Electroconvulsive Therapy: A Guide for Professionals and Their Patients

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

Author: Max Fink MD

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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 Oxford University Press, Inc., publishes works that further Oxford University’s objective of excellence in research, scholarship, and education. Oxford New York Auckland Cape Town Dar es Salaam Hong Kong Karachi Kuala Lumpur Madrid Melbourne Mexico City Nairobi New Delhi Shanghai Taipei Toronto With offices in Argentina Austria Brazil Chile Czech Republic France Greece Guatemala Hungary Italy Japan Poland Portugal Singapore South Korea Switzerland Thailand Turkey Ukraine Vietnam

Copyright © 2009 by Max Fink, M.D. Published by Oxford University Press, Inc. 198 Madison Avenue, New York, New York 10016 www.oup.com Oxford is a registered trademark of Oxford University Press All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of Oxford University Press. 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.

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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, memorystealing, 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 treatments 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 treatment 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 procedures 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 educate patients about what they can expect. This book is also meant to help students, medical practitioners, and mental health workers to intelligently 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 standards for effective treatment, culled from one doctor’s experience of over half a century in studying the mechanism of ECT and its clinical applications. 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 recommendations given here. When I discuss medications, I use their trade names as much as possible 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, electroseizure 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 connotation 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. Impressed 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 unsuccessful. 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 experimental 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 epileptic 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 necessary 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 electrotherapist 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 admitted 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 Robert Helen Dr. Rosenberg Sarah David Philip Gerald Jeffrey Monroe Jefferson Steven Eric Peter Claudia Donald Quinn

Depressive melancholia Psychotic depression in a 68-year-old scientist Pseudodementia and catatonia Suicide risk averted with treatment Acute manic episode Mania with psychosis Delirious mania in a 17-year-old adolescent Acute catatonia in a 20-year-old man Malignant catatonia: the neuroleptic malignant syndrome ECT in a patient with parkinsonian rigidity Acute psychotic episode in an 18-year-old Chronic schizophrenia Toxic psychosis and delirium in a 15-year-old Depression in a 16-year-old adolescent Mental retardation in a 23-year-old Self-injurious behavior in a 14-year-old 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 syndrome,5 toxic serotonin syndrome,6 pseudodementia,7 delirious mania,8 delirium,9 Tourette syndrome,10 catatonia,11 melancholia,12 and schizophrenia.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 appreciate 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, including 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 Hospital; Turan M. Itil and George Ulett at the Missouri Institute of Psychiatry; Richard Abrams, Michael A. Taylor, Jan Volavka, Jiri Roubicek, Rhea Dornbush, Peter Irwin, and Donald M. Shapiro at New York Medical 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 Rummans, Samuel Bailine, John Rush, and Mustafa Husain. My collaborations in the past decade with Michael A. Taylor in writing on catatonia and melancholia, with Jan-Otto Ottosson in writing on ethics in ECT, and my interest in the history of ECT, psychiatric classification, 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 International 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 University 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 placement 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, xv

75

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? thirteen

Is ECT Practice Ethical? Appendices, Notes,

129

Bibliography, Index,

121

153

139

115

111

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 epileptic 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 muscles 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 experiences 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 immediately 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 similar 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 disorders in patients of all ages, from children to the elderly, in people with debilitating 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 interferes 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 improve patients’ health as quickly and safely as possible, for many conditions 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 history 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, situational maladjustment, personality disorder, drug dependence, or sociopathy. 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 already 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 suffer 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 holiday was suggested. A family physician prescribed the latest antidepressant 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 recommend family therapy. If a child is diagnosed with attention deficit disorder or autism, families will consider special schooling. When self-injury, screaming, 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 unsuccessful courses of psychotherapy and medication. This delay is unfortunate because by the time ECT is begun the illness is fully established and difficult 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 medication 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 treatment 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 psychiatric 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 experience 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 circulatory 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 conditions 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 varieties 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 melancholia or a separate disorder identified as bipolar disorder is in dispute.5 Melancholic depression is present either in the same episode or in sequential episodes (Chapter Six). Catatonia is a motor syndrome characterized by mutism, negativism, posturing, staring, and repetitive acts.6 The syndrome is frequently recognized in patients with mania and depression, but catatonia is also a feature of some toxic states (Chapter Seven). Psychosis also improves with treatment, especially when it is a feature 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 identifiable 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 specialized care. For instance, the safe treatment of patients with recent myocardial 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 vascular malformation within the skull, once thought to be an absolute barrier 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 understood 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 treatment 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 substance 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 treatment. 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 procedure is uncommon in psychiatric practice, and was developed to address concerns about abuse at a time when public distrust of governmental authority was widespread and had affected the physician-patient relationship.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 discontinued at any time, even before the specified number of treatments is completed. This protection clause ensures that all treatments are accepted 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 psychiatrists 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 reports 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 “involuntary 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 procedures, devised for the protection of the mentally ill, may actually have detrimental consequences.7 They inhibit and delay the use of ECT, perhaps 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 increase its risks. The physician accordingly alters the medications used during 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 commonly 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 anesthesia. 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 treatment. 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 intravenous 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 electroencephalogram (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 saturation. 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 psychiatrist to record the duration of the muscular signs of the seizure. The doctor or the nurse usually explains the reasons for each connection: the chest (ECG) electrodes and blood pressure cuff permit continuous 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 concentration 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 systolic 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 electrocution 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 exercise. A mild analgesic like aspirin usually relieves this discomfort. A backache 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 activities and make sure that they are within the patient’s capacity. More difficult is determining when the patient is ready to make farranging 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 administered to severely psychotic patients. Some patients recovered from their illness but the effects on orientation and memory were severe, often requiring nursing care for feeding and toileting. Regressive ECT is no longer 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 occasionally 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 treatment resistance) does not affect the outcome of ECT or the number of treatments.11 Symptoms are often relieved by a few treatments, but sustained recovery 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 antidepressant medications were continued. For depressed patients who improved 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 restlessness 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 dissipate 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 another 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 patients 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 continuation 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 similar to the prescription of insulin for diabetes or the chemotherapy treatments 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 prescribed 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 sixmonth 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 medications now to be effective and to prevent a relapse. Years ago, reports of occasional 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 adequate 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 treatments at the first sign of symptom recurrence and continue until the benefits 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 psychotropic 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 recovery 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 melancholic 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 reduce 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 progressed 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 delusions, 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 treatments administered properly. Absence of quick relief indicates inadequate treatment or improper diagnosis.

