This case-based webinar will cover diagnostic testing and management of patients with common causes of binocular diplopia. Topics will include ocular motor cranial nerve palsies, myasthenia gravis, thyroid eye disease, and the sagging eye syndrome.
Lecturer: Dr. Karl Golnik, Neuro-ophthalmologist from the University of Cincinnati, Ohio USA.
DR GOLNIK: Well, greetings, everybody. And thanks for attending this Orbis Cybersight webinar. My last webinar, which was some months ago now, was on the diagnosis of patients with double vision. And there were a lot of questions at the end about: What’s the management of these patients? There was clearly not enough time to talk about both the diagnosis and the management at the same time. And so I thought: Well, why don’t we, for my next webinar, why don’t we talk about — concentrate on the management of the patient with double vision? So my goal, hopefully, when we’re done, is that you can describe the management of binocular double vision when we’re done with this. And again, we’re gonna cover, I’d said, some of the more common causes of double vision. We certainly can’t cover every single condition that causes double vision and its management in a one-hour webinar. So the outline here is just… I’m gonna harp again — emphasize again about this concept of determining the alignment. And then whether or not the double vision is isolated, that should be pretty brief. Then we’ll look at some specific causes of double vision and the management of these conditions. And so of course, when someone comes in with double vision, and the purpose of this webinar is to talk about the treatment of binocular double vision — because monocular double vision is never neurological. I’ve gone over some of these things before. There’s something called palinopsia. It’s a cortical problem where people may see something like a pot of flowers earlier in the day, and later, they see that pot of flowers superimposed on whatever they’re looking at. That’s not really what we think of as double vision, where you see the same thing doubled. And the assessment for monocular double vision is simple. Usually just a pinhole will correct the monocular double vision. But you can do all these other tests and so on. So we’re gonna dispense with monocular double vision. Because this is never gonna be neurologic. So before you start looking at alignment and making measurements, make sure it’s binocular, not monocular. And once in a while, I do see patients who come in with double vision, and they don’t know. It’s not… The double vision isn’t constant. It’s intermittent. They don’t know if it’s monocular or binocular. Obviously, we do the exam and we look for any misalignment, of course, they’re not having symptoms. So I tell them they have homework. And their homework is: Next time they have double vision, cover each eye in turn, and then call me and let me know. Is it monocular or is it binocular? Because the list of things that cause one or the other are very different. So I give them homework before we proceed with any further testing. The assessment of misalignment — we covered this last time, but again, I’m gonna emphasize that we have to assess the misalignment before we can even think about the diagnosis and the management. So the good news here is that cover/uncover testing and cross cover testing are our gold standards, really, for assessing misalignment. The Hirschberg test, which is looking at the corneal light reflex — I don’t want to hear about that test if the patient is able to fixate on a distant target. So of course, if someone has really terrible vision, and they can’t see the big letter at the end of the room, you may have to rely on corneal light reflex. Or if the patient is very young — of course, if they’re that young, they probably won’t be complaining of double vision either. But you can then look at the cornea light reflex to assess alignment. But if the person is a walking, talking individual who can look at a target, then I don’t want to hear — I don’t care what it looks — where the cornea light reflex appears to be. I want to know: Are they really misaligned? And that’s where cover-uncover and cross cover testing comes in. Let’s look at some examples to make sure we’re on the same page here. This is gonna be a polling slide. Don’t try to answer anything yet. And this patient is looking at a distant target. And we’re doing a cover-uncover test. And we’ll see what people think. In a minute, the poll will come on. But the question is: Is this an esophoria, an esotropia, an exophoria, or an exotropia? So the patient is looking at a distance target, the left eye is covered… The right eye is covered… Okay. Let’s go ahead and show the poll. So you can vote. As to which of these you think this is. Just so I can get a feel for people’s assessment of a cover-uncover test. Okay. So I have a pretty wide range of votes here. So when we’re doing the… I’m gonna leave that up on screen… When we’re doing the cover-uncover test, we are assessing really for a tropia. So if there’s no movement with the cover-uncover test, no movement, then there’s no tropia. All right? But if there’s movement, with a cover-uncover test, then there is a tropia. So as soon as you see movement in a cover-uncover test, you can eliminate answer number one and answer number three. Because this person has a tropia, not a phoria. Then, once you realize: Oh, there’s movement with the cover-uncover test, there’s got to be a tropia, then the question is simply: Well, is it an eso or an exo tropia? And in this case, every time you cover the patient’s right eye, the left eye — well, both eyes — move to the left. So the left eye moves out. That means this person is esotropic. Their eyes are relatively crossed. This person is fixating with the right eye. So when you cover the left eye, nothing happens. But when you make the person look with the left eye, both eyes move to the left. Left eye moves outwards, to find the target. Therefore it’s turned inward. And there is an esotropia. Okay. I’m gonna move on from there. So cover-uncover test — we’re looking for tropias. Let’s look at another patient with a cover-uncover test. And we’re looking at the eye that’s uncovered. You don’t look at the eye behind the hand. Just look at the eye that’s covered. Same idea. The person is looking at a distant target. And you can see in this video, I think, that there’s no movement of the uncovered eye. So in this case, the person has no tropia. But if the person’s having intermittent double vision, you want to know: Is there a phoria? So to find a phoria, once you find there’s no tropia, with a cover-uncover test, we do a cross cover test. And this eliminates the brain’s ability to use both eyes together, to fuse on the target at the end of the room. And so this again will be a polling slide in a moment. Let me play that video again. It’s supposed to be looping here. So now, with a cross cover test, we can see movement. Where this is the same person we just saw doing a cover-uncover test. No movement. Now with a cross cover test, there is movement. So let’s go ahead and put the polling slide up. And see what people think. Okay. All right. So good. So we have almost two thirds of people who got this right. So again, there’s no tropia. Because this is the same person on the previous slide who did a cover-uncover test. No movement. No tropia. So it’s got to be a phoria. So once you know it’s a phoria, the question is simple: Which way are the eyes moving? So in this case, whenever we uncover the eye, it moves in towards the nose. This is an exophoria. Okay. So that’s how we assess alignment. Now, ideally, we do more than just that. We also measure it. Ideally. Now, probably many of you don’t have prisms. I mean, that’s okay, I guess. If you see lots of double vision like I do, you definitely want prisms. But here we are, using a prism bar to neutralize the movement. And you can see here that now there’s really no movement. And you can then look at the side of your prism bar and say: Ah-ha! This patient, the same one, has a 10 prism diopter exophoria. And you can very quickly determine the pattern of misalignment by now simply telling the