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

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.

Autoantibodies associated with peripheral neuropathy

“…60 There are also reports that human anti-GM1 antibodies cause demyelination and conduction block when injected into rat nerve, 147,169 but conduction block was not observed by others following intraneural injection of anti-GM1 antibodies. 57,126 Variable findings have similarly been reported with regard to the effects of anti-GM1 antibodies on electrical activity of isolated nerve preparations in vitro. 2,61,160 Additionally, mouse phrenic nervehemidiaphragm preparations exposed to serum from MMN patients in vitro and in vivo, most of which contained anti-GM1 antibodies, exhibited an increased threshold of stimulation followed by complete conduction block in some experiments.…”

Acute Transverse Myelitis and Acute Motor Axonal Neuropathy Developed after Vaccinations against Seasonal and 2009 A/H1N1 Influenza

“…The lipopolysaccharide components of C. jejuni include ganglioside-like structures (15) and have been shown to induce production of anti-GM1 IgG antibodies (16), which are characteristic, and may or may not be directly causative (17,18), antibodies in AMAN. Interestingly enough, there have been a couple of cases of ATM that followed C. jejuni enteritis (19,20), in one of which serum anti-GM1 IgG and IgM were elevated (20).…”

Natural history of 46 patients with multifocal motor neuropathy with conduction block

“…26,32 There are reports of passive transfer of CB by injecting or directly applying serum of patients with GM1 ganglioside antibodies into or onto animal nerves, 29,30 but others have not been able to confirm this finding. 18,19 The disease appears to be slowly progressive in the majority of cases, but the rate of progression, degree of functional impairment, and mortality have not been adequately studied. Various forms of immunotherapy have not yet been fully investigated.…”