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The Processes Involved in Traumatic Axonal Injury

  • T. A. Gennarelli
  • D. I. Graham
  • L. E. Thibault
Conference paper

Abstract

Brain injury can be viewed as several clinical syndromes that result from various combinations of neural or vascular events occurring after mechanical distortion of the head. The primary traumatic events appear to be mediated by four basic mechanisms, the consequences of which are not instantaneous. Thus, brain injury involves processes that are set in motion at the time of head injury, but may require hours or days for completion. These four mechanisms of cellular dysfunction are receptor dysfunction, free radical effects, inflammatory events, and calcium-mediated damage and they have the potential for causing delayed cell dysfunction or delayed cellular death. These events, depending on whether they are primarily to the neural or vascular tissues, may produce additional events or epiphenomena, such as brain swelling, cerebral edema, and increased intracranial pressure (see Fig. 1). These types of events are similar in focal and diffuse brain injuries, but their effects may appear to be different because of a different mixture of neural versus vascular tissue involvement, and because of a different combination of the four principal mechanisms of cell damage. This paper addresses the manner in which axons are damaged after injury by these mechanisms.

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Copyright information

© Springer-Verlag Berlin Heidelberg 1997

Authors and Affiliations

  • T. A. Gennarelli
  • D. I. Graham
  • L. E. Thibault

There are no affiliations available

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