The primary injury, which can be correlated with prolonged coma and impaired motor response, was recognised by Strich in 1961 as a diffuse degeneration of the subcortical matter, subsequently termed diffuse axonal injury (DAI). Experimental work with primates confirms this to be a consequence of inertial loading of the head, with prolonged coronal angular acceleration. Microscopic pathological findings consist of small haemorrhages in the corpus callosum, septum pellucidum, deep grey matter of the cerebral hemisphere, and dorsilateral quadrant of midbrain and pons. Disrupted and swollen axons with globular ends known as "retraction balls of Cajal" are observed at an early stage. After a few weeks clusters of neuroglia form around the severed axons and wallerian degeneration of fibre tracts occurs.12 Clinically, diffuse axonal injury is thought to be responsible for a broad spectrum of injury from mild concussion in which no structural lesion can be demonstrated and complete clinical recovery ensues, to prolonged coma and death in instances of much greater angular acceleration.
The events leading to axonal disruption have recently been examined. Povlishock and others have shown that this is a process requiring several hours to complete and may be reversible before frank axonal disruption occurs, at least in some axons.13
It should of course be stressed that not all primary injury is diffuse. Focal contusions and lacerations are seen, especially after falls and blows to the head, often involving the inferior (orbital) surface of the frontal lobes and the anterior poles of the temporal lobes. Brain oedema around contusions may lead to late clinical deterioration as a result of mass effect and brain shift.
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