Cerebral hemodynamics is fundamentally regulated through the Circle of Willis (CoW), which redistribute flow via communicating arteries to stabilize perfusion under anatomical variations and vascular stenosis. In this study, a multiscale circulation model was developed by coupling a multiscale systemic hemodynamic framework with cerebral arterial network reconstructed from medical imaging. The model integrates a cerebral autoregulation mechanism (CAM) and enables quantitative simulation of flow redistribution across the CoW under normal, anatomically varied, and pathologically narrowing (stenosis) conditions. Baseline simulations at normal states reproduced physiological flow distributions in which the communicating arteries remained nearly inactive, showing negligible across-flow and agreement with clinical measurements, while two anatomical variations revealed distinct collateral activation patterns: the anterior communicating artery (ACoA) acted as the earliest and most sensitive functional collateral pathway, whereas the posterior communicating arteries (PCoAs) exhibited structure-dependent engagement. Progressive stenosis modeling further demonstrated the transition from a complete CoW to a fetal-type posterior cerebral artery (PCA) configuration, with early ACoA flow reversal followed by the ipsilateral PCoA activation, in agreement with experimental and transcranial Doppler observations. We further present a path-based quantitative analysis of source-to-sink flow contributions to quantitatively illustrates how the cerebral vascular network dynamically reconfigures collateral pathways in response to structural changes. Overall, the proposed framework provides a physiologically interpretable and image-informed tool for investigating cerebral flow regulations through the functional collaterals within the CoW, offering potential for clinical applications in the diagnosis, prognosis, and treatment planning of cerebrovascular diseases.
Liu et al. (Mon,) studied this question.
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