Lecture: Dysthyroid Optic Neuropathy, Management of 3rd Nerve Palsy & Neurovascular Imaging

At the completion of the lecture the participant should be able to: describe new vascular neuroimaging techniques, describe the approach to Thyroid Optic Neuropathy, and describe the management of isolated 3rd nerve palsy in adults.

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


Karl Golnik: All right, well greetings. And welcome to another Orbis Webinar, another Neuro-ophthalmology Webinar. Well, this is Dr. Karl Golnik, coming to you from my home in Cincinnati, Ohio, United States. It’s about 10:00 am, my time here. Welcome and there is a Q&A box that you probably all will see either at the top or bottom of your screen. Please feel free to write questions in there as we go through the course of the webinar. I am going to wait till the end of the webinar to answer the question. So, if you have questions don’t, maybe don’t write them right now because I may answer them during the webinar. But feel free to start writing questions.

And we’re going to talk about three different topics today, so, dysthyroid optic neuropathy, 3rd nerve palsy, and neuro-vascular imaging. So, sort of a potpourri of topics but I think it’s more interesting to cover a few topics than one long and boring topic. So, we’re going to start with my objectives when we’re done. I’m hoping that you will be able to describe the approach to thyroid optic neuropathy. You’ll be able to describe the management of isolated 3rd nerve palsy in adults that were specifically going to look at. And then you’ll be able to describe some new neuro-vascular imaging techniques that are fairly new, and I mean in the last couple few year kind of ballpark.

I have no financial conflicts with anything that we’re about to discuss. So, here’s a patient, we’ll start with she, the question I write here. Does she have a dysthyroid optic neuropathy? This is a 48-year-old woman who has swelling around both eyes, very obviously, she has blurry vision for the last couple of months. She was recently also diagnosed as being hyper thyroid. She is 20/20 however on exam, her visual fields are full to confrontation. And she is limited motility in all directions. Her fundus appearance is normal. And so I’m going to skip ahead to the next slide. So, the question is and this is an audience response question. I’m just trying to get a feel for what people think. Does this patient have dysthyroid optic neuropathy? Yes, no, or I need more information.

So, we will let you vote. You can click on the box that you believe is the correct answer. And then we will discuss your responses. And we’re going to give you, I don’t know 20 seconds or something like that. I can’t really see, oh there we go, I can see some of the responses coming in now. Oh, is this, I think the post I’m already sharing the poll results. So, it looks like the voting is done, sorry. So about two-thirds of people would like some more information, about a quarter think yes, and about 10% or so say no. And so we’re going to answer that question in the course of the next few slides. But I think the brief answer is three. We need more information. We don’t have enough yet to determine whether there is a thyroid optic neuropathy. Clearly she has thyroid, active thyroid eye disease but we don’t know enough yet to know if she has optic nerve dysfunction.

And so this is information and data from a paper published a couple of years ago. About 5% to 8% depending on what you read, a thyroid eye patients develop this thyroid optic neuropathy. They typically are male and older. But certainly you can be young, a young female and have on optic neuropathy. But the statistics show that is more likely if you’re male and older to develop this. So when I see a patient with the new onset of thyroid eye disease I usually talk about the spectrum of eye disease with optic neuropathy being sort of the most severe stage. And I tell them, you know, at most maybe one in 20 or so people will develop thyroid optic neuropathy if you look at all comers with thyroid eye disease.

Interestingly and I think importantly half to 70%, so at least half the patients have pretty good central visual acuity. So, 20/20 to 20/40, 6/6 to 6/12, so you can still have an optic neuropathy and not still at least half the people can have an optic neuropathy but have pretty good central visual acuity. So, the fact that the visual acuity is good does not mean the nerves working okay. And about 70%, it’s bilateral but of course it can be unilateral and my residents sometimes ask me, wait a minute, this is a systemic disease. Why would someone have a unilateral problem? And the answer, it happens. I get the same sort of questions about myasthenia. Why would myasthenia be unilateral, when it’s a systemic disease? I don’t know but it can be.

And then the fundoscopy only helps you of course if it’s abnormal. But at most 50% of patients will have abnormal fundoscopy. So, clearly you can have a normal fundus, a normal optic nerve and still have a compressive thyroid optic neuropathy. You can see of course in both of these fundus photos, there’re significant swelling of the- in this case the right nerve, there’s a little hemorrhage right here off the top of the disk. And the other eye you can see again moderate swelling of the nerve. You can also I think better appreciate in this fundus photo, these linear ridges or lines these are radial chorioretinal fold. So there’s something pushing on the back of the eye. In this case, in thyroid eye disease big extractor muscles can cause these radial retinal choroidal folds. So don’t forget to look for them.

Another way to look for this is using your red-free, so your direct ophthalmoscopes with the green filter. Sometimes these will pop out better. I’ve got some examples. I don’t think I’m showing here. So, keep in mind these characteristics when we talk about what do we need to know whether there is a dysthyroid optic neuropathy or DON. So, of course whenever we talk about optic nerve disease, we’re interested in whether there’s a relative afferent pupillary defect. But remember we just said that about 70% of people it’s bilateral and certainly in some percentage of those, it can be symmetric. And of course, if you have a symmetric optic neuropathy there will be no relative afferent pupillary defect.

So, although obviously, it’s very helpful if an RAPD is present that means that there’s got to be optic nerve dysfunction or some big retinal problem. But you can rule that out pretty quickly by looking at the retina. There’s got to be optic nerve problem if there is a relative afferent pupillary defect. But the lack of a relative afferent pupillary defect does not mean you’re good and the patient doesn’t have a problem with their nerves. If it’s symmetric, there will be no relative afferent pupillary defect and thyroid eye disease tends to be symmetric.

Color vision can be very helpful, usually people with any sort of optic nerve problem that affect central vision. Remember that’s key affect central vision, usually their color vision will be down, almost all ways. So, color vision testing can be very helpful. And you may have someone with very good vision 6/6 or 20/20 who may not see the color plates very well and that’s a hint that there is something going on with the nerve. But remember like the APD, if the color vision is normal and the visual acuity is normal, you could still have an optic neuropathy if there’s peripheral loss of vision. Okay, so color vision is helpful but if it’s normal that doesn’t mean again, there’s no optic nerve problem.

Ocular motility, it’s usually going to be very abnormal in thyroid optic neuropathy. So that I can’t even, I’m not sure I’ve ever seen a patient who had normal ocular motility, normal ocular motility in thyroid optic neuropathy. Because, why do you get the thyroid optic neurotic, you get big extra ocular muscles that usually are compressing. The orbital apex will show some examples in a moment. And so usually you’re clearly- you’re going to see significant ophthalmoplegia to developing dysthyroid optic neuropathy.

In visual fields, I said in the patient prior that the visual fields were normal to confrontation. But confrontational visual fields are a very gross testing mechanism. So here’s the most common type of field defect that’s reported with thyroid eye disease. It’s inferior field loss, I don’t know why but it is. That most of the patients I see have either constriction of the field centralize but most common pattern I see is inferior field loss, why? I don’t know why, it’s just more common inferior that you could imagine that in this patient’s visual field centrally they look pretty good. So, their central acuity is good. Their color vision is good. But they definitely have optic nerve dysfunction as evidenced by the visual field test.

