Treatment on the inpatient psychiatry unit at Rhode Island Hospital is predicated upon the biopsychosocial model elucidated by George Engel.1 This model posits that biological, psychological, and social factors are involved in the etiology of most illnesses, and that interventions should be directed toward problems in each of these domains. Thus, the program of care includes somatic therapies, individual psychotherapy, group psychotherapy, family therapy, occupational therapy, and mileau therapy.
One of the somatic therapies is electroconvulsive therapy (ECT). First developed in 1938, the practice of ECT has evolved into a sophisticated procedure.
The most common indication for ECT is an episode of major depression, an illness that has a lifetime prevalence of approximately 6% in the U.S. adult population. For this common illness, ECT is the most effective treatment available. A meta-analysis that compared the effectiveness of ECT to antidepressant medications found that the average response rate to ECT was 20% higher than that of tricyclic antidepressants and 45% higher than that of monoamine oxidase inhibitors.2 In every study that has compared ECT to a pharmacologic agent, ECT had either equal or superior antidepressant effects.3 Because newer antidepressant medications such as fluoxetine, venlafaxine, and nefazodone are no more efficacious than the tricyclics in treating major depression, it seems safe to state that ECT is as good or better than any antidepressant medication currently available.
The second most common indication for ECT is schizophrenia, and the related conditions of schizophreniform disorder and schizoaffective disorder. Other psychiatric indications for ECT include episodes of mania, catatonia, neuroleptic malignant syndrome, delirium, and affective and psychotic syndromes secondary to medical and neurologic disorders. In addition, patients with medication-resistant Parkinson's disease and epilepsy may benefit from a course of ECT; these effects are independent of antidepressant, antimanic and antipsychotic effects.
Although ECT is the most efficacious treatment for major depression, and useful for a variety of other diagnoses, it is underutilized. Ironically, the most efficacious treatment for depression is not our first-line treatment, and often not our second-line treatment. Several reasons account for this disparity. First, there is a general lack of knowledge about ECT, both in the community and even among physicians. Second, a stigma persists - the result of historical over-use, as well as Hollywood's negative portrayal of ECT. Finally, quasi-religious groups have used the media to broadcast unsubstantiated claims that all medical treatments of psychiatric illness, including ECT, are pernicious.12
Many of the patients receiving ECT at Rhode Island Hospital have comorbid medical illnesses, and some patients have serious multisystem problems and extensive medication regimens. ECT has been safely given to these patients, by taking advantage of the trained and experienced specialists available within an academic general hospital. In evaluating patients for ECT, our practice is to consult an internist (often a cardiologist) with regard to any contraindications for ECT. Particular attention is given to severe illnesses that present risks, including cardiovascular, neurologic, and pulmonary diseases. Other patients with specific risks for ECT include patients with a history of retinal detachment, glaucoma, orthopedic neck or back problems, gastroesophageal reflux, dental pathology, and pheochromocytoma. The pre-ECT evaluation also includes several laboratory tests: electrocardiogram, complete blood count with a differential count, and electrolytes. If any of these assessments yield abnormal data, additional tests may be necessary, including X-rays of the chest and spine, CT or MRI of the head, and electroencephalogram. In addition, women of childbearing age are assessed for pregnancy (ECT is generally safe for the fetus and pregnant mother). An anesthesiologist evaluates the patient, with an eye toward those medical conditions that are associated with substantial risk and are rated as a 4 or 5 on the 5-point physical status classification scale used by the American Society of Anesthesiologists.4
In performing ECT, each treatment begins with the staff verifying that the patient has had nothing to eat or drink for 6 to 8 hours prior to the treatment, except for necessary medications (e.g., antihypertensive medication) given with a small sip of water. An intravenous line is inserted, recording electrodes are placed upon the scalp to record a two-lead electroencephalogram during the treatment, and the two stimulating electrodes are then placed. (For bilateral ECT, the electrodes are placed in the bifrontotemporal position. For right unilateral ECT, one electrode is placed in the right frontotemporal position, and the other electrode is placed on the scalp overlying the right parietal lobe of the brain). A general anesthetic agent is then administered to render the patient unconscious. Methohexital is usually used for this purpose, at a dose of approximately 0.5-1.0 mg/kg. The patient then receives a muscle relaxant to reduce convulsive motor activity. The preferred agent is succinylcholine, a depolarizing drug, which is also given at a dose of approximately 0.5-1.0 mg/kg. The anesthetist continuously monitors cardiac and pulmonary function with an electrocardiogram and pulse oximetry, and administers oxygen. Once the patient is sufficiently anesthetized and paralyzed, the electrical stimulus is applied. The dose of the electric stimulus should be at least 50% above seizure threshold.5 The most precise method for quantifying seizure threshold is to empirically titrate the dose of the electrical stimulus, beginning with subconvulsive doses and then increasing the dose.6 The seizure itself should last from 20 to 120 seconds.
