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APA Task Force Report on Electroconvulsive Therapy

The Practice of Electroconvulsive Therapy:
Recommendations for Treatment, Training and Privileging
Second Edition (Completely Revised)

A Task Force Report of the American Psychiatric Association

Task Force on Electroconvulsive Therapy
Richard D. Weiner, M.D., Ph.D., Chair
C. Edward Coffey, M.D.
Laura J. Fochtmann, M.D.
Robert M. Greenberg, M.D.
Keith E. Isenberg, M.D.
Charles H. Kellner, M.D.
Harold Sackeim, Ph.D.
Louis Moench, M.D., Assembly Liaison

APA Staff: Harold Alan Pincus, M.D.
Laurie E. McQueen, M.S.S.W.

NOTE: The contributors have worked to ensure that all information in this book concerning drug doses, schedules, and routes of administration is accurate at the time of publication and consistent with the standards set by the U.S. Food and Drug Administration and the general medical community. As medical research and practice advance, however, therapeutic standards may change. For this reason and because human and mechanical errors sometimes occur, we recommend that readers follow the advice of a physician directly involved in their care or the care of a member of their family.

The findings, opinions, and conclusions of the report do not necessarily represent the views of the officers, trustees, or all members of the American Psychiatric Association. Each report, however, does represent the thoughtful judgment and findings of the task force of experts who composed it. These reports are considered a substantive contribution to the ongoing analysis and evaluation of problems, programs, issues, and practices in a given area of concern.

The Practice of Electroconvulsive Therapy:
Recommendations for Treatment, Training and Privileging
Second Edition (Completely Revised)

A Task Force Report of the American Psychiatric Association

APA Staff: Harold Alan Pincus, M.D.
Laurie E. McQueen, M.S.S.W.

TABLE OF CONTENTS

Appendix B

Consent forms and sample information patient information

Chapter 1. Introduction

Chapter 2. Indications for Use

Chapter 3. Contraindications and situations of high risk

Chapter 4. Use of ECT in special populations
* 1. Medically Ill
* 2. Elderly
* 3. Pregnancy
* 4. Children and Adolescents
Chapter 5. Adverse Effects

Chapter 6. Pre-ECT evaluation

Chapter 7. Concurrent medication

Chapter 8. Consent

Chapter 9. Staffing

Chapter 10. Location, equipment, supplies

Chapter 11. Treatment Procedures
1. Determination of inpatient and outpatient setting
2. Preparation of the patient
3. Airway management
4. Medications used with ECT
5. ECT devices
6. Stimulus electrode placement
7. Stimulus dosing
8. Physiological monitoring
9. Management of Missed, Abortive, and Prolonged Seizures
10. Postictal Recovery Period
11. Frequency and Number of Treatments
12. Multiple Monitored ECT Chapter 12. Evaluation of Outcome
1. Therapeutic response
2. Adverse Effects
Chapter 13. Continuation/maintenance treatment

Chapter 14. Documentation

Chapter 15. Education and Training in ECT

Chapter 16. Privileging in ECT

Credits

Chapter 1. INTRODUCTION

In 1990, the American Psychiatric Association (APA) published the first edition of The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging, a comprehensive set of recommendations for the practice of electroconvulsive therapy (ECT). This work was well received and influenced clinical practice in a number of meaningful ways, including the encouragement of guideline development by other groups within the U.S. (Fink et al. 1996) and elsewhere (Royal Australian & New Zealand College of Psychiatrists 1992; Royal College of Psychiatrists 1993; Gangadhar 1995). In the ensuing decade, the field of ECT has continued to advance, with a substantial amount of new scientific and clinical information forthcoming. Each year, hundreds of relevant publications have appeared, as interest in this treatment modality continues to expand.

Because of this growing knowledge base, APA gave the Task Force on ECT a mandate to undertake an update of this report. This revision has been an extensive process. A review of the available clinical literature included a search of all clinical citations related to ECT published between 1989 and 1998 that had been entered into the Medline database by December 1998. Supplementing, this literature review were suggestions received at a Task Force workshop at the 1996 APA Annual Meeting, and after subsequent presentations at Annual Meetings of the Association for Convulsive Therapy (ACT), as well as via informal input from experts and other interested parties. The Task Force’s efforts were made known to the APA membership on an ongoing basis through published summaries of component activities and by notification of the APA Assembly.

To help ensure that these recommendations would be clinically useful, as well as scientifically, ethically, and legally sound, the Task Force sought input from a large number of professional organizations (covering the fields of psychiatry, anesthesiology, nursing, nurse anesthesia, and psychology), individual experts in related areas (including child, adult, and geriatric psychiatry, neurology, psychology, anesthesiology, cardiology, obstetrics, medical ethics, and law), regulatory bodies (Joint Commission on Accreditation of Healthcare Organizations [JCAHO] and the Food and Drug Administration [FDA]), and major lay mental health organizations (see Appendix A). As the initial draft of the revised document neared completion, an article was published in Psychiatric News (the APA newspaper) soliciting the names of additional members with an interest in reviewing the draft. This request ensured that rank and file practitioners would also have the opportunity to have input. Finally, the APA’s own internal review process ensured that drafts were examined from a wide variety of perspectives. Input from these diverse sources was taken into account in the determination of the final product.

This revised volume offers a set of recommendations to assist practitioners and facilities in the safe and effective use of ECT. We have once more attempted to make the scope of the recommendations as comprehensive as possible, including coverage of the important issues of education, training, and privileging. In each section, recommendations are preceded by applicable background information, including pertinent literature citations(with a particular focus on recent work). This format differs from that of the original report, in which background information was placed in a separate Rationale section that was preceded by an overall Recommendations section. The goal of this change in format was an improved integration of the recommendations with their justification. As before, a Bibliography and Appendices provide additional source material of use to practitioners. Due to the growing importance of defined policy and procedure statements in clinical practice, an example of such a document is provided in Appendix E [not present in this Draft] and is designed to be in conformance with these recommendations. While it is not possible to highlight all the changes from the original volume, Appendix F [not present in this Draft] contains a list of major substantive differences between the present recommendations and those made in the 1990 volume.

Over the past 60 years, the practice of ECT has evolved into a complex procedure about which much has been learned, but many questions remain. In providing a comprehensive set of recommendations, it was necessary to include material based up on empirical findings as well as clinical consensus for those situations where well controlled clinical trials are either unavailable or not applicable. It was also apparent that in some cases reasonable alternative courses of action to those presented in these recommendations exist, and attempts have been made to describe a number of such alternative, where applicable. For these reasons, these recommendations should be viewed as suggestions rather than requirements.

In writing recommendations for a complex procedure such as ECT, it is impossible to cover all situations or deal with all possible exceptions. Accordingly, there will be times when overriding factors will lead a reasonable and prudent practitioner to alter practice from that recommended here. In addition, new clinically relevant information is continually appearing, and should be readily incorporated into clinical practice whenever it is shown to either maximize efficacy or minimize adverse effects.

To aid the practitioner in weighing the importance of individual recommendations, we have distinguished between recommendations that we believe are critical to the delivery of safe and effective treatment from those that we believe to be of lesser importance. The categorical term “should” is used to designate crucial recommendations, whereas other recommendations are described in more equivocal terms such as “encouraged,” “suggested,” “recommended,” or “considered”.

As a final caveat, the practitioner should be aware that legal regulations exist regarding ECT, particularly concerning informed consent procedures (see Chapter 8 ). These regulations vary considerably among jurisdictions and over time. Consequently, these recommendations may not always be compatible with all requirements of present or future statutes. Accordingly, practitioners should seek out information on applicable regulations before beginning practice of ECT and should be aware of substantive statutory changes as they unfold.

We encourage practitioners and trainees in psychiatry as well as those in related disciplines to read this document and to integrate its recommendations into their clinical practice. It is designed to offer a comprehensive yet practical overview of the safe and effective use of ECT, with recommendations that should be applicable across a wide spectrum of clinical settings.

Chapter 2: 2.1. Indications for Use

Convulsive therapy has been in continuous use for more than 60 years. The clinical literature establishing its efficacy in specific disorders is amongst the most substantial for any medical treatment (Weiner and Coffey 1988; Mukherjee et al. 1994; Krueger and Sackeim 1995; Sackeim et al. 1995; Abrams 1997a). Like other medical treatments, various sources of evidence support the efficacy of ECT in specific conditions. The indications for ECT have been defined by randomized controlled trials comparing ECT to sham interventions or treatment alternatives and similar trials comparing modifications of ECT technique. The indications for ECT have also been supported by reports of uncontrolled clinical series, case studies, and surveys of expert opinion.

The decision to recommend the use of ECT derives from a risk/benefit analysis for the specific patient. This analysis considers the diagnosis of the patient and the severity of the presenting illness, the patient’s treatment history, the anticipated speed of action and efficacy of ECT, the medical risks and anticipated adverse side effects, and the likely speed of action, efficacy, and safety of alternative treatments.

2.2. Referral for ECT

2.2.1. Primary use. There is considerable variability among practitioners in the frequency with which ECT is used a first-line or primary treatment or is only considered for secondary use after patients have not responded to other interventions. ECT is a major treatment in psychiatry, with well defined indications. It should not be reserved for use only as a “last resort.” Such practice may deprive patients of an effective treatment, delay response and prolong suffering, and may possibly contribute to treatment resistance. In major depression, the chronicity of the index episode is one of the few consistent predictors of clinical outcome with ECT or pharmacotherapy (Hobson 1953; Hamilton and White 1960; Kukopulos et al. 1977; Dunn and Quinlan 1978; Magni et al. 1988; Black et al. 1989b, 1993; Kindler et al. 1991; Prudic et al. 1996). Patients with longer duration of current illness have a reduced probability of responding to antidepressant treatments. The possibility has been raised that exposure to ineffective treatment or to a longer duration of episode actively contributes to treatment resistance (Fava and Davidson 1996; Flint and Rifat 1996).

The likely speed and efficacy of ECT are factors that influence its use as a primary intervention. Particularly in major depression and acute mania, substantial clinical improvement often occurs soon after the start of ECT. It is common for patients to manifest appreciable improvement after one or two treatments (Segman et al. 1995; Nobler et al. 1997). In addition, the time to achieve maximal response is often more rapid than that with psychotropic medications (Sackeim et al. 1995). Besides speed of action, the likelihood of obtaining significant clinical improvement is often more certain with ECT than with other treatment alternatives. Therefore, when a rapid or a higher probability of response is needed, as when patients are severely medically ill, or at risk to harm themselves or others, primary use of ECT should be considered.

Other considerations for the first-line use of ECT involve the patient’s medical status, treatment history, and treatment preference. Due to the patient’s medical status, in some situations, ECT may be safer than alternative treatments (Sackeim 1993, 1998; Weiner et al. in press). This circumstance most commonly arises among the infirm elderly and during pregnancy (see Sections 6.2 and 6.3). Positive response to ECT in the past, particularly in the context medication resistance or intolerance, leads to early consideration of ECT. At times, patients will prefer to receive ECT over alternative treatments, but commonly the opposite will be the case. Patient preferences should be discussed and given weight prior to making treatment recommendations.

Some practitioners also base a decision for primary use of ECT upon other factors, including the nature and severity of symptomatology. Severe major depression with psychotic features, manic delirium, or catatonia are conditions for which there is a clear consensus favoring early reliance on ECT (Weiner and Coffey 1988).

2.2.2. Secondary use. The most common use of ECT is in patients who have not responded to other treatments. During the course of pharmacotherapy, lack of clinical response, intolerance of side effects, deterioration in the psychiatric condition, the appearance of suicidality or inanition are reasons to consider the use of ECT.

The definition of medication resistance and its implications with respect to a referral for ECT have been the subject of considerable discussion (Quitkin et al. 1984; Kroessler 1985; Keller et al. 1986; Prudic et al. 1990; Sackeim et al. 1990a, 1990b; Rush and Thase 1995; Prudic et al. 1996). At present there are no accepted standards by which to define medication resistance. In practice, when assessing the adequacy of pharmacological treatment, psychiatrists rely upon factors such as the type of medication used, dosage, blood levels, duration of treatment, compliance with the medication regimen, adverse effects, nature and degree of therapeutic response, and type and severity of clinical symptomatology (Prudic et al. 1996). For example, patients with psychotic depression should not be viewed as pharmacological nonresponders unless a trial of an antipsychotic medication has been attempted in combination with an antidepressant medication (Spiker et al. 1985; Nelson et al. 1986; Chan et al. 1987). Regardless of diagnosis, patients who have not responded to psychotherapy alone should not be considered treatment resistant in the context of referral for ECT.

In general, failure of patients with major depression to respond to one or more antidepressant medications trials does not preclude a favorable response to ECT (Avery and Lubrano 1979; Paul et al. 1981; Magni et al. 1988; Prudic et al. 1996). Indeed, compared to other treatment alternatives, the probability of response to ECT among patients with medication-resistant depression may be favorable. This is not to say, however, that medication resistance does not predict clinical outcome of ECT. Patients who have not responded to one or more adequate antidepressant medication trials have a lower probability of responding to ECT compared to patients treated with ECT without having received an adequate medication trial during the index episode (Prudic et al. 1990, 1996; Shapira et al. 1996). In addition, medication-resistant patients may require particularly intensive ECT treatment to achieve symptomatic improvement. Consequently, the bulk of patients who fail to benefit from ECT are likely to also be patients who have received, and not benefited from, adequate pharmacotherapy. The relationship between medication resistance and ECT outcome may be stronger for tricyclic antidepressants (TCAs) than for selective serotonin reuptake inhibitors (SSRIs) (Prudic et al. 1996).

2.3. Major Diagnostic Indications

2.3.1. Efficacy in major depression. The efficacy of ECT in depressive mood disorders is documented by an impressive body of research, beginning with the open trials of the 1940s (Kalinowsky and Hoch 1946, 1961; Sargant and Slater 1954); the comparative ECT/pharmacotherapy trials of the 1960s (Greenblatt et al. 1964; Medical Research Council 1965); the comparisons of ECT and sham-ECT, both in the 1950s and in the more recent British studies (Freeman et al. 1978; Lambourn and Gill 1978; Johnstone et al. 1980; West 1981; Brandon et al. 1984; Gregory, et al. 1985; see Sackeim 1989 for a review); and the recent studies contrasting variations in ECT technique (Weiner et al. 1986a, 1986b; Sackeim et al. 1987a; Scott et al. 1992; Letemendia et al. 1991; Sackeim et al. 1993).

While ECT was first introduced as a treatment for schizophrenia, it was quickly found to be especially effective in patients with mood disorders, both in the treatment of depressive and manic states. In the 1940’s and 1950’s, ECT was a mainstay in the treatment of mood disorders, with response rates between 80-90% commonly reported (Kalinowsky and Hoch 1946; Sargant and Slater 1954). The results of these early, largely impressionistic studies have been summarized by the American Psychiatric Association (1978), Fink (1979), Kiloh et al. (1988), Mukherjee et al. (1994) and Abrams (1997a).

Post (1972) suggested that prior to the introduction of ECT, elderly patients with depression often manifested a chronic course or died of intercurrent medical illnesses in psychiatric institutions. A number of studies have contrasted the clinical outcome of depressed patients who received inadequate or no biological treatment to that of patients who received ECT. While none of this work used prospective, random assignment designs, the findings have been uniform. ECT resulted in decreased chronicity and morbidity, and decreased rates of mortality (Avery and Winokur 1976; Babigian and Guttmacher 1984; Wesner and Winokur 1989; Philibert et al. 1995). In much of this work, the advantages of ECT were particularly pronounced in elderly patients. For example, in a recent retrospective comparison of elderly depressed patients treated with ECT or pharmacotherapy, Philibert et al. (1995) found that at long-term follow-up rates of mortality and significant depressive symptomatology were higher in the pharmacotherapy group.

With the introduction of the TCAs and monoamine oxidase inhibitors (MAOIs), random assignment trials were conducted in depressed patients in which ECT was used as the “gold-standard” by which to establish the efficacy of the medications. Three of these studies involved random assignment and blind ratings, and each found a significant therapeutic advantage for ECT over TCAs and placebo (Greenblatt et al. 1964; Medical Research Council 1965; Gangadhar et al. 1982). Other studies also reported ECT to be as or more effective than TCA (Bruce et al. 1960; Kristiansen 1961; Norris and Clancy 1961: Robin and Harris 1962; Stanley and Fleming 1962; Fahy et al. 1963 ); Hutchinson and Smedberg 1963; Wilson et al. 1963; McDonald et al. 1966; Davidson et al. 1978) or MAOIs (King 1959; Kilo et al. 1960; Stanley and Fleming 1962): Hutchinson and Smedberg 1963; Davidson et al. 1978). Janicak et al. (1985), in a meta-analysis of this work, reported that the average response rate to ECT was 20% higher when compared to TCAs and 45% higher than MAOIs.

It should be noted that standards for adequate pharmacological treatment have changed over the decades (Quitkin 1985; Sackeim et al. 1990a), and that, by current criteria, few of these early comparative trials used aggressive pharmacotherapy in terms of dosage and/or duration (Rifkin 1988). In addition, these studies usually focused on depressed patients who were receiving their first biological treatment during the index episode. More recently, in a small study, Dinan and Barry (1989) randomized patients who did not respond to monotherapy with a TCA to treatment with ECT or the combination of a TCA and lithium carbonate. The ECT and the pharmacotherapy groups had equivalent efficacy, but the TCA/lithium, combination may have had an advantage in terms of speed of response.

No studies have compared the efficacy of ECT with newer antidepressant medications, including the SSRIs or medications such as bupropion, mirtazapine, nefazadone, or venlafaxine. However, no trial has ever found an antidepressant medication regimen to be more effective than ECT. Among patients who are receiving ECT as a first-line treatment, or who have received inadequate pharmacotherapy during the index episode due to intolerance, response rates continue to be reported in the range of 90% (Prudic et al. 1990, 1996). Among patients who have not responded to one or more adequate antidepressant trials, the response rate is still substantial, in the range of 50-60%.

The time to achieve full symptomatic improvement with antidepressant medications is typically estimated as 4 to 6 weeks (Quitkin et al. 1984, 1996). This delay until response may be longer in older patients (Salzman et al. 1995). In contrast, the average ECT course for major depression consists of 8-9 treatments (Sackeim et al. 1993; Prudic et al. 1996). Thus, when ECT is administered at a schedule of three treatments per week, full symptomatic improvement usually occurs more rapidly than with pharmacological treatment (Sackeim et al. 1995; Nobler et al. 1997).