And of course, CT and/or MRI, I think CT scan is perfectly fine for thyroid orbitopathy. If you’re sure someone has a thyroid eye disease, it’s cheaper, it’s usually faster to get a CT. You can even get a non-contrast CT pretty quickly, easier for everybody, cheaper and so on. So, typically I will order a CT in the setting of what looks to be known thyroid eye disease. And you can see of course in this sort of mid orbital cut, the enlarged muscles and again for reasons we don’t know or at least I don’t know, it’s inferior rectus most common than medial rectus than superior and then lateral. So, it’s just that’s the way you expect the muscles to be enlarged. You’d be very suspicious, if you saw just a big lateral rectus muscle, you want to think about other diagnostic entities.

And you can imagine that back in the orbital apex and I don’t think I’ve got that picture yet. In the orbital apex if those muscles are all big then that optic nerve is going to get squished because there’s bone 360 degrees in the back, in the around the orbit and around the nerve. So, these are the things that you want to think about when you’re really looking for dysthyroid optic neuropathy. Is there an APD? Is the color vision normal? How about the motility? You’re probably not going to see a dysthyroid optic neuropathy with good eye movements. Are the visual fields, automated visual fields normal or not? And then does a CT or an MRI show compression of the optic nerve in the orbital apex.

I showed this not for you to quickly write this down although you certainly can if you want. I thought it was kind of, I’m not sure what the right word is funny. This is a publication from just a couple of years ago where they looked at these at a way to predict whether there’ll be a dysthyroid optic neuropathy. They came up with this formula which interestingly you can see contains the things sort of we just talked about that. Is there a relative afferent pupillary defect? What about motility? What about the mean deviation (MD) on the automated visual fields? And then what about color vision. So here’s the way they fill in this formula. Is there an APD, yes or no? The combined limitation abductions, the mean deviation of the field and then the percent of color plates correctly identified.

And they said, basically if you plug all that information into this handy formula. If y is less than zero, it’s not dysthyroid optic neuropathy. If it’s greater than zero it is. So, I do not use this formula. I show it just because what it points out to you is what I tried to just point out in the previous slide. What’s important when we look at whether or not there’s a dysthyroid optic neuropathy, APD, motility, visual fields mean deviation and color vision. Those are the important things. Have I ever used this formula? No. Will I ever use it? No.

All right. So, let’s go back to this patient and the question now, I’m going to ask the same exact question for those who answered it, you have another chance. So, now the question is, we know I’ve given you a little bit of extra information and that is, that there is no APD. The acuity is normal. The fields are full to confrontation. But the automated perimetry is abnormal inferiorly in both eyes. And the motility is significantly limited in all directions. But the fundus is normal. So, now what do you think? Is there, does this patient have dysthyroid optic neuropathy, yes/no? Or do you still need more information other than the extra information which is the fields are abnormal, symmetrically inferiorly and there’s significant Ophthalmoplegia.

And all right, so very good. So, now that we’ve reversed things a little bit here. So, 68% are now saying yes there is. And so and the answer is yes, there is. They, the patient is abnormal automated perimetry in both eyes inferiorly, it’s relatively symmetric. So there’s no relative afferent pupillary defect and it doesn’t involve central vision which we know is common in dysthyroid optic neuropathy. But the combination of the abnormal visual fields that’s enough for me to say, okay she has a bilateral symmetric optic neuropathy. Now certainly, I would expect her imaging which I don’t talk about to show orbital, crowding in the orbital apex from enlarged extra ocular muscles.

Okay, I’m going to move on. And so that’s of course what we’ve been talking about. And here’s a good a nice axial CT scan and you can see here the medial and lateral recti. And you can easily understand how this optic nerve loses because you’ve got bone here, bone here, bone 360 degrees. But you’ve got too much tissue in the back of the orbital apex on both sides harder to see over here. But this person indeed has the kind of CT scan. I would expect to see with orbital apical compression in thyroid eye disease.

Now, I think written and we think that this – the path of physiology is compression of the nerve or the blood supply in the orbital apex in almost all the patients. But I have seen a rare patient who has no orbital apical compression but has, as you can see this nerve is just stretched out. So, if there’s a lot of fat in the orbit which there is here and this orbit is tight, they’ve got big muscles. I think there is such a thing as a stretch optic neuropathy, I think it’s pretty rare but I think I’ve seen a few times in 30 years, so rare. Usually, it’s compression of the nerve in the orbital apex.

So, how would you treat this patient? This is another audience response questions. The same patient we just talked about, she’s got a bilateral optic neuropathy, how you treat her with observation and we can go ahead and ask the audience this one if we’ve got the, yeah. So, would it be observation, oral corticosteroids, intravenous pulse corticosteroids, orbital decompression or radiation. And well, of course, we’ll be talking about the various forms of treatment after I just, I’m curious to see what people say about the answers to this question. We’re getting some votes. I’m assuming, I can’t see the votes as they’re tallied here. But let’s see what the audience says.

Okay, so we have a pop up variety. So, about half the people say intravenous pulse corticosteroids. About a third say oral corticosteroids and then, small percentage decompression, very small percent observation and radiation. So, all right let’s see what we’re going to do. I’m not going to tell you what I would do yet. But, so here’s what, at least what EUGOGO (the European Group On Graves Orbitopathy) would recommend as first line treatment for dysthyroid optic neuropathy, not just thyroid eye disease, you know, they have optic nerve compression at this point. And they recommend pulse IV methylprednisolone, you can see the dose 500 to a 1000 mg a day. Sorry that’s supposed to stay for three days. It doesn’t, there should be a three there, that’s a typo I missed. And then if there’s improvement after that shorter period of time, weekly pulses of IV methylprednisolone for at least the next six weeks, once a week for six weeks.

However, if there’s not fairly rapid improvement then orbital decompression, so if there’s no or very poor response in the first couple of weeks, go for orbital decompression. So, this is a sort of a consensus statement from four years ago now from 2016. And this consensus statement is based on a bunch of previous publications. Of course, most of these are all retrospective, you can see, one was a randomized controlled trial but there are only 15 patients in it. But most were all, almost all retrospective data and these are all the treatment trials for dysthyroid optic neuropathy that they used to help form this consensus.

What about since 2016, so they’ve been a couple of I think interesting studies although they’ve been retrospective. This one was interesting. In 85 patients they all received the EUGOGO recommendation, which was the 500 to 1000 mg per day for three days followed by the oral steroid, oral steroid taper. And then they repeated it, if it was no better. So, they got the three days no better, they repeated again three days. And then if no better, orbital decompression with an oral steroid taper, and the results I thought were fairly impressive. Sixty of the 85 whatever percent that works out, you know, more than two-thirds improved and did not go on to meet decompression surgery. I thought that was that was to me, it was pretty impressive. My feeling about steroids had been that they certainly can help. But, you know, once you get rid of the steroids the problem usually comes back. So, I was impressed.

So, about two-thirds didn’t require surgery. Of the 25 who did need surgery, 24 of the 25 improved. So, saying that the risk of waiting a couple of weeks was relatively small and they follow these people for about a year and a half. So, there seemed to be a lasting effect of the pulse steroids. And of course about a third did need surgery. And then this paper which is from 2018 as well also a retrospective paper looking radiation and steroids. Now, the key things here, remember these patients, they had a 104 patients with a 163 orbits. These were all patients that were cortical steroid responsive. These were not just patients with any old this thyroid optic neuropathy.

