REVIEW

What Is Brain Damage and Does Electroconvulsive
Therapy Cause It?
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Conrad M. Swartz, PhD, MD

Abstract: Surveys show public misperceptions and confusion about

WHAT DO PHYSICIANS REFER TO BY“BRAIN DAMAGE”

brain damage and electroconvulsive therapy (ECT). Fictional movies havemisrepresented ECT to suggest brain damage and to ridicule mental illness
and psychiatric patients. “Brain damage” has become a colloquial expression without consistent meaning. In contrast, brain injury is the medical
term for destruction of brain cells, such as from kinetic impact (concussion), hypoxia, or infection. Studies of both high-resolution magnetic resonance imaging (MRI) and enzyme assays find that causes of brain injury
are accompanied by observable structural changes on MRI and elevatedblood and cerebrospinal fluid levels of brain enzymes that leak from injured brain cells. Concussion is also followed by intracerebral bleeding,progressive brain atrophy, diffuse axonal injury, cranial nerve injury, and
2–4 fold increased risk for dementia. In contrast, there is no evidence that
ECT produces any of these. Studies of ECT patients find no brain edema,
structural change persisting 6 months, or elevated levels of leaked brain enzymes. Statistical comparisons between brain injury and ECT effects indicate no similarity ( P < 0.00000001). Moreover, the kinetic, thermal, andelectrical effects of ECT are far below levels that could possibly cause
harm. This robust evidence shows that there is no basis to claim that
ECT causes brain injury.

The expression “brain damage” is not used in publications by
neurologists or neurosurgeons in countries where English is theofficial language; rather, the term brain injury is used. “Brain damage” is occasionally used by other physicians indistinguishably frombrain injury. As used in the neurological literature, brain injury is a
detrimental change in brain structure beyond behavioral and psychological changes and complaints. Because behavioral and psychological effects can occur without brain injury, they are not evidence of it,
and the focus here is on brain measurements.
Brain injuries are commonly grouped into traumatic brain injuries (TBIs) and nontraumatic injuries, such as from hypoxia,
blood flow interruption, infection, tumor, or aneurysm. Causesof TBI noted include falls, collisions, assaults, and sports injuries,
producing an external force with kinetic energy that causes skull
damage (e.g., from a weapon) or brain movement inside the skull.2
Every cause and type of brain injury mentioned produces observable structural brain changes at least sometimes.

Key Words: ECT, electroconvulsive, therapy, brain damage, brain injury,
MRI, brain enzymes, concussion, traumatic brain injury, chronic traumatic
encephalopathy

WHAT DO THE PUBLIC AND NONPHYSICIANSREFER TO BY “BRAIN DAMAGE?”(J ECT 2024;00: 00–00)

THE BASIC QUESTION AND METHODSOF INVESTIGATION“Brain damage,” pain, cognitive difficulties, and simple fear
are common negative public perceptions about ECT.1 Large rapid
clinical improvement during a course of ECT in many patientssuggests that ECT produces changes in the brain; is damage partof this? What specifically is brain damage and does the ECT procedure cause it, separate from anesthesia concerns (e.g., hypoxia) andco-occurring medical conditions (e.g., coronary vascular illness)?
Google and PubMed searches on the terms “brain damage,”“brain injury,” “traumatic brain injury,” “MRI ECT,” “ECT brain injury,” and “ECT dementia” and then PubMed searches on “ECT”
with each specific brain cell enzyme produced the information
used. All studies found reporting verifiable observable brain structure or body fluid level data on these topics were reviewed.
From Somatics LLC, Venice, Florida.
Received for publication January 22, 2024; accepted February 23, 2024.
Reprints are not available (e‐mail: conrad.swartz@yahoo.com).
The author is a member of Somatics LLC, a manufacturer of ECT devices andsupplies, and a stockholder of Medtronic Corp.
Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.
This is an open-access article distributed under the terms of the Creative
Commons Attribution-Non Commercial-No Derivatives License 4.0(CCBY-NC-ND), where it is permissible to download and share the work
provided it is properly cited. The work cannot be changed in any way orused commercially without permission from the journal.
DOI: 10.1097/YCT.0000000000001019

