Electroconvulsive Theratw Current Concepts Chester Pearlman, M.D.

Abstract. Recent developments

in the practice and theory of ECT are reviewed. Indications, efficacy, and risklbenefit considerations are discussed with emphasis on the clinical utility and cost-effectiveness of increased and earlier usage of ECT in hospitalized patients. Treatment procedures are presented in some detail with listings of medical considerations, management of complications, and other applications to general hospital practice. Research on the mechanism of action, potential future developments, and some training issues are briefly discussed.

Following a 20-year period of enthusiastic use when it was the most effective treatment for serious psychiatric disorders, ECT underwent a similar period of excessive rejection associated with the advent of alternative treatments, accusations of inappropriate use, legal restrictions, and public protest. Subsequently, there has been a more systematic exploration of indications and risk/benefit considerations. For more thorough discussion of this phase, consult [l]. Historical, social, and political issues are described more extensively in [2]. A compendium of recent research appears in 131, and clinical issues were covered in the Review of Psychiat y [4]. An APA task force recently presented guidelines for current practice [5]. Convulsive Therapy is the standard clinical/research journal.

Efficacy and Indications Depression ECT continues to show the widest spectrum of efficacy in major depressive disorders [6]. Some early From the psychiatry Department, Tufts University School of Medicine, Boston, Massachusetts. Address requests for reprints to: Boston VA Medical Center (116A), 150 South Huntington Avenue, Boston, MA 02130.

128 ISSN 0163-8343/91/$3.50

comparisons with antidepressant drugs were biased in favor of ECT due to inadequate dosage and other flaws [1,7]. Similarly, the clinical lore that ECT works faster may be based upon early dopaminergic effects, like those of stimulants [8], which are unreliable predictors of final results. Nevertheless, in situations where the delay involved in a failed trial of antidepressants would be unwise, treatment of choice. ECT remains the ECT is also useful in those bipolar patients whose mood lability is exacerbated by antidepressants. In demented patients, ECT may greatly improve function by removing a depressive component (pseudodementia) [l] or may relieve life-threatening food refusal without alteration of cognitive function. Combined neuroleptic and tricyclic treatment of patients with delusions approaches the efficacy of ECT [9], and similar efficacy of lithium augmentation and ECT in some tricyclic-resistant patients has been reported [lo]. The significantly greater cost of hospitalization for patients who fail a drug trial before receiving ECT [ll], however, raises questions about routine use of the most effective treatment last. Just as maintenance drug treatment is recommended for 4-6 months, a similar use of ECT at intervals of l-4 weeks has been effective in managing patients who relapse following improvement [12]. Possible synergism between ECT and antidepressants was studied soon after the introduction of tricyclics and MAO inhibitors with contradictory results. It then became standard practice to discontinue MAO inhibitors before ECT because of an exaggerated fear of interaction with anesthesia [13] and tricyclics because of apparent lack of efficacy [l]. This question was recently reopened by a report of positive effects of the combination [14]. The package insert for fluoxetine General Hospital Psychiatry 13, 128-137, 1991 0 1991 Elsevier Science Publishing Co., Inc. 655 Avenue of the Americas, New York, NY 10010

Electroconvulsive Therapy: Current Concepts

contains a warning about possible prolongation of seizure duration, but this was not observed in a recent study [15]. Efforts to define reliable predictors of response to ECT have not been more successful than for drugs [l]. Atypical features, such as high mood reactivity, bulimia, and high anxiety suggest a poor response, but the many exceptions support a trial of ECT when other methods fail.

Mania Retrospective studies, reviewed in 151, have shown that ECT had roughly equivalent efficacy in manic episodes to lithium and neuroleptics. Two smaller prospective studies [16, cited in 11 found somewhat better results with ECT. Although ECT was also often useful for patients who did not respond adequately to these agents, the advent of other drugs [17] has reduced the necessity for ECT to the occasional patient who still fails to improve. Prolonged manic episodes are notoriously taxing, however, so that the utility of ECT before trials of these newer agents is similar to that for depression, although postrecovery prophylactic use of the drugs has been more extensively studied than ECT.