To get in this study where they were going to give radiation, you had to show that you were responsive to steroids. But the steroids did not hold you. So, in those patients they gave 2000 cGy in 10 fractions of 200 cGy per fraction and steroids, 98 out of 104. I mean almost everybody did not go on to require surgery. And so, this is further evidence that radiation for optic neuropathy in the setting of thyroid may be very helpful. It’s not we think that helpful for mild to moderate thyroid eye disease but rate in optic neuropathy perhaps helpful.

So, in summary for dysthyroid optic neuropathy, we look for these things, RAPD, color vision, fields, discs appearance, CT/MRI. We look for these to try to help us diagnose whether or not there’s an optic neuropathy. Keeping in mind that visual acuity and confrontation fields are not enough, we need visual automated perimetry at least and of course hopefully checking for color vision and the other things we mentioned. We then start, if there is, the first line treatment in my feeling is the intravenous pulse steroids. There is debate exist in regarding the best treatment at this point and we certainly need a randomized controlled trial to try to figure out what is the absolute best. But really all we have now are the retrospective type studies that I’ve described.

I just want to say one more word about thyroid eye disease in general. Now, this is not specific to thyroid optic neuropathy in any way. In fact, you wouldn’t use this as a first line treatment. But you might use this to prevent thyroid optic neuropathy, and that is this new medicine that was approved in the United States just back at the end of January 2020. Tepazza, it’s called teprotumumab. And as I say, approved in January in the US. It’s an insulin-like growth factor -1 inhibitor and it’s infusions. So, there’s initial infusion. And then there are seven additional infusions over the next 21 weeks – or well 24 weeks I guess total. So, there’s one infusion then three weeks later the seven start.

Now, I’m going to show you some data as to how effective this is. One of the problems with this medicine is at least in the United States, it’s $15,000 per vial and you probably unless you’re very, very light in terms of body weight, you’re going to need two vials per treatment. So, do the math, that’s $30,000 a treatment, except for the initial treatment. So, it’s expensive.

This is just some of the adverse reactions that report in the New England Journal of Medicine, not really anything to terrible I don’t think as compared to placebo certainly some of the things are a little more common. But this is the data that led to fairly rapid FDA approval. This is proptosis response, so the placebo groups the teprotumumab. This is the change in proptosis in millimeters. You could see huge differences in these curves. Clinical activity scores improved intepro with the drug overall response, double vision response even. And change from baseline quality of living scores much better for teprotumumab.

And they showed some pictures like this from the article which just showed impressive improvement. So, this is baseline and then after the 24 weeks of treatment I mean almost back to normal, remarkable I think. So, this is out there at least in the US, it’s approved. It’s very expensive. We are having some trouble getting it approved by insurance companies. But I’ve had a few patients who are in the midst of this treatment right now.

Okay, that’s what I have to say about that. We didn’t really talk about just run of the middle thyroid eye disease that much. I think the teprotumumab is definitely could be a major game-changer. It may mean a lot less optic neuropathy. It may be a lot less double vision and strabismus surgery, we’ll see.

So, I’m going to move on to the next topic which is management of acute isolated 3rd nerve palsy in adult. And I want to make sure that we understand here acute, so certainly not been going on for six months. Acute isolated in adults, I’m not talking about kids, not talking about chronic 3rd nerve palsy, I’m not talking about 3rd nerve palsy with other findings and we’ll talk about some of those things.

So, here’s a patient and let me just turn that sound off. And you could see this is an older gentleman in his late 70s. You can see that he has significant ptosis. He has a right 3rd nerve palsy with almost no elevation depression or reduction of the eye. You can see that his pupils are about the same size and very small. They both react okay. And his history, both the histories of these patients, sorry that his eyelids drooped over two days in each patient. There’s a mild ache around the right eye. I’m sorry, there’s a mild ache around the right eye in this patient. There’s a mild ache around the left eye in the patient below. So, I think I’m going to show you the next video. This should be mild ache around the left eye, there’re no symptoms of giant cell arteritis (GCA) in either patient.

The patient below is in his 50s. The patient above is in his 70s. Otherwise, it’s the fairly acute onset and you can see the eye movements and the patient below. The only difference is the patient below has some ache around the left eye. And you can see the pupils, it’s tough to see. But the patient below left pupils bigger than the right pupil. So the question for the audience is, is the management of these patients the same? Yes or no. Is the management the same? Meet management meaning, what’re you going to do? All right, let’s see what the audience say. So, the majority certainly say no. And then the minority say yes. So good, all right well let’s see we’re going to talk about management of 3rd nerve palsy here. That’s what this is about we’ll decide.

So, 3rd nerve palsy: incidence & etiology in one population-based studies in the United States anyway, there were 4.2 patients out of a 100,000 when you look at population base. And of course, well maybe not of course but not surprisingly 3rd nerve palsy were more common if you’re over 60 years of age then if you’re under 60 years of age. In this study of 145 cases presumed that microvascular were almost half about 10% had tumors, 10% were surgical, 6% were aneurysms.

Interestingly of the aneurysms, five of the eight where aneurysms of the cavernous sinus, which are a little bit different than posterior communicating artery aneurysms because cavernous sinus aneurysms don’t kill you, if they rupture you have a cavernous sinus fistula. And then there’s some less common things like giant cell arteritis, stroke, et cetera, et cetera that I listed at the bottom here, so certainly a wide variety of things.

But presumed microvascular by far the most common of these all of these various etiology. And remember when I say acute and that’s what this talk is about, I mean less than one month they come in and say, yeah I’ve had double vision for less than a month. And isolated which means no other neurologic symptoms or signs pains okay that people can have pain or discomfort with a microvascular 3rd or with aneurysm or other causes but no other sign. So, this assumes one has looked for the other signs and sometimes the signs are more subtle than others. So, let’s look and this will be a question for you, not yet though.

Let’s watch this video. And the question is does this fellow have an isolated 3rd nerve palsy. So, we’re looking first, that is right eye movements. I always tell my residents, don’t forget the eye that looks okay. Look at the other eye, make sure the eye movements look normal. So here’s the person looking up down, left and right. You can see that clearly there’s a significant left 3rd nerve palsy. The question is, is this isolated? Is there anything else going on when you look at this video? So, what do you think, yes this is an isolated left 3rd, or no, this is not an isolated? I’m not sure we gave you enough time to see. But you know that poll is covering his left, his left eye. But let’s see, we’ll look at it. We’re going to look at the answer in a moment, so ahead.

Okay, so about half, well not half 60/40. Okay, so let’s remove the pull. Let me just, so the answer is look at his left eye when he looks tries to look from up to down. We’ll wait for the video here, or maybe I’ll hurry the video along. So, when he looks from up to down, look at these blood vessels. They don’t move. Watch it, we’ll show it again in a moment at the end of the video. Up, down, there is no intorsion when he looks from up to down. If the 4th nerve is working, you will see an intorsion movement of that eye. And you’ll see those conjugal title blood vessels in toward. They’ll move downward but you don’t see that.

So, in the setting of a complete 3rd nerve palsy, the only way you can really look for 4th nerve function is so have the patient try to look up and then down and look for intorsion of those blood vessels immediately there and easily. So, this is not isolated. So this would not fit in our category of acute isolated 3rd nerve. This person had a metastases to cavernous sinus. And hold on, let me get rid of the – now this fellow of course was complaining of double vision. And that was all he was complaining of, well of course then his lid shut.

