Guillain-Barré syndrome has now become recognized as a clinical syndrome that may be due to several pathological entities, consisting of an acute inflammatory demyelinating polyradiculoneuropathy as well as an acute motor axonal neuropathy. Campylobacter jejuni infection is a common preceding event and, together with anti-ganglioside GM1 antibodies, is associated with axonal damage and a poor outcome. The mechanism by which such antibodies damage axons is not clear. The Miller Fisher syndrome is very closely associated with antibodies to ganglioside CQ1b that may be important in pathogenesis. Treatment of Guillain-Barre syndrome with intravenous immunoglobulin appears to be as effective as plasma exchange in one controlled trial. Two small series have reported a high incidence of early relapses following intravenous immunoglobulin, and its efficacy is being reexamined in a further controlled trial.
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