{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T11:56:49Z","timestamp":1792238209433,"version":"4.4.0"},"reference-count":39,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2023,9,27]],"date-time":"2023-09-27T00:00:00Z","timestamp":1695772800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Euro J of Neurology"],"published-print":{"date-parts":[[2024,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background and purpose<\/jats:title><jats:p>Nitrous oxide (N<jats:sub>2<\/jats:sub>O) induced neurological symptoms are increasingly encountered. Our aim is to provide clinical and diagnostic characteristics with a focus on electrodiagnostic studies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Patients with neurological sequelae due to N<jats:sub>2<\/jats:sub>O presenting in our hospital between November 2018 and December 2021 reporting clinical and diagnostic data were retrospectively reviewed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Seventy patients (median 22\u2009years) were included. Median N<jats:sub>2<\/jats:sub>O usage was 4\u2009kg\/week during 12\u2009months. Patients\u2019 history revealed a higher rate of sensory symptoms compared to motor (97% vs. 57%) and 77% walking difficulties. Clinical diagnosis was polyneuropathy (PNP) in 44%, subacute combined degeneration (SCD) of the spine in 19%, both in 37%. Median vitamin B12 level was low (159\u2009pmol\/L), normal in 16%. The median methylmalonic acid was increased (2.66\u2009\u03bcmol\/L). Electrodiagnostic abnormalities were observed in 91%, with 72% fulfilling axonal PNP criteria, 20% showing mild to intermediate slowing. One patient fulfilled demyelinating PNP criteria not related to N<jats:sub>2<\/jats:sub>O abuse (Charcot\u2212Marie\u2212Tooth type 1a). More prominent motor nerve conduction abnormalities were found; lower limbs were more affected. In 64% with normal conduction, myography showed signs of axonal loss. Magnetic resonance imaging showed cervical myelopathy in 58% involving generally five to six segments.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Nitrous oxide (N<jats:sub>2<\/jats:sub>O) leads to neurological symptoms by causing PNP and\/or SCD primarily involving the legs. Distinguishing PNP and SCD clinically was shown to be insufficient. Electrodiagnostic studies showed axonal PNP. Demyelinating PNP due to N<jats:sub>2<\/jats:sub>O abuse was not present in our cohort. Therefore, further diagnostic work\u2010up is warranted if demyelinating features are present.<\/jats:p><\/jats:sec>","DOI":"10.1111\/ene.16076","type":"journal-article","created":{"date-parts":[[2023,9,27]],"date-time":"2023-09-27T13:01:53Z","timestamp":1695819713000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Nitrous\u2010oxide\u2010induced polyneuropathy and subacute combined degeneration of the spine: clinical and diagnostic characteristics in 70 patients, with focus on electrodiagnostic studies"],"prefix":"10.1111","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1618-6340","authenticated-orcid":false,"given":"L. T.","family":"Hassing","sequence":"first","affiliation":[{"name":"HagaZiekenhuis, Department of Neurology  The Hague The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F. 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