title: Collateralization and ischemia in hemodynamic cerebrovascular insufficiency.
abstract: 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 < 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.
authors.affiliation: Department of Neurosurgery, Universitätsmedizin Charite, Berlin, Germany, marcus.czabanka@charite.de.
authors.forename: Marcus
authors.initials: M
authors.lastname: Czabanka
authors.forename: Gueliz
authors.initials: G
authors.lastname: Acker
authors.forename: Daniel
authors.initials: D
authors.lastname: Jussen
authors.forename: Tobias
authors.initials: T
authors.lastname: Finger
authors.forename: Pablo
authors.initials: P
authors.lastname: Pena-Tapia
authors.forename: Gerrit A
authors.initials: GA
authors.lastname: Schubert
authors.forename: Johann
authors.initials: J
authors.lastname: Scharf
authors.forename: Peter
authors.initials: P
authors.lastname: Martus
authors.forename: Peter
authors.initials: P
authors.lastname: Schmiedek
authors.forename: Peter
authors.initials: P
authors.lastname: Vajkoczy
mesh_terms: D000328:Adult; D015901:Angiography, Digital Subtraction; D002533:Cerebral Angiography; D002544:Cerebral Infarction / Q000209:etiology / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D002561:Cerebrovascular Disorders / Q000209:etiology / Q000503:physiopathology; D003097:Collateral Circulation; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D002537:Intracranial Arteriosclerosis / Q000150:complications / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009072:Moyamoya Disease / Q000150:complications / Q000503:physiopathology*; D015899:Tomography, Emission-Computed, Single-Photon