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Rothoerl, Ralf Dirk ; Schebesch, Karl-Michael ; Kubitza, Marion ; Woertgen, Chris ; Brawanski, Alexander ; Pina, Ana-Luisa

ICAM-1 and VCAM-1 expression following aneurysmal subarachnoid hemorrhage and their possible role in the pathophysiology of subsequent ischemic deficits

Rothoerl, Ralf Dirk, Schebesch, Karl-Michael, Kubitza, Marion, Woertgen, Chris, 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.

Date of publication of this fulltext: 05 Aug 2009 13:26
Article
DOI to cite this document: 10.5283/epub.1235


Abstract

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 ...

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. Copyright (c) 2006 S. Karger AG, Basel



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Details

Item typeArticle
Journal or Publication TitleCerebrovascular diseases (Basel, Switzerland)
Publisher:KARGER
Place of Publication:BASEL
Volume:22
Number of Issue or Book Chapter:2-3
Page Range:pp. 143-149
Date2006
InstitutionsMedicine > Lehrstuhl für Neurochirurgie
Identification Number
ValueType
16691023PubMed ID
10.1159/000093243DOI
KeywordsINTERCELLULAR-ADHESION MOLECULE-1; CEREBRAL VASOSPASM; CULTURED ENDOTHELIUM; GRANULOCYTE ADHESION; MONOCLONAL-ANTIBODY; CEREBROSPINAL-FLUID; ARTERIAL-WALL; E-SELECTIN; RATS; INFLAMMATION; adhesion molecules; intercellular adhesion molecule-1; vascular cell adhesion molecule-1; subarachnoid hemorrhage; vasospasm; ischemic neurological deficit, delayed
Dewey Decimal Classification600 Technology > 610 Medical sciences Medicine
StatusPublished
RefereedYes, this version has been refereed
Created at the University of RegensburgYes
Item ID1235

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