Fetal brain injury after maternal carbon monoxide intoxication: Clinical and neuropathologic aspects

Myron D. Ginsberg, Ronald E. Myers

Research output: Contribution to journalArticle

43 Scopus citations

Abstract

In a model of brain damage in the rhesus monkey fetus, carbon monoxide inhalation by the mother was used to produce graded fetal hypoxia. Four fetuses with arterial oxygen contents of 2.1 to 2.4 ml per 100 ml during the most severe insult hour appeared neurologically normal, and their brains contained no lesions. A single animal with an intermediate degree of hypoxia was moderately abnormal; its brain showed extensive necrosis of the basal ganglia. Four fetuses with arterial oxygen contents of 1.6 to 1.8 ml per 100 ml during the most severe insult hour showed profound clinical deficits, and on postmortem examination the brains were markedly swollen and showed an extensive hemorrhagic necrosis. The fetal brain exhibits a high threshold to the effects of sustained hypoxia, but once a critical level of deoxygenation is exceeded, extensive brain damage with early death results.

Original languageEnglish (US)
Pages (from-to)15-23
Number of pages9
JournalNeurology
Volume26
Issue number1
DOIs
StatePublished - Jan 1976

ASJC Scopus subject areas

  • Clinical Neurology

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