So, OCAPS, coming up, that's the purpose of this lecture. I think those of you that I've worked with closely are kind of aware of my philosophy of why we do OCAPS. It isn't just to terrorize you. We already think you're pretty smart folks or you wouldn't be in the program. I think its main purpose is to cause you to collect all the information you've kind of gone through in the course of the last year and for some of you in the last two or three years and put it together. And assimilate it and think about it. And I think for that purpose it is a useful exercise. Now in terms of stuff to go through, knowing where the muscles start thinking about pediatric ophthalmology things and the origins and insertions, you may get questions about which muscles, like which muscle does not originate which muscles from the annulus is in and there are two, inferior oblique, superior oblique, which do the nerves, blood vessels come from inside the cone, outside the cone, the insertion, how far the insertions are from the limbis. Those are all issues. There's usually a question about which muscle has the shortest tendon, that'd be inferior oblique. The longest obviously is superior oblique. And so that I think that just knowing, having an idea of what these numbers are, realizing that those of you who've spent time actually doing eye muscle surgery with us, realize that those numbers aren't exact. They vary, those are averages over large numbers of people. And I think that this idea of the location and Griffin touched on this in Grand Rounds the other day, Dr. Jardine, about this issue of the relationship of visual axis, the angle that the vertical rectus muscles make and the oblique muscles make because the oblique muscles, remember underneath this, this is looking from superior, the inferior oblique comes from the floor of the orbit nasally and wraps under the eye. Look at the parallel nature of the superior oblique, inferior oblique and the superior rectus, inferior rectus. That is what is responsible for this issue of separating the vertical function, superior rectus, inferior rectus and abduction, inferior oblique elevator, superior oblique depressor and abduction. And knowing those relationships and having an idea how all that works is important. And there's a lot of information on here. The thing that I would recommend that you remember, there may be a question about primary, secondary, tertiary functions of muscles. You may find something about this angle of orientation to the visual axis, which is the direction of pull. And this has to do with what we're just talking about with lining the eye up with the direction of action of the muscle. And when you're directly opposed to that, the vertical muscles, in contrast, have their major cyclorotatory function. Now, these axes of thick, this kind of shows up once in a while. The question might be which axis of thick do the horizontal rectus muscles rotate the muscle around? Well, that would be the Z axis. And if you're talking about the vertical rectus muscles, it would be the X axis and the torsional aspects are on the Y axis. You know, like pitch rolling yaw on an airplane, I don't use those terms commonly. You won't hear me use them, but they do show up. We're gonna run through this quickly if there's something that isn't clear that you have a question about, stop me, because the reason we're doing this is to try to go through this somewhat rapid fire to spur your thinking about things you might wanna review before you take that darn test. Now, monocular eye movements, ductions. We talk about superduction, infreduction, adduction, abduction, and then X cyclo. If you take a mark, make a mark at 12 o'clock on my left eye, rotate it out this way, X cyclo. And as in cyclo, and thinking about that in terms of your eyes and which way things go, is another thing we'll talk about when we review this three-step test that was touched on at Grand Rounds the other day. Binocular eye movements that involve both eyes going in the same direction. And that would be our versions. In versions, we talk about dextro and levo version, right and left gaze, superversion, infraversion. And you can also talk about the eyes rotating if I tip my head to the left to this dextro cyclo version. Although people don't usually use that, we usually think about torsion in terms of, you know, monocular, X cyclo, or encyclical movements. But that is used by some people. And then there are vergence movements, the dissimilar movements, which most typically are either convergence or divergence. I'll realize we have vergence movements that are both vertical and torsional as well to maintain fusion. Now, what about Herring's law? Herring's law is, you know, we get into physiology and doing muscle recordings. What happens is that the muscles that are called yoke muscles, the muscles that move the eye in the same direction, like my left lateral, right medial rectus, when I'm looking to the left, if you measure, do you get the same amount of neural input to each muscle? That is where primary and secondary deviations that we'll touch on come from. If you are fixing with a normal eye, you have a peretic lateral rectus, the smaller amount of esotropia, because it doesn't take a lot of neural input to maintain the normal eye. Fixing is a smaller esotropia because you're not having to use as much input. There isn't as much input going to the fellow eye. Whereas when you fix with the peretic eye, it requires a lot of effort from a lateral rectus that's not working very well, that also goes to the contralateral medial rectus. You wind up with a larger secondary deviation. So that's something, again, it might be a question about which is the primary deviation, which is the secondary deviation. Herring's law. Now, Sherrington's law, all that says is that when I take my right eye, I move it to the right, there's increased firing in my lateral rectus, decreased firing in my medial rectus. So that has to, and that comes into play when we think about things like Dwayne syndrome. In Dwayne syndrome, we talk about co-contraction. If I have Dwayne's type one in my left eye, the reason the lids look like they're closed, you get fish are narrowing on abduction is you wind up with firing of both muscles. So it's an aberration of what happens in Sherrington's law. Now, diagnostic positions of gaze. And the occasional would say, well, which of these are diagnostic positions of gaze? Diagnostic positions of gaze are where you can have a high likelihood of separating and having a single muscle be the mover of the eye. Right and left gaze, it's pretty easy. My right lateral rectus, abdux my right eye, the medial rectus my left eye, abdux the left eye. When I go straight up and down, it turns out it's a mix of superectus inferior oblique and superectus inferior rectus going down. And so straight up and straight down are not diagnostic. When you get in the oblique functions, that's where we separate the elevators and the depressors in each side. That's where that term comes from. And thanks for joining us. It's interesting outside, isn't it? Yeah, yeah. Wasn't sure my little car was gonna make it. I think my car tried to pole vault out and then my driveway and the trailer hits this morning as I slid down into the road. I'm feeling lucky to be here. Now this physiology, some of this stuff is useful. Some of it is useful only for OCAPs. All of it will kind of increase your understanding of how things work. And I think it's pretty cool stuff to think about at times. But we're gonna look here at the idea of retinal correspondence, the horopter, v-th-muler circle that does sometimes show up. Issues of stereopsis, sensory, motor fusion. And I'm not gonna talk about M&P systems that I don't find that really exciting. But anyway, the idea, as far as retinal correspondence, the idea is that when these eyes are looking at point F, every point on this circle, that's the v-th-muler circle, theoretically projects to a place in the retina in each eye that corresponds to each other. So that the representation on occipital cortex is of the same thing. And when things are lined up, and retinal correspondence is something that develops early in infancy. If your eyes are straight and work together in infancy, you will likely have normal retinal correspondence. If you develop strabismus later in life, you have a motorbike accident in Sir By Indonesia. Turns out they're very common, I was just there.  