Electroconvulsive Therapy and Brain Damage: Survey of the Evidence From a Philosophical Promontory

CHANGES IN BRAIN STRUCTURE

Multitudinous studies have examined whether ECT changes brain structure. Some scientific studies and reviews find no evidence of structural brain damage (Coffey et al., 1991; Weiner, 1984), supporting assertions of other prominent experts that ECT is safe and does not cause brain damage.

In recent years, the media has often parroted these claims, with one example being an article on the website of Discover magazine by popular science writer Carl Zimmer. The article calls ECT’s “safety questions put to rest” (Zimmer, 2012, para. 10). An article for The Atlantic by Dan Hurley, another popular science writer, contains an interview with psychiatrist Sarah Hollingsworth Lisanby and gives a mostly glowing depiction of the treatment in its contemporary form, with no mention of brain damage (Hurley, 2015). On March 17, 2016, Lisanby, in her professional role with the National Institute of Mental Health (NIMH), held a lengthy question-and-answer session about ECT through Facebook, in which she stated in answer to one question, “Research shows that ECT does not cause measurable brain damage” (NIMH, 2016). More interestingly, on January 17, 2017, Lisanby went on The Dr. Oz Show with celebrity doctor Mehmet Oz to further promote ECT (Sugarman, 2017). In a 2016 article for Boston Globe Media’s health news site STAT, psychiatry volunteer Kate G. Farber and financially conflicted psychiatrist and ECT specialist Charles H. Kellner write, “So where does the [ECT] ‘controversy’ come from? Mainly from a combination of outdated information and popular culture” (Farber & Kellner, 2016, para. 3). Ironically, not only is this article contributing to a pop culture understanding of ECT, but this statement is also a gross mischaracterization of the arguments of anti-ECT activists. It is an example of the straw man fallacy, the logical fallacy of misrepresenting an opponent’s argument as a weaker argument (straw man) than the one the opponent has actually given (Aikin & Casey, 2011; E. D. Cohen, 2009, pp. 383–386; Lewiński, 2011). Kellner and Farber also assert, “Severe memory loss is a rare side effect, while claims of brain damage are unfounded.” They never address the actual basis of those claims.

CHANGES IN SUBCELLULAR BRAIN CHEMISTRY

Changes in brain chemistry below the level of the cell give additional evidence for the issue of ECT-induced brain damage.

Growth factors are defined as proteins necessary for the growth and normal development of certain cells and which stimulate proliferation and differentiation in nearby cells (Campbell & Reece, 2005, Glossary). Neurotrophic factors (NTFs) are defined as molecules that enhance the growth and survival potential of neurons (Nature Publishing Group, 2016). Neurotrophins are conceived of as molecules which are both growth factors and a type of NTFs and which regulate neural development, survival, function, and plasticity (Chua, n.d.; E. J. Huang & Reichardt, 2001).

The neurotrophin or neurotrophic hypothesis proposes that repetitive neuronal activity enhances the expression, secretion, and actions of neurotrophins to modify synaptic transmission and connectivity, providing a connection between neuronal activity and synaptic plasticity, and implicating neurotrophins as having a key role in psychiatric disorders (Lang, Jockers-Scherübl, & Hellweg, 2004). Some studies and reviews show increases in neurotrophins or NTFs in the brains of animals after ECS and of patients after ECT, particularly brain-derived neurotrophic factor or BDNF (Sartorius et al., 2009; Taylor, 2008). This has further led researchers to the conclusion that ECT has beneficial physical effects on the brain.

But again, this change needs to be put into context, the proverbial forest through the trees. If the mechanism by which ECT works involves brain injury, then the enhancement in neurotrophins may not be enough to substantially restore the brain from the damage. Even if ECT does not cause brain damage, what can logically be concluded from the increases in neurotrophins?

Buttenschøn et al. (2015) looked at the roles of BDNF and vascular endothelial growth factor A (VEGF) in the pathophysiology of depression. The researchers investigated longitudinal associations between depression scores and serum levels of these NTFs during antidepressant treatment in 90 individuals with depression of at least moderate severity. They found no baseline or longitudinal correlations between depression scores and serum levels of BDNF or VEGF. They write, “Our results do not support the neurotrophic model of depression, since a significant decrease in serum BDNF and VEGF levels after 12 weeks of antidepressant treatment was observed.” Buttenschøn et al. note that their study’s finding is in agreement with three studies, but in disagreement with an equal number of others. Yet, there are differences in experimental design. To measure levels of the NTFs in blood serum, Buttenschøn et al. used the Quantikine Human VEGF or BDNF Immunoassay by R&D Systems, Inc., whereas they state that most of the other studies used the commercial ELISA kit from Promega. And they write that most of the other studies have small samples (between 10 and 56 depressed patients).