Journal of ECT • Volume 00, Number 00, Month 2024

Brain damage is a colloquial expression without consistentor specific meaning. In publications addressed to the public, its usage sometimes includes unverified—even unverifiable—beliefs.
The idea of “brain damage” has been used to provoke fear about
ECT, combining absence of knowledge about brain physiology andstructure, how the nervous system works, serious brain illness, andthe nature of electricity. For example, few people can identify what
voltage is, beyond something about electrons and wall sockets.
As a brain-related illustration, a survey found that a high proportion of the population has flatly incorrect ideas about the sequelae of TBI, and even health professionals who do not specialize in brain injury hold similar misconceptions.3 In this survey,
56% of respondents had at least some college education, 17%
had experienced brain injury, and nearly half knew people withbrain injury. However, 40% of respondents endorsed that sometimes a second head impact can help remember forgotten items,
a misconception presumably provoked by fictional televisionand movies.
Analogously, fictional movies and television mislead audiences by adversely depicting ECT and its consequences, as in“One Flew Over the Cuckoo's Nest (1975)” and “Death WishTwo (1982),” leaving the impression ECT causes permanent harmto the brain.4 “Cuckoo's” impact is so strong that recent movie
portrayals, as in “Don't Worry Darling (2022),” provoke conditioned fear reactions with minimal detail. Fictional comedy
movies and TV programs have misrepresented ECT to suggest
brain damage, and to comically ridicule mental illness and psychiatric patients, as in “The Beverly Hillbillies (1993),” “Strange
Brew (1983)” and “Mad TV (May 30, 2009),” and similarly in
Pink Floyd's famous song “Brain Damage (Dark Side of theMoon, 1973).”
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exposes-psychiatric-crimes.html, caution: this site attempts to install viruses). Likewise, British psychologist nonphysician John
Read6 wrote “brain cells receive electrical signals of a fractionof a volt. Subjecting them to 150 V inevitably causes damage, similar to traumatic brain injury.” Please consider what 150 volts and460 volts mean, then reconsider that a point of voltage represents
no power or energy without the presence of a second location ofdiffering voltage for electrons to flow between. In comparison,
the voltage difference across the cell body of a human brain neuron during the ECT stimulus is calculated as 0.006 volts7 and (by adifferent method) as less than 0.070 volts.8
In a litigation against psychiatrists, Dr. Peter Breggin mentioned working as a hired consultant (“expert witness”) for plaintiffs in about 80 lawsuits, and he claimed ECT causes brain damage.9 In that litigation, the plaintiff's brain images were interpreted
as normal before and after ECT. The jury rejected claims against
the defendant psychiatrist, noting plaintiff attorneys' inability toidentify that ECT caused harm. Breggin has authored numerous
books attacking psychiatry, e.g., “Toxic Psychiatry,” “Medication
Madness,” “Brain-Disabling Treatments in Psychiatry.” Previously, in a 1993 CBS network television program “Eye on
America,” Breggin said to the camera “We have a long history
in Psychiatry of damaging peoples' brains and claiming it helps.”
This same program shows a large banner displaying “SHOCKTREATMENT CAUSES BRAIN DAMAGE CITIZENS COMMISSION ON HUMAN RIGHTS (800)869-CCHR.”
Because the expression “brain damage” has no specificmeaning, claims about it also have no specific meaning or implications. In contrast, reports about brain injury can be understoodbecause it has specific meaning.
In a public internet survey of 1091 individuals who screened
positive for depression, many respondents stated they are frightened about ECT and concerned that it could cause brain damage
or pain. A large proportion were not aware that scientific evidence
for ECT is robust and it is a standard therapy for severe andtreatment-resistant depression.1

BRAIN INJURY FROM TBI

FIGURE 1. CCHR Placard Outside 2019 Annual APA Meeting.

