This brief will describe a representative sampling of the considerable documented evidence that ECT (electroconvulsive therapy) causes brain damage. The cited sources of information are publicly available medical journal articles of which abstracts can be found in the National Library of Medicine online database, with full texts from the publishers.
ECT is the process of applying electric shock to the head in order to provoke a brain seizure. The human brain has inherent resistance to such an attack. Homo sapiens evolved a skull to withstand penetrating trauma, but it is less effective at resisting electrical trauma. Electrical threats to the head were not a high priority, especially electric shocks received repeatedly, which would never occur in nature. Electric shock must be given at high enough power, and for long enough duration, to overcome the protective mechanisms of the brain, and this is relatively easy to accomplish.
Whereas a current in excess of 75 milliamperes (mAmps) prevents a grown man from releasing his grip on a live wire, ECT machines deliver between 750 and 900 mAmps. (Castellano, 2005 and Foris, 2018) When electric shock exceeds the brain’s seizure threshold, transmissions between brain cells degenerate into a pattern-less, entirely chaotic electrical storm. This generalized seizure activity is the goal of every ECT session.
Each person has a unique initial seizure threshold: the power and duration of the electroshock that it takes to provoke their first ECT seizure. The brain launches self-protective biochemical mechanisms after a seizure; similar to how it reacts to injuries caused by the sudden loss of blood supply, such as occurs after a stroke. (Stepień, et al, 2005) In the course of a typical series of ECT sessions, the brain tends to mobilize its biochemical defenses to increasingly resist each new shock. Thus the seizure threshold rises, meaning that in most patients, it takes progressively more electric power and progressively longer duration of shock in order to cause a seizure. (van Waardem et al, 2013) The more the shock power and duration are increased over the initial seizure threshold, the greater the cognitive side effects. For shock recipients, this manifests as an inability to think well, difficulty learning new things, and loss of memory. (McCall, et al 2000)
Physicians in the field of neurology are dedicated to the reduction or elimination of seizures. This is because there is abundant evidence that repeated seizures can be brain damaging, no matter how they come about. Seizures cause acute as well as chronically damaging inflammatory reactions in the brain. The damaged areas of the brain, in turn, increase the risk of more seizures. (Choi and Koh, 2008) Just as in epilepsy, brain inflammation is caused by ECT seizures. Studies that use MRI and sophisticated magnetic resonance spectography scans document significant ECT-induced inflammation of brain nerves. (Cano, et al, 2017)
Epilepsy is a disease in which there are recurrent seizures. One of the most common types of epilepsy originates in the temporal lobes located at the sides of the brain. In temporal lobe epilepsy the seizures spread out, causing degeneration of brain nerves in several other distinct brain areas. Particularly hard hit are the regions known collectively as the limbic system, including structures essential to memory and learning. In fact, neurodegeneration of limbic circuits is a hallmark of temporal lobe epilepsy. (Naegele, 2007) The goal of existing anti-epileptic therapy is to prevent seizures, and the newest research is directed at finding ways to reduce seizure-induced brain damage.
Seizures are known to produce a type of unstable oxygen molecule that destructively reacts (reactive oxygen species, ROS). ROS cause damage to genes and proteins, and can also directly cause cell death. (Williams, et al, 2015) Seizures provoke the activation of multiple other biochemical processes that hasten brain cell death. These have been found to include the ramping up of damaging enzymes, and switching on a genetic program to destroy the energy-production units inside the cells. (Niquet, et al, ed., 2012)
S100b – a biomarker of brain damage
A sensitive indicator of brain damage is the protein ‘S100b’, called a trauma biomarker. (Stavrinou , et al, 2011) This protein is normally beneficial to the brain in very small concentrations, but harmful when the concentrations increase. Escalating levels of S100b have been shown to result in abnormal brain nerve function or cell death. (Thelin, 2016) There have been many studies measuring blood levels of S100b after various forms of brain trauma. For example, an increase of just one-tenth of a microgram (per liter of blood) of S100b is a 96.7% predictor of a sports-related concussion. (Kiechle, et al, 2014) In one study on traumatic head injuries seen on brain scan, S100b was 100% sensitive, in that all patients with abnormalities on CT or MRI brain scans had elevated S100b. (Linsenmaier, et al, 2016)
A representative study looking at S100b levels after electroshock showed statistically significant increases in S100b measured one hour after ECT. (Arts, et al, 2006) However, in most of the studies that report significant elevations of S100b after ECT, the study authors chose to favorably characterize it as proof of therapeutic effectiveness. (Palmio, et al, 2010) In contrast, when S100b elevation is found in every other kind of brain injury, it is considered reliable proof of brain damage.
