4.3 Review

Guillain-Barre syndrome: An update

Journal

JOURNAL OF CLINICAL NEUROSCIENCE
Volume 16, Issue 6, Pages 733-741

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.jocn.2008.08.033

Keywords

Acute inflammatory demyelinating polyradiculoneuropathy; Acute motor axonal neuropathy; Acute motor and sensory axonal neuropathy; Guillain-Barre syndrome

Funding

  1. Motor Neuron Disease Research Institute of Australia (MNDRIA)
  2. National Health and Medical Research Council of Australia

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Guillain-Barre syndrome (GBS) is an acute polyneuropathy consisting of different subtypes. Acute inflammatory demyelinating polyradiculoneuropathy, the classic demyelinating form of GBS, accounts for 90% of all GBS cases in the Western world. Acute motor axonal neuropathy (AMAN) and acute motor and sensory axonal neuropathy (AMSAN) are axonal forms of GBS that are more prevalent in Asia, South and Central America, often preceded by infection by Campylobacter jejuni. AMAN and AMSAN may be mediated by specific anti-ganglioside antibodies that inhibit transient sodium ion (Na+) channels. The efficacy of plasmapheresis and intravenous immunoglobulin has been established in large international randomised trials, with corticosteroids proven ineffective. Although axonal demyelination is an established pathophysiological process in GBS, the rapid improvement of clinical deficits with treatment is consistent with Na+ channel blockade by antibodies or other circulating factors, such as cytokines. This review provides an update on the epidemiology, clinical features, diagnosis, pathogenesis and treatment of GBS. (C) 2008 Elsevier Ltd. All rights reserved.

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