CURRENT PERSPECTIVES
Electroconvulsive Therapy in Depression* E.
PERSAD, M.B., B.S. 1
Psychiatric Association (APA) task force on the use of ECT (4) lamented that the procedure was poorly controlled and inappropriately used. A similar state of affairs had been uncovered in the United Kingdom (5). Since then, the situation has improved, primarily as a result of activities within the profession to respond to public concerns. Public validation of ECT' s new found respectability was provided by the 1985 Clark Enquiry into the use of ECT in Ontario (6). In 1985, the National Institute of Mental Health convened a Consensus Conference on ECT in Washington, D.C. (7). Among its many findings, the Consensus Conference noted that "There is a continuing controversy concerning the mental disorders for which ECT is indicated, its efficacy, the optimal methods of administration, possible complications and the extent of its usage in various settings." The Conference statement continued, "ECT is demonstrably effective for a narrow range of severe psychiatric disorders in a limited number of diagnostic categories: delusional and severe endogenous depression and mania and certain schizophrenic syndromes. " Professional organizations such as the APA and the Royal College of Psychiatrists in the United Kingdom continue to monitor the usage ofECT, and both are due to release updated reports for their respective countries shortly. The use of ECT may be declining. In 1980,2.4% of all psychiatric admissions in the United States were given ECT (7). In the United Kingdom, a survey done in 1979 reported that 200,000 individual ECT treatments were administered, and 97% of these were in National Health Service Units (8). Thompson and Blaine (9) have reported that the use of ECT in the United States decreased by 46% between 1975 and 1980, and that the majority of patients receiving ECT (69.8%) were those suffering from affective disorders. Thompson and Blaine (9) also found that the diagnosis was more significant than sex in determining which patients received ECT. Fink (10) has questioned the conclusions of Thompson and Blaine regarding the decline of the use of ECT in the United States. It is Fink's belief that even though ECT may be declining in state hospitals, there is actually an increase in use in general public hospitals and in private psychiatric institutions. Fink (10) concludes that "the survey of Thompson and Blaine is a lagging indicator of ECT interest and usage. " In a recent Canadian sample (11) of 5,729 consecutive admissions in three general hospitals and one mental hospital, 21.5% of patients received ECT and half were for affective illnesses. This suggests that the use of ECT in at
Electroconvulsive therapy (ECT) has been in use for over 50 years and remains one of the most effective treatments in psychiatry. Effectiveness rates for ECT in depression range between 80% and 90%; no comparative study has shown any other intervention to be superior to ECT. ECT is also recommended for mania, schizophrenia and as a safe treatment for the elderly or medically ill depressed patient. This paper will deal with the use of ECT in depression. The areas to be covered are the clinical indications, the factors predictive ofresponse, the evidence for the efficacy ofECT, as well as theories of the mechanism of its action, side effects and guidelines for prescribing the procedure. Notwithstanding the efficacy, the safety· and perhaps an improved public acceptance, some observers have noted that there is a decline in the use ofECT. Others have suggested that such a decline may be evident only in the public sectors such as state and provincial psychiatric hospitals. Ongoing research is necessary to achieve further refinement ofECT, as well as enhance our understanding of this important treatment procedure.
E
lectroconvulsive therapy (ECT) has been in use for over 50 years and has remained one of the most effective treatments in psychiatry especially for the affective disorders (1). Notwithstanding its efficacy, the popular visual and print media tend to portray the procedure as a form of coercion to control helpless inmates of mental institutions. This representation of ECT evokes fear and apprehension in the minds of the general public. Such fear has been fuelled by controversial statements about ECT-induced brain damage made by a minority within the medical profession (1). Recently however, the print media has shown a more balanced point of view in reports on ECT. Whereas in 1980 Hapgood (2), writing in The Atlantic, argued for the abandonment of ECT and referred to it as one of those medical interventions that "subsequent generations will look back on as barbarous." In 1987 Squire, in the New York Sunday Times (3), wrote a more favourable piece entitled "Shock Therapy's Return to Respectability." The term "shock," however, perpetuates the image of ECT as an arbitrary and frightening procedure. Less than a decade ago, the American
*Manuscript received October 1989. 'Director of Education, London Psychiatric Hospital; Associate Professor of Psychiatry, University of Western Ontario, London, Ontario. Address reprint requests to: Dr. E. Persad, London Psychiatric Hospital, 850 Highbury Avenue, London, Ontario N6A 4H1
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least one Canadian study is approximately ten times that of the United States (7).
Indications for Use ECT was initially thought to be a treatment primarily for schizophrenia (12, 13) but as a result of clinical observation and open trials it became clear that ECT is indeed more appropriate in the treatment of depression. ECT is now regarded as the most effective treatment for certain types of depression, and that, further, no single controlled study has shown another form of treatment to be superior to ECT in the short term management of severe depression (7). ECT has also been found useful in mania (12) and in schizophrenia (14-16). According to Fink, the current APA task force will likely recommend that ECT should be considered the first line treatment for the following conditions: major depression, manic delirium and catatonia (17). There may be a limited role for ECT in other conditions in which psychotropic drugs may be contraindicated. For example, ECT has been reported as an alternative treatment in patients who develop neuroleptic malignant syndrome (18), and in medically ill patients (19). Case reports have suggested that ECT may have an ameliorating effect on tardive dyskinesia and on Parkinson's disease (17,20). This paper will focus on the use of ECT in depression.
The Use of ECT in Depression In practice, it is not unusual to recommend ECT in the treatment of depression after a failure of other interventions. In some situations the severity of the patient's clinical state, for example those in a depressive stupor or the highly suicidal patient, leads clinicians to a consideration of ECT as the first line of treatment. In addition, ECT should be considered in the following types of depressed patients: 1. Those with delusional depression. 2. Melancholiacs. 3. Elderly and medically ill depressed patients. 4. Those with treatment resistant depression. 1. Delusional Depression: Delusional depression is characterized by the presence of a depressed mood and delusions which are usually mood congruent but may also include delusions which may not be congruent with an affective state. These patients do not appear to benefit from antidepressants and some studies suggest that a combination of antidepressants and neuroleptics is the treatment of choice (21,22). However, several other studies (23,24) have shown that ECT is highly effective in the treatment of delusional depression and indeed it is superior to either antidepressants or neuroleptics used alone and is at least as effective as the combination of antidepressants and neuroleptics. Solan et al (25) found that ECT was equally effective in a psychotic and a nonpsychotic group of depressed patients, where neither group had responded to previous pharmacotherapy. The presence of psychotic symptoms may not enhance the degree of response to ECT (23).
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2. Melancholia: The severe endogenous or melancholic depressions are characterized by early morning wakening, marked weight loss, psychomotor retardation andlor agitation, diurnal variation and lack of reactivity. ECT is at least as effective as antidepressants and more effective than "sham" ECT in the short term treatment of these severe depressions (26). Ottoson (27) has indicated that ECT should be considered the treatment of choice for melancholia. It is his view that ECT is effective for the full syndrome in melancholia but that in other conditions such as mania, ECT's therapeutic benefit comes from nonspecific organic effects (27). There is also evidence of the efficacy of ECT in those endogenous depressives who have not responded to an adequate trial of antidepressants (24). 3. Depression in the Elderly: The treatment of depression in the elderly is becoming an increasingly important subject given the fact that the proportion of the population over age 65 is dramatically increasing (28). The incidence of affective disorders increases with age and the prognosis for depression in the elderly is less favourable with persistent and disabling symptoms in approximately one third of afflicted aged persons (28). This increased psychiatric morbidity is accompanied by an increased mortality rate in the depressed elderly. Pharmacotherapy in the elderly patient who is depressed has been widely considered to be safe and efficacious. In a series of 30 consecutive elderly depressed patients, ECT was found to be an effective treatment. ECT was also of benefit to some patients who were resistant to or who were unable to tolerate pharmacotherapy. This improvement was related to diagnosis; 92 % of patients with major depression improved and 69% showed complete symptom resolution. Burke and colleagues (28) indicated that the occurrence of adverse effects was concentrated in the oldest patients; that is, the complication rate correlated with the age to a significant degree and to health status, and they concluded that even though ECT is a safe treatment for the elderly, those who are older than 75 years or those with a history of cardiovascular disease are at increased risk for complications. 4. Treatment Resistant Depression: Paul and colleagues (29) reported on the use of ECT with treatment resistant depressed patients at the National Institute of Mental Health. Even though this was a small sample (nine patients), the authors found that despite the patients' poor prior response to a variety of pharmacological treatments, only one patient failed to show a complete response to ECT. This, and other studies (23, 24, 30, 31) of patients who are suffering from depression and who appear not to respond to pharmacotherapy, would indicate that ECT should be offered to those who are intractable. Some reports have also indicated that the treatment protocol should include bilateral ECT rather than unilateral ECT for those who appear to be treatment resistant (32). The fact that ECT appears to work where antidepressants have failed raises intriguing questions regarding mechanisms of action, to be discussed later.