patient… Turn your head to the left. Turn your head to the right. And you just leave the prism bar up there. Do your cross cover test. And you can measure to see: Is this a comitant misalignment? Which means about the same, no matter which direction you are looking. Or is this incomitant? Most acquired neurologic problems are incomitant. And so we’ll show some examples of that. I forgot to mention that certainly if there are questions, put them in the question and answer box. We’re gonna address those at the end of the webinar. I think it would be too hard to do that as we go through, although it might be optimal to do it that way. So that’s the deal with alignment. It’s pretty simple. The more you do it, like a lot of things, the simpler it gets. And another question, before we move on to management, is: Is it isolated? Is the double vision isolated? And so that’s important. Because certainly problems in your brain or maybe other neuro-ophthalmologic conditions — are the eyelids involved? Are the pupils involved, is there anything going on in the rest of the body? One of my neuro-ophthalmology tips is oftentimes, when I say to patients, is there anything else going on, other than the double vision, they say… Well, maybe it hurts a little bit. I don’t know. I say — not your eyes. The rest of you. Is there anything going on with your arms or your legs. I often use my arm and I do: The rest of you. I do this motion. Because you’re an eye doctor, right? And the patients don’t think you care anything about their arms or legs. But it may be important. And of course, are there multiple cranial nerves involved? And that gets back to the pupils and the lids and so on. So you want to know: Is there anything going on besides the double vision? All right. So what we’re gonna do now is look at some — sort of make this case-based, but then look at some conditions, and then talk about the management. Because this webinar — if you want to know more about how you diagnose all of these things, you can I think then access my last webinar, which was on the diagnosis of patients with double vision. This is on, primarily, the management. So here’s a patient. This will be a polling slide. This is a 71-year-old woman who complains of double vision for at least several months. It’s kind of a vague history. When did it start? Oh, I don’t know. It’s gotten a little worse. It was intermittent. Now it’s a little more constant. It’s mostly in the distance when I’m driving. There’s no real variability. It looks to be fairly isolated. The patient denies any ptosis. Although there was mild metric ptosis on the exam in the 71-year-old. There’s been no other problems in the rest of the body. They say… No, this is a really pretty much just… I’ve got this double vision. And I’d like to know why and I’d like to know what to do about it. And the person appeared to have relatively full adductions. I put a little cross hatch here. This is as we’re looking at the patient. Right gaze, left gaze, upgaze, downgaze. And you can see there’s a small esotropia, 4 prism diopters, it’s relatively comitant, so it’s a little bigger to the left and to the right, about the same up and down. So relatively comitant. Small esodeviation. And the polling question is: Which of these four deviations is this most consistent with? The history and the exam? And while you’re answering the poll, I usually tell people, after I take the history and the exam, there’s always two questions with double vision. Number one, why do you have it? Number two, what do we do about it? So the first webinar a few months ago was the why do you have it question. This is the what do we do about it question. Let’s see what people think. We can probably… Close the poll any time. All right. So we’ve got kind of a mixed group. So I’m gonna leave that up for a moment. I’m just gonna push it over to the side of mine. So the majority of people say myasthenia. There’s a close second, sagging eye syndrome, and thyroid eye disease and 6th nerve palsy. It could be almost any of these. I think the thing that would be least likely would be a 6th nerve palsy. Why? Because a 6th nerve palsy, although certainly that can cause a esotropia, it should be very incomitant. Right? So if you have a right 6th nerve palsy, the esotropia should get really big to the right. Less in the center. And then go away or be very small to the left. So I don’t like the 6th nerve palsy much. Thyroid eye disease — could be thyroid eye disease. You can see tight medial recti muscles. You could have a comitant esodeviation. Usually, though, if there’s ophthalmoplegia in thyroid eye disease, you’ll see some other findings of thyroid eye disease. And we’ve said this is pretty symmetric. Thyroid eye disease should cause lid retraction, usually exophthalmos. So I would say not as consistent with thyroid. Myasthenia is always a possibility. Because it can mimic anything. And I do say there’s a little ptosis. Although I think that was probably more just the patient’s age. There was no variability, fatigability, and so on. But myasthenia is definitely on the list. And this is, though, I think for me, the history in the exam room, is most consistent with what we call the sagging eye syndrome. And the sagging eye syndrome is… I think it’s not a great name. Patients don’t like that name, sagging eye. But this was something described almost ten years ago. Dr. Joe Demur at UCLA did a bunch of high resolution MRIs, and looked at the ligaments connecting the muscles to the globe. But he found: Hey, as we get older, guess what? These ligaments can stretch. A little bit. And he found abnormalities in the rectus pulley locations, the lengths of the lateral rectus and superior rectus band muscles. And oftentimes found a bit of superior ptosis. These are the bands we’re talking about. Sometimes these bands are broken up or not in communication. There was stretching of some of the pulleys and so on. And the idea behind this is simply mechanical. And the history in this case is very typical. It’s not sudden onset. Like four weeks ago today, I developed this problem. Myasthenia is often a little bit more definite. This is a rather vague sort of a history. Because it’s very slow. And he has shown that in this study, which was published just last year, that if you look at patients, he looked at all of his patients over the age of 40 with double vision, almost a thousand patients, and found that — guess what? As we get older, so less than 50, a small percentage of people have this. Whereas greater than 90, most of the patients had this. So you can see most commonly horizontal misalignments. Sometimes cyclo-vertical components as well. The management — and here I say consider myasthenia. This can mimic anything. So certainly in this patient, we have to consider myasthenia. It’s fairly easy for me to get a acetylcholine receptor antibody blood test, and do some other tests in the clinic. We’ll talk about those when we get to our myasthenia topic today. But consider myasthenia in any patient with double vision. I like to remeasure these patients at least once. So when they come in, this woman comes in, I said to her: Listen, this really — I did a good review of systems, to make sure there’s no other symptoms of myasthenia. Which means no drooping of the eyelids that gets worse at the end of the day, the double vision doesn’t really change much from morning to night. No systemic weakness of any sort, problems chewing, swallowing, breathing, no, nothing else. Depending, I might get the blood test. Certainly I’m going to look on the exam for other findings of myasthenia. But if the blood test is normal, there’s nothing else on exam, I’m still gonna tell her… Listen. Let’s see you in six to eight weeks. If this has been going on for some months, let’s see you in six to eight weeks, because I want to make sure there’s no variability on your exam that might make me feel more strongly about myasthenia. I want to make sure the measurements are fairly stable, because usually prism treatment in glasses… Whoops… Prism treatment is very, very effective. These patients usually don’t have big misalignments. They’re usually fairly comitant. So all of that