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Too often, the medical issues associated with traumatic brain injury are mistaken as psychiatric disorders, and patients are referred to psychiatrists for treatment, Gregory J. O’Shanick, MD, DLFAPA, told attendees of the 2021 

American Psychiatric Association Virtual Annual Meeting

O’Shanick, who is the medical director of the 

in Richmond, Virginia, urged psychiatrists to leverage their medical knowledge when assessing patients to determine when the diagnosis is a psychiatric disorder and when patients are presenting with medical mimics associated with traumatic brain injury (TBI). He shared his frustration with psychiatry’s loss of medical identity, especially as it related to brain injury medicine. In his 40-year career, he found “all too often, physicians, both MDs and DOs, psychiatrists, [were] missing basic neurologic issues that we as physicians should catch. If we are to be vocal regarding the necessity of having a MD and DO to ultimately provide oversight of care for those with behavioral disorders and writing prescriptions for psychotropic medications, we must not relinquish the use of those tools and skills that were taught to us in medical school.”

The prevalence of TBI has increased over the last 10 or so years, O’Shanick explained, although he acknowledged that the increase may be partially due to increased awareness. According to 

 from the Centers for Disease Control and Prevention, there was a 53% increase from 2006 to 2014 in TBI-related emergency department visits, hospitalizations, and deaths. In older adults and the very young, falls account for the number 1 cause of TBI.

 A combination of motor vehicle accidents, sports, falls, and other activities were the cause for the “very active” and maybe not as cautious young adult population (aged 15 years to 24 years).

Meanwhile, research has found a link between psychiatric disorders and TBI, O’Shanick noted, with an increase of disorders following TBI.

 Jennie Ponsford, PhD, and colleagues explored this phenomenon and found that only about 23% and 21% of individuals had a pre-TBI history of a mood disorder or anxiety disorder, respectively. They found an increase in psychiatric symptomology within the first year after TBI, with a stabilization at the 5-year point. Mood and anxiety symptoms were most common in patients with TBI, with 17.2% to 62% presenting with mood symptoms and 10.3% to 34.2% with anxiety symptoms. Interestingly, he noted depression is 4 to 6 times more common in patients with TBI than the general population, and is the most common cause of depression in men (as opposed to women, for whom menopause is the number one cause).

It is possible, he explained, that some of these mood disturbances and anxiety symptoms may be better explained as a medical consequence of TBI—or a signal of homeostatic disruption. In such cases, providing psychopharmacological treatment might help the patient with the symptoms, but will not address the underlying cause.

O’Shanick provided an example of a phobia being misattributed. He pointed to an individual who is afraid of a jumping off a diving board. They go up the stairs, walk to the edge, realize they are frightened, and go back down. They have conditioned themselves to be afraid—there is a learned component.

Next, he presented the case of an individual who has unrecognized balance and visual issues as a result of TBI. The person goes into a crowd and feels a sense of anxiety, because they have trouble feeling and remaining stable, and the learned component may be inappropriately linked to an anxiety disorder.

“As a physician, we need to figure that out,” O’Shanick emphasized.

Fortunately, a toolkit to help decipher these TBI-related medical mimics is relatively inexpensive, O’Shanick shared. All you need is a pen, index card, blindfold (or ask your patient to close their eyes), a sofa cushion, a tuning fork (which can be procured online for about $6), and a few questions. For example, to determine if the issue is 

 or a vestibular in nature, ask your patient if they need to touch the wall when closing their eyes in the shower to prevent falling. Or, if they feel anxious in a crowded area like a store or mall, does pushing a cart or stroller or holding on to someone make them feel better? If so, there are a few simple follow-up tests (eg, the Balance Error Scoring System and Fukuda Stepping Test) to help confirm the medical mimic. A referral for vestibular physical therapy and a neuro-ENT may prove useful for such patients.

Similarly, to determine if there is social phobia or vergence, ask your patient if they are having trouble seeing/reading books at a normal distance. Then, check near point convergence and conduct a cover test. A referral to a neuro-optometrist should be considered.

Sometimes a central auditory processing disorder may be confused with 

. It is especially important to decipher the difference, O’Shanick explained, because stimulants will worsen the central auditory processing disorder. Ask your patient if they have better sustained attention for visual vs verbal interactions, or if they have trouble understanding what people say if they cannot see their faces or mouths. Weber and Rinne tests can also prove useful, and a referral to an audiologist is indicated.