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Predictors of Response As has been noted in the foregoing, the clinical features of the depressed patient might be used as the indicators of response to ECT. However, there has been a continuing inquiry into other factors that might predict a favourable response to ECT in depressed patients (32-34). Biological predictors of ECT response have been extensively investigated. Scott (35) recently reviewed studies which used the following measures: resting electroencephalogram, neuroendocrine challenge tests, sedation and seizure thresholds, calcium levels and monoamine metabolites in peripheral body fluids. Scott's review (35) on biological measures indicates that there are no consistent physiological findings in depressed patients which carry a strong predictive value. Changes during ECT treatments have also been used to predict outcome. ECT has a profound effect on neuroendocrine functioning as measured by cortisol secretion and prolactin release. Neuroendocrine dysregulation associated with depression may be a valid indicator of ECT response, but as Fink (17) and Scott (35) have pointed out, certain biological factors may have general predictive values not specific to any particular somatic therapy. The duration of the seizure has been thought to predict outcome and a seizure duration of greater than 25 seconds has been recommended (4). Later studies examining the relationship between the duration of the seizure and outcome indicated that there was no relationship between individual seizure length measured either by observation, electroencephalograph (EEG) and clinical change, or outcome during the course of ECT (35). It may not be feasible to define a minimum length for a therapeutic seizure as time alone takes no account of the degree of spread of seizure activity over the cortex or throughout the brain. It has also been suggested that seizure threshold may playa role in outcome (36, 37). Careful clinical assessment remains the single most important step in the selection of depressed patients for ECT (27, 38, 39). Weight loss, early morning wakening and somatic delusions, the clinical features of endogenous depressive illnesses, may best predict a good outcome with ECT (39). Crow and Johnstone (26) raised the possibility that the only consistent clinical predictor of a specific response to ECT is the presence of delusions. Although a generalized tonic, clonic seizure is an essential component of successful ECT, endogenously depressed patients can experience satisfactory seizures and yet fail to recover with ECT (36).
Unilateral versus Bilateral ECT Electrode placement preferences in ECT have varied over the years. In the early years, bilateral ECT was the common method of administration. It was subsequently suggested that right unilateral ECT was just as effective and was preferable because of fewer cognitive side effects (4). There have been over 35 clinical trials dealing with this issue but the question remains unsettled (40-42). In one such study, involving double blind random assignment, the relative efficacy of bilateral and unilateral ECT with a low dose titration was assessed (36). The investigators reported that in
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52 patients (mean age 61.33 years) with primary major depressive disorder, bilateral ECT was markedly superior to right unilateral ECT in short term symptom reduction. The authors (36) pointed out that there was no difference between the two procedures, in the duration of generalized seizures or the number of treatments administered to achieve clinical response. The authors disagreed with the claim that the elicitation of a generalized seizure is sufficient for the antidepressant properties of ECT. It was their opinion that a dose in excess of seizure threshold may contribute to the efficacy of ECT, particularly with a right unilateral electrode placement. There is a wide interpatient variability as to seizure threshold. As well males, the elderly and patients on anticonvulsants have a higher seizure threshold (36). The Royal College of Psychiatrists is now recommending bilateral ECT using pulse current for the treatment of depression (43). The use of left unilateral electrode placement has not been adequately assessed. In clinical practice, the nondominant hemisphere (usually the right side) is used for the electrode placement.
The Efficacy of ECT in the Treatment of Depression ECT was introduced in an era when few other interventions were available for treating mental illnesses and that fact may have led to its widespread and somewhat indiscriminate use (4, 5). As clinicians gained experience with the treatment and refinements took place in the procedure, it was noted that ECT had a significant effect on patients suffering from melancholia. Kendell (8), in his review of the early clinical trials and impressions regarding ECT noted that it was regarded by some as almost "miraculous" in its effect on some patients. Comparison studies (44, 45) have generally found ECT to be comparable with other interventions. Some studies indicate that ECT may be superior to antidepressants (45). ECT and imipramine were compared in the treatment of depression in a large sample of patients (n=437) (24). The study was unique in that all 437 patients were given a trial of imipramine and the ECT group was composed of only imipramine failures. Among those with delusional depression 83% improved with ECT versus 40% with imipramine. Janicak and colleagues (40) analyzed several rigorously controlled studies that compared the efficacy of ECT with simulated ECT, placebo and antidepressants. A total of 19 studies were examined in which approximately 628 patients were involved. The overall efficacy of ECT was clearly supported by these studies. Combining the studies that compared ECT with any of the four other treatments resulted in an overall efficacy rate of 77.8% (simulated ECT 27.6%, placebo 37.6%, tricyclics 64.3% and MAOIs 32%). In this survey MAGIs were found to be less effective in endogenous type depression compared with depression where there is predominant anxiety, hypochondriacal or phobic syndromes. Put another way, MAOIs may be more appropriate for the atypical depressives. ECT is said to be ineffective in secondary depression (46).
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Rifkin (47) has pointed out that for conclusive statements to be made, comparison studies should be prospective with random assignment to treatment groups and blind assessment of outcome. Siris, Glassman and Steiner (48) reported that in 31 major studies comparing ECT and drugs in depression, 17 showed ECT to be clearly superior, eight appeared to give it a slight edge, four showed no difference and two were equivocal. These authors (48) commented on methodological problems in these studies, for example poor clinical descriptions of target symptoms as well as inadequate dose of drugs. Some studies have examined the effectiveness of combining ECT and antidepressant drugs in the treatment of depression but Siris and colleagues (48) found little evidence to support increased efficacy; as pointed out above, however, antidepressants may be necessary in the continuation phase to maintain the improvement already obtained with ECT. Rollin (49) stated that ECT was "the most significant advance in treatment of our time." As Kendell points out (8), by 1977 there was overwhelming evidence in favour of the effectiveness of ECT and its superiority over other interventions in the treatment of depression. The Royal College of Psychiatrists in the United Kingdom issued a statement in which the effectiveness of ECT as a treatment for depression was referred to as "substantial and incontrovertible" (8). Nonetheless, the criticism and doubts about the procedure persisted, expecially in North America, and this led to a series of double blind trials, all of which took place in the United Kingdom, in which patients were treated either with real or simulated (sham) ECT (50-53). Each study was different in electrode placement, in patient selection and in assessment of outcome. On balance the studies appear to give the edge to real ECT over simulated ECT, but there were some equivocal findings that led Kendell (8) in his review to question whether the four trials were comparable because of the differences in methodology. In one of the trials (53), there was a lack of any difference between real and simulated ECT groups at one and six months follow-up. Crow and Johnstone (39) summarized the findings from several outcome studies as follows: 1. The efficacy of ECT in the treatment of severe depression has been well established. 2. No study has clearly delineated the contribution to the therapeutic outcome of the nonconvulsive elements in the procedure. 3. In the sham versus real ECT studies, patients receiving sham ECT do show improvement over three to four weeks, but patients on real ECT improve to a greater degree. 4. ECT produces a rapid response but there is a limited duration of effect. 5. The only clinical indicator of ECT response in depression is the presence of delusions. It has long been accepted that high relapse rate with ECT is one of its most serious limitations. Any treatment modality for depression should take into consideration what is known about the natural course of the illness, and therefore the need for continuation and maintenance therapies once the acute symptoms have subsided. This is true of antidepressants and
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should also be true of ECT. The use of maintenance ECT has not been fully explored. ECT has also been found to reduce the length of hospitalization for depressed patients. In a recent study, Markowitz and colleagues (54) found that all patients treated with ECT responded, in contrast to only 49% of those who were treated with antidepressants. They also found that when the failed (drug) group was treated subsequently with ECT they all recovered. Markowitz and colleagues (54) concluded that patients treated with ECT stayed in hospital a mean of 13 fewer days, saving more than $6,400 U.S. a patient at then current rates. It must be noted that ECT is usually introduced after other measures have failed and therefore length of hospitalization may not convey a valid correlation with ECT usage and effectiveness. ECT has been shown to have an impact on suicide rates (55). Of 600 hospitalized patients, those who were treated with ECT had a better outcome though relapse rates were the same, but at follow-up after six months, the drug-treated group had displayed four to seven times more suicide attempts than the ECT group. The authors pointed out that this pattern persisted after three years. After review of several other studies, they concluded that ECT -treated patients had better chances of survival compared with patients treated with drugs. This investigation, however, has the shortcomings of being a retrospective chart review. ECT is not usually compared with psychotherapy in the treatment of depression, but one such study by Huston and Locher (56) found ECT more effective than a combination of psychotherapy, hydrotherapy and occupational therapy.
