This is the first of of two lectures designed to improve the participant’s ability to evaluate the patient with double vision. Part 1 covers the relevant portions of the history and examination, fusional disorders, and ocular motor cranial nerve palsies.
Lecturer: Dr. Karl Golnik
(To translate please select your language to the right of this page)
DR KARL GOLNIK: Greetings. This is Dr. Karl Golnik, coming to you from Cincinnati, Ohio, United States. For me, it’s 9:00 a.m.. Welcome to everyone from around the world, in whatever time it may be for you. Hopefully this is convenient as it is for me. Some of you may have attended my last webinar, when we talked about — I think it was part two of optic neuropathies, and I said we would try to do another optic neuropathies webinar. We will, but we already advertised this topic, ocular motility. So we’ll probably do a couple of webinars over the next couple of months on this topic, and then go back and finish up with optic neuropathies, including things like papilledema and toxic and nutritional optic neuropathies. But today, we’re gonna talk about ocular motility part 1. I’m hoping this will be part 1 of just two parts. And we’re gonna talk about the evaluation and about cranial nerve palsies. In particular, ocular motor cranial nerve palsies. As you know, you can type in questions throughout this talk, and we will try to address those at the end of the webinar. So my objectives are that when we’re done, you’ll be able to describe the pertinent portions of the history and exam for a patient with an ocular motility problem, and you’ll be able to describe an approach to a patient with ocular motor cranial nerve palsy. So I’m gonna start early on, with a polling question. And this is something that you will be able to answer with your keyboard. The question is — and don’t answer yet, I don’t think. We have to introduce the polling for you, I believe, on top of the slide, that the Orbis host will do. But the question is: What is the most — and let me move that out of the way, if I can. What is the… Okay. Sorry. Same question. What is the most important question for the patient who has double vision? So usually the reason we’re evaluating patients with ocular motility problems — usually — is that they have double vision. They come in and say: I’ve got double vision. That’s my chief complaint. So there’s always one question that is, to me, as a neuro-ophthalmologist, more important than all the other ones. So I would ask you to go ahead and vote. Is the most important question — is there any pain? That would be the first box. The second question: When did it start? Third question: Does it go away when you cover each eye? And fourth question: Is it present at distance and at near, both? So please vote. And I’m not sure if I can tell if you’re voting or not. If you are voting, I can’t see. So we’ll let you vote for a few more seconds, by clicking the appropriate box. Which just went away from my screen. Is there a way to… Ah-ha! And there are the answers that we have from some of you. And the majority of you indeed picked my favorite most important first question. At least, from a neuro-ophthalmology standpoint. And that is: Does it go away when you cover each eye? I think the other questions are all important questions. And certainly somewhere during the history I’m going to ask about those things. Thank you. We can put the polling slide away. So why is that the important question? So the first question is, of course: I ask them what I just said. Which is — does it go away when you cover either eye? Because you want to know — first thing is: Is this monocular double vision, or is it binocular? Because if it’s monocular, meaning I can close my left eye and it’s gone, but when I close my right eye, it’s still there — if it’s monocular, it is never neurologic. Never. So I wanna know, as a neuro-ophthalmologist. Now, as an ophthalmologist, you’re gonna wanna know, because you’re gonna be thinking about two completely different things. Whether it’s binocular or whether it’s monocular. So when it’s monocular, things like even just a little bit of uncorrected astigmatism can cause — I wear glasses on occasion. And when I done, I have a little monocular double vision. And when the patient says — oh, no, it’s only present in my right eye, I say I bet it’s sort of like a ghosting or superimposition of the images. It’s not two separate images. And the patient usually says yes, that’s right! You’re a good doctor. You know exactly, without even telling you, what it looks like. So monocular double vision is almost always gonna be a ghosting, a superimposition of the images, not two separate images. In fact, if the patient tells me it’s the right eye, and it’s two separate, separated images, then I ask them how they know it’s the right eye. Oh, because when I close my right eye, it goes away. What about when you close your left eye? I never tried that. So I think if they tell you it’s two widely separated images, it’s probably not monocular. So things like uncorrected astigmatism, anything that affects the cornea or lens could possibly do it, if they have an implant, an IOL, that’s misplaced or subluxed, that could do it. So the vast majority of monocular double vision is going to be refractive or media in nature. Rarely an epiretinal membrane can do it. So if you can’t find anything in the front of the eye, then look closely at the macula for an epiretinal membrane. And then there’s something called palinopsia. That is neurologic. It’s not really true double vision, though. That’s the phenomenon usually with parieto-occipital lesion, where people will say — yeah, I’ve got double vision. What do you mean? Well, this morning, I looked — there was a pot of flowers on my table. Now I can look over at that wall and there’s a pot of flowers superimposed on the wall. So they’re seeing two different things. Not two of the same thing. That’s palinopsia. As a neuro-ophthalmologist, practicing for 27 years, I don’t think I’ve ever seen a case of that. So you can imagine it’s fairly rare. And you can assess this pretty quickly, with just a pinhole. Even my patients, who are often sent to me being worried about a brain tumor or multiple sclerosis, can understand that when I throw up that little pinhole in front of their eye with the monocular double vision, and it goes away, they probably don’t have a brain tumor or something serious. Obviously you’re gonna refract them. If you have to, sometimes we’ll do corneal topography, looking for some sort of irregular astigmatism. Obviously we’re gonna look at the corneal surface in the lens and of course fundus, if you can’t find anything else causing the problem. But the bottom line with monocular double vision is don’t send that patient to a neuro-ophthalmologist, and don’t start measuring alignment and so on, because this is not gonna be a problem with ocular misalignment. And it’s not gonna be caused by a neurologic problem. So the rest of this talk will concentrate on binocular double vision. Meaning it goes away when I cover my left eye. It goes away when I cover my right eye. It’s only there with both eyes open. So once we ascertain that, I like to ask them — hey, is it horizontal or not? I mean, are the images right side by side, or are they in some other orientation? Why? Because if they say it is, you kind of eliminate all those wacky oblique muscles and the superior-inferior recti. It’s probably gonna be a problem with the horizontal recti muscles or other things that we’ll talk about. And then the other question is: Is it comitant or not? Now, comitant — obviously we don’t ask the patient is it comitant. Whoops, sorry. We ask the patient does the double vision change when you look left or right or up or down? Is there more misalignment? Now, patients don’t always know the answer to this. Sometimes I have engineers who bring me graphs and cosine-sine-tangent drawings of their double vision. But basically it means: Is there about the same amount of misalignment in each direction? So these figures I’m showing on the right — in the upper picture, the patient is looking straight ahead, and you can see that the person looks to have an esotropia. The right eye looks to be turned in slightly. When the person looks to the right, in the middle frame, now there’s a much larger misalignment of the eyes. But when the person looks to the left, there’s really no misalignment. So this would be an incomitant misalignment. Most neurologic misalignments are incomitant. And most — born with congenital problems — are relatively comitant. There are exceptions to both of those statements. And then don’t forget — oftentimes my residents will hear double vision and they’ll spend a real lot of time looking at the eye movements, which is fine. Looking at the alignment of the eyes is fine. But don’t forget what I call the fellow travelers. The fellow travelers are other parts of the eye exam that are very important. Why? Because