Citation

Langfitt TW, Gennarelli TA. J. Neurosurg. 1982; 56(1): 19-25.

Copyright

(Copyright © 1982, American Association of Neurological Surgeons)

DOI

10.3171/jns.1982.56.1.0019

PMID

7054418

Abstract

In the past few years, considerable progress has been made in describing patients with head injuries in such a manner that comparisons in morbidity and mortality can be made among neurosurgical centers according to the seriousness of the injury. Less progress had been made in classifying the type of pathology, especially by computerized tomography. The authors have introduced a classification that includes both the type and the seriousness of the injury. There appear to be two principal causes of the brian damage produced by head injury: 1) mechanical damage to neurons and their processes, especially axons and 2) ischemia. Mechanical damage produces axonal degeneration. Although central regeneration generally is quite limited, perhaps many of the axons damaged by head injury degenerate in continuity, a circumstance in which functional regeneration by axoplasmic outgrowth is much more likely to occur than in most experimental situations where the axons are physically divided. The ischemic brain damage that is so common in head injury appears to be mass lesions and brain swelling that both cause intracranial hypertension. The more the brain swells, and the higher the intracranial pressure, the more difficult it is to control the swelling and the pressure. In patients with acute subdural hematoma in particular, the brian swelling and the high mortality appear to be due to ischemic brain damage. There is recent evidence that the mortality rate in patients with acute subdural hematoma is a function of the time from injury to evacuation of the hematoma. Therefore, outcome from head injury can be improved by the earliest possible removal of space-occupying hematomas and by early, vigorous management of intracranial hypertension.

Language: en