But when I was checking him and holding his lids open like this. He said, you know, it’s funny I can’t, your thumb on my right eyelid feels different. It’s kind of numb. And I said, oh you can’t feel that very well. Now, it’s up that side of my forehead. So, the question is, is this an isolated 3rd nerve palsy? So then, he’s got a big pupil, you can see that. And it doesn’t work well. He’s got a complete looks like a pretty complete third. Let me see if I can, I don’t know if I haven’t look up and down, watch those vessels, yes there’s intorsion. Let’s just, so here’s an example of the 4th nerve working. Let’s just go to the end and when he looks from up to down, right, hold on, right now watch those blood vessels there they go in toward.

Okay, so let’s ask the question. Is this isolated? Okay, voting is, this one should theoretically be easy. Oh okay, well we can close the poll. So, what I, when I told you that he said, hey I can’t feel your finger on my eyelid very well, he’s telling you this is not an isolated 3rd nerve palsy. Your 3rd nerve does not innovate sensory, the skin on your forehead right, or your lid, your 5th nerve does. So, this person has a decreased sensation in the right V1. This is not an isolated 3rd nerve palsy. This is a right third and V1 division. This is someone who had squamous cell cancer that was removed about five years prior. They thought successfully and that squamous cell cancer crawl back down the 5th nerve and got the 3rd nerve in the cavernous sinus. This is not isolated. This is not the people that we’re talking about in this talk.

So, like I said if we’re talking about the differential diagnosis of an acute isolated third, you want to make sure you check the other cranial nerves. If the 4th nerve or the fifth or the sixth are not working, it’s not an isolated 3rd nerve palsy and the recommendation is different. Okay, so what about the management. Well, lots of different things could be potentially relevant and all of these things have been discussed in just at every big meeting, neuro-meeting, you’re going to go to, there’s going to be something probably on 3rd nerve palsy because the aneurysms can kill you. So, there’s the age, well, if you’re greater than 50 or less than 50, is that relevant? Well, it’s relevant because certainly it would be very unlikely to have a microvascular 3rd, if you’re less than 50. So, it’s relevant sure.

Can you have an aneurysm and be greater than 50? Sure. Pain, yes or no. Well that helps me almost not at all because the vast majority of third diabetic, 3rd nerve palsy, I see there’s pain. It’s ipsilateral I see pain with microvascular 3rd and 4th and 6th. It’s usually not terrible. Certainly, if the person’s got severe pain they’re going to get image but the presence of pain does not help me at all. Giant cell arteritis symptoms, well in the US at least depending on where you live in the world, we have a, you know, enough giant cell arteritis that we’re going to at least ask the patient if they’re over 50. We’re going to ask them about giant cell arteritis symptoms. That does not mean I’m going to get a sedimentation rate, C-reactive protein in the CBC and every patient with 3rd nerve palsy.

But if they have any symptoms of giant cell, I’m going to get those blood tests. I will document in my chart. I thought about giant cell arteritis, they have none of the other symptoms I’m not pursuing that. What about their past medical history? Well, certainly if there’s a history of cancer there’s a saying that I frequently use which is, if there is a history of cancer, it’s the cancer until you’ve proven otherwise. So, they have a history of cancer, I got to rule out cancer. Do they have vascular risk factors? Diabetes, high blood pressure, hypercholesterolemia, remember you don’t have to have diabetes to have a microvascular 3rd nerve palsy or 4th nerve or 6th nerve. You don’t have to have diabetes.

Is it complete? Well, is the 3rd nerve complete, so is the eyelid shut, is there no elevation depression or abduction as I showed in several cases or is it partial, like, I showed in the very beginning in the fellow with the lower of the two videos who had a mild 3rd nerve palsy? Is this the initial evaluation? When in the course of this 3rd nerve palsy are we seeing the patient? Is it they want? Is it because certainly a microvascular 3rd nerve palsy, if you see it the day after it starts and it’s partial it can definitely get complete over the next week. And I warn people, listen this could definitely get worse. Your lid could shut over the next one or two weeks. But if I see them three weeks out and it’s partial it’s probably not going to get worse if it’s microvascular, so if it does then I’m more worried.

Is there pupil involvement? So, we talk a lot, you hear a lot about. Is their pupil sparing? Well, if you have a complete 3rd nerve palsy and the pupil looks perfectly fine then you can say, there is pupil sparing. But what if it’s partial? Maybe the aneurysm isn’t quite pushing on that pupil yet but it’s, are the pupil fibers, is it pushing on the other fibers? My point here is that there’s a lot of things that go in to your decision-making process at least in the past. But I’m going to make it very simple for you. But all of those things are potentially relevant, so I don’t think there’s much controversy about age less than 50. The patients less than 50 you’re almost always going to image. I don’t think that’s controversial.

What about if there’s patient greater than 50 and they have diabetes and high blood pressure, is that controversial? Well, there’ve been a number of studies that have looked at that. So, here’s one from all 15/16 years ago, age greater than 50 acute isolated 3rd nerve palsy, this patient reported 29 patients, eight had complete 3rd nerve palsy with pupil sparing, all of these were microvascular. So that’s kind of reassuring. In this paper, they looked at 14 patients and this is from 2011, 14 patients with 3rd nerve palsy complete with pupil sparing, all were microvascular. And this patient, this paper was a little bit different, so they had 22, 3rd nerve palsy, four were complete with pupil sparing and one of them complete with pupil sparing. There was pituitary apoplexy which is a potentially deadly condition, if it’s not diagnosed. Their conclusion was, hey maybe we should image everybody with 3rd nerve palsy.

And, what about the imaging, well, this paper the first one I’m quoting here says that you’re certainly going to want to get some sort of blood vessel imaging, right? I mean that’s what we’re worried about. We’re worried about the aneurysm, that’s what’s probably going to kill you fastest, if you have one that’s not diagnosed. So, when you order imaging clearly you want A, MRA and MRI is not enough. A CT scan is not enough, so either one, an MRI, MRA or CT, CTA. So, when I say slightly less sensitive I’m referring to as compared to a CTA. I think this depends probably at least a bit or maybe a lot on where you are and what your institution has. Some institutes have great CTA, some have great MRA, some have both. So, it may depend on availability.

I think I would talk to the neuroradiologist hopefully that you have in your department or your institution and find out what do they think is their best way to detect small aneurysms or big aneurysms. The second paper I’m quoting here is basically they said, gee you know, it matters way more that you have a neuroradiologist on whether you can do CTA or an MRA because the neuroradiologist is needed. And I know there are a lot of places in the world that don’t have neuroradiologists and barely have radiologist. So that’s an issue. But clearly, you want to have a good neuroradiologist if you can.

And then another issue that comes up is what if the CTA or an MRA is normal but you have a really high suspicion. It’s a young person with no vascular risk factors with a partial pupil involving 3rd nerve palsy, you’ve done your CTA or you’ve done your MRA, and the basic thinking is then get cerebral angiogram to look for the small aneurysm that might be missed on an MRA or a CTA. Now, if you ask me, okay, when’s the last time I had to order an angiogram because we missed a small aneurysm on CTA or MRA? I can’t remember. It’s been more than a decade because we usually find them.

Nevertheless, the treatment- the recommendation is if you’re really concerned or let’s say you don’t have, you’re not real confident in your CTA, MRA or neuroradiologist then a cerebral angiogram is indicated. So, I got two slides and this sort of, it’s a little bit of a not sure, what, wait a second. But here’s what I teach. If the patients greater than 50 and they’ve got a 3rd nerve palsy, consider giant cell arteritis. If giant cell arteritis exists where you live, ask the right question, that doesn’t mean I get the blood test on everybody. But if they have any symptoms of giant cell, I get the blood test.

