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After many years of inaction, the FDA issued a final order on the classification of ECT devices in December, 2018.

 The very good news is that the order allows for ongoing availability of ECT devices in the US; the slightly less good news is that the new list of “on label” indications for ECT is shorter than in the past. To understand the implications of the new order, let’s review some of the background leading up to it, as well as the state of ECT in the US today.

The FDA regulates medical devices as well as drugs. As you might imagine, some aspects of this regulation are straightforward and easy to understand, but some are complicated, arcane, and highly bureaucratic. (For a review of earlier FDA actions leading up to the recent order, please see 

https://www.psychiatrictimes.com/electroconvulsive-therapy/fda-advisory-panel-reclassification-ect-devices

.) Medical devices are classified into three risk categories, with Class I considered the safest, Class III the riskiest.

Until now, ECT devices had been “grandfathered” into Class III for all indications, and the list of “cleared indications” was depression (unipolar and bipolar), schizophrenia, bipolar manic (and mixed) states, schizoaffective disorder, schizophreniform disorder, and catatonia. That list conforms well to the generally accepted uses of ECT in the US. The FDA needed to update the classification of all “grandfathered” devices, and the process (this is the complicated part) would require “premarket approval” for indications that would not be moved from Class III to Class II. Premarket approval typically requires new controlled clinical trials to demonstrate safety and efficacy, a requirement that would not be feasible, for both financial and ethical (the inappropriateness of subjecting very seriously ill psychiatric patients to placebos) reasons. Thus, it was crucial that some (at least one) of the previously “cleared indications” be moved to Class II, in order not to interrupt the availability of ECT devices for the US market.

The new ruling does just that: it moves two indications (depression and catatonia) into Class II, with “special controls.” The “special controls” are a series of requirements regarding technical parameters of the devices, labeling about adverse effects, practitioner training, and a few aspects of clinical practice.

So, what are the implications of the FDA order reclassifying ECT devices for ECT practice in the US? Most importantly, the move of the depression indication into Class II insures that the majority of ECT patients will continue to be treated without any change in their care. The way the order is written for this indication (that the depression should be “a severe major depressive episode associated with major depressive disorder or bipolar disorder in patients aged 13 years and older who have treatment resistance or who require a rapid response due to the severity of their psychiatric or medical condition”) mirrors closely clinical practice for the majority of patients referred for ECT in contemporary US practice.

The move of the indication “catatonia,” to Class II is also very important, but applies to a much smaller subset of ECT patients, perhaps no more than 5%.

 In my estimate, the two indications moved to Class II constitute 60% to 70% of current American ECT practice.

What about the other 30% to 40%? The FDA order makes it very clear that the FDA does not regulate clinical practice; they actually say this several times in the text accompanying the order: “FDA does not regulate the practice of medicine (see section 1006 of the FD&C Act [21 U.S.C. 396]). Diagnosis and treatment of patients are clinical decisions that fall within the practice of medicine.” In other words, practitioners are free to continue to prescribe ECT for any patient, regardless of diagnosis, whom they feel would benefit from the treatment.

This is similar to the freedom to use a medication for an off-label indication. The fact that the FDA chose to leave schizophrenia, schizoaffective disorder, and mania in Class III is perplexing and disappointing. Globally, schizophrenia may be the leading indication for ECT, and the clinical and research evidence base supports ECT as safe and effective for this illness.

One of the issues related to the FDA’s consideration of reclassification of indications is that they have a bundled, unitary concept of “safety and effectiveness.” Thus, their review panel may not have been convinced by the data for effectiveness of ECT in schizophrenia, but this has no bearing on safety. In fact, there is no reason to believe that the safety profile of ECT differs by psychiatric diagnosis.

Overall, the FDA order allows patients who need and want ECT, as well as practitioners who perform it, to breathe a sigh of relief. ECT will continue to be an important, albeit small, part of the psychiatric armamentarium landscape. From speaking with fellow ECT practitioners around the country, it is apparent that ECT use is increasing. The ongoing enthusiasm for transcranial magnetic stimulation and ketamine (intravenous or intranasal) has done little to decrease the demand and need for ECT; indeed, many of the patients whom we see in ECT consultation have tried those newer treatments but the treatments have failed.

The psychiatric community has a responsibility to support and promote treatments that are in the best interests of our patients, those treatments with a track record of safety and effectiveness. ECT certainly fits that bill. But organized psychiatry has always been a tad, or more, ambivalent about supporting ECT. Amazingly, there is no official path to training in ECT, there is no board certification, and it is unclear if the next generation of ECT practitioners will be large enough for the need. In a country with 49,000 psychiatrists, it is estimated that fewer than 1000 actually practice ECT.