Besides movie makers, antipsychiatry organizations such as
CCHR (“Citizens Commission” a Scientology organization affiliate) have long directed threatening claims about ECT to the public (Fig. 1). As an example, outside the main meeting hall of the2019 annual meeting of the American Psychiatric Association,
demonstrators carried color printed placards displaying in largebold font “ELECTROSHOCK TREATMENT. A FANCYWORD FOR 'KILL BRAIN CELLS'” with the organization name
CCHR Citizens Commission on Human Rights. (See photo). Referring to its downloadable video “Therapy or Torture: The Truth
about Electroshock,” the CCHR website5 states, “It hits the headwith the force of a 40-pound cinder block dropped seven and ahalf feet. It's been described by patients as a grenade going off
in your body. It's called electroconvulsive therapy.” This video presents a sequence of similarly threatening and distorted claims.
On its website, Scientology published a report of a CCHR
exhibit, “Psychiatry: An Industry of Death” stating “ECT...victims
are subjected to as much as 460 volts of electricity to the brain.”(https://www.scientologynews.org/press-releases/citizens-group-2

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Internet search for “brain damage” produces results mostly
concerning TBI related to common injuries from sports, vehicle
collisions, or falls. It may be surprising that TBI is far more likely
following rotational motion, i.e., shear, than from straight line impact.10 Moderate to severe concussion can immediately cause
bleeding inside the brain and then produce brain tissue loss ofabout 5% per year as atrophy, sometimes generalized and sometimes focal. This generalized atrophy is typically seen as wideningof cortical sulci, ventricular enlargement, and cortical thinning.11
Other examples of structural brain changes after TBI include
onset of epileptic (seizure) disorder, contusion (bruising, swelling), hematoma (bleed inside the skull), cranial nerve injury that
occurred together with TBI,12,13 and visible neurological signsof impaired motoric actions (e.g., paralysis) or reflexes (e.g., spasticity) associated with specific brain regions or illness.
Of concussion patients studied, 181 of 251 (72.1%) showedmagnetic resonance imaging (MRI) signs of diffuse axonal injury
within the first month of experiencing concussion with loss of
consciousness. These signs were visible on direct inspection of
the MRI. Patients with diffuse axonal injury showed significantly
worse functioning and neurocognitive outcomes compared toother patients, with personality changes, aggression, and major
depressive disorder.14 Chronic traumatic encephalopathy produced
visible atrophy of several frontal and temporal regions of brain cortex,
including orbital-frontal, dorsolateral frontal, superior frontal, anterior© 2024 The Author(s). Published by Wolters Kluwer Health, Inc.

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temporal, and medial temporal regions, as well as larger brain lateraland third ventricles.15
Dementia is increased 2- to 4-fold following moderate orworse TBI, according to a survey of publications.16 In a prospective longitudinal study of 208 patients with TBI, intracranial hemorrhage and hospitalization for at least 3 days was followed by increased incidence of dementia.17

BRAIN INJURY FROM TEMPERATURE ELEVATION

In its “Final Order on ECT” of December 2018,18 the US
FDA noted that direct brain injury from the ECT electrical stimulus would require temperature elevation in the brain to injurious
levels. This does not occur because most of the electrical current
is dispersed through the scalp and shielded by the skull, and isthereby short-circuited between the electrodes. Worst case calculation shows deep tissue temperature elevation is less than 0.092°
C,19 recently confirmed by measurements of scalp temperatures
corresponding to strong current shunting.7
Moreover, the hippocampus—the brain center for learningand memory—is distant from the location of ECT electrodes,
about as far as a brain region can be. Temperature injury in the hippocampus cannot occur in the absence of temperature injury
closer to the electrodes, and this does not happen.

