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included a Point/Counterpoint feature on electroconvulsive therapy (ECT). The feature elicited strong reactions from our readers. You can read the introductory essay, “Electroconvulsive Therapy: Obsolete and Dangerous or Still Just Misunderstood?” by Horacio A. Capote, MD, 

The authors of the original Point/Counterpoint have also continued their debate online. You can read a brief 

 for the opportunity to comment on the recent 

 articles in the April, 2021 issue on (ECT). The choice was presented as “

.” It is no choice at all: ECT is demonstrably safe and effective, but yes, still badly misunderstood.

ECT has evolved into a modern medical treatment for a limited number of psychiatric illnesses, primarily severe depression, but also psychosis and catatonia. ECT is what it is today, not what it was before modern general anesthesia, and needs to be objectively assessed, by true experts with recent experience in its use, and an understanding of the severity of the disorders it treats. We strongly support Michael E. Henry, MD’s position on ECT. He offers an accurate expert opinion based on evidence and experience. That is the information that should guide patients and physicians about ECT.

ECT has saved and improved countless lives, but as with any medical treatment or procedure, particularly one involving general anesthesia, there are risks and adverse effects; the decision to prescribe ECT always involves balancing those risks against potential benefits to the patient. That is the true, evidence-based process that expert ECT physicians follow when making a recommendation to consider ECT for a particular patient. Such a recommendation is never made cavalierly; it takes into account the severity and urgency of the psychiatric illness, the medical condition, and the treatment wishes of the patient. The informed consent process for ECT in the United States is comprehensive and follows modern ethical guidelines.

Unfortunately, misinformation perpetuates the stigma surrounding ECT. Attempts to discredit it are often based on ignorance of the realities of contemporary ECT, or worse, are ideologically driven and with questionable motives. ECT is not an ideology, a belief, or a religion. It is simply a medical procedure, with benefits and side effects. In truth there is no real point-counterpoint when one side is misinformation and distortions and the other side is medical fact.

Severe depression is disabling and sometimes life-threatening; until a worthy replacement for ECT is developed, patients and psychiatrists can be reassured that ECT is available when other treatments are ineffective. In knowledgeable medical circles, there is no controversy about that.

is the president of the International Society for ECT and Neurostimulation (ISEN). 

 is the chair of the Board of Directors of the ISEN.

A Psychiatric Times point/counterpoint feature on electroconvulsive therapy elicited strong responses.  

A Spirited Defense of ECT: From Our Readers

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, 

 have agreed to continue their debate online. Ms. Hancock, Cunliffe, and Dr Read argue that ECT is 

. 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 “

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 

 They failed to appreciate that when the authors compared the ECT patients to a risk-matched cohort, this finding did not meet statistical significance (

=.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 …”

 Similarly, Hancock and colleagues cite statistics from Duma and colleagues regarding 

 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.

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 

 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.

 They do not appear to have considered the data that show depression is associated with overactivity in these same brain regions.

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 

 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 (

 = .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.

 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.

 Although these latter results are from a separate study, the response rates are consistent with other medication studies in this population.

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.

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.

1. Henry ME. ECT: an effective and safe treatment. 

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. 

3. Peltzman T, Shiner B, Watts BV. Effects of Electroconvulsive Therapy on Short-Term Suicide Mortality in a Risk-Matched Patient Population. 

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. 

5. Gbyl K, Videbech P. Electroconvulsive therapy increases brain volume in major depression: a systematic review and meta-analysis. 

6. Fosse R, Read J. Electroconvulsive treatment: hypotheses about mechanisms of action. 

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. 

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. 

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. 

10. Tohen M, Vieta E, Calabrese J, et al. Efficacy of olanzapine and olanzapine-fluoxetine combination in the treatment of bipolar I depression. 

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. 

12. Pompili M, Verzura C, Trovini G, et al. Lurasidone: efficacy and safety in the treatment of psychotic and mood disorders. 

