Failure of anti‐GM1 IgG OR IgM to induce conduction block following intraneural transfer

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Abstract
In order to confirm the reported pathogenicity of human antibodies to monosialoganglioside GM1, immunoglobulin fractions with high anti‐GM1 IgG or IgM titers were prepared from patients with Guillain‐Barré syndrome and multifocal motor neuropathy respectively. These fractions were injected intraneurally into rat tibial nerves with fresh human complement. Neither the anti‐GM1 IgG nor the anti‐GM1 IgM fraction induced significant focal conduction block or slowing compared to a pooled fraction prepared from 5 normal individuals. In contrast, rabbit experimental allergic neuritis serum included as a positive control was highly active. Transverse sections of injected nerve failed to show evidence of demyelination. Staining for human immunoglobulin in cryostat sections showed the presence of injected anti‐GM1 antibody bound to nodes of Ranvier up to 6 days following intraneural transfer. These data fail to confirm previous reports of conduction block from intraneural transfer of anti‐GM1 serum and suggest that such electrophysiological effects may be the result of factors other than or in addition to anti‐GM1 antibodies. © 1995 John Wiley & Sons, Inc.