Guillain-Barré syndrome: multifactorial mechanisms versus defined subgroups.
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.
van der Meché
F G
FG
Department of Neurology, Erasmus Medical Center Rotterdam, The Netherlands.
Visser
L H
LH
Jacobs
B C
BC
Endtz
H P
HP
Meulstee
J
J
van Doorn
P A
PA
D001323:Autoantibodies / Q000097:blood; D002169:Campylobacter Infections / Q000150:complications; D016123:Campylobacter jejuni; D003586:Cytomegalovirus Infections / Q000150:complications; D005677:G(M1) Ganglioside / Q000276:immunology; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use; D007239:Infections / Q000150:complications; D010951:Plasma Exchange; D011129:Polyradiculoneuropathy / Q000145:classification* / Q000175:diagnosis / Q000209:etiology* / Q000628:therapy
D001323:Autoantibodies; D016756:Immunoglobulins, Intravenous; D005677:G(M1) Ganglioside