ECT is a highly structured treatment, involving a complex, repeatedly administered procedure that is accompanied by high expectations of therapeutic success. Such conditions may augment placebo effects. Given this concern, a set of double-blind, random assignment trials were conducted in England during the late 1970’s and 1980’s that contrasted ‘real’ ECT with ’sham’ ECT – the repeated administration of anesthesia alone. With one exception (Lambourn and Gill 1978), real ECT was found consistently to be more efficacious than sham treatment (Freeman et al. 1978; Johnstone et al. 1980; West 1981; Brandon et al. 1984; Gregory et al. 1985; see Sackeim 1989 for a review). The exceptional study (Lambourn and Gill 1978) used a form of real ECT, involving low stimulus intensity and right unilateral electrode placement, that is now known to be ineffective (Sackeim et al. 1987a, 1993). Overall, the real vs. sham ECT studies demonstrated that the passage of an electrical stimulus and/or the elicitation of a generalized seizure were necessary for ECT to exert antidepressant effects. Following the randomized acute treatment period, the patients who participated in these studies were free to receive other forms of acute or continuation treatment, including ECT. Consequently, information regarding the duration of symptomatic improvement with real versus sham treatment could not be obtained in this research.

Finally, there have been a host of studies in the treatment of major depression that have contrasted variations in ECT technique, manipulating factors such as stimulus waveform, electrode placement, and stimulus dosage. An important practical observation that emerged was that the efficacy of ECT is equivalent regardless of the use of sine wave or brief pulse stimulation, but that sine wave stimulation results in more severe cognitive impairments (Carney et. al. 1976; Weiner et al. 1986a; Scott et al. 1992). More critical in establishing the efficacy of ECT was the demonstration that the clinical outcome with ECT is dependent on electrode placement and the stimulus dosage (Sackeim et al. 1987a. 1993). These factors can dramatically impact on the efficacy of the treatment, with response rates varying from 17% to 70%. This work went beyond sham-controlled studies, since the forms of ECT that differed markedly in efficacy all involved electrical stimulation and the production of a generalized seizure. Thus, technical factors in ECT administration can strongly influence efficacy.

Prediction of response. ECT is an effective antidepressant in all subtypes of major depressive disorder. Nonetheless, there have been many attempts to determine whether particular subgroups of depressed patients or particular clinical features of depressive illness have prognostic value with respect to ECT’s therapeutic effects.

In the 1950’s and 1960’s, a series of studies showed impressive power to predict clinical outcome in depressed patients on the basis of pre-ECT symptomatology and history (Hobson 1953; Hamilton and White 1960; Rose 1963; Carney et al. 1965; Mendels 1967; see Nobler & Sackeim 1996 and Abrams 1997a for reviews). This work is now largely of historical interest (Hamilton 1986). While the early research emphasized the importance of vegetative or melancholic features as prognostic of positive ECT outcome, recent studies restricted to patients with major depression suggest that subtyping as endogenous or melancholic has little predictive value (Abrams et al. 1973; Coryell and Zimmerman 1984; Zimmerman et al. 1985, 1986; Prudic et al. 1989; Abrams and Vedak 1991; Black et al. 1986; Sackeim and Rush 1996). It is likely that the early positive associations were due to the inclusion of patients with “neurotic depression” or dysthymia in the sampling. Similarly, the distinction between unipolar and bipolar depressive illness has generally been found to be unrelated to therapeutic outcome (Abrams and Taylor 1974; Perris and d’Elia 1966; Black et al. 1986, 1993; Zorumski et al. 1986; Aronson et al. 1988).

In recent research a few clinical features have been related to ECT therapeutic outcome. The majority of studies that have examined the distinction between psychotic and nonpsychotic depression found superior response rates among the psychotic subtype (Hobson 1953: Mendels 1965a, 1965b: Hamilton and White 1960; Mandel et al. 1977; Avery and Lubrano 1979: Clinical Research Centre 1984; Kroessler 1985; Lykouras et al. 1986; Pande et al. 1990; Buchan et al. 1992; see also Parker et al. 1992: Sobin et al. 1996). This is of particular note given the established inferior response rate in psychotic or delusional depression to monotherapy with an antidepressant or antipsychotic medication (Spiker et al. 1985; Chan et al. 1987; Parker et al. 1992). To be effective, a pharmacological trial in psychotic depression should involve combination treatment with an antidepressant and an antipsychotic medication (Nelson et al. 1986; Parker et al. 1992; Rothschild et al. 1993; Wolfersdorf et al. 1995). However, relatively few patients referred for ECT with psychotic depression are administered such combination treatment in sufficient dosage and duration to be considered adequate (Mulsant et al. 1997). Multiple factors may be contributory. Many patients cannot tolerate the dosage of antipsychotic medications generally viewed as necessary for an adequate medication trial in this subtype (Spiker et al. 1985 Nelson et al. 1986). Patients with psychotic depression commonly have severe symptomatology, and are at increased risk for suicide (Roose et al. 1983). The rapid onset and high probability of improvement with ECT makes this treatment of particular value for these patients.

Several studies have also noted that, as with pharmacological treatment, patients with long duration of current episode are less likely to respond to ECT (Hobson 195 Hamilton and White 1960; Kukopulos et al. 1977; Dunn and Quinlan 1978; Magni et al. 1988; Black et al. 1989b. 1993; Kindler et al. 1991; Prudic et al. 1996). As already discussed, the treatment history of patients may provide a useful predictor of ECT outcome, with patients who have failed one or more adequate medication trials showing a substantial, but diminished, rate of ECT response (Prudic et al. 1990, 1996). In the majority of relevant studies patient age has been associated with ECT outcome (Gold and Chiarello 1944; Roberts 1959a, 1959b; Greenblatt et al. 1962; Nystrom 1964; Mendels 1965a, 1965b; Folstein et al. 1973; Stromgren 1973; Coryell and Zimmerman 1984: Black et al. 1993). Older patients are more likely to show marked benefit compared to younger patients (see Sackeim 1993, 1998 for reviews). Gender, race and socioeconomic status do not predict ECT outcome.

The presence of catatonia or catatonic symptoms may be a particularly favorable prognostic sign. Catatonia occurs in patients with severe affective disorders (Abrams and Taylor 1976; Taylor and Abrams 1977), and is now recognized in the DSM-IV as a specifier of a major depressive or manic episode (APA 1994). Catatonia may also present as a consequence of some severe medical illnesses (Breakey and Kala 1977; O’Toole and Dyck 1977; Hafeiz 1987), as well as among patients with schizophrenia. The clinical literature suggests that regardless of diagnosis, ECT is effective in treating catatonic symptoms, including the more malignant form of “lethal catatonia” (Mann et al. 1986, 1990; Geretsegger and Rochawanski 1987; Rohland et al. 1993; Bush et al. 1996).

Major depression which occurs in individuals with preexisting psychiatric or medical disorders is termed “secondary depression.” Uncontrolled studies suggest that patients with secondary depression respond less well to somatic treatments, including ECT, than those with primary depressions (Bibb and Guze 1972; Coryell et al. 1985; Zorumski et al. 1986; Black et al. 1988, 1993). Patients with major depression and a co-morbid personality disorder may have a reduced probability of ECT response (Zimmerman et al. 1986; Black et al. 1988). However, there is sufficient variability in outcome with ECT that each case of secondary depression must be considered on its own merits. For example, patients with post-stroke depression (Murray et al. 1986; House 1987; Allman and Hawton 1987; deQuardo and Tandon 1988, Gustafson et al. 1995) are believed to have a relatively good prognosis with ECT. Patients with major depression superimposed on a personality disorder (e.g. Borderline Personality Disorder) should not be denied ECT out of hand.

Dysthymia as the sole clinical diagnosis has been rarely treated with ECT. However, a history of dysthymia preceding a major depressive episode is common and does not appear to have predictive value with regard to ECT outcome. Indeed, recent evidence suggests that the degree of residual svmptomatology following ECT is equivalent in patients with major depression superimposed on a dysthymic baseline, i.e., “double depression”, and in patients with major depression without a history of dysthymia (Prudic et al. 1993).

Patient features, such as psychosis, medication resistance, and episode duration, only have statistical associations with ECT outcome. This information may be considered in the overall risk/benefit analysis of ECT. For example, a patient with a nonpsychotic, chronic major depression, who has failed to respond to multiple robust medication trials may be less likely to respond to ECT than other patients. Nonetheless, the probability of response with alternative treatments may be still lower, and the use of ECT justified.

2.3.2. Mania. Mania is a syndrome that, when fully expressed, is potentially life-threatening due to exhaustion, excitement, and violence. The early case literature first suggested that ECT is rapidly effective in mania (Smith et al. 1943; Impastato and Almansi 1943; Kino and Thorpe 1946). A series of retrospective studies comprised either naturalistic case series or comparisons of outcome with ECT to that with lithium carbonate or chlorpromazine (McCabe 1976; McCabe and Norris 1977; Thomas and Reddy 1982; Black et al. 1986; Alexander et al. 1988), Stromgren 1988; Mukherjee and Debsikdar 1992). This literature supported the efficacy of ECT in acute mania, and suggested equivalent or superior antimanic properties relative to lithium and chlorpromazine (see Mukherjee et al. 1994 for a review). There have been three prospective comparative studies of clinical outcome of ECT in acute mania. One study primarily compared ECT with lithium treatment (Small et al. 1988), another study compared ECT with combined treatment with lithium and haloperidol (Mukherjee et al. 1988. 1994), and in patients receiving neuroleptic treatment, one study compared real and sham ECT (Sikdar et al. 1994). While each of the prospective studies had small samples, the findings supported the conclusion that ECT was efficacious in acute mania, and likely resulted in superior short-term outcome than the comparison pharmacological conditions. In a review of the English language literature, Mukherjee et al. (1994) reported that ECT was associated with remission or marked clinical improvement in 80% of 589 patients with acute mania.

However, since the availability of lithium and anticonvulsant and antipsychotic medications, ECT has generally been reserved for patients with acute mania who do not respond to adequate pharmacological treatment. There is evidence from the retrospective and prospective studies that a substantial number of medication-resistant patients with mania benefit from ECT (McCabe 1976; Black et al. 1986; Mukherjee et al. 1988). For example, one of the prospective studies required that patients had failed an adequate trial of lithium and/or an antipsychotic medication prior to randomization to ECT or intensive pharmacotherapy. Clinical outcome was superior with ECT compared to combined treatment with lithium and haloperidol (Mukherjee et al. 1989). Nonetheless, the evidence suggests that, as with major depression, medication resistance predicts poorer response to ECT in acute mania (Mukherjee et al. 1994). While the majority of medication-resistant patients with acute mania respond to ECT, the response rate is lower than among patients in whom ECT is used as a first-line treatment.

The rare syndrome of manic delirium represents a primary indication for the use of ECT, as it is rapidly effective with a high margin of safety (Constant 1972; Heshe and Roeder 1975; Kramp and Bolwig 1981). In addition, manic patients who cycle rapidly may be particularly unresponsive to medications, and ECT may represent an effective alternative treatment (Berman and Wolpert 1987; Mosolov and Moshchevitin 1990; Vanelle et al. 1994).

Other than medication resistance, there have been few attempts to examine clinical features predictive of ECT response in acute mania. One study suggested that symptoms of anger, irritability and suspiciousness were associated with poorer ECT outcome. Overall severity of mania and degree of depression (mixed state) at preECT baseline were not related to ECT response (Schnur et al. 1992). In this respect, there may be some overlap between the clinical features predictive of response to ECT and lithium in acute mania (Goodwin and Jamison 1990).

2.3.3. Schizophrenia. Convulsive therapy was introduced as a treatment for schizophrenia (Fink 1979). Early in its use, it became evident that efficacy of ECT was superior in mood disorders than in schizophrenia. The introduction of effective antipsychotic medications markedly reduced the utilization of ECT in patients with schizophrenia. However, ECT remains an important treatment modality, particularly for patients with schizophrenia who do not respond to pharmacological treatment (Fink and Sackeim 1996). In the United States, schizophrenia and related conditions (schizophreniform and schizoaffective disorders) constitute the second most common diagnostic indication for ECT (Thompson and Blaine 1987; Thompson et al. 1994).

The earliest reports on the efficacy of ECT in patients with schizophrenia largely comprised uncontrolled case series (Guttmann et al. 1939; Ross and Malzberg 1939; Zeifert 1941; Kalinowsky 1943; Kalinowsky and Worthing 1943; Danziger and Kindwall 1946; Kino and Thorpe 1946; Kennedy and Anchel 1948; Miller et al. 1953), historical comparisons (Ellison and Hamilton 1949; Gottlieb and Huston 1951; Currier et al. 1952; Bond 1954) and comparisons of ECT with milieu therapy or psychotherapy (Goldfarb and Kieve 1945; McKinnon 1948; Palmer et al. 1951; Wolff 1955; Rachlin et al. 1956). These early reports lacked operational criteria for diagnosis and it is likely that the samples included mood-disorder patients, given the overinclusiveness of the diagnosis of schizophrenia in that era (Kendell 1971; Pope and Lipinski, 1978). Often, patient samples and outcome criteria were poorly characterized. Nonetheless, the early reports were enthusiastic regarding the efficacy of ECT, noting that a large proportion of patients with schizophrenia, typically on the order of 75%, showed remission or marked improvement (see Salzman, 1980; Small, 1985; Krueger and Sackeim 1995 for reviews). In this early work, it was also noted that ECT was considerably less effective in schizophrenic patients with insidious onset and long duration of illness (Cheney and Drewry, 1938: Ross and Malzberg 1939; Zeifert 1941; Chafetz 1943; Kalinowsky 1943; Lowinger and Huddleson 1945; Danziger and Kindwall 1946; Shoor and Adams 1950; Herzberg 1954). It was also suggested that schizophrenic patients commonly required particularly long courses of ECT to achieve full benefit (Kalinowsky, 1943; Baker et al. 1960a).

Seven trials have used a ‘real vs. sham ECT’ design to examine efficacy in patients with schizophrenia (Miller et al. 1953; Ulett et al. 1954, 1956; Brill et al. 1957, 1959a, 1959b, 1959c; Heath et al. 1964; Taylor and Fleminger 1980; Brandon et al. 1985; Abraham and Kulhara 1987; see Krueger and Sackeim 1995 for a review). The studies prior to 1980 failed to demonstrate a therapeutic advantage of real ECT relative to sham treatment (Miller et al. 1953; Brill et al. 1959a, 1959b, 1959c; Health et al. 1964). In contrast, the three more recent studies all found a substantial advantage for real ECT in short-term therapeutic outcome (Taylor and Fleminger 1980; Brandon et al. 1985; Abraham and Kulhara 1987). The factors that likely account for this discrepancy are the chronicity of the patients studied and the use of concomitant antipsychotic medication (Krueger and Sackeim 1995). The early studies focused mainly on patients with a chronic, unremitting course, while patients with acute exacerbations were more common in recent studies. All of the recent studies involved use of antipsychotic medications in both the real ECT and sham groups. As discussed below, there is evidence that the combination of ECT and antipsychotic medication is more effective in schizophrenia than either treatment alone.

The utility of monotherapy with ECT or antipsychotic medication was compared in a variety of retrospective (DeWet 1957; Borowitz 1959; Ayres 1960; Rohde and Sargant 1961) and prospective (Baker et al. 1958, 1960b; Langsley et al. 1959; King 1960; Ray 1962; Childers 1964; May and Tuma 1965, May 1968; May et al. 1976,1981; Bagadia et al. 1970; Murrillo and Exner 1973a, 1973b; Exner and Murrillo 1973, 1977; Bagadia et al. 1983) studies of patients with schizophrenia. In general, short-term clinical outcome in schizophrenia with antipsychotic medication was found to be equivalent or superior to that of ECT, although there were exceptions.

(Murrillo and Exner 1973a). However, a consistent theme in this literature was the suggestion that patients with schizophrenia who had received ECT had superior long-term outcome compared with medication groups (Baker et al. 1958; Ayres 1960; May et al. 1976, 1981; Exner and Murrillo 1977). This research was conducted in an era when the importance of continuation and maintenance treatment was not appreciated and none of the studies controlled the treatment received following resolution of the schizophrenic episode. Nonetheless, the possibility that ECT may have long-term beneficial effects in schizophrenia merits attention.

A variety of prospective studies have compared the efficacy of combination treatment using ECT and antipsychotic medication with monotherapy with ECT or antipsychotic medication (Ray 1962; Childers 1964; Smith et al. 1967; Janakiramaiah et al. 1982; Small et al. 1982; Ungvari and Petho 1982; Abraham and Kulhara 1987; Das et al. 1991). Relatively few of these studies involved random assignment and blind outcome assessment. Nonetheless, in each of the three studies in which ECT alone was compared with ECT combined with an antipsychotic, medication there was evidence that the combination was more effective (Ray 1962; Childers 1964; Small et al. 1982). With the exception of Janakiramaiah et al (1982), all studies that compared the combination treatment with antipsychotic medication monotherapy found the combination treatment to be more effective (Ray 1962; Childers, 1964: Smith et al. 1967; Small et al. 1982: Ungvari and Petho 1982; Abraham and Kulhara 1987; Das et al. 1991). This pattern held despite the dosage of the antipsychotic medication often being lower when combined with ECT. The few findings on the persistence of benefit suggested that there was a reduced rate of relapse in patients who had received the combination of ECT and antipsychotic medication as acute phase treatment. A new study has also found that combination ECT and antipsychotic medication is more effective as a continuation therapy than either treatment alone in patients with medication-resistant schizophrenia who respond to the combination treatment in the acute phase (Chanpattana et al. in press). These results support the recommendation that in the treatment of patients with schizophrenia and possibly other psychotic conditions the combination of ECT and antipsychotic medication may be preferable to the use of ECT alone.

In current practice ECT is rarely used as a first-line treatment for patients with schizophrenia. Most commonly, ECT is considered in patients with schizophrenia only after unsuccessful treatment with antipsychotic medication. Thus, the key clinical issue concerns the efficacy of ECT in medication-resistant schizophrenic patients.

There has yet to be a prospective, blinded study in which patients with medication-resistant schizophrenia are randomized to continued treatment with antipsychotic medication or to ECT (either alone or in combination with antipsychotic medication). Information on this issue comes from naturalistic case series (Childers and Therrien 1961; Rahman 1968; Lewis 1982; Friedel 1986; Gujavarty et al, 1987; Konig and Glatter-Gotz 1990; Milstein et al. 1990; Sajatovi and Meltzer 1993; Chanpattana et al. in press). This work suggests that a substantial number of patients with medication-resistant schizophrenia benefit when treated with combination ECT and antipsychotic medication. The safe and effective use of ECT has been reported when it has been administered in combination with traditional antipsychotic medications (Friedel 1986; Gujavarty et al. 1987; Sajatovi and Meltzer 1993) or those with atypical properties, particularly clozapine (Masiar and Johns 1991; Klapheke 1991a. 1993; Landy 1991; Safferman and Munne 1992; Frankenburg et al. 1992; Cardwell and Nakai, 1995; Farah et al. 1995; Benatov et al. 1996). While some practitioners have been concerned that clozapine may increase the likelihood of prolonged or tardive seizures when combined with ECT (Bloch et al. 1996), such adverse events appear to be rare.

