Recent publications have changed the management of several neuro-ophthalmic conditions. Topics will include optic neuritis and NMO, MOG, diagnostic evaluation of transient visual loss due to retinal arterial insufficiency, CRAO and BRAO and management of NAION.

Lecturer: Dr. Karl Golnik, Neuro-ophthalmologist, University of Cincinnati, Ohio, USA


DR GOLNIK: Greetings. This is Dr. Karl Golnik. I’m just trying to get my presentation up here for you to all see
And welcome. It’s morning time here for me in Cincinnati, Ohio, the United States, where it’s about -10 degrees Celsius, so it’s a cool morning for us. Welcome to everyone who has joined the webinar. There will be an opportunity for you to type questions in the question and answer box. I will address those at the end of the presentation. So be patient. If you have questions.
I also received about 35 questions in advance on a variety of topics. So depending on the time and so on, I will try to run through some of those questions, after, of course, answering any questions that might occur during this webinar. My objectives for the webinar: That when we’re done, you will be able to describe new developments in the diagnosis and treatment of some common neuro-ophthalmology problems.
And the three that we’ll concentrate on are transient monocular visual loss, non-arteritic ischemic optic neuropathy, and what’s been called atypical optic neuritis, and I’ll try to define that a bit better. But those are the three topics we’ll talk about. I’ll start with this patient, a 63-year-old gentleman with intermittent loss of vision in the left eye over the past few days.
The episodes are short. Just a few minutes at a time. Seem to be fairly random. This would seem to be transient monocular visual loss. He does have a history of diabetes and hypertension and high blood pressure.
Pupil are normal with no relative afferent pupillary defect, automated visual fields and ocular motility is normal, and funduscopic exam is pretty normal, one small hemorrhage temporal to the fovea, thought to be very early mild diabetic retinopathy.
So the question is: What do we do with this guy? I’ll come back to that question in just a moment. This is a review paper that was written a few years ago now, and they listed some causes of transient vision loss. Under monocular, vascular, embolic, thrombotic, like giant cell arteritis, is it vascular and related to narrowing of blood vessels? Could it be vasospasm or retinal migraine?
They talk of the category of monocular or binocular. Papilledema, optic disc swelling due to increased intracranial pressure can cause so-called transient visual obscurations, and Uhthoff phenomenon is another, people who had problems with the optic nerve, with optic neuritis, classically, can have transient visual loss when their temperature goes up.
I’m gonna talk mostly about acute retinal ischemia. Here you see three photographs with my arrows misplaced. I’m sorry. Hopefully you can see the arrow I’m controlling here. The arrow should be pointing at this embolus right up here. There’s a little hemorrhage maybe on the disc down here. Here’s another embolus. And in this case, a large area of retinal ischemia.
This is a person with a branch retinal artery occlusion and of course central retinal artery occlusions. And we’ll talk about what we do when we think it’s acute retinal ischemia. Of course, in patients with transient visual loss, we have to consider other entities. I have to show you a video. If you’ll look here, you’ll see an intermittent reflection.
That is a Holenhorst plaque. You don’t see it unless you put a little pressure on the eye. When you put pressure on the globe, it causes the blood to reflux, and it takes that Hollenhorst plaque and causes it to twist and reflect the light. But unless you put a little pressure on the eye in this case, you can’t see that Hollenhorst plaque. Hopefully we’ll see that again. But right there — nothing.
We treated this person with increasing their blood CO2 by having them blow into a brown paper bag, and here you can see that little reflectile whitish body. There’s the little blot hemorrhage we saw earlier. What’s happened is that Hollenhorst plaque has moved downstream, because when you breathe in that brown paper bag and your blood CO2 goes up, your blood vessels dilate.
The idea is to get that plaque to move downstream. I’m gonna show that again. Because it’s a tough video to obtain. It can be tough to see the findings. Look right here at the bifurcation. Nothing apparent, but you see that reflecting. Putting pressure on the eye, and the blood is pushing that Hollenhorst plaque back, twisting it enough, causing reflection. There’s an embolus, Hollenhorst plaque, in the blood vessel, and we had the patient increase their blood CO2, by breathing into a brown paper bag, and that allowed the blood vessel to dilate, and it moved the black downstream. Hopefully to affect less of the retina structure. And so here we are, later on. We’re further downstream. We’ll see that one little blot hemorrhage I mentioned down here. And right in here, you still don’t really see it, unless you put pressure on the eye.
01:06:45 So it’s kind of a cute case. Here we are, this is before the CO2, carbon dioxide breathing, without digital pressure and with digital pressure. And here we are afterwards. Now we’re further downstream, further into the retinal periphery, and again, you really only see that Hollenhorst plaque when you put a little digital pressure. So when we think about transient monocular visual loss, we have to think about things other than emboli.
Decreased perfusion, due to carotid or ophthalmic artery stenosis, retinal claudication. When people are exposed to bright light, they can have visual dimming or visual loss, because the retina is very metabolic. If there’s not quite enough blood supply and oxygen, that might affect the retinal function. And so it’s been called retinal claudication. I think this is pretty uncommon.
You have to have really bad stenosis of the blood vessels bringing blood to your eye. You of course could have reduced cardiac output. So if you have an arrhythmia, for instance, and your heart is not pumping well, you’ll probably get dizzy, but you could also have transient visual loss and systemic hypotension, for whatever reason, whether it’s blood loss or just very low blood pressure, again, could cause decreased perfusion of the retina and nerve and transient monocular — or if it’s systemic — binocular loss of vision. This is an interesting case. This is a patient who has intermittent monocular visual loss. Lasting in the sort of 10 to 15 minute ballpark. On the slide left, this is the way the retinal vascular structure looks when the patient is asymptomatic.
In slide center, this is actually during an episode. And you can notice this retinal arterial — most prominently, right here, inferiorly. I’m hoping you can see my mouse, as I’m moving the arrow. You can see how thin and narrow this looks, compared to the before picture. And of course the after picture, where it’s back to normal. This patient just happened to have a vasospasm, which I think it also probably the same thing as what’s been called retinal migraine. I think you want to be very hesitant to make a diagnosis of retinal migraine. This is very rare. Certainly this is not at the top of your list. But obviously if you can observe it, as we did, you can make that diagnosis. Calcium channel blockers may help reduce or eliminate these episodes of retinal migraine.
Papilledema, as I mentioned, so again, papilledema is usually bilateral optic disc swelling, but it has to be due to increased intracranial pressure. You can have transient monocular visual loss, TVOs, transient visual obscurations, oftentimes, elicited upon movement, bending over, standing up, sometimes even just eye movement. But it can happen without anything. Just sitting there, it can happen. Come and go.
