Cyanide holds great interest for neuropathologists because of its strong tendency to damage cerebral white matter selectively, both in experimental (1ndash;7) and in accidental (8) poisoning. In fact, the lesions of cyanide encephalopathy have been compared to those of Schilder's disease and Marchiafava-Bignami disease. Experimental cyanide encephalopathy has been studied for many years by light microscopy, and recent publications have described observations made by metallic impregnation and enzyme histochemistry (6, 7). Neuronal changes have been studied by electron microscopy (9). Nevertheless, certain problems arc unresolved. These include the nature and precise localization of the tissue spaces that give cyanide lesions in white matter a fenestrated appearance, the state of the axons, the role of the oligodendrocytes, the question of selectivity for myelin, and the time needed for lesion formation. The present study utilized the electron microscope to answer some of these questions. For this study, the older technics of repeated injections of potassium or sodium cyanide were inadequate because of the variable yield of lesions and the inability to time the onset of lesion formation. On the other hand, the administration of hydrogen cyanide by the respiratory route for a single short period yielded lesions of exactly timed onset, in a predetermined location (corpus callosum), in nearly all of the animals (5). There is no basic difference in neurotoxic effect between hydrogen cyanide and cyanide salts, inasmuch as the lesions produced by a single hydrogen cyanide exposure have been duplicated exactly by a single treatment with a cyanide salt under appropriate conditions (10).
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