Mechanism of Action ECT is an effective treatment modality for a variety of psychiatric conditions, which suggests a multiple mode of action. Ottoson (26, 57) is of the opinion that the antidepressant effect of ECT is due to the grand mal seizure, but the antimanic property of ECT results from the confusional and amnesic effects. The fact that ECT is beneficial in drug-failed depressed patients may also suggest a mechanism of action unlike that of antidepressants. Others (58) suggest that ECT has a unitary mechanism of action, and acts like an anticonvulsant. According to this theory, the traditional view of the role of the seizure is replaced by a view that the seizure leads to the therapeutic event in affective illnesses. A neuroendocrine mechanism of action has been postulated recently (59). According to this view, ECT produces generalized neuroendocrine effects, but these result in the production of a substance referred to as "antidepressin" by Fink and Nemeroff (59), a hypothalamic peptide, which is said to produce both the antidepressant and antipsychotic effects. The search for the therapeutic agent produced by ECT is not new. In the 1940s, Cerletti believed that convulsions were the main factor that led to the alleviation of symptoms; in the 1950s he believed that the injection of brain substances of electroshocked animals into mentally ill patients would eliminate the need for ECT and for convulsions (1). Cerletti believed that the injection of "acroagonines" would serve
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as a defense against subsequent illness (1, 60). Rudorfer (3), of the National Institute of Health, has recently echoed this opinion, and regards ECT as a "dirty drug" with a shotgun effect, and that future research should be directed towards the discovery of the substance or the therapeutic agent, generated by the ECT. In a study in which patients were assigned to treatment with either low energy, high energy pulses or high energy sinusoidal wave ECT, those patients on the higher dosage condition experienced greater therapeutic benefit (61). This may suggest a mechanism of action dependent on a stimulus intensity "therapeutic window" (61), only within which ECT is effective. The authors suggest that this might explain the findings of no difference between real and sham ECT reported in the Northwick Park trial (53). There is a trend in current practice to aim for suprathreshold energy rather than the minimal energy level required for a seizure (62).
Side Effects and Adverse Reactions to ECT ECT has a significant impact on the neurophysiology of patients undergoing the treatment. There is an increased permeability of the blood-brain barrier, as well as significant changes in neuroendocrine and cardiovascular measures. One of the myths associated with the treatment is that if ECT does work, it does so because of the evocation of fear, panic and anxiety that may accompany any stressful experience (I). Side effects and complications of ECT can occur during treatment as well as following treatment. Before modern improvements, the chief complications arising during the procedure especially in the clonic phase of the seizure were fractures and dislocations. These side effects are no longer common because of the use of muscle relaxant drugs. Patients coming to ECT should be medically clear and able to tolerate a general anesthetic as most of the problems which may arise during the treatment may be those secondary to reactions to the anesthetic procedure. The problems which might arise in the post-treatment period include onset of a confusional state. Fraser (63) in his review of several studies found that the most common complaint was memory impairment followed by headache, confusion, clumsiness, nausea or vomiting, eyesight problems and muscle pain. He pointed out that even though a number of patients were upset by the treatment, more than half agreed that they would readily have it again if necessary and over three quarters found the experience no more upsetting than going to the dentist. Crowe (64) reported however that almost all patients experience a transient confusional state immediately following ECT. Patients who are manic depressive run the risk of becoming manic if they are treated with ECT, as they do when treated with antidepressants. Such patients may be protected by continuing on lithium during the ECT. ECT, as has been noted earlier, can be used effectively in the treatment of both depression and mania. The major side effects noted with ECT are the cognitive changes that follow a course of treatment, and this is at the heart of the ECT controversy. Weiner (65) stated that a "nonselection assessment" of the data from a variety of meas-
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urements do not support the charge that ECT is the "purveyor of wholesale brain damage." In a later study, Weiner and colleagues (66) point out that unilateral nondominant electrode placement and brief pulse stimuli may produce fewer cognitive side effects. They do not rule out subtle, undetected changes with the high energy procedure. Critics of ECT are adamant that these changes represent irreversible brain damage, while proponents claim that they are temporary and reversible (7). Cognitive side effects can be minimized by giving unilateral rather than bilateral treatments, by reducing the dose of the electrical stimulation, by spacing between treatments and by limiting the number of sessions (7). There is some suggestion however that these precautions may reduce the effectiveness ofECT (62). There is no evidence that the effectiveness of ECT in alleviating depression is dependent upon the occurrence of cognitive changes as has been alleged by Breggin (67). The ECT Consensus Conference (7) has also reported that there was no evidence of cumulative deterioration, that the deficits found at the beginning of treatment were not worse by the end, and that there were no difficulties noted in the acquisition of new information over the course of treatment. These findings have been corroborated by others (68-70). A critical question regarding ECT-induced memory impairment is whether it persists. There have been several studies reviewing this and none could substantiate that ECT causes permanent memory loss. Some of the studies (8, 71) indicate that recall of patients pre-ECT was also generally worse than that of a matched control group. Interpretations of patients' complaints about memory loss following ECT may be affected by age and by depression (1).
ECT Mortality The incidence of deaths arising from ECT have been reviewed by Kendell (8) and Fink (72). Kendell (8) found that from 1956 to 1966 in England and Wales, there was an average of 3.6 deaths per year associated with ECT, but no figures were available for the size of the population treated. The ECT Conference (7) noted that in the least favourable recent series, there were 2.9 deaths per 10,000 patients. Fink (72) found that the incidence of death in ECT was variously reported from none in 8,500 treatments of 870 patients to 0.06%,0.08% and 0.8% of patients treated. According to Price (73), the best estimate of ECT fatalities is 0.03 % per patient treated, but it was unclear how this rate was calculated. Price (73) points out that this figure should be considered in perspective. For instance, mortality from short term barbiturate anesthetic is 3.3 per 100,000 procedures.
Guidelines for Prescribing ECT Patients and their relatives should be fully informed about the risks and benefits of ECT. Assessment of competence to give consent is essential. This has been one of the most difficult issues for patients who are severely depressed as they may not be considered competent to decide their treatment. Some centres use videotapes to assist patients and families in making an informed decision regarding ECT. In those
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clinical conditions which appear to fall outside the usual indicators, there should be a second psychiatric opinion, or if there is no response after 12 treatments for depression, or 15 treatments for schizophrenia (1). The procedure should be clearly documented including dosages of drugs used, whether the electrode placement was unilateral or bilateral and whether the seizure induced was bilateral or not. The clinician should also be aware of the relationship between the stimulus energy and waveform characteristics required for each patient to maximize benefit without increasing side effects. Recently attention has been directed to the treatment dosage as a therapeutic variable. Most modern ECT machines provide an electrical stimulus with a pulsatile square waveform. The continuous sine wave electric stimulus in the older ECT machines was associated with greater cognitive side effects. Treatment protocols vary widely even with the newer ECT machines. Guidelines for estimating the treatment dose include rule of thumb estimates such as one watt-second per year of patient age, or the addition of25 to 150% of energy above the seizure threshold (62).
Conclusions There is a danger that this procedure, which continues to generate controversy, may become increasingly underutilized by default or by lack of interest. Such a trend could be seen in a recent survey among senior psychiatric residents in Canada (74). However, ECT is one of the most effective treatments for affective disorders, especially the severe forms of depression. ECT has been effective in patients who have not responded to other interventions. Current research is directed towards the refinement of clinical criteria, and an improved understanding of the technical aspects of the procedure. Acknowledgements I wish to acknowledge my gratitude to Dr. Norman Endler, Ms. Elaine Cudmore and Mrs. Sharon Sanders for their help with the preparation of this manuscript.
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8. Kendell RE. The present status of electroconvulsive therapy. Br J Psychiatry 1981; 139: 265-283. 9. Thompson JW, BlaineJD. The use ofECT in the United States in 1975 and 1980. Am J Psychiatry 1987; 144: 175-180. 10. Fink M. Is ECT usage decreasing? Editorial. Convulsive Therapy 1987; 3: 171-173. II. Malia A. An epidemiological study of electroconvulsive therapy: rate and diagnosis. Can J Psychiatry 1986; 31(9): 824-830. 12. Fink M. Convulsive therapy: theory and practice. New York: Raven Press, 1979. 13. Cerletti U. L'electroshock. Rivista Sperimentale Di Freniatria 1940; 64: 209-310. 14. Small JG. Review: efficacy of ECT in schizophrenia, mania, and other disorders. Convulsive Therapy 1985; 1: 263-276. 15. Mirsky AF, Duncan CC. Etiology and expression of schizophrenia: neurobiological and psychosocial factors. Annual Review of Psychology 1986; 37: 291-319. 16. Shugar G, Hoffman B, Johnston D. Electroconvulsive therapy for schizophrenia in Ontario: a report on therapeutic polymorphism. Compr Psychiatry 1984; 25: 509-520. 17. Fink M. Academic Address: Mechanisms of action of ECT. London, ON: London Psychiatric Hospital, Departmentof Psychiatry Continuing Medical Education. University of Western Ontario, September 14, 1989. 18. Addonizio G, Susman YC. ECT as an alternative for patients with symptomsof neurolepticmalignant syndrome. J Clin Psychiatry 1987; 43: 102-105. 19. Regestein QR, Reich P. Electroconvulsive therapy in patients at high risk for physical complications. Convulsive Therapy 1985; I: 101-114. 20. Holcomb HH, Sternberg DE, Henniger GR. Effects of electroconvulsivetherapy on mood, parkinsonism, and tardive dyskinesia in a depressed patient: ECT and dopamine systems. Bioi Psychiatry 1983; 188: 865-873. 21. Kroessler D. Relative efficacy rates for therapies of delusional depression. Convulsive Therapy 1985; 1: 173-182. 22. Glasman RH, Kauter SJ, Shostak M. Depression, delusions and drug response. Am J Psychiatry 1975; 132: 716-719. 23. Rich CL, Spiker DG, Jewell SW, et al. ECT response in psychotic versus nonpsychotic unipolar depressives. J Clin Psychiatry 1986; 47: 123-125. 24. Avery D, Lubrano A. The DeCarolis study reconsidered. Am J Psychiatry 1979; 136: 559-563. 25. Solan WJ, Khan A, Avery D, et al. Psychotic and nonpsychotic depression: comparison of response to ECT. J Clin Psychiatry 1988; 49: 97-99. 26. Crow TJ, Johnstone EC. Controlled trials of electroconvulsive therapy. In: Malitz S, Sackeim HA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1986; 462: 5-11. 27. Ottoson JO. Clinical perspectives on mechanisms of action. In: MalitzS, SackeimHA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1986; 462: 357-365. 28. Burke WJ, Rutherford JL, Zorumski CF, et al. Elecroconvulsive therapy and the elderly. Compr Psychiatry 1985; 26: 480-486. 29. Paul MP, Extein I, Calil H, et al. Use of ECT with treatment resistant depressed patients at the National Institute of Mental Health. Am J Psychiatry 1981; 138(4): 486-489. 30. Akiskal HS. A proposed clinical approach to chronic and "resistant" depressions. J Clin Psychiatry 1985; 46: 32-36.
