 I have been assigned a really thrilling topic today. I'm going to talk about sensory and motor physiology and strobismus and ophthalmology in general. They like to ask lots of these questions on the boards and on the OCAPs and things. A horopter is the locus of points between, you know, in space, so the locus of points in space that fall on the same part of the retina, so, you know, where you will have singular vision because they're the same, you're gonna see the same out of either eye. However, Panem's area, whoops, I'll go back, is a little bit bigger and it's the area, it's the area where the points may lie on a little bit different part of the retina, but you're still just gonna see one because the eye can kind of move that way and bring it into one. So anything within Panem's area or within that horopter, you're just, you're gonna see one. Whereas things outside of that, you're gonna, you're gonna see double. This is just a little bit different way to diagram that where the horopter here is just this line here, so that's the area where you're looking at something that's gonna lie on the exact same part of the back of the retina. Whereas Panem's area is a little bit bigger and it's the area wherein you confuse your eyes together to bring one image together to get stereoscopic vision. So what is fusion? So fusion is the ability of your eye to see one. So it's your eye pulling two images, you know, looking at something out of one eye and then the other eye making it and your brain making it warm. They have to be similar in shape and size, which is why sometimes, you know, which is why when somebody's really anisomatropic it has a lot of myopia in one eye, especially if it's new after cataract surgery, they're gonna see two because they can't, their brain can't pull those images together. They also can't tolerate much dissimilarity between the images, which is something you would see in something like macular degeneration where the image out of one eye is gonna be a little wavy because they've got, you know, some exudate or something or diabetic retinopathy where their retinas are making things, you know, they look out of one eye and they, when they look at the Amzler grid, you know, they tell you there's wavy things. So the images are not the same with either eye and they can't pull them together and this can make it tough for people. Sometimes when they start having that, they start to get a little bit of strabismus, but even when you fix their strabismus, they're still intermittently diplopic because they can't pull those images together because they're not the same shape. And the receptive fields in the periphery are larger. I think that that means that the, that in the, in the periphery, your vision's not as clear in things and so you can, you can tolerate a little bit more dissimilarity. So sensory fusion is the relationship between the retinas and the visual cortex whereas images on corresponding retinal points combine to form a single image. That's kind of what I was talking about with that Panem's area. Even though they can be a little bit off, they can pull it together to make it one. Motor fusion. So sensory fusion talks about how they have to, you know, kind of be similar to be able to pull it into one. Motor fusion, you know, is something you see when you, when you put the prism bar up in front of one eye and you make the, you make the eyes exotropic and most people can pull it back in and make it one together. So their eyes can move to pull those images into a similar part of the retina so that they can make it one. Stereopsis is what we test with the TITMAS or with the RANDOT and it adds unique quality division, you know, binocular vision. What is that? So when you look at these, you know, here, the top dot in the, you know, usually, I can't always remember because I get these two confused because we have one in the clinic with nine and one in the clinic with ten and they're a little bit different. But these, the glasses that they wear are polarized, you know, for one eye and the other eye. So this top one, the right eye sees it a little bit differently than the left eye. But when their brain looks at it, it pulls it together, but gives it kind of an appearance of coming off the page. So it's, it's what, you know, the same, same concept as seeing a 3D movie. And, you know, as you go down, this TITMAS test only has nine, the RANDOT has ten, but, you know, the further you go down, the more fine their stereo is, the more, the less these images are dissimilar and the more that they can, they can pull it together. It's kind of a quick and easy way to tell if somebody, you know, hasster business, if they have amblyopia and things, because you have to have two good eyes to be able to see this. So someone who has, you know, amblyopia, significant amblyopia, they're not going to be able to see these images pull, coming out similarly with somebody with strabismus. Unless it's an intermittent strabismus, they're not going to be able to see these because they don't see well, you have to have two good, two good eyes to be able to see things in stereo. This is another thing I use in my clinic, the other guys don't use it so much, but it's a, you don't have to put glasses on and the kids can kind of see these and they're different. This is like 600 arcs, so it consists of 1200 arc seconds. Sometimes it's a little bit easier for the kids. Sometimes I like to use it in kids who have intermittent XT just to make sure that they do have stereos, a lot of those kids with intermittent XT do not become amblyopic. And so I just kind of follow them over time, especially if their control is pretty good, but just want to make sure they have stereo. Also, it's, you know, an easy way to see if somebody, if a kid has, before you dilate them, if they have amblyopia. Gross stereo is just the, you know, the fly usually 3000 seconds. You know, sometimes it's hard to tell if the kid really sees it or not. You can't ask him to the wing that wings pop up because most all kids will tell