We have tested serum samples from 24 patients with multifocal motor neuropathy (MMN) for reactivity to ganglioside GM1 and to Gal(β1–3)GalNAc-bearing glycoproteins isolated from human peripheral nerve and from Campylobacter jejuni (Cj) serotype O:19. IgM anti-GM1 antibodies were detected by ELISA in 11 patients (45.8%) with MMN and in only one subject (4%) from the control group. Western blots showed positive reactivity of sera from 6 patients (25%) with MMN to several Gal(β1–3)GalNAc-bearing glycoproteins from human peripheral nerve and from Cj O:19 isolates. Sera from three patients (12.5%) with MMN showed positively reactive bands with similar electrophoretic mobility in all isolates (60–62？kDa, 48–51？kDa, 42？kDa, and 38？kDa). All six patients showed positive reactivity to 48–52 kDa protein isolated from human peripheral nerve. Increased titer of IgG antibodies to 60–62？kDa protein isolated from Cj O:19 associated with Guillain-Barré syndrome was detected in three patients, and their serum showed also IgG positive reactivity to peripheral nerve antigen with the same electrophoretic mobility. One of these patients had a previous history of Cj infection which suggests the possibility that Cj may be also involved in the pathogenesis of MMN. 1. Introduction Multifocal motor neuropathy (MMN) is a chronic immune mediated neuropathy characterized by asymmetric, predominantly distal upper limb weakness, no sensory impairment, and by the presence of multifocal persistent partial conduction blocks on motor but not sensory nerves [1]. The muscle weakness related to individual motor nerve is associated with motor conduction block, at site distinct from common entrapment or compression syndromes [2]. Serum IgM antibodies to ganglioside GM1 were reported in 22–85% of patients with MMN, and these striking differences in reported prevalences may be explained by different laboratory techniques [3]. IgM antibodies against other gangliosides than GM1 have also been reported in MMN. Antecedent Campylobacter jejuni (Cj) infection has been implicated in the induction of Guillain-Barré syndrome (GBS) by a mechanism of molecular mimicry with the lipopolysaclharides (LPS) of Cj [4]. The pure motor axonal GBS is associated with antibodies to gangliosides GM1, GD1a, GalNAc-GD1a, GD1b, and GM1b [5–7]. We have previously shown the reactivity of anti-GM1 and asialo-GM1 antibodies from patients with MMN or chronic neuropathies with the LPS of Cj [8]. The possibility that Cj may also be involved in the pathogenesis of MMN has been supported by several reports of patients developing
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