 Okay, anyway, we're gonna talk about a bunch of stuff that hopefully will jog your memory and guide a bit of your reviewing. It's not, you know, in an hour to do an all-encompassing review of everything you need to know about paints, but that'll be a fair amount. It is useful, and there are some things, you know, the way I used to approach this was to think about what I would ask if I were writing the test. I think that's a useful, it was a useful strategy for me in terms of thinking about different things. And, you know, there are obvious things about blood vessels. One of the questions is what, as far as blood supply to muscles, talking about, you know, pediatric ophthalmology, what's different as far as blood supply to the rectus muscles? Just thinking of the rectus muscles. How many intercellular vessels do you have in each muscle? Two, except, I don't know, lateral rectus typically has one. Realize that when you're in the operating room, sometimes that isn't the case, but that's the answer for this purpose of this test. Another question might be, with nerve supply, which muscle does not have its nerve supply come from inside the muscle cone? Superbly. Yeah, and that is useful if you're talking about doing a complex orbital dissection and somebody's stinking around somewhere and you're worrying about not denervating a muscle. Otherwise, when you're reaching back in the orbit with retractors and hooks and various things, you can catch blood vessels and, you know, or if you were trying to do a procedure that I don't think ever should be done in humans, but called denervation and extirpation of the inferior bleak that some people think is a good thing to do, you need to know where the nerve supply to the inferior bleak is to destroy it. I'm not sure it's really offended me enough to destroy it, but some people don't agree. Now, the distance that the muscles are from the limbis, their insertion typically, and these are based on population studies where multiple things are measured, does show up at times, and this difference in distance going around from medial to superior rectus, going from about five and a half to almost eight, is called the spiral up to low that does show up. And the other thing that is useful in your understanding and of practical significance is this issue of the difference between the visual axis and the angle that these muscles, the vertical rectus, superior and inferior rectus make, and then the inferior bleak, which comes from the floor of the orbit up under the lateral rectus here, and inserts posteriorly, and the superior bleak, and the superior bleak, inferior bleak make an angle of 51 degrees with this visual axis and the rectus muscles 23 degrees. More importantly, when you turn the eye out, if you would see here, just to bring the visual axis out this way, you're gonna be more lined up with the vertical rectus muscles, and when you add up the eye, you're more lined up with the obliques. That is the reason when we talk about diagnostic positions of gaze that we're talking about the abducted eye separating the vertical function of the obliques, the abducted eye vertical function of the rectus muscles. And as far as another common question might be which muscle has the longest tendon? That would be the superior bleak. Which one has the shortest tendon? Inferior bleak, usually no tendon at all. And which ones originate from the annulus of zen? This table is taken right out of the home study course book, and I think it is useful. The other thing that is useful over here are the primary, secondary, and tertiary functions, realizing that with the oblique muscles, the primary functions are the cyclorotatory functions. And one way I try to remember this, if you remember that both of the oblique muscles, superior and inferior bleak, abduct, the vertical rectus muscles, superior and inferior rectus, adduct, and the muscles on top of the eye, both superior bleak and superior rectus or encyclotortors and the inferior muscles or encyclotortors. And, you know, because there could be a question conceivably asking you about that. We're thinking about these planes of our axi's effect are totally bogus except that it does give us a way to think about ways that the eye rotates, but knowing that one's X, one's Y, and one's Z has never really helped me take care of a patient. The one way to remember this is X kind of like a cross goes across and Y comes out at you and the Z is the other one. And, but using that like pitch roll and yaw, you can describe any movement of the globe, basically. And I think this is useful, for example, if we're talking about shifting the medial lateral rectus muscles for an eye that's hypotropic and what we're gonna do is rotate the eye around this X axis, this axis, to rotate it up by shifting the muscles horizontally, the horizontal muscles vertically and displacing them. And so I think it is useful to think about that, but eyes don't come with those labels. And then quickly, as far as ductions, ductions or monocular movements of an eye, adduction, abduction, superduction, infraduction. And you can also have X-Cyclo and Encycloprotations called extortion or X-Cycloduction, Encycloduction. And as far as binocular movements, we have movements of the both eyes in the same direction, dextro and lever version, up gaze, down gaze, and then movements that are not in the same direction, convergence and divergence, convergence being an active thing, and then divergence just basically, for most animal species being the absence of convergence, not an active process. There's no center in the brain that I'm aware of that subserves divergence. Now what about Herring's law? What does that tell us? Basically tells us that the yolk muscles, the muscles that move both eyes in the same direction. So if my eyes are looking off to my right lateral rectus, right medial rectus, get the same amount of innervation. Why is that? It explains a bunch of things. First of all, we use that at times to try to make it harder for one eye to move to increase the nerve, the innervational input to the other eye. Poster or fixation suture are just simply weakening, the muscle will do that, to try to get a lateral rectus that is heretic from a six nerve palsy to work better, to increase range of binocularity. That works there. And the other place that this plays a role are in primary and secondary deviations. Nico, what's primary deviation? Which eye are you fixing with? You're fixing with sound eye, that's correct. Secondary deviation is the predicate. So if I have a right six nerve palsy, when I fix with my left eye, I've got a relatively small amount of esotropia, right? But when I fix with my right eye, it requires a huge amount of effort to keep that eye straight. That same effort goes to my left medial rectus, which is why the secondary deviation, isn't that, is always larger than the primary deviation. That's how, that's one of the ways you can tell that you're dealing with one of two things. What's the other thing that'll cause a picture that looks just like that, Chris? You're increasing innervational input because it's really hard to keep the eye straight. Let's say I had had facial trauma. Cause like a restriction? Yeah, exactly. And I had a medial wall blow up. And you know, I may not have muscle trapped, it may just be that I've got scar tissue from bleeding in the orbit. But bottom line is that you can't separate those two exactly, just based on primary and secondary deviations. And we'll see this with restrictive changes in grave disease. You know, if I've got a tight inferior rectus on the right side, and I'm trying to look here, you know, my left eye will be way up at the ceiling and if I fix with the left eye, I'm gonna have a little bit of a right hypotropia. And so you see the same sort of phenomenon. And when you see eyes that are misaligned and they show you this on OCAPS, always ask yourself the question, which eye is the problem? Because it isn't always obvious. If they're fixing with the peretic eye, the sound eye can do all kinds of goofy things. They're probably not gonna show you that in OCAPS, but possible. Now, Sherrington's law, on the other hand, basically says that when antagonist muscles are involved, like my right lateral, right medial rectus muscle, when I abduct my right eye, I get increased innervational input to the lateral and decreased to its antagonist muscle, the muscle that pulls against it. That's important. What's the classic example of a situation where this does not occur? Explains, absolutely. Ding, ding, ding, you get that question right. And this I mentioned earlier, the idea you say, well, I always thought that this was pretty diagnostic looking up and down, but when you're looking up and you're looking down, you've got both the superior rectus and inferior bleak elevating the eye, inferior rectus super bleak compressing the eye, so you cannot separate those functions, whereas when we look here and we're looking up and right, the major elevator of this left eye is the inferior bleak, major elevator is the superior rectus. Those sorts of questions do show up from time to time. We're knowing about that. Again, the depressors here on my left eye down and right, and this is as you look at the patient, like when we're not as the patient is looking at their visual field, you're basically looking at the patient describing what, this is just what you see as you look at them. The major depressor and abduction is superior bleak, the