THE CANADIAN JOURNAL OF PSYCHIATRY Volume 37
Ottawa, Canada, December 1992
Number 10
POSITION PAPER
Electroconvulsive Therapy* MURRAY W. ENNS, M.D.' AND JEFFREY P. REISS, M.D., M.Sc. 2
Thefollowingpositionpaperwasapprovedby theBoardofDirectors of theCanadian Psychiatric Association on September 15,1992.
I
n 1980, the Canadian Psychiatric Association (CPA) published its first position paper on electroconvulsive therapy (ECT) which included a recommendation for periodic review of the position (I). During the past decade, a considerable amount of new research has been done. This has resulted in the need to update the position of the CPAon ECT. Electroconvulsive therapy remains an important part of the therapeutic armamentarium in contemporary psychiatric practice. Although the mechanism of action of ECT is not completely understood, over 50 years of clinical experience and a substantial volume of research have lead to the CPA's current recommendation that ECT should remain readily available as a treatment option. Like other significant medical interventions, ECT has clearly defined indications,demonstrated efficacy and safety, well known side-effectsand established standardsfor optimal practice. As such, the decision to use ECT in the treatment of an individual patient is a medical one, based on the psychiatrist's assessment of the patient's illness, an evaluation of the merits of ECT versus alternative treatments and involves the process of informed consent. With the passage of time and the accumulation of greater knowledge, ECT has developed into a complex treatment requiring the expertise of psychiatrists, anesthesiologists and frequently other medical specialists.As our understanding of mental illness grows, the specific treatments that are offered and the techniques of these treatments, including ECT, continue to evolve. The modem psychiatrist must keep abreast of this evolution.
Definition For the purposes of the CPA, electroconvulsive therapy
(BCT) is defined as a medical procedure in which a brief
electrical stimulus is used to induce a cerebral seizure under controlled conditions. Its purpose is to treat specific types of major mental disorders. History
In order to properly understand the origins of ECT, one must have an appreciation of the context in which it was developed. Prior to the 1930s, there were few treatments to offer severely disturbed psychiatric patients. They were provided with custodial care, sedation and some social support (2). In 1918, Von Juaregg (3) had developed malarial fever therapy for general paresis. He was awarded the Nobel Prize in medicine in 1927 for his accomplishment. Effective somatic therapy for functional psychosis was not yet available. During the 1930s four types of somatic therapies for schizophrenia were developed. The first three of these were insulin coma treatment introduced by Manfred Sakel in 1933 (4), psychosurgery (pre-frontal lobotomy) introduced by Egas Moniz in 1936 (5), and pharmacological convulsive therapy introduced by Ladislas VonMeduna in 1934(6). Von Meduna based his treatment on clinical and neuropathological studies which suggested to him a biological antagonism between epilepsy and schizophrenia. Technical problems with pharmacological convulsive therapy and the extremely uncomfortable sensations that conscious patients experienced pre-ictally, were the motivation for experimentation with other means of inducing seizures. In 1938, Ugo Cerletti and Lucio Bini pioneered the fourth innovative somatic therapy when they used electrical stimuli to induce seizures for the treatment of severe psychosis (7). Although they chose the term "electroshock" for their method,they used electricity only for the induction of convulsions, denying any effects of the electrical current, per se, on the psychotic illness. Electroshock, or ECT as it came to be known, is the only somatic therapy from that era that remains in widespread use today. While ECT was originally developed for the treatment of schizophrenia, it was not long after its introduction that it became widely recognized that the best results were obtained
"Manuscript received October 1992. lAssistant Professor of Psychiatry, University of Manitoba; Staff Psychiatrist, Mood Disorders Unit, 'Department of Psychiatry, Health Sciences Centre, Winnipeg, Manitoba. 2Associate Professor of'Psychiatry, University ofManitoba; Director, Health Maintenance Clinic, Department of Psychiatry, Health Sciences Centre, Winnipeg Manitoba. Addressreprintrequests to: Chief Administrative Officer, Canadian Psychiatric Association, 237 Argyle Avenue, Suite 200, Ottawa, Ontario K2P 188 Can. J. Psychiatry Vol. 37, December 1992
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in patients with major mood disorders, not those with schizophrenia. This observation has been borne out by controlled studies and is reflected in the contemporary diagnostic indications for ECT (8). Significant improvements in the technique of ECT have been made since its introduction. These have included succinylcholine induced muscular relaxation, short acting anesthesia, pre-oxygenation, the use of more efficient electrical stimulus wave forms, unilateral electrode placement, and more complete seizure monitoring (9). Despite these advances in technique, the popularity of ECT greatly diminished during the 1960s and 1970s. Both the introduction of effective pharmacological treatments and a vocal anti-ECT lobby likely contributed to this decline. Over the last 14 years however, the practice of ECT has undergone a turnaround. In 1978, the American Psychiatric Association (APA) published the report of the ECT task force under the chairmanship of Fred Frankel (10). This report formally recognized the role of ECT in contemporary psychiatric practice and in many ways became the standard for its use. Max Fink's monograph of 1979 (11) definitively summarized the topic from its beginnings to the mid-1970s. The Canadian Psychiatric Association published its own position paper on ECT in 1980 (1), also encouraging the availability of ECT "within the context of the usual doctor-patient relationship, the medical profession's most current understanding of mental illness and the most appropriate forms of treatment." Since then, several significant comprehensive and objective reports on the topic have been published. These have included the Ontario Ministry of Health's Report ofthe Electroconvulsive Therapy Review Committee (12) and the NIH/NIMH sponsored Consensus Conference Report (13). The most recent major report is the 1990 APA Task Force Report on ECT, chaired by Richard Weiner (8). Academic and research interest in ECT has grown under these developments as evidenced by the increasing number of publications on the topic and the establishment of a journal devoted exclusively to convulsive therapy issues (14). The previous position paper of the CPA on ECT (1) noted the lack of controlled double-blind studies and anticipated further research and clarification. Although unanswered questions about ECT remain, systematic research and study has more clearly established an ongoing role for electroconvulsive therapy in the treatment of incapacitating mental disorders (8,9). Indications The main diagnostic indications for ECT include major depression (single episode or recurrent), bipolar disorder (depressed, manic or mixed), non chronic schizophrenia (especially when affective or catatonic symptomatology is prominent), schizoaffective disorder and schizophreniform disorder. For these disorders there is either overwhelming evidence in the literature attesting to the efficacy of ECT, or a consensus among experienced psychiatrists as to its effectiveness (8,11,15).
