The Death of Electroconvulsive Therapy


Hanafy Youssef, D.M., D.P.M., F.R.C.Psych.
Ross Thomson Unit
Route Hospital
Ballymoney, County Antrim
Northern Ireland

Fatma Youssef, D.N.Sc., M.P.H., R.N.
Professor of Nursing Science
School of Health Professions
Marymount University
Arlington, Virginia, USA

ABSTRACT

In Italy, where it began more than 62 years ago, ECT has almost been abolished. In some countries, however, ECT is still used inappropriately, particularly in elderly patients. There is no medical, moral, or legal justification for ECT, and the new requirements of modern psychiatric practice can all be achieved without it. Like prefrontal lobotomy and all previous shock treatments, ECT is non-viable. The death of ECT will help promote mental health and put the treatment where it belongs - in the archaeology of science.

INTRODUCTION

The introduction of electroconvulsive therapy (ECT) into psychiatry and the enthusiasm with which it was adopted coincided temporally with the lack of other therapies for mental illness. Indeed, evidence that ECT has a beneficial effect is sparse. In contrast, there are many indications of its ineffectiveness and association with various forms of harm. The role of ECT in modern psychiatry needs re-evaluation, and the time may have come to abandon this unscientific treatment.1

By directive of the Minister of Health, use of ECT has been nearly abolished in Italy, where it began 62 years ago.2 Curiously enough, the Minister's instruction stirred no protest by that country's medical profession, and many psychiatrists welcomed the pronouncement. It is encouraging to know that ECT is nearly obsolete in Germany and Holland.

In Italy, the commission convened to evaluate ECT stated that the procedure was out of line with recent trends and was distinguished by improper use and abuse. Moreover, despite considerable research in recent decades, its mode of action had not been clarified. One commission member described ECT as belonging to the archaeology of science, adding that it should be acknowledged only for what it meant in the 1940s.

Notions that ECT could become more humane by legislation and the intervention of professional societies and colleges are an illusion. As a 1998 report stated, "Two thirds of ECT clinics fall short of the most recent college standards, particularly in relation to the frequency of Consultant attendance and training of junior doctors. These problems have not been fully resolved by 20 years of audit and college activity. There should be a continuing debate as to what future intervention might be considered."3

Is ECT Still Abused?

In the past, inappropriate uses of ECT were brought to light by patients and pressure groups. The history of ECT, its abuse, and resultant unfavorable publicity are responsible for its increasingly reduced use.1 We have been told that various bills introduced by legislators in the United States, professional societies, and the UK Royal College of Psychiatrists would make abuse a thing of the past.4,5 But it still exists, as this case report indicates. A 30-year-old patient committed suicide while undergoing ECT at Gartnaval Hospital in Scotland.6 Hospital records stated that he had refused ECT again and again. Health officials were accused of negligence leading to his death, and his family was awarded 50,000. This case exposed the UK's system of a required second opinion before use of ECT as a farce.

In spite of the Mental Health Act and various guidelines to safeguard against coercive treatments, an estimated 20,000 patients a year receive ECT in the United Kingdom, where many foreign doctors receive their psychiatric training. It is therefore not surprising that ECT is big business in private clinics and private hospitals in developing countries.

As the case report showed, ECT is not a suicide preventive.7 In fact, the mortality risk after ECT is higher than in patients who do not receive ECT.8 Death due to ECT may be rare, but the procedure can sometimes be fatal. A survey of all ECT treatments given with anesthesia in Denmark found a death rate of 1 in 22,000 treatments, ie, 4 to 5 unnecessary deaths per 100,000 treatments.9 In the past, when ECT was delivered without anesthesia, crush fractures of the vertebrae, among other fractures, occurred. Modified ECT with anesthesia and muscle relaxants is said to be safe; however, when death occurs, it is ascribed to the risk of anesthesia. Yet a significant proportion of anesthetists prefer not to become involved in ECT practice and research.10

Abuse of ECT in the young has surfaced in the past, but abuse in the elderly may go unnoticed.

