Clinical and electrophysiological characteristics of the experimental neuropathy caused by p-bromophenylacetylurea

J. Jakobsen, E. H. Lambert, G. Carlson, S. Brimijoin

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

Doses of p-bromophenylacetylurea (BPAU) ranging from 50 to 400 mg/kg were administered i.p., in dimethyl sulfoxide, to adult male Sprague-Dawley rats. Age- and weight-matched control rats were treated with equivalent volumes of solvent. After a latent period of 7 days, the test rats developed signs of peripheral neuropathy. The signs were dose related and ranged from modest hind limb weakness to total hind limb paralysis. The forelimbs were affected only by the highest dosage. Even in severely disabled rats there was no statistically significant decrease in the conduction velocity or amplitude of action potentials evoked in tail nerve. However, the maximum amplitude of potentials evoked in the anterior tibial muscles by in vivo stimulation of the sciatic nerve decreased to less than half of normal by 15 days after treatment with BPAU, 200 mg/kg. Muscle action potentials remained depressed for at least 60 days after treatment. The decrease in amplitude of the compound muscle action potential was strongly correlated with the clinically scored degree of disability (r = -0.82). Direct muscle toxicity was discounted because in vitro studies of the extensor digitorum longus showed a response to direct electrical stimulation even when miniature end-plate potentials and end-plate potentials were absent. The clinical observations and electrophysiologic findings are consistent with the conclusion that the distal extremities of the longest neurons are the primary locus of pathology in BPAU neuropathy.

Original languageEnglish (US)
Pages (from-to)158-172
Number of pages15
JournalExperimental Neurology
Volume75
Issue number1
DOIs
StatePublished - Jan 1982

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience

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