things that cause neurologic problems like third nerve palsies, myasthenia gravis, can affect other parts of the eye exam. In particular, the eyelid position, and the pupils. So we’re gonna look closely — and you can see in the upper diagram or photo there’s slight asymmetry. Now, you might say — is this left upper eyelid ptosis, or is this right upper eyelid retraction? That’s a good question. In this case, it was actually right upper eyelid retraction, in a patient with early thyroid eye disease. Although the patient thought there was a droopy left lid. The middle picture is supposed to show this conjunctival injection. Actually, there’s some arterialization of the conjunctival vessels, and this was a person who was treated for months with conjunction, and then they developed double vision, and they had a low flow cavernous sinus fistula, causing double vision in these arterialized conjunctival vessels in the left eye. And then the bottom photo is someone with more obvious exophthalmos, in addition to upper and lower eyelid retraction. And then sometimes just the head position of the patient will tell you they’ve got a head tilt, they’ve got a chin up or a chin down position, because they either are consciously or subconsciously putting their eyes in a position that minimizes or eliminates the double vision. And we’ll try to talk a bit more about that, as we go through the talks, this one, in part two. And just to make sure we’re all on the same page, when we talk about ocular motility, we talk about the ductions, which are the movements of one eye, when the other eye is covered, we talk about versions, which is when you ask the patient to look up, down, left, and right, with both eyes open, and then again, we talk about comitant, which I just defined. And when we talk about misalignment, we talk about esodeviation or ET, when the eyes are turning inward relative to one another, we talk about exotropia, the eyes turning outward relative to one another. I’m just gonna move — I can see myself here. I’m not sure — sort of in the way of people — I’m not sure you’re seeing this or not. I’m gonna try to get rid of it. And then we talk about hypertropias. Now, traditionally, and by convention, we usually label the hyper eye. That said, if I know for sure that the hypo eye is abnormal, I might call it a hypotropia. So obviously, if there is a vertical misalignment, you have to label right hyper, left hyper, or left hypo, or right hypo. If it’s esotropia or exotropia, you don’t have to necessarily label it left or right. So when someone says I have double vision, you need to know the pattern of ocular alignment. And the only way to know the pattern is to measure it in some way. Fortunately, our measurement methods are really simple, and it does not require a lot of technology. And the gold standards are the cover-uncover and the cross-cover testing. Now, Hirschberg testing, where you look at the corneal light reflexes, can be done, but I don’t wanna hear about Hirschberg if the patient has decent vision in both eyes, meaning they can fixate on a distant target, and if the patient is cooperative. So obviously in a baby, it may be hard to get them to fixate. If someone is blind in one eye, then a Hirschberg test is fine, because they can’t fixate with the other eye. But if the person is able to sit in your chair and is able to respond to your commands, I don’t wanna hear what the eyes look like. I want to know what the alignment is. People can look esotropic. They can look exotropic. I don’t care if they look it. I want to know: Are they? And the way you know are they is by doing cover-uncover and cross-cover testing, which I’ll try to demonstrate with videos. So here’s a patient who, if you look at her when she’s looking straight ahead, her eyes don’t really look crossed. And when I show this to neurologists, they say — her eyes look fine. But they aren’t fine. And so what’s happening here is she actually was born with a congenital esotropia. That’s not why I was seeing her. And I said… Let’s get a video, so I can try to demonstrate this principle. So the first step in checking alignment is to make sure that — I use their best correction, if they need correction. I have them look at a target at the end of the room. Usually a single letter. If you’ve got computerized eye charts, then isolate a single letter. If you don’t, then ask them to look at a single letter at the end of the chart. Obviously, the letter has to be big enough for them to see with each eye. So you can’t throw up a 20/20 letter if they’re 20/40 in one eye. You’ve got to throw up something — I usually throw up a letter that’s at least a couple lines bigger than their best corrected vision in the worse eye. So they can easily see it with each eye. I don’t just throw up the 20/400 or the 6/30 E, because if they have a small misalignment, that big letter may be as big as the misalignment. And you might not see movement of the eye. So I throw up a distant target and ask them to look at the target. I check with each eye to make sure — you can see that letter? Yes. I cover the other eye. Yes. I see it. And then every time I do a cover test, I ask the patient: You got it? Do you have it? Do you have it? Every time. Yes, I have it! But I ask them. Because some patients just won’t switch fixation. And my residents will say — yeah, that patient looks like they’re exotropic or esotropic, but, you know, there was no movement on the cover-uncover test. You have to verify that the patient is actually looking at the letter. They just won’t always do it. So in her case, what you’re seeing here is that she’s looking at that distant target. And every time we cover the left eye, nothing happens to the right eye. But every time we cover the right eye, both eyes move outward. Sorry, the left eye moves outward. Why? Because this person has an esotropia. It happens to be an amblyopic left esotropia. And she is choosing to fixate with the right eye. So when we cover the right eye, the left eye has to move out to find the target, and when we cover the left eye, nothing happens. Because the patient is choosing the right eye with the better visual acuity to fixate. So this is a cover-uncover test. Let’s look at another patient who has intermittent double vision. So there’s a young guy. Intermittent double vision. He’s not having double vision at the moment. So when we do the cover-uncover test, now with my hand instead of an occluder, you can see that if you watch the uncovered eye, there’s no movement. Don’t watch the eye behind your fingers! Sometimes people get confused. The cover-uncover test only requires you to look at the eye that is uncovered. When you take your hand away, you’re letting the patient refixate. That’s the difference between a cover-uncover and a cross-cover test, which I’ll demonstrate in a moment. So in this case, in this patient, the uncovered eye, the uncovered eye, doesn’t move. He is orthotropic. Orthotropic. Now, I’m gonna demonstrate — same patient. With a cross-cover test. So here’s the cross-cover test. What’s the difference? The difference is you’re not allowing the patient to regain fusion. And clearly, when you do a cross-cover test, you now see obvious eye movement, and the eye was moving inward. So this person has an exophoria. A latent misalignment. And in fact, they’re having double vision intermittently because the person was born with this exophoria, and on occasion, their brain, as he’s getting older, just can’t control it. And when he can’t control it, he gets an exotropia. So you can say that he has an intermittent exotropia. Right now, during our exam, it’s an exophoria. He’s controlling it, unless I do a cross-cover test. Now… If you have prisms, then you can measure how much exophoria does he have. And you simply put the prism bar up, and take a guess, initially, and you are trying to neutralize any movement. So you swing your hand back and forth. Got it. Got it. Got it. And when you see no movement, you now know that this is a 10-prism diopter exophoria. You can now very quickly determine whether this is comitant by simply turning the patient’s head to the left, doing your cross cover test — no movement. Turn the patient’s head to the right. No movement! Up and down! Ah. It is a comitant exophoria. Now, if there’s a little bit of movement, and you say — it’s 10 when he’s looking straight ahead, 12 when he looks to the left, 12 when he looks right — that’s relatively comitant. Okay. So that’s cover-uncover, and cross-cover testing. That’s the gold standard for measuring alignment. You all can do this. And should do this. So when we talk about double vision — so that’s when I’m gonna talk about the exam. I think… Is there anything else I wanna say? I don’t think much about the exam, except obviously you want to look for those fellow travelers. You’re gonna look at the eyelids closely. You’re going to look at the pupils closely. And that’ll become more apparent as we talk