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Failure of anti-GM1 IgG or IgM to induce conduction block following intraneural transfer
G K Harvey1, K V Toyka, J Zielasek
1Department of Neurology, Julius-Maximillians-Universität, Wurzburg, Germany.
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.
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.