Contrast that to the kid who's got infantile isotropia, whose eyes were never misaligned early in infancy. They never have normal retinal correspondence. The most that we can hope for in them is usually some aberration of anomalous correspondence where because the eyes are misaligned, I have my fovea in the left eye looking at things my right eye has turned in, part of my nasal retina thinks it's the fovea for the right eye. And so then you wind up with what is called a suppression scatoma, enough information ignored to avoid diplopia. That's what suppression's all about. It serves a useful purpose. If we could not straighten eyes, you had misaligned eyes early in childhood, you have a choice between, I'm gonna go through life seeing double all the time, that turns out not to be something that allows one to gather food, hunt animals, things of that sort, which was with our ancestors, those were important things. And so it's selected for people who could ignore that and that's likely how that all developed. Now, what else can we learn from this? There'll be a question often about looking at point F. If you're looking at a point here, or here, what is the patient's sense of things? And the idea, there is this range and it's narrow if you take a second point either in front or behind this point that we're looking at, where as you're looking at that point, you'll have a sense of depth because there's a little bit of disparity in the two eyes. Once you get outside that range in this area, you don't just see it as depth. You see two different things. You have double vision. If you wanna play with this yourself, take a couple of pieces of wire coat hanger, look at the coat hanger, and take things and move it back and forth and you can see where you see it and it looks like it's here and suddenly you're seeing two things. The second thing that'll happen is you'll notice that as you get farther away, you can go farther before you get that sense of I'm seeing double. And that's because this is required, there's the tolerances are much greater here than they are in the peripheral parts of the retina. These areas here are gonna be close to fixation. Now, normal retinal correspondence we touched on, there are sort of two variants of things didn't develop quite normally. One is what is called harmonious. The other is called nonharmonious. What that really refers to is changes in adaptation as a visual system develops. Let's say I was 50 ET for the first two years of life, then somebody did a little bit of surgery and I became 30 ET. So at the moment, my visual system is still thinking I'm 50 ET, but actually it looks like I'm 30 ET. That refers, that's really what's going on with nonharmonious retinal correspondence. If I am 30 doctors ET and my visual system thinks it's 30 ET, that's harmonious. And if there is some disparity due to whatever has happened, the term generally used for that is nonharmonious. And these are all without exception functions of I had early childhoods for business. If you see this in a patient on the neuro ophthalmology service, they've suddenly realized two in the morning that things aren't okay with their eyes and they show up and they want an MRI scan and somebody wants to do an LP and you're convinced they've got anomalous retinal correspondence, you can pretty certainly say this has been going on for years and it's among the suddenly noticed. And I know that some of you have been in that situation. I've seen an amblyopic adults that I've been asked to see down the road who suddenly on Saturday night reached up to get something and realized they didn't see out of this eye for the first time in their life. And had the major neural workup just to say, look, you have decreased vision, you have no stereopsis, your eyes are misaligned. This has been this way all of your life. It's a shame you didn't know it till now. And that is kind of amazing and probably says something about your innate thinking ability or observational skills, but there you are. Now, suppression. Suppression is a binocular function. If I'm suppressing from my left eye to avoid diplopia, when I cover my right eye and I do a visual field, everything's gonna be fine. It is only there under binocular viewing conditions. Monofixation refers to a situation where most of everything works together, probably not in exactly normal way, but works together and things correspond to one out of the other. There's very tiny suppression scatoma. This turns out to be a very stable arrangement in terms of alignment. This is what we wind up achieving in most kids with infantile, esotropia, some kids with infantile, exotropia, although it's harder to do. The advantage is they don't see double. They usually have pretty close to normal vision and their eyes don't wander greatly. They don't require additional surgeries. And then diplopia. And there are two things here that we, this idea of crossed and uncrossed diplopia that we need to understand to be able to make sense of what happens with those pictures that they show you with the bagelini lenses and the monofixation things, which still often show up on octopi caps, although they are virtually no practical use to anybody and no one uses them, except the torture residents and fellows in some institutions, well like Johns Hopkins and places like that, where I still think they drag, Dave Guyton drags his stuff out, but it isn't because it's useful to anybody. It's just because he can. And the idea, with esotropia, when the eyes are crossed, the image, if my right eye is turned in, is gonna project on the nasal retina. Does that make sense to everybody? And now normally, if you take, and when we talk about nasal retina, we're talking about everything that is nasal to the fovea, temporal retina, everything that's temporal to the fovea in my right eye. And normally, my nasal retina has to do with temporal visual space, correct? So if something is, my retinas correspond normally to each other, we turn my right eye in. If I have something in my nasal retina seeing the same thing that my left eye is looking at with its fovea, that nasal retina is gonna tell me that that object is often temporal space. Does that make sense? So that's where the idea of esotropia and uncrossed deplopia, the image from my right eye is gonna be off to the right. Contrast that to exotropia. When my right eye turns out, the object of regard is gonna fall on the temporal retina, everything from the fovea temporarily, and it's not from optic nerve, it's from the fovea. Everything out there in temporal retina is gonna tell me that it's on the nasal side, which is why you get crossed deplopia. So crossed deplopia, remember the cross and exotropia, crossed deplopia, if you can't just think through it, but some of these knowing how to think through it is what I'm trying to, where I'm trying to go with this, because I think that's a better way to approach life. Now, levels of binocularity, it goes from the I'm capable of seeing things with the two eyes at the same time to I'm kind of able to put them together to higher order, I can really put them together. And then lastly, I can perceive stereopsis, which basically just means that I've got a little bit different perspective of the world from the two eyes. And yes, it turns out that if you have hypertylerism, your stereopsis theoretically at least is better. And I used to give James Zimmerman's dad a hard time about this because nobody had more widely spaced eyes. I've never met a human with more widely spaced eyes. And so I told Paul that I thought he must have just superhuman stereopsis. He kind of operated like he did. So it was a good thing. He was very good under the microscope. And then, so again, simultaneous perception, sensory fusion and stereopsis are kind of the three levels they talk about in the home study course book. These things, these images share nothing in common. If you can put them together, that's simultaneous perception. If the patient tells you, you project slides independently to each eye in an amblyoscope. Now this, there are different things. And if this patient can superimpose the boats and come up with a different figures, that means that we're at a little higher level than I'm just seeing it with the two eyes. I can put those images on top of each other horizontally, vertically, torsionally, and see them at the same time. And then if I perceive stereopsis, it looks like the red arrow is sticking out because of that little bit of disparity that is here. That, again, is a higher level. Not gonna belabor that. I'm not gonna rest on that stuff. But now you'll, they'll talk at times about tests of binocularity. Claude Worth was a famous pediatric ophthalmologist or ophthalmologist. They didn't have pediatric ophthalmologists then. This test is named after him. And his, you know, this test basically where you take red lens before the right eye, R&R, green lens before the left eye, and then have this series of green, red, and white dots that you look at, allows you to assess whether the patient is binocular. It is not a test of stereopsis. And people usually use that to convince the patient that they're using the two eyes together to some extent and make themselves feel better after they've done surgery. Not that it really provides useful functional information for the patient. The bagelini lenses, Bruno Bagelini, was an Italian ophthalmologist who has these striated glasses that are mounted in a glasses frame and angles. It's the same thing as doing double-mattox rods. But you can see through it. So the patient isn't totally dissociated. And his idea with this, and this all has to do with this crossed, untrossed, oplopia suppression and things of that sort to figure those pictures out. We're gonna look at those. After image testing, with bagelini lenses, we're looking at a light source. That's what the little dot is in all those pictures. And you're doing it with both eyes open. After image testing, different scenario, what you're doing there is you're asking the patient to look a little target that isn't brightly lit while there's a light bulb that sticks out either way, either vertically or horizontally. You present it vertically to one eye. You present it horizontally to the other eye. If you have reasonably good vision and the patient has a fovea, the fovea will be looking at the target. So what you wanna think of the after image test is doing is tagging each eye. You're tagging the fovea and then you're asking the patient, where do you think your fovea is? Based on what's going on with your eyes. Whereas again, bagelini lenses, you've got both eyes open and it's done under binocular circumstances where with after image testing, I would stare at the thing for 30 seconds with my right eye. Then I would stare at it this way with my left eye for 30 seconds and then they say, what do you see? And that's why the after image and that horrible thing that you get after somebody flashes a flash bulb or a camera flash right in your face, that's what you see. And have I ever done that to a patient in the office? No, my attention span is not long enough to do that test. Now, we're at four dot, we've talked about a