ECT in the Elderly

ECT continues to be described as one of the most effective treatments for serious depressive disorders in the elderly, despite the memory disturbance and confusion that often accompany its use.11 An old person who refuses ECT may nevertheless be subjected to this procedure by formal certificate under the (UK) Mental Health Act. One defender of ECT in the elderly claimed that "Surgical procedures like mastectomy and episiotomy are accepted without any comments and ECT seems to be judged by different rules, often irrationally. So it is important that psychiatrists should not be apologetic about ECT."12 For this individual, who admits to no absolute contraindication to its use, ECT is even recommended as a treatment of dementia. Moreover, according to one survey, 20% of British psychogeriatricians have been administering maintenance ECT for many years.13 To justify its use, a video was prepared to educate the elderly. Some researchers judged that videos were unhelpful for this purpose.14

In the elderly, anxiety may increase and worsen with further treatment.15 Confusion is common. Undue confusion after ECT may be managed by lengthening the interval between treatments.16 Bilateral ECT causes lasting effects on memory,17 but in most cases, the elderly receiving ECT were provided no adequate explanation about possible risks.18 The widely used Ectron Series 5A machine has a maximum output of 700 millicoulombs (MC) but is underpowered for patients with a high seizure threshold, who are often elderly. These patients, it is claimed, need the 750- MC Thymatron DGX machine.19

When confusion intensifies with treatment and ECT fails, the fault is often laid at the feet of the elderly patient, who is characterized as hypochondriac and neurotic, with diminished intellect.20 The relapse rate of depressive illnesses is high unless therapy continues with antidepressant medications.21 ECT is given generally twice or thrice weekly, though the latter schedule conferred no advantage over the former.

The claim that ECT has a role in the care of the severely depressed elderly patient ignores the impairment in autobiographical memory of subjective experience related to melancholia. Memory loss was severe in some ECT patients but was not observed in those receiving antidepressants.23 The course of ECT is usually 6 to 12 treatments, and proponents of this procedure claim that the risks are related to anesthesia. One wonders how often these psychiatrists have had a general anesthetic to justify their anesthetizing elderly patients 12 or more times in 2 to 3 months.

Convulsion and Anticonvulsion in the Treatment of Affective Disorders

Cerebral electrical seizure is central to the claimed therapeutic effect of ECT. The issue becomes complicated when one takes into account the value of anticonvulsants, which are now used widely in the treatment and prevention of affective disorder. We thus have seizures and pharmacologic anticonvulsants exerting antidepressant effects.

Carbamazepine is reported to have antidepressant properties in some severely depressed patients.24 Controlled and uncontrolled trials estimated that about 65% of bipolar patients respond well to this drug.25 Sodium valproate also may have useful prophylactic effects in patients with refractory bipolar illness who show a poor response to lithium.26

The mechanisms of action of anticonvulsants that ameliorate mental disorders make sense according to biochemical models of depression.

Carbamazepine blocks neuronal sodium channels and, like lithium, facilitates some aspects of brain serotonergic function in humans.27 Sodium valproate can slow the breakdown of the inhibitory neurotransmitter of gamma-aminobutyric acid. Anticonvulsants affect the second messenger system (adenylate cyclase and phosphoinositide), which is linked to the central action of catecholamines,28 and act directly on monoamines, apparently reducing dopamine turnover.29

A mechanism of action of ECT has been pursued without success, although psychological and biological explanations have been proposed. The result is a strange situation in which psychiatrists attempt to treat the brain with drugs and electricity. Early psychological explanations included the "fear hypothesis" - shocking the brain to bring the patient face to face with a healthy reality 30 - and the "regression and punishment hypotheses" - in which treatment is rendered by a strict but forgiving father figure. Once treatment is concluded, guilt and fear are resolved.

Contemporary proponents claim that during ECT the seizure threshold of patients tends to increase.31 Shocking the brain with electricity may lead to changes in central neurotransmitter receptors and release of certain hormones.32 In rats, ECT alters noradrenaline pathways.33 These changes are short-lived, and the findings are pseudoscientific in that evidence for a lasting effect on the psychiatric illness is lacking. After more than 60 years, proponents admit that the mode of action is not known but aver that their clinical experience is more impressive than the philosophy of science. Indeed, this attitude provides further proof that "electricity is a form of treatment based on force and fraud, and justified by medical necessity.... It requires the sacrifice of the patient as a person, of the psychiatrist as a clinical thinker and moral agent."34

The ECT Debate

Five key questions form the debate about ECT.35

First, does ECT correct a dysfunctional neurophysiologic mechanism or merely cause neurologic dysfunction? ECT corrects nothing; it causes acute organic brain syndrome. Indeed, it can make the electroencephalograph difficult to interpret for a time, as each fit is followed by generalized theta and delta activity, which persists with successive electric treatments. As therapy proceeds, the disturbance becomes more widespread and involves higher voltage; alpha activity also may disappear.36