Modern ECT allows virtually all patients who need this modality to be treated safely, effectively, and with a level of tolerability previously unheard of. The proper understanding and contextualization of the (largely transient) cognitive effects of ECT suggests that exaggerated concerns about this adverse effect should not interfere with the appropriate prescription of a potentially life-saving treatment.

We believe that the adverse cognitive effects of ECT should be considered a tolerability and not a safety issue. In medicine, safety refers to the risk of physical injury or death. To elevate cognitive adverse effects to this level perpetuates the stigma surrounding ECT.

The most apt analogy to properly contextualize the seriousness of depressive illness weighed against the risks of ECT is cancer and chemotherapy. Many cancers are lethal, life-threatening illnesses for which treatments (surgery, chemotherapy, and radiation) carry considerable risks. Patients rarely categorically refuse cancer treatments because of concerns about adverse effects, yet this happens frequently with ECT. Our contention is that refusing ECT because of concerns about memory loss is equivalent to refusing cancer chemotherapy because of concerns about hair loss.

These effects are unpleasant and upsetting, but not worth risking one’s life over. Just as the side-effects of chemotherapy abate, so too do those of ECT; most of the hair grows back, most of the memories return, and the patient’s life is saved.

The FDA order removes what was a potentially dark cloud on the horizon of ECT. It continues to be the responsibility of our field to train an adequate number of ECT practitioners and to counter unsubstantiated attacks by the anti-psychiatry movement through education and ongoing contributions to the research evidence base for ECT.

Dr Kellner is Chief of Electroconvulsive Therapy (ECT), New York Community Hospital, Brooklyn, NY, and Adjunct Professor of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY. He reports that he has received research support from the NIMH, honoraria from UpToDate, Psychiatric Times, and Northwell Health, and royalties from Cambridge University Press.

 Food and Drug Administration. Neurological Devices; Reclassification of Electroconvulsive Therapy Devices; Effective Date of Requirement for Premarket Approval for Electroconvulsive Therapy Devices for Certain Specified Intended Uses. Final order. Fed Regist. 2018;83:66103-66124.

 McDonald WM, Weiner RD, Fochtmann LJ, McCall WV. The FDA and ECT. 

 Fink M, Kellner CH, McCall WV. Optimizing ECT technique in treating catatonia. 

 Fink M. Rediscovering catatonia: the biography of a treatable syndrome. 

 Leiknes KA, Jarosh-von Schweder L, HÃ¸ie B. Contemporary use and practice of electroconvulsive therapy worldwide. 

 Grover S, Sahoo S, Rabha A, Koirala R. ECT in schizophrenia: a review of the evidence. 

 Sanghani SN, Petrides G, Kellner CH. Electroconvulsive therapy (ECT) in schizophrenia: a review of recent literature. 

 Kellner CH, Greenberg RM, Ahle GM, Liebman LS. Electroconvulsive therapy is a standard treatment; ketamine is not (yet). 

 Kellner CH, Farber KG. Electroconvulsive therapy and cognition: a salutary reappraisal. 

This new FDA order now allows patients who need and want ECT, as well as practitioners who perform it, to breathe a sigh of relief.

The FDA on ECT: Supporting a Vital Treatment

The risk of cognitive adverse effects (eg, long disorientation duration, memory impairments), has been one of the factors that historically limited ECT use. However, modern modifications of ECT parameters have substantially limited these cognitive risks to a smaller portion of patients. For instance, the modern development and use of rectangular instead of sine wave pulse, ultra-brief instead of brief pulse, and right unilateral (RUL) instead of bilateral (BL) electrode placement have improved cognitive effects of ECT.

Further improvement of the cognitive adverse effects has been suggested by using a lower current amplitude than standard ECT, thus more focal stimulation as in Low AmPlitude Seizure Therapy (LAP-ST). Despite the more favorable cognitive effects compared with standard ultra-brief RUL ECT, similar efficacy has been shown in 2 preliminary studies on depression and suicidality.

 Moreover, further modifications in electrode shape and electrode placements might also be helpful for Focal Electrically Administered Seizure Therapy (or FEAST).

 These proof of concept studies provide additional promise to eliminating or markedly minimizing these adverse effects.

