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This page intentionally left blank
 PSYCHOTIC DEPRESSION

Psychotic depression is a distinct and acute clinical condition along the

spectrum of depressive disorders. It can manifest itself in many ways and
be mistaken for schizophrenia. It often induces physical deterioration,
mortally dangerous acts toward self or others, or completed suicide. This
book aims to help clinical practitioners and trainees describe their
observations of psychotic depression, formulate treatment, and express
expectations of recovery from illness. It focuses on all facets of the dis-
order, from clinical history to coverage of the current state-of-the-art
diagnostic and treatment protocols. Medical readers of this book will
come away able to diagnose and readily treat psychotic depression and
thus will be able to serve their patients better. Non-physician readers
will come away with the message that this is a terrible illness, but there
is hope. This book fills an important gap in the realm of psychiatric
literature.

Dr. Conrad M. Swartz is a board-certified psychiatry professor who has

written and lectured extensively on depression, anxiety, and the use of
electroconvulsive therapy for severe depression.

Edward Shorter is a historian of psychiatry who has written three books

on the history of psychiatry and psychosomatic illness.
 Also by Edward Shorter
A History of Psychiatry (1997)
Historical Dictionary of Psychiatry (2005)
Psychotic Depression

Conrad M. Swartz
Southern Illinois University School of Medicine

Edward Shorter
University of Toronto
CAMBRIDGE UNIVERSITY PRESS
Cambridge, New York, Melbourne, Madrid, Cape Town, Singapore, São Paulo

Cambridge University Press

The Edinburgh Building, Cambridge CB2 8RU, UK
Published in the United States of America by Cambridge University Press, New York
www.cambridge.org
Information on this title: www.cambridge.org/9780521878227

© Conrad M. Swartz and Edward Shorter 2007

This publication is in copyright. Subject to statutory exception and to the provision of

relevant collective licensing agreements, no reproduction of any part may take place
without the written permission of Cambridge University Press.
First published in print format 2007

ISBN-13 978-0-511-27833-4 eBook (EBL)

ISBN-10 0-511-27833-0 eBook (EBL)

ISBN-13 978-0-521-87822-7 hardback

ISBN-10 0-521-87822-5 hardback

Cambridge University Press has no responsibility for the persistence or accuracy of urls
for external or third-party internet websites referred to in this publication, and does not
guarantee that any content on such websites is, or will remain, accurate or appropriate.

Every effort has been made in preparing this book to provide accurate and up-to-date
information that is in accord with accepted standards and practice at the time of
publication. Nevertheless, the authors, editors, and publisher can make no warranties that
the information contained herein is totally free from error, not least because clinical
standards are constantly changing through research and regulation. The authors, editors,
and publisher therefore disclaim all liability for direct or consequential damages resulting
from the use of material contained in this book. Readers are strongly advised to pay careful
attention to information provided by the manufacturer of any drugs or equipment that
they plan to use.
To Cynthia and Anne Marie
 Contents

Preface page xi
Acknowledgments xv

Chapter 1 Introduction 1
Chapter 2 History of Psychotic Depression 21
Chapter 3 Diagnosis in Psychotic Depression 59
Chapter 4 Patients’ Experience of Illness 128
Chapter 5 Treatment in Historical Perspective 144
Chapter 6 Treatment: Pitfalls and Pathways 167
Chapter 7 Treatment: ECT, Medications, and More 192
Chapter 8 Treatment by Type of Psychotic Depression 235

