Objectives of this lecture are:

  • To describe the typical findings of 4th Cranial Nerve palsy or paresis.
  • To learn how to use the “Three Step Test” to diagnose cyclovertical muscle palsies.
  • Participants will understand why the third step confirms the diagnosis.

Lecture Location: on-board the Orbis Flying Eye Hospital in Bridgetown, Barbados
Lecturer: Dr. Rudolph Wagner, Rutgers – New Jersey Medical  School, Newark,  NJ  USA

Transcript

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DR WAGNER: So I’m gonna give a talk or a little presentation on superior oblique palsies or 4th nerve palsies. Some people call them — they’re not the same, but they refer to them differently. It’s really you have damage to the 4th cranial nerve, then you get weakness of the superior oblique muscle. But it’s sort of used interchangeably, the term, when you read about them. We’ll do the prequestions. Okay? Because we always do that with these lectures. So I’ll read it. Ocular torticollis, commonly named for head tilt, may occur in: Duane’s retraction syndrome, B, 4th cranial nerve palsy, C, congenital nystagmus, or D, all of the above. So you can see 38% with the 4th nerve palsy, because they were thinking that’s what the lecture’s about, so that’s why it’s gonna be the answer. But you can certainly get ocular torticollis or head positions in all of these conditions. Duane syndrome, they’ll present — if I have a left sided Duane syndrome with an abduction deficit in my left eye, I’m gonna turn my head to the left to keep me from needing to abduct that eye. If I have a congenital nystagmus, we had one in the clinic that had a null point or a neutral point where the nystagmus was less present. You turn your head in the opposite direction to keep the eyes — to allow you to look straight ahead without having the nystagmus, or improve your vision. So certainly all of these things can cause an ocular torticollis or head tilt or face turn, depending on how you want to use the terminology. But I guess if I purely said just a tilt, that would make me think more likely of a 4th cranial nerve palsy, because that’s where it is much more likely to occur. Next question: Significant overaction of the inferior oblique muscle is more likely to occur in an acute 4th nerve palsy than in a congenital type. And that’s a true or false. So which one is it more likely to occur? Is it more likely to occur in an acute type than a congenital type, that you would present with this overaction of the inferior oblique? And 43% said true, and 57% said false. Well, we’ll see as we go along why… To help you answer that question a little easier, and there are reasons. I’ll explain it as we go along. I don’t want to give away the answer right away, you know. The next one is: The upshoot or overelevation of the adducted eye in a patient with Duane’s retraction syndrome is secondary to inferior oblique muscle overaction. In other words, when you have a Duane’s syndrome, many times you’ll have an esotropia. Right? Type I. And when you then have the person bring their eye up to position and look up or down, you’ll get an upshoot. And it almost looks like the eye is just… Basically shooting up, as I said. In the adducted position. If you start them out when they’re looking down, you’ll often see it as a downshoot. So… The upshoot or elevation of the adducted eye in Duane’s retraction syndrome is secondary to inferior oblique muscle overaction. Is it? And you can see… Well, 54% say it is. The findings of a right hypertropia — so right hypertropia, my right eye is higher — worse in left gaze — for right hypertropia, which is worse when I look to the left. The right eye goes higher. And on head tilt to the right shoulder, so if I tilt my head to the right shouldered, the hypertropia increases… So I have a right hyper, worse in left gaze, and on head tilt to the right… Are typical of: A right inferior oblique muscle palsy, a right superior rectus muscle palsy, C, a right superior oblique muscle palsy, or D, a right inferior rectus muscle palsy? So most people think it’s right superior oblique muscle palsy, and most people are right on that one. So I’ll explain — during the lecture, I’m gonna explain to you how you can determine that, why it is that way. And there are easy ways to remember it, and there’s also ways to understand it too. If you understand it, then it’s even easier to remember it. So if you understand why this occurs, or what the reason for it is, it makes the whole thing easier. So the objectives really, in this lecture, are to describe the typical findings of a 4th cranial nerve palsy or paresis. If it’s totally paretic, that could mean that it’s not working at all, or you could have a palsy of the muscle too, or partially. To learn how to use the three-step test to diagnose cyclo-vertical muscle palsies, also referred to as the Bielschowsky head tilt test. And the participants will understand why the third step confirms the diagnosis. You need to go take it to the third step, in order to be sure of what you’re dealing with. Now, having said all of that, most of the patients that you will see with the head tilt and with the vertical strabismus are gonna have superior oblique palsies. It’s far more common than any of the others. I’ve maybe seen two or three inferior oblique palsies, which are hard to imagine that they occur, because that means you picked off an isolated branch of the 3rd nerve, going to the inferior oblique muscle. And the times I’ve seen it, one was a girl who woke up from anesthesia. We weren’t operating on her. She had some other anesthesia. And she woke up and she had double vision, and she indeed had an inferior oblique palsy. Something occurred, you know. We don’t know why. Maybe a small vascular incident. We’ll see it, but rarely. So anyway, what are the characteristics, really? We’ll talk about 4th or trochlear nerve palsy. Give it another name, now. Not only superior oblique. Now we call it the trochlear nerve. The 4th cranial nerve is the trochlear nerve. Congenital or following trauma. Certainly they can occur both ways. In congenital, if we suspect congenital, we often ask them to get family photos showing — which would usually show head tilt and large vertical fusional amplitudes. Well, the family photos — what happens is you ask them to bring in a picture, and you’ll often see, if it was an older person who came in, or young adult, and they have, when the were a child, very many times the whole family’s taking a picture straight ahead, and the person with the palsy, with this condition, is tilting his head way over. You see that, you don’t have to worry about a tumor or something unusual causing it. Most likely it’s just a congenital problem that they had. And by and large, those are the most common ones that