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I N PREVIOUS investigations of the pathophysiology of intracranial hypertension and cerebral swelling, we recorded intracranial pressure, cerebral blood flow, and several additional variables during expansion of a supratentorial balloon in the monkey2 ~,13 Among the phenomena observed were recurrent, marked rises in intracranial pressure. These pressure waves occurred spontaneously, were readily produced by hypoxia and hypercapnia, and could be aborted by hyperventilation with high oxygen mixtures. As pressure waves continued, the brain swelled, intracranial pressure ul t imately rose to tha t of arterial pressure, and cerebral blood flow ceased. There is evidence tha t the intermit tent brain swelling responsible for the periods of marked intracranial hypertension is due to cerebrovascular dilatation. We also believe tha t the end stage of the process, when intracranial pressure equals the arterial pressure and varies directly with it, is par t ly due to paralysis of cerebral vaso-constrictor tone. The purpose of this report is to present clinical confirmation of these earlier observations. The cerebral swelling which occurs following craniotomy frequently develops during the first ~4 hours. I f brain damage has not been severe, the pat ient improves rapidly following surgery. Rarely the initial postoperative improvement is followed by abrupt deterioration and death, which is often att r ibuted to a major vascular accident. However, this can be caused by acute brain swelling.
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Langfitt et al. (1966) studied this question.
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