Abstract
The intracranial pressure is implicated in many homeostatic processes in the brain and is a fundamental parameter in several diseases such as e.g. idiopathic normal pressure hydrocephalus. The presence of a small but persistent pulsatile intracranial pulsatile transmantle pressure gradient (on the order of a few mmHg/m at peak) has recently been demonstrated in hydrocephalus subjects. A key question is whether pulsatile intracranial pressure and displacements can be induced by a small pressure gradient originating from the brain surface alone. In this study, we model the brain parenchyma as either a linearly elastic or a poroelastic medium, and impose a pulsatile pressure gradient acting between the ventricular and the pial surfaces but no additional external forces. Using this high-resolution physics-based model, we use in vivo pulsatile pressure gradients from subjects with idiopathic normal pressure hydrocephalus to compute parenchyma displacement, volume change, fluid pressure, and fluid flux. The resulting displacement field is pulsatile and in qualitatively and quantitatively good agreement with the literature, both with elastic and poroelastic models. However, the pulsatile forces on the boundaries are not sufficient for pressure pulse propagation through the brain parenchyma. Our results suggest that pressure differences at the brain surface, originating e.g. from pulsating arteries surrounding the brain, are not alone sufficient to drive interstitial fluid flow within the brain parenchyma and that potential pressure gradients found within the parenchyma rather arise from a large portion of the blood vessel network, including smaller blood vessels within the brain parenchyma itself.