M.D.

PHILLIP R. SLAVNEY, M.D.

For Jean and Jacqueline
Preface ix

Acknowledgments xi

I / ASSESSMENT AND EXPLANATION IN PSYCHIATRY

1 / The Mind-Brain Problem and a Structure for Psychiatry 3

2 / Factionalism: The Other Source of Disarray in Psychiatry 18

3 / Classification in Psychiatry and the Method of DSM-IV 31

II / THE CONCEPT OF DISEASES

4 / The Disease Perspective: Its Premises, History, Strengths, and

Limitations for Psychiatry 45

5 / The Disease Concept Exemplified by Psychiatric Conditions

with Known Neuropathologies 54

6 / The Disease Concept Applied to Psychiatric Conditions without

Known Neuropathologies 63

7 / Manic-Depression: A Disorder in the Affective Realm 71

8 / Schizophrenia 82

III / THE CONCEPT OF DIMENSIONS

9 / The Dimensional Perspective: Graded, Quantitative,

Dispositional Distinctions 99

10 / Mental Subnormality: Distinctions within a Dimensional Feature

110
11 / Temperament, Affective Dimensions, and Personality
Disorders 126

12 / Emotions, Life Events, Traits of Temperament, and

Treatment 138

IV / THE CONCEPT OF BEHAVIORS

13 / The Behavior Perspective 151

14 / Characteristics of Motivated Behaviors 165

15 / The Causes of Behavioral Disorders 178

16 / Treatment Principles for Behavioral Disorders 195

17 / Bulimia Nervosa: A Behavior Treated through Stages of

Change 210

18 / Hysteria 223

19 / Suicide 238

V / THE CONCEPT OF LIFE STORIES

20 / The Life-Story Perspective 253

21 / The Application of the Life-Story Perspective in Practice:

Power, Process, and Pitfalls 268

VI / PRACTICAL IMPLICATIONS

22 / Practical Implications of the Perspectives 285

23 / Integrative Summary 294

Appendix. Reliability and Validity: The Processes of Verification 301

Notes 305

Index 325
The original version of this book (which served as a blueprint for our
teaching and research at Johns Hopkins) surveyed the sources,
principles, and disciplinary history on which psychiatrists base
diagnoses and treatments. We held that students with knowledge of
the basic patterns and constituent elements of psychiatric reasoning
could more easily absorb the details of the discipline, judge proposals
from its practitioners, and grasp the problems presented by patients.

This second edition expands on our original effort to describe

psychiatric thought-written now after our department has matured and
after more than a decade of comments, criticisms, and questions
about the book's thesis and specific components. We have revised
those portions of the text that proved obscure and have added new
chapters to illustrate our ideas.

Our aims are ambitious. We are aware of the amorphous, dispute-

ridden character of contemporary psychiatry and intend to forge a
conceptual structure on which better research and progressive,
coherent practices can arise. We hold that catalogues of diagnostic
terms-such as the Diagnostic and Statistical Manual of Mental
Disorders (DSM) of the American Psychiatric Associationand the
nonspecific, all-embracing "biopsychosocial" orientation toward the
discipline's elements do not advance such a structure but call
attention to its absence.

We do not intend to provide exhaustive descriptions of psychiatric

disorders, itemized lists of diagnostic criteria, or detailed prescriptions
for treatments. We are presenting not the entire informational content
of psychiatry but the ways that content is organized to permit clinical
assertions and case formulations to emerge.
 This book has six parts. The first part describes the overall domain
of psychiatric responsibility, the controversial aspects of psychiatric
explanation, and the vexing problem of psychiatric classification (with
particular emphasis on the rationale of DSM-III and DSM-IV). In that
part we argue that several different methods of reasoning are needed
to make sense of the different kinds of psychiatric patients. These
methods we have called perspectives in that they are distinct but
complementary ways of "looking" at mental disorders.

The next four parts analyze the perspectives of diseases,

dimensions, behaviors, and life stories. Each part includes a
consideration of those psychiatric conditions that most clearly
exemplify the explanatory power of the perspective under discussion.
We identify critical distinctions among the perspectives and
demonstrate fundamental differences in the disorders each
encompasses.

The final part is recapitulatory. In it we emphasize the implications

of seeing psychiatric conditions as differing in nature and how, based
on these distinctions, the approach to their treatment and
investigation must vary. We conclude by describing how knowledge
that is methodologically based and oriented toward research should
direct the future of psychiatry.

Thus, the second edition of this book has the same purpose and
organization as the first. It introduces psychiatric reasoning through a
series of chapters on explanatory methods and their application. It
brings structure to the thought and practice of the discipline, often by
rendering explicit what is implicit in psychiatric opinions. It presents a
framework for surmounting disputes and for clarifying experience.
And finally, it indicates how the field can evolve, dispelling ambiguities
about what psychiatrists know by specifying how they know it.
This second edition was encouraged and stimulated by the many
interactions between the authors and students of psychiatry whom
they encountered. Some of these were the medical students at Johns
Hopkins, who, employing the first edition as their primary psychiatric
text, demonstrated to us the many difficulties that had to be corrected
in a new edition. We are grateful to those many students from the
Johns Hopkins classes of 1986 to 2000 who worked so diligently with
us. As well, psychiatric residents and psychology trainees here at
Johns Hopkins studied and discussed the text with us almost daily
and in the process demonstrated to us its strengths and weaknesses.

The faculty of the Johns Hopkins Department of Psychiatry and

Behavioral Sciences as well as several psychiatrists and
psychologists from other schools of medicine contributed immensely
to this present edition both by general comments about the preceding
version and through their specific research in special areas of
interest. Most specifically, we thank Elizabeth Aylward, Jason Brandt,
John Breitner, Marshal John Lipsey, Constantine Lyketsos, Russell
Margolis, Peter Rabins, Adam Rosenblatt, Christopher Ross, and
Andrew Warren for their contributions to our understanding of
dementias, delirium, and amnesia. We thank J. Raymond DePaulo,
Jr., Kay Jamison, Melvin McInnis, Francis McMahon, and Sylvia
Simpson for their assistance in our understanding of affective
disorder, and we thank Patrick Barta, Karin Neufeld, Godfrey
Pearlson, Ann Pulver, Joseph Stephens, and Karen Swartz for their
help on the schizophrenia chapter. We thank Paul Costa, David
Edwin, Robert Gordon, Rudolf Hoehn-Saric, Geetha Jayaram, Gerald
Nestadt, and Julian Stanley for their thoughtful suggestions in the
domains of intelligence and temperament. We thank Arnold
Andersen, Nancy Ator, Fred Berlin, George Bigelow, Joseph Brady,
Peter Fagan, Marc Fishman, James Gibbs, Roland Griffiths, Angela
Guarda, Jill Jonnes, Michael Kaminsky, Ellen Ladenheim, Lee
McCabe, Betsy McCaul, John Meyer, Timothy Moran, David
Neubauer, Alan Romanoski, Gerald Russell, Thomas Schlaepfer,
Chester Schmidt, Jr., Gary Schwartz, Gerard Smith, Maxine Stitzer,
Eric Strain, Glenn Treisman, Jay Turkhan, and James Wirth for
helping immensely in clarifying the history, science, and clinical
issues of the behavior perspective for us. We thank Albert Dreyfus,
Theodore Feldberg, Michael Fox, Jerome Frank, Lauren Hodas, John
Imboden, Everett Siegel, Lex Smith, Mark Teitelbaum, and Barbara
Young for providing us with generous advice over matters of
psychotherapy and the life-story perspective. Our knowledge of child
psychiatry was greatly aided by the division directors of Child
Psychiatry here at Johns Hopkins: Joseph Coyle, Susan Folstein, and
Mark Riddle. James Harris, Paramjit Joshi, Alan Reiss, and John
Walkup also contributed generously to our child psychiatry concepts.
Many of the people already listed assisted us in thinking through the
basic approach of this book-often bringing us suggestions from their
broad scholarship and experience in teaching. Others who have done
likewise include William Breakey, Michael Clark, James Gibbons,
Jeffrey Janofsky, Jonathan Javitch, Marie Killilea, Thomas Koenig,
Edmond Murphy, Brian Poeschla, Ronald Rieder, Joseph Schwartz,
Michael Schwartz, and Thomas Wise.

Patricia Santora was absolutely essential to this second edition.

She devoted time and effort "beyond the call of duty" in seeing to its
evolution and composition. We are deeply in her debt.
Students of psychiatry have two tasks to accomplish as they seek to
master this discipline. They must become familiar with the features of
mental disorders and their treatments. Supervised experience with a
large number of patients provides this skill. But simultaneously they
must grasp implications embedded in the several methods of
explaining mental disorders that, when unacknowledged and
unordered, give this discipline a denominationalist disarray inimical to
progress.

As the title implies, the purpose of this book is not to review the
contemporary contents of psychiatry on which practice proceeds-
such as the identifying characteristics of schizophrenia, the regimens
and dosages of antidepressant medications, or psychotherapeutic
approaches for treating marital disharmony. Rather, our intention is to
consider and render explicit the forms in which those contents are
contained, that is, the basic patterns of thought and explanation by
means of which psychiatrists arrive at diagnostic and therapeutic
assertions. We plan to describe the principles, history, and sources of
confidence behind psychiatric practice rather than to provide a series
of miniessays on the major mental afflictions. In these first chapters
we present a justification of this plan and the obstacles it faces.

Obstacles for Beginners

Psychiatrists are physicians devoted to identifying and treating

human mental disorders. It is difficult to imagine a clinical subject
more intrinsically interesting or likelier to attract pupils. And yet, many
beginners are discouraged, almost to the point of disdain, by a
disquieting sense that their psychiatric teachers are indoctrinating
them into some arcane view of human nature and that they employ
specious reasoning to skirt vexing ambiguities in the subject matter.

The truth is that the teaching of psychiatry is anomalous. In contrast

to internal medicine, surgery, or pediatrics, psychiatry does not-
indeed, it cannot-emerge straightforwardly from the course of study in
physics, chemistry, and biology that medical students have followed
since college. As a result of this fact-an unavoidable effect of the
brain-mind problem-many students hold that psychiatrists come from
"left field," touting observations, opinions, and practices that demand
some idiosyncratic allegiance or peculiar initiation to embrace.

As teachers of psychiatry ourselves, we have learned, through hard

experience, to address a student's disquiet promptly so as to combat
skepticism and permit the natural appeal of this subject to emerge
and its practice to flourish.

Denominational Conflict: "Biology" or "Dynamics"?

Many beginners are troubled by denominational matters. They ask

whether they should assume a "biological" or a "psychodynamic"
orientation toward psychiatric patients. They have heard, usually in
college, that psychiatrists argue with each other over the "orientation"
(i.e., comprehensive point of view about patients) they have adopted.

We respond that every orientation is a partial understanding of this

discipline. These two familiar orientations, the biological and the
psychodynamic, dominate much of the debate in this field because
psychiatric patients differ among themselves in ways these two points
of view underscore.

Some psychiatric disorders are expressions of nature's power over

human life. The most obvious examples of such disorders are brain
diseases that break down psychological capacities such as memory,
mood, language, and perception. These disorders call for physical
and pharmacological measuresbiological by definition-to investigate,
treat, and, one hopes, cure.

Other psychiatric disorders are expressions of personal distress

due to life events. These are the emotional and behavioral effects of
conflict between a person's hopes, desires, and wishes and the
obstacles to their realization encountered in life. These disorders
depend not on nature's power but on human motives and their
capacity to produce distress when thwarted by experience. Disorders
from this source, the collision between human aims and life itself,
emerge from the emotional forces (i.e., the elements of
psychodynamics) released by such a collision and take the form of
disquieted moods and behaviors-anger, anxiety, depression.
Successful treatment will depend on understanding the patient as
someone in need of compassion and guidance.

The so-called orientations in psychiatry are ways of emphasizing

the importance of one source of mental disorder but may do so at the
expense of trivializing the other. The beginner does best to ignore
orientation and seize every opportunity to examine patients. Through
that experience, he or she will appreciate how biological and dynamic
explanations of the patients' mental states can complement each
other in practice and coexist without rancor in psychiatry.

More Information than Knowledge: What's Fundamental?

At an early stage in their study, most beginning students are struck

by the long lists of "diagnostic" criteria for psychiatric conditions that
many textbook authors claim they must remember. Students
recognize that little science seems to confer authority on these lists,
which derive from the fallible "consensus" of leading experts in
psychiatry. A sense of being stuffed with "factoids" that change with
every edition of an official text or manual can repel any student.
 We advise against a preoccupation with lists when starting the
study of psychiatry. We propose that students see many patients and
work to understand the methods that psychiatrists employ to assess
and explain mental disorders. This will provide the foundation for
"facts" to accumulate as experience grows. Memorizing lists for
diagnosis and treatment is anathema to us, and to most students,
primarily because information congealed in prescriptive recipes
hampers the growth of knowledge and the individualization of
treatment.

Is It Medicine?

As we psychiatrists start to teach our discipline to beginners, we

confront a qualm among some students that psychiatrists may not be
"real" doctors. "What else," we respond somewhat defensively, "might
we be?" "Well," comes the answer, "medicine is an applied natural
science directed toward sick people. Psychiatric patients seem not
sick but troubled, and psychiatric effort more guidance than curing.
Perhaps the natural associates of psychiatrists are not physicians
and surgeons but counselors, ministers, social workers, and even,
heaven forbid, lawyers."

We flinch at this view and sometimes turn cranky. After many

exchanges of this sort, we have found that the best answer to
skepticism about the medical nature of our discipline is to note the
path medicine followed in this century. We can then show that
psychiatry is proceeding along the same path, empirically and
methodologically, even as it confronts a fundamental problem in
science-the brain-mind discontinuity. As students gain knowledge of
the empirical and methodological approaches of psychiatry, their
concerns about orientations, disorganized and disconnected "facts,"
and the nature of psychiatry itself usually resolve. But one must know
the path of medical progress to follow it.

Understanding the Path

 All doctors work to understand human illnesses so as to rid people
of them. Historically, they began by describing and differentiating
illnesses. Thus, doctors were experts in diagnosis-the identification of
illnesses from the symptoms and signs that appeared in patients-long
before they could confidently explain, from causes and mechanisms,
the conditions they had identified.'

Nonetheless, with a proper diagnosis, doctors could help patients in

numerous ways: by distinguishing transient and trivial disorders from
persistent and mortal ones, by offering managements and medicines
discovered (usually by chance) to alleviate certain symptoms, and by
guiding patients toward recovery without imposing unnecessary
burdens on them. The ancient Hippocratic oath depicts the ethical
implications and use of such knowledge.

The last two centuries have seen medicine evolve from an

empirical, itemizing, diagnostic enterprise into a rational, causally
focused, bioscience-driven one. Biology, in its proper sense as the
scientific study of living things, became the foundation of medical
thought and practice. However, a fundamental, illuminating idea
emerged with this approach. One could gradually abandon thinking of
diseases as so many "entities" to be taxonomically catalogued like
specimens of Linnaean genera or species. Rather, one could
appreciate that diseases are, in truth, various modes of "life under
altered circumstances."

Do not underestimate this idea! It radically transformed practice and

research in medicine and surgery in our times. It now buttresses the
conceptual structure of these disciplines, affecting discourse,
investigation, and partnership.

Psychiatry is a branch of medicine that has not advanced as far

along this transforming pathway. Psychiatrists are adept at identifying
mental disorders. They can recognize the symptoms of anxiety and
depression. They know and can describe the distress and life
impairments these symptoms bring to patients. They can predict,
from long experience, how some of these symptoms will progress, to
recovery or to chronicity. They can even provide a variety of
treatments-most, it must be agreed, discovered by accident-that can
help patients by interrupting or ameliorating their symptoms.

However, psychiatry remains a medical discipline long on disorders

and short on explanations. In this sense, psychiatry is at a stage of
development other medical specialties passed through decades ago.
Psychiatrists, primarily because of the nature of their subject matter,
really know little about how the disorders they can identify derive from
the basic elements of life-physical or psychological-and even less
about how they can be conceived as "life under altered
circumstances." The immaturity of the discipline handicaps treatment,
prevention, and research.

Three Basic Questions for Psychiatrists

Anyone teaching psychiatry will at some time face three questions

from students who are acquainted with the path that medicine has
followed:

1. What is psychiatry's domain of study?

2. How can one make reliable and valid observations in that domain?

3. How is this domain generated by the brain?

These questions reveal the knowledge gap students of this

discipline must overcome. The questions do not necessarily occur to
the student in this sequence. However, they are best addressed in
this order, because as the answers take shape, they cohere, furnish
an understanding of psychiatric practices, and illuminate the linkages
between this clinical discipline and the basic sciences around it.

Question 1: What Do Psychiatrists Study?

THE SIMPLE ANSWER. Psychiatrists focus on troubles that appear
in people's thoughts, moods, and behaviors rather than in their skin,
bones, or viscera.

A MORE COMPLICATED ANSWER: A NATURAL BIOSYSTEM

CALLED THE MIND. The question merits an expanded answer as
well. The point of contact between the psychiatrist and the patient is
the patient's personal consciousness, or the mind. The psychiatrist's
job is to assess the contents of the patient's mind. Many would define
the term mind as the conceptualized repository of the conscious
experience encompassing a person's thoughts, moods, and
perceptions.

But the concept of the mind goes beyond what amounts to a

shorthand term for consciousness. The mind not only is the "site" of
conscious awareness but also consists of specific psychological
capacities such as memory, language, reasoning, perception, and
emotional responses. These capacities of the mind develop with
experience, change over time, and interrelate with one another.

Finally, the mind is the "setting" of executive purpose. Through

conscious evaluation, decision, and choice, a person directs his or
her behavior and selectively employs such capacities as memory,
thought, and language to interpret the world and to generate effective
action. This amalgamation of awareness, capacities, and executive
direction gives the mind a "system" character. This conception
improves on our definition.

A system is a group of diverse elements so combined as to form an

integrated whole functioning in unison and often to a purpose. The
cell, the brain, and the gastrointestinal tract are biosystems with their
own system-specific elements, dynamic internal actions, and lawful
relationships to other systems. Psychiatrists progress when they
construe the mind as a life system or biosystem made up of
psychological elements interacting lawfully with each other and with
other systems of the body.

OPERATIONS OF PSYCHIATRISTS IN ASSESSING THE MIND

FOR DISORDER. In assessing a patient with troubles in thoughts,
moods, or behaviors, psychiatrists attempt to find evidence for either
a disruption in specific elements of the mind or a general disturbance
in the efficient functioning of the mental system itself in life. For
example, a patient may arrive complaining to a psychiatrist that he
has become easily puzzled and distressed at work, and his family
reports that he cannot remember what has happened during the day.
The doctor, wondering whether an element of the patient's mental
system, such as memory, has been impaired, logically examines the
patient to discern whether he can learn and remember new things.
The psychiatrist's aim is to identify any loss of memory capacity in the
patient and then decide whether this loss, which explains the patient's
behavioral and emotional difficulties, is susceptible to treatment.

SUMMARY. The answer to the first question about psychiatry can be

summarized as follows: Psychiatrists study the mind, a distinct
system of capacities and functions expressed in human
consciousness as thoughts, moods, and decisions. Just like other
doctors, psychiatrists study this life system for evidence of disorders
that can be treated or prevented. The components of the mind can be
individually disordered (as with memory loss), the functional
interrelationships of the components can be troubled (as unmet
hopes can generate distress and fear), or the mind's customary goal-
achieving capacities may be thwarted (as habitual decisions go
awry). By a systematic assessment of the life and mental state of the
person, psychiatrists discern disorders and launch efforts to treat
them.

Question 2: Can This Life System Be Reliably Examined?

THE PROBLEM OF PRIVACY. Psychiatrists work to find disturbances
in the mind. However, the elements of consciousness, whether
normal or abnormal, are by nature "private" affairs. How can anyone,
let alone a doctor who sees a patient only briefly, have confidence in
assessing that patient's personal, uniquely private thoughts and
moods?

As people ourselves, however, we know our own thoughts and

moods "through and through." We experience them vividly. We do not
doubt our consciousness nor its ability to affect our actions. But can
we be as confident about such matters in others? Can psychiatrists
satisfy the public's legitimate demand for objectivity and impartiality in
clinical judgments while assessing the contents of a domain, the
mind, that is fundamentally personal, private, and internal, and thus
subjective?

ONE SOLUTION: BEHAVIOR. One approach is to employ

observations of "public" behavior to judge states of mind. For
example, we could infer that a person is conscious because he or she
responds attentively to commands or is anxious because he or she
trembles. This approach has been suggested and employed by some
investigators but is not without pitfalls, for example, in differentiating a
person with a tremor due to hyperthyroidism from one who is anxious.

A BETTER SOLUTION: PHENOMENOLOGY. A better approach is to

determine whether a patient's answers to a physician's inquiry (for
example, "What is your mood today?" "Are your thoughts clear?"
"What city are we in?") provide reasonable assessments of the
contents and capacities of that patient's mind. Karl Jaspers referred
to the results of eliciting and describing the per sonal mental
experiences of patients as the product of phenomenology, "the
empirical method of enquiry maintained solely by the fact of the
patient's communications."2
 We can assess the mental experiences of people through the
communicational capacities we share with each other. Our ability, for
example, to understand the feelings of our friends and relatives
demonstrates this clearly. Percy Bridgman, the founder of
operationalism, called these basic human capacities projection.3 All
these empirical, and projectionperhaps make too much of the simple
fact that we can learn how another person is thinking and feeling by
talking to that person.

A psychiatrist's mental status examination, sometimes called an

interview, is a systematic way of talking to patients. It is a way of
asking questions about their thoughts and feelings so as to reveal
them. How one asks such questions, follows up on the answers,
records the responses, and draws conclusions from them are skills to
be learned and practiced like any other means of examination, such
as auscultation of the heart or the application of the
sphygmomanometer. Just as with those skills, once the student
learns to conduct an effective mental status examination, he or she
can bring forth quite reliable and important information about patients
and their states of mind.

None of this is to deny that managing a mental status examination

can, like any medical skill, be difficult and calls for both experience
and effort from the physician. It also depends in part on the
cooperation and capacity of the patient to follow the physician's
questions. A mental status examination is more difficult to perform
with children and can be complicated if there are barriers between the
physician and the patient, such as language or cultural differences.4
However, there is a world of difference between an enterprise that is
difficult and one that is pointless.

The life system called the mind is distinct from the biosystems
studied by other medical specialties. However, its constituent
elements-thoughts and feelings-are real and can be described to
others and thus rendered objective enough to identify and treat.
SUMMARY. Psychiatrists can reliably examine a cooperating patient's
private and personal mental world by using a structured set of
questions and follow-up questions to facilitate communication about
the contents of the patient's conscious mind. The operative words are
cooperation, structure, and follow-up. By using this approach
systematically, one can draw reasonable conclusions about the
presence or absence of mental disorder.

Question 3: How Does the Brain Generate the Mind?

THE BRIEF ANSWER. We do not know how the brain produces the
mind.5.6

A CONTRAST WITH ANOTHER MEDICAL SPECIALTY. A contrast

between cardiology and psychiatry will emphasize this point and its
implications. The discipline of cardiology rests on a defined bodily
organ and its tributaries, a biosystem consisting of the heart and the
circulatory vessels. From the beginning of cardiology as a medical
specialty that recognized certain symptoms, such as breathlessness
and edema, as due to heart failure, cardiologists could predict that
understanding the physiological functions and capacities of the heart
would explain these symptoms and thus render them potentially
treatable.

The heart is vulnerable to disruptions of its muscles, valves, and

rhythmic pump action. The symptoms experienced by any cardiac
patient must derive from what is physiologically lost with a given
disruption and from what compensatory physiological events such a
loss initiates in the system as a whole. The study of symptoms thus
directs the diagnosis and management of the patient along rational
pathways extended by basic research into the heart's structure and
function. A beginner can start at almost any level within the elements
of the cardiovascular system, from the molecules that interact within
myocardial fibrils to the structural anatomy of the heart as an organ,
and conceptually encompass the discipline of cardiology and
appreciate how its practitioners explain and treat cardiac patients.

Like the cardiovascular system, the mind is also a system with

interactive elements such as thoughts, moods, and perceptions. The
mind and its elements are, however, products of the brain, and if we
reasoned directly from the cardiology example, we might conclude
that brain study could replace mind study with the great advantage of
assessing a physical object.

However, despite impressive advances in neuroscience, something

needed to explain how consciousness springs from brain tissue is
missing from its contributions. A person does not appear to be, and
certainly no one thinks of oneself as, the passive follower of the brain
and body. Each self thinks that it is, to some extent, in charge of the
body. "I" not only exist but also "tell" the brain what to focus on.
Mental life is "willful," a domain in which plans can be articulated,
actions directed, and results appraised, criticized, or regretted. If the
sense of "I" were not such an everyday experience that we take for
granted, it would be amazing. How does the material brain produce
such a thing as the self, "I," and how does the brain then relate to it?
As yet no scientist can connect this perception of the "I" and its
controlling capabilities totally to what is known of brain structure and
function. A disjunctive gap interrupts the path of explanation from
physical to psychological states.

THE BRAIN-MIND DISCONTINUITY. Because no similar disjunction

occurs in other branches of medicine, it must be described in more
detail in order to appreciate its implications for psychiatric teaching
and practice. Thoughts and moods occur through actions of neurons
and synapses and in no other way. We all assume that science will
eventually discover how the brain can deliver a directive self,
intentions, and vitality of mental experience. However, this discovery
will come about not simply by adding to the information we presently
have, but through a revolution in our understanding of properties that
can spring into existence from neural systems and material. This
revolution will bring us an entirely new conception of the biological
world and illuminate the place of freedom within it. The obliteration of
the brain-mind discontinuity demands something scientists cannot
imagine today. If this revolution occurs, then none of us,
neuroscientists or psychiatrists, will see the world as we do now.7

Thus, in contrast to cardiologists, psychiatrists cannot go directly

from knowing the elements of the brain (neurons and synapses) to
explaining the conscious experiences that are the essence of mental
life. At the frontier of brain and mind, wherever that may be, the
words we use change from tangibles (neurons and synapses) to
intangibles (thoughts, moods, and perceptions). One is not identical
to the other. Unlike cardiologists, psychiatrists are unable to go
directly from the molecular structure of a bodily organ to the
functional results of that organ's action.

There are several implications of this discontinuity. The most

fundamental implication is that this discontinuity renders impossible a
course of teaching and study that would seek to explain psychiatry
directly from neuroscience and thus from physics, chemistry, and
biology. Three other practical implications deriving from the brain-
mind discontinuity are discussed in the text that follows.

PSYCHIATRISTS BEGIN AT "THE TOP." The brain-mind

discontinuity justifies psychiatrists and their practices. Because of the
discontinuity in the links from brain to conscious experience, some
clinicians must identify and manage disorders emerging in
consciousness. In other words, psychiatry cannot be replaced by
neurology because brain facts cannot substitute for mind facts.

Psychiatrists are distinguished by working "top down"; that is, they

begin with consciousness and attempt to describe the events that
occur within it. Only after they have drawn out these features for
descriptive and analytic purposes do they turn to consider how events
in the brain, body, or environment can affect consciousness and
illuminate mental conditions.

CIRCUMVENTING THE BRAIN-MIND DISCONTINUITY.

Psychiatrists certainly do use the progress in neuroscience to make
sense of some mental disorders. However, the way they work with
this information is a means of circumventing the brain-mind
discontinuity, not eliminating it.

For more than a century, clinicians have been able to correlate the
occurrence of certain mental disorders, such as aphasia (the
disruption of language capacity), with injury to particular parts of the
brain. This is helpful information, as it guides clinicians in
understanding where damage in the brain may produce certain
mental symptoms. Specifically, psychiatrists now know that the
capacity to speak depends on neural activity in the left frontotemporal
regions and will be disrupted by any physical injury there.
Psychiatrists realize that they must examine the brain of a patient
who displays specific speech disorders. This examination may reveal
brain damage accessible to treatment. This explanatory approach
from symptoms to brain is an example familiar to doctors who
appreciate that they often correlate symptoms with evidence of bodily
breakdown.

Even though they know that certain language impairments are

associated with, emerge along with, and correlate in severity with
injury to the temporal lobe, clinicians still are not able to explain how
neural activity within this brain region produces our conscious sense
of choosing our words and directing our conversations. The
information provided by neuroscience permits clinicians to say that
this stretch of the brain is necessary but not how it is sufficient for
language.

To put it in simple terms: correlation is not explanation. The mind is

an experience; the brain is a physical structure. They are not
identical. How the actions of brain elements evoke the personal
experience of mental life and the intimate feeling of "minding" itself
(grasped in such expressions as "myself," "my ideas," "my wishes,"
and especially "my choices") does not emerge from even the most
advanced neuroscience.

PSYCHIATRISTS NEED SEVERAL METHODS OF EXPLANATION.

Not only is correlation not explanation, but also efforts to correlate
mental states and brain states cannot illuminate all of the clinical
conditions psychiatrists manage. Once again, people think their way
successfully through many challenges of life. Psychiatrists are
consulted when psychological disruptions interfere with this ability.
Some psychological symptoms derive from brain disease. However,
perfectly normal brains can bring forth maladaptive thoughts, feelings,
and decisions. Thus, people with brains that, so far as we know, are
structurally intact can misinterpret their situations, fear for their future,
and act improperly toward others.

An analogy may help clarify this simple but fundamental idea. In an

information-processing machine such as a computer, some problems
occur because a part of the machine breaks down (hardware
problems). These disorders will have a specific form depending on
their source and will call for a specific repair. Other problems occur
when the flow of information through the machine has been
misdirected by the instructions on which it functions (software
problems). The machine appears to operate properly but presents
"wrong answers" to questions and persists in these errors until a new
set of instructions for "correct answers" is provided to it. Both these
problems represent "pathology" in the system, but they differ
fundamentally in nature and treatment.

The brain, like the computer, can either have a broken part or take
up, through many influential routes, maladaptive instructions and thus
produce different mental conditions. Psychiatrists must learn to
recognize the differences between disorders resulting from "broken
parts" and maladaptive "instructions" in order to explain and treat
them appropriately.

All of these considerations mean that psychiatrists must employ

several distinct methods to understand the various disorders they
recognize in the mental lives of their patients. With each explanatory
method the definitions differ as to who is a patient, what is
psychopathology, what is meant by "normal, "and which treatments
are suitable. In fact, the fundamental question for psychiatric practice
is: What is the nature of the problem that a proposed therapy aims to
mend?

The Overall Answer in Perspectives of Psychiatry

Four standard methods for explaining mental disorders are implicit

in contemporary psychiatric thought and should be made explicit for
students. These methods (we shall call them perspectives, a visual
metaphor intended to emphasize that each method can illuminate
some aspects of psychiatric responsibility but will be blind to other
aspects) are the disease perspective, the dimensional perspective,
the behavior perspective, and the life-story perspective (figure 1).
Each finds utility with particular psychiatric conditions. Each has its
own concept of psychopathology and thus of what is "normal" and
"abnormal" in mental life.
 FIGURE 1. Perspectives of psychiatry.

1. The disease perspective rests on a logic that captures

abnormalities within categories. Psychiatrists employ the disease
perspective, just as all doctors have, by attempting to cluster patients
into separate groups defined by their impairments. Each group is
distinguished from other groups and from normal people by the
features that are the defining characteristics of the disease.
Embedded in the term disease is the idea that the ultimate
characteristic validating the category will be an identifiable
abnormality in the structure or function of a bodily part on which the
symptoms depend. For psychiatric diseases most abnormalities will
be found in the brain. The implication for practice is that diseases are
to be prevented or cured. This aim will be facilitated if and when the
abnormality in the bodily part provoking the symptoms of the disease
is discovered. A conceptual triad organizes the disease perspective:
clinical entity, pathological condition, and etiology.
 2. The dimensional perspective applies the logic of quantitative
gradation and individual variation to psychiatric assessments. This
perspective grapples with the fact that some patients are vulnerable
to mental distress because of their position on human psychological
dimensions of variation, such as intelligence or introversion that are
analogous to physical dimensions of variation, such as height or
weight. They occupy a position on the bell curve at some distance
from the mean. They are "abnormal" only in degree, not in kind. Their
distresses are those of any troubled person, just more easily
provoked by challenges others can manage. Their complaints and
symptoms are to be not "cured" but avoided. The treatment of these
patients focuses on discovering means of strengthening and guiding
them so they can manage their affairs more successfully in the future.
A conceptual triad organizes the dimensional perspective: potential,
provocation, and response.

3. The behavior perspective takes note of the goal-directed, goal-

driven (i.e., teleologic) features of human life and identifies some
abnormalities tied to these features. Thus, goal-directed behaviors
such as eating, drinking, sleeping, and sexuality are all aspects of
human life and depend on the bodily structure and learning through
maturation. The behavior perspective of psychiatry identifies
disorders emerging either because of unusual goals some people
come to crave (as in drug addiction) or because of excess in their
attempts to satisfy drives common to all (as in eating to obesity).
Abnormalities of the body may be provoking some of these
disordered behaviors, but anomalous learning experiences in the
form of cultural pressure and conditioning can also play a role. Some
behaviors depend not on physiological drive but on a combination of
psychiatric vulnerability and social learning. These behaviors include
hysteria, suicide, and crime. Physicians seek both psychological and
medical means to prevent, ameliorate, or interrupt these deranged
activities. Much of the success of treatment, directed at conversion,
not cure, will depend on physicians' winning the patient's cooperation
in these efforts. A conceptual triad organizes this perspective for
motivated behaviors: physiological drive, conditioned learning, and
choice.

4. Finally, the life-story perspective rests on the logic of narrative. A

distressed state of mind can be the natural, quite understandable,
result of a disturbing experience. Grief is an emotional expression of
loss, fear often follows a traumatic misadventure, and demoralization
is a result of a discouraging interpretation of life circumstances. A
narrative-a chronological recounting of setting, sequence, and
outcome-can make the evolution of these emotional states
comprehensible to patient and physician alike. The therapeutic
implications tied to this perspective include the need to comfort and
guide patients through a natural course of recovery, to assist them in
appreciating how they can act to avoid similar encounters in the
future, and to provide them with rescripted interpretations of their life
circumstances that provide more optimism and effective action. A
conceptual triad organizes the life-story perspective: setting,
sequence, and outcome.

Summary

Two implications about psychiatric thought and practice should now

be clear. These implications derive from the brain-mind discontinuity,
a fundamental obstruction that psychiatrists must circumvent as they
progress in their knowledge. First, psychiatrists must learn to
recognize the features of mental disorders, including the effects of
treatment of them. Only experience, under supervision, with a large
number of patients can provide this knowledge. Second, psychiatrists
must be familiar with several different modes of explanation
(perspectives) in order to comprehend both the diversity of mental
disorders found among their patients and the pitfalls of their
treatment. In fact, a study of method-methodology strictly speaking-is
essential for psychiatrists who would act effectively, avoid error,
defend their practice against critics, and extend the realm of
knowledge on which psychiatry depends through research.
 The chapters that follow attempt to show how the two aspects of
psychiatric thought on which rational treatment depends, the
description of mental symptoms and the explanation of their
generation, can be combined. In this way, psychiatry can start to
follow medicine in discerning how mental disorders are also
examples of "life under altered circumstances." Life can be altered by
what a patient "has" (diseases), what a patient "is" (dimensions), what
a patient "does" (behaviors), or what a patient "encounters" (life
stories).
If the mind-brain issue is the first and most fundamental problem
facing psychiatrists, then the long-standing factionalism dividing
psychiatric practitioners into partylike blocs, or "camps," according to
their beliefs about mental disorder is the second-and perhaps the
more distracting-issue obstructing progress. Over the last hundred
years, psychiatry has spawned many schools, or denominations,
within its ranks. The result is that psychiatry is the only discipline in
medicine in which it seems appropriate, even logical, to ask of a
practitioner his or her "orientation" or "philosophy." Such questions
denote that a professional identity is not sustained from one
psychiatrist to another in the way, for example, it is sustained from
one surgeon to the next.

Some claim that this factionalism is simply the result of new

discoveries that have not spread throughout the discipline and that
eventually every psychiatrist will be either "biological" or "dynamic,"
depending on the denomination the claimant champions. But this
argument seems unlikely, given that discoveries in psychiatry have
not been so many as to overwhelm anyone and as well most
subspecialties of medicine-such as cardiology-have little difficulty in
sustaining a professional identity in spite of the changes imposed on
their members by new discoveries. The Old Masters and the Young
Turks relate in a direct line of descent. Something more fundamental
must be at work. The mind-brain disjunction surely plays some role in
factionalism, given that a single source-our knowledge of neural
structure and function-cannot yet provide an explanation for all
aspects of mental disorders. Others must be sought.

The historical background of the denominations themselves reveals

much about their place and their power. They did not appear from
nowhere; nor did they spring unanticipated from the experience and
reflections of psychiatrists. We hold and teach that psychiatric
factionalism is actually an aspect of the more general divisiveness
over truth and human nature that has emerged over the last 200
years in Western thought. Because we also believe that the same
reasoning circumventing the mind-brain problem (and described in
the prior chapter) will help transcend factionalism, we now provide a
brief discursion into factionalism's historical background-into the
separate sources of ideas behind psychiatry's denominations-so as to
demonstrate how these problems came about.

Briefly, we see factionalism as derived from three major themes in

Western thought that have affected psychiatry since the work of Rene
Descartes in the seventeenth century. We shall refer to them as the
modern, postmodern, and antimodern ideas and expand on them in
the text that follows. Crucially, each has its own background, its own
set of leading historical figures, and its own contributions to
intellectual history in general and to psychiatry in particular.

Although, as will be apparent, they are at a fundamental level at

odds with one another, no one of them has overthrown the others.
Rather, they coexist competitively to this day, have strong champions,
and contribute mightily to the denominations of psychiatry. Any
proposal that hopes to unite the reasoning and practice of psychiatry
in order to provide its practitioners with a common foundation and a
professional identity must understand these ideas and know what
each has to bestow.

The Modern Conception and Psychiatry

 We shall entitle the set of ideas that emerged in Western history in
the mideighteenth century the modern conception. Its hallmark is the
Enlightenment, but it encompasses such historical events as the
American and French Revolutions and such practices and ideas as
the ascendence of empirical methods in science and technology, the
questioning of authority, the commitment to rationalism, the
accessibility of truth, and the freeing of humankind from subjection to
tyrannous social conditions. Its scientific leaders defined standards of
inquiry that opened the study of the physical world. Essentially,
human material progress rather than spiritual development became
the primary social goal to be sought and found through the
application of reason to human problems.

The Emergence of Modern Psychiatric Thought and Practice

As France was central at the outset of the Enlightenment, French

psychiatry was the first affected by it. In the 1790s Philippe Pinell
brought humane reforms to psychiatric care because he realized that
the mentally afflicted, the psychotic, the retarded, the demented, the
delirious, and so on, were suffering from natural processes-from
diseases rather than from moral failures or supernatural curses. This
conception was expanded by other French psychiatrists and
psychologists, such as Jean-Etienne Esquirol, Jean-Marc Itard,
Edouard Sequin, and their students. In their works there can be seen
a commitment to humane treatment of patients derived in part from
the ongoing empirical and experimental investigations of psychiatric
disorders and in part from the realization that crucial aspects of
human nature withstood the ravages of disease.2

Detailed considerations of the nature of psychiatric afflictions and

their proper treatments were enhanced by the efforts, experiments,
and clinical practices of nineteenth- and twentieth-century
investigators. Symptoms and signs were identified as formal
indicators of disorder, and these were relatedas particular forms of
disorder and injury-to particular mental capacities appreciated as
parts of normal mental life.

Leaders such as Wilhelm Wundt and Alfred Binet in psychology and

Emil Kraepelin, Eugen Bleuler, and Adolf Meyer in psychiatry
emerged. These leaders are all modernists, direct descendants of
Pinel, and, quite specifically, defenders of standards of practice and
reasoning-Kraepelin and Bleuler for observation, classification, and
differentiation of the signs and symptoms of mental disorder; Meyer
for a systematic examination permitting a comprehensive evaluation
of the patient and the patient's life.3.4

The contemporary expression of the modern way of psychiatry is

the operationalism and empiricism in classification in the Diagnostic
and Statistical Manual of Mental Disorders (III, III-R, and IV), which
are clearly neo-Kraepelinian, and the "biopsychosocial" concept, so
clearly neo-Meyerian.5 These recent expressions of modern
psychiatry are detailed in chapter 22.

Problems with Modernity

The natural sciences proved more effective in identifying various

forms of human psychological burdens than in acknowledging the
special qualities tied to human nature. Disease was something
moderns could define and grasp. Human consciousness and
especially the sense of purpose and freedom it evoked did not
register as incontrovertibly on modem scales. And yet human
purposes could be the source of some mental disorders, and certainly
it was human freedom that the Enlightenment intended to champion.

However, in many of modernity's social and ideological

expressionscommunism, fascism, Nazism-individual freedom was
considered quite negotiable when other social purposes were
projected. This sense of the contingency of the individual for
something else-the nation, the class, the Volk, the race, and today the
economy-was present in embryo at the start of the Enlightenment,
with its emphasis on human subjection to conditions and continues as
the dark side of modernity throughout the twentieth century.

Medicine and psychiatry were not spared this attitude of the

contingency of individuals. This aspect of modernity had one of its
most prominent expressions within biomedicine itself with the
eugenics movement of the early decades of this century and remains
as a shadow in the human genome project today. In particular,
German institutional psychiatry, with its focus on signs, symptoms,
and diagnosis, could not but contribute to a tendency to marginalize
through terminology, and through a warped combination of Darwinian
and Mendelian conceptions, the very people that modernity had, at its
start in the Enlightenment, seen as in need of help and protection.
These psychiatrists could define and differentiate impairments even
as the innate value of individuals, including sick persons, gradually
became less obvious. Thus, they began to speak of those carrying
the impairments of diseases as living "lives without value," lives that
proved susceptible to termination as other matters such as economic
considerations, public health opinions, racial "purity," or simply pity for
afflicted persons or their families became culturally dominant.6

This idea, first implemented in the form of involuntary sterilization of

psychiatric patients in many "advanced" nations of the West
(including thirty American states), played out to a "logical conclusion"
in Nazi Germany, where mentally ill patients were exterminated. As
had been noted by many others, this active governmental practice of
killing patients provided a sanction for the Holocaust. Both practices
were modern events, that is, dependent on modern technology,
supported by the laws of a modern state, and justified, at least in part,
by ideas stemming from modern bioscience.7

These justifications took some unintended sustenance from

utilitarian philosophers who, unwilling to defend freedom as a given in
human nature but rather as an idea that usually works for the greatest
good, left the implicit assumption that human freedom (and of course
life itself) is negotiable if and when it could be shown that the
"greatest good" could be obtained by taking it away. Dr. Kevorkian
and the contemporary Dutch physicians have carried this modern
idea of "death rather than illness" to such an extreme that they are
even prepared to pass rather quickly by the standards of diagnosis
Kraepelin established.

Absent a commitment to a "phenomenology" of human

consciousness where freedom as a given in our nature can be felt,
one might almost have predicted this deterioration in the standards of
psychiatry. As it turned out, the challenges to modernity (and its
psychiatric practices) came from these two sources: a more
advanced phenomenology of human mental life and a fundamentalist
commitment to the freedom of the individual in every situation.

Postmodern Conception and Psychiatry

We turn to phenomenology first. Emerging gradually, surreptitiously

at first and then in the last fifty years with great power and authority, is
a cultural and intellectual movement that, for want of a better term
and with many arguments about its limits, can be called
postmodernism. This movement is in fact best appreciated as an
extension of the modern ideas of the Enlightenment. Postmodernism
turns the rationalism and claims to honesty of modernity back on
themselves, even applying this critique to the standards and
certainties of the Enlightenment, to indicate that these ideas and
practices may be maneuvers of powerful, manipulative, self-serving
agents defending their authority.

Postmodern thinking can be best understood as a kind of modernity

gone sour on its own principles. But the critical ingredient that made it
possible was Friedrich Nietzsche's introduction of a phenomenology
of a particular kind, one provocative of disdain and particularly one
less impressed by either the cultural foundations of society or a
psychiatry of signs, symptoms, and diagnosis.

Nietzsche developed a psychology of the human "passions" and

their effects on all of our ideas. He saw them as hidden-indeed,
disguised-foundations behind our behaviors and our commitments.
He saw his role as exposing these foundations and so revealing base
origins of our "hitherto highest values."K His concept of the death of
God was a metaphor for not only the dissolution of religious faith but
also the dismissal of such modern ideas as progress, the perfectibility
of mankind, historical destiny, and universal morality. He announced
and glorified individuals whose power of reason was a match for their
passions, the Uebermenschen, postmodernists who could overcome
sentiment and tradition in drawing their own conclusions about the
truth and living life according to what applied to them.

Function versus Form in Psychiatric Practice

The premier postmodern psychiatric practitioner is Sigmund Freud,

who also based his conceptions on a "phenomenology of the
passions." For Freud, Kraepelin's diagnostic distinctions were
epiphenomena. Freud believed that Kraepelin's emphasis on formal
signs and symptoms in a search for diagnosis was a superficial
"descriptive psychiatry" that drew attention away from the study of the
true source of mental disorders: passions in conflict. Likewise, Freud
believed that the standards of thoroughness insisted on by Meyer
were excessive and distracting because they gave equal weight to
many aspects of a biography, underestimating the primacy of sexual
libido in the provocation and shaping of mental disorder.9

Freud followed the Nietzschean postmodern path of unveiling the

many dishonesties and rationalizations by which people got on with
life, blinding themselves to what they really thought or what really was
happening to them, even to the extent of suffering mental distress for
these rationalizations. For psychiatrists Freud brought an
appreciation that some mental disorders were outcomes of personal
attitudes-unintended but nonetheless inescapable outcomes of such
psychologically comprehensible emotions as anger, resentment, guilt,
and conflict. Mental disorders-and, for that matter, many other mental
phenomena, such as dreams, jokes, and slips of the tongue-were not
matters of form to be classified in some catalogue of pathology or
human mental events but rather represented the functioning of the
human mind as it managed the conflicts between its passions and
society's expectations.'()

Freud provided a clear advance for psychiatry beyond the modern

assumption that all mental disorders are products of nature,
explicable but impersonal, to be identified by their stereotypic signs
and symptoms. He found, rather, that some disorders are products of
the conflicted self bewildered by the collision of intentions and
experience-disorders that are understandable but private. Salutary
lessons for helping patients who are self-blind and unable to free
themselves from commitments to false ideas and false ideologies
emerged from Freud's conceptions. Psychiatrists today retain these
advances, attributable to Freud, in the importance they attach to how
empathic understanding of distressed and demoralized patients can
lead to methods of treatment that help them.

Another of Freud's conceptions that enhanced the craft of

psychotherapy was his attention to the emotional interactions
between patients and therapists wrapped up in his term transference.
For Freud, treatment sessions were not simply a form of professional
interaction but rather encounters shaped by the passions, wishes,
and hopes of both the patient and the therapist. Modem psychiatrists
of the Kraepelinian stamp, holding that treatment is a straightforward
technique, can underestimate the functioning of these emotive forces
and are surprised when they produce problems such as agitations
and noncompliance with treatment.
 Freud and his followers gave far-reaching scope to the idea that
mental disorders, and ultimately their resolution, are functions of the
person rather than forms of disease. He carried it from minor
distresses to a consideration of the psychoses. For example, Freud
said, "The delusional formation, which we take to be the pathological
product, is in reality an attempt at recovery, a process of
reconstruction."' 1 Carl Gustav Jung said, "Closer study of [deluded
individuals] will show that these patients are consumed by a desire to
create a new world system ... that will enable them to assimilate
unknown psychic phenomena and so adapt themselves to their own
world."12

Here is the vital heart of the controversy between modem and

postmodern psychiatry or, to use more familiar expressions, between
biological and dynamic psychiatry. It can be recognized right from the
start in the different terms psychiatrists of different orientations
employ to describe disorders. Some will choose terms such as states,
conditions, and mental events and emphasize forms of presentation
by indicating the presence of symptoms and signs. Others turn to
terms that imply a deeper meaning (i.e., function) behind the
manifestations of disorder and speak of processes, conflicts,
defenses, and latent and manifest contents.

When a psychiatrist begins by describing a distressing mental event

as a symptom or as a defense, he or she is moving down one, rather
than another road of reasoning, emphasizing either form or function.
The chosen emphasis evolves then from its beginnings into different
sets of explanatory and therapeutic implications even though the
identified mental event, as a phenomenon itself, is the same.
Because this choice of emphasis is seldom recognized,
acknowledged, or even understood as a choice for one path rather
than another, the mystifying conflict of implications over the nature of
psychiatric conditions is a result.
 One view of psychiatry tries to outplay the other in a call for
authority over explanations of disorder, patient care, and even the
"proper" way of thinking of psychiatrists. As can be seen from their
sources in modem and postmodern thought, each of these views is
encompassing, resting on certain assumptions of legitimacy and
importance. In fact, each develops in part in opposition to the other,
as Freud opposed Kraepelin. The debate between the proponents of
each idea may end simply in mutual repudiation-to the bewilderment
of our patients, our students, and our colleagues in medicine. Indeed,
when the sources of this conflict are unappreciated, people will ask,
"What are you psychiatrists fighting about?" We are fighting over what
is most important in assessing a patient's mental state: its formal
contents or its functional meanings.

But Freud went even further along the Nietzschean path, and the
concept of the transference added energy to his propositions. Like
Nietzsche, he preened himself on provocativeness and regularly
proposed that all arguments against him came from how his ideas
provoked the sense of impropriety about sexual matters in the
"unenlightened." He conceived the all-knowing, even visionary,
analyst who cuts through false leads and by dint of his insightful
authority is capable of helping patients understand the provocative
libidinal urges functioning behind the expressions of their disorders.
13.14

The Problem

Freud intended to emancipate psychiatry from the rigidities of

assessment and diagnosis and thereby sense a common logic behind
psychiatric disorders. In this useful exercise, however, he went very
far. Thus, the conception of an all-knowing, secret-discerning,
infallible guide and leader as the ideal psychiatrist eventually led to
overconfidence. The protective standards of evaluative thoroughness,
observational reliability, and empirical challenges to opinions brought
forth by such as Wundt, Kraepelin, and Meyer proved weak in the
face of Freudian assumptions. Freud's insinuations that the standards
these modern psychologists and psychiatrists claimed to defend were
fundamentally based on bad faith-an unwillingness to acknowledge
the passions, particularly the sexual drive and its social repression-
overpowered most of their students.

As these standards gave way and even academic institutions

surrendered to the Freudian faction, his followers became steadily
less rational and ultimately antirational. They claimed an authority-
indeed, an unimpeachable authority, because all questioning was
"nothing more than resistance"-resting on special insight into the
nature of the conflicts expressed in coded form in all human mental
disorder.

At first with Alfred Adler and Carl Gustav Jung, the transition from
Freud was simply a matter of emphasis, and these transitions might
have led to useful maturations of the dynamic psychology of hidden
conflicts if less had been at stake than claims to the secret of human
nature. But psychoanalysis lost interest in defining itself by its
methods as would a craft and turned away from any search for
external validation or dispute-resolving data as would a science.

Ultimately, psychoanalysis did not find a means for orderly

development of either theory or practice that could be publicly
examined, confirmed, or rejected. The visionary aspect of this
psychological movement-implying as it did that most psychiatric
symptoms were the functional outcomes of unresolved passions and
particular injurious encounters in life, most of which were buried as
latent contents in an unconscious realm waiting to be disinterred by
some expert-attracted imitators with a fervor driven by publicity,
faddish enthusiasms, and money. Splinter therapies such as
encounter groups, est, transactional analysis with its concern for the
"child within," and victimology right out to "past life" damage and
"alien abduction" got hearings even at university centers of
psychiatry. Thus, the circus of psychotherapists we have today
emerged-wild, changing, and often, it must be admitted, false to the
point of charlatanry and disdainful

A practice that considered the patient's reports of mental states as

nothing more than items to be looked through as the disguises of
repression, denial, reaction formation, and so forth-a basic
Nietzschean idea-rather than looked at as contents of human
consciousness was and remains the Achilles' heel of postmodern
psychiatry. It played a part in the recent violent reaction against both
modern and postmodern psychiatry represented by antimodem
fundamentalism.

Antimodern Fundamentalism and Psychiatry

In the last twenty-five to thirty years, essentially beginning in the

1960s, there has emerged a variety of claims that both modern and
postmodern thinking have damaged our society. These movements
note the corruptions visited on people by consumerism and the
preeminence of money-directing policies. But more than that, they
detect an ultimate immorality of treating people as things or of
supposing that their choices are always imposed by libidinal forces
they cannot control. These movements wish to reemphasize what are
best seen as traditional ideas: that human beings are special agents
dignified from their creation, often with a destiny that remains
mysterious, and endowed with freedom to make of themselves what
they can by their choices of a way of life. These movements can be
religious, as in religious fundamentalism, or nonreligious, as in some
forms of human rights fundamentalism.

In psychiatry the antimoderns were those who saw an authoritarian,

uncompromising rationalism in both modem and postmodern
psychiatrists that deprived people of liberty-or of the belief in liberty-in
the name of dubious treatment. These antimodern psychiatrists came
to believe that the institutions of psychiatry rather than the psychiatric
conditions were holding people hostage. The antimoderns claim to be
expressing the views of such modern philosophers as John Locke but
actually hold a fundamentalist commitment to liberty, presume a state
of freedom in all patients, and recommend (in the name of freedom)
the dissolution of all constraints on this liberty maintained by
psychiatric practice.

Psychiatrists such as Thomas Szasz, with his claims about "the

myth of mental illness" and his challenge to the psychiatric concepts
such as those addressing alcoholism and drug addiction, articulate
such an antimodem idea. They begin by viewing human nature as
free and thus human beings as capable of living many different kinds
of life. And they conclude that disordered ways of life must be
tolerated by a just society, as must many behaviors that rest on
choices, even deadly choices such as drug taking and suicide.
"Whose life is it, anyway?" ask these psychiatrists, a typical example
of the kind of talismanic utterances that function to protect antimodern
fundamentalists from accountability.

With Szasz we are dealing with a preacher-one keen most of all to

make an impression on an audience-not a teacher committed to
impart a rational, coherent, and progressive discipline to pupils
attentive to all the consequences of their practices. Liberty as an
absolute is the heart of Szaszian psychiatry. Specifically, it refuses to
accept the impairments on freedom from disease that modern
psychiatrists since Pinel have identified. The movement likewise
scoffs at "an excuse masquerading as explanation" when postmodern
psychiatrists try to explain behaviors such as addictions. Indeed,
Szasz refuses to acknowledge that advancing psychopharmacology
has detected disruptive lifealtering biological effects of chemical
substances distinct from life-terminating ones.16

To his credit, however, Szasz wishes to enjoin psychiatrists from

claiming too much both for disease categories that he sees as
arbitrary and for behavioral disorders that he sees as options. As
Szasz demonstrates in psychiatry, antimodernists are not to be
subsumed under simplistic political categories such as liberal or
conservative. Antimodernists can be found in both of these camps,
and simply equating orthodoxy or heterodoxy with antimodernism will
not grasp the movement in its essence.

For all that Szaszian psychiatry is a rejection of almost all the

history of modern thought about mental disorder-he would, after all,
put patients with schizophrenia back in the prisons from whence Pinel
rescued them-it does offer some useful countering contributions to
the imperialism of modem and postmodern psychiatry. It prizes
human dignity even in the midst of mental and behavioral chaos
provoked by psychiatric disorder. Considerable good is buried in its
rhetoric and plain tomfoolery. This good is the fundamentalist's good;
that is, something fundamental-essential, primary, vital, integral, and
indispensable-is often lost when we simply go about our business
unreflectively. From time to time we must be called to account for our
customs.

The Present Difficulty

As mentioned at the start of this chapter, these intellectual themes-

the modern, the postmodern, and the antimodern-exist side by side
today. One has not overthrown the other, but rather they are all alive,
competing, and contributing to psychiatric factionalism. In fact, the
unacknowledged commitment to one of these three intellectual
themes among competing points of view about psychiatric disorders
explains the restless confusions, unresolvable personal arguments,
and lack of progress that characterizes many psychiatric
conferences.

Within the general intellectual realm some transcending voices can

be heard. These spokespeople have much in common. They all see
the great achievements and solutions that modern science has
wrought. Not only do they celebrate the great advances in our
physical comforts from technology and medicine but they also
appreciate the advances in the sense of the fellowship of humankind
emphasized by postmodern thought. However, these transcending
individuals use phenomenology not only to unveil weaknesses but
also to appreciate that the shared subjective experiences of all
people provide a deeper understanding of the apt goals of human life.

Take, for example, this telling quote from this era's leading linguist,
Noam Chomsky: "If in fact man is an indefinitely malleable,
completely plastic being with no innate structures of mind and no
intrinsic needs of a cultural or social character, then he is a fit subject
for the `shaping of behavior' by the state authority, the corporate
manager, the technocrat, or the central committee. Those with some
confidence in the human species will hope this is not so and will try to
determine the intrinsic human characteristics that provide the
framework for intellectual development, the growth of moral
consciousness, cultural achievement, and participation in a free
community.""7

A Transcending Response for Psychiatry

Certain voices in psychiatry are similarly taking from modem,

postmodern, and even antimodern thought to reach a new synthesis.
The great exemplar is Karl Jaspers, who combined the rationalism of
modernity (expressed in the standards of psychiatric assessment)
with the central contribution of postmodernism, phenomenology. He
produced the first coherent study of methods of psychiatric reasoning
that emphasized their strengths, their weaknesses, and their apt
employment.'s

In such a way he could acknowledge the numinous aspects of

human nature-far more profoundly than the antimodernists-even as
he resolved misunderstandings that have led to the conflicts, indeed
imperialist wars, between modern and postmodern psychiatry. His
conception of psychiatry rested critically on several features of his
work: his defense of the study of the psyche in many different ways,
his commitment to science where science is appropriate, and his
defense of human beings as fundamentally free and radically
mysterious.

The influence of Karl Jaspers is obvious throughout this book. Its

fundamental aim is to provide a structure for the basic discourse of
this clinical discipline, and elements of modem, postmodern, and
even antimodern psychiatry can be found within it. We have
attempted to enlarge on his thought by further subdividing psychiatric
methods for study. However, exactly like him, we hold that faction in
psychiatry defeats its progress and must be transcended by
illuminating-indeed, making us all aware of-the methods psychiatrists
use to make sense of mental disorders. We consider fundamental the
perspectives of diseases, dimensions, behaviors, and life stories.

This book is more than an effort at classifying methods, resolving

data, and structuring the discipline in a reasonably effective way.
Specifically, we wish to combat the materialism of modernism and the
nihilism of postmodernism by emphasizing the ambiguity of
psychiatry itself derived from the mystery of the generation of
consciousness (see Chapter 1). Consciousness is the ultimate
experience of humankind on which the givens of our nature rest and
to which all of our social and personal interactions must be beholden.
Yet, as we repeatedly note, because we do not understand how it is
produced, we cannot claim to know its full potential.

Summary

The aim of this chapter has been to provide an orientation to the

sources of psychiatric factionalism-the issue second only to the mind-
brain problem obstructing the progress of this discipline. In fact, we
propose that the perspectives of psychiatry sketched out in the
previous chapter as ways of circumventing the mind-brain problem
are also methods of transcending the disarray of denominational
orientations in this field. They extract what is best from the modern,
postmodern, and antimodern expressions in psychiatry. In particular,
they attempt to address the form-versus-function standoff between
modem and postmodern psychiatrists by proposing perspectives in
which form and function vary in salience. Thus, in the disease
perspective, form is most dominant, expressed typically in terms of
symptoms, signs, and diagnosis; in the lifestory perspective, function
prevails as matters of conflicts of purpose and experience are
brought to light in explaining some aspects of mental distress and
disorder. All of which is simply to acknowledge the character of the
mind as a system-a place where events and purpose intertwine-in
which formal elements such as thoughts, moods, and perceptions
exist but interrelate functionally with aims, intentions, and drives.

We thus make a twofold claim for the perspectives of psychiatry.

They are both a means of circumventing the mind-brain problem in
making sense of mental disorder and a means of transcending-
indeed, resolving-the longstanding factionalism disrupting this
discipline. We now turn to explaining them one by one as methods of
reasoning, each with its own frame of reference, logical connections,
and sources of conviction. Only in that way can we hope to make our
twofold claim convincing.
Classification in psychiatry, as in any branch of medicine, is an effort
at matching patients to their presumed disorders-an enterprise from
whence effective investigations into common causes and
mechanisms can begin. However, with psychiatry, this effort raises
special problems. There is the usual difficulty in deciding how to
identify a disorder-what features of history, presentation, or cause to
use in differentiating one disorder from another. But as well, there is
some antipathy, occasionally rising to renunciation, for classification
itself in this discipline. Many psychiatrists feel that including a
condition under a psychiatric diagnosis is to judge it abnormal with
little or no more evidence than current prejudice. Others would go
even further, noting that the very idea that mental patients differ
among each other and in some categorical way from normal people
confronts a belief we all seem to share in the fellowship of
humankind. By this, they mean our sense of an abiding similarity of
sentiments among people, a belief in our common vulnerability to
misfortune and in the likelihood that we will feel and express our
difficulties in similar ways. This conviction provokes suspicion of
practices that cleave some people off into classes or categories of
mental disorders, labeling them in some way different-indeed,
pathologically different-from others.

The processes of classification and differential diagnosis must carry

a curse or bring stigma, it seems. Many enemies of these processes
point to the use of psychiatric terms, not as modes of understanding
and appreciation but as sophisticated forms of name calling (e.g.,
"He's paranoid," "She's hysterical," and "You're in denial"). Could we
not avoid these problems by abandoning categorical classification
and identifying psychiatric patients as troubled people whose
troubles, though varying in degree and in provocations, are
fundamentally all of the same kind? We should then be able to
understand each patient's difficulties as a natural response to a
specific ordeal and as well come to acknowledge and appreciate the
universal nature of human mental distress.

For all that one can appreciate the kindness motivating these
opinions, the claim that all psychiatric patients are the same, varying
only in what they have encountered and in the degree of their
disturbance, is an opinion that both oversimplifies the problem of
explanation and narrows the scope of psychiatric attention to those
individuals for whom such a claim could logically be defended. In fact,
we hold that to abandon differential diagnosis and classification is to
lose a convention and train of thought that has brought progress to
the understanding and treatment of abnormalities in other branches
of medicine. Unfortunately, one can despise and mistreat people for
many reasons and in many ways. If we categorize their disorders,
and think carefully about the implications of our methods, we can
minimize such harmful actions. However, even if we can agree to
accept the idea of diagnosis and classification in psychiatry as both
unavoidable and expedient, we do not solve either the problem of
stigmatizing by inclusion or the problem of finding a system of
classification that is coherent. In this chapter we shall address both of
these matters, approaching the issue of system first.

To classify psychiatric patients, one must confront the issue of their

constitution (i.e., their fundamental makeup). As mentioned in chapter
1, psychiatric disorders (problems of thought, mood, and behavior)
are not similar in kind. Some are the product of nature's power over
brains and bodies in a fashion identical to any medical disease. But
disordered mental states do not arise solely from that source, for
many are the product of human motivations, emotional and
behavioral disorders that emerge quite directly from a conflict
between what a person seeks in life and what reality delivers.
 No fundamental unifying conception can encompass all the
disorders that psychiatrists try to manage. Bioscience (most
thoroughly comprehended by molecular biology) is the foundation of
explanations in medicine, but psychiatric disorders derive from
several different foundations. Therefore, how to develop a
classificatory system that will help psychiatrists communicate with
each other about similar patients and at the same time take into
account the very different sources of human mental distress has been
a chronic and, it must be admitted, still incompletely resolved issue
today. The purpose of this chapter is to identify some of the basic
issues of classification itself and then consider how the present
Diagnostic and Statistical Manual of Mental Dis orders (DSM-IV),
which is the standard approach in the United States today, has coped
with these as well as with the problems inherent to psychiatry.'

Kinds of Categories

Categories differ in kind, and certain types of categories are

problematic if their conceptual foundations are not appreciated. By
kinds of categories, we mean not what is included in them, such as
symptoms or signs of disorder, but rather those distinctions between
categories that rest on the means of defining membership in the
category and, in particular, on how the criteria for membership are
assembled. The comprehensiveness of a category, its sense of unity,
and the ease of its communication depend especially on this last
characteristic.

Conjunctive Categories

The most satisfactory category, the conjunctive category,

accumulates its members by a "conjunction" of criteria. As an
individual is seen to hold progressively greater numbers of these
criteria, he or she is considered a member. The criteria are linked to
one another by the conjunction and, which permits the inclusion and
exclusion of individuals. Although the concept behind the category
may seem arbitrary, the criteria add together to clarify it. Thus, the
criteria for the category men (individuals of the male sex who are 18
years old or older) differentiate members of this category from infants,
boys, girls, and women. The term male sex can be expanded to
demand an XY chromosomal pattern and thus exclude a variety of
intersex individuals, if desired; but with each criterion the concept
becomes clearer and can be developed with increasing knowledge of
its elements.

Many medical categories are conjunctive in this sense. In fact, it is

on the hope of finding conjunctive categories of sick people that the
concept of disease rests. Thus we have the category measles, a
febrile illness, provoked by a particular virus, with an exanthem after
a known incubation period in an unimmunized individual. Each of
these characteristics is useful and necessary for defining the
members of the category more and more precisely until we are
confident that the essential characteristics are satisfied by the most
direct method: recognition of the infectious agent and the vulnerable
host. But the category, measles, is unambiguous from the start of our
observations, a condition in which a particular set of events occurs
regularly and for which some special agent common to all the events
and provocative of them is to be discovered.

Disjunctive Categories

Not all categories are conjunctive. There are disjunctive categories,

in which membership is given not on the basis of criteria that add up
to a more and more clearly defined example but on the basis of
criteria that allow the category to encompass a variety of rather
different individuals. A concept of membership lies behind the
category, but it is approached by criteria that can replace one another
in satisfying the requirements. Disjunctive categories have lists of
criteria linked by or rather than and. There is often considerable
debate about which criteria can replace others. Such a decision will
depend on the concept the category attempts to contain, which may
vary in its clarity among judges; the decision may eventually be made
arbitrarily.

A good example of a disjunctive category is the strike in baseball.

The batter is given a strike when he swings at a pitch and misses the
ball; or when he does not swing at a pitch that has passed over home
plate at a level between his knees and his upper arms; or when he
swings at a pitch and hits the ball, but the ball goes wide (foul) of the
ninety-degree arc between the first and third baselines; but only if he
has less than two strikes on record at the time, and so on.

Notice that there is a basic concept behind the category: namely,

the batter is penalized if he cannot hit the ball cleanly either when he
swings at it or when some judge (umpire) believes that it has been
pitched within his range. But it is a complicated category with much
sense of arbitrariness and is difficult to explain to someone
unfortunate enough not to have spent time contemplating this
pleasant game.

As you try to explain why a purposely bunted ball that runs foul
when the batter has acquired two strikes is called a third strike,
whereas other fouls in similar circumstances are not placed in the
count against the batter, you will appreciate at once why it may be
true that we abhor a disjunction as adding to the complications of our
study. In psychiatry, as in baseball, the effort at explaining the
disjunctive category often takes the form of repeatedly demonstrating
how any given criterion relates to the essential concept. An
opportunity to change a disjunctive to a conjunctive category is thus
usually welcomed.

There are many disjunctive categories in psychiatry, and most of

them have a similar awkwardness, sometimes to such a degree that
we wonder whether the category is real and useful, or arbitrary and
idiosyncratic. It is important to recognize that such questions of
category will remain even if the criteria can be easily identified and
reliably rated, because it is not so much the criteria themselves as
their collection and placement together as a category that are
questioned. A category is disjunctive whenever the criteria are
interchangeable, for example, when a category requires one criterion
from any three in group A, two from any six in group B, and none
from group C.

A good example of a disjunction in psychiatry has been the

category alcoholism. The traditional concept of alcoholism would
place in this category all those individuals who suffer or cause others
to suffer because of alcohol consumption. The or is already in the
definition. A person would by this definition be called alcoholic if he
drank enough to injure his health with cirrhosis of the liver; or if he
drank so much that he lost his job; or if he drank only occasionally,
but then to such a degree that he was arrested for dangerous driving.
These events would all constitute criteria for admission to the
alcoholism category, as already defined.

The category would have the utility of bringing together individuals

who stand in need of help with their drinking, but it might be
considered too broad, as it might encompass individuals with and
without physiological alcohol dependency (which could be another
category), or not broad enough, as it might overlook individuals-not
so uncommon, it turns out-who become so easily irascible and
aggressive when they drink even small amounts of alcohol that they
must learn to avoid it. Again, such arguments rest not on the reliability
with which the individual criteria can be identified but on the concept
behind the category proposed and for which these criteria are
collected.

A major portion of the difficulty in communicating and teaching in

psychiatry derives from the failure to appreciate the awkwardness
inherent in disjunctive categories and the regular need to explain
carefully the central concept behind a category, the features from
which it is constructed, and its utility. Disjunctive categories tend to
spring up and spread because they bring together under a single
term a variety of individuals otherwise difficult to classify. They reflect
the conceptual difficulty in the field. They must be used because we
have nothing better at the moment. But, their replacement with
conjunctive categories is usually sought; not only because an
element of arbitrariness may thereby be eliminated but also because
a hidden conjecture, wrapped in the original disjunction, may thus be
revealed.

Indeed, the disjunctive category of alcoholism has been confusing

when tied to questions such as whether alcoholism is a disease.
Because the category encompasses so many different phenomena, it
seems unlikely that all its mem hers will eventually prove to have an
identical condition. However, as we shall discuss more thoroughly in
the chapters on behavior, Griffith Edwards broke off a conjunctive
category-the alcohol dependency syndrome-from among those called
alcoholic and showed that the constancy of signs and symptoms
shared by all the members of that smaller group has a single cause:
psychological and pharmacological dependence on alcohol.2

The Diagnostic and Statistical Manual (DSM-III, -III-R, -IV)

The Diagnostic and Statistical Manual of Mental Disorders of the

American Psychiatric Association (abbreviated as the DSM) was first
organized as an effort to list the different disorders that psychiatrists
manage. In its early versions (DSM-I and DSM-II), it was simply a
classificatory list tied to the international classification system for
diseases and offered brief definitions of the disorders. Beginning with
the version published in 1980 (DSM-III), an effort was made to
provide the most up-to-date criteria-clear, distinct, and operational in
kind-employed by psychiatrists when they classified a patient as
suffering from a particular condition, such as schizophrenia,
dementia, antisocial personality, and the like. In this process, DSM-III
and the subsequent editions (DSM-III-Revised and DSM-IV) came up
against all the methodological problems inherent in psychiatric
nosology, including those that reflected some of the ideological
divisions in the discipline.

To be more specific, the disorders listed in DSM-111, like those of

DSM-I and DSM-II, were devised to reflect contemporary practice
concepts. With DSM-III and -IV the defining characteristics
considered suitable for each psychiatric diagnosis were first brought
up and then operationally refined by committees of experts. After
conceptual definitions had been reached by consensus, the
diagnostic categories-schizophrenia, dementia, and so on-that were
thought to capture these concepts along with the operational steps to
be followed in identifying a specific case were presented for use by
the profession. DSM-III was designed to be more than just an
updated version of its predecessors: its aim was to improve the
reliability of diagnostic practice in psychiatry by rendering the
definitions of the different disorders clear and then operationalizing
the identifying characteristics.

Reliability, not validity, is the primary goal of DSM-III (see the

appendix for a discussion of these distinctions). Certainly the hope is
that founding our diagnostic practice on reliable terms will encourage
investigations of these conditions and validate through research the
conceptions behind them. In fact, changes in classification from DSM-
III to DSM-IV represent some of the advances into the validation of
these diagnoses that occurred between 1980 and 1994. However,
these classifications still rest on present-day "consensus" about the
existence of such entities and not necessarily on proof. What DSM-III
and -IV provide are rules by which these presumed disorders can be
reliably recognized from occasion to occasion and from psychiatrist to
psychiatrist.

In this way DSM-III was an advance over DSM-11, but it also

illustrates the problems of a nosology for psychiatry, given that the
defining characteristics of psychiatric disorders are usually mental
events; the diagnostic categories are disjunctive in nature; and there
is little knowledge of mechanism and etiology to explain many of the
disorders, their differences from one another, and their natural
histories. Even "experts" can't get around these problems-and to
some extent the issue of who is an expert is itself a political decision,
as we shall discuss in relation to a few diagnostic entities forced into
the classificatory schema.

The Probabilistic Algorithm and DSM-III and -IV

As the authors of DSM-111 warmed to their task, they quickly came

to appreciate that the disjunctive character of most psychiatric
diagnoses represented a major obstacle to getting psychiatrists to
use them consistently and reliably. How could one have a reliable
method if the concept of a disorder were just as complicated as the
strike in baseball or, for that matter, such other disjunctions as the
characteristics of a citizen of a particular country? Idiosyncratic
conceptions of the disorder would arise from place to place in such a
fashion that a patient whose illness was called schizophrenic in one
center could well be called manic-depressive in another or even
simply "stressed out" in a third.

To get around this problem, improve the diagnostic reliability (such

that similar diagnostic terms would apply to similar patients from
place to place), and take into account differing opinions on the
fundamental features of certain disorders, the authors of DSM-111
chose a new method of approach, that of probabilistic algorithms, as
the best path for consensus. In this approach to diagnosis, an ill
person-X-is identified as an example of some conditionY-only if X
displays a critical sum of weighted features assumed by convention
to be manifestations of condition Y3

The DSM-III approach to diagnosis is probabilistic because it

assumes that particular patients with a given psychiatric disorder,
certain Xs of a Y, can have quite different signs and symptoms. Thus
(as it is often expressed in DSM-III), patients can qualify for the same
diagnosis if they have any three symptoms from group A, two from
group B, and none from group C. Such probabilistic rules define
specifically for each disorder what symptoms are acceptable for that
diagnosis, but they also permit different combinations of symptoms
from patient to patient within the diagnostic category (that is, several
different Xs all with the same Y)

That the DSM-III approach to diagnosis is algorithmic can be seen

in several of its features, two of which will be described here. First,
diagnoses are accepted or rejected after the summation of symptoms
by a prescribed formula. If the critical number of symptoms in an
acceptable combination is reached, the diagnosis is applied to the
patient. DSM-111 formulas are often impressive in their specificity and
multiplicity, but it is important to remember that the diagnoses they
produce reflect the conceptual conventions of present-day practice,
and do not on that account alone gain validation.

Second, the algorithmic nature of DSM-III is seen in its instructions

to give different weights to particular symptoms in a diagnostic
category. If, for a given disorder, three symptoms must be found from
a list of five in group A, but only two from a list of seven in group B,
then the symptoms of group A have greater weight in diagnosis. The
greatest weight comes from a single symptom that must be either
present or absent to permit a diagnosis to be made or excluded.
Many of the disorders in DSM-III are characterized by such weighting
of symptoms. Only if a prescribed sum is reached can a given
diagnosis be appropriately applied to the patient.

