An anesthetized sheep model of traumatic brain injury (TBI) has been developed to assess early changes in intracranial pressure (ICP) following closed head injury. Immediately after TBI, a transient (less than 10 min) hypertensive response occurred, followed by significant and prolonged systemic hypotension. ICP demonstrated a biphasic response, being seven times baseline values of 8 +/- 2 mm Hg 10 min after injury, decreasing to 25 +/- 2 mm Hg by 30 min, and then increasing to values exceeding 30 mm Hg by 4 h postinjury. ICP was always significantly higher than baseline values, which combined with hypotension, reduced cerebral perfusion pressure to less than 60 percent of normal. This early and sustained increase in ICP after craniocerebral trauma acutely alters cerebral perfusion pressure and brain oxygenation and provides a potential pathophysiological explanation for immediate clinical manifestations in humans following significant TBI. Abstract published by arrangement with John Wiley & Sons.