The character of the neurological injury is not clear. The disease onset is associated with high intake of cyanide from a diet of mostly bitter cassava, which is low in protein, particularly sulfur amino acids. These are essential for the detoxification in the body of cyanide to thiocyanate, which is removed in the urine. A number of studies implicate the combination of high cyanide intake from bitter cassava and low intake of sulfur amino acids as the cause. It has now been shown that the month by month incidence of<unk>  is significantly correlated with the percentage of children with high urinary thiocyanate content, which is a measure of their cyanide intake. The importance of an adequate supply of protein sulfur amino acids is shown from three unrelated<unk>  epidemics in Mozambique, Tanzania and DRC. People of the same ethnic group living only 5 km away from those with<unk>  had near zero<unk>  prevalence, because in Mozambique they lived near the sea, in Tanzania they lived near Lake Victoria and had access to fish and in DRC they lived near the forest and had access to animal protein. The dose–response relationship between<unk>  incidence and cyanide intake, together with the prevention of<unk>  in many villages by reducing cyanide intake from cassava (see below) and the importance of sulfur amino acids in prevention of<unk> , shows that<unk>  is very likely due to high cyanide/low sulfur amino acid intake in a diet of bitter cassava.<unk>  does not occur unless these conditions are met, which occurs only in remote villages in six tropical African countries. The total number of reported cases up to 2009 was 6788, but most cases are never reported and there was an estimate of 100,000 cases in DRC alone in 2002.<unk>  is spreading geographically as cassava is being grown in new areas where there is little knowledge of processing methods to remove cyanogens.<unk>  epidemics occur due to war which causes disruption of life in poor villages and drought, when the plant increases the cyanogen content of roots 2–4 times and the cyanide content of cassava flour also increases greatly.<unk>  is also endemic in certain areas. Traditional methods of processing cassava to remove cyanogens consist of sun drying and heap fermentation in East Africa, which are inadequate in removal of cyanogens even in a year of normal rainfall. In Central Africa soaking (retting) of cassava roots in water for 4–5 days is adequate, but short soaking for 1–2 days leaves large amounts of cyanogens in flour and leads to<unk> . In West Africa a roasted product called garri is produced by a different method than that used to produce flour, which reduces the total cyanide content to 10–20 ppm. There are no reported cases of<unk>  west of Cameroon. However another neurological disease called tropical ataxic neuropathy (TAN), occurs amongst older people in West Africa (including south-west Nigeria, and also Tanzania, Uganda, Kenya, West Indies and South India) and is probably due to long term intake of cyanogens from cassava at a lower level than that needed to cause<unk> .
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Onyalai