Optic disc drusen have been reported to cause transient monocular vision loss or blurring. I see a fair amount of optic disc drusen. I don’t see a lot of that, but if I have someone with that, and I see disc drusen, it probably is related. And then I mentioned Uhthoff’s phenomenon, presence of optic nerve dysfunction. There’s usually some evidence of optic nerve dysfunction. It decreased acuity, decreased color vision, maybe a small relative afferent pupillary defect, and this is a phenomenon noted hundreds of years ago — or a hundred years ago — where when your body temperature goes up, it could be a hot shower or bath, a hot day outside, I have a patient who had optic neuritis some years ago now, pretty much completely recovered,
but when he goes out and plays tennis, he plays his first set and he’s okay, but by the time he gets to the end of the set, his vision gets blurry. He sits down, drinks ice water, and plays the next set. This is not something that causes any damage to the nerve. It simply has to do with conduction along that nerve related to heat.
But what I really wanted to bring up was this topic. The acute retinal ischemia causing transient monocular vision loss. This is something that as ophthalmologists, at least in the past, we really hadn’t been following the guidelines. That were already existing out there. This is a review article from Emory University in the United States, published almost two years ago now,
and they note that both the US National Stroke Association and the American Heart Association define central nervous system infarction as brain, spinal cord, or retinal cell death attributable to ischemia. So it’s not just brain or spinal cord. It’s retinal cell death. And they said in their review article, the outdated belief that acute retinal ischemia is of less concern than cerebral ischemia, and therefore may not need emergent care, must be revisited. And there’s been at least one meta-analysis published a couple years ago, where they looked at a great number of studies, called advances in urgent evaluation and treatment of TIA, transient ischemic attack, decreased subsequent stroke risk. So this article, this meta-analysis, there is no debate regarding the obvious benefit of urgent assessment of TIA patients to decrease the risk of stroke recurrence, including patients presenting with acute vascular visual loss. So this is just as important and just as urgent as brain infarction. And you’re not meant to look at all of this data, but this is also from a review article, where they looked at these seven articles. Seven studies.
All of these studies were evaluating what you see when you get MRIs on patients with acute retinal ischemia. And basically the summary of those studies: The seven studies, more than 700 patients, with acute retinal ischemia. And in these patients, who all got MRIs, if there was a central retinal artery occlusion, up to 3/4 of the patients, even though they were otherwise asymptomatic, had silent strokes, silent strokes, on their MRIs. In patients with transient monocular vision loss, so these are patients who may have a normal-looking fundus, but just the history of transient monocular vision loss, up to about 1/3 had quote-unquote silent strokes on their MRIs. And so ideally you’re going to image these patients, who you think have transient monocular vision loss, due to acute retinal ischemia.
You’re gonna image these patients ideally with a brain MRI with DWI. DWI stands for diffusion weighted imaging. It’s simply one of the sequences that’s run. In the US, if you run a brain MRI, for whatever reason, you’re automatically gonna get DWI. That didn’t used to be the case, and might not be the case where you live. If you can order MRIs to where you live and you’re thinking about stroke, or any sort of ischemia, I would specifically ask them: Please do DWI. They should know what that is. They may already be doing it. But they may not automatically be doing it. This is the most sensitive way to pick up new ischemia in the brain. DWI images. The American Academy of Ophthalmology has a retinal and ophthalmic artery occlusion preferred practice pattern available.
If you Google this, you will come up with the AAO’s preferred practice pattern. And in that pattern, they say: Acute symptomatic posterior segment arterial occlusions represent an emergent ophthalmic condition, and require prompt evaluation. Acute symptomatic patients with retinal artery occlusions or giant cell arteritis, GCA, should immediately be referred to a cardiologist, emergency room, or stroke center at presentation. At presentation. And in a very recent editorial, a little more than a year ago, a good friend of mine, Tony Arnold, from the University of California, Los Angeles, wrote this editorial for the American Journal of Ophthalmology, about the urgent evaluation of a patient with acute central retinal artery occlusion.
And basically he said the paradigm for management of acute retinal ischemia, either transient or permanent, has changed. Ophthalmologists who manage these patients must recognize and institute the change, and probably everybody listening to this webinar, all ophthalmologists, will see patients with transient monocular visual loss.
So what should the ophthalmologist do? Well, you could offer same day appointments. Because depending on where you live in the world, that happens all the time or it doesn’t ever happen. But offering same day appointments, rule out non-vascular problems, and don’t forget about giant cell arteritis.
I know many of you live in areas where you don’t see much of that. I would caution that not seeing much of that maybe because you’re not thinking about it, and certainly there are differences in different populations, but don’t forget about giant cell arteritis. And if you really believe that this is an acute retinal ischemia, then refer to the ED, the emergency department, if you can, affiliated with a stroke center. And talk to them. And tell them: We think that this is acute retinal ischemia. Ideally you have a stroke specialist, a neurologist, assessment, and brain and vascular imaging with cardiac monitoring. That’s ideally what we would do these days.
So follow the guidelines. They’re out there. But I think as ophthalmologists, we have not been treating these patients with the sense of urgency that they deserve. So that’s topic number one. Acute transient monocular visual loss. And in particular, due to retinal ischemia. We did cover sort of the differential diagnosis of that as well.
And I’m gonna move on to topic number two. Here’s another patient. 68-year-old, Caucasian gentleman. Complained of blurred vision in the right eye for one week. You can see the right optic disc on top, the left optic disc on the bottom. The exam showed visual acuity 20/60, which would be 6/18 in the right eye. Normal in the left.
And there was a right relative afferent pupillary defect. And the question is: What’s the diagnosis? What’s the evaluation? And what if any is the treatment? And so this of course represents an AION. Anterior ischemic optic neuropathy. Which of course is characterized by sudden painless visual loss with disc swelling.
You cannot diagnose AION without disc swelling. The A is for anterior, which means you have to have disc swelling to make this diagnosis. Occasionally get a patient referred and they think it’s AION. But they don’t have disc swelling. If they don’t have disc swelling, it’s not AION. So most of my patients with AION have non-arteritic — and I suspect around the world that’s even more likely — because the other most common entity would be giant cell arteritis, which is not as common outside of the US and that subtype of population. And so for non-arteritic AION, NAION, of course, age — usually we talk about age greater than 50. Remember that people younger than 50 can have an AION. High blood pressure, diabetes, cholesterol. The things that affect your blood vessels.
There’s what we call the disc at risk. That is a small crowded disc. We think this is a compartment syndrome, and you can see in the photos below from our patient, when we look at the normal left optic disc that’s not swollen, you can see there’s essentially no cup. So this would clearly be what we call a disc at risk.
Sleep apnea I think has recently been well established as a risk factor for NAION. The thought would be that that you have sleep apnea. What happens when you have sleep apnea? You don’t exchange oxygen and carbon dioxide, and your blood oxygen level goes down. Which further decreases perfusion of your optic disc. So it makes sense, theoretically.
