MOGAD患者新发MRI亚临床病灶研究进展

Research Progress on New Subclinical MRI Lesions in MOGAD Patients

摘要: 抗髓鞘少突胶质细胞糖蛋白免疫球蛋白G抗体相关疾病(Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease, MOGAD)是一种中枢神经系统炎性脱髓鞘疾病，部分患者在临床缓解期存在新发亚临床MRI病灶，目前对此类病灶的定义、影像特征及其与疾病复发和预后的关系缺乏共识，临床管理多基于经验。本文通过系统回顾相关研究，总结其流行病学、影像学特征及临床意义，为临床决策提供循证参考。结果显示，MOGAD临床缓解期亚临床病灶总体发生率较低，好发于皮质下白质及深部灰质，常表现为边界模糊的T2/FLAIR高信号，钆强化罕见，且具有高度可逆性。现有证据提示此类病灶的出现与短期/远期临床复发风险及远期神经功能残疾进展缺乏明确且一致的相关性，相较于多发性硬化(Multiple Sclerosis, MS)的无疾病活动，MOGAD的亚临床病灶可能更多反映一过性、可逆的炎症过程，而非持续的疾病活动。目前不推荐将亚临床病灶作为启动或升级免疫抑制治疗的主要依据。MOGAD的临床管理应以临床症状为主，对亚临床病灶应采取审慎的个体化管理策略。

Abstract: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory demyelinating disorder of the central nervous system. Some patients develop new, asymptomatic magnetic resonance imaging (MRI) lesions during periods of clinical remission. Currently, there is a lack of consensus regarding the definition, imaging characteristics, and the relationship of these lesions with disease relapse and prognosis, leading to predominantly experience-based clinical management. This article provides a systematic review of relevant studies on subclinical lesions in MOGAD, summarizing their epidemiology, patterns of dynamic imaging evolution, and clinical significance to offer an evidence-based reference for clinical decision-making. The results indicate that the overall incidence of subclinical lesions during clinical remission in MOGAD is relatively low. These lesions show a predilection for the subcortical white matter and deep gray matter, typically appearing as ill-defined T2/FLAIR hyperintensities. Gadolinium enhancement is rare and characterized by a high degree of reversibility. Current evidence suggests that the appearance of such lesions lacks a clear and consistent correlation with both short-term and long-term risks of clinical relapse, as well as with the progression of long-term neurological disability. Unlike in multiple sclerosis (MS), subclinical lesions in MOGAD may reflect a transient, reversible inflammatory process rather than an indication of persistent disease activity. Consequently, it is currently not recommended to use the presence of subclinical lesions as a primary basis for initiating or escalating long-term immunosuppressive therapy. The clinical management of MOGAD should be primarily guided by clinical symptoms, adopting a prudent and individualized observation strategy for subclinical lesions.