reservoir from the modern concepts of
automaticity is that instead of being highly practiced routines that no longer require
the conscious exertion of control, psychoanalytic concepts of the unconscious are
unacceptable or unpleasant, such as feelings of pain, anxiety, or conflict. They are
unconscious because they are too painful to be dealt with consciously. They are
repressed, sublimated, and otherwise suppressed from awareness. Freud, in a manner
similar to modern learning theorists, believed that the unconscious influences behav-
ior and experience, even though we are unaware of these underlying influences. In
The Role of Automaticity in Therapy 73

the psychoanalytic model, these unconscious and maladaptive desires attempt to


break through to consciousness and cause all sorts of havoc. We expend a great deal
of psychic energy creating barriers to the expression of these impulses. As we have
seen, the concept and research around the concept of automaticity does away with
the need to conceptualize these maladaptive repressive forces.
While the differences may appear to be subtle, the implications are not. An
example might serve to clarify the difference: Mike is a dutiful husband and after
some discussion he agrees to replace his two-seater sports car, affectionately named
Mary for no particular sentimental reason, for a four-seater, sensible, family car. He
does so. About a week later, imagine it is raining rather heavily, and Mike, trying to
do the right thing, calls out to his wife that he is going to go get “Mary” and drive
her around front to pick her up. Mike’s upset wife is waiting out front and asks Mike
if he is unhappy about selling the original car, saying that she thinks he hates her
for encouraging him to do so. We are not going to get into the myriad of possible
psychoanalytic interpretations that would speak about Mike’s repressed anger.
Automaticity would indicate that Mike made the association between the word
“car” and the name “Mary” many times and, under the time pressure, produced the
typically occurring automatized response. No subordinated conflict-based interpre-
tation would be required.
It is not our intention to enter into a debate about which theoretical perspec-
tive might be correct. We have long ago decided the issue for ourselves. We do
not believe that the unconscious is solely the repository of maladaptive thoughts
and ideas that are too painful for conscious expression, and that the conscious-
ness contains mechanisms to suppress the expression of these undesirable
thoughts and impulses. The simple fact is that both adaptive and maladaptive
behaviors occur at the automatic level and that much of human behavior, good
and bad, occurs at the automatic level because the architecture and capacity of
the human brain require that practiced routines be conducted effortlessly and
efficiently.

The Role of Automaticity in Therapy

What then is automaticity in a learning theory context, and how might it be used
in therapy? Firstly, we provide the following definition: an automatic process is
one that, once initiated (regardless of whether it was initiated intentionally or
unintentionally), runs to completion with no requirement for conscious guidance
or monitoring (Moors & De Houwer, 2006). In addition, in agreement with Bargh
(1992), therapeutic intervention based on vertical brain-based learning theory is
conducted on the idea that all automatic processes are conditional. They are all
dependent on preconditions (e.g., the presence of a triggering stimulus, aware-
ness of the stimulus, the intention that the process takes place, a certain amount
of attentional resources, and the salience of the stimulus). Automatic processes
will vary with regard to the specific subset of preconditions they require. The
identification of these preconditions becomes an important element of the
74 8 Automaticity and Unconsciousness: What Are They and What’s the Difference?

therapeutic process. Essentially, the unconscious consists of routines stored in


working memory, which when triggered by conditioned environmental stimuli
run to completion without conscious awareness.

Therapy Process

We can now recognize that in most therapy processes, the emphasis is on identifying
these environmental triggers and altering the automatized response to them.
Different therapy approaches vary on what the triggers are, how to identify them,
and how to reprogram them, but all are in agreement that the task is the same: the
reprogramming of maladaptive automatized responses into adaptive ones. The sci-
entific questions to be derived from this are direct ones. Is there an efficient way to
perform this process? If there are several ways to achieve this end, is one more
efficient than the others? Is efficiency the goal, or is one process better at producing
greater knowledge acquisition at the expense of time? These are all questions that
deserve answers based on scientific inquiry. We do not seek to answer them or
answer any of them completely. What we do seek to clarify is what is now known,
and that is that the brain processes information in a predictable fashion. Therefore,
the question we seek to answer is whether there is a particular form of therapeutic
information provision that provides information in a manner that is consistent with
how the brain is going to process it. The answer is that there are specific principles
of brain-based learning that are directly applicable to the therapeutic process and
that these should be incorporated into standard therapeutic practice.
As indicated, the therapy process, which will be discussed in detail later,
emphasizes that automatized maladaptive behavioral and cognitive responses be
first made available for working memory and attention and systematically altered
with the resulting adaptive behavior re-automatized. Identifying the triggers (pre-
conditions) is an essential part of this process. For the most part, the maladaptive
responses and the reformulated adaptive ones are learned. They do not “come
preprogrammed at the factory.” They represent the interaction of core tempera-
mental characteristics (Chess & Thomas, 1967) and regulatory efficiency with
environmental experiences.

Does Therapy of a Mental Health Issue Imply That We Are


Treating a Disease?

The fact that they are learned (or shaped through an experiential process), can be
unlearned, and can adaptively be relearned means that for the most part, we are
not dealing with a disease process. A disease can be defined in several ways such
as “any impairment of normal physiological function affecting all or part of an
organism, esp. a specific pathological change caused by infection, stress, etc.,
Small-World Hub Models and Therapeutic Practice 75

producing characteristic symptoms; illness or sickness in general” (Reverso,


2014) or pathology (Perry et al., 2008). In either definition this implies that there
is some disruption of the normal.

Small-World Hub Models and Therapeutic Practice

Small-world hub models and the related construct of automaticity imply that the
network of connectionist hubs is unique to each human being. Some may be adap-
tive and some maladaptive, but the vast majority of these networks are based on the
system responses to the environmental stimuli it encounters. They are created by
learning and are the result of that learning. In recognizing that, it becomes important
to consider that learning and educational processes and principles should be utilized
when trying to alter them.
As regards automatization, therapy processes based on a small-world hub model
of brain organization would utilize an algorithm strengthening model (Anderson,
1996) that proposes one learning mechanism to account for automatization of all
routines. An algorithm is a mathematically understandable and expressible cogni-
tive process. The central theme of algorithm efficiency theories is that practice
improves the efficiency (speed and fluidity) of the underlying algorithmic processes
that compute interpretations of task stimuli (Rawson, 2010). In an algorithm
strengthening model, consistent practice is essential for the development of automa-
ticity. Improvement in terms of efficiency requires algorithms to remain consistent
with practice, even though aspects of the data they are practiced upon may change.
For example, when a student is learning addition, the algorithm (process) is the
same whether the number involved is a “2” or a “3” or a “45” (Carlson & Lundy,
1992). This principle would suggest that sound therapeutic process would involve
systematic and direct practice of the new skill (belief). This practice should include
behaviors that devolve from the expression of the belief. For example, if a person
comes to believe that yoga is beneficial, it is not sufficient to merely practice the
statement that yoga is beneficial, but it is usually required to practice the behaviors
(doing the yoga) that devolve from incorporating that belief. This principle would
also imply that the clearer the connection is between the belief and the practice, the
more efficiently it will be learned.
There are some additional aspects of these algorithmic models that have implica-
tions for therapeutic practice. The algorithm (processing) strengthening (Adaptive
Control of Thought or ACT) principle, in line with the connectionist models
reviewed earlier, hypothesizes that the same algorithms responsible for the initial,
nonautomatic stage of performance are also responsible for the skilled, automatic
stage of performance. In the latter stage, these algorithms are executed faster and
more efficiently with increasingly less conscious allocation of working memory and
control required. Hence, automatic and nonautomatic algorithms differ only with
regard to the features (such as speed and efficiency) they possess (Rawson, 2010).
This clearly implies that awareness and knowledge of how these algorithms operate,
both on a conceptual and neurophysiological level, are essential for the therapist
76 8 Automaticity and Unconsciousness: What Are They and What’s the Difference?

when designating intervention strategies because there is only one set of algorithms
that will control the sequence of the behavior both during the acquisition stage and
the demonstration stage. It also implies that a planned and purposeful creation of the
algorithms that has predictable outcomes would be preferable to a haphazard one.

Vertical Brain Models and Automaticity

Vertical brain-based therapy principles also emphasize the role of attention in


automaticity (Koziol & Budding, 2009). Attending to a stimulus is necessary to
encode it initially into working memory or to retrieve it from long-term memory.
Attention is a form of selection wherein the individual allocates working memory to
a specific stimulus (Shell et al., 2010). When a stimulus is either encoded or retrieved,
all information that was associated with it during a former presentation are attended
to as well. Both storage and retrieval are improved each time attention is focused on
the stimulus. Retrieval is done with less effort each time. In addition, as it is improved,
stronger retrieval cues are created, and automatic retrieval becomes ever more likely.
Automatization produces a shift in attention (rather than a reduction), with attention
being allocated to higher levels of organization. When components of a skill become
automatic with practice, attention is shifted from them to higher-level aspects of the
skill concerned with the integration of complex skills (Logan, 1992). The implica-
tions for therapy become clear. Older maladaptive behaviors are expressed automati-
cally in response to a variety of highly integrated stimuli. These stimuli must be
repaired with adaptive routines which are at first highly cognitive, unpracticed, and
rough. These new routines, which require considerable cognitive effort, are difficult
to learn and, at first, highly specific to the situation in which they are learned.
Successful therapy encourages the practice of these new adaptive routines until they
become widely responsive to a variety of cues, which are automatic, practiced, and
efficient. Automaticity would reciprocally improve the selection process as well. For
example, treatment, for a person with a negative outlook or depression, would
involve having a person spontaneously identify the positives or potential in a difficult
situation as opposed to seeing only the dangers.

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Chapter 9
Mental Illness

Mental illness, of course, is not literally a “thing” - or physical object - and hence it can
“exist” only in the same sort of way in which other theoretical concepts exist. Yet, familiar
theories are in the habit of posing, sooner or later — at least to those who come to believe
in them — as “objective truths” (or “facts”). During certain historical periods, explanatory
conceptions such as deities, witches, and microorganisms appeared not only as theories but
as self-evident causes of a vast number of events. I submit that today mental illness is
widely regarded in a somewhat similar fashion, that is, as the cause of innumerable diverse
happenings. As an antidote to the complacent use of the notion of mental illness, whether
as a self-evident phenomenon, theory, or cause, let us ask this question: “What is meant
when it is asserted that someone is mentally ill?”
Thomas Szasz (Szasz, 1960, p. 113)

Let us consider the following scenario: Little Joey has learned to belch by drinking
directly from the bottle of pop instead of pouring the pop into a glass. Little Joey has
learned this behavior while at his bachelor uncle’s house where your spouse took him
to watch football and hang out with “the guys.” Joey comes home to you and declares
that he has learned a new trick, shows you how to drink pop directly from the bottle,
and proudly finishes the demonstration with a large belch. He states proudly that all
of Uncle Biff’s friends who were watching football thought he was the best belcher
they had ever seen. You are not amused, immediately declare the behavior to be
unacceptable, and instruct little Joey in the proper way of drinking pop.
None of us would likely say that Joey’s maladaptive behavior was reflective of
a mental illness. In fact, in some cultures, this might be expected and approved of
behavior. Where, however, do we draw the line between the results of Uncle
Biff’s sophomoric behavioral instruction and a mental illness for little Joey? To
put it another way, when does little Joey’s following uncle Biff’s instructions
develop into a mental illness?
To demonstrate the point, let’s expand upon the above scenario a bit. Suppose that
little Joey refused to stop belching, declaring that it was fun, and began to drink out
of other containers and merrily belch whenever and wherever possible, including
school. He resists both your corrections and the teacher’s corrections by saying no he

© Springer International Publishing Switzerland 2016 79


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_9
80 9 Mental Illness

won’t change because Uncle Biff told him that real men make their own decisions
and don’t listen to a woman. Feeling his oats, Joey begins to refuse other instructions
such as taking a bath or brushing his teeth. Sometime later, after thinking about why
she didn’t see the warning signs about Uncle Biff previously, little Joey’s mother,
having tried everything she could think of including sending her husband and his
brother to Ms. Pickford’s School for Gentlemen, presents herself in your office. She
presents you with the litany of little Joey’s resistant and difficult behavior. You agree
to help her and inform her that this is her lucky day because you accept her insurance
coverage. You complete the form and when it comes to the section on diagnosis,
which must be completed so that little Joey’s mom can get her coverage, you write
down oppositional defiant disorder secure in the knowledge that he met the criteria.
But wait a minute; there are questions, serious questions, to be asked. According to
the assignment of that diagnosis, you now believe and assert that Joey now appar-
ently has a mental illness—an illness representative of defectively wired neural cir-
cuitry. At what point did this happen? Where in the behavioral response chain did
little Joey’s learned and reinforced refusal become an oppositional defiant disorder,
and more importantly, at what point did this behavior become an illness reflective of
permanently miswired neural circuitry?

Crossing the Line

As we shall see, there is a logic chain here that is fundamentally illogical. For the vast
majority of people, is it logical to draw a line and say when you cross it you are disor-
dered, or is it preferable to say that a person is in need of clinical help to address these
maladaptive behaviors? Current diagnostic labeling is an example of the former.

A Word About the DSM and the ICD 10

The Emperor was accordingly undressed, and the rogues pretended to array him in his new
suit; the Emperor turning round, from side to side, before the looking glass.
“How splendid his Majesty looks in his new clothes, and how well they fit!” everyone
cried out. “What a design! What colors! These are indeed royal robes!”
“But the Emperor has nothing at all on!” said a little child.
“Listen to the voice of innocence!” exclaimed his father; and what the child had said
was whispered from one to another.
“But he has nothing at all on!” at last cried out all the people. The Emperor was vexed,
for he knew that the people were right; but he thought the procession must go on now! And
the lords of the bedchamber took greater pains than ever, to appear holding up a train,
although, in reality, there was no train to hold (Andersen, 2008).

The Diagnostic and Statistical Manual of Mental Disorders (DSM) which houses
a currently used nosology (DSM 5) was developed out of a need for explicit
definitions of disorders as a means of promoting reliable clinical diagnoses
(American Psychiatric Association, 2014). The International Classification of
A Word About the DSM and the ICD 10 81

Diseases (ICD) is the international medical classification system established by the


World Health Organization. ICD codes are the international medical classification
system that identifies diseases, signs, symptoms, abnormal findings, complaints,
social circumstances, and external causes of injury or diseases. Both systems are
etiologically silent as regards many mental illnesses. In the DSM 5 numerous
changes were made to the classification (e.g., disorders were added, deleted, and
reorganized), to the diagnostic criteria sets, and to the descriptive text based on a
careful consideration of the available research about the various mental disorders
(American Psychiatric Association, 2014). There are ongoing and increasing con-
cerns regarding the use of the DSM system and its impact on research into mental
disorders. These include the argument that the DSM represents an unscientific and
subjective system (Lane, 2013). There are escalating concerns regarding validity
and reliability of the diagnostic categories, the reliance on superficial symptoms,
and as we have seen the use of artificial dividing lines between categories of mental
illness and normality. Possible cultural bias has been identified and the issue, high-
lighted in this book, of unnecessary medicalization of human behaviors raised.
Most importantly the DSM systems are etiologically silent by design.
As a result of both the DSM and ICD systems being etiologically silent by
design, when it comes to mental health issues, we use a unique process to establish
a diagnosis. In order to make a diagnosis, we decide that a certain volume of mal-
adaptive behavior has occurred and that the criteria have been met for volume, and
now this volume qualifies for a diagnosis. For example, either the DSM 5 or ICD 10
requires that an individual demonstrate six criteria out of nine in one of two catego-
ries in order to meet criteria for a diagnosis of ADHD. If you meet six criteria, you
have ADHD and are demonstrating the behavior reflective of a mental illness, but if
you have only five, you are not. You don’t even have to have the same six in order
to have the same illness, any six will do. To accomplish this slight of mind, we are
required to ignore all that usually comes with a diagnosis because what comes with
it is that the person who has reached that volume is now ill and that illness reflects
a biological underpinning. What then becomes most amazing is that once we declare
that a person meets the disorder criteria, we proceed to explain the diagnosis in
neurobehavioral terms. Having arrived at the conclusion based upon a heteroge-
neously constituted set of criteria, we attempt to explain with a homogeneously
neurophysiological or genetic model. In reality, when used in this manner, as
Thomas Szasz pointed out, “mental illness” is not the name of a biological condi-
tion whose nature awaits to be elucidated but is the name of a concept whose pur-
pose is to obscure the obvious. We would point out not only obscure but confuse.
This situation leads to a number of difficulties, not the least of which is that the
system creates heterogeneous disorder classes which confabulate research. As
pointed out by Karpur, Phillips, and Insel (2012), our understanding has been fur-
ther confused by a large number of statistically significant, but minimally differen-
tiating, findings as regards mental illness. Indeed, there are a myriad of reasons for
the disappointing progress in the nosology and diagnostics of mental illnesses, but
fundamentally the problem can be tracked to a lack of causal understanding of the
underlying biological mechanisms.
82 9 Mental Illness

If a significant portion of the difficulties that present themselves in a therapist’s


office are the result of an interaction between an individual’s genetically determined
temperament, constitution and environmental circumstance, are we best served by
describing the outcome as an illness? If these problems are learned behavior reflec-
tive of connectionist neurophysiologic white matter connections that can be system-
atically disconnected and reconnected to more adaptive behavior, is that reflective
of an illness? These questions lead to a number of other questions such as what is a
mental illness?

Defining Mental Illness

As with most terms in mental illness, when you go looking for an agreed-upon defi-
nition, you have trouble finding one (Fulford, 1989; Wakefield, 1992). The Merriam-
Webster Dictionary defines illness as “a condition of being unhealthy in your body
or mind: a specific condition that prevents your body or mind from working nor-
mally: a sickness or disease” (Merriam-Webster, 2014). According to the National
Institute of Health (NIH), a mental illness can be defined as a health condition that
alters a person’s thinking, feelings, or behavior (or a combination of all three) and
that causes the person distress and difficulty in functioning (National Center for
Biotechnology Information, 2007). The NIH goes on to state that as is the case for
most illnesses, symptomology can vary from mild to severe and that in some
instances of mild illness, the symptoms may not be noticeable. The careful reader
will notice that there is no attempt to ascribe the illness to the brain although most
would argue that the association is assumed. What is also not apparent but is
assumed is that the illness is caused by an underlying physiological process that has
somehow been altered or disrupted. The ensuing NIH discussion on diagnosis
makes that clear. “Unlike some disease diagnoses, doctors can’t do a blood test or
culture some microorganisms to determine whether a person has a mental illness.
Maybe scientists will develop discrete physiological tests for mental illnesses in the
future; until then however, mental health professionals will have to diagnose mental
illnesses based on the symptoms that a person has” (National Center for
Biotechnology Information, 2007). Quite without explanation, they substitute the
word disease for illness because when we think about the two, they are interchange-
able. The Merriam-Webster Dictionary defines the word disease in a medical con-
text to mean an “impairment of the normal state of the living animal or plant body
or one of its parts that interrupts or modifies the performance of the vital functions,
is typically manifested by distinguishing signs and symptoms, and is a response to
environmental factors (as malnutrition, industrial hazards, or climate), to specific
infective agents (as worms, bacteria, or viruses), to inherent defects of the organism
(as genetic anomalies), or to combinations of these factors” (Merriam-Webster,
2014). So in general, when you have a medical disease, you usually have an agent
or cause of that disease. But, as we have seen, when we speak of mental disease, that
is not the case. Since we do not know, or more specifically in the past we did not
Theories About the Etiology of Mental Illness 83

know, how mental disease occurs, symptoms, either behavioral manifestations or


verbal reports of internal states, are relied upon to reach a conclusion and a label as
to the exact nature of the disorder. Currently these lists of symptoms are enshrined
in the Diagnostic and Statistical Manual of Mental Disorders (5th ed.); (DSM 5)
(American Psychiatric Association 2013a, 2013b). In summary, to assess, diagnose,
and treat a mental illness, it is not required to have a conceptualization of how this
particular illness is caused, related to brain architecture, or developed. And we do
not have to know the physiology that underlies it. We merely must address the
symptomology and correct it in any way possible. This situation in and of itself is
not problematic. What happens next is, having made a diagnosis absent of an under-
standing of etiology, we behave, once the diagnosis is established, as though we
understand the etiology. We provide all manner of interpretations of causality after
essentially saying we don’t know the etiology.

Theories About the Etiology of Mental Illness

You cannot be faulted for thinking “Wait a minute. That can’t be true”. We have
many theoretical descriptions of the etiology of mental disorder. Certainly one must
be used in developing their etiological descriptions.” Let us examine one of the most
currently prevalent ones.
We know that there are neurotransmitters involved in the expression of many
mental disorders. What’s more is that we know that impacting these neurotransmit-
ter profiles often ameliorate the symptoms of many types of disorders. All of that
does not necessarily imply that these deficiencies in the operation of these neu-
rotransmitters are the cause of the disorder. In fact, there is evidence that they are
not (Faraone & Bierderman, 1998). The field of psychopharmacology is based on
the idea that we use drugs to treat disorders of the mind. We are told that the disor-
ders are caused by out of balance brain-based neurochemicals such as serotonin or
dopamine and that correcting these imbalances fixes the disorder; therefore, that
must be the explanation as to why the disorder occurs in the first place. Such theo-
ries of brain chemistry imbalance are collectively based on what is called the
monoamine hypothesis. The monoamine hypothesis states mental illness such as
depression is caused by the underactivity of monoamines such as serotonin, dopa-
mine, serotonin, or norepinephrine. While such explanations are very popular and
do provide some information which explains the effects of medications designed to
affect these monoamines, it remains the case that the science has not progressed
enough to provide a thorough explanation that describes how these psychopharma-
cological agents work upon the hypothetical disease process. In fact the opposite is
true. For example, “contemporary neuroscience research has failed to confirm any
serotonergic lesion in any mental disorder and has in fact provided significant
counterevidence to the explanation of a simple neurotransmitter deficiency”.
Modern neuroscience has instead shown that the brain is vastly complex and
poorly understood. While neuroscience is a rapidly advancing field, to propose that
84 9 Mental Illness

researchers can objectively identify a “chemical imbalance” at the molecular level


is not compatible with the extant science. In fact, there is no scientifically estab-
lished ideal “chemical balance” of serotonin, let alone an identifiable pathological
imbalance (Lacasse & Leo, 2005). It is also the case that as investigations progress,
the contribution of neurotransmitters such as dopamine or serotonin as causal fac-
tors in mental disorders becomes even less clear and for the most part reflects a
form of reasoning in the reverse. That logic can be faulty. For example, while it is
clear that increases in the level of aspirin in the blood stream decrease headache, it
does not mean that headache is caused by low levels of aspirin (Lacasse & Leo,
2005). As an example of the complexity involved in the development of mental
problems, recent research into schizophrenia suggested a framework that linked
risk factors, including pregnancy and obstetric complications, stress and trauma,
drug use, and genes, to increased presynaptic striatal dopaminergic function,
thereby providing a better understanding for the development of the disorder
(Howes & Kapur, 2009). Howes and Kapur (2009) go on to conclude that “a com-
plex array of pathological, positron emission tomography, magnetic resonance
imaging, and other findings, such as frontotemporal structural and functional
abnormalities and cognitive impairments, may converge neurochemically to cause
psychosis through aberrant salience and lead to a diagnosis of schizophrenia”
(p. 549). It appears increasingly the case that low levels of dopamine are the result
of learning, environmental, and structural factors (that may themselves be related,
in part, to learning) rather than the etiologic agents of the disorder. In other words,
low levels of monoamines may be symptoms as opposed to the cause. These neu-
rotransmitter anomalies are likely as not biomarkers similar to the behaviors that
are symptoms that characterize these hypothetical disorders. They may merely
reflect the functioning of the neural network that subserves the thoughts and behav-
iors associated with the disorder. It is the ability of the network recruited to sub-
serve the target behaviors that is in question. That ability of that network to operate
may be a function of signal strength across the network as reflected in dopaminer-
gic activity rather than a deficiency of dopamine itself.

Medication and Mental Illness

Yes, we know that some medications which target neurotransmitters are effective in
ameliorating symptoms of depression. Yes, we know that providing psychopharma-
cological support to improve the effectiveness of the functioning of the neurotrans-
mitters is efficacious in lessening the symptomology of depression. All of that is not
equivalent to saying the deficient dopamine or serotonin levels are the cause of
depression. It is entirely possible that the lower level of neurotransmitter is reflec-
tive of a poorly integrated white matter system created by faulty patterns of learn-
ing, association, or reinforcement (Gaffan & Harrison, 1987) or history of insult
(Batelle, Munoz-Moreno, Arbat-Plana, Figueras, & Gratacos, 2014). There is evi-
dence that suggests that this is a possibility in that it demonstrates that dopamine
Mental Health and White Matter Connections 85

changes associated with improved functioning in depressed patients occur as a


result of learning in treatment (Goldapple et al., 2004). In summary, we would
expect that the circuitry associated with performance of a particular task would have
a characteristic neurotransmitter signal profile. It would have to, in that all neuro-
cognitive performance would have a neurotransmitter profile because that is how
information is transmitted across neural circuits. To say that profile was causative is
an entirely different matter.
It remains the case that many in the field do not believe we are ready to discuss
nosology based on actual brain function. The National Institute of Health concluded
in 2007 that “the term mental illness clearly indicates that there is a problem with
the mind. But is it just the mind in an abstract sense, or is there a physical basis to
mental illness? As scientists continue to investigate mental illnesses and their
causes, they learn more and more about how the biological processes that make the
brain work are changed when a person has a mental illness.”
This state of affairs is unsettling. This is in part because the continuing reliance
on symptomology creates neurophysiologically heterogeneous classes of disor-
ders that do not lend themselves to basic science analysis. In addition, it hope-
lessly complicates the development of assessment instruments designed to assess
the various disease constructs (Wasserman & Wasserman, 2013). There is a rec-
ognition that the current nosology is necessary and will be altered when the basic
science catches up to what we have intuitively understood for some time. This has
begun to happen.