And I think studies now demonstrate that’s the case. So certainly in patients with NAION, we ask about snoring. Are you a big snorer? Being a big snorer doesn’t mean you have sleep apnea, but if you don’t snore, then you don’t have sleep apnea. Nocturnal hypotension is thought to be a risk factor. We know everyone in the early morning sleeping hours has their lowest blood pressure of the day.
The thought is that maybe that low pressure is the trigger, the straw that breaks the camel’s back, as we say, and that triggers the ischemia. Even though high blood pressure that triggers the narrowing of the arteries is a risk factor, maybe that low pressure is a factor. That’s one reason why people who are taking high blood pressure medicines should not be taking them at night.
Because that blood pressure medication at night can accentuate, can increase, that low blood pressure in the early morning sleeping hours. PDE-5 inhibitors like Viagra have been shown to slightly increase risk of NAION. Carotid artery stenosis does not. That is a big blood vessel problem. This is a small blood vessel problem. So not carotid artery stenosis. We know from the ischemic optic neuropathy decompression trial, where they looked at 200 patients with this, 100 patients who were treated with nothing, and this is what we found. 50% of patients had no change in vision forever. 43% of patients improved some. Not completely. And 7% worsen in the first six months. In that same study, they followed those 100 patients to see: How many have it happen in the other eye?
And they found that 15% had it happen in the other eye over the following five years. What about treatment? So this comes up a lot. And a number of the questions I received in advance of this webinar had to do with treatment of NAION. Well, for a while back some years ago now, optic nerve sheath fenestration — it was thought maybe that would help. But the study I just mentioned, the ischemic optic neuropathy decompression trial, looked at 200 patients. 100 got nerve sheath fenestration. 100 got nothing. People who got nothing did better than the people who got the nerve sheath fenestration. So we don’t do that anymore. What about steroids? That comes up very frequently. There are a number of questions about steroids, which is what I’m gonna address. So some years ago now, more than so, more than 10, Dr. Hayreh, a well known researcher and expert, published a paper where he retrospectively looked at 600 patients, and his habit had been to offer patients oral steroids, or not. And about half the patients took the steroids and about half didn’t. And he found that overall, if you looked at all the patients, there was no difference in visual recovery.
However, if you looked at a subgroup analysis of patients who were defined as, quote, “poor in visual acuity” at presentation, that would have been about 6/18 or worse, versus better than that, the people who got the steroids in the worse group seemed to do better. There are a lot of problems with this paper. There was a lot of debate about this paper.
But it led to this concept that… Hey, maybe steroids would help patients with NAION. Subsequently, there have been a number of papers — I would say none of them are great. But this one was a very recently reported paper, about a year ago, from India. This is a randomized controlled trial, where they had 38 patients with acute NAION.
One of the exclusion criteria was diabetes. So you couldn’t have diabetes and get in this study. It was double blind with two arms. One group got oral prednisolone in the schedule that you see. 80 for a couple weeks, 70, and so on, and decreasing. This was the protocol, I believe, that Dr. Hayreh used in his retrospective study. The other group got oral placebo. The primary outcome was best corrected visual acuity.
They also looked at visual evoked response and OCT at baseline, 1, 3, and 6 months. They looked at the consecutive series of NAION patients. They excluded 21 patients because 15, as I said, were diabetics, and that was exclusion. 2 had giant cell arteritis. 2 were already on steroids. And 2 declined to be in the study. That’s where they got their 38 patients. And at six months, they found no difference in the best corrected visual acuity.
There was no difference in the OCT nerve fiber layer. There was slightly better latency of the VER in the steroid group. Just going back to that slide, the problem, if you want problems — not problem, but the limitation, of course, of this study, was that although it was very well designed, 38 patients is not a lot of patients. And that’s the main issue here. The numbers were pretty small.
But since then, just in the last — I think it was from November of 2019, there was a meta-analysis done to look at this question of steroids versus no steroids. They looked at the 8 studies that they could find with 720 eyes, and basically the steroids did not improve vision. So I do not recommend the use of steroids in any form for NAION. And that’s the summary of sort of the new treatment, and so on, of non-arteritic anterior ischemic neuropathy.
Things that have changed in my practice: Number one, I no longer consider the steroids. Number two, I consider sleep apnea. At least a few papers now have identified sleep apnea as a risk factor. There’s also been a couple publications that looked at patients with sleep apnea and NAION in one eye, and asked the question: Hey, what about prevention of NAION in the opposite eye? Because one of the worst things we have to tell patients, when they come in with NAION in the first eye, is not only do we not have a treatment, in 2020, not only do we not have a treatment for this condition, but there’s a chance it could happen in your other eye. Which of course would be a whole big difference. Losing vision in one eye is nothing like losing vision in both eyes. So obviously patients are very concerned. There’s really been no studies that have shown anything decreases the risk in the other eye. But there have been a couple of small studies that have looked at sleep apnea. Patients with it who were treated for the sleep apnea, versus those who were not, and they showed a lower chance of fellow eye involvement in the patients treated for sleep apnea. So I recommend evaluation for it, if they’re snorers, and treatment. So that was our second topic. Moving on to our third topic.
31-year-old woman with blurred vision for two days, and discomfort. 20/60 in one eye, 20/30 in the other, she has relative afferent pupillary defect, and disc swelling of the right optic disc. Her past ocular history includes an episode of optic neuritis in 2016. She said I had something similar back then, they called it optic neuritis. She had an MRI of the brain at that time that was normal.
So the question is: What’s the diagnosis? I think that’s fairly obvious. She probably has a second episode of optic neuritis. But what about the evaluation and treatment? So this brings up a topic that’s fairly new, NMO spectrum disorders, defined as recurrent optic neuritis or extensive transverse myelitis. In investigation of patients with this problem, and of course, other investigations, they’ve identified a second antibody,
antibodies against the myelin oligodendrocyte glycoprotein. Versus the aquaporin 4 antibody. Same thing. Same thing as NMO antibody. The MOG is the different antibody. And in this study, published now more than five years ago, they looked at 215 patients, and found the majority of them with recurrent optic neuritis had NMO. A small percent had MOG. Patients with MOG were more likely to be men.
More likely to have bilateral optic neuropathy and single attacks with better recovery. So this was probably one of the first studies that looked at MOG and NMO. And that’s going to be the point of most of my talk about this condition, about optic neuritis. Especially depending on where you live in the world. These conditions can be more or less common.
And we know that the problem with optic neuritis, depending, again, on where you live, is differentiating: What kind of optic neuritis is this? Is this demyelinating optic neuritis? In other words, multiple sclerosis? Which we see a lot of in North America and in Western Europe. Or is it NMO? Or could it be MOG? We’ve got that now. So in this study, they wanted to try to see if there were MRI findings that might differentiate NMO optic neuritis from MS,
from demyelination. It was retrospective, but they looked at 26 patients with NMO and 26 patients with MS. And they found that in patients with NMO, you’re much more likely to have a longer segment of demyelination. So this — our lower image on the right — this whole right optic nerve, the little white arrow, this whole optic nerve is enhancing. You can see the left optic nerve is not enhancing.