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31. Fink M. Efficacy of ECT (letter). Lancet 1979; 2 (8155): 1303-1304. 32. Abrams R. Is unilateral electroconvulsive therapy the treatment of choice in endogenous depression? In: Malitz S, Sackeim HA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1986; 462: SO-55. 33. Hamilton M. Predictions of response to ECT. In: Abrams R, Essman WB, eds. Electroconvulsive therapy: biological foundations and clinical applications. New York: Spectrum Publications, 1982: 113-128. 34. Fink M. Predictors of outcome in convulsive therapy. Psychopharmacol Bull 1982; 18: SO-57. 35. Scott AIF. Which depressed patient will respond to electroconvulsive therapy? The search for biological prediction of recovery. Br J Psychiatry 1989; 154: 8-17. 36. Sackeim HA, Decina P, Kanzler M, et al. The efficacy of titrated low dosage ECT: the effects of electrode placement. Am J Psychiatry 1987; 144: 1449-1455. 37. Yatham L, Barry S, Dinan TG, et al. Which patients will respond to ECT? Letter to the Editor. Br J Psychiatry 1989; 154: 879. 38. Ottoson J. Electroconvulsive therapy of endogenous depression: an analysis of the influence of various factors on the efficacy of the therapy. J Ment Sci 1962; 108: 694-703. 39. Taylor MA. Indications for electroconvulsive treatment. In: Abrams R, Essman WB, eds. Electroconvulsive therapy: biological foundations and clinical applications. New York: Spectrum Publications, 1982: 2-40. 40. Janicak PG, Davis JM, Gibbons RD, et al. Efficacy of ECT: a meta analysis. Am J Psychiatry 1985; 142: 297-302. 41. D'Elia G, Raotma H. Is unilateral ECT less effective than bilateral ECT? Br J Psychiatry 1975; 126: 83-89. 42. Abrams R, Fink M. The present status of unilateral ECT: some recommendations. J Affective Disord 1984; 7: 245-247. 43. Pippard J. Book review of electroconvulsive therapy: the myths and realities. Convulsive Therapy 1989; 52: 197-198. 44. Avery DH, Winokur G. The efficacy of electroconvulsive therapy and antidepressants in depression. Bioi Psychiatry 1977; 12: 507-528. 45. Greenblatt M, Grosser GH, Wechsler H. Differential response of hospitalized depressed patients to somatic therapy. Am J Psychiatry 1964; 120: 935-943. 46. Coryell W, Pfohl B, Zimmerman M. Outcome for electroconvulsive therapy: comparison of primary and secondary depression. Convulsive Therapy 1985; 1: 10-14. 47. Rifkin A. ECT versus tricyclic antidepressants in depression: a review of the evidence. J Clin Psychiatry 1988; 49: 3-7. 48. Siris S, Glassman H, Steiner F. ECT and psychotropic medication in the treatment of depression and schizophrenia. In: Abrams R, Essman WB, eds. Electroconvulsive therapy: biological foundations and chemical applications. New York: Spectrum Publications, 1982: 91-111. 49. Rollin HR. The impact of ECT. In: Palmer RL, ed, Electroconvulsive therapy. Proceedings of the Leicester University Conference. Oxford: Oxford University Press, 1980. 50. Freeman CPL, Basson JV, Crichton A. Double-blind controlled trial of electroconvulsive therapy (ECT) and simulated ECT in depressive illness. Lancet 1978; i: 738-740. 51. Lambourn J, Gill D. A controlled comparison of simulated and real ECT. Br J Psychiatry 1978; 133: 514-519. 52. West E. Electric convulsion therapy in depression: a doubleblind controlled trial. Br Med J 1982; 282: 355-357.
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53. Johnstone EC, Deakin JFW, Lawler P, et al. The Northwick Park ECT trial. Lancet 1980; ii: 1317-1320. 54. Markowitz J, Brown R, Sweeney J, et al. Reduced length and cost of hospital stay for major depression in patients treated with ECT. Am J Psychiatry 1987; 144: 1025-1029. 55. Avery D, Winokur G. Suicide, attempted suicide and relapse rates in depression. Arch Gen Psychiatry 1978; 35: 749-753. 56. Huston P, Locher LM. Manic depressive psychosis: course when treated and untreated with electric shock. Arch Neurol Psychiatry 1948; 60: 37-48. 57. Ottoson J. Use and misuse of electroconvulsive treatment. Bioi Psychiatry 1985; 20: 933-946. 58. Post RM, Putnam F, Uhde TW, et al. Electroconvulsive therapy: implications for its mechanisms of action in affective illness. In: Malitz S, Sackeim HA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1986; 462: 376-388. 59. Fink M, NemeroffCB. A neuroendocrine view of ECT. Convulsive Therapy 1989; 5(3): 296-304. 60. Kalinowski L. History of convulsive therapy. In: Malitz SA, Sackeim HA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1986; 462: 1-4. 61. Robin A, Detissera S. A double blind controlled comparison of the therapeutic effects of low and high energy electroconvulsive therapies. Br J Psychiatry 1982; 141: 357-366. 62. Martin BA. Electroconvulsive therapy for depression in general psychiatric practice. Psychiatr J Univ Ottawa 1989; 14(2): 413-417. 63. Fraser M. ECT: a clinical guide. New York: John Wiley and Sons, 1982. 64. Crowe RR. ECT: a current prospective. N Engl J Med 1984; 311: 163-167. 65. Weiner RD. Does electroconvulsive therapy cause brain damage? The Behavioural and Brain Sciences 1984; 7: 1-53. 66. Weiner RD, Rogers HJ, Davidson JRT, et al. Effects of stimulus parameters on cognitive side effects. In: Malitz S, Sackeim HA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1988; 462: 315-325. 67. Breggin PRo Electroshock: its brain disabling effects. New York: Springer Publishing Company, 1979. 68. Squire LR. ECT and memory loss. Am J Psychiatry 1977; 134: 997-1001. 69. Squire LR. The question of long-term effects. Bethesda, MD: Paper presented at the NIMH Consensus Development Conference, June 1985. 70. Squire LR, Wetzel CD, Slater PC. Memory complaint after electroconvulsive therapy: assessment with a new self-reading instrument. Bioi Psychiatry 1979; 41: 791-801. 71. Freeman CP, Kendell RE. Patient's experience of and attitudes to electroconvulsive therapy. In: Malitz S, Sackeim HA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1986; 462: 341-352. 72. Fink M. Myths of shock therapy. Am J Psychiatry 1977; 134: 991-996. 73. Price TRP. Systemic effects of ECT. In: Electroconvulsive therapy: programme and abstracts. Washington, DC: Consensus Development Conference, National Institute of Mental Health, June 10-12, 1985.
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74. Goldbloom DS, Kussin D. Electroconvulsive therapy: attitudes training and experience among senior residents in psychiatry across Canada. Newfoundland: presented at the 39th Annual Meeting of the Canadian Psychiatric Association, September 22, 1989.
Resume La therapie convulsivante a I'electrochoc est en usage
depuis une cinquantaine d'annees et demeure I'un des traitements psychiatriques les plus efficaces. Son taux de succes dans les cas de depression est de l'ordre de 80% a 90% et, a ce jour, aucune etude comparative n 'a mis en evidence la superiorite d 'autres interventions. On recommande egalement la therapie convulsivante a I'electrochoc dans les cas de manie et de schizophrenie, et comme traitement sans
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danger chez les deprimes ages ou malades. Le present article traite de la therapie a l'electrochoc dans les cas de depression. L 'etude porte sur les indications cliniques, les facteurs permettant de prevoir les reactions du malade et les preuves d 'efficacite du traitement; on propose egalement des expliquations sur le mode d'action del'electrochoc et ses effets secondaires, ainsi que des directives pour la prescription du traitement. Malgre I'efficacite et l'innocuite de la therapie a l'electrochoc, et meme si celle-ci semble mieux acceptee par le public qu 'auparavant, certains observateurs notent que son usage est en declin. D 'autres pensent que ce declin se limite au secteur public, par exemple aux hopitaux psychiatriques federaux et provinciaux. II est necessaire de poursuivre les recherches en vue de raffiner la technique et d'en permettre une meilleure comprehension.
Electroconvulsive Therapy in Depression* E.
