Chen, John J.

Background: Data on corpus callosum involvement in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are limited. Objective: The objective of the study was to compare callosal lesions in MOGAD, multiple sclerosis (MS), and aquaporin-4-IgG positive neuromyelitis optica spectrum disorder (AQP4+NMOSD). Results: Callosal lesion frequency was similar in MOGAD (38/171 (22%)), MS (24/72 (33%)), and AQP4+NMOSD (18/63 (29%)). Clinical phenotypes included encephalopathy (47%) and focal supratentorial (21%) or infratentorial (45%) deficits. None had callosal-disconnection syndromes. Maximal callosal-T2-lesion diameter (median (range)) in millimeter was similar in MOGAD (21 (4–77)) and AQP4+NMOSD (22 (5–49); p = 0.93) but greater than in MS (10.5 (2–64)). Extracallosal extension (21/38 (55%)) and T2-lesion resolution (19/34 (56%)) favored MOGAD. Conclusions: Despite similar frequency and imaging overlap, larger lesions, sagittal midline involvement, and lesion resolution favored MOGAD.

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 = 17, 89%), and all improved, but 3 had CCE relapses. This study highlights the CCE spectrum and provides insight into its pathogenesis. ANN NEUROL 2023;93:297–302

Purpose To determine whether metabolic syndrome (MetS) is a risk factor for various forms of optic neuropathy including non-arteritic anterior ischaemic optic neuropathy (NAION). Methods This population-based analysis identified patients ≥40 years of age in Olmsted County, Minnesota, USA using the Rochester Epidemiology Project 2005–2018. Patients with MetS were identified if three or more of the five standard criteria for diagnosing MetS were present: systemic hypertension, hyperglycaemia, hypertriglyceridaemia, reduced high-density lipoprotein cholesterol (hypoalphalipoproteinaemia) and central adiposity defined by increased body mass index. Charts of patients identified as having an optic neuropathy were reviewed to record specific diagnoses and compared with patients without ocular pathology other than cataract. The odds ratio (OR) of association with MetS was calculated and adjusted for age, sex and race with multivariate analysis for the various optic neuropathies. Results Patients with MetS were more likely to have an optic neuropathy than those without (OR 2.2, p<0.001). After adjusting for age, sex and race, the only optic neuropathy found to be significantly associated with MetS was NAION (OR 6.17, p=0.002). For patients with NAION, though each individual component of MetS was individually significantly associated with MetS, further analysis suggested that hypertriglyceridaemia, hypoalphalipoproteinaemia and hyperglycaemia were likely the key drivers in the overall significance between NAION and MetS. Conclusion Patients with MetS were more likely to have NAION. Further studies are needed to determine whether MetS is a modifiable risk factor for NAION.