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From the Department of Neurology (Drs. Winbeck, Etgen, and Conrad), Technical University of Munich and Klinikum Chemnitz (Dr. Klingelhöfer), Germany.
Address correspondence and reprint requests to Dr. D. Sander, Department of Neurology, Technical University of Munich, Möhlstraße 28, 81675 Munich, Germany; e-mail: Dirk.Sander{at}neuro.med.tu-muenchen.de
Objective: — To evaluate the prognostic impact of early pathologic sympathetic activation after stroke.
Methods: — The authors examined 112 consecutive patients (mean age, 69 years; 60 men) with their first brain infarction. A pathologic sympathetic activation was presumed if the initial norepinephrine level exceeds 300 pg/mL. In addition, involvement of the insular cortex, nighttime blood pressure changes, and several cardiovascular risk factors were determined. One-year outcome measures were mortality rate, cardiovascular and cerebrovascular events, and activities of daily living (Barthel index and Rankin score).
Results: — Norepinephrine levels greater than 300 pg/mL, nighttime blood pressure increases, and insular involvement were associated with a lower Barthel index (p < 0.005) at the 1-year follow-up. By stepwise logistic regression analysis, insular infarction, serum norepinephrine concentration, right-sided infarction, and nighttime blood pressure increase were significant and independent predictors of an unfavorable functional outcome. Cox regression analysis showed a higher rate of cardiovascular and cerebrovascular events (hazard ratio, 2.9; 95% CI, 1.07; 6.83; p < 0.04) in patients with initially increased norepinephrine concentrations.
Conclusions: — The involvement of the insular cortex, the occurrence of a pathologic nighttime blood pressure increase, and an initially increased serum norepinephrine concentration are independent predictors of poor long-term outcome.
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