Events Triggered by Electrical Shock

The electricity passing through the brain causes massive, simultaneous excitation of vast numbers of neurons. The inhibitory mechanisms that normally hold neurons in check and shape the normal EEG rhythms are overwhelmed by the excitation. As the excitation builds and swamps the inhibitory mechanisms, it spreads throughout the brain. When the excitation reaches the motoneurons of all the body's muscles, there is massive, convulsive muscular contraction. The muscles contract so powerfully that tendons may be torn from the bones, the bones themselves may be broken, teeth chipped and broken, and so on. The massive requirements for oxygen and the interruption of breathing caused by the convulsion often causes anoxia. Accompanying the convulsion, there is a tremendous rise in blood pressure: changes in arterial pressure from 80mm Hg to 220mm Hg, or almost 200%, have been recorded (Plum, et al, 1968). This overall response resembles the "grand mal" seizure that occurs in epilepsy.

In recent years some of these consequences of the electrical shock have been ameliorated. The muscle contractions can be prevented by administration of a drug that blocks transmission of impulses from nerve to muscle. The ensuing paralysis protects bone and muscle, and also permits oxygen to be administered by artificial respiration. Under these conditions, the brain is well protected from anoxia. On the other hand, this procedure (paralysis) is frightening. Patients are therefore usually pretreated with barbiturate anesthetics so that their consciousness of their treatment is dulled or lost entirely. The effect of barbiturate anesthetic is to decrease the excitability of neurons in the brain. Larger shocks must, therefore, be employed to evoke a grand mal would be needed without the drugs. Thus, although the patient may gain from the paralysis and the administration of oxygen, he probably also loses by the higher voltage requirement. There is no evidence that these drug treatments substantially alter the electrical and chemical phenomena within the brain that I shall now describe.

Brain Changes During ECT

The massive neural activity evoked by the electrical shock causes and requires major changes in the metabolism and blood supply of the brain.

1. The neurons, because they are so active, require much more oxygen and nutrients. Therefore, with the onset of the seizure, cerebral blood flow rises dramatically -- as much as 400%. Cerebral oxygen consumption also rises as much as 400%. In accomplishing such massive increases in blood flow, the automatic mechanisms that normally regulate cerebral blood flow are overwhelmed. For the duration of the seizure and for sometime following it, blood flow to the brain becomes like that of must other tissues in the body -- proportional to the arterial pressure forcing the blood through the vessels. These changes accompanying ECT are not modified by the administration of anesthetic, paralytic drugs or oxygen (Plum, et al., 1968; Posner, et al., 1969).

2. The extremely high cerebral blood pressure and the breakdown in auto regulation of cerebral blood flow during the seizure frequently ruptures small, and occasionally large, vessels in the brain. Madow (1956) reviewed 42 cases of autopsy assembled from 26 published reports on patients who had recently received ECT. Twenty-five (60%) had either petechial hemorrhages or large infarcts. About three-quarter of these patients were over forty, but the frequency of hemorrhage in the group under forty was the same as for the older group. There seems every reason to suspect, therefore, that subarachnoid or intracerebral bleeding accompanies ECT about half the time. This is supported by numerous studies in animals autopsied after being subjected to ECT. For example, Alpers and Hughes (1942) found bleeding in 23/30 cats (77%); Heilbrunn(1943) found petechial or larger hemorrhages in all of the rats that convulsed in his experiments to ECT; Heilbrunn and Weil (1942) made similar findings in 17/21 (81%) rabbits. Wherever bleeding occurs in the brain, neurons lose their supply of oxygen and nutrients -- and die.

   Some studies failed to hemorrhages in animals following ECT, but most of these seem not comparable to the human cases. in two, the voltage applied was far below what is employed on humans (Masserman and Jacques, 1947; Winkleman and Moore, 1944). Others used only a single shock rather than, as is common for humans, a series of treatments (Windle, l948, Alexander and Lowenbach, 1944). Another study with negative findings.(Siekert, et al, 1950) used a small sample (5) of young monkeys (5-7 lbs., corresponding to an age of about one and a half years). Since damage is greater in older animals with less flexible vascular systems (Hartelius, 1952), this negative result on a small sample is not astonishing, nor does it contradict the many positive findings of damage. The positive findings cannot be attributed to poor preservation of the brains after death. While poor preservation makes difficult judging the condition of neurons or glia, it cannot cause bleeding within the brain. Nor can the bleeding be attributed to "old" methods of ECT (no paralysis or oxygen). One would expect under the old conditions the brain to be anoxic, with arrested circulation. This would lead to a lack of blood in the brain, the opposite of what is reported. Thus, the later modifications of ECT can relieve the threat of cerebral anoxia, but not the threat of high pressure, bleeding, loss of blood-brain barrier, or edema

3. The electrical shock causes damage to the blood-brain barrier. Aird, et al., 1956; Angel, et al., 1965; Lee and Olszewski, 1961). This has been shown experimentally in animals, and there is every reason to believe that it happens in humans as well. Whether this is caused by the huge rises cerebral blood pressure is unknown. Whatever the cause, the loss of this protective barrier exposes the brain tissue to components of the blood from. it is normally protected. For example, if a patient has been taking drugs of any kind, the brain may be exposed to much higher levels of the drugs than normally cross the blood-brain barrier.')