Whereas this is a patient with NMO. The image on the lower left, there’s an arrow that’s a little bit misplaced. This is right from the article. But right here, you see this little dot. There’s a little area of enhancement, of dye leakage on the MRI. This is more typical for demyelination. And so NMO, longitudinally more MRI enhancement. They found in their case that the cutoff was 17 millimeters,
which is quite a long section. This was fairly specific and sensitive for NMO. So I do pay attention. I think to me, if I see a patient with optic neuritis, their MRI shows enhancement of the nerve, if it’s a long segment, that makes me interested and I really start to then think… Okay, this is more likely gonna be NMO than typical demyelinating optic neuritis. If it’s a shorter segment, that doesn’t rule out NMO.
It’s somewhat helpful. I think a few patients who are thought to have demyelinating optic neuritis have MRI, and they show a long segment of deenhancement, and they’re shown to have anti-aquaporin, NMO antibodies. This study looked at patients and found bilaterally, not common in MS at all. Much more common in NMO or MOG. I rarely have seen a patient present with bilateral simultaneous optic neuritis that has turned out to be demyelinating.
Clearly if it’s simultaneous bilateral, that’s a big — we call it a red flag — a big caution. This is probably not demyelinating. The study also found that chiasmal and optic tract involvement were more common in NMO, and again, that longer segment involvement, not just more common in NMO, but also more common in MOG. This study was fairly recently done in the US, from Mayo Clinic, about a year and a half ago.
And they went back and looked at their patients who had recurrent optic neuritis. So they defined recurrent as at least two episodes. So this would be like our patient that I presented at the beginning of this section, who’s having her second episode of optic neuritis. And they had 246 patients, and they went back and looked at these patients, to see: How many had MOG or NMO? And I was pretty surprised.
this is in the US population. But 32%. So 19% MOG. 32% NMO. 32% of all comers with two or more episodes of optic neuritis had one of these two antibodies. And that was — to me, that was very impressive. I was surprised it was that high. They looked at the sort of subgroups, because they thought… Well, of these 246 patients, some of these patients just had visual problems.
So these patients, they said: Well, these are the patients likely to come and see an ophthalmologist. Whereas 186 of the 246 — whereas 60 had optic neuritis but also had other neurologic symptoms. So maybe these patients would not get to us, as ophthalmologists. They might get to the neurologists. When they looked at the 186 with just the vision problems, the percent was still pretty high. About 28% had one of these two antibodies.
They found that these patients with NMO had a worse visual prognosis, but the MOG patients more frequent recurrences. And they looked at the other group, the 60, with the neurologic, as you might imagine, more of these patients were positive. In fact, 38%, more than a third, were positive for the NMO antibody, and only about 7% for MOG.
And then this study, which was also recently reported at the end of 2018, looked at sort of what is MOG, what does optic neuritis look like? A very valuable study. They had 87 patients that are positive for the MOG antibody, a little bit higher women to men, but not much. 57 to 43. The median age was 47. But the range was 2 to 79. The age doesn’t help you that much. The vast majority, 86%, had disc swelling.
More than one third, it was bilateral and simultaneous. And I just mentioned, if we see patients with bilateral and simultaneous, it’s almost never demyelinating. And not only did they notice enhancement of the nerve on MRI, but very interestingly, these arrows in this image on the upper right show that the nerve sheath was enhancing. So we call this optic perineuritis. Optic perineuritis.
Sheath enhancement. You don’t see this with demyelinating — typically — or other forms of optic neuritis. So this is a very important finding if you see it. And they saw it more than a third of their patients. The average worst vision in these patients was counting fingers. Well past legal blindness. But the average visual recovery was 6/7.5. Does that work out to 20/25?
So the visual recovery was actually very good. Even though the average nadir, the average worst visual acuity, was counting fingers. And this is kind of a busy chart from a very recent — it’s actually an epub. It’s not been in print yet. In Current Opinion Neurology. Showing this table of the various characteristics on your left. Characteristics of MS, versus aquaporin 4, which is NMO, versus MOG.
And I’ve tried to highlight some of the things that are differentiating by my red circle. So you can see if we move down to steroid dependent — MS is not steroid dependent. NMO is not that steroid dependent. But MOG can be. This can be a steroid dependent optic neuropathy. The blindness. This gets to the chances of good visual recovery. We know in MS it’s pretty good and in MOG, it’s pretty good, but in NMO, the chance of visual recovery is rather poor.
ADM, acute disseminated encephalomyelitis — so this is an acute onset of other problems, multiple enhancing plaques in the brain, you can see this with MOG. So in a kid, with ADM, MOG is something that must be considered. Diencephalic syndromes and NMO. Things like hiccuping, weird symptoms that you can get in NMO. Some of these others are neurologic things that I haven’t bothered to comment on.
Length and location of the enhancement, as I mentioned. NMO — both NMO and MOG tend to have long segments of enhancement of the nerve. NMO tends to be more posterior, MOG more anterior, but I don’t think that really will differentiate the two. And the perineural enhancement, the perineuritis I mentioned, enhancement of the nerve sheath, if you see that, you should be thinking MOG.
So that’s a good — I don’t think it’s in print yet. I pulled this about a few weeks ago. And then what about treatment? So here’s… This is actually right from that review paper that I just cited. NMO optic neuritis. So the good news is: This is treated like lots of different kinds of optic neuritis. 3 to 5 days of intravenous methylprednisolone, followed by — not like demyelinating disease — followed by a slower, longer prednisone taper.
If we go down our right side, if there’s rapid improvement, then great. If they have NMO, though, usually, they’re going to be treated with long-term immunosuppression. Even after one episode of NMO optic neuritis, because another episode — they may be blind. Or they may have some other systemic permanent disability. So this is a bad actor, we say. This is a bad condition. And these patients are gonna get treated.
If you have a definitive diagnosis, they’re gonna get treated with chronic immunotherapy. Eculizumab in the US is the only approved treatment by the FDA for NMO, although the other things mentioned here are used. And here’s the difference in treatment for other forms of optic neuritis. If there’s no rapid improvement within the first few days, if they’re done with intravenous steroids and still have terrible vision, we personally usually use plasma exchange, plasmapheresis. Some might use intravenous immunoglobulin. Very expensive. And they’re gonna get chronic immunotherapy. You can see no matter, good improvement, poor improvement, they’re gonna get this chronic immunotherapy. And of course, I’m not the one prescribing the chronic immunotherapy. These patients are always going to be referred for neurologic evaluation, and hopefully treated by a neurologist familiar with this condition. So that’s NMO optic neuritis. The next slide will be similar for MOG. And this shows MOG IgG optic neuritis. Again, the same initial treatment. 3 to 5 days, a gram a day methylprednisolone, slow oral prednisone taper. If severe, and no recovery after the first week or two, consider the same thing. Plasma exchange. Or intravenous immunoglobulin.
