Cerebral circulation and the sympathetic nervous system in patients with traumatic brain injury or subarachnoid hemorrhage

Abstract

Maintenance of adequate cerebral microcirculation is necessary to avoid cerebral ischemia after severe traumatic brain injury and non-traumatic subarachnoid hemorrhage. After severe traumatic brain injury the blood-brain-barrier is disrupted and transcapillary leakage will contribute to the development of vasogenic brain edema. The edema causes a compromised microcirculation.Systemic complications and cerebral vasospasm observed after non-traumatic subarachnoid hemorrhage may be associated with an activated sympathetic nervous system. Although in-creased concentrations of plasma and urinary norepinephrine are found in patients following subarachnoid hemorrhage, this does not necessarily indicate an activated sympathetic nervous system. To adequately assess an activation of the sympathetic nervous system both release and removal processes of norepinephrine must be considered.A therapy focused on physiological principles for volume regulation and preserved microcir-culation following traumatic brain injury was evaluated in two clinical studies. Prostacyclin may improve cerebral microcirculation after severe traumatic brain injury due to its inhibition of platelet/leukocyte aggregation and adhesion to endothe-lium. Safety profile and outcome after prostacyclin administration was evaluated in the sec-ond study. With an isotope dilution technique the duration and magnitude of the sympathetic nervous activation in patients following subarachnoid hemorrhage was measured and the presumed inhibitory effect of clonidine on sympathetic nervous activation was tested.Favorable outcome after severe traumatic brain injury was 71% in both studies and the mor-tality rate was 13% and 3% respectively. Prostacyclin did not cause any severe side effects. Patients following subarachnoid hemorrhage exhibited an extreme elevation in sympathetic nervous system activity that persisted for at least one week after the insult. Contrary to what would be expected, clonidine did not reduce sympathetic nervous activation in patients fol-lowing subarachnoid hemorrhage.