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Acute and Chronic Cerebral White Matter Damage in Neonatal Hydrocephalus

Published online by Cambridge University Press:  18 September 2015

Marc R. Del Bigio ,
Marcia C. da Silva ,
James M. Drake  and
Ursula I. Tuor
Marc R. Del Bigio
Affiliation:
Neuropathology, the Hospital for Sick Children and University of Toronto, Toronto
Marcia C. da Silva
Affiliation:
Neurosurgery, the Hospital for Sick Children and University of Toronto, Toronto
James M. Drake*
Affiliation:
Neurosurgery, the Hospital for Sick Children and University of Toronto, Toronto
Ursula I. Tuor
Affiliation:
Neonatal Research, the Hospital for Sick Children and University of Toronto, Toronto
*
Division of Neurosurgery, Hospital for Sick Children, 555 University Avenu, Toronto, Ontario, Canada M5G 1X8
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Abstract:

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The neonatal cat model of kaolin-induced hydrocephalus is associated with progressive and severe ventriculomegaly. In this experiment we studied the evolution of the histopathological changes in hydrocephalic (n = 23) cats from 5–168 days after the induction of hydrocephalus along with age-matched controls (n = 10). In the periventricular white matter, extracellular edema and axonal damage were present within days of the onset of hydrocephalus. This was followed by reactive gliosis, white matter atrophy, and in some animals gross cavitation of the white matter. Even in the chronic, apparently compensated state there was ongoing glial cell death. Six cats were shunted an average of 23.6 ± 6.5 days after the induction of hydrocephalus because they were no longer able to feed independently. In spite of clinical improvement the white matter changes persisted. Overt cortical changes were minimal except where areas of white matter destruction encroached upon the deep layers. The white matter changes are very similar to those seen in periventricular leukomalacia and suggest that ischemia plays a role in neonatal brain injury caused by hydrocephalus.

Résumé:

Résumé:

Atteinte cérébrale aiguë et chronique de la substance blanche dans l’hydrocéphalie néonatale. Dans le modèle animal de l’hydrocéphalie induite par le kaolin chez le chat, on observe une ventriculomégalie progressive sévère. Nous avons étudié l’évolution des changements histopathologiques chez des chats hydrocéphalie (n = 23) et des contrôles appariés pour l’âge (n = 10), sur une période de 5 à 168 jours après l’induction de l’hydrocéphalie. L’oedème extracellulaire et l’atteinte axonale au niveau de la substance blanche périventriculaire étaient présents dans les jours suivant le début de l’hydrocéphalie. Ces changements étaient suivis d’une gliose réactionnelle, d’atrophie de la substance blanche et, chez certains animaux, de la formation de cavités importantes dans la substance blanche. Même à l’état chronique apparemment compensé, le processus de mort cellulaire se poursuivait au niveau des cellules gliales. Six chats ont subi une dérivation, en moyenne 23.6 ± 6.5 jours après l’induction de l’hydrocéphalie, parce qu’ils ne pouvaient plus se nourrir. Les modifications de la substance blanche ont persisté malgré l’amélioration clinique. Les changements corticaux étaient minimes, sauf dans les régions où la destruction de la substance blanche empiétait sur les couches profondes. Les modifications de la substance blache sont très semblables à celles observées dans la leucomalacie périventriculaire, ce qui suggère que l’ischémie joue un rôle dans les lésions cérébrale néonatales causées par l’hydrocéphalie.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 21 , Issue 4 , November 1994 , pp. 299 - 305
Copyright
Copyright © Canadian Neurological Sciences Federation 1994

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