Conduction abnormalities induced by sera of patients with multifocal motor neuropathy and anti-GM1 antibodies. Academic Article uri icon

Overview

abstract

  • Increased titers of anti-GM1 antibodies have been associated with motor neuron disease and motor neuropathy with or without conduction block. To investigate the pathogenetic role of anti-GM1 antibodies we injected into rat tibial nerves sera from patients with multifocal motor neuropathy and conduction block (MMN) or progressive spinal muscular atrophy (PMA), both presenting anti-GM1 antibodies. Sera of patients with MMN produced reduction of amplitude and dispersion of compound muscle action potential from proximal stimulation. Morphometry revealed demyelination in 6.2% of fibers. Sera of patients with PMA did not produce clear-cut electrophysiological or morphological changes. Differential effects of sera from patients presenting high-titer anti-GM1 antibodies, but with distinct clinical syndromes, might depend on differences in anti-GM1 antibody affinity, valency, or ability to fix complement. Alternatively, circulating factors other than, or in addition to, anti-GM1 antibodies present in sera of patients with MMN, but not of PMA patients, might be responsible for conduction abnormalities and reproduce them after passive transfer.

publication date

  • June 1, 1993

Research

keywords

  • Antibodies
  • Demyelinating Diseases
  • G(M1) Ganglioside
  • Motor Neuron Disease
  • Muscular Atrophy, Spinal
  • Neural Conduction

Identity

Scopus Document Identifier

  • 0027222922

Digital Object Identifier (DOI)

  • 10.1002/mus.880160606

PubMed ID

  • 8502258

Additional Document Info

volume

  • 16

issue

  • 6