Relapse in ECT

JAMA, March 14, 2001
Continuation Pharmacotherapy in the Prevention of Relapse Following Electroconvulsive Therapy

A Randomized Controlled Trial

Harold A. Sackeim, PhD; Roger F. Haskett, MD; Benoit H. Mulsant, MD; Michael E. Thase, MD; J. John Mann, MD; Helen M. Pettinati, PhD; Robert M. Greenberg, MD; Raymond R. Crowe, MD; Thomas B. Cooper, MA; Joan Prudic, MD

Context Electroconvulsive therapy (ECT) is highly effective for treatment of major depression, but naturalistic studies show a high rate of relapse after discontinuation of ECT.

Objective To determine the efficacy of continuation pharmacotherapy with nortriptyline hydrochloride or combination nortriptyline and lithium carbonate in preventing post-ECT relapse.

Design Randomized, double-blind, placebo-controlled trial conducted from 1993 to 1998, stratified by medication resistance or presence of psychotic depression in the index episode.

Setting Two university-based hospitals and 1 private psychiatric hospital.

Patients Of 290 patients with unipolar major depression recruited through clinical referral who completed an open ECT treatment phase, 159 patients met remitter criteria; 84 remitting patients were eligible and agreed to participate in the continuation study.

Interventions Patients were randomly assigned to receive continuation treatment for 24 weeks with placebo (n = 29), nortriptyline (target steady-state level, 75-125 ng/mL) (n = 27), or combination nortriptyline and lithium (target steady-state level, 0.5-0.9 mEq/L) (n = 28).

Main Outcome Measure Relapse of major depressive episode, compared among the 3 continuation groups.

Results Nortriptyline-lithium combination therapy had a marked advantage in time to relapse, superior to both placebo and nortriptyline alone. Over the 24-week trial, the relapse rate for placebo was 84% (95% confidence interval [CI], 70%-99%); for nortriptyline, 60% (95% CI, 41%-79%); and for nortriptyline-lithium, 39% (95% CI, 19%-59%). All but 1 instance of relapse with nortriptyline-lithium occurred within 5 weeks of ECT termination, while relapse continued throughout treatment with placebo or nortriptyline alone. Medication-resistant patients, female patients, and those with more severe depressive symptoms following ECT had more rapid relapse.

Conclusions Our study indicates that without active treatment, virtually all remitted patients relapse within 6 months of stopping ECT. Monotherapy with nortriptyline has limited efficacy. The combination of nortriptyline and lithium is more effective, but the relapse rate is still high, particularly during the first month of continuation therapy.

JAMA. 2001;285:1299-1307

Electroconvulsive therapy (ECT) is usually administered to patients with severe and medication-resistant major depression.1 The number of ECT procedures performed in the United States exceeds coronary bypass, appendectomy, or hernia repair.2 While the response rate to ECT in major depression is high,1, 3 relapse is a key problem.4 Naturalistic studies show that the relapse rate during the 6 to 12 months following ECT exceeds 50%.5-15

Electroconvulsive therapy is the only somatic treatment in psychiatry that is typically discontinued following response, yet patients untreated following ECT response have high rates of relapse.16-19 Studies in the 1960s suggested that continuation therapy with a tricyclic antidepressant (TCA) or monoamine oxidase inhibitor markedly reduced the 6-month post-ECT relapse rate.16-18 Post-ECT monotherapy with antidepressant medication is now standard.9, 20-23 However, the evidence supporting this practice is flawed, and the recent naturalistic studies document high relapse rates.

Post-ECT continuation pharmacotherapy has been based on 3 studies conducted in the 1960s.16-18 A primary goal of those studies was to determine whether concurrent treatment with TCAs or monoamine oxidase inhibitors reduced the number of ECT treatments needed. Following ECT, patients continued taking active medication or placebo or no subsequent treatment. Using 6-month follow-up periods, the findings were consistent. Patients who received a TCA or monoamine oxidase inhibitor during and following ECT had a relapse rate of approximately 20%, compared with 50% in the control groups. There are major concerns about this research.4, 24 At that time, ECT was a treatment of first choice.25, 26 Relevance for continuation therapy in medication-resistant ECT responders is uncertain. Second, some patients likely benefited from the concurrent antidepressant during ECT, and continued to benefit from the medication as continuation therapy. Since use of ECT now centers on medication-resistant patients,1, 21, 27 the relevance of this early research is questionable.

We conducted a randomized, double-blind, placebo-controlled trial of continuation pharmacotherapy following ECT response. The treatments were a TCA (nortriptyline hydrochloride), combination treatment with nortriptyline and lithium carbonate, or placebo. A placebo-controlled trial following ECT had never been conducted in the United States. This trial was justified since the relapse rates in recent follow-up studies5-15 often exceeded those seen with placebo in the controlled investigations from an earlier era.16-18 A placebo-controlled trial was also justified by our hypothesis that TCA monotherapy, the best documented treatment in post-ECT relapse prevention,16-18 has limited efficacy. Monotherapy with nortriptyline was tested since (1) early research suggested that TCA continuation therapy was effective in relapse prevention16-18; (2) concern that newer agents, such as selective serotonin reuptake inhibitors (SSRIs), may be less effective than TCAs in treatment of the severe episodes characteristic of ECT patients28-33; and (3) given the widespread use of SSRIs and other newer agents as first-line treatments, a low probability that ECT responders would have received an adequate TCA trial during the episode.34 We hypothesized, however, that the nortriptyline-lithium combination would be most efficacious, given the evidence that combined TCA-lithium treatment is particularly effective in medication-resistant major depression,35-41 and the supposition that regimens effective in the acute treatment of medication-resistant major depression exert protective effects as continuation treatment. Nortriptyline-lithium was also selected since few ECT remitters would have received this treatment during the episode.34, 42


Study Site and Study Participation

The study was conducted at the Carrier Foundation (Belle Meade, NJ), a private psychiatric hospital, and at university-based psychiatric facilities of the University of Iowa (Iowa City) and Western Psychiatric Institute and Clinic (WPIC; Pittsburgh, Pa). The New York State Psychiatric Institute (NYSPI; New York) was the coordinating and monitoring center. Using the Schedule for Affective Disorders and Schizophrenia,43 patients met the research diagnostic criteria44 for major depressive disorder. They had a pretreatment score of 21 or higher on the Hamilton Rating Scale for Depression (HRSD; 24-item scale).45 Patients were excluded if they had a history of bipolar disorder, schizophrenia, schizoaffective disorder, nonmood disorder psychosis, neurological illness, alcohol or drug abuse within the past year, ECT within the past 6 months, or severe medical illness that markedly increased the risks of ECT (eg, unstable or severe cardiovascular conditions, aneurysm or vascular malformation susceptible to rupture, severe chronic obstructive pulmonary disease).

Participants were recruited from those clinically referred for ECT. Over a 6-year period (1993-1998), 349 patients consented and participated in the pre-ECT screening (Figure 1). Patients who met inclusion/exclusion criteria for the open ECT phase were completers if they received at least 5 treatments or ended ECT earlier due to response and did not receive any psychotropic medication during the ECT course other than lorazepam (3 mg/d). Of the 59 patients who did not contribute to ECT outcome data, 17 patients were dropped before ECT due to diagnostic exclusions; 14 patients could not be withdrawn from psychotropics before (n = 7) or during (n = 7) ECT; 12 patients terminated ECT against medical advice prior to the fifth treatment; 9 developed an intercurrent illness so ECT was not initiated (n = 2) or was interrupted (n = 7) (all before the fifth treatment); 6 patients withdrew consent before ECT; and 1 dropped below the inclusion threshold (HRSD score of 21) before starting ECT. Only 2 of 59 dropouts (prohibited medications) should have contributed to ECT efficacy analyses, but end point evaluations were not obtained.

To enter the continuation trial, patients had to achieve at least a 60% reduction in HRSD scores relative to pre-ECT baseline, with a maximum score of 10 both at an assessment within 2 days of ECT discontinuation and reassessment 4 to 8 days following ECT termination, while free of psychotropic medication. Since the extent of residual symptoms is predictive of relapse following antidepressant treatment,46, 47 the remitter criteria were particularly stringent. These criteria required both a substantial symptomatic reduction and a low absolute score both immediately and 4 to 8 days following ECT. Patients with medical contraindications to nortriptyline or lithium were excluded. Patients provided separate informed consent for participation in the ECT and continuation pharmacotherapy phases, and capacity to consent was assessed at each time point. The institutional review boards at each enrollment site and the NYSPI approved the study. Assuming a relapse rate of 50% with placebo, the goal was to enroll at least 25 patients in each randomized treatment condition to have at least an 80% probability of detecting a significant advantage in relapse time for an active treatment in a primary, intent-to-treat, parametric survival analysis.

Study Design

Patients were withdrawn from psychotropic medications, other than lorazepam (up to 3 mg/d) as needed, before starting ECT. Methohexital (0.75-1.0 mg/kg) and succinylcholine chloride (0.75-1.0 mg/kg) were the anesthetic medications, with preadministration of an anticholinergic agent (0.4-6 mg of atropine or 0.2-4 mg of glycopyrrolate). Based on clinical judgment, patients received either right unilateral or bilateral ECT, using the d’Elia48 or bifrontotemporal21 placements, respectively. Electroconvulsive therapy was given 3 times per week with a customized MECTA SR1 device (MECTA Corp, Lake Oswego, Ore), which had double the maximal charge output of commercial devices in the United States. Seizure threshold was quantified at the first treatment using empirical titration.49 For right unilateral ECT, dosage at subsequent treatments exceeded initial threshold by at least 150%. Patients who did not show substantial improvement to right unilateral ECT within 5 to 8 treatments were switched to bilateral ECT. To be considered adequate, minimal seizure duration was 20 seconds of motor or 25 seconds of electroencephalogram manifestation.21 Length of the ECT course was determined on clinical grounds.

The ECT remitters were randomized to 3 continuation pharmacotherapy groups, stratified by classification of the index episode as psychotic depression; medication-resistant nonpsychotic depression; and nonpsychotic depression without medication resistance. Medication resistance was rated using the Antidepressant Treatment History Form.8, 34, 50 Medication-resistant nonpsychotic patients had to have received at least 1 adequate antidepressant trial prior to ECT. Patients with psychotic depression were not further stratified by resistance classification since only 4 (4.3%) of 92 such patients received an adequate combination antidepressant-antipsychotic trial during the episode.42

Using a randomly permuted block procedure consisting of blocks of 6 patients (within site and the 3 strata), each treatment condition was equally represented. The study psychiatrist who completed the Antidepressant Treatment History Form communicated the patient classification to the pharmacist who assigned the next available patient number within the stratum. Only the site pharmacist, the study coordinator at NYSPI, and the NYSPI laboratory conducting plasma level assays had access to the randomization code. The randomization code was generated by the study coordinator at NYSPI based on the randomization tables provided by Fleiss.51 Treatment teams, outcome assessors, and data analysts were blind to treatment assignment.

