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Experimental cerebral circulatory arrest: effect on electrocortical potentials.

S PONTANEOUS cerebral electrical potentials have been used clinically for prognosis following destructive cerebral lesions, and a persistently isoelectric electroencephalographic recording (EEG) has been considered one criterion of cerebral nonviability both for cessation of artificial maintenance of vital functions and for subsequent somatic organ transplantation. Prominent among causes of cerebral non-viability are those related to circulatory arrest, which include shock, arterial occlusive disease, cardiopulmonary insufficiency, and cardiac arrest. Diminution of cerebral blood flow as well as greatly increased intracranial pressure causes stagnant (ischemic) hypoxia, which in turn is reflected in profound EEG changes. These types of ischemic or anoxic cerebral insults may be reproduced experimentally and their effects on electrocortigraphic (ECoG) activity recorded. In such experiments, intrathoracic vascular occlusion causing immediate circulatory arrest has been produced to determine patterns of electrocortical silence, recovery, and the sensitivity of cortical electrical function related to survival. However, the preparation is not comparable to stepwise obliteration of the four major cervical vessels since simultaneous occlusion is difficult and a certain amount of cerebral damage can occur during experimental ligations, which make exact timing of anemia difficult. Also, a potentially large amount of collateral circulation exists. In man, for example, cases have been reported in which only minimal neurological dysfunction was caused following occlusion of all major cervical vessels, 8 although acute