MOG antibody syndrome presenting as aseptic meningitis: an evolving spectrum

Vibha, Deepti; Singh, Rajesh; Salunkhe, Manish; Dash, Deepa; Tripathi, Manjari

doi:10.1007/s10072-020-04558-4

Cited by 10 publications

(9 citation statements)

References 5 publications

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“…To the best of our knowledge, 7 cases of MOG-ADassociated meningitis, which were described to have fever, nausea, and nuchal rigidity, have been reported including our case (Table) (10)(11)(12)(13)(14)(15)(16). The mean age of these patients was 24.4 years (range: 3-55); four of these patients were male.…”

Section: Discussionmentioning

confidence: 76%

Myelin Oligodendrocyte Glycoprotein-antibody-associated Disorder Presenting with Corticomeningeal Encephalitis Prior to the Onset of Optic Neuritis

2021

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We herein report a case of myelin oligodendrocyte glycoprotein-antibody-associated disorder (MOG-AD) presenting with corticomeningeal encephalitis. The patient exhibited oral ulceration, a mild impairment of consciousness, fever, nausea, nuchal rigidity, positivity for human leukocyte antigen type B51, and neutrophil-dominant pleocytosis and interleukin-6 level in cerebrospinal fluid (CSF). Magnetic resonance imaging (MRI) revealed a right temporal lesion with leptomeningeal gadolinium enhancement. The initial diagnosis was neuro-Behçet's disease presenting with meningoencephalitis; however, a cell-based assay detected anti-MOG antibody in the serum and CSF and the patient also experienced bilateral optic neuritis. After administering steroid therapy, his neurologic symptoms and CSF abnormalities improved along with the disappearance of gadolinium enhancement and the lesion on MRI. This case suggests that MOG-AD may present with corticomeningeal encephalitis prior to the onset of optic neuritis.

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Section: Discussionmentioning

confidence: 76%

Myelin Oligodendrocyte Glycoprotein-antibody-associated Disorder Presenting with Corticomeningeal Encephalitis Prior to the Onset of Optic Neuritis

2021

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“…One case is that the patient can show brainstem encephalitis with pontine trigeminal root entry zone abnormality [2]. The second case is the patient with aseptic meningitis and optic neuritis [3]. And Spinal MRI showed lesions in the medulla oblongata, C2-T1, T4, T7, T11-T12, and spinal conus on T2 after progression of the disease the third case is similar to typical multiple sclerosis [4].…”

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Clinical characteristics of MOG antibody disease: two case reports

Guan

Zhang

et al. 2021

Neurol Sci

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“…Currently, approximately 11 aseptic meningitis cases accompanied by MOGAD have been reported ( Narayan et al, 2019 ; Suzuki et al, 2019 ; Leinert et al, 2020 ; Miller et al, 2020 ; Shi et al, 2020 ; Shen et al, 2021 ; Vibha et al, 2021 ; Zhang et al, 2021 ). Headache, fever, and ON were the most common symptoms, with mildly higher CSF cells, except in one case (1335/dL) ( Miller et al, 2020 ).…”

Section: Othermentioning

confidence: 99%

“…Acute disseminated encephalomyelitis is the most common clinical manifestation of MOGAD in children and is less common in adults than ON and myelitis ( Reindl et al, 2013 ; Reindl and Rostasy, 2015 ; Hacohen et al, 2017 ; Jurynczyk et al, 2017 ; Netravathi et al, 2020 ; Vibha et al, 2021 ). The results of Ramanathan’s study of 33 children and 26 adults with MOGAD found that 20% of the population presented with ADEM (exclusively in children), second only to ON (54%) ( Ramanathan et al, 2018 ).…”

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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MOG antibody syndrome presenting as aseptic meningitis: an evolving spectrum

Cited by 10 publications

References 5 publications

Myelin Oligodendrocyte Glycoprotein-antibody-associated Disorder Presenting with Corticomeningeal Encephalitis Prior to the Onset of Optic Neuritis

Myelin Oligodendrocyte Glycoprotein-antibody-associated Disorder Presenting with Corticomeningeal Encephalitis Prior to the Onset of Optic Neuritis

Clinical characteristics of MOG antibody disease: two case reports

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

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