Medication was administered in sealed capsules containing 25 mg of nortriptyline, 300 mg of lithium, or microcrystalline cellulose (placebo). The capsules containing nortriptyline or lithium were distinct in appearance, and each was matched with placebo capsules identical in size, weight, appearance, and taste. Each patient was given 2 sets of pills. On the first study day, 50 mg of nortriptyline or its placebo and 600 mg of lithium or its placebo were administered. Blood samples were obtained 24 hours later and estimates were determined for the oral dose needed to produce steady-state levels of 100 ng/mL of nortriptyline and 0.7 mEq/L of lithium.52-54 On days 3 and 4, depending on the estimate, oral doses were adjusted and maintained until plasma levels were again taken on days 9 through 11. The goal was to maintain nortriptyline levels between 75 and 125 ng/mL and lithium levels between 0.5 and 0.9 mEq/L. During the 24-week trial, plasma levels were determined on 10 occasions. A yoked-control procedure was used, with a psychiatrist at NYSPI reporting simulated nortriptyline and lithium values for patients receiving placebo, based on matching by sex, age, and weight with patients who were receiving active medication.

Patients were evaluated at weekly intervals for the first 4 weeks, at 2-week intervals for the next 8 weeks, and at 4-week intervals for the remaining 12 weeks. They were contacted by telephone at weekly intervals between visits. Clinical ratings during the continuation phase were obtained by the same blinded evaluator (continuous rater) who evaluated patients throughout the ECT course. During the continuation trial, a blinded study psychiatrist assessed adverse effects and vital signs, adjusted medication or placebo dosage (based on plasma levels reported by NYSPI and adverse effects), and completed clinical ratings. To evaluate the adequacy of the blinding, patients guessed their treatment assignment as placebo, nortriptyline, or nortriptyline-lithium at study exit. Patients who dropped out of the study or relapsed were offered clinical care by a psychiatrist at the research site not affiliated with the study or the follow-up evaluation of the particular patient.

Time to relapse was the main outcome measure. The criteria for relapse were a mean HRSD score (continuous rater and study psychiatrist) of at least 16 that was maintained for at least 1 week (over 2 consecutive visits) and a mean absolute increase of at least 10 points at 2 consecutive visits relative to continuation trial baseline. These criteria reflected a clinical worsening for which most clinicians would abandon the current treatment in favor of an alternative.

At the pre-ECT evaluation, a research nurse completed ratings on the Cumulative Illness Rating Scale55 to assess medical comorbidity. At all major time points (pre-ECT, post-ECT, start of continuation trial [day 0], week 12, week 24, and relapse), the HRSD, Clinical Global Impression,56 and Global Assessment Scale43 scores were completed by the continuous rater and the study psychiatrist. At each site, intraclass correlation coefficients for the 2 raters exceeded 0.97, 0.93, and 0.90 for HRSD, Clinical Global Impression, and Global Assessment Scale scores, respectively. A site-independent, time-blind clinician at NYSPI rated 239 videotapes of continuous rater interviews conducted at random intervals during the ECT and continuation phases. The intraclass correlation coefficients were 0.97, 0.96, and 0.95 for HRSD, Clinical Global Impression, and Global Assessment Scale scores, respectively. The HRSD, Clinical Global Impression, and Global Assessment Scale scores reported below are the continuous rater evaluations.

At each visit in the continuation phase, a blinded study psychiatrist completed the Treatment Emergent Symptom Scale.56 Forty-eight possible adverse effects were rated for severity, relationship to study medication, and action taken. Clinically significant adverse effects were defined as those rated as moderate in severity, possibly related to study medication, and, at minimum, those requiring increased surveillance.

Statistical Methods

Patients who met remitter criteria following ECT and who did or did not participate in the continuation trial were compared in demographic, clinical, and previous treatment features with t tests for continuous measures and 2 analyses for dichotomous variables. The randomized continuation pharmacotherapy groups were compared on baseline variables using analyses of variance or 2 analyses.

The primary analysis of the continuation trial used survival analysis for right-censored failure-time data. A simultaneous regression model was fit to the relapse-time data using the Weibull distribution.10, 15 Covariates in the regression model were the randomized treatment condition (3 levels), strata (3 levels), sex, and HRSD score at the start of the trial. In a secondary analysis, ECT treatment modality (right unilateral only vs right unilateral and bilateral ECT vs bilateral ECT only) and number of ECT treatments were added as additional covariates. To confirm the findings from the parametric analysis regarding treatment group differences, nonparametric estimates of the survival distribution function for each group were computed, using the Kaplan-Meier method57 and contrasted with the log-rank test (Mantel-Cox).58

Early in the study, 1 site (Carrier Foundation) was closed when the hospital discontinued its research division, so another site (University of Iowa) was added late. These 2 sites entered 21 patients in the continuation trial compared with 63 patients at WPIC. To determine whether the effects were not unique to WPIC, the Carrier Foundation and the University of Iowa were pooled for analysis. A site term (WPIC vs Carrier Foundation and University of Iowa) was entered into both secondary parametric and nonparametric survival analyses.

To assess the adequacy of pharmacotherapy, separate analyses of variances were conducted on the last plasma levels for nortriptyline and lithium obtained in completers (24-week or time of relapse), using the assayed values for active medication and the simulated values for placebo, and treatment group (3 levels) and relapse status as between-subject factors. A logistic regression was conducted on the patients’ guess of treatment condition with relapse status and actual treatment assignment as predictors.


Of the 290 patients who completed the ECT phase, 159 (54.8%) patients were remitters (Table 1 and Figure 1). There was no difference among the sites in remitter rate (22 = 3.75, P = .15). Immediately following ECT, 17 patients (5.9%) met initial remitter criteria, but not at the 4- to 8-day reassessment. The remitter rate may have been negatively influenced by the stringency of the remission criteria and the fact that 262 patients (90.3%) started with right unilateral ECT, with the minimum dosage only 150% above seizure threshold. Subsequent research has shown that the efficacy of right unilateral ECT improves at a higher dosage relative to seizure threshold.15, 59

Of the 159 remitters, 84 (52.8%) patients entered the randomized continuation trial. Of the 75 remitters who did not participate, 22.7% had medical exclusions for nortriptyline or lithium; 26.7% had travel limitations; and 50.7% preferred treatment by their referring physician, were receiving other medications or ECT, or were unwilling to receive placebo.

Comparisons of remitters who did or did not enter the continuation trial yielded no differences in pre- or post-ECT HRSD, Clinical Global Impression, or Global Assessment Scale scores, number of episodes, duration of current episode, number of ECT treatments, strength of the most potent antidepressant trial during the index episode, sum or average potency of all trials, number of trials, or number of adequate trials. The groups also did not differ in sex, race, history of previous ECT, use of right unilateral or bilateral ECT, or classification of medication resistance. Trial participants were younger (mean [SD], 57.4 [17.2] years) than nonparticipants (64.2 [16.3] years) (t157 = 2.54; P = .01); had more previous psychiatric hospitalizations (2.4 [2.6]) than nonparticipants (1.5 [1.6]) (t157 = 2.82; P = .005); a higher rate of psychotic depression (41.7% vs 16.0%) (21 = 12.54, P <.001); and less total medical burden (Cumulative Illness Rating Scale score, 6.1 [4.2] vs 8.0 [3.9]) (t157 = 2.91; P = .004). The medical exclusions for the continuation trial and travel limitations likely accounted for the higher age and greater medical burden of nonparticipants.

The continuation treatment groups were compared in demographic and clinical features (Table 2). There were no significant differences.

Eleven (13.1%) of the 84 patients dropped out of the trial before completing 24 weeks or meeting relapse criteria. The reasons for noncompletion are described in Figure 1. Dropout rates were evenly distributed among the 3 treatment groups (4 placebo, 2 nortriptyline, and 5 nortriptyline-lithium).

The overall model in the parametric analysis on survival time was significant (likelihood ratio, 26 = 27.3; P<.001) (Table 3). The treatment groups differed markedly (P<.001). Both nortriptyline alone (P = .01) and nortriptyline-lithium (P<.001) were superior to placebo in survival time, and nortriptyline-lithium was superior to nortriptyline alone (P = .04).

The Kaplan-Meier survival function was computed for each treatment group (Figure 2). Across the sample, 45 (61.6%) of 73 completers relapsed. This confirmatory nonparametric analysis yielded a log-rank 22 of 9.12 (P = .01). The relapse rates for completers were 84.0% (21/25) for placebo (95% confidence interval [CI], 70%-99%); 60.0% (15/25) for nortriptyline (95% CI, 41%-79%); and 39.1% (9/23) for nortriptyline-lithium (95% CI, 19%-59%). Only 1 patient relapsed while taking nortriptyline-lithium after 5 weeks, while relapse steadily continued with placebo and nortriptyline throughout the 24-week trial (Figure 2). Nonparametric survival analyses comparing each active treatment condition with placebo yielded a significant effect for nortriptyline-lithium (21= 8.52; P = .004), but only a trend for nortriptyline (21 = 3.33; P = .07).

The parametric survival analysis indicated that across the treatment conditions, medication-resistant nonpsychotic patients had a higher relapse rate than patients with psychotic depression. The relapse rates were 50.0% for psychotic patients (n = 28), 55.6% for nonpsychotic patients without medication resistance (n = 9), and 72.2% for nonpsychotic medication-resistant patients (n = 36). The significant effect of sex was due to a higher relapse rate among women (77.8%) than men (53.6%). Patients who relapsed had higher mean (SD) HRSD scores at trial entry (6.0 [3.1]) than patients who did not relapse (5.0 [2.8]). There were no additional significant effects in the parametric survival analysis when treatment with right unilateral, right unilateral and bilateral, or bilateral ECT (P = .89), and number of ECT treatments (P = .96) were entered as additional terms.

Study site (WPIC vs combined Carrier Foundation and University of Iowa) was entered as a term in both the parametric and nonparametric survival analyses. There were no site effects. The relapse rates at WPIC for placebo, nortriptyline, and nortriptyline-lithium were 88.9%, 60.0%, and 41.2%, respectively, and for the combined Carrier Foundation and University of Iowa they were 71.4%, 60.0%, and 33.3%, respectively.

The high rate of relapse across the treatments could have been due to excessively sensitive relapse criteria. Clinical ratings at continuation trial entry and end point were compared as a function of relapse status (Table 4). Relapsed patients showed marked symptomatic worsening. Fifteen (33%) of the 45 relapsed patients were hospitalized and received ECT, 6 patients (13%) received outpatient ECT, and all other relapsed patients (53%) were switched to other pharmacotherapies. The severity of relapse did not differ among the continuation treatments.