PERSAD, M.B., B.S. 1
Psychiatric Association (APA) task force on the use of ECT (4) lamented that the procedure was poorly controlled and inappropriately used. A similar state of affairs had been uncovered in the United Kingdom (5). Since then, the situation has improved, primarily as a result of activities within the profession to respond to public concerns. Public validation of ECT' s new found respectability was provided by the 1985 Clark Enquiry into the use of ECT in Ontario (6). In 1985, the National Institute of Mental Health convened a Consensus Conference on ECT in Washington, D.C. (7). Among its many findings, the Consensus Conference noted that "There is a continuing controversy concerning the mental disorders for which ECT is indicated, its efficacy, the optimal methods of administration, possible complications and the extent of its usage in various settings." The Conference statement continued, "ECT is demonstrably effective for a narrow range of severe psychiatric disorders in a limited number of diagnostic categories: delusional and severe endogenous depression and mania and certain schizophrenic syndromes. " Professional organizations such as the APA and the Royal College of Psychiatrists in the United Kingdom continue to monitor the usage ofECT, and both are due to release updated reports for their respective countries shortly. The use of ECT may be declining. In 1980,2.4% of all psychiatric admissions in the United States were given ECT (7). In the United Kingdom, a survey done in 1979 reported that 200,000 individual ECT treatments were administered, and 97% of these were in National Health Service Units (8). Thompson and Blaine (9) have reported that the use of ECT in the United States decreased by 46% between 1975 and 1980, and that the majority of patients receiving ECT (69.8%) were those suffering from affective disorders. Thompson and Blaine (9) also found that the diagnosis was more significant than sex in determining which patients received ECT. Fink (10) has questioned the conclusions of Thompson and Blaine regarding the decline of the use of ECT in the United States. It is Fink's belief that even though ECT may be declining in state hospitals, there is actually an increase in use in general public hospitals and in private psychiatric institutions. Fink (10) concludes that "the survey of Thompson and Blaine is a lagging indicator of ECT interest and usage. " In a recent Canadian sample (11) of 5,729 consecutive admissions in three general hospitals and one mental hospital, 21.5% of patients received ECT and half were for affective illnesses. This suggests that the use of ECT in at
Electroconvulsive therapy (ECT) has been in use for over 50 years and remains one of the most effective treatments in psychiatry. Effectiveness rates for ECT in depression range between 80% and 90%; no comparative study has shown any other intervention to be superior to ECT. ECT is also recommended for mania, schizophrenia and as a safe treatment for the elderly or medically ill depressed patient. This paper will deal with the use of ECT in depression. The areas to be covered are the clinical indications, the factors predictive ofresponse, the evidence for the efficacy ofECT, as well as theories of the mechanism of its action, side effects and guidelines for prescribing the procedure. Notwithstanding the efficacy, the safety· and perhaps an improved public acceptance, some observers have noted that there is a decline in the use ofECT. Others have suggested that such a decline may be evident only in the public sectors such as state and provincial psychiatric hospitals. Ongoing research is necessary to achieve further refinement ofECT, as well as enhance our understanding of this important treatment procedure.
E
lectroconvulsive therapy (ECT) has been in use for over 50 years and has remained one of the most effective treatments in psychiatry especially for the affective disorders (1). Notwithstanding its efficacy, the popular visual and print media tend to portray the procedure as a form of coercion to control helpless inmates of mental institutions. This representation of ECT evokes fear and apprehension in the minds of the general public. Such fear has been fuelled by controversial statements about ECT-induced brain damage made by a minority within the medical profession (1). Recently however, the print media has shown a more balanced point of view in reports on ECT. Whereas in 1980 Hapgood (2), writing in The Atlantic, argued for the abandonment of ECT and referred to it as one of those medical interventions that "subsequent generations will look back on as barbarous." In 1987 Squire, in the New York Sunday Times (3), wrote a more favourable piece entitled "Shock Therapy's Return to Respectability." The term "shock," however, perpetuates the image of ECT as an arbitrary and frightening procedure. Less than a decade ago, the American
*Manuscript received October 1989. 'Director of Education, London Psychiatric Hospital; Associate Professor of Psychiatry, University of Western Ontario, London, Ontario. Address reprint requests to: Dr. E. Persad, London Psychiatric Hospital, 850 Highbury Avenue, London, Ontario N6A 4H1
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least one Canadian study is approximately ten times that of the United States (7).
Indications for Use ECT was initially thought to be a treatment primarily for schizophrenia (12, 13) but as a result of clinical observation and open trials it became clear that ECT is indeed more appropriate in the treatment of depression. ECT is now regarded as the most effective treatment for certain types of depression, and that, further, no single controlled study has shown another form of treatment to be superior to ECT in the short term management of severe depression (7). ECT has also been found useful in mania (12) and in schizophrenia (14-16). According to Fink, the current APA task force will likely recommend that ECT should be considered the first line treatment for the following conditions: major depression, manic delirium and catatonia (17). There may be a limited role for ECT in other conditions in which psychotropic drugs may be contraindicated. For example, ECT has been reported as an alternative treatment in patients who develop neuroleptic malignant syndrome (18), and in medically ill patients (19). Case reports have suggested that ECT may have an ameliorating effect on tardive dyskinesia and on Parkinson's disease (17,20). This paper will focus on the use of ECT in depression.
The Use of ECT in Depression In practice, it is not unusual to recommend ECT in the treatment of depression after a failure of other interventions. In some situations the severity of the patient's clinical state, for example those in a depressive stupor or the highly suicidal patient, leads clinicians to a consideration of ECT as the first line of treatment. In addition, ECT should be considered in the following types of depressed patients: 1. Those with delusional depression. 2. Melancholiacs. 3. Elderly and medically ill depressed patients. 4. Those with treatment resistant depression. 1. Delusional Depression: Delusional depression is characterized by the presence of a depressed mood and delusions which are usually mood congruent but may also include delusions which may not be congruent with an affective state. These patients do not appear to benefit from antidepressants and some studies suggest that a combination of antidepressants and neuroleptics is the treatment of choice (21,22). However, several other studies (23,24) have shown that ECT is highly effective in the treatment of delusional depression and indeed it is superior to either antidepressants or neuroleptics used alone and is at least as effective as the combination of antidepressants and neuroleptics. Solan et al (25) found that ECT was equally effective in a psychotic and a nonpsychotic group of depressed patients, where neither group had responded to previous pharmacotherapy. The presence of psychotic symptoms may not enhance the degree of response to ECT (23).
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2. Melancholia: The severe endogenous or melancholic depressions are characterized by early morning wakening, marked weight loss, psychomotor retardation andlor agitation, diurnal variation and lack of reactivity. ECT is at least as effective as antidepressants and more effective than "sham" ECT in the short term treatment of these severe depressions (26). Ottoson (27) has indicated that ECT should be considered the treatment of choice for melancholia. It is his view that ECT is effective for the full syndrome in melancholia but that in other conditions such as mania, ECT's therapeutic benefit comes from nonspecific organic effects (27). There is also evidence of the efficacy of ECT in those endogenous depressives who have not responded to an adequate trial of antidepressants (24). 3. Depression in the Elderly: The treatment of depression in the elderly is becoming an increasingly important subject given the fact that the proportion of the population over age 65 is dramatically increasing (28). The incidence of affective disorders increases with age and the prognosis for depression in the elderly is less favourable with persistent and disabling symptoms in approximately one third of afflicted aged persons (28). This increased psychiatric morbidity is accompanied by an increased mortality rate in the depressed elderly. Pharmacotherapy in the elderly patient who is depressed has been widely considered to be safe and efficacious. In a series of 30 consecutive elderly depressed patients, ECT was found to be an effective treatment. ECT was also of benefit to some patients who were resistant to or who were unable to tolerate pharmacotherapy. This improvement was related to diagnosis; 92 % of patients with major depression improved and 69% showed complete symptom resolution. Burke and colleagues (28) indicated that the occurrence of adverse effects was concentrated in the oldest patients; that is, the complication rate correlated with the age to a significant degree and to health status, and they concluded that even though ECT is a safe treatment for the elderly, those who are older than 75 years or those with a history of cardiovascular disease are at increased risk for complications. 4. Treatment Resistant Depression: Paul and colleagues (29) reported on the use of ECT with treatment resistant depressed patients at the National Institute of Mental Health. Even though this was a small sample (nine patients), the authors found that despite the patients' poor prior response to a variety of pharmacological treatments, only one patient failed to show a complete response to ECT. This, and other studies (23, 24, 30, 31) of patients who are suffering from depression and who appear not to respond to pharmacotherapy, would indicate that ECT should be offered to those who are intractable. Some reports have also indicated that the treatment protocol should include bilateral ECT rather than unilateral ECT for those who appear to be treatment resistant (32). The fact that ECT appears to work where antidepressants have failed raises intriguing questions regarding mechanisms of action, to be discussed later.
