Amyloid precursor protein may be an acute-phase reactant to traumatic brain injury(5) and results in b-amyloid deposition in 30 per cent of fatal brain injuries. Apolipoprotein E (APOE) genotype may influence the degree to which amyloid is deposited, being greater in those with the e4 allele.(6)
Hydrocephalus following head injury may be due to cerebral atrophy, which may develop over the weeks and months following injury. Diffuse ventricular enlargement is often associated with atrophy of the corpus callosum, and is usually attributed to diffuse axonal injury. More localized atrophy is observed when contusions resolve to leave a loss of brain tissue.
Of greater importance is hydrocephalus resulting from the residual effects of subarachnoid blood interfering with the normal cerebrospinal fluid flow and preventing it from escaping into the venous system. This may require insertion of a ventriculo-peritoneal shunt to prevent deterioration in cognitive function.
Fractures to the floor of the skull, particularly if they are associated with cerebrospinal fluid leaks, may allow infection into the subarachnoid space, causing meningitis sometimes years after injury. Cerebral abscesses may take months before they become clinically evident.
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