No effects approached significance in the analyses of variances of nortriptyline and lithium levels on final visit. At final visit, the mean (SD) nortriptyline level was 89.9 (38.2) ng/mL for the nortriptyline group, 89.2 (32.2) ng/mL for the nortriptyline-lithium group, and the simulated levels reported for the placebo group averaged 93.0 (27.5) ng/mL. For lithium, the levels were 0.59 (0.2) mEq/L for the nortriptyline-lithium group, with simulated levels of 0.54 (0.2) mEq/L and 0.62 (0.2) mEq/L for the nortriptyline and placebo groups, respectively. Relapse was not associated with nortriptyline or lithium plasma levels.

A 1-way analysis of variance indicated that the treatment groups did not differ in the average number of clinically significant adverse effects (F2,80 = 0.13; P = .88). For the placebo, nortriptyline, and nortriptyline-lithium groups, the mean (SD) number of significant adverse effects per patient was 1.24 (1.8), 1.42 (1.7), and 1.21 (1.3), respectively. An analysis of variance in the completer sample (with treatment group and relapse status as between-subject factors) yielded no significant effects. The mean (SD) number of significant adverse effects among patients who relapsed (1.48 [1.7]) did not differ from nonrelapsed patients (1.32 [1.6]) (t70 = 0.39; P = .70). Table 5 presents the clinically significant adverse effects experienced by at least 3 patients.

At study exit, 63 of the 73 completers guessed their treatment assignment. The logistic regression analysis yielded a modest association between the treatment assignment and the patients’ guesses (24 = 9.68; P = .05) and a more robust association with relapse status (22 = 8.17; P = .02). Only 1 (4%) of the 25 patients who did not relapse believed he/she was treated with placebo, while this was true of 16 (42.1%) of the 38 patients who did relapse. Of the patients treated with placebo, 50% believed they received only placebo, while 31.8% and 18.2% believed that they had received nortriptyline and nortriptyline-lithium, respectively. For the nortriptyline group, the guesses were 29.4% for placebo, 23.8% for nortriptyline, and 52.4% for nortriptyline-lithium. For nortriptyline-lithium, these guesses were 5.0%, 30.0%, and 65.0%, respectively. While the patient blinding was imperfect, relapse status was a more powerful determinant of the guesses. The distributions overlapped considerably among patients treated with nortriptyline and nortriptyline-lithium.


Early research, based on first-choice use of ECT for major depression, indicated that half of the patients remain well in the 6 months following response without continuation therapy.16-18 We found that the relapse rate for placebo-treated patients was 84%. This suggests that the prognosis following ECT is more guarded today. Given the shift in use of ECT for severe, recurrent, and medication-resistant patients with higher risk of relapse,8, 15, 60 almost universal relapse should be expected without effective continuation therapy.

The early research suggested that continuation monotherapy with a TCA reduced the relapse rate to approximately 20%.16-18 We found that the relapse rate with nortriptyline continuation monotherapy was 60%, above the original projections for placebo. While TCAs are believed to be among the most effective antidepressant agents,27, 30, 33 our findings indicate that the efficacy of post-ECT TCA continuation monotherapy is not acceptable. Similarly, in a naturalistic study, Flint and Rifat61 found that continuation monotherapy with a TCA was ineffective in preventing relapse in psychotically depressed patients who responded to ECT.

The relapse rate for the combination of nortriptyline-lithium was 39.1%, which was superior to placebo and nortriptyline monotherapy. Similar results were reported in a naturalistic study at NYSPI, in which relapse rates over 1 year were markedly lower among ECT remitters who received TCA-lithium continuation therapy (35.3%) compared with patients who received continuation treatment with other pharmacological regimens (67.9%).15 It was noteworthy that the lithium levels in the present study were at the low end of what is considered the therapeutic range for acute or maintenance treatment (0.5-1.2 mEq/L).62, 63 This suggests that in combination with nortriptyline, lithium levels may only need to be greater than 0.5 mEq/L to prevent post-ECT relapse.

This study could not determine whether the advantage of the TCA-lithium combination was due to lithium alone or the synergism of lithium with the TCA. The only placebo-controlled trial of lithium following ECT in unipolar patients found that lithium did not have protective effects during the first 6 months following ECT.64, 65 Thus, it is likely that the advantage of nortriptyline-lithium was due to additive or synergistic effects and not lithium alone. Our findings encourage the use of nortriptyline-lithium as post-ECT continuation therapy. It is unknown whether similar protective effects would be obtained with a mood stabilizer other than lithium or antidepressants other than nortriptyline (in combination with lithium). This issue is important since SSRIs and other newer antidepressant agents have better tolerability than TCAs and are now more commonly used.

Patients with higher HRSD scores at the start of the continuation trial had shorter survival time. This is consistent with several studies of relapse during continuation pharmacotherapy following response to antidepressant medications46, 47 or ECT.8 Thus, concerted attempts should be made to maximize symptomatic improvement in patients receiving ECT. Women were more prone to relapse during the continuation phase. There is inconsistent evidence from naturalistic studies of a higher relapse/recurrence rate among women.14, 66-70 Studies of patients with psychotic depression suggested a high post-ECT relapse rate.6, 7 However, regardless of the treatment producing remission, no previous controlled study has compared relapse rates in psychotic and nonpsychotic depressed patients. We found that psychotically depressed patients had a lower relapse rate than medication-resistant nonpsychotic patients. Several studies have shown that medication resistance is especially predictive of post-ECT relapse.8, 15, 60 It is also possible that compared with medication-resistant nonpsychotic patients, patients with psychotic depression had less Axis II (personality disorder) pathology and better interepisode function. There is evidence that the post-ECT course is poorer in patients with significant Axis II pathology.71, 72

The major finding was that treatment with the nortriptyline-lithium combination produced a substantially lower relapse rate than treatment with placebo or nortriptyline alone. Nonetheless, the relapse with nortriptyline-lithium was high (39.1%). Two alternative strategies, which are not mutually exclusive, should be tested.4 Both strategies are suggested by the observations that relapse is heavily skewed to the period immediately following ECT. During the acute treatment phase, there is a several week delay before antidepressant and mood stabilizing agents exert therapeutic effects.73 Further, the abrupt discontinuation of effective somatic treatment is associated with potentiation of relapse,74-76 which is standard in terminating an ECT course. One strategy is to taper ECT over a few weeks, as is commonly done with pharmacological treatments, providing symptom suppression during the most vulnerable period. Second, the antidepressant medication used in continuation therapy may be started during the course of ECT, followed by post-ECT addition of lithium. All controlled studies in which ECT was combined with an antidepressant medication focused on whether response to ECT was improved,16-19 and not whether this strategy reduced post-ECT relapse. Nonetheless, a low post-ECT relapse rate was seen in studies in which patients began taking an antidepressant at the start of the ECT course.16-19 Thus, these 2 adjunctive strategies raise the possibility that the advantage seen with the nortriptyline-lithium therapy may be further improved and that the problem of the high rate of early relapse with continuation pharmacotherapy following ECT could be resolved.

Author/Article Information

Author Affiliations: Departments of Biological Psychiatry (Drs Sackeim and Prudic), Neuroscience (Dr Mann), and Analytical Psychopharmacology (Mr Cooper), New York State Psychiatric Institute, and the Departments of Psychiatry (Drs Sackeim, Mann, and Prudic and Mr Cooper) and Radiology (Drs Sackeim and Mann), College of Physicians and Surgeons, Columbia University, New York, NY; Western Psychiatric Institute and Clinic and the Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pa (Drs Haskett, Mulsant, and Thase); Carrier Foundation, Belle Meade, NJ (Drs Pettinati and Greenberg); Department of Psychiatry, University of Iowa, Iowa City (Dr Crowe). Dr Pettinati is now with the Department of Psychiatry, University of Pennsylvania, Philadelphia; Dr Greenberg, the Department of Psychiatry, St Francis Hospital, Jersey City, NJ.

Corresponding Author and Reprints: Harold A. Sackeim, PhD, Department of Biological Psychiatry, New York State Psychiatric Institute, 1051 Riverside Dr, New York, NY 10032 (e-mail:

Author Contributions: Study concept and design: Sackeim, Haskett, Mann, Pettinati, Cooper, Prudic.

Acquisition of data: Haskett, Mulsant, Mann, Pettinati, Greenberg, Crowe, Prudic.

Analysis and interpretation of data: Sackeim, Haskett, Mulsant, Thase, Cooper.

Drafting of the manuscript: Sackeim, Mann.

Critical revision of the manuscript for important intellectual content: Sackeim, Haskett, Mulsant, Thase, Mann, Pettinati, Greenberg, Crowe, Cooper, Prudic.

Statistical expertise: Sackeim.

Obtained funding: Sackeim, Haskett, Mann, Pettinati, Prudic.

Administrative, technical, or material support: Sackeim, Haskett, Mulsant, Thase, Mann, Pettinati, Cooper, Prudic.

Study supervision: Sackeim, Haskett, Mulsant, Thase, Mann, Pettinati, Prudic.

Funding/Support: This work was supported by National Institute of Mental Health grants R37 MH35636 (Dr Sackeim), R10 MH57009 (Dr Sackeim), R01 MH47739 (Dr Sackeim), R01 MH48512 (Dr Haskett), R01 MH49786 (Dr Mulsant), R01 MH52247 (Dr Mulsant), R01 MH 01613 (Dr Mulsant), R01 MH30915 (Dr Thase), R10 MH57804 (Dr Crowe), and R01 MH47709 (Dr Pettinati). The lithium carbonate used in this study was obtained through a grant from Solvay Pharmaceuticals Inc (Marietta, Ga). The electroconvulsive therapy devices used in this study were donated by the MECTA Corp.

Acknowledgment: We thank James J. Amos, MD, Donald W. Black, MD, Robert Dealy, MD, Diane Dolata, MSW, RN, Jennifer Dean, BA, Tracy Flynn, MEd, Janelle Gabel, RN, Stephen J. Hegedus, BS, Kevin M. Malone, MD, Mitchell S. Nobler, MD, Carrie J. Opheim, BS, Shoshana Peyser, CSW, PhD, Steven P. Roose, MD, Kerith E. Spicknall, BA, and Stephanie M. Stevens, RN, for assistance in carrying out this study.


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Figure 1:


Figure 2:







New UK report from Mind examines patient experiences

New UK report from Mind examines patient experiences

More than half of those in a recently completed survey of 418 ECT recipients said they did not realize they could refuse to give consent to the treatment.

The survey was conducted earlier this year in the UK by the mental health charity Mind, and concludes with several recommendations. Among those, Mind recommends that ECT should not be used against a person’s will.