Prediction of response. Since the earliest research, the clinical feature most strongly associated with the therapeutic outcome of ECT in patients with schizophrenia has been the duration of illness. Patients with acute onset of symptoms (i.e., psychotic exacerbations) and shorter illness duration are more likely to benefit from ECT than patients with persistent, unremitting symptomatology (Cheney & Drewry 1938; Ross and Malzberg 1939; Zeifert 1941; Kalinowsky 1943; Lowinger and Huddelson 1945; Danziger and Kindwall 1946; Herzberg 1954; Landmark et al. 1987; Dodwell and Goldberg 1989). Less consistently, preoccupation with delusions and hallucinations (Landmark et al. 1987), fewer schizoid and paranoid premorbid personality traits (Wittman 1941; Dodwell and Goldberg 1989), and the presence of catatonic symptoms (Kalinowsky and Worthing 19431; Hamilton and Wall 1948; Ellison and Hamilton 1949; Wells, 1973; Pataki et al. 1992) have been linked to positive therapeutic effects. In general, the features that have been associated with the clinical outcome of ECT in patients with schizophrenia overlap substantially with features that predict outcome with pharmacotherapy (Leff and Wing 1971; World Health Organization 1979; Watt et al. 1983). While patients with unremitting, chronic schizophrenia are the least likely to respond, it has also been argued that such patients should not be denied a trial of ECT (Fink and Sackeim 1996). The probability of significant improvement with ECT may be low in such patients, but alternative therapeutic options may be even more limited, and a small minority of patients with chronic schizophrenia may show dramatic improvement following ECT.

ECT may also be considered in the treatment of patients with schizoaffective or schizophreniform disorder (Tsuang, et al. 1979; Pope et al. 1980; Ries et al. 1981; Black et al. 1987c). The presence of perplexity or confusion in patients with schizoaffective disorder may be predictive of positive clinical outcome (Perris 1974; Dempsy et al. 1975; Dodwell and Goldberg 1989). Many practitioners believe that the manifestation of affective symptoms in patients with schizophrenia is predictive of positive clinical outcome. However, the evidence supporting this view is inconsistent (Folstein et al. 1973; Wells 1973, Dodwell and Goldberg 1989).

2.4. Other Diagnostic Indications

ECT has been used successfully in some other conditions, although this utilization has been rare in recent years (American Psychiatric Association 1978, 1990, Thompson et al. 1994). Much of this usage has been reported as case material, and typically reflects the administration of ECT only after other treatment options have been exhausted or when the patient presents with life-threatening symptomatology. Because of the absence of controlled studies, which would, in any event, be difficult to carry out given the low utilization rates, any such referrals for ECT should be well substantiated in the clinical record. The use of psychiatric or medical consultation by individuals experienced in the management of the specific condition may be a useful component of the evaluation process.

2.4.1. Psychiatric disorders. Besides the major diagnostic indications discussed above, the evidence for the efficacy of ECT in the treatment of other psychiatric disorders is limited. As noted earlier, major diagnostic indications for ECT may coexist with other conditions, and practitioners should not be dissuaded by the presence of secondary diagnoses from recommending, ECT when it is otherwise indicated, e.g., a major depressive episode in a patient with a pre-existing anxiety disorder. However, there is no evidence of beneficial effects in patients with Axis II disorders or most other Axis I disorders who do not also have one of the major diagnostic indications for ECT. Although there are case reports of favorable outcome in some selective conditions, evidence for efficacy is limited. For example, some patients with medication-resistant obsessive compulsive disorder may show improvement with ECT (Gruber 1971; Dubois 1984; Mellman and Gorman 1984; Janike et al. 1987; Khanna et al. 1988; Maletzky et al. 1994). However, there have been no controlled studies in this disorder, and the longevity of the beneficial effect is uncertain.

2.4.2. Mental disorders due to medical conditions. Severe affective and psychotic conditions secondary to medical and neurological disorders, as well as certain types of deliria, may be responsive to ECT. The use of ECT in such conditions is rare and should be reserved for patients who are resistant or intolerant to more standard medical treatments, or who require an urgent response. Prior to ECT, attention should be given to the evaluation of the underlying etiology of the medical disorder. It is largely of historical interest that ECT has been reported to be of benefit in conditions such as alcoholic delirium (Dudley and Williams 1972; Kramp and Bolwig 1981), toxic delirium secondary to phencyclidine (PCP) (Rosen et al. 1984; Dinwiddie et al. 1988), and in mental syndromes due to enteric fevers (Breakey and Kala 1977; O’Toole and Dyck 1977; Hafeiz 1987), head injury (Kant et al. 1995), and other causes (Stromgren 1997). ECT has been effective in mental syndromes secondary to lupus erythematosus (Guze 1967; Allen and Pitts 1978; Douglas and Schwartz 1982; Mac and Pardo 1983). Catatonia may-be secondary to a variety of medical conditions and is usually responsive to ECT (Fricchione et al. 1990; Rummans and Bassingthwaighte 1991; Bush et al. 1996).

When evaluating potential secondary mental syndromes, it is important to recognize that cognitive impairment may be a manifestation of major depressive disorder. Indeed, many patients with major depression have cognitive deficits (Sackeim and Steif 1988). There is a subgroup of patients with severe cognitive impairment that resolves with treatment of the major depression. This condition has been termed “pseudodementia” (Caine, 1981). Occasionally, the cognitive impairment may be sufficiently severe to mask the presence of affective symptoms. When such patients have been treated with ECT, recovery has often been dramatic (Allen 1982; McAllister and Price 1982: Grunhaus et al. 1983: Burke et al. 1985: Bulbena and Berrios 1986; O’Shea et al. 1987; Fink 1989). It should be noted, however, that the presence of pre-existing neurological impairment or disorder increases the risks for ECT-induced delirium and for more severe and persistent amnestic effects (Figiel et al. 1990; Krystal and Coffey, 1997). Furthermore, among patients with major depression without known neurological disease, the extent of preECT cognitive impairment also appears to predict the severity of amnesia at follow-up. Thus, while patients with baseline impairment thought to be secondary to the depressive episode may show improved global cognitive function at follow-up, they may also be subject to greater retrograde amnesia (Sobin et al. 1995).

2.4.3. Medical disorders. The physiological effects associated with ECT may result in therapeutic benefit in certain medical disorders, independent of antidepressant, antimanic, and antipsychotic actions. Since effective alternative treatments are usually available for these medical disorders. ECT should be reserved for use on a secondary basis.

There is now considerable experience in the use of ECT in patient’s with Parkinson’s disease (see Rasmussen and Abrams 1991; Kellner et al. 1994 for reviews). Independent of effects on psychiatric symptoms, ECT commonly results in general improvement in motor function (Lebensohn and Jenkins 1975; Dysken et al. 1976; Ananth et al. 1979; Atre-Vaidya and Jampala 1988; Roth et al. 1988; Stem 1991; Jeanneau, 1993; Pridmore and Pollard 1996). Patients with the “on-off” phenomenon, in particular, may show considerable improvement (Balldin et al. 1980 198 1; Ward et al. 1980; Andersen et al. 1987). However, the beneficial effects of ECT on the motor symptoms of Parkinson’s disease are highly variable in duration. Particularly in patients who are resistant or intolerant to standard pharmacotherapy, there is preliminary evidence that continuation or maintenance ECT may be helpful in prolonging the therapeutic effects (Pridmore and Pollard 1996).

Neuroleptic malignant syndrome (NMS) is a medical condition that has been repeatedly shown to improve following ECT (Pearlman 1986; Hermle and Oepen 1986; Pope et al. 1986-1 Kellam 1987; Addonizio and Susman 1987; Casey 1987; Hermesh et al. 1987; Weiner and Coffey 1987; Davis et al. 1991). ECT is usually considered in such patients after autonomic stability has been achieved, and should not be used without discontinuation of neuroleptic medications. Since the presentation of NMS restricts the pharmacological options for treatment of the psychiatric condition, ECT may have the advantage of being effective for both the manifestations of NMS and the psychiatric disorder.

ECT has marked anticonvulsant properties (Sackeim et al. 1983; Post et al. 1986) and its use as an anticonvulsant in patients with seizure disorders has been reported since the 1940s (Kalinowsky and Kennedy 1943; Caplan 1945, 1946; Sackeim et al. 1983; Schnur et al. 1989). ECT may be of value in patients with intractable epilepsy or status epilepticus unresponsive to pharmacological treatment (Dubovsky 1986; Hsiao et al. 1987; Griesener et al. 1997; Krystal and Coffey 1997).

RECOMMENDATIONS

2.1. General Statement

Referrals for ECT are based upon a combination of factors, including, the patient’s diagnosis, type and severity of symptoms, treatment history, consideration of the anticipated risks and benefits of ECT and alternative treatment options, and patient preference. There are no diagnoses which should automatically lead to treatment with ECT. In most cases ECT is used following treatment failure on psychotropic medications (see Section 2.2.2), although specific criteria exist for the use of ECT as a first-line treatment (see Section 2.2.1).

2.2. When Should a Referral for ECT Be Made?

2.2.1. Primary Use of ECT

Situations where ECT may be used prior to a trial of psychotropic medication include, but are not limited to, any of the following:

a) need for rapid, definitive response due to the severity of a psychiatric or medical condition

b) the risks of other treatments outweigh the risks of ECT

c) history of poor medication response or good ECT response in one or more previous episodes of illness

d) patient preference

2.2.2. Secondary Use of ECT

In other situations, a trial of an alternative therapy should be considered prior to referral for ECT. Subsequent referral for ECT should be based on at least one of the following:

a) treatment resistance (taking into account issues such as choice of medication, dosage and duration of trial, and compliance)

b) intolerance or adverse effects with pharmacotherapy which are deemed less likely or less severe with ECT

c) deterioration of the patient’s psychiatric or medical condition creating a need for a rapid, definitive response

2.3. Major Diagnostic Indications

Diagnoses for which either compelling data support the efficacy of ECT or a strong consensus exists in the field supporting such use:

2.3.1. Major Depression

a) ECT is an effective treatment for all subtypes of unipolar major depression, including major depression single episode (296.2x) and major depression, recurrent (296.3x) (American Psychiatric Association 1994).

b) ECT is an effective treatment for all subtypes of bipolar major depression, including bipolar disorder; depressed (296.5x); bipolar disorder mixed (296.6x); and bipolar disorder not otherwise specified (296.70).

2.3.2. Mania

ECT is an effective treatment for all subtypes of mania, including bipolar disorder, mania (296.4x); bipolar disorder, mixed (296.6x), and bipolar disorder, not otherwise specified (296.70).

2.3.3. Schizophrenia and Related Disorders

a) ECT is an effective treatment for psychotic exacerbations in patients with schizophrenia in any of the following situations:

1) when duration of illness from initial onset is short

2) when psychotic symptoms in the present episode have an abrupt or recent onset

3) catatonia (295.2x) or

4) when there is a history of a favorable response to ECT

b) ECT is effective in related psychotic disorders, notably schizophreniform disorder (295.40) and schizoaffective disorder (295.70). ECT may also be useful in patients with psychotic disorders not otherwise specified (298-90) when the clinical features are similar to those of other major diagnostic indications.

2.4. Other Diagnostic Indications

There are other diagnoses for which the efficacy data for ECT are only suggestive or where only- a partial consensus exists in the field supporting its use. In such cases, ECT should be recommended only after standard treatment alternatives have been considered as a primary intervention. The existence of such disorders, however, should not deter the use of ECT for treatment of patients who also have a concurrent major diagnostic indication.

2.4.1. Psychiatric Disorders

Although ECT has sometimes been of assistance in the treatment of psychiatric disorders other than those described above (Major Diagnostic Indications, Section 2.3), such use is not adequately substantiated and should be carefully justified in the clinical record on a case-by-case basis.

2.4.2. Psychiatric Disorders Due to Medical Conditions

ECT may be effective in the management of severe secondary affective and psychotic conditions displaying symptomatology similar to primary psychiatric diagnoses, including catatonic states.

There is some evidence that ECT may be effective in treating deliria of various etiologies, including toxic and metabolic.

2.4.3. Medical Disorders

The neurobiological effects of ECT may be of benefit in a small number of medical disorders.

Such conditions include:

a) Parkinson’s disease (particularly with the “on-off ‘ phenomenon b) neuroleptic malignant syndrome

c) intractable seizure disorder

Chapter 3. Medical Conditions Associated with Substantial Risk

ECT is often administered to patients with severe medical illness (see Chapter 4.1). In fact, it commonly is the treatment of choice in medically ill patients because of its speed of action and safety profile. There are no absolute medical contraindications to ECT. Instead, it is more pertinent to think in terms of degree of risk relative to the potential benefits of ECT.

Some conditions substantially increase the risk of treatment. For each patient, the attending physician and treating psychiatrist must undertake a risk-benefit analysis, including consideration of the seventy and duration of the illness and its threat to life; the likelihood of therapeutic success with ECT; the medical risks of ECT; and the benefits and risks of alternative treatments and of no treatment. After such an analysis, a choice can be made regarding the optimal intervention for an individual patient. In treating “high risk” patients with ECT, attempts should be made to improve and stabilize risk-related medical conditions (see Chapter 4.1). Careful medical evaluation is an essential component of this process and may include consultations with internists, cardiologists, neurologists, and other specialists (see Chapter 6).

The two organ systems of most importance when considering the medical risks of ECT are the cardiovascular system and the central nervous system. Most of the medical complications and mortality associated with ECT are referable to the heart. Recent myocardial infarction is believed to represent a risk for re-infarction during ECT (Applegate 1997). The concept of “recency” as it applies to this condition is difficult to define in the absence of relevant supporting data. The risks at six weeks following a mild myocardial infarction without adverse sequelae may be less than those present at six months following a severe, complicated infarction. In many cases of pre-existing cardiac disease the risks of ECT may be reduced by the use of short-acting intravenous antihypertensive agents (McCall et at. 1991) that diminish the hemodynamic changes that occur during the treatment or that exert other cardioprotective effects (set Chapter. 4.1).

Although there are little data to tie other specific cardiac disorders to substantially elevated morbidity and mortality with ECT, perioperative risk in general is believed to be greatly elevated in the presence of either uncompensated congestive heart failure or severe valvular heart disease (Dovinsky and Zyara 1997; Rayburn 1997). Again, pharmacologic means to diminish such risk exists (see Chapter 4.1). A similar situation can be said to exist with respect to vascular aneurysms. Here, lesions that are at increased risk of rupture with transient elevations in blood pressure are of particular concern, although, once more, data are lacking and the degree of risk can once more be minimized by appropriate acute antihypertensive prophylaxis (see Chapter 4.1).

Regarding the central nervous system, conditions associated with increased intracranial pressure, such as some brain tumors, are theoretically of great concern (Krystal and Coffey 1997). In the presence of these conditions, the rise in intracranial pressure that occurs with ECT could lead to brain herniation. However, such events are rare in practice (Kellner 1996). Most of the reports of dire outcomes are from the distant past when ECT technique was far less sophisticated (Maltbie 1980). The type and size of brain tumor also correlate with the degree of danger, smaller and slow-growing neoplasms posing less risk. For example, there are now several case reports of successful ECT in the presence of meningiomas (Fried and Mann 1988,- Greenberg et al. 1988: Hsiao 1984: Kellner and Rames, 1990; Malek-Ahmadi and Sedler 1989; Zwil et al. 1990). Clearly, clinical judgement needs to be exercised in determining the risk-benefit ratio in each individual case. Only rarely would one treat a patient with a known, large brain tumor, and likewise, only rarely would one need to avoid ECT in a patient with a small, stable meningioma. There is little information about the safety of ECT in other conditions associated with increased intracranial pressure, such as hydrocephalus or normal pressure hydrocephalus.

ECT may pose additional risks in patients who have recently suffered a cerebral infarct. Reports of stroke (either hemorrhagic or ischemic) during or shortly after ECT are surprisingly rare. Given the magnitude of hemodynamic changes, that occur during the treatment and the number of patients with cerebrovascular disease who receive ECT (Miller and Isenberg 1998; Zwil et al. 1992). This finding may be due to the brief duration of blood pressure and heart rate changes that are associated with ECT. Maintenance of blood pressure within a fairly narrow range is generally thought to be prudent, in order to avoid the potential risk of cerebral bleeding with severe hypertension or cerebral ischemia with hypotension (see Chapter 4.1).

Severe pulmonary conditions may lead to difficulties in airway management during and after the procedure. Consultation with anesthesiology or other staff regarding management (e.g. pre-ECT use of bronchodilators, attention to pre-treatment oxygenation) will often be indicated.

Patients with severe cardiopulmonary or other organ system disease that renders them high anesthesia risks (ASA level 4 or 5) also represents potentially high risk situations with ECT. Specialty consultations before ECT are often indicated to optimize the patient’s medical status (see Chapter 4.1 ).

In addition to medical conditions that increase the risks of ECT, certain medication regimens may also contribute to risk (see, Chapter 7).

RECOMMENDATIONS

1) There are no “absolute” medical contraindications to ECT.

2) Situations exist in which ECT is associated with an increased likelihood of serious morbidity or mortality. For such patients, the decision to administer ECT should be based upon the premise that their psychiatric condition is grave and that ECT is the safest treatment available.

3) Careful medical evaluation of risk factors should be carried out prior to ECT, with specific attention to modifications of the patient’s management and the administration of ECT which may diminish the level of risk (see Section 4.1).

4) Specific conditions that may be associated with substantially increased risk include the following:

a) unstable or severe cardiovascular conditions such as recent myocardial infarction, poorly compensated congestive heart failure, and severe valvular cardiac disease.

b) aneurysm or vascular malformation that might be susceptible to rupture with increased blood pressure.

c) increased intracranial pressure, as may occur with some brain tumors or other space-occupying cerebral lesions.

d) recent cerebral infarction.

e) pulmonary conditions such as severe chronic obstructive pulmonary disease, asthma, or pneumonia.

f) anesthetic risk rated as ASA level 4 or 5.