about various entities, as we go through why it’s important. All right. So when we think about double vision, I usually break it down into — there’s a whole bunch of different things. And I tell patients — I often give my residents five hours of lectures on double vision. Lots of things can cause it. So there can be fusional problems. There can be problems with any one of the ocular motor cranial nerves. There can be a problem with the extraocular muscles, like thyroid eye disease. There can be problems at the myoneural junction, like myasthenia gravis, and there can be problems with alignment related to inter or supranuclear problems, and in the next ocular motility part 2, we’ll cover muscle, myoneural junction, and inter and supranuclear problems. We won’t cover those today, because we only have one hour. So what about some of the fusional things? And I’m gonna talk about some of these I see fairly commonly. So there’s a decompensated phoria. Which is usually comitant. Something called divergence insufficiency. And convergence insufficiency. So let’s just take a look at a young patient. And this is actually a patient who… I’ll try to move that to the side. This is actually a patient who is younger. He has binocular horizontal double vision. He thinks it’s about the same, no matter where he looks, and it’s worse when he’s tired. Sometimes when doctors hear that — oh, worse when you’re tired? Isn’t that that myasthenia? Certainly not necessarily. So he thinks it’s worse when he’s tired. Maybe if he has an alcoholic drink or two, it might be worse. He has full ductions and versions. So there’s no deficits in the eye movements. He has a 14 prism diopter exotropia in primary position. It is comitant. So it’s 14 everywhere. So this would be a typical sort of a story of a broken down congenital phoria. He no longer can have this. And the history is often — yeah, you know, for some years, I’ve had an occasional double vision. Once in a while, someone will tell me — hey, your eye looks like it’s drifting out to the side. It’s usually that kind of a history. Gradual, but it’s just gotten worse and worse, and now it’s happening most of the time. And the treatment usually is — depending if it’s an exophoria, you might give him some exercises. It could be prism in glasses. It could be even some eye muscle surgery, depending on the patient and how they want to address it. So this is not gonna be neurologic. I’m not gonna order — if I see this story, and I have this exam, I’m not gonna be ordering neuroimaging. I’m not gonna be ordering testing for myasthenia, as long as I don’t see any other things or hear anything else that would be consistent with other diagnoses. So isolated. Been going on for a while. Getting worse. Full ductions and versions. Comitant. Misalignment. Exophoria. This is probably one of the more common things I see in patients over the age of 50 or so. The usual story is: You know, over some months, I don’t know how long exactly, but some months, I’ve been having some double vision. It’s only in the distance. When I’m driving, looking down the road, I see two. If they’re side by side, the stripes on the road cross together, sometimes. It definitely goes away. In fact, when it happens, I close one eye, so I can drive, and not have the double vision. Only in the distance. Never within arm’s length. On exam, the person has full ductions and versions. They have a small comitant esotropia only at distance. And so if we could bring in the audience polling slide, I’m gonna ask you what you think. What is the diagnosis? Is this convergence insufficiency? Is it divergence insufficiency? Is this consistent with a 6th nerve palsy? Or could this be myasthenia gravis? What’s the most likely diagnosis? Given the story. Some months, getting a bit worse, decided to see the doctor, because it’s bugging me. I’m tired of closing my eye, looking down the street. And we’ll give people a few more seconds to vote. 10, 9, 8, 7, 6, 5, 4, 3, 2, 1. Let’s close the polling and see what the audience says. So very good. About half of you had the correct answer, and that is divergence insufficiency. A small percent said 6th nerve palsy. Myasthenia and convergence insufficiency. So I think the only — my second choice, the thing that would concern me most, other than divergence insufficiency, would be myasthenia gravis. So if I had to pick my second one on this, I would put myasthenia. Why? Well, myasthenia can mimic any ocular misalignment. It can cause a comitant or incomitant misalignment. Certainly if someone has a unilateral 6th nerve palsy, it should not give you a comitant misalignment. You might have a 6th prism diopter esotropia in primary position, but if it’s a left 6th, in left gaze, it should get much worse. And in right gaze, it’ll probably go away, if it’s a mild 6th. Now, bilateral 6ths, which are pretty rare, could of course cause a comitant misalignment, but that wasn’t the option I gave you. And then convergence insufficiency, I think, would be the worst answer, because convergence insufficiency means your eyes aren’t going to converge well. So the symptoms are at near only. And it’s exodeviation. Not esodeviation. So that would be the answer that makes the least sense to me. All right. Let’s move on. So here’s a patient. Double vision. About a week’s worth. And then it went away. It went away because his eyelid closed. And so he is occluding the eye. And so you can see the thumb sign there. Which means I’m holding that eyelid open. I’m trying to show you his pupils. Hopefully you can see that. On my screen, it looks pretty good. He’s got significant anisocoria. Both pupils react a little bit, but certainly the right pupil is big. He’s got complete right upper eyelid ptosis, and as we saw in the… When we looked at his versions, which I think will loop, he has no elevation. He has no adduction, and no depression. But good abduction. So he has, I hope, what is a fairly obvious right 3rd nerve palsy, with pupil involvement. So hopefully for this audience, I don’t need to reiterate all of the anatomy, but I’ll review it briefly. As you know, the 3rd nerve contains the parasympathetics that run to the ciliary body and the iris sphincter. It also contains the innervation to the levator, and inferior and superior medial recti, in addition to the inferior oblique muscle. It starts in the brain stem. This is a cross section through the midbrain. Here is the 3rd nerve nucleus. It runs forward through the brain stem. When a cranial nerve in the brain stem — it’s not actually called the nerve. It’s called the fascicle. So this is the 3rd nerve fascicle. It becomes the nerve when it exits the brain stem here. But it’s a fascicle here. And you can have various brain stem syndromes, which we may talk a bit about in part 2. But if there’s a lesion in the shaded area too, this is the red nucleus. So this person is going to have a 3rd nerve palsy, because of the fascicular involvement, and a contralateral rubral tremor. So they like to ask this on examinations sometimes. If the lesion is here, and that’s, by the way, called Benedict’s syndrome. I’m not a big fan of eponyms, but… And if it’s a problem here, you get the corticospinal tract, and the 3rd nerve fascicle, and you get an ipsilateral 3rd nerve palsy, and a contralateral hemiparesis. This is also known as Weber’s syndrome. There’s another couple of syndromes I’m not gonna mention, because they usually aren’t on the exams. But you can look it up. There’s Nothnagel’s and Claude’s. That 3rd nerve then proceeds from the midbrain forward. It runs under the posterior clinoid process, it runs over the petroclinoid ligament into the cavernous sinus here, and then through the superior orbital fissure. You can see it runs right along with the 4th nerve, which we’ll talk about momentarily. Important part of the anatomy for us, and one of the reasons we worry a lot about 3rd nerve palsies, is that as it runs forward from the midbrain, it runs right under the origin of the posterior communicating artery. And you can see that artery retracted here. And you can imagine that if an aneurysm forms at the origin of the posterior communicating artery, if it points laterally and downward at all, it’s going to push on the 3rd nerve. And so that’s why we worry about acute 3rd nerve palsies, often painful, for aneurysms. And there’s the rule of the pupil, which I think is under some debate these days, as to how important that rule of the pupil is. But basically the rule is based on this pathology, and that is that the pupillomotor fibers, depicted here in the light blue, tend to reside on the outside of the 3rd nerve, in the inferomedial area, which is right where an aneurysm is going to push, if it forms. So in an aneurysmal 3rd, or a compressive 3rd, for other reasons, then those fibers on the outside of the nerve are most likely to be compressed. On the other hand, if you have the more common microvascular, diabetic, hypertensive 3rd nerve