Both hypotension and hypertension have been implicated in the production of cerebral ischemia and infarction. Although cerebral blood flow in the normal person is relatively independent of the systemic blood pressure down to levels of 50 to 60 mm. of mercury, it has been suggested that a lesser drop in blood pressure may produce cerebral ischemia when a significant obstruction is present in a vessel-leading to the brain.
A localized obstruction must reduce the vessel lumen by nearly 80 per cent to produce a significant distal drop in pressure, but luminal encroachment that extends over long distances theoretically could significantly decrease the distal arterial pressure with less severe grades of obstruction. However, the contribution to cerebral infarction of obstruction and distal decreases in blood pressure and flow is still an unsettled matter.
Thus, Marshall has reported that when patients with transient ischemic attacks were made briefly hypotensive with hexamethonium and tilting, nearly one half showed evidence of generalized cerebral ischemia only, and another one fourth developed evidence of generalized cerebral ischemia before any focal ischemia.
Failure to maintain the blood pressure may occur with cardiac arrhythmias and following myocardial infarction. The asystole that occurs in Stokes-Adams attacks, if prolonged, can reduce the cerebral blood flow so markedly that cerebral ischemia or infarction results.
The place of hypertension in the production of cerebral ischemia and infarction is less clear than that of hypotension. Rapid elevations of blood pressure evoke an increase in cerebrovascular resistance, and model experiments have demonstrated that stenosis coupled with this increased resistance significantly reduces blood flow. In animal experiments, marker hypertension causes constriction in small cerebral vessels leading, in turn, to areas of cerebral infarction.
The clinical evidence is less clear, al though bedside experience suggests that transient increases of blood pressure at the time of a cerebral ischemic attack may contribute to cerebral infarction.Other physiologic changes in cerebral hemodynamics may contribute to cerebral ischemia. Osteoarthritis in the cervical spine may compress the vertebral arteries so that extension, flexion, or rotation of the head can reduce vertebral artery blood flow to the point that ischemic symptoms occur. Cerebral ischemia will be augmented in these instances if anomalies or extensive atherosclerotic deposits compromise the circle of Willis.