major depressor and abduction is inferior rectus. And horizontally it's darn straightforward, but the reason they call these diagnostic positions in each of these six fields, there is one muscle that is the major mover of the eye in that direction, and you're looking at the function of that muscle. Now, sensory physiology, we're gonna kind of cruise through this, but questions do show up about this, about retinal correspondence, the horopter, which is a probably no other practical significance, in this v-fneuler circle, certainly of no other practical significance. Fusion is worth considering, and it does play a role particularly in sorting out how long one is heads for business and in deciding what to do with adults with strabismus to not give them terminal diplopia. Now, this is this picture again from the home study course, and this patient is looking at this point, f. And relative to that, there is a, you know, if everything, this is called the empirical horopter, this thing here, or this v-fneuler circle, and the idea is that on this circle, everything, every point along there while you're looking at f, is gonna be perceived and fall on corresponding areas in the retina in each eye. And so the idea is that anything on that plane, and it's basically not just a line, it is a surface, is going to appear to be single. It turns out on the other hand, there's this thing called panum space, and there have been questions before about this, and the question might be, if you're looking at object f and something is here or here, how is the patient perceive it? The idea is that in this space, if you're looking, and only if you're looking at f, because this only exists relative to that circumstance, anything that you see that isn't exactly on this plane is gonna be perceived to have stereo. Anything outside it is gonna be perceived to be double, relative to this point f. You can kind of see, and one of the things you wanna look at here is as you get farther from fixation, that space widens out quite a bit, where you can see something, and it'll look like it has depth and not appear to be double. If you take a piece of wire coat hanger, and you look at something, like the tip of a pencil, and you take the coat hanger, and you go back and forth, you'll see that the coat hanger looks single, then it looks double, then it looks single and double again, and you'll see, you can tell that it looks like it's farther away or closer than what you're looking at, and if you do it out here, it takes longer to get through that area. I mean, so this actually works, and is it of practical significance? It probably explains to some extent why when you look at patients in my clinic, and they are not perfectly straight. They're straight, give or take a little, and they've got stereopsis, they're not complaining of diplopia, and they're happy. You say, well, I thought we had to get their eyes absolutely perfectly straight, and the answer to that question is, we'd like them to be perfectly straight, but really what we're doing is getting them in a range where they can comfortably use their horizontal, vertical, and torsional fusion mechanisms, their ability to take an image and put the image together to do that comfortably and consistently so they can function. And then we've done our job in kids. It has to be close enough that they don't develop amblyopia. Now, interrupt if there are questions about any of this. These are things that, again, one of my philosophy and why you take OCAPs is that it causes you to collect all this information, the things you've been reading about. If you haven't been reading regularly, you are in deep stuff, but because that's something that you need to be doing, but bottom line is that it causes you to collect all this information, kind of organize your thoughts about it, and you do that once a year, and I think you turn out to be a better ophthalmologist. Now, retinal correspondence refers to, the idea is that there are points in each retina that relate at a cortical level to each other. If the situation is that things that should relate in right eye, the things in the left eye, then we have a situation of normal retinal correspondence. And if you grew up with a straight eyes, normal visual system, that is the circumstance. Anything else that involves anomalous retinal correspondence, whether it's harmonious or non-harmonious, we'll talk about that, implies that you had early childhoods for business because that is the only circumstance where you can develop anomalous retinal correspondence. So there might be a question that pertains to that. And we're gonna look at this just a bit more. Other issues, we're gonna talk about suppression, refers to the phenomenon, which is good if there was nothing we could do about strabismus, ambliopia and the like, where in infancy again, and childhood while the visual system is developing, you ignore enough information from one eye to not see a double. And that allows one to function and allow one hopefully to catch another mammoth, woolly mammoth or dinosaur or something and survive and pass that on. But in mono fixation, on the other hand, refers to a specific circumstance where you have subtle abnormalities in binocularity, usually very, very small angles for business. It may be small enough that you cannot even see it on cover testing, but it is a stable arrangement. And when we're talking about operating on children with infantile esotropia, infantile exotropia, this is the most likely desirable outcome. Rarely do we ever get those kids so they have straight eyes, normal binocularity. The usual outcome is mono fixation syndrome with good vision in each eye. And that has shown up as a question in OPACS before. Now, Nico, what if I wanted to test Becca for mono fixation syndrome? She came in, she had mild amblyopia and one eye. And her eyes looked perfectly straight and she didn't have anisomotropia. And you're saying, gosh, when I was on Peds, I learned that I'm supposed to come to some resolution as to how she developed amblyopia. How, what test, quick and dirty test you can do in any exam room once you have a box of prisons? Well, I was thinking, where's four dot if you do that test with the little teeny ones and you get far away and one of them disappears and you have a very observed patient will work. But let's say, let's stretch here and let's say she is a five-year-old. I'll make her a five-year-old first. Four-diameter base-out prism. And a four-diameter base-out prism test, what you're doing is you're just displacing the image on the fovea of the eye that you're placing it in front of. So while the patient is fixing, if I have mono-fixation syndrome and I've got a micro-tropi, I've got a little area that I'm suppressing in one eye, when I move the prism in front of their two things, normal situation, move that four-diameter base-out prism in front of one eye, you're gonna see a version movement. Both eyes are gonna move to pick up this new object, right? And then this eye, you're gonna realize, hey, I'm not looking at that, you're gonna see a virgins movement. And so you wanna look for both of those things, version and then the virgins movement to have both eyes looking at the same thing so that when I put this, let's say this eye is got a suppression scatoma, I move the prism here, I'm gonna see the version, but I'm not gonna see the versions. Let's, now when I put it in front of this eye because there's a suppression scatoma here and that's only there when I am binocular, when I do visual field testing, there's nothing wrong, right? I move it here, there's no movement at all. And that test actually works very well, but it is absolutely essential that you have a relatively small target because you gotta make the target disappear. You know, it's gotta be less than the size of their suppressant scatoma and a four-diameter base-out prism test and that test works. And so that, it's my favorite test to do for that, but you're right, if you do these, use the, there's a version of the, not the regular word four-dot, the word four-dot named after a guy named Claude Worth who's a famous, you know, strabizmologist of long ago, is it, we'll talk about it, it's a test of binocularity, not stereopsis and with the regular size spots, what you can do is you can walk to the end of the room with that and the farther you get away from the patient, suddenly they start suppressing one eye and that will work, that's good. You get points for that. I'm not sure that would be the right answer on the test. It might be both of those things. And then the other, this is a key kind of concept that you have to use to understand what patients are experiencing and it is worth spending just a moment kind of thinking through and also will play a key role in those goofy pictures from the Bagelini lenses, which are only pertinent to residents in OCAPs and the other issue are the after image test things because they're talking about two different things. The idea is which way things move when they become double, when you're esotropic or exotropic and you need to be able to think through this and remember, I wouldn't memorize it. I mean, you can memorize it. It's not a lot of information, but the idea is that if my right eye is esotropic and I am looking here at Nico, Nico's image, my left eye is gonna be on the fovea, isn't it? And some of the area around it because the image in Nico is gonna be a little larger than my fovea, but bottom line is that in my right