Patients’ Recollections Everyone is hesitant about the first treatment, so some trepidation is entirely 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 responsibilities. 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 published 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, staking 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, registering 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 pressure, 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

24 / Electroconvulsive Therapy 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 patient’s symptoms goes through an intellectual process similar to that of a detective solving a mystery. The doctor listens to the patient’s story, finding 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 disease, 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 administering anesthesia, in selecting the amount of electrical energy and the location of the electrodes for stimulation, and in monitoring bodily effects for safer treatments. The following descriptions are meant to answer questions 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 convulsion 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 himself, 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 metabolized 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 during treatment. A substance like Robinul or atropine, administered intravenously 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. Electricity 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 characteristics 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, gender, 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 quality 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 increasing 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 current 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 righthanded 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 electrodes 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 either 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 dominance 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 persons. 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 remission, 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 electrode 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 immediate effect of the electrical stimulus is to slow the heart rate. The developed 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 slowing 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 orientation, accepting the poorer remission rates of unilateral treatments. The additional weeks of illness and expense, and the physical demands of additional treatments, must be balanced by the immediate temporary reduction in confusion. Psychiatrists today differ in their recommendations for nonpsychotic depressed patients, some advocating unilateral ECT at maximum 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 systemically ill patients, in whom a quick result with a minimum number of treatments 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. Normal 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 normal 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 mercury (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 convulsion 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 interrupted 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 recorded 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. Careful 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 convulsion, 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 treatment 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 considers 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, attention to the treatment schedule is necessary. Daily treatments are often necessary, with a return to a more usual schedule when the severe symptoms 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 psychiatric 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 Psychiatric 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 treatment 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 excitement, 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 psychiatrist 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 relieved 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 sometimes 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 delivering 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 critical 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 patients 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 devastating 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 reason 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 anesthesia 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 committed 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 recovery. 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 treatment, recollections and memory test scores improve. An example of dramatic recovery of memory is seen in patients with pseudodementia, a severe form of melancholia in which memory is seriously impaired. With effective 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 preoccupied 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 associated 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 association of the treatment with its effects on memory is strengthened. Another cause of memory loss, though not often recognized or acknowledged, 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 sedatives 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. Recall may then be impaired for days. This is particularly true of the longeracting 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 disorientation. 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 reduced 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 already 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 confused 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 family, she may appear sleepy, vague, distant, and uninterested.


The anesthetic has both immediate and sustained effects on memory. 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 adequate levels of oxygen; patients sometimes stopped breathing for minutes, 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 concomitant 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 feature of treatment; in modern applications, the blood concentration of oxygen 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 technical 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 impairment 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 progressed 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 disconnections; as I have said, there was now something that resembled bifurcation of mood: lucidity of sorts in the early hours of the day, gathering murk in the afternoon and evening. . . . Rational thought was usually absent 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 highenergy 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, foreign 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 laughable. 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

Side Effects and Memory Issues / 41 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 completely closed, with one amusing exception. Several months afterwards, at a scientific meeting, I met a psychiatrist whose face seemed very familiar, 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 decades 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 outpatient 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 popular uses of the term “depression” is not what bothers me most. More important to me is being unable to think properly. Although I was receiving 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 behaviour 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 interventions 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 undetectable 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 developed 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 benefits, 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 sadness, 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 hopeless, 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 depression. These disorders require intensive treatment and almost always hospital care. A depressed patient is commonly unaware of the day’s events, registers little of what happens around her, and has a compromised memory. This form of depression can be difficult to distinguish from an Alzheimertype 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 withdrawal, 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 pseudodementia respond to tricyclic antidepressant drugs, but psychotic depressed patients require high doses of both antidepressant and antipsychotic medicines 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 suicide. 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 patients treated with ECT than among those treated with antidepressants (0% versus 10%) or those who had no history of such attempts (1.1% versus 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 cortisol levels normalize and, with relapse, became abnormal again. The connection 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 likelihood 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 cortisol 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 illness 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, responding once to medication and twice to ECT. In this episode, medications 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 treatment 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 planning 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 remained 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 responsive as melancholic depression, we cannot predict the necessary number of treatments. She received 12 treatments for a sustained effect 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 unsuccessful 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 patients hospitalized for depressive mood are psychotic.7 A delusional depression responds slowly and poorly to medications alone, even when administered in high doses of combinations of antidepressant and antipsychotic 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 delusional 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 recovered 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 failure 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 referred 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, contrary 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 disheveled, 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 condition 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 described 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 showered 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 attended 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 delusional melancholic depressive illness. Robert’s loss of weight, dehydration, 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. Relapse 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 ethical 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 patient 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 medical 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 irreversible 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 distinguishable 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 considered. 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 assess the history of a patient who seems to have rapidly developed dementia, 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 consideration 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 decrease 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 dementia 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 earlier, 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 incontinent of both bladder and bowel. Her husband retired from work to devote 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 rhythmic 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 noncommunicative, had lost weight, and had failed to care for herself or her family. Electroconvulsive therapy combined with unspecified antipsychotic


medications brought improvement. Five years later, she was again withdrawn 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 consequence 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 Haldol 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. Discharge 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, staring into space; she answered questions with “I don’t know,” and no longer 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 treatments, 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 characteristics 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 illness, 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 treatment 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 medications 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 psychiatric 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 psychoanalytic 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 National 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 support. Newspapers frequently report the suicide of public figures whose treatment was limited to psychotherapy or prescribed medications. Families 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

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atients suffering from mania are overactive, intrusive, excited, and belligerent. They may believe that they have special powers, are related to public figures, and can read the minds of others. They spend money lavishly. Voices on the radio or television are sometimes understood as personal communications. They speak rapidly, with illogical and confused thoughts, move constantly, and write page after page of nonsense. 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 parents are not their real parents, asserting that they have royal blood. They believe that they can predict the future. They know that others are watching 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 conceived 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 subtypes. The variety of symptoms that admit the diagnosis of bipolar disorder 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 manicdepressive 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 periods of depression, or occur as simultaneous mixed episodes of depression 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 solving 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 striking 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 inappropriately, is sometimes naked, and wanders about the streets. His hallucinations 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. Repetitive behaviors are prominent, such as the cycling behavior around the college 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 official classification as bipolar I disorder. About 80% of patients with mania have had or will have depressive episodes. Of the patients with depressive 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 medications, 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 verifiable diagnosis.5 Although ECT offers effective and rapid relief, especially for the severe forms of the illness, it is considered only as a last resort. The responsive conditions include the melancholic depressed phase or the manic phase of the conditions described as mania, mania with psychosis, or delirious 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 suicide. 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 behavior 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 Disorder) 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 intervention 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 patients (66%) remitted or showed marked clinical improvement.8 Indeed, for the psychotic, delirious, mixed depressive, rapid cycling, and catatonic 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 acknowledged 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 antipsychotic 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 protection, 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 medicines thinking they were no longer needed. At the hospital she was friendly, walked around the ward singing loudly, and laughing inappropriately. 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 nonsensical. 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 continued. 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 recalled 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 delirious 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, because 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 inappropriately 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 delusional thoughts, hallucinations, excitement, and aggression are characteristic 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 prescribed for manic patients, but lithium, anticonvulsants, and ECT are also accepted. A patient has much to gain from the multiple options for treating 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 hospitalized 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 psychiatric 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, showered, and asked for clean clothes. His demeanor improved. After 12 treatments, 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 treatment 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 neuroleptic 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 hospitalizations, 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 evolution, 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 pressure 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 neuroleptic 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

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atients with mental disorders exhibit a range of abnormal movements. 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 patient’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, unusual posturing, negativism (refusal to obey simple commands), mutism (persistent silence), echolalia (repetition of what has been said), echopraxia (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 sedative 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 Psychiatric 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 medical 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 neuroleptic 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 barbiturate 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 antipsychotic and hallucinogenic drugs. In recent surveys of patients admitted 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 staring 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 rejected 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 treatment, 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, insisting that he was well. He agreed to continue taking lithium. After two weeks in school, Gerald was brought back to the hospital, 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 manufacturing 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 recovery, and he refused further treatment. Since the benefits of ECT, like those of psychotropic medications, are transient, patients require continuing treatment for a sustained effect.

