Abstract
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 MRI’s 12 months apart, and >1 brain/spinal cord T2-lesion. The median (interquartile-range[IQR]) number of MRI’s (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-hypointesity decreased the likelihood (odds ratio[95% confidence interval]) 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) while 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 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.
- Received November 29, 2022.
- Accepted in final form April 17, 2023.
- © 2023 American Academy of Neurology
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