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

In Defense of ECT

 have agreed to continue their debate online. Below, Ms. Hancock, Ms. Cunliffe, and Dr Read argue that ECT is ineffective and unsafe. Representing the pro-ECT position, Dr Henry has responded to their article 

We thank Michael E. Henry, MD, for responding to our article electroconvulsive therapy (ECT): “

,” Henry challenges the conclusion of a recent review

 that there is no robust evidence to determine whether ECT is better than placebo: “The selection criteria used by Read and colleagues were limited to older studies (1956 to 1985).”

 The selection criteria were not time-limited. There simply have not been any placebo-controlled ECT studies since 1985.

 Furthermore the 11 pre-1986 studies were grossly flawed.

We agree with Henry that modern treatment approval requires rigorous, randomized, placebo-controlled methodology using the universally accepted standards of evidence-based medicine. ECT clearly lacks this sort of evidence-base.

Henry produces 3 traditional defences for this empirical data vacuum. First, he argues that studies without placebo control groups, such as comparing different electrode placements, are sufficient. A review of these non-placebo studies, however, revealed that none “produced robust evidence that ECT is effective for depression, primarily because at least 60% maintained ECT participants on medication, 89% produced no meaningful follow-up data beyond the end of treatment, and none investigated whether ECT prevents suicide.”

Second, Henry refers to “more than 75 years of clinical experience”

 as evidence of efficacy. Unfortunately, history is littered with treatments used for decades until deemed ineffective, harmful, or both.

Third, Henry brings up the “ethical dilemma of treating very ill patients with a placebo treatment.”

 But this assumes ECT is safe and more effective than a placebo, and that is precisely what is in question. Assuming its efficacy would position ECT proponents beyond the parameters of evidence-based medicine. Testing treatments in vulnerable populations is essential to establish efficacy, safety limits, and device regulatory protocols.

Henry portrays ECT-induced brain abnormalities, like hippocampal enlargement, as necessarily beneficial. However, a 2013 review of more than 100 imaging studies concluded “the temporarily improved scores on depression instruments following ECT reflect the combination of frontal and temporal lobe functional impairments and activation of the HPA axis and the mesocorticolimbic dopamine system. These effects as well as other detailed changes observed in structures such as the hippocampus appear consistent with those typically seen after severe stress-exposure and/or brain trauma.”

There is no evidence that ECT prevents suicide. A recent study found that 14,810 ECT patients were 1.3 times more likely to die by suicide than 58,369 ECT controls.

1. ECT provides only short-term symptom relief. There are no studies demonstrating ECT outperforms placebo beyond treatment termination, and none that it prevents suicide.

2. Between 12% and 55% of ECT recipients live with persistent memory loss,

 which is suffered disproportionately by women and older individuals, ECT’s target demographic groups.

3. Thymatron ECT device manufacturer lists 7 administration technique variables associated with risks of “

permanent brain damage and permanent memory loss

4. One in 50 ECT recipients suffer “major adverse cardiac events and death after ECT.”

5. Despite repeated requests, the US Food and Drug Administration acknowledges never receiving premarket PMA studies assessing safety or Product Development Protocols to establish 

 ECT research has still not produced any safety testing using modern clinical parameters, dosing limits, or universal administration technique protocols to reduce risks and enable replicable results.

6. Medicare reimburses ECT providers who fail to report quality data, without limits in the number of treatments provided or 

 The 34% increase in US hospitals providing ECT since device reclassification may reflect what happens when hospitals identify an unregulated income source.

7. No one knows how many Americans receive ECT each year, or how many treatments each individual receives, or 

8. ECT recipients are not provided legal informed consent regarding all risks.

9. ECT providers are not routinely assessing each patient for all known risks.

10. Repetitive intracranial mild traumatic brain injury has life-long consequence.

11. ECT recipients injured by treatment are rarely referred for comprehensive rehabilitation to improve quality of life.

12. ECT privileging requirements in the US do not include studying its 

 Without such training, psychiatrists cannot provide appropriate long-term follow-up as recommended by Thymatron device manufacturer.