NMS Variant of Malignant Catatonia The sudden onset of fever, motor rigidity, negativism, mutism, and instability 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 precipitant has been identified, usually one of the high-potency neuroleptic drugs like Haldol, Prolixin, or Navane. Cases have been observed in association with almost all neuroleptic drugs, including the atypical antipsychotic 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 decided to change his medication to a new atypical neuroleptic, Zyprexa. One month later Jeffrey became psychotic, and the traditional neuroleptic Trilafon was prescribed. He quickly became febrile, mute, and rigid, the diagnosis of NMS was made, and he was transferred to a tertiary care facility.


Neuroleptic medications were discontinued, and Jeffrey was treated on a medical service with large doses of Parlodel and Dentrium. His repetitive motor movements prompted the diagnosis of epilepsy, so anticonvulsants 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 administered every other day. After the fifth treatment, Jeffrey was alert, responsive, 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 exhibited 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 benzodiazepines and to consider ECT stemmed from the mistaken belief that NMS is a specific entity, separate from catatonia, with a different treatment algorithm. Whether NMS is a specific consequence of an excessive 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 treatment 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 unhappy 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 recognized as a response to some of the antidepressant drugs known as selective 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 infection. To separate the effects of ECT in parkinsonism from its effects in depression, Swedish scientists studied nondepressed hospitalized patients suffering from a severe form of parkinsonism. Using real and sham treatments, they found that real ECT relieved the rigidity of the syndrome 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 toileting. 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 parkinsonism, they gave their consent. He continued his antiparkinson medications 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 antiparkinson 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 released by the treatments. One week later the ECT treatments were reinstated, 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 period 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 continued 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, vascular or infectious disease, or prolonged use of neuroleptic drugs. Electroconvulsive 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 deficient in patients with parkinsonism.

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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

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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 (hallucinations, illusions) that are not based upon reality, and beliefs that others 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 frequently 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 notice, 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 helpful 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 “schizophrenia” 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 antipsychotic drugs were introduced in the 1950s. Comparisons of drugs and ECT3 and insulin coma4 found the treatments to be equally effective. 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 periods, 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 hospitalized 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 standard antipsychotic drugs.6 Despite these limitations, antipsychotic drugs are prescribed much more often than ECT. True, they are less expensive in time, cost, and effort. But when a drug course is ineffective, the physician may change to another medicine, combine medicines, or prescribe the latest product approved 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 melancholia 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 interface of seamless fatty membrane between the blood vessels and brain cells that prevents some substances from penetrating the cells. This interface, called the blood-brain barrier (BBB), prevents medications from reaching the brain cells of some patients. Physicians then must use massive drug doses to achieve even a minimal effect. Seizures, however, expand 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 cooperative 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 activities 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. During the summer he completed his freshman course requirements, and in the fall he returned to college. During the next three years he performed 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 medications 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 established 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, including trials of new medications, have failed.10

Chronic Schizophrenia Of the five types of schizophrenia identified in the psychiatric classification, 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, flattened 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 excitement. He first became ill during his second year at college and improved 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 bathing 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 Prolixin 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 difficult 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, including each newly discovered neuroleptic, have been tried in place of ECT, but without success. For more than 18 years, Steven has been in continuation treatment, with over 300 treatments by the year 2008.


comment. When Steven was first treated with ECT, we did not recognize the significance of the catatonic signs, nor did we prescribe benzodiazepines. Our later recognition of the importance of these signs led to his present regimen. Most electrotherapists would not have recommended 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 cannabis (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 necessitated continuous nursing protection. At times, he required physical restraint. A similar episode had occurred five months earlier. Eric had experienced a grand mal seizure and had been admitted to a community hospital, where he was described as belligerent, aggressive, and hypersexual. 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 recovered and returned to school after three weeks. At this admission, ECT was recommended, and with parental consent, Eric received three treatments in four days. By the second treatment, 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 allowed 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 suicidal 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 emotional 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 depression, 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. Congenital 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 medications. 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 certificate [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 improvement 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 complications. 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 during 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 particularly valuable for its ability to resolve such conditions rapidly and effectively.

Intractable Seizure Disorders Seizure disorders occasionally become intractable and persist as uncontrollable 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 associated 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 benzodiazepines or barbiturates. When these fail, profound and lengthy anesthesia requiring intubation and mechanical ventilation is induced with a barbiturate 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 induction 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 ongoing 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 neurological 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 intracranial masses and normal cerebrospinal fluid (CSF) pressures. In cases where increased intracranial pressure is suspected or measured, neurosurgical 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 poststroke 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

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Pediatric ECT

The child is father of the man. —Wordsworth1

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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 between 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 recommend 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 history 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 acetaminophen (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 consultations 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.

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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 interest 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 increased 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. Psychotherapy, 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 treatments 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 parents 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 disease. 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 reports. 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 periodically 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 cooperation 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 followup 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, catatonia, and intractable depression or mania not treatable by other means.

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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 treatments as do the psychiatric ill of average intelligence. Restraints and high doses of antipsychotic and sedative drugs are usually prescribed for uncontrollable 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 psychiatrists do not administer ECT to patients under guardianship, fearing disapproval 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 adverse conditioning therapy widely used among the mentally retarded. Those experiments, rightly condemned, are no longer in use, but reports still appear 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 misinformation 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 associated with somnolence. An EEG showed paroxysmal activity, and the anticonvulsant Tegretol was prescribed. A psychological evaluation assessed her intelligence test score at 50. Tantrums, aggression, and periodic uncontrollable excitement at age 16 warranted another EEG, which was normal. Claudia’s behavior 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. Although consultants considered ECT a reasonable course of treatment, as did her parents, no electrotherapist was willing to administer it, despite 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 depressed 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 appetite returned, she was tractable, and she responded to questions and directions. 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, taking 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.

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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. Electroconvulsive therapy allowed her to remain at home, and her parents, grateful for the treatment, willingly described their experience in a letter 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 slashing 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 patients 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. Donald’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 addition 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 disorders to preclude further treatment. Consent for ECT was obtained from his legal guardian.


After the sixth of twice-weekly treatments, the screaming, scratching, 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 progress. Anticonvulsants were prescribed, and no life-threatening behavior was evident for two years. comment. Self-injurious behavior is common in children and adolescents with intellectual disability and autism-spectrum disorders. Such behavior responds favorably to ECT. Good responses, however, are shortlived unless treatments are continued. It seems likely that the reported relapses occurred because of the short courses of ECT that were common before the 1990s. Continuation ECT is now more readily available, 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 belief 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. Apprehension about the abuse of the mentally ill with electricity that occurred 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

