The Guillain-Barre syndrome (GBS) is the most common form of acute neuromuscular paralysis in developed countries, but the pathogenesis is still largely unknown. The major clinical features of the syndrome were first united by J-B.O. Landry in 1859 (1). The syndrome was named after G. Guillain and J.A. Barre, two French army neurologists, who in 1916 described, together with A. Strohl, the typical findings in the cerebrospinal fluid (2). This 'dissociation albumino·cytologique', the combination of elevated protein and normal cell count, was in those days an important diagnostic feature that further distinguished the syndrome from other neurological diseases, like poliomyelitis. GBS was early recognized as a postinfectious disorder, although the infectious agents were not identified. Since then, major efforts have been made to elucidate the pathogenesis of GBS. In the last years, research in this field was dominated by the discovery that infections with the Gram negative curved rod Campy/abaeter jejunifrequently precede GBS and by the finding of antibodies against various peripheral nerve gangliosides in serum from GBS patients. This introduction will focus on these infections and antibodies, and will provide a background for understanding the studies described in this thesis.

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R. Benner (Robbert) , F.G.A. van der Meché (Frans)
Erasmus University Rotterdam
Prinses Beatrix Fonds, Willem H. Kroger Stichting
Erasmus MC: University Medical Center Rotterdam

Jacobs, B.C. (1997, October 22). Antecedent infections and anti-ganglioside antibodies in Guillain-Barré syndrome : their role in pathogenesis and heterogeneity. Erasmus University Rotterdam. Retrieved from