Mental Health and White Matter Connections

There is increasing recognition that a significant amount of what we call mental ill-
ness is related to structural and functional changes in white matter (Fields, 2008a,
2008b). For example, it is clear that certain aspects of depression result from mal-
adaptive stress-induced neuroplastic changes in specific neural circuits (Krishnan &
Nestler, 2008). White matter is what lies beneath the gray matter cortex. It is com-
posed of millions of bundles of axons (nerve fibers) that connect neurons in differ-
ent brain regions into functional circuits. The white color is associated with the
electrical insulation (myelin) that coats axons, essentially nerve tissue found in the
brain and spinal cord, which primarily contains myelinated fibers. White matter gets
its name from the fact that early imaging showed it as white in color (Fields, 2010).
Both white matter (Madden et al., 2004) and gray matter (Draganski et al., 2004)
have been shown to change in response to learning. Older connectionist models
demonstrated that learning involves changes in strength of synapses, the connec-
tions between neurons in gray matter. Newer research has demonstrated structural
changes in white matter after learning complex tasks, which raises the question of
whether white matter responds to experience in a manner that affects neuron func-
tion under normal circumstances, thereby affecting information processing and per-
formance (Fields, 2010). There is evidence that it does.
86 9 Mental Illness

White matter disruption and/or changes have been identified in a number of major
mental health diagnoses including attention deficit hyperactivity disorder (Overmeyer
et al., 2001; D’Agati, Casarelli, Pitzianti, & Pasini, 2010). As an example of just how
these white matter tracts might influence behavior, D’Agati et al. (2010), when looking
at individuals with ADHD, state that numerous types of motor abnormalities, including
motor overflow, have been identified in some children with attention deficit hyperactiv-
ity disorder (ADHD) including persistence of overflow movements, impaired timing of
motor responses, and deficits in fine motor abilities. They define motor overflow as
co-movement of body parts not specifically needed to efficiently complete a task. They
hypothesize that the presence of age-inappropriate motor overflow may reflect imma-
turity of the cortical systems involved in automatic motor inhibition. They note that
theories on overflow movements consistently implicate impairments in white matter
(WM) tracts, including the corpus callosum. They hypothesize that working memory
might be altered selectively in brain networks and thus influence motor behaviors.
They suggest that these abnormalities in motor/premotor circuits, which are important
for motor response inhibition, might be responsible for overflow movements in patients
with ADHD. This is important to note because vertical brain models identify these
motor circuits as involved with most cognitive activity, and dysregulation (or poor
performance) of these circuits would therefore be involved in most disorders of regula-
tion (Koziol & Lutz, 2013). White matter involvement has also been demonstrated in
depression (Thomas et al., 2002), bipolar disorder (Cullen & O’lim, 2014), obsessive–
compulsive disorder (Menzies et al., 2008), and anxiety disorder (Phan, 2009). In fact,
Stoodley (2015) identified white matter-based cerebellar dysfunction in several devel-
opmental disorders, including autism, attention deficit hyperactivity disorder (ADHD),
and developmental dyslexia, and pointed that damage to the cerebellum early in devel-
opment had long-term effects, through learning-based interaction with the environment
on movement, cognition, and affective regulation.
Central to any conception of vertical brain/small-world hub-based learning as the
etiology of some mental dysfunction would be the demonstration of normally occurring
white matter changes associated with learning. There is significant literature demon-
strating that such changes regularly take place (Scholz, Klien, Behrens, & Johansen-
Berg, 2009), and as we have noted, that learning in the form of a stress response has been
identified as an etiological factor in some forms of depression (Krishnan & Nestler,
2008). Fields (2008) noted that “myelination continues for decades in the human brain;
it is modifiable by experience, and it affects information processing by regulating the
velocity and synchrony of impulse conduction between distant cortical regions. Cell-
culture studies have identified molecular mechanisms regulating myelination by electri-
cal activity, and myelin also limits the critical period for learning through inhibitory
proteins that suppress axon sprouting and synaptogenesis” (p. 361). While these changes
in white matter have been noted, Zatorre, Fields, and Johansen-Berg (2012) observe that
“human brain imaging has identified structural changes in gray and white matter that
occur with learning. However, ascribing imaging measures to underlying cellular and
molecular events is challenging. Greater dialog between researchers in these different
fields would help to facilitate cross-talk between cellular and systems level explanations
of how learning sculpts brain structure” (p. 528).
Do Maladaptive Behaviors Constitute an Illness? 87

What does this all mean? It means that there are changes in white matter function
and structure that normally occur in response to learning, whether that learning
leads to adaptive behavior or maladaptive behavior. It implies that the neural path-
ways that subserve learning are not static but are constantly altering in response to
new learning. It also implies that neural connectivity that is reflective of maladap-
tive learning can be reoriented in response to learning that leads to adaptive behav-
ior. To us, this means that for the preponderance of problems termed as a mental
illness, the current constellation of brain structure is essentially a state rather than a
trait. If that is accurate, then for most people there is no such thing as a permanently
miswired brain or a brain that is being impacted by some toxic event or invasive
pathogen. Although undoubtedly these conditions do exist, the vast majority of the
problems termed mental illness are really nothing more than issues associated with
learning maladaptive responses for which the “cure” is to learn adaptive ones. This
does not imply that there aren’t factors that predispose an individual to develop
maladaptive responses to environmental stimuli. In fact there are. For example, cer-
tain variations in genes can predispose individuals to major depressive disorder as
genes help control the metabolism of neurotransmitters and their receptors, the
numbers of particular types of neurons and their synaptic connections, the intracel-
lular transduction of neuronal signals, and the speed with which all of these can
change in response to environmental stressors (Rot, Matthew, & Charnay, 2009).
The same genes that were producing adaptive responses are now contributing to
maladaptive responses as a result of learning. In addition recent research has pointed
to biomarkers that may lead to more precise diagnostic understanding of ADHD
subgroups (Faraone, Bonvicini, & Scassellati, 2014).

Do Maladaptive Behaviors Constitute an Illness?

So, we arrive at the question as to whether defining maladaptive responses as an


illness best describes the learning-based neurobiology that subserves them and best
serves the individuals who view themselves as ill. While we are mindful of Fulford’s
(1989) admonition that without the definition of these issues as an illness, medicine
in general and psychiatry in particular would be without appropriate conceptual
foundation for a discussion of the treatment of these issues. If we are talking about
normally distributed learning attributes and genetic predispositions and their inter-
action with environmental input, we believe not. What’s more, the continued reli-
ance on an outdated nosology, which was created because the illness model was not
conducive to the development of a firm etiological understanding and as a result
creates disorders by phenotype, leads to research that is counterproductive and
hopelessly confabulated. This has been pointed out before. “Diagnostic categories
based on clinical consensus fail to align with findings emerging from clinical neu-
roscience and genetics. The boundaries of these categories have not been predictive
of treatment response. And perhaps most important, these categories, based upon
presenting signs and symptoms, may not capture fundamental underlying
88 9 Mental Illness

mechanisms of dysfunction. One consequence has been to slow the development of


new treatments targeted to underlying pathophysiological mechanisms” (Insel
et al., 2010, p. 748). Furthermore, there are not only research-based difficulties with
the current system, and the continued use of the terms illness and disorder has nega-
tive social and emotional sequelae (Link & Phelan, 2001).

Research Domain Criteria

It is therefore past time to begin the development of new nosologies based upon
scientifically based, properly defined research criteria. There have already been
attempts in that direction. For example, the Research Domain Criteria (RDoC)
(Insel et al., 2010) classification scheme proposed by the National Institute of Health
conceptualizes mental illnesses in contrast to neurological disorders with identifi-
able lesions, as disorders of neural circuitry. The RDoC classification assumes that
the dysfunction in neural circuits can be identified with the tools of clinical neuro-
science and new methods for quantifying connections. Finally, the RDoC models
anticipate that data from related sciences such as genetics and clinical neuroscience
will yield biosignatures that will provide accurate clinical symptomology and signs
for clinical management. While we think the RDoC is a significant step forward, we
believe attention needs to be paid to the process of how those neural circuits are
established and maintained. That process for the most part does not require the ill-
ness model but does require a thorough understanding about the interaction between
an individual’s neural network and the environment in which it finds itself. We
believe that using the principles of neurodevelopmentally based learning outlined in
this book will support such an understanding.

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Chapter 10
Therapy

And so, it is not astonishing that, though the patient enters therapy insisting that he wants
to change, more often than not, what he really wants is to remain the same and to get the
therapist to make him feel better
― Sheldon B. Kopp, If You Meet the Buddha on the Road, Kill Him: The
Pilgrimage of Psychotherapy Patients

As a wise man once told me, the stuff you know is better than the stuff you don’t.
In context, this means that we prefer to stay the way we are. Change is threatening.
It is little wonder that people desire to stay the same as they are quite emotionally
invested in the choices they have made. That’s because it has taken them years of
time, effort, experience, and practice to get there.

Factors that Cause Us to Desire to Remain the Same

It takes a lot of work and factors operating together to produce a complex behavior
or emotion. A large body of research demonstrates that behaviors and experience
interact with physiological, cognitive, and emotional predispositions to produce
current behavior and that current behavior reflects the accumulation of all of these
interactive events (Atzaba-Poria, Pike, & Deater-Deckard, 2004; Buehler & Gerard,
2013). Rutter (2002) points out that a number of factors including susceptibility
genes, environmentally mediated causal risk processes, nature-nurture interplay, the
effects of psychosocial adversity on the organism, the causal processes responsible
for group differences in rates of disorder, and age-related changes in psychopatho-
logical characteristics all play a part in the development of complex adaptive and
maladaptive behavior.
Both adaptive and maladaptive behaviors have been practiced to the point of
automaticity. That means that these routines, no matter how seemingly complex to
the casual observer, can be performed effortlessly by the individual. They do not tax
cognitive resources. In essence, they are like an old shoe; they are comfortable and

© Springer International Publishing Switzerland 2016 91


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_10
92 10 Therapy

familiar although perhaps not very supportive and in many instances not good for
you to wear. Changing them requires cognitive effort. The new routines may be
painful and difficult to learn even though they might be better for you in the long
run. In order for these new routines to be successfully incorporated into our every-
day behavioral repertoire, they have to be broken in and practiced to the point
wherein you select them automatically. In other words you have to do as much work
and apply as much effort to learning the new routines as you did when you acquired
the old routines. This is difficult and in many cases frustrating. No wonder people
would prefer to stick with what they know.

Competence and Its Relationship to Emotional Status

The term competence has been used to refer to the result of these accumulated expe-
riences when a pattern of effective adaptation within an environment is achieved.
Competence results from complex interactions between a child and his or her envi-
ronment (Mastan & Coatsworth, 1998). In the context used herein, it implies that
the individual has (or lacking competence does not have) the capability to perform
well in a specific situation or groups of situations. The effects of lack of competence
have been shown to be observable early in development and also have long-term
escalating negative effect on social and emotional health (Denham, Blair, Schmidt,
& DeMulder, 2002). The process by which this occurs can be attributed to the fol-
lowing steps. An individual who lacks competence in an environment typically
becomes self-aware and engages in negative self-appraisals. These negative self-
appraisals are reinforced and reproduced regularly until they are automatically asso-
ciated with a specific class of behaviors. As we have seen elsewhere, it is highly
likely that these appraisals are linked with dedicated neural networks associated
with either reward (goal seeking) or avoidance (threat). These automatically associ-
ated appraisals are labeled as affect states such as depression and anxiety. That is in
part because the physiological responses associated with these affect states are also
associated, through the same principles of learning and over the neural networks to
the cognitions associated with the appraisals. These networks come on line when-
ever that stimulus is presented in the future.

Competence and Its Implication for Therapy

It seems easy to acknowledge that the complex learning-based interactions described


above are responsible for the development of behavior and thoughts. This makes it
all more confusing as to why, in the case of maladaptation, when discussing altering
these learned interactive results, we don’t include an understanding of utilization of
these same systems governed by the same principles. For example, it should be obvi-
ous by now that insight, absent behavior practiced to the point of automaticity, will
not produce either behavior or concomitant cognitive (including emotion) change
A Model for Learning Therapeutic Information 93

(Prochaska, DiClemente, & Norcross, 1992). It should also be obvious by now that
merely identifying a maladaptive influence, and on occasion reliving it, is not suffi-
cient to alter its influence (Norcross, Krebs, & Prochaska, 2011). This is because the
influence of that event has been shaped by multiple learning occasions in the envi-
ronment. Just as clearly, understanding how we arrived at certain conclusions and
emotional states will not automatically lead to the development of newly adaptive
responses. These new responses must be learned and practiced. In addition, maladap-
tive responses must be extinguished. That’s the only way human learning works.

Learning Therapeutic Material

If it is clear that there are numerous learned complex and interactive factors that
influence development of adaptive or maladaptive behavior, it also must be clear that
these influences must be processed through, and by, the human learning system.
There is not a single separate system that is exclusively dedicated to the information
processed as part of therapy. Like every other circumstance, there is only one system
composed of circuitry that is recruited in a task-specific manner to address the learn-
ing problem presented. These include recruited elements of brain cortical–subcorti-
cal networks that deal with arousal, both positive and negative, and reinforcement.
All human learning is the result of the efficient management of information by a
task-specific system. All information of any type is processed over the same net-
works and is encoded by the same memory, goal seeking, avoiding, and reinforce-
ment identifying systems. This system has the ability to process all sort of information
both positive and negative. Specific learning experiences govern the development of
the neural architecture to be sure, but the system properties and functioning are gov-
erned by a constant and unchanging set of operational rules. In more direct terms, all
learning is learned in the same way, and there are ways to make that learning efficient
and ways to correct it if it has gone astray. There is no exception made for therapy.

A Model for Learning Therapeutic Information

The therapy model that would devolve from this assumption is a blended connectiv-
ist–constructivist model when it comes to understanding the processes of learning
within a therapeutic (and every other) environment. That is because it recognizes the
importance of central themes (schemas) and understands the connectionist neural net-
works that govern how these schemas relate to one another. The model posits that
small-world model hubs (Bullmore & Sporns, 2009) represent the physiological mani-
festation of constructivist schemas and that the contribution of these schemas in a neu-
ral network is best represented by small-world hub networking models. Understanding
how these hubs interact with one another and change in relation to each other provides
us with the understanding about how to change the relationship of these hubs to one
another. The specifics of a small-world network model were discussed earlier.
94 10 Therapy

The model assumes that humans learn by using central themes (schemas) that are
used to provide basic pattern matches for incoming information. These central
themes are developed through a complex interaction between the individual’s
unique connectome and the environment. New neutral information is pattern
matched to the individual’s available schemata and assigned a place within an exist-
ing schema. That is, new information is classified according to the schemas (repre-
sented physiologically by hubs) that are available to the individual. This would help
us understand why for people experiencing depression, new information frequently
acquires a negative cast. All items within the schema to which it is matched are
already determined to have a negative cast and are processed over a network that
includes a subnetwork that processes negative information. These schemas are the
result of a complex and ever-evolving interaction between the individual’s connec-
tome and the environment.

The Essential Task of Therapy

In this model, changing the pattern matches and schema assignment of new infor-
mation becomes an essential task of therapy. In addition, changing the basic nature
of the schemas associated with negative affect is the ultimate goal of treatment. For
example, cognitive therapies would encourage the development of a class of events
entitled “Things I once thought were depressing but no longer are.” The therapist
would, by a process of dialectic exchanges have the client reinterpret negative
events, relabel them and understand that the original event was neutral. That would
be a very foundational goal of therapy. Even more importantly, the elegant goal of
therapy would be to understand how linguistic appraisals get accommodated into
schemas and to work to change the functioning of the original schema itself.
Analytic therapists who argue that the original traumatic event be reexperienced and
reinterpreted would conceptualize their work by understanding that everything that
has occurred since that original event would be the product of the event, its effect on
the developing connectome, and the subsequent experiences of the individual. Far
from being conceptually at odds, this model brings both perspectives into complete
alignment. The discussion, which could then be an empirical one, would be over the
best way to change the current connectome.

The Connectome and Therapy

On a network level that means changing how the hubs which represent concepts
relate to one another. Understanding how these hubs (concepts) are recruited in the
creation of thought and behavior is the goal of therapy. We therefore conclude that,
in order to be effective, every therapist must understand how the network processes
information and can articulate how the system learns and relearns information and
The Role of the Basal Ganglia in the Development of the Connectome 95

relationships between elements of information. More importantly, it is essential that


the therapist understand how information is pattern matched to schemas, and then
the neutral pattern match acquires a positive, negative, or neutral connotation. This
understanding is essential to creating the learning opportunities and environmental
circumstances that facilitate change. Even if you took the position that a therapist
should not choose the learning experience, it would still be essential to understand
how the learning experience provided by the client should be used to facilitate
changes in small-world organization.
As we saw, this pattern matching and schema development is best explained by a
model based on graphical analyses (connectionist models of cognition) (Bullmore &
Sporns, 2009). These suggest that all complex cognitive functioning, including those
associated with affectively laden content, are best represented by a connectionist
small-world model of neural networks. These small-world neural network models
are based on the concept of nodes which represent the confluence or connectivity
points of neurons, which on model is the physiological representation of a schema.
All brain networks have characteristically small-world properties of dense or clus-
tered local connectivity (nodes) with relatively few long-range connections to other
nodes. Nodes cluster together in small networks and vary to the degree of how cen-
tral they are to the connections to other small clustered networks within the system.
In this model these nodes are the physiological manifestation of the psychologi-
cal/constructivist schema. Clustered nodes represent complex schemas.
Anatomically, these nodes are complex networks containing billions of nerve cells
interconnected to other nodes by trillions of fibers. There are some important char-
acteristics of these small-world networks that potentially correlate to our under-
standing of the psychology of learning. For example, the nodes of a small-world
network have greater local interconnectivity or cliquishness than a random network,
but the minimum path length between any pair of nodes is smaller than would be
expected in a regular network. We have seen that small-world networks are valuable
models to use when evaluating the connectivity of nervous systems because the
combination of high-clustering and short path length between nodes provides a
capability for the network to perform both specialized and modular processing
in local neighborhoods and distributed or integrated processing over the entire net-
work (Achard, Salvador, Witcher, Suckling, & Bullmore, 2006).

The Role of the Basal Ganglia in the Development


of the Connectome

A key component of survival is the ability to learn which actions, in what con-
texts, yield useful and rewarding outcomes and which actions do not. Actions are
encoded in the brain in the cortex, but, as many actions are possible at any one
time, there needs to be a mechanism to select which one is to be performed.
These actions consist of stored and practiced routines. As you might imagine,
action selection is contextually specific. What might be the right thing to do in
96 10 Therapy

one situation might be the totally wrong thing to do in another. Suppose, for
example, you are quite used to going out to dinner in very casual attire and in
general do not care if people in the restaurant think you poorly dressed. On this
occasion though, you find out that a girl you want to meet is going to be in that
same restaurant and a mutual friend intends to introduce you. Your normal rou-
tine is no longer adaptive nor desirable and another must be selected. Failure to
do so would probably lead to an undesirable outcome. Similarly suppose your
child goes to the local school where your next-door neighbor is the principal.
Your families are very friendly and your 5-year-old child has taken to greet him
by calling him Uncle Ralph. The process of teaching your youngster where to
engage in one response and where not to would be important in this regard. The
therapeutic implications are important. Knowing how these decisions are made
will help us understand how a person selects a less desirable response (either
behavior, emotional, or both) when they knew that an alternative response was
better. In sum there has to be a mechanism that selects a response from among a
variety of available options including adaptive and maladaptive ones.

Action Selection and the Basal Ganglia

As we have indicated, the process of making a choice from among options is known
as action selection. This process of action selection is mediated by a set of nuclei
known as the basal ganglia. For the most part, humans are being bombarded by
environmental stimuli. These stimuli generate action requests from all over the cor-
tex. An action request is a complex pattern of signals encoding the action whose
overall level of activity (strength) represents the “salience” or urgency of the request.
These requests converge on the basal ganglia which are tasked to select the one that
is currently most important. Imagine you are attending an after-work cocktail recep-
tion and have gone directly to the reception. You haven’t eaten and you are hungry.
You enter the reception and spy the food; you also see your boss who is looking at
you and seemingly is expecting a greeting and you see the client you have been try-
ing to contact for a week. There are of course some of your friends from the office
who are waving to you as well. This is only a small subset of the stimuli impinging
on you at the moment. Clearly action selection is an important concept to under-
stand and highlight in therapy. Understanding both the perceived positive and nega-
tive valence of each choice will be critical for the client and therapist in understanding
why certain actions are selected.
The basal ganglia, also known as the basal nuclei, are a group of subcortical
structures which are strongly interconnected with the cerebral cortex, thalamus, and
brainstem, as well as several other brain areas. Functionally, the key components of
the basal ganglia are the dorsal striatum (caudate nucleus and putamen), ventral
striatum (nucleus accumbens and olfactory tubercle), globus pallidus, ventral pal-
lidum, substantia nigra, and subthalamic nucleus.
How We Decide 97

Basal Ganglia and Related


Structures of the Brain

basal ganglia
globus pallides
thalamus

substantia
nigra
cerebelium

Reproduced under the terms of the Creative Commons Attribution-ShareAlike License. Provided
by the US Food and Drug Administration.

How We Decide

Working out which action is selected is determined by the strength of the input from
each action request: The stronger the connection in the connectome between the
stimuli and the choice, the more important that action is deemed to be by the system.
In order to change the action (response) selected, the strength of connections
between various response options has to be altered so that the desired response is the
most strongly connected.
Understanding the impact of what is learned in therapy thus requires understand-
ing how that learning affects the relative strength of the outcome of each possible
action in relation to the stimuli (Gurney, Humphries, & Redgrave, 2015). Gurney
et al. (2015) built a computational model that demonstrates how the brain’s internal
signal for outcome (carried by the neurotransmitter dopamine) changes the strength
of these cortical connections to learn the selection of rewarded actions and the
suppression of unrewarded ones. Their framework links dopamine-modulated
cortico-striatal plasticity, phasic dopamine signals carrying environmental feed-
back, and the striatum’s role in reinforcement conditioned action selection. Their
model explains the important difference in instrumental learning tasks between
goal-directed and habitual behavior. An individual expressing goal-directed behav-
ior modifies that behavior in response to a change in the value of its outcome or in
the contingency between the action and the outcome; one expressing habit behavior
(automaticity) does not.
98 10 Therapy

This is then the goal of therapy, effecting action selection to produce adaptive
emotional and behavior outcomes. The model we have described shows how this
might be done. It recognizes that several known signals in the brain work together
to shape the influence of cortical inputs to the basal ganglia at the interface between
our actions and their outcomes.

The Knowledge Required to Be a Therapist

The job of the therapist is to first understand how this system operates, and how
through learned experience the connections and relationships between the various
nodes of the small-world hub network are altered. It would appear axiomatic to state
that if a person seeks to operate a system to enhance learning of any sort, it would
be judicious to understand how that system operated.
Let’s think about the example of an individual’s experience of post-traumatic
stress disorder as a result of a car crash. Our goal could be that instead of thinking
about car crashes when they see a car, this individual can ride in a car without
becoming effectively debilitated. There are many possible ways to go about it. One
way perhaps is that they could think about all the pleasant times they had riding in
a car before the crash. Another way perhaps is that they could evoke an image of a
car and do systematic desensitization to produce a relaxed state or still another
might be to recognize that the car crash was an example of the futility of becoming
independent from a constraining relationship. Whatever conjecture we believe, we
believe that in order to help a client make a change, it is incumbent upon us to
understand how the change can be made. This specifically means that we under-
stand what we can do to facilitate the disconnection of old interrelated small-world
nodes forming a maladaptive schema and facilitate the creation of a new pattern of
interconnectivity that produces increasingly adaptive behavior. We can then select
from the multiplicity of possibilities those that most effectively match out model of
how things are learned and maintained.

The Process of Therapy

At its core, therapy can be considered a process of increasing the likelihood of the
expression of adaptive behaviors and thought processes and weakening or unlearn-
ing maladaptive ones. Therapy in this perspective is about the therapist imparting
information and having the person use that information to change behavior and emo-
tional response sets. While there may be therapeutic environments that may make
certain individuals comfortable with the learning process, they cannot by themselves
substitute for a thorough understanding of how humans learn or a systematic use of
learning principles to help a person acquire and use the new material being offered.
We propose that it is not sufficient to be warm and supportive and leave the person
References 99

on a self-guided path of personal discovery. It is also not sufficient to understand the


principles of reinforcement without understanding how human goal-seeking cir-
cuitry interacts with reinforcement identifying circuitry to produce goal-directed
behavior. All therapy is learning and there are ways to make learning the material
associated with therapeutic change efficient, and there are ways to do it inefficiently.
We accept this idea without a second thought when it comes to education. We under-
stand that a student cannot learn math without directed and specific instruction.
Imagine if a person tried to learn physics using nondirective methods. No one would
accept that premise. We also know that mere rote practice of knowledge does not
produce effective learning. In most areas of learning, we strive to produce learners
who understand how they learn and can use that understanding to continually
enhance and develop their knowledge and effectiveness. We teach strategies based
upon learning principles. We somehow suspend that process for learning associated
with therapy. We act as if there are different rules or special neural circuits that are
associated with taboo or maladaptive knowledge or behavior. There are not.
Therapy is also a process by which one eliminates automatized maladaptive behav-
iors and thoughts and substitutes newly automatized adaptive behaviors and thoughts.
More specifically, in most instances, it is the process of taking previously maladaptive
automatic behaviors and thoughts, de-automatizing them and creating new adaptive
automatic behaviors and thoughts (responses) to life’s various situations. This would
of course ultimately, positively, impact an individual’s emotional state. Attaining ulti-
mate success in terms of self-fulfillment or realizing one’s potential would be in effect
a decision that an individual made when they were no longer engaging in identifiably
maladaptive behavior. Therapy, therefore, is about learning.
Learning in therapy is not different from learning in any other context. All learn-
ing is governed by the same principles and rules, many of which are well known and
we have spoken about earlier. What we want to highlight in this book is the connec-
tion of the underlying physiology and architecture of learning to the act of learning
things in therapy. By knowing these connections, the practicing therapist and client
will be able to select learning opportunities and design activities that will actually
serve to make learning adaptive behaviors and thoughts more efficient. The end
product is feeling well.

References

Achard, S., Salvador, R., Witcher, B., Suckling, J., & Bullmore, E. (2006). A resilient, small-world
human brain functionnal network with highly connected association cortical hubs. Journal of
Neuroscience, 26, 63–72.
Atzaba-Poria, N., Pike, A., & Deater-Deckard, K. (2004). Do risk factors for problem behaviour
act in a cumulative manner? An examination of ethnic minority and majority children through
an ecological perspective. Journal of Child Psychology and Psychiatry, 45(4), 707–718.
Buehler, C., & Gerard, J. (2013). Cumulative family risk predicts increases in adjustment difficul-
ties across early adolescence. Journal of Youth and Adolescence, 42(6), 905–920. doi:10.1007/
s10964-012-9806-3.
100 10 Therapy

Bullmore, E., & Sporns, O. (2009). Complex brain networks: Graph theoretical analysis of structural
and functional systems. Nature Reviews Neuroscience, 10(3), 186–198. doi:10.1038/nrn2575.
Chaytor, N., & Schmitter-Edgecombe, M. (2007). Fractionation of the dysexecutive syndrome in a
heterogeneous neurological sample: Comparing the Dysexecutive Questionnaire and the Brock
Adaptive Functioning Questionnaire. Brain Injury, 21, 615–629. doi:10.1080/
02699050701426949.
Denham, S., Blair, K., Schmidt, M., & DeMulder, E. (2002). Compromised emotional compe-
tence: Seeds of violence sown early? American Journal of Orthopsychiatry, 72(1), 70–82.
doi:10.1037/0002-9432.72.1.70.
Gurney, K., Humphries, M., & Redgrave, P. (2015). A new framework for cortico-striatal plastic-
ity: Behavioural theory meets in vitro data at the reinforcement-action interface. PLoS Biology.
doi:10.1371/journal.pbio.1002034.
Mastan, A., & Coatsworth, J. (1998). The development of competence in favorable and unfavor-
able environments. American Psychologist, 53, 205–220.
Norcross, J., Krebs, P., & Prochaska, J. (2011). Stages of change. Journal of Clinical Psychology,
67(2), 143–154. doi:10.1002/jclp.20758.
Prochaska, J., DiClemente, C., & Norcross, J. (1992). In search of how people change:
Applications to addictive behaviors. American Psychologist, 47(9), 1102–1114. doi:10.1037/
0003-066X.47.9.1102.
Rutter, M. (2002). Nature, nurture and development: From evangelism through science toward
policy and practice. Child Development, 73(1), 1–21.
Chapter 11
Historical Principles of Therapy
and Information Exchange

Words of comfort, skillfully administered, are the oldest therapy known to man.
Louis Nizer

The Oxford English Dictionary defines principle as “a fundamental truth or proposition


that serves as the foundation for a system of belief or behavior or for a chain of reason-
ing” or “a rule or belief governing one’s personal behavior” (Oxford English
Dictionary (US), 2014). When it comes to a discussion of therapy, the second defini-
tion is often more likely to be used in formulating the constructs identified. When
clinicians write about principles of therapy, they often talk about beliefs or principles
that guide their conduct during the therapy. The following, adapted from Finding the
Forest: Treating Survivors of Trauma Integrating Brief, Holistic, and Narrative
Techniques (Fowles, 2014), is a typical example of one such set of principles:
• The relationship between the therapist and client is not exactly a partnership after
all. It’s the therapist’s job to serve the client. Determining goals and (with assis-
tance) destination is the responsibility and right of the client, while the therapist
develops the road map.
• A therapist should be a visionary while remaining grounded in the present.
Therapists believe in possibilities, and their language should consistently reflect
faith in our client’s abilities to transcend their limitations and achieve their goals.
• Utilizing time creatively and flexibly is a standard by which the conscientious
therapist consistently operates.
• There is no ultimate formula for providing the best possible treatment to all
clients. That is because each client is unique.
• Therapists must never presume to have all the answers. When therapists offer
advice, they should consider the price their clients pay is their autonomy.
• The client, not the therapist, is ultimately responsible for the change.
• We can present, point out, clarify, and encourage; but we should never dictate.
Or this from Carl Rodgers: “For constructive personality change to occur, it is
necessary that the following conditions exist and continue over a period of time:

© Springer International Publishing Switzerland 2016 101


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_11
102 11 Historical Principles of Therapy and Information Exchange

• Two persons are in psychological contact.


