ECT Fink

Electroconvulsive Therapy
René Magritte: “La Clairvoyance.”
The voyage of discovery lies not in seeking new horizons

but in seeing with new eyes.
—Marcel Proust
Electroconvulsive
Therapy
A Guide for Professionals
and Their Patients
Max Fink, M.D.
3 2009
3
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Library of Congress Cataloging-in-Publication Data
Fink, Max, 1923 –
Electroconvulsive therapy: a guide for professionals and their patients / Max Fink.
p. ; cm.
Rev. ed. of: Electroshock: healing mental illness. 2003.
Includes bibliographical references and index.
ISBN 978-0-19-536574-0
1. Electroconvulsive therapy. I. Fink, Max, 1923 – Electroshock. II. Title.
[DNLM: 1. Electroconvulsive Therapy.
2. Mental Disorders—therapy. WM 412 F499e 2009]
RC485.E53 2009
616.89'122—dc22 2008020585
Originally published as Electroshock: Healing Mental Illness
135798642
Printed in the United States of America
on acid-free paper
To my teachers and my students,
who taught me much about both the care of my patients
and convulsive therapy.
This page intentionally left blank
Preface to the New Edition
Why This Book?
E lectroconvulsive therapy (ECT) is an effective and safe treatment for

those with severe mental illness. Yet, many consider it so dangerous
that they fear it as much as they fear the disease. It is often labeled “the
most controversial treatment in psychiatry.” The controversy is not about
its efficacy or its safety, which have been proved, but about the idea that
the treatment actually alters the brain, changing a person’s personality
and character. This mistaken perception has many roots—in the pain and
complications of ECT’s early use; in the confusion with the brain-altering
and ineffective treatments of insulin coma and lobotomy, which were
introduced at the same time but have long been discarded; and in fierce
philosophical and economic competition among psychotherapists.
Electroconvulsive therapy has undergone fundamental changes since
its introduction 75 years ago. It is no longer the bone-breaking, memory-
stealing, fearsome treatment pictured in films. Anesthesia, controlled
oxygenation, and muscle relaxation make the procedure so safe that the
risks are less than those accompanying the use of several psychotropic
drugs. Indeed, for the elderly, the systemically ill, and pregnant women,
ECT is a safer treatment for mental illnesses than alternatives.
Psychotropic drugs and psychosocial therapies are the primary treat-
ments that are offered the psychiatric ill, but are often inadequate. They
may fail to relieve the disorder, or fail to relieve it quickly enough, or they
vii
viii / Preface to the New Edition
may cause difficult or even dangerous side effects. In such cases, ECT is
certainly preferable.
When a physician recommends ECT (also known as electroshock or
convulsive therapy), family members and patients ask: Is this old treat-
ment still used? Is it safe? Is there a risk of brain damage? Will there be
memory loss? Usually a patient has been severely depressed for many
weeks, has not improved with the medicines that have helped for a
while, and is getting worse. Often the doctor has no other medications
to suggest.
More questions arise: What are the chances that the therapy will
work? Why didn’t the doctor suggest this treatment in the first place? And
occasionally, how does it work? This book answers such questions.
A decade ago, the first edition of this book was written to answer
these same questions. Why do we need a new edition? Treatment proce-
dures have improved, risks have been drastically reduced, and we have
learned more about the workings of the brain. We are better able to select
patients for good outcomes. At one time, fixed numbers of treatments
were prescribed, but we now know that some form of ongoing therapy
must be continued to keep patients well. Many doctors and patients now,
more than ever, readily recognize the value of ECT in reducing the drive
to suicide and in relieving many serious psychiatric illnesses.
This book is written for those faced with decisions about the use of
ECT and is meant to complement the DVDs that are available to edu-
cate patients about what they can expect. This book is also meant to
help students, medical practitioners, and mental health workers to intel-
ligently identify and prepare patients for treatment. My hope is that it
will answer questions that arise frequently about ECT; it is meant to be
a guide, answering questions about the who, what, why, when, and how
of the treatment.
The medical community’s experience with ECT is extensive and
sometimes contradictory. Like all medical specialties, ECT is not always
practiced the same way in every facility, so some of the information in
this book may differ from what other physicians recommend. Though
clinicians and researchers do not always agree about various aspects of
the therapy, the suggestions in this book are consistent with present stan-
dards for effective treatment, culled from one doctor’s experience of over
half a century in studying the mechanism of ECT and its clinical appli-
cations. Readers who are interested in learning more about the research
Preface to the New Edition / ix
conducted on ECT can consult the publications cited in the endnotes

and listed in the Bibliography. Those works support the recommenda-
tions given here.
When I discuss medications, I use their trade names as much as pos-
sible so that they will be more recognizable by lay readers. A table of trade
and generic names is included in Appendix Four.
Definitions
Because ECT is a technical discipline, it has spawned its own jargon.

Convulsive therapy, electroconvulsive therapy, ECT, electroshock, electro-
seizure therapy, and EST are all terms for the treatment. Some years ago,
psychiatrists began to abandon the term electroshock, in part because no
shock is involved, and, more important, because it carried the connota-
tion of pain caused by an electric current. But electroconvulsive therapy
and ECT, as well as electroshock, are the terms most widely used, even
though these labels are grating and frightening
In fact, the term electroshock is not accurate. When insulin was first
used to treat schizophrenia in 1933, the patients did show classic signs of
surgical shock: pallor, sweating, and lowered levels of consciousness. Im-
pressed with the similarity to the effects of surgical shock, practitioners
called it insulin shock treatment.1 Seizure therapy, introduced a year later,
was called convulsion treatment.2 A few years after that, when electricity
was used to induce the seizure, the Italian name l’elettroshock, translated
in the first English reports as electroshock, became popular.3 The term
electroconvulsive therapy, shortened to ECT, is of later coinage and is now
the preferred term to describe the treatment.
Electroconvulsive therapy, in which brain seizures are induced, is not
the same as electric shock, which refers to a form of psychological therapy
in which shocks are delivered to induce pain so that subjects will refrain
from performing an unwanted behavior. At one time, this practice was
used to stop the self-injurious behaviors of scratching, head banging, and
screaming of intellectually disabled patients. This use of electric shock
for aversive conditioning has been virtually abandoned and should not be
confused with ECT. Aversive conditioning is in disfavor as unsuccess-
ful. Yet, some “schools” still use this procedure and controversies often
flare up.4
x / Preface to the New Edition
Electroconvulsive shock or ECS is the term applied to the experimen-

tal induction of seizures in animals.
In a successful treatment, the brain will experience a sequence of
biochemical and electrical events that are expressed in the body as epi-
leptic seizures. A seizure is a coordinated brain and motor response that is
present in the newborn infant, is retained throughout life, and has been
observed in all animals. While it temporarily puts an animal at survival
risk, it has persisted, suggesting that the seizure has redeeming values to
the organism.
The term convulsion technically describes the outward muscular
manifestations of the seizure, even though these have been abolished in
ECT by modern techniques. Neurologists refer to a grand mal convulsion
or a grand mal seizure; other terms are epileptic fit, epileptic convulsion,
seizure, and fit.
In this book, I use seizure, grand mal seizure, and fit interchangeably
when referring to the electrical and biochemical events in the brain that
are essential for successful treatment. I use the word convulsion to refer
only to the observable movements of a seizure. A convulsion is not nec-
essary to ensure a good response, and since convulsions carry the risk
of bone fracture, modern ECT practice inhibits convulsive movements
through the use of muscle relaxants. In proper treatment the body remains
still.
A psychiatrist trained in ECT is occasionally known as an electro-
therapist or electroshock therapist, or—a term that makes us wince—as
shock doc.
Case Studies
I include several thumbnail sketches of the stories of patients as examples

of what is possible and what is probable. These accounts are based on my
experience as director of the ECT Service at University Hospital in Stony
Brook, New York, from 1980 to 1997. The adult in-patient facility admit-
ted about 500 patients each year; about 50 of these patients were treated
with ECT. Additional patient reports come from the ECT service at the
Long Island Jewish Hillside Hospital between 1997 and 2005, and some
vignettes come from my collaboration with Dr. Michael A. Taylor (now
at the University of Michigan Medical School) in writing textbooks on
Preface to the New Edition / xi
catatonia and on melancholia, two syndromes that are most responsive to

ECT. The patients’ real names have been replaced with pseudonyms and
identifying features have been changed to ensure their privacy, but the
treatment information is authentic. The patients’ names and conditions
are listed here to help readers find conditions of interest.
Almost all the examples come from the 1999 version of this book; those
that come from other sources are cited in a footnote at the presentation.
Mary Depressive melancholia
Robert Psychotic depression in a 68-year-old scientist
Helen Pseudodementia and catatonia
Dr. Rosenberg Suicide risk averted with treatment
Sarah Acute manic episode
David Mania with psychosis
Philip Delirious mania in a 17-year-old adolescent
Gerald Acute catatonia in a 20-year-old man
Jeffrey Malignant catatonia: the neuroleptic malignant
syndrome
Monroe ECT in a patient with parkinsonian rigidity
Jefferson Acute psychotic episode in an 18-year-old
Steven Chronic schizophrenia
Eric Toxic psychosis and delirium in a 15-year-old
Peter Depression in a 16-year-old adolescent
Claudia Mental retardation in a 23-year-old
Donald Self-injurious behavior in a 14-year-old
Quinn Catatonia in autistic spectrum disorder in a
17-year-old
On a final note, it will be interesting for nonmedical readers to learn
of the range of conditions for which ECT has been used in my services
and reported in the scientific literature. We have reported ECT to be
useful and safe in patients suffering from the neuroleptic malignant syn-
drome,5 toxic serotonin syndrome,6 pseudodementia,7 delirious mania,8
delirium,9 Tourette syndrome,10 catatonia,11 melancholia,12 and schizo-
phrenia.13 We have also applied ECT safely in patients with treatable
psychiatric syndromes who were simultaneously ill with severe anemia,14
auricular fibrillation,15 intracranial lesions,16 and mental retardation.17
xii / Preface to the New Edition
Broad experience with ECT in the elderly18 and in adolescents19 has been
presented in published reviews.
Electroconvulsive therapy has proven to be a remarkably versatile
treatment. My hope is that this book will help you to understand and ap-
preciate its potential to heal the severely psychiatrically ill.
Acknowledgments
T his book is the product of more than 55 years of clinical and research
interest in the convulsive therapies. I am indebted to the hundreds of
patients and their families who placed their faith in our research efforts.
Clinical studies are not possible without the support and faith of the
nurses and aides who are responsible for the daily care of our patients.
I am indebted to my teachers, from whom I have learned much, in-
cluding Morris B. Bender, Bernhard Dattner, Lothar Kalinowsky, William
Karliner, and Edwin A. Weinstein, all of New York; Jan-Otto Ottosson
of Sweden; and Max Hamilton of England. My colleagues in studies of
convulsive therapy have been Martin A. Green, Robert L. Kahn, Max
Pollack, Joseph Jaffe, Hyman Korin, and Donald F. Klein at Hillside Hos-
pital; Turan M. Itil and George Ulett at the Missouri Institute of Psy-
chiatry; Richard Abrams, Michael A. Taylor, Jan Volavka, Jiri Roubicek,
Rhea Dornbush, Peter Irwin, and Donald M. Shapiro at New York Medi-
cal College; and Walter Sannita, Morton Miller, Krishnareddy Gujavarty,
Larry Greenberg, Iaonnis Zervas, Georgios Petrides, Irene Carasiti, and
Avi Calev at SUNY at Stony Brook. In the past decade, I have been a
member of the CORE collaboration with Charles Kellner, Teri Rum-
mans, Samuel Bailine, John Rush, and Mustafa Husain.
My collaborations in the past decade with Michael A. Taylor in writ-
ing on catatonia and melancholia, with Jan-Otto Ottosson in writing on
ethics in ECT, and my interest in the history of ECT, psychiatric clas-
sification, and the role of neuroendocrines in psychiatry with Edward
Shorter of the University of Toronto have enriched my education and
xiii
xiv / Acknowledgments
writing. Alan Edelson, the publisher of Raven Press, encouraged me to

write a textbook and challenged me to launch a new journal, Convulsive
Therapy, despite the adverse public image of electroshock. An invitation
by John Schwartz, publisher of the Psychiatric Times, to write columns on
ECT has given me another outlet to express my interests.
My studies were encouraged by Israel Strauss, founder of Hillside
Hospital in New York, and Joseph S.A. Miller, its Medical Director;
Jonathan O. Cole at the National Institute of Mental Health; Alfred M.
Freedman at New York Medical College; Stanley Yolles at NIMH and at
SUNY at Stony Brook; and Prof. Dr. T. (Jack) Vossenaar of N.V. Organon
of Holland. For three decades my research was supported by the Interna-
tional Association for Psychiatric Research and in the past decade by the
successor Scion Natural Science Association.
This new edition has been edited by my wife, Martha, the historian
Edward Shorter, my associate Larry B. Greenberg, and the Oxford Uni-
versity Press editor Sarah Harrington.
The figures in this book are credited as follows:

Frontispiece © 2008 C. Herscovici, London/Artists Rights Society (ARS), New York.
Figures 2-1 and 10-2 are by Tom Dunne.
Figure 3-1 is from Letemendia et al.: “Therapeutic advantage of bifrontal electrode place-
ment in ECT” in Psychological Medicine 1993; 23:349–360.
Figures 10a-b are from American Scientist 2000; 88:162–167.
Contents
one
What Is Electroconvulsive Therapy? 3
two
The Patient’s Experience, 10
three
The Treatment Technique, 25
four
Side Effects and Memory Issues, 34
five
Depressive Mood Disorders, 43
six
Manic Mood Disorders, 57
seven
Movement Disorders, 67
eight
Other Uses: Psychosis,
Pregnancy, and Status Epilepticus, 75
xv
xvi / Contents
nine
Pediatric ECT, 85
ten
How Does ECT Work? 94
eleven
How Did Convulsive Therapy Originate? 103
twelve
Is Brain Stimulation an Alternative to ECT? 111
thirteen
Is ECT Practice Ethical? 115
Appendices, 121
Notes, 129
Bibliography, 139
Index, 153
o n e
What Is Electroconvulsive
Therapy?
Men ought to know that from nothing else but the

brain come joys, delights, laughter and sports, sorrows,
griefs, despondency and lamentations.
—Hippocrates1
E lectroconvulsive therapy (ECT) is an effective medical treatment for

severe and persistent psychiatric disorders. It relieves depressed mood
and thoughts of suicide, as well as mania, acute psychosis, delirium, and
stupor. It is usually applied when medications have given limited relief or
their side effects are intolerable. Electroconvulsive therapy is similar to
a surgical treatment. It requires the specialized skills of a psychiatrist, an
anesthesiologist, and nurses.
The patient receives a short-acting anesthetic. While the patient is
asleep, the physician, following a prescribed procedure, induces an epi-
leptic seizure in the brain. By making sure that the patient’s lungs are filled
with oxygen, the physician precludes the gasping and difficult breathing
that accompany a spontaneous epileptic fit. By relaxing the patient’s mus-
cles with chemicals and by inserting a mouth guard (not unlike those used
in sports), the physician prevents the tongue biting, fractures, and injuries
that occasionally occur in epilepsy. The patient is asleep, and so experi-
ences neither the painful effects of the stimulus nor the discomforts of
the seizure. The physiological functions of the body, such as breathing,
3
4 / Electroconvulsive Therapy
heart rate, blood pressure, blood oxygen concentration, and degree of

motor relaxation, are monitored, and anything out of the ordinary is im-
mediately treated.
Electroconvulsive therapy relieves symptoms more quickly than do
psychotropic drugs. A common course of ECT consists of two or three
treatments a week for two to seven weeks. To sustain the recovery, weekly
or biweekly continuation treatments, either ECT or medications, are
often administered for four to six months. If the illness recurs, ECT is
prescribed for longer periods. The duration and course of ECT are simi-
lar to those of the psychotropic medicines frequently used for the same
conditions.
For Whom Is ECT Useful?
Electroconvulsive therapy has been used safely to treat emotional disor-

ders in patients of all ages, from children to the elderly, in people with de-
bilitating physical illnesses, and in pregnant women. Emotional disorders
may be of short or long duration; they may be manifest as a single episode
or as a recurring event. Electroconvulsive treatment is an option when
the emotional disorder is acute in onset; when changes in mood, thought,
and motor activities are pronounced; when the cause is believed to be
biochemical or physiological; when the condition is so severe that it in-
terferes with the patient’s daily life; or when other treatments have failed.
Unfortunately, physicians commonly recommend ECT only as “the last
resort.” I hope to discourage such thinking, because if our goal is to im-
prove patients’ health as quickly and safely as possible, for many condi-
tions ECT should be an early rather than a last resort.
Many mental conditions, despite variations in their symptoms, can be
relieved. Among them are disorders of mood, in which patients suffer from
depression, mania, or overwhelming anxiety; and disorders of thought,
in which patients believe that others control their lives, influence their
minds, or plan their harm. Patients may be suspicious that spouses are
unfaithful, hear voices or see visions not based on real events, or suffer
severe guilt or feelings of worthlessness. Many patients are so wracked
by mental pain that they contemplate suicide, a frequent cause of death
among the psychiatrically ill.
Electroconvulsive therapy is also effective in treating disorders of
movement, such as mutism (refusal to speak), body rigidity, and the stupor
What Is Electroconvulsive Therapy? / 5
of catatonia, the excitement and sudden, purposeless movements of mania,

the hand wringing and restlessness of agitated depression, and even the
rigidity of parkinsonism. Such behaviors and conditions are relieved by
ECT regardless of any other concurrent psychiatric diagnosis the patient
may have (Appendix One).
Electroconvulsive therapy is not helpful for those with a lifelong his-
tory of mental and emotional dysfunction unless there has been an acute
and well-defined onset. Nor is it likely to help a patient with a neurosis, sit-
uational maladjustment, personality disorder, drug dependence, or socio-
pathy. If, however, such a patient evinces suicidal impulses, ECT should
be considered (Appendix Two).
When Might ECT Be Considered?
Most patients who are considered for ECT are so ill that they are al-
ready hospitalized. They may be depressed and threaten suicide, refuse
food and fluids, be so overactive that they risk exhaustion and self-injury,
threaten to harm themselves or others, or be in a melancholic stupor.
Elderly patients are often referred early, especially when they also suf-
fer from a systemic illness or do not tolerate their medications. Patients
referred for ECT have responded poorly to other treatments, or else their
daily life has been severely compromised, or they suffer unpleasant or
dangerous symptoms caused by the prescribed medications.
The life stories of the patients I’ve treated with ECT are remarkably
similar. The depressed patient is unable to work, and takes no pleasure in
relating to family or friends who may have sought to reassure him. A holi-
day was suggested. A family physician prescribed the latest antidepres-
sant medication or recommended formal sessions with a psychotherapist.
A religious leader was consulted. Following weeks or months of illness
with no relief, the family asks whether there is any other treatment. That
is when a physician suggests ECT.
Psychotic patients traverse much of the same ground. When a single
medication fails, combinations are tried. Because few doctors realize that
ECT can relieve thought disorders, ECT is considered only after the
patient’s behavior has become so disturbing that the hospital staff can no
longer deal with it or after the family insists on further help.
Manic and catatonic patients also endure one medication trial after
another, often in imaginative combinations. When aggression, screaming,
or excitement compels physical restraint or large doses of neuroleptic or

sedative medications, ECT is considered.
When adolescents and children experience psychiatric symptoms,
doctors frequently blame dysfunctional family interactions and recom-
mend family therapy. If a child is diagnosed with attention deficit disorder or
autism, families will consider special schooling. When self-injury, scream-
ing, excitement, aggression, mutism, and negativism make the family’s life
unbearable, the child is hospitalized. A psychiatrist may consider ECT in
these instances, but may find it difficult to overcome the common belief
that this treatment damages the developing brain. In fact, children and
adolescents who have been helped by ECT return to home and school,
learning and behaving in the same manner as others of their age—and
vastly improved. Prolonged illness, hospitalization, and the toxicity of
medications threaten progress in school far more than the side effects
of ECT.
The delay in such an effective treatment—and ECT is that, even
though patients and therapists favor medications and psychotherapy—
needlessly deprives the patient of a return to health. After weeks or months
of illness and poor response, there is every reason to turn to ECT.
For Whom Is ECT Appropriate?
Severely ill psychiatric patients are considered for ECT when they are
so ill as to need hospital protection and care. Electroconvulsive therapy
is commonly recommended after patients have experienced unsuccess-
ful courses of psychotherapy and medication. This delay is unfortunate
because by the time ECT is begun the illness is fully established and dif-
ficult to treat, with unpleasant social and family consequences, and with
the threat of suicide present for far too long.
The medical profession does acknowledge instances in which ECT
should be considered as soon as the illness is recognized instead of first
trying other therapies. A primary use of ECT (one without prior med-
ication and psychotherapy trials) is recommended “when there is a need
for rapid, definitive response because of the severity of a psychiatric or
medical condition; when the risks of other treatments outweigh the risks
of ECT; a history of poor medication response or good ECT response;
and [in response to] the patient’s preference.”2 Such guidelines are not
always adequate, but they do offer doctors some leeway in the choice of
treatment.
The more frequent use of ECT is secondary, after medication treat-
ment trials have failed, when the patient cannot tolerate the side effects of
prescribed medications, or when the condition has become life-threatening,
calling for a more definitive response.
Electroconvulsive therapy can be safely administered to most psy-
chiatric patients. In the elderly, the risks are those related to physical
deterioration associated with aging. Electroconvulsive therapy has been
safely administered to patients as old as 102. Although the list of systemic
problems in the elderly is long, none prevents the use of ECT. Some
conditions, however, make it more difficult to administer anesthetics
and maintain good oxygenation, but the technical aspects of ECT are
sufficiently well known that a safe treatment course can be provided.
Prudence dictates, of course, that elderly and systemically ill patients be
treated in a hospital by skilled practitioners.
For adolescents, the indications, efficacy, and safety of ECT have
been shown to be the same as for adults.3 The medical community’s expe-
rience with treating prepubertal children is limited to the few cases where
such conditions as catatonia or self-destructive acts are life-threatening.
More experience with such use of ECT is needed.
Electroconvulsive therapy has been safely administered in all stages
of pregnancy. It does not precipitate miscarriage, nor does it affect the
development of the fetus. When a pregnant woman suffers a severe mood
or thought disorder, antidepressant and antipsychotic drugs are usually
not prescribed, especially during the first three months of pregnancy,
because they pass from the mother through the placenta to the circula-
tory system of the fetus, possibly causing developmental complications.
During the first trimester of pregnancy, ECT is a safer treatment. During
the third trimester, special care must be taken to maintain a pregnant
woman’s airway. Management of ECT should be done by experienced
clinicians, who can also explain the risks associated with the treatment.
What Conditions Respond to ECT?
Since ECT was easy to apply, it was quickly tested in numerous con-
ditions and found to help the patients with mood disorders known as
manic-depressive illness. Adults who were melancholically depressed and

suicidal were saved, as were severely manic patients at risk of death by
dehydration and exhaustion. The conditions known to respond to ECT
are described in the following chapters, and case examples are given to
illustrate its typical uses.
Melancholia is the syndrome of severe depressive mood.4 Patients
are slowed in movement and thought or they are agitated. They sleep and
eat poorly, lose weight, and consider suicide. We identify many varie-
ties of melancholia, with melancholic depression, psychotic depression, and
pseudodementia being the most common (Chapter Five).
Mania is characterized by euphoria, grandiosity, and hyperactivity,
often overlapping with depression. Whether mania is a form of melan-
cholia or a separate disorder identified as bipolar disorder is in dispute.5
Melancholic depression is present either in the same episode or in se-
quential episodes (Chapter Six).
Catatonia is a motor syndrome characterized by mutism, negativism,
posturing, staring, and repetitive acts.6 The syndrome is frequently recog-
nized in patients with mania and depression, but catatonia is also a fea-
ture of some toxic states (Chapter Seven).
Psychosis also improves with treatment, especially when it is a fea-
ture of depression or mania.7 Persistent psychosis without an associated
mood disorder or a toxic cause is often called schizophrenia, an example
of a chronic psychosis (Chapter Eight).
The following chapters describe patients with these and other iden-
tifiable syndromes that are usefully treated with ECT.8
What Conditions Interfere with Effective ECT?
Are there systemic diseases that limit the use of ECT? We have learned
so much about how to ensure a safe procedure that there are no absolute
physical or medical conditions that rule out the treatment today. When
the patient’s psychiatric condition calls for ECT, a skilled team can offer
safe and effective treatment. Nonetheless, patients with life-threatening
medical conditions are considered high-risk cases, as they would be for
any complicated anesthetic and surgical procedure. They warrant special-
ized care. For instance, the safe treatment of patients with recent myocar-
dial infarction (heart attack), cerebrovascular injury (stroke), or cerebral
vascular malformation requires special attention to the control of blood

pressure, heart rate, and oxygenation. 9 The presence of a growth or vas-
cular malformation within the skull, once thought to be an absolute bar-
rier to the use of ECT, no longer bars its use.10 Some conditions, such as
severe obesity and third-trimester pregnancy, do make it more difficult to
maintain a good airway and adequate levels of blood oxygen. But when
treatment is indicated, the technical aspects of ECT are now well under-
stood and a safe therapeutic course can be ensured.
In considering whether to treat a depressed or psychotic patient who
also has a severe physical illness or complication, the anticipated benefits
of treatment must be weighed against the potential harm when treat-
ment is deferred. In severely suicidal patients or those in manic delirium
or malignant catatonia, the need for relief is balanced by the additional
physical risk of anesthesia and seizures. The clinical experience shows us
that ECT can be used safely in severely medically ill patients.11
Character pathology, alcoholism, and drug dependence impede a
successful outcome with ECT. These conditions interfere with treatment
compliance, just as they do for other treatments. A proper course of ECT
requires patient cooperation, which may not be achieved when illicit sub-
stance abuse is a prominent feature of the illness. These conditions are
the principal barriers to successful treatment.
t w o
The Patient’s Experience
With the modern technique of adequate anaesthesia

and relaxant drugs the patient loses consciousness
pleasantly and quickly and is aware of nothing until
he wakes up in the recovery room. For the next couple
of hours he feels a little unsteady and ataxic; in the
second series of treatments, though not in the first,
I felt nausea after treatment, and on two occasions
I have vomited after reaching home by car.
—A Practicing Psychiatrist1
T he popular images of electroshock presented in the media reflect

practices that were discarded more than 40 years ago. The films One
Flew Over the Cuckoo’s Nest and A Beautiful Mind portray imaginative
Hollywood images—not reality. The dramatic scene of a pleading patient
dragged to a treatment room, forcibly administered electric currents as his
jaw clenches, his back arches, and his body shakes while being held down
by burly attendants or by foot and wrist restraints, is false. Patients are not
coerced into treatment. They may be anxious and reluctant, but they come
willingly to the treatment room. They have been told why the treatment is
recommended, the procedures have been explained, and many have seen
DVD or video images of the procedures. Each patient has consented to
the treatment in writing, and in many instances, family members have
also agreed.
10
The Patient’s Experience / 11
Understandably, the patient may be hesitant about the first treat-

ment. He has seen those movies, so the procedures are explained again,
and, except for feeling a needle placed in his vein and electrodes and
measuring devices attached to his body, the patient is unaware of the
treatment as it occurs. One patient described his treatment this way: “It
is a nonentity, a nothing. You go to sleep, and when you wake up, it is all
over. It is easier to take than going to the dentist.”2
Many patients ask to be treated early in the morning so that they
can return to the day’s activities as soon as possible. It is not uncommon
for patients to reassure family members about the procedure. Doctors
frequently ask an experienced patient to explain the procedures and the
discomforts to a candidate; patients undergoing ECT have proved to be its
best advocates.
Patients Must Consent to Treatment
A consent form, voluntarily signed by each patient, is a necessary part of

electroconvulsive treatment in the United States.3 Such a consent proce-
dure is uncommon in psychiatric practice, and was developed to address
concerns about abuse at a time when public distrust of governmental au-
thority was widespread and had affected the physician-patient relation-
ship.4 In most venues, doctors accept the patient’s cooperation with
medication treatment and psychotherapy as consent. A formal statement
of the risks and benefits or alternative treatments is not usually required
for other psychiatric treatments, including the use of psychoactive drugs
that carry serious risks. In some states, such as Minnesota and Arizona,
a signed consent form is sought on admission to a psychiatric hospital
for medication treatments. The regulations seem not to require signed
consent in outpatient settings or in general medical hospitals.
The consent process for ECT begins when the doctor recommends
the treatment. He describes the benefits, the procedures, and the risks
of both ECT and alternative treatments to the patient and family. Some
institutions may offer an information booklet in addition to the consent
form, or an explanatory videotape or DVD may be shown to the patient
and family.5 When the patient agrees to undergo treatment, she signs the
consent form, under witness by a member of the medical staff and often
by a family member.
Consent is usually given for a specified number of treatments, but

not always. When more treatments are needed, the patient is asked to
sign a new form. It is not common practice to ask a patient for signed
consent before each treatment, although some states do mandate this.
The patient and family members are told that treatments may be dis-
continued at any time, even before the specified number of treatments
is completed. This protection clause ensures that all treatments are ac-
cepted voluntarily.
Doctors warn patients about risks, including the immediate effects
on memory. This warning is written into the consent form, and the patient
is asked to acknowledge his awareness of the risk. The fact that psychia-
trists offer such statements, even though the risk of persistent memory
loss is small, unfortunately promotes the common fear that memory is
severely altered by treatment.
Model consent forms are available from treatment facilities, in re-
ports of the American Psychiatric Association, and in textbooks. A sample
is presented in Appendix Three.
Involuntary Treatment
Understandably, patients want to make important decisions about their

own health care. Only when treatment is clearly necessary to preserve life
will the physician or family members seek to compel it by involving the
state in a court procedure.
When a patient is so ill that she requires continuing supervision to
prevent self-harm, or nursing care for feeding and preventing death by
inanition, state laws allow a judge to mandate treatment. Such “involun-
tary treatment” is infrequent.6 A physician, family member, or hospital
director petitions a court, and the patient and an attorney appear at the
hearing. The judge may (or may not) mandate the treatment, specifying
the number of treatments and other technical features.
Some states, such as California and Texas, have special laws about
consent for ECT. These laws prescribe the form of the consent, and the
descriptions of procedures and warnings, and stipulate the frequency of
consent renewal. There has been much debate about whether these pro-
cedures, devised for the protection of the mentally ill, may actually have
detrimental consequences.7 They inhibit and delay the use of ECT, per-
haps leading to prolonged illness and other complications.
When a patient refuses medical care, the physician, family, and court
are often unwilling to override that denial. Sadly, refusal is frequent in
patients with mania or paranoia. Since we recognize that the mentally ill
may not be able to assess the severity of their illness, we should consider
allowing physicians the same leeway in applying ECT that they have in
applying psychotropic drugs.
Pretreatment Examinations
Before administering anesthesia or ECT, the physician obtains a history

