SPONTANEOUS SEIZURES

It would appear that if seizures that were not previously evidenced appeared after ECT and persisted, permanent brain pathology must be inferred. There have been numerous cases of post-ECT spontaneous seizures reported in the literature and briefly reviewed by Blumenthal (1955, Pacella and Barrera (1945), and Karliner (1956). It appears that in the majority of cases the seizures do not persist indefinitely, although an exact perspective is difficult to obtain because of anticonvulsant medication employed and the limited follow-up information. another difficulty is, in all cases, definitively tracing the etiology to the ECT, since spontaneous seizures develop in only a very small proportion of patients given this treatment. Nevertheless, the composite of relevant literature does indicate that, at least in some patients, no evidence of seizure potential existed before treatment and post-ECT seizures persist for years.

An article that is one of the most systematic and representative in terms of findings is that of Blumenthal (1955) who reported on 12 schizophrenic patients in one hospital who developed post-ECT convulsions. Six of the patients had previous EEGs with four of them being normal, one clearly abnormal, and one mildly abnormal. The patients averaged 72 ECTs and 12 spontaneous seizures. The time from last treatment to first spontaneous seizure ranged from 12 hours to 11 months with an average of 2 and 1/2 months. The total duration of spontaneous seizures in the study period ranged from 1 day to 3 and 1/2 years with an average of 1 year. Following the onset of seizures, 8 of the 12 patients were found to have a clearly abnormal, and 1 a mildly abnormal EEG.

Mosovich and Katzenelbogen (1948) reported that 20 of their 82 patients had convulsive pattern cerebral dysrhythmia 10 months post ECT. None had such in their pre-treatment EEG. Nine (15%) of the 60 patients who had 3 to 15 treatments, and 11(50%) of the 22 patients who had from 16 to 42 treatments had this 10 month posttreatment dysrhythmia.

HUMAN BRAIN AUTOPSY REPORTS

In the 1940s and 1950s there were a large number of reports concerning the examination of brains of persons who had died following ECT. Madow (1956) reviewed 38 such cases. In 31 of the 38 cases there was vascular pathology. However, much of this could have been of a potentially reversible nature. Such reversibility was much less with the 12 patients who had neuronal and/or glial pathology. The following are the comments pertaining to the neuronal and glial pathology and the amount of time between last treatment and death: "Gliosis and fibrosis" (5 months); "Small areas of cortical devastation, diffuse degeneration of nerve cells", "Astrocytic proliferation" (1 hour, 35 minutes); "Small areas of recent necrosis in cortex, hippocampus and medulla", "Astrocytic proliferation" (immediate); "Central chromatolysis, pyknosis, shadow cells (15 to 20 minutes); "Shrinking and swelling. ghost cells", "Satellitosis and neuronophagia" (7 days); "Chromatolysis, cell shrinkage''. "Diffuse gliosis, glial nodules beneath the ependyma of the third ventricle" (15 days); "Increased Astrocytes" (13 days); "Schemic and pyknotic ganglion cells" (48 hours); "Pigmentation and fatty degeneration, sclerotic and ghost cells", "Perivascular and pericellular gliosis" (10 minutes); "Decrease in ganglion cells in frontal lobes, lipoid pigment in globus pallidus and medical nucleus of thalamus", "Moderate glial proliferation" (36 hours); "Glial fibrosis in marginal layer of cortex, gliosis around ventricles and in marginal areas of brain stem, perivascular gliosis in white matter" (immediate); "Marginal proliferation of astrocytes, glial fibrosis around blood vessels of white matter, gliosis of thalamus, brain stem and medulla" (immediate). In one case the author (Riese, 1948), in addition to giving the neuronal and glial changes, reported numerous slits and rents similar to that seen after execution. Needless to say, patients who died following ECT are not representative of patients receiving ECT. They tended to be in inferior physical health. Madow concluded, on the basis of these 38 cases and 5 of his own, "If the individual being treated is well physically, most of the neuropathological changes are reversible. If, on the other hand, the patient has cardiac, vascular, or renal disease, the cerebral changes, chiefly vascular, may be permanent."

CONCLUSION

A wide array of research and clinical based facts that provide suggestive to impressive evidence in isolation, provide compelling evidence when viewed in a composite fashion. Some human and animal autopsies reveal permanent brain pathology. Some patients have persisting spontaneous seizures after having received ECT. Patients having received many ECTs score lower than control patients on psychological tests of organicity, even when degree of psychosis is controlled for.

A convergence of evidence indicates the importance of number of ECTs. We have previously referred to the significant inverse correlations between number of ECTs and scores on psychological tests. It is conceivable that this could be a function of the more disturbed patients receiving more ECTs and doing more poorly on tests. However, it would be much more difficult to explain away the relationship between number of ECTs received and EEG convulsive pattern dysrhythmia (Mosovich and Katzenelbogen, 1948). No patients had dysrhythmia prior to ECTs. Also difficult to explain away is that in Table I of Meldrum, Horton and Brierley (1974), the nine baboons who suffered brain damage from experimentally administrated convulsions tended to have received more convulsions than the five that did not incur damage. (According to our calculations, U=9, p < .05 ) And, as already stated, Hartelius found greater damage, both reversible and irreversible, in cats that were given 11 to l6 than in those given 4 ECTs.

Throughout this review the vast individual differences are striking. In the animal and human autopsy studies there is typically a range of findings from no lasting effect to considerable lasting damage with the latter being more of the exception. Most ECT patients don't have spontaneous seizures but some do. The subjective reports of patients likewise differ from those of no lasting effect to appreciable, although usually not devastating impairment. The fact that many patients and subjects suffer no demonstrable permanent effects has provided rationale for some authorities to commit the non-sequitur that ECT causes no permanent harm.

There is evidence to suggest that pre-ECT physical condition accounts in part for the vast individual differences. Jacobs (1944) determined the cerebrospinal fluid protein and cell content before, during, and after a course of ECT with 21 patients. The one person who developed abnormal protein and cell elevations was a 57-year-old diabetic, hypertensive, arteriosclerotic woman. Jacobs recommended that CSF protein and cell counts be ascertained before and after ECT in patients with significant degree of arteriosclerotic or hypertensive disease. Alpers (1946) reported, "Autopsied cases suggest that brain damage is likely to occur in conditions with pre-existing brain damage, as in cerebral arteriosclerosis." Wilcox (1944) offered the clinical impression that, in older patients, ECT memory changes continue for a longer time than for younger patients. Hartelius (1952) found significantly more reversible and irreversible brain changes following ECT in older cats than younger cats. Mosovich and Katzenelbogen (1948) found that patients with pretreatment EEG abnormalities are more likely to show marked post-ECT cerebral dysrhythmia and to generally show EEGs more adversely affected by treatment.

In spite of the abundance of evidence that ECT sometimes causes brain damage, the Report of The Task Force on Electroconvulsive Therapy of the American Psychiatric Association (1978) makes a legitimate point in stating that the preponderance of human and animal autopsy studies were carried out prior to the modern era of ECT administration that included anesthesia, muscle relaxants, and hyperoxygenation. In fact, animals which were paralyzed and artificially ventilated on oxygen had brain damage of somewhat lesser magnitude than, although similar patterns as, animals not convulsed without special measures. (Meldrum and Brierley, 1973; Meldrum, Vigourocex, Brierley, 1973). And it could further be maintained that the vast individual differences stressed above argue for the possibility of making ECT very safe for the brain through refinement of procedures and selection of patients. Regardless of such optimistic possibilities, our position remains that ECT has caused and can cause permanent pathology.

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