• The first, whom we shall term the client, is in a state of incongruence, being
vulnerable or anxious.
• The second person, whom we shall term the therapist, is congruent or integrated
in the relationship.
• The therapist experiences unconditional positive regard for the client.
• The therapist experiences an empathic understanding of the client’s internal
frame of reference and endeavors to communicate this experience to the client.
• The communication to the client of the therapist’s empathic understanding and uncon-
ditional positive regard is to a minimal degree achieved” (Rogers, 1957) (pg. 97).
The above can best be described as a statement of conduct. It is aspirational and
describes how a therapist should relate to their clients. It describes how the therapist
and the client will interact and what the terms and expectations of that relationship will
be. They are familiar to almost anyone who has been trained to do therapeutic work.
What is interesting is that these principles do not describe how the therapist is
going to select from the information presented by the patient what issues will be
focused upon, what will be taught, and how it will be taught. More profoundly, these
principles are quite silent as to what will be learned or how it will be learned. Indeed
a careful reading of material on therapeutic process would suggest that, at least for
some models of therapy, the client would select the agenda and identify which stim-
uli and environmental factors were the important ones. In many forms of treatment,
it is left to the client to decide how to construct new knowledge and what conclusions
might be drawn. In other words, it seems that in many forms of therapy, it appears
that what is to be learned is left up to the client. While there are arguably some situ-
ations that this scenario would be preferable, it is hard to conceptualize how it makes
for an efficacious system of learning about things to change one’s own behavior.
Before you think that this statement might be an exaggeration, let’s look at the
definition of gestalt therapy obtained from the encyclopedia of mental disorders. “In
(Gestalt) therapy, clients become aware of what they are doing, how they are doing
it, and how they change themselves, and at the same time, learn to accept and value
themselves. Individuals, according to this approach, define, develop, and learn
about themselves in relationship to others, and that they are constantly changing.
Gestalt therapy is “unpredictable” in that the therapist and client follow moment-to-
moment experience and neither knows exactly where this will take them”
(Encyclopedia of Mental Disorders, 2014). How this awareness/learning takes
place, how it impacts which neural networks become involved, how those networks
are utilized and the component parts constructed, and what role of the therapist is in
utilizing these networks are neither discussed nor considered.
Consider, if you will, this statement from the American Psychoanalytic
Association: “Analysis can be viewed as an intimate partnership, in the course of
which the patient becomes aware of the underlying sources of his or her difficulties,
not simply intellectually but emotionally as well—in part by re-experiencing them
with the analyst. From the beginning of therapy, patient and analyst work together
to build up a safe and trusting relationship that enables the patient to experience
Learning Principles Associated with Education 103

aspects of his or her inner life that have been hidden because they are painful,
embarrassing, or guilt-provoking” (American Psychoanalytic Association, 2009).
All of these assumptions lead to a number of similar questions. How does this
awareness happen? What exactly does the patient become aware of or learn, and
how does the patient learn it? How does the patient use this new awareness to mod-
ify existing schema? How is all of this processed by the human brain? These ques-
tions are largely not addressed, but they need to be addressed.

Learning Principles Associated with Education

Most connectionist and constructivist models of learning, including the one utilized
in this book, would not take issue with the idea that new learning is created in the
mind of the learner and that learner’s participation and commitment are essential.
However, that would not lead to the assumption that the learning is almost exclu-
sively other directed. Contrast the above if you will, with another model of informa-
tion exchange directed at personal growth, the principles of teaching adapted from
Carnegie Mellon University, Eberly Center (2014):
“Teaching is a complex, multifaceted activity, often requiring instructors to jug-
gle multiple tasks and goals simultaneously and flexibly.
• Effective teaching involves acquiring relevant knowledge about students and
using that knowledge to inform course design and teaching. When one teaches,
they do not just teach the content, they teach the learner the content. If extended
to therapy practice the implication becomes clear. The teacher or in the case of
therapy, the therapist, must understand how the new information will be scaf-
folded onto the existing information of the client.
• Effective teaching involves aligning three major components of instruction:
learning objectives, assessments, and instructional activities. Teaching is more
effective and learning is enhanced when (a) instructors, articulate a clear set of
learning objectives (i.e., the knowledge and skills that we expect individuals to
demonstrate by the end of a learning experience); (b) instructional activities sup-
port learning objectives by providing goal-oriented practice; and (c) the assess-
ments provide opportunities for learners to demonstrate and practice the
knowledge and skills articulated in the objectives, and for instructors to offer
targeted feedback that can guide further learning.
• Effective teaching involves articulating explicit expectations regarding learning
objectives and policies. Articulating learning objectives (i.e., the knowledge and
skills that we expect learners to demonstrate by the end of a learning experience)
gives learners a clear target to aim for and enables them to monitor their progress
along the way.
• Effective teaching involves prioritizing the knowledge and skills chosen to focus on.
• Effective teaching involves adopting appropriate teaching roles to support learn-
ing goals. Even though learners are ultimately responsible for their own learning,
104 11 Historical Principles of Therapy and Information Exchange

the role a person assumes as instructor is critical in guiding the learners’ thinking
and behavior. The role chosen should be in service of the learning objectives and
in support of the instructional activities.”
This set of principles describes an active instructor whose goal is to impart a
focused set of learning objectives designed to increase knowledge in a predeter-
mined way. Here the role of the imparter of information is both directive and sup-
portive. There is no confusion as to what is to be learned, although it is understood
that the knowledge acquired may be put to different uses.
While these two sets of principles are not at odds, they certainly emphasize dif-
ferent things. One set of principles emphasizes the nature of the relationship
between two people, while the other emphasizes how information will be effec-
tively transferred from one person to another. While we do not quibble about the
importance of the relationship, it leaves us to wonder why the first did not recog-
nize that there is a merit to understanding how information is effectively trans-
ferred from one individual to another. In fact, some forms of therapy have taken the
idea to the extreme essentially advocating that the therapist is merely a backdrop
against which the client self-explores. Even if you do not believe that effective
treatment is about information exchange, you would have to agree that the role of
the therapist is to at least assist the client on a journey of self-exploration. If the
educational model has any relevance to the information exchange in the therapy
and how could it not, we would be left to wonder whether just being liked by them
is sufficient for that assistance to be effective.

All Therapies Have Learning Objectives

A major question for therapists therefore, becomes whether or not they believe
that there is a body of knowledge or a set of concepts, beliefs, and ideas that are
beneficial for the client to know and use. There is no doubt that for certain thera-
peutic interventions, that question is answered in the negative (Rogers, 2014),
while for others it is answered in the affirmative (Ellis & Harper, 1975). For
Rogers, testing of a learner’s achievement in order to see if some criteria held
by the instructor are met was directly contrary to the implications of therapy for
significant learning. For Ellis, therapy was an action-oriented process that
“teaches individuals to identify, challenge, and replace their self-defeating
thoughts and beliefs with healthier thoughts that promote emotional well-being
and goal achievement” (The Albert Ellis Institute, 2014). We believe that all
therapeutic systems, including those derived from the Rogerian tradition, have
a set of goals and objectives that entail beliefs and behaviors that so-called
“healthy” people would hold. These beliefs and behaviors are therefore legiti-
mate learning objectives and therefore subject to the same principles of learning
as is all other information acquisition.
Summary 105

Learning Theory

Let us finally contrast these therapeutic and educational principles with principles
often associated with learning theory:
• The principle of readiness posits that individuals learn best when they are physi-
cally, mentally, and emotionally ready to learn and do not learn well if they see
no reason for learning. Learners must both be excited to learn and willing to
concentrate on the new material. What is more, getting learners ready to receive
new information and creating interest in the information are the job of the instruc-
tor (Thorndike, 1932).
• The principle of exercise states that those things most often repeated are best
remembered (Thorndike, 1932).
• The principle of effect states that learning is strengthened when accompanied by a
positive reinforcer and that learning is weakened when associated with an aver-
sive event (Thorndike, 1932). One of the most important things that must happen
for new learning to be incorporated is that the person learning the new behavior
will be able to see evidence of progress and accomplish some degree of success.
• The principle of primacy states that those things of a class that are learned first
create a stronger impression and last longer. This also has clear implication for
the therapeutic process as unlearning maladaptive responses are more difficult.
• The principle of regency states that things most recently learned are more efficiently
remembered (Watson, 1925). Of course the opposite is also true in that the further in
time the learner is removed from a new fact, the more difficult it is to remember.
• The principle of intensity states that intensely taught material will be more likely
to be retained (Domjan, 2015).
• The principle of freedom states that things freely learned are learned best
(Weibell, 2011).
These principles describe how knowledge is processed and utilized in the brain.
These principles do not contradict the first two set of principles directly. They
describe how information is effectively processed in the human brain. They do have
implications for the process of therapy if that process is considered a process of
information exchange designed to alter behavior or thought.
We suggest that all three sets of principles have a role to play in the process of
therapy. We can look at all three sets of principles in a unified manner and think
about the first two sets of principles speaking to how we get information into a posi-
tion to be processed according to the third set of principles.

Summary

The book is being written based on the belief that all therapy is about the teaching
of adaptive strategies and behaviors, and that this teaching best occurs when the
principles of how the brain receives and processes information are understood and
106 11 Historical Principles of Therapy and Information Exchange

utilized to facilitate information exchange. Even if you are not a directive therapist,
we believe that it is still essential to understand how the exchange of ideas that occur
in the therapy is likely to be processed in the brain, cognitively and emotionally,
based upon these principles. No matter how well intentioned or supportive you may
be, if you do not understand these principles, the information exchange that occurs
in the therapy will be less than optimal at best, and ineffective at worst. If you are a
client, we believe it is essential for you to learn how you learn so that you can take
what you learn in the treatment and incorporate it into your daily behavior and
thinking. This process of incorporation is best served when it is purposeful and
directed as opposed to merely an accidental by-product of a discussion between two
positively regarding individuals.
We believe that all three types of principles must be incorporated into any thera-
peutic process in order for that process to be both efficient and successful. Therefore,
it is possible to create a list of principles that would be consistent with this belief and
help structure the therapeutic interaction to provide information that could be effec-
tively processed by the brain. It is to those principles that we now turn our attention.

References

American Psychoanalytic Association. (2009). About psychoanalysis. Retrieved from American


Psychoanalytic Association: http://www.apsa.org/About_Psychoanalysis.aspx
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tal Disorders: http://www.minddisorders.com/Flu-Inv/Gestalt-therapy.html
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Psychonotes_guiding_principles.htm
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Chapter 12
New Principles of Therapy

Go then, there are other worlds than these


Stephen King, The Gunslinger

Given that we now understand that all learning, whatever the topic or issue, occurs
over the same neural networks and follows the same laws governing working mem-
ory allocation, attention, and engagement, it is possible to develop a set of prin-
ciples that would facilitate learning in the therapeutic environment. As we have
indicated, these principles are not meant to supplant what we know about the value
of the therapeutic relationship. They are provided to help the therapist know what to
do after that relationship has been established.

The Therapist Must Focus on the Client and How They Will
Incorporate and Utilize New Knowledge

It is not sufficient to assess the state of the relationship between a therapist and a
client. While the relationship might be positive, as evidenced by the clients’ positive
regard of the therapist and vice versa, the client may in fact not be learning or under-
standing anything. Clients will seek to please a therapist and might describe the
relationship as positive even though nothing has in fact changed. What is most
important is that the therapist must understand where in the development of ideas
and concepts the client is, so that information can be presented that is accessible and
useable by the client. For this to occur, the therapist must understand how certain
constructs are developed and then be able to guide the client on a predictable path
to the healthy development of these constructs.
It is important to understand that all information is not useable all the time. There
are preconditions that exist that help determine whether new information will be
able to be incorporated by the client. Both Piaget (1977) and Vygotsky (1934/1986)
agree that the process of cognitive and related emotional change is initiated by a

© Springer International Publishing Switzerland 2016 107


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_12
108 12 New Principles of Therapy

cognitive conflict of sorts that occurs when an individual realizes a new idea does
not align with his current thinking or prior knowledge. For therapy to be successful,
we believe it is necessary for this moment of realization to be explicit, and for that
to occur, the client must first be cognizant and able to identify the components of a
current schema surrounding the construct and recognize that the new idea or fact is
discordant with the information already held. In other words, it is a necessary pre-
condition that the individual recognizes that the new information belongs to a cer-
tain class of information yet does not exactly correspond with what is already known
about that class. Piaget and Vygotsky both agree that when this moment occurs, an
individual will seek out answers in order to align his thinking and resolve the con-
flict. Piaget terms this conflict between what is known and what is new as the “just
right challenge” meaning that the new information was just difficult and challenging
enough to disturb an individual’s current conceptualization of how a certain class of
things are (current assimilatory schemata) and cause the changes in the target con-
cept (accommodations) required to lead to the next level of understanding and
expansion of the concept (equilibration) (Jardine, 2005). This notion of a “just right
challenge” implies that information that is too discordant with the existing informa-
tion or represents very significant differences between what is known and what is
new will represent too difficult a challenge for an individual to assimilate and will
be, therefore, rejected. As a result it is critically important that both the therapist and
the client examine the new information in relation to what is known and discuss how
it might be assimilated. Leaving this solely for the client to do implies that the new
information may or may not be included but rejected instead. In addition if it does
get included the way that it gets included, may be in fact neither what the therapist
intended nor desirable. The therapist should of course be aware that in some
instances, where beliefs are rigidly held, it is easier for an individual to reject the
new information to preserve the core belief. Think about the flat earth society or the
modern debate over global warming as examples of what might happen when new
information is rejected to preserve a cherished core belief.

There Is No Knowledge Independent of the Meaning


Attributed to Experience and Constructed by the Client

This principle relates to principle number one in that no information is processed by


an individual independently of what that individual already knows. As we have
seen, this principle is directly related to the known functioning of working memory.
New information is always appended to existing memory in order to be remem-
bered. This principle is also entirely consistent with constructivist learning models.
According to Piaget there are no pure facts if by “facts are meant phenomena pre-
sented nakedly to the mind by nature itself, independently respectively of the
hypothesis by means of which the mind examines them and of the systematic frame-
work of existing judgments into which the observer pigeon-holes every new
Learning in Therapy Is an Active Process in Which the Client (Learner) Gates… 109

observation” (Piaget, 1974, p. 33). Therefore, there are no essential truths. The best
we can hope for is a collection of commonly held adaptive beliefs. Before you think
that all commonly held beliefs are adaptive, we encourage you to consider the belief
that the earth is flat, which at one time was a very commonly held belief.
This principle has a number of implications, but especially highlights how the
therapist would benefit by understanding how new information is likely to be
received by the individual (the existing schema into which it will be incorporated).
If the therapist is going to provide information designed to alter a maladaptive
schema or set of beliefs (depression), it is necessary to identify for both the therapist
and the client how that existing schema works and how it distorts new information
to conform to its existing thought patterns. For example, how is talking about chil-
dren, even in a manner deemed healthy by the therapist, going to be interpreted in
the mind of a potential pedophile or a childless adult? How is talking about the fine
meal you had in the steak restaurant last night going to be interpreted in the mind of
a vegetarian as opposed to an omnivore?
There are a multitude of discussions that occur in any therapeutic encounter of
any sort that provide hypothetically neutral information that may be interpreted by
the client in any number of adaptive or maladaptive ways. Making these associa-
tions explicit and discussable is an essential task of therapy. The client or therapist
that does not understand this principle operates at considerable peril. The examina-
tion of how the existing schema encodes information should be the primary task of
the intervention and should occur before the actual attempts at altering are made.
Without this information, it is possible and in some instances likely, that those mal-
adaptive beliefs and behaviors will actually be reinforced by the therapeutic inter-
vention. For example, there is evidence that people grieve in different ways and as
a result, some grief therapies produce negative results for some people (Neimeyer &
Currier, 2009).

Learning in Therapy Is an Active Process in Which the Client


(Learner) Gates Sensory Input and Constructs Meaning
Out of It

Not everything said in therapy, or in life for that matter, is retained by the listener.
Studies suggest that as much as 30 % of the material provided during a lecture is
already lost by the conclusion of the lecture (Prince, 2004). Listeners actively
choose which information to attend to and remember. This process of selected atten-
tion to specific material, and the ignoring of other material, is termed gating. Gating,
which depends upon contribution of the reward system to the allocation of working
memory to specific stimuli, involves multiple brain systems operating in concert
(McGinty et al., 2011). Learning, which occurs when certain stimuli are selected
from the environment to be attended to therefore, is not a passive acceptance of
prepackaged knowledge which exists, but involves learners (clients) actively
110 12 New Principles of Therapy

engaging with the material and selecting from the material elements that are
meaningful to them in a purposeful and directed way. What is gated and what is not
is entirely dependent on the individual doing the gating, and the result is by no
means predictable by those individuals seeking to impart the knowledge. It is easy
to observe gating in action. Simply find a teenager and try to explain something to
them for which they have no interest.
As indicated, gating describes neurological processes of filtering out redundant
or unnecessary stimuli in the brain from all possible environmental stimuli.
Essentially, gating is the process which modulates input into the brain and insures
that the system is not overloaded. This is a crucial management process of the brain
because at any one point during the day there is more information coming into the
brain than can be effectively processed. Humans need a way to parse that informa-
tion down to critical elements to be attended to. This parsing is not a passive process
because the human brain actively selects the information it will attend to based upon
a number of variables. Among these variables are prior knowledge, past history of
reinforcement, and interest.

The Neurophysiology of Gating

The neurophysiology of gating is well known. The process of gating is centered on


the basal ganglia. The basal ganglia are a grouping of subcortical structures that
receive input from the prefrontal cortex and nearly all cortical regions, including
those originating in the associative and paralimbic regions of the neocortex. In addi-
tion to projection to the basal ganglia, the same segregated circuits are projected
back to their point of origin. These connections place the basal ganglia in a central
location in a network that exerts influence over a variety of mental functions includ-
ing the modulation of perception, cognition, affect, motivation, and action.
The basal ganglia is a massive inhibitory region of the brain, whose purpose is to
gate (select) the representations processed by the cortex determining which of the
representations can be either activated upon or inhibited (Frank, 2006). The basal
ganglia do this by telling regions of the cortex to become active through commands
processed through the frontal cortices. The complex involvement of the basal gan-
glia involves the processes of initiating, sustaining, switching, and inhibiting or
stopping behaviors (for a review of specific circuitry profiles, see Koziol & Budding,
2009). Therefore, the basal ganglia are an essential part of the brain’s executive
function system (Cameron, 2010) which have even been described as controlling
access to working memory (McNab, 2008).
There are of course, cortical systems that also contribute inhibition and rein-
forcement value to the gating process. There is a reciprocal relationship between the
subcortical basal ganglia and the pulvinar nuclei in the thalamus that in concert (or
as part of a gating network) functions as the gatekeeper, deciding which information
should be inhibited and which should be sent to other cortical areas.
Learning in Therapy Is an Active Process in Which the Client (Learner) Gates… 111

Sensory gating is differentiated to a degree by function. Gating functions are also


mediated by recruitment to the central network of the auditory cortex, prefrontal
cortex, and hippocampus (Mayer, 2009). Other areas of the brain that have been
identified as part of the gating network have been the amygdala, striatum, medial
prefrontal cortex, and midbrain dopamine networks. A discussion of the neurophys-
iology and neural architecture as well as various network models of gating is beyond
the scope of this book. Interested readers are encouraged to use the reference above
to begin their exploration of this topic.

The Role of Reward Recognition in the Gating Network

What gets gated or selected for action is highly dependent on the history of rein-
forcement associated with the action. In essence, the higher the probability of a
perceived reinforcement, the more likely it is that the stimuli associated with that
reinforcement will be gated to attention. In support of this fact, there is emerging
research concerning the integration of the reward recognition network with the gat-
ing system. In the gating system, “reward is a central component for driving
incentive-based learning, appropriate responses to stimuli, and the development of
goal-directed behaviors” (Haber & Knutson, 2010, p. 4).
There is substantial agreement concerning the cortical and subcortical network
structural participants for this complex human behavior. Specifically, Koziol and
Budding (2009) identified the subthalamic nucleus and ventral pallidum, the subic-
ulum and related hippocampal areas, the lateral habenula, the mesopontine rostro-
medial tegmental nucleus, the extended amygdala, the bed nucleus of the stria
terminalis, and the hypothalamus. As is true of other networks, the reward network
is not a fixed system. Koziol and Budding conclude by stating “one consistent point
that became apparent was that brain regions cannot be simply labeled as either con-
tributing, or not contributing, to motivated behavior; rather, it’s necessary to con-
sider the specific circumstances under which the region is being engaged” (p. 356).
Hart, Leung, and Balleine (2014) point out that “considerable evidence suggests
that distinct neural processes mediate the acquisition and performance of goal-
directed instrumental actions. Whereas a cortical-dorsomedial striatal circuit
appears critical for the acquisition of goal-directed actions, a cortical-ventral striatal
circuit appears to mediate instrumental performance, particularly the motivational
control of performance” (p. 104). This essentially means that as expected, automa-
tized behaviors and emotional responses have separate components of the reward
recognition network associated with them.
There are other subcortical structures that play a significant role in both gating
and reward recognition. One of these is the pedunculopontine nucleus (PPN) (also
referred to as pedunculopontine tegmental nucleus, PPTN or PPTg) which is located
in the brainstem, to the rear of the substantia nigra, and next to the superior cerebel-
lar peduncle. The PPN is historically identified as one of the main components of
the reticular activating system (Garcia-Rill, 1991). The PPN projects to a wide
112 12 New Principles of Therapy

variety of cortical and subcortical systems. The PPN plays a significant role in
gating both sensorimotor and reward-related behavior (Diederich & Koch, 2005).
Similarly, the nucleus accumbens (NAcc) has been identified as critical in the con-
trol of goal-directed behavior. Taha and Fields (2006) found that that a subset of
NAcc neurons demonstrated a long-lasting inhibition in firing rate, whose onset
preceded initiation of goal-directed sequences of behavior, and terminates at the
conclusion of the sequence. This firing pattern suggested that, when active, these
neurons inhibited goal-directed behaviors and that, when inhibited, these neurons
permissively gated those behaviors.
Other cortical structures such as the caudate nucleus are active when learning
relationships between stimuli and responses or categories. Seger and Cinotta (2005)
found that activity associated with successful learning was localized in the body and
tail of the caudate and putamen. Hippocampal activity was associated with receiv-
ing positive feedback, but not with correct classification. Successful learning cor-
related positively with activity in the body and tail of the caudate nucleus and
negatively with activity in the hippocampus.
The implications of reward circuit involvement, gating, and the therapeutic pro-
cess are clear. Clients will attend to what is interesting, rewarding, and understand-
able in terms of prior knowledge. In order to be learned, new information must first
be attended to, and in this regard, all information is not equal. The new information
is essentially competing with prior learned and reinforced behavior. Furthermore,
the new information has no history of reward associated with it. When new informa-
tion is offered within the context of the therapeutic relationship, it is clearly not
sufficient to assume that it will be associated with reward just because it is being
offered therapeutically. The therapist cannot be sure what information or portion of
the information is being attended to, how that information is being processed, and
how it is being used to alter existing knowledge.
We stated earlier that hippocampal activity was associated with receiving posi-
tive feedback but not with correct classification. This is a very important fact to
remember. It implies that the client will remember that they received positive feed-
back in a session, but not necessarily know why they received that feedback. They
may associate the positive feedback with any portion, relevant or irrelevant, of the
information it is associated with. More specifically, the client may remember that
the therapist was warm, supportive, and reinforcing but not remember exactly why
that support was provided.
Let’s take a look at an example of a potential therapist reply to a statement made
by their anxious client. The client says, “I went to the mall today to look for some
shoes before I came to this appointment.” One possible therapeutic reply is to say
“Tell me about that.” Now the client has a conundrum. Several schemata or classes
of response are possible based upon the client’s determination as to why the thera-
pist responded to this statement. In many systems of therapy, the client isn’t sure.
The client might think a variety of things including “Does my therapist think me
trivial for shopping” or “Is my therapist going to judge me by the store I went shop-
ping in?” or “Does my therapist think I was avoiding coming here?” or “Should I
talk about how I used to shop with my mother?” The possibilities are almost endless.
The Construction of Meaning in Therapy Is a Purposeful Activity 113

All of these appraisal systems would be put into play without a clear understanding
of why the question was asked or what the goal of asking it was. Compare that to a
system wherein the client knows that they are working on her fear of public spaces
by doing systematic exposure therapy to increasingly public spaces. The client has
been taught the principles of anxiety reduction and understands that if they remain
in the mall for a period of time, their anxiety will be reduced. This allows for the
proper schema to be accessed and modified based on new knowledge and experi-
ence. Furthermore, it permits the client to understand what they have learned from
the experience and how to use that knowledge in future situations. It targets the
learning experience and permits the formation of a practice experience to provide
reinforcement for a more adaptive behavior.
All of the above implies that the reinforcement and encouragement that occur
during the course of therapy must be directly tied to the stimuli the therapist desires
to highlight and hopefully change. This means that the more directed and purposeful
the information exchange, the surer the therapist can be that the information is being
used in the manner intended, and for the learning outcome specified. This is how
learning works and is effective, and there is no reason to assume that the learning that
takes place in therapy is different to any other form of learning in this regard. Leaving
the conclusions and inferencing to the client introduces a significant level of vari-
ability and uncertainty of outcome into the proceeding, making therapy done in this
manner inefficient. Nondirective approaches may actually result in incorrect pairings
between reinforcement and target and, in some cases, result in inappropriate assump-
tions and ideas being perceived by the client as reinforced.