There are clear advantages to DSM-III's approach to diagnosis.

Because it begins with the concepts and conventions of the day, it is
likely to be accepted for general use by the psychiatric community.
The individuals it identifies as patients are similar to those individuals
psychiatrists recognize as patients, and the diagnostic terms-
schizophrenia, major depression, antisocial personality-it employs are
reassuringly familiar. Then, too, the use of the probabilistic algorithm
is a neat way to finesse the disjunctive aspect of many psychiatric
diagnoses. DSM-III embraces the disjunctive in that it provides the
rules by which a diagnosis can be reached through several different
collections of symptoms, even though the basic concept behind the
diagnosis may remain difficult to grasp.

The most important advantages of DSM-III are those derived from

its clarity and criterion specificity. The rules of diagnosis-that is, which
symptoms must be found and which must be absent-are prescribed,
and, if properly employed, the rules can produce reliable diagnoses
from place to place and occasion to occasion. Reliable diagnosis is
crucial to any further advance in psychiatric understanding, and DSM-
111 (like several other approaches that share its fundamental
method) provides the basis for such reliability. The strengths of the
probabilistic algorithm rest on reliability, and reliability is an essential
feature of any good diagnostic system. But it is over issues of validity
that categories must eventually be tested, and the validity of a
psychiatric category is not established by finding a reliable method to
identify it.

As one might imagine given that the whole work begins with expert
testimony, the diagnostic categories that are the conceptual
foundation of DSM-11I were conceived before the algorithms were
designed. The algorithms serve to facilitate the reliable collection of
phenomena that the experts assume to be the expressions of those
categories. However-and this is not a trivial matteralthough a
diagnosis can be replicated from occasion to occasion, demonstrating
that the method of reaching the diagnosis is a good one, this
replication does not validate the condition. Indeed, the probabilistic
algorithm approach to diagnosis can create problems of its own.

Consider the following: we wish to base clinical diagnoses on

phenomena that can be clearly discerned in the mental states and
behaviors of patients. But such phenomena are limited in number,
and thus there will be a tendency for them to appear in more than one
category. The probabilistic algorithm not only cannot eliminate this
fact, it is vulnerable to compounding it. If, for example, a patient
satisfies the algorithms for narcissistic personality disorder, borderline
personality disorder, and histrionic personality disorder-all quite
disjunctive concepts and all resting on operationalized but rather
similar mental states and dispositions-the claim that he or she should
receive all three diagnoses provokes a sense of being entrapped
rather than enlightened by the logic of our methods. How was he or
she unlucky enough to be afflicted by three different disorders? The
crucial question for overlapping categories is what is nested in what,
and the probabilistic algorithm does not provide a satisfactory solution
to that question. We cannot tell whether there are several different
conditions that are difficult to separate on clinical grounds, or simply
several different diagnostic terms and algorithmic approaches to a
single underlying entity. This ambiguity is one of validity, and it is
telling. If several diagnostic formulas are satisfied by a patient's
clinical presentation, what does that mean about the fundamental
nature of the disorder, its treatment, and its prognosis?

There are several other problems tied to the use of probabilistic

algorithms in DSM-III. The need for clearly defined quantitative
criteria may occasionally fail to capture those qualitative features of a
patient's presentation that clini cians can use to decide on a
diagnosis. As well, the number and complexity of the rules for placing
patients in one diagnostic group rather than another sometimes grow
unwieldy for anything but a computer.

But these are minor objections to a method of categorizing

conditions that is an advance on previous methods. The fundamental
issue is that the categories derived from any method, even the
reliable method of DSM-III, need a more objective validation than
agreement with current diagnostic conventions. Some of the most
problematic features embedded in DSM-III and -IV derive from the
political sources of the initiating agreements over diagnostic
conventions. What constitutes a disorder and whether that disorder
really should be considered a disorder at all are issues that have
roiled the committees of DSM-III right from its start. For example,
whether to put homosexuality into or take it out of the diagnostic
classification was perhaps the most ferociously argued question for
DSM-III. Note that the reliability of the criteria for identifying someone
as homosexual was not the issue here. The issue was whether this
aspect of a person's sexual behavior constitutes a disorder, as
inclusion in the DSM-III would imply.

Several other diagnostic algorithms in DSM-III and -IV also

functioned to legitimize-by expert testimony and reliable criteria, but
ultimately by rhetoric-diagnoses that remain to this day contentious in
their nature and thus their existence. Post-traumatic stress disorder is
one such condition and the historical background for its emergence in
DSM-III and -IV was well described by Allan Young in his aptly titled
book The Harmony of Illusions: Inventing Post-traumatic Stress
Disorder.4 Multiple personality disorder is another condition in which
a behavior, acting as if one had several personalities, was given
legitimacy as a distinct disorder through the agency of a group of
determined practitioners. DSM-IV shifted the diagnostic label to
dissociative identity disorder in an effort to find some safe place for it
among the psychological concepts of the present era. But this
disorder remains, as it always has been, a behavioral condition that
thrives on the attention doctors give it (see chapter 18).

Even with probabilistic algorithms-indeed, in part because of their

seemingly comforting formulas-the problems of psychiatric
classifications remain. In particular, the need for close study of these
conditions in order to validate some of them and reject others
remains critical and often is overlooked because of the formulaic
diagnostic system. Validating evidence for the nature and existence
of each psychiatric disorder must be sought in domainspsychometric,
neurobiological, genetic, and so on-other than the patient's signs,
symptoms, and history.
 The source of the regularities in clinical presentations must be
identified from knowledge of biological mechanisms, dimensions of
personality, motivated behaviors, and responses to life events. When
we know how psychiatric categories relate to these domains, we will
understand them as we understand many other conditions in
medicine, and we will be able to speak with more confidence about
the great questions: How do these disorders come about? What
exactly is the nature of this particular disorder? How is this or any
other disorder to be avoided? What is necessary to help or cure those
afflicted by them? How does life under these particular conditions
proceed? These are questions that lie beyond categorization and
nosology at the moment.

Summary

DSM-111 and DSM-IV represent advances in diagnostic practice. A

reliable categorization is an important step in reasoning from initial
construals about psychiatric conditions. But this advance is
precarious because a DSM-III or -IV diagnostic category is likely to
represent a convention wrapped in a convention-a negotiated
terminology and diagnostic pathway intended to encompass a group
of patients whose clinical presentations reflect a conventionally
construed condition. Only the methods of validation will confirm some
of these conventions and reject others and so move psychiatry and
its classificatory systems ahead.

For all these reasons, this book attempts to look beyond DSM-III
and -IV at the conceptions of disorder and their fundamental
distinctions, with which these classificatory schemes have tried to
grapple. This is not to denigrate the classificatory effort but to claim
that the diagnostic manuals we have today codify rather than resolve
some of the major problems of this discipline, problems that will not
be understood if the classifications were considered definitive or
conclusive.
The concept of disease operates on an diseases are afflictions in
which an abnormality of a bodily part provokes the affliction's
characteristic symptoms, signs, and course. This disease-provoking
bodily abnormality may be one of structure (such as tumors and
infarcts) or one of function (such as excesses or deficiencies in
neuronal activity or endocrine secretion). The symptoms and signs of
the patients with a disease often indicate the nature of the bodily
abnormality, but the analysis of blood chemistries, radiological
images, electrocardiograms, and so forth, is usually necessary to
specify it.

Disease reasoning, in fact, combines a categorical method for

differentiating human afflictions, ultimately distinguishing them by
their underlying abnormalities (cardiac failure, hyperthyroidism, peptic
ulcer, etc.), with a coherent, well-marked path for tracking down their
causes (infection, vitamin deficiency, genetic mutation, etc.). The
categorical and explanatory aspects of disease reasoning operate in
tandem as a progressively clearer differentiation and understanding
of a disorder emerge.

For some students of psychiatry, the term disease is used

nonspecifically to identify almost any recognizable pattern of mental
or behavioral complaints. Such usage-as when the word is seen as a
compound of dis and ease and thus synonymous with discomfort-fails
to identify how disease reasoning applies to certain clinical disorders
and not to others.

For psychiatry, where stereotypic collections of mental and

behavioral symptoms are in need of explanation, and some of the
collections are diseases and some are not, this failure is particularly
problematic. It slights an approach that has brought clarity to general
medicine, and it sustains the amorphous, undifferentiated conceptual
structure of psychiatry that hinders the field's progress. Hence there
is a need for the review of the basic concept and in particular of the
stepwise logic that disease reasoning encourages for specifying the
bodily abnormalities and provocative etiologies underlying clinical
presentations in medicine generally and in psychiatry specifically.

A Brief History of the Concept

Although the term disease has a usage in which the concepts of

disorder, illness, and distress tend to mingle, the conceptual
approach that directs modem medical practice is customarily
attributed to Thomas Sydenham, a seventeenth-century English
physician who advanced an effective approach to identifying and
classifying clinical disorders. He urged physicians to make careful
observations of patients and particularly to note how the symptoms of
their illnesses unfolded so as to differentiate one from another
according to its nature.

Sydenham taught that symptoms customarily come in recognizable

clusters and that the course of development and remission of these
clusters is the best means of studying them and predicting the
outcome for a patient. He spoke of his work as would a naturalist:

In the first place, it is necessary that all diseases be reduced to

definite and certain species, and that, with the same care which we
see exhibited by botanists in their phytologies; since it happens, at
present, that many diseases, although included in the same genus,
 mentioned with a common nomenclature, and resembling one
another in several symptoms, are, notwithstanding, different in their
natures, and require a different medical treatment....

Something in the way of variety we may refer to the particular

temperament of individuals; something also to the difference of
treatment. Notwithstanding this, Nature, in the production of
disease, is uniform and consistent; so much so, that for the same
disease in different persons the symptoms are for the most part the
same; and the selfsame phenomena that you would observe in the
sickness of a Socrates you would observe in the sickness of a
simpleton. Just so the universal characters of a plant are extended
to every individual of the species; and whoever (I speak in the way
of illustration) should accurately describe the colour, the taste, the
smell, the figure etc., of one single violet, would find that his
description held good, there or thereabouts, for all the violets of that
particular species upon the face of the earth.5

This method of discriminating diseases by their characteristic

symptoms and course, so familiar to us now, had enormous
consequences for medical practice. As Henry Sigerist observed of
Sydenham:

Like Hippocrates, the basic principle of his medical thinking was the
humoral pathology, and like Hippocrates his general outlook upon
illness was that it was a natural healing process. Nevertheless there
lay a whole world between the two. The decisive difference between
them becomes plain in respect of their divergent outlook upon
illness as soon as they quit the domain of the general. Hippocrates
recognized only disease, not diseases. He knew only sick
individuals, only cases of illness. The patient and his malady were
for him inseparably connected as a unique happening, one which
would never recur. But what Sydenham saw above all in the patient,
what he wrenched forth to contemplate, was the typical, the
pathological process which he had observed in others before and
 expected to see in others again. In every patient there appeared a
specific kind of illness. For him maladies were entities, and his
outlook upon illness was, therefore, ontological. Hippocrates wrote
the histories of sick persons, but Sydenham wrote the history of
diseases.'

With Sydenham's teaching and influence came the modern medical

capacity for identifying and differentiating particular diseases. This
power opened the pathway and naturally evoked an interest in
physicians for discerning the mechanisms and causes of these
conditions that they could now separate and identify. The next
advance in the modern conception of diseases was led by the efforts
of Giovanni Battista Morgagni, an eighteenth-century Italian physician
who was the pupil of the anatomist Valsalva and successor to the
chair of Vesalius. Morgagni, more than anyone else, inaugurated the
method of clinicopathological correlation-the tying of particular clinical
signs and symptoms (Sydenham's identifying markers) to particular
pathological changes in the tissues of the body. This
accomplishment, according to Sigerist, "is what lifts Morgagni's works
up to so high a plane; is what gives their author an epoch-making
importance.... A symptom is no longer something that hangs vaguely
in the air. It is tracked down in the organism, is referred to the organs
upon whose disordered functioning it depends. Symptoms, symptom-
complexes, diseases, are strictly associated with the various organs.
Thus the conception of diseases as entities was strongly fortified."7

The identification of objective pathology through clinicopathological

correlation proved to be the springboard for the final conceptual step
in the modern mode of disease reasoning: the launching of a search
for causes, those etiological agencies provoking pathology in the
organs of the body. The study of anthrax by Robert Koch, a
nineteenth-century German physician, epitomizes this final step.
Koch not only extracted the anthrax bacillus from the inflamed tissues
of afflicted patients but also devised the fundamental rules by which
infectious diseases are to be discovered. Sigerist noted that with the
work of Koch and Louis Pasteur, "the infectious disorders had lost
many of their terrors. They were better known than they had ever
been before. They could, as it were, be seen face to face. The
struggle with them had become an open one. If we know our enemy,
we have far less reason to dread his power. That is why cancer is so
sinister, because it is an unknown adversary, one of whose nature we
still know little or nothing, so that we cannot attack it at the root. Most
of the infectious diseases, however, have now yielded up their
secrets. By the time of Koch's retirement from active work, it was
known, in the case of most of them, which was the best line, the best
point, of attack."s

The linkage of clinical presentations, pathological processes, and

etiological agents thus represents the deep intellectual contribution of
the pioneers of modem medicine. We now turn to the specifics of this
method to make its features clear and distinct for psychiatry.

Disease as a Conceptual Approach to Explanation

A disease is not a tangible thing; it cannot be observed apart from

its instances. Its essence is both conceptual and inferential. As a
concept, it rests on the proposition that a group of people who are
identical in such attributes as symptoms, signs, and laboratory
findings may be usefully viewed as sharing some biological
abnormality designated a disease. This criterion of abnormality
fundamentally distinguishes them as a group from patients with other
clinical attributes and from healthy people.

The diagnostic process tied to disease is an inferential exercise in

observation, differentiation, and classification. It culminates in the
decision to apply the term for the inferred common abnormality, the
disease, to the condition afflicting a particular patient. The
identification of some underlying abnormality of a bodily part-for
mental disorders more specifically some abnormality of the brain-
validates the assumption, derived from symptomatic appearance, that
the disorder is a disease.

This exercise in differentiation and validation proceeds stepwise

from the initial recognition of symptoms to the end point of defining a
cause for them. Thus, a relatively stereotyped collection of
observable signs and symptoms in the patient's presentation
identifies the clinical disease entity and distinguishes it from other
disease entities and from good health. From that beginning is
launched a search for the pathological change in the body, for the
cause of this change, and, of course, for treatments that can correct
or prevent this change. These steps can be represented in
operational terms.

Three-Step Approach

Disease categories can seem like sterile taxonomic exercises when

treatment is the aim and causes have yet to be found. But disease
reasoning focuses attention on the observable, and progress comes
in the three stages of identifying symptoms, linking the symptoms to a
pathology, and arriving at a cause.

Through documenting a patient's clinical history, conducting a

physical and psychological examination, and observing the progress
of symptoms over time, the physician can assess just how closely the
patient resembles other patients with similar symptoms and signs. We
can decide, particularly if the patient demonstrates some of the
cardinal or "defining" characteristics, that he or she is afflicted with a
clinical "syndrome" or clinical disease entity.`' Conditions such as
congestive heart failure and epilepsy are clinical syndromes in
general medicine with defining characteristics, whereas delirium,
dementia, manic-depressive illness, and schizophrenia are clinical
syndromes in psychiatry with their own particular characteristics.
 The ability to localize pathologies to bodily systems, organs,
tissues, cells, and now genes has permitted a further step in
reasoning from the clinical entities. As observations from the
pathological disciplines accumulated, it became evident that a
particular clinical syndrome could be the common expression of
several quite different bodily pathologies. For example, the symptoms
of congestive heart failure can be the clinical expression of infarction
of cardiac muscle, stenosis of the cardiac valves, constriction of the
pericardial lining, or a hyperactive thyroid gland (figure 2).

Although in each of these conditions the symptoms of congestive

failure can be recognized clinically, the identification of different
pathological mechanisms permits a designation of a variety of
specific pathological disease entities10 and allows a more rational
basis for prognosis and treatment. In fact, treatments that are
effective for some patients fail for others with seemingly identical
symptoms because of the pathological differences that underlie
clinical similarities. The defining criteria for a disease entity move with
this progress in knowledge from the stereotypic symptom clusters to
those identified features of abnormal bodily structure or function,
discerned through objective clinical laboratory techniques such as X
rays, biopsies, blood tests, EKGs, and EEGs. One speaks then, for
instance, less of congestive failure and more of mitral stenosis and its
complications that include congestive failure.
 FIGURE 2. Congestive heart failure.

Finally, based on pathological evidence, clinicians naturally begin to

ally themselves with basic biological scientists-geneticists,
microbiologists, neurochemists, neurophysiologists-in an effort to
discern the mechanisms and the provocative agencies that cause
these pathologies. (It has been said often that disease is an
"experiment of nature" in the sense that by disrupting some particular
capacity of the healthy organism, disease reveals the biological
underpinnings of physical and mental capacities. Disease thus
provides a comprehension of normal as well as abnormal biological
functioning. Notice that coronary artery disease provides an
appreciation of the role of coronary arteries in sustaining oxygen
supply to heart muscle just as it explains the course of cardiac
ischemia. For this reason, cardiologists ultimately become experts not
only in diseases of these coronary arteries but also in their
physiology. Similarly, a neuropsychiatrist after studying amnesic
patients often becomes an expert in the different aspects and
mechanisms of normal memory.)

Truly rational treatments, that is, treatments that do more than

ameliorate symptoms, can emerge only with the complete
understanding of the cause (etiology) of the pathological process.
Only through understanding how genes, bacteria, viruses, and so on,
can act to injure the structure or the function of the organ systems of
the body-and for mental disorders the brain more specifically-can we
claim that we know a disease through and through. Then measures
against gene action, against infectious processes, and against
biochemical states can proceed with our clear understanding of the
targets of the treatment and the expectations of outcome. Ultimately,
prevention-even though quite possible before all aspects of the cause
of a disease are graspedis best directed by the appreciation of the
etiology of the disease and the action of this etiology on the body.

In summary, diseases are the expression of biological changes that

can be understood as processes of nature. In figure 2 this concept is
diagrammed for congestive heart failure. With the appreciation of the
pathological entity constrictive pericarditis, for example, we
appreciate the role of tuberculous infection (cause) and the
inadequacy of ventricular filling (mechanism) behind the congestive
failure symptoms of the patient.

The strength of the disease reasoning-its focus on knowledge and

directing investigation in a search for hypotheses, theories, and laws-
is obvious. It begins with the most accessible and reliable
observations and then organizes them into the first approximation of
a classification. Success, usually first revealed by better prognostic
ability, encourages further study and ultimately leads to an
explanation of the disease and a rational basis for its treatment and
prevention.

Disease Reasoning in Psychiatry

The disease concept works in psychiatry just as it does in general

medicine. It proceeds in distinct stages of identification and
explanation. The first step, the recognition of a clinical syndrome, is
the identification of a characteristic cluster (syndrome) of
psychological signs and symptoms occurring in many patients. The
second step begins the process of explanation by correlating a
particular neuropathology with that syndrome. The search for a
neuropathology follows clues tied to the symptoms or signs of the
syndrome and relies on both clinical and laboratory efforts to identify
the nature, extent, and localization of the process in the brain. The
final step, the discovery of an etiological agency, is directed by the
emerging neurosciences reflected in such phenomena as
neurotoxicity, genetic mutation and its influence on neuronal
development and degeneration, neuropharmacology, and so on.
Once again, disease reasoning offers the promise of discovery and
ultimately of rational prevention and cure.

Strengths and Weaknesses of the Disease Concept Applied in

Psychiatry

Several obvious strengths of the disease concept make it a most

suitable beginning for the study of explanatory methods in psychiatry.
First, the entity or ontological approach (clinical syndrome-
pathological process-etiology) is familiar to most students of medicine
(figure 3). Second, the concept produces testable models in the
sense that it proposes a steplike path that can direct or redirect study
and in the past certainly has led to new knowledge. Third, the
concept encourages research and does so in an essentially clear and
linear fashion that tests the initial hypotheses and leads to discovery.
Fourth, the concept encourages ties to scientific disciplines and is
thus supportive of collaborative efforts between physicians and basic
scientists.

Several weaknesses of disease reasoning also need to be

appreciated. First, because of its emphasis on entities afflicting all
who have the hypothesized condition, this approach may neglect to
consider the individual and his or her unique vulnerabilities to
distress. Second, a proposed disease model to explain some form of
distress can be endlessly refined when research fails to confirm some
expected finding in pathology or etiology. The method thus can resist
refutation and run on the promise of future confirming information in a
speculative fashion. Third, the disease concept provokes the
temptation to presume a brain source for all matters of mental
distress-a twisted neuron for every twisted thought-and thus functions
in an imperial fashion within the discourse of psychiatry, dismissing
other themes of explanation.

This potential for overapplication also has clarifying ramifications.

Once disease reasoning is clearly understood, it is apparent that
biological science contributes more to psychiatry than simply its
evocation of disease reasoning. Biological foundations to personality
and to mechanisms of behavioral control will be subsequently
described. Thus, although all psychiatric disease-as with any
disease-rests on biological foundations of pathology and etiology, not
all biological sources of mental disorder emerge as diseases.

FIGURE 3. Disease perspective.

Summary

The concept of disease has a history in modern medicine and

functions as a means of categorizing conditions and studying them.
This method of reasoning about disorders has considerable value in
psychiatry, given that several psychiatric disorders are best
comprehended as diseases. Like all explanatory methods, disease
reasoning has clear advantages and disadvantages. It belongs
among the perspectives of psychiatry because of what it does but
also to distinguish it from other ways of explaining mental disorders.
In the following chapters we consider those conditions best
approached from the disease perspective either because their
pathological mechanisms and etiological sources are known or
because their presentations are so stereotyped from patient to patient
that a search for pathologies and etiologies seems apt.
The psychiatric conditions that best exemplify reasoning from disease
are those for which knowledge has extended far enough to permit
correlations between mental and neuropathological changes.
Illustrations of such conditions are the clinical syndromes dementia,
delirium, Korsakoff psychosis, and aphasia. Despite differing
presentations and neuropathologies among the disorders, the
disease concept provides an appropriate method of reasoning for
each of them. In each disorder a specific psychological function is
impaired, a deficit that permits the entity to be recognized and
differentiated from other conditions. With the identification of the
deficit, correlations between the clinical syndrome and particular
pathological states in the brain can be discerned, and in many
instances the clinicopathological correlation has opened the
syndrome to etiological study (see table 1).

Dementia

Dementia is distinguished from other mental disorders by three

characteristics. First, the patient presents evidence of a significant
decline in intellectual power from a previously established level. This
feature distinguishes the dementia syndrome from mental
subnormality, in which the disability is lifelong. Second, the patient
has in many aspects of intellectual life, including memory,
comprehension, and abstract reasoning. It is this global decline in
intellectual power that distinguishes the dementia syndrome from
other cognitive disorders, such as aphasia or Korsakoff syndrome, in
which the single mental functions of language or memory are affected
out of proportion to other capacities. Finally, the demented patient
shows no evidence of disturbance in consciousness. This last
characteristic differentiates the intellectual decline found in dementia
from that found in patients who are delirious.
 The characteristics defining this clinical syndrome are psychological
in nature. Dementia is thus a typical clinical syndrome in psychiatry,
and at this level of assessment nothing but the history and the mental
status examination is necessary to decide that the patient is
demented. The diagnosis is clinical and does not rest on the
discovery of a particular neuropathology. Once the psychiatric
syndrome has been recognized, however, the search for
neuropathology can be undertaken. This search is the next step both
in the diagnostic process and in reasoning from the disease concept.

Like all clinical syndromes, dementia has been associated with a

variety of pathological disease entities. These pathological processes
may be localized primarily within the brain or may affect cerebral
functioning secondarily. An excellent example of the
clinicopathological correlation inherent in the disease concept is
found in the work of Aloys Alzheimer.' At the beginning of this century,
Alzheimer found that some demented patients without obvious cause
for cerebral atrophy had microscopic changes in their brains (senile
plaques and neurofibrillary tangles) that could be reliably recognized.
Garry Blessed, Bernard Tomlinson, and Martin Roth demonstrated a
direct quantitative correlation between the dependent variable,
dementia, and the independent variable, the number of senile
plaques in the brain.2 While such changes in pathological anatomy
were being correlated with the clinical syndrome of dementia,
evidence was found for associated biochemical abnormalities. Thus,
for example, Elaine Perry and her associates reported that poor
cognitive performance and the number of senile plaques in the brains
of patients with dementia of the Alzheimer type are strongly
correlated with reduced cerebral levels of choline acetyltransferase,3
the enzyme involved in the synthesis of acetylcholine. The neurons
that carry much of the acetylcholine in the brain were then discovered
by Peter Whitehouse and colleagues to arise from the nucleus
basalis of Meynert and to have degenerated in Alzheimer disease.4
When Marshal Folstein and John Breitner used strict clinical criteria
for the diagnosis of Alzheimer disease, they found evidence for a
dominant hereditary transmission of the disorder.-5 Here, the
cumulative power of the disease concept is revealed as clinical
syndrome, neuropathology, biochemical abnormality, and genetic
etiology are interrelated and the direction of further research indicated
(figure 4).

With the recognition that distinct pathological disease entities could

produce the dementia syndrome, progress from identification to
explanation-a final step in the understanding of a disease-became
possible for some. In the dementia due to chronic subdural
hematomas, for example, the clinical syndrome, the responsible
neuropathology, and the etiological agency are evident, and a
particular treatment is clearly indicated. In other cases of dementia,
however, only the first two stages in reasoning from the disease
concept have been attained. Thus, in Pick dementia, though the
pathological disease entity is readily described, its cause is unknown
and its treatment palliative. There is even one type of dementia-the
type seen with the depression of manicdepressive illness-in which
there is still no evidence of cerebral dysfunction save the abnormal
mental forms themselves, yet even in that case the characteristic
clinical syndrome can be recognized and the process of
clinicopathological correlation begun.
 FIGURE 4. Dementia.

The occurrence of the dementia syndrome in the setting of manic-

depressive illness provides an interesting and controversial
application of the disease concept in psychiatry. Several
distinguished students of dementia have maintained that the global
decline in cognitive functions seen in some patients with affective
disorder should be called a "pseudodementia." The initial impetus for
this distinction arose from a desire to ensure proper diagnosis and
treatment for depressed patients, but its underlying assumption is that
"true" dementias occur only with demonstrable disturbances in the
brain's structure or metabolism. In manic-depressive illness no coarse
neuropathology or obvious pathophysiology has been regularly
demonstrated; following this reasoning, the dementia that sometimes
accompanies it must be not the real thing but only "the illusion of
involvement of the central nervous system."6

As we have said, dementia is best regarded as a clinical syndrome,

defined only by psychological features. Lack of knowledge about its
underlying pathology or cause should not exclude a given
presentation from the syndrome's compass if that presentation meets
appropriate clinical diagnostic criteria. This reasoning is fundamental
to the disease concept, in which identification and explanation are
separate stages. To say that a pseudodementia exists because there
is no demonstrable brain disturbance other than the syndrome itself
would be to say, if we turned the clock back seventy years, that
patients with petit mal epilepsy had pseudoseizures because no
anatomical changes had been found in their brains and because the
electroencephalogram, which eventually revealed a pathophysiology,
had not yet been invented.

We recognize that dementia may sometimes be simulated, as

paralyses or convulsions are, and that poor cognitive performance is
occasionally due to lack of motivation or to distraction; but to hold that
the dementia sometimes associated with depression is due only to
psychomotor retardation, for example, is to overlook the possibility
that the depressed mood, dementia, and psychomotor retardation are
all manifestations of the same underlying, but so far unidentified,
changes in the brain's functioning.?

Delirium

The mode of reasoning that uses the disease concept has also
been very helpful in our understanding of the clinical entities delirium,
Korsakoff syndrome, and aphasia. Delirium is that psychological
syndrome whose defining characteristic is impairment of
consciousness. By consciousness we refer to that dimension of
mental life that ranges from being fully alert to being comatose. We
chose the term consciousness for this characteristic rather than the
term attention because attention is an expression of consciousness
that can vary independently of it. One can be fully conscious yet
inattentive.

Since the days of Thomas Willis in the seventeenth century it has

been known that many pathological disease entities can produce
delirium,x but not until the 1940s was a mechanism suggested
through which states as different as hyponatremia and barbiturate
overdose, hypoxia and uremia, pneumonia, and head trauma could
act. George Engel and John Romano demonstrated a correlation
between the dependent variable-level of consciousness-and an
independent variable-cerebral pathophysiology-as reflected in the
slowing of brain activity recorded by the electroencephalogram.9
They found, in delirious states associated with many different
disorders, that progressive im pairment in consciousness was
attended by a progressive, diffuse slowing of the
electroencephalographic rhythms. This finding correlated a clinical
syndrome with a pathophysiological state rather than with a morbid
anatomy.

Several years later, Giuseppe Moruzzi and Horace Magoun

described the relationship of the brain stem reticular formation to the
activity of the electroencephalogram;10 thus, the disturbance of
consciousness found in delirium can be thought to depend on those
activating systems in the brain that maintain and modify arousal and
wakefulness. For delirium, as for dementia, the treatment and
prognosis are those of the underlying pathological disease entity. One
patient may be hypoglycemic from having taken too much insulin, a
condition that is readily treated and of generally excellent prognosis,
whereas another may be delirious from irreversible liver failure and
near to death.

Korsakoff Syndrome

Although memory is affected in the global intellectual decline

characteristic of dementia, it is much more specifically impaired in the
Korsakoff, or amnestic, syndrome. Here the characteristic
psychological deficit is in recent memory (the capacity to learn new
things), though recall of events prior to the onset of the illness is also
disturbed. Other cognitive functions (for example, abstract reasoning)
are often entirely spared, as are habitual skills such as reading and
writing. The essential preservation of cognitive skills unrelated to
memory distinguishes Korsakoff syndrome from dementia, and its
occurrence in clear consciousness differentiates it from delirium. The
memory loss is usually recognized from the history and mental status
examination, but psychological tests like the Wechsler Memory Scale
can be used both to document its presence and to follow its course.

Sergei Korsakoff, who recognized the syndrome in the late

nineteenth century, first described its occurrence in alcoholic patients,
though later papers documented its appearance in connection with
disorders characterized by persistent In the 1930s the role of
thiamine deficiency in all such cases was established, but the
identical psychological syndrome has also been found in association
with nonnutritional etiologies, such as bilateral infarction, infection, or
surgical removal of the hippocampal regions.

The correlation of psychological deficit and neuropathology is thus

anatomical because bilateral damage to the mammillary bodies, the
dorsal medial nuclei of the thalamus, or the hippocampi will all yield
the same clinical syndrome, whatever the etiology.12 Even if the
syndrome's cause is, like thiamine deficiency, completely reversible in
itself, once the structures just noted have been damaged, memory
loss may be permanent.

Aphasia

In aphasia, the final condition we will discuss to exemplify

psychological syndromes with known neuropathologies, the deficit is
in language. Though we often identify language with speech, the
aphasic patient's difficulty is not with the production of sounds
(aphonia) or the articulation of words (anarthria) but with language
itself, and it is a difficulty that can be reflected in the comprehension
as well as the expression of language, whether that language be
spoken, written, or communicated by gesture. Further, the
psychological deficit in aphasia affects propositional language
primarily, for even patients bereft of symbolic speech may be capable
of emotional expression.
 As in the amnestic syndrome, the psychological deficit in aphasia
emerges from localized brain pathology, and, again as in the
amnestic syndrome, that pathology can be of a variety of types (for
example, infarction, tumor, or abscess). The first descriptions of
clinicopathological correlations for aphasia are among the classics in
medicine, for they not only reveal aspects of language function but
also demonstrate that certain psychological capacities are dependent
on specialized regions of the brain. In the late nineteenth century,
Paul Broca and Carl Wernicke described the types of aphasia that
still bear their names. Broca observed that damage to the posterior
part of the left inferior frontal convolution leads to a particular difficulty
in spoken speech (called expressive, motor, or nonfluent aphasia),
though comprehension of language is relatively intact; 13 Wernicke
found that damage to the left angular gyrus of the temporal lobe
produces not only abnormal speech but also disruptions in the
comprehension of spoken and written language (receptive, sensory,
or fluent aphasia).14 Treatment and prognosis, as in other clinical
syndromes, depends on the underlying neuropathology; if that is
reversible, so is the aphasia.

For each of the conditions so far described, the appropriateness of

the disease concept should be clear. Dementia, delirium, Korsakoff
disorder, and aphasia all represent clinical syndromes distinguished
by their psychological features. It is the clustering of particular signs
and symptoms that identifies the syndromes and separates them
from one another, even though several syndromes may share a
symptom; for example, recent memory loss occurs in dementia,
delirium, and Korsakoff disorder. Once these syndromes were
identified, the process of explanation could begin, and for each a
variety of patho logical disease entities and etiological agencies has
been demonstrated. The process of explanation continues for all of
these conditions, however, because in many cases etiologies are
unknown and in all cases the brain-mind disjunction obscures the
mechanism whereby a particular brain lesion yields a certain
psychological effect.
 The clarity derived from the systematic application of the disease
concept to these entities leads us to deplore the practice of using the
term organic brain syndrome for any one of them. This practice
cripples diagnostic reasoning rather than advancing it. It inserts a
vague and essentially tautological reference to neuropathology into
the first stage of assessment.

There is more than one kind of mental disorder derived from

"organic" brain pathology. We have described dementia, delirium,
Korsakoff syndrome, and aphasia, but there are as well such others
as regional brain syndromes, pathological mental subnormality,
epileptic twilight states, and some symptomatic psychoses that we
will discuss later. Each of these conditions is organic but clinically
distinct from the others, and each has its own set of neuropathologies
and etiologies.

The specific terms dementia, delirium, Korsakoff syndrome, and so

forth, should be employed in the diagnostic formulation, thus keeping
distinct the differences among them in their presentations and
neuropathologies. To use the term organic brain syndrome when
dementia is meant obscures these distinctions and short-circuits the
process of clinical reasoning.

The Expression of Disease in the Individual

In this chapter we have shown that reasoning about diseases is

reasoning about forms. The discovery of a disease entity begins with
the recognition of a regular cluster of signs and symptoms occurring
in patient after patient. Thus, all demented individuals show a global
decline of cognitive functioning in clear consciousness. In each of
these patients, however, the total clinical picture will be somewhat
different, for in addition to the hallmark phenomena of the disease
there are others that reveal the individual's reaction to it. Diseases
are events experienced by persons, so in addition to fundamental,
stereotyped, and pathognomonic phenomena there are also
personal, variable, and pathoplastic ones. The disease is a part of the
patient's life story, and the patient responds to it as he or she does to
other crucial issues. Some responses will resemble those of other
patients of a given age, sex, socioeconomic class, occupation, and
personality, but many will be unique to the individual and will depend
on the particular meanings that the illness holds for him or her.

The reasoning from the disease concept draws our attention to the
objectorganism side of human beings and to the form of their
afflictions. In the process, though, we may identify the patient with the
disease, as if uttering its name were equivalent to uttering the
patient's name ("That's the dement in room seven"). Even in the midst
of disease, however, the patient remains a subject-agent, who thinks,
feels, intends, and behaves in response to the disease and to many
other things besides. It is often difficult to help a beginner see the
form of disease in an individual's unique presentation; it is sometimes
just as hard then to appreciate the responses derived from the impact
of disease on the individual's life story. Someone can be both
demented and demoralized.

Summary

This chapter identifies those mental disorders tied to

neuropathology and emphasizes the two interlocking aspects of the
disease perspective. The specific clinical entities-dementia, delirium,
and the like-provoke a search for their underlying pathologies and
etiologies. But, as well, table 1 listing some of the most salient
functions of the brain emphasizes disease as an "experiment of
nature" by demonstrating that each of these functions can be
separately injured with the implication that they are to some extent
separately organized in the brain itself. A study of these particular
psychiatric disorders can thus advance our knowledge of the forces
of nature that can injure the brain but also illuminates avenues of
investigation that may reveal how the brain is organized so as to
produce normal mental life.
 We close by emphasizing that any disease is a life event for the
individual and will therefore be expressed and even experienced
differently from patient to patient depending upon his or her individual
characteristics. In this way we emphasize that in clinical practice the
perspectives of psychiatry are not to be used exclusively of one
another but in combination. Our understanding of disease and its
course need not blind us to the life story source of the psychological
responses of the patient who suffers from it.
There are psychiatric conditions for which the disease concept is
deemed apt but which can as yet be described only as clinical
syndromes that remain invalidated by the discernment of underlying
pathological entities or etiological agencies. When faced with such
conditions, we must be clear about our terminology, not only because
we lack the corrective and confirming influences of morbid anatomy
and physiology but also because we must depend, to a degree that is
disconcerting in modern medicine, on our skill at differentiating
mental experiences from one another and at evaluating their
significance and relationship to the course of illness. Here more than
elsewhere our reasoning and its terminology can lead us astray.

Many patients who consult psychiatrists come because new,

disturbing, and uncontrollable mental experiences have intruded into
their lives. It appears as though a process expressed in moods,
thoughts, or perceptions has disrupted what had for them been an
integrated system of capacities and emotions. This process has
rendered many of their psychological experiences ineffective or alien.
Some of these patients, who also demonstrate paralyses or sensory
losses, can be recognized as suffering from pathological conditions
that disrupt brain function, and we appreciate their mental changes as
other symptoms of that pathology. But there are also patients with
similar mental symptoms for which a clear pathology cannot be
found. What of them? In the absence of demonstrable somatic
change, why use the disease concept rather than another'?

Disease denotes disruptions of the organism and of some part of it

in particular. In general medicine the symptoms indicative of
disruption are the appear ance of something unusual, such as pain,
or the disablement of some natural function, such as temperature
control (fever). Similarly, in psychiatry the construal of a disease is
prompted by evidence of the breakdown of normal capacities, such
as intelligence and consciousness, or by the appearance of new
forms of mental phenomena, such as hallucinations (perceptions
without stimuli) or delusions (fixed, false, idiosyncratic beliefs).

Again, in using the term form we refer to particular kinds of mental

activity, such as thinking, dreaming, perceiving, and calculating, as
well as to the connections linking perceptions with emotions or one
thought with another. All of these forms, or kinds of mental activity,
can be usefully distinguished from their content, that is, what the
individual is dreaming or thinking about or what specific perceptions
led to what particular emotional response.

Although many people seek psychiatric attention because of a

disturbance in mental content (for example, demoralization after
failure or anxiety with uncertainty), it is the patient with new and
unusual forms of mental experience who is most in need of an
explanation that goes beyond our appreciation of him or her as a
distressed subject. Thus, if the disturbance takes the form of
hallucinations, regardless of what the patient hallucinates about, that
experience of perceptions without stimuli must be explained. Other
disruptions in the form of mental life include delusions, the loss of
connections between thoughts (formal thought disorder), and
disturbances in the congruity of mood and behavior. The opinion that
these phenomena represent symptoms derived from disorders in the
organism is compelling, especially because identical phenomena are
provoked by conditions whose origin in brain dysfunction has been
discovered.

These changes in the forms of mental life are often called psychotic
phenomena, and the conditions in which they occur are called the
psychoses. But psychosis and psychotic are terms intended simply to
indicate that mental life has been disrupted in its capacities or forms;
they are ambiguous as to the degree and kind of that disruption. In
this way, psychosis is the modem equivalent of insanity, which had
itself replaced lunacy in professional and polite usage. Each of these
words indicates the disruption of mental life by a process that brings
new forms of psychological experience.

The term psychosis is thus broadly categorical and includes

subgroups within it. Dementia and delirium are psychoses because
they are characterized by disturbances in intellectual capacity and
consciousness. Affective disorder and schizophrenia are psychoses
because they disrupt the form of mental life with incomprehensible
moods, delusions, and hallucinations.

Occasionally the term psychosis is given a more special meaning, a

practice that we deplore because it usually renders vague what could,
with specific terminology, be clear. Thus, psychotic may be taken as a
synonym for schizophrenic, though the latter term is preferable
because there are many psychotic individuals (delirious people,
manic people, and so forth) who are not schizophrenic. When used
instead of delusional or hallucinated, psychotic obscures important
differences in psychopathology. Finally, the term psychotic can be
employed to mean intensely disturbed. This usage often carries the
hidden theoretical implication that all mental difficulties are a
continuum, with neurotic states approaching and becoming psychotic
ones as disturbance increases. If psychosis is merely a synonym for
severity, however, the distinctions possible between categories of
disorder may be lost, and with them clues to mechanism and etiology.
 In the next two chapters we discuss those conditions that appear
with incomprehensible moods, delusions, or hallucinations and as yet
lack a confirmed explanation as diseases. These syndromes, manic-
depressive illness and schizophrenia, are sometimes called functional
psychoses implying that they find purpose and meaning from an
individual's life. These functional psychoses are then contrasted with
organic ones, such as delirium and dementia, in which pathological
mechanisms and etiological agencies have been demonstrated.
However, psychiatric syndromes with and without recognized brain
pathology were noted in 1758 by William Battie, who wrote of
"consequential" and "Original" madness:

First then, there is some reason to fear that Madness is Original,

when it neither follows nor accompanies any accident, which may
justly be deemed its external and remoter cause. Secondly, there is
more reason to fear that, whenever this disorder is haereditary, it is
Original. For, altho' even in such case it may now and then be
excited by some external and known cause, yet the striking oddities
that characterise whole families derived from Lunatic ancestors,
and the frequent breaking forth of real Madness in the offspring of
such illconcerted alliances, and that from little or no provocation,
strongly intimate that the nerves or instruments of Sensation in such
persons are not originally formed perfect and like the nerves of
other men. Thirdly, we may with the greatest degree of probability
affirm that Madness is Original, when it both ceases and appears
afresh without any assignable cause.... Original Madness, whether
it be haereditary or intermitting, is not removable by any method,
which the science of Physick in its present imperfect state is able to
suggest. But altho' Original Madness is never radically cured by
human art, its ill-conditioned fate is however a little recompensed
sometimes by a perfect recovery, sometimes by long intervals of
sanity, without our assistance and beyond our expectation. Besides
Original Madness is in itself very little prejudicial to animal life....
Madness, which is consequential to other disorders or external
causes, altho' it now and then admits of relief by the removal or
 correction of such disorders or causes; yet in proportion to the force
and continued action of such causes, and according to the
circumstances of the preceding disorders, it is very often
complicated with many other ill effects of those causes and
disorders; and, tho' it may not in itself be prejudicial to bodily health,
any more than Original Madness, yet by its companions it becomes
fatal or greatly detrimental to animal life.'

That manic-depression and schizophrenia share many attributes of

Battie's "Original Madness" is clear, but in calling them functional as
opposed to organic disorders we should be wary not to conclude that
a neuropathology is nonexistent or that these disorders are produced
by some disturbance in the integrative "functioning" of the brain or
mind, perhaps entirely caused by psychological factors. Cryptogenic
or idiopathic might be better adjectives than functional, for manic-
depression and schizophrenia are major mysteries in medicine. They
are mysterious because although they provoke dramatic and
disabling symptoms, we know less about their causes or
mechanisms. We can recognize them, predict something of their
course, and symptomatically treat patients with empirically derived
methods, but neither rational therapy nor prevention is yet possible.
The relative stereotypy of symptoms and course has prompted
application of the disease concept to their study, but manicdepression
and schizophrenia so far remain clinical entities without pathological
mechanisms or etiological agencies that can be confidently assigned.

As a brief historical review makes apparent, even the recognition

and differentiation of these conditions have been problematic.

A Historical Note on Manic-Depression and Schizophrenia

The histories of the concepts of manic-depression and

schizophrenia are inextricably entwined. It is impossible to write of
one and not the other, and it is difficult to avoid turning a background
note on these conditions into a history of psychiatry.
 It is common teaching that Emil Kraepelin first separated manic-
depression and schizophrenia. The earlier masters-Philippe Pinel,
Jean-Etienne Esquirol, Wilhelm Griesinger, and Henry Maudsley-did,
however, recognize two clinical aspects of severe insanity: one
characterized by disturbed emotions (affectional insanity), the other
by disturbed thoughts and beliefs without a prominent change in
mood (ideational insanity). These leaders taught that affectional
insanity tended to have a periodic character in which depressed and
exalted moods could alternate and that it might completely remit, but
they also held that many patients with affectional insanity would go on
to develop ideational insanity as the second stage of an illness, the
stage at which it appeared in its incurable guise. Griesinger was
particularly insistent in his opinion that insanity is one disorder with
several stages (Einheitpsychose), in which the affective disorder
constitutes the first and recoverable form and the ideational illness
appears "only as consequences and terminations of the first, when
the cerebral affection has not been cured."2

Griesinger, whose Mental Pathology and Therapeutics (1845) can

still be read with pleasure, divided insanity into melancholia, mania,
monomania, and dementia, any one of which could be partial or
complete. Each of these was conceived of as a symptom cluster that
the disease, insanity, could assume at different periods in its course,
although every patient did not experience the whole course with the
same clusters or cluster order. With this approach Griesinger hoped
to avoid a meaningless proliferation of psychiatric entities based on
individual cases.

It may be that Griesinger and his contemporaries were encouraged

by their knowledge of the syphilitic condition, general paresis, to look
for a succession of stages from early affective change through to
dementia more broadly among psychiatric patients. But as the
syphilitic condition became steadily better understood as having a
particular neuropathology (chronic meningoencephalitis) and a
distinct etiology (syphilitic infection), it could no longer be employed
as suggestive of a unitary view of depressive and cognitive
progression where no such neuropathology was found.

The French psychiatrists Jean Pierre Falret and Jules Baillarger,

concentrating on "affective insanity," further crippled the concept of a
unitary condition by describing remissions and relapses in the course
of melancholic and manic conditions that they calledfolie circulaire
orfolie d doubleJbrme. They documented that this intermittent insanity
did not end in a continuous illness but was characterized by periods,
some apparently permanent, in which full health was restored.

Kraepelin recognized the implications of these developments for

concepts of mental illness, particularly the one he labeled manic-
depressive insanity, a term used to include under one disease entity
circular insanities, simple manias, melancholia, and even those
conditions in which more minor disturbances in mood occurred in a
periodic or continuous way without obvious relationship to a patient's
experiences.3 The common bond he saw in all forms of this entity
was a uniform prognosis: manic-depressive insanity never led to a
profound deterioration of personality or thinking, not even when
attacks continued for many years. Rather, all morbid manifestations
could completely disappear, either between attacks or permanently
after a series of them.

Kraepelin distinguished manic-depressive insanity from the

condition he called dementia praecox, a term first used by the French
psychiatrist Benoit Morel. In this syndrome, Kraepelin recognized a
variety of states in which a disturbance in thinking, emotion, and
volition led eventually to a destruction of the personality that was
peculiar to this condition itself.

Kraepelin's conception of these psychoses was heuristically

valuable. It focused attention on a salient feature of mental illness,
that some patients recover and others deteriorate, and it encouraged
genetic studies to discover whether the heredities of these conditions
were as distinct as their courses. Finally, it led Kraepelin and others to
attempt to define symptoms that would distinguish the two conditions
before the fulfillment of their prognoses. Such efforts continue to this
day.

Defining and prognosticating are unsatisfactory activities for

physicians if they do not lead either to an understanding of causes or
to effective treatment. The failure to discover a treatment that could
change the course of either manic-depressive insanity or dementia
praecox caused Kraepelin's concepts to be challenged.

Eugen Bleuler sought to further the Kraepelinian advance by

examining dementia praecox for a central, defining feature. He coined
the word schizophrenia for the condition, presumed there might be
many etiologies for the disorder (and thus spoke of the "group of
schizophrenias"), and attempted to explain its symptoms as the result
of some fundamental defect in the capacity of the mind to unify
thought processes and mental events.4 Bleuler's term schizophrenia
has stayed with the condition, probably because the word dementia is
used in another context and not all patients develop the illness while
young. Because thinking is disrupted in so many situations, however,
Bleuler's emphasis on thought disorder as central to schizophrenia
and his desire to recognize cases in their earliest and subtlest
manifestations perhaps led him and his followers to diagnose the
illness more often than Kraepelin would have done.

The major quarrels with Kraepelinian opinion that have

characterized psychiatry in the twentieth century have had less to do
with distinctions between manic-depression and schizophrenia than
with the issue of whether such conditions are best conceptualized as
diseases. Are they disorders qualitatively distinct from states of
mental health and produced by the action of some biological agent
leading to disruption of neural and therefore mental function? Or are
they more correctly viewed as reactions to life experiences in which
people differ from one another only in their degree of response?
 Several physicians have looked for functional explanations of these
psychoses through an appreciation of the life experiences and mental
conflicts of their patients. Sigmund Freud published his studies of
manic-depression and schizophrenia only after his initial
psychoanalytic work, perhaps because he began as a neurologist in
private practice and was involved primarily in the treatment of
neurotic patients. In fact, his major study of schizophrenia, the
Schreber case, was based on Schreber's published autobiography
rather than on a personal examination.5 Freud concentrated his
attention on the contents of Schreber's delusions and derived a
functional explanation of paranoid schizophrenia from the subject's
conflicts, particularly those over homosexuality. Freud ignored the
form of the delusional experiences and did not discuss how his
opinions could account for the deteriorating course of the illness. But
his meaningful explanations have survived, not only because he
founded the psychoanalytic movement but perhaps also because he
brought an encouraging and humane view of schizophrenic patients
to physicians who had to treat them through long periods of
therapeutic impotence. The same view can be taken of Freud's
attempt in "Mourning and Melancholia" to explain the symptoms of
affective disorder.6

Adolf Meyer likewise characterized manic-depression and

schizophrenia as reactions rather than as diseases.? He encouraged
the study of a patient's biography in order to see the condition as an
outcome of the patient's whole life experience. Again, Meyer's
opinions had the advantage of explaining disorder as derived from
issues best resolved through an understanding of the patient's
psychological needs and assets, but he also ignored the necessity for
such theories to account for the form of symptoms and their natural
history. His view, like Freud's, rested primarily on the plausibility of his
explanations.

Karl Jaspers was the first scholar in the field to make the point that
it might be difficult to choose a single position in such a controversy,
since similar psychological events might be produced by
circumstances in some patients and by disease in others. He
demonstrated this argument in a study of what has been called
morbid jealousy, pointing out that the symptom sometimes appears in
individuals in whom a lifelong trait of suspiciousness has
understandably progressed, owing to circumstances, into unfounded
excessive jealousy (for which we might use the term neurotic
jealousy), whereas in other patients the symptom appears
unanticipated by the previous personality and unrelated to life events;
the latter manifestation seems incomprehensible, a delusion with
jealousy as its content.8 It was this incomprehensibility that Jaspers
concluded to be characteristic of schizophrenic symptoms, and, as
his terms life break and process phenomena indicate, he believed
that such symptoms reflected the interruption of coherent mental life
and behavior by a somatic disorder. Since the psychopathology of
manic-depression is also incomprehensible in its form, however, it is
difficult to hold with Jaspers that such a characteristic is limited to
schizophrenic symptoms.

Attempts to see these conditions always as reactions have lost

momentum in the last few years with the appearance of symptomatic
treatments for manicdepression and schizophrenia and with the
recognition of similar conditions that are produced by agents that
affect the brain. But the continuing failure to identify a particular
cerebral pathology or pathophysiology in these disorders undermines
attempts to proclaim them as diseases with complete confidence.
They remain mysteries in the sense that a confirmation of their
essential nature is lacking. We hold that they are best viewed as
clinical entities within the disease perspective for which no certain
pathological entities or etiological agencies have as yet been
discovered. We are fortunate to have chanced upon treatments that
help, and in that regard we perhaps resemble William Withering after
his discovery of digitalis-grateful but astonished.
 Summary

The mentally crippling conditions manic-depression and

schizophrenia have been awkward to explain right from the time that
they were first recognized. We have presented a brief historical
review of these disorders and some of the original suggestions as to
their causes. Here, perhaps more vividly than in any other arena of
psychiatry, schools of thought have emerged in conflict. Those who
would identify these conditions as symptoms of brain disruption and
thus diseases have argued with those who would identify them as
emotional reactions provoked by a collision between an individual's
desires and how those desires were thwarted in life. The resolution of
this conflict awaits further scientific discovery.

Given the advances in pharmacology and longitudinal study of

patients with these conditions,9,"° we conclude that they are best
viewed as diseases in which the pathologic mechanisms and etiologic
agencies are not as yet fully discerned. We also emphasize that as
with any disease, these conditions interfere with the life story of the
afflicted and this interference will produce problems of its own that, as
discussed in chapter 5, must also be considered as a treatment plan
evolves.
Distressing changes in mood or emotion occur naturally in response
to life's events, and most do not prompt people to see a doctor, let
alone a psychiatrist. Of those patients who do attend a medical clinic,
one out of three will report being downhearted, sad, worried, and so
forth. The majority of these patients will be facing a serious life
situation-such as a medical illness with quite burdensome
implications-and the emotional states can be attributable to these
circumstances, disappearing if they are corrected. However, a
number of patients will be suffering not from some responsive mood
but from a fixed depressive state that overwhelms them, and has its
own particular characteristics distinct from ordinary discouraged
feelings. It must be recognized for what it is, major depression, a
disruption of affective life that psychiatrists know and treat as one of
the grievous forms of mental disorder. This chapter is devoted to
describing its symptoms and to identifying the growing evidence that
this condition is a disease with all of the implications for treatment,
prevention, and research linked to the concept of disease.'

Definitions

Manic-depression is a condition in which disruption of affect

regulation is the fundamental clinical feature-hence the perhaps more
appropriate designation, affective disorder. The terms affect, affective,
and a/fstivity need definition. Affect is defined as "feeling, emotion
and desire with an implication of their importance in determining
thought and conduct."2 Psychiatrists, fol lowing Bleuler's lead, have
identified an affective as distinct from a cognitive realm of mental life.
These two aspects of mind relate to each other, but it is not difficult to
appreciate that thoughts, reasons, perceptions, and thinking are
different from moods, emotions, drives, and feeling.

Affect is a broad term encompassing moods, emotions, motivations,

and such feelings as pleasure, confidence, depression, and
discouragement. Attempts to replace it with other words are usually
unsatisfactory. Mood describes a relatively persistent, dominating
affect; emotions are more fleeting affective events; and feeling is a
word confused with bodily sensation. The term affect is needed
because it encompasses this whole sphere of psychic life.

In normal mental life there is a coherent and natural relationship

between the domains of cognition and affect. Most thoughts are
accompanied by some feeling tone, and certain thoughts can produce
strong emotions, such as grief. In a similar way, most moods can
promote thoughts, as when fear leads to suspicion. The existence of
a class of disorders that strikes primarily at the affective aspect of
mental life and produces profound alterations in moods, emotions,
and drives reveals that a distinction between the cognitive and
affective realms represents an important aspect of mental-and
presumably brain-organization. The sense that some primary
disruption has occurred in the affective realm is the critical premise in
the category.

Symptoms and Course

Manic-depression must be approached as a clinical syndrome

because as yet no consistent abnormality of a bodily part can be
employed to define a pathology or etiology for it. The condition is
defined as it is described: by its symptoms and their course.
However, the course can be very variable, and the symptom cluster
that characterizes the disorder can have different expressions even
as it consists of three related and reliably elicited mental changes: a
disturbance in mood, a change in self-attitude, and a subjective
sense of alteration in mental energy and bodily health.

We must admit that even as we are restricted to clinical descriptions

in defining this condition, a marked heterogeneity-expressed in terms
of course, symptoms, and outcome-is found in the way the illness can
manifest itself in individuals. This heterogeneity will be better
explained when we understand the pathological mechanisms and
etiological agencies involved in generating the condition. However,
there is sufficient information to differentiate this condition from other
mental disorders including those with emotional components.

Course

The course of manic-depression is one of remissions and relapses,

the syndrome usually appearing in an unpredictable fashion and
persisting for a variable time. Each episode, even if untreated,
eventually abates, and the patient is restored to his or her premorbid,
symptom-free condition until the next attack. The most striking feature
of this course is that polar distinctions may occur in the affective
qualities of different episodes. With some attacks the mood is
depressive in character, whereas with others it is elated. There is
individual variety in this feature. Some patients alternate from
depression to elation in successive episodes. Others may show a
preponderance of one mood state over the other or throughout their
illness have attacks only of mania or only of depression. However, it
is the tendency of many patients to have attacks in both modes that
has led to the designation bipolar disorder that some investigators
prefer to the traditional manic-depression.

The course of manic-depression can be episodic, periodic, or

cyclical. A few patients suffer only a single attack (usually depression)
during their lifetime, whereas others have repeated bouts of
depression, mania and depression, or, least commonly, mania alone.
In most episodes, attacks occur unpredictably, though both
psychological and physical stresses can precipitate them; women
who experience the disorder may be at special risk in the postpartum
state.

The illness can also appear in specific times of the year, with
patients regularly becoming ill in fall or winter. The reason for this
seasonal variationthe condition now referred to as seasonal affective
disorder-is unknown, but must relate to seasonal change in the
intensity and duration of sunlight because an attack can be relieved
by having the patient sit before bright lights for a few hours each
day.3

Finally, in a small number of patients, manic-depression takes a

cyclical course, with attacks of mania and depression following one
another in a regular sequence. In such cases there may be a
predictable change from mania to depression and back again even as
frequently as every forty-eight hours.4 The occurrence of these
regular cycles supports the opinion that manic-depression is a
disease and that embodied mechanisms and etiologies lie at the root
of it.

Mood

The shift in mood toward either depression or elation/excitement is

the fundamental feature of the disorder and usually its clearest
characteristic. Occasionally the mood change is subtle and difficult
even for the patient to identify. The term depression is actually a
doctor's term and not one that patients tend to use when they are first
afflicted. They may describe their state as one of "disquiet," "worry,"
"lowness," or "shamed" when depressed or "frenzied," "wild,"
"energetic," or "tops" when elated.

However, after patients have had several attacks, they are more
able to distinguish these pathological and uncontrollable mood
changes from ordinary emotional reactions. They comment about the
odd and pervasive quality, unremitting nature, and remarkable,
almost stereotypic, similarity from one attack to another. Although
such patients have previously felt sad and happy in response to life
events, the mood during these episodes, whether of misery or
ecstasy, feels qualitatively different from those prior responsive
experiences. Many patients can promptly recognize a recurrence of
their illness because of this special, quite characteristic change in
mood, even though its severity may vary with each attack.

The affective change alters many features of mental life. When

depressed, the patients become withdrawn and lose interest in most
activities, including those that usually give them pleasure and
comfort. Even perceptions of the environment may become dulled,
and they can report that sounds are muffled, colors faded or
darkened, and food tasteless. Just the opposite happens in mania,
when energy increases, thoughts and ideas come quickly, social
activities increase, and perceptions become brighter and more
intense.

In whatever terms these changes are described, the critical feature

is that the patient's mood state is deviated and "fixed" in one direction
or the other. It is this feature that should prompt the diagnosis,
regardless of the words the patient uses to describe the feelings or
the thoughts that accompany it. The diagnostic psychological
disturbance of this clinical entity is a shift in mood of a sustained
character, one that is little influenced by the surroundings. Good news
or bad, supportive comments from friends or physicians, gains or
losses-none has much influence. Mood, usually a responsive feature
of mental life, here runs independently.

Complicated and subtle features of this mood change can be

reported by other observers of the patient. A common feature of
depression in adolescence is a shift in mood toward irritability, chronic
dissatisfaction, and even rebellion against parents. Minor difficulties
in family life are magnified, and attention of everyone is directed away
from the mood and toward some grievance. The expectation that
"adolescence must be stormy" or "teenagers are trouble" can delay a
proper diagnosis, sometimes with devastating effects. At the very
least, hard words can be exchanged among the family and for
recovery, time and effort are required to rehabilitate relations.

A depressive mood at different times of life will usually have

different expressions related to the general concerns and
relationships of these life periods. An agitated and fearful quality can
be predominant in middle life, a feature that for a time was thought to
define a subtype of depression, involutional melancholia. Elderly
patients often report a general loss of feeling in their depressions.
One patient, for example, noted with dismay that with depression her
customary feelings of heartfelt love on seeing her grandchild were
absent-a most distressing experience of affective loss for her.
Adolescent patients are often irritable.

In the evaluation of mood it is crucial to appreciate the many

different ways a mood change can be experienced and reported.
These "pathoplastic" aspects of manic-depression-derived from such
features as the age, life circumstances, habits, and personal
characteristics of the patient-should not distract one from the
"pathognomonic" feature of the shift of mood into a fixed and
unresponsive position.

Self-Attitude

The second fundamental symptom of manic-depression is a change

in selfattitude that usually parallels the change in mood and is in
some sense hard to differentiate from the mood itself. The manic
patient may believe that he is healthy, rich, talented, or powerful,
although, when depressed, he may feel diseased, poor, blameworthy,
unlovable, sinful, or useless.
 Such changes in self-attitude can be delusional. In the depressed
phase, the patient can come to believe that he is a notorious criminal,
that he is infected with venereal disease or filled with cancer, or that
he deserves public humiliation, even execution. In mania the patient
may believe that he is God, that he is a millionaire, or that he has the
knowledge and powers to save humankind. With these delusions and
as elaborations of them, the patient may think that others are trying to
harm him. Such delusions are felt by the patient to be deserved (as,
for example, a just punishment for his terrible crimes or the products
of envy for his extraordinary powers), a characteristic that can some
times help to distinguish the persecutory beliefs of affective disorder
from the paranoid delusions of a patient with schizophrenia, who
believes others to be oppressing him without justification.

Delusional changes in self-attitude may prompt destructive

behavior. The delusional fear and shame can lead to suicide (even to
family homicide if the patient believes that his relatives are tainted
with or face humiliation because of his evil). In mania, a delusional
belief in personal wealth may culminate in overspending to the point
of financial ruin. Such severe delusions are not the most common
kind of delusions experienced, however. Most are more subtle and
difficult to differentiate from responses to circumstances. During what
seems a mild depression, many of the patients will argue with the
doctors that their feelings of inadequacy as a student, of
incompetence as a partner, of stupidity as a scientist, of ugliness of
appearance, or of worthlessness as a family member are justified and
point to some event in the past for support.

Many observers can be taken in at this time, to the point of agreeing

with the patient even in some radical decision about the future such
as changing jobs or redirecting a career. Overconfident manic
workers have insulted their employers; underconfident depressed
students have resigned from colleges. The most radical decision of
course is suicide, a behavior in part prompted by a change in self-
attitude and the deep concerns of the patient it promotes. These
ramifications of self-attitude change are discussed more fully in the
later chapter on suicide (chapter 19).

To repeat, with the onset of an affective disorder a fundamental self-

attitude change can be a prominent symptom. The patients-accepting
the attitudinal opinions as axiomatic-will act and argue, sometimes
most cogently from these attitudes toward conclusions with
behavioral implications. The failure to appreciate the pathological
source of these changes, especially when they seem slight and
nondelusional in form, can be disastrous.

Change in Energy

A change in the patient's sense of mental energy and bodily health

is the third characteristic feature of manic-depression. In the
depressed phase the patient's thinking may be slow and inefficient.
He may complain of fatigue or physical discomfort, occasionally of
severe pain in a site of an old injury. On examination, the patient
appears ill, perhaps apathetic, with clear and demonstrable deficits in
the abilities to concentrate and to perform mental tasks.

If the depression worsens, all aspects of the patient's mental and

physical activity are slowed. He displays psychomotor retardation,
answering slowly if at all and walking with a gait, posture, rigidity, and
facial expression suggestive of parkinsonism. A stuporous condition
can be the most severe manifestation of this disorder, with the patient
bedridden, incontinent, mute, unable to feed or care for himself, and
in danger of death if not properly diagnosed and treated.

Again it is the more subtle forms of this energy loss that the better
diagnosticians tend to notice. The patient is not so clearly
psychomotor retarded as he is just a bit slow to respond. He reports
that he can work but that he is inefficient. He is not exactly stiff so
much as he is unanimated. These features of the patient, a change in
responsiveness and motility, the family come to recognize as
identifiable signs of relapse. A good rule: never doubt the spouse or
parent who says the patient shows the familiar signs of relapse, no
matter how vigorously the patient rejects the opinion.

In a manic phase the patient may experience his thoughts as

effortless and rapid and his body as healthy and filled with energy. As
this state worsens, the patient may become progressively more active
until his behavior takes on an uncontrollable hectic quality and his
thoughts become so rapid and chaotically responsive to every
distraction that sustained, goal-directed thinking is impossible.

The minor signs of this change can be simply a flush of health, a

vigor of response, perhaps with some tinge of condescension. These
features are again more promptly noticed by the people who live with
the patient. They may detect an early change in stance, facial
expression, or gesture that marks the onset of arrogance and
overbearing certitude that they have seen expand in the past into
irritability and imprudent actions.

Accompanying Symptoms

These defining symptoms are often accompanied by a variety of

affectrelated problems. The natural appetites, for example, are
altered during the illness, usually in a direction congruent with mood,
self-attitude, and sense of energy. In the depressed phase, a patient
usually has little appetite for food, loses weight, sleeps poorly, and is
uninterested in sex. During a manic attack, however, the same patient
may eat and drink with enthusiasm, sleep little but be refreshed by it,
and experience such an increase in sexual energy that both family
relationships and social reputation are endangered. Patients often
describe a diurnal variation in mood and sense of vitality; for
example, mornings are classically the worst time of day for patients
during the depressive phase of the disorder.
 Some patients experience hallucinations (usually auditory) that
have themes understandable in light of the mood change. Manic
patients may hear the voice of God praising their actions, whereas
depressed patients may hear voices encouraging them to die or
criticizing them as sinners.

Thought processes are almost always noted by the patient to be

alteredslow with depression, fast with mania. The expressions of the
thoughts in speech are also slow in the depressed phase of the
illness, but in mania pressured speech, rhymes, puns, and rapid
change of topic can occasionally progress to the point of total
incoherence.

Possible Mechanisms and Etiologies of Manic-Depression

The hypothesis that manic-depression is a disease carries the

implication that some as-yet-undemonstrated pathological
mechanisms and etiological agencies will emerge to explain the
heterogenous symptoms and course that are represented in the
clinical syndrome. Such discoveries of the "broken part," when they
occur, will as well increase our therapeutic and prognostic abilities. If
manic-depression joins dementia, delirium, Korsakoff syndrome, and
aphasia as a confirmed clinical disease entity, then the neural
substrate of affective life will be revealed and rational therapeutics
with preventive measures will be possible.

Neurological Evidence

The available data on which validation of manic-depression as a

disease depends, although still fragmentary, are strong enough to
bring confidence. One important piece of evidence is the finding that
the typical symptom cluster and even the bipolar course of manic-
depression can occur in disorders with known brain pathology.
Patients with Huntington disease, for example, often have, as their
first symptom, depression or mania.5 There is compelling evidence
that some 60 percent of patients with brain lesions in the left frontal
region, cerebral stroke most commonly, suffer from major depression.
This risk is increased if the lesion invades the basal ganglia and the
orbitofrontal cortex.6 Functional brain images using positron-emission
tomography also show diminished activity in the left frontal regions in
patients with spontaneously occurring major depression. These
observations imply that the affec tive syndrome, like dementia and
delirium, is a potential result of brain injury with some evidence that
dysfunction in the left frontal regions may be crucial.?

In the face of these observations, not only can we more confidently

expect confirmation of brain pathology behind manic-depression, but
we can also begin to think in these terms by definition. We can refer
to manic-depressive syndromes occurring in the setting of known
pathology as symptomatic in nature and can contrast them with the
idiopathic disorder. This mode of reference is analogous to that for
epilepsy, in which recurrent seizures "symptomatic" of particular brain
diseases are distinguished from idiopathic epilepsy, in which genetic
factors are critical.

Neurochemical and Neuropharmacological Evidence

Many current investigators in manic-depression concentrate on the

role of cerebral neurotransmitters. This area of research began in the
1950s with the clinical observation that reserpine, a drug used to treat
hypertension, could produce a classical depressive syndrome."
Animal studies demonstrated that reserpine depleted brain stores of
the neurotransmitters serotonin, norepinephrine, and dopamine.
Thereafter, the empirical discovery that monoamine oxidase inhibitors
and tricyclic compounds not only reverse depressive syndromes but
increase brain concentrations of the same neurotransmitters depleted
by reserpine reinforced the view that neurotransmitters were crucial.9
If reduction and increase of brain amines can produce and reverse
depression, then this may be the pathophysiology through which
genetic and other etiological agencies cause the spontaneously
arising disorder.

The gradual development of a rational pharmacology in manic-

depression has built on the idea that neurotransmitter changes are
basic to affective disorders. It goes beyond our purposes to describe
these investigations, but the planned development and remarkable
success of the selective serotonin reuptake inhibitors (SSRIs)
(fluoxetine, sertraline, etc.) and the suggestion and use of
anticonvulsants (carbamazepine, valproic acid, etc.) as mood
stabilizers are noteworthy recent advances. These treatments are
more than just symptomatic therapies because they try to influence
specific brain mechanisms of salience in manic-depression.

Genetic Evidence

Genetic factors have long been proposed to play an etiological role

in manicdepression. Thus, in 1953, Franz Kallmann demonstrated an
increasing risk for manic-depression in the relatives of patients
hospitalized with the He found rates of 16.7 percent for half-siblings,
22.7 percent for full siblings, 25.5 percent for dizygotic, or fraternal,
twins (like full siblings), and 100 percent for monozygotic, or identical,
twins. Although subsequent studies using different diagnostic
procedures and sampling techniques have found somewhat different
results (for example, higher risk for full siblings and less than perfect
concordance in monozygotic twins), a genetic factor is certainly
implicated in the pathogenesis of many cases of

It is still occasionally argued that environmental rather than genetic

causes are responsible for these family findings. The claim is that
increasing similarity of upbringing could account for the greater
concordance rates in monozygotic as opposed to dizygotic twins and
in full siblings compared with half-siblings. For this reason major
efforts have been exerted to link manic depression with a gene or
genes.
 This has not proven simple, and much of the problem may relate to
difficulties in distinguishing the phenotypic presentation of true
examples. Several initial scientific reports of linkage between specific
chromosomal locations and manic-depression could not be
replicated. One published report12 was specifically retracted13 when
further studies of afflicted families eliminated a correlation. Most
recently, though, a clear and confirmed linkage within some
pedigrees between members suffering manic-depression and a
region on chromosome 18 has been made. This linkage was
strengthened by concentrating on paternal inheritance in which allele
sharing between affected siblings ran to 70 to 80 percent. 14,15

Chromosome 18 is not the only site for genes responsible for

manicdepression, as Raymond DePaulo's group at Johns Hopkins
demonstrated. Francis McMahon showed that in contrast to the
families sharing some allele on chromosome 18, where paternal
lineage predominates, other sets of families show predomination of a
maternal rather than paternal inheritance-suggesting the possibility of
some role for genetic imprinting, mitochondrial inheritance, or other
female forms of transmission in manic Melvin McInnis made the
observation that clinical "anticipation" (worsening of the illness and
earlier age of onset by generation) occurs in bipolar affective disorder
families suggesting an expanding trinucleotide repeat sequence of
DNA as a possible etiological candidate gene or genes for manic-
depression.17

From all these data DePaulo suggested that the inheritance, as with
the manifestations of manic-depression, is likely to be
heterogeneous. Multiple genes, each with modest effects, may act in
concert to increase the susceptibility of individuals to affective
disorder. Although this conclusion is not the expected discovery of a
single gene that first promoted the study of the genome in manic-
depression, it could well explain such features as the clear evidence
of inheritance from twin and adoptive studies but the lack of a
Mendelian pattern. 111
Recapitulation

Although pathological entities and etiological agencies responsible

for most cases of manic-depression have not emerged with
compelling power, surely the data from symptomatic illnesses,
neurotransmitter studies, psychopharmacology, and genetics appear
to support the stepwise process of disease reasoning. A concept of
manic-depression, as a disorder of the affective mechanisms of the
brain, is emerging from them. These affective mechanisms are now
the subject of investigation by structural and functional brain-imaging
techniques. The brain states that represent the "broken part" in this
disease seem likely to be soon discovered.

Summary

The pathognomonic feature of the manic-depressive syndrome is

the deregulation of the affective domain of mental life, resulting in an
unrestrained dominance of mental activity by affect. Its construal as a
disease will be confirmed if and when we have a physiology and
pathophysiology of affect. Investigations to define the pathology and
etiology of manic-depression are vigorously under way, prompted by
the success that has already greeted this disease perspective
approach. A validating advance in neuroscience identifying the
pathology and etiology would certainly help explain the natural history
of the syndrome, its clinical heterogeneity, its distinction from affective
reactions such as grief, and its response to pharmacological and
physical treatments.
Schizophrenia is the great clinical challenge to psychiatry. A common
disorder in all cultures, schizophrenia has a prevalence of 1 percent
in the human population. It devastates psychological integrity and,
with a peak onset just as adult life is about to be launched (in men
between ages 15 and 25, a decade later in women), it represents a
tragic affliction-chronic, not fatal, breaking into the course of a life,
directing it away from promise and opportunity and toward
incoherence, frequent hospitalizations, and chaos. Some 50 percent
of patients with schizophrenia attempt suicide, and 10 percent
ultimately succeed. All are drawn by the disorder away from family
and community life into a state of isolation, self-absorption, confusion,
and distress.

These are the reasons schizophrenia is a condition of vital concern

to psychiatrists. It is also the condition that has revealed their relative
impotence and uncertainty over treatments. Time after time,
psychiatrists have changed their views about its fundamental nature
and its appropriate treatment. And time after time they have altered
public policy over its management-for some period encouraging
hospitalization, followed by another period seeing hospitalization as
an infringement on the patients' "freedom." These difficulties derive
from past failures of psychiatrists to agree about the fundamental
nature of the condition and what therefore constitutes the best
measures for managing and treating people with it. Fortunately, over
the past two decades, a stable consensus has gradually emerged
that schizophrenia is a product of disease of the brain-a consensus
that has led to advancing treatments and better social management
of these afflicted patients.' .2

In this chapter we describe the sound reasons for viewing

schizophrenia from the vantage point of the disease perspective, with
the implication that this clinical syndrome will eventually come to be
understood as the outcome of a pathological process or processes in
the brain (a "broken part") explained by some etiological agency or
agencies that injure that organ. Although this final achievement has
not been reached, its promise is clear and-based on contemporary
observations that we shall briefly review-evidence strongly suggests
that schizophrenia is due to a neurodevelopmental disruption of the
brain.