eye, it's gonna be on nasal retina. Normally, when I am looking at something with a fovea, everything in nasal retina so serves temporal space. Everything on the temporal to the fovea and you have to keep this in mind, not the optic nerve, the fovea, that's the zero point. Temporal retina, nasal visual space so that if my retinas are still working together normally, I have normal retinal correspondence and I'm esotropic, Nico falls on the nasal retina, which tells me he's over here. Now that's why with esotropia, you wind up with what's called uncrossed aplopia. Nico's image, if I turn my right eye in, the image from my right eye is going to move over here. Contrast that I'm now exotropic, okay? And I'm looking at Mike over here and bottom line is when I'm exotropic, he falls on temporal retina, which is gonna tell me that he's over here so Mike's image is gonna, from my right eye, is gonna move over here, it's crossed, okay? As opposed to uncrossed esotropia, crossed exotropia. Anybody not get that? Cause that is gonna be key to some things we're talking about. You need to, if it's, talk to me later, we'll draw pictures and make it make sense because otherwise a lot of what I'm gonna talk about in the next few minutes here isn't gonna make a lot of sense to you and there usually are questions about this on this test. Now, let's look at levels of binocularity and sidestep for a second. And there's sort of three levels of things we're talking about here. One is simultaneous perception. I'm seeing something at the same time out of two eyes. And fairly dense amblyobia can do that. The other is I can take the two images and put them together. And the third is I can tell subtle differences in where things are in space, stereopsis. Now in this picture here, there's nothing that is at all similar here or here, but if the chickens look like they're behind the chicken wire, I'm seeing both of those images. Simultaneous perception. Here there are differences in the two pictures. And if I can make it like this, I fuse those two images to make them one. I've had to overlap the ship in one with the other, the elephant in one with the other. And yet I'm picking up this and this that are different in the two pictures. On the other hand, if I present something where something is offset here and perceive it as being raised coming out of the page, I have stereo. And in this, sometimes there are questions about this in terms of the anatomy of the system that helps perceive this. And when we look at this, we have these different magnicellular and parbicellular systems that have to do with different parts of our vision. And that's kind of beyond the scope of what we're reviewing here this morning. But it's worth being aware of that at least. Now, Nico mentioned what I affectionately in clinic call the worthless four dot test. Basically, the worth four dot test is mainly used by people to show parents that they've done something wonderful for their kids when they've operated on them, because most kids after surgery will be able to say, yeah, I'm binocular. It's a test to say you're using both eyes. But I've not found that it gives me a lot of useful information. The bagelini lenses, Bruno Bagelini was an Italian ophthalmologist, maybe striated glasses. In the glasses, the lenses are, with the striations, oriented a certain way. You always put them in front the same way. There is one. I have one if you want to play with it and use. What you do is use the transluminator light and look at it. And similar to the Maddox rod that you have in clinic and use for double Maddox rod testing, you can use the bagelini lenses. And looking at where that pinpoint of light is, if the patient sees one light, they're binocular. Their eyes are lined up usually. And if they have diplopia, the position of the one from the right and the left eye sometimes give you information about whether they're isotropic or exotropic. For my money, you're better looking at the patient, cover testing, and measuring it. That's what we do. If you're trying to look at SHOPCO and the eye department, that test might be useful like the red glass test is where you hold the red lens in front of one eye, shine the light, and see where the white light and the red light are. And again, we see patients come in with that. I would urge you to go beyond that. And we're going to look at that bagelini lens thing as it appears in the test you're going to take. After image testing is actually a very cool test, takes a long filament in a long, skinny light bulb, and you put a piece of tape around the middle with a dot on it, and you ask the patient to look at it, one eye holding it vertical, one eye holding it horizontal. What you're doing is labeling the fovea in each eye, assuming the patient sees with each eye. You're saying, I'm going to tag the fovea here. I'm going to tag the fovea here. And then with both eyes open and they have the after image from that, I'm going to ask the patient where those things are in relation to each other and get useful information, which is different than this bagelini lens test where the patient has both eyes open. They're looking simultaneously, and we're talking about generally whether they have uncrossed or crossed the fovea, which is the way to answer those tests. And we're going to look at that. The ambioscope is a very elaborate device that allows you to directly measure horizontal, vertical, and torsional the fovea. I think there is one in the Moran graveyard, but we do not use it. You will likely never seen it used in our clinic, although Julie may, if I can find it, resurrect it just so you can all see what it looks like. Dr. Dries recently had a patient where he thought it might be helpful, so I'm going to see if it's not been sent to the scrap heap. I once threatened to use it for an anchor for my boat. And so we've talked about this. And this is Ilda Kapok. She is the chief of pediatric ophthalmology, Baskin Palmer. This was when she was, I think, a fellow with my buddy W. Elkhorn at Wilmer. And she posed for this picture that Dr. Geithan published. You put the red lens before the right eye, green lens before the left, and then you look at this combination of two green, one red, one white light. And if you see four lights, you're normal. If you see two red, you're suppressing the green. If you see three green, the white will look green. You're suppressing the right eye. And that may be a question about that. And if you see five dots, the patient is the pulpic. And if they have something that doesn't add up to five dots and they're seeing more than four dots, the patient is crazy. Or they're just jerking you around, or they can't count. But at that point, you're not going to get a lot of useful information from that test. Now, there's baglini lens test. And this is basically the normal situation. This black dot refers to the tip of the transilluminator light as you're looking at it. And so what we're looking at here is this pattern. And this is the right eye, where the right eye, the striations. So the striations are actually going this way to give you this similar to what happens with your Maddox rod. And vice versa for the left eye, normal situation. If we have a tiny suppression scatoma, mono fixation with one eye, you may have a very observant patient that can tell you there's a little break in the line. I've never found that to be a useful test personally. And if you've got normal retinal core, and this also is with normal retinal correspondence. Now, let's say we're esotropic. And we're going to pop down to this because these are the ones that they usually get you on. Notice here with esotropia, the image to the right eye shifted to the right. The image to the left eye shifted to the left. That is uncrossed or crossed? Uncrossed, right? And we just said for esotropia, you get uncrossed apopia. So look at where those are, and you can answer that. And the same here, the idea is that the image for the right is over on the left. The one on the left is over on the right. It's crossed. This is exotropia. When I was a resident, I spent a fair amount of time trying to make some significance out of whether these lines intersected above or below where the dots were. And it turns out that it's actually no significance at all. But there you are. And I didn't have anybody to tell me that this was just due to crossed or uncrossed apopia. So if you remember that concept, which is why I mentioned it, you will make sense of these. And now if you've got a large suppression scatoma, you can see something like this. If you suppress all one eye, you may see something like this. This test, there's a reason that it's not widely used. It's difficult to administer and interpret. Dr. Bagalini used it extensively, but I'm not sure that outside of his close circle in Italy, it received widespread acceptance. He was a very smart, capable pediatric ophthalmologist, kind of at the time, actually wasn't a pediatric, he was interested in strabismus. Long before there was anything called a pediatric ophthalmologist. Now after image testing, again, we do have one. If you have it, please let me know because it has disappeared. If you see it, it looks like a long fluorescent light tube with a core coming out of it. You plug it in, it used to light up when I saw it last. And it's kind of fun to play with. But that's the extent of it. And so with this again, this is a different concept than cross and uncrossed apopia. And the question might be, and