MRI STUDIES OF BRAIN STRUCTURE BEFORE AND
AFTER ECT
Early prospective brain imaging studies of ECT, using conventional MRI, showed no evidence of change in size of brain cortex, hippocampus, or ventricles between before and after a courseof ECT.20–22 One of the earliest nonconventional prospective MRI
studies used diffusion-weighted imaging, chosen for sensitivity tolocalized tissue changes from impaired energy metabolism, asfrom ischemia or prolonged seizure.23 Diffusion-weighted imaging showed no abnormalities after ECT.
More recent studies used high-resolution MRI scans to examine the hippocampus, a deep brain area involved with memory
function, and other limbic areas. These limbic regions are about as
distant from the scalp and ECT electrodes as a brain region can be,
so direct effects of the ECT electrical current are less likely thanelsewhere in the brain. As direct effects on brain structure do notoccur closer to the electrodes, there should be no direct effectsof ECT current on the hippocampus and other deep brain areas.
In one survey, 31 of 32 MRI brain-imaging studies of a totalof 467 patients and 285 controls found no evidence of brain injury
after ECT.24 More recent studies by this survey's authors foundthat all structural brain changes fade by 6 months after ECT; therefore, no detrimental changes persist. Specifically, after MRI brain
imaging in 18 severely depressed patients showed increased thickness in 26 cortical regions 6 days after ECT, imaging repeated 6
months later found all brain regions had returned to baseline thickness.25 In a later MRI study of 22 severely depressed patients, thesame investigators26 similarly observed initial increase in volumes
but no change between baseline and 6 months after ECT in bothright and left hippocampal dentate gyri, and in the volumes of
20 other major hippocampal regions.
Nordanskog et al27 observed that the volume of the hippocampus is the same 6 months after ECT as it was before ECT.
Measuring hippocampal volumes in 23 elderly patients, Bouckaert
et al likewise found no difference between 6 months after ECT and
before ECT.28
Jehna et al29 examined 12 depressed patients before, shortly
after, and 10 to 36 months after ECT. Before ECT patients had lessglobal brain volume, white matter, and peripheral gray matterthan healthy controls. After ECT, patients showed increased brain© 2024 The Author(s). Published by Wolters Kluwer Health, Inc.

What Is Brain Damage and Does ECT Cause It?

volumes but at 10- to 36-month follow-up, these increases had
faded to nonsignificant.
Studying MRI data in nine patients, Gyger et al30 observedthat water content does not increase with hippocampal volume after ECT, so there is no evidence that brain volume increase after
ECT is edema (swelling injury). Likewise, using data from ultrahigh field MRI measurements on 21 patients before and after 10
ECT sessions, Nuninga et al31 observed that edema is not partof hippocampal volume increases that accompany ECT.

LEAKAGE FROM BRAIN CELLS AFTER ECT
Besides MRI changes, brain injury can be detected bychanges in blood substances such as enzymes that leak from inside brain cells through damaged cell walls. Several study reports
describe that blood and cerebrospinal fluid (CSF) concentrationsof substances that show elevations after brain injury are not increased by ECT.
The brain isozyme (BB) of creatine phosphokinase (CPK) is
released rapidly into the circulation following stroke or transientischemic attack,32 seizure with prolonged loss of consciousness,and traumatic brain injuries whether mild, moderate, or severe—
including in amateur boxers. CPK-BB is also elevated in neurological diseases and malignancy. Blood samples taken shortly before ECT and 1, 2, and 6 hours following bilateral ECT in a seriesof 31 patients of age 23 to 70 showed no alteration in serum
CPK-BB concentrations, using a sensitive radioimmunoassay.33
CSF concentrations of three established markers of neuronaland glial generation were measured in nine patients before and after a course of six ECTs. These markers are CSF-tau protein, CSF
neurofilament, and CSF-100 beta protein, and none showed significant change with ECT. Moreover, the CSF/serum albumin ratio was unchanged; this ratio reflects blood-brain barrier dysfunction. The authors concluded that there is no biochemical evidenceof neuronal or glial injury or blood brain barrier dysfunction following ECT.34 Serum concentrations of S100B protein measured
in 22 depressed patients treated with ECT showed no change frombaseline to after the ECT course or 6 months later.35 Likewise,
S-100 protein levels were unchanged throughout courses of ECT
in 19 patients.36
Likewise, measurements of serum neuron-specific enolase
concentrations, a marker of neuronal injury that increases in the
bloodstream after generalized epileptic seizures and TBI, showed
no increase with ECT treatment. One study of seven patientsassayed serum enolase concentrations twice before ECT and at
16 different times after the first ECT, and again once before andafter later ECTs, finding no variations among these concentrations.37 Another study examined 14 patients before and along
the course of bilateral ECT, finding no elevation in enolase concentration.38 Later studies found no changes in serum enolase
concentration after ECT in 10 patients39 and in a different groupof 19 patients.36
Elevation of serum neurofilament light concentrations(sNfL) correspond to neuronal axonal injury in neurodegenerative
dementias and in multiple sclerosis.21 In clinical practice, neurologists judged sNfL as useful in confirming or excluding neurodegeneration in 59 of 109 patients, suggesting 53% of patients withneurodegeneration showed abnormalities.40 In two series of 15 patients each, concentrations of sNfL drawn both 24 hours and7 days after ECT remain unchanged from baseline, and these concentrations did not differ from healthy controls.41,42

