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  • Open Access

In moderate communicating hydrocephalus of human fetuses, ependymal denudation is a common feature that may result in abnormal neurogenesis

  • 1,
  • 1Email author,
  • 1,
  • 2,
  • 3,
  • 4 and
  • 1
Cerebrospinal Fluid Research20052 (Suppl 1) :S5

  • Published:


  • Hydrocephalus
  • Lateral Ventricle
  • Ventricular Cavity
  • Cerebral Aqueduct
  • Denude Area


Recent investigations carried out in natural and experimental mutant mice have provided strong evidence that a primary alteration of the ependymal cell lineage triggers a moderate foetal hydrocephalus [1, 2]. In human cases of hydrocephalus, however, ependymal loss has been regarded as resulting from the ventricular dilatation due to the accumulation of cerebrospinal fluid [3].

Materials and methods

The present investigation was carried out in 16–40 week old human foetuses with a communicating hydrocephalus and displaying a moderate dilatation of the ventricular cavities (n = 8), and foetuses of similar ages with no neuropathological alterations (n = 15). Paraffin sections throughout the walls of the cerebral aqueduct and lateral ventricles were processed for lectin binding and immunocytochemistry using ependyma, astroglia, neuroblasts and macrophague markers.


Large areas of ependymal denudation were found in the aqueduct and lateral ventricles of all foetuses developing a communicating hydrocephalus. At variance, no ependymal detachment was observed in non-hydrocephalic foetuses. In the youngest foetuses with hydrocephalus, denuded areas were not covered by astrocytes or other organized cell elements, leaving the neuropile directly exposed to the ventricular lumen. The area devoid of ependyma increased as the foetus developed. In the oldest foetuses studied, the denuded areas of the lateral ventricles were lined by a dense plexus of astrocytes. Under the denuded surface the presence of ependymal rosettes was observed. In the denuded areas of the lateral ventricles of hydrocephalic foetuses it was found (i) a loss of the germinal ependymal zone, (ii) disorganization of the subventricular zone and, (iii) abnormal migration of neuroblasts into the ventricular cavity.


The early loss of ependyma in human hydrocephalic foetuses would be associated to both, the hydrocephalic process and an abnormal migration of neuroblasts.



Supported by grants from FIS, PI 030756 and Red CIEN C/0306, Instituto de Salud Carlos III, and Servicio Andaluz de Salud, Spain to JMP-F; and Fondecyt 1030256, Chile to EMR.

Authors’ Affiliations

Departamento de Biología Celular, Genética y Fisiología, Universidad de Málaga, E-29071 Málaga, Spain
Servicio de Anatomía Patológica Hospital Carlos Haya, Málaga, Spain
Servicio de Neurocirugía Hospital Carlos Haya, Málaga, Spain
Instituto de Histología y Patología, Universidad Austral de Chile, Valdivia, Chile


  1. Jiménez AJ, Tomé M, Páez P, Wagner C, Rodríguez S, Fernández-Llebrez P, Rodríguez EM, Pérez-Fígares JM: A programmed ependymal denudation occurring during the embryonic life precedes development of congenital hydrocephalus in the mutant mouse hyh. J Neuropathol Exp Neurol. 2001, 60: 1105-1119.PubMedGoogle Scholar
  2. Davy BE, Robinson ML: Congenital hydrocephalus in hy3 mice is caused by a frameshift mutation in Hydin, a large novel gene. Hum Mol Genet. 2003, 12: 1163-1170. 10.1093/hmg/ddg122.View ArticlePubMedGoogle Scholar
  3. Sarnat HB: Ependymal reactions to injury. A review. J Neuropathol Exp Neurol. 1995, 54: 1-15.View ArticlePubMedGoogle Scholar


© The Author(s) 2005

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