of the symptoms and of bodily illnesses, performs a physical examination,
and may request laboratory tests. Blood tests for anemia, diabetes, and
thyroid disease, a urinalysis, and an electrocardiogram may be requested.
Spine and chest X-rays and an electroencephalogram were once routinely
done, but these are no longer considered necessary unless the patient’s
medical history suggests the need.
The patient’s medication records are examined, and medications
deemed useful are prescribed; patients with heart, lung, or brain disease
regularly take medicines that could affect the quality of treatment or in-
crease its risks. The physician accordingly alters the medications used dur-
ing ECT. Pregnancy tests may be performed in adult women. During the
first trimester of pregnancy, some medications are excluded lest they cause
a structural abnormality in the fetus. A dental examination is considered,
especially in the elderly. Some dental conditions require an individualized
plastic bite bloc, prepared by the dentist and used for each treatment. It
is similar to the mouth guard used by athletes in body-contact sports. The
anesthesiologist determines the patient’s past experiences with anesthesia
and describes what is about to happen. Sometimes anesthesiologists ask
for a separate signed consent form for this part of the treatment.
Preparation for Treatment
Treatments are usually given in the morning. In the first decades of ECT
use, treatments were given in the evening, allowing patients to return
home for a restful night, sedated by the treatment. Physicians also com-
monly treated patients on Saturday mornings, allowing patients to work
during the week. In present practice, personnel considerations mandate
morning treatments.
Patients are asked not to eat food or drink liquids after midnight the
night before treatment because nausea occasionally occurs during anes-
thesia. On awakening in the morning, patients may brush their teeth and
take the prescribed medicines with a sip of water. Some medicines, like
insulin in diabetes or lithium in mania, are often held until after the treat-
ment. A seizure alters the transfer of substances from the blood to the brain
cells. In patients with high serum levels of lithium, the amount transferred
may be so high as to elicit a transient toxic response of confusion and
disorientation. A seizure stimulates the release of brain hormones, and it
is possible that the insulin released by the seizure plus the treatment dose
will lower blood sugar excessively. To avoid extra weakness or dizziness,
insulin administration may be deferred until after the treatment.
A hospital patient changes into a loose gown; an outpatient comes to
treatment wearing loose-fitting clothes.
The patient is asked to empty the bladder and is then taken to the
treatment room, where she lies down on a stretcher. A nurse or physician
inserts a needle into a vein in the arm or foot, attaches a bottle of fluid
(usually sugar in water), and sets the fluid flowing at a slow rate. This in-
travenous line allows the easy and painless administration of medications
during the treatment.
Adhesive monitoring electrodes—flat, disposable pads or reusable
discs to which electrical connections can be made—are applied to the
skin, a painless procedure. Three electrodes are put in place for the elec-
troencephalogram (EEG); two stimulating electrodes for the electrical
stimulus; three for the electrocardiogram (ECG) and heart rate; and two
to measure motor movements during treatment. A recording electrode
placed on the patient’s finger or toe measures the blood oxygen satura-
tion. A blood pressure cuff on the arm measures the blood pressure, and
a second one may be placed as a tourniquet on a leg to allow the psychia-
trist to record the duration of the muscular signs of the seizure.
The doctor or the nurse usually explains the reasons for each con-
nection: the chest (ECG) electrodes and blood pressure cuff permit con-
tinuous monitoring of heart rate, blood pressure, and heart rhythms; the
head (EEG) electrodes monitor the brain’s electrical activity; the finger
electrode and one in the ventilating mask measure oxygen saturation in
the blood and the concentration of carbon dioxide in the exhaled air,
assuring the anesthesiologist that the oxygen in the blood is at the correct
level (Fig. 2–1).
Figure 2–1. Monitoring and stimulating electrodes for treatment.
The Treatment
After the preparations are complete, the patient is asked to breathe deeply
as 100% oxygen flows to the mask that covers the mouth and nose. Each
breath takes in much higher oxygen concentrations instead of the 20%
that is normal in room air. The anesthesiologist makes sure that oxygen
flows freely during the treatment and that the proper blood oxygen con-
centration is maintained.
A sedative medication administered through the intravenous line
quickly puts the patient to sleep. A muscle relaxant is injected, but before it
becomes active, the blood pressure cuff on the leg is inflated above the sys-
tolic blood pressure. A stimulator, applied to a nerve in the arm or leg before
the seizure, will show when the muscles are relaxed. When the twitches
stop, the muscles are properly relaxed for the treatment.
The mouth guard, made of rubber or plastic, is held in the patient’s

mouth by the anesthesiologist and prevents damage to the teeth or jaw
during the electrical stimulus. When the teeth need added protection, an
individualized device is made by the dentist.
The stimulus is given, and the treatment occurs. The patient is not
aware of any aspect of the treatment: neither the muscle relaxation nor
the passage of the current nor the seizure.
There is no reason to be concerned that a painful shock or electrocu-
tion will occur. Neither patients nor treatment team members have ever
been electrocuted in ECT.
Within three minutes after the treatment, the patient usually breathes
without assistance. On awakening, the patient is asked her name, the
date, and the name of the hospital. At first the patient is puzzled by the
questions, but awareness improves rapidly and the responses are usually
correct within 15 minutes. Within a half hour, the patient is aware of her
surroundings.
The return to awareness varies with the patient’s age and the amount
of medication that has been given. Young patients are usually fully alert
and oriented within a few minutes and are able to participate in normal
daily activities. Older patients, however, may require observation and care
for the rest of the treatment day. Occasionally, patients become agitated
when they first awaken in the treatment room. The restlessness is often
controlled by an intravenous dose of Valium or Ativan.
The patient awakens in a dreamy state, perhaps concerned about not
knowing where he is or what is expected of him. He may complain of a
headache or muscular soreness and stiffness similar to those after exer-
cise. A mild analgesic like aspirin usually relieves this discomfort. A back-
ache may be a sign that the dose of muscle relaxant needs to be adjusted.
Occasionally, nausea and vomiting occur as the anesthetic wears off.
Restrictions in Behavior After a Treatment
Formal restrictions are not usually placed on the daily activities after a
treatment, though the patient is advised to do only what can be done
safely. For instance, a patient should not drive a vehicle until she is
completely over the effects of the anesthetic and the treatment. Again,
recovery takes longer in older patients than in younger ones. It is up to
the caretaker (a friend or family member) to monitor the patient’s activi-

ties and make sure that they are within the patient’s capacity.
More difficult is determining when the patient is ready to make far-
ranging decisions, like those concerning finance, business, marriage, divorce,
and the signing of a will. A responsible adult who cares for the patient should
carefully supervise decisions that cannot be deferred until the patient is
well.8
Frequency of Treatments
The schedule of treatments has been developed through experience. At

first, treatments were given every three or four days. Treatment frequency
has varied from eight seizures in one day to a single seizure as an entire
course. Doctors once hoped that several seizures in a single day, under
one period of anesthesia—multiple monitored ECT (MMECT)—would
ensure clinical success without repeated use of anesthetics. But some
patients still suffered disorientation and confusion lasting for many days
without experiencing any additional benefits. Such schedules are not
encouraged today.
Daily treatments known as regressive ECT were sometimes adminis-
tered to severely psychotic patients. Some patients recovered from their
illness but the effects on orientation and memory were severe, often re-
quiring nursing care for feeding and toileting. Regressive ECT is no lon-
ger used.
Treatments are now usually given on alternate days in schedules of
either two or three treatments per week. In the elderly, two treatments a
week are often prescribed. Daily or twice-daily treatments are occasion-
ally required for patients who are acutely delirious, excited, or suicidal. As
soon as relief is attained, the customary treatment schedule continues.
Sometimes a single treatment is successful, but that is rare, even
noteworthy.9 Almost every patient requires more treatments for a lasting
benefit. It is difficult to predict how many treatments will be needed
for a successful course. It is even more difficult to predict the number
or frequency of continuation treatments required to sustain the benefit.
The response to treatment is determined by the severity and duration of
the illness, the patient’s response to medicine, and, most important, the
adequacy of each treatment. Physicians once thought that any seizure
was beneficial, but we now know that seizures vary in their efficacy. If
a fixed number of treatments are prescribed in advance, either by the
psychiatrist during the consent process or as mandated in some states,
the patient may receive an inadequate number of treatments and risk
early relapse.
The severity and duration of illness affect the number of treatments.
Paradoxically, the more severe the illness, the more rapid and effective
the response. The response in psychotic depression is more rapid than
in nonpsychotic forms.10 Prior mediation treatment failure (labeled treat-
ment resistance) does not affect the outcome of ECT or the number of
treatments.11
Symptoms are often relieved by a few treatments, but sustained re-
covery requires a greater number. For decades, doctors were so concerned
about the possibly detrimental effects on memory that they restricted the
number of treatments to the fewest needed to achieve improvement. As a
result, benefits were not sustained and relapse rates were painfully high.
Illness recurred in up to 20% of depressed patients within one month and
up to 50% within six months of a short course of ECT, even though anti-
depressant medications were continued. For depressed patients who im-
proved with ECT and then given no follow-up treatments, relapse rates
were as high as 80%.12
Recovery from the Illness
A depressed patient usually reports the return of appetite and restful

sleep first, followed by improvement in mood. Agitation and restless-
ness gradually disappear. Suicidal preoccupations and obsessive thoughts
take longer to change. The pace varies among patients. The changes are
most dramatic in those who have been severely ill; agitation, restlessness,
strange thoughts, and preoccupations with suicide and death usually dis-
sipate within the first week of treatment. The negativism, rigidity, and
mutism of catatonia are usually gone after two treatments. Disorders in
thought recede more slowly, often requiring more treatments.
Relief of the illness is a gradual process, with one feature after an-
other receding as the patient participates in more normal daily activities.
The end of a course of treatment is determined solely by the patient’s
clinical response. Patients frequently ask how many more treatments
will be needed, but improvement is best judged by reports of mood and

thought by the patient, the nursing staff, and family members.
Many depressed patients have abnormally high levels of the hormone
cortisol when depressed. As the depression is relieved, cortisol levels fall.
They rise again with relapse. Serum cortisol levels at 4 p.m. offer a useful
guide to relapse and the need for more continuation treatment.13
When everyone agrees that the course has been helpful, the options
can be evaluated. If the patient is to continue taking a medicine, it will
usually be prescribed during the last few sessions. For hospitalized pa-
tients a home visit is helpful, although careful monitoring during the visit
is very important, as it is a time of high risk for suicide. Once continua-
tion ECT has been recommended and an adult caretaker is on hand, the
patient can be discharged from the hospital and continue treatment as
an outpatient.
Continuation Treatment
Maintenance treatment is necessary after recovery to prevent relapse.

A course of ECT is not like a course of penicillin for an infection or a
single surgical procedure to stabilize a bone fracture. Rather, ECT is sim-
ilar to the prescription of insulin for diabetes or the chemotherapy treat-
ments that follow the surgical removal of a cancer. In these instances,
the patient’s condition is monitored by frequent visits and the dosing of
treatments is continually adjusted.
The federal government has funded two large multisite collaborative
studies in which severely depressed patients were treated with one of
two forms of ECT and then, after remission, with different continuation
treatments. For patients treated with right unilateral electrode placement
(RUL ECT), the remission rate was 55% among patients who completed
the treatment course; the six-month relapse rate was 80% for those pre-
scribed a placebo, 62% for those prescribed the single antidepressant
nortriptyline, and 36% for those prescribed lithium and nortriptyline,
(monitored for adequacy of blood levels).14 In the second study, patients
treated with bitemporal electrode placement (BT ECT) exhibited an
84% remission rate, with a 37% relapse rate for the same combination
of lithium and nortriptyline and a 39% relapse rate for those on a fixed
schedule of continuation ECT.15
For the delusional depressed, the relapse rates were equally high.
Longer courses of ECT followed by continuation ECT or continuation
pharmacotherapy are now commonly prescribed. An effective course of
treatment typically takes about six months.
This practice is similar to that used in pharmacotherapy, where a six-
month course is the minimum for the treatment of first episodes and much
longer periods for a recurrent illness. Lifelong prescription of medications is
not unusual for patients with psychosis, mania, or delusional depression.
Most patients come to ECT after having achieved limited benefit
from medications, so it is hardly reasonable to expect the same medica-
tions now to be effective and to prevent a relapse. Years ago, reports of oc-
casional success with continuation medications were confusing to those
who studied ECT, but a research group discovered that many of these
patients had originally received inadequate doses and received the proper
care only after successful ECT.16
Some depressed patients, however, come to ECT after seemingly ad-
equate doses of appropriate medications have had no sustained benefit. In
such cases, we cannot expect antidepressant medications to sustain the
benefits of successful ECT, and we must depend on its continuation. We
do not know how to prescribe the number or frequency of continuation
ECT, so the schedules cannot be prescribed arbitrarily. The schedules vary
widely according to symptom development. One approach is to offer treat-
ments at the first sign of symptom recurrence and continue until the ben-
efits are sustained. An alternative approach is to prescribe a fixed schedule
of treatments and add additional treatments when symptoms surface.
Continuation ECT is not a new practice. Before the present psy-
chotropic drugs were introduced, most treatments were given in office
settings. Patients continued working. They visited the doctor periodically,
and treatments were given when symptoms recurred.
The usefulness of continuation ECT was described by many authors
between 1943 and 1965. Based on this experience, a Task Force of the
Association for Convulsive Therapy assessed the safety and efficacy of
continuation ECT.17 Continuation ECT was revived when medications
were found not to sustain the benefits of ECT.
It is difficult to predict the number of treatments that will be required
after the initial course of ECT; some patients need weekly treatments for
many months or even years. One woman, for instance, began ECT when
she was 58 years old and continued outpatient treatments for a decade.18
Another patient, who was 31 when he began ECT for a complex form
of schizophrenia, has received more than 300 treatments.19 Such long
courses are unusual, but premature discontinuation of treatment is the
main reason for recurrence of illness. Follow-up office visits with the
patient and discussions with the family will determine the number of
treatments. If a patient has experienced no symptoms for several months,
treatment can be stopped.
Although the administration of ECT on an outpatient basis is not
difficult, many such courses of treatment have been cut short because of
the inconvenience of arranging for a caretaker—someone who is able to
take the patient to the treatment center and stay with her during recovery
from the effects of the anesthesia and the treatment. Another hurdle is
the need for a trained treatment team and treatment facilities, both of
which are in short national supply. An even greater hurdle is the prejudice
of family members and friends, many of whom harbor the mistaken belief
that the treatments are dangerous and dissuade the patient with overly
pessimistic projections or fears of permanent brain damage. My hope is
that this book will help to dispel those fears.
All patients fear that they will not get well and wonder how they and
their families will manage during the treatment course and the recov-
ery period. These concerns dominate their thinking, so it might benefit
families to meet with a psychiatrist or a mental health worker outside the
ECT sessions. Family group meetings can be very helpful. Sessions with
a psychotherapist are occasionally recommended for help in answering
practical questions during continuation treatment.
Expected Outcomes
Electroconvulsive therapy is prescribed for many illnesses. The melan-

cholic patient with anorexia, weight loss, and insomnia of recent onset
will, in almost all instances, recover after a few treatments, as will the
catatonic patient, whose motor symptoms are quickly relieved.
Some patients seek ECT only after months or years of ineffective
psychiatric and psychological treatments. Many have used sedative drugs
excessively and depend on alcohol, barbiturates, or benzodiazepines to
go through a normal day and achieve sleep. Every effort is made to re-
duce their drug use, since dependence on sedative medications compli-
cates the treatment. The good news is that after successful ECT, patients
sleep better and do not require their previous medications.
Melancholic patients with psychosis (psychotic depression) typically
respond rapidly and well. Unfortunately, they and their families are often
so pleased by the first signs of relief that they discontinue the treatment
before improvement is well established—a mistake that is also often made
with psychiatric medications. Psychotic depression is a malignant disease
that requires extensive treatment, perhaps months of continuation ECT.
It is a form that is difficult to identify properly, and two academic studies
showed that less than 5% of psychotic depressed patients were effectively
treated before referral for ECT.20
Patients with bipolar illness usually come to ECT treatment after all
other medications have failed and hospital care becomes necessary. The
treatment response is slow, and their recovery often can be sustained only
by months of treatment. By contrast, improvement is rapid for those with
a sudden onset of an intense form of mania, identified as manic delirium
or rapid cycling mania. Daily administration of ECT, often up to three or
four treatments per day, may be necessary for remission.21
Schizophrenic patients who have been ill for many months or years
usually require several weeks of treatment. When the illness has pro-
gressed to apathy, disinterest, and prolonged rumination—what are
known as the negative symptoms of psychosis—the efficacy of ECT (and
other treatments) is poor. For those with the positive symptoms of delu-
sions, hallucinations, and excitement, the response is better but slow,
often requiring more than 25 treatments to show a benefit.
Catatonic patients almost always find relief after two to four treat-
ments administered properly. Absence of quick relief indicates inad-
equate treatment or improper diagnosis.
Patients’ Recollections
Everyone is hesitant about the first treatment, so some trepidation is en-

tirely reasonable. Learning about the experiences of others is helpful.
Dr. Martha Manning, a psychotherapist and mother, became severely
depressed and consulted a psychotherapist, who prescribed medications
when her illness interfered with her family and professional responsi-
bilities. Despite months of psychotherapy and medication treatment, her
symptoms worsened and suicide dominated her thoughts. After half a

year, her therapist suggested ECT. The story of her experiences is pub-
lished in the book Undercurrents.22
On the morning of her first treatment, her physician introduced her
to the nurses and anesthesiologist. Then, she writes:
I am covered with hands. They take hold of different parts of me, stak-
ing out their territory. Voices tell me this is a dance done hundreds of
times before, so I need not be afraid. But their casual confidence, their
ease with my body, gives me no comfort. Just as I have lost so much
of myself in the past year, now I lose more. I offer myself up to these
strangers in exchange for the possibility of deliverance. Someone holds
my hand and slips needles under my skin. Another slides down my
gown and plants red Valentine hearts on my chest. Fingers anoint my
temples with cool ointment and fasten a plastic crown tightly around
my head. Wires connect me to machines that hum and beep, register-
ing the peaks and valleys of my brain and my heart. They cover my
mouth and nose with plastic and instruct me to breathe.
Dr. Manning successfully completed a course of treatment, returned to

work, and wrote her book.
A psychologist, Dr. Norman Endler, became depressed and was plagued
by suicidal thoughts. Psychotherapy was unsuccessful, and when he was
given antidepressant drugs he developed a racing and irregular heart rate,
difficulty in urination, pounding headaches, nausea, vomiting, high blood
pressure, and spells of weakness. After four months of failed medication
trials, he described his first treatment as an outpatient23:
I changed into my pajamas and a nurse took my vital signs (blood pres-
sure, pulse, and temperature). The nurse and other attendants were
friendly and reassuring. I began to feel at ease. The anesthetist arrived
and informed me that she was going to give me an injection. I was asked
to lie down on a cot and was wheeled into the ECT room proper. It was
about eight o’clock. A needle was injected into my arm and I was told to
count back from 100. I got about as far as 91. The next thing I knew I was
in the recovery room and it was about eight-fifteen. I was slightly groggy
and tired but not confused. My memory was not impaired. I certainly
knew where I was. I rested for another few minutes and was then given
some cookies and coffee. Shortly after eight-thirty, I got dressed, went
down the hall to fetch Beatty, and she drove me home. At home I had
breakfast and then lay down for a few hours. Late in the morning I got
dressed. I felt no pain, no confusion, and no agitation. I felt neither less
depressed nor more depressed than I had before the ECT.
Dr. Endler eventually recovered, returned to work, and published Holiday

of Darkness, a popular book on his experience.
t h r e e
The Treatment Technique
All things are difficult before they are easy.

—Fuller1
T he decision to recommend ECT is difficult, much like the decision

for a surgical operation. A physician seeking the source of the pa-
tient’s symptoms goes through an intellectual process similar to that of a
detective solving a mystery. The doctor listens to the patient’s story, find-
ing some conditions to be likely and others not. Physical signs of illness
are sought, and tests and special examinations that narrow the probability
to a specific illness are considered. When the doctor is able to put the
history, symptoms, signs, and test results together, a diagnosis is offered:
a solution to the mystery. In many cases, doctors are able to recommend
specific treatments that are effective and predict a good outcome. When
effective treatment is lacking, symptom relief is offered.
For the psychiatric symptoms caused by syphilis, diabetes, thyroid dis-
ease, and other medical illnesses, doctors verify the diagnosis with specific
tests and offer effective treatments. But for most psychiatric conditions
we do not understand the cause, nor do we have laboratory tests to narrow
the diagnoses.
In the past half century, the classification of psychiatric disorders
has grown to more than 300 conditions described mainly by clusters of
symptoms. For only a few disorders can we assure effective treatment. At
their best, the psychotherapies and medications relieve symptoms, but
none cure the disease. The same is true for ECT. It eases identifiable
25
syndromes, or clusters of symptoms. The relief is provisional, however,

requiring continued treatment to sustain the benefit.
Our abilities have progressively improved in selecting and administer-
ing anesthesia, in selecting the amount of electrical energy and the loca-
tion of the electrodes for stimulation, and in monitoring bodily effects for
safer treatments. The following descriptions are meant to answer ques-
tions about the techniques of treatment.
Anesthesia
Bone fractures were a principal risk of the treatments of the late 1930s
and 1940s. Physical restraint by a sheet over the chest and abdomen was
effective, but chemical relaxation of the muscles that inhibited the convul-
sion was better. By 1953, the synthetic chemical Anectine was shown to
block muscle contractions quickly and safely. Given intravenously, it acts
within a minute. It is also rapidly destroyed by the body, making it ideal for
the short time needed to relax the muscles during the treatment.
Not only the back and jaw muscles relax, but also the muscles that
control breathing. The patient under anesthesia, then, does not breathe on
his own; breathing is controlled by an anesthesiologist or nurse-anesthetist.
As the patient may have the sensation of being unable to breathe for him-
self, the anesthesiologist administers an anesthetic to block this panicky
feeling. The duration of anesthesia is very short and is induced chiefly by
the barbiturate Brevital, which, like the muscle relaxant, is rapidly me-
tabolized by the body.2 The period of anesthesia is usually no longer than
10 minutes.
Because breathing pure oxygen reduces the deleterious effects on
memory, a mask is placed over the patient’s nose and mouth so that very high
concentrations of oxygen are breathed. Occasionally, as when the patient is
obese or in the third trimester of pregnancy, a tube is inserted between the
mouth and the larynx to keep an open airway. Such intubation is done after
the patient is asleep and is removed before the patient wakes. Intubation, a
routine procedure in general anesthesia, causes no discomfort because the
patient is unaware of it, although a sore throat sometimes results.
Salivation increases, and the heart rate and blood pressure rise dur-
ing treatment. A substance like Robinul or atropine, administered intra-
venously in the treatment room just before the anesthetic, moderates
The Treatment Technique / 27
these changes. Some physicians prefer that the medication be given by

intramuscular injection about 30 minutes before the treatment.
The anesthesiologist, who is present during the entire treatment, makes
sure that the muscles are relaxed and that oxygenation is adequate.
Electrical Energy
The purpose of the electrical stimulus is to induce a brain seizure. Elec-

tricity is not essential for the treatment. Treatments were once given by
injecting chemicals (Metrazol) or by inhalation (Indoklon). An electrical
stimulus is favored because it is easier to administer and less expensive.
Electroconvulsive therapy devices enable the doctor to vary the char-
acteristics of the stimulus. A “square-wave” form of energy is used today,
replacing the alternating electrical currents that were popular for the first
two decades of ECT use.3
Since the energy that is needed depends in part on the resistance of
the skin, skull, and intervening tissues, ECT devices allow for an estimate
of the resistance between the stimulating electrodes, thereby ensuring
adequate and safe treatment. Amplifiers record the EEG and the ECG
during the seizure, permitting the doctor to evaluate the quality of each
treatment. The devices have circuitry to prevent the delivery of excessive
energy, so there is no reason to fear that electric currents may harm either
the patient or the doctor.
The energy level is individualized according to the patient’s age, gen-
der, and the type, amount, and duration of medications prescribed in the
days before ECT administration. We deliver more energy to older patients
than to younger ones and more to men than to women. As patients age, the
seizure threshold rises in a roughly linear correlation. The seizure threshold
is the level of energy needed to stimulate a seizure. It is the bar that must
be crossed to develop an effective treatment. One way to estimate dosing
is by consulting energy-dosage tables to set the level for the first treatment.
The settings for successive treatments are changed, depending on the qual-
ity of the seizure.
An alternate experimental method was developed by psychologists to
approximate the seizure threshold. During the first treatment an electrical
stimulus is applied, beginning with the first, which is too low, and increas-
ing until a seizure is produced. Successive treatments are given with energy
doses that are a fixed amount above the estimated threshold. The method
has inherent risks that are not necessary for effective results. The first
treatment is necessarily inadequate, eliciting an insufficient seizure. This
method is considered necessary when unilateral electrode placement (RUL
ECT) is used (dosage must be at least six times the ST for clinical efficacy)
but not with bilateral electrode placement (BT ECT), as the dose can be
effectively and safely determined from age and gender tables.
Electrodes
The stimulus is delivered through flat electrodes, usually one to two inches
in diameter, applied either to both temples (BT ECT) or to one temple
and the back of the head on the same side (RUL ECT). Some doctors
place the electrodes on the forehead, about three inches apart (bifrontal
electrode placement, or BF ECT). The efficiency of treatments and the
degree of side effects vary with electrode placement. To develop a seizure,
electric current must pass between the two electrodes. The electrodes
are either pasted on the scalp or held by an elastic band. Commonly used
electrodes today are flexible, encased in plastic, and usually pasted on the
scalp. Positioning the electrodes causes no pain or discomfort, and no cur-
rent flows through them until the patient is asleep and all arrangements
have been made for the treatment (Fig. 3–1).
The brain has a special center for each of its functions. In right-
handed individuals, the center for the control of speech and memory is
on the left side of the brain, the dominant side. In left-handed individuals,
the speech center is also generally on the left side of the brain, although
in a few individuals, it is on the right side. At first, when applying elec-
trodes for RUL ECT, handedness was determined and the nondominant
side selected. Such tests are no longer commonly used and are considered
unnecessary.
The influence of the currents on speech and memory, then, can be ei-
ther increased or minimized according to the side on which the energy is
delivered. Delivery of the stimulus on the nondominant side lessens the
immediate effects on orientation and recall on awakening. Since domi-
nance for speech and memory lies in the left hemisphere in more than
95% of the population, the unilateral electrodes are usually placed on the
right side, the non-dominant side for speech in more than 90% of per-
sons. This is called unilateral nondominant ECT (RUL ECT ).
Right unilateral
Bitemporal
Bifrontal
Figure 3–1. Electrode placements.

Unilateral ECT, however, is clinically less effective, and patients do

not improve as quickly as they do with BT ECT. The comparison is seen in
two large multisite government-sponsored studies which reported a 55%
remission rate for RUL ECT but an 84% rate for BT ECT. The average
number of treatments was 7.3 for BT ECT and 10.5 for RUL ECT to re-
mission, an average saving of three treatments and one week of illness.4
The memory measures in these studies showed no advantages for one
electrode placement over the other. An earlier comparison of both elec-
trode placements sought to increase RUL ECT efficacy by administering
energy at high multiples over the measured seizure threshold. When the
efficacies of RUL ECT and BT ECT were equated, the effects on memory
tests were not distinguishable.5
Treatments with unilateral electrode placement also require special
attention to energy dosing, as well as the use of medications to block the
effects of electric currents that do not induce a full seizure. The immedi-
ate effect of the electrical stimulus is to slow the heart rate. The devel-
oped seizure increases the heart rate. If the first effect, slowing of the
heart rate, is not canceled by the seizure, the rate may fall sharply, with
risk to the patient. Incomplete seizures are a necessary accompaniment of
measuring the seizure threshold, a procedure that is necessary to assure
adequate dosing for unilateral electrode placement. To prevent the slow-
ing of the heart rate, an anticholinergic medication that blocks cardiac
slowing is usually given with the anesthetic.
Because patients referred for ECT are severely ill, every effort is
made to ensure rapid and effective treatment. For more than 40 years,
practitioners sought to minimize the immediate confusion and poor orien-
tation, accepting the poorer remission rates of unilateral treatments. The
additional weeks of illness and expense, and the physical demands of ad-
ditional treatments, must be balanced by the immediate temporary reduc-
tion in confusion. Psychiatrists today differ in their recommendations for
nonpsychotic depressed patients, some advocating unilateral ECT at maxi-
mum energies and some bilateral ECT with dosing according to age. Some
doctors specifically recommend unilateral ECT in very young patients, the
physically healthy, those who express concerns about the possible effects
on memory and cognition, and when immediate relief is not necessary.6 In
treating psychotic, catatonic, and manic patients, and especially systemi-
cally ill patients, in whom a quick result with a minimum number of treat-
ments is desirable, most clinicians prefer bilateral ECT.
Physiological Monitoring
The actions of the heart, muscles, and brain change dramatically during
a seizure. At first, the heart rate slows and then becomes more rapid. Nor-
mal rates of 68 to 78 beats per minute (bpm) rise to 110 to 130 bpm and
remain elevated throughout the seizure. The rate quickly returns to nor-
mal as the seizure ends.
Blood pressure also rises with the seizure and falls when it is over. The
systolic blood pressure, usually between 110 and 160 millimeters of mer-
cury (mmHg), increases to 140 to 200 mmHg. Occasionally, the changes
in blood pressure or heart rate require adjustment by medication during
the treatment.
Blood oxygen saturation remains between 98% and 100%, with blood
carrying its maximum amount of oxygen. If the oxygen level in the blood
falls, the anesthesiologist administers more frequent breaths to maintain
the highest concentration in the lungs.
Seizure quality is determined by three measures. The motor convul-
sion is observed in a lower limb and recorded in the electromyogram
(EMG), the record of rhythmic changes in the electrical activity of the
muscles. The variation in heart rate is observed in the ECG, and the
brain’s electrical activity is recorded in the EEG.
Seizure durations in the muscles range from 20 to 60 seconds. The
changes in heart rate vary from 25 to 100 seconds, and those in the EEG
vary from 30 to 150 seconds. If the seizure in the EEG lasts for more than
180 seconds, longer than is needed for a good clinical effect, it is inter-
rupted by intravenous administration of a benzodiazepine. Valium, Ativan,
and Versed are commonly used.
An Effective Treatment
How do we judge whether a particular treatment will have the desired

effect? An effective treatment is defined by the changes in the EEG re-
corded during the treatment. At one time, the duration (in seconds) of
the seizure served as the index of effective treatment, with a minimum
of 25 seconds accepted for the motor seizure and at least 30 seconds for
the EEG. These criteria are no longer considered rigorous enough. Care-
ful measurement of the number of treatments needed for a good result
showed that the changes in the brain varied considerably with different
electrode placements and different energy levels. Effective treatment
today requires attention to the quality of the EEG as well as the length of
the seizure. Seizures of at least 25 seconds’ duration in the motor convul-
sion, 30 to 50 seconds in the heart rate increase, and 30 to 150 seconds
in the EEG are now accepted minimum standards. (An example of an
effective seizure pattern is shown in Chapter 10.) Another measure of
efficacy is the rise in the serum level of prolactin, a peptide released into
the blood with a seizure.7
In the depressed patient, the most reliable sign of an effective treat-
ment is the improvement in mood, appetite, sleep, and interest, as well as
more normal interpersonal behavior. Unless these improve within three
to five treatments, the treatment is considered weak. If there is no sign of
improvement, the doctor usually reconsiders the technical features of the
treatment or the diagnosis.
For the patient with thought disorder, sleep and appetite improve
first. Excitement and restlessness disappear next. Last, the patient con-
siders her thought disorders as strange experiences in the past.
Catatonia is sensitive to treatment characteristics. For the patient
who is mute, not eating, posturing, and refusing to carry out normal daily
activities, treatments may be given daily for three to four days to begin
the treatment process. Once the main symptoms have started to resolve,
a more conventional treatment schedule is instituted.
For manic patients, those with a mixed manic and depressive state,
or those who are cycling rapidly between mood states or are delirious, at-
tention to the treatment schedule is necessary. Daily treatments are often
necessary, with a return to a more usual schedule when the severe symp-
toms are relieved.
ECT-Qualified Psychiatrists
Psychiatrists who administer ECT are trained first as physicians and then
as psychiatrists. They gain their experience during their training in a psy-
chiatric hospital. When they seek additional training, they enroll in a
special fellowship program lasting for one to five days.
A psychiatrist who intends to administer ECT obtains permission
from the medical board of his institution to use the hospital’s facilities,
much as a surgeon obtains his privileges for surgery. To obtain the privilege
of using the hospital’s facilities, the physician must satisfy the institution’s
requirements, set according to standards suggested by the American Psy-
chiatric Association (APA) and the Joint Commission on Accreditation of
Health Care Organizations (JCAHO).
When a psychiatrist not trained in ECT decides that the treatment
is called for, he refers the patient to a qualified colleague who assumes
responsibility for the patient’s care during the ECT course. The latter
returns the patient to the referring physician for aftercare. Continuation
ECT is usually the joint responsibility of both therapists.
Where Is Treatment Carried Out?
Most patients are treated in a specially equipped unit in a hospital or

an ambulatory care center. Patients are allowed to go home after each
treatment. Nothing in the safe and expert administration of the treat-
ment necessitates the specialized care offered by a hospital. But hospital
care is necessary when the patient has a systemic illness that requires
continuous nursing attention. The infirm elderly, patients with suicidal
or homicidal preoccupations, and those in stupor, delirium, motor excite-
ment, and catatonia are usually treated in the hospital.
Not all ECT treatment facilities are equipped for a full treatment
course on an ambulatory basis. Outpatient treatment calls for the psychi-
atrist to establish relationships with consulting internists, dentists, and
anesthesiologists. The patient must have an adult caretaker to ensure
compliance with the medication regimen, to ensure that he takes no food
before the treatment, and to protect him until the effects of anesthesia
wear off. When such arrangements are difficult to provide, inpatient care
is necessary.
Electroconvulsive therapy requires special equipment to deliver the
controlled electrical energy necessary to induce a seizure, in addition to the
instruments for delivering anesthesia and for monitoring seizures. In many
hospitals, a treatment and recovery room suite is adjacent to, or part of, a
psychiatric inpatient treatment unit.
f o u r
Side Effects and Memory

Issues
We have all forgot more than we remember.

