{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T19:53:04Z","timestamp":1787169184847,"version":"build-2736575974"},"reference-count":8,"publisher":"BMJ","issue":"11","license":[{"start":{"date-parts":[[2021,11,28]],"date-time":"2021-11-28T00:00:00Z","timestamp":1638057600000},"content-version":"unspecified","delay-in-days":27,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["BMJ Case Rep"],"accepted":{"date-parts":[[2021,10,15]]},"published-print":{"date-parts":[[2021,11]]},"abstract":"<jats:p>Central pontine myelinolysis (CPM) develops due to acute hypernatremia from a normal baseline serum sodium in the setting of electrolyte abnormalities induced by topiramate use. Topiramate is a commonly used medication with several indications including migraines, myoclonic jerks and seizures. It has been reported to cause renal tubular acidosis and severe electrolyte abnormalities, which in turn predispose patients to neuropathology via renal concentration defects and osmotic shifts. Our patient is a 55-year-old woman with a history of multiple sclerosis and myoclonus on topiramate for several years who presented with weakness and was found to be profoundly hypokalemic. She went on to develop changes in mental status, motor deficits and evidence of CPM on MRI during her hospitalisation. Surprisingly, the patient never had hyponatremia; however, she had an acute rise in serum sodium from a normal baseline after fluid resuscitation with normal saline for hypotension during her admission.<\/jats:p>","DOI":"10.1136\/bcr-2021-245870","type":"journal-article","created":{"date-parts":[[2021,11,30]],"date-time":"2021-11-30T12:15:28Z","timestamp":1638274528000},"page":"e245870","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":3,"title":["Topiramate-induced severe electrolyte abnormalities and hypernatremia leading to central pontine myelinolysis"],"prefix":"10.1136","volume":"14","author":[{"given":"Luba","family":"Muaddi","sequence":"first","affiliation":[{"name":"Department of Medicine, Allegheny Health Network, Pittsburgh, Pennsylvania, USA"},{"name":"Division of Nephrology and Hypertension, Medicine Institute, Allegheny Health Network, Pittsburgh, PA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Omar","family":"Osman","sequence":"additional","affiliation":[{"name":"Department of Medicine, Allegheny Health Network, Pittsburgh, Pennsylvania, USA"},{"name":"Division of Nephrology and Hypertension, Medicine Institute, Allegheny Health Network, Pittsburgh, PA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6696-1424","authenticated-orcid":false,"given":"Barbara","family":"Clark","sequence":"additional","affiliation":[{"name":"Department of Medicine, Allegheny Health Network, Pittsburgh, Pennsylvania, USA"},{"name":"Division of Nephrology and Hypertension, Medicine Institute, Allegheny Health Network, Pittsburgh, PA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[2021,11,30]]},"reference":[{"key":"2025082803570848000_14.11.e245870.1","doi-asserted-by":"publisher","DOI":"10.3174\/ajnr.A3392"},{"key":"2025082803570848000_14.11.e245870.2","doi-asserted-by":"crossref","first-page":"30","DOI":"10.5049\/EBP.2015.13.1.30","article-title":"A case of osmotic demyelination presenting with severe hypernatremia","volume":"13","author":"Han","year":"2015","journal-title":"Electrolyte Blood Press"},{"key":"2025082803570848000_14.11.e245870.3","first-page":"284","article-title":"Lateral pontine and extrapontine myelinolysis associated with hypernatremia and hyperglycemia","volume":"8","author":"McComb","year":"1989","journal-title":"Clin Neuropathol"},{"key":"2025082803570848000_14.11.e245870.4","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.164.14.1561"},{"key":"2025082803570848000_14.11.e245870.5","doi-asserted-by":"publisher","DOI":"10.1016\/j.expneurol.2004.10.018"},{"key":"2025082803570848000_14.11.e245870.6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2125.2009.03521.x"},{"key":"2025082803570848000_14.11.e245870.7","doi-asserted-by":"crossref","first-page":"1482","DOI":"10.1016\/j.ekir.2018.07.014","article-title":"Hypokalemic nephropathy","volume":"3","author":"Yalamanchili","year":"2018","journal-title":"Kidney Int Rep"},{"key":"2025082803570848000_14.11.e245870.8","doi-asserted-by":"crossref","DOI":"10.1038\/srep18311","article-title":"Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus","volume":"5","author":"Khositseth","year":"2015","journal-title":"Sci Rep"}],"container-title":["BMJ Case Reports"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/syndication.highwire.org\/content\/doi\/10.1136\/bcr-2021-245870","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,8,28]],"date-time":"2025-08-28T10:57:15Z","timestamp":1756378635000},"score":1,"resource":{"primary":{"URL":"https:\/\/casereports.bmj.com\/lookup\/doi\/10.1136\/bcr-2021-245870"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2021,11]]},"references-count":8,"journal-issue":{"issue":"11","published-online":{"date-parts":[[2021,11,30]]},"published-print":{"date-parts":[[2021,11]]}},"alternative-id":["10.1136\/bcr-2021-245870"],"URL":"https:\/\/doi.org\/10.1136\/bcr-2021-245870","relation":{},"ISSN":["1757-790X"],"issn-type":[{"value":"1757-790X","type":"electronic"}],"subject":[],"published":{"date-parts":[[2021,11]]}}}