Abstract
Guillain-Barre 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 consid- erations, and prognosis of this disorder. inducing GBS as a complication. Sporadic cases of GBS can occur after surgeries, in patients with cancer, after transplan- tations, and in patients with HIV infection (11). The rather paradoxical occurrence of GBS, an autoimmune condition, in patients with immune depression is likely explained by a dysregulation of the mechanisms modulating immune re- sponses.
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