Failure to acknowledge adverse effects of ECT, with life altering consequences in some patients, creates insurmountable barriers to those injured who need appropriate rehabilitation interventions to improve quality of life after treatment. ECT’s immediate and long-term damage to so many far outweigh its temporary benefits for some individuals.

 is a nationally certified rehabilitation counselor and former Clinical Rehabilitation Counseling and Clinical Mental Health faculty member at San Diego State University. More than a decade ago, Sarah received 116 ECT treatments and now lives with long-term neurological sequalae of repeated exposure to high electrical fields.

is professor of clinical psychology at the University of East London. He is chair of the International Institute for Psychiatric Drug Withdrawal and editor of the scientific journal 

. He has authored several books and more than 200 research papers.

was a pediatrician in the UK until she left her job after undergoing ECT. She has become an advocate for other ECT patients. 

. 2021;38(4):4,7. Accessed April 16, 2021.

2. Read J, Hancock S, Cunliffe S, Henry ME. ECT: dangerous on either side of the pond. 

. 2021;38(4):4-6. Accessed April 16, 2021. 

3. Read J, Kirsch I, McGrath L. Electroconvulsive therapy for depression: a review of the quality of ECT versus sham ECT trials and meta-analyses. 

4. Gregory S, Shawcross CR, Gill D. The Nottingham ECT Study. A double-blind comparison of bilateral, unilateral and simulated ECT in depressive illness. 

5. Read J, Arnold C. Is electroconvulsive therapy for depression more effective than placebo? A systematic review of studies since 2009. 

7. Peltzman T, Gottlieb DJ, Shiner B, et al. Electroconvulsive Therapy in Veterans Health Administration Hospitals: Prevalence, Patterns of Use, and Patient Characteristics. 

Regulatory Update to Thymatron System IV Instruction Manual

. Somatics, LLC; 2018. Accessed May 6, 2021. 

9. Duma A, Maleczek M, Panjikaran B, et al. Major adverse cardiac events and mortality associated with Electroconvulsive Therapy: A Systematic Review and Meta-analysis. 

10. Food and Drug Administration. Reclassification of electroconvulsive therapy devices; effective date of requirement for premarket approval for electroconvulsive therapy devices for certain specified intended uses. Published online December 26, 2018. Accessed May 6, 2021. 

11. Centers for Medicare & Medicaid Services. Medicare program: fiscal year 2021 inpatient psychiatric facilities prospective payment system and special requirements for psychiatric hospitals for fiscal year beginning October 1, 2020. 42 CFR Parts 412 and 482. 2020;16990. 

12. Hancock SP. Whose finger is taking the pulse of America’s shock treatment controversy? Mad In America. July 16, 2020. Accessed May 6, 2021. 

13. American Psychiatric Association Committee on Electroconvulsive Therapy. 

The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging: A Task Force Report of the American Psychiatric Association. 2nd ed.

 American Psychiatric Association; 2001. Accessed May 5, 2021. 

ECT has been in use for decades, but does that mean it is safe or effective? 

Raising Doubts About ECT

                                                                                                     - Series Editor Gregory Eghigian, PhD

Eighty years ago, a mute man with paranoid schizophrenia, exhibiting delusions, hallucinations, and mannerisms, was found wandering the streets of Naples. On April 21, 1938, on the first floor of Rome Royal University Clinic for Nervous and Mental Illnesses, he became the first individual to be given what became known as electroshock treatment (electroconvulsive therapy or ECT) with 

 A turning point in psychiatric treatment, the psychiatrist who performed the treatment was Ugo Cerletti, MD, assisted by Lucio Bini, MD.

Ugo Cerletti (1877-1963) trained in psychiatry and neurology at leading European centers before becoming head of the Institute for Neuropsychiatry in Rome in 1935.

During a lengthy career, Cerletti distinguished himself with research in many areas. He conducted neuropathological studies on perivascular corpuscles (now known as 

), general paresis, and had a special interest in goitres—cretinism was prevalent in some parts of Italy—which he was still studying in his 80s. A creative and questioning mind, his interests extended beyond medicine; for example, he introduced white uniforms for Alpine troops and designed an advanced artillery missile.

