Guillain-Barré syndrome (GBS) was first described in 1916 (Guillain G, 1916) and 
is approaching its 100th anniversary. Our knowledge of the syndrome has hugely 
expanded since that time. Once originally considered to be only demyelinating in 
pathology we now recognise both axonal and demyelinating subtypes. Numerous 
triggering or antecedent events including infections are recognised and GBS is 
considered an immunological response to these. GBS is now considered to be a 
clinical syndrome of an acute inflammatory neuropathy encompassing a number of 
subtypes with evidence of different immunological mechanisms. Some of these are 
clearly understood while others remain to be fully elucidated. Complement fixing 
antibodies against peripheral nerve gangliosides alone and in combination are 
increasingly recognised as an important mechanism of nerve damage. New 
antibodies against other nerve antigens such as neurofascin have been recently 
described. Research databases have been set up to look at factors associated 
with prognosis and the influence of intravenous immunoglobulin (IvIg) 
pharmacokinetics in therapy. Exciting new studies are in progress to examine a 
possible role for complement inhibition in the treatment of the syndrome.