Atypical MOG antibody disease presenting with typical multiple sclerosis lesions

Dolbec, Katelyn; Chalkley, Joshua; Sudhakar, Padmaja

doi:10.1016/j.msard.2020.102342

Cited by 8 publications

(5 citation statements)

References 7 publications

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“…Our case, along with an increasing number of reports (Table 1), suggests a proportion of MOGAD with initial phenotypes suggestive of MS (2)(3)(4). The presence of lesions with shapes and distributions compatible with MS, as well as her OCB positivity led to the initial misdiagnosis of MS.…”

Section: Discussionmentioning

confidence: 60%

“…Herein, we report a case with findings initially concerning for multiple sclerosis (MS) yet subsequently diagnosed with MOGAD (Figure 1). Though rare, it is now recognized that patients with MOGAD could have typical MS attacks at onset (2)(3)(4). The major challenge, however, lies in the early recognition and correct diagnosis of such patients for an appropriate therapeutic strategy.…”

Section: Introductionmentioning

confidence: 99%

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Case Report: Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disorder Masquerading as Multiple Sclerosis: An Under-Recognized Entity?

Zheng

Cai

et al. 2021

Front. Immunol.

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Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) covers a wide spectrum of manifestations and is defined by the presence of MOG seropositivity. However, in a proportion of patients, there may be an overlap in some of the clinical and radiological manifestations between MOGAD and multiple sclerosis (MS). Being wary of this entity is critical to ensure appropriate therapy. Herein, we present a case with recurrent episodes of short-segment myelitis typical for multiple sclerosis, but later diagnosed as MOGAD by MOG antibody seropositivity. This case, along with previous reports, highlights an increasingly recognized subgroup in MOGAD with initial clinical phenotypes suggestive of MS, but later showing a disease course and therapeutic response compatible with MOGAD. Given the potential overlap of some clinical phenotypes in patients with MS and those with MOGAD, we recommend MOG antibody testing in all patients with recurrent short-segment myelitis, conus medullaris involvement, and those who demonstrated steroid dependence.

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Section: Discussionmentioning

confidence: 60%

Section: Introductionmentioning

confidence: 99%

Case Report: Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disorder Masquerading as Multiple Sclerosis: An Under-Recognized Entity?

Zheng

Cai

et al. 2021

Front. Immunol.

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“…Proteolipid protein (PLP), myelin basic protein (MBP), and myelin oligodendrocyte glycoprotein (MOG) proteins have been well-studied as self-antigens involved in demyelination in MS [ 28 ]. The autoimmune disease against MOG is called MOG antibody (MOG-IgG)-associated disease [ 29 ]. The clinical features are considered to reflect a unique disease with a different etiology from MS and optic neuritis, related to aquaporin-4 (AQP-4)-IgG [ 30 , 31 ].…”

Section: Ms and Environmental Factors (Immunity)mentioning

confidence: 99%

New Insights into Risk Genes and Their Candidates in Multiple Sclerosis

Shirai

Yamauchi

2022

Neurology International

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Oligodendrocytes are central nervous system glial cells that wrap neuronal axons with their differentiated myelin membranes as biological insulators. There has recently been an emerging concept that multiple sclerosis could be triggered and promoted by various risk genes that appear likely to contribute to the degeneration of oligodendrocytes. Despite the known involvement of vitamin D, immunity, and inflammatory cytokines in disease progression, the common causes and key genetic mechanisms remain unknown. Herein, we focus on recently identified risk factors and risk genes in the background of multiple sclerosis and discuss their relationships.

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“…Cobo-calvo’s case sequence showed that 80% (8 of 10) of MOGAD patients who presented with myelitis had LETM ( Cobo-Calvo et al, 2017 ). However, several MOGAD patients who present with recurrent short extensive myelitis have been reported ( Spadaro et al, 2016 ; Breza et al, 2019 ; Dolbec et al, 2020 ; Zheng et al, 2021 ). Kitley’s results showed that the proportion of MOGAD patients with conus involvement was significantly higher than that of NMOSD patients (75 vs. 17%, p = 0.02) ( Kitley et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Clinical Features and Imaging Findings of Myelin Oligodendrocyte Glycoprotein-IgG-Associated Disorder (MOGAD)

Liu

Wang

et al. 2022

Front. Aging Neurosci.

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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.

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Atypical MOG antibody disease presenting with typical multiple sclerosis lesions

Cited by 8 publications

References 7 publications

Case Report: Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disorder Masquerading as Multiple Sclerosis: An Under-Recognized Entity?

Case Report: Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disorder Masquerading as Multiple Sclerosis: An Under-Recognized Entity?

New Insights into Risk Genes and Their Candidates in Multiple Sclerosis

Clinical Features and Imaging Findings of Myelin Oligodendrocyte Glycoprotein-IgG-Associated Disorder (MOGAD)

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