Appendix 1 Summary Guide to Psychiatric Concepts 263

Appendix 2 Summary Guide to Psychotropic Medication
and Treatment 269
References 283
Index 305

ix
 Preface

Psychotic depression is an alloy of psychosis and depression

that is not separable into psychosis and depression. Psychosis is a
symptom that thought and behavior have become unrelated to reality. It
is, in other words, a symptom of madness just as biological as delirium.
Psychologists and psychodynamicists often understand illnesses as
psychological conditions, caused by psychological conflicts and blamed
on unconscious psychological mechanisms. Saying ‘‘illness’’ does not
denote ‘‘biological’’ to them. We should like readers to perceive the old-
time biological meaning of madness, not through the psychology of the
unconscious. Depression is an illness that includes, among other
symptoms, the loss of ability to think things through. Patients with
psychotic depression have an illness with symptoms of disordered
thought, behavior, and mood. They are both delusional and suffer a
mood disorder. They are truly physically ill, and their illness represents a
terrible suffering for patients and their families, worse so because they
cannot describe it. This book aims to help health care professionals find

xi
 preface

the words to describe their observations of psychotic depression, to work

together with their patients to formulate treatment, and to express
expectations of recovery from illness. The following pages contain the
past, the present, and the future of patient-centered concerns about
conventional, and some not entirely conventional, ideas concerning its
diagnosis and treatment.
We are trying to reach mainly physicians here, because it is upon
their shoulders that responsibility for diagnosis and treatment rests. But
we have tried not to make the book so forbiddingly ‘‘medical’’ as to be
inaccessible to those outside of medicine such as the patients themselves,
their friends and families, and all others interested in or curious about
psychiatric illness. It’s hard to write both for doctors and patients, for
obvious reasons. The pharmaceutical armamentarium so familiar to
physicians is a jumble of unfamiliar terms to everyone else. Physicians are
accustomed to thinking cooly about diagnoses that patients experience as
the horrors of hell and to rationally considering treatments that everyone
else deeply fears. The whole alphabet soup of instruments and proce-
dures that doctors take in with the mother’s milk of medical school is
usually entirely unfamiliar to patients, except terms such as ‘‘EEG’’ that
they have encountered in their own experience.
Thus, patients may not consume avidly every last line of the diagnosis
chapter because they are mainly interested in the one illness that they
have, not in the entire range of phenomena that they could conceivably
have but don’t. And physicians may smile indulgently at the chapter on
subjective aspects of psychotic depression – psychotic depression as the
patients experience it. But they should not. Knowing your patients’
experience of illness, and being able to succor and advise them appro-
priately, is part of the practice of medicine. At some level doctors realize
they do not feel what their patients experience until they go through the
same condition themselves or with a close relative. Of course, this
awareness is easily overlooked in the everyday demands of clinical
practice. Doctors, please do not imagine that you know all that your
patients go through, because you cannot.

xii
 preface

Medical readers of this book will come away able to diagnose and
readily treat psychotic depression, and thus be able to serve their patients
better. Nonmedical readers will come away with the message that this is
indeed a terrible illness, but that there is hope. This can be a precious
message.
Conrad Swartz is a practicing psychiatrist and an academic scholar
who has published on many subjects, and a specialist in medical treat-
ment, electroconvulsive therapy, and psychopharmacology. Much of his
research reflects his engineering PhD along with his MD. Edward
Shorter specializes in the history of psychiatry and psychopharmacology,
and is a PhD. Shorter comes to the story via the trail of age-old suffering;
Swartz has spent a lifetime treating patients. Both perspectives are useful
and offer a comprehensive picture of what one is up against in this
disease called psychotic depression.
Conrad M. Swartz
Edward Shorter

xiii
 Acknowledgments

S u s a n b
e la nge r , Heather Dichter, and Ellen Tulchinsky in the

History of Medicine Program of the University of Toronto have been of
great help in various aspects of the preparation of this book. We should
especially like to acknowledge the sage advice and practical experience
of Marc Strauss of Cambridge University Press and our copy editor
Anula Lydia.

