In 1944 Mosovich and Katzenelbogen studied the EEGs of 82 patients before and after ECT. Although the study is old, it is a model of good scientific work, particularly in that it studied patients before treatment and followed them for 10 months afterwards. The currents used were 300-600MA, within the range used today. The study showed that of 42 patients with normal EEGs before ECT, half (21) had abnormal EEGs following treatment. One-third of these abnormalities were severe "cerebral dysrhythmias". The EEG patterns resembled those commonly seen in epileptic patients in the periods between epileptic seizures. Of 40 patients with moderate EEG abnormalities before ECT, 13 showed cerebral dysrhythmia afterwards. To produce these changes a relatively few sessions sufficed, for they were found in 9/60 patients who had only 3-15 ECT. The frequency of damage increased with increasing number of shocks:. after 16-42 shocks, half the patients (11/22) showed cerebral dysrhythmia... These changes were often extremely long lasting. Thus, 68/82 patients showed the dysrhythmia the day following ECS, and 20 patients still had the pattern 10 months later. For all anyone knows, the changes were permanent (Mosovich and Katzenelbogen, 1944).

These findings have been confirmed in modern studies using anesthesia, oxygen, and muscle paralysis. For example, Abrams, et al. (1972) found significant slow delta waves when either bilateral or unilateral ECS was administered. When the shock was restricted to one side, the EEG changes were found on that side. Volavka, et al., (1972) showed that the amount of delta activity in the EEG was related to the number of shocks administered. These studies had the additional advantage that the EEG expert who read the records did not know how the patients had been treated, i.e., the readings were done "blind". (Abrams, et al 1., 1972) cite four additional studies done between 1965-1970 with similar EEG findings.

Summary and Conclusions Regarding the Effects of ECT on the Brain

1. During a seizure induced by ECT, there is a tremendous rise in blood pressure and a breakdown of the blood-brain barrier. These two events separately or in combination often cause hemorrhage, edema, and possibly toxic effects because the brain is exposed to chemicals in the blood from which it is normally protected. All of these phenomena cause the irreversible death of neurons in the brain (reviewed by Blackwood and Corsellis, 1976).

2. ECT alters the metabolism of brain proteins, RNA, and neural transmitters whose production is normally regulated carefully. Although the gross metabolism of these substances may later return to normal, their temporary alteration may have permanent effects in the brain. In fact, the very reason that hundreds of scientists around the world are studying the relation between these substances and memory is because small changes in their production might be the way that memories are stored.

3. EEG studies spanning a 28 year period show that ECT alters brain physiology from normal to abnormal. These changes, principally a slowing of the EEG waves, are similar to those found in epilepsy, mental deficiency, and other neuropathologies. The EEG changes associated with ECT appear to be extremely long-lasting very possibly they are permanent. They do not tell us whether a patient has lost his memory -- for that you have to ask the patient. They do tell us that ECT can cause profound alterations in brain function.

4. All of the changes that follow ECT vary from animal-to-animal and from person-to-person. Thus, blood pressure rises in one study were small in one case, only 23%, but large in others (up to 400%). Cerebrovascular hemorrhages are found commonly, but not invariably (about 60% of the time); similarly, about half the patients show EEG abnormalities.

Loss of Memory for Past Events Following ECT

Losses of memory for past events commonly occur following insult to the brain, for example, following mechanical injury or from chronic toxic states such as alcoholism (Russell, 1971; Whitty and Zangwill, 1966). It should not be surprising that memory loss also accompanies the damage done to the brain by ECT. Such losses have been documented in numerous case reports dating back to the 1940s (Levy, et al., 1942). In some cases the loss is catastrophically complete: memory is erased for professional skills as well as orientation to places and friends (e.g., Roueche, 1974). More commonly, the loss is "patchy": some events are lost while others are remembered; recent events are more likely to be lost than those in the distant past, but amnesia can extend backward for several years and can include events of early childhood that date back 20 to 40 years; some memories return while others do not (Janis, l948; A Practicing Psychiatrist, 1965; Brody, 1944; Valentine, et al, 1968; Medlicott, R.W., 1948; Squire, et al, 1975).

One's confidence that there must be substance to these case reports is strengthened by the hesitations of some physicians experienced in the use of ECT to employ it on patients engaged in intellectual work (e.g., Stromgren, 1973) and in the widespread adoption, especially in Europe, of unilateral ECT. In this method the electrodes are not placed on both temples, but on one side of the head only, in the frontal and parietal regions. The passage of current is therefore largely restricted to one side of the brain. The electrodes are usually placed on the so-called "non-dominant" side, the side concerned with spatial, rather than verbal tasks. With this treatment the EEC changes are limited to the non-dominant hemisphere, and patients, report fewer and less severe losses of memory for past events. Clearly, in order for there to be less memory and loss and less brain damage (EEC changes) with unilateral ECT, there must be substantial amounts of it with bilateral ECT (Abrams, et al., 1972; Stromgren, 1973; Valentine, 1968; Zinkin and Birtchnell, 1968; D'Elia, 1970; Heshe and Roeder, 1976; Lancaster, et al., 1958). Lest it be prematurely concluded that no damage is done by unilateral ECT to the "non-dominant" hemisphere, it is well to realize that the functions of this hemisphere are just beginning to be appreciated and that methods for assessing its function remain primitive (e.g., Ornstein, 1973).