—Fuller1
A s we have seen, ECT involves modest discomfort, minimal risk, and

almost no contraindications to its use. Headache, backache, nausea,
and vomiting are the most frequent immediate complaints. These are re-
lieved by mild analgesics and occasionally by the choice of anesthetic.
Spine fractures were a complicating risk of the early treatments, but they
are now prevented by muscle relaxation. In the past, seizures were some-
times prolonged and did not end promptly. Prolonged seizures are now
avoided by precise energy dosing and attention to anesthesia related to the
patient’s age. When a prolonged seizure does occur, it is readily recognized
and treated.
The risk of death during ECT is very low, less than that of women de-
livering spontaneous births.2 It is surprising that death is so rare since half
of the patients are elderly, many ill with severe systemic infirmities or criti-
cal illnesses. The low mortality rate reflects the inherent safety of modern
procedures. Indeed, some reports find that the lifetime death rates for
hospitalized psychiatric patients who have received ECT are lower than
the rates of those who have not. The mortality rate from natural causes
is lower for those treated with ECT than for those who have not. Suicide
rates are higher, however.3
34
Side Effects and Memory Issues / 35
Memory
The common memory loss associated with ECT is the main hurdle pa-
tients and their families face in accepting the treatment. Images of a
patient losing the memory of his past life, his work skills, the names of
his children and friends, and the ability to care for himself, much like a
patient with Alzheimer’s disease, are so prevalent that doctors hesitate to
recommend the treatment and many patients refuse permission even when
it may be their principal lifesaving option.
Such images are false.
The fear of memory loss is based largely on reports by patients who
were treated without anesthesia or ventilation with oxygen in the first
decades of the treatment’s use. Such treatments were accompanied by
severe, and often persistent, impairments in memory. Clinical practice
changed and our treatments are no longer associated with these devastat-
ing problems, as careful attention is now paid to oxygenation throughout
the procedure and to technical features that minimize the impact of the
stimulus, anesthesia, and the seizure on memory. There is no longer rea-
son to fear that ECT will permanently erase learned skills, the memory of
important life events, or the ability to recognize family members. Patients
are regularly able to return to work. With improvement, patients are again
interested in their families, and in social and political events, and have
the same abilities that they had before they became ill.
Concerns about memory are amplified by the experiences during the
days and weeks of actual treatment. Both the seizure itself and the anes-
thesia impair awareness of events during the days in the treatment cycle;
patients are usually confused and have difficulty recalling the experiences
of the treatment day. Since the treatments are repeated over weeks, the
events during the treatment course are poorly perceived and poorly com-
mitted to memory. The events are recorded as if through a haze, and when
these experiences are shared with visiting family members, they quite
naturally sympathize with the patient’s difficulties.
Age is the significant factor in the impact of ECT on memory. Younger
patients typically recover fully and quickly. Older patients have longer
recovery times, and their families often see them drowsy and confused.
These experiences are disturbing to patients, their families, nurses, and
caretakers and contribute to the popular notion that memory is severely
affected by the treatment.
Losses of memory are not necessary for recovery. In the initial years
of ECT use, psychoanalysts’ assumption that mental illness resulted from
hidden memories of unpleasant childhood events dominated psychiatric
philosophy. Acknowledging these events was considered the basis for re-
covery. Psychoanalysts, surprised by the rapid relief of the patients they
referred for ECT, believed that ECT suppressed early memories. These
theories are no longer tenable.4
Most patients come to treatment with impaired memories of recent
experiences resulting from preoccupation with their illness, inattention,
and the direct effects of their medications. As patients recover with treat-
ment, recollections and memory test scores improve. An example of dra-
matic recovery of memory is seen in patients with pseudodementia, a severe
form of melancholia in which memory is seriously impaired. With effec-
tive treatment, the impairments in memory and orientation are relieved.
Examples are found in Chapter Five.
Persistent Complaints of Impaired Memory
Some patients claim that their memories never fully return, that they have
gaps in recollections of specific personal memories, and that their work
skills are hampered. They sense feelings as if in a hazy cloud, or dreaming,
or distant from the immediate scene, and yet are capable of carrying on
normal daily activities using their pre-sickness and pre-treatment skills.
The few who voice their concerns report no recurrences of their illnesses
and successful careers in public advocacy and politics.5 Such complaints
are rare.
The portrayal of ECT in novels and films emphasizes the confusion
and disorientation that occur acutely with treatment, promoting the belief
that memory is severely affected. The campaigns against ECT by mental
health professionals who oppose the treatment keep the image of persistent
memory loss alive in the public mind. Family physicians, psychotherapists,
and mental health workers, with no direct knowledge of the treatment,
give voice to the popular images and keep the fear of memory loss alive.
Causes for Memory Complaints
When we are preoccupied by depressive and paranoid thoughts, when

our moods are distorted, when we feel hopeless and helpless, when we
harbor thoughts of self-harm, we register the events of our lives poorly.

Few events are associated with the emotional reminders necessary to
place memories in permanent memory storage to allow recall. At such
times, we misinterpret the motives and statements of family members
and friends. We distort the perceptions of daily events. We are so preoc-
cupied by the symptoms, pains, and discomforts of our illness that we
are vague, hesitant, and embarrassed when asked about recent events.
Our responses are slow, and we may even appear so demented that our
relatives fear that we have Alzheimer’s disease. The term pseudodementia
has been coined to describe these conditions, which are frequently as-
sociated with an affective or psychotic disorder.
Aging is important, as noted by Kitty Dukakis in a book she wrote
about her experiences with ECT.6 Many patients referred for treatment
are elderly, and many most likely experience regular “senior moments” of
failed recall. When these occur in persons who have had ECT, the asso-
ciation of the treatment with its effects on memory is strengthened.
Another cause of memory loss, though not often recognized or ac-
knowledged, is the influence of psychotropic drugs. All medicines that are
prescribed as treatment for psychiatric illnesses affect brain chemistry and
physiology, and the continuation of these treatments during the course
of ECT affects memory as well. Every biochemical change in brain cells
alters perception and recollection. These medications include the seda-
tives and sleep inducing agents Valium, Xanax, Ativan, Benadryl, Ambien,
Lunesta, chloral hydrate, and the barbiturates; lithium and the tricyclic
antidepressants Tofranil, Elavil, and Sinequan; and older antipsychotic
agents like Thorazine and newer agents like Clozaril and Risperdal.
Anxiolytic (antianxiety) and sedative drugs are often prescribed for
depressed patients to improve their sleep. The effects of such drugs on
orientation may persist until the day after they have been taken; even a
single dose may affect driving performance for 24 hours—or longer if the
dose is repeated. Tolerance to medications (whose efficacy diminishes as
the body learns how to metabolize and destroy them) develops rapidly,
encouraging the use of ever larger doses to achieve the desired effect. Re-
call may then be impaired for days. This is particularly true of the longer-
acting sedative drugs that are discarded slowly from the body.
Lithium affects memory, depending on its concentration in the
blood. Levels of lithium in the blood—and therefore in the brain—vary
during the day and night. Immediately after the drug is ingested, its level
in the blood rises to the point at which it clearly impairs concentration
and memory. The effects are more frequent in the summer, when people
become dehydrated with sweating and lithium passes through the body
more slowly.
Older tricyclic antidepressant medications affect concentration and
memory even in proper dosages. When these drugs are given along with
ECT, the combination may exaggerate the patient’s confusion and dis-
orientation. Motor excitement may occur when tissue and blood levels of
antidepressant drugs become high because of accidental or intentional
overdose. Even the newer antidepressants that are claimed to have a re-
duced influence on memory have noticeable effects.
Alcohol, whether as beer, whiskey, wine, or many other formulations,
even in small amounts, affects memory and recall. The patient who is al-
ready taking a sedative, lithium, or an antidepressant may sustain further
memory loss with the addition of alcohol.
Medical practitioners are well aware of the effects of psychotropic
drugs on memory. Since warnings about the effects of medications on
cognition and memory are not required in clinical practice, the matter is
rarely discussed, so the patient and her family are not prepared for such ill
effects. Doctors do not ascribe difficulties in recall to the medications, so
when medications and ECT are combined, as is common in continuation
treatment, their effects on memory are blamed solely on ECT, which then
carries the full burden of the public’s fear of every psychiatric treatment’s
cognitive effects.
Anesthetic Effects on Memory
The patient who is under an anesthetic during ECT will recall little that
took place in the treatment room. As the anesthetic wears off, she is con-
fused and restless. As she awakens further and recognizes the voices and
faces of the doctor and the nurse, she calms down. Quickly, she responds
to her name, identifies where she is, and recalls the date and time of day.
Disorientation about person is evident for 5 to 30 minutes; about place,
for an average of 10 to 40 minutes; about time, for up to one hour. These
periods are longer in older patients. When the patient returns to her room
following the treatment, she has difficulty perceiving her surroundings
and recalling events for several hours. And when she is visited by her fam-
ily, she may appear sleepy, vague, distant, and uninterested.
The anesthetic has both immediate and sustained effects on mem-

ory. It blots out the events of the treatment, often clouding recollection
of the minutes before it was given, and persists for hours, decreasing
slowly as the body sheds it. This effect of the anesthetic lasts longer in
older people and in those with liver and kidney disease, for these patients
eliminate the anesthetic more slowly.
Young adults questioned immediately after ECT recall occurrences
up to the moment of anesthesia. They are able to demonstrate intellectual
and performance skills—reading, writing, playing a musical instrument,
planning a play in chess or bridge—soon after the treatment. Such skills
are impaired longer or, in unusual instances, for days in elderly patients.
The degree of blood oxygenation also affects memory and recall. If
the anesthesiologist has difficulty sustaining the airway or filling the lungs
adequately with oxygen, the level in the blood and the brain may fall.
When ECT was introduced, little attention was given to preserving ad-
equate levels of oxygen; patients sometimes stopped breathing for min-
utes, their blood oxygen concentrations fell, and their skin turned blue.
Inadequate oxygenation of the blood led to inadequate oxygen in the
brain, which could not function properly. If the anoxia lasted for many
minutes, the patient suffered lasting memory impairment. So common
were these mishaps that memory loss was considered an inevitable con-
comitant of successful treatment. In a brilliant set of experiments, the
Swedish psychiatrist Gunnar Holmberg demonstrated that ECT given
with high concentrations of oxygen minimized the ill effects on memory.7
By the mid-1950s, continuous oxygenation had become a standard fea-
ture of treatment; in modern applications, the blood concentration of oxy-
gen is continuously monitored and any decrease is corrected quickly.
Individual Factors Affecting Memory
Memory is affected by the patient’s age, the duration and severity of the
illness, the presence and seriousness of bodily disorders, and such tech-
nical factors as current intensity, electrode placement, and the frequency
and number of treatments. Of these factors, age is the most relevant.
People experience, as part of aging, the frustrating loss of recent and
remote memory. The depressed elderly suffer the additional impediment
of fear about their illness.
Patients often come to treatment after lengthy periods of illness—

months, even years—during which fear has hindered their perception and
memory of life events. When they recover, often they cannot recall events
that took place during their illness, especially the phase that brought
them to ECT. This is true whether patients are treated by psychotherapy,
by medicines, or by ECT. Because those referred for ECT are usually the
most ill, and have been ill for the longest periods, their memory impair-
ment is the most severe.
William Styron, in his book Darkness Visible: A Memory of Madness,
wrote8:
But my behavior was really the result of the illness, which had pro-
gressed far enough to produce some of its most famous and sinister
hallmarks: confusion, failure of mental focus and lapse of memory. At
a later stage my entire mind would be dominated by anarchic discon-
nections; as I have said, there was now something that resembled bifur-
cation of mood: lucidity of sorts in the early hours of the day, gathering
murk in the afternoon and evening. . . . Rational thought was usually ab-
sent from my mind at such times, hence trance. I can think of no more
apposite word for this state of being, a condition of helpless stupor in
which cognition was replaced by that “positive and active anguish.” . . . I
had now reached that phase of the disorder where all sense of hope had
vanished, along with the idea of a futurity; my brain . . . had become less
an organ of thought than an instrument registering, minute by minute,
varying degrees of its own suffering.
Reports about adverse effects of ECT on memory dot the public

literature. A practicing psychiatrist received bilateral ECT with the high-
energy currents, in use decades ago, which was widely associated with
the reports that stigmatized the therapy.9 He wrote:
Memory for recent events, during the week or so preceding treatment,
appears to be the most severely affected. Memories for events of several
years ago seem to be impaired hardly at all. . . . When an event, entirely
forgotten, is brought to one’s notice, it sounds completely strange, for-
eign and unknown. One has the feeling that a confabulation is being
presented: the details of the account seem unnecessarily elaborate, as
if to make the story convincing, and the whole effect is almost laugh-
able. Then a fragment of the story rings true; a name is recognized, for
example, and . . . events or facts come suddenly to mind, in a linear
sequence. One is suddenly aware of a curious faculty to “feel one’s way”

along this sequence, as one element leads to the next.
He describes the difficulties in recall through an anecdote:

At the end of about two months the gaps in my memory had been com-
pletely closed, with one amusing exception. Several months afterwards,
at a scientific meeting, I met a psychiatrist whose face seemed very fami-
liar, though I could not remember his name nor where I had met him
before. I remarked on this to a friend, saying, “It must be a result of the
ECT.” The friend replied, “I’m not surprised, it was he who gave you
the treatment!”
The impact of the treatment on her memory is described by Kitty

Dukakis, the wife of a former governor of Massachusetts, in her book
Shock: The Healing Power of Electroconvulsive Therapy.10 After many de-
cades of depression, alcoholism, detoxification, abuse of sedative drugs,
and attempts at suicide, she was referred for ECT. She responded very
well, and in recent years she has undergone additional periodic outpa-
tient treatments. She describes difficulties in recalling people’s names
or specific events of the past: “Things I lose generally come back” with
prompting. Now that she receives continuation treatments, “the losses
have been less noticeable, less severe, after my recent ECT sessions. . . .”
She writes, “At the same time, I have learned ways to partly compensate
for whatever loss I still experience.” She calls family members and friends
to find missing telephone numbers. In another recollection she writes:
“Then there is the fact that I am sixty-nine. I like to forget that, but
I know my age has something to do with my forgetting people’s names,
directions, things like that.”
A literary writer and social scientist working in British mental health
clinics described her experience in a reminiscence titled “Choosing
ECT.”11 She had recurrent episodes of severe depression:
Although I was profoundly miserable, this misery that characterizes popu-
lar uses of the term “depression” is not what bothers me most. More
important to me is being unable to think properly. Although I was re-
ceiving medication, I was still unable to work, read, drive my car, make
even the simplest decisions or look after myself.
As with Dr. Manning, discussed in Chapter Two, her consideration

of ECT elicited statements about the evils of the treatment from her
friends and predictions that she would lose her memory and her ability to
write. After she had a course of ECT, she returned to work:
What is it like? Nothing really. I had an injection, went to sleep and then
woke up again a few minutes later. . . . I did have some memory problems
during the three-week course (could not remember who had visited and
so on). I think my friends found this more distressing than I did—if
I wanted to remember something I simply wrote it down. These effects
were not long-lasting: my job places heavy demands on my memory and
I was able to resume it shortly after my final treatment. Now, some three
months on, no one has complained about my forgetting anything.
She then noted:
One of the most irritating after-effects of having had ECT is the be-
haviour of those people who are so convinced that it causes irreparable
damage that they “test” my memory with their questions, or quiz me
and/or my friends concerning my state: “Are you/Is Rachel really all
right?” they ask in hushed and ominous tones, and apparently seem
unpersuaded by the answer “yes.”
After all else is said, a mental illness is a disorder of the brain,
the organ of mind and of memory. Our efforts—prescribing medicines
or eliciting seizures in the brain or easing the patient’s mental state by
psychotherapy—are intended to change the brain’s functions. No one
treated for a mental disorder with modern medicines or physical inter-
ventions escapes alterations in memory, and ECT is a powerful means of
affecting the mind’s functions. In modern clinical practice, the adverse
effects on memory have been minimized to the point of being undetect-
able by measurements six weeks after completion of treatment. In those
patients who suffer strange feelings and the slowing of thoughts more
than six weeks after treatment, there may be a recurrence of their illness,
or a bad reaction to continued medicines or, or patients may have devel-
oped a psychological response described as a somatization reaction, akin
to the more common posttraumatic stress disorder.12
Although improvements in our practice have eliminated or reduced
adverse effects in the thousands of patients treated with ECT, they are, like
all patients, subject to the risks attendant on every form of treatment. For
those considering ECT, the risk to memory is small compared to the ben-
efits, and our patients and we who treat them are fortunate in having this
treatment available.
f i v e
Depressive Mood Disorders
I want to die. I can’t believe I feel like this. But it is

the strongest feeling I know right now, stronger than
hope or faith or even love. The aching restlessness of
this depression is becoming unbearable.
The thoughts of suicide are becoming intrusive. It’s
not that I want to die. It’s that I’m not sure I can live
like this anymore.
—Manning1
E lectroconvulsive therapy is most often used to treat disorders of mood.

The internally experienced feeling is the emotional state reflected in
the way we present ourselves to others and in the ways we react to them.
Mood varies with daily circumstances and is sensitive to the conditions
of the body, particularly physical health, fatigue, hunger, and hormonal
activity.
Moods are experienced internally and fluctuate widely. Two disorders
are recognized. Depression, or depressive mood disorder, is dominated by sad-
ness, hopelessness, fear of the future, and the persistent thought that life
is not worth living. Mania, or manic mood disorder, is a state of excitement,
grandiosity, expansiveness, and feelings of increased power and energy. In
the present psychiatric classification, mania is labeled bipolar disorder and
the depressed phase is labeled major depression.2
In a depressive mood disorder, body functions are disrupted. Patients
are sleepless, appetite is poor, and weight loss may be pronounced, at
43
times amounting to 20% of the body weight within a few weeks. Work,
sexual activity, and family may be disregarded. The future appears hope-
less, patients believe they are helpless to affect it, and their thoughts are
filled with gloom. Threats of suicide reflect their distress. They are often
agitated and restless. Many meet the criteria for the malignant syndrome
of melancholia.3
Overwhelmed by feelings of helplessness, hopelessness, and
worthlessness, the depressed patient dwells on thoughts of suicide.
He may believe that others are watching or talking about him; voices
are heard when no one is present; and concerns that his spouse is
unfaithful dominate his thought. At times, the events depicted on the
television or movie screen seem to apply directly to him. Such strange
thoughts are delusions, and this severe state of depressed mood and
disorder in thought is labeled delusional depression or psychotic depres-
sion. These disorders require intensive treatment and almost always
hospital care.
A depressed patient is commonly unaware of the day’s events, regis-
ters little of what happens around her, and has a compromised memory.
This form of depression can be difficult to distinguish from an Alzheimer-
type dementia. When the symptoms of dementia are brought about by
depression, however, they can be reversed with treatment. The condition
is known as pseudodementia or reversible dementia.
Another common form of depressive illness is one dominated by with-
drawal, mutism, and negativism. Refusing to eat or drink, the depressed
patient sits rigidly in a chair or lies motionless on a bed, unresponsive to
questions and commands, seemingly in a stupor. The state is known as
catatonia or depressive stupor. This illness requires special treatment.
It is useful to identify the varieties of depression, because some call
for specific treatments. Melancholic patients and those with pseudode-
mentia respond to tricyclic antidepressant drugs, but psychotic depressed
patients require high doses of both antidepressant and antipsychotic med-
icines to achieve any benefit. Catatonic depressed patients respond to
the barbiturates and benzodiazepines. Different medications are offered
for the unipolar and bipolar depressions. Each disorder is responsive
to ECT.
A depressive mood disorder increases the likelihood of early death,
not only by suicide but also because the patient’s body undergoes systemic
changes associated with diseases like cancer and heart disease. In a large
Depressive Mood Disorders / 45
urban population, depressed patients were found to be more likely to die

within the one-year follow-up period than were patients who were not
depressed. The finding was corroborated by a large study of patients done
after 10 years and another study done after 16 years. The rate of death
during the two years after hospital treatment for a mental disorder is
higher for natural and accidental causes and for suicide.4 Higher suicide
rates are not limited to patients with depression; they are reported in all
psychiatric patients.
Effective treatment lowers mortality rates and the incidence of sui-
cide. Patients treated with ECT are more likely, during follow-up, to live
and to demonstrate greater clinical improvement than those treated with
pharmacotherapy. Suicide attempts are fewer in depressed patients treated
with ECT (0.8%) than in those treated with antidepressant medicines
alone (4.2%). Another study showed fewer suicide attempts among pa-
tients treated with ECT than among those treated with antidepressants
(0% versus 10%) or those who had no history of such attempts (1.1% ver-
sus 3.6%).5 Clearly, ECT’s effect on death rates among the mentally ill,
particularly those with mood disorders, is an important consideration.
In melancholic patients, serum cortisol, a hormone that regulates the
body’s response to stress, is abnormally elevated, especially in those ill
enough to be hospitalized. Surprisingly, with effective treatment, the cor-
tisol levels normalize and, with relapse, became abnormal again. The con-
nection between serum cortisol levels and suicide is unclear. A test of the
integrity of cortisol activity in the hypothalamic-pituitary-adrenal axis is
the dexamethasone suppression test (DST) developed in the early 1970s
by Bernard Carroll and his coworkers in Melbourne, Australia, and Ann
Arbor, Michigan.6 Patients with abnormal DST findings are more likely to
have made a recent suicide attempt and are more likely to make another
attempt. The rates of abnormal DST are higher in depressed patients
who subsequently kill themselves. A 13-year follow-up of hospitalized
depressed patients whose DST was recorded within a week of admission
reported that those with abnormal responses had a 14-fold increased like-
lihood of making a serious suicide attempt in the follow-up period.
Studies that do not find an association between nonsuppression and
suicide nevertheless report that suicide risk is associated with elevated cor-
tisol levels at 4 p.m., a time when levels should be low. Thus, a 4 p.m.
cortisol level assessment and a follow-up complete DST assessment
add important suicide prediction power once the patient is identified as
melancholic. Measures of cortisol provide independent assessments of

the severity of melancholia and the likelihood of self-harm.
Depressive Melancholia (Major Depression)
A depressive mood disorder is usually first noticed during adolescence or

early adulthood. It develops at a time of family or personal stress, such as
the death of a parent or spouse, a move from the family home, the loss
of a job, or the first experience of living away from home, as on entering
college. Episodes recur with the physiological stress of pregnancy or after
the birth of a child, during menopause, or with aging when physical ill-
ness or accident limits the person’s capacity to care for herself. When
psychotherapy or drug therapy fails, ECT is a realistic option.
MARY
Mary, a successful bookkeeper, retired after 27 years. Her husband had
died four years earlier, and she was living alone in a community in which
she had lived for more than three decades. She had a large circle
of friends, cared for herself, and frequently visited her two children and
three grandchildren.
For several months, though, her interest in friends and family
waned. She became unkempt, and her home was disorganized and
filled with litter. Although she was encouraged to visit her children and
grandchildren, she refused. When she went to her daughter’s home, she
remained in bed much of the day. She ate little and lost weight.
She had experienced three prior episodes of depressive illness, re-
sponding once to medication and twice to ECT. In this episode, medi-
cations were prescribed but achieved little benefit.
On her admission to the hospital, she was poorly groomed, slow in
speech, and in the previous two months had lost 12 pounds (8% of her
body weight). Low blood sugar, high blood pressure, a persistently irregular
heart rate, and an enlarged heart characterized her medical condition.
Stating that ECT had helped her before, she asked for the treat-
ment again. It was given three times the first week and twice weekly for
the next two weeks.
The day after the fourth treatment, Mary’s appetite returned and her
self-care improved. She no longer complained of insomnia or depression.
After the seventh treatment she was fully oriented, recalling telephone
numbers and names, and asked to be discharged.
She returned for outpatient ECT at weekly intervals. At the last
examination, her mood was cheerful and she had gained seven pounds,
had been to the hairdresser and was well groomed, and talked of plan-
ning to return to her apartment and her circle of friends.
After sustaining a normal mood for 14 months, however, Mary
again became depressed and returned for additional treatments. She was
readmitted to the hospital to receive four treatments in two weeks. She
returned home and had three additional outpatient treatments. She re-
mained well for the next two years, when contact was lost.
comment. While a depressive mood is usually treated with medicine,

because it is easy to prescribe and less expensive, ECT may be preferred
by patients who responded well to it during a previous episode or who had
observed its efficacy in others. Patient preference is an accepted reason
for selecting ECT even when the patient has not had a prior course of
medication.
In Mary’s case, it would have been difficult to determine at the
outset how many treatments she would need. Even in an illness as re-
sponsive as melancholic depression, we cannot predict the necessary
number of treatments. She received 12 treatments for a sustained ef-
fect in the first episode and required 7 in the second. Had she been
given a predetermined number of treatments—the usual number often
prescribed is six or eight—her course would have been evaluated as un-
successful and she would have been discouraged from pursuing further
treatment. Reliance on a prescribed number of treatments is a risky
decision and should not be accepted, even if requested, by patients and
their families.
Delusional Melancholia (Psychotic Depression)
Disorders of thought characterize severe depressive mood disorders. The

combination of mood disorder and thought disorder is now recognized
as the distinct clinical entity of delusional depression. This is a malignant
illness. Strange thoughts accompany morbid moods. About a third of pa-

tients hospitalized for depressive mood are psychotic.7 A delusional de-
pression responds slowly and poorly to medications alone, even when
administered in high doses of combinations of antidepressant and anti-
psychotic agents. In such cases, the broad activity of ECT, which treats
both aspects of this illness, is rapidly effective, making it the preferred
form of treatment.
There is good evidence supporting the effectiveness of ECT in delu-
sional depression. A study completed at Columbia University in the 1970s
showed that 9 of 10 delusional depressed patients responded well to ECT;
by comparison, only 3 of 13 responded to an antidepressant.8 This study
was replicated often. In one, 437 depressed hospital patients were treated
with Tofranil in doses of 200 to 350 mg/day for 25 days or longer (the dosage
and duration of treatment following standards for effective and adequate
treatment trials). Of these, 247 patients (57%) were evaluated as recov-
ered and were discharged. The remaining unimproved 190 patients were
treated with bilateral ECT, and of these, 156 (72%) recovered. In seeking
to understand why 43% of the depressed patients had not improved with
Tofranil, the authors examined these patients’ psychopathological features
and found that most of them were delusional as well as depressed.9
Patients with the delusional form of depression are most likely to have
severe abnormalities of neuroendocrine regulation, which may exacerbate
the bodily disturbances of the illness. For this reason, it is necessary to
use the most effective treatment at the earliest opportunity. Unfortunately,
recognition of this form of depression is difficult, and the frequent fail-
ure of medication treatment may reflect inadequate dosing for inadequate
periods of time. Two recent studies show that less than 5% of delusional
depressed patients had received sufficient drug treatment before being re-
ferred for ECT.10
ROBERT
Three years earlier, Robert, a 68-year-old scientist, had retired. When
his wife became bedridden, Robert was unable to manage their home.
He grew despondent, ate poorly, slept during much of the day, was up
much of the night, bathed irregularly, and complained of constipation
and body pains. He thought his food was poisoned and insisted, con-
trary to fact, that he had heart disease and would soon die. He accused
his wife of infidelity and refused to talk to her. He believed his neighbors
were spying on his home and watched the street from behind curtained
windows for hours at a time.
Brought to the hospital by an aide, Robert was unkempt and di-
sheveled, walking slowly. He had an unpleasant body odor, refused to
answer questions, and was reluctant to let the doctors examine him. He
accused them of plotting to steal his money. He insisted that his condi-
tion was hopeless and that treatment would be of no avail. At times, he
appeared to be hearing voices and muttering barely audible responses.
Clinical and laboratory examinations showed no signs of systemic
disease other than eczema and dermatitis resulting from poor skin care.
Robert refused medications, insisting that treatment was pointless, as
death was imminent.
Immediate treatment was deemed necessary. When the doctors de-
scribed the risks and benefits of ECT, Robert listened carefully, read the
consent form, and refused to sign it. His wife, with whom the course
of ECT was discussed, agreed to her husband’s treatment. The medical
director, noting the severity of Robert’s illness, the delusional content of
his thoughts, his severe weight loss and dehydration, poor self-care, and
refusal to take medications, also recommended ECT.
Although Robert refused to sign the consent form, he cooperated in
the examination and the administration of intravenous fluids. He came
willingly to the treatment room. The procedures were explained again,
and when he was asked to move onto the stretcher, he did so willingly.
With treatment he soon began to drink and eat, returned to a normal
sleep cycle, and showed greater interest in his personal care. He show-
ered when prompted, took his meals in the common room, applied the
medications prescribed for his skin, and drank fluids as requested. His
delusional thoughts persisted.
After 12 treatments, Robert was no longer sure that his wife was
unfaithful—indeed, he was sympathetic to her—and was puzzled as he
recollected his thoughts about his neighbors. After 15 treatments, he was
sufficiently improved to return home, with advice to continue ECT on
a weekly basis.
Eight additional treatments were given over the next three weeks.
Robert’s mood improved, and his weight increased by 15 pounds. He at-
tended to his bodily care, expressed puzzlement at the stories of his strange
thoughts, and went home to care for his wife.
During a friendly exchange as he was leaving the hospital, Robert

pointed out once again that he had never signed the consent form for
treatment and asked, with a smile, whether the psychiatrist would lose
his license as a result. He had accepted treatment, he said, because he
believed that his condition was hopeless and that he had no reason not
to be a “good guy” and cooperate.
One year later, Robert maintained his weight and slept well, and
his illness had not recurred.
comment. The patient’s depressed mood, weight loss, insomnia, and

thoughts of hopelessness, helplessness, and infidelity are signs of a de-
lusional melancholic depressive illness. Robert’s loss of weight, dehy-
dration, and unhealthy physical condition warranted more immediate
treatment than medications, and his improvement augured well for
continuation ECT. He received 23 treatments, after which his recovery
was sustained by an antidepressant medication alone.
How many treatments are needed to relieve delusional depression?
We cannot prescribe a fixed course, but delusional depressed patients
require many more treatments than the nondelusional depressed. Re-
lapse is frequent when the treatments just relieve the symptoms and the
course is short. Sustained improvement requires continuation treatment
over many months.
One may question the propriety of treating a patient without a
formal signed consent form, but in this instance the spouse’s consent
and the patient’s acquiescence to treatment were considered sufficient.
Robert’s cooperation with the treatment and his continued voluntary
compliance were evidence of consent. In treating this patient without
his written consent, yet with his acquiescence, in balancing the ethi-
cal principles of beneficence, nonmaleficence, autonomy, and justice,
priority is given to the principle of justice.11
Geriatric Depression and Pseudodementia
As some people grow old, they withdraw from their family and friends
and lose interest in their personal care. A severely depressed elderly pa-
tient may be thought to be suffering from the irreversible brain changes
that mark an Alzheimer’s syndrome when, in fact, the memory deficits
are the consequences of a severely depressed mood or the retardation of

catatonia. At first, such patients seem cantankerous and irritable, barely
responding to friendly overtures. Later, they shut the door to their home,
refuse to answer the telephone, and spend much of the day in bed. When
they respond to questions, they do so slowly. Family members, worrying
about an Alzheimer-type dementia, arrange for the patient to have medi-
cal and neurological examinations. An EEG exhibits irregular slowing, a
computed tomography (CT) scan of the brain reveals “regions of atrophy,”
or a magnetic resonance imaging (MRI) scan shows “diffuse, irregular
hyperintensities.” These “findings” are interpreted as evidence of irre-
versible brain pathology. The diagnosis is made of a structural dementia,
usually of an Alzheimer type.12
But laboratory test results are easily misinterpreted. At times, an
apparent dementia of recent onset may be a product of a depressive
mood disorder. The Australian psychiatrist Leslie Kiloh labeled such a
dementia-like syndrome pseudodementia.13 The condition is hardly dis-
tinguishable from the irreversible state of Alzheimer’s disease except by a
study of the history of earlier depressive episodes, a careful review of the
circumstances leading to the current disorder, and an effective clinical
trial of antidepressant therapy. If a dementia syndrome appears suddenly
in an adult, especially an elderly adult, pseudodementia should be con-
sidered. Such conditions of stupor and pseudodementia of depression
have been described as “benign stupors.” Before the advent of ECT, they
were common and often fatal.14
To avoid errors in diagnosis, the prudent physician will carefully as-
sess the history of a patient who seems to have rapidly developed demen-
tia, seeking earlier episodes of disturbed mood. Most patients are too ill to
give details when they come to medical attention, so the details are often
obtained from family members. A history of depressive illness should
prompt a more detailed examination for a mood disorder and consider-
ation of its treatment.
What is the risk in treating a patient with an irreversible structural
brain disease for a presumed depressive pseudodementia? Assume that
the patient is treated with antidepressant medications or ECT and the
dementia is not relieved; indeed, it worsens, and the worsening will de-
crease when the treatment stops. Yes, the patient may require intensive
nursing care for the few weeks it will take to return to the pretreatment
mental state. Then the care for dementia continues as before.
Assume, however, that the patient is suffering from a reversible de-

