 in terms of some of these weird nystagmus presentations, but they're tested quite frequently. So we'll talk about nystagmus, the different types of nystagmus, and really try and hit on some testable things. So we probably already know that nystagmus, just as kind of an involuntary movement of the eyes, there's different types, and we characterize it by how the eyes move. Do they move back and forth in a horizontal plane? Are they more circular or pendular? One of the real testable concepts is Alexander's Law, so they will ask you this at some point on some sort of test. But the speed of the nystagmus is greater when you look towards the fast phase. I don't know a great way to memorize that, except that it's the opposite of the null point, which is kind of how I remember it. So the null point we use clinically because the vision is better for these, even though someone who's had nystagmus from childhood or birth, they usually don't have ocelopsia, or the sensation that your world is moving, even though your eyes are. But they still do have more subtle symptoms in that their vision is better when their eyes are more still. And for many people, they do have a null point. Not everybody with nystagmus has a null point, but many people do. And their null point is the direction of gaze where the movement of their eyes is the least. So that's the opposite of Alexander's. So Alexander's would be the opposite of where their null point is. That's kind of one way to think about it. So we talk about nystagmus as how fast it is, how large are the movements and what direction are the movements when it's on over at all rotary or bleak. And when we're evaluating an infant with nystagmus, these are the new terms that sometimes I'll revert back to the old terms because these don't totally, they're not totally intuitive to me, but you can have kind of an idiopathic nystagmus which used to be called congenital kind of motor. And now they kind of call the infantile nystagmus syndrome. They call that, they lump all of these into it. So within that is the idiopathic where they're gonna have normal vision, normal vision development, normal dilated ism, normal refraction, they just have movement, eye movements. But then there can be kids with albinism. That's a big reason we see nystagmus in three, four month olds. Less commonly we'll see it early on with retinal diseases. Sometimes we can see it later. You certainly can see it early with like leavers and things. We just don't see that a lot. And then there's this fusion mild development syndrome which used to be called latent nystagmus. We'll go over that in a little bit. But essentially the things you wanna look for in a kid who has nystagmus, well you wanna know like are they tracking at all? Cause usually these kids are pretty young so you're not gonna get an actual visual acuity but can they see? Cause if they can see it's probably not some terrible degeneration of their retina. And then some of these retinal conditions like leavers and congenital stationary night blindness and some of these other retinal degenerative conditions have this thing called a paradoxical constriction of the pupil when you turn on the lights. So if the lights are dim, sorry when you turn off the lights. So if you dim the lights you would expect a normal pupil to dilate but they do the opposite thing. So that's not 100% sensitive for those conditions but it makes you think there's something going on of the retina if you see that. Do they have trans illumination defects in their iris that can be indicative of albinism? Do they have foveal hypoplasia? What's their light reflects like? Is there something that's just blocking their vision and that's why they can't see and they've developed nystagmus? So you really have to kind of, these are the things to focus on. And it all speaks to the differential that we've kind of talked about. Albinism is the thing, albinism we see a lot in eyes that look pretty normal except for that absence of the foveal light reflects but another big one we see is object nerve hypoplasia. Those are probably the biggest, most common reasons but certainly these other ones can be seen. And then we have kind of, they've looked this in now to the same category but really clinically you really want to differentiate a sensory nystagmus where they can't see to a nystagmus where they can see but their eyes shake and so you just have to kind of pay attention to that. They most often will be pendular if they're or kind of rotary without a pattern if they just can't see. And then the type of nystagmus that previously was called congenital motor nystagmus where their vision is normal. It's not associated with anything, any other health conditions or ocular abnormalities but the things that want to test you on is that it remains horizontal in all directions of gaze. And this is how they characterize it now. I think this is from, I can't keep up with when they update your BCSC but this was a recent BCSC book. So the congenital motor is now infantile nystagmus syndrome and but essentially this talks about kind of the same. So this is a nice way to highlight some of these features. I like to use this more than that other chart. The information's the same but convergence. So this is something I actually test in clinic. I look to make sure it's horizontal in all directions of gaze and then I see if it dampens with convergence that first one and you're not really gonna know if they have ocular option because usually you're seeing these kids so young. The null syndrome usually doesn't develop until kind of early childhood most often and it can change once it does develop. So you wanna look for that but it's not gonna be there any young kid. And then near visual acuity is usually better because their eyes shake less when they converge so you'll see that later on in these