Clinical spectrum and prognostic value of CNS MOG autoimmunity in adults

Cobo‐Calvo, Álvaro; Ruiz, Anne; Maillart, Élisabeth; Audoin, Bertrand; Zephir, Hélène; Bourre, Bertrand; Ciron, Jonathan; Collongues, Nicolas; Brassat, David; Cotton, François; Papeix, Caroline; Durand‐Dubief, Françoise; Laplaud, David‐Axel; Deschamps, Romain; Cohen, M.; Biotti, Damien; Ayrignac, Xavier; Tilikete, Caroline; Thouvenot, Éric; Brochet, Bruno; Dulau, Cécile; Moreau, Thibault; Tourbah, Ayman; Lebranchu, Pierre; Michel, Laure; Lebrun-Frénay, Christine; Montcuquet, Alexis; Mathey, Guillaume; Debouverie, M.; Pelletier, Jean; Labauge, Pierre; Derache, Nathalie; Coustans, M.; Rollot, Fabien; Sèze, Jérôme De; Vukusic, Sandra; Marignier, Romain

doi:10.1212/wnl.0000000000005560

Cited by 443 publications

(641 citation statements)

References 37 publications

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“…Typically, lesions appear as a small number (≤3) of poorly demarcated infratentorial lesions, 103 and thalamic and pontine lesions are distinctive MRI findings. 104 Supratentorial deep white matter lesions can be seen (Fig. 17).…”

Section: Brain Lesionsmentioning

confidence: 99%

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Magnetic resonance imaging diagnosis of demyelinating diseases: An update

Miki

2019

Clinical & Exp Neuroim

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Keywords acute disseminating encephalomyelitis (ADEM); demyelinating diseases; multiple sclerosis (MS); myelin oligodendrocyte glycoprotein (MOG) encephalomyelitis; neuromyelitis optica spectrum disorder (NMOSD) Correspondence AbstractMajor demyelinating diseases include multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), acute disseminated encephalomyelitis (ADEM) and myelin oligodendrocyte glycoprotein (MOG) encephalomyelitis. As treatment strategies differ among these diseases, precise diagnosis of demyelinating diseases is crucial, and magnetic resonance imaging (MRI) plays a pivotal role in the diagnosis. In the present review, MRI appearances of characteristic lesions of these demyelinating diseases, and differentiation between MS and other demyelinating diseases based on MRI findings are discussed.

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Section: Brain Lesionsmentioning

confidence: 99%

“…18). 104 Ogawa, et al 105 reported cases presenting with unilateral cortical encephalitis with epileptic seizure. Wang et al 106 reported that 21% of MOG-IgG-positive patients presented with encephalitis, and one-third of these patients also showed anti-N-methyl d-aspartase receptor antibody.…”

Section: Brain Lesionsmentioning

confidence: 99%

Magnetic resonance imaging diagnosis of demyelinating diseases: An update

Miki

2019

Clinical & Exp Neuroim

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“…Recently, Marignier et al . reported that among 49 adult anti‐MOG antibody‐positive patients with abnormal brain MRI findings, infratentorial lesions were located in the midbrain (10.2%), pons (34.69%), medulla oblongata (14.29%), cerebellar peduncles (18.37%) and cerebellum (4.08%), as well as adjacent to the fourth ventricle (22.45%) …”

Section: Discussionmentioning

confidence: 99%

“…Recently, Marignier et al reported that among 49 adult anti-MOG antibody-positive patients with abnormal brain MRI findings, infratentorial lesions were located in the midbrain (10.2%), pons (34.69%), medulla oblongata (14.29%), cerebellar peduncles (18.37%) and cerebellum (4.08%), as well as adjacent to the fourth ventricle (22.45%). 5 Therefore, lesions adjacent to the fourth ventricle that can involve cerebellar dentate nucleus might be one of the characteristic phenotypes of anti-MOG antibody-associated encephalitis. Further analysis is required to clarify the underlying pathophysiology and the clinical significance.…”

Section: Discussionmentioning

confidence: 99%

Cerebellar lesions in a patient with anti‐myelin oligodendrocyte glycoprotein antibody‐associated encephalitis

