Children with multiphasic disseminated encephalomyelitis and antibodies to the myelin oligodendrocyte glycoprotein (MOG): Extending the spectrum of MOG antibody positive diseases

Baumann, Matthias; Hennes, Eva-Maria; Schanda, Kathrin; Karenfort, Michael; Kornek, Barbara; Seidl, Rainer; Diepold, Katharina; Lauffer, Heinz; Marquardt, Iris; Strautmanis, Jurgis; Syrbe, Steffen; Vieker, Silvia; Höftberger, Romana; Reindl, Markus; Rostásy, Kevin

doi:10.1177/1352458516631038

Cited by 139 publications

(152 citation statements)

References 26 publications

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“…Anti-MOG antibody titers of monophasic ADEM patients declined or became negative over the course of months to years [6]. However, patients with persistently high anti-MOG antibody titers experienced a recurrent disease course [6, 7]. The anti-MOG antibody titer of the present case became negative and did not show recurrence.…”

Section: Discussionmentioning

confidence: 79%

Anti-MOG antibody-positive ADEM following infectious mononucleosis due to a primary EBV infection: a case report

et al. 2017

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BackgroundAnti-Myelin oligodendrocyte glycoprotein (MOG) antibodies are detected in various demyelinating diseases, such as pediatric acute disseminated encephalomyelitis (ADEM), recurrent optic neuritis, and aquaporin-4 antibody-seronegative neuromyelitis optica spectrum disorder. We present a patient who developed anti-MOG antibody-positive ADEM following infectious mononucleosis (IM) due to Epstein–Barr virus (EBV) infection.Case presentationA 36-year-old healthy man developed paresthesia of bilateral lower extremities and urinary retention 8 days after the onset of IM due to primary EBV infection. The MRI revealed the lesions in the cervical spinal cord, the conus medullaris, and the internal capsule. An examination of the cerebrospinal fluid revealed pleocytosis. Cell-based immunoassays revealed positivity for anti-MOG antibody with a titer of 1:1024 and negativity for anti-aquaporin-4 antibody. His symptoms quickly improved after steroid pulse therapy followed by oral betamethasone. Anti-MOG antibody titer at the 6-month follow-up was negative.ConclusionsThis case suggests that primary EBV infection would trigger anti-MOG antibody-positive ADEM. Adult ADEM patients can be positive for anti-MOG antibody, the titers of which correlate well with the neurological symptoms.

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Section: Discussionmentioning

confidence: 79%

Anti-MOG antibody-positive ADEM following infectious mononucleosis due to a primary EBV infection: a case report

et al. 2017

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“…Relapsing cases were assigned the following diagnostic categories: (1) multiple sclerosis, fulfilling the 2013 International Pediatric Multiple Sclerosis Study Group consensus criteria and the 2010 revised McDonald criteria; (2) NMOSD, fulfilling the 2015 Wingerchuk criteria; (3) multiphasic disseminated encephalomyelitis and ADEM‐optic neuritis fulfilling the 2013 International Pediatric Multiple Sclerosis Study Group consensus criteria; and (4) recurrent demyelination in a single central nervous system (CNS) area without evidence of clinically silent disease (for example relapsing optic neuritis).…”

Section: Methodsmentioning

confidence: 99%

“…More recently, MOG‐Ab have been reported in about 40% of children at first presentation of an acquired demyelinating syndrome, with two studies from the UK/France and the Netherlands suggesting that MOG‐Ab identified at onset are associated with a non‐multiple sclerosis disease course. Although initially reported in predominantly monophasic disease, MOG‐Ab have been detected in patients with multiphasic disseminated encephalomyelitis, recurrent optic neuritis, and acute disseminated encephalomyelitis (ADEM) followed by recurrent or monophasic optic neuritis, and in both adults and children with NMOSD without AQP4‐Ab. Two recent reports identified MOG‐Ab and AQP4‐Ab in 28 out of 35 and 34 out of 48 children with non‐multiple sclerosis relapsing demyelination.…”

mentioning

confidence: 99%

Myelin oligodendrocyte glycoprotein and aquaporin‐4 antibodies are highly specific in children with acquired demyelinating syndromes

Duignan

Wright

Rossor

et al. 2018

Develop Med Child Neuro

118

108

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Myelin oligodendrocyte glycoprotein antibodies (MOG-Ab) are highly specific for acquired demyelinating syndromes (ADS). Myelin oligodendrocyte glycoprotein antibodies are not identified in children with peripheral demyelination or genetic leukodystrophies/hypomyelination. Up to 48% of MOG-Ab ADS paediatric patients relapse, higher than previously thought. Seroconversion to MOG-Ab negative status is infrequent; patients may test MOG-Ab positive at follow-up sampling even when asymptomatic. Myelin oligodendrocyte glycoprotein antibodies status should only be used in conjunction with the clinical information to guide maintenance therapy.

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“…106 In pediatric cohorts, MOG-Ab was frequently found in patients with ADEM (up to 43%), most of whom had two or more episode of attacks (up to 100%). 117 …”

Section: Differential Diagnosis Of Nmosdmentioning

confidence: 99%

Differential diagnosis of neuromyelitis optica spectrum disorders

Kim

Lee

et al. 2017

Ther Adv Neurol Disord

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Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory disorder of the central nervous system (CNS) mostly manifesting as optic neuritis and/or myelitis, which are frequently recurrent/bilateral or longitudinally extensive, respectively. As the autoantibody to aquaporin-4 (AQP4-Ab) can mediate the pathogenesis of NMOSD, testing for the AQP4-Ab in serum of patients can play a crucial role in diagnosing NMOSD. Nevertheless, the differential diagnosis of NMOSD in clinical practice is often challenging despite the phenotypical and serological characteristics of the disease because: (1) diverse diseases with autoimmune, vascular, infectious, or neoplastic etiologies can mimic these phenotypes of NMOSD; (2) patients with NMOSD may only have limited clinical manifestations, especially in their early disease stages; (3) test results for AQP4-Ab can be affected by several factors such as assay methods, serologic status, disease stages, or types of treatment; (4) some patients with NMOSD do not have AQP4-Ab; and (5) test results for the AQP4-Ab may not be readily available for the acute management of patients. Despite some similarity in their phenotypes, these NMOSD and NMOSD-mimics are distinct from each other in their pathogenesis, prognosis, and most importantly treatment. Understanding the detailed clinical, serological, radiological, and prognostic differences of these diseases will improve the proper management as well as diagnosis of patients.

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Children with multiphasic disseminated encephalomyelitis and antibodies to the myelin oligodendrocyte glycoprotein (MOG): Extending the spectrum of MOG antibody positive diseases

Abstract: Children with MDEM and persisting MOG antibodies constitute a distinct entity of relapsing demyelinating events and extend the spectrum of MOG antibody-associated diseases.

Cited by 139 publications

References 26 publications

Anti-MOG antibody-positive ADEM following infectious mononucleosis due to a primary EBV infection: a case report

Anti-MOG antibody-positive ADEM following infectious mononucleosis due to a primary EBV infection: a case report

Myelin oligodendrocyte glycoprotein and aquaporin‐4 antibodies are highly specific in children with acquired demyelinating syndromes

Differential diagnosis of neuromyelitis optica spectrum disorders

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