Guillain-Barré Syndrome

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. Guillain-Barré syndrome (GBS, or better Guillain-BarréStrohl syndrome to recognize the three authors responsible for the first description of this disorder) [1] is an inflammatory polyradiculoneuropathy characterized by the acute development of diffuse weakness and areflexia. This syndrome encompasses various subtypes, the most common of which is acute inflammatory demyelinating polyradiculoneuropathy (AIDP). Less common are the axonal variants, acute motor axonal neuropathy (AMAN) and acute motor and sensory axonal neuropathy (AMSAN), and the atypical forms with more localized clinical expressions such as the Fisher syndrome [2]. AIDP is responsible for most cases of GBS in the United States and Europe [3,4]. Axonal forms are more common in China, Japan, and perhaps Central America [5,6].