makes prism usually the effective strategy. Now, strabismus surgery can be considered. It depends on the patient, of course. Most of the patients have glasses. Not everybody. Now, I can tell you I don’t wear glasses. I don’t like wearing glasses. And I would not like to have glasses for this condition. And I would personally — if it were me, and my choice was have double vision, have prism glasses, or have surgery, I might have the surgery. But so certainly surgery can be considered in those patients who just won’t consider the prism glasses. But of course, if they’re already wearing glasses, it’s usually a very easy choice for them to say: Sure. Just give me the new prescription. And I will use the prism. And I tell them: You know, like glasses, this may change. It may get a little worse over the years and decades. And you may need your prism tuned up. And that’s the management. And these people are usually very helpful. So I see the patients a second time. Typically the measurements over a couple months are very stable. If they’re not, then I’m worried about myasthenia. But if they’re very stable, I say: All right. Here’s the prism. I hope I never see you again. And I send them on their way. Of course, they get an annual eye exam from the regular ophthalmologist. Not from me. Because I don’t do cataracts and the rest of the stuff. But that’s what I do. And if they have a problem down the road and the double vision comes back, then I’m happy to see them again. So that’s the management for sagging eye syndrome. Okay. Here’s another patient. This will be a polling slide in a moment. Same sort of choices, I think. More or less. Maybe not the same, but similar choices. So this is a fellow who has had the fairly sudden onset of double vision. It started last week. So it’s been going on for just one week. He’s an older individual. In his 70s. And he has double vision. You can see his exam and his motility we’re looking at — so looking to the right, in downgaze. Looking to the left. And I think we showed you up somewhere. So you can see he has… Now I won’t say what he has. Because that’s the point in looking at the video. But we can go ahead with the polling slide. See what people think his exam and story is most consistent with. Okay. So certainly the majority of people said 3rd nerve palsy. Thyroid eye disease — this would be very unlikely to be thyroid eye disease. Right? He’s got an obviously droopy lid. Thyroid does not cause droopy lids. Sometimes patients say — they have ptosis. Could it be thyroid? No. It doesn’t cause droopy lids. So thyroid, I think, would be the worst answer. Sagging eye syndrome… I think that’s probably the second worst answer. And the reason I say that is that this is very, very asymmetric. So his right eye moves normally. And the left eye has significant limitations. Usually in the sagging eye syndrome, maybe I didn’t mention it — the eye movements are pretty good. It’s just a little change in the alignment. So sagging eye and thyroid eye would be two of the items that you should be able to very quickly dispense with, and say: No. Not either of those two. So you’re left, then, with 3rd nerve palsy or myasthenia. Well, I just said myasthenia can mimic anything. But this person has the sudden onset, one week ago. He’s got very, very significant ptosis. He’s got a deficit in elevation of the left eye. Adduction of the left eye. And depression of the left eye. So this would be most consistent with a unilateral left 3rd nerve palsy. Could it be myasthenia? It could. I have seen patients present with myasthenia that look like a 3rd nerve palsy. Of course, it would have to be pupil-sparing. And although I didn’t really show you his pupils, you can see his pupils. And they are the same size. And you’ll have to take my word that they were both moderately reactive, symmetrically reactive. So it could be myasthenia. So myasthenia would be the second best answer. But this is pretty classic 3rd nerve palsy. So let’s move on. I think I’ve got another polling slide. So here’s another patient with double vision. It’s been going on for a couple of weeks. A couple of weeks. And this one’s tougher. So let’s watch the video. And see in left gaze… Right gaze… Up. Down. And we’re actually looking at his pupils, which are kind of hard to see, because he’s got dark brown irises. Up. Left. Down. And to be fair, I’d have to tell you — I should tell you his alignment, I suppose. Because it’s not obvious. But when he looks up, he has a left hypotropia. Left hypo. When he looks down, he has a left hypertropia. When he looks to the right, he has an exotropia. So let’s put the polling slide up. And see what people think. Is this most consistent with myasthenia, sagging eye syndrome, thyroid eye disease, or 3rd nerve palsy? Okay. A little more. I would expect this to be a tougher question, because it’s more subtle than the last. So again, this is not sagging eye syndrome. Why not? It’s not sagging eye because I think there’s a clear cut problem with the left eye. So that left eye is not moving up. And I just said: In sagging eye, the eye movements are pretty good. And this person, when they look up, they have a left hypotropia. When they look down, they have a left hypertropia. When they look to the right, they have an esotropia. So this is not gonna be sagging eye. It’s also not gonna be thyroid eye disease. Thyroid eye disease certainly can cause a problem with adduction, a problem with elevation. And this person does have a problem with elevation of the left eye and adduction. If you look at the left eye, when he looks to the right, and compare it to the right eye, when he looks to the left, you’ll see that there’s still some sclera visible. So watch this. So when he looks to the… Hold on. When he looks down, the eye doesn’t move down well at all. That would not be… So a little sclera here, versus over here. He buries the sclera. So the pattern that we just described, hypo in upgaze, hyper in downgaze, exo in right gaze, 3rd nerve palsy. This is a 3rd nerve palsy. Hard to see his pupils, but this is a pupil involving 3rd nerve palsy. That left pupil is a bit bigger than the right. This could be an aneurysm. And it was. It was nasopharyngeal cancer that killed him. You wouldn’t normally look at him and say… Oh, his lid is shut. No, this is a partial 3rd nerve palsy, and that’s why the pattern of misalignment is so important. You do your cover-uncover testing, in left and right and up and down, you say… Oh, hypo in upgaze, hyper in downgaze, eso in contralateral gaze. And when someone may have a 3rd nerve palsy, we always want to do the appropriate testing, and we’ll talk about that in a moment. And then… So 3rd nerve palsy. So the problem — not problem — the issue with 3rd nerve palsy, whether someone has a very obvious 3rd nerve palsy, like our first patient, or a subtle 3rd nerve palsy, like the last patient, it could be that aneurysm that’s gonna kill them later today. Or a tumor, in his case. Nasopharyngeal cancer. It could be something bad. It could be something deadly. So if you see someone who may have a 3rd nerve palsy, then the evaluation is urgent. And in my country, at least, in the US, in my practice, I have the choice of getting an MRI. And MRA. Or CT/CTA. So the A, angiogram, what is gonna kill this person fast? An aneurysm that ruptures. So you need the A. So depending on where you live, I’m hoping that one or the other of these are available. But you need to rule out the aneurysm that could kill this patient later today. Or in the next two days or a week or whenever. So they need an urgent MRI. So if this patient walks into my office, and has the same history of… Oh, it’s been going on for a week or two weeks… And they have a 3rd nerve palsy, they go from my office to the hospital or wherever I’m gonna get this MRI/MRA, or CT/CTA. Now, here I say that if those studies are normal, the non-invasive studies, consider catheter angiogram if high suspicion. So that said, I don’t think… I’ve not ordered a catheter angiogram in years. Because MRA and CTA are so good. So in my patients where I have high suspicion, we find the problem on the MRA or the CTA, if it’s an aneurysm. I’ve not