xv
 1

Introduction

On june 20, 2001, Andrea Yates of Houston, Texas, drowned her five
children one by one in the bathtub in her home. She was clearly seriously
ill and had been treated with the drugs sertraline (Zoloft), olanzapine
(Zyprexa), haloperidol, and lorazepam among other remedies. Her
attending psychiatrist had rejected electroconvulsive therapy (ECT) for
her on the grounds that it was ‘‘for far more serious disorders’’ (Denno,
2003). She was said to have committed this terrible act in the grips of
major depression. But that cannot be right. ‘‘Major depression’’ is not a
specific illness. She had psychotic depression. She was improperly
diagnosed, evaluated, and certainly inadequately treated. Her illness gave
her an overwhelming compulsion or she would not have pushed the
heads of her children underwater in the delusive belief that she was saving
them from Hell.
Andrea Yates herself was caught in the jaws of Hell. An editorial
in the British medical weekly Lancet in 1940 called depression
‘‘perhaps the most unpleasant illness that can fall to the lot of man’’

1
 psychotic depression

(Lancet, 1940), and in the midst of a psychotic depression, Yates had

opportunity to experience this. Psychiatry could have rescued her, but
confusion about her diagnosis and her treatment interfered.
The Andrea Yates story had one more chapter, in which the reality of
her illness from psychotic depression was finally understood. An appeals
court overturned her original conviction because of inaccurate evidence
from Park Dietz, a forensic psychiatrist who had testified for the pro-
secution. In July 2006, Yates again went before a jury, which found her
not guilty. ‘‘The jury looked past what happened and looked at why it
had happened,’’ said her former husband. ‘‘Yes, she was psychotic.
That’s the whole truth.’’ This time Yates was sentenced to an indefinite
term in a maximum security hospital (Associated Press, 2006). Thus the
story had an end that lifted slightly the flap of public ignorance about this
disorder.
What happened to Andrea Yates between her 2002 and 2006
courtroom trials is also noteworthy. In 2002 she was physically fit. In
2006 she was hardly recognizable, flabby and overweight. In television
views of her in prison before the 2006 trial she was unkempt and poorly
groomed. Under psychiatric treatment her appearance strikingly dete-
riorated. What types of psychiatric treatments cause such deterioration,
and what do not? People avoid psychiatrists because they are afraid of
being stigmatized or controlled by psychiatric treatment. Success in
treatment includes avoiding stigmatization and behavioral deterioration
from the treatment.
Marc Cherry was the producer and scriptwriter of the TV series
Desperate Housewives. He said that, like Andrea Yates, his mother was at
the cusp of a similar experience. He and his mother had been watching
the news coverage of the Yates trial one evening and she grunted, ‘‘I was
once almost there myself.’’ Cherry was so surprised that he said to
himself, ‘‘If my own mother was once so desperate, then every woman
has probably felt the same thing’’ (Kreye, 2005).
But no! Andrea Yates killed her children in the grips of a delusional
depression. However stressed, every woman does not have a psychotic

2
 introduction

depression, any more that every woman has a pancreatic tumor or a

spinal infection. Psychotic depression is as much a medical illness as
tuberculosis. It is not a blip on the stress continuum. Mrs Cherry, at one
point, as her son said, set to throw her children out the car window, may
or may not have had a psychotic depression. But it is a disease, not a
normal response.

What is psychotic depression?

There is a classical psychiatric tradition of dividing depression into two

types.1 As Michael Shepherd, the dean of British psychopharmacology,
pointed out in 1959, there were hospital depressions and then there were
‘‘large groups of loosely termed ‘neurotic,’ ‘reactive,’ or ‘exogenous’
depression often admixed with the clinical manifestations of anxiety.
Many of them run a chronic, fluctuating course.’’ They were certainly
not suitable for admission to hospital. Most of these patients ‘‘do not
come to medical attention at all but rely rather on the advice of the
chemist [pharmacist] or on self-medication’’ (Shepherd, 1959).
In one type of depression – Shepherd’s hospital depression – brain
biology takes over. The depression happens out of the blue. The patients

