The etiology of acute brain swelling following experimental head injury.

Abstract

T hE pathophysiology of acute head injury has been studied in experimental animals by numerous investigators. Occasionally cercbrospinal fluid pressure has been recorded, usually from the lumbar subarachnoid space or cisterna magna, and there has been uniform agreement tha t prolonged, severe intracranial hypertension does not occur following experimental concussion. An initial sharp rise in intracranial pressure, concomitant with the blow, has been studied in some detail, but this is quite transient, and any subsequent rise in intracranial pressure has been found to be inconstant and moderate in degree. In contrast to the observations in animals, a marked increase in intracranial pressure secondary to brain swelling is commonly observed in patients with head injuries, and this has been generally a t t r ibuted to the rapid development of cerebral edema. If severe brain swelling occurs, intracranial pressure must increase, but we have been unable to find a previous explanation for the failure to observe significant intracranial hypertension following experimental head injury. In prior experiments we presented evidence that the rise in intracranial pressure produced by expansion of an intracranial mass causes cerebral vasodilatation. The vasodilatation increases cerebral blood volume and produces a further rise in intracranial pressure. As this process continues, a very great increase in intracranial pressure may occur rapidly due to intense cerebrovascular congestion. As the difference between the arterial and intracranial pressures decreases, cerebral blood flow falls, and irreversible cerebrovascular dilatation ultimately occurs due to ischemic vasomotor paralysis, l~ The purpose of this preliminary report of our experience with experimental