Abstract

Guillain-Barré Syndrome (GBS) is an acute polyneuropathy often triggered by inflammatory and probably autoimmune mechanisms. Development of GBS is in 2/3 of cases preceded by acute infection, typically with gastrointestinal or respiratory symptoms. Infectious agents related to GBS include cytomegalovirus, Epstein-Barr virus, Campylobacter jejuni, Mycoplasma pneumoniae and Haemophilus influenzae. Molecular mimicry seems to be responsible for GBS development after infection, through the synthesis of autoantibodies against myelin gangliosides. Autoimmune reactions develop only in a small fraction of all exposed individuals, depending on still unresolved factors. Different infections lead to forms of GBS differing in spectrum of autoantibodies and in frequency with which different clinical symptoms appear. This may be of some significance for early prognosis and in future possibly for choosing therapeutic options. An increased risk of GBS may be also related to vaccination, but with presently used vaccines this increase remains below one case of GBS per one million doses.