Guillain-Barré syndrome: multifactorial mechanisms versus defined subgroups

J Infect Dis. 1997 Dec:176 Suppl 2:S99-102. doi: 10.1086/513779.

Abstract

The clinical spectrum of Guillain-Barré syndrome (GBS) is summarized in relation to antecedent infections and anti-ganglioside antibodies. Associations exist between a pure motor form of GBS, diarrhea, Campylobacter jejuni infection, and anti-GM1 antibodies; between cranial nerve involvement and Miller Fisher syndrome, C. jejuni infection, and anti-GQ1b antibodies; and between variants, such as severe sensory involvement and cytomegalovirus infection. These three clinical variants are suggested to form the extremes of a continuous spectrum; they are discussed in relation to the more pathologically defined patterns of acute motor axonal neuropathy and acute motor-sensory axonal neuropathy. In particular, patients with a clinically pure motor variant of GBS, diarrhea, anti-GM1 antibodies, or C. jejuni infection seem to respond better to early treatment with high-dose immunoglobulins than to plasma exchange.

Publication types

  • Review

MeSH terms

  • Autoantibodies / blood
  • Campylobacter Infections / complications
  • Campylobacter jejuni
  • Cytomegalovirus Infections / complications
  • G(M1) Ganglioside / immunology
  • Humans
  • Immunoglobulins, Intravenous / therapeutic use
  • Infections / complications
  • Plasma Exchange
  • Polyradiculoneuropathy / classification*
  • Polyradiculoneuropathy / diagnosis
  • Polyradiculoneuropathy / etiology*
  • Polyradiculoneuropathy / therapy

Substances

  • Autoantibodies
  • Immunoglobulins, Intravenous
  • G(M1) Ganglioside