kids. And then one thing they love to test on is inversion of the optokinetic response. So we have that here. So if you look at the bottom, so a normal okay end drum, if you rotate it to the left, you're gonna get left pursuit and right jerk. That's just normal. And then for somebody with this type of nystagmus, let's say they have right jerk nystagmus so they're fast, you always name it by the fast phase which means their fast phase is to the right of horizontal jerk nystagmus. So they would either have less jerky right phase or they would actually switch to the left if they had this type of nystagmus. We can usually figure it out pretty well in clinic but so we don't often use this but they love to test it. The other things they love to test. So the slow phase, does anyone know this? What happens with this slow phase velocity for these kids? So they love to test that, good job guys. And then we already talked about dampened by convergence. So they like to call this one fusional mouth development syndrome but in clinic you'll hear us refer to this as latent nystagmus. And they call it fusional mouth development because now they think the source is related to just a poor development of binocularity. But essentially what you're gonna see is you look at the kid, they do not have nystagmus. You occlude one eye and they start to have nystagmus and it's usually a horizontal jerk nystagmus. It's also dampened by fusion and it's disrupted by increased by disruption of fusion which is why it comes out when you cover one eye. And it classically occurs in a triad with congenital esotropia and DVD. So this, I think this is more helpful. So the things they like to test you on. So when one eye is covered, the jerk nystagmus is present in, what the? Well it technically is present but you're not looking at the eye that's covered. So the point of this is the fast phase is it towards the covered or uncovered eye? They love to test this. Yeah so, and then we just talked about this. There's a classic triad if you, it's not always the kid. You can see latent nystagmus in other settings but you commonly see this in kids with what two other conditions. Yeah and then importantly, binocular visual acuity is better in these kids and we also find that it is better to test their vision with a frosted occluder. That's true for most forms of nystagmus rather than a completely opaque occluder. So and it's based on this principle and really the reason is because the shaking eye movements again often do not give them ocelopsia but they do degrade their visual quality. And then you see it with this one you see an exponential decrease in the velocity of the slow phase. So that's distinguishing it from the infantile nystagmus syndrome. This is a big one. I do see it from time to time and it's very testable. So this is acquired. It's usually acquired within the first few years of life and classically this is gonna have a shimmering characteristic to the nystagmus and if you haven't seen it before it literally looks like shimmering. It doesn't look like any nystagmus you've seen. It's usually really rapid shimmering and it's very, very often asymmetric. I don't think I've seen one that even looks symmetric. I mean, the degree of how asymmetric can vary but it is always asymmetric and it can be in any direction and sometimes intermittent. So and the reason we worry about this spasmus newtons is because it can be associated with other conditions that are bad. So to diagnose it, it's in a triad of head, sorry I added this stuff in to try and do a flipped classroom but then I forget and I just click it. So it's a triad of head bobbing and torticollis with a nystagmus and you do see the head bobbing. The torticollis, I mean their head position is always, it's just they're putting their head in a weird position and they're kind of like moving their head around and you see this shimmering nystagmus and so you do clinically see this triad. If it's truly a spasmus newtons, it disappears by five years of age and it's benign but it can be associated with chiasmal or super chiasmal tumors and so you always have to scan these kids and then if their scan is normal you just kind of wait it out. So periodic alternating nystagmus is when we don't see a lot but I have seen it a handful of times. It's usually really, really hard for patients because it's a jerk nystagmus that switches directions and you can see this in clinic. Their fast phase will be to the right and then it'll kind of slow down and then it'll ramp up on the left and their fast phase will go into the left. So they can't, you know, there's like no head position that really gives them a null point and it's just very debilitating visually and they can try and alternate their head posture to continually kind of chase that null but it's really hard to do so. The biggest thing about this is that they want to know that you know it can be associated with albinism, chiari, MS, and stroke. So for most of these other ones, the dangerous associations and the fact you should scan them are kind of the key things they're gonna test you on most often. I do have, this is one of my patients, but you can just follow the hemorrhage and you can see your eyes as they move then. And now it slows down, so she's, so she was actually gonna have a procedure, she was in the OR, so you can, but monocular nystagmus is never good. It can be spasmus, newtons, that's really asymmetric and I have seen that, but you always have to scan monocular nystagmus. It's not always associated with a brain abnormality, a glioma or something, but it's very possible. And then there is this Hyman-Belschalski phenomenon, I don't think they test that very often, but it's good to kind of have it in your mind that it's just basically a monocular nystagmus that's due to really bad vision in one eye for any number of