{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,11]],"date-time":"2026-10-11T04:11:09Z","timestamp":1791691869839,"version":"4.3.4"},"reference-count":50,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T00:00:00Z","timestamp":1775088000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T00:00:00Z","timestamp":1775088000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Epilepsia"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      Neonatal developmental and epileptic encephalopathy with movement disorder and arthrogryposis (NDEEMA) represents the most severe end of the gain\u2010of\u2010function (GOF)\n                      <jats:italic>SCN1A<\/jats:italic>\n                      disorder spectrum. Sporadic cases of congenital arthrogryposis have also been reported in individuals with\n                      <jats:italic>SCN2A\u2010<\/jats:italic>\n                      ,\n                      <jats:italic>SCN3A\u2010,<\/jats:italic>\n                      and\n                      <jats:italic>SCN8A<\/jats:italic>\n                      \u2010related developmental and epileptic encephalopathy. Here, we investigated whether NDEEMA occurs in other brain\u2010expressed sodium channelopathies and characterized its features.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Individuals with the clinical phenotype of NDEEMA were identified through internal databases, an international network of epileptologists and geneticists, and the literature. Their clinical and genetic information was analyzed. A literature survey was conducted to review studies describing the functional effects of the pathogenic variants.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Of 46 NDEEMA individuals, 25 harbored variants in\n                      <jats:italic>SCN1A<\/jats:italic>\n                      , 13 in\n                      <jats:italic>SCN2A<\/jats:italic>\n                      , one in\n                      <jats:italic>SCN3A,<\/jats:italic>\n                      and seven in\n                      <jats:italic>SCN8A<\/jats:italic>\n                      . Thirty\u2010five different pathogenic\/likely pathogenic missense variants were identified, all of which clustered in evolutionary conserved paralogous Na\n                      <jats:sub>V<\/jats:sub>\n                      positions. Five individuals died in utero. Thirty\u2010nine of 41 (95%) liveborn individuals developed neonatal epilepsy with tonic seizures and\/or apnea. Thirty\u2010one individuals tried sodium channel blockers, of whom 21 (68%) experienced seizure reduction. All individuals for whom information was available developed movement disorders, with myoclonus, dystonia, and tremor being the most common features. Literature review of functional studies revealed that nine NDEEMA variants, and the corresponding paralogues of 16 additional NDEEMA variants, have been biophysically characterized as GOF.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance<\/jats:title>\n                    <jats:p>\n                      This study expands the phenotype of NDEEMA from\n                      <jats:italic>SCN1A<\/jats:italic>\n                      to its paralogue sodium channel genes expressed in the brain:\n                      <jats:italic>SCN2A, SCN3A<\/jats:italic>\n                      , and\n                      <jats:italic>SCN8A<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/epi.70220","type":"journal-article","created":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T13:00:04Z","timestamp":1775134804000},"page":"3629-3643","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Neonatal developmental and epileptic encephalopathy with movement disorder and arthrogryposis: A shared phenotype across brain\u2010expressed sodium channelopathies"],"prefix":"10.1002","volume":"67","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7404-3631","authenticated-orcid":false,"given":"Sopio","family":"Gverdtsiteli","sequence":"first","affiliation":[{"name":"Department of Epilepsy Genetics and Personalized Medicine Danish Epilepsy Center, Member of the European Reference Network EpiCARE  Dianalund Denmark"},{"name":"Department of Regional Health Research Faculty of Health Sciences, University of Southern Denmark  Odense Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sebastian","family":"Ortiz","sequence":"additional","affiliation":[{"name":"Department of Epilepsy Genetics and Personalized Medicine Danish Epilepsy Center, Member of the European Reference Network EpiCARE  Dianalund Denmark"},{"name":"Department of Regional Health Research Faculty of Health Sciences, University of Southern Denmark  Odense Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tobias","family":"Br\u00fcnger","sequence":"additional","affiliation":[{"name":"Department of Neurology University of Texas Health Science Center at Houston  Houston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4893-9768","authenticated-orcid":false,"given":"Francesca","family":"Furia","sequence":"additional","affiliation":[{"name":"Department of Epilepsy Genetics and Personalized Medicine Danish Epilepsy Center, Member of the European Reference Network EpiCARE  Dianalund Denmark"},{"name":"Department of Regional Health Research Faculty of Health Sciences, University of Southern Denmark  Odense Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5445-5842","authenticated-orcid":false,"given":"Carmen","family":"Barba","sequence":"additional","affiliation":[{"name":"Neuroscience and Medical Genetics Department Meyer Children's Hospital IRCCS  Florence Italy"},{"name":"University of Florence  Florence Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Trine","family":"Bj\u00f8rg\u2010Hammer","sequence":"additional","affiliation":[{"name":"Department of Epilepsy Genetics and Personalized Medicine Danish Epilepsy Center, Member of the European Reference Network EpiCARE  Dianalund Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8484-5945","authenticated-orcid":false,"given":"Ingo","family":"Borggraefe","sequence":"additional","affiliation":[{"name":"Division of Pediatric Neurology Dr. von Haunersches Children's Hospital, Ludwig\u2010Maximilian University (LMU) Munich  Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0259-1046","authenticated-orcid":false,"given":"Roberto","family":"Caraballo","sequence":"additional","affiliation":[{"name":"Department of Neurology Hospital de Pediatr\u00eda J. 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