Unlike NMO, if it’s a single attack with good recovery, it may be reasonable to observe these patients. If it’s a single attack, full recovery, observation is reasonable. However, if there are recurrent attacks, steroid dependence, you try to taper, vision gets worse, you have to put them on more steroids, back and forth, if there’s incomplete recovery, then you’re gonna consider chronic immunotherapy, with some of the same types of medications that were just discussed. The Eculizumab has not been approved for this condition. So the take-home for NMO and MOG: If it’s recurrent optic neuritis, RON, NMO and MOG are common in the United States. About a third of patients are gonna have one or the other of these. In other countries, in other regions, it’s gonna be higher.
So in China, it’s much higher. NMO is more than half of the patients with optic neuritis. So this does depend on where you live. And so it would be helpful, depending on where you live, if you’re a neuro-ophthalmologist, to study this and find out: How common are these conditions? NMO, worse visual prognosis. MOG, more likely to recur. It’s crucial to differentiate these conditions from MS.
Because the treatment for MS, the long-term treatment, may actually be bad for patients with NMO and MOG. So hopefully you can obtain these antibodies. I know they’re not available everywhere. But I’ve recently been in a variety of countries where they are available. In some of the countries, they get results back faster than I do. So check NMO and MOG. Certainly if it’s recurrent optic neuritis. Depending on where you live, you may check it on every patient with optic neuritis. So in summary, for the webinar: Acute retinal ischemia is an emergency. You need to send them for emergent evaluation. They may be having a stroke as well. There’s no role for steroids in NAION. There is no proven treatment for NAION. In optic neuritis, you must check NMO and MOG. Certainly if optic neuritis is recurrent.
Depending on where you live, and how common these things are, maybe in every patient with optic neuritis. Okay. Let’s see now. I’m gonna open up my Q and A. And I will try to answer these questions in the order they were submitted. You can still submit questions if you wish. Okay. First question. How often do you CT scan optic nerve for optic neuritis? Only in diagnosis or follow-up too?
The answer is never, because I have easy access to an MRI, which is far superior. I shouldn’t say never. Obviously if my patient has a pacemaker or any metal in their body, anything that precludes — a contraindication, that is — for MRI, then I would have to get a CT. But in general, I’m gonna get an MRI. Can you please explain in what circumstance does Humphrey visual field SITA-standard need to be used compared to SITA-fast? I don’t care.
Either one. My routine is a Humphrey fast pack. We’re looking for patterns. Visual fields in neuro-ophthalmology are usually about recognition. I get a 20-42 fast pack. Sometimes SITA fast. I don’t usually get a SITA standard. Because they’re fast, and I want to torture the patient as little as possible, which also lets me get better results. Can you please explain again what to do in clinical practice to see the embolus?
Yeah. That was an unusual case. I show it because it’s kind of cool. But what we’re doing there is simply at the slit lamp, while you’re observing the fundus, you gently indent — you put a little digital pressure on their eye, back and forth. And when you do that, it causes the eye pressure to go up a little bit. It causes the blood to then reflux, and push that embolus and twist the embolus, and so you can see it. I mean, that’s a very rare case, I think. But I thought it was kind of cool to show. So it’s something that I will do in transient visual loss. Just a quick little pressure while I’m viewing the fundus to make sure I don’t see anything. How much do you value the OCT GCL? Well, that’s a big question. And I would say number one, I’m old. I’m an OCT dinosaur.
I don’t use OCTs a lot. I definitely have colleagues who use them for everything. All the time. Everyone gets an OCT. I just don’t find it helps me that much. So I’m probably not the right person to ask, honestly. But for me, it doesn’t help me much. Are there any routine recommendations for patients with no cup to disc… There isn’t. Because a fair percent of the people — a disc at risk is not just no cup.
Anywhere from a cup to disc of 0.0 to 0.2… Even 0.5 could be considered a disc at risk. So that’s a large part of the population. So it’s a lot of people. For a while, probably five or ten years ago, family practitioners were sending patients — because there had been a lot of press about Viagra, the PVE5 inhibitors, and they were sending all their patients that were about to start on Viagra for checks to see if they have the disc at risk.
I don’t think I would recommend that routinely. I don’t have any routine recommendations. What about addressing the underlying systemic conditions in AION. Definitely that needs to be done. When I said that there’s no proof that it’ll prevent it coming to the other eye, it’s because I don’t think there has been any proof. Clearly my main recommendation in somebody who I see with an NAION, and let’s say they’re a non-snorer, is: Please, if you haven’t had your vascular risk factors checked, meaning blood pressure, cholesterol, get them checked. I usually don’t have to do it myself, because the patient almost always has a family doc that they can go see, and usually they’ve seen the patient. But I have people who say… Oh, I’m healthy, but I haven’t seen a doctor in ten years. Clearly the first thing they need to do is get those vascular risk factors checked.
But there isn’t any data that I’m aware of that has proven that if you get those vascular risk factors under control it decreases your risk in the other eye. You prescribe aspirin in NAION patients? I talk to patients about aspirin. Of course, a lot of times, people are already on aspirin or something stronger. I think my philosophy… There’s not great data on aspirin. There have been a couple of studies that have looked at it.
One said it probably helps, the other said it doesn’t. And the question is: In this setting, will it decrease the risk in the fellow eye? There’s really not great data on that. That said, a lot of these patients have vascular risk factors. Blood pressure, cholesterol, diabetes. They’re older. It might help them to take an aspirin a day. There’s some debate about that. I tell them that if it were me, myself,
I probably would take a baby aspirin, 81 milligrams a day, unless I was having really frequent bruising or something like that. But I really don’t think there’s great evidence for it. I’m wondering how you differentiate PION from AION. Well, that’s a very simple question. The difference is that PION, posterior ischemic optic neuropathy, there is no disc swelling. In AION, there is. So by definition, there should be no problem differentiating these two conditions.
Because you can’t have AION without disc swelling and you can’t have PION with disc swelling. The hard pardon is PION, unlike NAION — it’s very common. If I see 100 people with NAION, I might see one person with PION. There’s a big difference in the differential diagnosis of PION and AION. AION, if I see 100 people with AION, probably 95 will have NAION. A few will have giant cell arteritis. And one or two might have blood loss or some other hypoperfusion problem.
PION is a totally different condition. Remember, NAION is a compartment syndrome. Because of the tight lamina cribrosa, the sclera. PION, idiopathic. You should never make that diagnosis. In other words, in a patient who has no history of blood loss, severe hypotension, on dialysis, with hypotension, giant cell arteritis, no history, none of those things, don’t make that diagnosis. It’s probably not. Idiopathic. PION. There’s no corollary to NAION.
