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In this observational retrospective study, we characterized 19 CCE patients (6.7% of our MOGAD cohort). Headache (n\u00a0=\u00a015, 79%), seizures (n\u00a0=\u00a013, 68%), and encephalopathy (n\u00a0=\u00a012, 63%) were frequent. Magnetic resonance imaging revealed unilateral (n\u00a0=\u00a012, 63%) or bilateral (n\u00a0=\u00a07, 37%) cortical T2 hyperintensity and leptomeningeal enhancement (n\u00a0=\u00a017, 89%). N\u2010Methyl\u2010D\u2010aspartate receptor autoantibodies coexisted in 2 of 15 tested (13%). CCE pathology (n\u00a0=\u00a02) showed extensive subpial cortical demyelination (n\u00a0=\u00a02), microglial reactivity (n\u00a0=\u00a02), and inflammatory infiltrates (perivascular, n\u00a0=\u00a01; meningeal, n\u00a0=\u00a01). Most received high\u2010dose steroids (n\u00a0=\u00a017, 89%), and all improved, but 3 had CCE relapses. This study highlights the CCE spectrum and provides insight into its pathogenesis. 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