Guillain-Barré syndrome (GBS) is an acute self-limited polyneuropathy named 
after Guillain, Barré, and Strohl, who first reported it in 1916. GBS was 
considered a demyelinating disease until the 1980s, when the acute axonal type 
of GBS was first reported. Since then, acute inflammatory demyelinating 
polyneuropathy and acute motor axonal neuropathy have been considered the two 
main subtypes of GBS. Autoimmunity underlies the pathogenesis of GBS. The 
presence of antibodies against various glycolipids in the acute-phase sera from 
patients with GBS has frequently been reported since the late 1980s. The 
effectiveness of plasmapheresis and intravenous immunoglobulin therapy has been 
established since the mid-1980s. However, severe or refractory cases still occur 
and further investigation is necessary for the development of novel treatments 
that are effective for such cases.