Abstract：
OBJECTIVE: Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is a distinct neuroinflammatory condition characterized by attacks of optic neuritis, transverse myelitis, and other demyelinating events. Though it can mimic multiple sclerosis and neuromyelitis optica spectrum disorder, distinct clinical and radiologic features which can discriminate these conditions are now recognized. This review highlights recent advances in our understanding of clinical manifestations, diagnosis, and treatment of MOGAD.
RESULTS: Studies have identified subtleties of common clinical attacks and identified more rare phenotypes, including cerebral cortical encephalitis, which have broadened our understanding of the clinicoradiologic spectrum of MOGAD and culminated in the recent publication of proposed diagnostic criteria with a familiar construction to those diagnosing other neuroinflammatory conditions. These criteria, in combination with advances in antibody testing, should simultaneously lead to wider recognition and reduced incidence of misdiagnosis. In addition, recent observational studies have raised new questions about when to treat MOGAD chronically, and with which agent. MOGAD pathophysiology informs some of the relatively unique clinical and radiologic features which have come to define this condition, and similarly has implications for diagnosis and management. Further prospective studies and the first clinical trials of therapeutic options will answer several remaining questions about the peculiarities of this condition.
RESULTS: Studies have identified subtleties of common clinical attacks and identified more rare phenotypes, including cerebral cortical encephalitis, which have broadened our understanding of the clinicoradiologic spectrum of MOGAD and culminated in the recent publication of proposed diagnostic criteria with a familiar construction to those diagnosing other neuroinflammatory conditions. These criteria, in combination with advances in antibody testing, should simultaneously lead to wider recognition and reduced incidence of misdiagnosis. In addition, recent observational studies have raised new questions about when to treat MOGAD chronically, and with which agent. MOGAD pathophysiology informs some of the relatively unique clinical and radiologic features which have come to define this condition, and similarly has implications for diagnosis and management. Further prospective studies and the first clinical trials of therapeutic options will answer several remaining questions about the peculiarities of this condition.
摘要：
目的：髓磷脂少突胶质细胞糖蛋白抗体病（MOGAD）是一种以视神经炎发作为特征的独特神经炎症性疾病，横贯性脊髓炎,和其他脱髓鞘事件。虽然它可以模拟多发性硬化症和视神经脊髓炎谱系障碍，现在已经认识到可以区分这些疾病的独特的临床和放射学特征.这篇综述强调了我们对临床表现的理解的最新进展，诊断,和治疗MOGAD。
结果：研究已经确定了常见临床发作的微妙之处，并确定了更罕见的表型，包括大脑皮层脑炎,这扩大了我们对MOGAD的临床放射谱的理解，并最终导致了最近发表的拟议诊断标准，对其他神经炎症性疾病的诊断进行了熟悉的构建。这些标准,结合抗体检测的进展，应同时导致更广泛的认识和减少误诊的发生率。此外,最近的观察研究提出了关于何时慢性治疗MOGAD的新问题，和哪个特工。MOGAD病理生理学提供了一些相对独特的临床和放射学特征，这些特征已经定义了这种情况。同样对诊断和管理也有影响。进一步的前瞻性研究和治疗选择的首次临床试验将回答关于这种情况的特殊性的几个剩余问题。
结果：研究已经确定了常见临床发作的微妙之处，并确定了更罕见的表型，包括大脑皮层脑炎,这扩大了我们对MOGAD的临床放射谱的理解，并最终导致了最近发表的拟议诊断标准，对其他神经炎症性疾病的诊断进行了熟悉的构建。这些标准,结合抗体检测的进展，应同时导致更广泛的认识和减少误诊的发生率。此外,最近的观察研究提出了关于何时慢性治疗MOGAD的新问题，和哪个特工。MOGAD病理生理学提供了一些相对独特的临床和放射学特征，这些特征已经定义了这种情况。同样对诊断和管理也有影响。进一步的前瞻性研究和治疗选择的首次临床试验将回答关于这种情况的特殊性的几个剩余问题。
