| Affiliation |
(AGL) Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, Texas; Professor of Ophthalmology, Weill Cornell Medicine, New York City, New York; (AC) Class of 2023, Baylor College of Medicine, Houston, Texas |
| Transcript |
Today we're going to talk about bilateral, either simultaneous or rapidly sequential, simultaneous or rapidly sequential, optic neuropathy, plus optic disc edema. So this scenario comes up a lot where you have a bilateral optic neuropathy, therefore you're going to have decreased visual acuity and decreased visual field. Usually it's going to be in a nerve fiber layer distribution, central scotoma very common, but also arcuate altitudinal. The thing that's interesting is when they have the disc edema. So when we have bilateral simultaneous and rapidly progressive disc edema in a young person, normally optic neuropathy, we're thinking about optic neuritis. And in an old older person you're thinking about NAION, and in a much older person you'd bethinking about giant cell arteritis. You still need to think in these general buckets for everybody. The younger person, optic neuritis is normally unilateral so the atypical feature is the bilaterality. So when it's bilateral we have to worry about fulminant IIH, which is pseudotumor cerebri, causing the bilateral disc edema. If it's unilateral: optic neuritis. If it's bilateral we still have to think about optic neuritis, but most MS-related optic neuritis is retro-bulbar, no disc edema. So when we have bilateral and a swollen disc, we're really thinking about the atypical optic neuropathies, and those are going to be MOG-myelin oligodendrocyte glycoprotein-and neuromyelitis optica in addition to the usual suspects sarcoidosis, syphilis, Lyme disease, the usual suspects. And the way we're going to differentiate these entities is we're going to start with an imaging study and that means MRI of head and orbit with gadolinium and fat saturation. Fat sat plus gadolinium, and what we're looking for is enhancement. So bilateral sequential NAION should not produce any enhancement, so that one can be can be knocked off the list fairly quickly if we have enhancement of the optic nerve. Giant cell-always in the differential even with the enhancement. So if they're an older patient we're still going to do the sed rate, the CRP. We're going to give all these people steroids, and we're going to do a temporal artery biopsy on that one. Normally this one is not hard to differentiate. However if the sed rate, CRP are normal, and we have enhancement then we're going to look at the pattern of the enhancement. So in MOG, the pattern is usually perineuritis. In NMO, longitudinally extensive. So the two patterns that we're looking for are optic nerve sheath enhancement, that's the perineuritis, perineuritis, it's around and longitudinally extensive enhancement in both NMO and MOG but especially in NMO. So the pattern of enhancement that we see on this study is what we're looking for in optic neuritis, and we're going to be ordering MOG and NMO. In fulminant IIH, the pattern is going to be the pattern of increased ICP, not enhancement, but fluid in the sheath, flattening of the globe, empty sella, narrowing of the sinus and we make sure that it's not thrombosis and that person is going to have to have a spinal tap to measure the opening pressure, do lumbar drain, get ready for surgery. If it's this bilateral optic neuritis, it still could be MS, but you've got to be thinking about the MS mimics: sarcoid, syphilis, lupus, the usual things and the MS-like illnesses, the antibody-mediated forms, and if we see sheath enhancement or perineuritis or longitudinally extensive enhancement, really you're in the MOG, MMO spectrum, and all these patients need intravenous steroids. NAION gonna be a diagnosis of exclusion, look for the enhancement, do a temporal artery biopsy in an older patient, and test for the usual suspects in the young patient. |