Ideas about using electricity on the nervous system go back to suggestions from the Greeks 2000 years ago. Cerletti was interested in the electrical provocation of seizures, which had already been used for 60 years. His electroshock machine, built by his associate Bini, was originally intended for research on epilepsy.

Giving live patients electric shocks could potentially stop their hearts, leading to death. Cerletti visited the Rome abattoirs and learned that the animals were first stunned by a current delivered across the temples, thus sparing the heart.

Of the biological therapies in the 1930s ECT was the most successful and lasting treatment. It had started with a serendipitous misconception that epilepsy and schizophrenia were mutually antagonistic. This led to the cardiazol therapy of Ladislas Meduna, MD, preceded by prefrontal leucotomy and 

 Some saw coma therapy as a progression from Julius Wagner-Jauregg, MD’s fever shock treatment for what was then called general paralysis of the insane. But cardiazol, although effective, had unpleasant side effects, including a terrible premonition of death before the seizure.

 Inducing the convulsion by electricity was cleaner, cheaper, and less cumbersome.

In his account of the first ECT treatment, Cerletti created a self-exalting myth. There were 3 failed attempts on the patient, each with a higher voltage, before getting a seizure. The hapless patient shouted “Another time is murderous ”before having his fit. It took a fortnight before Cerletti publicized his endeavor, suggesting some 

Cerletti believed that the therapeutic effect of ECT was produced by acroaginine (ECT in a bottle, according to Edward Shorter, MD) during the seizures and did extensive research on animals to isolate the substance, 

ECT was used to treat schizophrenia, but by the 1940s physicians realized that it was more effective for affective disorders, and the epilepsy/schizophrenia antagonism hypothesis was finally 

 Thus was born a new treatment in psychiatry that has saved countless lives despite the continuing stigma, myths, and 

Cerletti’s venture into electroshock was done when fascism was at its height. Italian psychiatry, although heavily influenced by German psychiatry, had its own character. From the start it regarded neurology as an equal partner with a strong focus on 

 It did not follow the German model of killing psychiatric patients, which presaged the horrors of the Holocaust.

 To his credit Cerletti did not support the fascist party, although it is reported that he read the literature.

It is ironic that the most life-saving treatment in psychiatry was discovered by someone who saw himself as primarily a neurologist—an indictment of the chasm that has grown between the 2 

Despite all of his successes, Cerletti, “the most renowned representative of Italian neuropsychiatry in the mid-twentieth century,” can be considered unlucky. Despite being twice nominated, he never won the Nobel Prize; it would have been 

 is Clinical Associate Professor at the Graduate School of Medicine, Wollongong University, Australia.

1. Cerletti U, Bini L. Electroshock *†. 

2. Rzesnitzek L. ‘A Berlin psychiatrist with an American passport’: Lothar Kalinowsky, electroconvulsive therapy and international exchange in the mid-twentieth century. 

Shock Therapy: A History of Electroconvulsive Treatment in Mental Illness

5. Berrios GE. The scientific origins of electroconvulsive therapy: a conceptual history. 

6. Burgese DF, Bassitt DP. Variation of plasma cortisol levels in patients with depression after treatment with bilateral electroconvulsive therapy. 

7. Babini VP. Looking back: Italian psychiatry from its origins to Law 180 of 1978. 

8. Piazzi A, Testa L, Del Missier G, et al. The history of Italian psychiatry during Fascism. 

9. Kotsaki K, Diamantis A, Magiorkinis E. Ugo Cerletti (1877-1963): an early Italian father of electroshock and a pioneer in many other ways. 

10. Sandrone S, Cambiaghi M. Ugo Cerletti (1877-1963). 

Against the backdrop of European fascism, an Italian physician pioneered a new treatment. 

The Man Who First Used ECT: Ugo Cerletti 

Psychiatry may be lagging behind other branches of medicine in an important way.

“In the rest of medicine, as you increase the acuity you increase the number of treatments,” Nolan Williams, MD, told the attendees of the 2021 American Psychiatric Association (APA) Annual Meeting, but in psychiatry, “as we increase acuity we actually lose treatment options.”