1 Aaron T. Beck seems to prefer, among possible polar depression types, the
‘‘distinction between endogenous and reactive depressions.’’ A. T. Beck. 1967.
Depression: Clinical, experimental, and theoretical aspects. New York: Hoeber/Harper
& Row, p. 66. For his discussion of the difference between ‘‘neurotic’’ and
‘‘psychotic’’ depressions, see pp. 75–86. See also David Goldberg and Peter Huxley.
1980. Mental illness in the community: The pathway to psychiatric care. London:
Tavistock. The authors argue that there may be a continuum in depressive illness.
Yet ‘‘ . . . [s]omewhere on this continuum the line must be drawn between those
whose mood disorder is impairing their social and psychological functioning, and
those in whom normal homeostatic mechanisms may be expected to operate.’’
(p. 15) See, e.g., P[er] Bech. 1988. A review of the antidepressant properties of
serotonin reuptake inhibitors. Adv Biol Psychiatry 17: 58–69; ‘‘We will analyze the
depressive inpatients and the depressive outpatients as two different diagnostic
entities’’ (p. 60).

3
 psychotic depression

are very sick and may have delusions and hallucinations or sink into
stupor. In 1920 German psychiatrist Kurt Schneider, then in Cologne,
proposed a term for this kind of depression in which the patients were
terribly slowed. He called it endogenous depression,2 borrowing from
the great German nosologist Emil Kraepelin the term ‘‘endogenous,’’ by
which Kraepelin meant biological, indwelling in the brain, and dom-
inating the body. Schneider contrasted endogenous depression with a
second type, which he called ‘‘reactive’’ depression, usually seen outside
of hospital settings. Reactive depression has almost nothing in common
with psychotic depression except maybe sadness. Yet reactive depression
can also be quite serious, the patients hovering on the brink of suicide.
But reactive patients are not psychotic nor do they experience the same
kind of ‘‘psychomotor retardation,’’ to use the technical term for
thought and action being slowed. There are two different illnesses here,
one involving a terrible, pathological slowing among other symptoms
and the other dependent on external events.
Whether there are two depressions or one – and, if two, whether they
may be divided into endogenous and reactive – has long been con-
troversial.3 We step into a snake pit here. But the massive evidence of
the history of psychiatric illness does indeed suggest that there are
two. For the sake of convenience we call them here endogenous and
reactive-neurotic, fully aware that future generations may find these

2 K. Schneider. 1920. Die schichtung des emotionalen lebens und der aufbau der
depressionszustaende. Zeitschrift fur die gesamte Neurol Psychiatr 59: 281–6. ‘‘Bei der
betrachtung der depressionszustaende gehen wir von den beiden, in ihren extremen
auspraegungen wohl characterisierten typen aus, der reinen motivlosen ‘endogen’
und der rein reaktiven depression’’ (In considering the types of depression, we use as
a basis the two forms that have been best characterized in their extreme forms, the
purely motiveless ‘‘endogenous’’ and the purely reactive depression; p. 283.)
3 Joe Mendels and Carl Cochrane (1968) began the revival of the endogenous-reactive
split: The nosology of depression: The endogenous-reactive concept. Am J Psychiatry
124 (Suppl): 1–11. Another important early contribution was I. Pilowsky et al. 1969.
The classification of depression by numerical taxonomy. Br J Psychiatry 115: 937–45.
See also the work of Michael Feinberg and Bernard J. Carroll. 1983. Separation of
subtypes of depression using discriminant analysis. J Affect Disord 5: 129–39.

