![]() There are blood tests that can test for MOG antibodies. NMDA receptor encephalitis is an autoimmune encephalitis that can cause psychosis, issues with memory and language, and seizures. MOG antibody disease can also occur in relation to another condition called anti-N-methyl-D-aspartate (NMDA) receptor encephalitis. When a relapse occurs, the diagnosis of MOGAD is confirmed. In some, the MOG antibody persists, and relapses may occur. In many children, the MOG antibody disappears within 1 year, and relapses do not occur. Those with MOG antibody disease are more likely to have both optic nerves affected at the same time, and if the symptoms are in only one eye, the other optic nerve may show subclinical atrophy.Ĭhildren can be found to have the MOG antibody in the setting of ADEM however, a positive MOG antibody test in the setting of ADEM does not necessarily imply a course of MOGAD. Paraparesis (weakness) of a limb or limbs.Paralysis (no motor function) of a limb or limbs.Loss or blurring of vision in one or both eyes.MOG antibody disease preferentially causes inflammation in the optic nerve, but can also cause inflammation in the spinal cord, brain, and brainstem. Furthermore, those with MOG antibody disease seem to be less likely to have other autoimmune disorders (such as rheumatoid arthritis, Hashimoto’s thyroiditis, etc.) than those with AQP-4 positive NMOSD. MOG antibody disease and AQP-4 positive NMOSD are thought to have distinct immunological mechanisms. AQP-4 is a water channel protein and those with NMOSD produce autoantibodies against AQP-4. Those with MOG antibody disease do not test positive for the NMO antibody called aquaporin 4 (AQP-4). Patients with persistently positive antibodies to MOG are at risk for recurrent events. Those with MOG antibody disease may previously have been diagnosed with neuromyelitis optica spectrum disorder (NMOSD), transverse myelitis (TM), acute disseminated encephalomyelitis (ADEM), optic neuritis (ON) or multiple sclerosis (MS) because of the pattern of inflammation it causes including brain, spinal cord and optic nerve damage. Those with MOG antibody disease should consider ongoing treatment with medications that suppress the immune system. Treatments are given at onset, and are typically intravenous steroids, plasma exchange (PLEX) or intravenous immunoglobulin (IVIG). The specific symptoms and severity of MOGAD can vary from one individual to another, but include issues with vision, symptoms associated with damage to the spinal cord, as well as seizures. The diagnosis is confirmed when MOG antibodies in the blood are found in patients who have repeated inflammatory attacks of the central nervous system. While the function of this glycoprotein is not exactly known, MOG is a target of the immune system in this disease. Myelin oligodendrocyte glycoprotein (MOG) is a protein that is located on the surface of myelin sheaths in the central nervous system. MOG antibody disease (MOGAD) is a neurological, immune-mediated disorder in which there is inflammation in the optic nerve, spinal cord and/or brain. Stay Informed With NORD’s Email Newsletter.Find a Rare Disease Patient Organization.Rare Disease Cures Accelerator (RDCA-DAP).Find Clinical Trials & Research Studies.Launching Registries & Natural History Studies.A Podcast For The Rare Disease Community.
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