If I see PION, I think about low blood pressure, low blood count. Are you on dialysis? Did your blood pressure bottom out? Giant cell arteritis? Those are the things I think about. How would you differentiate AION from demyelinating optic neuritis? It can be tough. Certainly if there’s demyelinating optic neuritis, 2/3 of the time there is no disc swelling, so then it’s easy.
One third of the time, there is disc swelling. In demyelinating optic neuritis, when there is disc swelling, it’s mild. There’s never hemorrhage. If there’s any hemorrhage, you could think about AION. Or you could think about atypical optic neuritis. If it’s a 23-year-old. I’m not gonna think about NAION. I’m gonna think about atypical optic neuritis. Demyelinating optic neuritis, the disc swelling must be mild, with no hemorrhage or exudate.
If it is anything else, it’s either atypical optic neuritis or NAION, possibly, in the right age range, or compression or something else. Could MOG neuritis be uniocular? For sure. Definitely. It’s common. In that study I showed you from Mayo Clinic, 63% it was unilateral. It’s more common to be unilateral. But compared to other optic neuritises, it’s way more common to be bilateral than those. But still the most common would be unilateral.
When would we send blood for aquaporin 4 and MOG? The answer depends a bit on where you live and how common these things are. In the United States, I don’t get NMO and MOG on every patient with their first episode of optic neuritis. If it’s not their first episode, I definitely do. Because the studies I showed you show that up to a third of patients will have one or the other in recurrent optic neuritis.
If the patient has poor recovery of vision, which is very unusual, for demyelinating or MOG, I’m definitely gonna get an NMO, because that commonly has poor recovery. So if there’s poor recovery, I check NMO. Of course, if there are other findings on MRI, if there’s a long segment of enhancement on the optic nerve, I’m gonna check NMO and MOG. If there is transverse myelitis, I’m gonna check NMO.
It’s kind of a tough question. In China, you’re gonna check NMO and MOG probably on every patient with optic neuritis, because more than half of the patients are gonna have one or the other of those things. So that’s why I say it depends a little bit on where you live. In countries where demyelinating disease is not common, these things are gonna be more common and you’re gonna find these things more often.
Are there NMO and MOG done on serum or CSF? There have been studies that show them positive in the serum and not in the CSF. So I usually get them on serum. How do you differentiate NMO versus MS clinically in a patient with the first episode? We sort of talked about that. It can be impossible. That’s why I don’t get MOG and NMO on everybody in my area of their first episode.
Because a lot of those people will be demyelinating. Whereas in a first episode in China, I will get them. Because common things are common. Depending on where you live. So again, if it’s the first episode, what am I looking for? I’m looking for long segments of enhancement. I’m looking for lack of improvement that you might see with the NMO. I’m looking also… I should reiterate the optic nerve sheath enhancement, which you can see in MOG.
That would help to differentiate. Those would be the main things. Had a patient with chronic kidney disease that developed NAION postdialysis. Can we avoid? Yeah, that’s the problem. If you see NAION or PION in a patient on dialysis, good chance it’s gonna be related to hypotension during dialysis. You’ve got to tell — because these patients are usually often very anemic.
So you’ve got this double — what we call a double whammy. You’ve got two factors. One, they already have a low blood count. They’re just not getting as much oxygen to their nerves for that reason. And then you lower their blood pressure during dialysis. So I tell the people doing dialysis: Listen, we’ve got to make sure that this blood pressure stays within a normal range, and I tell their hematologist do whatever you can do to keep their blood counts higher.
Those are the two main factors. In central retinal art occlusion, what is the most important intervention? I mean, they need the MRI to look for stroke and they need a vascular evaluation. In terms of intervention, there have been trials looking at intra-arterial and intravenous anticoagulation. These studies have not been shown to be of any significant benefit at this point.
What would you tell a young patient, less than 40 — thanks for defining that, since I’m much older than 40 — that’s okay. Patient with NAION and normal testing? Certainly I’m very hesitant to make a diagnosis of NAION in a patient less than 40. Now, it’s definitely been reported. But I’m not gonna be thinking NAION. I’m gonna be thinking optic neuritis. Or atypical optic neuritis.
So if there’s swelling, a lot of swelling with any hemorrhage, I’m gonna be thinking atypical optic neuritis. Now, if the patient is less than 40 and has juvenile diabetes, hypertension, obviously those are risk factors for NAION. But if it’s a healthy, less than 40-year-old person that you think has NAION, clearly I’m gonna be looking for vascular risk factors. So the usual. Blood pressure, cholesterol, diabetes. Sleep apnea.
It can be hard to differentiate NAION from optic neuritis in someone less than 40. Most of the time it’s not gonna be NAION. Especially if you say normal testing and you mean they have no vascular risk factors. Then I’m gonna be really hesitant and I’m gonna ask you: Why would you think it’s NAION? As opposed to some form of inflammation. Any role of intravitreal or anti-VEGF in NAION? No.
Are you recommending only contrast MRI or also no contrast? We usually get MRI — we say with and without contrast. What would you expect to see on DWI in the monocular visual loss case? So on diffusion weighted imaging, up to 30% of patients will actually have abnormalities, where on the DWI it looks like basically bright white enhancement. Enhancement is the wrong word. Bright white signal.
Where there’s restricted diffusion. Which means blood supply problem. In other words, either a stroke or what we call a silent stroke. Silent means they don’t have any systemic manifestations. So they actually have had a stroke and they need a regular stroke evaluation. Not just oh, you had a transient loss of vision. Don’t worry about it.
If there’s a patient with NAION, what should we give them besides check for… Well, there’s nothing to give them in the sense of treatment. Again, there is no treatment for NAION. But other than looking for the usual vascular risk factors, the sleep study for sleep apnea, if the patient snores. If there’s good proof that says they don’t even snore, they don’t have sleep apnea.
Do you recommend 30-2 or 24-2? Personally I do 24-2s. They’re faster than 30-2s. I don’t think I get any extra helpful information for any neuroophthalmologic condition. It’s just longer and torture for the patient. I need your email or somehow I can contact you. My email is simply my last name then my first name. So golnikkarl, with no punctuation, at And by the way, I should mention anybody can post a case to Cybersight. And if you post the case to Cybersight, and say it’s neuro-ophthalmology, I will probably be the one that reviews it. So either way. In NMO, when do you check NMO antibodies and MOG, before treatment? I’m not really sure about that question. If you know they have NMO, then you’ve probably already checked the NMO antibodies.