had any patients at least in the last decade where I’ve thought… Gee, the MRA is normal, the CTA is normal. I still think this is an aneurysm. They need a catheter angiogram. Because MRA and CTA have gotten so good, that’s why they don’t miss the aneurysm. They can detect very small aneurysms. That said, if the patient is over the age of 50, and they don’t have a lot of pain, usually aneurysms cause a lot of pain, but if they’re over 50, and the MRI or MRA or CT or CTA is normal, then almost every time this is gonna be what we call a microvascular or vasculopathic 3rd nerve palsy. And this will get better. The risk factors are age over 50, blood pressure, cholesterol, diabetes. So of course, if they don’t have a family doctor, if they have not had these things assessed in the last six months, they need them assessed. So if they say: No, I haven’t seen a doctor in five years, two years, I say all right. You need to get blood pressure, cholesterol, diabetes. Those things need to be checked. Because sometimes microvascular cranial nerve palsies, 3rd nerve palsies, can be the first sign of an underlying systemic condition that the patient has not… Does not know about. Most of the time, at least in the US, they have seen family doctors, they’re being followed, and they know whether or not they have these conditions. And a lot of the times, they say… Oh yeah, my diabetes isn’t under control. Sometimes they say: Gee, my diabetes has never been under better control. It can’t be related. And the answer is… It doesn’t mean your diabetes is under bad control or blood pressure or cholesterol. Just having those are risk factors. Sometimes that’s hard for patients to understand, why they’re well controlled risk factors — are still risk factors. So if they’re over age 50, probably microvascular. And then I’ll see the patient in six weeks. Make sure they’re getting better. Usually they are. I often tell them, if their lid is shut, the first thing that’s gonna happen is the lid will open. Then you’ll have double vision with the lid open. You’ll have to patch the eye or put some scotch tape on one of your lenses. And the patient comes back. Sure enough, the lid is open. You were exactly right. My lid opened up. I got double vision. You’re good. They like the doctor to predict what’s gonna happen. So that’s, I think, the short of it these days. In the past, there’s been lots of discussion about the rule of the pupil. Pupil sparing versus pupil involving. It’s true that pupil involving 3rd nerve palsies are much more likely to be the sign of some bad underlying pathology. But there’s so many caveats. And exceptions. And ifs and ands and buts. I teach at this point… Especially if you’re not someone seeing lots of 3rd nerve palsies, if you think they have a 3rd nerve palsy, just get the imaging study. All right. Here’s another polling question. This is a fellow in his 40s who was playing football and got tackled. And got double vision. And we’re looking at his versions. And you can see him looking down and to the left. Here he is looking down and to the right. Here’s the rest of his eye movements. And when he looks downward, that’s when his big problems occur with the double vision. He has a vertical misalignment of his eyes. It’s worse when he looks down. Better when he looks up. Worse when he looks to the… In this case, when he looks to the left. Better when he looks to the right. All right. Let’s show the polling slide. All right. What is this most consistent with? Myasthenia, third nerve palsy, fourth nerve palsy, sixth nerve palsy… Okay. Let’s see. All right. Okay. So three quarters of you had the correct answer. Which is fourth nerve palsy. Could it be myasthenia? It could. It could be myasthenia. I’ve seen myasthenia mimic a fourth nerve palsy. But it’s probably not. And the history, of course, would be very unusual for myasthenia. Right? I fell, hit my head playing football, and got double vision. That would be most consistent with an injury to a nerve. And the fourth nerve is the most commonly injured nerve. So that’s a big hint right off the bat. But he has the pattern of a right fourth nerve palsy. His eye will not move down and in well. So we’ll run that video again. He looks left and right, it looks pretty good. Up is good. But look when he looks down. This eye is not moving all the way down. And watch. Compare that eye to this eye, when it’s down and in. So I didn’t mention head tilt, because I thought that would be too much of a giveaway. So he has a traumatic right fourth nerve palsy. Sixth nerve… I said he had a vertical misalignment, worse in downgaze. That’s not the pattern of the sixth nerve palsy. Could it be a third nerve palsy? It would be very unlikely to be a third nerve palsy without any other findings. Just a depression deficit. And of course, the pattern is not really what you would expect. So let’s do… This will be another polling slide. So here’s a fellow who has double vision. As you can see, he’s in his 70s. He has I think high blood pressure. And he’s had double vision for a couple of weeks now. It’s horizontal. The images are side by side. He says that it really bugs him when he looks to the left. He’s pretty good — in fact, if he turns his head quite a bit, and looks way to the right, the double vision goes away. That when he looks way over to the right, it goes away. So let’s get the poll up there. I think this one… I think is pretty straightforward. Let’s see what people think. All right. Let’s close the polling. All right. So good. Again, three quarters… Could it be myasthenia? Yes, it could be myasthenia. Third nerve palsy, fourth nerve palsy, definitely not. So this fellow has a… Well, I would say a moderate… Whoops. A moderate left… I’ll play the video. Left abduction deficit. Now, is it a complete 6th nerve palsy? No. But like we saw with the 3rd nerve palsy, you don’t always see the complete scenario that you see in textbooks in patients. As they say, they haven’t read the textbook. So this person has a left abduction deficit. Compare that to when he looks to the right. I’ll do that in a minute. But there’s no vertical issues here. It’s simply a left abduction deficit. Worse when… Could this be myasthenia? Yes. It could be myasthenia. It’s always on the list. But this guy had a sudden onset double vision, moderate left abduction deficit. So the best answer is most consistent with 6th nerve palsy. Okay. So what about the management of 4th or 6th nerve palsies? Well, if the patient is over the age of 50, and there’s no history of trauma or anything else, and this is isolated, right, we’re talking about isolated now. You’ve looked, you don’t find anything else, then this is probably microvascular. Meaning risk factors of age over 50, blood pressure, cholesterol, diabetes. And in this scenario, I don’t get an MRI right off the bat. Or a CT scan. I say: Listen. Have you had your blood pressure, cholesterol, diabetes checked? Let’s get them checked if you haven’t. This should improve over 6 to 12 weeks. But 12 weeks — and I tell patients — 99.9% should be better in three months. If you are not, then you probably do not have a microvascular palsy. So I see them in 6 weeks. Oftentimes, the patients come back in 6 weeks and say: I am no better! And we repeat our measurements. And now instead of a 30 prism diopter esotropia, they have a 10 prism diopter. Well, guess what? For the patient, they either have double vision or they don’t. And so they say: I’m no better. But for us, we have a measurement. I can tell the patient — listen, last time — and I show them the prism bar. Last time, we had to use this really strong prism. Now you’re up here. You’re definitely getting better. Oh, okay. You’re the doctor. I guess you’re right. And I say: Listen. Come back in six weeks if you’re not better. But you’ll be better. And people never come back. Because 99.9 — I hate to say never. But 99.9, if it’s microvascular — now, what happens if they come back in six weeks and they’re no better? Oh, well, maybe it isn’t microvascular. Maybe it isn’t. So now I’m gonna consider getting that MRI. But if it’s improving — when I say better, I don’t mean resolved. I mean improved. How do you know it’s