this is where they get you, the answer, remember what we're doing is we're tagging the fovea in one eye and we're tagging the fovea in the other eye. The question often is the patient's got 65 diopters of esotropia, 10 diopters of right hypertropia, and 15 degrees of x-cycle of torsion. And you do after image testing, what does the picture look like? And guess what? No matter what the information they give you, if the patient has normal retinal correspondence, this is what they're gonna think when one fovea is doing relative to the other. Doesn't matter what their misalignment is. I mean, they're gonna beat the pulpic to beat the band, but when you label the fovea in one eye and you ask the patient where the fovea is in relation to the other eye, they're gonna put those, their brain's still gonna put those images together and it's gonna look like this. That question has shown up. Now it gets a little tricky here and you have to think back to what we went through to make sense of cross and uncrossed apopia. And it has to do with where the fovea thinks it is. Let's say I am esotropic and I've labeled the fovea in my right eye, but I have a pseudophobia, the thing that is looking at the object of regard, which is now in nasal retina, right? Right? What that makes my fovea now, the true fovea, which I've labeled, it thinks it's part of temporal retina. And you have to use that to go back to that analogy that the temporal retina has to do with things in the nasal side, right? And things in the nasal side, so that basically what it's gonna do is it's gonna do just the opposite of what happens with the uncrossed and crossed apopia. And that's where these things come from. And you need to sit down, think about that, make sense of it, if it isn't making sense, we can kind of draw it out together. So you're asking where the true fovea thinks it is relative to the real, you know, the pseudophobia, that's a term that I've made up to try to make sense of this. And this only occurs, this only occurs in the face of anomalous retinal correspondence where things are not relating as they were at the get-go. Otherwise, this will be the answer. And, yes? Question, in this test, does the distance of the target matter? The target is, it really doesn't, in that, I mean, the way people do it is they just hold it right here and they say, what you do is you say, stare at this, you have them look at it for like 30 seconds, then they look here for 30 seconds and you say, what do you see? And so, I think if it got, yeah, you could, if you had a suppression scatoma, you're correct, but I don't think anybody has used this test to try to detect suppression. And in fact, I don't think anybody, you know, the people that did this mainly were doctors who were at Wilmer who had maybe three patients a day that Dr. Geithen was seeing because he spent all day seeing them. And that's what he does. And Dave's a wonderful guy, but he doesn't see a lot of patients. And he's one of these really smart guys, scary smart, and then you met David Geithen. His dad was the guy that wrote Geithen's physiology. And he is a scary smart guy, but he doesn't see a lot of patients. It's kind of like the pediatric ophthalmology version of neuro-optimology clinic going wild. And it is, but this is something that's useful just to think through so you can make sense of it. Now, the other thing we didn't talk about with this was this issue, and I may come to this, I can't remember if it's in this slide set up, but harmonious, nonharmonious anomalous retinal correspondence. Let's say I measure with the amblyoscope that my eyes think that I'm 30 prison diopters, isotropic from a sensory standpoint, where my brain thinks it is. And when I do cover testing, I'm 30 prison diopters, isotropic. That's called harmonious. But if there is a difference in the two, from a sensory standpoint, I'm 20 diopters ET, when I measure it with prison and cover testing, I'm 40 prison diopters ET, that would be nonharmonious. And what that usually implies is that somewhere in development, alignment changed. We did surgery, they got glasses, their eyes were straighter for a while. And so they grew up in two different regimes as far as ocular alignment. And that's where nonharmonious ARC comes from. Develops over time. Now, the tests of stereopsis. TIPMAS test, watch for monocular clues. Grab a TIPMAS test in clinic, the one with the dots and the fly. Look at it with one eye and see how many of them you can get, asking the question, which one looks different. Then if you take the book and you hold the book as you're looking at it with the circles, you turn the book upside down, you'll notice that the dot that looks like it's stuck up, now looks like it sticks in. If a patient can tell you that without you prompting them, they've got true stereopsis for that test. That's a practical way that won't be on this test to sort that out. But otherwise, monocular clues, the smart kid who's answering the question, which one looks different because we ask that question all the time with children. Randot, which uses a different methodology, there are still some monocular clues just because of the way things are printed, but it isn't, and this is the TITMAS test, and this is the bone anchor, the amblyoscope. It looks like a research device. Notice the old-time switches and knobs. I don't think anyone has made one of those things in 50 years. They're not manufactured anymore and no one uses them practically. It takes forever to use it. It doesn't add a lot to change patient care. Now, what about amblyopia? You need to know, yeah, two to 4% depending on estimates, the population, and you could conceivably get a question because now there's a big push from the American Academy of Ophthalmology, American Academy of Pediatrics on preverbal amblyopia screening. And the question is, what is it based on? Might ask a question about that. And it is not based on asking, you know, measuring visual acuity. It is based on looking for amblyogenic factors. So you don't directly measure amblyopia, whereas if we're measuring visual acuity in a six-year-old, you find out that vision is 20, 20, and 2400 best corrected. You're directly measuring their amblyopia, the degree of amblyopia. In preverbal screening, most of these devices have something that will give you some sort of auto-refraction and some sense of ocular alignment, media opacity, some things of that sort, things that could cause amblyopia, amblyogenic factors. And I think that is important and it's now being recommended down to age one. And so every primary care doc and what has driven this unfortunately, the same thing that drives many things in medicine and that is someone developed a billing code. They can bill for doing it, therefore it's become a good thing to do. On the other hand, if you're talking about asking you to go out as a pediatrician and buy, you know, an eight or $10,000 device that you can't get any reimbursement for just because it's good for your patients, or they could take your family to Disney World, they're gonna go to Disney World every time. And so they need anyone. Now, strobismic, amblyopia that develops because of misalignment of the eyes, ignoring diplopia, developing a suppression scatoma, and isometropia, this is the circumstance where we have straight eyes, big difference in refractive area one eye compared to the other. And that is something that is the most commonly missed and what has really driven this early childhood screening that for bilateral or amatropic amblyopia, large hyperopia, astigmatism, for those of you who've been down to the Navajo reservation with us in the Southwestern Native American population, there is huge refractive area, usually combinations of myopia and astigmatism. And so a lot of these children will have amatropic amblyopia. The thing that's surprising to me and Chris and Nico and you guys have been down there with us, I think the idea is that why don't more of them have it? Because some of them actually function fairly well despite having huge amounts of astigmatism. So there's some piece of that puzzle that we're not still quite understanding that I'm gonna need your help to sort out. Couple of concepts. First of all, deprivation is the other kind but this crowding phenomenon, what's that referred to? That shows up as a question at times in some way. The idea with crowding phenomenon is a physiologic observation that in terms of visual physiology, system physiology, if you present single optotypes to an amblyopic eye, they will do better on the eye chart than if you present linear, multiple figures, optotypes, the little individual figures on an eye chart. And so you always want to present linear figures or use those surround bars you'll see on the HOTB test. And most of you now, we're brought up, I suppose, all using projected charts. Most of you don't have wall charts or anything that you're measuring patients on. So that you wanna be sure. I mean, my cake home message for you for this is know what the people who are measuring acuity for you are using. They are representing you and if they're not doing what you need done, it is easier with a four-year-old to take individual pictures and they go down and they miss amblyopia. So if they're gonna do that, use the surround bars and I think we may have a picture of that here somewhere we'll kinda, actually we may not but they're basically the little bars that occur around the optotype. You'll see those on the M&S