“However, given that it seems impossible to predict who will be adversely affected, and given the seriousness and permanent nature of the potential side-effects recorded above, we believe that it should no longer be able to be imposed without consent,” say the authors of the report.

Mind reports that during a three month period studied by the Department of Health (January through March 1999), 2,800 patients received 16,000 administrations of ECT. 700 (25%) of these patients were detained under the mental health act and only 29 percent of those consented to the treatment.

Other key findings from the Mind report:

* One-third (33%) of respondents had had ECT in the last 5 years.
* Depression was by far the most common diagnosis among respondents (53%).
* Over half (52.5%) of the total sample and over one-third (34%) of those given ECT most recently were not aware that they could refuse to give consent to the treatment.
* Almost three quarters (73%) of the total sample and almost two-thirds (60.5%) of those given ECT most recently were not, as far as they remember, given any information about possible side effects.
* Of those consenting to treatment in the last two years, 48% received, as far as they remember, no information about how the treatment would work and 44.5% no information about possible side effects.
* Only 8% of respondents (15% of those receiving ECT most recently) had the opportunity to consult an independent advocate before making a decision about ECT.
* 84% of respondents said that they had experienced unwanted side effects as a result of having ECT.
* 40.5% reported permanent loss of past memories and 36% permanent difficulty in concentrating.
* Among those receiving ECT within the last two years, 30% reported that it had resulted in permanent fear and anxiety.
* A third (32.5%) of recent recipients felt hopeful before having ECT but 29% felt terrified and 22% felt that they were being punished.
* In the short term, 36% of more recent recipients found the treatment helpful or very helpful and 27% unhelpful, damaging or severely damaging. However, in the long term, 43% of more recent recipients felt that it was unhelpful, damaging or severely damaging.
* 66.5% of the overall sample and 49% of those having ECT in the last 2 years would not agree to have it again.
* Respondents from black and minority ethnic communities were more likely to be detained under the Mental Health Act and to have received ECT without consent. They reported a more negative view of ECT than the overall sample with 50% finding it unhelpful, damaging or severely damaging in the short-term and 72% in the long-term.

Full report (MS Word format): UK-Mind-report-survey

ECT: does it prevent suicide?

Retrospective controlled study of inpatient ECT: does it prevent suicide?

Verinder Sharma
Journal of Affective Disorders
56 (1999) 183-187


Background: This study examined the use of ECT among inpatients who committed suicide at a provincial psychiatric hospital. Methods: A total of 45 psychiatric in-patients who committed suicide at a provincial psychiatric hospital were compared with a gender, age and admission diagnosis matched group of 45 hospitalized patients to examine the use of electroconvulsive therapy during the last 3 months of hospitalization. Results: No difference in the utilization of ECT was found in the two groups. Limitations: Retrospective design and small sample size. Conclusions: We failed to demonstrate that ECT had prevented suicide in hospitalized patients. Future prospective studies with large sample size are needed to further examine this question.

1. Introduction

Electroconvulsive therapy (ECT) is recommended as an initial treatment for suicidal depression (American Psychiatric Association, 1993). It is more effective than alternate treatments for severe depression and its rapid onset of action reportedly results in a reduction in the immediate risk of suicide (Goodwin and Jamison, 1990a). ECT is also an important treatment option in some bipolar patients but there is conflicting information whether it leads to acceleration of cycle frequency (Kukopulos et al., 1980; Winokur and Kadrmas, 1989). Studies have shown a lower incidence of suicide among depressed patients treated with ECT as compared with other treatment modalities (Avery and Winokur, 1976, 1978). ECT may also lower mortality and suicide risks in schizoaffective patients (Tsuang et al., 1979), however, the results of another study showed the treatment modality had little relationship with subsequent mortality including suicide (Black et al., 1989).

The utilization rate of ECT in patients who subsequently commit suicide is quite low. Only two of the 1397 suicide victims in Finland over a 12-month period were treated with ECT during the final 3 months. This figure is particularly low considering the prevalence of severe major depression at the time of suicide. A diagnostic study of a random sample of 229 suicides in this study showed a presence of major depression in 31% of the cases and 39% had been hospitalized at some point during the final three months. Given the extremely small number of patients committing suicide within 3 months of receiving ECT, the authors of this Finnish study concluded that ECT has a preventative effect on suicide (Isometsa et al., 1996). However, there was no control group and the base rate of ECT use in Finland during the study period was not specified. Barraclough et al. (1974) also reported that ECT had been neglected in some patients who eventually committed suicide, even though it had previously been successful.

In this study we present results of a case control study examining the use of ECT in a group of 45 in-patients who committed suicide at a psychiatric hospital during the period of 1969-1996 inclusive.

2. Material and methods

In a previous study we examined the risk factors for suicide among 44 in-patients at a provincial psychiatric facility who committed suicide between January 1969 and December 1995 by conspiring with an age and sex matched control group of 45 in-patients (Sharma et al., 1998). Sixty-five patients committed suicide during the study period but 21 patients who killed themselves 3 days or more after leaving the hospital on an authorized or unauthorized leave were excluded. This exclusion criteria was applied to enable us to carefully examine the course of the illness proximal to suicide. The study period for the current study was extended to December 1996. The patient admitted next after the suicide victim matched for gender, age (�5 years) and admission diagnosis (DSM-IV) served as the control. The hospital charts which included reports from previous hospitalizations were studied carefully and data extracted. The suicide and the control groups were compared using one-way analysis of variance (ANOVA) and chi-square on various sociodemographic and clinical variables such as age, sex, marital status, education, employment, living arrangements, number of previous hospitalizations, number of comorbid diagnoses, age at onset of psychiatric illness and length of index admission. The suicide and control groups were compared for the use of ECT during the three months prior to suicide or discharge including the number of patients receiving this treatment modality, the number of ECTs, the type of ECT and the time period between ECT and suicide or discharge.

3. Results

There were 31 males and 14 females in the suicide group. Twenty-one patients were single, 13 were married and 11 were divorced or separated. The mean age at the time of suicide was 38.9�4.6 years. The majority of the suicide victims suffered from mood disorders. Major depression was present in 19 (45.2%) and 12 (26.7%) patients were given the diagnosis of bipolar disorder. Schizophrenia was present in six (13.3%) patients and schizoaffective disorder in four (9%) patients. Four (8.9%) patients received a diagnosis other than the ones mentioned above. No significant differences were found between the two groups on sociodemographic: variables as shown in Table 1.

3.1. Electroconvulsive therapy

Fight patients in the suicide group and four in the control group received ECT during the index admission. One patient from the suicide group and two from the control group were excluded having received ECT mom than 3 months prior to the time of suicide/discharge. No patient among the 21 suicide victims who were excluded received ECT. Table 2 shows clinical data for the suicide victims and control subjects who received ECT during the 3 months before suicide or discharge respectively. Three patients committed suicide following completion of a course of ECT, two suicided during a course of ECT, one was receiving maintenance ECT, and in one patient ECT was discontinued due to lack of efficacy. Three patients had bilateral ECT, three had unilateral ECT and one had an unknown type of treatment. These patients had failed to respond to adequate trials of psychotropic drugs prior to receiving ECT Using one-way ANOVA, there was a trend for a significant difference for time between ECT and suicide/discharge (F = 4.2, P = 0.08) and number of ECTs during index admission (F = 4.0, P=0.09).

4. Discussion

Nearly 16% of suicide victims received ECT during the final three months. This figure is considerably higher than the one reported by Isometsa et al. (1996) who examined all completed suicides in Finland within a 12-month period. The number of patients hospitalized at the nine of suicide was not specified in this study. The higher rate of utilization of ECT in our study was likely due to two reasons. First, the majority of the patients suffered from a mow disorder especially major depression which is the commonest indication for ECT. Second, the psychiatric disorder was severe enough to require hospitalization. In another Canadian study of suicide amongst psychiatric in-patients, 13 out of 37 patients received ECT during the index admission (Roy and Draper, 1995). Eleven of these patients suffered from schizophrenia and had been in hospital for extended periods of time. However, there was no statistically significant difference between the number of suicide victims and controls receiving ECT.

All of the suicide patients (3) who completed ECT were considered non or partial responders. Only one control subject was considered to have shown a favourable response. It can be argued that the patients who committed suicide suffered a relapse after showing initial improvement but this was not the case. It is of note that dim of the partial/nonresponders to ECT had previously benefitted from this treatment Diminished response to subsequent trials of ECT has been noted in patients with histories of multiple episodes (Goodwin, and Jamison, 1990b).

Two patients committed suicide during the course of bilateral ECT which is generally considered more effective than unipolar ECT. Both of time patients were on lithium and one on the combination of lithium and carbamazepine prior to initiation of ECT. The rather abrupt discontinuation of mood stabilizers in these patients which was done to minimize the risk of confusion may have been a factor in exacerbating the risk for suicide. Both were highly apprehensive about ECT and refused to have further treatments due to memory impairment following the first treatment Suicide during the early course of ECT in a small number of patients was also reported by Barraclough et al. (1974). Suicidal patients who fail to respond to a trial of ECT or those who decline to have further treatments because of concerns regarding memory impairment should be viewed as high risk candidates. Patients may view ECT as the last resort and may be at a particularly high risk for suicide in case of a lack of favourable response to this treatment modality. The risk and benefit of discontinuation of mood stabilizers should be carefully weighed in patients receiving ECT.

In summary, findings of this study did not show a difference in the utilization, rate of ECT among hospitalized patients who committed suicide and a group of matched controls during the last three months of hospitalization. The majority of patients who committed suicide following completion of the course of ECT did so within a month and those who declined to have further treatment killed themselves within a week of the final ECT. This is the only controlled study to my knowledge to examine the utilization rate of ECT among inpatients who commit suicide. However, there are some methodological problems in this study including the retrospective design, small sample size and relatively low exposure to ECT yielding limited statistical power. Due to rather small number of patients in the two groups, it was not possible to compare the technical data on ECT.


Dr E. Persad is thanked for his help with the chart reviews and Karen Kueneman for her assistance in data collection and analysis.


American Psychiatric Association, 1993. Practice Guideline for Major Depressive Disorder in Adults Am J. Psychiatry 150(S), 1-23.

Avery, D., Winokur, G., 1976. Mortality in depressed patients treated with electroconvulsive therapy and antidepressants Arch. Gen. Psychiatry 33, 1023-1029.

Avery, D., Winokur, G., 1978. Suicide, attempted suicide and relapse rates in depression: occurrence after ECT and antidepressant therapy. Arch. Gen. Psychiatry 35, 749-753.

Barraclough, B., Bunch, J., Nelson, B., Sainsbury, P., 1974. A hundred cases of suicide: clinical aspects. Br. J. Psychiatry 125, 355-373.