reasons. And it's usually related to the hemliopia. We do see that, but if you just see a patient with monocular nystagmus, that's not your first thought, even though that's probably the most common thing, your first thought is you have to rule out a tumor. And then the same is true for CESA, which I'm sure you guys know. This one I've seen really rarely, but when you see it, it's completely obvious because they have kind of the CESA pattern of their eyes and usually when I see it, it's taking care of neurosurgery patients. And it's associated, because it's associated with brain lesions in the rostral midbrain or the supercellar area. And the thing they always will test you on is that it's a craniopharyngeoma in kids and they get by temporal defects. So that is very, very commonly tested, that association with the craniopharyngeoma. So convergence retraction nystagmus, you guys probably get this in aeroop because it's also seen commonly in adults. So you kind of know what the features are to look for, but in kids, you really wanna focus on the possibility of aqueductal stenosis or panhelloma. They really test that a lot. And then you probably already know from aeroop that it's really best elicited when the patient tracks the downward rotating okay syndrome. That's the best way to get kind of that paralysis of up gaze and the convergence retraction nystagmus that you see with. And it's usually really obvious. Have you guys seen that before? Okay, so obstacle clonus. This one, I just saw in clinic actually. You don't see it very often, but when you do in a kid it's pretty, I've never seen it not being neuroplastoma. Technically it can be post-infectious cerebellary taxia, viral etiologies, but I've never seen a kid with this that didn't have neuroplastoma. And the problem with this is that they do have ostealopsia because they didn't have nystagmus before and they had presumably normal vision development and now their eyes are like moving all over the place in a disorderly fashion. So it's very debilitating. And it's a perineoplastic syndrome but it's immune mediated. So it's kind of an autoimmune reaction to the tumor. But the problem is it doesn't always go away with treatment of the tumor. Sometimes they require lifelong immune suppression. And it's a syndrome we think of it most relating to the eyes, but they actually have a lot of spastic movements and ataxic movements. So it's kind of a full body ataxia essentially that if they're not on immunosuppression it won't return. So it's really difficult to treat these. I've worked with neurologists who've used like baclofen or anti-seizure medications and things like that. It seems like the immunosuppression is most effective but sometimes it goes away with treatment of the tumor but sometimes it doesn't. And then downbeat nystagmus can be heritable but it's most often thought to be bad. Proceedings by an Ocerabella degeneration. So they do, I remember studying for the boards and it may have just been that year but I was surprised on how much they hit on like what medications could cause things. I don't know if they're still doing that cause they go in phases but this is one that's classically associated with medications that people are commonly on. So I think it's thinking of degeneration or medication when you see downbeat nystagmus is kind of the best approach. Upbeat is most often associated with something like MS. And the Bruins nystagmus is something we see more in adults than the pediatric population mostly because of the association with CP angle tumors like schwannomas but they get this slow large amplitude nystagmus and towards the lesion and when they look away from the lesion their nystagmus totally changes to this rapid small amplitude nystagmus. I actually have never seen this. Have you guys seen it? Yeah, so they tested it a lot back in the day but I never actually saw it. So what do we do with nystagmus? So in infancy if the onset is really young which is when we're doing most of these nystagmus evaluations we look for signs of any other causes like ophthalmologic causes and that's, I don't know how, oh yeah, it's better up there. So anything that's disrupting their vision, their visual development, things like that can lead to ophthalmologic causes but if it's developing after infancy and or there are signs of neurologic problems then this is kind of your thought process. And this, I thought this was a fairly useful table to think about when to do a neurologic workup but I don't know that they're all, like I don't know abnormal pregnancy labor delivery that is so common. So I would just say normal eye exam, other motor delays, think about kind of a global. And then this, you guys get this already. I think you get this very thoroughly in neuro op but it is important to kind of more important in the adult population to distinguish these two things but in kids the place where I see it commonly is where they have traumatic injuries and then it involves their inner ear and things like that then they'll have new ones at nystagmus that is more peripheral and then it helps you know how to treat it and then it'll go away. Okay, so we, this we've kind of gone over when we talked about. So really quickly before we move to our next lecture we'll talk about how we treat these patients and not everybody has a null point but if they do have a null point it does give us a little bit of ability to surgically address their nystagmus. You can see in the chart, technically there are medications they try and use. Usually many of these medications are used by neurologists. We don't do a lot of it but I've never seen any of them work wonderfully but if you have nystagmus, I mean you want to try anything because some of these are certainly later onset so they're having ocelopsia and et cetera. So I don't know that there's a great medication but