Second, are the immediate documented benefits of ECT confirmed in long-term follow-up studies? Evidence of beneficial action of ECT is inadequate, and, as the Northwick Park Trial demonstrated, may be primarily a placebo effect.37 In that trial, 70 patients with endogenous depression were randomly allocated to eight real or eight simulated ECT treatments. No difference was found between the groups at 1- and 6-month follow-ups. The conclusion is that antidepressant effects of ECT are transient. The favorable response to simulated ECT highlights the importance of nursing, pharmacotherapy, and attention, even in severe cases of depression. No studies have documented that long-term prognosis improved with ECT. Long-term harm in some patients is well known, however.

Third, are present methods for obtaining informed consent sufficient? The long history of ECT abuse shows that the patient's freedom of choice is rare - a state of affairs described as "shameful."38 Coercion has involved the threat of detention and the promise of discharge. A patient who consents to ECT is deemed capable of understanding its nature, purpose, and likely effect in spite of coexisting memory disturbance, anxiety, and pessimism. Refusal of ECT, on the other hand, triggers a second opinion from another medical practitioner and forcible use of the procedure.

Fourth, can the alleged life-saving function of ECT be fulfilled by another treatment at less cost to the patient's well-being? Modern psychiatry favors a biological approach to treating mental illness. There is no need to shock the brain with electricity and call it a life-saving therapy.

Fifth, are the observable side effects the only side effects, and is their diminution over time more apparent than real? Those who administer ECT may accept anxiety, headache, confusion, nausea, and vertigo as minor problems. The issue of ECT-induced brain damage has been compared with that from boxing.39

CONCLUSION

There is no medical, moral, or legal justification for ECT. Like prefrontal lobotomy and all previous forms of shock treatment, ECT is nonviable. The debate about ECT is political, not scientific. Old Psychiatry armed with ECT was an attempt at social and political control. Contrary to one view, ECT is an assault on the patient's brain.40 In this millennium, psychiatrists will make use of knowledge in social sciences, psychiatric epidemiology, and psychopharmacology. They will not need to know about better ECT machines and weigh spurious claims of a proven worth in clinical experience.

The measures against ECT in Italy and other European countries show that this is a dying therapy. Nothing less than a total ban will help promote mental health and close this shameful chapter in the history of psychiatry.

REFERENCES

1. Youssef HA, Youssef FA. Time to abandon electroconvulsion as a treatment in modern psychiatry. Adv Ther. 1999;16:29-38.

2. Bourne H. Electroconvulsive therapy ending where it began. Psychiatr Bull. 1999;23:505.

3. Duffet R, Elliot P. Auditing electroconvulsive therapy. The third cycle. Br J Psychiatry. 1998; 172:401-405.

4. American Psychiatric Association. Task Force on Electroconvulsive Therapy. Report 14. Washington, DC: American Psychiatric Association; 1978.

5. Royal College of Psychiatrists. Memorandum on the use of electroconvulsive therapy. Br J Psychiatry. 1977;131:261-272.

6. Daly M. Electric shock victim wins historic victory. The Big Issue. 1999;10:5.

7. Fernando S, Storm V. Suicide among psychiatric patients of a district general hospital. Psychol Med. 1984;14:661-672.

8. Babigian HM, Gurrmacher LB. Epidemiological consideration in electroconvulsive therapy. Arch Gen Psychiatry. 1984;41:246-253.

9. Heshe J, Roeder I. Electroconvulsive therapy in Denmark. Br J Psychiatry. 1976;128:241-245.

10. Haddad DM, Benbow SM. Anaesthetists' views of electroconvulsive therapy clinic. Psychiatr Bull. 1993;17:655-657.

11. Clyma EA. Unilateral electroconvulsive therapy. How to determine which hemisphere is dominant. Br J Psychiatry. 1975;126:372.

12. Wilkinson D. ECT in the elderly. In: Holmes L, Howard R, eds. Advances in Old Age Psychiatry: Chromosomes to Community Care. Worthing, UK: Wrighton Biomedical Publishing; 1977:161-171.

13. Benbow SM. Old age: psychiatrists' views on the use of ECT. Int J Geriatr Psychiatry. 1991;6: 317-322.

14. Baxter L, Roy-Byrne D, Liston E, et al. Informing patients about electroconvulsive therapy: effects of video-tape presentation. Convuls Ther. 1977:2:25-29.

