Department of Neurology, Poznan University of Medical Sciences, 49 Przybyszewskiego Street, 60-355 Poznan, Poland.
Department of Neurology, Division of Neurochemistry and Neuropathology, Poznan University of Medical Sciences, 49 Przybyszewskiego Street, 60-355 Poznan, Poland.
Int J Mol Sci. 2020 Dec 24;22(1):100. doi: 10.3390/ijms22010100.
Myelin oligodendrocyte glycoprotein (MOG)-associated disease (MOGAD) is a rare, antibody-mediated inflammatory demyelinating disorder of the central nervous system (CNS) with various phenotypes starting from optic neuritis, via transverse myelitis to acute demyelinating encephalomyelitis (ADEM) and cortical encephalitis. Even though sometimes the clinical picture of this condition is similar to the presentation of neuromyelitis optica spectrum disorder (NMOSD), most experts consider MOGAD as a distinct entity with different immune system pathology. MOG is a molecule detected on the outer membrane of myelin sheaths and expressed primarily within the brain, spinal cord and also the optic nerves. Its function is not fully understood but this glycoprotein may act as a cell surface receptor or cell adhesion molecule. The specific outmost location of myelin makes it a potential target for autoimmune antibodies and cell-mediated responses in demyelinating processes. Optic neuritis seems to be the most frequent presenting phenotype in adults and ADEM in children. In adults, the disease course is multiphasic and subsequent relapses increase disability. In children ADEM usually presents as a one-time incident. Luckily, acute immunotherapy is very effective and severe disability (ambulatory and visual) is less frequent than in NMOSD. A critical element of reliable diagnosis is detection of pathogenic serum antibodies MOG with accurate, specific and sensitive methods, preferably with optimized cell-based assay (CBA). MRI imaging can also help in differentiating MOGAD from other neuro-inflammatory disorders. Reports on randomised control trials are limited, but observational open-label experience suggests a role for high-dose steroids and plasma exchange in the treatment of acute attacks, and for immunosuppressive therapies, such as steroids, oral immunosuppressants and rituximab as maintenance treatment. In this review, we present up-to-date clinical, immunological, radiographic, histopathological data concerning MOGAD and summarize the practical aspects of diagnosing and managing patients with this disease.
髓鞘少突胶质细胞糖蛋白(MOG)相关疾病(MOGAD)是一种罕见的、以抗体为介导的中枢神经系统(CNS)炎症性脱髓鞘疾病,具有多种表型,从视神经炎开始,通过横贯性脊髓炎到急性播散性脑脊髓炎(ADEM)和皮质脑炎。尽管这种疾病的临床表现有时与视神经脊髓炎谱系障碍(NMOSD)相似,但大多数专家认为 MOGAD 是一种具有不同免疫系统病理学的独特实体。MOG 是一种存在于髓鞘外膜上的分子,主要在大脑、脊髓和视神经中表达。其功能尚未完全阐明,但这种糖蛋白可能作为细胞表面受体或细胞黏附分子发挥作用。髓鞘的最外层位置使其成为脱髓鞘过程中自身抗体和细胞介导反应的潜在靶标。视神经炎似乎是成人中最常见的首发表现型,而 ADEM 则在儿童中更为常见。在成人中,疾病过程呈多相性,随后的复发会增加残疾。在儿童中,ADEM 通常表现为一次性发作。幸运的是,急性免疫疗法非常有效,且严重残疾(活动和视力)的发生率低于 NMOSD。可靠诊断的一个关键要素是使用准确、特异和敏感的方法检测致病性血清抗体 MOG,最好使用优化的细胞基础测定法(CBA)。MRI 成像也有助于将 MOGAD 与其他神经炎症性疾病区分开来。随机对照试验的报告有限,但观察性开放标签经验表明,大剂量类固醇和血浆置换在急性发作的治疗中有效,而免疫抑制治疗,如类固醇、口服免疫抑制剂和利妥昔单抗作为维持治疗也有效。在这篇综述中,我们介绍了关于 MOGAD 的最新临床、免疫学、影像学、组织病理学数据,并总结了诊断和管理这种疾病患者的实际方面。