palsy, it tends to be more of a core infarction, which can spare these fibers on the outside of the nerve, which have other collateral blood supply. And so we talk about pupil sparing, versus pupil-involving 3rds. I think I have an example of a fellow with an almost complete 3rd. Here he is diabetic, he is 70-something. You can see that his left eye does not move up well. It does not adduct well. And it does not depress well. It does a little bit. He’s got trace elevation, trace depression, trace adduction, maybe. Good abduction. Significant ptosis. You’ll notice — I’m not showing you his pupils specifically, but you’ll notice when his eyes are open that his pupils are the same size, and they do indeed react symmetrically. So this is an almost complete pupil-sparing 3rd nerve palsy, in a 75-year-old diabetic. He has mild to moderate pain. This is someone who I don’t image. If this is an acute, sudden onset, in this age range, pupil-sparing complete or nearly complete 3rd, I don’t image it. Pretty much I’m gonna image most other people. That’s the debate. Jeez, you image everybody with any kind of 3rd nerve palsy. I still reserve imaging for people who don’t fit in this guy’s category. Let’s take a look at another patient. So this is gonna be an audience — we don’t put the poll in yet. These are gonna be your choices when we put the poll in. So this is a video of another fellow with double vision. And I’m not gonna really describe much. I’m gonna let you watch the video. We’ll let it loop at least once. And I’m gonna ask you… What do you think this patient has? Is it myasthenia? Graves’ disease? Left 3rd nerve palsy? Left 4th nerve palsy? He’s got dark brown irises. I’m trying to show you those irises. I will give you — since it may be hard to see, because of the color — he does have a bit of anisocoria. The left pupil slightly larger than the right. They both react symmetrically. And you can see his eye movements. So let’s go ahead and throw the poll in, if we could. And let’s see what you guys think about this. Is this myasthenia? Is this Graves’ disease? Is this a left 3rd nerve palsy? Is this a left 4th nerve palsy? And… Give you another 10 seconds. 9, 8, 7, 6, 5, 4, 3, 2, 1. Close the poll. And let’s see what people say. All right. So kind of a variety. So this is indeed — the majority of you are correct. Although it’s not a huge majority. This is a left 3rd nerve palsy. Now, this goes along with the rule of — it doesn’t always look like it does in the textbook. So if you’ve got an aneurysm, or you’ve got a tumor, this fellow happened to have nasopharyngeal cancer — pushing somewhat on his left 3rd nerve. It’s not gonna be the complete 3rd nerve palsy. And as you watch this guy, you’ll notice, of course, the anisocoria. He’s got some ptosis. But when he looks up, that left eye just doesn’t quite elevate all the way. And when he looks — it does abduct all the way. When he looks down — look at the right eye. It doesn’t quite depress all the way. And when he looks to the right — look at the sclera. He buries the sclera when his right eye adducts. But when his left eye tries to adduct, it does not. Now, how would you… Those of you who weren’t sure, and said — well, maybe that’s a 3rd — how would you be sure? You would look at his alignment. In primary position. He has got a small exotropia. Because his left eye is not adducting fully. When he looks upward, so you simply put the chin down, do your cover-uncover test, he’s got a left hypotropia. When you put his chin up, and he looks down at the chart, he now has a left hypertropia. That is the pattern of a 3rd nerve palsy. So whether he’s got a complete 3rd nerve palsy, like our other guy, who had a trivial microvascular 3rd, diabetic, it’s gonna get better — this guy’s got something that killed him. But it’s mild. So it’s not gonna necessarily look like the textbooks and be complete. This is when you want to try to catch the problem as early as possible. So you need to look for patterns. And his pattern is the pattern of a left third nerve palsy, with pupil involvement. All right. We have another person. This guy has… Guess what? Double vision. His story is he’s about 40. He was playing football. European, not American. He got tackled. And he hit his head, and he got double vision. Almost right away. His double vision is oblique. It’s sort of up and down and side by side. And you are seeing a quick video, and I should have put a different… I just really wanted you to look at his eye movements. I’m gonna run the ductions — or sorry, the versions again. Let’s just look at his versions. And I’m not gonna ask — this is not a polling question. But I’m gonna let you look at it. And I keep having him look down and to the left, down and to the right. There’s a reason for that. Let me just run those versions one more time, and we’ll look at his alignments in a minute. So this is probably the most common — one of the more common things I see. When they see a neurologist, and the neurologist says his eyes look fine! Why does he have double vision? And he has a right 4th nerve palsy. We’ll come back to him in a minute. Okay. This is a good question. This is a polling question. And the question — and this may be a little — we’ll see if it’s a little bit tougher. The question is, if you know your anatomy, a left 4th nucleus lesion causes which of the following? So a left — I laser your left 4th nerve nucleus, or you have a smaller lacunar infarct or an MS plaque — does that cause a left hypertropia, a right hypertropia, incyclotorsion, or none of the above? So a left 4th nerve nucleus. 10 more seconds. 10, 9, 8, 7, 6, 5, 4, 3, 2, 1. Call it. All right. Well, the majority is still in the right. So why does a left 4th nerve nuclear lesion cause a right hypertropia? Let’s look at the answer. You can remove that polling thing, if you could. So… It of course has to do with the anatomy. So here’s the anatomy. Here’s the 3rd nerve nucleus. We just talked about that. In the midbrain. Here’s the 4th nerve nucleus. Now, unlike any other cranial nerve, right, the 4th nerve exits the brain stem posteriorly. Not only does it exit the brain stem posteriorly — it comes back, goes through the superior medulla cerebellum, and goes like this. So when we see what looks like a right 4th nerve palsy, if we’re talking about the peripheral nerve, right — that right 4th nerve started in the left midbrain. In the nucleus. So a nuclear 4th is gonna give you what looks like a contralateral 4th nerve palsy, clinically. So that’s the bit of information you need to know to get that preceding question correct. And then that 4th nerve — and I’ll show you a better schematic in a moment. It comes out, it loops around, and here it comes forward, right near the 3rd nerve, right near the cavernous sinus. Here it is with the 3rd nerve. It’s very small. And that’s why the 4th nerve, one of the reasons why the 4th nerve is susceptible to head injury. It’s a very thin nerve. It’s a very long nerve. It loops all the way around your brain stem from the back. It resides with the 3rd nerve in the lateral wall of the cavernous sinus. Not within the body of the cavernous sinus. In the lateral wall. It proceeds forward through the superior orbital fissure outside of the annulus of Zinn. So here’s the trochlear nerve. And then here’s that anatomy. So the 4th nerve comes out the back of the brain stem, it decussates here, in the superior medulla cerebellum, comes out, and loops around. So what looks like the left 4th nerve starts in the right 4th nerve nucleus. And here’s a schematic I think is helpful to sort of memorize, when you’re thinking about what does the 4th nerve and the superior oblique muscle do? As you know, the 4th nerve only goes to the superior oblique. So if you look at the center image here, you can see — and if you think about the force vector, what happens when that muscle contracts, that muscle is inserted behind this midline. So when the force contracts, the eye is gonna depress. And it’s inserted temporal, lateral, to this midline. So you’re gonna have incyclotorsion. And indeed, the main function of the superior oblique muscle is incyclotorsion. The secondary action is depression. However, when the person is looking towards the nose, now that force vector is acting totally as a depressor. And that’s why when you see a deduction deficit, the deduction deficit’s most apparent looking down and toward the nose. Or looking down and away from the 4th nerve palsy. When the person is looking out towards the temple, now the force vector is almost entirely torsion. But you don’t see torsion when you look at the eye. You don’t see it. You don’t see a duction deficit, because it’s hard to see the torsion. So if you can remember that anatomy, that force vector, and how that trochlea works, the trochlea being the pulley that the superior oblique muscle or tendon goes through. So let’s look back at our guy. His eye movements look pretty good, except when he looks