HISTOLOGICAL EXAMINATION
No cell death or injury occurred the brains of laboratorymonkeys after the electroconvulsive shock procedure,43 thewww.ectjournal.com

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laboratory animal model of ECT. Several reports describe brain
autopsy examination of elderly patients who had received large
numbers of ECT treatments. An 89-year-old woman with recurrent episodes of mania and documented history of more than
1250 bilateral ECT treatments showed no signs of brain injury
on microscopic (histological) and macroscopic (gross anatomical)
examination.44 Postmortem brain examination of a 92-year-old
woman after 91 ECT treatments showed no pathological changes
that could be attributed to ECT, including in the hippocampus.
Moreover, her cognition was intact as shown by perfect score on
Mini-Mental State Exam 6 days before death.45 Likewise, postmortem examination of an 84-year-old man after 422 ECT treatments showed no pathological changes attributable to ECT. Examination included thickness and deep structures, such as basal ganglia,
thalami, ventricles, hippocampus, amygdala, and brainstem.46
Microscopic postmortem examination of hippocampus from
12 patients who had received ECT for depression within 5 years ofdeath revealed no substantial cell loss, structural changes, or signsof inflammation, and likewise for age-matched non-ECT patientsand healthy controls47; all groups showed similar mild age-relatedchanges. Patients included a 100 year old who received over 176
ECTs since age 90 and a 58 year-old who received more than69 ECTs. Several studies cited above report brain growth and cell
additions during the first few months after ECT,25,26 pointing
away from injury and demonstrating that the adult brain remains
capable of growth, i.e., mitosis.

DEMENTIA ONSET
There is no evidence of increase in dementia incidence in patients who received ECT. After an average of 34 years of followup on 1089 consecutive depressed inpatients treated with ECT,
dementia was not more common than in 3011 matched depressed
inpatients who did not receive ECT,48 and age had no effect. Another follow-up study of 5901 patients 2.4 to 7.8 years after ECT
reported that in those younger than 70 years, ECT was not associated with greater incidence of dementia than in age-matched patients not given ECT. For patients at least 70 years old, ECT was
associated with significantly lower rate of dementia.49

DISTINCTIONS BETWEEN TBI AND ECTThe kinetic energy of an object is calculated by the formula
1/2 of mass times velocity squared. This represents the ability ofan impact to produce changes. High kinetic energy requires rapid
physical movement but there is only slight to no physical movement during routine modern ECT, which is given under anesthesia, so produces virtually no kinetic energy. In ECT, there is no
physical force that can produce skull injury or brain movement.
Moreover, TBI is far more likely following rotational motion(i.e., shear) than a straight impact,10 and there is no rotational motion during ECT. Before the ECT electricity is applied, patients are
so deeply paralyzed they cannot breathe, and an anesthetist must
provide ventilation.
In contrast to studies of TBI consequences, studies of patients before and after ECT have found no evidence of brain
shrinkage, diffuse axonal brain injury, bleeding into the brain, cranial nerve injury, onset of epileptic seizure disorder, or signs of
impaired motor actions or reflexes. Accordingly, ECT is notfollowed by any sign of brain injuries that accompany TBI.
The studies of MRI brain imaging cited above include all
known reports of imaging both pre-ECTand again at least 6 months
afterward; these examined a total of 87 patients, none of whomshowed persisting brain changes. The higher incidence of brainchanges after TBI shows that it is a different condition. Statisticallycomparing 0 of 87 ECT patients against 181 of 251 traumatic brain

