CONDUCTION ABNORMALITIES INDUCED BY SERA OF PATIENTS WITH MULTIFOCAL MOTOR NEUROPATHY AND ANTI-GM1 ANTIBODIES

Increased titers of anti-GM1 antibodies have been associated with moto r neuron disease and motor neuropathy with or without conduction block . To investigate the pathogenetic role of anti-GM1 antibodies we injec ted into rat tibial nerves sera from patients with multifocal motor ne uropathy and conduction block (MMN) or progressive spinal muscular atr ophy (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 demy elination 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 antibodi es, 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 p atients, might be responsible for conduction abnormalities and reprodu ce them after passive transfer.