ABSTRACT
The fact that the axons might be damaged in a head injury was first demonstrated nearly 50 years ago by Strich, who performed a neuropathological study of the brains of patients who had been vegetative after a head injury. Systematic neuropathological studies employing this antibody have shown that a degree of damage to axons probably occurs in the vast majority of head injuries and that the subsequent clinical picture is dictated by the amount and distribution of that damage. Experimental work shows that extreme forces are necessary for axons to rupture immediately and that in virtually all head injuries, axotomy is likely to be a secondary, delayed event after injury as a result of damage to the axonal cytoskeleton. Biomechanical conditions conducive to diffuse traumatic axonal injury (dTAI) may also cause vascular shearing of the microvasculature of the white matter in both the forebrain and brainstem.