end up coming in to see ophthalmologists. And they come in at different ages. It’s not like — I mean, sometimes they’re recognized early on, because they have the head tilt. Some people have it, and family members don’t even recognize that it’s there, although it’s pretty prominent when you see it. But that’s the way it is. Some people come in when they’re older, complaining of double vision, because they were able to control this, and their fusional vergences break down, and they’re no longer able to control it, and the phoria that they had becomes a tropia, and then it’s bothersome. So they’ll come in because of that. The large vertical fusion amplitudes. This goes into what you normally see in kids or people that had congenital superior oblique palsies. Because over the years, they’ve been able to control that vertical deviation, either by tilting their head or by stimulating this fusional mechanism to allow them to control it. You know, normally a person really — if you have never had a strabismus, and we put a prism in front of you, a vertical prism of 4 or 5 diopters, you’re gonna have double vision. You’re not gonna be able to fuse that. Most of the time. You can maybe get 2 or 3, but beyond that, unlikely. Whereas these people, they could come in, and their eyes could be in alignment, and you could keep adding and adding prism, and they may eat up prism, we call it, as much as 20 prism diopters, sometimes. They have these huge, huge fusional vergence amplitudes, which must have been developed over time, because there was constant stimulation for that to occur. And that’s also a benefit in them that have surgery, because after surgery, if you operate, they can still use those fusional amplitudes to help correct the deviation, even if there’s a residual after surgery. It’s one of the reasons why, with the inferior oblique palsies, or superior oblique palsies, we don’t really… Sometimes… What do we say? The enemy of good is perfect? And if you try to get something perfect and do more surgery than necessary, or really correct the full deviation, you may have a little trouble if you overcorrect them. So it’s wise to use these fusional vergences. And they work, but they don’t work so great if you change them from a hyper to a hypo, because then they’re using a totally different mechanism to fuse that. It’s not the same. Whereas a little residual hyper, that started out as a hyper, they can fuse very well, and not have too much difficulty with it. So it’s something to keep in mind. So these large fusional amplitudes, they generally occur in people that have had congenital or long period of time superior oblique palsy. And you can develop that in one following trauma, but that would then — the history would be a little bit different. They would say they usually had head trauma, they didn’t do anything about it, and over years, they developed some fusional… And they could control it. But by and large, generally, the congenital ones have the fusional vertical amplitudes, and the acute — certainly the acute ones don’t. The acute ones will present differently. They’ll usually present with — from acute head trauma, they’ll usually present with double vision and underaction of the inferior oblique. So a person that has acute trauma to the superior oblique, to the 4th nerve, with a vertical — they’ll complain of double vision, and more often, they’ll complain not only of a vertical diplopia, but of torsional diplopia, because they usually get extorsion when this occurs. Because you all know the superior oblique is an intorter, and when that’s paretic or paralyzed, it causes the eye to extort, and they complain of that. But what I was driving at with that is that when they have the — when you examine a person that is complaining of double vision, and they look like they have a vertical strabismus, and you suspect that they have a superior oblique palsy, if you take them — if it’s my right eye, and you take me into left gaze, it will overelevate, but if it’s more acute, when you take them right and down to the left, you’ll really see an underaction of the right superior oblique. And you’ll see a much larger vertical deviation in downgaze, in down and to the left, than you might in upgaze. And it’s just the opposite in the congenital types. Because the inferior oblique has been overacting and overacting against this paretic muscle, they often have an overelevation of the inferior oblique and a much greater vertical deviation in upgaze, and especially to the opposite side. So that helps you. It helps you to categorize it a little bit. Most of the people that I’ve seen that have had superior oblique trauma or injury to the 4th cranial nerve, they have a history of a pretty good shock to the head, but not necessarily being unconscious or… You know, not like neurologic trauma. I always grade them this way: The worst neurologic trauma or head trauma produces 3rd nerve palsies. Second would be a 6th nerve palsy. And the people that have 3rd nerve palsies usually have significant other abnormalities, neurologically. 6th nerve palsy — if it’s from trauma, they’ve usually got a pretty good shock. They get them from hypertension, strokes, diabetes. That’s different. But if they get them from trauma, it usually takes a pretty good one to produce that. Maybe an automobile accident. And they have more significant head trauma. But the 4th nerve palsies usually have the least significant head trauma, when they give you their story of what happened to them. They remember. They say — oh, you know, I was playing football. I got knocked over, stunned for a few seconds, but then they come back, and they realize they’re seeing double vision, and it’s very common that you’ll see it that way. So they’re not often coming in acutely, as a big problem, unless you get them right away. And of course, I mentioned the inferior oblique muscle overaction, which occurs over time. It may be bilateral or unilateral. The bilateral ones are more difficult to diagnose, because they present primarily with extorsion, and don’t have much of a deviation in the primary position. They may have a little bit of a vertical in one, because very rarely do you get damage to both of them symmetrically. You may have a greater weakness on one than the other, of the superior oblique muscles. So they might present with a small vertical deviation in one eye, but if you take them through the three-step test, you’ll find that if it’s bilateral they’ll often have a small vertical deviation in the right eye. If you go into left gaze, you get a larger right hypertropia, and if you go into — excuse me. Larger left hypertropia if you go to right gaze. If you go to left gaze, you actually get a right hypertropia. So we’ll get into that a little bit too. But it’s one of the ways of