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NEUROLOGY 1988;38:435
© 1988 American Academy of Neurology

Studies on the etiology and pathogenesis of motor neuron diseases. II.

Clinical and electrophysiologic features of pyramidal dysfunction in macaques fed Lathyrus sativus and IDPN

J. Hugon, MD, A. Ludolph, MD, D. N. Roy, DSc, H. H. Schaumburg, MD and P. S. Spencer, PhD

From the Institute of Neurotoxicology (Drs. Hugon, Ludolph, Roy, Schaumburg, and Spencer), Departments of Neuroscience (Dr. Spencer), Neurology (Dr. Schaumburg), and Pathology (Drs. Schaumburg and Spencer), Albert Einstein College of Medicine, Bronx, NY; the Department of Neurology (Dr. Hugon), Limoges University Hospital, Limoges, France; and the Department of Neurology (Dr. Ludolph), University of Muenster, Muenster, West Germany.

A primate model of lathyrism has been produced in well-nourished male cynomolgus monkeys chronically fed a fortified diet composed of Lathyrus sativus (chickling or grass pea) and given daily per os an alcoholic extract of this legume. Animals given a diet of non-neurotoxic Cicer arietinum (chick pea) cross-matched with the nutritional properties of the experimental diet served as controls. Another group of animals received the same diet and oral doses of beta, betá-iminodipro-pionitrile (IDPN), a reference compound that has been termed an "experimental neurolathyrogen. " Monkeys fed Lathyrus developed clinical and electrophysiologic evidence of corticospinal deficits after 3 to 10 months of feeding. Animals administered IDPN showed clinical and/or electrophysiologic changes in the PNS and CNS motor and sensory pathways, and signs of cerebellar dysfunction. Since the two primate disorders are separable on clinical and electrophysiologic grounds, further use of the term "experimental neurolathyrogen" to describe the neurotoxic properties of IDPN seems inappropriate. These findings demonstrate the feasibility of developing a model of early human lathyrism in adequately nourished nonhuman primates.

Address correspondence and reprint requests to Dr. Spencer, Institute of Neurotoxicology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461.

Supported by U. S. Public Health Services grant NS 19611, the Fondation pour la Recherche Médicale, Paris, France, and Deutsche Forschungsgemeinschaft, Bonn, West Germany.

Received March 24, 1986. Accepted for publication in final form June 11, 1987.






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