FAILURE OF ANTI-GM(1) IGG OR IGM TO INDUCE CONDUCTION BLOCK FOLLOWING INTRANEURAL TRANSFER

In order to confirm the reported pathogenicity of human antibodies to monosialoganglioside GM(1), immunoglobulin fractions with high anti-GM(1) IgG or IgM titers were prepared from patients with Guillain-Barre syndrome and multifocal motor neuropathy respectively. These fractions were injected intraneurally into rat tibial nerves with fresh human complement. Neither the anti-GM(1) IgG nor the anti-GM(1) 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-GM(1) 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-GM(1) serum and suggest that such electrophysiological effects may be the result of factors other than or in addition to anti-GM(1) antibodies. (C) 1995 John Wiley and Sons, Inc.