Yes, I guess… I think the answer to this question is: If you’re suspecting NMO, or if the person has optic neuritis, I’m gonna check them right away. I’m gonna start treatment. Because if I think they have optic neuritis, the good news is, whether it’s demyelinating optic neuritis or any form of optic neuritis, pretty much, it’s fine for the initial treatment to be 3 to 5 days of intravenous methylprednisolone. The problem is, at least for me,
I don’t get the results of the NMO or MOG in the first five days, which is when I would like the result. Because as you saw, on the treatment of optic neuritis, in either of these conditions, if there’s not fast recovery, you should consider plasmapheresis. So I would love to have the results fast. But the other thing to point out is if the patient has been treated with big bunches of steroids, that could potentially affect the NMO and MOG antibody results. Prescribe aspirin… I already answered that. Hopefully you heard that. The answer is I don’t usually prescribe it. I might discuss it. I said personally I might take a baby aspirin, 81 milligram aspirin per day, but there’s not really great evidence for that recommendation. How to differentiate between parainfectious and demyelinating other than history? Certainly if the parainfectious optic neuritis can cause hemorrhage at the disc, it can cause exudate, it can cause macular edema. None of those things should be seen in demyelinating optic neuritis. The problem is you don’t necessarily see those things in parainfectious. But if you do see… You’re thinking optic neuritis, and you look at the nerve, it’s very swollen, there’s hemorrhage, exudate, fluid in the macula, there’s a star of exudate, any of those things, parainfectious has to go way up on your list.
It’s not gonna be typical optic neuritis. If a patient complains of a few episodes of transient visual loss but everything seems fine on exam, what advise would you give in the case of a future episode? So if a patient says… I had a few episodes, and the most recent was in the last week, I send them to the emergency room. They need a stroke evaluation. If they say I had a few episodes over the last year, and the last one was a few months ago, I’ll say… Let me know if you have another episode and we’ll send you to the emergency room. Have you seen young asymptomatic athletes with extremely thin neuroretinal rims? I’m not sure about young asymptomatic athletes. I definitely see patients with thin neuroretinal rims who don’t have glaucoma, who just have big optic nerves and big optic disc cups with nerve fiber layers. I haven’t seen that, no. Do you order MOG IgG titer routinely? As I said, I don’t routinely order it in first episodes of optic neuritis. Second episode or more, definitely. Any of those things we talked about. Perineural enhancement of the sheath, long segment of the sheath. I would order it. If you live in an area where there’s a lot of MOG, but a lot of areas don’t know if that’s the case or not. You
Could you explain why differentiation between optic neuritis and NMO is important? There’s really no difference in the first five days, but if you think someone has demyelinating optic neuritis, it’s not steroid response — you treat them and 90%-plus improve. A short oral steroid taper, maybe a week or two, and that’s it. In the case of NMO, they’ll get a prolonged oral prednisone taper, and if they’re not improving rapidly, they’re gonna get plasmapheresis. Hi, Chinyere. There was no question there. Does your line of investigation differ according to ethnicity of patients? Um… I guess it depends. The answer is… Not a lot. In the United States. Again, of course this is a very open question. Because you’re not speaking specifically for any particular condition. Just trying to think of conditions where my line of investigation differs,
depending on ethnicity, and the answer is probably not. Certainly if I have an Asian with optic neuritis, I’m gonna be more likely to think about NMO than if they’re not Asian, I guess. That would probably be about all I would say. If an optic neuritis patient is highly suspicious to have NMO/MOG but negative blood tests… If there’s enhancement, it’s their second or more episode…I would consider repeating that. The blood test. Yes. Especially let’s say the blood was drawn as we talked about earlier, when they were being treated with any sort of immunosuppressive. I would consider then checking it off the immunosuppressives. What do you do in patients not improved after optic neuritis with no detected cause? I guess it depends on the timing.
If someone comes in and says… Well, I was told I had optic neuritis a year ago, and I never got better, they had imaging and all that, I’m not gonna do anything. If the patient is not improved after the first couple weeks, let’s say they got intravenous steroids, you sent their blood for NMO/MOG, they came back negative, they got their intravenous steroids, maybe a short course of oral prednisone, and they’re no better, I would consider retreating with intravenous steroids once, to see if that makes any difference. But remember, 7% of people with typical optic neuritis don’t get better. So not everybody gets better. How important is serum homocysteine level in NAAION? There have been a number of papers written about that. I think there’s some debate. I honestly don’t check it.
Let’s see. That’s not a question. What is the role of hyperbaric oxygen therapy? No proven role. Is there a protocol for diagnosis of toxic optic neuropathy due to anti-TB drugs? There is no, I would say, evidence base for that. The way that ethambutol works — it chelates metal ions. You need metal ions in enzymes, the electron transport chain. I usually do supplement them with copper and zinc.
In the US, we have something called OcuVite, vitamins that have a lot of copper and zinc. It is not proven. It is theoretical. Is MRI needed? I mean… I usually don’t get an MRI if it’s typical. The person comes in, they’ve been on ethambutol for a couple months or more, they have bilateral symmetric central loss of vision, sometimes it can look on field testing like bitemporal defects. Then of course I do get an MRI. If it looks bitemporal.
I’ve had people that really looked like they had bitemporal field defects that had normal MRIs. And it’s all the ethambutol. When is my next Congress in Europe? Oh, boy. Let’s see. Well, I’m gonna be in Romania. That’s gonna be more of a medical education sort of lecture. Not neuro-ophthalmology. I’m just trying to think of my next time in Europe, other than… I’m gonna be in Tunisa. That’s northern Africa. That doesn’t count.
Trying to think. Europe? I’m gonna be in Jakarta in a couple weeks if anybody wants to go to Indonesia. A big general ophthalmology meeting, but a few neuro-ophthalmology sessions. Europe? I don’t know. I would have to pull up my travel list. But I think the European Society of Ophthalmology meeting is not until 2021. I’ll be there. That’ll be in Prague, I believe.
Would you order MOG routinely? Kind of discussed that a few times already. I don’t think I’m gonna reiterate. Does that mean… Does that mean in your practice you treat every optic neuritis with IV methylprednisolone? Yes. Would the titer — that’s not a question there. Would titer of MOG correspond with severity or recurrence of the disease? I don’t know that that’s specifically been looked at, and I don’t care.
I guess… I mean, either it’s positive or not. At least at this point. So I don’t think it really helps. Let’s see. Not a question. Not a question. How do we differentiate diabetic… Oh, so that’s a tough one. I think for a while people weren’t sure there was a difference. I think there is a difference between diabetic papillopathy. It can be either unilateral or bilateral. It’s usually mild disc swelling.
Usually the visual loss is much less severe than the NAION, but you can see NAION with minimal loss of vision. I think to me the main thing that really differentiates it is the duration of disc swelling. So in my patients with NAION, I always tell them: Listen, in four to eight weeks, the swelling should be gone. In diabetic papillopathy, you can have disc swelling for months and months and months.
It’s been reported up to 18 months. Now… Who cares if there’s a difference? Well, I care, I guess. The problem is of course there’s no treatment for either one. What’s gonna happen is gonna happen. And so from a treatment standpoint, it doesn’t really make any difference. Because there is no treatment.
