A Model of Pulsations in Communicating Hydrocephalus

Abstract

The traditional theory of communicating hydrocephalus has implicated the bulk flow component of CSF motion; that is, hydrocephalus is generally understood as an imbalance between CSF formation and absorption. The theory that the cause of communicating hydrocephalus is malabsorption of CSF at the arachnoid villi is not substantiated by experimental evidence or by physical reasoning. Flow-sensitive MRI has shown that nearly all CSF motion is pulsatile, and there is substantial evidence that hyperdynamic choroid plexus pulsations are necessary and sufficient for ventricular dilation in communicating hydrocephalus. We have developed a model of intracranial pulsations based on the analogy between the pulsatile motion of electrons in an electrical circuit and the pulsatile motion of blood and CSF in the cranium. Increased impedance to the flow of CSF pulsations in the subarachnoid space redistributes the flow of pulsations into the ventricular CSF and into the capillary and venous circulation. The salient features of communicating hydrocephalus, such as ventricular dilation, intracranial pressure waves, narrowing of the CSF-venous pressure gradient, diminished cerebral blood flow, elevated resistive index and malabsorption of CSF, emerge naturally from the model. We propose that communicating hydrocephalus is the result of a redistribution of CSF pulsations in the cranium.

Development of hydrocephalus and classical hypothesis of cerebrospinal fluid hydrodynamics: Facts and illusions

“…A similar hypothesis was proposed (Egnor et al, 2002) in which the cause of CH was the redistribution of CSF pulsations inside the cranium. The redistribution should be the result of the dissipation of arterial pulsation into the subarachnoid space, and the flow of the stronger arterial pulsations to the choroid plexus and capillary and venous circulation.…”

“…The explanation cannot be found in light of the classical hypothesis of CSF hydrodynamics, and therefore, in recently presented research of CH in adult rats with kaolin obstruction, Li et al (2008) concluded that the obtained experimental results do not support the theory by which mechanical obstruction of CSF absorption causes hydrocephalus. It seems that the development of CH could be a result of the redistribution of CSF pulsation in the cranium (Egnor et al, 2002;Greitz, 1993;Nagra et al, 2008) which significantly differs between the higher ventricular system pulsations and the lower subarachnoid space pulsations.…”

Effect of infusion tests on the dynamical properties of intracranial pressure in hydrocephalus

“…Consequently, the arterial pulse pressure transmitted to the capillary circulation would be stronger [45]. In this study, we observed that the state of intracranial hypertension induced by…”

“…The transmission of arterial pulsations through the CSF is also linked to the windkessel effect [45]. This mechanism involves a progressive dampening of arterial pulsations, mostly through the CSF, in order to reach the capillary bed of the brain as a nonpulsatile flow [45,46].…”

“…This mechanism involves a progressive dampening of arterial pulsations, mostly through the CSF, in order to reach the capillary bed of the brain as a nonpulsatile flow [45,46]. In normal cerebral blood flow this occurs as a consequence of a close coupling between CSF oscillations and arterial pulsations, which leads to a resonance state [46].…”