Abstract
In susceptible individuals, one of a variety of known or unknown precipitants affects the arachnoid villi so as to produce a large increase in CSF outflow resistance, R a. This increase in R a raises CSF pressure (CSFP), which rise provokes a redistribution of arteriovenous pressures across the cerebrovascular bed. The end result is a measurable increase in cerebral blood volume, compression of the ventricular system and compromise of the convexity subarachnoid space, which further increases CSF outflow resistance. Ultimately, a new steady state CSFP is attained.
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