<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>89(2)</volume><submitter>Ramanathan S</submitter><funding>The Petre Foundation</funding><funding>Brain Foundation</funding><funding>Sydney Research Excellence Initiative 2020 Neuroimmunology Group</funding><funding>The National Blood Authority IVIg Grant</funding><funding>National Health and Medical Research Council</funding><funding>The National Blood Authorit IVIg Grant</funding><funding>Multiple Sclerosis Research Australia</funding><pubmed_abstract>&lt;h4>Objective&lt;/h4>We characterised the clinical course, treatment and outcomes in 59 patients with relapsing myelin oligodendrocyte glycoprotein (MOG) antibody-associated demyelination.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/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</pubmed_abstract><journal>Journal of neurology, neurosurgery, and psychiatry</journal><pagination>127-137</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5800335</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Clinical course, therapeutic responses and outcomes in relapsing MOG antibody-associated demyelination.</pubmed_title><pmcid>PMC5800335</pmcid><pubmed_authors>Merheb V</pubmed_authors><pubmed_authors>Patrick E</pubmed_authors><pubmed_authors>Gill D</pubmed_authors><pubmed_authors>White OB</pubmed_authors><pubmed_authors>O'grady G</pubmed_authors><pubmed_authors>Thompson J</pubmed_authors><pubmed_authors>Clark D</pubmed_authors><pubmed_authors>Fraser C</pubmed_authors><pubmed_authors>Ware T</pubmed_authors><pubmed_authors>Caruana P</pubmed_authors><pubmed_authors>Vucic S</pubmed_authors><pubmed_authors>Barnett MH</pubmed_authors><pubmed_authors>Subramanian G</pubmed_authors><pubmed_authors>Yiannikas C</pubmed_authors><pubmed_authors>Mohammad S</pubmed_authors><pubmed_authors>Marriott M</pubmed_authors><pubmed_authors>Pilli D</pubmed_authors><pubmed_authors>Shah U</pubmed_authors><pubmed_authors>Cairns A</pubmed_authors><pubmed_authors>Freeman J</pubmed_authors><pubmed_authors>Ouvrier R</pubmed_authors><pubmed_authors>Tantsis E</pubmed_authors><pubmed_authors>Calvert S</pubmed_authors><pubmed_authors>Kothur K</pubmed_authors><pubmed_authors>Spooner C</pubmed_authors><pubmed_authors>Australasian and New Zealand MOG Study Group</pubmed_authors><pubmed_authors>Ramanathan S</pubmed_authors><pubmed_authors>Brilot F</pubmed_authors><pubmed_authors>Broadley S</pubmed_authors><pubmed_authors>Orr C</pubmed_authors><pubmed_authors>Yiu E</pubmed_authors><pubmed_authors>Grattan-Smith P</pubmed_authors><pubmed_authors>Hardy T</pubmed_authors><pubmed_authors>Webster R</pubmed_authors><pubmed_authors>Chelakkadan S</pubmed_authors><pubmed_authors>Shuey N</pubmed_authors><pubmed_authors>Barton J</pubmed_authors><pubmed_authors>Ryan M</pubmed_authors><pubmed_authors>Zou A</pubmed_authors><pubmed_authors>Parratt J</pubmed_authors><pubmed_authors>Burrow J</pubmed_authors><pubmed_authors>Nosadini M</pubmed_authors><pubmed_authors>Riminton D</pubmed_authors><pubmed_authors>Lopez J</pubmed_authors><pubmed_authors>Fung VSC</pubmed_authors><pubmed_authors>Lechner-Scott J</pubmed_authors><pubmed_authors>Andrews P</pubmed_authors><pubmed_authors>Nguyen TK</pubmed_authors><pubmed_authors>Tea F</pubmed_authors><pubmed_authors>Thomas T</pubmed_authors><pubmed_authors>Reddel SW</pubmed_authors><pubmed_authors>Ling S</pubmed_authors><pubmed_authors>Gupta S</pubmed_authors><pubmed_authors>Rodriguez-Casero V</pubmed_authors><pubmed_authors>Butzkueven H</pubmed_authors><pubmed_authors>Scheffer I</pubmed_authors><pubmed_authors>Troedson C</pubmed_authors><pubmed_authors>Malone S</pubmed_authors><pubmed_authors>Dale RC</pubmed_authors><pubmed_authors>Henderson APD</pubmed_authors><pubmed_authors>Riney K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Clinical course, therapeutic responses and outcomes in relapsing MOG antibody-associated demyelination.</name><description>&lt;h4>Objective&lt;/h4>We characterised the clinical course, treatment and outcomes in 59 patients with relapsing myelin oligodendrocyte glycoprotein (MOG) antibody-associated demyelination.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/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</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Feb</publication><modification>2026-06-17T07:06:18.956Z</modification><creation>2026-06-17T03:10:24.854Z</creation></dates><accession>S-EPMC5800335</accession><cross_references><pubmed>29142145</pubmed><doi>10.1136/jnnp-2017-316880</doi></cross_references></HashMap>