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September 11, 2001; 57 (5) Articles

Prognostic relevance of pathological sympathetic activation after acute thromboembolic stroke

D. Sander, K. Winbeck, J. Klingelhöfer, T. Etgen, B. Conrad
First published September 11, 2001, DOI: https://doi.org/10.1212/WNL.57.5.833
D. Sander
MD
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K. Winbeck
MD
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J. Klingelhöfer
MD
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T. Etgen
MD
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B. Conrad
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Citation
Prognostic relevance of pathological sympathetic activation after acute thromboembolic stroke
D. Sander, K. Winbeck, J. Klingelhöfer, T. Etgen, B. Conrad
Neurology Sep 2001, 57 (5) 833-838; DOI: 10.1212/WNL.57.5.833

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Abstract

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.

  • Received September 28, 2000.
  • Accepted April 19, 2001.
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