if they do have a null point you can shift their central vision to the null point. We'll talk about that and you can also because like congenital motor improves with convergence you can induce convergence with base out prisms and I've done that from time to time and it's worked in certain patients. The surgical treatment of nystagmus is called the Kestenbaum Anderson because of the two people that kind of collectively thought to do this but in reality what we more often do is we use the Marshall Parks and he's the kind of the grandfather of pediatric ophthalmology is what he's called but he kind of innovated mostly the dose but essentially you're doing a recess-resect procedure on each of the horizontal rectus muscles simultaneously and you're doing that to move the eyes in the direction of the head turn but you only can do this when there's a null because you're trying to place their null centrally so they're still gonna look towards their null but now that's gonna make them look in the center and so this is just the dosage and things like that so if there's no null point there are less options but there is a disinsertion, reattachment, surgery, or a sense-keep procedure both of which I've done because these were advocated also by Marshall Parks and the person I trained with trained with Marshall Parks and some kids, so the disinsertion, reattachment, you literally take the muscles off and you put the back on and there's this guy in Pittsburgh who does all this nice diagnostic research with electrodes and things and his data show that that just resets kind of the neurologic inputs to the muscles and can dampen the nystagmus and what's interesting is for some kids I have seen dramatic results from that like one pediatrician was calling me and like how did you get this nystagmus to go away and I was like, oh, you know, sometimes it works, sometimes it doesn't and we just have no idea and then other kids it's like, well, it looks like I did nothing, so great, and so we have no idea why it can work so miraculously for some kids and other kids not at all. So the sense-keep procedure, that one you actually, you don't just disinsert the muscles so that's like the next step if you don't see an effect with just disinsertion, reattachment and they wanna try something else. The sense-keep procedure, you literally take the muscles off the eye wall and let them fly, you do not reattach them all for rectus, horizontal rectus muscles and I don't do that a lot because well, some people do, I know you're laughing because it sounds extreme but the person I trained with is one of the most famous people in the field and he does this routinely. And he actually helps people quite a bit. The problem, so it does work but it doesn't always make the nystagmus completely go away but it does make it better for the vast majority of patients but the problem is that the lateral will have more action when it reattaches to the globe than the medial just because of the arc of contact of those two muscles naturally on the globe so you tend to get an XT after this and so what he does now, he's modified it so he actually sews the lateral rectus to the orbital ribs to completely get rid of all of its function and just lets the medials fly and he has less exotropia with that and then they have less nystagmus. They cannot move their eyes a lot but they can move them somewhat and their nystagmus is better so yeah, it's not something I do a lot but there's a lot of very, very highly respected people who are innovating this procedure and I think there's a certain patient population that are just so debilitated by their nystagmus that this is attractive to them so keep that in mind maybe someday we'll innovate it further and be able to do even more. All right, so let's, the other topic we were supposed to cover today is this vision and ambliopia testing in infants and children and so I think you guys have some familiarity with this but not all of you have done the piece rotation so let's just talk about what we expect. At birth we want them to react to light, just blink and that's usually present by about 30 weeks of age and then at six weeks we want them to look at faces that's most often what they're gonna do, faces. Three months we want them to fix and follow on like a lighted toy and then by about two to three years we'd really like to see if we can get them matching some of the palindromic eye chart images for those of you familiar with how we test kids the HOTB and the Lea symbols are palindromes they're a mirror image of each other left to right and that there's a developmental phase around this age that where there's left-right confusion just normally and so it kind of gets rid of that component of visual testing and then by about five years we want them to read a full smell and light the first two are kind of self-explanatory but how do we characterize the fix and follow? I do know that the standard practice here is to write the text right fix and follow. However, you'll see us doing a lot of other things to kind of characterize vision and I think that some of those things in a pre-verbal child tell us more about visual development and so the indirect assessments are listed first and then you can do optokinetic nystagmus with the OKN drum you can do teller cards and you can do VEP testing to really understand how the nerve is working in the brain but we'll go over all of the pros and cons so fix and follow you just wanna, this is my mentor this is the one who did this who does the Simsky and wrote this book but you guys all know what this is but don't forget to test each eye individually but then I think this is much more meaningful central steady maintain and really in the field this is more correct a more correct way to do it and so central is under monocular conditions so if, can their eye just look straight