Some studies have not reported increases in S100b after ECT, but a closer look at study design reveals an explanation for the conflicting findings. S100b is a very short-lived chemical, with half of it disappearing within as soon as 25 minutes. (Ghanem, et al, 2001) Therefore, studies that measure S100b more than an hour after ECT can be predicted to not to find anything. Some studies have tested at the 1-hour mark, but the S100b levels were combined with the levels measured at 3-hours, 6-hours, and later time points, even up to 2 days after ECT, and then reported as “mean” levels or averages. This statistical manipulation would obscure any real increase at the early time point. (See for example Agelink, et al, 2001 and Maier, et al, 2018)
Anatomical brain changes
Pictures of the brain are less sensitive than biochemical measurements, but can reveal much about the cumulative brain-damaging effects of electroshock, particularly on the frontal lobes. The frontal lobes are necessary for higher mental processes such as thinking, problem solving, judgment, decision-making and planning. A review of 26 studies that reported brain scan changes after ECT concluded, “The ECT response is associated with decreased frontal perfusion, metabolism, and functional connectivity…” (Abbott CC, et al. 2014) In lay terms, this means the brain scans routinely showed that ECT reduces blood flow, slows metabolism, and suppresses nerve-to-nerve impulses in the frontal regions of the brain.
The effects of ECT on brain anatomy are all over the map. For example, a study done in the earliest days of routine CT scanning reported remarkable loss of brain tissue after patients underwent a series of electroshock treatments. This is a condition called atrophy, where the brain actually shrinks. (Weinberger, et al, 1979) The same has been repeatedly demonstrated in the subsequent decades: a 1986 CT study found that ECT recipients were twice as likely to have a measurable loss of brain tissue in the front area of the brain and a tripling of the incidence of a loss of brain tissue in the back of the brain, compared to depressed patients who did not get ECT. (Dolan, RJ, et al, 1986) In the 1990s brain shrinkage from ECT was again corroborated, this time by MRI scans, with a strong correlation between the numbers of previous ECT treatments with the loss of brain tissue. (Andreasen, et al, 1990)
Yet other studies report growth of new brain tissue after ECT. This kind of response is also seen after a traumatic brain injury, in which setting it is universally interpreted as an effort to replace injured or threatened brain cells. In contrast, many ECT researchers declare that new brain growth is a sure sign of the desired treatment effect. (for example Gbyl and Videbech, 2018) However their pronouncement is not borne out by conflicting findings in other studies, which report that brain enlargement after ECT is not related to clinical improvement in the patient. (see for example Sartorius, et al 2018) Another recent study measured changes in 5 distinct brain regions after ECT, and concluded, “None of the brain imaging measures correlated to the clinical response.” (Jorgensen, et al, 2016)
A typical twist on the interpretation of brain damage caused by ECT is exemplified in this report from a major university: researchers detailed the abnormalities on MRI in 5 out of 35 patients within 6 months of treatment. The authors arbitrarily chose to assign the brain damage to “progression of ongoing cerebrovascular disease” rather than to their treatment. (Coffey, et al, 1991)
In summary, there is abundant objective evidence – anatomic and biochemical – of the brain damaging effects of ECT, which give rise to the exceedingly common complaints of ECT recipients regarding difficulty thinking, deciding, and remembering.
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