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If you’re getting a visual recovery within 24 to 48 hours with IV steroids, I’m very suspicious for MOG. One of the things that we’ll see with MOG is a very rapid response. We talked about a lack of response as being a marker maybe for NMO. Especially for the pediatric cases routinely admitted, 1 of the things I’ll look for is an early response to treatment. If they are not better, then we look to plasmapheresis. Rod Foroozan, MD: Yeah, I was going to ask you the same thing. If they’re not better then, I’m looking at pheresis. If after 3 days of IV steroids they’re not better, I give them 2 more days. I admit all these patients now, so that I can get the imaging of the cord done right away, and I can see their response. But if you see a patient who fits the clinical profile of optic neuritis, and that optic nerve is swollen and there are hemorrhages, the index of suspicion for NMO goes up very high and also for anti-MOG. The old teaching about optic neuritis was that the patient couldn’t see anything, and when the doctor looked in, the optic nerve looked normal. Sergott, MD: One of the tip-offs for MOG disease that we’ve seen is a lot of swelling on fundoscopic examination. Now we have a spectrum of disease that initially was only considered to be MS and now it has branched into at least 2 other forms, MOG and NMO. And they can signify in older patients a risk for recurrent optic neuritis or what was previously termed CRION, for chronic relapsing idiopathic optic neuritis. In our experience, probably about one-third of patients at Texas Children’s Hospital who develop optic neuritis who are children will have MOG antibodies present. And what was noted is a group of patients who had optic neuritis that often was very responsive to steroids were found to have these positive antibodies.Įxactly what their role is in the pathogenesis of optic neuritis is not clear, but it is a marker in a group of patients, and that includes younger patients, pediatric patients, who develop optic neuritis. Actually, what was found was that MOG was found to be used in an experimental model causing experimental autoimmune encephalitis, so an animal model of MS, and subsequently the antibody became available a few years ago more commercially and for research purposes several years before that. Rod Foroozan, MD: Yeah, so the MOG story actually dates back a little earlier, when it was thought to be using antibodies against MOG that were thought to be maybe somehow protective treatment for MS. Rod, tell us about that, especially in children. Sergott, MD: Let’s talk about this anti-MOG variety of NMO.