This article is part of the supplement: 51st Annual Meeting of the Society for Research into Hydrocephalus and Spina Bifida

Oral presentation

VEGF-R2+ activation in the caudate: an adaptive angiogenic response to hypoxia in chronic hydrocephalus?

Abhishek Deshpande, Stephen M Dombrowski and Mark G Luciano

Department of Neurological Surgery, S-80, Pediatric and Congenital Neurological Surgery, CSF Physiology Laboratory, The Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA

author email corresponding author email

from 51^st Annual Meeting of the Society for Research into Hydrocephalus and Spina Bifida
Heidelberg, Germany. 27–30 June 2007

Cerebrospinal Fluid Research 2007, 4(Suppl 1):S2doi:10.1186/1743-8454-4-S1-S2

Published:	20 December 2007

First paragraph (this article has no abstract)

Chronic hydrocephalus (hydrocephalus) is characterised by impaired gait, and associated with decreased cerebral blood flow and oxygen delivery. We investigated the role of chronic hypoxia in the caudate which is a known motor nucleus involved in gait control. Also, increased ICP and vascular compression as the result of enlarged ventricles may be directly responsible for the gait problems in hydrocephalus. VEGF, which is triggered by ischemic/hypoxic events causes associated adaptive angiogenesis and also plays a critical role in neuronal protection. Previously, using an experimental model of hydrocephalus, we have shown decreased cerebral blood flow, oxygen delivery and increased capillary density. Here we investigated whether neuronal and glial VEGF-R2 expression is associated with an adaptive angiogenesis in the caudate.