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J Clin Neurosci. 2009 Jun;16(6):733-41. doi: 10.1016/j.jocn.2008.08.033. Epub 2009 Apr 7.

Guillain-Barré syndrome: an update.

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1
Prince of Wales Medical Research Institute and Prince of Wales Clinical School, University of New South Wales, Randwick, New South Wales, Australia. s.vucic@powmri.edu.au

Abstract

Guillain-Barré 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.

PMID:
19356935
DOI:
10.1016/j.jocn.2008.08.033
[Indexed for MEDLINE]
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