bit and this is Ilda Kapo who is a pediatric ophthalmologist in Miami when she was just a bit younger and showing the red green glasses and these are the targets. So this is what they're looking at and you've got two green, one red and this light can either be seen as green, red or pink or kind of off green. Different people do different things but if they see some combination of four dots chances are they're binocular and they're normal. If on the other hand they see just green dots it means they're suppressing the right eye. If they see just red dots they're suppressing the left eye. If they see more than four dots and you see some combination of the three and the two like five dots, you're to pulpic and if they see six or more either they need a refraction or they're crazy. Now the bagelini lenses talked about and these are the pictures and this again comes back to this issue simply and these are the pictures they show you and they'll show you a patient with esotropia or exotropia and the question here comes down to whether this is only really useful in the patient who's got normal retinal correspondence and then you've made the eyes misaligned and you're saying what happens and this comes back to this crossed and uncrossed apulopia so that this is the dot of light and this is what you need to think about where the dot is and with esotropia we said they have uncrossed apulopia the image from the right is gonna go to the right it has it's moved over to the right that's where this picture comes from whereas with exotropia you've got crossed apulopia the image from the right eye is gonna move over to the left side which it has here. I when I was a resident tried to figure this out in some terms related to whether these lines crossed above or below and it makes absolutely no sense don't do that I never could make sense of it until I just dod not immediate what they're doing these are just if you're looking at the trans illuminator light tip whether the light looks like it's gone this way or that way and the rest of it follows this and the other issues here if you've got a very small suppressed scatoma the eye that has that you'll see a small gap in the line most patients can't appreciate it and if they've got a huge like dense amblyopia chances are they're not gonna see the line at all so that I don't really find this to be a useful thing in the clinic what you will see in my clinic is using the bagelini lenses to do a real world measurement of torsion I think they're elegant for that where you make the lines horizontal and then have the patient adjust things so things look level and that again because it doesn't dissociate I find more useful in planning surgery than using the double Maddox rods but you need to realize that that is not a universal concept and there's not general agreement about that even in our division after image testing and again with this the issue comes down with these pictures when you look at this and this is the opposite with the patient who is ET where we're stimulating nasal retina thinking it's the fovea you wind up with cross-topopia for the same reason you had cross non-cross-topopia and the patient's isotropic because what you're doing is you're asking where you're labeling the real fovea assuming they've got good vision and then you're asking where does the eye think that fovea is and the idea with this patient who's got, if you've got normal retinal correspondence the other question they'll show with this is they'll take a patient who's got 100 diopters of ET and 50 diopters of hyper and 20 diopters of encyclopedia rotation and they'll say the patient has normal retinal correspondence what does the after image test look like and what the after image test is gonna look like is it's gonna look like this because the fovea is corresponding to the fovea in the other eye the patient is diplopic when the eyes are open realized we're labeling each eye on its own and then asking the patient where you think it is and so that's a trick question and that does show up if they've got normal retinal correspondence this is what you're gonna see and it doesn't matter whether they're misaligned or not and now if you've got isotropia this patient who is isotropic what happens is that I'm labeling the fovea but now because my eye is turned in and there's something in the nasal retina that thinks it's the fovea when I'm binocular the idea is that the fovea is behaving as if it is part of my temporal retina and we stimulate temporal retina most commonly when we're isotropic that's the way I sort these things out and so when we're isotropic we have crossed the plopia and hence we see the image from the right eye over here on the left side or crossed the plopia and it's just the opposite sit down and think through that that is the way to make sense of this it's what's going on it's a matter of when I stimulate labeled fovea looking at just one eye and then I let the patient be binocular if my eyes work together normally this is what's gonna happen even if they're misaligned but if we've got anomalous retinal correspondence when you're monocular you're still gonna label a fovea but then with your brain sorting it out because the anomalous retinal correspondence it's gonna look as if it is part of wherever it thinks the fovea is and it's weird and again, does this help us in clinic? No, it really doesn't Now, Titmus test, brand dot test so the Titmus wash from monocular clues brand dot test because there aren't monocular clues most of the time is probably more accurate but there's some people's brains who just will not do it that turn out to have pretty good stereopsis and this is the Titmus test the idea to go back to this with this monocular clues the idea is if you look at that book with one eye without the glasses on I can get six of those things right just asking the question, which is different not does it stick up? If you wanna find out if they're doing that what you do is with the glasses on turn the book upside down the things that stuck up should look like they go in and if they don't there's something not right and suspect it where I picked this up is when I have my staff tell me a patient has eight out of nine circles or seven out of nine circles and a patient who's got 50 diopters of constanisotropia and I know the patient doesn't have good stereopsis and then you say how did this result happen? In the idea, I'll just grab the book put the glasses on them and say does that stick up? They say no, does it stick down? No, but I can tell you that one's different and it's a useful thing to think about now, let's ramble through this the amblyoscope you don't need to know about it makes a great boat anchor we have one around somewhere in a storage room I think Kathleen DeGree had it for a while and played with it in Neuroclinic but I don't use it now amblyopia just to kind of you know there'll be questions about this it is important to know about as well this is the incidence these are the different entities in the way I kind of think about as far as Strobismic and Isomatropic Amatropic meaning both eyes out of focus deprivation, there's something preventing vision like a scar lid down with a hemangioma and basically we eliminate the causes create equal clear images do occlusion or penalization occlusion, patching and one of the things they may ask you about you can do up to about a week of full-time occlusion per year of age without having to recheck a child or you're gonna cause occlusion, amblyopia that does show up so that if they were to say well you're gonna see this two month old you're gonna patch them full-time which nobody does anymore but it'll still show up on here and see them back in six months that would be a bad thing to do I would not recommend it now, Strobismus different types of deviations I think we're all on board with that Angle Kappa is one of the things that often shows up with a question about Angle Kappa the way to remember this is that in rep not prematurity we see positive Angle Kappa the question is does it look like they're XT and which one is which in ROP where usually the fovea is dragged temperately causing the eye to look like it's turned out even though it's lined up that's positive Angle Kappa and if you remember that you can figure out the Angle Kappa question and I mean it is fascinating I have a parcel of kids I follow who when you do cover testing they are clearly esotropic all post-premies with bad ROP but when you look at them they look like they're 40 diapters XT and so then you have a conversation with the parents and you say I could make your child look really funny and our eyes would work together better because then what you're gonna do to fix the esotropy is make her look more XT and very few patients will take you up on that and I don't think I would either as a parent that'd be bad oh let's back up here for a second and so the other we're gonna touch on this three step test in just a bit and keep rambling here now as far as esotropia infantile, accommodative ET, parietic and then there are the really cool things like Dwayne syndrome, spasm near divergence paralysis deprivation, dissociated horizontal deviation remember there are three parts of the dissociated stir business complex vertical, x-cycle rotation and an outturning all of which are a function of early abnormal binocularity that's the only place you develop any of that dissociated stir business so when you see DVD that means you had misaligned eyes early in life exotropia, intermittent far and away the most common thing and there is a huge disparity in terms of geographic and racial distribution of stir business in Asia nine out of 10 patients I see with stir business are exo it is rare to see esotropia in Sir by Indonesia or in Kathmandu, Nepal on the other hand, here accommodative