GUILLAIN-BARRE-SYNDROME - MULTIFACTORIAL MECHANISMS VERSUS DEFINED SUBGROUPS

The clinical spectrum of Guillain-Barre syndrome (GBS) is summarized i n relation to antecedent infections and anti-ganglioside antibodies. A ssociations exist between a pure motor form of GBS, diarrhea, Campylob acter jejuni infection, and anti-GM(1) antibodies; between cranial ner ve involvement and Miller Fisher syndrome, C. jejuni infection, and an ti-GQ(1b) antibodies; and between variants, such as severe sensory inv olvement 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 a cute motor axonal neuropathy and acute motor-sensory axonal neuropathy . In particular, patients with a clinically pure motor variant of GBS, diarrhea, anti-GM(1) antibodies, or C. jejuni infection seem to respo nd better to early treatment with high-dose immunoglobulins than to pl asma exchange.