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injuries with MRI abnormalities,14 Fisher's exact test shows negligible chance ( P < 0.00000001)—as close to zero as statistical testing
permits—that TBI and ECT are similar. To illustrate the strength ofthese results, consider the imaginary circumstance that brain abnormalities appear post-ECT in 5 of 87 ECT patients from undiagnosed deteriorative conditions such as head injury from a fall during
the course of ECT treatment. Still, Fisher exact statistical test continues to show the same negligible chance, P < 0.00000001, of
TBI and ECT similarity.
The studies of brain cell leakage cited above examined a totalof 142 patients after ECT, and none showed cell leakage. Studiesof blood markers after TBI show significant enzyme elevations
but only one study found identified the incidence of these elevations.50 It reported that sNfL in all of 14 boxers were elevatedand higher than controls, with no overlap. Those experiencing severe head impact showed higher sNfL levels. Likewise, sNfL in allof 28 concussed professional hockey players were higher thancontrols with no overlap.50 This totals sNfL elevation in 42 of
42 concussions. Statistically comparing 0 of 142 ECT patientswith 42 of 42 concussed athletes, Fisher exact test shows whatamounts to no chance ( P < 0.00000001)—as low as statistical
testing can find—that TBI and ECT are similar. Even these statistical results are understated; consider the imaginary circumstancethat five athletes with concussions do not show sNfL elevations
but 5 of 30 ECT patients do. Again, Fisher exact statistical test
yields the same result, no chance P < 0.00000001 that TBI andECT are similar. Likewise, comparing 0 of 30 ECT patients showing sNfL elevations with 59 of 109 neurodegeneration patients40
again reveals no chance ( P < 0.00000001) of similarity.
As further contrast between ECT and TBI, as noted above,
TBI is followed by increased incidence of dementia but ECT isnot. Moreover, ECT is not followed by structural brain changes
or brain cell enzyme leakage as accompany interruption of bloodflow or oxygen to the brain, brain toxin exposure, brain infection,or brain bleeds or tumors, and there is no logical rationale for ECT
to produce these. Thereby, and including concussion, ECT has
nothing in common with events, diseases, or agents that produce
brain injury.

LIMITATIONS
The analyses are limited by the data available, technology,
and ethical considerations. The TBI data were not from randomized controlled studies, but deliberately exposing subjects to TBI
is not ethical. The MRI imaging resolution and brain enzyme
measurements are limited by the current state of technology;
new different or more detailed measurements may produce otherevidence. This study was limited to measurements of verifiablephysical evidence indicative of brain structure. Cognitive performance and complaints and other subjective symptoms were notconsidered relevant and were not examined.

CONCLUSIONS
Numerous studies show that all effects of ECT on brain structure are only temporary, disappearing within 6 months. Separately,
there is no evidence of enzyme leakage from brain cells after ECT.
Accordingly, there is no evidence of permanent structural changes
or brain cell injury following ECT. In contrast, all known causes ofbrain injury produce persisting visible structural deteriorative
brain changes and brain cell enzyme leakage in at least some people, and statistically significant differences from them show that
ECT is not like any of them. Moreover, the sensitivity of identifying structural brain deteriorative changes is high enough to findthey accompany major depression itself and also exposure to antipsychotic drugs commonly used in treating major depression.
© 2024 The Author(s). Published by Wolters Kluwer Health, Inc.

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Claims that ECT causes “brain damage” or brain injury are notconsistent with scientific understanding or knowledge, and dissemination of such claims amounts to misleading provocation offear and alarm.
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