15. Abram R. Electroconvulsive Therapy. Oxford: Oxford University Press; 1988.

16. Sackeim HA. Use of electroconvulsive therapy in late life depression. In: Schneider LS, ed. Diagnosis and Treatment of Depression in Late Life. Washington, DC: American Psychiatric Press; 1994:259-277.

17. Squire LR. Memory function as affected by electroconvulsive therapy. Ann N Y Acad Sci. 1966; 466:307-314.

18. Freeman CP, Kendell RE. ECT: patients' experience and attitude. Br J Psychiatry. 1980;137:8-16.

19. Galloway J, Blakey A. Correspondence: ECT in the elderly. Psychiatr Bull. 1998;22:714.

20. Hobson RF. Prognostic factors in electric convulsive therapy. J Neurol Neurosurg Psychiatry. 1953; 16:275-281.

21. Sackeim HA, Prudie J, Devanand DP, et al. The impact of medication resistance and continuation of pharmacotherapy on relapse following response to electroconvulsive therapy in major depression. J Clin Psychopharmacol. 1990;10:96-104.

22. Gangadhar BN, Janakiramiah N, Subbakrishna DK, et al. Twice versus thrice ECT in melancholia: a double blind prospective comparison. J Affect Disord. 1993;27:273-278.

23. Peretti CS, Danion JM, Grange D, Moubarek N. Bilateral ECT and autobiographical memory of subjective experience related to melancholia: a pilot study. J Affect Disord. 1996;41:9-15.

24. Post RM, Utide TW, Roy-Byrne PP, Joff RT. Antidepressant effects of carbamazepine. Am J Psychiatry. 1990;143:29-34.

25. Post RM. Anticonvulsants as adjuncts or alternatives to lithium in refractory bipolar illness. In: Amsterdam JD, ed. Advances in Neuropsychiatry and Psychopharmacology, II. Refractory Depression. New York: Raven Press; 1991:155-165.

26. McElory SL, Keck PM, Pope HG. Sodium valproate: its use in primary psychiatric disorders. J Clin Psychopharmacol. 1987;8:16-24.

27. Elphick M, Young JD, Cowen PJ. Effects of carbamazepine on dopamine and serotonin mediated neuroendocrine responses. Arch Gen Psychiatry. 1990;47:135-140.

28. Post RM, Weiss SR, Chung DM. Mechanism of action of anticonvulsants in affective disorders: comparison with lithium. J Clin Psychopharmacol. 1992;12:23s-35s.

29. Maitre L, Ballzer V, Mondadori C. Psychopharmacological and behavioural effects of anti-epileptic drugs in animals. In: Emrich HM, Okuma T, Muller A, eds. Anticonvulsants in Affective Disorders. Amsterdam: Elsevier Science; 1984:3-13.

30. Cook LC. Convulsion therapy. J Ment Sci. 1944;90:435-464.

31. Sackeim HA, Prudie J, Devanand DP, et al. Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med. 1993;328:839-848.

32. Grahame-Smith DG, Green AR, Costain DW. Mechanism of the antidepressant action of electroconvulsive therapy. Lancet. 1978;i:254-256.

33. Green AR, Heal DJ, Goodwin GM. The effect of electroconvulsive therapy and antidepressant drugs on monoamine receptors in rodent brain: similarities and differences. In: Antidepressants and Receptor Function. Chichester, UK: Wiley; 1986;123:246-267. Ciba Foundation Symposium.

34. Szasz TS. From the slaughter house to the mad house. Psychother Theory Res Pract. 1971;8:64-67. 35. Taylor JR, Carrol JL. Current issues in electroconvulsive therapy. Psychol Rep. 1987;60:747-758.

36. Lishman WA. Organic Psychiatry: The Psychological Consequences of Cerebral Disorder. London: Blackwell Scientific; 1987:111.

37. Johnstone EC, Deakin JF, Lawler P, et al. The Northwick Park Electroconvulsive Therapy Trial. Lancet. 1980;ii:1317-1320.

38. ECT in Britain: a shameful state of affairs. Lancet. 1981;ii:1207. 39. Templer DI. ECT and brain damage: how much risk is acceptable? Behav Brain Sci. 1984;7:39.

40. Fink M. ECT - Verdict: not guilty. Behav Brain Sci. 1984;7:26-27.