systems. There, once you get to that, you can put those on there and I'd urge you to use that because you will miss less. It simulates linear optotypes. So you wanna eliminate the causes. You wanna achieve equally focused images due either occlusion or penalization. There are new things that probably won't show up on OCAPS but you'll hear about using stimulation of both eyes and various sorts of circumstances to treat amblyopia, exciting stuff and that is something though that is coming probably not to show up in a test like this though at the moment. And now, let's run through strabismus, terminology, types of deviations and whatnot and this angle cap of things so that you can figure out the answer because there is often a question about that and a question about the three-step test. So, as far as terminology, ET, XT, you know, right hypertropia, RHT, left hypertropia, go right out the word hypo. If there's parenthesis around the T, what does that imply? An intermittent deviation. And what about angle kappa? What's that all about? If there's displacement of the fovea, making it look like the patient is strabismic and the classic and the way I would remember that is in RLP, the fovea is almost always dragged temporally. Simulating now, if I drag my fovea temporally, my eye is going to turn out like this to put that temporally dragged fovea looking right here at NICO, isn't it? And so, it looks like, and I have seen kids, post premature kids, more than several, that look like their eyes are looking east and west, if they've had dragging of the retina in both eyes. But when you do cover testing, they're moving out like this to pick up fixation. So, they're from a motor standpoint, alignment standpoint, they're isotropic. From an appearance standpoint, they already look funny and their eyes are turned out. And so, when you talk to parents and say, well, I could give her a little better chance of using the two eyes together if we made her eyes straighter this way, but it's going to make her look real funny. And they never opt for that of smart parents. But it's really funny how that works. And so, the thing you don't want to do is look at that post premature kid and say, well, obviously the eyes are turned out, they look like they're turned out to me, and I'm going to straighten them out because you're going to make the patient worse in the standpoint of esotropia. And you're likely going to cause them to lose vision as a result. They're going to develop angliopia. That's one of the reasons that we wait and we look and measure and re-measure and make sure we know what the heck's going on. Three-step test will go through if it doesn't show up here in the next few slides here. Now, infantile esotropia, accommodative, peretic, and other, and this includes Dwayne's, all of these issues, and let's, and intermittent exotropia. Now, exotropia, let's back up for, well, intermittent XT, infantile, infantile exotropia, similar to infantile ET, both of these disorders have large angle misalignment showing up in the first six months of life. They don't have significant refractive error, probably due to a failure in the process of acquiring binocularity, and they benefit from early surgery in getting some sort of stable alignment, but you cannot make it as if they never had the problem. Then sensory deviations, we're going to talk about just a little bit as well here. Vertical deviations, when you're thinking through this, think about dissociated vertical deviation, thyroid, oblique dysfunction, and then the role of the vertical muscles in A and V patterns, mainly the superior oblique and inferior oblique. Now, how do we separate dissociated vertical deviation, this up, down from a true hyper deviation? With a true hyper, you're going to have a hyper-hypo relationship. When I go from one eye to the other, I'm going to do this, and if you don't see a true hyper-hypo relationship where we alternate when we're doing our cover testing, all I see is I go from this side to this side, I'm saying this happened, this happened, and if you look carefully, you will often see a little x-cyclo and a little x-so movement as well. This is what's called dissociated stir business complex. All three of those things are part of this. Mike Brodsky's related DVD to, and he's at Mayo now, was in Oklahoma, the Dorsal Writing Reflex and Fish. He's another one of these scary smart guys like Dave Guyden, who sits and thinks about things, and it makes sense to him. I've listened to him talk about it several times, and I still can't quite get on board with it, but he thinks it's really cool. So, worth reading about. Now, let's look at some things here for show and tell, and I want to go through these. What's this patient have? Type of deviation? Esotropia, which eye is fixing? So this would be right, esotropia. And let's look here, and then we're gonna look here. Now, what's this patient have? Exotropia. You look at where the corneal leg reflexes is shifted, and you can't tell which eye, I mean, you say does the patient have INO or a third nerve palsy? Well, they could, but nothing to support a third nerve palsy, and without looking at movements and the speed of saccades and that, you can't tell. Wait a second. Let's go back here to this patient. On the other hand, if you look carefully, let's hear a list of things. What's wrong with this patient? Just describe what you see, right? You got left hypo, and the left eye, I think, is also a little exo. Is the lid down a little bit? Is there a little bit of anisecoria? Okay, and so, can you put that together? Third nerve palsy. So this is a third nerve palsy. This is a kid with a brain tumor, okay? So this is the right answer for this kid would have been to get an urgent neuroimaging study, which was actually done the day this photo was taken, and then it was turned over to neurosurgery and the oncology services. This is classic, this beautiful picture of an intermittent deviation. Straight eyes, top, E.T., right E.T. here at the bottom, after the cover is removed. So this isn't aphoria. Remember, for you, my eyes are misaligned only when I prevent binocularity. This is an intermittent tropia because her eyes became misaligned and when you take the cover away, they stay crossed for a bit. And then, she'll straighten out. And so that is an intermittent desatropy is not that common a problem. Whereas intermittent dexatropy, as you're already aware, is probably the most common or second most common type of strabismus that we deal with here, all across almost everywhere you go in Asia, intermittent dexatropy is by far the most common type of deviation, hands down. You'll see 10 intermittent, or maybe 15 or 20 intermittent dexity patients for every patient with accommodated E.T. or infantile E.T. There are regional differences. When I was a fellow in Indiana, we saw tons of kids with infantile dexatropy. Most of these tropes in our practice here are accommodated E.T. Why? I am not sure. Probably not good to be in Indiana. Now, this patient is the patient that gets sent in because of this difference in the appearance of the two eyes. Wide inter-campo distance and we have the same child later without the appearance of pseudo-esatropia and still having perfectly straight eyes. If you look at this patient, you could look at corneal light reflex testing. More elegantly, you could look at the Brookner test, simultaneous red reflex assessment, which would be symmetric. You could do cover testing, all of which will be normal. So this is a problem with looking crossed and how the child looks. You don't get that sense, that gestalt that the eyes are still crossed and this is the angle Kappa issue that we mentioned and we'll go beyond that. This is this red lens test that I talked about that they do at Shotco in the eye department. And you look here and what the child sees is this white light, one eye, the red line. And if the red is before the right eye and it's shifted off to the right side, are they E.T. or X.T., E.T., right? Uncross the plopio. And if it's off to the left side, it's crossed and you can use it to sort that out. But you have better means at your disposal. Where something like this might be helpful is when you see the patient after the adult patient after cataract surgery and they're complaining of double vision, you do cover testing, you look at them, you don't see anything going on. I mean, what I do with those patients is I put a little bit of vertical prism because usually it's vertical prism and you put a little bit base down, put a little bit base up and suddenly they say, ah, that's it. No more double vision. And you know which way it was off because subtle vertical changes often do to some sort of toxicity of an injected anesthetic with the inferior rectus muscle, usual culprit. This is the HES screen where you can map out the deviation who ran off with my length, the equipment for this and I've never seen it since and she didn't know any knowledge of it so I don't think that one's gonna surface. It's probably in somebody's office and this is an after image tester. And you look at this right here, you look at this and this is about as large as it looks when it's the right distance from you, Niko. And it occupies a lot of visual space. Now, this is, what's our concern gonna be? What is this, first of all? Yeah, that's a capillary hemangioma. Would you be worried about this and wanna do something with it? Okay, and what is the best current treatment option for this child? What's