you that anyway. But if they really kind of go to try to grab the wings or if they kind of try to scoop up the wings, we say it's positive. If they just put their hand on it and go straight down into it, we usually say it's negative, but sometimes it can be a little tricky to know exactly if they're seeing it or not. Because somebody doesn't see things on that, on the, on the stereopsis. If they don't have stereopsis, if they don't, if they can't see any of those images popping up, it doesn't mean that they don't have depth perception and parents always get that confused. There are lots of other things that can contribute to depth perception. You know, these kids can still be, you know, still be athletes and do those kinds of things. They probably won't be like a major league baseball player or something because I think that there's something that goes with seeing that spin on that ball or things that, you know, you have to have really fine stereo. I mean, I think it'd be an interesting test to look at, like, major league baseball players or look at really good tennis players or things. I bet they all have an excellent stereo acuity. But, you know, it's not synonymous with stereopsis. You know, there's lots of other things like image over, object overlap, object size, highlights and shadows, perspective. There are lots of other things that get contributed to depth perception. So when a kid comes in and, you know, the parents say, oh, they don't have any depth perception, they do have some depth perception. It's maybe not the same. And I think some of these kids are slower to walk, are slower to get some of those stereo skills. Probably aren't going to be a stellar athlete either, but it doesn't mean that they don't have depth perception. Because what we're talking about with that, you know, that stereopsis test is just this binocular sensation of relative depth perception caused by that tiny horizontal disparity. You know, you can see it when you look with one eye or look with both eyes. There's a little difference, but it's not a huge difference between them. You still have some depth perception if you just have one eye. And the truth is, after you get out about 10 or 20 feet, you're really relying on monocular cues, not so much that binocular vision. You know, as you guys know, your eyes are at the front of your head and your brain, where you process the image of things is at the back. So, you know, those radiations have to travel a long way, which is why most kids who have any kind of neurologic issue often have strabismus, because anything that affects, you know, the brain, sometimes those radiations don't get all the way to the back and they don't have great binocular vision, and I think that's why, you know, where they start to drift in or out. They also, you know, have this decensation where the outside fibers do not cross and the inside fibers usually, you know, do cross. One area where they don't is albinism, and those kids usually do not have great stereo vision. You know, some of them do have some stereo vision because they're varying degrees of that. You know, there are some kids with albinism who have pretty close to 20-20 vision, and then there are other kids who have 2200, and I think the amount of decensation goes with the severity of the disease, but they usually in general don't have as good of a binocularity because those radiations don't travel the same way. And as you know, those, you know, goes through the eye, through the lateral genica nucleus, through, you know, through the brain to the back, or to the visual cortex where things are interpreted. I never think about these, but they always like to put them in those books. I never saw, I remember seeing any questions on any of the tests about any of these, but the magnocellular cells are represented in peripheral retina. They're especially sensitive to moving stimulant. They're insensitive to color, whereas the parvocellular ones are the ones that are usually located more in the fovea, which have your high-res info about borders and color. Important for seeing detail and the conial cellular are the ones that they don't know much about, maybe related to seeing the color blue. When you're born, your vision is not normal. Some of that is because your fovea is not totally formed, which can make some of these tests kind of difficult, especially, you know, Dr. Creole has that test where he uses the fact that those kids with albinism, those fibers don't decussate, the nasal fibers don't decussate in kids with albinism. And so he measures the time from, you know, stimulus to the back of the brain and he notices a difference in that wavelength in these kids with albinism. But some of these kids, these tests are not usually are often not conclusive when they're in really young kids, because things are still developing right after birth. So the fovea is covered by multiple cell layers, you know, you can't often see a great foveal reflex, which can make it even tougher to diagnose things like an albinism because you don't see a fovea in a normal kid, so you don't know that you're looking at an albinism, especially if they're really young, because you haven't developed any of that in a stagmus yet. Some of those kids with albinism don't develop in a stagmus. But the photoreceptors move around a little bit and the cones really concentrate in that foveal area. The white matter, you know, starts myelinating during the first two years, which is why those kids then can be able to walk neurons in the lateral geniculate nucleus, lateral geniculate body, increased in size, and things continue to change through the first few years of life. While this is developing and changing, any disruption of that can lead to amblyopia, so a cataract, anything that blurs the visual axis, anisomatropia, that's significant or strabismus, that's significant. They've also found that in monkeys that have had their eyelids sutured to simulate amblyopia, their lateral geniculate lamina shrink mildly. So it is, you know, and this is kind of