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Under exceptional circumstances, ECT may also be considered a treatment option for disorders not included in the above list. When considering ECT for unusual indications, the psychiatrist should be aware that compelling evidence of the effectiveness of ECT is lacking and should thoroughly consider the available standard treatments before offering ECT. Consultation with a psychiatric colleague is also recommended when ECT is being considered for an unusual indication. A small number of medical disorders have also been treated successfully with ECT - neuroleptic malignant syndrome (16), Parkinson's disease (17,18) and refractory epilepsy (19,20), among others (8). The clinical utility of ECT in these disorders should not be considered firmly established. However, patients who suffer from one of these disorders in addition to a major diagnostic indication for ECT (for example, Parkinson's disease and major depression) may experience improvement in both disorders with ECT (17). The decision to use ECT in the treatment of an individual patient is based on the consideration of a number of factors in addition to diagnosis. These factors include the patient's prior treatment response, the severity of the disorder, the relative need for rapid response to treatment, the risks and benefits of ECT in comparison with other appropriate treatments and the patient's preferred treatment modality. Although ECT is frequently used as a second line treatment after psychotropic medications have failed, the use of ECT need not be restricted to this setting. Consideration of some of the factors noted above may lead the psychiatrist to offer ECT as a primary treatment modality. Contraindications It has been stated in the past that the only absolute contraindication to ECT is an intracranial neoplasm (21). Since then, experience in the administration of ECT to patients with a variety of serious medical conditions has accumulated. Techniques have been developed to reduc.e the risks associated with ECT in these conditions so that no contraindication to ECT is currently considered absolute (8,15). Instead, recent reports refer to specific conditions in which there is significantly increased risk. These conditions include: space occupying intracranial lesions or other conditions associated with elevated intracranial pressure, recent myocardial infarction with cardiac decompensation, severe underlying hypertension especially if related to a pheochromocytoma, evolving strokes and other risk factors for intracerebral hemorrhage, retinal detachment, and any condition in which the anesthetic risk is rated as American Society of Anesthesiologists (ASA) level 4 or 5 (8,9,15). Pregnancy is not considered a contraindication to the use of ECT. Numerous case reports suggest that ECT is a low risk and highly efficacious in treating depression at any stage of pregnancy (8). As in all applications of ECT, the decision to treat a patient in the presence of one of these conditions should be made only after careful consideration of the risks and benefits of ECT, alternative treatments, or no treatment. Particular care should be taken
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to optimize the patient's medical condition prior to the administration of ECT and to modify the treatments in such a way as to minimize the risk (8,9). This preparation should include consultation with an anesthesiologist and other medical or surgical specialists, as appropriate. Adverse Effects When ECT was originally introduced, up to 40% of patients suffered from complications of various types (13). Most frequently this involved compression fractures of the vertebrae (11). Early use of ECT was also associated with a significant mortality rate - approximately one per 1,000 patients (13). Contemporary use of ECT including pre-oxygenation, brief anesthesia, muscular relaxation and physiologic monitoring is associated with a very low rate of morbidity and mortality. The majority of deaths associated with ECT are due to cardiorespiratory causes (22). This is consistent with the higher mortality found in patients whose cardiac function is already impaired (15). Several recent reviews of ECT related mortalities suggest a rate of 2.0 to 4.5 deaths per 100,000 treatments (23-25). It should be recognized that this mortality rate is comparable to that reported for brief general anesthesia in minor surgery (8,11). With the advent of present day techniques, many of the significant medical complications of ECT have been eliminated. A complication rate of one per 1,400 treatments has recently been suggested (13). These complications include laryngospasm, prolonged apnea, prolonged seizures, tooth damage arid circulatory insufficiency (13). Cardiac arrhythmias are frequent during the treatment and immediately postictally, however the majority of these are benign and resolve without intervention (22,26). Nausea, headache and muscle soreness are commonly reported but these symptoms respond to symptomatic treatment (11). To objectively evaluate the significance of these adverse effects, it must be remembered that pharmacological treatments may have both serious and minor adverse effects as well. As examples, tachyarrhythmias, hypotension, cardiac conduction disturbances, anticholinergic toxicity and death due to overdose or idiosyncratic effects of the drugs are among the serious side-effects of heterocyclic antidepressants (27,28). The principal adverse effect of ECT, which has been the root of much controversy, is memory impairment. Four types of cognitive impairment related to ECT can be discerned (9). Immediately following an ECT treatment there is a period of post-ictal confusion. After clearing of the post-ictal confusion, retrograde amnesia (forgetting of events prior to the seizure) and anterograde amnesia (forgetting of events after the seizure) can be demonstrated using a variety of neuropsychological tests. A small minority of patients also experience longer lasting subjective memory impairment which may be difficult to objectively detect. Anterograde and retrograde amnesias subside over an interval of one to six months following a course of ECT
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(15,29). Although some specific memories of events during the months before and after ECT may be permanently lost (30), acquisition and retention of new memories and longer term memory are not persistently impaired (30,31). Subjective memory impairment following ECT may be persistent. Some cases may be explained on the basis of residual psychopathology, increased awareness of essentially normal forgetfulness, or secondary gains related to the complaint of memory loss (15). However, the basis of these complaints is incompletely understood and it is possible that persistent subtle, though genuine, memory difficulties may not be adequately detected with available neuropsychological tests. The foregoing discussion of memory side-effects of ECT refers to ECT in a general way. However, it is important to note that the severity of adverse cognitive effects of ECT is dependent upon the specific technique used. Bilateral electrode placement, higher stimulus intensity, sine wave stimulus waveform, more frequent treatments, concomitant psychotropic drug use and higher anesthetic dose are all factors associated with greater cognitive side-effects than unilateral nondominant electrode placement, moderately supra threshold intensity, brief pulse waveform, less frequent treatments given without concomitant psychotropics and more moderate anesthetic dose (8,32-34). IfECTis administered using a brief pulse stimulus on the nondominant hemisphere, patients may have no detectable memory impairment after a few days post-ECT treatment (29). Claims have been made that ECT causes "brain damage" (35). A recent comprehensive and objective review of a large number of studies concluded that ECT, as administered today, causes no detectable evidence of irreversible structural brain damage (36). However, the possibility remains that subtle deficits occur which cannot be objectified with currently available techniques. Efficacy A number of authors have comprehensively summarized the studies which demonstrate the effectiveness of ECT (9,11,24). No attempt will be made here to review all of the data. Instead, a summary of the conclusions which can be made on the basis of available data will be presented. It has been clearly demonstrated in double-blind controlled studies that genuine ECT is substantially more effective than sham ECT in the treatment of major depression (37-39). In a small number of methodologically sound studies it has been demonstrated that ECT is also superior to moderate doses of antidepressant drugs (40-42). In a large number of studies, albeit with methodological flaws, this same conclusion has been reached (43). However, Abrams (9) notes that optimal drug therapy using serum level monitoring and possibly higher doses, has not been directly compared with ECT. Mania generally responds very well to ECT (9). The number of controlled studies documenting the effectiveness of ECT in mania is small, probably because of its good
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response rate to pharmacological treatment. In recent years, two controlled prospective studies of ECT in the treatment of mania have been reported. Both of these studies found that ECT resulted in more rapid resolution of symptoms than the combination of lithium and neuroleptics (44,45). Some authorities recommend bilateral ECT as the preferred treatment in this patient group (46,47). The effectiveness of ECT for schizophrenia is more difficult to evaluate than it is for mood disorders. Much of the difficulty arises because the schizophrenic patients included in the relevant studies were diagnosed using a wide variety of diagnostic criteria and had widely disparate symptomatology (9). Recent studies have demonstrated that genuine ECT causes more rapid resolution of schizophrenic symptoms than sham ECT (48,49). Chronic patients were excluded and patients with affective symptoms were allowed in these studies. Several prospective studies of the treatment of non chronic schizophrenia have compared ECT with neuroleptics finding no significant difference between the two treatments (50-52). In addition, some studies have suggested that the combination of ECT and neuroleptics results in quicker recovery for non chronic schizophrenia than treatment with neuroleptics alone (53,54). Earlier studies of genuine versus sham ECT, using groups of chronic schizophrenics, failed to find any difference between the two treatments (55,56). In summary, some selected groups of schizophrenic patients, particularly those with a brief duration of illness and/or prominent affective symptoms, may respond as well to ECT as they do to neuroleptics. Patients with chronic schizophrenia, on the other hand, respond no better to genuine ECT than sham ECT. Taken together, the data indicate that ECT has a more limited role in the treatment of schizophrenia than in the treatment of mood disorders. As a second line treatment for schizophrenia, ECT still has value in contemporary psychiatric practice. The number of treatments required for an effective course of ECT varies substantially between individuals. Typically, patients with depressive illness require six to 12 treatments, while patients with mania or schizophrenia may require a somewhat higher number (8,9). However, some patients may improve dramatically with only a few treatments. Once the patient has achieved full remission, no further benefit results from the administration of additional treatments (57,58). When patients show a slow or insignificant response to a series of treatments, it requires the clinical judgment of the psychiatrist to determine when to recommend termination or modification of the treatments. This judgment takes account of such factors as the nature and severity of the patient's symptoms, the magnitude of cognitive side-effects, history of response to ECT, and the response obtained thus far. It is therefore difficult to provide specific guidelines for the maximum allowable number of treatments. Nevertheless, the following recommendations are made. If after six to eight treatments there is minimal improvement, consideration should be given to changing the technique of ECT. These
