Rothoerl, Ralf Dirk and Schebesch, Karl-Michael and Kubitza, Marion and Woertgen, Chris and Brawanski, Alexander and Pina, Ana-Luisa (2006) ICAM-1 and VCAM-1 expression following aneurysmal subarachnoid hemorrhage and their possible role in the pathophysiology of subsequent ischemic deficits. Cerebrovascular diseases (Basel, Switzerland) 22 (2-3), pp. 143-149.
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Other URL: http://dx.doi.org/10.1159/000093243
BACKGROUND: The pathophysiology of ischemic cerebral lesions following aneurysmal subarachnoid hemorrhage (SAH) is poorly understood. There is growing evidence that inflammatory reactions could be involved in the pathogenesis of such delayed occurring ischemic lesions. The aim of this study was to evaluate adhesion molecules with regard to these lesions following SAH. METHODS: Serum and cerebrospinal fluid (CSF) samples were taken daily from 15 patients up to day 9 after SAH and evaluated for intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1). RESULTS: CSF and serum samples correlated well during nearly the whole time course (p < 0.0001). A secondary increase in ICAM-1 and VCAM-1 in the serum and CSF correlated with an increase in flow velocity in the transcranial Doppler (p > 0.0001 and p < 0.007) but not to a delayed lesion in the CT scan. CONCLUSION: We believe that inflammatory processes are involved in the pathogenesis of cerebral vasospasm but they might only be a part of a multifactorial pathogenesis.
|Institutions:||Medicine > Lehrstuhl für Neurochirurgie|
|Keywords:||Adhesion molecules; Intercellular adhesion molecule-1; Vascular cell adhesion molecule-1; Subarachnoid hemorrhage; Vasospasm; Ischemic neurological defi cit, delayed|
|Subjects:||600 Technology > 610 Medical sciences Medicine|
|Refereed:||Yes, this version has been refereed|
|Created at the University of Regensburg:||Yes|
|Deposited On:||23 Mar 2007|
|Last Modified:||20 Jul 2011 20:52|