Black, D.W., Winokur, G., Mohandoss, E., WooIson, R.F., Nasralab, A., 1989. Does treatment influence mortality in depressives? A followup of 1076 patients with major affective disorders. Am. Clin. Psychiatry 1, 165-173.

Goodwin F.K., Jamison, K.R., 1990a. Manic-Depressive Illness. Oxford Press, New York, p. 778.

Goodwin, F.K., Jamison, K.R., 1990b. Manic-Depressive Illness. Oxford Press, New York. pp. 660-661.

Isometsa, E.T., Henrikisson, M.M., Heikkinen, ME, Lonnqvist, J.K, 1996. Completed suicide and recent electroconvulsive therapy in Finland. Convuls. Ther. 12 (3), 152-155

Kukopulos A, Reginaldi D, Laddomada P, Floris G, Serra G, Tondo L., 1980.
Related Articles Course of the manic-depressive cycle and changes caused by treatment. Pharmakopsychiatr Neuropsychopharmakol.. 13:156-67.

Roy, A., Draper, R., 1995. Suicide among psychiatric hospital in-patients. Psychol. Med. 25, 199-202,

Sharma, V., Persad, E., Kueneman, IC, 1998. A closer look at inpatient suicide. J. Affect. Disord. 47, 123-129.

Tsuang, M.T., Dempsey, G.M., Fleming, J.A., 1979. Can ECT prevent premature death and suicide in ‘schizoaffective’ patients? J. Affect. Disord. 1, 167-171.

Winokur G., Kadrmas, A., 1989. A polyepisodic course in bipolar illness: possible clinical relationships. Comp. Psychiatry 30 (2), 121-127.


Does Electroconvulsive Therapy Prevent Suicide?

Convulsive Therapy
2(1):3-6, 1986

Does Electroconvulsive Therapy Prevent Suicide?

Victor Milstein, Ph.D., Joyce G. Small, M.D., Iver F. Small, M.D., and Grace E. Green, B.A.

Larue D. Carter Memorial Hospital and Indiana University School of Medicine.
Indianapolis, Indiana, USA.

Summary: To examine the issue of whether or not electroconvulsive therapy (ECT) protects against suicidal death, we followed a complete population of 1,494 adult hospitalized psychiatric patients for 5-7 years. During that time there were 76 deaths of which 16 or 21% were by suicide. Cause of death was not significantly related to age. gender or research diagnosis. Patients who committed suicide were more apt to have received ECT than those who died from other causes, but this difference was not significant. A control group of living patients matched for age, sex, and diagnosis had very similar exposures to ECT. which further indicates that ECT does not influence long-term survival. These findings combined with a close examination of the literature do not support the commonly held belief that ECT exerts long-range protective effects against suicide.

At the recent Consensus Development Conference on Electroconvulsive Therapy (ECT) sponsored by the National Institutes of Health and Mental Health, there was much argument concerning whether ECT does or does not reduce the risk of suicide. At first, this concern would appear to be superfluous as ECT is known to be an effective form of treatment for severe depression and other illnesses that are associated with a significantly elevated risk of suicide. The conference report (Consensus Development Conference, 1985) states that “the immediate risk of suicide (when not manageable by other means) is a clear indication for consideration of ECT.” However, factual data in support of this contention are not readily obtainable.

Studies by Tsuang et al. (1979) and Avery and Winokur (1976) often are quoted as showing that ECT is associated with lower mortality rates than is drug therapy or institutional care in the treatment of patients with schizoaffective disorder or depression. However, their data show reduced mortality from all causes but no significant reduction in suicidal death per se. Avery and Winokur (1976) found that death from suicide was not different in patients receiving ECT compared with those receiving other treatment modalities. Later, these same authors (1978) demonstrated that patients who were treated with ECT made significantly fewer suicide attempts ova a 6-month follow-up period than did patients who did not receive ECT. However, Babigian and Guttmacher (1984) failed to demonstrate that ECT exerts a protective influence against suicidal death. Eastwood and Peacocke (1976) did not find an interrelationship between suicide, hospital admissions for depressive illness, and ECT.

Review of the early literature also reveals conflicting findings. Ziskind et al. (1945) reported that treatment with ECT or pentylenetetrazol (Metrazol) reduces death from suicide. Huston and Locher (1948a) found that none of their patients with involutional melancholia treated with ECT committed suicide, whereas 13% of untreated patients did. The same authors reported a lower rate of suicide in manic depressive patients treated with ECT than in untreated patients (1948b). However, two subsequent studies (Bond, 1954; Bond and Morris, 1954) found no significant protective effect of ECT against suicide in patients with either involutional psychosis or manic depressive illness.


In an effort to cast light on this still unresolved question, we report our findings from follow-up studies of a series of 1,494 patients. They consisted of all consecutive adult admissions to Larue D. Carter Memorial Hospital during the years 1965-72. Further details concerning the facility and patient sample appear elsewhere (Small et al., 1984). From contacts with families and attending physicians and cross-referencing of patients’ names listed on Indiana death certificates, we ascertained that 76 patients had died during the 5- to 7-year follow-up period. Thus, 5.1% of the total sample had died by the time of follow-up, and of these, 16 or 21% were the result of suicide. Causes of death were examined in relation to age, sex, retrospective research diagnosis (Feighner et al., 1972), and whether or not the patient had received ECT during the index hospitalization or at any time in the past. These data are summarized in Table 1.

Neither age nor gender was significantly related to suicidal versus nonsuicidal deaths. There were no significant associations with research diagnoses grouped in terms of affective disorder, schizophrenia, or other conditions. Forty-four percent of the patients who committed suicide had been treated with ECT during the index hospital admission, whereas 32% of patients who died from other causes had received ECT. These differences were not statistically significant.

In view of these negative findings, we next evaluated a control group of patients who were still alive at follow-up. The patients comprising this group were individually and exactly matched for sex and research diagnosis (Feighner et al., 1972) with those who had died. They also were matched for age as-closely as possible and for date of admission to the hospital. When we examined the ECT experience of these living matched control patients and compared them with those of the patients who had died, we found no statistically reliable differences (Table 1).


The results of this retrospective study do not support the contention that ECT exerts long-term protective effects against suicide. Although not statistically significant, more of the patients whose death was ascribed to suicide had received ECT during their index hospital admission than those who died from other causes (44 vs. 32%). Similarly, when their previous ECT experience was added, more patients who died as a result of suicide had received ECT (50 vs. 40%). The matched control group revealed very similar percentages, suggesting that ECT has minimal impact on long-range survival. To consider the early studies demonstrating that ECT exerts a protective effect against suicidal death, the published data must be reworked to determine whether differences were significant. Ziskind et al. (1945) followed 200 patients for a mean of 40 months (range 6-69 months). Eighty-eight patients were treated with either Metrazol or ECT. The remaining 109 patients either refused convulsive therapy (n = 43), had symptoms too mild to warrant this treatment (n = 50), or had a condition contraindicating ECT (n = 16). There were 13 deaths in the control patients with 9 by suicide, compared with 3 deaths with 1 suicide in the convulsive therapy patients. These data yield a Fisher’s exact probability of 0.029, indicating a significant association between treatment/nontreatment and suicide/other causes of death. However, the conditions of the 16 patients with contraindications to ECT and whether they contributed disproportionately to the suicides are unknown.

Huston and Locher (1948a) compared patients with involutional psychosis untreated and treated with ECT. They found that none of the patients in the convulsive therapy group committed suicide, whereas 13% of those untreated did. Interpretation of this study is complicated by the fact that they followed the ECT-treated patients for a mean of 36 months (range 1-48 months) and the untreated patients for 77 months (range 2 days to 180 months). In a subsequent report on manic depressive psychosis treated with ECT or not, the same authors ( 1948b) found that the ECT-treated patients, followed for a mean of 36 months, had a 1% suicide rate, while the control patients, followed for a mean of 82 months, had a 7% suicide rate. Examining the association of ECT/no ECT and death from suicide/other causes yielded a nonsignificant probability using fisher’s exact method. In studies of patients with involutional psychosis (Bond, 1954) and manic depressive illness (Bond and Morris, 1954) examined 5 years after treatment with ECT or no treatment, analysis of these data does not reveal a significant protective effect against suicide of ECT compared with nontreatment.

Thus, we are able to point to only one study, the very early report of Ziskind et al. (1945), which indicates a significant protective effect of ECT against suicide. The remainder of the evidence is overwhelmingly negative. It appears to us that the undeniable efficacy of ECT to dissipate depression and symptoms of suicidal thinking and behavior has generalized to the belief that it has long-range protective effects. In one sense, it is reassuring that this very effective somatic therapy does not exert long-reaching influences on future behavior, in another, it is disappointing that it does not.

Acknowledgment: This work was supported in part by a grant from the Association for the Advancement of Mental Health Research and Education. Inc., Indianapolis. IN 46202. U.S.A.


Avery, D. and Winokur, G. Mortality in depressed patients treated with electroconvulsive therapy and antidepressants. Arch. Gen. Psychiatry: 33:1029-1037. 1976.

Avery, D. and Winokur, G. Suicide, attempted suicide, and relapse rates in depression. Arch. Gen. Psychiatry. 35:749-7S3, 1978.

Babigian H. M., and Guttmacher, L. B. Epidemiologic considerations in electroconvulsive therapy. Arch. Gen. Psychiatry. 41:246-2S3. 1984.

Bond, E. D. Results of treatment in psychoses with a control series. II. Involutional psychotic reaction. Am. J Psychiatry. 110:881-885. 1954.

Bond, E. D. and Morris, H. H. Results of treatment in psychoses with a control series. III. Manic depressive reactions. Am. J Psychiatry: 110:885-887. 1954.

Consensus Conference. Electroconvulsive therapy. JAMA. 254:2103-2108,1985.

Eastwood, M.R. and Peacocke. J Seasonal patterns of suicide, depression and electroconvulsive therapy. Br. J. Psychiatry. 129:472-47S. 1976.

Feighner, J. P.. Robins, E.R., Guze, S. B.. Woodruff. R. A. Jr.. Winokur, G. and Munoz, R. Diagnostic criteria for use in psychiatric research. Arch. Gen. Psychiatry: 26 57-63, 1972.

Huston, P.E. and Lecher, L. M. Involutional psychosis. Course when untreated and when treated with electric shock. Arch. Neurol. Psychiatry. 59:385-394, 1948a.

Huston. P. E. and Locher. L. W. Manic-depressive psychosis. Course when treated and untreated with electric shock. Arch. Neurol. Psychiatry: 60:37-48, 1948b.

Small, J G., Milstein, V., Sharpley; P. H., Klapper. M. and Small, J. F. Electroencephalographic findings in relation to diagnostic constructs in psychiatry. Biol. Psychiatry: 19:471-478, 1984.