diagnosing that. So this is a patient — maybe Dr. Vaughan remembers. We saw this one — this is one from Jamaica that we ended up helping out, I think, that had… This is years ago, where she was really… This is her preferred head position. That’s a significant, significant head tilt. Many people don’t have it that way. But you can see why. As soon as you get her head to the straight position, she’s got this big, huge left hypertropia. So this is something that you’ll see with that, and if you tilt her more, it’ll go even higher. Very common. You know, kids very rarely complain of double vision. Almost never. Because if they have these types of conditions, like a Duane syndrome or a 4th nerve palsy, they can find a position where their eyes are not… Where their eyes are lined up. Okay? So they find it automatically. No one has to tell them that. We see kids all the time that have postviral 6th nerve palsies, that the parents will say… You know, just yesterday he started just looking at everything with his head turned to one side. And you examine them, and you see that they can’t abduct fully, and in many cases, if there was no injury or tumor — you’ve got to rule things out — but you’ll see that. So they don’t complain of double vision, but they show it to you by trying to maintain binocular vision. Now, that’s as opposed to comitant strabismus. Most of the kids that have comitant strabismus, there’s no position where their eyes are in alignment. Right? But even they don’t complain of double vision. They might, sometimes, the intermittent exotropias do, but very shortly, if they’re young enough, maybe less than 7 or 8, if they develop a strabismus, they invoke these — what we call sensory adaptations, which are mechanisms to eliminate the double vision. These include suppression and anomalous retinal correspondence or abnormal retinal correspondence. That’s a whole lecture in itself, but the point being that those kids that don’t have a spot where their eyes — where they can maintain normal binocular vision — will usually then develop suppression, sometimes go on to amblyopia. Whereas these kids that can get a position where their eyes are not crossing, or they don’t see double, will not. And they maintain their binocularity, because of this. So if we talk about isolated cyclo-vertical muscle palsies, the step test can be useful in diagnosing any of the cyclo-vertical muscles. It doesn’t work for the… Well, it works for all the verticals. And it can help you to determine what you’re dealing with. Now, the first step is called the Bielschowsky test. Marshall Parks was an ophthalmologist in the United States that basically was the father of pediatric ophthalmology, not only — pretty much internationally. Because before he came along, there were strabismus surgeons, but there were no pediatric ophthalmologists. Nobody did exclusively that. And it was more based on just strabismus. But then they started breaking it off as a subspecialty, because so many of the kids had strabismus that you started seeing other problems that children had, and then it became a subspecialty, and now there’s — the fellowships are generally called fellowships in pediatric ophthalmology and adult strabismus, because we tend to do that. So someone like myself, that all I do is pediatric ophthalmology and strabismus, probably about 10% to 15% of my patients are adults that are eye muscle disorders, whereas most of them are children. In the children, we do everything else. So it’s a good specialty. You don’t have to just do strabismus if you do pediatric ophthalmology. You can do other things that children have. As opposed to all the other specialties in ophthalmology, where you’re more organ-specific. Your cornea or your… Well, neuro-ophthalmology is sort of similar. But retina, you’re doing the retina. So it’s nice if you want a balance of it. So step one: What eye is higher in primary gaze? So where is the right — which eye is higher? And, you know, we define these things by the hypertropia, by the higher eye. However, certainly I’ve seen people present that have had a right superior oblique palsy, present with a left hypotropia. For some reason, they prefer to use their right eye, either because it’s the better seeing eye in many cases, even though they had an injury to the nerve — it might be that their vision is just better in that eye, the other eye might be amblyopic. Whatever reason. So they could present the same way. However, they will follow in the same steps of the test. But you base it on the hypertropia, not on the hypotropia. So you have to take that into consideration when you do your measurements. And then step two is: Where is the hypertropia greater? Is it greater in lateral gaze, to the right or to the left? And then the third step is: Is the hypertropia greater on head tilt toward the right shoulder or toward the left shoulder? And these are the elements of the three-step test. And that’s what you go through when you have a patient. So here’s somebody who wants to keep her head tilted to the right side. And I’ll show you — that does have a left hypertropia. You can see where she’s going. She’s going to the OR to have it fixed. But I took some pictures right before that. So here we are. So we have her looking to the right. And looking to the left. So I think it’s pretty clear that she has a right hypertropia, which is worse… Excuse me. A left hypertropia in gaze to the right. So she had a left hypertropia in primary gaze, and she has a left hypertropia in gaze to the right, and really looks pretty much okay in gaze to the left. So if you then tilt her to the right and to the left, you can see that the left hypertropia is greater on head tilt toward the left shoulder. You can see here, if you use the inferior limbus as your guide, there’s no conj seen here, or very minimal, whereas here you can see more extensive conjunctiva showing. So that’s your indication that the left eye is higher than the right. So she has, if we go back, she’s got a left hypertropia, which you don’t see so well on this primary, because — the reason you don’t see it, by the way, is I always — I should have taken a better picture. I have some that will. You always want to force them, when they present with head tilt, when you try to get the deviation in primary, you’ve got to force them to hold their head straight. I call it forced primary gaze. You’ve got to hold the head straight, because if you don’t do it, it won’t show up. But if you get them straight, and their nose is pointing right where you want them to, they’re not tilting, you will see the vertical if they have it. So it’s very important to do that, which I didn’t do in this one. But you can still see the right hypertropia, and certainly this is overaction of the left inferior oblique, when