that? Bay blocker. Bay blocker, and what do you wanna make sure that this child doesn't have so you do not kill the child when you institute Bay blockers? Basis syndrome? Know about that, that could potentially show up in this circumstance because that's one of those things where if they've got that, and if they've got that, what you need to do is you probably need to get pediatric cardiology involved. It's gonna be a cardiac dent. And so the idea is that what we do here, we have a system that was set up on one of our dermatologists in conjunction with ER docs and Susan Ethridge from Pediatric Cardiology to admit kids and rapidly get them up to speed on systemic beta blockers. You can also use topical beta blockers if it's a period, but this thing's got enough thickness that for my money, you wanna be on a propranolol and it is a magic bolt. I mean, these things shrink. The idea is, and as far as ways this can cause amblyopia, the obvious one is that it's blocking vision. But the other ways, if it extends into the orbit, it can cause hypotropia. So misalignment of the eyes, it also can push on the eye, usually causing astigmatism, so anisomatropia. So always, always, always, you see a kid with something like this refractive. Now, this kid, this is a child who's got isotropia. He's straight in the glasses. What's your diagnosis? Okay, now, looking at this picture, question might be, what is the appropriate surgical procedure initially? And the answers might be, let's say they give you A, medial rectus precession, both eyes, B, recessed for sec procedure, free stroke of your left eye, C, lateral rectus precession, both eyes, or D, no surgery is appropriate at this time, which is, what's the answer? B, yeah, no surgery. Why will a patient's eyes are straight with the glasses? That's what you're trying to accomplish. And they will try to trip you up with things like that. Now, this patient has a high ACA ratio, high ratio of accommodative convergence to accommodation, meaning that when they accommodate for an object at near, they get more convergence per unit of focusing, per diopter of focusing. Ordinarily, you focus about three diopters to focus on things at near. You should get just enough convergence to allow you to keep both eyes looking at what you're looking at. If you get excess convergence, what happens is you wind up with extra esotropia, like this patient has here through the top of the glasses, and the eyes are much straighter through this cheap, I was made at JC Penney's executive bifocal. Don't ever do that to a patient. That's a terrible thing to do with a patient. This patient has equal vision. You can see he's fixing right eye, fixing left eye, alternating esotropia. What would be the best initial surgical procedure? Yes. And so what you want to do with that question is you want to eliminate, first of all, the ones that would move the eye in the wrong direction. When they say lateral rectus recession, both eyes, that would win a quick trip to risk management and they write out the check kind of a situation that would not be good. And they might have inferior oblique myectomy, both eyes, or superior oblique tuck. But you want to find something that A makes sense and then figure out which ones could potentially work and say, which would be the best for this because there may be some of those gray line kind of discussions. Now, this patient has dense amblyopia in this eye because of this and what is this? It's a morning glory optic nerve, basically without the pigment. It's an optic nerve cobalt. So this is sensory, meaning I see poorly out of this eye esotropia. So if they ask you for surgery on this patient, and this could be a question, the question is to make the eye look straight. First of all, do you do a recess, resect procedure on this eye, or do you operate on both medial rectus muscles? Yes, the reason you limit the surgery to this eye is you've got a normally seeing left eye and you've got an eye that might have finger counting vision in this eye and you don't want to operate on that normal eye to subject it to even a small amount of risk. Again, now this patient, this patient has sensor esotropia and actually this shows kind of this Brueckner test to its extreme. This is what 20 diopters of anisotropia looks like for this young lady who has monocular aphakia who is kind enough to take her contact lens out for me for this photograph. This patient has poor vision in one eye and someone recommended that they have medial rectus precession bilaterally for esotropia. Esotropia is there and they came for you to see you for a second opinion. First of all, is everything normal as the referring doctor described in the funds? No, what's wrong? What's the diagnosis? What's wrong here? Is there anything wrong? You look at this. This looks like the optic nerve is out here, right? Or maybe even here, but actually it's this little nubbin of stuff here. This is optic nerve hypoplasia, okay? So this raises some other issues. First of all, you know why the right eye is always the one that's turned in or left eye rather, I'm sorry, left eye is always turned in. And then the other thing though, there's some important questions you need to ask these parents. Is the child growing normally? Have they had an MRI scan? You look for midline pernial defects. And the other thing that everybody else forgets that you need to remember is there also is an association between optic nerve hypoplasia and basal encephalosil. And I've gotten our neurosurgeons here at primary more than once on that where I've insisted that the radiologists look for a basal encephalosil and then to see John Castle fixing the basal encephalosil and having him say, how did you know this kid had this? And it's a known association. I mean, it's not huge, but it's one of those questions to ask so that every time I see a kid with optic nerve hypoplasia, I ask them how they are doing in terms of their physical growth. If they're not where they should be on the growth chart, they need to see an endocrinologist. And some of these kids, I mean, the ones that have big problems, often they come to us from endocrinology knowing that they have panhypotuitourism and we need to probably ramble and let you guys get on with your day. The rest of this slide set Elaine has had for quite a while. So look through the pictures. This is a pretty picture. This is one of twins I took care of with these beautiful lens opacities. This kid, they'll show you one of these. Those are blood vessels in this white thing up against the back. The technical term for this appearance is what local cornea, what's this kid have? The kid's got, this kid's got retinoblastoma. That is a group E. I'm slamming the lens right up against the cornea and I believe this child also had iris neovascularization and then I became a past specimen. I went to the other Dr. Mandelos's lab. But they're gonna want a differential diagnosis so think through a differential diagnosis for that. And this patient, this patient has a left third nerve palsy. Now this is what you don't wanna do and somebody sent me this photo a long, long time ago and one of the take home messages that probably won't show up on OCAPS but when you've got a child with congenital cranial nerve palsy, do not patch the preferred eye all day or you'll create this situation. We talked about primary and secondary deviations and this patient has got a secondary deviation fixing with this is how she likes to fix with her peretic eye and this right eye way up here and it has 2,200 best correct vision and it was the previous normal eye and they came to see somebody because they've been patched too much and suddenly and once they switch fixation you will never get them back. So this is the one circumstance with a congenital cranial nerve palsy where you're never gonna make a binocular with a third nerve palsy. You wanna patch them just enough to keep that vision reasonable so for their only eye they can function but if you do too much patching you're gonna cause a big problem. So, an hour or two a day at most and follow them closely. What's this kid have? If anybody has to run feel free you don't need to stay here on my account otherwise I'll hang and run through a few more of these. This child is fixing with the right eye large angloisotropia, he's about five months old. What's the most likely diagnosis? Wayne syndrome, infantile estropia, the cognitive eti, infantile eti. Now, this is my daughter. This is how she looked when actually she presented at 18 months of age with misalignment of her eyes. Notice that her brookner test looking at the red reflex here is asymmetric, it's brighter from the more misaligned eye and she has estropia. She's now a nurse over primary. You'll see her when we make rounds in the NICU. And this is her, just you don't think of a bad parent when I put her in glasses and she does have 2015 acuity in good stereo. And you know, and so I put her in glasses. What's her diagnosis? Accommodative estropia. This is a child just to show you that people can have as one of my mentors said, lice and fleas, this patient has the appearance and this patient had been told by one pediatrician, the one the parents stopped going to that he just had a wide inter-campal distance and he was normal. And I'm here to tell you, when you look at this, look at where the light reflex is here. This eye is looking at you and these light reflexes aren't quite where they should be because the camera flash is not