Theoretical justification for use of ECT in PTSD and proposed mechanism of action

Hippocampal neurogenesis has been shown to contribute to the clearances of artificially induced long-term potentiation (a cellular model of learning and memory). This mechanism may have a role in treatment-resistant PTSD and related memories if clearance of hippocampal memory traces in the contextual fear conditioning can be accomplished. Since ECT induces neurogenesis, it might have a role in treatment of PTSD (

ECT has been suggested to induce neurogenesis and neuroplasticity in both brain imaging and in brain pathology studies. Olsen and collegues

 measured the number of newly formed neurons in the hippocampal subgranular zone in adult rats exposed to chronic restraint stress and electroconvulsive stimulation alone or in combination. This study found that chronic stress induced depression-like behavior without changing neurogenesis in the hippocampus, while electroconvulsive stimulation prevented stress-induced depression-like behavior and increased neurogenesis.

The role of ECT in inducing neuroplasticity in both animals and humans is best detailed in a comprehensive review by Bouckaert and colleagues.

 Since hippocampal neurogenesis has also been shown to ameliorate PTSD symptoms, it is plausible to hypothesize that ECT might help PTSD by inducing hippocampal neurogenesis.

Hippocampal neurogenesis may not be the only mechanism. Other mechanisms related directly to memory deconsolidation might also be possible, where ECT could cause more improvement in PTSD symptoms if delivered right after reconsolidation of the traumatic memories.

In one study patients with severe treatment-resistant PTSD were administered 6 sessions of ECT after retrieving either traumatic (n = 4) or a neutral memory (n = 4).

 Study findings indicate that post traumatic-retrieval ECT tended to produce better reductions in skin conductance responses and subjective reactivity to the traumatic imagery (

 = .026). Thus, supporting the theory that ECT may have its effects augmented if delivered right after reconsolidation of traumatic memories.

Further investigation is warranted, not only from a therapeutic standpoint, but also from mechanistic perspectives. Despite plausibility of these hypotheses, it must be stressed that these hypotheses need to be further tested to be proven or disproven in a well-powered controlled clinical trial, given the preliminary evidence.

Wider availability of ECT in facilities that treat a substantial number of patients with treatment-resistant PTSD and depression, such as VA hospitals, would not only improve care for patients with disorders indicated for ECT (according to the standard of care), but also provide a chance to investigate the potential role of ECT in treatment-resistant PTSD (or PTSD with depression) given that the number of patients needed for such a trial would be unlikely to be obtained by any one center or hospital.

Standard therapeutics fall short of helping many patients with PTSD

Several medications and combinations of medications, including SSRIs and other antidepressants have been studied for treatment of PTSD. For instance, 80% of veterans with PTSD seen at the VA receive pharmacologic treatment (with or without psychotherapy), of these, 89% are prescribed antidepressants.

Most of the studies have been positive for the FDA-approved medications, paroxetine and sertraline, although the therapeutic effect size of antidepressants has been small.

 Moreover, the results of a large multicenter randomized trial of post-FDA-approved sertraline were not positive.

Prazosin has shown evidence of efficacy in some well-designed clinical trials for nightmares (and some other PTSD symptoms).

 However, a recent, large multicenter clinical trial did not show benefit for nightmares or other PTSD symptoms in veterans with chronic PTSD.

 Neither did another study that examined prazosin for PTSD (but not nightmares).

Trauma-based therapies such as cognitive processing therapy and prolonged exposure are considered the gold standard treatments for PTSD. However, despite all available standard therapeutics, a high percentage of patients still do not achieve remission (or response) from multiple trials of both pharmacotherapy and psychotherapy.

Traumatic memories generate some of the most persistent memories and are the hardest to erase. This might be explained by the cellular mechanism for encoding durable memories that also involve structural change. At the intranuclear level, a recent review by our group suggests that the effect of these traumatic memories may even be passed to the next generations via epigenetic methylation effects.17 These persistently encoded memories might be, at least in part, why so many patients with PTSD are treatment-resistant or partial responders.

Many patients with treatment resistance suffer the burden of impairment, elevated risk of suicide and violence, and higher incidence of all-cause mortality. This obviously creates significant family and societal burden. Common PTSD psychiatric comorbidities include depression and substance use disorders. In addition, there are high rates of other psychiatric and physical illnesses including hypertension and cardiovascular events.

Preliminary evidence for the role of ECT in treating PTSD

A serious look at innovative solutions as well as established interventions that are known to be highly effective in other treatment-resistant disorders is needed. Modern ECT has a high level of safety compared with older techniques, not only in terms of anesthesia and muscle relaxation, but also in terms of the improvements in electric parameter modifications, and electrode placements.

In disorders where ECT is indicated, ECT generally has the advantage of working faster than medications and psychotherapy with an effectiveness rate that is usually at least twice as high as standard therapeutics. It also frequently works in more severe and treatment-resistant cases.

The literature that examined the role of ECT in treating PTSD in humans is scant and totals four preliminary studies (

). (The reader interested in more details on the topic is referred to a recent synthesis of the existing evidence of the role of ECT in PTSD.

