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Neonatal status convulsivus, spongiform encephalopathy, and low activity of Na+/K(+)-ATPase in the brain.

Authors
  • Renkawek, K
  • Renier, W O
  • de Pont, J J
  • Vogels, O J
  • Gabreëls, F J
Type
Published Article
Journal
Epilepsia
Publication Date
Jan 01, 1992
Volume
33
Issue
1
Pages
58–64
Identifiers
PMID: 1310285
Source
Medline
License
Unknown

Abstract

The first and second child of a family died from neonatal seizures with no detectable brain malformation, metabolic, infectious, or chromosomal etiology. Neuropathological examination of the brain of the second child who died at 11 days revealed a widespread spongy state and a selective vulnerability of the astrocytes characterized by numerous enlarged bare astrocytic nuclei and different forms of astrocyte degeneration. The glial cells were strongly positive for glial fibrillary acidic protein and vimentin immunocytochemical reaction. Cortical measurement of Na+/K(+)-ATPase revealed very low enzyme activity. We hypothesize that a defect of Na+/K(+)-ATPase of the astrocytes could be the common pathogenetic factor for the congenital status convulsivus and for the spongy state.

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