If there is an acute isolated 3rd nerve palsy at any age with any risk factors with pupil sparing or pupil involvement get an MRI, MRA or this the CTA, everybody. Why? You’re going to get MRI/A and CTAs on people with microvascular 3rd, but how many 3rd nerve palsies do you see in a year, if you’re not a neuro-ophthalmologist. Will you remember all these little caveats and then there’s always that occasional patient with an aneurysm with a pupil sparing third. Are you willing to take that risk? Just get the imaging. Don’t worry about pupil sparing, age of patient, just imaging with MRI/MRA or CTA. And if it’s normal and you have a really high suspicion, get the cerebral angiogram.

Now, what do I do? It’s not what I do. So, I do the same as what I just said. If the patient is less than 50, if there’s cancer, if there’s no vascular risk factors, if there’s pupil involvement, if it’s incomplete, no matter the age, I get it. However, I don’t image if they’re greater than 50, if they have vascular risk factors, if there’s complete and its pupil sparing unless there’s no improvement in six weeks. So, I see lots of 3rd nerve palsies. I think most neuro-ophthalmologists do. If I see, you know, a 75-year-old diabetic, hypertensive with a sudden onset of a 3rd nerve palsy, and pupil sparing and it’s complete, I will, I don’t imaging.

What do I recommend for comprehensive ophthalmologist, image everybody. Why don’t I do it? I see lots of 3rd nerve palsies. In the United States at least healthcare spending is not sustainable. We need to do what we can do to limit spending. In my experience, I looked at my last, I don’t know 20 years, 430 of those 3rd nerve palsies of the 430 more, well more than half were microvascular. If I got imaging in everyone, you can multiply how much it costs for the MRI/MRA, which is probably a lot more in the United States and where you may live, but cost of medicine, at least in the US, not sustainable.

All right, that’s what I have to say about 3rd nerve palsies. I’m going to move on to our last topic and hopefully we’ll have time for some questions, we will. What’s new in vascular neuroimaging? So, this is a little more esoteric, I think. Just my objectives for this section are that we will discuss the pros and cons of CT/CTA, MRI/MRA, describe at least two developments in neuro-vascular imaging that have changed clinical practice, at least where I live, it’s changed clinical practice. I think these things are probably things you all know, the CT basically versus MRI.

CT is usually fast. It’s more readily available. There’s low susceptibility to motion. Of course, it’s faster. It’s not as claustrophobic. It’s good for bone and calcification. It doesn’t matter, well, you’ll see artifacts from metal but it’s not contra indicated, if you have metal. It’s good for looking at blood. MRI is traditionally not as good as blood although some of the new imaging sequences which I’m going to mention SWI is also good for blood. Of course, CT involves radiation. There is none in MRI. There’s also Iodinated contrast which they’re a percentage of people with allergies to this. Gadolinium or Gadopentetate is generally better tolerated.

It’s lower resolution in general in MRI and it’s not as good for acute ischemia, whereas an MRI, the DWI (diffusion weighted imaging) can detect acute ischemia and as little as just a few minutes of ischemia. And here’s an example of this, a patient that was sent to me from the emergency room with visual changes and imbalance, and it occurred shortly after waking up one morning, he went to the emergency room, they got the CT scan and said, oh good news, it sounds like a stroke but your CT is normal. Well, I saw him he had a monomers I mean obviously this is of course a stroke in his cerebellum which is causing the imbalance and this was not seen acutely on CT scan. So, somebody with an acute stroke within 24 hours, the CT may well be normal.

What about CTA versus MRA? Well, CTA, you have to have contrast. You can’t do a CTA without contrast. MRA, the contrast makes it a bit better but you don’t need the contrast, so you can do an MRA without contrast unless you’re interested in the aortic arch or in carotid stenosis, you can fine aneurysms and find vascular lesions without contrast on an MRA. It’s probably not quite as good resolution as a good CTA. That’s the data that shown here, highly specific and sensitive for small aneurysms.

Here’s one of the new things that we’re doing perfusion CT or PCT. This is more sensitive than CT for ischemia. I just showed you how CT can be very insensitive for acute ischemia. Here’s a CT scan on the bottom left, bottom left, looks pretty normal. The PCT, the blue area here is showing areas that are not as well perfused, if you compare to the other side. And here’s the CTA which shows lack of big blood vessels to this hemisphere. So, the PCT which is very fast, the PCT is more sensitive.

And one of the ways that we’re using it is, the person gets this very rapid CT scan. I mean it takes just minutes literally to do the scan. They’re having a stroke. They’re in the emergency room. Here’s the core infarct, which is in red. This is area that probably is not salvageable. But then here’s the green which what you see on the PCT, you can see how the green area is much larger than the red. So, all if you subtract out the red which is probably damaged, look at the green that may be damaged if you don’t intervene with blood thinning, so there’s all this brain that might be saved.

So, here you can see all, even way up in these cuts, there is a way down in this, sorry, down in this case and up, there’s areas that are not dead where the core infarct is. So, all the green, if you subtract the red from the green all that extra brain could potentially be saved. So, this can be, I, this is actually emailed or texted to the stroke specialist in the ER from radiology to determine how important it is to treat this patient.

Another thing that we’re using is MR-vessel wall imaging that helps differentiate vasculitis from atherosclerosis from dissection and vasoconstriction. So, aneurysm wall enhancement (AWE). Here’s a patient with a lesion. In this case, an aneurysm that’s obvious from the MRA, but in this case there’s some enhancement of the wall and this has been shown AWE (aneurysm wall enhancement) has been shown to be a risk factor for rupture. So, if you see AWE with the contrast enhancement, enhancement of the wall of the aneurysm that is much more worrisome than if you do not. And these days you know, we don’t treat every aneurysm. Smaller aneurysms are followed and observed, if they’re asymptomatic. That’s the whole another webinar.

And then here’s a patient with vessel wall imaging. Here’s their non-contrast CT. You can see the acute hemorrhage, that’s where the MRI usually is not as good. Here’s a 3D Time of Flight MRA showing occlusion of the M2 segment right here. Here’s a T1 MRI, showing this blockage in the blood vessel, and here’s post-contrast. So, it’s actually enhancing indicating that this is actually a young person with a spontaneous intracerebral hemorrhage and they had vasculitis. So, this is vessel wall imaging. These are all, you know, software programs.

And then I mentioned this briefly about detecting blood. So, here’s a patient. They get their MRI, the DWI shows all of the white is acute ischemia. Now, you don’t want to anti-coagulate this patient if there’s bleeding, right? Because then they’re risk for cerebral hemorrhage. Well, how do you tell if there’s hemorrhage? Here’s the SWI (susceptibility weighted imaging) showing hemorrhage in the midst of the infarction, so if this was not present, you would anti-coagulate or treat with platelet inhibitors. But because of the hemorrhage, you don’t treat because, you know, the data shows that if you treat this patient that their stroke could get much worse, there could be more bleeding and it’s contra indicated, so SWI.

So, in summary for what’s new, you must know the pros and cons of CT versus MRI, of course just to get your, the best test. CT-perfusion imaging has definitely improved our treatment for stroke. An MR vessel wall imaging is aiding in our – how we approach aneurysms and diagnose vasculitis and so on. All right, so that’s what I have to say about those three topics. I’m going to stop sharing my screen and I’m going to pull up the Q&A, which at where I can see there are a short 43 questions apparently. Let’s see if they’re all questions.

