Abstract

Hydrocephalus can be obstructive or communicating. In cases of communicating hydrocephalus, patients will typically have enlarged brain ventricles. It has long been thought that the reason for this is obstruction to the outflow of cerebrospinal fluid from the subarachnoid space, which also results in raised intracranial pressure (ICP). However, there are several clinical and anatomic observations that are not well explained by this idea. These are for example, the conditions of Normal pressure hydrocephalus (NPH) which has normal ICP but ventriculomegaly, and idiopathic intracranial hypertension (IIH) which has raised ICP but normal sized ventricles. This hypothesis states that the mechanism for raised ICP and large ventricles seen in communicating hydrocephalus (ventriculomegaly) are different and seeks to explain the cause of ventriculomegaly using illustrative examples. It also suggests explanations for why ventriculomegaly occurs in NPH, infectious or carcinomatous meningitis, but is absent in IIH, or dural venous sinus thrombosis. Based on operative neurosurgical observations it states that the arachnoid membranes in the basal cisterns serve as part of a directional CSF flow mechanism consisting of fluid diodes, or “Tesla valves” of arachnoid membrane, containing CSF that is propelled by brain pulsations from the point of exit from the 4th ventricle to its points of absorption. This hypothesis suggests explanations for the physiologic appearance of a near uniform subarachnoid space, as well as the occurrence of the syndrome of the trephined and external hydrocephalus seen following a decompressive craniectomy. Also suggested are avenues of further research testing with MRI phase contrast CSF flow studies, classification of anatomic and peri-operative observations and rationale for creation of novel experiments to test the hypothesis, and aid diagnosis and treatment of a number of cranial CSF disorders.

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