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changes may include switching to bilateral electrode placement, increasing the electrical dose, or pharmacologically augmenting the elicited seizures (8). When patients with depressive illness do not show substantial improvement after 12 to 14 treatments, another psychiatrist's opinion should be obtained before administering further treatments. Likewise, when patients with mania or schizophrenia show little improvement after 14 to 16 treatments, a second psychiatric opinion should be obtained before proceeding further. ECT is usually administered two or three times per week, although double ECTs (two seizures per session) or daily treatments are sometimes used early in the course oftreatment in an attempt to speed the recovery of extremely ill patients (8,9,11). In the past, some clinicians used "regressive ECT" in which a prolonged and intensive course of treatment was used in order to induce a sustained delirium. The objective of this practice was to create a "regressed state" and subsequently reconstruct the patient's character. This practice has not received scientific support and as such should not be used. The above discussion deals with the acute treatment of psychiatric disorders. However, these disorders can be recurrent. In particular, follow-up studies of patients treated for depression, especially those with delusional or treatmentresistant depression (two common indications for ECT) , have high relapse rates in the year after acute treatment (59,60). For this reason, some form of maintenance treatment is indicated to prevent relapses after a course of ECT (9,61). Controlled studies directly comparing maintenance ECT to maintenance pharmacotherapy are lacking. A number of clinical studies however, have reported that maintenance ECT reduces the rate of relapse and recurrence of mood disorders (62-64). Although further prospective study is needed, maintenance ECT may be useful in selected patients who cannot tolerate pharmacotherapy or who continue to relapse despite appropriate pharmacotherapy. Assessment and Documentation Prior to the administration of ECT, a thorough evaluation of the patient's psychiatric and medical status is required. This involves a psychiatric history, mental status examination including objective assessment of cognitive functions, medical history, and physical examination. Essential laboratory investigations include a complete blood count, serum electrolytes and renal function tests. Patients over 45 years of age should also receive an electrocardiogram and possibly a chest radiograph. When the patient has co-existing medical conditions or is of advanced age, further investigations and consultations should be obtained as discussed under contraindications. The results of this complete evaluation should be documented in the patient's record prior to commencing ECT. The record must also contain documentation of informed consent and the indications for ECT. The physician's orders for ECT should indicate treatment dates and desired electrode placement. Patients should fast for eight hours prior to treatment.
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Between ECT treatments, the psychiatrist should reassess and document changes in target symptoms and the occurrence of adverse effects. Objective testing of cognitive functions is an important part of this process. The physician who administers the ECT should keep a record of each treatment including stimulus parameters the doses of anesthetic and muscle relaxant used, and the quality and duration of seizure activity elicited. After the course of ECT has been terminated, a summary note should be completed for the medical record. Technique It is beyond the scope of this paper to discuss details of the technique of ECT; complete descriptions are available elsewhere (8,9,11). However, it is worth emphasizing that the specific technique used in ECT is a matter of considerable consequence. Electrode placement, stimulus intensity and waveform, treatment frequency, concomitant psychotropic drugs and anesthetic medications have been mentioned previously as factors affecting the severity of cognitive sideeffects. The clinical effectiveness ofthe elicited seizure is also affected by some of these parameters. As examples of how technique can affect outcome, a brief discussion of electrode placement and stimulus-intensity and waveform will be presented. Since the introduction of unilateral ECT, there has been considerable controversy over the merits of unilateral versus bilateral electrode placements. The two central issues are memory impairment and efficacy. Bilateral treatments have been clearly associated with greater memory impairment (11,15). Reports on the relative efficacy of the two electrode placements have been much more divided. In about one-half of the reports the treatments were found to be comparable, and in the other half bilateral ECT was found to be superior (9). 'Therefore, unilateral ECT may be advantageous when it is especially important to reduce cognitive side-effects. Bilateral ECT, on the other hand, may be preferred if there is a greater treatment urgency or if unilateral ECT fails (8), More recently it has been demonstrated that there is an interaction between electrode placement and stimulus intensity affecting the efficacy of ECT. Barely suprathreshold, brief pulse unilateral ECT is remarkably ineffective (65). However, increasing the stimulus intensity increases the efficacy of brief pulse unilateral ECT (65,66). In the case of bilateral ECT, barely suprathreshold stimuli remain effective, but increasing the stimulus intensity may speed the clinical response (66,67). The earliest ECT devices employed a sine wave current to elicit seizures (7). This type of electrical current administers a substantial amount of energy below the patient's seizure threshold, thereby increasing memory impairment, but not enhancing therapeutic effects (68). For this reason, sine wave currents are generally considered obsolete and brief pulse currents are the accepted standard (8,9). The question of what constitutes the optimal technique for administering ECT is not completely answered. Therefore, the clinician administering or prescribing ECT must make
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decisions about various aspects of the treatment technique based on an ongoing assessment of the relative risks and benefits. Mechanism of Action
A large number of hypotheses on the mechanism of action of ECT have been proposed (19,20,69-72). These hypotheses have included both psychological and biological explanations of the effects of ECT. Psychodynamic theories have generally emphasized the importance of fear in the patient, the role of guilt and punishment for imagined wrongdoing, and amnesia for the causes of depression (69). Although the importance of psychological factors in ECT treatments should not be completely overlooked, such purely psychological explanations lack empirical support and have been abandoned by psychiatric investigators. In contrast, biological theories of the action of ECT have been the subject of much recent investigation. Neurochemical, neuroendocrine, electrophysiological and neuropsychological hypotheses have been advanced (19,20,70-72). The role of the cerebral seizure is central to most contemporary theories of the action of ECT. A considerable amount of research supports the contention that epileptiform discharges in the brain are necessary and sufficient for efficacious ECT (68,73). Recent work challenges this view and suggests that the occurrence of a generalized seizure of "adequate duration," by itself, may not be sufficient to ensure maximally effective treatment. In particular, the use of barely suprathreshold electrical stimulation results in diminished therapeutic response, especially with unilateral ECT (65,67,73). It appears that some aspect of the process of seizure generalization may be more closely related to the therapeutic effect of ECT than the occurrence and duration of cerebral seizures (9,15). Research has greatly increased our knowledge about the biological effects of ECT. As with most biological treatments in psychiatry, however, we still do not know precisely why ECT works. As such, ECT remains an empirical treatment. Nevertheless, this does not detract from its efficacy and safety . as a therapeutic modality in psychiatric practice. Consent to Treatment
For the most part, the process of obtaining informed consent for ECT is no different than the consent procedure for other significant medical interventions. The attending psychiatrist or other designated medical personnel must be directly involved in obtaining informed consent. The physician should provide realistic information about the nature of the condition being treated, the expected benefits and possible risks of ECT, as well as the benefits and risks of other reasonable alternative treatments, or no treatment (74). The physician should also ensure that the patient has understood the information provided as part of the assessment of the patient's competence to consent to treatment. Consent must be obtained from the patient unless the patient is clearly incompetent to participate in the process. For incompetent
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patients, substituted consent should be obtained in accordance with the requirements of provincial legislation and facility regulations. Whenever possible, the substituted consent procedure should include obtaining the views of family members and significant others, as well as a second psychiatric opinion. It should be emphasized that informed consent is a process that begins with the provision of information and the signing of a consent document, and continues through the entire course of treatment. Therefore, consent may be withdrawn at any time. The issue of consent should be reviewed in an ongoing manner.