, posttraumatic neuroendocrine (PTNE) disorders may be relatively common in patients with TBI,

 and mood symptoms are associated with PTNE, O’Shanick explained. Psychiatrists should inquire about changes in menses, sex drive, cold intolerance, and skin and hair dryness to elucidate if PTNE is a potential cause of the mood symptoms. Lab studies should be considered, including 

, TSH, FSH, LH, IG-1, estradiol/testosterone, and am/pm cortisol. In considering TBI in these cases, O’Shanick reminded attendees that they should not overlook 

Finally, O’Shanick illuminated inherent biases in the Minnesota Multiphasic Personality Inventory-2, which might lead to an incorrect diagnosis. For instance, stomach trouble and headaches score positively on the hypochondriasis scale, but both may be related to TBI and TBI treatments. Similarly, positive scores on the hysteria scale result from noting they are unable to work, feel sad, and have trouble sleeping, all of which are associated with TBI.

Ultimately, the psychiatrist is the ideal position to leverage their medical and behavioral knowledge to support these patients.

“Hopefully this will allow you to think a little bit differently when patients come into your office,” O’Shannick concluded. “Maybe ask some increased questions when it comes to injury related issues, concussion related issues… and to see if there is some other types of medical issues behind some of the anxieties that your patients have. At the end, you may just find that you’re practicing … much more successfully and ultimately helping your patients.”

1. CDC. Surveillance report of traumatic brain injury-related emergency department visits, hospitalizations, and deaths. 2014. Accessed May 2, 2021. 

https://www.cdc.gov/traumaticbraininjury/pdf/TBI-Surveillance-Report-FINAL_508.pdf

2. Ponsford J, Always Y, Gould KR. Epidemiology and natural history of psychiatric disorders after TBI. 

3. Beyer C, Zaytsev J, Donegan D, et al. 

The effects of traumatic brain injury on pituitary function: a systematic review and meta-analysis

Too often, the medical issues associated with traumatic brain injury are mistakenly diagnosed as psychiatric disorders. A few simple questions and tests can elucidate the real culprit and lead to appropriate treatment.

Is It a Psychiatric Disorder or TBI Medical Mimic?

In the 1930s and 1940s, researchers identified childhood autism as a unique condition. At the same time, many believed that children became autistic because they had cold, intellectual, emotionally withholding mothers.

But Clara Park, a woman whose daughter had autism, set out to understand autism differently and, along with other families and dedicated researchers, she upended the medical establishment’s view of her daughter’s condition.

In this Mental Health Minute, Marga Vicedo, PhD, discusses her recent book, 

Intelligent Love: The Story of Clara Park, Her Autistic Daughter, and the Myth of the Refrigerator Mother

. Along with telling Park’s story, the book shows how medical research can both reflect social attitudes and change them.

is professor of the history of science and medicine in the Institute for the History of Philosophy of Science and Technology at the University of Toronto. She is the author of 

Has the history of psychiatry informed your practice? 

Share comments with your colleagues by emailing 

. Comments may be shared online pending review and editing for style.

A mother’s quest to understand her child revolutionized our understanding of autism. 

What Causes Autism?

John J. Miller, MD, gives an overview of functioning across neuronal systems. 

is medical director, Brain Health, Exeter, NH; editor in chief,

; staff psychiatrist, Seacoast Mental Health Center, Exeter, NH; consulting psychiatrist, Exeter Hospital, Exeter, NH; consulting psychiatrist, Insight Meditation Society, Barre, MA.

A message flowing through the brain, across neuronal systems... where is it headed?

The Bigger Picture: Across Neuronal Systems

A classification system to identify communication between brain regions brings us closer to predicting and diagnosing attention deficit hyperactivity disorder (ADHD) with better precision than ever before, according to a 

In this Q&A, we speak with lead author of the study, Chris McNorgan, PhD. Dr McNorgan is assistant professor, Department of Psychology at the University at Buffalo, State University of New York, and director of Computational Cognitive Neuroscience Laboratory, in the Department of Psychology at the University at Buffalo — SUNY.

Psychiatric Times (PT): You talk about task-based functional connectivity as a biomarker of ADHD. Can you tell us more about that?