Chapter 5. Adverse Effects

5.1. Medical Complications

Precise rates of mortality attributable to ECT are difficult to determine due to methodological issues intrinsic to studies of medical mortality, such as uncertainty as to cause of death, time frame for linking death to ECT, and variability in reporting requirements. The mortality attributed to ECT is estimated to be approximately the same as that associated with minor surgery (McCabe 1985 Warner et al. 1993; Brand et al. 1994; Badrinath et al. 1995: Hall et al. 1997). Published estimates from large and diverse patient series over several decades report up to 4 deaths per 100,000 treatments (Heshe and Roeder, 1976; Fink, 1979; Weiner 1979; Babigian and Guttmacher, 1984; Crowe, 1984; Kramer, 1985: Abrams 1997b; Reid et al. 1998). Despite the frequent use of ECT in patients with significant medical complications and in the elderly (Sackeim 1993, 1998; Weiner et al. in press), rates of mortality appear to have decreased in recent years. A reasonable current estimate is that the rate of ECT-related mortality is 1 per 10,000 patients. This rate may be higher in patients with severe medical conditions. The rate of significant morbidity and mortality is believed to be lower with ECT than with treatment with some types of antidepressant medication (e.g., tricyclics) (Sackeim 1998). There is also evidence from longitudinal follow-up studies that mortality rates following hospitalization are lower among depressed patients who received ECT than patients who received alternative forms of treatment or no treatment (Avery and Winokur, 1976; Philibert et al. 1995)

When mortality occurs with ECT, it typically happens immediately following the seizure or during the postictal recovery period. Cardiovascular complications are the leading cause of death and of significant morbidity (Pitts 1982; Burke et al. 1987; Welch and Drop 1989; Zielinski et al. 1993; Rice et al. 1994). Despite the short-lived increases in cerebral blood flow and intracranial pressure, cerebrovascular complications are notably rare (Hsiao et al. 1987). Given the high rate of cardiac arrhythmias in the immediate postictal period, the majority of which are benign and resolve spontaneously, ECG should be monitored during and immediately following the procedure (see Section 11.8) and patients should not be taken to the recovery area until there is resolution of significant arrhythmias. Vital signs (pulse, systolic and diastolic pressure) should be stable prior to the patient’s leaving the recovery area (Section 11.10). Patients with pre-existing cardiac illness are at greater risk for post-ECT cardiac complications (Prudic et al. 1987; Zielinski et al. 1993; Rice et al. 1994). Indeed, there is evidence that the type of pre-existing cardiac disease predicts the type of complication that may be encountered following ECT. For example, ventricular arrythmias are more common in patients with pre-existing ventricular abnormalities than in patients with ischemic heart disease (Zielinski et al. 1993). Management of cardiac complications is discussed in Chapter 11.

Two other possible sources of morbidity are prolonged seizures and tardive seizures (Weiner et al. 1980a). Management of prolonged seizures is described in Section 11.9. Failure to terminate seizures within a period of 3 to 5 minutes may increase postictal confusion and amnesia. Inadequate oxygenation during prolonged seizures increases the risk of hypoxia and cerebral dysfunction, as well as cardiovascular complications. In animal studies, seizure activity that is sustained for periods exceeding 30-60 minutes, regardless of steps taken to maintain appropriate levels of blood gases, is associated with an increased risk of structural brain damage and cardiovascular and cardiopulmonary complications (Meldrum et al. 1974; Ingvar 1986; Meldrum 1986; Siesjo et al. 1986; O’Connell et al. 1988; Devanand et al. 1994).

Prolonged seizures and status epilepticus may be more likely in patients receiving medications that lower seizure threshold or interfere with seizure termination (e.g. theophylline, even at therapeutic levels) (Peters et al. 1984; Devanand et al. 1988a; Abrams, 1997a), in patients receiving concomitant lithium therapy (Weiner et al. 1980b), in patients with pre-existing electrolyte imbalance (Finlayson et al. 1989), and with the repeated induction of seizures within the same treatment session (e.g., multiple monitored ECT) (Strain-and Bidder 1971, Maletzky 1981).

There has been concern as to whether the rate of spontaneous seizures is increased following the course of ECT (Assael et al. 1967; Devinsky and Duchowny 1983). The evidence indicates, however, that such events are extremely rare and probably do not differ from population base rates (Blackwood et al. 1980; Small et al. 1981). There are no data concerning rates of tardive seizures, i.e., seizures that occur following termination of the ECT-induced seizure, but experience indicates that these are also rare events. As noted in Section 11.9, prolonged or tardive seizures occurring during the immediate postictal period are often not accompanied by motor manifestations, underscoring the need for EEG seizure monitoring (Rao et al. 1993). Nonconvulsive status epilepticus may also occur in the interictal period, with an abrupt onset of delirium, unresponsiveness, and/or agitation as distinguishing clinical features (Grogan et al. 1995). Cessation of EEG abnormalities and improved cognitive function following short-acting anticonvulsant treatment (e.g. intravenous lorazepam or diazepam) may prove diagnostic (Weiner and Krystal, 1993).

Prolonged postictal apnea is a rare event that occurs primarily in patients with a pseudocholinesterase deficiency resulting in slow metabolism of succinylcholine (Packman et al. 1978). Maintaining adequate oxygenation is critical in instances of prolonged apnea, which will usually resolve spontaneously within 30 to 60 minutes. When prolonged apnea is encountered, it is helpful to obtain a dibuciane number assay or a pseudocholinesterase level prior to the next treatment in order to establish etiology. At subsequent treatments, either a very low dose of succinylcholine may be used or a non-depolarizing muscle relaxant, such as atracurium, may be substituted (Hickey et al. 1987; Hicks, 1987; Stack et al. 1988; Kramer and Afrasiabi 1991; Lui et al. 1993).

To some extent, medical adverse events can be anticipated. Whenever possible, the risks of such events should be minimized by optimization of the patient’s medical condition prior to ECT and/or modifications in ECT procedures. Patients with preexisting cardiac illness, compromised pulmonary status, a history of CNS insult, or medical complications following prior courses of anesthesia or ECT are especially likely to be at increased risk (Weiner and Coffey 1988; Zieliniski et al. 1993). ECT psychiatrists should review the medical work-up and history of prospective ECT patients (see Chapter 6). Specialist consultations or additional laboratory studies may be called for, as well as changes in medication regimens. In spite of careful pre-ECT evaluation, medical complications may arise which have not been anticipated. ECT facilities should be staffed with personnel prepared to manage potential clinical emergencies and should be equipped accordingly (see Chapters 9 and 10). Examples of these events include cardiovascular complications (such as cardiac arrest, arrythmias, ischemia, hyper- and hypotension), prolonged apnea, and prolonged or tardive seizures and status epilepticus.

Major adverse events that occur during or soon after the ECT course should be documented in the patient’s medical record. The steps taken to manage the event, including specialist consultation, use of additional procedures, and administration of medications, should likewise be documented. As cardiovascular complications are the most likely source of significant adverse events and are seen most frequently in the immediate post-ECT period, the treatment team should be capable of managing the major classes of cardiovascular complications. A set of predetermined procedures for dealing with instances of prolonged or tardive seizures and status epilepticus are helpful.

5.2. Systemic Side Effects

Headache is a common side effect of ECT and is observed in as many as 45% of patients during and shortly following the postictal recovery period (Devanand et al. 1995; Freeman and Kendell 1980; Gomez 1975; Sackeim et al. 1987d: Tubi et al. 1993; Weiner et al. 1994). However, the precise incidence of postECT headache is difficult to determine due to methodological issues such as the high baseline (preECT) occurrence of headache in patients with depression, the potential effects of concurrent medication or medication withdrawal, and differences between studies in the assessment of headache. PostECT headache appears to be particularly common in younger patients (Devanand et al. 1995) and especially in children and adolescents (Rey and Walter 1997; Walter and Rey 1997) It is not known whether pre-existing headache syndromes (e.g., migraine) increase the risk of postECT headache, but ECT may exacerbate a previous headache condition (Weiner et al. 1994). The occurrence of postECT headache does not appear to be related to stimulus electrode placement (at least bifrontotemporal vs. right unilateral) (Fleminger et al. 1970; Sackeim et al. 1987d; Tubi et al. 1993; Devanand et al. 1995), stimulus dosage (Devanand et al. 1995), or therapeutic response to ECT (Sackeim et al. 1987d; Devanand et al. 1995).

In most patients the postECT headache is mild (Freeman and Kendell 1980; Sackeim et al. 1987d), although a sizable minority will report severe pain associated with nausea and vomiting. Typically the headache is frontal in location and has a throbbing character.

The etiology of postECT headache is not known. Its throbbing character suggests a similarity with vascular headache, and ECT may be associated with a temporary change in quality of headache from muscle-contraction type to vascular type (Weiner et al. 1994; Weinstein 1993). Indeed, ECT upregulates 5-HT2 receptors and 5-HT2 receptor sensitization has been associated with development of vascular headache (Weiner et al. 1994). Other suggested mechanisms include electrically induced temporalis muscle spasm or acute increase in blood pressure and cerebral blood flow (Abrams 1997a; Weiner et al. 1994).

Treatment of postECT headache is symptomatic. Aspirin, acetaminophen, or non-steroidal anti-inflammatory drugs (NSAIDs) typically are highly effective, particularly if given promptly after the onset of pain. Sumatriptan, a serotonin 5HTID receptor agonist, has also been effective at doses of 6 mg subcutaneously (DeBattista and Mueller 1995) or 25 – 100 mg orally (Fantz et al. in press). Some patients will require more potent analgesics (e.g. codeine), although narcotics may contribute to associated nausea. Most patients also benefit from bed rest in a quiet, darkened environment.

PostECT headache may occur after any ECT treatment in a course, irrespective of its occurrence at any prior treatment. Patients who experience frequent postECT headache may benefit from prophylactic treatment, such as aspirin, acetaminophen, or NSAIDs given as soon as possible after ECT, or even immediately prior to the ECT treatment. Subcutaneous sumatriptan 6 mg given several minutes prior to ECT was also found to provide effective prophylaxis in a patient with severe, refractory postECT headache (DeBattista and Mueller 1995).

Estimates of the prevalence of nausea following ECT vary from 1.4% – 23% of patients (Gomez 1975; Sackeim et al. 1987d), but the occurrence is difficult to quantify because of methodological issues noted above for headache. Nausea may occur secondary to headache or its treatment with narcotics, particularly in patients with vascular-type headache. It may also occur independently either as a side effect of anesthesia or via other unknown mechanisms. When nausea accompanies headache, the primary treatment should focus on the relief of headache as outlined above. PostECT nausea is otherwise typically well controlled with dopamine-blocking agents, such as phenothiazine derivatives (e.g. prochlorperazine and others), butyrophenones (haloperidol, droperidol), trimethabenzamide, or metoclopramide. If nausea is severe or accompanied by vomiting these agents should be administered parenterally or by suppository. All of these agents have the potential to cause hypotension and motoric side effects, and may lower seizure threshold. If nausea does not respond to these treatments or if side effects are problematic, the serotonin 5HT3 receptor antagonists ondansetron or dolasetron may be useful alternatives. These medications may be given in single intravenous doses of 4 mg and 12.5 mg respectively, several minutes before or after ECT. The greater expense of these medications and their lack of proven superiority over traditional anti-emetics in the setting, of ECT may limit their routine use. If problematic nausea routinely follows the use of a particular anesthetic, an alternative anesthetic may be considered.

5.3 ). Treatment Emergent Mania

As with pharmacological antidepressant treatments, a small minority of depressed patients or patients in mixed affective states switch into hypomania or mania during the ECT course (Devanand et al. 1988b; Andrade et al. 1988b, 1990; Angst et al. 1992; Devanand et al. 1992). In some patients, the severity of manic symptoms may worsen with further ECT treatments. In such cases, it is important to distinguish treatment emergent manic symptoms from delirium with euphoria (Devanand et al. 1988b). There are a number of phenomenological similarities between the two conditions. However, in delirium with euphoria patients are typically confused and have pronounced memory disturbance. The confusion or disorientation should be continuously present and evident from the period immediately following the treatment. In contrast, hypomanic or manic symptomatology may occur in the context of a clear sensorium. Therefore, evaluating cognitive status may be particularly helpful in distinguishing between these states. In addition, states of delirium with euphoric are often characterized by a giddiness in mood or “carefree” disposition. Classical features of hypomania, such as racing thoughts, hypersexuality, irritability, etc. may be absent. In cases of delirium with euphoria an increase in the time between treatments, a decrease in the stimulus intensity, or a change to unilateral from bilateral electrode placement may lead to resolution of the condition.

There is no established strategy on how to manage emergent manic symptoms during the ECT course. Some practitioners continue ECT to treat both the mania and any residual depressive symptomatology. Other practitioners postpone further ECT and observe the patient’s course. At times, manic symptomatology will remit spontaneously without further intervention. Should the mania persist, or the patient relapse back into depression, reinstitution of ECT may be considered. Yet other practitioners terminate the ECT course and start pharmacotherapy, often with lithium carbonate or other mood stabilizer, to treat emergent manic symptomatology.

5.4. Objective Cognitive Side Effects

The cognitive side effects produced by ECT have been the subject of intense investigation (Squire 1986; Sackeim 1992; McElhiney et al. 1995) and are the major complications limiting its use. ECT psychiatrists should be familiar with the nature and variability of cognitive side effects, and this information should be conveyed during the consent process (see Chapter 8 ).

The cognitive side effects of ECT have four essential features. First, the nature and severity of cognitive alterations rapidly change with time from last treatment. The most severe cognitive side effects are observed in the postictal period. Immediately following seizure induction, patients experience a variable, but usually brief, period of disorientation, with impairments in attention, praxis, and memory (Sackeim 1986). These deficits recede at variable rates over time. Consequently, the magnitude of deficits observed during the course of ECT will be a function, in part, of the time of assessment relative to the last treatment and the number of treatments received (Daniel and Crovitz, 1983a; Squire et al. 1985).

Second, the methods used in ECT administration profoundly impact on the nature and magnitude of cognitive deficits. For example, the methods of ECT administration will strongly determine the percentage of patients that develop delirium, characterized by continuous disorientation (Miller et al. 1986; Daniel and Crovitz 1986; Sackeim et al. 1986, 1993). In general, as described in Table 1, bilateral electrode placement, sine wave stimulation, high electrical dosage relative to seizure threshold, closely spaced treatments, larger numbers of treatments, and high dosage of barbiturate anesthetic agents are each independently associated with more intense cognitive side effects compared to right unilateral electrode placement, brief pulse waveform, lower electrical intensity, more widely spaced treatments, fewer treatments, and lower dosage of barbiturate anesthesia (Miller et al. 1985; Sackeim et al. 1986; Weiner et al. 1986b: Sackeim et al. 1993; Lerer et al. 1995; McElhiney et al. 1995). Optimization of these parameters can minimize short-term cognitive side effects and likely reduce the magnitude of long-term changes (Sobin et al. 1995). In patients who develop severe cognitive side effects, such as delirium (Summers et al. 1979; Miller et al. 1986; Mulsant et al. 1991), the attending physician and ECT psychiatrist should review and adjust the treatment technique being used, such as switching to unilateral ECT, lowering the electrical dosage administered, and/or increasing the time interval between treatments, and decrease the dosage or discontinue any medications being administered that may exacerbate cognitive side effects.

Third, patients vary considerably in the extent and severity of cognitive side effects following ECT. There is limited information about the factors that contribute to these individual differences. There is evidence that among depressed patients without known neurological disease or insult, the extent of preECT global cognitive impairment, i.e., mini-Mental State Exam (MMSE) scores, predicts the magnitude of retrograde amnesia for autobiographical information at long-term follow-up. While ECT typically results in improvement in global cognitive status in these patients, as a function of symptomatic response, nonetheless, these same patients may have greater persistent amnesia for personal memories (Sobin et al. 1995). Similarly, there is evidence that the duration of disorientation immediately following the ECT treatment is independently predictive of the magnitude of retrograde amnesia for autobiographical information. Patients who require prolonged periods to recover orientation may be at greater risk for more profound and persistent retrograde amnesia (Sobin et al. 1995). Patients with pre-existing neurological disease or insult (e.g., Parkinson’s disease, stroke) may also be at increased risk for ECT-induced delirium and memory deficits (Figiel et al. 1991). Magnetic resonance imaging (MRI) findings of basal ganglia lesions and severe white matter hyperintensities have also been linked to the development of an ECT-induced delirium (Figiel et al. 1990). Some medications may exacerbate ECT-induced cognitive side effects. These include lithium carbonate (Small et al. 1980; Weiner et al. 1980b), and medications with marked anticholinergic, properties, particularly in elderly patients.

Fourth, ECT results in highly characteristic cognitive changes. Across diagnostic groups, prior to receiving ECT, many patients have deficits in attention and concentration that limit their capacity information (Byrne 1977; Pogue-Geile and Oltmanns, 1980; Cornblatt et al. 1981; Sackeim and Steif, 1988). For example, patients with severe psychopathology often have deficient recall of information that was just presented to them (immediate memory). In depressed patients, these deficits are most marked for unstructured material that requires effortful processing in order to impose organization (Weingartner and Silberman 1984; Roy-Byrne et al. 1986). However, such patients are considerably less likely to have deficits in retaining the new information that they do learn (delayed memory) (Cronholm and Ottosson 1961; Sternberg and Jarvik 1976; Steif et al. 1986). With symptomatic response following ECT, the deficits in attention and concentration usually resolve. Consequently, measures of immediate memory are either unchanged or improved within a few days of ECT termination (Cronholm and Ottosson, 1961; Steif et al. 1986; Weiner et al. 1986b; Rossi et al. 1990; Sackeim et al. 1993). Since attention and concentration are essential to many aspects of cognitive function, it is not surprising that shortly following completion of the ECT course improvement may be observed in a wide variety of neuropsychological domains, including global cognitive status (Sackeim et al. 1991; Sobin et al. 1995) and measures of general intelligence (IQ) (Huston and Strother 1948; Stieper et al 1951; Squire et al. 1975; Malloy et al. 1981; Sackeim et al. 1992). There is no evidence that ECT results in impairments of executive functions (e.g., the capacity to shift mental sets), abstract reasoning, creativity, semantic memory, implicit memory, or skill acquisition or retention (Weeks et al. 1980; Frith et al. 1983; Squire et al. 1984; Taylor and Abrams 1985; Jones et al. 1988).

Against this background of unchanged or improved neuropsychological performance, ECT selectively results in anterograde and retrograde amnesia. The anterograde amnesia is characterized by rapid forgetting of newly-learned information (Cronholm and Ottosson 1961; Squire 1986; Steif et al. 1986; Weiner et al. 1986b; Frith et al. 1987; Sackeim et al. 1993). As noted, compared to preECT baseline, a few days following ECT patients may recall more items in a list that was just presented. However, recall after a delay will often be impaired (Korin et al. 1956; Cronholm and Ottosson 1961; Cronholm and Molander 1964; Squire and Miller 1974; Steif et al. 1986; Weiner et al. Squire and Chace 1975; d’Elia 1976; Robertson and Inglis 1978, 1986b; Calev et al. 1989b; Sackeim et al. 1993). The extent and persistence of this rapid forgetting of newly learned information varies among patients and should be taken into account when making recommendations regarding the postECT convalescence period. Until there is substantial resolution of the anterograde amnesia, returning to work, making important financial or personal decisions, or driving may be restricted. The anterograde amnesia rapidly resolves following the termination of ECT. Indeed, no study has documented anterograde amnestic effects of ECT more than a few weeks following the ECT course (Strain et al. 1968; Bidder et al. 1970; Heshe et al. 1978; Jackson, 1978; Fraser and Glass, 1980; Weeks et al. 1980; Gangadhar et al. 1982; Frith et al. 1983; Weiner et al. 1986b; Sackeim et al. 1993). It is unlikely that ECT has any long-term effect on the capacity to learn and retain new information.

