{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T03:31:32Z","timestamp":1790652692292,"version":"4.1.0"},"reference-count":22,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2017,12,30]],"date-time":"2017-12-30T00:00:00Z","timestamp":1514592000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000272","name":"National Institute for Health Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000272","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000272","name":"National Institute for Health Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000272","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000317","name":"Action Medical Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000317","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000381","name":"Multiple Sclerosis Society","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000381","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000272","name":"National Institute for Health Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000272","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Develop Med Child Neuro"],"published-print":{"date-parts":[[2018,4]]},"abstract":"<jats:sec><jats:title>Aim<\/jats:title><jats:p>To review the demographics and clinical and paraclinical parameters of children with myelin oligodendrocyte glycoprotein (<jats:styled-content style=\"fixed-case\">MOG<\/jats:styled-content>) antibody\u2010associated relapsing disease.<\/jats:p><\/jats:sec><jats:sec><jats:title>Method<\/jats:title><jats:p>In this <jats:styled-content style=\"fixed-case\">UK<\/jats:styled-content>\u2010based, multicentre study, 31 children with <jats:styled-content style=\"fixed-case\">MOG<\/jats:styled-content> antibody\u2010associated relapsing disease were studied retrospectively.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Of the 31 children studied, 14 presented with acute disseminated encephalomyelitis (<jats:styled-content style=\"fixed-case\">ADEM<\/jats:styled-content>); they were younger (mean 4.1y) than the remainder (mean 8.5y) who presented with optic neuritis and\/or transverse myelitis (<jats:italic>p<\/jats:italic>&lt;0.001). Similarly, children who had an abnormal brain magnetic resonance imaging (<jats:styled-content style=\"fixed-case\">MRI<\/jats:styled-content>) at onset (<jats:italic>n<\/jats:italic>=20) were younger than patients with normal <jats:styled-content style=\"fixed-case\">MRI<\/jats:styled-content> at onset (<jats:italic>p<\/jats:italic>=0.001) or at follow\u2010up (<jats:italic>p<\/jats:italic>&lt;0.001). \u2018Leukodystrophy\u2010like\u2019 <jats:styled-content style=\"fixed-case\">MRI<\/jats:styled-content> patterns of confluent largely symmetrical lesions was seen during the course of the disease in 7 out of 14 children with a diagnosis of <jats:styled-content style=\"fixed-case\">ADEM<\/jats:styled-content>, and was only seen in children younger than 7 years of age. Their disability after a 3\u2010year follow\u2010up was mild to moderate, and most patients continued to relapse, despite disease\u2010modifying treatments.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">MOG<\/jats:styled-content> antibody should be tested in children presenting with relapsing neurological disorders associated with confluent, bilateral white matter changes, and distinct enhancement pattern. Children with <jats:styled-content style=\"fixed-case\">MOG<\/jats:styled-content> antibody\u2010associated disease present with age\u2010related differences in phenotypes, with a severe leukoencephalopathy phenotype in the very young and normal intracranial <jats:styled-content style=\"fixed-case\">MRI<\/jats:styled-content> in the older children. This finding suggests a susceptibility of the very young and myelinating brain to <jats:styled-content style=\"fixed-case\">MOG<\/jats:styled-content> antibody\u2010mediated mechanisms of damage.<\/jats:p><\/jats:sec><jats:sec><jats:title>What this paper adds<\/jats:title><jats:p>\n<jats:list list-type=\"bullet\">\n\n<jats:list-item><jats:p>Myelin oligodendrocyte glycoprotein (MOG) antibody\u2010associated demyelination manifest with an age\u2010related phenotype.<\/jats:p><\/jats:list-item>\n\n<jats:list-item><jats:p>Children with MOG antibody and \u2018leukodystrophy\u2010like\u2019 imaging patterns tend to have poor response to second\u2010line immunotherapy.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><\/jats:sec>","DOI":"10.1111\/dmcn.13649","type":"journal-article","created":{"date-parts":[[2017,12,30]],"date-time":"2017-12-30T05:36:40Z","timestamp":1514612200000},"page":"417-423","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":119,"title":["\u2018Leukodystrophy\u2010like\u2019 phenotype in children with myelin oligodendrocyte glycoprotein antibody\u2010associated disease"],"prefix":"10.1111","volume":"60","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8490-9657","authenticated-orcid":false,"given":"Yael","family":"Hacohen","sequence":"first","affiliation":[{"name":"Department of Neuroinflammation Queen Square MS Centre UCL Institute of Neurology London UK"},{"name":"Department of Paediatric Neurology Great Ormond Street Hospital for Children London 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