Citation

Povlishock JT. Ann. Emerg. Med. 1993; 22(6): 980-986.

Affiliation

Department of Anatomy, Medical College of Virginia, Virginia Commonwealth University, Richmond.

Copyright

(Copyright © 1993, American College of Emergency Physicians, Publisher Elsevier Publishing)

DOI

unavailable

PMID

8503536

Abstract

STUDY OBJECTIVES: Although diffuse axonal injury is recognized as a consistent feature of traumatic brain injury, there is confusion regarding its pathogenesis. To provide insight into its pathogenesis, animal models of traumatic brain injury complemented by post mortem human analyses were used. DESIGN: In animals, anterograde tracers together with antibodies targeting the neurofilament subunits were used in light and electron microscopic analyses of axonal injury. In humans, antibodies to the neurofilament subunits also were used to follow diffuse axonal injury. Animals were followed from minutes to months after injury, whereas humans were studied from six hours to 59 days after injury. MEASUREMENTS AND MAIN RESULTS: In neither animals nor humans did traumatic brain injury cause direct axonal tearing. Instead, the traumatic brain injury triggered focal intra-axonal change in the 68-kd neurofilament subunit, which became disordered in its alignment and resulted in impaired axoplasmic transport. This caused axonal swelling and disconnection. The sequence of axonal change was similar in animals and man; however, its temporal progression was slower in humans. CONCLUSION: Traumatically induced axonal damage is triggered first by focal intra-axonal change involving the neurofilament subunits. This neurofilament change is due to either direct mechanical failure of the axonal cytoskeleton or the initiation of a biochemical event that causes neurofilament disassembly. In general, the temporal progression of the intra-axonal changes that lead to ultimate disconnection is influenced by the severity of the traumatic injury and the species evaluated.

Language: en