Donald I. Templer and David M. Veleber
Clinical Neuropsychology (1982) 4(2): 62-66

Literature relevant to the question of whether ECT permanently injures the brain was reviewed. Similar histological findings of epileptics and patients who had received ECT were discussed. Experimental research with animals seems to have demonstrated both reversible and nonreversible pathology. Psychological test findings, even when attempting to control for possible pre-ECT differences, seem to suggest some permanent cognitive deficit. Reports of spontaneous seizures long after ECT would appear to point to permanent brain changes. Human brain autopsies sometimes indicate and sometimes do not indicate lasting effects. It was concluded that vast individual differences are salient, that massive damage in the typical ECT patient is unlikely, and that irreversible changes probably do occur in some patients.

This review centers around five areas germane to the question of whether electroconvulsive therapy (ECT) causes permanent brain pathology. Relatively indirect evidence is provided by two of these areas, the brain condition of epileptics and the examination of animal brains after experimental ECT. The other three areas are psychological testing findings with history of many ECTs, spontaneous seizures, and autopsy findings. The review does not concern the extensive literature that shows that ECT temporarily impairs cognitive functioning. Such literature eventually shows impairment beginning with the first ECT and becoming progressively worse with succeeding treatments. Improvement occurs following the course of ECT, sometimes with the tested functioning actually being higher than the pretreatment level, which is presumed to have been impaired by psychopathology such as thought disorder and depression. Reviews of this literature can be found elsewhere (American Psychiatric Association, 1978; Campbell, 1961; Dornbush, 1972; Dornbush and Williams, 1974; Harper and Wiens, 1975), as can reviews indicating that the unilateral ECT (applied to the right side) in increasing usage in recent years causes less impairment than bilateral ECT (American Psychiatric Association, 1978; d'Elia, 1974; Hurwitz, 1974; Zamora and Kaelbing, 1965). This literature is really not very relevant to the central issue of our review. It has never been disputed that cognitive impairment occurs after ECT. Even the most fervent and excathedra defenders acknowledge that "temporary" impairment occurs. It is the issue of permanency that has been controversial.

THE BRAINS OF EPILEPTICS

It would seem that if an epileptic grand mal seizure produces permanent brain changes, then an electrically induced convulsion should also do so. In fact, inspecting the evidence with respect to epileptics may provide us with a conservative perspective in regard to ECT since the latter could produce damage from the externally applied electrical current as well as from the seizure. Experimental research with animals has shown that the electric shocks (not to the head) produce more deleterious effects in the central nervous system than any other locality or system of the body. More pertinent are the studies of Small (1974) and of Laurell (1970) that found less memory impairment after inhalant induced convulsions than ECT. And, Levy, Serota and Grinker (1942) reported less EEG abnormality and intellectual impairment with pharmacologically induced convulsions. Further argument provided by Friedberg (1977) is the case (Larsen and Vraa-Jensen, l953) of a man who had been given four ECTs, but did not convulse. When he died three days later, a subarachnoid hemorrhage was found in the upper part of the left motor region at the site where an electrode had been applied.

A number of post-mortem reports on epileptics, as reviewed by Meldrum, Horton, and Brierley (1974) have indicated neuronal loss and gliosis, especially in the hippocampus and temporal lobe. However, as Meldrum et al. pointed out, on the basis of these post-mortem reports, one does not know whether the damage was caused by the seizures or whether both were caused by a third factor intrinsic to the epilepsy. To clarify this issue, Meldrum et al. pharmacologically induced seizures in baboons and found cell changes that corresponded to those in human epileptics.

Gastaut and Gastaut (1976) demonstrated through brain scans that in seven of 20 cases status epilepticus produced brain atrophy. They reasoned that "Since the edema and the atrophy were unilateral or bilateral and related to the localization of the convulsions (unilateral or bilateral chronic seizures), the conclusion can be drawn that the atrophic process depends upon the epileptic process and not on the cause of the status."

A common finding in epileptics and ECT patients is noteworthy. Norman (1964) stated that it is not uncommon to find at autopsy both old and recent lesions in the brains of epileptics. Alpers and Hughes (1942) reported old and recent brain lesions associated with different series of ECT.