[Guillain-Barré syndrome: clinical features, immune mechanisms, and therapies].

Guillain-Barré syndrome (GBS) is an acute, inflammatory, demyelinating disease of the peripheral motor nerves and nerve roots. The cause of GBS is unknown; it is though to be immune-mediated. The following seven clinical features usually distinguish this syndrome: 1) the neurological symptoms are preceded 1 to 3 weeks by an antecedent event. 2) symptoms and signs progress rapidly for several days up to 2 weeks, followed by a period of stability before gradual improvement to normal function after several months, 3) there is symmetric weakness, 4) there is a loss of tendon reflexes, 5) cerebrospinal fluid protein is elevated, 6) conduction velocity in motor nerves is reduced and F-waves are absent, and 7) most patients recover functionally. There are variants of this common presentation, such as acute motor axonal neuropathy and acute motor and sensory axonal neuropathy, of the many variants, the most aberrant is Fisher syndrome. The clinical criteria for diagnosis of Guillain-Barré syndrome and the electrodiagnostic criteria for demyelination of the peripheral nerve are described. Circulating antineural antibodies directed at a number of antigens have been demonstrated in GBS, occasionally against P2 protein (P2), galactocerebroside, and ganglioside GM1. We studied peripheral blood samples from patients with acute phase GBS using flow cytometry. The proportion of activated T cells (CD4 + HLA-DR +) was increased in comparison to the proportion in healthy controls. The helper-inducer (CD4 + CD29 +) subset was also increased; the suppressor-inducer (CD4 + CD45RA +) subset was neither increased nor decreased. Activated T cells and helper-inducer cells may play a crucial role in the onset of GBS. Lymphocytes sensitized to P2 were demonstrated in the acute stage of GBS, but not in any other neurological diseases. The lymphocytes recognized the P2 residues 60-78. We also demonstrated a significant relationship between GBS and IILA-A2, B61, Cw3, and DR6 antigens. Early plasmapheresis has been proved to be useful for patients with GBS. Intravenous immunoglobulin therapy appears to be as effective as plasmapheresis. Corticosteroids can no longer be considered useful therapy for GBS. Two randomized, controlled trials, one using conventional doses of prednisolone and high-dose intravenous methylprednisolone have shown no benefit.