Educationand Research Over the years ECT has become an increasingly complex treatment. The modern psychiatrist must therefore acquire a high level of knowledge and sophistication in order to use the treatment optimally. The educational process should begin in medical school, so that graduates have an appreciation of the role of ECT in contemporary psychiatric practice. Residents in general psychiatric programs should have both didactic teaching and practical experience in the use of ECT. When ECT is performed by a psychiatric resident, adequate supervision must be provided. Psychiatrists who prescribe or administer ECT should keep their knowledge and practical skills up to date through the use of continuing education programs and/or attention to clinical and research reports in the psychiatric literature. Research and clinical experience have already provided much information on which to base the practice of ECT. Nevertheless, much remains to be learned. Although awareness of the way treatment technique can affect outcome has increased, it is still not known how to select the ideal form of treatment for a given patient. Furthermore, a great deal has been learned about the neurophysiological effects of ECT, but it remains to be determined which of these effects, if any, is responsible for the therapeutic response. These examples serve to highlight the need for ongoing research and publication on the topic of ECT.
Summaryand Recommendations 1. When used properly, ECT is a safe and effective treatment which should continue to be available as a therapeutic option for the treatment of mental disorders. 2. ECT should be used only on the recommendation of a psychiatrist, and should preferably be administered by a psychiatrist. 3. The main conditions for which ECT is indicated are major mood disorders and non chronic schizophrenia, particularly when affective or catatonic features are prominent. A second psychiatric opinion is recommended if ECT is to be used for an unusual indication. 4. A medical history, physical examination and appropriate laboratory investigations are necessary in order to detect any significant medical illness prior to the administration of ECT. If an active medical disorder is present, steps
should be taken to treat the disorder and/or to further modify the technique of ECT in order to minimize the possible risks. Consultation(s) from an anesthesiologists and other medical specialists should be obtained, if indicated. 5. During a course of ECT, the psychiatrist should regularly reassess and document changes in target symptoms and the occurrence of adverse effects. Objective testing of cognitive functions is part of this process. 6. Modification of ECT with brief anesthesia, muscle relaxants and pre-oxygenation should be accomplished by a suitably qualified physician, unless specific contraindications to the use of these modifications are present. 7. The decision to use ECT is a medical one, and requires informed consent. If the patient is incompetent to give this consent, a consultation from another psychiatrist with regard to the use of ECT should be obtained. Following this, the psychiatrist can decide whether to seek substituted consent for ECT or to pursue another course. 8. ECT is a complex medical intervention. Practitioners require considerable knowledge and practical skills in order to optimally perform the procedure. Psychiatric residencies should include training in ECT and psychiatrists should keep up-to-date with advances in the theory and practice of ECT. 9. Continuing basic and clinical research is encouraged in order to delineate the mechanism of action of ECT and to further improve the clinical application of the treatment. 10. The position of the CPA on ECT should be periodically reviewed, as dictated by changes in our knowledge and understanding of the treatment of major mental illness.
References 1. Pankratz WJ. Electroconvulsive therapy: the position of the Canadian Psychiatric Association. Can J Psychiatry 1980; 25(6): 509-514. 2. Endler NS. The origins of electroconvulsive therapy. Convulsive Therapy 1988; 4: 5-23. . 3. Von Juaregg W. The treatment of general paresis by inoculation of malaria. J Nerv Ment Dis 1922; 55: 369-375. 4. Sakel M. Neue Behandlungsmethode der schizophrenie. Moritz Perles, Wien und Leipzig, 1935. 5. Moniz E. Tentatives operatoires dans le traitement de certaines psychoses. Paris: Masson et de, 1936. 6. Fink M. Meduna and the origins of convulsive therapy. Am J Psychiatry 1984; 141: 1034-1041. 7. Cerletti U. L'electroshock. Revista Sperimentale di Freniatria 1940; 64: 209-310. 8. The practice of ECT: recommendations for treatment, training and privileging. Task force report on ECT. Washington DC: American Psychiatric Press, Inc., 1990. 9. Abrams R. Electroconvulsive therapy. Oxford: Oxford University Press, 1988. 10. Electroconvulsive therapy, task force 14. Washington DC: American Psychiatric Press, Inc., 1978. 11. Fink M. Convulsive therapy: theory and practice, New York: Raven Press, 1979. 12. Report of the electroconvulsive therapy review committee. Toronto ON: Ontario Ministry of Health, 1985.
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13. Consensus conference, electroconvulsive therapy. JAMA 1985; 254: 2103-2108. 14. Fin~ M. Convulsive therapy. New York: Raven Press, 1985. 15. Weiner RD. Electroconvulsive therapy, fifth edition. In: Kaplan HE, Sadock BJ, eds. Comprehensive text of psychiatry. Baltimore MD: Williams and Wilkins, 1989: 1670-1678. 16. ~earIman CA. Neuroleptic malignant syndrome: a review of the literature. J Clin Psychopharm 1986; 6: 257-273. 17. ~ouyon R, Serby M, Klutchko B, et al. ECT and Parkinson's disease revisited: a naturalistic study. Am J Psychiatry 1989; 146: 1451-1455. 18: Abrams R. ECT for Parkinson's disease. Am J Psychiatry 1989; 146: 1391-1393. 19. Post RM, Putnam F, Uhde TW, et al. Electroconvulsive therapy as an anticonvulsant. Ann N Y Acad Sci 1986; 462: 376-388. 20. Sa~keim HA, Decina P, Prohovnik I, et al. Anticonvulsant and antIdepressant properties of electroconvulsive therapy: a proposed mechanism of action. Bioi Psychiatry 1983' 18: 13011310. ' 21. Kalin?wsky LB. Pharmacological, convulsive and other somanc treatments in psychiatry. New York: Grune and Stratton, 1969. 22. Welch CA, Drop LJ. Cardiovascular effects ofECT. Convulsive Therapy 1"989; 5: 35-43. 23. Babigian HM, Guttmacher LB. Epidemiologic considerations In electroconvulsive
Ottawa, Canada, December 1992
Number 10
POSITION PAPER
Electroconvulsive Therapy* MURRAY W. ENNS, M.D.' AND JEFFREY P. REISS, M.D., M.Sc. 2
Thefollowingpositionpaperwasapprovedby theBoardofDirectors of theCanadian Psychiatric Association on September 15,1992.
