ECT Has No Known Mechanism of Action: A Review of the Literature

The original theory of ECT was that seizures and mental disease could not coexist in the same brain. This justified the brutal act of subjecting a person to electric shock to the point of inducing a seizure, after which the patient would be more manageable and their behavior deemed more socially acceptable. (Piazzi, et al. 2011) It is now known that persons with epilepsy are more likely than the general population to have a concurrent mental diagnosis. (Beletsky and Mirsattari, 2011)

An early psychoanalytic explanation for changes in behavior after ECT supposed that it satisfied a need for punishment that was supposedly craved by the mental patient. Another theory credited ECT for causing regression to an infantile state, which was declared to be an improvement compared to the patient’s pre-treatment mental anguish.  Others suggested that patients responded positively to the immense fear surrounding the procedure, which induced them to suppress their unacceptable behaviors, or to simply quit complaining. (McCall et al, 2014) Modern ECT procedure delivers shocks while the person is under general anesthesia, but up to one-third of recipients will still admit to fear and coercion inherent in the treatment milieu. (Chakrabarti et al. 2010)

The earliest psychological explanations of ECT responses were pinned on the concept of ‘beneficial brain damage’. This was due to the finding that Rorschach (ink blot) tests after ECT were similar to those seen after any other form of brain damage. (Summerskill et al., 1952) It corresponded with the observation that formerly excitable people became docile after traumatic head injury or suffering a stroke, or undergoing ECT.  Another psychological explanation that is still popular today credits ECT-induced amnesia with providing relief to the distressed patient, essentially wiping their memory of upsetting events. (Miller, 1967)

ECT is the process of applying electricity to the head in sufficient amount and for long enough to overcome brain protective mechanisms, with the goal of causing a generalized brain seizure. This is characterized by chaotic electrical activity (electrical storm), and would result in limb flailing and powerful muscle jerks, if they were not masked by paralyzing drugs and general anesthesia.

The amount and duration of electric shock typically has to be increased for each successive ECT session. This is called the ‘anti-convulsive effect’ of ECT. It is simply a primitive survival reaction, in which the brain reflexively mounts increasingly strong defenses to each successive electrical attack, throughout a series of ECT sessions. This anticonvulsant effect has been attributed to be the way ECT works – a theory that is more of an observation than any kind of explanation of therapeutic effect. (Sackeim et al. 1983) Furthermore, it does not explain why there is not an anti-depressant effect from administering conventional anti-seizure medications, which would be a much less traumatic way of conveying an anti-convulsive effect.

ECT causes temporarily reduced brain blood flow and slows metabolism in the brain, with both responses also seen in other forms of brain damage.  ECT enthusiasts have tried to spin this into a positive, supposing that reduced blood flow and slowed metabolism are somehow beneficial for the upset and apparently hotheaded patient. (Nobler et al., 1994) One of America’s earliest mental doctors, Benjamin Rush, used a crude variation of this with his “tranquilizing chair” that shackled the patient to a chair and submerged him in freezing cold water. (NIH, 1994)

An ECT recipient can stay dull and emotionally blunted for weeks and months, usually taken as a positive therapeutic response. Brain wave tests show pronounced slow wave activity in between ECT sessions, which can persist for weeks after a course of ECT. This is thought to be a reflection of reduced connectivity – literally reduced transmission of normal electrical flow from one brain neuron to another. Slowed brain activity is credited with the reason the patient appears pacified after ECT. (Sackeim et al, 1996) The slow waves are characteristic of the brain wave pattern of sleep. This gives rise to a related theory that the sleep-like state is soothing to the disturbed brains. (Charlton, 1999) Nonmedical observers are more likely to call it zombie-ism.

The early era of brain imaging by CT scans revealed that brain shrinkage (atrophy) was common after a series of ECT. Atrophy is also a prominent feature of dementia, but this did not detract from the conclusion that brain shrinkage must be how ECT worked. (Dolan, 1986) Did mental patients somehow have too much brain tissue?  More modern imaging techniques of MRI and PET scanning, combined with the timing of brain scanning earlier on (immediately or within one week of ECT) have shown the opposite – ECT initially caused new neuron growth, and temporary enlargement of various areas of the brain. (Gbyl and Videbech, 2018) The conflicting findings seem to be an artifact of the timing of the scans. In the brain injury field, it is well documented that cell repair and growth activities initially go into overdrive after a injury; if they cannot compensate for the damage done, then scar tissue forms and atrophy sets in. This would not be seen until scans done months later.

Much is published on the biochemical brain changes that occur after ECT, with corresponding theories about how up-regulation or down-regulation of this or that brain chemical could be the way ECT works. A particularly sensitive indicator of brain damage is the protein ‘S100b’, so reliable that it is called a trauma biomarker. (Stavrinou, et al, 2011) S100b initiates brain repair activities. It is elevated immediately after any form of brain damage, including electroshock. At first, elevated S100b was cited as a possible therapeutic effect of ECT. This was difficult to spin positively because it is tantamount to saying that ECT causes brain damage since a brain repair chemical is released. So researchers then designed studies to show that S100b was not increased from ECT after all. They did this by measuring for S100b two hours or more after the electroshock – a sure way to get negative results because the protein is so short lived, most of it is gone within an hour after the shock. (Ghanem, et al, 2001)

There is no consistency to the reports of various neurotransmitter levels, up or down, after ECT. (Grover, et al 2005) Studies are very poor because of design flaws, such as too few subjects and lack of a comparison group that did not get ECT.  Measurement of neurotransmitters in the peripheral blood (by a blood draw from an arm vein) is not an accurate reflection of the neurotransmitter levels in the brain; for example, blood serotonin level has no relationship to brain serotonin level. (Pietraszek, 1993)There is rarely a study that controls adequately for potential confounders – factors that would influence the findings and give spurious results. The most common of these is concomitant use of a myriad of psychotropic medications, any of which change the neurotransmitter levels as well as PET scan activity, or recently having started or stopped psychotropic medication, which profoundly affect not only neurotransmitter levels but also mental state. In addition, invalid statistical analyses that skew the results are common when the study authors have a pet theory to support.

An especially insidious form of reporting is to state results in terms of trends and tendencies. This is an intentional strategy to obscure the fact that measured biochemical levels were not statistically significantly different from control subjects or from baseline measurements. These ‘almost-but-not-quite’ findings all too often get cited in subsequent publications as if they were definitive positive results. (Grover, et al 2005)

In summary, there is no known mechanism of action of ECT. This basic fact should be a part of full informed consent for anyone being offered ECT.

References:

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Dolan RJ, P. Calloway SP, Thacker PF, Mann AH, ‘The cerebral appearance in depressed subjects’ Psychol Med 1986;16:775-779.

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Piazzi, A., Testa, L., Missier, G. D., Dario, M., & Stocco, E. (2011). The history of Italian psychiatry during Fascism. History of Psychiatry, 22(3), 251–267.

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