Increased Vulnerability of the Traumatized Brain to Early Ischemia

Abstract

Hypoxia and arterial hypotension are the most frequent causes of secondary brain damage in head injured patients and contribute significantly to morbidity and mortality (1,2,3). Early ischemia due to a delay in hospital admission is difficult to document and even more difficult to study in humans. However, laboratory studies have recently demonstrated that early secondary hypotension and hypoxia increases both mortality and morbidity following experimental head trauma (4). Yet, it is unclear whether this is the result of a direct effect on the brain or upon peripheral systems of the animal. Therefore, an increased vulnerability of the brain to ischemia or hypoxia following trauma has not been demonstrated to date. An increased vulnerability of the traumatized brain to ischemia may result from a number of factors. First, impairment of the responsiveness of the cerebral circulation as the result of trauma (1,2,5,6) may increase the risk of cerebral ischemia in patients with secondary hypotension and hypoxia. Second, metabolic derangements which result directly from the primary traumatic insult may increase the vulnerability of the brain to hypoxic and ischemic damage. Finally, peripheral reactions to trauma, hemorrhagic hypotension, or apnea may alter the response of the traumatically damaged CNS to hypoxia and ischemia. The present study was undertaken to examine the effect of an early “secondary” ischemic insult upon the function and structure of the traumatized brain. The response of the normal brain to the same level of ischemia was studied for comparison. The purpose of the current study was to test the hypothesis that a traumatic insult renders the CNS more vulnerable to cerebral ischemia.