There is a, there, I’m going to probably not answer questions that are not relevant to the topics we just discussed. There’s one on managing 3rd nerve regeneration. There’s you know, I sent him just for business urgency what they can do. There’s no great way to do it. But I’m not going to try to answer those. All right, let’s, let me scroll through. What is the management of 3rd nerve palsy due to birth trauma with a normal delivery? Well, we didn’t talk about kids, of course. I mean, the management would be, are you sure it’s due to birth trauma? So, I think that would require imaging in a newborn, and then I would wait and hope that it gets better, and then of course, the usual, you know, if it doesn’t, if the lead is shut, you know you’ve got to worry about amblyopia for business et cetera.

After the completion of this lecture, certificate will be offered to the participants? I don’t know the answer to that perhaps Orbis will let you know. Someone says yes, you’ll get a certificate. Can color vision be normal and inflammatory optic nephritis? So, the answer is yes, I just had one of my young attending present a patient to me and said, well, you know, the person’s younger I was thinking it was optic neuritis but the color vision is normal. And I said, well, what is their acuity, 20/20. I said, well, again color vision should be affected in any optic nerve problem if the central vision is not normal. But if the central vision is normal and there’s a peripheral field defect, the color vision can be normal and they can still have optic neuritis.

Let’s see, oh, that’s not related to this. Is, does thyroid optic neuropathy have a relation — a relation with T3, T4, TSH? The answer is not that I’m aware of. It doesn’t, and I always talk to patients about, you know what, I tell, well, I start telling about thyroid eye disease, I said I’m going to talk about thyroid eye disease and thyroid blood disease and the two don’t necessarily have anything to do with one another. So, of course we want to fix your thyroid blood disease but that may have no bearing on your thyroid eye disease. I certainly see people who, 10% of people have no thyroid blood disease ever. So, and I see people who are hyperthyroid 20 years ago, had thyroidectomy, their blood levels great. They come in with acute onset of thyroid eye disease 20 years later. So, it’s related to the immune response, of course, not to the other markers.

But why should we do a visual field division is 10 of 10 and the fundus is normal because when thyroid compresses your optic nerve in the orbital apex, you don’t necessarily get swelling. You should do that if there’s a tumor, same thing. There’s a tumor compressing the optic nerve in the orbital apex, you can have normal color vision, you can have normal confrontational vision, you can have definitely have a normal fundus and you can have of significant optic neuropathy, and you want to make sure they don’t get to the point where they’ve lost central vision and so on.

In many cases were unable to discern the cause of the isolated 3rd nerve with negative imaging angiogram blood work, right? I mean I think that the point is that probably if you can’t think, if the imaging, you have good imaging, and the imaging is normal, it’s probably microvascular. That’s why in that one study where I showed a 140 something patients, 43 has said presumed microvascular, why presumed? Well, because either they were the right age or all the studies were normal. So, I don’t know that you can say normal imaging in any person with the third means, it’s microvascular.

I think if the person is over 50 and they have normal vascular imaging, I’m going to probably assume it’s microvascular. I’m going to file follow them and watch for improvement. I didn’t mention but the vast majority of people with microvascular 3rd get better. I mean 99%, right, so if they don’t get better over six to twelve weeks that’s going to make me nervous and I’m going to have to look harder, make sure their imaging, they had good imaging of their brain with contrast. In a younger person clearly I want and not just the A, not just the angio but I want to look at the tissue for things that might not kill you today, like an aneurysm but I want dye. I never ordered MRI of the brain without dye, never.

How do you clinically differentiate muscle enlargement of the thyroid eye disease from other radiologist such as oral and formal IgG4 disease, so that can be difficult because I don’t necessarily believe all this stuff about tendon sparring et cetera. I think you know if it obviously, if the person has other findings of thyroid eye disease externally lid retraction and so on and then they have the typical pattern of extra ocular muscle involvement medial, inferior and then medial I’m going to assume that it’s thyroid eye disease. If there’s something, anything atypical about it there’s no external signs of thyroid eye disease, lid retraction and so on. If there’s weakness of the muscle as opposed to restriction, right? So, remember thyroid eye disease causes double vision by restricting movement, not by paralyzing as lymphoma might or IgG4 that would be a clue. If it doesn’t fit the pattern, there’s just a big superior rectus or there’s just a big lateral rectus. There’s probably going to get blood studies and probably biopsy of the muscle.

Just with abnormal visual fields and thyroid eye disease, can we say it’s just thyroid optic neuropathy even though there’s no RAPD? No, I mean, should we not ask for CT? Yes, so, I think if the visual fields are abnormal, of course I’d want to make sure they’re reproducible because I see, you know, the first time someone does a field I see garbage all the time, so I’d like to be reproducible. If it’s asymmetric, let’s say there’s terrible field on one side, normally and there’s no APD that would make no sense. I’d want to repeat that.

If, and I’m going to get certainly before I’m going to treat them for thyroid optic neuropathy, I’m going to get a CT or their orbits, or at least I’m going to get one at the same time, if they come in with an obvious thyroid optic neuropathy and crappy vision, I’m going to start the IV steroids.. But I’m always going to get a CT because some of the patients may need orbital decompression and they’re going to get, they need a CT to look anyway. But if there’s any question at all, clearly they need a CT. I didn’t mean to say I wouldn’t get a CT.

How often do you perform an MRI as steroid response control? I think that means in the setting of thyroid eye disease, do we get an MRI to look at the change in my, never. I mean, I don’t care what the MRI shows. I only care if the nerve is working better. I think that answers that. Could the visual field defect and thyroid eye disease caused by restriction of extra-ocular motility? Well, I don’t think I can be caused by restriction of motility. I think it’s either big muscles that are restricting utility but causing compression in the orbital apex. I don’t think, I mean that’s an interesting idea somehow. I don’t, I have never heard or read of that.

Can the VEP be of some help in early diagnosis? Probably referring to thyroid, I suppose it might. I mean I think the other things are adequate. And for me, VEP can be, I see a lot of junk comes out of VEP that I can’t explain well, so I’m not a big fan of VEP. I ordered a VEP maybe once every 20 years, just in general. I mean, I only, the only time I ordered pretty much if it’s, I think the patient is non-organic vision loss, almost, sometimes if there’s a question of old optic neuritis.

What are laboratory examination we need to evaluate and dysthyroid optic neuropathy patients? Well, usually by the time someone is diagnosed with dysthyroid, of course they don’t develop, you know, dysthyroid optic neuropathy over a week. They have, they usually already had the evaluation at least where I’m from, maybe not everywhere but yeah, I mean I’m going to check a thyroid stimulating hormone, a T3, T4, and a thyroid stimulating immunoglobulin.

Would you do electro diagnostic? So, I think we just talked about that. The answer is I don’t. Is dysthyroid optic neuropathy, what are the signs of response? So, improvement in the fields or the acuity or the color vision, and all of those things that you would measure, all of the various measurements of function of the optic nerve. If the patient does not have optic nerve [indiscernible] [00:58:07], can we still give IV steroid? So, the answer is yes. We didn’t talk about just moderate thyroid eye disease but there’s a lot of data that shows that once-a-week intravenous steroid either usually it’s either 500 mg methylprednisolone or 1000 mg once a week for six weeks. So, I will often, if the person has pretty active looking thyroid eye disease and double vision, pain and irritation, I’ll give them once a week for six weeks and then repeat it sometimes, if they’ve got a good response but it seems to flare up, I’ll repeat it another six weeks.