In neuroscience, the role of BDNF is being shown to be complex, with continuing debate about how this neurotrophin affects epilepsy and other health conditions. Is it a good thing? Is it a bad thing? Is it good sometimes and bad others? It appears that context matters.

In a 2013 commentary on the research of the role of BDNF in epilepsy, Scharfman writes,

There may be times when BDNF becomes “too much of a good thing,” to use the very words of Binder, Croll, Gall, and Scharfman (2001). In fact, one study of transgenic mice genetically engineered to overexpress BDNF indicated that “overexpression of brain-derived neurotrophic factor in the brain can interfere with normal brain function by causing learning impairments and increased excitability. The results also support the hypothesis that excess brain-derived neurotrophic factor could be pro-convulsant in the limbic system” (Croll et al., 1999, p. 1491). A second study of transgenic mice engineered for BDNF overexpression demonstrated that “chronic BDNF overexpression in the central nervous system (CNS) causes learning deficits and short-term memory impairments, both in spatial and instrumental learning tasks” (Cunha et al., 2009). Another study analyzed genetic variation and plasma levels of BDNF in rats and in U.S. Army Special Operations soldiers deployed during the Iraq and Afghanistan wars (Zhang et al., 2014). Stressed rats and soldiers who had probable posttraumatic stress disorder (PTSD) had allelic differences in the BDNF gene (Val66Met) associated with increased BDNF expression, indicating that “stress results in BDNF overexpression in the hippocampus” and suggesting “a BDNF-related compensatory mechanism” (p. 10).

Thus, increases in BDNF after ECT may actually be a medical sign of brain injury or impairment or trauma.

CHANGES IN ELECTRICAL FUNCTIONING

There is some evidence that ECT can disrupt the normal healthy electrical activity of the human brain. A recent study by a small group of neurology researchers identifies five patients who received maintenance ECT and developed “florid temporal epileptiform abnormalities on electroencephalography (EEG)” and other seizure activity, even though they had no history of epilepsy (Bryson, Gardner, Wilson, Rolfe, & Archer, 2016). The abnormalities ceased after cessation of ECT. The researchers hypothesize, “Maintenance ECT may predispose to epilepsy with a seizure focus in the temporal lobe.”

Bryson and colleagues’ (2016) article was met with skepticism (Asadi-Pooya, 2017). However, they logically defended their work, noting that prior research that did not find an association between ECT and epilepsy involved patients tending to have received a much smaller number of ECT treatments and/or no EEG was recorded (Archer, Bryson, Gardner, Wilson, & Rolfe, 2017). They also report that they “have observed temporal lobe epileptiform discharges in several other patients.”

Reisner’s (2003) review also identifies several older studies that found EEG abnormalities after ECT (pp. 210–211). This author was not able to find records of most of those. On a side note, although Reisner’s review is extremely comprehensive in its list of studies summarized, he often gives uncritical acceptance of study conclusions, especially of more recent research, and he glosses over the significance of the many historical findings of pathology in his own conclusions.

BRAIN DAMAGE IN AUTOGENOUS SEIZURES

When ECT is performed as intended for inducing a therapeutic effect, a seizure is always involved. Therefore, a pertinent question is whether naturally occurring seizures cause brain damage. There is disagreement over this issue among neurology experts, although seizure duration and frequency are believed to affect whether brain damage occurs. A 2015 Web page on the site of Epilepsy Action, which is described as “the UK’s leading epilepsy organisation,” states that seizures (either single or in clusters) that last longer than 30 minutes can cause damage to the brain. This is the duration the organization uses as a standard for status epilepticus, although other definitions have been noted (Lawson & Yeager, 2016). Several dictionary definitions do not apply any minimum time frame, instead defining the term similarly to that of Merriam-Webster, “A single prolonged seizure or a series of seizures without intervening full recovery of consciousness” (Status epilepticus, n.d.). The seizure duration in present-day forms of ECT in the United States is often less than 60 s (Mayo Clinic Staff, 2015), which implies that ECT seizures do not necessarily cause brain damage.

But some neurology experts have expressed beliefs that autogenous seizures are harmful to the human brain (Bronen, 2000; Carroll, 2003; Childs, 2008; Young & Jordan, 1998).