something I sometimes say to parents when they don't understand why the glasses aren't fixing the amblyopia. Because amblyopia is a brain disease, so they can actually look at those monkeys and see that those kids with those monkeys with amblyopia don't have the same brain on either side because it hasn't grown and they can see that microscopically. You know, and they start to narrow these ocular dominance columns start to narrow. What happens in these amblyopic monkeys is that the open eye starts growing neurons to occupy areas that were usually where the neurons from the deprived eye usually are. So the amblyopic eye, I mean the strong eye starts taking over the space where there usually was, were neuronic connections from the amblyopic eye. But there's no real benefit to having more, you know, to having these neurons grow because the visual acuity, I mean although it's usually 2020-2015, it doesn't seem to have the bionic or any better than a normal eye. They've also shown that, you know, PET scans have shown that there's increased blood flow to and glucose metabolism during stimulation of the amblyopic eye. And this, and when they leave it that way and then open the eye, these cells, you know, you know, cannot be regenerated. So in a normal eye, with a normal patient with two eyes, you know, the cells are, are, both eyes are driving it, but in the amblyopic eye it's only being driven by one eye. So this critical period is the time during which, in the monkey studies, so they've done lots of studies on monkeys and kittens where they suture one eye shut, they leave it shut for a few weeks and then they open it up and then they look at their brain and see what is this exact critical period. So it's the, it's the time during which they can open up the eye that they've sutured and try to get normal vision back. We don't always know what this is. In kids, you know, they used to think it was about eight years old that we couldn't treat amblyopia past, but now they did a study a couple years ago where even kids up to 13 years old when they treated anisopatropic amblyopia with glasses or patching if they hadn't been treated before they could improve the vision. They've also shown, you know, they've also done some studies where even people who, you know, have an amblyopic eye and then they have injury, they have ruptured glow or something and lose vision in their good eye. The vision in that amblyopic eye, even in adults, can improve a little bit. When they've done trials to try to do that improve it by patching in adults. Usually they can improve it a tiny bit, but when they stop patching it goes away. So there is some plasticity even in adults, but we don't know exactly what this critical period is in kids and that can always make things difficult because parents will always want to stop patching, but you never know when you stop patching are you out of the critical period or not. As they get older it gets less, but you don't really know exactly what that is because it varies with the kind of amblyopia they have and the severity of the amblyopia they have. So you often kind of have to stop, try tapering off and then and then seeing, but you know it's somewhere between 8 and 13, but some of those kids where they come in with dense, dense amblyopia because they've had a cataract removed and they didn't patch after they lost the contact for a long time. That critical period is closed even sooner. So this is always a difficult thing because we don't know exactly when this is. So what is amblyopia? Like I said it's a brain disease. So it's decreased visual acuity in a normal, when you do an exam on a kid and they have decreased acuity in one eye and versus the other eye, but there's nothing structurally going on that explains it and and then you deduce that it's from the brain. Usually in those kids you can explain it though. You know I have a couple of kids where I you know they have amblyopia and I don't know why and you know you assume they've probably had some anisomotropy or something that they grew out of but sometimes you just really don't know. But the biggest causes are strabismus where the eyes aren't aligned so they choose one and ignore the other. Anisomotropic and it's much more in hyperopic kids than in much more when you have a hyperopic difference than if you have a myopic difference you know if you have a kid with a plus 1 and a plus 3 they're much more likely to develop amblyopia than that minus 1 minus 3 kid and high bilateral refractive errors. So these are people with high plus prescriptions less likely high minus prescriptions but can happen with that too and then kids who have four five six diopters of the stigmatism. So anisomotropia why does that cause why does that cause amblyopia? Because you know when a kid's a plus 1 and a plus 3 they got to work harder to use that plus 3i so they just won't they'll use the plus 1i so that plus 3i is going to stay two diopters defocused it's going to be two diopters blurry and that their just their brain's going to learn to see two diopters blurry out of that eye. Has a later onset critical period than than strabismic amblyopia that's like what I was saying the kids with cataracts you know their amblyopia usually if you don't treat it in the first you know months to years of life there they're never going to develop normal vision whereas this you have a couple more years even those kids that were 13 years old who had anisomotropic amblyopia you could treat at that age and usually a stigmatism doesn't cause amblyopia in the first year and may not develop until age three this is kind of a funny one because now insurance companies are reimbursing for the use of those vision screeners in the clinics and they always pick up a couple diopters and stigmatism and send them to you but when I see kids one or two or three of just the stigmatism I just watched them because a lot of these kids have a stigmatism their eyelids are tight so they're pushing on their eye causing that I'd have a stigmatism especially at 90 and but it's