estropia is the norm we see accommodative estrokes coming out of our ears when I was in Indiana we saw infantile esotropia many more times and we saw accommodative ET why they did is I'm not sure but it probably says something about Hoosiers sensory deviations that I put up there basically a sensory deviation means that there is something wrong with vision in the eye and the crossing developed secondary to not seeing well turns out that early in infancy most eyes will turn in whereas if I developed optic neuritis and lost vision in my right eye over time my right eye would probably turn out and it has to do with relative accommodative and convergent tone at different points in life now what was on that slide okay, vertical deviations we touched on DVD thyroid disease is the answer most common acquired vertical deplopia in adults actually most common acquired deplopia in adults it would still be thyroid disease oblique dysfunction superior bleak palsy being far and away the most common and separating this issue of congenital and acquired is really important because of the various CNS lesions that can go along with that and then we'll touch on A and B patterns a bit although we just talked about that the other day in grand rounds so I'm not gonna belabor it now show and tell and we'll flip through these so what's going on here esotropia, right? right, esotropia exotropia what's going on here so how many different things do you see wrong with that patient? yeah, at least three the eyes turned out it's down there's a little bit of ptosis and there's some anisocorrhea so this kid's got a third nerve palsy and a brain tumor okay, and that's the reason we worry about these things and whether things are congenital whether they're acquired and in terms of pattern recognition in picking out cranial nerve palsies every time you see a patient with strabismus although we kind of get complacent we see them in Pete's clinic and most kids we see have a combative esotropia when I get a call from a pediatrician saying, little Susie's eyes are suddenly crossed usually it's just that they've got a comedy DVT and parents noticed it but the reason we have them come up and we see them today is because we do see kids who they've got a posterior fossa tumor that got increased intracranial pressure and bilateral six nerve palsy, swollen nerves and they need to see the neurosurgeons in the oncologist right away and separating those the only way I've found to do that is to take a look at them and do it urgently now this is an intermittent deviation where when we've taken this patient who has straight eyes we've covered this eye this eye is remaining crossed so this isn't just aphoria aphoria as soon as you take the cover away things are going to go back to normal they're going to maintain fusion this is an intermittent deviation this patient is very interesting and this is the same child photos taken years apart and when you look it sure looks like that left eye could be isotropic as it turns out the eyes are perfectly straight here they are still perfectly straight here and that is pseudoisotropia with resolution of the appearance because you no longer get the sense in that bottom photo that the eyes are crossed angle kappa we touched on this red lens test is done by people at Walmart everywhere and not by many other folks I'm not a fan I think that as ophthalmologist we should be able to sort things out a little more accurately this is I'm trolling for some misalignment and you should be able to look at the patient do cover testing and do it in more elegant fashion or I'll be disappointed in you so the idea is you have them looking at a white light source with the Maddox rod they're going to see a line through it if the light source and the Maddox rod line up there's a good chance that their eyes are lined up that's what you're trying to answer and this has red-green goggles the idea is the question is where does the patient think things are compared to what the examiner is showing them I do have a set of these goggles Judith Warner has them somewhere I haven't seen them in about 15 years and I'm not sure that she still has them but they are She's been on the ramp for a while trying to find them Yes and that's usually when I've asked her if anyone has seen my Lancaster red-green ones because she knows she has them obviously I don't use them very much and we talked about this this is the after image tester so you look at this thing and then this light shows through this and I have one somewhere in my office I think Nero had that for a while that I did get them to give back and bring it out once in a while for show and tell but the bulb doesn't work anymore so it's not nearly as exciting this is a vascular lesion ambliopia would be the big culprit and if you wanted to treat this kid systemically with something what would be the treatment of choice for pranolone, right? Now, and you'd worry about what do you want to make sure the patient doesn't have so you don't kill them? Faces, that's right and that may show up on here as well P-H-A-C-E-S for those that aren't familiar with that and that's why we admit children at the hospital to start beta blocker treatment it turns out that it was observed in kids who were on beta blockers who had vascular lesions that the vascular lesions regressed that's where that came from it was a fortuitous observation the same way that a child who was getting steroids people noticed, you know that's where the idea of injecting steroids interlesionally or using systemic steroids was a fortuitous observation as well in any event causing the lesion to regress so that it isn't blocking vision pushing on the eye causing anisomatropia or causing misalignment of the eyes all of which can cause amblyopia in this patient, what have we got here? patient has crossed eyes this is esotropia, right, right esotropia left eye is looking at you the eyes look straighter with these hyperopic spectacles, diagnosis accommodated VT now this patient who is straight at distance but through the top of the glasses has massive esotropia through these bifocals looks much straighter what have we got? Well, you've got a accommodative esotropia with a high ACA ratio meaning accommodative conversions to accommodation what that means is that per unit of focusing I get more crossing and so those are folks the only way you can sort that out is with them in their full cyclopage refraction knowing they're straight at distance and they're crossing it near the idea of looking at them in the office saying well it looks to me like they're 30 ET at distance and they're 40 ET at near I'm gonna put them in bifocals don't go there put them in their full cyclopage refraction with this idea of a high ACA ratio the appropriate treatment for that is to put them in the bifocals and then try to wean them over a number of years now this patient basically what we're seeing here is just alternating fixation in a child who's got infantile esotropia this child, this is this eye this eye is crossed all the time somebody told him it would go away as a child grew and didn't they came to see you what is this? What part of the eye is that? That's the optic nerve is it normal? No, it's an optic nerve colobone that's a morning glory type optic nerve colobone it doesn't have a lot of pigment on it but it is resulted in non-recoverable very poor vision in this eye you can try to make it better try patching them it probably won't work and at some point when they start getting picked on at school you want to straighten that eye out and make it look straight what's the other really important intervention for this patient? Safety glasses and you want to put them in safety glasses because the idea is protecting that other eye from injury is important now this patient is a unilateral AFAKE this is the most asymmetric Brookner test you're ever going to see she has sensory esotropia associated with amblyopia associated with her monocular AFAKE we'll straighten that eye out but it is not going to make her binocular this again is what part of this is the optic nerve this is where you should see the nerve and it turns out that this is really the nerve right here and not all of that is nerve what is this? Optic nerve hypoplasia congenital cataract can cause this is a really pretty one and now this child this is another reason that we see kids urgently with new onset strabismus that's been noticed and when you look here you notice blood vessels here right and this mass that's retinoblastoma it's a large retinoblastoma and so again something to be aware of and this patient what we're looking at here is primary and secondary deviation it turns out that she has a right third nerve palsy and there's some imbalance between up and down which is why the eye is going up not down which is what you might typically expect when she fixes with her normal left eye she's got a fairly large exotropia but look what happens when she fixes with the parietic right eye the left eye is right out of the picture so this is the primary deviation this is the secondary deviation secondary deviation is when you fix with the parietic eye you'll probably see something about that infantile ET again this is my daughter she's now a nurse over at primary this was taken a few years ago and this is with her glasses she has a combative ET and her eyes are straight she's got normal vision of binocularity it does work and again infantile esotropia just to show you that not everybody with wide intercanthal distance and epicanthal folds has pseudo-esotropia people can have lice and fleas and this child clearly has issues now what are we looking at here what do you see in this picture after we take the cover away what's going on with that right eye it's up okay this is dissociated vertical deviation and it's at