Fujimori

Nakashima

2019

Clinical & Exp Neuroim

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“…There is variable support in the literature for the relevance of persistent MOG antibody status for predicting recurrent disease . However, prevention of recurrence in the face of repeated neuroinflammatory events prevent future disability.…”

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confidence: 99%

Rituximab in children with myelin oligodendrocyte glycoprotein antibody and relapsing neuroinflammatory disease

Albassam

Longoni

Yea

et al. 2019

Develop Med Child Neuro

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ABBREVIATIONS IVIGIntravenous immunoglobulin MOG Myelin oligodendrocyte glycoproteinThe aim of this study was to evaluate tolerability of and response to rituximab in children with myelin oligodendrocyte glycoprotein (MOG) antibody-positive relapsing neuroinflammatory disease. This was an observational study of prospectively collected data on 12 consecutive children (eight females, four males; median age at onset 10y 6mo [interquartile range {IQR} 7y 2mo-12y 5mo], median follow-up 2y 1mo [IQR 1y 7mo-2y 6mo]) with central nervous system inflammation and persistent serum MOG immunoglobulin G positivity more than 12 weeks after clinical presentation. Patients received a standardized rituximab treatment protocol. MOG antibody testing was performed following standardized cell-based methods. Median clinical follow-up after rituximab induction was 2 years (IQR 1y 7mo-2y 10mo). The relapse rate in the first 12 months posttreatment was 0 (IQR 0-0). After rituximab, two patients relapsed during B-cell suppression and four showed clinical or radiological disease recurrences at B-cell reconstitution. Mild-to-moderate infusion related adverse events occurred in two patients. Leukopenia developed in seven patients and serum immunoglobulin suppression in five patients with no significant age effect on the risk of their development. None developed severe life-threatening events. Rituximab-induced B-cell suppression was associated with absence of relapses in 10 patients who were MOG-positive with recurrent disease. Rituximab was well tolerated. The most frequent adverse effects were hypogammaglobulinemia and leukopenia. We recommend monitoring of complete blood counts and immunoglobulins in this population.Myelin oligodendrocyte glycoprotein (MOG) antibodies are seen in the serum of 25% to 58% of children who present with a first acquired demyelinating syndrome, 1-5 and may also be seen in adults presenting with acute neuroinflammation (4-15%). 3,5-7 Twenty-five per cent to almost 75% will continue to have high titers of MOG antibodies after presenting acutely, 8 with considerable risk of relapse. 9 In one adult-based cohort of 252 patients in the UK with elevated MOG antibodies, 36% had relapses within a median duration of 16 months. 8 Steroids, intravenous immunoglobulin (IVIG), and plasma exchange 10 may be beneficial in reducing symptomatology at the time of an acute event, but are unlikely to decrease the risk of relapse.There is variable support in the literature for the relevance of persistent MOG antibody status for predicting recurrent disease. 11,12 However, prevention of recurrence in the face of repeated neuroinflammatory events prevent future disability. Given the potential for irreversible neurological disability, 13 and the robust response of other antibody-mediated conditions to B-cell suppression with rituximab therapy, 14 we used a standardized treatment protocol using rituximab in children with recurrent central nervous system (CNS) inflammatory disease and persistent MOG antibody positivity 12 weeks or more af...

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Clinical spectrum and prognostic value of CNS MOG autoimmunity in adults

Abstract: In adults, MOG-Ab-associated disease extends beyond clinical and radiologic abnormalities in the optic nerve and spinal cord. Despite the relapsing course, the overall visual and motor outcome is better compared with AQP4-Ab-positive patients.

Cited by 443 publications

References 37 publications

Magnetic resonance imaging diagnosis of demyelinating diseases: An update

Magnetic resonance imaging diagnosis of demyelinating diseases: An update

Cerebellar lesions in a patient with anti‐myelin oligodendrocyte glycoprotein antibody‐associated encephalitis

Rituximab in children with myelin oligodendrocyte glycoprotein antibody and relapsing neuroinflammatory disease

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