Catntonic

States

Although due to a variety of causes, catatonic states generally respond better to ECT than to neuroleptics [l]. The role of benzodiazepines in such situations is a subject of current interest [18] that is further discussed below. The type of catatonia, which follows a period of maniclike excitement, is a specific indication for ECT [19].

Atypical Psychoses This heterogeneous group characterized by isolated delusions and/or hallucinations and a recurrent or cyclic course sometimes responds to ECT after failure to benefit from neuroleptics or other drugs.

Schizophrenic

Disorders

Neuroleptics supplanted the use of ECT in these conditions before the development of current diagnostic criteria so that the potential role of ECT is unclear [1,4]. Although the response of chronic schizophrenics has generally been poor, some recent studies have suggested synergistic effects of neuroleptics and ECT [20,21]. The possible role of

ECT in treating complications be discussed below.

of neuroleptics

will

Misceflaneous Beneficial effects of ECT in delirium due to many causes have been reported [4,22], but no clear indications are apparent even for experimental use. A paradoxical benefit in intractable seizures [23] or episodic dyscontrol[24] may be related to anticonv&ant effects of ECT. ECT was also beneficial in some cases of phencyclidine psychosis that had not responded to neuroleptics [25]. The potential role of ECT in Parkinson’s disease will be discussed below [26].

Risk/Benefit

Considerations

The mortality associated with ECT is about l/10,000 patients [l], similar to other minor procedures involving anesthesia. The principal potential morbidity results from the cardiovascular stimulation and increased intracranial pressure associated with ECT. Since there are no longer any absolute contraindications [5], the indications and absence of alternatives would be the determining factors in such situations. An advantage of ECT is that the exposure is punctate and in a setting where medical complications are best handled in contrast to drugs whose potentially serious complications may occur when medical intervention is not possible. This factor supports greater usage in the elderly and has a specific application in mania during the first and third trimesters of pregnancy. In the absence of suicidal or similar danger or when the acute illness has subsided, outpatient ECT is quite feasible if an adequate support system is available to escort the patient and report evidence of relapse or complications. The principal long-term morbidity of ECT involves memory disturbance. Although current technology has allowed great reduction in incidence and severity of this complication, it remains a concern and will be discussed below.

Treatment Procedures Protocols for the general hospital appear in [1,4]. Anesthetic considerations are discussed in [1,27,28]. A check list is provided in Table 1. The pre-ECT work-up is similar to that for other procedures involving anesthesia. This includes 129

C. Pearlman

Table 1. Medical Considerations

for ECT

HEENT Increased intracranial pressure (relative contraindication) Recent stroke, aneurysm (avoid hypertension) Epilepsy (hold daily anticonvulsants until after ECT) Skull defect (adjust electrode placement to avoid it) [29] Retinal detachment treated by permanent buckle may be harmed by intraocular pressure during ECT (eye consultation) Glaucoma (check anterior chamber and medication) [ 301 Loose or damaged teeth (may need special mouth guard) Cardiovascular Recent myocardial infarct or heart failure (relative contraindications) Arrhythmias (pre-ECT oxygenation; have lidocaine, atropine, defibrillator available) Pacemaker (switch to fixed mode when appropriate) Aneurysm, valve replacement, aortic graft (avoid hypertension) ECT may cause benign T-wave inversion (suggestive of subendocardial infarct) Respiratory Infection (postpone ECT until resolved) COPD (high theopylline level may prolong seizures) [ 311 Asthma (have theophylline, epinephrine ready) Gastrointestinal Active GI bleeding (relative contraindication) Urological Prostatic hypertrophy (insure bladder emptying before ECT) Bones and joints Susceptibility to pathological fracture (increase succinylcholine for complete paralysis) [32] Rheumatoid arthritis (cervical spine X-ray to assess erosion of odontoid process) Systemic Personal or family history of low pseudocholinesterase (measure blood level; use test dose of 2 mg succinylcholine) Endocrine Diabetes (hold insulin until after AM ECT; l/3 normal AM dose for Pheochromocytoma (adequate beta-adrenergic blockade)

PM

ECT)