Williams and his fellow presenters at a panel on rapidly acting medications

 all had the same question: How can psychiatrists design treatments to respond to sudden-onset conditions?

Williams, assistant professor of psychiatry and behavioral sciences at Stanford University Medical Center, described the situation as “emergency room purgatory.” Because of slow-acting treatments and limited hospital capacity, “the whole process of going through the inpatient unit can take several months,” he said. “The only treatment that we have available for these folks is ECT [electroconvulsive therapy.” But ECT is available in only 10% of US hospitals.

However, psychiatrists might have other options for fast-acting treatments. He shared 

showing that accelerated theta burst repetitive transcranial magnetic stimulation (r-TMS) had positive results for mood disorders, including MDD.

 R-TMS treatment works by stimulating the left dorsolateral prefrontal cortex (DLPFC). In MDD, the DLPFC may be failing to inhibit the subgenual cingulate, and the result of this network failure is cognitive impairment and inwardly directed negative thoughts,” Nolan explained. “By stimulating DLPFC, r-TMS corrects the mood imbalance and restores mood regulation.”

In initial numbers from his study of patients with a treatment-resistant mood disorder (TRD), Nolan found that after 5 days of sessions (10 hourly sessions at 1800 theta-burst pulses per hour), participants improved. On the Montgomery Asberg Depression Rating Scale (MADRS), he found an 80% average reduction of participants MADRS scores.

Another options for fast-acting treatment is ketamine. Charles DeBattista, MD, professor of psychiatry and behavioral sciences at Stanford University, presented evidence for its efficacy for TRD. He noted that ketamine is an anesthetic agent, a μ-opioid agonist, and while its effects on TRD are rapid, making it potentially helpful in psychiatric emergencies. “Often within a couple of hours to a day, patients experience a significant improvement, and the effects were sustained for a week or so,” he said. These effects did decrease after a week, but there is also evidence that repeated injections may lead to 

DeBattista also presented the option of esketamine, which has been fast tracked by the US Food and Drug Administration for treating TRD and acute suicidality in MDD. Multiple studies have found that it rapidly 

New mothers represent another population that might benefit from fast-acting medications. “Maternal mental health is something that’s been an enormous problem forever,” said Samantha Meltzer-Brody, MD, MPH. “Those of us that have the privilege of working with perinatal women are always struck by how debilitating PPD [postpartum depression] can be.” Rapidly acting medications could reduce mortality and morbidity, she said, and allow for more positive interactions between mothers and their newborns.

Although many selective serotonin reuptake inhibitors are approved to treat PPD, she pointed out that their initial effects may not be felt for weeks or even months, and many women’s symptoms do not respond to them. Meltzer-Brody, the Assad Meymandi Distinguished Professor and Chair in the University of North Carolina Department of Psychiatry, also considers an alternative to these medications: neurosteroids like brexanolone.

In a 2018 paper, Meltzer-Brody and her coauthors found brexanolone to be effective for

 Using the HDRS for measurement, the researchers found an average 8- to 10-point reduction in 12 hours, and around an 18-point reduction at 60 hours, the study’s primary endpoint. At day 30, participants average reduction remained, on average, 16 points down from baseline. The paper hypothesized that brexanolone works by increasing γ-aminobutyric acid (GABA) function, which appears to be inhibited during PPD.

With these new options, it seems psychiatry may not lag behind other branches of medicine for long. 

1. Williams N. Developing rapidly acting antidepressants: neurosteroids, dissociative agents (Ketamine Analogues and Psilocybin), and Accelerated Theta Burst r-TMS. Paper presented at: American Psychiatric Association Annual Meeting; May 1-3, 2021; virtual.

2. Nettekoven C, Volz LJ, Kutscha M, et al. Dose-dependent effects of theta burst rTMS on cortical excitability and resting-state connectivity of the human motor system. 

3. Li CT, Chen MH, Juan CH, et al. Efficacy of prefrontal theta-burst stimulation in refractory depression: a randomized sham-controlled study. 

4. Yip AG, George MS, Tendler A, et al. 61% of unmedicated treatment resistant depression patients who did not respond to acute TMS treatment responded after four weeks of twice weekly deep TMS in the Brainsway pivotal trial. 

