title: A 3D numerical study of the collateral capacity of the Circle of Willis with anatomical variation in the posterior circulation.
abstract: BACKGROUND
  The Circle of Willis (CoW) is the most important collateral pathway of the cerebral artery. The present study aims to investigate the collateral capacity of CoW with anatomical variation when unilateral internalcarotid artery (ICA) is occluded.
  
  
  METHODS
  Basing on MRI data, we have reconstructed eight 3D models with variations in the posterior circulation of the CoW and set four different degrees of stenosis in the right ICA, namely 24%, 43%, 64% and 79%, respectively. Finally, a total of 40 models are performed with computational fluid dynamics simulations. All of the simulations share the same boundary condition with static pressure and the volume flow rate (VFR) are obtained to evaluate their collateral capacity.
  
  
  RESULTS
  As for the middle cerebral artery (MCA) and the anterior cerebral artery (ACA), the transitional-type model possesses the best collateral capacity. But for the posterior cerebral artery (PCA), unilateral stenosis of ICA has the weakest influence on the unilateral posterior communicating artery (PCoA) absent model. We also find that the full fetal-type posterior circle of Willis is an utmost dangerous variation which must be paid more attention.
  
  
  CONCLUSIONS
  The results demonstrate that different models have different collateral capacities in coping stenosis of unilateral ICA and these differences can be reflected by different outlets. The study could be used as a reference for neurosurgeon in choosing the best treatment strategy.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Ren
authors.forename: Qiang
authors.initials: Q
authors.lastname: Chen
authors.forename: Zhi-Yong
authors.initials: ZY
authors.lastname: Li
mesh_terms: D002560:Cerebrovascular Circulation; D002941:Circle of Willis / Q000033:anatomy & histology* / Q000473:pathology / Q000502:physiology* / Q000503:physiopathology; D003251:Constriction, Pathologic / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D008953:Models, Anatomic