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 meas ured ICP increase varies linearly with the peak tangential load of the se experiments. These experiments point to possible alterations in cer ebral blood flow. This paper investigates the possible etiology of thi s particular phenomenon, and presents a simple analytical model that c ould 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 arter ies following venous constriction. Passive release of cerebrospinal fl uid (CSF) is believed to mediate the long-term decay of intracranial p ressure and possibly contribute to local hyperemia.