at you if it's the only eye looking which is most often true they have nystagmus, they're not gonna have steadiness of fixation that's also under monocular conditions but something like nystagmus, you would put unsteady and then M is really the important one because this means can they maintain fixation and alignment under binocular so if they're tropic, meaning when they look at you with both eyes one of their eyes isn't straight, just spontaneously you don't have to do anything, it's just not straight so if they're tropic, the M is not they're not, they don't have the M they're un-maintained is how we put it but they could still be central because most of those kids who are tropic they have vision and if you occlude their fixing eye, they will straighten their tropic eye and look at you so they could be central under monocular conditions but not under binocular, which is the M this is in the field considered the better way to characterize vision and then it's all based on this fact that we need equal visual input to the two eyes to have equal visual development and not develop amblyopia so building on that the CSM kind of touches on are there risk factors for their vision not developing equally but then how can we actually tell if they have early amblyopia and their vision is not developing equally well if they're tropic then and they always fix with the same eye so they're not alternating it's not like sometimes they're right eye straight sometimes they're left eye straight it's pretty equally one or the other but it's always their left eye's out the right eye's straight, it never changes you don't need to do a test you can't really do in a preverbal child you can't really do fixation preference testing because they're already showing you what their fixation preference is their left eye is not fixing their right eye is fixing but if they have straight eyes and they have anisometropia like one eye has a different prescription than the other you don't know from looking at them that one eye might have amblyopia their eyes are straight they're gonna track together so how can you tell that in a preverbal child which is really important because it would inform whether you give them glasses or start patching and so you can do it with the cover preference testing like this picture shows like if they're really upset when you cover one eye but they're totally fine when you cover the other eye then you might think that in this child it would be their left eye would be the fixing eye because if their preferred eye is covered they're upset if their bad eye is covered they don't care is the idea but in reality kids just don't like you messing with them so this is not a very sensitive test a better test that those of you who've worked with me in clinic have seen me do is this induced tropia test so again if they're already tropic you can't really use this but you already know what their fixation preference is if their eyes are straight you can use the induced tropia test and it's a really effective way to tell you if they have an eye preference or amblyopia potentially in one of their eyes so the principle is that you give them double vision by this is a base down prism usually I use a 20 but in anything from about 10 to 20 is okay you want the images you're basically giving them two images and you want them to be able to see both of the images so if you give them like a 40 the images are gonna be so separated they're not gonna be able to appreciate there's two images so that's why the magnitude of the prism matters and you have to have them fixing you can do this at distance or near but usually I have them more reliably fixing at near and so you want a toy that they really are interested in and you want them to be visually engaged with that toy and then what you'll see so you can see here in this kid that the eyes kinda look like they're looking up at the toy and that's because you're seeing two images with this right eye and a higher and a lower image because the prism's there and he's fixing on the higher image which can only be seen with this right eye because that's the eye with the prism so he's using the right eye and in this image he's looking straight he's not looking up and that means he's not looking at the higher image he's just looking straight ahead and so that means he's still just looking at the image that his right eye is seeing and so this is the classic way to say okay he's not, he's preferring to use the right eye not the left eye this eye is suspicious for amylobia and then you look at all of the amylobia risk factors you assess them for all those and figure out why he might have amylobia and but sometimes it's more subtle than this like in a perfect world if they have no amylobia you would see usually what you see is they look at your toy and then they look up because they're noticing like oh there's another image there and then you put it on the prism on the other side and they look at your toy and then they look up because they're just noticing that other image so that's kind of a normal test but then sometimes they will just use the eye without the prism each time so they never look up but they are each time you move the prism they still are fixing with that eye without the prism so that's also normal because they're using each eye does that make sense? so there can be different iterations of this and if you understand the principle of what you're testing you can kind of interpret but basically what you're looking for is you want them to use both eyes and so how can we actually those things are most useful to me in a preverbal child because some of this other testing is just not as sensitive not very feasible very time consuming like an ok and drum you know sometimes I'll do this if there's like no tracking and you just think wow this kid really can't see anything like