MOGassociated

MOG-associated disease (MOGAD) is an autoimmune demyelinating disorder of the central nervous system defined by the presence of immunoglobulin G antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) in serum. It is diagnosed by a cell-based assay for MOG-IgG and by excluding other causes of CNS demyelination.

MOGAD is distinct from multiple sclerosis and from aquaporin-4-IgG–positive neuromyelitis optica spectrum disorder (NMOSD), though clinical features can overlap. The diagnosis relies on positive MOG-IgG testing and an appropriate clinical and radiologic context, with careful exclusion of alternative diagnoses.

Clinical features vary with age. In children, MOGAD often presents as an acute disseminated encephalomyelitis–like illness with multifocal neurologic symptoms and sometimes encephalopathy. In adults, optic neuritis and transverse myelitis are common presentations. A relapsing course occurs in a substantial subset of patients, underlining the need for long-term management in some cases.

Imaging typically shows involvement of the optic nerves, spinal cord, or brain. MRI patterns can include optic nerve head involvement, cortical or juxtacortical lesions, and brainstem or deep gray matter involvement, with spinal cord lesions that can be extensive but are not universal. Cerebrospinal fluid findings may show mild inflammation; oligoclonal bands are less frequent than in multiple sclerosis.

Treatment and prognosis: during acute attacks, high-dose intravenous corticosteroids are standard; plasma exchange is considered for steroid-refractory cases. For relapsing disease, immunotherapy such as rituximab, mycophenolate, or azathioprine may be used to reduce relapses. Intravenous immunoglobulin is used in some pediatric cases. Most patients recover from individual attacks, but relapses can occur; disease-modifying therapies effective in MS are generally not used for MOGAD.