Special situations Pregnancy (fetal monitoring) [33] Paraplegia, muscle trauma, extensive burns (use curariform for relaxation to avoid hyperkalemia with succinylcholine) Hemodialysis (treat day after dialysis when K+ normal) [34] Drug interactions Echothiopate (topical anticholinesterase for glaucoma) should be stopped 3 weeks before ECT or use curariform for relaxation MAO inhibitors, digitalis, quinidine, several gram-negative antibiotics, and cyclophosphamide also may potentiate succinylcholine Lithium may cause neurotoxicity [35] Lidocaine greatly decreases seizure duration (possibly reduced efficacy) Anticoagulants (theoretical increased risk of bleeding); maintain prothrombin time at 1.5-2 times control or switch to heparin and give ECT at trough level (361 Reserpine (severe hypotension) should be stopped 48 hr before ECT

130

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items such as possible adverse reaction to barbiturates or anticholinergic drugs and evidence or family history of abnormal response to succinylcholine (drug interactions, prolonged apnea, malignant hyperthermia). The presence of relative contraindications listed in Table 1 would trigger the risk/benefit considerations discussed above. When feasible, pretreatment hypertension should be controlled by appropriate medication. Alternatives are discussed below. Informed consent is complicated by the inherent nature of psychiatric disorders. Detailed guidelines for issues to be covered are listed in [5]. These include such items as a range of the likely number of treatments, description of the procedure, and the indications, alternative treatments, and possible complications. The process generally involves discussion with the patient and family, consultation with other psychiatrists when indicated, and occasional court appearances when local statutes require judicial approval for treatment of incompetent patients. Legal issues are reviewed in [1,2,37]. Educational videotapes [38,39] may be helpful for persons who have been influenced by anti-ECT propaganda or negative imagery in popular films. ECT is best performed in an area devoted to procedures involving brief anesthesia with access to a recovery suite. The anxiety involved in taking a patient from a psychiatric unit to this area can be minimized by preanesthetic medication and the presence of nursing personnel known to the patient. Pentobarbital 50-100 mg, given i.m. about an hour before ECT, is usually effective for sedation. Benzodiazepines should be avoided for this purpose because of possible interference with ECT efficacy [40]. Patients receiving regular treatment with these agents should be switched to one without active metabolites, and none should be given for 8 hours before ECT. Occasional patients who are normotensive, who have labile hypertension not requiring treatment, or whose hypertension is poorly controlled, become significantly hypertensive just before or following ECT. Although the absence of reported stroke or cardiac infarction or failure in such cases is reassuring [41], prudence suggests efforts to modulate the blood pressure elevation associated with ECT. When pulse is significantly elevated, a short-acting beta-blocker, such as labetalol, may be given i.v. immediately before ECT. When pulse is not elevated, i.v. hydralazine before ECT will reduce peripheral resis-

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tance. Sublingual nifedipene has also been useful [42]. The ECT stimulus produces a vagal discharge that is ordinarily counteracted by the sympathoadrenal activity accompanying a convulsion. Preanesthetic administration of an anticholinergic agent is indicated to avoid prolonged asystole when beta-blockers are used, especially in cases involving subconvulsive stimuli, which may be accidental or part of the determination of convulsive threshold [43]. Routine use of anticholinergics is not indicated, but they may be helpful in managing excessive secretions and in patients with partial A-V block. Negative aspects of anticholinergics are increased hypertensive reaction [ 11 and possibly increased posttreatment confusion in the elderly [44]. Thus, such use should be decided on an individual basis [5]. The standard anesthetic agent for ECT is methohexital although thiopental is also acceptable. The occasional patient who is allergic to barbiturates can be anesthetized with etomidate [5]. The standard muscle relaxant for ECT is succinylcholine except in a few medical conditions noted in Table 1. Although succinylcholine is known to provoke malignant hyperthermia in susceptible individuals, no case has ever been reported with ECT despite the likelihood that hundreds of patients were at risk in view of the estimated incidence of l/16,000 procedures [45]. Pharmacokinetic aspects of the use of succinylcholine for ECT [46] may be responsible for this situation. Total paralysis is generally required in patients susceptible to pathological fractures, which should be monitored by a nerve stimulator. Even with optimal paralysis, however, the ECT current causes contraction of jaw muscles so that a flexible block between the jaws is necessary to avoid tooth damage [l]. Residual muscle activity during the convulsion also produces carbon dioxide so that hyperventilation during the postictal period is necessary to prevent hypercapnia [47]. Continuous cardiac monitoring should be used as for any procedure involving anesthesia. The question of EEG monitoring remains unresolved [5]. Its clinical utility is clear only in cases requiring total paralysis or the rare example of persistent CNS seizure without motor signs, but its use is consistent with the current tendency to study effects of ECT on CNS activity more carefully [l]. Brief pulse technology, which permits seizure induction with much less electrical energy than with the sine-wave current available from electric outlets, has become standard in the most widely used ECT machines [l]. With these machines, low131

