Cerebrospinal Fluid Facilitation of Cerebral Blood Flow: A Windkessel Analysis of Intracranial Hypertension

Due to the rigidity of the skull and intracranial compartment, cerebral blood flow (CBF) and its link to intracranial hypertension is not well understood. It is hypothesized that the cerebrospinal fluid (CSF) flow out of the cranium facilitates a windkessel mechanism, which allows for venous blood flow to be minimally pulsatile, and thus the inertance of the system to be relatively low. The disruption of this mechanism may lead to pulsatile venous flow, increased venous inertance, and eventual increased intracranial pressure (ICP) caused by autoregulated vasodilation. In this research, a windkessel model is developed to represent the intracranial compartment including systemic compliance facilitated by the translocation of CSF. The element parameters of this model are fit to clinical cerebrovascular pressure and flowrate data corresponding to a nominal state as well as an increased ICP state. By comparing the calculated parameters from each state, the hypothesized mechanism leading to increased ICP is confirmed. The increased ICP state exhibits lower CSF-facilitated capacitance, higher venous inertance, and decreased arterial resistance, which results in increased ICP compared to the nominal state. These results have broad implications for the understanding of intracranial hypertension and may lead to improved techniques for diagnostics and treatment of these symptoms.