4
 introduction

terms inadequate. Yet the present state of science does not permit us to
go beyond them, and whatever one chooses to call them the fundamental
reality is that two classes of depressive illness exist, as unalike as chalk and
cheese. Most practitioners will probably agree with this, even though
they are forced into the procrustean one-depression bed by the official
diagnostic schema – the Diagnostic and Statistical Manual (DSM) of the
American Psychiatric Association – that is now current.
One distinguished believer in the two-depression concept is
Joe Schildkraut at Harvard. In 1965 Schildkraut devised one of the most
influential ever biological theories in psychiatry. He said that affective
disorders (depression and mania) result from disturbances in the
metabolism of the neurotransmitter norepinephrine. Chemically, nor-
epinephrine belongs to the ‘‘catecholamine’’ class of neurotransmitters,
and Schildkraut’s ideas became famous as the ‘‘catecholamine hypoth-
esis of affective disorders.’’4 Schildkraut, as other observers, saw that
there were two kinds of depression. Later, he characterized the endo-
genous disorders as ‘‘running out of gas depressions’’ and the reactive as
‘‘chronic characterological depressions.’’ (He actually did not use the
term reactive but rather ‘‘depressions with much more in the way
of . . . self-pity and histrionics.’’ Yet it means the same thing: a chronic
character meets a distressing environmental event.) Schildkraut called
the endogenous concept ‘‘more a European notion, a notion that might
be called by some vital depressions, because you didn’t have to have a
depressed mood. It was based on having a loss of vitality, anergia,
anhedonia and psychic retardation.’’ He said that such depressions,
unlike the reactive, ‘‘did not readily change with ongoing interpersonal
interactions or environmental events. It was a kind of fixed-stuck
disorder.’’5

4 Joseph J. Schildkraut, interview. 2000. The catecholamine hypothesis. In David

Healy (ed.) The Psychopharmacologists, vol. 3. London: Arnold, pp. 111–34, at p. 131.
5 See note 4.

5
 psychotic depression

A tradition exists of calling endogenous depression melancholia.

Psychiatrists once resisted the term melancholia because it harked
back to the days when deep depression was associated with humoral
theories of ‘‘black bile’’ and the melancholy constitution. Yet the term
melancholia has such historical heft that many prefer it to the rather
jargonish-sounding ‘‘endogenous.’’ Bernard Carroll affirmed emphati-
cally in 1982, after discovering that a biological test (the dexamethasone
suppression test) was relatively specific for melancholia, ‘‘Our results
give unequivocal support to the view that melancholia is a categorically
distinct entity from non-endogenous depression’’ (Carroll, 1982). In
2006 Michael Alan Taylor and Max Fink re-endorsed in a compre-
hensive overview the existence of melancholia as a separate diagnosis
(Taylor and Fink, 2006). In our view, melancholia is one type of
endogenous depression, but when speaking generalistically the two
terms are interchangeable.
There are various types of endogenous depression. In catatonic
depression, the extreme form of which is stupor, movement and speech
are slowed. In melancholic depression, the patient has a sickly persona,
and movement and speech may also be ‘‘retarded.’’ In this book, we are
interested in the type of endogenous depression called ‘‘psychotic,’’
characterized by delusions and hallucinations. As Chapter 3 explains,
there are various forms of psychotic depression that are really more or less
independent illness entities in their own right. Psychotic depression is not
actually a disease of its own but a collective term for a number of illnesses
having the common properties of depression and psychosis. Of hospi-
talized patients with endogenous depression, about half are psychotic.6
Psychotic depression is highly dangerous. The patients’ thinking
becomes so delusive that, having lost contact with reality, they

6 Of 225 patients with primary unipolar affective disorders admitted to the Iowa
University Psychiatric Hospital between 1935 and 1940 (part of the ‘‘Iowa 500
Study’’), 52% revealed delusions. See William Coryell and Ming T. Tsuang. 1982.
Primary unipolar depression and the prognostic importance of delusions. Arch Gen
Psychiatry 39: 1181–4.