Tsuang, M. T., Dempsey, G. M. and Fleming, J A. Can ECT prevent premature death and suicide in schizoaffective patients? J. Affect.. Disorders. 1:167-171, 1979.

Ziskind, E., Somerfeld-Ziskind, E. and Ziskind, L. Metrazol and electric convulsive therapy of the affective psychoses. Arch. Neurol. Psychiatry. 53:212-217.1945.

TABLE 1. Patient characteristics by outcome
  Patients who died Living controls
matched to death
  Suicide Other Suicide Other
n 16 60 16 60
n 6:10 23:37 -  
% 38:63 38:62 - -
Research diagnosis (n/%)        
Affective 4 25 21 35 - -
Schizophrenic 4 25 12 20 - -
Other 8 50 27 45 - -
Mean age (yrs) 32 43 31 44
ECT during index admission (n/%)        
Yes 7 44 19 32 8 50 21 35
No 9 56 31 68 8 50 39 65
ECT: index plus history (n/%)        
Yes 8 50 24 40 9 56 29 48
No 8 50 36 60 7 44 31 52

Review of Consumers’ Perspectives on Electro Convulsive Therapy – SURE

The SURE – Service User Research Enterprise – report on consumer views in the UK.

Download PDF file (1.2 mb) consumerperspectives.pdf

Effectiveness rates in electroconvulsive therapy

Effectiveness rates based onelectrode placement and electricity amount

Placement Dosage Effectiveness

* low dose: just enough electricity to produce convulsion

** suprathreshold: 2.5 times the amount electricity needed to produce convulsion

* low dose: just enough electricity to produce convulsion
** suprathreshold: 2.5 times the amount electricity needed to produce convulsion

Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy
Authors: Sackeim HA, et al.
N Engl J Med — 1993 Mar 25;328(12):882-3

BACKGROUND. The efficacy of electroconvulsive therapy in major depression is established, but the importance of the electrical dosage and electrode placement in relation to efficacy and side effects is uncertain.

METHODS. In a double- blind study, we randomly assigned 96 depressed patients to receive right unilateral or bilateral electroconvulsive therapy at either a low electrical dose (just above the seizure threshold) or a high dose (2.5 times the threshold). Symptoms of depression and cognitive functioning were assessed before, during, immediately after, and two months after therapy. Patients who responded to treatment were followed for one year to assess the rate of relapse.

RESULTS. The response rate for low-dose unilateral electroconvulsive therapy was 17 percent, as compared with 43 percent for high-dose unilateral therapy (P = 0.054), 65 percent for low-dose bilateral therapy (P = 0.001), and 63 percent for high-dose bilateral therapy (P = 0.001). Regardless of electrode placement, high dosage resulted in more rapid improvement (P therapy (59 percent) relapsed, and there were no differences between treatment groups.

CONCLUSIONS. Increasing the electrical dosage increases the efficacy of right unilateral electroconvulsive therapy, although not to the level of bilateral therapy. High electrical dosage is associated with a more rapid response, and unilateral treatment is associated with less severe cognitive side effects after treatment.
Electroconvulsive therapy in the treatment-resistant patient.
Authors: Devanand DP, Sackeim HA, Prudic J
Psychiatr Clin North Am
1991 Dec

In medication-resistant patients with major depressive disorder, the response rate with bilateral electroconvulsive therapy (ECT) drops to 50% from the expected range of 80% to 90%. Relapse rates following ECT are high in medication- resistant depressed patients and are clustered in the first 4 months following clinical response. Medication resistance during the index episode predicts a high rate of relapse, whereas those patients who have not received an adequate medication trial prior to ECT are less likely to relapse. If a patient who fails an antidepressant trial then responds to a course of ECT, alternative pharmacologic strategies or maintenance ECT should be considered to decrease the likelihood of relapse. Patients who do not respond to a traditional course of bilateral ECT may respond subsequently to longer courses of bilateral ECT at markedly suprathreshold stimulus intensity, or may respond to a different class of antidepressant medication from that which they failed previously.

Patient selection and remission rates with the current practice of electroconvulsive therapy in Germany
Authors: Kornhuber J, Weller M
Convuls Ther 1995 Jun;11(2):104-109 /TD>

Disorder Treated Effectiveness of ECT
Unipolar 31.9%
Bipolar 38.3%

The current practice of German psychiatric hospitals restricts electroconvulsive therapy (ECT) to patients with profound disability and failure to respond to pharmacotherapy. We studied clinical features and seizure parameters in 63 patients who received ECT in a 3-year period at a German university hospital. Patients with unipolar and bipolar disorder (depressed) (n = 47) showed a complete or partial recovery as assessed 2 weeks after completion of the ECT course in 31.9 and 38.3%, respectively. Multiple linear regression analysis performed on several clinical and ECT seizure parameters failed to identify strong outcome predictors in our selected sample of patients. Most patients who eventually responded did so early in the course of ECT, while there was little improvement when 10 ECT treatments were given. Our report highlights the efficacy of ECT in the management of severe psychiatric disorders even in a highly selected sample of patients previously found to be resistant to alternative modes of psychiatric treatment.

The impact of medication resistance and continuation pharmacotherapy on relapse following response to electroconvulsive therapy in major depression.
Authors: Sackeim HA, Prudic J, Devanand DP, Decina P, Kerr B, Malitz S
J Clin Psychopharmacol 1990 Apr;10(2):96-104

After clinical response to electroconvulsive therapy (ECT), 58 patients with major depressive disorder were followed for 1 year or until relapse. The rate of relapse was substantially higher in patients who had failed adequate antidepressant medication trials prior to ECT than in patients not determined to be medication resistant. Adequacy of post-ECT pharmacotherapy was only marginally related to likelihood of relapse. The subgroup of patients who appeared to benefit from adequate post-ECT pharmacotherapy were those who did not receive an adequate medication trial prior to ECT. The findings call into question the common practice of administering as continuation pharmacotherapy following ECT the same class of medications that patients had failed with during the acute episode prior to ECT. The findings also indicate that resistance to antidepressant medication is a strong predictor of relapse following response to ECT.
Electroconvulsive therapy in the treatment-resistant patient.
Authors: Devanand DP, Sackeim HA, Prudic J Psychiatr Clin North Am 1991 Dec;14(4):905-923

In medication-resistant patients with major depressive disorder, the response rate with bilateral electroconvulsive therapy (ECT) drops to 50% from the expected range of 80% to 90%.

Relapse rates following ECT are high in medication-resistant depressed patients and are clustered in the first 4 months following clinical response. Medication resistance during the index episode predicts a high rate of relapse, whereas those patients who have not received an adequate medication trial prior to ECT are less likely to relapse. If a patient who fails an antidepressant trial then responds to a course of ECT, alternative pharmacologic strategies or maintenance ECT should be considered to decrease the likelihood of relapse. Patients who do not respond to a traditional course of bilateral ECT may respond subsequently to longer courses of bilateral ECT at markedly suprathreshold stimulus intensity, or may respond to a different class of antidepressant medication from that which they failed previously.

EEG Monitoring in ECT: A Guide to Treatment Efficacy

EEG Monitoring in ECT: A Guide to Treatment Efficacy

by Max Fink, M.D., and Richard Abrams, M.D.

Psychiatric Times, May 1998

For over 50 years we clinicians have administered electroconvulsive therapy with little to guide us in deciding whether or not a particular induced seizure is an effective treatment. At first we thought that piloerection or pupillary dilatation predicted the efficacy of a seizure, but these signs were difficult to assess and were never subjected to controlled experiments.

The duration of the motor seizure was examined next, and in evaluations of the seizures in unilateral and bilateral ECT, it seemed reasonable to opine that a minimum of 25 seconds defined a good seizure (Fink and Johnson, 1982). In studies of unilateral and bilateral ECT with threshold and suprathresh-old energy dosing, motor seizure durations were greater than 25 seconds, yet the threshold-unilateral condition yielded ineffective courses of treatment (Sackeim et al., 1993). Indeed, the new experience finds that longer seizures are not necessarily better for determining efficacy (Nobler et al., 1993; Krystal et al., 1995; McCall et al., 1995; Shapira et al., 1996). The occurrence of a prolonged, poorly developed, low-voltage seizure of indeterminate length and poor postictal suppression is a clear call for restimulation at a higher dose, with the expectation of inducing a shorter, better developed and clinically more effective seizure.

The Seizure EEG

Modern brief pulse ECT devices provide the facility to monitor the seizure by an electroencephalogram, an electrocardiogram, and lately, an electromyogram. For a decade it has been feasible to examine the electrographic characteristics of the EEG seizure as well as its duration. The EEG usually develops patterned sequences consisting of high voltage sharp waves and spikes, followed by rhythmic slow waves that end abruptly in a well-defined endpoint. In some treatments, however, spike activity is poorly defined and the slow waves are irregular and not of particularly high voltage. It is also difficult to define the endpoint, with the record showing a waxing and waning period followed by an imprecise termination. Could these patterns be related to treatment efficacy?

One suggestion was that bilaterally induced seizures were characterized by greater midseizure ictal amplitude in the two to five hertz frequency band than those induced by unilateral ECT (Krystal et al., 1993). Moreover, the seizures in bilateral ECT showed greater interhemispheric symmetry (coherence) during the seizure and more pronounced suppression (flattening) of EEG frequencies in the immediate postictal period. In other words, bilaterally induced seizures were more intense and more widely distributed throughout both hemispheres than seizures induced with unilateral stimulation.

The clinical relevance of these observations derives from the frequently reported therapeutic advantage of bilateral over unilateral ECT in the relief of depression (Abrams, 1986; Sackeim et al., 1993). The apparent validity of these observations led others to specifically examine the clinical predictive value of the described EEG patterns.

The EEG data of Nobler et al. (1993) came from studies of patients receiving either unilateral or bilateral ECT and energy stimulation either at threshold or two and one-half times threshold (Sackeim et al., 1993; 1996). The patients who received threshold unilateral ECT fared poorly compared to those who received bilateral ECT. Regardless of the electrode placement, however, those patients who exhibited greater midictal EEG slow-wave amplitude and greater postictal EEG suppression experienced greater clinical improvement and relief of depression (Nobler et al., 1993), confirming the observations by Krystal et al. (1993). Greater immediate post-stimulus and midictal EEG spectral amplitudes, greater immediate post-stimulus interhemispheric coherence and greater postictal suppression were reported with higher dose stimuli (two and one-half times threshold) compared to barely suprathreshold stimuli (Krystal et al., 1995). In another study, clinical improvement in depression correlated best with evidence for an immediate postictal reduction both in EEG amplitude and coherence (Krystal et al., 1996).