not going to be amblyo amblyogenic at this age and those kids are going to want to keep their glasses on and their vision is usually going to develop normally and oftentimes they'll grow some of that of stigmatism so even if it's anisomotropic I usually sit on it for a little while they use it like in the nine month old but it's often wrong because the kids don't look fix it on that target so it's kind of a bad test because then the just sends more kids out right that they usually don't have anything and the truth is when they have even when they have anisomotropia I'm not going to do anything about it I usually sit on it for a while and the pediatric ophthalmology group doesn't have like no no we haven't gotten together to make it of that you know and those vision screeners are a little bit different in terms of I have had some practice at least one practice that's emailed me their cutoffs to tell me what they would do for it and I just kind of said well I wouldn't do it in the young kids because it's just not accurate but no and there's no consensus nationwide I don't have to do those either but everybody's doing it now because they're going to pay for it so they take a check of that reimbursement so they like using them now but the truth is these young kids when they pick up I've only had a couple that were good or even if they are there I sit on them for a while and don't do anything it's in the map for a while. Strabismus you know those things are supposed to pick up on Strabismus too but if they're not fit you know and how do they do that they can tell that there's a different reflex when one eye is crossed but you know the pediatrician should be able to pick up on that but honestly in my experience parents are better than pediatricians. I mean pediatricians send me a couple students to do Strabismus a day and usually the parents are better than the kids on the student Strabismus but you know Strabismus why do they get amblyopia because they're not their phobias aren't lined up you know they're using one eye and phobias lined up and the eye that's crossed is not using that phobia and it's critical periods earlier too so and Bob always says this too that these anti-symmetropic amblyopia are much easier to treat than these Strabismus amblyopia so when they have a mix of that you know patch patch patch patch patch and you're still not sometimes can't get it can't get that vision 2020 it's just really hard suppression is what happens you know it's an adaptation really you know when it's when your Strabismus evolutionarily you would want to get rid of the image that's giving you double vision so those kids who are born with Strabismus they're starting to turn that eye off which leads to amblyopia so you know why why do they get amblyopia well it's it's an evolutionary adaptation but doesn't it's not always a good one if we can treat it so they start to turn off that eye so those kids have an area where they they aren't able to they turn off the image and they don't see it the thing that's weird is why with crossing ET do they get amblyopic and with XT they rarely get amblyopic I don't know but most of those kids with bad XTs still are 2020 each eye and still have stereo vision but those ET's don't so patients with Strabismus and normal retinal correspondence without Diplopia suppressed so this just means that if you've got a kid with Strabismus who comes in and tells you they don't have double vision it's because they're turning that one eye off so you want to try to treat that treat that suppression and usually with kids with amblyopia we start by putting them in the right glasses if they're still not equal in their vision that we start doing patching and or atropine trouble you know atropine seems easier but for those dense cases you wonder like the atropine is only blurring them up close unless they're you know got a high hyperopic prescription and if you are blurring them enough to make it you know to make the good eye the bad eye you know it may not be working although they've shown that even when it doesn't blur it enough so even when they look up close with it when they were they're using atropine and their good eye is still clearer than their bad eye they still do have some improvement in their vision other trouble with atropine is you can't flip kids and so if you don't see it back enough you can make their good eye their bad eye and if they keep using that atropine it's just gonna get worse and worse and worse and then you know there is some thought even these kids when you haven't fully treated the amblyopia the thought is if you do surgery to try to get their eyes straighter is that going to treat the amblyopia is getting rid of that strabismus to make them straighter you know usually the general teaching is treat the amblyopia make that vision better and and then you know the straighter they're more likely to stay straight after surgery but you know the flip side of that is sometimes doing surgery makes that eye closer so you know a kid who has a huge esotropia that takes him a lot of effort to flip between the two eyes if you get him pretty close and they're only flipping a little bit they're going to use that amblyopica a little bit more treating that suppression is a little bit tougher on these kids that aren't able to fuse because they're always these are kids who even when you do surgery they still have a little bit of a tropia and like I said those are the ones that are harder to treat because they really never use their eyes together and almost retinal correspondence just means that they when they when they're at when they do when they are using their eyes together their retinas aren't corresponding with the same spot so they're the phobia and one eye is not matching up with the phobia in the other eye and so it acquires an anomalous common visual direction with a peripheral retina element in the deviated eye so the deviated eye there's a little area off the phobia that you know that corresponds to the phobia in the other eye and these are like