Guillain-Barre syndrome is an acute autoimmune polyradiculoneuropathy with
a clinical presentation of flaccid paralysis with areflexia, variable senso
ry disturbance, and elevated cerebrospinal fluid protein without pleocytosi
s. Although Guillain-Barre syndrome previously had been viewed as a unitary
disorder with variations, it currently is viewed as a group of syndromes w
ith several distinctive subtypes. These include the principal subtype preva
lent in the Western world (acute inflammatory demyelinating polyradiculoneu
ropathy, and others, each with distinctive electrodiagnostic and pathologic
features, including acute motor axonal neuropathy), acute motor-sensory ax
onal neuropathy, Miller Fisher syndrome, and perhaps others. The clinical a
nd pathologic features of these Guillain-Barre syndrome subtypes are review
ed, and the role of antecedent infections, particularly Campylobacter jejun
i gastroenteritis, and the role of antiganglioside antibody responses are r
eviewed with respect to pathogenesis. Treatment of Guillain-Barre syndrome
includes both important supportive measures and immunotherapies, specifical
ly high-dose intravenous immunoglobulin and plasma exchange.