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of mood and slowing of movements. Autism had been diagnosed at age four, and Quinn received educational, speech, and social-skill interventions 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. Abnormal 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 facial expression were further slowed. Over the next four months he spoke less and exhibited frequent motor tics, rapid blinking, and head turning. 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 “watching 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 labeled 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 spontaneously, 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 antagonism between mental illness and seizures, an antagonism we no longer consider credible. But though we may smile at this belief, we acknowledge 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, evaluate 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 symmetrically 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 functions that go awry are those that are controlled by the body’s neuroendocrine 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 illness 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 consider diabetes, a systemic disorder that follows the failure of the specialized 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, norepinephrine, acetylcholine, serotonin, and dopamine have been identified as active neurotransmitters in the intercellular spaces. A stimulated nerve cell momentarily releases the chemical at its ends; then the next cell is stimulated (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 (peptides) 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, specialized cells in the pancreas, and the sex glands of the ovary and testes (Fig. 10–2). These two systems, neurotransmitter and neuroendocrine, are intimately 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 normal 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 disappear. (Only to reappear when the traveler again crosses time zones as he returns home.) Dysfunction in any endocrine gland has consequences. If the thyroid 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 electrical 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 systemic and mental effects have been associated with deficiencies or excesses 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 hypothalamus to discharge its hormones at the same time that the brain’s central 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 materials they need to function properly. During ECT, large amounts of hypothalamic 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 hypothalamus 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 released by seizures become available to brain cells. The brain consists of two large hemispheres that sit atop a central brain stem. These hemispheres 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 (choroid 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 select 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 availability 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 prescribe 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 dopamine, 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 thyrotropin-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 fluids be examined before and after seizures to find substances that either appear anew or are changed in amount. The identification of such substances will mark those that we may ethically search for in patients. Such a search should make possible the development of an effective replacement 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 neuropsychiatrists had identified three mental illnesses that dominated the clinical scene: neurosyphilis (described as dementia paralytica), dementia praecox (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, restraining 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 hospitals 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 relieve severe depressive and agitated states. Agitated patients were kept in a stupor for days with continuing high doses of barbiturates, with periods

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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 procedures. 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 become 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 pasteurization 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 developed 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 Medicine in 1927.5 Inducing relapsing fever instead of malaria, or seeking to develop protein sensitivity by injections of gonococcal or typhoid vaccines, tuberculin, 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, circulatory collapse, cerebral anoxia, and surgical shock—led to high death rates. Despite the low success rate and the high incidence of complications 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

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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 antagonism 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, however, 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 seizureinducing 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 Psychiatric Research Institute, believed that dementia praecox was an irremediable inherited genetic disorder. That dementia praecox might be treatable was academic heresy. Fearing criticism, Meduna moved his research activities 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 psychotic, 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 symptoms were sufficiently relieved to allow him to return home. A recent examination 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 visitors from Italy, Germany, India, Australia, and the United States. In May 1937, he discussed Metrazol treatment at an international meeting organized by the Swiss Neuropsychiatric Society.14 He was invited to lecture 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 designed 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 became 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 psychotic 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 effective in relieving psychosis. The coup de grâce came with the publication 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 Thorazine became a principal treatment for the psychoses. Lobotomy (leucotomy) was introduced following reports that surgical removal of the brain’s frontal lobes pacified chimpanzees. The Portuguese neurologist Egas Moniz, who developed the procedure in Lisbon in 1935, thought that such surgeries would tranquilize agitated and obsessive 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 lobotomy, 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 lobotomy. 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 treatments 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 lobotomy 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 centers to reestablish ECT and practitioners to join together in an advocacy group, the International Association for the Advancement of Electrotherapy, 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 secondary 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 figures. 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 dismay 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 somatic 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 insensitivity 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 unproven treatments of the psychoneuroses and psychoses. In the absence of sound principles on the causes and bodily effects of psychiatric illnesses, it is to be expected that the trials are highly imaginative. Devotees of the talk therapies turn to psychoanalysis, individual and group therapies, 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 deprivation, continuous sleep, electrosleep, acetylcholine infusions, nitrous oxide and ether inhalation, histamine injections, megavitamins and complex diets, atropine and scopolamine coma, hemodialysis, intravenous lysergide (LSD), methamphetamine and megimide, hypothermia, photoshock, 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 administered seizure (FEAST) and nonseizure (FEAT) therapy, cortical electrical stimulation (CES), transcranial direct electrical current (tDEC), and responsive neurostimulation (RNS). More recently, imaginative brain stimulation methods labeled transcranial 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 followed popular science beliefs in the potency of electricity alone and administered 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 innovative. 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. Isoelectric 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 depression 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 enthusiastically promoted as replacements for ECT, that is, as ways to induce 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 details 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 sustained 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 threshold, 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, compared 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 magnetic 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 device discharges low-voltage stimulations similar to those of the pacemakers 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 stimulating 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 commercial use over the disapproval recommended by the FDA staff and consulting committees. This aberrant approval was the subject of hearings by the Grassley Committee of the U.S. Senate.14 After these hearings, 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 patients 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 patients 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 stimulation 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 treatment 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 immediate risks of the treatment, for the risks and death rates are extremely low—almost certainly lower than the risks acknowledged for the psychoactive 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’ perception. Conflicts between believers in the biological basis of mental illness 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 Germany and the Soviet Union during the Second World War incited a worldwide 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 patient 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 appropriate 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 psychiatric treatments, consent is implied in the patients’ voluntary admission 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 opportunity regardless of age, gender, color, religion, or wealth).

Beneficence As we have seen in the previous chapters, ECT is an effective treatment 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 mitigated by sedation and anesthesia, just as they are for invasive medical procedures. 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 methods of treatment that select minimal energies, careful electrode placement, 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 principle 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 judgments, 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 treatment, 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 treatment. 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 trials, 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 unduly 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 benefits of ECT are well defined, offering severely ill patients a chance for recovery. The risks are few, and even a transitory loss of personal memories 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 professional ignorance of its benefits and by exaggerated fears of its risks. Because the primary medical obligation is to preserve life, it may be necessary 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 insurance support of medical care. By setting artificial guidelines on the number 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 treatment 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, nonmaleficence, 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 Substance-related disorders Anxiety and somatiform disorders Factitious disorders Dissociative disorders Sexual dysfunctions Sleep disorders Impulse disorders Adjustment disorders Personality disorders

123

[293.0, 290.xx, 294.xx] [303.xx, 291.x, 304.x, 292.x] [300.xx] [300.xx] [300.1x, 300.6] [302.xx, 625.8, 608.89, 607.84, 608.89, 625.8] [307.xx, 780.xx] [312.3x] [309.xx] [301.xx]


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 helping 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 recovery 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 patients 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 special 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 numbers, 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 occurring 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 Amidate Amytal Anapsine Anectine Artane Ativan Benadryl Brevital Cardiozol Clozaril Cogentin Dentrium Depakote

zolpidem etomidate amobarbital droperidol succinylcholine trihexyphenidil lorazepam diphenhydramine methohexital pentylenetetrazol clozapine benztropine dantrolene valproic acid, sodium valproate propofol venlafaxine amitriptyline isoflurane haloperidol

soporific anesthetic anesthetic/sedative anesthetic muscle relaxant antiparkinson sedative sedative anesthetic induces seizures atypical antipsychotic antiparkinson muscle relaxant anticonvulsant

Deprivan Effexor Elavil Forane Haldol

anesthetic antidepressant antidepressant (TCA) anesthetic antipsychotic (Continued)