improved? The best way is that you’ve got a measurement. You can judge their duction deficit. -1, -2, -3, -4. And you can do that, if you don’t have a way to measure with prism. If they’re no better, then I image them. Now, if they’re less than 50, and of course, don’t have risk factors, so healthy young person, they get an MRI right off the bat. Because that would be unlikely, that they would have a microvascular 4th or 6th nerve palsy in a young person, with no other risk factors. Now, if they have a long history of high blood pressure or diabetes, that’s another story. But they could have a tumor, they could have multiple sclerosis, they could have something else causing a problem with these cranial nerves. I definitely see people — because one of the most common causes of 4th nerve palsy is that they had it when they were born. And they were compensating. They were able to fuse it. And at some time during their life, whether it be 20, 40, or 60, now they no longer can fuse. They no longer can compensate for this misalignment. So these patients often have very large vertical fusional amplitudes. I think we covered that in our last webinar. So sometimes it is old. With 4th nerve palsies. Not 6th. 4ths. So if the person has the sudden onset of double vision, we wait. We follow them. We read the measurements. And if they come back and they’re no better, then we often will image them. Unless we have good evidence that it’s old. If the imaging is normal, I continue to follow them. I think about myasthenia. And might do testing for myasthenia. But ultimately, sometimes the 4th nerve palsy — we think was just present in the past. But not… The person was phoric, not tropic. When I ask these patients — I say this is gonna sound like a funny question. You’re 50 years old. But back when you were a young adult, did you ever notice that when you would close one eye, close the other eye, back and forth, the thing you were looking at would jump up and down? Yeah, of course. Isn’t that normal? No! But they’re telling me — what is it when they’re closing one eye back and forth? They’re doing a cross cover test. So any phoria you have, I blink back and forth, like I’m doing… Hopefully you can see on the video… Any phoria, they’ll see a jump. And I have people frequently say: Oh yeah. That’s how it’s always been. Things always jump up and down when I close one eye quickly back and forth. They think it’s normal. It is normal for them. And that’s good evidence that this is just decompensation of something that’s old. And of course I mention: Consider myasthenia if it’s variable and if it’s not improving. Okay. How are we doing on time? We need to speed up a little. Here’s another polling slide. This person has had double vision for about a month now. And we’re looking at his versions here. Don’t forget to look for fellow travelers. Fellow travelers are… Is this just an eye movement problem? Or is something else going on? Let’s go ahead with the polling slide. Since we’re… So is this myasthenia? Sagging eye? Thyroid eye? 6th nerve palsy? It’s kind of hard, unless you see the obvious finding… All right. So we’ve got a spectrum. So certainly this person has bilateral abduction deficits. Bilateral. Abduction is poor in both directions. And they are esotropic. So this could be bilateral 6th nerve palsy. But I’m gonna stop the video right there. Look at his eyelids. He’s got marked bilateral eyelid retraction. I don’t even need to see the eye movements to tell you: This guy’s got thyroid eye disease. I mean, this is… Just looking at the still photo, he has got thyroid eye disease. Nothing else causes this appearance. And of course, when you add it in with the bilateral abduction deficits, because of bilateral medial rectus tightness, enlargement, you’ve got findings on this slide alone… Basically that are pathognomonic for thyroid eye disease. Thyroid eye disease. And not only that. He’s got lid lag. When he looks down, his lid doesn’t move down. In downgaze… Watch. See? Look at those lids. Thyroid, every time. And so thyroid certainly can look a variety of different ways. It can be this active, angry, in the left upper photo, the more quiet bulging eyes with upper and lower lid retraction. It can be unilateral. Why? I don’t know. Myasthenia, thyroid, they can be unilateral. They can be unilateral. But if you see lid retraction, it’s almost always thyroid. So management… Well, if they smoke tobacco, tell them to stop. Because that’s really the only modifiable habit that people have, that actually has been proven again and again in studies to exacerbate thyroid eye disease. So just one more reason not to smoke tobacco. If the alignment is stable and mild, meaning 20 prism diopters or less, you can use prism. Prism is not always super successful, because in thyroid eye disease, the misalignment is often not very comitant. Comitant. So that means that depending on where they’re looking, there’s different amounts of alignment. Any time there’s different amounts of alignment, prism is less effective. Because if you give them exactly what they need in primary position, but as soon as they look to the left or the right or up and down a little bit, they’ve got… Different misalignment — the prism won’t work. In those patients, they’ll get the prism, and if they hold their head straight and look straight ahead, it’s one. But anywhere else, it’s two. They’re gonna close their eye and say… These glasses don’t work. If it’s relatively comitant and stable, so I’m gonna see these patients at least a couple times, because we know that thyroid eye disease often is not stable… But if it is, I see them in two months, no change, I see them in two more months, no change, all right. We can try prism with the understanding that if you change, the prism might not work anymore. And if they’re willing to accept that, then we can give them some prism. Strabismus surgery certainly can be considered. And it’s often considered in thyroid eye disease. Again, you want them to be relatively stable. And so I tell people with thyroid eye disease who have mild to moderate thyroid eye disease, without optic nerve involvement — we’re not talking about that. That’s another topic. But mild to moderate with double vision, our treatments are… Our success of our treatments are dependent on stability. So I’m gonna see you every two months, until you’re stable. Or… Well, until you’re stable, basically. Eventually, they will get stable. Now, recently, there’s been a new treatment. And steroids sometimes are used for thyroid eye disease. Very unhelpful, in my opinion. In double vision. So I’ve not had anybody treated with steroids where it really helped the double vision. It can help other parts of thyroid eye disease. But that’s a whole nother topic. And you probably will have a webinar on that. But there is a new medicine that’s been in the US at least approved called teprotumumab. It’s an insulin-like growth factor 1 inhibitor. It’s an intravenous infusion. There are 8 of these over a total of 21 weeks. The studies really are very promising, and we’ve used this. This has been approved for use in the United States for the last year and a half, almost two years, at this point. One of the problems, at least in the United States, is that’s the cost. $120,000 to $225,000. Now, as you can imagine, I have no patients who can afford that. But insurance will cover it if they meet the right criteria. You can imagine that this is not something that most anywhere in the world — any patient anywhere in the world — is gonna be able to afford. So the question is: Are they gonna be able to get the cost of this way, way down? But here’s the data. And I’m not gonna go over each of these charts. But the dark bold line are patients randomized to teprotumumab. The light gray line are patients randomized to placebo. And you can see that the proptosis response, how active the disease is, the double vision response, is much, much better in the teprotumumab group. Here’s just an example of a patient from the New England Journal of Medicine publication. In someone before and then after their first dose, and their eight infusions of the teprotumumab. And you can see almost resolution