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From the Department of Neuroimmunology (Drs. Hadden and Hughes), Guy’s, King’s and St. Thomas’ School of Medicine, and the Statistics Unit (Dr. Swan), Public Health Laboratory Service, London, UK; the Department of Neurology (Drs. Hadden, Hartung, Zielasek, Weishaupt, and Toyka), Institute for Hygiene and Microbiology (Dr. Karch), and Institute for Virology and Immunobiology (Drs. Weissbrich and Schubert), Julius Maximilians University, Würzburg, Germany; the Department of Neurology (Dr. Hartung), Karl Franzens University, Graz, Austria; and the Department of Neurology (Dr. Cornblath), Johns Hopkins University, Baltimore, MD.
Address correspondence and reprint requests to Dr. R.D.M. Hadden, Department of Neuroimmunology, Guy’s, King’s and St. Thomas’ School of Medicine, Hodgkin Building, Guy’s Hospital, St. Thomas’ St., London SE1 9RT, UK; e-mail: rob.hadden{at}doctors.org.uk
OBJECTIVE: To test the hypothesis that different preceding infections influence the neurophysiologic classification and clinical features of Guillain–Barré syndrome (GBS).
METHODS: We tested pretreatment sera, 7 ± 3 (mean ± SD) days from onset, from 229 patients with GBS in a multicenter trial of plasma exchange and immunoglobulin, for serological markers of infection, adhesion molecules, and cytokine receptors, and compared these with neurophysiologic and clinical features.
RESULTS: Recent infection by Campylobacter jejuni was found in 53 patients (23%), cytomegalovirus in 19 (8%), and Epstein–Barr virus in four (2%). Patients with C. jejuni infection were more likely than others to have neurophysiologic criteria of axonal neuropathy or inexcitable nerves, antiganglioside GM1 antibodies, pure motor GBS, lower CSF protein, and worse outcome. Patients with cytomegalovirus infection were younger and more likely than others to have raised serum concentrations of molecules important in T lymphocyte activation and migration, soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble leukocyte selectin, and soluble interleukin-2 receptor (sIL-2R). Concentrations of sICAM-1 and soluble tumor necrosis factor receptor were higher in patients with inexcitable nerves than those with demyelinating neurophysiology. Logistic regression analysis showed death or inability to walk unaided at 48 weeks were associated with diarrhea, inexcitable nerves, severe arm weakness, age over 50, raised sIL-2R concentration and absence of immunoglobulin (Ig) M antiganglioside GM1 antibodies.
CONCLUSIONS: Subtypes of GBS defined by preceding infections were only approximately associated with different patterns of clinical, neurophysiologic, and immunologic features. A single infectious agent caused more than one type of pathology in GBS, implying interaction with additional host factors. Most patients had no identified infection.
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