Summary
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.
Similar content being viewed by others
References
Commins BT, Lawther PJ (1965) A sensitive method for the determination of carboxyhaemoglobin in a finger prick sample of blood. Br. J Industr Med 22:139–143
Foncin JF, Le Beau J (1978) Myélinopathie par intoxication oxycarbonée. Neuropathologie ultrastructurale. Acta Neuropathol (Berl) 43:153–159
Ginsberg MD, Myers RE (1974) Experimental carbon monoxide encephalopathy in the primate. I. Physiologic and metabolic aspects. Arch Neurol 30:202–208
Ginsberg MD, Myers RE, McDonagh BF (1974) Experimental carbon monoxide encephalopathy in the primate. II. Clinical aspects, neuropathology, and physiologic correlation. Arch Neurol 30:201–216
Grinker RR (1925) Über einen Fall von Leuchtgasvergiftung mit doppelseitiger Pallidumerweichung und schwerer Degeneration des tieferen Großhirnmarklagers. Z Ges Neurol Psychiatr 98:433–456
Lapresley J, Fardeau M (1967) The central nervous system and carbon monoxide poisoning. II. Anatomical study of brain lesions following intoxication with carbon monoxide (22 cases). Prog Brain Res 24:31–74
Okeda R, Funata N, Takano T, Miyazaki Y, Higashino F, Yokoyama K, Manabe M (1981) The pathogenesis of carbon monoxide encephalopathy in the acute phase. Physiological and morphological correlation. Acta Neuropathol (Berl) 54:1–10
Okeda R, Funata N, Song S-J, Higashino F, Takano T, Yokoyama K (1982) Comparative study on pathogenesis of selective cerebral lesions in carbon monoxide poisoning and nitrogen hypoxia in cats. Acta neuropathol (Berl) 56:265–272
Palay SL, Palay CV (1974) Cerebellar cortex: cytology and organization. Springer, Berlin Heidelberg New York
Author information
Authors and Affiliations
Additional information
Supported by the Nissan Science Foundation and The Adult Disease Clinic Memorial Foundation
Rights and permissions
About this article
Cite this article
Okeda, R., Song, S.Y., Funta, N. et al. An experimental study of the pathogenesis of Grinker's myelinopathy in carbon monoxide intoxication. Acta Neuropathol 59, 200–206 (1983). https://doi.org/10.1007/BF00703204
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF00703204