of the findings. So pretty exciting. And really a game changer in the treatment of this condition. Okay. There’s our last patient to have a polling system on. He’s in his mid-50s. He’s had double vision for a week. He has good acuity, pupils are normal. He has a mild deficit in depression of the right eye. Which I’m not really showing you. But when he looks down, he has a right hypertropia. A right hypertropia. And so the question is: What am I showing you? Because I’m not showing you that, really. So I want you to look at his left upper eyelid, as he looks from down to up. And open the polling slide, please. And I think we can close the polling slide in the interests of time. All right. So the vast majority think myasthenia. Not sagging eye. This person on the video I’m trying to show has ptosis. On the left. A little bit on the right too. But on the left, more prominent. And when he looks from down to up, there’s a little movement of his eyelid back downward. If you look from down to up, and you still keep looking up, your lid won’t do this. This is a form of Cogan’s lid twitch. This person has myasthenia gravis. Clearly not the pattern of a 6th nerve palsy. Which is a right hypertropia in downgaze. Not the pattern of thyroid. It would be a hypotropia in upgaze. And certainly not sagging eye syndrome. So this is myasthenia. And there are different ways to assess myasthenia in the clinic that are very inexpensive. And one way is what’s called the sleep or rest test. And this was described as a 30-minute rest. It doesn’t have to be sleep. But the bottom line is you tell the patient: Keep your eyes closed for the next 30 minutes. Do not open them. And here’s a patient with obvious ptosis. He had some double vision. And here he is before the 30 minute rest. Here he is after the 30 minute rest. Because myasthenia is fatigable. And when you rest the muscle for a short time — this won’t last for long. But you basically tell them to rest. Tell them: I’m coming back in the room. Don’t open your eyes ’til I tell you. Open your eyes, blink once, and look straight ahead. So 30 minutes. The problem is: Who’s got 30 minutes these days? So the other test we can do is an ice test. So here in the video, watch the left eyelid. See how droopy it is. Here’s our fancy ice pack. A rubber glove with ice in it. Two minutes. Two minutes, no longer. It gets cold. Two minutes go by. And remove the eye pack and say: Blink once and look straight ahead. Boom. Very positive ice test. Fairly specific and very sensitive for myasthenia. What else? Of course I mentioned earlier in this webinar — in the US, we’ll usually always check acetylcholine receptor antibodies. EMG can be helpful, but usually not so much with ocular myasthenia, unless you’ve got someone who’s doing single fiber EMG of the orbicularis muscles. And I don’t personally in my institution have that. So usually we rely mostly on ice tests, which are short, and acetylcholine circulating antibodies, and of course, our clinical suspicion. So with management of myasthenia… Well, I always get neurology involved. Why? Because when a patient presents with ocular myasthenia of short duration, there’s a fairly good chance — not 100%, by any means — but a fairly good chance they may develop generalized systemic myasthenia. I don’t do stuff like that. And if they have problems chewing, swallowing, breathing, can’t walk, that’s not me. That’s a neurologist. So I tell them: I know you’re not having symptoms in the rest of your body, but I want you to get a neurologist. Have at least one exam so they know you. It can be hard to get a neurologist at short notice. So let’s just set up an appointment with a neurologist. Not an emergency. We get a chest CT scan to rule out thymoma. Honestly, it’s extremely rare. Maybe in 30 years, once I’ve found a thymoma. Do we really need it? Well, that’s the teaching. They’re rare. I usually start with one of two medicines. The mainstays. Pyridostigmine or corticosteroids. So pyridostigmine is 30 milligrams, three times a day. I tell the patient: Don’t take it right before bed. You don’t need it while you’re sleeping. Right? So one in the morning. More or less when you get up. One four hours or so before bed. And then split the difference. I do tell them: Listen, the reason why it’s three times a day is because it doesn’t last long. So that’s kind of a pain. I tell them the main side effect, if there’s a side effect, is diarrhea. That’s why we usually start at 30 milligrams. And my prescription reads: Half a pill, three times a day, increase as tolerated to a full pill, three times a day, over 7 to 10 days. And I see them back in a month to see how they’re doing. Corticosteroids can be used as well. But the corticosteroids again, depending on the patient and other medical problems, have potentially more and worse side effects. Sometimes I’ll use pyridostigmine. It works okay. But then I’ll add a little prednisone or corticosteroids in. To try to blast them and get them under control. Then taper the corticosteroids. Now, most ophthalmologists in the US do not treat myasthenia. As a neuro-ophthalmologist, I see it a lot. So I treat it. But most ophthalmologists don’t. They let the neurologists treat it. Now, if the pyridostigmine and corticosteroids don’t work, there are other medicines that could be considered. Mycophenolate mofetil, azathioprine — I don’t prescribe these. I just don’t have enough experience. And the last category, and unfortunately there is a category of unknown. And so I definitely have patients where I’m not entirely sure what they have. They don’t have a specific cranial nerve pattern. It doesn’t fit any particular pattern. They don’t have obvious myasthenia. So I usually will get the MRI in that setting. Get an acetylcholine receptor antibody in that setting. And I tell them: Listen. A negative acetylcholine receptor antibody doesn’t mean you don’t have myasthenia. In other words, there is no test that rules out myasthenia. About 40% of people with myasthenia have a negative acetylcholine receptor antibody. So it still could be myasthenia. Sometimes I will try, because of that. I’ll say… Listen. We’ve got a medicine, pyridostigmine. It only works for myasthenia. So if you get better on the pyridostigmine over a month or so, if I try it, I give them one month, and if they come back, no better, I say… Okay. Stop taking it. But if they get better on pyridostigmine, well, it must be myasthenia. It only works for myasthenia. So I’ll repeat the exam. See if something changes. See if I get clued in to what’s going on, despite the negative testing that we’ve done. Sometimes if I’m really worried, let’s say they’ve got a partial abduction deficit, it’s getting worse, I might repeat the imaging, looking for something that might have been missed the first time around. Hopefully that’s not a lot of patients, but I definitely have patients where I’m not entirely sure of the diagnosis. So in summary, make sure it’s not monocular. Everything we just talked about does not pertain to monocular double vision. You have to determine the pattern to really know what you’re dealing with. Right? You have to consider myasthenia in every patient with double vision or ptosis. All right. So I am going to stop sharing. And look at the Q and A. The first question. What can cause comitant diplopia besides a phoria? A good question. One of the things you want to keep in mind: Phoria does not mean congenital. Phoria simply means there’s a small enough misalignment that that particular patient can control it. They can fuse it. So you could have a problem with a tumor pushing on your 6th nerve, but just barely. And they might be phoric. So you need to get rid of the idea that phoria means benign and tropia means bad. Not true at all. Now, if you have a comitant phoria, it is often benign. Because most of the acquired problems that we’ve talked about are incomitant. So in that patient with a 6th nerve palsy in the phoria, they may be phoric in primary position. It may be a bigger phoria towards the size of the 6th nerve palsy and they may be orthophoric in left gaze. And that’s still not comitant. That’s why you have to check in different gazes to know. So what can cause comitant double vision? So I’ve seen thyroid eye disease do it. Sagging eye syndrome. We just mentioned the patient who had a fairly comitant misalignment. But certainly cranial nerve palsies shouldn’t be comitant. So the first case — it was exotropia but you called it esotropia? It wasn’t an exotropia. It was an esotropia. So the eye in that case — if you do a cover/uncover test, if the eye that you uncover goes outward, that is an eso deviation. Eso deviation. Is vision therapy effective for the management of double vision? Well… Certainly that depends… Well, let’s see. It depends completely on what’s causing the double vision. Right? No, vision therapy is not effective for neurologic causes of double vision. I mean, I never recommend vision therapy, unless it’s something like conversion insufficiency, or something up close. That can help in younger people. But that’s not a neurologic issue. So I would qualify my answer to say that no, I don’t think vision therapy is effective in anything neurologic.
