GBS is a postinfectious, immune-mediated disease. Infection with C jejuni is one of the most common recognized risk factors for developing GBS. Cellular and humoral immune mechanisms probably play a role in its development. Most patients report an infectious illness in the weeks prior to the onset of GBS. Many of the identified infectious agents are thought to induce production of antibodies that cross-react with specific gangliosides and glycolipids, such as GM1 and GD1b, which are distributed throughout the myelin in the peripheral nervous system.
The pathophysiologic mechanism of an antecedent illness and of GBS can be typified by C jejuni. The virulence of C jejuni is thought to be based on the presence of specific antigens in its capsule that are shared with nerves. Immune responses directed against lipopolysaccharide antigens in the capsule of C jejuni result in antibodies that cross-react with ganglioside GM1 in myelin, resulting in immunologic damage to the peripheral nervous system. This process has been termed molecular mimicry.
For more on the pathophysiology of GBS, read here.
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Cite this: Stephen Kishner. Fast Five Quiz: Test Your Knowledge of Guillain-Barré Syndrome - Medscape - Nov 02, 2016.