A retrospective chart review investigated the use of ECT in veterans with PTSD.

 The statistical analysis included 26 veterans with both MDD and PTSD. PTSD severity was assessed by the PTSD Checklist (PCL) and depression severity by the Montgomery-Asberg Depression Rating Scale (MADRS).

 Patients had significant reduction in both depressive and PTSD symptoms (

 < .001) after the ECT course. However, only 35% of patients had reduction in symptoms on the PCL. The major limitations of this study are the retrospective nature (which could have cofounded the findings) and the small sample size.

A retrospective case-control study compared patients with comorbid PTSD and MDD who were treated with an ECT course (n = 92) to those with matched controls that did not receive ECT (n = 3393).

 PTSD and MDD symptoms improved as assessed using the Clinical Global Impression (CGI) scale. The ECT group improved more than those who did not receive ECT but were on antidepressant medications (P = .001).

The most recent retrospective case-control study compared patients treated with ECT who had MDD and comorbid borderline personality disorder, PTSD, or both (n = 75), and a matched group but with MDD alone without comorbidities (n = 75).

 The medical records were reviewed to determine treatment response and estimate CGI-improvement (CGI-I). Study findings showed no statistically significant difference in the CGI-I response rates between the 2 groups (

 > .017). Limitations of the study were that no specific measures of PTSD were used other than the c-CGI-I, the retrospective design, and that the group of interest was heterogeneous (with comorbid borderline personality disorder, PTSD, or both).

The only clinical trial available in the literature for ECT in PTSD is an open-label non-controlled trial.

 Participants (N = 20) had severe, chronic, and treatment-resistant PTSD as evidenced by failure to respond to 4 or more adequate antidepressant trials, as well as 12 sessions of cognitive behavior therapy. This is also the only study that measured PTSD with the Clinician-Administered PTSD Scale (CAPS) as the primary measure. CAPS scores for the sample mean decreased by 34% (

 < .001). The authors also reported that the correlation between improvement in CAPS and MADRS was low, suggesting that benefits for PTSD were independent from depression improvement.

This data seems encouraging; however, the overall evidence is still limited as this study was small and uncontrolled. No randomized controlled clinical trials exist so far. Thus, routine clinical use of ECT for PTSD cannot be recommended, at least not yet. The available studies either have small sample size or design limitations or both. However, most available evidence is positive, although publication bias could not be ruled out. The available evidence warrants further research in this area to provide definitive answers.

The preliminary data on the role of ECT in PTSD seems promising. However, I would caution that (although most studies are positive suggesting a helpful effect of ECT in PTSD), the studies so far are preliminary and publication bias (where negative studies may not have been published) cannot be ruled out.

Thus, definitive, well-powered, randomized controlled clinical trials to confirm or revoke the initial results are warranted, given the severe burden, grave suffering, and lack of remission with standard therapeutics in many patients with PTSD. Modification of the clinical trials using the innovative technique of trauma memory arousal to deconsolidate memories shortly before an ECT session may prove to be more fruitful in future clinical trials.

On the clinical side, there is not enough evidence to support the use of ECT for PTSD. However, since PTSD is commonly comorbid with other disorders where ECT is clinically indicated (such as depression and schizophrenia), comorbid PTSD should not dissuade the clinician from treating patients with ECT who are otherwise clinically appropriate to benefit from ECT.

 The views expressed are those of Dr. Youssef and do not represent Medical College of Georgia or the Department of Veterans Affairs.

Dr Youssef is Associate Professor Department of Psychiatry & Health Behavior, Medical College of Georgia at Augusta University, and Psychiatry Educator for medical students at the office of Academic Affairs, Augusta, GA.

Dr. Youssef is the principal investigator (PI) of the Low AmPlitude Seizure Therapy (LAP-ST) randomized clinical trial and prior PI on a proof of concept LAP-ST clinical trial. He is currently a co-investigator on the FEAST ECT study funded by MECTA, but did not receive any monetary or salary support from MECTA or other device or pharmaceutical companies (past 5 years) for any of the studies. Dr. Youssef received research support from the Veterans Administration, and a grant from ABR Corporation, and the NIH (past 5 years).

 Youssef NA, Sidhom E. Feasibility, safety, and preliminary efficacy of Low Amplitude Seizure Therapy (LAP-ST): a proof of concept clinical trial in man. 

 Youssef N, McCall WV, Patel C, et al. Speed of remission of suicidality for low amplitude seizure therapy (LAP-ST) versus right unilateral ultra-brief ECT. 

 Nahas Z, Short B, Burns C, et al. A feasibility study of a new method for electrically producing seizures in man: focal electrically administered seizure therapy [FEAST]. 

