Guillain-Barré syndrome: An update

Steve Vucic, Matthew C. Kiernan, David R. Cornblath

Research output: Contribution to journalReview articlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)733-741
Number of pages9
JournalJournal of Clinical Neuroscience
Volume16
Issue number6
DOIs
StatePublished - Jun 1 2009

Keywords

  • Acute inflammatory demyelinating polyradiculoneuropathy
  • Acute motor and sensory axonal neuropathy
  • Acute motor axonal neuropathy
  • Guillain-Barré syndrome

ASJC Scopus subject areas

  • Surgery
  • Neurology
  • Clinical Neurology
  • Physiology (medical)

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