127

Table Appendix 4 –1 (Continued) Brand Name

Chemical Name

Use

Indoklon Ketalar Klonipin Lamictal Lithobid Lunesta Metrazol Miltown Moban Nardil Navane Norpamin Pamelor Parlodel Paxil Pentothal Prolixin Prozac Risperdal Robinul Sinemet Sinequan Tegretol Tofranil Trilafon Ultiva Valium Versed Wellbutrin Xanax Zoloft Zyprexa

flurothyl ketamine clonazepam lamotrigine lithium eszoplicone pentylenetetrazol meprobamate molindone phenelzine thiothixene desipramine nortriptyline bromocriptine paroxetine thiopental fluphenazine fluoxetine risperidone glycopyrrolate l-dopa doxepin carbamazepine imipramine perphenazine remifentanil diazepam midazolam bupropion alprazolam sertraline olanzapine

induces seizures anesthetic sedative anticonvulsant anti-manic soporific induces seizures anxiolytic antipsychotic antidepressant (MAOI) antipsychotic antidepressant (TCA) antidepressant (TCA) dopamine agonist antidepressant (SSRI) anesthetic antipsychotic antidepressant (SSRI) atypical antipsychotic anticholinergic dopamine agonist antidepressant (TCA) anticonvulsant antidepressant (TCA) antipsychotic anesthetic sedative sedative anxiolytic anxiolytic antidepressant (SSRI) atypical antipsychotic

MAOI, monoamine oxidase inhibitor; SSRI, selective serotonin reuptake inhibitor; TCA, tricyclic antidepressant.

Notes

Preface to the New Edition 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.

Sakel 1938. Meduna 1937. Cerletti 1950, 1956. Kaufman 2007. Greenberg and Gujavarty 1985; Fricchione et al. 1990. Fink 1996. Bright-Long and Fink 1993. Fink 1999b. Fink 2000b; Malur et al. 2000. Trivedi et al. 2003. Fink and Taylor 2003. Taylor and Fink 2006. Gujavarty et al. 1987; Fink and Sackeim 1996. LaGrone 1990. Petrides and Fink 1996a. Greenberg et al. 1986, 1988. Thuppal and Fink 1999. Greenberg and Fink 1990. 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 twosyndrome model is described in Goodwin and Jamison (1990, 2007). The history of these developments is presented by Healy (2008). 6. Fink and Taylor 2006. 7. Fink and Taylor 2003; Taylor and Fink 2006. 8. The overlap of these syndromes suggests an interesting speculation. A syphilitic infection of the nervous system elicits many behavior syndromes, including 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 presentation 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 Hospital 1999; Dartmouth Hitchcock 2002; and Osborne 2006. 6. In Texas and California, where doctors are required to report ECT treatments, 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

8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23.

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). APA 2001; Abrams 2002. Rich, 1984; Abrams 2002. Petrides et al. 2001; Taylor and Fink 2006. Rasmussen et al. 2007. Sackeim et al. 2001. Fink 2005; Taylor and Fink 2006. Sackeim et al. 2001. Kellner et al. 2006. The results and conclusions are assessed by Fink and Taylor 2007. Prudic et al. 1990; Sackeim et al. 1990. Fink et al. 1996. Chapter Five, patient Helen. Chapter Eight, patient Steven. Mulsant et al. 1997; Rasmussen et al. 2006. Fink 1999b; Taylor and Fink 2006. Manning 1994. 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. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

Fuller 1732. Abrams 1997, 2002. Munk-Olsen et al. 2007. Shorter 1997; Shorter and Healy 2007. Rouechè 1974; Donahue 2000. These, and other examples, are discussed in Fink 2007. Dukakis and Tye 2006. Holmberg 1953. Styron 1990. A Practicing Psychiatrist 1965. Dukakis and Tye 2006, Chapter 9, pp. 156–63. Perkins 1996. Fink 2007.

Chapter Five: Depressive Mood Disorders 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.

Manning 1994. APA 1980; Taylor and Fink 2006. Taylor and Fink 2006. Taylor and Fink 2006. Taylor and Fink 2006. Carroll et al. 1981. Taylor and Fink 2006. Glassman et al. 1975. Avery and Lubrano 1979. Mulsant et al. 1997; Rasmussen et al. 2006. Ottosson and Fink 2004. Coffey et al.1991. Kiloh 1961. Hoch 1921. Fink 1999a; Bright-Long and Fink 1993. 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. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Duke 1992. Meduna 1950; Bond 1980; Fink 1999b; Taylor and Fink 2006. Nasar 1998. Goodwin and Jamison 1990; Taylor and Fink 2006, 2008; Fink and Taylor 2007. Taylor and Fink 2006, 2008; Fink and Taylor 2007; and the earlier critiques by Goodwin and Jamison 1990. Hermesh et al. 1992; Fink and Taylor 2003. Goldberg et al. 2007. Mukherjee et al. 1994. Ottosson and Fink 2004. Fink and Sackeim 1996. The augmentation of clozapine with ECT has case study support (Braga and Petrides 2005). 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. 2. 3. 4. 5. 6. 7.

Carpenter 1912. Fink and Taylor 2003. Fink and Taylor 2003; Mann et al. 2003; Caroff et al. 2004. Fink and Taylor 2003; Mann et al. 2003; Caroff et al. 2004. Ottosson and Fink 2004. Andersen et al. 1987. Zervas and Fink 1991; Faber and Trimble1991.

Chapter Eight: Other Uses: Psychosis, Pregnancy, and Status Epilepticus 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Shakespeare 1938. Petrides et al. 2001; Taylor and Fink 2006. Fink and Sackeim 1996. Fink et al. 1958. Kane et al. 1988. Kane 2004. Fink and Sackeim 1996. Christison et al. 1991; Wyatt 1991. Lieberman et al. 2005. 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. Indeed, 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 placenta 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, despite repeated seizures, with a failure of the biochemical inhibitory mechanisms 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 prolactin 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 termination 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. 2. 3. 4. 5. 6.

Shakespeare Wm: Hamlet, Act IV, Scene 3. Klaesi 1922. Scull 2005. Terry 1939. Wagner-Jauregg 1918. Dattner 1944; Duffy 1995.

136 / Notes 7. 8. 9. 10. 11. 12.

13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28.

Duffy 1995. Meduna 1985; Shorter and Healy 2007. Meduna 1937, 1985. Meduna 1935, 1985. Meduna 1985. 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 seizures were common in these early patients. Meduna 1937. Katzenelbogen 1938. Meduna, 1985. Weigert 1940. Cerletti 1950, 1956; Bini 1938, 1995. Cerletti 1956. Jessner and Ryan 1941. Abrams 1988; Shorter and Healy 2007. Fink 2003; Doroshow 2007; Shorter and Healy 2007. Fink et al. 1958; Fink 2003. Valenstein 1986; El-Hai 2005. Fink 1991; Shorter 1997. APA 1978. APA 1990, 2002. European Forum for ECT, Nordic Association for Convulsive Therapy. 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 enthusiasm for lobotomy is explored in many books including Valenstein 1986 and Pressman 1998.

Chapter Twelve: Is Brain Stimulation an Alternative to ECT? 1. 2. 3. 4. 5. 6. 7. 8. 9.

Santayana 1954. Finger 2006; Finger and Zaromb 2006. Parent 2004. Ulett et al. 1954; Fink 1979; Palmer 1981. Reynolds and Sjoberg 1971. Langer et al. 1985, 1995. Greenberg et al. 1987. George and Belmaker 2000; Lisanby 2004; Shorter and Healy 2007. Eranti et al. 2007.

