Reaction of the cerebral venous sinus system to acute intracranial hypertension.

Abstract

A acute intracranial hypertension develops, the cerebral blood flow (CBF) invariably falls. Langfitt and coworkers 8 have shown that CBF reduction depends upon the degree of intracranial pressure (ICP) elevation and the rapidity with which it develops. The precise anatomical site of vascular obstruction or physiological alteration leading to failure of CBF in the presence of adequate arterial perfusing pressures has not, however, been conclusively demonstrated. Coincident with rising ICP and falling CBF, a separate and well-documented vascular phenomenon occurs. Cerebral vasodilation, as graphically demonstrated by Wolff and Forbes, 1~ can be observed through a cranial window concomitant with experimentally elevated ICP. The simultaneous occurrence of apparent dilation and falling CBF remains an unexplained vascular paradox. Conventional hemodynamic teaching would associate vasodilation with increased flow, and it has been explained as a physiological adjustment of the vascular bed to accumulated hypoxic acid metabolites. In the course of flow studies Marshall, et al., ~~ found that severe injury reduces or abolishes cerebral vasomotor tone and autoregulation. When the traumatized vascular system is subjeeCed to epinephrine-induced systemic hypertension the cerebral arterioles fail to constrict normally. This phenomenon may in part explain cerebral vasodilation, in which an increased blood mass may be presented to the capillary-venous system during arteriolar dilatation. However, faulty auto-regulation during intracranial hypertension does not explain falling CBF. Arteriolar failure should elevate the CBF in a manner analogous to that observed during hypercapneic states. T,~I Since the mechanism of falling CBF cannot be attributed to restriction of vascular