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Guillain-Barré syndrome in adults: Clinical features and diagnosis

Francine J Vriesendorp, MD
Section Editors
Jeremy M Shefner, MD, PhD
Ira N Targoff, MD
Deputy Editor
John F Dashe, MD, PhD


The acute immune-mediated polyneuropathies are classified under the eponym Guillain-Barré syndrome (GBS), after the authors of early descriptions of the disease. GBS is a heterogeneous condition with several variant forms. Most often, GBS presents as an acute, monophasic paralyzing illness provoked by a preceding infection.

The clinical features and diagnosis of GBS in adults will be reviewed here. Other aspects of GBS are discussed separately. (See "Guillain-Barré syndrome in adults: Treatment and prognosis" and "Guillain-Barré syndrome in children: Epidemiology, clinical features, and diagnosis" and "Guillain-Barré syndrome in children: Treatment and prognosis".)


The pathogenesis of Guillain-Barré syndrome (GBS) is reviewed here briefly and discussed in detail elsewhere. (See "Guillain-Barré syndrome: Pathogenesis".)

GBS is thought to result from an immune response to a preceding infection that cross-reacts with peripheral nerve components because of molecular mimicry. The immune response can be directed towards the myelin or the axon of peripheral nerve, resulting in demyelinating and axonal forms of GBS. (See "Guillain-Barré syndrome: Pathogenesis", section on 'Mechanisms'.)

Campylobacter jejuni infection is the most commonly identified precipitant of GBS. Cytomegalovirus, Epstein-Barr virus, human immunodeficiency virus (HIV), and Zika virus have also been associated with GBS. (See "Guillain-Barré syndrome: Pathogenesis", section on 'Antecedent events'.)

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Literature review current through: Oct 2017. | This topic last updated: Aug 21, 2017.
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