Carroll’s (2003) news article for The New York Times states “mounting evidence now suggests that repeated seizures can indeed harm the brain—or, in rare cases, even lead to death.” Among the neurology professors Carroll interviewed are Marc Dichter, Timothy Pedley, and Thomas P. Sutula, who all speak with great concern about the dangers of epilepsy being minimized. They speak of the syndrome Sudep (sudden unexpected death in epilepsy patients), damage to the hippocampus, swelling of the hippocampus, loss of neurons, and permanent changes that increase the probability of having a seizure again.

In the article by Childs (2008), Orrin Devinsky, director of the epilepsy program at New York University, is quoted as saying, “Recurrent seizures injure the brain, and the memory centers are particularly vulnerable.”

Bronen, a doctor at Yale University School of Medicine, writes, “A number of experimental animal and clinical imaging studies support the idea that seizures by themselves cause brain damage,” (p. 1782) specifying hippocampal damage, decreases in gray matter, metabolic dysfunction, swelling of neurons and glial cells, and more.

Doctors Young and Jordan write that nonconvulsive seizures damage the brain, citing sources on cognitive impairment, recurring seizures, and neuronal death. Generally, modern American ECT uses only nonconvulsive seizures because the treatment is modified to prevent full-body convulsions. “Unmodified” ECT is ECT without anesthesia or muscle relaxants and is still practiced in other parts of the world, where reports of abuse and public controversy have ensued even in recent years (Lewis, 2014; Shukla, 2000).

Referring back to the changes in subcellular brain chemistry following ECT, it should be repeated that increased expression of BDNF has been recorded after general seizure activity, meaning production of the NTF is increased (Binder et al., 2001). If one is to believe that an increase in NTFs after ECT is a sign that the treatment is beneficial to the brain, then it is logically consistent to also believe that an increase in NTFs after autogenous seizures is a sign that naturally occurring seizures are beneficial. This would contradict the opinions of Devinsky, Dichter, Pedley, Sutula, Young, and Jordan, and other experts who consider autogenous seizures to be harmful. If one does not accept that proposition as true, yet one still believes that the increase in NTFs after ECT is a sign of benefit to health, then one must be prepared to answer this question: How is the increase of NTFs after ECT any better than the increase of NTFs after autogenous seizures?

CLEAR CASES OF BRAIN DAMAGE

There are a few cases of patients with clear brain damage subsequent to ECT. Considering older cases, Reisner (2003) refers to a 1963 case of evident brain damage in a 23-year-old man (p. 209), cited originally by McKegney and Panzetta (1963). The patient was described as “in apparently good physical health” but with catatonic schizophrenic symptoms (McKegney & Panzetta, 1963). It is interesting to note the historically dated, questionable diagnoses given to this man, such as a “character disorder” of “passive dependent and homosexual type” (p. 398). (As noted earlier in this article, homosexuality is one example of medicine’s blunders and reversals because the trait was for several years considered a mental disorder by the majority of psychiatry.) On the same page, the article states, “He first manifested evidence of brain damage immediately following his first ECT and died after a progressively deteriorating course of 2 months.” This was despite the apparent use of anesthesia and oxygenation, alterations to modern ECT intended to prevent full-body convulsions and anoxia (inadequate oxygen in body tissue).