I
n 1980, the Canadian Psychiatric Association (CPA) published its first position paper on electroconvulsive therapy (ECT) which included a recommendation for periodic review of the position (I). During the past decade, a considerable amount of new research has been done. This has resulted in the need to update the position of the CPAon ECT. Electroconvulsive therapy remains an important part of the therapeutic armamentarium in contemporary psychiatric practice. Although the mechanism of action of ECT is not completely understood, over 50 years of clinical experience and a substantial volume of research have lead to the CPA's current recommendation that ECT should remain readily available as a treatment option. Like other significant medical interventions, ECT has clearly defined indications,demonstrated efficacy and safety, well known side-effectsand established standardsfor optimal practice. As such, the decision to use ECT in the treatment of an individual patient is a medical one, based on the psychiatrist's assessment of the patient's illness, an evaluation of the merits of ECT versus alternative treatments and involves the process of informed consent. With the passage of time and the accumulation of greater knowledge, ECT has developed into a complex treatment requiring the expertise of psychiatrists, anesthesiologists and frequently other medical specialists.As our understanding of mental illness grows, the specific treatments that are offered and the techniques of these treatments, including ECT, continue to evolve. The modem psychiatrist must keep abreast of this evolution.
Definition For the purposes of the CPA, electroconvulsive therapy
(BCT) is defined as a medical procedure in which a brief
electrical stimulus is used to induce a cerebral seizure under controlled conditions. Its purpose is to treat specific types of major mental disorders. History
In order to properly understand the origins of ECT, one must have an appreciation of the context in which it was developed. Prior to the 1930s, there were few treatments to offer severely disturbed psychiatric patients. They were provided with custodial care, sedation and some social support (2). In 1918, Von Juaregg (3) had developed malarial fever therapy for general paresis. He was awarded the Nobel Prize in medicine in 1927 for his accomplishment. Effective somatic therapy for functional psychosis was not yet available. During the 1930s four types of somatic therapies for schizophrenia were developed. The first three of these were insulin coma treatment introduced by Manfred Sakel in 1933 (4), psychosurgery (pre-frontal lobotomy) introduced by Egas Moniz in 1936 (5), and pharmacological convulsive therapy introduced by Ladislas VonMeduna in 1934(6). Von Meduna based his treatment on clinical and neuropathological studies which suggested to him a biological antagonism between epilepsy and schizophrenia. Technical problems with pharmacological convulsive therapy and the extremely uncomfortable sensations that conscious patients experienced pre-ictally, were the motivation for experimentation with other means of inducing seizures. In 1938, Ugo Cerletti and Lucio Bini pioneered the fourth innovative somatic therapy when they used electrical stimuli to induce seizures for the treatment of severe psychosis (7). Although they chose the term "electroshock" for their method,they used electricity only for the induction of convulsions, denying any effects of the electrical current, per se, on the psychotic illness. Electroshock, or ECT as it came to be known, is the only somatic therapy from that era that remains in widespread use today. While ECT was originally developed for the treatment of schizophrenia, it was not long after its introduction that it became widely recognized that the best results were obtained
"Manuscript received October 1992. lAssistant Professor of Psychiatry, University of Manitoba; Staff Psychiatrist, Mood Disorders Unit, 'Department of Psychiatry, Health Sciences Centre, Winnipeg, Manitoba. 2Associate Professor of'Psychiatry, University ofManitoba; Director, Health Maintenance Clinic, Department of Psychiatry, Health Sciences Centre, Winnipeg Manitoba. Addressreprintrequests to: Chief Administrative Officer, Canadian Psychiatric Association, 237 Argyle Avenue, Suite 200, Ottawa, Ontario K2P 188 Can. J. Psychiatry Vol. 37, December 1992
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in patients with major mood disorders, not those with schizophrenia. This observation has been borne out by controlled studies and is reflected in the contemporary diagnostic indications for ECT (8). Significant improvements in the technique of ECT have been made since its introduction. These have included succinylcholine induced muscular relaxation, short acting anesthesia, pre-oxygenation, the use of more efficient electrical stimulus wave forms, unilateral electrode placement, and more complete seizure monitoring (9). Despite these advances in technique, the popularity of ECT greatly diminished during the 1960s and 1970s. Both the introduction of effective pharmacological treatments and a vocal anti-ECT lobby likely contributed to this decline. Over the last 14 years however, the practice of ECT has undergone a turnaround. In 1978, the American Psychiatric Association (APA) published the report of the ECT task force under the chairmanship of Fred Frankel (10). This report formally recognized the role of ECT in contemporary psychiatric practice and in many ways became the standard for its use. Max Fink's monograph of 1979 (11) definitively summarized the topic from its beginnings to the mid-1970s. The Canadian Psychiatric Association published its own position paper on ECT in 1980 (1), also encouraging the availability of ECT "within the context of the usual doctor-patient relationship, the medical profession's most current understanding of mental illness and the most appropriate forms of treatment." Since then, several significant comprehensive and objective reports on the topic have been published. These have included the Ontario Ministry of Health's Report ofthe Electroconvulsive Therapy Review Committee (12) and the NIH/NIMH sponsored Consensus Conference Report (13). The most recent major report is the 1990 APA Task Force Report on ECT, chaired by Richard Weiner (8). Academic and research interest in ECT has grown under these developments as evidenced by the increasing number of publications on the topic and the establishment of a journal devoted exclusively to convulsive therapy issues (14). The previous position paper of the CPA on ECT (1) noted the lack of controlled double-blind studies and anticipated further research and clarification. Although unanswered questions about ECT remain, systematic research and study has more clearly established an ongoing role for electroconvulsive therapy in the treatment of incapacitating mental disorders (8,9). Indications The main diagnostic indications for ECT include major depression (single episode or recurrent), bipolar disorder (depressed, manic or mixed), non chronic schizophrenia (especially when affective or catatonic symptomatology is prominent), schizoaffective disorder and schizophreniform disorder. For these disorders there is either overwhelming evidence in the literature attesting to the efficacy of ECT, or a consensus among experienced psychiatrists as to its effectiveness (8,11,15).
