Does Electroshock Therapy Cause Brain Damage?

There has long been a controversy over whether ECT causes brain damage. At one time, the medical consensus was that electroconvulsive therapy achieves its effects through brain damage, but that opinion has undergone a complete reversal in the last 60 years. The official view, today, is that ECT causes no brain damage whatsoever, although adverse cognitive effects (sometimes lasting years) are associated with the procedure.

The American Psychiatric Association’s sample information sheet (representing suggested wording for informing patients abut ECT) includes the following language:

During ECT, a small amount of electrical current is sent to the brain. This current induces a seizure that affects the entire brain, including the parts that control mood, appetite, and sleep. ECT is believed to correct biochemical abnormalities that underlie severe depressive illness. We know that ECT works . . .

The phrase “a small amount of electrical current” is misleading, because the amount of current involved (typically 0.9 amps at 450 volts) is known to be fatal if applied to other parts of the body. Likewise, the statement “ECT is believed to correct biochemical abnormalities” is blatantly fraudulent, since there is no consensus view on how ECT achieves its effects. Indeed, the consensus view is that ECT’s mechanism of action is not understood. 

When consent is granted based on this kind of misinformation, it cannot be considered “informed consent.” Also, when consent forms fail to mention that there is no difference in outcome, after one month, in patients who receive sham ECT versus real ECT (except for fewer side effects with sham), patients are seriously misled.

Adverse cognitive effects are well known to be associated with ECT, and this is another area in which patients are under-informed. In spite of repeated claims (for 50 years) that ECT is safe, the first large-scale prospective study of cognitive outcomes following ECT did not occur until 2007, when outspoken ECT advocate Harold Sackeim, et al. (2007; for a complete list of references, go here) found that autobiographical memory was significantly (p < .0001) worse in patients both immediately after ECT and six months later. At both time points, the degree of impairment was significantly correlated to the number of shocks, with women and older patients particularly impaired. Impairment was also greater among those who received bilateral ECT rather than unilateral ECT, prompting Sackeim to conclude “there appears to be little justification for the continued first-line use of bilateral ECT in the treatment of major depression.” (Despite this, bilateral ECT remains the most common form of ECT in use today.) 

 

A 1980 study (Freeman et al., 1980; again, see references here) produced the longest followup data to date. ECT patients performed worse than non-recipients on ability to recall famous personalities from the 1960s and also on personal memories from early childhood; the average time since ECT was 8.4 years. Most people would consider this permanent memory damage.

In addition to significant retrograde amnesia, there are reports of ECT resulting in anterograde amnesia (the inability to retain newly learned information; a learning disability). The American Psychiatric Association report (2001) cites 11 studies demonstrating anterograde amnesia in the first few weeks after ECT, concluding that during this time, “returning to work, making important financial or personal decisions, or driving may need to be restricted.” Nevertheless, the APA report states “no study has documented anterograde amnesia effects of ECT for more than a few weeks,” which is blatantly false. Feliu et al. (2008) found that anterograde amnesia persists for four weeks. Two studies (Porter et al., 2008; Squire & Slater, 1983) showed that anterograde memory is degraded for at least two months. Halliday et al. (1968) demonstrated anterograde memory deficits lasting three months. 

 

For many years, it has been claimed that ECT produces no brain damage. And yet, in the 1940s it was commonly accepted that ECT owes its effects to brain damage. In 1941, Walter Freeman, in a paper called “Brain-damaging therapeutics,” wrote: “The greater the damage, the more likely the remission of psychotic symptoms. [...] Maybe it will be shown that a mentally ill patient can think more clearly and more constructively with less brain in actual operation” (Freeman, 1941). A review in the Lancet (Alpers, 1946) described ECT-induced hemorrhages and concluded that “all parts of the brain are vulnerable—the cerebral hemispheres, the cerebellum, third ventricle and hypothalamus.” In two memory tests used to assess brain damage, Goldman et al. (1972) found that ECT patients scored worse than a non-ECT control group at both 10 and 15 years after ECT, which “suggests that ECT causes irreversible brain damage.” 

 

According to Read and Bentall (2010), “In the 1940s and 1950s autopsies consistently provided evidence of brain damage, including necrosis (cell death).” 

 

In a review of the first twenty years of autopsies, Allen (1959) concluded: “damage to the brain, sometimes reversible but often irreversible, occurred in the course of electric shock treatments.” 
 

CT scans have demonstrated frontal lobe atrophy among ECT patients (Calloway et al., 1981; UK ECT Review Group, 2003). One review acknowledged that “both anterograde and retrograde memory impairment are common” (Rami-Gonzalez et al., 2001). The same review documented various forms of neurobiological dysfunction underlying the subtypes of ECT-induced memory dysfunction: Retrograde amnesia was found (not surprisingly) to be a consequence of electrochemical dysfunction of the limbic-diencephalic subcortical areas involved in information retrieval; while in anterograde amnesia, the medial temporal lobe is most affected. 

The medical literature thus strongly suggests that ECT causes brain damage, which is the only reasonable way to explain the persistent and often irreversible cognitive deficits that occur in patients who have been repeatedly shocked. But again, consent forms leave out this important information, throwing into question the notion that any ECT patient has ever truly given “informed” consent.

John Read and Richard Bentall, in their review of the literature (Read & Bentall, 2010), observed: “The continued use of ECT . . . represents a failure to introduce the ideals of evidence-based medicine into psychiatry. This failure has occurred not only in the design and execution of research, but also in the translation of research findings into clinical practice.” Their conclusion was that “the cost-benefit analysis for ECT is so poor that its use cannot be scientifically justified.” On this basis, and because consent forms do not accurately portray the risks of electroconvulsive therapy, continued use of ECT in a therapeutic setting can only be considered unethical.

For a complete list of references to all studies mentioned here and in previous posts, see the book Hack Your Depression or go online here. 

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