the people who you know some have like mono fixation or things like that so it's an adaptation that's an evolutionary adaptation to restore some amount of binocularity despite their stir business and sometimes it can make things a little bit tricky after surgery when you line them up they see a little bit of Diplopia but usually it kind of goes away you can test for this so by putting a red lens in front of you know in front of the oh so if their love phobias are so this is their pseudophobia and this is the phobia here and somebody who has this you have them look through a red lens here and they see this light as pink whereas you know this would be somebody who has an almost retinal correspondence because they're looking at their pseudophobia and their phobia whereas this is somebody who you know they're using their phobia and their phobia and you put you know a prism in here you put a base out prism to make them exotropic and then you put a red lens here as well and so what you're finding here is that they have crossed so they're gonna have crossed the phobia they're looking with their real phobia so this is this is an official this is one with a lot less retinal correspondence I have to think about these things too because we never really use them but this is the red glass test that looks for anomalous retinal correspondence and somebody with ET so this is somebody who's looking at an image here they've got a right ED of 20 prism diopters they're looking here with their phobia here and they've got uncrossed diplopia which you know corresponds with esotropia or they they suppress depending on which side they're looking at if you correct some of that esotropia with you know five prism diopters but you know that they're really 20 then they start to see one so you're only correcting some of it but they're you know they're starting to they aren't the public at all whereas if you correct the whole 20 prism diopters you know which is sometimes why you should you know when you're testing these people you know you do a cover-on-cover test you do the ultimate prism cover test you're trying to build up as most the biggest number you can because you're trying to figure out what you should operate on for surgery you you get up to a 20 you put the 20 there and and then they start seeing crossed diplopia which is you know make means that they're XT so this is just somebody who you know they're 20 prism diopters esotropic however when you put a 20 prism diopters when you put a 20 diopter prism in front of them you know you make an exotropic so that they're when you're lying when you line them up with their actual physiologic phobias they're having double vision this is just the same thing telling you that so and usually crossed diplopia is exotropia and uncrossed is esotropia is somebody with normal retinose correspondence and so when they're looking off their looking off their phobia they're seeing things correctly worth four dot is something I like to use in clinical act especially in adults and things you want to know if they can't use if they are a fuser and you know you put these glasses on the red over the right eye the green over the left eye the right eye they see two red with the left eye they see three green and then you just ask them what they see usually for these kids who you know and they should see four up close and for a distance where as these ambiopic kids are going to see you know whichever if their right eyes crossed they're going to see three green up close and far away some of them are a little bit intermittent some of them is kind of hard because they'll tell you they see all of them but they don't really see them all at the same time they're suppressing and alternating between the two the other thing you can figure out too is if they have a mono fixation syndrome so if they have some amount of where their phobia in one eye lines up with a little bit of the peripheral phobia in the other eye and they will usually fuse up close but suppress far away so that's the way you can tell about mono fixation so if they see five lights they don't usually have suppression but you have to figure out are they seeing five lights at the same time or they crossed and flipping between the two eyes and they see three you know they see two red and three green three green and that's kids that's usually what it is they usually are not to pull the kids are not usually to pull pick if they're to pull pick there's a problem because it means it's a new it's a new sensory service mess and you know to pick up on mono fixation syndrome they usually suppress a distance of fuse in here and some of these are kind of tricky because sometimes when you do the alternate prism cover test they often won't like move so you can't tell but it's you know kids are coming in like a 2020 2030 40 in the other eye they usually don't have that battle flip of ambiopia they usually have some amount of you know peripheral fusion with a little skatoma they usually sometimes have stereo cutie but it's usually reduced they have a little bit of ambiopia it's considered a good outcome after stir business surgery so these are the kids that you operate for congenital E.T. of 40 or 50 and then after they have an E.T. of like eight to ten they aren't straight but their brain can't make them straight. This is what Bob likes to use I don't really ever use these but they have these dots here and they usually put the right eye at 135 and the left eye at 45 and then you know in the people who are normal they'll see an X if they're suppressing the left eye they're only going to see the one you know the right eye that goes this way I don't know how you would tell this I don't know that people would really be able to tell you this but I've never really used this test so I don't know but you know in those mono fixators where they have that compression skatoma in one eye they might tell you that there's a break in that eye in the middle then you know if you have esotropia with normal retinal correspondence you're going to have