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, A. Ludolph, D. N. Roy, H. H. Schaumburg, P. S. Spencer

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

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, beta'-iminodipropionitrile (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.

Original languageEnglish (US)
Pages (from-to)435-442
Number of pages8
JournalNeurology
Volume38
Issue number3
StatePublished - 1988

Fingerprint

Lathyrus
Motor Neuron Disease
Macaca
Lathyrism
Primates
Diet
Peas
Cicer
Cerebellar Diseases
Efferent Pathways
Macaca fascicularis
Poaceae
Fabaceae
Haplorhini

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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. / Hugon, J.; Ludolph, A.; Roy, D. N.; Schaumburg, H. H.; Spencer, P. S.

In: Neurology, Vol. 38, No. 3, 1988, p. 435-442.

Research output: Contribution to journalArticle

@article{98de59ead5724926a14c15ced4a5b4fb,
title = "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",
abstract = "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, beta'-iminodipropionitrile (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.",
author = "J. Hugon and A. Ludolph and Roy, {D. N.} and Schaumburg, {H. H.} and Spencer, {P. S.}",
year = "1988",
language = "English (US)",
volume = "38",
pages = "435--442",
journal = "Neurology",
issn = "0028-3878",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - 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

AU - Hugon, J.

AU - Ludolph, A.

AU - Roy, D. N.

AU - Schaumburg, H. H.

AU - Spencer, P. S.

PY - 1988

Y1 - 1988

N2 - 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, beta'-iminodipropionitrile (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.

AB - 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, beta'-iminodipropionitrile (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.

UR - http://www.scopus.com/inward/record.url?scp=0023833862&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023833862&partnerID=8YFLogxK

M3 - Article

C2 - 3347349

AN - SCOPUS:0023833862

VL - 38

SP - 435

EP - 442

JO - Neurology

JF - Neurology

SN - 0028-3878

IS - 3

ER -