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Under exceptional circumstances, ECT may also be considered a treatment option for disorders not included in the above list. When considering ECT for unusual indications, the psychiatrist should be aware that compelling evidence of the effectiveness of ECT is lacking and should thoroughly consider the available standard treatments before offering ECT. Consultation with a psychiatric colleague is also recommended when ECT is being considered for an unusual indication. A small number of medical disorders have also been treated successfully with ECT - neuroleptic malignant syndrome (16), Parkinson's disease (17,18) and refractory epilepsy (19,20), among others (8). The clinical utility of ECT in these disorders should not be considered firmly established. However, patients who suffer from one of these disorders in addition to a major diagnostic indication for ECT (for example, Parkinson's disease and major depression) may experience improvement in both disorders with ECT (17). The decision to use ECT in the treatment of an individual patient is based on the consideration of a number of factors in addition to diagnosis. These factors include the patient's prior treatment response, the severity of the disorder, the relative need for rapid response to treatment, the risks and benefits of ECT in comparison with other appropriate treatments and the patient's preferred treatment modality. Although ECT is frequently used as a second line treatment after psychotropic medications have failed, the use of ECT need not be restricted to this setting. Consideration of some of the factors noted above may lead the psychiatrist to offer ECT as a primary treatment modality. Contraindications It has been stated in the past that the only absolute contraindication to ECT is an intracranial neoplasm (21). Since then, experience in the administration of ECT to patients with a variety of serious medical conditions has accumulated. Techniques have been developed to reduc.e the risks associated with ECT in these conditions so that no contraindication to ECT is currently considered absolute (8,15). Instead, recent reports refer to specific conditions in which there is significantly increased risk. These conditions include: space occupying intracranial lesions or other conditions associated with elevated intracranial pressure, recent myocardial infarction with cardiac decompensation, severe underlying hypertension especially if related to a pheochromocytoma, evolving strokes and other risk factors for intracerebral hemorrhage, retinal detachment, and any condition in which the anesthetic risk is rated as American Society of Anesthesiologists (ASA) level 4 or 5 (8,9,15). Pregnancy is not considered a contraindication to the use of ECT. Numerous case reports suggest that ECT is a low risk and highly efficacious in treating depression at any stage of pregnancy (8). As in all applications of ECT, the decision to treat a patient in the presence of one of these conditions should be made only after careful consideration of the risks and benefits of ECT, alternative treatments, or no treatment. Particular care should be taken
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to optimize the patient's medical condition prior to the administration of ECT and to modify the treatments in such a way as to minimize the risk (8,9). This preparation should include consultation with an anesthesiologist and other medical or surgical specialists, as appropriate. Adverse Effects When ECT was originally introduced, up to 40% of patients suffered from complications of various types (13). Most frequently this involved compression fractures of the vertebrae (11). Early use of ECT was also associated with a significant mortality rate - approximately one per 1,000 patients (13). Contemporary use of ECT including pre-oxygenation, brief anesthesia, muscular relaxation and physiologic monitoring is associated with a very low rate of morbidity and mortality. The majority of deaths associated with ECT are due to cardiorespiratory causes (22). This is consistent with the higher mortality found in patients whose cardiac function is already impaired (15). Several recent reviews of ECT related mortalities suggest a rate of 2.0 to 4.5 deaths per 100,000 treatments (23-25). It should be recognized that this mortality rate is comparable to that reported for brief general anesthesia in minor surgery (8,11). With the advent of present day techniques, many of the significant medical complications of ECT have been eliminated. A complication rate of one per 1,400 treatments has recently been suggested (13). These complications include laryngospasm, prolonged apnea, prolonged seizures, tooth damage arid circulatory insufficiency (13). Cardiac arrhythmias are frequent during the treatment and immediately postictally, however the majority of these are benign and resolve without intervention (22,26). Nausea, headache and muscle soreness are commonly reported but these symptoms respond to symptomatic treatment (11). To objectively evaluate the significance of these adverse effects, it must be remembered that pharmacological treatments may have both serious and minor adverse effects as well. As examples, tachyarrhythmias, hypotension, cardiac conduction disturbances, anticholinergic toxicity and death due to overdose or idiosyncratic effects of the drugs are among the serious side-effects of heterocyclic antidepressants (27,28). The principal adverse effect of ECT, which has been the root of much controversy, is memory impairment. Four types of cognitive impairment related to ECT can be discerned (9). Immediately following an ECT treatment there is a period of post-ictal confusion. After clearing of the post-ictal confusion, retrograde amnesia (forgetting of events prior to the seizure) and anterograde amnesia (forgetting of events after the seizure) can be demonstrated using a variety of neuropsychological tests. A small minority of patients also experience longer lasting subjective memory impairment which may be difficult to objectively detect. Anterograde and retrograde amnesias subside over an interval of one to six months following a course of ECT
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(15,29). Although some specific memories of events during the months before and after ECT may be permanently lost (30), acquisition and retention of new memories and longer term memory are not persistently impaired (30,31). Subjective memory impairment following ECT may be persistent. Some cases may be explained on the basis of residual psychopathology, increased awareness of essentially normal forgetfulness, or secondary gains related to the complaint of memory loss (15). However, the basis of these complaints is incompletely understood and it is possible that persistent subtle, though genuine, memory difficulties may not be adequately detected with available neuropsychological tests. The foregoing discussion of memory side-effects of ECT refers to ECT in a general way. However, it is important to note that the severity of adverse cognitive effects of ECT is dependent upon the specific technique used. Bilateral electrode placement, higher stimulus intensity, sine wave stimulus waveform, more frequent treatments, concomitant psychotropic drug use and higher anesthetic dose are all factors associated with greater cognitive side-effects than unilateral nondominant electrode placement, moderately supra threshold intensity, brief pulse waveform, less frequent treatments given without concomitant psychotropics and more moderate anesthetic dose (8,32-34). IfECTis administered using a brief pulse stimulus on the nondominant hemisphere, patients may have no detectable memory impairment after a few days post-ECT treatment (29). Claims have been made that ECT causes "brain damage" (35). A recent comprehensive and objective review of a large number of studies concluded that ECT, as administered today, causes no detectable evidence of irreversible structural brain damage (36). However, the possibility remains that subtle deficits occur which cannot be objectified with currently available techniques. Efficacy A number of authors have comprehensively summarized the studies which demonstrate the effectiveness of ECT (9,11,24). No attempt will be made here to review all of the data. Instead, a summary of the conclusions which can be made on the basis of available data will be presented. It has been clearly demonstrated in double-blind controlled studies that genuine ECT is substantially more effective than sham ECT in the treatment of major depression (37-39). In a small number of methodologically sound studies it has been demonstrated that ECT is also superior to moderate doses of antidepressant drugs (40-42). In a large number of studies, albeit with methodological flaws, this same conclusion has been reached (43). However, Abrams (9) notes that optimal drug therapy using serum level monitoring and possibly higher doses, has not been directly compared with ECT. Mania generally responds very well to ECT (9). The number of controlled studies documenting the effectiveness of ECT in mania is small, probably because of its good
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response rate to pharmacological treatment. In recent years, two controlled prospective studies of ECT in the treatment of mania have been reported. Both of these studies found that ECT resulted in more rapid resolution of symptoms than the combination of lithium and neuroleptics (44,45). Some authorities recommend bilateral ECT as the preferred treatment in this patient group (46,47). The effectiveness of ECT for schizophrenia is more difficult to evaluate than it is for mood disorders. Much of the difficulty arises because the schizophrenic patients included in the relevant studies were diagnosed using a wide variety of diagnostic criteria and had widely disparate symptomatology (9). Recent studies have demonstrated that genuine ECT causes more rapid resolution of schizophrenic symptoms than sham ECT (48,49). Chronic patients were excluded and patients with affective symptoms were allowed in these studies. Several prospective studies of the treatment of non chronic schizophrenia have compared ECT with neuroleptics finding no significant difference between the two treatments (50-52). In addition, some studies have suggested that the combination of ECT and neuroleptics results in quicker recovery for non chronic schizophrenia than treatment with neuroleptics alone (53,54). Earlier studies of genuine versus sham ECT, using groups of chronic schizophrenics, failed to find any difference between the two treatments (55,56). In summary, some selected groups of schizophrenic patients, particularly those with a brief duration of illness and/or prominent affective symptoms, may respond as well to ECT as they do to neuroleptics. Patients with chronic schizophrenia, on the other hand, respond no better to genuine ECT than sham ECT. Taken together, the data indicate that ECT has a more limited role in the treatment of schizophrenia than in the treatment of mood disorders. As a second line treatment for schizophrenia, ECT still has value in contemporary psychiatric practice. The number of treatments required for an effective course of ECT varies substantially between individuals. Typically, patients with depressive illness require six to 12 treatments, while patients with mania or schizophrenia may require a somewhat higher number (8,9). However, some patients may improve dramatically with only a few treatments. Once the patient has achieved full remission, no further benefit results from the administration of additional treatments (57,58). When patients show a slow or insignificant response to a series of treatments, it requires the clinical judgment of the psychiatrist to determine when to recommend termination or modification of the treatments. This judgment takes account of such factors as the nature and severity of the patient's symptoms, the magnitude of cognitive side-effects, history of response to ECT, and the response obtained thus far. It is therefore difficult to provide specific guidelines for the maximum allowable number of treatments. Nevertheless, the following recommendations are made. If after six to eight treatments there is minimal improvement, consideration should be given to changing the technique of ECT. These
