A SIMPLE MATHEMATICAL-MODEL OF THE INTERACTION BETWEEN INTRACRANIAL-PRESSURE AND CEREBRAL HEMODYNAMICS

A simple mathematical model of intracranial pressure (ICP) dynamics or iented to clinical practice is presented. It includes the hemodynamics of the arterial-arteriolar cerebrovascular bed, cerebrospinal fluid ( CSF) production and reabsorption processes, the nonlinear pressure-vol ume relationship of the craniospinal compartment, and a Starling resis tor mechanism for the cerebral veins. Moreover, arterioles are control led by cerebral autoregulation mechanisms, which are simulated by mean s of a time constant and a sigmoidal static characteristic. The model is used to simulate interactions between ICP, cerebral blood volume, a nd autoregulation. Three different related phenomena are analyzed: the generation of plateau waves, the effect of acute arterial hypotension on ICP, and the role of cerebral hemodynamics during pressure-volume index (PVI) tests. Simulation results suggest the following: 1) ICP dy namics may become unstable in patients with elevated CSF outflow resis tance and decreased intracranial compliance, provided cerebral autoreg ulation is efficient. Instability manifests itself with the occurrence of self-sustained plateau waves. 2) Moderate acute arterial hypotensi on may have completely different effects on ICP, depending on the valu e of model parameters. If physiological compensatory mechanisms (CSF c irculation and intracranial storage capacity) are efficient, acute hyp otension has only negligible effects on ICP and cerebral blood flow (C BF). If these compensatory mechanisms are poor, even modest hypotensio n may induce a large transient increase in ICP and a significant trans ient reduction in CBF, with risks of secondary brain damage. 3) The IC P response to a bolus injection (PVI test) is sharply affected, via ce rebral blood volume changes, by cerebral hemodynamics and autoregulati on. We suggest that PVI tests may be used to extract information not o nly on intracranial compliance and CSF circulation, but also on the st atus of mechanisms controlling CBF.