6
 introduction

contemplate suicidal behavior, taking poison perhaps to kill off the

hallucinated bug infestation (although it kills them). As London psy-
chiatrist Thomas A. Munro, a psychiatrist at Guy’s Hospital in London,
pointed out in 1949, ‘‘The treatment of depression is always a great
responsibility. The patient’s life is at stake’’ (Munro, 1949).
Psychotic depressions can also be risky for others. As with Andrea
Yates, periodically there are terrible stories of psychotically depressed
parents who murder their children to save them from the fires of Hell or
the doom the parents know lies ahead. Thus, the English Drug and
Therapeutics Bulletin advised in May 1965 as follows: ‘‘Another reason
for admitting severely depressed patients to hospital is that on occasion
they murder relatives or friends in an attempt to spare them imagined
pain.’’7
In psychotic depressive illness we are therefore discussing a variety of
endogenous depression, depressions that may end up in hospital.
Reactive depressions, on the other hand, come on slowly, under stress,
and are filled with anxiety, anger, or dissatisfaction. The symptoms of
reactive depressions tend to be vague, formless, and primarily subjective.
In today’s psychiatry, reactive distress tends to be called by a range of
terms that are really all over the map, from adjustment reaction, major
depression, depression ‘‘not otherwise specified,’’ or dysthymia, to the
whole anxiety spectrum, such as generalized anxiety disorder or some
other anxiety diagnosis, to personality disorders such as borderline
personality, or even dissociative disorder. The term neurosis formerly
applied in many cases. The psychoanalysts once considered these
patients, perhaps not incorrectly, as having a character disorder. A
number of additional conditions doubtless huddle under the shelter of
reactive distress, including chronic fatigue syndrome (formerly neur-
asthenia), weltschmerz, and the emotional consequences of poverty,
pain, and threatening medical illness.

7 See May 28, 1965, Antidepressant therapy, Drug and Therapeutics Bulletin 3(11):
pp. 41–3, at p. 42.

7
 psychotic depression

In the vast mass of ‘‘depression’’ diagnoses that are handed out today,
many patients will have such a reactive depression: the depression comes
on in response to bad news rather than out of the blue. The patients’
thought and movement are not abnormally slowed as in endogenous
depression. Unlike psychotic depression, which answers readily to ECT,
reactive depressions do not respond so well to ECT. The phrase ‘‘reactive
depression,’’ by the way, was abolished in 1980 in American psychiatry
with the advent of a new recipe-based classification manual called DSM-
III. Yet, the term reactive depression delineates a basin of distressed
patients with a mixture of sadness, weariness, and anxiety that is difficult
to circumscribe well, and there is no reason why it should not soldier on.8
Endogenous depression is an entirely different beast. The patients are
not necessarily sad but slowed in thought and deed, sometimes to the
point of stupor. The patients complain that their minds move slowly and
their movements are laborious and painful. In the psychotic variety of
endogenous depression the patients are not always slowed, and may have
a hint of mania, exhibiting such features of agitation as pacing and
repeating ‘‘It’s my fault, it’s my fault.’’ Yet the main point is that the
patients are tormented by delusions of various kinds; in an earlier era
their delusive thoughts often involved their irremediable sinfulness;
today, hypochondriac delusions about one’s organs turning to concrete
and the like come to the fore. Endogenous illness does not have the same
favorable promise of remission that is lent to reactive depression,
although after about 8 months most untreated endogenous patients get
over it (for the time being). Patients with endogenous depression are
often inclined to seek oblivion, so that suicide is always to be feared, as

8 It is true that reactive depression has not been without its critics. As Swiss
psychiatrist H. J. Bein put it, ‘‘It must, of course, be borne in mind that . . . in all the
so-called reactive depressions, the qualifier ‘reactive’ is only a reflection of the
investigator’s empathy for a given situation.’’ H. J. Bein. 1978. Prejudices in
pharmacology and pharmacotherapy: Reserpine as a model for experimental
research in depression. Pharmakopsychiatrie Neuropsychopharmakologie 11: 289–93, at
p. 291.

