Cerebrovascular Networks and Collateral Circulation
The cerebrovascular system distributes blood through a hierarchical network that extends from major cerebral arteries to arterioles and capillaries. Alternative collateral pathways can redistribute flow when a primary arterial route is compromised. We develop image-based and synthetic vascular-network models to quantify how vascular connectivity, geometry, and collateral configuration affect cerebral pressure, flow, and tissue perfusion. These models support controlled evaluation of anatomical variability and compensatory flow under stenotic and ischemic conditions.
Image-Based and Synthetic Cerebrovascular Networks
Major cerebral arteries can be reconstructed from clinical vascular imaging, but smaller vessels remain below the available image resolution. We extend the image-derived arteries with synthetic vascular trees that represent the unresolved arteriolar network. The tree-generation algorithm accounts for local tissue demand, proximity between vessels and supplied tissue, and the mechanical cost of maintaining blood flow.
In the tissue-growth-based approach, vascular and tissue domains develop concurrently. An increase in the supplied tissue volume and its metabolic demand triggers the addition and adaptation of vascular branches. The resulting network connects nearby tissue regions while satisfying prescribed flow demand and minimum-work constraints.
Hemodynamic Coupling across Vascular Scales
We solve one-dimensional blood-flow equations in the explicitly represented arteries, arterioles, and collateral vessels and couple the terminal branches with a continuum representation of tissue perfusion. Terminal vascular pressures provide boundary information to the tissue domain, while tissue flow demand is transferred back to the vascular network. The iterative coupling maintains consistency between network hemodynamics and regional perfusion.
Circle of Willis Anatomy and Flow Redistribution
The Circle of Willis provides major communicating pathways among the anterior and posterior cerebral circulations. Its anatomy varies substantially among individuals, and incomplete or asymmetric configurations can alter the redistribution of flow when cerebral inflow is reduced. We construct patient-specific three-dimensional models with physiologically informed boundary conditions to examine how anatomical variants and autoregulatory responses affect cerebral pressure and flow.
Current research evaluates the coupled effects of Circle of Willis anatomy, arterial stenosis, and autoregulatory capacity on patient-specific cerebral hemodynamics. The objective is to determine how vascular connectivity modifies pressure and flow redistribution under impaired inflow conditions.
Computational Modeling of Collateral Circulation
Collateral vessels provide alternative connections between vascular territories and may redirect blood toward regions affected by arterial stenosis or occlusion. We generate collateral pathways between adequately supplied and hypoperfused branches and systematically vary their caliber, density, and spatial distribution. This approach allows the effects of individual collateral-network properties to be evaluated under controlled conditions.
Effects of Collateral Caliber and Density
Under the investigated conditions, collateral caliber has a stronger influence on perfusion recovery than collateral number alone. Small-caliber collateral networks provide limited additional flow even when their density is increased, whereas larger vessels form lower-resistance pathways and produce a greater hemodynamic effect. The relative contribution of collateral circulation also increases as primary arterial stenosis becomes more severe.
Network Response in Ischemic Tissue
We combine subject-specific arterial geometry, synthetic downstream networks, collateral pathways, and tissue-perfusion models to examine blood-flow redistribution under ischemic conditions. Comparisons among baseline, stenotic, collateral, and vasodilated configurations allow the individual and combined contributions of structural and active compensatory mechanisms to be assessed. The arteriolar side of that response is treated in Cerebral Perfusion and Autoregulation; here the emphasis is on network connectivity and collateral morphology.
Model Evaluation and Scope
We evaluate synthetic vascular morphology through comparisons with high-resolution imaging and anatomical measurements. Simulated flow and perfusion patterns are compared with physiological ranges, literature data, and arterial spin-labeling MRI where available. These comparisons assess the plausibility of the reconstructed networks but do not establish direct clinical diagnostic accuracy.
The current collateral model represents intraparenchymal arterial and arteriolar networks. Pial arterial networks, pial-to-pial collaterals, and collateral pathways involving the external carotid circulation are not explicitly represented.
Selected work
Annals of Biomedical Engineering
Computer Methods and Programs in Biomedicine 244:107956
Tissue-growth based synthetic tree generation and perfusion simulation
Biomechanics and Modeling in Mechanobiology 22:1095–1112
Computational analysis of cerebral hemodynamics: effects of autoregulation and Circle of Willis anatomy
Computers in Biology and Medicine