{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["89(2)"],"submitter":["Ramanathan S"],"funding":["The Petre Foundation","Brain Foundation","Sydney Research Excellence Initiative 2020 Neuroimmunology Group","The National Blood Authority IVIg Grant","National Health and Medical Research Council","The National Blood Authorit IVIg Grant","Multiple Sclerosis Research Australia"],"pubmed_abstract":["<h4>Objective</h4>We characterised the clinical course, treatment and outcomes in 59 patients with relapsing myelin oligodendrocyte glycoprotein (MOG) antibody-associated demyelination.<h4>Methods</h4>We evaluated clinical phenotypes, annualised relapse rates (ARR) prior and on immunotherapy and Expanded Disability Status Scale (EDSS), in 218 demyelinating episodes from 33 paediatric and 26 adult patients.<h4>Results</h4>The most common initial presentation in the cohort was optic neuritis (ON) in 54% (bilateral (BON) 32%, unilateral (UON) 22%), followed by acute disseminated encephalomyelitis (ADEM) (20%), which occurred exclusively in children. ON was the dominant phenotype (UON 35%, BON 19%) of all clinical episodes. 109/226 (48%) MRIs had no brain lesions. Patients were steroid respons"],"journal":["Journal of neurology, neurosurgery, and psychiatry"],"pagination":["127-137"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5800335"],"repository":["biostudies-literature"],"pubmed_title":["Clinical course, therapeutic responses and outcomes in relapsing MOG antibody-associated demyelination."],"pmcid":["PMC5800335"],"pubmed_authors":["Merheb V","Patrick E","Gill D","White OB","O'grady G","Thompson J","Clark D","Fraser C","Ware T","Caruana P","Vucic S","Barnett MH","Subramanian G","Yiannikas C","Mohammad S","Marriott M","Pilli D","Shah U","Cairns A","Freeman J","Ouvrier R","Tantsis E","Calvert S","Kothur K","Spooner C","Australasian and New Zealand MOG Study Group","Ramanathan S","Brilot F","Broadley S","Orr C","Yiu E","Grattan-Smith P","Hardy T","Webster R","Chelakkadan S","Shuey N","Barton J","Ryan M","Zou A","Parratt J","Burrow J","Nosadini M","Riminton D","Lopez J","Fung VSC","Lechner-Scott J","Andrews P","Nguyen TK","Tea F","Thomas T","Reddel SW","Ling S","Gupta S","Rodriguez-Casero V","Butzkueven H","Scheffer I","Troedson C","Malone S","Dale RC","Henderson APD","Riney K"],"additional_accession":[]},"is_claimable":false,"name":"Clinical course, therapeutic responses and outcomes in relapsing MOG antibody-associated demyelination.","description":"<h4>Objective</h4>We characterised the clinical course, treatment and outcomes in 59 patients with relapsing myelin oligodendrocyte glycoprotein (MOG) antibody-associated demyelination.<h4>Methods</h4>We evaluated clinical phenotypes, annualised relapse rates (ARR) prior and on immunotherapy and Expanded Disability Status Scale (EDSS), in 218 demyelinating episodes from 33 paediatric and 26 adult patients.<h4>Results</h4>The most common initial presentation in the cohort was optic neuritis (ON) in 54% (bilateral (BON) 32%, unilateral (UON) 22%), followed by acute disseminated encephalomyelitis (ADEM) (20%), which occurred exclusively in children. ON was the dominant phenotype (UON 35%, BON 19%) of all clinical episodes. 109/226 (48%) MRIs had no brain lesions. Patients were steroid respons","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Feb","modification":"2026-06-17T07:06:18.956Z","creation":"2026-06-17T03:10:24.854Z"},"accession":"S-EPMC5800335","cross_references":{"pubmed":["29142145"],"doi":["10.1136/jnnp-2017-316880"]}}