Model for short-term intracranial pressure changes following traumatic injury.

Results from primate studies show a transient increase in intracranial pressure (ICP) after a nonimpact inertial loading condition. The measured ICP increase varies linearly with the peak tangential load of these experiments. These experiments point to possible alterations in cerebral blood flow. This paper investigates the possible etiology of this particular phenomenon, and presents a simple analytical model that could explain the changes in intracranial pressure. The model combines the effects of cerebral venous constriction, arterial dilatation, and raised mean blood pressure to yield the characteristic immediate rise and exponential decay of ICP. The main contributor to the increase in intracranial pressure is believed to be vasodilation of cerebral arteries following venous constriction. Passive release of cerebrospinal fluid (CSF) is believed to mediate the long-term decay of intracranial pressure and possibly contribute to local hyperemia.