Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD Panel proposed criteria

Banwell, Brenda; Bennett, Jeffrey L.; Marignier, Romain; Kim, Ho Jin; Brilot, Fabienne; Flanagan, Eoin P.; Ramanathan, Sudarshini; Waters, Patrick; Tenembaum, Sílvia; Graves, Jennifer; Chitnis, Tanuja; Brandt, Alexander U.; Hemingway, Cheryl; Neuteboom, Rinze F.; Pandit, Lekha; Reindl, Markus; Sáiz, Albert; Sato, Douglas Kazutoshi; Rostásy, Kevin; Paul, Friedemann; Pittock, Sean J.; Fujihara, Kazuo; Palace, Jacqueline

doi:10.1016/s1474-4422(22)00431-8

Cited by 425 publications

(512 citation statements)

References 105 publications

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“…A study by Wendel et al found that patients with declining anti-MOG antibodies have a significantly lower risk of relapse [ 61 ]. The pathognomonic feature of 40–90 % of cases of neuromyelitis optica depending on the demographic is the presence of disease-specific aquaporin-4 (AQP4) antibody, which plays a key role in the pathogenesis of the disease [ 62 ]. Also, 10–40 % of cases with negative AQP4 antibody have positive MOG antibody which is mostly present in ADEM [ 61 ].…”

Section: Discussionmentioning

confidence: 99%

“…Based on the new criteria, MOGAD is typically linked to acute disseminated encephalomyelitis, optic neuritis, or transverse myelitis, and is less frequently connected with cerebral cortical encephalitis, brainstem presentations, or cerebellar presentations. MOGAD may manifest as either a monophasic or relapsing disease course, and diagnostic accuracy relies on the use of MOG-IgG cell-based assays [ 62 ]. It is essential to exclude diagnoses such as multiple sclerosis, although not all patients with multiple sclerosis require screening for MOG-IgG [ 62 ].…”

Section: Discussionmentioning

confidence: 99%

“…MOGAD may manifest as either a monophasic or relapsing disease course, and diagnostic accuracy relies on the use of MOG-IgG cell-based assays [ 62 ]. It is essential to exclude diagnoses such as multiple sclerosis, although not all patients with multiple sclerosis require screening for MOG-IgG [ 62 ]. In differentiating the diagnosis of ADEM from infectious meningoencephalitis, evidence of meningismus together with the examination of CSF cytology and PCR might be helpful.…”

Section: Discussionmentioning

confidence: 99%

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Acute disseminated encephalomyelitis (ADEM) following COVID-19 vaccination: A systematic review

Nabizadeh

Noori

Rahmani

et al. 2023

Journal of Clinical Neuroscience

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Acute disseminated encephalomyelitis (ADEM) following COVID-19 vaccination: A systematic review

Nabizadeh

Noori

Rahmani

et al. 2023

Journal of Clinical Neuroscience

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“…In MS, progressive patients have higher GFAP both in serum and CSF compared to RRMS and HC (59). Conversely, oligodendrocytes are variably lost in all three diseases, while in MOGAD, progenitor cells are preserved as they do not yet express MOG (49,50,58,62).…”

Section: Histopathological Findingsmentioning

confidence: 98%

Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease

Corbali

Chitnis

2023

Front. Neurol.

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Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) is a spectrum of diseases, including optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and cerebral cortical encephalitis. In addition to distinct clinical, radiological, and immunological features, the infectious prodrome is more commonly reported in MOGAD (37–70%) than NMOSD (15–35%). Interestingly, pediatric MOGAD is not more aggressive than adult-onset MOGAD, unlike in multiple sclerosis (MS), where annualized relapse rates are three times higher in pediatric-onset MS. MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross blood brain barrier (BBB). MOGAD lesions show a perivenous confluent pattern around the small veins, lacking the radiological central vein sign. Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden antigen-presenting cells and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. CD4+ T cells, unlike CD8+ T cells in MS, are the dominant T cell type found in lesion histology. Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses. MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. Stimulation of peripheral MOG-specific B cells through TLR stimulation or T follicular helper cells might help differentiate MOG antibody-producing plasma cells in the peripheral blood. Neuroinflammatory biomarkers (such as MBP, sNFL, GFAP, Tau) in MOGAD support that most axonal damage happens in the initial attack, whereas relapses are associated with increased myelin damage.

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“…Up to 42% of AQP4 IgG negative patients harbor IgG antibodies to Myelin Oligodendrocyte Glycoprotein (MOG) ( 54 ). There may be overlap with or genuine MOG antibody associated disease (MOGAD) ( 55 ). AQP4 is found mainly in the central nervous system on astrocytes near the blood-brain barrier and function as a water channel, whereas the binding of AP4-Ab to AQP4 channels causes their downregulation.…”

Section: Complex Immunological Role Of B Cells In Ms Nmosd and Mogadmentioning

confidence: 99%

B cell targeted therapies in inflammatory autoimmune disease of the central nervous system

et al. 2023

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Cumulative evidence along several lines indicates that B cells play an important role in the pathological course of multiple sclerosis (MS), neuromyelitisoptica spectrum disorders (NMOSD) and related CNS diseases. This has prompted extensive research in exploring the utility of targeting B cells to contain disease activity in these disorders. In this review, we first recapitulate the development of B cells from their origin in the bone marrow to their migration to the periphery, including the expression of therapy-relevant surface immunoglobulin isotypes. Not only the ability of B cells to produce cytokines and immunoglobulins seems to be essential in driving neuroinflammation, but also their regulatory functions strongly impact pathobiology. We then critically assess studies of B cell depleting therapies, including CD20 and CD19 targeting monoclonal antibodies, as well as the new class of B cell modulating substances, Bruton´s tyrosinekinase (BTK) inhibitors, in MS, NMOSD and MOGAD.

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Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD Panel proposed criteria

Cited by 425 publications

References 105 publications

Acute disseminated encephalomyelitis (ADEM) following COVID-19 vaccination: A systematic review

Acute disseminated encephalomyelitis (ADEM) following COVID-19 vaccination: A systematic review

Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease

B cell targeted therapies in inflammatory autoimmune disease of the central nervous system

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