These analyses of the seizure EEG show promise of defining a clinically effective seizure. The available brief pulse ECT devices allow visual examination of the seizure record so that we can estimate the presence and duration of spike activity and the development of rhythmic high voltage slow wave activity, measure the duration of total seizure activity, and evaluate the endpoint of the fit (precise or imprecise).

In recent research studies, the methods of EEG analysis have been complex. Investigators often use sophisticated multichannel instrumentation recorders and EEG-analytic computer systems that are not usually available in clinical settings, but their elegant findings are consistent with the visual observations of the records provided by clinical ECT devices.

EEG Seizure Measurement

ECT device manufacturers provide some quantification of the EEG changes. The clinical Thymatron� DGx device made by Somatics Inc. provides three quantitative measures of the seizure EEG: seizure energy index (integration of total energy of the seizure), postictal suppression index (degree of suppression at end of the seizure) and endpoint concordance index (a measure of the relation of the endpoints of the EMG and the EEG seizure determinations when simultaneously recorded).

In 1997, Somatics introduced a proprietary computer-assisted EEG analysis system for use with their ECT device to obtain the EEG power spectral and coherence analytic measures for routine clinical use.

In their new Spectrum 5000Q device, the Mecta Corporation makes available the EEG algorithms derived from research by Krystal and Weiner (1994) and licensed from Duke University to assist clinicians in better determining the quality and efficacy of individual seizures. The clinical significance of these measures has not been prospectively examined, yet the measures provide accessible quantitative indices of the seizure EEG which hold the promise of clinical application and provide the means for establishing their validity (Kellner and Fink, 1996).

For immediate application, clinicians can visually examine the available EEG outputs for evidence of good seizure intensity and generalization. The present criteria for an effective seizure include a synchronous, well-developed, symmetrical ictal structure with high amplitude relative to baseline; a distinct spike and slow wave midictal phase; pronounced postictal suppression; and a substantial tachycardia response. These are reasonable criteria based on present experience. Another measure, that of interhemispheric coherence (symmetry), can be roughly estimated visually from a two-channel EEG recording when care is taken to position the recording electrodes symmetrically over both hemispheres.

Examples of inadequate and adequate seizures are shown in Figures 1, 2a and 2b. These samples are derived from an ongoing study involving energy dosing estimates in the first treatment of a 69-year-old man with recurrent major depression. In the first two stimulations, 10% (50 millicoulombs) and 20% (100 millicoulombs) energies were applied. In the third application, 40% (201 millicoulombs) energy was applied. Electrode placement was bilateral.

Interseizure EEG

In patients receiving a course of ECT, EEG recordings made in the days after treatments showed profound and persistent effects. With repeated seizures, the EEG showed a progressive increase in amplitudes, a slowing and greater rhythmicity of frequencies, and the development of burst patterns. These changes in EEG characteristics were related to the number of treatments, their frequency, type of energy and electrical dosage, clinical diagnosis, patient age and clinical outcome (Fink and Kahn, 1957).

The improvement in patient behavior from the Fink and Kahn (1957) study (observed as a decrease in psychosis, lifting of depressed mood and decrease in psychomotor agitation) was associated with the development of high degrees of EEG change. The EEG characteristics predicted which patients had improved and which had not.

The association was quantitative�the greater the degree of slowing of EEG frequencies and the earlier that “high degree” slowing appeared, the earlier and more dramatic was the change in behavior. Elderly patients developed EEG changes early while younger adults were often slow in showing the changes. In some patients the EEG did not slow despite many treatments, except when the treatments were given more frequently during the week.

The association between ECT-induced interictal EEG slowing and improvement in depression was confirmed by Sackeim et al. (1996). EEG records were examined at different times during the treatment course in 62 depressed patients who received either unilateral or bilateral ECT at threshold or high-dose energies. ECT produced a marked short-term increase in delta and theta power, the former of which resulted from effective forms of ECT. The changes in the EEG were no longer present at two-month follow-up. The authors concluded that the induction of EEG slow-wave activity in the prefrontal cortex was tied to the efficacy of ECT.

An important clinical application of EEG methodology is in determining the adequacy of a course of ECT. When a clinical change does not occur in a timely fashion, the interseizure EEG can be examined visually or by computer analysis. Failure of the EEG from the frontal leads to show well-defined delta and theta activity after several treatments suggests that the individual treatments were inadequate. At such times, the treatment technique should be reexamined for adequacy (i.e., sufficient electrical dosage, choice of electrode placement, concurrent drug use), or the frequency of the treatments should be increased. If the patient fails to improve despite apparently sufficient EEG slowing, the diagnosis and treatment plan should be reexamined.

The renewed interest in the seizure EEG as a marker of seizure adequacy, and in the interseizure EEG as a marker of ECT course adequacy is likely to underlie the next phase of research into the physiology of ECT.

Dr. Fink is professor of psychiatry and neurology at the State University of New York at Stony Brook. He is the author of Convulsive Therapy: Theory and Practice (Raven Press), and founder of the quarterly journal, Convulsive Therapy.

Dr. Abrams is professor of psychiatry at the Chicago Medical School. He has conducted basic science and clinical research on ECT for more than 25 years and has written over 70 articles, books and chapters on ECT.


Abrams R (1986), Is unilateral electroconvulsive therapy really the treatment of choice in endogenous depression? Ann N Y Acad Sci 462:50-55.

Fink M, Johnson L (1982), Monitoring the duration of electroconvulsive therapy seizures: �cuff� and EEG methods compared. Arch Gen Psychiatry 39:1189-1191.

Fink M, Kahn RL (1957), Relation of EEG delta activity to behavioral response in electroshock: Quantitative serial studies. Arch Neurol Psychiatry 78:516-525.

Kellner CH, Fink M (1997), Seizure adequacy: does EEG hold the key? Convuls Ther 12:203-206.

Krystal AD, Weiner RD (1994), ECT seizure therapeutic adequacy. Convuls Ther 10:153-164.

Krystal AD, Weiner RD, Coffey CE (1995), The ictal EEG as a marker of adequate stimulus intensity with unilateral ECT. J Neuropsychiatry Clin Neurosci 7:295-303.

Krystal AD, Weiner RD, Gassert D et al. (1996), The relative ability of three ictal EEG frequency bands to differentiate ECT seizures on the basis of electrode placement, stimulus intensity, and therapeutic response. Convuls Ther 12:13-24.

Krystal AD, Weiner RD, McCall WV et al. (1993), The effects of ECT stimulus dose and electrode placement on the ictal electroencephalogram: An intraindividual crossover study. Biol Psychiatry 34:759-767.

McCall WV, Farah BA, Raboussin D, Colenda CC (1995), Comparison of the efficacy of titrated, moderate-dose and fixed, high-dose right unilateral ECT in elderly patients. Amer J Ger Psychiatry 3:317-324.

Nobler MS, Sackeim HA, Solomou M et al. (1993), EEG manifestations during ECT: effects of electrode placement and stimulus intensity. Biol Psychiatry 34:321-330.

Sackeim HA, Luber B, Katzman GP et al. (1996), The effects of electroconvulsive therapy on quantitative electroencephalograms. Relationship to clinical outcome. Arch Gen Psychiatry 53:814-824.

Sackeim HA, Prudic J, Devanand D et al. (1993), Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 328:839-846.

Shapira B, Lidsky D, Gorfine M, Lerer B (1996), Electroconvulsive therapy and resistant depression: Clinical implications of seizure threshold. J Clin Psychiatry 57:32-38.

Study: Shock Therapy Faulted

Study: Shock Therapy Faulted


CHICAGO (AP) – Patients who underwent electroshock therapy for depression had an unexpectedly high relapse rate in a study that has refocused attention on the procedure 25 years after “One Flew Over the Cuckoo’s Nest” made it seem like torture.

The treatment fell out of favor after that Oscar-winning movie, a satirical look at life in a mental hospital. But it has since made a comeback, with 100,000 Americans a year now getting it, according to the National Mental Health Association.

Electroconvulsive therapy, or ECT, is most commonly used to treat severe depression that has not responded to medication or psychotherapy.

A study of 84 patients in Wednesday’s Journal of the American Medical Association found that without follow-up medication, depression returned in 84 percent of patients within six months. Among patients who received antidepressant and anti-psychotic medication after ECT, 39 percent relapsed.

Previous research reported relapse rates of 20 percent with medication and 50 percent without.

The higher-than-expected relapse rates in the latest study reflect a debate over the procedure’s benefits and risks.

Columbia University psychiatry professor Harold Sackeim, who led the study and is one of ECT’s most vocal supporters, said that it remains the most effective treatment for depression but that his findings illustrate the need for accompanying medication.

Dr. Peter Breggin, a Bethesda, Md., psychiatrist, called the study “an open admission that electrical shock is worthless.”

He said the high relapse rate supports critics’ theory that ECT causes brain damage that for a few weeks prevents patients from expressing sadness or depression, while leading to possible long-term memory loss.

Dr. Richard M. Glass, a deputy JAMA editor, said in an accompanying editorial that the study highlights the need “to bring electroconvulsive therapy out of the shadows.”

Major depression affects about 10 percent of Americans 18 and older yearly, or about 17 million adults, according to government estimates. It has a mortality rate as high as 15 percent, mostly from suicide, Glass said.

“The results of electroconvulsive therapy in treating severe depression are among the most positive treatment effects in all of medicine,” relieving symptoms in 50 percent to 90 percent of cases, Glass said.

Still, he wrote, “on the face of it, producing convulsions with electric current seems like a strange way to treat illness.” And more than 60 years after ECT was introduced, doctors still do not know exactly how it works.

Patients typically receive three shocks weekly, under anesthesia, for up to a month, followed by medication.

ECT is endorsed by the AMA, the National Mental Health Association and the American Psychiatric Association, which recently published a report that says there is no evidence ECT causes brain damage.

Linda Andre, director of the anti-ECT group Committee for Truth in Psychiatry, criticized Sackeim for failing to investigate ECT’s side effects and said it is because of his ties to the industry.

The study was funded by the National Institute of Mental Health. Manufacturer MECTA Corp. donated the ECT equipment. Sackeim said he has worked for MECTA as an unpaid consultant but has no financial interest in the company.

Most relapses in the study occurred soon after ECT, suggesting that drug treatment should perhaps begin during ECT instead of afterward, Sackeim said. ECT also could be gradually tapered off instead of abruptly stopped.

Jerry Kirk said he has had ECT every three weeks since 1995 to control manic depression, even though he claims it has caused long-term memory loss and learning difficulties. Kirk did not want to reveal his location and employer because of the stigma of electroshock – one so great it forced vice presidential candidate Thomas F. Eagleton off George McGovern’s ticket in 1972.

“It’s a trade-off,” said Kirk, an executive with a six-figure salary. “Six, seven years ago, I couldn’t work or hold down a job.”

