| Affiliation |
(AGL) Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, Texas; Professor of Ophthalmology, Weill Cornell Medicine, New York City, New York; (JA) Class of 2023, Baylor College of Medicine, Houston, Texas |
| Description |
Summary: Optic neuritis • Demyelinating inflammation of the optic nerve • Most common cause of an acute unilateral optic neuropathy in young people • Multiple sclerosis is most common cause of optic neuritis, especially in Caucasian women o Testing for multiple sclerosis done via MRI o If MRI checking for enhancement of the nerve is negative for multiple sclerosis, must consider atypical optic neuritis, such as NMO or MOG; Atypical optic neuritis • Caused by demyelinating inflammation of optic nerve from something other than multiple sclerosis, notably antibodies • NMO - Neuromyelitis Optica o Associated with antibodies against aquaporin-4 channel • MOG ¬Myelin oligodendrocytic glycoprotein o Antibodies against MOG • Signs of atypical optic neuritis that suggest pathology other than MS o Atypical enhancement -Longitudinally enhancing -Bilateral -Chiasmal o Swollen disc o Older and/or non-Caucasian and/or male patient o Intractable hiccups o Nausea, unexplained o Vomiting, unexplained o Symptomatic narcolepsy • Treatment o Intravenous steroids o IVIG or plasma exchange o Chronic immunosuppressive therapy [Questions] "How should MOG be treated?" Answer: Acute MOG is typically treated with corticosteroids, IVIG, or plasma exchange. Immunosuppression may also be used long-term. |
| Transcript |
Today we're going to be talking about NMO and MOG. NMO, neuromyelitis Optica, an optic neuritis associated with a myelitis, and MOG, myelin oligodendrocytic glycoprotein. You need to know about NMO and MOG in patients with optic neuritis because the most common cause of an acute unilateral loss of vision with an RAPD and a normal fundus or a swollen nerve in a young person is an optic neuropathy. That most common optic neuropathy is optic neuritis, and normally multiple sclerosis is the most common cause of optic neuritis, especially in young females who are Caucasian. The old paradigm was, we would get the clinical history and do the exam, we would do an MRI scan, it would show enhancement of the optic nerve, and what we're looking for is periventricular, multifocal white matter lesions, which may or may not enhance consistent with demyelinating lesions like the Dawson's fingers. If the MRI was negative for multiple sclerosis, we'd be good. You could give intravenous steroids. You could give nothing. You could give oral steroids. The optic neuritis treatment trial showed intravenous steroids sped the rate of recovery but didn't change outcome. So, that was the end of that. However, now you need to know that if the MRI scan is negative for multiple sclerosis, that might not be a good thing, because what it means is not likely to be MS. Not zero, but less likely. If it's not MS, it could be something that looks like MS and is producing the optic neuritis but is actually something far more sinister: antibodies. Antibodies against the aquaporin-4 channel or antibodies against myelin oligodendrocytic glycoprotein. What that means for you clinically is, the outcome, the treatment, and the prognosis are going to be completely different from an optic neuritis related to MS versus an optic neuropathy related to NMO or MOG. And so, when someone has optic neuritis and their MRI is positive for MS, we just do what we always did. But if it's negative for MS, or if there are features that suggest that it is NMO or MOG - for example, clinically with patients with NMO they might have intractable hiccups or nausea and vomiting unexplained or symptomatic narcolepsy. These are super weird questions that we have to ask every patient with optic neuritis now that we didn't have to ask before. We're going to be asking and looking for myelitis in those patients and if the antibody NMO IgG aquaporin-4 channel is positive, not only do we have to consider intravenous steroids in the acute phase, but thinking about plasma exchange or IVIG followed by chronic immunosuppressive therapy like rituximab to prevent the myelitis from coming if a person is NMO positive. Likewise with MOG, even though it's not as bad as NMO, it's kind of like NMO-light. If we see longitudinally enhanced extensive enhancement on the MRI after gadolinium, or if it's chiasmal disease, or if it's bilateral, or if the disc is swollen, or if there's anything about this optic neuritis that is atypical clinically - an older person, a non-Caucasian person, a non-Caucasian older, Asian male - we should be thinking about things that look like optic neuritis but are not from MS. Those are the patients we're going to do NMO and MOG on. So, in summary, yes, optic neuritis is still the most common cause of an acute unilateral optic neuropathy in young people. Yes, still do an MRI looking for an enhancement of the nerve and yes, keep looking for MS. But if we don't see MS, we see something weird about the enhancement - bilateral, longitudinally enhancing, or chiasmal - or if we don't see any evidence of MS and the patient has any of those weird symptoms - intractable hiccups, nausea, vomiting, myelitis symptoms, symptomatic narcolepsy - or if the imaging shows peri-neuritis or shaggy enhancement, then we should be ordering NMO and MOG. But if it looks like a duck and flies like a duck and quacks like a duck, it's probably multiple sclerosis. |
