This may include IVIG and medication, such as azathioprine, myucophenolate mofetil, or rituximab. However, some patients may experience recurrent attacks and need a long-term management plan. Many individuals with anti-MOG syndrome will recover fully after their first treatment and never relapse. In rare cases, if high-dose steroids are not effective, patients may undergo intravenous immunoglobulin (IVIG) treatment. Intravenous corticosteroids are the first line of treatment. Treatment for acute symptoms of demyelination involves reducing inflammation. Symptoms of acute disseminated encephalomyelitis may include: Clinical interest in myelin-oligodendrocyte glycoprotein (MOG) autoantibodies has increased remarkably in the past decade, and the term MOG antibody-associated disease (MOGAD) has been coined to include several clinical and radiological syndromes, most of which are demyelinating, that occur in individuals with these antibodies. Individuals with anti-MOG syndrome may experience optic neuritis, transverse myelitis, and/or acute dissemination encephalomyelitis, depending on which parts of their nervous system are affected. Myelin oligodendrocyte glycoprotein (MOG) is a protein that is located on the surface of myelin sheaths in the central nervous system. Department of Translational Neuroscience.Department of Physical Medicine & Neuro-Rehabilitation.Department of ENT and Skull Base Surgery.The diseases are bizarrely different AQP4 targets astrocytes while MOG targets oligodendrocytes yet the phenotypes look quite similar. For example, in patients with recurrent optic neuritis, the visual outcomes are better with MOG-associated disease than AQP4-associated disease. Barrow-ASU Center for Preclinical Imaging It may actually indicate a more favorable prognosis.Core Facilities and Biobank Show submenu.Bioskills & Neurosurgery Research Laboratory.Grand Rounds, Publications, & Media Show submenu.Neuroscience Fellowship Programs Show submenu.Rehabilitation Psychology Residency Program.Neuroscience Residency Programs Show submenu.Parkinson’s Disease & Movement Disorders.This condition can cause seizures, as well as symptoms that are typical of. Center for Transitional Neuro-Rehabilitation One way MOG can manifest is called acute disseminated encephalomyelitis (ADEM).In this review, we examine the history of the MOG antibody and its relevance to demyelinating disease, as well as compare the clinical, radiographic and serological profiles of patients with MOG antibody with patients with AQP4 antibody.Ĭopyright © 2018 Elsevier B.V. MOG antibody disease has thus recently emerged as a distinct entity carved out of the patient population diagnosed with NMOSD. In recent studies around the world where MOG testing is available, up to 42% of NMOSD patients who test seronegative for the AQP4 antibody test positive for MOG antibodies. In addition, acute disseminated encephalomyelitis (ADEM) is a well-recognized phenotype of MOG antibody disease in children. Clinically, the disease resembles neuromyelitis optica spectrum disorders in the predilection for relapses of optic neuritis and transverse myelitis. MOG is a glycoprotein expressed on the outer membrane of myelin and solely found within the central nervous system, including in the brain, optic nerves and spinal cord. MOG antibody disease is an autoimmune disease of the central nervous system associated with a serological antibody against MOG, myelin oligodendrocyte glycoprotein.
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