Literature DB >> 22834894

Insular stroke is associated with acute sympathetic hyperactivation and immunodepression.

U Walter1, S Kolbaske, R Patejdl, V Steinhagen, M Abu-Mugheisib, A Grossmann, C Zingler, R Benecke.   

Abstract

BACKGROUND AND
PURPOSE: Post-stroke immunodepression has been related to brain lesion size but not a specific lesion location. Here, we studied the influence of lesion location within middle cerebral artery (MCA) territory on parameters related to activation of sympathetic adrenomedullar pathway, immunodepression, and associated infection.
METHODS: We analyzed clinical, brain imaging, and laboratory data of 384 patients (174 women; mean age 70.8 ± 12.9 years) consecutively admitted to the stroke unit no later than 24 h after onset of acute ischaemic stroke involving the MCA territory.
RESULTS: Patients with lesion affecting >33% of MCA territory had increased serum metanephrine and normetanephrine levels, elevated neutrophil counts but decreased eosinophil, helper T lymphocyte, and cytotoxic T lymphocyte counts compared to patients with lesion in <33% of MCA territory. Patients with large infarctions had increased frequency of infections within 14 days after stroke, especially chest infections (P < 0.001). Considering only patients with non-lacunar infarction in <33% of MCA territory, those with insular lesion had significantly higher normetanephrine levels, higher neutrophil but lower eosinophil and helper T lymphocyte counts than those with non-insular lesion, despite similar lesion diameters. This coincided with an increased frequency of chest infections (P < 0.01) in patients with insular lesion. Whilst patients with right insular lesion showed decreased heart rate variability, lesion laterality had no impact on laboratory findings or infection frequency.
CONCLUSION: These findings suggest a specific role of insular lesion in the pathogenesis of stroke-induced sympathetic hyperactivation and immunodepression. Neuroimaging studies applying lesion volume calculation techniques are warranted to confirm these findings.
© 2012 The Author(s) European Journal of Neurology © 2012 EFNS.

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Year:  2012        PMID: 22834894     DOI: 10.1111/j.1468-1331.2012.03818.x

Source DB:  PubMed          Journal:  Eur J Neurol        ISSN: 1351-5101            Impact factor:   6.089


  36 in total

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