mentia and the antidepressant treatment is effective. The patient, relieved
of the pseudodementia of depression, returns home and is again part of a
family and a community. The effort has been outstandingly worthwhile,
for a life has been saved. Such favorable odds surely argue for a course of
effective antidepressant treatment in elderly patients with a diagnosis of
dementia, especially if the condition made a sudden appearance.15 The
following case is an example of such a gamble that paid off.
HELEN
Helen, a 58-year-old married woman, was referred to our geriatric service
for confirmation of the diagnosis of Alzheimer’s disease. Nine years ear-
lier, she had been depressed, sleepless, and withdrawn and had refused to
eat. Helen showed an immediate response to treatment with Elavil, but
two weeks later she became confused, wandered aimlessly, and withdrew
from family and friends. A CT X-ray study was interpreted as showing
cortical atrophy, a diagnosis of Alzheimer’s disease was made, and the
family was advised that further intervention was useless.
For nine years, Helen’s husband and her five daughters cared for
her at home. Her weight dropped to 75 pounds, and she became incon-
tinent of both bladder and bowel. Her husband retired from work to de-
vote himself to her care, and received support from their daughters and
friends.
On examination Helen was thin and pale, stared aimlessly, kept
her arms wrapped around herself or moved an arm and a leg in rhyth-
mic motions, and engaged in self-stimulatory actions, like a mechanical
doll. She appeared oblivious of others in the room. As the examination
progressed, her perplexity and anxiety increased. She touched paintings
on the wall and picked up magazines to glance at them momentarily.
Cognitive screening was time-consuming because her speech was slow
and halting, but Helen did show that she knew her name, even though
she said that the year was 1976 instead of 1985.
Helen was admitted to the hospital’s inpatient psychiatric unit, and
a detailed history, obtained from her husband, showed previous episodes
of depressive illness. At age 42, she had been withdrawn and noncom-
municative, had lost weight, and had failed to care for herself or her fam-
ily. Electroconvulsive therapy combined with unspecified antipsychotic
medications brought improvement. Five years later, she was again with-
drawn and unable to care for herself or her family. She received a second
course of ECT and once more recovered. Then, when she was 49, she
again became ill and was admitted to our hospital. These experiences
suggested that her dementia was depressive in origin, not the conse-
quence of a structural brain lesion.
Admission laboratory evaluations and a CT scan of the head were
normal. The antidepressant Pamelor (75 mg/day) was prescribed. Helen’s
appetite improved, and she engaged in brief conversations. When she
appeared to respond to internal auditory stimuli, the antipsychotic Hal-
dol was added, and she received the combined treatment for three weeks.
Her appetite improved further; she became continent and minimally
verbal. She remained depressed, however, and ECT was begun.
After the fifth treatment, Helen was alert and communicative.
After 13 treatments, she was fully oriented, took care of her daily needs,
and achieved a maximum score on the cognitive Mini-Mental Test. Dis-
charge from the hospital was recommended, with both ECT and the
antidepressant Pamelor as continuation treatments.
Over the next four months, Helen received ECT once every six
days. Between treatments, she cared for herself, cooked for her family,
and enjoyed the company of her grandchildren. She traveled with her
husband and attended softball games, keeping score and cheering for
her favorite team.
In the following years, Helen’s symptoms returned periodically. On
each occasion, she became hesitant about decisions and progressively
less able to work or cook. She would stand still for many minutes, star-
ing into space; she answered questions with “I don’t know,” and no lon-
ger dressed herself or cared for her home. This sequence occurred over
two to five days. At these times she was withdrawn and perplexed and
performed poorly on cognitive tests. For 10 years, she received 10 to
16 ambulatory treatments each year. Lithium therapy with serum levels
between 0.7 and 0.9 mmol/L replaced Pamelor in the second year. In
1995, Ativan in daily doses of 0.5 mg three times a day was added. For
the next five years, Helen remained well and required no further ECT.
comment. How is one to explain the abnormal CT scan at the start

of Helen’s illness and the normal CT scan at the later examination?
Although brain imaging by CT and MRI is said to reflect permanent
characteristics of brain structure, scans do vary. The state of hydration,

the position of the head for imaging, and the exposure characteristics
alter images. In this instance, the diagnosis of Alzheimer’s disease on the
basis of a CT reading of cerebral atrophy was incorrect.
Over the decade during which Helen received outpatient treat-
ments, her condition recurred despite medication and more than 170
ECT treatments. The features of staring, puzzlement, posturing, and
mutism were prominent throughout the course of her illness, but they
were not considered significant until they were recognized as character-
istics of catatonia. After the benzodiazepine Ativan was prescribed in
regular and large doses, she no longer required continuation ECT.
Suicide
Electroconvulsive therapy decreases the risk of suicide. More than 50% of

suicides occur during an episode of depressive illness. Recent assessments
report rates of about 9% of successful suicide for those ever hospitalized
and a lifetime risk of 2% to 4% for all persons with depressive illness.
These figures are four to eight times greater than the rates of suicide from
other causes. Melancholic patients who are agitated and anxious, who are
psychotic, or who have been hypomanic are at the greatest risk.
Suicide is more frequent in persons over age 50, greater for men than
for women, greater in those using alcohol in large amounts, and greater in
those with severe physical illnesses, especially illnesses that have a poor
prognosis for recovery or require painful treatments.
Antidepressant agents reduce the number of depressive episodes.
Lithium substantially reduces the long-term risk of suicide in affectively
ill patients. It is the best- documented medication to minimize the risk of
suicide. Naturally, the more rapid and effective the resolution of the ill-
ness, the lower the suicide risk.
An anxious and agitated melancholic patient, especially one who
is despondent enough to have devised and described a suicide plan, is
best treated in a hospital, where 24-hour protection can be assured. In a
national multisite collaborative study of depressed patients referred for
ECT, one-third expressed persisting suicidal thoughts or reported suicidal
acts. With ECT, the thoughts of suicide were rapidly reduced—after one
week in 38%, after two weeks in 61%, and at the end of the course in
81% of patients.16 Another similar multisite collaborative study showed

the same reduction in suicide risk with effective ECT.17
The need to immediately reduce the risk of suicide justifies the use
of ECT, particularly when psychopharmacological or psychological treat-
ment will not take effect quickly enough. A particularly poignant story
illustrates the benefits of treatment.
DR. ROSENBERG
A former dean of Yale University Medical School, Dr. Leon Rosenberg
described his recurrent depressive illness and his suicide attempt. After
retiring from his academic position at age 65, he suffered from a feeling
of numbness for weeks; nothing seemed important. Insomnia, irritability,
loss of concentration, and despondency followed. Antidepressant medi-
cations offered little benefit. He checked into a local hotel, sat on the bed
washing down one antidepressant pill after another with vodka, and went
to sleep anticipating his death. Awakening 12 hours later, he called his
wife, who had been frantically looking for him. On admission to the psy-
chiatric ward of a local hospital, he was offered ECT. He was surprised,
thinking that it had been abandoned years before. His negative view of
the treatment, developed by images from the 1950s and from movies, had
been reinforced by his experiences at Yale, then a center of psychoana-
lytic practice and theory. Nevertheless, he consented to treatment.
“After the fourth ECT,” he reported,“I was noticeably less depressed.
My appetite returned, as did my ability to sleep. After eight treatments,
my mood was fully restored. I experienced no confusion, memory loss,
headache or any other symptom sometimes attributed to ECT.” Six weeks
after the suicide attempt, he took a train to Washington, D.C., and
presented a report of the Institute of Medicine to the leaders at the Na-
tional Institutes of Health (NIH). “My comments were well received,
and the committee’s report to NIH . . . was well received . . . I am quite
certain that none of the people I addressed that day knew that I had
recently lost and then retrieved my mind.”
comment. This episode was the fourth that Dr. Rosenberg recalled,
the others occurring in 1959, 1965, and 1980, each at a time when he
changed his academic position. The remission of his depressed moods
with ECT encouraged him to testify to the benefits of this treatment.
The risk of suicide in the psychiatrically ill patient is a continuing

concern for families and clinicians, and clinical practice offers little sup-
port. Newspapers frequently report the suicide of public figures whose
treatment was limited to psychotherapy or prescribed medications. Fam-
ilies are intimidated and are unwilling to restrict the patient’s activities
or to take the simple precaution of removing firearms from the home and
office. Vigilance is essential if the risks of self-harm are to be reduced.
s i x
Manic Mood Disorders
The mania started with insomnia and not eating

and being driven, driven to find an apartment, driven
to see everybody, driven to do New York, driven to
never shut up.
—Duke1
P atients suffering from mania are overactive, intrusive, excited, and

belligerent. They may believe that they have special powers, are re-
lated to public figures, and can read the minds of others. They spend
money lavishly. Voices on the radio or television are sometimes under-
stood as personal communications. They speak rapidly, with illogical and
confused thoughts, move constantly, and write page after page of non-
sense. They typically sleep and eat poorly, have little interest in work,
friends, or family, and often require restraint or seclusion. Suicide is a
perpetual threat. Some manic patients are likable, while others are angry
and frightening.
Psychosis is a frequent feature. Manic patients believe that their par-
ents are not their real parents, asserting that they have royal blood. They
believe that they can predict the future. They know that others are watch-
ing or talking about them, and they hear voices when no one is present.
Delusional mania requires more intensive treatment and almost always
hospital care.
In older classifications of psychiatric illnesses, these patients were
considered to be suffering from a manic-depressive illness. In modern
57
classification, this term has been discarded and the illness is now con-
ceived as bipolar disorder for patients with manic and depressive features
and major depression for those with depressive symptoms only. Bipolar
disorders, ranging from mild to severe, are divided into numerous sub-
types. The variety of symptoms that admit the diagnosis of bipolar dis-
order has led to a virtual epidemic of diagnoses of the condition. Many
patients so labeled do not exhibit the sleep difficulty, loss of appetite, and
loss of weight, or the severity of illness, that were the criteria for manic-
depressive illness.
In manic-depressive illness, the manic episode persists for hours, days,
weeks, or months and interferes with normal living. Once the episode
resolves, it may suddenly recur; or manic episodes may alternate with pe-
riods of depression, or occur as simultaneous mixed episodes of depres-
sion and mania. When the shift in mood from mania to depression takes
place within one or a few days, the condition is labeled rapid cycling, a
particularly malignant form of the illness.
Like depressive mood disorder, mania is associated with disturbances
in eating and sleeping, thinking, memory, and movement. Manic patients
sleep and eat poorly, lose weight, and have trouble concentrating on solv-
ing problems and planning the day’s activities. Memory is impaired, often
severely. Some patients are so disorganized as to appear demented and
delirious. A good characterization of this illness is melancholic mania.
Delirious mania (manic delirium, oneirophrenia) is a particularly strik-
ing form of mania. A previously normal person suddenly becomes excited
and restless, sleeps poorly, believes that neighbors are watching him, and
is easily frightened. He hides in the house or in a closet, dresses inap-
propriately, is sometimes naked, and wanders about the streets. His hal-
lucinations are vivid and his thoughts disorganized. Confusion alternates
with catatonia. This state is associated with physical exhaustion to the
point of a risk to life.2
More than a third of manic patients show catatonic features. They
posture, stare, and alternate between talkativeness and mutism. Repeti-
tive behaviors are prominent, such as the cycling behavior around the col-
lege courtyard hour after hour by the Nobelist Dr. John Nash described
in the biography and film A Beautiful Mind.3
Manic periods that alternate with depression are identified in the of-
ficial classification as bipolar I disorder. About 80% of patients with mania
have had or will have depressive episodes. Of the patients with depres-
sive episodes, 20% exhibit manic symptoms during the course of their
Manic Mood Disorders / 59
illness. The two forms of the illness, melancholic depression and mania,
are manifestations of the same sickness.4
While many treatments are recommended, from psychotherapies to
complex polypharmacy (the concurrent administration of many different
psychotropic medications), none are very effective. Among the medica-
tions, lithium, the anticonvulsants Tegretol, Depakote, and Lamictal, and
antipsychotic drugs are all recommended. Unfortunately, the diagnosis
of bipolar disorder lacks a basis in measurable tests of body physiology,
chemistry, or structure. Bipolar disorder as presently defined is not a veri-
fiable diagnosis.5
Although ECT offers effective and rapid relief, especially for the se-
vere forms of the illness, it is considered only as a last resort. The respon-
sive conditions include the melancholic depressed phase or the manic
phase of the conditions described as mania, mania with psychosis, or de-
lirious mania.
Until the 1930s, the main treatment for mania was sedation with
opioids, bromides, or chloral. These were poorly effective, and patients
frequently died of starvation, infection, excitement and exhaustion, or sui-
cide. Electroconvulsive therapy was the first effective treatment, indeed a
lifesaving one, and within a few years, ECT was widely prescribed. When
Thorazine and other antipsychotic drugs were introduced, these were
largely substituted for ECT, often in heroic doses, to control manic behav-
ior in rapid neuroleptization. This procedure calls for repeated intravenous
doses of a neuroleptic like Haldol to induce a speedy response. Doses are
administered hourly or every few hours until the patient is drowsy and
inhibited in movement. Such treatment carries a high risk of inducing the
toxic form of catatonia known as the neuroleptic malignant syndrome.6
Lithium therapy became the next popular treatment, and after a few
decades, interest shifted to the anticonvulsant drugs. These have been
highly touted in the public and professional press, but the evidence for
their efficacy is poor. A large multisite, federally supported national study
(STEP-BD- Systematic Treatment Enhancement Program for Bipolar Dis-
order) compared lithium, valproate, bupropion, paroxetine, lamotrigine,
risperidone, inositol, tranylcypromine, and three behavioral interventions
(cognitive- behavioral therapy, family-focused therapy, interpersonal and
social rhythms therapy). The study failed to find specificity for any inter-
vention leaving treatment recommendations as confused as before.7
Even with this array of medications, some patients remain ill, and
ECT is once again recognized as an effective alternative. A review of the
reports of manic patients treated with ECT found that 371 of 562 pa-
tients (66%) remitted or showed marked clinical improvement.8 Indeed,
for the psychotic, delirious, mixed depressive, rapid cycling, and cata-
tonic forms, ECT is the most effective and rapid intervention.
The main impediment to ECT in treating mania is the difficulty in
obtaining consent; indeed, this requirement is a special hurdle with these
patients, one that is often insurmountable. Manic patients are grandiose.
They deny that they are ill and see no reason to consent to treatment. Even
when manic patients do give consent, they often do not take the prescribed
medicines consistently. The distinction between the use of medications,
for which acquiescence alone is needed, and the use of ECT, for which
written consent is needed, restricts the use of ECT despite its acknowl-
edged efficacy and safety. Treatment of a patient without written consent
requires an order from a state court, but obtaining the court order can be
slow and expensive.9 Many judges refuse to order ECT in the mistaken
belief that it is dangerous. As a result, in present clinical practice, ECT is
considered after the failure of extensive treatment with medications that
are prescribed in extraordinarily large doses and odd combinations. It is
not unusual for a manic patient to be secluded, restrained, and given anti-
psychotic and sedative medications for many weeks before a court order is
obtained. Unfortunately, the order may arrive so late that the condition has
deteriorated and become life-threatening due to failure to eat and drink,
weight loss, infection, and fever.
Acute Manic Episode
Some manic episodes develop so rapidly that they warrant hospital pro-
tection, seclusion, and physical restraint. During the patient’s periods of
excitement, care must be taken to prevent her from injuring herself, other
patients, and the professional staff.
The following case describes the treatment of an acute manic episode.
SARAH
A 32-year-old married schoolteacher became grandiose, intrusive, and
silly. She spent money freely and claimed that God had selected her from
among all women for special attention. She slept poorly and was unable
to conduct her classes. The police had found her mumbling and singing
to herself in a village mall, where she had made expensive purchases.
At the hospital emergency room, she laughed mischievously and spoke
aloud to God.
Sarah had been in this state for three weeks. For 10 years, she
had had periods of sadness and withdrawal interspersed with periods of
heightened mood. Her response to the prescription of lithium, Prolixin
and Tegretol had been good, enabling her to continue teaching.
A few weeks earlier, Sarah had stopped taking her prescribed med-
icines thinking they were no longer needed. At the hospital she was
friendly, walked around the ward singing loudly, and laughing inap-
propriately. She walked into other patients’ rooms, took their clothing
and books, and then dropped them in the hall or in the next room.
The melodies of her songs were recognizable, but the words were non-
sensical. Her attire was gaudy, and she embraced and kissed everyone
she met. Her attitude was so friendly and pleasant that her audience
laughed with her.
Lithium and Tegretol were discontinued but Prolixin was contin-
ued. Two treatments of bilateral ECT were given the first day and a
single treatment on each of two successive days. Sarah became calm and
less intrusive, and by the third day she was oriented, slept through the
night, and ate ravenously. At times, she was incontinent of urine and re-
called recent events poorly. Therapy was continued on alternate days for
nine additional treatments.
After five weeks of hospital care, Sarah was discharged to aftercare
with a prescription of maintenance lithium therapy. She no longer sang
or was intrusive, nor did she speak to God. She was chagrined about
her purchases. Her appetite and sleep returned. She was oriented to
time, date, and place and remembered the events leading to her illness.
One month later she returned to work, and at the follow-up visit after
18 months she was doing well.
comment. Sarah’s case exemplifies the efficacy of ECT in treating de-

lirious mania even when the condition has been unresponsive to drug
therapy. When ECT is considered, lithium and anticonvulsants are
usually discontinued but neuroleptic drugs are still given if they were
already part of the treatment. Lithium is discontinued, or the dosage is
reduced or monitored before a course of ECT, to avoid the possibility of
a confusional syndrome, which may occur in patients with high serum

lithium levels. Tegretol and other anticonvulsants are also discontinued
because their anticonvulsant effects interfere with the production of an
effective seizure.
Manic patients are treated with bilateral electrode placement, be-
cause it brings about rapid clinical effects. The treatments are first given
on a daily schedule, even though such short interseizure periods may
lead to confusion, disorientation, and occasional incontinence. As the
time between treatments is lengthened, the confusion is relieved; it is no
longer present after the treatment course is completed.
Recurrent Angry Mania with Psychosis
In another variety of mania, the patient is angry, irritating, and unfriendly;

he relates poorly to others and is shunned and isolated. Because his
thoughts are disordered, he is widely misunderstood as he responds inap-
propriately to questions and comments. His frustration is high.
Early in the course of this illness, it is difficult to distinguish a manic
mood disorder from the chronic psychosis of schizophrenia, since delu-
sional thoughts, hallucinations, excitement, and aggression are character-
istic of both conditions. The proper diagnosis depends on the course of
the illness; bipolar patients have remissions and relapses, while those with
schizophrenia remain ill without relief.
A diagnosis of schizophrenia limits the treatment options, which are
broader for those diagnosed with mania. Antipsychotic medications are
the principal treatment for the schizophrenic patient. They are also pre-
scribed for manic patients, but lithium, anticonvulsants, and ECT are also
accepted. A patient has much to gain from the multiple options for treat-
ing manic disorder and little to lose. The experienced physician does not
claim to distinguish between these disorders early in a patient’s illness.
DAVID
A 38-year-old single high school dropout had been repeatedly hospi-
talized for impulsive and destructive behavior during the preceding
20 years. He was sure that his neighbors and family were watching him,
and he often directed aggressive outbursts at his parents and siblings.
Once found wandering in the streets of the village, mumbling, kicking

objects, and threatening bystanders, David was brought to a psychiat-
ric emergency room. Disheveled, argumentative, loud, and angry, he
grandiosely stated that God had spoken to him. After he was medically
sedated, a reading of his record of previous care indicated that he had
been hospitalized four times in the preceding 13 months, each time for
a similar outburst.
Three weeks before the current incident, David had been discharged
from the hospital with prescriptions for lithium, Divalproex, Tegretol,
and Thorazine. In the hospital, the lithium and anticonvulsants in his
blood were below effective levels. He had been unable to deal with the
complexity of dosing with four different medications.
David was unkempt and angry, lashing out at his roommate when
he passed too near. Sometimes he spoke in a low voice when no one
was in the room. Voices, he said, were telling him that his parents were
not his real parents and that God was watching over him. He was well
oriented for time and place, and examination found him to be below the
standard body weight.
Electroconvulsive therapy was recommended and accepted. All
medications except Thorazine were discontinued. Bilateral ECT was
begun on an alternate-day schedule. The sedative Ativan was given two
hours before the first treatment, and despite David’s insistence that he
did not need treatment he came voluntarily to the treatment room.
His response was slow. After the eighth treatment, he shaved, show-
ered, and asked for clean clothes. His demeanor improved. After 12 treat-
ments, he no longer appeared to be listening to voices. On a brief leave
from the hospital with his brother, he acted normally, ate in a restaurant,
and shopped in the local mall. Treatment with lithium was begun, and
blood serum levels were maintained at 0.5 to 0.6 mEq/L, a dose considered
adequate to maintain the patient’s mental state while ECT continued.
By the sixth week, David was cooperative, well oriented, and less
hostile. Arrangements were made for him to live in an adult home. The
lithium dose was increased and Thorazine continued. He has not been
hospitalized for more than two years.
comment. A mental illness that has gone untreated for weeks or

months is far more difficult to manage than one of recent appearance.
The repeated hospital admissions and the complex medication regimen
in this patient’s record indicated that he required more intensive treat-

ment than had been offered. Electroconvulsive therapy combined with
Thorazine returned him to a less hostile, marginally competent state,
one in which he was able to live in the community. Had ECT and neu-
roleptic medications been offered earlier in the course of his psychotic
illness, especially within two years of the disease onset, the outcome
might have been better.10
In some of David’s many hospitalizations, the diagnosis was bipolar
disorder with psychosis rather than schizophrenia, and both antimanic
and antipsychotic medications were prescribed. In other instances, the
diagnosis was schizophrenia, and only antipsychotic medications were
given. These periods of incomplete treatment contributed to the patient’s
deterioration. It was the failure of a resolution, despite multiple hospi-
talizations, that led the doctors to decide on ECT. David was granted
an opportunity to undergo treatment regardless of the psychopathology,
and the gamble proved successful.
Delirious Mania (Mania with Psychosis)
In clinical psychiatry, opportunities for dramatic intervention are few.

Most patients come to the psychiatrist after long and complex experience
with their conditions. Delirious mania, with its acute onset, rapid evolu-
tion, and life-threatening aspects, is an exception. It is highly responsive to
ECT, but failure to recognize the condition often leads to the prescription
of such large doses of neuroleptic drugs that seizures or life-threatening
conditions like the malignant neuroleptic syndrome result. The striking
feature of delirious mania is the lack of awareness of the environment, the
patient appearing as if “in a dense fog.”
PHILIP
A 17-year-old adolescent, after a weekend of partying, became delirious,
a condition that his parents ascribed to overindulgence in alcohol. For
two weeks Philip remained at home, refused to go to school, slept and
ate little, and closeted himself in his room, listening to rock music. By
the third week, he had become so excited that his parents brought him
to the community hospital. He was unkempt and talked continuously,
singing, and beating rhythms with his hands. Sedation with Ativan
proved inadequate; he needed physical restraints. After an injection
of the antipsychotic Haldol, he developed the toxic syndrome of fever,
rigidity, elevated blood pressure, and rapid heart rate. Withdrawal of
medication resolved the acute syndrome, but he remained psychotic and
manic and was transferred to our academic inpatient unit.
On admission, Philip was agitated, confused, and incoherent, with
slurred, disorganized speech. He believed that he had strange powers,
that his parents, who accompanied him and were present, were not his
real parents, and that he had been selected for a spectacularly successful
career in finance. For minutes at a time he stared past the interviewer,
not answering questions. Although he seemed oriented to time, place,
and person, he could not recall the names of three objects after five
minutes. His ability to do numerical calculations was poor, and he was
unaware of current events. His temperature, heart rate, and blood pres-
sure were normal.
Electroconvulsive therapy was recommended, and both his parents
and Philip agreed. All medications except lithium were discontinued.
On the fourth day in the hospital, he was treated with bilateral ECT
under combined Ketalar and Anectine anesthesia. An adequate seizure
was induced, and recovery was uneventful.
Within an hour Philip was rational and oriented, neither overactive
nor delusional, and no longer in need of restraint. Later that afternoon
he relapsed to his manic state, and each of the next two daily treatments
followed the same pattern. After the fourth treatment his thoughts, mood,
and affect were appropriate, his delusional ideas had disappeared, his
self-care was normal, and he appeared well. He was discharged after the
sixth treatment with a prescription for lithium and biweekly outpatient
ECT. He received four additional treatments. Once he returned to school,
he soon made up the work that he had missed. The lithium therapy was
sustained for four months, and Philip was then discharged from the clinic
as recovered.
comment. The syndrome of delirious mania is poorly recognized, as the

patients are treated for acute psychosis or schizophrenia.11 When neuro-
leptic medications are administered to an excited patient, particularly
one who has catatonic features and is dehydrated, a toxic neuroleptic
malignant syndrome may develop, especially when the neuroleptic is
given by intramuscular injection. Electroconvulsive therapy is a safer

and more effective treatment. Philip’s catatonic signs were repetitive
stereotyped movements, staring, and periodic negativism. Catatonic
features are common in patients with mania (and depression); indeed,
they occur more often in patients with mood disorders than in those
with schizophrenia.
s e v e n
Movement Disorders
Every new movement or manifestation of human

activity, when unfamiliar to people’s minds, is sure
to be misrepresented and misunderstood.
—E. Carpenter1
P atients with mental disorders exhibit a range of abnormal move-

ments. The severely depressed are given to hand wringing, pacing,
and restlessness. Others lie in bed, stare into space, and posture for hours
or days. At times, this behavior is so extreme as to be a stupor. Psychotic
patients exhibit tremors or peculiar facial and body movements described
as parkinsonism, dystonia, or dyskinesia. Manic patients are in constant
motion. Children and adolescents bang their heads and pick at their skin,
injuring themselves.
Little attention is paid to such behavior unless it overwhelms the pa-
tient’s life, but it does distress the patient, the family, and the community.
These motor symptoms often bring psychiatric patients to medical care.
Catatonia
Catatonia is the motor syndrome characterized by muscular rigidity, un-

usual posturing, negativism (refusal to obey simple commands), mutism
(persistent silence), echolalia (repetition of what has been said), echo-
praxia (imitation of movements), and repeated stereotyped mannerisms.2
67
It appears suddenly and quickly immobilizes the patient or it appears

insidiously. When it dominates behavior and threatens the patient’s life
by the failure to eat or drink, treatment becomes compulsory. Forced
feeding, bedsores resulting from immobility, muscular atrophy, bladder
catheterization and consequent infection, and blood clots in immobilized
limbs all take a terrible toll. If the clots move to the lungs or brain, stroke
or death may ensue.
Catatonia was first described as a consequence of intense emotional
anguish and tension. Although the movements frequently respond to sed-
ative drugs, ECT is a more complete and effective treatment.
The condition is frequently seen in patients with affective illnesses—
both depression and mania—in patients with systemic disorders, and in
those with toxic brain states caused by hallucinogenic drugs. For decades,
the prevailing belief in psychiatry was that each instance of catatonia
represented a type of schizophrenia. The major classification systems in
psychiatry—the Diagnostic and Statistical Manual of the American Psychi-
atric Association and the International Classification of Diseases—assigned
to all patients with catatonia the diagnosis of schizophrenia, catatonic
type. As a consequence, few patients were treated with anticonvulsant
sedatives or with ECT, because those treatments were not recognized
as effective in schizophrenia. This error was rectified to a small extent in
the 1994 classification system of the American Psychiatric Association
(DSM-IV), which recognized a form of catatonia as secondary to a medi-
cal illness and as a feature of mood disorders.
Catatonia is defined by two or more characteristic motor signs in a
patient with a mental disorder. It appears in many guises. A retarded, or
slowed, motor form is common. An acute form with high risk for rapid
death is labeled pernicious, lethal, or malignant catatonia. The neuroleptic
malignant syndrome (NMS), which follows the administration of neuro-
leptic drugs, is a special instance of malignant catatonia.3
Many catatonic patients are referred to neurologists and internists,
as the first presentations are of an acute systemic medical illness, a toxic
response to medicines, or an infectious illness. But when systemic causes
are ruled out and the condition persists, accompanied by psychotic
thoughts or delirium, the patients are referred to psychiatrists. Regardless
of the cause or form of catatonia, the syndrome responds well to barbi-
turate or benzodiazepine sedation. When these medications fail, as they
do in about 10% of patients, ECT quickly relieves the syndrome, usually
within three treatments.
Movement Disorders / 69
Though catatonia is generally considered a form of schizophrenia

in the psychiatric classification, it is more often encountered in patients
with depression and mania, and in toxic states following the use of anti-
psychotic and hallucinogenic drugs. In recent surveys of patients admit-
ted to psychiatric treatment units and emergency rooms, about 10% are
found to exhibit catatonia.
GERALD
A 20-year-old college student studied intensively for end-of-semester
tests and got little sleep. Found by his parents sitting like a statue star-
ing at the television screen, Gerald did not answer questions, nor did
he sleep, eat, or bathe. In the psychiatric emergency room, he remained
seated, rigid, silent, and staring into space. An intravenous injection of
Ativan relieved his mutism, and he spoke of voices instructing him not
to speak, of messages directed at him from the television set, and of his
fear that he would soon die. Within an hour he was again mute, staring
and unresponsive.
No evidence of toxic drugs was found in Gerald’s urine and blood.
Repeated intravenous injections of Ativan enabled him to maintain his
feeding and toileting. After a physical examination and laboratory tests
showed no systemic cause for his behavior, acute schizophrenia of the
catatonic type was diagnosed. The use of antipsychotic drugs was re-
jected due to concern about the development of NMS in a patient with
signs of catatonia. At that point, the risks and benefits of ECT were
discussed with Gerald’s parents, who consented to the treatment.
Bilateral ECT began, and later in the morning after the third treat-
ment, Gerald was responsive, pleasant, cooperative, and bewildered by
the descriptions of his recent behavior. He recalled hearing voices but
could not explain their origin. He asked to be allowed to return to school,
and though continuation treatments were recommended, he refused, in-
sisting that he was well. He agreed to continue taking lithium.
After two weeks in school, Gerald was brought back to the hospi-
tal, rigid, staring, and posturing. Ativan again relieved the immediate
syndrome but did not sustain the relief. Electroconvulsive therapy once
more brought relief, this time after five treatments. At this point, Gerald
agreed to outpatient treatments. He returned home, and received four
weekly treatments and then six additional biweekly treatments while
he attended a day hospital program. Lithium and Ativan were also
prescribed, and after four months he returned to school, where he kept

up his regular classwork.
Almost a year later, however, Gerald’s parents brought him back to
the hospital with the same syndrome, which was relieved this time by
a course of 11 ECT treatments. Because a urine examination showed
signs of kidney dysfunction, Tegretol was prescribed in place of lithium.
Gerald decided not to complete his schooling and took a job in a manu-
facturing assembly plant, where he had kept his position for more than
two years at the time of his last visit.
comment. Gerald’s rapid improvement was misinterpreted as recov-

ery, and he refused further treatment. Since the benefits of ECT, like
those of psychotropic medications, are transient, patients require con-
tinuing treatment for a sustained effect.
NMS Variant of Malignant Catatonia
The sudden onset of fever, motor rigidity, negativism, mutism, and insta-
bility of heart and respiration rates are components of NMS, which may
appear after the administration of antipsychotic drugs. The syndrome is
indistinguishable from malignant catatonia, except that a specific pre-
cipitant has been identified, usually one of the high-potency neuroleptic
drugs like Haldol, Prolixin, or Navane. Cases have been observed in asso-
ciation with almost all neuroleptic drugs, including the atypical antipsy-
chotic agents Clozaril and Risperdal. All neuroleptic drugs put patients at
risk. Like catatonia, this syndrome is responsive to ECT when supportive
fluids, rest, and withdrawal of the offending substances fail.
JEFFREY
A 40-year-old man had been treated for psychosis since age 16. Now
that he was stabilized on Thorazine and lithium, Jeffrey’s therapist de-
cided to change his medication to a new atypical neuroleptic, Zyprexa.
One month later Jeffrey became psychotic, and the traditional neuro-
leptic Trilafon was prescribed. He quickly became febrile, mute, and
rigid, the diagnosis of NMS was made, and he was transferred to a ter-
tiary care facility.
Neuroleptic medications were discontinued, and Jeffrey was treated

on a medical service with large doses of Parlodel and Dentrium. His re-
petitive motor movements prompted the diagnosis of epilepsy, so anticon-
vulsants were administered. Ativan, prescribed in low doses, controlled his
infrequent agitation. Jeffrey remained mute and rigid and required total
nursing care. A gastrostomy was done to permit feeding, and he developed
pulmonary and bladder infections that required antibiotic treatment.
After Jeffrey had been in intensive medical care for four months, a
visiting lecturer and consultant made the diagnosis of catatonia. Ativan
at doses higher than had been used earlier was recommended, and when
the dose was increased to 12 mg/day, the patient responded to commands
and smiled at his parents, though he remained mute.
Electroconvulsive therapy was recommended but was not available
at that tertiary care center, so Jeffrey was transferred to our university
medical center. When his mother consented to ECT, she recalled that
her son had had a similar episode of psychosis, rigidity, and mutism at
age 16, and he had responded well to ECT.
Ativan was reduced to 6 mg/day and bilateral ECT was adminis-
tered every other day. After the fifth treatment, Jeffrey was alert, respon-
sive, and friendly. He recognized his parents, smiled, was less rigid, and
took oral feedings. By the ninth treatment he was verbally responsive.
The four months of rigidity and forced bed rest, however, had left him
with limb strictures and such badly impaired movement that he was
unable to stand or to use his hands to feed himself.
Ativan was increased to 8 mg/day and ECT was spaced at weekly
intervals. When Jeffrey was no longer psychotic and no longer exhib-
ited catatonia, he could use both of his hands and was able to stand,
with some residual restriction in movement. After 22 treatments he was
transferred to a rehabilitation center. The prognosis for recovery was
deemed good.
comment. Jeffrey’s condition is an example of persistent catatonia and

inadequate treatment. The failure to prescribe adequate doses of benzo-
diazepines and to consider ECT stemmed from the mistaken belief that
NMS is a specific entity, separate from catatonia, with a different treat-
ment algorithm. Whether NMS is a specific consequence of an exces-
sive reduction in the amount of brain dopamine or whether it is a type
of catatonia is still undetermined. Those who see it as a specific disorder
in dopamine activity seek to increase brain dopamine by prescribing