 The challenge with using behavior to diagnose cognitive disorders is that behavior is extremely variable, even within individual patients. Behavioral indicators commonly used to identify ADHD might meet a subjective threshold on one day, but not during a follow-up test, leading to diagnostic instability.

 detects or confirms the presence of a condition of interest by virtue of covarying with the condition: If the biomarker is present, then so is the condition. ADHD is associated with atypical activity patterns, and because the brain does not rewire itself every day, we expected to find persistent differences between ADHD and controls in the connectivity that governs those activity patterns. 

Although a computer is required to represent the complex connectivity patterns that distinguished between controls and ADHD, the high classification accuracy for these machine-learning models establishes that these connectivity patterns provide sufficient evidence to reliably identify ADHD.

PT: What new information does the study provide?

 Ours was not the first study that assumed ADHD can be identified by characteristic functional connectivity. However, the substantial improvement in prediction accuracy over previous studies tells us a few things. First, that task-based functional connectivity within a brain network involved in a task that taxes inhibitory control appears to be more predictive of ADHD than resting state connectivity collected while individuals let their minds wander.

The second finding is more of an analytic innovation, explicitly tying diagnostic accuracy to performance on a relevant behavioral task. The 

 (IGT) was developed under a particular theory about the role of inhibitory processing in ADHD. However, just because it is theoretically tied to ADHD does not make it so. 

Because the classifiers had to identify both IGT performance and ADHD diagnosis from the same set of functional connections, it had to find which connections, if any, were predictive of both. Successfully solving the problem established that performance on the IGT is relevant to ADHD by virtue of the fact that the same functional connections predict both. The study provides a template for similarly linking other diagnostic measures to outcomes.

PT: What can you tell us about the future of machine learning in predicting ADHD with diagnostic accuracy?

 Although task-based connectivity was more diagnostic than resting-state, running an experimental task in an MRI scanner will not be a practical diagnostic tool anytime soon. However, by explicitly linking neuroimaging results to easily administered behavioral tasks, models like this might be used in the future. They may translate a particular behavioral performance profile into a likely connectivity profile confirmed by MRI if need be. These results might inform the choice of intervention. 

ADHD diagnoses have been described as unstable: The same individual may fall above or below threshold at different times. So the fact that childhood ADHD diagnoses were 

 in fMRI scans taken from young adults is remarkable, and I think points to the disorder as something that is deeply ingrained at the neurological level, although it may appear much more transitory at the behavioral level. We do not have information about severity in the participants at the time of the scan, but even if we assumed all of them were symptom-free, their brains are clearly doing something identifiably different.

Finally, these models are remarkably accurate because they make use of many different data points. The optimal precision was calculated based on 4 individual fMRI scans per participant. There may be different subtypes that could be identified by an extension of this paradigm using new tasks. All this points to the general idea that having more information on-hand leads to better evaluations, though the information required to achieve very high accuracy may take a computer to process it.

PT: Did you find anything in your research that was unexpected?

 In hindsight, finding subgroups seems obvious, but we were not looking for different connectivity profiles for high- and low-scorers on the IGT. This was purely for a proof-of-concept, and to make it easier to argue that the classifier had identified activity that was related to inhibitory control. This got us thinking about how this sort of approach might be useful for identifying subpopulations.

PT: Can you tell us about future directions in this research?

 There are a few interesting directions that immediately suggest themselves. Clinical endpoints may be based on subjective self-report. As a surrogate, the 

 must not only be correlated with the condition, but evidence of a causal link must be established between the condition and the biomarker. Research that examines whether and/or which interventions lead to related changes in functional connectivity and in clinical endpoints might establish functional connectivity as a surrogate endpoint. This would allow connectivity to provide additional context for interpreting subjective patient reports.

A second direction would be to link diagnostically predictive connectivity patterns to other commonly used behavioral indicators. We found different connectivity profiles for those with ADHD that scored uncharacteristically high on the IGT, which is commonly used in an experimental setting. This indicates that individuals with ADHD may be differentiated by different patterns of hyper- or hypo-connectivity, and these differences may inform choice of intervention, eg, a drug that targets the hypo-connected circuit. 

 to performance on other tasks more commonly used in a clinical setting may lead to more effective treatment of ADHD in patients who show atypical performance on 1 or more clinically relevant measures.

1. McNorgan C, Judson C, Handzlik, Holden JG. Linking ADHD and Behavioral Assessment Through Identification of Shared Diagnostic Task-Based Functional Connections. 