you see that eye turning that way. So here’s one. Here’s a lady, she wants to keep her head tilted a little bit to the right. And again, in this one, we did force her to hold her head straight, and I think you can see that there’s a left hypertropia in that eye. And if we then… So let’s take it through — let’s go step by step. Okay? So we have a left hypertropia in the left eye. Okay? So that means that all four vertical muscles could still be involved in this patient right now. Okay? The elevators of the… I shouldn’t say all four. Yeah, yeah. Well… Yeah. Four can be. So let’s say… Let’s say this: The elevator of the right eye is the… Of the left eye is left superior rectus, and the left inferior oblique. Okay? The depressors of the right eye are the right inferior rectus and the — excuse me, left. Everything’s left. Left inferior rectus and left inferior oblique. The elevators are just the opposite here. So if I have a left hypertropia, meaning that my left eye is too high, if I alternate cover, if I cover the right eye, the left eye will come down to pick up fixation, and I’ll now have a right hypotropia. So if I have a problem with a left hypertropia, it could be because both depressors in the left eye are not working properly. The inferior rectus or the superior oblique. Or both elevators of the left eye are not working properly. The left inferior oblique… Right inferior oblique and the right superior rectus. So all that first step tells you is that. It tells you about those four muscles. So if we look at the diagrammatically, we know that these are the four muscles that could be involved in this patient. She’s got a left hyper, or a right hypo. So it’s either the left inferior rectus, the right inferior oblique, or the left superior oblique and the right superior rectus. But where do these — in which — the next step, the second step is: Going to gaze, lateral gaze, and it’ll give you the answer. It’ll eliminate two of these, based on which direction the hypertropia is greater. So… When you look to the right, the left superior oblique is the elevator of the left eye. And the right superior rectus is the elevator of the right eye. Correct? When you look to the right. When I look to the left, the elevator of the left — excuse me — the depressor of the left eye, because you have a left hypertropia, is the left inferior rectus. In that position. Or the right inferior oblique, which is supposed to elevate the — excuse me. That’s the elevator of the right eye. So where is the… So we’re talking about either a right hypo, a left hyper, or a right hypo. So where is the deviation greater, in right gaze or left gaze? So we have this patient that has a left hypertropia, and we go to her. And we see that in step two, the left hypertropia is worse in right gaze, whereas in left gaze, things are okay. So now we know that the two muscles that were working in right gaze in her, that were involved in the vertical movements, were the left superior oblique, which is the depressor, right? Or the right superior rectus, which is the elevator of the right eye. Does that make sense so far? So we could either have… That means we could either have a left superior oblique palsy or weakness, or a right superior rectus palsy. So if you understand that, you know — you’ve eliminated the LIR and the RIO for that reason. So those are the last two left. So the third step is the tilt. And the left hypertropia in her case was greater on left head tilt. And there’s some elevation here, but it’s certainly greater there. Now, once you see that, then you know pretty much that we have a left hypertropia worse in head tilt to the left, and you look at the third step in the test. You know we’re down to these two muscles: The left superior oblique and the right superior rectus. And you need to know which muscles are active when you tilt your head to the opposite side. So what you need to know is that when you tilt your head to the left, you actually… What happens is that when you tilt your head to the left… Why does the left eye overelevate in this particular patient? Well… What happens is: When you tilt your head, you know how, if you’re watching television or something, and you tilt your head so much to the side, you can still see everything straight ahead? That’s because your torsional movements in your eyes are allowing you to do that. That’s only for a certain degree. If you go 180 degrees, you can’t do it. But you can tilt your head a certain amount and still see okay with both eyes together. That’s because you have these torsional movements. And you need to know that the intorters in both eyes are the superior muscles, the superior rectus and the superior oblique. The extorters are the inferior rectus and the inferior oblique. And by intorsion, we mean moving the 12:00 position toward the nose. By extorsion, we mean moving the 12:00 position away from the nose. And that way — like, if you had a line through the middle of the cornea, and that’s the axis that you’re rotating your eye about. So that’s what happens. So I’m gonna say this about four different ways, but so what’s happening here is that she’s tilting her head to the left. Okay? So that means that in order… If you do that normally, that would mean that you would need to intort your left eye, in order for you to see properly. But her superior oblique muscle is not working, so the other muscle, the superior rectus muscle, kicks in, in order to try to correct that intorsional or that torsional diplopia. When that happens, because the primary action of the superior rectus muscle is to elevate the eye, you get an overelevation. So when you have a superior oblique palsy or weakness, and the same side, the superior rectus, causes the overelevation, when you tilt to the same side that the palsy is — you know, part of it is that the inferior oblique is not working either, to depress the eye. But it is a combination, kind of, of the two, that causes that. And the reason you get the big elevation is because the superior rectus is firing in order to correct that. So step three is then: In this case, where is the left hypertropia worse? And it was worse on head tilt to the right. And it couldn’t be… It wouldn’t be the right superior rectus, because when you tilt your head to the right, you would need to intort the right eye to see better. Right? And we know that the muscle that we’re talking about, the right superior rectus, is the muscle that — is the only potential muscle causing this problem. So there would be no cause for the right superior rectus to fire when you tilt your head to the right, because you would need to intort — to intort, not extort it. Kind of makes sense, if you think about it? So that’s how you do it. There’s easier ways to do this, but if you can think about it, and