 Olesen MV, Wortwein G, Pakkenberg B. Electroconvulsive stimulation, but not chronic restraint stress, causes structural alterations in adult rat hippocampus: a stereological study. 

 Bouckaert F, Sienaert P, Obbels J, et al. ECT: its brain enabling effects: a review of electroconvulsive therapy-induced structural brain plasticity. 

 Youssef NA, McCall WV, Andrade C. The role of ECT in posttraumatic stress disorder: a systematic review. 

 Andrade C, McCall WV, Youssef NA. Electroconvulsive therapy for post-traumatic stress disorder: efficacy, mechanisms and a hypothesis for new directions. 

 Corchs F, Vermes JS, AraÃºjo ÃC, et al. Targeting the reconsolidation of traumatic memories with electroconvulsive therapy and prolonged exposure therapy in posttraumatic stress disorder. 

 Mohamed S, Rosenheck RA. Pharmacotherapy of PTSD in the U.S. Department of Veterans Affairs: diagnostic- and symptom-guided drug selection. 

 Hoskins M, Pearce J, Bethell A, et al. Pharmacotherapy for post-traumatic stress disorder: systematic review and meta-analysis. 

 Friedman MJ, Marmar CR, Baker DG, et al. Randomized, double-blind comparison of sertraline and placebo for posttraumatic stress disorder in a Department of Veterans Affairs setting. 

 Raskind MA, Peskind ER, Hoff DJ, et al. A parallel group placebo controlled study of prazosin for trauma nightmares and sleep disturbance in combat veterans with post-traumatic stress disorder. 

 Raskind MA, Peterson K, Williams T, et al. A trial of prazosin for combat trauma PTSD with nightmares in active-duty soldiers returned from Iraq and Afghanistan. 

 Raskind MA, Thompson C, Petrie EC, et al. Prazosin reduces nightmares in combat veterans with posttraumatic stress disorder. 

 Raskind MA, Peskind ER, Chow B, et al. Trial of Prazosin for post-traumatic stress disorder in military veterans. 

 Petrakis IL, Desai N, Gueorguieva R, et al. Prazosin for veterans with posttraumatic stress disorder and comorbid alcohol dependence: a clinical trial. 

 Youssef N, Lockwood L, Su S, et al. The effects of trauma, with or without PTSD, on the transgenerational epigenetic DNA methylation alterations in human offspring. 

 Watts BV. Electroconvulsive therapy for comorbid major depressive disorder and posttraumatic stress disorder. 

 Forbes D, Creamer M, Biddle D. The validity of the PTSD checklist as a measure of symptomatic change in combat-related PTSD. 

 Montgomery SA, Asberg M. A new depression scale designed to be sensitive to change. 

 Ahmadi N, Moss L, Simon E, et al. Efficacy and long-term clinical outcome of comorbid posttraumatic stress disorder and major depressive disorder after electroconvulsive therapy. 

 Kaster TS, Goldbloom DS, Daskalakis ZJ, et al. Electroconvulsive therapy for depression with comorbid borderline personality disorder or post-traumatic stress disorder: a matched retrospective cohort study. 

 Margoob MA, Ali Z, Andrade C. Efficacy of ECT in chronic, severe, antidepressant- and CBT-refractory PTSD: an open, prospective study. 

Given the severe burden, grave suffering, and lack of remission with standard therapeutics in many patients with PTSD, preliminary data on the role of ECT seems promising.

Treating Recalcitrant PTSD With ECT: Are We There Yet?

The recent increase in suicides, including those of Kate Spade and Anthony Bourdain, highlights the urgent need for better treatment of severe depression. Recent data from the CDC document an alarming trend: suicide is up by nearly 30% since 1999.

 It is now the 10th leading cause of death, with 45,000 suicides in 2016. While the antecedents of suicide are multifactorial, at least half of the people who attempt/complete suicide have a psychiatric illness, mostly a mood or psychotic disorder.

, Richard A. Friedman, a psychiatrist, noted, “last year, the National Institutes of Health spent more money researching dietary supplements than it did suicide and suicide prevention. Any other disease that comes close to killing as many Americans as suicide does, like HIV and heart disease, gets marquee recognition as a public health menace and major federal research funding . . . the simple reason suicide has been neglected for so long is stigma.”

 Benedict Carey, in a New York Times article about the same CDC suicide data, wrote, “one of the few proven interventions [to reduce suicides] is unpalatable to wide swaths of the American public: reduced access to guns.”

 We believe that another intervention proven to reduce suicidality, ECT, is underused because it is similarly stigmatized and considered “unpalatable.”