they're not fixing at all they're four months old like I don't know sometimes I'll use an ok and drum just to see wow will they look at anything but in theory you can kind of approximate their visual acuity by whether or not they track the ok and drum but we don't otherwise do that a lot and then I guess sorry and then the teller cards forced preferential looking is all this is called but they're teller cards which I thought I had a thing on I don't know where it went but essentially I don't know if you've seen these in the clinic we use them very infrequently but it's like this giant thing that the examiner looks through a peephole and they're showing each card is like this big and you're including an eye or not I mean depending on the kid but you basically it's it's a more and more fine grade of contrast stimulus like just lines basically and with a very large contrast large lines large black and white space that's kind of correlating with low sensitive visual acuity and then the finer the lines are the more fine your visual acuity is so if the kid keeps looking at the finer and finer lines with one eye but not the other eye then that eye doesn't see as well but you can imagine how long I mean literally the examiner the tack is like behind here looking through the peephole trying to figure out where the kid's looking I just don't it's not practical that really we do it in very rare circumstances and then the VEP you guys know what a VEP is but clearly we're not doing those on all kids we just do them if we have a concern for visual processing but I would say we do kind of want to think about doing a VEP because many times it is requiring sedation and if these kids are already delayed so dating them is not doing them any favors because anesthesia can not be good for brain development and neurodevelopment and what are we really have to be clear about the benefit of what the information we're getting if we know the kid has a bad brain for example and they're not tracking is a VEP gonna tell us a lot more that VEP is gonna be abnormal because a VEP takes into account how your brain actually processes the information in your occipital cortex if that brain is abnormal that VEP is gonna be abnormal and what is that telling you and there is no data to follow these over time so even in kids with gliomas where in my mind it seems like it would be more useful to have some understanding of how to follow these longitudinally because you have a tumor on the nerve there's still no data to suggest that you even should follow these longitudinally with VEPs so definitely in a kid with a bad brain it's gonna be abnormal it's not gonna inform your treatment because what are you gonna do you already know their vision is abnormal and their brain is abnormal and it could potentially harm their brain development given that they already have so many challenges so that's just my soapbox about that so here's the teller card so you can kinda see how silly this is this woman looking behind here and then the kid trying to see I think the principle is sound but it is very logistically intense to do that and I don't know, there's only rare circumstances where you really want that actual visual acuity information you really more so need to know ampliopia, yes, no, risk factors, yes, no let's treat that and then by two years of age or three usually we get them with these palindromes and only pictures are okay they're not palindromes and they often overestimate the visual acuity so that's fine but I mean, I think one thing is you wanna make sure you're testing them with the same method each time and not like one-time Allen pictures one-time Lee assembles, one-time HOTV because their visual acuity can vary just by the test itself and so these are the palindromic ones and I like these the best I don't really have a preference HOTV versus Leah but I do like to stick with the same one for each kid, each visit and I like to use matching a lot because some of these kids are really shy even if they know the letters and crowding bars can be used for both really and we'll mention that a little bit but the crowding phenomenon is one I'm sure you've heard about you can get that with a single image with crowding bars or you can get that with a line of text and it's a phenomenon whereby an amblyopic eye will have poor visual acuity because of the crowding phenomenon but a normal eye will be unaffected by that so it is a way to critically assess the vision and whether you need to continue your amblyopia treatment and then by five years we want them to read the Snellen chart they should have 2020 to 2030 vision at this age those are usually the parameters so when we get these failed vision screen all the spot screeners which we'll talk about in a minute usually they're cut off as 2030 if they're using the eye chart and then we'll talk about how the spot screeners flag these kids and then obviously you want to do one eye at a time and I like to patch up you'll see a lot of our texts doing that if they're squirrely kids because they will cheat and we see this very commonly they'll be peeking out from behind the occluder and they'll think this vision makes no sense to me and it's just because they were peeking and if you put a sticky patch on they can't do that so if the visions have normal you guys kinda know this but you have to do a very detailed structural exam checking everything even things that on first pass look normal you just wanna make sure you're really critically evaluating things and not just checking the most common or because sometimes you'll just find the most bizarre things in these kids but so certainly they can have structural abnormalities amblyopia is a big one cortical visual impairment you have to consider that if they have an abnormal brain and then sometimes kids really do just have delayed visual