down and in, down and to the left. Watch how this eye, compared to the other eye — look how far down that eye gets down, compared to the other eye. And let me — I’ve still got that — I should have edited that. So let’s look at that one more time. This is all you’re gonna see. You’re not gonna see much more than this in a 4th nerve palsy. Look at that. Look at this eye. Compare it to that eye. Right 4th nerve palsy. Now, of course, you’re going to do tests of alignment. So in primary position, he’s looking at a distant target, he’s got a very small right hyper. Hard to even see. I’m gonna do a cross-cover testing, to bring it out a little better, so you can see it. See that? Eye up. Down. Eye goes up. Eye goes down. That’s it. That’s it. That may be all you see with a 4th nerve palsy. This is a partial 4th nerve palsy. It’s not gonna hit you over the head. So a tiny right hyper. What are you gonna do? You’re gonna quickly determine the pattern. Now he’s got more misalignment. And in the patient who’s with it, he’ll say — oh, those letters got further apart! So he’s got a bigger right hyper in downgaze. What happens when he looks up? So he puts his chin down. Oh, those letters went together. Now there is no misalignment. What about when he tilts his head to the right? Well, bigger. See? The misalignment — watch. Now, I’m doing a cross-cover test, because it’s just easier for to you see it in the video. He is tropic with a cover-uncover test. What about when he tilts his head to the left? The letters come together. And he has no significant misalignment. So why does that happen? I think it happens because when you tilt your head to the… Let’s think about this. A right 4th nerve palsy… So when you tilt your head to the right, both eyes are going to compensate, and your left eye is going to excyclotort, and your right eye is going to incyclotort. So when your brain says — incyclotort! Your 4th nerve is supposed to be working and your superior oblique muscle is supposed to do it. But it doesn’t. There’s a problem. It won’t incyclotort. So the misalignment is bigger. But when you tilt your head to the left, now you’re asking your right eye to excyclotort. Well, that’s what it’s doing, because you’ve got a 4th nerve palsy. So it minimizes the imbalance. Now, why does the vertical misalignment get bigger when you tilt your head towards the 4th nerve palsy? Your brain says… Incyclotort, right eye! And your superior oblique muscle is not working. Because the 4th nerve is not working. There’s another muscle that is an incyclotorter. The superior rectus. But the primary action of the superior rectus is elevation. So what happens? The superior rectus fires. Intorts and elevates. More misalignment. Now, here’s a patient you might see also had a head injury. And she has no vertical misalignment in primary position. But her story is — my vision very blurry when I look straight ahead. However, I can get rid of the blur by covering either eye. So there’s something going on binocularly. Now, watch when she looks to the right and the left. When she looks to the left, she has a right hyper. And when she looks to the right, she has a left hyper. So let’s… She’s a little eso. So look at this. This eye is here. This eye is not moving downward. You confirm that with your cover-uncover testing. And look here. Neither eye depresses well in adduction. This is a bilateral 4th. Why does she have no vertical misalignment? Because they’re pretty symmetric. And when you have a unilateral 4th, the eye in question will go up. Bilateral, they both go up. Why is she having blurry vision if there’s no vertical misalignment? Because the torsion adds up. So the eye goes up. And this. And the other eye goes up. And this. So now she’s got this. She’s got these overlapping but torsional problems. That’s why when you cover either eye, it gets better. So don’t be fooled by bilateral force. Look at the alignment. You’ve got to determine the pattern. If you see what we call shifting hypers, left hyper in right gaze, right hyper in left gaze, think about bilateral 4ths. Here’s another patient with bilateral 4ths. She’s got no misalignment in primary. But watch what happens when we tilt her head in each direction. Right hyper in right head tilt. And left hyper in left head tilt. It’s subtle. But it’s there. So bilateral 4ths. Motor vehicle accident. Closed head injury. So remember this? And you can figure out what you need to figure out about 4th nerve palsies, I think. Another fellow, older individual. With double vision. I don’t think I have a polling slide for this. I don’t think. I might. Hold on. Let me just see. No, I don’t. Okay. Let me play this video again. So what do we think? Double vision. It is horizontal. It is binocular. Started one week ago. So this is pretty subtle. And it’s so subtle, I’m gonna look at this and say… Well, the eyes look pretty good. I think maybe there’s a mild abduction deficit on the left. How do I know for sure? I’m gonna look at his misalignment. Look at the letter at the end of the room. Yes, he’s a little esotropic in primary position. When he looks to the left, he has a bigger esotropia. And when he looks to the right, he’s orthotropic. So he has the pattern of a mild left 6th nerve palsy. 6th nerve. So now we’re down in the brain stem, further down in the pons. You can see here is the 6th nerve nucleus. Here’s part of the 5th nerve nucleus and part of the 7th nerve nucleus. Hold on. Where are we? Yeah. And so all of these nuclei start in the same general place. Or live in the same general place. The 6th nerve runs forward through the PPRF, the horizontal gaze center. And through the corticospinal tract, so you can see other brain stem syndromes with 6th nerves and contralateral hemiparesis. You can see gaze palsies. That’s the subject of part 2 of ocular motility. Next month, I think. Unlike the 3rd and 4th nerve, it exits the brain stem here in the pontomedullary junction. It runs up this bone, the clivus, underneath the petroclinoid ligament, also known as Gruber’s ligament, through a canal — for extra credit, called Dorello’s canal — into the cavernous sinus. Now, you can see that in this area right here, you can imagine the other side of the brain stem. There’s a place in here on the clivus where both 6th nerves exist in relative isolation. So occasionally, I will see metastases to the clivus, clival chordomas, presenting with just isolated bilateral 6ths. Bilateral 6ths. If you see something you think is bilateral 6ths, look closely at the clivus. It runs forward, as I mentioned, not in the lateral wall, but in the body of the cavernous sinus. So processes like cavernous sinus fistulas that affect primarily the cavernous sinus body are more likely to cause 6th nerve palsies. Here’s another fellow. Let’s look at his eye movements. He’s got horizontal, binocular, double vision. It started a few weeks ago. And hopefully you’ll see that there is a mild right abduction deficit. You can prove that by doing your cover-uncover testing. Here we are in primary position. He’s got an esotropia. He’s sort of switching fixation. He prefers to fixate with the right eye. He’s got better acuity in the right eye. And when he looks to the left, his misalignment goes away, and indeed, he said — yay! The double vision went away. When he looks to the right, he has a larger esotropia. So he’s got a mild right abduction deficit, compatible with the right 6th nerve palsy. He’s in his 60s. He has hypertension. It’s been going on for a couple weeks. So my last polling question, I believe, is this: The patient on the preceding slide most likely has which of the following? A microvascular 6th, related to possibly diabetes and hypertension? A compressive 6th nerve palsy, something pushing on that nerve? Myasthenia gravis? Or giant cell arteritis? 