Tropic ataxic neuropathy

Several investigations have suggested that consumption of residual cyanide in cassava products causes paralytic disorders, such as konzo (Spencer, 1994 Tylleskar, 1994) and tropical ataxic neuropathy (Osuntokun, 1994 Spencer, 1994). In both conditions, the pathogenic mechanism is still unknown. In addition, there are indications that the long-term effects of increased cyanide consumption might include diabetes (Akanji, 1994). 

Cyanide poisoning has been reported8 from eating chokecherries, bitter almonds, and apricot pits. In addition, cyanide is found in lima beans and cassava beans and roots. Cassava is a staple in certain countries and is blamed for the high incidence of tropical ataxic neuropathy in those areas. 

Despite the apparent effectiveness of traditional methods of preparing cassava dishes in reducing the cyanide content, there is evidence to indicate that a tropical disease known as ataxic neuropathy may be associated with the consumption of cassava (31, 32, 33). One of the metabolic routes whereby cyanide is detoxified involves the formation of thiocyanate as shown in Figure 7. Elevated levels of thiocyanate in blood plasma have been observed in individuals who suffered from ataxia neuropathy and who had a history of high consumption of cassava. Rats fed boiled or fermented cassava also showed high levels of thiocyanate in plasma and developed clinical signs of ataxia neuropathy. The mechanism whereby cyanide or its metabolic product, thiocyanate, are involved in the pathogenesis of this disease remains to be elucidated. 

Much of the toxicological interest in cyanide relating to mammals has focused on its rapid lethal action. However, its most widely distributed toxicologic problems are due to its toxicity from dietary, industrial, and environmental factors (Way 1981, 1984 Gee 1987 Marrs and Ballantyne 1987 Eisler 1991). Chronic exposure to cyanide is correlated with specific human diseases Nigerian nutritional neuropathy, Leber s optical atrophy, retrobulbar neuritis, pernicious anemia, tobacco amblyopia, cretinism, and ataxic tropical neuropathy (Towill etal. 1978 Way 1981 Sprine etal. 1982 Beminger et al. 1989 Ukhun and Dibie 1989). The effects of chronic cyanide intoxication are confounded by various nutritional factors, such as dietary deficiencies of sulfur-containing amino acids, proteins, and water-soluble vitamins (Way 1981). 

Makene WJ, Wilson J. 1972. Biochemical studies in Tanzanian patients with ataxic tropical neuropathy. J Neurol Neurosurg Psychiatry 35 31-33. 

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