Notes / 137 10. 11. 12. 13. 14. 15.

O’Reardon et al. 2007. Lisanby 2004. Lisanby 2004. Nahas et al. 2005; Rush et al. 2005. Grassley and Baucus 2005. Lisanby 2004; Kopell and Greenberg 2008.

Chapter Thirteen: Is ECT Practice Ethical? 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Holmes 1915. APA 2001; Abrams 2002; Shorter and Healy 2007. Breggin 1979; Friedberg 1976; Sackeim 2000. Shorter 1997; Ottosson and Fink 2004; Dukakis and Tye 2006; Shorter and Healy 2007. Shorter 1997; Braslow 1998; Pressman 1998; El-Hai 2005; Scull 2005. APA 1978. The summary text by Beauchamp and Childress (2001) is the basis for the discussion by Ottosson and Fink (2004). Bolwig and Madsen 2007; Manganas et al. 2007. APA 1997, 1999, 2000, 2002, 2004. Angell 2004; Healy 2004; Medawar and Hardon 2004.


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Index

Page numbers followed by f indicate illustrations. Adolescents acute toxic syndrome, 81–82 autism, 92–93 catatonia, 92–93 delirious mania, 64 –66 depression, 86 –87 ECT use, 85–86 safety, 7 self-injury, 91–92 typical patient history, 6 Adverse effects. See Side effects Age, memory loss and, 35, 37, 39 Alcohol consumption, memory impairment and, 38 Alcoholism, as contraindication, 9 Aldini, Giovanni, 111 Alzheimer’s disease, 44, 50–52 American Psychiatric Association (APA) Diagnostic and Statistical Manual, 68 Electroconvulsive Therapy Task Force, 108–109, 116 practice standards, 33 Amnesia. See Memory loss/ impairment

Anesthesia, 13, 15, 26 –27, 38–39 Anesthetic agents, 26, 131n2(ch3) Anger, manic, 62–64 Antianxiety drugs, memory impairment and, 37 Anticonvulsants, for mania, 59, 61–62 Antidepressants introduction, 108 memory impairment, 37, 38 toxic serotonin syndrome, 72 Antipsychotic drugs. See Neuroleptic drugs Anxiolytic drugs, memory impairment and, 37 APA. See American Psychiatric Association Association for Convulsive Therapy, 109 Attention deficit disorder, 6 Autism, 6, 92–93 Autonomy, ethics and, 118 Aversive conditioning therapy, ix, 89 Barbiturates, 26, 68 A Beautiful Mind, 10, 58

153

154 / Index Bender, Lauretta, 88 Beneficence, ethics and, 117 Benzodiazepines, 31, 68, 81 Bergland, Richard, 100 Bifrontal electrode placement (BF ECT), 28 Bilateral electrode placement. See Bitemporal electrode placement ECT Bini, Lucio, 107 Bipolar disorder, 8, 22, 43, 57–60. See also Mania Bipolar I disorder, 58 Bite bloc. See Mouth guard Bitemporal electrode placement ECT (BT ECT ), 19–20, 28–30 Blood-brain barrier, 77 Blood pressure changes, 31 monitoring, 14 Bone fractures, 26 Brain electrical activity monitoring, 14 functional centers and anatomy, 28, 100 stimulation therapies, 111–114 tumors, 84 BT ECT. See Bitemporal electrode placement ECT California legislation, 12, 108–109, 130n6(ch2) Camphor-in-oil injections, 105–106, 136n12(ch11) Cannabis-induced toxicity, 81–82 Carroll, Bernard, 45 Case studies, x–xi acute catatonia, 69–70 acute manic episode, 60–62 acute psychosis, 78–79

autistic spectrum disorder, catatonia in, 92–93 catatonia, in child, 88 chronic schizophrenia, 79–81 depression in adolescent, 86 –87 depressive melancholia, 46 – 47 malignant catatonia, 69–70 mania, recurrent, with psychosis, 62–64 mania with psychosis, 64 –66 mental retardation, self-injury in, 91–92 mental retardation, outbursts and catatonia in, 89–91 neuroleptic malignant syndrome, 70–72 outbursts and catatonia, in mental retardation, 89–91 parkinsonism, 73–74 pseudodementia and catatonia, 52–54 psychotic depression, 48–50 self-injury in mental retardation, 91–92 suicidal intention, 55–56 toxic psychosis and delirium, 81–82 Catatonia, 67–70 autism, 92–93 case histories, 69–70 characteristics of, 44, 67–68 in children, 88 classification of, 68 ECT effectiveness in, 8, 32, 68, 71–72 in mania, 58, 59, 60, 65–66 medications, 68 rapid neuroleptization, 59, 65–66 treatment outcomes, 22 typical patient history, 5–6 Cerebrospinal fluid (CSF), 95–96, 100–101

Index / 155 Cerletti, Ugo, 107 Chemical convulsive therapy, 27, 105–106 Children catatonia, 88 ECT, 4, 87–88 Mental retardation, 89–92 safety, 7 self-injury, 67, 91–92 typical patient history, 6 Comorbid conditions, xi–xii, 8–9 Computed tomography (CT ), 53–54 Confusion, 17, 35, 36, 38, 62 Consent concept, 109 Electroconvulsive Therapy Task Force and, 116 Form, 125–126 in mania, 50, 60 requirements, in ECT, 11–12, 116 Continuation treatment, 19–21 Contraindications, 8–9 Controversy, ECT and, vii, 115–116, 119 Convulsion, defined, x Convulsion treatment, ix Convulsive therapy. See Chemical convulsive therapy; Electroconvulsive therapy Convulsive Therapy, 109 Cortisol, 19, 45– 46, 99 Court mandated involuntary treatment, 12–13, 60, 130n6(ch2) CSF. See Cerebrospinal fluid CT (computed tomography), 53–54 Darkness Visible: A Memory of Madness (Styron), 40 Death risk in depression, 44 – 45 ECT and, 34

Deep brain stimulation (DBS), 114 Definitions, ix–x Delirious mania, 22, 58, 59–60, 64 –66 Delusional depression, 8, 20, 22, 44, 47–50 Dementia, reversible. See Pseudodementia Dementia paralytica, 103. See also Neurosyphilis Dementia praecox, 103. See also Schizophrenia Depression, 43–56 in adolescents, 46, 86 –87 autobiographical description, 40 case histories, 46 – 47, 48–50, 52–54, 55–56 characteristics, 43– 44 cortisol levels, 45– 46 delusional, 8, 20, 22, 44, 47–50 ECT effectiveness, 8, 32, 45, 48, 54 –55 geriatric, 44, 50–54 major, 43, 46 – 47, 58 medications, 44, 45, 48, 50, 54 memory impairment, 40 postpartum, 82–83 relapse rates, collaborative study, 19–20 risk of death, 44 – 45 stroke, 84 suicide, 45– 46, 54 –56 treatment outcomes, 21–22 types, 44 typical patient history, 5 Depressive mood disorder. See Depression Depressive stupor. See Catatonia Dexamethasone suppression test (DST), 45 Diabetes, 96 –97