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changes may include switching to bilateral electrode placement, increasing the electrical dose, or pharmacologically augmenting the elicited seizures (8). When patients with depressive illness do not show substantial improvement after 12 to 14 treatments, another psychiatrist's opinion should be obtained before administering further treatments. Likewise, when patients with mania or schizophrenia show little improvement after 14 to 16 treatments, a second psychiatric opinion should be obtained before proceeding further. ECT is usually administered two or three times per week, although double ECTs (two seizures per session) or daily treatments are sometimes used early in the course oftreatment in an attempt to speed the recovery of extremely ill patients (8,9,11). In the past, some clinicians used "regressive ECT" in which a prolonged and intensive course of treatment was used in order to induce a sustained delirium. The objective of this practice was to create a "regressed state" and subsequently reconstruct the patient's character. This practice has not received scientific support and as such should not be used. The above discussion deals with the acute treatment of psychiatric disorders. However, these disorders can be recurrent. In particular, follow-up studies of patients treated for depression, especially those with delusional or treatmentresistant depression (two common indications for ECT) , have high relapse rates in the year after acute treatment (59,60). For this reason, some form of maintenance treatment is indicated to prevent relapses after a course of ECT (9,61). Controlled studies directly comparing maintenance ECT to maintenance pharmacotherapy are lacking. A number of clinical studies however, have reported that maintenance ECT reduces the rate of relapse and recurrence of mood disorders (62-64). Although further prospective study is needed, maintenance ECT may be useful in selected patients who cannot tolerate pharmacotherapy or who continue to relapse despite appropriate pharmacotherapy. Assessment and Documentation Prior to the administration of ECT, a thorough evaluation of the patient's psychiatric and medical status is required. This involves a psychiatric history, mental status examination including objective assessment of cognitive functions, medical history, and physical examination. Essential laboratory investigations include a complete blood count, serum electrolytes and renal function tests. Patients over 45 years of age should also receive an electrocardiogram and possibly a chest radiograph. When the patient has co-existing medical conditions or is of advanced age, further investigations and consultations should be obtained as discussed under contraindications. The results of this complete evaluation should be documented in the patient's record prior to commencing ECT. The record must also contain documentation of informed consent and the indications for ECT. The physician's orders for ECT should indicate treatment dates and desired electrode placement. Patients should fast for eight hours prior to treatment.
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Between ECT treatments, the psychiatrist should reassess and document changes in target symptoms and the occurrence of adverse effects. Objective testing of cognitive functions is an important part of this process. The physician who administers the ECT should keep a record of each treatment including stimulus parameters the doses of anesthetic and muscle relaxant used, and the quality and duration of seizure activity elicited. After the course of ECT has been terminated, a summary note should be completed for the medical record. Technique It is beyond the scope of this paper to discuss details of the technique of ECT; complete descriptions are available elsewhere (8,9,11). However, it is worth emphasizing that the specific technique used in ECT is a matter of considerable consequence. Electrode placement, stimulus intensity and waveform, treatment frequency, concomitant psychotropic drugs and anesthetic medications have been mentioned previously as factors affecting the severity of cognitive sideeffects. The clinical effectiveness ofthe elicited seizure is also affected by some of these parameters. As examples of how technique can affect outcome, a brief discussion of electrode placement and stimulus-intensity and waveform will be presented. Since the introduction of unilateral ECT, there has been considerable controversy over the merits of unilateral versus bilateral electrode placements. The two central issues are memory impairment and efficacy. Bilateral treatments have been clearly associated with greater memory impairment (11,15). Reports on the relative efficacy of the two electrode placements have been much more divided. In about one-half of the reports the treatments were found to be comparable, and in the other half bilateral ECT was found to be superior (9). 'Therefore, unilateral ECT may be advantageous when it is especially important to reduce cognitive side-effects. Bilateral ECT, on the other hand, may be preferred if there is a greater treatment urgency or if unilateral ECT fails (8), More recently it has been demonstrated that there is an interaction between electrode placement and stimulus intensity affecting the efficacy of ECT. Barely suprathreshold, brief pulse unilateral ECT is remarkably ineffective (65). However, increasing the stimulus intensity increases the efficacy of brief pulse unilateral ECT (65,66). In the case of bilateral ECT, barely suprathreshold stimuli remain effective, but increasing the stimulus intensity may speed the clinical response (66,67). The earliest ECT devices employed a sine wave current to elicit seizures (7). This type of electrical current administers a substantial amount of energy below the patient's seizure threshold, thereby increasing memory impairment, but not enhancing therapeutic effects (68). For this reason, sine wave currents are generally considered obsolete and brief pulse currents are the accepted standard (8,9). The question of what constitutes the optimal technique for administering ECT is not completely answered. Therefore, the clinician administering or prescribing ECT must make
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decisions about various aspects of the treatment technique based on an ongoing assessment of the relative risks and benefits. Mechanism of Action
A large number of hypotheses on the mechanism of action of ECT have been proposed (19,20,69-72). These hypotheses have included both psychological and biological explanations of the effects of ECT. Psychodynamic theories have generally emphasized the importance of fear in the patient, the role of guilt and punishment for imagined wrongdoing, and amnesia for the causes of depression (69). Although the importance of psychological factors in ECT treatments should not be completely overlooked, such purely psychological explanations lack empirical support and have been abandoned by psychiatric investigators. In contrast, biological theories of the action of ECT have been the subject of much recent investigation. Neurochemical, neuroendocrine, electrophysiological and neuropsychological hypotheses have been advanced (19,20,70-72). The role of the cerebral seizure is central to most contemporary theories of the action of ECT. A considerable amount of research supports the contention that epileptiform discharges in the brain are necessary and sufficient for efficacious ECT (68,73). Recent work challenges this view and suggests that the occurrence of a generalized seizure of "adequate duration," by itself, may not be sufficient to ensure maximally effective treatment. In particular, the use of barely suprathreshold electrical stimulation results in diminished therapeutic response, especially with unilateral ECT (65,67,73). It appears that some aspect of the process of seizure generalization may be more closely related to the therapeutic effect of ECT than the occurrence and duration of cerebral seizures (9,15). Research has greatly increased our knowledge about the biological effects of ECT. As with most biological treatments in psychiatry, however, we still do not know precisely why ECT works. As such, ECT remains an empirical treatment. Nevertheless, this does not detract from its efficacy and safety . as a therapeutic modality in psychiatric practice. Consent to Treatment
For the most part, the process of obtaining informed consent for ECT is no different than the consent procedure for other significant medical interventions. The attending psychiatrist or other designated medical personnel must be directly involved in obtaining informed consent. The physician should provide realistic information about the nature of the condition being treated, the expected benefits and possible risks of ECT, as well as the benefits and risks of other reasonable alternative treatments, or no treatment (74). The physician should also ensure that the patient has understood the information provided as part of the assessment of the patient's competence to consent to treatment. Consent must be obtained from the patient unless the patient is clearly incompetent to participate in the process. For incompetent
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patients, substituted consent should be obtained in accordance with the requirements of provincial legislation and facility regulations. Whenever possible, the substituted consent procedure should include obtaining the views of family members and significant others, as well as a second psychiatric opinion. It should be emphasized that informed consent is a process that begins with the provision of information and the signing of a consent document, and continues through the entire course of treatment. Therefore, consent may be withdrawn at any time. The issue of consent should be reviewed in an ongoing manner.