Patients sometimes present conditions that necessitate changing the procedure and making special accommodations. Two cases treated within our program illustrate this point. In the first case, the patient's obesity was so severe that it compromised airway management, and the patient required elective intubation for each ECT treatment. In the second case, the patient had von Willebrand's disease, which presented a theoretical risk for cerebral hemorrhage due to the increased blood pressure that occurs during each ECT treatment. The patient's father had a similar bleeding disorder and he had suffered a cerebral hemorrhage. Our patient's bleeding time was checked one-half hour prior to each ECT treatment, and an antihypertensive medication was used to control the patient's blood pressure during each ECT treatment.
In administering ECT, research has established a dose-response relationship between the magnitude of the electrical stimulus that is used to induce the seizure, and the response rate.7 Numerous studies have consistently shown that these two variables are directly related.5 Unfortunately, the incidence of adverse cognitive effects is also directly related to the magnitude of the electrical stimulus. Although seizure duration has little relationship to efficacy, a successful treatment requires a seizure lasting at least 15 seconds as measured by duration of motor movements and an electroencephalographic recording.
The number of treatments that constitutes a full course of ECT for psychiatric disorders such major depression has not been empirically established. We offer anywhere from 3 to 20 treatments, administered three per week. Patients are assessed daily, and when clinical improvement plateaus, the course of ECT is completed. An average course of treatment will consist of 6 to 12 treatments. All patient receiving ECT begin their treatment as inpatients. For some patients, the acute course of ECT is finished as an outpatient.
Mortality as a result of ECT is very rare, and is approximately the same as that associated with minor surgery and childbirth. The best current estimate is that the rate of death related to ECT is 1 per 10,000 patients, or 1 per 80,000 treatments.1 Death related to ECT is usually due to cardiac arrythmia, myocardial infarction, congestive heart failure, prolonged apnea, status epilepticus, and cerebral herniation. The overall baseline medical status of the patient is probably related to mortality.
Two of the most common side effects are memory impairment and postictal delirium. In one study7 that assessed postictal delirium, the mean (SD) time to recovery of orientation ranged from 21 (11) minutes to 41 (17) minutes, depending on whether study patients received high-dose unilateral ECT or high-dose bilateral ECT (discussed below). Memory impairment has been heavily studied, and many factors independently determine how cognition is adversely affected, including electrode placement, stimulus waveform, stimulus intensity, spacing of treatments, number of seizures per individual treatment session, concomitant psychotropic medications, and anesthetic medications. ECT often results in both anterograde and retrograde amnesia, with the former resolving more quickly than the latter. Self-reports of memory impairment usually show poor association with objective tests and strong association with measures of psychopathology.5
Other adverse effects of ECT occur with varying probabilities, and include elevated blood pressure, tachycardia, bradycardia, asystole, apnea, status epilepticus, postictal delirium and agitation, memory impairment, headache, oral lacerations, dental injuries, myalgia, nausea, and bone fractures. Despite these problems, about 80% of the patients who receive ECT want another course of ECT if they become sick again.5
Following a successful course of ECT, the issue arises as to how to prevent relapse or recurrence of the illness. In particular, major depressive disorder is a highly recurring illness, with the majority of patients suffering multiple episodes of major depression. For patients who recover from an episode of major depression, nearly two-thirds will suffer at least one recurrence during the subsequent 10 years; on average, each patient will suffer two recurrent episodes during 10 years of follow-up.8 Thus, the large majority of patients who successfully complete an acute course of ECT subsequently receive pharmacotherapy as prophylaxis. Recent research has evaluated the use of such pharmacotherapy to prevent relapse of major depression. In one study9 patients with major depression were treated openly with ECT: those who remitted were entered into a randomized, double-blind, placebo-controlled trial that compared the efficacy of continuation treatment with placebo vs. nortriptyline vs. the combination of nortriptyline plus lithium. Over the 24-week trial, the relapse rate for placebo was 84%; for nortriptyline, 60%; and for nortriptyline-lithium, 39%. Although the combination was markedly more efficacious than placebo, the relapse rate for those receiving nortriptyline-lithium was still high.
As a result of such high rates of relapse and recurrence despite optimal pharmacotherapy, some patients receive continuation and maintenance ECT, with a frequency varying from one ECT treatment every two weeks to one treatment every 3 months. These continuation and maintenance treatments are usually performed on an outpatient basis, and the use of these treatments is supported by observational studies. In one study, patients with major depression who responded to an acute course of ECT were significantly more likely to remain free of depression if they received maintenance ECT rather than antidepressant medications.10 For those receiving maintenance ECI, the cumulative probability of recurrence was 7% at two years and 27% at five years. For those receiving maintenance antidepressant medications, the cumulative probability of recurrence was 48% at two years and 82% at five years. Ongoing controlled trials are evaluating the efficacy of such treatments; it is anticipated that these studies will further establish their benefits.