156 / Index Diagnoses, effectiveness of ECT for, 4 –5, 7–8, 121–123 Diagnostic and Statistical Manual [DSM] (APA), 68 Diagnostic process, 25 Disorientation, 17, 35, 36, 38, 62 Dopamine in neuroleptic malignant syndrome, 71–72 in parkinsonism, 74, 101 Dopamine toxicity, 73 Drug dependence, as contraindication, 9 Drugs. See Medications DST (dexamethasone suppression test), 45 Dukakis, Kitty, 37, 41 Dyskinesia, 67, 76. See also Movement disorders Dystonia, 67. See also Movement disorders ECG. See Electrocardiogram ECS. See Electroconvulsive shock ECT. See Electroconvulsive therapy EEG. See Electroencephalogram Effective treatment, 31, 96 –96 Efficacy, compared to other treatments, vii–viii, 4 Elderly persons depression, 44, 50–54 ECT, 4, 5, 7 memory loss, 35, 37, 39 recovery, 17 treatment schedule, 17 Electrical stimulus, characteristics of, 27–28, 131n3(ch4) Electricity, medical research on effects of, 111–112 Electric shock, for aversive conditioning, ix, 89

Electrocardiogram (ECG), 14, 31 Electroconvulsive shock (ECS), x Electroconvulsive therapy (ECT). See also specific topics applications, xi, 3, 4 –6, 7–8, 121–122 history, 94, 106 –107, 108–109 misconceptions, vii, ix, 89, 92, 115–116 primary vs. secondary use, 6 –7 procedures. See Treatment, ECT terminology, ix–x Electroconvulsive Therapy Task Force (APA), 108–109, 116 Electrodes ECT, 28–30, 29f monitoring, 14, 15f Electroencephalogram (EEG) changes in, during and after treatment, 95, 96f interseizure, 80, 134n11(ch8) monitoring of treatment, 14 Electromyogram (EMG), 31 Electroseizure therapy (EST). See Electroconvulsive therapy Electroshock, ix. See also Electroconvulsive therapy Electroshock therapists, x, 32–33 Electrotherapists, x, 32–33 EMG (electromyogram), 31 Endler, Norman, 23–24 Endocrine glands, 98 Endocrine system, 95–99 Epileptic seizure, x, 105 EST (electroseizure therapy). See Electroconvulsive therapy Ethics, 115–120 balancing principles, 119 beneficence, 117 code of medial ethics, 116 –119 consent, 116

Index / 157 controversial image of ECT, 115–116, 119 ECT availability and, 72, 118–119 justice, ethics, 118–119 medical insurance, 119 medications evaluation and, 119–120 nonmalfeasance, ethics, 117 Examinations, pretreatment, 13 Facilities for ECT, 33 Facility standards, ECT availability, 72, 118–119 Fever therapy, 104, 136n28(ch11) Film portrayals of ECT, 10 Fit, defined, x Fractures, 26 Generic names of medications, 126 –127 Georgetown mantra, ethics and, 116 –119 Geriatric depression, 44, 50–54 Government regulations, 12, 108–109, 116, 130n6(ch2) Grand mal seizure, x, 84, 95, 99, 111–112 Heart monitoring, 14 Heart rate, changes in, 31 History, 103–110 chemical convulsive therapy, 105–106 concept of voluntary consent, 109 current innovative therapies, 109–110 early treatments, 103–106 electroconvulsive therapy, 94, 106 –107, 108–109 fever therapy, 104 insulin coma, 107 lobotomy, 108 prolonged sleep therapy, 103–104

psychopharmacology, 108–109 shock therapies, 107–108 Holiday of Darkness (Endler), 24 Holmberg, Gunnar, 39 Hormones, 14, 95, 96, 97, 100 Hospitalization for treatment, 19, 33 ICT. See Insulin coma therapy Ill patients, safety in, 7, 8–9 Indications for ECT, xi, 3, 4 –6, 7–8, 121–122 Informed consent. See Consent Innovative therapies, current, 109–110 Insulin, 14, 96 –97 Insulin coma therapy (ICT ), ix, 76, 107–108, 115 Intellectually disabled children. See Mental retardation International Psychiatric Association for the Advancement of Electrotherapy, 109 Interseizure electroencephalogram, 80, 134n11(ch8) Intracranial masses, 84 Intubation, 26 Involuntary treatment, 12–13, 60, 130n6(ch2) Isoelectric narcotherapy, isoflurane anesthesia and, 112 Joint Commission on Accreditation of Health Care Organizations ( JCAHO), 33 Justice, ethics and, 118–119 Kiloh, Leslie, 51 l-Dopa, 101 Lithium, 14, 37–38, 54, 59, 61–62 Lipótmezö, 105 Lobotomy, 108, 115

158 / Index Magnetic seizure therapy (MST ), 113 Maintenance treatment. See Continuation treatment Major depression, 43, 46 – 47, 58 Malaria fever therapy, 104 Malignant catatonia, 68–70. See also Neuroleptic malignant syndrome Mania, 57–66 acute episodes, 60–62 adolescents, 64 –66 bipolar disorder, 57–59 case histories, 60–62, 62–64, 64 –66 catatonia in, 58, 59, 60, 65–66 characteristics, 57 delirious, 22, 58, 59–60, 64 –66 ECT effectiveness, 8, 32, 59–60, 61–62, 64 medications for, 59, 61–62 melancholic, 58 one-syndrome vs. two-syndrome models, 130n5(ch1) with psychosis, 57, 62–66 treatment outcomes, 22 treatments, 59–60 typical patient history, 5–6 Manic delirium. See Mania, delirious Manic-depressive illness, 57–58, 103. See also Bipolar disorder Manic mood disorder. See Mania Manning, Martha, 22–23 Marijuana-induced toxicity, 81–82 Mechanism of action, 94 –102 early theories, 94, 105 neuroendocrine theory, 99–102 neurohormonal system, 95–97 neurotransmitters and neurohormones in mental illness, 97–99 seizure as therapeutic event, 94 –95 Medical ethics, code of, 116 –119 Medical experimentation, 116

Medical insurance, 119 Medications antipsychotic. See Neuroleptic drugs for catatonia, 68 consent for, 11 for depression, 44, 45, 48. See also Antidepressants ECT compared to, vii–viii, 4 evaluation of, 119–120 history of use, 108–109 limitations, vii–viii for mania, 59, 61–62, 64, 65–66 memory impairment, 37–38 names of, trade and generic, 126 –127 for neuroleptic malignant syndrome, 71–72 for parkinsonism, 73, 74 pretreatment evaluation, 13 for psychosis, 76 –77. See also Neuroleptic drugs in relapse prevention, 20 for status epilepticus, 84 withholding, during ECT, 14 Meduna, Ladislas, 94, 105–106, 135n3(ch10), 136n12(ch11) Melancholia. See Major depression Melancholic mania, 58 Memory loss/impairment, 34 – 42 age, 35, 37, 39 anesthesia, 38–39 collaborative study, 30 electrode placement, 28 exaggerated fears of, 12, 35–36 individual factors, 39– 42 persistent, 36 personal experiences, 40– 42 prevention by oxygenation, 26, 35, 39 psychiatric disorders, 36 –37, 40 psychotropic drugs, 37–38 during treatment, 35, 42