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resistance contact between electrodes and scalp is a critical factor. Adequacy of this contact should be tested before the patient is anesthetized and repeated immediately before the ECT stimulus. Contact can be improved by vigorous pressure with hand-held electrodes. In addition, situations involving relatively low impedance, such as a patient with a narrow skull receiving bilateral stimulation, require a longer stimulus duration to reach the convulsive threshold [l]. Fortunately, these new machines have sufficient energy output to induce seizures in almost all patients, although exceptions occur because of the arbitrary limit of about 100 joules. The conventional definition of an adequate seizure is 25 seconds of motor activity [48], and animal [49] and human [l] studies have suggested a rough correlation between stimulus energy and seizure duration. Shorter seizures, however, do not necessarily reduce efficacy [5], and as discussed below, seizure duration may be more relevant for unilateral stimulation. Seizure prolongation may be achieved by hyperventilation [50] or use of caffeine [51]. Whereas a seizure is a necessary concomitant of effective ECT, the nature of the optimal stimulus is much less clear 1481, as is discussed below. The optimal frequency of treatment is also unclear [52]. The standard practice of three per week in this country and two per week in Europe was established empirically long before the advent of knowledge about expected treatment course with psychotropic drugs. The only direct comparison of thrice versus twice weekly ECT for depression in matched patient samples showed no significant difference in improvement after 4 weeks 1531. Preliminary results of a prospective controlled study of this issue noted equivalent efficacy after 4 weeks, but suggested more rapid improvement with thrice weekly ECT [54]. More rapid improvement with four versus two ECT treatments per week had previously been reported [55]. A switch from thrice to twice weekly at our facility in 1984 supported the impression of similar ultimate improvement, but assessment of rate of improvement is still under investigation. Occasional logistic problems, which resulted in a patient receiving ECT only once per week near the beginning of treatment, were more clearly associated with delayed improvement. A recent study of manic patients showed no difference between three and five treatments per week [56], and we have had good results with two ECT treatments per week. The related question of greater rapidity of antidepressant effects by pro132

ducing several seizures during a single session (multiple-monitored ECT) remains controversial. The literature is reviewed in [l] with methodologic criticisms, which were addressed in a recent study [57]. Beneficial effects of two seizures per session were noted in some depressed patients who had not responded to one seizure per session [58]. The controversy concerning relative efficacy of unilateral and bilateral electrode placement [l] has been clarified by two recent reports. One showed that use of stimulus intensities near the convulsive threshold with unilateral placement was associated with greatly reduced efficacy 1591. The other noted that development of prominent right-sided EEG slowing with right unilateral stimulation was similarly associated with reduced efficacy [60]. Determination of the convulsive threshold is a bit cumbersome as is formal EEG study to detect unilateral slowing, and the degree of suprathreshold stimulation necessary to achieve equivalent efficacy with unilateral placement is still being studied. Moreover, much less cognitive disturbance is associated with bilateral brief-pulse stimulation than that which occurred with sine-wave equipment [61], although the importance of moderately suprathreshold stimulation for optimal efficacy was recently noted [62]. Thus, the advice to use unilateral stimulation except when the risk associated with failure was high has shifted [48]. One strategy is to begin with bilateral brief-pulse stimulation and to switch to unilateral after signs of improvement [l] or if troublesome cognitive side effects appear. If evasion of memory disturbance is a prime consideration [5], one can begin with right unilateral stimulation estimated to be moderately suprathreshold with adjustment of stimulus energy to produce seizures lasting 40-120 seconds. In general, this requirement is higher for men than women and increases with age [43]. If no improvement is noted after 2 weeks, switching to bilateral placement is advised. Cognitive side effects may also be reduced with twice weekly ECT. The time-course of improvement with ECT resembles that of antidepressant drugs-occasional remission after 1-2 treatments, modal results after 3-4 weeks, and occasional maximal response following 20 or more ECT treatments. If no response has occurred after 12 ECT treatments, however, benefit from more is unlikely [l]. Most patients will not relapse once improvement has reached a plateau. Drug treatment, however, is generally continued for 4-6 months, and neurotransmitter receptor alterations produced by both drugs and