coaxial with the camera's viewpoint but this kid's got leftiesetropia in addition to the appearance. So he's got pseudo estropia and true estropia. And so yes, Asian kids with epicampal folds can get infantile estropia. And I've seen quite a few of them. And so beware that circumstance and look carefully from your own opinions. Now this patient, this is cool here. What we're seeing here is updrifting a little bit in interning, but updrifting mainly that right eye, this is manifest. It's staying there when we took the cover away, DVD. And this child here, this is very cool. If you look here, you'll see under the cover, the left eye go up here, the right eye go up here. This is latent DVD. We only operate on DVD if it is noticeable, causing problems, it doesn't cause amblyopia and operating on it, it doesn't make the kid see any better. So if they're getting picked on at school, you can operate on it. And it typically shows up as kids get into school age. Now this, three step test. This child walking down the cereal aisle at Smith's Food King, you look at this kid come down the aisle like this and you stop mom and you say, pardon me, your child has a, yeah, on which side? With that head tilt? Yes, absolutely. And why? Well, what happens is when he tips his head to the right, well, you remember our, we're not getting, it's the encyclorotation of the eye that's driving the head tilt, because what happens is when I come over here, there are two encyclorotators. Superbly, superrequisites, right? It turns out that the suprarectis is not nearly as good because it has so much less angle than the suprarectis on the globe. So when you tip your head here, the suprarectis tries to do the encyclorotation but it really overshoots with the vertical at the same time. And so that uplifting that you see when you tip the head, the greater hyper on the, the epsilon head tilt is from the other muscle taking on the cyclorotory function. So that slammed up for those who haven't gone through, you know, the idea with this, if you remember right, left, right, left, right, left. So if you wind up with a right hypertropia that is worse in left gaze and on right head tilt, that's a right posterior puzzle. And the other way to think about this at times, typically what you will see is three things. You're gonna see a head tilt. You're gonna see a face turn. You're gonna see a chin down thing. So we're gonna be like this. Okay, and the idea is that I'm going to tip my head to the right with that right forward. I'm also gonna turn my head a bit, my face a bit to the left, drop my chin down. Why I want my right eye is far away from where the suprarectis is acting as possible. So you'll see those three things. Kind of again, like pitch rolling yawn, that X, Y, and Z thing. If we talk about chin up, chin down, face turn right, face turn left, head tilt right, head tilt left, you can describe any head position. So with superior bleak palsy, this kid is tipping his head because it allows him to maintain binocular and equal vision. So that don't try to get the parents to hold the head straight, have good daycare. And the idea is that if you haven't do that, they're gonna be misaligned, they're gonna lose vision. And so the idea is you wanna take care of the problem because otherwise with this kid, what's gonna happen is by the time he is a teenager, he's gonna have permanent changes in his facial bones. And he's gonna wind up with changes that we can't make better in terms of the head tilt maybe just permanent, even if we straighten the eyes out later. And so the other thing you see in this photo is that when we have this head tip to the left, like he is here, the eyes are straight. And look at that right eye winging up towards the ceiling when he tips his head off to that right side. Isn't that cool? This is an adult with the same thing and he is showing you a little bit. Now he's got his head tipped to the right and he's got his face turned to the right and he's got a little bit of a chin down head position. All three of the things that I mentioned. And it's kind of fun to do this when people come into clinic and you kinda look at them as they walk by and you say, hmm, what's that patient have? And odds are you're right. The other issue you can look at is fundus torsion. The phobia should be up here and it is excite low rotated. And in a patient who's nonverbal, you can do this. I've also used this in the operating room and in a phasic adult to look at the torsion and try to get things level because he was telling me things were like this but he couldn't tell me with the double, the baggling, the loose baggling lenses that I used to measure torsion when he was level. It was a frustrating experience for him. This is that more magnification. Now, what's this kid got? He's looking straight ahead here. Yep, up and right, up and left, brown syndrome. And that is due to either a congenital contracture, super oblique tendon, or an acquired abnormality, usually inflammatory around the trophia, often seen with ethmoid sinusitis, sometimes seen with other systemic inflammatory conditions that cause one to see the uveitis service. Now, this patient is trying to look up and right, straight up and up and left. And this left eye doesn't go up well in any of those circumstances. What is the new term for this disorder? Sort of monocular elevation deficiency or double elevator palsy. That's what this is. And it's due to either a weakness in elevating the eye or restriction down below or both. It isn't due to a primary neurologic insult or something you can point a finger to and is often, if not always, present from birth. And we operate, if something's tight, we take care of that, usually the impure rectus. And if not doing a transposition, medial lateral to the superectus, we'll take care of the innervational issues. And I have seen things just beware if you see a patient that has had ptosis surgery. Our ptosis, our oculoplastic surgery colleagues can cause something that looks just exactly like this just by creating abnormal attachments between superectus and leviatorapinorosis. So if they've had ptosis surgery, go in and look there first and free everything up and you'll probably fix the patient. What's this? Now this patient has got a little bit of a left face turn and when he looks to his right a little bit, this is what you see. When he looks to the left, this is what you see. Notice this, notice this. What's this? Dwayne's, which one? Type one. He's got, and is it more common in this eye or this eye? Left eye and little girls. But it's like, you know, 49, 51. So it's not a huge difference, but that question does show up. And this is, we're trying to show here a secondary deviation in this patient who I believe actually has a six nerve palsy and not planes, but here he is fixing. And when he fixes with this eye, here he's fixing with his sound right eye, small angle estropia, fixing with the left eye, large angle estropia. And there we've got primary secondary deviation and this is Dwayne's type three as we go through things here and this eye isn't going in or out. Those eyes, you can do some surgery to make them straighter but you cannot make them binocular. What's this guy got? Yeah, you say, sir, how long have you had thyroid troubles? When he walks in and sits in the chair and they kind of look at you and say, how did you know? So it was kind of obvious. But, and this is more obvious and this is another patient with Graze disease. Now, this patient on the other hand, there's a family picture of this child and about 10 relatives. And they're all sitting like this, looking down their noses in the family picture, kind of looks like the folks on the fortune deliverance. But on the other hand, it is, and what do they have? Well, they probably have fibrosis syndrome and congenital fibrosis syndrome and that occurs in a number of varieties. Elizabeth Engle is probably the world's foremost authority on it and she's done a bunch of stuff with genetics of this and that work that you're interested in this disorder. But I think that with this, you can't make them binocular. You can make the eyes straight. All of these muscles are really tight. The surgery is incredibly difficult and if you're contemplating operating a kid this call me so I can talk you out of it because you will not have fun. But doing ptosis surgery to let them, because they're back here like this, not because of the eye misalignment, it's a ptosis driving it because when they're here, their lids are down blocking everything. So get the lids fixed, get their eyes straightened out as much as you can and hope for the best and follow them closely. Now this patient comes in and this patient at times has complete left ptosis, has complete right ptosis, sometimes a ZT, sometimes XT and they've seen five different doctors, got five different answers and you walk in and you say, I know what you've got. Let's prove it, what do they have? Myostenia, absolutely. And so does this patient. Now, this is myostenia and this is I believe with the tensilon and look at that nut. Tensilon can do other weird things so please don't use it randomly in clinic, particularly in my clinic without talking to me ahead of time. It wouldn't be a good thing. I would probably send them down to the RTU or have an neurology, you want it somewhere where they're monitored. And this patient has always got this flat kind of effect and the eyes don't move from side to side. He's got some funny furrows in his