Guillain-Barré syndrome (GBS) is clinically defined as an acute peripheral 
neuropathy causing limb weakness that progresses over a time period of days or, 
at the most, up to 4 weeks. GBS occurs throughout the world with a median annual 
incidence of 1.3 cases per population of 100 000, with men being more frequently 
affected than women. GBS is considered to be an autoimmune disease triggered by 
a preceding bacterial or viral infection. Campylobacter jejuni, cytomegalovirus, 
Epstein-Barr virus and Mycoplasma pneumoniae are commonly identified antecedent 
pathogens. In the acute motor axonal neuropathy (AMAN) form of GBS, the 
infecting organisms probably share homologous epitopes to a component of the 
peripheral nerves (molecular mimicry) and, therefore, the immune responses 
cross-react with the nerves causing axonal degeneration; the target molecules in 
AMAN are likely to be gangliosides GM1, GM1b, GD1a and GalNAc-GD1a expressed on 
the motor axolemma. In the acute inflammatory demyelinating polyneuropathy 
(AIDP) form, immune system reactions against target epitopes in Schwann cells or 
myelin result in demyelination; however, the exact target molecules in the case 
of AIDP have not yet been identified. AIDP is by far the most common form of GBS 
in Europe and North America, whereas AMAN occurs more frequently in east Asia 
(China and Japan). The prognosis of GBS is generally favourable, but it is a 
serious disease with a mortality of approximately 10% and approximately 20% of 
patients are left with severe disability. Treatment of GBS is subdivided into: 
(i) the management of severely paralysed patients with intensive care and 
ventilatory support; and (ii) specific immunomodulating treatments that shorten 
the progressive course of GBS, presumably by limiting nerve damage. High-dose 
intravenous immunoglobulin (IVIg) therapy and plasma exchange aid more rapid 
resolution of the disease. The predominant mechanisms by which IVIg therapy 
exerts its action appear to be a combined effect of complement inactivation, 
neutralisation of idiotypic antibodies, cytokine inhibition and saturation of Fc 
receptors on macrophages. Corticosteroids alone do not alter the outcome of GBS.