|Author: ||B. O. Osuntokun|
|Keywords: ||Cassava, Manihot esculenta, clinical neurology, epidemiology|
In the 1930s, Moore described a syndrome of visual loss, glossitis, angular stomatitis and eczema of the scrotum in adolescent boys in an institution in Nigeria.
The diet based on cassava was blamed for the problem because the condition improved when the cassava component of the diet was reduced.
Clark (1936) first attributed the cause specifically to the high content of cyanogens in cassava.
Extensive clinical, biochemical and epidemiological studies in Nigeria between 1966 and 1980 produced a wealth of circumstantial evidence to support the hypothesis that dietary cyanogens were the most important causal factor of chronic cyanide intoxication.
The geographic distribution and high prevalence of the disease corresponded with the consumption of large amounts of cassava.
In patients, plasma thiocyanate, cyanide and urinary thiocyanate levels were raised but these levels fell on a cassava-free diet.
Plasma levels of sulfur-containing amino-acids were reduced.
Liver rhodanese, the major enzyme for detoxifying cyanide, was normal.
Vitamin B12 metabolism was normal and plasma concentrations of most other vitamins, were normal; levels of thiamine and riboflavin were low.
Not all members of vulnerable populations succumb to the disease; mechanisms of genetic predisposition, and reasons for the apparent long latency between exposure and onset of symptoms, are unknown.
The prevalence of the disease appears to have fallen in some parts of south-western Nigeria following substitution of cassava by other foods as the staple diet.
Since 1981, epidemics of a cassava-related acute spastic paraparesis named konzo have been reported in drought-stricken areas of Mozambique, Zaire and Tanzania.
It would appear that severe acute or sub-acute chronic cyanide intoxication causes acute or sub-acute spastic paraparesis; a less severe but chronic cyanide intoxication causes a more chronic degenerative neuropathy.
The cassava-induced neurological syndromes are quite different from HTLV-1-associated myelopathy which has been described in various parts of the Tropics and in non-endemic areas in temperate climates.
There is need for further experimental investigation of the pathogenesis of the disease; especially the possibility that cyanide causes neuropathologic lesions by interalia potentiating the toxicity of endogenous excitotoxic amino-acids.
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