Research/Cerebrovascular and Brain Mechanics/01 / 02

Cerebral Perfusion and Autoregulation

Cerebral perfusion depends on the interaction among large-vessel hemodynamics, microvascular resistance, tissue demand, venous drainage, and active vascular regulation. We develop patient-specific multiscale models that connect image-derived vascular networks with three-dimensional tissue-perfusion domains. These models incorporate physiologic supply–demand relationships, passive vessel mechanics, and arteriolar autoregulation to quantify how systemic pressure, posture, vascular stiffness, and arterial stenosis affect regional cerebral blood flow.

A brain with its arteries and tissue perfusion field, systemic pressure changing, arteriolar diameter answering, and perfusion returning to its regulated range
Cerebral blood flow through the whole brain, reconstructed from the arterial and venous trees and shown in mL per 100 g per minute.

Physiologic Flow Distribution and Perfusion Territories

Realistic cerebrovascular simulations require boundary conditions that represent the blood-flow demand of the supplied brain tissue. We estimate subject-specific flow distributions by associating image-derived cerebral arteries with surrounding tissue regions. The required flow for each territory is determined from tissue mass and regional cerebral blood-flow demand and is distributed through a one-dimensional vascular model.

The model is evaluated by comparing estimated arterial flow distributions and perfusion territories with reported physiological data and perfusion imaging. The supply–demand formulation also reduces sensitivity to variations in segmented vessel caliber compared with geometry-only flow allocation.

MRI and MRA → vessel and tissue segmentation → artery–tissue association → perfusion territories coloured and labelled as territories, not as flow → the resulting flow distribution across the major arteries
From MRI and MRA to vessel and tissue segmentation, the assignment of each tissue region to the artery supplying it, and the flow each major artery must carry.

Multiscale Cerebral Perfusion Modeling

Cerebral vessels below the resolution of clinical imaging cannot be reconstructed directly. We extend image-derived arteries with synthetic vascular trees and couple one-dimensional blood-flow equations with a three-dimensional tissue-perfusion model. This multiscale formulation transfers pressure and flow between the explicit vascular network and the tissue domain and provides spatial estimates of cerebral perfusion.

The synthetic vascular network, the arterial pressure distribution along it, and the three-dimensional cerebral blood-flow field — with simulated perfusion set against arterial spin labeling MRI on one shared colour scale
Simulated cerebral perfusion set against measured perfusion for four subjects, in three dimensions and slice by slice, on one shared colour scale.

Autoregulatory Coupling under Pressure and Postural Changes

Cerebral autoregulation modifies arteriolar resistance to stabilize blood flow under changes in systemic and local conditions. We incorporate active arteriolar dilation and constriction into a multiscale model that includes arterial and venous networks, pre- and postcapillary compartments, and a three-dimensional perfusion domain. This framework allows the coupled effects of aortic pressure, gravity, vessel-wall stiffness, and metabolic demand to be examined.

Under the investigated conditions, active autoregulation maintains cerebral blood flow within a relatively narrow range by adjusting arteriolar diameter. Arterial deformation and total vascular volume are affected by systemic pressure and gravity, whereas venous volume is primarily sensitive to posture. Increased vascular compliance amplifies posture-dependent volume changes and the corresponding autoregulatory response.

Supine, upright and inverted side by side, each with arterial and venous pressure and total vascular volume beneath, and autoregulation enabled against disabled as two curves
The same model upright, supine and inverted. The top row carries arterial pressure; below it, perfusion with the passive response alone and with active regulation included.

Autoregulatory Response to Ischemia

Arterial stenosis reduces downstream pressure and produces a mismatch between tissue supply and metabolic demand. We model arteriolar vasodilation as a reduction in downstream vascular resistance in response to local hemodynamic and metabolic stimuli. This mechanism allows the contribution of active regulation to perfusion recovery to be quantified under controlled stenosis conditions.

Under the investigated stenosis conditions, arteriolar vasodilation produces a larger improvement in tissue perfusion than sub-resolution collateral vessels alone. The contribution of collateral circulation remains dependent on vessel caliber, density, and stenosis severity, and is treated in Cerebrovascular Networks and Collateral Circulation.

Normal vessels with baseline perfusion, the same tissue under stenosis with the hypoperfused region marked, and perfusion after arteriolar vasodilation
Cortical perfusion at 0, 50, 70 and 90 per cent middle cerebral artery stenosis, with the affected territory and its branches coloured by the arteriolar dilation needed to sustain flow.

Model Evaluation and Interpretation

We evaluate cerebral perfusion models through comparisons with physiological flow ranges, vascular morphology data, perfusion territories, and medical perfusion imaging. These comparisons assess whether the models reproduce plausible pressure, flow, and tissue-perfusion patterns. The resulting simulations provide mechanistic estimates rather than direct clinical diagnoses and remain dependent on assumptions regarding sub-resolution vasculature, tissue properties, and autoregulatory capacity.

Cerebrovascular and Brain Mechanics2 topics in this area
Cerebral Perfusion and AutoregulationCerebrovascular Networks and Collateral Circulation