Definition

Psychiatrists have had difficulty agreeing on a definition of

schizophrenia. This is not only because its characteristics are mental
changes lacking a defined pathology, for such is also true of manic-
depressive disorder, but also because schizophrenia has no unifying
psychological feature that is fundamental to its nature and aids in its
recognition. There can be no diagnosis of dementia without a decline
in intelligence, of delirium without alteration in consciousness, or of
manic-depressive illness without change in affectivity. But in
schizophrenia, there is no such central psychological characteristic.
Any consideration of schizophrenia must begin with a long clinical
description, which is the only form of definition anyone can so far
provide, forming in this way a most disjunctive diagnostic category.

This definition, though, identifies schizophrenia as a clinical

syndrome distinguished from others by symptoms and natural history.
Its course is not uniform. Schizophrenia can appear insidiously and
progress slowly and relentlessly or it can begin suddenly and
continue with exacerbations and remissions. The most dramatic
features occur during active phases of the disorder and take the form
of hallucinations and delusions. Odd modes of thinking, peculiar
incongruities of mood, and a loss of mental energy varying from
minimal to severe can develop gradually or during an acute attack but
may not recover after the attack. The disorder often renders the
patient's personality cold and unpredictable, and it may lead to a
disappearance of finer sensibilities and capacities for affection. There
is good evidence that a mild form of cognitive deficit, a dementia,
develops in schizophrenic patients.

The symptoms of schizophrenia can be conveniently divided into

positive and negative symptom groups. The positive symptoms-so
called because they represent the appearance of new features in
mental life-include the hallucinations, delusions, and formal thought
disorder more commonly seen in the acute attack of the disorder. The
negative (or "deficit") symptoms are those that represent a diminution
of normal psychological capabilities. They include the loss of mental
energy, reduction in goal-directed capacities, the peculiarities of
interest and behavior, and the disappearance of feelings of warmth
and affection toward others. A patient can have almost any
combination of positive and negative symptoms. Each symptom is a
devastating disturbance of mental life and behavior. Pertinently, the
diagnosis of schizophrenia must be reserved for those patients with
these symptoms but without evidence of brain disease or of affective
disorder. It is thus a clinical syndrome diagnosed by exclusion.

Schizophrenia usually begins in late adolescence or young adult

life, although onset even after 60 occurs. In general, the illness
produces a deterioration of cognition and personality, so even if
delusions, hallucinations, and formal thought disorder abate, patients
remain intellectually and emotionally crippled, with poverty of thought,
a narrowed range of interests, and a life isolated from others. This
deterioration is not inevitable, however, for even before the discovery
of neuroleptic drugs, remissions were reported in 10 to 25 percent of
cases, a figure that improved with the emerging principles of effective
pharmacological and psychotherapeutic treatments and with
programs of social rehabilitation.3

Among the signs and symptoms that mark the onset of a

schizophrenic illness, none can be agreed on as characteristic of the
disorder. Emotional unrest, uncertainty, and perplexity can be found
in many conditions, so the diagnosis of schizophrenia cannot rest on
them alone. As Kurt Schneider pointed out, however, a number of
mental changes are found more often in schizophrenia than in the
other disorders. These phenomena can usefully be divided into
abnormal mental experiences and disturbed modes of expression, an
early attempt at what has more recently been made explicit in the
form of "positive" and "negative" symptoms.4 The abnormal mental
experiences, which Schneider referred to as "first-rank symptoms,"
are better evidence of the illness only because they are more reliably
elicited and are less dependent on observers' interpretations than are
the changes in expression. However, they are not seen in every
schizophrenic patient and can occur in other disorders.

Abnormal Mental Experiences

Hallucinations and delusions are the most vivid schizophrenic

mental experiences, though it must be remembered that these
symptoms also occur in delirium, dementia, and manic-depressive
illness. Although hallucinations can arise in any sensory modality,
auditory hallucinations are the most common, and in the absence of
affective disorder or coarse brain disease certain types of auditory
hallucinations are almost diagnostic of schizophrenia. Thus, the
patient who hears voices arguing with one another (often referring to
him in the third person), voices commenting on his every action, or
voices repeating his thoughts, experiences hallucinations most typical
of schizophrenia.

Delusions in schizophrenia can begin as vague, fearful

interpretations or "half-beliefs" and then develop into incorrigible
convictions that are well formed and persistent. A delusion coming on
suddenly, not prompted by an hallucination or previous delusion and
not related in any obvious way to the patient's mood, is called a
"primary" or "autochthonous" delusion and is highly suggestive of
schizophrenia.
 Many other characteristic schizophrenic experiences are of
delusional form but have such individual features that they have been
named separately. In one, somatic passivity, the patient ascribes
bodily sensations to some external agency. The sensation may be
rooted in an obvious physical process or in an hallucination. A patient
of C. S. Mellor's had injured his right knee in a fall, but reported, "The
sun-rays are directed by a U.S. army satellite in an intense beam
which I can feel entering the centre of my knee and then radiating
outwards causing the pain."5 In all of these phenomena the patient
reports unwilling subjection to experiences that seem completely real,
terrifying, and perplexing. The inexplicability of these phenomena has
led to consideration of them as symptoms of disease.

Symptoms of Disturbed Expression

Disturbances in the patient's modes of expression include "positive"

symptoms-formal thought disorder-and "negative" symptoms-loss of
motivation and emotional warmth-that often appear together in
various combinations in different patients. Formal thought disorder is
one of the cardinal schizophrenic symptoms, however. The term
refers to a disturbance in the form of the patient's thought rather than
in its content.

The relationship of ideas to one another is the abnormal feature, not

the truth or falsity of a given opinion or idea. Grammar, syntax, and
words themselves can get jumbled, but the main difficulty in
schizophrenic thought disorder is a failure in the discursive features
of thought and language. The expressed thoughts do not follow one
another in a coherent goal-directed fashion but emerge almost
randomly, poorly related to one another, and any meaningful linkage
of the thoughts to a communicable idea is lost. The clumsiness of
word selection or of grammatical structure adds to the problem but
are not the major difficulty as in aphasia.
 The patient with schizophrenia seems unable to monitor the
direction of his discourse. He seems to overrespond distractedly to
the secondary meanings of his words, is derailed by inessentials, and
loses sight of the initiating goal of his discourse to follow several
others that are themselves soon lost in a confusion of phrases and
expressions. Because the patient often acts throughout this
performance as though he understood himself and the intended
direction of his responses, any observer-particularly a physician who
is examining the patient-can at first wonder whether the
communication problem was provoked by some vagueness in the
initiating assessment questions. Only after repeatedly stopping the
patient and attempting to restart a more coherent answer does it
become clear that the problem lies with the patient's responses, not
the doctor's questions.

A good example of this phenomenon is provided by Eliot Slater and

Martin Roth, whose patient wrote: "It is a tragedy perhaps, I find
practically all the foreign human beings had this knowledge, and
perhaps at least certain of our own Nationality such as myself had
not, even my friends, comrades, where aware as the State Authorities
must have been, which I feel you will accept as to be Sts-in all
aspects revalent to deliberary to try and induce, such as been my lot,
constant body, head, Activation numerical strong, and distance Voice
face and body barrage."6

Formal thought disorder resembles the other abnormalities of

expression in being a disturbance described in dimensional rather
than categorical terms. Thus, whereas patients are either
hallucinating or not (a categorical distinction), the expression of their
thoughts can be ranged along a continuum from logical and goal-
directed to incoherent and lost. Difficulty in recognizing thought
disorder comes not when it is extreme but in examples of milder
incoherence where one examiner's threshold for vagueness in the
discourse of a patient may be higher or lower than another's. Thought
disorder then may be difficult to distinguish from difficulties in
language facility or differences in expression derived from one's
culture or education. Indeed, disturbed modes of expression in
schizophrenia are less reliably rated than are abnormal mental
experiences,7 an issue that should be considered in the weights
given to these symptoms during a diagnostic exercise. Disordered
mental experiences such as delusions and hallucinations should be
vigorously sought in any diagnostic interview.

Disturbances in the patient's emotions are other examples of the

negative symptoms of schizophrenia. Early in schizophrenia the
patient may appear inexplicably angry, perplexed, or ecstatic, and
although questioning may reveal that such feelings are due to
delusions or hallucinations, more often the patient is unable to
account for them. His emotional state may also seem incongruous to
the thoughts he is expressing; thus, he may laugh while saying he is
miserable and frightened. Finally, and especially after an acute attack
of schizophrenia with its positive symptoms subsides, the patient may
remain oddly cold and distant, whatever the circumstances. These
disturbances in emotional expression may be the patient's most
disconcerting symptom and even when mild can be baffling and
distressing to his family.

Other abnormal modes of expression occasionally found in

schizophrenia are those disturbances in activity, posture, and mobility
called catatonic symptoms. (Again, it is important to note that such
symptoms are not diagnostic of schizophrenia, as they can also occur
in affective disorder and coarse brain disease.) Gestures may be stiff,
slow, and mannered; movements repetitive or incomplete; postures
unnatural and maintained for long periods. Some patients make facial
grimaces or speak with peculiar accents, others manifest echolalia
(involuntary repetition of words spoken to the patient) or echopraxia
(involuntary repetition of gestures made in the patient's presence).
Still others become mute and immobile.
 During the active phase of schizophrenia, abnormal mental
experiences, formal thought disorder, and catatonic symptoms are
usually most prominent; during the chronic phase, disturbances in
emotional expression may be more evident. Although at times
patients seem free of residual symptoms, with many a careful
examination will usually reveal mild disturbances in thinking and
emotional responsiveness.

The issue of dementia in schizophrenia-a decline in cognitive

power-has been long debated, with many psychiatrists believing that
the difficulties in thinking were due to the patients' being distracted by
hallucinations or delusions during cognitive testing or by an overall
lack of motivation to concentrate on mental tasks. Careful
psychological studies, with apt control subjects, have demonstrated
that schizophrenic patients show deficits in those tasks tied to
concept recognition and those requiring shifts of attention or shifts of
cognitive "set." These patients do especially badly on such problem-
solving, set-shifting tasks as the Wisconsin Card Sorting Test. They
also show deficits in verbal memory, vigilance, and visual attention.8
Intriguingly, some of these cognitive deficits are more common in
relatives of schizophrenic patients who themselves do not have
schizophrenia.`'.'"

Diagnosis and Classification

When Emil Kraepelin developed his concept of dementia praecox in

the late nineteenth century, he included presentations earlier
described as separate entities by Franz Kahlbaum (catatonia), Ewald
Hecker (hebephrenia), and L. Snell (paranoid psychosis, or
monomania). Despite their differing symptomatic features, Kraepelin
grouped them in a single clinical disease category because they
shared a chronic deteriorating course, in contrast to the episodic,
remitting course of manic-depressive illness. The classical subtypes
of schizophrenia were thus distinguished by their predominant
symptoms: in the catatonic form, psychomotor changes; in the
hebephrenic, thought disorder and incongruity of mood; in the
paranoid, delusions; and in the simple, loss of affective
responsiveness and disturbances in will and drive.

At the onset of their illness, many patients present clinical pictures

that fit these classical descriptions, but most eventually manifest such
a mixture of symptoms that assigning them to one or another of these
subtypes seems arbitrary. This fact has led to other attempts at
distinguishing among schizophrenic illnesses for clues to etiology and
outcome (for example, process versus reactive schizophrenia;
schizophrenia versus schizophreniform states), but none has proven
entirely satisfactory. We are almost certainly dealing with what Eugen
Bleuler called the group of and await biological rather than
psychological markers to develop a classification for types of
schizophrenia that is both valid and clinically useful.

The fundamental feature of the symptoms of schizophrenia is that

they are mental events in whose form it is impossible to perceive the
cause and effect relationship that can be appreciated in normal
psychological experience. We see perceptions without stimuli
(hallucinations), beliefs without justification (delusions), thinking
without logical connections (thought disorder), and emotions without
issues and issues without emotions (the incongruous split of affective
states from thought contents).

All the particular psychological experiences Schneider called first-

rank symptoms belong here in a list of mental phenomena in which
no glimmer of psychological cause and effect can be perceived. It is
impossible, for example, to see such a connection in the experience
of patients who hear voices comment on their actions or who believe
their thoughts are broadcast to the world. Symptoms and signs
described by other psychiatrists as typically schizophrenic, Bleuler's
thought disorder or Ewen Cameron's overinclusiveness, also share
this lack of an obvious causal connection.
 These experiences are called schizophrenic only when the patient
shows no signs either of a primary change in affect or of coarse brain
disease. When such evidence is present, the symptoms should
always be ascribed to manicdepressive illness, delirium, or dementia.
Schizophrenic symptoms are psychological events without
explanations, and without is the operative word. It is clear that the
ascription of a symptom as schizophrenic is an opinion based on
exclusion rather than on positive evidence.

If a symptom can be called schizophrenic only if it is without

explanation, then clearly the first responsibility of diagnosticians is to
be sure that they cannot attribute it to another disorder. Because all
the abnormal mental experiences and disturbances of expression
described as symptoms of schizophrenia can be seen in manic-
depressive illness, delirium, and dementia, those illnesses must be
carefully excluded when a patient is presented for diagnosis and
therapeutic planning. Further, because disturbances in expression
can occur in vulnerable people under stress, a consideration of the
patient and his or her circumstances is required before it can
confidently be stated that a symptom is inexplicable. An anxious and
preoccupied person may, for example, have fragmented thinking; a
naturally reserved, introverted individual can appear distant or cold;
and a person of a different cultural heritage may express emotions in
a manner unfamiliar to the psychiatric observer.

Many of these diagnostic problems, though, can be resolved by

adding a careful longitudinal assessment of the onset and progress of
the condition to the cross-sectional interview done upon admission to
the clinic. A detailed evaluation of any progressive change in a
patient's personality and situation, best done with help from other
informants such as family members or friends, should be made
before a clinical presentation and set of symptoms are confidently
diagnosed as manifestations of schizophrenia. Sometimes a
longitudinal assessment in a hospital is required. Of note is the fact
that the nurses caring for the patient through the day are usually
more capable of picking up the subtle forms of "negative" symptoms
that elude the doctors seeing the patient for a cross-sectional
interview.

From this reasoning it is obvious that the identification of a patient

as suffering from schizophrenia represents minimal understanding of
his condition. Such a diagnosis indicates only that he suffers from a
madness that is identified as an explanation for his troubles after
other conditions have been considered but excluded.

Psychiatrists do well to make the diagnosis of schizophrenia

cautiously. There is not only the danger of overlooking other
conditions with different prognoses and treatments but also the risk
that when a diagnosis resting on exclusion is used other things may
often be excluded too easily. The diagnosti cian's goal must be to
find, if possible, a positive explanation for the patient's symptoms in
other disorders or reactions. To do so requires a detailed history,
repeated mental status examinations, observations from several
sources of informants (family members, nurses, occupational
therapists, social workers, and so on), and the readiness to consider
a variety of formulations and to try a variety of treatments.

Pathologies and Etiologies

Disease reasoning is now fundamental to schizophrenia. However,

only its progress beyond the clinical description will validate
schizophrenia as a disease. There is enough emerging evidence to
bring confidence to anyone holding the presumption that it is a
disease, and evidence related to the pathology and the etiology of
schizophrenia is advancing apace.

Brain Pathology and Schizophrenia

Characteristic clinical phenomena of schizophrenia and even

aspects of its course can be produced by known brain diseases. In
their extensive review, K. Davison and C. R. Bagley listed conditions,
ranging from epilepsy to encephalitis and from Wilson's disease to
cerebral trauma, that can evoke a schizophrenialike state in patients
without genetic predisposition.12 Further, it is not brain damage in
general that appears to be associated with this "symptomatic"
schizophrenia but lesions in the temporal lobes and basal ganglia in
particular.

Even more telling has been the evidence for neuropathology in

schizophrenia that has come from better methods of studying the
brain. In the past, abnormalities seen in postmortem brain tissue and
pneumoencephalograms of patients with schizophrenia were
challenged as artifacts-perhaps of long hospitalization or various
forms of treatment. By combining reliable approaches to the clinical
diagnosis of schizophrenia (thus limiting the cases studied to those
most likely to be examples) with more careful postmortem studies,
rather consistent abnormalities in the medial inferior temporal lobe
(hippocampus, entorhinal cortex, and parahippocampal gyros) in the
form of shrunken tissues and disrupted neuron patterns are found.13
Neuronal disruptions have also been identified in the frontal cortex.14

The introduction of computerized axial tomography in the late 1970s

enhanced confidence in a neuropathology of schizophrenia. Eve
Johnstone and colleagues in Britain, Godfrey Pearlson and
associates, and Daniel Weinberger and associates in the United
States identified ventricular enlargement and sulcal widening in the
brains of patients with schizophrenia. These structural images could
not be dismissed as artifacts of neuroleptic medication or of long as
they were made early in the onset of the disorder and often before
treatments began.

Further advances in brain-imaging techniques, such as positron-

emission tomography (PET), have made functional images of the
activity of the brain possible in conscious subjects. With these
techniques schizophrenic patients can be studied while they are
attempting to solve problems or when they report hallucinations. A
major discovery was that in many schizophrenic patients the frontal
regions of the brain do not become active under test circumstances,
such as the Wisconsin Card Sorting Test, that customarily exercise
the frontal lobes. This functional "hypofrontality," as Weinberger
called it, may be a vital explanation for the loss of direction and
inactivity of patients with schizophrenia. Indeed these particular
features can be construed as symptoms of damage to "executive"
functions in schizophrenia-functions that in normal people are
represented by their capacity to make decisions, differentiate
between alternatives, and progress with some confidence along a line
of reasoning toward a goal. Loss of executive capacity may be
fundamental to some of the negative symptoms of

Patrick Barta and Godfrey Pearlson identified (with magnetic

resonance imaging) the region of the planum temporale, the superior
temporal gyrus, and the auditory cortex around Wernicke's region of
the cerebral hemispheres as often reduced in volume and altered in
symmetry in schizophrenic patients. In fact, they could correlate the
degree of atrophic disruption of this brain region with the severity of
the auditory hallucinations and thought disorder the patients
experienced. This was a critical observation because not only did it
support the hypothesis that schizophrenia is a brain disease but it
provided evidence that, like in focal epilepsy, the particular positive
symptoms of a schizophrenic patient could be linked to discrete sites
of damage in the brain. 19

Psychopharmacology and Schizophrenia

Advances in psychopharmacology provide another body of

suggestive work encouraging the hypothesis that schizophrenia is a
brain disease. Here, as in manic-depressive illness, cerebral
neurotransmitters are of great interest, and here, again, research was
stimulated when specific drugs were observed to provoke a set of
symptoms closely resembling those that emerge in schizophrenia.
Amphetamine or cocaine use, especially if chronic, can induce a
paranoid syndrome in individuals without genetic predisposition to
schizophrenia-a paranoid syndrome in clear consciousness with
delusions and hallucinations.20 In fact, a dose-response relationship
correlates the amount of dextroamphetamine taken with the severity
of the paranoid symptoms.21 Amphetamine and cocaine increase the
synaptic levels of dopamine.22

This fact took on even greater significance as it was realized that

neuroleptics effective in relieving schizophrenic positive symptoms
block postsynaptic dopamine receptors, especially the dopamine D2
and D4 receptor types.23-25 These two sets of observations-the
provocation of symptoms and their treatment both with drugs
affecting dopamine-generated the hypothesis that dopamine excess
could lie behind some of the features of schizophrenia and that
abnormalities in dopamine release, reuptake, or reception may
represent the pathological disease mechanisms responsible for a
subgroup of schizophrenic illnesses.26

Etiological Studies

As a variety of potential pathologies and pathological mechanisms

in schizophrenia emerge, efforts to relate them to etiological agencies
have followed. The etiological approach to schizophrenia, as with
manic-depressive illness, has been long directed at genetic
causation. Investigations into the way schizophrenia may be inherited
and how this inheritance functions pathogenetically (that is, the
mechanisms by which genotype could become phenotype) are in
progress.

Family studies have repeatedly demonstrated an increasing risk for

schizophrenia with increasing proximity of blood relationship to a
proband with the disorder. Adoption studies also encourage the
opinion that schizophrenia is inherited. In Leonard Heston's pioneer
research, for example, the psychiatric status of two groups of
adoptees were compared: (1) the children of schizophrenic biological
mothers raised in normal adoptive homes and (2) the children of
psychiatrically normal mothers raised in comparably normal adoptive
homes.27 The rate of schizophrenia in the children of schizophrenic
mothers was found to be significantly higher than that in the controls,
indicating that it was not adoption but biological inheritance that links
to schizophrenia. A total national population sample of legally
adopted adults in Denmark was studied by Seymour Kety and his
colleagues, whose findings confirmed the importance of genetic
factors in the etiology of schizophrenia.28

An intriguing observation from twin studies with schizophrenia was

made when monozygotic twins discordant for schizophrenia were
followed by Einar Kringlen and Gunnar Cramer. Monozygotic twins of
schizophrenics, who did not express the disorder themselves,
nonetheless had an increase in schizophrenia in their offspring. This
provided a suggestion that distinct etiological factors, genetic and
environmental, may combine to produce schizophrenia.29

The discovery that people born in the winter and spring months
have a higher incidence of schizophrenia than those born in the
summer and fall was thus most intriguing. This fact-repeatedly
confirmed-holds true across countries and cultures-and most crucially
in both the Northern and Southern Hemispheres, where winter and
summer are reversed in the calendar. This seasonal factor in
schizophrenic births powerfully suggests some injury to the
developing brain by an infection in the mother during the cold
season.30,31

The most recent hypotheses about the etiology of schizophrenia

combine genes of pathogenic potential with brain-damaging events in
pregnancy or the perinatal period, a combination of damage that may
itself have only the most subtle effects in childhood but gives rise to
the schizophrenic symptoms with maturation. Thus, a "broken part" in
the brain generated by a combination of genes and environmental
pathogens affecting fetal brain development is proposed to be the
mechanism behind schizophrenia. This requirement of a combination
of genetic and environmental pathogens could explain the
nonMendelian inheritance of the condition and the discordant
monozygotic twins.

There is good evidence that the neuropathology of schizophrenia is

of the kind that would be produced during brain development. The
disruptions in the medial inferior temporal regions are of exactly this
kind. Abnormal sulcalgyral patterns on the surface of the brain of
schizophrenics suggest abnormal neuronal cell migration from the
deeper regions of the brain to the cortex during the formation of the
neocortex. (Some failure of neuronal cell proliferation or an excessive
destruction of neurons during development cannot be excluded, given
the ventricular dilatation in schizophrenic patients.)

There certainly has emerged some physical evidence that, at least

in some schizophrenic patients, disruptions-genetic or otherwise-have
affected them in utero. Many schizophrenic patients have high arched
palates, low set ears, and fingerprint variants that identify them as
suffering from some pathological process in development that affects
the ectodermal structures, including the brain.32

A powerful support for an early life injury to brain development

showing up as schizophrenia in adult life comes from the prospective
epidemiological studies in Great Britain, the National Survey of Health
and Development and the National Child Developmental Sample, that
examined all children born in the United Kingdom during a defined
time period. Both studies identified children who as adults developed
schizophrenia. They could thus report on their childhood
appearances and behaviors. Those children who were to be future
cases of schizophrenia differed from the other children in being
significantly delayed in reaching their developmental "milestones."
They walked and talked late, had frequent speech problems and
poorer motor coordination. They scored significantly lower on IQ
measures as compared to their peers and demonstrated a preference
for solitary activities and play, avoiding other children.33.34 In other
studies, more serious signs were identified in a few preschizophrenic
children, including abnormal posture, involuntary movements, and
bodily hemineglect resembling patients with parietal lobe injuries.35

The Neurodevelopmental Hypothesis

Daniel Weinberger in the United States and Robin Murray in the

United Kingdom, from these observations, proposed that
schizophrenia be viewed as a brain disease with a developmental
component.36,37 Although the actual brain damage is produced in
fetal life, its effects are not immediately obvious; but it does disrupt
the program of development, so years later as the brain reaches
maturity a loss of psychological integration due to damage in these
areas becomes manifest-"unmasked" decisively in adolescence or
early adult life-to produce schizophrenic symptoms. Christopher Ross
and Godfrey Pearlson offered the intriguing hypothesis from their
brain-imaging studies that the heteromodal association cortex is the
brain system capable, if injured, of showing just such delayed
symptoms.38

Schizophrenia differs from most other genetic or infectious diseases

that occur in fetal life and affect the developing brain. These others,
such as phenylketonuria or congenital rubella, produce obvious
symptoms right from infancy. With schizophrenia, only the slightest
symptoms can be identified at first-and those often only
retrospectively-the full clinical picture emerging only in adolescence
and early adulthood.

This powerful hypothesis has the advantage of making sense of

many features of schizophrenia and incorporating many of the facts
around this condition revealed by epidemiological, neuropathological,
and genetic investigation.39 Like any good hypothesis, it generates
energy for further investigative work needed to bring more clarity to
the explanation of all the symptoms of this condition and the
differences among patients who suffer from it. But for our purposes its
great advantage is the encouragement it gives to the concept of
schizophrenia as a brain disease-one that may soon be identifiable
on the basis of some pathological marker that will permit the
diagnosis of schizo phrenia to move with confidence beyond a listing
of symptoms and provide the means to prevent it.

Summary

Our purpose in this chapter has been to show how the disease
perspective could organize information about a condition that can as
yet be defined only by its clinical symptoms and course. If diagnosis
must depend on such phenomena, then only the most reliable ones
should be emphasized. When we understand the disorder at the level
of pathology or etiology and have biological markers as in brain
images or from gene products, then the most reliably recognized
symptoms may in fact prove to be less important indicators of the
condition, but until that time they are the best we have.

As a category, schizophrenia is disjunctive. It is hard to grasp even

its conceptual essence beyond the fact of it as insanity. That there
are suggestions of its essence as a disorder of "executive" function
tied to frontal lobe dysfunction, and that there are emerging links
between the hallucinatory features and damage to particular brain
regions certainly encourage a continuing close study of patients and
the employment of methods for demonstrating both structural and
functional neuropathology. The concept that schizophrenia may have
symptomatic and idiopathic (i.e., genetic) forms remains strong, as
the symptomatic schizophrenias from amphetamine and cocaine
abuse bring suggestions about mechanisms.

The organization of information through use of disease reasoning

does not end the argument over the nature of schizophrenia, because
even the powerful evidence that we now have cannot be confidently
applied to all cases. However, it strongly supports the idea that the
eventual explanation of the condition will be found in brain pathology-
and the corollary that schizophrenia as an experiment of nature will
teach us about the organization of the brain in relationship to the
development of normal mental functioning.

The conditions discussed in chapters 7 and 8 do not exhaust all the

psychiatric disorders for which the disease concept may be suitable.
Evidence is available that panic anxiety and some forms of
obsessional illness (all conditions without demonstrable
neuropathology) may also be viewed in this way. On the other hand,
disease should not be thought synonymous with symptoms such as
pain or delusions, because the symptoms are the events to be
explained by the construct. It should not be used to account for
emotions such as anger or frustration, construed as the responses of
a subject to stressful circumstances; nor should it be chosen to
explain those personal vulnerabilities, such as timidity or attention-
seeking, that reflect constitutional temperament and developed
character. Certainly the disease concept should not be employed for
behaviors such as delinquency or alcoholism, in which the actions of
individuals with particular intentions are crucial.

In conclusion, we wish to keep the traditional concept of disease

separate from other explanations of human distress and abnormality.
These other explanations can combine biological with other
predisposing and precipitating features. But when we reason in terms
of disease, we seek cause in a particular kind of disordered biology-a
"broken part"-thus identifying the power of nature to mar the contents,
capacities, and course of human mental life. To hold to disease as the
sole explanation of psychiatric conditions would be to overlook the
other ways of evoking mental distress and behavioral disorder, as
through varying combinations of motives, constitution, learning, and
conflict of purpose with experience.
The dimensional perspective rests on two facts everybody knows.
First, people differ in mind just as they differ in body. Some are bright,
others dull; some are bold, others shy; some are moody, others
serene. Second, those people who are very different falter where
others flourish. They struggle and often need help in life. These facts
are so familiar that they frame the plots of novels and embolden the
predictions of astrologists, palmists, and fortune-tellers. I The
ancients, noting the irritability of the "choleric" and the sullenness of
the "melancholic," ascribed their differences to bile.

Since the middle of the nineteenth century, psychiatrists have

generated other labels for psychological deviations (often using
awkward terms such as moral idiocy or narcissism). But they did try
to help patients and families, even though their explanations for the
deviants were often as fashion bound (toilet training had its vogue) as
those of the ancients.

The science of psychometrics brought quantitation and graded

measurement to human psychology and, as well, observations and
defining concepts more amenable to brain-based explanations of
human psychological differences. This science, springing from
everyday observations, strengthened psychiatric services for patients
whose emotional and behavioral difficulties derived from their
character, cognition, or temperament. This chapter aims to show how
all this came to pass.
 We plan to clarify definitions and measurements of psychological
variation, demonstrate how deviation to an extreme in a measurable
psychological feature relates to distress and disorder, and identify
principles of treatment that take these factors into account. The
easiest place to begin is with the psycho logical variable intelligence
and with the clinical problems of patients limited in intelligence-
cognitively subnormal persons, whom we will discuss in detail in
chapter 10.

Background

Any attempt to explain psychological differences, either from brain

structure or from upbringing, needed methods to identify and
measure them. Francis Galton, the nineteenth-century English
polymath who pioneered in psychometrics, made this telling remark
about the conventional views on human psychological differences:
"An ordinary generalization is nothing more than a muddle of vague
memories of inexact observations. It is an easy vice to generalize. We
want lists of facts, every one of which may be separately verified,
valued and revalued, and the whole accurately summed."2

Galton began his studies of individual differences and psychological

performance by assessing perception, mental imagery, and word
associations. As R. E. Fancher noted, it is from Galton that we have
"the very idea that tests could be employed to measure psychological
differences between people.... He thus elevated the scientific study of
individual differences to the level of a major psychological specialty
with important social implications."3

The tasks Galton began are not finished. However, psychologists

who followed after him added the assessment of psychological
potentials and dispositional features, such as intelligence and
extraversion. With this new interest, new problems for psychology
emerged. Definitions were disputed when dispositional features such
as intelligence were considered. Validation questions that emerged
over test design asked whether any test measures the psychological
feature it claims. The early efforts at measuring intelligence illuminate
these problems and their solutions.

Intelligence: Defining a Psychological Disposition

Many definitions of intelligence have been proposed-for example,

mental efficiency, mental capacity, that quality required for scholastic
success-but none has proven completely satisfactory. Some critics
would say that like beauty, intelligence is in the eye of the beholder.
The problem is that intelligence is not a tangible object, not
something physical such as height, weight, shape, or facial structure.
Intelligence is an innate potential, latent, not mani fest-more like the
solubility of a substance or the electrical resistance of a wire-useful in
describing differences that emerge only with testing.4 Intelligence is
brought to light (and its potential made evident) when abstract
thinking, problem solving, or new learning is demanded. Intelligent
people deal with these tasks more quickly and efficiently than do less
intelligent people.

Intelligence is easier to appreciate in action than to define. Many

other psychological differences share this problem of definition, as
they are also examples of potentials evoked by circumstance. But it is
in the domain of cognition that the issue was first confronted and at
least partially resolved by psychologists.

To estimate a person's intelligence (cognitive potential), examiners

present the subject with tasks, the performance of which can be
considered an aspect of intelligence in action, and score the results.
From these scores inferences can be made about a person's
intellectual potential and how it compares with that of others, all
without explicitly defining intelligence. A progressively more confident
estimate of cognitive potential emerges as more and more such
scorable tasks are studied.
 Defining intelligence in practice is part of daily life. We all estimate a
person's intelligence by observing such things as the use of
language, grasp of situation, and speed of response. We call people
bright or dull, estimate their capacity for managing difficult situations,
and predict something of their future, all from our experience with
others. At one time or another, though, we learn that in this judgment
we can be misled, over- or underestimating individuals because of
stereotypes tied to such incidentals as manner of speech, accents, or
emotional expressions.

Psychologists are doing nothing fundamentally different. Rigor in

their appraisals brings confidence to their judgments. For example,
they add scope by insisting on several different tasks before drawing
their opinions. They add precision by scoring the responses and
comparing scores across many subjects. And they remove biases
from their tests whenever they discover them. These are good things,
but the fact remains that psychologists have but transformed the
ordinary way of estimating a person's potential into a technique. If this
is kept in mind, then test scores and the judgments based on them
will not be overvalued.

History

Alfred Binet, in France, developed the first psychological tests of

intelligence early in the twentieth century. His work was prompted by
his responsibilities to a governmental committee trying to improve the
education of mentally defective children. He thought that
measurements of the mental capabilities of children were needed in
order to plan for them.

Binet and his collaborator, Theodore Simon, began by presenting

cognitive tasks of progressive difficulty to groups of children ranging
in age from 3 to 12 years. They noted which tasks were successfully
accomplished by most children in each age group. They then used
this knowledge to define the "mental age" of any individual child by
noting the tasks the child could master and determining whether the
child was advanced or retarded by comparing the mental age against
the chronological age.5

William Stern first suggested a step enhancing the conception of

intelligence beyond the notion of mental age. He proposed that a
child's mental age (MA) be divided by the chronological age (CA) and
then multiplied by 100 to determine the intelligence quotient (IQ). For
example, the average child-by definition, one with a mental age
identical to the chronological age-has an IQ of 100, while an 8-year-
old child with a mental age of 10 has an IQ of 125. These
psychologists quickly demonstrated that this score stays fairly
constant for an individual after age 7 or 8.6

Galton had noted normal bell-shaped distributions when the mental

characteristics of a population were displayed. These were similar to
the distributions of human physical characteristics such as height and
weight discerned by the Belgian statistician Adolph Quetelet (1796-
1874). IQ scores of children, better than mental age calculations,
were also distributed in a "normal" bellshaped way in the population.
This observation opened the way to intelligence tests for adults. For
them, test items were selected so that the scores obtained in a large
population follow a normal curve. By retaining the convention of an IQ
score of 100 as the mean, the commonly used tests show only small
differences in their standard deviation (Stanford-Binet standard
deviation is 16; Wechsler Adult Intelligence Scale standard deviation
is 15).

Nature-Nurture: The Problem of Explaining Human Differences

We would certainly like to know why human beings vary in

intelligence. The quantitative and graded scores provided by IQ are a
first step toward this goal, because scores can be correlated with
other quantitative variables. Measurable differences in brain structure
and function can be correlated with IQ in an effort to find such
relationships. Such an effort, fundamental to a neurobiology that aims
to make sense of psychological potentials, has had some success.
Modest correlations between IQ and the size of the frontal lobes have
been found.? Similarly, IQ seems to correlate with reaction times to
stimuli," implying some relationship to the speed of neural
transmission. A clear understanding of the cerebral substrate of
intelligence still eludes us.

Other correlations with IQ have been informative. For example,

Lewis Terman and his colleagues demonstrated that intellectually
gifted people (IQ above 135) tend to be emotionally stable, personally
effective, courageous, and empathetic, a finding that challenges their
popular stereotype as shy, introverted, psychologically unstable
"nerds."9

The recognition of measurable intellectual differences and the

attempt to explain them brought on the "nature versus nurture"
controversy-with a vengeance and directly from the initial forging of
IQ tests. Francis Galton, the pioneer of psychometrics, defined the
terms of this conflict: "The phrase `nature and nurture' is a convenient
jingle of words, for it separates under two distinct heads the
innumerable elements of which personality is composed. Nature is all
that a man brings with himself into the world; nurture is every
influence that affects him after his birth. The distinction is clear: the
one produces the infant such as it actually is, including its latent
faculties of growth of body and mind; the other affords the
environment amid which the growth takes place, by which natural
tendencies may be strengthened or thwarted, or wholly new ones
implanted.""'

Recent Progress

The study of intelligence since Galton's time has documented that

nature and nurture combine in developing intellectual potential.
Exactly how these factors interact remains unknown, but for any
given individual either nature or nurture can have a greater or lesser
responsibility in the outcome. Key questions for psychology are how
human beings acquire intelligence and what experiences maximally
stimulate it. Correct answers would benefit education and child
rearing. Incorrect answers have been disastrous, as exemplified by
the immigration policies and the state-supported sterilization and
eugenics efforts of the United States in the 1920s.

A hereditary component to intelligence is The strongest evidence

comes from family, twin, and adoption studies that show that IQ
scores and biological relatedness are positively correlated. Identical
(monozygotic) twins are most comparable in their intelligence. A
recent Swedish-British-American collaborative study of same-sex
twins gave an estimate of 62 percent for general intelligence
heritability.12

Intelligence, like height, has a polygenic heredity. Support for this

view comes from a phenomenon (yet another of Galton's
observations) that is found in all smoothly graded polygenic traits:
regression toward the mean between generations. Individuals who
deviate from the mean in a certain characteristic will, on average,
have children who revert toward the average for that characteristic.
Bright parents will have children who, on average, are not as bright
as they-often a source of considerable distress in families of high
intellectual achievement, and dull parents will have children who, on
average, are brighter than they are-often a source of great
satisfaction.

For intelligence, the degree of reversion is approximately 30

percent of the deviation from the mean of the parental partners. Thus,
if the mother has an IQ of 135 and the father an IQ of 125 (their
mean, 130, being 30 points above the population mean), their
children will distribute their IQ around a mean of 121. Conversely, if
the mother has an IQ of 80 and the father an IQ of 70 (their mean, 75,
being 25 points below the population mean), their children will
distribute their IQ scores around a mean of 82.5. Reversion to the
mean also works in the opposite direction. Very dull and very bright
children have parents who tend, on average, to be closer to the
population mean in IQ.

All these reversions are statistical features tied to the regular

reproduction of a stable, bell-shaped IQ curve in the population,
generation after generation. However, because bright individuals
presumably provide a stimulating environment for their offspring,
these findings of reversion undermine the view that all intellectual
capacity derives from its nurture. A multifactorial, polygenetic
explanation best serves these observations.

Heredity cannot be the sole explanation for an individual's

intelligence. Environmental factors clearly play some formative
function. Anything that damages the brain-such as maternal
alcoholism during embryogenesis, anoxic obstetrical complications at
birth, or exposure to lead in childhoodwill hurt intelligence.

Environmental influences, especially social ones, that enhance

intelligence are more difficult to specify, but that they exist is certain.
One telling example is the increase in IQ scores (as much as 12
points) in children adopted out of dysfunctional families in infancy.'3
Another is the increase in the mean IQ scores that have occurred in
most countries in this century. Read Tuddenham was first to
demonstrate this last point by showing that significant increases
occurred in mean IQ scores in American soldiers from World War I to
World War II without any other obvious explanation than
improvements in nutrition, hygiene, and education of the American
population as a whole.14 Such improvements seemed to be
associated with the overall average increase in height in the same
population. However, a better education during the formative years of
childhood may well have been crucial. L. R. Wheeler demonstrated a
similar value of environment by linking enhanced IQ scores in
children in one region of Tennessee to improved social conditions.15
 This early work culminated in that of James R. Flynn, who, following
up on intelligence testing in the U.S. military, found that scores on
virtually every type of IQ test have risen roughly 3 points per decade
in the population of this country in this century.'6 In fact, scores from
both Wechsler and StanfordBinet tests rose 24 points in the United
States between 1918 and 1989.17

Flynn demonstrated similar increases in other countries that have

historic records on their population's IQ. These generational
increases in IQ are evident with tests that have the least
contamination from cultural or educational advantage, such as the
Raven's Progressive Matrices, which probe the ability to recognize
abstract patterns and solve nonverbal challenges.18 This remarkable
observation has been called the Flynn effect by Richard Herrnstein
and Charles Murray.19 These authors dismissed the phenomenon as
a curiosity. However, it is a striking demographic observation and has
occurred over a briefer time than could gene action. It gives
encouragement to efforts at increasing educational experience,
especially for infants and children. In fact, all these results support the
value of national programs such as Head Start that attempt to
accelerate the intellectual development of children in poverty who are
at risk for mental subnormality.20

The Flynn effect indicates either that early experience is crucial to

intellectual potential or that IQ tests measure other things than an
innate trait. Both implications are likely: intelligence, like many other
brain-based traits, can be enhanced by experiences that stimulate
neural growth during formative years, and IQ tests are sensitive to
training-by exposure either to tests themselves or to specific
experience with test material in school. What is clear is that
presentday students have intellectual potentials their parents did not
have.

Social Controversy Generated by IQ Testing

 Perhaps the most socially disruptive controversies in psychology
have emerged from cross-ethnic and cross-class studies using IQ
tests. These issues, fundamentally issues of cross-cultural validity of
IQ tests, are unresolved but remain a source of argument between
hereditarians and environmentalists over the generation and
implications of IQ.

We hold and will argue in the following text that as with the
generation of bodily height, it is likely that an individual's genetic
inheritance sets some limit on ultimate cognitive potential but that
environmental circumstances, when adverse-as in nutritional or
educational deprivation-can impose a much lower limit. In fact, as H.
J. Butcher pointed out, societies can be so different from one another
that "what is given at birth" may assume almost any degree of relative
importance for the eventual development of intelligence.21

We can be more explicit about this awkward matter. The nature-

nurture problem devolves into several arguments. Even the most
vociferous opponents tend to agree that individuals are possessed of
a general mental capacity called intelligence, which is sometimes
designated by the letter g. This capacity is reflected to some degree
in all the diverse types of cognitive talents we can measure. The strict
hereditarian would hold that differences in this general intellectual
capacity (g) among individuals and among groups of individuals are
the result of genetic differences. The strict environmentalist, on the
other hand, would propose that although individuals may inherit all
sorts of different specific talents, any general intellectual endowment,
if it exists, is identical for each individual; thus, all differences in
cognitive abilities for individuals as well as for groups are the result of
different experiences.

The most recent data on intelligence and heredity demonstrate that

neither the pure hereditarians nor the pure environmentalists can be
correct. Some 62 percent of the IQ variance among individuals
depends on their genetic variance, and thus some 38 percent of their
cognitive variance depends on environmental variance.22

This split means that in the argument about ethnic or other group
differences, a middle ground can fit what data are available. This view
holds that individuals inherit different genetic endowments for
intelligence. But, large human groups such as nations or races do not
necessarily differ significantly among each other in their genetic pools
for intellectual capacity. All intergroup differences in cognitive ability
can be the result of those environmental and experiential differences
that distinguish one group from another. Further, whatever the
proportion of variance in intelligence we ascribe to heredity, for
practical purposes society can act and plan as though environmental
influences are crucial.

Implications of Intelligence for Life Success

Herrnstein and Murray, in their book on intelligence mentioned

earlier, made a point: "Measures of intelligence have reliable
statistical relationships with important social phenomena but they are
a limited tool for deciding what to make of any given individual.... IQ is
not a synonym for human excellence."23 Many students of IQ make
similar points in relationship to the ultimate achievement of
competence by individuals who work to learn.

The correlation between IQ and scholastic achievement is high (r =

.5), but this figure indicates that IQ in fact explains only 25 percent of
the scholastic variance among students. Presumably other personal
features, such as persistence, energy, interest, and luck, play
important roles in achievement. Julian Stanley has noted from his
experience with hundreds of gifted children that intellectual potential
represented by high IQ is not necessarily associated with mental
energy. A high IQ does not guarantee success nor a lower IQ failure
in schoolwork or in life. As Stanley has said, "You can't major in IQ."
24
 IQ is not destiny but rather an indicator of potential, enhancing or
reducing the odds of success. Again and again in The Bell Curve
Herrnstein and Murray showed that IQ correlates with success and
failure in our society but does so as but one of several factors-an
important one, no doubt, and one more easily measured than some
others-but not the sole one. Furthermore, all the social problems they
tied to low IQ-poverty, unemployment, crime, and so onwere
problems for the minority, not the majority, of people with a low IQ.
When not burdened by racial bias and discrimination, the majority of
people in the lower ranges of IQ are able to find employment, stay
employed, avoid poverty, and sustain family life. Such facts should
encourage teachers, social workers, psychologists, and psychiatrists
who attempt to help people achieve just such social goals. Low IQ
puts a person at risk for failure, but this risk can be mitigated with the
development and encouragement of protective factors such as
education and family harmony.

Another fact relating IQ to independent living is that the demands

on intellectual potential are greatest in the acquiring of a skill or
occupation. Once such a skill is learned, its regular employment-as in
a daily job-is usually less demanding intellectually. This fact
encourages remedial work and extra vocational training for people
with lower intellectual potential because they can usually sustain the
employment level that they have needed help to achieve.25 Finally,
the availability of social safety nets and early assistance are
important to the vulnerable. This assistance permits them to regain
their stability, occupation, and social integration much more swiftly
when misfortune or mistakes happen than they would if required to
depend on their own capacities to cope and plan. All these
implications are tied to the concept of IQ as cognitive potential rather
than fate.

A Final Advantage of a Valid IQ Measure in Clinical Settings

 Intelligence is a potential. It is expressed in the skills learned in life
and developed through experiences in a family, an occupation, a
school, and so forth. These skills are acquired more rapidly in the
highly intelligent and more slowly and more limitedly in the less
intelligent. Nonetheless, lifetime competency is the outcome not of
intellectual endowment alone but of what was endowed and what was
acquired.

In the history of standardized intelligence testing, a celebrated

achievement was to identify individuals who were educationally
backward because of a lack of teaching and distinguish them from
those who were intellectually defective.26,27 Differentiating
educationally backward from defective children engendered better
efforts at remediation of both problems. This discovery also
emphasized the importance of watchful efforts to guarantee adequate
education to all children-regardless of class, race, ethnicity, poverty-to
open the pathways to their success and fulfillment.

Although intelligence test scores may be abused to further handicap

individuals and may, if improperly understood, lead to social policies
one can deplore, clinical evaluative judgments would be more difficult
without them. To rely solely on personal and perhaps idiosyncratic
judgments of intelligence is to risk underestimating the capacities of
individuals thought unintelligent because of such extraneous features
as race, social class, or physical appearance.

Also, without some form of testing, we would overlook and deny

assistance and remedial opportunities to those with intellectual
deficits. Such special effort can enhance their skills and knowledge,
guide them into situations where they can work and be protected from
exploitation, and make clear the links between their emotional
reactions and provocative situations-such as accidents, losses, and
economic demands-that test their intellectual powers.

Summary
 Intelligence testing, however controversial, has been valuable as
long as its limits have been recognized. Its achievements in
predicting scholastic performance and in differentiating the
educationally backward from the intellectually subnormal were major
stimuli for the development of other psychological tests. As a
quantitative, graded measure of potential, IQ represents an important
predictor of social security and a dignified social existence. A lower
intellectual potential renders a person more vulnerable to failure and
more serious consequences in the face of bad luck or misfortune.

Obviously, when possible, intelligence should be enhanced and

protected. However, IQ does not determine social success. Skills
derived from education, which a higher IQ makes easier to acquire,
are decisive. Individuals with lower IQ scores are helped by remedial
measures that enhance the skills that their lesser potential renders
more difficult for them to achieve. They also may need extra support
and assistance when misfortune strikes so as to mitigate its
deleterious effects.

Although not originally designed to aid psychiatrists, the definition

and measurement of intellectual potential have illuminated several
mental and behavioral disorders. These advances are most obvious
for mental subnormality, a subject to which we now turn.
People at the lower end of the IQ dimension-cognitively subnormal
persons-elicit psychiatric attention because they face many problems
in adjusting to life, given their limitations. These problems include
difficulty in the acquisition of skills needed for independent living and
a vulnerability to distressing and persistent emotional states when
faced with failure or misfortune. The processes of identification and
treatment of patients with lower IQs bring to light general principles of
the dimensional perspective that apply to psychiatric practice.

Definitions

The defining feature of mental subnormality is a lifelong deficit in

intellectual potential. Individuals with this deficit are slow to learn,
have difficulty in abstract reasoning, and are vulnerable to social
failure and exploitation. They need extra assistance, such as in
education in order to strengthen such occupationally critical skills as
reading and arithmetic. They also need thoughtful guidance in the
choice of their life paths. Strengthening and guiding are the operative
terms for helping these patients. With such help, many of them are
capable of an independent, contented, and dignified life.

For centuries, people with lifelong deficits in intellect have been

distinguished from others with other mental difficulties. As John Locke
observed: "Madmen put wrong ideas together, and so make wrong
propositions, but argue and reason right from them; but idiots make
very few or no propositions, and reason scarce at all."' Locke's
statement distinguishes between someone with the delusions of
schizophrenia, a mental disease, from someone cognitively
subnormal. Note, however, that such stigmatizing terms as idiot
emerge in the description and derive from a categorical or typological
approach to classifying subnormal patients. The dimensional method
of defining subnormality and subtypes has replaced Locke's method
with many advantages.

Recognition and Differentiation in the Dimensional Perspective

Mental subnormality was recognized and some of the burdens

faced by subnormal people appreciated long before intelligence tests
and IQ scores were developed. However, with such scores it is
possible not only to employ a quantitative definition of subnormality
but also to appreciate the problematic issue of subnormality's
classification and subclassification.

The standard practice is to restrict the class of mentally subnormal

individuals to those who fall two standard deviations below the mean
IQ for the population. Customarily, depending on whether the
Stanford-Binet or the Wechsler Adult Intelligence Scale is used,
anyone with an IQ below 68 or 70 is classified as subnormal. Given
this distribution around the mean, terminology would suggest that
subnormal is preferable to retarded or learning disabled as a means
of identifying these people.

"Normality" and "Abnormality" as an Issue for Dimensional

Characteristics

This technique of classification by an IQ score is helpful for some,

but not all, clinical purposes. As we have described it and as IQ
scores reflect, intelligence is a smoothly graded dimensional variable
in the human population with no clear cutoffs or abrupt discontinuities
separating one group of people from another. It is a trait recognizable
in its greater or lesser power in everyone. Where to say the "normal"
population ends and the "abnormal" people emerge is arbitrar even
though an individual extremely deficient in intelligence is usually
obvious.

To make this arbitrary aspect clear consider, for example, a man

with an IQ of 75. By definition, he falls within the unimpaired group
because he is only 1.5 standard deviations below the mean. But
because a variation of 6 points on repeated testing is not unusual,
would a second test score of 69 then make him impaired? This
question reveals the awkward matters of definition of normality and
abnormality that are inherent to the dimensional perspective, its
measurements, and its definitions.

We are dealing with a matter of "more or less" rather than "all or

none." We have drawn a distinction in the population at a
conventional and convenient mathematical point on an unbroken
curve, a distinction that identifies a group of people that clinical
experience has shown often has trouble because of what is
represented by their position on such a curve. That is, emotional
problems and social malfunction will more certainly derive from a
patient's limited cognitive potential when this potential falls below two
standard deviations from the mean. Likewise, emotional and
behavioral difficulties attributable directly to intellectual limitations will
be less frequent in people whose cognitive powers are higher.

How to explain and manage the problems experienced by people

with cognitive subnormality rests on issues other than simply the
measurement of their IQ. How this lowered potential for planning and
abstract reasoning puts such people at risk for emotional distress and
disorder is fundamental to an understanding of the dimensional
perspective.

Potential-Provocation-Response

The implication is that psychological potentials interact with life

circumstances to produce emotional distress and behavioral disorder.
This interaction applies in all "dimensional" disorders and encourages
efforts at drawing distinctions in smoothly graded traits within the
population. Yet, as we have said, it is most easily exemplified by the
study of patients with mental subnormality.

A low IQ in itself is not the problem. IQ is a measure of cognitive

potential, the weakness of which becomes apparent in an
intellectually subnormal individual only when he or she is faced with a
cognitively demanding task. The person may cope more or less well
with any particular task. However, if demanding enough, such a
challenging stimulus can provoke a distressing emotional reaction in
the individual as he or she struggles against failure. This reaction, not
the low IQ, is what attracts psychiatric attention, identifies the person
as a patient in need of explanation and treatment.

As the cognitive potential falls among people (as indicated by

measured IQ), then more and more individuals will find challenging
the matters of decision, judgment, and learning presented by daily
experience. Individuals at the lower levels of IQ will find many
ordinary demands of life such as basic education to be emotionally
taxing. Challenges that defeat the person will provoke intense but
familiar human responses to failure such as depression, anxiety, and
irritability.

Central to this idea is that the psychological responses of

depression, anxiety, and so forth are not expressions of low IQ
directly. They are the distressing states of mind provoked in anyone
struggling with a challenge that exceeds his or her capacity.

By this reasoning it follows that identical psychological responses

will emerge in individuals with "normal" IQ faced with a challenge that
overwhelms them. Certainly psychiatrists recognize emotional
distress derived from a sense of failure, even among those whose IQ
scores do not fall below the arbitrary two-standard-deviations
criterion, when they are struggling with a complicated problem. It is
the struggle that produces the reaction. The struggle is the outcome
of the relative weights of two factors: the individual's IQ and the
difficulty of the task. It is in this combination that we identify the
emotive paradigm: potential (IQ), provocation (cognitive challenge),
and response (the emotional states tied to a struggle for success).

To summarize, individuals whose IQs fall two standard deviations

below the mean will usually find difficulty with relatively
straightforward tasks such as elementary school education and show
their distress in struggling with such tasks. Individuals at the mean for
IQ (100) will, if they attempt to tackle a career in high science such as
advanced physics or chemistry, have similar difficulties with such
complicated studies and again show distress as they struggle with the
material and fight against failure. The synergistic interaction of
potential, provocation, and response-a paradigm for explanation in
the psychiatry of dimensions that in future we shall refer to as the
emotive paradigm-is most clear in cognitively subnormal patients. We
revisit this concept in the subsequent chapters of part III.

Subclassification of Subnormality by IQ Score

The IQ scores do more than identify a general potential for difficulty;

they permit an approach to subclassifying the mentally subnormal
that has useful prognostic features. Subclassification of the
population of people with lower IQ into mild (IQ 69-55), moderate (54-
40), severe (39-25), and profound (24 and below) subnormalities
makes categories out of groups of patients in each of standard
deviation units below an IQ of 70. These arbitrary divisions of deficit
identify progressive weakness in cognitive potential and greater risk
for emotional distress and behavioral disorder.
TABLE 2. Lewis IQ Table
Source: Data from Penrose LS: The Biology of Mental Defect, 3rd ed.
London, Sidgwick and Jackson, 1963, pp. 49-50.

For example, although mildly subnormal persons need guidance in

periods of distress, they can acquire many basic educational skills,
such as reading and writing, and are capable, with extra training, of
social and vocational functioning that brings a degree of self-support,
up to complete independence. Many such people by adulthood are
indistinguishable from the rest of the community and may not then be
recognized as subnormal unless they are examined.2 Moderately
subnormal persons are trainable in social and vocational skills but will
usually need direction and sheltering, as their educational capacities
seldom reach beyond the second-grade level and their social
judgment is poor. Severely disabled persons do not profit much from
education, but can develop self-protective skills and habits of
cleanliness that allow much independence within a protective
environment. Profoundly subnormal persons need nursing care,
being only minimally able to look after themselves. As will be
discussed further, profoundly subnormal persons are usually
burdened by neurological symptoms and signs that indicate brain
disease as the source of their cognitive impairment.

Subclassification of Mentally Subnormal Persons by Pathological

and Physiological "Types"

Profoundly intellectually subnormal patients call attention to another

waytied to the cause of their subnormality-of classifying patients that
has critical implications for prognosis, treatments, and prevention.
Although for purposes of definition we have focused on the smoothly
graded distribution of intelligence in the population, the IQ curve for
the population is not perfectly symmetrical. There are more
individuals two standard deviations below the mean than there are
two standard deviations above it. This observation can be made
whenever a total population sample is drawn into IQ assessment,
taking care not to miss any individual, including those in chronic care
institutions.

E. 0. Lewis pointed out in his survey of an English county that this

asymmetry is produced mainly by finding a larger number of
individuals among more severely defective persons (below IQ 50)
than would be expected from a perfect Gaussian curve (figure 5).3
Table 2 shows the percentages that Lewis found in various IQ
categories and compares them with the percentages predicted from a
perfectly normal distribution. The percentage of the population found
in the 50-70 IQ group is essentially what would be expected from a
normal distribution. But there are six times as many people as would
be expected in the lower categories. Lewis could explain these
findings only after examining the individuals. Then he observed that
two different groups are found among the intellectually subnormal
persons.

One group, people whom he called subculturally or physiologically

subnormal, is made up of individuals who are the counterparts of the
intellectually gifted in the population. They have apparently intact
nervous systems, are mostly mildly subnormal (clustering in the 50-
70 IQ range), and are the expected occupants of the lower end of the
"normal" distribution. They have parents who are on the low side of
the mean for IQ, and they are much more heavily represented among
socially deprived families. A multiplicity of genetic and environmental
factors seems to have contributed to their deficits. They represent the
majority (75-80 percent) of the group of mentally subnormal persons.

The other group consists of individuals who have brain damage.

This damage may be due to a faulty gene or to brain injuries
produced during gestation, delivery, or early development. Lewis
called these individuals pathologically subnormal, and though they
are the minority (no more than 25 percent of the subnormal
population), most have IQs of 50 and below.

These latter patients carry neurological signs and symptoms and

physical stigmata (microcephaly, facial deformities, and the like) along
with their subnormality. They are burdened by palsies, epileptic
seizures, and sensory deficits including blindness or deafness, as
well as by a lowered intellectual potential. Their parents are
distributed more equally around the mean for IQ, and they are not
overrepresented among socially deprived persons.

It is the second group that gives the asymmetrical character to the

IQ curve. In fact, the asymmetry of the IQ curve is best understood as
a form of bimodality in the population on this dimension of human
variability-intelligence. At the lowest end there is a small "mode,"
consisting mostly of braindamaged individuals and very few
undamaged ones. As the dimension is ascended, the brain-damaged
individuals drop out and the major mode of the intelligence capacities
of the undamaged individuals appears, peaks at IQ 100, and comes
down to a normal tail at the high end.

We have, in fact, one trait-intelligence-but within the population

displaying that trait there are two groups of people: one group
representing the normal distribution and another group, people with
brain disease. This observation of a subgroup with disease buried
within a "normal" distribution and distorting its shape is not restricted
to psychological measurements. The same phenomenon is found in
the distribution of blood pressure measurements in the population:
the upper range of the normal distribution is inflated by patients with
diseases such as pheochromocytoma and renal artery occlusion.

Clinical Problems of Pathologically Mentally Subnormal Persons

 Persons with a pathologic mental subnormality are most often the
subject of intensive psychiatric attention. In this group are patients
with many brain diseases, particularly those related to problems of
development and birth. They include genetic anomalies, infections,
malformations, traumatic injuries, asphyxia, endocrine disorders, and
the effects of toxins.

These people suffer from neurological symptoms that vary with the
severity, nature, and location of their pathology. These symptoms
include epileptic seizures; motor-sensory impairments; perceptual
disorders; and abnormalities of growth, bodily structure, and physical
appearance.

Their burdens derive from more than just their intellectual

impairment. They are often physically deformed and dysplastic in
various ways-some standard and recognizable at a glance, some
unique to the individual. They have symptoms that impair their
movements, their interactions with others, and their independence.
They often have a "splintering," or asymmetry, of psychological
interests and capacities and an autistic quality of troubling
strangeness and inaccessibility to their demeanor.4

Although a complete consideration of all the forms of brain disorder

that can adversely affect the development of cognitive potential goes
beyond our purposes, three particular causes, which are examined in
the next three sections, of pathological mental subnormality
demonstrate important principles for managing and preventing these
disorders.

Genetic Disorder as a Source of Pathological Mental Subnormality

In the population of pathologically mentally subnormal persons,

single-gene disorders are frequent. The afflicted are usually
homozygous for a recessive gene. Dominant gene disorders are
seldom found among mentally subnormal persons because if they
appear as mutations, they are quickly eliminated from the genetic
pool owing to the reduced fertility of individuals who are mentally
subnormal. Recessive genes, manifesting symptoms only when
present in the homozygotic form, are preserved longer in the genetic
pool because heterozygotes are relatively unaffected.

A classical example of such a recessive condition is

phenylketonuria. In this disorder, the homozygotic individual is
deficient in phenylalanine hydroxylase, an enzyme critical to the
formation of tyrosine and thus to several important neurotransmitters.
Without the enzyme, phenylalanine accumulates because it cannot
be metabolized. These patients show high levels of phenylalanine in
their blood and cerebrospinal fluid and spill the metabolic products of
that amino acid in their urine. They can be protected from developing
the clinical manifestations of the disease (which include small stature,
convulsions, and eczema in addition to severe mental subnormality) if
they maintain a diet low in phenylalanine during childhood and
adolescence.

This condition exemplifies many of the issues raised by recessive

genetic disorders. First, such disorders produce a severe mental
subnormality if no treatment is found. Second, a biochemical
abnormality accompanies the individual's symptoms and is usually
attributable to the lack of some vital enzyme in a metabolic path.
Third, such recessively inherited conditions are more common in
consanguineous matings, because individuals who share a common
genetic pool are more likely to share a rare gene arising from a
common ancestor than are unrelated individuals. Fourth, the search
for carriers of the recessive gene (heterozygotes) has great
importance for genetic counseling.

The people carrying a recessive gene are usually not easy to

identify-a distressing feature, given that their offspring can have such
severe subnormality. However, in phenylketonuria it is possible to
identify heterozygotesif there is any warning-because with only one
normal gene for the enzyme and thus a smaller amount of it,
heterozygotes are slower than normal in metabolizing phenylalanine
(although not so slow as to be injured by it). For phenylketonuria and
similar disorders, there is a need to learn how the biochemical
abnormalities affect the developing brain so that still better modes of
protection can be found.

Chromosomal Abnormalities as a Source of Pathological Mental

Subnormality

The group of pathologically subnormal individuals with gene

disorders should be distinguished from the group with abnormalities
in the number or structure of their chromosomes. The development of
standard cytological tech niques for separating and typing
chromosomes has made possible the identification of hundreds of
chromosomal disorders.

The most common of these to produce severe mental subnormality

is Down syndrome (trisomy 21). Here, the extra chromosome 21
misdirects the development of the brain, impairing intelligence, just as
it affects the development of other parts of the body, causing defects
in stature, appearance, and dentition and often altering the structure
and function of the musculoskeletal, cardiac, and gastrointestinal
systems.

A form of mental retardation linked to a morphological abnormality

on the X chromosome called fragile X syndrome accounts for a large
number of mildly to moderately subnormal males (and some
females). This condition is now appreciated as due to an inherited
DNA section on the X chromosome that "expands" in gametogenesis
generation after generation and produces more and more severe
affliction. This portion of the genome at the tip of the X chromosome
consists of an unstable trinucleotide repeat.5 It alters the physical
appearance of the X chromosome (when stained properly) such that
the tip seems only loosely adherent to the body of the chromosome,
hence the name fragile X.

This condition produces mental retardation and a typical dysplastic

physical appearance. Its inheritance follows that of a typical X-linked
disorder, but worsening over generations. Fragile X syndrome may be
sufficiently common to explain much of the excess of males in the
subnormal population.6

Pathological Subnormality Due to Toxic Fetal Environment

Alcohol consumption by pregnant women is the most common

teratogen to which the developing fetus is likely to be exposed.
Because alcohol passes freely through the placenta, the fetal brain is
exposed to blood levels as high as those the mother experiences. In
fact, some 10 to 20 percent of alI pathologic mental subnormality may
be attributable to maternal use of alcohol. Alcohol may have multiple
effects on the developing brain, such as impairing the migration of
cells during embryogenesis. Useful distinctions have been made by
separating patients with fetal alcohol syndrome (FAS) from those with
some of the same abnormalities but not as seriously affected (fetal
alcohol effects, or FAE).7

Among the typical features of FAS are mental subnormality,

microcephaly, craniofacial anomalies, and developmental retardation.
One in 1,000 babies born in the United States has FAS. This most
common form of pathological mental subnormality is totally
preventable by abstinence from alcohol during pregnancy, a point
made by the U.S. surgeon general.

Treatment and Care of Pathologically Mentally Subnormal Persons

Pathologically subnormal persons have brain pathology derived

from a variety of etiological agencies. Their injury appears not only in
their lessened cognitive potential but also in the intrusions of other
symptoms and signs of brain disease and in the imperfect and
unequal development of their executive and emotive controls, which
impairs their social adaptation.

Treatment usually must begin with management of the symptoms

and signs of the neurological impairments. Adequate treatment of
epileptic seizures is particularly crucial because measurable
improvement in intellectual capacity and a considerable improvement
in overall energy and responsiveness occur in the patients so treated.
In like fashion, treatments and rehabilitative services for spasticity,
speech disorders, and sensory losses enhance independence and
competence of these patients.

Pathologically subnormal persons are also at increased risk for

particular behavioral and emotional disorders. Symptom clusters
resembling infantile autism, attention deficit disorder, and pervasive
developmental disorder are common among these patients. James
Harris has spoken of "behavioral phenotypes"8 in relation to
particular pathological conditions and pointed out how such
stereotypic syndromes emerge. In fact, the high incidence of
symptoms such as autism and self-injury among persons who are
syndrome-specific pathologically subnormal is some evidence that a
brain pathology often underlies these behaviors when expressed in
other mentally subnormal children.

Close follow-up of individuals with Down syndrome revealed their

risk of developing a dementing illness with the neuropathological
changes of Alzheimer's disease in middle age.9 Data from the
Camberwell Study also indicate that the prevalence of schizophrenia
is greater among pathologically mentally subnormal persons than
among the rest of the population.10 Affective disorder, both
depression and mania, also occurs with increased frequency among
these patients. In subnormal individuals, delirium, dementia, manic-
depressive illness, and schizophrenia can be diagnosed by their
usual clinical criteria. As A. H. and others have pointed out, however,
the verbal skills of people with IQ below 45 are often insufficient to
permit the easy recognition of characteristic abnormal mental
experiences. With patients in this IQ range, such diagnoses must
often rest on changes in overt behavior and emotional expression (for
example, periodic variations in socialization, activity level, and sleep
could suggest manic-depressive illness). For similar reasons, the
treatments for these disorders need especially careful monitoring in
subnormal patients because they can contribute less than other
people to reporting progress of their recovery.

Mentally subnormal persons with superimposed emotional or

behavioral disorders have a double burden to bear. However, once
adequately evaluated, these patients, like all others, can respond well
to treatment. Examples of useful pharmacological treatments include
stimulants for attention deficit disorder, tricyclic or serotonin-reuptake-
inhibiting antidepressants, and neuroleptic medications for
schizophrenic symptoms. Social and behavioral training and
treatments are also invaluable for these patients. It is often difficulties
in this realm-as with self-injurious behavior, social withdrawal, food
refusal, and aggression-that frighten the families of these patients
and bring them to specialists.

Efforts to find the best treatments for patients with these interactive
impairments and dysfunctions can result in remarkable improvement
in their social integration and happiness. Their families, in particular,
appreciate the gains from apt psychiatric formulations, diagnoses,
and treatments because such actions greatly reduce the burdens of
caring for these patients and enhance the pleasure of the family's and
patients' lives together. Such enterprise represents a most satisfying
form of psychiatric practice.

Physiological (Subcultural) Mental Subnormality

Physiological subnormal individuals differ from "normal" people only

by their reduced intellectual capacity and do not carry extra burdens
and identifying signs such as epilepsy, paralysis, or sensory
impairment. Their difference is quantitative and seldom more than
moderate in degree. Their physical appearance is indistinguishable
from others: they may be tall or short, handsome or plain. Their
cognitive deficiency may not be evident until they face tasks, such as
school or employment, that demand a certain level of abstract
reasoning and learning skill.

It may not be until they enter school as young children that their
relative lack of intelligence is recognized. Their earlier developmental
milestones, such as talking, walking, and toilet training, are usually
attained at suitable ages or recognized as delayed only in retrospect.
Their problems appear only when they are faced with the necessity of
learning abstract concepts. They show difficulty in learning to read or
compute, and they need special help to progress.

The therapeutic implications are obvious. These patients with

limited intellectual potential need intensified instruction not only in
scholastic subjects where they are particularly weak but also in
socialization, manual and vocational skills, and home economic
competence. These treatment needs and methods have been
appreciated since Edouard Sequin and Maria Montessori.12 Leo
Kanner emphasized in 1952 how important the emotional state of the
patient is for the success of educational efforts.13 A great need
continues to exist for trained evaluators, social workers with some
advanced education in methods of measurement, to assess the
context of the lives and school performances of these patients. Also
highly beneficial are teachers who appreciate the importance of
helping these people achieve any small gain in social skills and
education.

If protected and assisted during childhood and adolescence, the

mildly subnormal person may disappear from clinical attention. This is
particularly likely if the person's life enters into a settled routine of
interaction with others as a member of a supportive family and as an
employee in a manageable job. Then only with misfortunes or
accidents that disrupt such situations (the death of a spouse or the
closing of an industry) do the impairments of these people again
become apparent. In the periods of life marked by the need for
analysis, learning, and planning, such individuals demonstrate their
vulnerabilities, are at risk for emotional distress, and often need
psychiatric attention and care.

The "Emotive Triad" and Principles of Treatment for the Problems of

Mentally Subnormal Individuals

We have considered treatments that assist mentally retarded

patients either by attending to the symptoms derived from a brain
disorder or by providing appropriate guidance during development so
as to optimize their opportunities to live as independently as possible.
Now we shall describe the principles of treatment for symptoms that
emerge later in life and bring these patients to psychiatric attention
anew.

It is crucial, however, to appreciate that simply being mentally

subnormal does not translate directly into being a psychiatric patient.
Mentally subnormal people in the other aspects of their character and
their capacities, such as devotion to a job or a family or their potential
for good and for evil, are as various as people with higher cognitive
powers. Many of them are capable of independence and a life of
contribution to others. In fact, it is in their similarity to others that
mentally subnormal individuals are vulnerable to feelings of
discouragement and to emotional expressions of anxiety, depression,
and frustration if what they intend is thwarted by circumstances or if
their inability to formulate a plan interferes with their recovery from
misfortune. These feelings of theirs are exactly like anyone else's.
The vulnerability is simply to the lower degree of challenge they can
sustain.
 Anxiety and frustration certainly do act to reduce still further, albeit
temporarily, their cognitive efficiency. Prompt efforts to help a patient
in such a circumstance are necessary to keep matters from
worsening further. Nothing that we are saying, though, should be
interpreted as implying that these emotional reactions are unique to
mentally subnormal persons. Their emotional states are not
pathological in themselves but exactly the kind experienced by
anyone demoralized by failure.

Misfortune such as an accident can launch a downward spiral of

failure, discouragement, further failure, and intense emotional
distress. This cluster of problems is often discernible as one listens to
the history of recent events and the patient's worries and hears from
the patient how they relate to the patient's aims and what ideas he or
she has had to resolve them.

The confusion of purposes, the particulars of challenge (inability to

balance a checkbook, deal with a teacher, avoid exploitation, and so
on), and the sense of being frightened, overwhelmed by
circumstances, paralyzed by indecision, and depressingly isolated
are characteristic problems that emerge during a sympathetic,
thorough interview and represent manifestations of demoralization
and discouragement. Intellectual subnormality makes the patient
vulnerable to this reaction, but circumstances provoke it.

Again, this formulation exemplifies the "emotive paradigm" to

explain the discouraging and demoralized states of mind that these
patients suffer. Given the concept of potential-provocation-response,
a rational treatment plan must have two interactive aspects. First,
relief must be provided for the immediate problem (i.e., the patient's
presenting distressful response and its provocative stimulus).
Sometimes the patient will be helped by some mild tranquilizing
medication for anxiety or grief while plans are developed to deal with
a pressing challenge. A patient may benefit from brief hospitalization
for respite from some exploitative situation. This first aspect of
treatment brings the encouragement of support to the patient and
usually reduces demoralization, the sense of isolation, and agitation.
This phase of treatment also interrupts the downward spiral of further
confusion and incompetency that the emotional state has provoked.

The second aspect of therapy consists of efforts at counseling for

the future to help the patient avoid such situations that strike at his or
her vulnerability as that provoking the recent trouble. Sometimes this
step requires a better placement at school, protection from failure and
better pacing for slower learning. Sometimes it demands a better
coordination of family and community resources in order to eliminate
aspects of isolation and exploitation of the patient. Mostly it requires a
thoughtful consideration of the place of the patient in life and of the
presenting, here-and-now, challenges that threaten and defeat him or
her.

Knowledge of the vulnerability of the patient to troubles encourages

these efforts. Also, the potential-provocation-response concept will
encourage the testing of treatment plans and their revision when they
do not succeed. A treatment plan of strengthening and guiding has
different implications from a treatment aiming at cure. One of these
implications is considering many alternative paths to a goal and often
reconsidering the goal itself. Given a demoralized patient, his or her
premorbid social stability, particularly a stable employment history, is
a good predictor of final recovery. But a thorough assessment of the
present provocation and what it has done to the patient is needed.

Thus, the overall goals of treatment are two. First, help the
immediate emotional and behavioral reaction. Second, strengthen the
patient against subsequent failure (through instruction and
remediation of skill deficits) and guide the patient toward activities
and circumstances where the vulnerable potential is less exposed.
With the dimensional perspective, both of these aspects of treatment
require follow-up in the form of periodic counsel and redirection to
keep "the good times going" and to avoid new challenges to the
patient's vulnerabilities.

Summary

Mental subnormality illustrates psychiatric disorders that relate to

dimensions of human variation. Intelligence is the dimensional feature
and patients at the lower end, mentally subnormal persons, often
need psychiatric assistance. Mental subnormality can be provoked by
brain disease-pathological mental subnormality-or can encompass
people who naturally make up the lower end of the "bell-shaped"
curve-physiologically subnormal persons. Patholog ically subnormal
individuals have neurological deficits as well as a reduced cognitive
potential.

Patients with mental subnormality are at risk for emotional distress

in the face of what seem to be modestly challenging circumstances.
This distress can worsen the performance of these compromised
individuals and is usually explained by the interaction of potential,
provocation, and response that we have dubbed the emotive
paradigm. Treatment of the distress resolves into two interrelated
aspects: relief of the emotional responses to the current provocations,
and strengthening, counseling, and guiding the patient so as to avoid
similar provocative situations in the future.
A traditional but rough-and-ready psychological distinction divides
conscious mental life into its cognitive and affective components, that
is, into one arena of thoughts, perceptions, memory, language, and
so on, and into another of emotions, moods, and drives. We
encountered this distinction in the disease perspective on recognizing
that the fundamental problem in the clinical syndrome, dementia, was
a global collapse of cognitive ability, whereas that of manic-
depression was a disruption of affective control.

As with any division of consciousness, the boundaries between

these two domains are not well defined. A person's thoughts certainly
alter his or her moods, and an intense emotional state will impair
anyone's capacity to think through a problem. Nonetheless, these
realms of mental life are clear enough to sustain a commonsense
distinction if not a sharply analytic one. The premise of this chapter is
that just as individuals differ in cognitive character-varying in a
smoothly graded fashion from dull witted to bright-so individuals vary
in their proneness to certain emotions, moods, and drives-from
emotionally stable and unresponsive to emotionally labile and
intense. As we used the term intelligence to encompass the cognitive
dispositional dimension, we shall use the term temperament to
identify differences in affective disposition among people.