 2020;11:583005. Accessed April 13, 2021. 

https://www.frontiersin.org/articles/10.3389/fphys.2020.583005/full

New research brings us closer to linking diagnostically predictive connectivity patterns in patients with ADHD.

Advances in Predicting and Diagnosing ADHD

An international group of experts analyzed findings from a large pool of select studies and developed an updated consensus statement with declarations about attention deficit hyperactivity disorder (ADHD). They curated a collection of validated statements, addressing questions on topics ranging from nutrition, neuropsychiatry, and nonpharmacologic treatments. The 

Lead author Stephen V. Faraone, PhD, joins us in this Q&A to talk about the study. Dr Faraone is Distinguished Professor in the Departments of Psychiatry and Neuroscience and Physiology, Psychiatry Research Division, SUNY Upstate Medical University, Syracuse, New York. He is President of the 

Psychiatric Times (PT): What prompted the consensus guidelines and why are they important now?

Despite a large scientific literature about ADHD, much misinformation about ADHD is spread by the internet and other media. This creates 

 and leads to treatment decisions that are not in the best interests of patients. Our consensus provides clinicians, patients, and family members evidence-based results they can use to make informed decisions.

I asked thought leaders from ADHD professional associations from around the world to nominate authors for the project.

PT: Since this is a worldwide consensus statement with 27 countries represented, what sort of differences did you find internationally? How does the United States

compare with other countries in terms of recognition and treatment?

The prevalence of ADHD, the symptoms of the disorder and its outcomes are essentially the same around the world, with some small exceptions. The main difference is in how often ADHD is appropriately diagnosed and treated. Diagnosis and treatment rate are better in countries with well-developed health care systems compared with other countries. The United States has higher rates of diagnosis compared with other high-income countries, although ADHD in adults is underdiagnosed in the United States and around the world.

PT: The article talks about stigma of both patients with ADHD and the health professionals who treat the disorder. Can you tell us more about that?

For patients diagnosed with ADHD, stigma leads to decreased self-esteem, less acceptance by peers, social isolation, and lower self-perceptions of confidence. When treatments are stigmatized, patients and parents are less likely to seek appropriate treatment. Moreover, clinicians are less likely to provide those treatments. This leads to unnecessary distress and disability and costs to society.

PT: The piece came up with 208 empirically supported statements about ADHD. Which ones were most impactful? What new information does the paper provide?

The degree of impact will vary with the reader. Learning about what treatments do and do not work for ADHD can be life changing for patients and families. Learning that ADHD costs societies billions of dollars each year will motivate policy makers to improve access to care. Learning about the medical conditions associated with ADHD will be of much interest to primary care clinicians.

By definition, strong evidence cannot be “new” because it arises from published scientific studies. But I expect that much of this information will be new to most nonprofessional readers and for those professionals that are new to 

PT: Of what clinical relevance is the consensus statement, and does it offer teaching points for readers?

In a nutshell, clinicians will learn that ADHD is a well-defined condition that can be diagnosed at any age; untreated ADHD has many, many serious consequences ranging from school failure in childhood to criminality in adulthood; and the medications for treating ADHD are much more effective than nonmedical treatments for relieving ADHD symptoms.

• ADHD is not an invention of modern society. The syndrome had been reported in medical writings in Europe as early as 1775.

• ADHD is rarely caused by a single genetic or environmental risk factor, but most cases of ADHD are caused by the combined effects of many genetic and environmental risks each having a very small effect.

• Neuroimaging studies find small differences in the structure and functioning of the brain between people with and without ADHD. These differences cannot be used to diagnose ADHD.

I was surprised to learn that ADHD puts people at increased risk for many medical disorders including obesity, asthma, allergies, diabetes mellitus, hypertension, sleep problems, psoriasis, epilepsy, sexually transmitted infections, abnormalities of the eye, immune disorders, and metabolic disorders.

Our next goal is to disseminate the International Consensus Statement as widely as possible. It has been translated into Spanish, French, and German and we also have a summary in Welsh. Colleagues are currently in the process of translating it into Mandarin, Turkish, Portuguese, Arabic, Hindi, Dutch, Japanese, and Italian. These translations will be available at the World Federation of ADHD website.

Readers can learn more about the Consensus Statement from Dr Faraone via Twitter: 

1. Faraone SV, Banaschewski T, Coghill D, et al. The World Federation of ADHD International Consensus Statement: 208 Evidence-based Conclusions about the Disorder. 