reason it out, it’s much better, because then you really won’t forget. So why is it, then, to say it another way: Why is it the left superior oblique? Why? Well, as I said, the intorters are the superior oblique and the superior rectus. The extorters, the inferior oblique and the inferior rectus. When you tilt your head toward the left shoulder, your left eye must intort, and your right eye must extort. Is that right? Yes. But if the left superior oblique is paretic, the other intorter, the left superior rectus, fires, and also elevates the right eye, which causes the left hypertropia. There’s no reason, as I said, for the right superior rectus to fire, because the right eye needs to extort, not intort. So that’s when you tilt your head to the left, I should say. So really, if it was just the opposite, if it was worse when you tilt your head to the right, then the right superior rectus would be the answer. But I can tell you: Very, very rarely are you gonna see a right superior rectus palsy. Same reason. That means you picked off an isolated muscle. Now, I did see a case of a woman who had trauma to the superior rectus muscle individually, and it did become paretic, I guess, because… You know, the nerves enter — the rectus muscle length is about 40 millimeters. The nerves enter about a third of the way from the origin, the apex. So you could, you know… Strabismus surgeons, we never get involved in the nerves of those muscles. We’re never anywhere near that when we’re operating, hopefully. But you could have an injury in the orbital fracture, orbital floor, orbital groove, that could damage the nerve to the superior rectus muscle, and I have seen patients that had superior rectus palsies that satisfied the criteria of the three-step test. But very, very rarely. So step three, like I said, it shows you another way. When left head tilt is greater, left hypertropia is greater on left head tilt, the left superior rectus fires to intort, and causes the left hypertropia. This is intorsion, toward the nose. That’s extorsion, away from it. So that helps you kind of understand a little bit about what it’s all about, and how it works. So what are your surgical options, once you’ve determined that this is indeed what you have? Well, if there’s a big overaction of the inferior oblique, you can certainly weaken the inferior oblique in some way. One way or the other. There’s a couple different ways to did it. Maybe three or four. You can tuck or strengthen the superior oblique tendon. Sometimes you can recess the inferior rectus in the opposite eye, because if I have a right hypertropia and a left hypo, I can recess the left inferior to bring that eye up to balance it. Sometimes you get what’s called a spread of comitance, meaning that the vertical deviation is pretty much similar in all fields of gaze, and you might need to recess the superior rectus on the same side where you have the palsy. And a lot of this is based on what’s called the Knapp classification. I don’t have a slide of that. And the Knapp classification — I don’t have a slide of it — basically is — you draw a box. I might have it in one of my other lectures. You draw a box in, like, a table, like, for a tic-tac-toe thing, and you look for where is the hypertropia greatest. And it turns out that most commonly, if it’s greatest in upgaze and to the opposite side, that’s the inferior oblique overacting, and that’s the muscle that you operate on. So by and large, 90% of the superior oblique muscles that I operate on — I operate on the inferior oblique. And the inferior oblique is the best muscle to operate on for a lot of reasons. It’s very forgiving, in the sense that it doesn’t cause overcorrections. It’s usually self-adjusting. You do the operation, and after a period of time, it gets even better, most of the time, when you correct the vertical deviation. And so it’s really… If you can do that procedure, I prefer to do it. Once in a while, you have a situation where there’s a vertical deviation, there’s big underaction of the superior oblique, and there is no overaction of the inferior oblique, and then you kind of have to do something with the superior oblique. Most of the time — even some of those you could get away a little bit with doing the inferior rectus in the other eye. But most of the time in those cases, you do. And then you have to do something with it. Most of the time what I do is I tuck it, if it’s a unilateral case. And what you’ll find — you know, the superior oblique is by far the least operated-on muscle by anybody. I do a lot of surgery, and I do maybe — if I do three or four a year, that’s a lot. Just because it doesn’t present that way, that it needs to be done, that often. I’ve had operations where people come in, that they’ve had superior oblique palsies, they’ve had the inferior oblique done, they’ve had the opposite inferior rectus done. They still have a vertical deviation. They have torsion. You’ve got to do it. You have to do something in those cases. And what I have found is, when you approach the superior oblique, and you hook it, if it is a paretic muscle, it’s very, very floppy and inelastic. As opposed to a superior oblique when we’re doing an A pattern, where they have a tight superior oblique. It’s totally different. Those muscles are pinned against the globe. You get under it, sometimes you can barely distinguish the thin fibers from the sclera. But when it’s paretic muscle and you’re doing the right procedure, it makes you feel good when I see that, because I know I’m doing the correct procedure if I see this floppy muscle. When you hook it, you can actually lift it up and look at it, and then you can tuck it. And by tucking it, you basically fold it over on itself, shorten it, bring it over, put it under the superior rectus muscle, and it works well when you have it — if you tuck it too much, you can get a Brown syndrome. You can induce a Brown syndrome, which is underelevation in the adducted position. If you don’t tuck it enough, it doesn’t work. But no one can tell you how much you have to do it. You do it sort of by feel. And you convert it from being a floppy muscle to being somewhat — looks like a normally — normal tension in the muscle itself. So that’s why people don’t do it as much, because it’s somewhat… A little bit less predictable. And so here’s a typical kind of case that you like. This is a guy with a right hypertropia, a little bit of a head tilt to the left, big overaction of his right inferior oblique muscle. You can see that. And when you tilt him, not big overaction, but certainly a right hypertropia, worse on head tilt to the right, and no vertical deviation on head tilt to the left. So he’s a perfect candidate for inferior oblique recession. And indeed, that’s what we did. Here he is after