| Transcript |
For common optic neuropathies, this is for example the 14-year-old who has been referred for papilledema but you can see it's clearly drusen, lumpy and bumpy appearance in the disc with autofluorescence. The scan that we can see the drusen on is CAT scan. CAT scan looks at calcification really well and we can see the hyper density in the optic nerve head right there so it's one of the few reasons where a CT scan might be helpful. Ultrasound is better in general for looking for buried drusen, however if it's not calcified it won't show up on ultrasound and it won't show up on CT. So, in contrast if you have a patient who has headache, pulse synchronous tinnitus and transient visual obscuration, and has real disc edema rather than pseudo papilledema. it also produces a hyper intense lesion at the disk edge but this time it's from leakage into the true papilledema. So, we see the flapping of the globe here on this MRI scan and so the post contrast imaging study is showing the true disc edema as opposed to the pseudo papilledema from the CAT scan. And the radiographic findings of increase in strain of pressure include this empty sella right here. We can also see the fluid in the sheath which forms this hyper intense tram-tracking and the flattening of the globe as seen before, as well as narrowing of the transverse sinus. These are the radiographic features that we see in increased intracranial pressure from any cause but especially pseudotumor cerebri. You should be able to compare and contrast the cat scan and the MRI. Both have a hyper dense or hyper-intense disk, but in MRI that's contrast enhancement from leakage from true papilledema and in cat scan that's calcification. So, here's a twenty-year-old female who has acute unilateral loss of vision, RAPD, and normal fundus. Of course, that's the stem for optic neuritis, and so the imaging study of choice MRI had orbit gadolinium with fat suppression. If you don't give the contrast you won't see anything. So that's my house there at night. And fat suppression allows us to suppress the normal fat. This is a T1-weighted study pre contrast. You can see the fat is very bright but it's too bright on T1 of the orbit. We don't want to see that fat so if we don't put fat suppression, the fat is very bright and it's going to block our view of the contrast. So, in this post-contrast study you can see the contrast in the nose. You can't tell if that nerve is enhancing because you have white on white, and so that MRI scan is going to be read as normal and the question is why? Because white stuff on white stuff equals white stuff--polar bears. So, what we'd like to do is suppress that fat. You can see in this T1 post-contrast when you suppress the fat now, we can see the enhancement of the optic nerve--both on the coronal study here with the arrow and the axial study there. And the same thing here, post contrast T1 we have suppressed the fat and we can see the enhancement of the optic nerve now. Fat suppression takes away the fat. Now we can see that the optic nerve is enhancing. A similar type of suppression sequence is present in MRI called flare fluid attenuation inversion recovery, and basically the fluid cerebrospinal fluid is too bright on T2 so just like the fat is too bright on T 1 the CSF is too bright on T2. We'd like to use an inversion recovery sequence to attenuate the fluid, in this case the cerebrospinal fluid, so we can see the paraventricular white matter lesions. So, we can see the white matter lesions without flare on these T2 studies, but it's so much easier if we suppress the CSF. And if we look at this Kupersmith paper you can see that if you do a contrast enhanced MRI scan, right there, only about 5% of the cases don't have enhancement. So, if we don't see enhancement of the optic nerve on the MRI it's really bothersome. And once again, 5.6 percent of the patients had no enhancement, but the rest of the patients have variable degrees of enhancement. So, we really are looking for enhancement in the optic nerve as the distinctive radiographic feature of optic neuritis. In addition, we can see the T2 change in the nerve. The nerve can be enlarged with edema or the sheath itself can show hyperintensity. And so when we see T1, the muscles are enhancing--post contrast enhancement of the nerve--that's different than the T2 signal that we see around the nerve for the sheath and also in the nerve when it's edema. And so when we see T2 change in the nerve but there's no enhancement, then that's old. So, the T2 change that we see on the T2 coronal flare is just indicative that some type of optic neuropathy happened--but you don't know which one--versus the T1 post-contrast study is going to show enhancer. In addition, you need to know whether the enhancement is in the nerve itself or in the sheath. So, you can see here this black thing in the middle is the nerve and the sheath is what's enhancing--and that's peri neuritis--versus when the nerve itself is enhancing. So, when we see the enhancement, we want to know is it in the nerve or around the nerve. So, going back to this patient who has the retrobulbar optic neuritis, if it's the sheath rather than the nerve itself, that's peri neuritis in the acute setting. And in the chronic setting, the most common sheath is sheath meningioma. So, that would be not a duck. So, it's got to quack like a duck, look like a duck and fly like a duck. Typical optic neuritis enhances in the parenchyma, not the sheath. And so if we just change one thing in this stem and make it bilateral, that bilateral already is a clinical clue that something's not right and that's not quacking properly. And so if we see enhancement bilaterally or enhancement in the chiasm--chiasmitis--that's a big red flag that it's not a duck, not typical optic neuritis, and we should be worried in this setting for the things that could mimic MS related optic neuritis that's neuromyelitis optica (NMO) and myelin oligodendrocyte glycoprotein (MOG). And what we're looking for in the MR in NMO, neuromyelitis optica is areas that are aquaporin 4 rich areas and so if we see T2 change in the peri ependymal region or in the area post rima--the hypothalamus or any of the areas that are highlighted here in green--those are the aquaporin 4 rich areas that are affected in NMO. And what that means for us clinically is every patient with optic neuritis, we have to ask about hypothalamic symptoms like symptomatic narcolepsy, area post rima symptoms like intractable hiccups and persistent nausea and vomiting. And we're going to be looking for chiasmal involvement with enhancement or bilateral longitudinally extensive unilateral or bilateral enhancement. And finally, we want to know about MOG. So, MOG, the sheath, and also the fat, so it goes outside of the optic nerve the MOG--myelin oligodendrocytic glycoprotein--the MOG doesn't enhance just in the nerve but also in the sheath of the surrounding tissue. So, when we see these atypical imaging patterns, you should really be thinking about NMO, NOG, sarcoidosis and the usual inflammatory infectious mimics of optic neuritis. And so here's just another example where we have extensive enhancement. It's bilateral and it's involving the sheath. This would be a very atypical feature for demyelinating optic neuritis, and it suggests that it's some sort of inflammatory granulomatous infiltrative or MS optic neuritis mimic like NMO or MOG. And then finally if you have a chronic and progressive version of it a 20-year-old acute loss of vision, painlessly progressing, however has a RAPD in this optic ciliary shunt vessel, which is actually a retinal choroidal venous collateral. This is the stem for a patient with sheath meningioma. And so again the radiographic feature is going to be enhancement to the sheath rather than the parenchyma itself, as opposed to optic peri neuritis which is acute and painful. This is going to be chronic and progressive, and we may or may not see that retinal choroidal venous collateral--the optic ciliary shunt vessel. So, if you just know these main imaging parameters for optic neuritis, I think that you'll have a lot better way to divide up the patients who are presenting with optic neuritis. And if it doesn't quack like a duck, look like a duck and fly like a duck--especially radiographically--you should be thinking about the mimics. |