 2021;S0149-7634(21)00049-X. Accessed April 4, 2021. 

https://www.sciencedirect.com/science/article/pii/S014976342100049X#abs0010

A collection of validated statements addresses overarching topics ranging from nutrition, neuropsychiatry, and nonpharmacologic treatments.

Consensus Statement Revises Previous Assertions About ADHD

has identified a potential new mechanism for treating depression. 

The study, conducted by researchers at the Icahn School of Medicine at Mount Sinai, used the drug ezogabine to open the KCNQ2/3 potassium channels in participants’ brains. The results showed significant improvements in 

 Because anhedonia is associated with poor response to antidepressant medication, worse overall outcomes, and increased suicide risk, this finding is especially important. 

“Our study is the first randomized, placebo-controlled trial to show that a drug affecting this type of ion channel in the brain can improve depression and anhedonia in patients,” said the paper’s lead author, James Murrough, MD, PhD, associate professor of Psychiatry and Neuroscience at the Icahn School of Medicine at Mount Sinai. “Targeting this channel represents a completely different mechanism of action than any currently available antidepressant treatment.”

The study included 45 participants with high levels of anhedonia and divided them into 

 The treatment lasted 5 weeks, with clinical measures of depression and anhedonia taken at weekly visits. Although the study did not meet its primary endpoint at the 5-week mark, it found that participants on ezogabine had increased reward anticipation and large improvements on the Montgomery-Åsberg Depression Rating Scale (MADRS) and the Snaith-Hamilton Pleasure Scale (SHAPS), compared with the placebo.

The United States Food and Drug Administration approved ezogabine in 2011 as an anticonvulsant for epilepsy, but this is the first study to test it as a depression treatment. The drug acts on the KCQ2/3 channel, which affects brain cell function by regulating the movement of electrical charges across cell membranes.

A previous study led by co-author Ming-Hu Han, PhD, found that changes in KCNQ2/3 potassium partially determined whether mice showed 

signs of depression and anhedonia following stress

 Mice with increased KCNQ2/3 channels in their brains appeared resistant to depression. When the mice were given drugs to increase KCNQ2/3 channel activity, previously depressed mice no longer showed depressive or anhedonic behaviors.

“The fundamental insight by Dr Han’s group that a drug that essentially mimicked a mechanism of stress resilience in the brain could represent a whole new approach to the treatment of depression was very exciting to us,” said Murrough.

 The previous study by Han’s group paved the way for the current study.

“I think it’s fair to say that most of us on the study team were quite surprised at the large size of the beneficial effect of ezogabine on clinical symptoms across multiple measures related to depression,” Han said of the current study.

 “We are greatly encouraged by these findings and the hope they offer for the prospect of developing novel, effective treatments for depression and related disorders.”

1. Mount Sinai Health System. Researchers identify brain ion channel as new approach to treating depression. 

. March 1, 2021. Accessed April 7, 2021. 

https://www.newswise.com/articles/researchers-identify-brain-ion-channel-as-new-approach-to-treating-depression?sc=dwhr&xy=5013482

2. Costi S, Morris LS, Kirkwood KA, et al. Impact of the KCNQ2/3 channel opener ezogabine on reward circuit activity and clinical symptoms in depression: results from a randomized controlled trial. 

3. Friedman AK, Juarez B, Ku SM, et al. KCNQ channel openers reverse depressive symptoms via an active resilience mechanism. 

Opening certain potassium channels in the brain reduces depressive symptoms and anhedonia. 

Is There a New Mechanism for Treating Depression?

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. 

Treatment-resistant bipolar depression: a randomized controlled trial of electroconvulsive therapy versus algorithm-based pharmacological treatment

4. Kellner CH, Husain MM, Knapp RG, et al; CORE/PRIDE WOrk Group. 

A novel strategy for continuation ECT in geriatric depression: phase 2 of the PRIDE study

5. Alpers BJ. The brain changes associated with electrical shock treatment; a critical review. J Lancet. 1946;66(11):363-369.

7. Chen W, Zhongsheng Z, Lee RC. Supramembrane potential-induced electroconformational changes in sodium channel proteins: a potential mechanism involved in electric injury. 

