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Perivenous demyelination: Association with anti‐myelin oligodendrocyte glycoprotein antibody
Author(s) -
Misu Tatsuro,
Takai Yoshiki,
Takahashi Toshiyuki,
Nakashima Ichiro,
Fujihara Kazuo,
Aoki Masashi
Publication year - 2020
Publication title -
clinical and experimental neuroimmunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.297
H-Index - 15
ISSN - 1759-1961
DOI - 10.1111/cen3.12569
Subject(s) - myelin oligodendrocyte glycoprotein , neuromyelitis optica , acute disseminated encephalomyelitis , optic neuritis , medicine , pathology , multiple sclerosis , immunology , oligodendrocyte , antibody , demyelinating disease , myelin , experimental autoimmune encephalomyelitis , central nervous system
By the discovery of an antibody to aquaporin 4 (AQP4), the clinical and radiological findings of neuromyelitis optica (NMO) such as diffuse cerebral or longitudinally extended spinal cord lesions had been clarified as distinct features from multiple sclerosis (MS). Pathological studies in NMO demonstrated loss of immunoreactivity to AQP4 and glial fibrillary acidic protein but a relative preservation of myelin basic protein, especially at the lesions with perivascular deposition of immunoglobulins and complements, suggesting autoimmune disease against astrocytes. In recent years, the antibody against myelin oligodendrocyte glycoprotein (MOG) has been studied for its association with acute demyelinating diseases such as acute or multiphasic disseminated encephalomyelitis (ADEM/MDEM), optic neuritis, AQP4 antibody–negative NMOSD, and brainstem or cerebral cortical encephalomyelitis. We could identify the dominance of perivenous inflammatory demyelination like ADEM in our biopsied case series with MOG antibody. In recent brain‐biopsied cases with MOG antibody, the deposition of humoral immunity, perivascular inflammation, and perivenous demyelination were observed especially in atypical cases including cortical encephalitis or disseminated encephalitis. In this review, we focus on MOG antibody–related diseases, which we considered it as a differentiated disease from MS by means of the disease‐specific autoantibody and the distinct pathophysiology.