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II. Clinical Aspects, Neuropathology, and Physiologic Correlation

Myron D. Ginsberg, MD; Ronald E. Myers, MD, PhD; Bernard F. McDonagh, PhD

Arch Neurol. 1974;30(3):209-216.

Abstract
Fourteen of 19 juvenile rhesus monkeys that had received 0.1% to 0.3% carbon monoxide (CO) for 75 to 325 minutes 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 five days. Another three 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 two 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.

Author Affiliations
Bethesda, Md

From the Laboratory of Perinatal Physiology, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Public Health Service, Dept of Health, Education, and Welfare, Bethesda, Md. Dr. Ginsberg is now with the Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia.

Footnotes
Accepted for publication Sept 11, 1973.

Read in part before the 97th annual meeting of the American Neurological Association, Chicago, June 14, 1972.

Reprint requests to Department of Neurology, Hospital of the University of Pennsylvania, 3400 Spruce St, Philadelphia 19104 (Dr. Ginsberg).

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