A recent series of articles and editorials documents the current state of ECT use (actually underuse) in the US. Herein, we review the new data and make suggestions about “right sizing” ECT in contemporary American psychiatric practice.

 wrote an editorial, which accompanied an important study that demonstrated that inpatients with mood disorders who received ECT had half the rate of hospital re-admission in 30 days than those who were treated with medications.

 More recent findings indicate that only 0.25% of patients with mood disorders in a large health care database received ECT.

 Similarly, in a cohort of over 11,000 veterans with psychiatric illness, only 50 received ECT (0.45%).

Because of its speed and effectiveness, ECT may actually be a cost-saving intervention; this benefit is in addition to its ability to relieve suffering and save lives. The cost-effectiveness of ECT was investigated in a major health economics study.

 Six alternative strategies for incorporating ECT into depression treatment were modeled based on data drawn from multiple meta-analyses, randomized trials, and observational studies of patients with depression. The researchers concluded that an optimal cost-effective strategy is to offer ECT after two failed pharmacotherapy trials, not relegating it to a “last resort” position after innumerable trials. Furthermore, they found, “over 4 years, ECT was projected to reduce time with uncontrolled depression from 50% of life-years to 33% to 37% of life-years, with greater improvements when ECT is offered earlier.”

How much is the right amount of ECT for optimum mental health outcomes? If ECT were used more often, would some suicides be prevented? Let’s start by addressing what we know about how much ECT is now done in the US. Unfortunately, in contrast with many European countries where national health databases provide accurate epidemiological data about the utilization of most medical procedures, including ECT, the US lacks such data.

ECT utilization rates have been shown to vary widely, both between regions in the US and between countries around the world.11 In a review, Leiknes and colleagues

 collected data about ECT utilization worldwide. They reported that, despite wide variability, the average ECT treated person rate (TPR) approximates 2.2 per 10,000 resident population per year. (In selected countries, where ECT may be less stigmatized, the rate is higher. For example, the TPR in Belgium is ~4.5 per 10,000 residents.) In the US, a TPR of 3 would equate to approximately 90,000 ECT patients per year. This accords well with an estimate derived from one of the best sources of population data in the US, the Medicare database.

 A similar extrapolation from this database is that approximately 450,000 to 500,000 ECT procedures are done annually in the US.

There are 49,000 psychiatrists in the US, but only 1216 were found in the 2016 Medicare database as having performed ECT.

 The International Society for ECT and Neurostimulation (ISEN), has about 300 members.

 There is a gender gap among ECT practitioners, with only 19% being female, despite the fact that psychiatry residency classes for the past decade have been more than 50% female. Only 14% of ECT procedures performed in the US are done by women psychiatrists.

The ambivalence with which ECT is regarded derives from multiple sources, but the media, with its sensationalized and anachronistic portrayals, has been the major influencer. Unfortunately, ambivalence also comes from within the psychiatric profession, where residency experience in ECT is woefully lacking, leading to practitioners who are uncomfortable prescribing it.

Modern ECT has been refined to the point that its morbidity and mortality are remarkably low. A recent systematic review and meta-analysis found a mortality rate of 2.1/100,000 procedures, making it among the safest treatments performed under general anesthesia.

 The technical advancement of ultrabrief pulse right unilateral ECT allows many seriously ill patients to recover with very few cognitive effects.

 ECT practice and research are advancing in the US and abroad. PubMed contains over 15,000 citations for ECT. And, ECT research continues around the world as we mark the 80th anniversary of the invention of ECT.

Despite the enthusiasm with which newer brain stimulation techniques have been embraced, ECT remains alone; no other modality can come close to ECT for antidepressant/antipsychotic efficacy, speed of response, and clinical track record of utility. We do a disservice to our seriously ill patients when we conflate ECT with other “neurostimulation” techniques.

Taken together, the above data suggest that ECT is, in fact, vastly improved, but still underutilized. We believe that greater, and earlier, prescription of ECT in appropriately selected patients would lead to better mental health outcomes, including fewer suicides. While an exact right-sized figure is hard to come by, we speculate that closer to 250,000 ECT patients per year (resulting in about 1.5 million ECT procedures) in the US is a more appropriate number for optimal mental health outcomes and reduced suicides. Currently, it is easier to get a gun than a prescription for ECT in the US. Fortunately, this may now be changing. ECT-marginalized for decades-is regaining its rightful place in the treatment armamentarium of contemporary psychiatric medicine.

Dr Kellner is Chief of Electroconvulsive Therapy (ECT), New York Community Hospital, Brooklyn, NY and Adjunct Professor of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY. Ms Patel is an undergraduate at Emory University. 