For clarity and emphasis, let us again emphasize the word

disposition as the aspect of human psychology under study in the
dimensional perspective. Terms such as intelligent, stable, or
emotionally labile identify dispositional features of a person. These
features are not obvious attributes such as being tall or short, being
male or female, or even being young or old. They are not simple
states of mind such as anger, depression, or elation; nor are they
straightforward psychophysiological attributes such as visual acuity,
motor reaction times, or galvanic skin conductance responses. A
dispositional feature, such as intelligence or extraversion, is a
constitutional proclivity that may underlie many different psychological
states and responses but can be identified only under specific
circumstances. It is a latent feature until brought into action (where its
contribution can be witnessed) by some challenge.

Inherent, latent attributes are hardly restricted to the psychological

or even to the biological realm. Such features can be found in
physical objects, examples being the electrical resistance of a
metallic wire or the solubility of a crystalline substance. Operationally
(and grammatically) the existence of a dispositional feature is
revealed by a sentence that begins with an "if" clause and ends with
a "then" clause. Consider several examples: IfX volts are placed
across this wire, then Y amps will flow through it, demonstrating its
characteristic Z Ohms of resistance. Ifthis patient is given this series
ofXcognitive tests, then he will, on average, get Y correct
demonstrating his Z level of IQ. If this person is challenged by an
inconsistent superior, then he will often decompensate with anxiety,
demonstrating his high levels of introversion and neuroticism.

The dimensional perspective thus encompasses those individuals

who deviate to an extreme in their affective disposition (temperament)
and who often suffer and turn for psychiatric assistance because of
the emotional and behavioral problems evoked by challenging
circumstances. We are applying, now in the affective domain, the
same logic we used to explain how problems can emerge from life's
challenges in individuals who deviate downward in their cognitive
disposition (intelligence).
 This chapter aims to describe methods that reveal affective
dispositional dimensions and to identify their clinical implications. In
particular, we shall describe how the concept of disorder emerges
from assessments about the affective constitution of an individual-
documenting again how the "emotive paradigm" directs diagnosis,
prognosis, and treatment.

Personality Types

Since the ancient Greeks, people have noted constellations of

affective dispositions among their fellows. The descriptions of these
"personality types," such as sanguine and choleric, are apt enough to
make them recognizable today. The astrologers also offer typological
distinctions among people, groupings of temperamental
characteristics so tellingly apt that many accept the absurd
presumption that these different types, Gemini, Leo, Sagittarius, and
so on, derive from the dominant constellation of the zodiac at the time
of the individual's birth.

But we need not go back to ancient history and fortune-tellers to

find a typological approach to temperament. Axis II of DSM-III and
DSM-IV employs a typology. It notes that people who are cautious
and self-doubting may well also be neat and worryingly perfectionistic
(a cluster of attributes designated as the compulsive personality type
if such people seek psychiatric help). Those who are emotionally
labile and self-centered also tend to be theatrical (the hysterical or
histrionic personality type).' A given individual may have prominent
emotional attributes of several "types" and receive a whole list of
diagnostic labels-histrionic, borderline, narcissistic-when assessed by
psychiatrists. This can bewilder any student seeking clarity in
psychiatric assessment. Indeed, a group of individuals chosen to be
representative of a certain personality type will always include
examples whose personality characteristics seem to merge with the
"normal" population of people. Several problems of the typological
approach to temperament diagnosis are listed in the following
paragraphs.

First, it proposes categories that are awkwardly disjunctive. We

sense a central concept behind the type but may be unable to agree
on the various criteria that identify it. Thus, the diagnosis of hysterical
personality indicates that the patient has a combination of
dispositional affective characteristics that include self-dramatization,
emotional lability, and egocentricity. The essence of the problem
these features encompass remains elusive, but, as with other
personality types, one attribute is selected to identify the cluster of
traits. In DSM-III, the American Psychiatric Association changed the
term from hysterical to histrionic in order to clarify the category,
emphasizing the shallow theatricality of the emotional presentations
of these patients.2 Jaspers, in a similar attempt to find the central
feature of the type, proposed that such individuals "crave to appear ...
as more than they are." 3

As in any effort to grasp the concept behind a disjunctive category,

these approaches help explain what is implied by the chosen terms.
Because they are not categories like diseases, linked to pathological
mechanisms and etiological agencies that can be objectively detected
by laboratory examinations, these diagnostic terms must be used
cautiously. Thus, the second objection to typology: types are poorly
tied to phenomena beyond themselves. They are not conducive to
explanations that can be tied to brain or behavioral science from
whence progress in understanding and management can come.

These objections are just another way of saying that typologies are
difficult to validate (see the appendix). The difficulty accounts for the
multiplicity of distinct types of personality that have been described.
Each type is often vividly portrayed by its originator, who may even
propose operational criteria for the recognition of its features. But
operationalism is not validation. The proposal that features of
temperament make up a coherent cluster rather than an arbitrary
collection of random characteristics is not validated by simply
describing how each feature is identified.

A third objection: a type cannot usually be identified from a

presenting mental state but only from historical evidence of the
patient's characteristic emotional responses on prior occasions.
Knowledge of a patient's dispositions is best derived from reports
from some other informant than the patient. However, this informant
may mislead by over- or underemphasizing a feature of temperament
in describing the patient.

From Types to Dimensions

Despite these problems tied to types, such categories do grapple

with human affective differences, sensing that people differ in their
vulnerability to emotional distress depending on their constitution.
However, psychiatric information about these types is for the most
part derived from patients who are seeking psychiatric help. We need
some knowledge of the dispositional traits of the entire population in
order to understand how these types and their clinical problems
emerge. Alfred Binet realized the same point when he attempted at
the turn of the century to make sense of mentally subnormal people
in France. He recognized that only a study of the variation in
intelligence within the whole population would bring about a
conception of the nature of impaired people. As described in chapter
9, he devised objective measures of intelligence that could be applied
to everyone. In that way he revolutionized the science of
psychometric assessment of human characteristics. A similar history
has emerged in the psychometrics of temperament.

Even the personality types of DSM-III represent extensions of

general human variation. Gerald Nestadt and colleagues in the U.S.
Epidemiologic Catchment Area (ECA) Study, looked for the features
tied to the diagnoses of antisocial personality type, compulsive
personality type, and histrionic personality type in the population of
Baltimore.4 They demonstrated that these features, far from being
restricted to those people who satisfied the criteria for these mental
disorders, were common among people who were not defined as
patients. Those people who received a specific DSM-III diagnosis
simply carried more of these common features than did others. They
were separated from the "normals" by the arbitrary rules in DSM-III
that require the diagnosis to be applied after a sum of characteristics
had been exceeded.

TABLE 3. Prevalence of DSM-III Compulsive Personality Traits

Weighted to the General Population

Source: Data from Nestadt G, Romanoski AJ, Brown CH, Chahal R,

Merchant A, Folstein MF, Gruenberg EM, McHugh PR: DSM-III
compulsive personality disorder: an epidemiological survey. Psychol
Med 21:461-471, 1991.

To be specific, Nestadt and colleagues demonstrated that such

features as perfectionism, worrying, and work devotion-all cardinal
features of the compulsive personality type-were in fact to be found in
more than 20 percent of the population of Baltimore (table 3).5 Whom
to identify as disordered with the "compulsive personality" type
diagnosis was an arbitrary decision on a graded dimension of
variation encompassing many people (figure 6).

The same facts held true for antisocial and histrionic personality
typesthey also were arbitrarily distinguished from the population
depending solely on the number of features they displayed-all of
which were shared with others. From these data one might speak of a
greater or lesser compulsive tendency or antisocial inclination for any
particular person, but the decision to attach a typological label
(namely, antisocial, compulsive disorder) was arbitrary. One was
simply drawing a diagnostic line across a graded set of human
features.

An increased number of these features did predict greater clinical

difficulties and did so in a graded, essentially "dose response,"
fashion. Thus an increasing compulsivity score correlated with an
increasing risk for DSM-III generalized anxiety disorder and a
diminishing risk for alcoholism. In a similar fashion increasing
antisocial features correlated with an increasing risk for alcoholism
and a decreased risk for generalized anxiety disorder.6 These
observations that dispositions were graded in the population at large
but carried an increasing vulnerability to particular kinds of emotional
and behavior disorder at the extremes were very similar to the
observations of Binet that graded reduction in intelligence predicted
progressively more severe educational difficulties.
FIGURE 6. Distribution of compulsivity scores in the general
population. The shaded area indicates DSM-III compulsive
personality disorder. Source: Nestadt G, Romanoski AJ, Brown CH,
Chahal R, Merchant A, Folstein MF, Gruenberg EM, McHugh PR:
DSM-111 compulsive personality disorder: an epidemiological study.
Psycho! Med 21: 461-471, 1991, p. 465.
 More Basic Dimensions of Affective Disposition

All this work with types and the dissection of their features
emphasizes that vulnerability to emotional distress can derive from
abiding dispositional features of an affective kind. Temperament is the
term to describe these dispositions, identifying an individual's
tendencies to react to circumstances in a particular emotional
fashion. When the term temperament is used in this way-emphasizing
tendencies and varying reactions-it is clear that we are implicitly
comparing one individual with others and that the constituent traits of
a personality can be considered as dimensions along which people
vary in much the same way as they vary in other dimensional
characteristics, such as height or intelligence. Just as people are
taller or shorter, brighter or duller, so, too, they are more or less
optimistic or pessimistic, dependent or independent, conscientious or
carefree, suspicious or trusting.

This implication generated the efforts to discern the dimensional

traits along which people vary rather than types into which they are
filed. It also carries the assumption that assessments of temperament
will rest on comparisons of people with one another developed in the
same way as are estimates of intelligence: from study of the general
population.

As with the concept of intelligence, progress in the definition and

assessment of personality traits has occurred amid theoretical
disputes and methodological problems. Can traits be assessed by
questionnaire or only be observed when their potentials are brought
into action? Are the various techniques for assessment reliable and
valid? Another major problem psychologists face is that there are
thousands of words in English that are appropriate as trait names.?
Which are clinically relevant? One solution to these questions came
from the statistical techniques whose development began with
Galton. Factor analysis provides a means whereby many separate
measurements can be correlated and from them traits derived that
more parsimoniously account for variations observed. The technique
of factor analysis has been used productively by many workers, but
by none more successfully than Hans Eysenck and his associates.

Eysenck's group began with psychiatrists' ratings of thirty-nine

personality traits in 700 neurotic military men.8 A factorial study of the
intercorrelations of these traits revealed two major dimensions of
variation: neuroticism-stability and introversion-extraversion,
personality dimensions that had previously been described by such
psychologists as Wundt and Jung and that have subsequently been
replicated in general populations.

The dimensions of neuroticism-stability and introversion-

extraversion are important. Like the dimension of intelligence, they
can be identified throughout the population and thus assessed in both
normal individuals and patients by using test instruments (such as the
Eysenck Personality Inventory) of acceptable reliability. These two
dimensions actually measure a group of very fundamental affective
dispositional features. Once these features are appreciated, then the
graded characteristics-introversion-extraversion and
neuroticismstability-begin to make sense of much of human affective
variability but also make sense of the different types identified in
clinical populations.`'

The introversion-extraversion dimension separates individuals

according to the character of their emotional responses. Extraverts
are individuals who have quick emotional reactions to life events,
reactions that relate to the present implications of the events.
Extraverts thus tend to be sociable, warm, and responsive to
circumstances-to be quick to anger and quick to recover their
composure. Introverts, on the other hand, tend to have slow
emotional reactions to life events-reactions that relate mostly to the
implications of the events in the light of the future or the past.
Introverts therefore tend to be less sociable and may even seem shy;
they are more cool and slow to warm up in situations and likewise
slow to change either in response to others or in recovery after an
emotional irritation has been established.

An intriguing feature of the distinction across the introversion-

extraversion dimension is that extraverts tend to be more influenced
by rewards than by punishments and are slower to develop Pavlovian
conditioned reflexes. Introverts tend to be more influenced by
punishment than by rewards and are more prompt in developing
conditioned

The neuroticism-stability dimension of Eysenck is an easier

dimension of affectivity to explain than the introversion-extraversion
dimension. It is an estimate of the variation in strength of the
characteristic emotional responses of the individuals. Some
individuals characteristically respond intensely to events whereas
others respond weakly. By this dispositional feature we do not mean
that a severely stressful event would not produce a strong reaction in
anyone; rather, we mean that the neuroticism dimension identifies
those individuals who tend to have intense emotions when others do
not. Thus, the neuroticismstability dimension can be given other more
operational titles. Some refer to it as the unstable-stable dimension of
human affectivity; others refer to it as the strong-weak dimension of
emotional reactivity.

These two dimensions (introversion-extraversion and neuroticism-

stability) are in fact orthogonal dimensions in the sense that one's
position on one dimension does not predict one's position on the
other. This idea is displayed in figure 7, derived from Eysenck,
showing that with these two dimensions the population can be divided
into four groups: persons who are unstable extraverts (the choleric),
unstable introverts (the melancholics), stable extraverts (the
sanguine), and stable introverts (the phlegmatic). The capacity of
these two dimensions to reconstruct the ancient "typology" provides
powerful validating information about the dimensional construct. Table
4 divides the types according to these different dimensions.12
FIGURE 7. Eysenck circle. The inner circle of this diagram shows the
famous doctrine of the four temperaments; the outer circle shows the
results of numerous modem experiments involving ratings and self-
ratings of behavior patterns of large groups of people. It can be seen
that there is considerable agreement and that a considerable part of
personality can be described in terms of two major dimensions, here
labeled introverted/extraverted and unstable/ stable. Source: Eysenck
HJ: Principles and methods of personality description, classification
and diagnosis, chapter 3 in Readings in ExtraversionIntroversion, I.
Theoretical and Methodological Issues, Eysenck HJ (ed). New York:
Wiley-Interscience, 1970, p. 36.

TABLE 4. Four Temperaments

Clinical problems tend to occur among those individuals with the

"strong" emotional tendencies-hence the aptness of the term
neuroticism. In fact, various DSM-III diagnoses of personality types
tend to fall into one of these two unstable quadrants: Cluster B, or the
narcissistic, borderline, antisocial, and histrionic types, being all
unstable extraverts, and the Cluster C group, or the avoidant,
dependent, and obsessive-compulsive types, being all unstable
introverts. A disposition toward weak emotional reactions tends to
protect the person from behaviors and states of mind that need
psychiatric guidance.

Of considerable interest is that certain pharmacological treatments

move an individual along one or other of these dimensions
temporarily. 13.14 Beverage alcohol tends to move everyone in the
direction of extraversion. This is probably its main use among social
drinkers: releasing emotional responsiveness to the immediate
situation. For those of an unstable, extraverted temperament, such
further relaxation of their emotional inhibitions can be disastrous,
leading to explosions of rage and violence after only a small amount
of alcohol ingested.

Ritalin, among most children and some adults, tends to move the
consumer in the direction of The serotonin reuptake inhibitors and
lithium tend to move people down on the neuroticism-stability
dimension; that is, they reduce the intensity of the emotional
responsiveness of individuals, whether they are extraverted or
introverted.'6'7

Validity

Despite all these observations, the validation of traits such as

introversionextraversion and neuroticism-stability remains under
study. We do not have an ultimate validation, such as the
demonstration of a correlation of these traits with some aspect of the
brain or of the genome. Important converging evidence, however,
does support Eysenck's dimensions. Although there exist many
theoretical and technical differences among the measures developed
by Hans Eysenck, Raymond Cattell, and J. P. Guilford, all three of
these investigators produced empirical results that reveal these two
basic dimensions of personality. Eysenck's neuroticism correlates
with Cattell's anxiety and Guilford's emotional health; Eysenck's
extraversion corresponds to Cattell's exvia and Guilford's social
activity. 18

Another piece of convergent evidence validating these constructs

as enduring traits is the demonstration that they actually endure. In
fact, the scores an individual achieves at one time on these measures
predict the scores he or she will achieve at some later time. Paul
Costa and Robert McCrae give evidence in the form of retest
correlations of .73 in the Guilford characteristics over twelve-year
intervals in adults. Such high correlations are evidence of both the
stability of these measures and the validity of the enduring trait
construct itself. 19

Stability of Affective Dispositions

In recent years psychologists have debated whether personality is

best accounted for by trait theory, which posits relatively stable
characteristics that have a causal role in behavior and depend on
factors "inside" the person, or by social-learning theory, which seeks
to account for behavioral tendencies through concepts such as
operant conditioning and factors "outside" the person. As N. S. Endler
and D. Magnusson set the question: "Is behavior consistent across
situations, or is it situation-specific?"20 As in the nature-nurture
debate over intelligence, the best answer seems to be both.

Despite the crucial role the environment plays in provoking the

manifestation of emotion, to some important degree the potential for
certain reactions is present from birth. Support for that view comes
from studies that demonstrate differences in autonomic reactivity and
behavior in neonates21 and from genetic research that suggests a
strong hereditary component to personality in monozygotic twins
raised apart.22.23 As with intelligence, however, we cannot assume
that what seems given before life experience cannot be changed by
that experience. As teaching produces an educated person, guidance
through experience generates the control of responses identified by
the concept of character. In every person both constitution and
circumstance can be assessed for their relative contributions to an
individual's vulnerability to distress and ability to manage situations
that challenge him or her.24

The advantages that accrue from the trait approach to temperament

and from the identification of dimensions such as introversion-
extraversion and neuroticism-stability are identical to those found in
the identification of the intelligence dimension. This perspective
provides a powerful conceptual framework for understanding
individual vulnerabilities without becoming lost in the endlessness of
individuals themselves. Much is explained, though much remains
open to discovery.25.26

Summary

Individuals vary dispositionally in their affective constitution in

exactly the way they vary in their cognitive constitution. Just as
individuals vary across the dimension of intelligence in the population,
so do they vary across such dimensions as introversion-extraversion
and neuroticism-stability. Those individuals who deviate to an
extreme in the affective dimensions have problems just as do those
individuals who deviate (are low) in the intelligence dimension.
Essential to emphasize is that just as with intelligence where
individuals can be distributed according to their power and swiftness
of reasoning, so these dimensions divide patients according to their
characteristic emotional responses to events-quick responses,
focused on the present for extraverts; slow responses, focused on the
future for introverts; strong responses for the unstable; weak
responses for the stable.

The affective dispositional constitution (temperament) is thus as

crucial as the cognitive dispositional constitution (intelligence) and is
the substrate for emotional distress and behavior vulnerabilities.
Treatments here in contrast to treatments for disease relate to
guidance and strengthening of the individuals so as to protect them
from their vulnerabilities rather than to cure them of some "broken
part." In the next chapter we review the emotional reactions
themselves that these dispositional temperaments facilitate.
In the last chapter we described how deviation along certain
dimensions of affective disposition, especially toward the "unstable"
(that is, "neurotic") pole of the neuroticism-stability dimension,
renders an individual vulnerable to emotional distress upon facing
incidents that conflict with or challenge his or her expectations or
purposes. In this chapter we elaborate on this concept, the emotive
triad, by focusing on the nature of the emotional responses provoked
by such life events. Our point will be that the dispositional potentials
and situational provocations vary independently as each provides
some proportionate influence in evoking any given emotional
reaction. Thus, a person who diverges to an extreme along the
neuroticism dimension will respond with a dysphoric emotion such as
anxiety when facing a challenge that would not trouble a less
affectively vulnerable individual. Employing this information in
treatment has its own complications-quite different from those in
treating a disease.

Life Events as Provocative of Emotions

In chapter 11 we indicated some of the complexities tied to

dimensional dispositions. Life events may be even more complicated,
as they include not only disasters such as bereavement or injury but
also conflict-laden situations so subtle and symbolic that their
challenge or threat to the individual is not immediately obvious.

Thus, certain situations-of loss, defeat, injury, or imposition-provoke

emotional responses of anxiety or misery in anyone.' But, for some
people, less extreme circumstances-again, usually ones that
challenge the person's emotional control-elicit these same responses.
Psychiatric attention is drawn to the vulnerability of these people
because their emotional reactions to these circumstances are so
prompt and their intensity and duration so disproportionate. Thus, the
responses themselves are "normal," indeed familiar, in their nature
and character. It is their frequency and magnitude that identify them
as problematic.

This approach to emotional states is different from that of the

disease concept, in which the primary focus is on mental events so
unusual in their form, such as hallucinations and delusions, that they
prompt a search for some broken part or functional derangement of
the brain. With those symptoms we are induced to employ the
concept of disease with its logical development from clinical entity to
etiological agency in order to explain these unusual symptoms and to
direct treatment or research.

The success of the disease method should not, however, make us

overlook the limitations of its applicability. There are many clinical
situations in which the patient's difficulty is characterized, not by the
appearance of foreign symptoms, but by the distressing excess of
some familiar emotion, by a quantitative rather than a qualitative
abnormality. The patient and his family complain that he is more often
anxious than others or that he is discouraged, demoralized, or
uncertain more frequently than seems warranted.

Here, the disease method may mislead. What is most apparent is

not a stereotyped set of specific symptoms with a relentless course
indicative of some pathological process, but a troubled person
expressing natural feelings and complaining that they are excessive
and distressing. How are we to appreciate these issues, and how can
we devise explanations that accomplish as much for the troubled
person as the concept of disease does for impaired persons?
 This is the area of psychiatry in which the method of understanding
shifts from the determinism of biology to the appreciation of meaning
in human behavior. We turn from the language of organisms
(disease, symptoms, natural history, mechanism, cause) to a
language of subjects (feelings, intentions, assessments, actions,
responses). We attempt to understand these patients as people with
intelligible, if misguided, plans and with comprehensible, if excessive,
responses, all derived from personal dispositions and life
circumstances. On the basis of the patients' dispositions and
circumstances, we expect to understand some of the attitudes they
have, the choices they make, and the emotions they express. We
conceive of treatment in terms of guidance through persuasion and
the strengthening of alternative attitudes through clarification and
interpretation-rather than in terms of cure, repair, or replacement.

Neurosis as a Problematic Term

It is this book's point that although no psychiatry is complete without

an appreciation of the patient as both an organism vulnerable to the
powers of nature and a subject responsive to circumstances, the
conceptual distinctions between these views of the patient should not
be blurred, no matter how intermingled their expressions become on
a clinical level. In this blurring lies a great source of confusion in
psychiatry, in which the contributions from disease are muddled with
those from personal conflicts or vice versa. Thus, the word neurosis,
often used to identify conflict-driven emotional responses, is derived
from such source terms as nervous and nerves, a linkage
emphasizing elements of the organism in the very situations in which
they seem less pertinent.

In fact, few words in psychiatry have presented so many conceptual

problems as neurosis. For some students neurosis implies a discrete
entity, separate from psychosis but also qualitatively separate from
normal mental life. For others neurosis is given a critical place in a
theory of mental disorders-a condition of mild abnormality partway
between a normal state and the severely abnormal psychotic states-
implying that all mental disorders are on a continuum of severity with
a common etiology. This idea presumed that the neurotic disorders
were states that emerged as borderline conditions between the
normal and the schizophrenic or manic-depressive states.

DSM-III and its subsequent editions rejected the noun neurosis, but
retained the adjective neurotic as a shorthand expression for
quantitatively excessive emotional responses. We follow that practice
as well and point to the emotive triad for an explanation of these
emotional responses. Within this framework, the neurotic emotional
responses are not disease entities such as schizophrenia but rather
modes of individual affective expression provoked by some conflict
between events and purposes, between expectations and reality. A
full explanation of the increased frequency and intensity of these
emotional responses takes into account the affective disposition as a
potential generating them. Thus, personality dispositions are the
potentials, life circumstances are the provocations, and "neurotic"
emotive symptoms are the responses-all to be assessed and
accounted for in these clinical situations.

The Emotive Triad Tied to Affective Dispositions

The concept of personality often implies circumstances. For

example, the term paranoid personality implies an individual who
responds with suspiciousness and feelings of persecution to settings
so minimally threatening that they seldom provoke such responses in
others. As the concept of disposition indicates, the attitudes to which
the person remains vulnerable will disappear when that person is in a
setting free of threats.

This combination of a vulnerable individual and stressful

circumstances is central to reasoning about psychiatric disorder from
the perspective of dimensional dispositional differences. Although
there are circumstances that everyone finds stressful-prolonged
combat, natural disaster, the death of a loved one-psychiatrists
seldom see patients under the provocation of such universal events.
Much more often, psychiatrists see people who although complaining
about their situations, turn out to have some particular dispositional
vulnerability that renders them liable to emotional distress in
circumstances where others would not be as upset.

For example, a mentally subnormal person is distressed by

demands on his or her powers of abstract thinking that someone of
normal intelligence would master without difficulty; a very dependent
person becomes upset and suicidal at the end of a relationship
whose termination might have gladdened most people; an extremely
fussy person is angered and frustrated when dealing with a
subordinate whose performance most supervisors would find
adequate. Ernst Kretschmer termed the events that elicit a
characteristic response from a particular vulnerability "key
experiences" because individuality and situation fit together like a lock
and key to release an emotional reaction.2

The best ways of appreciating all these observations is to grasp that

the affective disposition, particularly dispositions tending toward the
strong or unstable pole of the neuroticism-stability dimension,
represents the vulnerability to emotional responses. The emotive triad
of potential, provocation, and response is fundamental to our
reasoning. Certain potentials as represented in personality when
faced with provocations in the form of life challenges or circumstance
can evoke responses in the form of "neurotic" symptoms such as
anxiety and depression that call for psychiatric attention (figure 8).

FIGURE 8. Emotive triad.

Anxiety as an Example
 To exemplify this approach, we will consider the emotional state of
anxiety. Before we begin, we should acknowledge that anxiety can be
a symptom of any number of psychiatric disorders. In particular, it can
be a feature of major depression and give an episode of that illness
an agitated quality. Anxiety can also be the cardinal feature of attacks
of the panic-anxiety state, a psychiatric condition that has been
documented as probably a disease by demonstrating its heritability.

We are not considering these symptomatic manifestations of

anxiety but rather here will describe how it can be a universal
experience in situations of threat and uncertainty. In fact, the
relationship among potential, provocation, and response has been
thoroughly studied for anxiety and is one of the classical examples of
reasoning about neurotic disorders.3

That anxiety is not a completely destructive and inappropriate

emotion is shown by the classical Yerkes-Dodson law-the "inverted
U" relationship between arousal and performance skills. This
relationship indicates that for any given task the presence of some
anxiety, with its accompanying arousal and attentiveness, improves
performance. But as anxiety increases, the skillfulness of the
performance peaks and then rapidly declines. The difficulty of the
task determines the turning point. In easy tasks anxiety improves skill
even when tension is considerable, but in difficult tasks only a small
amount of anxiety is needed to cripple performance.4

Anxiety is thus to some degree useful and is occasionally

experienced by everyone. It can be mild or severe depending on
circumstances and personality characteristics, but all people, though
varying in proneness to anxiety, can be incapacitated if a threatening
environment is thrust upon them for a prolonged period. During
intense and protracted military combat, all soldiers will eventually
show disabling anxiety.5
 Anxiety is distinguished from fear only by convention, with fear
being the term for a transient, intense, and focused response to a
particular and immediate threat and anxiety the term for a more
sustained and variable emotion developed in the face of a more
subtly threatening and prolonged situation. Anxiety's earliest
manifestations are a sense of vigilance and tension, features bringing
with them alertness and a sense of stimulation that are not
necessarily unpleasant. These manifestations can include an element
of excitement and can be sought out in a spirit of adventure. Their
discharge and relief, for example, in a successful performance, can
be a source of enjoyment.6

With increasing anxiety, however, dysphoric qualities increase. All

efforts become fatiguing, and persistent exhaustion is a regular
complaint. Tension, vigilance, and arousal give way to worry,
agitation, distractibility, jumpiness, the odd state of
derealization/depersonalization, and a loss of mental and physical
efficiency. Autonomic features of anxiety, such as tachycardia,
stomach cramps, and dry mouth add considerably to the dysphoria.
Many anxious people report a pervasive feeling of "air hunger"
leading to overbreathing. This overbreathing by reducing circulating
carbon dioxide from the blood can increase the sense of
depersonalization and can add feelings of light-headedness and
"floating." The overbreathing occasionally even induces tetany. The
final result is an incapacitated and demoralized person in severe
emotional and physical distress.

Dysphoric anxiety is a most miserable state, suitable resolutions

varying with circumstances and individuals. Obviously the most
immediate way of eliminating anxiety is to leave the situation and to
avoid it in the future. This is only occasionally a realistic solution. It is
impossible, for example, to run from combat without risking new
dangers or to leave a job without disrupting other commitments.
Effective teaching on the job diminishes the severity of occupational
anxiety and should eventually replace it with the enjoyment of skill, a
phenomenon recognized by teachers everywhere. Effective
leadership in combat can modify the intensity of anxiety by similarly
increasing skill, confidence, and esprit de corps. In these situations,
mastery of the situation rather than its avoidance reduces both its
provocative threat and the anxious response. Mastery of a situation is
a successful way of managing anxiety, but it demands the capacity to
differentiate and assess the threatening elements as well as the skill
to overcome them. This is not an easy feat to accomplish on one's
own, so it is scarcely surprising that most of us at various times
require help from others to master some of the challenges life
presents us.

Avoidance and mastery of circumstances are two ideal solutions to

anxiety. When these solutions are unavailable or must be deferred,
any of several other modes of dealing with the emotion itself may be
used. These secondary approaches fundamentally are efforts to
modify anxiety as a distressing experience. Some people discover
that sedatives such as alcohol reduce tension, a discovery that brings
temporary relief but also carries with it the risk of sedative abuse if
anxiety is chronic. Physician-prescribed sedatives likewise can help
with a transient anxious state, and, when used under supervision and
along with other means for remediating the life situation prompting
this emotional response, the benzodiazapine anxiolytics are most
useful.

People can also deal with anxiety (and particularly its unpleasant
feelings of frustration, weakness, and defeat) by replacing it with
another, more active state, such as anger or aggression. These
transformations often occur so automatically that the individual may
be unaware that anxiety is involved at all. The experience and
expression of anxiety can be altered in many other ways, but in each
case there are contributions from the individual, the situation, past
experience, and sociocultural expectations. These latter influences
will determine not only whether anxiety is mastered but also whether
the anxious person turns to psychiatrists for assistance. Bruce and
Barbara Dohrenwend and their colleagues have shown that many
people in the general population have emotional distress
indistinguishable in degree and kind from that reported by psychiatric
patients.? Such people may not seek professional help, in part
because they are not, in Jerome Frank's term, demoralized by their
suffering;8 because their social networks are such that the assistance
of family and friends is sufficient; or because their cultural
perspectives do not acknowledge the problem as one needing a
physician's attention.9

In summary, the mental state of anxiety is not difficult to recognize.

Its provocation through conflict between expectations and
circumstance can be described by the patient. The dispositions that
lead to these conflicts and which are represented in other affective
tendencies of the individual can be identified by a psychiatrist either
through some extended experience with the patient as in
psychotherapy or through the descriptions from the patient or his
family of his emotional responses in situations, such as school,
employment, and marital life, that everyone encounters. The
treatment methods include guiding the patient through the
circumstances that have provoked the anxiety so as to relieve its
threat and to strengthen the patient's capacity to face similar
situations without such a response in the future. Symptomatic relief
for the emotional response itself is a useful, if necessarily temporary,
approach aiding the guidance and strengthening efforts of
psychotherapy. The ultimate aim is to help patients develop a sense
of responsibility and control-responsibility for many of the life
situations they face and control of the way they respond to them.

Dimensional Triad with Other Emotions and Traits of Temperament

This close look at anxiety can be repeated for a series of other

states of mind in which the paradigm of potential, provocation, and
response can be appreciated. In explaining each of these states of
mind, we link a subject, a particular situation, and an emotional
response together through our capacity to empathize with
(understand and appreciate) the natural feelings of others, even
those feelings that are so intense as to go beyond our own personal
experience. As the elements of the emotive triad can themselves be
empirically identified, so the meaningful, empathically supported
linkages between them can direct apt psychotherapeutic and
pharmacological interventions.

In the introvert faced with circumstances he or she perceives as

threatening, we can understand the appearance of anxious
withdrawal and sometimes selfmedication with alcohol and can offer
better alternatives. In the same way, for the self-dramatizing,
extraverted, and emotionally labile individual called histrionic, we
understand how an environment perceived as neglectful can provoke
anger, depression, and self-injurious behavior. The self-doubting,
perfectionistic, and introverted person, in a situation viewed as
changing and unsettled, risks the development of anxiety, frustration,
and fussy obsessions in ways that again we can understand and
appreciate. The affectionless and adventure-seeking personality in a
poorly structured community may, we can see, manifest the behavior
of delinquency, whereas an unstable, aggressive individual in
challenging circumstances may become violent. These are
paradigms of regular occurrence; the linkages between their
elements are grasped by our capacity for meaningful understanding,
and their treatment via guidance and redirection forms a large part of
psychiatric practice.

The application of this method of understanding emotional

responses has several common characteristics. First, the central
issue is an exaggeration of a normal emotional response. Second,
the patients are distinguished by a dispositional feature varying in a
quantitative rather than a qualitative way from normal individuals.
Although we are all capable of emotional responses we are not all
neurotic, because we are not prone to excessively strong or
persistent emotional responses to life circumstances.

Third, a satisfactory causal explanation for any particular patient's

problem will be complicated; it will rest ultimately on appreciating
linkages among inherited dispositional characteristics and the habits
of emotional response generated by prior experiences, as well as by
the presenting life context. The same symptoms may appear in
different situations because the individual perceives a similar threat in
each of them. Fourth, diagnosis, too, is individual and depends on the
appreciation of a multiplicity of different features in a given patient,
including an assessment of the patient's strengths as well as his or
her vulnerabilities; the threats perceived and the responses that
result; the patient's physical condition; and the brevity or duration of a
stressful situation. A diagnosis demands a weighing of all these
contributions and does not easily devolve into a label. Diseases are
categories that fit well into a labeling nosology; when dealing with
neurotic reactions, in contrast, a paragraph is needed to characterize
each patient's problem.

Fifth, in neurotic disorders prognosis is uncertain for two reasons:

personality traits do provide enduring dispositional vulnerabilities; and
circumstances, important in provoking and maintaining the emotional
state, are often unpredictable. Sixth and finally, therapy must be tailor
made for each patient despite symptomatic similarity. Although two
people complain of depression, one may be a dependent and self-
dramatizing elderly widow in poor health who must move from her
daughter's house, whereas the other might be a perfectionistic and
self-doubting adolescent who has left home for difficult college work.
Although they share certain emotional complaints (distress in their
new situation), their personalities and situations are so dissimilar that
the goals and methods of achieving insight, environmental change,
and symptom relief may be quite different.
 Common to helping both, however, will be a good faith effort to
grasp the meaningful nature of the links between the emotion and its
provocations and in particular the contribution of the personality's
dispositions. Because any treatment takes the form of guidance and
redirection, it will demand a foundation based on some mutual
appreciation and respect between the patient and the therapist, some
decision about which goals are possible (and which order they should
be approached) for this individual at this time, and some instruction
(that is, "role induction") of the patient into the very processes of the
psychotherapeutic relationship. 10-12

Questions such as the following will naturally arise: Does this

patient need and can he be prepared for radical insight, change, and
new acceptance? Would he be better provided with simpler tactics to
resolve the present situation, pharmacological assistance to restore
his equilibrium, and then reconsider the more radical approach to
review his disposition, his circumstances, and his responses? A
discussion of these matters of designing a psychotherapeutic plan
and its associated psychopharmacological supports goes beyond our
purposes here.

Summary

The explanation of neurotic states presented in this chapter rests on

an appreciation of the connections linking potentials, provocations,
and responsesconnections that do not take the form of biological laws
and do not act to compel an identical response in every instance.
These connections lack such powerful predictive force and are in fact
not intended for prediction. They provide a mode for understanding
people in emotional difficulty. The explanatory relationships between
potentials, provocations, and responses are meaningful rather than
determinative. These relationships identify the complex, interactive,
and dynamic elements that make sense of disorders that derive not
from nature's power but from the capacities of people to respond to
life's challenges and disappointments with emotional and behavioral
distress. We grasp their significance from our ability to appreciate or
empathize with them.

These emotional conditions, their dispositional potentials and

provoking events do not fit easily into a categorical diagnostic system
such as that of DSM-III and DSM-IV. A diagnostic formulation of some
paragraphs rather than a label encompasses the situation and directs
the suitable treatments. Such a formulation-employing as it does
assessments of the dispositional potential, the circumstantial
provocation, and the emotional response and inspired as it must be
by an empathic understanding of the interactions among these
elements-finds therapeutic and prognostic power in its
comprehensive grasp of issues arising from within and impinging
from without on a given patient at a given time.

These matters are the fundamental ingredients of the dimensional

perspective. This arena of study will advance in the future by
identifying such contributions as the genetic foundations of traits, the
structure and functions of the brain systems that analyze
circumstances and evoke emotions, and the place of learning and
development in constructing a mature character from the
temperamental underpinnings identified here.

But even as this information expands, its place in treating a patient

will depend on the capacity of a therapist to understand the complex
links among the person, the situation, and the responses-that is, to
grasp how these troubles emerge from who the patient is, what he or
she is facing, and how he or she reacts. More knowledge will
increase the power of our explanations but will not change the
implications of this treatment.
Psychiatrists treat a large and heterogeneous group of people not for
what they "have" but for what they are "doing." A maladaptive
behavior-such as alcoholism, drug addiction, anorexia, or paraphilia-
has become a warped "way of life" for these people and they either
seek or, more commonly, are brought to psychiatrists for help. This
chapter addresses disorders of this nature and the conceptual
dilemmas they present.

Behaviors are so basic to life that they virtually disappear from

attention unless one of them gets in the way of others. For most of
humankind each day consists of a smooth succession of behavioral
actions that shift, almost unnoticed, from one to the next. A typical
day might run from arising refreshed from sleep in the morning,
through a series of meals that intermittently interrupt periods of effort
at work or school, followed by a family recreational gathering in the
evening before finally returning to sleep at night. None of these
undertakings or their sequential successions draws much attention as
all seem so natural.

Behaviors encompassing eating, drinking, sleep, sex, or maternity

emerge in response to felt need, choice, and circumstance. Satiation
brings a homeostatic control to some of these behaviors so that each
stays within bounds and one behavior replaces another as, for
example, the interest in sleep, eating, drinking, or sex is transiently
reduced by its own expression.

Embedded within the sequences of these basic, life-sustaining

behaviors and emerging naturally from them through interest and
psychological energy are those other goal-directed behaviors tied to
social roles, values, and purpose, such as work, school attendance,
home maintenance, worship, and recreation. These behaviors
depend more on social learning than on the waxing and waning of
some appetite and yet over time become habituated responses to
daily life and shape the expressions and sequences of the more basic
behaviors.

Thus, expectations eventually develop about all these behaviors

and their place-the basic, "driven" (or, as physiological psychology
has termed them, motivated) behaviors and the socially learned,
purposeful behaviors. We acknowledge the need for sleep but still
accept the obligations of work or school attendance. Social learning
shapes the expression of the driven behaviors; for example, the
culture imposes etiquette rules on meals, and it is expected that
everyone will learn these rules and adults will heed them.

Fundamentally, every organized society takes account of the

insistence of the motivational drives and provides for them. It
recognizes that some of these behaviors are not completely voluntary
undertakings and thus require both time for their expression and
institutions such as marriage for their sanction. But each society
monitors these behaviors and through its agencies such as the family,
the school, and the church helps young people learn the importance
of ordered conduct in a life, a structure within which benefits can
emerge.

Certainly each of these behaviors, driven or learned, brings

benefits, including the immediate hedonic rewards and relief of
pressured appetites and the sense of mastery from practicing a
learned task. The same driven and learned behaviors also bring long-
term benefits as health from apt nutrition, and the cohesion of
intimate sexual partners that sustains a base for child rearing. Every
one of these benefits depends on combining a response to a drive
with prudence and moderation. Ultimately-and, fortunately, more
often than not-through the guided trials and errors of childhood and
adolescence emerges a responsible adult capable of avoiding
injurious, offensive misdirections and of building on the opportunities
that good health, a strong family, and competence bring.

The ordinariness of these behavioral aspects of daily life makes

them inapparent even as they represent the intriguing, ever changing,
interactive influences of physiological appetites and life experience.
To illuminate the challenge they present to psychiatry and to
comprehend the nature of the clinical abnormalities that turn up in this
domain, we will now turn to more specific definitions and descriptions.

A Definition of Behavior and Two Behavioral "Triads "

The term behavior applies to any motor-sensory activity linked to a

goalordinary goals such as working for a living or sleeping for rest,
and disordered goals such as suicide, alcoholic intoxication, or
paraphilic sexual actions. Within many driven behaviors-both normal
and abnormal-influences, difficult to isolate from each other, come
from three sources: a driving, impelling physiology; conditioned
learning; and choice (inclined by culture, opportunity, or preference).
Throughout these chapters we shall make reference to these
interwoven influences-drive, conditioning, and choice-as a behavioral
triad (figure 9). We shall demonstrate how they contribute to normal
behaviors and how they provide avenues for the treatment of deviant
ones.

As will be discussed, learning plays a role in all behaviors, but this

triad applies primarily to the driven, or "motivated, " behaviors, which
rest on physiologically based hungers and appetites. As we discuss
later, some behaviors do not come from these appetites but develop
from the social contexts in which people live. These behaviors
develop over time as responses shaped by social antecedents and
consequences. A distinct triad for socially learned behaviors is shown
in figure 10, and its implications for disorder and treatment are
discussed along with motivated behaviors in subsequent chapters.
 We later discuss matters of drive and of learning, describing in that
process how in many disorders they are combined to produce the
behavioral presentations. But before we elaborate on these matters, it
remains crucial to recognize behavior as distinct from simple motor
activity. As an example of how motorsensory activities form discrete
goal-directed behaviors, notice that humans learn to coordinate hand,
eye, and mouth for many purposes, but we readily distinguish those
actions employed in the behavior of eating because they lead to food
consumption. When we consider all the activities that eventuate in
food consumption and are encompassed by the concept of eating
behavior, we must include those actions tied to food acquisition and
preparation, those related to choices of sequence in presenting and
consuming food, and those interactions with meal companions that
follow culture specific, socially enforced etiquette rules. All of the
motor-sensory actions, none of them exactly the same from occasion
to occasion, are responses to some hunger for food with learned
choices of what and how to eat. An understanding of eating behavior
(its provocations, directions, frequency, periodicity, quantities
consumed, and abnormal variations) must link influences extending
from the physiological drives to the personal and cultural experiences
that teach what is expected.

FIGURE 9. Components of driven behaviors.

 FIGURE 10. Components of socially learned behaviors.

Because of these multiple and interactive controls that emerge from

vital organismic needs and which are shaped by experience and
social expectations, the perspective of behavior can seem more
complex than the other three perspectives of psychiatry. Nonetheless,
it is simple in its definition. Behavior is defined by "what is taking
place," that is, the teleologic design unfolding from a person's activity.
When one can see "what is taking place," specifically, when one has
identified the goal direction to which all the observable motorsensory
actions contribute, then one can explore factors encompassing
physiology, past experience, learning, and choice that reveal "what is
going on." But even identifying what is taking place and thus picking
out a goal-directed aspect of observable activity is not always easy.

A Natural Example

To clarify the problems of identification tied to the concept of

behavior, consider this regular occurrence in nature. The California
gray whale lives for most of the year in the region of the Bering Strait.
Each winter it travels thousands of miles along the North American
coast to the Baja peninsula. The animals breed and bear young in the
warm lagoons of that portion of California and, in early spring, travel
again thousands of miles back to their northern habitat.

During their trips the whales display many spectacular capacities

and activities. They swim, spout, chase, and sound-overtly displaying
the wonders they are. A casual whale watcher on a day's excursion
from the piers of Los Angeles would not be aware of the ultimate
domination of all their activities by a goal-direction. That dominance
lies hidden unless the animals are observed over time with their fixed
destination and the seasonal recurrence of their passage identified.

The whales are migrating, not just aimlessly swimming. Migration is

what's taking place. To discover what's going on to produce migratory
behavior in each of these animals, we must learn much more about
the California gray whale. In particular, we must discern which
physiological features of the whale provide it with a sense of place
and direction (a map and a compass), a capacity to distinguish
climatic changes from transient weather events, and an awareness of
the behavior of its conspecifics. Then we can claim a more
comprehensive understanding of the behavior, migration, which
directs and modifies the whale's activities until it reaches its
destination. Thus, behavior is a term emphasizing the congruence of
a pattern of activity for a stable purpose. Recognition of migratory
behavior demands first descriptive and then analytic efforts (what's
taking place followed by what's going on) that we would not
undertake if, for example, our sole interest were directed not at what
the whale was doing but at the reflexes coordinating its fins.

Behavior is a crucial and distinguishing feature of animal existence.

Many natural scientists and psychologists have devoted their careers
to observing its several phenomena in many species so as to
appreciate how behaviors fit an animal into the earth's biosphere with
all the dynamic changes the biosphere presents.

For all that behavior is a most intriguing area of study, the

phenomena represented by it and the explanations offered for these
phenomena have historically been a source of scientific quarreling
extending to ideological and philosophical disagreements. One of the
great chronicles of the natural sciences over the last century recounts
the story of these disagreements and their gradual resolution.

A History of Behavioral Research

Charles Darwin (1809-1882)

Charles Darwin was the first modern scientist to take note of the
place of behavior in relation to an animal's fitness to its habitat. Many
earlier naturalists had identified "instincts" as built-in features of
animal existence employed in sustaining either the individual life
(such as eating or drinking behaviors) or the species survival (such
as sexual and maternal behaviors). These naturalists presumed that
instincts needed no further explanation beyond their sustaining
functions. These predecessors of Darwin have been referred to
disparagingly as "finalists" (that is, those who confuse the question
"what for?" with the question "how?"). They seemed to believe that by
demonstrating (or even just presuming) some species-protective or
species-preserving goal for a behavior they have resolved the
question of its mechanism and cause.

Darwin was not a finalist in any sense. He emphasized that instincts

and the behaviors by which they were identified were biological
features resting on structural and physiological mechanisms open to
natural selection and evolutionary change. They were as suitable for
study and for detailed, constructive explanations as any anatomical or
physiological feature of a species.'

Sigmund Freud (1856-1939)

Sigmund Freud was encouraged by Darwinian thought, among

other influences, to describe the psychological phenomena behind
"instincts" and experienced as "motivation" or "drive." He thus
advanced the psychological science of his day by directing attention
toward the affective and provocative psychological experiences
(hungers, longings, preoccupations, and so on) that were self-
reported by human subjects while under the influence of their
instincts. These dynamically changing, "driven" features of normal
psychological life had been neglected by the pioneers in psychology
of his time. Their interests were directed toward the study of cognitive
phenomena such as perception, language, and memory rather than
the differing contexts of drive and motivation in which these
phenomena occur.

Freud articulated these matters early in his psychological

investigations and first described his ideas in his "Project for a
Scientific Psychology": "With an (increasing) complexity of the interior
(of the organism), the nervous system receives stimuli from the
somatic element itself-endogenous stimuli-which have equally to be
discharged. These have their origin in the cells of the body and give
rise to the major needs: hunger, respiration, sexuality. From these the
organism cannot withdraw as it does from external stimuli.... They
only cease subject to particular conditions, which must be realized in
the external world. (Cf., for instance, the need for nourishment.) In
order to accomplish such an action ... an effort is required ... since the
individual is being subjected to conditions which may be described as
the exigencies of life."2 Later, in "Instincts and Their Vicissitudes,"
Freud defined instincts in a way that emphasized their bodily origins:
"a concept on the frontier between the mental and the somatic, as the
psychical representative of the stimuli originating from within the
organism and reaching the mind, as a measure of the demand made
upon the mind for work in consequence of its connection with the
body."3

A fundamental aspect of Freud's descriptions was his effort to

define how a subject's "attitude" toward his environment changed
under the dominating influence of a particular "instinctive" affective
state. Under that influence, a subject now noticed-and with a
progressing interest-aspects of his environment that he had
previously ignored. Indeed, his perceptions, thoughts, and
remembrances took up this interest in a fashion that led to action.

Freud was pointing out something that seems obvious. For

example, a hungry person sees food where others do not and seeks
to consume what others (not hungry) would ignore. And, after eating,
the sated subject disregards those preparations that attract others to
eat. Thus, Freud noted that behaviors emerge with distinct "attitudes"
toward the surrounding environment. These attitudes, described by
human subjects and deducible from their actions, represent the
psychological experiences that accompany motivated behaviors.

These concepts of drive and attitude provoked controversy in

psychology. They seemed to depend solely on self-reports and
interpretations rather than identified bodily mechanisms or easily
manipulated stimuli from the environment. Freud presumed and
predicted that some brain-based, biological mechanism would
eventually come to light and make sense of changing drives and the
central role of attitude in altering sequentially the salience to the
subject of environmental objects and events. The neuroscience of his
times, however, was too primitive. Freud's ideas and their
development into explanations for psychopathology rested on the
hope that science would ultimately confirm them.

John B. Watson (1878-1958)

Freud's ideas were quickly challenged because they lacked a

physical foundation in a biological substructure. John B. Watson, the
outspoken behaviorist, held that Freud's ideas were overelaborations
of the instinct concept and unnecessary in explaining behavior
including both its goal-directed form and its attitudinal features.4,5

Watson held that the antecedent and consequential reinforcements

tied to environmental events that surround every sensory-motor act
shaped spontaneous activity into goal-directed patterns by a process
similar to trial-anderror learning. He also held that these
reinforcements generated the attitudes that Freud considered vital to
his theories. Although Watson did accept the concept of instincts as
built-in energizers of activity, he held firm to the opinion that
environmental consequences of activity turned what were best
viewed as "inner unrests" into goal-directed, purposeful behaviors.
 The Watsonian opinion of the crucial role of learning through an
interaction between the organism and the environment was inspired
by the conditioning studies of Ivan Pavlov and supported by the
"operant" behaviorism ultimately developed by B. F. Skinner. These
investigators certainly demonstrated the power of reinforcement in
shaping the expression of behaviors both by events that precede an
activity (e.g., Pavlov's bells before a feeding), and events that follow
spontaneous activity as consequences of it (e.g., painful shocks or
food delivery upon pressing a lever).

Pavlov, Watson, Skinner, and their many students were committed

to the role of the environment as the major influence on behavior.
Learning from experience could, they thought, explain all the manifest
expressions of a goaldirected behavior-stating in essence that to the
question "What is going on?" the answer is "learning, in all its various
forms."

Although the conflict between Freud and Watson now may seem
more a battle of emphasis over two entwined features of behavior
(the former proposing drives that rest on endogenous mechanisms,
and the latter learning from environmental reinforcement of
responses), it raged for years because each side lacked some vital
element to resolve the disagreement. The Freudians needed
biophysiological mechanisms for their proposals in order not to seem
mythmakers proposing inner "ghosts" steering outer actions. The
behaviorists needed to explain how attitude and drive fluctuated in
spontaneous daily rhythms and how activity susceptible to learning
emerged without obvious external provocations.6

Curt Richter (1894-1988)

Into this standoff came a group of physiological psychologists such

as John Brobeck, Eliot Stellar, and Frank Beach. They sought what
Freud had presumed-the embodied physiological mechanisms
providing a machinery for the sequences of arousal, satiation, and apt
placement of behaviors such as feeding, drinking, and sexuality into
daily life. They also were prepared to accept that these behaviors
should be responsive to the environment and shaped by learning, as
Pavlov, Watson, and Skinner had demonstrated. Thus, they sought
biophysical sources for the generation and ultimate regulation of
these behaviors but expected to discern how such mechanisms were
open to environmental stimuli that would influence their expressions.

A most dramatic, and perhaps prototypic, example of this resolving

psychophysiology was pioneered by Curt Richter, who began in
Watson's laboratory at Johns Hopkins University. Richter produced
observations and experimental results that began to resolve the
controversy between the champions of inner drive and those of
environmental shaping.?

Richter came to Hopkins in 1919, joining Watson as a young and

untutored graduate student. When he asked Watson for direction, he
was told to do a good piece of research but nothing more. After some
days of aimless wandering around the Hopkins classrooms and
laboratories, Richter arrived at his desk one morning to find that
someone-a technician, he later discovered-had placed a cage
containing rats in his cubicle. More days passed with Richter sharing
his space with these animals and little more of note.

However, after several days Richter noticed a simple fact.

Sometimes the rats were active and other times inactive. He asked,
Why is it that the rats are sometimes active and sometimes inactive?
Is there anything regular about these matters or are they random
actions of the animals? If they are organized rather than chaotic, what
physiological mechanisms could account for the organization? No
one, including Watson, seemed to know the answers to these simple
questions, and as a result Richter launched a research program that
has had far-reaching influence to the present day.
 To begin, Richter demonstrated that a rat's activity occurred in quite
regular cycles, with most of its activity occurring in the darkness of
night. He followed this observation by demonstrating that even if a rat
were blind and unable to appreciate light from dark, its activity
remained cyclical with periods of activity and rest following each other
in a sequence that approximated twentyfour hours but did depart from
this strict time in ways that were individual. Some rats fell into a cycle
that was a bit under twenty-four hours and thus became active earlier
and earlier each day. Other rats fell into a cycle slightly longer than
twenty-four hours and so became active later and later each night.

Ultimately, Richter demonstrated that lesions in the anterior

hypothalamus would totally disrupt all expression of a rhythmic
diurnal activity cycle in the rat such that a random-indeed, chaotic-
form of stopping and starting periods of activity occurred throughout
the day and the night. Robert Y. Moore (and simultaneously Irving
Zucker) demonstrated that a small nucleus in this region, the
suprachiasmatic nucleus, generated the regular diurnal sequence of
activity and inactivity in rats and other mammals.8.9 This nucleus has
efferent connections to the brain but has its afferent input (the retinal-
hypothalamic tract) from the eyes. Daylight registers on the retina,
thus influencing the neural output of the suprachiasmatic nucleus in a
fashion to fit the rat's activity to light and dark sequences in its
environment.

This investigation discerned that behind a regularly occurring

behaviorindeed, a clocklike rhythm of arousal and rest-was a bodily
part that generated it: the suprachiasmatic nucleus. The special
feature of this bodily component was that it was "open" to the critical
feature of the environment, appearance and disappearance of
sunlight, that was pertinent to the rat's nocturnal habits. The onset of
sunlight registered on the retina would "reset" the suprachiasmatic
nucleus, and the rat would remain a nocturnal animal following
closely the seasonal alterations in the duration of sunlight in its
natural environment.
 This investigation, which began with Richter's discerning a
regulated pattern of behavior-nocturnal activity (what's taking place)-
was followed by discovering physiological machinery, open to the
influence of the surrounding environment, generating this pattern
(what's going on). Such a discovery confirmed that both the Freudian
claims for endogenous drive and the Watsonian emphasis on
environmental shaping are entwined in producing apt behavior. A
biophysiology capable of arousing a drive but open to and interacting
with the environment explained these two aspects of an instinctive
behavior.

We chose this example from physiological psychology because its

message is clear. Many other laboratories investigating other
behaviors (drinking, eating, sleep, sexuality, and the like) continue to
demonstrate how endogenous bodily mechanisms function to evoke
goal-directed activities that can be shaped by antecedents and
consequences from the environment.'0 What had previously seemed
conflicting concepts about behavior can now be seen as providing
different components to the development of a behavior pattern. All
studies of motivated behaviors seek a similar template: embodied
elements (for drive) open to the surrounding environment (for
learning). A diagram of this idea is shown in figure 11.

This model's critical implication for psychiatry needs underlining. As

any motivated behavior rests on two entwined elements-an embodied
feature that elicits and reelicits a drive in cycles over time and an
access feature for the environment to shape the responses to that
drive by learning-then one can expect that behavioral disorders may
arise from either element. Some disorders may be due to "overdrive,"
others to "maladapted learning," and still others to some combination
of both. Physiological psychology has delivered a conception of the
systems behind motivated behaviors on which to seek explanations
for disorders and rational approaches to their treatment.
 FIGURE 11. The interactive components of motivated behaviors.

Goal-Directed Behaviors: Some Driven, Others Learned

The discoveries just discussed have done more than illuminate the
clinical issues of the motivated, or driven, behaviors. As it became
clear that these behaviors tied to the vital organismic needs for food
and water, sleep, sex, and maternal actions are comprehensible
through the combination of drive and learning, it likewise became
clear that these behaviors are fundamental to life itself. There are
other goal-directed behaviors that are connected to social roles and
rules represented by the day-to-day actions of people in a
communitytheir occupational activities, their sources of amusement,
and their compliance with the customs and beliefs of their society.

It seems forced to place these latter behaviors on a driven basis,

except indirectly as they provide means to satisfy the drives. Social
learning through the interactions of antecedents, responses, and
consequences brings these behaviors into efficient functioning, and
much of social psychology is devoted to discussing the learning of
these behaviors. For psychiatrists, several behavioral disorders can
be seen to rest primarily on social learning. These include hysteria,
suicide, and delinquency, which are behaviors because they are
goaldirected activities but not motivated behaviors because they do
not rest on some intrinsic instinctive drive. The implications for these
distinctions for explanation and treatment are discussed in
subsequent chapters.

Behavior as a Site for Clinical Concern

Before we turn to a closer consideration of particular behavioral

disorders, we should identify two general advantages tied to
identifying behavior as a specific domain of psychiatric attention.
First, the concept of behavior provides psychiatrists with answers to
several questions. For example, Is homosexuality a disease? No, it is
a behavior in which an individual finds satisfaction of erotic needs
from members of the same sex rather than the opposite sex. What is
hysteria? It is a behavior in which the symptoms and signs of disease
are imitated for social and psychological benefits. How do
psychiatrists treat suicidal patients? Activities aimed at terminating
one's life arise in several clinical circumstances. Treating suicidal
patients depends on formulating a diagnostic impression that directs
treatment. These treatments can range from psychotherapy for
demoralization to electroconvulsive therapy for manic-depression.

The second advantage to recognizing behavior as a specific

domain of life study comes from appreciating that disorders in this
realm can be distinguished from disorders that are tied to the bodily
instruments of activity such as the arms or legs. In fact this distinction
in attention may help distinguish aspects of psychiatry from aspects
of neurology. To be specific, neurologists attend to palsies of limb,
lameness in gait, incoordinations and tremors of arm or leg. Behavior,
goal-directed activity, calls medical (i.e., psychiatric) attention to
disorders that can appear with uncompromised musculoskeletal
capacities.

The disordered aspect of a behavior may, for example, be tied to its

goals. Suicide, with death as a goal, is a prime example. But drug
dependence and sexual perversions also can be seen as behaviors
with disordered goals. Recognizing these forms of human behavior
provokes the obvious question: Why do these goals-in the case of
suicide, self-injury, and death-preoccupy the patient? What if any
could be a role for drive in suicide, what is a role for learning?

The means to reaching a goal represent another way in which a

behavior can be deviant and disordered. Examples here include the
use of dangerous sedatives for sleep; the indulgence in delinquency,
truancy, and bullying for play; or the interest in exhibitionism for
sexual expression. These features raise the question of why such
means came to be chosen when the goals-sleep, play, sex-can be
achieved, with benefits, in more usual ways. What predisposition and
reinforcements have shaped these choices? What mechanisms may
have gone awry? Thus the totally blind person, deprived of
sensations from diurnal light and dark cycles, can have serious sleep
and wakeful change explicable from the disconnection of the
suprachiasmatic nucleus."

The consequences of some behaviors identify them as dangerous

and injurious. Examples include lung cancer from cigarette smoking,
HIV infection with particular sexual practices, and coronary artery
disease and obesity with high-fat dietary preferences. They arouse
questions about how physicians can interrupt these dangerous
behaviors or, when that proves too difficult, protect people from their
consequences.

Finally, the provocations of a behavior can identify disorder.

Although behaviors can be propelled by delusions or manic
excitement, the mental phenomenon referred to as "craving"-
experienced in consciousness as an insistent, overpowering hunger
or demand-gives the addictions and disorders in sexual or other
appetites their disruptive dominance. Cravings, derived from powerful
physiological drives (overdrive?) combined with conditioned learning,
overwhelm an individual's capacity to direct and modify his or her
actions.12 Any behavior in which control and choice are impaired is
abnormal by definition and thus a source of clinical concern.

Summary

Our purpose in this chapter has been to introduce the domain of

behavior, note how vital issues of life are encompassed within it, and
demonstrate the scientific concepts that explain it. The issues of
identification, explanation, and treatment of specific anomalous
behaviors and particularly the importance of craving as a
manifestation of disorder are considered in more detail in subsequent
chapters. But critical to this introduction to the behavior perspective is
an attempt to emphasize that motivated (driven) behaviors develop
through a combination of (1) specific embodied physiological features
that arouse the drive and respond to its satisfaction with (2) learning
through the influence of the environment on the responses generated
by the drive. Thus, disorders of motivated behaviors could come
either from some disruption of the drive mechanisms or from a
maladaptive set of life experiences that misdirected the learned
response patterns. Rational treatments would follow the identified
source or sources of the problem.

An appreciation of behavior as a domain of psychiatric concern

does bring a number of implications to practice that are encountered
in subsequent chapters. In particular, the treatment of behaviors runs
into a series of issues not found in treatment of diseases. The task is
the redirection of a way of life-conversion, not cure-and this brings
with it a number of conflicts of belief and attitude. These conflicts are
usually between psychiatrist and patient, as the main task is to win
the patient's agreement for change. However, other conflicts with
social groups and advocates emerge here and fundamentally depend
on moral issues concerning how human life should be lived.
When appraising behaviors (what people are doing), psychiatrists
must reconfront the issue of abnormality, a matter much more
problematic here than with disease. Psychiatrists could resolve
disagreements over psychiatric diseases (what people have) by
pointing to bodily pathology, a broken part. But when they claim that a
behavior is disordered and in need of treatment, psychiatrists have
been accused, on the one hand, of denying people the right to live as
they choose, and, on the other, of exonerating antisocial dissipations
with a medical excuse.

In this chapter we revisit the triad of drive, learning, and choice to

demonstrate how to identify disorders among the motivated, or
driven, behaviors, explain what we know, and document what we still
have to learn about them.

Definitions and Understanding Motivation

Motivational states are identified by subjective experiences such as

hunger, thirst, and sexual arousal. These drive states are affects, that
is, companions of moods and emotions within the affective domain.
Dispositional states is another term for affects and applies to hunger,
thirst, sexual arousal, and so on, in that they foster certain attitudes
and behaviors. They can be powerful and pressing, dominant and
engulfing, or moderate and deferrable. These dispositions, resting on
a brain-based physiology, give motor-sensory activity the goal-
directedness that defines behaviors. Thus, dispositional drives are
psychological expressions that respond, among other prompts, to
deprivation. They, and the responses they promote, are modified by
learning especially in the form of conditioning to circumstances
evoking or inhibiting them. The expressed behavior emerges as a
choice for actions that vary in their character from occasion to
occasion in reaching a goal.

The behaviors can differ in the specificity of their goals. Some goals
are general, such as sustaining activity itself in a diurnal rhythm,
waxing and waning in relation to time of day. Other goals are more
particular, such as aggression or defense, manifested as either fight
or flight. Finally, some goals are sharply defined, such as food
consumption, water drinking, or sexual congress.

These dispositionally driven, goal-directed behaviors have the

adaptive functions first identified by the instinct psychologists and
appreciated as lifepreserving components of existence. Eating,
sleeping, defense, and sexuality relate in a hierarchy, one
superseding the other, as circumstances change or satisfactions are
achieved with the effect that the individual is seldom locked into a
persistent or dangerous activity by the domination of an inappropriate
motivation. In fact, failure to find apt release from a drive is often a
feature of abnormality. Inhibition (satiation) is as critical as excitation
(arousal) in healthy motivated behaviors. Indeed, the integrative
sequence of arousal and satiation renders motivated states such as
hunger or thirst variable, intermittent, and coherent psychological
manifestations.

In summary, each motivated behavior, resting on a unique

neurobiology that provokes a cyclical arousal of its appetite, is open
to shaping by experience and, in its healthy form, is expressed,
integrated, and elaborated as a lifesustaining, enriching activity.
Three aspects of motivation-psychological experience, expressed
behavior, and physiology-can be profitably examined.

The Psychological Experience

 Affective dispositions tied to motivated behaviors are familiar and
accessible to psychiatric investigation. For example, an individual can
describe hunger as it waxes and wanes before and after meals during
a typical day. Through this description, psychiatrists learn the insistent
power of affective dispositions and how they are shaped by
experience and maturation. People report how these affects can
dominate them by altering their sensitivity to stimuli, promoting their
search for satisfactions, and distracting them from other activities.
One of the best examples is the emergence of sexual interest with
puberty, where stimuli previously only mildly interesting become
arousing and preoccupying. Adults describe sexual arousal as an
appetite for pleasure and an urge for release from tension. Both
aspects occur simultaneously and have been built into causal
theories for behavior such as the "pleasure principle" or "drive
reduction." The predominant psychological experiences with sex
include an arousal of interest and susceptibility to sexual actions,
which can become pressing, and the temporary reduction of sexual
interest following a consummation.

A critical point about motivated behaviors is that prolonged

deprivation will increase their power to the point, with some, that they
can supplant all other concerns. In particular, prolonged deprivation of
life-sustaining drives such as hunger and thirst will customarily lead to
abandonment of all projects other than those devoted to reaching
food or drink.

The affective disposition underlying and promoting a goal-directed

motivated behavior is far from trivial. Choosing to eat or drink is not
like choosing which tie matches one's shirt. A person's interests
become progressively more dominated by a drive, a domination
reflected in preoccupations, dreams, and eventually, some aspect of
activity. The dispositional pressure can become so intense that it may
overwhelm strong resistance. A capacity and sense of choice
remains, but becomes progressively more narrow as drive increases.
Behavior Itself

The behavioral expressions of these affective dispositions have

been studied by physiological psychologists, such as Frank Beech
and Eliot Stellar.'.2 These studies divided activities preparing for such
behaviors as eating, drinking, or sexuality from their final expressions.
The preparatory activities, such as the searching for food and the
courting of a mate, are called the appetitive behaviors and the
ultimate expressions, such as food ingestion or sexual congress, the
consummatory behaviors. The appetitive actions show great variety
within a goal-seeking behavior because they are expressed under
differing circumstances from occasion to occasion. The
consummatory actions are much more stereotyped and simple,
ingestion and copulation being straightforward species-specific
maneuvers in themselves.

The behavioral expressions of drive, especially in their appetitive

stage, are always modified by learning. Immediate circumstances and
past experience tied to the expression of any behavior can shape its
present and subsequent manifestations. For example, through
preparing meals and eating them, people become intrigued by the
opportunities meals present for enhancing the pleasure of eating.
This promotes in some the interests and skills of gourmet cooks.

An intriguing domain of psychology today is the study of how

consummatory behavior, that which produces satiety, also has long-
term sensitizing effects that encourage subsequent behavioral
expressions and preferences. There is a dual aspect to the
consummatory expression of a drive: the prompt but temporary
reduction or satiation of the drive but simultaneously the
enhancement of interest in indulgence of the behavior with
subsequent opportunities.3 This enhancement of behavior by its own
expression was overlooked by such psychologists as Sigmund Freud
when they assumed that all manifestations of behavior were
prompted by drive discharge and reduction, an idea that led these
psychologists to counsel against behavioral inhibitions as leading to
"drive-damming" and ultimate "breakthrough" expressions. We now
know that expressions of drive can actually strengthen the drive over
time and may lead to lessened control.

These observations amplify on classical (Pavlovian) and operant

(Skinnerian) conditioning explanations of behavioral change. They
speak to the role of certain cultural patterns in different human
societies where an interaction between drive for a behavior and the
expressions encouraged by the culture can enhance or suppress
certain activities. For instance, cultural anthropologist Richard Sipes
challenged the Freudian model of drive reduction by comparing
overall aggressiveness in warlike societies with that in peaceful
societies. He worked with the assumption that if war would give
release to an aggressive drive, then other aggressive expressions-
such as combative sports, body mutilations, and harsh treatments of
deviants-should be lessened in warring tribes and increased in pacific
ones. In fact, just the opposite proved true. The practice of war is
accompanied by an increase rather than a decrease in all forms of
aggressive behavior, which implies that aggressive responses
enhance aggressive behavior overall.4

In other words, the expression of a motivated behavior-feeding,

fighting, or sex-does more than satisfy the drive of the moment. It
enhances receptiveness to the behavior itself and to the settings for
its display-sustaining an interest in it, impelling its repetition, and
encouraging other forms of its display. In these ways, satiating
experience can both amplify the power of the drive and shape the
choices in subsequent expressions. Both normal and abnormal
behaviors derive power and pattern from this reciprocation of
endogenous drive and the instruction of experience. We tend to
become what we enact.

This, admittedly, is a frightening prospect-one that social policy

must take into account. For example, a frequently heard defense for
prostitution and pornography is that these means of expressing the
sexual drive relieve inner "pressures" liable to "break through"
inappropriately without them and thus encourage better behavior in
other circumstances. It is as likely that these means of satisfying sex
build an appetite that coarsens character, injures social bonds, and in
some individuals provokes paraphilia.

The realization that satisfactions can give behaviors a growing

power over us has led to such concepts as "sexual addiction." On
close inspection, "sexual incontinence" fits better as a description of
the problem. In certain men, past experience encouraged sexual
interest in inappropriate people and in inappropriate places-leading,
for example, to sexual harassment of office mates-without any
evidence of an increase in sexual drive compared to other men.

However, there is no iron determinism in these matters. As an

individual comes to appreciate how these powerful motivational
dispositions promote attractions and behavior, he can also appreciate
that the expressions are under some control of his will and
consequentially subject to influence from his intentions, aspirations,
and commitments. He can be expected to become responsible for his
actions.

Motivational dispositions can be pressing and provocative but can

be suspended by choosing incompatible activities or through
conscious refusal to act on the drive. Such a refusal may be tied to
human values, culture, or interpretation (celibacy among the clergy;
the ascetic denials of religious ceremony associated with Yom Kippur,
Lent, Ramadan; and even the self-starvation to death of political
prisoners). Influenced by their contexts, their past expressions, and
their encultured meanings, motivated behaviors may expand or
contract for many reasons but they are not irrepressible responses to
stimuli such as the knee jerk. The place of choice in shaping the
expression of behaviors include the following: Etiquette rules tend to
be learned and then obeyed even by hungry people. Sexual interests
can be withheld from action so that they do not disrupt the lives of
others. Sleepiness is ignored by mothers accepting nursing
responsibilities to a newborn.

Profound implications for humankind rest on the fact that the

expressions of motivated behaviors are neither automatic nor fixedly
predesigned. A place for learning, deliberation, and choice remains
despite insistence of drive, amplification from expression, and power
of habit. Through maturation, guidance, and example from others,
and reflections on trials and errors, most people learn to control their
behavior and achieve a life of fidelity, satisfaction, and promise.
Failures to accomplish these developmental tasks, however, often
bring people to psychiatrists and are discussed later on.

Underlying Physiology

Motivated behaviors (eating, drinking, sleep, sexuality, etc.) have

physiological mechanisms that arouse and satiate them. The drives
depend on elements of biology: genes, molecules, receptors,
neurons, and neuro-anatomical systems. The limbic-hypothalamic
system of the brain is a critical site for the organization and
integration of the provocative and inhibitory signals behind motivated
behaviors.

In the previous chapter we described how Richter, Moore, and

Zucker revealed that the hypothalamic site encompassing the
suprachiasmatic nucleus controlled activity rhythms and was open to
the influence of light perception from the environment. Similar
physiological studies have revealed how embodied mechanisms
control other drives. With most drives-hunger and thirst, in particular-
investigations have distinguished integrative responsibilities for
"peripheral" mechanisms (that is, bodily functions, in the form of
visceral events, hormonal release and reception, and autonomic
neural signals), and "central" mechanisms (that is, brain functions
formed from neural systems and neurotransmitter actions).
 For example, Paul McHugh, Timothy Moran, Paul Robinson, and
Gary in a series of investigations, related the peptide hormone
cholecystokinin, to gastric distention in controlling food intake. They
demonstrated that this hormone, released by the entry of nutrients
into the small intestine, is picked up by receptors on the pyloric
muscles and vagus nerve. By causing pyloric constriction, this
reception acts to slow the gastric emptying of food, enhancing and
sustaining stomach fullness. As well, the receptors on the vagus
amplify the afferent signals from gastric stretch receptors to the brain.
Through these physiological effects provoked by this hormone, meal-
ending satiety is gradually brought about as food is ingested.

A more complete description of this work goes beyond our

purposes here. But it represents another example of just how stimuli
produced by a behavior (here the gradual but increasing distention of
the stomach with eating) can be integrated physiologically to bring a
behavior to a controlled end (here to replace hunger with satiety).

Peripheral signals that control motivated behaviors ultimately reach

the limbic hypothalamic system, where they are integrated and
influenced by other signals. This region plays an important role in the
arousal of behavior and in the pleasure that behavioral expressions
bring. In particular, the mesolimbic dopamine pathway may provide
the reinforcing, hedonic sensations tied to many consummatory
behaviors such as food ingestion and sexual activity.

The mesolimbic dopamine path-linking the midbrain regions (where

sensations from the peripheral body first arrive) with the limbic
forebrain areas (such as the nucleus acumbens), where its neurons
release the neurotransmitter dopamine-can form a system for
reinforcing motivations generally." In addition, a rich array of opiate
receptors in the midbrain region have been discovered that may
amplify the peripheral signals to the mesolimbic dopamine path. This
receptor field presents a means for endogenous opiates to integrate
with peripheral sensations and add to their rewarding character.
 Our purpose in briefly mentioning these basic neuroscience
discoveries is to show the existence of embodied features capable of
arousing, sustaining, and inhibiting drives. These features not only
provide the biological substrate for normal motivations but also point
to sites that can sustain pathological injury and affect control of
motivations.

Features of Abnormality Tied to Motivated Behaviors

As noted earlier in this chapter, selecting criteria to define a

behavior as abnormal is a vexed issue because of social
expectations and values. One may long for the objective evidence
that a "broken part" gives to validating a disease.

Some behaviors, however, may be prompted by a disease-such as

alcoholic drunkenness or sexual misdirections provoked by an attack
of mania. That these behaviors are disordered is seldom contended
as they are so obviously symptomatic of the underlying disease and
disappear with its treatment. These examples, however, constitute a
tiny minority of the behavioral problems needing explanation and
treatment. More common are those behaviors that emerge in
individuals who have no obvious diseases or defects. Their behaviors
raise the issues of what should be called abnormal and considered a
legitimate topic for psychiatric assessment and treatment.

