{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T15:05:26Z","timestamp":1787065526560,"version":"build-2736575974"},"reference-count":52,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T00:00:00Z","timestamp":1777852800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T00:00:00Z","timestamp":1777852800000},"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":["Ann Clin Transl Neurol"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>The study aimed to characterize the clinical features, etiologies, and outcomes of isolated, first\u2010time pediatric ON in the post\u2010MOG\u2010IgG era.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This was a single\u2010center retrospective cohort study at Texas Children's Hospital of patients diagnosed with first\u2010time ON between 2018\u20132024, with follow\u2010up data collected through 2025. Inclusion criteria required monocular or binocular subacute vision loss with supportive paraclinical signs. Subjects were excluded if they had a prior history of demyelinating disease or extra\u2010orbital demyelinating lesions on initial brain\/spine MRI. Primary outcomes were the proportion of MOG\u2010IgG seropositivity, retinal nerve fiber layer thickness, and visual acuity at onset and most recent follow\u2010up.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Of 73 children with ON, 38 met criteria for isolated first\u2010time ON. Etiologies included MOGAD (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200927, 71.1%) and idiopathic\/monophasic (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u20099, 23.7%), while none of the 38 subjects were later diagnosed with multiple sclerosis. MOGAD\u2010ON was associated with less severe vision loss at presentation (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.01) compared to idiopathic cases. At most recent follow\u2010up, both groups achieved excellent functional recovery, yet both demonstrated significant retinal nerve fiber layer thinning from ON presentation. Linear regression revealed worse presenting LogMAR significantly correlated to thinner follow\u2010up RNFL (F(1,18)\u2009=\u20098.467, R\n                      <jats:sup>2<\/jats:sup>\n                      \u2009=\u20090.32,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.01). One (3.7%) MOGAD\u2010ON patient relapsed during follow\u2010up.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>In isolated pediatric ON, no patients were diagnosed with MS, and MOGAD is the predominant etiology. The linear correlation between initial LogMAR and subsequent RNFL atrophy suggests a permanent reduction in neurological reserve dependent on the degree of functional severity at ON onset.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/acn3.70422","type":"journal-article","created":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T11:53:31Z","timestamp":1777895611000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["<scp>MOGAD<\/scp>\n                    Is the Most Common Cause of Isolated Optic Neuritis in Children"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0009-0005-7048-7912","authenticated-orcid":false,"given":"Chaitanya","family":"Aduru","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Section of Neurology and Developmental Neuroscience Baylor College of Medicine and Texas Children's Hospital  Houston Texas 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Section of Neurology and Developmental Neuroscience Baylor College of Medicine and Texas Children's Hospital  Houston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8213-2941","authenticated-orcid":false,"given":"Alexander J.","family":"Sandweiss","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Section of Neurology and Developmental Neuroscience Baylor College of Medicine and Texas Children's Hospital  Houston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,5,4]]},"reference":[{"issue":"1","key":"e_1_2_11_2_1","doi-asserted-by":"crossref","first-page":"89","DOI":"10.1016\/S1474-4422(22)00187-9","article-title":"Optic Neuritis and Autoimmune Optic Neuropathies: Advances in Diagnosis and Treatment","volume":"22","author":"Bennett J. 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