Parlodel or Sinemet and to relieve muscular rigidity and fever through
the use of muscle relaxants. Neither of these treatments is specifically
effective. Electroconvulsive therapy is the definitive and effective treat-
ment for NMS.4
Because the tertiary care center to which Jeffrey was sent did not
have the resources for administering ECT, he was transferred once
again. At the first center, the staff had not considered ECT for Jeffrey
because it was not within their experience. That a tertiary care hospital,
licensed to treat mentally ill patients, could not provide ECT is an un-
happy comment on the lack of understanding of the treatment’s merits.
It is unethical for a psychiatric hospital that offers broad services as a
tertiary care center not to have facilities for ECT. Such a lack fails the
ethical criterion of justice, the availability of interventions regardless of
age, gender, and economic status.5
Another syndrome, the toxic serotonin syndrome, has been recog-
nized as a response to some of the antidepressant drugs known as selec-
tive serotonin reuptake inhibitors (SSRIs). Prozac, Zoloft, and Paxil are
some of the best-known medicines in this class, and the syndrome has
been reported with each of them. The motor and mental changes, and
the effective treatment, are similar to those of NMS.
Parkinsonism
Many depressed patients, especially elderly ones, are slow and hesitant
in movement, rigid in posture, and tremulous. When they are treated for
depression, both the motor signs and the depressed mood are relieved.
The signs of this motor syndrome are hardly distinguishable from those
of Parkinson’s disease caused by cerebrovascular change or systemic in-
fection. To separate the effects of ECT in parkinsonism from its effects
in depression, Swedish scientists studied nondepressed hospitalized pa-
tients suffering from a severe form of parkinsonism. Using real and sham
treatments, they found that real ECT relieved the rigidity of the syn-
drome but not the tremor.6 Electroconvulsive therapy is occasionally used
to relieve the motor signs of parkinsonism when it is marked by severe
rigidity independent of the presence of a mood disorder.7
MONROE
A 63-year old retiree developed bilateral parkinsonism. Treatment with
antiparkinson agents was successful for about seven years, but then the
medications gave Monroe only a few hours of relief. He spent his time
mainly in bed or in a chair and needed assistance in feeding and toi-
leting. Although depressed, he did not express thoughts of self-harm,
nor did he develop psychosis or melancholia. He was alert and well
oriented, even though he could not stand or walk unaided and could
speak only slowly, in a hoarse, uncertain voice. Examination found no
signs of other systemic illness.
When Monroe and his wife were told of an experimental protocol
approved by the university for a trial of ECT in patients with parkinson-
ism, they gave their consent. He continued his antiparkinson medica-
tions at the full dosage.
Immediately after the third bilateral ECT treatment, Monroe spent
a full day out of bed. He was able to feed and care for himself and to
speak more clearly. That night, however, he had nightmares, and the
next day he was delirious, frightened, and unable to say where he was.
His heart rate was rapid and his blood pressure was elevated. The anti-
parkinson medications were discontinued, and the syndrome abated. By
the third day he was once again well oriented, though stiff.
The delirium Monroe had experienced was ascribed to dopamine
toxicity caused by the combination of continued Sinemet (which is
changed in the body to brain dopamine) and the brain dopamine re-
leased by the treatments. One week later the ECT treatments were re-
instated, and his motor rigidity was eased. After three treatments, he was
able to walk with assistance and to leave his bed at will. The mental
disturbances did not recur.
After 11 treatments given twice a week, Monroe went home and
continued outpatient ECT at alternating weekly and biweekly sessions
for four months. Throughout the course of treatment, except for the pe-
riod of acute toxicity, he remained oriented. He occasionally complained
of forgetfulness. An avid card player, he continued to play gin rummy
(and win as before). With the arrival of winter he moved to Florida,
where his outpatient care was maintained. The treatments were given less
frequently until, after 10 months, they were stopped. Monroe’s symptoms
of parkinsonism were relieved with lower doses of Sinemet, and he con-

tinued his home-bound life with tolerable rigidity and tremor.
comment. Repeated seizures stimulate the tissues to liberate increased

amounts of brain neurotransmitters. Dopamine is the brain transmitter
that is deficient in patients with parkinsonism, caused by aging, vascu-
lar or infectious disease, or prolonged use of neuroleptic drugs. Electro-
convulsive therapy relieves the rigidity due to each of these causes. The
application of ECT in treating rigidity is considered experimental, but
it is useful in severely ill patients. Now that the risks of delirium from
full-dosage antiparkinson agents are recognized, these medications are
reduced before ECT is begun.
An explanation of the benefit of parkinsonian rigidity comes from
the experimental literature. Seizures liberate increased amounts of brain
neurotransmitters, including dopamine, the neurotransmitter that is de-
ficient in patients with parkinsonism.
e i g h t
Other Uses: Psychosis, Pregnancy,

and Status Epilepticus
There are more things in heaven and earth, Horatio,

Than are dreamt of in your philosophy.
—W. Shakespeare1
A lthough ECT was developed as a treatment for schizophrenia, its

ease of use, its safety, and the lack of effective treatments for many
psychiatric conditions encouraged experimentation with this therapy to
treat other disorders. These explorations define a cluster of conditions—
acute and chronic psychosis, psychiatric disorders in pregnancy and the
postpartum period, and intractable seizure disorders—in which ECT has
a clinical role.
Psychosis (Thought Disorders)
Strongly held beliefs (delusions), abnormal sensory experiences (hallu-

cinations, illusions) that are not based upon reality, and beliefs that oth-
ers are paying special attention or plotting harm to the subject (paranoid
thoughts) impair social functioning and disrupt family life. Thought
disorders are the central peculiarity of schizophrenia but are also fre-
quently found in patients with depression, mania, toxic states, and brain
disorders. Regardless of the cause or the associated signs and symptoms,
75
treatment can reduce the psychosis. This benefit is often given small no-
tice, however, because ECT is widely regarded as an antidepressant, not
an antipsychotic, treatment.
The relief of psychosis afforded by ECT varies with the underlying
condition. Disorders in thought in patients with depression or mania are
readily relieved. Indeed, the more severe form of psychotic depression is
relieved more rapidly than nonpsychotic depression.2 When ECT is used
to treat patients with malignant catatonia and delirium, the psychosis is
relieved at the same time as the toxic state. When psychosis dominates
the clinical condition without other features, schizophrenia is the usual
diagnosis. For acute schizophrenia dominated by the positive symptoms
of paranoia, catatonia, or excitement, ECT is quite helpful. It is not help-
ful for the chronic varieties dominated by passivity and withdrawal, the
negative signs of the illness.
The clinical approach to the diagnosis of a psychotic condition is to
exclude other causes for psychosis first and reserve the label “schizophre-
nia” for the residue of “not otherwise diagnosed” psychotic conditions.
While we are able to ameliorate the psychoses in mood disorders and toxic
states, palliation and symptom reduction are the best that we can offer
other psychotic patients.
Electroconvulsive therapy and insulin coma therapy were the main
treatments for psychosis at the time when Thorazine and other new an-
tipsychotic drugs were introduced in the 1950s. Comparisons of drugs
and ECT3 and insulin coma4 found the treatments to be equally effec-
tive. The lesser cost, ease of administration, and greater acceptability of
medicines led to their preferred use. In time, however, the limitations of
the medications were recognized as patients failed to improve despite
extended courses of treatment with many different medications. Doses
of antipsychotic medications were often increased until rigidity, tremor,
fixed facial expression, or slowed walking occurred. Then the doses were
lowered slightly. When patients are treated in this manner for long peri-
ods, they develop persistent movement disorders—parkinsonism (slowed,
shuffling gait, vacant expression, tremors), dystonia (persistent peculiar
posturing), and dyskinesia (repetitive abnormal movements of the mouth,
tongue, face, and trunk). Dyskinesias occur at the rate of 4% per year
of exposure for men and 5% per year of exposure for women.5 As more
and more examples of patients with medication side effects piled up in
Other Uses: Psychosis, Pregnancy, and Status Epilepticus / 77
doctors’ practices, ECT was reconsidered as a less toxic alternative. Its

benefits compel its consideration today, especially in severely ill and hos-
pitalized patients.
When treatment with antipsychotic medications is discontinued,
the psychosis so often reappears that present practice recommends that
the medicines be taken for years. The newer atypical antipsychotic drugs
do not produce the same difficult side effects of rigidity and dyskinesias
caused by the older antipsychotic medications, but they reduce the signs
of psychosis in only about 30% of those who do not respond to the stan-
dard antipsychotic drugs.6
Despite these limitations, antipsychotic drugs are prescribed much
more often than ECT. True, they are less expensive in time, cost, and ef-
fort. But when a drug course is ineffective, the physician may change to
another medicine, combine medicines, or prescribe the latest product ap-
proved for marketing. When ECT is finally considered, it is usually as a
costly last resort and is almost always prescribed for far too short a period.
The improvement brought about by ECT in delusional melancho-
lia and mania is rapid, occurring with 8 to 15 treatments. In patients
with schizophrenia, however, the improvement is slow, and more than
20 treatments are usually required for a benefit. Relapse is frequent when
the treatments stop. To achieve a persistent benefit, treatments usually
continue as long as there are residual symptoms. A minimum course of
ECT for effective relief of psychosis is one that continues for at least six
months. The reluctance of psychiatrists to prescribe adequate courses of
treatment and the patient’s refusal to complete the recommended course
are the main reasons for relapse after successful remission.
Antipsychotic drugs and ECT are synergistic in their effects—that
is, they act in combination—so the combination may be more effective
than either treatment alone. Antipsychotic medications reach the brain
cells by active transport across cell membranes. There is, however, an in-
terface of seamless fatty membrane between the blood vessels and brain
cells that prevents some substances from penetrating the cells. This in-
terface, called the blood-brain barrier (BBB), prevents medications from
reaching the brain cells of some patients. Physicians then must use mas-
sive drug doses to achieve even a minimal effect. Seizures, however, ex-
pand the spaces within the BBB, allowing the excluded molecules to
cross more easily from the blood to the brain cells.7
Acute Psychosis
The following case describes the relief of thought disorder by ECT.
JEFFERSON
When an 18-year-old college freshman returned home for the Christmas
holidays, he did not call his high school friends. Jefferson spent most of
the time in his room, mumbling to himself and paying little attention to
his family. While watching television, he would argue with the images
on the screen and talk of his fear that the world would soon end. His
appetite was not impaired, and he slept normally. A skilled piano player,
he practiced for many hours but did a poor job of following the score;
melodies were introduced in strange juxtapositions.
When the holidays were over, Jefferson refused to return to college,
and his parents brought him to a psychiatric hospital. He was coopera-
tive and alert. He appeared to listen to messages, saying that his father’s
voice was talking to him even though his father was not present. He
could not relate the content. Although he could list his school courses
and the names of his teachers, he could not recall the homework that had
been assigned over the holidays. He denied being sad or ill, but he agreed
to remain in the hospital.
Jefferson denied using hallucinogenic drugs, and neither the urine
nor blood examination showed traces of such substances. He was not
physically ill. The diagnosis of acute paranoid schizophrenia was made,
and his family was told that the treatment options were neuroleptic drugs
or ECT. The risks, benefits, and potential rate of improvement with each
course of treatment were described, and Jefferson and his parents signed
the consent form for ECT.
After the eighth treatment, Jefferson participated in ward activi-
ties and played pleasant piano pieces for the patients and visitors. After
11 treatments, he went home. For the remainder of the semester, he
lived at home and attended psychotherapy sessions twice a week. Dur-
ing the summer he completed his freshman course requirements, and
in the fall he returned to college. During the next three years he per-
formed all the work for his bachelor’s degree and then moved to New
York City, where he composed popular music. For seven years, there
was no recurrence.
comment. Many psychiatrists are concerned that a persistent psychosis

may leave scars in the brain that will permanently affect thought and
behavior.8 Since ECT is rapidly effective for psychosis, the belief that
every psychotic patient must first be treated with neuroleptic medica-
tions should be questioned. If the first medication trial is ineffective
after six to eight weeks, it seems more reasonable to consider ECT than
to prescribe a succession of neuroleptic drugs since none have estab-
lished superiority over the others.9 Unfortunately, few psychotic patients
are given the option of ECT in place of repeated neuroleptic trials, as
the expert algorithms for treatment of psychosis developed by official
committees do not consider ECT until many medication trials, includ-
ing trials of new medications, have failed.10
Chronic Schizophrenia
Of the five types of schizophrenia identified in the psychiatric classifica-

tion, the paranoid form, dominated by delusions and hallucinations, and
the catatonic form, characterized by rigidity, mutism, and negativism, may
improve with ECT. These are the positive signs of schizophrenia. The
negative signs of schizophrenia are apathy, lack of volition and drive, flat-
tened affect, disorganized thoughts, and little interest in self-care, in the
events around the patient, or in the patient’s future. These are labeled the
disorganized, residual, and undifferentiated types. They appear after long
periods of illness. At this point in the illness, the patterns of abnormal
behavior and brain changes are fixed; minimal benefit is achieved with
ECT. Yet, some patients with a mixture of positive and negative signs may
benefit from ECT.
STEVEN
During the 13 years before he reached the age of 31, Steven had been
hospitalized 22 times for delusional thoughts, hallucinations, and ex-
citement. He first became ill during his second year at college and im-
proved with antipsychotic drugs. During his third episode at age 20,
he responded to ECT and returned to college for one semester. When
illness recurred, the psychiatrist concluded that ECT had failed and
did not consider it again. Over the years, Steven’s parents sought the
advice of many consultants, one of whom suggested that ECT be tried

once more.
On admission, Steven was bearded and unkempt, mumbling to
himself, posturing in a crucifixion stance, and alternating between
mutism and slow, hesitant responses to inquiries. He asserted that he
was Jesus Christ, that the Lord spoke often to him, and that he was
bringing His message to the world. He was cooperative except for bath-
ing and shaving. Psychological testing showed his intelligence quotient
to be high; EEG and blood measures were normal.
Medications were discontinued and bilateral ECT was begun.
After the third treatment, Steven recognized his parents and asked
about his sister. His mutism and posturing abated, but his psychotic
symptoms persisted despite more than 18 treatments. Because of his
lack of response, an interseizure EEG recording was done.11 Since it
did not show the slowing of frequencies and the increased amplitudes
associated with effective ECT, we concluded that the benefits of ECT
had not yet developed and continued the course.
On the day after the 23rd treatment, Steven showered, shaved off
his beard, and asked to visit a barber. He was alert, oriented, and said he
had no delusional thoughts. When he was reminded of his statements
about Jesus and God he was surprised, though he did recall thinking of
God. After a visit by his parents, he was puzzled by the date; he had lost
track of the years during which his sister had graduated from college,
married, and had two children.
Treatments were continued once a week, with the neuroleptic Pro-
lixin prescribed as maintenance treatment. As preparations were made for
Steven to return to the community, he had to face his lack of social and
work skills. He remained fully oriented for time, place, and date and was
aware of his family’s activities. Because he had read very little, it was diffi-
cult to see how he could return to college. He did not accept the suggestion
of acquiring training in manual skills and returned to his residence in a
state-sponsored adult home. There he participated in group activities and
cared for himself. Biweekly continuation ECT inhibited his delusional
thoughts and mutism. Ativan at a dose of 3 to 4 mg/day was prescribed as
additional treatment for the catatonic signs. Various medications, includ-
ing each newly discovered neuroleptic, have been tried in place of ECT,
but without success. For more than 18 years, Steven has been in continu-
ation treatment, with over 300 treatments by the year 2008.
comment. When Steven was first treated with ECT, we did not rec-
ognize the significance of the catatonic signs, nor did we prescribe ben-
zodiazepines. Our later recognition of the importance of these signs led
to his present regimen. Most electrotherapists would not have recom-
mended the combination of the sedative anticonvulsant lorazepam with
ECT, but our experience with other patients after Steven, and our later
understanding of how to achieve effective ECT using EEG criteria, led
us to use both treatments concurrently.
Acute Toxic Syndromes
The hallucinogenic drugs cocaine, amphetamine, lysergide (LSD), and can-

nabis (marijuana) elicit acute and often severe states of excitement with
delusional thoughts. The acute manic and psychotic symptoms of these
states are responsive to ECT.
ERIC
A 15-year-old boy became irritable, with inappropriate verbal outbursts
and unprovoked aggressive behavior, slept and ate excessively, and
gained 10 pounds in a few weeks. Following an intravenous injection
of Amytal, Eric said that he had been smoking marijuana during the
weekend. He expressed thoughts of death, and threats of suicide neces-
sitated continuous nursing protection. At times, he required physical
restraint.
A similar episode had occurred five months earlier. Eric had ex-
perienced a grand mal seizure and had been admitted to a community
hospital, where he was described as belligerent, aggressive, and hyper-
sexual. The urine examination was positive for cannabinoids. He was
treated with antipsychotic drugs, but even with low doses he became
rigid, mute, and febrile. When the medications were withheld, he re-
covered and returned to school after three weeks.
At this admission, ECT was recommended, and with parental con-
sent, Eric received three treatments in four days. By the second treat-
ment, the depressed mood and delusional thoughts had disappeared
and he spoke spontaneously. After the third treatment, he was bright,
cheerful, friendly, and pleasant, with a good appetite and normal sleep
rhythms. Observation for an additional nine days without relapse al-

lowed him to be discharged to home and school.
Eric continued in psychotherapy. He told his therapist that each
time he smoked marijuana he had become ill, so he had not used it since
his last hospitalization. He performed well in high school, graduating in
the upper quarter of his class. Four years later he was married, working,
and the father of a child.
comment. Eric suffered from a cannabis-induced psychosis with sui-

cidal and catatonic features. He did not tolerate neuroleptic drugs, as
they induced the motor signs of malignant catatonia. Similar success
with ECT has been reported in treating toxic delusional states caused by
LSD and Sernyl (phencyclidine, PCP).12
Psychiatric Disorders During Pregnancy
Pregnancy is a period of severe stress, and mothers with a history of emo-

tional illness often exhibit recurrences. The immediate postpartum period
is particularly risky, for the mother has to deal not only with the physical
stresses of motherhood, but also with the drastic changes in hormones
as the sources from the baby and the placenta are suddenly expelled and
a new body hormonal balance needs to be reestablished. At such times,
severe depressive and delirious episodes are common.
The combination of debilitating loss of energy, spells of crying, and
a feeling of being incompetent to care for the child is termed postpartum
blues. It is an almost universal occurrence. More severe forms of depres-
sion, marked by delusional thoughts and delirium, also occur, especially
in mothers who have had a prior depressive episode. The most severe
illnesses are less frequent now, probably as a result of better medical care
during the delivery and the greater safety of cesarean delivery in mothers
with very difficult births.
During the first three months of pregnancy, the developing fetus is
considered unusually sensitive to medications taken by the mother. Con-
genital abnormalities are a persistent fear when chemicals are taken by
the mother and then enter the blood circulation of the infant through the
placenta. During this time, ECT with the minimal use of medicines is a
reasonable option.
As it is still unclear whether medications will adversely affect the

fetus in the second three months of pregnancy, some practitioners rely on
medications and others on ECT. In the final three months of pregnancy
the fetus is considered fully formed, and most practitioners prefer medi-
cations. Electroconvulsive therapy is recommended when medications
fail to control the illness or when the patient has had a good result with
the treatment in an earlier episode.
The impact of ECT is described in a British report from the
1940s:13
A married woman of 32 years was admitted to hospital under a certifi-
cate [involuntary admission] in April 1938. Three to four weeks after the
birth of her seventh child she had become depressed and sleepless. At
admission, “tears were trickling down her face” and she was auditorily
hallucinating, the voices saying that she was bad and was to be burnt
alive. She remained apathetic, retarded and asocial. A little improve-
ment was noticed in November 1944. In August 1945 she was given a
course of ECT and at the end of this was greatly improved, mixing on
the wards, talking freely, etc. She was discharged in December 1945.
Since then she has had two further children with no psychiatric com-
plications. When interviewed in 1962, she could remember little of her
stay in hospital during the 7 years prior to being given ECT, but much
of the few months following.
Electroconvulsive therapy is a practical and effective treatment dur-

ing pregnancy.14 It is particularly valuable in the postpartum period. At
such times, especially considering the physical state of the mother after
carrying the child to delivery and the stresses of the delivery, it is par-
ticularly valuable for its ability to resolve such conditions rapidly and
effectively.
Intractable Seizure Disorders
Seizure disorders occasionally become intractable and persist as uncon-

trollable fits known as status epilepticus (SE). Two forms are recognized—
one in which convulsions are prominent (convulsive status epilepticus,
SE) and one in which the motor manifestations are hidden but the brain
events occur and are demonstrated on the EEG (nonconvulsive status
epilepticus, NCSE). Status epilepticus is an emergency condition associ-

ated with high morbidity and a mortality rate of 20% in adults. Treatment
is difficult. The customary treatment calls for increases in anticonvulsant
medications to therapeutic levels and supplementation with benzodiaz-
epines or barbiturates. When these fail, profound and lengthy anesthesia
requiring intubation and mechanical ventilation is induced with a bar-
biturate or with Deprivan. Such treatment is known as pharmacologic
coma. It has high morbidity and mortality rates.15
Electroconvulsive therapy offers an alternative treatment. The in-
duction of a full grand mal seizure (or repeated grand mal seizures) by
ECT will often call the brain’s shut-off mechanism into play, terminating
SE. Electroconvulsive therapy was first used to treat SE in 1943, and
isolated clinical reports attest to its benefits.16 An interesting theoretic
explanation of why inducing a seizure in an ongoing SE ends the ongo-
ing seizures comes from our understanding of the biochemical events of
induced seizures.17
Other Neurological Conditions
Many textbooks caution against inducing seizures in patients with neuro-

logical conditions, particularly in those with intracranial masses. The fear
is that the treatment will increase the pressure of the brain fluids inside
the skull and compress the brain, causing death. This fear is unfounded.
Seizures have been induced safely and effectively in patients with intra-
cranial masses and normal cerebrospinal fluid (CSF) pressures. In cases
where increased intracranial pressure is suspected or measured, neuro-
surgical treatment takes precedence. The prejudice against ECT use in
patients with normal CSF pressures is poorly justified.18
Severe depression may follow the debilitating effects of a stroke when
the blood to part of the brain is shut off or a hemorrhage occurs. In post-
stroke patients with severe depression, ECT has been applied safely and
usefully. Electroconvulsive therapy has also been safely used in patents
with Huntington’s chorea, multiple sclerosis, tardive dyskinesia, and
other debilitating neurological disorders when the psychiatric symptoms
were considered severe and probably responsive to ECT.19
n i n e
Pediatric ECT
The child is father of the man.

—Wordsworth1
T he role of ECT in the treatment of adolescents and children is not

well understood. The experience is limited and poorly documented,
especially in pre-pubescent children. For much of the twentieth century,
child and adolescent psychiatrists believed that the mental disorders of
children and adolescents are psychologically, not biologically, determined.
Psychological attitudes and family interactions were considered the cause
of the pathology of the disorders. In the past two decades interest has
shifted to biological causes and treatments. Depression and mania, autism,
anorexia nervosa, and attention deficit hyperactivity disorder (ADHD) are
now recognized in children and adolescents with increasing frequency.
These shifts in attitude encourage greater interest in medication trials,
and with these, increasing tolerance for trials with ECT.
ECT in Adolescents
The renewed interest in the role of ECT in pediatric patients was shown
at a 1994 conference when experts reported an additional 62 case reports
beyond the 94 that had been described in publications.2 Patients be-
tween 14 and 20 years of age with major depressive syndromes, delirious
mania, catatonia, or acute delusional psychoses had been successfully
85
treated with ECT, usually after other treatments had failed. No reports of
harm to age-related faculties, such as impaired maturation, growth, and
the capacity to learn, were presented. On the contrary, the resolution of
their mental disorders encouraged the young people to complete school
and continue their education.
No adjustments to the adult ECT protocol were required except that
close attention was given to energy dosing. Adolescents require very little
energy to induce an effective seizure. No reporter described instances of
uncontrolled seizures.
Some clinicians, faced with seriously ill adolescents with features
that would encourage ECT if the features were seen in adults, now rec-
ommend ECT. Examples of the successful treatment of melancholia,
psychosis, mania, and catatonia dot the literature.3 Efficacy is reported in
patients with severe mental retardation and in those with self-injurious
repetitive behavior and catatonia grafted onto various forms of autism.4
These reports are sufficiently encouraging to loosen the usual injunctions
against the use of ECT in adolescents. In 2004, the American Academy
of Child and Adolescent Psychiatry offered official practice guidelines
for the use of ECT in adolescents that closely follow the guidelines for
treatment in adults.5
Depressed Adolescent
PETER
A 16-year-old boy was admitted to the hospital after a two-year his-
tory of depressed mood, feelings of worthlessness and incompetence,
isolation, and withdrawal from school. One year earlier, he had been
hospitalized after an attempted suicide with an overdose of acetamino-
phen (Tylenol) and aspirin. Peter was referred to a residential school,
continued individual psychotherapy, and was prescribed antidepressant
medications. But thoughts of suicide persisted, so after numerous con-
sultations and medications, he was referred for ECT.
Peter was lean, well groomed, and alert, obsessed by thoughts of
helplessness, dying, and the inability to maintain his schoolwork. He had
lost 40 pounds in four months (25% of his body weight). He wanted
help but was terrified by the fear that if ECT failed, there was no other
recourse.
Pediatric ECT / 87
On the ward, Peter remained in his room, slept late, missed meals,
and took no part in ward activities. Neuropsychological testing showed
a superior intelligence quotient; on the Wechsler Intelligence Scale for
Children-III (WISC-III) his verbal score was 129, his performance score
was 106, with a full-scale IQ of 121.
After he and his parents signed the consent form, Peter received
seven treatments. He rapidly lost his depressed mood and expressed in-
terest in returning to school. He remained fully oriented, showed an
interest in reading, and participated, using his age-related skills, in the
occupational and group-therapy programs.
After he returned home, Peter received outpatient ECT twice
weekly and then weekly throughout the summer. When school began,
however, he again became depressed. The treatment frequency was in-
creased to three times a week for two weeks, and his feeling of well-being
returned.
Four months after his first treatment, and following 25 treatments,
Peter showed no signs of depression. He conscientiously took the mood
stabilizer lithium and the antidepressant Nardil, and he attended weekly
psychotherapy sessions. One year later, performing at his normal grade
level in school, he was able to discontinue his medications. He acquired
a girlfriend and took part in normal adolescent activities.
comment. Peter suffered from a major depressive mood disorder. Psycho-

therapy, medications, and special schooling had been ineffective. During
the index ECT course and in continuation treatment, his improvement
in mood and behavior was indistinguishable from that of an adult.
Peter’s parents at first had been adamantly against the use of drug
therapy and ECT. Then, disheartened by the inefficacy of ongoing treat-
ments and their son’s suicidal threats, they consented to ECT as a last
resort. Given the success of the treatment they had most feared, the par-
ents considered themselves fortunate to have been referred to a pediatric
psychiatrist with an eclectic approach in his practice.
ECT in Prepubertal Children
Psychiatrists have less experience with ECT in prepubertal children than

in other age groups. The earliest description of various somatic therapies
in children was reported in the 1940s by Lauretta Bender at New York’s