Occasionally the answer seems obvious. Just as self-injury and

suicide are considered disturbed behaviors on the basis of their
disastrous consequences, so should alcohol consumption when it is
carried to the point of bodily illness and social dilapidation. This
handy definition of abnormality-if it hurts you, it's bad-has two
problems, however. First, it does not address the behavior directly for
evidence of its own abnormality but only sees abnormality in its
consequences. Second, as has been frequently said by people
risking the dangers of cigarette smoking, "Whose life is it, anyway?"
 Another unsatisfactory but logically consistent way of defining
abnormality rests on the social nature of some behaviors. Because
they involve actions in society, they are thus subject to society's laws.
The inability of a person to conform his or her behavior to the
constraints of law identifies the individual as requiring some form of
control, perhaps from physicians. This issue is exemplified in laws
that identify and constrain such behaviors as public drunkenness. Yet
the difficulties are many with generalizations from such a rule. Legal
definitions of abnormality have led to stigmatizing, and even to
hospitalizing as mentally ill, persons engaging in political activities
that challenge the status quo.

A better criterion for regarding a behavior as a matter for clinical

concern rests on some judgment that either the individual in question
or others suffer from its expression. This also is a serviceable
standard but one that tends to founder on the issue of suffering-who
is suffering and from what, how much suffering is acceptable, and
when does the suffering reflect a clinically relevant problem. For
example, is a hangover enough to indicate that the prior evening's
drinking was deviant?

A solution to the dilemma of defining behavioral abnormality

emerged when clinicians began to study behaviors themselves and to
appreciate how some of their expressions could fall away from control
and hamper other life tasks. The close study of beverage alcohol first
brought forth these concepts. We shall describe these observations
and their conclusions because they are a model example of
behavioral epidemiology and encourage similar approaches to
disorders of other motivated behaviors.

Alcohol consumption is so common in the adult population of the

United States that drinking itself cannot be considered abnormal,
risky but not deviant. Contemporary epidemiological surveys indicate
that between 65 and 70 percent of adult Americans drink alcohol in
any year, 30 to 35 percent drink weekly, and 4 to 6 percent drink
heavily (consume five or more drinks on at least one occasion every
week).12 These data do not define where significant problems with
alcohol consumption emerge nor who from among all these people
should be considered alcoholics. Measuring the quantity of alcohol
consumed against some arbitrary standard, identifying bodily damage
as in liver cirrhosis, and differentiating the particular modes of alcohol
consumption certainly provide some sense of the problems and risks
tied to alcohol use but do not identify abnormal drinking itself.

The concept that there is not one condition, alcoholism, but a

variety of individuals with drinking problems emerged with the work of
Griffith Edwards, and his colleagues at the Institute of Psychiatry in
London in the 1970s.13 Data from a large U.S. household probability
sample indicate that problem drinkers number approximately 7.4
percent of the population, or close to 14 million Americans. They
congregate in two groups, with different behavioral disorders and
different treatment needs.

Approximately one-third of problem drinkers have the alcohol

dependency syndrome. This is a driven, stereotypic behavioral
condition resting on physiological dependence to alcohol developed
from prolonged and excessive consumption. Patients with the alcohol
dependency syndrome demonstrate a dominating, indeed
overwhelming, motivated drive. They are preoccupied with plans for
getting more alcohol when abstinent and make sustaining a steady
supply of alcohol their primary daily occupation. If alcohol is withheld
from them, they will quickly show signs of physical dependence, with
trembling, nausea, and sometimes delirium. Alcohol consumption, at
pharmacological doses, dominates their life despite the appearance
and worsening of serious bodily and social damage from its effects.
Those with the alcohol dependency syndrome are alcohol addicts
driven by a hunger for alcohol that overpowers them.

The other two-thirds of problem drinkers are not physiologically

dependent on alcohol but have a habit of using alcohol
inappropriately, often but not necessarily in excessive quantities.
Their condition, aptly called alcohol abuse disorder, encompasses
those who seek and indulge in alcohol for its tranquilizing, euphoric,
or disinhibiting features heedless of consequences. For example,
they will drink alcohol while driving, when at work, or when they
should attend to domestic responsibilities. Their alcohol consumption
disrupts their analytic capacities and their emotional control, leading
to accidents, domestic disharmony, and violence.14 Despite repeated
disruptions to their social and interpersonal life, these individuals
minimize the role of alcohol in these problems and do little or nothing
to avoid further inappropriate drinking. Because they are not
physiologically dependent, they usually do not show other
problematic symptoms beyond uncomfortable "hangovers."

Alcohol abuse disorder is a learned habit precipitated and sustained

by predispositions of temperament and by the psychologically
rewarding consequences of ethanol. A whole variety of social and
psychological factors, not the addictive hunger driving the alcohol
dependency syndrome, support this habit. The combination of self-
centered immaturity and a preference for companions who drink like
them will be found frequently among the patients with this disorder.

These two behavior syndromes, the addicted state of alcohol

dependency and the indulgent habits of alcohol abuse, represent
clear distinctions among all those who drink alcohol. The many
adverse physical and social injuries tied to alcohol consumption
derive from these syndromes and are best studied as consequences
rather than as definitions of deviance. The sense of patients' needing
treatment for physiological dependency and for habit control emerges
from these behavioral distinctions.

We offer these epidemiological observations on alcohol use and its

disorders not only for their own value but also as a model for
approaches to identifying deviance in other motivated behaviors such
as eating, sexuality, sleep. Deviance can be appreciated either as an
expression of excessive and overpowering drive (dependency) or as
an inapt use of a common faculty (abuse). In our following review of
the phenomenology, expression, and physiology of other behaviors,
we describe similar forms of dependency or abuse.

The Psychological Experience

The most persuasive criterion for the existence of dependency lies

in its dispositional, affective presentation. A transformation of the
customary subjective experience of drive into one of dependence
takes the form of a "craving" for Such cravings can be relatively
benign: for example, the desires of a pregnant woman for an unusual
food, desired not for its nutritive value but for some other and
seemingly irresistible quality such as its salty or savory flavor can be
pressing but little more than inconvenient. More distressing and
potentially dangerous are sexual cravings, in which particular sexual
activities, such as pedophilia or sadistic activity, become the sole
focus of thoughts and plans, dominating all other considerations of
sexual expression, including a sense of affection for and adherence
to a partner.

In all its various presentations, a persistent craving divorces the

affective interest in a behavior from the coordinated biological,
psychological, and social elements that customarily enrich and
control it. With craving, sexual activity becomes ritualized and
stereotyped. The term paraphilia is most appropriate in describing the
patient's fixed craving and misdirection of sexual urge, away from
feelings of affection for another person and sense of his or her
irreplaceability as a loved person, toward a stereotyped hunger for
selfgratification in which a kind of consumption is the sole aim and the
human objects of the desire are equivalent and replaceable as means
to the end.

A craving is not only stronger and more difficult to control than other
motivated states, but also, as Jaspers pointed out, it is often
experienced as something as alien as it is compelling. Its behavioral
expression, as it is almost pure consumption, produces no long-term
satisfaction or relief from its insistent psychological pressure. Indeed,
many individuals with cravings report their obsessive quality and
strength as sharply different from normal drives. The patient defines
himself or herself as abnormal because he or she is distressed and
overmastered by craving.'6 Thus, cravings constitute the best
categorical evidence for an abnormal dependency syndrome in a
motivated behavior and as well the best justification for medical
intervention. Craving drives some sexual perversions, the bulimic
bouts of bulimia nervosa, and the alcohol and drug dependency
syndromes.

In contrast to the dependency syndromes, abuse behaviors emerge

as expressions not of craving but of adventure seeking and self-
indulging attitudes tied to a diminished concern for consequences.
Sexual adventures with prostitutes or binges of alcoholic
drunkenness in college fraternities are often provoked by
combinations of opportunities; impulsive, nonreflective features of
immaturity; and peer pressure rationalized as "initiations."

Although these expressions can sometimes lead to sustained

dependency, most do not. With guidance from others and from
personal reflections on the shameful implications and dangers of
abuse behaviors, most adults abandon the attitudes and companions
that support these impulses. However, a casual view of these
behaviors as benign "rites of passage" is unwarranted. Even if we
prescind, for the moment, from the moral and legal objections to
these behaviors-in fact we hold those objections to be legitimate and
compellingthere are medical and psychiatric reasons to reject the
behaviors. Not only are they dangerous to the health of the
adventurous (such as through infections from sexual behaviors and
accidents with drunkenness), but also these common but sporadic
abuse behaviors of many adolescents can become coarsening habits
of a few, who will later need attention from psychiatric services.
The Behavior Itself

In contrast to normal motivated behaviors, where a consummatory

expression is followed by a period of disinterest in the activity, in the
dependency forms of abnormal behaviors this satiety feature is
abbreviated and may even be absent. This is another persuasive
indicator of deviance.

An absence of satiation is particularly obvious in cocaine addiction.

Here the addict, preoccupied with a hunger for cocaine, discovers
that after each injection he is immediately preoccupied with a drive to
repeat it. The sequence of preparation, consumption, and further
preparation of cocaine will continue either until the stocks are
exhausted or all the money of the addict has been spent.

Another example of a behavior in which satiation is attenuated is

the binge and vomit cycle in patients with bulimia nervosa. These
patients can consume and then dispose of huge quantities of food.
Some can persist throughout the day, running up massive grocery
bills that threaten a family's economy. This activity resembles the
"sham feeding" demonstrations of Pavlov, who, by forming an
esophageal fistula in dogs through which ingested food and water
drained, caused these animals to eat and drink without pausing. The
bulimic vomiters, like these experimental animals, persist in food
consumption because by emptying their stomachs they evade the
visceral signals for satiety.

The sexual perversion of "exhibitionism" represents a learned

behavior that can be best construed as an abusive and deviant form
of courtship ritual. The behavior is played out despite considerable
danger to the individual. Perhaps because it has no consummatory
feature from which satiation can come, exhibitionism will often be
repeated with many victims during the time the patient commits to the
behavior's expression and turns out to be quite difficult to treat.
 Prostitution, in contrast to the dependency- and abuse-driven
behaviors mentioned so far, is a sexual behavior with a commercial
purpose. Certainly the sexual actions of the prostitute are not driven
by erotic motivation or by an insatiable craving for experience. In fact,
they are not driven at all but are learned behaviors, modeled from
others, and taken up for financial reasons. The generation and
commercial organization of prostitution, sex as a market, is a vicious
exploitation of women. The damages tied to prostitution go far
beyond the usual complaints of the spread of venereal infections. Any
society that tolerates the treatment of human beings as consumable
goods is in chaotic disarray.

The Underlying Physiology

An abnormality in a motivated behavior must depend on the

subversion of some normal physiological mechanisms, both those
that evoke a drive and those that shape its expression through
conditioned learning. The search for these features has been a major
focus of drug addiction studies. In the course of such studies, some
remarkable features of neurobiology have emerged of interest to
understanding both normal and abnormal behaviors.

We mentioned the discovery of opiate receptors in the brain.17,18

These function normally to influence the effects of physical stimuli on
behavior. Their discovery promptly led to the identification of
endogenous "opiates" that function in a variety of activities. As well,
this discovery opened up a whole new domain of
psychopharmacology. In particular, it makes sense of why a plant
product-opium-can generate a dependency syndrome. Exogenous
botanical opiates stimulate the physiological receptors in the brain
normally responsive to endogenous opiates, and with this artificial
stimulation the number and sensitivity of receptors is changed such
that a craving for abnormal, exogenous supplies can emerge.
 The mesolimbic dopamine pathway responsible for the experience
of pleasurable reinforcement and linking the limbic midbrain area to
the limbic cerebral structures is most likely involved in cocaine
dependence. Cocaine blocks the reuptake of dopamine in the
synapses within this system and produces a powerful reinforcing
experience.19 Thomas Schlaepfer and his associates demonstrated
with brain imaging that the nucleus accumbens, a major end point of
the mesolimbic pathway, is activated by cocaine.20

Furthermore, many drug abuse behaviors can become conditioned

responses through their pharmacological properties of relieving
anxiety or evoking a relaxed and unconflicted state of mind. The
neurophysiology of these effects may rest on pharmacological
inhibition of frontal lobe activity, where longterm planning and the
appreciation of implications are generated.

Undoubtedly, other aspects of brain organization tied to learning

can lead to sustained deviant behaviors as through early exposure to
consummatory experiences-drug ingestion, sexual experience, food
fads. Exactly what the brain mechanisms are for this critical
conditioning of behavior and what the long-term effects of
consummatory actions on the brain are represent major enterprises
now in neuroscience. Discernment of these mechanisms will enhance
considerably our appreciation of the abuse liability of addictive drugs
and as well illuminate just how early experience can have powerful
effects on later expressions of motivated behaviors. We all await the
discoveries in this arena of neuroscience.

Summary

We described how motivated behaviors can be a site for disorders

by differentiating normal behaviors from their abnormal expressions,
particularly those that take the form of dependency or abuse
syndromes. In the dependency disorders, an intense drive blocks out
other interests and overwhelms the patient. In the abuse syndromes,
the patient indulges a habit or learned behavior for its rewards. Our
purpose has been to define those features that give these behaviors
a deviant character, such as craving, habitual repetition, and
physiological reinforcement. In the next two chapters we review the
genesis of behavioral disorders and their treatments.
People with behavioral disorders are patients because of what they
are doing, not what they have. They present their psychiatrists with a
more difficult explanatory task: How does this behavior arise, what
has caused it to be disordered, and why would this patient behave in
this way? We attempted to offer some answers in the preceding
chapter by discussing those disordered behaviors tied to motivational
systems-disorders of hunger, sexuality, and alcohol use, for example.
We also attempted to demonstrate how abnormalities can be
recognized in the psychological experience and the behaviors
themselves, and we pointed out that these disorders rest on some
misdirection of the physiology underlying motivated drives.

The implication of that chapter, like the chapter that preceded it, is
that the triad of choice, drive, and learning can represent normal as
well as abnormal expressions of behavior but that closer inspection of
behaviors themselves demonstrates that most abnormalities are
either characterized by an overpowering drive (dependency), a
learned habit of indulging the pleasures of the behavior (abuse), or-
perhaps most commonly-some combination of the two factors. In this
chapter we wish to look more closely at the several kinds of causal
mechanisms that can lead to deranged behaviors and as well
consider some of the psychological proposals offered to explain what
psychological purposes-that is, functions-some behaviors serve and
how those purposes are thought to sustain the behavior even in the
face of damage and danger.

We begin with a brief consideration of those behavioral disorders

that are obviously symptoms of some disease. These are few in
number but often dramatic in their presentations because the disease
has in some way damaged the controls on drive or has amplified
drive beyond the capacity of the patient to manage. Brain lesions,
chromosome abnormalities, and genetic variation have all produced
some impressive clinical syndromes-with behavior in "overdrive"
represented among the symptoms and ultimately explained by a
disruption of the embodied controls on the motivational system-the
"broken part."

Nevertheless, most behavioral disorders do not emerge as

symptoms of some underlying disease. Rather, they are the products
of some combination of development, polygenic influence, and
learning. The main body of this chapter is devoted to considering
provocative factors that determine aspects of these conditions'
incidence in the population, even though the factors do not unfailingly
produce a behavioral disorder as does the presence of an embodied
broken part.

Finally, we consider those explanations couched as answers to the

question of purpose behind a behavior: Just why does this patient act
in this way? The "why" answers bring us to consider the work of
psychodynamic psychiatrists and of the behaviorists. They offer
distinct "why answers" to the question of the causes of behavior and
thus provide different ways of understanding it.

Disease as a Provocative Factor in Some Behavioral Disorders

Some behaviors are caused by diseases and have a syndromic

character in which disease reasoning functions appropriately. That is,
with these conditions, a cluster of features-including behavioral
features-is recognizable as a recurrent clinical entity. In such cases, a
search for pathological mechanisms and etiological agents is
rewarded by discerning a fundamental disruption or dyscontrol of the
embodied mechanisms normally directing the basic drive.
Symptomatic behavioral disorders can involve many drives, but
particularly eating behavior and sleep.
Brain Disease

Injuries to certain strategic regions of the brain have been

recognized to provoke particular behavioral disorders. The
hypothalamus, the region at the base of the brain surrounding the
third ventricle, is such a region. Any pathology-neoplastic, traumatic,
inflammatory, and so on-that damages the medial hypothalamus can
produce a remarkable state of overeating. Gross obesity associated
with pituitary hormonal deficiency was first described in such patients
by the German neurologist Alfred Frohlich, and to this day is
sometimes referred to as Frohlich syndrome.' It is probably best to
simply include this syndrome as one variant of the expression of
hypothalamic hyperphagia and obesity.2 The patients are totally
preoccupied with eating and become enraged and aggressive when
their food is restricted. They recover normal behavior with relief of the
offending hypothalamic lesion. This form of overeating and obesity is
best construed as a behavioral symptom of an underlying brain
disease.

Chromosome Abnormality

Another form of disease that can produce behavioral symptoms

relates to chromosomal abnormality. Chromosomal disorders,
discussed in chapter 10, usually produce mental retardation, but at
least one produces as well a gross abnormality in the control of food
intake. Prader-Willi syndrome has been tied to translocation of
chromosomal material from chromosome 15. Other cytogenetic
injuries to the genome are possible in some examples of Prader-Willi.
However, in all the patients the most disabling feature is obesity and
overeating; hyperphagia that goes so far as to provoke food stealing,
raiding of refrigerators, and even the prowling of garbage collections
is standard. Upon closer study, this indiscriminant food taking is
associated with a failure of the satiety controls in these patients. As
the child matures, he or she becomes totally preoccupied by food and
reports worrying about having enough food in the home and where
the next meal will be coming from.3

The patient with Prader-Willi syndrome usually dies early from the
effects of hyperphagia, becoming grossly and incapacitatingly obese.
Again, this is an example of a behavioral symptom of disease. In this
case, the broken part identified as pathological is chromosome 15
where both translocations and deletions have been found. Exactly
how a lesion in this chromosome interferes with the customary
controls on food intake is as yet unknown. Therefore, the treatments
have so far been all symptomatic. Some help from naloxone
treatment has been reported, as have behavioral management
techniques. But none has been fully successful.

Gene Disorder

Perhaps the most distinctive motivated behavior syndrome with a

clear genetic basis-indeed dominant inheritance-is narcolepsy. Here
the mecha nisms controlling the natural sequences of sleep are
disordered and a constellation of features-narcoleptic sleep spells,
cataplexy, hypnagogic and hypnopompic hallucinations, and sleep
paralysis-afflicts patients.

The study of sleep is a major division of scientific investigation of

motivated behaviors, and it has revealed that in narcolepsy the
several symptoms can be explained by the intrusion and dyscontrol of
the rapid eye movement (REM) phase of sleep. The patients may
enter REM sleep inappropriately during the day or experience
aspects of REM when they should be fully awake. Hypnagogic
hallucinations of narcolepsy are dream experiences associated with
REM, sleep paralysis is muscle paralysis normally produced in sleep
by REM now experienced in wakefulness, and the narcoleptic spells
are expressed by a tendency to drift into REM sleep quickly when not
stimulated during the day. Sleep studies with an
electroencephalograph (EEG) reveal this tendency to quickly enter
REM sleep.4

The rare recessive condition Lesch-Nyhan syndrome is an inborn

error of purine metabolism in which self-injury is a prominent
behavioral symptom. The disorder is X chromosome linked and thus
only affects males. Compulsive self-injury, including amputation of
fingers by self-biting and loss of lip tissue from the same behavior, is
common in the youngest victims. But selfhitting and head banging
also are common behavioral presentations. These symptoms-along
with mental retardation and choreoathetosis-are so extreme and so
resistant to redirection and counseling that the patients often need
physical restraint to keep from lethal self-injurious behavior.

The fundamental biochemical defect is in the metabolism of

hypoxanthine, resulting in excesses of uric acid. Exactly how this
produces self-injurious behavior is not known. Treatment measures
have included behavioral treatment protocols, including aversive
management. Naloxone treatment has also been tried. Again, without
a better appreciation of the mechanisms linking the etiological lesion
to the behavioral symptoms, we are left with unsatisfactory
symptomatic approaches.5

Behaviors Associated with Psychiatric Diseases

Certain psychiatric diseases often provoke behaviors that will not be

seen when these diseases are in remission. For example,
homosexual behavior is occasionally seen in people only when they
are suffering from mania. Their behavior under these circumstances
is but one expression of the heightened sexual drive that sometimes
accompanies the disorder and that may take other forms as well.
Likewise, excessive consumption of alcohol, with its phys iological
consequences, can occur in manic patients experiencing an increase
in all their appetites, although never when they are euthymic.
 It is crucial to recognize those examples of a behavior that are
symptomatic of particular diseases, because the treatment of the
behavior and its prognosis depend on the underlying cause. To
mistake the alcoholic behavior of a depressive individual, who
requires pharmacological treatment or electroconvulsive therapy, for
the binge behavior provoked by romantic disappointment in a
dependent and dramatic person who needs psychotherapy is to
overlook a fundamental distinction. Symptomatic behaviors are
recognized by the company they keep with other symptoms of a
psychiatric disease. The possibility of a relationship between disease
and behavior should be considered in all examples of the sudden
appearance of activities uncharacteristic of the individual. That
behaviors and diseases sometimes occur together raises the issue of
whether certain behaviors should themselves be regarded as
diseases. This position has been affirmed by several advocacy
groups, especially those concerned with alcohol abuse and
dependence.

The use of the term disease for alcoholism seems to us to be

metaphoric: it signifies and dramatizes the craving over which
alcoholic persons have little control, it acknowledges the chronic
remitting and relapsing nature of the disorder, and it emphasizes that
brain processes are involved in alcohol addiction. Though calling
alcoholism a disease has had beneficial effects, including the
enhancement of tolerance toward alcoholic persons in the society
and a willingness to provide more services for them, we hold that this
metaphor for a behavioral disorder is ultimately not helpful. We
should not restrict our thinking about alcohol addiction to the disease
concept, because it will reduce our understanding of the behavior
itself and how it derives from the linkages between brain
mechanisms, life choices, and learning.

The disease concept progresses in a logical way from clinical

syndrome to pathological disease state to etiological agency. It
describes a process of reasoning as well as a set of facts. Although it
can be applied to a syndrome like mania, in which alcohol abuse
occurs (that is, "pushed" by the increase in all the appetites) and may
eventually explain a subset of alcoholic persons who could have a
genetic feature or defect rendering them vulnerable to ethanol
addiction (that is, "pulled" by some physiologically based,
extrareinforcing feature of alcohol's effect on their body or brain), the
category of disease does not do justice to all of the varied
manifestations and causes of excessive alcohol consumption.

The act of drinking is the sine qua non of alcoholism. Though large
amounts of alcohol consumption can cause pathological disease
states and clinical syndromes such as cirrhosis and delirium tremens,
the drinking of alcohol is itself an action demanding some willful
choice, just like the smoking of cigarettes. Indeed, drinking alcohol
and smoking cigarettes are purely matters of choice at first. The
addicted individual who is entrapped in a behavior prompted by a
multiplicity of genetic, sociocultural, and developmental forces is no
less a victim of an overmastering and powerful influence than is a
person with a disease-but the place of choice and of learning in the
behavioral triad offers special opportunities to treat, prevent, and
explain these disorders in ways unique to themselves. Indeed,
medicine and psychiatry are not the sole sources of opinion here.
Moral concerns, legal constraints, and intense social controversy also
emerge in the considerations of these disorders, the settings that
enhance them, and the means-including medical and psychiatric-to
manage and treat them. The theme of moral concerns and social
conflicts repeatedly appears in the behavior perspective. Such
controversies, however, do not change our opinion that behaviors can
cause diseases and diseases can cause behaviors, but the terms are
not interchangeable.

Genetic, Developmental, and Environmental Causes

Examples of behavior as a product of disease are rare. We need to

turn to other explanations and other mechanisms for the common
behavioral disorders that psychiatrists treat. For instance, we do not
expect to find a disease of the brain that sheds light on why an
adolescent chooses to smoke nor why any particular person turns to
prostitutes for sexual activity. Instead, we must turn to the more
general influences on human beings and appreciate how they interact
in provoking abnormal behaviors in some people.

Genetics, development, and social environments combine in the

most helpful explanations of the incidence and prevalence of these
behaviors in a population. In this chapter we review some of the
current investigations in these matters because they reveal the extent
of the problem of prevention and, through an understanding of risk
factors, give us some idea of what issues tend to predispose and
which to protect individuals from these particular psychiatric
abnormalities.

Genetic Contributions to Behavioral Disorders

The genome harbors the fundamental forces that ultimately lead to

any behavior. It is at the genetic level, for instance, that the
programming of normal development is to be found. From this
program of development emerge, on schedule, the neural structures
that serve functions like eating and sleeping. As well, the genome
holds the program that schedules the emergence of life stages such
as puberty that are important in sexual behavior.

We can relate overeating and obesity directly to a specific portion of

the genome in Prader-Willi syndrome. Similarly and rarely there are
conditions such as Lesch-Nyhan syndrome in which a recessive gene
explains a persisting behavior of self-injury. One of the most common
familial syndromes of motivated behavior is narcolepsy. These, as
mentioned, are examples of behavioral syndromes where disease
reasoning applies and where the patients are examples of a specific
and categorically identifiable condition.
 In most populations, behaviors such as alcoholism and delinquency
emerge as graded features, with some individuals showing more or
less of the behavior at different times. A confident identification of
genetic influence might seem difficult with such conditions, but
considerable progress has been made in demonstrating a genetic
contribution to these issues.

Mendelian heredity patterns have not been found for these

behaviors. However, twin, family, population, and adoption studies
have all been employed to reveal some genetic-presumably
polygenic-role in many behaviors. Franz Kallmann, for example,
found a concordance rate of 100 percent in male monozygotic twins,
one of whom was identified as homosexual, whereas the rate of
concordance for male dizygotic twins was much less.6 In a later
systematic survey of the literature, Leonard Heston and James
Shields concluded that the concordance rate was closer to 50 percent
for monozygotic twins?-still an impressive figure if homosexual
behavior were regarded as determined purely by environment and
choice.

Eliot Slater and Valerie Cowie proposed that in the European-

American culture of the present era genetic factors play some role in
the production of homosexual behavior, but they also point out that
sexual behavior is molded by many influences, including "acquired
tastes" (or learning) closely related to the culture in which the
individual develops.8 Thus, in ancient Greece, where homosexuality
was not considered a deviation, the genetic contribution to the
behavior was submerged within cultural mores.

Presently, two different ways of understanding the origins of

homosexuality compete with one another. One view considers
homosexuality to be "constructed" out of a culture's traditions and
beliefs about sexual roles and behaviors. This constructionist view is
opposed by "essentialists," who hold that some innate quality of
individuals-presumably carried by the genetic makeup-drives the
erotic life toward either the opposite or their own sex.9 It is likely that
both the constructionists and the essentialists have a piece of the
explanation. It is possible, Slater and Cowie point out, to picture a
future in which homosexual behavior will be so much in the cultural
experience of every individual that the genetic contribution will
become undetectable. On the other hand, such historical events as
the AIDS epidemic may, by emphasizing risks tied to homosexual
behaviors, alter cultural attitudes and suppress homosexual activity.

Very similar methods, results, and reasoning apply to the

contribution made by genetics to criminal behavior and delinquency.
That there is a genetic contribution was powerfully demonstrated by
Johannes Lange in his study of twins, published with the fearsome
title Crime as Destiny. In this study, only three of thirteen monozygotic
pairs were discordant for criminal records, whereas only two of
seventeen dizygotic same-sex pairs were concordant.10 K. 0.
Christiansen, in a more recent, population-based study (rather than
the selected samples employed by Lange) of nearly 6,000 twin pairs,
yielded lower concordance rates for monozygotic twins (35.8% for
monozygotic pairs versus 12.3% for dizygotic pairs), but an important
genetic contribution is still

Studies demonstrating a genetic factor in criminality have also

acknowledged cultural/environmental influences shaping the
behavior. For example, in the twin study of A. J. Rosanoff, L. M.
Handy, and 1. R. Plesset, though a higher concordance rate for adult
criminality was again found in male monozygotic twin pairs when
compared to male dizygotic pairs, the rate for juvenile delinquency
was quite similar for monozygotic and dizygotic These results
suggest that influences such as the home, school, or neighborhood
play the major role in provoking juvenile delinquency, whereas
hereditary factors may be more crucial in the development of later,
adult crime. A similar interaction of genetic and environmental effects
has been observed using the adoption-study technique. B. Hutchings
and S. A. Mednick, for example, found that although hereditary
factors seemed to be more influential in promoting criminal behavior
in male adoptees, both nature and nurture played a role (table 5)."

A genetic contribution to alcoholism was discerned in the family

studies of Manfred Bleuler.14 The objection that alcoholism might be
simply the result of shared family life rather than of shared genes has
been answered by the systematic adoption studies of Donald
Goodwin and his colleagues, which demonstrated that the sons of
alcoholics raised by unrelated, nonalcoholic adoptive parents were
four times likelier to become alcoholic than were adopted-out sons of
nonalcoholics.15 This work, confirmed in other studies,'6 indicates
that a specific susceptibility to alcoholism rather than to other
psychiatric disorders, including antisocial behavior, is transmitted
from parent to child, even if the child is not exposed to the alcoholic
parent.

TABLE 5. Hutchings and Mednick on Criminal Behavior

Source: Data from Hutchings B, Mednick SA: Registered criminality in

the adoptive and biological parents of registered male adoptees. In
Mednick SA, Schulsinger F, Higgins J, Bell B (eds.): Genetics,
Environment and Psychopathology. Amsterdam, ElsevierlNorth-
Holland, 1974, pp. 215-227.

Such studies are indicators of a role for genetics in these and other
behavioral disorders. What is also clear is that the mechanisms for
such genetic actions have yet to be explained. Even when a specific,
genetically determined enzyme defect is known, as in Lesch-Nyhan
syndrome, how that defect is related to the particular-in this case,
self-injurious-behavior is not understood. In other instances, what is
inherited may not be a mechanism specific to a behavior but rather
something related to qualities of that person that render him or her
more vulnerable to social influences. Thus, in certain environments
one's bodily habitus may make one more attractive to homosexual
encouragement or more likely to be sought out for the strength and
agility required for certain active criminal pursuits.

Without the clear indications offered by Mendelian characteristics,

the genetic contributions to behavioral disorders as presently defined
are likely polygenic. Although some gene may have a particularly
strong influence, the additive effects of a large number of genes,
some predisposing and some protecting the individual, interact with
other forces shaping his development, reinforcing his inclinations, and
providing his milieu. That genes have a role in behavior can be
demonstrated; that behaviors are influenced by other forces is also
certain, particularly learning through models, instructions, and
rewards from the sociocultural environment.

Sociocultural Forces Influencing Behavior

Cultural forces play important roles in many behaviors and do so by

several different modes of action. The most obvious is by providing
opportunities for the expression of behaviors. For instance, the
eighteenth-century British political decisions to encourage local
distillers of gin and to raise taxes on the imported product made
highly concentrated grain alcohol available to large numbers of
people at low cost, an availability that was a major contribution to an
increase in the prevalence of alcohol abuse.17 The rise in alcohol-
related social, medical, and psychiatric problems promoted the
temperance movement (vigorously supported by psychiatrists such
as Emil Kraepelin, Eugen Bleuler, and Adolf Meyer), a social force
that was effective in leading several countries to restrict the
distribution of alcohol. A sharp decrease in alcohol abuse and its
consequences occurred in the Prohibition era in the United States
and after the introduction of bar- and liquor-licensing laws in Great
Britain during World War 1. 18

But society, besides providing an opportunity for the expression of

behavior, can incite it. Alcohol consumption, smoking, and early
sexual behavior can be encouraged by such sociocultural
phenomena as peer pressure, advertising, and the provision of role
models. Advertising is often underestimated in its power and even
unrecognized, such as when a hidden prompt of behaviordress,
sexual behavior, smoking-is embedded in a cinematic story. Is there
any parent who does not sometimes despair of his or her ability to
influence a child's behavior in the face of these forces?

Finally, more general social conditions can affect the expression of

several behaviors at once. Emile Durkheim, the great sociologist,
examined the social factors provoking suicide. He found that this
behavior was more common among people poorly integrated into
their social milieu, such as immigrants, and that such burdensome
social factors as poverty and isolation seemed to encourage both
suicide and delinquency.19 We devote a later chapter to suicide.

The problem with resting the etiology of behavioral disorders on

cultural and social forces alone is that these forces act on many
members of the community, only a minority of whom demonstrate the
behavior in question. Unless some appreciation of personal
vulnerability is also provided, the development of a behavioral
disorder in any given individual cannot be understood. Sheldon and
Eleanor Glueck demonstrated that in the delinquent population clear
personality characteristics can be used to predict to some extent
which individuals in particular social environments will become
delinquent.20 From early childhood, delinquent individuals can be
seen to be assertive, selfcentered, adventure-seeking, easily bored,
and explosive individuals who tend to be limit testing and suspicious
of authority. These characteristics make them more prone to take up
activities that challenge society's rules and standards. The Gluecks
pointed out a sharp distinction between those individuals and others
in the same family and culture who do not become delinquent despite
experiencing the same social disruptions. The outstanding
characteristics of nondelinquent individuals are a sense of concern
about others' appraisal of their conduct, a capacity for guilt, and an
ability to worry over consequences that is exhibited in all aspects of
their lives, not just in relation to law.

It is impossible to consider social and cultural forces as sufficient

causes for a particular behavior in a given individual. It is likely,
however, that they are among the more important determinants of the
number of people expressing and troubled by a particular behavior,
because with increasing social pressure less and less vulnerability is
required to provoke the behavior and learn how to practice it.

Development and Its Role in Generating Behaviors

If genetic and social elements combine to provoke and shape

behaviors, they customarily do so in a developing (i.e., maturing)
person. The concept of development relates genetic to psychological
and social causes and provides a means of partitioning these causes
over a lifetime. Development influences behavior sequentially, so a
given experience or event at one stage in life will affect-even shape-
the expression of later experience and behavior.

Animals, but not humans, have quite strict periods in which

behaviorally important events must occur for later species-specific
behaviors to appear normally. The critical period and imprinting
displayed in such animals as dogs and birds are examples of these
phenomena. In human beings, the evidence is less compelling that
such sharp critical periods exist. But a sensitivity to the shaping of
behavior by experiences is likely. Certainly this is true of the capacity
to learn a language, which tends to wane in facility after about age 8.
In the realm of motivated behaviors, John Money and his associates
believed that gender identity emerges early in infancy in response to
the actions of others and that it affects later sexual behavior.21
Emphasizing the role of learning in shaping a motivated behavior,
these investigators may not have given sufficient attention to the role
of prenatal genetic and hormonal influences in organizing brain
development and influencing the embodied elements of sexual drive
on which later sexual attitudes, later interests, and a later sense of
gender ultimately depend. John Bowlby employed an ethological
concept of attachment to explain the natural development of parental
bonds, which, if disrupted early in life, may be hard to replace later.22
Yet none of these concepts has the iron determinism of critical
periods in animals, and they have all been challenged by other
observations.

It is well established that biological events have an important

influence on human behavior when they occur at particular stages in
development. For example, though the formation of male gender
identity and behavior can be influenced by sociocultural factors,
prenatal exposure of the brain to androgens seems not only crucial in
the process but outweighs the sociocultural factors. This fact became
clear when infants born with ambiguous genitalia were all surgically
corrected with female structures and raised as girls. With maturation,
some individuals with a male genetic constitution (Y chromosome)
have rebelled against their female identification and sought help to be
restored as males.2;

In normal males the Y chromosome initiates the production of

androgens, imposing on the organism the program for male pituitary
secretions and eventually for masculine sexual activity. Females,
lacking the Y chromosome, follow a different course of development,
but that course can be changed if females are exposed prenatally to
androgens. Sometimes this occurs when their mothers are given
hormones such as progestin during pregnancy, but it can also happen
in adrenogenital syndrome, in which the fetal adrenal gland produces
an androgenic steroid rather than cortisol.

John Money and Anke Ehrhardt studied patients whose

adrenogenital syndrome was diagnosed and treated early, so they
looked like and were appropriately raised as girls.24 In spite of the
early treatment, however, many of them later chose play objects more
traditionally associated with boys (guns, automobiles) than with girls
(dolls) and preferred in their play to join boys in vigorous sports,
rather than to play with female friends, as control girls did.

Money and Ehrhardt also studied males whose cells were

insensitive to the androgens secreted by their testes.25 These
genetic males with the androgen insensitivity syndrome responded to
the relatively small amounts of circulating estrogen normally
produced in males, and therefore they developed and seemed to be,
behaviorally as well as in their outward appearance, women.

The effects of hormonal changes on behavior are not limited to the

fetal period. In normal puberty, behavior is altered, though in the
direction prepared by previous development. In the patients studied
by Julianne ImperatoMcGinley and her associates, puberty produced
or permitted a more fundamental change.26 These patients were
genetic males with a fetal deficiency of dihydrotestosterone, so they
had ambiguous external genitalia and were brought up as girls, but
did not have surgical "correction." With the increased secretion of
male hormones at puberty, obvious features of male genital and
physical anatomy emerged, and these adolescents were able to shift
to a masculine role, a behavioral change that prevailed over their
gender of rearing. Thus, sexual identity and behavior rest not simply
on the individual's chromosomal constitution but also on his or her
particular developmental passage through a sequence that includes
intrauterine hormonal exposure, gender attribution in early childhood,
learning, and pubertal hormonal surges.
 Although biological factors in development are of great interest,
they seem to account for only a small number of patients seen with
problematic behaviors. Patients who have not met developmental
timetables that are based on sociocultural expectations can also have
difficulties as documented by such behavioral problems as school
refusal. In fact, an assessment of the interactions among genetic,
developmental, and sociocultural factors is required to explain and
distinguish among behaviors that have superficial resemblances. For
example, children can be brought to psychiatric attention because
they do not willingly attend school, and though their behavior is the
same, the underlying reasons are different.

Some of these children are truants: they do not attend school, but
neither do they stay home. They seek others of like mind and spend
their time in play or sometimes in crime. Other children refuse school
by staying home. This group can be further differentiated into children
who do so because they fear some aspect of the school situation
(school phobia) and those who stay home because they fear leaving
their mothers (separation anxiety). In this last group we can find an
immature child, whose dependent and often conflicted relationship
with his or her mother is threatened by the necessity of meeting a
developmental schedule imposed by society. Though members of all
these groups refuse to attend school, the underlying causes of and
treatments for their behaviors are different, distinctions best reflected
in the differing designations of each of the behaviors in the
category.27

Meaningful Answers to the Problem of Explanation

We have reviewed the ways in which a behavior depends on a

neural apparatus that can be damaged by disease but is customarily
built from the genetic constitution, how that behavior is responsive to
hormonal and other biological influences, and how it is modified by
circumstances and sociocultural forces. In all these explanations,
though, the sense of meaning and purpose that is behavior's most
obvious characteristic-and that may be partially explained by offering
a story of a self or agent in action-has been ignored. The sense of an
agent intending to reach some desired goal remains a vital part of the
phenomena of behavior. It is at least a challenge and often a rebuke
to the adequacy of any explanation based on mechanisms and
etiologies. How can we incorporate the experience of subjective
insistence into our understanding of patients and their behavioral
problems?

Freudian Meaningful Understandings

For the Freudians and all derivative psychodynamic theorists,

drives are the explanation. Freud described and then incorporated
drives into his theories of human behavior. The insistent quality of
drive explained the resistance of mental disorders to change despite
admonitions, advice, and experience. The pathological rigidity,
implacability, and repetitiveness of the life stories of his patients could
not have come from choice, reason, or will, Freud argued, but are just
what could arise from motivated drives, drives that are
unacknowledged and disguised but nonetheless relentless and
recurrent.

Sandor Lorand, in his explanation of the functions served and

meanings revealed in the food refusal found in anorexia nervosa,
presented a typical drive formulation. The symptoms express the
following meanings:

1) Loss of appetite: Food implies oral and sexual gratification

identified with early phantasies of impregnation. Thus are revived
strong feelings of guilt necessitating denial by rejection of food.
Food usually is excessively charged with importance in an
environment where a patient anorexia nervosa. It is the vehicle of
love and also of punishment....
 2) The denial of adulthood, in general and especially in sexuality:
Adult problems cannot be handled because of constant
preoccupation with the problems of food around which the earliest
difficulties of the child centered. This preoccupation also excludes
adult adjustment to sexual needs. Then too, genitality has to be
denied because of desires and guilt centering around the early
Oedipus relationship.

3) Wasting away: It expresses strong suicidal desires....

4) Menstrual disturbances: Cessation of menstruation is an attempt

to eliminate the problem of being preoccupied with genital function
which in adulthood implies thoughts of sexual relationship and
pregnancy. At times amenorrhea means permanent impregnation,
and then again complete rejection of femininity. These are defenses
against Oedipal guilt.

5) Guilt and atonement: Since the symptoms are used to obtain

revenge and attention, they become charged with guilt, at the same
time the suffering acts as expiatory self-punishment.28

This is a remarkable stance. The conception of a hidden motivation

behind the multiplicity of conscious acts is armed against objections.
It gives a comprehensive meaning both to the sense of purpose
experienced by the patient and to the pathological rigidity of the
symptoms. It sustains the confidence of the therapist in his or her
practice, whether the therapist relieves the symptoms or not. Jung,
Adler, and all the other schismatics broke away from Freud over what
they imagined to constitute the underlying, unconscious motivations,
but the centrality of motivation itself remained in their reasoning.
Methodologically, they were the same; only the emphasis changed.

Clinical success may come from the encouragement these beliefs

give to sustaining and informing the psychotherapeutic relationship.
When applied to individuals, they cultivate an attitude that can be
helpful and insightful. But the theorists overplay their hands when
they generalize from a few patients to humankind. Then they make
every action and capacity of human beings an expression of the
identical motivation, a flowering of guises that attracts some by its
apparent explanatory power but which strains the credulity of others
who see more choice and complexity in human affairs.

Behaviorist Explanations of Behavioral Disorders

Behaviorists approach behaviors differently from Freudians. Though

they also acknowledge the phenomena of the motivated drives and
may even credit Freud with emphasizing them, they propose that the
subjective feature as well as the observable behavior must be
explained. They reject as the answer to the question "Why does this
man drink water?" the response "because he is thirsty," because it
seems to make the explanation rest on an element that they consider
part of the behavior itself-the thirst that provokes an operant
resolution.

Like other behaviorists, B. F. Skinner believed that all behaviors are

ultimately the lawful and direct outcome of past experiences, but he
saw this past experience in a more dynamic way than did his
predecessors.29 Behavioral expressions do not derive solely from the
antecedent stimuli to a responsethe original Pavlovian or classical-
conditioning paradigm. Rather, interaction occurs between the
organism and the environment such that actions (operants) of the
organism that are at first no more than random, spontaneous
elements from the organism's activity repertoire (for example,
pecking, pushing, scratching, and biting) act on the environment to
provoke a change in it. This change can in turn affect the organism: it
may provide food, make sound, or cause pain. The environmental
event thus acts as a reinforcement, increasing or decreasing the
frequency of the initiating activities, which now become "behavioral
operants." Thus, the environmental consequences "shape" the
originally random activity into sustained, goal-directed, and effective
sequences of actions. The inner, mental states of purposefulness,
desire, fright, and so on, are parts of these sequences that can be felt
"within the skin" but which, like the overt behavior, depend for their
meaning and apparent goal-directedness on the shaping influence of
experience.

Skinner acknowledged that inner states of hunger, thirst, affection,

and fear occur in the organism and have an insistent power. Some of
the motivated feelings, for example, emerge with deprivation,
because they are tied to innate physiological mechanisms. But, such
feelings, Skinnerians believe, become identified and incorporated into
the goal-directed aspects of behavior in the immature organism
because of their past successful relief by apt, reinforced actions. All
aspects of behavior-its unique pervasive teleologic quality, its goal
direction, its associations with inner states of mind, its capacity for
sequential complexity-can be explained from the Skinnerian position,
the appreciation of the interactions at the interface between the
organism and the environment, which is encapsulated in the phrase
"past experience."

This is more than just a plausible proposal. The shaping of behavior

can be demonstrated. Behaviorism forms the conceptual and
technological basis of an extensive enterprise in research and has
provided fresh insight into some psychiatric disorders. As an
example, it proposes that some phobic conditions develop as
aberrations of avoidance behavior, which normally serves to remove
the individual from danger. Previously, such conditions had often
proven refractory to both the insights of psychotherapy and the
biological changes of drug treatments. The view that phobias were
abnormally sustained, conditioned emotional responses that could be
reshaped by "extinction" brought a new method of treatment with
demonstrable success. This treatment of phobia was also a vigorous
challenge to the view that every symptom is a disguised
manifestation of latent, unconscious motives and drives. The relief of
phobic symptoms was not followed by the appearance of others, as
that view would logically propose.30

Yet the difficulties with behaviorism are also evident. Behaviorism

promises more than it has delivered, as do most encompassing
positions. In particular, the neglect of the issue of drive made
behaviorism blind to the "overdrive" conditions, even while
behaviorists became ever more expert in the schedules of
reinforcement that generate learning. Not all behavioral disorders
derive from drive, just as not all behavioral disorders derive from
misguided learning. Most are a mixture of troubles from both sources.

Behaviorism does without the notion of a self who chooses and is

thus accountable. It thus cannot offer guidance to people struggling to
find ways of life that make sense of their moral feelings and their
purposes. Moreover, even at the level of learning, species
generalizations from rats and pigeons to humans and the
environment generalizations from Skinner boxes to the world cannot
be justified. For example, the attempt to explain language in
behavioral terms that would ignore the intentionality and creativeness
of human thinking and communication has been contradicted-indeed,
discredited-in Noam Chomsky's classical review of Skinner's views
on language development.31

Summary

In this chapter we have briefly reviewed the domains of explanation

tied to the perspective of behavior. We have described the few
conditions in which a behavior disorder is a symptom of a disease,
the behavior emerging as one of the several symptomatic features of
a clinical syndrome based on a disruption of the bodily controls on a
basic drive. Hypothalamic obesity and narcolepsy are two examples.

We have documented how in most behavioral disorders the causal

factors combine polygenic inheritance, developmental deviance, and
pathogenic social environments. We discussed how these factors
influence the incidence and prevalence of behavioral disorders and
noted how these disorders differed fundamentally from diseases. We
commented briefly on the use of the term disease as a description of
alcoholism and why we prefer to think of this condition more in
relation to the behavioral dependency and abuse syndromes.

Finally, we briefly reviewed the "why" explanations offered by

psychiatrists for some behavior disorders; that is, what concepts or
theories are considered informative when the question "Why is this
patient behaving abnormally?" is asked. Both Freudian and
Skinnerian answers were briefly considered.

Eventually, efforts at the prevention of behavioral disorders call

attention to matters of choice and preference. These efforts, often led
by psychiatrists, lead to conflicts in society. For example, psychiatrists
who challenge provocative factors such as the availability of alcohol,
the advertisements for smoking, or the glamorization of promiscuous
sexuality will encounter opposition from many vested interests in the
commercial world. Conflicts of will between psychiatrists and others
indeed are regular parts of the behavior perspective. The next
chapter reviews the treatment commonalities of various disorders as
they exemplify the similarities of an approach derived from reasoning
about them as behaviors.
The treatment of behavior differs from that of disease in that it tries to
stop what people are "doing," not cure what they "have." And yet,
what they are "doing" is no passing fancy but a "way of life" so stark
that it brands them as alcoholics, addicts, anorexics, or paraphilics.
Such people are patients because they persist in enslaving activities
even as psychiatrists, among others, strive to get them to spring free.
This conflict of aims between patients and psychiatrists is the crux of
the clinical problem in the behavior perspective. Treatment calls for a
coherent view of behavioral disorders, a sound idea about what can
and cannot be expected from treatment, and great powers of
forbearance. The crucial point is that with behavior the goal of
treatment is not cure of a disease but conversion from one way of life
to another. This explains much of the difficulty and as well much of
the rewards of success.

In chapter 15 we described psychological and social influences on

the choices and learning paths that forge behavior disorders. Most
patients offer meaningful explanations for their alcoholism, their
anorexia, or their drug taking: "I'm worried about money and the
cocaine temporarily relieves my mind," "I feel misunderstood at home
and drinking vodka with pals cheers me up," or "My parents are
weight conscious and I'm worried about meeting their standards."
Why not begin by addressing these "causes," perhaps adjusting
these feelings, and expect the behavior to evaporate just as fever,
cough, and chest pain disappear with antibiotic treatment of
pneumonia? Because this approach, modeled on diseases, does not
work. Behaviors are not diseases. When a psychiatrist slights the
self-sustaining power of a behavior while struggling to correct some
putative underlying cause or reason for it, alcoholics continue to
drink, anorexics to starve, and exhibitionists to cruise. Only effort
directed at the behavior itself will succeed. Exactly how this can be
accomplished is the subject of this chapter.

The model for behavior-attentive treatments has several sources

but the most prominent was the emergence in the 1930s of Alcoholics
Anonymous (AA). This patient-led group challenged the
psychomedical treatments then in vogue by claiming that alcoholism
is both the problem and the explanation: alcoholics drink to excess
because they are alcoholic. I Furthermore, once patients admit to
being alcoholic they can recover-particularly if joined with other
alcoholics prepared to help them refrain from drinking for "just one
day." This approach worked-not every time, but with more patients
than any other could claim.

Psychiatrists risk seeming to argue with success when they ask for
the source of AA's achievement. The question is crucial if such
success is to be applied generally in other behavioral disorders. As
we see it, to diagnose a patient as alcoholic is to say that a drive,
provoking a craving for alcohol, possesses the patient and has led
him or her to learn ways to satisfy it. Treatment aimed at those
physiologically induced hungers and conditioned habits that together
encourage surrender to the behavior-rather than at dubious
psychological reasons proffered to "explain" it-makes sense. To
attack these forces, their expression in the patient's resistance, and
their power to generate relapse is to confront the behavior directly
and move patients away from choices driven by hunger and habit and
toward recovery.2

The general principles drawn from the behavior-attentive treatments

of AA can thus be understood and applied to other disorders. In
particular, with every behavioral disorder, the triad of choice, drive,
and habit becomes the target of therapy.

Treatments for Choice

 We consider choice first because every treatment for a behavior
disorder will depend on it. Although patients are "driven" toward
drinking or drug-taking behavior, the drive needs compliance-a
choice-for fulfillment. Even when the drive is so subjectively
compelling that resistance to it is agony, a small element of will
remains in surrender. As described in chapter 14 this surrendering act
differentiates behavior from stereotyped reflexes.

The presence of choice in behavior makes possible therapeutic

intervention "betwixt the cup and the lip." Indeed, the sense of choice
encourages the AA adage of holding off a drink "just for today." Even
treatments attacking the physiology of drive and the conditioned
habits demand that the patient choose them as alternative responses
to intense hungers and ingrained habits.

Certainly the choice for treatment is not easy for individuals with
these disorders. The family or friends, often more aware of the
damage the behavior has brought even as the patient continues to
surrender to it, are usually the ones who prompt an intervention. A
mnemonic adage holds that alcoholics do not seek but are dragged
into treatment by one of the four Ls: Loved ones (for friends and
family), Liver (for any physical symptom of alcohol abuse), Livelihood
(for the financial threat that alcoholism brings), or Law (for such
issues as arrest for driving while intoxicated).

Similar agents pull patients with anorexia nervosa into treatment.

Family members usually insist that the patient seek medical help
having witnessed her growing weakness and emaciation.
Occasionally physical complications of starvation-fainting, debility,
and confusion-overcome the patient and bring her to the clinic.

Only the rare patient awakens spontaneously to sense that he or

she is in thrall to a behavior. External insistence of some kind-
confronting patients with how they are out of control-is usually
required to prompt the choice for treatment.
The Physician's Role in Prompting Choice for Recovery

Physicians can exert considerable influence over behavior. For

example, many have helped their patients stop smoking by pointing
out its link to cancer and lung disease. In the same way physicians
can draw for patients the connection between physical complications
and the abuse of alcohol, and so foster treatment. Physicians are
also exposed to many patients who complain about a complication of
a behavior but ignore its source. One of the cautionary tales in our
department features the intravenous drug addict who, without
accessible veins, was injecting cocaine into his carotid artery. He
came to the clinic and asked, "Doctor, every time I inject cocaine into
this pulsing vein, I get a headache. Do you have anything for
headache?"

Here, in the extreme, is a patient whose treatment objectives

diverge so far from those of his physician as to be farcical. However,
divergence of aims in behavior is ever an issue. The patient wants
relief from the burdens despite the behavior. The physician knows
that the behavior and its burdens are so entwined that only ceasing
the behavior will cure the "headaches." The future depends on
resolving that divergence in intentions.

Differentiating Patients by Readiness to Change

Experienced psychiatrists all realize that people differ in their stance

toward behavioral change, a difference reflected in how "clients" differ
from "patients." Clients negotiate with their physicians to minimize the
burdensome consequences and yet retain some of their behavior
("just a couple of drinks won't hurt"). Patients agree with the clinician
and, acknowledging their behavior to be out of control, try to follow
prescriptions.

A more operational division, which classifies candidates for

treatment according to their readiness for change, was advanced by
James Prochaska and Carlo DiClemente. They differentiated patients
into (1) those in a precontemplative stage, where no thoughts of
changing behavior were present; (2) those in a contemplative stage,
where they were considering change but were not ready to accept the
implications for the way of life that such a change would demand; and
(3) those in an action stage, who were ready to act against the
behavior and change and now sought help in overcoming the
psychological and social obstacles such a change would entail.3
Physicians who recognize these differences among people can, as a
first step in treatment, bring them to move toward the patient status
and the action stage.

But, resistance to both diagnosis and prescription often hinders a

patient from choosing help. This resistance can be so extreme that
the patient rejects treatment, usually claiming that it is unnecessary or
impossible. Overcoming such resistance-"All women want to be thin.
I'm like everyone else and not anorexic"-requires persistence. Getting
relatives to understand the goal of treatment and how they can
facilitate the patient's persistence in treatment is often necessary. All
these efforts, though, confront the basic problem in behavioral
disorders: the drive behind the patient's choice. Again, these
behaviors are not simple choices from among several pleasant
alternatives. Either drive-sensed as craving-or habit-sensed as
readiness to respond-seizes the patient's attention, promotes
disorder, and hinders recovery.

Groups Foster the Choice for Change

Physicians need to sustain the patient's commitment to change in

the face of such drives and habits. AA demonstrated the value of
group therapy for resisting the surrender to drink. Group therapy,
bringing together people at different stages in recovery and with
different attitudes toward change, provides crucial help, first by
holding the patient back from taking that drink today, and later by
calling the patient's attention to his many rationalizations for
succumbing to his impulses.

Group members can identify situations prompting relapse and

methods for avoiding them by discussing their own disastrous
experiences with alcohol. They offer support when an individual feels
the resurgence of craving and is tempted to relapse. The group can
show how the individual is repeating the failures of many others. The
sharing of experience in a group provides fellow feelings and
mitigates the sense of stigma that patients under treatment for
behavior disorders will almost always feel.

All these psychological methods help the patient accept treatment

and resist craving. But direct attacks on drive and habit are available
for some behaviors.

Treatments of the Physiology of Drive

Many physicians attempting to treat behavioral disorders have

made efforts to relieve craving. They have had success with two
particular disordersopiate addiction and sexual paraphilia-in finding a
means for satisfying or reducing a drive in a way to promote
abstinence. Methadone treatment for opiate addiction and
antiandrogen treatment for sexual paraphilias are two celebrated
success stories. Both describe pharmacological measures aimed at
the drive itself.

The Methadone Treatment Program

With the epidemic of heroin addiction in the 1950s, the concept of

medicalization with morphine maintenance emerged when
counseling, social services, and group therapy did not succeed. In
several European countries registered addicts were supplied a
controlled amount of morphine or heroin each day, and some success
in reducing social problems (for example, criminal activity) was
reported. There was less success in the United States, for reasons
unknown. Here addicts consumed amounts of morphine that
rendered them immobile, and medically supplied heroin was traded in
the criminal markets.

Vincent Dole and Marie Nyswander of Rockefeller University in New

York City began to treat heroin addicts with the synthetic opiate
methadone in the 1960s.4 This compound, with a longer half-life than
morphine and heroin, did not provoke addicts to consume so much as
to sink into apathy. The doctors also demonstrated that a single daily
oral dose of methadone, capable of reducing opiate craving, liberated
addicts from constant drug-seeking behavior. Many returned to work,
family life, and school and benefited from counseling, group therapy,
and social services. Arrests fell, and productive lives were restored.
These results led to a qualified acceptance of methadone treatment
under controlled supervision throughout the United States.

More details about patient selection, methadone dosage, and the

coordination of adjunctive psychological and social services go
beyond our purposes. A methodone program is, however, the prime
example of a pharmacological treatment directed against a self-
induced drug hunger. It led to sustained treatment and rehabilitative
success as well to the waning of the heroin epidemic in the 1970s.
Now in the 1990s the combination of buprenorphine, an opiate
agonist-antagonist, with naltrexone, an opiate antagonist-in a single
pillshows even greater promise for heroin addiction and less abuse
liability than methadone.5

Success with methadone not only encouraged other

pharmacological approaches to heroin addiction but pharmacological
treatment in other addictions as well. For example, reducing the
hunger for cigarettes and thus promoting smoking cessation were
achieved when pharmacologists developed a chewing gum and
transdermal patches to deliver nicotine.
Antiandrogen Treatment of Paraphilias

Another psychopharmacological approach to drive reduction

derived from the proposal that elevated sexual drive supported many
paraphilias such as pedophilia. John Money and Fred Berlin of Johns
Hopkins suggested that some patients might respond to androgen
reduction or blockade with a reduction in sexual drive.6 They first
offered paraphiliac patients treatment with medroxyprogesterone
acetate (Depo-Provera, a progestational hormone) and then offered
leuprolide acetate (Lupron Depot, a blocker of pituitary stimulation of
androgens). Berlin has followed and demonstrated the effectiveness
of treatment in more than 600 patients,7 and a recent comparison
study confirmed the effectiveness of these treatments in controlling
paraphiliac behavior.8

Berlin held that pharmacological treatment was no panacea. Its

prescription must be preceded by a careful patient assessment and
his willingness to cooperate in a treatment program. Only
overmastered paraphiliacs, not criminal offenders (distinctions made
in relationship to the behavioral contexts and responses), were to be
his subjects. He also reiterated that pharmacological treatment must
be supplemented with psychological treatment and supervision.
Group therapy proved helpful for these sexual behavioral disorders,
especially when groups were led by individuals experienced in
drawing out from patients their sexual preoccupations and in devising
combinations of pharmacological and psychological therapies to
address them.

Other Treatments of Disordered Drive

Other indirect pharmacological approaches have found utility in

behavior programs. A good example is disulfiram (Antabuse), which
encourages abstinence in alcoholics essentially by setting up a
situation in which the indulgence of the behavior will be punished.
This treatment, blocking the natural metabolism of alcohol and
provoking sickening amounts of acetaldehyde if alcohol is consumed,
depends on the patient choosing to take disulfiram each day and
therefore on some commitment to abstinence. Disulfiram has been
shown to reduce the number of days in a year a patient drinks, and
some alcoholics may gain more benefit from it than others. But it has
proven difficult to demonstrate a long-term value of disulfiram
independent of other evidence of commitment to recovery such as
attending group meetings.`'

Recently, the opiate antagonist naltrexone has helped recovering

alcoholics. In a study employing double-blind placebo controls, this
medication, added after alcoholic detoxification, significantly reduced
the number of patients relapsing back into alcoholism. I(' The
presumptive explanation for this success is that endogenous opiates
must reinforce alcohol consumption. Naltrexone, by blocking the
reception of alcohol-provoked opiate surges, would deprive the
patient of a physiological "reward" for drinking. Because most
alcoholics will eventually try a drink and these trials represents a
common avenue of relapse, naltrexone by rendering these responses
"unrewarding" can encourage and may indeed sustain abstinence.
Naltrexone thus may work against the behavior by evoking extinction
of the drinking response through the removal of its hedonistic reward.

Another treatment features an intriguing approach to overeating and

obesity. Gastrointestinal surgery intends to enhance the satiation
derived from meal taking, thus reducing hunger for food. These
treatments were prompted after observing sustained weight loss in
patients following partial gastrectomy for peptic ulcers. Different
intestinal "bypass" methods have been tried with only temporary
success and many medical complications. The safest and more
enduring treatment is "gastric stapling," in which the gastric volume is
reversibly reduced. Because gastric distention is one of the signals of
satiety, this method, by which the gastric volume is reduced to but a
few cubic centimeters, provokes satiety signals with small meals and
thereby induces significant weight loss. Such a radical invasive
treatment can be recommended only for individuals with life-
threatening "morbid" Future trials with "keyhole" surgery may hold a
promise for less severely obese patients. One caveat is that already
several patients with the eating disorder bulimia nervosa, have
persuaded unsuspecting surgeons to carry out this gastric bypass in
them so as to achieve their overvalued ideal of thinness. A careful
history, with external informants, must be taken in any patient seeking
bypass surgery.

Problems Associated with Treatments of Drive

The point raised at the end of the last section leads directly into a
consideration of other problems tied to pharmacological and surgical
treatments of behavior disorders. Some fail because, advertised as a
"magic bullet," they are not combined with adjunctive psychological
treatment. In others, a placebo response may be mistaken for a more
permanent treatment.

Even effective pharmacological treatments present problems. The

efforts in Switzerland to provide addicts with heroin openly in certain
districts of the city ultimately ended in social disorder. Addicts were
drawn from elsewhere to the freer environment of Switzerland, the
local "needle parks" became filled with used needles and other
dangerous refuse, and new addicts were encouraged by tolerance.
The Swiss government now offers heroin treatment under closer
supervision and only to addicts who can demonstrate that they have
failed in other treatment programs such as methadone. Even this
approach has a problematic aspect. It has transformed a medical
service from one making every effort to encourage recovery and
health into a government agency dismissing a troublesome group of
people from social concern by, in essence, leaving them to their fate.

Some treatments directed toward drive reduction have proved

dangerous. Recently it was demonstrated that the combination of
phentermine and fenfluramine (phen-fen) for obesity produced fatal
pulmonary hypertension and life-threatening cardiac valve
malformations in some patients. 12-14 Pharmacological measures for
behavioral disorders customarily require prolonged treatment
exposures and thus must be rigorously assessed for damaging side
effects before being released and for some years afterward.

Recapitulation

As the drive for these abnormal behaviors rests on physiology, so

treatments aimed at physiology are logical and occasionally helpful.
With each treatment, however, the patients must be carefully chosen
and must themselves be ready to persist in the program. This
persistence is bolstered by adding other treatments, such as group
psychotherapy to sustain the resolve for recovery and measures to
encourage the extinction of the old habits. We now turn to this aspect
of treatment.

Treatments of the Learned Elements in a Behavior

Although a physiological embodied mechanism may be necessary

for craving, the conditioned learning of a response pattern may
enhance it. Failure to consider aspects of learned habits is a common
reason for treatment failure. Patients describe pleasures tied to the
accoutrements of their behaviors, noting how they miss the activities,
companions, and settings that sustained them and how revisiting
these experiences and settings leads to relapse. The issues of
learning and habit must be addressed in order to support the choice
for treatment.

Classical- and Operant-Conditioning Features of Habit

A common experience of patients trying to stop cigarette smoking

underscores this point. These patients discover that the first few
weeks of abstinence are most difficult because of nicotine withdrawal
symptoms-notably headache, tension, distractibility, and craving.
These physical symptoms abate after the first few weeks, as does
much of the craving. There is, however, a crucial exception. Patients
will notice, months after abandoning cigarettes, that a strong urge to
smoke reappears in every setting where smoking was enjoyed in the
past. These settings at first are those close to home: at breakfast
time, in the automobile traveling to work, after dinner at night, and so
forth. Special effort to resist smoking is required in each of these
settings to extinguish the habit.

After patients experience the extinction of craving in local sites, then

less commonly visited sites turn out to have a similar relapse-
promoting power. For example, a visit to a theater, favorite restaurant,
or club can trigger the hunger for a cigarette even years after
smoking has ceased. The power of the urge can come as a great
surprise to the patient. Triggering events such as these make clear
that extinction of a learned behavior demands facing, resisting, and
ultimately extinguishing all the stimuli previously tied to it.

A similar mystifying return of drug hunger and relapse was

described in heroin addicts by Abraham Wickler.15 His patients had
stayed drug free for several years in the federal facility in Lexington,
Kentucky, and claimed they had lost all interest in heroin. On
reentering their old neighborhoods in New York City, they
experienced the return of drug craving with overpowering force.
Wickler thought he may have discovered a new physiology in opiate
addiction in which long-dormant physical dependency and withdrawal
symptoms resided. These addicts, however, probably were
experiencing a conditioned craving for heroin prompted by signals of
its availability.

These returns of craving, for cigarettes or for heroin, can be viewed

from both Pavlovian (classical) conditioning and Skinnerian (operant)
conditioning theories. The settings where cigarettes or heroin were
previously used may elicit the sense of drug hunger just as the bell of
Pavlov produced saliva in his conditioned dogs. As well, the craving
has in the past been satisfied by the operants of the cigarette or the
needles for drug injecting and will do so again in the same way as the
hungry animal in a Skinner box learns that pressing a lever brings
food and relief from starvation.

Treatment for the Habit Features of Behavior

These observations indicate great relapse vulnerability in patients

long after a physiological drive has abated. Conditioned learning tied
to a behavior, just like the physiologically based drive, acts to push
the patients toward surrender. Indeed, conditioning and physiology
act synergistically to evoke craving and promote behavior. Hence,
treatments for the extinction of the habit play as important a role as
does the treatment for drive and must where possible be combined
with it.

The Behavioral Pharmacology Research Unit of the Department of

Psychiatry, led at Johns Hopkins by George Bigelow, Maxine Stitzer,
and Roland Griffiths, has demonstrated the various ways that
behavioral and pharmacological treatments can be combined to
promote recovery from addictions to alcohol, nicotine, and opiates.
Their treatment proposals emerged from doubleblind, multiple-
placebo trials in which advantageous combinations were

For example, this group showed how polydrug abuse can be

treated by combining methadone treatment with behavioral rewards
for being free of the other drugs. The relief that the patient receives
from the opiate hunger with methadone can be given or withheld
depending on compliance over other drugtaking behaviors such as
cocaine or barbiturates. In another study these investigators
demonstrated that voucher rewards reinforced compliance in
treatment for cocaine addiction. The patients were rewarded with
vouchers that could be translated into money for each day they could
provide a urine sample free of cocaine and any other drug of
 Compulsory behavioral treatment should not be scorned. Colin
Brewer and John Smith showed that the compulsory features of
parole supervision, with its expectations of continuing abstinence and
evidence of employment in order for criminal addicts to stay out of
prison, was more successful in sustaining recovery than were either
repeated hospitalizations or incarcerations. Combina tions of
interventions-parole supervision, methadone maintenance, and AA
attendance-that change a patient's entire response relationship to the
stimuli in his or her environment are more likely to produce
abstinence.'K

Monitoring Behavioral Compliance

A critical observation that emerged from these and other studies in

behavioral deconditioning is the importance of monitoring the
patient's behavior whenever possible. This information can be
employed to reinforce compliance by means of apt rewards or
punishments. The monitoring measures in addictive disorders include
urine testing or Breathalyzer tests for evidence of drug or alcohol
consumption. The patients' knowledge that they are being monitored
and that the results show everyone whether they have succeeded in
overcoming temptation in the interval between visits turn out to help
patients stay abstinent.

The important effects of monitoring behavior have been applied in

treatments of conditions less destructive than alcoholism and drug
addiction. The treatment of obesity, particularly as organized by the
Weight Watchers group, has as a central part of the treatment the
weekly weigh-in. The simple recording of the weight gain or loss by
the program director on a written record in the patient's possession
acts as a stimulus in maintaining the dietary program between visits.
To act in such a way as to record a satisfactory report turns out to be
its own reward.
 Monitoring behavior in treatment programs is more than a policing
effort, although in some settings it is that as well. Monitoring provides
both actual and anticipatory rewards and punishments. The very
recording of evidence of abstinence is a stimulus for compliance and
its power can be amplified by a whole variety of contingent incentives
up to and including greater freedom between treatment sessions as a
reward or more restrictive environments and closer supervision as
punishment.

Interactions between the Behavior Perspective and Other

Perspectives of Psychiatry

For all that the fundamental therapeutic issues can be tied to the
behavioral triad, the other perspectives of psychiatry can, in individual
cases, offer important therapeutic guidance. Some of these are rare
and extraordinary complicating issues. Others are common and
significant in any program of behavioral treatment.

Abnormal Behaviors Associated with Brain Pathology

A rare but recognized provocative cause of a behavior disorder is

brain pathology-particularly a pathological process affecting the limbic
regions, where neural controls on emotions and drives reside, or
affecting the frontal lobes responsible for inhibiting impulsive actions.
We mentioned that a tumor affecting the medial hypothalamus can
produce intense hunger and gross obesity in the patient. This kind of
"symptomatic" behavior responds to treatment of the provocative
lesion as does any symptom to the cure of its disease.

In like fashion, the several reports of distorted and excessive sexual

appetites in patients early in Alzheimer's disease or after cerebral
infarctions can represent distressing symptoms. These "symptomatic"
behavioral disorders do enhance confidence that there is a
physiology behind drive and its expression. But the rare occasions in
which a disease process can disrupt all control over behavior are
distressing and demand a variety of pharmacological trials
(gonadotrophin suppression, neuroleptics, and so on) and close
supervision.

Interactions between Behavioral and Mood Disorders

Many patients begin to abuse alcohol in the midst of either a

depressive or manic affective disorder. A depressive syndrome is
particularly frequent in female alcoholics. Such terms as comorbidity
and dual diagnosis have been employed in these situations, though
not always with clarity. The crucial matter is to differentiate a
"symptomatic" depressive state (DSM-IV substanceinduced mood
disorder) provoked by alcohol from a major depression inducing
alcohol consumption for relief of painful agitation and anxiety.

Just how drinking and a depressive mood relate to each other

should be carefully assessed in every case where they are combined.
This assessment will have crucial treatment implications. Those
patients in whom the alcoholism follows the course of depression
should receive ongoing treatment for major depression, not only
during their alcohol treatment but long after the control of alcohol
consumption has been achieved. The proposal to add antidepressant
medication to the treatment of an alcoholic has occasionally run afoul
of those AA programs that assume that all symptoms in an alcoholic
are either consequences of drinking or rationalizations for it. Only
recently, with better awareness of depression as a distinct disease
entity, have AA leaders and sponsors accepted the combination of
antidepressant treatment and AA treatment for some patients.

Obviously, to make these distinctions requires a full knowledge of

the patient. In those patients who are intoxicated from alcohol no
such thorough knowledge is possible until they are sober and free of
withdrawal symptoms. Because some of these patients are abusing
other drugs, an accurate appreciation of their full problem may
require several clinic visits and longer periods of sobriety.
 Many of the same points should be made about anorexia nervosa,
a condition that also has complicated links to depression. As with
intoxicated addicts a confident understanding of depression, either as
symptomatic of the starvation or as amplifying typical self-despising
anorexic preoccupations, can emerge only after the patient has
recovered from her starvation.

Interactions between Behaviors and Temperament

Personality features provide a major contribution to behavior

disorders. The person with an antisocial temperament-that is, an
unstable extravert with less than ordinary concerns for others-is often
launched into drug taking and alcohol abuse given that he or she is
less influenced by either social controls or self-reflections. As "people
of the moment," they are more responsive to daring opportunities,
peer models, and the promises of excitement than are others. 19

Persuading such people to change their behavior is intrinsically

more difficult, and essentially impossible if they are under the
influence of drugs or alcohol. Sometimes only the compulsion of law
can bring them into therapy. As mentioned earlier, legal compulsions
in the form of parole and close monitoring of behavioral compliance
and social integration have proven of value in sustaining these
patients in a remission from alcoholism and drug addiction.

Further help in managing the behavior of these patients with

complicating antisocial personality traits has emerged from specific
programs of psychotherapy. A more confrontational, group therapy
treatment addressing the tendency of these patients to minimize their
responsibilities and justify their behaviors has been tried. For
example, Daytop Village and Phoenix Housegroup treatment
programs for drug addicts who were also criminals-had more success
than other programs with these patients because of the form that the
group treatment took. Elements including group leaders who
themselves had been addicts and the use of the "hot seat" for
confronting the patient seemed to lead to more honesty about
behavior. These groups held up the patient's patterns of dodging
responsibility, recognized as familiar to the veteran addicts in the
group, to derision. Ultimately, guidance came through aggressive
efforts-sometimes backed up by legal compulsions-at strength ening
in these patients a commitment to truth about themselves and their
problems.20

Emotionally labile patients are often difficult to engage in treatment.

They may expect that any treatment will first address their feelings of
distress so as to make them "ready to change" and thus keep the
burden for treatment on the shoulders of the therapists. This
expectation on the part of patients is but another version of the
common error "treat the causes and the behaviors will melt away."
These patients must learn that stopping the behavior rather than
emotional relief is the first goal of treatment. Very often until the
behavior is controlled, the patient's emotions, responding to conflicts
of will with the treatment team, remain unstable and brittle, justifying
relapse. Group therapy, again, provides the best means for teaching
the patient how preoccupation with these feelings hinders recovery.
"Behavior first, feelings second" becomes the byword in the program.

Summary

This chapter has attempted to identify the practical problems of

treating behavioral disorders, reemphasizing that the goal cannot be
construed in terms of cure, as with disease, but in terms of
conversion from one way of life to another. Successful programs for
motivated behavioral disorders address the triad of choice,
physiological drive, and conditioned learning in a "staged" fashion,
attempting (1) to draw patients, some with compulsion, into therapy;
(2) to solve problems and sustain resolve for recovery with group and
individual counseling; (3) to provide apt psychopharmacological relief
for drive; (4) to monitor compliance, watching for relapse; (5) to
organize a behaviorally responsive system of reinforcements; and (6)
to begin rehabilitation with restructuring the life patterns that
contribute to the behavior in the patient.

The appreciation that behavior disorders can be differentiated into

those that rest on drive and those that rest on social learning leads to
the choice of certain apt adjunctive treatments, several of which have
proven of great value. Thus for the "driven" disorders, treatment may
include (1) satisfaction replacements (methadone, nicotine patch), (2)
drive reduction (medroxyprogesterone acetate [Depo-Provera]), (3)
response punishment (disulfiram [Antabuse]), (4) reinforcement
blockage (naltrexone), and (5) harm reduction (needle exchange).
For those behaviors with critical socially learned elements such as
anorexia nervosa, hysteria, or delinquency, treatment measures may
include (1) redirection with psychotherapy to better aims and better
consequences, (2) rewards for appropriate choices and responses
(token economies), and (3) social restructuring and rehabilitation
(family therapy).

