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The author reviews the history of research into its pathogenesis and treatment to highlight promising avenues for future research.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This is a nonsystematic personal review.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Since the early 1900s, the clinical picture of GBS has been illustrated in multiple series culminating in the ongoing International Guillain\u2013Barr\u00e9 Syndrome study of 2000 patients. In the 1950s and 1960s, the inflammatory nature of the commonest form, acute inflammatory demyelinating polyradiculoneuropathy (AIDP), was described. In the 1990s, two axonal forms, acute motor\u2013sensory axonal neuropathy and acute motor axonal neuropathy, were recognized. In the 1990s and early 2000s, these forms were shown to be due to antibodies against\n                      <jats:italic>Campylobacter jejuni<\/jats:italic>\n                      glycans cross\u2010reacting with glycolipids on axonal membranes. The pathogenesis of AIDP remains unknown, but T\u2010cell responses to the compact myelin proteins, P2 and P0, which cause experimental autoimmune neuritis, suggest that T cells are important. Randomized controlled trials in the 1970s and 1980s showed no benefit from corticosteroids. Trials in the 1980s showed benefit from plasma exchange and in the 1990s from intravenous immunoglobulin.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Future research should seek biomarkers to identify subgroups with different treatment responses, define the true natural history of the disease with population\u2010based epidemiological studies, study the pathology in autopsies early in the disease, seek causative antibodies and confirm autoimmune T\u2010cell responses in AIDP, and expand treatment trials to include anti\u2010T\u2010cell agents.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/ene.16346","type":"journal-article","created":{"date-parts":[[2024,5,16]],"date-time":"2024-05-16T07:39:56Z","timestamp":1715845196000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":45,"title":["<scp>Guillain\u2010Barr\u00e9<\/scp>\n                    syndrome: History, pathogenesis, treatment, and future directions"],"prefix":"10.1111","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5251-3797","authenticated-orcid":false,"given":"Richard A. 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