Electroconvulsive

ECT return to baseline about 2 weeks after discontinuation. Thus, relapse within a few weeks after a successful course of ECT may occur [5]. Several studies have shown that subsequent use of tricyclics or lithium prolonged the interval between depressive episodes [1,63]. It has been suggested, however, that since most patients currently receiving ECT have already failed one or more drugs, the indications for such treatment are questionable [64]. Nevertheless, prophylactic benefit despite inability to treat an acute episode is possible, and the continual advent of new agents requires testing in patients who have failed other drugs. ECT at intervals of 1-4 weeks has also been used to treat such relapses 15,121. We have had similar results with this practice. Most patients are able to discontinue treatment after 4-6 months, but as with an occasional patient who reantidepressants, lapses whenever the treatment is stopped appears to benefit from indefinite maintenance ECT. Posttreatment complications are usually mild, such as headache related to the transiently increased intracranial pressure. Uncommon but serious problems, such as allergic reactions, bronchospasm, arrhythmias, and prolonged apnea due to low pseudocholinesterase can be treated in collaboration with the anesthesiologist. The occasional occurrence of prolonged seizures should be managed with continued hyperventilation and i.v. use of a benzodiazepine [5]. Severe posttreatment agitation can be managed with mechanical restraint and use of i.v. midazolam. Some patients may respond better to i.m. haloperidol 1 hour before ECT. This complication also shows puzzling variability, ranging from an isolated occurrence to occurrence during only one of several ECT series to increasing severity during a single course [65]. EEG effects of ECT are reviewed in [l]. ECT-related cognitive and memory disturbance has been extensively studied [1, 3-51 and is commonly linked to concern that ECT may produce brain damage. Although there is considerable individual variability, such impairment usually becomes apparent after about six treatments and varies from amnesia for the procedure to a spotty memory loss for names and similar information. Occasional patients become quite confused. These problems typically clear within a few weeks. Some patients complain of persistent memory disturbance but show no objective evidence of dysfunction. Pre- and posttreatment testing with sophisticated measures of autobiographical memory has shown persistent amnesia for some experi-

Therapy:

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ences or personal details occurring within a few years before bilateral treatment with sine-wave stimulation. Such disturbance was less extensive with brief-pulse stimulation and was not found with unilateral treatment [61]. The question of brain damage has been studied with pre- and posttreatment CT and MRI scans [66-681, enzyme markers, and cerebral blood flow and metabolism without evidence of ECT-related pathology except for transiently increased permeability of the bloodbrain barrier [1,3,4]. The memory dysfunction seems related to consolidation and/or retrieval processes [69]. Vasopressin has been suggested to be involved in such processes but was ineffective in treating ECT-induced disturbance [70]. Nootropic agents, such as piracetam and related compounds, have been reported to reverse amnestic effects of electrically induced seizures (ECS) in animals [71] but have not yet been tested with ECT.

Mechanism

of Action

Research in this area is active, but, as with psychotropic drugs, the absence of suitable animal models is a severe obstacle. The wide spectrum of ECT effects (antidepressant, antimanic, antipsychotic) also complicates these efforts. One approach has focused on effects of ECS in rodents with a schedule similar to that of ECT [72,73]. The results have generally resembled those of antidepressant drugs on measures of noradrenergic receptor function. Studies of serotonin function have shown up-regulation of cortical 5-HTz receptors in contrast to the down-regulation conventionally observed with drugs. Although this finding may not be clinically relevant [73], current hypotheses of antidepressant action that involve facilitation of 5HT,, function by down-regulation of 5-HT, activity [74] imply that 5-HTz up-regulation might be involved in the antimanic effect of ECT. Similar 5HT, up-regulation was found with the antimanic agent, valproate, although not with carbamazepine [75]. An alternative hypothesis for moodstabilizing action has proposed possible limbic anticonvulsant effects [3,23,24,76]. Repeated ECS generally produced down-regulation of muscarinic cholinergic receptors in contrast to no effect with tricyclics. This was suggested as a possible mechanism for ECT-induced amnesia [77]. Nootropic agents also have been found to counteract amnesia induced by a single ECS or scopolamine injection [78]. Unlike most antidepressants except stimulants, ECS showed a clear facilitation of many 133

