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  • Oral presentation
  • Open Access

Lymphatic cerebrospinal fluid absorption is impaired in a kaolin-induced hydrocephalus model in the rat

  • 1,
  • 2,
  • 2,
  • 2,
  • 3 and
  • 1Email author
Cerebrospinal Fluid Research20074 (Suppl 1) :S43

  • Published:


  • Hydrocephalus
  • Human Serum Albumin
  • Kaolin
  • Evans Ratio
  • Basal Cistern


It has been assumed that the pathogenesis of hydrocephalus includes a cerebrospinal fluid (CSF) absorption deficit. Since a significant portion of CSF absorption occurs into extracranial lymphatic vessels located in the olfactory turbinates, the purpose of this study was to determine if CSF absorption was compromised at this location in a kaolin-induced hydrocephalus model in rats.

Materials and methods

Kaolin (n = 10) or saline as control (n = 9) was introduced into the basal cisterns of Sprague Dawley rats and the development of hydrocephalus was assessed using MRI. The degree of ventriculomegaly was calculated for each animal as the Evans ratio. Human serum albumin (125I-HSA) was injected into the lateral ventricles. The enrichment of 125I-HSA in the olfactory turbinates at 30 minutes post injection provided an estimate of CSF transport through the cribriform plate into the nasal lymphatic vessels.


Injection of kaolin produced hydrocephalus in the majority of animals. The average Evans ratio in the kaolin group (0.48 ± 0.02) was significantly greater than that in the saline injected animals (0.35 ± 0.01; p = 0.0042). The CSF tracer enrichment in the olfactory turbinates (expressed as percent injected/gm tissue) in the kaolin rats averaged 0.99 ± 0.39 and was significantly lower than that measured in the saline controls (5.86 ± 0.32; p = 0.0019). A plot of the Evans ratio versus lymphatic transport revealed a significant negative correlation (p = 0.0002) with the largest degree of ventriculomegaly associated with the lowest levels of lymphatic CSF uptake.


We conclude that lymphatic CSF absorption pathways are compromised in a kaolin hydrocephalus model suggesting an important role for extracranial lymphatic vessels in this CSF disorder.

Authors’ Affiliations

Department of Laboratory Medicine and Pathobiology, Sunnybrook HSC, University of Toronto, Toronto, M4N 3M5, Canada
Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI 48201, USA
Department of Radiology, State University of New York at Stony Brook, Stony Brook, NY 11794-8460, USA


© Nagra et al; licensee BioMed Central Ltd. 2007

This article is published under license to BioMed Central Ltd.