作者: Kazue Ogawara , Satoshi Kuwabara , Masahiro Mori , Takamichi Hattori , Michiaki Koga
DOI: 10.1002/1531-8249(200010)48:4<624::AID-ANA9>3.0.CO;2-O
关键词:
摘要: To clarify the relations of axonal form Guillain-Barre 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% motor neuropathy (AMAN) 38%. Frequent IgG class against GM1 (40%), GD1a (30%), GalNAc-GD1a (17%), GD1b (21%). Identified infections C. (23%), cytomegalovirus (10%), Mycoplasma pneumoniae (6%), Epstein-Barr virus (3%). There was a strong association between AMAN GM1, GD1a, GalNAc-GD1a, or GD1b. Almost all with at least one these had pattern rapid resolution conduction slowing/block possibly because early-reversible changes on axolemma. infection frequently associated antibodies, but more than half jejuni-negative. These findings suggest that three phenomena "axonal dysfunctions (AMAN failure)," "IgG GD1b," "C. infection" are closely microorganisms other trigger an response elicit GBS.