maturation you see this a lot in pre-me's but other kids can have it too and this is where they have totally normal eyes they're usually otherwise normal kids that have this and then they often get better with time and they just have taken a little longer to develop their visual system but usually it ends up catching up in the end so you always have to consider if this kid is cooperative with your exam because we have so many kids that they'll not do a great job when we're testing their vision but they can do other things they want to do just fine so amblyopia is a big deal if you don't catch it early you don't get a redo the period of visual maturity is where your brain is learning vision is birth to about seven or eight years and that's the period where they're susceptible to amblyopia and also the period where we can treat amblyopia most effectively because once the brain has completed that visual learning it's hard to change it and rewire it to learn about our vision because essentially amblyopia is brain damage and so it's preventable there are the classes so the classes really speak to their respectors you can have refractive either bilateral high refractive error or anisomatropic refractive error you can have stravizmic or deprivation from cataract or other opacities and then you can't really differentiate it based on vision the crowding phenomenon is helpful APD you can get in really severe amblyopia and it can coexist with structural problems like someone with an object nerve hypoplasia that's mild that represents a difference if it's unilateral in that eye between the other eye so the vision might be mildly affected by the hypoplasia but then that could be compounded and worsened if the brain perceives that that eye is not as good as the other eye so in severe hypoplasia where they just have no vision they have nystagmus and they really just can't see out of the eye I don't think there's a role for patching but there is mild hypoplasia where the nerve is mildly affected and they may have mild visual deficits but you have to be aware that that can worsen because amblyopia can be added on top so you wanna consider that and then I mean with these kids you just have to kinda check them and check them again over time because there's variability to how they wanna participate in the test and how their ability to participate in the test and so you just have to do it again and again and then I think the basic things are look at fixation behavior and use linear crowding bar testing to really sort out amblyopia you can get mild, moderate or severe and it usually correlates to the etiology but not always and then we treat it with glasses and often removing the amblyopia risk factor so sometimes glasses will do that sometimes you have to take out a cataract, et cetera so glasses are interesting because this guy at Vanderbilt has done a lot of work on what is the amblyopic range of refractive error and so I usually adhere to I mean he's done some really nice work on this and so I always assess whether the child has amblyopia and it does seem like if there's a family history of amblyopia the kids are more susceptible you at a relatively lower risk factor like lower magnitude or refractive error you can see amblyopia in a kid that's more susceptible based on family history than you would in a kid who has no amblyopia in their family history, I have no idea why but it's not all black and white, just follow the chart but this is a very informative chart on when you should prescribe glasses and then certainly you guys know that we also use penalization therapy glasses themselves have been shown to improve amblyopia by up to three lines I've seen glasses do much more than three lines so unless it's a severe amblyopia I usually start with glasses let the kid get used to those let the family get used to those see how much visual improvement we've gotten and then decide if we need a penalization therapy because these things are stressful for families today especially in their two year old and so those penalization therapies include patching you can do atropine, you can do optical occlusion with like a banger foil or something that blurs one of their lenses and the younger they are the more they respond to this treatment and this just highlights that the older they get the harder it is however we have done many studies and this ATS3 study these are all PDIG studies have you guys heard of PDIG? PDIG is Pediatric Eye Disease Investigation Group Mimi is our, Mimi Young is our Utah leader for that but it's a multi-centered clinical investigative group that they design all these trials so they did all the infantile cataract trials the infantile glaucoma trials I mean they do all the big trials that inform our clinical care so I'm one of the participants I think Bob is and Mimi's our leader and so we have had some of these trials come through we are limited private groups actually private clinics can also have some of these trials and they use the PDIG IRB to approve the protocol because they are not associated with an academic institution whereas we use our IRB which is fine our IRB is fine but it takes a lot longer so we don't get as many of the trials here you won't see as many kids enrolled in these trials here because usually by the time our IRB approves it they're like no we're only enrolling for like six more months so but this trial showed you may see some of these trials come through they're very good, well-designed interesting trials that highly inform our clinical care this one showed that older kids up to 14 I think can see benefit from patching if their amblyobia is caught late and they do not have a significant history of patching previously if they've patched and patched and then they stopped patching when they were nine and now their vision is still bad restarting patching will not get