Those who work to treat behavioral disorders must take a long-

range view of these patients and develop much forbearance in the
face of relapse. Endurance and equanimity are sorely tested in
providing these treatments, and not every psychiatrist is willing to
persist in this work. The rewards of those who do come from those
patients-some of whom had initially seemed the most unlikely of
prospects-who do achieve a stable recovery. We exemplify all these
treatment concepts with a specific patient in the next chapter.
In this chapter we present a patient with a remarkable variant of
bulimia nervosa, describe her condition, follow her treatment, and
explain its rationale. Our aim is to demonstrate the practical
employment of the behavior perspective. As we have stated
repeatedly, there is a radical implication related to cause that
distinguishes behavior from disease. With disease, the symptomatic
manifestations are the outcome of an underlying pathology; it is
pathology that we strive to attack, expecting the signs and symptoms
of the disease to melt away. We look "into" a disease to find the
causal mechanisms forging the symptoms.

With behavior, we identify activities drawn by a goal. Alcoholics

drink to get drunk; anorexics starve to get thin. An explanation for
behavior is therefore found in its goal-directed presentations and
rewards. Looking into the behavior's manifestations as though they
were "symptoms" forged by some specific mechanism rather than
looking "out" at the goal and at the readiness or unreadiness of the
patient to abandon that goal will misdirect the therapy. Indeed, the
major disappointments in psychiatric treatment of alcoholism,
anorexia, and so forth, derived from the assumption that addressing
all the demoralizing life conflicts of these patients would lead to the
melting away of the behavior, just as symptoms melt away when
pathology is cured. The shift of psychiatric attention to the behavior
itself, to the readiness of the patient to change, and to efforts at
interrupting it (if "only for a day") increased therapeutic success by
revealing self-sustaining features of behavior as a critical aspect of its
explanation and its intractability.

Addressing behavior to interrupt it is the first and most crucial issue

in therapy. Only later in the course of treatment-after the patient has
accepted some responsibility and taken action to interrupt the
behavior and bring it under some control-does extensive work on the
individual demoralizing issues have pertinence as an aspect of
rehabilitation.

Efforts to interrupt behavior challenge the patient's willingness to

accept treatment. Most patients come to treatment to avoid the
burdens of behavior, not necessarily to give it up in its entirety. This is
where the conflict of wills appears-the patient negotiating for aspects
of the behavior, the psychiatrist fighting to stop it. This is also where
relapses begin as the patient rationalizes his or her choices. And
finally this is where the problem is solved-not by cure but by
conversion, from contemplations to actions.

This treatment method has increased psychiatric effectiveness with

behavioral disorders and has been rediscovered for condition after
condition over time. For disorders such as alcoholism, anorexia, and
drug addiction, calling the patient's attention to the behavior and
insisting that some of the responsibility for it is the patient's led to
success. In this chapter we shall consider a patient with a long-
standing form of bulimia nervosa and describe how a staged
approach to her behavioral condition-beginning first with efforts to
bring her into an action mode against the activity and only then
followed by efforts at treating sustaining factors in her life and in her
body-succeeded where other efforts had failed.2.3

Case Report

The Problem
 A young woman was admitted to our Eating Disorder Service with a
fourteen-year history of bulimia that she had gradually transformed in
the last few years into a habit of oral rumination of food. In solitary
stints lasting hours each day, she would chew and then spit out large
amounts of sweet foods. This behavior came to dominate her daily
life and the purchase of these sweets became a serious drain on her
household finances.

Background

The patient was the product of a normal pregnancy and delivery but
was born into a family with affective disorder in several members.
She herself had had several periods of depression during her late
adolescence and early adult hood, mostly experienced as diminished
mood, a loss of confidence and selfesteem, and lack of energy. Her
eating disorder, however, seemed separate from the depressions. It
began after a surgical procedure at age 14 that led to her losing some
45 pounds of weight (she went from 170 to 125 pounds). The effect of
this weight loss on her appearance pleased her, brought praise from
others, and prompted her to try to stay thin by dieting.

The Behavior

Her dieting rapidly turned to binge eating and self-induced vomiting

when she learned the discomforts of food restriction. The vomiting
ultimately caused her bodily damage, including severe tooth decay
and a rectal prolapse requiring surgical repair. These physical
consequences of her behavior, along with continuing beliefs that
fatness was unacceptable and that she must control her caloric
intake, led her to shift gradually to her present eating habits of
prolonged bouts of tasting and expectorating sweet foods.

This became an almost daily activity for her. The process involved a
trip to her local bakery to get cakes and donuts, especially those
glazed with sugar. She hid these goods in the house until she could
be alone (when her husband was at work or asleep). Then she would
go into the kitchen, collect the food around her, and for several hours
steadily expend the entire supply: masticating it, savoring the sweet
flavor, and swallowing as little as possible by spitting remnants into a
bowl or disposable plastic bag.

The Experience

She reported several experiential features surrounding and

sustaining this behavior. First, what she enjoyed was the flavor of
these foods: the more sugary sweet, the better. Second, she tried to
restrict her consumption of other food during the day because the
hungrier she was when she began a stint of rumination, the more
pleasurable she found the sweets. Third, once started, she persisted
until the sweets were all consumed, persisting not only because the
taste was pleasurable but also because a mental state-which she
described as "zoning out," that is, comforted, relaxed, and detached
from daily cares-took her over as she proceeded.

She reported suffering from periods of depression during the last

several years. She could not say whether these were worsened by
her eating disorder, but she was sure that the stints of rumination did
comfort her when she was depressed and seemed to her to be more
frequent during her depressive phases.

Prior Treatment Efforts

She did not so much seek treatment as she was forced into it
because her family lost patience. On arrival on our service, she
pointed out that she had received much psychotherapy and
outpatient, inpatient, and day hospital treatment elsewhere during the
last decade. These treatments had proposed to her explanations for
acting as she did-proposals that she could accept as enhancing her
understanding of herself and the behavior. But this information did not
change her activity. She came to Johns Hopkins just as badly
afflicted, craving sweets and indulging her habit, as she had been
over the last several years.

Presentation

The treatment team found her to be cooperative on admission. She

was neatly dressed, neither obese nor overly thin, but slightly
apprehensiveadmitting that she was demoralized by her family's
criticisms and unsure whether she could maintain her marriage, given
the enjoyment she took from her behavior. She vividly described the
pleasure that chewing and spitting sweet foods gave her. She noted
that she developed little or no food satiety during this activity.
Occasionally, the prolongation of the sweet tasting would make her
slightly nauseated. Only that sensation, or, more usually, the
exhaustion of the food supply, would lead her to stop a particular
stint.

She was not convinced that she wanted to give up this behavior. It
was just so enjoyable. However, she lost much in life because of the
time and money it consumed. She had sacrificed her advancing
education, her job, and the goodwill of her husband to it. At the same
time, she was weary of therapy and could not imagine how more
would help her abandon this habit.

The Treatments

She was informed that initially treatment would concentrate on her

attitude toward change itself, followed by assessment and treatment
of her affective lability and her present life circumstances, all with the
purpose of getting her to stop this behavior. Group and individual
therapy along with antidepressant medications and perhaps other
pharmacological treatments directed at the eating behavior itself
would be tried. She was requested to take part in the program with an
open mind and with a cooperative spirit.
 The prime treatment was group therapy. The group challenged her
attitudes about change and regarded her attempts to review
endlessly the putative meaningful explanations for her behavior as
resistance to change and, indeed, an effort to dodge accountability
for choosing to behave as she did. The group insisted that she turn
away from expressing feelings about her life and begin to think about
her responsibility for this disordered, indeed perverse, activity. It was
held that she was merely contemplating change and was not yet in
the "action" phase. She was started on lithium to stabilize her mood
and on naltrexone to block the "bliss" that may have reinforced her
behavior.

As she listened and responded, it did seem that she entered into an
action mode-ready to assume responsibility for her behavior and now
seeking help in doing so rather than seeking explanations for why she
failed. With this shift in her attitudes, she was transferred to the day
hospital and given a series of home visits from people involved in the
treatment setting. Meetings with her husband revealed some aspects
of the marital relationship that could stand correction. She herself
began to appreciate that psychological issues that may well have
precipitated or initiated her eating disorder (on which she had
previously devoted much attention) were not the issues sustaining it
now. Therefore, she agreed to turn her attention away from long
reviews of her past life and continual expressions of "feelings" as
though her feelings must be resolved for her to recover. Instead, she
was directed toward considering those aspects of her present life that
might have sustained her interest in this behavior and conditioned its
regular repetition. She was told that her feelings mattered less than
her behavior because they would improve when her behavior was
under control.

Her affective temperament as an unstable extravert also came to

light. It was thought that this disposition rendered her emotional
responses to frustrations more intense. An added treatment was
developed around guiding her in managing the friction of daily life-at
home, school, and work-more successfully in order to diminish the
emotionally provocative events that prompted her to surrender to the
ruminative behavior. Again the emphasis was "control the behavior;
your feelings will follow."

With a continuation of this approach-psychotherapy for issues in the

"here and now," medications for affective disorder and opiate
rewards, and a daily reminder that her behavior was ultimately hers to
control regardless of her "feelings"-she has remained abstinent for
months. She continues to visit the program as an outpatient, takes
part in group and individual therapy with the original aims, and
remains on the medications prescribed: lithium and naltrexone.

Discussion

This is an example of a patient with a most peculiar and destructive

pattern of behavior. The behavior dominated her life (pushing aside
work, family, and health, and so on) and rested on a "craving" or
compelling drive tied to hunger and eating, but was a response that
broke the linkage between eating behavior and its customary aims
(that is, between food consumption and nourishment). In such a case,
the judgment of abnormality in behavior rests on recognizing how its
indulgence is impoverishing the person, physically, psychologically,
and financially.

There is, and always will be, a strong vein of moral criticism in any
decision identifying a behavior as abnormal. After all, it is at one level
a token of preference to adjudge abnormal what another person
chooses to do. A judgment of this sort may be supported by
suggestions that the person is not choosing freely but is compelled
(enslaved) to the activity. But even then such a judgement usually
encompasses what one believes to be an appropriate way to live. If,
as with this patient, the highest concern to which she devotes herself
is a maximization of sweet-tasting experience, if this devotion has the
compelling feature of a craving, and if the responses undermine all
other capacities of the patient, then most people and all psychiatrists
will agree that this behavior is a disorder suitable for treatment.

Psychiatrists can explore four sources of information when

searching for evidence of behavioral disorder: (1) the particular
characteristics that demonstrate a behavior's most obvious
distinctions from normal, (2) predisposing psychologic features that
support the disorder, (3) the place of maladaptive learning
engendering the behavior, and (4) the linkages to physiological
mechanisms that may reveal a biologic substrate for abuse. These
issues were explored in developing an explanation and a treatment
program for this patient.

Behavioral Features

Gerald Russell's criteria for anorexia nervosa and bulimia nervosa

indicated that both disorders involve a "morbid fear of fatness"
directed either at the restriction of food intake in anorexia nervosa, or
the overeating, vomiting, and purging of bulimia nervosa.4.5 This
morbid fear of fatness has the characteristics of an overvalued idea,
that is, a thought shared with others in the society but in the patient
held with the intense emotional commitment capable of provoking
dominating behavior in its service. Terms such as fanaticism or a
ruling passion grasp the concept of overvalued idea. Thus many
normal people have worries about gaining weight but the overvalued
idea-one cannot be too thin-is the ultimate concern of eating disorder
patients that drives their actions and replaces all other interests and
affairs.

The epidemiological evidence about these eating disorders indicate

aspects of their nature. They are afflictions of (1) youthful females in
(2) upper classes of (3) developed countries in (4) the contemporary
era. In a sense these conditions are much like dress fashions, with an
added overvalued idea. Notice that these eating disorders are not
found among all human populations, as are diseases. Rather, these
disorders seem culture bound-resting in some way on the
psychological motives and conflicts generated in maturing women by
our particular sociocultural milieu.The patient learns these behaviors
through example and experience.6

What psychological matters sustain eating disorders and give them

salience for the patient? This question has been a perennial issue for
psychiatrists. Sometimes they have considered the restriction of
eating to be the feature needing explanation, sometimes the vomiting.
Meaning was sought in these features, presuming that they
represented responses to conflicts over sexual matters. Thus,
anorexic restriction suggested unconscious beliefs in oral
impregnation, and bulimic vomiting suggested repressed sexual
disgust. These concepts were detailed in chapter 15 in the quote from
Lorand.7

Most of these interpretations now seem forced, go beyond any

data, and usually are sequentially and regularly replaced by some
other conception of the mental life of women imagined by male
psychiatrists. The patients themselves tend to describe their struggles
for thinness as generated and sustained by comparing themselves to
other women. They note and envy the thinness of others, seeing it as
an attractive physical feature, and-believing that thinness indicates a
capacity for self-control-learn behaviors that will produce thinness in
themselves despite the urgency of hunger.

This patient often commented about women in the mall and

compared herself unfavorably to the thinner ones. She also was
particularly engaged by her own image in the mirror and focused on
what "parts" she could make thinner. This "comparison
preoccupation" of anorexic women can explain the increased risk for
these disorders in ballet dancers and fashion models, who are
occupationally committed to construct a bodily appearance more
striking than others. Women comparing themselves with other women
seems as likely a motivation behind eating disorders as any sexual
conflict.

Predisposing and "Comorbid" Features

With severely starved anorexic patients the first step in treatment is

the relief of their starvation. This restores the patient's capacity to
understand and contribute to the next stages. With an inpatient
service this lifesaving step is not too difficult. We can with the help of
conscientious nurses produce steady gains of weight in emaciated
patients of from three to five pounds per week. Although our patient
was not starved, a program to address her dietary hygiene was
launched, as will be discussed further.

Several "comorbid" psychologic conditions are associated with

anorexia nervosa or bulimia nervosa. They may provide some of the
individual predispositions to the disorders and need direct treatment.
In particular, an affeclive disorder is common amongst patients with
eating disorders. This condition needs treatment with antidepressant
medications, (lithium in our patient), and close monitoring. Obsessive-
compulsive dispositional features also can complicate eating
disorders. These features need direct attention and may respond to
pharmacological treatment.K

A link between these comorbid psychologic predispositions and the

eating disorders seems plausible. Again if a comparison of the self
with other women is fundamental to these behaviors, then the
negative self-attitudes of depression and the perfectionism of
obsessive-compulsive attitudes would give more power to the
sociocultural pressure for thinness as an ideal. Once an eating
disorder began, these comorbid features, if untreated, would sustain
it, interfering with recovery.

Other common psychologic features well known to be associated

with these eating disorders are abnormalities of temperament,
unstable introverts for anorexia nervosa and unstable extraverts for
bulimia nervosa. An important sustaining feature may be the relative
ease with which an introvert develops conditioned emotional
responses. This form of learning may play a crucial role in sustaining
anorexia nervosa because these patients-who are mostly introverts-
develop strong conditioned aversive responses toward fatty foods
and thus direct their food choices away from those edibles with more
calories.

Maladaptive Learning

A historical change in eating disorders in the United States

suggested a role of social modeling and instruction behind these
behaviors. Whereas in the 1940s eating disorders were rare (and
mostly exemplified by anorexia nervosa where patients restricted
their caloric intake), beginning in the 1960s bulimia nervosa emerged
as a new condition and spread to become the more common eating
disorder. This progression, implying powerful social learning at a time
when thinness became fashionable, was first noted by Gerald
Russell.9 A critical psychological reward that sustains patients within
an eating disorder may be the sense of self-efficiency that learning to
control calories and bodily appearance can bring.

Our patient learned a new behavior with which she could satisfy her
tasting desires without gaining weight. She progressed from classical
bulimia nervosa to this odd variant of "rumination" in which she was
spared the pain of vomiting. With this transformation, she could enjoy
sweet foods for hours with no concern for gaining weight and with
none of the physical exertions of forced vomiting.

Physiological Substrate for Abuse Liability

Our knowledge of the embodied controls on the hunger drive

suggested a path followed by this patient in learning her new
behavior and as well identified a potential adjuvant treatment for it.
She reported that if she could get very hungry, she could enjoy the
behavior even more. Also, because taste was the reinforcer of her
activity, we reviewed how taste of sweetness-a crucial element in the
physiology of normal eating-could be linked to the hedonistic
pleasures of food consumption. A thorough consideration of the
psychophysiology of taste was therefore launched in seeking an
explanation for her "rumination."

TASTE AND ITS PHYSIOLOGY. Taste is an important part of the

psychoneural system responsible for controlling and directing food
intake. The reinforcing character of sweet taste is built into
mammalian physiology. It functions both as a means of distinguishing
foods from nonfoods and as a reward sustaining food ingestion until
satiety supervenes. By discerning sweetness from other tastes
people can be encouraged to consume nutritious food (for example
ripened fruit) and thus maintain good health with the satisfaction of
hunger.

This patient had taken the taste function, learned to isolate it, and
made its stimulation an activity that dominated her. She developed a
compelling "craving" for its indulgence-an indulgence that produced a
blissful, relaxed, sensual, or, as she put it, "zoning out" state of mind.
In so doing, she perverted taste from its customary function of
directing and sustaining balanced nutritious dietary habits.

BRAIN MECHANISMS REINFORCING TASTE. The

psychophysiology of taste suggests how the taste of sweetness might
provide an avenue for craving, such as that seen in this patient. The
mesolimbic dopamine pathway is the brain system for pleasure and
hedonistic behaviors in general. This is the path that when stimulated
electrically will produce "self-stimulation" in rats and monkeys. It is
also the path that "lights up" in PET scanning of humans taking
addictive drugs such as cocaine. I"
 The cell bodies of this path are imbedded in the ventral midbrain
and its axones extend to and synapse with neurones in the limbic
system releasing dopamine from their terminals. One input to these
cell bodies in the midbrain comes from the hindbrain, where taste
sensations are first received in the brain. As well, the mesolimbic cell
bodies are surrounded with opiate receptors. Neural activity from the
hindbrain, evoked by taste sensations, can thus play on the
mesolimbic dopamine cells and may release endogenous opiates.
This may be the neural substrate for the hedonistic and reinforcing
features of tasty foods. 11.12

There is pharmacological evidence that supports the importance of

the mesolimbic dopamine pathway in taste-driven behavior. Earlier
this evidence depended on the model of "sham" feeding first
designed by Pavlov but in recent years has been employed with great
success in demonstrating physiological controls on feeding behavior
by Gerard P. Smith and his collaborators at Cornell Medical College.
In sham feeding a fistula is formed in the stomach of a rat so that all
that it ingests promptly flows out of the stomach and neither distends
that organ nor passes into the intestine. As a result such animals will
persist in consuming a liquid food without interruption for many hours.
Their rate of consumption will vary directly with the sweetness of the
solution. Thus, the rate of sham feeding is a good measure of the
consumptive drive of the animal.

Intriguing to our point with this patient is Timothy C. Kirkham and

Steven J. Cooper's demonstration that sham feeding for sucrose in
rats was reduced by naloxone-the blocker of opiate reception."
Gerard Smith provided a similar demonstration that sucrose-driven
sham feeding was reduced by giving pimozide, a dopamine receptor
blocker.14 Thus, pharmacological agents that act either to block
opiate reception arousing the mesolimbic dopamine path (naloxone)
or to block dopamine reception in the limbic system (pimozide)
significantly reduced the consumption of sucrose in experimental
studies. These observations led to a therapeutic trial with this patient.
THERAPEUTIC APPLICATIONS OF THIS INFORMATION. Many
observers of bulimia nervosa have commented on its resemblance to
sham feeding, and certainly this patient's ruminative chewing and
expectorating sweet foods were much like it. Sucrose glazed on or
baked into food was the substance she sought. The energy and taste
pleasure were enhanced by fasting. She persisted in the
consummatory behavior until all was chewed, because no natural
satiety supervened. That she developed during this behavior an
intriguing blissful state of mind, a kind of inebriation encouraging her
intemperance, was also noteworthy.

For these reasons and given these animal studies on sham feeding
for sucrose, her physicians wondered if endogenous opiates were
helping to sustain her behavior. She was offered naltrexone to see if it
might reduce the pleasure she obtained from taste and thus reducing
the reinforcement of her behavior. This medication would not deal
with all the provocative and sustaining features of her behavior.
However, given the oddness of this variant and its inebriationlike
psychological accompaniment, a trial of naltrexone seemed
warranted. The patient claimed at discharge that her thinking about
sweets had lessened-a self-report that needs other challenges to test
but nonetheless one that matched the therapeutic hypothesis.

Given her report of the role of hunger in her behavior, her

therapeutic program included the insistence that she never let herself
become very hungry. In the hospital she was given three modest-
sized meals to eat per day, and it was demonstrated to her that she
did not gain weight on this regimen. In this way she was reassured
that hunger satisfaction would not produce huge weight gain but
would prevent an appetite spurred into overdrive. This simple matter
of dietary hygiene further reduced her interest in rumination.

Stages in the Treatment of a Behavioral Disorder

 The treatment program with this patient is typical of standard
treatments for behavior in that it was "staged"-that is, the program
was broken down into components, each with its own therapeutic aim
and followed by a subsequent stage only when the aim was reached.

The goal of the first stage was to have the patient acknowledge
responsibility for the behavior and commit herself to change. This
proved, as is often true, the most difficult stage of treatment, with the
patient's arguing that her behavior was due to her uncontrolled
feelings and burdensome life circumstances that the doctors must
relieve before they could expect her to improve. The therapeutic
group rejected these ideas of the patient and confronted her (with a
smile) with her unwillingness to take responsibility for her activity. She
complained bitterly about this interpretation and presented much
resistance to the shift of attention from her feelings to her choices; on
one occasion she threatened to leave.

We came to believe that she had entered the "action" phase of

recovery when she finally was willing to discuss the pleasures and
rewards of the behavior that had made it so enticing to her and would
be difficult to abandon. It seemed, but we were never certain, that this
shift occurred after she had been repeatedly confronted by the failure
of the many therapeutic efforts in the past that had concentrated on
her feelings. She seemed to realize that she was running out of
resources, her husband was running out of patience, and the group
would not give up identifying her rationalizations. Then, she admitted,
"the time has come to change."

The next stage of treatment-following her willingness to "own" the

behavior and fight against it-included treatments that were explained
to her as adjunctive and were directed at her dietary hygiene, her
comorbid depression, and the opiatelike potentiation of her ruminative
activity. These were treatments directed at what seemed sustaining
elements to her behavior and were intended to help her with her
resolve. As well, here we launched a challenge against the social
learning behind her striving for thinness, such as her continuing
modeling of herself against other women. Group members who had
struggled against the overvalued idea of thinness themselves could
help her acknowledge its irrationality.

Her temperamental difficulties of emotional intensity and inability to

defer her gratifications were also addressed as issues that led to her
surrendering too promptly to her behavior. She was encouraged to
learn to manage her emotions better. In this stage the patient
continued with group therapy and began to contribute to the
assimilation of other patients introduced into the service who, as she
had some weeks before, needed confrontation over their
rationalizations and needed to move into the action phase of
recovery. This augmented her learning of a new approach to her own
behavioral problems.

In the final stage of treatment, as discharge approached, a

consideration of her present life circumstances and how they
contributed to her behavior was begun. In particular, her husband
was brought into meetings with her therapists so that his justifiable
concerns could be addressed but also so that he could understand
something more about her responses to frustration and thus make it
possible for them to work together in avoiding conflicts.

She remains now in ambulatory follow-up treatment guarding

against relapse and continuing with rehabilitative efforts directed at
her marriage and her employment. The future is not settled, but
further therapeutic efforts reviewing her confused thinking about her
body and guiding her away from frustrations are continuing. Her
resolve to overcome the difficulties with recovery remains high.

Summary

This case was chosen to exemplify treatment of a behavioral

disorder, emphasizing the entwined elements of learning and bodily
mechanisms in its causation and the staged approach to its treatment
and rehabilitation. The initial task was helping the patient realize that
the behavior ultimately was her responsibility and that recovery could
only occur when she was ready to be accountable for it. The
therapists would then help her with some of the precipitants and
provocations, such as comorbid depressions, emotional instability,
poor dietary hygiene, and intrinsic reinforcing factors. But
permanently interrupting the behavior depended on her readiness to
take action against it.

In particular, her expectations that the behavior must await her

emotional stability or the resolution of her marital difficulties were
confronted as rationalizations against action in group therapy. She
was given to understand that improvements in her feelings would
come with recovery rather than produce it and that any efforts to
resolve her marital problems would be thwarted if the behavior
continued. Her attitude about thinness was addressed by other
members in the group who had held similar thoughts. This attitude
was recognized as a conditioned phenomenon that could be
extinguished if it were not indulged. Finally rehabilitative efforts
directed toward her family life and social integration through work
were launched.

This patient who came to the service only contemplating change

and carrying a number of particular learned and physiological
reinforcements for her habit was successfully brought into an action
mode toward recovery. All help that followed this crucial first step in
her treatment was concentrated on solving with her the issues that
she had previously neglected and providing treatments that might
help sustain her resolve. This was not a cure but a conversion, and,
like all conversions, had to begin with a will to change.
Some behavior disorders are not propelled by an embodied drive but
emerge from social contexts that give them meaning and direction.
Psychiatrists regularly manage two of them, hysteria and suicide-
behaviors, by definition, in that they are goal-directed activities;
disorders because the goals are deviant. But they are not "motivated
behaviors," as we are using that phrase from physiological
psychology, because they are not expressions of an intrinsic hunger
or appetite but deviant actions some people learn to resolve problems
they face.

Definitions and Distinctions

Hysteria is one of the great words of psychiatry-right up there with

mania, delirium, and dementia. But that may be its biggest problem.
The noun hysteria suggests something a patient has-an illness or
disease. But hysteria is not something a patient has; it is something
the patient does; that is, it is a behavior. The hysterical patient acts in
such a way as to imitate the symptoms or signs of a somatic or
psychologic disorder.'

Hysteria is a general term for a large class of activities that have as

their common feature mimicry of medical or psychiatric conditions,
false portrayals formed by complaints of affliction or displays of
dysfunction. The boundaries of this class are not sharp, merging
imperceptibly, on the one hand, with hypochondriasis, in which
patients repeatedly bring transient symptoms to medical attention
because they are anxious worriers and, on the other with factitious
behavior in which patients injure themselves to obtain medical
attention.2 The practice of distinguishing "conversion" hysteria from
"dissociative" hysteria followed in DSM-III and DSM-IV is unprofitable,
we believe, a vestige of outdated psychodynamic reasoning. The
motor-sensory manifestations of the former and the psychological
manifestations of the latter do not represent critical distinctions in
their nature but derive from what can pass muster as a believable
portrayal of "sickness." In some social contexts, neurological signs
have currency; in others, psychological manifestations are trumps.

Consider this more comprehensive definition: hysteria is a behavior,

engaged in more or less unwittingly, that imitates a medical, surgical,
or psychiatric disorder through such actions as complaining of
"symptoms" or producing "signs" of affliction, all with the goal of
achieving the social status of a "sick person," where certain
privileges, considerations, and attitudes from others can be expected.
Even this definition needs some elaboration to resolve the remaining
ambiguities tied to the behavior.

Because hysteria can appear in many guises, the definition does

not specify its presentations. A list of its guises could be as long as
the catalogue of human illness. Hysterical patients can complain of
pains, weakness, nausea, or amnesia. They can act as if paralyzed,
blind, deaf, or mute. They can fall into faints or seizures, writhe with
choreiform movements, or portray several different "personalities."
Indeed, they can produce any display that means "illness" to them
and captures the attention of others empowered to provide them the
benefits of being "sick."

Physicians are the usual providers of "sick benefits," and therefore

specialist physicians intrigued by diagnostic problems are often the
audience before whom these behaviors are displayed. But anyone
who can supply sympathy, support, and protection may be the target
and perhaps the unwitting sustainer of this behavior. This group
includes spouses, parents, siblings, colleagues, employers, and
teachers.

The "more or less unwittingly" phrase bracketed within our definition

broaches the idea that these people are not frauds or malingerers.
The human power of self-deception can bring many people to believe
in the validity of symptoms that offer them advantages. They are not
so much trying to deceive the doctors as deceiving themselves and
everyone else with the idea that they are sick. Hysteria is a behavior
derived from patients' false beliefs that they are victims of some
disease, injury, or disorder. The goal of appearing sick is not
calculatedly chosen so much as it is gradually assumed as beliefs are
delineated, advantages emerge, implications are felt, and
encouragement is received. The patients learn the behavior that
manifests their belief in their supposed affliction. This explains why
many manifestations develop and change over time-shaped by the
responses of observers-and why many patients, on recovery, report
that they had to struggle to retain their own belief in their "sickness."
Beliefs are to hysteria what cravings are to addiction.

Finally, the goal of the behavior is itself ambiguous. The person may
already be "sick," as with a depression, intoxication, or dementia-
conditions that distort attitudes, reasoning, and judgment. Why seek a
goal that has already been achieved without, one might say, any
effort? Here, however, the goal is a search not for the burdens but for
the benefits of "sickness"-particularly benefits encompassing
protection, attention, and support.

The sociologist Talcott Parsons elucidated the benefits embedded

within the status of being ill when he spoke of the privileges that our
culture offers to one in the "sick role."3.4 These privileges include
release from work, notice and concern from others-amplified if the
depicted disorder can convey a theme of "victimhood" (as did the
hysterical behavior of "possession" that ignited the Salem witch
trials)-and deliverance from conflicts and demands. From Parsons's
concept of the sick role, David Mechanic and Issy Pilowsky
developed the expression "abnormal illness behavior" as an
improvement on We use the terms interchangeably-accepting the
advantages of the behavioral emphasis from Mechanic and Pilowsky
but holding to the traditional term, hysteria, for ready reference.
 In summary, the definition of hysteria has such ambiguities that a
confident separation of hysterical patients from others cannot be
derived from it. However, the concept itself-comprehending
complaints provoked by beliefs and represented as "abnormal illness
behavior"-is settled enough to permit a consideration of the
manifestations of the behavior, its rational explanation, and its
treatment.

Acute and Chronic Expressions

An acute hysteria is usefully differentiated from a chronic form.

Acute hysteria-subsumed in DSM-IV as conversion and dissociative
disorders-is the relatively abrupt appearance of an artifactual set of
signs and symptoms that call attention to themselves. Many of the
phenomena relate to neurological functioning and include weakness
or paralysis in a limb, sensory loss in an arm or leg, sudden blindness
or deafness, odd athetotic or choreiform movements, or convulsive
activity resembling epilepsy. Acute hysteria can equally often appear
in a psychological guise-as the sudden loss of speech, loss of
memory (including a loss of awareness of one's own identity), visual
or auditory hallucinations, or multiple personalities.

Patients with chronic hysteria-the form subsumed in DSM-IV as

somatization disorder or Briquet's syndrome-are characterized by
lifelong complaints of symptoms such as pains, faintness, abdominal
cramping, nausea, coughing, and shortness of breath that turn out to
be groundless and artifactual. They also have occasional complaints
suggestive of neurological dysfunction, such as double vision,
impaired coordination, and amnesia, but these are less common.
However, over their lifetime these patients complain about the
function of almost every one of their bodily systems. The
gastrointestinal tract may be most favored as a site of complaints
(cramps, nausea, and vomiting, for example), but the patients also
have pulmonary, cardiac, orthopedic, genitourinary, and neurological
symptoms-all of which may have led to strenuous searches for
pathology because they are so vividly recounted. These searches,
which can include exploratory surgery, fail to reveal confirmatory
pathology.8

A physician familiar with the patient may come to realize that the
"complaining behavior" worsens with new life burdens to the patient-a
depression recurs, a conflict with a significant person appears, or a
financial crisis ensues. Then subtle symptoms of a functional sort
within any of the bodily systemsgastrointestinal, genitourinary,
musculoskeletal-become overpowering, anxious preoccupations
driving the patient from doctor to doctor.

The opinion that hysteria is disappearing is incorrect. At Johns

Hopkins Hospital about 2.5 percent of the patients seen in psychiatric
consultation have some form of hysteria. The chronic variety is more
commonly seen on the medical services while the acute form shows
up on the neurological and psychiatric wards. Hysteria is not
disappearing but has taken on less conspicuous guises, as people
learn what can pass as disease today. The common expressions of
motor-sensory dysfunctions as in convulsions and choreoathetotic
writhings have been replaced with subtle disorders of psychological
functions such as amnesia or alterations in consciousness.

Multiple personality disorder is the best contemporary example of

the trend. Before 1957 this presentation was a most rare form of
hysteria. But a miniepidemic followed the publication and
dramatization of the manifestations in the book The Three Faces of
Eve, by C. H. Thigpen and H. Cleckley.9 This epidemic recurred
nationwide with the force of a craze after the publication of the book
Sybil, by Flora Rheta Schreiber.1° The latter book had a greater
impact because it delivered the status of "victim" to anyone displaying
multiple personality disorder. The book claimed that the "condition"
was a common and natural response to forgotten sexual abuse in
childhood, the memory of which had been repressed and dissociated
into one of the "alter" personalities. This idea was not only potent fuel
for patients but gained sustenance from contemporary political ideas
and "gender wars."

Identifying and Explaining Hysterical Behaviors

To identify and make sense of a hysterical presentation, one should

consider evidence from (1) the manifestations; (2) the dispositions as
revealed by the patient's temperament and past behaviors; and (3)
the physical, psychological, and social provocative circumstances. A
diagnostic formulation may not find support from all three of these
evidentiary sources, but each should be systematically explored
preferably with help from a person who knows the patient-a family
member always, a prior physician when possible.

Manifestations

Although almost any somatic or psychological illness can be

imitated in hysteria, the exactness of the counterfeit depends
considerably on what the patient knows of medicine or can learn.
Thus, nurses and doctors can produce more compelling facsimiles
than But any patient who interacts with doctors over time can learn to
produce convincing imitations.

The features of acute hysteria are always vivid-taking the form of

paralyses, limb contractures, seizures, sensory losses, faints, and
fugue states. Their artifactual nature is usually clear in that the
neurological signs do not conform to anatomical paths; the seizures
do not have electroencephalographic accompaniments; the faints and
fugues never injure. Indeed, the dysfunctions of acute hysteria are
those that burden others-nurses, doctors, and family memberswhile
symptoms such as urinary incontinence, that would burden the
patient, tend not to appear. Henry Head wrote a classical review of
the many artifactual features of pseudoneurologic hysterical
presentations. 12 Certain psychologic presentations can always be
considered hysterical artifacts: multiple personalities a prime
example.

The vaguer, subjective manifestations of chronic hysteria tend to

afflict either the head and neck or the abdomen and lower back.
Despite being vividly described, pains will lack a precise site of origin
and will spread idiosyncratically across limbs without regard to natural
physiological boundaries. Because these complaints may have
prompted some concerned surgeon to operate on the patient,
symptoms from adhesions or other scars from previous surgery may
complicate the presenting picture. This potential for worsening the
problem is reason for recognizing hysteria early and treating it as
behavior, not as disease. This admonition is, of course, a counsel of
perfection because these patients are so convinced that they are ill
that they may encourage, indeed demand, ordeals such as invasive
procedures and surgical explorations.

Dispositions and Predispositions

The natural hosts of hysterical behaviors are people who are the
immature, dependant, burdened, or emotionally unstable-those
predisposed to fears and conflicts who may lack the capacity to find
efficient ways to solve their problems and are thus ready to grasp at
beliefs and behaviors that demand attention. They may be
predisposed to conflict and inclined to imagine mistreatment. Some
may be especially prone to influence and suggestion, a personality
disposition correlated with being highly hypnotizable. 13

Karl Jaspers noted a zeal for exaggeration and drama among these
patients and characterized them as "craving to appear, both to
themselves and others, as more than they are and to experience
more than they are ever capable of."14 Fascination with one's self
and its corollary preoccupation with how one is viewed by others are
embedded in this temperament. Such people-often but not always
youthful-are prone to opinions and behaviors that, they believe, mark
them as having some special social standing-in particular giving them
the glamour of intellectual complexity, spiritual depth, or dramatic and
unsuspected suffering. The conjunction of this disposition with life
circumstances in which the individual feels neglected or senses
disinterest from others can promote hysterical demeanors that cry out
for attention.

When suffering from debilitating physical or psychiatric illnesses,

many patients have a lessening of their powers of resistance to
suggestion. An affliction of judgment due to the unsuspected advent
of such diseases as dementia or major depression should be
considered when disease-imitating behavior appears in mature adults
who have never displayed such ways of dealing with conflicts.

Intoxication from prescribed or self-indulged medications may help

to provoke and sustain hysteria. Indeed, in the recent epidemic of
false memories of Satanic ritual abuse, most of the patients
"recovering" these memories were receiving intoxicating doses of
benzodiazapine sedatives that rendered them vulnerable to
suggestions from the leaders of this psychiatric misdirection.
Detoxification from these sedatives often led to their rejection of these
beliefs and their recovery.

In chronic hysteria an intriguing combination of the dispositional

traits of emotional instability, self-dramatization, and obsessionality is
often found. Michael Kaminsky and Phillip Slavney, who first pointed
out this pathogenic combination of temperamental features, proposed
that it evokes the "complaining behavior." They suggested that these
patients ruminate in an anxious way about their problems-particularly
minor somatic sensations and symptomsand because they are also
self-dramatizing and attention seeking, they do not bear their
problems silently but complain often and loudly to their family and
their physicians. They insist on being seen and treated as "sick."' 5.16
 Historical review may identify these dispositional features in a given
patient. That previous complaining behavior led to unrevealing
medical investigations or to surgery without issue can suggest that a
presenting episode is of the same kind and should be approached
psychosocially rather than physically.

Circumstances

The circumstances from which both acute and chronic hysterical

symptoms emerge are typically those that induce moods of
depression or frustration. Sometimes such moods are a product of
major depressive illness; more often they are the result of the
patient's perceptions of burden, neglect, or conflict in life. Whatever
its source, these moods can support a feeling of ill health and open
the patient to suggestive influences from the environment.

The cultural environment provides the basic support for a "sick role"
by offering acceptable models and examples of disease and
disablement. In fact a whole set of socially and culturally derived
experiences can be expropriated, amplified, and shaped by
predisposed individuals into the behavioral guise of disease. Thus,
the patient may witness sickness and envy some of its social
advantages through contact with disabled individuals at home or in
hospitals. A depressed nurse caring for a paralyzed patient may
develop a weakness of a similar kind. A discouraged student viewing
a teaching film on amnesia may begin to sense memory problems of
his or her own.

Several social agents can provoke hysteria. All act to teach-indeed,

to seduce-patients into self-deceptions about their health. These
agents may provide models of disease, act as transmitting vectors
that amplify social concerns about danger and disorder, or shape
preexisting concerns of patients into dramatic manifestations. As an
example, one person with hysteria can act so dramatically as to
"infect" others with the belief that they also are sick, producing
astonishing but usually short-lived epidemics of acute hysteria in a
school, an office, or a convent. Unsuspecting physicians may suggest
symp toms in the course of examining troubled patients-as did Jean-
Martin Charcot, who, when directing the Parisian mental hospital, the
Salpetriere, in the 1880s, evoked the behavior of "hysteroepilepsy" in
many of the patients as he studied them. 17,18

More malevolent provocateurs include witch hunters, conspiracy

theorists, mesmerists, and true believers in anything from a personal
Satan, to reincarnation, to invaders of earth from interstellar space.
These agents of hysteria, all of whom believe that evil is afoot,
suggest symptoms, signs, and courses of behavior to patients. In
fact, if the student of amnesia who sensed memory difficulties of his
own happened to be taking a psychology class led by a teacher
fascinated by the concept of "repressed memory," he might be drawn
into believing that his "memory" problem reflected some "forgotten"
sexual abuse. 19

An amplifying and sustaining role for learning must be added to

these provocative circumstances in order to understand hysteria.
That is, the social context not only provides the goal-the sick role-but
also can provide directions to it. These directives can come with (1)
models, as might come from witnessing illness in others or from
reading books such as The Three Faces of Eve; (2) rewards, as by
repetitive demonstration of professional interest in certain
"symptoms"; and (3) explicit instructions, as in books describing how
to review one's feelings and sensations when worrying about such
poorly defined conditions as chronic fatigue syndrome or "repressed
memories."

The role of learning behind a hysterical presentation is often evident

when a careful history of its progression is taken. Such a history will
reveal how the "symptoms" first appeared in a slight, almost
insignificant way-perhaps a little unsteadiness afoot, a ticlike twitch, a
vague "memory"-only to progress over time as they draw the
attention of examining doctors into paralysis, choreoathetotic
movement, memories of sexual abuse in satanic rituals or spacecraft
abductions.

Preexisting physical disorders can start the learning process. Thus,

pseudoseizures occur most commonly among people with epilepsy.
The distress of illness, autosuggestions prompted by experiencing
seizures, and inhibitions lowered by sedative medications may
combine with other predisposing factors to encourage a patient to
learn and assume an even more dramatic presentation of his or her
condition.20'2'

Hysterical behaviors-regardless of their provocations and

predispositions-are sustained by the effects these behaviors have on
those who observe them. Physicians and psychotherapists especially
may have played a critical role in suggesting a disorder. Others, for
example, fellow members of "sur vivor" groups, who review the
justifying "symptoms," may reinforce the patient's loyalty and
commitment to the behavior.

But the crucial sustaining ingredient, the one that produces fury in
the patient against skeptics, is the patient's own wish (or sensed
need) to remain consistent to the beliefs and guises of the illness
assumed. For consistency's sake many patients will continue a
hysterical behavior long after the provocative circumstances have
disappeared. Compliance with a suggestion, followed by consistency
to its consequences, is the formula for sustaining abnormal illness
behavior.22

Recapitulation

The manifestations of hysteria are artifactual representations of

somatic or psychological disorders. For example, pseudo-neurologic
or pseudopsychologic signs and symptoms are displayed by a patient
who believes that he or she is sick and in need of treatment.
 The patients' beliefs and their particular manifestations are
produced by suggestion and sustained by the attention of others.
These suggestions and encouraging attentions also derive from
beliefs-contemporary beliefs and concepts about disease and mental
disorder that are held within the patient's community and are
disseminated to patients and others by the media or by influential
figures such as physicians or therapists. Hysteria is thus a
psychosocial condition in which patients troubled by a variety of non-
specific psychological conditions that include adjustment disorders,
personality deviations, and even some co-morbid mental or physical
diseases, respond to sociocultural prompts that suggest and specify
manifestations and explanations that can serve as evidence of
"sickness" to others.

The patients' beliefs are developed from the community's beliefs

and then are amplified and sustained by the rewarding attention that
the manifestations receive from observers. In this way we can
understand the historical epidemics of hysteria as in the witch craze
of the sixteenth and seventeenth centuries, the outbreak of hysterical
manifestations provoked by Anton Mesmer in the 1780s, the hystero-
epilepsy of Charcot, and the recent outbreak of multiple personality
disorders and "recovered" memories. Beliefs of the patients and
beliefs in the community reinforce and sustain each other.

Harold Merskey has cogently proposed that hysterical disorders be

referred to as doxogenic conditions. His term is derived "from the
Greek doxe, meaning opinion, and genon, to produce."23 This
expression emphasizes that the patients' complaints are determined
by ideas about illness which arise from the interaction between the
patient and the culture.
 FIGURE 12. Interactive social provocations of hysterical behaviors.

Hysteria thus is a behavior resting on psycho-social foundations.

The prevalence of particular manifestations of hysteria will wax and
wane with the cultural attitudes and belief systems in which patients
are located-the very concept of "sickness" being a socially recognized
status.

Thus hysteria is a behavior "pushed" by beliefs of patients that

some medical condition afflicts them but "pulled" through unwitting
pathogenic instruction by significant social agents who believe in the
existence of processes or pathologies in the patient that need to be
identified and attended to. The beliefs of the patient and the beliefs of
the observers coincide with contemporary socio-medical concepts to
provoke and sustain "abnormal illness behavior" (see figure 12).

Implications for Diagnostic Practice

A diagnosis of hysteria cannot be settled simply by providing a

thorough evaluation of its manifestations, its provocative
circumstances, and the dispositions of the patient. Many medical
conditions that have changing symptoms and signs can be
overlooked. A cardinal diagnostic rule is: the only compelling
evidence of hysteria is the relief of its features through psychosocial
measures and countersuggestion.

This point (among others indicating the pitfalls tied to the diagnosis
of hysteria) was emphasized by Eliot Slater and Eric Glithero in 1965.
By following patients initially considered hysterical in a neurological
clinic over time, these authors demonstrated that many (certainly
more than diagnosticians can contemplate comfortably) developed
evidence of a neurological or psychiatric disease.23 The following
procedures protect against the error of overlooking a hidden medical
illness while permitting the treatment of hysterical behavior to
proceed with confidence.

A formal ward conference should be called when a hysterical

diagnosis is under consideration. At this conference all members of
the treatment team are invited to suggest any other condition-
including the most esoteric-that might be confused with the patient's
presentation. These conditions are then listed so as to identify the
noninvasive examinations or laboratory tests that might lead to their
verification. A pact is made among the group: if these diagnostic
assessments-which could include lumbar punctures, muscle biopsies,
and brain imaging-are negative, then the patient will be treated for
hysteria. This treatment will continue-without further doubts,
hesitations, and diagnostic suggestions-until either a new sign
appears (rather than a new symptom) or the patient fails to improve
within a specified period of time. The diagnostic conference should
then be reconvened and the process repeated. In these ways,
treatment proceeds and concerns about the diagnosis are
appropriately acknowledged until either the patient recovers or a
correct diagnosis emerges.

Pseudoexplanations

Hysteria is a formidable term-in medicine not only because of its

antiquity but also because of the many explanatory misdirections it
has prompted. What is most intriguing is the fundamental similarity in
the errors of explanation. They all rest on assuming that the
manifestations of hysteria reveal the actions of some inner process,
just as symptoms of a disease reveal a pathological physiology or
emotional states such as grief relate to specific provocations.

Indeed, the term hysteria is derived from the ancient belief that the
symptoms reflect uterine (from the Greek hystera) dysfunction. In one
iteration of this theme the uterus was believed to wander through the
body in search of "satisfaction," bumping against the other organs
and causing symptoms. Pressure within a bodily space invaded by a
wandering uterus was thought to explain such hysterical complaints
as chest fullness, headache, and abdominal pains.

The absurdity of the uterine explanation can divert attention from

the methodological flaw that it represents. The explanation presumes
that the expressed features of hysteria derive from some intrinsic
biological or psychological dysfunction-in the same way, for example,
that edema accumulates in the body when the heart fails. But hysteria
is a behavior, not a disease. Its features are neither signs nor
symptoms shaped by a process in patients but are representations
adopted by patients to convince themselves and others that they are
victims of some medical misfortune.

Investigators who attempt to discern mechanisms that shape

symptoms from within rather than identify a behavior from its effects
without often stretch contemporary beliefs about the body or mind
beyond bounds in proposing explanations for hysteria. Some of their
proposals turn out to be as fantastic as the uterine hypothesis, all the
result of efforts at understanding applied in the wrong direction.
Indeed, the classical explanations of hysteria follow a historical line of
descent from the wandering uterus, to possession by demons, to evil
spells of witches, to the "animal magnetism" theory of Franz Mesmer,
to the physiological propositions of Charcot, to Freud's opinion that
the features are symbolic "conversions" of sexual conflicts. A present
fashion holds that multiple personality disorder hides forgotten early
life sexual abuse by compartmentalizing the memories into "alter
personalities" through "robust repression" or "dissociation."2'27

The mistreatment of hysteria follows the same historical line,

including heating the genitals (to draw back the uterus), exorcisms to
drive out the demons, charms to protect against witches' spells,
catharsis to relieve conflicted feelings, and hypnosis to "recover" the
memories of abuse so as to "rejoin alter personalities." All derive from
the erroneous proposition that there are inner dysfunctions to be
cured rather than a belief to be corrected and a behavior to be
terminated.

The provocative psychosocial factors sustaining hysterical

behaviors are those that enhance suggestibility, make the goal of the
sick role desirable, and emphasize features that count as disease.
These provocative attitudes, beliefs, assumptions, and so on, can
derive from any source but are all of the kind that make the goal
direction comprehensible. No specific pathologies (or
psychopathologies) lie behind this behavior, no spells or demons
generate it, and no traumatic life encounters or psychosexual
struggles regularly provoke it. Its manifestations have no more
symbolic or other functional significance than is needed for patients to
find solutions to demoralization by imitating an illness.

This methodological analysis has several practical implications. If

the problem is not primarily the expression of some specific inner
pathology or psychological process but a behavioral act of a
distressed person that is prompted by belief that is enhanced by
learning, and that is rewarded by attention, then the treatments must
follow this analysis. The emphasis should not be on attempts to cure
a pathology, resolve an unconscious conflict, or bring some special
events to mind as though these were fundamental to the issue.
Rather, efforts at altering the belief in "sickness" (by some form of
countersuggestion or relearning) should be the first steps, followed by
guiding the patients toward more effective ways of managing all their
troubles.

Treatment

Before reviewing the treatment of hysteria, we should acknowledge

that a patient imitating a disease may annoy physicians more than
intrigue them. However, if those doctors can see something of the
human-indeed, the selfdeceptive and theatrical-side of these
presentations, they may be able to enjoy extricating patients from this
behavior.

Treatment of hysteria rests on persuasion and countersuggestion.

The doctor is persuading the patients that their beliefs are erroneous
and the behaviors based on those beliefs interfere with their lives. To
some extent, this is a contest of wills-a point that can be made about
the treatment of most behavior disorders. But with this disorder, the
contest is between the patient who insists that he or she has a
particular disease and the doctor who denies it. The trick is to keep
this contest of wills from becoming so confrontational that the patient
flies from treatment.

Occasionally, if doctors simply turn their attention away from the

presenting features to focus on the life circumstances of these
patients, they succeed. An example of this approach might be a
remark such as "You have been sick, but now you are recovering.
Even though full relief of these symptoms has not arrived you will not
be troubled much further by them. Now we must attend to what is
upsetting you at home so as to help you." If a patient can come to
believe that the doctor will assist with any initiating troubles, this
redirection of attention may be all that is needed.

With multiple personality disorder, the turning aside of attention is

crucial. The physicians and the nurses must not converse with the
"alternative personalities" as though they were real. Such actions
would only reinforce the beliefs and consolidate the hysterical
behavior, just as giving a white cane to a patient with hysterical
blindness would sustain that manifestation. The treatment team might
say, "We've learned it is not helpful to communicate with `alters'-you
must talk to us yourself and about the matters we choose" and then
terminate each therapeutic session until the patient learns to follow
this direction.

Patients with chronic hysteria will ruminate and expand on their

symptoms if they do not receive some response from the physicians
about their condition. We have learned that (after winning their
confidence during assessment) we can teach patients how their
condition matches the description of somatization disorder or
Briquet's syndrome found in DSM-IV. Many patients seem satisfied
that their problem is a known-indeed, an eponymous-one. They do
not sense the stigma that doctors often tie to a behavioral diagnosis.
And with this information, they usually cooperate with the therapeutic
program. After all, they have had their sense that something is wrong
confirmed, even though its therapeutic implications turn out to be
psychosocial ones rather than the medicosurgical ones they
expected.

Some hysterical phenomena need a more direct approach.

Psychosocial difficulties cannot be addressed as long as gross
hysterical features persist. Patients who writhe in a choreoathetotic
way or who cannot walk must stop the behavior before they are ready
to consider their life circumstances or their problematic dispositions.

Sometimes a treatment plan suffices in which a doctor lays out the

expectation to the patient that he or she will recover function
progressively each day through physiotherapy. This expectation can
be conveyed by the doctor's prescribing to the patient the exercises
the nurses and physiotherapists will follow. Again, the message to the
patient is that the treatment is one of rehabilitation in which his or her
cooperation is expected. We have seen the signs of paralysis
dissipate on schedule as the patient learns that the "sickness" is
acknowledged, recovery is expected, and treatment is under way.

Sometimes, however, it is necessary to enhance the doctor's power

of persuasion by increasing the suggestibility of the patient. For this
purpose either hypnosis-now used not to delve for "hidden problems"
but to increase the readiness of the patient to accept a
countersuggestion-or intravenous amobarbital sodium-given to the
point where the patent is mildly intoxicated with slurred speech-can
produce a state of mind in which severe hysterical features can be
eliminated. A patient with a hysterical paraplegia can be encouraged
to rise from the chair and walk. If such a patient can be led out into
the public to demonstrate his recovery to others, the paralysis often
will not return. The therapeutic conversation can next turn toward
those life circumstances that prompted the beliefs and the behavior
originally.

When psychiatrists assure the patient that the underlying distress

will be addressed, hysterical symptoms relieved by suggestion are
seldom replaced. This is especially true if the hysterical symptoms
have been long persistent, sustained more by the patient's need for
behavioral consistency than by a continuing life problem, and the
patient is offered through the persuasive power of countersuggestion
the opportunity to relinquish these symptoms without embarrassment.
Then, if the patient is promptly started on psychological and social
rehabilitation, the return of the expression can be prevented. Crucial
to this effort would be the diagnosis and apt treatment of any
provocative psychiatric illness such as major depression or panic
disorder that sustained the attitudes tied to the hysterical
manifestations.

The long-term management of the patient with chronic hysteria, or

Briquet's syndrome, is best accomplished by a mutual understanding
of the problem by the patient and the doctor. These patients need
physicians who can continue to be interested in them. Only a
persisting treatment program-one that promptly recognizes the
reemergence of new complaints, appreciates their source, interrupts
any precipitant such as reappearance of depression, and finds these
kinds of behavioral problems interesting-can save these patients from
needless medical and surgical interventions and bring them through
relapses swiftly and economically.

Summary

Hysteria is a behavior in which medical and psychiatric conditions

are imitated by people who, believing they are victims of some
disease or injury, generate complaints or physical signs. It appears in
two common forms: (1) acute hysteria with sudden appearance of
dramatic "signs" of disorder and (2) chronic hysteria represented by a
lifelong habit of medical complaining.

In both forms, the goal of the behavior is to persuade others to

accept the patients' beliefs in their "sickness." This concept averts
explanatory and therapeutic misdirections by putting the
psychological precipitants and the manifestations into proper
methodological alignment. The psychological precipitations and
provocations are general, nonspecific issues but of the kind for which
abnormal illness behavior and the sick role could be solutions.

Hysteria is diagnosed by an assessment of the form of the

presenting features, the setting in which they developed (including
the associated psychological or medical conditions, recent life events,
and contexts of learning or suggestion), and the dispositional features
of the patient. The management of hysteria in both its forms is a
matter of carrying out a prompt diagnosis, removing the patient from
pathogenic instruction, introducing countersuggestion, and providing
psychological rehabilitation. This last aspect of treatment,
rehabilitation, follows the interruption of the deviant manifestations by
relieving persisting distress and teaching the patient to manage
without recourse to abnormal illness behavior in the future.
Some disordered behaviors are produced when a natural drive-
hunger, sex, sleep, and so forth-is subverted, occasionally by disease
but often by experience. These we call the motivated behavior
disorders and include within them drug addiction and alcoholism as
self-induced drives.

We also recognize disorders of behavior not tied to an intrinsic drive

but learned by psychologically predisposed (usually demoralized)
people interacting with social forces (some obvious, some subtle) that
promote goal-directed actions. Hysteria is one such example. Suicide
is another in which psychological predispositions and social
encouragement interrelate. In this chapter we elaborate on this
interrelationship. Our aim is to emphasize that suicide-like bulimia
and hysteria-is a behavior in which personal choice and social
influences are enmeshed.

Definition and Statistics

Suicide is the behavior of actively seeking self-destruction. It varies

in its life-threatening intensity among the individuals who display it.
Essentially all of them are suffering from one or another psychiatric
condition that predispose them to the behavior. With many suicidal
persons a recent adverse life event has provoked feelings of loss and
hopelessness. As well there are several sociocultural and
demographic factors that add to a person's suicidal risk.

Suicide is the ninth leading cause of death in the United States. The
behavior is responsible for more than 30,000 deaths each year and
many more thousands of attempts that fail but leave patients
damaged.' Although some psychiatrists wish to place all life-
threatening behaviors into a suicidal context-an idea championed by
Karl Menninger in his book Man against Him.selfz-we hold this to be
a succumbing to metaphoric reasoning in psychiatric thought. It
glosses over how suicidal behavior is directed at self-destruction,
whereas cigarette smoking, fast automobile-driving, alcohol
consumption, and so forth have their own provocations and goals.3

In any particular example of suicide, individual and collective

proclivities tend to combine. Consequently, the attempt to make
sense of the several contributions-identifiable psychiatric disorder,
specific personal events, and sociocultural factors-has been the
regular work of psychiatrists and sociologists in this century. This
effort has produced information about suicidal patients-as well as
methods for treating them-but there has been little if any reduction in
overall suicide rates, a discouraging fact indicating we have more to
learn.

Psychiatric Factors

Psychiatric investigations on suicide have demonstrated that mental

disorder is common in both those who commit suicide and those who
attempt it but fail. Eli Robins and his associates at Washington
University did careful psychiatric histories on a series of suicides
retrospectively through family and friend informants. They discovered
that 95 percent of suicides had a diagnosable psychiatric disorder.
Major depression was the most common condition, but
schizophrenia, panic anxiety, alcoholism, and personality deviations
also occur.4

Clare Harris and Brian Barraclough, who searched the scientific

literature for increased rates of suicide among persons with specific
psychiatric and medical disorders, demonstrated such increases in
every psychiatric condition with the exception of mental retardation.5
In a companion study, they showed that with medical conditions high
suicide rates were found in those disorders either with major
depression as a cardinal symptom-such as Huntington's disease-or
with alcoholism such as alcoholic hepatic cirrhosis. They could not
conclude that suicide rates in medical illnesses were linked directly to
the physical burdens of diseases, given that there was no increase in
suicide among patients with amyotrophic lateral sclerosis or crippling
arthritis nor among those with hepatic cirrhosis based on viral
hepatitis. The seemingly burden some condition of pregnancy and the
first year of motherhood is associated with a three- to eightfold
decrease in suicidal rates.6

Many investigators of suicide have recognized that older people

appear to make more vigorous suicidal efforts than do younger ones
and that patients with certain psychiatric conditions may make more
dangerous efforts at selfdestruction than patients with other mental
disorders. In an examination of these features, Paul McHugh and
Helen Goodell graded barbiturate selfpoisoners according to suicidal
severity in a consecutive series of 100 patients admitted to New York
Hospital, where resuscitation methods were highly developed and
thus drew severely poisoned patients through the emergency
services. In this study, patients who scored highest on ratings of
dangerousness in their suicidal efforts were most commonly suffering
from a major depression and were older. Those whose acts were less
life threatening most commonly had an unstable personality and were
facing a frustrating social conflict. These psychiatric diagnoses did
not account for all the patients as a sizable number of them-varying
across severity of self-poisoning-were those in the midst of a serious
life predicament such as a major medical illness or a financial crisis.
Again, older age was associated with more dangerous suicidal
behavior in that subgroup.'

Suicide does, as many investigators have noted, involve aggression

and is often impulsively carried out, and individuals who commit or
attempt suicide do have a greater lifetime history of aggression and
impulsivity in other settings. This observation may have been
employed in the past to suggest that suicide expresses a "death
instinct."8 A better explanation of this association of aggressive
impulsivity and suicide came with the discovery that low levels of the
neurotransmitter serotonin in the brain are correlated with a
dispositional tendency to all forms of aggression including suicide.
Maria Asberg and her associates demonstrated that the
cerebrospinal fluid (CSF) in individuals who had made serious suicide
attempts had lower levels of the serotonin metabolite 5-HIAA. This
discovery, replicated both in individuals who attempt suicide and
those who accomplish it, was followed by the demonstration that
similarly low levels of CSF 5-HIAA were found in criminals and other
individuals with histories of impulsive, externally directed aggression.
These observations led to the hypothesis that a neurobiologically
specifiable predisposition toward aggression-whether directed against
the self as in suicide or against property and other persons as in
arson and assaults-may characterize these people.¢13

Further work demonstrated that postsynaptic serotonin receptors

appear to be increased specifically in the prefrontal cortex of suicide
victims, suggesting a compensatory upregulation of receptors
responding to reduced serotonin neuronal activity. These receptor
changes are even more pronounced in the ventral prefrontal cortex,
that region of the brain noted for its responsibility in inhibiting
impulsive actions. A concept of a suicidal propensity-which can be
associated with other expressions of impulsivity and aggression-is
thus strengthened by these

This hypothesis could help answer some questions that emerge

with clinical experience. For example, if the primary provocation for
suicide were the distressful meanings (correct or delusional)
assumed about life by the patient, one could explain the association
between suicide and the presence of delusional hopelessness and
self-disdain-but not why this association is weak. A more complete
view would propose that delusional beliefs act indirectly by provoking
a depressive attitude that then facilitates the expression of the
impulsive, aggressive disposition in suicide. A familial increase in
suicide might demand the simultaneous concurrence of genes for
depression and those for low serotonin activity. The need for a
"double hit" in which the onset of depression unveils the genetic
propensity for impulsivity could explain why equally depressed
individuals are not equally suicidal. A history of prior aggression and
impulsivity, as well as a family history of suicide, would indicate an
enhanced suicidal risk in any patient with depression.

A major hope tied to these studies is that pharmacotherapy,

particularly with serotonin reuptake blockade, may enhance
psychiatric treatments of suicidal behavior. A clear means of
identifying this hyposerotonergia in people generally and psychiatric
patients in particular-a kind of biological marker for suicidal risk-would
provide a means of singling out and protecting more people from
suicide. The search for such a marker, now restricted to CSF
measures of 5-HIAA levels, encourages functional brain imaging for
serotonergic activity and studies for genetic polymorphisms tied to
serotonin functioning. A neurobiological test to detect patients at high
risk for suicide would be a great boon for

As psychiatric knowledge of suicide-a behavior driven by mental

disorders and dispositions-increases, the concept of euthanasia and
physicianassisted suicide becomes more suspect. The doctors
supporting euthanasia emphasize the patient's medical burdens and
assumptions about life and death but tend to overlook how underlying
and treatable psychiatric conditions lead to these assumptions. By
overidentifying with the patient's distorted and depressive attitude
about the future, these doctors may well be encouraging both
demoralization and aggression against the self. Many euthanasia
advocates hold that the psychiatric issues of chronically, terminally ill
people are "beside the point." We obviously disagree with such an
opinion-dismissing as it does all present (and future) knowledge
about the psychiatric underpinnings of suicide. We believe that
neglect of this information turns physician-assisted suicide into a
betrayal of patients and an abuse of power.

Sociological Explanations of Suicide

 Social scientists have devoted more efforts to suicide than any
other maladaptive behavior save crime and delinquency. Major
sociocultural provocative and sustaining factors have been
discovered. To reflect on the generation and control of this behavior,
one must evaluate the sociocultural factors along with individual
psychobiographical ones.

Sociocultural Factors

Increased rates of suicide correlate with certain kinds of social

disorder. This correlation can explain some of the variance in suicide
found from nation to nation, from time to time, even from
neighborhood to neighborhood. The behavior of suicide, said Peter
Sainsbury, has an ecologic

The classic initial studies on suicide and society were those of

Emile Durkheim, a founder of scientific sociology. Durkheim's great
monograph Le Suicide was first published in 1897.19 He launched
the careful study of the social correlates of suicide in France and
described the social conditions that engender the behavior.
Sainsbury, in his influential monograph, Suicide in London, confirmed
and expanded on Durkheim's observations and concepts. In addition,
many investigators who have looked for the social contexts of suicide
in England, the United States, and Scandinavia have come to agree
that the social elements that generate suicide are similar from country
to country and from place to place.2023 We next expand on the
descriptions of Durkheim, identifying links between social contexts
and suicide.

EGOISTIC SUICIDE. By using the term egoistic suicide, Durkheim

emphasized the various social circumstances that contribute to a
morbid individualism conducive to suicide. He saw the relaxation of
value-laden social controls on people ordinarily derived from
religious, familial, and political circumstances as crucial. This
relaxation led to such individual self-absorption that life seemed
meaningless when one's hopes were thwarted.

Durkheim's evidence was the increase in suicides among those he

believed lacking in these social influences. This is how he interpreted
the higher rate of suicides among Protestants and "free thinkers" as
compared to Roman Catholics. Similarly, the increased rates of
suicide among the single and divorced as compared to the married
and especially the married with children (the more kids, up to five, the
more the reduction in suicide rates), he felt supported his view of
social controls providing protection. Harris and Barraclough, in their
demonstration that pregnancy protects against suicide, also
suggested that circumstances drawing attention to others-here a new
life-pulls a person out of self-absorption and away from suicide.24

Durkheim also noted, as some confirmatory evidence for the

influence of social forces encouraging a morbid individualism and
suicide, the prompt reduction in the overall suicide rate in a country
when the political situation called for solidarity during wartime. Then,
he believed, people faced with a common enemy came out of their
"individual shells" to support the effort-an action that turned their
attention away from themselves and toward their allegiances and
importance to others.

ANOMIC SUICIDES. Durkheim derived anomic suicides from times of

loss and social disintegration, for instance, during economic
depressions. These social periods produce unemployment,
bankruptcy, and despair. Durkheim refuted the idea that simple
poverty was the explanation for these suicides by demonstrating that
in such periods of economic depression, the indigenous or
established poor do not have an increase in suicide but that the more
affluent who undergo a loss of employment and a change in
expectations are those who show the increase.
 Further development of the concept of anomie (from the Greek
word for lawlessness) came as other sociologists expanded upon
Durkheim's initial grapplings with the idea. The concept of anomie
was extended to explain the increase in suicides in city
neighborhoods characterized by weak or absent standards of conduct
and by an increase in social isolation or social anonymity. Ruth
Cavan, for example, demonstrated high suicide rates in four Chicago
neighborhoods with shifting populations of transient males. The
habitations of these neighborhoods consisted mostly of cheap hotels
and rooming houses, where weak social links, instability of
relationships, and impersonality were the norm.25

There have been some suggestions that suicides found among

college students may be explained by a loss of social integration
precipitated on young people by leaving home and attempting to set
up life in a challenging, competitive, and somewhat alienating
environment. College dormitory life is not always the supportive and
coherent environment that is imagined by the person before
admission. Given the challenge of studies and the potential for failure,
the college setting could be thought to have both anomic and egoistic
elements combined. However, it is also true that major depression as
an illness has its appearance during these same years of life, and the
best evidence would indicate that the increase in college suicides
may not be any greater than the increases in suicides among 15- to
24-year-olds noted since 1960.26 This fact indicates that careful
psychiatric evaluations of students complaining of depression and
suicidal thinking are required before assumptions are made about the
source of their difficulties.27

ALTRUISTIC SUICIDES. The final relations of suicide to social

circumstances recognized by Durkheim were those he considered to
be socially encouraged suicides, or, as he put it, altruistic suicides. By
this concept he meant that for some suicides the force of society, and
in particular society's values and institutions, can be such as to
overpower the individual's own claim to life, engulfing him or her in its
force. This engulfment may be expressed by a feeling of a duty to
destroy one's life to support the group or the group's ideals. Durkheim
encompassed within these suicides the custom of suttee in which the
Hindu widow willingly is cremated at her husband's funeral pyre in
order to indicate her devotion to him and the hara-kiri of Japanese
samurai in disgrace with his company. In Western culture, altruistic
suicides include suicide pacts in which a female will accept death
along with her suicidal mate-an example being the consort of writer
Arthur Koestler, who took poison with him. Herbert Hendin holds, we
believe correctly, that in these pacts a man who wishes to end his life
subtly coerces a woman to "prove her love" by joining him.28.29

With altruistic suicides social engulfment transforms the patient's

consciousness, leading him or her to believe death is suitable.
Simultaneously, the society or cultural group encouraging this suicidal
activity presents rationalizations that support its subtle pressure on
the individual. Almost every culture provides such pressures,
instrumentalizing them in various forms. The contemporary exercises
of physician-assisted suicides in Holland and in some American
states are examples of this "altruism." This activity will continue as
long as the rationalizations for it can be defended-by noting general
neglect of pain and suffering in the chronically and terminally ill or
until the abuses of physician authority that the assisted suicide
represents remain unappreciated. 30

Psychiatric and Demographic Factors

Durkheim held that social factors are the exclusive causes of

suicide, but these will not suffice to explain individual cases. We have
described the psychiatric factors that surely play an important role in
every one of these circumstances. As we note in chapter 16, social
forces alone cannot provide a complete explanation for any behavior,
because although these forces play on everyone only a minority
respond. Those who do attempt suicide must have other predisposing
features that amplify the influence of social forces.
 There are demographic factors to appreciate as well. Males kill
themselves more frequently than females, older people more
frequently than younger, and urban dwellers more than rural dwellers;
individuals who have attempted suicide but failed do ultimately kill
themselves at a rate much higher than those who have never tried.31

Sociodemographic and Psychiatric Profile

The facts already discussed resolve into a profile of the individual at

highest risk for suicide: an aging male, single or divorced, living alone
in an urban district lacking much social integration, who has suffered
a setback from a prior status as in loss of money, employment, or
physical health and who has attempted suicide on at least one
occasion. If to this collection of factors are added alcoholic
inebriation, some depression, and teaching about suicide with social
encouragement, modeling, and even instructions (such as found in
Final Exit, by Derek Humphrey, wherein is described in detail a highly
lethal method of using a plastic bag over the head along with
barbiturate sedatives or alcohol and that since its publication has led
to increased suicides with this method),32 likelihood of suicide is very
high.

Evaluation, Treatment, and Prevention

Sainsbury pointed out that the sociologists' findings are not

irreconcilable with the findings of psychiatrists.33 Sociology deals
with the behavior of groups, psychiatry with individuals. Each
approach can justifiably follow its own methods and provides its own
observations. An integrated explanation of suicide appreciates both
the effects of social situations and psychological states or traits.
Treatments and preventions depend on the recognition of these
synergistic, indeed amplifying, elements.

Evaluations
 It is crucial for psychiatrists to recognize suicidal patients. This is a
complicated matter, that goes beyond our purposes to discuss fully,
but there are several straightforward points that need emphasis. An
assessment of a patient's inclination toward suicide should be a
regular part of every initial examination and of follow-up examinations
with patients who have those conditions in which suicide is frequent
(major depression, alcoholism, schizophrenia, and those who have
made a previous attempt). A family history of suicide and a personal
history of impulsivity should increase evaluative concern.

Common sense can apply in determining the extent to which this

assessment is pursued. With the initial evaluation of an individual
seeking guidance about some life conflict and more anxious for help
than depressed and demoralized, how the patient responds to a
question about plans for the future may be sufficient to indicate that
he or she is thinking in terms of living and working out the problems.
With any patient who reports depressive and discouraged feelings,
some question directed toward the patient's feelings about death
should be routine. This can take such form as "Do you still feel your
life is worthwhile?" or, more specifically, "Some people when they are
feeling like you are feeling, get the thought that if they did not awaken
one morning it would be all right. Do you ever have such thoughts?" If
the answers here are "Of course, I feel worthwhile" or " I'm not that
low, Doctor," one can have some confidence that suicide is not
imminent. If, however, the patient replies in more equivocal ways,
then a sequence of standard questions-attempting to assess the
degree of the suicidal inclination and the need for intervention-is
required.

These questions are in order of specificity and logical sequence:

"Have you been feeling so bad that you've thought about ending your
life?" If the answer is again "Oh, I am not that downhearted" or
"Things are not that bad for me, Doctor," then the physician can be
reassured and this line of questions can cease. If the answer is "Well,
yes, the thoughts do come to my mind," then the next question-
intended to assess the seriousness of the inclinations-"Have you
thought about how you might end your life?" is logical and apt. Again
the patient may reply, "I'm not that bad off, Doctor" or "Things haven't
gone that far," but other replies, such as "Yes, I might take pills" or "I
could use a gun" or even "Well, I did look into that book Final Exit,"
must be followed with some actions to protect the patient, such as
discovering whether he has pills or firearms available, and beginning
to involve his family members and other supporters in protecting him
and appreciating the distress and dangers he faces. Again, this step
may prompt some reassuring responses from the patient, such as
"These are just thoughts or dreams," but they should be followed by
such questions as "Have you tried any of these dangerous things-
taken a few pills, cut yourself, picked up a plastic bag?" Any positive
answers indicate an intensity of suicidal inclination that demands
protection of the patient and if necessary hospitalization.

As with the assessment of any behavioral inclination, no absolutely

foolproof method is available. The patient, even if asked may not
inform anyone of his or her goal. However, by asking questions of this
sort with such preambles as "I'm very concerned about your state of
mind" this form of screening exploration of the patient's thoughts
becomes routine and acceptable-a kind of good faith effort on the
parts of both the patient and the physician to reach decisions on this
important matter. Vigilance and concern by the doctor may not protect
the patient from acting on a sudden impulse, but they do turn out to
be appreciated by many patients as efforts of a protective sort.

Management and Treatment

We are dealing with a human behavior. The goal of self-destruction,

prompted as it may be by psychiatric states and predispositions, is
nonetheless one in which the will of the patient is involved. A conflict
of wills over a behavior is once again a critical issue. It emerges when
the psychiatrist evaluates the patient's state of mind and impedes his
or her inclinations. Just as with drug abuse, bulimia, and hysteria, the
patients may offer complex justifications for their actions that take
substance from the Zeitgeist. Such comments as "Whose life is it,
anyway?" reflect a common thread in behavior disorders, where the
physician's effort to thwart the behavior and obstruct the goal can be
challenged as an arbitrary imposition of moral judgment.

Preventing suicide certainly rests on a moral judgment, as do many

decisions on behavior disorders. This conflict is a regular feature of
the psychiatric treatment of behaviors-a conflict that other people may
try to join. Psychiatrists add to their moral judgment and act to
prevent suicide because they recognize the mental disorders
confusing patients and encouraging the behavior. In any given case,
the justification for the psychiatrist's efforts emerges only after proper
treatment is given to the depressive symptoms that have prompted
the suicidal thoughts and actions. Then most patients are grateful to
be alive.

However, right from the start in caring for a suicidal patient,

psychiatrists can find support for their efforts at protection. Not only
can the physician identify the mental disorder that is provoking the
behavior but most specifically with the "whose life" question, it is
usually not difficult for the psychiatrist to point out the many
individuals surrounding the patient who will be devastatingly injured-
sometimes materially, always psychologically-by the patient's death.
Any psychiatrist who has had a patient commit suicide can describe
the grief and sense of regret that such a death evokes in
everyoneincluding the doctor.

There are many zealots for patient rights to suicide, even some who
turn to their own personal experience and claim that they were
unfairly thwarted from death-a death they still claim they should have
achieved even as they now are active in a productive life and no
longer suicidal. We see these claims for a right to suicide from these
people as most paradoxical.
 However, we are not surprised that such proposals circulate around
this behavior just as they do with drug addiction and sexual
paraphilias. Behavior disorders and their treatments always provoke
conflicts of opinion among psychiatrists, patients, and others.
Psychiatrists work to redirect-more specifically convert-patients from
a destructive line of reasoning: one that may be supporting
addictions, paraphilias, eating disorders, or suicide. We can be called
upon to defend our opinions-why, for example, do we not offer free
access to addictive drugs, liposuction to anorexics, or death to the
depressed and demoralized? Long experience has taught us that if
our profession supports these behaviors as rational, it misleads
patients, misdirects the public, and collaborates with the pathologic
social forces that encourage them.

