From the Department of Neurology and Mayo Clinic Center for Multiple Sclerosis and Autoimmune Neurology (L.C., V.R., J.J.C., S.B.S.-M., J.-M.T., S.J.P., E.P.F.), Mayo Clinic, Rochester, MN; Vita-Salute San Raffaele University (L.C., M.A.R., M.F.); Neuroimaging Research Unit (L.C., M.A.R., M.F.), Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy; Department of Ophthalmology (J.J.C.), and Department of Radiology (P.M.), Mayo Clinic, Rochester, MN; Department of Medical, Surgical and Experimental Sciences (E.S.), University of Sassari, Italy; Department of Neurology (A.S.L.-C.), Mayo Clinic, Jacksonville, FL; Neurology Unit (M.A.R., M.F.), Neurorehabilitation Unit (M.F.), and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; and Laboratory Medicine and Pathology (S.J.P., E.P.F.), Mayo Clinic, Rochester, MN.
Neurology. 2023 Sep 26;101(13):e1376-e1381. doi: 10.1212/WNL.0000000000207478. Epub 2023 Jun 19.
To determine the timing and predictors of T2-lesion resolution in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).
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).
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], = 0.002; large: 0.30 [0.16-0.55], < 0.001), whereas acute steroids favored resolution of large T2-lesions (1.75 [1.01-3.03], = 0.046). Notably, 32/55 (58%) T2-lesions resolved without treatment.
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.
确定髓鞘少突胶质细胞糖蛋白抗体相关性疾病（MOGAD）中 T2 病灶消退的时间和预测因素。
这项回顾性观察性研究使用标准治疗数据，纳入标准为 MOGAD 诊断、12 个月内至少 2 次 MRI 且至少有 1 个脑/脊髓 T2 病灶。每位患者的中位数（四分位距 [IQR]）MRI 数量（疾病发作时为 82%）为：脑部，5（2-8）；脊柱，4（2-8）。使用年龄和性别调整的广义估计方程评估 T2 病灶消退的预测因素，并按 T2 病灶大小（小 <1 cm；大 ≥1 cm）分层。
我们研究了 55 例患者的 583 个 T2 病灶（脑，512 [88%]；脊髓，71 [12%]）。在最后一次 MRI（中位随访 54 个月 [IQR 7-74]）时，455 个 T2 病灶（78%）消退。中位（IQR）消退时间为 3 个月（1.4-7.0）。小 T2 病灶比大 T2 病灶消退更频繁且更快。急性 T1 低信号降低了 T2 病灶消退的可能性（大小无关的比值比 [95%CI]）：小病灶：0.23（0.09-0.60）， = 0.002；大病灶：0.30（0.16-0.55）， < 0.001），而急性类固醇有利于大 T2 病灶的消退（1.75 [1.01-3.03]， = 0.046）。值得注意的是，55 例患者中有 32 例（58%）T2 病灶未经治疗而消退。
高频率的自发 T2 病灶消退表明这代表了 MOGAD 的自然史。T2 病灶消退的速度以及大小、皮质类固醇和 T1 低信号对这一现象的影响，使我们深入了解了 MOGAD 的发病机制。