uncrossed apopia and a V here whereas if you have exotropia you're going to have crossed apopia you know so you're you're seeing your right eye over here and your left eye over here these tests are kind of hard because unless you use them a lot you can have to sit and think about it for a minute and then you when you're seeing them on a test you kind of will overthink them sometimes so but they do like to ask them after image testing is another way of doing the same thing where you you know Shina you label the phobia by shining some lights and then have them you know see the after image in their eyes in somebody with normal retinal correspondence they're going to bring it cross here these are from your book your those AAL books but this test this one's a little bit funny so these are people with anomalous retinal correspondence where you know they have they they are seeing things off here but I don't like this image because I never like to think about things in terms of anomalous retinal correspondence but this is somebody who so if they are right over here this is really they're seeing an exotropic but they are esotropic so it's just off amblyoscope we don't have one of these sometimes on the boards they like to show you weird devices and say what is this but it's a way that you can have somebody sitting there and dial things in to really figure out what their ocular alignment is it can be really helpful for torsional diplopia and you know you you have that you dial them in to figure out exactly you know what their eye alignment is in a certain direction of gaze and you can also use it for some people use it for like building up amplitudes in terms of fusion or divergence amplitudes so it neutralizes the torsion it can tell why somebody can't fuse you know in some of these cases is it because of their retina or is it because they've got a huge amount of torsion torsion can be tricky because people you know they can have you like especially for the bilateral superior obliques you can be looking at them and they can have you know you do a cover-on-cover test and they have no deviation in down gaze maybe they have a tiny ET of three or four but they tell you that they you know something's off with their vision and sometimes they can't even tell you that it's double vision or anything but the reason that they're not seeing is because of torsion so you know you really do need to check for torsion especially in cases where you have a little bit of a hyper because the torsion may be the problem and sometimes they cannot tell you that they can't verbalize that ambioscopy like I said you can use it for some exercises to overcome suppression which can be a bad thing and some people some people are not able to fuse and they're suppressing and if you get rid of that suppressant scatoma then they're going to be very angry at you because they can't you know they're always going to be diplopic don't matter this is one I usually like to use you know you usually use a red lens and a white lens and then have the person dial in things to make things parallel with the ground or you know or this I usually do parallel with the ground and parallel with each other sometimes that they're fusing it together you can put a prism in there to make them you know based down prison to make one higher than the other and then you just make them parallel with each other so that they're not fusing it together and then what you read off there is what they are so if this lens is this way you know in this side they're x-cycletorted in this side you know if they're x-cycletorted in this side and in cycletorted in this side those are going to be parallel so it's not an issue but if they got a bunch of x-cyclo in both eyes you know that's where your problem is you can die you can tolerate somewhere six seven diopters of torsion usually but much more than that starts to be a problem Lancaster red green these are this is a test where you this is the person giving the test and this is the person taking the test you know they have these lights on here and she she shines a beam on on a wall and then you you know the person taking the test should line it up and make it you know make it on top of each theoretically make it on top of each other but it's a way that you can tell you know patterns you can't really tell how many diopters somebody's off but you can tell so this is somebody that's fixing and usually the red is the red and the left is the sorry the red is the red and this was the left eye so you can see that this person's misalignment is much more in down gaze and their torsion also you know up here they're not so tortued down here they have quite a bit more torsion and quite a bit more isotropia and this is actually patient with it so it's a v pattern bilateral superior bleak policy so this is somebody were in primary gaze they aren't looking you know and these are the different directions of gaze they aren't so bad but when they start looking in down gaze they get really tortued and in and horizontal misalignment and that's it a lot of talking but in general if your eyes are lining up you know you're either going to get double vision or you're suppressing and you know these are different ways to kind of try to tease out what's going on you know you are going to see these people with head trauma that tell you that something's off and look at them and think oh they're they look pretty straight I don't know what they're talking about but you know sometimes if you aren't measuring in all positions of gaze they may have a little you know quite a bit of torsion and just trying to figure that out can be a little bit tricky so these tests that sometimes help us tell that you know in general we don't do a whole lot of these tests because you know even the suppression tests so much there's so much of a element of Cosmesis in strabizma surgery so oftentimes we'll do surgery and try to get them straight and if they have a little bit of almost retinal correspondence that we try to deal with that after so that's about it