Guillain-Barré syndrome (GBS) is an autoimmune acute peripheral neuropathy. 
Frequently a flu-like episode or a gastroenteritis precede GBS, and the 
cross-reactivity between microbial and neural antigens partly explains the 
pathophysiology of the disease and the possible detection of antiganglioside 
antibodies. The weakness reaches its nadir in 2-4 weeks: the patients may be 
chair- or bed-bound, may need artificial ventilation and frequently experience 
dysautonomic dysfunction; 5-15% of the patients die and more patients are left 
with a disabling motor deficit and/or fatigue. Electrophysiology and 
cerebrospinal fluid evaluation support the diagnosis. The treatment of GBS is 
multidisciplinary, and both plasma exchange and high dose immunoglobulin (IVIg) 
are effective in reducing both the severity of the disease and the residual 
deficits. Finally, steroids are not effective in GBS.