Experimental Carbon Monoxide Leucoencephalopathy in the Cat

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Abstract
After left common carotid artery ligation, cats were exposed to different CO gas concentrations for different periods, and the cerebral lesions were examined by light and electron microscopy at different intervals after exposure. Exposure to the higher concentration produced severe cardiopulmonary disturbances and resulted in light staining of the myelin, dilatation of the extracellular spaces, and swelling of astrocytes in the white matter on the ligated side. This change was maximal at 1 to 3 days after exposure and subsided within one week. In cats exposed longer, necrotic or cystic lesions were observed on the ligated side. Prolonged exposure to the lower concentration resulted in edema and reactive and degenerative axonal changes, followed by disintegration and phagocytosis of myelin sheaths, predominantly on the ligated side. Edema subsided within one week. Later, confluent patches of demyelination, such as are seen in Grinker's leucoencephalopathy, were observed on the ligated and, to a lesser degree, on the non-ligated side. These lesions in the cerebral white matter may be related to the degree and duration of anoxic or histotoxic anoxia, or both, induced secondarily by the effects of the CO gas on cardiopulmonary function, and to the survival intervals after exposure. We postulate that the pathological change in experimental Grinker's leucoencephalopathy may be due to Wallerian degeneration or a dying-back process, rather than to true demyelination.

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