Dr Kellner reports that he has received research support from the NIMH, honoraria from UpToDate, Psychiatric Times, and Northwell Health, and royalties from Cambridge University Press. Ms Patel reports no conflicts of interest concerning the subject matter of this article.

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The recent increase in suicides highlights the urgent need for better treatment of severe depression. ECT is an intervention proven to reduce suicidality, yet it is underused because of the associated stigma.

The Role of ECT in the Suicide Epidemic

ECT is a highly effective treatment for depression, but a portion of patients fail to respond as hoped. Clinical variables have overall limited utility as a predictor of response. Is inflammation the key?

Inflammation and Response to ECT in Treatment-Resistant Depression

is Associate Professor of Psychiatry, Kennedy Krieger Institute, Johns Hopkins School of Medicine, Baltimore, MD

is Chief of Electroconvulsive Therapy, New York Community Hospital, Brooklyn, NY

 is Professor Emeritus, Departments of Psychiatry and Neurology, Stony Brook University, Stony Brook, NY.

Since its introduction 8 decades ago, ECT has been a standard treatment for severe affective and psychotic illness, as well as less common indications including catatonia, 

, neuroleptic malignant syndrome, and status epilepticus. A new indication for ECT has 

 for intractable self-injurious behavior (SIB) among individuals with autism and intellectual disabilities.

 Response to ECT is typically swift and robust, with great benefit for patients and their families.

SIB is defined as any act toward the self that causes physical injury, and has been recognized for decades to occur among individuals with autism spectrum disorders and intellectual disability. Estimates of SIB prevalence vary widely, with higher rates usually found among those with greater cognitive and communication impairments, and psychiatric and medical comorbidities. Common manifestations of SIB include head banging; hand-to-head, knee-to-head, and hand-to-body hitting; self-pinching; scratching and biting; and body slamming against hard surfaces. The frequency of SIB varies widely, from occasional, to daily, hourly, or even a per-minute basis. Frank bodily injury is common and includes bleeding, bruising, swelling, fracture, infection, disfigurement, traumatic ossification, cataract development, retinal detachment with associated loss of vision, and concussion or intracranial damage. Other deleterious consequences of SIB include reduced social, educational, family, and occupational functioning, with higher risk of placement in more restrictive settings and limited life opportunities.

Standard treatments of SIB in autism and intellectual disability are behavioral and psychopharmacological interventions. While many individuals respond to these modalities, there has long remained a subgroup of treatment-refractory patients who have exhausted dozens of psychotropic medications, years of intensive behavioral therapy, and multiple out-of-home placements and hospitalizations. Such patients may be padded and immobilized head-to-toe in protective equipment, and frequently receive psychotropic medications as chemical restraint-often with limited benefit and high risk of adverse effects. Despite such efforts, these patients often sustain permanent injuries including blindness from retinal detachment and cerebral hemorrhage.

Recent suggestions that SIB might be one of many symptoms of catatonia in autism spectrum disorders-including mutism, negativism, posturing, rigidity, and repetitive speech and acts-led to treatment trials with ECT, the long-recognized effective treatment for catatonia, with 

Jay is a 19-year-old man with autism and intellectual disability. He was initially hospitalized at age 12 after several years of severe head- and body-directed SIB with frequent facial bleeding, as well as aggressive behaviors toward his family, caregivers, and school staff. SIBs were so intense that a caregiver inadvertently broke Jay’s arm while attempting to block hand-to-head striking. Jay also displayed mood instability with sobbing and wild laughter, irritability, physical hyperactivity, agitation, and insomnia.

He had exhausted multiple drug trials from all US-available psychotropic classes, as well as years of intensive behavioral services. He demonstrated affective and behavioral improvement of a few months’ duration on lithium carbonate, aripiprazole, and riluzole, but deteriorated again with such behavioral dyscontrol that his parents feared their only option to maintain his safety was placement in a locked residential facility.

A trial of 3 times per week bilateral ECT was initiated. Jay demonstrated dramatic reduction in SIBs after just a few treatments, as well as improved sleep and more stable mood. ECT frequency was gradually reduced while monitoring for recurrence of SIB or mood deterioration; ultimately, a maintenance ECT regimen of every 9 or 10 days was established.

Jay was able to remain at home, where he participated fully and safely in family life with his parents and 2 siblings. He continued in a program emphasizing community-based living and functioning activities, and was able to master skills never thought possible for him before, such as independent grocery shopping from a list, followed by check-out with a debit card and meal preparation.

He tolerates ECT well and is able to go to school without incident after early-morning treatment. He remains on a concomitant regimen of lithium and aripiprazole; SIB is limited to rare incidents of hand-biting with no resultant injuries. Jay has received an estimated 290 sessions of ECT over the past 8 years.