Another issue in ECT research is the placement of the two stimulating electrical leads;11,13 that is, whether the initial arc of current passes through only one cerebral hemisphere or both hemispheres. When the initial ate of current passes through one hemisphere-unilateral ECT-the seizure in that hemisphere is propagated across the corpus collosum to the other hemisphere, and then this hemisphere seizes. For unilateral ECT, the hemisphere that is selected to receive the initial arc of current is the one that is nondominant for language; this is almost always the right hemisphere for right-handed patients and is usually the right hemisphere in left-handed patients. In bilateral ECT, the leads are placed in the bifrontotemporal position, with the result that the initial arc of current passes through one hemisphere, across the corpus collosum, and through the other hemisphere. Bilateral ECT may be more efficacious than unilateral ECT, but is associated with significantly more cognitive morbidity.
Related to the issue of lead placement is the question of dose, that is, the magnitude of the electrical stimulus used to induce the seizure. Bilateral ECT has generally been regarded as more efficacious than unilateral ECT, and bilateral ECT is also associated with more side effects, primarily cognitive impairment. Recent research suggests that right unilateral ECT at a high dose may be as effective as a moderate dose of bilateral ECT, with less severe and persistent cognitive effects.11
In summary, ECT is one of several treatments for patients with severe psychiatric disorders. Our experience has shown that ECT can play an important part in helping many patients recover from some of these debilitating illnesses. Primary care physicians, who treat patients with major depression, are in a position to help reduce the stigma that has accrued to ECT. Although ECT may seem primitive and has been negatively depicted in films and on television, it nevertheless is an efficacious procedure that is often life-saving.
REFERENCES
1. Engel GL. The clinical application of the biopsychosocial model. Am J Psychiatry 1980; 137:535-44.
2. Janicak PG, Davis JM, Gibbons RD, et al. Efficacy of ECT. Am J Psychiatry 1985; 142:194-206.
3. Sackheim HA, Devanand DP, Nobler MS. Electroconvulsive therapy, in Psychopharmacology: The Fourth Generation of Progress. Edited by Bloom F, Kupfer D. New York, Raven, 1995, pp 1123-42.
4. American Society of Anesthesiologists: New classification of physical status. Anesthesiol 1963; 24:111.
5. American Psychiatric Association, Committee on Electroconvulsive Therapy. The practice of electroconvulsive therapy, second edition. Washington, DC, American Psychiatric Association, 2001, pp 27- 30.
6. Sackheim HA, Decina P, Kanzler M, et al. Effects of electrode placement on the efficacy of titrated, low-dose ECT. Am J Psychiatry 1987; 144:1449-55.
7. Sackheim HA, Prudic J, Devanand DP, et al. Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. NEJM 1993; 328:839-46.
8. Solomon DA, Keller MB, Leon AC, et al. Multiple recurrences of major depressive disorder. Am J Psychiatry 2000; 157:229-33.
9. Sackheim HA, Haskett RF, Mulsant BH, et al. Continuation pharmacotherapy in the prevention of relapse following electroconvulsive therapy. JAMA 2001; 285:1299-307.
10. Gagne Jr GG, Furman MJ, Carpenter LL, et al. Efficacy of continuation ECT and antidepressant drugs compared to long-term antidepressants alone in depressed patients. Am J Psychiatry 2000; 157:1960-5.
11. Sackheim HA, Prudic J, Devanand DR et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral electroconvulsive therapy at different stimulus intensities. Arch Gen Psychiatry 2000; 57:425-34.
12. Swart C, Abrams R. What you need to know about electroconvulsive therapy. Somatics LLC, Lake Bluff, Il, 1994.
13. Tew Jr JD, Mulsant BH, Haskett RF, et al. A randomized comparison of high-charge right unilateral electroconvulsive therapy and bilateral electroconvulsive therapy in older depressed patients. J Clin Psychiatry 2002;63:1102-5.
David A. Solomon, MD, is Associate Professor of Psychiatry and Human Behavior, Brown Medical School.
Rendueles Villabla II, MD. Position previously cited.
CORRESPONDENCE:
David A. Solomon, MD
Department of Psychiatry, Rhode Island Hospital, 593 Eddy Street, Providence, RI 02903-4970
Phone: (401) 444-5110
Fax: (401) 444-6180
e-mail: DASolomon@Lifespan.org
Copyright Rhode Island Medical Society Oct 2003
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