5. Murrough JW, Perez AM, Pillemer S, et al. Rapid and longer-term antidepressant effects of repeated ketamine infusions in treatment-resistant major depression. 

6. Canuso CM, Singh JB, Fedgchin M, et al. Efficacy and safety of intranasal esketamine for the rapid reduction of symptoms of depression and suicidality in patients at imminent risk for suicide: results of a double-blind, randomized, placebo-controlled study. 

7. Fu DJ, Ionescu DF, Li X, et al. Esketamine nasal spray for rapid reduction of major depressive disorder symptoms in patients who have active suicidal ideation with intent: double-blind, randomized study (ASPIRE I). 

8. Meltzer-Brody S, Colquhoun H, Riesenberg R, et al. Brexanolone injection in post-partum depression: two multicentre, double-blind, randomised, placebo-controlled, phase 3 trials. 

What treatments could handle both psychiatric emergencies and long-standings mental health conditions—in a hurry?  

Fast-Acting Options for Mood Disorders and Psychiatric Emergencies

B. ECT is a viable treatment and I would recommend it in some cases

C. ECT is use an approved treatment but I would not recommend it

Is ECT a viable or a dangerous treatment for psychiatric disorders? Is there a middle road? Share your thoughts in our poll.

PsychPoll: ECT, Yay or Nay?

The article by John Read, PhD, and colleagues argues in favor of suspending the use of electroconvulsive therapy (ECT) due to a lack of efficacy data and unacceptable adverse effects, specifically, brain damage.

 Unfortunately, the analysis is based on studies conducted prior to the modern era of ECT, and it draws on a limited slice of the available safety and efficacy data for ECT. More recent studies have found key areas of efficacy (

The selection criteria used by Read and colleagues were limited to older studies (1956 to 1985) and critiques of the quality of the data. Thus, the piece is judging clinical trial designs from the 1980s and earlier, using 2019 standards. It is no surprise that the included studies do not utilize methodology developed after the studies were completed. More importantly, the analysis did not include reports that compare different types of ECT, and comparisons of ECT with pharmacotherapy were also not included. This excludes most of the recent meta-analyses and clinical trials of ECT, which have used state-of-the-art clinical trial design. For example, a recent meta-analysis conducted by 

 compared ultrabrief pulse right unilateral (RUL) ECT with brief pulse RUL ECT.

 They found remission rates of 44.9% for brief pulse right unilateral ECT vs 33.8% for ultra-brief pulse RUL ECT (OR, 0.71; 95% CI, 0.51-0.99; P = .045). Their meta-analysis showed that brief pulse caused more cognitive adverse effects than ultrabrief pulse, but there were no data after the acute course.

Since ECT is considered to be an established treatment, it can be used as an active comparator in a noninferiority paradigm, avoiding the ethical dilemma of treating very ill patients with a placebo treatment. As such, Helle K. Schoeyen, MD, PhD, and colleagues 

 brief-pulse RUL ECT to algorithm-based pharmacology in a cohort of patients with treatment-resistant bipolar depression.

 At the end of a 6-week trial, the Montgomery-Asberg Depression Rating Scale scores in the ECT group were 6.6 points lower than those of the pharmacological treatment group (95% CI, 2.5-10.6; P = .002). In a 

, Charles Kellner, MD, and colleagues compared continuation ECT augmented by venlafaxine with lithium plus venlafaxine in geriatric depression.

 At 24 weeks, the ECT group had statistically significantly lower depression scores (Hamilton Depression Rating Scale score, 4.2; 95% CI, 1.6-6.9) than the medication only group. If ECT were not more effective than placebo, as Read and colleagues proposed, there would be no difference in the efficacy of different types of ECT, nor would ECT perform better than standard pharmacology. Taken together, these studies support the acute and sustained clinical efficacy of ECT and are inconsistent with the lack of efficacy proposed by Read and colleagues.

