THE TROPICAL or nutritional ataxic neuropathy as seen in Nigerian patients is characterized by bilateral optic atrophy, bilateral nerve deafness, and predominantly posterior column myelopathy with or without peripheral neuropathy. The clinical, biochemical, and electrophysiologic features of this syndrome have been described,1 but there is no pathologic study of the disease in Nigeria. The natural history of the disease is one of slow progression, and there has been no fatal case among the patients studied. There is evidence that chronic cyanide intoxication from dietary sources may be an etiologic factor.1,2 The effects of chronic cyanide intoxication on the nervous system in man and in experimental animals have been well documented; these include, among other things, diffuse demyelination. It is believed that the tropical ataxic neuropathy is a demyelinating disease. The evidence for this is scanty and, to date, has been based on the findings of
Williams AO, Osuntokun BO. Peripheral Neuropathy in Tropical (Nutritional) Ataxia in Nigeria: Light and Electron Microscopic Study. Arch Neurol. 1969;21(5):475–492. doi:10.1001/archneur.1969.00480170047005
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