The resolution of SIB with ECT was first documented in a 1982 report of a 25-year-old man with severe mental retardation and head-directed SIB of several years’ duration.

 In 1999, a report presented a 14-year-old boy with mental retardation whose persistent head-banging and self-scratching were alleviated by ECT, which allowed discharge after many months in a restricitve institutional setting.

The relationship between self-injury, catatonia, and ECT was first questioned in the 2008 case report of an autistic girl with posturing, rigidity, mutism, stupor, grimacing, food refusal, and global skill regression, alternating with bursts of extreme self-injury that led to bilateral traumatic cataract formation and retinal detachment.

 ECT resulted in resolution of catatonic symptoms, as well as nearly complete eradication of SIB, which allowed for vision preservation in one eye.

The following year, the case of an 8-year-old autistic boy with ongoing agitation and stereotyped movements (in the form of nearly 110 SIBs per hour) was reported.7 After treatment with ECT, he averaged only 20 SIBs per hour. It was postulated that his SIB was a manifestation of catatonia.

 proposed that self-injury in autism represented a variant of catatonia. They reviewed the history of these conditions, exploring self-injury as a stereotypy common to both catatonia and autism, and further connecting catatonia, autism, tic disorders, and the self-injury that occurs in the 3 conditions. Subsequent reports have continued to call for recognition of repetitive SIB as a sign of catatonia, with clear implications for the use of ECT in its treatment.

ECT for adolescents with autism spectrum disorder and SIB includes standard ECT protocols of general anesthesia with propofol or methohexital, muscle relaxation with succinylcholine, and continuous oxygenation via face mask. Flumazenil, the benzodiazepine reversal agent, may be used at the time of treatment when patients have recently taken these medications. 

 is typically bilateral, and stimulation is with modern brief-pulse devices.

Moderately suprathreshold stimulus dosing takes into account the lower seizure threshold of younger patients. Seizure adequacy is monitored by the duration and quality of the recorded EEG. The ECT course begins with seizures 3 times per week, until SIB frequency has been markedly reduced; ECT frequency is then gradually reduced over the ensuing weeks, while monitoring for sustained SIB reduction. For these patients, ECT is a procedure analogous to renal dialysis, with frequency of treatment guided by objective symptom evaluation, and the need to optimize the quality of patient and family life.

While the mechanism of the relief of catatonia by ECT is unclear, the neuroendocrine studies of melancholia offer potential clues. Studies of cortisol and thyroid functions in these patients find chemical abnormalities that resolve with repeated ECT, suggesting that seizures normalize the hypothalamic-pituitary-adrenal axis and other endocrine functions. While we know little about the specific neuroendocrine disturbances in autism spectrum disorder or in catatonia, there are likely commonalities in the underlying physiology between these disorders and melancholia. At present, the best understanding of the mechanism of the beneficial effect of ECT in adolescents with SIB is the neuroendocrine explanation developed for melancholia. Additional mechanistic theories are enhanced neurogenesis, angiogenesis, and neuronal connectivity.

ECT came into widespread use at a time when psychodynamic thinking dominated child and adolescent psychiatry and the application of the somatic therapies was considered anathema. Since the 1990s, this attitude hurdle has been slowly overcome with the realization that some severe childhood and adolescent disorders-notably, melancholia, mania, and catatonia-are safely and effectively relieved by modern ECT procedures. Recognizing SIB in autism spectrum disorder as a form of catatonia has encouraged this application. Indeed, ECT has been documented as nothing short of lifesaving for many children and young adults with autism spectrum disorder who were previously wholly incapacitated by SIB.

Wachtel L, Shorter E. Self-injurious behaviour in children: a treatable catatonic syndrome. 

Wachtel L, Dhossche D. ECT for self-injurious behavior. In: Ghaziuddin N, Walter G, eds. 

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 Bates WJ, Smeltzer DJ. Electroconvulsive treatment of psychotic self-injurious behavior in a patient with severe mental retardation. 

 Wachtel LE, Kahng S, Dhossche DM, et al. ECT for catatonia in an autistic girl. 

Wachtel LE, Contrucci-Kuhn SA, Griffin M, et al. ECT for self-injury in an autistic boy. 

Wachtel L, Dhossche D. Self-injury in autism as an alternative sign of catatonia. 

 Fink M. The mechanism of action of ECT. In: Ghaziuddin N, Walter G, eds. 

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Optimizing ECT technique in treating catatonia

ECT has been found effective in mitigating the deleterious consequences of SIB.

ECT for Self-Injurious Behavior in Autism: A New Indication


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