I guess in this day and age, you would have to think about the sleep apnea and all of that. But I think it’s important to diagnose sleep apnea no matter what, because it’s been associated with all sorts of other medical conditions. In NMO after treatment, when would you repeat MRI? Well, never. If there’s no symptoms. Now, if it’s NMO optic neuritis, well… If they have a positive NMO blood test, and they have just an episode of optic neuritis, I always send them to neurology for a systemic neurological evaluation. I mean, every patient. I’m not the one that’s gonna start these chronic immunosuppressives, and I’m not the one that’s gonna take care of these other systemic problems. So the neurologist usually will decide that.
Will you be in WOC? Definitely will be there and definitely will be in some… I’m not sure how many, but I’ll definitely be in some of the neuro-op sessions. Please say hello. I’ll be in Romania at the end of May. We’re having a two day meeting on improving teaching ability. Training of residents and so on. One question regarding immediate management of CRAO. What is the role of paracentesis and oral acetazolamide?
If it’s immediate management, both have a big role. You want to lower intraocular pressure for the reasons we’ve talked about. We want to try to dilate the retinal arterioles, and one of the factors is intraocular pressure. So if you lower the intraocular pressure by paracentesis, and oral acetazolamide, then theoretically, you might dilate that arteriole enough to allow the embolus to travel downstream, and damage less retina.
And finally, is there any role for Citicoline in NAION? There’s no proven role for it. It’s been studied, but I don’t believe it’s proven and I don’t use it personally. And I think that’s the end. That was 50 questions! And I mentioned earlier on that I would look at other questions. And I don’t know that we really have time. We’re already way over.
And I’m trying to do… There we go. End my slide show. I don’t know… I don’t really know how many people are still on here. Let me just quickly look at… For maybe 10 minutes, we can look at some of these other questions. Some of these have nothing to do. These were all questions that were submitted prior to knowing what was really in this webinar.
Let me just try to answer a couple of these things. Is it possible to diagnose IAH with disc swelling? I’m not sure what that question means. Usually you have optic disc swelling. Usually you can have IAH without optic disc swelling. Papilledema is not part of the diagnostic criteria for IAH. The criteria are elevated intracranial pressure on spinal tap and no cause present on MRI or CT imaging.
What line of treatment for head or facial trauma? There are no good studies looking at this. I usually do if there are no contraindications use steroids, either intravenous or oral, but there’s no education… Excuse me. No evidence base for me to give you an answer to that question. Double vision and lateral rectus palsy. Yes. Not sure what the question is.
Indications… If someone needs prism glasses? I’m not sure about the question. What is the protocol for optic neuritis. We discussed that in the webinar. Approach to management of common cranial palsies… So this is somewhat controversial. I would say this: In third — excuse me, fourth and sixth nerve palsies that I think are microvascular, that take some experience, I usually don’t image them. If they are isolated fourth or isolated sixth nerve palsy, over 50.
Age less than 50, they get imaged. If it’s a third nerve palsy, my teaching is image all third nerve palsies, MRI, MRA, CTA, look at the blood vessels, rule out aneurysm. Papilledema management? That’s a long question. I won’t go into that now. You can get the answer to that from previous webinars. I told you about my opinion of the NAION treatment. I don’t do surgery on infants. Answered that, answered that.
Management of carotid cavernous fistula — favorite topic of mine. It depends on many different factors, whether it’s direct or indirect fistula. Direct fistulas generally are gonna be treated intravascularly. By intervention of a radiologist. Indirect or low flow fistulas, you can observe them with no treatment at all, and 50% spontaneously resolve, to all sorts of other treatments. That’s a long topic.
First episode of suspected… I think that should say neuritis need MRI, yes. Ocular myasthenia, that’s not a question. How often is it related to bilateral optic neuritis? Virtually never. I’m not sure I’ve ever had a patient come in with bilateral optic neuritis that was MS in 30 years. Talked about NMS-OSD, young male patient with sudden bilateral vision loss with optic disc swelling.
That’s a fairly big differential. But I would think about toxic things. Methanol poisoning. Atypical optic neuritis. You can think about increased intracranial pressure and papilledema, even though they don’t usually have severe visual loss suddenly. Those would be things I would think about off the bat. Some light on ophthalmoplegic migraine.
It happens. The general rule is that you don’t want to make that diagnosis in an adult without history of the same when they were a child. Interestingly, lots of people with ophthalmoplegic migraine who are now getting imaged with MRI contrast have enhancement and enlargement of the third nerve. It’s common. It’s not a tumor. Don’t try to remove it.
This has to do with traumatic optic neuropathy and steroids. We don’t use super megadoses of steroids in traumatic optic neuropathy. I sometimes use a gram of solumedrol, that is, methylprednisolone a day, for a few days, if there are no contraindications. One contraindication would be of course other injuries, the patient is on a respirator and they’re at risk for infection.
Causes of NAION post dialysis, typically combination of anemia and low blood pressure. Some patients also go to optic atrophy, I don’t know what that means. Wolfram syndrome and glaucoma. Diabetes insipidus, diabetes mellitus… Optic atrophy and deafness. I don’t know. That’s a rare condition. I have a few patients with it. They don’t have glaucoma. The problem is: What if they have an optic nerve problem? And they have glaucoma?
There is nothing you can do for Wolfram syndrome. I would manage their glaucoma. Typically Wolfram is gonna give you central vision loss primarily, so I would look at progressive cupping, progressive loss of vision, and lower the pressure. What are the most frequent diagnostic challenges? That’s a huge topic. Diplopia, acquired nystagmus, management… There’s a webinar on that already that I did last year, that’s recorded on Cybersight.
Have you already seen in your practice pediatric optic neuritis with anti-HPV vaccination? I have not. I would not be surprised. But I don’t see a lot of kids. Apart from cranial MRI, what other investigations should be done for children with optic neuritis? Depending on where you live, NMO and MOG can be done. How do you treat it in immunocompromised patients? Same as in immunocompetent patients.
Idiopathic intracranial hypertension in a 23-year-old woman with irregular menstrual cycle? I don’t think the irregular menstrual cycle has anything to do with it. But that’s a big question. Blood pressure and AION. High blood pressure is a risk factor. Low blood pressure can precipitate the event. I’m done with that. So thanks, everybody, for attending this long webinar and question and answer. If there are ideas for other neuro-ophthalmology topics that I haven’t
already done, where the webinar is recorded, please let us know, and with that, I am going to stop sharing my screen. I wish everyone a good day or night. And thanks for attending this Orbis webinar.
DR GOLNIK: The question is… Is there any role of brimonidine? So there was a study that started looking at brimonidine and NAION, and the problem was no one ever saw enough patients acutely enough to start the brimonidine, and so although there’s theoretical reasons that brimonidine might help, I do not use brimonidine in NAION. So clearly there’s no evidence base. There’s no data that supports using it.
no data that says it doesn’t work either. But that goes for lots and lots of treatments. So I don’t use it.
And I think with that, I will say so long.

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