Axonal Guillain-Barr� syndrome: Relation to anti-ganglioside antibodies andCampylobacter jejuni infection in Japan

TLDR

The study aimed to clarify the relationships between axonal Guillain‑Barré syndrome, anti‑ganglioside antibodies, and Campylobacter jejuni infection. The authors examined 86 consecutive Japanese GBS patients. Among the 86 patients, 38 % had acute motor axonal neuropathy, 36 % had acute inflammatory demyelinating polyneuropathy, and IgG anti‑ganglioside antibodies (GM1, GD1a, GalNAc‑GD1a, GD1b) were strongly associated with AMAN, while Campylobacter jejuni infection was common but not exclusive, indicating that axonal dysfunction, anti‑ganglioside antibodies, and C. jejuni infection are closely linked yet other pathogens can also trigger the antibody response.

Abstract

To clarify the relations of the axonal form of Guillain-Barré syndrome (GBS) to anti-ganglioside antibodies and Campylobacter jejuni infection, 86 consecutive Japanese GBS patients were studied. Electrodiagnostic criteria showed acute inflammatory demyelinating polyneuropathy in 36% of the patients and acute motor axonal neuropathy (AMAN) in 38%. Frequent anti-ganglioside antibodies were of the IgG class and against GM1 (40%), GD1a (30%), GalNAc-GD1a (17%), and GD1b (21%). Identified infections were C. jejuni (23%), cytomegalovirus (10%), Mycoplasma pneumoniae (6%), and Epstein-Barr virus (3%). There was a strong association between AMAN and IgG antibodies against GM1, GD1a, GalNAc-GD1a, or GD1b. Almost all the patients with at least one of these antibodies had the AMAN pattern or rapid resolution of conduction slowing/block possibly because of early-reversible changes on the axolemma. C. jejuni infection was frequently associated with AMAN or anti-ganglioside antibodies, but more than half of the patients with AMAN or anti-ganglioside antibodies were C. jejuni–negative. These findings suggest that the three phenomena "axonal dysfunctions (AMAN or early-reversible conduction failure," "IgG antibodies against GM1, GD1a, GalNAc-GD1a, or GD1b," and "C. jejuni infection" are closely associated but that microorganisms other than C. jejuni frequently trigger an anti-ganglioside response and elicit axonal GBS. Ann Neurol 2000;48:624–631