Why is rituximab concentrate and decider of optic nerve any mechanism we should worsen neuropathy? I don’t know the answer to that. I certainly have never used it. But I don’t know. What is your experience with, oh, intraorbital steroid injections for thyroid eye disease? I have none. Although I know there are paper too, I think from, mostly from Latin America that have advocated for that. I certainly don’t think there’s been any sort of clinical trial though as best as I know. And so, I have zero experience with intraorbital steroid injections. Is there a serological biomarker for thyroid eye disease? Well, I mean I think you know usually, usually there will be signs of hyperthyroid or the blood test for hyperthyroidism will be abnormal. But again, if not, you look for euthyroid is greatest that look for thyroid-stimulating immunoglobulin primarily.

Why is there red desaturation? Good question, but color vision is typically affected if central vision is. I don’t know why exactly. That’s an interesting question. What precautions do we take with methylprednisolone treatment? I mean it’s pretty safe. I don’t, there are no, I mean obviously if the person’s diabetic, they would be the same problems. I mean, you know, like, we’ve given intravenous steroids for a long time for optic neuritis and the studies have shown very little bad side effects. I mean the main side effects in those studies are sleep disturbance and mood swings, basically, a couple of people got depressed.

But I mean, we think in generally otherwise healthy people, there aren’t many. I think in a, you know, a frail little old lady which are not usually the people I treat that you might want to admit them for the IV steroids. Most of patients we treat is outpatients, they go in once a day for three days in setting of dysthyroid optic neuropathy or if it’s just the moderate thyroid eye disease, they go in once a week. They start an IV, they get their dose, and they go home.

It’s a nice paper from Dr. Frederick and Joy on why classic dysthyroid optic nerve presents most commonly with an inferior visuals you do, do the superior muscle being closest to the optic nerve vision which is in. Interesting, thank you. That’s from Orbit 2017 August edition for those of you who want to read more about that. And I am not sure if that’s proven or theory, but maybe that inferior rectus which is the biggest, usually the biggest was pushing it towards them. Okay, but that’s makes sense. What is the dosage mentioned of steroid in your practice? Well, it’s exactly what we talked about. So, if it’s, if they come in and we say that you have a dysthyroid optic neuropathy, it’s a gram of methylprednisolone a day for three days, and then followed by once a week. If it does, if the person is not responding meaning their vision is getting better, their visual fields getting better, et cetera, in two weeks then orbital decompression.

There’s a question about watching this conference, I believe these are all recorded and available on the Cybersight’s website in the very near future. So, just to confirm if the age is more than 50 and the patient having diabetes and even feel sparing, we must image. I mean, I, that’s what I’m teaching. I mean I think if you see tons of 3rd nerve palsies. But again it’s got to be age more than 50, patient is diabetic, hypertension, it’s acute, you know this is going on for a week. I woke up, my lid was shut, and my lid shut, not this is gradually getting worse and it’s got to be isolated, right? No 4th nerve palsy, no 5th nerve palsy, no other symptoms, you know, that’s when I don’t image. But I know what to look for I know the questions to ask to determine if it’s isolated and I see a lot of 3rd nerve palsy. I think everyone else who sees the occasional 3rd nerve palsy its way safer to just image.

What is the schedule for tapering a systemic surgery of brain recurrence? So, that would be recurrence of thyroid optic neuropathy, the- so what I do is what we just mentioned which is, if it’s- if they have dysthyroid optic neuropathy they get the three days, a gram a day methylprednisolone every day. Then they get once a week, as long as they’re improving they get once a week for the six more weeks, and that’s the taper.

What is SWI? So, susceptibility weighted imaging is just a, it’s a software computer program that allows the MRI to detect blood, acute blood in the setting of an ischemic stroke. So, the problem is if you have an ischemic stroke sometimes there’s bleeding within the stroke, and if you have bleeding you don’t want to treat with anti-platelet agents because studies show that it’s worse. You can cause that hemorrhage to increase and kill the patient, maybe or make their stroke worse. So the SWI specifically will show you in that stroke that’s shown by the DWI if there’s blood.

Is there any role in systemic steroids and isolated 3rd nerve palsy of microvascular cause? Absolutely not. Some comments I won’t read out loud here. They’re good. I love you too. Let’s see, can we only do MRI rather than going for MRA as that is interventional? Well, I’m not sure what you mean. MRA is not interventional. And if you were talking about 3rd nerve palsy, what is the thing we’re really, really worried about, an aneurysm. Will MRI show you that? Probably not, certainly not as well as an MRA or a CTA, and it’s not interventional in the sense that you can do an MRI, and MRA or MRI without contrast. You cannot do a CTA without contrast. So by interventional you mean an intravenous injection then an MRA does not have to be done with dye, you can do it without.

In which case are you recommending radiation? Well, that’s interesting because you know that article about radiation is, I have not recommended radiation recently and I don’t think I’ve had many dysthyroid optic neuropathy in the last year or so but it does that one study does give you pause. I mean, I think radiation might be certainly in an older patient, anybody at risk for oral decompression but again if they’re failing the steroids, right now I recommend oral decompression. If the person says to me and they do I won’t have surgery, I’m 80 years old. I don’t want the risk of surgery. Then I say all right, we’ve got radiation. But I guess that’s the way I’m using it right now. I don’t think I have switched to the radiation, but there may be data I’m hoping there’s data that comes out that changes that approach for me.

Who’s to decide the special forms of imaging? Yeah, well, that stuff I mean, these are new things. And so I think what I would do is make sure as usual, make sure the radiologist knows what are you looking for. This patient presented acutely, I think they might have a stroke. I’m looking for a stroke. I’m also looking to see if there’s blood, you know, associated with it and then they’ll recommend it. So, I think the radiologist almost always are going to probably know more than the ophthalmologist about what to get. How to learn interpreting neuroimaging is ophthalmologist? Well, I mean there’s a lot of different things you might want to learn. There are certainly, I think there are textbooks written on neuroimaging for ophthalmology. I think there is, I think I gave a webinar on that. That should be recorded on Cybersight’s website. That would be a start, I suppose.

How to decide an old optic disc pallor is due to resolve just I read optic neuropathy if someone’s history. Well, as I tell all my patients and I see lots of patients that are sent to me with optic atrophy, right? They have a pale disk. They have an APD. If it’s unilateral I tell them all the same thing. When I look at your pale disc, it’s kind of like if you’re driving home today and you see a car that hit a telephone pole you could say that, well there’s been damaged. There’s an accident there but you can’t tell me if that car got running off the road by another car, if the driver fell asleep, if the driver hit a patch of oil, you can’t look at optic atrophy and say I know what caused this, and so you’ve got to investigate for the various causes of optic atrophy. We published a paper years ago now. We looked at ‘90, I think it was ‘95 or ‘97 patients with unexplained optic atrophy, they all got MRIs, a quarter of them had tumors that were previously not diagnosed, so we image all patients with optic atrophy if it’s unexplained.

What is the management of ischemic 3rd nerve palsy? If you’re convinced that it’s ischemic, if- I asked the patient have you had a general physical examination with your internal- your family doctor in the last six months? If you haven’t, you need to tune up. Go get blood pressure, cholesterol, diabetes checked. If you have and you’re doing well, I’ll see you in six weeks to make sure your microvascular 3rd nerve palsy is getting better, and as long as it’s improving, well, maybe see in six more weeks make sure it gets better all the way.