tongue. What is the diagnosis? What? Well it looks a little like the alcohol syndrome, doesn't it? But it's not. It's medius. Yeah, medius sequence. Yeah, and these kids have a bilateral gaze palsy. They can't move their eyes in either direction. It isn't a bilateral six nerve palsy which has been reported to occur. I take exception to that, it isn't bad. But these kids, you can get their eyes straight, you cannot get them to move normally. And then this patient, this patient has, first of all, tell me what the diagnosis is. And then second is where is the lesion on the patient's MRI? And on which side? Yes, I don't know. Yep. Then lastly, A and B patterns. So A patterns, you're either turned out more or you are have less ET in down gaze. A pattern, B pattern, you have more ET or, B pattern, you have less ET or more XT in up gaze. And so what we've got here with an A pattern is you're gonna have greater ET or less XT in up gaze. So there's disparity between up and down. And question maybe, first of all, what kind of pattern is it? When we look at this patient, this patient is small angle ET in up gaze, large angle XT in down gaze, what kind of pattern is this? A. And this patient is essentially ortho in down gaze, large angle XT in up gaze. That's a D pattern, isn't it? And so when we look here, the thing that often goes with D patterns is in this patient has XT in up gaze, their ET in down gaze notices up drifting of the right eye. What is the major elevator of the eye and adduction in fear of leak? So this is right in fear of leak overaction, left in fear of leak overaction. And the answer when they ask you about this with a V pattern with in fear of leak overaction and they'll ask you to choose between a number of surgical options is weak in the in fear of leaks if they've got in fear of leak overaction and then do horizontal surgery that makes sense for the primary position deviation. If they don't have any, just do the in fear of leaks. Now contrast, let's say this patient doesn't have any in fear of leak overaction and we're gonna shift medium rectus muscles, which way do we shift them with a V pattern down towards the apex and you shift the laterals towards the open end of the V. Now, the same thing happens with an A pattern. You're always gonna shift with an A pattern if you're operating on medium rectus muscles, whether you're doing a recession or a recession, you shift it towards the apex and laterals towards the open end. And you do that if you don't have oblique dysfunction. If you've got oblique dysfunction, do the obliques. Now A patterns travel with superior oblique overaction. Let's see, I don't think I've got a picture of an A pattern there. And this is quickly ROP. And one of you guys, I've got to wander over in about five minutes to primary to do the surgery. But what does this patient have? This is a neonate with blood vessels and this white thing behind the lens. Yeah, stage five ROP. This is where the term retro-lental fibroplasia came from and realized when they first described this in the 1940s, the only instrumentation, scapins did not develop the injury. They had a direct ophthalmoscope. That's what they were examining these babies in the NICU. And so when you think about that, put yourself in their shoes, take the direct ophthalmoscope the next time you go to do a consult in the NICU and see how much of the fund is you think you could see. That's what the initial epidemic of ROP. So when we look at ROP, these are the zones. Zone one is a circle whose radius is twice that this is some optic nerve depovia. Zone two, the radius becomes optic nerve to nasal or a serata. And zone three is what is left outside of that. Staging, one is a line. Instead of just normal vascularization progressing, you have a line where normal vascularization stops and beyond is a vascular retina, a raised ridge, stage two, extra retinal fibro proliferative tissue three and either extra foveal for A or involves the fovea for B and like the MAC on, MAC off thing, we heard about grand rounds. I think it was last week. These do have implications. If your fovea is off, the outcome is never very good in terms of having sharp reading vision. Can a child still recover useful vision, be able to navigate non-familiar surroundings? You bet it's always worth trying to save vision. And stage five, total detachment. And whether it's open funnel or closed funnel matters greatly if you are the pediatric vitro retinal surgeon trying to put instruments in through paris plana or in that circumstance, paris placata and not just destroy the retina with them. And so if it's closed funnel, unless you've got, there are some things, Mike Tracy has this magic substance that he developed in Detroit that they used to peel membranes in to try to separate things. But the visual outcomes in those cases are not nearly as good as the dramatic anatomic successes that they've been able to achieve in some kids. So this is stage one ROP. You've got, you can loosen a little line. Notice you don't see corretal background as well where you have a vascular retina. And this is a little bit more stage one, maybe early stage two here. This is definitely a raised three dimensional structure. This is stage two. Notice the striking difference with the vascular retina. This is stage three. Yeah. And the, this is just detached stage three as well here. Again, where there was stage three, things have grown out farther. When you see these big vessels as you hit the periphery, you'll always see something out here like the pot of gold at the end of the rainbow. This shows a four A detachment for B. The phobia is now detached. This is a total exudative detachment and a kid with very, very posterior zone one ROP. An official photo taken here, unfortunately at the University of Utah. Paula Morris who retired here a while ago. Anybody here? Remember you guys know Paula? Yeah Paula, what we did is brought kids from the NICU over to Moran was then clinic eight in university hospital and put them on a mail stand on their side with a lid speculum in and took pictures with the Zeiss big Zeiss camera. There was no ret cam and the Kaua camera, I could get pictures the size of an indirect holding it by hand using the indirect lens but they weren't the quality they wanted for the study. So Paula graciously took those photos and deserves credit for that. This is plus disease. This is the standard photo in the original iCrop description. This is republished in 88, the first publication of that I think was in 85 and in a later clarified now, meaning that you have two quadrants thinking of and this is a left eye super nasal, infer nasal, super temporal, infer temporal either venous, engorgement, arterial or tortuosity in the posterior pole by definition two quadrants or more for plus disease. This is more fulminant plus disease for quadrants involved. I think everybody called this plus disease. This is dilated to iris vessels. There are no significance with ROP other than when you get them, often the pupil doesn't dilate well making it really difficult. And this is very posterior flat, aggressive posterior ROP change in zone one. Plastic treatment was either eight non contiguous or five continuous clock hours of stage three with plus disease and cryo rap. Now type one and you do need to know this, this may well show up is if you've got any ROP with plus disease in zone one, no matter what it is, that's type one meaning I need treatment. If in zone one you've got stage three with or without plus disease, they get treated. And out in zone two, stage two or three with plus disease and this is dramatically different. Remember that the eight non contiguous and five continuous clock hours, we used to sit and wait and you say, well I think it's four and a half, it's not really five, we're not gonna treat them now. If you've got one clock hour, you get treated. And that is a big difference. And I was involved heavily in this study and in writing, help write the paper that laid all this stuff out so that this stuff is near and dear to me. If you have questions about it, talk to me. But the idea with this and the reason we came up with this type one type two thing was that the study that led to this, the E. Trote study, early treatment of ROP study, we used a computer modeling program that said you're either at high risk or low risk. If you're at high risk, you got treated at low risk, we watched you. And the bottom line is that we had a choice of either saying anybody who did ROP had to have this computer nomogram with their fingertips and be calculating and putting all this data in or could we fit something else to the data? And the type one type two schema came from this. And type two is I've got ROP, but it isn't type one. That's type two ROP. And so there you are. And my apologies if it isn't there, but if we've got again in zone one, stage one or stage two ROP without plus disease, watch these kids like a hawk. They probably need to be seen more than weekly. Out in zone two, if you've got some stage three without plus disease, use your judgment. Typically we'll just follow them once a week. And so if you are type one or if you reach conventional threshold, something got missed, they were really sick and couldn't be examined. We treat them and we follow the type twos very closely. I'm gonna stop there. I've got to get over the primary. What questions do you guys have? Otherwise, good luck with old cats. I'm glad it's you and not me. And there you are.