surgery. Maybe a week after. And you can see certainly that vertical overaction that we see here is gone. And even sometimes you get a little bit of an underaction, in cases like this, which is okay. Because as I said, it’s somewhat self-adjusting. So this is the ideal case that you want. Now, I wrote here a 14-millimeter recession. And that’s usually what I do. And this Dr. Parks that I mentioned earlier, he was the one that described what the 14-millimeter recession is. And we’ll get back to that in a minute. I think I’m gonna talk about it, but I want to see if… Yeah, I better talk about it now. So on my other slide, I have slides that actually show you how to do it. The other lecture. But basically for you that are here today, what you do is you hook the — you find the inferior oblique muscle. And the way I usually do it — and I’m gonna do a case — is we bring the eye into elevation, in adduction, I usually do an inferotemporal — we call it a fornix or cul-de-sac incision. Through that incision, I’ll hook the inferior rectus, and then locate the inferior oblique in that quadrant. I’ll usually insert just below the lateral margin of the inferior rectus. The lateral rectus. And when you hook it, you put sutures through it, and you can then disinsert it and you can reposition it. And what I do is I go back along the inferior rectus muscle, right where the inferotemporal vortex vein is, and reattach it at that point. You can also just do a myectomy, where you just cut it loose, where it inserts. It works. My only concern is: Sometimes it’s so floppy, the inferior oblique, that it looks like it might just go back to where you left it when you cut it, and it’s possible. It’ll usually retract. I used to do this wild procedure, which I stopped doing, the denervation and extirpation, where you get the inferior oblique, you trace it all the way back to where it penetrates Tenon’s capsule, you look for the notch. On one side of it, you can see where the nerve enters, and you sort of extend it out. You pull it as much as you can, get cautery, you cauterize the vascular bundle and cauterize the nerve, and you cut it below the nerve, if you can. More posterior to it. And then you just take this big chunk of muscle out. And then you can let it retract inside the Tenon’s, and you can suture the Tenon’s closed, if you want. I haven’t done that in about 20 years. Because other things seem to work, and that was before they developed the anteriorization procedure, where you can sometimes — you can put the — you can convert the inferior oblique from an elevator to a depressor, and you can actually attach it just next to the insertion of the inferior rectus, either a little bit in front of it, behind it, or right at it, and that’s another lecture that I’m gonna give, why you would do that, and why it’s advantageous. It happens to work quite well, if you have a combination of both inferior oblique overaction and DVD. You can solve both problems by using that in some cases. You almost always do that procedure symmetrically, because if you do one inferior oblique anteriorization, you’re almost certainly gonna induce some vertical deviation in the other eye, in many cases. Not necessarily in the cases with the bad superior oblique palsy, but in some of them that have just minor problems or minor elevation issues, or DVDs, or something like that. So you’ve got to be careful. If you… Let me see. What else about it? Oh, to give you an idea, I had a patient that had trauma, had a lacerated inferior rectus muscle, from an injury, which retracted back somewhere behind Tenon’s into the globe, and we didn’t want to go look for it. It was not good. It was a huge vertical. So in her case, since we didn’t have any inferior rectus to work with, we actually did a nice anterior transposition of the inferior oblique, put it a couple millimeters anterior to the insertion, where the insertion of the inferior rectus would have been, because you can still see that. It was lacerated behind it. But there was just a tendon attached to the insertion. So we knew we could locate it. And that worked quite well. I think I also recessed the superior rectus too. But it did give you some depression, just from that. So it gives you an idea that it could be a pretty powerful depressor when it’s put in a particular position. So it’s useful in some cases like that, when you think about — you’re trying to do something more unusual that needs to be done. And so we talked about this the easy way, to remember which palsy you’re dealing with. We say RLR, right hyper, worse in left gaze, and on right head tilt. So RLR equals RSO. Right superior oblique. So therefore, if RLR is right superior oblique, you missed the part where we described how you do it the right way. But if you do it this way, conversely, if RLR is right superior oblique, then LRL is left superior oblique. Now, because the last step came down to between the superior oblique and the opposite superior rectus, if you have RLL, then you know it’s the opposite superior rectus, and therefore LLR is the opposite superior rectus. For that one. This one’s pretty easy. Right hyper, worse in right gaze, right head tilt. It’s really the left inferior oblique, and there of course you’re dealing more with a hypotropia. Because the inferior oblique is an elevator. So therefore LLL is right inferior oblique, and the last step — same thing. You would use that to get it. But as I told you, clinically, most of the time you’re gonna see this, those two up there. You will see some bilaterals. On our board examination, even in the US, most of the time they ask you about superior oblique palsies. They ask about bilateral — they always ask about bilateral superior oblique palsies, always, and they sometimes — if they really want to give you a hard time, will give some kind of an unusual vertical deviation. So it’s something to keep in mind. Now, I did mention earlier about something, about Duane’s syndrome, in that there often are upshoots and downshoots, which may mimic inferior oblique overaction, or downshoots that may mimic superior oblique overaction. When you have a Duane syndrome, if I have — say in left eye, more in left than right, let’s say, I have a left esotropia, and I can’t abduct past the midline, or very slightly past the midline — there’s variability in there. Some can move more than others. But then you come into the adducted position, and you get retraction of the globe, and narrowing of the fissure, on attempted adduction. Well, if you start them coming in a little bit in the adducted position in the upgaze, some of them will shoot up, and then others will shoot down. If you start in the inferior position. Most of the time, they attribute this to lateral rectus muscle slipping on the globe, and that causes the