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Collateralization and ischemia in hemodynamic cerebrovascular insufficiency

Background Moyamoya disease and atherosclerotic cerebrovascular occlusive disease lead to hemodynamic impairment of cerebral blood flow. One major differentiation between both disease entities lies in the collateralization pathways. The clinical implications of the collateralization pathways for the...

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Bibliographic Details
Published in:Acta neurochirurgica 2014-11, Vol.156 (11), p.2051-2058
Main Authors: Czabanka, Marcus, Acker, Gueliz, Jussen, Daniel, Finger, Tobias, Pena-Tapia, Pablo, Schubert, Gerrit A., Scharf, Johann, Martus, Peter, Schmiedek, Peter, Vajkoczy, Peter
Format: Article
Language:English
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Summary:Background Moyamoya disease and atherosclerotic cerebrovascular occlusive disease lead to hemodynamic impairment of cerebral blood flow. One major differentiation between both disease entities lies in the collateralization pathways. The clinical implications of the collateralization pathways for the development of hemodynamic ischemia remain unknown. The aim was to characterize collateralization and ischemia patterns in patients with chronic hemodynamic compromise. Methods Hemodynamic compromise was verified using acetazolamide-stimulated xenon-CT or SPECT in 54 patients [30 moyamoya and 24 atherosclerotic cerebrovascular disease (ACVD)]. All patients received MRI to differentiate hemodynamic ischemia into anterior/posterior cortical border zone infarction (CBI), inferior border zone infarction (IBI) or territorial infarction (TI). Digital subtraction angiography was applied to evaluate collateralization. Collateralization was compared and correlated with the localization of ischemia and number of vascular territories with impaired cerebrovascular reserve capacity (CVRC). Results MM patients showed collateralization significantly more often via pericallosal anastomosis and the posterior communicating artery (flow in the anterior-posterior direction; MM: 95 %/95 % vs. ACVD: 23 %/12 %, p  
ISSN:0001-6268
0942-0940
DOI:10.1007/s00701-014-2227-1