Objective: Impaired blood pressure regulation in the acute phase of stroke has been associated with less favorable outcome. Mechanisms and effects of blood pressure dysregulation in stroke are not well understood; however, central autonomic impairment with sympathetic overactivity and baroreflex involvement are discussed. Baroreflex sensitivity (BRS) in spontaneous intracerebral hemorrhage has not been investigated. We sought to examine BRS in patients with intracerebral hemorrhage and evaluate the relationship between BRS and short-term outcome measures. Design: An open, prospective study. Setting: Neurocritical care unit and stroke unit in a university hospital. Patients and Measurements: We studied 45 patients with acute intracerebral hemorrhage within 72 hrs from onset of symptoms and 38 control subjects. BRS was measured noninvasively using a hemodynamic monitoring device. Beat-to-beat blood pressure variability was derived. The effects of the BRS, hemorrhage volume, intraventricular blood, and admission scores on outcome at 10 days were studied using a multivariate regression model. Main Results: Compared with the control group, patients with intracerebral hemorrhage had significantly decreased BRS (p = 0.002) and significantly increased systolic, diastolic, and mean beat-to-beat blood pressure variability (p < 0.0001, p = 0.007, p = 0.015). After adjusting for age, National Institute of Heath Stroke Scale at admission, volume of intracerebral hemorrhage and presence of intraventricular blood in a multivariate regression model, BRS gain was an independent predictor of outcome at 10 days. Conclusions: We found that BRS was decreased in patients with acute intracerebral hemorrhage and correlated with increased beat-to-beat blood pressure variability. BRS independently predicted outcome at 10 days. Modulation of baroreceptor reflex sensitivity may represent a new therapeutic target in acute stroke and warrants future studies.

Background and Purpose— Autonomic dysfunction, including increased sympathetic drive and blunted baroreflex, has repeatedly been observed in acute stroke. Of clinical importance is that the stroke-related autonomic imbalance seems to be linked to worse outcome after stroke. Here, we discuss the role of baroreflex impairment in acute stroke and its possible pathophysiological and therapeutic relevance. Summary of Review— Possible mechanisms linking baroreflex impairment with unfavorable outcome in stroke may include increased cardiovascular morbidity and mortality, promotion of secondary brain injury due to local inflammation, hyperglycemia, or altered cerebral perfusion. Conclusions— We suggest therefore that the modifying of autonomic functions may have important therapeutic implications in acute ischemic as well as in hemorrhagic stroke.

Background and Purpose— Impaired baroreflex sensitivity (BRS) has been previously shown to be of prognostic value in patients with cardiovascular disease and stroke. Because baroreflex seems to be blunted by both carotid atherosclerosis and by lesions affecting central processing, controversy exists regarding the etiology of stroke-related baroreflex changes. The insula may play a central role in baroreflex modulation. The aim of the study was therefore to examine BRS in patients with acute stroke with regard to carotid atherosclerosis and insular involvement. Methods— We evaluated spontaneous BRS in 96 patients with acute stroke within 72 hours of ictus and 41 control subjects using a sequential crosscorrelation method. Results— Fifty-two patients with ischemic stroke and 44 patients with intracerebral hemorrhage, mean age 58.4 years, were included. With comparable carotid atherosclerosis profiles, patients with stroke had significantly lower BRS than control subjects (3.3 versus 5.3, P <0.001). Carotid atherosclerosis had no influence on variance of the BRS values in the acute stroke group. Patients with insular involvement had significantly lower BRS than patients with no insular involvement (2.55 versus 4.35, P =0.001) or control subjects (2.55 versus 5.3, P <0.001). Furthermore, patients with left insular involvement had significantly lower BRS than patients with right insular involvement (2.3 versus 3.5, P =0.049). There was no significant difference between patients with no insular lesions and control subjects ( P =0.263). Conclusions— We demonstrated that baroreflex impairment in acute stroke is not associated with carotid atherosclerosis but with insular involvement. Both insulae seem to participate in processing the baroreceptor information with the left insula being more dominant.

Background and Purpose—: High infection rate after severe stroke may partly relate to brain-induced immunodepression syndrome. However, the underlying pathophysiology remains unclear. The aim of the current study was to investigate the role of autonomic shift in increased susceptibility to infection after acute intracerebral hemorrhage (ICH). Methods—: We retrospectively analyzed 62 selected patients with acute ICH from our prospective database. Autonomic shift was assessed using the cross-correlational baroreflex sensitivity (BRS). The occurrence and cause of in-hospital infections were assessed based on the clinical and laboratory courses. Demographic and clinical data including initial stroke severity, hemorrhage volume, intraventricular blood extension, history of aspiration, and invasive procedures such as mechanical ventilation, surgical hematoma evacuation, external ventricular drainage, central venous and urinary catheters, and nasogastric feeding were recorded and included in the analysis. Results—: We identified 36 (58%) patients with infection during the first 5 days of hospital stay. Patients with infections had significantly lower BRS, higher initial NIHSS scores, larger hemorrhages, and more frequently had intraventricular blood extension and underwent invasive procedures. In the multivariate regression model, decreased BRS (OR, 0.54; 95% CI, 0.32–0.91; P =0.02) and invasive procedures (OR, 2.32; 95% CI, 1.5–3.6; P <0.001) remained independent predictors for an infection after ICH. Conclusions—: Decreased BRS was independently associated with infections after ICH. Autonomic shift may play an important role in increased susceptibility to infections after acute brain injury including ICH. The possible therapeutic relevance of autonomic modulation warrants further studies.

Background and Purpose—: Hemicraniectomy has been shown to be an effective treatment of life-threatening edema (LTE) in malignant middle cerebral artery infarction when performed early. Identifying patients who will develop LTE is therefore imperative. We hypothesize that autonomic shift toward sympathetic dominance may relate to LTE formation. We aimed to investigate the predictive potential of baroreflex sensitivity (BRS) as a marker of autonomic balance for calculating the course of large middle cerebral artery infarction. Methods—: Patients with middle cerebral artery infarction >2/3 of the territory and BRS measurement at admission were analyzed. BRS was estimated using the cross-correlational method. Demographic, clinical, and radiological data including stroke severity, infarct size, and basal ganglia involvement were recorded. Malignant course with LTE was defined as clinical deterioration and midline shift ≥5 mm in the first 48 hours. Results—: Eighteen (62.8%) patients developed LTE. Patients with LTE had lower BRS (2.3 versus 4.4 mm Hg/ms, P =0.007), larger infarcts (214 versus 144 mL, P =0.03), more frequent involvement of the basal ganglia (14 versus 4, P =0.03), and more often underwent thrombolysis combined with endovascular intervention (6 versus 0, P =0.04). In a multivariate model, BRS (OR, 0.36; CI, 0.14–0.93; P =0.03) and basal ganglia involvement (OR, 11.53; CI, 1.15–115.9; P =0.04) were independent predictors for LTE. This model correctly classified 86.2% of the malignant cases. Conclusions—: Decreased BRS, mirroring sympathetic activation, and basal ganglia involvement were associated with development of malignant course with LTE in large middle cerebral artery infarction. The predictive relevance of our findings needs to be confirmed in further studies.