Timing and Predictors of T2-Lesion Resolution in Patients With Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease
Laura Cacciaguerra, Vyanka Redenbaugh, John J. Chen, Pearse Morris, Elia Sechi, Stephanie B. Syc‐Mazurek, A. Sebastian López‐Chiriboga, Jan‐Mendelt Tillema, Maria A. Rocca, Massimo Filippi, Sean J. Pittock, Eoin P. Flanagan
Abstract
<h3>Objectives</h3> To determine the timing and predictors of T2-lesion resolution in myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD). <h3>Methods</h3> 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). <h3>Results</h3> 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], <i>p</i> = 0.002; large: 0.30 [0.16–0.55], <i>p</i> < 0.001), whereas acute steroids favored resolution of large T2-lesions (1.75 [1.01–3.03], <i>p</i> = 0.046). Notably, 32/55 (58%) T2-lesions resolved without treatment. <h3>Discussion</h3> The high frequency of spontaneous T2-lesion resolution suggests that this represents MOGAD9s natural history. The speed of T2-lesion resolution and influence of size, corticosteroids, and T1-hypointensity on this phenomenon gives insight into MOGAD pathogenesis.