Annals of Neurology · 1993 · 153 citations · 26 references
Life SciencesNeurologyNeuroscienceAutoimmunityNeuroimmunologyNeuropathologyAutoantibodiesAutoimmune Neurological DisordersDemyelinating DiseasesDemyelinating DisordersNervous System PathologyNeurologic PathophysiologyAntibodiesAntibody-mediated Neurologic DiseaseAssayGuillain-barré Syndrome PathogenesisMyelin AntigensPeripheral Nervous System MyelinSerological DetectionSerum Biomarkers
Serum antibodies to monosialoganglioside (GM1), disialoganglioside (GD1b), and Campylobacter jejuni, measured by enzyme-linked immunosorbent assay and serum antibodies to peripheral nerve myelin, measured by the C1 fixation and transfer assay, were studied in 58 acute-phase patients with Guillain-Barré syndrome (GBS), 42 disease controls, and 29 normal controls. Anti-peripheral nerve myelin antibodies were elevated in 57 of 58 patients with GBS compared with controls, whereas only 8.6% had increased antibody titers to GM1 and 10.3% to GD1b. Only low antibody titers (GM1) or no antibodies (GD1b) were found in controls. More GBS patients (17.2%) than controls (7%) had antibodies to C jejuni. Poor recovery with inability to walk at 1 year after onset of symptoms was seen in 3 (5%) of the patients with GBS. All 3 patients had serological evidence of recent C jejuni infection but no antibodies to GM1 or GD1b. GBS patients with antibodies to GM1 or GD1b had excellent recovery. Our data indicate that antibodies to GM1 or GD1b do not necessarily mediate the extensive axonal damage seen in these severely affected patients.
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A treatable multifocal motor neuropathy with antibodies to GM1 ganglioside
Alan Pestronk, David R. Cornblath, Amjad A. Ilyas et al. · Annals of Neurology · 1988 · 609 citations
Medicine, Neurology, Neuroscience +17