There is also a case of death and brain damage from 2015, which wasn’t widely publicized until 2016 (Armstrong, 2016; Prince, 2016; Silfverskiold, 2016). Seventy-one-year-old Elsie Tindle, an involuntary patient with a learning disability who was suffering depression and downward physical health, was forced to have ECT at Sunderland Royal Hospital in Sunderland, England. After only three ECT treatments from February to March 2015, she had an unexpected spontaneous seizure, ending in her demise on April 4, 2015. The inquest was presided over by Sunderland Coroner’s Court HM Senior Coroner Derek Winter, whereas the postmortem examination was done by Home Office pathologist Nigel Cooper. Cooper “concluded the formal cause of death as anoxic-ischemic brain damage, due to status epilepticus, due to electroconvulsive therapy” (Prince, 2016; Silfverskiold, 2016). This case especially raises questions of what other interventions could have been tried before the drastically invasive and often traumatizing procedure of involuntary ECT (Breeding, 2016; Burstow, 2006; Froede & Baldwin, 1999; Johnstone, 1999; Spikol, 2006), which this author has also personally experienced. Ironically and illogically, despite Tindle’s death, the jury ruled that her involuntary ECT was “lawful and necessary” (Armstrong, 2016; Prince, 2016) as though the only options were ECT or no treatment. This is a logical fallacy concerning ethics similar to the fallacy of the alternative disjunct concerning physical truth. The fallacy has complex, somewhat varied forms (Tomić, 2013). But put simply, the false dilemma fallacy is belief in a false dichotomy or false set of alternatives (Boone, 1999, p. 6), the fallacy of thinking there are only two options, or not considering all of the choices available in an ethical dilemma (Texas State University, Department of Philosophy, n.d.). Treatments for depression include several classes of oral and injectable medication, some with long-term effectiveness, and some for short-term emergencies; other technologies such as transcranial magnetic stimulation (TMS), cranial electrotherapy stimulation (CES), transcranial direct current stimulation (tDCS), and low-field magnetic stimulation (LFMS); nutritional and micronutrient therapies; clinical social work, peer support, various talk therapies, emotional regulation techniques, and psychosocial interventions; temporary physical restraints; and intravenous medication or nourishment. There are also novel treatments under investigation, such as precision-medicine biologics meant to replace missing brain proteins (Hamill, 2016; Pan et al., 2017). In addition, sham ECT (anesthesia only) may be effectual for many patients because some research has shown (Ross, 2006). (See “Placebo and Nocebo Effects” and “Anesthesia, Muscle Relaxants, and Postelectroconvulsive Therapy Medication” sections for hypotheses about potential confounding by placebo effects and the effects of anesthetics and other drugs used during or after ECT.)

CONFOUNDING VARIABLES

A confounding variable (confounder) is a variable in research that can interfere with truthful assessment of the relationship between an independent variable and a dependent variable, such as ECT and any measure of brain health or dysfunction. There are various confounders that could interfere with research on whether ECT causes brain damage.

THE 2011 U.S. FOOD AND DRUG ADMINISTRATION EXECUTIVE SUMMARY ON ELECTROCONVULSIVE THERAPY HAS SIGNS OF BIAS

The aforementioned includes scientific, real-world, and logical evidence that ECT causes brain damage. The 2011 FDA review of ECT is in some ways superficial and even contains indications of confirmation bias and selection bias. The report’s statement that “there is no evidence to suggest that ECT causes brain damage” (p. 37) is clearly false because it dismisses or disregards so much. Although this author has opined that all human thought is biased, the report’s deviations from objective evaluation are unacceptable coming from a governmental agency with oversight on medical laws and regulations. Instead of merely excluding the unmentioned studies with important findings from its report, the FDA should have explained why those studies were deemed lacking in rigor or reliability. What standards were used to define scientific rigor and to exclude certain research as lacking in rigor or completely lacking in value? But perhaps the FDA failed to mention those studies not just because of bias, but because of simple ignorance. Moreover, although the FDA report has detailed sections on memory and cognitive adverse events, neuropathological findings, and death, the report almost completely ignores the long history of negative patient accounts showing that ECT, especially involuntary ECT, is often dehumanizing and psychologically traumatic (Breeding, 2016; Burstow, 2006; Froede & Baldwin, 1999; Johnstone, 1999; Spikol, 2006). Such accounts also indicate that patients with negative experiences may be less likely to report those experiences and more likely to be invalidated, ignored, and dismissed by psychiatric professionals.

“DISSENTING” EXPERTS

There have been neurologists, psychiatrists, psychologists, and related health professionals who have opined that ECT causes brain damage. They stand in contrast to the apparent predominant opinion of the present day, but their views are not based on flights of fancy and they should not be dismissed without serious consideration.

A 1977 article by neurologist John Friedberg, cited by Reisner and earlier here, asserts that ECT results in neuropathology and “brain disease.” Friedberg also had a book published in 1976 that attacked electroshock as dangerous, cruel, and ineffectual, and presented interviews with patients expressing serious complaints. Friedberg passed away in 2012. An obituary for Friedberg notes he had trained at Yale University and University of Rochester School of Medicine. He was “well known for his courageous opposition to abuse by the psychiatric establishment” (San Francisco Chronicle, 2012).

In a 2000 letter in Nature, neuroscience professor Peter Sterling disputes the insistence of financially conflicted psychiatrist Max Fink that brain damage from ECT is a merely a myth promoted by antipsychiatrists. Sterling states,

In a 2002 article, philosopher and psychology professor James Giles (PhD in Philosophical Psychology) lays out the history and philosophy of ECT, ideas about it from proponents and critics, and accounts for the long list of known side effects, including long-term cognitive damage, summarizes evidence of brain damage, and describes the severe problems with research on ECT. The result is an unsettling sense of inhumane treatment that enables psychiatrists to exert power and control, with Giles concluding that ECT is qualified for the “title of the blood-letting of our time” (p. 82).

