Key result
Intravenous pulse methylprednisolone therapy led to rapid clinical improvement and resolution of MRI lesions in a woman who developed MOGAD following adenovirus meningitis shortly after childbirth.
Why the study?
It is unknown at what point in life MOGAD develops or how autoimmune mechanisms trigger it.
Case Report (n=1)
No
This case suggests that adenoviral infection early after childbirth may trigger MOGAD, which can be effectively treated with early high-dose corticosteroid therapy.
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a group of central nervous system (CNS) demyelinating diseases caused by autoantibodies against myelin oligosaccharide protein (MOG), a myelin sheath component protein, and present with a variety of symptoms, including optic neuritis, myelitis, acute disseminated encephalomyelitis (ADEM), brainstem encephalitis, and corticobasal encephalitis. It is currently unknown at what point in life MOGAD can develop or how it can be triggered by autoimmune mechanisms. Here, we report a case of a mature woman who suffered from adenoviral meningitis one month after childbirth and developed MOGAD but was able to return to child rearing with high-dose methylprednisolone therapy. This case suggests that the risk of developing MOGAD early after childbirth may be increased. The case also suggested that adenoviral infection may be involved in the development of MOGAD.
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Saito et al. (2023) conducted a case report in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) (n=1). Intravenous pulse methylprednisolone (IVMP) was evaluated on Clinical and radiological improvement. Intravenous pulse methylprednisolone therapy led to rapid clinical improvement and resolution of MRI lesions in a woman who developed MOGAD following adenovirus meningitis shortly after childbirth.
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