10, 9, 8, 7, 6, 5, 4, 3, 2, 1. Close the poll. See what we say. All right. So the majority of you — 80% — say microvascular. A few say compressive. A few say giant cell, and no one said myasthenia. Could it be myasthenia? Yes. Myasthenia could mimic a 6th. It’s not in this case. Could it be giant cell arteritis? Yes. In this case, it wasn’t. But you definitely want to ask those questions. And I know some people, depending on where you live, may not see a lot of giant cell arteritis. But certainly in my practice, I’m gonna ask anybody over 50 with double vision and cranial nerve palsy — I’m gonna ask them the giant cell arteritis questions. Could it be compressive? It could be. It’s only been a few weeks. Could be compressive. But certainly that’s more of a typical story for a microvascular. However, we can close the polling… I kind of tricked you. So one of the things you want to make sure you do is look for fellow travelers. And if you see something that looks like a 6th nerve palsy, the fellow travelers are V and VII. So you want to check orbicularis strength. And in trying to demonstrate that his orbicularis strength really just isn’t as good on the right, and when he wrinkled his forehead, it wasn’t as good on the right, and when I checked his facial sensation, it wasn’t as good on the right. So guess what? This is no longer the differential diagnosis of an isolated 6th. This is the differential diagnosis of a right 5th, 6th, and 7th. And so clearly, when you have multiple cranial nerves involved, you’re gonna get an MRI, which we did. We’re looking for something perhaps in the brain stem or thereabouts. Because of the anatomy. And sure enough, I got a call from the radiologist. The radiologist said — yeah, we found the problem. It looked like he had a little lacunar infarct in the pons. I said… Well, I guess that could cause it. They said… Yeah, right in the left pons. This little… You can see where the red arrow is. I said… Left pons? I saw him a couple days ago. I’m pretty sure he had a right 5th and 6th and 7th. And they said — oh, no, this is the left. I said — are you sure you labeled the film right? They didn’t like that very much. So I said send me the MRI, which I always say, and my assistant, who went to high school, looked at this MRI and she said… What’s this? And I said… I don’t know. But it’s not good. And this was metastatic lung cancer. In a guy that did not know he had lung cancer, which killed him. So you’ve got to look for those fellow travelers, and more or less never trust the radiologic interpretation. Look at it yourself, and make sure that the radiologist knows exactly what you’re looking for. And then our last patient is this woman who’s got double vision, complete ptosis, and generalized ophthalmoplegia. Interestingly, the left pupil is smaller than the right pupil. And that’s because she’s got a left Horner syndrome, in addition to III and IV and VI. She also has decreased facial sensation on the left and has what we would call a cavernous sinus syndrome. All of those things run through the cavernous sinus. The sympathetics, III, IV, V, and VI. So this would be called a cavernous sinus syndrome. And here I don’t think this — this doesn’t depict the sympathetic fibers, but again, a problem in here — she had a cavernous sinus aneurysm, causing that compilation of findings. Now, if I told you this person also has a left relative afferent pupillary defect, in addition to all the other findings, she no longer has a cavernous sinus syndrome. Why not? Because the optic nerve does not run in the cavernous sinus. She now has, by definition, an orbital apex syndrome. In the orbital apex, of course, you’ve got all the stuff from the cavernous sinus, plus the optic nerve. So if the optic nerve is involved, along with those other cranial nerves, you call it an orbital apex syndrome. All right. So summary. Part 1 of ocular motility. You have to differentiate monocular from binocular double vision immediately, or you’re gonna waste a lot of time. And maybe money. Determine the pattern of the misalignment. It will help you determine: Is it a 3rd? Is it a 4th? Is it a 6th? Check the fellow travelers. Lids and pupils — I should say, of course, cranial nerves V and VII, if you think you’re dealing with a 6th nerve palsy. And remember that not all cranial nerve palsies are complete. They’re not all gonna look like what you see in the textbook. You’ve got to look for the pattern. Okay. So that is the conclusion of this webinar. Now, there are questions that I will attempt to answer. And I think I just have to open up… And I’m gonna run through these in order from beginning to end. I think. Hold on. Let me just… Let me go to the beginning. Here we go. Okay. So there’s a question: What is palinopsia? I hope I described that, and maybe you asked before I said it, but it is the phenomenon, usually a parieto-occipital problem, where a person sees something they saw earlier, superimposed on whatever they’re seeing. So it shouldn’t be mistaken for true double vision. In my clinic, all specialists refer patients to do MRI… Hold on. Yeah. In my clinic, all specialists refer patients to do MRI of the brain. They say even for monocular and for binocular, it’s a neurologic cause. Is it necessary for patients to have MRI of the brain with — absolutely not. It is a total waste of time and money. In fact, what happens when a patient is sent to me with double vision, the patient sometimes calls the office and says — my doctor wants me to see Dr. Golnick because I have double vision. My staff says to the patient: Does it go away when you cover either eye? No. It doesn’t go away when I cover my left eye. It is only present in my right. Dr. Golnick will not see you, because you do not have a neurologic problem. Have your doctor call him and explain why they are sending a non-neurologic problem to a neuro-ophthalmologist. It’s gonna be refractive or media, almost every time. So absolutely positively no. Total waste of money and time. That said, the ophthalmologist should try to figure out what’s causing the monocular double vision. Do you recommend doing an MRI of the brain for patients greater than 60 years presenting with pupil sparing 3rd nerve palsy? So what I do with that patient is… If they present — the easiest answer is: If they present with a complete — it’s been one week. One day. They have a complete — lid is shut. Eye does not move up, down, or in. Pupil is spared. They have any of the following: Hypertension, cholesterol, diabetes. They have no severe pain. Mild or moderate pain — okay. I don’t image them. If they come in and they say — over the last three months, my vision — I’ve been getting double vision. My lid’s been drooping shut. So if they give a history of a progressive thing, they get imaging. If they have really bad pain, nausea, vomiting, they get imaged. If they have a partial 3rd nerve palsy, so they have a little ptosis, like the guy that we saw, except pupil sparing, then it depends a bit on the patient. I probably — if they have vascular risk factors, and it’s only been a couple days, I might have them come back in the next few days to make sure they don’t develop pupil involvement. There are some people who would image that person. There are some people who would argue — I image every 3rd nerve palsy, pupil sparing or not. I don’t care if they’re 80. Because you might miss something. I’m not in that group. In fact, I’ll be at the Asian Pacific Academy of Ophthalmology in a few weeks, and I was asked to be part of one of the mini-debates, and the debate is: Do you image everybody with an isolated oculomotor cranial nerve palsy? And they assigned me the pro. Which means I have to argue that I would. Even though I wouldn’t. But tune in there, if you happen to be in Singapore. All right. Let me… Sorry. Let me find the next question here. Examination room lighting level during your assessment? I mean, the only time I dim the lights would be to look at the pupils. And then I’m gonna dim them significantly, if I can. You know? I hope that answers that question. I don’t dim them or do any lighting as far as the ocular motility part. Do you recommend doing cerebral angiography in a young patient with 6th nerve palsy when the MRI brain with contrast came to be normal? Definitely not. Extremely rare that a 6th nerve palsy is gonna be caused by a vascular lesion in a young person. In fact, I don’t even order an MRA. I’m assuming when you say MRI brain — I mean, if you’re worried, you could do an MRI and an MRA, or a CTA, if you’re really interested in looking at blood vessels. I cannot remember the last time I ordered a cerebral angiogram outside of a cavernous sinus fistula. A decade? If you have amblyopia, the cover test is not reliable, because the amblyopic eye can fixate in an eccentric way. Um… I partially agree with that. If they have anomalous retinal — I partly agree with that statement. That said, the vast majority of patients that I see with strabismic amblyopia you can measure it by doing a cover-uncover and cross-cover test. Or really just cross-cover, because it’s gonna be a tropia. Is there any way you differentiate between exophoria versus intermittent exotropia? Well, the only difference between exophoria and intermittent exotropia is that in a patient with an intermittent exotropia, they have a phoria that they can’t always control. So, for instance, in that young guy that I showed the video of, he was not diplopic when I saw him. But his history was: When he gets tired, and when he drinks a few drinks, he gets double vision. I’m quite sure that what’s happening is he’s losing control of that phoria. So I would call him an intermittent exotropia. Do I have objective proof? No. I have his history that says he gets occasional double vision. And I think it’s just breaking down. On the other hand, if the patient is in your chair, and sometimes they’re tropic and sometimes they’re phoric, then you could say that’s an intermittent XT or ET. Whatever it happens to be. And it has nothing to do with the angle. It has to do with: Can the person control it or not? And it also has