De- chaume and Chambon, 1947) by the repeated subcutaneous injection of cyanides.Some have considered these lesions to show features similar to the spontaneous demyelinating diseases occurring in man and possibly in certain other mammalia, such as the monkey, sheep, dog, horse, moose, and fox.The present report describes similar lesions produced by this means experimentally in the rat, and contrasts them with the lesions which resulted from experimental chronic carbon monoxide poison- ing, and from experimental capillary embolism and disseminated capillary thrombosis which were successfully produced, perhaps for the first time, in this species.These cyanide lesions in the rat develop only in the central white matter of the cerebrum and show a certain selectively demyelinating character unlike any of the other lesions achieved in this animal in these experiments.They have a remarkable histo- logical similarity to the rare Marchiafava-Bignami disease of man, and indeed some similarity to Schilder's disease.This experimental cyanide lesion in the rat brain is the only spontaneous or experimental lesion in this animal which is at all reminiscent of demyelinating disease.Furthermore, the rat appears to be quite insusceptible to the " experimental ' allergic' encephalomyelitis " which we have studied in the guinea-pig, and it is apparently completely resistant to hypersensitization lesions like -the cerebral Arthus phenomenon (Lumsden, 1949).The production, therefore, of this entirely artificial demyelinating disease in the rat, bearing as it does such a close similarity to that produced in the same way in the other species mentioned, suggests the existence of some fundamental biological mechanism in the brains of mammalia.Though it is much too premature as yet to say what this mechanism B is, the obvious inference is that it may be an enzymatic mechanism peculiar to the oligodendro- cyte-myelin sheath complex.
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CHARLES E. LUMSDEN (1950) studied this question.