Timing and Predictors of T2-Lesion Resolution in Patients With Myelin-Oligodendrocyte-Glycoprotein-Antibody-Associated Disease

Objectives To determine the timing and predictors of T2-lesion resolution in myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD). Methods This retrospective observational study using standard-of-care data had inclusion criteria of MOGAD diagnosis, ≥2 MRIs 12 months apart, and ≥1 brain/spinal cord T2-lesion. The median (interquartile range [IQR]) number of MRIs (82% at disease onset) per-patient were: brain, 5 (2–8); spine, 4 (2–8). Predictors of T2-lesion resolution were assessed with age- and sex-adjusted generalized estimating equations and stratified by T2-lesion size (small <1 cm; large ≥1 cm). Results We studied 583 T2-lesions (brain, 512 [88%]; spinal cord, 71 [12%]) from 55 patients. At last MRI (median follow-up 54 months [IQR 7–74]) 455 T2-lesions (78%) resolved. The median (IQR) time to resolution was 3 months (1.4–7.0). Small T2-lesions resolved more frequently and faster than large T2-lesions. Acute T1-hypointensity decreased the likelihood (odds ratio [95% CI]) of T2-lesion resolution independent of size (small: 0.23 [0.09–0.60], p = 0.002; large: 0.30 [0.16–0.55], p < 0.001), whereas acute steroids favored resolution of large T2-lesions (1.75 [1.01–3.03], p = 0.046). Notably, 32/55 (58%) T2-lesions resolved without treatment. Discussion The high frequency of spontaneous T2-lesion resolution suggests that this represents MOGAD's natural history. The speed of T2-lesion resolution and influence of size, corticosteroids, and T1-hypointensity on this phenomenon gives insight into MOGAD pathogenesis.