{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Valencia-Sanchez C"],"funding":["National Institute of Neurological Disorders and Stroke","NINDS NIH HHS"],"pagination":["297-302"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10107670"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["93(2)"],"pubmed_abstract":["Cerebral cortical encephalitis (CCE) is a recently described myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) phenotype. In this observational retrospective study, we characterized 19 CCE patients (6.7% of our MOGAD cohort). Headache (n = 15, 79%), seizures (n = 13, 68%), and encephalopathy (n = 12, 63%) were frequent. Magnetic resonance imaging revealed unilateral (n = 12, 63%) or bilateral (n = 7, 37%) cortical T2 hyperintensity and leptomeningeal enhancement (n = 17, 89%). N-Methyl-D-aspartate receptor autoantibodies coexisted in 2 of 15 tested (13%). CCE pathology (n = 2) showed extensive subpial cortical demyelination (n = 2), microglial reactivity (n = 2), and inflammatory infiltrates (perivascular, n = 1; meningeal, n = 1). Most received high-dose steroids (n "],"journal":["Annals of neurology"],"pubmed_title":["Cerebral Cortical Encephalitis in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease."],"pmcid":["PMC10107670"],"funding_grant_id":["R01NS113828"],"pubmed_authors":["Budhram A","Guo Y","Valencia-Sanchez C","Kunchok A","Chen JJ","Dubey D","Krecke KN","Elsbernd PM","Redenbaugh V","Tillema JM","Sechi E","Pittock SJ","Flanagan EP","Lucchinetti CF","Montalvo M","Lopez-Chiriboga S"],"additional_accession":[]},"is_claimable":false,"name":"Cerebral Cortical Encephalitis in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.","description":"Cerebral cortical encephalitis (CCE) is a recently described myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) phenotype. In this observational retrospective study, we characterized 19 CCE patients (6.7% of our MOGAD cohort). Headache (n = 15, 79%), seizures (n = 13, 68%), and encephalopathy (n = 12, 63%) were frequent. Magnetic resonance imaging revealed unilateral (n = 12, 63%) or bilateral (n = 7, 37%) cortical T2 hyperintensity and leptomeningeal enhancement (n = 17, 89%). N-Methyl-D-aspartate receptor autoantibodies coexisted in 2 of 15 tested (13%). CCE pathology (n = 2) showed extensive subpial cortical demyelination (n = 2), microglial reactivity (n = 2), and inflammatory infiltrates (perivascular, n = 1; meningeal, n = 1). Most received high-dose steroids (n ","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2025-04-26T05:03:02.127Z","creation":"2025-04-06T11:21:36.643Z"},"accession":"S-EPMC10107670","cross_references":{"pubmed":["36372941"],"doi":["10.1002/ana.26549"]}}