{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,24]],"date-time":"2026-01-24T02:56:54Z","timestamp":1769223414772,"version":"3.49.0"},"reference-count":39,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2021,8,31]],"date-time":"2021-08-31T00:00:00Z","timestamp":1630368000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Epilepsia"],"published-print":{"date-parts":[[2021,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objectives<\/jats:title><jats:p>Status epilepticus (SE) can be associated with neuronal surface antibodies (NS\u2010Abs) but NS\u2010Ab detection rate remains unknown in patients with SE of unclear etiology at symptom presentation but suspected of having an autoimmune etiology (SE suspected autoimmune). We aimed to determine the NS\u2010Ab detection rate and the clinical features that predict the presence of NS\u2010Abs in patients with SE suspected autoimmune.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We retrospectively reviewed the clinical information of 137 patients with SE suspected autoimmune who underwent testing for NS\u2010Abs between January 2007 and September 2020. NS\u2010Abs were examined in both serum and cerebrospinal fluid (CSF) obtained at symptom onset with established assays. We classified brain magnetic resonance imaging (MRI) findings into unremarkable, autoimmune limbic encephalitis (ALE) (bilateral abnormalities highly restricted to the medial temporal lobes), ALE\u2010Plus (ALE pattern and additional extramedial temporal lobe abnormalities), multifocal cortico\u2010subcortical (MCS), or other pattern. We compared the clinical features between patients with and without NS\u2010Abs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Forty\u2010four patients (32.1%) had NS\u2010Abs, including 35\u00a0<jats:italic>N<\/jats:italic>\u2010methyl\u2010<jats:sc>d<\/jats:sc>\u2010aspartate receptor (NMDAR) (one with concurrent \u03b3\u2010aminobutyric acid B receptor [GABAbR] and \u03b1\u2010amino\u20103\u2010hydroxy\u20105\u2010methyl\u20104\u2010isoxazolepropionic acid receptor [AMPAR]), 5 \u03b3\u2010aminobutyric acid A receptor (GABAaR), 2 leucine\u2010rich glioma\u2010inactivated 1(LGI1), 1 GABAbR, and 1 unknown antigens. Compared with NS\u2010Ab\u2010negative patients, NS\u2010Ab\u2010positive patients were more likely to have a preceding headache (56.8% vs 26.7%), preceding psychobehavioral or memory alterations (65.9% vs 20.4%), involuntary movements (79.5% vs 16.1%), CSF pleocytosis (81.8% vs 62.0%), elevated immunoglobulin G (IgG) index (45.2% vs 15.6%), oligoclonal bands (51.5% vs 9.5%), tumor (47.7% vs 8.6%), and higher APE2\u00a0score (median of 9 vs 7), and they were less likely to have an ALE\u2010Plus pattern (2.3% vs 23.7%). However, preceding fever and ALE or MCS pattern were not different between the two groups of patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Significance<\/jats:title><jats:p>When an autoimmune etiology was suspected, there was a relatively high likelihood (one of three patients) of identifying NS\u2010Abs. Some clinical features (preceding symptoms, inflammatory CSF) predict a higher likelihood of finding NS\u2010Ab positivity, but the ALE\u2010Plus MRI pattern is more likely suggestive of NS\u2010Ab negativity.<\/jats:p><\/jats:sec>","DOI":"10.1111\/epi.17055","type":"journal-article","created":{"date-parts":[[2021,8,31]],"date-time":"2021-08-31T07:26:00Z","timestamp":1630394760000},"page":"2719-2731","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Status epilepticus suspected autoimmune: Neuronal surface antibodies and main clinical features"],"prefix":"10.1111","volume":"62","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5465-6297","authenticated-orcid":false,"given":"Hiroki","family":"Suga","sequence":"first","affiliation":[{"name":"Department of Neurology Kitasato University School of Medicine Sagamihara 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Japanese Red Cross Otsu Hospital Otsu Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masahiro","family":"Hayashi","sequence":"additional","affiliation":[{"name":"Department of Neurology Hiroshima City Hiroshima Citizens Hospital Hiroshima Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuya","family":"Onozawa","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory Kitasato University Hospital Sagamihara Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naomi","family":"Nagata","sequence":"additional","affiliation":[{"name":"Department of Neurology Kitasato University School of Medicine Sagamihara Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Juntaro","family":"Kaneko","sequence":"additional","affiliation":[{"name":"Department of Neurology Kitasato University School of Medicine Sagamihara 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