{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T13:18:57Z","timestamp":1762003137580,"version":"build-2065373602"},"reference-count":13,"publisher":"BMJ","content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["BMJ Case Reports"],"accepted":{"date-parts":[[2017,12,22]]},"abstract":"<jats:p>An 81-year-old man presented with fever, confusion and rapidly-progressive flaccid tetraparesis. Clinical presentation and neurophysiology were consistent with a severe axonal polyneuropathy. Anti-GM1 and<jats:italic>Campylobacter<\/jats:italic>serology were both positive, consistent with postinfectious axonal-variant Guillain-Barr\u00e9 syndrome (GBS). GBS is characterised by albuminocytological dissociation, where an elevated protein and acellular cerebrospinal fluid are typical. However, in this case, CSF analysis revealed an exaggerated pleocytosis (72 white blood cells (WBC)\/mm<jats:sup>3<\/jats:sup>). No source of central nervous system infection or inflammation was identified despite thorough investigation. The patient was treated with intravenous immunoglobulin and intensive rehabilitation.<\/jats:p><jats:p>Albuminocytological dissociation classically distinguishes GBS from infective causes of flaccid weakness (eg, enteroviruses, flaviviruses and HIV). Diagnostic criteria frequently cite a pleocytosis of &lt;50 WBC\/mm<jats:sup>3<\/jats:sup>as required in the diagnosis of GBS. However, this case demonstrates that pleocytosis exceeding this level can occur in the presence of convincing evidence of GBS and without demonstrable neurotropic infection.<\/jats:p>","DOI":"10.1136\/bcr-2017-222995","type":"journal-article","created":{"date-parts":[[2018,1,6]],"date-time":"2018-01-06T13:05:15Z","timestamp":1515243915000},"page":"bcr-2017-222995","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":8,"title":["Guillain-Barr\u00e9 syndrome with exaggerated pleocytosis and anti-GM1 ganglioside antibodies"],"prefix":"10.1136","volume":"2018","author":[{"given":"Gabriel T.","family":"Doctor","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4284-6704","authenticated-orcid":false,"given":"Sian K","family":"Alexander","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aleksandar","family":"Radunovic","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"239","published-online":{"date-parts":[[2018,1,6]]},"reference":[{"key":"2025042702251075000_2018.jan06_1.bcr-2017-222995.1","unstructured":"Guillain G , Barr\u00e9 JA , Strohl A . 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