![]() Some scholars have concluded that the anterior optic nerve is significantly more likely to be involved in MOGAD patients, which is different from AQP-4 antibody-positive patients ( Kitley et al., 2014 Ducloyer et al., 2020). Rempe’s study showed that compared with NMOSD patients, MOGAD patients with ON were more prone to bilateral optic nerve involvement (6/11 vs. However, that study was very small and lacked sufficient statistical power.īilateral involvement of the ON is usually present, but sometimes it may be unilateral ON ( Akaishi et al., 2019 Rempe et al., 2021). (2014) showed that among 9 MOGAD patients, none were diagnosed with ON alone, and 4 patients were diagnosed with ON plus myelitis simultaneously or successively. Significantly, retrospective analysis results of Kitley et al. Other studies have reported similar results ( Cobo-Calvo et al., 2017, 2021 Li et al., 2021 Rempe et al., 2021). (2020) analysis of 263 CNS demyelination episodes in 93 MOGAD patients showed that 121 (45.8%) were ON. Compared with patients with MS or NMOSD, those with MOGAD present with isolated ON without additional CNS lesions ( Wingerchuk et al., 2015). (2019) found that out of 166 MOGAD episodes in 85 patients, 67.5% were ON (bilateral neuritis was 18.7%). (2020) prospectively observed 65 patients diagnosed with acute ON within 1 year, 14% of whom were MOG-IgG positive. Optic neuritis (ON) is the most common symptom of MOGAD in adults, occurring in approximately 54-61% of patients ( Biotti et al., 2017 Hacohen et al., 2017 Cobo-Calvo et al., 2018 Carandini et al., 2021 Kunchok et al., 2021b). This paper discusses the typical symptoms and atypical symptoms of MOGAD through literature retrieval to improve the ability to identify potential patients. Many atypical symptoms or complications have been reported ( Fujimori et al., 2021 Peters et al., 2021 Wildemann et al., 2021). Additionally, there is no unified standard regarding the clinical manifestations and magnetic resonance imaging (MRI) characteristics of MOGAD. ![]() Although the specific pathophysiologic mechanism remains inconclusive, MOGAD usually manifests as direct demyelinating pathological changes that are similar to MS, unlike NMOSD, in which astrocytes are first damaged and then demyelinated ( Salama et al., 2019 Mader et al., 2020). Typical symptoms of MOGAD include ON and myelitis, which overlap with multiple sclerosis (MS) and NMOSD ( Carandini et al., 2021). MOGAD is a demyelinating disease of the central nervous system (CNS). With the popularization of cell-based assay detection methods, MOGAD has been separated from NMOSD ( Wingerchuk et al., 2015 Thompson et al., 2018). ( Fujimori et al., 2021 Peters et al., 2021 Wildemann et al., 2021). MOG-IgG can lead to ON, myelitis, and ADEM and are currently associated with anti-n-methyl-d-aspartate (NMADA) antibody encephalitis, teratoma, COVID-19, etc. Myelin oligodendrocyte glycoprotein (MOG) is widely present on the surface of oligodendrocytes and the myelin sheath of the nervous system, and its role may be similar to that of a cell adhesion molecule, maintaining the stability of the surface of oligodendrocytes and regulating the complement response ( Bernard et al., 1997 Johns and Bernard, 1999). The purpose of this review is to discuss the clinical manifestations, imaging features, outcomes and prognosis of MOGAD. Currently, there is a lack of clinical randomized controlled trials on the treatment and prognosis of MOGAD. Approximately 44-83% of patients undergo relapsing episodes within 8 months, which mostly involve the optic nerve, and persistently observed MOG-IgG and severe clinical performance may indicate a polyphasic course of illness. Compared to NMOSD, MOGAD generally responds well to immunotherapy and has a good functional prognosis. ![]() Attention should be given to screening patients with atypical symptoms. ![]() Some studies have revealed the presence of brainstem lesions, encephalopathy or cortical encephalitis. MOG-IgG have been found in patients with peripheral neuropathy, teratoma, COVID-19 pneumonia, etc. Usually, optic neuritis (ON), myelitis or acute disseminated encephalomyelitis (ADEM) encephalitis are the typical symptoms of MOGAD. MOGAD occurs in approximately the fourth decade of a person’s life without a markedly female predominance. In one study, 31% of NMOSD patients with negative aquaporin-4 (AQP-4) antibody were MOG-IgG positive. The detection of MOG-IgG has been greatly improved by the cell-based assay test method. Myelin oligodendrocyte glycoprotein-IgG-associated disorder (MOGAD) is a nervous system (NS) demyelination disease and a newly recognized distinct disease complicated with various diseases or symptoms however, MOGAD was once considered a subset of neuromyelitis optica spectrum disorder (NMOSD).
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