In a 2003 op-ed, psychiatrist Loren Mosher and professor of social work David Cohen write that ECT is not safe and not necessary. They cite the words of electroshock survivors Leonard Roy Frank, Thomas Hsu, and Jackie Mishra, who in turn call ECT brain-damaging, violating, and impairing. The article notes that Mosher was formerly chief of the Center for Studies of Schizophrenia at the NIMH and served as first editor-in-chief of Schizophrenia Bulletin, whereas Cohen received the 2003 Eliot Freidson Award from the American Sociological Association for outstanding publication in medical sociology.

In a lengthy 2010 review of the research on ECT, psychology professors John Read and Richard Bentall found “strong evidence (summarized here) of persistent and, for some, permanent brain dysfunction” (p. 333). They also write that in the 1940s it was commonly accepted that ECT “works” by causing brain damage and that in the 1940s and 1950s many autopsies showed evidence of brain damage (p. 344). Cited studies and reviews include that of Alpers (1946). This author could not find database records of the others, although a Web search indicated Read and Bentall are not the only ones to cite them. Read and Bentall refer to more recent studies they believe indicate brain damage, including the study by Calloway et al. (1981) and a 2001 study by Rami-Gonzalez et al. whose aim was “to review different subtypes of memory dysfunction associated with ECT from a neuropsychological perspective.”

Psychiatrist Peter Breggin has multitudinous times written that ECT is brain-damaging (Breggin, 1998, 2007, 2010, 2011; van Daalen-Smith, Adam, Breggin, & LeFrançois, 2014). Breggin has received research grants from Harvard Medical School and NIMH and has testified as a medical expert in more than 90 cases since 1987 (Breggin, n.d.). One was the 2007 case Salters v. Palmetto Health Alliance, in which former nurse practitioner Peggy Salters won $625,177 in damages for cognitive injuries sustained from ECT. This was found to be caused by the medical negligence of Dr. Eric Lewkowiez, who referred her for ECT but failed to report her increasing memory difficulties to the ECT specialist, resulting in Salters becoming “completely unable to function” at work or home (Anderson, Kittredge, & Short, 2007).

RELEVANCE TO LAW

In United States law, burden of proof is the obligation of a party in a legal case to provide evidence that will convince the court or jury in support of a contention. It dictates the degree of certainty that judges or juries must have to decide in favor of a party (Bergman, 2015). Ascending standards of burden of proof include “preponderance of the evidence,” “clear and convincing evidence,” and “beyond a reasonable doubt.”

In judicial cases, a burden of proof must be satisfied to answer legal questions of fact, which are distinct from questions of law in that they may be determined without reference to any legal rule or standard (Brown, 1943).

Prima facie is an adjective and legal term meaning plain, clear, or self-evident; strong enough to establish as fact unless disproven or rebutted (Legal Information Institute, n.d.); or presenting sufficient evidence at first glance for a plaintiff to win a case (NOLO, 2016).

The evidence reviewed here shows a near certainty of brain damage in some individual cases and indicates a rational likelihood that all ECT causes some degree of brain damage. Therefore, it can be reasonably concluded that the claim that ECT never causes brain damage does not meet the standard of proof as defined by clear and convincing evidence. There is not even a preponderance of evidence to prove the claim. The contention cannot legally be established as a fact by prima facie evidence because that evidence would be overturned by the evidence against it. Rather, there is clear and convincing evidence that ECT has caused brain damage in some individuals.

Furthermore, placebo and nocebo effects in ECT may affect legal liability if a patient were to sue their treatment providers for medical malpractice over an ECT-induced brain injury. An article in Psychological Injury and Law discusses how contextual factors can influence a patient’s expectations about his or her recovery from a brain injury and how both the accident and negligence-related nocebo effects can create legal liability (Vanderploeg, Belanger, & Kaufmann, 2014). Thus, poor care of a patient before, during, and/or after ECT may add to legal liability and increase the chances of winning a case on the partial basis of establishing brain damage. Involuntary ECT could add to this liability.

SUMMARY AND CONCLUSION

Psychiatric authorities and governmental agencies, including the FDA, have concluded ECT does not cause brain damage. However, the research on this issue has been deeply flawed, with researchers sometimes analyzing data using erroneous reasoning and drawing hasty conclusions, often reflecting researchers’ confirmation bias and at times even logical fallacies.