The treatment measures for suicidal patients go on simultaneously

with these management issues. The treatments are directed first at
any major disease that may lie behind the behavior, such as major
depression or schizophrenia. A consideration of an impulsive feature
along with depression would logically prompt the use of serotonin
reuptake inhibitors. But, as well, much psychotherapeutic efforts of
the cognitive-behavioral kind are crucial here and will reveal the
distortions of attitude and presumption that patients have either
developed on their own or, more likely, picked up from the models
and instruction about the act of suicide from their social environment.

Treatment of a multifactorial kind that combines psychotherapy and

pharmacotherapy is critical given the evidence we have. The
separation of the two forms of treatment-psychotherapy and
pharmacotherapy-into different hands and different professional
services may endanger suicidal patients, especially if launched early
in the evaluative and therapeutic processes. This practice of
separating psychotherapy and pharmacotherapy may be now
mistakenly encouraged by economic forces of "managed care" and
be still another social process endangering vulnerable people.
Protective Actions

In considering a human behavior in which goal directedness and

impulsivity combine to end a life, then measures to impede the
behavior or make it temporarily impossible are crucial. After all, a
mistake in this matter is permanent. Gun control and particularly the
removal of firearms from the homes of potentially suicidal people are
obvious steps for psychiatrists. Moreover, advocacy for social policies
that remove lethal means from households is a logical practice of
psychiatrists.34 They can point to the clear evidence of a reduction in
suicide in Britain when poisonous carbon monoxide gas was removed
from the municipal supply of cooking gas.35 Placing obstacles in
public tall buildings and other high places has been criticized as just
sending the suicidal patients to other settings for their acts. But
certainly these obstacles have impeded the sudden impulsive suicidal
act, have occasionally permitted a rescue as a patient struggles
around an obstacle, and as Herbert Hendin pointed out, have
provided a clear statement that our society does not encourage
selfdestructive behavior. A similar concern for patients leads to the
screening of stairwells in hospitals and clinics.

Psychiatrists should recognize how modeling and instruction act to

encourage suicidal behavior, just as they do other forms of behavior.
They can then challenge these examples of persuasion wherever
they appear. Confronting the misdirected authors supported by the
Hemlock Society with the damage they have done will help. Similar
challenges to suicidal instructions can come from calling attention to
Hendin's demonstrations of how "physician-assisted suicide" has led
to abuse in the Netherlands.36 It may be enough to point out how
these practices bring out the most ferocious forms of paternalistic
attitudes in doctors. Knowledge of the care available for the terminally
ill in hospices, where psychiatric distress is directly treated and pain
and discomfort minimized, can also prove reassuring to members of
the community who are being frightened into suicidal planning by
false assumptions about the management of dying.
 Psychiatrists can help bring information about depression to
everyone in the society and how this mood disorder often is at the
root of suicidal behavior. They should teach people to realize that
depression is a disease of nature, that it is often associated with an
irrational view of the world, that it is eminently treatable, and that, far
from an indication of some lack of moral fiber, it is a condition that has
afflicted some of the heroes and heroines of our civilization.37

Summary

All psychiatric disorders, with the exception of mental retardation,

are associated with some increase in suicide. Depression,
alcoholism, and schizophrenia have the highest rates. Those
neurological and medical conditions with high suicide rates are those
that either encompass within their symptoms a depressive syndrome
or are themselves products of alcohol abuse.

Two psychiatric features tend to combine in successful suicides.

One feature derives from the mental disorders themselves; the other
is a disposition toward aggression and impulsivity correlated with low
brain serotonin. Therefore, both of these features should be sought in
patients who are being evaluated for suicide. The potential for a
biological marker for suicide risk was noted.

The social circumstances encouraging suicide, first recognized by

Durkheim, still exist and still do their damaging work. They are a
constellation that either deny patients social support or encourage
them in their suicidal thinking. "Physician-assisted" suicide is simply
our culture's form of altruistic suicide.

Suicide remains a great personal tragedy of many psychiatric

patients. Progress in its study will eventually arm psychiatrists with
more understanding and with the means for treating it. However,
much of the difficulty and controversy that surrounds suicide will not
disappear with more information. These controversies come directly
from its nature as a behavior. Many of the issues-conflicts of will,
moral judgments, and social challenges-have been seen in the other
behavior disorders and included in discussions of them.

Behavior is a special arena of concern for psychiatrists, and until

there is greater social uniformity of opinion about humankind and the
place of personal responsibility and social influence in the way lives
are led, the treatment of behavior disorders and their identification as
abnormal will remain contested. These are not conditions that
psychiatrists are trying to cure; they are behaviors they are trying to
stop provoked by attitudes they are trying to change. Moral
judgments are involved and cannot, indeed should not, be ignored.
Psychiatrists, who can appreciate these issues as embedded within
the behavior perspective are not surprised by conflict. They act in
society's interest by explaining to the public exactly why their
treatments and managements of suicidal patients afflicted by the
dangerous combination of mental disorder and social influence are of
the kind they are.
So far we have drawn from sciences such as pathology,
psychometrics, integrative physiology in explaining disorders of
mental life. However, when faced with patients who are grief stricken,
demoralized, angry, and so forth, psychiatrists, usually without
reflecting on the process, use a method of explanation quite distinct
from that of science. They fall back on the most natural method of
reasoning humans have: they explain the problem with a story. That
is, they see the patient as a subject responding to a set of
circumstances and understand the distressing symptoms as reactions
to misfortune.

Where do they get this approach and any confidence in its

conclusions? A narrative is often the first way we explain almost any
set of unfamiliar events to each other. And, of course, storytelling and
epic writing are ancient ways of teaching and explaining human
experiences and how life events shaped them. But-and surely it is a
telling point, obvious once made-this method of explanation, through
the composition of a story of setting, sequence, outcome, is the
method of historians, taken up by psychiatrists because it is a natural
way of understanding someone else.

In this chapter we review the distinctive characteristics of historical

reasoning and show that the life-story approach in psychiatry is
essentially the same method. We teach how to identify this method in
all of its presentations and as well reveal how the method
psychiatrists employ most easily and with many advantages has
particular complications long known to historians.

Life-Story Reasoning Is Historical Reasoning

 Historians offer compelling explanations of human thoughts, plans,
and behaviors, which indicates that natural science is hardly the only
source for helping people understand one another. Modern German
philosophers have differentiated scientific from historical explanations
terminologically as erklaeren and verstehen ("explanation" and
"understanding," as these words are usually translated). These
terminological distinctions, the subtleties of which go beyond the
scope of this book, do emphasize that in studies of human beings-
their actions, motives, and consequences-an apt mode of explication
distinct from that of the scientist has always been at hand.

By employing a historian's approach to the crucial features of the

subject's life, a psychiatrist can make some sense of the subject's
psychological distress and complaints and even render them obvious
outcomes, sometimes inevitable, given what is known and
emphasized. This understanding, transmitted from psychiatrist to
patient as a set of interpretative explanations during psychotherapy,
can provide information useful in avoiding similar, emotion-generating
conflicts in the future. The historical method, however, is not without
its own problems. These very problems are not avoided, and may
indeed be enhanced, when psychiatric topics are addressed.

The Historical Method and Its Implications

Ingredients

What do we mean by history? Historians seek to learn the facts and

reason about the past so as to explain how things came to be. At first,
they bring no special faculties or techniques to this enterprise-no
microscopes, no chemical analyses, no X rays-but rather work to
develop as skills those rational faculties available in anyone. These
skills include collecting facts, differentiating significant from
insignificant past events, and distinguishing familiar from unexpected
outcomes. 1-3
 Historians also identify and take note of influences such as the
economic, geographic, and cultural forces that shape the flow of
events in a crucial fashion. They mark particular leaders who direct
history in one way rather than another. From these efforts, historians
transmit their knowledge to students through compelling narratives of
settings, sequences, and outcomes. The composition of these
persuasive historical narratives depends on a capacity for judgment,
a weighing of alternatives, and a critical stance toward the sources of
information and the conclusions. Always, whether in describing or
explaining, the historian holds up facts and processes that illuminate
one another. Satisfying historical narratives are those that make
sense of situations and outcomes by demonstrating aspects of
human nature and responses to circumstances with which, on
reflection, we can all identify. We hear and we understand.

All this is not without two major problems. The first is that the
historian has difficulty extracting personal biases from narratives. The
second (actually an aspect of the first) is that the identification of the
force or energy directing the course of historical events-that gives the
account momentum along the way, marked in the narrative as setting-
sequence-outcome-can seem arbitrary, inadequate, or even contrived
to make the narrative plausible.

History's First Problem: Bias

Consider first the issue of bias. Every historian's narrative

explanation depends on the arrangement and differential emphasis of
many facts from the past. The narrative is constructed to make a
point; it does not simply emerge from the facts. As the distinguished
historian Pieter Geyl pointed out (in his book Napoleon: For and
Against), the result is that history can seem "an argument without
end" among individuals, each of whom is passionate about one point
of view but blind to some other aspect of the past.4 Most historians
when revising a prior point of view on an epoch revisit the source
material and amend the narrative line-thus altering our attitudes
toward and in some sense our relationship to people influential in
history.

Revisionist historians may base their efforts on a careful restudy of

the documents from the past, recognizing previously ignored nuances
in them-as, for example, did the British historian A. J. P. Taylor in
composing his controversial book The Origins of the Second World
War.5 Other historians may take up a new attitude toward a historical
and previously esteemed figure because of their passionate
conversion to some new tenets with contemporary salience. An
example is the recent demeaning of Christopher Columbus and his
voyages of discovery because of their devastating effects on Native
Americans.

The realization that narratives may shape attitudes in ways that

others deplore can often provoke anger and rejection of a new
history, even when a historian is just bringing out a few previously
ignored facts about an event. For example, in 1995 the Smithsonian
Institution's Air and Space Museum, in a fifty-year retrospective study,
attempted to launch an exhibit encompassing the complex attitudes
felt by American leaders about the wisdom of using the atomic bomb
on the city of Hiroshima. The curators brought to light official memos
of the time demonstrating that moral concerns weighed, admirably
one might say, on the President and the Secretary of War. But a
public protest to ban the exhibition was led by some World War II
veteran groups who believed this exhibit challenged the rightness of
the final decisions. This protest ultimately employed political pressure
to deny the presentation of the exhibit-pressure that eventually cost
the museum director his job. Such was the fear of a historical review
that would add nuance and greater understanding of this crucial
event of World War II, an event with profound effects on the postwar
world.6

History's Second Problem: Causation Contrived

 History is not a science; nor are the standard skills of a historian
truly scientific. But these are earnest skills-those of a craft demanding
a critical and trained intelligence applied to matters of perception,
memory, attitude, and no small dose of skepticism.

The historian customarily acquires and then arranges, contrasts,

organizes, and processes past events into some form of narrative
ultimately reducible to setting-sequence-outcome. A good portion of
the "argument without end" derives from the emphasis given by the
historian to forces that purport to explain how the sequences followed
one another and led to the outcome.

For some historians, an interest in such a deeper explanation is

weak-they may even suspect the interest as a source of bias-and
thus their narratives are more like chronicles of events in which one
leads to another in some temporally linear path along which accidents
and chance tend to dominate the outcome. Other historians place
their emphasis on personal causal forces such as the motives and
character of political leaders-the will and ambition of Napoleon, for
example-as giving the direction to the course history has taken and
the sequence of events that has been compiled. Still others
emphasize as deeper causal forces aspects of culture and cultural
attitudes-such as the role of the Protestant ethic in the rise of
capitalism in Europe as it provided the moral fiber that sustained the
laws of contract essential to the contemporary economic system of
the West.

Finally, there are those "ultimate historians"-separate from the

specialistswho offer to explain the general causal forces that direct
history overall, that are represented in the outcomes of all cultures of
the past, and that can be adduced in the present and contemporary
culture with predictions for the future. The best representatives of the
ultimate historians are Karl Marx and Arnold Toynbee. Marx
emphasized the modes of production as generating the relationships
among people, giving dynamic force to their conflicts and, ultimately,
as capitalism followed feudalism, leading to revolution and
communism. Arnold Toynbee saw common features of growth and
decay in every civilization, a kind of pattern in history within which
certain stages or recurrent "rhythms" of response to challenge can be
recognized. He used this perspective to make sense of contemporary
events and to predict the future of Western civilization. Both Marx and
Toynbee conceived of their roles as analogous to that of Charles
Darwin, who explained the diversity of biology and anatomy from
evolutionary theory. They explained the diversity of history from some
pervasive power over humankind. Both of them saw the fundamental
problem for history as discerning the force that gives it direction.

Leo Tolstoy (see the second epilogue in War and Peace) thought all
these efforts of historians at defining the force behind the sequences
of recorded events in history were failures. "What force moves the
nations?"7 he asked, and he concluded that no one had succeeded
or would succeed in defining a power behind the immense variety of
human choices and behaviors that history records. The critical point
for us is not who is right and who wrong, nor what is the penetrating
approach to causation and what is the trivial, but how historians hold
various views about the causal heart at the center of a historical
process. Each one of them can quicken our interest and draw our
attention to a set of events-appreciated as setting, sequence, and
outcome-especially as they emphasize aspects that others did not
and even when they also turn out to need correction.

Persuasion as a Historian's Intent

No one could hope to understand humankind without the help of

historians. Yet everyone who studies their contributions recognizes
that an understanding of history and humankind is a method prone to
advances and retreats, assertions and retractions, emphases and
corrections. Its power depends less on facts or data and more on
interpretation, emphasis, and persuasion. "History," said Ved Mehta,
"was not objective (possessing a hard core of facts) but subjective
(possessing a hard core of interpretation). "8

Historical opinions have not all stayed at home in books and in the
schoolroom. They have had their own effects on history itself, in the
work of Karl Marx such a powerful effect that governments and
nations have been created and destroyed because of his
interpretations of what lay behind settingsequence-outcome. Thus,
many a historical narrative, deriving coherence from how it deciphers
human relationships and what it claims about them, actually does
more than inform readers. It is concerned with persuasion, a
transactional function that by changing people's understandings and
relationships with the past can alter the way they will act in the future.

Recapitulation

History is an approach to understanding human affairs that is a craft

rather than a science. It functions by seeing linkages between
settings, sequences of events, and outcomes and by drawing out
those linkages in narrative form. However, no historical narrative is
complete. All the facts can never be known, many of the source
documents can receive different interpretations, and with the
exception of the simplest of narratives the forces connecting setting,
sequence, and outcome are myriad, many obscure, and all debatable
in priority.

From these qualities springs the idea that history is ever an

argument without end. Nonetheless, most presentations of the
argument can approximate the truth and, at least for a time, have
powerful effects on all of us. Although it may not be their paramount
purpose, many historians-far from content with providing a body of
information about the past-intend to provide interpretations and
dramatic narrations that will have an effect on the present and the
future.
 It is our point in the rest of this chapter that the skills of the historian
are employed by psychiatrists in the life-story perspective to acquire
information and to illuminate the setting, sequences, and outcomes
behind the distressing symptoms experienced by the patient. In a
real-not an analogous-sense, psychiatrists using this perspective act
as personal historians to their patients intending to influence them
and their future. As such, they should understand that narratives must
rest first and foremost on the careful identification of the biographical
facts of the patient. But even then the narratives may provoke
arguments over an arbitrary selection and emphasis among the facts
and over conclusions that depend on presumptive forces that cannot
be objectively documented. However, psychiatrists also understand
that this method permits them to appreciate aspects of human life not
obvious to science. Moreover, it provides them with a natural path for
their paramount purpose: launching psychotherapy and so relieving
distress by altering the present and the future life of the patient.

A Natural Process of Psychiatric Explanation

Patients ask their physicians to explain their mental distress. In

practice, psychiatrists work first to acquire information about the
backgrounds, life experiences, and mental states of patients. Then
they may discover that a story provides a useful way of tying these
facts together. Easily, directly, and with nothing added, just arranged
into setting-sequence-outcome, a story can seem to flow out of the
information acquired (see figure 13). This is particularly true for those
mental states of discouragement, disappointment, worry, and
frustration that Jerome Frank tied together under the felicitous term
demoralization.9

For example, a psychiatrist treating a patient who complains of lack

of confidence and withdrawal when faced with new challenges as
from school or employment might indeed feel that this was an almost
expected outcome if she discovered that as a child the patient was
harshly criticized by perfectionistic parents so that he never felt he
measured up to their expectations. The quite simple story with a
childhood setting and sequence and their psychological effects
(outcome) provides a persuasive understanding of the problem. In
more complicated stories, the disrupting sequences may derive from
the person's wishes and attitudes. A lonely young man who frequently
is rejected in his courtship efforts turns out to be clumsy in
interactions with young women because with each encounter he
suffers from ambivalent attitudes, looking for companionship but
fearing intimacy and its power.

The story method permits the psychiatrist to apprehend and

describe human distress by identifying the person in a life-a person
with particular characteristics and with particular intentions and thus
with particular vulnerabilities. Such stories will customarily describe
some role for the patient in the generation of the problem. All this is to
say that a story, with its ingredients of setting, sequence, and
outcome, particularly as these are given direction by the patient's fully
conscious or less clearly sensed intentions or assumptions, can be a
powerful way of comprehending many states of distress. This is
particularly true of those states that are the universal human forms of
distress, such as grief, homesickness, or jealousy, where the simplest
arrangement of setting sequence-outcome is readily comprehended.
The story is a coherent way of knowing these experiences for the
human plights they are.

FIGURE 13. Narrative triad and presumptive forces in life-story

reasoning.

Power
 Every person is a story, and every story has the capacity to teach
something about every one of us. There are as many stories as there
are lives, and there are many stories within each life. The particular
story that will be chosen by a psychiatrist, of course, is one thought to
illuminate the clinical issue at hand. Again, this can be an obvious
story, such as that of grief emerging from loss of a cherished person.
When it is so obvious, there is usually immediate confirmation and
support of the story from the patient and from others. The
psychiatrist, like the historian, tries to fill in the gaps in the narrative
when connections of events to outcomes are not obvious. The aim is
to help the patients make sense of their suffering. Sometimes the
best and most acceptable story is hard to find; then there may be
disagreement between patients and physicians about what should be
emphasized and what changed.

If the person, the person's intentions, and their effects on setting,

sequence, and outcome are the ingredients of psychiatric life-story
reasoning, the power of conviction-the illuminating and irresistible
belief in the inferences of the story-emerges from its narrative line.
The narrative carries power because it gives its selected facts and
sequences of responses a sense of inevitability.

Occasionally, someone develops a hypothesis from a specific

individual's story and tests it on numerous subjects through the
empirical-deductive method of science to find how good a
generalization it is. But this is rare and never the source of the same
feeling of conviction. The story, with its interpretation of the person in
a life of intentions, assumptions, and conflicts, is powerful and
persuasive simply because to the listeners the story "makes sense."

The art of telling the best story for a particular patient often depends
on a capacity for imaginative reconstruction of his life circumstances,
his "assumptive world,"10,11 and his deepest wishes, hopes, and
fears, a faculty richly developed in Freud and expressed in
paradigmatic stories of psychoanalysis such as those of Dora and
Little Hans. Such a skill can be taught, improved with practice, and
helped by supervision from experienced psychotherapists.

What stories tend to be told? Stories usually take advantage of

themes that can enhance the plausibility of their linkage of setting-
sequence-outcome with an easily recognizable force giving it
direction. Thus, the concept of development, so crucial to our
understanding of motivated behaviors and so obvious an aspect of
human life, can be employed in the simplest vignettes of maternal
separation and childhood distress, of pubescent shyness and sibling
rivalry. More elaborate and more problematic stories derived from the
same source might link a young woman's anorexia nervosa to her
unwillingness to face the challenge of sexuality, to her rejection of her
mother's care, to her primitive views on conception, or to any other
such conflict with the power of biological development and its social
implications.

What is sought as a story is what can fit, illuminate, and, most

crucially, be accepted in sustaining an interaction between patient
and therapist. In this regard, plausibility is certainly as important as
historical truth-an issue noted most clearly by Donald Spence, who
would differentiate "narrative truth" (what makes sense and is useful
in therapy) from historical truth (which may never be

On the other hand, this is a formula for an argument without end

because if the truth is not established, the narrative that will win out
will be that told by the most powerful of authorities or supported by
the powerful ideologies of the times. The struggle to define a
presumptive force behind the elements of setting-sequence-outcome
has been and remains today the major source of contention in
psychiatry and is the cause for its division into camps of one school of
psychotherapy after another.

Finally, a successful, persuasive story explanation will not stay in

the mind of the psychiatrist but will be transformed into a treatment
program for the patient. This, after all, is the whole point of the
exercise. The treatment will rest on the issues that the story brings to
light-particularly those issues and distressing outcomes that the
patient played a role in generating. The patient's role, expressed
through intentions felt, assumptions sustained, and obstacles
unresolved, are revealed best through the life-story perspective. With
this appreciation and with further help from the psychiatrist, the
patient can revisit and revise those intentions, alter the assumptions,
make more effective decisions, and take charge of his or her life.

Comparison with Historical Reasoning

It is now worth reprising the identity of the life-story method with

historical reasoning. In both there is the attempt to make sense out of
situations by bringing to light issues that preceded them and may
have provoked them. Life stories work well in attempting to explain a
specific happening and are much less successful in finding general
laws that explain all happenings, even similar ones. That is, the
psychiatrist with the life story may understand a particular case of
depression but will not discern from this method some general cause
of depression. Likewise, historians may grasp some of the causes of
a particular war but are mostly ignorant about the causes of war in
general, as Tolstoy repeatedly proclaimed.

In the process of attempting to understand patients, psychiatrists

find that using this method does encourage their development of
skills in assessment and inquiry about the facts. For psychiatrists
these skills include those needed to put patients at ease so as to
draw out their feelings and assumptions in relation to the facts. But,
as well, the psychiatrist must retain the critical attitude necessary to
judge the reliability of the patient's reports of the facts and what
further efforts must be made to confirm them.

Eventually, with this information the patient "comes alive" as a

person in a world for the psychiatrist, just as a historian permits us to
see the people of the past as struggling like us with the forces of
nature and society. People understanding other people is the
essence of this method whether used by psychiatrists or historians. In
matters of credibility psychiatrists and historians sharing the same
method carry the same burden. They must be prepared to defend the
factual foundations of their opinions, describe how these facts were
ascertained, and revisit them if challenged.

When the interpretations of psychiatrists or historians-making sense

of setting-sequence-outcome-are simple, they provoke little
controversy and receive general acceptance. When, however, as in
more complex clinical or historical situations, they introduce
interpretive schemes resting on underlying theoretical and thematic
forces (for example Freudian forces in psychiatry, Marxist forces in
history), then for all that the story can be enriched with coherence
these interpretive emphases provoke questions and disagreements
fundamentally impossible to resolve by this method alone. Arguments
resting on power and plausibility (usually translated into compatibility
with the ruling fashions) will usually persist "without end." Just as
Tolstoy noted that there was no single satisfactory answer to his
question "What force moves the nations?" so we must admit that
psychiatrists of our century trying to find a single answer to the
question "What force moves mankind?" have succeeded only in
disagreeing.

Finally, because this method depicts aspects of human nature and

the plights we are all heir to in a way no other method can match, the
opinions generated do not rest in sterile repositories but are pressed
forward by their authors in efforts to persuade listeners to understand
their implications and act on them. For a few historians-a recent
example is Michel Foucault 15-this can go so far as to encourage
social change, even revolution. For psychiatrists, this persuasive
aspect of the method is the purpose of the exercise. It is employed in
building and forwarding a therapeutic plan by which a person can
take the interpretations of the story as appropriate explanations for
present troubles and use them to rescript his or her attitudes and
approaches to the future. A state of demoralization explained as an
unintended consequence of now understood psychological forces is a
state that can be overcome and replaced with a sense of mastery and
control in the future.

For all these reasons, we hold that psychiatrists and historians use
the same method. Some psychiatrists detect a nuance of
disparagement in the term story, but we chose it primarily to draw out
the nature of the process of explanation employed by masters of the
narrative in the clinic as well as the history classroom. We wish to
emphasize narrative itself-its strengths and drawbacks. It is to these
that we now turn.

Strengths

It is easy to appreciate the power of the life-story method, a power

that links the self, its intentions and assumptions, with their
consequences. To see these playing out their themes in a narrative is
to see them in the most natural way. In a clinical story almost any
psychological feature can be employed to make a narrative
meaningful. The elements of mental life that we have considered
previously, such as the subject's distinctive temperament, cognitive
capacities, or motivations, add clinical comprehensiveness to the
story. These phenomena become part of the characterization of the
person and help to clarify aspects of the person's intentions and
assumptions. As well, the onset of some diseasemedical or
psychiatric-can be crucial in a life story, and the whole purpose of the
story would then be to appreciate how this illness is affecting this
particular individual and how to help the person manage it better.
Demoralization can come from many sources, and the life story can
be combined in a formulation of explanation that can take these other
perspectives of psychiatry into account.
 A story is a vivid way to capture a part of reality, reality as it is
experienced and lived. No other method can give this sense of
immediacy. In addition, the story provides for the sense of complexity
in mental life. Because stories are endless in their variety, they are
immune to the criticism that "things are more complicated than any
science can imagine." If such a point is made about a particular story,
it is answered with a more detailed narrative that further develops the
various themes in the story's plot.

The story is the best way to enhance our natural sympathy for the
patient because it views the patient as being caught up in life's
processes. Our ability to help her and even our desire to help her
depend to a considerable degree on this response. No alien object is
the protagonist of the story; the patient is always a person like us,
with hopes, fears, and intentions that affect the person's future. The
story provokes optimism in both the patient and the therapist. After all
if the decisions of the self were in the past influencing the succession
of events that provoked the problem, then efforts to alter those
decisions in the present can generate a different succession of
events solving the problem.

The story usually fits the times, a characteristic that can account for
both its contemporary persuasiveness and the eventual replacement
of one story with another. Some of the power of the Freudian vision
rested on its mixture of classical mechanics, romantic imagery, and a
secular worldview compatible with the attitudes of the liberal
intellectual middle-class community of his time. That the Jungian
analytic psychology was less popular originally may be attributable in
part to its unfashionable emphasis on the mystical and the
supernatural; yet now many people find insights about their lives in
the Jungian conception.

The story method is being proposed at a time when physicians

claim the importance of appreciating the "whole" patient or "holistic"
medicine. It is clearly an improvement in our understanding of any
individual to see not only the diseased state but also the person's
sense that she is in the midst of a crucial situation in her life. Holistic
medicine is fundamentally the combination of knowledge of the
patient's disease and personal story. By giving the patient time to tell
the story as she sees it, and through an appreciation of other stories
like hers, the physician can understand and assist the patient with
emotional and behavioral reactions.

Drawbacks

The drawbacks of the story method are largely the obverse of its
strengths, as might be expected. First, the patient's story is
appreciated and written by authors who see and hear from the patient
some things and not others. The story method brings out professional
conflicts in a way other methods do not. This phenomenon certainly
contributed to the remarkable personal animosities between Freud,
Jung, and Adler. Similarly, not only do observers of psychiatric
practice hold that what story you find in your patients determines
what type of practitioner you are (Freudian, Jungian, and so on), but
also it can sometimes seem that opting for the story method can mark
you as a good psychiatrist in some communities and a bad
psychiatrist in others.

Next, psychiatrists are not immune to the herd instinct that can
bedevil all storytellers. They may see forces in their patients that
others tell them they should see. Psychiatrists, like journalists, may
repeat a version of the same story on occasion after occasion
because a harmony with the spirit of the times may be as crucial for
therapeutic purposes as for satisfying publishers and editors.

Stories are encountered, written, and experienced. They are difficult

to refute or even to challenge. The story is often crucial to the
psychotherapeutic process, but whether the particular story is more
important than the sense of caring and optimism in the practitioner
(perhaps generated by this commitment to the story he or she tells)
has been difficult to determine. The work of Jerome Frank again
suggests that it is more the sense of caring a story brings that counts
in therapeutic success, not the historic accuracy.

The story presents us with a dictum about the patient. It may disrupt
rational argument because criticism of its logic or complaints about its
biases can be interpreted either as missing the point or as
"resistance" on the part of the critic. Nonetheless, the story method is
vulnerable to two potential errors: the choice of the story method
rather than another category of explanation, and the choice of an
erroneous story by getting the facts and linkages wrong in the
patient's life.

The erroneous choice of the story perspective for a patient with a

disease does more than deprive the patient of the strengths of the
disease method (specific treatment and prognosis); it burdens the
clinical situation with the limitations of the story method without
conferring its advantages. The most obvious of these limitations is felt
by members of the patient's family. Because of its power to create
symbols, the story can transform relatives into passive figures or role
players in the patient's life story, a transformation that renders them
relatively impotent in contributing to the patient's recovery. They may
sense a collusion of patient and therapist in an interpretation of all
their actions and opinions. They often feel trapped by a set of
conceptions about them that treats, by a kind of "looking-glass logic,"
each of their efforts as an expression of the same predetermined,
story-designated role. The resentments and sense of ill usage that
this application provokes injure the network of support the patient with
a disease needs to carry through the illness and convalescence.

A similar set of problems can be felt by everyone if an erroneous

story is asserted and then sustained by theory. The recent craze over
"recovered" memories as a way of generating a story to explain
patients with depressions and eating disorders revealed this problem
most vividly. The therapists, always insisting that it was not their
obligation to find the "truth," nonetheless took very susceptible
patients and told them that their symptoms were the outcome of a
setting of severe sexual abuse during their childhood, the memory of
which they had "repressed." These stories themselves then produced
distressing emotions in the patients that were interpreted by the
therapists as "to be expected with realization of your betrayal." Long
periods of therapy and long arguments over matters of interpretation
especially by those falsely accused produced still more hardship. The
accused faced the difficulty of "proving the negative" even as every
effort on their part to do so was again interpreted as efforts at
"denial." This was an example of the story method run wild, and
resolutions did not come until the patient left the therapist and began
to rebuild a coherent understanding of the problem.

Summary

The purpose of this chapter has been to introduce the simplest

ingredients, along with some critical interpretation, that distinguish the
method of the lifestory perspective. Recognizing it as a form of
historical reasoning makes clear the source of some of its power and
its problems. This method will give the clearest understanding of the
fellow-suffering of our patients and help us relate to them
therapeutically. On the other hand, it is not a scientific method from
which we can expect a steady advance of general knowledge and
new, irrefutable discovery. It is a method that can provide great help
to patients, even though it also can provoke disagreement as one set
of interpretive schemata battles with others in a never ending
argument over truth and values. Once it is appreciated that the life-
story perspective uses the method of historians, then several
implications are obvious-implications that must be drawn in order to
employ this perspective appropriately both for the patients and the
profession.

First and perhaps most critically, as implied by the terms setting,

sequence, and outcome-and depicted in figure 13-the story organizes
information in a linear, temporal chain of events. Although the
outcome may provide a setting for a subsequent sequence, knowing
the outcome does not permit the psychiatrist to know the original
setting or sequence. In contrast to the bidirectionality of the
information that forms the other three perspectives, one cannot be
sure in the life-story perspective how the outcome was generated
without some separate investigation to determine its antecedents.
With this method, it is critical for psychiatrists to learn how to access
the factual past of the patient with accuracy in composing an
appropriate story. This, of course, is exactly the demand of any
historical discipline. The investigator must make some reason able
effort to determine the facts on which he or she will ultimately build a
narrative. Psychiatry, like history, is full of examples where
assumptions of the facts-from unreliable sources or through a
commitment to theory-led to a mistaken point of view and a
misdirected narrative.

More detailed aspects of the method and particularly its application

in psychotherapy are the subject of the following chapter.
The life-story perspective provides both an understanding of
psychological distress and an ingredient for psychotherapy. How can
a method lacking much of a scientific foundation (and so vulnerable
to bias) deliver these practical benefits? The answer to this question
emerges as one considers what emotionally distressed patients need.

The life-story perspective presumes that much distress stems from

events. The support for such a premise is plain. Grief surely comes
from loss, homesickness from displacement, and discouragement
from failure. At the same time, psychotherapists assume that patients
benefit from those interpretations of their mental woes that help them
understand and surmount them. Again this assumption seems
straightforward. Resolutions are better than predicaments.

Nonetheless, deciding which patients need psychotherapy and

which system of life stories to choose-Freudian, Jungian, Adlerian,
and so forth-are issues that remain ambiguous and debated. We
hold, as we explain in this chapter, that every psychiatric patient,
regardless of the basic nature of his mental condition, can at some
time in the course of his disorder profit from psychotherapy. As well,
the particular version makes less difference than the patient's
reassuring experience, developed during therapy, that an expert in
psychological maladies knows that some aspects of his condition are
treatable. These matters of the appropriate patient and the
appropriate story are far from straightforward.
 The Patients

Because the life-story perspective presumes distressing mental

states to be the outcome of life events, this perspective and its
therapeutic procedures can be combined with the perspectives
previously discussed. That is simply to say that disorders tied to
diseases, dimensional vulnerabilities, or behaviors are themselves life
events with distressing implications. For example, the diagnosis of a
disease such as manic-depression in any patient is a significant
incident with discouraging connotations. For this reason, a
psychiatrist not only must provide such a patient with the apt
medicinal treatments for the disease but also must provide her with
practical psychological support during an attack. This support
includes differentiating for the patient those emotions that are
symptoms of the condition and those that are responses to reflections
on their implications. After an attack and during a remission, the
psychiatrist must help the patient place this problematic matter of a
remitting and relapsing condition into her life in a way that minimizes
its damage and abbreviates its recurrences.

By teaching the patient about this disease, the psychiatrist can help
her develop a coherent life plan that will take her vulnerability into
account and at the same time not overstress it to the point of
invalidism. In this process, aspects of the patient's personality, life
circumstances, and support (family, work, and education) can be
reviewed, considered as sources of vulnerability or strength, and if
necessary reordered with advantages. This form of psychotherapy is
fundamentally a rehabilitative effort-Samuel Guze referred to it as
rehabilitative psychotherapy-that attempts to help the patient manage
her life and future as she recovers from her illness.'

In a similar fashion, psychotherapy based on the life-story

perspective provides a means of educating and guiding patients
vulnerable to distress and disorder because of their dimensional
vulnerabilities. Such psychotherapy will emphasize how unreflective,
emotion-laden, habitual responses to circumstances in the past have
led to unintended consequences that might with reflection be avoided
in the future. The psychotherapy of the behavior disorders also will
use the life story to remind patients of past choices and past disasters
derived from succumbing to addictions or from venturing into
circumstances that provoke their cravings. The story will be a crucial
way to move the patients through the contemplative and toward the
action phase of their recovery by helping the patients see just how
they have chosen their behavior path in the past.

Beyond adding to the other perspectives, the life-story perspective

can be the primary way of comprehending some presentations of
emotional distress. These include grief, homesickness, jealousy, and
discouragement-in fact, any of the specific and general forms of
misery that are common outcomes of distressing settings and
sequences in human existence.

Some of these miseries arise from acute and obviously traumatic

events, such as battle, accident, injury, or loss. Others are the
outcomes of more insidious combinations of misaligned personal
expectations and experiences. These might include a sequence of
recurrent failures in schoolwork, employment, or courtship.
Uncertainty in aims, misunderstanding of customs, or lack of
appropriate responses may have deprived the individual of direction
or understanding, which has led to a sense of isolation, grievance, or
misery.

All these experiences are capable of provoking in patients a sense

of being overcome, defeated, or frustrated by circumstances. Terms
such as discouragement, fearfulness, hopelessness, loneliness, or
resignation may be used to describe the specific emotional responses
of particular patients. As we will elaborate on further, the most useful
generalization describing such states was that coined by Jerome
Frank. He recognized that all these patients were to some degree
overwhelmed, defeated, or overmastered by the circumstances of
their life settings and sequences. Their diverse states of mind he
incorporated under the term demoralization. He interpreted the
patients' fundamental psychological needs to be regaining some
sense of control and "mastery" of the future.2

This concept of the similarity of patients in need of psychotherapy

has relieved much ambiguity and has specified the responsibilities of
psychiatrists. These responsibilities include the differentiation of the
causal elements of demoralization in any clinical presentation and an
appreciation of how different aspects of life stories-circumstances,
personal expectations, attitudes, or habitual responses-can lead to a
fundamentally similar outcome in patients.

Regardless of its source, demoralization is the prime focus of

psychotherapy. It is appreciated as an outcome of an individual's life
story. We now shall address the characteristics of life stories, their
composition by the psychiatrist, and their inherent pitfalls.

The Stories

What can seem truer than a story depicting an emotional state as

the outcome of events that thwarted the hopes and aspiration of an
individual? However, a psychiatrist drawing an explanation from a life
story is usually not just collect ing events and recapitulating them in
chronological order. Similar to the historian, the psychiatrist, with
contributions from the patient, reconstructs the events in a way that
appreciates the present as an evolving part of the patient's life. Thus,
a process of judgment turns a chronicle of events into a narrative in
which the clinical issues faced are illuminated by the sense of
direction a story brings.

What stories tend to be told? Those that tie setting-sequence-

outcome together in a coherent, directed way. As mentioned in
chapter 18, development, so obviously a vital and progressive aspect
of every existence, is an apt element for life stories. It has both
temporal direction and a compelling character. The issue of
development, however, should be construed broadly to include not
only its biopsychological aspects as in the emergence of the attitudes
of adolescence with puberty but also how decisions and choices
made at critical life junctures shape subsequent events. Individuals
can open or close certain pathways in life by choice and develop
particular environments for themselves.

People are not totally passive objects either of their biodevelopment

or their environments but play some role in selecting environments
that either foster later success and happiness or ultimate
disappointment and frustration. Development conceived in these
terms will emphasize the activity of the person as well as the species-
specific, genetically endowed program of growth and differentiation.
Thus, a more advanced conception of development that can
encompass the constitutional (read genetic) factors promoting
particular attitudes and the social environments (some quite actively
chosen, others passively accepted, and still others imposed as if by
fate) should be used in the composition of a life story. With any given
patient, the story should emerge from a thorough assessment of the
patient's biography with particular emphasis on the interrelationship of
the universal elements of every human life (family of origin, schooling,
employment, sexual emergence, and so on). Then the role of choice
and chance at crucial stages can make better sense of his presenting
state and of his particular needs in treatment.

Many life stories useful in explaining demoralization and

overmastery are simple. The recognition of a patient who has
experienced a recent loss or injury and who arrives with apt emotions
of misery and grievance is a story that almost writes itself. On the
other hand, the best story may not be a straightforward description of
current events and their immediately comprehensible consequences
but rather a proposal in narrative form of the interaction between the
intentions or assumptions of this patient and what has happened over
a lifetime to frustrate and defeat him. The composition of the most
therapeutically useful story will often depend on an emerging
appreciation of the character of the patient, on his capacity to sense
his own contributions to his problems, and ultimately on identifying
the core values in forming his own goals and aspirations.

There are pitfalls tied to this method. Occasionally a therapist,

motivated by theory or aiming to simplify psychotherapy, forces a
story on a patient, constructing it backward, as though one can know
the story from the symptom. Such examples include the view that
obsessional adults must have been the victims of oppressive toilet
training in infancy or that a forgotten episode of child abuse must be
present when anorexia nervosa emerges in a young woman.

The observations on which the setting-sequence-outcome

explanation is based must be genuine. Otherwise the power of the
narrative to influence a patient's attitudes and assumptions may be
destructively misguided. In other words, in caring for patients one
cannot have both the license of fiction to imagine any story and as
well the security of fact on which to direct a treatment program. We
shall consider these matters in more detail.

Psychiatrists may reveal another characteristic of stories as they

propose some underlying force to render setting-sequence-outcome
coherent: they compose their stories and choose their facts by
evoking some generalization about humankind. These
generalizations-distinctly different in character from scientific
proposals-resemble proverbs and maxims. They seldom are tested
hypotheses or laws whose limits in accounting for thoughts,
emotions, and behaviors are known.

Many psychotherapists quote maxims such as Josef Breuer and

Sigmund Freud's statement "Hysterics suffer mainly from
reminiscences"3 and Harry Stack Sullivan's dictum "The obsessional
neurotic has never had the satisfaction of outstanding success in
interpersonal relations."4 The distinguished psychiatrist and
psychotherapist Elvin Semrad was memorialized by his students in a
book of his collected maxims about patients and psychotherapy.5
Such a product is a typical achievement of a psychotherapy leader
and differs fundamentally from the achievement of an empirical
scientist.

Not only are individuals and their circumstances more complex than
any maxim can encompass-an issue the statistical approach of the
empiricist acknowledges-but also an awkward feature of maxims is
that their opposites are equally true. For all that it may seem that
"absence makes the heart grow fonder," it is equally evident that "out
of sight is out of mind." Maxims thus do not provide proof for an
opinion nor confident support for a treatment but may offer
rationalizations for stories composed or treatments launched.

In summary, the life story has a special place in the understanding

of distressed states of mind. It functions persuasively and it makes
use of biographical information. In particular, it tries to tie these
biographical facts to some coherent force that makes sense of the
direction from which the outcome, manifested in symptoms, emerges.
It is to considerations of the force behind the story that we now turn.

The Selfs Intentions or Assumptions as Basic Elements of Stories

Much of the driving force within a story rests on the recurring acts
and choices of the person, products of such intentional features as
plans, purposes, and wishes. If these intentions and the assumptions
behind them were fully appreciated, then the story and its outcome in
behavior or emotional conflict would be clear. To make sense of the
life story, the psychiatrist must place the personal intentions and
assumptions of the patient properly in their setting and sequence,
often filling the gaps with interpretations (occasionally imaginations)
when facts are not forthcoming.
 Such constitutional matters as intelligence, temperament, and
drives are crucial to consider first because these certainly do
predispose and tend to delimit a person's intentions. But within
intentions, we denote the specific thoughts and feelings that are tied
to a patient's biographical situation and its difficulties. These may
include aims and ambitions, attitudes toward family members or
occupational colleagues, and moral values and their ramifications.
These thoughts and feelings are the basic elements of most coherent
life stories in psychiatry and quickly become the focus of
psychotherapy.

It is often possible to discern a network of interrelated attitudes and

assumptions that constitute a person of particular inclinations and
character. Although many thoughts and feelings are easily identified
by asking the patient about them, some emerge only on further
acquaintance; that is, only with repeated encounters in the course of
psychotherapy do her habitual responses and thoughts become
evident. Their nature, though, may emerge as well from the
descriptions of her characteristic emotional and behavioral responses
witnessed and reported by collateral informants such as her family
members and friends.

Intentions-represented in plans, attitudes, feelings, and so forth,

and which are so important in making sense of a life story-are almost
limitless in their variety. This variety provokes an urge among
psychiatrists to reduce the intentions to a basic few, by implying that
most conscious intentions derive from a small set of powerful
attitudes such as those tied to sexuality or aggressiveness. This
reduction of a manifold of intentions marks the practice of the
originators of dynamic psychiatry-Freud, Jung, Adler, and so on. In
fact, these psychiatrists' systematic proposals of an unconscious,
underlying, intentional core of drive provoking all actions and thus
fundamental to mental distress made them and the stories they told
so interesting.
 Thus, the central Freudian concept that holds throughout his work,
both in his case studies and in his elaborated theories, is the idea that
the manifest contents of consciousness, including the stated
intentions of the self, are distorted elements derived from an
unconscious and latent realm. In this realm a primitive motivated
drive tied to sexuality is held back from consciousness by the
repressive, defensive forces forged within the unconscious by social
pressure. In certain critical situations and unguarded moments, these
repressed drives emerge to direct the patient's mental life and
behavior. The process of transforming unconscious motives and
intentions into conscious concepts and choices-thus avoiding the
distressing and inexplicable mental disorders derived from eruptions
of unconscious motivations-is the essence of the Freudian story.

Every story for Freud and his followers, even if they disagree about
which drives are paramount, is an exercise in hermeneutics: a
reading of the books of consciousness and behavior for their hidden-
"Freudian"-meanings, an unveiling of the purposes and functions of
the self. This reading is done by someone who knows what is to be
found and who makes of each clinical encounter a reiteration rather
than a test of the vision. That which is known is rediscovered in a new
story to encourage the knower in his or her opinion and to enhance
his or her commitment to what was assumed at the start.

Again in this way the originating schools of psychodynamics

resemble the schools of political thought in which, for example,
Marxist interpretations (such as the labor theory of value) seem to
explain all aspects (including the disorders) of society and history to
his followers and often are used to exclude alternative explanations
and ideas. It remains our point that the most important recent
advance in psychotherapy-one that we will detail later-was the
realization that what patients needing psychotherapy actually share
are not their stories nor some essential, unconscious, and hidden set
of intentions but their states of demoralization. This state is a
common outcome of many different settings, sequences, and
intentional forces in life.6

With this realization clinicians have returned to a simpler and more

direct approach to the link between intentions and psychological
consequences. Their fundamental assumption is that there are
unwanted, unsought, and distressing consequences that are almost
inevitable with certain intentions. Much of contemporary
psychotherapy based on life-story reasoning strives to demonstrate
how such "unintended consequences" emerge from intentional
actions that vary in their conscious appreciation. Specifically, this
translates into the opinion that there are ways of construing oneself
and others that make one vulnerable to losing friendships; being
exploited; or feeling disappointed, angry, or ineffective.

Systematic techniques for exploring these linkages among

intentions have emerged over the last few decades with great
advantage to psychotherapeutic practice. These technical advances
do not attempt to reduce all intentions to a central few but identify for
each patient the intentions that have played the major role in his or
her distress. Particularly, these techniques attempt to demonstrate
and make explicit how certain assumptions and intentions shape a
person's construal of his or her circumstances; how they lead to
unintended consequences; and how specifiable, alternative ways of
thinking and responding to events would be just as true to the facts of
a life and yet produce more confidence and happiness. The best
examples of this method of reasoning and practice are George Kelly's
personal construct analysis and Aaron Beck's cognitive-behavioral
The details of these practices go beyond our purposes here but the
innovative descriptions of their originators and the mounting evidence
of their effectiveness with patients can be consulted with advantages
in a still better understanding of the life-story method and the
coherent psychotherapy that it encourages.

Purpose of Stories
 The psychiatric story works to make sense of the present troubles
as derived from some aspects of the patient's intentions and resultant
life events so as to inspire the patient to change. Stories thus are not
simply concerned with information; their paramount purpose is
persuasion-trying to bring to light problems tied to intentions and
attitudes in order to promote change in demeanor, assumptions, and
habitual responses. Such change can lead to more effective ways of
living than those that brought the patient to the consulting room.

For example, a psychiatrist might eventually be able to show and

say-on the basis of learning about the anxiety and discouragement
the patient experiences at work: "This distress and problem for which
you seek help is an example of a common human urge-perhaps, for
you, exaggerated-to con trol others and get them to do your bidding.
We have seen its expression in your relationships with your family
and friends. Alternative ways of relating to others in some of these
circumstances would likely be more successful, be less fraught with
anxiety and irritation, and lead to clearer recognition by others of your
skills. Let us look together at some of these situations and how your
thoughts and responses in them could have been different and so
produce different feelings on your part and different reactions from
your associates."

As one can see from even such a vignette, stories are not data, the
raw material or elemental observations that form a strong basis for an
inference or an interpretation in science. Stories are themselves
interpretations that relate, in narrative form, events from the patients'
lives to their current symptoms in a way that makes the development
of those symptoms seem explained.

Although stories are not facts, they certainly should be based on

facts to the extent possible-some to be discerned through external
informants. The story constructs linkages between events, combining
facts and presumptions, some of which are reported by the patient
and others assumed by the psychiatrist. In truth, the story with a
therapeutic aim is an argument the psychiatrist presents to the
patient-often directly, sometimes subtly-on the basis of information
derived from what the psychiatrist chooses to emphasize in the
patient's biography. It links up facts and presumptions to make a point
about the generation of mental distress.9

Stories are persuasive abstractions from biographical facts and a

patient's clinical presentation. They often include not a little
conjecture. As such, each story can differ in its linkage to the facts of
the biographies, some tied more closely to events than others. In
each, the effort is to appreciate the force or forces that drive the triad
of setting-sequence-outcome forward. In this fashion, every story
expresses what cold logic may struggle to grasp: the reality of inner
conflicts, incompatibilities, and tensions.

Some students of medicine dedicated to objectivity and truth are

dismayed by the intermingling of observations, interpretations,
presumptions, and collateral information in the themes and stories
advanced in psychotherapy. These students may assume that they
must choose from among different presentations of psychotherapy
such as Freud's or Jung's or reject the entire exercise as simply a
conflict of ideologies. They may overlook the situations that the
psychiatrists' stories produce for patients, for instance, being
understood and given help by an authority, and how that feature
rather than the absolute truth of the stories may be the story's
purpose.

A story with its ingredients of setting-sequence-outcome-informed

by an appreciation of the place of the patient's intentions in directing
this set of events-can be a primary way of comprehending a state of
distress and encouraging its resolution or better management. This is
true particularly of those states that are the universal human forms of
distress: grief, homesickness, jealousy, and the like. As such, stories
will customarily describe a role for the patient himself in the
generation of the story both from the self's capacity for directing a life
plan and for reflecting on the outcome, and they will have a clear
connection to a treatment program for the patient. This treatment will
rest on the issues the story brings to light: namely, that to some
extent the patientthrough intentions felt and expressed and through
obstacles struck and unresolved-influenced the outcome.

With this appreciation, the patient can revisit and revise those
intentions, take charge of his life, and make more effective decisions.
He can come to think of himself less as a victim of circumstances and
more as an agent responsible for his future and in control of his
feelings, prepared to produce a better story in the future with the
information he has learned from his past.

Psychotherapy Is for Demoralization

In exactly this fashion, the empirical investigations of Jerome Frank

on psychotherapy, mentioned earlier, have proven useful and
illuminating. He examined many patients who had come for
psychotherapy at Johns Hopkins. He discovered that the patients did
not share the same life experiences, selfattitudes, or particular
unconscious intentions, such as the Freudian, Jungian, or Adlerian
teachers of psychotherapy proposed. Rather, they were similar in the
psychological condition for which they sought help. They were all
"demoralized" in the sense of being overmastered and discouraged
by some aspect of their lives. Sometimes the symptoms of manic-
depression had discouraged them. Sometimes they were entrapped
by their habits of behavior, and sometimes they were responding to
recurring unpleasant encounters with family members or employers in
which they saw themselves as powerless.

Frank also demonstrated that these patients could be helped by

many different persuasive life stories, but that the more persuasive
ones depended not so much on some secret knowledge of human
nature as on how they linked the patient and the therapist in a
meaningful psychological exploration of the role of the patient in
these outcomes. In particular, the stories and explanations that
seemed most helpful were those that engaged the patient emotionally
and were transmitted by the therapist, whom the patient could endow
with some author ity over psychological matters and who was
prepared to instruct the patient and provide assistance in
restructuring her intentions and plans.

Almost any story that helped the patient take on a meaningful

approach to her difficulties-that is, to see how her intentions and
assumptions interacted with her life experiences and thereby made
sense of her distress-was welcome. And if this psychological
approach restored in the patient a sense of direction and
responsibility for effective living-mastery was Frank's term for this
aim-therapy worked in relieving distress and bringing confidence
where there had been discouragement.

The schools of psychotherapy that incorporated the life-story

perspective and had a divisive influence on psychiatry have, with
Frank's observations and concepts, been appreciated in a radically
different way. Any one of them might help patients, particularly if they
can transmit some sense of concern to the patient in the process.
The relationship counts more than the story. We have learned to see
that the psychotherapy patients are similar in their mental states and
their sense of demoralization rather than similar in their life stories or
in their unconscious conflicts. When treating a patient, a
psychotherapist should choose a story as close as possible to the
interactions between the patient's intentions and his or her life
experiences rather than attempt to force the patient into a story that
fits the theories of Freud, Jung, Adler, or anyone else. In particular,
the story should stick close to verifiable facts and the psychiatrist
should beware of wild stories that come from the Zeitgeist. There is
nothing wrong with using external informants when trying to establish
events in the patient's life. This work, of course, is usually done
during the initial evaluation of the patient, though it can be enhanced
and corrected later.
 This most liberating idea of finding an explanation for
demoralization explains why the persuasive power of a given story
may be its most telling feature, more critical than its permanent and
absolute linkage to the ultimate facts of a biography. This power of
persuasion may depend as crucially on the relationships between the
author of the explanation and its recipient as on the composed
narrative. Recognizing from what sources persuasion derives its
power is the fundamental meaning behind Donald Spence's helpful
distinction between "narrative" and "historical" truth in psychotherapy.
We understand him as appreciating that narratives fill in the gaps in
the record and function effectively for patients, even though later
information may lead to their modification. Frank also reported how
many patients after receiving considerable help from one story
ultimately-as they become skillful in their own psychological
assessment-modify the story in the light of better reflections on the
sources of setting and sequence. This phenomenon, the final story
found only late and after a previous version has succeeded in helping
the patient, brings us back to the problem of fact and fiction in the life-
story perspective and in psychotherapy.

The Issue of Fiction

Crucial to these views of Spence and Frank is the idea that the life-
story perspective is not scientific reasoning but that the stories can,
like history, be modified and corrected with further assessment of the
patient and the reappraisal of his or her psychological states and
biographical background. Although not necessarily grasping all the
truth on each iteration, when practiced correctly the life-story
approach is not the writing of fiction.

Just as history is not fiction but a rational discipline reflecting on

many different sources for its narratives and demanding effort by its
practitioners to confirm the facts on which the narratives are built, so
here in the realm of psychiatry what is depicted in the life story and
employed in psychotherapy must be what corresponds to some
biographical material that can be referenced, displayed, and critically
reassessed by any interested party. It is crucial to make this point
because the process of therapy is an attempt to persuade a
vulnerable person to see his or her life in a particular fashion-one in
which he or she has overlooked opportunities to take charge-and
truth is important.

Most patients begin psychotherapy ready to accept what the

therapist will offer. Why else have they come? If a story with little or
no foundation is composed and urged on the patient in
psychotherapy (and if all attempts by the patient to reject the story
are considered "resistance"), then it is possible to build up any story
and any set of new assumptions. Forcing an interpretation on a
patient is not an acceptable technique and has great danger. Here
fiction of the most destructive kind can be written and imposed as fact
on patients.

The recent outbreak among a sizable group of patients in

psychotherapy of false memories-"memories" of infantile sexual
abuse and wild ideas of satanic cults and alien abduction-depended
on the recurring error that stories could be composed backward
simply from the symptoms and then forced on the patient. Patients
with severe depression were told that their depression represented
the effects of sexual trauma suffered when they were infants and
young children, repeated and continuing abuses they had forgotten or
"repressed" because they were so devastating. These stories were
composed with little effort to consider either alternative diagnoses for
the patients' depressions or stories that might better explain their
presenting complaints. Even less effort was expended to confirm the
presumed, past and forgotten, provocative traumas. "Narrative truth"
seemed to rule without any effort at establishing "historical truth."

Much injury to patients and their families resulted, and only now are
protective guidelines against such practices-all of them restatements
of what thoughtful therapists had long known-being widely
promulgated. All of this could have been avoided had the therapists
thought about the method of the life story they were using. Therapists
who realize that they are responsible for the story because not only
are they its authors but they are also its promoters-the ones who
have made the crucial professional decision that the story method
itself and indeed a particular story offers the most apt treatment
approach for this patient-will be cautious and make good faith efforts
to confirm the facts and interpretations on which the story is built.
Those therapists who do not realize that at a most fundamental level
they are the "owners" of the story and responsible for judging its
suitability both as explanation and as treatment are capable of doing
great harm and are often surprised when their responsibility for this
damage is pointed out to them.

Ultimate Concerns

Last, an aspect of the life story expressed in its practical

expressionpsychotherapy-should be made explicit because it is often
lost in the medical overtones of the term therapy. It is a distinction in
the way this method conceptualizes its tasks in relation to the patient,
his present state, and his future.

The concept of disease presumes the action of a pathological

process that causes symptoms in the present and that constrains the
patient's future in predictable ways. The best treatment will interrupt
that process, and its success will be unambiguous: relief of current
symptoms and freedom from their return as products of the disease in
question.

Psychotherapy and the story method that informs it begin with

present complaints but consider them and any prediction of the future
primarily in terms of the patient's past. Present and future derive not
from the effects of some ongoing process but to a considerable
degree from the poorly conceived or conflicted decisions of the
patient. These decisions are what bring about unintended and
unfortunate consequences.

Whereas in the disease construct the pathological process evokes

a crippled future, the story attempts to show that the self's intentions
and assumptions lead to the consequences seen in the present and,
if unchanged, are to be expected in the future. Psychotherapy is not
an effort to interrupt a process that has a specified character and a
predictable course; it is an effort to help a person choose to live more
successfully in the present and to confront any future more effectively.
Its aim is a person perfected, in the sense of an understanding more
fully developed, rather than a disease cured or an injury healed.

This is a shift of premise with many implications, two of which need

emphasis. First, the life-story method is suited for its aim because it
provides the patient and the therapist with a dramatized and
memorable way of discovering the interaction of events and
intentions that led to the present. It also provides illumination and
inspiration that can facilitate the mutual effort to discern more
effective approaches to the future. Second, the criteria for success in
this enterprise are elusive and value laden because they rest, not on
the demonstration of a future free from the effects of a specific
process, but on the reports of satisfaction by the self and on abstract
comparisons of paths of life to be chosen or rejected.

Because psychotherapy and the life-story technique are based on

satisfaction and intentional choices, they are brought into a dialogue,
if not a confrontation, with "ultimate concerns." It goes beyond our
purpose in this short book to mediate in that dialogue, but it remains a
crucial though seldom-discussed aspect of this domain. The ultimate
concerns promulgated by a story-based psychiatry can and should be
compared with those from other encompassing views about
humankind, such as the philosophical and the religious. Although this
comparison invokes a domain of challenge and accountability
unfamiliar to and usually unsought by physicians, it remains true that
values here are often propagated by insinuation rather than by direct
argument. In discussions about the best way to live a life,
psychiatrists do not, simply by virtue of their professional educations,
have the final jurisdiction.

Summary

The purpose of this chapter has been to demonstrate the clinical

issues the life-story perspective brings to light and how it leads
directly into psychotherapy. Our major points are that patients in
psychotherapy are similar in their states of demoralization and not in
their stories. Demoralization can come from many sources, including
those covered in the other perspectives of psychiatry. But the
composition of a life story with the patient is a most helpful approach
toward an explanation of demoralization.

The composition of a life story demands a thorough assessment of

the patient from which emerges an adequate formulation that
considers both matters of diagnosis and of the interactions of crucial
biographical events with the patient's intentions and assumptions.
From such information an individual story that approximates a true
depiction of the life in the form of a persuasive argument can develop,
from such a story a therapist can encourage the patient to see how
her intentions helped precipitate the emotional consequences. This
approach can lead the patient to see her contribution to her troubles
and to rescript her approach to life circumstances.

Demoralization is overcome as the patient develops, from a

meaningful appreciation of the events and their linkages in her life,
the ability to move beyond the injuries she has suffered and the
mistakes she has made so as to take charge of her future. The
mastery of life's direction is the aim of psychotherapy. It is facilitated
by learning how events of the past and aspects of one's own
character have conspired to produce prior frustrations and recurrent
demoralization. By cultivating more appropriate responses to events,
this learning can foster a better group of settings, sequences, and
outcomes for the future.

The decision to use the life-story perspective and what story to

develop with the patient, however, are far from trivial matters. They
are critical professional decisions, and the psychiatrist is responsible
for their consequences. Therefore, the psychiatrist not only should
use prudence in these decisions-by carefully considering alternative
perspectives-but also should show continuing good faith efforts at
confirming the facts and judgments on which the decisions for the life
story were made, reviewing them regularly when patients are either
worsening or not improving during treatment, in order to revisit the
initial decisions. The psychiatrist, like the historian, "owns" the story
and will surely be professionally held responsible for it and its
consequences.
The perspectives described in the preceding chapters bring three
practical benefits to contemporary psychiatry: they add structure and
coherence to the discipline overall, they disclose and contrast the
strengths and limitations of treatments, and they draw psychiatry to
the sciences and clinical specialties that surround it. These benefits
of the perspectives, each to be discussed further in this chapter, help
embed psychiatry in the culture of science and enhance its position
as a subdiscipline of medicine.

Additions to the Present Structural Elements of Psychiatry

Currently, much of American psychiatric practice rests on

undertakings launched in the late 1960s. The most celebrated
achievement was the fashioning of a reliable approach to naming and
classifying psychiatric disorders that culminated in the 1980 edition of
the American Psychiatric Association's Diagnostic and Statistical
Manual of Mental Disorders (DSM-III). This feat encouraged
psychiatry programs to commit to research in a more collaborative
and progressive spirit.

Thus, for example, they began to invest in technical instruments of

huge size and expense, such as positron-emission tomography (PET)
scanners that might previously have been considered equipment for
neurology departments. Symbolic of this new direction has been the
vigorous involvement of the National Institute of Mental Health
(NIMH) in a research campaign for the 1990s entitled the "Decade of
the Brain." As well, American psychiatrists abandoned allegiances to
narrow explanatory theories about mental disorders. Many
acknowledge a breadth of informative sources by enthusiastically
supporting the encompassing "biopsychosocial" approach proposed
by George Engel.',2

DSM-III and the biopsychosocial concept were attempts to settle

some of the general uneasiness in the discipline provoked in the
1960s by such issues as the unexpected, specific power of
psychopharmacology; the awkward randomness in diagnostic
practices; and the embarrassing "house divided" character of the
discipline, whereby "biological" and "dynamic" factions contended.
These new proposals partially succeeded in their corrective aims and
had much to recommend them. Each took a compromising stance
toward contemporary practice and opinion. DSM-III admitted to its
canon any entity that could be "operationally" defined by its
champions, and the biopsychosocial orientation embraced any
explanatory concept within its ample hierarchical arms.

But the problems of the contemporary positions are not hard to find.
In attempting to steer clear of the disputes that had riven the
discipline, the authors of DSM-III devised a classificatory system
committed to empiricism. For all its advantages at one stage in a
discipline's growth, empiricism is admittedly-and with DSM-111
almost boastfully-a form of ignorance. By posing the existence of
conditions, DSM-III calls out for their validation and explanation. That
call certainly encourages research, but DSM-III is a catalogue, not a
guide, and thus cannot recommend a path.

The biopsychosocial concept looks, at first glance like the source of

information to answer this call from DSM-III. However, for all its good
sense and feeling of rightness to psychiatrists, its problems are not
far from the surface. Figure 14 shows the "systems hierarchy" that
Engel laid out in one of his original papers.3 He placed the "person"
squarely in the middle of conceptualized strata of knowledge layered
both below and above. He thus in a picture revealed how restrictive
any formulation of a clinical disorder would be if it were confined to
matters biological (below the person), psychodynamic (within the
person), or social (above the person)-hence the term
biopsychosocial.

But, this systems approach is so broad in its scope and so

nonspecific in its relation to any particular disorder that it can do no
more than remind psychiatrists to look at everything. In particular, the
proposal skips over the problems of linking its strata together. For
example, the relationship of the brain to the mind is presented in this
figure as a step like that between cells and tissues or between the
person and the family. One suspects that explanations for disorder
may be cobbled together by trivializing the many problems at the
interfaces between the hierarchical strata.
FIGURE 14. Engel's hierarchy of natural systems. Source: Engel, GL:
The clinical application of the biopsychosocial model. Am J
Psychiatry 137: 535544, 1980, p. 537. Reprinted with permission.
 In fact, the biopsychosocial approach offers no rules, directions, or
logical pathways to explain the patient groupings of DSM-III. In this
way, the biopsychosocial concept is heuristically sterile. It denotes the
ingredients but provides no recipes to specify the use of these
ingredients in explaining mental disorders.

Finally, the biopsychosocial idea is not new. It is Adolf Meyer's

concept of psychobiology renamed. It retains all the strengths and
limitations of that previous version. In Adolf Meyer's Thomas W.
Salmon Memorial Lectures of 1932, he also embedded the person in
a hierarchy of stratified systems (interactive levels of integration was
his term) from the atom to the society.4 In proposing an explanation
for any disorder, he encouraged a complete study of each patient's
body, brain, and biography. Every mental disorder, he believed,
stemmed from the responses of the person encountering the issues
of a lifetime. He persuaded psychiatrists to seek within their "critical
common sense" the explanations and treatments of mental disorders.

Meyer's energies derived from his opposition to simplicities and

fatalistic implications that he discerned within the diagnostic
framework that came from Emil Kraepelin. He wished to show that
mental disorders could be better understood as reactive outcomes of
the workings of a given person in a life. Meyer debunked the method
of fixed entity diagnoses, calling them sterile labels. He promoted
individualized formulations in descriptive, explanatory paragraphs for
patients with mental illnesses.

Meyer's concept of the formulation brought discernment and

individualization to psychiatric practice, but now we need better
means for building a formulation than the critical common sense
Meyer recommended. This need is not met by the biopsychosocial
reiteration of Meyer's ideas. Rather, the lack of a better means to
formulate a clinical problem is simply underlined. To appropriate
Meyer's terms, we need the means to appreciate the "workings"
behind the presentations of psychiatric disorders and how they are
expressed by individual patients.

It certainly was no coincidence that Engel's biopsychosocial

concept, a restatement of Meyer's position, emerged in the same
decade as DSM-III. It met and satisfied the same felt need as had its
predecessor: to move from diagnostic labels to more discerning
formulations of patients.

Organized American psychiatry is replaying a set of themes from

earlier in this century. It is both neo-Kraepelinian and neo-Meyerian.
But how these reappropriations of the past can steer our present
activities into a more satisfactory future is not obvious.

In practice, a temporizing modus vivendi has been struck. Clinicians

accept DSM-III for records and research, but teach and practice by
local preference for either "biological" or "dynamic" reasoning and
formulations just as before. By regularly repeating in almost
mantralike manner, "We use the biopsychosocial approach," they
cloak their persisting life in a house divided.

We hold that working with the perspectives of psychiatry presented

in this book-differentiating psychiatric conditions according to their
natures and supplying a set of critical concepts for explanation,
treatment, and researchcan help terminate this temporizing approach
and unite the discipline. Thus, they provide in an assimilable form the
pertinent elements of the psychiatric formulation. They offer the neo-
Kraepelinian DSM-III clear and distinct pathways for organization,
treatment, and research. They sustain the ecumenical tenor of the
neo-Meyerian biopsychosocial idea by introducing contributions to
psychiatry from different sources. With their employment, the house
divided character of psychiatry, represented by the so-called
biological and dynamic orientations, can be surmounted.

Therapeutic Implications Tied to Each Perspective

 Again, diseases, dimensions, behaviors, and life stories are the four
perspectives we advance. Each of these perspectives supports a
particular kind of treatment that must be studied for itself. However, in
every treatment beneficial and burdensome features are inextricably
intermingled. These features must be clearly described in order to
maximize the benefit and minimize the burdens inherent in any
treatment protocol. These benefits and burdens tied to each
perspective's treatments are outlined in figures 15 and 16 but need
further definition here.

FIGURE 15. Therapeutic aims.

FIGURE 16. The "red ink" in therapies: an implication of the

perspectives.

Disease Perspective

The essence of disease-reasoning is that the signs and symptoms

of the patient emerge from some "broken" bodily part. Treatment
seeks to cure or alleviate such broken parts. For psychiatric diseases,
the treatments are usually pharmacological-although some physical
treatments such as electroconvulsive therapy and some forms of
psychosurgery are available.

All medications and all physical treatments have damaging side

effects. Medications are toxic at some level, and physical treatments
cannot be offered free of any injurious features-most of them fleeting
but all distressing. A treatment protocol must acknowledge these
burdens of treatment to the patient so that the side effects do not
come as surprises and do not disrupt the program. A watchful
understanding of this aspect of the disease perspective is critical.

Dimensional Perspective

The essence of the dimensional perspective is that the patient's

mental and behavioral difficulties are due to vulnerabilities resting on
his or her position at some extreme on a dimension of human
psychological variability, such as cognitive ability and affective
temperament. Treatment of these patients evolves around
strengthening and guiding them-as in remedial education and
vocational training for cognitively vulnerable persons and in character
construction and therapeutic supervision for affectively vulnerable
persons.

The "red ink" in these treatments is the rather obvious paternalism

of guidance and the sense of the arbitrary in the ultimate values
behind the therapeutic supervision. Only an ongoing treatment plan
that balances the proposals of the psychiatrist against the wishes of
the patient will not founder on these particular problems.

Behavior Perspective

With the behavior perspective we recognize that disorders of goal-

directed behaviors rest on some combination of physiological need,
conditioned learning, and choices. Treatments are focused on
stopping the behavior by helping the patient choose to act against it,
help most effectively delivered through group therapy. Recourse to
such methods as pharmacological management of the drive
(methadone, nicotine patch, naltrexone, antiandrogens, and so forth),
interrupting the conditioning that sustains the behavior, and
treatments for comorbid conditions can assist the process.

The problem associated with the treatments of behavior is that of

stigmatization. One cannot attempt to stop a behavior without at
some level deploring it, and this stigmatization must ultimately be
justified to patients and others. Again, group therapy in which patients
are encouraged to identify themselves as persons with a behavioral
problem (for example, the Alcoholics Anonymous protocols of
introduction: "I'm Bill; I'm an alcoholic") acknowledges the stigma and
indeed may employ it therapeutically.

Life-Story Perspective

The life-story perspective functions to explain common emotional

responses with narratives that evoke the triad of setting, sequence,
and outcome to explain the distressing state. Treatment thus
becomes an attempt to interpret to the patient just how this outcome
could be expected-ideally, predictedgiven the setting and sequence.
Most crucial in this treatment is the therapist's effort to help the
patient see how in minor or major ways he or she contributed to these
consequences and can avoid them in the future.

These interpretive efforts of the therapist all depend on an alliance

with the patient that will encourage their acceptance. However, all
interpretations carry the hostility of condescension (that is, "I know
you better than you know yourself"). A strong supportive relationship
between the therapist and the patient is needed to blunt this sharp
edge of interpretations and permit them to accomplish their
rescriptive role.

Facilitation of Linkages to Surrounding Disciplines

 The final benefit of the perspectives is their aid in developing a
collaborative relationship to neighboring disciplines, particularly for
research and the sharing of information. Most medical disciplines,
such as cardiology, advance as the problems of the patients reveal
issues related to the biological sciences, such as electrophysiology,
endocrinology, and genetics. For psychiatrists to take similar
advantages, they must distinguish among their patients those for
whom specific aspects of biology might apply. By implication, they
also must distinguish those psychiatric disorders that have less of a
biological foundation, resting as they do on conflicts between what is
intended and what is encountered in life itself.

As shown in figure 17, the investigator who understands the

fundamental distinctions among psychiatric patients is aptly
positioned to bring questions to and find help from the surrounding
professional groups. The members of these groups become more
effective collaborators once a structure for psychiatry becomes clear
to them.

For example, consider the intriguing multidisciplinary research

carried out in the Department of Psychiatry at Johns Hopkins by
Robert G. Robinson and his collaborators on the depressions
associated with cerebral infarctions. These depressions were known
to clinicians as a frequent complication of strokes, and they had
always been interpreted from a life-story perspective as outcomes to
be expected in anyone faced with the disabilities and threats tied to
cerebrovascular disease. However, when Robinson recognized that
these depressions resembled major depression, he launched a
collaboration with neurologists and neuroscientists to study the matter
more closely.5•6 This collaboration, which depended on a shift to the
disease perspective, confirmed among other facts that these
depressions were susceptible to treatment with the same medications
that work in major depression.? This work established that lesions in
the left anterior frontal region of the brain were the ones most
commonly producing depression. This observation was soon picked
up by scientists interested in functional imaging of the brain, who
eventually demonstrated that with other depressions the left frontal
regions were hypoactive.8 We had advanced in our understanding of
stroke and how its lesions could disrupt the affective neurological
controls in the brain.

FIGURE 17. The linkages of psychiatry.

All progress in psychiatric investigation will depend on the

facilitation of similar linkages between psychiatrists and other
investigative workers. All will derive from an appreciation of
fundamental distinctions in psychiatric disorders made explicit by the
perspectives described in this book.

Summary

The practical benefits of the perspectives of psychiatry are not hard

to find. They provide more structure and conceptual coherence to this
discipline by making explicit aspects of reasoning about patients that
are often left implicit and vague. They define and differentiate the
treatments psychiatrists provide to patients and so identify both the
appropriateness of each of these treatments and their intertwined
side effects and burdens. They present a structural foundation to
psychiatric practice that encourages and facilitates collaborative
efforts with the professional groups that surround psychiatry. These
practical benefits are also associated with several conceptual
advantages, to which we turn in the next chapter.
At the start of this book we identified two special obstacles hindering
the advance of psychiatry toward full status as a subspecialty of
medicine. These are (1) the mind-brain problem, which hinders
understanding of just how mental phenomena-the psychiatrists'
subject matter-emerge from the brain; and (2) the ferocious
factionalism (that is, orientations) over the nature of mental disorders
that is itself derived from the conflicting approaches to truth fashioned
in our times. Throughout the book we have made a twofold claim. We
hold that these perspectives-differentiating patient groups according
to the nature of their disorders with implications for treatment-can
circumvent the mind-brain problem and can transcend and ultimately
reconcile the factionalism of psychiatry. We conclude by drawing out
a few more implications of this approach to psychiatry and its
predicament.

Ultimate Implications

Lack of Homogeneity

If psychiatrists must employ several different methods of reasoning

(the different perspectives) in comprehending their discipline, then
psychiatric patients cannot be a homogeneous group. In fact, some
are individuals damaged as organisms and constrained in their
thoughts and behaviors by the misdirections of delusions and
hallucinations. Others suffer from emotional reactions differing in
frequency and degree but not in kind from those everyone suffers.
Still others are those whose emotions and behaviors represent the
outcome of conflicts between what they wished or hoped for and what
life delivered. It is the task of psychiatry to recognize and distinguish
these patients from each other and from "normal" people.
 Thus, no unifying concept applies to all psychiatric patients and
their disorders-no "unified field theory"; no ultimate reductive
foundation such as molecular biology provides contemporary
medicine; and certainly no fundamental psychological issue, such as
Freud, Jung, or Adler proposed-at the heart of all this diversity. Put as
simply as possible, we cannot-and at this juncture are unable to even
imagine how we might-derive all the information encompassed in the
practice of this discipline from a single source.

