lathyrism/manihot esculenta

Konzo (caused by consumption of improperly processed cassava, Manihot esculenta) and neurolathyrism (caused by prolonged overconsumption of grass pea, Lathyrus sativus) are two distinct non-infectious upper motor neurone diseases with identical clinical symptoms of spastic paraparesis of the legs.

Although both konzo and neurolathyrism are diseases associated with diet, we know surprising little about the diets of the groups at risk. The objective of this paper is to discuss methods for assessing dietary intake in populations at risk for konzo and lathyrism. These methods include weighed food

Both neurolathyrism and konzo are associated with the nutritional dependence of human populations on a single plant food. These diseases express themselves as chronic disorders of upper motor neurones, leading to signs and symptoms that characterise amyotrophic lateral sclerosis (motor neurone

Neurological disorders have been reported from parts of Africa with protein-deficient populations and attributed to cyanide (CN-) exposure from prolonged dietary use of cassava, a cyanophoric plant. Cyanide is normally metabolized to thiocyanate (SCN-) by the sulfur-dependent enzyme rhodanese.

Konzo and lathyrism are associated with consumption of cassava and grass pea, respectively. Cassava consumption has also been associated with a third disease, tropical ataxic neuropathy (TAN). This review presents a new unifying hypothesis on the causative agents for these diseases: namely, that

Epidemics of neurotoxic disease in developing regions of the world are often associated with dietary dependence on plant components with inherent toxic potential or which have spoiled and become contaminated with mycotoxins. Diseases triggered by plant toxins include lathyrism and cassavism, types

Environmental chemicals involved in the etiology of human neurodegenerative disorders are challenging to identify. Described here is research designed to determine the etiology and molecular pathogenesis of nerve cell degeneration in two little known corticomotoneuronal diseases with established

Tropical neurology began less than two centuries ago. Consumption of dietary toxins predominated at the beginning and gave birth to the geographic entity. The story moved from lathyrism through Jamaican neuropathy to cassava-induced epidemic neuropathy, which was contrasted with Konzo, also

Tropical myeloneuropathies include tropical ataxic neuropathy and tropical spastic paraparesis. These disorders occur in geographic isolates in several developing countries and are associated with malnutrition, cyanide intoxication from cassava consumption, tropical malabsorption (TM), vegetarian

Since the beginning of this century, the concept of tropical neuromyelopathy (T. N. M.) was progressively elaborated in tropical areas. This disorder is constituted by three main clinical syndromes (e.g.: polyneuropathy, spastic paraplegia, ataxia). Abnormal clinical, electrophysiological and

The epidemiology of tropical spastic paraparesis/human T lymphotropic virus I (HTLV-I)-associated myelopathy (TSP/HAM) is frequently inconsistent and suggests environmental factors in the etiology of these syndromes. The neuropathology corresponds to a toxometabolic or autoimmune process and

Although neurotoxic models for progressive degeneration of both the anterior horn cell and the Betz cell do not exist, (neuro)lathyrism and neurocassavism (konzo) are examples of self limiting neurotoxic disorders that predominantly target the Betz cell. Both disorders are caused by the continuous

A large number of causal agents produce spinal cord lesions in the tropics. Most etiologies found in temperate regions also occur in the tropics including trauma, herniated discs, tumors, epidural abscess, and congenital malformations. However, infectious and nutritional disorders occur with higher

Experimental cyanide exposure in animals causes demyelination and circumstantial clinical and laboratory evidence suggest that there are human parallels. In Leber's hereditary optic atrophy there appears to be a defect in the conversion of cyanide to thiocyanate because of deficient rhodanese

BACKGROUND A wide range of plants, seeds and fruits used for nutritional and medicinal purposes can give rise to neurotoxic symptoms. METHODS We review the neurological pathology associated with the acute or chronic consumption of plants, seeds and fruits in human beings and in animals. Of the