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Predictors of Response As has been noted in the foregoing, the clinical features of the depressed patient might be used as the indicators of response to ECT. However, there has been a continuing inquiry into other factors that might predict a favourable response to ECT in depressed patients (32-34). Biological predictors of ECT response have been extensively investigated. Scott (35) recently reviewed studies which used the following measures: resting electroencephalogram, neuroendocrine challenge tests, sedation and seizure thresholds, calcium levels and monoamine metabolites in peripheral body fluids. Scott's review (35) on biological measures indicates that there are no consistent physiological findings in depressed patients which carry a strong predictive value. Changes during ECT treatments have also been used to predict outcome. ECT has a profound effect on neuroendocrine functioning as measured by cortisol secretion and prolactin release. Neuroendocrine dysregulation associated with depression may be a valid indicator of ECT response, but as Fink (17) and Scott (35) have pointed out, certain biological factors may have general predictive values not specific to any particular somatic therapy. The duration of the seizure has been thought to predict outcome and a seizure duration of greater than 25 seconds has been recommended (4). Later studies examining the relationship between the duration of the seizure and outcome indicated that there was no relationship between individual seizure length measured either by observation, electroencephalograph (EEG) and clinical change, or outcome during the course of ECT (35). It may not be feasible to define a minimum length for a therapeutic seizure as time alone takes no account of the degree of spread of seizure activity over the cortex or throughout the brain. It has also been suggested that seizure threshold may playa role in outcome (36, 37). Careful clinical assessment remains the single most important step in the selection of depressed patients for ECT (27, 38, 39). Weight loss, early morning wakening and somatic delusions, the clinical features of endogenous depressive illnesses, may best predict a good outcome with ECT (39). Crow and Johnstone (26) raised the possibility that the only consistent clinical predictor of a specific response to ECT is the presence of delusions. Although a generalized tonic, clonic seizure is an essential component of successful ECT, endogenously depressed patients can experience satisfactory seizures and yet fail to recover with ECT (36).
Unilateral versus Bilateral ECT Electrode placement preferences in ECT have varied over the years. In the early years, bilateral ECT was the common method of administration. It was subsequently suggested that right unilateral ECT was just as effective and was preferable because of fewer cognitive side effects (4). There have been over 35 clinical trials dealing with this issue but the question remains unsettled (40-42). In one such study, involving double blind random assignment, the relative efficacy of bilateral and unilateral ECT with a low dose titration was assessed (36). The investigators reported that in
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52 patients (mean age 61.33 years) with primary major depressive disorder, bilateral ECT was markedly superior to right unilateral ECT in short term symptom reduction. The authors (36) pointed out that there was no difference between the two procedures, in the duration of generalized seizures or the number of treatments administered to achieve clinical response. The authors disagreed with the claim that the elicitation of a generalized seizure is sufficient for the antidepressant properties of ECT. It was their opinion that a dose in excess of seizure threshold may contribute to the efficacy of ECT, particularly with a right unilateral electrode placement. There is a wide interpatient variability as to seizure threshold. As well males, the elderly and patients on anticonvulsants have a higher seizure threshold (36). The Royal College of Psychiatrists is now recommending bilateral ECT using pulse current for the treatment of depression (43). The use of left unilateral electrode placement has not been adequately assessed. In clinical practice, the nondominant hemisphere (usually the right side) is used for the electrode placement.
The Efficacy of ECT in the Treatment of Depression ECT was introduced in an era when few other interventions were available for treating mental illnesses and that fact may have led to its widespread and somewhat indiscriminate use (4, 5). As clinicians gained experience with the treatment and refinements took place in the procedure, it was noted that ECT had a significant effect on patients suffering from melancholia. Kendell (8), in his review of the early clinical trials and impressions regarding ECT noted that it was regarded by some as almost "miraculous" in its effect on some patients. Comparison studies (44, 45) have generally found ECT to be comparable with other interventions. Some studies indicate that ECT may be superior to antidepressants (45). ECT and imipramine were compared in the treatment of depression in a large sample of patients (n=437) (24). The study was unique in that all 437 patients were given a trial of imipramine and the ECT group was composed of only imipramine failures. Among those with delusional depression 83% improved with ECT versus 40% with imipramine. Janicak and colleagues (40) analyzed several rigorously controlled studies that compared the efficacy of ECT with simulated ECT, placebo and antidepressants. A total of 19 studies were examined in which approximately 628 patients were involved. The overall efficacy of ECT was clearly supported by these studies. Combining the studies that compared ECT with any of the four other treatments resulted in an overall efficacy rate of 77.8% (simulated ECT 27.6%, placebo 37.6%, tricyclics 64.3% and MAOIs 32%). In this survey MAGIs were found to be less effective in endogenous type depression compared with depression where there is predominant anxiety, hypochondriacal or phobic syndromes. Put another way, MAOIs may be more appropriate for the atypical depressives. ECT is said to be ineffective in secondary depression (46).
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Rifkin (47) has pointed out that for conclusive statements to be made, comparison studies should be prospective with random assignment to treatment groups and blind assessment of outcome. Siris, Glassman and Steiner (48) reported that in 31 major studies comparing ECT and drugs in depression, 17 showed ECT to be clearly superior, eight appeared to give it a slight edge, four showed no difference and two were equivocal. These authors (48) commented on methodological problems in these studies, for example poor clinical descriptions of target symptoms as well as inadequate dose of drugs. Some studies have examined the effectiveness of combining ECT and antidepressant drugs in the treatment of depression but Siris and colleagues (48) found little evidence to support increased efficacy; as pointed out above, however, antidepressants may be necessary in the continuation phase to maintain the improvement already obtained with ECT. Rollin (49) stated that ECT was "the most significant advance in treatment of our time." As Kendell points out (8), by 1977 there was overwhelming evidence in favour of the effectiveness of ECT and its superiority over other interventions in the treatment of depression. The Royal College of Psychiatrists in the United Kingdom issued a statement in which the effectiveness of ECT as a treatment for depression was referred to as "substantial and incontrovertible" (8). Nonetheless, the criticism and doubts about the procedure persisted, expecially in North America, and this led to a series of double blind trials, all of which took place in the United Kingdom, in which patients were treated either with real or simulated (sham) ECT (50-53). Each study was different in electrode placement, in patient selection and in assessment of outcome. On balance the studies appear to give the edge to real ECT over simulated ECT, but there were some equivocal findings that led Kendell (8) in his review to question whether the four trials were comparable because of the differences in methodology. In one of the trials (53), there was a lack of any difference between real and simulated ECT groups at one and six months follow-up. Crow and Johnstone (39) summarized the findings from several outcome studies as follows: 1. The efficacy of ECT in the treatment of severe depression has been well established. 2. No study has clearly delineated the contribution to the therapeutic outcome of the nonconvulsive elements in the procedure. 3. In the sham versus real ECT studies, patients receiving sham ECT do show improvement over three to four weeks, but patients on real ECT improve to a greater degree. 4. ECT produces a rapid response but there is a limited duration of effect. 5. The only clinical indicator of ECT response in depression is the presence of delusions. It has long been accepted that high relapse rate with ECT is one of its most serious limitations. Any treatment modality for depression should take into consideration what is known about the natural course of the illness, and therefore the need for continuation and maintenance therapies once the acute symptoms have subsided. This is true of antidepressants and
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should also be true of ECT. The use of maintenance ECT has not been fully explored. ECT has also been found to reduce the length of hospitalization for depressed patients. In a recent study, Markowitz and colleagues (54) found that all patients treated with ECT responded, in contrast to only 49% of those who were treated with antidepressants. They also found that when the failed (drug) group was treated subsequently with ECT they all recovered. Markowitz and colleagues (54) concluded that patients treated with ECT stayed in hospital a mean of 13 fewer days, saving more than $6,400 U.S. a patient at then current rates. It must be noted that ECT is usually introduced after other measures have failed and therefore length of hospitalization may not convey a valid correlation with ECT usage and effectiveness. ECT has been shown to have an impact on suicide rates (55). Of 600 hospitalized patients, those who were treated with ECT had a better outcome though relapse rates were the same, but at follow-up after six months, the drug-treated group had displayed four to seven times more suicide attempts than the ECT group. The authors pointed out that this pattern persisted after three years. After review of several other studies, they concluded that ECT -treated patients had better chances of survival compared with patients treated with drugs. This investigation, however, has the shortcomings of being a retrospective chart review. ECT is not usually compared with psychotherapy in the treatment of depression, but one such study by Huston and Locher (56) found ECT more effective than a combination of psychotherapy, hydrotherapy and occupational therapy.
