TY - JOUR
T1 - Timing and Predictors of T2-Lesion Resolution in Patients with Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease
AU - Cacciaguerra, Laura
AU - Redenbaugh, Vyanka
AU - Chen, John J.
AU - Morris, Pearse
AU - Sechi, Elia
AU - Syc-Mazurek, Stephanie B.
AU - Lopez-Chiriboga, A. Sebastian
AU - Tillema, Jan Mendelt
AU - Rocca, Maria A.
AU - Filippi, Massimo
AU - Pittock, Sean J.
AU - Flanagan, Eoin P.
N1 - Publisher Copyright:
© American Academy of Neurology.
PY - 2023/9/26
Y1 - 2023/9/26
N2 - ObjectivesTo determine the timing and predictors of T2-lesion resolution in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).MethodsThis 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).ResultsWe 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.DiscussionThe 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.
AB - ObjectivesTo determine the timing and predictors of T2-lesion resolution in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).MethodsThis 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).ResultsWe 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.DiscussionThe 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.
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U2 - 10.1212/WNL.0000000000207478
DO - 10.1212/WNL.0000000000207478
M3 - Article
C2 - 37336767
AN - SCOPUS:85166781769
SN - 0028-3878
VL - 101
SP - E1376-E1381
JO - Neurology
JF - Neurology
IS - 13
ER -