{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T07:33:31Z","timestamp":1792740811848,"version":"4.5.0"},"reference-count":35,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2022,7,16]],"date-time":"2022-07-16T00:00:00Z","timestamp":1657929600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100007735","name":"DGN","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100007735","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008087","name":"Guthy-Jackson Charitable Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008087","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2022,9]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>Patients with myelin oligodendrocyte glycoprotein antibody (MOG\u2010IgG)\u2010associated disease (MOGAD) suffer from severe optic neuritis (ON) leading to retinal neuro\u2010axonal loss, which can be quantified by optical coherence tomography (OCT). We assessed whether ON\u2010independent retinal atrophy can be detected in MOGAD.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Eighty patients with MOGAD and 139 healthy controls (HCs) were included. OCT data was acquired with (1) Spectralis spectral domain OCT (MOGAD: <jats:italic>N<\/jats:italic>\u00a0=\u00a066 and HCs: <jats:italic>N<\/jats:italic>\u00a0=\u00a0103) and (2) Cirrus high\u2010definition OCT (MOGAD: <jats:italic>N<\/jats:italic>\u00a0=\u00a014 and HCs: <jats:italic>N<\/jats:italic>\u00a0=\u00a036). Macular combined ganglion cell and inner plexiform layer (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL) were quantified.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>At baseline, GCIPL and pRNFL were lower in MOGAD eyes with a history of ON (MOGAD\u2010ON) compared with MOGAD eyes without a history of ON (MOGAD\u2010NON) and HCs (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001). MOGAD\u2010NON eyes had lower GCIPL volume compared to HCs (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001) in the Spectralis, but not in the Cirrus cohort. Longitudinally (follow\u2010up up to 3\u2009years), MOGAD\u2010ON with ON within the last 6\u201312\u00a0months before baseline exhibited greater pRNFL thinning than MOGAD\u2010ON with an ON greater than 12\u00a0months ago (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001). The overall MOGAD cohort did not exhibit faster GCIPL thinning compared with the HC cohort.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>Our study suggests the absence of attack\u2010independent retinal damage in patients with MOGAD. Yet, ongoing neuroaxonal damage or edema resolution seems to occur for up to 12\u00a0months after ON, which is longer than what has been reported with other ON forms. These findings support that the pathomechanisms underlying optic nerve involvement and the evolution of OCT retinal changes after ON is distinct in patients with MOGAD. ANN NEUROL 2022;92:476\u2013485<\/jats:p><\/jats:sec>","DOI":"10.1002\/ana.26440","type":"journal-article","created":{"date-parts":[[2022,6,15]],"date-time":"2022-06-15T12:21:07Z","timestamp":1655295667000},"page":"476-485","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":61,"title":["Longitudinal Retinal Changes in <scp>MOGAD<\/scp>"],"prefix":"10.1002","volume":"92","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4906-5983","authenticated-orcid":false,"given":"Frederike Cosima","family":"Oertel","sequence":"first","affiliation":[{"name":"Experimental and Clinical Research Center Max Delbr\u00fcck Center for Molecular Medicine and Charit\u00e9 \u2013 Universit\u00e4tsmedizin Berlin, corporate member of Freie Universit\u00e4t Berlin and Humboldt\u2010Universit\u00e4tzu Berlin  Berlin Germany"},{"name":"NeuroCure Clinical Research Center Charit\u00e9 \u2013 Universit\u00e4tsmedizin Berlin, corporate member of Freie Universit\u00e4t Berlin and Humboldt\u2010Universit\u00e4t zu Berlin  Berlin Germany"},{"name":"Department of Neurology University of California San Francisco  San Francisco CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8812-1637","authenticated-orcid":false,"given":"Elias S.","family":"Sotirchos","sequence":"additional","affiliation":[{"name":"Department of Neurology Johns Hopkins University School of Medicine  Baltimore MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0276-8051","authenticated-orcid":false,"given":"Hanna G.","family":"Zimmermann","sequence":"additional","affiliation":[{"name":"Experimental and Clinical Research Center Max Delbr\u00fcck Center for Molecular Medicine and Charit\u00e9 \u2013 Universit\u00e4tsmedizin Berlin, corporate member of Freie Universit\u00e4t Berlin and Humboldt\u2010Universit\u00e4tzu Berlin  Berlin Germany"},{"name":"NeuroCure Clinical 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