Ventricular size in pseudotumor cerebri and the theory of impaired CSF absorption.
The purpose of this theoretical study is to determine whether the absence of ventricular enlargement in pseudotumor cerebri (PTC) is consistent with the theory that PTC is caused by reduced absorption of cerebrospinal fluid (CSF), either from increased outflow resistance at the arachnoid villi or from obstruction of the dural venous sinuses. We model the brain as a thick spherical shell of parenchyma, enclosing a CSF-filled ventricular system, and surrounded by a thin cerebral subarachnoid space (CSAS). We treat the parenchyma as a porous solid matrix, filled with interstitial fluid and blood vessels. We subject the model to a uniform increase in CSF pressure (CSFP) and solve the equations of poroelasticity for the resulting displacements of parenchymal tissue. The effect of a rise in CSFP on ventricular size depends on the response of the cerebral blood vessels and the degree to which the pia is tethered to the dura. If the cerebral vessels decrease in caliber with increasing CSFP, a rise in CSFP causes the ventricles to contract and the CSAS to expand if the pial surface is free to move inward, but causes slight ventricular enlargement if the pia is tethered to the dura. If, instead, the vessels dilate, the ventricles contract and the CSAS becomes effaced. Small, normal, or slightly enlarged ventricles in PTC are consistent with the theory of reduced CSF absorption.
Levine
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DN
Department of Neurology, New York University School of Medicine, RIRM-311, 400 East 34th Street, New York, NY 10016, USA.
D001932:Brain Neoplasms / Q000134:cerebrospinal fluid* / Q000473:pathology*; D002552:Cerebral Ventricles / Q000473:pathology*; D006801:Humans; D011559:Pseudotumor Cerebri / Q000134:cerebrospinal fluid* / Q000473:pathology*