Pharmacotherapy Following Electroconvulsive Therapy

Pharmacotherapy Following Electroconvulsive Therapy: JAMA, March 14
This new study in JAMA highlights something that has tried to focus attention upon from its first day on the net:

ECT is a short-term solution to a long-term problem.

You can read the study for yourself, but here are some highlights:

Basically, Harold Sackeim, Ph.D., took a group of patients recruited by his research organization and divided them into three groups: placebo; nortriptyline; nortriptyline and lithium.

Although he says in his opening paragraphs that ECT has a relapse rate of 50 percent or better, his own study shows a relapse rate of 84 percent – of those who responded to ECT in the first place. The group that received nortriptyline alone had a relapse rate of 60 percent, and the third group (nortriptyline and lithium) had a relapse rate of 39.1 percent.

It’s not mentioned in the body of the article, but if you examine Figure 1, you’ll see that of 290 people who completed ECT, 114 (40 percent) did not respond.

Additionally, the patients received 200 percent of the maximal charge output, requiring special machines (supplied by Mecta Corp.). This is an extremely high dose of electricity, and one that is not available to practitioners who are not participating in research studies.

That rate of 60 percent efficacy using a double dose of electricity is a far cry from the oft-quoted 80 to 90 percent efficacy rate of ECT.

Some questions about this study are now being raised by the media due to discrepancies from Harold Sackeim:

* First there is the Mecta issue. By federal law, Dr. Sackeim was required to disclose to JAMA that he has financial ties to this manufacturer, yet it isn’t mentioned. Linda Andre, director of the ECT survivor group Committee for Truth in Psychiatry has documentation to show that he is in fact a paid consultant to Mecta, despite his continued protests that he isn’t.
* Second, Linda has documents gathered under the Freedom of Information Act that include Sackeim’s progress notes to NIMH, the funder for this study. According to her there are several discrepancies between the numbers in the published study and in his notes to NIMH. Hopefully Dr. Sackeim will publicly address these discrepancies, and would be willing to publish any statements from him, unedited.

Stunningly quick results often fade

USA Today Series

Stunningly quick results often fade

Does shock therapy work?

Many psychiatrists and patients are supporters of shock therapy because of the startlingly quick changes it usually produces.

Shock therapy lifts 70% to 95% of patients out of depression, according to most studies. That compares favorably with the most popular anti-depressants: Prozac (51%) and Zoloft (59%), according to a recent study of those drugs.

And shock therapy often seems to work on people who don’t respond to drugs. It’s also frequently used on high-risk patients – the elderly, those with AIDS, multiple sclerosis, Alzheimer’s, pregnancy, even heart transplants – who should avoid anti-depressants because they could interact badly with other medications.

But, unlike drugs, shock therapy’s benefits fade quickly.

Researchers have been unable to document any anti-depressant effect from shock that lasts longer than four weeks – a fact not disclosed to patients in educational literature or consent forms.

The standard measure of shock therapy’s effectiveness is the Hamilton Depression Score. A severely depressed person would have a score of 30 or more; a nondepressed person, less than 10.

If, after shock, the depression score goes down, the shock is judged a success.

It’s been proven repeatedly that shock therapy lowers the scores.

The American Psychiatric Association information sheet for patients says: “We know ECT works: 80% to 90% of depressed people who receive it respond favorably, making it the most effective treatment for severe depression.”

But the APA doesn’t mention that this success disappears as quickly as it comes.

Two controlled studies have been done to track how long shock’s effect lasts. The two studies compared depressed patients who were shocked with a similar group who had “fake shock” – given anesthesia and muscle relaxants but not shocked.

The results:

In a 1980 study, shocked patients’ depression scores were 26% lower than patients who received fake shock.

But one month later, there was no difference in depression scores between the two groups. A six-month follow-up also found no difference.

A 1984 study found shock patients were less depressed at two and four weeks than those receiving fake shock. But there was no difference at 12 weeks or 28 weeks.

No study has addressed the subject since. Shock researchers now consider it unethical to do studies with placebos (fake shock) on the grounds that it would be withholding treatment from a sick patient.

Shock therapy is strongly recommended to help suicidal patients.

Electroconvulsive Therapy, the textbook written by the owner of shock machine manufacturer Somatics Inc., says suicidal patients should be shocked as the first treatment, before drugs or other therapies. And a suicide threat is a common justification for giving forced shock to patients who don’t want it, under court order, according to University of Kansas sociologist Carol Warren.

But the studies show shock therapy doesn’t stop people from killing themselves.

A 1986 study involving 1,494 patients found no difference in suicide rates between shocked and non-shocked depressed patients. The study, published in Convulsive Therapy, then reviewed all previous studies on shock and suicide.

“A close examination of the literature does not support the commonly held belief that ECT exerts long-range protective effects against suicide,” the study concludes.

By Dennis Cauchon, USA TODAY

Video and audio clips about electroconvulsive therapy


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Electroshock as violence against women:
Dr. Bonnie Burstow explores electroshock as a form of violence against women. She is a feminist therapist, an anti-psychiatry and anti-fascist activist. She is also the former co-chiar of the Ontario Coalition Against Electroshock and is the author of Radical Feminist Therapy: Working in the Context of Violence. Listen

Weekly Paul Henri Thomas updates:
WGBB radio has vowed that it will carry weekly updates until Paul Henri is no longer at risk of forced electroshock treatments. You may listen to the show live on the net on Monday nights at 7 pm Eastern time. I will try and record the shows for those who miss them:

  • Feb. 26, 2001: WGBB on Long Island, New York carried a GREAT program that featured Sherry Taub, a New York activist, and PAUL HENRI THOMAS! (He’s the man at Pilgrim being forcibly electroshocked currently) He’s difficult to understand at times due to his French accent and the effects of the THIRTEEN psychiatric drugs he’s on, but it’s a great interview. A MUST LISTEN! (30 minutes)
  • March 5, 2001: The second show featuring advocate Anne Kraus talking about the hearing and the latest news on Paul Henri. (29 minutes)
  • March 12, 2001: The third show featuring Sherry Taub and Laura Ziegler talking about the latest legal news concerning Paul Henri. (38 minutes)
  • April 2, 2001: Another show, featuring Linda Andre of CTIP and Anne Kraus. (11 minutes)

My interview on CKLN Radio in Toronto, where I discussed ECT, the Kathleen Garrett case, forced ECT and other issues in September, 2000. (25 minutes)

Feb. 26, 2001: KUCI in Irvine, California has a weekly show on Mondays called Mind…Your Own Business, where they discuss mental health issues. I was the guest for this show and talked about ECT, Paul Henri, forced ECT and more. (50 minutes)

Three excerpts from the recent series by Gary Null ( on ECT and the use of force.

  • Gary interviews a number of ECT survivors, who speak about their experiences and talk about the issues surrounding ECT. Listen (45 minutes)
  • Gary speaks to psychiatrist Dan Fisher of the National Empowerment Center, who discusses issues, plus talks about why ECT isn’t an effective treatment. Dr. Fisher says 50 percent of psychiatrists are opposed to ECT. (The audio on this is a little fuzzy). Gary also discusses the current state of research and does an exhaustive lit review. Listen (22 minutes)
  • Gary interviews more ECT survivors and continues his series. Listen (57 minutes)

Dr. Max Fink on informed consent issues and protecting yourself against lawsuits (if you’re an ECT doc). (3 minutes)

Dr. Max Fink sums up how psychiatrists are given the power to play god: “The judgment is yours. Society says….YOU’RE the psychiatrist…” (1 minute)


The issues

Channel 11 in St. Louis reports on HB134 which would require ECT reporting. (48 seconds)

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An interesting clip from 60 Minutes II. (24 seconds) Oh boo hoo, CBS had the video removed.
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The Extra news show explores the issues surrounding ECT. This segment interviews Liz McGillicuddy, who lost much of her memory from electroshock in 1994. (3:47 minutes)

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It also includes interviews with Dr. John Friedberg, neurologist in California, who talks about the fact that the FDA has NEVER required safety testing of the machines, and they interview Harold Sackeim, PhD, shock proponent extraordinaire. In his interview, he *admits* that the famous 1 in 200 statistic is not based in science!
Here, Harold Sackeim admits the truth – the statistic is not based in science! (30 seconds)

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Gordon Elliot Show

Diann’a Loper discusses how a bill she helped create has helped other ECT patients. This kind of reporting MUST be made mandatory across the USA. Lobby your legislators! (30 seconds)

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Diann’a Loper fell into a post-partum depression. Her psychiatrist pushed her into ECT, and she lost everything – her marriage, her new baby, and most of her life. Says Diann’a, “I wish they would have killed me.” (2:30 minutes)

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Hope Morgan received ECT when she began suffering from insomnia. Her doctor diagnosed depression. “My life was in a shambles,” says Hope, referring to the devastation following the ECT. (3:10 minutes)

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Marcia Fink says ECT turned her life around. “I do things anyone else can do.” She says the only memory loss she suffered was three months’ worth. (1:47 minutes)

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Hal Haralson says ECT in the state hospital 40 years ago turned his depression around. (43 seconds)

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A doctor from the audience speaks against ECT, and the role of insurance companies. (1:02 minutes)

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Dr. Charles Kellner blatantly lies about the current stimulus dosing used in today’s ECT! BUSTED! (1 minute)

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More from Charles Kellner
When questioned about his financial ties to Mecta, one of the shock machine manufacturers, Dr. Charles Kellner attempts to change the subject. (32 seconds)

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Here, Dr. Kellner says the tragic experiences of patients like Hope and Diann’a are “unfortunate” and goes on to say that most people will be cured by ECT. He fails to mention the now-admitted high relapse rate, or the need for continuation/maintenance ECT. (30 seconds)

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Dr. Charles Kellner misleads the public about the effectiveness of ECT. (1 minute)

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Dr. Charles Kellner makes up a story about how ect works. The truth is, nobody knows, and he’s CAUGHT ON TAPE fabricating a nice tale. (50 seconds)

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Dr. Peter Breggin discusses the role of the FDA in the ECT controversy, and how they dropped the ball. (1 minute)

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Dr. Breggin talks about the literature, and why some people become *more* depressed after ECT. (35 seconds)

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Dr. Breggin explains how the perception of ECT has changed, and how the longstanding theory that “brain damage was helpful” has been given a new spin. (50 seconds)

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Dr. Peter Breggin sums it all up: View the clip (10 seconds)

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Scottish Documentary on Ewen Cameron, who worked with the CIA to brainwash and erase memory using electroshock. In three parts.
Part 1

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Part 2
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Part 3
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News stories on Christian Hageseth and his legal woes

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Video clips from the Mecta lawsuit, Harold Sackeim testimony