Educationand Research Over the years ECT has become an increasingly complex treatment. The modern psychiatrist must therefore acquire a high level of knowledge and sophistication in order to use the treatment optimally. The educational process should begin in medical school, so that graduates have an appreciation of the role of ECT in contemporary psychiatric practice. Residents in general psychiatric programs should have both didactic teaching and practical experience in the use of ECT. When ECT is performed by a psychiatric resident, adequate supervision must be provided. Psychiatrists who prescribe or administer ECT should keep their knowledge and practical skills up to date through the use of continuing education programs and/or attention to clinical and research reports in the psychiatric literature. Research and clinical experience have already provided much information on which to base the practice of ECT. Nevertheless, much remains to be learned. Although awareness of the way treatment technique can affect outcome has increased, it is still not known how to select the ideal form of treatment for a given patient. Furthermore, a great deal has been learned about the neurophysiological effects of ECT, but it remains to be determined which of these effects, if any, is responsible for the therapeutic response. These examples serve to highlight the need for ongoing research and publication on the topic of ECT.
Summaryand Recommendations 1. When used properly, ECT is a safe and effective treatment which should continue to be available as a therapeutic option for the treatment of mental disorders. 2. ECT should be used only on the recommendation of a psychiatrist, and should preferably be administered by a psychiatrist. 3. The main conditions for which ECT is indicated are major mood disorders and non chronic schizophrenia, particularly when affective or catatonic features are prominent. A second psychiatric opinion is recommended if ECT is to be used for an unusual indication. 4. A medical history, physical examination and appropriate laboratory investigations are necessary in order to detect any significant medical illness prior to the administration of ECT. If an active medical disorder is present, steps
should be taken to treat the disorder and/or to further modify the technique of ECT in order to minimize the possible risks. Consultation(s) from an anesthesiologists and other medical specialists should be obtained, if indicated. 5. During a course of ECT, the psychiatrist should regularly reassess and document changes in target symptoms and the occurrence of adverse effects. Objective testing of cognitive functions is part of this process. 6. Modification of ECT with brief anesthesia, muscle relaxants and pre-oxygenation should be accomplished by a suitably qualified physician, unless specific contraindications to the use of these modifications are present. 7. The decision to use ECT is a medical one, and requires informed consent. If the patient is incompetent to give this consent, a consultation from another psychiatrist with regard to the use of ECT should be obtained. Following this, the psychiatrist can decide whether to seek substituted consent for ECT or to pursue another course. 8. ECT is a complex medical intervention. Practitioners require considerable knowledge and practical skills in order to optimally perform the procedure. Psychiatric residencies should include training in ECT and psychiatrists should keep up-to-date with advances in the theory and practice of ECT. 9. Continuing basic and clinical research is encouraged in order to delineate the mechanism of action of ECT and to further improve the clinical application of the treatment. 10. The position of the CPA on ECT should be periodically reviewed, as dictated by changes in our knowledge and understanding of the treatment of major mental illness.
References 1. Pankratz WJ. Electroconvulsive therapy: the position of the Canadian Psychiatric Association. Can J Psychiatry 1980; 25(6): 509-514. 2. Endler NS. The origins of electroconvulsive therapy. Convulsive Therapy 1988; 4: 5-23. . 3. Von Juaregg W. The treatment of general paresis by inoculation of malaria. J Nerv Ment Dis 1922; 55: 369-375. 4. Sakel M. Neue Behandlungsmethode der schizophrenie. Moritz Perles, Wien und Leipzig, 1935. 5. Moniz E. Tentatives operatoires dans le traitement de certaines psychoses. Paris: Masson et de, 1936. 6. Fink M. Meduna and the origins of convulsive therapy. Am J Psychiatry 1984; 141: 1034-1041. 7. Cerletti U. L'electroshock. Revista Sperimentale di Freniatria 1940; 64: 209-310. 8. The practice of ECT: recommendations for treatment, training and privileging. Task force report on ECT. Washington DC: American Psychiatric Press, Inc., 1990. 9. Abrams R. Electroconvulsive therapy. Oxford: Oxford University Press, 1988. 10. Electroconvulsive therapy, task force 14. Washington DC: American Psychiatric Press, Inc., 1978. 11. Fink M. Convulsive therapy: theory and practice, New York: Raven Press, 1979. 12. Report of the electroconvulsive therapy review committee. Toronto ON: Ontario Ministry of Health, 1985.
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13. Consensus conference, electroconvulsive therapy. JAMA 1985; 254: 2103-2108. 14. Fin~ M. Convulsive therapy. New York: Raven Press, 1985. 15. Weiner RD. Electroconvulsive therapy, fifth edition. In: Kaplan HE, Sadock BJ, eds. Comprehensive text of psychiatry. Baltimore MD: Williams and Wilkins, 1989: 1670-1678. 16. ~earIman CA. Neuroleptic malignant syndrome: a review of the literature. J Clin Psychopharm 1986; 6: 257-273. 17. ~ouyon R, Serby M, Klutchko B, et al. ECT and Parkinson's disease revisited: a naturalistic study. Am J Psychiatry 1989; 146: 1451-1455. 18: Abrams R. ECT for Parkinson's disease. Am J Psychiatry 1989; 146: 1391-1393. 19. Post RM, Putnam F, Uhde TW, et al. Electroconvulsive therapy as an anticonvulsant. Ann N Y Acad Sci 1986; 462: 376-388. 20. Sa~keim HA, Decina P, Prohovnik I, et al. Anticonvulsant and antIdepressant properties of electroconvulsive therapy: a proposed mechanism of action. Bioi Psychiatry 1983' 18: 13011310. ' 21. Kalin?wsky LB. Pharmacological, convulsive and other somanc treatments in psychiatry. New York: Grune and Stratton, 1969. 22. Welch CA, Drop LJ. Cardiovascular effects ofECT. Convulsive Therapy 1"989; 5: 35-43. 23. Babigian HM, Guttmacher LB. Epidemiologic considerations In electroconvulsive