8. Traumatic Brain Injury Advisory Board meeting minutes. California Department of Rehabilitation. August 26, 2019. Accessed February 12, 2021. 

https://www.dor.ca.gov/Content/DorIncludes/documents/TBI/ TBI Full Committee Meeting Minutes 8-26-19.docx

9. Abrams R.And there’s no lasting proof of brain damage. 

10. Weiner R, Reti I. Key updates in the clinical application of electroconvulsive therapy. 

Hippocampal volume changes following electroconvulsive therapy: a systematic review and meta-analysis

Biol Psychiatry Cogn Neurosci Neuroimaging.

12. Oltedal L, Narr KL, Abbott C, et al. Volume of the human hippocampus and clinical response following electroconvulsive therapy. 

Electroconvulsive therapy increases brain volume in major depression: a systematic review and meta-analysis

14. Luccarelli J, McCoy TH Jr, Seiner SJ, Henry ME. Maintenance ECT is associated with sustained improvement in depression symptoms without adverse cognitive effects in a retrospective cohort of 100 patients each receiving 50 or more ECT treatments. 

15. Tørring N, Sanghani SN, Petrides G, et al. 

The mortality rate of electroconvulsive therapy: a systematic review and pooled analysis

16. Abrams R. The mortality rate with ECT. 

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

ECT: An Effective and Safe Treatment

Although electroconvulsive therapy (ECT) is still used on about a million individuals annually, a recent review found “large variation between continents, countries and regions in utilization, rates and clinical practice.”

 in usage between the highest and lowest utilizations regions of England.

In June 2020, this article’s first author published his fifth review of the ECT literature since 2010.

 evaluated the quality of 5 meta-analyses that claimed ECT was effective and safe, as well as the quality of the placebo-controlled studies that had been cited by the meta-analyses. (In these studies, placebo included the general anesthetic without the electric shock.) There have only been 11 placebo-controlled studies of ECT for depression, all of which were conducted before 1986.

The 5 meta-analyses often cited by critics, which included between 1 and 7 of the 11 studies, paid little or no attention to the studies’ multiple limitations (

The quality of most SECT-ECT studies is so poor that the meta-analyses were wrong to conclude anything about efficacy, either during or beyond the treatment period . . . Given the high risk of permanent memory loss and the small mortality risk, this longstanding failure to determine whether or not ECT works means that its use should be immediately suspended until a series of well designed, randomized, placebo controlled studies have investigated whether there really are any significant benefits against which the proven significant risks can be weighed.

The review’s conclusion that there is no evidence ECT prevents suicide, as often claimed, has been unequivocally confirmed by a study of 14,810 patients who received ECT and 58,369 controls.

 Patients in the ECT group were 16 times more likely to attempt suicide over 12 months than the non-ECT patients. Even after controlling for a range of mediating variables, the ECT patients were still 1.3 times more likely to die by suicide (not a statistically significant difference).

The exact incidence of brain damage remains unknown. If brain damage is defined as memory loss persisting at least 6 months after the last ECT, findings range from 12% to 55%.

 This damage is more common in women and older individuals,

 and these groups receive ECT disproportionately.

 While there are many accounts of devastated lives on social media, examples in the published scientific literature are less common. One example 

With each shock treatment, I felt more and more of myself slipping away. I couldn’t remember things, particularly the immediate past, but eventually even the more distant past had been erased. I was frightened by this. I thought, ‘if I don’t know what I’ve done or where or I’ve been, then who am I? A person’s memories are her identity. Take them away, and you take away her sense of self.’

Advocates of ECT treatment deny it causes brain damage, although a manufacturer of ECT machines includes “permanent brain damage” as a risk.

 Others acknowledge memory loss but blame the depression, not the electricity, even after a review concluded that “There is no evidence of a correlation between impaired memory/cognition after ECT and impaired mood, much less a causal relationship,”

 a conclusion subsequently confirmed in a 

The class action lawsuit currently being prepared in the United Kingdom (UK) is focused not on the memory loss and brain damage per se, but on the failure of psychiatrists to 

The risk of death is greater than 1 per 10,000 patients noted by organizations like the American Psychiatric Association.

 The leading cause of death is cardiovascular failure.

 A review of 82 studies with more than 100,000 patients, found that 1 in 50 patients experienced “major adverse cardiac events.”

 In addition, there are other mortality risks, which are higher for older individuals in the target age group for ECT, and are associated with general anesthetic procedures.

No one has precise data about how many Americans receive ECT each year, let alone how many treatments each patients receives or how closely providers space treatments. This is a troubling dilemma, according to the authors.

Neuropsychiatry