least part of the time manifest it is right now and so likely that this child the next question is how old were you when you had your first eye muscle operation did you have misaligned eyes as a child you'll occasionally see this where there isn't any history of that but that's rare now this patient again what we're looking at here is under the cover right now the left eye is covered it's looking at the ceiling the right eye is covered it's looking at the ceiling when he looks right at you his eyes are straight this is latent dvd and this child again just looking at this picture when you look here you should wonder does that child have a fourth nerve palsy and remember the way that with fourth nerve palsy right left right left right left meaning with right fourth nerve palsy you've got a right hypertrophy that is worse than left gaze and on right head tilt and so this child is a left head tilt as he looks at you because he's trying to fix his right hyper that he has when he tips his head to the right which eye has the peretic fourth nerve right right okay very good and then this guy tips his head to the right drops his chin down a bit which is his peretic fourth nerve left and what this shows is the x-cycle rotation of the fundus that you will often see particularly in patients who have congenital fourth nerve palsy magnified you that this you should be able to draw a line from center of optic nerve that phobia should be here and it has shifted this far in patients who are a phasic I've actually used that to do a heredito procedure we try to affect just torsion and adjusted that in the operating I'm looking with the indirect ophthalmoscope to try to level things out to get rid of torsional diplopia and a guy who could tell me that things were tilted but he couldn't express how much they were you know with bagel any lenses to measure things so I just looked at him in the operating room and he was actually quite happy afterwards so you can use this at times for patients benefit and now this patient what is this this patient is straight when he looks straight ahead looks up and right he looks good when he looks up and left this right eye doesn't go up two things that could be causing this one restrictive one not lack of elevation in adduction brown syndrome that's the number one diagnosis but until you know it's tight what else should be lifting the eye in adduction which muscle okay so if you had a right in fearably heresis could cause a similar picture and until you know that's tight you take a hold of the eye and move it you can't separate the two worth remembering and that might be something that would show up now this patient this left eye doesn't go up when he looks up and right it doesn't go up when he looks straight up and it doesn't go up much at all when he you know it still goes up a little bit but not much when he looks up and left so what is this condition in contrast to brown delval elevator palsy also known as monocular elevation deficiency with current terminology now this patient this kid when he looks straight ahead he's got small angle leftisotropia with a little bit of a face turn he actually fuses when this left eye is adducted notice the height of the palpable fissure and when he tries to look to his left look at how wide that fissure is open what's he got which eye which eye is the abnormal eye which one has the narrowing in the widening fissure left that's the one that's got the joints it's got co-contraction what's going on there is that when he tries to look to his right both his medial and lateral contract that's the co-contraction pulls the eye posteriorly tell people fissures look like the narrow when he tries to go to his left the medial relaxes and lets the eye come forward the lateral doesn't pull that's it just passively pushes the lids open as the eye comes forward and notice you'll see parents at least you know six or seven out of ten kids with dwayne's type one in the left eye will show up with a parent telling you that the right eye is crossing that is almost always the case and this is why i had uh... kid i saw who was in his late teens when i was a fellow who was the only child mom and dad sat in the same place at the dinner table all a child's life mom kept saying his eyes crossed dad kept saying no it's not dad was a physician so he won the argument supposedly then they had him looked at when he was about eighteen and i said well you're both kind of right it turns out that mom looked from this perspective she sat on the kid's right dad looked, i mean whether dad looked over here mom sat over here every time the kid looked at mom things look really funky so did they ever think of switching places at the dinner table? not the best and then there's this patient here and what we're looking at here again is that this patient has small-angle esotropia when he is fixing with this right eye when he fixes with the left eye he has large-angle esotropia and this is acquired it's not dwayne's syndrome, what does he got? if you looked at his ductions and versions and you'd have to add, you know, I want to see his ductions and versions this left eye does not abduct and this started suddenly uh... after a head bump he's got six nerve paul's, this is a six nerve paul's and then dwayne's, basically again dwayne's, this right eye is not going out it is not in primary position things look pretty good and we look to the left it doesn't go in so in type three dwayne's there's no abduction and abduction, I didn't have another picture, I apologize for taking one out of the book but I wanted to show one and what does this wide-eyed stare thyroid disease, absolutely as does this now this kid there's a whole series of people in his family all of whom lift their head like this, they look down the end of their nose, they have ptosis, their eyes don't go up what do they got? not CPOE, they've got fibrosis syndrome they've got congenital fibrosis, the extractinomuscle, CPOE what you're going to see there, kind of a variant of what you see with current seer kids where you wind up with a mitochondrial myopathy whereas these kids it is an abnormality in genesis of the muscles including the levator so they all kind of look like the folks from deliverance, you know on the porch and they line up for a family photo and you get a family picture and they've all got their chin up and they've got various I've had some sort of surgery to fix things you can't make this kid normal what you can do is you can try to give him with eye muscle surgery and lid surgery a more normal appearance so he isn't tortured at school and I think it's our obligation to do that, I'm not making fun of him but it is funny when you look at the family photo and grandma will be there and she'll say, well what's wrong? He looks just like Uncle Henry I don't want to fix this and this patient who intermittently has this really droopy-eyed appearance and then sometimes has a bright bushy-eyed appearance and sometimes comes in and the eyes are turned in and sometimes are turned out what have we got? Myostena, absolutely the same with this guy I saw a patient again when I was a fellow Debbie Alcorn who's now my counterpart at Stanford that Dr. Table will get to work with Debbie called me and she said, boy you must have had a bad day you looked at this kid and said the kid had left-sided ptosis and fifty diacres of XT I'm seeing him today the kid has right-sided ptosis and he's fifty diacres ET and it turned up, yes he had myostena we were both right now this child here we've got this very, this kid doesn't smile he's got a furrowed tongue and notice the eyes, he's got small-angle esotropia and his eyes do not move from side to side at all what's he got? maybe a sequence and in this this is a bilateral lateral gaze ptosis it is not bilateral just six nerve palsies if it was bilateral six nerve palsy the kid could adduct normally and their eyes just don't move normally at all horizontally and you can try to make them straight by doing eye muscle surgery but they will you cannot make them binocular it's a kind of a sad disorder now what's going on with this patient patient hears this as basically right gaze primary position and left gaze patient had optic neuritis ten years ago they've got a funny-looking MRI scan it's an I-N-O and where what part of the brain stem is the lesion that caused this MLF, that's right on the right, so that is something that is worth, now A and B patterns again just this would be what kind of pattern? A and good and these are similar, this is basically an A pattern where if you see this we've got this sort of configuration which is where that description came from and this patient in contrast has this sort of configuration the pattern and this is a patient who has a large angolietian down gaze exo and up gaze over elevation and adduction and so if we were to fix this we would operate to take care of any misalignment in primary position horizontally and would you shift muscles or would you weaken the offending oblique? work on the obliques okay and those questions do show up what they'll do though usually is they're not going to call for subtle judgments they're going to put in things that are just plain wrong like for esotropia doing medial rectus resection or a suprableectonotomy or something like that so that you know just say is this a reasonable thing to do for this patient not is it absolutely what I would do but is it a reasonable thing to do and that's probably the answer and what they're looking for is just your ability to think through things this is a totally detached retina and you see ciliary processes this patient has stage five end-of-game ROP and again just to review demarcation line, ridge, extra retinal tissue stage three and the stage is a retinal detachment, extra foveal foveal involving and