Bellevue Hospital, where she treated more than 100 children who had
been hospitalized for aggression, tantrums, suicidal acts, uncontrolled
mania, and thought disorders. Many may have had structural brain dis-
ease. This was a time before the introduction of psychotropic drugs, so
Dr. Bender treated uncontrollable behavior with ECT, insulin coma, and
experimental hallucinogens. Electroconvulsive therapy was helpful, but
follow-up studies showed the benefits to be temporary.
Catatonia in a Prepubertal Child
The experience with ECT in children is limited to individual case re-

ports. Psychiatrists at the University of Iowa described their experience
with an 8½-year-old girl who came to them after a month of persistent
low mood, tearfulness, feelings of worthlessness, social withdrawal, and
indecision.6 She spoke in a whisper and answered questions only with
prompting. Her movements were slow, and she needed help in eating and
toileting. She repeatedly scratched her arms until she drew blood. When
she refused to eat, she required nasogastric tube feeding. She was peri-
odically mute, exhibited bodily stiffness, was bedridden much of the day,
and often wet the bed. The diagnosis was catatonia in a depressive mood
disorder. Treatment with psychotropic medications was unsuccessful.
After her parents gave their consent for a course of ECT, she was
treated following an adult protocol. She quickly showed greater coopera-
tion in her daily activities. She began to feed herself, and the nasogastric
feedings ended after the 11th treatment. After eight additional treatments
and physical recovery, she was ready to go home; the antidepressant Prozac
was prescribed for aftercare. She quickly adjusted to school. In a follow-
up note in 2007, the senior author of the case study reported that the
young woman had had no recurrence and is now enrolled at a university.
A similar experience of the successful resolution of catatonia in an
11-year old girl has recently been reported.7 The child responded well to
six sessions of ECT, exhibiting hypomania that warranted continuation
mood stabilization. In a one-year follow-up she was performing very well
in school and athletics, no longer requiring medication.
At present, ECT is used in prepubertal children with psychosis, cata-
tonia, and intractable depression or mania not treatable by other means.
Pediatric ECT / 89
ECT in the Intellectually Disabled
The mentally retarded are prone to the same psychiatric disorders that
plague the rest of the population, and they respond to the same treat-
ments as do the psychiatric ill of average intelligence. Restraints and high
doses of antipsychotic and sedative drugs are usually prescribed for un-
controllable outbursts and self-injurious behavior. When these fail, ECT
is applied, with occasional relief.
There is much prejudice against the use of ECT in patients with
intellectual disability, and it is not limited to the public. Many psychia-
trists do not administer ECT to patients under guardianship, fearing dis-
approval or anticipating legal difficulties for undertaking what may be
perceived as a controversial treatment.
Much of the reluctance to administer ECT in the mentally retarded
comes from the confusion between the electricity in ECT and the use of
painful electric shocks to condition behavior in an animal or a human. In
fact, electric shocks—delivered with devices known as cattle prods—to
teach a child or animal that certain acts will be painful was once an ad-
verse conditioning therapy widely used among the mentally retarded. Those
experiments, rightly condemned, are no longer in use, but reports still ap-
pear from time to time.8 Apprehension about the abuse of the mentally
ill with electricity was so widespread that it is still difficult for doctors to
apply any electrical treatment to these patients. The public misinforma-
tion is tragic.
Among the reports of successful and safe use of ECT in patients
with mental retardation is the following case report.
CLAUDIA
A 12-year-old girl with mental retardation exhibited temper tantrums as-
sociated with somnolence. An EEG showed paroxysmal activity, and the
anticonvulsant Tegretol was prescribed. A psychological evaluation as-
sessed her intelligence test score at 50.
Tantrums, aggression, and periodic uncontrollable excitement at
age 16 warranted another EEG, which was normal. Claudia’s behav-
ior worsened, and lithium therapy elicited a calming effect. After four
months of depressed mood, failure to eat, and weight loss at age 19, she
was hospitalized for the first time. Antidepressants and neuroleptic drugs
were added to the continued treatment with the Tegretol and lithium,
but because of neurotoxicity, these medications were replaced by the
anticonvulsant Depakote. Claudia exhibited severe dystonia, however,
and all the medications were discontinued.
Over the next two years, Claudia was hospitalized on four occasions
for two to five weeks each and was treated with several medications. Al-
though consultants considered ECT a reasonable course of treatment,
as did her parents, no electrotherapist was willing to administer it, de-
spite the pleas of her parents, who were her appointed legal guardians.
Episodes of mutism and rigidity alternated with outbursts when she
would run off unless restrained. Claudia once impulsively dived into the
family swimming pool even though she was unable to swim.
When she was admitted to our hospital, Claudia’s parents pleaded
with us to consider ECT. Their daughter, who looked her stated age of 23,
would stand and stare, not speaking, for long periods. She would assume
postures imitating others or after the examiner moved her limbs. The
catatonic signs were accompanied by screaming and aggressive outbursts,
so she often required restraint. She appeared depressed, refused to eat,
and was incontinent. Her speech was unintelligible to everyone but her
mother.
Brain imaging studies showed no abnormality. The EEG exhibited
extensive low-voltage fast activity without spike activity or seizure-type
bursts. These signs were interpreted as secondary to the effects of the
drugs. None of the tests supported the earlier diagnosis of epilepsy.
High doses of Ativan diminished the catatonic behavior, but de-
pressed mood, excitement, and incontinence continued as before. When
the treating psychiatrist agreed to a course of ECT, both parents signed
the consent form.
After two treatments, Claudia’s mood and sleep improved, her appe-
tite returned, she was tractable, and she responded to questions and direc-
tions. After the third treatment, the signs of catatonia were gone and her
behavior was well controlled. She was discharged to her parents’ home for
continuation Ativan and weekly ECT. She was sustained at home, tak-
ing part in a day-treatment program for patients with mental handicaps.
She required no additional medications. After five months, the treatments
were discontinued and Claudia remained in the community with Ativan
as the principal medication.
Pediatric ECT / 91
comment. The syndrome of behavior outbursts, depression, mania, and

catatonia in a patient with intellectual disability does not differ from the
syndrome recognized as mixed bipolar disorder in those without such
disability. Psychotropic and anticonvulsant medications served Claudia
well for a few years, but intolerance precluded their continued use. Elec-
troconvulsive therapy allowed her to remain at home, and her parents,
grateful for the treatment, willingly described their experience in a let-
ter to the Texas legislature when it considered banning ECT for all of
its citizens. (The Texas legislature had already banned ECT in anyone
under the age of 16. They considered a ban on ECT for all patients but
decided against it.)
Self-Injurious Behavior
Repetitive compulsive acts mark a number of abnormal mental states—the

hand washing of patients with obsessive-compulsive disorder, the slash-
ing of wrists of patients with borderline personality disorder, the repetitive
face scratching and head banging of patients with intellectual disability,
and the compulsive acts of patients with Tourette’s syndrome. These pa-
tients are usefully treated as suffering from catatonia and are occasionally
responsive to ECT.
DONALD
A 14-year-old intellectually disabled boy was admitted to our university’s
inpatient facility because of persistent head banging, which required
him to wear a protective helmet and be restrained most of the day. Don-
ald’s mental age was measured as 4.3 years. He communicated mainly
by interpretable guttural sounds. Repetitive head banging and skin
scratching began at age 10 and persisted despite medication use and
both positive and negative reinforcement. He wore large gloves in addi-
tion to the helmet and was sedated to control his high-pitched wailing
and prolonged screaming. After four years of failed treatment, Donald
was evaluated for ECT.
On admission to the hospital, the examination found no bodily dis-
orders to preclude further treatment. Consent for ECT was obtained from
his legal guardian.
After the sixth of twice-weekly treatments, the screaming, scratch-

ing, and head banging were reduced. By the 10th treatment, Donald no
longer needed the helmet, gloves, or restraints. Treatments were reduced
to once weekly, and after 16 treatments he was returned to his residence.
For another two months, treatments were given once every two weeks
and then stopped, because the psychiatrists were satisfied with his prog-
ress. Anticonvulsants were prescribed, and no life-threatening behavior
was evident for two years.
comment. Self-injurious behavior is common in children and adoles-

cents with intellectual disability and autism-spectrum disorders. Such
behavior responds favorably to ECT. Good responses, however, are short-
lived unless treatments are continued. It seems likely that the reported
relapses occurred because of the short courses of ECT that were com-
mon before the 1990s. Continuation ECT is now more readily avail-
able, and the benefits can be better sustained. In Donald’s case, the
treatments were spread over four months, a period known to be effective
in patients with such severe conditions. We lack acceptable guidelines
for how long treatments must be continued.
Donald’s court-appointed legal guardian only reluctantly, and after
much persuasion, allowed ECT to be administered. In stating his be-
lief that this therapy was dangerous and abusive to his client, he was
reflecting the common confusion about ECT and the use of high-energy
electric shocks to condition behavior in an animal or a human. Ap-
prehension about the abuse of the mentally ill with electricity that oc-
curred in the past has been so broadly circulated that it is still difficult
for doctors to apply the treatment.
Catatonia in Autism
A common form of catatonia, dominated by mutism, refusal of food, and

slowing of movements in an adolescent with autism, may be resolved
with ECT, as demonstrated by the following case.
QUINN
A 17-year-old boy with a history of autism, recurrent depressive illness,
and mild intellectual disability was hospitalized with progressive worsening
Pediatric ECT / 93
of mood and slowing of movements. Autism had been diagnosed at age

four, and Quinn received educational, speech, and social-skill interven-
tions throughout his school years.
A severe decline, marked by mutism and reduced food intake, began
at age 14, when Quinn became progressively slower in movement and
had to be prompted to dress himself and eat. He would stand or sit alone
for long periods, undertaking no spontaneous activities. Much time was
spent in the bathroom, washing his hands or looking in the mirror. Ab-
normal blinking, eye rolling, and jerking of his neck were repeatedly
observed.
When Quinn returned from a few weeks at summer camp, he had
lost weight, his speech had become sparse, and his movements and fa-
cial expression were further slowed. Over the next four months he spoke
less and exhibited frequent motor tics, rapid blinking, and head turn-
ing. Laboratory investigations did not find abnormalities of a general
medical or neurological illness.
A diagnosis of obsessive-compulsive disorder and depressive mood
disorder led to the prescription of various medications with little benefit.
His movements slowed further, described by Quinn’s parents as “watch-
ing a movie in slow motion.”
Catatonia was diagnosed, and in the hospital Quinn received a
course of bilateral ECT, which led to dramatic improvement in his
movements, speech, appetite, and interpersonal interactions. He became
more verbal, his movements were more spontaneous, and he was able to
perform the activities of daily living. Antidepressants were prescribed,
and his improvement was maintained. Quinn’s family considered his
response to ECT to be lifesaving.
comment. Similar cases are reported in medical journals.9 Indeed,

awareness is seeping through the profession that the repetitive, often
self-injurious behaviors found in patients with disorders diversely la-
beled autism, mental retardation, and Tourette’s syndrome are usefully
considered variations of catatonia.
The relief of diverse behavior syndromes in adolescents brings with
it welcome improvement in social relations, schooling, and the quality
of home life. The prejudice against the use of ECT in this population
warrants reconsideration.
t e n
How Does ECT Work?
The scientist is always wrong; he is essentially a rebel;

he only postulates his “laws” for them to be
broken by himself or others.
—Walter1
T he major puzzle in ECT is its mechanism of action. How do seizures,

which can be dangerous and damaging when they occur spontane-
ously, change a dysfunctional brain into one that performs normally?
Why do repeated epileptic seizures relieve psychiatric disorders? The
originator of the therapy, Ladislas Meduna, believed in a biological antag-
onism between mental illness and seizures, an antagonism we no longer
consider credible. But though we may smile at this belief, we acknowl-
edge that it led Meduna to devise methods to induce seizures safely,
select patients who were likely to benefit, develop a plan for a successful
course of treatments, demonstrate the safety of inducing seizures, evalu-
ate the merits and risks of seizures as treatment, and convince others
to continue his work.2 His observations have been repeatedly verified,
leaving little doubt about the effectiveness of ECT in treating mental
illnesses.3
We know a great deal about the essential features of a successful
course of ECT. The generalized brain seizure is the central therapeutic
event. The biochemical and physiological consequences of the seizure are
the basis for the behavioral effects; neither anesthesia nor electric current
alone is useful, nor, except rarely, is a single seizure.4 To be of benefit,
94
How Does ECT Work? / 95
seizures must be repeated two or three times a week for many weeks. The
more recent the mood, thought, or movement disorder, the more fully it
can be relieved. Illnesses involving lifelong problems, character pathology,
neuroses, and the mood disorders secondary to the abuse of drugs are not
amenable to this treatment. We know how to avoid the risks of anoxia,
unmodified convulsions, and prolonged seizures, and we recognize that
these aspects of the treatment course do not explain how ECT works.
Evidence of Brain Seizure
Two aspects of the brain seizure have been extensively studied. The EEG
records electrical activity of the brain under electrodes that are symmetri-
cally placed over the scalp. Immediately after the stimulus, the “seizure”
EEG is recorded on a moving strip (Fig. 10–1). The electrical waves show
a sharp buildup of frequencies and amplitudes, then the frequencies slow,
mixtures of slow brain waves and sharp spike-like waves appear, with ever
higher amplitudes and slower waves in runs and bursts. Suddenly the
frequencies cut off and the record becomes flat, with a gradual return to
baseline frequencies.5 After the last treatment, the EEG changes in the
brain persist for up to two months, gradually decreasing in prominence as
the individual brain rhythms are reestablished.
The release of brain hormones into the CSF and into the blood is the
second measure of brain seizure activity. An example is the increase in
prolactin, a product of the pituitary gland, which peaks 20 to 40 minutes
after a seizure. The prolactin surge is sufficient evidence that a grand mal
brain seizure has taken place rather than a pseudoseizure.6 Prolactin is
only one of the many brain hormones that are released after an effective
grand mal seizure.
Many theories have been proposed to explain the beneficial effects
of ECT, but none have been proven by experimental studies. A logical
theory is based on the effect of seizures on the body’s endocrine system,
the interacting glands that maintain the body’s balance in biochemistry
and physiology.
In severe psychiatric illnesses, the mood, thought, and motor func-
tions that go awry are those that are controlled by the body’s neuroendo-
crine system, the glands of the brain (hypothalamus and pituitary) and
the body (thyroid, adrenal, testis, ovary, and parathyroid). Endocrine and
(a)
(b)
Figure 10–1a, 10–1b. Electroencephalographic evidence of an effective treatment.
physiological functions are grossly abnormal; they normalize when the ill-
ness is relieved and become abnormal again when the symptoms recur.7
The body’s glands produce chemicals (hormones) that are distributed
to all the cells of the body through the blood circulation. The hormones
are also distributed throughout the brain by the circulation of the brain’s
own CSF, a clear water-like fluid that bathes all the brain cells.
To help us understand the causes of a mental illness we should con-
sider diabetes, a systemic disorder that follows the failure of the special-
ized cells in the pancreas to produce the hormone insulin. Insulin regulates
the release and storage of sugars in the body. Scientists first identified the
missing hormone in 1922, and substituted it with insulin from animals and
later with chemically synthesized insulin. Diabetes is now controlled by
daily substitution of insulin injections and diet. The substitution does not
cure the deficiency, but it does ameliorate the symptoms of the illness by
replacing a hormone necessary for life. Similar hormone deficiencies are
probably the basis for the severe psychiatric syndromes, especially those
that respond to ECT.
Neurotransmitters and Neurohormones
Neurotransmitters and neurohormones are chemicals that enable the

communication between the neurons (the controlling brain cells) and
the tissues of the body.
Communication among and between brain cells is accomplished
by the release of neurotransmitters, chemicals that are discharged at the
points of contact (synapses) of the brain cells. Their release stimulates or
inhibits the actions of neighboring brain cells. Epinephrine, norepineph-
rine, acetylcholine, serotonin, and dopamine have been identified as ac-
tive neurotransmitters in the intercellular spaces. A stimulated nerve cell
momentarily releases the chemical at its ends; then the next cell is stimu-
lated (or inhibited), and the neurotransmitter is immediately inactivated.
The actions are local, immediate, and momentary. Neurotransmitters are
not distributed to the body. Modern psychoactive drugs are believed to
influence the release and persistence of the neurotransmitters, chiefly
serotonin and dopamine.8
Hormones, by contrast, are the proteins or protein fragments (pep-
tides) produced by glands in the brain and in the body. Master hormones
originate in the hypothalamus and pituitary, the centrally located glands
at the base of the brain. The chemicals stimulate the release of hormones
from other glands in the body, the best known being the thyroid and
parathyroid in the neck, the adrenal glands above the kidneys, special-
ized cells in the pancreas, and the sex glands of the ovary and testes
(Fig. 10–2).
These two systems, neurotransmitter and neuroendocrine, are inti-
mately related. Connections between the hypothalamus and the pituitary,
for example, are both direct (through the release of neurotransmitters)
Figure 10–2. Brain–endocrine gland connections.
and indirect (through peptides circulating to the pituitary gland). These

intimate connections are among the more remarkable discoveries of
twentieth-century neuroscience.
Endocrine glands play dominant roles in our lives. They control life’s
cycles, from maturation from fetus to infant to adult, daily feeding and
sleeping, pregnancy and birth, and senescence and death. The glands
discharge their hormones into the bloodstream to be distributed to all
the cells of the body. The substances of one gland affect the release and
activity of the others. They operate in an interacting rheostatic system,
with hormones released as pulsatile discharges in daily rhythms, rising
with wakefulness and falling with sleep.9
A common example of the interactions of hormones and behavior is

seen as an air traveler crosses time zones and tries to maintain his nor-
mal behavior. Because his sleep cycle is interrupted, he becomes drowsy,
sad, and anxious, is fatigued, cannot concentrate his thoughts, and recall
and memory are impaired. These functions are controlled by cortisol, the
adrenal hormone that is stimulated by the adrenocorticotrophic hormone
(ACTH) of the pituitary gland. The amount of cortisol in the blood and
in the urine changes with the sleep-wake cycle—highest when we are
awake and lowest just as we fall asleep. At first, the cortisol cycle follows
the home times, but once the traveler adjusts to the new time cycle,
the cortisol release cycle is reestablished, the unpleasant symptoms dis-
appear. (Only to reappear when the traveler again crosses time zones as
he returns home.)
Dysfunction in any endocrine gland has consequences. If the thy-
roid fails to produce enough of its hormones, hypothyroidism results. If
that defect occurs in early childhood, the outcome is mental deficiency.
In an adult, myxedema occurs. Fluids accumulate in the body tissues,
mental activity lags, muscles become weak, and reflexes and the electri-
cal rhythms of the brain slow. The subject is depressed, and has poor
memory and paranoid thoughts. Coma, even death, may follow. On the
other hand, if the thyroid gland secretes excessive amounts of hormones,
behavior is marked by excitement, mania, and grandiosity. Similar sys-
temic and mental effects have been associated with deficiencies or ex-
cesses of the hormones produced by the pituitary, hypothalamus, adrenal,
parathyroid, testis, and ovary glands.
A Neuroendocrine View of ECT
What does this tell us about ECT? How does a seizure cause such profound
changes in physiology? Although epileptic fits may arise from any portion
of the brain, only those that come from the central part of the brain—the
brain stem, or what are known as centrencephalic structures—are essential
to the favorable effects of ECT. The hormonal cells of the hypothalamus
sit right above, and are intimately related to, the cells of the pituitary gland.
In ECT the currents from the stimulating electrodes on each temple pass
maximally through the central parts of the brain, stimulating the hypo-
thalamus to discharge its hormones at the same time that the brain’s cen-
tral structures elicit a grand mal seizure. These hormone levels are readily
measured in the blood within a few minutes of the seizure and remain
elevated for hours. The substances circulate throughout the body, affecting
all the body’s cells—a compelling and welcome sign of recovery.
Mental disorders arise when specialized brain cells lack the materi-
als they need to function properly. During ECT, large amounts of hypo-
thalamic and pituitary hormones are “squeezed out,” and new levels are
measurable in the CSF and the blood within a few minutes.
In some courses of ECT, the beneficial change to normal endocrine
function continues after the treatment course ends. In other courses,
the glands revert to their abnormal activities and the signs of the mental
disorder again become evident. Repeated stimulation of the hypothala-
mus and the pituitary is needed to sustain normal brain functions and a
normal mental state.
The brain’s structure helps us understand how the chemicals re-
leased by seizures become available to brain cells. The brain consists of
two large hemispheres that sit atop a central brain stem. These hemi-
spheres are not solid structures, like the liver or spleen, but are hollow.
The sac-like structures known as the lateral ventricles are fluid-filled
spaces that are connected to another sac (the third ventricle), which lines
the space between the two hemispheres. Behind these, and connected
to them, is a fourth ventricle, sitting above the brain stem and below the
cerebellum. The fluid-filled ventricles are also connected to the spaces
on the surfaces of the brain and the full length of the spinal cord. These
intricate sacs and pathways allow all the brain’s cells to be bathed by the
clear, watery CSF, which is rich in peptides, amino acids, sugars, salts,
and proteins. These chemicals come from brain cells and from the body’s
endocrine glands via the bloodstream. The fluid is produced continuously
in the brain, and circulation is assured by highly vascular structures (cho-
roid plexus) in the ventricles that absorb CSF and pass it to the blood.
Richard Bergland, a neurosurgeon, asked what role the CSF and the
brain’s ventricular system may play in the brain’s physiology.10 Using paper
chromatography, a method that separates substances dissolved in a fluid,
he observed more than 300 different peptides and amino acids in the
CSF. He induced seizures in sheep, extracted CSF from the ventricles,
and found these substances to substantially increase in variety and in
amount after seizures.
The brain’s ventricular system makes the substances carried in the
CSF accessible to all brain cells, which extract what they need to function
properly. Picture the CSF as a conveyor belt, allowing brain cells to pick
up this peptide now, another later, and more of yet another as the cell
demands. That is what you and I do when we go to a food buffet; we se-
lect what we need now and pass up other offerings. At another time, our
selections differ as our needs change. It is not strange that ECT corrects
so many different disorders, since it unselectively increases the availabil-
ity of many different substances that are needed for different specialized
functions.
An example of this process is seen in the relief of parkinsonism.
Motor rigidity, tremors, and hesitant gait result when the brain’s cellular
aggregate known as the substantia nigra lacks dopamine. Physicians pre-
scribe large doses of l-dopa, a precursor of dopamine, to encourage the
brain to produce more dopamine. When the prescription is successful,
brain dopamine levels increase, the rigidity that inhibited proper easy
movement decreases, and body movements become smooth again. When
l-dopa treatment fails, ECT is used; it also floods the CSF with dopa-
mine, relieving the rigidity and hesitant gait of parkinsonism.
For many patients, the effects of a small series of treatments persist
for long periods after the course ends. For other patients the brain cells
again function poorly and the mental disorder reemerges. In such cases,
ECT is continued to sustain normal brain cell functions and a normal
mental state.
This theory assumes that the brain’s secretion of substances that
regulate mood and thought are abnormal in the mentally ill.11 Admittedly,
we have not yet identified a specific substance with effects on mood and
thought that is analogous to insulin in its effect on sugar metabolism,
thyroxin’s effect on cellular metabolism, and parathormone’s effect on
calcium metabolism. The most promising candidate has been thyrotro-
pin-releasing hormone (TRH), a tripeptide released by the hypothalamus.
It has euphoriant and antidepressant effects when given parenterally to
humans. Because it is rapidly metabolized, however, its action is short.
A congener of TRH with robust resistance to metabolic denigration is a
reasonable target of chemical research. Such congeners to other brain
peptides—for beta-endorphin, des-Tyr-γ-endorphin12 and for vasopressin,
desglycinamide ariginine vasopressin13—are examples of modified brain
peptides with longer durations of action than the natural compounds.
Our failure to identify the behavior-regulating substances is often
cited as a criticism of this hypothesis, but we cannot deny the empirical
evidence that such substances exist. It is reasonable that ventricular flu-

ids be examined before and after seizures to find substances that either
appear anew or are changed in amount. The identification of such sub-
stances will mark those that we may ethically search for in patients. Such
a search should make possible the development of an effective replace-
ment for ECT.
We have less experience with the hormone changes associated with
psychosis or catatonia than we do with the changes in depression. But,
considering the efficacy of ECT, it is probable that a parallel abnormality
in the hormone system is a determining factor. The diversity of theories
about the effectiveness of ECT notwithstanding, its remarkable success
in altering abnormal behavior compels our interest and encourages the
continuing search for an understanding of the mechanism.
e l e v e n
How Did Convulsive

Therapy Originate?
Diseases desperate grown, by desperate appliance are

relieved; Or not at all.
—Hamlet1
I n the second half of the nineteenth century, European neuropsychia-

trists had identified three mental illnesses that dominated the clinical
scene: neurosyphilis (described as dementia paralytica), dementia prae-
cox (schizophrenia today), and manic-depressive insanity (now known
as the two disorders of major depression and bipolar disorder). These
diseases were devastating, often fatal, and no effective treatments were
known. Caretakers of the mentally ill commonly resorted to chains, re-
straining chairs, cold and hot baths, and seclusion to control aggressive
behavior. Morphine and other sedative chemicals kept patients asleep
but did little to heal their illnesses. The mentally ill who were dangerous
to themselves or to others were housed in large state-supported hospi-
tals managed by hospital superintendents with full authority to treat the
inmates. Lacking effective remedies, they permitted many experimental
and unsafe interventions.
Prolonged sleep was an experimental treatment that seemed to re-
lieve severe depressive and agitated states. Agitated patients were kept in
a stupor for days with continuing high doses of barbiturates, with periods
103
of alertness for feeding and toileting. While some died of pneumonia, the
few who recovered their senses encouraged these trials.2 Body infections
were once thought to cause mental disorders, so to cure mental disease,
the teeth, tonsils, gallbladder, and large sections of the colon were often
removed even though there was no credible evidence to justify the pro-
cedures. Many patients died. The patients suffered further humiliation
when hospitals did not provide false teeth to help them chew their food.
Surgical removal of sexual organs was another “treatment.” Eugenicists
argued for sterilization of the mentally ill, especially those who had be-
come burdens on society. It is estimated that more than 18,000 people
in psychiatric institutions were surgically sterilized during the first half of
the twentieth century.3
The discovery of bacteria as the cause of infectious febrile illnesses
was a great accomplishment of medical research in the nineteenth
century. The French chemist Louis Pasteur’s demonstration that high
temperatures would destroy bacteria, an observation that led to the pas-
teurization of foods, also suggested that fevers could have a therapeutic
benefit in bodily infections. This theory was supported by improvement
of psychosis in patients who survived infections with smallpox or typhoid
fever.4 In one experiment conducted in 1917, blood from a patient with
active malaria was injected into nine patients with neurosyphilis; they de-
veloped cycles of fever every 48 to 96 hours. Remarkably, the psychiatric
symptoms of three patients remitted. This report galvanized interest in
malaria fever therapy for neurosyphilis. Despite remission rates of 8% to
51% and death rates of 2% to 47%, Julius Wagner-Jauregg, the Austrian
physician who reported the findings, received the Nobel Prize for Medi-
cine in 1927.5
Inducing relapsing fever instead of malaria, or seeking to develop
protein sensitivity by injections of gonococcal or typhoid vaccines, tuber-
culin, or milk were not much better. Elevating core body temperatures by
using electric blankets and enclosed cabinets heated by electric lights were
equally dangerous. The complications of fever therapy—dehydration, cir-
culatory collapse, cerebral anoxia, and surgical shock—led to high death
rates. Despite the low success rate and the high incidence of complica-
tions and death, so feared was neurosyphilis as a mental illness and as a
fatal disease that fever therapy was internationally accepted until it was
replaced by penicillin in 1944.6
How Did Convulsive Therapy Originate? / 105
Chemical Convulsive Therapy
Patients with dementia praecox who developed epileptic seizures after

a head injury or after encephalitis were occasionally relieved of their
mental disorder. Because this experience suggested a biological antago-
nism between dementia praecox and epilepsy, some physicians sought
to halt intractable epilepsy with transfusions of the blood of psychotic
patients, hoping that a chemical product of the psychosis in the blood
would counteract and treat epilepsy. These efforts failed.7
In the early 1930s Ladislas Meduna, a physician trained in neurology
and neuropathology, was examining cadavers at the Hungarian Psychiatric
Research Institute in Budapest.8 He observed that the brains of patients
with schizophrenia had fewer than the normal number of neuroglia cells,
the basic supporting brain cells. In the brains of those with epilepsy, how-
ever, the number of glia was increased. (The neuroglia are branched cells
in the central nervous system that provide the structural communicating
network for the neurons, the cells that are the basis for thought, memory,
emotion, and action.) Meduna theorized that the deficiency was a sign
of dementia praecox and inferred that amelioration of the symptoms of
dementia praecox in patients who developed epileptic seizures must be
due to the increase in the number of neuroglia.9
Could artificial seizures increase the number of glia cells and ease
the symptoms of schizophrenia? Meduna experimented with seizure-
inducing chemicals in animals and settled on the intramuscular injection
of camphor-in-oil. After 15 to 60 minutes, a grand mal convulsion was
elicited that neither incapacitated nor killed the animal test subjects.
The technique seemed applicable to humans.10
But many clinicians, including the director of the Hungarian Psychi-
atric Research Institute, believed that dementia praecox was an irremedi-
able inherited genetic disorder. That dementia praecox might be treatable
was academic heresy. Fearing criticism, Meduna moved his research ac-
tivities from the Institute to a state hospital for the long-term mentally ill
at Lipótmezö, outside Budapest.
Among Meduna’s patients was a 33-year-old man who had been psy-
chotic, mute, and withdrawn for four years, suffering from a catatonic form
of psychotic illness. He required feeding through a tube to the stomach, and
since all other measures had failed, was deemed suitable for experimental
treatment. On January 23, 1934, Meduna injected camphor-in-oil into

an arm muscle, and “after 45 minutes of anxious and fearful waiting the
patient suddenly had a classical epileptic attack that lasted 60 seconds.”
Meduna repeated the injections at three- to four-day intervals and
. . . two days after the fifth injection, on February 10 in the morning,
for the first time in four years, he got out of his bed, began to talk,
requested breakfast, dressed himself without help, was interested in
everything around him, and asked about his disease and how long he
had been in the hospital. When we told him he spent 4 years at the
hospital, he did not believe it.11
Injections were repeated on three more occasions, and the patient’s symp-
toms were sufficiently relieved to allow him to return home. A recent ex-
amination of this patient’s records at Lipótmezö showed that he relapsed
after many months and needed further treatment.12
Learning that intravenous injections of the chemical Metrazol safely
induced seizures in animals, Meduna tried this compound in place of
camphor. Metrazol was easier to use, as it induced seizures immediately
and more predictably. It quickly became the principal induction agent.
In two years Meduna treated 110 patients, and in 1937 he reported
relief and remission of mental illness in 53.13 The remission rate was
higher among those who had been ill for less than four years. The seizures
elicited by Metrazol and those elicited by camphor were equally effective,
suggesting that the improvement was due to the seizure, not the mode of
induction. That conclusion led directly to the notion of using electricity
to induce seizures.
Within a few months of his 1935 publication, Meduna received visi-
tors from Italy, Germany, India, Australia, and the United States. In May
1937, he discussed Metrazol treatment at an international meeting or-
ganized by the Swiss Neuropsychiatric Society.14 He was invited to lec-
ture throughout Europe, South America, and the United States. Meduna
learned of the Nazi invasion of Austria-Hungary while in South America,
and he sought asylum in the United States. He worked in Chicago until
his death in 1964.15
Electroconvulsive Therapy
The induction of a seizure by Metrazol was a frightening procedure. Within

a few minutes after the intravenous injection, the patient’s thoughts began
to race, the heart beat more rapidly, and he experienced feelings of terror
and impending doom—and then suddenly lost consciousness.16 When
he awoke his muscles and back ached, his tongue and lips were often
bleeding, and he had a violent headache. Many patients refused further
treatment. Making the procedure less unpleasant was imperative.
Electric currents were tested in many animal experiments as an
alternative method of seizure induction. A successful method was de-
signed in Rome by Ugo Cerletti and Lucio Bini.17 On April 11, 1938, a
39-year-old man suffering from a manic and psychotic episode became
the first person in whom a seizure was safely induced electrically. The
team headed by Cerletti and Bini initially applied a current that did not
induce a seizure. A second induction, at a higher setting, was successful.
Seizures were repeated on alternate days over the next three weeks, and
the patient recovered.18
The interest in Metrazol convulsive treatments had already galvanized
psychiatric practice; the description of electricity in its stead stimulated
further interest. By 1940, Metrazol treatment was reported in 3000 cases
in the United States and 2011 in Europe.19 When physicians emigrated
from Italy to England and the United States, they brought with them the
instruments they had used or they had instruments built in their new
locations according to the original designs.20 By 1940 ECT was as widely
used as Metrazol convulsive therapy, and in the ensuing decades it be-
came established as the principal method of clinical seizure induction.
Other Drastic Interventions
Two other dramatic treatments collectively called the shock therapies

were introduced between 1933 and 1935. Insulin coma therapy (ICT),
introduced by Manfred Sakel in Vienna in 1933, followed the discovery
of the hormone insulin.21 Large doses of insulin were injected into psy-
chotic patients, who then developed comas that relieved the symptoms
of psychosis in some of them. The comas were ended with injections
of sugar. Patients underwent up to 50 comas in a prescribed treatment
course. The relief rates were variable, with considerable morbidity and
mortality. Insulin coma therapy was widely used in the 1940s and 1950s
until it was shown that the antipsychotic medication Thorazine was ef-
fective in relieving psychosis. The coup de grâce came with the publica-
tion of a study of patients referred for insulin coma treated with either
ICT or Thorazine. The efficacy rates of the two treatments were similar,
but Thorazine was considerably safer and much less expensive.22 Thora-
zine became a principal treatment for the psychoses.
Lobotomy (leucotomy) was introduced following reports that surgi-
cal removal of the brain’s frontal lobes pacified chimpanzees. The Portu-
guese neurologist Egas Moniz, who developed the procedure in Lisbon
in 1935, thought that such surgeries would tranquilize agitated and ob-
sessive psychiatric patients. His optimistic report encouraged others to
subject patients to surgical brain cutting despite appalling complications
and high death rates. Antipsychotic drugs also replaced this treatment.
Moniz was awarded the Nobel Prize for Medicine in 1949.23
Because ECT was developed around the same time as ICT and lo-
botomy, the three were intimately related in the minds of the public and
the profession. When neither insulin coma nor lobotomy was found to
be effective, each was supplanted by the psychotropic drugs introduced
in the 1950s. In the 1970s, when ECT was once again called on to treat
medication-resistant cases, its image had been tarnished by the almost
universal confusion with the two abandoned interventions.
Psychopharmacology
New medications to treat schizophrenia, depression, mania, and anxiety