them better than their best vision that they achieved when they were younger so if they only got to 2070 when they were nine and that was the best they ever got and now they're like 2100 and they don't get better with an updated refraction you might argue that you could get them back to 2070 but you wouldn't be able to get it better but if they'd never patched and they were 2100 in your clinic they could probably get better than 2070 by patching so amblyobia treatment it's more of an art than a science I mean it's based on science but kids are all different what are they gonna work best with are they compliant with patching do the parents have a desire to force their child to patch if not should we try atropine penalization atropine penalization is very effective in certain populations but not in every population because it works on the principle of psychopathic blurring of the dominant eye and that is more effective if that eye is hyperopic if that eye is myopic it's not as blurred to that child so it's less likely to induce them to want to use their non-preferred eye at near which is what you actually want them to do and so atropine is great but it doesn't work equally in all populations I have used a banger foil so for kids that are good glasses wearers but they just will not patch they're not good candidates for atropine because of their refractive error putting a little foil that fits into the lens frame and our optical shops can kind of order them and fit them they come in different powers so if their bad eye is like 2200 you can get a 2200 banger foil and put that on their good eye and do that for four hours a day or something to try and get them to use their non-preferred eye so there are lots of options and it's just a trial and error to see what dose of treatment will the child respond to what treatment will they actually do I don't know if this is a screening so the screening let me make sure we have time to talk okay so the pediatricians there is a contention in the field of how we should screen these kids I think the best thing is what's supported by the AEO APOS, which is the pediatric ophthalmology group and the AAP, the pediatricians so the pediatricians do great jobs with red reflex testing and visual acuity testing at three to four years of age and things like that but they also, so we know what these are and I think by and large pediatricians do a really good job this was a patient I had at MUSC when I was a fellow there he said, he thought everyone had a bad eye but refractive ambly ups are the ones that are missed because their eyes are straight they don't have any visual complaints because their good eye takes over they don't have blurred vision and so these are the kids that are now picked up really effectively when they're pre-verbal with these photo screeners that a lot of pediatrician offices have that are really great and so they estimate refractive error and they also, which is I think why most kids are referred to us but they also look at ocular alignment and things like that so they can pick up sure business so two of the biggest they can also pick up cataract because they will pick up if there's a clouding but usually the pediatrician has picked that up just with their flashlight before that time but pediatricians really have a hard time picking up an isometrope so this is the population that has benefited most from these screeners and there are groups that advocate for comprehensive IACMs for kids like every year and it was interesting because one study by that Shondan Huy at Vanderbilt said that for the number of newborns per year that would be 20 million I exams, $75 an exam it'd be like $2 billion a year and we don't have the people to provide this service nor is it needed and when kids are screened in this way which still happens to some extent they tend to get glasses prescriptions that they don't need so in this study also by Shondan Huy he looked at preschool age children who did not have amylogenic factors and he said how often so these kids were normal how often did they get glasses even though everything was normal and you can see in the chart he looked at optometry comprehensive ophthalmology and pediatric ophthalmology in terms of who prescribed glasses for these really low refractive errors that are not within an amblyopic range and so I think if we do all these comprehensive exams we'll get more of that and I think cost wise it's not beneficial but the other thing is that kids are normally hyper-opic and there's a normal hyper-opic range and we feel like that's important for them to reach imagropization and we know there's a lot of other factors that influence that in terms of whether they'll eventually become myopic or whatever but we do feel like especially at the younger ages where some of these kids were given glasses that hyper-opic nature of their eyes does inform the level of accommodation that they have and that level of accommodation is what we think plays into how your eye reaches imagropization and if you give them glasses you're fundamentally screwing with that and so it could be harmful not just cost ineffective so the spot screeners these are old picture, older pictures but these are really good there's different ones they're not always accurate but they usually don't miss kids that need to see us and so this is by far the biggest thing that we're seeing coming in from those vision screens but they're really a good change to the field to really pick up all the kids that really need to see us so I think we made both lectures do you guys have questions about what we'll go over it all to as you guys come through with the exception of Rachel you've already done these but Theresa we can talk about how this goes into our actual practice and as you guys all come through we'll put it into practice for you okay thanks guys thank you