Abstract

AbstractGuillain–Barré syndrome (GBS) is an acute self‐limited polyneuropathy. The original paper was reported by Guillain, Barré and Strohl in 1916. GBS was considered to be a demyelinating disease of the peripheral nervous system, called acute inflammatory demyelinating polyneuropathy. In the 1980s, the acute axonal type of GBS was first reported. This subtype was later called acute motor axonal neuropathy. In addition to acute inflammatory demyelinating polyneuropathy and acute motor axonal neuropathy, several subtypes including Miller Fisher syndrome were reported. GBS was shown to be an immune‐mediated disease. The frequent presence of antibodies against various glycolipids have been reported in the acute‐phase sera from GBS patients since the end of the 1980s, including anti‐GM1 antibody in acute motor axonal neuropathy and anti‐GQ1b antibody in Miller Fisher syndrome. The efficacy of plasmapheresis and intravenous immunoglobulin therapy has been established since the mid 1980s. However, despite those therapies, there are still severe or refractory cases. Further investigation is necessary for the development of novel therapeutic strategies.

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