were rapidly introduced in the 1950s. As these were tested, medications
like Thorazine were found to be as successful as insulin coma and lo-
botomy. Antidepressants seemed to be as effective as ECT for depressive
illnesses, and by the mid-1960s, medications had largely replaced these
physical treatments.
But for many patients these medications did not suffice, and they
were again referred for ECT. Many responded rapidly, and interest in ECT
was renewed. Treatment procedures and instruments had been improved,
but strong public and professional resistance discouraged doctors from
recommending or using ECT.24 As the number of medication-resistant
cases mounted, clinicians were encouraged by their patients to seek treat-
ments outside the pharmacy. An interest in ECT had been maintained by
a small academic community, mainly in the United States. The passage
by the California legislature in 1973 of a law making ECT and lobot-
omy illegal in the state galvanized the American Psychiatric Association
to establish a Task Force on ECT. Its report supported the efficacy and
safety of the treatment.25 That report encouraged academic medical cen-
ters to reestablish ECT and practitioners to join together in an advocacy
group, the International Association for the Advancement of Electrother-
apy, which was transformed in the 1980s into the academic Association
for Convulsive Therapy. In 1985 a scientific journal, Convulsive Therapy,
was established. Revisions of the American Psychiatric Association’s Task
Force report occurred in 1990 and 2002.26 As interest heightened in the
United States, the same concerns about medication treatment failures
encouraged psychiatrists in other countries to establish ECT centers and
ECT societies in Europe.27 As patients searched for effective alternatives,
ECT was recalled, and by the mid-1990s, the role of ECT as the second-
ary treatment and even as the primary treatment for severe psychiatric
illnesses was reestablished.
Reprise
The audacity of Wagner-Jauregg, Moniz, Meduna, Cerletti, Bini, and the

many others who sought to alter the course of mental illness by physical
means was abetted by their patients’ view of doctors as paternalistic fig-
ures. It was assumed that the doctors’ efforts were always for the benefit
of their patients. The doctors’ boldness was encouraged by the hopeless
nature of mental disorders as well as the willingness of patients to endure
any hardship, suffer any risk, and pay any price for relief.28 But many
patients were treated unwillingly, despite their protests. Once a patient
was admitted to a psychiatric facility, consent for treatment was assumed
and any refusal was given little heed. Reports of abuse led to public dis-
may and anger that spurred legislative attempts to interdict psychiatric
treatments and limit their use to voluntary, mentally competent patients
who could and did consent. The concept of voluntary consent for so-
matic treatment of the mentally ill was initially shaped by the consent
procedure for ECT drawn up by a Task Force appointed by the American
Psychiatric Association in 1978.
Like the desperate interventions developed for neurosyphilis and
schizophrenia, innovative treatment methods are often applied without
scientific testing for efficacy or safety. The same bravado and insensi-
tivity to ethical and scientific principles mark the incessant flood of
opportunistic interventions that sprout willy-nilly as “treatments” for

mental illness today.
The medical literature contains claims for many untested and un-
proven treatments of the psychoneuroses and psychoses. In the absence
of sound principles on the causes and bodily effects of psychiatric ill-
nesses, it is to be expected that the trials are highly imaginative. Devotees
of the talk therapies turn to psychoanalysis, individual and group thera-
pies, family therapy, milieu and psychosocial therapies, behavior therapy,
client-centered psychotherapy, cognitive therapy, hypnotherapy, existential
therapy, and marital therapy, none experimentally proven to be effective.
Physical manipulations are equally imaginative, including sleep dep-
rivation, continuous sleep, electrosleep, acetylcholine infusions, nitrous
oxide and ether inhalation, histamine injections, megavitamins and com-
plex diets, atropine and scopolamine coma, hemodialysis, intravenous
lysergide (LSD), methamphetamine and megimide, hypothermia, photo-
shock, regressive electroshock, subcoma insulin, cerebral pneumotherapy,
high-dose reserpine, acupuncture, and light therapy. Less well known but
equally imaginative and unproven therapies are focal electrically admin-
istered seizure (FEAST) and nonseizure (FEAT) therapy, cortical electri-
cal stimulation (CES), transcranial direct electrical current (tDEC), and
responsive neurostimulation (RNS).
More recently, imaginative brain stimulation methods labeled trans-
cranial magnetic stimulation (TMS), magnetic seizure therapy (MST),
vagus nerve stimulation (VNS), and deep brain stimulation (DBS) challenge
the profession. These treatments are the subject of Chapter Twelve.
t w e l v e
Is Brain Stimulation an
Alternative to ECT?
Those who cannot remember the past are

condemned to repeat it.
—Santayana1
I nterest in electricity in medicine, especially in psychiatric conditions, is

as old as our knowledge of electricity as a controllable phenomenon. At
the end of the eighteenth and the beginning of the nineteenth centuries,
Benjamin Franklin and Anton Mesmer were among many students who
used electric currents to stimulate paralyzed limbs and to relieve hysterical
states.2 Giovanni Aldini, the nephew of Luigi Galvani, a principal early
student of electricity, applied electric currents to mentally ill patients.3
In the original Aldini publication, the figures show one electrode applied
to the top of the head and a second to the hand. The text states that the
electrodes were connected to earrings. Much of Aldini’s work was done
on fresh cadavers to show that electricity stimulated motor movements.
There is no evidence that he produced seizures for therapeutic purposes.
From the onset of the introduction of ECT, the importance of the
grand mal seizure to the treatment has been questioned. Many people fol-
lowed popular science beliefs in the potency of electricity alone and ad-
ministered low-energy electric currents without inducing a seizure. When
scientists compared sham treatments to real ECT in seeking benefits for
patients, they found the sham currents to be ineffective.4 Low-energy
111
electric currents delivered from a battery with electrodes on the scalp to

either alert or sleeping subjects (electrosleep) were without benefit.5
Some applications of electricity in medicine have been truly innova-
tive. At the end of every grand mal seizure, brain waves (measured by the
EEG) flatten out, with markedly reduced rhythmic activity. Such activity
can be simulated by anesthesia using a chemical called isoflurane. Iso-
electric narcotherapy (isoflurane anesthesia therapy) is a brain-stimulation
technique that seeks to induce long periods of electro-cerebral silence or
markedly decreased electrical activity in the brain.6 An hour of isoelectric
brain electrical activity under anesthesia was once thought to relieve de-
pression in a fashion similar to ECT, but an attempt at replication in six
subjects failed.7 Without independent confirmation, the technique has
been abandoned.
In the past two decades, three physical interventions have been en-
thusiastically promoted as replacements for ECT, that is, as ways to in-
duce the same benefits without seizures. The central claim is that these
treatments are as effective as ECT without side-effects on cognition and
memory.8
Transcranial Magnetic Stimulation (TMS)
A recently introduced technology applies repetitive magnetic pulses to

the head without inducing a seizure. Anesthesia is not needed. The de-
tails of the stimulation currents, number and frequency of pulses, and
stimulating paddle location are under continuing study. The variations
in placement of the stimulating paddle, and the number and frequency
of stimulations, are many, but as of mid-2008, no study had shown sus-
tained benefit for any variation of TMS in a psychiatric illness.
In one study, depressed patients were treated with a 15-day course
of daily TMS stimulation to the left dorsolateral prefrontal cortex. Of the
patients who received either TMS or ECT, 59% of those treated with
ECT achieved remission compared to 17% of those treated with TMS.
The greater efficacy of ECT was demonstrated despite the fact that a less
effective treatment, RUL ECT at 2.5 times the measured seizure thresh-
old, was used for comparison.9
In another large multisite study of daily real TMS and sham TMS over
six weeks (30 sessions), a 50% reduction in mood scores was recorded in
Is Brain Stimulation an Alternative to ECT? / 113
18% and 24% of real-treated patients at weeks 4 and 6, respectively, com-

pared to 11% and 12% of sham-treated patients. These efficacy rates are
comparable to improvement rates in similar patient populations treated
with placebo in multisite medication studies.10
Transcranial magnetic stimulation is not approved for clinical use in
the United States, but it is widely used experimentally.
Magnetic Seizure Therapy (MST)
An accidental seizure is a hazard of TMS. A few grand mal seizures have

been experimentally induced in patients using very high-energy mag-
netic currents. Magnetic seizure therapy has been offered to patients as
a treatment under experimental protocols. It is recommended as a more
focused stimulation of the brain, again, hopefully, with lesser effects on
cognition.11 The EEG records of these experiments do not demonstrate
the full seizure patterns that are characteristic of effective ECT; they are
similar to the partial patterns shown in underpowered unilateral ECT
experiments. A study comparing MST with ECT has yet to be reported.
Vagus Nerve Stimulation (VNS)
In this opportunistic extension of the experience with cardiac stimulators,

a device is surgically implanted in the chest. The stimulating electrodes
are surgically applied to the left vagus nerve, located in the neck. The de-
vice discharges low-voltage stimulations similar to those of the pacemak-
ers implanted in cardiac patients to regulate abnormal heart rhythms.12
The vagus nerve arises in the brain stem and travels in the neck to the
chest and abdomen, where it monitors the functions of body organs. Once
the electrodes are attached, the frequency and strength of the stimulat-
ing electric currents are programmed for retrograde stimulation of the
brain stem. The patient is not conscious of these pulses. Although case
reports enthusiastically support the use of VNS for a variety of psychiatric
symptoms, no credible scientific study has shown a benefit in patients for
whom ECT is considered the effective treatment.13
Although no clinical benefit was demonstrated in clinical trials for
the treatment of therapy-resistant depression, the commissioner of the
Food and Drug Administration (FDA) approved these devices for com-
mercial use over the disapproval recommended by the FDA staff and
consulting committees. This aberrant approval was the subject of hear-
ings by the Grassley Committee of the U.S. Senate.14 After these hear-
ings, the FDA commissioner resigned.
The failure to demonstrate reliable efficacy for VNS has led most
medical insurers to refuse to pay for implantation of the device or for
monitoring continued stimulation, despite the approval by the FDA.
No study comparing the benefits and risks of VNS and ECT for pa-
tients recommended for ECT had been published by the summer of 2008.
Its use is best considered experimental and unproven as a replacement
for ECT.
Deep Brain Stimulation (DBS)
This surgical technology places electrodes deep within the brain and a
stimulator is implanted under the skin, as with VNS. The researchers
seek to implant the electrodes in brain centers believed to be abnormal in
depressive mood disorder or psychosis. Effective sites for the location of
the electrodes are yet to be determined.15 Similar experiments have been
done in patients with severe parkinsonism, with the electrodes implanted
in the brain centers known to be abnormal. So far, few psychiatric pa-
tients have participated in the DBS experiments, and the procedure is at
best considered experimental.
In more than two centuries of interest, no method of brain stimula-
tion that does not induce a seizure has equaled the efficacy of ECT in
relieving severe psychiatric disorders.
t h i r t e e n
Is ECT Practice Ethical?
Our system of morality is a body of imperfect social

generalizations expressed in terms of emotion.
—Holmes1
E lectroconvulsive therapy is widely considered a controversial treat-

ment in psychiatry. Many cite it as the most controversial treatment
in medicine.2 It is not its efficacy that is controversial, however; as we’ve
seen, it offers effective relief for severe psychiatric illnesses even when
other interventions have failed. Nor is the controversy about the imme-
diate risks of the treatment, for the risks and death rates are extremely
low—almost certainly lower than the risks acknowledged for the psycho-
active agents that are the core of modern pharmacotherapy. No systemic
illness or medical condition limits its use.
The controversy is based on the belief that inducing seizures by
electricity permanently damages the brain, causing such severe losses of
personal memory that the patient is no longer recognizable as the person
known before.3 This belief is unfounded, and any effects on memory and
cognition have been shown to be limited to the time during and directly
before treatment (as discussed in Chapter Four).
The roots of the controversial image are many, not the least of which
is the unfortunate conflation of ECT with lobotomy and insulin coma.
The poor portrayal of the treatments by the media inflames viewers’ per-
ception. Conflicts between believers in the biological basis of mental ill-
ness and those with the psychological interests of psychoanalysis and
115
clinical psychology roiled psychiatry throughout the twentieth century.

As a result, governmental regulations for ECT, especially those limiting
its use in children and adolescents, and requirements for written consent
(in some venues for each treatment), have restricted its use.4
Ethical guidelines for the relationship between physician and patient
have a long history, the Hippocratic Oath developed by the ancient Greeks
being the most widely acknowledged guide. The shameful evidence of
medical experimentation on unwilling prisoners by physicians in Ger-
many and the Soviet Union during the Second World War incited a world-
wide reassessment of the patient-doctor relationship. Until the 1970s,
no limitation on experimental intervention with psychiatric patients was
envisioned. Treatments without a scientific basis were lauded and then
discredited when the adverse consequences were shown to be greater than
the benefits. Treatments were applied in institutions where the patients
had an utterly dependent role, and assigned treatments were mandated at
the discretion of the institution director.5
Informed voluntary consent first became a feature of psychiatric care
when the American Psychiatric Association, the professional body that
seeks to guide psychiatric practice, approved the recommendations of the
1978 Electroconvulsive Therapy Task Force.6 That report recommended
that a voluntarily signed written consent form be obtained from every pa-
tient prior to ECT. The consent form was to describe the procedure, the
anticipated benefits and risks, the alternatives that were considered and
their benefits and risks, the names of the responsible physician(s), and
the clear statement that the patient may, at any time, withdraw consent.
For patients who lacked comprehension and competence to make such
decisions, approval for the treatment was to be obtained from the appro-
priate judicial authority according to individual state laws. An example of
this consent form is published in Appendix Three.
To this day, ECT requires signed voluntary consent. For other psy-
chiatric treatments, consent is implied in the patients’ voluntary admis-
sion to a hospital, their continuing attendance at psychotherapy sessions,
and their agreement to take the prescribed medications. No description
of treatment risks is required.
A code of medical ethics that can be applied to ECT is based on what
is known as the Georgetown mantra, the work of the faculty at Georgetown
University beginning in 1979.7 Four principles are enunciated as the basis
for an ethical relationship: beneficence (do good), nonmaleficence (do not
Is ECT Practice Ethical? / 117
harm), autonomy (respect for individual wishes), and justice (equal op-
portunity regardless of age, gender, color, religion, or wealth).
Beneficence
As we have seen in the previous chapters, ECT is an effective treat-

ment inducing remission of symptoms in specific illnesses. Efficacy is
demonstrated even in patients in whom other interventions have failed.
In earlier chapters, I have described the lifesaving benefits of ECT for
patients with suicide intent, melancholic stupor, delirious mania, and
malignant catatonia. An interesting new finding is that inducing seizures
increases the growth of new brain cells in the hippocampus, the part of
the brain that is responsible for retention of memories. (Neurogenesis,
the increased growth of neurons, has been demonstrated in animals and
humans.8)
The fact that ECT causes remission of serious psychiatric illnesses,
even when other treatments have failed, argues that this treatment is
beneficent.
Nonmaleficence
The immediate fears and panic that accompany a new treatment are miti-
gated by sedation and anesthesia, just as they are for invasive medical pro-
cedures. The low risk of death and the minimal side effects demonstrate
the lack of harm of ECT. After more than half a century of research, the
failure to demonstrate evidence of “brain damage” puts this allegation
into its proper perspective. It is not a barrier to the use of ECT.
The greatest fear engendered by ECT is that of memory loss, the fear
that one’s personality will be permanently damaged. With present meth-
ods of treatment that select minimal energies, careful electrode place-
ment, and physiologic monitoring, the impact on memory is localized to
the treatment period, although a few patients complain of effects in the
months after the treatment course. On balance, the benefits far outweigh
the risks.
The proper application of ECT is not an infringement of the prin-
ciple of nonmaleficence.
Autonomy
Electroconvulsive therapy is administered in patients who are deemed

competent to make personal judgments about their care and who agree to
the treatments. For patients deemed incompetent to make personal judg-
ments, society assures necessary treatment as authorized by a state court.
Facilities vary in the ways that they inform patients about the benefits
and risks of ECT, but the principle is well established and the means for
education are widely available. Explanations of the treatment by trained
personnel, information pamphlets and descriptive media presentations
(DVD, video), and meetings with patients and family members in the
course of treatment are methods of informing patients.
The proper application of ECT is not an infringement of autonomy.
Justice
The principle of justice requires the availability and application of ECT

based on equal opportunity regardless of age, gender, color, religion, or wealth.
Unfortunately, present psychiatric practice fails to meet this standard.
Few physicians and fewer psychiatrists have been trained to decide
the merits of ECT for individual patients. Consequently, the identification
of patients with the potential to benefit from ECT is severely limited. We
lack national certification standards for competence in delivering the treat-
ment, thereby failing to assure effective and safe treatment. Psychiatric
hospitals licensed to care for the mentally ill are not required to have the
facilities or the trained personnel to deliver this essential psychiatric treat-
ment. This lack is especially notable in community-supported facilities
that are responsible for the care of the poor, the elderly, and children.
The prevailing practice that considers ECT as the last resort is unjust,
as it consigns patients to weeks, months, and even years of inadequate
care. The professional algorithms for the treatment of major depression
consign patients to a minimum of three failed medication treatment tri-
als, each for at least six weeks, before ECT is considered.9 Considering
the suicide risk that is inherent in a melancholic depression, requiring the
patient to undergo four or more months of travail is unjust.
The treatment algorithms for bipolar disorder and schizophrenia do
not consider ECT in the line of treatments but suggest its consideration
when all other treatments have failed.
Is ECT Practice Ethical? / 119
Electroconvulsive therapy assures remission rapidly and effectively

in hospitalized melancholic and delirious patients, in febrile patients with
malignant catatonia, and in acute psychotic patients. Earlier treatment
than the “last resort” standard is warranted. Electroconvulsive therapy in
adolescents, the mentally retarded, the pregnant, and the elderly is un-
duly discouraged, doing a disservice to these populations, for whom the
evidence of successful treatment is compelling.
The practice of ECT does not meet the principle of justice.
Balancing Ethical Principles
Medical practice seeks to optimize benefits and minimize risks. The ben-
efits of ECT are well defined, offering severely ill patients a chance for
recovery. The risks are few, and even a transitory loss of personal memo-
ries is considered, by most patients who have received ECT, a small price
to pay for the relief of a severe disorder.
At times, the decision to use ECT is hampered by public and pro-
fessional ignorance of its benefits and by exaggerated fears of its risks.
Because the primary medical obligation is to preserve life, it may be nec-
essary to override the principle of autonomy in treating psychiatrically
incompetent patients. Treatment decisions are matters between patients
and their doctors; I consider the intercession of families and courts to be
an unnecessary intrusion into this relationship.
A more serious impediment in the United States to ethical health care
is the increasing control of treatments by bureaucrats who manage the in-
surance support of medical care. By setting artificial guidelines on the num-
ber and frequency of treatments, these lay managers ensure that patients
receive inadequate courses of continuation treatment. Low payments for
physicians’ services drive physicians out of practice. With the legislative
impediments in some states, the availability of ECT is decreasing despite
the increasing evidence of its efficacy and improvements in its safety.
Ethical issues in the assessment of medications for psychiatric treat-
ment have recently roiled the profession. The evidence that pharmaceutical
companies design the drug efficacy and safety studies, manage the data
and the analyses, write the reports, and then seek a compliant academic
figure to lend his or her name to the report as published with industry
encouragement in a prestigious medical journal has recently upset the
medical community. Concerns about increased suicide risk in adolescents
when newer antidepressants are used have shown that the assessment
of medications for marketing is subject to undue influence by industry,
academic assessors, and political leaders.10
The practice of ECT meets ethical standards for beneficence, nonma-
leficence, and autonomy but not for justice.
a p p e n d i x o n e
Diagnoses in Which ECT

Is Considered Effective
Major depression
Single episode [296.2x]*
Recurrent [296.3x]*
Bipolar major depression

Depressed [296.5x]*
Mixed [296.6x]*
Not otherwise specified [296.70]*
Mania (bipolar disorder)

Mania [296.4x]*
Mixed type [296.6x]*
Not otherwise specified [296.70]*
Atypical psychosis [298.90]
Schizophrenia
Catatonia [295.2x]
Schizophreniform [295.40]
Schizo-affective [295.70]
Catatonia
Schizophrenia, catatonic type [295.2x]
Catatonic disorder due to medical condition [293.89]
121
122 / Appendix One
Malignant catatonia [293.89]

Neuroleptic malignant syndrome [333.92]
Delirium
Due to a general medical condition [293.0]
Due to substance intoxication [specify substance]
*Especially when associated with delusions.

Source: American Psychiatric Association DSM-IV (1994).
a p p e n d i x t w o
Diagnoses in Which ECT

Is Considered Ineffective
Dementia and amnestic disorders [293.0, 290.xx, 294.xx]

Substance-related disorders [303.xx, 291.x, 304.x, 292.x]
Anxiety and somatiform disorders [300.xx]
Factitious disorders [300.xx]
Dissociative disorders [300.1x, 300.6]
Sexual dysfunctions [302.xx, 625.8, 608.89,
607.84, 608.89, 625.8]
Sleep disorders [307.xx, 780.xx]
Impulse disorders [312.3x]
Adjustment disorders [309.xx]
Personality disorders [301.xx]
123
a p p e n d i x t h r e e
Sample ECT Consent Form
Consent for Electrotherapy
I, _______________________, M.D. (and _______________________, M.D.)

recommend electroconvulsive therapy for your present mental symptoms.
These treatments have been given to thousands of mentally ill patients since
1938, with many improvements in the treatments and greater success in help-
ing patients since then.
Treatments are given in the mornings before breakfast, in a specially
equipped treatment room. You will be attended by an anesthetist, a nurse,
and a psychiatrist.
A needle will be placed in your vein (as you may have had when samples
were taken for blood tests) and an anesthetic will be injected. You will become
drowsy and fall asleep. Other medicines will be given to relax your muscles.
The anesthetist will help you breathe with pure oxygen through a mask.
The treatment is given while you are asleep. Momentary electric currents
are passed through electrodes on the scalp to stimulate the brain. A grand mal
seizure and muscular contractions for up to two minutes follow; with proper
relaxation, the contractions are barely measurable.
The treatments take only a few minutes. You are then moved to the recov-
ery room, where you will wake up as after a deep sleep. You may feel groggy,
and probably have muscular aches, like after exercises, and a headache. You
return to your room, usually within an hour of the treatment. You will be given
your breakfast and spend the rest of the morning on the ward with your nurse
or attendant.
125
126 / Appendix T hree
Treatments are given every other day for up to 12 treatments. Many pa-
tients improve rapidly and require fewer treatments. Some require more than
12, but these will not be given without another discussion with you and your
family.
The treatment has risks. The treatments are given in a room where spe-
cial equipment and supplies for your protection are available. Patients often
become confused and may not know where they are when they awaken. This
may be frightening, but the confusion usually disappears within a few hours.
Memory for recent events, mainly for the period of illness and the treatment,
may be disturbed. Dates, names of friends, public events, telephone num-
bers, and addresses may be difficult to recall. In most patients, the memory
difficulty is gone within four weeks after the last treatment; but rarely, the
problems remain for months and even years. Death is a rare complication oc-
curring no more frequently than death in mothers giving spontaneous birth.
Equally uncommon with modern anesthesia are bone fractures, broken or
lost teeth, and spontaneous seizures after the treatment is over, but these
may occur.
You may discontinue the treatments at any time, although you will be
encouraged to continue until an adequate course is completed.
I, ___________________________, have read this description of the
treatments and these have been explained to me by ____________________.
I agree to have the treatments and understand that Dr. ______________
will be the physician in charge of my treatment.
Dated: _____________________ Agreed ______________________

Witness: ________________ Relationship to Patient _____________
a p p e n d i x f o u r
Medication Names and Uses
Table Appendix 4–1
Brand name Chemical name Use
Ambien zolpidem soporific

Amidate etomidate anesthetic
Amytal amobarbital anesthetic/sedative
Anapsine droperidol anesthetic
Anectine succinylcholine muscle relaxant
Artane trihexyphenidil antiparkinson
Ativan lorazepam sedative
Benadryl diphenhydramine sedative
Brevital methohexital anesthetic
Cardiozol pentylenetetrazol induces seizures
Clozaril clozapine atypical antipsychotic
Cogentin benztropine antiparkinson
Dentrium dantrolene muscle relaxant
Depakote valproic acid, anticonvulsant
sodium valproate
Deprivan propofol anesthetic
Effexor venlafaxine antidepressant
Elavil amitriptyline antidepressant (TCA)
Forane isoflurane anesthetic
Haldol haloperidol antipsychotic
(Continued)
127
Table Appendix 4 –1 (Continued)
Brand Name Chemical Name Use
Indoklon flurothyl induces seizures

Ketalar ketamine anesthetic
Klonipin clonazepam sedative
Lamictal lamotrigine anticonvulsant
Lithobid lithium anti-manic
Lunesta eszoplicone soporific
Metrazol pentylenetetrazol induces seizures
Miltown meprobamate anxiolytic
Moban molindone antipsychotic
Nardil phenelzine antidepressant (MAOI)
Navane thiothixene antipsychotic
Norpamin desipramine antidepressant (TCA)
Pamelor nortriptyline antidepressant (TCA)
Parlodel bromocriptine dopamine agonist
Paxil paroxetine antidepressant (SSRI)
Pentothal thiopental anesthetic
Prolixin fluphenazine antipsychotic
Prozac fluoxetine antidepressant (SSRI)
Risperdal risperidone atypical antipsychotic
Robinul glycopyrrolate anticholinergic
Sinemet l-dopa dopamine agonist
Sinequan doxepin antidepressant (TCA)
Tegretol carbamazepine anticonvulsant
Tofranil imipramine antidepressant (TCA)
Trilafon perphenazine antipsychotic
Ultiva remifentanil anesthetic
Valium diazepam sedative
Versed midazolam sedative
Wellbutrin bupropion anxiolytic
Xanax alprazolam anxiolytic
Zoloft sertraline antidepressant (SSRI)
Zyprexa olanzapine atypical antipsychotic
MAOI, monoamine oxidase inhibitor; SSRI, selective serotonin reuptake inhibitor; TCA,
tricyclic antidepressant.
Notes
Preface to the New Edition

1. Sakel 1938.
2. Meduna 1937.
3. Cerletti 1950, 1956.
4. Kaufman 2007.
5. Greenberg and Gujavarty 1985; Fricchione et al. 1990.
6. Fink 1996.
7. Bright-Long and Fink 1993.
8. Fink 1999b.
9. Fink 2000b; Malur et al. 2000.
10. Trivedi et al. 2003.
11. Fink and Taylor 2003.
12. Taylor and Fink 2006.
13. Gujavarty et al. 1987; Fink and Sackeim 1996.
14. LaGrone 1990.
15. Petrides and Fink 1996a.
16. Greenberg et al. 1986, 1988.
17. Thuppal and Fink 1999.
18. Greenberg and Fink 1990.
19. Moise and Petrides 1996.
Chapter One: What Is Electroconvulsive Therapy?

1. Hippocrates 1947. Quotation as cited in 1947.
2. APA 2001.
3. Abrams 2002; APA 2001; Fink and Taylor 2003; Taylor and Fink 2006.
129
130 / Notes
4. Parker and Hadzi-Pavlovic 1996; Taylor and Fink 2006.

5. The one-syndrome concept is detailed in Taylor and Fink (2006). The two-
syndrome model is described in Goodwin and Jamison (1990, 2007). The
history of these developments is presented by Healy (2008).
7. Fink and Taylor 2003; Taylor and Fink 2006.
8. The overlap of these syndromes suggests an interesting speculation. A syphi-
litic infection of the nervous system elicits many behavior syndromes, includ-
ing paranoia, depression, mania, delirium, and catatonia. Patients also exhibit
diverse neurologic signs, such as failure of eye pupils to respond to light,
tremors, paralyses, and peculiar walking gaits. Syphilis is “the great imitator.”
The diverse forms of this disease are responsive to penicillin.
When we examine the many conditions that respond to ECT we find
great overlap, supporting the belief that a common pathophysiology is the
basis for these syndromes, one that is relieved by repeated induced seizures.
Monitoring the response to ECT to identify populations of diverse pre-
sentation with a common pathophysiology is a strategy for a clinical-based
classification of psychiatric disorders (Fink and Taylor 2008).
9. Abrams 1989, 2002; APA 2001.
10. Greenberg et al. 1986, 1988; Ghaziuddin et al. 1999; APA 2001; Abrams 2002.
11. APA 2001; Abrams 2002; Fink and Taylor 2003; Ottosson and Fink 2004;
Taylor and Fink 2006.
Chapter Two: The Patient’s Experience

1. A Practicing Psychiatrist 1965.
2. Fink 1986.
3. The history of the consent procedures and the background for the unique
position of ECT in psychiatric treatment is described by Ottosson and
Fink 2004 and Shorter and Healy 2007. (Also see Chapter Thirteen of this
volume.)
4. APA 1978; Ottosson and Fink 2004; Shorter and Healy 2007.
5. Information booklets are available from the National Institute of Mental
Health (Sargent 1986) and Somatics Inc. (Abrams and Swartz 1991). The
DVD (videotape) presentations are referenced as Fink 1986; Hillside Hospi-
tal 1999; Dartmouth Hitchcock 2002; and Osborne 2006.
6. In Texas and California, where doctors are required to report ECT treat-
ments, less than 3% of patients are treated under court mandates. Ottosson
and Fink 2004.
7. Parry 1981; Roy-Byrne and Gerner 1981. For a layman’s description of how
California’s laws interfered with one patient’s treatment see Wyden 1998,
Chapter 20.
Notes / 131
These regulations are even more restrictive for adolescents and interfere
with the continuation treatments that are needed to sustain a benefit (Wachtel
et al. 2008).
8. APA 2001; Abrams 2002.
9. Rich, 1984; Abrams 2002.
10. Petrides et al. 2001; Taylor and Fink 2006.
11. Rasmussen et al. 2007.
12. Sackeim et al. 2001.
13. Fink 2005; Taylor and Fink 2006.
14. Sackeim et al. 2001.
15. Kellner et al. 2006. The results and conclusions are assessed by Fink and
Taylor 2007.
16. Prudic et al. 1990; Sackeim et al. 1990.
17. Fink et al. 1996.
18. Chapter Five, patient Helen.
19. Chapter Eight, patient Steven.
20. Mulsant et al. 1997; Rasmussen et al. 2006.
21. Fink 1999b; Taylor and Fink 2006.
22. Manning 1994.
23. Endler 1990.
Chapter Three: The Treatment Technique

1. Fuller 1732.
2. Commonly used alternatives are Amidate (etomidate), Deprivan (propofol),
Ketalar (ketamine), Pentothal (thiopental), and Ultiva (remifentanil). The
favorable characteristics are rapid onset and very short duration.
3. The frequency of the square waves used in present-day treatments varies
from 30 to 70 cycles per second, with pulse widths of 0.3 to 2.0 milliseconds.
The duration of stimulation varies between 0.2 and 8.0 seconds and delivers
25 to 500 millicoulombs (mC) of energy in approved U.S. devices. Modern
devices allow variation of these parameters and also include monitors for
EEG and heart rate.
Between 1938 and 1980 the sinusoidal form of electrical energy was
widely used. It is commonly available from a conventional wall outlet in the
United States at 110 volts; it is reduced to 70 volts or increased to 170 volts
by a transformer in the device. A clock, graduated from 0.1 to 1.0 second,
controls a measured amount of energy for the treatment. Such energy is less
efficient and is associated with greater immediate changes in orientation and
awareness. The use of these forms of current is no longer recommended.
4. Sackeim et al. 2001; Kellner et al. 2006.
5. McCall et al. 2000.
132 / Notes
6. Abrams 2002.
7. Fink 2000; Abrams 2002.
Chapter Four: Side Effects and Memory Issues

1. Fuller 1732.
2. Abrams 1997, 2002.
3. Munk-Olsen et al. 2007.
4. Shorter 1997; Shorter and Healy 2007.
5. Rouechè 1974; Donahue 2000. These, and other examples, are discussed in
Fink 2007.
6. Dukakis and Tye 2006.
7. Holmberg 1953.
8. Styron 1990.
9. A Practicing Psychiatrist 1965.
10. Dukakis and Tye 2006, Chapter 9, pp. 156–63.
11. Perkins 1996.
12. Fink 2007.
Chapter Five: Depressive Mood Disorders

1. Manning 1994.
2. APA 1980; Taylor and Fink 2006.
6. Carroll et al. 1981.
8. Glassman et al. 1975.
9. Avery and Lubrano 1979.
10. Mulsant et al. 1997; Rasmussen et al. 2006.
11. Ottosson and Fink 2004.
12. Coffey et al.1991.
13. Kiloh 1961.
14. Hoch 1921.
15. Fink 1999a; Bright-Long and Fink 1993.
16. Kellner et al. 2005. Not all patients completed the treatment course, some
withdrawing early as soon as they achieved some relief. That the relief was
not assured and that more treatment was needed was shown by two patients
who attempted suicide when prematurely discharged.
17. Prudic and Sackeim 1999.
Notes / 133
Chapter Six: Manic Mood Disorders

