Guillain-Barre syndrome: An update of acute immune-mediated polyradiculoneuropathies

BACKGROUND - Guillain-Barre syndrome (GBS) is a clinically defined syndrome leading to acute flaccid paralysis, which is attributed to an autoimmune process that targets cranial nerves, peripheral nerves, and spinal roots. Since its description more than 80 years ago, the concept of GBS has evolved into a heterogeneous syndrome. SUMMARY - This article gives an outline of the natural history and typical clinical presentation of acute inflammatory demyelinating polyradiculoneuropathy. It also covers the axonal forms of GBS, including acute motor axonal neuropathy, acute motor sensory axonal neuropathy, and Fisher's syndrome. The systemic clinico-pathologic study of early GBS cases from northern China has confirmed the existence of axonal variants and enhanced understanding of the underlying immune mechanisms. Much attention is currently focused on the preceding infection with Campylobacter jejuni and the concept of molecular mimicry to explain the immunopathogenesis for the various forms of GBS. Mortality from GBS has been reduced 10-fold by improvements in modern critical care. Two equally effective immunomodulatory therapies (plasma exchange and intravenous human immunoglobulin) have proven benefit in terms of shortening recovery times. CONCLUSION - This review is intended to provide an up-to-date account of GBS and its clinical management.