The Construction of Meaning in Therapy Is a Purposeful


Activity

Clients learn to learn as they learn. This is because as they learn they construct sys-
tematically more advanced and complex adaptive schema, and the construction of the
schema determines how new knowledge is both interpreted and potentially incorpo-
rated. At the same time, they are subconsciously rehearsing and refining these new
schemata and related strategies and moving them toward automaticity (Thatch, 1997).
At the beginning of therapy, a client will present with a number of problem behav-
iors and/or ideas which are causing them difficulty. These behaviors and ideas are the
result of a complex and extensive learning history that, through the continuing inter-
action between existing schema and new information in the environment, produced
the current automatic default state. Learning in therapy consists both of constructing
meaning and constructing systems of interrelated meaning. The goal of this learning
is to develop a system of adaptive behavior and thought. In most instances this new
system of adaptive behavior and thought will be at odds with the existing and
entrenched system of maladaptive behavior and thought. In order to make therapeu-
tic progress, the new system of adaptive behavior and thought must be reinforced and
encouraged to the point of automaticity, while the existing maladaptive schema must
114 12 New Principles of Therapy

be made nonautomatic. This is a two-pronged process. The new adaptive system


must be purposefully selected and practiced, while at the same time the old maladap-
tive system must be purposefully deselected and not practiced.
All of this requires precision in definition and in identifying therapeutic behav-
ioral and emotional outcomes. It also requires the client to understand and partici-
pate in the process of constructing new and adaptive schema. This is because at the
beginning of treatment, new adaptive learning will create a new response schema
that is poorly developed, skeletal, poorly generalized, and interconnected. The cli-
ent will not spontaneously use the new information outside of the therapeutic envi-
ronment. This new schema must be purposefully developed and practiced to the
point of automaticity. In line with learning theory, this is best accomplished with
clear learning outcomes and specific teaching strategies designed to reach those
outcomes. Individuals learn better and develop efficient subconscious rehearsal
strategies when goals are clearly articulated (Dijksterhuis & Aarts, 2010). They can-
not clearly articulate the outcome and processes unless those things are identified
and taught in the context of therapy.

A Word About Outcomes

While this book is not about the development of teaching strategies, although devel-
oping teaching strategies in therapy may not be a bad idea, it may serve at this point
to have an idea as to what constitutes a good learning outcome, at least in education.
A good learning outcome is a statement as to what your client will be able to do
once that outcome is attained. The outcome should be observable and measurable
and not just reportable. Arguably, this implies getting a client to report that they feel
better is not a legitimate learning outcome for therapy. This does not mean that it
cannot be a goal, although it does imply that the success or failure of therapy should
not solely be judged on a subjective report.
Learning outcomes are generally organized around three basic principles:
1. What information should the client learn through the therapeutic exchange?
What specific terms, rules, procedures, and systems will be taught that the client
should be able to clearly state?
2. What skills should the client learn through therapy? What tasks, skills, or com-
petencies should the client be able to demonstrate?
3. What cognitive or developmental changes should the client be able to demon-
strate as a result of therapy? How should the client’s thinking have changed
(Martin, 2007)?
Therapy therefore should be about the development or modification of schemata
to produce a rich and broadly generalized set of behaviors and cognitions that are
employed automatically when the situation requires.
Human Learning Consists of Pattern Matching. Each Meaning We Construct Makes Us… 115

Human Learning Consists of Pattern Matching. Each


Meaning We Construct Makes Us Better Able to Give
Meaning to Other Stimuli Which Can Match
with a Previously Identified and Categorized, Similar Pattern

When we encounter a new stimulus, the brain immediately begins to attempt to


match it with what is already known. Humans pattern match between crucial
issues in the environment and elements of mental schemata to determine which
schemata will be accessed and used to append the new information (Endsley &
Garland, 2000). Classes of stimuli are grouped together in the brain. As we have
seen, these schemata are best represented in the brain by small-world hub brain
models. Essentially, each hub is the center of an integrated unit of neurons that
fire collectively when stimulated. These hubs are characterized by a number of
features that insure efficient communication with other hubs representing similar
concepts. Network studies of structural connectivity have revealed a number of
highly nonrandom network attributes of these small-world systems. These
include high clustering and modularity of member neurons combined with high
efficiency and short path length both within the hub and between hubs represent-
ing similar constructs. The combination of these attributes simultaneously pro-
motes high specialization and high integration within a modular small-world
architecture (Sporns, 2011). We can rather easily conceptualize these groups of
neurons that respond similarly to specific stimuli as the neurophysiological rep-
resentation of schemata. Member items of a particular schema are usually
responded to similarly. Think about an individual who is afraid of spiders when
they first encounter a spider. Their response doesn’t depend on the situation or
the type of spider. Seeing a spider produces anxiety and fear. There are many
examples of these types of responses. As another example, think about a staunch
political response to a member of another party.
Clients seeking treatment often have whole classes of stimuli (schemata) to
which they react poorly. This is not always however, the case. Sometimes, increas-
ing exposure and information can amend the schemata or split it into two related
schemata. Suppose you took the time to learn about spiders and found out which
ones were dangerous and which were not. Eventually you would develop two
highly related schemata, spiders which were dangerous and spiders which were
not. The response patterns to these schemata would be different. Therapy should
work in a similar fashion. The goal of treatment should be to make the response
patterns of individuals to specific schema explicit so that they can be examined
and modified. Maladaptive responses should be deconditioned, and adaptive
responses practiced and automatized.
116 12 New Principles of Therapy

The Crucial Action of Constructing Meaning Is


Neurophysiologically Based and Involves Brain Circuitry
Dedicated to Learning and Reinforcement Recognition

All information to be learned and then incorporated into long-term memory store is
processed over the same neural networks. We reviewed those networks in the chap-
ter How We Learn. There is no separate system for material learned in therapy,
although there may be, as a result of the emotional valence of the material, different
brain regions recruited for specific elements of what is discussed in treatment. These
regions responsible for emotional valence and reward recognition are not the exclu-
sive domain of the material learned in therapy. These regions are recruited by any
activity which is accompanied by a level of arousal. As we have seen, these regions
which are responsible for reward recognition are critical in the gating process.
“Converging data demonstrate two parallel neural networks within the Prefrontal
Cortex (PFC) one, including the dorsolateral PFC (DLPFC), involved in working
memory (WM) and planning and the other, including the ventral PFC (VPFC) and
to some extent the ventral medial areas (MPFC), associated with reward sensitivity
and motivation” (Pochon et al., 2002, p. 5669).
The working memory system is a cerebral network that includes a storage buffer
mediated by the parietal cortex, a subvocal rehearsal system mediated by the left infe-
rior PFC, and an executive component mediated by the DLPFC. The motivational
component involves monitoring and adaption to the perception of reward functions.
Research has identified the medial frontopolar area role in the monitoring of reward
and determining the contextual value of an ongoing cognitive task. In addition, a
closely interconnected limbic and paralimbic system which includes the VPFC and
MPFC also plays a key role in behavioral response to reward context. This paralimbic
system includes those networks associated with episodic memory, including the para-
hippocampal cortex, hippocampus, and prefrontal cortex, and structures linked more
specifically to emotional processing, including the amygdala, orbitofrontal cortex,
and anterior cingulate cortex (Smith, Henson, Dolan, & Rugg, 2004).
In most instances of learning, both of these separate networks, reward recognition
and working memory, must be engaged for learning to take place and long-term mem-
ory store to be activated. Research has in fact demonstrated that motivational engage-
ment (reward recognition) and cognitive processes networks are linked by a specific
neural system, designed to improve efficiency and speed of learning (Pochon et al.,
2002). The lateral frontopolar area appears to serve this function. This integrated cir-
cuitry is involved in any and all learning, either adaptive or maladaptive, including
emotional deregulatory disorders such as depression (Simpson et al., 2000).
Clearly, the degree to which the relationship between the therapist and the client
produces an environment for encouragement and support is important. It is clear
that the therapists’ approval and support is a source of reinforcement that is used by
all therapists to guide and shape the course of learning. What is learned in the
context of this relationship is that information exchanged is processed over the net-
works described above, and learned in the same way as all other learning. There are
Learning in Therapy Is a Social Activity Involving an Analysis of Our… 117

not separate rules for the information contained in a therapy session. If you
understand how these networks operate, you can structure the information exchange
to work effectively. If you do not understand how these networks operate, you can-
not appropriately structure the presentation of information in a manner that would
allow the person receiving it to effectively use it. It is as simple as that.

The Language We Use Influences Learning. Language


and Learning Are Inextricably Intertwined

Language can impact and even restructure cognition. This is true for both language-
based and nonlanguage (visual-spatial) tasks (Diessel, 2014; Majid, Bowerman, Kits,
Haun, & Levinson, 2004). There is also research that demonstrates that language use is
a collaborative process that influences the representation of meaning in the speaker, the
listener, and the collective that includes both the speaker and listener (Holtgraves &
Kahima, 2008). This implies that both the client and the therapist would have meaning
modified as a result of the language-based interaction that is therapy and that the thera-
pists’ participation is essential to the modification of meaning for the client. The words
we use and how we use them impact the way we feel and behave (Pennebaker &
Francis, 1996). Finally, there is research that clearly identifies language as the scaffold-
ing device unto which new thought is structured and developed (Clark, 2006).
What all of this implies is that language is a critical tool for the shaping and
reshaping of thought and related emotional states. The directed, purposeful, and
structured use of language is important for imparting information designed to
change cognition. The haphazard or inefficient use of this tool would produce less
than optimal results. Therefore, those systems that make purposeful use of language
are to be preferred to less directed systems where the expected impact of language
is not planned, or in fact the use of language itself is minimalized.

Learning in Therapy Is a Social Activity Involving an Analysis


of Our Relationships with Other Important Human Beings
in Our Lives. To Be Useful, Knowledge Acquired in Therapy
Must Be Applied and Practiced Within the Context of Both
New and Existing Relationships

There are two separate points here, the first of which is that learning is a social pro-
cess with at least two active participants, and the second is that new learning must
be practiced in those social contexts for which it was intended. This practice must
be purposeful and directed. The learning outcome for the practice should be known
to the learner so that the result of the practice can be integrated into the appropriate
body of existing knowledge. The goal is automaticity of new behavior into the rep-
ertoire of the individual.
118 12 New Principles of Therapy

A further point should be added in that learning without interaction between the
person acting (the learner) and the social world as initially represented by the thera-
pist, is ineffective. To put it another way, it is not enough to just think about it, or
talk about a new behavior or idea in the office. New behavior must be practiced in
the social world for it to be incorporated into the automatic repertoire of the learner.
Such practice represents the core of a planned and purposeful therapy process.
Vygotsky viewed cognition as socially constructed and shared and language as
the critical link between the social and the psychological planes of human function-
ing (Berk & Winsler, 1995). There is increasing recognition that cognition origi-
nates in basic motor movements and develops largely in social interaction shaped by
cultural and environmental processes. These processes are central rather than inci-
dental to cognitive development (Watson-Gegeo, 2004).
The relationship between a therapist and a client can be conceptualized within
this framework. The goal of the therapy is to provide a secure place in which new
initial learning can take place that is free from threat and conducive to experimenta-
tion and practice. In this environment, the therapist encourages, challenges, and
then provides feedback on the progress of the learning. While a casual reading of
Vygotsky’s works might suggest that the teacher is a facilitator, this does not mean
that this facilitation is accomplished without specificity and direction. Facilitation is
directive and guiding, with specific goals in mind.

Learning in Therapy Is Contextual. We Learn in Relationship


to What Else We Already Know and What We Already Believe

In therapy it is not desirable to append adaptive knowledge to maladaptive pre-


existing knowledge. To be effective, new skill sets and their associated cognitions
must be developed and practiced. In practice, this is difficult to do because humans
show a strong tendency to hold onto prior knowledge and discount new knowledge
that is not in agreement with prior knowledge. In other words, if the new knowledge
disagrees with what I already know, I have a strong tendency to reject the new
knowledge to protect my existing beliefs (Chinn & Brewer, 1993; Lipson, 1982).
Indeed, it can be argued that one purpose of knowledge is to develop attitudes and
belief systems that are resistant to change and that this rejection of new knowledge
serves a valuable protective function (Woods, Rhodes, & Biek, 1995).
In order to understand how this process works, it is important to know that, as we
have discussed, humans learn by pattern matching. When we first encounter a novel
stimulus, we search what we know, looking for similar patterns or constructs to relate
it to (Carmicheal & Hayes, 2001). We then look at this information in light of what
we already know. We can do of three basic things with this new knowledge. We can
accept it and alter what we already know. We can reject it and protect what we
already know. Or we can consider it and see how it fits in with what we already know.
As we have seen, humans have a propensity to protect what we already know,
and therefore, the most likely scenario when confronted with new information is to
reject it outright. The second most likely event is to consider it and see how it fits in
It Is Not Possible to Assimilate New Knowledge Without Having Some Structure... 119

with what we already know, and the least likely outcome is to accept the discordant
new information and throw away or irrevocably alter what we already know. Much
of what the layperson thinks about when they think about therapy is defined by this
last most unlikely outcome. People believe that the therapist will say something,
and on the basis of that statement, a transformation of the maladaptive body of
knowledge will occur. As we have just learned, this is both unlikely and counter to
the actual tendency of people when they process information.
What is more likely, and in fact therapeutically desirable, is that the client
(learner) engages in the middle option. They will use the new information to see
how it relates to what they already know. We do know a few things about how this
occurs. One of the most important things is that for this objective analysis to occur,
the learner must be motivated to do the comparison and dispassionate about the
analysis. The stronger the attitude is held, the more difficult the comparison is to
make (Woods et al., 1995). In addition, beliefs associated with strong affect states
lead to strongly held attitudes which are more resistant to change.
All of this goes to the point that in order to change the strongly held, emotionally
laden belief systems that characterize the thinking of people with emotional prob-
lems, the clients must be encouraged to do a systematic and dispassionate analysis
of those belief systems in an environment, or in a manner, that does not threaten the
client and cause the client to withdraw. Based on constructivist principles such as
the “just right challenge” (Vygotsky, 1934/1986), new information must be just dif-
ferent enough and minimally threatening enough to enable the client to process it,
while at the same time, be both novel and interesting enough to encourage the allo-
cation of working memory. This calls for a careful and thoughtful assessment of the
type of new information, its purpose, and how it will be offered to the client. This
argues persuasively that the clients should not be left to their own devices to filter
the information provided in a therapeutic exchange because their natural tendency
will be to reject new information or avoid comparison or questioning their passion-
ately held attitudes. The job of the therapist is, with the learning outcome clearly in
mind, to systematically prepare the stimuli so that they meet the just right challenge
and create an environment wherein the client is open to, and engaged in, confronting
maladaptive attitudes and beliefs. By a process of shaping and desensitization, the
therapist should present new information designed to challenge the existing attitude,
while at the same time not being threatening to it.

It Is Not Possible to Assimilate New Knowledge


Without Having Some Structure Developed from Previous
Knowledge Upon Which to Build

Learning is incremental; the more we know, the more we can learn. Therefore, any
effort to teach must be connected to the state of the client and must provide a clear,
direct, and unambiguous path into the subject for the learner that emanates from the
learner’s (client’s) previous knowledge. This implies that adaptive beliefs and
120 12 New Principles of Therapy

constructs should form the basis of new learning and that therapy should be directed
toward both creating the functional beliefs, attitudes, and skills sets and then prac-
ticing those skills sets in multiple environments.
There is research that clearly indicates that learning occurs when potential
responses to internal representations of environmental occurrences are reweighted,
with some responses being made more likely and other responses becoming less
likely. This data suggests that the older conceptions, that the internal representations
are changed, were incorrect (Petrov, Dosher, & Lu, 2005). This implies that the
predictive weights of the response are reweighted, resulting in some responses
being much more likely than others. In other words, learning occurs when some
responses are trained and selected, and others are not trained and are deselected.
Learning is effective when this process is directed and specific, with the learning
paths specified and reinforced. Learning is then enhanced through a process of
refinement of, and automation of, these selected responses (Neches, 1987).

Learning New Ideas and Ways of Behaving in Therapy Is Not


Instantaneous

Learning requires both practice and rewards. Learning theory identifies this as the
laws of effect/exercise (Thorndike, 1932). Meaningful and utilitarian learning
requires the revisiting of ideas in many contrasts and situations. Clients must recog-
nize old ideas as maladaptive and actively seek to replace them with new ideas
based upon a foundation of new learning and successful application. Research has
suggested that learning new skills or changing existing cognitive schema is
enhanced, in terms of increased automaticity, when new concepts are pulled into
working memory and then used in multiple applications (Logan & Klapp, 1991). In
order to create these various applications, guided practice enhanced with behavioral
practice improves learning efficiency (Felder & Brent, 2003).
There is a delicate balance required when learning complex material in therapy.
Research indicates that cognitive load-reducing methods are effective to reach high
rates of retention of information and behavior for complex tasks. These cognitive
load-reducing methods include low variability of presentation, complete guidance,
and feedback. Once the new information is acquired, it is precisely these methods that
hinder the transfer of learning to new situations. In order to effect generalization,
methods that induce appropriate and increasing cognitive load, such as high variabil-
ity and limited guidance or feedback, increase effective learning (van Merriënboer,
Kester, & Paas, 2006). In other words, to effect learning and generalization of new
constructs in therapy, highly structured and guided instruction is necessary to create
the new schema. Only after the new schema is constructed is it beneficial to reduce
guidance and structure, which will then increase the cognitive demand on the client
and thereby facilitate generalization and application of the new skill.
People assume that during the course of treatment, a therapist will say something
and all of a sudden a magic moment of realization and awareness will occur. It will
Motivation Is a Key Component in Learning. Not Only Is It the Case that Motivation... 121

be sudden and often occur in response to a single thing the therapist has said. This
is referred to as the “Aha” moment. Is there then an “Aha” experience in therapy?
The easiest answer is both yes and no. Yes, because after sufficient guided instruc-
tion, the client will develop a new way of looking at things and begin to change their
behavior as a result of the new perceptual set. From that moment on, things will not
be thought of in the same way as they had been in the past. No, because the change
does not come easily or in fact suddenly. It is hard won and the result of initially
structured and focused guided practice and repetition.
Consider our well-practiced schema about our solar system and the planets in it.
In 2006, however, astronomers announced that Pluto was no longer a planet because
of its size and lack of domination of its orbital environment. It had been reclassified.
We all went to bed one night safe in the notion that we knew Pluto was a planet and
woke up to find out that it wasn’t. It was an “Aha” moment to be sure, but it couldn’t
have occurred without us first knowing what a planet was and having a basic under-
standing of the solar system. Much as Piaget and Vygotsky suggested, there came a
moment when new information altered our schema of the solar system and planet
Pluto. But, we needed to have a schema in the first place in order for it to be altered.
An example of a maladaptive diagnostic schema would be one wherein “refrigerator
mothers” were once conceptualized as the etiology of autism (Demaria, Aune, &
Jodlowski, 2008).
Therapy works the same way. In order to alter a maladaptive schema, repetition
and practice of new ways of thinking and new constructs must occur. The moment
of change in the schema is sudden, but in reality it is the result of all that practice.
For those of you who are concerned about the fate of poor Pluto, there is good news.
There is a movement to try to have it reinstated as a planet. We all might wake up
one morning and have to have another “Aha” experience. For clinicians, imagine the
process you go through in order to correct the residual schema of the parent blaming
either themselves or their partner for their child being on the autism spectrum.
Research on therapy process has begun to identify this course of schema change
as part of therapy and develop ways to assess it. For example, the assimilation model
(Stiles, Meshot, Anderson, & Sloan, 1992) proposes and evaluates for a systematic
sequence of changes in the representation of a problematic experience during psy-
chotherapy. The model is supported by research that indicates increasing degrees of
assimilation of insights as therapy progresses.

Motivation Is a Key Component in Learning. Not Only Is It


the Case that Motivation Helps Learning, It Is Essential
for Learning

Recent research clearly identifies that reinforcement plays a crucial role as to what
is selected for attention and what is not. The reward recognition circuit is essential
for gating (selecting) knowledge to be attended to and subsequently learned
122 12 New Principles of Therapy

(Wasserman & Wasserman, 2015). This is because what is gated (attended to) is
what is admitted to working memory and also determines what it retrieved from
long-term store by pattern recognition (Shell et al., 2010).
“Reward is a central component for driving incentive-based learning, appropriate
responses to stimuli, and the development of goal-directed behaviors. In order to under-
stand the role reward recognition has for learning new things, it is important to understand
how the different brain regions are recruited to work together to evaluate environmental
stimuli and transform that information into actions” (Haber & Knutson, 2010, p. 4).
There is substantial recognition of both cortical and subcortical contributions to learning
(Koziol & Budding, 2009). Motivation, which we define as the contribution of the reward
system to the allocation of working memory, involves multiple brain systems operating
in concert. McGinty et al. (2011) identified the subthalamic nucleus and ventral pallidum,
the subiculum and related hippocampal areas, the lateral habenula, the mesopontine ros-
tromedial tegmental nucleus, the extended amygdala, the bed nucleus of the stria termi-
nals, and the hypothalamus as contributing to the reward recognition network.

Dopamine Pathways Serotonin Pathways

Frontal
cortex Striatum

Substantia
nigra

Functions
Mood
Functions Memory
Nucleus
Reward (motivation) processing
accumbens VTA
Pleasure, euphoria Sleep
Motor function Hippocampus Cognition
(fine tuning)
Compulsion Raphe nucleus
Perseveration

This image is in the public domain because it contains materials that originally came from the
National Institutes of Health

McGinty et al. conclude by stating “one consistent point that became apparent was
that brain regions cannot be simply labeled as either contributing, or not contributing,
to motivated behavior; rather, it's necessary to consider the specific circumstances
under which the region is being engaged” (p. 356). Reinforcement can be looked at as
motivation in that by the recruitment brain systems, it serves to orient and behavior-
ally direct the individual to a particular subset of environmental stimuli.
Maladaptive Behavior and Thought Is Based Upon Automaticity 123

Hart et al. (2014) point out that “considerable evidence suggests that distinct
neural processes mediate the acquisition and performance of goal-directed instru-
mental actions. Whereas a cortical-dorsomedial striatal circuit appears critical for the
acquisition of goal-directed actions, a cortical-ventral striatal circuit appears to medi-
ate instrumental performance, particularly the motivational control of performance”
(p. 104). While they point out that these distinct circuits of learning and performance
constitute two distinct “streams” controlling instrumental conditioning, the interface
between these two streams or circuits might represent a juncture for a limbic–motor
interface. They posit that the basolateral amygdala, which is heavily interconnected
with both the dorsal and ventral subregions of the striatum, coordinates this interac-
tion providing input to the final common path to action. We propose that this inter-
face represents the intersection of the reward circuitry that creates and maintains
motivation and engagement (Wasserman & Wasserman, 2015).
There are models of how specifically, reward recognition participates in the devel-
opment of a learning response. For example, Roelfsema and Ooyen (2005) describe
attention-gated reinforcement learning (AGREL) which describes the rules that govern
the changes that occur in the connections between neurons as a result of learning. They
define these changes as plasticity. They indicate that there are two factors that deter-
mine synaptic plasticity: (1) a reinforcement signal that is homogeneous across the
network and depends on the amount of reward obtained after a trial and (2) an atten-
tional feedback signal from the output layer that limits plasticity to those units at earlier
processing levels that are crucial for the stimulus–response mapping. In other words, in
order for learning to occur, the desired signal must be reinforced and thereby strength-
ened, while at the same time, the non-desired signal must not be reinforced and there-
fore suppressed. We will speak more about this idea of strengthening and suppression
in the next section. It should come as no surprise to anyone that unmotivated, or poorly
motivated clients will not learn. What is crucial to remember, is that motivation is not
an abstract concept, but apparently highly task specific. Motivation is not the product
of a mystical personality trait that certain individuals either have in abundance or in
which they are deficit. Motivation reflects the operation of the reward recognition cir-
cuit which is either more or less efficiently integrated with behavioral circuits. The
implication of all this is that in therapy, a client may state that they are motivated to
change, but in the particular may be unmotivated to engage in the behaviors necessary
to facilitate that learning. They desire the outcome, but the component behaviors are
not rewarding and therefore not engaged. It is also important to remember that success
brings reinforcement, and the increased likelihood the action will continue to be
selected in the future. Therapeutic progress, therefore, is facilitated when a planned
program of increasingly complex actions is engaged in and reinforced.

Maladaptive Behavior and Thought Is Based


Upon Automaticity

Automaticity is the goal of human learning (Aarts & Dijksterhuis, 2000;


Bargh & Chartrand, 1999). In this regard, maladaptive thought and resulting beha-
vior are no different than any other type of thought, including adaptive thought.
124 12 New Principles of Therapy

It is learned in the same way and expressed behaviorally in the same way. Neural
circuitry involved in its learning is the same neural circuitry that is involved in
all other learning. This leads to an interesting likelihood; in many instances
where behavioral definitions of mental health issues are utilized, there are not
brains that are defectively permanently wired, or permanently damaged. In addi-
tion it is not guaranteed that a person with an emotional dysregulation issue has
a badly wired brain. It implies that the current patterns of connectivity are the
result of reinforcement patterns that have not produced adaptive behavior.
Luckily, in most instances, this is not permanent. These pathways supporting
maladaptive behavior can be altered by the same processes that supported their
formation in the first place.
We have seen research indicating that learning occurs when potential responses
to internal representations of environmental occurrences are reweighted with
some responses being made more likely, and other responses becoming less
likely (Petrov et al., 2005). Both working memory and processing speed effi-
ciency, which impacts the quality or quantity of information represented, play
important roles in this process. Deselection and reselection depends on the abil-
ity to suppress (deselect) newly identified task-irrelevant information as well as
the ability to activate (select) newly identified task-relevant information (Brewin
& Beaton, 2002). Interestingly, increased working memory and processing speed
efficiency are both associated with fluid intelligence, and are associated with the
ability to suppress unwanted stimuli and impulses. The more efficient a person
is, and the more efficient working memory is, results in material being held in
working memory for a greater period of time and available for modification.
Fluid intelligence refers to the ability to solve novel problems and adapt to new
situations (Horn & Cattell, 1967). Increased flexibility implies increased ability
to evaluate novel solutions and consider new responses. It also suggests increased
ability to select a new response to make automatic. All of this suggests that fluid
intelligence would be intimately and positively correlated with mental health.
There is in fact some evidence that this might be the case, at least in populations
of older individuals (Perlmutter & Nyquist, 1990).
Deselection and reselection of a new process to make automatic is at first a
conscious and planned process. This is because conscious processes are focused
and convergent, drawing heavily on limited working memory resources
(Dijksterhuis & Meurs, 2006). In addition, there is data that suggest that perfor-
mance degradation, in terms of efficiency and fluidity, can occur when too much
attention is allocated to processes that usually run more automatically (Bielock,
Jellison, Rydell, McConnell, & Carr, 2006). This suggests that an individual who
is attempting to eliminate a maladaptive, automatized process will struggle and
perhaps become even more inefficient and ineffective as they shift from their
maladaptive strategies to newer, potentially effective but not yet automatic cogni-
tive processes. This moment in therapy will be highly discomforting to the client,
and the therapist must be prepared with strategies to continue to encourage the
transition. Without planned and purposeful support, clients are likely to return to
the previously automatized, but maladaptive processes.
Learning Is About Connections in that What Is Stored Together Stays Together in Memory 125

Learning Is About Connections in that What Is Stored


Together Stays Together in Memory

Learning occurs in context. What is learned is associated and remembered in the


context of what was around it the time it was encountered. Appropriate or socially
acceptable responses can be stored with socially unacceptable responses should that
association be reinforced. This is the basis for many fetishes and phobias. Given the
right set of motivational circumstances, inappropriate responses can be stored.
Therapy should be designed to identify these maladaptive contextual pairings and,
where appropriate, work to repair appropriate emotional responses with acceptable
behavioral outcomes.
These fourteen principles reflect what is known from both learning theory and
neuropsychological research. They are applicable in any situation where something
is to be learned. They are not suspended in the special instance of learning in therapy.
Whatever you call the result, self-actualization, behavioral change, spiritual growth,
destruction of maladaptive gestalts, or behavior change, the result of therapy should
be that the individual engages in more adaptive behavior at the end than when they
began. This inevitably means that the individual has learned new ways of behaving.
While we do not argue with those who say that the relationship between the cli-
ent and the therapist is crucial, we would certainly argue that the relationship is not
the sole requirement, nor sufficient element, for progress to take place. A positive
relationship is certainly conducive to learning, but things still have to be learned,
and neuropsychologically speaking, all humans learn them in the same way. The
therapist that emphasizes the relationship but does not know how knowledge is
transmitted and learned does so at their own and their client’s peril.