nothing to do with the underlying cause. You can have a small… You can have an exophoria and have a 3rd nerve palsy. So if you have a mild 3rd, you may not have an exotropia in primary position. You may have an exophoria. If you have a mild 6th, you may have a small esotropia in left gaze, and you might be phoric in primary. It just depends on how good the patient’s brain is at controlling the misalignment. Some brains are good. Some brains are not good. Someone says… There should be diurnal variation in myasthenia. The answer is… Yeah. You would like to hear there’s — yeah, the classic story is: Every morning I think I’m cured. Later in the day, I’m not. I’ve had patients with myasthenia who were worse in the morning. And worse in the evening both. So I think that… Yes, textbook… You love to hear that. Yeah, you know, I’m pretty good in the morning. I get worse as the day goes on. If they don’t say that, does that rule out myasthenia? Absolutely not. How do you differentiate between skew deviation and 4th nerve palsy? Oh, that’s a good question. So if I see someone… You want to know the pattern, right? So skew deviation, which is kind of a wastebasket term for vertical misalignment of central nervous system origin with no other, like, no orbital problems — it’s got to be central nervous system — and it’s usually gonna be somewhere… Could be cerebellum, could be somewhere in the brain stem. We’re gonna talk more about skew when we do part 2 of ocular motility. I think the way I would differentiate it is that typically a 4th nerve palsy — you’re gonna see what looks like the pattern of a 4th nerve palsy. You’re gonna see worsening with head tilt to the same side. You’re gonna see improvement with head tilt to the other side. You’re gonna see the pattern of 4th nerve that we described. Do you start your patients with ocular myasthenia on steroids to reduce the chance of generalized myasthenia gravis? The answer is… Usually yes. There is not really good evidence for that. And we’ll talk more about it in part 2. So what causes the downshoot on adduction? So I’m not sure in what scenario we’re talking about. Downshoot on adduction. So I’m not sure I can answer that question. Because you probably wrote it when we were talking about some specific thing. How do you predict and avoid the risk of postop double vision when doing muscle surgery in adult strabismus? Well, that’s certainly a question not for me, since I don’t do double vision surgery or strabismus surgery. I think the way you do it, obviously, is — number one, you learn through experience. As I tell my patients who I send for eye muscle surgery. It’s an art, not a science. Number two, some docs will — and it’s a preference by the strabismus surgeon. Will do adjustable sutures. So they’ll leave the suture hanging out in the eyelid. Get the patient up and around. Have them look at the eye chart. See how their alignment is. And tighten or loosen the suture. While the patient is awake, looking at the eye chart. But I think probably the really good answer to that would be an answer, I assume, sometime… There will be an Orbis webinar on strabismus surgery and probably congenital strabismus. Okay. Could you give us more lectures about imaging? Ah. Yeah. I mean, I think that would be a great topic for a future lecture. I think we’ve got the next couple… The next couple set up. Let me just make a note about imaging. And maybe we could do that and maybe Orbis could write that down too. We could do that as a future webinar. Do you recommend neuroimaging for patients presenting with 4th nerve palsy even when there’s a history of microvascular pathology? So this is a little bit easier than the 3rd nerve problem. Mostly it’s easier because there are less… Typically less severe things, I feel, that cause 4th nerve palsy, as compared to 3rd. So the answer is: It depends. If the person is under 50, and there’s no long history of — yeah, I’ve had head tilt since I was a kid. Here are the photos — they’re gonna get imaged. Unless they’re, say, a juvenile diabetic. I might wait. If they’re over 50, and they’ve got vascular risk factors, and they have an isolated 4th nerve palsy, I usually don’t image them, unless they say — yeah, I’ve had double vision for 6 months. Because the microvascular stuff should really get better in 3 months. Certainly in 6 months. And so my routine, if I think it’s microvascular, would be… See you in 6 weeks. Repeat my measurements. And I’m gonna make sure I have a measurement, at least in primary position, to compare it. Because guess what happens at 6 weeks? They come back — I’m no better. And I make the measurement. Oh, you had a 10 prism diopter right hypertropia. Now you have a 3 prism — you are getting better. To you, it’s either you have double vision or you don’t. To us, it’s a question of degree. That’s why you need that measurement. Now, if they come back in 6 weeks, whether it’s a 3rd, a 4th, a 6th, and there is no change, or it’s worse, they get imaged. How often do I have to do that? I can’t remember doing that in 20 years. What is the main cause of double vision in children? Well, children don’t always get double vision. I avoid seeing children, when possible. I’ve got 7 pediatric ophthalmologists at Cincinnati Children’s Hospital. I only see kids under 10 if one of the pediatric ophthalmologists sends me the patient. So in terms of what’s the main cause, I really don’t know. I would probably defer that, ask that when they do that strabismus webinar I mentioned they should do. When a patient presents with pupil-involving 3rd nerve palsy, what do you advise? MRI brain or MRA? Certainly if a patient presents with a pupil-involving 3rd, they need both a look at the brain and a look at the blood vessels. Depending on where you live and what your resources are, hopefully you have an MRI and an MRA, or CT and CTA, and then I would say use either one if you think and you know one happens to be better than the other where you live. Then order it. In my world, they’re pretty interchangeable. The question then becomes: What if the CTA, what if the MRA and the… What if the scans show no reason for this pupil-involving 3rd? Do you then order a catheter angiogram? And the answer is… In a patient, a younger patient, yes. In someone with diabetes and hypertension, I’m probably gonna follow that patient. Because in my world, it’s very rare that you would miss an aneurysm on our MRA or CTA. And so to my knowledge, we’ve not missed one at least in ten years. So I’ve not had to order a catheter angiogram for that reason. Thank you for touching on the role of the superior rectus and increasing… That’s not a question. Okay. What is the role of alternate occlusion in 6th nerve palsy? Absolutely none. One of my life’s goals is to stop doctors from telling patients to alternate the patch. It just makes you offbalance, every time you alternate the patch. I don’t think there’s any role whatsoever. You cannot exercise a nerve. I discourage alternate occlusion. Except in amblyopia, which is another topic. What about double vision? 35 prism diopter esotropia, 10-year-old patient, after contusion of the left eye? So that would then bring up a number of possibilities. And again, telling me there’s a 35 prism diopter esotropia of a 10-year-old — you haven’t told me the whole part of the exam. Does it go away when they look to the right, and does it get worse when they look to the left? Is it comitant? Probably it’s not comitant, would be my bet. But if it’s not, then does it look like a 6th nerve palsy? You can have a 6th nerve palsy from a head injury. You can have muscle injury, bruising contusion, from a head injury. You could have breakdown of a preexisting esophoria from a head injury. Clearly that kid is going to be imaged. You are gonna wanna look at their orbit and you’re gonna wanna look at their brain. And that would be what I would do in that setting. What would you do if you find a patient with a partial 3rd nerve palsy and pupil involvement, but all MRIs come out normal? Right. The symptoms… Oh, and the symptoms improve in one week. Wow. That’s very, very short. We didn’t really talk about that, but when I see someone who… I’m thinking microvascular. And again, pupil involvement, technically it shouldn’t be. But if I’m thinking microvascular, they usually don’t get better in one week. And to me, that’s kind of a red flag. So for me, whenever I hear double vision — if the person’s over 50, and the double vision is either transient — like, I had three episodes that lasted 20 minutes — or it’s present, but goes away in a couple weeks or less, it really raises my suspicion for giant cell arteritis or some other vascular problem. And so in this patient, I don’t know their age — I would definitely want to know — ask them all the questions about giant cell, and probably check a CBC, a sedimentation rate, and a C-Reactive protein. I would be interested in this patient if the MRA looked at the neck or if it was