To determine the timing of T2-lesion resolution and its predictors in myelin-oligodendrocyte glycoprotein antibody-associated disease (MOGAD).

MOGAD T2-lesions often resolve over time, differing from other demyelinating disorders. Studies assessing the timing and predictors of T2-lesion resolution are lacking, yet may improve our understanding of its pathophysiology and guide the timing of follow-up MRI.

We retrospectively included 63 patients (pediatric-onset 17, 27%) with a MOGAD diagnosis, >2 MRIs, and >1 brain or spinal lesion. A lesion-diameter of ≥1 cm was required to avoid non-inflammatory lesions. T2-lesion resolution was assessed on all available scans. The association between patient and intrinsic lesion factors and lesion resolution over 12 months was assessed with age-, sex- and lesion diameter/length-adjusted generalized estimating equations.

We studied 404 T2-lesions (brain, 314[78%]; spinal cord, 90[22%]). Median (interquartile range) follow-up duration and number of scans per patient were 46 (13-74) months, 5 (3-8) brain and 4 (2-8) spinal cord, respectively. At last MRI, 287 lesions (71%) resolved, with a median (interquartile range) time-to-resolution of 4 months (2-12). Among patient factors, concomitant optic neuritis was associated with a lower likelihood of resolution (odds ratio [95% confidence interval] -0.93 [-1.76; -0.10], p=0.028). Acute treatment (steroids, immunoglobulins or plasma-exchange) had no effect (-0.57 [-1.21; 0.07], p=0.08), and in those receiving no acute treatment spontaneous resolution occurred in 17/35 lesions (49%). Among intrinsic lesion features, deep grey matter location increased the likelihood of resolution (1.08 [0.25; 1.91], p=0.011), while T1-hypointensity (-1.21 [-1.82; -0.59], p<0.001) decreased the likelihood of resolution. High-antibody titer, pediatric-onset, location in brain vs. spinal cord, and oligoclonal bands were not predictive of lesion resolution.

MOGAD T2-lesions usually resolve within one year irrespective of acute treatment. This likely reflects the distinct pathogenesis of MOGAD rather than treatment response and may help in differentiating from multiple sclerosis.