then total detachment and to back up hang on here for just a second zone one the circle whose radius goes from optic nerve twice the distance from there to the fovea your vessels are just inside here this is zone one the area outside that where the radius of the circle goes from optic nerve to nasal or a serata that zone two and what's left is zone three that you need to remember there often is some sort of question about that these are arbitrary things that when this was arrived at in a hotel room in Calgary, Alberta people thought that most people could look at and fairly reliably say where these things are there isn't a landmark in the eye but you can see the optic nerve, you can see the fovea and you can see the nasal or a serata which is why when you do exams with me I pick on everybody so much about finding the nasal or a serata because until you can find the nasal or a you can't really play the ROP game and figure out what's going on with an individual patient and I'm going to stop there for a second because I do want to go through one patient example just to hit something because there often also is a three-step test question on here that isn't a fourth neuro palsy and how do we go through thinking about that so I'm gonna hit this close this and I'm going to go back here and go to this and then I want to come down to so when the cause is not super oblique palsy where are we this patient if you go through what we said about right left right left right left left hypertrophy but this left hypertrophy is clearly worse in left gaze not right gaze and it is worse on left head tilt so how do we sort through this what I do and what I recommend you do if you've got some scratch paper there is you draw yourself a little picture of these and this is looking at right eye left eye with the superectus infir bleak as the elevators infir rectus superectus depressors and so the first question is going to be with this left hypertrophy which muscles if they were peretic could cause left eye to be up there and what about could the upper ones on the right cause the right eye to be down the left eye to be up so let's look at that and so gosh that's what we did and so let's mark that okay so that's one the first thing that we do then the question is going to be is it worse off to the left and right where what we're going to do is circle some groups of muscles one side it'll either be these two or these two and this was worse off to the left side wasn't it so you want to circle those off to the left let's do that we'll put a line there and so now we've narrowed things down to four to basically two possible contenders haven't we and so the issue here then is it a right inferior oblique peresis or a left inferior rectus peresis then the issue of this head tilt thing and it's worse on head tilt left isn't it you can just say well i've got the head tilt left i'm going to take things to the left here i'm going to draw lines here the thing that also makes sense to me with this when you think about is it worse on left head tilt to right head tilt to say which muscles are doing it and what i do is i tip my head and say if it's worse on left head tilt is it the encyclotortors or x-cyclotortors i'm worried about and on my left eye when i tip my head to the left i have to encyclorotate to keep things level don't i right i has to x-cyclorotate so we know which muscles on my if i now with left head tilt here is worse on left head tilt i've got my encyclotortors and i've got my so on the left eye my encyclotortors are which muscles superior rectus superior bleak so still works we're tipping to the left here and then on my right eye when i tip to the left i've got an x-cyclorotate and you know that both inferior bleak and inferior rectus are the paired x-cyclorotators correct so we're going to make this sort of come on machine don't let me down now there we go and so and then you look for something that you've basically marked that's in blue that has two arrows there and the candidate here is a inferior bleak paracus and this actually doesn't happen that infrequently i operate probably once every couple of months on somebody with an inferior bleak paracus the best course of action is to recess the contralateral superior rectus because it turns out that they're worse in left gaze if you recess that superior rectus that's going to have most of its vertical effect in left gaze and gaze left and up where their eye doesn't go so you're balancing out their deviation so again does that make sense how to work through that think through that and i think that's where i'm going to leave you uh... with i guess it was one of the thing let me just look at this stuff right here because i think i have a let's just go through these for just a second i want to look there is a patient who's got i think i put in here not that patient this is not the sixth... okay so this patient here this is a head tilt so we're in the fourth nerve palsy territory and this is a patient with a patient who's got a right hyper worse in left gaze and probably has increases on right head tilt there's no question he's got a fourth nerve palsy right the question then we got this patient and this is basically patient who's this exam and this does show up one of the thing is to think about in this is a patient when you first look at this you say well g the patients got a right hyper it's worse over here in left gaze it's worse on right head tilt uh... although i didn't say that here uh... but there are a couple of things that should raise a red flag here actually three that i can see one is that we've got isotropy and down gaze two is this flick left hyper in gaze down and right which doesn't make sense with the right fourth nerve palsy and then there's this issue twenty degrees of excite excite low so what's going on here it's bilateral and when they show you a fourth nerve palsy i want you to remember to look ask yourself could this be bilateral if you see a v-pattern if you see more than about twelve thirteen degrees of excite contortion or if you see and they'll show you know large amounts of this and then this flick or or maybe one left hyper in gaze down and right and just to try to trick you bilateral fourth nerve palsy now is this a practical significance you bet it is because in this patient if you don't acknowledge it and either let the parents know that you might have to come back and do something if it's a child or let the patient know if it's an adult or deal with bilateral surgery i mean to give you an example i saw a little girl in serbia when i was in indonesia they want to be an operator she had a very large left head tilt with her right superior blink palsy she also had very dramatic overaction of her left inferior blink and she had esotropian down gaze and she had lots of fun distortion and it turns out she had a bilateral fourth now it turns out that when you operate in fourth nerve palsy if you want to get rid of the head tilt you'll probably have more luck if you do something with the superior blink so i tucked her right superior blink but i also recessed her left inferior blink because otherwise what would come up right after surgery is the parents would see this left eye up here that's going to be accentuated by the browns that i'm going to induce when i tighten the right superior blink so i did that to try to get a better outcome and save my colleagues in serbia from having to try to sort out because otherwise if you don't tell them ahead of time people think you caused the problem with the other eye not that they had a bilateral palsy you know if you tell them how things might not turn out just the way they want they think you're a smart doctor if they wait and they tell you or grandma tells you that you screwed up they don't think you're very smart good luck with this test if there are questions that come up as you're going through this and some things that make sense it's okay to call me and uh... i uh... get out of this and otherwise what questions do you have about any of this any pediatric ophthalmology strabismus related topics uh... uh... that you've been coming across in your study you guys just are you all in the midst of trying to review things and go through stuff it's you know i think it's purposely causing you to review this stuff is in fact a good thing you know i don't look at it is is evil i think when i was in your shoes i thought it was evil i would recommend that you study i tried not studying my second year residency i just said i'm gonna take it see what i know what i found out was that if you're being tested against people who are studying their hardest in reviewing things you're not going to look very good and uh... it wasn't a happy experience discussing that with my department chairman because i was already on the bad list have a great weekend


