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  • Neuro-Ophthalmology/Orbit

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

    Banwell B, Bennet J, Marignier R, et al. The Lancet: Neurology, March 2023

    Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a neuroinflammatory disorder that causes demyelination primarily of the optic nerve, as well as areas of the brain, brainstem, and/or spinal cord, and which can present similarly to diseases like multiple sclerosis (MS). Based on a comprehensive review of available data, new criteria are proposed for the diagnosis of MOGAD that rely on MOG serum antibodies (MOG-IgG) and specific clinical features of this neurodegenerative disease.

    Study design

    This comprehensive literature review of 378 articles summarized the currently available data on MOGAD with a focus on the clinical, serological, and imaging features that differentiate this condition from other demyelinating diseases, specifically MS and neuromyelitis optica spectrum disorder (NMOSD). Using this data, the authors propose criteria to help guide physicians in the correct diagnosis of MOGAD, particularly when trying to differentiate this condition from MS.


    The proposed MOGAD diagnostic criteria include:

    1) The presence of a core clinical demyelinating event more commonly seen in patients with MOGAD than those with MS or NMOSD, including optic neuritis (31%–58% of patients with MOGAD vs <5% of patients with MS) or transverse myelitis that extends 3 or more vertebral segments in length (>60% of patients with MOGAD, rare in MS).

    1. A positive live or fixed cell-based serum assay for MOG antibodies (MOG-IgG).
    2. A clear positive is considered diagnostic without additional supporting features.
    2) A low positive titer, positive assay without a reported titer, or serum negative but cerebrospinal fluid–positive assay requires additional supporting clinical or MRI features, such as optic neuritis (bilateral, longitudinal optic nerve involvement and/or perineuritis on MRI, optic disc edema), longitudinally extensive myelitis (>3 vertebral segments, lesions often involving the central spinal cord [H-sign] or conus), and/or involvement of the brain, brainstem, or cerebellum (multiple ill-defined white matter lesions, often with deep grey matter involvement).

    3) Exclusion of better diagnoses.


    These criteria reflect the current understanding of MOGAD; as diseases evolve, so the criteria used to diagnose diseases can be expected to change as well. Moreover, the advancement of technology and increased sensitivity of lab testing over time may affect the interpretation of serological tests.

    Clinical significance

    The proposed criteria need to be further validated, but they provide an excellent starting point for the development of a framework for diagnosing MOGAD. Making an accurate diagnosis is crucial to achieving a better outcome, as appropriate treatment differs from one demyelinating disease to another. This comprehensive overview of MOGAD-specific clinical, serological, and radiographic features, especially in comparison to those of MS and NMOSD, should help physicians to better identify MOGAD and distinguish it from other similar diseases.

    Additionally, using a titer to quantify MOG antibody levels can be a useful positive predictive indicator of the condition. However, it is important to understand that MOG antibody positivity does not, in and of itself, confirm the diagnosis of MOGAD. Multiple diseases can involve MOG-IgG positive assays, so caution should be exercised when ordering MOG antibody testing; it should only be done in cases that otherwise fit the baseline criteria for MOGAD and should not be used for general screening. If a physician only relies on MOG-antibody positivity without considering supporting features, false-positive diagnoses may occur, and the diagnosis of another condition may be missed.

    Financial Disclosures: Dr. Danah Albreiki discloses no financial relationships.