Following ECT, patients also display retrograde amnesia. Deficits in the recall of both personal (autobiographical) and public information are usually evident, and the deficits are typically greatest for events that occurred temporally closest to the treatment (Janis, 1950; Cronholm and Molander 1961; Strain et al. 1968; Squire 1975; Squire et al. 1975, 1976, 1981; Weeks et al. 1980; Sackeim et al. 1986; Wiener et al 1986b; Sackeim et al 1993; McElhiney et al. 1995). The magnitude of the retrograde amnesia is greatest immediately following the treatment. A few days following the ECT course, memory for events in the remote past is usually intact, but there may be difficulty in recalling events that transpired several months to years prior to ECT. The retrograde amnesia over this time span is rarely complete. Rather, patients have gaps or spottiness in their memories of personal and public events. Recent evidence suggests that the retrograde amnesia is typically greater for public information (knowledge of events in the world) as compared to personal information (autobiographic details of the patient’s life) (Lisanby et al. in press). The emotional valence of autobiographical events, i.e., memories of pleasant or distressful events, is not related to their likelihood of being forgotten (McElhiney et al. 1995).

As time from ECT increases, there is usually substantial reduction in the extent of retrograde amnesia. Older memories are more likely to be recovered. The time course for this shrinkage of retrograde amnesia is often more gradual than that for the resolution of anterograde amnesia. In many patients the recovery from retrograde amnesia will be incomplete, and there is evidence that ECT can result in persistent or permanent memory loss (Squire et al. 1981; Weiner et al. 1986b; McElhiney et al. 1995; Sobin et al. 1995). Owing to a combination of anterograde and retrograde effects, many patients may manifest persistent loss of memory for some events that transpired in the interval starting several months before and extending to several weeks following the ECT course. There are individual differences, however, and, uncommonly, some patients may experience persistent amnesia that extends back several years prior to ECT. Profound and persistent retrograde amnesia may be more likely in patients with pre-existing neurological impairment and patients who receive large numbers of treatments, using methods that accentuate acute cognitive side effects (e.g., sine wave stimulation, bilateral electrode placement, high electrical stimulus intensity).

To determine the occurrence and severity of cognitive changes during and following the ECT course, orientation and memory functions should be assessed prior to initiation of ECT and throughout the course of treatment (see Chapter 12 for details).

5.5. Adverse Subjective Reactions

Negative subjective reactions to the experience of receiving ECT should be considered adverse side effects (Sackeim 1992). Prior to ECT, patients often report apprehension; rarely, some patients develop intense fear of the procedure during the ECT course (Fox 1993). Family members are also frequently apprehensive about the effects of the treatment. As part of the consent process prior to the start of ECT, patients and family members should be given the opportunity to express their concerns and questions to the attending physician and/or members of the ECT treatment team (see Chapter 8 ). Since much of the apprehension may be based on lack of information, it is often helpful to provide patients and family members with an information sheet describing basic facts about ECT (see Chapter 8 ). This material should be supplemental to the consent form. It is also useful to make available video material on ECT. Addressing the concerns and educational needs of patients and family members should be a process that continues throughout the course. In centers that regularly conduct ECT, it has been found useful to have ongoing group sessions led by a member of the treatment team, for patients receiving ECT and/or their significant others. Such group sessions, including prospective and recently treated patients and their families, may engender mutual support among these individuals and can serve as a forum for education about ECT.

Shortly following ECT, the great majority of patients report that their cognitive function is improved relative to their pre-ECT baseline (Cronholm and Ottosson 1963b; Shellenberger et al 1982; Frith et al 1983; Pettinati and Rosenberg 1984; Weiner et al 1986b; Mattes et al 1990; Calev et al 1991; Sackeim et al. 1993 ); Coleman et al 1996). Indeed, recent research has shown that two months following completion of ECT the memory self-ratings of former patients are markedly improved relative to their pre-ECT baseline and indistinguishable from healthy controls (Coleman et al. 1996). In patients who have received ECT, memory self-ratings show little association with the results of objective neuropsychological testing (Cronholm and Ottosson 1963b; Frith et al 1983; Squire and Slater 1983; Weiner et al 1986b; Squire and Zouzounis 1988; Calev et al 1991a; Coleman et al 1996). Likewise, in healthy and neurological samples, subjective memory assessments have generally shown weak or no association with objective neuropsychological measures (Bennett-Levy and Powell 1980; Broadbent et al. 1982; Rabbitt 1982; Larrabee and Levin 1986; Sackeim and Stem 1997). In contrast, strong associations are observed between mood state and memory self-ratings among patients who have received ECT, as well as other populations (Stieper et al. 1951; Frith et al 1983; Pettinati and Rosenberg 1984; Weiner et al. 1986b; Mattes et al 1990; Coleman et al. 1996). In essence, patients who benefit the most from ECT in terms of symptomatic response typically report the greatest improvement in subjective evaluations of memory.

A small minority of patients treated with ECT later report that they have suffered devastating consequences (Freeman and Kendell 1980, 1986). Patients may indicate that have dense amnesia extending far back into the past for events of personal significance and/or that broad aspects of cognitive function are impaired such that they are no longer able to engage in former occupations. The rarity of these subjective reports of profound cognitive deficits makes determination of their absolute base rates difficult. Multiple factors likely contribute to these perceptions by former patients.

First, in some patients self-reports of profound ECT-induced deficits may be accurate. As noted, as with any medical intervention, there are individual differences in the magnitude and persistence of ECT’s cognitive effects. In rare cases, ECT may result in a more dense and persistent retrograde amnesia that extends back to years prior to the treatment.

Second, some of the psychiatric conditions treated with ECT result in cognitive deterioration as part of their natural history. This may be particularly likely in young patients in their first psychotic episode (Wyatt 1991, 1995), and in older patients where ECT may unmask a dementing process. While in such cases, cognitive deterioration would have occurred inevitably, the experience of transient short-term side effects with ECT may sensitize patients to attribute the persistent changes to the treatment (Squire 1986; Sackeim 1992).

Third, as noted above, subjective evaluations of cognitive function typically show poor association with objective measurement and strong association with measures of psychopathology (Coleman et al. 1996). Only one study recruited patients with long-term complaints about effects of ECT and compared them to two control groups (Freeman et al. 1980). Objective neuropsychological differences among the groups were slight, but there were marked differences in assessments of psychopathology and medication status. Patients who reported persistent deficits due to ECT were less likely to have benefited from the treatment, and were more likely to be presently symptomatic and receiving psychotropic treatment (Freeman et al. 1980; Frith et al. 1983).

Recommendations

5. 1. General

a) Physicians administering ECT should be aware of the principal adverse effects which may accompany its use.

b) The type, likelihood, and persistence of adverse effects should be considered on a case-by-case basis in the decision to recommend ECT and in the informed consent process (see Chapter 8 ).

c) Efforts should be made to minimize adverse effects by optimization of the patient’s medical condition prior to treatment, appropriate modifications in ECT technique, and the use of adjunctive medications (see also Section 4.1).

5.1.1. Cardiovascular Complications

a) The electrocardiogram (ECG) and vital signs (blood pressure, pulse, and respiration) should be monitored during each ECT treatment to detect cardiac arrythmias and hypertension (see Section 11.8).

b) b) The ECT treatment team should be prepared to manage the cardiovascular complications known to be associated with ECT. Personnel, supplies, and equipment necessary to perform such a task should be readily available (see Chapters 9 and 10).

5.1.2. Prolonged Seizures

Each facility should have policies outlining the steps to be taken to terminate prolonged seizures and status epilepticus (see Section 11.9.4).

5.1.3 Prolonged Apnea

Resources for maintaining an airway for an extended period, including intubation, should be available in the treatment room (see Chapters 9 and 10).

Systemic Side Effects

Headache and nausea are the most common systemic side effects of ECT. Systemic side effects should be identified and symptomatic treatment considered.

5.3 Treatment Emergent Mania

Instances in which patients switch from depressive or affectively mixed states into hypomania or mania during a course of ECT should be identified, and a determination to continue or suspend further treatment with ECT.

5.4. Cognitive Dysfunction

a) Orientation and memory function should be assessed prior to ECT and periodically throughout the ECT course to detect and monitor the presence of ECT-related cognitive dysfunction (see Section 12.2.1 for details). This assessment should attend to patient self-reports of memory difficulty.

b) Based on the assessment of the severity of cognitive side effects, the physician administering ECT should take appropriate action. The contributions of medications, ECT technique, and spacing of treatments should be reviewed. Potential treatment modifications include changing from bilateral to right unilateral electrode placement, decreasing the intensity of electrical stimulation, increasing the time interval between treatments, and/or altering the dosage of medications, or, if necessary, terminating the treatment course.

Table 1. Treatment factors that may increase or decrease the severity of adverse cognitive side effects

Treatment factor
Associated with increased
cognitive side effects
Steps to be taken to reduce
cognitive side effects
Stimulus waveform
Sine wave
Change to brief pulse
Electrode placement
Bilateral
Change to right unilateral
Stimulus intensity
Grossly suprathreshold
Decrease electrical dose
Spacing of treatments
ECT administered 3-5 times
per week
Decrease frequency or stop
ECT
Number of seizures per session
Multiple (two ore more) seizures
per session
Change to conventional
ECT
Concomitant psychotropic
medications
Lithium, benzodiazepines,
neuroleptics, antidepressants
Reduce dose or stop
psychotropics
Anesthetic medications
High dose may contribute to
amnesia
Reduce dose as appropriate for
light level of anesthesia

Chapter 6. Pre-ECT Evaluation

Although components of the evaluation of patients for ECT will vary on a case-by-case basis, each facility should have a minimal set of procedures to be undertaken in all cases (Coffey 1998). A psychiatric history and examination, including past response to ECT and other treatments, is important to ensure that an appropriate indication for ECT exists. A careful medical history and examination, focusing particularly on neurological, cardiovascular, and pulmonary systems, as well as upon effects of previous anesthesia inductions, are crucial to establishing the nature and severity of medical risks. Inquiry about dental problems and a brief inspection of the mouth, looking for loose or missing teeth and noting the presence of dentures or other appliances should be carried out. The evaluation of risk factors prior to ECT should be performed by individuals privileged to administer ECT and ECT anesthesia. Findings should be documented in the clinical record by a note summarizing the indications and risks and suggesting any additional evaluative procedures, alterations in ongoing medications (see Chapter 7), or modifications in ECT technique that may be indicated. Procedures for obtaining informed consent should be carried out (see Chapter 8 ).

Laboratory tests required as part of the pre-ECT workup vary considerably. Young, physically healthy patients may not require any laboratory evaluation. Nevertheless, common practice is to perform a minimum screening battery of tests, often including a CBC, serum electrolytes, and an electrocardiogram. A pregnancy test should be considered on women of childbearing age, although ECT is not generally of increased risk in pregnant women (see Section 4.3). Some facilities have protocols whereby laboratory tests are specified on the basis of age or certain medical risk factors such as cardiovascular or pulmonary history (Beyer et al. 1998). Spine x-rays are no longer routinely necessary, now that the risk of musculoskeletal injuries with ECT has been largely obviated by the use of muscular relaxation, unless pre-existing disease affecting the spine is suspected or known to exist. EEG, brain computed tomography (CT), or magnetic resonance imaging (MRI) should be considered if other data suggest that a brain abnormality may be present. There is now some evidence that abnormalities found on structural brain images or EEG may be useful in modifying treatment technique. For example, since subcortical hyperintensities on MRI have been linked to a greater risk of post-ECT delirium (Coffey 1996; Coffey et al. 1989; Figiel et al. 1990), such a finding might encourage the use of right unilateral electrode placement and conservative stimulus dosing. Likewise, the finding of generalized slowing on a pre-ECT EEG, which has been linked to greater post-ECT cognitive impairment (Sackeim et al. 1996; Weiner 1983) might also encourage the above technical considerations. The potential use of pre-ECT cognitive testing is discussed elsewhere (See Section 12.2).

Although no data exist on the optimal interval in time between the pre-ECT evaluation and the first treatment, the evaluation should be performed as close as possible to the initiation of treatment, keeping in mind that it often must be spread over a number of days, due to need for specialty consultations, waiting- for laboratory results, meetings with patient and significant others, and other factors. The treatment team should be aware of pertinent changes in the patient’s condition over this time interval and should initiate further evaluation as indicated.

The decision to administer ECT is based on the type and severity of the patient’s illness, treatment history, and a risk-benefit analysis of available psychiatric therapies, and requires agreement among attending physician, ECT psychiatrist, and consentor. Medical consultation is sometimes used to obtain a better understanding of the patient’s medical status, or when assistance in the management of medical conditions is desirable. To ask for “clearance” for ECT, however, makes the assumption that such consultants have the special experience or training required to assess both risks and benefits of ECT as compared to treatment alternatives — a requirement that is unlikely to be met. Likewise, determinations made by individuals in administrative positions regarding the appropriateness of ECT for specific patients are inappropriate and compromise patient care.

RECOMMENDATIONS:

Local policy should determine the components of the routine pre-ECT evaluation. Additional tests, procedures, and consultations may be indicated, on an individual basis. Such a policy should include all the following:

1. psychiatric history and examination to determine the indication for ECT. The history should include an assessment of the effects of any prior ECT.

2. a medical evaluation to define risk factors. This should include medical history, physical examination (including assessment of the teeth and mouth), and vital signs.

3. an evaluation by an individual privileged to administer ECT (ECT psychiatrist –Section 9.2), documented in the clinical record by a note summarizing indications and risks and suggesting any additional evaluative procedures, alterations in ongoing medications, or modifications in ECT technique that may be indicated.

4. anesthetic evaluation, addressing the nature and extent of anesthetic risk and advising of the need for modification in ongoing, medications or anesthetic technique.

5. informed consent (see Chapter 8 ).

6. appropriate laboratory and diagnostic tests. Although there are no absolute requirements for laboratory tests in a young, healthy patient, a hematocrit, serum potassium and an electrocardiogram should be considered in most patients. Consideration should be given to performing a pregnancy test in women of childbearing age prior to the first ECT. More extensive laboratory evaluation may be indicated, depending on the patients’ medical history or current status.

Chapter 8: Consent for ECT

8.1 General

“The core notion that decisions regarding medical care are to be made in a collaborative manner between patient and physician” has, over the last few decades, evolved into a formal legal doctrine of informed consent (Appelbaum et al. 1987, p. 12). Such doctrine serves to focus on a number of important questions regarding the nature of consent to treatment. What is informed consent? Who should provide consent, and under what circumstances? How, and by whom, should capacity for consent be determined? What information should be provided to the consentor and by whom? And how should consent be managed with incompetent or involuntary patients? General reviews of informed consent issues as they relate to ECT can be found in Parry (1986), Roth (1986), Taub (1987), and Winslade (1988), while capacity for consent and the use of ECT in incompetent and/or involuntary patients is specifically addressed in Roth et al. (1977), Salzman (1977), Culver et al. (1980), Roy-Byrne and Gerner (1981), Gutheil and Bursztajn (1986), Mahler et al. (1986), Applebaum et al. (1987), Wettstein and Roth (1988), Levine et al (1991), Reiter-Theil (1992), Martin and Bean (1992), Martin and Clancy (1994), Bean et al (1994), and Boronow et al (1997).

The psychiatric profession, both in the United States and elsewhere, has made a number of attempts to offer practical guidelines for the implementation of consent in the clinical setting. In this regard, the conceptual requirements for informed consent posed by the 1978 APA Task Force on ECT are still applicable; 1) a patient who is capable of understanding and acting reasonably upon such information, 2) the provision of adequate information, and 3) the opportunity to consent in the absence of coercion (American Psychiatric Association 1978). Specific recommendations concerning consent for ECT often reflect a trade-off between the preservation of the autonomy of the patient and the assurance of the patient’s right to receive treatment (Ottosson 1992).

A crucial hallmark of informed consent is the quality of interactions between the consentor and the physician, particularly since consent for ECT is an ongoing process. In general, the more the physician keeps the consentor abreast of what is transpiring and involves the consentor in everyday decision making, and the more he/she is sensitive to the consentor’s concerns and feelings regarding, these decisions, the fewer problems there will be with the consent process.

8.2 The Requirement for Consent.

Since informed consent for ECT is mandated, both ethically and by regulation, it is incumbent upon facilities using ECT to implement and monitor compliance with reasonable and appropriate policies and procedures. Although the practitioner legally obliged to follow state and local regulatory requirements concerning consent for ECT, judicial and political efforts should be made to correct overregulation (Winslade et al. 1984; Taub 1987). In this regard, ECT should not be considered different from other medical or surgical procedures with comparable risks and benefits. Regulations should not unduly obstruct the patient’s right to treatment, since unnecessary suffering, increased physical morbidity, and even fatalities may result if procedures to provide ECT to incompetent or involuntary patients (see below) are needlessly prolonged (Mills and Avery 1978; Roy-Byrne and Gerner 1981; Tenenbaum 1983; Walter-Ryan 1985; Miller et al. 1986; Johnson 1993).

8.3 When and by Whom Should Consent Be Obtained?

As with consent for medical and surgical procedures, the patient should provide informed consent unless lacking capacity or otherwise specified by law. The involvement of significant others in this process should be encouraged (Consensus Conference 1985) but not required (Tenenbaum 1983).

ECT is unusual, but not unique, among medical procedures in that it involves a series of repetitive treatments over an appreciable time period (typically 2 to 4 weeks for an acute ECT course). Because it is the series of treatments, rather than any single treatment, that confers both the benefits and adverse effects of ECT, consent should apply to the treatment series as a whole (unless otherwise required by state law).

Since an ECT course generally extends over multiple weeks, the informed consent process should continue across this period. Patient recall of consent for medical and surgical procedures is commonly faulty (Roth et al. 1982; Miesel and Roth 1983; Herz et al 1992; Hutson and Blaha 1991; Swan and Borshoff 1994). For patients receiving ECT, this recall difficulty may be exacerbated by both the underlying illness and the treatment itself (Sternberz and Jarvik 1976; Squire 1986). For these reasons, the consentor should be provided ongoing feedback regarding clinical progress and side effects and any questions should be addressed. Particularly if the consentor expresses reluctance about receiving ECT, h/she should be reminded of his/her right to accept or refuse further treatment.

Continuation/maintenance ECT (see Chapter 13) differs from a course of ECT in that (1) its purpose is the prevention of relapse or recurrence, (2) the patient’s clinical condition is improved compared to that preceding the index ECT course, and (3) it is characterized by both a greater inter-treatment interval and a less well-defined endpoint. Because the purpose of continuation/maintenance treatment differs from an acute course of ECT, a new informed consent process should be initiated, including the signing of a separate consent form. As a series of continuation ECT typically lasts at least 6 months, and because continuation/ maintenance ECT is provided to individuals who are clinically improved and already knowledgeable about the treatment, a 6-month interval is adequate before readministration of the formal consent document (unless state law requires otherwise).

Ideally, the consent process involves discussions with the consentor about general aspects of ECT and information unique to the patient, as well as the signing of the informed consent document. The information essential to consent to ECT should be provided by a knowledgeable physician. Ideally, this person should also have a therapeutic alliance with the patient. In practice this requirement can be accomplished by the attending physician, treating psychiatrist, or other knowledgeable physician acting individually or in concert. It may also be helpful for other, professional staff to provide further information to the consentor. Consent for anesthesia may either be included in the ECT consent process or separately obtained by an anesthetist.