Hello everybody and welcome to the second video of the Fusion Research lecture. You remember that last time I gave a historical overview about the early time of fusion research and one of the important messages from last time was that pinches to the configurations which were researched at the beginning of fusion research are not suitable for fusion reactors. One solution to overcome the problems with pinches were proposed by those three men shown in the picture here. On the left hand side we have Lyman-Spitzer, one of the fathers of the Hubble Space Telescope program. Then we have Igor Tam and Andrei Sakharov from the Soviet Union. And what they suggested was add a strong axial magnetic field to get a better confinement. So the solution proposed by them was add an additional strong axial magnetic field. The solution by Lyman-Spitzer from the US was using coils only. That is called the Stellarator. There the magnetic field is completely produced by coils. And the other solution suggested and pursued by the Soviet colleagues was the Tokamak. And that is also produced by induction. And the additional strong axial magnetic field results in a twisted magnetic field lines. Now why do we need twisted magnetic field lines? That is an important question. Why do we need twisted field lines? That is a good question. Let's look at the case if we would not have twisted field lines. What would happen to them? Let's try to draw a cross-section. Something like this. This is a cross-section where we have the magnetic field pointing into this direction. We have a magnetic field gradient pointing into this direction. And in the fluid picture, you remember that from Plasma Physics 1 lecture, in the fluid picture we have the diamagnetic drift. The diamagnetic drift which describes the drift motion being caused by a pressure gradient and a magnetic field. And since we have a pressure gradient here, so in that cross-section the Plasma pressure is the highest in the center. And we have a magnetic field direction. And this is divided by the charged particles density and the square of the magnetic field. And from the diamagnetic drift motion, the diamagnetic current follows. Which can be written as minus, again it's the pressure gradient and the cross product of the magnetic field. Divided by the squared of the absolute value of the magnetic field strength. Now, if we draw the magnetic, sorry, the diamagnetic current into the cross-section. And since it depends on the square of the magnetic field, sorry, on the inverse of the square magnetic field, it is larger on the output side. So this is the direction of the current, remember there's a minus in front of the fraction. And so maybe something like this, right? I've tried to draw a thick arrow here, so this is supposed to be the J-diah, the diamagnetic current. And on the other side, it's a bit smaller indicated here by a thinner arrow. So this is also J-diah, so-called diamagnetic current. And this current, which is stronger on the output side than on the inverse side, would now lead to charge separation. Having positive charge on the upper side and negative charges on the bottom side. Meaning, if we come back to the original question, why do we need twisted field lines? If we do not have the twisted field lines, we would get charge separation. Charge separation, which generates an electric field. So I've only drawn here the charges. But of course, you know that this makes an electric field like this. This is an electric field, E. And the electric field and the magnetic field, that results in E cross B drift, as you know. E cross B drift. And you know that this is a charge-independent drift, meaning it pushes the whole plasma to the output side. If you make a cross product of the two quantities, you see that the plasma is pushed to the wall. So pushes plasma to wall. And thus we would have no confinement. So not suitable for a fusion reactor, no confinement. Now obviously, twisted field lines are a solution to that. Twisted field lines are a solution to that. And why is that the case? We come back to our cross-section here and extend that plot a little bit by trying to draw another cross-section here. And then trying to make a plot where these are connected. These are two cross-sections, right? Something like this. And if we... So this is the same cross-section magnetic field now pointing outwards, but we would have the same charge separation here with plus and minus. And now adding twisted field lines. So let me try to draw a field line on the torus here. If it's twisted, it might look for example like this. So this is a magnetic field line here, giving the direction of the magnetic field line at each point. And this field line allows now for the charges to freely move along them and thus to compensate for the charge accumulation. So the twisted field lines are therefore necessary to compensate for the charge accumulation. Since they allow currents to flow along the field lines. Allow currents along the field lines. And these currents have a name and they are called furschlüter currents. And since these are quite important, give them a yellow box. And by the way, I have derived the necessity for twisted field lines here in the fluid picture. But you can do the same in the particle picture. Then you would need the gradient drift and the curvature drift. But the result would be the same. Okay, now we see that we need twisted field lines. And one solution suggested 1951 by Spitzer was the so-called figure 8 accelerator. Named figure 8 for obvious reasons as you see in the picture below. Figure 8 accelerator in Princeton. That was suggested by Lyman-Spitzer. And you can see one thing in the picture which I have included here. That the experiments at that time could be brought to the conferences actually. So they fit on the table, which is really nice thing. An interesting or funny story is how Lyman-Spitzer got interested in fusion research. Was actually by some science face news. Because in 1951 an Austrian physicist working in Argentina claimed a breakthrough in fusion research. And Lyman-Spitzer once said in an interview that his father-in-law called him in his skiing vacations. Pointing him to that news press article about the fusion breakthrough, which was false. And this got Lyman-Spitzer interested in fusion research. And legend says that the shape of his stellarator, which here looks like an 8 and is a bit twisted. Was inspired by the form of a pretzel, which he had when he went skiing. So here the twisted field lines are achieved by twisting the whole torus. Another way to realize the twisted magnetic field lines is instead of twisting the torus. Using twisted helical coils as depicted on this slide. Here are two realizations of that. On the left hand side is the classical stellarator. On the right hand side the torsotron or heliotron. So let's first briefly talk about the classical stellarator. Where you can see that you have helical coils winding around the torus here, right? Some helical coils winding around the torus. And in these coils the current flows in opposite directions. So the classical stellarator we have oppositely directed currents in the helical coils. That requires the use of additional toroid field coils. We will discuss that in the magnetic configuration section. Here in the drawing these are indicated by the blue color. So we need toroid field coils in addition. In the torsotron or heliotron on the other hand, we also have helical coils winding around the torus as you can see here. But now in these helical coils the current flows in the same direction. So it's equally directed currents in helical coils. And as you can see already maybe in the drawing there are additional type of coils in green. These are vertical field coils which we need here. We need vertical field coils. And again we will discuss that in more detail in the magnetic configuration section. Okay, now these are some nice drawings but let's look at a few stellarator realizations. Here we have the model C stellarator. Model C stellarator, a very early device in being an operation in Princeton. Princeton from 1961 until 1969. If you look at the photography you can see here somebody sitting or standing. So to give you an idea of the size the stellarator is located here. And you can also see it is somewhat elongated. So this is approximately the plasma shape I would say. So it's a racetrack configuration with a length of the racetrack of approximately 1.2 meters. And the plasma had radius of something on the order of 6 centimeters. Not only Princeton stellarators were built but also in Garching in Germany near Munich. So here are some first experiments at the IPP Garching at the Institute for Plasma Physics Garching. You can see a few stellarators here on the bottom. This one, this is also a racetrack configuration. This is Wendelstein 1A. Then here we have another one, this is a linear device. Wendelstein 1B. And by the way if you wonder about the name Wendelstein, Wendelstein is a mountain near Garching. And this was inspired by the Americans who named this stellarator program Matterhorn. So here we have another stellarator. Now this is a circular one. This is Wendelstein 4. And again if you look at the photography you see two scientists sending there to give you an idea about the size of the experiment that they were rather small at that days. Another one, a more recent one. This is a picture from last year, a stellarator called TJK. This is a TJK stellarator. And this is located at the University of Stuttgart. So I have included it here because this is where I work. And this is actually to be more precise a torsaton. And it is a low-temperature stellarator which can be operated at the University because you can see here, you can see that it is a low-temperature stellarator because it emits light in the visible range. Fusion-relevant parameters usually mean that you have temperatures too high for light in the visible range, but rather in the X-ray range. Okay, a very important concept in the stellarator research was the development of modular coils, modular coils. In the year you see two drawings. If you first look at the left drawing here you see the helical coils winding around the torus producing the magnetic field that you need. And on the right drawing you see modular coils. And these modular coils produce the same magnetic field as on the left-hand side. Now this has the advantage that in case of any damage the coils can be repaired. So it's repairable in case of damage, repairable in case of damage. And in addition, that is maybe even more important, you have more flexibility in your magnetic field configuration and designing your magnetic field configuration, more flexibility. And we will see that this is an important part in stellarator research when we