C. Pearlman

measures of dopaminergic function, although the effects on dopaminergic receptors are more complex [79]. Similar studies have been performed for opiate and other peptidergic receptors and secondmessenger effects involving cyclic AMP and phosphatidyl inositol [80]. Neuroendocrine effects have also been studied in both animals and humans, but without clear implications [ 1,3,4]. Another series of studies focused on the possible relationship between neurophysiologic mechanisms involved in the EEG alterations associated with ECT and the therapeutic effects [81]. A third approach has considered ECT as a form of brain stimulation instead of just a convenient way to produce a convulsion. Thus, beneficial effects were ascribed to increased secretion of a peptide, euthymesin, produced by stimulation of hypothalamic/limbic structures [82]. A pharmacologic basis for this idea is found with partial agonists. When the basal output of a transmitter is deficient, such agents act as agonists, but when the basal output is high, their competition with the transmitter for receptor sites has antagonist effects [cf. 831. A similar intracellular hypothesis is discussed in [84].

General Discussion The facilitation of dopaminergic function by ECT has suggested application to Parkinson’s disease, where improvement in both mood and movement disturbance has frequently been noted [26,85]. Possible mechanisms are reviewed in [79]. ECT has also been found to counteract psychotomimetic effects of dopaminergic agents, which had been a limiting factor in the treatment of some patients with Parkinson’s disease [86]. Finally, ECT counteracts neuroleptic-induced Parkinsonism [87], and ECS does not produce striatal dopamine-receptor supersensitivity like neuroleptics nor tardive dyskinesia. Thus, maintenance ECT also deserves further study either as an adjunct or alternative to neuroleptics in schizophrenic and schizoaffective disorders. A related issue is the management of patients with neuroleptic malignant syndrome (NMS). Although this complication is rare, it is much more prevalent in patients with affective disorders, like other extrapyramidal side effects [88]. Use of ECT is reviewed in [89]. Although most recent severe cases of NMS have responded to treatment with dopamine agonists and/or muscle relaxants, occasional examples that have subsequently responded 134

only to ECT have suggested possible coexistence of NMS and a catatonic state that is difficult to differentiate from neuroleptic-induced muscular rigidity. Although benzodiazepines have been useful in catatonic states [18], and animal work has suggested a model for benzodiazepine antagonism of muscular rigidity due to dopamine deficiency, this effect is unpredictable due to the complexity of the relevant receptor relationships [SS], and benzodiazepines have not been useful in Parkinson’s disease. Accordingly, ECT seems indicated in catatonic patients who have not responded to benzodiazepines. Guidelines for treatment of patients who fail to respond to ECT are unclear. Contrary to previous impressions, medication resistance in depressed patients was recently noted to be associated with ECT resistance [90]. One study noted substantial persistence of depressive symptoms for the next 6 months despite drug treatments [91], whereas another found good response to antidepressants, especially clomipramine [92]. Some cases of improvement after addition of lithium to antidepressants have also been reported 1931. Diagnostic review of three of our cases suggested that the target symptoms of major depression or atypical psychosis had been distorted by borderline personality disorder. A few other patients with a history of depressive episodes responsive to ECT, which then failed, improved with methylphenidate and/or an MAO inhibitor. These situations may be confounded by treatment order effects and the natural history of depressive episodes. For example, a patient who had failed outpatient drug treatment, a course of 20 ECT treatments, and several additional trials of drugs and psychotherapy during a year of hospitalization, had a remission after a course of six ECT treatments. An area with little data is the use of ECT in children and adolescents. Anecdotal results in depressive and manic syndromes are reviewed in [1,94]. Guidelines are presented in [5]. From a training perspective, there is a disparity between advances in ECT and resident interest in mastering it compared to psychopharmacology. Persons drawn to psychiatry are less interested in minor surgical procedures like ECT. Although the division of labor between internists and surgeons works well enough, application to psychiatry is complicated by the necessity for repeated induction of ECT over a period of weeks in conjunction with monitoring of the clinical course. Thus, when the responsible psychiatrist does not perform ECT, the

