For example, we know that only about 20 percent of people with recurrent episodes of optic neuritis have the MOG or the AQP4 antibody. What other antibody tests might become available? Many of these patients might have one or two optic neuritis attacks over five years and have normal visual outcomes. But whether all of these patients should be put on heavy-hitting immune suppression isn't 100 percent clear. The persistence of the MOG antibody might indicate a need for medication to prevent disease relapse and possibly reduce disability progression. In general, we would treat each attack, maybe aggressively, with steroids. This is a very interesting phenomenon and quite unusual in the field of autoimmune neurology. But if the antibody persists, the patient is at higher risk of another attack. Those patients are at low risk of another attack. Many of these patients will see a very rapid drop in MOG antibodies and test negative within six months. We've also found that the persistence of the MOG antibody is associated with disease relapses. We are planning a study to learn more about these phenotypes. 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. It may actually indicate a more favorable prognosis. How does the presence of the MOG antibody affect disease course? 10 percent of patients with recurrent optic neuritis and 2 percent of patients with a single optic neuritis.20 percent of patients with a longitudinally extensive transverse myelitis.30 percent of patients with neuromyelitis optica who lack the AQP4 antibody.60 percent of pediatric patients and 40 percent of adult patients with acute disseminated encephalomyelitis.

Our work indicates that testing is positive in: Which inflammatory disease phenotypes are associated with the MOG antibody? Sagittal T2 FLAIR image nine months later after immunotherapy shows almost complete resolution of the T2 hyperintense lesions. Sagittal T2 fluid-attenuated inversion recovery (FLAIR) image of an adult patient demonstrates multifocal T2 hyperintense lesions in the frontal, occipital and temporal lobes, the corpus callosum, and the brainstem (arrows), consistent with acute disseminated encephalomyelitis. It uses a completely novel method of flow cytometry developed by Mayo Clinic to identify patient antibody binding to the MOG protein that is expressed on living cells.įLAIR image of adult patient demonstrates multifocal T2 hyperintense lesionsĪ1. Our test has great sensitivity and specificity.

An optic neuritis seems to be a very common presentation of MOG. Patients who have more than one episode of optic neuritis absolutely should have testing. Which patients would benefit from this antibody testing?Īny patient who suddenly presents with vision loss, significant disk edema or recurrent optic neuritis should consider testing for both MOG and AQP4 antibodies. Combined testing allows for the most comprehensive evaluation for patients with recently diagnosed demyelinating diseases. Mayo Medical Laboratories offers testing for both MOG and AQP4 antibodies, either separately or in combination.

Yet some MS medications have been reported to worsen diseases that mimic MS. That's important because diseases associated with the MOG antibody - as well as diseases associated with the water channel aquaporin-4 (AQP4) antibody, which was discovered at Mayo Clinic - are commonly misdiagnosed as MS. Testing positive for the MOG antibody indicates that a patient doesn't have classical MS. The MOG antibody can distinguish a spectrum of autoimmune demyelinating diseases from multiple sclerosis (MS). How does this test help with the diagnosis of inflammatory demyelinating diseases? Mayo Clinic has developed the first test available in the US to identify the myelin oligodendrocyte glycoprotein (MOG) antibody in patients' blood.

Anti mog antibody