Neurocognitive Learning Therapy

Since we have now spent some time looking at a treatment paradigm that incorpo-
rated the ideas and principles in this book, we thought it might be interesting to name
a therapeutic approach that would embody these principles. We, at first, resisted this
idea because we believe that the elements we are speaking about should be utilized
in all therapeutic encounters with clients. We would not want to do anything to sug-
gest that we think it would be a good idea to ignore these principles of learning.
On the other hand, having all the principles embodied in a single system would
create a powerful approach that would enable both clinical intervention and research
methodology improvement. Such a powerful system would deserve recognition,
and since all human learning incorporates pattern matching, such a system should
have an identifiable pattern called a name. It is of course also possible that some
practitioners might actually prefer to label themselves as proponents of the model,
and it is to these individuals that we offer the name Neurocognitive Learning
Therapy (NCLT).
126 12 New Principles of Therapy

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Stiles, W., Meshot, C., Anderson, T., & Sloan, W. (1992). Assimilation of problematic experiences: The
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Taha, S., & Fields, H. (2006). Inhibitions of nucleus accumbens neurons encode a gating signal for
reward-directed behavior. Journal of Neuroscience, 26(1), 217–222.
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Thatch, W. (1997). Context-response linkage. International Review of Neurobiology, 41, 599–611.


doi:10.1016/S0074-7742(08)60372-4.
Thorndike, E. (1932). The fundamentals of learning. New York: Teachers College Press.
van Merriënboer, J., Kester, L., & Paas, F. (2006). Teaching complex rather than simple tasks:
Balancing intrinsic and germane load to enhance transfer of learning. Applied Cognitive
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Vygotsky, L. (1934/1986). Thought and language. Cambridge, MA: MIT.
Wasserman, T., & Wasserman, L. (2015). The misnomer of attention deficit hyperactivity disorder.
Applied Neuropsychology Child, 4, 116–122.
Watson-Gegeo, K. (2004). Mind, language, and epistemology: Toward a language socialization paradigm
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sequences (pp. 283–313). New York: Psychology Press.
Chapter 13
Tell Me How You Feel

Is it really possible to tell someone else what one feels?


Leo Tolstoy, Anna Karenina

In our model, neurocognitive learning therapy (NCLT), a model which presupposes


a trusting relationship, where both semantic and emotional content have pride of
place, what do we mean when we ask a patient the inevitable, how they felt about
something, or how something made them feel?
In this model we mean that we are asking the client to describe, in detail, all of the
thoughts, physiological responses, and emotional labels for those physiological
responses and behaviors that are brought from long-term memory to working memory.
We are cognizant of the fact that, when the follow-up question of “What is happening
that causes you to feel this way” comes, clients will search their memories and pick the
likely candidates that match the emotion they are describing. We are doing this in order
to identify elements associated around the particular feeling in the individual’s connec-
tome. All of this enables us to determine which of these responses are adaptive, which
of these responses are maladaptive, or which response is dystonic and which is not.
The therapist is not asking this question to determine the etiology of the pattern of
responses. We know that they are all learned. And it does not necessarily matter how
they were learned within the neuropsychological model, other than if the learning
that led to the maladaptive responses was still continuing. Again, we know they were
learned through association and automatization. We understand that validating the
client’s emotional state is important to the therapeutic process because it is designed
to ensure that the client feels both heard and understood. We also understand that this
same process of validation can be both dangerous and destructive as it runs the
chance of reinforcing the very maladaptive behaviors we are seeking to change.
This supportive therapeutic step should not however be confused with maintain-
ing our sights on the larger umbrella of understanding how this person came to
these maladaptive and distressing issues: the neurophysiological process is the same
for all and all are subject to the learning principles outlined throughout this book.

© Springer International Publishing Switzerland 2016 129


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_13
130 13 Tell Me How You Feel

We do not want people to explore their feelings and then dwell on them. We want to
begin to identify the particular experiences that we will have to provide in order to
weaken the associations with the established and automatized pattern of maladap-
tive behavior and corresponding emotions in order to strengthen new and adaptive
responses. We of course also want to know if something other than the automatized
responses themselves is currently maintaining the behavior.

Tell Me What You Think About That

You would be correct if you were thinking that asking a person what they were
thinking about yielded information in a similar manner to the “Tell me what you are
feeling” question. In an NCLT perspective, this is quite true. The therapist is asking
for the cognitions or thoughts that are associated with a particular issue. Going back
to the small-world hub model, we discussed earlier what you are really trying to do
as a therapist is to clearly establish all of the associated thoughts and feelings so that
you have a clearer picture concerning the modifications to be made.

An Example

In order to make the point clearer, let’s look at a highly exaggerated situation. Susi
is a new client that comes to you complaining of anxiety responses when she has to
visit each of her divorced parent’s homes. Both parents accompany her to your ses-
sion. She is 12 and her parents have been divorced since she was 8. She recalls that
the divorce has been rather amicable and her parents are quite supportive of her time
sharing with the other parent. Susi and her parents report that the first couple of
years were uneventful, but after that Susi began experiencing mild anxiety when she
alternated between her parent’s homes. It has worsened recently to the point that
Susi was asking to go to boarding school as a way of alleviating stress.
Upon questioning to establish all of the associations, Susi provides the following
information: Susi loves both her parents dearly and, as is typical, wants them to get
together and reunify. She says she accepts the fact that they won’t, but nevertheless, she
still hopes for reunification. She reports that when she visits either parent and they have
a talk to seek to catch up, the parents will tell her about their new relationships and ask
about the spouse in the same vein. Each parent has told her to please not discuss their
particular relationship status with the other parent as that is for the parent to do when
necessary. Recently, the parents have been more active in the dating world, and each
has developed a relationship. Susi reports that she does not know whether the new
person will be there when she arrives. Susi also reports that she is increasingly anxious
on the car ride to a particular parent’s home, often feels nauseous, and has headaches.
On one or two occasions, the headaches have been so severe that she has used them as
an excuse to cancel a visit. Susi says that she loves both her parents and has spoken to
them about her wishes. She does not want to hurt either one.
An Example 131

Clearly, there are many issues involved here, to name a few, abandonment,
betrayal of trust, making demands on others, failure to nurture, putting parental
needs ahead of those of the children, asking children to keep secrets, loss of parental
affection, sharing the parent with a stranger, and a general lack of security. Each of
the above list is theme and each has an associated set of thought and feelings.
Traditionally, schools of therapy would have spent a good deal of time arguing
about which of these problems represented a core issue and therefore receive primacy
in the order of intervention. NCLT would point out that, because of the small-world
hub organization of neural networks, they are not discrete issues and that they are all
interrelated. Primacy is not a valuable construct in this regard. They are all primary
because they are all one. NCLT would help the client to recognize and identify all of
these issues and understand that they are all interconnected. It would certainly recog-
nize that it is, for this client, an emotionally frustrating and insecure situation to be in.
Then it would get to work at giving the client skills to handle her anxiety, and tools to
handle her cognitions and feelings. It would help the client first separate out what she
could control, and what was for the moment outside of her control. Those who are out
of their control might use cognitive therapy techniques to address any unrealistic
demands, dialectical behavior therapy techniques to address the emotionality associ-
ated with the demands, and mindfulness techniques to provide skills that would help
counter the physiological states associated with the anxiety.
For those of you who are saying that this is merely eclecticism at work, we
would strenuously disagree. Eclectic therapists are fond of saying “I do what
works,” but are in general bereft of a model that tells them why they should target a
behavior or why this issue was there in the first place. Many, in our experience,
claim to be atheoretical. Throughout the world, if you ask a psychologist or coun-
selor what their theoretical orientation is, the most frequently given response is
integrative or eclectic (Norcross & Goldfried, 2005). If you are an NCLT therapist,
you know exactly why you are picking a particular intervention and exactly how
that intervention will generate information that can be used by the clients learning
network. The two approaches could not be more different.
Eclecticism is the best recognition that no one current treatment model is effec-
tive enough. The fact that integrative approaches are required or even recommended,
is a tacit admission of the field (a) that mirroring the mind–body split, we have
models that fail to integrate a picture of mental health and the processes involved
and (b) that the single disease entity model currently in use in the mental health field
is inadequate to predict effective treatment.
The NCLT model is designed to assist in the integration of understanding the
human mind, mental health, and mental disorders. This integration is long over-
due. In the United States, many people suffer from more than one mental disor-
der at a given time. Almost half (45 %) of those with any mental disorder meet
criteria for two or more disorders (The Kim Foundation, 2014). To us, this
reflects the fact that our current disease label no longer adequately describes the
problems. While it is of course possible that an individual might have two disor-
ders, we believe that it is more likely that the overall disorder is not adequately
identified or described by the current nosology.
132 13 Tell Me How You Feel

Many Techniques Generate Useful Information

The reader will undoubtedly know that there are established techniques that would
be quite useful in this process if they are used in the context described above. For
example, cognitive behavior therapy techniques that challenge maladaptive thought
processes (Beck, 2011; Ellis & Harper, 1997) or techniques that highlight the inter-
dependency of thoughts and their associated emotions (Van Dijk, 2013), could both
be effectively employed to identify maladaptive thought-feeling associations and
begin to create learning experiences to support the acquisition of adaptive responses
to stimuli. These approaches challenge the client to create a new adaptive narrative
to a stimulus that previously was associated with negativity. In fact, almost every
therapeutic approach can generate potentially useful information. There is, for
example, a vast amount of clinical opinion, but a striking lack of empirical evidence
that catharsis is effective as a clinical intervention. Within the context of neurocog-
nitive learning therapy, there is some indication that even simple catharsis can serve
to identify components of an individual’s response scheme (Kosmicki & Glickauf-
Hughes, 1997) and be used to establish and strengthen new patterns of association.
Traditional psychotherapeutic approaches have placed great emphasis on how a
therapist will relate to the client while we are getting this information, and how safe
the client feels when providing it. Much less emphasis has been placed on what the
therapist or client will be actually doing with it. As we have pointed out, there are
even approaches that suggest that we ought not to tell the client what to do with it,
but we should let the client figure out that piece by themselves. As Carl Rogers was
often quoted as saying “In my early professional years I was asking the question:
How can I treat, or cure, or change this person? Now I would phrase the question in
this way: How can I provide a relationship which this person may use for his own
personal growth” (Rogers, 2015). However, even Rogers recognized that all human
knowledge was processed in the same way. “In a person who is open to experience
each stimulus is freely relayed through the nervous system, without being distorted
by any process of defensiveness” (Rogers, 2015).
We believe that recent research has clearly demonstrated that all information is
processed in relation to what has already been learned and is therefore never free
from interpretative bias. We would rush to point out the following; how the informa-
tion which has already been processed and retained in long-term memory is elicited
in therapy and is much less important to the therapeutic process than the use it is put
to after it is elicited.

Any Way into the Connectome Is a Good Way

Recently therapeutic approaches, such as dialectical behavior therapy, have been


developed that attempt to integrate the emotional responsivity of the individual within
a cognitive treatment model (Van Dijk, 2013). These approaches recognize that many
An Educated Client Is the Best Client 133

individuals respond to their emotions more readily than they do their thoughts. NCLT
would recognize these emotional expressions as the identifications of elements of the
connectome and treat them as learned associations much in the same way as it would
look at semantic information. There are indications that others have begun to recog-
nize this fact as well, recognizing that all therapeutic learning can be explained by a
connectionist process. For example, in describing the benefits of a group of these
emotionally oriented treatments, Gard et. al. (2015) points out, “if you practice some-
thing, then you are going to get enhanced connectivity in neural structures” (p. 55).

Neurocognitive Learning Therapy Integrates All Models

We recognize that most forms of treatment would describe themselves as therapeu-


tic approaches that have a component detailing with how humans become dysfunc-
tional. In our view, they are describing segments of an individual’s learning and
epigenetic history. For example, cognitive behavior therapy, according to its detrac-
tors, has been described as looking at the here and now minimizing the importance
of personal history, while psychodynamic psychotherapy has been described as
looking to address the root causes of psychological issues. The detractors of psy-
chodynamic therapy claim that many of these factors are outside the client’s aware-
ness and therefore cannot influence behavior (Spencer, 2010). Cognitive behavior
therapy has been described as coldly logical, ignoring the emotional component that
is so richly utilized in psychodynamic interventions.
NCLT holds all learning in equally high regard. It understands that most human
learning reflects itself in highly automatized routines that are by definition below the
threshold of awareness. It recognizes the importance of the interactive effects of both
cognitively and emotionally regulated learning on the development of these routines
within the connectome. NCLT has an understanding about how we become dysfunc-
tional and how to go about creating adaption. Without attempting to overreach, we
believe NCLT permits the effective unification of a variety of treatment models based
on what was before now, competing models of the nature of mental health.

An Educated Client Is the Best Client

All of this occurs in the context of a fully informed and educated client. Clients in
NCLT are educated in the connectionist model and to some extent how small-world
hub models work. In this way NCLT clients understand why questions are being
asked and for what purpose an activity is encouraged. The discussions in NCLT
revolve around strengthening adaptive connectionist networks and weakening mal-
adaptive ones. A discussion of pathology is not required, and in many senses coun-
terproductive, in that the idea of a pathological trait might serve as an impediment to
corrective action on the part of the client. The client understands why the questions
134 13 Tell Me How You Feel

are being asked and to what purpose the replies will be put. They understand that
each time they identify a maladaptive response or thought, they will be asked to plan
some activity designed to decrease the probability of its reoccurrence.

In Summary

What we have demonstrated is that it is possible to create a therapeutic system that


is based on, and integrates, the neuropsychology and neurophysiology of learning.
We have demonstrated that this learning is not only semantic and logical but involves
emotional responsivity as well. We have shown that you do not need to have two
systems for learning and that the traditional mental processes can easily be explained
by an integrated neurophysiologically grounded model. All systems are valid as
techniques within this integrated system to generate information to be used.

References

Beck, J. (2011). Cognitive behavior therapy. New York: Guilford Publications.


Ellis, A., & Harper, R. (1997). A guide to rational living. New York: Willhire Book Company.
Gard, T., Taquet, M., Dixit, R., Hölzel, B. K., Dickerson, B., & Lazar, S. W. (2015). Greater wide-
spread functional connectivity of the caudate in older adults who practice kripalu yoga and
vipassana meditation than in controls. Frontiers in Human Neuroscience, 9, 137. doi:10.3389/
fnhum.2015.00137. eCollection 2015.
Kosmicki, F., & Glickauf-Hughes, C. (1997). Catharsis in psychotherapy. Psychotherapy: Theory,
Research, Practice, Training, 34(2), 154–159. doi:10.1037/h0087724.
Norcross, J. S., & Goldfried, M. R. (2005). Handbook of psychotherapy integration (2nd ed.).
New York: Oxford University Press.
Rogers, C. (2015). Carl Rogers quotes. Retrieved from Brainy Quote: http://www.brainyquote.
com/quotes/authors/c/carl_rogers.html
Spencer, R. (2010). CBT or psychodynamic therapy? Retrieved from Dr Rene Spencer: cbtvspsy-
chodynamic.com
The Kim Foundation. (2014). The Kim Foundation. Retrieved from Statistics: Mental Disorders in
America: http://www.thekimfoundation.org/html/about_mental_ill/statistics.html
Van Dijk, S. (2013). DBT made simple. New York: New Harbinger.
Chapter 14
Case Studies

Life is a purposeful action


Asa Don Brown

The following are designed to be case examples demonstrating how to incorporate


the model we are describing into the everyday consultative practice of the practitio-
ner. They are designed to demonstrate how the learning principles and underlying
neurophysiology are incorporated into everyday practice.

Little Mary Sue

Our first example involves a young girl named Mary Sue. Mary Sue is 5 years old.
Your intake indicates that Mary Sue was born into the Smith family, which is com-
prised of Mr. and Mrs. Smith and two older siblings. Mary Sue was delivered fol-
lowing a full term, uncomplicated gestation. Mary Sue was described as having
been difficult to soothe and was diagnosed with colic. Mrs. Smith held Mary Sue
almost constantly through the first 6 months of life. Gross motor, fine motor, and
language developmental milestones were obtained well within normal limits. First
words were spoken at 9 months and Mary Sue was fully ambulating by 12 months
of age. Mary Sue went to preschool at 3 years of age and her teachers described her
as bright and active. Now, at age 5, Mary Sue’s mother is concerned about her
behavior. At home, Mary Sue continues to be difficult to pacify. She frequently
loses her temper and decompensates into tantrums that can last for an hour. Your
questions reveal Mrs. Smith’s confusion regarding her ability to predict Mary Sue’s
response at any given time. Your refined questions hone in on the major sources of
difficulty: that the rages are usually preceded by Mary Sue not getting something
that she had planned to get or when her schedule is disrupted. For example, if Mary
Sue was told that she cannot watch TV tonight because of her poor behavior, a tan-
trum would ensue. Mary Sue loves to watch her favorite video. She will often watch

© Springer International Publishing Switzerland 2016 135


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_14
136 14 Case Studies

it over and over. Obviously, during the course of the day, Mrs. Smith must try to get
Mary Sue to turn off the video. Often, When Mary Sue is asked to turn off the video,
Mary Sue will respond with a tantrum. Temper tantrums of this sort occur daily, and
when they happen, it is difficult to calm Mary Sue. Additional questioning indicates
that Mrs. Smith describes Mary Sue as requiring a great deal of her attention. For
example, Mary Sue will often ask the same questions over and over. These ques-
tions relate to what is going to happen during the day. Once Mary Sue has a sched-
ule in her head, she appears mollified although, as noted, this quickly changes once
that schedule is altered. Mrs. Smith states that Mary Sue’s tantrums are disrupting
the home and wants to work to make sure that they don’t continue.
Mrs. Smith continues to describe Mary Sue as quite active. She is often unable to
continue with a selected activity for very long. These reports are confirmed by the
preschool teacher who indicates that while Mary Sue is doing satisfactorily aca-
demically, she is, however, immature and might profit from another year of pre-
school instead of progressing to kindergarten. During the intake Mrs. Smith also
asks you to advise her about the benefit of providing Mary Sue another year of
preschool. She is especially concerned because Mary Sue is scheduled to attend an
academically competitive private elementary school where her two older siblings
are already successfully enrolled.
In order to get a comprehensive assessment, you administer several behavior
checklists. The elevations across the checklists are clinically significant and consis-
tent. Mary Sue meets criterion for ADHD combined type. In addition, your direct
observation of, and interview with, the child confirms the parent reports of a highly
active little girl who flits around your office and has difficulty sitting still. She also
has difficulty staying focused on what you are talking about and any tasks you give
her. The diagnostic conclusion being rather straightforward, you meet with the fam-
ily, review the results, and discuss the definition and behaviors associated with
attention deficit disorder. You also discuss the pros and cons of cognitive behavior
therapy and psychopharmacology. Mary Sue’s parents being diligent choose both
options, and a week later she is in your office and you are developing a behavioral
intervention plan, while at the same time she is on a trial dose of a stimulant medica-
tion provided by a pediatrician who has confirmed your findings.

The Alternative Model

Knowing what you now know, how does one adopt the model being proposed in this
book into the client–therapist relationship? What would be different and what would
remain the same?
The major difference would emerge after the checklists are completed or perhaps
after the diagnostic intake is completed, if the data provided is very clear. The dis-
cussion would go something like this:
We would begin to explain to the parent: “We talked about Mary Sue having a
diagnosis of attention deficit hyperactivity disorder. However, you can see that it is
The Alternative Model 137

not her attention per se that is problematic as Mary Sue can watch the same video
for extended periods of time. And although Mary Sue is generally highly active, she
can sit in one place while watching her favorite video over and over. In fact, she gets
upset when you try to break that highly focused attention to the video. We therefore
think about children like Mary Sue a little differently.”
With regard to her attention problem, we would explain that Mary Sue does not
have an attention deficit. Rather, we would say that Mary Sue has difficulty paying
attention to what we want her to pay attention. We would talk about Mary Sue having
a narrow band of interest and that the things that she is interested in have a strong pull
on her attention. In other words, we would talk about the attention problem in terms
of orientation to task and the selection of stimuli to be gated. The materials we are
presenting her with are of limited interest. That is, her reward center is not engaged,
or “turned on,” by the materials presented, for example, in the classroom circle time
wherein the teacher teaches a lesson. This has resulted in a “reward history” in which
Mary Sue is not internally reinforced for attending to this type of information or
activity. Our job then is to find ways to increase the reward valence of these activities
and the curriculum material in order to make it of higher reward value to Mary Sue,
thereby increasing her motivation and, subsequently, her attention.
As regards Mary Sue’s rigidity and tantrums, we would say that rather than being
related to an attention deficit, we would discuss it in terms of a regulatory one. It is
very clear from what the parent has shared that Mary Sue has a history of poorly
regulating her behavior and becoming quickly overwhelmed. It is also clear that
getting overwhelmed is her first and, in most cases, only response to confronting
unexpected situations or those which are divergent from her expectations. Once
Mary Sue is confronted with unexpected situations, she becomes overwhelmed.
Once overwhelmed, it is difficult for her to regain control of herself. It is also appar-
ent that Mary Sue gets anxious when things are not as she has planned them to be
and relies on organization and predictability to keep that anxiety in check.
If you look back, Mary Sue has a history of this poor ability to self-regulate from
the time she was born. It is clear that she had difficulty regulating herself emotion-
ally and bringing herself under control. What you saw were the resulting behaviors
such as the tantrums. This difficulty regulating has continued and gotten worse as
the demands on her have increased and the number of things that can deviate from
expectancy multiplies. As a result, Mary Sue’s resulting default behavior became
tantrum. It is a behavior she “has practiced” for so long and what is now demon-
strated automatically. She has not yet practiced alternative behaviors that would
help her regulate herself.
The impact of this model on intervention is now almost monumental. Traditionally,
the clinician would be talking about this child’s attention weaknesses and so all
subsequent interventions would have been geared toward improving Mary Sue’s
attention and outbursts. Traditional recommendations would have been geared
toward, for example, reinforcing Mary Sue for remaining seated in her class or
complying with directives. The new model allows us to explain to teachers and
parents how Mary Sue is not having a conduct problem; she is anxious and does not
regulate her anxiety well. She has poor coping skills and decompensates. Now the
138 14 Case Studies

intervention has to incorporate a program to address these issues, building skills to


provide our “attention deficit” youngster with skills to help her internally with plan-
ning, problem solving, and, ultimately, resilience.
At this point you would begin a discussion of automaticity and how humans rely
on automaticity to function. You would then explain that Mary Sue’s tantrum are her
automatic response to unexpected environmental variation and that the job in front
of us was to de-automatize the undesirable response, teach a new response, and then
automatize the new response.
For certain parents this discussion might be accompanied by a discussion of
neural networks particularly the interface with target selection and reward history,
but this would depend on how well the parent was taking this all in. We would fol-
low the discussion of automaticity with a discussion of neural networks and recruit-
ment of networks. We would talk about efficiency of recruitment of networks. We
would offer a basic explanation of how the difficulty is Mary Sue’s poor ability to
recruit networks efficiently and how this is impacting emotional arousal, impacting
her working memory, and impacting the allocation of working memory through
reward identification. The provision of information could go on over the course of
several sessions. This is as much about educating the parents as it is about teaching
skills to the children.
The model now requires that we go through three steps. The first is that we are
going to help de-automatize Mary Sue’s maladaptive response, the second is we are
going to teach her an adaptive response, and the third is that we will then help her
automatize the new response. In reality, we will be doing this all at the same time,
but you will understand that there are these three components.
To the client you might present the following intervention designed to provide a
prompt, provide exposure to a relevant stimulus, and provide the strategies for suc-
cessful addressment of the difficulty: “So, let me tell you about this game we will
teach Mary Sue to play. It’s called surprise time. Surprise time is a simple game.
Each day one person, preferably you, Mrs. Smith, because you now understand
what we are trying to do, will pick one moment to “surprise” Mary Sue. That is, we
will prompt Mary Sue that surprise time is coming soon in order to allow her to
begin to suppress the “default” setting and allow her to begin to use thoughts/words
(a template provided by the therapist) to construct a new response. Mary will know
what is going to happen. When the surprise comes, you will purposefully disrupt her
schedule. We will teach Mary that when a change in schedule is going to happen,
she will use words and help to form a new plan. (Allow a brief time between the
prompt and the “surprise” trial. After a selected amount of time and number of
practices, the prompt will be dropped. Then, if she does this when the surprise hap-
pens, she will earn a reward (preferred activity, access to a preferred item, etc.). If
successful, she will be told that she passed the game for today and the reward will
be given. If not successful, she will be told that it is surprise time and will be helped
to practice. Over the next few weeks, we will expand surprise time to three times a
day. Mary Sue will always have to guess whether the disruptive event that is hap-
pening is planned or not. After this skill has been practiced, we will add another
person (to assist with generalization) and keep doing it until Mary Sue is always
The Alternative Model 139

pausing and deciding whether this is a surprise time event or not. Then we will keep
going until automaticity is installed for both pausing and selecting the adaptive
strategy. At that point we will select another target.”
The parent leaves the office with a new strategy, an understanding of why the
strategy was selected and the learning principles involved, a very rudimentary begin-
ning understanding of the underlying circuitry involved and an initial target and
training strategy. That may seem like a lot, but in fact, it is quite accomplishable in
an hour. Training then is focused on skill acquisition and widening of adaptive skills.
The focus in this model is on both education and skill improvement (for both the
parent and the child) and not about modifying maladaptive behavior that occurs as
a result of an illness. In fact, you will notice that the word illness is not used, and
conceptualizing the current behavioral status of the individual as disordered is not
required. The focus is on the interaction with the constitutionally derived function-
ing of Mary Sue’s circuitry and how it has interacted over time with environmental
exigencies to produce the current profile of her behavior. When you think about it in
this way, you will readily see that describing her as having a mental disorder called
ADHD adds little to the discussion other than perhaps to understand that she has the
propensity to poorly regulate environmental input and inefficiently use target selec-
tion strategies. You can use it, but it isn’t really critical that you do so.
If you are thinking that this is classic behavior therapy, you are of course in many
respects correct. As we have consistently pointed out, the laws of learning are the
laws of learning, and these laws apply to the brain and to “emotional” responsivity
equally. It would be explained to Mary Sue’s parents that we needed to help Mary
Sue select the proper response from the variety of options available, and then we
needed to train that response. It would then focus on identifying situations for train-
ing. The difference here is that classic behavior therapy did not tie itself back to the
underlying neural networks. It did not concern itself with the interaction between
the underlying neurophysiology and how information is processed. We do not rule
out the possibility that as we have described previously, there is an underlying prob-
lem that prevents the physiology from engaging efficiently. For example, in Mary
Sue’s case, other children may have better ability to shift their behaviors and emo-
tionally regulate. In this case, that would include the failure of motor inhibition and
the poor epigenetically based development of desirable inhibition skills. They did
not, in general, concern themselves with automaticity and allocation of memory and
related attention. This model does planning on responses and of course reinforce-
ment for the purposes of establishing automaticity of the newly learned behavior.
If you are thinking this sounds somewhat like sensory integration, we suppose
that it does. Sensory integration argues that individuals have difficulty regulating
sensory input, and that by increasing the system’s ability to process that input, we
improve the individual’s ability to function. We take the epigenetic position that at
first this might be true in that the young child with this propensity will have diffi-
culty developmentally regulating. We differ in that we believe that this poor regula-
tion leads to a set of automatized maladaptive responses that themselves prevent the
development of adaptive responses. These adaptive responses will not be spontane-
ously uncovered upon improvement of the system processing capacity. In fact, we
140 14 Case Studies

are not sure at this point whether or not that is even possible. We are sure that by
teaching adaptive methods of coping with input, you improve the operation of the
network. In fact, most successful sensory integration approaches include the teach-
ing of adaptive responses, but do it with only a rudimentary understanding of the
role of automaticity.
If you are thinking of these things, it is because these are therapeutic approaches
which, in part, address the issues presented. The NCLT model is designed to incor-
porate all of these approaches into an integrated model.

