Citation

Gennarelli TA. J. Emerg. Med. 1993; 11(Suppl 1): 5-11.

Affiliation

Department of Neurosurgery, University of Pennsylvania, Philadelphia 19104.

Copyright

(Copyright © 1993, Elsevier Publishing)

DOI

unavailable

PMID

8445204

Abstract

Head injuries vary widely in their etiology, pathophysiology, clinical presentation, and optimal treatment strategies. Broadly speaking, there are two categories of brain injury: focal injuries and diffuse injuries. Focal brain injuries, which are usually caused by direct blows to the head, comprise contusions, brain lacerations, and hemorrhage leading to the formation of hematoma in the extradural, subarachnoid, subdural, or intracerebral compartments within the head. Diffuse brain injuries, which are usually caused by a sudden movement of the head, comprise classical brief cerebral concussion and more prolonged posttraumatic coma, also known as diffuse axonal injury. Primary traumatic effects involve neural or vascular elements of the brain, which can be affected by delayed effects such as deafferentation or secondary events such as ischemia, swelling, cerebral edema, and increased intracranial pressure. Axonal damage at the node of Ranvier results in a traumatic defect in the axonal membrane that causes the excessive accumulation of calcium ions within the intracellular compartment of the axon. Brain ischemia can result in a similar effect, further increasing the accumulation of calcium ions, which can lead to axonal degeneration. Injury-specific treatments are now being designed to alter the various pathophysiological mechanisms of brain injury.

Language: en