8.4 Information to Be Conveyed

The use of a formal consent document for ECT ensures the provision of essential information to the consentor. Earlier task force recommendations (American Psychiatric Association 1978, 1990), other professional Guidelines, and regulatory requirements (Mills and Avery 1978; Tenenbaum 1983); Winslade et al. 1984; Taub 1987; Winslade 1988) have encouraged the use of comprehensive written information about ECT as part of the consent process. Such material may either be contained wholly within the formal consent document, or included as a patient information supplement. In either case, informational material should be given to the consentor to keep. In surgical patients, patient information supplements have been shown to significantly enhance recall of information provided prior to surgery (Askew et al 1990).

Sample consent forms and supplementary patient information material are included in Appendix B. If these documents are used, appropriate modifications should be made to reflect local requirements. It is also suggested that reproductions be in large type, to ensure readability by patients with poor visual acuity. To further enhance the understanding of ECT, many practitioners now augment written materials with use of videotapes designed to cover the topic of ECT from the layman’s perspective (Baxter et al. 1986; Guze et al. 1988; Battersby et al. 1993; Dillon 1995; Westreich et al. 1995). A listing of such materials has been included as part of Appendix C.

However, to rely entirely upon such generic materials as the sole informational component of the informed consent process would be ill advised. Even with considerable attention to readability, many patients understand less than half of what is contained in a typical medical consent form (Roth et al. 1982). In this regard, it is interesting to note that psychiatric patients do not perform more poorly than medical or surgical patients (Miesel and Roth 1983). Because of this situation, in addition to written information given to the patient, a discussion between the consentor and a knowledgeable physician should take place. This discussion should summarize the main features of the consent document, provide additional information applicable to that individual, and allow a further opportunity for the consentor to express opinions and have questions answered. Examples of individual-specific information include: the rationale for ECT, reasonable treatment alternatives, specific benefits and risks, and any major alterations planned in the ECT procedure. This discussion should also be briefly summarized in the patient’s clinical record.

Substantial alterations in the treatment procedure or other factors having a major effect upon risk-benefit considerations should be conveyed to the consentor on a timely basis and documented in the patient’s clinical record. The need for ECT treatments exceeding the typical range (see Section 11.11) and the switching of stimulus electrode placement (see Section 11.6) represent two such examples.

Informational material provided as part of the consent process should be sufficient in scope and depth to allow a reasonable person to understand and evaluate the risks and benefits of ECT as compared to treatment alternatives. Since individuals vary considerably in education and cognitive status, efforts should be made to tailor information to the consentor’s ability to comprehend such data. In this regard, the practitioner should be aware that too much technical detail can be as counterproductive as too little. The readability of consent forms should be no greater than at a 10th grade level to optimize comprehension (some contemporary word processing software packages capable of easily determining readability – the consent documents in Appendix B meet this criterion).

Topics to be covered in the consent document generally include the following:

1) a description of the ECT procedure, including the times when treatments are given (e.g., Monday, Wednesday, Friday mornings , general location of treatment (i.e., where treatments will take place), and typical range for number of treatments to be administered

2) why ECT is being recommended and by whom

3) that there is no guarantee that ECT will be effective

4) that there is generally a substantial risk of relapse following ECT, and that continuation treatment of some sort is nearly always indicated

5) a generic mention of applicable treatment alternatives

6) the likelihood (e. g., “extremely rare,” “rare,” “uncommon,” or “common”), and anticipated severity of major risks associated with the procedure (see Chapter 5), including mortality, adverse effects upon cardiovascular and central nervous systems (including both transient and persistent amnesia), and common minor side-effects. In light of the accumulated body of data dealing with structural effects of ECT (Devenand et al 1994), “brain damage” should not be included as a potential risk.

7) an acknowledgement that consent for ECT also implies consent for appropriate emergency treatment in the event that this is clinically indicated
a description of behavioral restrictions that may be necessary during the pre-ECT evaluation period, the ECT course, and the recuperative interval

9) 10) a statement that consent for ECT is voluntary and can be withdrawn at any time

11) 10) an offer to answer questions at any time regarding the recommended treatment and the name of whom to contact for such questions

8.5 Capacity to Provide Voluntary Consent.

Informed consent requires that a patient be capable of understanding and acting reasonably upon information provided to him/her about the procedure. For the purpose of these recommendations, the term “capacity” reflects this criterion. There is no clear consensus as to what constitutes “capacity to consent.” Criteria for capacity to consent have tended to be vague, and formal “tests” of capacity are only now under active investigation (Bean et al 1996; Grisso and Appelbaum 1995; Martin et al 1994). It is suggested, instead, that the individual obtaining consent consider the following general principles in making a determination. First, capacity to consent should be assumed to be present unless compelling evidence to the contrary exists. Second, the occurrence of psychotic ideation., irrational thought processes, or involuntary hospitalization do not in themselves constitute such evidence. Third, the patient should demonstrate sufficient comprehension and retention of information so that he/she can reasonably make a decision whether or not to consent for ECT.

Unless otherwise mandated by statute, a determination of capacity is generally made by the attending physician. First, the attending physician is in an excellent position to assess the patient’s ability to meet the above three criteria for capacity to consent. Also, the attending physician is likely to be aware of how the patient’s mental illness affects these criteria. Finally, the attending physician is generally the one who makes such determination with respect to other medical and surgical procedures. Should the attending physician be in doubt as to whether capacity to consent is present, use may be made of an appropriate physician consultant not otherwise associated with the patient’s care.

There is concern that attending physicians may be biased to find that capacity to consent exists when the patient’s decision agrees with their own. In this regard, however, ECT is no different from other treatment modalities. Fixed requirements for a priori review of capacity to consent for ECT by consultant, special committee, appointed lawyer, or judicial hearing are impediments to the patient’s right to treatment and are inappropriate.

Patients who have previously been adjudicated legally incompetent or medical purposes usually have consent provided by a legally appointed guardian or conservator, although this may vary depending upon jurisdiction.

For patients with capacity to consent, ECT should only be administered with the agreement of the patient. To do otherwise would infringe upon the right to refuse treatment. Situations where the patient lacks capacity to consent for ECT are generally covered by regulations which include how and from whom surrogate consent may be obtained. In such instances, all the information typically provided regarding ECT and alternative treatment should be shared with this individual.

Informed consent is defined as voluntary when the consentor’s ability to reach a decision is free from coercion or duress. Since the treatment team, family members, and friends all may have opinions concerning whether or not ECT should be administered, it is reasonable that these opinions and their basis be expressed to the consentor. In practice, the line between “advocacy” and “coercion” may be difficult to establish. Consentors who are either highly ambivalent or are unwilling or unable to take full responsibility for the decision (neither of which are rare occurrences with patients referred for ECT) are particularly susceptible to undue influence. Staff members involved in clinical case management should keep these issues in mind.

Threats of involuntary hospitalization or precipitous discharge from the hospital due to ECT refusal clearly represent undue influence. However, consentors do have the right to be informed of the anticipated effects of their actions on the clinical course and the overall treatment plan. Similarly, since physicians are not expected to follow treatment plans which they believe are ineffective or unsafe, an anticipated need to transfer the patient to another attending physician should be discussed in advance with the consentor. It is important to understand the issues involved in a consentor’s decision to refuse or withdraw consent. Such decisions may sometimes be based upon misinformation or may reflect unrelated matters, e.g., anger towards self or others or a need to manifest autonomy. In addition, a patient’s mental disorder can itself limit the ability to cooperate meaningfully in the informed consent process, even in the absence of psychosis.

A number of suggestions have been offered to help guarantee the right of involuntarily hospitalized patients to accept or refuse specific components of the treatment plan, including ECT. Examples of such recommendations include the use of psychiatric consultants not otherwise involved in the patient’s care, appointed lay representatives, formal institutional review committees, and legal or judicial determination. While some degree of protection is indicated in such cases, overregulation will serve to limit unnecessarily the patient’s right to receive treatment.

RECOMMENDATIONS

8. 1. General

a) Policies and procedures should be developed to assure proper informed consent, including when, how, and from whom it is to be obtained, and the nature and scope of information to be provided.

b) These policies and procedures should be consistent with state and local regulations.

8.2. The Requirement for Consent

a) Informed consent should be obtained from the patient except in situations where the patient lacks capacity to do so (see Section 8.5.3).

b) Informed consent for ECT is given for a specified treatment course or for a period of continuation/maintenance ECT (see Section 13.3).

c) Consent for future treatments may be withdrawn at any time, including, between ECT treatments, by the individual providing consent.

8.3. When and by Whom Should Consent Be Obtained?

a) Informed consent for ECT, including the signing of a formal consent document, should be obtained before beginning an ECT treatment course or a period of continuation or maintenance ECT. In the latter case, the consent process should be repeated at least every six months.

b) Informed consent should be obtained by the patient’s attending physician, treating psychiatrist or other physician knowledgeable about both the patient and ECT (unless otherwise specified by law).

c) When separate informed consent for ECT anesthesia is required, it should be obtained by a privileged or otherwise authorized anesthesia provider.

d) The consentor should be provided ongoing feedback regarding clinical progress and side effects and any questions or concerns should be addressed.

e) If the consentor expresses reluctance about the treatment at any time prior to or during the ECT course, h/she should be reminded of his/her right to accept or refuse treatment.

8.4. Information to Be Conveyed

8.4.1. General Considerations

a) Information describing ECT (see below) should be conveyed in a written consent document. This document and/or a summary of general information related to ECT should be given to the consentor to keep (examples are provided in Appendix B). The use of a separate consent document may be required for anesthesia with ECT in certain settings.

b) The use of appropriate video format patient information on ECT is encouraged.

c) In addition to the written consent document an overview of general information on ECT and individual-specific data should be presented orally by the attending physician, treating psychiatrist, or other knowledgeable physician. Further information may also be provided by other staff members.

d) The consentor should be informed if substantial alterations in the treatment procedure arise that may have a major effect upon risk-benefit considerations.

e) Significant discussions with the consentor regarding these issues should be documented in the clinical record.

f) All information should be provided in a form understandable to the consentor, and should be sufficient to allow a reasonable person to understand the risks and benefits of ECT and to evaluate the available treatment options.

g) The consentor should have an opportunity to ask questions relevant to ECT or treatment alternatives.

8.4.2. Specific Information Provided

The consent document should provide:

a) a description of ECT procedures including:

1) when, where, and by whom the treatments will be administered

2) a range of the number of treatment sessions likely

3) a brief overview of the ECT technique itself.

b) a statement of why ECT is being recommended and by whom, including a general consideration of treatment alternatives.

c) a statement that, as with any treatment modality, therapeutic (or prophylactic) benefits associated with ECT may be absent or transient.

d) a statement indicating the need for continuation therapy.

e) a statement as to the likelihood and severity (in general terms) of the risks related to anesthesia and seizure induction: including mortality, cardiac dysfunction, confusion, acute and persistent memory impairment, musculoskeletal and dental injuries, headaches, and muscle pain.

f) a statement that, as with any other procedure involving general anesthesia, consent for ECT also implies consent to perform appropriate emergency medical interventions in the unlikely event that this proves necessary during the time the patient is not fully conscious.

g) a statement that consent is voluntary and can be revoked at any time before or during the treatment course.

h) a statement that the consentor is encouraged to ask questions at any time regarding ECT, and whom to contact for such questions.

1) a description of any restrictions on patient behavior that are likely to be necessary before, during,, or following ECT.

8.5. Capacity to Provide Voluntary Consent

8.5.l. General Considerations

a) The use of ECT requires voluntary consent from an individual with capacity to make such a decision.

b) Individuals with mental illness are considered to have the capacity to consent to ECT unless the evidence to the contrary is compelling. The presence of psychosis, irrational thinking, or involuntary hospitalization do not in themselves constitute proof of lack of capacity.

c) Unless otherwise specified by statute, the determination of capacity to consent should generally be made by the patient’s attending physician, with use of an appropriate physician consultant not otherwise associated with the patient’s care in cases where the attending physician is uncertain as to whether capacity to consent is present.

d) In the event of refusal or withdrawal of consent to ECT, the attending physician and/or treating, psychiatrist should inform the consentor of anticipated effects of this action upon clinical course and treatment planning.

8.5.2. Patients Having the Capacity to Provide Consent

In this case, ECT should only be administered in the presence of voluntary patient agreement, including signing of a formal consent document.

8.5.3. Patients Lacking the Capacity to Provide Consent

State and local law covering consent to treatment for patients lacking the capacity to provide such consent should be followed, including statutes pertinent to emergency situations where a delay in treatment may lead to death or serious impairment in health. Applicable legal requirements vary considerably by jurisdiction and are subject to revision over time. Surrogate decision makers should be provided with the information described above. Consideration should be given to any positions previously expressed by the patient when in a state of determined or presumed capacity, as well as to the opinions of major significant others.

12. Evaluation of Outcome

12.1. Therapeutic Response

Before beginning an acute or index course of ECT, each patient should have a documented treatment plan, indicating specific criteria for remission. The type and severity of prominent symptomatology should be described. It is helpful for therapeutic goals to take into account the aspects of symptomatology that are expected to improve. For example, some patients with schizoaffective disorder present with relatively chronic forms of thought disturbance (e.g., delusions), with prominent superimposed episodes of affective symptomatology. In a number of these patients, ECT may ameliorate the affective component without influencing the chronic thought disturbance. Prolonging the ECT course because of persistent thought disturbance may result in unnecessary treatment. In contrast, many patients with mood disorder present with chronic dysthymia preceding a clear-cut episode of major depression. Some practitioners may be uncertain whether remission of a major depressive episode is associated with return to the chronic dysthymia or whether dysthymic symptomatology also responds to ECT. There is evidence that the extent of residual symptomatology shortly following ECT does not differ among patients with a double depression(i.e., major depression superimposed on dysthymia) and patients with major depression without a history of dysthymia (Prudic et al. 1993). Thus, in patients with double depression, basing treatment termination only on resolution of the major depressive episode may result in incomplete treatment, and possibly heighten the risk of relapse.

After the start of ECT, clinical assessments should be performed and documented attending physician or designee after every one or two treatments. To allow for clearing of acute cognitive side effects, it is preferable to conduct these assessments at least 24 hours following a treatment. Assessments should document changes in the disorder being treated with ECT, both in terms of improvement in the signs and symptoms that were present initially and the emergence of new symptomatology. Although infrequent, switches from depression to mania may occur during the course of ECT. In this context, it is important to distinguish between mania and a delirium with euphoria (Devanand et al. 1988b) (see also Section 5.3). Serial assessments of cognitive function may help in making this differential diagnosis.

In patients treated for catatonia, the nature of other symptoms may have been difficult to discern at pretreatment due to mutism or negativism. After catatonic symptoms improve with ECT, other aspects of psychopathology may become evident and should be assessed and documented. Other patients may have experienced delusions or hallucinations before or during the ECT course, but these symptoms may have been difficult to verify due to patient guardedness or other factors. With clinical improvement, additional symptoms may become apparent, impacting on future treatment.

Some practitioners find it useful to use a standardized rating instrument when assessing symptomatic change. Changes in rating scale scores over time are particularly helpful in determining whether the degree of improvement has accelerated, decelerated, or plateaued and in documenting the extent of residual symptomatology at the completion of ECT. For patients with major depression, the Hamilton Rating Scale for Depression (HRSD, Hamilton 1967) is a commonly used instrument. The 24-item version of the HRSD contains items assessing symptoms of hopelessness, helplessness, and worthlessness, features that are particularly common in patients receiving ECT. An alternative instrument is the Montgomery-Asberg Depression Rating Scale (MADRS) (Montgomery and Asberg 1979). For patients with psychotic disorder, clinician assessments of symptomatology may be performed with the Brief Psychiatric Rating Scale (Overall and Gorham 1962). The Young Mania Rating Scale (Young et al. 1978) may be used for patients with acute mania. It should be noted that the instructions used with instruments such as the HRSD traditionally assess symptomatology over the past week. Since symptomatic change with ECT is often rapid and requires more frequent assessment, it is useful to reduce the interval being examined to a few days.

Prior to ECT, clinician and self-report assessments of depression severity show only moderate correlation (Sayer et al. 1993). This discrepancy is largely attributable to a subgroup of patients who clinicians rate as moderately or severely depressed, but have low levels of symptomatology by self-report. These patients most commonly present with psychotic depression (Sayer et al. 1993). Following completion of ECT, the degree of agreement between self- and clinician-rated assessments is considerably greater. Some clinicians find that a formal self-report instrument is of supplemental value in documenting the effects of ECT on symptomatology. The Beck Depression Inventory II (Beck et al. 1996; Dozois et al. 1998) may be used, with the period being assessed modified from two weeks to at most one week. An alternative self-rating instrument is the Inventory Depressive Symptomatology (IDS-SR, Rush et al. 1985), which has the advantage of having a complementary clinician rated version. It should be noted, however, that self-ratings of depression seventy are supplemental, and should never substitute for clinician evaluations.

Before using ECT as a continuation treatment, the type and severity of residual symptomatology following acute phase treatment should be ascertained. As with acute phase treatment, the ECT physician should interview the patient before each continuation treatment to determine changes in symptoms and cognition. Emergence of symptoms suggestive of potential relapse should trigger consideration of changes in treatment frequency and/or technique.

12.2. Adverse Effects

Cognitive changes. The impact of ECT on cognition, particularly orientation and memory, should be assessed both in terms of objective findings and patient report during and following the ECT course (see Sections 5.4 and 5.5). This assessment should be conducted before the start of ECT to establish a baseline level of functioning, and should be repeated at least weekly throughout the ECT course. It is suggested that cognitive assessment, like assessment of therapeutic change, be conducted at least 24 hours following an ECT treatment to avoid contamination by acute postictal effects.

The evaluation of cognitive function may include either bedside assessment and/or formal neuropsychological measures. In either case, cognitive assessment should minimally include evaluations of orientation, anterograde amnesia, and retrograde amnesia. For bedside or informal assessment, orientation in the three spheres (person, place and time) should be determined. Informal assessment of anterograde and retrograde amnesia can be conducted by discussion with the patient of events in the recent and distant past (e.g., events associated with the day of the interview, recent trips or special occasions, and memory for personal details, such as address, phone number, etc.).

Formal testing instruments provide quantitative measures for tracking change. To assess global cognitive functioning, including orientation, an instrument such as the Mini-Mental State exam (MMSE, Folstein et al. 1975) may be used. Significantly diminished MMSE scores (e.g., reductions of 20% or more) may reflect or suggest the development of a sustained delirium and lead to consideration of modifications in ECT technique. Similarly, such reductions following the end of the ECT course may have implications for discharge planning and for the level of supervision required following ECT. It should be noted, however, that changes in global cognitive status, as measured by the MMSE, are not necessarily associated with the degree of anterograde or retrograde amnesia. Patients may show unchanged or improved MMSE scores and still manifest considerable amnesia (Sobin et al. 1995).

