In Defense of ECT

Article

Research data shows that ECT is often more effective than alternative treatments, and safe too.

Prostock-studio/AdobeStock

Prostock-studio/AdobeStock

Editorial note: the April issue of Psychiatric TimesTM included a Point/Counterpoint feature on electroconvulsive therapy (ECT). You can read the introductory essay, “Electroconvulsive Therapy: Obsolete and Dangerous or Still Just Misunderstood?” by Horacio A. Capote, MD, here.

The authors of the original pro and con articles have agreed to continue their debate online. Ms. Hancock, Cunliffe, and Dr Read argue that ECT is ineffective and unsafe. Representing the pro-ECT position, Dr Henry has responded to their article below.

I would also like to thank Sarah Hancock, MS, CRC, Sue Cunliffe, MBchB, RCPCH, John Read, PhD for responding to my article “ECT: An Effective and Safe Treatment.”1

Their objections to electroconvulsive therapy (ECT) are primarily focused on the cognitive side effects, which they feel are caused by ECT-induced brain damage, and methodologic issues with studies supporting the efficacy of ECT. The main problem with their critique is that they appear to misinterpret the statistics they are presenting.

For example, when they discussed the findings of Peltzman and colleagues, they reported that the study found that ECT patients in the Veterans Health Administration (VHA) were 1.3 times more likely to die by suicide than controls.2,3 They failed to appreciate that when the authors compared the ECT patients to a risk-matched cohort, this finding did not meet statistical significance (P=.095), despite the large sample size of 14,810 ECT patients and 58,369 controls. They also failed to mention the authors’ conclusion that the “use of ECT in the VHA is rare. Patients who receive ECT have a complex and high-risk profile …”3 Similarly, Hancock and colleagues cite statistics from Duma and colleagues regarding major cardiac events following ECT.4 In their meta-analysis of the major cardiac events, the authors conservatively excluded 28 of 82 studies because they reported no adverse events. Without inclusion of this group the incidence of cardiac deaths and all-cause mortality were 0.18 and 0.33 per 1000 patients, respectively. When this group of studies was included, the incidence of cardiac deaths and all-cause mortality dropped to 0.04 and 0.13 per 1000 patients. They also did not consider that in the Veterans Health cohort, the risk ratio of all-cause mortality for the ECT group was a statistically non-significant 0.88, less than the non-ECT group.2,3

My previous response to the question of whether ECT causes brain damage has already highlighted the findings and conclusions of Gbyl and Videbech, who reviewed 32 imaging studies of ECT with a total of 467 patients and 285 controls. They reported that none of the studies they reviewed found evidence of brain damage.5 Hancock and colleagues point to EEG, PET, SPECT, and fMRI data that show relative decreases in the activity of the frontal and temporal lobes after ECT as evidence that ECT causes brain damage.6 They do not appear to have considered the data that show depression is associated with overactivity in these same brain regions.7

In addition to failing to present a balanced interpretation of the safety data for ECT, Hancock and colleagues ignore converging lines of evidence that support the efficacy of ECT. For example, they reject a study such as that published by Helle and colleagues, for lack of a placebo control.8 In this study, the authors used a randomized parallel treatment design with blinded raters to compare brief-pulse RUL to algorithm-based pharmacology in 73 subjects with bipolar depression. They found a significantly higher response rate of 73.9% for the ECT group versus 35.0% for the medication group (P = .01). These results are remarkably similar to those of Perugi and colleagues, who treated 522 consecutive patients with treatment-resistant bipolar disorder with ECT and found response rates of 68.1 for bipolar depression, 72.9% for mixed state, 75% for mania and 80% for catatonia.9 To provide some context for these response rates, one of the pivotal clinical trials for the olanzapine/fluoxetine combination treatment for bipolar depression reported a response rate of 56.1% for the active drug versus 30.4% for the placebo treatment arm.10 Although these latter results are from a separate study, the response rates are consistent with other medication studies in this population.11,12

Most importantly, we should not forget that the treatment options for individuals afflicted with severe depression, many of whom actively contemplate suicide frequently, are limited. Hancock and colleagues should apply balanced, rigorous scientific scrutiny to the available data before they advocate against ECT. Their analysis to date has not met that standard.

Dr Henry is the head of ECT and lecturer on psychiatry at Massachusetts General Hospital. He receives salary support from a National Institutes of Health grant on ECT.

References

1. Henry ME. ECT: an effective and safe treatment. Psychiatric Times. 2021;38(4):4,7.

2. Peltzman T, Gottlieb DJ, Shiner B, Riblet N, Watts BV. Electroconvulsive Therapy in Veterans Health Administration Hospitals: Prevalence, Patterns of Use, and Patient Characteristics. J ECT. 2020;36(2):130-136.

3. Peltzman T, Shiner B, Watts BV. Effects of Electroconvulsive Therapy on Short-Term Suicide Mortality in a Risk-Matched Patient Population. J ECT. 2020;36(3):187-192.

4. Duma A, Maleczek M, Panjikaran B, Herkner H, Karrison T, Nagele P. Major Adverse Cardiac Events and Mortality Associated with Electroconvulsive Therapy: A Systematic Review and Meta-analysis. Anesthesiology. 2019;130(1):83-91.

5. Gbyl K, Videbech P. Electroconvulsive therapy increases brain volume in major depression: a systematic review and meta-analysis. Acta Psychiatr Scand. 2018;138(3):180-195.

6. Fosse R, Read J. Electroconvulsive treatment: hypotheses about mechanisms of action. Front Psychiatry. 2013;4:94.

7. Dale E, Pehrson AL, Jeyarajah T, et al. Effects of serotonin in the hippocampus: how SSRIs and multimodal antidepressants might regulate pyramidal cell function. CNS Spectr. 2016;21(2):143-161.

8. Schoeyen HK, Kessler U, Andreassen OA, et al. Treatment-resistant bipolar depression: a randomized controlled trial of electroconvulsive therapy versus algorithm-based pharmacological treatment. Am J Psychiatry. 2015;172(1):41-51.

9. Perugi G, Medda P, Toni C, et al. The role of electroconvulsive therapy (ECT) in bipolar disorder: effectiveness in 522 patients with bipolar depression, mixed-state, mania and catatonic features. Curr Neuropharmacol. 2017;15(3):359-371.

10. Tohen M, Vieta E, Calabrese J, et al. Efficacy of olanzapine and olanzapine-fluoxetine combination in the treatment of bipolar I depression. Arch Gen Psychiatry. 2003;60(11):1079-1088.

11. Bahji A, Ermacora D, Stephenson C, et al. Comparative efficacy and tolerability of adjunctive pharmacotherapies for acute bipolar depression: a systematic review and network meta-analysis. Can J Psychiatry. 2021;66(3):274-288.

12. Pompili M, Verzura C, Trovini G, et al. Lurasidone: efficacy and safety in the treatment of psychotic and mood disorders. Expert Opin Drug Saf. 2018;17(2):197-205.

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