CLINICAL ARTICLE - VASCULAR Collateralization and ischemia in hemodynamic cerebrovascular insufficiency Marcus Czabanka & Gueliz Acker & Daniel Jussen & Tobias Finger & Pablo Pena-Tapia & Gerrit A. Schubert & Johann Scharf & Peter Martus & Peter Schmiedek & Peter Vajkoczy Received: 18 July 2014 /Accepted: 1 September 2014 /Published online: 25 September 2014 # Springer-Verlag Wien 2014 Abstract Background Moyamoya disease and atherosclerotic cerebro- vascular occlusive disease lead to hemodynamic impairment of cerebral blood flow. One major differentiation between both disease entities lies in the collateralization pathways. The clin- ical implications of the collateralization pathways for the de- velopment 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 hemody- namic ischemia into anterior/posterior cortical border zone infarction (CBI), inferior border zone infarction (IBI) or territorial infarction (TI). Digital subtraction angiog- raphy was applied to evaluate collateralization. Collateralization was compared and correlated with the localization of ischemia and number of vascular terri- tories 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 <0.05). ACVD patients demonstrated collateralization via the anterior and posterior communicating arteries (flow in the posterior- anterior direction, MM: 6 %/5 % vs. ACVD: 62 %/88 %, p <0.05). Patterns of infarction were comparable (aCBI: MM: 36 % vs. ACVD: 35 %; pCBI: MM: 10 % vs. ACVD: 20 %; IBI: MM: 35 % vs. ACVD: 41 %; TI: MM: 13 % vs. ACVD: 18 %). The number and localization of vascular territories with impaired CVRC were comparable. Conclusions Despite significant differences in collateralization, the infarct patterns and severity of CVRC impairment do not differ between MMV and ACVD patients. Cerebral collateralization does not allow reaching conclusions about the localization of cerebral ischemia or severity of impaired CVRC in chronic hemodynamic impairment. Keywords Moyamoya angiopathy . Atherosclerotic cerebrovascular disease . Hemodynamic cerebrovascular insufficiency . Cerebrovascular reserve capacity . Cerebral collateralization . Stroke Introduction Moyamoya vasculopathy (MMV) represents a model disease for occlusive cerebrovascular pathology with chronic This study was presented at the Annual Meeting of the German Neurosurgical Society (DGNC) 2014. M. Czabanka (*) : G. Acker : D. Jussen : T. Finger : P. Vajkoczy Department of Neurosurgery, Universitätsmedizin Charite, Berlin, Germany e-mail: marcus.czabanka@charite.de P. Pena-Tapia : P. Schmiedek Department of Neurosurgery, University Hospital Mannheim, University of Heidelberg, Heidelberg, Germany G. A. Schubert Department of Neurosurgery, University of Aachen, Aachen, Germany P. Martus Institute for Clinical Epidemiology and applied Biometrics, University Medical Center, Tübingen, Germany J. Scharf Department of Neuroradiology, University Hospital Mannheim, University of Heidelberg, Heidelberg, Germany Acta Neurochir (2014) 156:2051–2058 DOI 10.1007/s00701-014-2227-1