MOGAD

MOGAD, or myelin oligodendrocyte glycoprotein antibody-associated disease, is a spectrum of inflammatory demyelinating disorders of the central nervous system linked to antibodies against the MOG protein. It is considered distinct from multiple sclerosis and from aquaporin-4 antibody–positive neuromyelitis optica spectrum disorder, though it can share clinical features with those conditions. MOG-IgG is detected in serum and supports the diagnosis when the clinical presentation is compatible.

Clinical features vary by age. In optic neuritis, patients may experience eye pain and vision loss; in myelitis, there can be limb weakness or sensory loss with bladder dysfunction; acute disseminated encephalomyelitis–like presentations are more common in children and involve encephalopathy and multifocal symptoms. Relapses are possible, and the disease course ranges from monophasic to relapsing.

Diagnosis relies on detection of MOG-IgG in serum using cell-based assays. CSF findings are nonspecific; oligoclonal bands are often absent. MRI findings can include optic nerve or chiasmal inflammation, spinal cord lesions that are often longitudinally extensive, and variable brain lesions. The overall pattern helps distinguish MOGAD from other demyelinating diseases, though overlap can occur.

Management focuses on treating attacks and reducing relapse risk. Acute episodes are typically treated with high-dose intravenous corticosteroids; plasmapheresis may be used for severe or refractory relapses. For prevention of relapses, immunosuppressive therapies such as azathioprine, mycophenolate mofetil, or rituximab are commonly used, with intravenous immunoglobulin as an option in some cases. The choice of long-term therapy is individualized, and some multiple sclerosis–specific therapies may be ineffective or unsuitable. The prognosis is generally favorable for many patients, though relapses can occur and outcomes depend on lesion location and severity.