Abstract:

Guillain-Barré syndrome (GBS) is caused by an inflammatory polyradiculoneuropathy, which most commonly results from acute demyelination produced by a CD4 T-cell mediated response against myelin proteins. Axonal forms have also been recognized. Molecular mimicry between components of the bacterial wall of Campylobacter jejuni and gangliocytes in the membranes of peripheral axons may be responsible for some cases of axonal GBS. Immune therapy with plasma exchange or intravenous immunoglobulin is the standard of care for the treatment of patients with acute GBS. This review summarizes available information regarding the pathophysiology, clinical manifestations, therapeutic considerations, and prognosis of this disorder.