Mechanism of Action ECT is an effective treatment modality for a variety of psychiatric conditions, which suggests a multiple mode of action. Ottoson (26, 57) is of the opinion that the antidepressant effect of ECT is due to the grand mal seizure, but the antimanic property of ECT results from the confusional and amnesic effects. The fact that ECT is beneficial in drug-failed depressed patients may also suggest a mechanism of action unlike that of antidepressants. Others (58) suggest that ECT has a unitary mechanism of action, and acts like an anticonvulsant. According to this theory, the traditional view of the role of the seizure is replaced by a view that the seizure leads to the therapeutic event in affective illnesses. A neuroendocrine mechanism of action has been postulated recently (59). According to this view, ECT produces generalized neuroendocrine effects, but these result in the production of a substance referred to as "antidepressin" by Fink and Nemeroff (59), a hypothalamic peptide, which is said to produce both the antidepressant and antipsychotic effects. The search for the therapeutic agent produced by ECT is not new. In the 1940s, Cerletti believed that convulsions were the main factor that led to the alleviation of symptoms; in the 1950s he believed that the injection of brain substances of electroshocked animals into mentally ill patients would eliminate the need for ECT and for convulsions (1). Cerletti believed that the injection of "acroagonines" would serve
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as a defense against subsequent illness (1, 60). Rudorfer (3), of the National Institute of Health, has recently echoed this opinion, and regards ECT as a "dirty drug" with a shotgun effect, and that future research should be directed towards the discovery of the substance or the therapeutic agent, generated by the ECT. In a study in which patients were assigned to treatment with either low energy, high energy pulses or high energy sinusoidal wave ECT, those patients on the higher dosage condition experienced greater therapeutic benefit (61). This may suggest a mechanism of action dependent on a stimulus intensity "therapeutic window" (61), only within which ECT is effective. The authors suggest that this might explain the findings of no difference between real and sham ECT reported in the Northwick Park trial (53). There is a trend in current practice to aim for suprathreshold energy rather than the minimal energy level required for a seizure (62).
Side Effects and Adverse Reactions to ECT ECT has a significant impact on the neurophysiology of patients undergoing the treatment. There is an increased permeability of the blood-brain barrier, as well as significant changes in neuroendocrine and cardiovascular measures. One of the myths associated with the treatment is that if ECT does work, it does so because of the evocation of fear, panic and anxiety that may accompany any stressful experience (I). Side effects and complications of ECT can occur during treatment as well as following treatment. Before modern improvements, the chief complications arising during the procedure especially in the clonic phase of the seizure were fractures and dislocations. These side effects are no longer common because of the use of muscle relaxant drugs. Patients coming to ECT should be medically clear and able to tolerate a general anesthetic as most of the problems which may arise during the treatment may be those secondary to reactions to the anesthetic procedure. The problems which might arise in the post-treatment period include onset of a confusional state. Fraser (63) in his review of several studies found that the most common complaint was memory impairment followed by headache, confusion, clumsiness, nausea or vomiting, eyesight problems and muscle pain. He pointed out that even though a number of patients were upset by the treatment, more than half agreed that they would readily have it again if necessary and over three quarters found the experience no more upsetting than going to the dentist. Crowe (64) reported however that almost all patients experience a transient confusional state immediately following ECT. Patients who are manic depressive run the risk of becoming manic if they are treated with ECT, as they do when treated with antidepressants. Such patients may be protected by continuing on lithium during the ECT. ECT, as has been noted earlier, can be used effectively in the treatment of both depression and mania. The major side effects noted with ECT are the cognitive changes that follow a course of treatment, and this is at the heart of the ECT controversy. Weiner (65) stated that a "nonselection assessment" of the data from a variety of meas-
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urements do not support the charge that ECT is the "purveyor of wholesale brain damage." In a later study, Weiner and colleagues (66) point out that unilateral nondominant electrode placement and brief pulse stimuli may produce fewer cognitive side effects. They do not rule out subtle, undetected changes with the high energy procedure. Critics of ECT are adamant that these changes represent irreversible brain damage, while proponents claim that they are temporary and reversible (7). Cognitive side effects can be minimized by giving unilateral rather than bilateral treatments, by reducing the dose of the electrical stimulation, by spacing between treatments and by limiting the number of sessions (7). There is some suggestion however that these precautions may reduce the effectiveness ofECT (62). There is no evidence that the effectiveness of ECT in alleviating depression is dependent upon the occurrence of cognitive changes as has been alleged by Breggin (67). The ECT Consensus Conference (7) has also reported that there was no evidence of cumulative deterioration, that the deficits found at the beginning of treatment were not worse by the end, and that there were no difficulties noted in the acquisition of new information over the course of treatment. These findings have been corroborated by others (68-70). A critical question regarding ECT-induced memory impairment is whether it persists. There have been several studies reviewing this and none could substantiate that ECT causes permanent memory loss. Some of the studies (8, 71) indicate that recall of patients pre-ECT was also generally worse than that of a matched control group. Interpretations of patients' complaints about memory loss following ECT may be affected by age and by depression (1).
ECT Mortality The incidence of deaths arising from ECT have been reviewed by Kendell (8) and Fink (72). Kendell (8) found that from 1956 to 1966 in England and Wales, there was an average of 3.6 deaths per year associated with ECT, but no figures were available for the size of the population treated. The ECT Conference (7) noted that in the least favourable recent series, there were 2.9 deaths per 10,000 patients. Fink (72) found that the incidence of death in ECT was variously reported from none in 8,500 treatments of 870 patients to 0.06%,0.08% and 0.8% of patients treated. According to Price (73), the best estimate of ECT fatalities is 0.03 % per patient treated, but it was unclear how this rate was calculated. Price (73) points out that this figure should be considered in perspective. For instance, mortality from short term barbiturate anesthetic is 3.3 per 100,000 procedures.
Guidelines for Prescribing ECT Patients and their relatives should be fully informed about the risks and benefits of ECT. Assessment of competence to give consent is essential. This has been one of the most difficult issues for patients who are severely depressed as they may not be considered competent to decide their treatment. Some centres use videotapes to assist patients and families in making an informed decision regarding ECT. In those
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clinical conditions which appear to fall outside the usual indicators, there should be a second psychiatric opinion, or if there is no response after 12 treatments for depression, or 15 treatments for schizophrenia (1). The procedure should be clearly documented including dosages of drugs used, whether the electrode placement was unilateral or bilateral and whether the seizure induced was bilateral or not. The clinician should also be aware of the relationship between the stimulus energy and waveform characteristics required for each patient to maximize benefit without increasing side effects. Recently attention has been directed to the treatment dosage as a therapeutic variable. Most modern ECT machines provide an electrical stimulus with a pulsatile square waveform. The continuous sine wave electric stimulus in the older ECT machines was associated with greater cognitive side effects. Treatment protocols vary widely even with the newer ECT machines. Guidelines for estimating the treatment dose include rule of thumb estimates such as one watt-second per year of patient age, or the addition of25 to 150% of energy above the seizure threshold (62).
Conclusions There is a danger that this procedure, which continues to generate controversy, may become increasingly underutilized by default or by lack of interest. Such a trend could be seen in a recent survey among senior psychiatric residents in Canada (74). However, ECT is one of the most effective treatments for affective disorders, especially the severe forms of depression. ECT has been effective in patients who have not responded to other interventions. Current research is directed towards the refinement of clinical criteria, and an improved understanding of the technical aspects of the procedure. Acknowledgements I wish to acknowledge my gratitude to Dr. Norman Endler, Ms. Elaine Cudmore and Mrs. Sharon Sanders for their help with the preparation of this manuscript.
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8. Kendell RE. The present status of electroconvulsive therapy. Br J Psychiatry 1981; 139: 265-283. 9. Thompson JW, BlaineJD. The use ofECT in the United States in 1975 and 1980. Am J Psychiatry 1987; 144: 175-180. 10. Fink M. Is ECT usage decreasing? Editorial. Convulsive Therapy 1987; 3: 171-173. II. Malia A. An epidemiological study of electroconvulsive therapy: rate and diagnosis. Can J Psychiatry 1986; 31(9): 824-830. 12. Fink M. Convulsive therapy: theory and practice. New York: Raven Press, 1979. 13. Cerletti U. L'electroshock. Rivista Sperimentale Di Freniatria 1940; 64: 209-310. 14. Small JG. Review: efficacy of ECT in schizophrenia, mania, and other disorders. Convulsive Therapy 1985; 1: 263-276. 15. Mirsky AF, Duncan CC. Etiology and expression of schizophrenia: neurobiological and psychosocial factors. Annual Review of Psychology 1986; 37: 291-319. 16. Shugar G, Hoffman B, Johnston D. Electroconvulsive therapy for schizophrenia in Ontario: a report on therapeutic polymorphism. Compr Psychiatry 1984; 25: 509-520. 17. Fink M. Academic Address: Mechanisms of action of ECT. London, ON: London Psychiatric Hospital, Departmentof Psychiatry Continuing Medical Education. University of Western Ontario, September 14, 1989. 18. Addonizio G, Susman YC. ECT as an alternative for patients with symptomsof neurolepticmalignant syndrome. J Clin Psychiatry 1987; 43: 102-105. 19. Regestein QR, Reich P. Electroconvulsive therapy in patients at high risk for physical complications. Convulsive Therapy 1985; I: 101-114. 20. Holcomb HH, Sternberg DE, Henniger GR. Effects of electroconvulsivetherapy on mood, parkinsonism, and tardive dyskinesia in a depressed patient: ECT and dopamine systems. Bioi Psychiatry 1983; 188: 865-873. 21. Kroessler D. Relative efficacy rates for therapies of delusional depression. Convulsive Therapy 1985; 1: 173-182. 22. Glasman RH, Kauter SJ, Shostak M. Depression, delusions and drug response. Am J Psychiatry 1975; 132: 716-719. 23. Rich CL, Spiker DG, Jewell SW, et al. ECT response in psychotic versus nonpsychotic unipolar depressives. J Clin Psychiatry 1986; 47: 123-125. 24. Avery D, Lubrano A. The DeCarolis study reconsidered. Am J Psychiatry 1979; 136: 559-563. 25. Solan WJ, Khan A, Avery D, et al. Psychotic and nonpsychotic depression: comparison of response to ECT. J Clin Psychiatry 1988; 49: 97-99. 26. Crow TJ, Johnstone EC. Controlled trials of electroconvulsive therapy. In: Malitz S, Sackeim HA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1986; 462: 5-11. 27. Ottoson JO. Clinical perspectives on mechanisms of action. In: MalitzS, SackeimHA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1986; 462: 357-365. 28. Burke WJ, Rutherford JL, Zorumski CF, et al. Elecroconvulsive therapy and the elderly. Compr Psychiatry 1985; 26: 480-486. 29. Paul MP, Extein I, Calil H, et al. Use of ECT with treatment resistant depressed patients at the National Institute of Mental Health. Am J Psychiatry 1981; 138(4): 486-489. 30. Akiskal HS. A proposed clinical approach to chronic and "resistant" depressions. J Clin Psychiatry 1985; 46: 32-36.