upshoot and downshoot. Not the inferior oblique overaction. It can look like it, but it generally is not, because it wouldn’t make sense. Why would the inferior oblique be involved, unless there was some other miswiring which occurred? Which I guess can occur, but it’s less likely. And the way we often solve that is by doing what’s called a Y-splitting procedure, to eliminate this leash effect. So you take the inferior oblique, lateral rectus, you get at the insertion, and you actually use two sutures, two double armed sutures. You place them so that you can split the lateral rectus in the middle. And you can then transpose up one end of it, superiorly. This will happen inferiorly. And that seems to work in some cases. It’s an easier way to eliminate some of the upshoots and downshoots than doing some of the more radical procedures. So here’s a Duane’s type 3, which means that — most of the Duane’s type 3 don’t have much deviation in primary. You know, type 1 is abduction deficit. Type 2 is adduction. Type 3 is both. But this guy has definitely poor abduction. He certainly has some widening of the palpebral fissure on attempted abduction, which you can see clearly, and when he looks to the left, the palpebral fissure narrows on adduction. So this is both reduced adduction and reduced abduction. And while I’m at it, if you look at… All Duane’s patients, even the type 1s that have abduction deficits, they all have a very small — some — a small adduction deficit also. That’s what differentiates — that’s one of the things that helps you differentiate a Duane’s from a 6th nerve palsy. 6th nerve palsies don’t have that. And the way you look for it — and I think I have a lecture on that too — but the way you look for it is: If I have a left Duane syndrome, if you measure me in straight ahead gaze, again, you’ve got to do the forced primary, gotta hold my head straight, because they really want to turn their head, people with Duane’s, to see. You hold their head straight, and you can measure the esotropia. If you then try to turn their head to the left to measure the esotropia in left gaze, it’s gonna be very difficult. Because they can hardly abduct. So you can see it’s gonna be a huge eso. But if you turn their head way to the opposite side, to get the eye in the adducted position, and you alternate cover, you’ll often get a small XT. An exotropia. Which you won’t get in a 6th nerve palsy. You’ll only get that in a Duane’s syndrome. And when you see that, that really helps you confirm the diagnosis. You can also check it by convergence. They almost all have convergence insufficiency, Duane’s. When you bring the convergence card closer, they’ll go out. Whereas a 6th nerve palsy should not. In fact, they should keep going in, unless you had convergence insufficiency before the 6th nerve palsy. But that would be giving them two diseases, which we don’t like to do. But those happen sometimes. But anyway, this is the palpebral fissure widens. This one, the palpebral fissure narrows on adduction. And when he overshoots in this case — when he tries to look up — you’ll see this big overelevation of the left eye, which could look like an inferior oblique palsy, if you don’t — I mean, inferior oblique overaction, if you didn’t really know the patient and see what he was doing prior to that. So just keep that in mind, that they believe the lateral rectus slides, and this causes this overelevation. Where if you start them in the downward gaze, it slides up and gives you the depression. And I’m sure that’s what happens. One time, when I was a resident… This guy… We had a case of bilateral Duane’s that really looked for all the world like it had superior oblique palsy. And it was a person — superior oblique overaction. Downshoots from Duane. But we thought it was that, not Duane’s. So we said… Let’s just try and see what happens. So we weakened the superior oblique, and lo and behold, nothing happened at all. It was amazing. I mean, it still had the exact same kind of a downshoot, even though it was gone. So at least in that one particular case, it didn’t seem like it was the cause, for sure. So other vertical deviations. I know we have thyroid ophthalmopathy, which is one of the more common things that I deal with in adults. The inferior rectus and the medial rectus are most frequently involved. Where I work, the orbital surgeons do a lot of orbital decompressions, and orbital decompressions equal big time strabismus, with usually restrictive strabismus. Something happens to the dynamics, I think, when they change the orbital dynamics. These thick muscles, they change their — they make them more fibrotic, or more in a position where it’s difficult for them to act normally, so certainly they get — many of them have strabismus, which needs to be operated on at that point. And for those of you that watched the surgery today, some of those patients look like that, the muscles, the thyroid muscles. Not all of them. But some of them have really tight muscles, which are difficult to operate on. Hard to even get a hook underneath. You have to resort to all these kinds of methods that we were using to do that. But you’ll see that. Orbital floor fractures. You know, those are rough. You often will get a hypotropia in primary, and they may have a combined palsy and restriction of the inferior rectus muscle, which I think happens a lot in these cases. They come in and they present with a hypotropia, because they have an entrapped inferior rectus muscle. And you can’t… They can’t look up so tight, and you’re not sure what they’re doing, looking at downgaze, because it’s sort of restricted in movement too. So the orbital surgeon then goes in, and frees up the fracture, repairs the fracture, frees up the muscle, and the next day, they have a huge hypertropia, because they’ve had trauma or injury to the inferior — to the nerve, most likely to the inferior rectus in that fracture site, or behind it, or wherever the fracture occurred. Now, many and many of those will actually get better over time. Put them on steroids, sometimes. If it was related to inflammation, and the repair occurred reasonably close to when the injury occurred, they sometimes will recover that, and you don’t have to deal with it if that happens. So you’ll see vertical deviations in floor fractures. Sometimes they’re difficult to fix. Vertical strabismus following cataract surgery — that’s a whole nother issue. There used to be quite a few from retrobulbar anesthesia procedures, attributed to — very many. And what happens is: If you inject a retrobulbar, you get into the muscle itself, it’s very toxic to the muscle, and it causes fibrosis. I don’t think I have a slide about that here, but one of my other lectures I do, maybe. But believe it or not… You all know about