just brain. I would possibly even look at the — do an echocardiogram and look at the heart. Personally, I have never seen that scenario. I have never seen a 3rd nerve palsy with pupil involvement resolve over one week. Never. Hypertension, controlled patient, two episodes of blurry and double within one week. Would you ask for an MRI? I would probably ask for an MRI and an MRA. Because what you’re describing — if they’re sure that it’s binocular double vision, what they’re describing is potentially a transient ischemic attack. I would ask them questions about giant cell arteritis, depending on where you live and how common that is and the age of the patient. But if nothing else was coming up and the patient’s a good historian, I would consider this to be consistent with a posterior circulation TIA. Carotid Dopplers won’t do it. They’ll look at your carotid arteries. Well, guess what? That’s not where the blood’s coming from to your brain stem. So you need to get an MRA or a CTA. I would look at their neck and brain, and then if nothing comes up? I would even consider an echocardiogram again, looking for an embolic source. How do you differentiate between decompensated 4th nerve palsy and acquired? Well, it can be tough. But what you can look for is large vertical fusional amplitudes. So in a patient with a longstanding 4th, often — not always — often they develop very large vertical fusional amplitudes. Now, you can check your own vertical fusional amplitudes by throwing up vertical prism. See how much you can fuse. In other words, how much you control before you get double vision. And the answer is usually maybe 2, maybe 3, unlikely 4 prism diopters. Certainly if I see someone who can control more than 5, that’s strongly suggestive of two things. One of two things. One, longstanding misalignment. And most commonly, a congenital 4th. Now, the way I’ve been burned with that, thinking — oh, this must be old — is in myasthenia. Because myasthenia can vary. Even while they’re sitting in your chair. And I’ve had at least a couple patients — I said wow! Like at that! Now they’re fusing all that misalignment! And they turned out to have myasthenia. Okay. How much do you rely on your technicians to do motility and pupil testing? Zero. My technicians are not allowed to put drops in eyes. I do not even ask them to look at eye movement testing. Now, I’m a big believer in ophthalmic technicians. I’m the past president of JCAHPO, which is the technician training group that works around the world. But… For me, as a neuro-ophthalmologist, you know, I rely zero. How much do I rely on my residents? Zero. They have to look. But I don’t let my residents dilate patients. When one of my colleagues sends me a patient from my office, and I know… They say gee, you know, there’s no relative afferent pupillary defect, but the person is count-fingers, and they don’t have a retinal detachment… I say… I will not see the patient today. Because I’m sure you already dilated the patient. Yes. I’m sure your technician checked. Yes. They said there’s no APD. Right. Do you believe them? No. Well… Why did you let them check their pupils? Do you prefer MRA instead of CTA? Only, again, as I said, some institutions have really good CTA. Some have really good MRA. I don’t care which. If you have good — both. Can you expand on your questions for suspected GCA? Sure. So, you know, I think in my practice, which is straight neuro, I think about GCA in every patient I see who’s over 50. Virtually every patient. And we always get, hopefully, a negative review of systems for giant cell arteritis. So the questions we ask are: The most specific symptom is jaw claudication. Now, not all jaw pain is jaw claudication. Jaw claudication occurs with progressive chewing. It’s ischemia of the muscles of mastication. So if a person says — yeah, I open my mouth wide — it hurts! That’s probably not jaw claudication. My first bite, it hurts. Probably not jaw claudication. Remembering that jaw claudication is not just pain. It can be weakness. So I ask for any problems with chewing. Weakness or pain. They say — yeah, I chew okay for a little, and then my jaw gets weak or painful. Cramping. That is something very specific for giant cell arteritis. New onset headaches in someone over 50. It’s unusual to have a new onset headache for someone over 50. If they say — oh yeah, I get headaches. I’ve had them my whole life. Any change? No. Not interesting to me. Scalp tenderness. So a good history of scalp tenderness. Make sure if you’re thinking about giant cell that you palpate their temporal arteries. I see patients sometimes with not much hair, like me. Big superficial temporal artery. Hey, did the doctor that sent you palpate — no. By the way, it’s a lot bigger than it used to be, and when I do this, it’s tender! Ugh! Palpate those arteries! It takes five seconds. Other questions. Unexplained weight loss. Fatigue. Malaise. Transient loss of vision. Transient binocular double vision. What was I thinking of? And then the blood tests — we look for microcytic… I’m sorry. Normocytic, normochromic anemia. We look for elevated platelet count. We look for elevated sed rate, elevated C-reactive protein. Remembering that sed rate is dependent on age and gender. So normal sed rate for a female, age plus 10, divided by 2. For a man, age divided by 2. Can you prescribe them with anything at all while waiting for patients with palsies? Yes. Occlude them. So I take — the least expensive medical device known to mankind. Opaque scotch tape. And I slap it on their glasses. It’s amazing how many people say… Wow! No one told me this! It’s amazing! I see fine! Some people don’t like the tape. I tell them the tape is like taking cold medicine for a cold. Cold medicine is not curing your cold. It’s to try to make you feel better while you’ve got it. If you don’t like taking cold medicine, don’t take it. If you don’t like the patch, don’t patch. Don’t switch the patch! Okay. On the previous case, the patient was over 60. The MRA only covered the brain. Improvement… Oh, mainly in the ptosis. So this was our… Let me just go back and check the name here. But this was our patient who presented with an isolated 3rd nerve palsy… With pupil involvement. Improved over a week. The ptosis improved. So the rest of it didn’t improve. Okay. I thought you meant it went away completely in a week. I always tell patients with microvascular 3rds the first thing that’s gonna get better is the lid. And when it gets better, if your lid’s closed, you’re gonna have double vision or you’re gonna have a patch on one eye. Right now, you’ve got an autopatch. So if the lid was improving, that would reassure me a bit about a microvascular 3rd with pupil involvement. Now, the teaching is that if the pupil’s involved, it’s not microvascular. I see patients — at least a patient every… Probably 6 months with a pupil-involving 3rd that’s microvascular. Now, that doesn’t mean you shouldn’t worry about all the bad things we talked about, but it happens. It happens. So I would suspect that this person is going to have gradual improvement. Now, when I see people with pupil-involving 3rds that don’t improve, usually if something isn’t gonna get better, it’s the pupil. Which fortunately doesn’t really big people much. All right. Let’s see. We’re getting towards the… My voice is getting toward its end. Okay. One last question. Oh, I have no question. Okay. That’s the end of the questions. So… Have a great day. Or night. Or wherever you happen to be. Oh, wait a minute. I’ve got one more question. So what about the use of Fresnel prisms? Do you send to your orthoptist related to double vision? So certainly I talk to patients about Fresnel prism in microvascular cranial nerve palsies in general is because I’m expecting it to get better. And if you put them in a Fresnel prism, it might work for a week or two, and then it doesn’t work. So it depends a bit. If the patient’s rich, and doesn’t mind possibly changing their Fresnel prism every two weeks or three weeks, then I say… Sure. We can do that. But most people in my practice say — well, if I have to do it every few weeks, I don’t really want to. In the United States, if I send them for a Fresnel prism, they’ll get charged about $50US for the prism. But yeah. I think if the person knows the downside to the Fresnel prism, and the fact, of course, that we think you’re gonna get better, then we don’t use it. Okay. That’s the last question. I’m gonna call it there. I see no more. I hope we’ll see you at the next webinar. When is it? In March. Anybody who’s gonna be at the All-India Ophthalmology Society meeting next week, I’ll be there. If you see me, say hello. If you’re gonna be in Singapore, likewise. I look forward to meeting anybody who’s tuning into these webinars. Thanks again. And have a great day. And good luck with your ocular motility.
February 8, 2017
1 thought on “Lecture: Ocular Motility I”
Very enjoyable! This is my study break!!