Lathyrism, one of the oldest neurotoxic diseases known to Man, results from excessive consumption of the chickling pea, Lathyrus sativus, and certain related species. Once prevalent throughout Europe, N. Africa, Middle East and parts of the Far East, the disease is presently restricted to India, Bangladesh and Ethiopia.
Lathyrism is a form of irreversible, non-progressive
spastic paraparesis associated with poorly understood degenerative changes in spinal cord. Domestic animals, notably the horse, also develop hindlimb
paralysis after prolonged feeding on lathyrus fodder. Experimental animal models of
lathyrism have been reported but none has been satisfactorily investigated, and concurrence between these experimental diseases and the human condition is unproven. The culpable agent in lathyrus species that precipitates
paralysis also is unknown. Current attention is focused on the
glutamate analog, beta-(N)-oxalyl-amino-
L-alanine acid (BOAA). While this compound is present in those lathyrus species that induce
spastic paraparesis and, in large doses, reportedly causes neuropathological changes similar to
glutamate neurotoxicity, there is little to compare these neuropathological changes with those found in human
lathyrism. Chronic primate feeding studies utilizing BOAA need to be carried out to determine whether this agent is responsible for human
lathyrism. Some species of lathyrus, notably Lathyrus odoratus, are unable to induce human
lathyrism but contain a compound,
beta-aminopropionitrile (
BAPN), that induces pathological changes in bone ("osteolathyrism") and blood vessels ("angiolathyrism") of experimental animals without damaging the nervous system. However, related compounds,
dimethylaminopropionitrile (DMAPN) and
beta, beta'-iminodipropionitrile (IDPN), are chronic
neurotoxins in humans and animals, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)