talk about the stellarator in more detail. So more flexibility in magnetic configuration. And the first realization of a modular stellarator was the W7AS stellarator in 1990. W7AS, you see it in the drawing on the left-hand side. And this was the first stellarator with modular coils. And this is what the A stands for in the name for advanced. And that refers to using modular coils. And it was located at IPP. Okay, as a next important experiment I'd like to list here LHD, the large helical device which was put into operation in 1989 in Japan. The picture on the left-hand side, you can see first that it is a heliotron because the coil binds around the torus only in one direction, current flowing in one direction. You see Japanese scientists standing around and engineers here to give you an idea about the size of the experiment. So it is a very large stellarator. It has a large radius of 3.5 meters, an average plasma radius of 0.6 meters. And if you look on the photography on the right-hand side, you see the experiment hidden underneath in a lot of heating systems there. It has superconducting coils. And this allowed for very long-piles operations for conducting coils. And so this was basically an experiment where you could operate plasma-infusion-relevant parameters in steady state. So that was and is still a very important experiment. The next one in the list for the stellarators is W7X, which is an optimized stellarator. And what optimized means, we'll tell you that later. For now optimized here means that losses are reduced. So in that way optimized. To give you an idea about the size, look at the drawing on the left-hand side. In the center there is a human being standing. So it is really a huge device which has of course also superconducting coils to allow for basically steady state operation. It has a large radius of 5.5 meters and the average plasma radius is 0.53 meters and it also uses modular coils. W7X was put into operation in 2015. So 2015 the first plasma was achieved in W7X. And if you look on the photographies on the left-hand side, here you can see the chancellor, Angela Merkel, pushing the button to start the first plasma. Here you can see the head of the Max Bank Institute, Professor Sibel Günder. That was a big press event and the German fusion program got a lot of positive press there. The other photographies, the first plasma is shown top left, the magnetic field lines top right, the plasma. And as I said, that was a very successful experiment so far. Okay, that's it for a brief historical overview about these accelerators. Let's now briefly talk about the tokamak. Tokamak, oops, tokamak. To start with let's first briefly outline the concept of the tokamak because you might know that already based on induction. So we use the transformer principle and what we now try to do is first draw a transformer where we have some kind of primary winding. So some wire winding here around this iron core, something like that. So this is supposed to be the primary winding of the transformer primary winding. This is the original concept where we use an iron core. Now this is the primary winding here and the plasma now is the secondary winding. So we have here some kind of toroidal shaped plasma which might look like this. And around that there are the toroidal field coils, which we had seen earlier. So a lot of coils here. And if we now ramp up a voltage or a current in the primary winding that induces a current in the secondary winding, which is the plasma, it produces a current thus it produces a magnetic field. Together with a magnetic field from the toroidal field coils we get the twisted magnetic field lines necessary for confinement. Now that is the concept with the iron core. In modern devices often we realize the tokamak without an iron core, and let's quickly try to draw that. So again we have some kind of plasma looking like this. And then now we have not an iron core but an air core and we are using a central solenoid as primary winding. So in the center we have some kind of central solenoid. This is supposed to be a long solenoid as you can, I'm sure, easily imagine, right? So this is now the primary winding. Then we of course also have the coils producing the toroidal field here around it. So if we ramp up a current in the primary winding it induces a current in the plasma together with the current from the toroidal field coils we get our twisted magnetic field lines. Now a slightly improved version of the drawing can be seen here. Again in the center the central solenoid divided into several sections as you can see. To being able to ramp up the current in different parts to get a profile inducing a current in the plasma here and then the blue coils here producing the toroidal field together giving us a twist that we need in the field lines. So the tokamak is based obviously on induction. That has a few consequences. One first consequence is that it is an inherently pulsed device, right? It's a pulsed operation because we can only induce a current in the plasma if we ramp up or down a voltage. Now in addition, which is a very big advantage is that driving a current in the plasma provides also a heating mechanism. That is omic heating. Omic heating however has unfortunately the problem that it is, or the drawback that it is not sufficient to achieve fusion parameters alone. So alone it is unfortunately not efficient, sorry not sufficient for fusion parameters to achieve fusion parameters. Now why is that the case? Because when we increase the temperature on the plasma the resistivity drops and thus the heating efficiency from omic heating drops as well. Okay, a bit of an historical overview and the day to start with is certainly 1949 where a Soviet soldier who had basically no, I think he even had no high school diploma if I'm not wrong, Oleg Lavrientiev and I'm pretty sure I pronounced that wrong, I'm sorry, he sent a letter to Stalin proposing the original tokamak concept. Stalin forwarded that to his chief scientist and they found the idea very appealing, slightly adopted it and realized the first tokamak experiments from that. The Kurchatov Institute was founded in Moscow at that name, it was not named like that but nowadays it's known as Kurchatov Institute where a lot of major breakthroughs in tokamak research were achieved. Among others in 1968 where they achieved the remarkable temperature of 2 kilo-electron volt at the T3 tokamak and when they presented their results at conferences the other scientists from the other countries basically didn't believe them, they did not thought the Soviet scientists did something wrong, it was just much better than their values. So the Soviet scientists invited the scientists from the world to their experiment and actually a team of British scientists came over bringing their own diagnostic installing them at the T3 tokamak and they confirmed these values. So this was a much better performance than the Stellarators at that time. So a much better performance much better performance than Stellarators and this is the reason why many labs around the world then decided to switch from Stellarators to tokamaks. In 1973 at the IAEA conference in Novosibirsk the Intor concept was first discussed and proposed and that was the first concept for an international reactor basically if you wanted to predecessor of ETA. However before we come to working fusion reactors the next important reactor to mention or experiment to mention sorry is certainly JET, the joint European Taurus which was put into operation in 1983 and JET really is a massive device. First of all you see it has an iron core then here you see a human being standing there and this gives you an idea of the size of it. The major radius is 2.96 meters the average plasma radius is 1.25 meters and JET is located in Southern England in Cullham and it is also important because it allowed for DT operation. In this photography you see this is showing the inside of JET and again to give you an idea of the size of scientists standing there on the left hand side working on it. That gives you another good idea about the size of JET. JET allowed for real fusion experiments so it was designed for DT operation, so daterium trisium operation and in that sense it is a real fusion experiment and JET holds the record for the highest amount of fusion power released in an experiment which is on the order of 16 megawatt. The next step is ETA the International Thermal Experimental Reactor. ETA is even larger with a radius of 6.2 meters and a small plasma radius of about 2 meters and ETA is designed for the first time to release more energy via fusion processes than was initially needed to heat up the plasma. You can get an idea about the size of ETA looking at the picture on the drawing sorry on the left hand side where you see here a scientist standing next to a human being and ETA is located in southern France. It is a joint international project China, European Union, India, Japan, Korea, Russia and the US are part of it representing half of the world population designing, constructing and building ETA together. Here is a recent photography of the construction site so taken in February. ETA is scheduled to have its first plasma in 2025, first plasma in 2025 and 2035 the full power DT operation will take place so that will be the date when as I said for the first time more power will be released by fusion than was initially needed to heat up the plasma. That will be a remarkable date in fusion research and as you can see it's not too far away and you are right in the place to contribute and help getting making ETA a successful achievement. That's it for the historical overview about Stellarator and Tokamak and in the next video we will talk about key parameters relevant to describe fusion. See you in the next video.