Experimental Carbon Monoxide Encephalopathy in the Primate: II. Clinical Aspects, Neuropathology, and Physiologic Correlation

Myron D. Ginsberg, Ronald E. Myers, Bernard F. Mcdonagh

Research output: Contribution to journalArticle

107 Scopus citations

Abstract

Fourteen of 19 juvenile rhesus monkeys that had received 0.1% to 0.3% carbon monoxide (CO) for 75 to 325 min survived the intoxication and were studied clinically and pathologically. Three animals suffered severe deficits, including limb paralysis, alterations of muscle tone, blindness, and deafness. In one case, the deficit evolved following a delay of 5 days. Another 3 monkeys exhibited only mild motor disturbances. The salient brain lesion was a bilaterally symmetrical, destructive leukoencephalopathy, most extensive in the frontal and posterior parietal regions. Lesions of the globus pallidus and of the hippocampus each occurred in 2 brains. The size of the white matter lesions correlated with the degree of metabolic acidosis and systolic hypotension sustained during CO exposure but not with the extent of hypoxia per se, suggesting that the lesion, while requiring hypoxia as a precondition, was crucially determined by other factors.

Original languageEnglish (US)
Pages (from-to)209-216
Number of pages8
JournalArchives of neurology
Volume30
Issue number3
DOIs
StatePublished - Mar 1974
Externally publishedYes

ASJC Scopus subject areas

  • Arts and Humanities (miscellaneous)
  • Clinical Neurology

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