The main safety concern raised by Read and coauthors is that ECT causes brain damage. Specifically, they argued that the changes to autobiographical memory and the memory difficulties reported by patients following ECT treatment are evidence of brain damage. They also cited “microvascular, neuronal, voltage-gated ion channel damage that is visible on standard brain scans” as further buttressing this argument.

 The piece also leverages an article from 1946,

 and the minutes from a traumatic brain injury advisory board meeting8 to support the brain damage claim. However, it does not appear that the more recent studies that fail to show chemical or structural evidence of brain damage with ECT,

 nor those that suggest improvement in cognitive function relative to baseline following ECT.

Perhaps the most interesting finding regarding the memory effects of ECT is that the hippocampal volume, which has been shown to 

 in major depression, increases following a course of ECT treatment.

 This finding has been supported by 2 recent studies. Leif Oltedal, MD, PhD, and colleagues reported results from a multicenter imaging trial of the effects of ECT on hippocampal volume using structural magnetic resonance imaging in 281 patients from the Global ECT-Magnetic Resonance Imaging Research Collaboration.

 Their results showed an increase in hippocampal volume in participants receiving unilateral or bilateral ECT, while the 95 control participants who did not receive ECT did not show changes between the 2 scans.

This finding was corroborated by a systematic 

 of ECT’s effects on the brain’s structure by Krzysztof Gbyl, MD, and Paol Videbech, MD, DMSc.

 They reviewed 32 studies with 467 patients and 285 controls, and drew a number of interesting conclusions. None of the studies they reviewed reported evidence of brain damage. Instead, the studies found that hippocampal volume as well as other cortical and subcortical regions showed increases in volume. The authors noted that the increases in brain volume tended to occur in regions of the brain thought to be involved in the pathophysiology of depression.

 They also reviewed 5 diffusion tensor magnetic resonance imaging studies with a total of 92 patients and 62 controls, and the changes they found indicated increased, not decreased, white matter integrity between the frontal and temporal lobes after ECT. These finding are also consistent with results from a retrospective chart review study by my research group. We were able to identify 100 patients who had received at least 50 ECT treatments, 36 of whom received 100 ECT treatments as part of an acute course of ECT that transformed into maintenance treatment. Cognitive function as measured by the Montreal Cognitive Assessment essentially did not change in either group.

 In short, in an illness thought to result from decreased prefrontal cortical activity and connectivity to limbic structures, there is consistent evidence of increased volume and connectivity, not atrophy, following state-of-the-art modified ECT, which is corroborated by the available cognitive data.

The other safety concerns raised were an increased risk of major cardiac adverse events and an increased risk of death from ECT. While ECT does cause dramatic swings in heart rate and blood pressure, these effects are transient and well known. Further, the swings can be managed with thoughtful pretreatment, assessment, and careful monitoring during the procedure. Consistent with this approach, Niels Tørring, MSc, PhD, and colleagues 

 a systematic review and pooled data analysis from 15 studies and found a death rate of 2.1 per 100,000 treatments.

 This is a decrease from the 4 per 100,000 treatments previously reported.

 Given the population that typically receives ECT, this decline in mortality likely reflects improvements in the medical management of chronic medical conditions and anesthetic technique. These data clearly do not support the assertion of an increased risk of death with ECT.

In summary, the concerns that were raised about ECT are commonly shared by the general public, and they are based on data from older studies that used the methodology now considered outdated both in terms of ECT practice and analytic techniques. Read and colleagues did not consider more recent, state-of-the-art clinical trial data that corroborate more than 75 years of clinical experience supporting the efficacy of ECT in a population of patients who suffer significant disability, increased medical comorbidity, and increased mortality.

1. Read J, Kirsch I, McGrath L. Electroconvulsive therapy for depression: a review of the quality of ECT versus sham ECT trials and meta-analyses. 

2. Tor P-C, Bautovich A, Wang MJ, et al. 

A systematic review and meta-analysis of brief versus ultrabrief right unilateral electroconvulsive therapy for depression

3. Schoeyen HK, Kessler U, Andreassen OA, et al. 

There is consistent evidence of benefits following state-of-the-art modified ECT.

Electroconvulsive Therapy

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