A variety of instruments are available to assess delayed recall of newly learned information. These include subtests of the Weschsler Memory Scale III (WMS-III, Weschsler, 1997) which provides age-adjusted norms for delayed memory components. Unfortunately, there are no alternative versions of the WMS-III, and repeated assessment may be confounded by practice effects. In contrast, the Randt Memory Test (Randt et al. 1980; Randt and Brown, 1983)subscales that assess delayed memory for verbal and pictorial material have shown sensitivity to the anterograde amnesia associated with ECT (Zervas and Jandorf, 1993), and this instrument has five alternative forms. When used with a delay recall procedure, the Buschke Selective Reminding Test (Hannay and Levin 1985), is also useful for repeated assessment (Sackeim et al. 1993). Tasks involving delayed copying of complex figures (Lezak, 1995), delayed recognition memory for unfamiliar faces, and the Benton Visual Retention Test (Benton. 1950; Sivan, 1992) have shown sensitivity to ECT associated anterograde amnesia for nonverbal information (Meyendorf et al. 1980; Steif et al. 1986; Weiner et al. 1986; Sackeim et al. 1993).

Brief and valid assessment instruments to gauge the extent of retrograde amnesia are less readily available. Tests that formally assess recall and/or recognition of famous people or public events (e.g., Butters and Albert 1982; Goldberg and Barnett, 1985) have been used (Squire 1986; Weiner et al. 1986). However, most of these instruments categorize events in relation to the decade of their prominence (e.g., 90=s, 80=s, 70=s). The retrograde amnesia resulting from ECT displays a temporal gradient, such that events closest in time to the treatment course are most vulnerable to memory loss and remote events are spared (Squire et al. 1975; Squire 1986; Sackeim 1992). Consequently, these instruments are unlikely to be sufficiently sensitive.

An alternative approach has been to assess amnesia for autobiographical or personal memories (Weiner et al. 1986; Sackeim et al. 1993; McElhiney et al. 1995: Sobin et al. 1995). Memory loss for events in the patient’s life is often the most distressing aspect of ECT’s cumulative side effects. Unfortunately, the instruments shown to be sensitive in research are lengthy and generally not amenable to routine clinical use. Efforts are underway to validate a brief instrument that may be sensitive to ECT-induced retrograde amnesia for autobiographical information.

When cognitive status is assessed formally or informally, the patient’s perception of cognitive changes should also be ascertained. This assessment may be done by informally inquiring whether the patient has noticed any changes in the ability to concentrate (e.g. to follow a television program or a magazine article), to remember visitors or events of the day, or to recall more remote events. Patient perception of memory functioning may also be examined using a quantitative instrument. The Squire Memory Complaint Questionnaire (Squire et al. 1979) has been used most commonly with patients receiving ECT.

As noted in Section 5.5, recent studies have repeatedly found that patients report fewer memory complaints shortly following the ECT course relative to their preECT baseline (Coleman et al. 1996). T he changes in self-reported cognitive function are independent of changes in objective neuropsychological measures, but correlate substantially with degree of improvement in depressive symptomatology (Cronholm and Ottosson 1963; Frith et al 1983; Squire and Slater 1983; Weiner et al 1986; Squire and Zouzounis 1988; Calev et al. 1991; Coleman et al. 1996). Some concerns have been raised about the reliability of the Squire Memory Complaint Questionnaire, as it requires patients to assess their current cognitive functioning relative to their functioning prior to onset of the psychiatric episode, a complex judgment (Coleman et al. 1996). The Cognitive Failures Questionnaire (Broadbent et al. 1982) is an alternative self-report instrument, with a broader sampling of aspects of cognitive function.

In the event of substantial deterioration in orientation or memory functioning during the ECT course that is unresolved upon hospital discharge, a plan should be made for follow-up of cognitive status. The plan should include a description of when follow-up assessment would be desirable, as well as the specific domains of cognitive function to be assessed. Most commonly cognitive functioning recovers markedly in within days of the end of the ECT course (Stelf et al. 1986) and patients should be reassured that this will likely be the case.

It should be kept in mind that the suggested evaluation procedures provide only gross measures of cognitive status. Furthermore, interpretation of cognitive change may be subject to a number of difficulties. Patients frequently have cognitive impairments before receiving ECT (Sackeim and Steif 1988) and therapeutic response may be associated with improvement in many cognitive domains (Weeks et al. 1980; Malloy et al. 1982; Frith et al. 1983; Sackeim et al. 1992, 1993). However, while some patients show improved scores relative to their preECT baseline, they still may not have fully returned to their baseline level of cognitive functioning (Steif et al. 1986). This discrepancy may be a basis for complaints about lingering cognitive deficits. In addition, the procedures suggested here only sample limited aspects of cognitive functioning, for example, deliberate (conscious or intentional) learning and retention of information. Patients may also have deficits in incidental (unattended) learning. Likewise, the suggested procedures concentrate on verbal memory, although both right unilateral and bilateral ECT produce deficits in memory for nonverbal material (Squire 1986).

Other adverse effects. During the ECT course, any onset of new risk factors, or significant worsening of those present before ECT, should be evaluated prior to the next treatment. When such developments alter the risks of administering ECT, the consentor should be informed and the results of this discussion documented. Patient complaints about ECT should be considered carefully. The attending physician and/or a member of the ECT treatment team should discuss these complaints with the patient, attempt to determine their source, and ascertain whether corrective measures are indicated.

RECOMMENDATIONS

12. Evaluation of Outcome

12.1. Therapeutic Response

a) Each treatment plan should indicate specific criteria for remission.

b) Clinical assessments should be performed by the attending physician or designee and documented prior to ECT and after every 1-2 ECT treatments, preferably at least 24 hours following the treatment.

c) Formal clinical rating instruments may be useful in to documenting changes in symptomatology over the ECT course.

12.2. Adverse Effects

12.2.1. Cognitive Changes

a) During a course of ECT the presence and severity of disorientation, anterograde amnesia, and retrograde amnesia should be monitored in terms of both objective findings and self-report (see Sections 5.4 and 5.5). This evaluation should consist of bedside assessment of orientation and memory (both retention of newly learned material and recall of recent and remote events) and/or administration of formal neuropsychological measures.

b) Assessment should be carried out prior to ECT and at least weekly throughout an ECT course. When possible, cognitive assessment should be performed at least 24 hours following an ECT treatment.

c) Modifications of the ECT procedure should be considered, if there is substantial deterioration of orientation and/or memory during an ECT course (see Section 5.4.(b)). If such effects remain following completion of the ECT course, a plan should be made for postECT follow-up assessment.

12.2.2. Other Adverse Effects

Any sudden onset of new risk factors, or worsening of previously identified risk factors, should be evaluated prior to the next ECT treatment (see Chapter 5). In this regard, patient complaints concerning ECT should be considered carefully.

CHAPTER 13: Management of Patient’s Post-ECT Course

13. Management of Patient’s Post-ECT Course

13.1. Continuation therapy is traditionally defined as the provision of somatic treatment over the 6 month period following, the onset of remission in an index episode of mental illness (National Institute of Mental Health Consensus Development Panel 1985; Prien & Kupfer 1986; Fava & Kaji 1994). However, individuals referred for ECT are particularly likely to be medication resistant and to display psychotic ideation during the index episode of ‘illness, and the risk of relapse remains high (50-95%) throughout the first year following completion of the ECT course (Spiker et al. 1985; Aronson et al 1987; Sackeim et al 1990a,b, 1993; Stoudemire et al. 1994; Grunhaus et al. 1995). For this reason, we will operationally define the continuation interval as the 12 month period following successful treatment with ECT.

Regardless of its definition, continuation treatment has become the rule in contemporary psychiatric practice (American Psychiatric Association 1993, 1994, 1997). Following completion of the index ECT course, an aggressive program of continuation therapy should be instituted as soon as possible. Occasional exceptions include patients intolerant to such treatment and possibly those with a history of extremely long periods of remission (although compelling evidence, for the latter is lacking).

13.2. Continuation pharmacotherapy. A course of ECT is usually completed over a 2- to 4-week period. Traditional practice, based in part on earlier studies (Seager and Bird 1962; Imlah et all. 1965; Kay et al. 1970) and in part on clinical experience, has suggested continuation treatment of patients with unipolar depression with antidepressant agents (and possibly antipsychotic agents in the presence of psychotic symptoms), patients with bipolar depression with antidepressant and/or mood stabilizer medications; patients with mania with mood stabilizer and possibly antipsychotic agents, and patients with schizophrenia with antipsychotic medications (Sackeim 1994). However, some recent evidence suggests that a combination of antidepressant and mood stabilizer pharmacotherapy might improve the effectiveness of continuation therapy for patients with unipolar depression (Sackeim 1994). It may also be beneficial to discontinue antidepressant medications during the continuation phase of treatment for patients with bipolar depression (Sachs 1996). For patients with major depression episodes, medication dosages during continuation treatment are maintained at the clinically effective dose range for acute treatment, with adjustment up or down depending upon response (American Psychiatric Association 1993). For patients with bipolar disorder or schizophrenia, a somewhat less aggressive approach is utilized (American Psychiatric Association 1994, 1997). Still, the role of continuation therapy with psychotropic drugs after a course of ECT continues to undergo assessment (Sackeim 1994). In particular, disappointingly high relapse rates, especially in patients with psychotic depression and in those who are medication resistant during the index episode (Sackeim et al. 1990a: Meyers 1992; Shapira et al. 1995; Flint & Rifat 1998), compel reevaluation of present practice, and suggest consideration of novel medication strategies or continuation ECT.

13.3. Continuation ECT. While psychotropic continuation therapy is the prevailing practice, few studies document the efficacy of such use after a course of ECT. Some recent studies report high relapse rates even in patients complying with such regimens (Spiker et al. 1985, Aronson et al. 1987; Sackeim, et al. 1990, 1993); Stoudemire et al. 1994). These high relapse rates have led some practitioners to recommend continuation ECT for selected cases (Decina et al. 1987; Kramer 1987b; Jaffe et al. 1990b; McCall et al. 1992). Recent reviews have tended to report surprisingly low relapse rates among patients so treated (Monroe 1991; Escande et al. 1992; Jarvis et al. 1992; Stephens et al. 1993; Favia & Kaji 1994; Sackeim 1994; Fox 1996; Abrams 1997a; Rabheru & Persad 1997). Continuation ECT has also been described as a viable option in contemporary guidelines for long-term management of patients with major depression (American Psychiatric Association 1993), bipolar disorder (American Psychiatric Association 1994), and schizophrenia (American Psychiatric Association 1997).

Recent data on continuation ECT have primarily consisted of retrospective series in patients with major depression (Decina et al. 1987; Loo et al. 1988; Matzen et al. 1988; Clarke et al. 1989; Ezion et al. 1990; Grunhaus et al. 1990; Kramer 1990; Thienhaus et al. 1990; Thornton et al. 1990; Dubin et al. 1992; Puri et al. 1992; Petrides et al. 1994; Vanelle et al. 1994; Swartz et al. 1995; Beale et al. 1996), mania (Abrams 1990; Kellner et al. 1990; Jaffe et al. 1991; Husain et al. 1993; Vanelle et al. 1994; Godemann & Hellweg 1997), schizophrenia (Sajatovik & Neltzer 1993; Lohr et al. 1994; Hoflich et al. 1995; Ucok & Ucok 1996; Chanpattaria 1998), and Parkinson’s Disease (Zervas & Fink 1991; Friedman & Gordon 1992; Jeanneau 1993; Hoflich et al. 1995; Aarsland et al. 1997; Wengel et al. 1998). While some of these investigations have included comparison groups not receiving continuation ECT or have compared use of mental health resources before and after implementation of continuation ECT, controlled studies involving random assignment are not vet available. Still, suggestive evidence that continuation ECT is cost-effective, in spite of the cost per treatment, is particularly promising (Vanelle et al. 1994; Schwartz et al. 1995; Steffens et al. 1995; Bonds et al. 1998). In addition, an NIMH-funded, prospective multi-site study comparing continuation ECT with continuation pharmacotherapy with the combination of nortriptyline and lithium is presently underway (Kellner – personal communication).

Because continuation ECT appears to represent a viable form of continuation management of patients following completion of a successful course of ECT, facilities should offer this modality as a treatment option. Patients referred for continuation ECT should meet the following indications: 1) history of illness that is responsive to ECT; 2) either resistance or intolerance to pharmacotherapy alone or a patient preference for continuation ECT; and 3) the ability and willingness of the patient to receive continuation ECT, provide informed consent, and comply with the overall treatment plan, including the behavioral restrictions that may be necessary.

Since continuation ECT is administered to patients who are in clinical remission, and because long inter-treatment intervals are used, it is typically administered on an ambulatory basis (see Section 11.1). The specific timing of continuation ECT treatments has been the subject of considerable discussion (Kramer 1987b; Fink 1990; Monroe 1991; Scott et al. 1991; Sackeim 1994; Petrides & Fink 1994: Fink et al. 1996; Abrams 1997; Rabheru & Persad 1997; Petrides 1998), but evidence supporting any set regimen is lacking. In many cases, treatments are started on a weekly basis with the interval between treatments gradually extended to a month, depending upon the patient’s response. Such a plan is designed to counteract the high likelihood of early relapse noted previously. In general, the greater the likelihood of early relapse, the more intensive the regimen should be. The use of psychotropic agents during a series of continuation ECT remains an unresolved issue (Jarvis et al. 1990; Thornton et al. 1990; Fink et al. 1996; Petrides 1998). Given the resistant nature of many such cases, some practitioners supplement continuation ECT with such medication in selected cases, particularly in those who have limited benefit from continuation ECT alone. In addition, some practitioners believe that the onset of symptoms of impending relapse in ECT responsive patients undergoing continuation pharmacotherapy alone may represent an indication for a short series of ECT treatments for a combination of therapeutic and prophylactic purposes (Grunhaus et al. 1990), although controlled studies are not yet available to substantiate this practice.

Before each continuation ECT treatment, the attending physician should 1) assess clinical status and current medications, 2) make a determination as to whether the treatment is indicated, and decide the timing of the next treatment. A monthly assessment may be used if continuation treatments are occurring at least twice monthly and the patient has been clinically stable for at least 1 month. In any case, the overall treatment plan, including the role of ECT, should be updated at least quarterly. Informed consent should be renewed no less frequently than every 6 months (see Chapter 8 ). To provide an ongoing assessment of risk factors, an interval medical history, focusing on specific systems at risk with ECT, and vital signs should be done prior to each treatment, with further assessment as clinically indicated. In many settings, this brief evaluation is accomplished by the ECT psychiatrist or anesthetist on the day of the treatment. A full anesthesia pre-operative exam (see Section 6) should be repeated at least every 6 months, and laboratory tests at least annually. Although cognitive effects appear to be less severe with continuation ECT than with the more frequent treatments that are administered during an ECT course (Ezion et al. 1990; Grunhaus et al. 1990; Theinhaus et al. 1990; Thornton et al. 1990; Barnes et al. 1997), monitoring of cognitive function should be done at least every 3 treatments. As discussed in Chapter 12, this may consist of simple bedside assessment of memory function.

13.4. Continuation psychotherapy. For some patients, individual or group psychotherapy may be useful in dealing with underlying psychodynamic issues, in facilitating better ways to cope with stressors that might otherwise precipitate a clinical relapse, in assisting the patient to re-organize his/her social and vocational activities, and in encouraging a return to normal life.

Maintenance therapy. Maintenance therapy is empirically defined herein as the prophylactic use of psychotropics or ECT longer than 12 months past the onset of remission in the index episode. Maintenance treatment is indicated when attempts to stop continuation therapy have been associated with symptom recurrence, when continuation therapy has been only partially successful, or when a strong history of recurrent illness is present (Loo et al. 1990; Thienhaus et al. 1990; Thornton et al. 1990; Vanelle et al. 1994; Stiebel 1995). The specific criteria for maintenance ECT, as opposed to maintenance psychotropic therapy, are the same as those described above for continuation ECT. The frequency of maintenance ECT treatments should be kept to the minimum compatible with sustained remission, with re-evaluation of the need for extension in the treatment series and repeated application of informed consent procedures performed at the intervals listed above for continuation ECT.

RECOMMENDATIONS

13.1. General Considerations

a) Continuation therapy, typically consisting of psychotropic medication or ECT, is indicated for virtually all patients. The rationale behind decisions not to recommend continuation therapy should documented.

b) Continuation therapy should begin as soon as possible after termination of the ECT course, except when presence of adverse ECT effects, e.g., delirium, necessitates a delay.

c) Unless countervened by adverse effects, continuation therapy should be maintained for at least 12 months. Patients with a high risk of recurrence or residual symptomatology will generally require longer-term maintenance therapy.

d) The aim of maintenance therapy is to prevent recurrence of new episodes of the index disorder. It is typically defined as treatment continuing longer than 12 months following completion of the most recent ECT course. Maintenance therapy is indicated when therapeutic response has been incomplete, when a recurrence of clinical symptoms or signs has occurred, or where a history of early relapse is present.

13.2. Continuation/Maintenance Pharmacotherapy

The choice of agent should be determined by the type of underlying illness, a consideration of adverse effects, and response history. In this regard, when clinically feasible, practitioners should consider a class of pharmacologic agents for which the patient did not manifest resistance during the treatment of the acute episode.

13.3. Continuation/Maintenance ECT

13.3.1. General

a) Continuation/Maintenance ECT should be available in programs administering ECT.

b) Continuation/maintenance ECT may be given on either an inpatient or outpatient basis. In the latter case, the recommendations presented in Section 11.1 apply.

13.3.2. Indications for Continuation ECT

a) history of recurring episodic illness which has been responsive to ECT; and

b) either 1) pharmacotherapy alone has not proved effective in preventing relapse or cannot be safely administered for such a purpose; or 2) patient preference; and

c) the patient is agreeable to receive continuation ECT, and is capable, with the assistance of others, of complying with the treatment plan.

13.3.3. Delivery of Treatments

a) Various formats exist for delivering continuation ECT. The timing of treatments should be individualized for each patient, and should be adjusted as necessary with consideration of both beneficial and adverse effects.

b) The duration of continuation ECT should be guided by the factors described in 13.1(b) and 13.1(c).

13.3.4. Maintenance ECT

a) Maintenance ECT is indicated when a need for maintenance treatment (Section 1-3.1(d)) exists in patients already receiving continuation ECT (Section 13.3.2).

b) Maintenance ECT treatments should be administered at the minimum frequency compatible with sustained remission.

c) The continued need for maintenance ECT should be reassessed at least every three months. This assessment should include consideration of both beneficial and adverse effects.

