Clinical phenotype, radiological features, and treatment of myelin oligodendrocyte glycoprotein-immunoglobulin G (MOG-IgG) optic neuritis

摘要

Purpose of review To review the clinical characteristics, radiological manifestations and treatment of myelin oligodendrocyte glycoprotein (MOG)-immunoglobulin G (IgG) optic neuritis. Recent findings Serum antibodies to MOG have recently been found to be a biomarker of MOG-IgG-associated disorder (MOGAD), a demyelinating disease distinct from both multiple sclerosis (MS) and aquaporin-4-IgG neuromyelitis optica spectrum disorder (AQP4-IgG-positive NMOSD). The phenotype of MOGAD is broad and includes optic neuritis, transverse myelitis, and acute demyelinating encephalomyelitis (ADEM). Optic neuritis is the most common presentation in adults, whereas ADEM is the most common presentation in children. Clinical characteristics suggestive of MOG-IgG optic neuritis include recurrent optic neuritis, prominent disc edema, and perineural enhancement of the optic nerve on magnetic resonance imaging. Although the nadir of vision loss is severe with MOG-IgG optic neuritis, the recovery is typically better than AQP4-IgG optic neuritis and therefore has a favorable overall prognosis. Patients with relapsing disease will often need chronic immunotherapy. Rituximab, azathioprine, mycophenolate mofetil, and monthly intravenous immune globulin are the most commonly utilized treatments. MOGAD is a unique entity that is separate from both MS and AQP4-IgG-positive NMOSD. Recognition of the clinical and radiologic features allow for the correct diagnosis. Future randomized trials will determine the optimal treatment for MOGAD.