Joseph

In many ways Joseph was the ideal 11-year-old until the incident happened. He was
the product of a full-term gestation and achieved all of his developmental mile-
stones well within normal parameters. His parents, Mark and Martha Jones, consid-
ered themselves blessed. Joey’s preschool teacher announced that she thought that
Joey was quite academically advanced and recommended testing for “gifted pro-
gramming” upon entering kindergarten. Joey did quite well on the tests and was
placed into the desired program and thrived. Everything was going along quite well
and all was as it should be.
Things changed when in March of Joey’s 11th year, he and his friend Ben were
walking home from school. They were on the sidewalk when a car’s tires screeched
and Joey turned to see a truck swerve to avoid a car that had suddenly emerged from
a driveway. The truck headed right for the boys and Joey called out to Ben, who
engrossed in a text message on his phone had not even looked up, to warn him. Joey
jumped and tried unsuccessfully as it turned out, to push Ben out of the way. He
failed, and Ben was struck by the truck and died right in front of Joey.
Everything seemed okay after the accident. After Ben’s funeral, Joey returned
to school. His parents, ever cautious and diligent, hired a grief counselor to help
Joey process his feelings around the accident. Problems began to emerge how-
ever, slight at first, but rapidly escalating. It started when Joey became anxious
about walking home from school. He jumped at every car noise and was con-
stantly checking and rechecking the street traffic. He eventually became so anx-
ious that he stopped walking home and had to be picked up. That worked for a
while until his anxiety about being in a car escalated and now, at age 13, he was
refusing to go to school. School refusal was only part of it as most days he
would refuse to leave his house and become agitated when leaving the house
was suggested. His parents note that he has become more somber and less
related. Desperate now, they have turned to you for help. We will assume for the
purposes of our discussion that this is a clear-cut example of post-traumatic
stress disorder and eliminate a discussion about how we substantiated our clini-
cal opinion.
Joseph 141

A Word About Grief Therapy

Outside the scope of this book, there is a healthy scientific debate about the efficacy of
Grief Therapy in general and a clear recognition that Grief Therapy might not be an
effective intervention for some people (Sword, 2012). What is well within the scope of
this book is the basis of the connection that in some cases, Grief Therapy can have
deleterious outcomes. Sword (2012) points out that in general, the traditional Grief
Counseling approaches return to the narrative of the trauma that happened and then try
to desensitize a person to the enduring impact of the event. In relation to treatment for
post-traumatic stress disorder, Joey must relive the trauma over and over again.
Sword (2012) points out that while this may be an effective treatment for some,
it is more often detrimental. Reliving trauma is something that the individual with
PTSD does every moment of every day, awake or asleep, all by themselves; they
don’t need the therapist to help them. For our discussion this means that the painful
event is essentially automatized and in some ways legitimatized. If therapy is about
creating adaptive responses, this does not appear to be a judicious way to do it.
Research into alternative models of intervention for grief and PTSD is continuing,
and newer models emphasize the creation of adaptive skills and helping clients
reframe their “illness” as a “mental injury” (Zimbardo, Sword, & Sword, 2012).’
We would conceptualize post-traumatic stress disorder as the development of a
highly automatized maladaptive behavioral and cognitive set of responses that are
utilized in connection with an ever-expanding set of specific initial event-related
stimuli. Initial anxiety responses are attached to a widening set of stimuli that are all
associated. In order to address this problem, the same formulation would be
required. You must reduce and eliminate the maladaptive responses while at the
same time increasing the adaptive ones. In this instance we would deem it critically
important to provide the client with a cognitive schema for both the development of
the maladaptive response set and the system we are going to use to address it.
If you were thinking, “This is a good place for a discussion about the role of medi-
cation” we would agree. What about giving medication to reduce the anxiety? This
appears perfectly reasonable to us and represents a much targeted use of psychophar-
macology in support of a planned program of learning. It could of course be argued
that by reducing the anxiety, you would be reducing the system drivers and the strength
of connections for the post-traumatic stress disorder-related behavior, and we would
agree as well. We think this would be helpful and, in fact if continued for a long
enough period of time, might reduce the atomicity of the anxiety response in reaction
to specific stimuli. We believe, however, that utilizing pharmacology in support of a
neurophysiologically based learning program would be much more efficient.
After inviting Joey and his parents into the treatment room, you would begin by
explaining the etiology and development of the complex set of behaviors learned in
association with the anxiety resulting from the condition known as post-traumatic
stress disorder. You would perhaps discuss how your developmental history indicated
that Joey had a history of anxiety-based respondency and that, in any event, the ini-
tial event was quite anxiety producing and elevated the potential for Joey’s responding
142 14 Case Studies

with anxiety whenever a similar event occurred. You would go on to explain that
Joey’s initial reaction to the out of control car and his friend’s death was (understand-
ably) quite strong, and that was sufficient enough to produce a set of responses that
became quickly automatized as the avoidance behavior quickly and effectively
reduced the anxiety. You would go on to describe how through a process of schema
development the world of things that Joey responded anxiously to expanded (a sim-
ple discussion of Piagetian-based schema development would help here). After that
you would describe how these new reactions had become automatic, and the goal of
treatment was to de-automatize them and make new, adaptive responses automatic.
You would indicate that you were going to do this either by desensitizing Joey to the
formerly anxiety-producing responses or by developing and practicing new responses
that were mutually exclusive to the undesirable ones. (The selection of which
approach to use would depend on the circumstances and whether the stressor was
amenable to systematic desensitization techniques.) Initially, you would target a
newly added or peripheral behavior that had been added to the repertoire so that Joey
could have some initial success and develop a sense of competence. You would work
on each maladaptive response until they were eliminated.
It is important to point out that we recognize that Joey is an 11-year-old child
who has feelings attached to what happened to Ben and to him. Joey will need a
therapist he can trust and who he thinks is empathic. How this talk therapy proceeds,
however, will either strengthen Joseph’s arousal and propensity for anxiety or help
him to reduce his automatic anxiety response by providing him with alternative
responses. This will be determined by the path and interventions chosen by the
therapist, based upon their conceptualization of how the disorder was created, what
it impacted, and how to “override” it.

Randy

To put it bluntly, Randy was always difficult. There was no other way to describe
him. From the moment he was born, he was difficult to soothe. He was stubborn.
His outbursts rattled his parents. This came as somewhat of a shock to his easy-
going parents who were kind and loving people and believed that if they were warm
and supportive, their child would grow and flourish. They responded to Randy’s
outbursts by trying to soothe him or give him what they thought he needed.
The story would of course have the same ending if Randy’s parents were ineffec-
tive discipliners, distracted parents, and two working parents who left Randy in the
care of a safe but indifferent care taker or parent who were just busy resulting in
young Randy having to tantrum to get their attention. In short, this is a story of a
youngster who was born with some difficulty regulating stress and then was placed
in an environment that shaped his behavior from there. In case you are suspicious
about the assertion that there are individuals born with a reduced capacity for stress
tolerance check Kajantie & Räikkönenc, (2010) or Badynaev, (2005). In summariz-
ing this position, Badynaev points out that stress-induced effects and stress-resistance
Randy 143

strategies often persist for several generations through mechanisms related to


maternal, ecological, and cultural inheritance. These trans-generational effects, along
with both the complexity of developmental systems and stressor recurrence, are
thought to underlie genetic assimilation of stress-induced effects. In addition, Parsons
(1990) noted that genetic disruptions include intense directional selection within spe-
cific genes which could then be further disrupted by environmental factors. Finally,
research has demonstrated a normal variation in the human infant adrenocortical
system in the production of cortisol in reaction to stress (Gunnar, 1992). Suffice it to
say that there is ample evidence to demonstrate that humans are born with geneti-
cally based predispositions for managing stress, and this predisposition interacts with
the environment in which it finds itself to produce the idiosyncratic stress tolerance
for a particular individual.
The parents continue; Randy became completely demanding as he got older. By
age six he directly challenged and threatened his parents if he did not get his way.
He was routinely oppositional and defiant, mostly at home, but increasingly at
school. His first-grade teacher had just requested a conference to discuss his behav-
ior when the parents called you for assistance.
After doing the standard diagnostic interview where you uncovered the facts
outlined above, you have the parents complete a variety of behavior checklists and
also have Randy’s teachers fill out the teacher’s version of the same checklists. The
replies are pretty uniform, indicating that Randy demonstrates the behaviors consis-
tent with a diagnosis of oppositional defiant disorder. You note that there are aggres-
sive behaviors noted and a diagnosis of conduct disorder is also possible. You
inform the parents that it is most likely an oppositional defiant disorder and recom-
mend therapy to help address the difficulty.
What does that therapy consist of? Well depending on your “orientation,” belief
system or training, it could be lots of things ranging from improving Randy’s ability
to form empathic attachments to modifying his maladaptive behavior. Methods used
might include play, where appropriate behaviors would be modeled to behavior
modification where negative behaviors would be punished and positive one rein-
forced. With the exception of cognitive behavior therapy, it would be hard to go into
the literature and find empirical support for many of the potential intervention tech-
niques other than direct parent training programs (Eyberg, Nelson, & Boggs, 2008;
Kendall, 2006). We would suggest that the cognitive behavior therapy target the
maladaptively learned responses rather than focusing on the defective nature of a
hypothetically independently developing cognitive system. Targeting the maladap-
tively learned responses would focus heavily on parent training which has been
found to be efficacious in addressing the behavior of children with oppositional
defiant disorder (Brestan & Eyberg, 1998). Eyberg et al. (2008) identified 16 treat-
ments approached as being empirically valid, and many of them share similar fea-
tures such as a heavy parent training emphasis practicing to the point of automaticity
adaptive behavior and eliminating maladaptive previously automatic responses.
After some deliberation you select the approach advocated by Forehand and
McMahon (1981). This treatment was designed for preschool and early school-age
children (ages 3–8 years) who demonstrate noncompliant behavior. It is provided to
144 14 Case Studies

families individually as a secondary prevention program. The parent and child are
generally seen together for 10 weekly sessions (60–90 min each) with a therapist.
Parents are instructed in skills aimed at disrupting the coercive cycle of parent–child
interaction, which include increasing positive feedback to the child for appropriate
behaviors, ignoring minor negative behaviors, giving children clear directions, and
providing praise or time-out following child compliance and noncompliance,
respectively. Parents learn skills through a variety of techniques designed to provide
them mastery and automaticity. These parent training techniques include modeling,
role-plays, and in vivo training in either the clinic or home and progress in skill
acquisition as each skill is mastered. To reinterpret the above into the framework,
we are suggesting, through instruction, the parents are taught to identify the mal-
adaptive responses which are targeted for extinction, while at the same time, adap-
tive behaviors are heavily reinforced to the point of automaticity. Such practice
takes place under instruction in the environment in which the disruptive behaviors
occur and in which the new behaviors are supposed to be performed.
It is important to note that diagnosing the set of the behaviors as an illness, or a
disorder, had little or nothing to do with the treatment for the child. Treatment was
based on an understanding about how the behaviors were learned and maintained
through a pattern of epigenetic interaction between genetic predispositions and
environmentally provided learning experiences. These learning experiences follow
a predictable and knowable set of rules that should be used to govern what happens
in treatment designed to create adaptive behavioral responses.
A word should be said here about the idea of disorder. The reader will note that
the term disordered was used in the previous discussion. Disordered behavior was
described as maladaptive behavior which produces less than desirable outcomes. It
is not clear whether having disordered behavior means that the individual has a
disorder. It is even less clear that individuals who manifest a uniquely individual-
ized set of disruptive behaviors have the same disorder as other behaviorally pheno-
typically similar individuals as is suggested by the current nosology. Each individual
experiences a unique set of environmental influences that create a highly individual-
ized learned pattern of respondency. The commonality that binds these things
together is the principle by which these maladaptive behaviors are learned and by
which the hope for adaptive behavior is acquired.

Grand Rounds

Your patient is a divorced, middle-aged woman who currently lives alone by choice.
She had been in therapy for years, since her early twenties, and while she reports
that she thinks the experience benefitted her, she remains somewhat mired in her
current emotional state which has persisted for some time. She came from an intact
family, but characterized her relationship with her mother as poor, and her mother
as emotionally distant. Starting when she was a young child and extending until
early adolescence, her mother became physically abusive. She reported that she was
Randy 145

never able to tell whether her mother was angry or not. When the mother left, your
client assumed the caretaking role for the family. Your client reported that she went
on to marry an abusive partner. She finally left him after the threat of physical vio-
lence escalated. Currently, she reports that she is fearful of being alone. She sleeps
with the lights on. She is barely able to get to social events, which will get her
involved in her new community. She describes most current events as “horrific” and
as a result does not watch TV or own a computer. She will not tell her family or
friends about her history because in her mind it reflects an abnormal family, which
in turn makes her abnormal. She perceives most men and women she meets as supe-
rior to her intellectually, socially, and in overall attractiveness. She describes a daily
aura of depression and derives little pleasure from interactions with others.

What Is Your Diagnosis of This Woman?

There are certainly lots to choose from. She fits the avoidant personality disorder
criteria. This personality disorder is characterized by a pervasive pattern of social
inhibition, feelings of inadequacy, and a hypersensitivity to negative evaluation. She
presents with low self-esteem, feelings of shame and inadequacy, detachment, and
negative affect. She is constantly afraid others will criticize her and perceives her-
self as inferior to them.
Or perhaps she fits post-traumatic stress disorder. She was exposed to direct
threats over years and has intrusive memories, low self-esteem, and intense anxiety.
She has persistent negative emotions of guilt and shame. She feels alienated and
detached. She has constricted affect, blames herself, and is often unable to experi-
ence positive emotions.
Or would we best diagnose a generalized anxiety disorder and comorbid depres-
sion or perhaps several of these things.
Based upon your diagnosis, how would you begin treatment? What are you
expecting the “process” to look like? What are your goals?
Some therapies might focus on the interaction between the mother and daughter
and its subsequent impact on your client’s personality development. Some therapies
might rely on what the patient brings to the forefront with each session. Some thera-
pies might focus on cognitive distortions.
Some of this is clearly necessary in order for the therapist to establish a relation-
ship, allow the therapist to gather background and historical information, and allow
the patient to be in a safe place to vent their feelings and concerns.
However, how therapy is delivered depends upon one’s conceptualization of the
case. Our model does not require a conceptualization of arrested development or a
battle between drives. It requires educating a person as to how they maintain their
emotions, beliefs, and behaviors which continue to influence their lives by under-
standing their own neurophysiology.
For example, remember that we are our experiences and that new experiences get
“matched” with our prior experiences. And so the danger becomes that allowing
your patient to engage in prolonged free style talking creates an additional “connec-
146 14 Case Studies

tion” between their history and their account, thus strengthening the development of
maladaptive schema that is often recruited when talking about families or relation-
ships. The response circuitry that contains this maladaptive response would be
engaged when cognitive processing around this topic occurs. This in turn strength-
ens the emotional arousal that results from this connection sequence. The connec-
tion sequence might go something like this; the patient recounts the multiple
episodes of being told to approach their parent and later their husband. They
approach and are “punished” for some wrongdoing. They internalize the message.
Now they are recounting those episodes further strengthening the connections
between their perceived fault and subsequent guilt, anxiety, and shame.
The current authors believe that in order for therapy to be successful, we want to
identify the maladaptive schema that contains all the deficient responses to similar
situations. We want to create a new and adaptive set of responses and have the client
practice these responses in therapy to the point of automaticity. We want to tamp
down the existing neuro-circuit sequence that recruits the maladaptive schema and
begin to replace it with a healthier one which includes adaptive responses and the
cognitions that go with them.
In this case, we would attack the faulty perceptions of guilt and responsibility
directly. We would explain how these messages were delivered to this patients
developing mind and how schemas were created which have become her “default”
settings. Whenever she experiences a similar situation, she automatically elicits her
overly rehearsed messages that this, whatever “this” is, is her fault. We would teach
her to challenge the automatic thoughts or schema, with the understanding that this
will impact and necessitate new learning of new connections.
Perhaps, rather than allowing the patient to continue to assume “responsibility”
for whatever happened, we might ask the patient to define the role of a parent.
Almost invariably, the response is that a parent is supposed to protect their children
and teach them so that they can be healthy adults. And therein begins the chip that
leads to a wedge between former connections and new engagements which create
healthy alterations in the (neuro-circuit) process. The changes will become apparent
in the patient’s emotional arousal levels, their cognitive explanations, and, ulti-
mately, in their behavior, allowing new sets of competencies and skills and how
readily they can access them.
Your patient might be describing herself as a weak person, afraid of everything.
We would be attacking that concept of herself as weak. We would be explaining to
that person how her neurophysiological defenses have gone awry. That is, fear as
emotional arousal can be lifesaving. If we encounter a bear while walking in the
woods, becoming fearful and alert is good. It prepares us to defend ourselves or
leave the situation (fight or flight). However, as a young person, she could not fight
nor get out. And her constant heightened fear led to a pattern resulting in a lifetime
of anxiety (hypersensitivity neurophysiologically) she can no longer easily turn off.
We would teach how to challenge the old schema with the intent of creating new
schema and hubs which can become competitive with the old neuro-circuitry, and as
more and more practice of the new schema takes place, the adaptive schema can
achieve greater automaticity.
References 147

This becomes observable in your patient as the frequency, intensity, and duration
of the old schema or maladaptive responses are replaced with new schema. The dem-
onstrations or reports of those new schemas would be highlighted and reinforced by
the therapist, thereby increasing the likelihood of them being recruited again as
needed. By challenging the old schemas, by reinforcing new connections, we increase
the likelihood of the recruitment of healthy responses, increase the automaticity of
the new and healthy responses, and help create a more resilient person.

References

Badynaev, A. (2005). Stress-induced variation in evolution: From behavioural plasticity to genetic


assimilation. Proceedings of the Royal Society B: Biological Sciences, 272, 877–886.
doi:10.1098/rspb.2004.3045.
Brestan, E., & Eyberg, S. (1998). Effective psychosocial treatments of conduct-disordered chil-
dren and adolescents: 29 years, 82 studies, and 5,272 kids. Journal of Clinical Child Psychology,
27(2), 180–189. doi:10.1207/s15374424jccp2702_5.
Eyberg, S., Nelson, M., & Boggs, S. (2008). Evidence-based psychosocial treatments for children
and adolescents with disruptive behavior. Journal of Clinical Child & Adolescent Psychology,
37(1), 215–237. doi:10.1080/15374410701820117.
Forehand, R., & McMahon, R. J. (1981). Helping the non complaint child: A clinician’s guide to
parent training. New York: Guilford Press.
Gunnar, M. (1992). Reactivity of the hypothalamic-pituitary-adrenocortical system to stressors in
normal infants and children. Pediatrics, 90(3), 491–497.
Kajantie, E., & Räikkönenc, K. (2010). Early life predictors of the physiological stress response
later in life. Neuroscience & Biobehavioral Reviews, 35(1), 23–32.
Kendall, P. (2006). Child and adolescent therapy: Cognitive behavioral procedures. New York:
Guilford Press.
Parsons, P. (1990). Fluctuating asymmetry: An epigenetic measure of stress. Biological Reviews,
65(2), 131–145.
Sword, R. (2012, November 22). Why reliving your trauma only goes so far. Retrieved
from Psychology Today: https://www.psychologytoday.com/blog/the-time-cure/201211/
why-reliving-your-trauma-only-goes-so-far
Zimbardo, P., Sword, R., & Sword, R. (2012). The time cure: Overcoming PTSD with the new
psychology of time perspective therapy. New York: Wiley.
Chapter 15
The Takeaway

“I have tried to show that the notion of mental illness has outlived whatever usefulness it
might have had and that it now functions merely as a convenient myth. As such, it is a true
heir to religious myths in general, and to the belief in witchcraft in particular; the role of
all these belief-systems was to act as social tranquilizers, thus encouraging the hope that
mastery of certain specific problems may be achieved by means of substitutive (symbolic-
magical) operations (Szasz, 1960, p. 117).” However;
Miracle Max: Whoo-hoo-hoo, look who knows so much. It just so happens that your
friend here is only MOSTLY dead. There’s a big difference between mostly dead and all
dead. Mostly dead is slightly alive. With all dead, well, with all dead there’s usually only
one thing you can do.
Inigo Montoya: What’s that?
Miracle Max: Go through his clothes and look for loose change. (The Princess Bride, 1987)

We wrote this book for several reasons. We hoped to demonstrate that both psychology
and neuroscience have progressed sufficiently that, working together, they can pro-
vide answers regarding both the etiology of and treatment for those issues that have
been labeled mental disorders. We have provided an introduction to a model that
offers the potential to do just that. We also wrote this book out of a concern that the
current state of affairs is no longer scientifically useful. We hoped to demonstrate that
a science based on a phenotype is a science built on sand. The current science around
mental disorders has developed in response to our past inability to understand the
etiology of the issues we were facing. In response to our attempt to understand by
classifying groups of symptoms or behaviors, we have developed phenotypical clus-
ters and attempted to understand each of these clusters as if they are a specific form of
medical disease. We have attempted to demonstrate that the imposition of a disease
model, over what is in many cases merely maladaptive behavior, has necessitated the
creation of a diagnostic system and treatment methodologies that demand a disease
interpretation. As we have seen, this logic is both circuitous and flawed.
There would be significant difficulties with the existing paradigm even if the
problems ended there, but they do not. What is more egregious is that, all but
ignoring our knowledge of how these phenotypical clusters were derived, we then

© Springer International Publishing Switzerland 2016 149


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1_15
150 15 The Takeaway

go on to take what are no more than behavioral constructs and clinically treat them
as diseases. We have researched them as single entity diseases and we speak about
them in the same manner. We talk about disease types and treatment for these types
of disease as if there isn’t significant confabulation in the description. We expect
cures because that’s what disease requires. Diseases have cures, and all that is nec-
essary is to apply the correct cure and the problem is resolved. All of this has led to
disastrous consequences for ongoing research and treatment.

Self-Deception

In order to accomplish this sleight of mind, we have to engage in a massive process


of self-deception. In order to understand how we accomplish this self-deception, we
must understand the system upon which is based. That system is the nosology used
to identify the various things that are classified as illnesses. For mental disorders
that system is now the ICD 10 which is remarkably similar to the American
Psychiatric Associations Diagnostic and Statistical Manual or DSM 5. While both
these systems have different codings, they both essentially discuss the same pheno-
typically derived disorders. The goal of the DSM 5, the new manual, as with all
previous editions, is to provide a common language for describing psychopathol-
ogy. Having a common language does have its benefits. It enables us to develop a
shorthand to discuss the issues that confront the science. While this is an admirable
goal, the problem is that clusters of co-occurring maladaptive behaviors (symp-
toms) were grouped together and provided with a label often obscuring the “symp-
toms” which differentiate the individual based upon which sub-straits are involved
or recruited. The result of this process is that things with similar occurring behaviors
are grouped together under the same label. This is much like grouping all food cre-
ations with dough on the bottom and cheese on the top as pizza. For a science this
creates significant problems. “While DSM has been described as a “Bible” for the
field, it is, at best, a dictionary, creating a set of labels and defining each. The
strength of each of the editions of DSM has been “reliability”—each edition has
ensured that clinicians use the same terms in the same ways. The weakness is its
lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or
AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symp-
toms, not any objective laboratory measure. In the rest of medicine, this would be
equivalent to creating diagnostic systems based on the nature of chest pain or the
quality of fever. Indeed, symptom-based diagnosis, once common in other areas of
medicine, has been largely replaced in most medical disciplines in the past half
century as we have understood that symptoms alone rarely indicate the best choice
of treatment” (Insel, 2013). The symptom-based disease descriptions have led to a
number of anomalies. One with crucial negative consequences for the field has been
the idea that certain mental disorders only emerge in adulthood. It is more likely that
these “late-emerging” disorders had developmental trajectories that, because of the
constraints imposed by the diagnostic system, were neither researched nor
Is There a Place for the Medical Model? 151

identified. It is past time to end the artificial distinction between disorders of


childhood and disorders emerging in adulthood. We should direct our research
toward understanding the developmental trajectories of all mental health issues and
acknowledge that some disorders may be developing long before they become clini-
cally identifiable (National Institute of Mental Health, 2015).
We believe that we have demonstrated that a large number of issues listed as
mental disorders in the currently used nosology are the results of the interaction
between the connectome, environment, and individual learning experiences. In
some instances the result of this learning is faulty implementation which has been
learned and then automatized. As we have attempted to show, there are clear small-
world hub models that account for this learning and do a wonderful job modeling
how the brain processes information. More importantly, these models point the way
to methodologies that can correct this maladaptive learning and replace them with
adaptive responses instead. The principles by which this change can be made were
outlined in this book.

Is There a Place for the Medical Model?