13.3.5. Pre-ECT Evaluation for Continuation/Maintenance ECT

Each facility using continuation/maintenance ECT should devise procedures for pre-ECT evaluation in such cases. The following recommendations are suggested, with the understanding that additions to or increased frequency of evaluative procedures should be included whenever clinically indicated.

a) Prior to each treatment:

1) interval psychiatric evaluation (this evaluation may be done monthly if treatments are at an interval of 2 weeks or less AND the patient has been clinically stable for at least 1 month)

2) interval medical history and vital signs (this exam may be done by the ECT psychiatrist or anesthetist at the time of the treatment session), with additional examination as clinically indicated

b) Updating of overall clinical treatment plan at least every three months.

c) Assessment of cognitive function (see Section 12.2.1) at least every three treatments.

d) At least every six months:

1) consent for ECT (see Chapter 8 )

anesthesia preoperative examination

e) Laboratory tests (see Chapter 6) at least yearly.

13.4 Continuation/Maintenance Psychotherapy

Psychotherapy, whether on an individual, group, or family basis, represents a useful component of the clinical management plan for some patients following an index ECT course.

APPENDIX B

Sample ECT Consent Documents

1. Consent Form : Acute Phase
2. Consent Form: Continuation/Maintenance ECT
3. Patient Information Sheet

Electroconvulsive Therapy (ECT) Consent Form:
Acute Phase

Name of Patient:__________________

My doctor, ___________________________, has recommended that I receive treatment with electroconvulsive therapy (ECT). This treatment, including the risks and benefits that I may experience, has been fully described to me. I give my consent to be treated with ECT.

Whether ECT or an alternative treatment, like medication or psychotherapy, is most appropriate for me depends on my prior experience with these treatments, the features of my illness, and other considerations. Why ECT has been recommended for me has been explained.

ECT involves a series of treatments, which may be given on an inpatient or outpatient basis. To receive each treatment I will come to a specially equipped area in this facility. The treatments are usually given in the morning. Because the treatments involve general anesthesia, I will have had nothing to eat or drink for several hours before each treatment. Before the treatment, a small needle will be placed in my vein so that I can be given medications. An anesthetic medication will be injected that will quickly put me to sleep. I will then be given another medication that will relax my muscles. Because I will be asleep, I will not experience pain or discomfort or remember the procedure. Other medications may also be given depending on my needs.

To prepare for the treatment, monitoring sensors will be placed on my head and body. Blood pressure cuffs will be placed on an arm and leg. This monitoring involves no pain or discomfort. After I am asleep, a carefully controlled amount of electricity will be passed between two electrodes that have been placed on my head.

I may receive bilateral ECT or unilateral ECT. In bilateral ECT, one electrode is placed on the left side of the head, the other on the right side. In unilateral ECT, both electrodes are placed on the same side of the head, usually the right side. Right unilateral ECT (electrodes on the right side) is likely to produce less memory difficulty than bilateral ECT. However, for some patients bilateral ECT may be a more effective treatment. My doctor will carefully consider the choice of unilateral or bilateral ECT.

The electrical current produces a seizure in the brain. The amount of electricity used to produce the seizure will be adjusted to my individual needs, based on the judgment of the ECT physician. The medication used to relax my muscles will greatly soften the contractions in my body that would ordinarily accompany the seizure. I will be given oxygen to breathe. The seizure will last for approximately one minute. During the procedure, my heart, blood pressure, and brain waves will be monitored. Within a few minutes, the anesthetic medications will wear off and I will awaken. I will then be observed until it is time to leave the ECT area.

The number of treatments that I will receive cannot be known ahead of time. A typical course of ECT is six to twelve treatments, but some patients may need fewer and some may need more. Treatments are usually given three times a week, but the frequency of treatment may also vary depending on my needs.

ECT is expected to improve my illness. However, I understand that I may recover completely, partially, or not at all. After ECT, my symptoms may return. How long I will remain well cannot be known ahead of time. To make the return of symptoms less likely after ECT, I will need additional treatment with medication, psychotherapy, and/or ECT. The treatment I will receive to prevent the return of symptoms will be discussed with me.

Like other medical treatments, ECT has risks and side effects. To reduce the risk of complications, I will receive a medical evaluation before starting ECT. The medications I have been taking may be adjusted. However, in spite of precautions, it is possible that I will experience a medical complication. As with any procedure using general anesthesia, there is a remote possibility of death from ECT. The risk of death from ECT is very low, about one in 10,000 patients. This rate may be higher in patients with severe medical conditions.

ECT very rarely results in serious medical complications, such as heart attack, stroke, respiratory difficulty, or continuous seizure. More often, ECT results in irregularities in heart rate and rhythm. These irregularities are usually mild and short lasting, but in some instances can be life threatening. With modern ECT technique, dental complications are infrequent and bone fractures or dislocations are very rare. If serious side effects occur, the necessary medical care will be provided.

The minor side effects that are frequent include headache, muscle soreness, and nausea. These side effects usually respond to simple treatment.

When I awaken after each treatment, I may be confused. This confusion usually goes away within an hour.

I understand that memory loss is a common side effect of ECT. The memory loss with ECT has a characteristic pattern, including problems remembering past events and new information. The degree of memory problems is often related to the number and type of treatments given. A smaller number of treatments is likely to produce less memory difficulty than a larger number. Shortly following a treatment, the problems with memory are greatest. As time from treatment increases, memory improves.

I may experience difficulties remembering events that happened before and while I received ECT. The spottiness in my memory for past events may extend back to several months before I received ECT, and, less commonly, for longer periods of time, sometimes several years or more. While many of these memories should return during the first few months following my ECT course, I may be left with some permanent gaps in memory.

For a short period following ECT, I may also experience difficulty in remembering new information. This difficulty in forming new memories should be temporary and typically disappears within several weeks following the ECT course.

The majority of patients state that the benefits of ECT outweigh the problems with memory. Furthermore, most patients report that their memory is actually improved after ECT. Nonetheless, a minority of patients report problems in memory that remain for months or even years. The reasons for these reported long-lasting impairments are not fully understood. As with any medical treatment, people who receive ECT differ considerably in the extent to which they experience side effects.

Because of the possible problems with confusion and memory, I should not make any important personal or business decisions during, or immediately following, the ECT course. During and shortly after the ECT course, and until discussed with my doctor, I should refrain from driving, transacting business, or other activities for which memory difficulties may be troublesome.

The conduct of ECT at this facility is under the direction of Dr. ____________________

I may contact him/her at ___________ if I have further questions.

I am free to ask my doctor or members of the ECT treatment team questions about ECT at this time or at any time during or following, the ECT course. My decision to agree to ECT is being made voluntarily, and I may withdraw my consent for further treatment at any time.

I have been given a copy of this consent form to keep.

Date Signature

_________ _________________________

Person Obtaining Consent:

Name Signature

_________ _________________________

Electroconvulsive Therapy (ECT) Consent Form:
Continuation/Maintenance Treatment

Name of Patient:

My doctor, ____________________________ has recommended that I receive continuation or maintenance treatment with electroconvulsive therapy (ECT). This treatment, including, the risks and benefits that I may experience, has been fully described to me. I give my consent to be treated with continuation ECT.

I will receive ECT to prevent relapse of my illness. Whether ECT or an alternative treatment, like medication or psychotherapy, is most appropriate for me at this time depends on my prior experience with these treatments in preventing, the return of symptoms, the features of my illness, and other considerations. Why continuation/maintenance ECT has been recommended for me has been explained.

Continuation/maintenance ECT involves a series of treatments with each usually separated in time by one or more weeks. Continuation /maintenance ECT is usually given for a period of several months or longer. These treatments may be given on an inpatient or outpatient basis.

To receive each continuation/maintenance treatment I will come to a specially equipped area in this facility. The treatments are usually given in the morning. Because the treatments involve general anesthesia, I will have had nothing to eat or drink for several hours before each treatment. Before the treatment, a small needle will be placed in my vein so that I can be given medications. An anesthetic medication will be injected that will quickly put me to sleep. I will then be given another medication that will relax my muscles. Because I will be asleep, I will not experience pain or discomfort or remember the procedure. Other medications may also be given depending on my needs.

The electrical current produces a seizure in the brain. The amount of electricity used to produce the seizure will be adjusted to my individual needs, based on the judgment of the ECT physician. The medication used to relax my muscles will greatly soften the contractions in my body that would ordinarily accompany the seizure. I will be given oxygen to breathe. The seizure will last for approximately one minute. During, the procedure, my heart, blood pressure, and brain waves will be monitored. Within a few minutes, the anesthetic medications will wear off and I will awaken. I will then be observed until it is time to leave the ECT area.

The number of continuation/maintenance treatments that I will receive will depend on my clinical course. Continuation ECT is usually given for at least six months. If it is felt that continuation ECT is helpful and should be used for a longer period (maintenance ECT), I will be asked to consent to the procedure again.

ECT is expected to prevent the return of my psychiatric condition. While for most patients ECT is effective in this way, I understand that this cannot be guaranteed. With continuation/maintenance ECT I may remain considerably improved or I may have a partial or complete return of psychiatric symptoms.

ECT very rarely results in serious medical complications, such as heart attack, stroke, respiratory difficulty, or continuous seizure. More often, ECT results in irregularities in heart rate and rhythm. These irregularities are usually mild and short lasting, but in some instances can be life threatening. With modem ECT technique, dental complications are infrequent and bone fractures or dislocations are very rare. If serious side effects occur, the necessary medical care will be provided.

The minor side effects that are frequent include headache, muscle soreness, and nausea. These side effects usually respond to simple treatment.

When I awaken after each treatment, I may be confused. This confusion usually goes away within an hour.

I understand that memory loss is a common side effect of ECT. The memory loss with ECT has a characteristic pattern, including problems remembering past events and new information ion. The degree of memory problems is often related to the number and type of treatments given. A smaller number of treatments is likely to produce less memory difficulty than a larger number. Shortly following a treatment, the problems with memory are greatest. As time from treatment increases, memory improves.

I may experience difficulties remembering events that happened before and while I received ECT. The spottiness in my memory for past events may extend back to several months before I received ECT, and, less commonly, for longer periods of time, sometimes several years or more. While many of these memories should return during the first few months following continuation ECT, I may be left with some permanent gaps in memory.

For a short period following each treatment, I may also experience difficulty in remembering new information. This difficulty in forming new memories should be temporary and will most likely disappear following completion of continuation/maintenance ECT.

The effects of continuation/maintenance ECT on memory are likely to be less pronounced than those during an acute ECT course. By spreading treatments out in time, with an interval of a week or more between treatments, there should be substantial recovery of memory between each treatment.

Because of the possible problems with confusion and memory, it is important that I not drive, or make any important personal or business decisions the day that I receive a continuation/maintenance treatment. Limitations on my activities may be longer depending on the side effects I experience following each treatment, and will be discussed with my doctor.

The conduct of ECT at this facility is under the direction of Dr. _________________

I may contact him/her at ___________if I have further questions.

I am free to ask my doctor or members of the ECT treatment team questions about ECT at this time or at any time during or following the ECT course. My decision to agree to continuation/maintenance ECT is being made voluntarily, and I may withdraw my consent for future treatment at any time.

I have been given a copy of this consent form to keep.

Date Signature

_________ _________________________

Person Obtaining Consent:

Name Signature

_________ _________________________

Sample Patient Information Booklet

Electroconvulsive Therapy

What is Electroconvulsive Therapy?

Electroconvulsive therapy (ECT or shock treatment) is an extremely safe and effective medical treatment for certain psychiatric disorders. With this treatment, a small amount of electricity is applied to the scalp and this produces a seizure in the brain. The procedure is painless because the patient is asleep, under general anesthesia.

Who is Treated with ECT?

ECT has been used for over 60 years. In the United States, about 100,000 individuals are estimated to receive ECT each year. ECT is most commonly given when patients have severe depressive illness, mania, or some forms of schizophrenia. Frequently, ECT is given when patients have not responded to other treatments, when other treatments appear to be less safe or difficult to tolerate, when patients have responded well to ECT in the past, or when psychiatric or medical considerations make it particularly important that patients recover quickly and fully.

Not all patients improve when treated with medications or psychotherapy (talk therapy). Indeed, when illnesses such as depression become particularly severe, it is doubtful that psychotherapy alone will be sufficient. For some patients, the medical risks of medications are greater than the medical risks of ECT. Typically, these are people with serious medical problems, such as some types of heart disease. When patients have life-threatening psychiatric problems, such as suicidal tendencies, ECT is also often recommended because it usually provides faster relief than medications. Overall, about 70 to 90% of the depressed patients treated with ECT show substantial improvement. This makes ECT the most effective of the antidepressant treatments.

Who Administers ECT?

A treatment team gives ECT. The team consists of a psychiatrist, an anesthesiologist, and nurses. The physicians responsible for administering ECT are experienced specialists. ECT is administered in a dedicated suite at the (name of facility) The suite contains a waiting, area, a treatment room, and a recovery room.

How is ECT Given?

Before ECT is administered, the patient’s medical condition is carefully assessed. This includes a complete medical history, physical examination, and medical tests, as needed. The treatments are usually given three times per week in the morning on Monday, Wednesday and Friday. Before each treatment, the patient should not eat or drink anything after midnight. Patients should also try to refrain from smoking during the morning prior to the treatment.

When the patient comes to the ECT treatment room, an intravenous line is started. Sensors for recording, EEG (electroencephalogram, a measure of brain activity) are placed on the head. Other sensors are placed on the chest for monitoring EKG (electrocardiogram). A cuff is wrapped around an arm for monitoring blood pressure. When everything is connected and in order, an anesthetic medication (methohexital) is injected through the intravenous line that will cause the patient to sleep for 5 to 10 minutes. Once the patient falls asleep, a muscle relaxant (succinylcholine) is injected. This prevents movement, and during the seizure there are only minimal contractions of the muscles.

When the patient is completely asleep and the muscles are well relaxed, the treatment is given. A brief electrical charge is applied to electrodes on the scalp. This stimulates the brain and produces the seizure that lasts for about a minute. Throughout the procedure, the patient receives oxygen through a mask. This continues until the patient resumes breathing on his or her own. When the treatment is completed, the patient is taken to a recovery area for monitoring by trained staff. Usually within 30 to 60 minutes, the patient can leave the recovery area.

How Many Treatments are Needed?

ECT is given as a course of treatments. The total number needed to successfully treat psychiatric disturbance varies from patient to patient. For depression, the typical range is from 6 to 12 treatments, but some patients may require fewer and some patients may require more treatments.

Is ECT Curative?

ECT is extremely effective in providing relief from psychiatric symptoms. However, permanent cures for psychiatric illness are rare, regardless of the treatment given. To prevent relapse following ECT, most patients require further treatment with medications or with ECT. If ECT is used to protect against relapse, it is usually administered to outpatients on a weekly to monthly basis.

How Safe is ECT?

It is estimated that death associated with ECT occurs in one of 10,000 patients. This rate may be higher in patients with severe medical conditions. ECT appears to have less risk of death or serious medical complications than a number of the medications used to treat psychiatric conditions. Because of this strong safety record, ECT is often recommended for patients with serious medical conditions. With modem anesthesia, fractures and dental complications are very rare.

What are the Common Side Effects of ECT?

The patient will experience some confusion on awakening following, the treatment. This is partly due to the anesthesia and partly due to the treatment. The confusion typically clears within an hour. Some patients have headaches following the treatment. This is usually relieved by Tylenol or aspirin. Other side effects, such as nausea, last for a few hours at most and are relatively uncommon. In patients with heart disease, there is an increased risk of cardiac complications. Cardiac monitoring and other precautions, including the use of additional medications if required help to ensure a safe treatment.

The side effect of ECT that has received the most attention is memory loss. ECT results in two types of memory loss. The first involves rapid forgetting of new information. For example, shortly following the treatment, patients may have difficulty remembering conversations or things they have recently read. This type of memory loss is short-lived and has not been shown to persist for more than a few weeks following the completion of ECT. The second type of memory loss concerns events from the past. Some patients will have gaps in their memory for events that occurred in the weeks to months and, less commonly, years prior to the treatment course. This memory loss also reverses following the completion of ECT. However, in some patients there may be permanent gaps in memory for events that occurred close in time to the treatment. However, like with any treatment, patients differ in the extent to which they experience side effects, and more extensive memory loss has been reported by a minority of individuals. It is known that the effects on memory are not necessary to obtain the benefits of ECT.

Many psychiatric illnesses result in impairments of attention and concentration. Consequently, when the psychiatric disturbance improves following ECT, there is often improvement in these aspects of thinking. Shortly following, ECT, most patients show improved scores on tests of intelligence, attention, and learning.

Does ECT Cause Brain Damage?

The scientific evidence strongly speaks against this possibility. Careful studies in animals have shown no evidence of brain damage from brief seizures, like those given with ECT. In the adult, seizures must be sustained for hours before brain damage can occur, yet the ECT seizure lasts only for about a minute. Brain imaging studies following ECT have shown no changes in the structure or composition of the brain. The amount of electricity used in ECT is so small that it cannot cause electrical injury.

How Does ECT Work?

Like many other treatments in medicine, the exact process that underlies the effectiveness of ECT is uncertain. It is known that the benefits of ECT depend on producing a seizure in the brain and on technical factors in how the seizure is produced. Biological changes that result from the seizure are critical to effectiveness. Most investigators believe that specific changes in brain chemistry produced by ECT are the key to restoring normal function.

Considerable research is being conducted to isolate the critical biochemical processes.

Is ECT Frightening?

ECT has often been portrayed in the movies and TV as a painful procedure, used to control or punish patients. These portrayals have no resemblance to modem ECT. One survey found that following ECT most patients reported that it was no worse than going to the dentist, and many found ECT less stressful. Other research has shown that that the vast majority of patients report that their memory is improved following ECT and that if needed, they would receive ECT again.

ECT is an extremely effective form of treatment. It is often safer and more effective than medications or no treatment at all. If you have any questions about ECT, please discuss them with your physician. You may also wish to read one of the following books. Both books were written by psychologists who were against people having ECT until they each had a severe depression and needed the treatment. Drs. Endler and Manning describe their illness, their experience in treatment with medication and psychotherapy, and their experience with ECT.

HOLIDAY OF DARKNESS
by Norman S. Endler
Wall & Thompson, Toronto
1990

UNDERCURRENTS: A THERAPIST’S
RECKONING WITH DEPRESSION
by Martha Manning
Harper, San Francisco
1995

Added: July 22, 2006 at 12:44 pm
Categories: Position Statements

Comments (8)

Al SylvesterNovember 16th, 2008 at 2:12 pm

chapt 9, 10, 11 seem to be missing from this.

Cindy DeLa CruzJanuary 15th, 2009 at 5:19 pm

Yes, the information I searching for was in Ch. 9, 10, and 11. This is very unfortunate that these chapters are missing.

Dr. Paul F. WhiteJanuary 21st, 2009 at 8:55 pm

How do I obtain the missing sections (Chapter 11)? I need to reference the recommendations regarding use of caffiene to prolong seizure times. Thank you for your prompt reply.

Dr. Paul F. WhiteJanuary 21st, 2009 at 8:57 pm

How do I obtain a copy of Chapter 11 (Treatment). I want to reference the APA recommendations regarding the use of caffeine to prolong ECT-evoked seizures. Thank you for your prompt reply.