Explain exo and iso. So I’m not sure about iso. You might have meant eso. So exo means that the eyes are turning outward, relative to one another. So in an exotropia, if you cover one eye, this eye is looking straight ahead, this eye is gonna come in. Right? You cover this eye. The eye will turn inward. For them to take up fixation. In eso, the eye turns outward. In which situations is MRA or CTA more suitable? So I would say it’s more suitable depending on what you have available and what — if you know your institution, or where you get the scans, there are some places where they think: Oh, the CTAs are definitely better. And there are some people who don’t have CTA, and then the MRA is better. If you good MRA and CTA at your institution, I would probably get the CTA. They’re slightly more sensitive. But most important is to know: Do they do good MRAs and CTAs? And if one of them is better, then pick the one that’s better. For third nerve palsy, do you get imaging if the pupil is not involved? My understanding is that imaging is only if the pupil is involved. So… Or if the palsy is incomplete. Right, so that’s sort of my point about the caveats. So the answer to your question: Do I get imaging if the pupil is not involved? If the patient is under 50, yes. Without risk factors. So if the patient is young and their pupil is not involved, and they don’t have juvenile diabetes, I get imaging. If the patient is over 50, and they have a complete third nerve palsy with pupil sparing, the answer is I personally do not get imaging. Now, that’s not what I teach non-neuro-ophthalmologists. Because I see lots of third nerve palsies. And so I think because MRI — excuse me — MRA and CTA are so safe, my teaching is: Get the MRI and the MRA or the CTA. Because there’s so many caveats to the rule of the pupil. What about if it just started yesterday? It’s incomplete? So the bottom line is… No, I don’t. If I see someone who is 65 with diabetes and they have a complete pupil sparing third nerve palsy, I don’t get imaging. I see them in six weeks and I send them for the vascular evaluation to their family doctor. Blood pressure, cholesterol, diabetes. And make sure that those things are under control. So I think in that setting, greater than 50, sudden complete third nerve palsy with pupil sparing, it would be reasonable to — if you’re sure — it would be reasonable to not get the imaging. The second question, I think, is the same. I was taught that patients over 50 with a non-pupil… Right. So again, if it’s complete, and pupil sparing, then I would agree that if they’re over 50, you could probably wait. Yeah. All right. Please be definitive in the diagnosis considering the differential so we know the diagnosis in each stage. Okay. I’m not sure how to answer that one. I see some patients come with lagophthalmos, with facial deviation, after they have their teeth pain. Lagophthalmos… So it sounds like if they have lagophthalmos, they have orbicularis weakness. And it sounds like you’re saying they have a 7th nerve palsy. So if a person has an unexplained 7th nerve palsy, they need an MRI with and without contrast. And by the way, when I say MRI, I always mean with and without contrast. I never order an MRI without contrast for double vision. And for that matter, I almost never order MRI without contrast for anything of the head. If you don’t give contrast, you cannot rule out everything you want to rule out. You’ve got to give contrast. What do you mean fellow travelers? That just means… What other part of the exam do you really want to pay close attention to, with someone with double vision? And the answer is pupils and eyelids. Because pupils are important if it’s a 3rd nerve palsy, and eyelids are important if it’s a 3rd nerve palsy or if it’s myasthenia, because of droopy lids, or if it’s thyroid eye disease, because of lid retraction, like that one patient we saw. Do you use botulinum injections in thyroid eye disease? So I assume you mean injections into the extraocular muscles for double vision? I don’t. I don’t use botulinum toxin. I don’t think any of our strabismus surgeons do. Sometimes they’ll use botulinum toxin intraoperatively if there’s a really — if the muscles are really super tight. Or they think there’s scarring of the muscle. I don’t. Let’s see. When you lay ice over the closed eye — so this is for possible myasthenia — aren’t you in fact rest testing? The answer is yes. And in fact, when we published the paper, Golnik and Associates, on ice testing, back in 20… One or two years ago. One of the criticisms is — wait a minute. Just what you said. You’re really doing a two-minute rest test. So maybe it’s just the rest. And the answer is — and I didn’t show you — but that patient that I showed you, with the very positive ice test — we did a rest test right before we did the ice test in that same patient. No change during the rest test. And then immediately after the rest test… Well, not immediately. Within some minutes after the rest test, we did the ice test. In that same patient I showed you. So the answer is: I prefer the ice for two reasons. One, it takes two minutes. Two, I’ve had negative rest tests and positive ice tests. So — prefer. Can you recommend any book? Well, for neuro-ophthalmology? I don’t think there’s really necessarily any books specifically for double vision. There’s a very in depth, complicated book by David Zee on eye movements. But that’s not probably what you want. I think for neuro-ophthalmology, I like… Well, I like the American Academy of Ophthalmology’s Basic and Clinical Science book, one in the series. And that’s relatively inexpensive. But it’s a paperback, it’s about 400 pages. I just actually bought the most recent one, because they change it and update it every five years, and I do a lot of teaching of residents in the United States, and I want to make sure that I’m teaching what they’ve got in the book. Because that’s what’s on their board exams and so on. But that’s a fairly inexpensive book. The other book that I like is a larger hard cover book. The authors are Liu and Volpe. And I think it’s just called Neuro-ophthalmology. I have a copy of it somewhere on my bookcase, but don’t see it immediately. Please explain the sagging eye syndrome. Basically it simply means that as we age, the ligaments that hold our eyeballs in place stretch. Or may stretch. And when they stretch, it just creates a little different force vector, and that can create little amounts, small amounts, of misalignment. It doesn’t cause any big duction or version deficit. But they get small amounts of misalignment. By far the most common is a little eso deviation. And the history is often… Boy, you know, the last some number of months, I had a little bit of… Way in the distance. Like, if I’m driving, I’ll see two headlights, two sets of taillights, side by side. But now it’s… I’m starting… Like television distance. I’m starting to have some double vision there too. And they have these small, relatively comitant esotropias in the distance. Was the thymoma removed from the patient in which you found it? Yes. Did it make a difference? No. And so at some point, maybe I won’t