Partial versus complete urge significance. Well, I mean it is significant. Again, if I see, I said that what do I do, and maybe it’s different than what I teach. If I see a 70-year-old who comes in and says, yeah, you know, a day, yesterday I woke up, my left lid was droopy. By the end of day, it was closed. He comes in. He’s got a complete 3rd with pupil sparing. Okay, complete 3rd pupil sparing over 24 hours. I’m not imagining that person. I wouldn’t fault anyone for doing it, who’s not intra-ophthalmology, I wouldn’t fault them. But I’m not going to do it.

On the other hand, let’s say they come in and they got a partial 3rd nerve palsy and it’s been going on for couple of days. Maybe that aneurysm hasn’t pushed on that pupil fibers yet, it should theoretically. But maybe it hasn’t, so either, if I’m convinced it’s going to be ischemic, I’m going to say come back in a few days because I want to see that lid shuts and your pupils not involved. And that’s part of the problem. A partial 3rd nerve palsy with pupil sparing may just be because whatever is causing it hasn’t affected those pupil fibers yet.

Any role the OCT and the diagnosis of optic neuropathy, sure, I mean, I think, OCT can help remember acutely. It won’t unless you’re not sure if they’re swelling of the nerve or not. But let’s say it’s a retrobulbar optic neuropathy like thyroid and it’s relatively new, and OCT won’t help because you hopefully haven’t damaged any of your nerve fibers and you’ll have a normal OCT. So, that said, if there’s damage and you lost nerve fibers it can help tell you that there’s the problems is at the nerve.

Let’s see. Good morning and- does, thyroid optic neuropathy, what if the patient has systemic disease that makes steroids not the best choice? Yes, so that would be, if the steroid, let’s say the person just can’t, the steroids are going to kill this person because they’ve got diabetes. Well then, I would definitely go right to orbital decompression. And if they were so fragile that that wouldn’t work, I would go to radiation. What’s the management of congenital 3rd nerve palsy. They’re probably all in the United States, they’re all going to get imaged and then it’s going to be I’d send them to the pediatric ophthalmologists and say, what can we do to try to rehabilitate the eye.

I think I answered the protocol for just thyroid optic neuropathy. Does the risk of dysthyroid optic neuropathy related to clinical activity score? Yes, I think it does. I mean, you, as I tell patients you’re not going to have a normal looking eye with no motility problems and have a dysthyroid. I mean that would be very rare. In fact, we just had a patient who came in with acute loss of vision, big APD, NLP, big extra ocular muscles, history of thyroid eye disease, big muscles, no lid retraction, acute loss of vision. She had sarcoidosis, biopsy-proven sarcoidosis. So, I think the clinical activity score, yes that’s important.

Place of oral corticosteroids, I think if you can’t get intravenous, you can give oral. You can even give big dose oral. But in general, things have trended towards the best treatment being the pulse steroids intravenous. MRA, DSA, when it will be the first investigation? I mean I never do just, you know, catheter, cerebral angiogram is a first step because MRA and CTA are really good. I said I would get a cerebral angiogram only if MRA or CTA were normal. And I was really concerned about an aneurysm. How- when was the last time I had to do that, I can’t even remember, more than a decade ago. But if you don’t have good MRA, CTA, then you would get the angiogram sooner than I would.

Do other acute isolated granular palsies four or six have unique ideologies isolated third? So, you’re not as worried about aneurysms because of the anatomy that posterior communicating artery aneurysm is right next to the third. That’s why aneurysms, it’s just where aneurysms like to form. So, you’re certainly not anywhere near is worried about a critical acute, you know, intracranial hemorrhage with a 4th or 6th. So, 4th and 6th are different in that respect. But yeah, I mean they have unique ideologies, I mean I don’t know unique but they certainly 4th and 6th microvascular are still probably the most common, certainly microvascular 6th is the most common, 6th nerve palsy I see. Microvascular 4th are pretty common but they can be seen of course after trauma, most commonly, and they can be congenital with breakdown later on in life.

All right, we’re running out of time here. I’m not going to get, there’s still a 129 open questions. I’ll go for one more minute. For suspected vascular problems CTA or MRA, which is better? It really depends I think on your institution. I would ask your neuro-radiologist if you have one, which do you prefer, which do you think is more sensitive? The study showed that good CTA is a little more sensitive than good MRA. Can a mild thyroid eyes be present with just [indiscernible] [01:13:02]. Well, sort of by definition is not mild but the answer is no. I really would expect them to have significant obvious thyroid eye disease. You say suspicion of aneurysm palsy 3rd if normal and right, what is the point of CTA?

Well, I think that depends. I mean if you’re radiologists say that hey the MRA is normal but the CTA is better, let’s get one. I’d get one. But if, I’d get whatever the best non-invasive studies first and then, I don’t think in my setting I’d get, if I got a normal MRA, I don’t think you’d get a CTA, I’d get the angiogram. Because again there is an issue of timing too we want to find the aneurysm and fix it. Do you do thyroid antibody tests in cases of new thyroid cases? Yes. In case of the 3rd nerve palsy with, will eye moving exercise help? No.

How do we manage this thyroid optic neuropathy stretch? So, that’s a good question. There’s certainly, no, no one’s ever really looked at it because there’s not enough cases but probably it would be orbital decompression. Maybe, you know, I didn’t mention fat. Sometimes people will remove fat from orbits, not usually so much for thyroid optic neuropathy but for exophthalmos, you could consider those. I’m not sure about the prognosis honestly. I literally have seen less than a handful of cases in my career.

Do you use navigation to optimize outcome of orbital decompression? I don’t do orbital decompression and I sent them to my oculoplastic people, so I’m not sure exactly how they’re doing it, sorry. Is 6th nerve palsy association with other nerves like 3rd and 4th? Sure, I mean cavernous sinus lesions right, 3rd, 4th and 6th and 5, B1, B2, we should be looking for that combination. Answered that one. Who will, what will you manage the pupil sparing 3rd nerve palsy patient was less than 50 and has, yeah, I image them if they’re less than 50, I don’t care if they, you know, if they have diabetes or not. I’ve definitely seen microvascular cranial, a 3rd nerve palsy is in juvenile diabetics. You know they’re 50 or they’re 45, but they’ve had diabetes for 30 years, so you can see it. I still image them.

Let’s see, all right, I think we’re running out of time here. So it’s 11:16, my time. Thanks, I’m sorry I couldn’t answer all the questions. They’re still now 133 open questions, maybe we should have a webinar just questions. But I thank everybody for participating and again this will be- this has been recorded, it will be available on Cybersight, so I appreciate everybody’s attendance. Good luck with your neuro-ophthalmology.

Hopefully, I’ve helped at least with a few conditions, a little bit. And if you want to look at old Cybersight’s webinars that I’ve done and I’ve done a bunch they should all be recorded.

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May 18, 2020

Last Updated: October 31, 2022

3 thoughts on “Lecture: Dysthyroid Optic Neuropathy, Management of 3rd Nerve Palsy & Neurovascular Imaging”

  1. Hi Surekha – we do have some lectures on these topics already. See links below:

    Lecture: Scleral Lens Assessment and Fitting

    Lecture: Orthokeratology: Troubleshooting Patient Cases

    Lecture: Rigid Gas Permeable Lens Assessment and Fitting: It’s Not That Hard

    Lecture: Therapeutic Contact Lenses: Management of Ocular Surface Disease

    Hope this helps!


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