1. Duke 1992.
2. Meduna 1950; Bond 1980; Fink 1999b; Taylor and Fink 2006.
3. Nasar 1998.
4. Goodwin and Jamison 1990; Taylor and Fink 2006, 2008; Fink and Taylor
2007.
5. Taylor and Fink 2006, 2008; Fink and Taylor 2007; and the earlier critiques
by Goodwin and Jamison 1990.
6. Hermesh et al. 1992; Fink and Taylor 2003.
7. Goldberg et al. 2007.
8. Mukherjee et al. 1994.
10. Fink and Sackeim 1996. The augmentation of clozapine with ECT has case
study support (Braga and Petrides 2005).
11. In the older literature, the syndrome was labeled oneirophrenia, a dreamy
state of poor awareness. No effective treatment was known until ECT was
developed (Meduna 1950; Fink 1999b; Fink and Taylor 2003).
Chapter Seven: Movement Disorders

1. Carpenter 1912.
3. Fink and Taylor 2003; Mann et al. 2003; Caroff et al. 2004.
4. Fink and Taylor 2003; Mann et al. 2003; Caroff et al. 2004.
6. Andersen et al. 1987.
7. Zervas and Fink 1991; Faber and Trimble1991.
Chapter Eight: Other Uses: Psychosis, Pregnancy,

and Status Epilepticus
1. Shakespeare 1938.
2. Petrides et al. 2001; Taylor and Fink 2006.
3. Fink and Sackeim 1996.
4. Fink et al. 1958.
5. Kane et al. 1988.
6. Kane 2004.
7. Fink and Sackeim 1996.
8. Christison et al. 1991; Wyatt 1991.
9. Lieberman et al. 2005.
10. APA 1997.
134 / Notes
11. The studies of the changes in the EEG during the course of ECT found
progressive slowing and increased amplitudes of the EEG frequencies in the
interseizure EEG, done usually 24 to 30 hours after a treatment. If such
slowing did not occur, the treatment course was found to be ineffective. The
development of significant EEG slowing was a sign of effective treatment. In
this instance, the lack of slowing encouraged us to continue the treatments
(Fink 1979).
12. Fink1995.
13. Protheroe 1969; abstracted from Taylor and Fink 2006, p. 35.
14. Some practical concerns about how to deliver ECT safely during pregnancy
are reflected in the literature (Abrams 2002). Some writers recommend
monitoring the fetus’s heart rate during the treatment. Such monitoring has
shown no adverse effect on the fetus by the anesthesia or the seizure. In-
deed, it is a remarkable experience to see how well the fetus is protected by
following the changes in the heart rates of the fetus and mother. During the
minutes of the seizure the mother’s heart rate increases, but the fetus’s rate
remains undisturbed.
In treating a woman during the third trimester, when the fetus and pla-
centa may be large and interfere with breathing, the anesthesiologist usually
positions the patient on her side so that he can move the diaphragm more
easily. Occasionally, in obese women, intubation of an airway into the trachea
may be necessary.
15. Fink 2004; Anschel and Fink 2005.
16. Griesemer et al. 1997.
17. The pathophysiology of SE is the persistence of a low seizure threshold, de-
spite repeated seizures, with a failure of the biochemical inhibitory mecha-
nisms to increase sufficiently to terminate a seizure (Fink 2004). In SE the
seizures, although frequent, are not robust, as has been found in studies of
prolactin in the blood serum. In a robust seizure, like that developed during
ECT and like many epileptic seizures, the concentration of prolactin in the
blood increases markedly (Abrams 2002). The measurement of serum pro-
lactin in the hour after a seizure differentiates true epileptic seizures from
hysterical seizures or pseudoseizures (Trimble 1978). In SE, prolactin levels
do not rise; indeed, they remain normal both in adults and in children. This
failure of patients in SE to release large amounts of prolactin suggests that
their seizures are incomplete and cannot stimulate a robust inhibitory termi-
nation process. But maximal seizures can be elicited with ECT even in SE,
which makes SE a reasonable alternative to pharmacologic coma (Fink 2004;
Anschel and Fink 2005).
18. Greenberg et al. 1988; APA 2001; Abrams 2002.
19. Abrams 1989, 2002.
Notes / 135
Chapter Nine: Pediatric ECT

1. Wordsworth 1875.
2. Schneekloth et al.1993; Moise and Petrides 1996; Rey and Walter 1997;
Walter and Rey 1997; Cohen et al. 1997.
3. Fink 1999b; Fink and Taylor 2003; Taylor and Fink 2006.
4. Moise and Petrides 1996; Thuppal and Fink 1999; Dhossche et al. 2006;
Wachtel et al. 2008.
5. Ghaziuddin et al. 2004.
6. Cizadlo and Wheaton 1995.
7. Chung and Varghese 2008.
8. Kaufman 2007.
9. Dhossche et al. 2006; Wachtel et al. 2008.
Chapter Ten: How Does ECT Work?

1. Walter 1956.
2. Meduna 1935, 1937, 1950, 1985.
3. The remarkable story of convulsive therapy is reported by Meduna in his
autobiography, published posthumously (Meduna 1985). Two recent books
detail his history and the subsequent developments in convulsive therapy
(Shorter and Healy 2007; Dukakis and Tye 2006).
4. Fink 1979, 1999a.
5. Fink 1979, 2000a.
6. Trimble 1978.
7. Fink 2000a; Taylor and Fink 2006.
8. Hales 2005.
9. Nemeroff and Loosen 1987.
10. Bergland 1985.
11. Nemeroff and Loosen 1987; Wolkowitz and Rothschild 2003.
12. GK-78, Organon. Fink et al. 1981.
13. Org 5667, Organon. Westenberg et al. 1994.
Chapter Eleven: How Did Convulsive Therapy Originate?

1. Shakespeare Wm: Hamlet, Act IV, Scene 3.
2. Klaesi 1922.
3. Scull 2005.
4. Terry 1939.
5. Wagner-Jauregg 1918.
6. Dattner 1944; Duffy 1995.
136 / Notes
7. Duffy 1995.
8. Meduna 1985; Shorter and Healy 2007.
9. Meduna 1937, 1985.
10. Meduna 1935, 1985.
11. Meduna 1985.
12. Baran et al. 2008. The records also showed that Meduna had experimented
with camphor injections in ten earlier patients, beginning on January 2,
1934. Nine of the first 11 patients presented with catatonia; three improved
with treatment. Meduna sought an effective dosing schedule. Missed sei-
zures were common in these early patients.
13. Meduna 1937.
14. Katzenelbogen 1938.
15. Meduna, 1985.
16. Weigert 1940.
17. Cerletti 1950, 1956; Bini 1938, 1995.
18. Cerletti 1956.
19. Jessner and Ryan 1941.
20. Abrams 1988; Shorter and Healy 2007.
21. Fink 2003; Doroshow 2007; Shorter and Healy 2007.
22. Fink et al. 1958; Fink 2003.
23. Valenstein 1986; El-Hai 2005.
24. Fink 1991; Shorter 1997.
25. APA 1978.
26. APA 1990, 2002.
27. European Forum for ECT, Nordic Association for Convulsive Therapy.
28. For a description of the enthusiasm with which fever therapy was accepted,
despite its risks and poor results, see Duffy 1995 and Braslow 1998. The en-
thusiasm for lobotomy is explored in many books including Valenstein 1986
and Pressman 1998.
Chapter Twelve: Is Brain Stimulation an Alternative to ECT?

1. Santayana 1954.
2. Finger 2006; Finger and Zaromb 2006.
3. Parent 2004.
4. Ulett et al. 1954; Fink 1979; Palmer 1981.
5. Reynolds and Sjoberg 1971.
6. Langer et al. 1985, 1995.
7. Greenberg et al. 1987.
8. George and Belmaker 2000; Lisanby 2004; Shorter and Healy 2007.
9. Eranti et al. 2007.
Notes / 137
10. O’Reardon et al. 2007.

11. Lisanby 2004.
12. Lisanby 2004.
13. Nahas et al. 2005; Rush et al. 2005.
14. Grassley and Baucus 2005.
15. Lisanby 2004; Kopell and Greenberg 2008.
Chapter Thirteen: Is ECT Practice Ethical?

1. Holmes 1915.
2. APA 2001; Abrams 2002; Shorter and Healy 2007.
3. Breggin 1979; Friedberg 1976; Sackeim 2000.
4. Shorter 1997; Ottosson and Fink 2004; Dukakis and Tye 2006; Shorter and
Healy 2007.
5. Shorter 1997; Braslow 1998; Pressman 1998; El-Hai 2005; Scull 2005.
6. APA 1978.
7. The summary text by Beauchamp and Childress (2001) is the basis for the
discussion by Ottosson and Fink (2004).
8. Bolwig and Madsen 2007; Manganas et al. 2007.
9. APA 1997, 1999, 2000, 2002, 2004.
10. Angell 2004; Healy 2004; Medawar and Hardon 2004.
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Index
Page numbers followed by f indicate illustrations.
Adolescents Anesthesia, 13, 15, 26 –27, 38–39

acute toxic syndrome, 81–82 Anesthetic agents, 26, 131n2(ch3)
autism, 92–93 Anger, manic, 62–64
catatonia, 92–93 Antianxiety drugs, memory
delirious mania, 64 –66 impairment and, 37
depression, 86 –87 Anticonvulsants, for mania, 59, 61–62
ECT use, 85–86 Antidepressants
safety, 7 introduction, 108
self-injury, 91–92 memory impairment, 37, 38
typical patient history, 6 toxic serotonin syndrome, 72
Adverse effects. See Side effects Antipsychotic drugs. See Neuroleptic
Age, memory loss and, 35, 37, 39 drugs
Alcohol consumption, memory Anxiolytic drugs, memory impairment
impairment and, 38 and, 37
Alcoholism, as contraindication, 9 APA. See American Psychiatric
Aldini, Giovanni, 111 Association
Alzheimer’s disease, 44, 50–52 Association for Convulsive Therapy, 109
American Psychiatric Association (APA) Attention deficit disorder, 6
Diagnostic and Statistical Manual, 68 Autism, 6, 92–93
Electroconvulsive Therapy Task Autonomy, ethics and, 118
Force, 108–109, 116 Aversive conditioning therapy, ix, 89
practice standards, 33
Amnesia. See Memory loss/ Barbiturates, 26, 68
impairment A Beautiful Mind, 10, 58
153
154 / Index
Bender, Lauretta, 88 autistic spectrum disorder,

Beneficence, ethics and, 117 catatonia in, 92–93
Benzodiazepines, 31, 68, 81 catatonia, in child, 88
Bergland, Richard, 100 chronic schizophrenia, 79–81
Bifrontal electrode placement depression in adolescent, 86 –87
(BF ECT), 28 depressive melancholia, 46 – 47
Bilateral electrode placement. malignant catatonia, 69–70
See Bitemporal electrode mania, recurrent, with psychosis,
placement ECT 62–64
Bini, Lucio, 107 mania with psychosis, 64 –66
Bipolar disorder, 8, 22, 43, 57–60. mental retardation, self-injury
See also Mania in, 91–92
Bipolar I disorder, 58 mental retardation, outbursts and
Bite bloc. See Mouth guard catatonia in, 89–91
Bitemporal electrode placement ECT neuroleptic malignant syndrome,
(BT ECT ), 19–20, 28–30 70–72
Blood-brain barrier, 77 outbursts and catatonia, in mental
Blood pressure retardation, 89–91
changes, 31 parkinsonism, 73–74
monitoring, 14 pseudodementia and catatonia,
Bone fractures, 26 52–54
Brain psychotic depression, 48–50
electrical activity monitoring, 14 self-injury in mental retardation,
functional centers and anatomy, 91–92
28, 100 suicidal intention, 55–56
stimulation therapies, 111–114 toxic psychosis and delirium, 81–82
tumors, 84 Catatonia, 67–70
BT ECT. See Bitemporal electrode autism, 92–93
placement ECT case histories, 69–70
characteristics of, 44, 67–68
California legislation, 12, 108–109, in children, 88
130n6(ch2) classification of, 68
Camphor-in-oil injections, 105–106, ECT effectiveness in, 8, 32, 68,
136n12(ch11) 71–72
Cannabis-induced toxicity, in mania, 58, 59, 60, 65–66
81–82 medications, 68
Carroll, Bernard, 45 rapid neuroleptization, 59, 65–66
Case studies, x–xi treatment outcomes, 22
acute catatonia, 69–70 typical patient history, 5–6
acute manic episode, 60–62 Cerebrospinal fluid (CSF), 95–96,
acute psychosis, 78–79 100–101
Index / 155
Cerletti, Ugo, 107 Deep brain stimulation (DBS), 114

Chemical convulsive therapy, 27, Definitions, ix–x
105–106 Delirious mania, 22, 58, 59–60,
Children 64 –66
catatonia, 88 Delusional depression, 8, 20, 22,
ECT, 4, 87–88 44, 47–50
Mental retardation, 89–92 Dementia, reversible. See
safety, 7 Pseudodementia
self-injury, 67, 91–92 Dementia paralytica, 103. See also
typical patient history, 6 Neurosyphilis
Comorbid conditions, xi–xii, 8–9 Dementia praecox, 103. See also
Computed tomography (CT ), 53–54 Schizophrenia
Confusion, 17, 35, 36, 38, 62 Depression, 43–56
Consent in adolescents, 46, 86 –87
concept, 109 autobiographical description, 40
Electroconvulsive Therapy Task case histories, 46 – 47, 48–50,
Force and, 116 52–54, 55–56
Form, 125–126 characteristics, 43– 44
in mania, 50, 60 cortisol levels, 45– 46
requirements, in ECT, 11–12, 116 delusional, 8, 20, 22, 44, 47–50
Continuation treatment, 19–21 ECT effectiveness, 8, 32, 45, 48,
Contraindications, 8–9 54 –55
Controversy, ECT and, vii, 115–116, 119 geriatric, 44, 50–54
Convulsion, defined, x major, 43, 46 – 47, 58
Convulsion treatment, ix medications, 44, 45, 48, 50, 54
Convulsive therapy. See Chemical memory impairment, 40
convulsive therapy; postpartum, 82–83
Electroconvulsive therapy relapse rates, collaborative study,
Convulsive Therapy, 109 19–20
Cortisol, 19, 45– 46, 99 risk of death, 44 – 45
Court mandated involuntary stroke, 84
treatment, 12–13, 60, suicide, 45– 46, 54 –56
130n6(ch2) treatment outcomes, 21–22
CSF. See Cerebrospinal fluid types, 44
CT (computed tomography), 53–54 typical patient history, 5
Depressive mood disorder. See
Darkness Visible: A Memory of Madness Depression
(Styron), 40 Depressive stupor. See Catatonia
Death risk Dexamethasone suppression test
in depression, 44 – 45 (DST), 45
ECT and, 34 Diabetes, 96 –97
156 / Index
Diagnoses, effectiveness of ECT Electrocardiogram (ECG), 14, 31

for, 4 –5, 7–8, 121–123 Electroconvulsive shock (ECS), x
Diagnostic and Statistical Manual Electroconvulsive therapy (ECT).
[DSM] (APA), 68 See also specific topics
Diagnostic process, 25 applications, xi, 3, 4 –6, 7–8,
Disorientation, 17, 35, 36, 38, 62 121–122
Dopamine history, 94, 106 –107, 108–109
in neuroleptic malignant misconceptions, vii, ix, 89, 92,
syndrome, 71–72 115–116
in parkinsonism, 74, 101 primary vs. secondary use, 6 –7
Dopamine toxicity, 73 procedures. See Treatment, ECT
Drug dependence, as terminology, ix–x
contraindication, 9 Electroconvulsive Therapy Task Force
Drugs. See Medications (APA), 108–109, 116
DST (dexamethasone suppression Electrodes
test), 45 ECT, 28–30, 29f
Dukakis, Kitty, 37, 41 monitoring, 14, 15f
Dyskinesia, 67, 76. See also Electroencephalogram (EEG)
Movement disorders changes in, during and after
Dystonia, 67. See also Movement treatment, 95, 96f
disorders interseizure, 80, 134n11(ch8)
monitoring of treatment, 14
ECG. See Electrocardiogram Electromyogram (EMG), 31
ECS. See Electroconvulsive shock Electroseizure therapy (EST). See
ECT. See Electroconvulsive therapy Electroconvulsive therapy
EEG. See Electroencephalogram Electroshock, ix. See also
Effective treatment, 31, 96 –96 Electroconvulsive therapy
Efficacy, compared to other Electroshock therapists, x, 32–33
treatments, vii–viii, 4 Electrotherapists, x, 32–33
Elderly persons EMG (electromyogram), 31
depression, 44, 50–54 Endler, Norman, 23–24
ECT, 4, 5, 7 Endocrine glands, 98
memory loss, 35, 37, 39 Endocrine system, 95–99
recovery, 17 Epileptic seizure, x, 105
treatment schedule, 17 EST (electroseizure therapy). See
Electrical stimulus, characteristics of, Electroconvulsive therapy
27–28, 131n3(ch4) Ethics, 115–120
Electricity, medical research on balancing principles, 119
effects of, 111–112 beneficence, 117
Electric shock, for aversive code of medial ethics, 116 –119
conditioning, ix, 89 consent, 116
Index / 157
controversial image of ECT, psychopharmacology, 108–109

115–116, 119 shock therapies, 107–108
ECT availability and, 72, 118–119 Holiday of Darkness (Endler), 24
justice, ethics, 118–119 Holmberg, Gunnar, 39
medical insurance, 119 Hormones, 14, 95, 96, 97, 100
medications evaluation and, 119–120 Hospitalization for treatment, 19, 33
nonmalfeasance, ethics, 117
Examinations, pretreatment, 13 ICT. See Insulin coma therapy
Ill patients, safety in, 7, 8–9
Facilities for ECT, 33 Indications for ECT, xi, 3, 4 –6, 7–8,
Facility standards, ECT availability, 121–122
72, 118–119 Informed consent. See Consent
Fever therapy, 104, 136n28(ch11) Innovative therapies, current, 109–110
Film portrayals of ECT, 10 Insulin, 14, 96 –97
Fit, defined, x Insulin coma therapy (ICT ), ix, 76,
Fractures, 26 107–108, 115
Intellectually disabled children. See
Generic names of medications, Mental retardation
126 –127 International Psychiatric Association
Georgetown mantra, ethics and, for the Advancement of
116 –119 Electrotherapy, 109
Geriatric depression, 44, 50–54 Interseizure electroencephalogram,
Government regulations, 12, 80, 134n11(ch8)
108–109, 116, 130n6(ch2) Intracranial masses, 84
Grand mal seizure, x, 84, 95, 99, Intubation, 26
111–112 Involuntary treatment, 12–13, 60,
130n6(ch2)
Heart monitoring, 14 Isoelectric narcotherapy, isoflurane
Heart rate, changes in, 31 anesthesia and, 112
History, 103–110
chemical convulsive therapy, 105–106 Joint Commission on Accreditation
concept of voluntary consent, 109 of Health Care Organizations
current innovative therapies, ( JCAHO), 33
109–110 Justice, ethics and, 118–119
early treatments, 103–106
electroconvulsive therapy, 94, Kiloh, Leslie, 51
106 –107, 108–109
fever therapy, 104 l-Dopa, 101
insulin coma, 107 Lithium, 14, 37–38, 54, 59, 61–62
lobotomy, 108 Lipótmezö, 105
prolonged sleep therapy, 103–104 Lobotomy, 108, 115
158 / Index
Magnetic seizure therapy (MST ), 113 Medical insurance, 119

Maintenance treatment. See Medications
Continuation treatment antipsychotic. See Neuroleptic drugs
Major depression, 43, 46 – 47, 58 for catatonia, 68
Malaria fever therapy, 104 consent for, 11
Malignant catatonia, 68–70. See also for depression, 44, 45, 48. See also
Neuroleptic malignant syndrome Antidepressants
Mania, 57–66 ECT compared to, vii–viii, 4
acute episodes, 60–62 evaluation of, 119–120
adolescents, 64 –66 history of use, 108–109
bipolar disorder, 57–59 limitations, vii–viii
case histories, 60–62, 62–64, 64 –66 for mania, 59, 61–62, 64, 65–66
catatonia in, 58, 59, 60, 65–66 memory impairment, 37–38
characteristics, 57 names of, trade and generic,
delirious, 22, 58, 59–60, 64 –66 126 –127
ECT effectiveness, 8, 32, 59–60, for neuroleptic malignant
61–62, 64 syndrome, 71–72
medications for, 59, 61–62 for parkinsonism, 73, 74
melancholic, 58 pretreatment evaluation, 13
one-syndrome vs. two-syndrome for psychosis, 76 –77. See also
models, 130n5(ch1) Neuroleptic drugs
with psychosis, 57, 62–66 in relapse prevention, 20
treatment outcomes, 22 for status epilepticus, 84
treatments, 59–60 withholding, during ECT, 14
typical patient history, 5–6 Meduna, Ladislas, 94, 105–106,
Manic delirium. See Mania, delirious 135n3(ch10), 136n12(ch11)
Manic-depressive illness, 57–58, 103. Melancholia. See Major depression
See also Bipolar disorder Melancholic mania, 58
Manic mood disorder. See Mania Memory loss/impairment, 34 – 42
Manning, Martha, 22–23 age, 35, 37, 39
Marijuana-induced toxicity, 81–82 anesthesia, 38–39
Mechanism of action, 94 –102 collaborative study, 30
early theories, 94, 105 electrode placement, 28
neuroendocrine theory, 99–102 exaggerated fears of, 12, 35–36
neurohormonal system, 95–97 individual factors, 39– 42
neurotransmitters and persistent, 36
neurohormones in mental personal experiences, 40– 42
illness, 97–99 prevention by oxygenation, 26, 35, 39
seizure as therapeutic event, 94 –95 psychiatric disorders, 36 –37, 40
Medical ethics, code of, 116 –119 psychotropic drugs, 37–38
Medical experimentation, 116 during treatment, 35, 42
Index / 159
Mental illness Neuroleptic drugs. See also

classification, 25, 130n8(ch1) Neuroleptic malignant syndrome
history of treatments. See History bipolar disorder, 59
memory impairment, 36 –37, 40 delirious mania, 64, 65–66
neurotransmitters and ECT and, 61–62, 77
neurohormones, 97–99 movement disorders and, 76
pregnancy, 82–83 schizophrenia, 62, 64
severity, duration, and number of usage of, 76 –77
treatments, 18 Neuroleptic malignant syndrome
theory of causes, 101 (NMS), 59, 64, 65–66, 70–72
treatments, vii–viii, 103–106, 109– Neurological conditions, ECT in, 84
110. See also Medications Neurosyphilis, 103, 104
Mental retardation, 89–92 Neurotransmitters, 97
Metrazol injections, 106, 107 NMS. See Neuroleptic malignant
Misconceptions, vii, ix, 89, 92, syndrome
115–116 Nonmaleficence, ethics and, 117
MMECT (multiple monitored ECT), 17
Monitoring, physiological, 14, 31 One Flew Over the Cuckoo’s Nest, 10
Monitoring electrodes, 14, 15f Oneirophrenia, 58, 133n11(ch6). See
Moniz, Egas, 108 also Delirious mania
Mood disorders, 4, 7–8, 43. See also Outcomes, 21–22
Depression; Mania Outpatient treatment, 11, 20, 33
Mortality Oxygen administration, in reduction
depression and, 44 – 45 of memory effects, 26, 35, 39
ECT and, 34 Oxygen monitoring, 14, 15, 31
Mouth guard (bite bloc), 13, 16
Movement disorders, 67–74 Parkinsonism, 67, 72–74, 101
antipsychotic medications, 76 –77 Patient experiences
catatonia. See Catatonia Dukakis, 41
indication for ECT, 4 –5 Endler, 23–24
neuroleptic malignant syndrome, film portrayals, 10–11
59, 64, 65–66, 70–72 Manning, 22–23
parkinsonism, 67, 72–74, 101, 114 practicing psychiatrist, 10
MST (magnetic seizure therapy), 113 Styron, 40
Multiple monitored ECT (MMECT), 17 Patient selection, 4 –5
Muscle relaxants, 15, 26 Pediatric patients. See Adolescents;
Children
Nash, John, 58 Personality disorders, 9
Neuroendocrine system, 95–97, 98f Pharmaceutical industry, 119–120
Neuroendocrine theory, 99–102 Pharmacologic coma, 84
Neurohormones, 97 Physicians, ECT qualification for, 32–33
160 / Index
Physiological monitoring, 14, 31 Recovery period, 16

Postpartum depression, 82–83 Recurrence of illness. See Relapse
Post-treatment restrictions, 17 rates
Pregnancy, 7, 13, 82–83, 134n14(ch8) Refusal of treatment, 12–13
Pretreatment examinations, 13 Regressive ECT, 17
Procedure for ECT, 3– 4, 15–16, Regulations. See Government
27–31 regulations
Prolactin, 95, 134n17(ch8) Relapse prevention, 19–21
Prolonged sleep therapy, 103–104 Relapse rates, 18, 19–20, 30
Pseudodementia, 8, 36, 37, 44, 51 Reversible dementia. See
Psychiatric disorders. See Pseudodementia
Mental illness Right unilateral electrode
Psychiatric treatment, consent placement ECT (RUL ECT),
and, 11, 116 19–20, 28–30
Psychopharmacology history, 108–109 Rigidity, in parkinsonism, 73–74, 114
Psychosis, 75–77 Risk, consent and, 12
acute, 8–9, 78–79 Rosenberg, Leon, 55
acute toxic syndromes, 81–82 RUL ECT. See Right unilateral
case histories, 78–82 electrode placement ECT
in chronic schizophrenia, 79–81
ECT for, 8, 76 –77 Safety of ECT, vii, 7, 34, 134n14(ch8)
insulin coma therapy, 76 Sakel, Manfred, 107
mania, 57, 62–66 Salivation, 26
medications, 76 –77 Schizophrenia
typical patient history, 5 catatonic type, 68
Psychosocial therapies, limitations chemical convulsive therapy,
of, vii–viii 105–106
Psychotherapy sessions, during chronic, case history, 79–81
treatment, 21 ECT effectiveness, 8, 76
Psychotic depression. See Delusional neuroleptic drugs, 62, 64
depression positive and negative signs, 79
Psychotic disorders. See Thought treatment outcomes, 22
disorders Sedative drugs, memory
Psychotropic drugs. See Medications impairment and, 37
Public prejudice against ECT, 21, Seizure disorders, 83–84
108, 119 Seizures
chemical induction, 27, 105–106
Rapid cycling mania. See Delirious defined, x
mania drug levels, 14
Rapid neuroleptization, 59 duration, 31
Index / 161
electrical stimulus for induction, Symptom relief

27–28, 107 vs. cure, 25–26
electroconvulsive shock, x and treatment length, 18–19
hormone release, 14, 99–102 Syphilitic infection, 103, 104,
monitoring, 31, 95–96 130n8(ch1)
physiological changes during, 31 Systemic illness, safety in, 7, 8–9
as therapeutic agent, 94 –95
Seizure threshold, 27, 30, Taylor, Michael A., x
134n17(ch8) Terminology, ix–x
Selective serotonin reuptake inhibitors Texas legislation, 12, 130n6(ch2)
(SSRIs), 72 Thorazine, 59, 76, 107–108
Self-injury, in mental retardation, 91–92 Thought disorders, 4, 32, 75–79. See
Shock: The Healing Power of also Psychosis; Schizophrenia
Electroconvulsive Therapy Thyrotropin-releasing hormone
(Dukakis), 41 (TRH), 101
Shock therapies, 107–108 Toxic serotonin syndrome, 72
Side effects, 34, 40– 41. See also Toxic syndromes, acute, 81–82
Memory loss/impairment Trade names of medications,
Sleep, prolonged, 103–104 126 –127
Speech, minimizing effects on, 28 Transcranial magnetic stimulation
SSRIs (selective serotonin reuptake (TMS), 112–113
inhibitors), 72 Treatment, ECT
State laws. See Government delays in, 5–6
regulations duration, 4
Status epilepticus, 83–84, effectiveness criteria, 31–32
134n17(ch8) frequency, 17–18
STEP-BD (Systematic Treatment guidelines, 6 –7
Enhancement Program for maintenance. See Continuation
Bipolar Disorder), 59 treatment
Stroke, depression after, 84 outcomes, 21–22
Stupor preparation, 13–15
depressive. See Catatonia procedure described, 3– 4, 15–16,
pseudodementia, 51 27–31
Styron, William, 40 scheduling, 13
Suicide Treatment, of mental illness
cortisol levels, 45– 46 options, vii–viii
depression, 45– 46, 54 –56 psychotropic drugs. See
efficacy of ECT in prevention, Medications
54 –55, 56 rejected, 103–106
risk factors, 54 unproven, 109–110
162 / Index
Treatment facilities, 33, 72, 118–119 Unilateral nondominant ECT. See

Treatment resistance, 18 Right unilateral electrode
TRH (thyrotropin-releasing placement ECT
hormone), 101
Tricyclic antidepressants, memory Vagus nerve stimulation ( VNS),
impairment, 37, 38 113–114
Ventricular system of brain, 100
Undercurrents (Manning ), 23 Voluntary consent. See Consent
Unilateral electrode placement.
See Right unilateral electrode Wagner-Jauregg, Julius, 104
placement ECT Women, pregnant. See Pregnancy

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Electroconvulsive Therapy

René Magritte: “La Clairvoyance.”

The voyage of discovery lies not in seeking new horizons

Max Fink, M.D.

Oxford New York

Copyright © 2009 by Max Fink, M.D.

Published by Oxford University Press, Inc.

Originally published as Electroshock: Healing Mental Illness

E lectroconvulsive therapy (ECT) is an effective and safe treatment for

conducted on ECT can consult the publications cited in the endnotes

Because ECT is a technical discipline, it has spawned its own jargon.

Electroconvulsive shock or ECS is the term applied to the experimen-

I include several thumbnail sketches of the stories of patients as examples

catatonia and on melancholia, two syndromes that are most responsive to

writing. Alan Edelson, the publisher of Raven Press, encouraged me to

The ﬁgures in this book are credited as follows:

Men ought to know that from nothing else but the

E lectroconvulsive therapy (ECT) is an effective medical treatment for

heart rate, blood pressure, blood oxygen concentration, and degree of

For Whom Is ECT Useful?

Electroconvulsive therapy has been used safely to treat emotional disor-

of catatonia, the excitement and sudden, purposeless movements of mania,

When Might ECT Be Considered?

or excitement compels physical restraint or large doses of neuroleptic or

For Whom Is ECT Appropriate?

What Conditions Respond to ECT?

manic-depressive illness. Adults who were melancholically depressed and

What Conditions Interfere with Effective ECT?

vascular malformation requires special attention to the control of blood

The Patient’s Experience

With the modern technique of adequate anaesthesia

T he popular images of electroshock presented in the media reﬂect

Understandably, the patient may be hesitant about the ﬁrst treat-

Patients Must Consent to Treatment

A consent form, voluntarily signed by each patient, is a necessary part of

Consent is usually given for a speciﬁed number of treatments, but

Understandably, patients want to make important decisions about their

Before administering anesthesia or ECT, the physician obtains a history

Preparation for Treatment

Figure 2–1. Monitoring and stimulating electrodes for treatment.

The mouth guard, made of rubber or plastic, is held in the patient’s

Restrictions in Behavior After a Treatment

the caretaker (a friend or family member) to monitor the patient’s activi-

The schedule of treatments has been developed through experience. At

Recovery from the Illness

A depressed patient usually reports the return of appetite and restful

will be needed, but improvement is best judged by reports of mood and

Maintenance treatment is necessary after recovery to prevent relapse.

Electroconvulsive therapy is prescribed for many illnesses. The melan-

Everyone is hesitant about the ﬁrst treatment, so some trepidation is en-

symptoms worsened and suicide dominated her thoughts. After half a

Dr. Manning successfully completed a course of treatment, returned to

Dr. Endler eventually recovered, returned to work, and published Holiday

The Treatment Technique

All things are difﬁcult before they are easy.

T he decision to recommend ECT is difﬁcult, much like the decision

syndromes, or clusters of symptoms. The relief is provisional, however,

these changes. Some physicians prefer that the medication be given by

The purpose of the electrical stimulus is to induce a brain seizure. Elec-

Figure 3–1. Electrode placements.

Unilateral ECT, however, is clinically less effective, and patients do

How do we judge whether a particular treatment will have the desired

Where Is Treatment Carried Out?