order CTs of the chest. I mean, for ocular myasthenia. If it’s systemic, that’s another story. How long do we give the oral corticosteroid? So what I usually do in myasthenia is… If I’m using the steroid, I tell the patient: Listen, we want to try to use the steroids for a couple few months at most. So we’ll start on the steroids maybe… In the range of a half a milligram per kilogram of prednisone. I’m not sure if I can translate that into all the other steroid preparations. And I’ll use it for a month. See them in a month. Oh, you have a great response. Okay. Let’s gradually taper that over the next two months and try to get you off and see what happens. If they’re not… If they’re just using the steroids, and they’re not on pyridostigmine, and they flare up on the steroid taper, I’m gonna add in the pyridostigmine. You can use both together. But if they need long-term treatment, then I try to get them on the pyridostigmine long-term, and not on the steroids long-term. Hang on. I’m just gonna watch the clock here. I was told I need to stop pretty soon. Is 6th nerve palsy and nasopharyngeal mass related? Well, certainly a nasopharyngeal cancer might cause a 6th nerve palsy. It could cause any 3rd or 4th or 6th, depending on how it’s growing. How do you suspect a skew as opposed to a 4th nerve palsy? Okay. So that’s a good question. Usually skew deviations — the ductions and versions are full. A skew by definition is an asymmetric input to the vertical gaze centers. A 4th nerve palsy — you should fit a pretty specific pattern. Right? We didn’t talk in detail. Although I think we did talk about this in my other webinar. One of the tests for skew is measuring misalignment in seated position, versus lying down position. I must say, I don’t do that much. Skew deviations are usually due to brain stem pathologies. I don’t see a lot of skews. And usually when I do, they’re either comitant or incomitant, but they don’t fit the pattern. So if you can really do your alignment testing and do left head tilt and right head tilt and it fits the pattern of a 4th nerve palsy, I mean, I think it almost always is gonna be a 4th nerve palsy. Now, I could ask this: Does it matter? Whether they have a skew or a 4th nerve palsy? Because if it’s a young person who comes in with double vision, and they have a vertical misalignment, you’re gonna image them. And so that would be the imaging — that would be the management for a skew. You want an MRI. Brain. With and without contrast. If they have a 4th nerve palsy, without any obvious cause, that’s the management. If it was an older individual, and you thought it was a 4th nerve palsy and decided to wait a bit, and it wasn’t getting better, then you would image them. How important is it to determine the site of a lesion in a 3rd nerve palsy? Well, not very important. In the sense that if they have a 3rd nerve palsy, and we talked about the management — you get an MRI. The MRI will — if there’s a lesion, the MRI will show you where the lesion is. I think you can clinically sometimes tell where the lesion is. But I don’t think it’s that important from a management standpoint. Right? It’s either microvascular, which means it’s in the nerve, or it’s somewhere else. Which hopefully will show up on the MRI. What are the indications for prism therapy? How many prism diopters are allowed to be managed? Well, so there are two ways to give prism. One, you can grind it into the lenses. And two, you can use temporary press-on prisms, Fresnel prisms. The Fresnel prisms, you can correct a large amount of misalignment. Of course, the Fresnel prism sticks to the lens. And if you close your eye without the Fresnel, then it’s gonna be blurry. So usually we use them temporarily. Hopefully temporarily. Either we fix them — people with big misalignments, often we do strabismus surgery. But if you can’t, I mean, you can use a Fresnel prism indefinitely. So the downside to the Fresnel is it definitely makes your vision a bit blurry in the eye with the Fresnel. You would never ever use Fresnels — I’ve seen people with Fresnels on both sides. That makes no sense. The main limitation, though, of the ground-in prism, number one, is you can probably… Certainly more than 20 prism diopters would be very difficult to put in glasses, grind into the lenses. And then the other issue with prism, whether it’s Fresnel or ground-in, is what I mentioned. And that is: If the misalignment is very incomitant, people just don’t like the prism very much. And then strabismus surgery, if it’s stable, strabismus surgery is something that could be considered. So the indications for prism therapy would be stable, comitant misalignments. That would be the best indication. The patient you showed an eso 6 prisms, both sides could have bilateral 6th? I think that may be the fellow with thyroid. He definitely had bilateral abduction deficits that look… If you just look at the motility, look like bilateral 6th. But his eyelids told you that he’s got thyroid eye disease. How often do you recommend Hess tests to be done? So I never do Hess tests. When I was a resident, I did it a lot. If you have a Hess screen, it can be very helpful, if you know how to use it. That’s probably another talk. But I never use a Hess screen. Because number one, I don’t have one. But I’m certainly not looking for one. I didn’t — someone noticed that I did not mention edrophonium, otherwise known as Tensilon testing. In the US, at least, it’s hard to get it. We used to get little small amounts, like single use amounts. Now you have to buy a big bottle that expires and you have to throw it away if you don’t use it. Also, edrophonium can stop your heart. I had a couple of people we did that to, doing Tensilon tests in the office. I haven’t done a Tensilon or edrophonium test in at least 15 years, maybe 20. I rely on the other methods that we talked about. That doesn’t mean you can’t do them. You do have to be cognizant that the patient’s heart might stop. Sometimes people, whether you do an ice test, they say… Oh, this is getting cold. And I say… Oh, we have a medicine that we can use, but it might stop your heart. That shuts them up pretty fast. What is conjunctival epithelial melanosis? Very good question. I probably couldn’t give you a very erudite answer to that, because I’m not an anterior segment doc. And so I will decline to answer that question. It definitely has nothing to do with double vision. Does the management depend on the site of the lesion of 3rd nerve palsy? Not really. It’s either a nerve, peripheral nerve — so microvascular — or something pushing on the intracranial nerve. Aneurysm, tumor, or possibly a brain stem issue. So I don’t think the management depends on the site. It depends on what’s causing the problem, though. How can we order Fresnel prism? I don’t know the answer. I mean, in the US, what I do is I send them to the optician. With a prescription that says: Fresnel prism. Sorry. I don’t know if there’s a way. You probably would have to Google that. The problem, of course, is… If you’re gonna give Fresnel, you need all sorts of different strengths. So when you’re using prisms, you put the correction to one eye, not dividing the amounts. Yes. If you’re grinding the prism into the lenses, it’s just easier to make the glasses symmetric. So if they need 10 prism diopters, base-out prism, I give 5 base-out, OU. If it’s Fresnel prism, though, you don’t split it. Because then they’re gonna have blurry vision in both eyes. Because the Fresnel gives them blur, when you look through the Fresnel. That is the end of the questions. So thanks, everybody, for participating. And I look forward to further neuro-ophthalmology webinars. I would, if you’re interested in neuro-ophthalmology, take a look at old Cybersight webinars. I’ve done probably… I don’t know. A dozen or thereabouts. They should all be recorded. So thanks very much for your attention. Have a great rest of the day. However much of the day that might be. And we’ll see you in the future around the world or on Cybersight webinars.
2 thoughts on “Lecture: Management of Neuro-ophthalmic Causes of Diplopia”
This was really enlightening
Everything is good but I have a question