An experimental study of the pathogenesis of Grinker's myelinopathy in carbon monoxide intoxication
- Cite this article as:
- Okeda, R., Song, S.-., Funta, N. et al. Acta Neuropathol (1983) 59: 200. doi:10.1007/BF00703204
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The change of Grinker's myelinopathy in carbon monoxide (CO) poisoning occurs not only in patients with the clinically diphasic type of CO-poisoning but is also found around the destructive lesions in patients with the acute form of CO-poisoning. The distribution of this myelinopathy is similar to that of the acute form of CO-poisoning. The cerebral change of experimental acute CO-encephalopathy is a sort of hypoxic-ischemic encephalopathy. Based on these findings an experiment was conducted to analyze the pathogenesis of Grinker's myelinopathy as follows: 43 cats were separated into four groups. Group A was subjected at first to inhalation of 0.3% CO/Air gas lasting for 2 h and then 2 or 3 days later to hypotension ranging from 60 to 90mm Hg for 1 h under the state of slight hypoxia (PaO2: 50–80 mm Hg). Group B was also exposed to CO-gas and hypotension similarly to Group A, but hypoxia was not imposed during hypotension. Groups C and D were subjected only to hypotension and to CO-gas, respectively. Myelin pallor was found selectively in the cerebral white matter of all cats of Group A and 18 of the 23 cats of Group B, and the subcortical U-fibers and perivascular myelin were spared. This was similar to Grinker's myelinopathy. The myelin pallor was investigated by light and electron microscopy and considered to be due to edema and separation of the myelin sheath and axon. In Groups C and D such a change was either absent or only slight. The conditions necessary for the onset of Grinker's myelinopathy were discussed, and it was proposed that the patients recovering from acute CO-poisoning should be kept in hospital for several weeks so that their blood pressure and blood gas could be monitored continuously.