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31. Fink M. Efficacy of ECT (letter). Lancet 1979; 2 (8155): 1303-1304. 32. Abrams R. Is unilateral electroconvulsive therapy the treatment of choice in endogenous depression? In: Malitz S, Sackeim HA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1986; 462: SO-55. 33. Hamilton M. Predictions of response to ECT. In: Abrams R, Essman WB, eds. Electroconvulsive therapy: biological foundations and clinical applications. New York: Spectrum Publications, 1982: 113-128. 34. Fink M. Predictors of outcome in convulsive therapy. Psychopharmacol Bull 1982; 18: SO-57. 35. Scott AIF. Which depressed patient will respond to electroconvulsive therapy? The search for biological prediction of recovery. Br J Psychiatry 1989; 154: 8-17. 36. Sackeim HA, Decina P, Kanzler M, et al. The efficacy of titrated low dosage ECT: the effects of electrode placement. Am J Psychiatry 1987; 144: 1449-1455. 37. Yatham L, Barry S, Dinan TG, et al. Which patients will respond to ECT? Letter to the Editor. Br J Psychiatry 1989; 154: 879. 38. Ottoson J. Electroconvulsive therapy of endogenous depression: an analysis of the influence of various factors on the efficacy of the therapy. J Ment Sci 1962; 108: 694-703. 39. Taylor MA. Indications for electroconvulsive treatment. In: Abrams R, Essman WB, eds. Electroconvulsive therapy: biological foundations and clinical applications. New York: Spectrum Publications, 1982: 2-40. 40. Janicak PG, Davis JM, Gibbons RD, et al. Efficacy of ECT: a meta analysis. Am J Psychiatry 1985; 142: 297-302. 41. D'Elia G, Raotma H. Is unilateral ECT less effective than bilateral ECT? Br J Psychiatry 1975; 126: 83-89. 42. Abrams R, Fink M. The present status of unilateral ECT: some recommendations. J Affective Disord 1984; 7: 245-247. 43. Pippard J. Book review of electroconvulsive therapy: the myths and realities. Convulsive Therapy 1989; 52: 197-198. 44. Avery DH, Winokur G. The efficacy of electroconvulsive therapy and antidepressants in depression. Bioi Psychiatry 1977; 12: 507-528. 45. Greenblatt M, Grosser GH, Wechsler H. Differential response of hospitalized depressed patients to somatic therapy. Am J Psychiatry 1964; 120: 935-943. 46. Coryell W, Pfohl B, Zimmerman M. Outcome for electroconvulsive therapy: comparison of primary and secondary depression. Convulsive Therapy 1985; 1: 10-14. 47. Rifkin A. ECT versus tricyclic antidepressants in depression: a review of the evidence. J Clin Psychiatry 1988; 49: 3-7. 48. Siris S, Glassman H, Steiner F. ECT and psychotropic medication in the treatment of depression and schizophrenia. In: Abrams R, Essman WB, eds. Electroconvulsive therapy: biological foundations and chemical applications. New York: Spectrum Publications, 1982: 91-111. 49. Rollin HR. The impact of ECT. In: Palmer RL, ed, Electroconvulsive therapy. Proceedings of the Leicester University Conference. Oxford: Oxford University Press, 1980. 50. Freeman CPL, Basson JV, Crichton A. Double-blind controlled trial of electroconvulsive therapy (ECT) and simulated ECT in depressive illness. Lancet 1978; i: 738-740. 51. Lambourn J, Gill D. A controlled comparison of simulated and real ECT. Br J Psychiatry 1978; 133: 514-519. 52. West E. Electric convulsion therapy in depression: a doubleblind controlled trial. Br Med J 1982; 282: 355-357.
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53. Johnstone EC, Deakin JFW, Lawler P, et al. The Northwick Park ECT trial. Lancet 1980; ii: 1317-1320. 54. Markowitz J, Brown R, Sweeney J, et al. Reduced length and cost of hospital stay for major depression in patients treated with ECT. Am J Psychiatry 1987; 144: 1025-1029. 55. Avery D, Winokur G. Suicide, attempted suicide and relapse rates in depression. Arch Gen Psychiatry 1978; 35: 749-753. 56. Huston P, Locher LM. Manic depressive psychosis: course when treated and untreated with electric shock. Arch Neurol Psychiatry 1948; 60: 37-48. 57. Ottoson J. Use and misuse of electroconvulsive treatment. Bioi Psychiatry 1985; 20: 933-946. 58. Post RM, Putnam F, Uhde TW, et al. Electroconvulsive therapy: implications for its mechanisms of action in affective illness. In: Malitz S, Sackeim HA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1986; 462: 376-388. 59. Fink M, NemeroffCB. A neuroendocrine view of ECT. Convulsive Therapy 1989; 5(3): 296-304. 60. Kalinowski L. History of convulsive therapy. In: Malitz SA, Sackeim HA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1986; 462: 1-4. 61. Robin A, Detissera S. A double blind controlled comparison of the therapeutic effects of low and high energy electroconvulsive therapies. Br J Psychiatry 1982; 141: 357-366. 62. Martin BA. Electroconvulsive therapy for depression in general psychiatric practice. Psychiatr J Univ Ottawa 1989; 14(2): 413-417. 63. Fraser M. ECT: a clinical guide. New York: John Wiley and Sons, 1982. 64. Crowe RR. ECT: a current prospective. N Engl J Med 1984; 311: 163-167. 65. Weiner RD. Does electroconvulsive therapy cause brain damage? The Behavioural and Brain Sciences 1984; 7: 1-53. 66. Weiner RD, Rogers HJ, Davidson JRT, et al. Effects of stimulus parameters on cognitive side effects. In: Malitz S, Sackeim HA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1988; 462: 315-325. 67. Breggin PRo Electroshock: its brain disabling effects. New York: Springer Publishing Company, 1979. 68. Squire LR. ECT and memory loss. Am J Psychiatry 1977; 134: 997-1001. 69. Squire LR. The question of long-term effects. Bethesda, MD: Paper presented at the NIMH Consensus Development Conference, June 1985. 70. Squire LR, Wetzel CD, Slater PC. Memory complaint after electroconvulsive therapy: assessment with a new self-reading instrument. Bioi Psychiatry 1979; 41: 791-801. 71. Freeman CP, Kendell RE. Patient's experience of and attitudes to electroconvulsive therapy. In: Malitz S, Sackeim HA, eds. Electroconvulsive therapy: clinical and basic research issues. Annals of the New York Academy of Sciences 1986; 462: 341-352. 72. Fink M. Myths of shock therapy. Am J Psychiatry 1977; 134: 991-996. 73. Price TRP. Systemic effects of ECT. In: Electroconvulsive therapy: programme and abstracts. Washington, DC: Consensus Development Conference, National Institute of Mental Health, June 10-12, 1985.
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74. Goldbloom DS, Kussin D. Electroconvulsive therapy: attitudes training and experience among senior residents in psychiatry across Canada. Newfoundland: presented at the 39th Annual Meeting of the Canadian Psychiatric Association, September 22, 1989.
Resume La therapie convulsivante a I'electrochoc est en usage
depuis une cinquantaine d'annees et demeure I'un des traitements psychiatriques les plus efficaces. Son taux de succes dans les cas de depression est de l'ordre de 80% a 90% et, a ce jour, aucune etude comparative n 'a mis en evidence la superiorite d 'autres interventions. On recommande egalement la therapie convulsivante a I'electrochoc dans les cas de manie et de schizophrenie, et comme traitement sans
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danger chez les deprimes ages ou malades. Le present article traite de la therapie a l'electrochoc dans les cas de depression. L 'etude porte sur les indications cliniques, les facteurs permettant de prevoir les reactions du malade et les preuves d 'efficacite du traitement; on propose egalement des expliquations sur le mode d'action del'electrochoc et ses effets secondaires, ainsi que des directives pour la prescription du traitement. Malgre I'efficacite et l'innocuite de la therapie a l'electrochoc, et meme si celle-ci semble mieux acceptee par le public qu 'auparavant, certains observateurs notent que son usage est en declin. D 'autres pensent que ce declin se limite au secteur public, par exemple aux hopitaux psychiatriques federaux et provinciaux. II est necessaire de poursuivre les recherches en vue de raffiner la technique et d'en permettre une meilleure comprehension.