Much like Miracle Max, we have also come to understand that there is a place for
the medical model within a modern understanding for mental disorders. As we have
shown, there are some cognitive and emotional maladaptations that are caused by
disease process and could be addressed by interventions based on a disease model.
The cognitive decline of dementia, the cognitive and emotional limitations of
Alzheimer’s patients, and the emotional and faulty appraisal systems associated
with schizophrenia are all examples of disorders that involve the faulty regulation of
cognition and emotion that have clear biological/medical cause. Perhaps it is time
for these disorders to be looked at differently or classified as distinct from the
greater majority of disorders that reflect the effect of learning on an individual’s
unique connectome. Perhaps the medically caused group could be labeled as disor-
ders of mental illness, while the interactive learning/connectome models could be
labeled as disorders of mental health. That might be a good place to start.
The beauty of an evolving science is that it constantly redefines itself. Along the
way it develops apparently self-evident truths that are later discovered to be less than
obvious and less than true but never the less contain valuable insights which can be
integrated into an evolving increasingly reliable and accurate whole. In that vein we
believe the concept of mental health needs to be reevaluated and that Szasz while par-
tially right was also in fact partially wrong. Szasz was right to point out that most of
what we consider to be a reflection of illness is in fact a reflection of learning. He was
right to point out that medicalization of the idea of a learned maladaptive response,
which required the development of a phenotypical coding system, would lead us in the
wrong direction both as a science and as a service. We would add to that argument that
the medicalization of what are conditions of maladaptive learned responses has led to
unfortunate consequences including the clouding and confabulation of research into
etiologically recognizable disorders and effective treatments.
152 15 The Takeaway

Science has now developed to the point where we can recognize that there are
disorders that represent a connectome disrupted or broken by disease (Infectious
Disease and Mental Illness, 1997), injury (Schwarzbold et al., 2008), or pathogen
(Wenner, 2008) that can be truly considered an illness that requires medical attention.
We would rush to point out that the existing nosologies are not always helpful here
either in that they group phenotypically similar problems that might actually reflect
the interrelationship of experience and learning with these physical problems.
It would be fair game to ask which problems would represent illnesses and which
do not. Which problems would require medical intervention as a first-line interven-
tion in order to repair the dysfunction? We recognize that the field as a whole is still
quite confused regarding the division of learned behavior and physical abnormality
or disease. For example, take this statement from the National Alliance on Mental
Illness, “A mental illness is a medical condition that disrupts a person’s thinking,
feeling, mood, ability to relate to others and daily functioning. Just as diabetes is a
disorder of the pancreas, mental illnesses are medical conditions that often result in
a diminished capacity for coping with the ordinary demands of life” (National
Alliance on Mental Illness, 2014). Here the problem is easily seen in practice; dia-
betes is caused by pancreatic dysfunction. What is the cause of mental illness?
Current mental health models describe the results. Using the same system would be
like saying that if diabetes causes jaundice, then treat the jaundice and claim we
have treated the disorder.
It is clear that diabetes is a disorder of a dysfunctional pancreas, and it is just as clear
that in many instances, mental illness is not the result of a structurally dysfunctional
brain. The brain of an individual with a maladaptive learned response is not permanently
dysfunctional or broken. The connectome on which the learned behavior is based can be
modified through further learning to produce more adaptive responses. No conception
of illness is required to accomplish this modification, but a firm scientifically based
knowledge of how the brain learns and relearns is. Put simply, you don’t have to be ill
to behave maladaptively, and you don’t have to be cured in order to behave better.
We also wrote this book because we believe it is past time for the mental health field
to catch up with the rest of science and begin to explore the etiology of the various
issues we are attempting to address. It is only by truly understanding how the behaviors
and cognitions that comprise adaptive response to the environment are developed that
we can design effective interventions to correct the maladaptive response. We believe
that the emerging science in connectionist small-world hub modeling coupled with
what is clearly known about how the brain learns can, when integrated, offer an effec-
tive explanation for much of what is termed mental illness. We believe we have shown
one way that might be done in this book. We are certain that as we begin this process
of redefining maladaptive behavior, many of the phenotypically derived labels we have
come to rely upon and love will have to be discarded.
We believe that we have shown that for a large number of people who seek out
services, the medicalization of mental health is unnecessary and may be leading
research in the wrong direction. Research based on behaviorally similar phenotypes
will not lead us to an understanding of the etiology that leads individuals to engage in
maladaptive behavior. Current research clearly indicates that behavior is the result of
Dissolving the Dichotomy of Mind and Body 153

nature and nurture operating interdependently to produce an ever-evolving connec-


tome that subserves both learning and the expression of that learning which we call
behavior. Simple solutions that point to either behavior or genetics no longer suffice.
For example, research on violent behavior revealed that a monoamine oxidase A
(MAOA) low-activity genotype (contributing to low dopamine turnover rate) as well
as the CDH13 gene (coding for neuronal membrane adhesion protein) is associated
with extremely violent behavior (Tiihonen et al., 2014). The authors stress however
that most people with this genotype do not go on to commit violent crime. There are
environmental and behavioral patterns that serve to increase the probability that a per-
son will actually engage in violent behavior. Even when violent behavior is expressed
and the connectome established to produce the undesirable final behavior, relearning
appropriate behavior can alter the connectome and produce more adaptive behavior.
We have attempted to demonstrate that the basis for the advancement of both
research and treatment in the field of mental health should rely on a firm understand-
ing of how individuals learn adaptive and maladaptive behavior, and how that learning
interacts with the existing connectome of the individual doing the learning. We must
acknowledge that this connectome is based on a genetically determined core that
expands and develops through interaction with the environment. We have suggested
that the Research Domain Criteria (RDoC) which attempts to transform diagnosis by
incorporating genetics, imaging, cognitive science, and other levels of information to
lay the foundation for a new classification system represents one model. We are not
alone in identifying these targets as critical for our understanding of the etiology of
“mental health.” The National Institute of Health in its new strategic plan states “Over
the past 6 years, large, replicated genomic studies have revealed many common and
rare variants associated with the most heritable conditions (e.g., schizophrenia, bipo-
lar disorder, autism). We have gone from few clues to many. However, we still cannot
explain the root cause(s) of mental illnesses. The task now is to sort through the com-
plex patterns of genomic variation to define and elucidate how these variations confer
risk. This strategy should not only identify critical pathways and circuits but potential
new therapeutic targets. Nongenetic factors (e.g., environment, experience, the micro-
biome, to name just a few) have also been shown to increase the risk of mental ill-
nesses. How does the interplay of genetic and environmental factors influence the
development of mental illnesses? By understanding genomic, epigenomic, and other
nongenomic factors and their interplay, we can begin to explain how our brain gener-
ates adaptive and maladaptive behaviors—predicting, interpreting, and responding to
a complex world”(National Institute of Mental Health, 2015).

Dissolving the Dichotomy of Mind and Body

It is acknowledged that we do not have the information to develop either a working


model of a typical connectome or models of atypically developed connectomes at the
current time. We certainly do not yet have a comprehensive diagnostic model that
154 15 The Takeaway

relates to the basic science related to the connectome. An important reason for this is
in part, because the DSM model has homogenized and therefore distorted our
research on mental health for many years. Research must evolve away from the DSM
model of the science for it to proceed. Research must evolve toward a model that
recognizes that for the most part, problems of adaption reflect a complex interaction
of learning, genetics, cognition, and neuroscience. To do this the existing borders
between specialties must be dissolved and a new science of cognitive neuroscience,
psychologically developed learning theory, and genetics be developed to address the
challenges ahead. The persistence of the mind–body problem has allowed us to con-
tinue to develop separate fields for the treatment of mental health issues. It is time for
this to end. For those of us that inhabit the world of the mind and have been able to
ignore the interaction with the connectome, this might seem a formidable task. It is
Knowing that may imply structural changes in the way individuals are prepared to
engage in mental health practice. On the other hand, just because there are physio-
logical processes involved does not imply that the science of mental health belongs
to medicine. Neuropsychologists and experimental psychologists have long demon-
strated that well-trained scientists and practitioners in the psychological field can
work successfully with physiologically based constructs. Insel (2013), in discussing
the National Institutes of Health decision to direct research away from a symptom-
based understanding of psychopathology, stated that for the past half century, we
have understood that “symptoms alone rarely indicate the best choice of treatment.
Patients with mental disorders deserve better.” We agree.

Treatment Techniques Must Understand the Epigenetic


Nature of Mental Health

It is not enough to just understand the genesis of psychopathology and how the
human connectome functions to support it. We must design treatment techniques
that respond to the various etiological factors that contribute to the development and
maintenance of psychopathology. These treatment techniques must target either the
functionality of the connectome or the modification of the connectome. That means,
in our opinion, that there will continue to be a place for medical interventions
designed to improve the functionality of the existing connectome. Similarly, there
will continue to be a place for verbally based therapies designed to provide experi-
ences that would alter the pattern of white matter connectivity. As we have endeav-
ored to point out, these verbally based therapies, while being respectful of the
importance of the therapeutic relationship, must be altered to recognize that therapy
is essentially a process of learning adaptive behaviors and unlearning maladaptive
ones. We must teach therapists to conduct treatment in accordance with sound prin-
ciples of learning having specifically defined learning objectives.
It can of course be argued that people come to therapy for other reasons not
necessarily associated with helping them explain the genesis of poor behavior and
decisions. In some instances, they might be feeling bad and not know why. In these
Does Conceptualizing People as Being Mentally Ill Add Anything to the Treatment… 155

instances it is argued the goal of therapy is not behavior change, but understanding
and acceptance. While this argument appears unlikely, as the desire to understand
implies a desire to change, the argument still leads to an approach based on aware-
ness and learning. Research has demonstrated that individuals perform norm-
violating behaviors based on a nonconsciously activated goal elicit negative affect
(Oettingen, Grant, Smith, Skinner, & Gollwitzer, 2006). This research suggests
that when we do something we recognize that breaks a social or personal norm, and
we do not specifically identify a reason for doing so, we become sad. That is
because people regularly engage in a behavior or a thought automatically, and only
after it occurs and becomes significant do they seek an explanation for its occur-
rence. That explanation is often post hoc, and in many cases arbitrarily assigned
from readily available environmental stimuli. The reasons assigned as to causality
of the behavior do not necessarily relate to the actual cause. Additional research
suggests that when a positive explanation as to causation is assigned to the behav-
ior, the person responds by positively emoting (Parks-Stamm, Oettingen, &
Gollwitzer, 2010). Their research also indicated that applicable conscious goals are
indeed used to interpret nonconsciously activated goal striving and that this inter-
pretation occurs automatically rather than consciously. In summary, if we can help
a person make positive attributions concerning their behavior, it is likely that, even
if they recognize that they do not like the outcome, they will think positively about
their actions. If these attributions are made automatic, then the individuals’ mood
state should improve. This suggests that a positive, directed approach to learning
these adaptive attributions would produce the most success. The principles that
governed the learning of these attributions would be the same as those that gov-
erned all other learnings.

Does Conceptualizing People as Being Mentally Ill Add


Anything to the Treatment Process?

Ultimately, we believe that people come to treatment in order to change maladaptive


behaviors and cognitions, and the resulting feelings, and change in these behaviors
and thoughts must be the ultimate yardstick against which the efficacy is judged. We
believe that this change is best achieved through the use of techniques that are based
on clearly established principles of learning that will create changes in how infor-
mation is processed in the connectome. As we have said, patients deserve better
than what they have been receiving, and this is the way to give it to them. In the end,
the benefit of viewing individuals as mentally ill adds nothing to the treatment pros-
pects and as such should be discarded in the vast majority of the cases for which it
is now used.
All of this implies that many of the forms of treatment for mental disorders may
be ineffective and will have to be replaced by newer treatments that are based on
how the brain processes information. These treatments will have to be delivered by
practitioners who are knowledgeable about these processes. The inevitably will
156 15 The Takeaway

imply that some forms of treatment currently in vogue will fall by the wayside.
While it is clear that some will lament their passing, it is also clear that they will
represent the cost of an emerging science. As we have said, it is long past time.

References

Infectious Disease and Mental Illness. (1997). Retrieved from Mental Health and Illness: http://
www.mentalhealthandillness.com/infectiousdiseaseandmentalillness.html
Insel, T. (2013, April 29). Directors blog: Transforming diagnosis. Retrieved from National
Institute of Mental Health: http://www.nimh.nih.gov/about/director/2013/transforming-
diagnosis.shtml
National Alliance on Mental Illness. (2014). Mental illness. Retrieved from National Alliance on
Mental Illness: http://www.nami.org/Template.cfm?Section=By_Illness
National Institute of Mental Health. (2015, March). NIMH strategic plan for research. Retrieved
from National Institute of Mental Health: http://www.nimh.nih.gov/about/strategic-planning-
reports/index.shtml
Oettingen, G., Grant, H., Smith, P. K., Skinner, M., & Gollwitzer, P. M. (2006). Nonconscious goal pur-
suit: Acting in an explanatory vacuum. Journal of Experimental Social Psychology, 42, 668–675.
Parks-Stamm, E., Oettingen, G., & Gollwitzer, P. (2010). Making sense of one’s actions in an
explanatory vacuum: The interpretation of nonconscious goal striving. Journal of Experimental
Social Psychology, 46, 531–542.
Schwarzbold, M., Diaz, A., Martins, E., Rufino, A., Amante, L., Thais, M., . . . Walz, R. (2008).
Psychiatric disorders and traumatic brain injury. Neuropsychiatric Disease and Treatment, 4,
797–816.
Szasz, T. (1960). The myth of mental illness. American Psychologist, 15, 113–118.
The Princess Bride. (1987). The Princess Bride. Retrieved from IMBD: http://www.imdb.com/
character/ch0003789/quotes
Tiihonen, J., Rautiainen, M., Ollila, H., Repo-Tiihonen, E., Virkkunen, M., Palotie, A., . . . Paunio, T.
(2014). Genetic background of extreme violent behavior. Molecular Psychiatry, 28. doi:10.1038/
mp.2014.130, http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2014130a.html
Wenner, M. (2008). Infected with insanity: Could microbes cause mental illness? Scientific
Amercian, 8, 5.
Neurocognitive Learning Therapy:
Clinical Teaching Guide

Introduction

Depathologizing psychopathology can be a valuable addition to programs that train


mental health practitioners because it outlines the fundamental principles of how
clients learn in therapy, demonstrates how that learning is processed over the human
connectome, and provides a specific guideline for the course of treatment. While the
principles in the book appear to argue in favor of more directive approaches to treat-
ment, they are in fact applicable to all types of interventions. That is because all
learning is accomplished in the same manner regardless of the style in which the
information is imparted. In these times of empirically verified treatment, what
should concern the therapist is the speed in which the new information is learned
and incorporated into existing cognitive schema and available to generalize to novel
experiences.
The principles detailed in the book not only form the basis of an empirically veri-
fiable therapy but offer the possibility of serving as the basis of a reformulation of a
diagnostic nosology for disorders affecting mental health.
As we have pointed out in the book, if these principles are utilized in a specific
clinical paradigm, they then form the basis of an intervention we have termed
Neurocognitive Learning Therapy, a treatment that integrates cognitive behavior
therapy, learning theory, and the neurophysiological substrates of learning to
enhance delivery of effective interventions. Neurocognitive Learning Therapy
(NCLT) is a current, innovative form of treatment that is the first treatment para-
digm designed to utilize neuropsychologically based principles of learning as its
foundation.
Depathologizing psychopathology can be used either as the basis of a standalone
course in principles of psychotherapy or as part of a fundamentals of psychotherapy
course. This guide is designed to provide the reader with some suggestions as to

© Springer International Publishing Switzerland 2016 157


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1
158 Neurocognitive Learning Therapy: Clinical Teaching Guide

Table 1 Compliance with therapy learning principles in the general practice of major therapy
systems
Cognitive
Nondirective behavior Behavior Psychodynamic
Principle NCLT therapies therapies therapy therapies
The therapist must focus X X
on the client and how they
will incorporate and utilize
new knowledge
There is no knowledge X X X X
independent of the
meaning attributed to
experience and constructed
by the client
Learning in therapy is an X X X X
active process in which the
client (learner) gates
sensory input and
constructs meaning out of it
The construction of X X
meaning in therapy is a
purposeful activity
The crucial action of X
constructing meaning is
neurophysiologically based
and involves brain circuitry
dedicated to learning and
reinforcement recognition
The language we use X X
influences learning.
Language and learning are
inextricably intertwined
Learning in therapy is a X X X X
social activity involving an
analysis of our
relationships with other
important human beings in
our lives. To be useful,
knowledge acquired in
therapy must be applied
and practiced within the
context of both new and
existing relationships
Learning in therapy is X X X X
contextual. We learn in
relationship to what else
we already know and what
we already believe
(continued)
Therapy Reimagined 159

Table 1 (continued)
Cognitive
Nondirective behavior Behavior Psychodynamic
Principle NCLT therapies therapies therapy therapies
It is not possible to X X
assimilate new knowledge
without having some
structure developed from
previous knowledge upon
which to build
Learning new ideas and X X X X X
ways of behaving in
therapy is not
instantaneous
Motivation is a key X
component in learning. Not
only is it the case that
motivation helps learning; it
is also essential for learning
Maladaptive behavior and X X X
thought are based upon
automaticity
Learning is about X X
connections in that what is
stored together stays
together in memory

how that might be accomplished. This guide is divided into content area sections
that can be used for one or more lesson depending on the depth of instruction
required. Each section provides the description for a series of lectures.

Therapy Reimagined

Central Thesis

Historically, therapeutic intervention for mental health problems placed great


emphasis on the clearly established fact that the nature of the relationship between
the client and their therapist is an essential element to the therapeutic process. We
do not seek to take issue with the value of the therapeutic relationship. We do seek
to point out that what occurs in the context of this relationship is governed by the
same laws of learning as in any other interaction between an individual and their
environment. We believe that in the therapeutic relationship as it exists, it is the role
of the therapist to choose which ideas and behaviors are, or are not, reinforced. All
learning is learning, and learning is governed by the same principles whether it is
learning how to drive an automobile, learning about the history of our country, or
learning about ourselves.
160 Neurocognitive Learning Therapy: Clinical Teaching Guide

Regardless of the type of therapeutic relationship one prefers, all learning occurs
over brain networks that are recruited for specific tasks, but the connective proper-
ties of these networks are always the same. Learning about ourselves in therapy is
no different than any other kind of learning in this regard. It is a synthesis of our
neurophysiologically based learning networks and the environment in which it
operates.

Classroom Discussion

Review and discuss the implications of Chap. 1. Discuss the different types of things
that are learned in therapy and demonstrate that these things are learned by the same
brain-based learning system.

Questions

What is the mind–body problem and how does it relate to modern therapeutic
practice?
How has the continuation of the mind–body problem created problems for therapy
practice?
What is the role of relationship in modern therapy practice?
Is a therapeutic relationship the sole precondition for success of treatment?

Modern Conceptions of Mental Pathology

Central Thesis

What do we mean when we talk about mental illness? Increasingly everyday prob-
lems that cause stress are being made into medical disorders which then require a
form of medical intervention to resolve. In our current paradigm, medical knowl-
edge and perspective are applied to human conditions and problems which become
increasingly defined and treated as medical conditions and thus become the subject
of medical study, diagnosis, prevention, or treatment. Is this desirable or even scien-
tifically accurate?

Classroom Discussion

What do we mean when we say that a problematic mental condition, such as adoles-
cent antisocial behavior, a child’s defiant behavior toward a parent, intense sadness,
intense worry, intense shyness, failure to learn to read, or heavy use of illicit drugs,
Classroom Discussion 161

is not merely a form of normal, albeit undesirable and painful, human functioning,
but indicative of psychiatric disorder? Read and discuss the implications of Chap. 2.

Questions

Is it necessary to conceptualize all negative issues of everyday life as reflective of an


illness in order to devise effective treatment approaches?
What is the concept of medicalization and how does it relate to the modern-day
conceptions of mental health/mental illness?
Why is the number of mental illness diagnoses growing?
Is the medical model the best model to use when talking about what causes mental
illness?
Is there another model that might be useful in conceptualizing the etiology of men-
tal illness?

How We Learn: Connectionism and Constructivism

Central Thesis

Learning is about creating new connections between bodies and elements of knowl-
edge. One vector for this learning is the connection between new information and
existing information, but that is not the only one. Another vector is the connections
created between elements or bodies of existing knowledge. This is the basis of
creativity, looking at things from new and differing perspectives. Still another vec-
tor is looking at existing information and creating inferential constructs.
Connectionist theory provides the basis for understanding how the human connec-
tome learns and retains information. Connectionist theory is not sufficient for
understanding how humans categorize and classify information. In addition to
focusing on expanding connections between elements of knowledge, therapy should
also concern itself with identifying and/or establishing key learning concepts or
schemata that form the basis for future learning. Constructionist theory is required
to do that.

Classroom Discussion

Discuss the relative contributions of constructivism and connectionism to the devel-


opment of an integrated model of how people learn in therapy. Discuss the follow-
ing constructivist learning principles and their implications for treatment:
1. Learning in therapy is an active process in which the client (learner) gates sen-
sory input and constructs meaning out of it. It is not a passive acceptance of
162 Neurocognitive Learning Therapy: Clinical Teaching Guide

knowledge which exists, but involves the learner (client) actively engaging with
the material in a purposeful way.
2. Clients learn to learn as they learn: they construct systematically more advanced
and complex schema. Learning in therapy consists both of constructing mean-
ing and constructing systems of meaning. Because human learning consists of
pattern matching, each meaning we construct makes us better able to give
meaning to other sensations which can fit a similar pattern.
3. The crucial action of constructing meaning is neurophysiologically based and
involves brain circuitry dedicated to learning and reinforcement recognition.
4. The language we use influences learning. Language and learning are inextrica-
bly intertwined.
5. Learning in therapy is a social activity involving an analysis of our relationships
with other important human beings in our lives. To be useful, knowledge
acquired in therapy must be applied and practiced within the context of our new
and existing relationships.
6. Learning in therapy is contextual. We learn in relationship to what else we
already know and what we already believe. In therapy we cannot append adap-
tive knowledge to a set of maladaptive preexisting knowledge. New skill sets
must be developed and practiced.
7. It is not possible to assimilate new knowledge without having some structure
developed from previous knowledge upon which to build. The more we
know, the more we can learn. Therefore, any effort to teach must be con-
nected to the state of the client and must provide an unambiguous path into
the subject for the learner that emanates from the learner’s (client’s) previous
knowledge.
8. Learning is not instantaneous. Significant learning requires the revisiting of
ideas in many contrasts and situations. Clients must recognize old ideas as mal-
adaptive and actively seek to replace them with new ideas based upon a founda-
tion of new learning and successful application.
9. Motivation is a key component in learning. Not only is it the case that motiva-
tion helps learning, it is essential for learning. The reward recognition circuit is
the essential gating in selecting knowledge to be learned.
10. Maladaptive behavior and thought are based upon automaticity. The adaption
of new schema implies that the old schemas are no longer automatically
selected. This at first is a conscious and planned process of selection.

Questions

1. What are the fundamental principles of connectionism?


2. What are the fundamental principles on constructionism?
3. How does connectionism and constructivism inform therapy process?
A Learning Model for Therapy 163

A Learning Model for Therapy

Central Thesis

The three basic principles of learning and their implications for therapeutic
learning:
1. Learning is a product of working memory allocation.
2. Working memory’s capacity for allocation is affected by prior knowledge.
3. Working memory allocation is directed by motivation.
Additional principles of learning are based upon the neurobiology of learning
and are incorporated into the therapeutic interaction for a vertical brain model.
These are as follows:
1. New learning requires attention. Only those items that are being attended to will
be candidates for working memory store.
2. Learning requires repetition. Learning is a pattern recognition. Those patterns
that are recognized and routinely retrieved from store are utilized and general-
ized. We would add that those patterns are associated by repetition and reinforce-
ment to the arousal centers located in the limbic system. Any new learning is
attached to existing schemas, and each set of these existing schemas (represented
neuroanatomically and neurophysiologically as small-world hubs) has a motiva-
tional and emotional response associated with it.
3. Learning is about connections, in that what is stored together stays together in
memory. Appropriate or socially acceptable responses can be stored with socially
unacceptable responses should that association be reinforced. Given the right set
of motivational circumstances, inappropriate responses can be stored.
4. Some learning is effortless and some requires effort. The goal of learning is
automaticity. That is, the goal of learning is to have some complex connections
between elements of data available to the learner without effort. People will
automatically associate and continue to associate emotional states with events
without cognitive effort to change those associations. The goal of therapy is to
make new, essential connections as efficient and automatic as possible.
5. Learning is learning. While all neurons learn in exactly the same way, people
utilize these processes idiosyncratically. Motivation is particular to the
individual.
Basic knowledge related processes that govern the process of therapy.
1. If knowledge in long-term memory is retrieved, the strength of association
between these items in working memory is increased. How things are presented
and grouped in working memory determine what procedures will be developed.
2. If a knowledge chunk is retrieved, all other chunks to which it is connected are
retrieved, and all connections between these retrieved chunks are strengthened
(small-world hubs).
164 Neurocognitive Learning Therapy: Clinical Teaching Guide

3. If parts of retrieved knowledge match to working memory contents, they are


strengthened. If parts of retrieved knowledge do not match to contents in work-
ing memory, they are weakened and inhibited. Therefore, establishing new pat-
tern matches (schemata) is an essential component in therapy.
4. Episodic learning is easy. Semantic knowledge is difficult.
5. If an action is successful, its connection to the knowledge of the situation in
which it occurred is strengthened. If an action is unsuccessful, its connection to
the knowledge of the situation in which it occurred is weakened or inhibited.
New procedures must be understood and conscientiously practiced.
6. If knowledge has been retrieved, new information in working memory will be
connected to this knowledge. This is the basis of establishing new adaptive
procedures.
7. Any active knowledge in long-term memory is accessible to working memory.

Classroom Discussion

Discuss how these principles can be used in therapy by giving case examples. For
example, talk about the role of action potentials in the assignment of attention and
how that relates to a diagnosis of attention deficit hyperactivity disorder. Give
examples of phobias that might be caused by emotional and physiological
responses being paired with unusual stimuli. Read and discuss the implications of
Chap. 4.

Questions

What is the Unified Learning Model and how does it inform therapy process?
What is epigenetics?
What is the future role of epigenetics in the treatment of mental illness?
What will be the role in therapy in a model that is based on epigenetics?
What does the term competence mean in the context of therapy?

The Effect of Learning on the Connectome


(For Those Instructors That Include a Discussion
of the Neurophysiology of Learning)

Central Thesis

The connectome is a term used to describe a comprehensive map of the neural white
matter connections in the brain. It is the result of a complex developmental trajec-
tory. Aberrations in the development of any of the networks that comprise the
Classroom Discussion 165

connectome contribute to psychopathology. Research has shown a high level of


functional connectivity within resting-state networks of the brain, which suggests
the existence of direct neuroanatomical connections between these functionally
linked brain regions that subserve ongoing interregional neuronal communication.
Research has shown that clearly identifiable white matter tracts interconnect at least
eight of the nine commonly found resting-state networks. Humans are born with
these networks in rather fundamental form and they are developed through a process
of interaction with the environment. It is these networks that are recruited as needed
when we are asked to perform a specific task.
Complex cognitive functioning is best represented by a connectionist small-
world hub model of neural networks. Small-world neural network models are based
on the concept of nodes which represent the confluence or connectivity points of
neurons. Research has demonstrated that brain networks have characteristically
small-world properties of dense or clustered local connectivity (nodes) with rela-
tively few long-range connections to other similarly dense nodes.

