Impaired neurogenic cerebrovascular control and dysautoregulation after stroke.

Abstract: Impaired Neurogenic Cerebrovascular Control and Dysautoregulation After Stroke • Cerebral autoregulation was tested in 32 patients with various anatomical locations and stages of ischemic cerebrovascular disease. Cerebral perfusion pressure (CPP) was raised or lowered in a standard manner by the use of head-up tilting (induced hypotension) and head-down tilting (induced hypertension). Any impairment of cerebral autoregulation was analyzed quantitatively by the ratio of the change in cerebral blood flow (CBF) over the change in CPP. There was significant correlation between the degree of dysautoregulation whether CPP was increased or decreased. An inverse correlation was shown between the degree of dysautoregulation and the duration after the ischemic episode during both induced hypotension and hypertension. Patients with brainstem lesions including those with transient ischemic attacks (TIAs) showed a greater impairment of autoregulation which persisted longer than those with hemispheric lesions. Patients with severe cerebral hemispheric infarction showed greater impairment of autoregulation than those with minor hemispheric lesions. Dysautoregulation also was greater in patients with subcortical lesions compared to those with cortical lesions. Hypertensive patients showed significantly greater decreases in CBF and effective MABP during induced hypotension than normotensive patients although autoregulation index was the same. Thus, symptoms are more frequent in hypertensives because of greater changes in CPP. Paradoxical responses in CBF to changes in CPP occurred in six patients. These were noted in moderately severe lesions in relatively young patients with hypertension and deeply located cerebral or brainstem lesions in the subacute stage. The mechanisms which control cerebral autoregulation were discussed and the nervous structures situated in the deep cerebral regions and brainstem, possibly the central structures of the autonomic nervous system, were proposed to control autoregulation of CBF.