Abstract
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). The detection of MOG-IgG has been greatly improved by the cell-based assay test method. In one study, 31% of NMOSD patients with negative aquaporin-4 (AQP-4) antibody were MOG-IgG positive. MOGAD occurs in approximately the fourth decade of a person’s life without a markedly female predominance. Usually, optic neuritis (ON), myelitis or acute disseminated encephalomyelitis (ADEM) encephalitis are the typical symptoms of MOGAD. MOG-IgG have been found in patients with peripheral neuropathy, teratoma, COVID-19 pneumonia, etc. Some studies have revealed the presence of brainstem lesions, encephalopathy or cortical encephalitis. Attention should be given to screening patients with atypical symptoms. Compared to NMOSD, MOGAD generally responds well to immunotherapy and has a good functional prognosis. 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. Currently, there is a lack of clinical randomized controlled trials on the treatment and prognosis of MOGAD. The purpose of this review is to discuss the clinical manifestations, imaging features, outcomes and prognosis of MOGAD.
Highlights
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)
Gao et al (2021) recently used ophthalmological indicators to analyze the structural and functional changes after optic neuritis (ON) in Myelin oligodendrocyte glycoprotein-IgG-associated disorder (MOGAD) patients, and the results showed that the AQP-4 group exhibited lower indicator values than the healthy control group, but there was no difference in the values between the MOGAD group and the control group, which may be the reason why MOGAD patients usually had a better prognosis
The clinical manifestations of adult MOGAD patients and AQP-4 antibody-positive patients have been compared, and the results showed that MOGAD patients had a lower probability of visual acuity (VA) of 20/100 (HR 0.23, 95% CI 0.07–0.72, p = 0.012) and severe initial VA loss (HR 1.52, 95% CI 1.12–2.05, p = 0.007) (Cobo-Calvo et al, 2018)
Summary
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). (Fujimori et al, 2021; Peters et al, 2021; Wildemann et al, 2021). With the popularization of cell-based assay detection methods, MOGAD has been separated from NMOSD (Wingerchuk et al, 2015; Thompson et al, 2018). Typical symptoms of MOGAD include ON and myelitis, which overlap with multiple sclerosis (MS) and NMOSD (Carandini et al, 2021). 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 demyelinated (Salama et al, 2019; Mader et al, 2020). Many atypical symptoms or complications have been reported (Fujimori et al, 2021; Peters et al, 2021; Wildemann et al, 2021). This paper discusses the typical symptoms and atypical symptoms of MOGAD through literature retrieval to improve the ability to identify potential patients
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