Classroom Discussion

Read Chap. 5 and discuss how the human brain is organized to process information.
Also discuss how what we learn impacts the development of the brain and the impli-
cations for the development of maladaptive behavior.

Questions

What is the connectome?


What does the book hypothesize about the relationship of the connectome to mental
illness?
How does knowing about the connectome change your conceptualization of the
etiology of attention deficit hyperactivity disorder? How does it affect your con-
ceptualization of depression?
What is a small-world hub?
What does the book hypothesize in the relationship of the concept of a small-world
hub and schemas?
What is a neural network?
What is the relationship of neural networks to learning?
How does learning affect the organization of neural networks?
According to the book, how is learning, the connectome, and mental health
related?
166 Neurocognitive Learning Therapy: Clinical Teaching Guide

The Role of Emotion in Learning

Central Thesis

There are potentially hundreds of emotional response types being grouped under the
term emotion. Research indicates that there are differing neural networks (defined
as recruited elements) in play for differing emotional states. Limbic circuits are
responsible for regulating stress responses that intersect with circuits that are
responsible for memory and reward, providing a means to demonstrate learning of
the stress response with respect to prior experience and anticipated outcomes. This
implies that the underlying physiology of classes of stress-related states is the same
but that experience and reward value determine the label we put on these reactions.
There is neural network capacity devoted to, in response to a stimulus, generating
certain physiological responses, “feeling states,” which are then cognitively
appraised with an environmentally contextual label. This forms the basis of emo-
tional responsivity.
One key goal in therapy is the downregulation of emotional states. In general we
want people to become calmer and better focused and to be able to handle perceived
threats in a more mindful manner.

Classroom Discussion

Read Chap. 6. What is the definition of emotion in the context of therapy? Review
appraisal theory and discuss its implications for therapy. Describe how the human
connectome regulates emotional states.

Questions

When we talk about emotion, exactly what do we mean?


Have the number of human emotions been clearly established?
What is the relationship of emotional regulation to the concept of mental health?
What are the roles of distraction in emotional regulation?
What is the role of upregulated and downregulated emotional responses to mental
health?
What are perceived threat and reward valuation and how are these concepts related
to mental health?
What do we mean when we talk about hijacked attention?
What strategies are identified that help a person regulate their emotional states and
how do they relate to known systems of therapy?
Classroom Discussion 167

Biologically Based Disorders of Mental Illness

Central Thesis

There are disorders of mental health that have as their basis purely biological-/
genetic-based dysfunction. There is emerging evidence that there are disorders of
mental health that have at least a very strong biological/genetic contribution to their
etiology. In particular, disorders such as schizophrenia, bipolar disorder, and autism
fit a biological model very well. That is, there are disorders of mental health that are
based on brain-based dysfunction that an individual is born with and then manifest
themselves either at birth or soon after (e.g., autism) or at a point later in an indi-
vidual’s development (e.g., manic depressive disorder, psychosis).
There are also models that posit that a damaged connectome is the etiological
foundation of most mental illness. Major depressive disorder and autism are exam-
ples of diseases whose etiology is credited to a damaged connectome. The study of
human brain networks with in vivo neuroimaging techniques coupled with advances
in both network science and graph theory has given rise to the field of connec-
tomics. Connectomics focuses on how whole-brain computational models can help
generate and predict the dynamical interactions and consequences of brain
networks.
Both biological and preexisting damaged connectome models argue that for all
disorders, the outcome was inevitable. The patterns of connections are fixed and
immutable and unerringly lead to a specific mental disease. In short, everybody that
has a particular pattern of connectivity at birth, or that everyone with a particular
pattern of genome, goes on to develop a particular mental disorder. Secondly, it
argues that environmentally based learned experiences would have no effect on the
outcome. The eventual architecture of the developed connectome would then be
predictable from the outset.
Even in the disorders with a clear genetic basis, there is evidence of the interac-
tion of neural architecture with environmental experience. In addition, fixed damage
models, biological or connectomic, fail at the current time because not all individu-
als who have the neurophysiologic architecture do not go on to display the maladap-
tive behavior associated with the disorder. Through its emphasis on epigenetics,
NCLT accounts for the fact that people with similar neuro-architecture have differ-
ing emotional response sets.

Classroom Discussion

Read Chap. 7 and have the class discuss the role of genetics in the development of
emotional disorders. Discuss the implications of epigenetics on the future of mental
health. Discuss how a life course model of mental health might be useful for under-
standing how to development treatment methodology.
168 Neurocognitive Learning Therapy: Clinical Teaching Guide

Questions

What are damaged connectome models? How are these models used to explain
disorders of mental health?
Describe the serotonin hypothesis of depression and how it relates to models of the
development of mental illness?
While at the current time it appears that there might be groups of disorders that do
not have a clear genetic predisposition, is this state of affairs temporary?
Will the genetic contribution of all issues identified as problems of mental health be
identified in the fullness of time?
For the disorders with clear generic contribution, what is the role of environmen-
tally based learning on the expression of the disorder?
If the outcome of development is not predetermined, what experiences would
encourage healthy development and which would not?

Automaticity and Unconsciousness

Central Thesis

The purpose of this automaticity is to free the individual of the need to expend
executive management resources in the performance of a particular task. This is
necessary because working memory and executive resources are limited, and this
process of automatization frees the cognitive resources of an individual for process-
ing novel tasks. As a result of practice and experience, we engage in many behaviors
and feel many emotions without actively thinking about them. Automaticity then is
the basis of what was considered the unconscious. Automaticity preserves our
resources for more important and emergent tasks. An understanding of automaticity
is therefore essential for both understanding the development of what is termed
mental dysfunction and the system of intervention required to address it.
Automaticity is not necessarily limited to observable behaviors. It also refers to the
learning of cognitive processing routines which require attention, focus, and work-
ing memory. Both positive and negative maladaptive behavior and emotional states
can become automatic as well. It all depends on what is learned and processed as a
result of the individuals’ interaction with the environment. Research demonstrates
that the regulation of emotions is in many aspects highly automatized.
Much of what is currently defined as constituting mental disorders reflects (a) the
development of maladaptive behaviors which have become automatic and (b) the
inappropriate application of these habitual or automatic behaviors onto novel situa-
tions. This creates a cycle in which there is strengthening of the automaticity of the
habitualized behaviors, which in turn results in outcomes which cause emotional
and mental distress because of misapplication.
Mental Illness 169

Classroom Discussion

Discuss the implication of automaticity to the therapeutic process. How does the
concept of automaticity align with classic therapeutic concepts of the unconscious?
Read Chap. 8 and discuss how to use the concept of automaticity in the therapeutic
process. For example, discuss the automatic components of anxiety responses or
how automaticity impacts your responses when you become angry.

Questions

What is the role of identifying environmental triggers for automatic behaviors in the
process of therapy?
What is the role of automaticity in the development of models of mental illness?
How are the constructs of automaticity and unconscious related?
Are automatized thought and cognitive routines available for therapeutic work?
How does understanding that most emotional responses highly automatized inform
therapy work?

Mental Illness

Central Thesis

There is increasing recognition that a significant amount of what we call mental ill-
ness is related to structural and functional changes in white matter. Research has
demonstrated structural changes in white matter after learning complex tasks and
that white matter responds to experience in a manner that affects neuron function
under normal circumstances, thereby affecting information processing and perfor-
mance. White matter-based cerebellar dysfunction has been identified in several
developmental disorders, including autism, attention deficit hyperactivity disorder
(ADHD), and developmental dyslexia. Damage to the cerebellum early in develop-
ment has long-term effects, through learning-based interaction with the environ-
ment on movement, cognition, and affective regulation.
Central to any conception of vertical brain/small-world hub-based learning as the
etiology of some mental dysfunction would be the demonstration of normally
occurring white matter changes associated with learning. There is significant litera-
ture demonstrating that such changes regularly take place.
There are changes in white matter function and structure that normally occur in
response to learning, whether that learning leads to adaptive behavior or maladaptive
behavior. It implies that the neural pathways that subserve learning are not static, but
are constantly altering in response to new learning. It also implies that neural con-
nectivity that is reflective of maladaptive learning can be reoriented in response to
learning that leads to adaptive behavior. In the preponderance of problems termed as
170 Neurocognitive Learning Therapy: Clinical Teaching Guide

a mental illness, the current constellation of brain structure is essentially a state


rather than a trait. For most people there is no such thing as a permanently miswired
brain, or a brain that is being impacted by some toxic event or invasive pathogen.
Although undoubtedly these conditions do exist, the vast majority of the problems
termed mental illness are really nothing more than issues associated with learning
maladaptive responses for which the “cure” is to learn adaptive ones.

Classroom Discussion

Read Chap. 9 and review the current models of mental illness. Discuss their strengths
and weaknesses. Discuss how changes in small-world hub architecture could lead to
maladaptive behavior classified as reflective of mental illness.

Questions

What are the weaknesses of the serotonin hypothesis of mental illness?


How do white matter changes reflect learning?
How does the process of diagnosis impact the conceptualization of mental illness?
What is the relationship of learned behavior to the development of mental illness?
What role does learned behavior play in the behaviors of a person diagnosed with a
mental illness?
As it exists today, is it required to have a conceptualization of how this particular
illness is caused, related to brain architecture, or developed in order to treat it?
Does a positive response to a medication imply that the cause of the disorder being
treated was caused by a problem corrected by that medication?
Are changes in white matter structure or function related to changes in mental
health?
What changes in white matter have been associated with attention deficit disorder?
Obsessive–compulsive disorder?
Do maladaptive behaviors constitute a mental illness? State your opinion and justify
it from the information provided in the book.
What are research domain criteria and how do they relate the therapy?

Therapy

Central Thesis

Research demonstrates that behaviors and experience interact with physiological, cog-
nitive, and emotional predispositions to produce current behavior and that current
behavior reflects the accumulation of all of these interactive events. Adaptive and mal-
adaptive behaviors have been practiced to the point of automaticity. That means that
All Forms of Therapy Have Learning Objectives 171

these routines, no matter how seemingly complex to the casual observer, can be
performed effortlessly by the individual. They do not tax cognitive resources.
Changing them requires cognitive effort. The new routines may be painful and diffi-
cult to learn even though they might be better in the long run. In order for these new
routines to be successfully incorporated into our everyday behavioral repertoire, they
have to be tried and practiced to the point you select them automatically. In other
words, you have to do as much work and apply as much effort to learning the new
routines as you did when you acquired the old routines. This is difficult and in many
cases frustrating. This is the work of therapy. At its core, therapy can be considered a
process of increasing the likelihood of the expression of adaptive behaviors and
thought processes and weakening or unlearning maladaptive ones. The goal of therapy
is effecting action selection to produce adaptive emotional and behavior outcomes.

Classroom Discussion

Read Chap. 10. Discuss the work of therapy. Discuss the role of insight in therapy
and whether insight alone is sufficient for a client to profit from therapy.
Discuss the important role of action selection in the process of selection of
behavioral response and in the process of therapy. Give examples or have students
generate examples.

Questions

What is the role of the concept of competence in the process of therapy?


Is the concept of central themes important in therapy?
What is the primary job of the therapist?
What is the essential task of therapy?
How does Neurocognitive Learning Therapy use a client’s history of depression in
the treatment of their current depression?
What is action selection and how does it relate to the choices that we make?
What is the role of the basal ganglia in the development of behaviors associated
with mental illness?

All Forms of Therapy Have Learning Objectives

Central Thesis

All therapeutic systems have a set of goals and objectives that entail beliefs and
behaviors that so-called “healthy” people would hold. These beliefs and behaviors
are therefore legitimate learning objectives and therefore subject to the same prin-
ciples of learning as in all other information acquisition.
172 Neurocognitive Learning Therapy: Clinical Teaching Guide

Classroom Discussion

Discuss how educational learning objectives, classic therapy learning objectives,


and learning theory all interact and are relevant to the process of therapy. Discuss
how Thorndike’s principles of learning impact the process of therapy.

Questions

What is the principle of exercise?


What is the principle of readiness?
What is the principle of effect?
What role do these and other principles have in the process of therapy?
Can the principles of learning used in education inform the work of a therapist?

New Principles of Therapy

Central Thesis

There are learning principles that are fundamental to the process of therapy.
These are:
1. The therapist must focus on the client and how they will incorporate and utilize
new knowledge.
2. There is no knowledge independent of the meaning attributed to experience and
constructed by the client.
3. Learning in therapy is an active process in which the client (learner) gates sen-
sory input and constructs meaning out of it.
4. The construction of meaning in therapy is a purposeful activity.
5. Human learning consists of pattern matching. Each meaning we construct
makes us better able to give meaning to other stimuli which can match with a
previously identified and categorized similar pattern.
6. The crucial action of constructing meaning is neurophysiologically based and
involves brain circuitry dedicated to learning and reinforcement recognition.
7. The language we use influences learning. Language and learning are inextrica-
bly intertwined.
8. Learning in therapy is a social activity involving an analysis of our relationships
with other important human beings in our lives. To be useful, knowledge
acquired in therapy must be applied and practiced within the context of both
new and existing relationships.
9. Learning in therapy is contextual. We learn in relationship to what else we
already know and what we already believe.
Classroom Discussion 173

10. It is not possible to assimilate new knowledge without having some structure
developed from previous knowledge upon which to build.
11. Learning new ideas and ways of behaving in therapy is not instantaneous.
12. Motivation is a key component in learning. Not only is it the case that motiva-
tion helps learning; it is also essential for learning.
13. Maladaptive behavior and thought are based upon automaticity.
14. Learning is about connections in that what is stored together stays together in
memory.
Both gating and reward recognition are important constructs to the process of
therapy. Clients will attend to what is interesting, rewarding, and understandable in
terms of prior knowledge. In order to be learned, new information must first be
attended to, and in this regard, all information is not equal. The new information is
essentially competing with prior learned and reinforced behavior. When new infor-
mation is offered within the context of the therapeutic relationship, it is clearly not
sufficient to assume that it will be associated with reward just because it is being
offered therapeutically. The therapist cannot be sure what information or portion of
the information is being attended to, how that information is being processed, and
how it is being used to alter existing knowledge. This implies that the reinforcement
and encouragement that occur during the course of therapy must be directly tied to
the stimuli the therapist desires to highlight and hopefully change. The more directed
and purposeful the information exchange, the surer the therapist can be that the
information is being used in the manner intended and for the learning outcome
specified.

Classroom Discussion

Discuss the role of gating and reward recognition in the process of therapy. Discuss
directive and nondirective forms of treatment and how they differ with respect to
action selection, reward recognition, and gating. What is Neurocognitive Learning
Therapy and how does it incorporate all of the above principles?

Questions

How can a therapist be certain that the information proffered during therapy is put
to the use it is intended?
What information should the client learn through the therapeutic exchange?
What skills should the client learn through therapy? What tasks, skills, or competen-
cies should the client be able to demonstrate?
What cognitive, processing, or emotional changes should the client be able to dem-
onstrate as a result of therapy? How should the client’s thinking have changed?
Describe the role of reward recognition and gating in therapy.
174 Neurocognitive Learning Therapy: Clinical Teaching Guide

What is the value of specificity to the therapeutic process?


What is the definition of motivation used in the book?
Describe the neural circuits involved with motivation and how they are important in
therapy.
How is, from a neurophysiological and learning theory perspective, motivation
related to the therapeutic process?
What is Neurocognitive Learning Therapy?
Describe how a neurocognitive therapist would treat the following:
Attention deficit disorder
Depression
Obsessive–compulsive disorder
Schizophrenia

Tell Me How You Feel

Central Thesis

Validating a client’s emotional state is important to the therapeutic process because


it is designed to ensure that the client feels both heard and understood. This same
process of validation can be both dangerous and destructive as it runs the chance of
reinforcing the very maladaptive behaviors that are targeted for change.
From a NCLT (Neurocognitive Learning Therapy) perspective, the therapist is
asking for the cognitions or thoughts and feeling that are associated with a particular
issue to determine the neuro-architecture (connections) associated with the particu-
lar schema being discussed. The therapist is really trying to establish all of the
associated thoughts and feelings so that you have a clearer picture concerning the
modifications to be made. It is the learned pattern of associations we are trying to
impact.
NCLT asserts that, because of the small-world hub organization of neural net-
works, these associated thoughts and feelings are not discrete issues; they are all
interrelated. Determining which thought or feeling is primary is not important.
Primacy is not a valuable construct in this regard. They are all primary because they
are all in one network, and the entirety of that network is accessed every time a
thought is evoked about any part of it. NCLT strategically helps the client to recog-
nize and identify all of these issues, understand that they are all interconnected, and
work to change the interactions between them.
To accomplish this NCLT therapist, use many different techniques depending on
the research-supported effectiveness of that technique on the behavior, thought, or
emotion being targeted. This is different than eclecticism in that NCLT has a very
definite understanding about the nature and etiology of mental disorder. Eclecticism
does not.
Case Examples 175

Classroom Discussion

Discuss the reason why we collect a history from a client. The difference between
traditional reasons for collecting information and the reasons that an NCLT thera-
pist would collect the same information. NCLT therapists collect information to
identify patterns of interconnection, thereby pinpointing triggers for how the infor-
mation is stored in long-term memory.

Questions

How does the model described in the book impact the concept of dual diagnosis?
Does having two diagnoses imply that you have two different diseases?
Should clients be informed about the process of therapy?

Case Examples

Read Chap. 14 and discuss the implications of the treatment model described.
Discuss the vital role of parents in the treatment of children. Discuss and critique the
cases presented. Discuss how an NCLT therapist would address specific clinical
issues of interest to the class. Discuss the strengths and weaknesses of the concept
of dual diagnosis.
Index

A target selection strategies, 139


Adaptive and maladaptive behaviors, 169, 170 therapeutic approaches, 140
Adaptive Control of Thought (ACT) and therapy, 72, 73
principle, 75 treatment, 145
Adolescent antisocial behavior, 160 Automaticity and unconsciousness
Alzheimer’s disease, 61 central thesis, 168
Appraisal theory, 47 classroom discussion, 169
Attention deficit hyperactivity disorder questions, 169
(ADHD), 8, 86, 136, 164, 169
Automaticity, 28–29
adaptive responses, 140 B
definitions, 69 Bifurcation of reality, 14
depression, 145 Biology
disordered behavior, 144 depression, 59
disruptive behaviors, 144 learning-based model, 59
emotional arousal, 138 Blended connectionist model, 23
environmental variation, 138 Brain-derived neurotrophic factor
executive management resources, 70 (BDNF), 60
in learning theory, 73
instrumental learning, 70
learning principles, 139 C
maladaptive behavior and thoughts, Common disease/common variant (CDCV), 63
123–124 Competence, 26
maladaptive behaviors and emotions, Connectionism and constructivism
71–72 central thesis, 161–162
and mental health, 72 classroom discussion, 161–162
mental health issue, 74–75 questions, 162
observable behaviors, 71 Connectionist models, 19–20
operant/instrumental conditioning Connectionist theory, 161
models, 70 Connectome, 164–165
personality disorder, 145 description, 33
post-traumatic stress disorder, 145 effect of learning
procedural/implicit system, 70 central thesis, 164–165
sensory integration, 139 classroom discussion, 165
social knowledge structures, 71 questions, 165

© Springer International Publishing Switzerland 2016 177


T. Wasserman, L.D. Wasserman, Depathologizing Psychopathology,
DOI 10.1007/978-3-319-30910-1
178 Index

Connectome (cont.) G
higher-order cognition and information Genetic predisposition, 11
analysis, 34 Grief Therapy
interregional neuronal communication, 35 post-traumatic stress disorder, 141
and psychopathology, 34, 35 psychopharmacology, 141
resting-state networks, 35 stress tolerance, 142
white matter tracts, 34
Connectome models, 58
Constructivism, 16–18 H
Constructivist models of learning, Hierarchies, 30
18, 103 Hijacking attention, 52
Critical thinking, 30, 31 Historical connectionism, 19
Huntington’s disease, 61

D
Declarative knowledge, 28 I
Depathologizing psychopathology, 157 Idiosyncratic stress tolerance, 143
Diagnostic and Statistical Manual Information exchange, 103–106
of Mental Disorders (DSM 5), Integrated brain circuitry, 37, 38
80, 83 International Classification of Diseases (ICD),
Dialectical behavior therapy, 132 9, 80–81
Dorsal attention network (DAN), 51 Intrinsic connectivity networks (ICNs), 58
Downregulating emotion, 50
DSM nosology (DSM 5), 8
K
Knowledge, 26
E
Emotion
adaptive behavior, 48 L
agreement, 45 Learning
antecedent-focused strategy, 48 analyses and classifications, 15
appraisal theory, 47 behaviors, 15
cognitive labels, 47 components, 16
cognitive threat assessment, 47 emotional engagement, 14
consensual conceptualization, 46 landscape, 15–16
emotion-generative process, 48 neural networks, 15
human–product interactions, 45 stimulation and processing data, 15
neural networks, 46–47 Learning and emotion
operationalization, 46 central thesis, 166
reappraisal, 48 classroom discussion, 166
regulation strategies, 48 questions, 166
strategies, 52–53 Learning Principles Associated with
suppression, 48 Education, 103
Emotion and learning Learning theory, 105, 120
central thesis, 166 Learning-based neurobiology, 87
classroom discussion, 166 Limbic circuits, 166
questions, 166
Epigenetic models, 63–64
Episodic memory, 27 M
Major depressive disorder (MDD), 61
Medial prefrontal cortex (mPFC), 52
F Medical model
Fixed models, 58–59 cognitive and emotional maladaptations, 151
Freudian model, 67 connectome, 152
Index 179

emotional and faulty appraisal Mental pathology, modern conceptions


systems, 151 central thesis, 160
medicalization, 151 classroom discussion, 160–161
Medicalization, 10 questions, 161
Medicalization of mental health, 7–8 Mind–body problem, 3–4, 13–14, 62–63
Memory chunk, 29, 30
Mental disorders
biologically based N
central thesis, 167 National Institute of Mental Health (NIMH), 4
classroom discussion, 167–168 NCLT. See Neuro-Cognitive Learning Therapy
questions, 168 (NCLT)
DSM IV, 8 Network recruitment, 49
obsessive–compulsive disorder, 9 Neural networks, 50–51
Mental health Neurobiological vulnerability, 11
cause of, 61–62 Neurocognitive learning model, 19
disorders, 60–61 Neurocognitive learning therapy, 125
effect of learning, 40–42 Neuro-cognitive learning therapy (NCLT),
and neural networks, 38–39 157, 158, 167, 173–175
practitioners, 157 clients learning network, 131
Mental illness, 57–58 emotional labels, 129
adaptive and maladaptive human learning, 133
behaviors, 153 informed and educated client, 133, 134
automatic thoughts/schema, 146 maladaptive behavior, 130
central thesis, 169–170 maladaptive thought process, 132
child’s attention weaknesses, 137 neuropsychological model, 129
classroom discussion, 170 pathology, 133
client–therapist relationship, 136 physiological responses, 129
cognitive explanations, 146 psychodynamic therapy, 133
connectionist small-world hub psychotherapeutic approaches, 132
modeling, 152 schools of therapy, 131
diagnostic labeling, 80 small-world hub model, 130
diagnostic model, 153 therapeutic approaches, 133
diagnostic system and treatment Neurophysiology
methodologies, 149 of learning, 25
disease types and treatment, 150 stimulant medication, 136
DSM, 81
environmental and behavioral
patterns, 153 O
etiology, 83, 84, 152 Oppositional defiant disorder, 143
explanatory conceptions, 79
ICD systems, 81
learning, 125 P
maladaptive learned response, 152 Paradigm shifts
maladaptive responses, 87 conception, 2
maladaptive schema, 146 homosexuality, 2
medications, 84, 85 learning and neurophysiology, 2
mental disorders, 155 mental health, 2, 4
nosology and diagnostics, 81 mental illness, 3
questions, 170 neurophysiology, 3
self-deception, 150, 151 neurotransmitters, 2
symptomology, 82 nondirective treatments, 4
symptoms/behaviors, 149 therapeutic relationship, 4, 5
treatment techniques, 154–155 Personality-related factors, 11
and white matter connections, 85–87 Piagetian-based schema development, 142
180 Index

Post-traumatic stress disorder (PTSD), 8 healthy development, 107


Procedural knowledge, 28 learning language, 117–119
Psychiatric dysfunction, 51–52 learning model
Psychoanalytic theory of personality, 72 basic principles, 163
central thesis, 163–164
classroom discussion, 164
R questions, 164
Recruited elements, 166 learning objectives
Research Domain Criteria (RDoC), 88, 153 central thesis, 171
Reward-driven behaviors, 47 classroom discussion, 172
questions, 172
learning therapeutic material,
S 93, 94
Semantic knowledge, 27 limbic–motor interface, 123
Sensory gating, 111 maladaptive system, 114
Serotonin hypothesis, 60 neurological processes of filtering, 110
Small-world hub models, 75 neurophysiology of gating, 110
Small-world hub-based learning, 86 on connectome, 39, 40
Small-world neural network models pattern matches and schema assignment, 94
graphical analysis, 35 post-traumatic stress disorder, 98
specialized and modular processing, 36 principles
Substance Abuse and Mental Health Services central thesis, 172–174
Administration (SAMHSA), 8 classroom discussion, 173–174
questions, 173–174
psychopathological characteristics, 91
T questions, 171
Therapy, 171–174 realization and awareness, 120
action selection and basal ganglia, 96 reward recognition circuit, 121
action-oriented process, 104 reward recognition network, 122
adaptive and maladaptive behaviors, 91 reward recognition, gating network,
adaptive behaviors, 98 111–113
assimilatory schemata, 108 schema construction, 113
automatized maladaptive behaviors and small-world hub brain models, 115
thoughts, 99 stimuli and environmental factors, 102
brain circuitry, learning and reinforcement teaching strategies, 114
recognition, 116–117 therapeutic behavioral and emotional
central thesis, 170–171 outcomes, 114
classroom discussion, 171 therapeutic intervention, 109
clustered nodes, 95 thought processes, 98
cognitive load-reducing methods, 120 Therapy re-imagined
cognitive/developmental changes, 114 central thesis, 159–160
competence, 92–93 classroom discussion, 160
complex behavior/emotion, 91 questions, 160
compliance with learning principles, Thorndike’s principles of learning, 172
158–159
computational model, 97
connectome, 94–95 U
constructivist learning, 108 Unconscious thought theory (UTT), 68
dopamine-modulated cortico-striatal Unconsciousness
plasticity, 97 automatic processing, 68
environmental occurrences, 120 cognitive processes, 68
etiology, autism, 121 cognitive psychology, 67
gating, 109 social psychology, 67
goal-directed behavior, 99 working memory, 69
Index 181

Unified Learning Model (ULM) V


human learning, 24 Ventral attention network (VAN), 51
integrated current theory, 23 Vertical brain-based therapy principles, 76
long-term memory, 24
neurocognitive learning model, 24
rules of learning, 25 W
stimulus, 24 Working memory, 51