Among the several subimplications to be drawn from this idea is the

practical consequence that the initial evaluation of any patient cannot
be abbreviated by focusing solely on some aspect of his or her
history or mental status examination construed as the fundamental
source of all psychiatric troubles. Thus, one cannot expect the
explanation of every disorder to emerge from a consideration of
conflicts during development, from a survey of sexual drive and its
expression, or from an assessment of feelings of inferiority and their
resolution. One cannot expect that laboratory tests useful in one set
of patients will of necessity explain anything about others. Nor can
one even expect that some scientific advance at such fundamental
molecular biological levels as synaptic transmitters and membrane
receptors will ultimately explain the course of development of all
mental disorders and provide for their treatments.

A capacity to gather a comprehensive body of information on every

patient from history, mental state, physical examination, and
laboratory studies (as described in standard textbooks of psychiatry
such as that of Willy MayerGross, Eliot Slater, and Martin Roth)' must
be a fundamental skill of a competent psychiatrist and one demanded
by a discipline without a unified field theory. The perspectives of
psychiatry offer a means of organizing (that is, formulating) this
information in ways that will draw out matters of cause, treatment,
and prognosis. As the metaphor of a perspective implies, if one
method of considering information proves inadequate then another
"point of view" that reformulates the information is justified.
 Each perspective of psychiatry has its own set of premises, store of
facts, modes of research, and methods of treatment that are, to a
degree remarkable in medicine, distinct from the others. Yet each
must be considered for its potential benefit in every clinical encounter
and reconsidered as more information, as from the course of the
condition or the response to treatment, is acquired. We have
attempted to depict their separate (even though potentially
interlocking) character in the preceding chapters and so to
demonstrate how psychiatry must ally itself with multiple sources of
scientific knowledge and investigation in order to advance.

An important advantage of reasoning from distinct perspectives in a

nonhomogeneous population is that category errors in assessment
and treatment can be promptly appreciated and avoided. For
example, an approach to the study of major depression should follow
a different course from an approach to the understanding of grief. To
construe the regular remitting and relapsing course of major
depression as a reaction to life circumstances would dismiss
prematurely its likely etiologies in genetics and its production through
misaligned brain mechanisms. Similarly, to view grief as a peculiar
form of brain disease would be to work with the wrong premises
about its place in human affective and social life.

Clear features distinguish major depression from grief. A

comprehensive assessment of a patient in whom these two
conditions are under consideration would attempt to identify those
features and then account for them in terms of genetics and brain
pathophysiology for depression and the species-specific reactions to
life events for grief. This is required even though aspects of the
presentation of each go beyond the disease or life-story explanation.

Thus, in depression, aspects of personality, past experience, and

current life circumstances will determine the content of a patient's
worries and may influence a patient's expressed behavior during a
depressive phase, as in encouraging a more agitated appearance in
some individuals than in others. Similarly, in grief, the relatively
stereotyped experiences of anorexia, insomnia, and driven
restlessness suggest some "built-in" biobehavioral mechanisms
mediating this particular human psychological response to life
circumstances.

Because no single explanatory source is available to answer clinical

questions, psychiatrists build their opinions from a comprehensive
gathering of information from each patient and then organize this
information for practical purposes of treatment and prognosis. We
hold that many of the organizational principles employed by
psychiatrists have been more implicit than explicit and thus more
difficult to teach and defend-hence this effort to explicate the
perspectives.

Problems of Classifications

Because several distinct perspectives are employed to make sense

of the different psychiatric disorders, classificatory systems are often
unsatisfactory in psychiatry, no matter how well the issues of
operationalism, reliability, and validity are addressed. A classificatory
system, if it is any kind of "system" at all, must find some consistent
concept for its framework.

DSM-III was an advance over DSM-11. It argued for publicly

accessible criteria in diagnosis and for categories that are strict and
conceptually clear. It incorporated empirical research about
psychiatric conditions into classification. Recognizing these changes,
it can be appreciated that DSM-Ill's strengths are most obvious in the
categorical conditions such as the diseases but that it labors to cope
with clinical situations in which the individual contributions from
personality, behaviors, and life circumstances intermingle.

Continuing Sources of Conflict

 Psychiatry may always find itself involved in battles, most often and
most injuriously from partisans of one perspective who fail to give
legitimacy to another. The claims of the "antipsychiatrists" were
examples of this vulnerability in a discipline of multiple perspectives.

The "death of psychiatry" wing of the antipsychiatrist movement

proposes that because the major disease categories will likely prove
to have brain pathology, the care of patients with such illnesses will
devolve to neurologists. Because a medical degree is not required to
provide psychotherapy, patients with symptoms not caused by
diseases will be treated by psychologists, social workers, nurses, and
lay therapists. There will be nothing left for psychiatry to call its own,
and it will therefore wither away.

The syllogism succeeds only by defining psychiatry as a discipline

that ignores diseases of the brain (for example, dementia, delirium,
and mental retardation) and that approaches the issues of personality
disorder, behavior, and life encounters solely in terms of therapy (not
in terms of differential diagnosis, prognosis, and scientific
investigation). A psychiatry that sees itself as a discipline of several
distinct perspectives has been overlooked by this view. Such a
psychiatry will grow and prosper only with further knowledge of the
brain and from psychometric investigations, behavioral science
studies, and an appreciation of distinctions in methods of explanation.

Psychiatry's critics often cite forensic issues and condemn

psychiatrists who confine patients involuntarily or who offer reasons
to mitigate the punishment of certain individuals who break the law.
These arguments again tend to assume that all behaviorally disturbed
patients are fundamentally the same and differ from normal only in
degree. Therefore, in fairness, the law should not treat them
differently from other people: none should be placed in a hospital
without his or her agreement, and all should suffer the full penalty of
the law for their expressed behaviors.
 Once again, the response to this view is that psychiatric patients
are far from a homogeneous group. Some are misdirected by
delusions and hallucinations. Others have not learned methods of
controlling their emotions and behaviors. A democratic society can
legitimately decide how it will apply these distinctions in its law, and
psychiatrists should help.

Choice of Perspectives and Its Implication

We have delineated four perspectives that attempt to make sense

of the clinical presentations of patients: diseases, dimensions,
behaviors, and life stories. Although they can often be intermingled in
formulating a clinical problem, it should now be clear that each
depends on different grounds: disease, for example, on the
demonstration of pathology within a bodily part; dimensions, on
discriminable distributions and the prediction of future performance
from positions on the dimensional axis.

Psychiatrists can choose any perspective or construe new ones to

explain a patient's symptoms. They can call on the disease
perspective if they think that neurobiological information, present or
future, will discern the structural or functional disorder at the heart of
the symptoms. They can propose a life story if they think it illuminates
the relationship between events and emotional responses.

A psychiatrist is free to choose or to change perspective, but the

choice, once made, always presents a set of demands that extend
from the particular patient to a defense of the choice itself. A change
of perspective is not a release from responsibility; it is only a shift to a
different set of demands. One understands a perspective and can be
accountable for its choice when one can define the relevant domains
of information and knowledge from which its validation should emerge
and can describe the explanatory themes and treatment methods that
this perspective supports.
 By insisting on this kind of reasoning, psychiatry can encourage
ingenuity and creative insight without fearing a continuation of its
history of acrimony and denominational warfare. Indeed, one can go
further and note that as these perspectives make sense of
differences among psychiatric patients, similar ways of reasoning are
not restricted to psychiatry. Internal medicine is familiar with these
ways of thought. A good internist appreciates that elevated blood
pressure may be a symptom of a pathology (pheochromocytoma),
evidence of a polygenically explicable deviation along a dimension of
human variation, or due to the anxiety of entering a hospital setting.
The same physical feature can have different causes and different
implications.

We hold that psychiatrists must make these distinctions more

explicit than internists do. We hope through this approach to arrive at
a time when we have so precisely clarified the presumptions about
what we know and how we know it that we can place everyone, but
especially patients and their families, on more equal terms with us.
They then can ask questions and receive answers about our
assumptions, practices, and plans and so contribute more
discerningly to their recovery. The Perspectives of Psychiatry is our
attempt to hasten that day.
Operationalism has an enduring legacy: a concern for verification
represented by the processes of reliability and validity. Reliability is
the verification of observations. Validity is the verification of
presumptions. Both take sustenance from operationalism but develop
their power from logic, statistics, and the hypothetico-deductive
process of science.

Reliability, or observational verification, estimates the consistency

with which one can make an observation. Reliability is demonstrated
by the correlations between the results of observers who use the
same technique to make that observation. The techniques may range
from an element of the physical examination to a portion of the
psychiatric interview to responses based on questionnaires.

The reliability of some psychiatric observations is high. This

indicates that psychiatrists can agree-though perhaps incorrectly
agree-about whether a patient does or does not have abnormal
mental states such as delusions and hallucinations. Reliability studies
also indicate that agreements improve with the psychiatrist's training;
some aspects of a patient's behavior such as affective responses can
be more difficult to agree about; and certain approaches to an
interview are better for some observational purposes than for
Although any observation that depends on the communication
between physician and patient has several sources of error, our
confidence in the reproducibility of many observations is high enough
to employ them in the construction of explanatory concepts.

Validity verifies the constructions built on these observations.

Through the processes of reliability, we assess our capacity to
observe. Through those of validity we challenge the concepts put
forth to explain consistency in a set of observations. With this
challenge we hope to confirm what begins as a presumption: that
underlying a particular pattern of results derived from a given means
of observation there is a comprehensible construct or testable
concept that explains the results. The observations (scores on test
instruments, patterns of symptoms) are the indicators of the
construct, but they are not synonymous with the construct, as strict
operationalism might imply.

The construct is a conceived relationship among domains (such as

psychological, biological, social, and historical), each of which is
potentially a source of observations that make the construct testable.
A disease is a construct that conceptualizes a constellation of signs
and symptoms as due to an underlying biological pathology,
mechanism, and cause. The validation of a disease entity rests not
simply on the reliability with which signs and symptoms can be
observed, nor on the operational language by which it is defined, but
also on the development of empirical methods that investigate the
underlying anatomical and pathophysiological domains from which
the consistency of those signs and symptoms is derived.

It is easy to see that verification of an observational method

(reliability) is a finite task. Once done, the process soon becomes the
repetition of an achievement. Verification of a construct (validation) is
never "done." Validation is an ongoing process of demonstrating,
through the exploration of as many related domains as possible, that
the construed explanation of an observable consistency continues to
survive.

There are many ways such explanations can fail to be validated. An

original set of results may have derived from the use of an
inappropriate technique or from the study of the wrong group, so
similar results are not found when the technique is changed or
another group is studied.
 Constructs are never proven. They survive challenges that establish
their applicability, but they are replaced when better explanations
come alongbetter in the sense of surviving more challenges,
accounting for more aspects of consistency, and encouraging better
methods of observation. Constructs are also not things given in
nature. They are conceptualized networks of relationships that derive
from observations and assumptions. They are hypotheses that make
sense of observational consistency. The best constructs are those
that explain much but can be challenged by simple tests of validation,
some of which the construct survives but all of which demonstrate the
confidence limits within which the construct must be held. Constructs
that explain all observables but cannot be challenged are doctrines;
constructs that explain little and are quickly refuted are the hunches
of the day. Advances in the field lie with those constructs between
doctrines and hunches and with those investigators who appreciate
the activity of validation as generative of continually improving
constructs.

The process of validation and the techniques of reliability and

validity are valuable for the data they yield and also for the spirit of
confidence and fellowship they give to our judgments. In a field where
there is seldom an autopsy to confirm a clinical opinion, explicit
concern for reliability and validity is necessary.

By reviewing the assessment of mental phenomena, we intend not

only to reassure ourselves that the interview-with its mental status
examination-is a basic tool for psychiatrists and is dependable as a
means of discerning real events but also to prepare the ground for an
inquiry into methods of explanation, approaches that will allow us to
understand why someone is stuporous, hallucinated, or anxious.
These issues as applied to DSM-III and DSM-IV are elaborated in
chapter 3.
 Chapter 1: The Mind-Brain Problem and a Structure for Psychiatry

1. King LS: Transformations in American Medicine: From Benjamin

Rush to William Osler. Baltimore, Johns Hopkins University Press,
1991.

2. Jaspers K: General Psychopathology (vol 1), Hoenig J, Hamilton

MW (trans). Baltimore, Johns Hopkins University Press, 1997, p 55.

3. Bridgman PW: The Way Things Are. Cambridge, Harvard

University Press, 1959, p 220.

4. Leff JP: Psychiatrists' versus patients' concepts of unpleasant

emotions. Br J Psychiatry 133:306-313, 1978.

5. Slavney PR, McHugh PR: Psychiatric Polarities. Baltimore, Johns

Hopkins University Press, 1987, pp 9-25.

6. Searle JR: The Mystery of Consciousness. New York, New York

Review of Books, 1997.

7. McHugh, PR: Psychiatry and its scientific relatives: "A little more
than kin and less than kind" (editorial). J New Ment Dis 175:579-583,
1987.

Chapter 2: Factionalism

1. Pinel P: Traite medico-philosophique sur !'alienation mentale, 2nd

ed. Paris, Brosson, 1809; Ist ed. 1801, pp 252-253.

2. Lane, Harlan: The Wild Boy of Aveyron. London, Biddies, 1977.

 3. Ackerknecht EH: A Short History of Psychiatry, Wolff S (trans),
2nd ed. New York, Hafner Publishing, 1968.

4. Shorter E: A History of Psychiatry: From the Era of the Asylum to

the Age of Prozac. New York, John Wiley & Sons, 1997.

5. McHugh PR: A structure for psychiatry at the century's turn: The

view from Johns Hopkins. J Royal Soc Med 85:483-487, 1992.

6. Hoche A, Binding K: Die Freigabe der Vernichtung

lebensunwerten Lebens. Leipzig, Meiner, 1920.

7. Proctor RN: Racial Hygiene: Medicine under the Nazis.

Cambridge, Harvard University Press, 1988.

8. Stern JP: Nietzsche. London, Fontana Press, 1978.

9. Freud S: Five lectures on psychoanalysis. In Strachey J (ed): The

Standard Edition of the Complete Psychological Works of Sigmund
Freud (vol London, Hogarth Press, 1957, p 49.

10. Ricoeur P: Freud and Philosophy. New Haven, Yale University

Press, 1970, p 4.

11. Freud S: Psychoanalytic notes on an autobiographical account

of a case of paranoia (dementia paranoides). In Strachey J (ed): The
Standard Edition of the Complete Psychological Works of Sigmund
Freud (vol 12). London, Hogarth Press, 1957, p 71.

12. Jung CG: The Collected Works (vol 3). London, Routledge &
Kegan Paul, 1953-1971, p 189.

13. Roazen P: Freud and His Followers. New York, Da Capo Press,
1992.

14. Shorter E: A History of Psychiatry: From the Era of the Asylum

to the Age of Prozac. New York, John Wiley & Sons, 1997, chap 5, pp
145-189.

15. McHugh PR: William Osler and the new psychiatry. Ann Int Med
107:914-918, 1987.

16. Szasz TS: The Myth of Mental Illness, rev ed. New York, Harper
& Row, 1974; 1st ed 1960. Quote p xiii.

17. Chomsky N: Language and Freedom. New York, Abraxus Press,

1970.

18. Jaspers K: General Psychopathology (vol 1), Hoenig J, Hamilton

MW (trans). Baltimore, Johns Hopkins University Press, 1997.

Chapter 3: Classification in Psychiatry and the Method of DSM-IV

1. Diagnostic and Statistical Manual of Mental Disorders, Fourth

Edition (DSM-Iii). Washington, DC, American Psychiatric Association,
1994.

2. Edwards G, Gross MM: Alcohol dependence: Provisional

description of a clinical syndrome. Br Med J 1:1058-1061, 1976.

3. Smith EE, Medin DL: Categories and Concepts. Cambridge,

Harvard University Press, 1981.

4. Young A: The Harmony of Illusions: Inventing Post-Traumatic

Stress Disorder. Princeton, Princeton University Press, 1995.

Chapter 4: The Disease Perspective

1. Scadding JG: Diagnosis: The clinician and the computer. Lancet

2:877-882, 1967.

2. Kendell RE: The concept of disease and its implications for

psychiatry. Br J Psychiatry 127:305-315, 1975.
 3. Kraupl TF: The medical model of the disease concept. Br J
Psychiatry 128:588-594, 1976.

4. Wing JK: Reasoning about Madness. Oxford, Oxford University

Press, 1978, pp 21-42.

5. Sydenham T: The Works of Thomas Sydenham, M.D. (vol 1).

London, Sydenham Society, 1848, pp 13-17.

6. Sigerist HE: The Great Doctors. New York, WW Norton, 1933, p

181.

7. Ibid., pp 233-234.

8. Ibid., pp 371-372.

9. Krliupl TF: Psychopathology (rev ed). Baltimore, Johns Hopkins

University Press, 1979, p 5. 10. Ibid., p 8.

Chapter 5: The Disease Concept Exemplified by Psychiatric

Conditions with Known Neuropathologies

1. Alzheimer A: Ober eine eigenartige Erkrankung der Hirnrinde.

Allgemeine Zeitschrift fur Psychiatrie 64:146-147, 1907.

2. Blessed G, Tomlinson BE, Roth M: The association between

quantitative measures of dementia and of degenerative changes in
the cerebral grey matter of elderly subjects. BrJ Psychiatry 114:797-
811, 1968.

3. Perry EK, Tomlinson BE, Blessed G, Bergmann K, Gibson PH,

Perry RH: Correlation of cholinergic abnormalities with senile plaques
and mental test scores in senile dementia. Br Med J 2:1457-1459,
1978.
 4. Whitehouse PJ, Price DL, Clark AW, Coyle JT, DeLong MR:
Alzheimer's disease: Evidence for selective loss of cholinergic
neurons in the nucleus basalis. Ann Neurol 10:122-126, 1981.

5. Folstein MF, Breitner JCS: Language disorder predicts familial

Alzheimer's disease. Johns Hopkins Med J 149:145-147, 1981.

6. Kiloh LG: Pseudo-dementia. Acta Psychiat Scand 37:336-351,

1961.

7. McHugh PR, Folstein MF: Psychopathology of dementia:

Implications for neuropathology. In Katzman R (ed): Congenital and
Acquired Cognitive Defects. New York, Raven Press, 1979, pp 17-30.

8. Lipowski ZJ: Delirium: Acute Brain Failure in Man. Springfield,

111, Charles C Thomas, 1980, pp 14-15.

9. Romano J, Engel GL: Delirium: I. Electroencephalographic data.

Arch Neurology and Psychiatry 51:356-377, 1944.

10. Moruzzi G, Magoun HW: Brain stem reticular formation and

activation of the EEG. Electroencephalog and Clin Neurophysiol
1:455-473, 1949.

11. Victor M, Adams RD, Collins GH: The Wernicke-Korsakoff

Syndrome. Philadelphia, FA Davis, 1971, p 4.

12. Ibid., pp 166-170.

13. Broca P: Nouvelle observation d'aphemie produite par une

lesion de la moitie posterieure des deuxibme et troisieme
circonvolutions frontales. Bulletins de to Societe Anatomique de Paris
6:398-407, 1861.

14. Wernicke C: Der aphaisische Symptomencomplex:

Einepsychologische Studie aufanatomischer Basis. Breslau, Cohn &
Weigert, 1874.

Chapter 6: The Disease Concept Applied to Psychiatric Conditions

without Known Neuropathologies

1. Hunter R, Macalpine 1: Three Hundred Years of Psychiatry, 1535-

1860. London, Oxford University Press, 1963, pp 406-407.

2. Griesinger W: Mental Pathology and Therapeutics. New York,

William Wood & Co, 1882 (trans. CL Robertson & J Rutherford), pp
144-145.

3. Kraepelin E: Manic-Depressive Insanity and Paranoia. New York,

Arno Press, 1976.

4. Bleuler E: Dementia Praecox or the Group of Schizophrenias.

New York, International Universities Press, 1950.

5. Freud S: Psychoanalytic notes on an autobiographical account of

a case of paranoia (dementia paranoides). In Strachey J (ed): The
Standard Edition of the Complete Psychological Works of Sigmund
Freud (vol 12). London, Hogarth Press, 1957, pp 9-82.

6. Freud S: Mourning and melancholia. In Strachey J (ed): The

Standard Edition of the Complete Psychological Works of Sigmund
Freud (vol 14). London, Hogarth Press, 1957, pp 243-258.

7. Meyer A: Substitutive activity and reaction-types. In Lief A (ed):

The Commonsense Psychiatry of Dr. Adolf Meyer. New York,
McGraw-Hill, 1948, pp 193-206.

8. Jaspers K: Eifersuchtswahn, Ein Beitrag zur Frage: "Entwicklung

einer Personlichkeit oder Prozess." Zentralblatt fur die Gesamte
Neurologie and Psychiatrie 1:567-6673, 1910.
 9. Stephens JH, McHugh PR: Characteristics and long-term follow-
up of patients hospitalized for mood disorders in the Phipps Clinic,
1913-1940. J New Ment Dis 179:64-73, 1991.

10. Stephens JH, Richard P, McHugh PR: Long-term follow-up of

patients hospitalized for schizophrenia, 1913-1940. J New Ment Dis
185:715-721, 1997.

Chapter 7: Manic-Depression

1. Goodwin FK, Jamison, KR: Manic-Depressive Illness. Oxford,

England, Oxford University Press, 1990.

2. Webster's New International Dictionary of the English Language,

2nd ed. Springfield, Mass, G & C Merriam, 1950, p 42.

3. Rosenthal, NE, Wehr, TA: Seasonal affective disorders.

Psychiatric Ann 17:670-674, 1987.

4. Bunney WE, Jr, Hartmann EL, Mason JW: Study of a patient with
48-hour manic-depressive cycles. II: Strong positive correlation
between endocrine factors and manic defense patterns. Arch Gen
Psychiatry 12:619-625, 1965.

5. Folstein SE, Folstein MF, McHugh PR: Psychiatric syndromes in

Huntington's disease. In Chase TN (ed): Advances in Neurology (vol
23). New York, Raven Press, 1979, pp 281-289.

6. Robinson RG, Starkstein SE, Price TR: Post-stroke depression

and lesion location. Stroke 19:125-126, 1988.

7. Baxter LR, Jr, Schwartz JM, Phelps ME, Mazziotta, JC, Guze,
BH, Selin, CE, Gerner, RH, Sumida, RM: Reduction of prefrontal
cortex glucose metabolism common to three types of depression.
Arch Gen Psychiatry 46:243-250, 1989.
 8. Quetsch RM, Achor RWP, Litin EM, Faucett RL: Depressive
reactions in hypertensive patients. Circulation 19:366-375, 1959.

9. Schildkraut JJ: Neuropsychopharmacology and the Affective

Disorders. Boston, Little, Brown, 1969, pp 7-37.

10. Kallmann F: Heredity in Health and Mental Disorder. New York,

WW Norton, 1953, pp 128-129.

11. Gershon ES, Berrettini W, Nurnberger J, Jr, Goldin LR: Genetics

of affective illness. In Meltzer HY (ed): Psychopharmacology: The
Third Generation of Progress. New York, Raven Press, 1987, pp 481-
491.

12. Egeland JA, Gehard DS, Pauls DL, et al.: Bipolar affective
disorders linked to DNA markers on chromosome 11. Nature
325:783-787, 1987.

13. Kelsoe JR, Ginns EI, Egeland JA, Gerhard, DS, Goldstein, AM,
Bale, SJ, Pauls, DL, Long, RT, Kidd, KK, Conte, G: Re-evaluation of
the linkage relationship between chromosome loci and the gene for
bipolar affective disorder in the old order Amish. Nature 342:238-243,
1989.

14. Berrettini W, Ferraro TN, Goldin LR, Weeks DE, Detera-

Wadleigh S, Nurnberger J1, Gershon ES. Chromosome 18 DNA
markers and manic-depressive illness: Evidence for susceptibility
gene. Proc Nall Acad Sci USA 91:5918-5921, 1994.

15. Stine OC, Xu J, Koskela R, McMahon FJ, Gschwend M, Friddle

S, Clark CD, McInnis MG, Simpson SG, Breschel TS, Vishio E, Riskin
K, Feilotter H, Chen E, Shen S, Folstein S, Meyers DA, Botstein D,
Marr TG, DePaulo JR. Evidence for linkage of bipolar disorder to
chromosome 18 with a parent-of-origin effect. Am J Human Genetics
57:1384-1394, 1995.
 16. McMahon F1, Stine OC, Meyers DA, Simpson SG, DePaulo JR:
Patterns of maternal transmission in bipolar affective disorder. Am J
Human Genetics 56:1277-1286, 1995.

17. McInnis MG, McMahon FJ, Chase GA, Simpson SG, Ross CA,
DePaulo JR: Anticipation in bipolar affective disorder. Am J Human
Genetics 53:385-390, 1993.

18. Gelernter J: Genetics of Bipolar Affective Disorder: Time for

another reinvention? Am J Human Genetics 56:1262-1266, 1995.

Chapter 8: Schizophrenia

1. Gottesman II, Shields J (eds): Schizophrenia: The Epigenetic

Puzzle. New York, Cambridge University Press, 1982.

2. Henn FA, Nasrallah HA (eds): Schizophrenia as a Brain Disease.

New York, Oxford University Press, 1982.

3. Enna SJ, Coyle JT (eds): Neuroleptics: Neurochemical,

Behavioral and Clinical Perspectives. New York, Raven Press, 1983.

4. Schneider K: Clinical Psychopathology, 5th rev ed. New York,

Grune and Stratton, 1959, pp 132-135.

5. Mellor CS: First rank symptoms of schizophrenia. Br J Psychiatry

117:15-23, 1970.

6. Slater E, Roth M: Clinical Psychiatry, 3rd ed. Baltimore, Williams

and Wilkins, 1969, plate viii.

7. Luria R, McHugh PR: The reliability and clinical utility of the

Present State Examination. Arch Gen Psychiatry 30:866-871, 1974.

8. Gur RC, Ragland JD, Gur RE: Cognitive changes in

schizophrenia: A critical look. Int Rev Psychiatry 9:449-457, 1997.
 9. Cannon TD, Zorrilla LE, Shtasel D, Gur RE, Gur RC, Marco EJ,
Moberg P, Price RA: Neuropsychological functioning in siblings
discordant for schizophrenia and healthy volunteers. Arch Gen
Psychiatry 51:651-661,1994.

10. Kremen WS, Seidman LJ, Pepple JR, Lyons MJ, Tsuang MT,
Faraone SV: Neuropsychological risk indicators for schizophrenia: A
review of family studies. Schizophr Bull 20:103-119, 1994.

11. Bleuler E: The prognosis of dementia praecox: The group of

schizophrenias. Ailgemeine Zeitschrift fir Psvehiatrie 65:436-464,
1908. Translated in The Clinical Roots of the Schizophrenia Concept:
Translations of Seminal European Contributions on Schizophrenia.

12. Davison K, Bagley CR: Schizophrenia-like psychoses

associated with organic disorders of the central nervous system: A
review of the literature. In Herrington RN (ed): Current Problems in
Neuropsychiatry (Br J Psychiatry Special Publication No 4). Ashford,
Kent, Royal MedicoPsychological Association, 1969, pp 113-184.

13. Bogerts B, Meertz E, Schonfeld-Bausch R: Basal ganglia and

limbic system pathology in schizophrenia. Arch Gen Psychiatry
42:784-791, 1985.

14. Brown R, Coulter N, Corsellis J, et al.: Post-mortem evidence of

structural brain changes in schizophrenia. Arch Gen Psychiatry
43:36-42, 1986.

15. Johnstone EC, Crowe TJ, Firth DC, Husband J, Creel L:

Cerebroventricular size and cognitive impairment in schizophrenia.
Lancet 2:924-927, 1976.

16. Pearlson GD, Veroff AE, McHugh PR: The use of computed
tomography in psychiatry: Recent applications to schizophrenia,
manic-depressive illness and dementia syndromes. Johns Hopkins
Med J 149:194-202, 1981.
 17. Weinberger DR, DeLisi LE, Perman GP, Targum S, Wyatt RJ:
Computed tomography in schizophreniform disorder and other acute
psychiatric disorders. Arch Gen Psychiatry 39:778783, 1982.

18. Pearlson GD, Marsh L: Section on "Brain Imaging" in American

Psychiatric Association Annual Review of Psychiatry (vol 12), Oldham
JM, Riba MB, Tasman A (eds). Washington, DC, American
Psychiatric Association, 1993.

19. Barta PE, Pearlson GD, Powers RE, Richards SS, Tune LE:
Auditory hallucinations and smaller superior temporal gyral volume in
schizophrenia. Am JPsychiatry 147:1457-1462, 1990.

20. Connell PH: Amphetamine Psychosis (Maudsley Monograph No

5). London, Chapman and Hall, 1958.

21. Griffith JD, Cavanaugh J, Held J, Oates, JA:

Dextroamphetamine: Evaluation of psychotomimetic properties in
man. Arch Gen Psychiatry 26:97-100, 1972.

22. Snyder SH, Banerjee SP, Yamamura HI, Greenberg D: Drugs,

neurotransmitters and schizophrenia. Science 184:1243-1253, 1974.

23. Seeman P, Lee T, Chau-Wong M, Wong K: Antipsychotic drug

doses and neuroleptic dopamine receptors. Nature 261:717-718,
1976.

24. Snyder, SH: The dopamine hypothesis of schizophrenia: Focus

on the dopamine receptor. Am J Psychiatry 133:197-202, 1976.

25. Meador-Woodruff JH: Update on dopamine receptors. Ann Clin

Psychiatry 6:79-89, 1994.

26. Kahn RS, Davis KL: New developments in dopamine and

schizophrenia. In Bloom FE, Kupfer DJ (eds): Psychopharmacology:
The Fourth Generation of Progress. New York, Raven Press, 1994,
pp 1993-1204.

27. Heston LL: Psychiatric disorders in foster home reared children

of schizophrenic mothers. J Ment Science 112:819-825, 1966.

28. Kety SS, Rosenthal D, Wender PH, Schulsinger, F, Jacobsen, B:

Mental illness in the biological and adoptive families of adoptive
individuals who have become schizophrenic: A preliminary report
based on psychiatric interviews. In Fieve RR, Rosenthal D, Brill H
(eds): Genetic Research in Psychiatry. Baltimore, Johns Hopkins
University Press, 1975, pp 147-165.

29. Kringlen E, Cramer G: Offspring of monozygotic twins

discordant for schizophrenia. Arch Gen Psychiatry 46:873-877, 1989.

30. Pulver A, Sawyer J, Childs B: The association between season

of birth and the risk of schizophrenia. Am J Epidemiol 114:735-748,
1981.

31. Pulver A, Liang, Kung-Yee, Brown CH, Wolyniec P, McGrath J,

Adler L, Tam D, Carpenter WT, Childs B: Risk factors in
schizophrenia: Season of birth, gender and familial risk. Br J
Psychiatry 160:65-71, 1992.

32. Green MF: Preliminary evidence for an association between

minor physical abnormalities and second trimester neurodevelopment
in schizophrenia. Psychiatry Research 53:119-127, 1994.

33. Jones P: The early origins of schizophrenia. Br Med Bulletin

1:135-155, 1997.

34. Crow TJ, Done DJ, Sacker A: Cerebral lateralization is delayed

in children who later develop schizophrenia. Schizophrenia Research
3:181-185, 1996.
 35. Walker EF, Lewine RR, Neumann C: Childhood behavioral
characteristics and adult brain morphology in schizophrenia.
Schizophrenia Research 22:93-101, 1996.

36. Weinberger DR: Schizophrenia: From neuropathology to

neurodevelopment. Lancet 346:552-557, 1995.

37. Pilowsky LS, Kerwin RW, Murray RM: Schizophrenia: A

neurodevelopmental perspective. Neuropsychopharmacology 1:83-
91, 1993.

38. Ross CA, Pearlson GD: Schizophrenia, the heteromodal

association neocortex and development: Potential for a neurogenetic
approach. Trends in Neuroscience 19:171-176, 1996.

39. Jones P: The early origins of schizophrenia. Br Med Bulletin

53:135-155, 1997.

Chapter 9: The Dimensional Perspective

1. Allport GW: Personality. New York, Henry Holt, 1937, pp 65-85.

2. Galton F: Measurement of character. Fortnightly Rev 42:179-185,

1884.

3. Fancher RE: Pioneers of Psychology. New York, WW Norton,

1979, p 254.

4. Miles TR: Contributions to intelligence testing and the theory of

intelligence. I: On defining intelligence. Br J Educ Psychology 27:153-
165, 1957.

5. Binet A, Simon T: Methodes nouvelles pour le diagnostic du

niveau intellectuel des anor mauy. Annee Psvchologique 11:191-244,
1905.
 6. Stem W: The Psychological Methods of Testing Intelligence.
Baltimore, Warwick and York, 1914.

7. Reiss AL, Abrams MT, Singer HS, Ross JL, Denckla MB: Brain
development, gender and IQ in normal children. Brain 119:1763-
1774, 1996.

8. Neisser U, Boodoo G, Bouchard TJ, Wade BA, Brody N, Ceci Si,

Halpern DF, Loehlin JC, Perloff R, Sternberg R, Urbina S:
Intelligence: Knowns and unknowns. Am Psychologist 51:77101,
1996.

9. Terman LM, Oden MH: The Gifted Child Grows Up. Stanford,
Stanford University Press, 1947, pp 377-378.

10. Gallon F: English Men of Science. London, Macmillan, 1974, p

12.

1 1. Plomin R, Petrill SA: Genetics and intelligence: What's new?

Intelligence 24:53-77, 1997.

12. McClearn GE, Johansson B, Berg S, Pendersen NL, Ahern F,

Petrill SA, Plomin R: The proportion of the variance in intelligence
attributable to genetic variance. Science 276:1560-1563, 1997.

13. Neisser U, Boodoo G, Bouchard TJ, Wade, BA, Brody, N, Ceci,

SJ, Halpern, DF, Loehlin, JC, Perloff, R, Sternberg, R, Urbina, S:
Intelligence: knowns and unknowns. Am Psychologist 51:77-101,
1996.

14. Tuddenham RD: Soldier intelligence in World Wars I and II. Am

Psychologist 3:54-56, 1948.

15. Wheeler LR: A comparative study of the intelligence of East

Tennessee mountain children. J Educ Psycho! 33:321-334, 1942.
 16. Flynn JR: The mean IQ of Americans: Massive gains, 1932-
1978. Psychological Bulletin 95:29-51, 1984.

17. Horgan J: Get smart, take a test. Scientific American 273:12-14,

November 1995.

18. Flynn JR: Massive gains in fourteen nations: What IQ tests

really measure. Psychological Bulletin 101:171-191, 1987.

19. Hermstein RJ, Murray C: The Bell Curve: Intelligence and Class
Structure in American Life. New York, Free Press, 1994.

20. Campbell FA, Ramey CT: Effects of early intervention on

intellectual and academic achievement: A follow-up study of children
from low income families. Child Development 65:684-698, 1994.

21. Butcher HJ: Human Intelligence: Its Nature and Assessment.

London, Methuen, 1968, p 271.

22. McCleam GE, Johansson B, Berg S, Pendersen NL, Ahern F,

Petrill SA, Plomin R: The proportion of the variance in intelligence
attributable to genetic variance. Science 276:1560-1563, 1997.

23. Hernstein RJ, Murray C: The Bell Curve: Intelligence and Class
Structure in American Life, New York, Free Press, 1994, p 21.

24. Stanley JC: Varieties of intellectual talent. J Creative Behavior

31:93-119, 1997.

25. Hunt E: The role of intelligence in modem society. American

Scientist 83:356-368, 1995.

26. Burt CL: Experimental tests of general intelligence. Br J

Psychology 3:94-177, 1909.

27. Burt CL: The evidence for the concept of intelligence. Br J Educ
Psychology 25:158-177, 1955.
 Chapter 10: Mental Subnormality

1. Clarke AM, Clarke ADB: Criteria and classification of

subnormality. In Clarke AM, Clarke ADB (eds): Mental Deficiency, 3rd
ed. New York, Free Press, 1974, p 15.

2. Kushlick A, Blunden R: The epidemiology of mental subnormality.

In Clarke AM, Clarke ADB (eds): Mental Deficiency, 3rd ed. New
York, Free Press, 1974, p 36.

3. Penrose LS: The Biology of Mental Defect, 3rd ed. London,

Sidgwick and Jackson, 1963, pp 49-50.

4. Wing L: The Autistic Spectrum. London, Constable, 1996.

5. Ross CA, Mclnnis MG, Margolis RL, Li S-H: Genes with triplet
repeats: Candidate mediators of neuropsychiatric disorders. Trends
Neurosci 16:254-260, 1993.

6. Jacobs PA, Glover TW, Mayer M, Fox P, Gerrard JN, Dunn HG,
Herbst DS: X-linked mental retardation: A study of 7 families. Am J
Med Genetics 7:471-489, 1980.

7. Rosett HL, Weiner L: Alcohol and pregnancy: A clinical

perspective. Ann Rev Medicine 36:73-80, 1985.

8. Hams JC: Behavioral phenotypes in mental retardation:

Unlearned behavior disorders. Adv Developmental Disorders 1:77-
106, 1987.

9. Burger PC, Vogel FS: The development of the pathologic

changes of Alzheimer's disease and senile dementia in patients with
Down's syndrome. Am J Pathology 73:457-468, 1973.

10. Corbett JA: Psychiatric morbidity and mental retardation. In

James FE, Snaith RP (eds): Psychiatric Illness and Mental Handicap.
London, Gaskell Press, 1979, pp 11-25.

11. Reid AH: Psychoses in adult mental defectives. 1: Manic-

depressive psychosis. BrJPsychiatry 120:205-212, 1972.

12. Lane H: The Wild Boy ofAveyron. London, Biddies, 1977.

13. Kanner L: Itard, Sequin, Howe: Three pioneers in the education

of retarded children. Am J Mental Deficiency 65:2-10, 1960.

Chapter 11: Temperament, Affective Dimensions, and Personality

Disorders

1. Lazare A, Klerman GL, Armor DJ: Oral, obsessive and hysterical

personality patterns. J Psychiat Res 7:275-290, 1970.

2. Diagnostic and Statistical Manual of Mental Disorders, Third

Edition (DSM-III). Washington, American Psychiatric Association,
1980, pp 313-315.

3. Jaspers K: General Psychopathology. Chicago, University of

Chicago Press, 1963, p 443.

4. Nestadt G, Romanoski AJ, Brown CH, Chahal R, Merchant A,

Folstein MF, Gruenberg EM, McHugh PR: DSM-111 compulsive
personality disorder: An epidemiological survey. Psychol Med 21:461-
471, 1991.

5. Nestadt G, Romanoski AJ, Samuels JF, Folstein MF, McHugh PR:

The relationship between personality and DSM-III Axis I disorders in
the population: Results from an epidemiological survey. Am J
Psychiatry 149:1228-1233, 1992.

6. Ibid.
 7. Allport GW, Odbert HS: Trait-names: A psycholexical study.
Psycholog Monographs 47: (Whole No 211), 1936.

8. Eysenck HJ: Dimensions of Personality. London, Routledge &

Kegan Paul, 1947.

9. Eysenck HJ: The Dynamics of Anxiety and Hurteria: An

Experimental Application of Modern Learning Theory to Psychiatry.
New York, Praeger, 1957.

10. Franks CM: Conditioning and personality: A study of normal and

neurotic subjects. J Abnormal Soc Psychology 52:143-150, 1956.

1 I . Gray JA: The Psychology of Fear and Stress, 2nd ed.

Cambridge, Cambridge University Press, 1987, pp 349-356.

12. Roback AA: The Psychology of Character: With a Survey of

Temperament. New York, Harcourt, Brace, 1928, p 68.

13. Eysenck HJ: The Dynamics of Anxiety and Hysteria: An

Experimental Application of Modern Learning Theory to Psychiatry
New York, Praeger, 1957, pp 223-249.

14. McDougall W: The chemical theory of temperament applied to

introversion and extraversion. J Abnormal Soc Psychology 24:293-
309, 1929.

15. Eysenck HJ: The Dynamics of Anxiety and Hysteria: An

Experimental Application of Modern Learning Theory to Psychiatry.
New York, Praeger, 1957, pp 223-249.

16. Rifkin A, Quitkin F, Carrillo C, Blumberg AG, Klein DF: Lithium

carbonate in emotionally unstable character disorders. Arch Gen
Psychiatry 27:519-523, 1972.
 17. Stein DJ, Hollander E, Liebowitz MR: Neurobiology of impulsivity
and the impulse control disorders. J Neuropsychiatry and Clin
Neurosciences 5:9-17, 1993.

18. Costa PT, Jr, McCrae RR: Still stable after all these years:
Personality as a key to some issues in adulthood and old age. In
Baltes PBB, Brim OG (eds): Life Development and Behavior (vol 3).
New York, Academic Press, 1980, pp 65-102.

19. Costa PT, Jr, McCrae RR: Personality stability and its
implications for clinical psychology. Clin Psyehol Rev 6:407, 1986.

20. Endler NS, Magnusson D: Personality and person by situation

interactions. In Endler NS, Magnusson E (eds): Interactional
Psychology and Personality. New York, John Wiley & Sons, 1976, p
1.

21. Bridger WH, Birns BM, Blank M: A comparison of behavioral

ratings and heart rate measurements in human neonates.
Psychosomat Med 27:123-134, 1965.

22. Shields J: Heredity and psychological abnormality. In Eysenck

HJ (ed): Handbook of Abnormal Psychology. San Diego, Robert R
Knapp, 1973, pp 565-571.

23. Plomin R: Behavioral genetics. In McHugh PR, McKusick VA

(eds): Genes, Brain, and Behavior. New York, Raven Press, 1991.

24. Lochlin JC, Willerman L, Horn JM: Human behavior genetics.

Ann Rev Psych 39:101-133, 1988.

25. Mischel W: On the interface of cognition and personality:

Beyond the person-situation debate. Am Psychol 34:740-754, 1979.

26. Plomin R, DeFries JC, McCleam GE, Rutter M: Behavioral

Genetics, 3rd ed. New York, Freeman, 1997.
 Chapter 12: Emotions, Life Events, Traits of Temperament, and
Treatment

1. Finlay-Jones R, Brown GW: Types of stressful life event and the

onset of anxiety and depressive disorders. Psychol Med 11:803-815,
1981.

2. Kretschmer E: A Text-Book of Medical Psychology. London,

Oxford University Press, 1934, p 195.

3. Slater E: The neurotic constitution: A statistical study of two

thousand neurotic soldiers. J Neurology and Psychiatry 6:1-16, 1943.

4. Lader M, Marks 1: Clinical Anxiety. New York, Grune and

Stratton, 1971, p 8.

5. Swank RL: Combat exhaustion: A description and statistical

analysis of causes, symptoms and signs. J New Ment Dis 109:475-
508, 1949.

6. Lader M, Marks I: Clinical Anxiety. New York, Grune and Stratton,

1971, p 8.

7. Dohrenwend BP, Dohrenwend BS, Gould MS, Link B,

Neugebauer R, Winch-Hitzig R: Mental Illness in the United States:
Epidemiological Estimates. New York, Praeger, 1980.

8. Frank JD: Psychotherapy: The restoration of morale. Am J

Psychiatry 131:271-274, 1974.

9. Eisenberg L: What makes persons "patients" and patients "well"?

Am J Med 69:277-286, 1980.

10. Orne MT, Wender PH: Anticipating socialization for

psychotherapy: Method and rationale. Am J Psychiatry 124:1202-
1211, 1968.
 11. Hoehn-Saric R, Frank JD, Imber SD, Nash EH, Jr, Stone AR,
Battle CC: Systematic preparation of patients for psychotherapy. I:
Effects on therapy behavior and outcome. J Psychiatr Res 2:267-281,
1964.

12. Frank JD, Frank JB: Persuasion and Healing: A Comparative

Study of Psychotherapy, 3rd ed. Baltimore, Johns Hopkins University
Press, 1991.

Chapter 13: The Behavior Perspective

1. Darwin C: The Expression of the Emotions in Man and the

Animals. London, John Murray, 1872.

2. Freud A: Project for a scientific psychology. In Strachey J (ed):

The Standard Edition of the Complete Psychological Works of
Sigmund Freud (vol 1). London, Hogarth Press, 1957, pp 296297.

3. Freud S: Instincts and their vicissitudes. In Strachey J (ed): The

Standard Edition of the Complete Psychological Works of Sigmund
Freud (vol 14). London, Hogarth Press, 1957, p 121.

4. Watson JD: Psychology as the behaviorist views it. Psychological

Review 20:158-177, 1913.

5. Watson JD: Behaviorism. Chicago, University of Chicago Press,

1930, chap 5.

6. Herrnstein RJ: Nature as nurture: behaviorism and the instinct

doctrine. Behaviorism 1:2352, 1972.

7. Richter CP: Animal behavior and internal drives. Q Rev Biol

2:307-343, 1927.

8. Moore RY, Eichler UB: Loss of a circadian adrenal corticosterone

rhythm following suprachiasmatic lesions in the rat. Brain Research
42:201-206, 1972.

9. Stephan FK, Zucker I: Circadian rhythms in drinking behavior and

locomotor activity of rats are eliminated by hypothalamic lesions. Proc
Natl Academy Science USA 69:1538-1586, 1972.

10. Toates F: Motivational Systems. Cambridge, Cambridge

University Press, 1986.

11. Klein T, Martens H, Dijk DJ, Kronauer RE, Seely EN, Czeisler
CA: Circadian sleep regulation in the absence of light preception:
Chronic non-24-hour circadian rhythm sleep disorder in a blind man
with a regular 24-hour sleep-wake schedule. Sleep 16:333-343, 1993.

12. Jaspers K: General Psychopathology (vol 1), Hoenig J, Hamilton

MW (trans). Baltimore, Johns Hopkins University Press, 1997, pp
323-324.

Chapter 14: Characteristics of Motivated Behaviors

1. Hinde RA: Animal Behaviour: A Synthesis of Etiology and

Comparative Psychology, 2nd ed. New York, McGraw-Hill, 1970.

2. Thorpe WH: Learning and Instinct in Animals. London, Methuen,

1963.

3. Hinde RA: Animal Behaviour: A Synthesis of Etiology and

Comparative Psychology, 2nd ed. New York, McGraw-Hill, 1970,
chap 24, pp 594-603.

4. Sipes RG: War, sports, and agression: An empirical test.

American Anthropologist 75:64-86, 1973.

5. McHugh PR, Moran TH: The accuracy of the regulation of caloric

ingestion in the rhesus monkey. Am J Physiology 235:R29-R34,
1978.
 6. McHugh PR, Moran TH: Calories and gastric emptying: A
regulatory capacity with implications for feeding. Am J Physiology
236:8254-R260, 1979.

7. Robinson PH, Moran TH, McHugh PR: Gastric cholecystokinin

receptors and the effect of cholecystokinin on feeding and gastric
emptying in the neonatal rat. Ann NYAcad Sci 448:627629, 1985.

8. McHugh PR, Moran TH: The stomach, cholecystokinin and

satiety. Fed Proc 45:13841390, 1986.

9. Schwartz GJ, Moran TH, McHugh PR: Autoradiographic and

functional development of gastric cholecystokinin receptors in the rat.
Peptides 11:1199-1203, 1990.

10. Schwartz GJ, McHugh PR, Moran TH: Integration of vagal

afferent responses to gastric loads and cholecystokinin in rats. Am J
Physiology 261: R64-R69, 1991.

11. Nauta WJH, Feirtag M: Fundamental Neumanatomy. New York,

Freeman, 1986, p 218.

12. U.S. Department of Health and Human Services: Ninth Special

Report to the U.S. Congress on Alcohol and Health. Washington, DC,
U.S. Department of Health and Human Services, NIH Publication No.
97-4017, 1997.

13. Edwards G, Gross MM: Alcohol dependence: Provisional

description of a clinical syndrome. Br Med J 1:1058-1061, 1976.

14. Vaillant GE: The Natural History ofAlcoholism Revisited.

Cambridge, Harvard University Press, 1995, pp 26-28.

15. Ludwig AM: Understanding the Alcoholic's Mind: The Nature of

Craving and How to Control It. New York, Oxford University Press,
1988.
 16. Jaspers K: General Psychopathology (vol 1), Hoenig J, Hamilton
MW (trans). Baltimore, Johns Hopkins University Press, 1997, pp
323-324.

17. Goldstein A, Lowney LJ, Pal BK: Stereospecific and nonspecific

interactions of the morphine congener levorphanol in subcellular
fractions of mouse brain. Proc Nall Acad Sci USA 68:1742-1747,
1971.

18. Snyder SH: A model of opiate receptor function with implications

for a theory of addiction. In Snyder SH, Matthysse S (eds): Opiate
Receptor Mechanisms. Cambridge, MIT Press, 1975, pp 137-141.

19. Cooper JR, Bloom FE, Roth RH: The Biochemical Basis of
Neuropharmacology, 7th ed. New York, Oxford University Press,
1996, p 304.

20. Schlaepfer TE, Pearlson GD, Wong DF, Marenco S, Dannals

RF: PET study of competition between intravenous cocaine and
Raclopride at dopamine receptors in human subjects. Am J
Psychiatry 154:1209-1213, 1997.

Chapter 15: The Causes of Behavioral Disorders

1. Erdheim J: Ueber hypophysengangsgeschwulste and

Hirncholesteatome. Sitzungsb d.k. Akad d. Wass Math-naturw. Cl.
Wien 113:537-726, 1904.

2. Powley TL: The ventromedial hypothalaminic syndrome, satiety,

and a cephalic phase hypothesis. Psycho! Rev 84:89-126, 1977.

3. Clarren SK, Smith DW: Prader-Willi syndrome: Variable severity

and recurrence risk. Am J Dis Child 131:798-800, 1971.

4. Parkes JD: Sleep and Its Disorders. Baltimore: WB Saunders,

1985.
 5. Wilson JM, Young AB, Kelly WN: Hypoxanthine-quanine
phosphoribosyl tranferase deficiency: The molecular basis for the
clinical syndromes. New Engl J Med 309:900, 1983.

6. Kallmann FJ: Comparative twin study on the genetic aspects of

male homosexuality. J New MentDis 115:283-297, 1952.

7. Heston LL, Shields J: Homosexuality in twins: A family study and

a registry study. Arch Gen Psychiatry 18:149-160, 1968.

8. Slater E, Cowie V: The Genetics of Mental Disorders. Oxford,

England, Oxford University Press, 1971, p 121.

9. Mondimore FM: A Natural History of Homosexuality. Baltimore,

Johns Hopkins University Press, 1996, pp 97-100.

10. Lange J: Crime and Destiny. New York, Charles Boni, 1930, pp
45-46.

11. Christiansen KO: Crime in a Danish twin population. Acta Genet

Med Gemellol 19:323326, 1970.

12. Rosanoff AJ, Handy LM, Plesset IR: The Etiology of Child
Behavior Difficulties: Juvenile Delinquency and Adult Criminality with
Special Reference to Their Occurrence in Twins (Psychiatric
Monograph [California] No I). Sacramento, Department of Institutions,
1941.

13. Hutchings B, Mednick SA: Registered criminality in the adoptive

and biological parents of registered male adoptees. In Mednick SA,
Schulsinger F, Higgins J, Bell B (eds): Genetics, Environment and
Psychopathology. Amsterdam, Elsevier/North-Holland, 1974, pp 215-
227.

14. Bleuler M: Familial and personal background of chronic

alcoholics. In Diethelm 0 (ed): Etiology of Chronic Alcoholism.
Springfield, III, Charles C Thomas, 1955, pp 110-166.

15. Goodwin DW, Schulsinger F, Hermansen L, Guze SB, Winokur

G: Alcohol problems in adoptees raised apart from alcoholic
biological parents. Arch Gen Psychiatry 28:238-243, 1973.

16. Cadoret RJ, Cain CA, Grove WM: Development of alcoholism in

adoptees raised apart from alcoholic biologic relatives. Arch Gen
Psychiatry 37:561-563, 1980.

17. Zinberg NE, Harding WM: Control over Intoxicant Use:

Pharmacological, Psychological and Social Considerations. New
York, Human Sciences Press, 1982, p 151.

18. Terris M: Epidemiology of cirrhosis of the liver: National

mortality, data. Am J Public Health 57:2076-2088, 1967.

19. Durkheim E: Suicide: A Study in Sociology. Glencoe, III, Free

Press, 1951.

20. Glueck S, Glueck E: Unravelling Juvenile Delinquency. New

York, Commonwealth Fund, 1950.

21. Money J, Tucker P: Sexual Signatures: On Being a Man or a

Woman. Boston, Little Brown, 1975, pp 86-118.

22. Bowlby J: The making and breaking of affectional bonds. 1:

Aetiology and psychopathology in the light of attachment theory. Br J
Psychiatry 130:201-210, 1977.

23. Diamond M, Sigmundson HK: Sex reassignment at birth: long-

term review and clinical implications. Arch Pediatr Adolesc Med
151:298-304, 1997.

24. Money J, Ehrhardt AA: Man & Woman Boy & Girl: The
Differentiation and Dimorphism of Gender Identityfrom Conception to
Maturity. Baltimore, Johns Hopkins University Press, 1972, pp 96-
103.

25. Ibid., pp 108-114.

26. Imperato-McGinley J, Peterson RE, Gautier T, Sturla E:

Androgens and the evolution of male-gender identity among male
pseudohermaphrodites with 5 a-reductase deficiency. New Engl J
Med 300:1233-1237, 1979.

27. Hersov LA: School refusal. In Hersov LA, Rutter M (eds): Child
Psychiatry: Modern Approaches. Oxford, Blackwell Scientific
Publications, 1977.

28. Lorand S: Anorexia nervosa. Psychosomat Med 5:282-292,

1943.

29. Skinner BF: About Behaviorism. New York, Alfred A Knopf,

1974.

30. Goodwin DW: Phobia: The Facts. Oxford, Oxford University

Press, 1983.

31. Chomsky N: Review of BF Skinner's Verbal Behavior. Language

35:26-58, 1959.

Chapter 16: Treatment Principles for Behavioral Disorders

1. Kurtz E: Not-God: A History q/Alcoholic:s Anonymous. Center

City, Minn, Hazelden Educational Materials, 1979.

2. Monti PM, Abrams DB, Kadden RM, Cooney NL: Treating Alcohol
Dependence: A Coping Skills Training Guide. New York: Guilford
Press, 1989.
 3. Prochaska JD, DiClemente CC: Toward a comprehensive model
of change. In Miller WR, Heather N (eds): Treating Addictive
Behaviors: Processes of Change. New York, Plenum Press, 1986, pp
3-27.

4. Jones J: Hep-Cats, Nares, and Pipe Dreams: A History of

America c Romance with Illegal Drugs. New York, Scribner, 1996, pp
285-295.

5. Bickel WK, Stitzer ML, Bigelow GE, Liebson IA, Jasinski DR,
Johnson RE: A clinical trial of buprenorphine: Comparison with
methadone in the detoxification of heroin addicts. Clin Pharmacol
Ther 43:72-78, 1988.

6. Berlin FS, Meinecke CF: Treatment of sex offenders with

antiandrogenic medication: Conceptualization, review of treatment
modalities, and preliminary findings. Am J Psychiatry 138:601-607,
1981.

7. Berlin FS, Hunt WP, Malin HM: A five year plus follow-up survey
of criminal recidivism within a treatment cohort of 406 pedophiles,
exhibitionists, and 109 sexual aggressives: Issues and outcome. Am
J Forensic Psychiatry 143:5-28, 1992.

8. Roster A, Witztum E: Treatment of men with paraphilia with a

long-acting analogue of gonadotropin-releasing hormone. New Engl J
Med 338:416-422, 1998.

9. Fuller RK, Branchey L, Brightwell DR, Derman RM, Emrick CD,

Iber FL, James KE, Lacoursiere RB, Leek K, Lowenstann 1:
Disulfiram treatment of alcoholism: A Veterans Administration
cooperative study. JAMA 256:1449-1455, 1986.

10. Volpicelli J, Alterman A, Hayashida M, O'Brien C: Naltrexone in

the treatment of alcohol dependence. Arch Gen Psychiatry 49:876-
880, 1992.
 11. Halmi K: Gastric bypass for massive obesity. In Stunkard AJ
(ed): Obesity. Philadelphia, WB Saunders, 1980, pp 388-394.

12. Weintraub M: Long-term weight control: The National Heart,

Lung, and Blood Institute funded multimodel intervention study. Clin
Pharmacol Ther 51:581-646, 1992.

13. Mark EJ, Patalas ED, Chang HT, Evans RJ, Kessler SC: Fatal
pulmonary hypertension associated with short-term use of
fenfluramine and phentermine. New Engl J Med 337:602-606, 1997.

14. Connolly HM, Crary JL, McGoon, MD, Hensrud DD, Edwards
BS, Edwards WD, Schaff HV: Valvular heart disease associated with
fenfluramine-phentermine. New Engl J Med 337:581588, 1997.

15. Wickler A: Conditioning factors in opiate addiction and relapse.

In Wilner DI, Kassenbaum GG (eds): Narcotics. New York, McGraw-
Hill, 1965.

16. Stitzer ML, Bigelow GE, Gross J: Behavioral treatment of drug

abuse. In Treatments of Psychiatric Disorders (vol. 2). Washington,
DC, American Psychiatric Association, 1989.

17. Silverman K, Higgins ST, Brooner RK, Montoya ID, Lone EJ,
Schuster CR, Preston KL: Sustained cocaine abstinence in
methadone maintenance patients through voucher-based
reinforcement therapy. Arch Gen Psychiatry 53:409-415, 1996.

18. Brewer C, Smith J: Probation linked supervised disulfiram in the

treatment of habitual dnmken offenders: Results of a pilot study. Br
Med J 287:1282-1283, 1983.

19. Rouser E, Brooner RK, Regier M, Bigelow GE: Psychiatric

distress in antisocial drug abusers: relation to other personality
disorders. Drug and Alcohol Dependence 34:149-154, 1994.
 20. Smart RG: Outcome studies of therapeutic community and
halfway house treatment for addicts. Int J Addict 11:143-159, 1976.

Chapter 17: Bulimia Nervosa

1. Prochaska JO, DiClemente CC: Toward a Comprehensive Model

of Change in Treating Addictive Behaviors: Processes of Change.
New York, Plenum Press, 1986, pp 3-27.

2. Andersen AE: Practical Comprehensive Treatment of Anorexia

Nervosa and Bulimia. Baltimore, Johns Hopkins University Press,
1985.

3. Romanoski AJ: Alcohol and Drug Dependence. In Stobo JD,

Hellmann D, Ladenson P, Petty B, Traill T (eds): The Principles and
Practice of Medicine, 23rd ed. Stamford, Conn, Appelton and Lange,
1996, pp 927-936.

4. Russell GFM: Anorexia nervosa: Its identity as an illness and its

treatment. In Price JH (ed): Modern Trends in Psychological Medicine
(vol. 2), 1970, pp 131-164.

5. Russell GFM: Bulimia nervosa: An ominous variant of anorexia

nervosa. Psychological Med 9:429-448, 1979.

6. Szmukler GI, Patton G: Sociocultural models of eating disorder. In

Szmukler GI, Dare C, Treasure J (eds): Handbook of Eating
Disorders: Theory, Treatment and Research. Chichester, England,
John Wiley & Sons, 1995, pp 177-192.

7. Lorand S: Anorexia nervosa. Psychosomatic Med 5:282-292,

1943.

8. Herzog DB, Keller MB, Sacks NR, Yeh CJ, Lavori PN: Psychiatric
co-morbidity in treatment-seeking anorexics and bulimics. J Am Acad
Child Adolesc Psychiatry 31:810-818, 1992.
 9. Russell GFM: Anorexia nervosa: Its identity as an illness and its
treatment. In Prince JH (ed): Modern Trends in Psychological
Medicine (vol 2), 1970, pp 131-164.

10. Schlaepfer TE, Pearlson GD, Wong DF, Marenco S, Dannals

RF: PET study of competition between intravenous cocaine and
raclopride at dopamine receptors in human subjects. Am J Psychiatry
154:1209-1213, 1997.

11. Smith GP: Dopamine and food reward. Prog Psychobiol Physiol
Psychol 16:83-144,1995.

12. Giraudo SQ, Grace MK, Welch CC, Billington CJ: Naloxone's
anorectic effect is dependent upon the relative palatability of food.
Pharmacol Biochem Behav 46:917-921, 1993.

13. Kirkham TC, Cooper SI: Attenuation of sham feeding by

naloxone is stereospecific evidence for opioid mediation of
orosensory reward. Physiol and Behav 43:845-847, 1988.

14. Smith GP: Dopamine and food reward. Prog Psychobiol Physiol
Psychol 16:83-144, 1995.

Chapter 18: Hysteria

1. Slavney PR: Perspectives on "Hysteria. " Baltimore, Johns

Hopkins University Press, 1990.

2. Reich P, Gottfried LA: Factitious disorders in a teaching hospital.

Ann Intern Med 99:240247, 1983.

3. Parsons T: Social Structure and Personality. New York, Free

Press, 1964, pp 274-275.

4. Parsons T: The Social System. Glencoe, III, Free Press, 1951, pp

436-437.
 5. Mechanic D, Volkart EH: Stress, illness behavior, and the sick
role. Am Sociological Review 26:51-58, 1960.

6. Pilowsky 1: Abnormal illness behavior. Br J Med Psychology

42:347-351, 1969.

7. Pilowsky 1: A general classification of abnormal illness behaviors.

Br J Med Psychology 51:131-137, 1978.

8. Slavney PR: Perspectives on "Hysteria. " Baltimore, Johns

Hopkins University Press, 1990, pp 34-55.

9. Thigpen CH, Cleckley H: The Three Faces of Eve. New York,

McGraw-Hill, 1957.

10. Schreiber FR: Sybil. Chicago, Henry Regnery, 1970.

11. Reich P, Gottfried LA: Factitious disorders in a teaching hospital.

Ann Intern Med 99:240247, 1983.

12. Head H: The diagnosis of hysteria. Br Med J 1:827-829, 1922.

13. Spiegel H: The Grade 5 Syndrome: The highly hypnotizable

person. Int J Clin Exp Hypnosis 22:303-319, 1974.

14. Jaspers K: General Psychopathology. Baltimore, Johns Hopkins

University Press, 1997, p 443.

15. Kaminsky MJ, Slavney PR: Methodology and personality in

Briquet's syndrome: A reappraisal. Am J Psychiatry 133:85-88, 1976.

16. Kaminsky MJ, Slavney PR: Hysterical and obsessional features

in patients with Briquet's syndrome (somatization disorder).
Psychological Medicine 13:111-120, 1983.

17. Guillain G: J.M. Charcot: His Life, His Work, Bailey P (trans).
New York, Paul B Hoeber, 1959.
 18. Babinski J, Froment J: Hysteria or Pithiatism and Reflex
Nervous Disorders in the Neurology of War, Rolleston JD (trans).
London, University of London Press, 1918.

19. McHugh PR: Witches, multiple personalities and other

psychiatric artifacts. Nature Medicine 1:110-114, 1995.

20. Merskey H, Buhrich TH: Hysteria and organic brain disease.

BrJMed Psychology 48:359366, 1975.

21. Roy A: Identification and hysterical symptoms. Br J Med

Psychology 50:317-318, 1977.

22. Cialdini RB: Influence: How and Why People Agree to Things.
New York, Quill Press, 1984.

23. Merskey H: The Analysis of Hysteria: Understanding Conversion

and Dissociation, 2nd ed. London: Gaskell, 1995, p 308.

24. Slater E, Glithero E: A follow-up of patients diagnosed as

suffering from "hysteria." J Psychosomatic Research 9:9-13, 1965.

25. Veith I: Hysteria: The History of a Disease. Chicago, University

of Chicago Press, 1965.

26. Kenny, M: The Passion ofAnsel Bourne: Multiple Personality in

American Culture. Washington, DC, Smithsonian Institution Press,
1986.

27. Loftus E, Ketcham K: The Myth of Repressed Memory. New

York, St Martin's Press, 1994.

28. Fatty, Thomas A: The diagnosis of multiple personality disorder:

A critical review. Br J Psychology 153:597-606, 1988.

Chapter 19: Suicide

 1. Center for Disease Control and Prevention: Advance report of
final mortality statistics, 1990. Monthly Vital Statistics Report 41:1-52,
1993.

2. Menninger K: Man against Himself. New York, Harcourt Brace

and World, 1938.

3. Schmidt CW Jr, Shaffer JW, Zlotowitz HI, Fisher RS: Suicide by

vehicular crash. Am J Psychiatry 134:175-178, 1977.

4. Robins E: The Final Months: A Study of the Lives of 134 Persons

Who Committed Suicide. New York, Oxford Press, 1981.

5. Harris EC, Barraclough BM: Suicide as an outcome for mental

disorders: A meta-analysis. Br J Psychiatry 170:205-228, 1997.

6. Harris EC, Barraclough BM: Suicide as an outcome for medical

disorders. Medicine 73:28 1296, 1994.

7. McHugh PR, Goodell H: Suicidal behavior: A distinction in

patients with sedative poisoning seen in a general hospital. Arch Gen
Psych 25:456-464, 1971.

8. Freud S: Beyond the Pleasure Principle. New York, WW Norton,

1975.

9. Asberg M, Thuren P, Traskman, L. Bertilsson L, Ringberger V:

Serotonin depression: A biochemical subgroup within the affective
disorders. Science 191:478-480, 1976.

10. Brown GL, Ebert MH, Goyer PF, Jimerson DC, Klein NJ, Bunney
WE, Goodwin FK: Aggression, suicide, and serotonin: Relationship to
CSF amine metabolites. Am J Psychiatry 139:741-746, 1982.

11. Van Praag HM: CSF 5-HIAA and suicide in non-depressed

schizophrenics. Lancet 2:977978, 1983.
 12. Linnoila M, Virkkunen M, Scheinin M, Nuutila, A, Rimon, R,
Goodwin, FK: Low cerebrospinal fluid 5-hydroxyindoleacetic acid
concentration differentiates impulsive from nonimpulsive violent
behavior. Life Sciences 33:2609-2614, 1983.

13. Virkkunen M, Nuutila A, Goodwin FK, Linnoila, M: Cerebrospinal

fluid monoamine metabolite levels in male arsonists. Arch Gen
Psychiatry 44:241-247, 1987.

14. Mann JJ, Underwood MD, Arango V: Postmortem studies of

suicide victims. In Watson SJ (ed): Biology of Schizophrenia and
Affective Disease. Washington, DC, American Psychiatric
Association, 1996, pp 197-220.

15. Arango V, Underwood MD, Gubbi AV, Mann JJ. Localized

alterations in pre- and postsynaptic serotonin binding sites in the
ventrolateral prefrontal cortex of suicide victims. Brain Research
688:121-133, 1995.

16. Stein DJ, Hollander E, Liebowitz MR: Neurobiology of impulsivity

and the impulse control disorders. J Neuropsychiatry Clin
Neuroscience 5:9-17, 1993.

17. Mann JJ: The neurobiology of suicide. Nature Medicine 4:25-30,

1998.

18. Sainsbury P: Suicide in London: An Ecological Study. New York,

Basic Books, 1956.

19. Durkheim E: Suicide: A Study in Sociology, Spaulding J,

Simpson G (trans). New York, Free Press, 1951.

20. Stengel E, Cook WG: Attempted Suicide. New York, Oxford

University Press, 1958.
 21. Dublin LI: Suicide: A Sociological and Statistical Study. New
York, Ronald Press, 1963.

22. Hendin H: Suicide and Scandinavia. New York, WW Norton,

1965.

23. Hendin H: Suicide in America: New and Expanded Edition. New

York, WW Norton, 1995.

24. Hams EC, Barraclough BM: Suicide as an outcome for medical

disorders. Medicine 73:281-296, 1994.

25. Cavan RS: Suicide. Chicago, University of Chicago Press,

1928.

26. Schwartz AJ, Whitaker LC: Suicide among college students:

Assessment, treatment and intervention. In Blumenthal SJ, Kupfer DJ
(eds): Suicide over the Life Cycle. Washington, DC, American
Psychiatric Association, 1990, pp 303-340.

27. Themstrom M: Hatay Heaven: Diary ofa Harvard Murder. New

York, Doubleday, 1997.

28. Noyes R, Frye S. Hartford C: Single case study: Conjugal

suicide pact. J Nerv Mental Dis 165:72-75, 1977.

29. Mehta D, Mathew P, Mehta S: Suicide pact in a depressed

elderly couple. JAm Cancer Soc 136:136-158, 1978.

30. Hendin H: Seduced by Death: Doctors, Patients, and the Dutch

Cure. New York, WW Norton, 1997.

31. Hendin H: Suicide in America: New and Expanded Edition. New

York, WW Norton, 1995.

32. Marzuk P, Tardiff K, Hirsch CS, Leon AC, Stajic M, Hartwell N,

Portera L: Increase in suicide by asphyxiation in New York City after
the publication of Final Exit. New Engl J Med 329:1508-1510, 1993.

33. Sainsbury P: Suicide in London: An Ecological Stud: New York:

Basic Books, 1956.

34. Marzuk PM, Leon AC, Tardiff K, Morgan EB, Stajic J, Mann 11:
The effect of access to lethal methods of injury on suicide rates. Arch
Gen Psychiatry 49:451-458, 1992.

35. Hendin H: Suicide in America: New and Expanded Edition. New

York, WW Norton, 1995 p 23.

36. Hendin H: Seduced by Death: Doctors, Patients, and the Dutch

Cure. New York, WW Norton, 1997, p 29.

37. Jamison KR: Mood disorders and patterns of creativity in British

writers and artists. P.cvchiatrv 52:125-134, 1989.

Chapter 20: The Life-Story Perspective

1. Evans RJ: In Defense of History. London, Granta Books, 1997.

2. Hobsbawn E: On History. New York, New Press, 1997.

3. Mehta V: Fly and the Fly Bottle: Encounters with British

Intellectuals. New York, Columbia University Press, 1983.

4. Geyl P: Napoleon, For and Against. Harmondsworth, England,

Penguin Books, 1949.

5. Taylor, AJP: The Origins of the Second World War. London,

Hamilton, 1961.

6. Harwit M: An Exhibit Denied: Lobbying the History of Enola Gay.

New York, SpringerVerlag, 1996.
 7. Tolstoy, L: War and Peace. Translated by Louise and Aylmer
Maud. New York: Simon and Schuster, 1942, p 1317.

8. Mehta V: Fly and the Fly Bottle: Encounters with British

Intellectuals. New York: Columbia University Press, 1983, p 129.

9. Frank, JD, Frank JB: Persuasion and Healing: A Comparative

Study of Psychotherapy, 3rd ed. Baltimore, Johns Hopkins University
Press, 1991.

10. Cantrill H: The "Why" of Manc Experience. New York,

Macmillan, 1950.

11. Frank JD, Frank JB: Persuasion and Healing: A Comparative

Study of Psychotherapy, 3rd ed. Baltimore, Johns Hopkins University
Press, 1991, pp 26-34.

12. Spence, DP: Narrative Truth and Historical Truth: Meaning and
Interpretation in Psychoanalysis. New York, WW Norton, 1982.

13. Spence, DP: Narrative truth and theoretical truth. Psychoanalytic

Quarterly 51:43-69, 1982.

14. Spence, DP: Tough and tender minded hermeneutics. In Messer

SB, Isaid LA, Woolfolk RL (eds): Hermeneutics and Psychological
Theory. New Brunswick, NJ, Rutgers University Press, 1987.

15. Foucault M: Madness and Civilization: A History of Insanity in

the Age of Reason. New York, Pantheon, 1965, pp 3-7.

Chapter 21: The Application of the Life-Story Perspective in Practice

1. Guze, SB: Why Psychiatry Is a Branch of Medicine. New York,

Oxford University Press, 1992, pp 80-83.
 2. Frank JD, Frank JB: Persuasion and Healing: A Comparative
Study of Psychotherapy, 3rd ed. Baltimore, Johns Hopkins University
Press, 1991.

3. Breuer J, Freud S: On the psychical mechanism of hysterical

phenomena: Preliminary communication. In Strachey J (ed): The
Standard Edition of the Complete Psychological Works of Sigmund
Freud (vol. 2). London, Hogarth Press, 1955, p 7.

4. Sullivan HS: Clinical Studies in Psychiatry. New York, WW

Norton, 1956, p 238.

5. Rako S, Mazer H (eds): Elvin Semrad: The Heart of a Therapist.

Northvale, NJ, Jason Aronson, 1983.

6. McHugh PR: A structure for psychiatry at the century's turn: The

view from Johns Hopkins. J Royal Soc Med 85:483-487, 1992.

7. Kelly GA: The Psychology of Personal Constructs: A Theory of

Personality (vol 1). New York, WW Norton, 1955.

8. Beck AT: Cognitive Therapy and the Emotional Disorders. New

York, International Universities Press, 1976.

9. Spence, DP: The Freudian Metaphor: Toward Paradigm Change

in Psychoanalysis. New York, WW Norton, 1987.

Chapter 22: Practical Implications of the Perspectives

1. Engel GL: The need for a new medical model: A challenge for
biomedicine. Science 196:129-136, 1977.

2. Engel GL: The clinical application of the biopsychosocial model.

Am JPsychiatry 137:535544, 1980.

3. Ibid.
 4. Winters EE, Bowers AM (eds): Adolf Meyer, 1866-1950. In
Psychobiology: A Science of Man. Springfield, Ill, Charles C Thomas,
1957.

5. Robinson RG, Bolduc P, Price TR: A two year longitudinal study

of post-stroke depression. Diagnosis and outcome at one and two
year follow-up. Stroke 18:837-843, 1987.

6. Starkstein SE, Robinson RG, Price TR: Comparison of cortical

and subcortical lesions in the production of post-stroke mood
disorders. Brain 110:1045-1059, 1987.

7. Lipsey JR, Robinson RG, Pearlson GD, Rao K, Price TR:

Nortriptyline treatment of poststroke depression: A double blind study.
Lancet 1:297-300, 1984.

8. Mayberg HS: Neuroimaging studies of depression in neurologic

disease. In Depression in Neurologic Disease, Starkstein SE and
Robinson RG (eds). Baltimore, Johns Hopkins University Press,
1993.

Chapter 23: Integrative Summary

1. Mayer-Gross W, Slater E, and Roth M: Clinical Psychiatry, 3rd ed.

Slater E and Roth M (eds). London, Bailliere, Tindall & Cassell, 1969.

Appendix

1. Kreitman N, Sainsbury P, Morrissey J: The reliability of psychiatric

assessment: An analysis. J Ment Sci 107:887-908, 1961.

2. Luria R, McHugh PR: The reliability and clinical utility of the

Present State Examination. Arch Gen Psychiatry 30:866-871, 1974.

3. Andreasen NC: Affective flattening and the criteria for

schizophrenia. Am J Psychiatry 136:944-947, 1979.
 4. Rutter M, Cox A: Psychiatric interviewing techniques. I: Methods
and measures. Br J Psychiatry 138:273-282, 1981.