{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T16:17:49Z","timestamp":1788884269814,"version":"build-2803163510"},"reference-count":27,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JNS"],"published-print":{"date-parts":[[2013,12]]},"abstract":"<jats:p>Symptomatic shunt malfunction without ventricular enlargement is known as slit ventricle syndrome (SVS). Patients presenting with this syndrome are not a homogeneous group. Of the 5 different types classified by Rekate, Type 1 is caused by CSF overdrainage and is associated with low pressures; Types 2 and 3 are associated with shunt blockage and elevated CSF pressures; Type 4 is cephalocranial disproportion that increases brain parenchymal pressure but not CSF pressure; and Type 5 is headache unrelated to shunt function. The low and normal CSF pressure types are relatively well understood, but the high-pressure forms are more problematic. In the high-pressure forms of SVS it is said that the lack of ventricular dilation is related to a reduction in brain compliance analogous to idiopathic intracranial hypertension or pseudotumor cerebri. Despite this, there is little evidence in the literature to support this conjecture. With this in mind, 3 cases of SVS associated with elevated CSF pressure are presented. The MR venogram findings and hemodynamics of these 3 cases are shown to be identical to those of pseudotumor cerebri. A literature review indicates that an underlying venous impairment may be functioning in the patients who re-present with small ventricles following shunt malfunction.<\/jats:p>","DOI":"10.3171\/2013.7.jns13390","type":"journal-article","created":{"date-parts":[[2013,8,30]],"date-time":"2013-08-30T14:02:29Z","timestamp":1377871349000},"page":"1503-1510","source":"Crossref","is-referenced-by-count":32,"title":["Hypertensive slit ventricle syndrome: pseudotumor cerebri with a malfunctioning shunt?"],"prefix":"10.3171","volume":"119","author":[{"given":"Grant A.","family":"Bateman","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1754","reference":[{"key":"b1-jns13390","series-title":"J Clin Neurosci","doi-asserted-by":"publisher","first-page":"402","DOI":"10.1016\/j.jocn.2007.03.018","article-title":"Arterial inflow and venous outflow in idiopathic intracranial hypertension associated with venous outflow stenoses","volume":"15","author":"Bateman","year":"2008"},{"key":"b2-jns13390","series-title":"AJNR Am J Neuroradiol","first-page":"1180","article-title":"Vascular hydraulics associated with idiopathic and secondary intracranial hypertension","volume":"23","author":"Bateman","year":"2002"},{"issue":"6 Suppl","key":"b3-jns13390","series-title":"J Neurosurg","first-page":"439","article-title":"Idiopathic hydrocephalus in children and idiopathic intracranial hypertension in adults: two manifestations of the same pathophysiological process?","volume":"107","author":"Bateman","year":"2007"},{"key":"b4-jns13390","series-title":"J Neurosurg","doi-asserted-by":"publisher","first-page":"446","DOI":"10.3171\/2008.6.17609","article-title":"A mathematical model of idiopathic intracranial hypertension incorporating increased arterial inflow and variable venous outflow collapsibility. 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