Abstract

Based on a proposed pathophysiology of slit ventricle syndrome (SVS), we have hypothesized that lumboperitoneal shunting exerts effects in SVS patients by increasing the buffering capacity for raised intracranial pressure (ICP) via an increase in cerebrospinal fluid drainage from the cerebral subarachnoid space (SAS). We describe 3 SVS patients with patent lumbar subarachnoid drainage but under-functioning ventriculoperitoneal shunts (VPS) who presented with ventriculomegaly (not SVS), and persistence of shunt malfunction like symptoms. Revision of the VPS resulted in complete resolution of symptoms despite a finding of low pressure in the ventricular space. This supports the hypothesis that lumboperitoneal shunting preferentially drains the SAS over the intraventricular space and in these cases allows the ‘SVS’ ventricles to enlarge by creating a pressure gradient from ventricles to SAS through the cortical mantle.

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