8
 introduction

actually happens in perhaps one in seven of the untreated cases. (But in

nonendogenous depression too the patients may attempt suicide, and
the psych emergency wards are very familiar with them.)
‘‘Endogenous depression should be looked upon as an acute disease,
like appendicitis; it cannot wait,’’ one Swedish psychiatrist told a
Scandinavian symposium from the floor in 1960. He remembered a
patient from his practice in Linköping, referred with the following
information, ‘‘The patient is recommended for examination at a psy-
chiatric clinic.’’ There was nothing more. ‘‘We phoned the doctor but he
was not in, and then we wrote – as we usually do – requesting details of
the case. Three days passed before we got any news and the same day the
patient committed suicide, taking with him a daughter of five years.’’9
Finally, endogenous depression is ‘‘autonomous’’; it does not
get better with good news.10 Your lover has just moved back in?
Guess what, your psychotic depression has not improved. As psycho-
pharmacologist Donald Klein once told Robert Spitzer, the mastermind
of DSM-III, in a moment of irritation, ‘‘I think that the distinction
between the relatively autonomous depression and the relatively reactive
depression is a strikingly important one that should be present in this
edition [the forthcoming DSM-III-R in 1987]. That also speaks for the
utility of a mood-reactive depressive disorder.’’11
DSM-IV in 1994, no longer under Spitzer’s control, did incorporate
the notion of mood reactivity, but made it a characteristic of major
depression with ‘‘atypical features,’’ meaning what is often called ‘‘aty-
pical depression.’’ Yet the disease designers included alongside ‘‘mood
reactivity,’’ ‘‘interpersonal rejection sensitivity,’’ which means basically

9 Gerdt Wretmark, in discussion. In Erik S. Kristiansen (ed.) 1961. Depression:

Proceedings of the Scandinavian Symposium on Depression, 26–28 October 1960.
Copenhagen: Munksgaard, pp. 138–9.
10 Pioneering the distinction between ‘‘autonomous’’ and ‘‘reactive’’ depressions was
English psychiatrist R[obert] D[ick] Gillespie. 1929. The clinical differentiation of
types of depression. Guy’s Hospital Reports 79: 306–44.
11 Klein to Spitzer, March 19, 1986; American Psychiatric Association, Williams
Papers, DSM-III-R, box 2.

9
 psychotic depression

thin skin (American Psychiatric Association, 1994). The disease

designers had in effect asserted that thin skin is the autonomous
dimension of major depression.
The basic problem with DSM, though, is that it fails to recognize
endogenous depression. The manual styled itself as ‘‘atheoretical,’’
meaning making no assumptions about causation. But by dismissing
causality, DSM is more agnostic than diagnostic. In all other fields of
medicine, causality is crucial in diagnosis and intimately tied to evidence
and scientific observation. Psychiatrists must not be so totally agnostic (if
they want to be effective or to practice on the basis of modern science).
After Kraepelin lumped mania and depression together in 1899 as a
single illness,12 ‘‘manic-depressive psychosis,’’ for about the next half
century endogenous depression often was referred to as manic-depres-
sive illness. Yet the majority of patients had no evidence of mania, and
many patients with mania had no history of depression. Today, authors
distinguish between genuine manic-depressive illness, also called
‘‘bipolar-1’’ disorder, and unipolar disorder (depression without mania).
This book is mainly about unipolar disorder and about psychosis in the
depressive phase of bipolar illness. But, to be frank, some clinicians think
that sooner or later many of the depressed hospitalized patients will
develop an episode of mania, and that on a lifetime basis the distinction
between unipolar endogenous depression and bipolar disorder is
meaningless.13
To recap, this basic distinction between endogenous and reactive
depression has today almost been lost sight of. Since Kurt Schneider, the
classification of depression has become rather a parlor game for insiders,
with countless varieties being proposed. In particular, the all-encom-
passing amorphous label of major depression and a pseudospecific

12 Emil Kraepelin. 1899. Psychiatrie: Ein Lehrbuch für Studirende und Aerzte, vol. 2, 6th
edn. Leipzig: Barth, pp. 359–425.
13 See, e.g., Heinz E. Lehmann. 1971. Epidemiology of depressive disorders. In Ronald
R. Fieve (ed.) Depression in the 1970’s. Amsterdam: Excerpta Medica, pp. 21–30;
proceedings of a conference held in 1970.

