IgG Anti‐GM1 antibody is associated with reversible conduction failure and axonal degeneration in guillain‐barré syndrome

Abstract

To investigate the pathophysiological role of anti-GM1 antibody in Guillain-Barré syndrome (GBS), we reviewed sequential nerve conduction studies of 345 nerves in 34 GBS patients. Statistically significant correlation between IgG anti-GM1 antibodies and electrodiagnoses was found. Sixteen IgG anti-GM1-positive patients were classified as having acute motor or acute motor sensory axonal neuropathy (AMAN or AMSAN) (12 patients), as having acute inflammatory demyelinating polyneuropathy (AIDP) (3 patients), or as undetermined (1 patient) by electrodiagnostic criteria. Besides axonal features, there was rapid resolution of conduction slowing and block. In 3 patients initially diagnosed as having AIDP, conduction slowing was resolved within days, and 1 of them and 3 AMAN patients showed markedly rapid increases in amplitudes of distal compound muscle action potentials that were not accompanied by prolonged duration and polyphasia. The time courses of conduction abnormalities were distinct from those in IgG anti-GM1-negative AIDP patients. Rapid resolution of conduction slowing and block, and the absence of remyelinating slow components, suggest that conduction failure may be caused by impaired physiological conduction at the nodes of Ranvier. Reversible conduction failure as well as axonal degeneration constitutes the pathophysiological mechanisms in IgG anti-GM1-positive GBS. In both cases, immune-mediated attack probably occurs on the axolemma of motor fibers.

Increased circulating T cell reactivity to GM1 ganglioside in patients with Guillain–Barré syndrome

“…[ [27] In the present study, there was an increased frequency of elevated anti-GM1 antibody levels in those GBS patients demonstrating increased T cell reactivity to GM1, although this failed to reach statistical significance. GM1 is relatively enriched in human ventral roots compared with dorsal roots, 28 and antibodies specific to GM1 are commonly associated with motor neuropathy, especially axonal forms of GBS, 27 CIDP and multifocal motor neuropathy.…”

“…GM1 is relatively enriched in human ventral roots compared with dorsal roots, 28 and antibodies specific to GM1 are commonly associated with motor neuropathy, especially axonal forms of GBS, 27 CIDP and multifocal motor neuropathy. As the majority of our patients had demyelinating forms of GBS, we were unable to examine the frequency of GM1 reactive T cells in axonal forms of GBS.…”

Carbohydrate mimicry between human ganglioside GM1 and Campylobacter jejuni lipooligosaccharide causes Guillain–Barré syndrome

“…Limb weakness in some GBS patients is quickly cured by plasmapheresis, indicating that autoantibody causes physiological conduction failure in the motor nerves before any pathological change occurs (26). The nerve terminal lacks a blood-nerve barrier; therefore, Abs have easy access to neuronal membranes, the presumed sites of injury.…”

Clinical Assessment of Self-Reported Acute Flaccid Paralysis in a Population-Based Setting in Guatemala

“…"Mild" GBS has been described previously, 14,15 and the first case, who developed weakness but remained functionally independent and did not seek medical care, suggests that "mild" AFP may occur in the community and not come to medical attention. Electrodiagnostic studies performed on this individual over 1 year after illness were normal; however, reversible electrophysiologic changes have been observed in GBS, and ultimate long-term electrophysiologic improvement in mild illness has not been defined.…”