Pathophysiology and Clinical Significance of ICP Course in Comatose, Patients with Severe Head Injury

Intracranial pressure (ICP) levels in comatose, severe head injury patients can vary considerably during the initial 7–10 days after trauma (Miller et al. 1977). Intracranial hemorrhage and hydrocephalus are among the entities known to drive the ICP up but they can often be successfully treated (Galbraith and Teasdale 1981). However, posttraumatic brain edema, a frequent cause of intracranial hypertension, is sometimes difficult to control and may result in brain death (Bruce et al. 1981). In a consecutive series of patients with severe head injury vigorously treated by a standard protocol that included emergency evacuation of mass lesions and intensive care (Becker et al. 1977) we identified four ICP courses that were associated with different patient outcome categories. To gain insight into the pathophysiological substrate that contributes to these ICP courses and the significance of ICP levels to brain function following severe head trauma we analysed the interaction of cortical and brain stem evoked potentials (EP), CT scan, neurological examination, autopsy and operative findings, admission blood pressure, arterial blood gases, secondary systemic and CNS complications and patient outcome in each of the four ICP courses identified.