Electroconvulsive

potential for inefficient or inappropriate care arises. While refusal of ECT may often be ascribed to the patient, family, or public opinion, the possible effect of a psychiatrist who is unable to explain convincingly the risk/benefit issues or to conduct the treatment also deserves consideration. Training issues are further discussed in [5].

References

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6.

7. 8.

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10.

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13.

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1.5.

16.

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AJ: Alternatives to lithium for 17. Prien RF, Gelenberg preventive treatment of bipolar disorder. Am J Psychiatry 146:840-848, 1989 and cata18. Menza MA, Harris D: Benzodiazepines tonia: An overview. Biol Psychiatry 26:842-846, 1989 19. Mann SC, Caroff SN, Bleier HR, et al: Lethal catatonia. Am J Psychiatry 143:1374-1380, 1986 20. Gujavarty K, Greenberg LB, Fink M: Electroconvulsive therapy and neuroleptic medication in therapyresistant positive-symptom psychosis. Convulsive Ther 3:185-195, 1987 21. Dodwell D, Goldberg D: A study of factors associated with response to electroconvulsive therapy in patients with schizophrenic symptoms. Br J Psychiatry 154:635-639, 1989 22. Hsiao JK, Messenheimer JA, Evans DL: ECT and neurological disorders. Convulsive Ther 3:121-136, 1987 23. Sackeim HA, Decina I’, Prohovnik 1, et al: Anticonvulsant and antidepressant properties of electroconvulsive therapy: A proposed mechanism. Biol Psychiatry 18:1301-1310, 1983 24. Schnur DB, Mukherjee, S, Silver J, et al: Electroconvulsive therapy in the treatment of episodic aggressive dyscontrol in psychotic patients. Convulsive Ther 5:353-361, 1989 25. Dinwiddie SH, Drevets WC, Smith DR: Treatment of phencyclidine-associated psychosis with ECT. Convulsive Ther 4:230-235, 1988 26. Douyon R, Serby M, Klutchko B, et al: ECT and Parkinson’s disease revisited: A “naturalistic” study. Am J Psychiatry 146:1451-1455, 1989 27. Selvin BL: Electroconvulsive therapy-1987. Anesthesiology 67:367-385, 1987 28. Marks RJ: Electroconvulsive therapy: Physiological and anaesthetic considerations. Can Anaesth Sot J 31:541-548, 1984 29. Hartmann SJ, Saldivia A: ECT in an elderly patient with skull defects and shrapnel. Convulsive Ther 6:165-171, 1990 30. Nathan RS, Dowling R, Peters JL, et al: ECT and glaucoma. Convulsive Ther 2:132-133, 1986 31. Devanand DP, Decina I’, Sackeim HA, et al: Status epilepticus following ECT in a patient receiving theophylline. J Clin Psychopharmacol 8:153, 1988 32. Levy SD: “Cuff” monitoring, osteoporosis, and fracture. Convulsive Ther 4:248-249, 1988 33. LaGrone D: ECT in secondary mania, pregnancy, and sickle cell anemia. Convulsive Ther 6:176-180, 1990 34. Pearlman C, Carson W, Metz A: Hemodialvsis, chronic renal failure, and ECT. Convulsive ?her 4:332-333, 1988 35. Penney JF, Dinwiddle SH, Zorumski CF, et al: Concurrent and close temporal administration of lithium and ECT. Convulsive Ther 6:139-l-25, 1990 36. Tancer ME, Evans DL: Electroconvulsive therapy in geriatric patients undergoing anticoagulation therapy. Convulsive Ther 5:102-109, 1989 37. Rozovsky FA: Consent to Treatment. Boston, Little, Brown, 1989 38. Fink M: Informed ECT for Patients and Families. Lake Bluff, IL, Somatics Inc, 1986

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