10
 introduction

subtype called atypical depression enjoy popularity at the moment. Yet

there are not countless varieties. There are really only two master illness
entities here. Schneider’s distinction between endogenous and reactive
has a solidity that has withstood the test of time. This book is about
psychotic depression in its varieties because it is threatening, yet
repairable.
There are commonalities between the two depressions. They may
have sadness in common or a diminished sense of self-worth and over-
arching distress. Both may be triggered by stress, but endogenous
depression must also have a biological trigger, not just a psychological
one. Jet lag, high cortisol, insomnia, starvation, and stimulant drug
abuse may all serve as behavioral disturbances that provoke the physical
brain changes of endogenous depression. As L. G. Kiloh and R. F.
Garside at the University of Durham observed in 1963 in a classic article,
‘‘It is often correctly pointed out that many attacks of endogenous
depression are precipitated by adverse circumstances and are therefore in
this sense reactive, but this does not necessarily indicate that the pre-
cipitants play an important causal role’’ (Kiloh and Garside, 1963).
And sin! While psychotically depressed patients are covered in it,
patients with community depression feel they deserve to be treated
better. They do not dread punishment for having sinned unforgivably in
the eyes of God, or fear that they are dead.
Thus, two diseases. It is just as tuberculosis and pneumonia are two
different diseases, although they may have fever and coughing up
phlegm in common. Lumping the diseases of endogenous and reactive
depression together as ‘‘depression’’ makes about as much sense as
lumping tuberculosis and pneumonia together: They have different
prognoses, entirely different responses to treatment, and presumably
different biochemistry and genetics. That means we are talking about
utterly different diseases, not variations on a theme.
In this book we look at the whole question of the diagnosis and
treatment of psychotic depression afresh, without the preconceptions of
industry-marketed psychopharmacology and DSM-nonspecific nosology

11
 psychotic depression

that have made psychiatry today a field that needs upstanding principles
instead of accommodating every viewpoint. It is not as though we had a
huge conventional wisdom about psychotic depression to overturn,
because in the past 30 years psychiatry has not paid much attention to the
condition (nor has psychiatry bothered much about the other kinds of
endogenous depressions either). But psychiatry has paid inordinate
attention to the public marketing of what is officially called ‘‘major
depression,’’ which is a mixture of melancholia and dissatisfaction, or of
psychotic depression and reactive depression if one will. A single class of
drugs – the selective serotonin reuptake inhibitors (SSRIs) – has been
offered by industry as the treatment of choice of major depression,
although the drugs are not effective for serious depressions.14
So there is a conventional wisdom out there: the SSRIs as the ideal
treatment for major depression. And the conventional wisdom is wrong.
There is no specific thing as major depression, and the SSRIs are poor
antidepressants, although they have efficacy in treating other types of
mood changes, such as worry. The enormous success of the SSRIs as the
treatment of choice for major depression – a nontreatment for a non-
illness – has left many clinicians frustrated as their patients fail to recover
until their illnesses have run their natural cycle. It has also left the
patients chasing futilely one ineffective treatment after another rather
than receiving accurate diagnoses and therapies that might make them
genuinely better.

14 In an unguarded moment, Robert Temple, head of the Office of Drug Evaluation

I of the Food and Drug Administration (FDA), admitted in front of a microphone
at a meeting of an advisory committee, ‘‘[We need] to find out whether the [SSRI-
style] drugs actually provide some benefit, even in people who seem to be doing well
on them . . . I mean, as Tom [Laughren] has pointed out repeatedly, the failure of
most of the drugs to show effectiveness doesn’t mean they don’t work. On the other
hand, we don’t have evidence that they do work, and that is not irrelevant either.’’
FDA Archives, Joint Meeting of the CDER Psychopharmacologic Drugs Advisory
Committee and the FDA Pediatric Advisory Committee, September 14, 2004,
transcript p. 55. Although the meeting was given over to pediatric suicide with
antidepressants, Temple made this comment in the context of the treatment of
adults. Laughren was head of the psychopharmacology evaluation unit of the FDA.

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