Index / 159 Mental illness classification, 25, 130n8(ch1) history of treatments. See History memory impairment, 36 –37, 40 neurotransmitters and neurohormones, 97–99 pregnancy, 82–83 severity, duration, and number of treatments, 18 theory of causes, 101 treatments, vii–viii, 103–106, 109– 110. See also Medications Mental retardation, 89–92 Metrazol injections, 106, 107 Misconceptions, vii, ix, 89, 92, 115–116 MMECT (multiple monitored ECT), 17 Monitoring, physiological, 14, 31 Monitoring electrodes, 14, 15f Moniz, Egas, 108 Mood disorders, 4, 7–8, 43. See also Depression; Mania Mortality depression and, 44 – 45 ECT and, 34 Mouth guard (bite bloc), 13, 16 Movement disorders, 67–74 antipsychotic medications, 76 –77 catatonia. See Catatonia indication for ECT, 4 –5 neuroleptic malignant syndrome, 59, 64, 65–66, 70–72 parkinsonism, 67, 72–74, 101, 114 MST (magnetic seizure therapy), 113 Multiple monitored ECT (MMECT), 17 Muscle relaxants, 15, 26 Nash, John, 58 Neuroendocrine system, 95–97, 98f Neuroendocrine theory, 99–102 Neurohormones, 97

Neuroleptic drugs. See also Neuroleptic malignant syndrome bipolar disorder, 59 delirious mania, 64, 65–66 ECT and, 61–62, 77 movement disorders and, 76 schizophrenia, 62, 64 usage of, 76 –77 Neuroleptic malignant syndrome (NMS), 59, 64, 65–66, 70–72 Neurological conditions, ECT in, 84 Neurosyphilis, 103, 104 Neurotransmitters, 97 NMS. See Neuroleptic malignant syndrome Nonmaleficence, ethics and, 117 One Flew Over the Cuckoo’s Nest, 10 Oneirophrenia, 58, 133n11(ch6). See also Delirious mania Outcomes, 21–22 Outpatient treatment, 11, 20, 33 Oxygen administration, in reduction of memory effects, 26, 35, 39 Oxygen monitoring, 14, 15, 31 Parkinsonism, 67, 72–74, 101 Patient experiences Dukakis, 41 Endler, 23–24 film portrayals, 10–11 Manning, 22–23 practicing psychiatrist, 10 Styron, 40 Patient selection, 4 –5 Pediatric patients. See Adolescents; Children Personality disorders, 9 Pharmaceutical industry, 119–120 Pharmacologic coma, 84 Physicians, ECT qualification for, 32–33

160 / Index Physiological monitoring, 14, 31 Postpartum depression, 82–83 Post-treatment restrictions, 17 Pregnancy, 7, 13, 82–83, 134n14(ch8) Pretreatment examinations, 13 Procedure for ECT, 3– 4, 15–16, 27–31 Prolactin, 95, 134n17(ch8) Prolonged sleep therapy, 103–104 Pseudodementia, 8, 36, 37, 44, 51 Psychiatric disorders. See Mental illness Psychiatric treatment, consent and, 11, 116 Psychopharmacology history, 108–109 Psychosis, 75–77 acute, 8–9, 78–79 acute toxic syndromes, 81–82 case histories, 78–82 in chronic schizophrenia, 79–81 ECT for, 8, 76 –77 insulin coma therapy, 76 mania, 57, 62–66 medications, 76 –77 typical patient history, 5 Psychosocial therapies, limitations of, vii–viii Psychotherapy sessions, during treatment, 21 Psychotic depression. See Delusional depression Psychotic disorders. See Thought disorders Psychotropic drugs. See Medications Public prejudice against ECT, 21, 108, 119 Rapid cycling mania. See Delirious mania Rapid neuroleptization, 59

Recovery period, 16 Recurrence of illness. See Relapse rates Refusal of treatment, 12–13 Regressive ECT, 17 Regulations. See Government regulations Relapse prevention, 19–21 Relapse rates, 18, 19–20, 30 Reversible dementia. See Pseudodementia Right unilateral electrode placement ECT (RUL ECT), 19–20, 28–30 Rigidity, in parkinsonism, 73–74, 114 Risk, consent and, 12 Rosenberg, Leon, 55 RUL ECT. See Right unilateral electrode placement ECT Safety of ECT, vii, 7, 34, 134n14(ch8) Sakel, Manfred, 107 Salivation, 26 Schizophrenia catatonic type, 68 chemical convulsive therapy, 105–106 chronic, case history, 79–81 ECT effectiveness, 8, 76 neuroleptic drugs, 62, 64 positive and negative signs, 79 treatment outcomes, 22 Sedative drugs, memory impairment and, 37 Seizure disorders, 83–84 Seizures chemical induction, 27, 105–106 defined, x drug levels, 14 duration, 31

Index / 161 electrical stimulus for induction, 27–28, 107 electroconvulsive shock, x hormone release, 14, 99–102 monitoring, 31, 95–96 physiological changes during, 31 as therapeutic agent, 94 –95 Seizure threshold, 27, 30, 134n17(ch8) Selective serotonin reuptake inhibitors (SSRIs), 72 Self-injury, in mental retardation, 91–92 Shock: The Healing Power of Electroconvulsive Therapy (Dukakis), 41 Shock therapies, 107–108 Side effects, 34, 40– 41. See also Memory loss/impairment Sleep, prolonged, 103–104 Speech, minimizing effects on, 28 SSRIs (selective serotonin reuptake inhibitors), 72 State laws. See Government regulations Status epilepticus, 83–84, 134n17(ch8) STEP-BD (Systematic Treatment Enhancement Program for Bipolar Disorder), 59 Stroke, depression after, 84 Stupor depressive. See Catatonia pseudodementia, 51 Styron, William, 40 Suicide cortisol levels, 45– 46 depression, 45– 46, 54 –56 efficacy of ECT in prevention, 54 –55, 56 risk factors, 54

Symptom relief vs. cure, 25–26 and treatment length, 18–19 Syphilitic infection, 103, 104, 130n8(ch1) Systemic illness, safety in, 7, 8–9 Taylor, Michael A., x Terminology, ix–x Texas legislation, 12, 130n6(ch2) Thorazine, 59, 76, 107–108 Thought disorders, 4, 32, 75–79. See also Psychosis; Schizophrenia Thyrotropin-releasing hormone (TRH), 101 Toxic serotonin syndrome, 72 Toxic syndromes, acute, 81–82 Trade names of medications, 126 –127 Transcranial magnetic stimulation (TMS), 112–113 Treatment, ECT delays in, 5–6 duration, 4 effectiveness criteria, 31–32 frequency, 17–18 guidelines, 6 –7 maintenance. See Continuation treatment outcomes, 21–22 preparation, 13–15 procedure described, 3– 4, 15–16, 27–31 scheduling, 13 Treatment, of mental illness options, vii–viii psychotropic drugs. See Medications rejected, 103–106 unproven, 109–110

162 / Index Treatment facilities, 33, 72, 118–119 Treatment resistance, 18 TRH (thyrotropin-releasing hormone), 101 Tricyclic antidepressants, memory impairment, 37, 38 Undercurrents (Manning ), 23 Unilateral electrode placement. See Right unilateral electrode placement ECT

Unilateral nondominant ECT. See Right unilateral electrode placement ECT Vagus nerve stimulation ( VNS), 113–114 Ventricular system of brain, 100 Voluntary consent. See Consent Wagner-Jauregg, Julius, 104 Women, pregnant. See Pregnancy

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