When examining changes in brain structure after ECT, researchers have been inclined to attribute brain atrophy to depression rather than ECT. Several brain imaging studies have found increases in brain volume after ECT, but they have not adequately considered and answered the possibility that such volume increases may be caused by swelling from electrical brain injury, rather than beneficial brain growth or regeneration, with at least one study’s analysis engaging in the logical fallacy of affirming a disjunct.

Nonpsychiatric neuroscience research indicates that neurons in the human brain undergo pruning with age, such that less gray matter in the cortex is actually associated with better cognitive performance. This has implications for ECT research because researchers have often concluded that the increase in brain volume found after ECT must be beneficial, rather than detrimental. Quantity of brain tissue may not be a good indicator of quality of neurocognitive functioning.

Several studies have found some type of neurogenesis occurs after ECT, but at least a few have found neurodegeneration, and it is unclear if the neurogenesis found is actually beneficial to health or a sign of injury. Many historical animal studies, and a few human studies, found signs of pathology, although ECT was often performed differently or unmodified at the times of those studies. A modern interventional nonhuman primate study that found neurogenesis and no sign of cell death after ECT used a very small sample, a short duration of treatment, and its analysis shows some confirmation bias. One of the study authors, who now works at NIMH, was later sent a warning letter by a department of the FDA for violations of research protocols.

A poorly designed recent observational study with a small sample of patients found a short-term increase in hippocampal volume after ECT, like several other studies, but the authors overlooked how their data showed that after 12 months mean hippocampal volume had decreased slightly from its original measurement. This provides evidence of long-term brain damage.

Some research has found an increase in neurotrophins or NTF after ECT and after ECS, an animal analog of ECT, especially BDNF. Scientists have hastily concluded this is a sign of therapeutic benefit. However, several neuroscience studies show that the role of BDNF is complex. Research on the neurotrophic hypothesis that depression and other psychiatric disorders are caused by low quantities of neurotrophins has had mixed findings. Research with rodents suggests that overexpression of BDNF, rather than being beneficial to health, causes cognitive impairment, may be epileptogenic, may be a response to seizures in general, and at least one human study indicates that increased expression of BDNF is a response to trauma. This suggests that increases of this NTF after ECT are actually a sign of harm.

A recent study by a small group of neurology researchers recorded epileptiform abnormalities on EEG in five patients who received maintenance ECT, and there are older studies with similar findings.

Although neurology experts have expressed disagreement over whether autogenous seizures alone cause brain damage, many have indeed stated that seizures damage or injure the brain.

There is strong evidence bordering on proof that ECT has caused brain damage in some individuals, including a recent case in which an involuntary patient died from a spontaneous seizure, and the pathologist concluded the cause of death as brain damage because of status epilepticus, caused by ECT. This case also raises ethical questions because it shows how psychiatric professionals often do not consider all available treatment options but rush to ECT, violating the dignity of the patient and endangering patient safety.

There are many variables that likely confound research on whether ECT causes brain damage, including brain scan inaccuracy; placebo and nocebo effects; cognitive reserve; anesthesia, muscle relaxants, and post-ECT medication; and cognitive biases and statistical biases.

A lengthy 2011 FDA review of ECT has signs of selection bias because multiple studies that could indicate brain damage were omitted. The FDA report also contains some language indicating confirmation bias in its evaluation of the studies cited. The report’s statement that “there is no evidence to suggest that ECT causes brain damage” is false.

Although the present consensus among psychiatrists seems to be that ECT does not cause brain damage, there have been several dissenting professionals from neurology, psychiatry, psychology, and related health fields. Their observations and arguments have been at times compelling.

From a standpoint of legal burden of proof, there is clear and convincing evidence that ECT has caused brain damage in some individuals. Legal liability may be increased when poor care of an ECT patient leads to nocebo effects.

This author concludes that ECT likely always causes some form or degree of brain damage. The primary mechanism by which it works probably involves brain damage, with resulting memory loss and cognitive impairment the means by which it relieves depression, disabling the overall functioning of the patient in ways that may outweigh whatever psychiatric disability the patient had, or continues to have if the treatment is ineffectual. Beneficial physical effects are more likely because of placebo effect and anesthetics than because of electricity or seizure. Involuntary ECT likely often works as torture and social control, which this author has experienced. Even voluntary ECT with perceived informed consent can be traumatizing. Patients who have positive subjective experiences of the treatment are probably unaware of much of the damage and disability inflicted in them and/or accept it because of social conditioning and iatrogenic anosognosia.