Botox, right? Botox toxin? You know, it was developed by Dr. Alan Scott in San Francisco, who tried different toxins to weaken the muscles. You had snake venom. A few other things. He tried concentrated aminoglycosides, because they can damage muscles. All kinds of things that didn’t work. Botox he settled on, because it was low dose, it was controllable, and things like that. So he is always — he’s a great thinker. He’s still practicing. He’s probably in his late ’80s, I would say. But only about 4 or 5 years ago, he started thinking about… Gee. Since people get retrobulbar anesthesia, when they inject the inferior rectus, they actually get this restriction of the muscle, this tightening. What happens is — when you inject it, similar to what I said with the floor fractures — so let’s say you inadvertently inject the inferior rectus muscle. Okay? And I’ve seen this clinically with patients that have had this done after cataract surgery. In the short term, when they first come in, they actually have a hypertropia. Because they’ve had an injection right into the muscle, which weakened it. But over weeks, as the fibrosis occurs from the damage, from the injection, into the muscle, they get progressive hypotropias. And the eye comes down and down and down. So after six or eight weeks, many of them have a vertical deviation that was opposite what they had right after the procedure, and it’s due to an inferior rectus fibrosis or restriction. So Dr. Scott has been using this to strengthen or augment some muscles. So he’ll inject the muscle with Botox, with bupivacaine, right? He’ll inject it into the muscle, and that will cause some fibrosis. Sometimes he figures he can cause restriction of the muscle with — inject marcaine or bupivacaine, and then inject the antagonist with Botox, and try to control the deviation somehow. So these are all kind of wild ideas, but I can think of cases where it could be useful. You know, in some things. But it just gives you an idea — it’s just interesting, how inadvertently, the muscle is getting injected — caused him to realize that perhaps you could take advantage of that fibrosis that’s induced by the anesthetic agents, and use that to modify muscle position. You’ll hear and read about it. There are now articles popping up about treating different conditions and strabismus with injection into the muscle. You know, most of these injections, in my experience, they work okay for certain things, but they don’t have — they don’t usually give you a definitive long-term effect, in many of them. Except I like — I do some acute 6th nerve palsies, where I’ll inject the medial rectus muscle, banking on the fact that it’s gonna wear off in a little while, and maybe give them the chance to recover some of their 6th nerve. So there are some things. That’s a whole nother topic too. Left orbital floor fracture here. That’s what I was talking about. All the damage over there. Muscles entrapped. Presents with a hypotropia, can’t elevate the eye. This one didn’t have an issue afterward, no paresis of the nerve. Left pretty good, pretty well. But, you know, they refer to — I don’t know if you’ve ever heard this term, but in children, there’s a term they call “white orbital fractures”. And what it means is that, just like this guy, children, they often get these fractures, they don’t have signs. No ecchymosis, no bruising around the orbit, and it can occur. To give an extreme example, I got called in the hospital, inpatient, to see a kid who had double vision and a vertical strabismus. And they called me and said: We think he’s got a neurologic issue. We’re not sure why. We can’t find any reason for the double vision. So I go to the hospital, and they did an MRI scan of the brain. Didn’t really look at the muscles. They just looked at the brain. And they said… He doesn’t have a tumor, so he must be okay. I said… Gee, for all the world, he looks like he had a fracture. He can’t elevate his eye. This is acute. What else can cause that? You know? It was a normal scan of the brain. And I started talking to the kid, and he said… I keep telling these people, I was playing with my brother, and I rolled over, and I think I hit my knee, when I did a somersault or tumble over it. I thought I hit my knee on the bottom of my lid, and it hurt. You know? I didn’t say anything until I went home, and anyway… So he said… Let’s get a CAT scan. So we got a CAT scan of the orbit, and sure enough, he had a fracture. But he had absolutely no signs of external trauma that would lead you to suspect that. So that’s the story of the white orbital fractures that occur in children, frequently. I guess because the bones are more fragile, and they can blow out more easily. So anyway, so I think that’s gonna be it for this lecture. But we’ll have to go over the objectives and the questions again. So to describe the typical findings of 4th cranial nerve palsy or paresis, we did. Learn how to use the three-step test to diagnose cyclovertical muscle palsies. I think we’ve accomplished that. And then understand why the third step confirms the diagnosis. So let’s go back to the questions. I think that’s what we’re gonna do. And number one… Everybody have their answering things out? Okay, good. Okay. Ocular torticollis, head tilt, may occur in Duane retraction syndrome, fourth cranial nerve palsy, congenital nystagmus, or all of the above. And if anybody gets this wrong, I’ll never get invited back to Orbis again, so please try to do your best. So let’s see. That looks pretty good. Let’s see what we got. So good. We got 100%. All of the above. Certainly they can all cause head tilt or head position tilt. Okay. Good. There’s two more questions, though. Actually, three more. The next question: Significant overaction of the inferior oblique muscle is more likely to occur in an acute 4th cranial nerve palsy than in a congenital type. True or false? So somebody still says it’s true. Probably the person that walked in a little late from lecture. I talked about this right at the very beginning. And just to go over that, the reason that it happens is that, over time, the congenital types generally develop fusional vergences that produce these large overactions of the inferior oblique, whereas the acute types don’t have the time for that to happen. Understand? And let’s go quickly to the next one. The upshoot or overelevation of the adducted eye in Duane’s syndrome is secondary to inferior oblique muscle overaction. True or false? Well, for the sake of speed, we’ll do it. And 50% still say true, 50% false. It is not. Like I said, it’s due to the lateral rectus sliding on the globe. Okay? One more. I guess that’s it. So very good.

 

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May 25, 2018

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