Autonomic nervous dysfunction during acute cerebral infarction

Central autonomic impairment due to acute cerebral infarction is known to lead to excessively high blood pressure and tachycardia. The mechanism by which these symptoms occur in patients with supratentorial lesions has not been elucidated. The objective of this study was to evaluate the autonomic dysfunction that occurs in these patients.

Seventy-seven ischemic stroke patients (65·8 years) with an acute ischemic cerebral infarction underwent comprehensive clinical evaluation that included laboratory tests and a 24 hour electrocardiogram. These patients were classified into one of the following two groups: those with either a single, supratentorial symptomatic small-vessel occlusion (lacunar infarction; n=47; Group S), or a large-artery atherosclerosis (n=30; Group A); 31 unimpaired subjects served as controls (Group C).

High frequency power spectrum (HF), which is thought to be a reflection of parasympathetic activity, was significantly reduced in all patient groups (p<0·01) at the time of admission compared to controls. Seven days later, only the HF values in Group A were still reduced. The correlations between the patients' NIHSS scores and their HF were statistically significant in each group, and multiple adjusted relative risk of HF value was 1·31 (95% CI: 1·02-2·11). The HF in Group S was found to be particularly diminished in patients who had an infarction in either the putamen or thalamus so that these ganglia may be key lesions of central autonomic network.

Our data suggest that patients with a supratentorial acute stage cerebral infarction may display a reduced parasympathetic regulation and relative increase in sympathetic output.